Exam 5: Chapter 29, 30, 31, 32 Flashcards

1
Q

Upper GI bleeding causes

A

bleeding varices, peptic ulcers, mallory-weiss tear

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2
Q

Lower GI bleeding causes

A

polyps, cancer, inflammatory disease, hemorrhoids

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3
Q

Sx of Gi bleeding

A

melena, decreased Hct and Hgb, tachycardia, hypotension, change in LOC, hematemesis, diarrhea

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4
Q

Pathophysiology of GERD

A

reflux of chyme through LES; decreased LES tone

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5
Q

Causes of GERD

A

increased abdominal pressure, delayed gastric emptying, and certain foods

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6
Q

Sx of GERD

A

heartburn, indigestion, acid regurgitation, dysphagia, cough, chest pain, asthma, abdominal pain with eating

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7
Q

Complications of GERD

A

esophageal cancer (Barretts tumor)

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8
Q

Pathophysiology of hiatal hernia

A

part of the stomach protrudes through diaphram into the thorax

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9
Q

Sx of hiatal hernia

A

GERD, esophagitis, dysphagia, epigastric pain

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10
Q

Pathophysiology of acute gastritis

A

usually superficial erosions due to injury to the mucosal barrier by drugs and chemicals like NSAIDs and aspirin

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11
Q

Pathophysiology of chronic gastritis

A

thinning and degeneration of the stomach wall; more in the elderly population

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12
Q

Pathophysiology of chronic fundal gastritis

A

the worst; leads to gastric atrophy, decreased acid secretion, pernicious anemia

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13
Q

Pathophysiology of peptic ulcer disease

A

a break or ulceration in the mucosal lining in the lower esophageal, stomach, or duodenum; exposed to gastric secretions and autodigestion

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14
Q

Causes of gastric ulcers

A

H. pylori and NSAIDs

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15
Q

Risk factors for gastric ulcers

A

chronic gastritis, decreased PG synthesis, duodenal reflux of bile and pancreatic enzymes

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16
Q

Causes of duodenal ulcers

A

H. pylori and NSAIDs; there is increased acid and pepsin secretion

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17
Q

Complications of duodenal gastritis

A

intestinal obstruction, bleeding, perforation, and death

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18
Q

Causes of a stress ulcer

A

an acute peptic ulcer related to severe illness, trauma, or neural illness

19
Q

Pathophysiology od dumping syndrome

A

rapid emptying of hypertonic chyme into duodenum 10-20 min after eating

20
Q

Sx of dumping syndrome

A

cramping pain and diarrhea

21
Q

Pathophysiology of anemia related to post-gastrectomy

A

iron is malabsorbed and related to decreased acid production or no duodenum

22
Q

Cholelithiasis

A

gall stones

23
Q

Sx of cholelithiasis

A

abdominal pain, pain radiating to the right shoulder, jaundice, pruritus, heartburn, food intolerance especially fatty food

24
Q

Cholecystitis

A

inflammation of gallbladder usually from gall stones stuck in cystic duct

25
Q

Sx of cholecystitis

A

abdominal pain, fever, increased WBC, and rebound tenderness

26
Q

Pathophysiology of acute pancreatitis

A

obstruction of outflow of pancreatic enzymes; enzymes are activated and autodigestion occurs

27
Q

Causes of acute pancreatitis

A

alcoholism and biliary tract obstruction

28
Q

Sx of acute pancreatitis

A

abdominal pain, vomiting, and abdominal distension

29
Q

Causes of chronic pancreatitis

A

chronic alcoholism, fibrosis, continued inflammation, calcification, and cysts

30
Q

Complications of chronic pancreatitis

A

pancreatic cancer

31
Q

Pathophysiology of alcohol detoxification

A

alcohol turns into acetaldehyde and hydrogen. acetaldehyde damages hepacyte mitochondria, inhibits removal of proteins from liver, and alters metabolism of vitamins and minerals

32
Q

Pathophysiology of portal hypertension

A

obstructed blood flow through portal system

33
Q

Causes of portal hypertension

A

thrombosis, inflammation, and fibrous changes in liver

34
Q

Pathophysiology of esophageal varicies

A

increased portal vein pressure that causes development of collateral vessels; usually occurs in the lower esophagus, stomach, and rectum

35
Q

Pathophysiology of ascites

A

increased hydrostatic pressure in mesenteric tributaries of the portal vein that leads to water in peritoneal cavity

36
Q

Sx of ascites

A

abdominal distension, wt gain, SOB, and spider angioma

37
Q

Complication of ascites

A

bacterial peritonitis

38
Q

3 phases of HAV

A

prodromal: 2 wks after exposure and causes general sx
icteric: 1-2wks later jaundice, dark urine, clay colored stool, and enlarged liver
recovery: 6-8 wks after exposure. sx diminish, liver still enlarged and tender. liver normal 2-12 wks after exposure

39
Q

Cirrhosis of the liver

A

irreversible and inflammatory disease

40
Q

Fatty Liver

A

mildest form; reversible when drinking is stopped

41
Q

Alcoholic Hepatitis

A

inflammation, degeneration and necrosis of liver cells; infiltration by leukocytes and lymphocytes

42
Q

Cirrhosis

A

fibrosis of liver

43
Q

Sx of alcohol cirrhosis

A

wt loss, anorexia, enlarged liver and spleen, ascites, GI hemorrhage, hepatic encephalopathy, esophageal varicies

44
Q
A