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Some common problems in General Medicine Prof Judy Savige The University of Melbourne, Northern Health General comments • Medicine is changing rapidly so do not believe everything you read in books! • Your teachers tend to have firm opinions and do not always agree – so listen, question and decide for yourselves • Develop screening examinations for diabetes and CNS Your approach to the patient • Always treat your patients with respect • They are sick and worried • Watch how they walk into the room or wake up, and how they answer your questions • Close the curtains, introduce yourself, and address the patient appropriately • Examine the patient thoroughly and not with their clothes on! Ward rounds each day • • • • • Ask the patient how they are Ask about their illness and progress Examine for signs of recovery Check medications Check test results and see what they tell you about the patient • Don’t just ignore an abnormal test White nails • Only in female medical students • Never in a patient! Beau’s lines • Fingernails grow 1 mm a week • Severe illness interrupted nail growth 8 weeks ago CNS screening examination Complete neurological examination • when there is a history of neurological disease • when neurological disease is suspected • when you find an abnormality on screening examination Neurological assessment • • • • How patient walks into the room, posture Speech How they answer questions History itself Neruological signs patients are unaware of • Memory loss • Small, unequal pupils (glaucoma treatment, cataract removal) • Nystagmus • Visual field loss, neglect • Bell’s palsy • Previous stroke – posture, weakness, brisk reflexes • Parkinson’s disease – cogwheeling in upper limb • Cerebellar disease - nystagmus, past-pointing, heeltoe gait • Cervical spondylosis – brisk reflexes in limbs • Peripheral neuropathy – absent ankle jerks and vibration sense • Absent ankle jerks – old age CNS examination • Higher cortical function – history taking • Cranial nerves – Quality of talking – Facial asymmetry, ptosis, – Visual fields and neglect – Horizontal nystagmus and double vision – Raising eyebrows, smiling – Uvula midline, tongue pointing midline Lower limbs • • • • • • Heel-toe walking Stand on toes, squat Romberg’s test Ankle reflexes Vibration sense at ankles Sensory examination may be hard to interpret Upper limbs • • • • • ‘Play the piano’ Parietal drift, neglect Tone including ‘unrolling the fingers’ Biceps reflex Finger-nose test to a fixed point- looking for past-pointing and intention tremor Diabetes Remember: Diabetes is a vascular disease Diabetes assessment • 30% of all medical inpatients • 90% all diabetics have type 2 disease and sometimes have complications at presentation Screening questions for diabetics • Who looks after you? – GP, endocrinologist, diabetes nurse educator, dietician, coordinated clinic, ophthalmologist, podiatrist • Do you smoke? Check list for diabetics • Type I or 2, LADA, duration and treatment • Who is responsible for your care? What is control like? Blood sugar record, hypo- and hyperglycemia, HbA1C • What has BP control been like? Lipids? • Any complications? Complications of diabetes • • • • Hypertension – 70% Dyslipidemia – 70% Macrovascular disease – IHD, PVD, CVD Microvascular – Nephropathy – 20% – Retinopathy – 33% – Peripheral neuropathy –50% Macrovascular disease • • • • • Af, BP lying and standing S1 and S2, bruits, JVP Carotid bruits, old stroke Renal , iliac, and femoral bruits Dorsalis pedis, posterior tibial pulses Diabetic foot • Joint deformities, bunions, callus, ulcers, hairlessness, muscle wasting, tinea, nails • Capillary return, peripheral pulses 9both together) • Peripheral neuropathy – ankle jerk and VS • Shoes Diabetic eyes • • • • Cataracts – polar and cortical Glaucoma Macular degeneration Diabetic retinopathy – Background (haemorrahge and exudates) – Proliferative (new vessel formation) retinopathy – Laser burns Macular degeneration • Commonest irreversible cause of blindness in the world • Risk factors are age, smoking, hypertension Result of treatment for diabetes • Laser burns • Treatment protects the macula and central vision Check list for diabetics during admission • • • • FBE, U and E, LFT HbA1c (aim for HbA1c < 7) Cholesterol/triglycerides Urinary albumin:creatinine Advice to smokers • Don’t ignore it • You can tell them – Most powerful addiction known – Most patients stop by going ‘cold turkey’ – Most do not succeed the first time – Even reducing the number of cigarettes reduces lung damage – Champix, nicotine patches and smoking cessation clinics Hypertension • • • • • • Obesity, alcohol, stress Diabetes Renal artery stenosis – renal doppler Chronic renal disease – renal ultrasound, cr Glomerulonephritis – urinary RBC, cr Conn syndrome – aldo renin ratio – on prazosin and amlodipine • Phaeo – 24 hour – NOR, AD, DOP Hypertension assessment • 24 hour BP monitoring • ECG • Cardiac echo – for LVH and diastolic dysfunction • • • • HbA1C Cholesterol and triglycerides Urine alb:cr U and E Treatment of hypertension • Weight loss • Exercise • More vegetables, less alcohol, less salt and less fast food • Walk the dog, get a dog! • Meditation, yoga, prayer Treatment of hypertension • ACE inhibitor • Ca channel blocker • Prazosin – very effective but BD • Aldomet – should not be used long term • Avoid thiazides Treating pain • Non-pharmacological methods first – heat, rest and acupuncture • Panadol – 2 when pain is max then try one every 2 hours to max of 4 g a day • Add in a NSAID – and watch closely, eg Nurofen • Only then consider codeine-based medications – oxycontin and oxynorm • Codeine – based meds have too many sid effects and are becoming our commonest drug of addiction • Avoid tramadol in the elderly GORD • Non-pharmacological measures – Avoid foods that precipitate pain - spicy, acidic (tomatoes, OJ), fatty – Reduce weight – Reduce alcohol – Stop smoking – Avoid large and late meals – Raise head of bed on blocks • PPI for 8 weeks at dose that reduces symptoms • Try stopping PPI after that if a good response. Recommence treatment if symptoms recur within 3 months. Recurrences after 3 months can be treated with further short courses. Or use for symptoms only • Endoscopy only for continuous treatment to exclude Barrett’s oesophagus or atypical features Urinary tract infections • Cystitis versus pyelonephritis • Males with pyelonephritis may have a prostatic nidus • Most antibiotics do not enter the prostate – need to use ciprofloxacin or norfloxacin Heart failure Patient with CCF • What is the underlying cause? • Why has this patient presented now? • If you don’t know the answers to these questions, you can’t treat the patient appropriately What else do you want to know? • • • • • • • Recent chest pain Sinus rhythm, or bradycardia, Af or tachycardia Anaemic Septic JVP, crepitations, peripheral or sacral oedema BP- lying and standing Weight now and previously when euvolemic What is the underlying cardiac abnormality? • Ischemic heart disease – in many • Hypertension – in many too • Other types of cardiomyopathy – eg inherited, viral, drugs, alcohol, amyloid, haemochromatosis, thyrotoxicosis • Valvular disease – rheumatic, aortic stenosis How do you know it’s IHD? • • • • History of angina, infarct, stents or CAGs ECG changes Echo – segmental dysfunction Troponin elevation What are precipitants of CCF? • • • • • • • • • • Not taking tablets Progressive disease Further ischemia or infarct AF, bradycardia or other arrhythmia Fever Thyrotoxicosis Fluid, salt overload Anaemia Pulmonary embolism Drugs – b blockers, NSAIDs What treatment? • Not taking tablets • Side effects of tablets • Further ischemia or infarct • Progressive disease • Supervise, explain, box • Stop these • Treat ischemia, angioplasty, increase antianginal meds • Optimise meds • • • • • • • • • • • • AF Fever Thyrotoxicosis Fluid, salt overload Anaemia PE Control rate or revert Treat infection Make euthyroid Diurese, fluid restrict Transfuse Anticoagulate Treatment for CCF • Increasing diuretics is not always best treatment • Work out patient’s base weight – from asking them or from chart • Patients often respond to pulses of diuretics – aim for previous well weight, ankle oedema means 3 – 5 Kg in XS, sacral oedema is > 5 kg Treatment for CCF • • • • • Fluid and salt restrict – but hard for patients Diuretics, K supplements ACE inhibitors, ARB b-blockers – sotalol, bisoprolol Spironolactone Treatment for severe fluid overload • • • • • • Fluid restriction to 1.5 or 1 L a day Extra pulses of lasix Lasix, chlotride, amiloride/aldactone Strict bed rest Stockings Try to maintain blood pressure - risk of acute renal failure from reduced intravascular volume Combination of heart failure and renal failure (end-stage CCF) • Aim is to have patient free of symptoms • Not SOB, not uremic (sleepy or confused) and not dizzy when they stand up (postural hypotension) • Don’t worry too much about the serum creatinine (symptoms correlate better with urea level) • Takes days to sort out compartments • Best done at home by GP if at all possible • Generally poor outcome How do you tell the difference between heart failure and pneumonia? • Clinical signs may be identical • Pneumonia – Look toxic – Yellow-green sputum – Fever at any time since presentation – High CRP – CXR – localised alveolar opacity, no upperlobe diversion • CCF and pneumonia commonly coexist Pneumonia that does not improve How do you know a patient is improving • Ask them • Improvement usually starts within 12 hours of starting antibiotics • Less sputum • Fever starts to subside • Crepitations start to clear • Arterial saturations improve, less need for O2 • Lack of progression • CRP falls quickly • Finally radiological abnormalities clear When pneumonia does not improve • • • • • • • • • • • • Wrong antibiotic eg atypical pneumonia Pneumonia too extensive – often in middle-aged men Wrong disease eg acute cholecystitis CCF present too Continued aspiration Poor sputum drainage – helped by physiotherapy Elderly, frail, comorbidities impairing immune status Pleural effusion, abscess, empyema Bronchiectasis TB Cancer Bronchiolitis-obliterans organising pneumonia (COP) Acute renal failure • Once renal function is abnormal, it will continue to deteriorate (‘hyperfiltration hypothesis’) • Must try to get renal function back to base line to prevent deterioration to chronic renal failure • Rapidly progressive glomerulonephritis – a medical emergency – glomerular haematuria and RBC casts Acute or chronic renal failure? • Ask the patient about renal function, refer to old records • Small kidneys in CRF on ultrasound • Hb, Cr and Urea and Ca/P are not always helpful, PTH takes too long • Often acute-on-chronic renal failure - work out baseline renal function and hope to recover to this Tests in RPGN • • • • • • • • • • ANCA antiGBM antibodies ANA and antidsDNA antibodies ASOT and antiDNase B Hepatitis B and C serology Cryoglobulins antiPLAR2 antibodies IgA C3 and C4 Renal biopsy Treatment of ARF • Treat underlying cause – hypotension, sepsis, obstruction • Stop or monitor all renally-excreted drugs • Low protein, low K diet • Treat fluid overload - fluid restriction • Treat hyperkalemia, acidosis • Dialysis – fluid overload, K, acidosis, uremia Diagnostic tests • You should use tests to confirm your clinical suspicions • Do not ignore an abnormal test but think it means • Always have a reason for requesting a test – there is no need to repeat FBE and U/E more than twice weekly in stable hospital inpatients • CRP is a very useful test – indicates inflammation is present and the amount of inflammation • All medical admissions warrant FBE, U/E, LFT, Ca, P, RBS/HbA1C and usually CRP. Vit D is often worthwhile. We have no good test for malnutrition. Iron deficiency • • • • Lethargic Anaemic, peptic ulcer disease, aspirin use Have a high index of suspicion Hb and MCV may be normal Iron deficiency • Aspirin – even low dose for cardiac disease • Dieting • Menstruation, pregnancy, breast feeding • Renal failure • Coeliac disease • Gastrointestinal tract ulceration, GORD • Ca bowel Examination • • • • • Conjunctival pallor – Hb < 100 Koilonychia, brittle nails Hair loss, stomatitis, dull skin BP lying and standing Abdominal examination, epigastric tenderness • PR examination Treatment • Ferrogradument/VitC – one a day for at least 4 months • Blood transfusion • Iron infusion • Proton pump inhibitor • Lower dose aspirin or clopidigrel • Check ferritin level 3 months after end of treatment Rapid fall in haemoglobin • • • • Wrong blood sample Haemodilution Blood loss Anaemia of chronic disease/active inflammation • Laboratory variation Microcytic anaemia • Iron deficiency • Anaemia of chronic disease • Thalassemia – MCV – constant thru’ life Anaemia of chronic disease • • • • • Lowish haemoglobin Normal or low MCV Unable to use iron, high ferritin High CRP Together with iron deficiency – low-N ferritin, may respond to iron infusion Macrocytosis • • • • • • • Liver disease Alcohol Hypoxemia B12/folate deficiency Medications eg azathioprine Myelodysplasia Reticulocytosis, hypothyroidism, cold agglutinins B12 deficiency • • • • • • • 20% due to pernicious anaemia B12 malabsorption Gastrectomy Vegans Terminal ileal disease Pregnancy, OC Myeloma, elderly Pernicious anaemia • Blood film – larger RBC, hypersegmented neurotrphils, cytopenias • Intrinsic factor antibodies, • High serum gastrin • Schilling’s test – rarely performed now • Holotranscobalamin II Haemolysis • • • • • • • Uncommon Fall in haemoglobin Increase in unconjugated bilirubin Increased reticulocytes Increased LDH Low haptoglobins Specific tests for cause Haemolysis • Blood film is really helpful – Hereditary spherocytosis – spherocytes – AIHA – spherocytes – G6PD deficiency – bite and blister cells – TTP – fragmented RBC – Sickle cells – Cold AIHA – agglutinated cells Neutropenia • • • • Medications Sepsis Infections Marrow infiltration Neutrophilia • Stress/steroids • Infections • PRV Thrombocytopenia • • • • • • Severe sepsis Medications – cytotoxics, alcohol, heparin ITP Aplastic marrow Hypersplenism Marrow infiltration Thrombocytosis • • • • Inflammation Iron deficiency Acute blood loss Essential thrombocystosis/PRV C reactive protein • Monocytes, macrophages release cytokines that cause liver to produce CRP • CRP binds foreign pathogens and damaged cells, activates complement and is chemotactic for monocytes • Marker of inflammation • Highest in bacterial infections (>100 mg/L) • Increased in rheumatoid arthritis, inflammatory bowel disease, malignancy, after surgery, gout • Not affected by anaemia, CCF, polycythemia (unlike ESR) • Earlier rise, falls more quickly than ESR