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First Aid GIT > FA GIT II > Flashcards

FA GIT II Flashcards

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Git Commands flashcards
1
Q

Lab Levels?

A

Deposition of hemosiderin (iron), caused by iron deposition.

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2
Q

How much can total body iron reach in hemochromatosis

A

50 g, enough to set off metal detectors at airports

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3
Q

How do you treat hereditary hemochromatosis?

A

Repeated Phlebotomy Deferoxamine

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4
Q

Hemochromatosis HLA Type Association

A

Associated with HLA-A3

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5
Q

What happens in secondary biliary cirrhosis? How does it present? Labs? Complicated by?

A

Extrahepatic biliary obstruction (gallstone, biliary stricture, chronic pancreatitis, carcinoma of the pancreatic head)-> increased pressure in intrahepatic ducts-> injury/fibrosis and bile stasis

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6
Q

What happens in primary biliary cirrhosis? Presents? Labs? Associated with?

A

Autoimmune reaction-> lymphocyte infiltrate + granulomas. Increase in serum mitochondrial antibody, including IgM

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7
Q

What is Primary Sclerosing Cholangitis? Presents? Labs? Associated with? Can lead to?

A

Unknown cause of concentric “onion skin” bile duct fibrosis-> alternating strictures and dilation with “beading” of intra and extrahepatic bile duts on ERCP

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8
Q

Gallstones causes and what are the types?

A

Caused by increased cholesterol and/or billirubin, decreased bile salts and gallbladder stasis all cause stones.

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9
Q

Cholesterol Stones? What percentages? Causes?

A

Radiolucent with 10-20% Opaque due to calcifications- 80% of stones, associated with obesity, Crohn’s disease, cystic fibrosis, advanced age, clofibrate, estrogens, multiparity,rapidd weight loss, and native american origin.

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10
Q

Pigment Stones

A

Radiopaque- seen in patients with chronic hemolysis, alcoholic cirrhosis, advanced age, and biliary infection.

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11
Q

What can gallstones cause?

A

can most often cause cholecytisis, also ascending cholangitis, acute pancreatitis, and bile stasis

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12
Q

How do you diagnose and treat gallstones

A

Diagnose with ultrasound. Treat with cholecystectomy.

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13
Q

What are some risk factors for gallstones?

A

Female, Fat, Fertile, and Forty. 4F’s

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14
Q

What is murphy’s sign

A

Inspiratory arrest on deep palpation due to pain.

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15
Q

What is charcot’s triad of cholangitis?

A

Jaundice, Fever, Right Upper Quadrant Pain

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16
Q

Cholecystitis

A

Inflammation of gallbladder, usually from gallstones. Rarely ischemia or infectious (CMV).

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17
Q

What happens in acute pancreatitis? Causes? Presentation, Labs, Can lead to?

A

Autodigestion of pancreas by pancreatic enzymes.

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18
Q

What can chronic pancreatitis lead to

A

Can lead to pancreatic insufficiency, steatorrhea, fat-soluble vitamin deficiency, and diabetes mellitis

19
Q

Chronic Calcifying Pancreatitis is strongly associated with? Increased risk of?

A

Alcoholism and Smoking, Increasing Risk of Pancreatic Cancer

20
Q

Presents with?

A

Prognosis averages 6 months or less, very aggressive, usually already metastasized at presentation, tuors more common in pancreatic head (obstructive jaundice).

21
Q

Name some proton pump inhibitors, Mechanism of action, and clinical use?

A

Omeprazole and lansoprazole

22
Q

Name some H2 blockers, Mechanism of action, Clinical Use

A

Cimetidine, Ranitinde, Famotidine, Nizatidine

23
Q

What are some of cimetidine’s side effects?

A

Potent inhibitor of P450, antiandrogenic efffects (prolactin release, gynecomastia, impotence, decreased libido in males), can cross blood brain barrier (confusion, dizziness, and headaches) and placenta. Decreases renal excretion of creatinine.

24
Q

What are ranitidine’s side effect?

A

Decreased renal excretion of creatinine.

25
Q

Bismuth, Sucrafalate Mechansim and Clinical Use?

A

Binds to ulcer base, providing physical protection and allows HCO3- secretion to reestablish pH gradient in the mucous layer.

26
Q

What is the triple therapy of H. pylori ulcers

A

Metronidazole, Amoxicillin (or tetracycline), Bismuth

27
Q

Misoprostal mechanismn, clinical use, toxicity

A

PGE1 analog, increased production and secretion of gastric mucous barrier, decreases acid production

28
Q

What are muscarinic antagonists names? mechanisms? clinical use? toxicities/

A

Pirenzepine, Propantheline

29
Q

Ocreotide Mechanism? Use? Toxicities?

A

Somatostatin Analog

30
Q

Infliximab Mechanism, Clinical Use, Toxicity

A

A monoclonal antibody to TNF, proinflammatory cytokine

31
Q

Sulfasalazine Mechanism, Clinical Use, Toxicity

A

Combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory). Activated by colonic bacteria.

32
Q

Ondansetron Mechanism, Clinical Use, Toxicity

A

5-HT3 Antagonist, powerful central-acting antiemetic.

33
Q

Metoclopramide Mechanism, Use, Toxicity? Drug interaction with? Contraindicated in?

A

D2 receptor antagonist, increases resting tone, contractility, LES TONE, motility

34
Q

How does antacids work?

A

Affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric empthing.

35
Q

What can overuse of some antacids cause

A

Aluminun hydroxide- constipation and hypophosphatemia, proximal muscle weakness, osteodystrophy, seizures

36
Q

What are problems with all antacids

A

Can cause hypokalemia and can chelate and decrease effectiveness of other drugs (tetracycline)

37
Q

Discuss possible etiology of Crohn’s vs. Ulcerative colitis

A

Crohn’s - disordered response to intestinal bacteria

38
Q

Location of Crohn’s vs. Ulcerative Colitis

A

Crohn’s- Any portion of the GI tract, usually the terminal uleum and colon, Skip lesions, and rectal sparing

39
Q

Gross morphology of Crohn’s versus ulcerative collitis?

A

Crohn’s: Transmural inflammation. Cobblestone mmucosa, creeping fat, bowel wall thickening (“string sign” on barium swallow x-ray), linear ulcers, fissures, fistulas

40
Q

Microscopic Features of Crohn’s versus Ulcerative colitis

A

Crohn’s- Noncaseating granulomas, lymphoid aggregates

41
Q

Complications of Crohn’s versus UC

A

Crohns- strictures, fistulas, perianal disease, malabsorption, nutritional depletion, colorectal cancer

42
Q

Intestinal Manifestations of Crohn’s versus UC such as Diarrhea?

A

Crohns- Diarrhea that may or may not be bloody

43
Q

Extraintestinal manifestations of Crohns vs UC?

A

Crohns- Migratory polyarthritis, erythema nodosoum, immunological disorders

44
Q

Treatment of Crohns vs. UC?

A

Crohns- Corticosteroids, Infliximab

First Aid GIT (2 decks)

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