Gi Physiology And Pathology, Usmle Step 1 - Not Mine

Front 1

What is the source, action, and regulation of gastrin? What two amino acids are super potent stimulators of gastrin? In which syndrome is gastrin increased?

Back 1

SOURCE: G cells in antrum of stomach
ACTION: increases gastric H+ secretion, increases growth of gastric mucosa, increases gastric motility.
REGULATION: decreased by stomach pH < 1.5. increased by stomach distention, aa's, peptides, vagal stimulation (through GRP).
PHENYLALANINE and TRYPTOPHAN are potent stimulators.
Gastrin is increased in ZE syndrome.

Front 2

What is the source, action, and regulation of cholecystokinin. Why does pain in cholelithiasis worsen after fatty food ingestion?

Back 2

SOURCE: I cells (duodenum, jejunum)
ACTION: increase pancreatic secretion, increase gallbladder contraction, decrease gastric emptying
REGULATION: increased by FA, aa's.
Pain worsens after fatty food ingestion in cholelithiasis due to increased CCK.

Front 3

What is the source, action, regulation, and purpose of secretin?

Back 3

SOURCE: S cells in duodenum
ACTION: increases pancreatic bicarb secretion, decreases gastric acid secretion, increases bile secretion
REGULATION: increased by acid, FA's in lumen of duodenum
PURPOSE: secretin causes pancreas to release bicarb, which neutralizes gastric acid in the duodenum, allowing pancreatic enzymes to function.

Front 4

What is the source, action, and regulation of somatostatin? What is it used to treat?

Back 4

SOURCE: D cells (pancreastic islets, GI mucosa)
ACTION: decrease gastric acid and pepsinogen secretion, decrease pancreatic and small intestinal fluid secretion, decrease gallbladder contraction, decrease insulin and glucagon release.
REGULATION: increased by acid, decreased by vagal stim.
Secretin is used to treat VIPoma and carcinoid tumors. It has anti-growth hormone effects, and is an inhibitory tumor.

Front 5

What is the source, action, and regulation of GIP?

Back 5

SOURCE: K cells in duodenum, jejunum
ACTION: exocrine - decreases H+ secretion; endocrine - increases insulin release.
REGULATION: increased by FA's, aa's, oral glucose.
b/c of GIP, an oral glucose load is used more rapidly than the equivalent given by IV.

Front 6

VIP (vasoactive intestinal polypeptide) - what is the source, action, and regulation? What is a VIPoma?

Back 6

SOURCE: parasympathetic ganglia in sphincters, gallbladders, small gut
ACTION: increase intestinal water and lyte secretion; increase relaxation of intestinal smooth muscle and sphincters
REGULATION: increased by distention and vagal stim; decreased by adrenergic input.

Front 7

What is the source, action, and regulation of motilin?

Back 7

SOURCE: small intestine
ACTION: migrating motor complexes (MMC's)
REGULATION: increased in fasting state

Front 8

Which cells produce intrinsic factor and gastric acid?

Back 8

parietal cells

Front 9

How is gastric acid regulated?

Back 9

gastric acid is increased by histamine, ACh, and gastrin.
gastric acid is decreased by somatostatin, GIP, prostaglandin, and secretin.

Front 10

What is the source, action, and regulation of pepsin? How is pepsinogen activated --> pepsin?

Back 10

Pepsin is made in the chief cells of the stomach; it's involved in protein digestion; it's increased by vagal stim and local acid; inactive pepsinogen is converted to pepsin by H+

Front 11

What effect does atropine have on parietal cells and G cells?

Back 11

Atropine blocks vagal stimulation of parietal cells b/c they use ACh as their transmitter, so you can't make acid or intrinsic factor; however, atropine has no effect on vagal stimulation of G cells, because GRP isused as the transmitter, not ACh.

Front 12

Discuss the roles of salivary amylase, pancreatic amylase, and oligosaccharide hydrolases in carbohydrate digestion.

Back 12

SALIVARY AMYLASE: starts digestion, hydrolyzes alpha-1,4 linkages to yield disaccharides (maltose, maltotriose, and alpha-limit dextran)
PANCREATIC AMYLASE: highest concentration in duodenal lumen; hydrolyzes starch to oligosaccharides and disaccharides
OLIGOSACCHARIDE HYDROLASES: at brush border of intestine, the rate-limiting step of carbohydrate digestion, produce monosaccharides from oligo-and disaccharides.

Front 13

As far as carb absorption is concerned, what three things can enterocytes absorb?

Back 13

Only monosaccharides (glucose, galactose, and fructose) can be absorbed by enterocytes. Glucose and galactose are taken up by SGLT1 (Na+ dependent). Fructose is taken up by facilitated difusion by GLUT-5. All are transported to the blood by GLUT-2.

Front 14

Where is iron absorbed, and in what form?
What about folate?
B12?

Back 14

iron is absorbed as Fe2+ in the duodenum. Folate is absorbed in the jejunum. B12 is absorbed in the ileum, as is bile.

Front 15

What are the three most common salivary tumors?

Back 15

Salivary tumors are usually benign, and occur in the parotid gland.
Pleomorphic adenoma - ductal and myoepithelial cells (can also have cartilage or even bone!!!)...most common tumor, painless, movable mass. benign w/ high rate of recurrence.

Warthin's tumor - epithelial and lymphoid components, M>F, smokers 8x more likely to get it. benign, w/ heterotopic salivary gland tissue trapped in a lymph node, surrounded by lymphatic tissue. 10% of Warthin's tumors are bilateral, and 10% are multifocal.

Mucoepidermoid carcinoma (most common malignant tumor).

Front 16

With hepatocellular jaundice, what type of hyperbilirubinemia will you have? Will the urine bilirubin be increased or decreased? What about the urine urobilinogen?

Back 16

Conjugated/unconjugated
Urine bilirubin will be increased
Urine urobilinogen will be nl or decreased

Front 17

With obstructive jaundice, what type of hyperbilirubinemia will you have? Will the urine bilirubin and urine urobilinogen be increased or decreased?

Back 17

Conjugated
Urine bilirubin will be increased
Urine urobilinogen will be be decreased

Front 18

With hemolytic jaundice, what type of hyperbilirubinemia will you have? Will the urine bilirubin and urine urobilinogen be increased or decreased?

Back 18

Unconjugated
Absent urine bilirubin (acholuria)
Increased urine urobilinogen

Front 19

What is Gilbert's Syndrome?

Back 19

Gilbert's syndrome is an asymptomatic, condition in which the patient has a mildly decreased UDP-glucuronyl transferase or decreased bilirubin uptake; they present with an elevated conjugated bilirubin. Associated w/ stress. No clinical consequences

Front 20

What is Crigler-Najjar Syndrome? What is the difference between type I and type II?

Back 20

Crigler-Naijjar syndrome is the absence of UDP-glucuronyl transferase. It presents early in life, with death within a few years. High unconjugated bilirubin. Pt has jaundice, kernicterus (bilirubin in brain).
Type I Crigler-Naijjar syndrome is lethal, try to treat w/ plasmapheresis and phototherapy. Type II is less severe, and responds to phenobarbital, which increases liver enzyme synthesis.

Front 21

What is Dubin-Johnson Syndrome?

Back 21

Benign condition in which conjugated bilirubin is elevated due to defective liver excretion. Grossly black liver.

Front 22

Rotor's Syndrome?

Back 22

Benign condition (even more so than Dubin-Johnson Syndrome) and does not cause black liver.

Front 23

What is Wilson's Disease (Hepatolenticular degeneration)? How is it inherited? What do you treat it with?

Back 23

Wilson's disease is a mutation in an ATPase (ATP7B gene) that is needed to transport Cu into the bile and to incorporate it into ceruloplasmin (basically you can't get rid of copper). Copper accumulation --> toxic liver injury through production of ROS via the Fenton equation. Copper also accumulates in brain, cornea, kidney, and joints. Symptoms include asterixis, basal ganglia degeneration (parkinsonian symptoms), low ceruloplasmin, cirrhosis, corneal deposits (kayser-fleischer rings), copper accumulation, HCC, choreiform movements, dementia, hemolytic anemia, and increased urinary Cu excretion.

Inheritance is autosomal recessive.

Treat w/ penicillamine.

Front 24

What is the difference between hemosiderosis and hemochromatosis? What symptoms does hemochromatosis present with/what are some complications?
What would the iron studies show?
How do you treat it?

Back 24

Hemosiderosis is the deposition of hemosiderin (iron), whereas hemochromatosis is the disease caused by the iron deposition. have micronodular cirrhosis, diabetes mellitus, bronze skin, CHF, increased risk of HCC, and pseudogout due to deposition of iron and calcium pyrophosphate in joints. Disease may be primary (AR) or secondary to chronic transfusion therapy (beta thalassemia major). iron studies would show increased ferritin, increased iron, decreased TIBC --> increased transferrin saturation.
It is associated w/ HLA-A3.
Treat w/ phlebotomy and deferoxamine.

Front 25

What are some features of primary sclerosing cholangitis? What lab value is elevated? What do you see on ERCP? What are the symptoms?

Back 25

Primary sclerosing cholangitis can be intra- or extra hepatic. Have inflammation and fibrosis of bile ducts --> alternating strictures and dilation w/ "beading" on ERCP. Concentric "onion skin" bile duct fibrosis. Super high ALP may be only sign, or may have fatigue, jaundice, and pruritis. 70% of PCS pts also have ulcerative cholitis.

Front 26

What is primary biliary cirrhosis? Who is it most common in? What do you see histologically? What does it present with? What lab values might you see? What is it associated with?

Back 26

Intrahepatic. Primary biliary cirrhosis is an autoimmune disorder that is most common in middle-aged women. Histologically, see chronic granulomatous inflammation around medium-sized intrahepatic bile ducts. Symptoms include severe obstructive jaundice (--> high conjugated bili), increased serum mitochondrial Abs, steatorrhea, pruritis, and hypercholesterolemia (xanthoma). Associated w/ CREST and scleroderma.

Front 27

What is secondary biliary cirrhosis?

Back 27

Due to extrahepatic biliary obstruction. Increased pressure in intrahepatic ducts --> injury/fibrosis. Often complicated by ascending cholangitis (bacterial infection), bile stasis, and bile lakes. increased ALP, increased conjugated bili.

Front 28

When would you expect pigment stones (radioopaque) v. cholesterol stones.

Back 28

Pigment stones are more likely in pts w/ chronic RBC hemolysis, alcoholic cirrhosis, and biliary infxn.

Front 29

What are pirenzepine and propantheline?

Back 29

Pirenzepine and propantheline are muscarinic antagonists. they block M1 receptors on ECL cells (decreasing histamine secretion) and block M3 receptors on parietal cells (decrease H+ secretion). They are used (rarely) for peptic ulcers. Toxicities include tachycardia, dry mouth, difficulty focusing the eyes.

Front 30

What are some side effects of overusing aluminum hydroxide?

Back 30

hypophosphatemia, constipation, proximal muscle weakness, osteodystrophy, seizures

Front 31

What are some side effects of overusing magnesium hydroxide?

Back 31

Diarrhea, hyporeflexia, hypotension, cardiac arrest.

Front 32

What are some side effects of overusing calcium carbonate?

Back 32

hypercalcemia, rebound acid.

Front 33

What is a common side effect of ALL antacids (aluminum hydroxide, magnesium hydroxide, calcium carbonate).

Back 33

hypokalemia

Front 34

What is infliximab, what is it used to treat, and what are three toxicities?

Back 34

Infliximab is a monoclonal Ab against TNF. It is used to treat Crohn's disease and Rheumatoid arthritis. Toxicities include respiratory infxns (including reactivation of TB, fever, and hypotension).

Front 35

What is sulfasalazine, what is it used to treat, and what are 4 toxicities?

Back 35

Sulfasalazine is a combination of sulfapyridine (an antibacterial) and mesalamine (an anti-inflammatory). it must be activated by colonic bacteria. It is used to treat ulcerative colitis and Crohn's disease. It can cause malaise, nausea, reversible oligospermia, and sulfonamide toxicity.

Front 36

What is ondansetron, when is it used, and what are two toxicities?

Back 36

Ondansetron is a powerful 5-HT3 antagonist. it's a central-acting anti-emetic. used to control vomiting post-operatively and in pts undergoing cancer chemo. Common AE's include HA and constipation.

Front 37

What is metoclopramide? When is it used? What are some AE's?

Back 37

Metoclopramide is a D2 receptor ANTAGonist that increases resting tone, contractility, LES tone, and motility. It does NOT influence colon transport time. It is used in diabetic and post-surg gastroparesis. Toxicities include parkinsonian effects, restlessness, drowsiness, fatigue, depression, nausea, diarrhea. Drug interactions w/ digoxin and diabetic agents. Contraindicated in pts w/ smal bowel obstruction.