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MEDICINE EVALS 4 rationalization

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(December 03, 2012)

1. HEPATIC UPTAKE unconjugated bilirubin + albumin ---> transported to liver ---> hepatic uptake w/o albumin via process that partly involves carrier - mediated membrane transport in hepatocyte cytosol - unconjugated bilirubin coupled predominantly to Glutathione S- transferase (formerly ligandin)

2. CONJUGATION in endoplasmic reticulum: bilirubin is solubilized by CONJUGATION to glucuronic acid forming BILIRUBIN MONOGLUCURONIDE and DIGLUCURONIDE conjugation of glucuronic acid to bilirubin is catalyzed by bilirubin uridine - diphosphate (UDP) glucuronosyltransferase

3. EXCRETION - bilirubin glucoronides are excreted across the canalicular membrane into the bile canaliculi by ATP dependent transport process mediated by canalicular membrane protein called multidrug resistance associated protein2 (MRP2)

4.    80-90% urobilinogens: excreted in feces either unchanged or oxidized to orange derivatives - UROBILINS 10-20%: passively absorbed, enter venous blood and re-excreted by liver small fraction < 3 mg/dl: escapes hepatic uptake: filters across renal glomerulus and excreted in urine

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UNEXPLAINED ENIGMAS IN JAUNDICED PATIENTS WITH LIVER DISEASE - can be explained by prolonged half-life of albumin 1. Some patients with conjugated hyperbilirubinemia do not exhibit bilirubinuria during the recovery phase of their disease because bilirubin is bound to albumin and therefore not filtered by renal glomeruli. 2. Elevated serum bilirubin levels decline more slowly than expected in some patients who otherwise appear to be recovering satisfactorily. Late in recovery phase of hepatobiliary disorders - all conjugated bilirubin may be in albumin linked form - value in serum falls slowly because of long half-life of albumin

6. Bilirubinura is suggestive of: a. overproduction of bilirubin b. impaired hepatic uptake c. impaired conjugation d. decreased bile excretion 7. A. Benign Recurrent Intrahepatic Cholestasis (BRIC) Rare disorder characterized by recurrent attacks of pruritus and jaundice Familial recessive pattern of inheritance Jaundice and pruritus may be debilitating and prolonged BRIC type 2- mutation in bile salt excretory protein (BSEP)

Increased bilirubin production Hemolysis Ineffective erythropoesis III. DUBIN-JOHNSON SYNDROME defect is a point mutation in the gene for canalicular multispecific organic anion transporter (+) altered excretion of bilirubin into bile ducts 9. DISORDERS OF BILIRUBIN METAB leading to UNCONJUGATED HYPERBILIRUBINEMIA I. initially episodic. A. serum bilirubin: 6-25 mg/dl Treatment: phenobarbital-induces UDP glucuronosyl transferase activity (+) marked jaundice but survives into adulthood with intercurrent illness (surgery) ---> kernicterus B. ROTOR’S SYNDROME (+) problem with hepatic storage of bilirubin C.B. CRIGLER-NAJJAR TYPE I exceptionally rare condition in neonates complete absence of bilirubin UDP glucuronosyl transferase activity ---> unable to conjugate and excrete bilirubin characterized by severe jaundice o (bilirubin > 20 mg/dL) + neurologic impairment 2º kernicterus frequently leads to death in infancy or childhood only effective treatment: orthotopic liver transplantation D. Decreased Hepatic Bilirubin Clearance Crigler Najjar TypeI Decreased Hepatic uptake Crigler Najjar Type II Impaired conjugation Gilberts syndrome Physiologic Neonatal Jaundice Acquired Conjugation defects . major bile canalicular exporter of bile acids ( BSEP –bile salt excretory protein) 8. Progressive Familial Intrahepatic Cholestasis (FIC) Phenotypically related syndromes Byler disease: progressive FIC type I presents in early infancy as cholestasis.glycoprotein. CRIGLER-NAJJAR TYPE II more common than type I mutation in bilirubin UDP glucuronosyl transferase gene causes reduced but not completely absent enzyme activity patients live to adulthood. male predominance 2-7:1 D. & 10. GILBERT’S SYNDROME marked by impaired conjugation of bilirubin due to reduced bilirubin UDP glucuronosyl transferase activity mild unconjugated hyperbilirubinemia < 6 mg/dL serum bilirubin levels may fluctuate and jaundice often identified only during periods of fasting very common: 3-7%. mutation in FIC1 gene Type2: mutation in protein sister of p. DUBIN-JOHNSON SYNDROME defect is a point mutation in the gene for canalicular multispecific organic anion transporter (+) altered excretion of bilirubin into bile ducts C. Hereditary Defects in Bilirubin Conjugation II.

calcium carbonate intake “rock -like” stools) Emotional state Prolonged travel Presence of blood in stools Weight loss Family background for malignancy *history for Sexual Preference is NOT NEEDED… . AST c.ask for: Diet (low residue.indicates severe hepatocellular injury 13. which lab test will most likely be significantly increased? a. asthma) Subdiaphragmatic lesions (e. ALT b. GGT d. Falsely Decreased Liver Span: Pneumothorax Emphysema 16. abscess) Aberrant lobe of the liver (Riedel’s lobe) Extremely thin or relaxed abdominal muscles Occasionally present in normal persons 14. PALPABLE LIVER WITHOUT HEPATOMEGALY Right diaphragm displaced downwards (e. HISTORY OF PATIENT W/ CONSTIPATION. A patient with family background for colonic malignancy should undergo: COLONOSCOPY 17. and alcoholic stools. In a jaundice patient presenting with pruritus.DISORDERS of BILIRUBIN METAB leading to CONJUGATED HYPERBILIRUBINEMIA Familial Defects in Hepatic Excretory Function Dubin-Johnson syndrome (DJS) Rotor’s syndrome Benign Recurrent Intrahepatic Cholestasis (BRIC) Progressive Familial Intrahepatic Cholestasis (FIC) 11. Falsely Increased Liver Span: Consolidation (pneumonia) Atelectasis/fibrosis Pleural effusion 15. low water intake. FAILURE OF PROTIME TO CORRECT WITH PARENTERAL VITAMIN K . emphysema. Alkaline Phosphatase 12.g.g. tea colored urine.

Constipation may be attributed to the intake of: Drugs: Antacids (calcium containing antacids) Anticholinergics hematinics (iron containing vitamins) 22. stenosis) *least pertinent PE for Px w/ constipation: Peri-orbital/ bi-pedal edema 19. Constipation: Reduction in frequency of defecation Constant sensation of rectal fullness Feeling of incomplete evacuation Painful defecation or “dyschezia” Stools are small Encopresis (“paradoxical diarrhea in constipation”) 20. Passage for fresh blood admixed with stools.look for: Neurological deficits (including autonomic function) Signs of weight loss Bowel sounds Tender areas Masses Abnormal digital rectal examination findings (fissures. more frequent BM’s. Electrolyte replacement c.18. hypogastric pain 24. AOTA e. prominent tenesmus. Fluid. bloody/ mucoid. Encopresis is best managed by: a. NOTA . LARGE STOOL DIARRHEA - SMALL STOOL DIARRHEA - small intestinal origin less frequent BM’s absent tenesmus watery greasy foul smelling stools periumbilical pain large intestinal origin. Intestinal antiseptics d. PE FOR PATIENT W/ CONSTIPATION. Constipation may result from: Excessive mucosal absorption of water Motor dysfunction due to electrolyte disturbance Luminal obstruction 21. Lab procedure least likely indicated is: FECAL OCCULT BLOOD TEST – not needed since the blood in the stool can be observed 23. Anticholinergics b.

 acarbose (a-glucosidase inhibitor) active secretion into the lumen by:  laxatives (castor oil. irritable bowel  Relief by bending forward– retroperitoneal source/ hemo/ pneumoperitoneum 33. usually bloody and mucoid large intestinal origin 26. dysuria. Coli) 29. Landmarks in doing digital rectal examination: Genital Structures Ano-rectal ring Sacro-spinous ligament 31. bacterial) mucosal sloughing (amoebiasis. vesicles/pustules) Day-care facilities and institutions– shigella and giardia (low inoculum). Shigella. Osmotic Diarrhea Secretory Diarrhea Exudative Diarrhea – non-absorbable solute  laxatives (lactulose.25. intra-abdominal masses Test for rebound tenderness 30. stools are usually: type of small stool diarrhea. biliary obstruction. prostaglandins)  toxins (seafood/shellfish. fungi overgrowth (candida species) Travel– ETEC. prominent tenesmus. Palpation of abdomen in a patient presenting with abdominal pian entails: Light palpation for muscle spasm/rigidity Deep palpation for size of liver. High risk groups for Diarrhea:     Antibiotic use– pseudomembranous colitis (c. kidneys. spleen. enteroinvasive E. defficile). carbohydrate fermentation. “gay bowel syndrome”– herpes simplex proctitis (tenesmus. senna)  other drugs (metformin. rotavirus Homosexuals. biliary ascariasis  Post-prandial onset– PUD. pancreatitis. Salmonella. bisacodyl. rota/adeno viruses (easy to spread) 28. Hallmark symptoms of AMOEBIASIS: bloody and mucoid (+) tenesmus 27. In Dysentery. shigellosis. Common manifestation of abnormal GI motility mostly revealed by INSPECTION: DISTENTION . Mg(OH)2). PERTINENT HISTORICAL DATA:  Evolving pattern (visceral to parietal)– acute appendicitis and acute cholecystitis  Disproportionate pain (more pain. ano-rectal ulcers. less PE findings)– ischemia. & 32.

Acute Diverticulosis involving the sigmoid colon. ileus. CLINICAL FEATURES OF VOMIT  No antecedent nausea– CNS origin (tumor)  Voluntarily induced– gastric outlet obstruction  Fecaloid odor– intestinal obstruction. A bruit in the setting of severe abdominal pain and shock is suggestive of: AORTIC ANEURYSM 44. Slowly progressive evolving pattern of pain over a long period of time in an elderly is a hallmark manifestation of: MESENTERIC ISCHEMIA 43. Perforated peptic ulcer ---ito nasa answer key E.34. Cause of abdominal distention wherein abnormal intestinal motility is least expected to play a role: a. Acute Pyelonephritis D. Disproportionate pain (more pain. Acute cholecystitis *** Evolving pattern (visceral to parietal)– acute appendicitis and acute cholecystitis …pero bat hindi E ang sagot? Or di ko lang alam na correct pala talaga. early visceral pain is usually felt over: HYPOGASTRIC 37. gastric outlet obstruction (with bacterial overgrowth)  Succussion splash (clappotage)– gastric outlet obstruction  Vomiting and pain sequence– vomiting first (medical abdomen).  41. Must be considered when pain and fever is heralded by dysuria: PYELONEPHRITIS 42. flatus c. Sudden change in the pattern of long standing visceral pain to a parietal type in an elderly strongly points to the possibility of: A. tumor 38. pain then vomiting (surgical) . HINTS IN GENERAL SURVEY: Pallor: vasoconstriction in shock OR anemia due to hemorrhage 40. less PE findings)– ischemia. fluid d. biliary ascariasis 39. feces b. Visceral pain in early stages of Acute Appendicitis is usually felt over the: UMBILICAL 35. Biliary ascariasis C. Visceral pain in early stages of Acute Cholecystitis is usually felt over the: EPIGASTRIC 36. Acute pancreatitis B.

Most likely diagnosis is: a. Gastric malignancy e. biliary tract disease b. alcohol. A 45 y. HEMORRHAGIC & EROSIVE GASTROPHATHY . GERD d. female w/ history of melena. Mallory-Weiss Tear c. AOTA .o. Hematemesis in a 61 y.o. with fever. retching or coughing preceding hematemesis 48. EGD and colonoscopy revealed unremarkable findings.ingestion of NSAIDs. Bilous Vomitus is at least suggestive of: a. A 21 y. Large intestines b. GERD d. colonic malignancy c. male medical student came in due to hematochezia and diarrhea of less than 1 week duration assoc. inflammatory bowel disease d. do not cause major bleeding . A 61y. alcoholic meal assoc. esophagus e. GERD c.45. AOTA 51. esophageal varices b. irritable bowel syndrome b. PUD MALLORY – WEISS TEARS:  Tears which are usually on the gastric side of the GE junction  Vomiting. STOMACH d. acute pancreatitis c. stress 50. male alcoholic with history of vomiting of previously ingested food preceding hematemesis.o. ESOPHAGEAL VARICES *Esophageal Varices: Liver disease. Amebic colitis 47. male. with jaundice and ascites is most likely due to: a. PUD b. poorer outcome c.mucosal. What is the most likely cause of hematemesis? a. AOTA e. Most likely source of bleeding is: a. with gnawing epigastric pain is most likely due to: a. Melena ing 21 y.o. PUD d. NOTA 46. peptic ulcer d. smoker. Gastric malignancy 49. Gastric malignancy b.endoscopically visualized subepithelial hemorrhages and erosions .o. Small intestines c.

blood has been present in the GI tract for at least 14 hours. Hematemesis with early satiety. more proximal bleeding site HEMATOCHEZIA . ung may malignacy na sagot. USUAL PRESENTATIONS OF GI BLEEDING:  HEMATEMESIS – Vomiting of fresh blood from esophageal varices. & 59. . – UGI bleeding above the ligament of treitz  MELENA . Melena c.a lower GI source of bleeding. 57.. AOTA e. epigastric pain and weight loss: GASTRIC MALIGNANCY –usually basta may weight loss. . Hematochezia d. usually associated with hemodynamic instability and dropping haemoglobin .usually due to hemorrhoids  60. Small amount of GI bleeding which can only be detected by stool chemical testing: a. 58. with change in bowel habit and weight loss: COLONIC MALIGNANCY 55. NOTA *Occult GI bleeding can only be detected by chemical testing. Most common cause of lower GI bleeding in general population: ANAL FISSURES/HEMORHOID 54.massive upper GI bleeding.52. Hematochezia assoc. Hematemesis b. Best way to assess a patient with GI bleeding initially: CHECK HR AND BP 56. :)) 53.