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1.2 Question 1 As an obstetric SHO, you are presented with a primigravida who is 41 weeks + 2 days pregnant. She has had an uneventful pregnancy but has been admitted to hospital for induction of labour. you for advice. She is unsure how to prepare a feed of formula milk. She asks List four pieces of practical advice you would give her on how to prepare a feed. Any four of the following; •Hands must be washed and absolutely clean before handling the bottles and teats • Suitable bottles and teats must be thoroughly washed and sterilised before use •Water should be boiled before it is used to make a feed •Information on how much water and the number of scoops of formula powder needed for a feed for a baby of various ages can be found on the back of the manufacture’s formula milk container. •Water should be put into the bottle FIRST and accurately measured in the bottle by using the fluid ounces/mls guide at the side of bottle. •The correct number of scoops of formula powder should be put into the bottle AFTER the water has been added •A clean knife should be used to scrape off any excess powder in each scoop to ensure the correct amount of formula powder is in each scoop •The bottle filled with water and formula powder should be GENTLY shaken to ensure adequate mixing •The milk should be allowed to cool and tested on the back of the hand before giving it to the baby •The milk, once prepared can be stored in the fridge for up to 24 hours. •The best way to warm a refrigerated bottle is by placing it in a jug of warm water. Take great care if you heat the feed in a microwave oven because of the risk of hot spot burning. Question 2 A mother presents to the GP clinic and is concerned about when and how to wean her 20 week old baby. a. What is the current recommended age for weaning a baby? 6 months (recommended by department of health) 1 b. List three signs are suggestive that a child is ready for weaning? The baby is hungrier and cries more for food The baby wakes up for a feed more time during the night than previously The baby shows more interest in food The baby starts to make chewing motions with their mouth c. What types of foods can be initially introduced to the baby? List two. Baby Rice cereal mixed in with breast or formula milk (recommended by the department of health as a starter) Pureed fruit (e.g. Banana) Pureed cooked vegetables ( e.g potatoes, carrots broccoli, peas, parsnips) d. List two types of food you would advice the mother to avoid in the first stages of weaning Gluten containing products (if weaned before 6 months) Don't add sugar or salt to any foods Don't feed hot spices in the first 12 months Avoid (until 12 months) raw or soft eggs, patè, soft cheeses such as brie, honey( in rare cases it can lead to infant botulism Avoid peanut butter until 12 months or 3 years if allergies run in the family, Avoid whole nuts until 6 years (due to the dangers of choking). e. The mother asks you ‘What about milk, do I have to discontinue that now?’ What will you reply? Give a reason for your answer. You should reply ‘No’ The reason for this is that babies still rely on milk for most of their energy (calorie) intake. 1.2 Feeding By the end of the course students should be able to: • make and give a feed • give advice to parents about infant feeding and weaning 2 1.5 Question 1 A two-day-old term infant on a postnatal ward has had bilious vomits after every feed since birth. The baby is hungry and feeds well but is yet to pass meconium. Clinical examination reveals a dysmorphic child with a flat occiput, large tongue, low set ears and single palmar crease. A plain abdominal film was taken and showed a double bubble appearance in the stomach. a. What is the ‘double bubble appearance’ indicative of? Duodenal atresia b. What genetic condition does this child have that accounts for his dysmorphic features? Down’s Syndrome c. List three further investigations you would perform and give a reason for each investigation stated Karyotype: To confirm the diagnosis of chromosomal abnormality Upper gastrointestinal (GI) contrast study: There has been no passage of meconium for 48 hours Echocardiogram: Congenital heart disease should be actively looked for in babies with Down’s syndrome d. Give three possible short term or long term complications of this condition that may necessitate intervention. Any three of the following: Congenital heart disease Duodenal atresia Severe learning disability Small stature Recurrent respiratory infections Hearing impairment from acute otitis media Visual impairment from cataracts, squints Increased risk of leukaemia Atlanto-axial subluxation (rare) Hypothyroidsm 3 Alzheimer’s disease e. What information, support or advice can be given to the parents at the time of diagnosis and thereafter? Any one of the following: Written explanation of condition and its cause Information about the short term and long term implications of diagnosis Information about national charities and self help groups e.g Down Syndrome Association Professional counselling to help deal with feelings of guilt, disappointment or anger Antenatal diagnosis for future pregnancies Question 2 Ben aged two months is admitted with tachypnoea following an upper respiratory tract infection. On examination there is a thrill, a loud (grade4/6) pansystolic murmur at the left sternal edge and the liver is palpable 4 cm below the costal margin. a. What is the most likely cause of his clinical condition? Heart failure, probably precipitated by an upper respiratory tract infection b. What is the most likely underlying diagnosis? Ventricular septal defect (VSD) c. A chest x-ray was performed. Name 3 signs on the x-ray that may be indicative of your chosen diagnosis Cardiomegaly, Enlarged pulmonary arteries, Increased pulmonary vascular markings Pulmonary oedema d. What single diagnostic investigation would you perform now? Echocardiography e. Outline 2 important aspects of management that may be considered in this condition and give a reason for performing each intervention 1) Drug therapy – furosemide, thiazide, spironolactone, ACE inhibitors Reason – To treat symptomatic heart failure 2) Surgery Reason: Severe symptoms with failure to thrive OR Reason: Pulmonary hypertension with possible progression to pulmonary vascular 4 disease and subsequent Eisenmenger’s syndrome. 3.) Monitoring and observation (symptoms, signs, CXR, echocardiography) Reason: This is acceptable in asymptomatic patients. By the age of 2 years at least 50% of small and moderate sized VSDs undergo sufficient partial or complete spontaneous closure to make intervention unnecessary. 1.5 Congenital Abnormalities By the end of Phase II , students should be able to: • recognise and explain to parents the principles of management of the commoner congenital abnormalities 5 1.6 1. Nick and Judith have been blessed with a bouncing baby boy, Gavin. What three measurements are plotted on his centile growth chart? Head circumference Weight Height Being distinctly average, he follows the 50th centiles. What would be noted on his chart to constitute mild failure to thrive? Mild failure to thrive is a fall across two centile lines. (Severe failure to thrive is a fall over three centile lines) Name two Organic and two Non-Organic causes of failure to thrive. Organic: Inability to feed Poor retention of food Illness-induced anorexia Impaired nutrient absorption Increased energy requirements Metabolic causes Chromosomal disorders/syndromes Congenital infection Non-Organic: Feeding problems Maternal stress Lack of stimulation and undernutrition Munchausen’s syndrome by proxy Three years later, Gavin’s parents tell you he has reached all his developmental milestones at the correct age. Name three of the five developmental areas that are measured. 6 Gross motor Fine motor Vision Hearing and Speech Social behaviour At what median age are the following milestones achieved? Crawls – 8-9 months Has a mature pincer grip – 10 months Smiles responsively 6 weeks What screening tool is used for testing hearing in infants? The Distraction test At what age would this tool be used? 6-9 months 2. Child X has cerebral palsy. Name two ways in which cerebral palsy might present. Abnormal tone and posturing Feeding difficulties Delayed motor milestones Abnormal gait when walking is achieved Language and social developmental delay The management of Child X’s cerebral palsy will involve a multidisciplinary team approach. Name four members who might be involved. 7 Paediatrician General Practitioner Eric’s Family Physiotherapist Occupational therapist Speech and language therapist Social worker Health visitor Surgeon (e.g. fundoplicaiton for recurrent oesophageal reflux) 1.6 Developmental child health By the end of Phase II , students should be able to: • recognise failure to thrive, its common causes and initiate management • make a developmental assessment of the infant and toddler • recognise delay in speech and in walking • examine a child for hearing loss, including distraction testing • examine a child for reduced visual acuity and squint • outline to parents the facilities available for children with learning difficulties • outline to parents the facilities available for children with mobility difficulties • recognise short stature and refer appropriately • recognise delayed puberty and discuss the causes and investigation with patients and parents 8 1.7 JB is a child who has been diagnosed with cystic fibrosis. This requires daily medication, frequent visits to hospital and several hospital admissions for respiratory illness. When he is 3 he is admitted to hospital for 2 weeks. During this time his parents are unable to visit. 1) What are the stages of the acute separation response in young children? Protest Despair Detachment 2) What factors in family life can have a negative impact on the psychological wellbeing of a child? Give 6 examples. Parental mental illness Inconsistent, unpredictable discipline Divorce Inappropriate expectations/responsibilities for age. Abuse Intrusive overprotection. Bullying. 3) What are the common disorders of psychological development that could present in any child at age <5 yrs, 5-10 years old and as an adolescent? Give 3 examples for each. - Age <5 yrs Meal refusal Sleeeping problems (night terrors, nightmares, waking at night) Breath-holding attacks (Aggressive behaviour, Autism, Tantrums). - 5-10 years old Nocturnal enuresis Hyperactivity School refusal (Anxiety, antisocial behaviour, Tics, Faecal soiling) - Adolescence Anorexia nervosa 9 Chronic fatigue syndrome Deliberate self-harm (Drug misuse, depression) JB starts at nursery, and the nursery nurse expresses concerns that he may have features of an autistic spectrum disorder. 4) What are the three main features of autism? Poor social interaction Lack of imagination Poor communication skills. 5) What other behaviour patterns can be seen in autism? Give 2 examples. Obsessive behaviours Repetitive behaviours When JB is 9 he starts refusing to go to school. 6) What are the two main causes of school refusal? Separation anxiety persisting beyond the toddler years. School phobia – anxiety provoked by an aspect of school. 7) Name 3 professional groups who could be involved when an older child refuses to go to school. Teachers Educational psychologist Educational welfare officer 8) Name 6 behavioural features that might suggest attention deficit disorder. Fidgeting Continually interrupts Instructions never obeyed Blurts out answers Behind with schoolwork Short attention span. 10 9) What are the social and emotional issues that JB might face when he becomes a teenager? Low self esteem Problems gaining independence from parents Rebelling against medication regime. Problems conforming with peer group because of limitations of illness. Depression Anxiety Alcohol and drug misuse 1.7 Child Psychiatry By the end of Phase II , students should be able to: • recognise the common presentations of psychiatric disorder in children and distinguish the common causes • recognise the interaction between child and family upon the psychological disorders of childhood • discuss attachment theory • recognise the common disorders of childhood psychological development • recognise the impact on children of physical/mental illnesses in a parent • recognise the psychological aspects of chronic physical illness in children • discuss school refusal with a child and its parents • recognise the social and emotional issues in adolescents with chronic illness 11 1.10 1) You are a house officer in A+E and you see an 8 month old child who has had vomiting and diarrhoea for 2 days. What signs would you look for to assess hydration? (6 marks) Any 6 of: Sunken fontanelle Prolonged capillary refill time Dry mucous membranes Reduced skin turgor Sunken eyes/tearless Oliguria Tachypnoea Tachycardia Reduced level of consciousness Hypotension How would you clinically assess severity of dehydration in terms of body weight loss? (3 marks) Mild dehydration < 5% Moderate dehydration 5-10% Severe dehydration >10% Name some routes through which rehydration therapy be administered? (2 marks) Oral NG tube Intravenous Intra-osseous Name a micro-organism that commonly causes gastroenteritis in children in developed countries? (1 mark) Any of: 12 Viruses –Rotavirus, Adenovirus, Coronavirus Bacteria – Campylobactor, Shigella, E.Coli, Staphylococcus, Salmonella 2) A 2 year old boy is given the diagnosis of coeliac disease in outpatient clinic. What symptoms and signs would suggest this diagnosis? (6 marks) Any of: Failure to thrive Abnormal stools/diarrhoea – foul smelling, pale, frequent and bulky Vomiting Weight loss Constipation Short stature Abdominal distension Buttock wasting Irritability Delayed motor milestones Glossitis, angular stomatitis Dermatitis Herpetiformis What serological investigations would you consider? (2 marks) Any of: Anti-gliadin antibodies Anti-endomysial antibodies Anti-tissue transglutaminase antibodies Anti-reticulin antibodies What advice would you give to parents about the long term management and implications of coeliac disease? (2 marks) 13 Any of: Removal of all products containing wheat, rye and barley from the diet for life Referral to a dietician Possibility of a gluten challenge later in childhood to reassess the susceptibility of the jejunum to damage by gluten Life long follow-up Increased risk of complications in later life Extended questions: What other diseases are patients with coeliac disease more prone to in later life? (1 mark) Any of: Small bowel malignancy Enteropathy associated T cell lymphoma Increased risk of other autoimmune disorders – thyroid, adrenal, pancreas, SLE, RA Osteoporosis Ulcerative jejunoileitis The gold standard investigation for diagnosis of coeliac disease is jejunal biopsy. What histological features would you expect to see in the jejunum of a patient with coeliac disease? (2 marks) Any of: Lymphocyte infiltration Subtotal villous atrophy Crypt atrophy Increased intra-epithelial cells 3) A 4 year old child presents with constipation. What are the symptoms which would suggest a diagnosis of constipation? (2 marks) Any of: Child passes <1 motion every 3 days 14 Passage of stools that are hard, small or pellet like Stools that are difficult or painful to pass What lifestyle changes would you suggest to parents to help manage the constipation? (2 marks) Any of: Increase fluid intake Diet high in fibre, fruit and vegetables Regular toileting What is encopresis, and how can affect a child and their family? (3 marks) Encopresis is the passage of stools in unacceptable places in a child over the age of 4 years old. Any sort of bio-psycho-social answer eg. Increased washing of clothes, teasing/bullying at school, increased risk of abuse, Name two different types of laxatives available and give an example of each? (4 marks) Any of: Bulk forming laxatives – Ispaghula Husk (Fybogel, Fibrelief) Stimulant laxatives – Senna (or Bisacodyl, Dantron, Sodium Picosulfate, Glycerol) Faecal softeners – Liquid paraffin (or arachis oil) Osmotic laxatives – Lactulose (or macrogols, magnesium salts, phosphates, sodium citrate) Bowel cleansing preparations – Picolax (or Klean-prep, Citramag) Extended question: Name some organic causes of constipation (2 marks) Any of Hypothyroidism Hypercalcaemia Hirschprungs disease 15 Urinary concentrating defect Anorectal stenotic lesions Anal Fissures Spinal/Neuromuscular disease 1.10 Gastrointestinal Disease By the end of Phase II , students should be able to: • recognise the common causes of feeding difficulty and initiate management • discuss feeding difficulties with parents • recognise dehydration and the associated biochemical changes • recognise the common causes of vomiting in infancy, childhood and adolescence and initiate management • recognise the common causes of acute and chronic diarrhoea in infancy, childhood and adolescence and initiate management • recognise the common causes of constipation in infancy, childhood and adolescence and initiate management • give advice to parents on gastroenteritis • recognise and assess obesity • make an initial assessment of a child with acute abdominal pain and refer appropriately • recognise the common causes of chronic abdominal pain • recognise the common causes of an abdominal mass in infancy, childhood and adolescence 16 1.11 A 4 year old Asian boy presents with a history of swelling around his eyes, most noticeable in the morning for the preceding 5 days. His parents have noted that his urine appears frothy and is reduced in volume. Q1. What is the most likely diagnosis? Nephrotic syndrome Q2. Apart from peri-oribital and ankle swelling what other areas would you look for swelling particularly if this was a severe case? Swelling of scrotum On examination there is dullness to percussion and reduced breath sounds at the right base. Q3. What are these clinical findings suggestive of and why has it happened? Pleural effusion which is secondary to hypoalbunimaemia Q4. What initial investigations would be implemented to confirm this diagnosis? Urine dipstick U+ E albumin levels microscopy and culture Q5. What is the treatment for this patient and how long should the patient be treated for? 17 Oral steroids – prednisolone 60mg/m2/day for a period of 10days Q6. What are the side-effects of these drugs in children? Name 2. Growth stunting and immunosuppresion Q7. What are the serious complications which may occur with this condition? (2) Hypovolaemia (intravascular compartment becomes depleted) Thrombosis ( hypercoaguable state due to urinary loss of antithrombin and increased blood viscocity from raised haematocrit predisposes to thrombosis). Q8. What prophylaxis should be given in the acute phase of this condition and why? Pencillin prophylaxis is given in acute phase to prevent pneumococcus infection due to urinary loss of immunoglobulins increasing susceptibility to infection 1.11 Renal/urinary By the end of Phase II , students should be able to: • recognise oedema in infancy, childhood and adolescence, discuss its causes and management with parents • recognise a history of haematuria, and initiate investigations • recognise polyuria and initiate investigations • identify the commoner causes of bedwetting and give advice to parents • fit a urine bag, obtain a specimen for testing • explain the need for suprapubic aspiration to parents • recognise and interpret the urine abnormalities in urinary infections 18 1.12 Qu. 1. Lucy is a 2 year old girl who presents to A & E. The parents are very worried, they say that Lucy has been ill with a temperature for a few days and this morning just after breakfast she had a ‘fit’ which lasted about quarter of an hour. a) List three causes of Lucy’s fit in your differential diagnosis: Febrile convulsion Meningitis with a febrile convulsion. Infantile spasm (3-12 months of age). b) To help you distinguish which of your differentials is most likely list 6 things you would specifically want to rule out on examination? Photosensitivity, Neck stiffness. Fever, Purpuric rash, Signs of shock Positive Brudzinski’s/Kernig signs c) Your SHO performs a lumbar puncture on Lucy. What changes would you expect in the CSF for both bacterial and viral meningitis? 1) Bacterial: Turbid CSF, increased (!!) polymorphs, increased proteins, increased (!!) glucose. 2) Viral: Clear CSF, Lymphocytes increased, Normal or increased (!) protein, normal or increased (!) glucose. d) What are the main causative agents of meningitis? 1 month-6 years: Neisseria meningitides Streptococcus pneumoniae. Haemophilus influenzae e) What is the immediate management for meningitis? Step 1 is done for you. 19 1) ABC Start antibiotics - Third generation Cephalosporin (Cefotaxime) plus either Rifampicin or Vancomycin whilst waiting for CSF culture results.. CSF lumbar puncture (ideally CT first ) Check antibiotic regime against CSF results and change if necessary. Establish if there are any contacts. Reassess f) List 4 complications of meningitis: Hearing loss. Local vasculitis - cranial nerve pathology. Local cerebral infarction.- epilepsy. Hydrocephalus. Other: Cerebral abcess and Subdural effusion. Extended: What antibiotic would you give to anyone Lucy may have had contact with who is at risk? Rifampicin. Qu.2. Dave is a 15 year old boy who presents to his GP with his mum. Whilst shopping his mum witnessed Dave having a ‘fit’. She explains that he suddenly dropped to the floor and at first was still but then started to shake. When he came round he was sleepy and spent the rest of the day in bed. His mum is very worried. a) What extra information would be useful to know? Was he incontinent? Has it happened before? Did he have any preceding aura or warning sign. Is he on any medication? Does he use recreational drugs? Does he drink alcohol? b) Name 5 different types of generalised epilepsies. Absence seizures. 20 Myoclonic seizures. Tonic seizures. Tonic-clonic seizures. Atonic seizures. c) Dave admits that this is his fourth fit. His friends had seen two of the previous three fits and had described the same fit in the same way as his mum. What investigations are required? Blood tests checking electrolytes. Serum glucose. EEG. CT or MRI. d) Name three anticonvulsant drugs that you could prescribe for generalised tonic-clonic seizures? Sodium valporate. Carbamazepine. Lamotrigine. e) Dave explains that once has finished school he wants to join the army. Mention 5 things you would want to cover with Dave and his mum? Provide written information (Leaflets) on epilepsy. Give details of support groups. 3) Educate both Dave and his mum about the recovery position and how rectal diazepam is useful and how it should be administered. 4) Explain that there are driving restrictions imposed by the DVLA regarding how long he must be free of fits before he is allowed to drive. He should look these up when he wants to learn to drive. He will need to contact the army to see if he will be eligible to join. 1.12 Central Nervous System By the end of Phase II , students should be able to: • take a history of febrile fits • take a history of epilepsy in infancy, childhood and adolescence 21 • outline to parents the nature and treatment of febrile fits and epilepsy • examine a floppy baby and discuss the nature of the problem with parents • recognise the possibility of meningitis and initiate management • recognise and interpret the CSF abnormalities of meningitis • recognise the common causes of abnormalities in gait in infancy, childhood and adolescence 22 1.13 A 7 year old boy presents to A&E with after concerns from school about the extent of continuous bruising on the buttocks and legs. Q1. What would concern you about this pattern of bruising illustrated in Figure 1? Unexplained injuries to protected parts of the body such as the buttock may indicate the presence of non-accidental injury. The presence of bruises that have various ages may signify multiple episodes of injury caused by ongoing physical abuse Q2.What other areas of the body if bruised would raise your suspicions of a diagnosis of bruising caused by non-accidental injury? Thighs, torso, frenulum, ears and neck Q3. How can you make a rough estimate the age of the bruising in this picture? By the colour of the bruise. The picture shows yellow/brown colour indicating that these bruises are older than a day. A bruise of within a day will be erythematous Q4. What is the difficulty with determining the bruise age by colour? 23 Determining the bruise's age by its color must take into account the individual patient's skin tone, the bruise's location (whether overlying soft tissue or bone), the patient's relative nutritional state or other indeterminate factors. Q5. What investigation may be indicated in the presence of suspicious bruising? Platelet count and coagulation screen to exclude thrombocytopaenia and other bleeding diatheses which often presents with multiple and excessive bruising. Q6. How would you proceed with this case and whom should you inform? If child abuse is suspected in the UK the Social Services Child Family department must be informed. A decision must be made whether the child requires immediate protection either hospital admission or placement in foster home. In most cases further management will involve evaluation of the family by social workers and Child Protection Conference. Q7. Who should be present at the Child Protection Conference? Paediatrician, GP, health visitor, social worker, police, nursing staff, representatives from school and parents. 1.13 Haematology By the end of Phase II , students should be able to: • assess anaemia in infancy and childhood • assess a child with bruising 24 1.14 SW is a 5-year-old male who presented to A&E with severe vomiting, abdominal pain, and drowsiness. This had lasted for approximately 4 hours and was preceded by 1 week history of flu like illness. On examination he had signs of weight loss and dehydration. A) What would be your main differential in SW? Give two other examples of differential diagnoses. Diabetic Ketoacidosis Gastroenteritis Appendicitis B) After initial ABC management, give three other management steps. Rehydration with fluids (normal saline over 48-72hrs) Insulin administration (sliding scale starting at 0.1units/kg/hr) Potassium infusion. (metabolic acidosis should correct itself following fluid administration). C) SW was newly diagnosed with insulin dependent diabetes mellitus following this incident. Give an example of how you would explain to his parents what this condition is and how it needs to be managed. “Your son has been diagnosed with diabetes which means that he is not producing insulin within his pancreas, which we all need to regulate our blood sugar. This is due to an autoimmune process, where there is destruction of the islet cells within the pancreas which produce the insulin. Unfortunately he will need to be put on insulin, and will need daily injections throughout his life. If his condition is managed effectively then he will almost certainly lead a normal life.” D) SW is responding well to treatment, give two regular investigations that his parents 25 could perform at home to monitor his diabetes. Blood glucose. Urine dipsticks (to check for protein and ketones). E) List 3 key members of the diabetes team which will be essential in providing continuing care throughout SW’s childhood. -Consultant Paediatrician (with an interest in diabetes) -Diabetic specialist nurse -Paediatric dietician F) SW needs to be placed upon an insulin regime. Give 2 examples of possible regimes: Twice-daily regimen – Twice daily short acting and intermediate acting insulin Basal-bolus regimen – Three times daily short acting boluses and one or two medium acting basal boluses of insulin. 1.14 Diabetes By the end of Phase II , students should be able to: • diagnose and assess diabetes • outline to 'parents' in a role play situation the management of childhood diabetes • perform ward-based blood and urine tests and interpret the results 26 1.15 A 1 year old boy, DS, is brought to the GP by his mother with an itchy rash, which is diagnosed as atopic eczema. 1) What are the other possible diagnoses. Give 4. Contact dermatitis Pityriasis rosea Fungal infection Psoriasis Urticaria Chickenpox 2) What features would you expect to find on examination of this child’s rash. Give 4 points present mainly on face and scalp. (Occurs mainly on flexure surfaces in older children) excoriation weeping rash crusted rash erythematous rash Dry skin. 3) What type of illnesses is this child at increased risk of developing? Atopic disease – hayfever, asthma. 4) What is the underlying pathological reaction. Type I Hypersensitivity Increased IgE production in response to common environmental allergens. 27 5) What has caused this serious exacerbation of this child’s eczema? Infection with Herpes Simplex Virus 6) What else could cause an exacerbation of this child’s eczema? Give 5 points Staph aureus infection Contact with an irritant/allergen Psychological stress Idiopathic Environment (heat, humidity) 7) What simple advice could you give to DS’s mother for managing this child’s eczema? Give 4 points. 28 Avoid soap and detergents Avoid nylon and wool clothing next to the skin Cut nails short (to reduce damage from scratching) Avoid any precipitating allergens. 8) What medical treatments are available for the treatment of eczema? Give 5. Emollients Topical corticosteroids Occlusive bandages Antibiotics H1 histamine antagonists 1.15 Skin disease By the end of Phase II , students should be able to: • recognise the common skin conditions in infancy, childhood and adolescence • outline to parents the management strategies available 29 1.16 PW is a 2 year old girl who presents to A&E with a painful swollen right arm. Give 3 salient points that you would ask within the history. -What was she doing at the time of injury? -Any previous history of injury to the arm? -Any other injuries? What investigations would you order? X-ray of site of injury. Blood results (coagulation disorders, calcium and phosphate levels, copper deficiency) What type of fracture is shown in the radiograph above? Greenstick fracture of the right radius 30 A CxR taken at the same time is shown below: What abnormality is shown by the arrows? healed rib fractures What other points in the history may aid a diagnosis of NAI? Previous injuries in unlikely areas e.g. skull fractures, facial bruising, cigarette burns. Inconsistent stories Social circumstances e.g. underlying drug / alcohol abuse within the family. If you do suspect non-accidental injury, who else would you involve in the investigation and management? List three. Social services Health worker GP Community Paediatrician Police in severe cases Give one other important diagnosis which may produce the picture seen in radiograph B, and what other examination findings may substantiate this diagnosis. 31 Osteogenesis imperfecta Blue sclera Skeletal deformities Short stature Joint laxity (Excellent question) Give the pathophysiology of this condition. Osteogenesis imperfecta is a condition resulting from abnormality in the type I collagen. Type I collagen fibers are found in bones, organ capsules, fascia, cornea, sclera, tendons, meninges, and dermis. Structurally, this protein is composed of a left-handed helix formed by intertwining of pro-a1 and pro-a2 chains. Mutations in the loci coding for these chains result in osteogenesis. 1.16 Fractures in Children By the end of their teaching the students should be able to: • recognise those fracture patterns that occur in children and their possible aetiological factors • order appropriate investigations • be aware of non-accidental injury and know the outline strategy for the handling of non accidental injuries • act as part of the team in the immediate and definitive care 32 1.17 Question 1 Harry, a 7 year-old boy has had pain in the right leg since he woke up this morning. He finds it difficult to walk on the leg due to pain, which has been getting worse throughout the day. His teachers at school said that he was unable to join in his P.E lesson because he was in too much discomfort and his mother was asked to pick him up early from school since the pain was getting significantly worse. The pain is in the groin, front of the thigh and radiates down to the knee; is exacerbated by movements at the hip and weight bearing. Harry does not have any pain in any other joints, and he otherwise feels fit and well. There is no history of trauma; Harry was playing happily the previous day. He had a moderately severe viral upper respiratory tract infection 2 weeks ago; but has now fully recovered. All other past medical history was unremarkable. Harry is afebrile. ◦ List 3 differential diagnoses on the basis of this history: transient monoarticular synovitis (TMS) septic arthritis (SA) juvenile rheumatoid arthritis (others to consider; osteomyelitis, leukaemia and other malignancies) ◦ What findings on examination would you look for to aid your diagnosis? Assess gait and ability to weight bear (TMS – able to walk despite discomfort; SA – severe pain, tenderness to palpation, spasm, and refusal to walk) Examination of the hip: TMS – no signs of trauma; mild, or no effusion unlikely to be obviously swollen; mild restriction of hip motion, especially abduction and internal rotation. (cf. SA or bacterial infection – hip is held in a flexed, abducted and externally rotated position and severely painful to move) Vital signs: TMS – afebrile; SA – usually febrile (>38.50C) ◦ Are there any particular features of the history that give you a clue to the diagnosis? **Past history of non-specific viral upper respiratory infection – Approximately 70% of involved children have a history of prodromal symptoms indicative of a viral URTI 7-14 days before onset of TMS of the hip Other features consistent with this diagnosis: Sex: male-to-female ratio is 2:1; Age: mean age of onset is 6 years, most patients are 3-8 years of age; distribution and character of symptoms: monoarticular, acute onset, 33 progressive pain exacerbated by active movement at the joint but still able to weight bear; otherwise in good health, no systemic symptoms associated; no history of trauma. Harry’s mother persuaded him to rest as much as possible and gave him some pain relief, which eased his discomfort. However, after two days, Harry felt able to mobilise again and was keen to get back to school and play football in the playground with his friends. After one day back at school, running around, Harry’s hip became extremely painful once again and he was unable to weight bear on it by the evening. His mother took him to their GP the following day for further review. ◦ Given the progression of symptoms, what now seems to be the most likely diagnosis? Transient monoarticular synovitis (hip) ◦ What investigations would you instigate? 1st line: Blood tests (FBC, U&E’s, LFT’s) AP and lateral pelvic x-rays Others to consider: Aspiration of fluid if moderate effusion present – may improve symptoms and improve local blood flow Bone scans may help to differentiate a septic process ◦ What advice would you give Harry and his mother meanwhile to help ease the discomfort? Bedrest and non-weight bearing until the pain resolves, followed by limited activities (for 1-2 weeks) Important to communicate that rest is essential even following resolution of pain – if the child returns to normal activities too early, exacerbation of the symptoms can occur NSAID’s can help for symptomatic relief Advised to return to the GP for further evaluation if there is lack of improvement/worsening of symptoms despite adequate rest to eliminate other, more serious disorders. Question 2 John is 5 years old. His mother is concerned because she has noticed him walking with an increasingly obvious limp for the last 3 weeks. He does not complain of discomfort when running or walking but has reported intermittent “soreness” of the leg from time 34 to time. When asked where it hurts, he points to the front of his right thigh. John is otherwise in good health, has no recent history of illness and all other joints are non painful and normally active/non-restrictive. There is no history of trauma and review of all systems was unremarkable – he is afebrile. On examination John appeared short for his age, and walked with a limp – minimal weight bearing on the right leg. There was no discrepancy of leg length, swelling, signs of trauma or localised tenderness on palpation. There was decreased range of movement at the hip – poor abduction and internal rotation and muscle spasms were seen in the quadriceps of the right leg. Examination of the left leg and hip was normal. Investigations showed John to have delayed bone age. ◦ What is the most likely diagnosis? Perthes disease – idiopathic avascular necrosis (osteonecrosis) of the capital femoral epiphysis (CFE) and the associated complications in a growing child. Caused by interruption of the CFE blood supply. ◦ What issues should be discussed with John and his mother about problems that could occur in later life given the suspected diagnosis? The short-term prognosis concerns femoral head deformity at the completion of the healing stage. Development of late degenerative arthritis occurs; the incidence is essentially 100% in children who are 10 years of age or older at onset. This rate is in contrast to a negligible risk in children 5 years or younger and a 38% risk when onset occurs between 6 and 9 years of age. Therefore, discussion should focus on the potential that there is a moderate risk but the age of onset is of good prognostic value. Long-term prognosis involves the potential for osteoarthritis of the hip in adulthood ◦ What features of the history suggest that there is a good prognosis? Age – 5 years old (The age related risk is associated with premature CFE closure. Early intervention to prevent deformity of the femoral head prior to closure reduces the likelihood of degenerative changes occurring, reducing the incidence of later complications/joint disease and the associated morbidity in early adulthood.) ◦ Which specific investigation would help determine the severity of the condition? AP and lateral pelvic x-ray – technique of choice for determining the extent of CFE involvement, useful for following disease progression and identifying CFE collapse and extrusion and assess response to treatment. 35 Occasionally additional procedures such as arthrography, bone scans, and MRI may be useful. Bone scans and MRI are helpful in recognising early perthes disease but are of limited value in assessing the extent of CFE involvement or following the disease progression. ◦ What interventions could be considered (possibly not immediately) to improve John’s prognosis and avoid complications in later life? Surgical and non-surgical “containment” - the femoral head is contained within the acetabulum, which acts as a mold for the reossifying CFE. Perthes disease is a local, self-healing disorder – treatment focuses of prevention of femoral head deformity and secondary osteoarthritis. Containment is indicated for children 6 years of age or older in whom more than half the CFE is involved. This is accomplished by non-surgical containment using abduction casts and orthoses or by surgical containment with proximal femoral varus osteotomy – long term results are 85-90% satisfactory. Objective 1.17 The Limping Child By the end of their teaching the student should be able to: • examine the child with the painful hip or knee • consider the conditions of irritable hips, synovitis, systemic rheumatoid arthritis, slipped upper femoral epipyhsis, Perthes disease, septic arthritis, osteomylitis and tumour • initiate appropriate investigations • outline treatment to the child and family 36 2.2 Miss AB is a 26 year old woman who has been to her GP with concerns that her period is 3 weeks late. 1. Give two other symptoms which could be obtained form the history, and may suggest that she is pregnant. (2 points) breast tenderness vomiting 2. There are several clinical signs which can be seen on examination of a pregnant woman (later gestation), name 4. (4 points) Striae gravidarum linea nigra areolae pigmentation chloasma montgomery’s tubercles (on the breast) 3. A urine pregnancy test is suggested. What substance does this investigation detect, what is it produced by and what role does it play in pregnancy. (3 points) ßhCG (human chorionic gonadotrophin) produced by the trophoblast it maintains the corpus luteum which secretes progesterone to maintain the pregnancy 4. Routine ultrasound scan is performed at 11-14 weeks; suggest one use that this has. (1 point) confirm gestational age identify multiple pregnancies nuchal thickness in Down’s Syndrome 37 2.2 Diagnosis of pregnancy By the end of Phase II , students should be able to: • diagnose pregnancy on clinical grounds • use tests of pregnancy appropriately • recognise the role of ultrasonography in the diagnosis of pregnancy 38 2.3 Mrs J is a 30 year old lady who has come to ask about starting a family. She has no medical problems but smokes 20 cigarettes a day. 1. State 2 factors which you would advise her about and for each give a reason why. (4 points) Smoking cessation: Any of; associated with IUGR, premature labour, miscarriages Folic acid supplements: reduce the risk of neural tube defects 2. What important advice would you give if Mrs J had a pre-existing condition such as diabetes or epilepsy? (1 point) Ensure optimum management of pre-existing maternal disease prior to pregnancy if possible and address potential teratogenic medications (question not quite fit in: debate role of screening for genetic disease and be able to take a family hx with reference to genetic disease) 2.3 Pre-pregnancy counselling and care By the end of Phase II , students should be able to: • recognise the importance of pre-pregnancy counselling in particular groups • debate the role of screening for genetic disease • take a simple family history with reference to genetic disease 39 2.4 A 35 year old lady presents to her GP saying that she has carried out a home pregnancy testing kit and it has revealed a positive result. She wants to confirm whether or not she is pregnant and how far she has progressed through her pregnancy. Name five likely symptoms of pregnancy noticed in the first trimester of pregnancy, that this lady may mention. Morning sickness. Fatigue. Frequency of micturition. Heartburn. Constipation. Breast changes. Emotional lability. This lady tells you that the date of her last menstrual period (LMP) was on the 7 th September 2005. Calculate using Naegle’s Rule the estimated date of delivery (EDD). Estimated date of delivery (EDD) = Last menstrual period (LMP) + 9 mnths 7 dys = 7th September + 9 mnths 7 dys = 14th September 2005 + 9 mnths = 14th June 2006 Give one reason directly associated with the menstrual cycle, that could affect the accuracy of this calculated EDD. Some women have longer than average length of menstrual cycles. Variation in the length of the proliferative phase of the menstrual cycle. List three other confounding factors could affect EDD accuracy. Assumption of 40 weeks gestation (280 days). Assumption of conception occurring two weeks after first day of LMP (14 days into cycle ovulation occurs, assumption of conception 40 occurring on this day, but could have occurred any time between then and next date of expected menstrual period). Break through bleeding could confuse the date of LMP. Bleeding from recent IUCD use could confuse date of LMP. Break through bleeding and irregularity of cycles after cessation of oral contraceptive pill could confuse date of LMP. Describe the basis of a standard pregnancy test. B human chorionic gonadotrophin (B hCG) secreted from placenta and trophoblastic tissue is excreted in the maternal urine. This is detected by monoclonal antibodies to it, tagged to latex or red cells. A visible colour change in the detection probe is noticed by this reaction which confirms the pregnancy. What visible changes may be noticed on speculum examination in a pregnant woman? Bluish tinge to the vagina and cervix. Give three ultrasound parameters that may be noted with respect to the foetus, to verify pregnancy dates. Presence and size of gestation sac. Foetal crown-rump length. Foetal bipareital diameter. Foetal head circumference. Foetal abdominal circumference. Foetal femur length. List five potential risk factors for abnormality in pregnancy. Maternal age. Previous miscarriage. Consanguineous marriage between parents. Alcohol abuse. Drug abuse. Teratogen ingestion. Maternal illness (including infections such as HIV). 41 Poor folic acid intake. There is concern from an ultrasound scan that this woman’s child may have Down’s Syndrome. A “triple test” is carried out on maternal serum. Name the three factors tested, and indicate whether these would be high or low if the foetus does have Down’s Syndrome. Human chorionic gonadotrophin levels raised. Decreased alpha fetoprotein levels. Decreased unconjugated oestradiol levels. Name and give a brief description of three investigations used to detect foetal abnormalities (other than the “triple test” and ultrasound scanning). 1 Amniocentesis – fine needle used to aspirate amniotic fluid from the mother’s uterus, under ultrasound real time guidance. Cells shed from foetal gut and skin can then be used for further tests such as karyotyping. 2 Chorionic villus sampling – sample of actively dividing trophoblast cells allows rapid karyotyping. Done in 1 st trimester by transabdominal/transcervical route. 3 Placental biopsy – sample of actively dividing trophoblast cells allows rapid karyotyping. Done in 2nd/3rd trimester by transabdominal route. 4 Foetal Tissue Sampling – done under real time ultrasound guidance, involving skin or liver or other organ tissue extraction depending on indication.. 5 Antenatal foetal blood sampling – done under USS guidance transabdominally (placental cord, foetal intrahepatic vessels, foetal heart). Name a foetal abnormality that could be responsible for raised alpha fetoprotein levels in maternal serum. 42 Neural tube defect (anencephaly, spina bifida). Give three other reasons for raised alpha fetoprotein in maternal serum. Exomphalos. Gastroschisis. Polycystic kidneys. Foetal death (tissue autolysis). Foetal teratoma (AFP secreted from tumour). Duodenal/oesophageal atresia. A younger pregnant woman mentions a long term problem with acne vulgaris, for which she had roaccutane treatment. What sort of drug is this and why is this of relevance with respect to her unborn child? It is an isotretinoin medication derived from vitamin A and is highly teratogenic. 2.4 Ante natal care By the end of Phase II , students should be able to: • assess pregnancy by a detailed obstetric and general medical history • calculate the expected date of delivery and allow for the possible confounding effects of irregular menstruation and the effects of the oral contraception • identify normal pregnancy • identify the possibility of abnormality in pregnancy 43 2.5 A PRHO clerks a 16 year old girl who presented to the A&E department with acute abdominal pain. The girl gave a history of generalised lower abdominal pain for 3 days, worsening over the past 24 hours and being more localised over right iliac fossa. On examination she has rebound abdominal tenderness in right iliac fossa. 1) Give four likely differential diagnoses. Gastrointestinal – appendicitis, mesenteric adenitis, Meckel’s diverticulum, inflammatory bowel disease, gastroenteritis, peritonitis. Reproductive – Ectopic pregnancy, salpigitis/pelvic inflammatory disease, endometriosis, mittelschmerz. Renal – UTI, ureteric colic(stones). Pain from adjacent areas 2) The PRHO then performs a pregnancy test: a) What hormone is measured to test for pregnancy? Beta - Human chorionic gonadotrophin. b) Specifically which cells secrete it? Trophoblast cells. c) When is it first measurable in the urine? 2 weeks after implantation. 3) The hormone level is >1000 IU/L and the uterus is empty on ultrasound scan. Give two possible explanations for this and underline the most serious one. Early intrauterine pregnancy (<5weeks). Ectopic pregnancy. 44 4) With regards to this serious problem, what factors may predispose to this? Give two. Previous tubal surgery. Fertility treatment (IVF, GIFT). Previous Ectopic pregnancy. Congenital abnormalities (diverticula). IUCD. Progesterone only pill. Emergency contraceptive. 5) Give one medical and one surgical treatment options. Medical –methotrexate either systemically or direct injection into fallopian tube under USS guidance. Surgical – laparoscopy and salpingectomy or salpingostomy. 6) How would you follow this patient up? Beta-HCG and TV USS every 1-2 days to ensure termination. Give all rhesus negative women anti-D. 7) In a 16 year old girl specifically, what advise would you give regarding contraception? 2.5 Major problems of pregnancy By the end of Phase II , students should be able to: • recognise, and initiate management of • spontaneous miscarriage • ectopic pregnancy • trophoblastic disease • abruptio placentae • placenta praeva • unclassified antepartal haemorrhage • recognise pre-eclampsia 45 • initiate investigation of gestational hypertension • explain the consequences of pre-eclampsia • outline to a patient the management of pre-eclampsia and gestational hypertension 46 2.6 You are a GP at your local practice. An extremely anxious 40-year-old woman comes to see you after reading a news paper article about the risks of Downs Syndrome in older women. You know this patient well. You diagnosed her pregnancy last month after she missed her last two periods. The pregnancy test was positive and her last menstrual period (LMP) was 10 weeks ago. You and the patient discuss prenatal screening with particular reference to Downs Syndrome. What investigation can reveal the gestational age of the fetus more reliably than a history of her LMP? Ultrasound What four main types of prenatal screening are available to detect Downs Syndrome? Maternal serum screening (blood) or Triple Test. Ultrasound Amniocentesis Chronic Villus Sampling Which three markers are assessed by the Triple Test. AFP (alpha fetoprotein) Oestriol HCG. Explain why the cut off for high vs low risk of Downs Syndrome via the Triple Test is set at 1 in 250? If the risk is 1 in 250 or less, the risk of having a baby with Down syndrome is greater than the risk of having a miscarriage from the amniocentesis. If the risk is more than 1 in 250, the risk of having a miscarriage from amniocentesis is greater than the risk of having a baby with Down syndrome. 47 What abnormalities may be found on Ultrasound to indicate Downs Syndrome? List 3. Any three of…. Nuchal translucency Choroid plexus cyst Echogenic bowel Echogenic intracardiac focus Dilatation of kidneys The fetus was determined to be high risk of Downs Syndrome by Triple Test. What two further investigations can give a more reliable assessment and at what gestational age can they be performed? Note: They both allow fetal chromosomal analysis. Amniocentesis at 14-18 weeks, and Chronic Villus Sampling at 10-12 weeks. List 5 side effects/ risks for these investigations? Cramps Bleeding Infection Leak amniotic fluid Increased risk of misscariage. This patient asks you if medication can be harmful during pregnancy. Below are six common drugs. List one major side effect to the fetus in each. Warfarin: Neonatal haemorrhage Tetracyclines: Abnormal bone growth or Teeth discoloration ACE inhibitors: Renal damage Benzodiazepines: NSAID: Phenytoin: Amiodarone: Neonatal withdrawal Delayed closure of ductus arterious Cleft palate or cardiac abnormalities Neonatal goitre. 48 2.6 Fetal growth, development and disease By the end of Phase II , students should be able to: • recognise and interpret discrepancy in uterine size for gestational age • outline to patients the role of blood tests, ultrasound amniocentesis and chorionic villus sampling in the establishment of fetal health • describe the role and methods of fetal assessment in pregnancy • recognise the potential adverse effects of drugs in pregnancy • debate the benefits and costs of prenatal screening 49 2.7 A 32-year-old multiparous woman presents at 10 weeks’ gestation to the antenatal clinic. She has a blood pressure of 140/90 mmHg. 1.) Name 3 causes for this BP (3 marks) Essential hypertension Chronic hypertension Secondary hypertension 2.) What examinations should be performed? (2 marks) Repeat BP measurements Fundoscopy – assesses severity of hypertension 3.) What investigations should be performed? (4 marks) FBCs U+Es LFTs 24-hour urinary protein concentration 4.) How should this condition be managed? (2 marks) Treatment should be aimed at controlling the BP. Drugs that have been used include methyldopa, labetolol and nifedipine. These drugs can be used as single agents or in combination. (Important to remember that labetolol and nifedipine have been known to cause fetal and neonatal bradycardias. Methyldopa may cause abnormal LFTs and depression). 50 A 26-year-old woman who is now 37 weeks pregnant has been attending the antenatal clinic since she was 14 weeks pregnant. A routine FBC performed by the midwife at 36 weeks shows the following abnormal results: Hb = 8.2 g/dl MCV = 68.4 fl WBC = 9.0 x 109 1.) What is the diagnosis? (1 mark) Microcytic anaemia 2.) What are the reasons for this diagnosis? (2 marks) Low Hb, low MCV 3.) What other symptoms may she present with? (3 marks) Breathlessness easy fatiguability asymptomatic palpitations tinnitus symptoms from underlying cause. e.g. GI bleed- malaena, rectal bleed 4.) What further investigation will you perform on her? (2 marks) Serum ferritin 5.) Assume she has iron deficient anaemia what 2 treatment options may you recommend for her at this stage? (2 marks) Parenteral iron, blood transfusion A glucose tolerance test was performed on a pregnant woman who previously had a stillbirth at 39 weeks. The results are shown below: 51 Fasting = 5.5 mmol/l 60 minutes = 12.4 mmol/l 120 minutes = 10.5 mmol/l 1.) What is the diagnosis? (1 mark) Impaired glucose tolerance 2.) What treatment will you recommend for her? (2 marks) Dietary control in the first instance, if unsuccessful, insulin should be started 3.) What are the complications of the condition during pregnancy? (3 marks) Fetal macrosomia, unexplained intrauterine death, polyhydramnios 4.) When is the baby most likely to be delivered? (1 mark) At 38 weeks gestation 5.) If the mother is placed on insulin, what must be done after delivery? (1 mark) Stop the insulin and return her to her pre-pregnancy status; without any treatment) 6.) What advice will you give this woman about the long-term implications of this condition? (2 marks) She has a higher risk of developing adult-onset diabetes mellitus and therefore will require frequent screening Mrs PB attended for routine antenatal care at 28 weeks gestation when she was found to have a + protein in her urine. She had no symptoms. An MSU grew E. Coli for which she was treated successfully. On 2 subsequent visits she was found to have proteinuria and an MSU showed significant showed significant bacterial growth but she remained asymptomatic. 52 1.) What is this condition called? (2 marks) Asymptomatic significant bacteruria 2.) What is the sequelae if this is untreated? (1 mark) Symptomatic UTI 3.) What 2 causes of this condition need to be excluded? (2 marks) Urinary tract abnormalities kidney stones pyelonephritis 4.) What treatment would this patient benefit from? (2 mark) Antibiotics with either trimethoprim, ampicillin or nitrofurantoins 5.) What further investigations need to be performed on her? (2 marks) Ultrasound scan of kidneys, intravenous urogram 3-4 months after delivery 2.7 Medical problems in pregnancy By the end of Phase II , students should be able to: • initiate management of the common self-limiting problems in pregnancy • recognise the potential adverse effects of intercurrent disorders such as anaemia, asthma, cardiac disease, diabetes, hypertension, renal and thyroid disease • initiate appropriate investigations for these disorders • appreciate the risk of thromboembolic disease in pregnancy • participate in the long-term management of these conditions 53 2.8 Mrs G has conceived after her third IVF attempt. She has just had an USS at 6 weeks and has been told she has triplets. a. What three possible first trimester complications may she have? Miscarriage Hyperemesis gravidarum Vanishing triplet syndrome. b. What prophylactic drugs must she have during pregnancy? Name 2. Iron tablets folic acid. c. What would be the most common complication in the second half of pregnancy? Preterm labour d. What three other maternal complications may arise? Anaemia Hypertension Preeclapsia pressure symptoms. e. What precautions might be taken to reduce risk and complications of prematurity? Admission into hospital for bed rest. Antenatal steroids to reduce the severity of respiratory distress syndrome in the babies. f. How may the babies be delivered? The most common way is by C-section but vaginal delivery is possible. 54 2.8 Multiple pregnancy By the end of Phase II , students should be able to: • recognise the likelihood and make the diagnosis of multiple pregnancy • recognise the complications of multiple pregnancy during pregnancy, parturition and the puerperium • outline to patients the possibility of preterm labour and the early symptoms 55 2.9 A woman was admitted to the delivery suite at 38 weeks gestation with absent fetal movements for 24 hours and fetal heart was not picked up on CTG. a) How would you confirm the diagnosis of intrauterine fetal death? (1 mark) Ultrasound scan b) How would you counsel the mother? (3 marks) Explain the diagnosis to the mother in an empathic way explain need to deliver the fetus explain need to investigate the cause of intrauterine death c) Name 4 investigations you would perform on the mother. (4 marks) Coagulation profile thyroid function test HbA1c Kleihauer test lupus anticoagulant and anticardiolipin antibodies infection screen d) Name 2 investigations you would perform on the fetus. (2 marks) Swabs from nose, throat ear and mouth Skin biopsy for karyotype Autopsy 2.9 Intrauterine and neonatal deaths By the end of Phase II , students should be able to: • recognise the antecedents and methods of prevention of intrauterine and neonatal death 56 • recognise on clinical grounds the possibility of intrauterine death and initiate appropriate investigations • communicate with patients in a role play situation about the diagnosis of intrauterine death • participate as a team member in the counselling of parents sustaining an intrauterine or neonatal death 57 2.10 A gravida 0, aged 37 women, comes to see you for advice as she is planning to start a family. She has heard that there are risks associated with starting a family later in life. a) List 2 maternal risks of elderly primigravida. (2 marks) Any of: Increased risk of ectopic pregnancy Increased spontaneous loss Molar pregnancy Thromboembolism Mortality. b) Give 2 obstetric risks associated with increased age at first delivery. (2 marks) 2 of: abruptio placenta (HTN, fribroids) placenta previa increased rate of c-section uterine infection (postpartum endometriosis). c) What are the foetal risks? Give 2. (2 marks) Increased incidence of twinning Iatrogenic preterm delivery Aneuploidy Non-chromosomal anomalies/ autosomal dominant mutations (due to increased paternal age). d) What is the aim of prenatal diagnosis? (2 marks) Identification of abnormalities to prepare the parents Offer termination Identify conditions which may influence the timing of delivery Enable adequate paediatric support to be available Identify foetuses that may benefit from in utero treatment. e) Name 2 prenatal tests and what they are used for. (2 marks) Maternal serum -feto protein – neural tube defects Triple test (HCG, MSAFP, oestriol) – aneuploidy 58 Ultrasound scan – soft markers (nuchal translucenecy in Down’s, echogenic bowel in CF), structural abnormalities (congenital heart disease, abdominal wall defects). Amniocentesis: tissue sampling and karyotyping Chorionic villus sampling: tissue sampling and karyotyping. A 13 year old girl comes to see you with a 8 week history of amenorrhoea. f) What are the possible diagnoses? Pregnancy Emotional disturbances (stress, exams) Weight loss/athleticism PCOS Drugs (OCP) Hyper/hypothyroidism Hyperadrenalism g) What first line investigation would you do? Pregnancy test h) What are the issues associated with an adolescent pregnancy? (2 marks) Lack of concordance with prenatal care. Nutritional issues – growth demands of adolescence Vitamin deficiency Iron deficiency (poor diet, heavy erratic periods) Alcohol and drugs Body image and dieting Infections - UTI STD Other - lack of social support (partner, home, school) Infant disadvantage. A 34-year-old lady comes to see you as she has a positive pregnancy test. She has 7 children. i) Define grand multiparity. (1 mark) 59 5 or more pregnancies carried to viability. j) What risks are associated with this? Abruptio placenta (due to age/HTN) Placenta previa (due to previous scarring) Post partum haemorrhage (due to atony and therefore lack of contraction) Precipitate delivery k) What social issues need to be considered? Childcare during and after pregnancy Socio-economic factors Contraceptive advice. Mrs J, a 25 year old G2 P0 is referred to you in the antenatal clinic. She is a known to have a problem with alcohol abuse and her midwife is concerned that she is continuing to drink throughout her pregnancy. l) List 3 facial features of Foetal Alcohol syndrome. Absent/hypoplastic philtrum Broad upper lip Flattened nasal bridge Micrognathia Micropthalmia Short nose Short palpebral fissures m) List 5 other features of Foetal Alcohol Syndrome. Hyperactivity/irritability Developmental delay Growth deficiency Mental retardation Poor coordination Congenital heart and joint defects n) Give one other effect of drinking during pregnancy. Increased spontaneous abortion 60 Restricted foetal growth Preterm birth Ms H G1 P0 is pregnant. She works as a nurse and had a needle-stick injury 1 year ago. Having never been vaccinated, she contracted acute hepatitis B and has recently had a blood test showing presence of Hepatitis B E antigen. o) Is her foetus at risk of vertical transmission? Yes (up to 90% if HBeAg present) p) By what routes may Hep B be transmitted to Ms H’s baby? Intrapartum exposure Haematogenous Transplacental Breastfeeding. q) What management plan would you follow? Advise to abstain from alcohol/hepatotoxins Notify staff on labour ward Ensure baby receives Hep B immunoglobulin and vaccine LFT’s ?amniocentesis ?delivery route discuss breastfeeding Mrs K is HIV positive and pregnant with her first child. r) What maternal factors affect vertical transmission? Advanced maternal disease Low CD4 count High viral load Genital tract HIV viral load Genital tract infections s) What obstetric factors effect transmission? Mode of delivery (reduced in c-section) 61 Duration of membrane rupture Prematurity t) What interventions would you recommend? Antiretroviral therapy Elective c-section Formula feeding u) What antiretroviral therapy would you prescribe? Triple therapy – zidovudine, lamivudine and nevirapine v) How would you manage the neonate? Treat with antiretroviral therapy (depending on mothers viral load) Diagnostic testing: HIV PCR at day 1, 1 month, 3 months, 6 months, 12 mnth HIV antibody at 18 months BCG not given until after 18 months. 2.10 Special situations By the end of Phase II , students should be able to: • recognise that special obstetric risks are associated with grand multi-parity, elderly primigravidae, adolescent pregnancies and pregnancies in drug and alcohol abusers • recognise the particular risks to patients and staff in circumstances of Hepatitis B and HIV infection 62 2.11 Ms K is a 25 year old primigravida of 29 weeks gestation who presented with an abdominal ‘tightening’ sensation which were becoming more painful and more frequently in nature. Define premature labour. Premature labour is defined as labour occurring after 24 weeks and before 37 weeks gestation. Describe five characteristics of a woman who is at increased risk of developing premature labour. Body mass index <19 Low social class Extremes of reproductive age (under 20 and over 35) Domestic violence Previous preterm labour Others to mention – unsupported, smoking, previous preterm labour, bacterial vaginosis and chronic medical conditions. Name five possible causes of Ms K’s premature labour Infection eg. Chorioamnionitis, maternal pyelonephritis, appendicits. Uteroplacental ischaemia eg. Abruption Uterine overdistension eg. Polyhydramnios, multiple pregnancy. Cervical incompetence Foetal abnormaility Upon initial examination of Ms K in the EAU department describe what you would do. Assess mother to see if she is stable (? shocked from a large abruption) Assess for signs of a precipitant of preterm labour e.g. sepsis, polyhydramnios, and severe pre-eclampsia, obstetric cholestasis. 63 Determine frequency and regularity of contractions Sterile speculum examination – check for dilatation of the cervix Begin foetal monitoring – CTG Ascertain foetal presentation (cephalic/breech) Inform paediatricians Ultrasound examination – abnormal lie and presentation common in preterm labour. What investigations would you carry out? Blood tests MSU and urinalysis High vaginal and endocervical swabs Assess for liquor using nitrazine sticks (PH – sensitive) – turn black, if it is not obvious. False positives from infected vaginal discharge, semen, blood and urine It was discovered that Ms K membranes were not ruptured, cervix was approx 1 cm dilated. There was no obvious precipitant or cause. What treatment should be initiated at this stage? Corticosteriods – betametasone or dexamethasone 12mg/12h IM twice promotes foetal surfactant production, lowering mortality and complications of Respiratory Distress syndrome. Use before 34 weeks only. Antibiotics – to be used if membranes rupture or obvious infection Consider tocolysis Monitor maternal pulse, BP, temperature, contractions and foetal heart rate. Tocolytic therapy was initiated. Name two known drugs and describe its mode of action. Ritodrine/salbutomol – beta agonist, act on beta – receptors in myometrium to cause relaxation. Nifedipine – calcium channel blocker – block calcium channels in the myometrium, interrupting contraction. 64 Mention a side effect of each named drug. Ritodrine – pulmonary oedema, tachycardia, hyperglycaemia and hypokalaemia. Nifedipine – potential to alter uteroplacental bloodflow causing foetal compromise. Maternal side-effects headache, flushing and tremor. 2.11 Preterm labour By the end of Phase II , students should be able to: • recognise the circumstances when preterm labour may occur • outline management to the patient 65 2.12 Mandy, aged 27, is expecting her first baby. No known complications are identified. Early in her pregnancy, she discusses the delivery options with her midwife. Initially Mandy is in favour of a home birth. But she later changes her mind, choosing to deliver the baby in hospital. A) Suggest two reasons why Mandy may have decided to opt for a hospital based birth. (any 2 from below) Primigravid women are more likely to experience failure to progress in the first or second stages of labour than multigravid women. This would require hospital transfer. Regional anaesthesia, Resuscitation of the newborn, Management of postpartum complication are all more difficult at a home delivery, compared with a hospital delivery. In her 39th week of pregnancy Mandy attends the maternity unit. She is experiencing contractions at a rate of one every 5-10 minutes and believes that she is in labour. B) List 3 symptoms may Mandy have experienced, which herald the onset of labour? Regular uterine contractions. Rupture of membranes. Show. C) What is the definition of labour? The occurrence of regular uterine contractions accompanied by cervical dilatation. The midwife confirms that Mandy has started the first stage of labour. D) Define the three stages of labour. 66 First stage: From the onset of labour until the cervix is fully dilated. Second stage: From full cervical dilation to birth of the baby. Third stage: From birth of the baby to delivery of the placenta. The midwife initiates monitoring of the progress of Mandy’s labour using a partogram. E) What four factors are recorded on a partogram? Cervical effacement. Cervical dilatation. Descent of presenting part. Uterine contractions The wellbeing of Mandy and her foetus are also monitored. F) List two parameters used to assess maternal wellbeing during labour, and two to assess foetal wellbeing. Maternal (any 2 of below): Blood pressure Pulse Temperature Pain relief Fluid balance Foetal (any 2 of below): Foetal heart rate Colour of liquor Foetal scalp pH A short cardiotocograph recording is taken on admission. G) What parameters should be used to interpret a cardiotocograph recording? Remember: “BRAVADO” 67 BR The baseline rate. A Acceleration. VA Variability. D Decelerations. Overall impression. F) Indicate two findings on a cardiotocograph that may indicate foetal distress. (any 2 of following) The baseline rate <110 or >160 beats/minute. Accelerations absent for over 20 minutes. Variability <5 beats/minute. Decelerations not associated with contractions. Overall impression non-reassuring. F) List 4 indications for continuous cardiotocograph monitoring. (any 4 of following) Preterm infant (<37 weeks completed gestation). Foetuses that are or are suspected to be small for gestational age. Multiple pregnancies. Women with epidural analgesia. Women with Syntocinon augmentation of labour. Women who have been induced. Women who are hypertensive. Women with major medical disorders, including diabetes. Women who develop meconium staining of the amniotic fluid during labour. Women who undergo a trial of uterine scar. If a foetal heart abnormality is recorded with the Pinard stethoscope/sonicaid. G) Which drug is routinely given during for the third stage of labour? When should it be administered? Syndometrine. Administered with the delivery of the anterior shoulder. 68 2.12 Normal labour By the end of Phase II , students should be able to: • describe the environments in which normal labour may be conducted and their relative benefits and risks • acknowledge the wishes of the mother in this decision • recognise the onset of labour • manage normal labour under supervision • identify the drugs commonly used in labour and their benefits and risks • participate in fetal surveillance in labour • recognise the common signs of fetal distress 69 2.14 Louise, a 25 year old woman, has successfully delivered her first baby, a healthy male, by normal full term delivery. Normal third stage has completed, though she needed repair of a third degree tear. She is wishing to breast feed but is experiencing some difficulty. Define the puerperium 6 week period from the completion of the 3rd stage of labour What physiological changes take place during the puerperium? e.g.s Genital tract: Uterine involution Lochia Endometrium regeneration and return of menstruation CVS: Fall in plasma volume and cardiac output Return of BP to normal (if raised in pregnancy) Blood: Increased coagulability due to rise in platelets and clotting factors U+E return to normal Rise in HB and haematocrit with haemoconcentration Urinary tract: Reduction of physiological dilatation GFR fall to normal Reduced bladder sensitivity to over-distension List benefits of breast feeding To mother To baby (from Lifespan;) Benefits to mother: 70 post-partum recovery- uterine involution, less weight gained, figure and physical fitness psychological- bonding. Measure of success by society Long-term health- lower risk osteoporosis, ovarian ca post-menopausal, breast cancer Benefits to baby: Species specificity Nutritional benefits Emotional- bonding Enhanced immunity- less infection Lower risk cot death Lower risk allergies Coats gut- lower risk gastroenteritis Cost For what maternal related reasons may breast feeding be difficult? Mastitis Abscess formation Postnatal depression/ psychosis Multiple births Exhaustion What advise would you give to a mother such as Louise who is learning for the first time to establish successful lactation? Louise asks you about postnatal contraception. She has used the OCP previously, but has heard that some drugs should not be given whilst breastfeeding, and wonders if breastfeeding alone will be enough to protect her. What contraceptive advice would you give her? What are her options and when should any measures be started? Lactation not adequate alone Start contraception 4-6 wks post-delivery OCP contraindicated if breastfeeding- suppresses lactation Progesterone-only pill or depot is safe when breastfeeding IUD safe- insert at end of 3rd stage or at 6 weeks (infection screen first). 71 drugs that should be avoided during breastfeeding, and their potential effect on the baby With your help, Louise successfully starts breastfeeding. She is managed on the ward for a few days. What routine assessments should be made daily postnatally? What common problems in the puerperium should be identified? Assess: Uterine involution and lochia Blood pressure Temperature Pulse Perineal wound Common problems: Infection Thrombo-embolism Poor wound healing Urinary incontinence Urinary retention Faecal incontinence Feeding problems Post-natal depression and psychosis Louise develops pyrexia. What are the most likely sources/causes? How would you assess and manage it? Sources/causes: Genital tract infection- endometritis (± retained products of conception) Urinary tract infection Breast- Mastitis 72 Wound infection Lung infection DVT Examine- abdo, breasts, IV access sites, chest, legs Cultures- Blood, urine, high vaginal, fetal Broad spectrum antibiotics Louise returns home with her new baby. A few days later, she is visited by her midwife. What symptoms might suggest post-natal depression? What are the risk factors? Tiredness Guilt Feelings of worthlessness RF: Social/emotional isolation Previous history Pregnancy complications What measures might you take in treatment Social support Psychotherapy Antidepressants 2.14 Normal puerperium and lactation By the end of Phase II , students should be able to: • make routine assessments of patients to identify infection, thrombosis and feeding problems and assess wound healing • recognise the factors leading to the establishment of successful lactation 73 • advise patients on the use of drugs in lactation • recognise the possibility of post-natal depression and psychosis 74 2.15 Mrs S is a 35 year old primigravida at 40+10 weeks gestation. She has been admitted to the labour ward for induction of labor. 1) What is the rationale for induction at this timing? Due to increased perinatal mortality rates/Caesarean section after 42 weeks. 1 mark 2) Give 3 circumstances where induction of labor would be contraindicated? Previous caesarean section, Multiple Pregnancy, Maternal Cardiac disease, Pre-eclampsia. 3 marks The progress of labor was monitored using the Bishops score. 3) Name 4 of the criteria examined for a bishops score. Dilation, Consistency, Length, Station, Position. 4 marks Mrs S progressed through to the 2nd stage of labor. Her blood pressure (110/70), pulse (75bpm), and temperature (37.1ºC) were all monitored. minutes. Contractions were 3 in every 10 During her contractions, fetal heart rate was monitored by CTG, and fetal distress was noted. 4) List 3 signs of fetal distress that can be observed on a CTG. Unprovoked decelerations, 75 Decreased variability, Fetal bradycardia(<110bpm)/tachycardia(>175bpm), Slow recovery of fetal heart rate following a deceleration. 3 marks Due to the fetal distress and a prolonged 2 nd stage, assisted ventouse delivery was attempted. 5) Give two complications of a ventouse delivery, and 2 complications of a forceps delivery. Ventouse: Cephalo/skull haematoma, Scalp laceration, Vaginal tears, Neonatal jaundice. Forceps: Vaginal tears, Ruptured uterus, Facial nerve palsy. 4 marks Following successful delivery, Mrs S was noted to have lost 500ml of blood and was continuing to lose blood. 6) Give 3 causes of post partum haemorrhage Caesarean section, Atonic uterus, Retained placenta, Trauma during delivery. 3 marks 7) What drug is commonly used at the end of the 2nd stage of labor to aid the progress of the 3rd stage, and what is it a combination of? Syntometrine, combination of Ergometrine and Oxytocin. 2 marks 76 2.15 Abnormal labour By the end of Phase II , students should be able to: • describe the role of induction of labour and the possible methods • recognise common fetal and maternal problems in the first stage of labour • participate in the management of delay in the first stage of labour including the use of oxytocin and monitoring techniques • recognise delay in the second stage of labour and the circumstances when it may occur • recognise the common complications of the third stage of labour and describe how they may be prevented • recognise and participate in the immediate management of post-partum haemorrhage • discuss with patients the need for operative delivery including Caesarean Section • debate critically the role of Caesarean Section 77 3.2 Mr Phillips, a 68 year old retired gardener comes to see you his GP complaining of difficulty passing water which has been blood stained. After skilfully eliciting the history, you suspect the prostate to be the cause of Mr Phillips’ troubles a) Apart from examining Mr Phillips’ abdomen, which examination is indicated here? Digital rectal examination b) List four other indications of when to perform the examination mentioned in a. Suspected lower GI prostate cauda equina/ back injury Rectal bleeding Severe constipation Pain in the anal or rectal area Suspected enlarged prostate gland Suspected rectocele. c) List four things you would normally inspect for whilst performing this examination (in any case, not just for Mr Phillips). Rectal prolapse fistulo-in-ano skin tags anal fissure anal warts haemorrhoids anal carcinoma pruritus ani excoriation from diarrhoea 78 d) Give two distinguishing features for each of prostatitis, prostatic carcinoma and BPH upon palpation of the prostate gland. Hard and nodular in prostatic carcinoma boggy and tender in prostatitis smooth and diffusely enlarged in BPH e) Assessment of anal tone is an important aspect of digital rectal examination. Which type of muscle comprise the internal and external sphincters of the anus and what is their respective innervation? Internal is involuntary smooth muscle, sympathetic innervation via the hypogastric and pelvic plexus External is striated voluntary muscle. The proximal aspect is in intimate relationship with the puborectalis muscle. The pudendal nerve, specifically the inferior rectal branch, innervates the external anal sphincter. Question 2 Mrs Wilson is a 56 year old school teacher. She has two children and is overweight with a BMI of 28. She has come to see you the HO in A&E with a 3 month history of RUQ/epigastric pain, colicky in nature and is occasionally relieved by food. She also has a previous history of a peptic ulcer. a) List two likely differential diagnoses that fit with Mrs Wilson presenting complaints. Chronic cholecystitis Biliary colic Duodenal/gastric ulcer GORD b) Name two treatments for Mrs Wilsons’ symptoms? 79 Lifestyle and diet modification – avoid spicy food, stop smoking, weight loss Simple antacids - gaviscon Proton pump inhibitor – omeprazole H2 Receptor antagonists – ranitidine c) List two further investigations required at this stage to identify the cause for Mrs Wilsons problems. H-pylori testing: CLO test or Urea Breath test Upper GI endoscopy Ultrasound scan abdomen d) List 4 indications for upper GI endoscopy apart from weight loss and age. Symptoms > 4 weeks Dysphagia/odynophagia Persisting symptoms despite treatment Relapsing symptoms Persisting vomiting GI bleeding e) Outline 3 of the potential complications of upper GI endoscopy Problems related to sedation/medication Bleeding Perforation f) Following the upper GI endoscopy, Mrs Wilson became unwell with abdominal pain made worse by coughing. What does her chest x-ray show and what is the commonest cause of this condition. 80 X-ray shows pneumoperitoneum (gas shown under both sides diaphragm) Commonest cause is from perforated gastroduodenal ulcer. 81 Question 3 Mr Hughes, a 34 year old stock broker, attends A&E with a 11 day history of yellowing of his skin and abdominal pain. He has noticed darkening of his urine and his motions have become putty coloured in the last three days. a) Give four likely differential diagnoses for this patient? Pancreatitis Alcoholic liver disease Acute hepatitis Choledocholithiasis (gallstone in CBD) Drugs (paracetamol) Ascending cholangitis His liver function blood results are as follows LFT: Bilrirubin (conjugated) – 68 (3-17mol/L) Alkaline Phosphatase – 300 (40-120u/L) ALT – 40 (3-35u/L) b) What do these blood results imply is the likely pathological process? And what other biochemical parameters would you like to know? Diagnosis - Obstructive/cholestatic jaundice Biochemical parameters - Gamma GT & Serum Amylase c) State one further investigation you would arrange to determine the cause. Abdominal ultrasound scan ERCP d) Mr Hughes has an ERCP arranged by your registrar. Give two indications for this test and state three complications that can occur. 82 Indications (diagnostic) Cholangitis Jaundice with intra hepatic duct dilatation Jaundice with normal ducts and a non diagnostic biopsy Recurrent pancreatitis Post cholecystectomy pain Indications (therapeutic) Sphincterotomy for CBD stones Stenting for malignant strictures Complications Acute pancreatitis Bleeding Cholangitis Perforation Extended Question Briefly outline the normal metabolism of bilirubin. Bilirubin is breakdown product of haemoglobin. It is conjugated with glucuronic acid by hepatocytes and becomes water soluble. The conjugated bilirubin is secreted into bile and then passes in to the gut. Some is taken up by the liver (enterohepatic circulation) with the remainder being converted to urobilinogen by gut bacteria. Urobilinogen is either reabsorbed or excreted by the kidneys, or converted stercobilin which colours faeces brown 83 3.2 Investigations By the end of Phase II students should be able to: • perform and interpret digital rectal examination • recognise the radiological features of intra-peritoneal air, obstructed bowel and correct placement of naso-gastric tubes • explain to a patient the reasons for conduct of and possible complications of upper gastro-intestinal endoscopy, colonoscopy ERCP and contrast radiography • request abdominal ultrasound and plain abdominal radiographs and chest radiographs appropriately seeking advice where necessary • interpret liver function tests and routine liver serological and immunological investigations relate the results to the underlying pathology 84 A 68 year old gentleman presents with a 3 month history of nocturia, poor stream, increased frequency, urgency and hesitancy. The SHO suspects Benign Prostatic Hyperplasia and feels she needs to perform a digital rectal examination (DRE). How would you perform a digital rectal examination whilst maintaining dignity for the patient? Fully explain the procedure to the patient. Make sure you will not be interrupted Ensure the patient is kept as comfortable and warm as possible. Lie patient on their left side with knees pulled to chest. Use gloves and lubricant. Part the buttocks. Ask the patient to take a deep breath and gently insert your finger into the anus. Feel with finger pad and twist with finger tip. When finished, wipe anus. Inspect glove for faeces, blood. You palpate the prostate gland. Typically, how would you differentiate between a patient with BPH and a patient with Prostate Cancer? A normal prostate is the size of a walnut. In BPH-the gland may still feel smooth, yet is enlarged. In prostate cancer, the gland may show asymmetrical, nodular enlargement. It may feel characteristically stony hard and irregular with obliteration of the median sulcus. Name 5 differential diagnoses which would require a DRE to be performed? BPH Prostate Cancer Cauda Equina Syndrome- assess anal tone by asking patient to squeeze your finger. Bowel Cancer- feel for masses and inspect glove for blood Chronic Constipation- feel for impacted faeces and inspect glove for faeces. . Objective: Digital rectal examination 85 3.4 1. A 35 year old gentleman presents to his GP complaining of recent onset dyspepsia a) Name 5 likely differentials to consider Duodenal ulcer Gastro-oesophageal reflux Functional dyspepsia MI Gastric ulcer Gastric malignancy Gallstones Gastritis Oesophagitis Pneumonia b) What do you understand by the term dyspepsia? A non-specific group of symptoms related to the upper GI tract including epigastric pain related to hunger, eating specific foods or time of day; associated bloating; heartburn which may be associated with acid reflux. c) On further history taking he revealed he suffered with epigastric pain which was worse before meals and at night and relieved by eating and drinking milk; he denied any ‘alarm’ symptoms. What is the most likely diagnosis? Duodenal ulcer (but don’t rely on history alone) d) What are the main risk factors involved? Helicobacter pylori* Smoking Increased gastric acid secretion Drugs (aspirin, NSAIDs, steroids)* Blood group O Increased gastric emptying *Major factors 86 e) Under what circumstances is referral for urgent endoscopy necessary? Patients of any age with dyspepsia when presenting with any of the following: Chronic GI bleeding Progressive unintentional weight loss Progressive difficulties swallowing Persistent vomiting Iron deficiency anaemia Epigastric mass Suspicious barium meal Also patients aged 55 years and over with unexplained and persistent (4-6/52) recent onset dyspepsia alone. f) Explain possible initial pharmacological therapies for this patient (mention 3). Initial strategy proton pump inhibitor (PPI) full dose for a month Testing for and treating H.pylori. H.pylori can be initially detected using either a carbon-13 urea breath test or a stool antigen test. If positive start eradication programme ‘triple therapy’, a 7 day twice daily course of: full dose PPI (e.g. lansoprazole 30mg bd) + metronidazole 400mg + clarithromycin 250mg; or full dose PPI + amoxicillin 1g and clarithromycin 500mg (Insufficient evidence to guide which should be offered first, NICE guidelines 2004) If no response to above try H2 receptor antagonists (ranitidine or cimetidine) or a prokinetic; No response to above treatments refer for 2nd opinion g) Before beginning pharmacological therapies what initial advice may you offer? Review medications for possible causes of dyspepsia (steroids, NSAIDs, Ca antagonists, nitrates, theophyllines, bisphosphonates). Use of simple antacids Stop smoking Reduce alcohol intake Avoid food that worsens symptoms Weight reduction 87 h) Peptic ulcer surgery (including antrectomy with vagotomy and subtotal gastrectomy with Roux en Y) is nowadays rarely performed due to the success of medical therapy. However you may encounter patients who are now experiencing the long-term complications of ulcer surgery. Briefly describe 3 of these long-term complications. Dumping syndrome – fainting, vertigo, sweating, which may be due to the osmotic effect of rapid transit of food from the stomach into the small intestine. Fluid is reabsorbed into the jejunum causing temporary hypovolaemia. Anaemia – may be due to iron deficiency because hydrochloric acid is needed for iron absorption or due to vitamin B12 deficiency because intrinsic factor is required. Both hydrochloric acid and intrinsic factor are absent after partial gastrectomy. Steatorrhoea and diarrhoea Bile reflux and vomiting Small stomach syndrome Recurrent ulceration and malignancy in gastric remnant Osteomalacia i) What do you understand by the term ‘non-dysfunctional dyspepsia’? Functional means symptoms occur in the absence of any demonstrable abnormalities. Functional dyspepsia can present with a range of symptoms including upper abdominal pain/discomfort, fullness/early satiety, bloating and nausea. 2. A 67 year old gentleman presents to his GP complaining of a 3-4 month history of epigastric pain/discomfort and unintentional weight loss. a) What other features in the history may suggest a gastric carcinoma, mention 3? Anorexia Dysphagia Upper GI bleed Metastatic disease Vomiting Anaemia 88 Mass in abdomen b) What clinical signs may be evident, name 5? Epigastric mass Hepatomegaly Jaundice Ascites Troissier’s sign (Virchow’s node) Acanthosis nigricans c) What risk factors are associated with gastric carcinoma, name 5? Diet – nitrosamines, pickling methods Blood group A Pernicious anaemia Smoking Alcohol H.pylori infection Atrophic gastritis d) Name 3 types of tumour which can be found in the stomach Adenocarcinoma (commonest) Lymphoma Leiomyomas Leiomyosarcomas neurofibromas GI stromal tumours (GISTs) e) Describe what you may find on macroscopic examination? Polypoid, ulcerating or infiltrative (Borrmann classification) If widespread can cause linitis plastica (leatherbottle stomach) f) How and where may gastric carcinomas spread? Direct invasion 89 Lymphatic spread – Virchow’s node Haematogenous spread – liver, lung, brain Transcoelomic e.g. to ovaries (Krunkenberg tumour) g) What investigations may this patient undergo, name 5? Urgent upper GI endoscopy – diagnostic - multiquadrant biopsy of all gastric ulcers Bloods – FBC (anaemia), LFTs (mets) Barium meal CT/MRI – staging Bone scan – staging Endoscopic ultrasound – assess depth of gastric invasion and local lymph node involvement Diagnostic laparoscopy – used to exclude undiagnosed peritoneal or liver secondaries prior to consideration of resection. 3) A 45 year old lady presents to A&E with severe right upper quadrant pain and vomiting? a) What differential diagnoses would you consider? Biliary colic Acute cholecystitis Pancreatitis Peptic ulcer disease Hepatitis Ruptured aneurysm b) On further history taking she reveals she has experienced similar episodes of pain over the past few months but never as severe and as prolonged as the current pain. The pain radiates to the right tip of the scapula and is precipitated by fatty foods. On examination the patient is lying still with shallow breathing. What other signs may you find on examination? Tenderness Guarding Murphy’s sign 90 Tachycardia Low grade pyrexia Mass Jaundice (if stone moves into CBD) c) Name the most important investigation and likely findings. Abdominal ultrasound scan - shows gallstones, thickened gallbladder wall, checks dilatation of biliary tree indicative of obstruction. d) How would you manage this patient? NBM IV fluids Strong analgesia e.g. pethidine Antibiotics e.g. cefuroxime and metronidazole Surgery – controversial issue regarding timing of surgery for patients with acute cholecystitis. OHCM states in suitable candidates do cholecystectomy within 72h, Early surgery is associated with fewer complications. If delayed, relapse occurs in 18%. Otherwise cholecystectomy deferred for 6-12 weeks until the inflammation has settled. Percutaneous cholecystostomy - elderly or high risk patients unsuitable for surgery e) Name 5 complications of gallstones. Biliary Colic Acute cholecystitis Chronic cholecystitis Empyema Gangrene/perforation Cholestatic jaundice Ascending cholangitis Acute pancreatitis Gallstone ileus 4) A 58 year old gentleman presents to his GP complaining of retrosternal pain 91 exacerbated by lying down and drinking alcohol and associated with regurgitation of gastric contents. a) Name the most likely diagnosis to consider? Gastro-oesophageal reflux disease (GORD) b) Name 5 risk factors associated with this disorder. Hiatus hernia Obesity Pregnancy High caffeine intake Alcohol Smoking Systemic sclerosis Increased gastric volume (large meals, delayed gastric emptying) Drugs (TCA, anti-cholinergics, Ca channel blockers, Nitrates) c) Briefly describe the underlying mechanisms responsible for this disorder. Normally reflux of acid is prevented by the lower oesophageal sphincter (LOS) angle of His crural fibres of the diaphragm prominent mucosal folds positive intra-abdominal pressure acting on the LOS Therefore failure of one or more of these mechanisms or if hiatus hernia present allows gastric contents to reflux into the oesophagus causing oesophagitis. d) Briefly describe 4 complications Oesophagitis – ulceration of oesophageal mucosa (mild to severe) Barrett’s oesophagus – a premalignant disorder, metaplastic change from normal squamous to columnar epithelium Barrett’s ulcer – may bleed or perforate Iron deficiency anaemia – blood loss from severe oesophagitis Stricture – fibrosis may result from healing oesophagitis 92 Oesophageal malignancy – adenocarcinoma e) Name 3 investigations and possible findings. Upper GI endoscopy – directly visualise, biopsy and cytological brushings to confirm presence of oesophagitis and to grade its severity and exclude malignancy. Barium swallow – can show structural abnormalities 24h oesophageal pH monitoring – significant reflux if pH <4 for >4.7% of time. f) Briefly describe lifestyle advice? Weight loss Raise bed head Small regular meals Avoid hot drinks, alcohol and eating <3h before bed Avoid drugs affecting oesophageal motility (nitrates, anticholinergics, TCA) or that damage the mucosa (NSAIDs) g) How would you further manage this patient? Initially try antacids or alginates. If symptoms persist for >4wks (or weight loss; dysphagia; excessive vomiting; GI bleeding) refer for GI endoscopy. Oesophagitis confirmed – try PPI Pro-kinetic drugs Surgery – Nissen fundoplication if symptoms are very severe and there is radiological or pH-monitoring evidence of severe reflux. 3.4 Dyspepsia By the end of Phase II students should be able to: • recognise and distinguish between peptic ulcer disease, gastro-oesophageal reflux disease and functional dyspepsia clinically and on investigation including investigation for H. pylori infection 93 • initiate management for these conditions including treatment for H. pylori infection • communicate to a patient the diagnosis of peptic ulcer disease with an explanation of the management including life-style changes • recognise the possibility of gastric cancer in older patients with upper abdominal symptoms • recognise the possibility of gall bladder disease in patients with upper abdominal pain and to initiate appropriate investigations 94 3.6 You are called to see a 53year old man in A & E who looks unwell with a large, distended abdomen and jaundice. He is unkempt and smells strongly of alcohol. a) At what plasma bilirubin level is jaundice visible? (1mark) 35mol/L b) Give a brief description of bilirubin metabolism. (3marks) Formed from breakdown of Hb Conjugated with Glucoronic acid by hepatocytes to make it water soluble Conjugated bilirubin secreted into bile & out into gut Some passes into enterohepatic circulation Rest converted to Urobilinogen by gut bacteria Urobilinogen either: Reabsorbed and excreted by kidneys Converted to stercobilin which colours faeces brown Jaundice can be classified by the site that is causing the problem. State the 3 types and give an example of each. (3marks) Pick one of the types and fill in the table below to show what you would expect to find when testing LFT’s – State if the level would be increased, decreased or within the normal range. (2marks) Pre-hepatic Hepatocellular Post-Hepatic Bilirubin ↑ ↑ ↑ AST N ↑ ↑ ALP N ↑ or N ↑ GGT N ↑ ↑ PRE-HEPATIC Physiological = neonatal Haemolysis Glucuronyl transferase deficiency = Gilbert’s syndrome, Crigler-Najar syndrome LFT’s: Bilirubin (micromoles/l) 50-150 (normal range 3-17) AST I.U. < 35 (normal range <35) 95 ALP I.U. <250 (normal range <250) Gamma GT I.U. 15-40 (normal range 15-40) HEPATOCELLULAR Viruses = Hep. A, B, C, CMV, EBV Drugs = Paracetamol overdose, Anti-TB (RIP), Sodium Valporate etc. Alcoholic hepatitis Cirrhosis Hepatic Metastases Haemochromatosis Wilson’s Disease Budd-Chiari syndrome Dubin-Johnson syndrome 1-antitrypsin deficiency Toxins = carbon tetrachloride LFT’s: Bilirubin (micromoles/l) 50-250 (normal range 3-17) AST I.U. 300-3000 (normal range <35) ALP I.U. <250-700 (normal range <250) Gamma GT I.U. 15-200 (normal range 15-40) CHOLESTATIC (OBSTRUCTIVE) Gallstones in common bile duct Pancreatic cancer Drugs = Antibiotics (flucloxacillin, fusidic acid, co-amoxiclav), Oral contraceptives, Clorpromazine etc. Cholangiocarcinoma Sclerosing cholangitis Primary biliary cirrhosis Biliary atresia LFT’s: Bilirubin (micromoles/l) 100-500 (normal range 3-17) AST I.U. 35-400 (normal range <35) ALP I.U. >500 (normal range <250) Gamma GT I.U. 30-50 (normal range 15-40) You want to take a history from this man. List 4 pertinent questions that you would like to ask. (4marks) 96 Blood transfusions IV Drug Use Body piercing/tattoos Sexual Hx Travel abroad Alcohol consumption FHx of jaundice Medications Contact with other jaundiced people From the history you discover that this man has been drinking heavily for the past 10years. State the most likely diagnosis and two things might you expect to find on examination of this man. (2marks) Diagnosis = Alcoholic liver disease causing cirrhosis/hepatic failure. Palmar Erythema Spider naevi Gynaecomastia Bruising Scratch marks Dupytren’s contracture Clubbing Leuconychia Testicular atrophy Hepatomegally Ascites Based upon your most likely diagnosis from (e), what investigations would you like to carry out for this patient? (3marks) Bloods FBC Folate & B12 LFT’s – Alk. Phos., ALT, AST, Bilirubin GGT Albumin PT/INR 97 WCC Platelets Virology – rule out infective cause Ascitic Tap Liver USS You diagnose alcoholic liver cirrhosis. How would you manage this patient’s ascites? (2marks) Fluid restriction Spironolactone (100mg/24h PO, every 48rs to 400mg/24h) Add Furosemide (<120mg/24h PO) Monitor U & E’s, Cr Chart weight loss = aim for 0.5kg/day You hear your consultant talking about portal hypertension and porto-systemic anastomoses. What is portal hypertension and how does it occur? (1mark) Damage to liver causes a raised pressure in the venous portal system. Raised pressure stimulates expansion of collaterals between the portal and systemic system Name the four sites of porto-systemic anastomoses. (2marks) Oesophagus = Haematemesis Umbilical = Caput medusa Anus = Haemorrhoids (rectal bleeding) Retro-peritoneal 3.6 Jaundice & hepatomegally By the end of Phase II students should be able to: - distinguish pre-hepatic, hepatic, post-hepatic jaundice on clinical & biochemical grounds - distinguish between infectious and mechanical causes of biliary obstruction - initiate appropriate investigations - distinguish the common causes of hepatomegally on clinical grounds - initiate investigations for hepatomegally 98 - recognise the manifestations of chronic liver disease including encephalopathy and portal hypertension - recognise the situations associated with acute hepatic failure, the signs of hepatic failure and initiate immediate management 99 Mr Best, who admits to an alcohol intake of 20 cans of lager per day, has a 3 month history of jaundice, abdominal swelling, shortness of breath and itching. Looking through his previous admission notes you see that cirrhosis of the liver was diagnosed. What is cirrhosis Loss of normal liver architecture with diffuse fibrosis and nodular degeneration which is usually irreversible In late cirrhosis, a small liver can be found. However, earlier on in the disease a patient may have hepatomegaly. Apart from cirrhosis name 3 causes of hepatomegaly. CCF Infectious causes e.g. acute hepatitis, weils disease, Epstein barr virus Carcinoma, neoplasm Cholangitis Haematological -Leukaemia, lymphoma, thalassaemia Vascular – e.g. amyloid Reidel’s lobe Reye’s syndrome Abcess, cyst Tricuspid incompetence (pulsatile) As well as alcohol abuse, name three causes of cirrhosis Infection Hepatitis – viral, autoimmune, fungal Autoimmune Primary sclerosing cholangitis Autoimmune liver disease Genetic causes alpha 1 antitrypsin deficiency Haemochromatosis Copper deposition (wilson’s disease) 100 drugs – e.g. amiodarone, methyldopa, methotrexate hepatic venous outflow obstruction: venoocclusive disease, Budd Chiari "cardiac cirrhosis" from constrictive pericarditis What abnormalities in blood results (FBC, LFT etc) would you expect in someone with chronic liver disease associated with alcohol abuse(values not required) FBC –mean cell volume increase Decreased platelets and WCC Increased gamma GT Increased AP and AST Decreased albumin Increased bilirubin (jaundice) INR/PT increase State the test you would perform to confirm your suspicion of ascites on examination One of: Shifting dullness Fluid thrill (‘Dipping’ may also be done to look for masses underlying ascites) What other investigations would you carry out in suspected ascites Ultrasound Diagnostic paracentesis Name three ways in which ascites is managed? Bed rest 101 Fluid restriction Low salt diet Spironolactone (frusemide added if no response) Observation: daily weights, U&E, creatinine (stop diuretics if Na↓ or creatinine ↑) Paracentesis (with albumin infusion) Mr Best has signs of encephalopathy and portal hypertension. Name two presentations for each. Encephalopathy: Liver flap Confusion Restlessness Slurred speech, incoherent speech Coordination problems Drowsiness, stupor Coma Foetor hepaticus hyperreflexia Portal hypertension: ascites - with low plasma albumin porto-systemic shunts - e.g. caput Medusae, oesophageal varices haematemesis or melaena - due to rupture of gastro - oesophageal varices venous hum of abdomen haemorrhoids peripheral oedema (increased risk of hepatocellular carcinoma) Name three hand signs of liver disease Palmar erythema Brusing 102 Terry’s nails Dupytren’s contracture Gynecomastia Clubbing Asterixis leuconychia Objective: Chronic liver disease 103 3.7 Whilst working in A&E as a newly qualified F1 doctor you are presented with Ruddiger a 52 year old male. From the history you ascertain that Ruddiger has had an alcohol problem for the past 10 years following the loss of a jackpot winning lottery ticket. He has recently been drinking even more following the loss of his trusted Labrador, Wotsit. On examination the most striking finding is his distended abdomen which you suspect is due to ascites. List 2 clinical signs you would look for to demonstrate ascites? Shifting dullness Fluid thrill Abdominal distension List 2 signs associated with ascites that you would look for? Abdominal wall venous distension Ankle oedema Distension of the neck veins Divarifacation of the recti Your examination has clearly demonstrated that Ruddiger has ascities. medical student attached to your firm asks you what ascites is. An inquisitive What would be your response? Ascites is the presence of free fluid within the peritoneal cavity What investigation would you order to determine the nature of the fluid within his abdomen? Diagnostic paracentesis / ascites tap List 2 things that this fluid would be analysed for? 104 Protein Malignant cells Infection Blood / white cells The fluid can either be a transudate or an exudate. What is the difference and list 2 causes for each? Transudate = protein <25 g/L Exudate = protein > 25 g/L Transudate – cardiac failure, liver failure, cirrhosis, hypoproteinaemia Exudate – Intra-abdominal malignancy, infection, pancreatitis Investigations show the fluid to be a transudate. You suspect the ascites is due to damage to Ruddiger’s liver from the excessive alcohol. List 4 things that your management would include to relieve the ascites? Bedrest Fluid restriction (<1.5 L/day) Low salt diet Diuretic – spironolactone Diuretic – furosemide Therapeutic paracentesis / ascites tap Alcohol avoidance advice 3.7 Ascites By the end of Phase II students should be able to: • detect ascites clinically • initiate appropriate investigation having regard to the likely causes • initiate management of hepatic ascites 105 3.9 A 26 year old medical student comes to you complaining of abdominal pain and explosive diarrhoea that has been getting worse for the past 7 days. She has noticed some blood mixed in with her stool and is now very concerned. She reports that she has been travelling around Thailand for the previous 3 weeks. a) What is the likely cause of her bloody diarrhoea? Any of : b) Pancreatitis, Campylobacter, Shigella, Salmonella, E.coli (1) inflammatory bowel disease, antibiotics, malabsorption and thyrotoxicosis are all causes of chronic diarrhoea, but can you name 2 other bacteria, protazoa and viruses that cause acute diarrhoea (½ for each)? Bacteria Clostridium difficile Mycobacterium tuberculosis vibro choleae. (1) Protazoa Entamoeba Histolytica Giardia lamblia (1) Viruses Rotavirus (Grp A) Astrovirus Norwalk-like virus enteric adenovirus calicivirus (1) c) What investigation and treatment would you recommend ? Stool culture +/- parasite screen (1) Rehydration using isotonic oral fluids containing electrolytes and glucose (1). (Intravenous fluid replacement may be indicated in patients with persistent vomiting) Ciprofloxacin 500mg bd or Erythromycin 500mg qds for 1 week is indicated as her diarrhoea is persistent.(1) Anti diarrhoeal drugs should be avoided here to avoid prolonging the infection. d) She returns 2 months later complaining of severe constipation and she has not had 106 her bowels open for 10 days. Give 3 different drugs used in the treatment of constipation and briefly mention how they exert their effects: (½ each 3max) Lactulose/Magnesium sulphate - Osmotic laxative (1) Senna/Docusate sodium - Motility agent (1) Ispaghula Husk/Fybogel - Bulk forming laxative (1) Extended Question – The defecation reflex occurs in response to distension of the rectal wall mediated by mechanoreceptors, can you describe the stages involved ? Contraction of the rectum Relaxation of the internal and external sphincter An initial contraction of the external anal sphincter Increased peristaltic activity in the sigmoid colon Relaxation of the external anal sphincter Expulsion of faeces (27 extra marks if you remember all this) 3.9 Diarrhoea and constipation By the end of Phase II students should be able to: • appreciate likely diagnoses in patients with acute and chronic diarrhoea and how they may be distinguished on clinical grounds • initiate appropriate investigation • assess the physiological effects of severe diarrhoea • explain the importance of oral rehydration solutions • distinguish the common causes of constipation on clinical grounds • initiate appropriate investigations for constipation 107 • manage constipation 108 3.10 A 15 year old girl newly diagnosed with Inflammatory bowel disease. Q1. How might she have presented? Diarrhoea with blood / mucus RIF mass Abdo pain Weight Loss Signs of anaemia Systemic signs E.g Skin and Eyes Fever Q2. How would you investigate her (she presented with diarrhoea)? FBC – Anaemia, white cell count, raised platelets LFT’s – albumin, alk phos U/E’s – potassium Inflammatory markers – CRP, ESR Anti-endomysial antibodies – (celiac) Stool sample – infective cause Endoscopy – histology and macroscopic appearance Q3. On histology how would you differentiate between UC and Crohns? UC Crohns Confined to Mucosa Skip lesions with multiple biopsies Crypt abscess Transmural Cell displasia Granulomas and giant cells Macrophages, lymphocytes and plasma cells Q4. What are the macroscopic differences? UC Crohns Rectum to iliocaecal valve Mouth to Anus (occasionally backwash ileitis) Skip lesions 109 Superficial ulceration Rose thorn fissures Pseudopoylpos Cobblestone appearance Fistulae and Abscesses After 5 years she has had repeated exacerbations and presents to A&E with bloody diarrhoea occurring fifteen times a day and lower abdominal pain, for the last 3 weeks She is very distressed and feels she has no quality of life Q5. Give your acute management? ABC IV fluids Admit IV steroids NBM AXR – ? abscess +/- antibiotics ASA e.g sulphasalazine Analgesia After 1 week she is showing signs of improvement but still does not feel that she is able to cope at home. Q6. Discuss her options (for each disease) UC Crohnes Medically – aziothioprine If localised – can operate steroids Otherwise – aziothioprine ASA’s steroids Surgically – remove affected area ASA’s o Panproctocolectomy Q7. She opts for a surgical approach to discuss the issues 110 UC Positives Negatives Reduced colon cancer risk Major Surgery – anaesthetic risk Symptom resolution Stoma – possibly life long Long term incontinence post reversal Crohns Positives Negatives Possible reduction in symptoms Reduced chance of perforation Recurrence of Disease Adhesions Fistula formation Q8. When wanting to assess disease control other than GI symptoms what else might you question her about (systemically) Eyes – Uveitis o Irritis o Episcleritis Skin - Rashes – erythema nodosum, pyoderma gangrenosm Joints- Ankylosing spondylitis o Liver- Sacroilitis PSC Gall Stones Q9. (Extended) Her brother suffers from Ankylosing spondylitis. What genetic factor might they share? HLA B27 111 3.10 Inflammatory bowel disease By the end of Phase II students should be able to: • recognise the possibility of inflammatory bowel disease in patients presenting with lower gastrointestinal symptoms • initiate appropriate investigations in a patient with a suspected inflammatory bowel disease • initiate appropriate management in a patient with inflammatory bowel disease • recognise the differences in presentation between Crohn's disease and ulcerative colitis, and how these relate to the underlying pathology • recognise the possibility of systemic symptoms associated with inflammatory bowel disease • explain to patients the nature of and the rationale for maintenance treatment for inflammatory bowel disease 112 3.12 A 42 year old man presents to his GP with a 4 day history of bloody diarrhoea. The blood is fresh in appearance. The patient has been diagnosed as suffering from FAP since his early 20's. The patient also complains of abdominal pains which subside once he goes to the toilet. He is mildly short of breath and looks pale in appearance. Question 1a What is FAP and explain why you are worried this patient has cancer of the large bowel? People with Familial Adenomatous Polyposis, a rate autosomal dominant disorder, almost always develop cancer of the intestine by age 35. It is characterised by thousands of polyps growing in the large intestine. It is a pre-malignant condition. Question 1b Explain the breathlessness. The patient is likely anemic due to chronic blood loss. Question 2 What are the 4 layers of the large bowel and for that matter the rest of the GI system? Mucosa, Submucosa, Muscularis Propria/Externa, Serosa Question 3 Name 1 other symptom you might expect the patient to complain about if he indeed has cancer of the large bowel. 113 Unexplained weight loss Question 4 What is the most common colon cancer cell type? Adenocarcinoma (which accounts for 95% of cases). Question 5 Which classification is used to stage cancer in the large bowel? Briefly explain each stage. Duke's A: invaded submucosa and muscle layer of the bowel but confined to the wall. Duke's B: breached the muscle layer and bowel wall but no involvement of local lymph nodes. Duke's C1: spread to immediately draining pericolic lymph nodes. Duke's C2: Spready to higher mesenteric lymph nodes. Duke's D: Distant visceral metastases. Extended Question 6 Name 5 factors which increase a person's risk of developing Colo-rectal cancer. Any 5 of: Smoking Diet high in fats Diet high in carbohydrates Diet low in fibre Suffering from Inflammatory bowel diseases (i.e. Crohn's, UC) as these conditions are pre-malignant. 114 Family Hx of Bowel Cancer Age. The risk of developing colorectal cancer increases with age. Most cases occur in the 60s and 70s, while cases before age 50 are uncommon unless a family history of early colon cancer is present. HNPCC (Hereditary Non-Polyposis Colorectal Cancer) Extended Question 7 Name 2 investigations you would like to see carried out to assess the extent of disease in this patient's bowel? Barium Enema Colonoscopy +/- Biopsy 3.12 Bowel cancer By the end of Phase II students should be able to: • recognise the possibility of colonic cancer in patients with disturbed bowel habit, rectal bleeding or anaemia • initiate appropriate investigations to confirm the diagnosis and extent of disease • suggest a prognosis based on staging and other factors • outline to patients the possible management strategies for bowel cancer • outline to a patient the management of a colostomy 115 3.13 Peter, a 58 year old gentleman presents to accident and emergency with a 6 hour history of acute abdominal pain. As the surgical house officer you are called. On arrival in A+E Peter has a pulse of 100bpm, is pyrexial and in obvious distress. Q1 As you are walking to A+E what are your top 4 differential diagnoses for acute abdominal pain. Perforation Bowel Obstruction Acute Pancreatitis Dissecting Aortic Aneurysm Mesenteric Vascular Obstruction Acute appendicitis Acute Cholecystitis Kidney Stones Diverticulitis Peptic Ulcer On taking a history you find that he has a 6 hour history of severe epigastric pain, waking him from his sleep, which is associated with nausea and vomiting. history of gallstones and hypertension. There is a Peter attributes his symptoms to food at his daughters wedding the day before. Q2 What initial investigations would you carry out and why (be specific, not just ‘blood test’)? FBC: Raised WCC (infection) U+E’s: Dehydration (N+V), General kidney function (management) CRP, ESR: inflammatory markers 116 LFT’s: Raised AST secondary to Gallstones, Albumin for severity of ?pancreatitis Amylase: May be raised in pancreatitis Glucose: Severity of ?Pancreatitis Bone (Ca): Severity of ?Pancreatitis ABG: Severity of ?Pancreatitis Erect CXR – Perforation? Air under the diaphragm? AXR – Kidney stones? Sentinal Loop present? Psoas shadow? ECG Q3 Apart from gallstones, give 4 other common causes of pancreatitis? If gallstones are not the cause, what do you think is the most likely cause in this case? Alcohol Drugs Trauma ERCP Autoimmune GET SMASHED – causes such as scorpion sting not common in this country! Alcohol and diuretics most likely cause – due to daughters wedding the night before, at which he may have been drinking, and history of hypertension, which may be treated with diuretics. Q4 In pancreatitis you would expect an increase in amylase, name 3 other causes of an increased amylase. Upper GI tract perforation Leaking AAA Mesenteric Ischaemia Acute cholecystitis Renal Failure 117 Q5 What parameters would you use to assess the severity of an individual such as Peter who is suffering from pancreatitis? And what is the name for this scoring system? Modified Glasgow Criteria PaO2 < 8 kPa (PANCREAS) Age >55 years Neutrophils >15x109/L Ca < 2mmol/L uRea >16mmol/L Enzymes – LDH >600iu/L, AST >200iu/L Albumin<32g/L Sugar (glucose) > 10 mmol/L Peter scores 4 on this scale and your consultant admits him of ITU. Q6 In your further management what complications would you look for? ARDS Diabetes Mellitus Pseudocysts Pleural effusions Organ failure Pancreatic abscess Ascites Sepsis Extended Q 118 What signs would you look for on abdominal examination in severe pancreatitis and what are they called? Cullens sign – Peri-umbilical bruising Grey-turners sign – Bruising of the flanks 3.13 Acute abdominal pain By the end of Phase II students should be able to: • recognise localised and generalised peritonitis and begin to distinguish the common causes • appreciate the causes of a ruptured viscus and how they may be begin to be distinguished • investigate, assess and initiate management of acute pancreatitis • appreciate the common causes of pain in the right iliac fossa and how they may be distinguished • initiate appropriate investigations in a patient with upper abdominal pain • recognise the possibility of bowel obstruction • initiate appropriate investigations and initiate intravenous fluid replacement and appropriate pain relief 119 A 52-year-old man presents to A&E with a four-day history of severe epigastric pain radiating to the back. The patient describes the pain as a sharp constant pain present in the epigastric region radiating to the back in a band like fashion. The pain was made worse on eating and drinking alcohol and relieved slightly by sitting forward. The patient described associated symptoms of vomiting and nausea. Question 1: What are the main differentials for the patient’s presentation? Acute pancreatitis Peptic ulcer Acute cholecystitis GI obstruction Question 2: What investigations would you order? Bloods – FBC, U&E, Amylase, LFT’s, and CRP Abdominal x-ray Ultrasound of gallbladder Question 3: After investigation the patient’s serum amylase was found to be 3045u/mL, LFT’s were normal, WCC was 11.5 and CRP was 105. Nothing abnormal was detected on Ultrasound and on abdominal x-ray; there was no psoas shadow. Given these results, what is the most probable cause of the patient’s presentation? Acute pancreatitis Question 4: What are the commonest causes of acute pancreatitis? G – Gallstones E – Ethanol T – Trauma S – Steroids M – Mumps A – Autoimmune – PAN S – Scorpion venom H – Hyperlipideamia/Hypercalcaemia/Hypothermia 120 E – ERCP D – Drugs – azathioprine, asparaginase Question 5: What common signs may be found on examination with a patient with acute pancreatitis? Tachycardia Fever Jaundice Shock Generalised abdominal tenderness Periumbilical discolouration – Cullen’s sign – around the umbilicus Grey Turners sign – at the flanks Question 6:What are the criteria for predicting the severity of acute pancreatitis? P – PaO2 < 8 kPa A – Age > 55 N – Neutrophils > 15*10power9/L C – Calcium < 2 mmol/L R – Renal function – Urea > 10mmol/L E – Enzymes – LDH > 600iu/L and AST > 200iu/L A – Albumin < 32 g/L S – Sugar – Glucose > 10 mmol/L Question 7: What would be the management plan for this patient? Nil by mouth Set up IVI and give plasma expanders and 0.9% saline until vital signs are satisfactory and urine flow > 30mL/L. Check weight daily and insert a catheter. Analgesia: Pethidine 75-100mg/4h IM, or morphine (may cause the sphincter of oddi to constrict more) Hourly pulse, BP and urine flow Daily FBC, U&E, glucose, amylase, blood gas. 121 If worsening, take to ITU. Question 8: What are some of the complications of acute pancreatitis? Early: Disseminated Intravascular Coagulation Renal failure Respiratory failure Haemorrhage Thrombosis – may occur in the splenic and gastroduodenal arteries, or in the colic branches of the superior mesenteric artery, causing bowel necrosis. Late: > 1 week – P Pancreatic necrosis Pseudocyst Objective: acute pancreatitis 122 3.14 Lindsay, a 23 year old previously healthy woman presents to her general practitioner with a 3 month history of generalised abdominal pain. On looking at her previous attendance and notes she was last seen for back pain 5 months ago. Q1 List 6 further questions you would want to ask about her presenting complaint. Change in bowel habits Change in consistency PR bleeding/mucus Diet/relationship to food Relieving/aggravating factors Bloating/flatus Tenesmus PV bleeding/LMP/cyclical/discharge On further questioning, Lindsay reports a change in bowel habits, primarily constipation. Q2 Give 4 causes of constipation which may be applicable in this case? Decreased dietary fibre Hypothyroidism Hyperparathyroidism Anxiety/depression IBS Drugs (codeine based – may have been used to treat previous back pain) Other common causes are less likely due to the young age and previous good health. 123 On further questioning, she reports an associated bloating feeling. She also believes she leads a healthy lifestyle. On examination of Lindsay there is nothing remarkable found. Q3 What investigations would you do, if any? There are no real indications for any investigations, however if other symptoms were present to indicate hypothyroidism or parathyroidism then the following would be indicated: Thyroid function tests Plasma Ca All tests come back normal. Q4 Give steps to your management of Lindsay. Description of IBS Reassurance Patient own management eg increase dietary fibre, increase exercise, decrease stress Medical therapy – osmotic laxative eg lactulose, anti spasmodic eg Mebeverine Q5 Name one complication of this disorder? Colonic diverticulae 124 3.14 Irritable bowel syndrome By the end of Phase II students should be able to: • recognise the presentations of irritable bowel syndrome • appreciate other common causes of chronic abdominal pain and how they may be distinguished • explain to a patient the nature of irritable bowel syndrome and its relationship to precipitants such as stress. 125 3.17 MP is a 35 year old man who was diagnosed with Type 1 diabetes mellitus at the age of 14 after presenting to his GP with polyuria, polydipsia and weight loss. Urine dipstick demonstrated the presence of glucose and ketones, which is not diagnostic of diabetes mellitus, but indicates the need for further investigation. Name three blood tests used to diagnose diabetes mellitus and the values that indicate presence of the disease. Random blood glucose > 11.1 mmol/L Fasting venous plasma glucose ≥ 7.0 mmol/L 2 hour oral glucose tolerance test > 11.1 mmol/L NOTE: These values refer to venous plasma levels, rather then that of venous whole blood. Diabetes mellitus increases the risk of cardiovascular disease. Which other co-existent cardiovascular risk factors can be screened / assessed in a diabetic patient? (Name 3) Blood pressure Cholesterol Smoking history Diabetic control (BMs, HbA1c) When Mr P was initially diagnosed he was educated on his condition, advised about the importance of diet, referred to a dietician, and started on insulin. You are concerned that Mr P is non-compliant. You are worried that he is not following your dietary advice with a large alcohol intake, and is not regularly taking his insulin. Which investigation can be used to determine a patient’s glycaemic control? What is the target value? What does this value indicate? HbA1c < 7 % Glycosylated haemoglobin levels relate to the mean glucose level over the previous 8 weeks (i.e. RBC half life) Later that week Mr N was found at home drowsy and a little confused following a late night where he consumed a lot of alcohol. Earlier that day he had complained of feeling shaky, sweating, pallor, heart pounding, and irritability. What is the likely diagnosis? 126 Hypoglycaemia Name two other ways that this condition may present. Coma Seizures Temporary paralysis You measure his blood glucose as 2.5. What management would you like to initiate? Oral sugar e.g. fruit juice, sugar lump, followed by long acting starch e.g. toast How would your management differ if he was unresponsive? Call an ambulance Glucose 25-50g IV or glucagon 0.5-1mg SC/IM – should see some improvement following this. Repeat after 20 minutes if no improvement If prolonged hypoglycaemia, may want to give dexamethasone 4mg/4hr IV to combat cerebral oedema. 3.17 Insulin dependent diabetes By the end of Phase II students should be able to: • identify patients with insulin-dependent diabetes • screen patients for co-existent cardiovascular risk factors • screen for diabetes-related complications • initiate management of a patient with IDDM, including the appropriate use of long- and short-acting insulins • determine a patient's degree of metabolic control • recognise diabetic ketoacidosis • participate in the management of diabetic ketoacidosis • recognise and manage hypoglycaemia • outline to patients the dietary principles of the management of IDDM 127 3.19 A long standing insulin dependent diabetic Mr B, presents at your clinic having recently been diagnosed with hypertension. You realize that the combination of long standing diabetes and hypertension puts Mr B at greater risk of cardiovascular complications; hence you decide to examine his cardiovascular system. Name 6 signs or symptoms you might expect to find on Mr B? Intermittent claudication angina pain reduced exercise tolerance diminished peripheral pulses reduced capillary refill, cold peripheries ischaemic skin changes poor healing and ulcers. How would you treat Mr B’s hypertension in order of preventing the development of cardiovascular complications? Treatment is dependent upon the BP; <145/80 and no microalbuminuria check BP every 6months >140/80 an <160/100 and no microalbuminuria, treat with antihypertensives; ACE inhibitor, beta-blocker or a thiazide >140/80 with microalbuminuria should be treated with either an ACE inhibitor or angiotensin 2 antagonist, with a target BP of 135/75 In addition to examining Mr B’s cardiovascular system you decide to perform fundoscopy to detect any retinal changes of diabetic retinopathy. Name the 4 stages of diabetic retinopathy with the key features of each? Background, diabetic maculopathy, pre-proliferative and proliferative Explain why these retinal changes develop in diabetic patients? 128 These changes are the result of microvascular disease, with an increase in the thickness of the basement membrane, and increased permeability of the retinal capillaries. The result is the formation of microaneurysms that haemorrhage and later lead to new vessel development. Diabetic retinopathy is one of the complications that can develop in a diabetic patient. List 4 other complications of diabetes and whether they are microvascular or macrovascular changes? Neuropathy – microvascular Nephropathy – microvascular Peripheral vascular disease –macrovascular Ischaemic heart disease –macrovascular Stroke - macrovascular What are the pathological differences between microvascular and macrovascular changes? Microvascular disease involves the small vessels in the retina, glomerulus and vasa nervorum, whilst macrovascular involves the larger vessels. In microvascular disease there is progressive narrowing of the vascular lumina due to hyperglycaemia-induced microvascular hypertension, basement membrane thickening and increased vascular permeability. Macrovascular disease involves atherogenesis; the infiltration of lipid in the intimal layer resulting in plaque formation and occlusion of the vessel. Finally, you decide to manage Mr B with a multidisciplinary approach. Name 4 health professionals/ agencies that could be involved in his care? Endocrinologists/ GP/ diabetic nurse/ chiropodist/ophthalmologist/renal physician/orthopaedic surgeon 3.19 Long term complications By the end of Phase II students should be able to: • recognise the long term cardiovascular complications of diabetes • manage hypertension appropriately in diabetics 129 • recognise renal disease in diabetics and refer appropriately • recognise diabetic neuropathy • recognise autonomic neuropathy • recognise the potential importance of skin lesions in diabetics • recognise diabetic retinopathy and refer appropriately • describe the mechanisms underlying these complications and the potential for their prevention 130 3.23 Alice is a 66-year-old housewife who complains of weakness and episodes of fainting, which makes her spend most day in bed. She also complains of nausea, vomiting and abdominal pain. Alice also mentions in passing that her friends have been commenting on her tan, even though she has not been on holiday. a) what could be the diagnosis? (name 2) Addison’s disease Congenital adrenal hyperplasia a) give two common causes for this condition? Autoimmune Tuberculosis HIV/AIDS Metastatic carcinoma Bilateral adrenalectomy b) what is the name of the test that will confirm your diagnosis and give a brief explanation of the procedure? Short ACTH Stimulation test (Synacthen Test) Do plasma cortisol, inject tetracosactide IM (exogenous ACTH), plasma cortisol after 30 minutes. Cortisol remains low in Addison’s disease, but if above 600nmol/l then exclude Addison’s disease c) name two drugs that may be given to this patient? Glucocorticoid replacement with either hydrocortisone or prednisolone Mineralocorticoid replacement with fludrocortisone 131 Alice was given treatment. 2 years later she complained of being overweight, easy bruising, excess hair growth and purple marks on her stomach. d) what is the name of this condition? Cushing’s syndrome EXTENDED Why has Alice got a ‘tanned’ appearance to her skin? Lack of adrenal hormones causes feedback on the hypothalamo-pituitary axis to increase CRH and therefore ACTH production. ACTH contains MSH-like sequences that cause pigmentation due to stimulation of melanocytes. OBJECTIVES 3.23 Adrenal gland hormones By the end of Phase II students should be able to: • recognise the symptoms and signs of Addison's Disease • confirm the diagnosis of Addison's Disease • initiate the immediate management of Addisonian crisis • recognise symptoms and signs of Cushing's Syndrome • confirm the diagnosis of Cushing's Syndrome • participate in the long term management of Addison's Disease and Cushing's Syndrome 132 3.24 Dr Patel thrusts another rather large set of notes and asks you to see Mr PA in the side room. On glancing at the GP letter you read: ‘This 45yr old gentleman has been complaining of long term headaches and visual field disturbances suggestive of a pituitary lesion. The results of his glucose tolerance tests (GTT) are consistent with acromegaly. I would be grateful if you could review his care’ Which type of visual field loss would you expect to find in this patient? (1 mark) Bi-temporal hemianopia (tunnel vision) List four other clinical features you would expect to find during a physical examination on this patient other then those already mentioned. (2 marks) prominent eyebrow ridge increased interdental space Prognathism, greasy skin, large tongue, spade like hands, features relating to carpel tunnel syndrome (diff from Prognathism) husky voice enlarged feet Briefly describe how you would perform a glucose tolerance test? (2 marks) Overnight fasting Oral glucose 75mg taken at T 0 mins Monitor BM and growth hormone at timed intervals, 0>30>60>90>120 mins Absence of GH suppression suggests acromegaly. Suggest two non-biochemical investigations you may carry out to assess the severity of Mr PA’s main condition. (2 marks) MRI brain: assess size and spread of pituitary lesion 133 X-ray feet and hands: looking for osteophytes and increased joint space ( Mr PA condition is a pit adenoma causing excessive levels of GHRH and thus GH causing acromegaly. Carpel tunnel is not his main problem thus nerve conduction tests are not investigations you would order yet. ) Dr Patel, being impressed with your answers so far, asks how you would treat this patient with acromegaly. (Assume he is otherwise fit and well). (3 marks) Surgery (hypophysectomy) is gold standard with adjunct radiotherapy to shrink the lesion. (If unfit for surgery then somatostatin analogues (octeotide) and dopamine agonists (bromocriptine) are effective) Regular pituitary function tests are essential. Extended question Describe the clinical features you would expect to find if Mr PA’s condition was left untreated (E3 marks) Acromegaly > Hypopituitarism. Hypothyroidism features Androgen deficiency (loss libido, hypogonadism, loss of muscle bulk) Corticotrophin deficiency (postural HT, weight loss, low sodium) 3.24 Pituitary gland hormones By the end of Phase II students should be able to: • recognise the circumstances when hypopituitarism may occur • recognise the possibility of hypopituitarism in patients with 'non-specific' symptoms • initiate investigations for posterior pituitary function in patients with polyuria • initiate investigations of the cause of hypopituitarism • recognise acromegaly • initiate investigations for acromegaly • outline to patients the possible treatments for acromegaly 134 1) A)-Mr A is a 49-year-old widower and has just joined your GP’s practice. The practice nurse has referred him because during his enrolment check-up, a BP of 173/90 was recorded. You repeat his BP and it is 176/101. What is the difference between essential and secondary hypertension? (1 mark) Essential hypertension has no specific underlying cause, lifestyle plays a large part, and secondary hypertension is the result of a range of pathological processes. B)-Give 4 possible causes of secondary hypertension: (4 marks) (Any 4 of below) Renal parenchymal disease eg chronic pyelonephritis, glomerulonephritis, polycystic disease Renal artery disease eg atherosclerosis, fibromuscular dysplasia, vasculitis Obstructive uropathy eg hydronephrosis 2 to stone/tumour Congenital eg coarctation of the aorta Drugs eg combined oral contraceptive pill, NSAID’s Endocrine eg phaeochromocytoma, hyperaldosteronism, Cushing’s syndrome, acromegaly C)-At this first consultation, you are struck by Mr A’s large facial features including his jaw, nose, brow and large hands. You suspect that Mr A maybe suffering from acromegaly. Name 4 other signs or symptoms of acromegaly other than the ones mentioned above: (4 marks) Interdental separation, headaches, excessive sweating, visual deterioration, tiredness, wt gain, amenorrhoea/oligomenorrhoea, galactorrhoea, impotence, poor libido, deep voice, hirsutism, goitre, breathlessness, tingling in hands/carpel tunnel syndrome, polyuria/polydipsia, muscular weakness, joint pains, thick greasy skin, tight rings. D)-Describe one of the aetiologies for acromegaly: (1 mark) Benign pituitary tumour secreting GH (commonest) Pituitary carcinoma Carcinoid tumours that secrete hypothalamic GH-releasing hormone. 135 E)-In the history Mr A went on to confirm that he had been experiencing headaches and had noticed a change in his appearance but put it down to his age. In view of his possible diagnosis, name 3 investigations would you like to do and why? (6 marks) (3 of any, 1 mark for investigation, 1 mark for reason) GH levels – excessive circulating levels of GH, although this is non-diagnostic on its own because transient raised levels are normal during stress IGF-1 levels – almost always raised in acromegaly as a result of increased GH levels Glucose tolerance test – GH is measured during a GTT, in healthy individuals, GH is undetectable during the test, because hyperglycaemia inhibits GH secretion. MRI scan of pituitary – pituitary neoplasm is commonly the cause Prolactin levels – frequently, the adenoma secretes both GH and prolactin Assessment of visual fields – bitemporal hemianopia caused by pressure on the optic chiasm by the tumour. CXR and/or ECG – left ventricular hypertrophy secondary to hypertension F)-A diagnosis of acromegaly is eventually made. What are the risks to Mr A if his condition goes untreated? (2 marks) Any hypertension related illness, eg coronary heart disease, heart failure, cerebrovascular disease, PVD Increased risk of neoplasia, especially large bowel tumours G)-Discuss the treatment options available? (4 marks) (Any 2; 1 mark for treatment, 1 mark for a relevant point) Surgery – Trans-sphenoidal route is usually used, 90% of microadenomas are cured. Complications include hypopituitarism, meningitis, intra-operative bleeding and death Radiotherapy- Often used if attempts at surgery do not reduce GH levels. Hypopituitarism may occur. Medical therapies – Most effective is Octreotide, a somatostatin analogue, which inhibits GH secretion in 60%. Bromocriptine, dopamine agonist reduces GH release, less effective Extended Question H)-Explain the mode of secretion and physiological action of GH (4 marks) 136 GH is secreted by the anterior pituitary GH acts directly on tissues, but most effects are mediated via IGF-1 (insulin-like growth factor), produced mainly from the liver after stimulation from GH. Stimulates cell growth and replication by accelerating the rate of protein synthesis Increase uptake of amino acids, especially after a meal Virtually every tissue responds, skeletal muscle and chrondrocytes especially Counter regulatory to insulin, i.e., increases blood glucose via stimulating hepatic gluconeogenesis and inhibiting glucose uptake by muscle Secretion of GH occurs in bursts, in response to dual control by GHRH and GHRIH; it is stimulated by low blood glucose and high blood amino acids, and during REM sleep. Objective: pituitary gland abnormalities 137 3.25 John is 18-years-old and is walking through the park when he sees some school friends playing football. They ask if John would like to join in and hesitantly, because he hasn’t done any exercise for years, he agrees to make up the numbers. Towards the end of the game John is very sweaty, his hands are shaking and collapses on the floor. At hospital John is diagnosed as being in a hypoglycaemic coma. a) define hypoglycaemia in relation to plasma glucose levels? <2.5mmol/l b) give five causes of hypoglycaemia?(any 5) Unexpected or unusual exercise Alcohol Insulin/ oral diabetes drugs overdose Malabsorption Addison’s disease Hypopituitarism Congenital adrenal hyperplasia Liver failure Alcohol abuse Hypothermia Insulinoma and other metastatic disease c) what other signs and symptoms may his friends have noticed? Sweating Hunger Drowsiness Personality change Fits Anxiety Confusion Headache 138 Nausea Tiredness d) how would you treat such a patient? ABC 50-100ml 50% dextrose IV fast followed by 0.9% saline flush as dextrose harms veins Glucagon 1mg IM if no venous access EXTENDED What is Whipple’s triad and which condition does it diagnose? Diagnoses insulinomas by symptoms are associated with fasting or exercise hypoglycaemia is confirmed during these episodes glucose relieves the symptoms 3.25 Hypoglycaemia By the end of Phase II students should be able to: • recognise the possibility of hypoglycaemia and the circumstances under which it may occur • initiate appropriate initial investigations • initiate immediate management of hypoglycaemia 139 A 21 year old female presents to A&E with a GCS of 9, abdominal pain and vomiting. She is hyperventilating. She appears quite thin. Her friend tells you she has been drinking heavily all evening but mostly soft drinks with little alcohol. The nurse calls you over to show you she has an insulin pen in her jacket. You ask for a blood glucose measurement which comes back at 26mmol/L. 1. Give the most likely cause of her symptoms [1 mark] Diabetic ketoacidosis (DKA) 2. List 3 factors which may precipitate this condition [3 marks] Infection Poor compliance Recent diagnosis 3. You decide to investigate further. List 5 investigations that would be suitable in the acute phase. (be specific, don’t just put ‘blood test’) [5 marks] FBC HbA1c U+E Glucose Blood gases Serum amylase CXR Ketones in urine or blood 4. Give 3 interventions to manage this patient [3 marks] Insulin Sliding Scale Fluid replacement Potassium supplementation Nil by mouth Treat precipitating cause if any 140 5. Explain why the Type 1 diabetic with severe hyperglycaemia will enter a ketotic state while the Type 2 diabetic will tend towards the hyperosmolar nonketotic state. [5 marks] Low insulin prevents the uptake of glucose into tissues. This prevents cells using glucose as an energy source. Alternatives are required. Energy is gained by producing fatty acids from lipolysis. These are converted into ketones by the liver. These are present in the circulation and produce a ketotic state In Type 2 diabetics there is plenty of insulin present but there is resistance to it’s action. The blood glucose produces a hyper osmolar circulation which produces its clinical effect due to osmotic pressures leading to cellular dehydration Ojective: HONK and DKA 141 3.26 Sidney is a 55 year old bus driver. He presents to A+E with non-specific symptoms of headache, confusion and drowsiness. Bloods results: serum Na levels of 102mmol/l (130-145mmol/l) Q1: Name 3 medical disorders causing ↓Na: Hypothyroidism Addisons’ disease SIADH ↑ extracellular volume (heart failure, liver failure) Q2: Treatment generally involves correcting the underlying cause. But how would you manage this patient acutely? Mild: Fluid restriction. Moderate: IV saline and frusemide. Severe (emergency): IV 0.9% saline or hypertonic 1.8% saline. Gradually ↑Na. can combine with frusemide. Caution in heart failure. Q3: What other investigations would you consider, to establish the cause? Hypothyroidism (TFTs) Addisons’ disease (blood plasma, synacthen test) SIADH (plasma osmolality, urine osmolality, U&Es) heart failure, liver failure ( BNP level, CXR, ECG, LFTs) 142 Deepak presents to his GP with a hx of polydipsia and polyuria. Investigations show he has a ↑ serum Na level of 158mmol/l. Q1: Name 4 causes of ↑Na: Diabetes insipidus, ↓ Water intake, ↑ Fluid loss with less Na loss (vomiting, diarrhoea, burns) Incorrect IV fluid replacement (excessive saline) Primary aldosteronism Renal disease (ATN) Q2: how would you initially manage this (relating management to both hypovolaemia and hypervolaemia): Hypovolaemia: Give water orally, or 5% dextrose IV slowly (guided by urine output, and plasma Na. Avoid hypotonic solutions! Hypervolaemia: diuretics to remove Na and ↑ fluid loss. Q3: He was later found to have Diabetes insipidus, what test confirms the diagnosis of this condition? How is it performed, and how would you interpret the results? Water deprivations o Deprivations of water for ~9hours o Injection/intranasal administration of ADH (Desmopressin) o Measure urine osmolarity after hourly intervals (also can take serial plasma samples) Central DI: urine osmolarity increases Nephrogenic DI: urine osmolarity changes very little 143 Rose has recently been diagnosed with type I diabetes mellitus. She presents to A+E with signs and symptoms consistent with DKA. Blood results show that her serum potassium is 6.7mmol/l. Q1: Why do you get ↑K in DKA? Metabolic Acidosis in DKA, causes redistribution of electrolytes to help minimise acidosis. K:H exchanger (↑ extracellular K, ↑ intracellular H) Q2: List 4 other causes of ↑K levels. Renal failure: main cause, due to oliguria Drugs: K sparing diuretic (main), ACEi, β-blockers, excess K therapy, massive blood transfusion. Redistribution to ECF: Acidosis-(K:H exchanger), cell lysis (crush injury, haemolysis, strenuous exercise, rhabdomyolysis, burns). Endocrine: hypoaldosteronism (Addison’s disease) Artefact: haemolysis of RBC’s in collecting bottle, delayed analysis-leakage of K. Q3: What ECG changes would you expect to see with increasing K levels? Tall/tented T waves, small/flat P waves, wide QRS complex, VF. Q4: List 5 options in treating K levels >6.5mmol/l? 10ml calcium gluconate. This provides cardio-protection, doesn’t lower K levels!! Insulin + glucose: moves K into cells, via Na:K: Nebulised salbutamol: moves K into cells. Consider Calcium resonium PO or PR to bind K in the gut, SE: constipation. Sodium bicarbonate: corrects acidosis. High dose frusemide Haemodialysis: 144 Jaswinder has a past hx of hypertension, controlled by use of a diuretic. On routine bloods his serum potassium was 2.4mmol/l. Q1: name some other causes of low serum K? Drugs: diuretics (main cause), β-adrenergic stimulation (salbutamol) Mineralcorticoid excess: Conn’s syndrome, Cushing’s syndrome, corticosteroids, ectopic ACTH, hyperaldosteronism. Redistribution: alkalosis (K:H exchanger), excessive insulin. Vomiting (pyloric stenosis, bulimia nervosa), Diarrhoea Q2: What ECG changes are associated with ↓ K? Prolonged P-R interval, small or inverted T waves, prominent U waves (after T wave), depressed ST segment. Q3: How would you manage K levels <2.5mmol/l? IV KCl not more than 20mmol/h (never give a fast bolus, peripheral vein damage) 3.26 Abnormalities of sodium and potassium By the end of Phase II students should be able to: • initiate investigation of hypo and hyper natraemia and hypo and hyper kalaemia • initiate management of these conditions 145 4.3 You are a doctor working in an Emergency Department, you are called to see Miss HG a 15 year old girl who has fallen from her horse. She has been triaged and sent for investigations. Question 1: What is this investigation, what is it of and what does it show? [3] X –Ray, Clavicle, Fracture of distal 1/3. Question 2: When presenting an X ray what are the important features? [4] Patients name, age, penetration,type of X ray, eg PA view of shoulder Question 3: How may the injury in question 1 be managed? [3] Pain relief, broad sling or collar and cuff, review in around 3 weeks. Will not usually require any surgery. While you are seeing Miss HG she complains of an odd feeling in her wrist, you examine it. Question 4: What features are you looking for on examination of the wrist? [4] Neurovascular compromise (wiggle your fingers, can you fell me touching this, distal 146 pulses). Any painful areas, deformity/swelling, open fractures, bruising. Extended Question: What are the stages of bone healing? [4] Haematoma –Granulation Tissue – Callus Formation – Bony consolidation Remodelling - Extra notes: Other Fractures You May see: Colles Fracture: Forearm fractures account for 55% of childrens fractures. May result in dinner fork deformity. 147 Scaphoid fracture: If suspected (e.g. pain in anatomical snuff box) but not visible on initial X ray then put in plaster and re Xray after 2 weeks Ankle Fracture: High impact, will always require treatment, from plaster of paris backslab to internal fixation. 148 Anterior Shoulder Dislocation: Trauma, pain, loss of movement and shoulder contour. Objective 4.3 Investigations By the end of Phase II students should be able to: • recognise the radiological features of fractures in general and the specific features of the commoner fractures seeking advice where necessary • recognise the radiological features of subluxation and dislocation 149 4.4 1. A 25 year old man trips on a tree branch as he walks down a steep incline and falls awkwardly. He immediately experiences severe pain in his left leg and is unable to weight bear on standing. a. State 4 clinical features of a fracture Pain Loss of function Tenderness Deformity Swelling Crepitus (grating of the broken ends) b. You check his airway, breathing and circulation and find that he is not shocked. You find that there are no abrasions to the skin overlying the fracture. What would be your first 4 steps in the immediate first aid care of this fracture? Step 1 Immobilise the fracture Step 2 Remove tight clothing such as boots, or anything that may impede circulation Step 3 Check circulation, sensation and motion beyond fracture site Step 4 Give pain relief c. What is the main investigation of choice? Plain radiograph left leg d. What 2 features are you looking for on this investigation of choice? Alignment (displacement, angulation, rotation) Bone pathology ( If open wound, look for trapped air and foreign body) e. You find that there is a closed transverse fracture to the lower third of this man’s left fibula. It is poorly aligned. What should be done to manage this fracture? Reduction (under anaesthesia) Fixation Immobilisation 150 f. ‘Fracture disease’ follows immobilization – what 3 clinical features are associated with this condition? Muscle atrophy Osteoporosis Stiff joints g. Post-operatively this man is doing well and is about to be discharged home when he experiences pain in his left calf. What are you concerned this may be a symptom of? Compartment syndrome h. And signs would you look for to ascertain this diagnosis ? Name 3. (3 of the following) Redness Skin mottling Blisters Swelling Pain on passive muscle stretching i. What is the pathological process behind this condition? (5 points) and what is the surgical management for this condition? Vicious cycle of pressure (from limbs own dead weight when immobile) vascular occlusion hypoxia necrosis increased pressure Surgical management: j. Fasciotomy He recovered and was later discharged home. This very very unlucky man suddenly starts to experience breathlessness 10 days after his accident. What is ur differentials? (name 2) Fat embolism Pulmonary embolism k. choose one of the above differentials you have mentioned, what other signs might you be looking for? Name 3. For fat embolism: Dyspnoea Confusion 151 seizures Coma pyrexia Hypoxia For pulmonary embolism: Dypnoea Tachycardia cyanosis Raised JVP Pleural rub hamoptysis l. Thankfully, this man makes a full recovery and on follow up his check plain radiograph shows a well healed fracture. What are the pathological steps that lead to bone healing? 5 points Haematoma formation (1) vascular granulation tissue subperiosteal osteoblast stimulation bone matrix endochondral ossification deformable woven bone (callus) (1) Replacement by lamellar bone (1) Remodeling (1) Fracture union (trabecular) (1) m. What 5 factors may delay or even arrest the repair of a fracture? Movement Interposed soft tissues Gross misalignment Infection Pre-existing bone disease 4.4 Fractures-general 152 By the end of Phase II students should be able to: • manage the immediate first aid care of a fracture • describe when the possibility of fracture should be suspected and request appropriate radiological investigations • apply a Plaster of Paris backslab to upper and lower limbs • describe to a patient the management of the commoner fractures • describe how the processes of healing may be promoted or retarded • recognise the possibility of acute compartment syndrome and fat embolism 153 4.5 Mrs OL is a 70 year old lady that has been brought to the Emergency department. She has had a fall. She complains of pain in her right leg and right wrist. Question 1: What signs may be found if her neck of femur is fractured? [2] External rotation and leg shortening. Question 2: Outline some tests that should be conducted prior to surgery?[3] X-Rays (especially lateral views), bloods (FBC and U&E). Look at this investigation. Question 3: What is the name and resulting deformity of this common fracture in postmenopausal women?[2] Colles fracture and dinner fork deformity. Question 4: Aside from increasing age name 4 other causes of osteoporosis? [4] Anorexia, alcoholic, steroid use, Cushings disease, hyperparathyroidism, thyrotoxicosis, myleoma, primary biliary cirrhosis, rheumatoid arthritis. 154 Question 5: Name, aside for osteoporosis, two causes of pathological fractures? Pagets disease (increased bone turnover associated with hypernucleated ostroclasts, causing bone remodelling, enlargement and weakness) and secondary deposits (common cancers include breast, lung, thyroid, kidney, prostate, cervix, bowel, and from multiple myeloma). Extended Question: What is the blood supply to the femoral head and why is this relevant in this case? Lateral circumflex femoral artery and medial circumflex femoral artery and the artery to the femoeal head which is useless in older people. That is why a fracture can disrupt the arterial supply and lead to avascular necrosis of the femoral head. N.B: Bits I couldn’t fit in HRT and menopause, intertrochanteric and intracapsular fractures. 4.5 Fractures-the Elderly By the end of Phase II students should be able to: • recognise those fracture patterns particular to the elderly • recognise the underlying aetiological factors predisposing to fracture in the elderly • request appropriate radiographic examinations • recognise the possibility of significant underlying disease which may influence definitive treatment of the fracture and initiate appropriate investigation 155 4.7 27 year old male presents in A&E having sustained a compound fracture of the tibia bone following an RTA. 1. What is his immediate management? Airway- check airway patent. If not, try jawthrust or headtilt and chin lift. Insert geudal airway if needed or other airways (ET, tracheostomy) if it is severely compromised. Breathing- check RR, pulse oximeter to check O2 sats. Circulation- check BP, pulse, capillary refill. 2x IV cannula insertd and infuse fluid (type of fluid depends on hospital and severity of the patient) if needed. 2. a) Outline the treatment/ management of compound fractures. Emergency theatre within 6 hours. The wound should be covered (and compressed) with an antiseptic dressing and the limb immobilised using a splint (whilst waiting for theatre). (Injury should be photographed so repeated examination is avoided). If there is gross deformity, manipulation under sedation may be needed before splinting. The neurovascular status must be checked before and after this is carried out. In theatre, the wound is thoroughly washed out and any contaminated or dead tissue is debribed. This is to avoid infection and better union for healing. The fracture is assessed and stabilised (usually by internal or external fixation) b) Which 2 drugs should you consider broad spectrum antibiotics (such as cefazolin, or clindomycin if there is pencillin allergy) tetanus booster should be given 3. Eight hours later he is complaining of continued pain in his lower leg and his posterior tibialis and pedis dorsalis pulses are absent. Write a note on your diagnosis and management. Compartment syndrome. As pressure rises within a fascial compartment in the limb (due to e.g. haemorrhage), the capillary blood flow to the tissues decreases. Ischaemia occurs when the capillary pressure is less than the compartment/ tissue pressure. Management: Elevate the limb, remove all bandages and split the cast all 156 the way to the skin. If this fails to relieve the pain, remove the plaster. If symptoms continue then a fasciotomy maybe needed to relieve the pressure. 4. What are the immediate, early and late complications of a compound fracture? Immediate Haemorrhage Neurovascular and visceral damage Early Compartment syndrome Infection (worse if associated with metal work) Late Problems with union (delayed, non- and malunion) Thromboembolic events (prolonged immobilisation) Avascular necrosis Sudek’s atrophy / reflex sympathetic dystrophy Myositis ossificans Joint stiffness Growth disturbance 5. Write a note on the physiological process of bone healing. 5 stages: Bleeding into the fracture An inflammatory reaction is set up and granulation tissue forms The cells proliferate and early bone and cartilage form – callus This then consolidates – as woven bone which then transforms to stronger lamellar bone The bone then remodels to the normal stresses its placed under 4.7 Open Fractures 157 By the end of Phase II the student should be able to: • recognise an open fracture • apply the principles of immediate stabilisation and wound coverage • prescribe tetanus toxoid and antibiotic appropriately • have an understanding of the importance of debridement • act as part of the team in the definitive care for these fractures • recognise the possibility of complications such as chronic osteomylitis 158 4.7 A 32-year-old man is brought by paramedics to A&E after being involved in a motorcycle accident; impact occurred at 65 miles per hour. (ABCs) assessment, x-rays of the lateral C-spine, chest, and pelvis have been obtained. No injuries are detected. The patient is hemodynamically stable. Upper limb examination normal. Examination of the left hip, knee, and ankle is normal, and the distal neurovascular exam is intact. Examination of the right lower extremity reveals a 12-cm break in the skin, with exposed bone and periosteum on the anteromedial aspect of the leg. There is an obvious deformity of the leg. An anterior-posterior and lateral x-ray of the tibia and fibula is taken. The patient has a midshaft tibia/fibula fracture with moderate comminution. How would you dress the wound? A sterile dressing such as dilute Betadine should be applied in A&E and should not be removed until the patient arrives in surgery. Multiple examinations of the wound should be avoided to prevent nosocomial contamination and infection. Would you start him on antibiotics or wait until he goes to surgery? Antibiotics should be started as soon as possible. At our institution, a first-generation cephalosporin such as cefazolin 1 g every 8 hours and an aminoglycoside such as gentamicin 80 mg every 8 hours are the antibiotics of choice. At other institutions, cefazolin, vancomycin, and gentamicin, alone or in combination, are used. The patient's last tetanus booster was 7 years ago and he completed the initial 159 series as a child. The current wound appears dirty. What would you do now? In this case, a tetanus booster is warranted (Td 0.5 cc IM). What is the most important aspect of caring for open fractures? Debridement of all necrotic, nonviable tissues including skin, subcutaneous tissue, muscle, tendon, and bone are crucial to the successful management of open fractures. If tissues are devitalized, antibiotics and nutrients, which are important in fighting bacteria and in wound healing, will not reach them. The devitalized tissues will become necrotic and become a nidus for infection. What are the two forms of fixation avaliable to stabilise a fracture of this sort? Exteranal fixation - An external fixator is indicated for bad soft tissue injury with or without gross contamination, because dirt can enter the canal during nailing. Internal fixing (intramedullary nail)- An intramedullary nail is ideal because it will not cause further soft tissue damage. The downside of a nail is that you disrupt the intramedullary blood supply of bone, which could have an effect on the healing of the fracture. 4.7 Open Fractures By the end of Phase II the student should be able to: • recognise an open fracture • apply the principles of immediate stabilisation and wound coverage • prescribe tetanus toxoid and antibiotic appropriately • have an understanding of the importance of debridement • act as part of the team in the definitive care for these fractures • recognise the possibility of complications such as chronic osteomylitis 160 4.8 Tom is 35-year-old man who presents to A&E with an injured knee. He was tackled whilst playing football, and fell twisting his knee. It started hurting immediately, and has since become swollen; he is finding it difficult to weight bear. i) Describe the structures that help to stabilise the knee. Anterior - the tendon of quadriceps femoris Lateral - the ilio-tibial tract + tendon of biceps femoris Posterior - popliteus + semimembranosus Medial - tendons of sartorius, gracilis + semitendonosus. Or Static stabilisers = intrinsic static stabilisers are the anterior + posterior cruciate ligaments. Extrinsic static stabilisers are the medial + lateral collateral ligaments. Dynamic stabilisers = Quadriceps – rectus femoris Vastus lateralis/medialis/intermedius Hamstrings – Biceps femoris Semitendonosus Semimembranosus. ii) In an injury resulting from a side impact on the knee, how might the soft tissues of the knee joint be affected? May result in an ‘unhappy triad’ of injuries, namely a torn anterior cruciate ligament, a torn medial/tibial collateral ligament and a torn medial meniscus. iii) What features of the menisci and ligaments make the above set of injuries more likely? The medial collateral ligament is firmly attached to the medial meniscus, which means that frequently tearing of the ligament also results in tearing or detachment of the meniscus. Meniscal tears more commonly involve the medial meniscus as it is more firmly fixed to the tibia, compared to the lateral meniscus. 161 iv) You examine the knee; name two tests that you would use to investigate whether an effusion was present in Tom’s knee. Patella tap test – if there is a substantial effusion then the patella will spring back against your fingers. Bulge sign – useful for smaller effusions. v) You continue your examination with the following tests – describe in the case of Tom, what you might expect to find on examination? McMurray’s test? If there is a cartilage tear, its engagement between the tibia and femur during this manoeuvre leads to severe pain, and sometimes locking. Anterior draw test? Rupture of the anterior cruciate ligament will allow the tibia to slide anteriorly on the femur to a greater extent than on the unaffected side. Posterior draw test? As the posterior cruciate ligament in unlikely to be affected in this injury, a positive posterior draw test is unlikely. vi) You decide that Tom has indeed ruptured is anterior cruciate ligament, and torn his medial meniscus – which surgical procedure may he benefit from? Explain to him what it involves and what the complications may be. Trimming or repair of the torn meniscus is essential; this is done via an arthroscopy. Surgical intervention reduces the recurrent pain, locking and swelling but not the risk of secondary osteoarthritis. An arthroscopy involves a general anaesthetic, and the examination of the inside of the knee joint via a camera inserted through a small incision. During the procedure repair and trimming of the cartilage can be undertaken using ‘keyhole’ surgical techniques. The complications include bleeding, infection, knee swelling, recurrence of symptoms, and reaction to the anaesthetic. vii) What is the definition of a strain, and a sprain? Sprain – injury to a ligament, caused by sudden overstretching. As the ligament is not severed it gradually heals but may take several months. Should be treated by cold compress. Strain - Excessive stretching of a muscle resulting in pain and swelling. What are the treatment options for patients diagnosed with a sprain or strain? 162 RICE – rest, ice, compression, elevation Analgesia/anti-inflammatories Use of supports vii) A patient presents with a painful swollen knee, apart from trauma what are some of the differential diagnoses? Septic arthritis Osteoarthritis Gout Osteomyelitis Haemathrosis What investigation(s) could you perform to differentiate between causes of knee swelling? pyrexial? FBC + Clotting screen Blood cultures – often positive in septic arthritis Joint x-ray Joint aspirate – microscopy + cultures; crystals in gout, gram stain + culture may isolate infective organism Serum urate – usually raised in gout >600umol/L viii) How may a joint become infected and what factors may make an individual more prone? direct injury blood-borne infection from an infected skin lesion, or other site by haematogenous spread. Chronically inflamed joints are more prone to infection e.g. RA, as are artificial joints Immunosuppressed patients – drug induced/AIDS Elderly Alcohol + drug abuse. 163 4.8 Soft Tissue Injuries By the end of Phase II the student should be able to: • distinguish clinically between strain, sprain, and rupture of ligaments and muscles • assess traumatic knee effusions • initiate investigations in patients with soft tissue injuries • initiate management of soft tissue injuries • recognise the common underlying aetiological factors predisposing to infection in soft tissue injuries and wounds • identify infection in soft tissue injuries • request appropriate radiographic examinations and other investigations as required to assess the extent of soft tissue infections • recognise the possibility of a gas-forming infective organism being present, the significance of this to the patient's health and the principles of investigation and management of this infection • assess skin lacerations, including the recognition of foreign bodies, perform simple suturing under local anaesthesia and dress wounds • initiate surgical management of soft tissue injuries 164 4.9 Mr Willow, 25 years old presented in A&E having sustained a chain saw injury to his left hand. a) What further questions would you ask? When, where, how? Dominant hand? Occupation? Hobbies? Previous hand injuries and disability? b) On examination list 3 features you would look for on; i. Inspection Hand posture, where the lacerations are, what is underneath it (tendons, vessels, nerves), is hand/finger perfused? Is there soft tissue loss? ii. Palpation ulnar and radial pulses present, is hand/fingers cold, is sensation normal distal to injury. range of movement From the examination you suspect he has injured a flexor tendon in his hand. c) Name the two tendons you are concerned about? flexor digitorum superficialis flexor digitorum profundus d) How could you test the integrity of these tendons? FDS inserts into middle phalanx, FDP inserts into distal phalanx. Failure to flex the DIP joint against resistance indicates divided FDP. If this is intact 165 but flexion at PIP joint is affected then division of FDS. You have also noticed he has a laceration at the wrist. e) Which nerves are you concerned he may have damaged? Median ulnar f) Give the clinical findings for each nerve stated if injured. median – unable to oppose thumb (paralysis of thenar muscles), fine control of 2 nd and 3rd is impaired (first two lumbricals impaired). APE HAND on trying to make a fist. Sensory lost over thumb and adjacent two and half digits. ulnar – difficulty making a fist because of paralysis of most intrinsic hand muscles (these muscles put fingers into a position of flexion at MCP and extension at interphalangeal joints) and unopposed long flexors. CLAW HAND . Sensory loss over medial one and half digits. g) What clinical signs would suggest a vascular injury? Pulselessness, temperature, colour, capillary refill, venous return, swelling. Note absent distal pulsation or pulsating haematomas. Consider the management of this patient h) What are the indications for surgical repair? Name 3 tendon injury (open). Nb. Closed rupture of for example extensor tendon (mallet finger) can often simply be splintered. nerve injury i) Outline the need for hand rehabilitation to the patient, 166 Rehabilitation involves protected mobilization allowing early movement without excessive stress on the tendon repair. Wear a splint. It restores gliding function, minimising adhesions and increases tensile strength. Greatly aiding restoration of function. 4.9 Limb Injuries By the end of Phase II the student should be able to: • diagnose nerve and tendon injuries in the hand • identify injuries needing operative repair • discuss • identify vascular injury in the upper and lower limbs • identify division of tendons in the upper limb rehabilitation in broad outline with the patient with the injured hand 167 4.10 You are a member of an air ambulance team attending to a 28 year old man with multiple injuries at the site of a road traffic accident. 1. State, in order of priority your measures to ensure patient survival until transfer to a trauma centre Ensure airway patency and adequate ventilation by administering supplementary oxygen. Intubate and ventilate manually if necessary Immobilise cervical spine and place patient on a long spine board. Restore circulatory blood volume by crystalloids, plasma expanders and colloids as necessary with pulse, BP, JVP monitoring Commence head injury observations. Alleviate pain with narcotic analgesics (5 marks) 2. Whilst you are attempting to stabilize the patient, he becomes increasingly breathless. i) State the two probable causes for his progressive respiratory failure Tension Pneumothorax Haemothorax (2 marks) ii) List the clinical signs you would elicit to confirm your diagnoses. Cyanosis Tracheal shift Hyper-resonance or dull to percussion, with diminished or absent breath sounds in the chest Evidence of injury to chest wall on gently springing the rib cage. (4 marks) iii) What would be your immediate management of a tension pneumothroax? 168 Wide bore cannula incision in the mid clavicular line, 2 nd intercostals space on the affected side. (2 marks) iii) State one blood investigation that would be particularly useful to monitor his condition (if you had available facilities). Arterial Blood Gases (1 mark) 3. The patient is trapped in the wreckage of his vehicle and his transfer is delayed by three hours. i) Discuss your supportive measures. Prevent hypothermia, administer oxygen and support ventilation. Set up iv infusion and maintain normal blood pressure Maintain constant verbal and tactile communication and reassure the conscious patient. Treat life and limb threatening emergencies as facilities permit. (4 marks) ii) What is meant by “the golden hour” The golden hour is the 60 minutes after the initial trauma when fairly severe injuries can still be treated and lives saved. (2 marks) Extended question: Draw and label a chest drain. (5 marks) 169 4.10 Multiple Trauma By the end of Phase II • the students should be able to: identify the basic principles of resuscitation in the multiply traumatised patient according to ATLS guidelines • be aware of the injury severity grading systems • describe the importance of the 'golden hour' • identify the range of investigative procedures in a patient with multiple trauma such as radiographs, peritoneal lavage and urethography and be aware of the indications for these • identify the indications for immediate life support procedures such as endotracheal intubation, needle thoracocentesis or insertion of chest drain and drainage of cardiac tamponade 170 4.11 Mr Segaren, a 25 year old jack the lad, is brought to the A&E department having sustained a closed head injury from a blow to the back of the head outside Evolve in Leamington. 1. i) What is meant by “coup” and “contrecoup” injury with reference to closed head injuries? Coup injury is damage to the brain at the site of the blow. Contrecoup injury represents damage to the brain on the opposite side to the blow due to brain movement within the rigid skull. (2 marks) ii) What is the difference between primary and secondary brain injury? Primary brain injury is damage that occurs to the brain immediately as the result of trauma and is directly related to the amount of force applied to the head. Secondary brain injury results from complications associated with the initial trauma. (2 marks) iii) List four complications that can contribute to secondary brain injury. Respiratory complications eg hypoxia, hypercapnia, airway obstruction) Hypovolaemic shock Intracranial bleeding Cerebral oedema Epilepsy Infection (4 marks) 2. i) you asses his level of consciousness. He opens his eyes only in response to pain, he is making random words but no conversational exchange and he flexes his limbs on painful stimulus. What does he score on the Glasgow coma scale? 3 points for motor response – flexor response to pain 3 for inappropriate speech 171 2 for eye opening in response to pain total of GCS= 8. ii) Assuming he is unconscious, list the physical signs you would elicit to establish the extent of the intracranial injury Blood pressure, pulse and respiration Pupillary sizes and reflexes Reflexes – Babinski Fundoscopy for papilloedema (4 marks) iii) List the types of intracranial bleeding that may be present and state one investigation that would demonstrate the lesion. Extradural / Subdural / Subarachnoid / intracerebral CT/MRI head scan. (2 marks) 3. Mr Segaren is found to have an extra-dural haematoma. Write short notes on your management of him. (5 marks) Protect the airway Exclude cervical spine injury Quarter hourly obs of BP and pulse Intracranial pressure monitoring Daily ABG/FBC/U&E Mannitol infusion preoperatively Surgical evacuation of haematoma with placement of intra-cranial pressure monitoring device. Postoperative antibiotic therapy. (5 marks) 4.11 Head injury By the end of Phase II students should be able to: 172 • make an initial assessment of the patient taking into account the mechanism of injury • calculate the Glasgow coma scale • participate in the management of head injury and recognise the importance of prevention of secondary brain ischaemia 173 4.12 Whilst working in the Paediatric Assessment Unit, a 5 year old boy attends with extensive scalding on his lower limbs and buttock area. How would you estimate the extent of the burn? Chart (Lund & Browder) as appropriate for age. (1) Briefly describe the appetence of 1st, 2nd and 3rd degree burns. (3) 1st – minor, painful erythema 2nd – painful, blistering, partial thickness, non-blanching 3rd – White, brown or black. Absent sensation. No blisters. They are extensive 3rd degree burns in this child. Name 2 lab investigations you wish to carry out (2) FBC 174 U&E Glucose Group and Save/ X-match Urinalysis Coagulation Name 3 things to be included in your initial management (3) Analgesia e.g. morphine Anti- emetic e.g. Cyclizine Ensure airway patent/protected Oxygen IV fluids Antibiotics Tetanus prophylaxis Urinary catheter Mention 3 complications of serious burns in any patient (3) Hypovolaemic Renal failure Sepsis/toxic shock Stress Ulcers Pulmonary dysfunction Cardiac arrest Post-traumatic stress Scarring/Keloid formation 3 Days after admission, the patient become pyrexial, hypotensive and complains of nausea. What is the likely reason for this? (1) Toxic shock syndrome/Sepsis What is the organism most commonly responsible? (1) Staphylococcus aureus Extended Question What may make you suspect non-accidental injury in a child in terms of burns? Mention one (1) 175 Explanation unlikely Late presentation Other injuries also present Scalds on the buttocks, lower limbs and hands Small, circular (cigarette burns) 4.12 Burns By the end of Phase II students should be able to: • assess the extent and depth of a burn • plan appropriate investigations for a patient with severe burns • initiate immediate management of a patient with burns, recognising the possible complications of burns, including airways obstruction and the occurrence of toxic shock syndrome in children • be aware of burns as a form of non-accidental injury • discuss with patients the physical and mental effects of burns • discuss management of burns with physiotherapists and occupational therapists 176 4.13 A 78 year old lady presents with hip pain which she has had for many years and has worsened over the past few months. She has pain in the hip, which is typically worse at the end of the day and after doing her housework and other activities. She also finds that she has stiffness in the morning but this is better by the end of the day. These problems also severely affect her mobility and gait and have made her prone to several falls in the past. 1) The following radiological pictures show the classical features of a particular condition. Name the condition and describe the major radiological changes that occur with this condition (5 marks). Osteoarthritis Reduced joint space Marginal osteophytes Sclerotic bone changes Cyst formation 2) What signs are found on examination? Joint tenderness Crepitus on movement 177 Limitation of range of movement Joint instability Joint effusion and variable levels of inflammation Bony swelling Wasting of muscles 3) Briefly outline the pathphysiological changes associated with the condition (8 marks). The essential feature is degeneration of the cartilage: Fibrillation (cracks in the surface cartilage) Loss of cartilage matrix Chondrocyte proliferation and death Fibrous repair tissue fills the cracks in the cartilage Subchondral bone cysts form from exposure to synovial fluid pressure Loss of cartilage with eburnation (ivory like thickening and polishing) of bone surface Osteophyte formation (Heberden’s nodes – osteophytes at the DIP) Synovitis caused by fragments of cartilage in joint space. 4) What typical investigations would you do for this disease? Blood tests. There is no specific test; the ESR and CRP are normal. Rheumatoid factor only when the damage is advanced. X-rays. As above. These are only abnormal when the damage is advanced. MRI. This demonstrates early cartilage and subchondral bone changes. Arthroscopy. This reveals early fissuring and surface erosion of the cartilage. 5) Describe the major treatment options available? Physical measures Weight loss and exercise for strength and stability. Walking aid held in contralateral hand in hip arthritis and in ipsilateral hand if it’s the knee. Regular exercises (e.g. quadriceps exercises in knee OA) and keep active. 178 Medication Should only be used with severe disease. Simple analgesia first e.g. paracetamol and if no good NSAIDs but prescribe with adequate explanation of side effects and can be left off on good days. Surgery Total hip replacement arthroplasty for severe OA, reduces pain and stiffness and greatly increases function. 179 Q1) The clinical and radiological pictures shown in picture 1a and 1b) and picture 2a and 2b) of hands show two different conditions. Picture 1a Picture 1b 180 Name the condition in picture 1a) and 1b) above and describe some of the salient features. Osteoarthritis of the hands Hand joint involvement showing bony thickening of the DIP (Heberden nodes) and PIP joints (Bouchard nodes). Picture 2a Picture 2b The above hands (2a and 2b) are those of a 65 year old lady who has had this problem with her hands for many years and describes how her hands are often very swollen, painful and stiff, especially in the morning. This eventually involved her larger joints i.e. ankles, knees, hips, elbows, shoulders, cervical spine and TMJ. debilitated with this condition. She is thus very She also suffers with breathing difficulties and has problems with her eyes. Q2) Name the condition in picture 2a) and 2b) above and describe some salient features that you find in the hands with this condition? Rheumatoid arthritis of the hands 181 Sausage shaped fingers and MCP joint swelling. Later on, ulnar deviation and volar subluxation (partial dislocation) at MCP joints Boutonniere and swan-neck deformity of the fingers or z-defromity of the thumbs. The wrist subluxes and the radial head becomes prominent (piano-key). Extensor tendons in the hand may rupture and adjacent muscles waste. Findings on xrays: Soft tissue, juxta-articular osteoporosis; ↓joint space. Later on: bony erosions (+/- subluxation) and (+/- complete carpal destruction).A Q3) Briefly outline the pathophysiology of this condition. The essential feature in joints is chronic nonsuppurative inflammation of the synovial membrane that can destroy the articular cartilage, bone, and adjacent tissues. Chronic inflammatory synovitis Synovial membrane is thickened with villous outgrowth (hypertrophic villous synovitis) Proliferating synovial tissue extends over the surface of the articular cartilage as “pannus”. Pannus covers the cartilage, eroding into cartilage and bone Neutorphils are prominent in the joint fluid B and T lymphocytes (especially CD4 helper cells) are found in the synovial stroma Synovial antigen presenting cells (dendritic cells and macrophages) are activated Pannus comes to resemble a piece of highly vascular, active, cellular lymphoid tissue Osteoclastic activity in underlying bone results in osteoporosis and bone erosions Inflammation of tendon sheaths and other synovium-lined tissues. Q4) Outline the major investigations for this condition. No one specific laboratory test is diagnostic of RA. The diagnosis is made primarily 182 on the clinical features (an arthritis involving small peripheral joints) but blood test can be done with the following features:along with: ↓ HB (Normochromic or hypochromic anaemia, and other indicators of a chronic systemic acute phase response e.g. elevated globulins, decreased albumin). ESR CRP Rheumatoid factor (often negative in the start and becoming positive in 80%). NB also raised with other conditions. ↓WCC ANA (+ve 30%) Radiology: Plain radiographs, occasionally CT and/or MRI Biopsy: Q5) Synovium, skin, nodules, vessels, lymph nodes – rarely necessary. Outline the treatment options associated with this condition The aim is to minimize symptoms and improve prognosis Multidisciplinary approach Regular exercise Physiotherapy Occupational therapy Household aids and personal aids (orthoses) e.g. wrist splints. Intra-lesional steroids (joint injection) Surgery – to improve function, not for cosmetic effect. Simple analgesics or NSAIDs ( no affect on long term outcomes) 2nd Line DMARDs (disease modifying anti-rheumatic drugs) Start these if there is persisting synovitis for more than 6 weeks. Sulfasalazine is the first choice in the UK 183 Sulfasalazine: s/e nausea, headaches, ↓marrow, sperm count and hepatitis. Methotrexate: s/e nausea, diarhoea, cough, SOB, cirrhosis. Ciclosporin: s/e nausea, tremor, gingival hypertrophy, hypertension. s/e ↓marrow, proteinuria. Gold: Azathioprine: Penicillamine: s/e ↓marrow, nausea, LFTs, oncogenic. s/e ↓marrow, proteinuria. Hydroxychloroquine: s/e permanent retinopathy with high doses, tinnitus, headache. Adjunctive therapy with corticosteroids For severe systemic illness, intermittent and troublesome mono/pauciarticular inflammation +/- vasculitis. e.g.methylprednisolone inflamed joints. Steroids may be given as intermittent pulses 80-120mg im or 500-1000mg iv or can injected into Or can be used until the DMARDs take effect. Have numerous s/e especially osteoporosis and potential for opportunistic sepsis. Biological agents Target pro-inflammatory cytokines e.g. TNF and IL1 Chimeric monoclonal antibodies (infliximab) Fc fusion proteins with soluble TNF receptor (etanercept) Expensive but highly effective More recently recombinant IL-1 receptor antagonists are also an effective agent. 184 4.13 Investigations By the end of Phase II • students should be able to: interpret the major radiological changes of osteoarthritis of the hip and of rheumatoid arthritis of the hand • request and interpret routine investigations for auto-immune disease • relate these changes to the underlying pathology 185 4.14 A 75 year old gentleman presents in A&E complaining of an excruciatingly painful left knee. The pain came on suddenly the previous night and he has never suffered from similar symptoms before. There is no recent history of trauma to the knee. 1. What is your differential diagnosis? Crystal arthropathy (e.g. gout, pseudogout) Septic arthritis Monoarthritic presentation of a polyarticular disease (e.g. OA, RA) 2. On examination he has a red, hot, swollen knee with significantly reduced range of movement due to pain. You decide to aspirate joint fluid. What 3 other investigations would you perform on him? Take blood for: FBC (looking for ↑WCC), ESR/CRP (inflammatory markers), U&E (renal status important in gout), serum urate level Blood cultures (if sepsis is possible) Knee X-ray – look for erosions, calcification, widening/loss of joint space, changes in underlying bone (e.g. sclerotic areas, osteophytes) 3. Joint aspiration reveals turbid, yellow synovial fluid, rich in neutrophils. No organisms have been identified in culture. Microscopy reveals negatively birefringent needle-shaped crystals. What is the diagnosis and how would you manage this condition in the acute setting? Goutut. NSAIDs (e.g. ibuprofen, naproxen) – analgesic/anti-inflammatory effect [If NSAIDs are contra-indicated, e.g. due to peptic ulcer, give colchicine PO] Joint aspiration (reduces pressure) NB: NSAIDs & colchicine are problematic in renal failure – steroids can be very effective but not without side-effects! 186 4. What are the predisposing factors for the above condition? chronic renal disease drugs (e.g. thiazide diuretics, low-dose aspirin) hypertension lead toxicity alcohol genetic (e.g. glucose-6-phosphate deficiency) idiopathic gout increased purine turnover (myeloproliferative disorders, e.g. polycythaemia vera – lymphoproliferative disorders, e.g. leukaemia – others, e.g. carcinoma) genetic (e.g. Lesch-Nyhan syndrome) 5. How would you prevent similar attacks in the future? Avoid purine-rich foods (e.g. offal, oily fish), obesity & alcohol excess Consider long-term allopurinol (↓ serum urate) but not until 3 wks after an attack know allopurinol’s mode of action, dose, side-effects! Control hypertension, avoid diuretics and aspirin E. If microscopy of the synovial fluid had revealed positively birefringent rhomboid-shaped crystals what would the diagnosis be? What are the risk factors for this condition? Pseudogout. Risk factors: Old age Dehydration Hyperparathyroidism DM Acromegaly Haemochromatosis Wilson’s disease ↓ PO4/ ↓ Mg 187 A 35-year old gentleman presents in A&E with an acutely painful knee. The pain came on over the last 24 hours and he is also feeling feverish and generally unwell. His doctors suspect that he might be suffering from septic arthritis. 1. What are the possible micro-organisms responsible for this condition? (in order of decreasing prevalence) Staph aureus Streptococci (mainly – Strep pneumoniae, Group A strep) Gram –ve bacilli (mainly – H. influenzae, E. coli) Neisseria gonorrhoea Anaerobes 2. What are the 3 possible routes by which the joint becomes colonised? Direct inoculation (e.g. during joint surgery/aspiration) Spread from infected peri-articular tissue (e.g. spread from osteomyelitic focus) Haematogenous spread (due to transient/persistent bacteraemia, e.g. skin/lung/bladder infection) 3. Name 3 host factors that can predispose to non-gonococcal septic arthritis Increasing patient age Decreased immunocompetence (e.g. diabetes) Pre-existing joint disease (e.g. RA patients) 4. You decide to aspirate synovial fluid from the patient’s knee and send it for culture. How would you treat his condition while awaiting culture results? Ask for advice from orthopaedic surgeons and microbiologists! Start empirical antibiotic treatment depending on suspected organism (e.g. for staphs – flucloxacillin & benzylpenicillin IV until sensitivities are known) Rest affected joint (no bearing of weight) 188 Encourage early joint mobilisation as symptoms subside – vigorous physio! 4.14 Acute onset joint pain By the end of Phase II the students should be able to: • recognise the symptoms of infection of bone or soft tissue • initiate diagnostic procedures and treatment of the condition • recognise the possibility of septic arthritis • recognise the indications for surgery • discuss the prognosis and rehabilitation with the patient or parents • recognise acute and chronic gout and initiate management 189 4.15 Mr L is a 65 year-old man who presented to his GP with unremitting chest pain that is particularly worse at night. His worried wife, who accompanied him, has also noticed that he has lost weight recently. His significant past medical history comprises of successful management of prostatic carcinoma by brachytherapy 3 years ago. a. What is brachytherapy? Radiotherapy administered by implanting radioactive wires or grains into or close to a tumour b. Name 3 differential diagnoses for his presenting complaint rib tumour, primary or metastatic muscular strain rib fracture The GP was concerned that Mr L may have bone metastases from his prostatic carcinoma. c. Which investigations would you carry out to confirm or refute the presence of bone cancer? Serum alkaline phosphatase Calcium Prostate specific antigen d. Name 2 types of primary malignant neoplasms of bone Osteosarcoma Fibrosarcoma Chondromas e. Name three treatment options for Mr L. Analgesics 190 Anti-inflammatory drugs Local radiotherapy Hormonal therapy Internal fixation of pathological fracture 4.15 Bone and Soft Tissue Tumour By the end of Phase II • the student should be able to: identify the broad pathological types of bone and soft tissue tumours which affect the musculo-skeletal system • recognise the possibility of underlying bone or soft tissue tumour in patients presenting with musculoskeletal symptoms • detect major abnormalities on examination suggestive of bone and soft tissue tumour • recognise the importance of staging and how this may be performed • be aware of the concepts of treatment of bone and soft tissue tumours 191 Mrs JR, a 76 year old female, presents to your GP clinic with a 2 day history of a painful left knee. 1. List four possible causes of a painful solitary large joint trauma Septic arthritis Gout/pseudogout Gonococcal arthritis Haemophilia Rheumatoid arthritis The following is found on examination Left knee examination shows: overlying skin red and warm swollen, painful left knee joint pain on all left knee movement – with diminished movements due to pain and spasm 2. What additional features would you expect on general examination that would suggest a infective aetiology Swinging pyrexia Tachycardia 3. From the clinical findings what is the most likely diagnosis Septic arthritis 4. What predisposing factors need to be considered in any patient with this condition? debilitating disease infection elsewhere such as an infected leg ulcer rheumatoid arthritis 192 immunosuppression/corticosteroids diabetes mellitus recent joint surgery joint prostheses penetrating injury 5a) What is your immediate management? Admit to hospital as risk of rapid joint damage 5b) What investigations should be ordered? blood cultures full blood count for leucocytosis erythrocyte sedimentation rate C-reactive protein aspiration of synovial fluid - usually purulent with a neutrophil count above 50,000 per mm3, and low glucose concentration anti-streptolysin O titre Plain X-ray of left knee What radiological findings would expect? None at this stage, first radiological changes appear after 2-3 weeks. 5. What radiological features may you find in 2-3 weeks? Narrowed joint space, and patchy rarefaction 6. What aetiological agents are likely to be isolated from your investigations name 2. Staphylococcus aureus is the most common agent. Others may include: Streptococcus pyogenes pneumococcus Haemophilus influenzae, although most likely in those under three years gonococcus gram negative rods, such as E. coli, Pseudomonas 193 All the above are primary causes, but may be secondary to osteomyelitis of an adjacent bone. 7. What immediate antibiotic agents would you expect to be administered? Should check local protocol, and most recent BNF, but likely agents include clindamycin alone or flucloxacillin and fusidic acid if Haemophilus influenzae then give amoxicillin or cefuroxime 8. What complications could arise from this condition? chondrolysis septic dislocation avascular necrosis shortening late degenerative change Objective: painful solitary large joint 194 4.16 A 29 year old woman presents to medical outpatients with a 3 month history of painful, swollen proximal interphalangeal joints associated with early morning stiffness and malaise and lethargy. What is the likely cause of her arthopathy? (1 mark) Rheumatoid arthritis Name 3 investigations that you may wish to conduct and the likely finding if it is the diagnosis suggested in question 1? (6 marks) Blood count – low Hb, high platlets, Rheumatological marker- high rheumatoid factor, Inflammatory markers – high ESR, high CRP X-ray – periarticular erosion, soft tissue swelling, angular deformatity, osteoperosis In the categories below list an associated feature which may occur in this disorder 1) eyes, 2)skin 3) respiratory 4) cardiovascular 5)renal: Sjogrens syndrome (dry eyes and mouth), scleromalacia Rheumatoid nodules , vasculitic rash Pleural effusion, rheumatoid nodules, pulmonary fibrosis Pericarditis, pericardial effusion Chronic renal failure, secondary to amyloidosis or drugs Outline the pharmaceutical medical management of this condition Analgesia – paracetamol, NSAIDS Anti-inflammatory – NSAIDS Corticosteroids- prednisolone DMARDS (Disease Modifying Agents of Rheumatological Diease) D-penacillamine, gold salts, sulphazalazine Immune modulatory – anti TNF (Infliximab) Extended 195 Breifly outline the role of 2 members of the MDT in the care of this patient Physician -patient education of disease, medical management, referral management Physiotherapist – maintain joint mobility through exercise Occupational therapist – evaluate impact of disease on life, advise easier ways to perform daily tasks and design and prescribe assistive devices Orthotist- provide and fit splints and other aids Surgeon- perform joint replacement Others you can mention: Social worker, Specialist nurse, GP 196 An obese 67y old woman presents to her GP with a 4 month history of increased swelling , pain and stiffness in her right knee. She suffered a comminuted fracture of her distal right femur in a road traffic accident 15 years ago? What is the likely diagnosis? osteoarthritis. List 3 risk factors for the development of this condition Family history of OA Herediatry disorders (Ehler Danlos) Metabolic conditions – haemachromatosis, agromegaly Concominant bone disorders (Pagets, Perthes) Trauma – previous fractures Obesity Repeatative trauma/ occupation (footballers, atheletes, ballet dancers) For each of the following features place either RA (for rheumatoid arthritis) or OA (for osteoarthritis) – for which ever condition it is commonly associated with. Number 10 is done for you. 1. Loss of joint space on xray 6. Bouchards node 2. Feltys syndrome 7. Initial synovial inflammation 3. HLA DR1 8. Swan neck deformity 4. Z deformity of the thumb 9. Subchondral cysts 5. Osteophyte formation 10. Ulnar deviation RA Answers below: OA-1,5,6,9 RA- 2,3,4,7,8,10 Briefly outline the management of this condition 197 Conservative/supportive: Patient education (explanation of disease and its management). Lifestyle changes (weight loss, exercise) Physiotherapy (maintain joint moment, increase muscle strength), Occupational therapy to supply aids and appliances to aid mobility Medical: Pain relief and NSAIDS. Steroid injections Surgical: Debridement (removal of dead tissue within the joint) Artherodesis (fusing a joint) Osteotomy Arthroplasty 4.16 Chronic Inflammatory and Degenerative Joint Disease By the end of Phase II the student should be able to: • recognise rheumatoid arthritis and distinguish active from inactive disease • describe the immunological basis of rheumatoid arthritis • recognise the multi-system manifestations of many auto-immune processes • diagnose and assess the severity of degenerative disease of the hip and knee • initiate appropriate investigations • initiate appropriate management, especially the relief of pain • discuss with patients the range of aids to daily living that are available • describe the referral pathways for patients to physiotherapy and occupational therapy • recognise the need for surgical assessment • be able to discuss with patients the treatment options available, the role of rehabilitation and possible complications of surgical treatment 4.18 A 23 year old man who had previously fractured his leg is now on crutches. He has noticed that since the use of his crutches, he has experienced loss of sensation and 198 weakness in his hands. On examination a diagnosis of radial nerve palsy is made. Q) which actions of the upper limb would he find difficult to perform? extension of fingers, wrist and elbow Q) What area of sensation would be lost? Dorsum of hand – lateral 3 ½ digits with sparing of finger tips Q) How did the radial nerve become affected? Compression of nerve in the axilla by incorrect use of crutches A 42 Year old female is seen by her GP complaining of pain and numbness in her hands. She notices that her symptoms are classically worse at night and during the day, during prolonged flexion of the wrist e.g typing or knitting. Q) What is the diagnosis ? Carpal tunnel syndrome Q) What are features on examination? Wasting of thenar eminence, weakness of thumb movements Q) What test can be done to confirm the diagnosis? Tinnels Test (tapping over median nerve at the wrist to reproduce the symptoms) Q) What are the causes of this condition? Median nerve compression as it passes under flexor retinaculum (in carpal tunnel). Much more common in females than in males and associations are pregnancy, rheumatoid arthritis, hypothyroidism, acromegaly, trauma and idiopathic in post menopausal women ? 199 Q) What is the treatment for this condition? Conservative – using splints Medical – local steroid injections Surgical – decompression of the flexor retinaculum 4.18 Nerve Compression By the end of Phase II the student should be able to: • recognise nerve compression in the upper limb • initiate investigations for a patient with nerve compression • be aware of the role of surgery and radiotherapy in the relief of nerve compression 200 4.19 During a neonatal health check, performed the first day after birth, a baby is diagnosed with developmental dysplasia of the hip (DDH) Q) Which clinical tests would be carried out to diagnose this? Ortolani and Barlow Manoeuvre Q) Name 3 risk factors for DDH? Breech birth, +ve family history, increase in birth weight, post maturity, Oligohydramnios Q) What imaging technique can be used as a screening tool for DDH? Ultrasound Q) Briefly outline the treatment of this condition? Use double nappies – reassess in 3 wks with ultrasound If still problem – splint hips in abduction 6 – 18 mths closed reduction – frame /gallows before 6 yrs – open reduction (surgery) 4.19 Congenital Problems By the end of Phase II the students should be able to: • detect scoliosis, fixed flexion, kyphosis, varus and valgus deformities • detect deformity present in the knee, hip, shoulder and the small joints of the hand • consider the possibility of congenital dislocation of the hip and talipes equinovarus • perform the diagnostic procedures available at birth and early life to detect these conditions 201 • outline the diagnosis, management and prognosis to the family 202 4.21 Mrs S is a 47 year old woman that presents to her GP. Her mother has suffered from osteoporosis and Mrs S wants advice on how she can help prevent osteoporosis. Q1. What steps can Mrs S take to help prevent herself getting osteoporosis? Dietary – Calcium supplementation, Vitamin D supplementation Regular Weight bearing exercise (30 mins 3 times per week) Smoking cessation Avoid excess alcohol Q2. Give four risk factors for Osteoporosis. Hip protectors to reduce fall risk Female sex, increasing age, family history of osteoporosis, early menopause, smoking, excessive alcohol, immobility, lack of exercise, malabsorption, 4 prolonged steroid therapy, Cushing’s disease, Hyperparathyroidism,marks Myeloma, Hypogonadism in men. Q3. Give four treatment options for Osteoporosis. 4 Oestrogen therapy via HRT in postmenopausal women marks Biphosphonates Vitamin D (Calcitriol) Calcium supplementation Calcitonin Androgens for Hypogonadal men 4marks Q4. Osteomalacia and Osteoporosis may both present with subclinical 4 fractures. What blood tests would help differentiate osteomalacia from marks osteoporosis? 4 In osteoporosis, Serum alk phos, plasma calcium and serum phosphate are all marks normal. In osteomalacia, serum alk phos is high, plasma calcium is low or low normal and serum phosphate is low. marks 4 203 4.21 Metabolic bone disease By the end of Phase II students should be able to: • recognise the circumstances where osteoporosis is likely to occur • be able to give advice to patients about preventing osteoporosis and outline treatment strategies • recognise the circumstances when osteomalacia may occur • initiate investigation of osteomalacia • recognise the circumstances when hypercalcaemia may occur • initiate the management of hypercalcaemia 204 4.22 A 62 year old lady presents to her GP. She has been feeling non-specifically unwell for nearly 3 months. She has been suffering pain and stiffness in her shoulders, neck, hips and lumbar spine (limb girdle pattern) which is worse first thing in the morning upon waking and makes getting out of bed difficult. For the past 2 days she has suffered a severe constant headache affecting her right temporal scalp. She has also noticed tenderness in this same area. Q1. What is the likely diagnosis? Polymyalgia Rheumatica with concurrent Temporal Arteritis (Giant cell arteritis/Cranial arteritis). Q2. Which investigations should be carried out and what is the definitive marks diagnostic test for this condition? FBC may demonstrate mild anaemia ESR characteristically very elevated CRP raised LFT’s – Serum alk phos and γ-glutamyltransferase may be raised 2 Definitive diagnostic test is Temporal Artery Biopsy Q3. How should this condition be initially managed? 4 marks High dose Corticosteroids PO 2 Q3. Name 3 other conditions associated with vasculitis. marks Rheumatoid Arthritis SLE Scleroderma Polymyositis/Dermatomyositis Goodpastures Syndrome Inflammatory Bowel Disease Paraneoplastic Subacute Infective Endocarditis 3 marks 4.22 Other conditions By the end of Phase II students should be able to: 205 • recognise, investigate and initiate management of cranial arteritis • recognise and refer cauda equina compression • recognise progressive cervical myelopathy • recognise common dermatological manifestations of rheumatic disease 206 3.1 & 5.2 Mr Bogg is an unfortunate 65 year old man who has attended the ward prior to a right hemicolectomy for a longstanding colonic tumour. history. He has a longstanding medical He has had diabetes mellitus for the past 48 years for which he is currently using insulin and notes that he has good control and has no known complications. He also suffers from hypertension that he diligently checks at home and at his GP’s and notes is within the ‘normal range’. He is otherwise well on the day of admission. (a) Given his medical history what ASA grade would you assign him and state what features in his history suggest this particular grade. What does the ASA grading system predict? (3 marks) Class II: “a patient with mild to moderate systemic disease that does not limit the patient’s activities in any way”. Known hypertensive and diabetic both of which are well controlled and have no significant complications. Predicts perioperative mortality. (b) Name 3 pre-operative investigations that would be appropriate in this patient (3 marks) Bloods (FBC, U&E, Cr, BM, HbA1c) PA CXR 12-Lead ECG (c) What steps would take to optimise his pre-operative glucose levels. account (exact numerical details are not required). Give a detailed (7 marks) Liaise with surgeon and anaesthetist Put patient first on list Refer to local policy Stop LA insulin the night before Setup a sliding scale (50U of SA insulin with 50mL N/saline) Check BM every hour and adjust sliding scale Aim for a BM of between 7 – 11mmol/L during surgery Continue sliding scale until px eats second meal – check BM every 2 hours Switch back to normal regimen On the day of his operation, Mr Bogg was transferred from the ward to the anaesthetic 207 room. Following pre-oxygenation and initial iv induction with propofol the medical trouble maintaining a seal and therefore the anaesthetist asked him to put in an oral airway. student was asked to ventilate him by bag and mask. He was having (d) How do you size a guedel airway in an unconscious patient? (1 mark) An estimate of the airway size required is given by comparing the airway length with the vertical distance between the patient’s incisor teeth and the angle of the jaw (e) Describe the process of inserting an oral airway (2 marks) Start with airway upside down Place into oropharynx in this position, advance to the hard palate Rotate the airway 180o Fully insert until opening lies in front of teeth (f) What is the main problem that one must warn the patient of during propofol administration – especially if they are of an anxious disposition? (1 mark) Often administered with local anaesthetic due to pain on injection He was then paralysed prior to intubation. The anaesthetist used rocuronium to facilitate this. (e) What is the mechanism of action of rocuronium and how could its effects be reversed if the surgeon broke a fingernail and decided to cancel the procedure. (2 marks) Rocuronium is a non-depolarizing competitive neuromuscular blocking agent that competes with acetylcholine for post-synaptic binding sites. It is commonly reversed using an anticholinesterase such as neostigmine to overcome the block. (f) Name 2 methods to confirm that the ETT was in the correct place. Give 4 complications of intubation. (6 marks) To confirm correct placement either: ventilate the chest and watch it rise symmetrically auscultate over the stomach during ventilation and hope not to hear bubbles with ventilation. 208 Complications: (Any from below) Oesophageal intubation Right main-stem bronchus intubation Gastric aspiration Airway trauma Dental trauma Cervical cord injury (g) How does one prevent gastric aspiration during induction of anaesthesia? How does it work? What is the complication that may arise from forgetting to do this (especially in a trauma situation)? Where would such a patient go in the post-operative period? (4 marks) Use cricoid pressure Cricoid is the only complete ring of cartilage in the larynx therefore occludes oesophagus with application of direct anterior pressure Aspiration pneumonia Send to ITU for monitoring and management 5.1 Pre-operative assessment for anaesthesia By the end of Phase II students should be able: • to order appropriately pre-operative blood tests, chest radiographs and ECGs. • to recognise patients who have an increased risk of peri-operative morbidity and mortality • to participate in the pre-operative work-up regimes for high risk patients • to liaise with the anaesthetist in the management of a diabetic patient having surgery 5.2 General anaesthesia By the end of Phase II students should be able to: • recognise the properties of some of the commoner drugs used in anaesthesia and their side effects • perform venous cannulation competently • recognise some of the complications which may occur during an anaesthetic including, hypertension, bradycardia and tachycardia, myocardial infarction, aspiration of stomach contents • care for an unconscious patient 209 5.3 Question 1 A post-operative patient is in recovery. State 3 risk-factors that increase the chance of post-operative nausea and vomiting. (3 marks) Female gender Obesity Young age Positive history Surgery to middle ear, posterior cranial fossa, intra-abdominally, hysterectomy Severe pain Administration of opioid analgesics, nitrous oxide (ketamine, isoflurane) Hypoglycaemia, hypoxia, uraemia, hypotension. Gastric dilatation e.g. from bag and mask ventilation State 2 different anti-emetic drug groups and the generic name for 1 drug from each. (2 marks) Anti-histamine e.g. chlorphenamine, loratidine, cyclizine. Dopamine antagonist e.g. metoclopramide, domperidone. 5HT3 antagonist e.g. granisetron, ondansetron. Anti-cholinergic e.g. hyoscine, atropine Where in the body can the receptors for these drugs be found? (2 marks) Histamine (H1) receptors, found mainly in the vestibular labyrinth. Dopamine receptors are found in chemoreceptor trigger zone 5HT3 receptors are predominantly found in the GI tract. Cholinergic receptors are found in the vestibular labyrinth and chemoreceptor trigger zone Question 2 Post-surgery a patient is sent to the ward on patient-controlled analgesia (PCA). Name 2 advantages of PCA over infusion or i.m. injection. (2 marks) 210 Increased patient satisfaction. Increased ability to match the dose with the patient’s perceived pain level. Reduced work-load for nursing staff. Elimination of painful repeated i.m. injections. Greater certainty of plasma opiate levels as given i.v. Name 2 disadvantages of PCA over infusion or i.m. injection. (2 marks) Initial cost of pump Not suitable for children under 5-7 years, confused, frail or elderly patients. Potential for overdose remains. What instructions would you give to the nursing staff regarding safe monitoring of PCA? (3 marks) Regular observations, especially sedation score (neuro) and respiratory rate. Pain score. Written-up prescription for naloxone. Check syringe volume with actual consumption – stop PCA if discrepancy. Nurse on open ward rather than side room. Prescription for breakthrough anti-emetic. Later, you check the patient, but they are unresponsive, have a respiratory rate of 7 breaths per minute and pin-point pupils. What do you do? (4 marks) Call for help Stop the PCA ABCs giving O2 via bag-and-mask ventilation Give naloxone State the generic name and dose of the reversal agent given in this situation. (2 marks) Naloxone, 0.8-2mg i.v. every 2-3 mins until respiratory rate is adequate, to a maximum of 10mg. 5.3 Postoperative problems By the end of Phase II students should be able to: 211 • treat post-operative nausea and vomiting • appreciate the likely causes and initiate management of post-operative confusion • recognise and initiate management of post-operative respiratory failure • understand the importance of effective post-operative analgesia • manage i.v. patient controlled analgesia and epidural analgesia and their side effects • prescribe strong, intermediate and minor analgesics in the post-operative period having regard to the operation and to appropriate doses, routes of administration, side effects and contra-indications • perform intravenous, intramuscular and subcutaneous injections competently 212 5.4 Question 1 Pulse oximetry is commonly used to monitor hospital patients. Describe 2 advantages and 3 limitations of this technique. (5 marks) Advantages: Small and portable Continuous monitoring Non-invasive Simple to use Fast results Limitations: Does not measure C02 levels Carboxyhaemoglobin gives falsely high readings Methaemoglobin gives falsely low readings In respiratory failure a high FiO2 may give misleadingly high SpO2% Inadequate pulse e.g. hypoperfusion, hypovolaemia, hypothermia, peripheral vasoconstriction. Excessive patient movement can disturb Nail varnish, nicotine and henna can prevent reading Methylene blue (thyroid surgery) gives false low readings In anaemia the SpO2 may be high, but there may be inadequate tissue delivery of oxygen Below 10kPa, a small drop in PaO2 produces a large drop in saturation reading due to the haemoglobin dissociation curve Readings <70% are inaccurate (machines are calibrated against healthy human volunteers – they don’t let them get this hypoxic apparently!) Question 2 Name 2 vessels appropriate for introducing a central venous catheter. (2 marks) Internal jugular vein Subclavian vein Basilic vein at antecubital fossa (only 60% chance of success) 213 State 4 complications that can potentially arise from central venous catheterisation. (4 marks) Air embolus Pneumothorax Scepticaemia Local infection at catheterisation site Arterial puncture and haemorrhage Venous thrombosis Thoracic duct injury (left side) Injury to brachial plexus, phrenic or recurrent laryngeal nerve 5.4 Monitoring By the end of Phase II students should be able to: • recognise the need for central venous cannulation and the associated complications • measure a patients CVP using a water manometer • recognise the need for pulmonary artery catheterisation and its uses • use and interpret pulse-oximetry • recognise the need for cardiac monitoring 214 5.5 While working as a house officer on the cardiology ward, Mr S a 75-year-old man with a history of ischaemic heart disease, mistakenly arrives at the ward for his outpatient appointment. While you are showing him to the outpatient department he collapses in the corridor with central crushing chest pain and quickly becomes unresponsive. Using simple manoeuvres you open his airway but find he is not breathing and has no pulse. After calling for the resuscitation team you return to him to begin basic life support until help arrives. 1) According to the 2005 resuscitation council guidelines, at what ratio should chest compressions to rescue breaths be given to an adult? (1) 30:2 Help quickly arrives and a defibrillator is attached to assess his heart rhythm and IV access is gained. A) B) C) D) 2) Assuming they are all pulseless, name the ECG rhythms A-D (4) A) Pulseless electrical activity (PEA) / electromechanical dissociation (EMD) B) Asystole C) Ventricular fibrillation (VF) D) Ventricular tachycardia (VT) 3) Mr S is found to be in the same rhythm shown in C. According to the advance life support algorithm 2005 how should this be treated? (4) 1 x defibrillator shock 215 2mins of CPR (30:2) Adrenaline 1mg IV each cycle Reassess rhythm 4) What other rhythm is treated this way (use the letter A-D as above)? (1) D 5) Name one drug other than adrenaline that can be used in order to correct rhythm C and your answer to question 4 (1) Amiodarone 6) Name four reversible causes of cardiac arrest (4) Hypoxia Hypovolaemia Hypothermia Hyper/hypokalaemia (metabolic) Tension pneumothorax Thromboembolism Toxic Tamponade, cardiac Eventually the resuscitation attempts are successful and Mr S returns to sinus rhythm but does not regain consciousness. He is taken to the intensive care unit due to his poor condition. His condition continues to deteriorate and a decision is needed on whether to attempt to resuscitate Mr S, should he experience anther cardiac arrest. 7) Under what circumstances is it appropriate to issue a do not attempt resuscitation order (DNAR) in an incompetent / unconscious patient? (3) When CPR will to restart the patient’s heart and breathing - Futile When there will be no benefit gained by restarting the patient’s heart and breathing – Patient will die now or next time they arrest When the expected benefits of CPR are outweighed by the burdens – co-morbidity 216 will cause poor or no quality of life 8) Who is ultimately responsible for decision-making regarding resuscitation orders for incompetent / unconscious patients? (1) The consultant / GP in charge of the patients care (Where care is shared consensus is needed) The resuscitation council 2005 guidelines can be accessed here. 5.5 Cardio-pulmonary resuscitation By the end of Phase II students should be able to: • Diagnose and initiate management of asystole, ventricular fibrillation, pulseless ventricular tachycardia and electro-mechanical dissociation according to established guidelines • Operate a defibrillator competently • Discuss the ethical dilemmas surrounding resuscitation and how they may be resolved 217 5.8 Miss S, a 20 year old women attends A&E and admits to taking an overdose of pills. 1. What essential questions must you ask at this point? What have you taken? Including drugs and alcohol. How much have you taken? When did they take them? Why did they take them? 2. She tells you that she has taken 16 paracetamol tablets, no alcohol, roughly an hour and a half ago. What is your immediate management plan? IV access Bloods – FBC, U&E, LFT, Clotting/INR Paracetamol levels taken at 4 hours post OD ABG Activated charcoal – according to local protocol Senior advise 3. What is the specific antidote/treatment for paracetamol overdose? N-acetyl cysteine (Trade name is Parvolex) 4. When would you decide to use it? Refer to Paracetamol OD chart found in all A&E departments Table shows two treatment lines for plasma-paracetamol concentration against time (in hours) since the OD. Most patients will receive N-aceyl cysteine if their plasma-paracetamol level is above the normal treatment line. 5. There are two treatment lines on the paracetamol overdose chart, one for normal/low-risk patients and one for high-risk patients. When would you use the high-risk treatment line? Malnourished patients e.g. anorexia, alcoholism, HIV positive Patients taking enzyme-inducing drugs e.g. carbemazepine, phenobarbitone, phenytoin, rifampicin, alcohol. 218 6. What would you like to ask Miss S to determine her suicide risk? What happened today to make her take the OD? Was the self-harm/attempted suicide premeditated or opportunistic? Did she leave a note? Did she intend to kill herself? Does she regret her actions or would she do this again? Any history of psychiatric disorders? E.g. depression, schizophrenia. Previous suicide attempts? Assess support network. 7. What are the long term consequences of paracetamol overdose? Liver failure & encephalopathy Renal failure 5.8 Acute poisoning By the end of Phase II • students should be able to: recognise the commoner inhalants and ingestants responsible for accidental and deliberate poisoning • initiate immediate resuscitation if appropriate • participate in the management of the commoner poisonings • make an assessment of the underlying social and psychiatric factors in deliberate self-harm and the likelihood of a repetition 219 5.9 You are the Surgical HO on call. You are asked as she has an increasing Mews Score. by the nursing staff to assess Mrs B, Mrs B had a right hemicolectomy two days ago for a colonic carcinoma. 1. Define shock? Circulatory failure resulting inadequate organ perfusion. 2. List four types of shock and a specific example, not including neurogenic shock. Cardiogenic shock – post-MI Hypovolaemic shock – bleeding from trauma, ruptured AAA, ruptured ectopic pregnancy fluid loss from vomiting, diarrhoea, burns, third space losses Anaphylatic shock – Type I hypersensitivity reaction Septic shock – Endotoxins released from Gram negative bacteria e.g. E.coli Endocrine shock – Addisonian crisis, hypothyroidism Iatrogenic shock – from anaesthetics, antihypertensives 3. What signs would suggest shock in a patient? List six. Systolic BP <90 mm Hg heart rate/tachycardia Capillary refill respiratory rate urine output/oliguria Pallor Faint/collapse Confusion Mrs B has the following observations: Temp: 38.4C Heart rate: 108bpm BP: 92/74 mm Hg O2 Sats: 97% 220 On examination she has warm peripheries and capillary refill is <2 seconds. The pulse is rapid but bounding. 4. What type of shock is Mrs B likely to be suffering from? Septic shock 5. What other observation would be useful to aid management? Urine output Fluid balance 6. What would be your immediate management plan? IV access, if not already got it IV fluid, colloid or crystalloid Blood, urine and wound swab cultures Antibiotics: Cefuroxine 1.5g TDS IV, Metronidazole 500mg QDS IV, Gentamicin 5mg/kg OD IV (blind treatment) Senior review 5.9 Shock By the end of Phase II • students should be able to: recognise and initiate immediate investigation and management of hypovolaemic shock • recognise and initiate immediate investigation and management of septic shock and its complications • recognise the pathophysiological disturbances which accompany shock • monitor and assess the response to treatment 221 5.11 Mrs D, an 80 year-old lady is brought to the Emergency department by her daughter who is very concerned about her mother’s sudden onset of acute confusion. Her mother lives alone independently but recently complained of a fever and has spent the last few days in bed. List 3 possible differential diagnoses for her acute confusional state (3) Infection - LRTI UTI Septicaemia Metabolic - Hypoglycaemia of hyperglycaemia Hyponatraemia Alcohol Uraemia Hypothyroidism or hyperthyroidism CNS - Meningitis CVA Post-ictal Drugs - Tranquillizers Lithium, Digoxin Benzodiazepines You are unable to obtain a history from Mrs D. On examination Mrs D is very confused, pyrexial 38ºC with a respiratory rate of 32 breaths/min, SATS 85% on air, BP 150/60 mmHg. Bronchial breathing is noted at the right lower lobe. Abdomen examination is unremarkable. What is the most likely diagnosis? (1) LRTI List 3 immediate investigations you wish to do. (3) CXR ABG Blood cultures Blood tests (urea, WCC, CRP) Bm 222 An ABG comes back for you to interpret it paO2 7 KPa paCO2 4KPa pH 7.47 HCO3- 20 BE 1 What does it show? (2) Type I RF What is your immediate management? (5) High flow (60%) oxygen IV access IV fluids IV antibiotics Analgesia Monitor ABGs regularly over the next few hours Inform anaesthetist Mrs D subsequently improves over the next few hours and is moved to a ward. What potential complications could result from pneumonia? (2) Lung abscess Empyema End of Question Total 16 Marks 5.11 Acute confusional state By the end of Phase II students should be able to: • recognise and distinguish the common causes • initiate investigation and management of the commoner causes 223 5.13: Whilst on your respiratory rotation, you are called by the nurses to see a 26 year old man, with a known history of asthma, because he is complaining of shortness of breath! When you reach his bed he is agitated and confused. He is tachpnoeic (RR = 24). His most recent blood gas results are shown below. ABG's: pH = 7.36 kPa pO2 = 7.8 kPa pCO2 = 3.2 kPa HCO3 = 24 mmol/l BE = -2.0 mmol/l SaO2 = 92% on air Temperature = 38.1oC 1. What is your assessment of this patient? ABG's show hypoxia. All other values are within normal parameters. ? Exaccerbation of asthma. Patient is suffering from Type 1 respiratory failure. Causes include: Pneumonia Pulmonary oedema Pulmonary embolism Asthma Emphysema Fibrosing alveolitis ARDS 2. What is your management? A,B,C etc..... Auscultate - wheezing? Start highflow oxygen (35 - 60%) by face-mask to correct hypoxia 224 Salbutamol nebuliser Position patient comfortably Check hydration, pulse, BP, temperature etc. Look for underlying cause of respiratory failure: Order CXR FBC; U and E's; CRP Repeat ABG's. Sputum and blood cultures (esp. if febrile) Check medication and time of last dose. Look up the BTS guidelines on step-wise approach to asthma management in adults (Beta 2 agonist, Inhaled steroid, Lk receptor agonist, Aminophylline etc). Don't forget to get Senior help early, particularly if there is a chance his condition could deteriorate! i.e. anaesthetists/ITU Having done the above the patient improves so you go back to bed. However, 3 hours later you are called back to the same ward because another patient has "gone off". You stroll merrily back! On arrival, the patient is a 56 year old man with an 80 pack-year smoking history and a known COPD sufferer. He is cyanosed, sleepy and has a bounding pulse. His most recent ABG results are as follows: pH = 7.32 pO2 = 7.1 kPa pCO2 = 7.0 kPa HCO3 = 26 mmol/l BE = 4 SaO2 = 89% on 2l O2 via nasal cannulae 3. What is you assessment? ABG's show Respiratory acidosis with Type 2 respiratory failure. Type 2 respiratory failure is defined as Hypoxia (PaO2 < 8kPa) with Hypercapnia (PCO2 > 6.5kPa). This is caused by alveolar hypoventilation with or without V/Q mismatch. Causes include: 225 Pulmonary disease (COPD, asthma, pneumonia, pulm. fibrosis, obstructive sleep apnoea) Reduced respiratory drive (sedative drugs, CNS tumour, trauma) Neuromuscular disease (cervical cord lesion, diaphragm paralysis, polio, Guillain-Barre syndrome) Thoracic wall disease (kyphoscoliosis, flail segment). 4. What is your management? Some debate on this one! - Most consultants say...... A,B,C's as normal. Start high-flow oxygen as hypoxia will kill you quicker than hypercapnia. This is because high-flow oxygen will "knock-off" the patient's respiratory drive which is driven by hypoxia instead of hypercapnia. (The reason for this is becasue the patient has been suffering from a chronic resp. disease, resulting in higher-than-normal blood CO2 levels. The central respiratory centre is therefore relatively insensitive to CO2 levels, "resets" to a higher CO2 level and as a result hypoxia drives respiration. By giving lots of O2, pO2 levels rise and respiration reduces. This raises CO2 levels to dangerous levels and causes acidosis. In addition, hypoxia will also occur due to the lack of respiration). CALL ANAESTHETISTS/ITU CONSULTANT!!! - The OHCM says...... Treat underlying cause Controlled O2 therapy: start at 24% re-check ABG's after 20 mins. If PCO2 is steady or lower, increase O2 to 28%. If PCO2 has risen > 1kPa and the patient is still hypoxic, consider a respiratory stimulant e.g. Doxapram 1.5 - 4 mg/min IV or assisted ventilation e.g NIPPV. If this fails consider intubation and ventilation i.e. CALL ANAESTHETISTS/ITU CONSULTANT!!! Guide to colours of Venturi valves: Venturi valve Flow rate Oxygen delivered colour (l/min) (%) Blue White 2 4 24 28 226 Yellow 6 35 Red 8 40 Green 12 60 Which mask for which patient? Nasal cannulas: Patients with normal vital signs—for example, postoperative, slightly low oxygen saturations, long term treatment with oxygen at home Simple face masks and masks with a reservoir bag: Higher concentrations of oxygen are required and controlled oxygen is not necessary—for example, severe asthma, acute left ventricular failure, pneumonia, trauma, or severe sepsis. (Masks should always be set to a minimum of 5 l/min because significant rebreathing of CO2 can occur when exhaled air is not adequately flushed from the mask) Venturi masks: Controlled treatment with oxygen required in people with chronic respiratory failure—for example, COPD 5.13 Respiratory failure By the end of Phase II • students should be able to: make a rapid assessment and initiate management in the patient with acute respiratory distress • recognise a patient in respiratory failure • assess the cause, severity and type of respiratory failure and initiate management • interpret arterial blood gas results • prescribe oxygen and oxygen delivery systems appropriately 227 6.1 + 6.2 Miss P.V Bleed presented to her G.P with long standing menorrhagia. She went on to explain that recently she had been feeling tired all the time and on occasions becomes quite breathless. On examination the G.P noted she was pale, tachycardic and had spoon shaped nails. He decided to undertake some routine blood tests, one of these being a full blood count. Which 2 components of the full blood count are we most interested in when classifying Miss P.V Bleeds anaemia? (1) Haemaglobin MCV Miss P.V Bleeds full blood count results were as follows. Haemoglobin 9.8g/dL Mean Corpuscular volume (MCV) 72fl Mean Corpuscular Hb (MCH) 23 pg From these results, how would you classify Miss P.V Bleeds anaemia? (1) Microcytic anaemia Given her history and above blood results, Miss P.V Bleed is most likely to be suffering from Iron deficiency anaemia as a result of her chronic blood loss. List three other causes of Iron deficiency anaemia (3). malabsorption low dietary Fe intake Pregnancy (increased requirement) Hypothyroidism chronic gastrointestinal bleed What two following blood tests could you request the lab to run on Miss P.V Bleeds blood related to her condition of Iron deficiency anaemia to confirm your diagnosis? (2) 228 Serum ferritin Serum Iron What is the appropriate treatment for Miss P.V Bleed given her Hb level is 9.8 g/dL (1) Oral Fe, ferrous sulphate, I.M Fe if unable to tolerate oral. How would you initially manage her if the Hb level was 4.8 g/dL? (1) Blood transfusion List 3 hazards for this initial treatment of correcting a low Hb level (3). Transfusion reactions (cross reaction between donor and recipient) transmission of infection, Hep B, C, HIV Circulatory overload leading to heart failure, electrolyte disturbances from large volumes in transfusion. Following her Gynae outpatient appointment Miss P.V Bleed’s menorrhagia was treated and her iron deficiency anaemia corrected itself with the above treatments. Unfortunately 6 years later she developed a gastric carcinoma and required a gastrectomy. After her operation she returned to her G.P with similar symptoms as before, pallor, exhaustion and lethargy. Her Hb was 9g/dL. How would the red cells appear on a blood film taken from Miss P.V Bleeds blood? (1) Macrocytic Based on her history, what form of anaemia is Miss P.V Bleed most likely suffering from now? (1) Pernicious anaemia. 229 What is required for Vitamin B12 to be adequately absorbed by the terminal ileum? (1) Intrinsic factor The Schillings test is often used to confirm a diagnosis of Vitamin B12 deficiency anaemia, briefly describe this test (4) Patient given a loading dose of 1000mg of Vit B12 intramuscularly, followed by small doses of radioactive vit B12 and excretion is then measured in the urine. Vitamin B12 malabsorption is corrected by giving intrinsic factor with labelled vitamin in pernicious anaemia, but persists despite the use of intrinsic factor in intestinal disease. How would you wish to manage Miss P.V Bleed if the schillings test was positive for Vit B12 deficency anaemia and her Hb was around 9 g/dL? (2) IM hydroxycobalamin 3 times weekly for 2 weeks and then once every 3 months for life. Name 4 other causes of macrocytic anaemia. Alcohol Folate deficiency Liver disease Drugs , e.g. azathioprine Reticulocytosis hypothyroidism 230 6.1 Investigations By the end of Phase II students should be able to: • obtain a blood sample by venepuncture • interpret a full blood count report • explain to patients the nature and value of a bone marrow aspiration and biopsy 6.2 Anaemia By the end of Phase II • students should be able to: recognise the significance of a low haemoglobin taking into account the age and sex of the patient • distinguish the type of anaemia from the blood count and together with the clinical information from the patient determine the likely cause • evaluate the cause of iron-deficiency anaemia • treat iron-deficiency anaemia • distinguish between iron-deficiency anaemia, the anaemia of chronic disease and thalassaemia trait and either treat or make appropriate referral • distinguish between macrocytic and megaloblastic anaemia • determine the cause of macrocytic anaemia clinically and with appropriate laboratory investigation • use laboratory investigation to identify the cause of megaloblastic anaemia and to institute treatment with appropriate urgency • initiate investigation of normochromic, normocytic anaemia and make appropriate referrals • recognise the possibility of and likely causes of haemolytic anaemia from laboratory investigation and clinical evidence and make appropriate referrals • recognise and institute management of acute complications of sickle cell anaemia 231 6.3 Miss F is an 18 year old female who presented with acute shortness of breath. On further questioning she has a 3- 4 month history of malaise and night sweats which has worsened over the last two weeks. She also complains of frequent nose bleeds, heavy periods and easy bruising. On examination the positive findings are pallor, a temperature of 380c, pulse of 105, BP: 135/79, respiratory rate of 18 per minute. You suspect a Leukaemia. A) Name four features you would expect to see on a blood test. Any four from: Anaemia Leucopenia Thrombocytopenia Hyperuricaemia (due to break down of cells) Reduced clotting times B) Apart from a blood test, name four other investigations you would carry out. Any four from: Peripheral blood film Bone marrow aspirate/trephine Immunophenotyping (identify cell type by looking at cell surface) Cytogenetics (to look for Philadelphia Chromosome which is found in Acute Lymphoblastic and Chronic Myeloid Leukaemia). Cytochemical studies (to identify cell types by looking at enzymes in cells). Chest X-ray (to rule out lymphoblastic lymphoma which would cause a mediastinal mass which would be identified on the chest x- ray). C) As part of her treatment you give her a blood transfusion. Name two complications of a blood transfusion. Immunological complications: Haemolytic transfusion reaction. Non- haemolytic transfusion reaction (febrile reaction) Alloimmunisation 232 Incompatibility Transfusion related acute lung injury (TRALI) Anaphylaxis (plasma protein incompatibility) Non immunological complication: Transmission of infection Circulatory failure because of volume overload Iron overload, with repeated transfusions Electrolyte change (K+ particularly) with massive transfusion Thrombophlebitis Air embolism D) The studies show she has acute lymphoblastic leukaemia and you begin chemotherapy to induce remission. During chemotherapy there is a risk of Tumour Lysis Syndrome. What is this and how can it be prevented? It is the rapid necrosis of tumour cells due to the chemotherapy which results in hyperuricaemia and raised potassium and phosphate levels. It can cause renal failure due to the deposition of uric acid and calcium phosphate crystals in the renal tubules. It is often exacerbated by a low intravascular volume. It can be prevented by ensuring the patient has normal uric acid levels by prescribing Allopurinol and by ensuring diuresis is established with I.V. fluids. E) Apart from Tumor Lysis Syndrome name three short term and three long term effects of chemotherapy: Short term: (any three) Myelosuppression Nausea and Vomiting Alopecia Oral ulceration Long term: (any three) Infertility Second malignancy Cardiac Arrhythmias and cardiomyopathy Pulmonary fibrosis Cataracts 233 F) Leukaemic blast cells can infiltrate the brain and lungs resulting in coma and respiratory failure respectively. If the blast cell count in the peripheral blood is very high (> 100x 109/L) that patient may need leukophoresis. What is leukophoresis? Blood is collected from a vein and centrifuged to remove the leukaemic cells. The red blood cells and plasma are then returned to the patient via another vein. It prevents sludging of blast cells in the capillary beds. 6.3 Haematological malignancies By the end of Phase II • students should be able to: recognise the possibility of a malignant disorder of the lympho-haemopoietic system on clinical grounds and from the blood count • make an appropriate estimate of the urgency of referral • undertake investigations to confirm myeloma as a cause of a raised plasma viscosity • describe to patients in outline the potential benefits and possible side effects of radiotherapy, chemotherapy and hormonal therapy in lymphoma 234 6.4 (answers not provided for this question) Clinical Scenario: You receive the following lab data at the end of clinic and turn up these values: Haematocrit: 49% RBC; 6.4 x 106 microlitres MCV: 76fL WBC 14 000 per microlitre Platelet count 480 000 per microlitre The white cell differential is normal. The patient is a middle aged woman who has come in for a yearly check up, she does not smoke or drink. She appeared well and physical examination was normal. 1. Are these results normal? 2. Are these separate abnormalities or part of a patter 3. What separate abnormalities would cause similar results? 4. If you consider the data together, what disease comes to mind? 5. What would be your plan at this stage? The patient returned in 2 months and re examination revealed a spleen tip. 6. What is your thought now? This same patient returns with a swollen left leg. Doppler studies have revealed she has a femoral vein thrombosis. Her laboratory results return as follows: HCT: 50% WBC: 18 000 per microlitre Platelet count: 850 000 per microlitre MCV: 72 fL 7. There are many causes of venous thrombosis. Does any possibility seem obvious from this data? 8. What treatment would you offer her? 6.4 Polycythaemia 235 By the end of Phase II students should be able to: • recognise an abnormally high haemoglobin • use clinical examination and a full blood count to determine the cause • investigate and refer appropriately • participate at an appropriate level in venesection treatment 236 6.5 (answers not provided for this question) A 12-year-old girl visits the GP following concerns about her first menstrual period. The flow was very heavy and persisted for two weeks. On further discussion she reported having always bruised easily and suffered with nose bleeds as a young child. What other information should be sought if a bleeding disorder is suspected? You suspect this is a congenital bleeding disorder. What blood tests will you need to carry out for the haematologist? If she is diagnosed with a bleeding disorder what 3 interventions should her GP avoid? Bleeding disorders are rarely congenital and are more commonly acquired, complete the following table regarding common disease states and the coagulation deficit they cause: Disease state Pathophysiology Malabsorption Vitamin K deficiency Decreased synthesis of coagulation factors Bacterial septicaemia Thrombotic disorders: Mr RB is a 58-year-old businessman who has come to see his GP with some pain and swelling in his left calf. He has recently been on a long haul flight to New York and is worried about deep vein thrombosis (DVT) What else do you need to ask about in the history? If you suspect a DVT what would you look for on examination? After a full history and examination are carried out Mr RB is sent for investigations that confirm a DVT and anticoagulation therapy is commenced. 237 As the F1 on call you are asked to start Mr RB on warfarin, what dose will Mr RB be started on, and how will the treatment be monitored? What else does Mr RB need to know about starting anticoagulation therapy? What is the target international normalised ratio for treatment of a one off DVT or pulmonary embolism? Mr RB returns to the GP after a minor episode of bleeding following a tooth extraction during the treatment period, the results of a blood test show an INR of 5, he is also complaining of bleeding gums. What 3 measures are recommended management strategy for this type of patient? 6.5 Disorders of bleeding and thrombosis By the end of Phase II students should be able to: • recognise a bleeding tendency on history and examination • manage at an appropriate level an acute haemorrhagic state • interact appropriately with the haematologist in the management of patients with chronic problems of haemostasis • recognise the possibility of a pro-thrombotic state on clinical grounds and make an appropriate referral • initiate and monitor anticoagulant therapy with warfarin and heparin according to published guidelines • counsel patients on anticoagulant therapy • recognise over-anticoagulation on clinical and laboratory grounds and be able to initiate management after appropriate discussion 238 6.8 Jane Smith is a 52 year old lady receiving chemotherapy for cancer. She has undergone 2 cycles with an interval of 6 weeks between them. She finished the latest chemotherapy 2 weeks ago. Reviewing her blood results it is clear that she has the following abnormalities: Anaemia Thrombocytopaenia Leucopenia Q1) what has happened and why? EXPERIENCING BONE MARROW FAILURE ?SECONDARY TO CHEMOTHERAPY. Q2) what are the risks associated with this picture? INCREASED BLEEDING, INCREASED SUSCEPTIBILITY TO INFECTION Q3) how do chemotherapy drugs work? AFFECT DNA SYNTHESIS OR REPAIR PROMOTES CELLULAR APOPTOSIS The rest time between the cycles of chemotherapy allow the normal cells such as bone marrow and the GI tract to recover from the toxicity. Q4) what precautions should be taken (haematological) before commencing chemotherapy? REVIEW PERIPHERAL BLOOD FILM Q5) what can be given to accelerate the recovery of the white cell count after chemotherapy GROWTH FACTOR G-CSF 239 Q6) A cytotoxic drug (such as Alkylating drug) when used in combination with extensive irradiation, can result in what possible haematological disorder? Increased incidence of ACUTE NON-LYMPHOCYTIC LEUKAEMIA Q7)Give two factors that can increase the incidence of blood dyscrasias in a patient? INREASING AGE DOSE OF DRUG DURATION OF DRUG USE 6.8 Drug interactions By the end of Phase II • students should be able to: recognise a haematological problem as being a possible consequence of concomitant drug therapy especially in patients on chemotherapy • recognise patients who are at risk of severe sequelae to drugs because of underlying haematological diseases 240 7.2 & 7.3 Barry, a previously well sixty two year old butcher from Barton on the Beans presents with a 3 day history of swollen ankles and shortness of breath. He is a poorly controlled diabetic and has been so for at least 18 years, and has poorly controlled hypertension. During his work up he has the above PA x-ray taken and an ECG. 1. Give 3 pathological findings you can see on this x-ray? Cardiomegaly: The cardio thoracic ratio is greater than 50%. Pulmonary Oedema: Bat wing appearance (Caused by the initial narrowing of the lower lobe vessels and widening of the upper lobe vessels). Pulmonary Effusion (blunting of the costophrenic angles) *** Also to look for in real life are KERLEY B LINES: 1-2 cm long horizontal lines which meet the pleura at right angles. They are usually seen up the side of the lungs beginning at the costophrenic angle. They are due to interlobular lymphatics which have been distended by fluid or tissue classically secondary to left ventricular failure or mitral stenosis. *** 2. Why is it important to know if this is a PA or AP film and which is most useful in this case? 241 When x-rays enter the chest anteriorly and are detected posteriorly, the heart, which is anterior in the chest, casts a bigger shadow than in PA films. PA films are thus more accurate in the assessment of cardiomegaly. When a large heart shadow isn’t necessarily cardiomegaly: In an AP x-ray In expiration: A pregnant patient. One with ascites. An obese patient A disobedient patient In these cases patients may not be able to take a full inspiration which might make the heart look bigger than it actually is. Eight to nine posterior ribs showing is a good inspiration. 3. Considering the history, what are the likely causes each of the 3 pathological findings? Cardiomegaly: Caused by hypertrophy of the myocardium as a result of years of uncontrolled hypertension Pulmonary Oedema: Caused by fluid leaking into the interstitium due to ↑ hydrostatic pressures as a result of left ventricular failure and pulmonary venous congestion. Pleural Effusion: A Transudative pleural effusion also caused by raised hydrostatic pressure as above. 242 One of WMS’s medical students suggested to the Consultant cardiologist that an ECG might be useful. Below is the patient’s ECG [Sorry the ECG does not fit the case perfectly; I couldn’t find one that did] 4. Where and what are the abnormalities, and hence where and what is the cause? Bradycardia of 50 bpm (Often associated with MI) S-T segment changes: ST elevation in leads II, III, and aVF suggesting inferior wall MI. Reciprocal changes (ST segment depression) in leads V1 and V2. In addition there is ST elevation in lead V6 suggesting lateral wall involvement. Lateral infarction produces changes in leads I, avL and V5/6. T Waves: Tall, (>75% of R waves) especially in Lead III and AVF which can be caused by myocardial ischemia. Inverted T waves in V1, V2 V3 These changes suggest an infarction affecting the inferior aspect of heart. 5. What is the likely diagnosis? Be specific about where in the heart the problem is. Inferior lateral MI (Silent) 243 6. From your basic understanding of ECG’s, explain why is there S-T depression in leads V1 and V2, and S-T elevation in leads II, III and aVF? The ST depression is basically S-T elevation when viewed from the other side of the heart. S-T Elevation represents MI in the inferior aspect of the heart. When viewed from the V1 and V2 leads, the opposite picture is seen. E 7. Why might our patient not have any chest pain despite the likely diagnosis? A long term Diabetic, especially one who is poorly controlled may have diabetic neuropathy. The damage to nerves caused by hyperglycaemia may mask the usual symptoms of infarction, causing a silent MI. Florence, a 72 year old women with a 15 year history of COPD presents to you with an acute exacerbation of shortness of breath. She also has fevers and rigors and pain associated with breathing and coughing. Her cough is productive of rusty coloured sputum. She has a chest x-ray shown below: 8. What can you see? How does this support the likely diagnosis? The right upper lobe (RUL) is showing an increased density. 244 There are linear lucencies in the right upper lobe (air bronchogram). This is due to consolidation consistent with a lobar pneumonia. Explanation: On a normal CXR, we can visualize the air-filled trachea, mainstem bronchi and initial portions of the lobar bronchi. Further branches should only be seen with the injection of contrast during a bronchogram. When air can be visualized in the more peripheral intrapulmonary bronchi, this is known as the ‘air-bronchogram sign’. This abnormality is usually caused by an infiltrate/consolidation that surrounds the bronchi. Dave Is a 66 year old man who has been getting progressively more breathless over a period of years. He is a life long non smoker, is phobic of pigeons and only tried slate mining once for a few minutes as a teenager (and he did not inhale). He has no medical history except for long standing and severe rheumatoid arthritis. 9. Describe what you can see in this x-ray that may be related to Dave’s breathlessness. State in general terms the diagnosis: Fine nodular and streaky linear shadowing (reticularnodular pattern) which is worse in the lung basis. Poor definition of cardiac border (Due to adjacent lung fibrosis) Fibrosis Blunted costophrenic angle indicative of pleural effususion. 245 A spirometry is requested to investigate Dave’s lung function. A Leicester medical student who is writing up Dave for a portfolio intercepts the results and finds that Dave’s FEV1:FVC ratio is 0.88. Having a vague recollection of the importance of the ratio being over 0.70 He asks you if he can tell Dave the good news, that all is well. 10. What do you say? Explain your answer, especially the relevance of a ratio being > than 0.75. No you can’t. A ratio of >0.75 indicates that there is no obstructive airway disease, so we can only rule out diseases such as COPD and Asthma. To interpret the results fully you will need the rest of the results. 11. When you get the results you find that Dave’s Vital capacity is only 55% of the predicted for his age and height. What can you conclude about the pattern of lung disease now? This is a restrictive pattern of disease. The vital capacity is reduced by fibrosis, and the FEV1: FEV ratio is normal because there is no obstruction. E 12. Years later Dave presents with worsening breathlessness and swollen ankles. What is the likely cause? Dave’s rheumatoid related lung fibrosis has caused right heart failure (cor-pulmonale). Pulmonary vasoconstriction due to alveolar hypoxia or blood acidemia and/or anatomic compromise of the pulmonary vascular bed in lung disease eventually causes pulmonary hypertension, which eventually causes right heart failure. A women presents to A+E acutely unwell: Her arterial blood gases are measured, and the results are shown below: Normal Values pH 7.25 7.35-7.45 pCO2 kPa 7.12 4.7-6 246 pO2 kPa HCO3 13. 9.1 mmol/l >10.6 25 What do they indicate? 22-28 (State respiratory/metabolic alkalosis/acidosis) Respiratory acidosis 14. Suggest a Cause: Severe asthma COPD Decreased GCS (CVA) 19 year old Sarah presents to you, her GP, with shortness of breath. She has had an irritating cough at night for a month. 15. You decide to get her to do a peak flow. Explain how you would explain to her what to do: Make sure the peak flow dial is at zero. Stand up if possible and take in as deep a breath as you can. Then place your mouth around the mouthpiece of the meter and form a tight seal with your lips. Blow out through your mouth as hard and fast as you can until you can not blow out any longer. This will move the main flow indicator up the scale and the number listed beside the indicator is your peak flow. While chatting to Sarah she tells you that she recently spent 6 months working and travelling in the Indian sub continent. She stayed with a family for three months in a remote village. She left in a rush and burnt all her belongings when she found out that 2 of the adults had TB, and she is worried she has caught it. Sarah has had all her due vaccinations. 16. Would a tuberculin test such as the mantoux test be useful in ruling out TB infection? Explain. No. If she has had a BCG vaccination she should react to the tuberculin protein regardless of whether she has contracted TB. [Incidentally, the vaccination only 247 provides 80% protection, and only for the first 15 years after the vaccination, so she could have TB despite having a BCG] E. 17. What would be the most useful investigation to rule out pulmonary TB, especially in someone with a non productive cough? Chest X-ray. (In TB Typically shows patchy or nodular shadows in the upper lobes, loss of volume and fibrosis with or without cavitation) An abnormal chest x-ray is often found in asymptomatic patients, but the reverse is very rare. Alan, a 56 year old Social Science lecturer presents with central crushing chest pain on exertion. The pain only comes when he is exercising and has been getting slightly worse over a period of 2 years. He smokes 20/day and has a 5 year history of hypertension, which he attributes to a particularly stressful module he teaches at his university’s medical school. 18 Which two important investigations would you do at this early stage? ECG Cardiac Enzymes Both these tests were normal. His blood tests are normal except cholesterol which comes back as 7.9 mmol/l. 19. What other non-invasive test would you like to do? Stress electrocardiography. 20. How would you explain this test to Alan? Stress electrocardiography is an measurement of your hearts electrical activity taken while you are exercising. The purpose is to analyse the changes in your hearts 248 electrical pattern as it does more work. Some patterns which indicate a lack of oxygen reaching your heart are not visible until the heart is stressed. Below is Alan’s stress ECG 21. Is the exercise test positive or negative? Explain. There is S-T segment depression, indicating a positive exercise test and probable IHD. not actually have IHD). (5% may In particular the segment of S-T depression is flat or even slightly down sloping which is much more likely to be due to IHD than up sloping S-T depression (see Oxford Hand book). 22. What are Alan’s risk factors for IHD? Smoking, Hypertension, Hyperlipidaemia, sex, age, stress. 23. Alan is diagnosed with Angina. What would you prescribe for him to take when he experiences the same chest pain on exertion again. 249 Sublingual glyceryl trinitrate tablet (0.5 mg) or GTN spray. 24. In the longer term how would you treat him? Give life style and medical management. Weight loss Stop Smoking Take gentle exercise Diet (low fat, low salt) Relaxation Decrease alcohol (if appropriate) Medical: Asprin (75-150mg /24hrs PO unless contraindications) Beta blockers Nitrates (atenalol 50-100mg/24hr PO) (GTN spray or sublingual tablets up to every ½ hour) (as prohylaxis 10-30mg oral nitrates BD such as isosorbide mononitrate) Calcium antagonists Statin 25. (amlodipine 5mg/24hr, diltiazem-MR 90-180mg/12 hr PO) (Aim to reduce cholesterol to <5mmol/l) Alan is scheduled for coronary angiography. Explain to him what this entails and how it may benefit him. This involves insertion of a catheter into the heart via a blood vessel in your leg. Contrast can be introduced into the coronary allowing visualisation of the anatomy and thus patency - of the coronary arteries. Obstructed blood vessels can be unblocked in various ways in the same procedure if appropriate. Objectives: 250 7.2 Investigations By the end of Phase II • students should be able to: recognise the basic radiological features of cardiac enlargement and pulmonary oedema and relate them to the underlying pathophysiology • perform an ECG • understand the basic principles of electrocardiography and interpret major abnormalities. • be able to explain stress electrocardiography, echocardiography, and coronary and femoral angiography to a patient. • recognise the basic radiological features of consolidation, pleural fluid, lung collapse, carcinoma and lung fibrosis, seeking advice where necessary and relate them to the underlying pathology • obtain and interpret a spirograph and recognise the changes in obstructive and restrictive lung disease • interpret blood gas abnormalities • use and explain the use of a peak flow meter • interpret tuberculin tests 251 7.3 Angina pectoris By the end of Phase II students should be able to: recognise angina initiate investigations to confirm the diagnosis and assess the severity of underlying coronary artery disease recognise the risk factors in individual patients initiate immediate management 252 7.3 Daisy, an 80 year old lady presents to her GP following a few episodes of chest pain she has experienced whilst out walking. This is particularly noted on colder days and the pain is relieved by sitting on a nearby park bench. The GP informs her that she may have a condition known as ‘Angina Pectoris’. Question> What is the definition of Angina pectoris (also known as stable angina)? Central chest pain (caused by myocardial ischaemia) which is brought on by exertion and relieved by rest. Question> The GP mentions that a cold environment, exercise, eating a large meal and emotional stress can play a role in initiating an angina pectoris attack. As well as these triggers, list 6 risk factors associated with coronary artery disease? Hypertension diabetes mellitus smoking hyperlipidaemia high BMI family history exercise (lack of) age, sex of the individual ethnicity socio-economic status alcohol. Question> The GP after taking a detailed history, begins an examination (with a chaperone). In particular, he looks for signs of anaemia, thyrotoxicosis and hyperlipidaemia. He then auscultates the chest for heart sounds. In particular, he listens for murmurs associated with aortic stenosis and aortic regurgitation. What role would aortic stenosis play in someone with angina pectoris? If the individual exerts themselves, the cardiac output would increase. However, if there is an obstruction to left ventricle emptying, then the coronary arteries will not receive the perfusion they are now requiring with exertion, thus exacerbating angina 253 pectoris. Can you draw the features of an aortic stenosis murmur on this diagram? HS HS I----------II------------I I111111111II------------I (ejection pan-systolic murmur) The GP refers Daisy for an ECG. Question> Name 2 positive findings on an ECG that would indicate Daisy was suffering with an acute attack of angina pectoris? ST depression, T wave inversion and T wave flattening. Question> Name 2 positive findings that would indicate previous ischaemic heart disease (IHD)? Left bundle branch block pathological Q waves left ventricular hypertrophy (i.e. left axis deviation, left ventricular strain, large R waves in V5 and large S waves in V2). Question> The GP refers Daisy for an Exercise Tolerance Test (ETT). The cardiologist reviews the ETT-ECG for any of the ECG changes aforementioned. If there are no positive ECG changes and no symptoms experienced whilst on the treadmill, does this mean Daisy does not have angina pectoris? No. Angina pectoris is a clinical diagnosis and the ETT is only 70% sensitive and 80% specific. The diagnosis of angina pectoris is a clinical one, derived after a combination of history, examination and investigations. With a normal ETT, the GP wants to refer Daisy for a diagnostic Coronary angiography, where therapeutic treatment may also occur; PTCA (Percutaneous transluminal coronary angioplasty i.e. ballooning) and/or a stent may be inserted. Depending on the results, a distant option is a coronary artery bypass graft (CABG). Question> In the meantime, the GP puts Daisy on a β-antagonist. What is the 254 mechanism of action in angina pectoris? A β antagonist acts on the β1 receptors in the blood vessels and heart to reduce heart rate (negative chronotropic effect) thus allowing greater filling of the coronary arteries during diastole. β antagonists also reduce contractility of the ventricles (negative inotropic effect) and thus reduce the oxygen demand on the heart. Non-cardioselective β antagonists will also act on β 2 receptors in the lungs and cause broncho-constriction. Question> Name two other classes of medication that are used to relieve symptomatic angina pectoris? Calcium receptor antagonists nitrates Potassium receptor agonist (e.g. Nicorandil). Extended Question> Name 2 additional types of angina (other than angina pectoris) and state their definition? Crescendo angina. The amount of effort to invoke symptoms decreases with time, although symptoms do not occur at rest. Unstable angina. Symptoms appear unpredictably either with minimal exertion or at rest. Nocturnal angina. Symptoms appear at night and can awake the patient. Decubitus angina. Onset of symptoms occurs when the patient is lying down. The GP also notes that treatment will be a holistic one with an aim of reducing all cardiovascular risk factors. 7.3 Angina pectoris By the end of Phase II • students should be able to: recognise angina 255 • initiate investigations to confirm the diagnosis and assess the severity of underlying coronary artery disease • recognise the risk factors in individual patients • initiate immediate management 256 7.4 1) A) 65 years old Mr. E presented with acute onset of central crushing chest pain 2 hours ago. He said that the pain came on suddenly while he was sitting and reading a book and since then the pain persisted. otherwise was not breathless. He looked generally unwell but Apart from acute coronary syndrome (ACS), list 4 other possible causes for his symptoms: (any 4) Pericarditis Dissecting aortic aneurysm Pulmonary embolism Gastroesophageal reflux Musculoskeletal pain Pancreatitis Perforated peptic ulcer B) Hopefully you know you will need to do a 12 lead ECG. What ECG patterns would indicate ST elevated myocardial infarction (STEMI) that fits the criteria for thrombolysis? More than 1 mm elevated ST segment in 2 or more contiguous limb leads, or More than 2 mm ST elevated in two or more contiguous chest leads. C) You have diagnosed him as having ST elevated myocardial infarction (STEMI) and decided to prescribe thrombolytic drugs. List five contraindications to the prescription of thrombolytic drugs. (any 5 from below) History of haemorhagic stroke at anytime in the past Active or recent gastric ulcer or any active internal haemorrhage Suspected aortic dissection 257 Recent major surgery with the last 6 weeks e.g laparotomy Head injury Previous allergic reaction to fibrinolytic agents Non haemorrhagic stroke within the past 1 year Previous streptokinase exposure Pregnancy or post partum C) what other immediate investigations will you do for Mr. E ? Bloods- FBC, U&Es, LFTs, D- dimer, glucose, lipid profile, cardiac enzymes (CK, Troponin T 12 hours after the onset of chest pain) Chest xray ABG Later management( arrange Echo) D) At the mean time, you will need to control his pain. what analgesia, apart from GTN, will you use, what dose and what route? Diamorphine IV 2.5-10mg C) C) what are the three factors that might contribute to thrombus formation in Mr. E’s coronary artery? Virchow’s triad: Damage in the intimal surface of the vessel changes in the pattern of blood flow hypercoagubility D) Few hours later Mr. E had a cardiac arrest and you were called in by the nurses. The cardiac nurses were doing the chest compression and a Guedal airway was in place. Another nurse now showed you the following ECG pattern. What is your diagnosis? What do you do next? 258 Diagnosis: ventricular fibrillation Attach defibrillator and defibrillate (joules depending on the machines) and check pulses in between. Give adrenaline every 3 mins accordingly, IV 1 mg. 7.4 Acute myocardial infarction By the end of Phase II • students should be able to: recognise acute myocardial infarction and use appropriate investigations to confirm the diagnosis • act appropriately to ensure that those patients likely to benefit receive thrombolysis as quickly as possible • control the pain of myocardial infarction • recognise ventricular fibrillation and carry out immediate management • recognise the need for further active management in the medium to long term • describe the features of the underlying pathophysiological changes which can be used to develop treatment and prevention strategies 259 A fifty-five year old man, Mr. Askew, presents in A&E with sudden onset of severe chest pain persisting for one hour. He describes his chest pain as “crushing”, with no radiation. He admits to having similar chest pains lasting for around 15 minutes over the last 5 months. These pains usually occur when he is exercising and are relieved by rest. Rest does not relieve his chest pain today. He feels sweaty, breathless and nauseous. He does not smoke. 1 What features of the history suggest a cardiac origin for his chest pain? Central, crushing chest pain with sweating, breathlessness and nausea. 2 What chest pain features would be suggestive of aortic dissection? Sudden tearing chest pain, may radiate to the back. 3 Give two likely cardiac causes of Mr. Askew’s chest pain. Unstable angina. Acute myocardial infarction. 4 Which pathological process commonly underlies these two diagnostic possibilities? Thrombus formation on an atherosclerotic plaque. 5 What biochemical markers would you assay to distinguish between your two diagnostic possibilities given in question 3? Cardiac enzymes – creatine kinase (MB), aspartate transferase (AST), lactate dehydrogenase (LDH). Cardiac troponins (troponin T and/or I). 6 Mr. Askew’s ECG shows ST elevation and development of pathological Q waves in leads V1-6, I and aVL. What diagnosis do these ECG findings suggest? Acute anterior myocardial infarction. 7 What would you expect to find at cardiac catheterisation in this patient? Lesion causing blockage in/narrowing of left anterior descending coronary artery. 8 Mr. Askew is given 300mg oral aspirin. What is the mode of action of aspirin? Irreversible acetylation of platelet cyclo-oxygenase enzyme, preventing thromboxane A2 formation, leading to inhibition of long-term platelet activity/aggregation. 260 9 Give the four phases of clot formation. Vasoconstriction Platelet activation Clotting Clot lysis and scarring 10 Name three other substances you would prescribe, in addition to aspirin, as part of Mr. Askew’s immediate management. Oxygen Diamorphine/morphine Glyceryl trinitrate 11 What non-modifiable risk factors for coronary heart disease does Mr. Askew have? Male sex Age 12 List five modifiable risk factors for coronary heart disease. Smoking Hypertension Hypercholesterolaemia Diabetes mellitus Obesity 13 Mr. Askew has a body mass index of 26.9kg/m2. What does this indicate? Patient is overweight. 14 Name two drugs that may be used in obesity treatment to achieve weight reduction. Orlistat. Sibutramine. 15 Mr. Askew receives thrombolysis. List five contraindications to thrombolysis. Coagulation defects, including anticoagulant treatment. Stroke within last six months. Possible aortic dissection. Acute/recent gastrointestinal bleeding. Surgery/major trauma within last two weeks. 16 One UK National Service Framework states patients suitable for thrombolysis should 261 receive this within 60 minutes of symptoms onset. Name the process that could be used to evaluate whether current practice is meeting this standard. Clinical audit. A few hours later, Mr. Askew suddenly feels unwell. His ECG is shown below. (Source: http://www.ecglibrary.com) 17 What does this ECG show? Ventricular fibrillation. 18 Name two drugs that you might need to use as part of your immediate management of this condition. Adrenaline Amiodarone 19 List five early complications of myocardial infarction. Arrhythmias Sudden death Cardiogenic shock Ruptured papillary muscle or chordae tendinae Pericarditis 20 Mr. Askew has a total blood cholesterol of 8.1mmol/l. Which type of drug would you consider prescribing? Statin. 262 21 Give two side effects of this type of drug. Myalgia Myopathy 22 What lifestyle advice would you give Mr. Askew as part of secondary prevention? Diet – decrease saturated fat intake, decrease salt intake, increase fibre intake (fruit and vegetable intake). Exercise – advise programme of cardiac rehabilitation leading to at least 30 minutes of aerobic exercise three times per week. Smoking – remain abstinent. 23 Another patient dies 3 days after having a myocardial infarction. What histological features would you expect to find in the myocardium at post mortem? Marked necrosis and inflammation is seen 2-4 days post-MI. 24 The relatives of the deceased patient are grieving. Name and outline one psychological model which attempts to explain this process. Worden’s four-stage model of grieving: Stage 1- Accept the reality of the loss Stage 2- Experience the pain of grief Stage 3- Adjust to an environment without the deceased person Stage 4- Withdraw emotional energy from the deceased person and reinvest this in other relationships Topic “ACUTE CORONARY SYNDROME” 7.3 Angina pectoris By the end of Phase II students should be able to: •recognise angina •initiate investigations to confirm the diagnosis and assess the severity of underlying coronary artery disease •recognise the risk factors in individual patients •initiate immediate management 7.4 Acute myocardial infarction By the end of Phase II students should be able to: 263 •recognise acute myocardial infarction and use appropriate investigations to confirm the diagnosis •act appropriately to ensure that those patients likely to benefit receive thrombolysis as quickly as possible •control the pain of myocardial infarction •recognise ventricular fibrillation and carry out immediate management •recognise the need for further active management in the medium to long term •describe the features of the underlying pathophysiological changes which can be used to develop treatment and prevention strategies. 264 7.5 Rose, is an 83 year old lady, who presents to the same GP, requesting a ‘medical’. Rose needs a medical certificate to satisfy the requirements for a local charity bungee-jump. One of the first actions performed by the GP was to take Rose’s blood pressure. Question> What are the diastolic and systolic values of a blood pressure reading, above which, constitute hypertension? Controversial numbers but essentially 140(systole) / 90 (diastole). The GP notes that Rose has a large arm but the GP only has a small blood pressure cuff, as the room had previously been used for a paediatric clinic. Question> If the GP were to progress with the blood pressure recording using this equipment, what effect would it have on the blood pressure reading, and why? Blood pressure reading would be inaccurate and the reading (both systolic and diastolic) would be higher than the actual blood pressure. The small cuff would not occlude the brachial artery even at a high cuff pressure, thus giving a false high reading. In search of the correct equipment, the GP comes across an automated oscillometric blood pressure device (e.g. ‘Dinamap’). Question> State one limitation of this device? Does not measure diastolic pressure (it calculates it using systolic pressure and mean arterial pressure). The machine may not be automated. Need electrical/battery supply. Requires user education. Requires blood pressure recording to be done twice consecutively for a more accurate measurement. Is less accurate with arrhythmias. The GP thinks Rose may have hypertension, so advises her to return to the surgery on 2 more occasions. 265 If Rose expresses anxiety associated with attending the doctor’s surgery, the GP may want to investigate her blood pressure using a 24 hour blood pressure monitor. Question> With a diagnosis of hypertension, the GP wants to assess end-organ damage. He looks into her eyes with a fundoscope. List the 4 stages of hypertensive retinopathy outlining a characteristic feature of each. Grade 1. Silver wiring; tortuous retinal arteries with increased reflectiveness. Grade 2. Grade 1 plus arterio-venous (A-V) nipping; thickened retinal arteries passing over retinal veins. Grade 3. Grade 2 plus haemorrhages and soft exudates (i.e. cotton wool spots); small infarcts. Grade 4. Grade 3 plus papilloedema (blurring of optic disc margins). Question> Apart from the eyes, list 3 other organs potentially at risk from uncontrolled hypertension? Brain; six times more likely to suffer with a Stroke. Heart; 3 times more likely to have coronary artery disease. Kidneys; renal failure. Peripheral blood vessels; twice as likely to develop PVD. At an increase risk of aortic dissection. Question> Although in over 90% of cases, the cause of hypertension is unknown (‘essential hypertension’), the GP would like to exclude any secondary causes of Rose’s hypertension. Can you name 4 causes of secondary hypertension? Renal causes: diabetic nephropathy, chronic glomerulonephritis, polycystic disease, tubulointerstitial nephritis and renovascular disease (e.g. renal artery stenosis). Endocrine causes: conn’s, adrenal hyperplasia, phaeochromocytoma, cushing’s and acromegaly. Congenital causes: coarctation of the aorta. Medication: oral contraceptive, NSAID’s, steroids, vasopressin, carbenoxolone, liquorice derivatives, and sympathomimetics. Pregnancy. 266 Question> The GP initiates Rose’s hypertension management by giving her some lifestyle advice. List 4 such interventions that will aid Rose’s hypertension and reduce her risk of complications. Weight reduction (BMI<25 ideally). Low fat (especially saturated fat) diet. Low sodium intake (<6g/day). Smoking cessation. Limit alcohol consumption to advisable units (<14 (women) and <21 (men)/week). Partake in exercise. Eat fruit, vegetables and fish regularly. Question> Despite this good advice, it is clear Rose may still need medication to reduce her blood pressure. List 4 categories of first line medication that can be used to achieve a reduction in blood pressure? ACE Inhibitor β antagonist Calcium channel blocker Diuretic. Angiotensin II receptor antagonist. α antagonists. Extended Question> What is Malignant Hypertension and name 2 symptoms that may occur in someone with malignant hypertension. A recent and severe rise in blood pressure that, if left untreated, could be life threatening (>220/120mmHg). It carries an 80%+ mortality rate at 1 year if left untreated. Symptoms include: severe headache, visual disturbances, seizures, transient loss of consciousness, reduced urine output, blood in the urine, symptoms of heart failure (i.e. frothy white sputum cough, dyspnoea, swollen ankles, orthopnoea, paroxysmal nocturnal dyspnoea, anorexia, fatigue and nausea). Rose wasn’t too bothered when the GP advised against performing the bungee jump, she had done 10 jumps already. 267 7.5 Hypertension By the end of Phase II • students should be able to: appreciate the importance of recognising and treating hypertension to reduce the risk of morbidity and mortality from its complications • diagnose hypertension having regard to the variability in blood pressure and possible errors in its measurement • look for possible remediable causes • recognise end organ damage • manage a patient with hypertension having regard to modification of other factors, the place of non-drug methods, the risks and benefits of pharmacological intervention and problems of compliance 268