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GI Flashcards

1
Q

What is the taste sensation to the tongue?

A

Anterior 2/3 of the tongue= chordi tympani (CNVII)

posterior 1/3 = glossopharyngeal nerve

throat = vagus

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2
Q

What nerves provide pain sensation to the tongue?

A

anterior 2/3 = CNV3 mandibular

posterior 2/3= glossopharyngeal

throat = vagus

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3
Q

What are the 2 types of chronic gastritis?

A

autoimmune chronic gastritis and chronic H. pylori gastritis

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4
Q

What are the 2 types of gastric carcinoma

A

intestinal and diffuse type

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5
Q

Most common causes of an upper GI bleed?

A

duodenal ulcer and esophageal varices

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6
Q

Most common caues of a lower GI bleed

A

upper GI bleed, diverticulosis, and angiodysplasia

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7
Q

What is angiodysplasia?

A

acquired malformation of mucosal and submucosal capillary beds, arises in the cecum and right colon due to high wall tension.

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8
Q

What is hereditary hemorrhagic telangiectasia?

A

AD d/o with thin-walled blood vessels, espcially in the mouth and GI tract. Rupture presents as bleeding.

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9
Q

Plummer-Vinson Syndrome?

A

Plumbers DIG

Dysphagia (esophageal webs), Iron deficiency anemia, and Glossitis. (can lead to SCC)

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10
Q

Annular pancreas?

A

pancrease forma a ring around duodenum, risk of duodenal obstruction. bilious vomiting.

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11
Q

What type of necrosis occurs in acute pancreatitis?

A

liquefactive hemorrhagic necrosis and fat necoriss of peripancreatic fat

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12
Q

What are the major risk factors of acute pancreatitis?

A

alcohol and gallstones, maybe trauma

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13
Q

Major risk factors of chronic pancreatitis?

A

alcohol and recurrent bouts of acute pancreatitis. Cystic fibrosis in children.

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14
Q

What are the major risk factors of pancreatic adenocarcinoma?

A

smoking and chronic pancreatitis

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15
Q

What is the serum marker of pancreatic adenocarcinoma?

A

CA 19-9

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16
Q

Biliary atresia?

A

failure to form or early destruction of extrahepatic biliary tree, common bile duct is absent! Biliary obstruction presents in first 2 months of life. Jaundice, leads to cirrhosis.

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17
Q

3 risk factors of cholelithiasis (gallstones)?

A

(1) supersaturation of cholesterol or bilirubin (2) decreased phospholipids like lecithin and decreased bile acids (3) stasis

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18
Q

Most common type of gallstone?

A

cholesterol stones

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19
Q

Are cholesterol stones radiolucent or radiopaque?

A

radiolucent (cannot see on xray)

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20
Q

How does estrogen effect gallstone formation?

A

Estrogen upregulates HMG-CoA reductase which leads to increased levels of cholesterol, increased LPL receptors and increased cholesterol uptake. At greater risk for developing gallstones when at a fertile age

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21
Q

Are bilirubin stones radiopaque or radiolucent?

A

radiopaque (show on XR)

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22
Q

Which microorganisms predisopose to bilirubin gallstones?

A

Ascaris lumbricoides, E.coli, and Clonorchis sinensis

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23
Q

How do bacterial infections lead to increased risk for bilirubin stones?

A

they can deconjugate the bilirubin which increases the risk for precipitation of bilirubin

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24
Q

Where is the pain in acute cholecystitis?

A

RUQ pain that radiates to the right scapula

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25
Q

Common lab finding of acute cholecystitis?

A

increased serum alkaline phosphatase (in the epithelial cells that line the gallbladder, released as the epithelium is destroyed)

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26
Q

What is a common histologiacl finding in chronic cholecystitis?

A

Rokitansky-Aschoff sinus; herniation of the gallbladder mucosa into the muscular wall

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27
Q

What is a late complication of chronic cholecystitis?

A

porcelin gallbladder with a shrunken, hard gallbladder due to chronic inflammation, fibrosis and dystrophic calcification.

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28
Q

What is choledocolithiasis?

A

gallstone stuck in the biliary ducts

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29
Q

What is the major risk factor and most common presentation of gallbladder adenocarcinoma?

A

procelain gallbladder and cholecystitis in an elderly woman

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30
Q

What enzyme conjugates bilirubin?

A

uridine glucouronyl transferase (UGT)

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31
Q

What is the defect in physiologic jaundice of the newborn?

A

Transiently low levels of uridine glucuronyl transferase, so increased UCB in the blood which can deposit in the fat in the basal ganglia and cause kernicterus.

Tx: phototherapy which makes UCB soluble!

32
Q

Gilbert syndrome?

A

AR, Mildly low UGT, high UCB in the blood and presents as jaundice during stress e.g. infection

33
Q

Crigler-Najjar syndrome?

A

Absence of UGT, results in kernicterus, fatal

34
Q

Dubin-Johnson syndrome?

A

Deficiency of bilirubin canalicular transport protein, so cannot excrete, increased CB whcih is water soluble. **Dark liver, **otherwise not clinically significant

35
Q

Rotor Syndrome?

A

similar to Dubin-Johnson syndrome, **but lacks liver discoloration **

36
Q

What must be present for an infection of HDV to take place?

A

Must have a pre-exisitng HBV infection (superinfection, very severe), or a coinfection simultaneously with HBV

37
Q

What is like the only thing you need to know about HEV infection?

A

Occurs in pregnant women and is associated with fulminant hepatitis (liver failure with massive liver necrosis)

38
Q

Symtpoms of acute viral hepatitis?

A

jaundice with increased UCB and CB, with dark urine, fever, malaise, nausea, and elevated liver enzymes (ALT>AST). **apoptosis of hepatocytes. **

39
Q

What are the symtpoms of chronic hepatitis?

A

sxs longer than 6 months, inflammation predominantly or portal tract, risk of cirrhosis

40
Q

What mediates fibrosis of liver in cirrhosis?

A

TGF-beta released from fibroblasts

41
Q

Histological/gross findings of liver in cirrhosis?

A

disruption of normal hepatic parenchyma by bands of fibrosis and egenerative nodules of hepatoctes

42
Q

What are the clinical features of cirrhosis?

A

portal HTN leads to ascites, congestive splenomegaly/hyperspelnism, portosystemic shunts. Rapidly developing renal failure

43
Q

What changes are seen in the liver in alcohol related liver disease?

A

fatty liver

44
Q

What causes the damage in alcoholic hepatitis?

A

binge drinking leads to buld up of acetaldehyde whihc mediates damage. Hepatocytes swell and see formation of Mallory bodies, necrosis and acute inflammation

45
Q

What are mallory bodies?

A

damage cytokeratin filaments that are seen in Alcohol-Related Liver Disease

46
Q

Based on lab values, how can you differentiate between viral and alcohol hepatitis?

A

Viral: ALT>AST

Alcohol: AST>ALT (AST is in the mitochondira, which is mainly damaged in this situation)

47
Q

Non-alcoholic Fatty Liver Disease?

A

Fatty change, hepatitis, and or cirrhosis that develops w/o alcohol. Associate with obesity (ALT>AST)

48
Q

What is the mutation in hemochromatosis?

A

HFE gene, usually C282Y (cystein replaced by tyrosine)

49
Q

What is Wilson’s disease?

A

AR defect in ATP-mediated hepatocyte copper transport, copper does not enter the blood therefore low ceruloplasmin

50
Q

What is the treatment for Wilson’s disease?

A

D-penicillamine- chelates copper

51
Q

What is primary biliary cirrhosis?

A

autoimmune granulomatous destruction of intrahepatic bile ducts

52
Q

Autoantibody associated with primary biliary cirrhosis?

A

antimitochondrial antibody

53
Q

Primary Sclerosing Cholangitis?

A

inflammation and fibrosis of intrahepatic and extrahepatic bile ducts. Increased risk for cholangiocarcinoma

54
Q

what do the extrahepatic and intrahepatic bile ducts look like in PSC?

A

periductal fibrosis with **onion-skin **appearance, beaded appearance

55
Q

What disease is primary sclerosing cholangitis associated with?

A

Ulcerative colitis- p-ANKA +

56
Q

What is associated with hepatic adenoma?

A

benign tumor of hepatocytes associated with oral contraceptive use; regresses upon cessation of drug.

57
Q

What is the serum tumor marker for HCC?

A

alpha-fetoprotein

58
Q

Reye Syndrome?

A

Fulminant liver failure and encephalopathy in children with viral illness who take asprin. Related to mitochondrial damage of hepatocytes. Hypoglycemia, elevated liver enzymes, nausea with vomiting, progess to coma and death. Microvesicular fatty change

59
Q

What nerve innervates the muscles of the tongue?

A

CN XII hypoglossal (EXCEPT for palatoglossus which is innervated by CNX)

60
Q

What artery supplies the proximal lesser curvature of the stomach?

A

Left gastric artery which originates from the celiac artery

61
Q

What artery supplies the distal lesser curvature of the stomach?

A

Right gastric artery, originating from the proper hepatic which came from the comon hepatic from the celiac artery

62
Q

What artery supplies the proximal greater curvature of the stomach?

A

Left gastroepiploic artery from the splenic artery

63
Q

What artery supplies the distal greater curvature of the stomach?

A

Right gastroepiploic artery from the gastroduodenal artery from the common hepatic and celiac

64
Q

What artery supplies the proximal greater curvature of the stomach above the splenic artery?

A

Short gastric arteries originating from the splenic artery

65
Q

What are the symptoms of an HBV infection?

A

serum sickness-like prodrome (malaise, fever, rash, pruritis, lymphadenopathy and joint pain). Once symtoms start to go away, will get an elevated ALT/AST and then rises in bilirubin and ALP

66
Q

Is HCV usually symtomatic or asymptomatic?

A

asymptomatic

67
Q

Major risk factors for squamous cell carcinoma of the oral cavity?

A

tobacco and alcohol

68
Q

Is leukoplakia or erythroplakia more suggestive of squamous cell dysplasia (precursor lesion)?

A

Erythroplakia

69
Q

What is a pleomorphic adenoma?

A

biphasic tumor (stroma and epithelial tissue), parotid, high recurrence rate due to incomplete removal during surgery.

MOST COMMON TUMOR OF SALIVARY GLAND

70
Q

What is a Wartharin tumor?

A

cystic tumor w/lymphoid tissues.

2ND MOST COMMON TUMOR OF SALIVARY GLANDS

71
Q

What is the most common malignant tumor of the salivary glands?

A

Mucoepidermoid Carcinoma (facial nerve involvement indicates malignancy)

72
Q

Where does esophageal carcinoma spread (location dependent)?

A

upper 1/3- cervical nodes

middle 1/3- mediastinal or tracheobronchial nodes

lower 1/3- celiac and gastric nodes

73
Q

What is the function of statins?

A

inhibit HMG-CoA reductase and also increases LDL receptors on hepatocytes

74
Q

How can gallstone formation be prevented in patients on total parenteral nutrition?

A

Administer exogenous CCK (not secreted due to loss of stimulation from entering the stomach)

75
Q

How is copper excreted from the body?

A

secreted into bile and excreted into the stool, which is the primary route for copper elimination

76
Q

WHat is diphenoxylate?

A

opioid antidiarrheal, slows gastric motility

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