SAS/Review Flashcards
1
Q
Which one of the following is NOT a risk factor for developing hepatocellular carcinoma?
- Hepatitis C viral infection
- Alcoholic liver disease
- Hemochromatosis
- Herpes virus
- Diabetes, type 2
A
d. Herpes virus
* Non-hepatotrophic viruses do not cause chronic infection
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
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
4
Q
Which systemic disease is characterized by mucin in the bile ducts?
A
Cystic fibrosis
5
Q
A
A - Acute hemorrhagic gastritis
Erosion of the superficial mucous layer (no mucous cells left) with lots of neutrophils and vascular congestion
6
Q
Which hepatotrophic virus increases risk of HCC, even without cirrhosis?
A
Hepatitis B virus
7
Q
PBC or PSC?
Affects small biliary ducts (intrahepatic)
A
PBC
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
9
Q
Which pattern of gastric motility is active during the inter-digestive state?
A
Migrating motor complex
(Interdigestive = between meals)
10
Q
Where is alpha-1 antitrypsin synthesized?
A
Liver
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
12
Q
Which antibody is associated with primary biliary cholangitis?
A
Anti-mitochondrial antibody
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
14
Q
Which strcture is labeled by A?
A
Arcuate line of the rectus sheath
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
16
Q
Which artery is labeled by F?
A
Common hepatic artery
(Not labeled right above it is the right gastric arteries)
17
Q
Which enzyme deficiency is characterized by hepatocytes with PAS+ diastase resistant inclusions?
A
Alpha-1 anti-trypsin deficiency
-> Cirrhosis, emphysema
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
19
Q
Which artery is labeled by E?
A
Right gastroepiploic artery
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)
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
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
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
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
25
Fluid can pass from the lesser peritoneal sac to the greater peritoneal sac under which structure?
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
26
Which artery is labeled by G?
Gastroduodenal artery
27
How will cirrhosis affect drug clearance?
* 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**
28
What esophageal pathology is shown?
Achalasia
This is the "bird's beak" sign
29
Which strcture is labeled by C?
Linea alba
30
Basal metabolic rate (BMR) makes up what percentage of energy expenditure?
65%
31
What results from a gallstone at location **D**?
Describe the presentation
**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)
32
Why does ursodeoxycholic acid help patients with cholestasis?
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**
33
What results from a gallstone at location **C**?
Describe the presentation
**Acute cholecystitis**
* Post-prandial RUQ pain
* Positive Murphy's sign
* Unremarkable liver function tests
| (Blockage of the cystic duct)
34
B - Hypochlorhydria and high gastrin
* Chronic autoimmune gastritis destroys parietal cells
* -\> lower HCL secretion
* -\> No negative feedback to G cells
* -\> High gastrin
35
Why are duodenal ulcers more likely in antral-predominant H. pylori gastritis?
Antrum = D cells and G cells are here
H pylori preferentially destroys D cells
- \> No brakes on acid secretion
- \> Acid leakage into duodenum
36
C
* B12 is in animal products and enriched flour
* Deficiency -\> neuropathies, fatigue, memory impairment
37
What results from a gallstone at location **E**?
Describe the presentation
**Choledocholithiasis**
* Colicky RUQ pain
* Intermittent jaundice
* Elevated Alk-phos, GGT, unconjugated bilirubin
A.
B.
C. Cholecystitis
D. Cholelithiasis
E. Choledocholithiasis
F. Pancreatitis
| (Gallstone stuck in the common bile duct)
38
Which genetic mutation is most likely to predispose to acute pancreatitis?
**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
Which artery is labeled by A?
Left gastric
40
Which vitamin deficiency is associated with cardiomegaly?
Thiamine (B1)
41
42
What results from a gallstone at location **F**?
Describe the presentation
**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
Describe the “typical” patient with primary sclerosing cholangitis
* Young man
* Ulcerative colitis
* Most people with PSC have UC
44
Interpret the serology:
HBsAG(-), total anti-HBc(-), HBsAb(+)
**Immune due to vaccination**
* HBsAG(-) =\> Not actively infected
* total anti-HBc(-) =\> No past infection
* **HBsAb(+) =\> Immune to future infection**
45
Which congential syndrome is characterized by a complete absence of UDP-GT?
Crigler-Najjar syndrome Type 1
Very severe
46
D
47
Which liver pathology is characterized by **concentric periductal fibrosis**?
Primary sclerosing cholangitis (PSC)
48
What is the serologic difference between chronic and acute HBV infection?
**Both: HBsAg (+), _total_ anti-HBc (+)**
* Acute: _IgM_ anti-HBc (+)
* Chronic: _IgM_ anti-HBc (-)
* Has been converted to _IgG_ anti-HBc (-)
49
A patinet has cirrhosis due to alpha-1 anti-trypisin deficiency
What non-GI symptoms woudl you expect?
* Edema
* Cough/shortness of breath due to emphysema
* Ascites
50
The digestion of which nutrient is most directly reliant on stomach acid?
Proteins
* H+ stimulates pepsinogen secretion from chief cells
* Acidic environment facilitates the hydrolysis of pepsinogen to pepsin
51
What is the prevalent cause of GERD?
Transiet relaxation of the lower esophageal sphincter
52
Which artery is labeled by I?
Pancreaticoduodenal
53
Which artery is indicated by the red arrow?
Common hepatic artery
* Splits into the **gastroduodenal** (down) and **proper hepatic** (up)
54
C
* Birth weight should double in 4-5 months
* Triple in 1 year
55
Liver specimen
What kind of inflammatory cells dominate around the portal tract?
Does this represent an acute or chronic process?
**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
What endoscopic finding can distinguish Eosinophilic esophagitis from GERD?
EoE will have **linear furrows** and esophageal rings
* Linear furrows are pretty specific for EoE
57
C - Linea semilunaris
58
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
Which liver pathology is characterized by **florid duct lesions**?
Primary biliary cholangitis (PBC)
## Footnote
**granulomatous destruction of the bile ducts**
60
Which structure is labeled by D?
Lateral arcuate ligament
61
E - inhibits prostaglandin synthesis
(This is NSAIDs, not H. pylori)
62
Diffuse foveolar hyperplasia + excess TGF-alpha are characteristic of which gastric disorder?
What macronutrient my be deficient?
Menetrier's disease
Protein (often causes hypoproteinemia)
Note: **Characterized by massive overgrowth of mucous cells** (foveola) in the mucous membrane lining the stomach, resulting in large gastric folds
63
Describe the actions of CCK on the:
* Gallbladder:
* Pancreas:
* Stomach:
* Sphincter of Oddi:
What is the overall purpose of CCK?
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
What is involved in the conjugation of bilirubin?
Unconjugated (direct) bilirubin is **glucoronidated by UDP-glucuronyltransferase** to form conjugated (indirect) bilirubin
65
Which artery is labeled by H?
Proper hepatic artery
66
D
* IgA deficiency
* Anti-TtG IgG
* Check this in anyone with suspected celiac and IgA deficiency
67
Which strcture is labeled by E?
Medial arcuate ligament
68
Describe the "typical patient" with primary biliary cholangitis
* Older woman
* Anti-mitochondrial antibody
*Vs. PSC; young men with ulcerative colitis*
69
What would we expect to see in the biopsy of a patient with Whipple's disease?
Lamina propria filled with:
* **Macrophages containing bacilli that stain with periodic acid-Schiff (PAS-D) reagent**
* Foamy histiocytes
70
Which strcture is labeled by B?
Linea semilunaris
71
PBC or PSC?
## Footnote
**Histology may show florid duct lesions in early stages**
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
Thermic effect of food (TEF) makes up what percentage of energy expenditure?
10%
73
C
* DQ2/DQ8 is strongly associated with celiac disease
74
Which liver pathology is characterized by **reduced interlobular bile ducts?**
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
Which gene is most commonly mutated in pancreatic cancer?
K-Ras
76
What is the utility of alpha-fetoprotein (AFP) in the diagnosis and/or management of hepatocellular carcinoma?
* 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
E - Dendritic cells
| (They are everywhere)
78
D - Macrovesicular steatosis
* All of these can be found in steatohepatitis (inflammation)
* Macrovesicular steatosis can occur before inflammtory changes
79
C - Dental caries
* Sjogren's
* -\> Less saliva
* -\> Less bicarbonat
* -\> Cannot neutralize acids produced by bacteria in the oral cavity
* -\> Dental caries (cavities)
80
Stomach
* No villi
* Parietal cells are pink
* Chief cells are blue
81
Which artery is labeled by D?
Left gastroepiploic artery
82
Does liposuction result in systemic health benefits?
Explain
No systemic health benefits
Liposuction reduces cutaneous fat, but the visceral fat is what causes obesity-related health problems
83
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?
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
Interpret the serology:
HBsAG(+), total anti-HBc(+), HBsAb(+)
**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
How would gastric levels of the following substances change with proton-pump inhibitor use?
* HCl:
* Gastrin:
* Histamine:
* Secretin:
* HCl: **decrease**
* Gastrin: **increase**
* Histamine: **increase** (2/2 to increased gastrin)
* Secretin: **decrease** (hypothetically, but maybe no change)
86
Which HBV antibody indicates immunity to future infection?
HB**s**Ab (+)
Aka has Anti-HB**s**
87
Which artery is labeled by B?
Short gastric arteries
88
Which artery is labeled by C?
Splenic artery
