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Review / Wrong Answers > DIT review - GI 3 > Flashcards

DIT review - GI 3 Flashcards

1
Q

Describe the function of the pancreas

A
  • Fat digestion:
    • Lipase, Colipase, Phospholipase A
  • Protein digestion:
    • Proteases (trypsin, chymotrypsin, elastase, carboxypeptidase)
  • Activation of zymogens:
    • Trypsinogen
      • Trypsinogen is produced by the pancreas and converted to its active enzyme, trypsin, via enterokinase/enteropeptidase produced by the small intestine
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2
Q

What is the effect of CCK on the pancreas?

A
  • From small intestine
  • Stimulates gallbladder contraction and pancreatic secretion
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3
Q

What is the effect of Secretin on the pancreas?

A
  • From small intestine
  • Stimulates pancreas to secrete bicarb
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4
Q

Effects of cystic fibrosis on the pancreas

A
  • Mutated CFTR - reduced luminal Cl- secretion and increased luminal sodium absorption (decreased water content = dehydrated, viscous mucus)
  • This causes thick pancreatic secretions, causing the pancreatic ducts to get plugged
    • Malabsorption of fats and proteins
    • Malabsorption of fat soluble vitamins
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5
Q

Causes of acute pancreatitis

A
  • Autodigestion of pancreas by pancreatic enzymes
  • Causes:
    • Most common:
      • Gallstones
      • Alcohol
    • I GET SMASHED:
      • Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypertriglyceridemia/Hypercalcemia, ERCP, Drugs (e.g. Sulfa, NRTIs, protease inhibitors)
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6
Q

What is Trousseau Syndrome

A
  • Hypercoagulability
  • Venous thrombosis
  • Migratory thrombophlebitis
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7
Q

Tumor markers of pancreatic adenocarcinoma

A

CA19-9

CEA

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8
Q

What is the portal triad

A

Hepatic artery, portal vein, bile duct

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9
Q

What is the difference in blood being carried by the hepatic artery vs. portal vein

A
  • Hepatic artery - carrying oxygenated blood
  • Portal vein - carrying blood rich in nutrients and drugs that were absorbed in the GI tract
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10
Q

Describe the metabolism of bilirubin, including the conjugating enzyme

A
  • Hemoglobin broken down into heme and globin
  • Heme then broken down into iron and protoporphyrin
  • Protoporphyrin converted into unconjugataed bilirubin
  • UCB binds to albumin to be brought to the liver
  • Liver conjugates UCB into CB
    • UDP glucuronyl transferase (UGT) is the enzyme in the hepatocytes that conjugates bilirubin
  • CB dumped into bile canaliculi to be sent to the gallbladder
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11
Q

What is the cause of physiologic jaundice of the newborn

A
  • Newborn livers have low UGT activity, leading to increased UCB
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12
Q

What is kernicterus

A
  • Too much fat soluble UCB can deposit in the basal ganglia of the brain, leading to kernicterus
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13
Q

How does phototherapy work for treatment of jaundice

A
  • Phototherapy – makes UCB water soluble
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14
Q

Describe Gilbert Syndrome (defect, elevated CB vs. UCB, presentation)

A
  • Autosomal recessive
  • Mildly low UGT activity
    • Due to mutation in promoter region
  • Slight elevation of UCB
  • Benign and asymptomatic; slight jaundice during stress
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15
Q

Describe Crigler-Najjar syndrome (defect, elevated Cb vs. UCB, presentation)

A
  • Absence of UDP-GT
  • Elevated UCB and jaundice
  • Kernicterus is usually fatal
  • Treatment:
    • Phototherapy, Plasmapheresis (to remove UCB), liver transplant
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16
Q

How do you differentiate Type I vs. Type II Crigler-Najjar syndrome

A
  • Type I vs. Type II
    • Type I is more severe
    • If you give phenobarbital, it will cause decreased UCB in Type II and no change in Type I
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17
Q

Describe Dubin-Johnson syndrome (defect, elevated CB vs. UCB, presentation)

A
  • Deficiency of bilirubin canalicular transport protein
    • Cannot transport CB from liver to bile ducts
  • Black liver (due to build up of bilirubin in hepatocytes)
  • Increased CB
  • Clinically benign
18
Q

What are the 3 stages of alcoholic liver diseas?

A

Hepatic steatosis

Alcoholic hepatitis

Alcoholic cirrhosis

19
Q

Describe histology and lab values of alcoholic hepatitis

A
  • Inflammation of liver – swollen and necrotic hepatocytes
  • Mallory bodies – intracytoplasmic eosinophilic inclusions of damaged keratin filaments
  • AST > ALT (THINK: A Scotch and Tonic)
20
Q

Why would you see bleeding and bruising in liver failure?

A
  • Loss of coagulation factors - Coagulopathy and elevated PT and PTT
21
Q

Why would you see edema and ascites in liver failure?

A
  • Loss of albumin - decreased osmotic pressure causing to fluid to leak out of vessels
22
Q

What is the cause of confusion, delirium, hypersomnia, coma, and death in liver failure?

A
  • Inability to metabolize toxins (e.g. ammonia) - hepatic encephalopathy
23
Q

What is the cause of spider telengectasias is liver failure?

A
  • Inability to inactivate steroids - elevated estradiol levels
    • Testicular atrophy, gynecomastia
    • Spider telengiectasias
    • Palmar erythema
24
Q

Signs and symptoms of portal HTN

A
  • Portosystemic shunts – anastomoses between portal venous system and systemic veins in order to relieve pressure
    • Esophageal varices
    • Caput medusae (around the umbilicus)
    • Anorectal varices – hemorrhoids
  • Hepatomegaly
  • Splenomegaly
  • Ascites
    • Spontaneous bacterial peritonitis (SBP)
    • Treat with diuretics or peritonitis
25
Q

How do you treat esophageal varices

A
  • Octreotide
  • Endoscopic banding
  • Propranolol or Nadolol
  • TIPS procedure: Transjugular intrahepatic portosystemic shunt
26
Q

What is the cocktail of drugs usually given to patients with cirrhosis

A
  • Diuretics – ascites and edema
  • Beta-blocker – prevention of bleeding esophageal varisces
  • Vitamin K – to maximize clotting
  • Lactulose – excrete ammonia
27
Q

What is nutmeg liver and what causes it?

A

Nutmeg liver = backup of blood into liver

Caused by Budd Chiari or R heart failure

28
Q

Cause and presentation of Budd Chiari syndrome

A
  • Caused by occlusion of IVC or hepatic veins - decreased outflow of blood leaving the liver - congestive liver disease
  • Presentation:
    • Hepatomegaly, ascites, abdominal pain
    • No JVD
      • Liver congestion + JVD = R heart failure
29
Q

What is the mechanism behind Reye Syndrome

A
  • Hepatic encephalopathy in children treated with aspirin for a viral infection
  • Aspirin metabolites decrease beta-oxidation by reversible inhibition of mitochondrial enzymes
30
Q

What is the defect in Wilson disease and what does it cause (presentation, lab values)

A
  • Autosomal recessive
  • Mutation in hepatocyte copper-transporting ATPase (ATP7B gene)
  • Inadequate copper excretion into bile and blood
    • Decreased serum ceruloplasmin
    • Increased urine copper
    • Copper accumulation in: liver, brain, cornea, kidney, joints
  • Presentation:
    • Liver disease, Kayser-Fleischer rings, renal disease (Fanconi syndrome)
31
Q

Treatment of Wilson disease

A
  • Chelation with Penicillamine
32
Q

Causes of hemochromatosis

A
  • Primary:
    • Recessive mutation in HFE gene - abnormal iron sensing - increased intestinal absorption
  • Secondary:
    • Chronic transfusion therapy
33
Q

Lab values in hemochromatosis (ferritin, iron, TIBC, transferrin saturation)

A

Increase ferritin, increased total serum iron, decreased TIBC, increased transferrin saturation

34
Q

Presentation of hemochromatosis

A

Classic triad:

Cirrhosis, Diabetes mellitus, Skin pigmentation

(“bronze diabetes”)

35
Q

Treatment of hemochromatosis

A
  • Phlebotomy
  • Chelation with Deferoxamine
36
Q

Cause of lung and liver disease in alpha-1-antitrypsin deficiency

A
  • Lungs:
    • Decreased a1-antitrypsin - uninhibited elastase in alveoli - decreased elastic tissue - panacinar emphysema
  • Liver:
    • Misfolded gene produce protein aggregates in hepatocellular endoplasmic reticulum - cirrhosis with PAS (+) globules
37
Q

Diseases of what body systems will cause increased Alkaline phosphatase?

A

Liver, biliary, bone

38
Q

What are associated risk factors for hepatic adenoma?

A

oral contraceptive, anabolic steroid use

39
Q

What are associated risk factors for hepatic angiosarcoma

A

exposure to arsenic or vinyl chloride

40
Q

What are associated risk factors for Hepatocellular carcinoma

A
  • Hepatitis B
  • Hepatitis C
  • All associations with cirrhosis
  • Hemochromatosis
  • A1-antitrypsin deficiency
  • Aflatoxin from Aspergillus
41
Q

What lab value will be elevated in hepatocellular carcinoma

A

Elevated a-fetoprotein

Review / Wrong Answers (140 decks)

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