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NOTES: GI Review by Minnie (she/her) > SAS/Review > Flashcards

SAS/Review Flashcards

1
Q

Which one of the following is NOT a risk factor for developing hepatocellular carcinoma?

  1. Hepatitis C viral infection
  2. Alcoholic liver disease
  3. Hemochromatosis
  4. Herpes virus
  5. Diabetes, type 2
A

d. Herpes virus
* Non-hepatotrophic viruses do not cause chronic infection

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2
Q

Interpret the serology:

HBsAG(-), total anti-HBc(+), HBsAb(+)

A

Immune due to past infection (that has been cleared)

  • HBsAG(-) => Not actively infected
  • total anti-HBc(+) => Infected in the past
  • HBsAb(+) => Immune to future infection
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3
Q

Which cells of the antrum can be thought of as the “gas” and the “bakes” for gastric acid secretion?

A
  • Gas: G cells - secrete Gastrin
    • Gastrin increases gastric acid secretion indirectly through action on ECL cells, and directly by acting on parietal cells
  • Brakes: D cells - secrete Somatostatin
    • Somatostatin in hibits gastrin release from G cells and histamine release from ECL cell
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4
Q

Which systemic disease is characterized by mucin in the bile ducts?

A

Cystic fibrosis

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5
Q
A

A - Acute hemorrhagic gastritis

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6
Q

Which hepatotrophic virus increases risk of HCC, even without cirrhosis?

A

Hepatitis B virus

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7
Q

PBC or PSC?

Affects small biliary ducts (intrahepatic)

A

PBC

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8
Q

A 50-year-old patient presents with acute onset abdominal pain and elevate lipase and amylase (3 x ULN). Which of the following is the most appropriate next step?

A

Get a gallbaldder ultrasound

  • Presentation + elevated lipase and emylase 3xULN
    = acute pancreatitis
    • ​Don’t need additional imaging to diagnosis
  • Need to get an ultrasound to see if it is caused by a gallstone
    • ​Informs next steps of treatment
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9
Q

Which pattern of gastric motility is active during the inter-digestive state?

A

Migrating motor complex

(Interdigestive = between meals)

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10
Q

Where is alpha-1 antitrypsin synthesized?

A

Liver

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11
Q

How do the actions of CCK and secretin differ with respect to the pancreas?

A
  • CCK acts on acinar cells to upregulate release of pancreatic enzymes
    • ​Also relaxes the sphincter of Oddi to allow for enzyme release
  • Secretin acts on ductal cells to upregulate release of bicarbonate
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12
Q

Which antibody is associated with primary biliary cholangitis?

A

Anti-mitochondrial antibody

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13
Q

After diagnosis of HCC, how is the approach to treatment determined?

A

Careful measurement of the size and number of tumors

  • Do not need to biopsy! Risk of bleeding or seeing tumor spread
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14
Q

Which strcture is labeled by A?

A

Arcuate line of the rectus sheath

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15
Q

What is the most likely pathophysiology behind acute pancreatitis after binge drinking?

A

Dysregulation of trypsin

  • Trypsin is supposed to convert pancreatic proenzymes to active enzymes in the duodenum
  • Binge drinking can precipitate dystregulation of trypsin activation, resulting in pancreatic enzyme activation before secretion
    • ​-> Injury to pancreatic tissue
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16
Q

Which artery is labeled by F?

A

Common hepatic artery

(Not labeled right above it is the right gastric arteries)

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17
Q

Which enzyme deficiency is characterized by hepatocytes with PAS+ diastase resistant inclusions?

A

Alpha-1 anti-trypsin deficiency

-> Cirrhosis, emphysema

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18
Q

Which cells are the “pacemakers” of smooth muscle cells in the intestine?

A

Interstitial cells of Cajal

  • Note: Cannot initiate contraction on their own - additional stimulus is required
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19
Q

Which artery is labeled by E?

A

Right gastroepiploic artery

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20
Q

Which transporter is responsible for active absorption of glucose through the brush border?

A

SGLUT-1

(Secondary active transport, driven by Na+/K+ ATPase)

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21
Q

List the layers of the hollow organs of the digestive system, from inside to outside

A
  • Mucosa
    • Epithelium
    • Lamina propria
    • Muscularis mucosa
  • Submucosa
  • Muscularis propria
  • Serosa/Adventitia
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22
Q
A

A - Ascending colon

  • The midgut herniates throught the umbilical cord
  • The ascending colon is part of the midgut
    • Midgut = distal duodenum -> proximal transverse colon
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23
Q

What is the result of increased cAMP in intestinal cells?

A

Secretory diarrhea

  • Increased cAMP
  • -> Phosphorylation of the CFTR channel
  • -> Increased Cl- secretion
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24
Q

List 2 complications after acute pancreatitis

How are they managed?

A

Interstitial pancreatitis

Necrotizing pancreatitis

  • Both can be removed surgically, but important to let them develop into plseudocyst/walled off necrosis before intervening
    • ​Chance that they will resolve on their own
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25
Q

Fluid can pass from the lesser peritoneal sac to the greater peritoneal sac under which structure?

A

Under the lesser omentum

  • The lesser omentum is made up of the hepatogastric and hepatoduodenal ligaments
  • The epiploic (aka omental) forament is closest to the hepatoduodenal ligament
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26
Q

Which artery is labeled by G?

A

Gastroduodenal artery

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27
Q

How will cirrhosis affect drug clearance?

A
  • High extraction drugs
    • Clearance will be impaired because cirrhosis reduces blood flow -> drug levels in the blood will be higher
  • Low extraction drugs
    • Clearance will not be impaired by decreased blood flow, but the hepatocytes also won’t work as well, which may result in decreased clearance; monitor drug levels
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28
Q

What esophageal pathology is shown?

A

Achalasia

This is the “bird’s beak” sign

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29
Q

Which strcture is labeled by C?

A

Linea alba

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30
Q

Basal metabolic rate (BMR) makes up what percentage of energy expenditure?

A

65%

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31
Q

What results from a gallstone at location D?

Describe the presentation

A

Cholelithiasis

  • RUQ pain after fatty meals that goes away
  • Unremarkable liver function tests
  • Generally no serious symptoms until it gets stuck at:
    • C = Acute cholecystitis
    • E = Choledocholithiasis
    • F = Acute pancreatitis

(A gallstone in the gallbladder)

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32
Q

Why does ursodeoxycholic acid help patients with cholestasis?

A

It makes teh bile pool more hydrophilic

  • Ursodeoxycholic acid is a more hydrophilic bile acid than what we produce
    • Less toxic to the body
  • Supplementing bile acid decreases endogenous bile acid production
    • Less of it will get stuck in the biliary tree
      +
    • Fewer hydrophobic bile acids synthesized
    • Less damage
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33
Q

What results from a gallstone at location C?

Describe the presentation

A

Acute cholecystitis

  • Post-prandial RUQ pain
  • Positive Murphy’s sign
  • Unremarkable liver function tests

(Blockage of the cystic duct)

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34
Q
A

B - Hypochlorhydria and high gastrin

  • Chronic autoimmune gastritis destroys parietal cells
  • -> lower HCL secretion
  • -> No negative feedback to G cells
    • -> High gastrin
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35
Q

Why are duodenal ulcers more likely in antral-predominant H. pylori gastritis?

A

Antrum = D cells and G cells are here

H pylori preferentially destroys D cells

  • > No brakes on acid secretion
  • > Acid leakage into duodenum
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36
Q
A

C

  • B12 is in animal products and enriched flour
  • Deficiency -> neuropathies, fatigue, memory impairment
37
Q

What results from a gallstone at location E?

Describe the presentation

A

Choledocholithiasis

  • Colicky RUQ pain
  • Intermittent jaundice
  • Elevated Alk-phos, GGT, unconjugated bilirubin

(Gallstone stuck in the common bile duct)

38
Q

Which genetic mutation is most likely to predispose to acute pancreatitis?

A

PRSS1

  • Also SPINK1, but this is more disease modifying (won’t cause acute pancreatitis on its own, but makes it more likely in the setting of tobacco, alcohol, etc)
39
Q

Which artery is labeled by A?

A

Left gastric

40
Q

Which vitamin deficiency is associated with cardiomegaly?

A

Thiamine (B1)

42
Q

What results from a gallstone at location F?

Describe the presentation

A

Gallstone pancreatitis (Acute pancreatitis)

  • Sever epigastric pain radiating to the back
  • Amylase and/or lipase elevated 3xULN

(Gallstone blocks the common biliary/pancreatic outflow, resulting in bile in the pancreas)

43
Q

Describe the “typical patient” with primary sclerosing cholangitis

A
  • Young man
  • Ulcerative colitis
    • Most people with PSC have UC
44
Q

Interpret the serology:

HBsAG(-), total anti-HBc(-), HBsAb(+)

A

Immune due to vaccination

  • HBsAG(-) => Not actively infected
  • total anti-HBc(-) => No past infection
  • HBsAb(+) => Immune to future infection
45
Q

Which congential syndrome is characterized by a complete absence of UDP-GT?

A

Crigler-Najjar syndrome Type 1

Very severe

47
Q

Which liver pathology is characterized by concentric periductal fibrosis?

A

Primary sclerosing cholangitis (PSC)

48
Q

What is the serologic difference between chronic and acute HBV infection?

A

Both: HBsAg (+), total anti-HBc (+)

  • Acute: IgM anti-HBc (+)
  • Chronic: IgM anti-HBc (-)
    • Has been converted to IgG anti-HBc (-)
49
Q

A patinet has cirrhosis due to alpha-1 anti-trypisin deficiency

What non-GI symptoms woudl you expect?

A
  • Edema
  • Cough/shortness of breath due to emphysema
  • Ascites
50
Q

The digestion of which nutrient is most directly reliant on stomach acid?

A

Proteins

  • H+ stimulates pepsinogen secretion from chief cells
  • Acidic environment facilitates the hydrolysis of pepsinogen to pepsin
51
Q

What is the prevalent cause of GERD?

A

Transiet relaxation of the lower esophageal sphincter

52
Q

Which artery is labeled by I?

A

Pancreaticoduodenal

53
Q

Which artery is indicated by the red arrow?

A

Common hepatic artery

  • Splits into the gastroduodenal (down) and proper hepatic (up)
54
Q
A

C

  • Birth weight should double in 4-5 months
  • Triple in 1 year
55
Q

Liver specimen

What kind of inflammatory cells dominate around the portal tract?

Does this represent an acute or chronic process?

A

Lymphocytes (basophilic)

Represents a chronic process

(Specifially, this was chronic HCV)

  • Neutrophils = neutral pink cytoplasm, weird purpleish/reddish nucleus
    • => acute process
  • Eosinophils = brighter red
56
Q

What endoscopic finding can distinguish Eosinophilic esophagitis from GERD?

A

EoE will have linear furrows and esophageal rings

  • Linear furrows are pretty specific for EoE
57
Q
A

C - Linea semilunaris

58
Q
A

E - Low gastric pH

  • Gastrin serves to increase HCl release from parietal cells, resulting in a more acidic environment (lower pH)
  • Low pH = negative feedback that inhibits gastrin release

Exception: Gastrinoma! Will continue secreting gastrin regardless of gastric pH

59
Q

Which liver pathology is characterized by florid duct lesions?

A

Primary biliary cholangitis (PBC)

60
Q

Which strcture is labeled by D?

A

Lateral arcuate ligament

61
Q
A

E - inhibits prostaglandin synthesis

(This is NSAIDs, not H. pylori)

62
Q

Diffuse foveolar hyperplasia + excess TGF-alpha are characteristic of which gastric disorder?

What macronutrient my be deficient?

A

Mentrier’s disease

Protein (often causes hypoproteinemia)

63
Q

Describe the actions of CCK on the:

  • Gallbladder:
  • Pancreas:
  • Stomach:
  • Sphincter of Oddi:

What is the overall purpose of CCK?

A

CCK causes:

  • Gallbladder: contraction (to push out bile)
  • Pancreas: acinar secretion (more enzymes!!)
  • Stomach: reduced emptying
  • Sphincter of Oddi: relaxation (to let enzymes + bile through)

NOTE: no action on HCO3 secretion!
Secretin->ductal cells take care of this

64
Q

What is involved in the conjugation of bilirubin?

A

Unconjugated (direct) bilirubin is glucoronidated by UDP-glucuronyltransferase to form conjugated (indirect) bilirubin

65
Q

Which artery is labeled by H?

A

Proper hepatic artery

66
Q
A

D

  • IgA deficiency
  • Anti-TtG IgG
    • Check this in anyone with suspected celiac and IgA deficiency
67
Q

Which strcture is labeled by E?

A

Medial arcuate ligament

68
Q

Describe the “typical patient” with primary biliary cholangitis

A
  • Older woman
  • Anti-mitochondrial antibody

Vs. PSC; young men with ulcerative colitis

69
Q

What would we expect to see in the biopsy of a patient with Whipple’s disease?

A

Lamina propria filled with:

  • Macrophages containing bacilli that stain with periodic acid-Schiff (PAS-D) reagent
  • Foamy histiocytes
70
Q

Which strcture is labeled by B?

A

Linea semilunaris

71
Q

PBC or PSC?

Histology may show florid duct lesions in early stages

A

PBC

  • Florid duct legion = lymphoplasmacytic inflammation with or without granuloma
    • Lymphocytes are purple (basophilic)
    • [in lecture they indicated the part above the little hole but tbh I really don’t know what we’re looking at]
72
Q

Thermic effect of food (TEF) makes up what percentage of energy expenditure?

73
Q
A

C

  • DQ2/DQ8 is strongly associated with celiac disease
74
Q

Which liver pathology is characterized by reduced interlobular bile ducts?

A

Alagille syndrome

  • Mutation in notch signaling pathway -> Narrow/malformed bile ducts that don’t allow for bile flow
    • -> Bile back-up causes liver damage
75
Q

Which gene is most commonly mutated in pancreatic cancer?

76
Q

What is the utility of alpha-fetoprotein (AFP) in the diagnosis and/or management of hepatocellular carcinoma?

A
  • AFP (+) strongly indicates HCC, however, not all HCC tumors secrete AFP
  • If a tumor is AFP (+), can measure AFP levels to deptermine treatment efficacy/response
77
Q
A

E - Dendritic cells

(They are everywhere)

78
Q
A

D - Macrovesicular steatosis

  • All of these can be found in steatohepatitis (inflammation)
  • Macrovesicular steatosis can occur before inflammtory changes
79
Q
A

C - Dental caries

  • Sjogren’s
  • -> Less saliva
  • -> Less bicarbonat
  • -> Cannot neutralize acids produced by bacteria in the oral cavity
  • -> Dental caries (cavities)
80
Q
A

Stomach

  • No villi
  • Parietal cells are pink
  • Chief cells are blue
81
Q

Which artery is labeled by D?

A

Left gastroepiploic artery

82
Q

Does liposuction result in systemic health benefits?

Explain

A

No systemic health benefits

Liposuction reduces cutaneous fat, but the visceral fat is what causes obesity-related health problems

83
Q

A patient with chronic HBV infection has been asymptomatic for the past few years; they report strict adherence to their medications. At their next checkup, they are found to have:

  • Total bilirubin 3x ULN
  • ALT 4x ULN
  • Very low HBV DNA viral load

What cause of these abnormal labs is most important to rule out?

A

HDV superinfection

  • Suspect in anyone with chronic HBV who is aherent to medication who suddenly develops abnormal labs
    • Esp if HBV DNA viral load is low
84
Q

Interpret the serology:

HBsAG(+), total anti-HBc(+), HBsAb(-)

A

Chronic HBV infection

  • HBsAG(+) => Actively infected
  • Total anti-HBc(+) => has seroconverted to chronic infection
    • We would expect this to be IgG in a chronic infection
    • Anti-HBC IgM rises with acute infection, falls as the immune system fails to clear (taken over by IgG)
  • HBsAb(+) => Immune to future infection
85
Q

How would gastric levels of the following substances change with proton-pump inhibitor use?

  • HCl:
  • Gastrin:
  • Histamine:
  • Secretin:
A
  • HCl: decrease
  • Gastrin: increase
  • Histamine: increase (2/2 to increased gastrin)
  • Secretin: decrease (hypothetically, but maybe no change)
86
Q

Which HBV antibody indicates immunity to future infection?

A

HBsAb (+)

Aka has Anti-HBs

87
Q

Which artery is labeled by B?

A

Short gastric arteries

88
Q

Which artery is labeled by C?

A

Splenic artery

NOTES: GI Review by Minnie (she/her) (38 decks)

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