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CCP 64. Constipation: Infrequent bowl movements (~3 or less times weekly) or passing stools less often than person’s own normal habit, or with difficulty, straining, or pain + Rome criteria. Bowel structure and function: -Alimentary canal is used to process, digest, gain essential amino acids, vitamins, mineral, protein, fat and carbohydrates from food/water and excrete waste products -Large bowl is sight of mineral and water absorption -Motility due to -segmental contractions by taenia coli (longitudinal muscles) -peristalsis with distension initiating contractions and vagal inhibitory and excitatory fibres controlling movement, involving outer longitudinal and circular smooth muscles (Meissner’s and Auerbach’s plexuses) -mass movement -Mucus is also secreted to aid passage of faeces -Defecation urges come from cholinergic parasympathetic nerves of pelvis and go to higher centres with voluntary external anal sphincter (striated muscle) relaxation occurring thereafter as well as the involuntary internal anal sphincter (smooth muscle). A reflex response of distension of the distal rectum occurs. Intact Auerbach’s and Meissener’s plexuses necessary for this reflex relaxation to occur. An increase in intra-abdominal pressure will then be achieved to expel faeces. Causes of constipation: Colorectal carcinoma -Aetiology -3rd most common cancer in UK for men and women -Most are adenocarcinomas which advance from polyps -Risk factors of family history of colorectal carcinoma under 60, HNPCC, inflammatory bowel disease, FAP (APC tumour suppressor gene mutation), Peutz-Jeghers syndrome, Diet (rich in meat and fat, low in fibre, folate and calcium, smoking, sedentary lifestyle, hormonal factors (nulliparity, early age of menopause), diabetes mellitus, history of small bowel cancer, ovarian or breast cancer -Symptoms/signs -Right colon cancers: weight loss, anaemia, occult bleeding, mass in right iliac fossa, disease more likely to be advanced at presentation. -Left colon cancers: often colicky pain, rectal bleeding, bowel obstruction, tenesmus, mass in left iliac fossa, early change in bowel habit, less advanced disease at presentation. -Rectal bleeding, change of bowel habit and anaemia are the most common symptoms/signs -Jaundice, hepatomegaly and ascites in advanced disease -Diagnosis -LFTs+FBC -Sigmoidoscopy/Colonscopy. Colonoscopy is gold standard as most cancers detectable this way -CT colongraphy -Liver USS, CT/MRI -The Dukes' staging classification is now gradually being replaced by the tumour/node/metastases (TNM) classification: -TX: primary cannot be assessed. -T0: no evidence of primary carcinoma in situ (Tis) - intraepithelial or lamina propria only. -T1: invades submucosa. -T2: invades muscularis propria. -T3: invades subserosa or non-peritonealised pericolic tissues. -T4: directly invades other tissues and/or penetrates visceral peritoneum. -NX: regional nodes cannot be assessed. -N0: no regional nodes involved. -N1: 1-3 regional nodes involved. -N2: 4 or more regional nodes involved. -MX: distant metastasis cannot be assessed. -M0: no distant metastasis. -M1: distant metastasis present (may be transcoelomic spread). -Management -Surgery: r/l hemicolectomy, sigmoid colectomy, anterior resection, abdominoperitoneal resection, can provide pre-operative brachytherapy) -Radiotherapy -Chemotherapy: mainly for metastatic disease with varying regimes, can be used in conjunction with monoclonal antibodies (cetuximab and bevacizumab) -Palliative therapy -Around half the people diagnosed with colorectal carcinoma will survive for at least 5 years after diagnosis Hypecalcaemia (Hyperparathyroidism) -Aetiology -Parathormone (PTH) & other cause of Ca2+ increase, e.g. sarcoidosis -Amyloidosis -Renal failure -Addison’s disease (adrenal calification) -TB nodes; Toxoplasmosis (CNS) -Histoplasmosis (e.g. in lung) -Overdose of vitamin D -Raynaud’s-associated disease e.g. CREST (calcification in skin or CNS vessels); dermatomyositis -Muscle primaries/leiomyosarcomas -Ossifying metastases (ostesarcoma) or ovarian mets (to peritoneum) -Nephrocalcinosis -Endocrine tumours (e.g. gastrinomas) -Symptoms/signs -Bones, stones and psychic moans -Abdominal pain -Vomiting -Constipation -Polyuria -Polydypsia -Depression -Anorexia -Weight loss -Tiredness -Weakness -Hypertension -Confusion -Pyrexia -Renal stones -Renal failure -Ectopic calcification -Cardiac arrest -ECG: QT interval decreased -Diagnosis -Distinguish between malignancy (↓albumin, ↓Cl-, alkalosis, ↓K+, ↑PO43-, ↑alk phos.) and hyperparathyroidism (↑PTH). Also FBC, protein electrophoresis, CXR, isotope bone scan, 24hr urinary Ca2+ excretion Hypothyroidism -Aetiology -Common (4/1000/yr) -Female to male ratio ~ 6:1 -Autoimmune causes: primary atrophic hypothyroidism, Hashimoto’s thyroiditis -Other causes: iodine deficiency, post-thyroidectomy or radioiodine treatment, drug-induced, subacute thyroidits. Secondary hypothyroidism due to not enough TSH (hypopituitarism, rare). -Associated with Down’s and Turner’s syndrome, CF, primary biliary cirrhosis, ovarian hypertimulation, POEMs syndrome -Pregnancy complications: eclampsia, anaemia, prematurity, ↓birthweight, stillbirth, PPH -Symptoms/signs -Tired; sleepy ;depression; cold intolerance; weight gain; constipation; menorrhagia; hoarse voice; cramps; weakness; dementia; myalgia; reduced memory/cognition -BRADYCARDIC;reflexes relax slowly; ataxia (cerebellar);dry thin hair/skin; yawing/drowsy/coma; cold hands +/- reduced temperature; ascites +/- non-pitting oedema (lids;hands;feet) +/- pericardial or pleural effusion; round puffy face/doublechin/obese; defeated demeanour; immobile +/- ileus, CCF (also neuropathy; myopathy; goitre) -Diagnosis -TFTs; TSH ↑, T4 ↓ (in rare secondary hypothyroidism T4 ↓& TSH ↓). Macrocytosis + cholesterol & triglycerides ↑ -Management -Levothyroxine, amiodarone. Hirschsprung’s disease -Aetiology -Aganglionic megacolon - Congenital; lack of migration of neural crest cells to nervous plexuses in bowel -Complications of GI perforation, bleeding, ulcers -Symptoms/signs -Delayed passage of meconium -Abdominal distension -Constipation (absolute) - Chronic enterocolitis -Megacolon -Faeces felt per abdomen -Diagnosis -Barium enema or sigmoidoscopy/biopsy of aganglionic section, staining for acetyl-cholinesterase-+ve nerve excess -Management -Excision of aganglionic segment +/- colostomy. Doesn’t always lead to immediate recovery Other causes: - Laxative abuse -Drug related e.g. aluminium antacids, antimuscarinics (e.g. procyclidine, oxybutynin), antidepressants (most commonly tricyclic antidepressants, but others may cause constipation in some individuals), antiepileptics (some): carbamazepine, gabapentin, oxcarbazepine, pregabalin, phenytoin, sedating antihistamines, antipsychotics, antispasmodics: dicycloverine, hyoscine, calcium supplements, diuretics, iron supplements, opioids, verapamil -Constitutional/dietary Pharmacology of laxative, motility stimulants and constipating agents: -Bulk forming -Increases bulk in similar process to fibre -Unprocessed bran + other supplements such as isphagula (psyllium) taken as part of diet -Increases bulk of faeces by absorbing more water -Stimulant -Increase motility of the bowel -Senna, bisacodyl etc. -Osmotic -Retain fluid in large bowel by osmosis -Lactulose and macrogols (polyethylene glycols) -Faecal softeners -Does what it says on the tin -Bulk forming laxatives have similar action -Docutase sodium (has weak stimulant action as well), liquid paraffin etc. Motility stimulants -Metoclopramide: increases local Ach release increasing gastric motility -Domperidone: dopamine-receptor antagonist increases gastric emptying and duodenal peristalsis through unknown mechanism Constipating agents -Antidiarrhoeal drugs -Glucose and sodium chloride to replace electrolytes (dioralyte etc.) -Opiods: act on mu receptors on myenteric neurons reducing peristalsis -Antispasmodics -Muscarinc receptor antagonists: decrease muscle tone by inhibiting parasympathetic activity in alimentary canal (e.g. dicyclomine, propantheline) -Mebeverine acts directly on GI smooth muscle causing it to relax