MEDICINE EVALS 4 rationalization:

(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

5.

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)

B. 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. 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 2 kernicterus frequently leads to death in infancy or childhood only effective treatment: orthotopic liver transplantation D. Progressive Familial Intrahepatic Cholestasis (FIC) Phenotypically related syndromes Byler disease: progressive FIC type I presents in early infancy as cholestasis, initially episodic; mutation in FIC1 gene Type2: mutation in protein sister of p- glycoprotein, major bile canalicular exporter of bile acids ( BSEP bile salt excretory protein)

8.

A. 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, 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. ROTORS SYNDROME (+) problem with hepatic storage of bilirubin C. GILBERTS 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%, male predominance 2-7:1 D. 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. & 10.

DISORDERS OF BILIRUBIN METAB leading to UNCONJUGATED HYPERBILIRUBINEMIA I. Increased bilirubin production Hemolysis Ineffective erythropoesis III. Hereditary Defects in Bilirubin Conjugation II. Decreased Hepatic Bilirubin Clearance Crigler Najjar TypeI Decreased Hepatic uptake Crigler Najjar Type II Impaired conjugation Gilberts syndrome Physiologic Neonatal Jaundice Acquired Conjugation defects

DISORDERS of BILIRUBIN METAB leading to CONJUGATED HYPERBILIRUBINEMIA Familial Defects in Hepatic Excretory Function Dubin-Johnson syndrome (DJS) Rotors syndrome Benign Recurrent Intrahepatic Cholestasis (BRIC) Progressive Familial Intrahepatic Cholestasis (FIC)

11. In a jaundice patient presenting with pruritus, tea colored urine, and alcoholic stools, which lab test will most likely be significantly increased? a. ALT b. AST c. GGT d. Alkaline Phosphatase

12. FAILURE OF PROTIME TO CORRECT WITH PARENTERAL VITAMIN K - indicates severe hepatocellular injury

13. PALPABLE LIVER WITHOUT HEPATOMEGALY Right diaphragm displaced downwards (e.g. emphysema, asthma) Subdiaphragmatic lesions (e.g. abscess) Aberrant lobe of the liver (Riedels lobe) Extremely thin or relaxed abdominal muscles Occasionally present in normal persons

14. Falsely Increased Liver Span: Consolidation (pneumonia) Atelectasis/fibrosis Pleural effusion

15. Falsely Decreased Liver Span: Pneumothorax Emphysema

16. A patient with family background for colonic malignancy should undergo: COLONOSCOPY

17. HISTORY OF PATIENT W/ CONSTIPATION- ask for: Diet (low residue, low water intake, 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

18. PE FOR PATIENT W/ CONSTIPATION- look for: Neurological deficits (including autonomic function) Signs of weight loss Bowel sounds Tender areas Masses Abnormal digital rectal examination findings (fissures, 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. Constipation may result from: Excessive mucosal absorption of water Motor dysfunction due to electrolyte disturbance Luminal obstruction

21. Constipation may be attributed to the intake of: Drugs: Antacids (calcium containing antacids) Anticholinergics hematinics (iron containing vitamins)

22. Passage for fresh blood admixed with stools. Lab procedure least likely indicated is: FECAL OCCULT BLOOD TEST not needed since the blood in the stool can be observed 23. LARGE STOOL DIARRHEA
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SMALL STOOL DIARRHEA

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small intestinal origin less frequent BMs absent tenesmus watery greasy foul smelling stools periumbilical pain

large intestinal origin, more frequent BMs, prominent tenesmus, bloody/ mucoid, hypogastric pain

24. Encopresis is best managed by: a. Anticholinergics b. Fluid, Electrolyte replacement c. Intestinal antiseptics d. AOTA e. NOTA

25. In Dysentery, stools are usually: type of small stool diarrhea, prominent tenesmus, usually bloody and mucoid large intestinal origin

26. Hallmark symptoms of AMOEBIASIS: bloody and mucoid (+) tenesmus

27. High risk groups for Diarrhea: Antibiotic use pseudomembranous colitis (c. defficile), carbohydrate fermentation, fungi overgrowth (candida species) Travel ETEC, Shigella, Salmonella, rotavirus Homosexuals, gay bowel syndrome herpes simplex proctitis (tenesmus, dysuria, ano-rectal ulcers, vesicles/pustules) Day-care facilities and institutions shigella and giardia (low inoculum), rota/adeno viruses (easy to spread)

28. Osmotic Diarrhea Secretory Diarrhea

Exudative Diarrhea

non-absorbable solute laxatives (lactulose, Mg(OH)2), acarbose (a-glucosidase inhibitor) active secretion into the lumen by: laxatives (castor oil, bisacodyl, senna) other drugs (metformin, prostaglandins) toxins (seafood/shellfish, bacterial) mucosal sloughing (amoebiasis, shigellosis, enteroinvasive E. Coli)

29. Palpation of abdomen in a patient presenting with abdominal pian entails: Light palpation for muscle spasm/rigidity Deep palpation for size of liver, kidneys, spleen, intra-abdominal masses Test for rebound tenderness

30. Landmarks in doing digital rectal examination: Genital Structures Ano-rectal ring Sacro-spinous ligament

31. & 32. PERTINENT HISTORICAL DATA: Evolving pattern (visceral to parietal) acute appendicitis and acute cholecystitis Disproportionate pain (more pain, less PE findings) ischemia, biliary ascariasis Post-prandial onset PUD, pancreatitis, biliary obstruction, irritable bowel Relief by bending forward retroperitoneal source/ hemo/ pneumoperitoneum

33. Common manifestation of abnormal GI motility mostly revealed by INSPECTION: DISTENTION

34. Visceral pain in early stages of Acute Appendicitis is usually felt over the: UMBILICAL

35. Visceral pain in early stages of Acute Cholecystitis is usually felt over the: EPIGASTRIC

36. Acute Diverticulosis involving the sigmoid colon, early visceral pain is usually felt over: HYPOGASTRIC

37. Cause of abdominal distention wherein abnormal intestinal motility is least expected to play a role: a. feces b. flatus c. fluid d. tumor

38. Disproportionate pain (more pain, less PE findings) ischemia, biliary ascariasis

39. HINTS IN GENERAL SURVEY: Pallor: vasoconstriction in shock OR anemia due to hemorrhage

40. Sudden change in the pattern of long standing visceral pain to a parietal type in an elderly strongly points to the possibility of: A. Acute pancreatitis B. Biliary ascariasis C. Acute Pyelonephritis D. Perforated peptic ulcer ---ito nasa answer key E. 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.

41. Must be considered when pain and fever is heralded by dysuria: PYELONEPHRITIS

42. Slowly progressive evolving pattern of pain over a long period of time in an elderly is a hallmark manifestation of: MESENTERIC ISCHEMIA

43. A bruit in the setting of severe abdominal pain and shock is suggestive of: AORTIC ANEURYSM

44. CLINICAL FEATURES OF VOMIT No antecedent nausea CNS origin (tumor) Voluntarily induced gastric outlet obstruction Fecaloid odor intestinal obstruction, ileus, gastric outlet obstruction (with bacterial overgrowth) Succussion splash (clappotage) gastric outlet obstruction Vomiting and pain sequence vomiting first (medical abdomen), pain then vomiting (surgical)

45. Bilous Vomitus is at least suggestive of: a. biliary tract disease b. acute pancreatitis c. peptic ulcer d. AOTA e. NOTA

46. A 21 y.o. male medical student came in due to hematochezia and diarrhea of less than 1 week duration assoc. with fever. Most likely diagnosis is: a. irritable bowel syndrome b. colonic malignancy c. inflammatory bowel disease d. Amebic colitis

47. A 61y.o. male alcoholic with history of vomiting of previously ingested food preceding hematemesis. What is the most likely cause of hematemesis? a. Gastric malignancy b. Mallory-Weiss Tear c. GERD d. PUD MALLORY WEISS TEARS: Tears which are usually on the gastric side of the GE junction Vomiting, retching or coughing preceding hematemesis

48. Melena ing 21 y.o. male, smoker, with gnawing epigastric pain is most likely due to: a. esophageal varices b. GERD c. PUD d. Gastric malignancy

49. HEMORRHAGIC & EROSIVE GASTROPHATHY - endoscopically visualized subepithelial hemorrhages and erosions - mucosal, do not cause major bleeding - ingestion of NSAIDs, alcohol, stress

50. A 45 y.o. female w/ history of melena. EGD and colonoscopy revealed unremarkable findings. Most likely source of bleeding is: a. Large intestines b. Small intestines c. STOMACH d. esophagus e. AOTA

51. Hematemesis in a 61 y.o. alcoholic meal assoc. with jaundice and ascites is most likely due to: a. PUD b. ESOPHAGEAL VARICES *Esophageal Varices: Liver disease, poorer outcome c. GERD d. Gastric malignancy e. AOTA

52. Hematemesis with early satiety, epigastric pain and weight loss: GASTRIC MALIGNANCY usually basta may weight loss.. ung may malignacy na sagot. :))

53. Most common cause of lower GI bleeding in general population: ANAL FISSURES/HEMORHOID

54. Hematochezia assoc. with change in bowel habit and weight loss: COLONIC MALIGNANCY

55. Best way to assess a patient with GI bleeding initially: CHECK HR AND BP

56, 57, 58, & 59. USUAL PRESENTATIONS OF GI BLEEDING: HEMATEMESIS Vomiting of fresh blood from esophageal varices; UGI bleeding above the ligament of treitz MELENA - blood has been present in the GI tract for at least 14 hours, more proximal bleeding site HEMATOCHEZIA - a lower GI source of bleeding, - massive upper GI bleeding, 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. Hematemesis b. Melena c. Hematochezia d. AOTA e. NOTA *Occult GI bleeding can only be detected by chemical testing.