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Block 5 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

MRI imaging for liver and gallbladder

  1. T2 weighted MRI is best for imaging …
  2. T1 Weighted MRI is best for imaging…
  3. MRCP is best for imaging… and can diagnose….
A
  1. darker liver parenchyma, brighter gallbladder / common bile duct
  2. brighter liver parenchyma, darker gallbladder / common bile duct
  3. visualization of biliary tree (NON-INVASIVE bc does not require IV contrast) → for diagnosing Choledocholithiasis (stones in bile ducts)
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2
Q
  1. What imaging technique is used for cirrhosis?
A
  1. ultrasound
  2. look at outline of liver- this shows cirrhosis
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3
Q
  1. What imaging technique is best used for cholelithiasis (gallstones)?
A
  1. ultrasound - stones leave dark shadows (white arrows)

second image …

  • Black arrow show gallstones at gallbladder neck
  • Blue arrow show thickened wall of gallbladder
  • White dotted arrow show pericholecystic fluid
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4
Q

how do you differentiate focal nodular hyperplasia and hepatocellular carcinoma on CT imaging?

A
  1. Focal nodular hyperplasia (FNH) is a benign liver lesion that is composed of a proliferation of hyperplastic hepatocytes surrounding a central stellate scar.
  2. hepatocellular carcinoma does not have the stellate center
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5
Q

Pancreatitis on CT or MRI - what should you look out for in imaging

A
  1. peripancreatic fluid (asterisk - this is MRI image)
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6
Q

Necrotizing pancreatitis on CT - how do you know it is necrotizing pancreatitis?

A
  1. White tissue (white arrow on left image) - shows the leftover viable tissue, the tissue to left is necrotic
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7
Q
  1. What are pancreatic pseudocysts?
  2. How are they seen on imaging (CT)?
A
  1. well-circumscribed collections of homogenous fluid attenuation - most common complication of pancreatitis
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8
Q

How does chronic pancreatitis look different from acute pancreatitis in imaging?

A
  1. parenchymal fibrosis / fatty change / calcifications
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9
Q

How does pancreatic adenocarcinoma look like on imaging (ultrasound)?

A
  1. irregular margins of mass in pancreas (outlined by arrows)
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10
Q

Label what each image is

A

image

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11
Q

What does this image show in intestines?

A

toxic megacolon

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12
Q

Hepatitis A

  1. DNA/RNA?
  2. transmission?
  3. vaccine?
A
  1. RNA (non-enveloped, (+) ssRNA, linear, icosahedral)
  2. fecal-oral
  3. yes
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13
Q

Hepatitis B

  1. DNA/RNA?
  2. transmission?
  3. vaccine?
A
  1. DNA (enveloped, partially dsDNA, circular, icosahedral)
  2. body fluids
  3. yes
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14
Q

Hepatitis C

  1. DNA/RNA?
  2. transmission?
  3. vaccine?
A
  1. RNA (enveloped, (+) ssRNA, linear, icosahedral)
  2. body fluids
  3. NO
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15
Q

Hepatitis D

  1. DNA/RNA?
  2. transmission?
  3. vaccine?
A
  1. RNA (enveloped, (-) ssRNA, circular genome)
  2. body fluids
  3. NO
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16
Q

Hepatitis E

  1. DNA/RNA?
  2. transmission?
  3. vaccine?
A
  1. RNA (non-enveloped, (+) ssRNA, linear, icosahedral)
  2. fecal-oral
  3. Not in US
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17
Q
  1. What are some symptoms of viral hepatitis (infection of liver which leads to chronic liver inflammation)
  2. AST > or < ALT
  3. Bilirubin levels
A
  1. often asymptomatic or fever, GI symptoms, RUQ pain, jaundice, itching (due to bile salts in skin), dark urine, clay-colored stools (due to lack of of bilirubin excretion)
  2. ALT>AST - both are increased
  3. Increased bilirubin
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18
Q

Hepatitis A

  1. how is it diagnosed?
  2. is vaccine activated or inactivated?
  3. infection is chronic or self limited?
A
  1. anti-HAV IgM antibodies + symptoms OR anti-HAV IgG antibodies (IgM are first antibodies body makes to fight infections and IgG are antibodies that take a while to make so it indicates infection was not so recent)
  2. inactivated IM injection
  3. self limited
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19
Q

Hepatitis B

  1. Incubation period?
  2. what type of vaccine is available for this?
  3. Is this mostly self limited or chronic?
  4. extrahepatic manifestations? (2)
A
  1. long incubation period: 1-4 months
  2. recombinant HBsAg (to make anti-HBsAg antibodies w/o HBc or HBe antibodies)
  3. Can be either but chronic is common in infant children - and risk progression to cirrhosis, liver failure, hepatocellular carcinoma
  4. polyarteritis nodosa (a rare multi-system disorder characterized by widespread inflammation, weakening, and damage to small and medium-sized arteries) and glomerular disease
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20
Q

Hepatitis B

  1. What does HBsAg mean
  2. What does HBcAg mean
  3. What does HBeAg mean
A
  1. Hep B surface antigen (A protein on the surface of hepatitis B virus)
  2. Hep B core antigen (an inner core protein)
  3. Hep B e antigen (a secretory protein processed from the precore protein)
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21
Q

HBV antigens and antibodies help tell you the infection status of person.

  1. What do you find in a person that is immunized the HBV?
A
  1. IgG antibody - Anti-HBs (antibody against surface antigen of HBV)
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22
Q

HBV antigens and antibodies help tell you the infection status of person.

  1. What do you find in a person that has acute HBV infection? (3)
A
  1. HBsAG (HBV surface antigen)
  2. HBeAG (HBV e antigen - indicates significant viral replication/highly infectious)
  3. Anti-HBc (antibody against core antigen - IgM)
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23
Q

HBV antigens and antibodies help tell you the infection status of person.

  1. What do you find in a person that is in their window period (The time between exposure and when antibodies can be detected) of HBV infection? (1)
  2. What is undetectable? (2)
  3. When does this window period happen?
A
  1. anti-HBc (IgM) - antibody against core antigen)
  2. HbsAG (surface antigen) and anti-HBsAG (antibody against surface antigen)
  3. After HBsAG and HBeAG have peaked and fallen + after symptoms BUT before the peak of anti-HBs (plus presence of other two antibodies)
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24
Q

Out of the three antigens in HBV which ones are detectable in serum?

A
  1. only “e” and surface antigens. Core antigen is not found in serum.
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25
Q

HBV antigens and antibodies help tell you the infection status of person.

  1. What do you find in a person that is in chronic (high infectivity) portion of HBV infection? (3)
A
  1. HBsAG, HBeAG, and Anti-HBc (IgG)
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26
Q

HBV antigens and antibodies help tell you the infection status of person.

  1. What do you find in a person that is in chronic (low infectivity) portion of HBV infection? (3)
A
  1. HBsAG, anti-HBe, and Anti-HBc (IgG)
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27
Q

HBV antigens and antibodies help tell you the infection status of person.

  1. What do you find in a person that is in the recovery portion of HBV infection? (3)
A
  1. Anti-HBs, Anti-HBe, Anti-HBc (IgG)
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28
Q

HBV antigens and antibodies help tell you the infection status of person.

  1. What do you find in a person that is immunized to HBV? (2)
A
  1. Anti-HBs and Anti-HBc (IgG)
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29
Q

NRTI (nucleoside/tide reverse transcriptase inhibitors)

  1. For what hepatitis type is this used for?
  2. Name of drugs in this category?
  3. Mechanism of action? (how do the two drugs act differently?)
A
  1. chronic Hep B
  2. Entecavir and tenofovir
  3. Inhibition of reverse transcriptase to prevent virus production → Entecavir (guanosine analogue) and Tenofovir (adenosine analogue)
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30
Q

Interferon Alpha 2a/Alpha 2b

  1. For what hepatitis type is this used for?
  2. Mechanism of action?
A
  1. chronic hep B
  2. inhibits viral penetration and induces proliferation of macrophage and helper T cell for immune defense
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31
Q

Ribavirin

  1. For what hepatitis type is this used for?
  2. Mechanism of action?
  3. special instructions?
  4. side effects? (5)
A
  1. Chronic Hep C
  2. Inhibits replication of HCV but mechanism not clear
  3. monotherapy is ineffective. Needs to be combined with interferon or DAA (direct acting antiviral)
  4. hemolytic anemia, MI, depression, fatigue, rash
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32
Q

Direct Acting Antivirals (DAA)

  1. For what hepatitis type is this used for?
  2. Mechanism of action?
A
  1. Chronic Hep C
  2. direct inhibition of the function of HCV specific proteins
    3.
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33
Q

What are the three different “products” within the category of Direct Acting Antivirals (DAA) → MOA, drug name, and suffix for (BLANK)

  1. (BLANK)
  2. NS5A inhibitor
  3. NS5B polymerase inhibitor
A
  1. NS3 /4A protease inhibitors
  2. -previr suffix (simeprevir)
  3. NS3/NS4A is responsible for cleaving and processing the HCV encoded polyprotein which is important for HCV viral life cycle
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34
Q

What are the three different “products” within the category of Direct Acting Antivirals (DAA) → MOA, drug name, and suffix for (BLANK)

  1. NS3 /NS4A protease inhibitors
  2. (BLANK)
  3. NS5B polymerase inhibitor
A
  1. NS5A inhibitor
  2. -asvir suffix (ledipasvir)
  3. NS5A is a viral phosphoprotein that has a role in replication, assembly, and release ← inhibiting this
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35
Q

What are the three different “products” within the category of Direct Acting Antivirals (DAA) → MOA, drug name, and suffix for (BLANK)

  1. NS3 /NS4A protease inhibitors
  2. NS5A inhibitor
  3. (BLANK)
A
  1. NS5B polymerase inhibitor
  2. End in suffix -buvir (sofosbuvir)
  3. NS5B polymerase - important for replication

used in combo with NS5A inhibitor

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36
Q

What are kupffer cells in the liver?

A
  1. fixed tissue macrophages within sinusoids (vascular channels that receive blood from terminal branches of the hepatic artery and portal vein at the periphery of lobules and deliver it into central veins)
  2. they phagocytose cell debris and old RBCs
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37
Q
  1. Endothelial cells of liver form a barrier between what two structures?
  2. What is the purpose of the endothelial cells creating a fenestrated barrier?
A
  1. sinusoids and space of disse
  2. allow passage of macromolecules w/out allowing blood cells through
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38
Q

Stellate (Ito) Cells – (HSC)

  1. What are they and what is their function?
  2. Where do they reside?
  3. What does it store?
  4. Complications from overactivation of these cells?
A
  1. They are quiescent fibroblasts are activated by inflammatory mediators to commence collagen synthesis. upon liver injury, stellate cells transform into fibroblast like cells and can do scar tissue generation → can make type I/III collagen + remodel ECM
  2. space of disse
  3. vitamin A (in large fat droplets within the cell)
  4. fibrosis/cirrhosis
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39
Q
  1. What is found within a portal triad in the liver?
  2. What does the central vein drain into?
A
  1. branch of hepatic artery
  2. branch of portal vein
  3. bile duct
  4. central vein drains into IVC
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40
Q

The organization of the liver can be described in 3 different formats. Describe what each format means

  1. Hepatic lobule
  2. Portal lobule
  3. Zones of Portal Acinus
A
  1. Hepatocytes drained by a single central vein and hepatocyte is surrounded by 6 portal triads (hexagon shape)
  2. three hepatocytes are drained by a single bile duct (makes a triangle between 3 central veins)
  3. There are three zones within the hepatocyte based on ATP levels and oxygenation of blood
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41
Q

Zones of Portal Acinus (based on ATP and oxygenation levels)

  1. Zone I - describe ATP and O2 levels + alternative name
  2. Zone II - describe ATP and O2 levels + alternative name
  3. Zone III - describe ATP and O2 levels + alternative name
A
  1. High ATP, High O2 — Periportal
  2. mid — transitional
  3. Low ATP, Low O2 — Pericentral (by central vein)
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42
Q
  1. What reactions are more likely to happen near periportal side (4)
  2. What reactions are more likely to happen near pericentral side
A
  1. Periportal - reactions that require ATP (such as gluconeogenesis, AA catabolism, urea cycle, albumin synthesis)
  2. Pericentral - don’t require much ATP (such as glycolysis, FA synthesis, Toxin metabolism)
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43
Q
  1. What zone is more susceptible to ischemia?
  2. Why?
A
  1. zone III
  2. Zone III is more susceptible to ischemia because it has less O2 concn
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44
Q
  1. What zone of liver is most affected by viral hepatitis?
  2. What zone is where alcoholic hepatitis occurs?
  3. What is the metabolite of ethanol that affects liver?
  4. What is the metabolite of acetaminophen that affects liver?
A
  1. Zone I
  2. Zone III
  3. acetaldehyde
  4. NAPQI

these to metabolites of toxins affect/injure liver

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45
Q

What is phase 1 reactions vs phase 2 reactions in metabolism of toxins in livers?

A
  1. phase 1 reactions - make primary metabolite under the P450 enzymes. Some toxins are able to be excreted in urine or bile after this first phase I reactions.
  2. Phase 2 reactions - when primary metabolite (that is still unable to be excreted) undergoes another reaction to make secondary metabolite to make it ionized and able to be excreted via urine or bile
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46
Q
  1. What vitamins are stored by liver?
  2. What vitamins are activated in liver?
  3. What is the liver’s interaction with copper?
A
  1. Vitamin A and Vitamin B12
  2. Vitamin D activation (D3 → 24 ‘-OH)
  3. allows for copper metabolism. Exports copper into blood via attachment to ceruloplasmin → then it can be excreted into stool via bile
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47
Q

What proteins are formed in the liver? (4)

A
  1. albumin (hypoalbuminemia happens in advanced cirrhosis for this reason)
  2. lipoproteins
  3. prothrombin (increased PT is seen in liver dysfunction for this reason)
  4. transferrin
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48
Q

How does liver help in excretion of bilirubin?

A
  1. conjugation of bilirubin occurs in hepatocytes which allows for proper excretion. Once conjugated it can be actively transported into bile canaliculi by MRP2 transporter
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49
Q
  1. Hemolytic Jaundice - excessive RBC breakdown → leads to increase in [unconjugated/conjugated] bilirubin
  2. Hepatocellular jaundice - liver injury → leads to increase in [unconjugated/conjugated] bilirubin
  3. Obstructive Jaundice - obstruction in bile or pancreatic ducts → leads to increase in [unconjugated/conjugated] bilirubin
A
  1. unconjugated
  2. both
  3. conjugated
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50
Q
  1. Where is bile made?
A
  1. liver
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51
Q
  1. Where are bile canaliculi?
  2. In what direction does bile move in relation to periportal and pericentral
A
  1. Bile canaliculi also known as bile capillaries are thin tubes that receive bile secreted by hepatocytes. The bile passes through canaliculi to the hepatic bile ducts and then into the common hepatic duct which drains directly into the duodenum.
  2. from pericentral to periportal
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52
Q
  1. Why do hepatocytes have a frothy appearance?
  2. are nuclei small or large?
A
  1. because of the glycogen content
  2. large nuclei
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53
Q

In portal triad you have hepatic arteriole, portal venule, and bile ductule

  1. What is the oxygenation levels of blood coming in through hepatic arteriole and portal venule
A
  1. Hepatic arteriole is fully oxygenated (comes from caval system)
  2. Portal venule is partially oxygenated (comes from portal system)
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54
Q

Gallbladder

  1. What is the purpose of gallbladder in terms of bile?
A
  1. epithelial cells absorb ions, extracts water → this leads to bile becoming 10X more concentrated
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55
Q

Gallbladder

  1. What cells are found in mucosa? What is the histological marker of gallbladder?
  2. special structures of submucosa and muscularis mucosa
  3. is gallbladder is covered by adventitia or serosa
A
  1. very tall simple columnar epithelial cells - highly folded mucosa (appearance of bridges)
  2. there is no submucosa or muscularis mucosa
  3. majority is covered with serosa but liver attachment is covered with adventitia
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56
Q

Function of the pancreas

  1. exocrine
  2. endocrine
A
  1. exocrine secretion - secretion of digestive enzymes into duodenum
  2. endocrine secretion - secretion of hormones into blood stream
57
Q

Pancreas

  1. pancreas is divided into (BLANK A) by connective tissue septa
  2. How are serous acini and intercalated duct related?
  3. How are interlobular ducts related to the two structures in #2
A
  1. lobules
  2. serous acini are glands that secrete zymogens → this is dumped into intercalated ducts
  3. pancreas secretions are eventually dumped into interlobular ducts and then this goes into pancreatic duct
58
Q
  1. What does intercalated duct do to the pancreatic secretion/solution?
  2. What are centroacinar cells
A
  1. secrete HCO3 (alkaline secretions)
  2. these cells are found in the opening of intercalated ducts - stain lighter than surrounding serous acini
59
Q
  1. What is the function of the islets of langerhans in pancreas?
  2. List the 4 types of islet cells
A
  1. Produce many hormones and secrete them directly into blood
  2. alpha cells, beta cells, delta cells, minor islet cells
60
Q

Islets of langerhans in pancreas - what hormones do these secrete?

  1. alpha cells
  2. beta cells
  3. delta cells
  4. minor islet cells
A
  • Alpha cells - produce glucagon
  • Beta cells - islet cells, produce insulin
  • Delta cells - produce somatostatin and VIP
  • Minor islet cells - produce gastrin, pancreatic peptide, and ghrelin
61
Q
  1. Which glut transporter is not insulin dependent?
  2. Why is this essential for insulin secretion?
A
  1. GLUT2
  2. This brings glucose into beta cells and signals insulin to be released within 3 minutes. Then insulin can lead to even more glucose absorption (decreasing blood glucose)
62
Q

What is the most common primary liver tumor?

A

hepatocellular carcinoma

63
Q

Hepatocellular carcinoma

  1. what are some risk factors for this cancer (3)
  2. symptoms (4)
  3. How is it diagnosed? (3)
A
  1. History of HepB or HepC, alcoholic cirrhosis, hemochromatosis and more
  2. asymptomatic many times but can show hepatomegaly, hypoglycemia, erythrocytosis (increased amount of RBC)
  3. elevated AFP (alpha fetoprotein) in blood + CT scan + biopsy
64
Q

Budd chiari syndrome

  1. pathophysiology
  2. symptoms (4)
  3. What can cause this syndrome? (3)
A
  1. Thrombosis of hepatic vein (what central vein flows into) → this causes back up of blood into liver → can lead to liver cirrhosis which can then lead to hepatocellular carcinoma
  2. abdominal pain, ascites, hepatomegaly, zone III congestion and necrosis
  3. pregnancy, hypercoagulable state, Hepatocellular carcinoma and more
65
Q

Hepatic adenoma

  1. Morphology of lesion
  2. risk of malignancy
  3. risk factors
A
  1. circumscribed lesion in liver, a solitary mass, shows cords of normal hepatocytes with absent portal triads/tracts
  2. these are benign liver tumors common in young women
  3. contraceptive use, anabolic steroids (exposure to sex hormones)
66
Q
  1. What is a cavernous hemangioma?
  2. What is a hepatic angiosarcoma
  3. What exposure is hepatic angiosarcoma associated with?
A
  1. common benign liver tumor - composed of vascular spaces (happens when capillaries swell and form a noncancerous mass called an angioma)
  2. a particularly rare, non-cirrhotic, primary malignancy of the liver - vascular tumor
  3. vinyl chloride or arsenic exposure
67
Q

Pancreatic Adenocarcinoma

  1. Where does it occur and its Prognosis?
  2. Risk factors? (4)
  3. Gene mutations?
  4. symptoms? (5)
  5. Tumor markers? (2)
A
  1. in the head and has very poor prognosis, avg survival is 1 year after dx
  2. >50 years, smoking, diabetes, chronic pancreatitis
  3. KRAS (most common) - but also BRCA2 and SMAD4
  4. PAINLESS JAUNDICE (since many occur in head and this is close to bile duct it can block it and create jaundice)- dark urine - abdominal pain - clay colored stools - steatorrhea
  5. CA-19-19 and CEA (but CEA is just used to measure treatment response
68
Q

Pancreatic Adenocarcinoma - signs on examination/screening

  1. What is the courvosiier’s sign?
  2. What is trousseau’s syndrome?
A
  1. enlarged, non-tender gallbladder with jaundice
  2. migratory superficial thrombophlebitis (redness on skin that migrates)
69
Q
  1. What is the whipple procedure
  2. What is it used to treat?
A
  1. remove the head of the pancreas, the first part of the small intestine (duodenum), the gallbladder and the bile duct.
  2. pancreatic adenocarcinoma
70
Q

Gallbladder adenocarcinoma

  1. arises from what in the gallbladder?
  2. Risk factors?
  3. Classic presentation?
A
  1. glandular epithelium of gallbladder
  2. gallstones (esp. porcelain gallbladder)
  3. new-onset cholecystitis in elderly women
71
Q
  1. AST is located in..? (of hepatocytes)
  2. ALT is located in…? (of hepatocytes)
  3. What does increase in AST>ALT indicate?
  4. What does increase in ALT>AST indicate?
A
  1. mitochondria of hepatocytes
  2. cytoplasm of hepatocytes
  3. alcohol hepatitis
  4. cell damage hepatitis
72
Q
  1. What does elevated alkaline phosphate mean in liver tests?
  2. What does elevated GGT along with elevated Alk phosphate mean?
A
  1. obstructed bile flow (cholestasis)
  2. confirms hepatobiliary cause of increased Alk Phos
73
Q

What are the three types of alcoholic liver disease?

A
  1. Hepatic steatosis
  2. alcoholic hepatitis
  3. alcoholic cirrhosis
74
Q

Alcoholic liver disease - hepatic steatosis

  1. pathophysiology under this
  2. symptoms
  3. Where does injury begin (zone 1-3)?
  4. Is it reversible with cessation of alcohol?
A
  1. accumulation of FAs within hepatocytes
  2. Often asymptomatic - can present with hepatomegaly
  3. fatty infiltration begins at zone III
  4. yes it can be reversed
75
Q

Alcoholic liver disease - Alcoholic Hepatitis

  1. pathophysiology under this
  2. symptoms
  3. What special structure is found under microscopy and what is it?
  4. What causes the injury to hepatocytes?
A
  1. a more severe, inflammatory type of liver injury characterized by swollen, dying hepatocytes, neutrophilic infiltration, and Mallory-Denk bodies.
  2. Fever, jaundice, RUQ pain after heavy binge drinking in alcoholics
  3. Mallory Bodies (image) - cytoplasmic inclusions of damaged intermediate filaments in hepatocytes
  4. Caused by toxic effects of acetaldehyde (ethanol → acetaldehyde in liver)
76
Q

Alcoholic liver disease - Alcoholic Cirrhosis (Same as Cirrhosis generated via other form that is not alcohol)

  1. pathophysiology under this/histology of liver
  2. symptoms (5)
  3. What hormone is elevated in end stage liver disease/cirrhosis?
  4. What does this elevated hormone lead to? (clinical presentations) (3)
A
  1. Due to chronic liver injury - fibrosis occurs and disrupts normal liver structure. This leads to histology of liver showing mix of fibrosis in tissues and regenerative nodules
  2. Hyperammonemia (leads to asterixis, confusion, comma) , jaundice, hypoglycemia, coagulopathy, hypoalbuminemia (leads to edema and ascites)
  3. Estrogen
  4. gynecomastia (men), spider angioma, palmar erythema
77
Q

Cirrhosis

  1. What do stellate (ito) cells secrete to begin the fibrosis of the liver
  2. How is cirrhosis diagnosed? (3)
A
  1. TGF-beta
  2. liver biopsy – small, nodular liver on CT - presence of ascites+spider angiomata
78
Q

Non-Alcoholic Fatty Liver Disease

  1. pathophysiology of disease
  2. special structure in the histology of liver
  3. AST>ALT or AST
A
  1. Fatty infiltration of hepatocytes which may be due to high BMI, high blood lipid levels, diabetes, eating habits, and genetics
  2. Ballooning of hepatocytes (imaging)
  3. AST>ALT
79
Q
  1. Cardiac Cirrhosis is (BLANK A) heart failure that leads to chronic liver edema which can cause cirrhosis
  2. In this condition the liver takes on a mottled appearance known as (BLANK B)
A
  1. right heart failure
  2. nutmeg liver
80
Q

Reye’s Syndrome

  1. pathophysiology
  2. what type of patient does this present in?
  3. how to prevent this
A
  1. rapid, severe liver failure/swelling of liver
  2. children with viral infections who have taken aspirin
  3. avoid aspirin in children
81
Q

Alpha 1 antitrypsin deficiency

  1. describe what this is?
A
  1. an inherited condition that raises your risk for lung and liver disease. Alpha-1 antitrypsin (AAT) is a protein that protects the lungs. The liver makes it. If the AAT proteins aren’t the right shape, they get stuck in the liver cells and can’t reach the lungs
82
Q
  1. What antibodies are seen in autoimmune hepatitis
  2. What type of patient is typically seen to have autoimmune hepatitis
A
  1. anti-nuclear antibody + anti-smooth muscle antibody (this is specific for autoimmune hepatitis)
  2. middle aged women
83
Q

tylenol (Acetominophen) overdose

  1. What organ does this mainly affect?
  2. What lab test/value can tell you it is Acetominophen overdose?
  3. What treatment is used for this? (2)
A
  1. liver - acute liver failure
  2. AST/ALT >1000
  3. activated charcoal or N-acetylcysteine (replenishes glutathione to metabolize NAPQI, the metabolite of acetaminophen)
84
Q

Shock liver (ischemic hepatitis)

  1. What zone is most affected and can lead to necrosis?
  2. What lab test/value indicate shock liver?
A
  1. Zone III (this region already has low O2 levels)
  2. AST/ALT > 1000
85
Q

Wilson’s Disease

  1. Pathophysiology?
  2. Autosomal recessive or dominant
  3. Gene mutation?
A
  1. ATP7B is mutated so this protein is unable to incorporated Copper into ceruloplasmin for excretion transport via bile. This is lack of copper excretion so copper accumulates in liver and creates free radicals. - liver injury-
  2. autosomal recessive
  3. ATP7B gene mutation
86
Q

Wilson’s Disease

  1. clinical presentation (5) (hint: some are movements, some are appearances, some are tests)
  2. Dx (2)
  3. Tx (2)
A
  1. cirrhosis, Parkinsonian movements, dyskinesia (uncontrolled involuntary movements), Kayser-Fleischer Rings (in eyes), Coombs negative hemolytic anemia
  2. reduced ceruloplasmin level, high urinary copper excretion
  3. Penicillamine or oral zinc
87
Q

Hereditary Hemochromatosis

  1. Pathophysiology?
  2. Autosomal recessive or dominant
  3. Gene mutation?
A
  1. unregulated absorption of heme and non-heme iron so iron accumulates in various parts of body. This unregulated absorption is bc there are low hepcidin levels which normally inhibits too much iron absorption.
  2. autosomal recessive
  3. mutation in HFE gene
88
Q

Hereditary Hemochromatosis

  1. Why do women show symptoms later than men?
  2. What clinical presentations can iron accumulation lead to? (Hint: pancreas, skin, heart, joints, glands)
  3. What things must be avoided and why?
A
  1. women lose iron during menstruation so they have an extra way of iron excretion than men
  2. iron in pancreas can lead to diabetes — can lead to bronze color skin — dilated cardiomyopathy — arthropathy —atrophy of pituitary gland
  3. alcohol bc this accelerates liver damage AND vitamin C bc this increases iron absorption
89
Q

Hereditary Hemochromatosis

  1. how is it dx (2)
A
  1. genetic testing for C282Y mutation in HFE gene
  2. prussion blue staining ( the blue is iron)
90
Q

Secondary Hemochromatosis

  1. what causes this?
  2. What can treat this?
A
  1. iron accumulation due to excessive blood transfusion - such as in hematologic disorders (thalassemia major, sickle cell, leukemia)
  2. phlebotomy (removes iron) and iron chelating agents
91
Q

Cholethiasis

  1. what is this?
  2. What are the different types?
A
  1. gallstones (stones in gallbladder)
  2. cholesterol and pigment (bilirubin)
92
Q

Cholesterol gallstones

  1. what three pathways/occurences cause this?
A
  1. excess estrogen- this promotes cholesterol synthesis
  2. underproduction of bile salts - this decreases cholesterol solubility
  3. decreased reabsorption of bile salts - this decreases cholesterol solubility
93
Q

Bilirubin (pigment) stones

  1. is this unconjugated or conjugated bilirubin that make up the stones
  2. what three processes lead to bilirubin stones/unconjugated bilirubin
A
  1. unconjugated
  2. extravascular hemolysis (increases bilirubin and overwhelms conjugation enzymes) — cirrhosis/chronic liver disease (impaired bilirubin conjugation) — recurrent biliary tree infections
94
Q

Biliary Colic

  1. what is unique about this pain description?
  2. what causes this pain?
A
  1. POSTPRANDIAL RUQ pain that radiates to right shoulder blade (no inflammation)
  2. Pain occurs when CCK stimulates gallbladder to contract and it contracts against stone in outlet duct
95
Q

Acute Cholecystitis

  1. What is this a complication of?
  2. what is unique description of the pain related to this?
  3. What physical maneuver can you do to test for this?
  4. What complications can occur?
A
  1. gallstone obstructing the cystic duct leads to bile build up and inflammation of gallbladder.
  2. RUQ pain that radiates to right scapula
  3. Murphys sign - press on RUQ, ask pt to inspire but pt stops due to pain
  4. rupture of gallbladder, peritonitis → this is why it is tx with urgent sx
96
Q

Chronic cholecystitis

  1. what is this?
  2. What does the gallbladder appear like in this disease?
A
  1. long - standing untreated cholecystitis leads to chronic inflammation
  2. Porcelain gallbladder - due to calcification of gallbladder this leads to porcelain appearance o nX-ray

high risk of gallbladder carcinoma

97
Q

Choledocolithiasis

  1. What is this?
  2. What test results will indicate this? (4)
A
  1. Gallstone obstructing common bile duct (biliary obstruction)
  2. jaundice — very increased ALK phos — increased AST/ALT — progression to cholangitis (swelling of the bile duct system)
98
Q

Ascending Cholangitis

  1. What is this?
  2. What symptoms can occur with this (there is a triad and a pentad of symptoms)
A
  1. gallstone blocks flow of bile - this allows bacteria to “ascend” biliary tree
  2. Charcot’s Triad: fever, abdominal pain, juandice
  3. Reynold’s Pentads: Charcot’s triad PLUS confusion and hypotension (can also have sepsis due to infection)
99
Q

Ascending Cholangitis

  1. what bacteria are typically involved?
A
  1. gram negatives (Like E. Coli and Klebsiella)
100
Q

What is gallstone ileus?

A
  1. massive gallstone erodes through the gallbladder wall and creates a fistula with small intestine
101
Q

Gallstone pancreatitis is due to obstruction of (BLANK A) with a gallstone

A
  1. common bile duct
102
Q

Biliary Atresia

  1. What is this
  2. Typical patient
  3. symptoms (4)
A
  1. a condition in infants in which the bile ducts outside and inside the liver are scarred and blocked - lack of biliary duct formation
  2. neonates
  3. jaundice, dark urine, pale stools - absent gallbladder on ultrasound
103
Q

Primary biliary cirrhosis/cholangitis

  1. what is this?
  2. typical patient
  3. symptoms
  4. dx (5)
A
  1. disease in which the bile ducts in your liver are slowly destroyed (lymphocytes and granulomas in bile ducts). It is an autoimmune disease that causes liver damage → but no extrahepatic injury
  2. middle aged women
  3. itching (increase bile acids in skin), fatigue
  4. anti-mitochondrial antibodies, elevated Alk Phos, elevated ANA, mild AST/ALT elevation, may have cholesterol > 1000 (lead to xanthomas)
104
Q

Primary Sclerosing Cholangitis

  1. what is this?
  2. symptoms
  3. lab findings (4)
  4. dx/imaging findings (2)
A
  1. Stricture/inflammation/fibrosis of the bile duct - autoimmune disorder that involves intra and extra hepatic bile ducts.
  2. RUQ pain, fatigue, jaundice
  3. elevated IgM, p-ANCA, elevated Alk phose, elevated conjugated bilirubin
  4. onion skin fibrosis of bile ducts and beading on cholagiogarm
105
Q

Secondary biliary cirrhosis/cholangitis

  1. what is this?
A
  1. extrahepatic biliary obstruction (due to gallstones or strictures) that leads to liver fibrosis and bile stasis
106
Q

Acalculous cholecystitis

  1. What is this
  2. What is caused by (2)
A
  1. Cystic duct obstruction caused by gallbladder ischemia. With ischemia the gallbladder wall thickens and this leads to obstruction. NOT CAUSED BY GALLSTONES
  2. Caused by burns or severe trauama
107
Q

Acute Pancreatitis

  1. pathology
  2. what are the causes of this (Hint: I GET SMASHED)
A
  1. There is a block of flow of enzymes out of the pancreas. When inciting event occurs it induces premature activation of pancreatic enzymes within the gland itself → this leads to autodigestion of pancreas → INFLAMMATION, LIQUEFACTIVE NECROSIS, HEMORRHAGE
  2. Idiopathic
  3. gallstones
  4. ethanol
  5. trauma
  6. steroids
  7. mumps
  8. autoimmune
  9. scorpion sting
  10. Hypercalcemia
  11. Hypertriglyceridemia
  12. ERCP
  13. Drugs
108
Q

Acute pancreatitis

  1. symptoms
  2. Amylase and lipase?
  3. CT imaging shows?
  4. ALK phos?
  5. AST/ALT?
  6. BUN?
A
  1. epigastric pain that radiates to the back, nausea, vomiting, fever, tachy, etc
  2. elevated amylase and lipase (3X normal)
  3. image (edema surrounding pancreas)
  4. very increased ALK phos IN GALLSTONE CAUSED PANCREATITIS
  5. increased AST/ALT IN GALLSTONE CAUSED PANCREATITIS
  6. Elevated BUN (aggressive hydration is needed)
109
Q

How is acute pancreatitis dx? there is a criteria

  1. (BLANK A) pain consistent with disease
  2. (BLANK B and/or BLANK C) >3X the upper limits of normal
  3. Findings on imaging
  4. (BLANK D) out of the 3 have to be positive to dx with acute pancreatitis
A
  1. abdominal
  2. amylase and/or lipase
  3. pancreatic edema / pancreatic necrosis / bile duct stones / bile duct dilation
  4. 2 out of 3
110
Q

What are some complications of acute pancreatitis? (5)

A
  1. DIC -systemic inflammation leads to endothelial dysfunction and activation of coagulation
  2. ARDS- there are a lot of inflammatory chemicals that are secreted into the blood stream. These chemicals create inflammation throughout the body, including the lungs.
  3. Pseudocyts - walled off collection of edema
  4. pancreatic abscess - infection of pseudocysts
  5. Fat necrosis - necrosis spreads to surrounding fat of pancreas
111
Q

What is the treatment of Acute Pancreatitis

A
  1. NPO status (no food or liquid)
  2. IV fluids to maintain BP
  3. Pain control
112
Q
  1. What are the causes of chronic pancreatitis? (2)
  2. clinical presentation
  3. what happens to pancreas with chronic pancreatitis?
A
  1. alcoholism or cystic fibrosis in children
  2. chronic abdominal pain, weight loss, steatorrhea bc of pancreatic insufficiency
  3. calcification of pancreas (seen on imaging), pancreatic duct dilation, atrophy of parenchyma
113
Q

How do you treat someone that has pancreatic insufficiency (shows steatorrhea) (4)

A
  1. low fat meals
  2. insulin
  3. pancreatic enzymes
  4. stop alcohol and tobacco
114
Q
  1. splenic vein thrombosis often shows up due to what pathology?
  2. What does this lead to?
A
  1. chronic pancreatitis
  2. gastric varices, upper GI bleed, and enlarged spleen
115
Q

What are lifestyle treatment plan options for a person with Non-alcoholic fatty liver disease?

A

image

116
Q

What is the dx of Hep B in each scenario?

A

image

117
Q
  1. What causes portal hypertension (obstructed blood flow through liver due to portal resistance) (3)
A
  1. cirrhosis, vascular obstruction, intrahepatic vasoconstriction (w/loss of NO)
118
Q

High portal pressure leads to opening of venous collaterals (portal-systemic vein connections) - what are these collaterals that become enlarged due to portal hypertension? (5)

A
  1. left gastric vein (portal)+esophageal branch of azygous vein (systemic) → esophageal varices that can cause hematemesis
  2. left gastric/splenic vein (portal) → gastric varices that can cause melena
  3. paraumbilical vein (portal)-epigastric veins (systemic) → caput medusa (enlarged veins around umbilicus)
  4. superior rectal vein (portal) - inferior rectal vein (systemic) → internal hemorrhoids
  5. Engorgement of spleen due to splenic vein back-up → hypersplenism
119
Q
  1. What is ascites?
  2. What two things cause it and explain why?
A
  1. accumulation of fluid in peritoneal cavity
  2. portal hypertension and hypoalbuminemia
  3. Portal hypertension - pressure in portal vein leads to fluid leaking out and into abdomen
  4. Hypoalbuminemia - less protein leads to less oncotic pressure of vessels so fluid is not retained as easily in vessels. - fluid goes into abdomen
120
Q

SAAG (Serum ascites albumin gradient) - diff between serum albumin - ascites albumin

  1. SAAG >1.1g/dL -?
  2. SAAG <1.1g/dL -?
A
  1. portal hypertension
  2. malignant ascites - leaky vasculature due to malignancy
121
Q

How do you treat ascites? (4)

A
  1. Na restriction (bc with more sodium you keep more water)
  2. spironolactone (K+ sparing diuretic - to get rid of fluid/water)
  3. loop diuretics
  4. Paracentesis - getting fluid directly out of cavity
122
Q
  1. direct bilirubin is (unconjugated/conjugated) bilirubin
  2. indirect bilirubin is (unconjugated/conjugated) bilirubin
  3. which one is the cause of dark urine
A
  1. conjugated - water soluble
  2. unconjugated - water insoluble
  3. direct/conjugated bilirubin is cause of dark urine
123
Q

Explain how heme from RBC hemolysis gets excreted via urine and feces (5+ steps)

  1. When RBCs are at 120 days they get “eaten” by macrophages which breaks the RBC into heme and globin
    1. Heme is split into Fe and Protoporphyrin
    2. Protoporphyrin is converted to unconjugated bilirubin (this is still in macrophage)
  2. UCB is bound to albumin and moves through the circulatory system to get to the liver where hepatocytes convert UCB to CB via UGT enzyme
  3. (BLANK A) is secreted out to the bile canaliculi to go to the gallbladder
  4. Gallbladder then secretes bile for food digestion - this bile has (BLANK A) in it
  5. In small intestine, (BLANK A) is converted to urobilinogen (UBG)
    1. UBG is converted to (BLANK B) which is responsible for brown color of feces
    2. Some UBG is reabsorbed into blood and spontaneously oxides into (BLANK C)
    3. (BLANK C) is sent to the liver and the kidney. Via the kidney it is excreted in the urine making urine yellow color
A
  1. When RBCs are at 120 days they get “eaten” by macrophages which breaks the RBC into heme and globin
    1. Heme is split into Fe and Protoporphyrin
    2. Protoporphyrin is converted to unconjugated bilirubin (this is still in macrophage)
  2. UCB is bound to albumin and moves through the circulatory system to get to the liver where hepatocytes convert UCB to CB via UGT enzyme
  3. CB is secreted out to the bile canaliculi to go to the gallbladder
  4. Gallbladder then secretes bile for food digestion - this bile has CB in it
  5. In small intestine, CB is converted to urobilinogen (UBG)
    1. UBG is converted to stercobilin (SB) and SB is responsible for brown color of feces
    2. Some UBG is reabsorbed into blood and spontaneously oxides into urobilin (UB)
    3. Urobilin (UB) is sent to the liver and the kidney. Via the kidney it is excreted in the urine making urine yellow color
124
Q

Explain how heme from RBC hemolysis gets excreted via urine and feces (5+ steps)

  1. When RBCs are at 120 days they get “eaten” by (BLANK A)** which breaks the RBC into **(BLANK B) and (BLANK C)
    1. (BLANK B) is split into Fe and Protoporphyrin
    2. Protoporphyrin is converted to unconjugated bilirubin (this is still in macrophage)
  2. UCB is bound to albumin and moves through the circulatory system to get to the liver where hepatocytes convert UCB to CB via UGT enzyme
  3. CB is secreted out to the bile canaliculi to go to the gallbladder
  4. Gallbladder then secretes bile for food digestion - this bile has CB in it
  5. In small intestine, CB is converted to urobilinogen (UBG)
    1. UBG is converted to stercobilin (SB) and SB is responsible for brown color of feces
    2. Some UBG is reabsorbed into blood and spontaneously oxides into urobilin (UB)
    3. Urobilin (UB) is sent to the liver and the kidney. Via the kidney it is excreted in the urine making urine yellow color
A
  1. When RBCs are at 120 days they get “eaten” by macrophages which breaks the RBC into heme and globin
    1. Heme is split into Fe and Protoporphyrin
    2. Protoporphyrin is converted to unconjugated bilirubin (this is still in macrophage)
  2. UCB is bound to albumin and moves through the circulatory system to get to the liver where hepatocytes convert UCB to CB via UGT enzyme
  3. CB is secreted out to the bile canaliculi to go to the gallbladder
  4. Gallbladder then secretes bile for food digestion - this bile has CB in it
  5. In small intestine, CB is converted to urobilinogen (UBG)
    1. UBG is converted to stercobilin (SB) and SB is responsible for brown color of feces
    2. Some UBG is reabsorbed into blood and spontaneously oxides into urobilin (UB)
    3. Urobilin (UB) is sent to the liver and the kidney. Via the kidney it is excreted in the urine making urine yellow color
125
Q
  1. When RBCs are at 120 days they get “eaten” by macrophages which breaks the RBC into heme and globin
    1. Heme is split into Fe and (BLANK A)
    2. (BLANK A) is converted to unconjugated bilirubin (this is still in macrophage)
  2. UCB is bound to (BLANK B) and moves through the circulatory system to get to the liver where hepatocytes convert UCB to CB via (BLANK C) enzyme
  3. CB is secreted out to the bile canaliculi to go to the gallbladder
  4. Gallbladder then secretes bile for food digestion - this bile has CB in it
  5. In small intestine, CB is converted to urobilinogen (UBG)
    1. UBG is converted to stercobilin (SB) and SB is responsible for brown color of feces
    2. Some UBG is reabsorbed into blood and spontaneously oxides into urobilin (UB)
    3. Urobilin (UB) is sent to the liver and the kidney. Via the kidney it is excreted in the urine making urine yellow color
A
  1. When RBCs are at 120 days they get “eaten” by macrophages which breaks the RBC into heme and globin
    1. Heme is split into Fe and Protoporphyrin
    2. Protoporphyrin is converted to unconjugated bilirubin (this is still in macrophage)
  2. UCB is bound to albumin and moves through the circulatory system to get to the liver where hepatocytes convert UCB to CB via UGT enzyme
  3. CB is secreted out to the bile canaliculi to go to the gallbladder
  4. Gallbladder then secretes bile for food digestion - this bile has CB in it
  5. In small intestine, CB is converted to urobilinogen (UBG)
    1. UBG is converted to stercobilin (SB) and SB is responsible for brown color of feces
    2. Some UBG is reabsorbed into blood and spontaneously oxides into urobilin (UB)
    3. Urobilin (UB) is sent to the liver and the kidney. Via the kidney it is excreted in the urine making urine yellow color
126
Q
  1. Hemolysis leads to increased amount of unconjugated or conjugated bilirubin?
  2. biliary obstruction leads to increased amount of unconjugated or conjugated bilirubin?
  3. Primary liver disease leads to increased amount of unconjugated or conjugated bilirubin??
A
  1. unconjugated/indirect
  2. conjugated bilirubin
  3. total bilirubin (both conjugated and unconjugated)
127
Q

Biliary obstruction leads to increased amount of conjugated/direct bilirubin

  1. how does this affect stool color
  2. how does this affect urine color
  3. ALK phos levels
  4. ALT/AST levels
A
  1. clay colored stools - there is no stercobilin to make brown color
  2. dark urine (conjugated/direct bilirubin is WATER SOLUBLE so it can still go into urine but makes it dark
  3. very increased
  4. increased
128
Q

Fill in the blanks

A

image

129
Q

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A

image

130
Q

Fill in the blanks

A

image

131
Q

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A

image

132
Q

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A

image

133
Q

Fill in the blanks

A

image

134
Q

Pathophysiology of Dubin-Johnson Syndrome

  • indicate mutation, urine appearance, the mechanism that leads to pathology
A
  • Dubin-Johnson syndrome - deficiency in MRP2 which is a transporter that moves CB from the hepatocyte to the bile canaliculus to get CB to the gallbladder
    • CB builds up in hepatocytes and causes upregulation of MRP3 transporter which moves CB to the circulatory system instead and this path leads to CB being excreted via urine (very dark urine)
135
Q

Mucinous Cystic Neoplasm (MCN)

  1. is it more often in men or women?
  2. where is this found in relation to the pancreas?
  3. is it connected to pancreatic ductal system?
  4. Associated dysplasia and/or invasive carcinoma?
A
  1. women
  2. body or tail
  3. no
  4. dysplasia can be low, moderate, or high grade - up to ⅓ of cysts can be associated with invasive carcinoma
136
Q

Intraductal papillary mucinous Neoplasm (IPMN)

  1. is it more often in men or women?
  2. where is this found in relation to the pancreas?
  3. is it connected to pancreatic ductal system?
  4. Associated dysplasia and/or invasive carcinoma?
A
  1. men
  2. head
  3. yes - main pancreatic duct or a major branch
  4. yes. dysplasia can be low, moderate, or high grade - a subset can be associated with invasive carcinoma
137
Q

Serous Cystadenoma

  1. is it more often in men or women?
  2. What organ is this found in?
  3. Description?
A
  1. Female
  2. pancreas
  3. usually composed of unilocular (or at times multilocular) cysts filled with clear watery fluid.
138
Q
  1. what is Cholangiocarcinoma
  2. is this common?
  3. Risk factors?
  4. symptoms
A
  1. a type of cancer that forms in the slender tubes (bile ducts) that carry the digestive fluid bile
  2. 2nd most common primary malignant liver tumor after HCC
  3. Primary Sclerosing Cholangitis, liver fluke infections
  4. present late with fatigue, weight loss, abdominal pain

Block 5 (7 decks)

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