Week 5 knowledge check.
Gastrointestinal and Hepatobiliary
Disorders
hepatitis markers – answer IgG: G=gone (infection is gone)
IgM: M=antibody made Minute infected (acute infection)
HBsAg: hep B surface antigen = infection
Anti-HBs: hep B surface antibody = immunity
after HP shots - answer
gastroesophageal reflux disease (GERD) - answer-backflow of contents of the stomach
into the esophagus, often resulting from abnormal function of the lower esophageal
sphincter, causing burning pain in the esophagus
-risk: obesity, hiatal hernia, drugs/chemicals that relax the LES (Anticholinergics,
nitrates, calcium channel blockers, nicotine), delayed gastric emptying (Gastroparesis,
ulcers)
-s/sx: pain after 1 hr fo eating, worse pain if lies down or ABD pressure increase r/t
coughing, vomiting, straining
-dx: esophageal endoscopy, tissue biopsy to assess dysplastic changes
-tx: PPIs, weight loss, smoking cessation, elevate head, no tight clothing
pancreatitis - answer-between ages 50-60, more in blacks
-risk: Obstructive binary tract disease, alcoholism, peptic ulcers, hyperlipidemia,
smoking and genetics
-acute and chronic
Acute live failure - answer-very rare, from severe impairment of liver cells without
preexisting liver disease or cirrhosis
-Acetaminophen is leading cause
-death of hepatocytes may be viral or toxic injury
-will develop 6-8 weeks after viral hepatitis or 5 days to 8 weeks after acetaminophen
OD
-elevated conjugated and unconjugated bilirubin
chronic liver failure - answer
, gall bladder disease - answer-includes inflammation, infection, stones, or obstruction of
the gallbladder
-UQ abd pain
-Cholelithiasis=gallstone
-Cholecystitis=inflammation of the gallbladder
diverticulitis - answer-inflammation of the diverticula
-predisposing factors: older age, genetics, obesity, smoking, ASA/NSAIDs
-can occur anywhere in the GI tract
-s/sx: pain in lower ABD, diarrhea
tx: ultrasound, sigmoidoscopy, colonoscopy, increase fiber intake to increase stool
weight to lower colonic pressures
jaundice - answer-yellow pigmentation of the skin caused by hyperbilirubemia (>2.5-3)
-cause: obstruction to bile flow (gallstones), intrahepatic obstruction (Cirrhosis),
excessive hemolysis of RBCs
bilirubin - answerorange-yellow pigment in bile; formed by the breakdown of hemoglobin
when red blood cells are destroyed
upper GI bleed - answer-in the esophagus, stomach, duodenum
-frank, bright red blood
-causes: Bleeding esophageal or gastric varies, a Mallory-Weiss tear at the esophageal-
gastric junction on , NSAIDs, ASA,
lower GI bleed - answer-bleeding from the jejunum or ileum of the small intestine, colon,
rectum
-causes: polyps, IBD, diverticular disease
hectic encephalopathy - answer-neurologic syndrome, impaired behavioral, cognitive
and motor function
-3 types: Type A (rapidly during acute fulminant hepatitis), Type B (after portosystemic
bypass or shunting w/out liver dx) and type C (slowly with cirrhosis)
-combo of biochemical and neurotransmission alterations, Free neurotoxins going to
brian
-most hazard is Ammonia which is the end products of intestinal protein digestion
-s/sx: memory loss, irritability, lethargy
dx: test ammonia levels
tx: correct F/E levels
intra-abdominal infections - answer
Gastrointestinal and Hepatobiliary
Disorders
hepatitis markers – answer IgG: G=gone (infection is gone)
IgM: M=antibody made Minute infected (acute infection)
HBsAg: hep B surface antigen = infection
Anti-HBs: hep B surface antibody = immunity
after HP shots - answer
gastroesophageal reflux disease (GERD) - answer-backflow of contents of the stomach
into the esophagus, often resulting from abnormal function of the lower esophageal
sphincter, causing burning pain in the esophagus
-risk: obesity, hiatal hernia, drugs/chemicals that relax the LES (Anticholinergics,
nitrates, calcium channel blockers, nicotine), delayed gastric emptying (Gastroparesis,
ulcers)
-s/sx: pain after 1 hr fo eating, worse pain if lies down or ABD pressure increase r/t
coughing, vomiting, straining
-dx: esophageal endoscopy, tissue biopsy to assess dysplastic changes
-tx: PPIs, weight loss, smoking cessation, elevate head, no tight clothing
pancreatitis - answer-between ages 50-60, more in blacks
-risk: Obstructive binary tract disease, alcoholism, peptic ulcers, hyperlipidemia,
smoking and genetics
-acute and chronic
Acute live failure - answer-very rare, from severe impairment of liver cells without
preexisting liver disease or cirrhosis
-Acetaminophen is leading cause
-death of hepatocytes may be viral or toxic injury
-will develop 6-8 weeks after viral hepatitis or 5 days to 8 weeks after acetaminophen
OD
-elevated conjugated and unconjugated bilirubin
chronic liver failure - answer
, gall bladder disease - answer-includes inflammation, infection, stones, or obstruction of
the gallbladder
-UQ abd pain
-Cholelithiasis=gallstone
-Cholecystitis=inflammation of the gallbladder
diverticulitis - answer-inflammation of the diverticula
-predisposing factors: older age, genetics, obesity, smoking, ASA/NSAIDs
-can occur anywhere in the GI tract
-s/sx: pain in lower ABD, diarrhea
tx: ultrasound, sigmoidoscopy, colonoscopy, increase fiber intake to increase stool
weight to lower colonic pressures
jaundice - answer-yellow pigmentation of the skin caused by hyperbilirubemia (>2.5-3)
-cause: obstruction to bile flow (gallstones), intrahepatic obstruction (Cirrhosis),
excessive hemolysis of RBCs
bilirubin - answerorange-yellow pigment in bile; formed by the breakdown of hemoglobin
when red blood cells are destroyed
upper GI bleed - answer-in the esophagus, stomach, duodenum
-frank, bright red blood
-causes: Bleeding esophageal or gastric varies, a Mallory-Weiss tear at the esophageal-
gastric junction on , NSAIDs, ASA,
lower GI bleed - answer-bleeding from the jejunum or ileum of the small intestine, colon,
rectum
-causes: polyps, IBD, diverticular disease
hectic encephalopathy - answer-neurologic syndrome, impaired behavioral, cognitive
and motor function
-3 types: Type A (rapidly during acute fulminant hepatitis), Type B (after portosystemic
bypass or shunting w/out liver dx) and type C (slowly with cirrhosis)
-combo of biochemical and neurotransmission alterations, Free neurotoxins going to
brian
-most hazard is Ammonia which is the end products of intestinal protein digestion
-s/sx: memory loss, irritability, lethargy
dx: test ammonia levels
tx: correct F/E levels
intra-abdominal infections - answer
