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81 Cards in this Set
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Leukoplakia
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White thickening on the tongue or oral mucosa, idiopathic cause. It is pre-malignant!
Oral hairy leukoplakia is a shaggy white patch on the side of the tongue caused by EBV (seen in HIV). |
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Aphthous ulcers
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Causes: Crohn’s disease/coeliac disease, trauma, erythema multiforme, lichen planus, pemphigus/pemphigoid, infections (Herpes simplex, syphilis, Vincent’s angina).
Symptoms: shallow painful ulcers on the tongue/oral mucosa. Heals without scars. Treat.: Is difficult. Hydrocortisone on the ulcer/tetracycline mouthwash may help. If the ulcer does not heal in 3 weeks, perform biopsy to exclude malignancy. |
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White intra oral lesions
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Can be:
- Idiopathic keratosis - Carcinoma - Leukoplakia/hairy oral leukoplakia - Lichen planus - SLE - Poor dental hygiene - Smoking - Candidiasis - Aphthous stomatitis - Squamous papilloma - Secondary syphilis |
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Candidiasis
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Cause: Appear in high ages, DM, antibiotics, immunosuppression (long term corticoster., corticoster. inhalers, cytotoxics, malignancy, HIV). Oral candidiasis in a healthy patient may suggest HIV.
Symptoms: White patches/erythema on the buccal mucosa that may be hard to remove and bleed when scraped. Treat.: Nystatin/amphotericin/fluconazole |
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Cheilitis/angular stomatitis
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Fissuring on the angles of the mouth
Cause: denture problems, candidiasis, iron/riboflavin (B2) deficiency. |
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Gingivitis
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Cause: poor oral hygiene, drugs (phenytoin, cyclosporine, nifedipine), pregnancy, vitamin C-deficiency (scurvy), acute myeloid leukemia, Vincent’s angina.
Symptoms: Inflammation of the gums+hypertrophy. |
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Microstomia
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Cause: small mouth due to thickening+tightening of the perioral skin after burns, epidermolysis bullosa or systemic sclerosis.
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Oral pigmentation
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Cause: Perioral brown spots suggests Peutz-Jegher syndrome. Pigmentation anywhere in the mouth suggest Addison’s disease/drugs (antimalaria). Malignant melanoma. Telangiectasis of the oral mucosa suggests systemic sclerosis or Osler-Weber-Rendu syndrome. Creamy yellow spots at the border of the oral mucosa and the lips are sebaceous cysts which are common and benign. Black tongue indicates Aspergillus Niger colonization.
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Teeths
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Blue line at the gum-tooth margin indicates led poisoning. Yellow-brown discoloration indicates prenatal/childhood treatment with tetracycline.
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Tongue
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Furred/dry in dehydration or medication with tricyclics, after radiotherapy, Crohn’s/Sjögren’s/Mikulicz’s syndrome.
Glossitis: smooth red sore tongue caused by deficiency of iron, folate or vitamin B12. Local loss of papillae that leads to ulcer like lesions that change color and size indicated “geographic tongue” (harmless migratory glossitis). Macroglossia: Too big tongue seen in myxedema, acromegaly, amyloid. Tongue cancer: appears on the edge of the tongue as a raised ulcer with firm edges. On ant. 1/3 of the tongue spreads to submental nodes, middle 1/3 spreads to submandibular nodes and post. 1/3 spreads to deep cervical nodes. Riskfactors are smoking and alcohol. |
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Dysphagia
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Cause: Mechanical block (malign/benign strictures), extrinsic pressure, motility disorders.
Symptoms: difficulty swallowing. Cachexia, anemia, supraclavicular nodes (left->Virchow’s node in intra-abdominal cancer), systemic disease (syst. sclerosis, CNS). Diagn.: Ask the following questions: Problem swallowing solids and liquids from start? Yes->motility disorder (achalasia, neurological), pharyngeal cause. Or was it first solid, then liquid? (benign/malign stricture).Difficult making the swallowing movement? (bulbar palsy, espec. if cough on swallowing). Painful swallowing? (cancer, severe esophagitis, achalasia, esophageal spams). Is the problems intermittent (esophageal spasm) or constant (malignant stricture). Does neck bulge on drinking? (pharyngeal pouch.) Diag.: Blood (CBC [anemia], urea+electrolytes [dehydr.]), thorax-Xray (fluid level in mediastinum, absent gastric bubble, aspiration), barium swallow test, endoscopy+biopsy, esophag. manometry |
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Diffuse esophageal spasm
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Cause: corkscrew esophagus, nutcracker esophagus
Symptoms: intermittent dysphagia+chest pain Diagn.: Barium swallow test (abnormal contraction, corkscrew esophagus). Non-propulsive contraction indicates cork-screw esophagus and suggest motility disorder. Nutcracker esophagus is a distal peristaltic contraction (>180mmHg) that causes pain that’s relieved by nitrates (sildenafil) or sublingual nifedipine. |
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Achalasia
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Cause: failure to relax the lower esophag. sphincter due to degeneration of plexus myentericus.
Symptoms: dysphagia, regurgitation, substernal cramps, ↓weight. Diag.: Barium swallow test shows dilated esophagus. Treat.: endoscopic balloon dilatation, Heller’s cardiomyotomy and then PPI (omeprazole). If not indicated for surgical procedures, perform botulinum toxin injections. |
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Benign esophageal strictures
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Cause: GERD, corrosive substances, surgery, radiotherapy, esophageal cancer. Associated with GERD, Barrett’s esophagus, tobacco, alcohol, achalasia, Paterson-Brown-Kelly syndrome [post-cricoid web+iron deficiency].
Treat.: Endoscopic balloon dilatation |
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Nausea and vomiting
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Causes: GI-tract (peptic ulcers, pyloric stenosis, intestinal obstruct. paralytic ileus, acute cholecystitis/pancreatitis), CNS (migraine, ↑intracran. pressure, brainstem lesions, motion sickness, labyrinthitis), metabol.(uremia, hypercalcem., hyponatrem., pregnancy, diabet. ketoacid., Addison’s), drugs (antibiotic., digoxin, opiates, cytotoxics), others (MI, autonomy. neuropathy, UTI)
Diag.: Blood (CBC, livertests, Ca2+, glucose, amylase, gases [metabol. hypochloremic alkalosis from loss of gastric content]), abdom. Xray (bowel obstruct.), endoscopy. Treat.: Use pre-operative care for post-op symptoms. Try oral route first. 1/3 of patient will require two anti-emetics, but avoid drugs in pregnancy/children. Give i.v. fluids+K+ if severely dehydrated. |
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Anti-emetic drugs
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H1-antagonists: Cyclizine
D2-antagonists: Cinnarizine, metoclopramide 5HT3 antagonists: Domperidone, prochlorperazine, haloperidol, ondansetron Others: Dexamethasone, Midazolam |
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Dyspepsia
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Cause: Non-ulcer dyspepsia, duodenal/gastric ulcer, duodenitis/gastritis, gastric malignancy, GERD, esophagitis.
Symptoms: Epigastric pain related to hunger, specific foods or time of day. May be associated with bloating and fullness after meal and heartburn. Alarming symptoms are anemia, ↓weight, anorexia, recent progression of symptoms, melena/hematemesis, swallowing difficulty, tender epigastrium, abdominal mass, supraclavicular nodes. Diag.: Test for H. pylori with carbon dioxide breathing test, antigens in feces, endoscopic biopsy. Treat.: Antacids+antireflux 4 weeks. Persisting symptoms, test for H.pylori. If positive, eradicate H. pylori. If negative, give PPI. Review symptoms after 4 weeks. |
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Duodenal ulcer
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Cause: H.pylori, drugs (aspirine, steroids), ↑gastric secretion, ↑gastric emptying (->↑duodenal pH), bloodgroup 0, smoking.
Symptoms: 50 % are asymptomatic. Epigastric pain before meals or during night. Pain relieved by eating/drinking milk. Epigastric tenderness. Diag.: Endoscopy (stop PPI 2 weeks before), test for H. pylori, measure gastrin levels when off PPI (Zollinger-Ellison syndrome). Diff. diagnosis: Non-ulcer dyspepsia, duodenal Crohn’s, TBC, lymphoma, pancreatic cancer. |
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Gastric ulcer
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Cause: high age (ulcer on curvature minor, usually benign. Ulcer on other locations are often malignant), smoking, NSAID, duodenal reflux, delayed gastric emptying, stress, neurosurgery (Cushing’s ulcer) or burns (Curling’s ulcer).
Symptoms: Asymptomatic/epigastric pain related to meals, relieved by antacids. Diagn: Endoscopy (malignancy exclusion) with multiple biopsies from ulcer rim+base (histology and H.pylori) and brushing (cytology). Treat: Life style change (stop smoking), eradicate H.pylori if positive, antacids (PPI [lasoprazole], H2-rec. block [cimetidine, ranitidine]), stop NSAID/use PPI, surgery. Complications: bleeding, perforation, malignancy, gastric outflow obstruction. |
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GERD
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Causes: dysfunction of lower esophageal sphincter ->reflux (may cause esophagitis, ulcer, benign esophageal stricture, Barrett’s esophagus, adenocarc., iron deficiency). Associated with smoking, hiatus hernia, pregnancy, obesity, large meals, achalasia surgery, drugs (tricyclics/anticholinergics/nitrates), systemic sclerosis, H. pylori.
Symptoms: Heartburn at meals/lying down/leaning forward. Relieved by antacids. Belching, excessive salivation, painful swallowing, nocturnal asthma. Diag.: Endoscopy if symptoms > 4 weeks, dysphagia, persistent/relapsing sympt. despite treatment, ↓weight. Treat.: Lifestyle (↓weight, stop smoking, raised head when resting, small regular meals, avoid hot drinks, alcohol, late meals, nitrates, anticholinergics, tricyclics, calcium channel blockers, NSAID). Antacids or alginates relieve symptoms. PPI if esophagitis. Prokinetics (metoclopramide). Surgery (Nissen fundoplication) in severe symptoms resistant to medical treatment+pH-evidence of severe reflux |
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Hiatus hernia
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Cause: Divides into sliding hiatus hernia (Gastro-esoph. junction above diaphr.) and rolling hiatus hernia (gastro-esoph. junction remains in abdomen).
Symptoms: 50% have symptomatic GERD. Diagn.: Barium swallow test, endoscopy (for complications but cannot reliably exclude hernia). Treat.: ↓weight, treat symptoms of reflux (antacids, alginates, PPI, prokinetics). Surgery if persistent symptoms or recurrent stricture. |
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Symptoms of diarrea
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>200 ml of watery stool/day with ↑stool frequency. Steatorrhea is defined as increased watery stool with ↑amount of fat (pale, foul smelling, hard to wash away). Differentiated from fecal urgency (rectal cancer).
Symptoms: Large bowel symptoms (watery stool+blood/mucus, pain relieved by defecation, tenesmus, urgency), small bowel symptoms (periumbillical pain not relieved by defecation, watery stool, steatorrhea), pus, blood, mucus, constipation, ↓weight, clubbing, oral ulcers, dehydration, anemia |
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Causes of diarrea
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Cause: Acute diarrea (gastroenteritis), chronic diarrea with alternating constipation (IBD),"", chronic pancreatitis, organic cause (suggested by anorexia, nocturnal diarrea, anemia), celiac disease, gastrinoma/VIPoma, pellagra, amyloidosis, bloody diarrea (Campylobacter, Shigella, Salmonella, E.coli, amoeba, UC/Crohn’s, colorect. cancer, colonic polyps, pseudomembranous colitis, ischemic colitis), mucous (IBD, colorectal cancer, polyps), pus (IBD, diverticulitis, fistula/abscess), non-GI-causes (PPI, antibiotics, cimetidine, propranolol, cytotoxics, NSAID, digoxin, alcohol, laxatives, thyrotoxicosis, autonomic neuropathy, Addison’s, carcinoid).
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Diagnosis of diarrea
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Clinical signs, rectal examination, fecal culture+fat+antigens [C. difficile]. Blood (CBC, urea+electrolytes,↓K+,↑ESR [cancer, IBD], ↑CRP [infection, IBD], ↓TSH [thyrotoxicosis], coeliac serology), rigid sigmidoscopy+biopsy, colonoscopy/barium enema [malignancy, colitis]
Treat.: Treat causes. Oral rehydration [saline+K+] (better than i.v.), avoid antibiotics except in infective causes with systemic illness (risk of antibiotic resistance) |
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Constipation, causes, symptoms and diagnosis
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Passage of stool <3 times/week or difficulty passing stool+straining+discomfort.
Causes: General (poor diet, ↓fluid intake, IBD, immobility, old age, post-op), anorectal disease (anal fissure, anal stricture, rectal prolaps), intestine. obstruct. (colorect. carcinoma, strictures [Crohn’s], pelvic mass, diverticulosis [rectal bleeding], pseudo-obstruct.), metabolic/endocrine (hyper-Ca2+, hypothyr., hypo-K+, porphyria, lead poisoning), drugs (opiate analgetics, anticholinergics, iron), neuromusc. (spinal/pelvis lesion, aganglionosis [Chaga’s, Hirschsprung’s], syst. sclerosis, diabet. neuropathy), other (chronic laxative abuse, idiopat. slow transit, idiopat. megarectum, psycholog.). Symptoms: blood/mucus alternating with diarrea, changed bowel habit. Diagn.: Mostly tests are not needed unless >40 years old, changed bowel habit, associated symptoms (↓weight, mucus, blood, tenesmus). Blood (CBC, urea+electrolytes, Ca2+, thyroid.), sigmoidoscopy+biopsy, barium enema/colonoscopy (malignancy) |
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Treatment of constipation
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Treat cause. Advice exercise+↑fluid intake (↑fibres might cause bloating without helping constipation). If this fails, consider medication for a short period. Bulking agents (methylcellulose) ↑fecal mass and stimulates peristaltism within a few days. Taken with lots of fluids. Contraindicated in intest. obstruct., colonic atony, fecal impaction. Stimulant laxatives (glycerol, danthron) ↑intest. motility (don’t use in intest. obstruct. or acute colitis), avoid prolonged use (can cause colonic atony, hypokalemia). Stool softeners (liquid paraffin) are helpful in painful anal conditions (fissures), but should not be used for long time (lipoid pneumonia, malabsorption). Osmotic laxatives (lactulose) retain fluid in the bowel, useful in hepatic encephalopathy.
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Causes of jaundice
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Yellow pigmentation of skin+sclera+mucosa due to ↑plasma bilirubin.
Pre-hepatic jaundice: ↑bilirubin prod. (hemolysis, dyserythropoesis)/↓liver uptake/conjugation (glucuronyl transferase deficiency [Gilbert, Crigler-Najjar])-> unconjugated bilirubin in circulation but not in urine. Hepatocellular jaundice is caused by damage to the hepatocytes by virus (hepatitis, CMV, EBV), drugs, alcohol, cirrhosis, livermetastases/abscess, haemochromatosis, autoimmunity, septicemia, leptospirosis, alfa-1-antiytypsin deficiency, Budd-Chiari, Wilson, Dubin-Johnson, Rotor, right heart failure, toxins, fungi. Obstructive jaundice appears when the common bileducts is obstructed ->overspill of conjugated bilirubin in circulation (dark urine+pale feces[+pruritus]). This is caused by gallstone, panc. cancer, porta hepatis lymphnodes, drugs, cholangiocarcinoma, primary sclerosing cholangitis, primary biliary cirrhosis, choledochal cyst, biliary atresia, Mirrizi’s syndrome |
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Causes of jaundice in a previously stable cirrhosis patient
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Sepsis from UTI or pneumonia
Alcohol Drugs Malignancy (hepatocellular carcinoma) GI-bleeding Look for signs of decompensation such as ascites, dilated abdominal veins, neurological upset or peripheral edema. |
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Drug-induced cause of jaundice
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Hemolysis: antimalarias, dapscine
Hepatitis: paracetamol overdose, anti-TBC (isoniazid, rifampicin, pyrazinamide), statins, sodium valproate, MAO-inhib., halothane Cholestasis: Antibiotics, anabolic steroids, oral contraceptives, chlorpromazine, sulfonylurea, gold |
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Diagnosis of jaundice
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Ask about: blood transfusions, i.v. drugs, piercing/tattoos, sexual activity, trips, jaundice contacts, family history, alcohol, medications. Signs of chronic liver disease (leuchonychia, Terry’s nails, clubbing, palmar erythema, hyperdynamic circulation (↑NO->vasodilat), Dupuytren’s contracture, spider naevi, xanthelasma, gynecomastia, atrophic testis,↓bodyhair, parotid enlargement, hepatomegaly, small liver [late disease]), hepatic encephalopathy, lymphadenopathy, splenomegaly, ascites, palpable gallbladder, pale stool, dark urine.
Tests: Screening (serology [EBV, CMV, HBV+HCV], iron [hemochromatosis: ↑ferritin+↑iron], alfa-1-antitrypsin defici., ↓serum copper+ceruloplasmin [Wilson], ANA+ ANCA, immunoglobulines, direct+indirect bilirub.), Blood (CBC, coag., Coomb’s, urea+ electrolytes, liver test), urine (no bilirub. in prehepatic, no urobilinogen in obstruct.), ultrasound (dilat. bileducts, gallstones, metastases, pancreatic mass), ECRP (dila. bileducts+unimproved livertests), biopsy, CT/MRI |
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Upper GI-bleeding
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Causes: ulcers, liver disease, esophageal varices, drugs (NSAID, aspirine, steroids, thrombolytics, anticoag.), alcohol, gastritis/duodenitis, malignancy, bleeding disorders, portal hypertensive gastropathy, haemobilia, Meckel’s diverticulum, Peutz-Jegher syndrome, Osler-Weber-Rendu syndrome.
Symptoms: hematemesis (bright red or coffee grounds), melena (black blood in stool), shock. Diag.: History (dyspepsia, ulcers, liver disease, esophageal varices, dysphagia,vomiting, ↓weight, drugs, alcohol, cardiovasc./respir. disease, hepatic/renal disease, malignancy), rectal palpation (melena), signs of shock (cold, clammy skin, capil. refill >2s., ↓GCS, ↓urine output, tachycardia, hypotension, postural BP-drop >20 mmHg [syst],), blood (CBC, Hb, urea+electrolytes, liver tests, coag., cross match). |
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Acute management of upper GI-bleeding
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Protect airways and give highflow O2. Insert two large-bore cannulae (14-16 G) and take blood (CBC, urea+electrolytes, liver tests, coag., cross match, gases). Give 1 unit blood/unit Hb under 14 g/dl. I.v. crystalloid to ↑intravasc. volume while waiting for cross match (if decompensating despite i.v. fluid, give 0 neg. blood). Put catheter for CVP in order to monitor and guide fluid replacements according to venous pressure. Insert urinary catheter and monitor urinary output every hour. Take thorax-Xray and ECG. When cross match is done, transfuse until hemodynamically stable.
Correct coag. abnorm. (fresh frozen plasma, K-vitamin, platelets), monitor pulse, BP, CVP (>5 cm H2O) hourly. Arrange urgent endoscopy. Give omeprazole i.v. after endoscopy (reduces risk of rebleeding [mortality 40%] and need for surgery). Re-examine after 4 h and give fresh frozen plasma if >4 units of blood have been given. Keep Hb at >10g/dl, keep 2 units in reserve. Check biochemistry and blood values daily. |
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Causes and prophylaxis of variceal bleeding
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Causes: Cirrhosis, schistosomiasis, sarcoidosis, myeloproliferative disease, congenital hepatic fibrosis, portal vein/splenic vein thrombosis, Budd-Chiari’s syndrome, right heart failure, constrictive pericarditis, veno-occlusive disease. All of them leading up to a portal pressure gradient of >10mmHg.
Riskfactors of variceal hemorrhage are ↑portal pressure, variceal size, endoscopic features, Child-Pugh score. Primary prophylaxis (before initial bleeding) are beta-blockers (propranolol), repeated endoscopic banding ligation. Secondary prophylaxis (after initial bleeding) are the ones named above and Transjugular Intrahepatic Portosystemic Shunting (TIPS) or surgical shunting. Risk assessment for variceal bleeding are done with Child-Pugh’s score. |
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Causes and symptoms of liver failure
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Causes: Infections (viral hepatitis, yellow fever, leptospirosis), drugs (paracetamol overdose, halothane, isoniazide), toxins (amanita phalloides mushroom, carbon tetrachloride), vascular (Budd-Chiari’s syndrome, veno-occlusive disease), others (alcohol hepatitis, primary biliary cirrhosis, haemochromatosis, autoimmune hepatitis, alfa-1-antitrypsine deficiency, Wilson’s disease, fatty liver, pregnancy).
Symptoms: Jaundice, hepatic encephalopathy, asterixis, constructional apraxia (ask patient to draw a 5-pointed star). |
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Diagnosis and treatment of liver failure
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Diagn.: Blood (culture, CBC, urea+electrolytes, liver test, coag. [↑INR/PT], glucose, paracetamol levels, serology [hepatitis, CMV, EBV], ferritin, alfa-1-antitrypsin, ceruloplasmin, autoantibodies), urine (culture), ascites tap (>250 neutrophiles/mm3 indicates spontaneous bacterial peritonitis), Thorax-Xray, abdominal ultrasound.
Treat.: Rest with 20° head elevation, protect airways (intubation), place nasogastr. tube. Insert urinary catheter+CVC. Monitor temp, respir., pulse, BP, pupils, urine output hourly. Blood values daily (CBC, urea+electrolytes, liver tests, INR). Give 10 % dextrose 1L/12h for hypoglycemia, test blood glucose every 4 h. Make sure patient are well nourished (↑calories, ↓proteins). Treat cause. Hemofiltration/dialysis if renal failure develops. Avoid sedatives/drugs with hepatic metabolism, opiates, diuretics, oral hypoglycemic, saline-containing fluids. Effect of warfarin are enhanced. PPI for prophylaxis of stress ulcers+treat seizures with lorazepam. |
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Hepatotoxic drugs
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Paracetamol, methotrexate, phenothiazines, isoniazid, azathioprine, estrogen, salicylates, tetracycline, mitomycin
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Treatment of complication of liver failure
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Bleeding (vitamin K, fresh frozen plasma, platelets), infections (ceftriaxone until antibiogram are ready [avoid gentamicin]), ascites (fluid restriction, low salt diet, daily weight, diuretics), hypoglycemia (regular blood glucose check. Give 50 ml 50% glucose if glucose <2 mmol/L or symptomatic), encephalopathy (avoid sedatives, rest with 20° head elevation, lactulose, regular enema [↓nitrogen-forming bowel organism]), cerebral edema (mannitol + hyperventilation).
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Grading of hepatic encephalopathy
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Grade I: Altered mood/behavior, sleep disturbance
Grade II: Increased drowsiness, confusion, slurred speech Grade III: Stupor, incoherence, restlessness, significant confusion Grade IV: Coma |
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Cirrhosis
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Cause: Irreversible liver damage (loss of hepatocytes with fibrosis and nodular regeneration) caused by chronic alcohol abuse, HBV/HCV, autoimmunity (primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis), genetic disorders (Hemochromatosis, alfa-1-antitrypsin, Wilson’s), others (Budd-Chiari [hepatic vein thrombosis]), drugs (amiodarone, methyldopa, methotrexate).
Symptoms: Asymptomatic, increased liver values or end-stage liver disease. |
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Symptoms and complications of chronic liver disease
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Symptoms: Leuchonychia (white nails with undemarcated lunulae), hypoalbuminemia (Terry’s nails [proximal white, distal 1/3 reddened by teleangiectasis]), clubbing, palmar erythema, hyperdynamic circulation (↑NO->vasodilat.), Dupuytren’s contracture, spider naevi, xanthelasmata, gynecomastia, atrophic testis, ↓body hair, parotid enlargement, hepatomegaly/small liver (late stage).
Complications: Hepatic failure with coagulopathy (↓factor II, VII, IX, X+↑INR), encephalopathy, asterixis, confusion, coma, hypoalbuminemia, sepsis (pneumonia, septicemia), spontaneous bacterial peritonitis, hypoglycemia. Portal hypertension with ascites, splenomegaly, portosystemic shunt (esophageal varices+caput medusae). Increased risk of hepatocellular carcinoma. |
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Diagnosis and treatment of chronic liver disease
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Blood (↑/↓bilirubin, ↑AST+ALT+Alk. phosphatase↑ and later ↓albumin and↑INR). Finding the cause with ferritin, iron, total iron binding capacity, serology (hepatitis), immunoglobulines, autoantibodies (ANA,AMA,SMA), alfa-fetoprotein, ceruloplasmin, alfa-1-antitrypsin. Ultrasound, MRI, ascitic tap (neutrophils >250/mm3 indicates spontaneous bacterial peritonitis).
Treat.: Good nutrition, low salt, alcohol abstinence. Avoid NSAID+sedatives+opiates. Treat pruritus with cholesthyramine (increases bile salt excretion). Interferon improves liver values and slow progression to hepatocell. carcinoma in HCV-cirrhosis. Penicillamine in Wilson’s. Overall 5-years survival is 50%. Poor prognostic markers are encephalopathy, Na+<110mmol/L, albumin <25g/L, ↑INR. |
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Treatment of complications to chronic liver disease
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Ascites are treated with bedrest, fluid restriction (<1.5 L/day), low salt, spironolactone to calm down the RAAS-system. Monitor weight daily, aim for ½ kg weightloss/day. If poor response, add furosemide. Check urea+electrolytes often. Paracenthesis with concomitant albumin infusion can be tried.
Spontaneous bacterial peritonitis (E.coli, Klebsiella, Strept.) are considered in patients with ascites who deteriorate fast. Give Cefotaxime for 5 days until antibiogram are done. Prophylaxis to high risk patients (↓albumin,↑INR) or to patient with earlier episodes. |
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Hereditary hemochromatosis
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Cause: Inherited disorder (chromosome 6) of iron metabolism-> increased intestinal iron absorption->iron deposits in organ (joints, liver, heart, pancreas, pituitary, adrenals, skin).
Symptoms: Initially asymptomatic, then tired, arthralgia (large joints, MCP), grey skin pigmentation, DM (Bronze diabetes), chronic liver failure, hepatomegaly, cirrhosis, dilat. cardiomyopathy, hypogonadism (pituitary dysfunct./cirrhosis), osteoporosis, hyporeninemic hypoaldosteronism. Diag.: Blood (↑ livertest, ↑serum ferritin+serum iron, transferrin sat. >80%, glucose), genotyping, liver biopsy. MRI, ECG+echo (cardiomyopathy). Screening of family members. Treat.: Iron-low diet, tea+coffee+red wine (↓iron absorpt.), venesect (removal of 1 U blood/week until mildly iron deficiency [Htc <0.5, ferritin <100microg/L, transferr. sat. <40%], might need this for life e.g. 1U blood/2-3 month), control of diabetes (HbA1c might be false low due to venesection). Prognosis good with venesection. |
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Secondary hemochromatosis
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Cause: any hematological disease where many transfusions have been given (40 L).
Treat.: Find out if pathology responds to alternative treatment (erythropoetin administration or bone marrow transplantation) before the iron accumulation have become irreversible. |
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α-1-antitrypsin deficiency
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Cause: Is a serine protease inhibitor who control inflammatory cascades. The deficiency is caused by a mutation in chromosome 14 and transmission is autosom. recessive.
Symptom: children: liver disease. Adults: emphysema (dyspnea), chronic liver disease+cirrhosis+cholestatic jaundice+hepatocell. carcinoma. Diag.: Blood (↓serum levels of α-1-antitrypsin) , liver biopsy, phenotyping, DNA (prenatal diagn. in week 11-13), lung density on CT. Treat.: Supportive for emphysema and liver complications, stop smoking. If FEV1 <80% without smoking consider addition of α-1-antitrypsin from human plasma, liver transplantation. Prognosis: Male gender and obesity predisposes to advances liver disease. Emphysema is main cause of death. |
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Wilson’s disease/hepatolenticular degeneration
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Cause: autosom. recessive disease (chromos. 13) with toxic accumulation of copper (due to failed excretion in liver) in liver and CNS (basal ganglia).
Symptoms: Children: liver disease (hepatitis, cirrhosis, fulminant liver failure). Young adults: CNS signs (tremor, dysarthria, dysphagia, dyskinesia, dystonia, dementia, parkinsonism, micrographia, ataxia/clumsiness), affective signs (depression, ↓/↑libido, personality change), cognitive (↓memory+IQ, anger, delusions, mutism), Kayser-Fleischer rings (copper deposits in iris), others (hemolysis, blue nails, polyarthritis, hypermobile joints, grey skin, abortion, hypoparathyr.). Diag.: Blood (↓serum copper+ceruloplasmin), urine (24 h copperexcretion), liver biopsy, MRI. Treat.: Lifelong penicillamine, monitor CBC and copper excretion, livertransplantation, screening of siblings. Prognosis: Pre-cirrhotic liver disease is reversible but not neurological disease. Death due to liver failure, variceal hemorrhage or infection. |
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Primary biliary cirrhosis
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Cause: Interlobular bile duct lesion through chronic granulomat. inflammat. causes progressive cholestasis+cirrhosis+portal hypertension. Possibly autoimmune, associated with thyr. disease, RA, Sjögren’s, keratoconjunctivitis sicca, systemic sclerosis, renal tubular acidosis, membranous glomerulonephritis.
Symptoms: Asymptomatic (↑alkal. phosphate. on routine test)/lethargy, pruritus, jaundice, xanthelasma/xanthoma, hepatomegaly/splenomegaly Diag.: ↑alkal. phosphate., mildly ↑AST+ALT. Late disease-> ↑bilirubin,↓albumin, ↑Prothr. time, pos. AMA (anti-mitoch. ab), ↑IgM, ↑cholesterol, ↑TSH. Ultrasound+ERCP, liver biopsy. Treat.: Cholestyramine/rifampicin for pruritus, codein for diarrea, prevent. of osteoporosis, supply of fatsoluble vitamins (A,D,K). Liver transplantation for end stage liver disease/resistant pruritus. Complic.: Osteoporosis, malabsorpt.->osteomalacia+coag.pathy, portal hypert., ascites, hepat. encephalopathy Prognosis: <2 y. if jaundice. Better with liver transplant. |
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Primary sclerosing cholangitis
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Cause: idiopathic cause with inflammation, fibrosis and strictures of intra-and extrahepatic bile ducts. Associated with ulcer. colitis, Crohn’s disease and HIV infection.
Symptoms: Asymptomatic (find ↑alkal. phosphatase in routine test)/jaundice, pruritus, abdominal pain, hepatomegaly, portal hypertension, fatigue. Diag.: Blood (↑Alkal. phosphatase, ↑bilirubin, hypergammaglobulinemia, pos. ANA+ANCA, neg. AMA), ERCP/MRCP, liver biopsy. Ultrasound to detect cholangiocarcinoma. Colonoscopy screening every year for those with ulc. colitis (↑risk of colorect. carcinoma). Treat.: Cholestyramine/rifampicin for pruritus, Antibiot. as prophylaxis against bacterial cholangitis, liver transplantation for end-stage disease. Complic.: bacterial cholangitis, cholangiocarcinoma, ↑risk of colorectal cancer. Prognosis. Worst for those with IBD since it increase the risk of colorectal cancer post. transplant. |
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Autoimmune hepatitis
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Cause: idiopathic inflammatory liver disease characterized by defect in T-suppressor cells and antibodies against hepatocytes. Associated with pernicious anemia, autoimmune hemolysis/thyroiditis, UC, DM, glomerulonephritis and primary sclerosing cholangitis.
Symptoms: Young middle aged women with acute hepatitis+signs of autoimm. disease (fever, malaise, urticarial, polyarthritis, pleurisy, pulm. infiltr., glomeruloneph.). Others are more insidious/asymptomatic and diagnosed incidentally with chronic liver disease. Diag.: no labtest/pathognomonic sign, so is a diagnosis of exclusion. Overlaps with primary biliary cirrhosis, primary sclerosing cholangitis and chronic viral hepatitis. Treat.: Immunosuppression (prednisolone, azathioprine [steroid sparing]), if sideeffects of steroids, give cyclosporine, budesonide, methotrexate, cyclophosphamide. Liver transplant for decomp. cirrhosis Complic.: Associated with cirrhosis and therapy. Prognosis: 80% survival in 10 years, lower in cirrhosis. |
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Liver tumors
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Causes: secondary metastases from breast, bronchus or GI-tract. Less common with primary malignant tumors (Hepatocellular carcinoma, cholangiocarcinoma, angiosarcoma, hepatoblastoma, fibrosarcoma, leiomyosarcoma).
Symptoms: Benign are asymptomatic (Cyst, adenoma, haemangioma, fibroma, leiomyoma). Fever, malaise, anorexia, ↓weight, right upper quadrant pain, late jaundice (except in cholangiocarcinoma). Hepatomegaly, signs of chronic liver disease+evidence of decompens. (jaundice, ascites), abdominal mass, bruits over liver (hepatocell. carcinoma.). Diag.: Blood (CBC, liver test, serology [hepatitis], α-1-antitrypsin defic.), ultrasound, MRI (benign/malign), ERCP, biopsy (histology. diagnosis. Risk of seeding along biopsy tract!), mammography, thorax-Xray, colonoscopy, bone marrow biopsy. Liver metastases indicate advanced disease. Treat.: Vary depending on the primary tumor and presence metastases. Chemotherapy, resection. Most of them are palliative. Prognosis: < 6 months. |
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Hepatocellular carcinoma
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Cause: Malignant tumor of hepatocytes caused by viral hepatitis (persistent B or C), cirrhosis, hemochromatosis, primary biliary cirrhosis, aflatoxin, parasites(clonorchis sinensis), anabolic/contraceptive steroids.
Treat.: Resection solitary tumor <3 cm increased 3 y. survival to 59%, but 50 % have recurrence in 3 y. Chemotherapy, percut. ablation, tumor embolization are alternatives. Prevent.: HBV vaccination, use clean needles, screen blood products/samples. Screening with ultrasound and α-fetoprotein. Prognosis: < 6 months, 5 y. mortality is 95%. Better prognosis is occur in children/young adults (5 y. survival 60%). |
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Cholangiocarcinoma
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Cause: malign tumor in the biliary tree caused by parasites (Chlonorchis), primary sclerosing cholangitis, congen. biliary cyst, biliary-enteric drainage surgery.
Symptoms: Fever, abdominal pain, ascites, malaise, ↑bilirubin, much ↑ alkal. phosphatase. Treat.: 70 % unfit for surgery (major hepatectomy+extrahepat. bile duct excision+caudate lobe resection), 76% recurrence in resection. Post-op complic. are liver failure, bile leak, GI-bleeding. Palliative stent for obstructed bile duct (percutan. or via ERCP) improve life quality. Prognosis: around 5 months, 5 y. survival is 30% |
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Haemangioma
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Cause: benign tumor in the liver. Found incidentally on ultrasound/CT, require no treatment. Avoid biopsy because if high risk of bleeding.
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Adenoma
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Cause: common benign liver tumor caused by anabolic steroids, oral contraceptives and pregnancy.
Treat.: Only if symptomatic |
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Causes and symptoms of ulcerative colitis
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Relapsing and remitting inflammatory disorder of unknown cause in the colonic mucosa (hyperemic/hemorrhagic granular mucosa with pseudopolyps+punctate ulcers [normally not transmural]) extending from rectum and proximally (proctitis, left sided colitis, pancolitis). Never spreads proximally of ileocecal valve (unless backwash ileitis).
Symptoms: Gradual onset of diarrea±blood+mucus, crampy abdominal discomfort, tender abdomen, bowel frequency correlates with disease gravity, systemic symptoms (fever, tachycardia, anorexia,↓weight), urgency, tenesmus (proctitis). Extra-int. signs are clubbing, aphthous oral ulcers, erythema nodosum, pyoderma gangrenosum, conjunctivitis/episcleritis/iritis, large joint arthritis (sacroileitis, ankylos. spondylitis), fatty liver, cholangiocarcinoma, renal stones, osteomalacia, nutritional defects, amyloidosis. |
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Diagnosis and complications of ulcerative colitis
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Blood (CBC, ESR, CRP, urea+electrolytes, culture), stool, abdom. Xray (mucosal thickening, no fecal shadows, colonic dilat.), erect Xray (perforation), sigmoidoscopy (inflamed friable mucosa), rectal biopsy, barium enema (loss of haustra, shortened colon. Never perform during severe attack or for diagnosis!!)
Complic.: Perforation, bleeding, toxic dilat. of colon, venous thrombosis, colon cancer (colonoscopy every 2-4 year). |
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Remission induction in ulcerative colitis (UC)
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Mild: if <4 feces/d+patient well, give prednisolone (20-40 mg/d)+mesalazine. Hydrocortisone/prednisolone foam for proctitis. If symptoms improve, ↓steroids gradually. If doesnt improve after 2 weeks, treat as moderate UC.
Moderate: If 4-6 feces/d+patient well, give oral prednisolone (40 mg/d) for a week, then ↓to 30 mg/d for a week, then 20 mg/d for 4 weeks. Add 5-ASA+perform steroid enema x2/d. If improving, ↓steroids, if no improvement after 2 weeks, treat as severe UC. Severe: If systemically unwell+>6 feces/d, give i.v. fluids+hydrocortisone (100mg/6h), rectal steroids (100 mg hydrocortisone), monitor temp+pulse+BP. Record stool frequency. Exam twice/day for distention, bowel sounds and tenderness. Perform blood tests daily (CBC,ESR,CRP,urea+electrolytes±abdominal Xray). Consider blood transfusion if Hb<10g/dl. If well after 5 days, transfer to oral prednisolone 40mg/d + 5-ASA (sulfasalazine) to maintain remission. If CRP>45 on day 3, consider cyclosporine/infliximab/surgery |
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Maintaining remission in UC
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5-ASA such as sulfasalazine (side effects oligospermia, pancreatitis, hepatitis) are first line while mesalazine or osalazine are used if the person is intolerant to sulfasalazine or if the person is young and oligospermia from sulfasalazine treatment is a great problem. Azathioprine are given as steroid-sparing treatment to those who have big side effects of steroids or those who relapse quickly once steroids are reduced. Monitor CBC every 4-6 weeks.
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Causes and symptoms of Crohn’s disease
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Cause: Chronic inflammatory GI-disease with transmural granulomatous inflammation in any part of the gut (mostly terminal ileum+proximal colon) with healthy mucosa between the damaged areas (“skip lesions”/”cobble stone pattern”). Cause in unknown, but associated with high sugar low fibre diet, altered cell-mediated immunity, smoking and NSAID (exacerbations).
Symptoms: Diarrea, abdominal pain+tenderness, ↓weight, aphthous ulcers, mass in right iliac fossa, perianal abscess/fistulae, anal/perianal strictures, symptoms of active disease (fever, malaise, anorexia). Extra-intestinal signs are clubbing, erythema nodosum, pyoderma gangrenosum, conjunctivitis/episcleritis/iritis, large joint arthritis (sacroileitis, ankyl. spondylitis), fatty liver, primary sclerosing cholangitis, cholangiocarcinoma, renal stones, osteomalacia, malnutrition, amyloidosis. Complic.: small bowel obstruct., toxic dilat., abscess, fistulae, perforation, rectal hemorrhage, colonic carcinoma. |
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Diagnosis of Crohn’s disease
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Blood (CBC, ESR, CRP, urea+electrolytes, liver tests, culture, anemia tests [iron, B12, folate]). Markers of activity are ↓Hb+albumin, ↑temp., ↑ESR+CRP+leukocytes. Sigmoidoscopy+rectal biopsy if the mucosa looks normal. Capsule endoscopy. Small bowel enemas for ileal disease, barium enema for cobble stone pattern+colonic strictures. Colonoscopy are preferred before barium enema (can take biopsies). MRI ***** pelvic disease.
Severity is harder to assess than ulcerative colitis |
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Treatment of Crohn’s disease
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Mild attacks (symptomatic but systemically well): Prednisolone 30 mg/d oral for 1 week, then 20 mg for 1 month. Examine every 2-4 weeks. If symptoms resolve, decrease prednisolone by 5 mg every 2-4 weeks and stop when parameters are normal.
Severe attacks: i.v. steroids+fluids followed by i.v. hydrocortisone (100mg/6h), topical steroids for rectal affection, metronidazole (perianal disease/infection), monitor of temp., pulse, BP and stool frequency. Exam twice/d for CBC, ESR, CRP, urea+electrolytes and abdom. Xray. Blood transfusion if Hb<10g/dl. If improving after 5 days, transfer to oral prednisolone (40 mg/d). If no response/deterioration, seek surgical care. Additional therapy: Azathioprine (steroid-sparing if steroid side effects/rapid relapse), methotrexate, infliximab (anti-TNF-ab, 1 dose can induce remission)[+cyclosporine/tacrolimus], surgery (for obstruction, perforation, fistulae, abscess, but is never curative). Sulfasalazine not useful for maintaining remission in Crohn’s. |
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Irritable bowel syndrome (IBS)
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Cause: a heterogeneous group of abdominal symptoms without organic cause. Probably causes are disorder of intest. motility or enhanced visceral perception (“gut-brain axis”).
Symptoms (>6 months): Central/lower abdominal pain relieved by defecation, bloating, altered bowel habits (constip.+diarrea), tenesmus, rectal mucus, nausea, pain in back/thigh/chest, urinary frequency, depression. They are exacerbated by stress, menstruation and gastroenteritis. Normal physical examination with general abdomen. tenderness. Signs indicating other disease than IBS: age >40 y., symptoms <6 months, anorexia, ↓weight, waking up at night with pain/diarrea, mouth ulcers, ↑CRP and ↓Hb. Treat.: Exclude other diagnoses. Medical therapy rarely works, usually symptomatic, but reassurance is important. Exclude foods if intolerant, ↑fiber intake if constip., bulking agents in diarrea, antispasmodics (mebeverine) in colic and bloating, metoclopramide in dyspepsia, psychological therapy. |
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Causes and symptoms of pancreas carcinoma
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Causes: mostly ductal adenocarcinoma (early metastasis) where 60 % are in the pancr. head, 25% in body and 15% in tail. A few are in ampulla of Vater and others in pancreatic islets (insulinoma, gastrinoma, glucagonoma, somatostinoma or VIP-oma), all with better prognosis. Riskfactors are smoking, alcohol, DM, chronic pancreatit. 95% have mutation in KRAS2-gene.
Symptoms: Tumor in the head causes painless obstructive jaundice, tumors in the body/tail present with epigastric pain that radiates towards the back/relieved by leaning forward. Other symptoms are anorexia, ↓weight, DM, acute pancreatitis, migratory thrombophlebitis, ↑Ca2+, marantic endocarditis, portal hypertension (splenic vein thrombosis), nephrosis (renal vein metastases). Signs are jaundice+palpable gallbladder (Courvoisier’s law), epigastric mass, hepatomegaly, splenomegaly, lymphadenopathy, ascites. |
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Diagnosis, treatment and prognosis of pancreas carcinoma
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Blood (cholestatic jaundice), ultrasound/CT (pancreatic mass, dilat. biliary tree, hepatic metastases), endoscopic ultrasound (most accurate for panc. masses),biopsy, MRI/MRCP, ERCP.
Treat.: Often metastases on presentation, 10% suitable for radical surgery: pancreatoduodenectomy (Whipple’s) if tumor <3cm without metastases (high post-op morbidity)+post-op chemotherapy (↓progression). Endoscop./percut. stents in bile tree for jaundice and anorexia. Large dose opiates/radiotherapy/celiac plexus infiltration with alcohol for pain. Prognosis: < 6 months, 5 y. survival <2%. After surgery 5 y. survival 5-14%. Better prognosis if tumor <3cm, no involved nodes, negative resection margins at surgery, tumor in ampulla of Vater/islets. |
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Scurvy
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Cause: lack of vitamin C.
Symptoms: listlessness, anorexia, cachexia, gingivitis, loss of teeth, foul-smelling breath, bleeding gums/nose/hairfollicles/into joints/bladder/gut. Diag.: no test is satisfactory. ↓ascorbic acid. Treat.: Dietary education, ascorbic acid 250 mg/d orally. |
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Beriberi
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Cause: Lack of vitamin B1 (thiamine) caused by alcoholism, malnutrition, prolonged vomiting (chemotherapy), GI-malignancy, hyperemesis gravidarum.
Symptoms: Heart failure with general edema (wet beriberi) or neuropathy (dry beriberi). Treat.: Thiamine administration, have resuscitation close at hand since there are risk of hypersensitivity to thiamine. |
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Pellagra
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Cause: Lack of nicotinic acid such as in carcinoid syndrome and anti-TBC drugs (isoniazide).
Symptoms: classical triad with diarrea, dementia, dermatitis (±neuropathy with depression, insomnia, tremor, rigidity, ataxia, seizures). Treat.: education, electrolyte replacement, administration of nicotinamide 100 mg/4h orally |
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Xerophtalmia
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Cause: vitamin A deficiency
Symptom: blindness, dry conjunctive with oval/triangular spots, cloudy and soft cornea. Treat.: Administration of vitamin A 200.000 IU orally, repeat in 24 h and a week later. Careful in treatment of pregnant since vitamin A can cause embryopathy. |
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Carcinoid tumor
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Cause: Big tumorgroup of cells with enterochromaffin origin (produce 5HT and other substances) commonly appearing in appendix, ileum, rectum, testis/ovaries, bronchi. Tumors >2cm will metastasize so they are therefor considered malignant.
Symptoms: Initially few symptoms. GI-tumors: appendicitis, intussusception, obstruction. Hepatic metastases cause pain in right upper quadrant. Secretion of bradykinin, substance P, VIP, gastrin, insulin, glucagon, ACTH, parathyr./thyr. hormone. Treat.: Important to find primary tumor, resection is possible. Embolization/radiofrequency ablation of hepatic metastases can ↓symptoms but they require octreotide cover to avoid carcinoid crisis. The crisis appears when mediators escape into the blood stream ->vasodilat., hypotens., tachycardia, bronchoconstr. and hyperglycemia. Treat with high dose octreotide+support+ fluids. Prognosis: 38 months if metastases, 5-8 y. if not (and may be much longer, up to 20 y. even if metastases are present.) |
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Carcinoid syndrome
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Occurs in 5% of patient with carcinoid tumor and implied involvement of the liver.
Symptoms: bronchoconstriction, paroxysmal flushing in upper body, diarrea, congestive heart failure (tricusp. regurg.+pulm. stenosis from 5HT-induced fibrosis). Diagn.: ↑24h urine measurement of 5-hydroxyindleacetic acid, octreoscan (radiolabeled octreotide), PET. Treat.: Octreotide (somatostatin analogue) blocks release of tumor mediators and counter peripheral effects. The effect disappears with time. Loperamide/cyproheptadine for diarrea, α-interferon as addition to octreotide. |
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Gastrointestinal malabsorption
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Symptoms: diarrea, ↓weight, lethargy, steatorrhea, anemia (↓iron,B12,folate), bleeding disorders (↓vitamin K), edema (↓proteins), metabolic bone disease (↓vitamin D), neuropathy.
Diag.: Blood (CBC [↓/↑MCV], ↓Ca2+, ↓B12+folate, ↓iron, ↑INR, lipidprofile, coeliac serology ), stool, barium follow through (diverticula, Crohn’s, radiation enteritis), breath hydrogen analysis (proves bacterial overgrowth by giving glucose an measure an ↑in exhaled hydrogen), endoscopy+biopsy |
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Tropical sprue
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Cause: Unknown cause. Causes villous atrophy and malabsorption
Symptoms of gastrointestinal malabsorption. Treat.: Tetracycline 250 mg/6h orally+folic acid 15 mg/d orally+optimal nutrition. |
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Coeliac disease
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Cause: T-cell mediated autoimmunity in small bowel where prolamin-intolerance causes villous atrophy and malabsorption. Associated with dermatitis herpetiformis.
Symptoms: Steatorrhea, abdominal pain, bloating, nausea+vomiting, aphthous ulcers, angular stomatitis, ↓weight, fatigue, weakness, iron-deficiency anemia, osteomalacia, failure to thrive. Diagn.: Antibodies against transglutaminase and gliadin, anti-endomysial-Ab (IgA-ab, 95% specificity if not IgA-deficient), duodenal biopsy (subtotal villous atrophy+crypt hyperplasia that’s reversed on gluten-free diet). Treat.: lifelong gluten-free diet. Can eat rice, maize, soya, potatoes, oats and sugar. Verify diet with anti-endomysial-ab test. Complications: anemia, lactose-intoll., T-cell lymphoma, malignancy (gastric, esophageal, bladder, breast, brain), myopathies, neuropathies, hyposplenism, osteoporosis. |
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Chronic pancreatitis
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Causes: alcohol, familial, CF, hemochromatosis,pancreatic duct obstruction (stones,tumor), congenital (pancreas divisum).
Symptoms: epigastric pain that drills itself through the back (relieved by sitting leaning forward), bloating, steatorrhea, ↓weight, brittle diabetes. The symptoms come and go. Diag.: Ultrasound, CT, MRCP, ERCP, abdominal Xray (calcifications). Treat.: Analgesia (coeliac plexus block), lipase, fat-soluble vitamins, insulin. Diet with no alcohol+low fat, surgery (pancreatectomy/pancreaticojejunostomy) for resistant pain/narcotic abuse,↓weight. Complications: Pseudocyst, DM, biliary obstruction, local artery aneurysm, splenic vein thrombosis, gastric varices. |
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Vitamins- and metal deficiencies and their syndromes
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Vit. A: Xerophtalmia
Vit. B1: Beriberi, Wernicke’s encephalopathy Vit. B2: Angular stomatitis, cheilitis Vit. B6: Polyneuropathy Vit. B12: Macrocytic anemia, neuropathy, glossitis Vit. C: Scurvy Vit. D: Rickets, osteomalacia Vit. E: Hemolysis, neurological deficit Vit. K: Bleeding disorder Folic acid: Macrocytic anemia Nicotinamide: Pellagra Copper: Menkes’ kinky haird syndrome Fluoride: Caries Iodide: Goiter, cretinism Iron: Microcytic anemia Phosphate: osteoporosis, anorexia, weakness Selenium: Cardiomyopathy Zinc: Acrodermatitis enteropathica, poor wound healing |
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Causes of gastrointestinal malabsorption
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Usual: Coeliac disease, chronic pancreatitis, Crohn’s disease
↓Bile: primary biliary cirrhosis, ileal resection, biliary obstruction, colestyramine Panc. insuff.: pancreatic cancer, CF Small bowel mucosa: Whipple’s disease, tropical sprue, radiation enteritis, small bowel resection, brush border enzyme deficiency (lactase), drugs (metformin, neomycin, alcohol), amyloid Bacterial overgrowth: spontaneous in jejunal diverticula. Infection: Giardiasis, strongyloidiasis Intestinal hurry: Post-gastrectomy with dumping, post-vagotomy, gastrojejunostomy. |
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Symptoms and diagnosis of alcoholism
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Symptoms and diagnosis of alcoholism
Symptoms: Liver: acute+reversible fatty liver and alcoholic hepatitis that can both->cirrhosis. CNS: ↓memory+cognition, cortical atrophy, retrobulbar neuropathy, seizures, wide-based gait neuropathy,confabulation, Korsakoff’s syndrome, Wernicke’s encephalopathy. GI-tract: Obesity, diarrea, gastric erosions, peptic ulcers, varices, pancreatitis (acute/chronic), carcinoma, oral mucosa lesion. Blood: ↑MCV, anemia (bone marrow depression, GI-bleeding, folate deficiency, hemolysis), sideroblastic anemia. Heart: Arrhythmias, ↑BP, cardiomyopathy, sudden death. Diagnosis: denial is an important feature of alcoholism, so question also the relatives. Blood (↑or very ↑γ-GT [non-specific]), liver biopsy (Mallory bodies±neutrophil infiltr.). |
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Treatment of alcoholism
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Multiple high potency vitamin injection i.m. can reverse CNS affection (↓memory+cognition)
Treat.: Group therapy/self-help. Relapse (50% relapses in the beginning of treatment) are treated with acamprosate for anxiety, insomnia and craving. Start as soon as acute withdrawal is over and continue for 1 year. Disulfiram can be used for chronic alcoholism, causes extreme effects when drinking (flushing, headache, palpitations). |
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Alcoholic hepatitis
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Symptoms: Anorexia, tender hepatomegaly±jaundice, bleeding, ascites. Severe hepatitis are indicated with jaundice, encephalopathy and coagulopathy.
Diag.: Blood (↑WCC, ↓INR, ↑AST, ↑MCV, ↑urea) Treat.: Stop alcohol consumption! For withdrawal symptoms give chlordiazepoxide (if not possible, give i.m. lorazepam). High dose i.v. vitamin B, keep resuscitation equipment close to hand. Optimize nutrition (35-40 kcal/kg/d+1.5 g proteins/kg/d) for prevention of sepsis and encephalopathy. Measure weight every day, take blood (liver test, urea+electrolytes, INR). No water restrictions of hyponatremia., can make it worse. Take ascitic fluid for culture (spontaneous bacterial peritonitis). Start steroid therapy (prednisolone 40mg/d for 5 d.) if Maddrey Discriminant Factor >32. Prognosis: Mild episodes have low mortality. Severe hepatitis can have 30 d. mortality of 50%. 40% mortality 1st year. |
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Symptoms and treatment of alcohol withdrawal
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Symptoms: ↑pulse, ↓BP, tremor, confusion, seizures, visual or tactile hallucination (“delirium tremens”)
Treat.: Admit to hospital. Check vital signs every 4 h, beware of ↓BP. Give generous of chlordiazepoxide first 3 d and decrease dose during following 7-14 days. Alternative is diazepam. Clomethiazole causes addiction! Administer vitamins if needed. |
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Patterns in different liver diseases
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Alcoholic liver disease: very ↑ AST, ↑ALT, AST/ALT-ratio >2, MCV very↑
Hepatitis C: ↑/normal AST, very ↑ALT, AST/ALT-ratio<1, normal MCV Non-alcoholic fatty liver syndrome: ↑AST, very ↑ALT, AST/ALT-ratio<1, MCV↑or normal |
