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Patho Units 7-10 > Unit 7 Review > Flashcards

Unit 7 Review Flashcards

1
Q

what is the source of H2O and electrolytes that are secreted in digestive secretions?

A

Enterocytes in the crypts of Lieberkuhn

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2
Q

What is the function of H2O and electrolytes secreted in digestive secretions?

A

serves as a vehicle for absorption for the chime as it comes in contact with villi

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3
Q

three major GI hormones

A

Ach, gastrin, histamine

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4
Q

what does Ach, gastrine and histamine do in GI tract

A

stimulate the release of acid

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5
Q

gastrin stimulates ( ) to secrete ( ) to promote ____ and ___

A

gastric gland ……. hydrochloric acid

growth of gastric mucosa and promote gastric motility

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6
Q

homone that increases GI motility

A

motilin

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7
Q

stimulated by chime in the duodenum, stimulates gall bladder to eject bile and pancreas to secrete alkaline fluid, slows gastric emptying

A

Cholecystokinin

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8
Q

hydrolysis: hydrogen and hydroxyl ions removed/added, splitting up food into basic parts

A

digestion

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9
Q

monosaccarides are broken down from what

A

carbs

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10
Q

fats are broken down into

A

fatty acids and glycerol

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11
Q

proteins are broken down into

A

amino acids

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12
Q

the transport of particles through and to the cells, active transport, diffusion or solvent

A

absorption

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13
Q

what bacteria is involved in the development of chronic gastritis and peptic ulcers

A

helicobacter pylori

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14
Q

H pylori cause ( ) with release of ________ ________ and reactive O2 metabolites that damage mucosal epithelial cells and cause loss of protective mucosal barrier

A

inflammation

inflammatory cytokines

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15
Q

what are methods for diagnosing H. pylori

A

cultures, histological staining, mucosal biopsy

urea breath tests, serum antibodies, stool and serum antigen, and gastric biopsy

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16
Q

protect stomach lining–stimulate the secretion of mucus and bicarbonate and by inhibiting secretion of acid

A

prostaglandins

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17
Q

destructive effect on prostaglandin synthesis

A

ASA and NSAIDS

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18
Q

Gram negative infectious agent

A

H. Pylori

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19
Q

treatment for H. pylori

A

bismuth, combination of abx w/vit. C to prevent relapse

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20
Q

peptic ulcers r/t increased gastrin: a gastrinoma (gastrin secreting neruoendocrine tumor) of the pancreas or duodenum stimulates proliferation of gastric parietal cells and chronic secretions

A

Zollinger-Ellison syndrome

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21
Q

2 out of 3 symptoms x3 months: change in bowel habits, abdominal pain, bloated feeling, mucus in stool, gas, diarrhea or constipation

A

IBS

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22
Q

inflammation anywhere in digestive tract, RLQ pain, colon thickened rocky appearance, ulcers deep and may extend into all layers of bowel wall, rectal bleeding not common

A

Crohn’s Diseases

23
Q

colon is affected site, inflammation is continuous, not patchy, pain in LLQ, colon wall is thinner and shows inflammation, ulcers only on inner lining of intestinal walls, bleeding during BMs

A

ulcerative cholitis

24
Q

tests for colon CA

A

colonoscopy, sigmoidoscopy, fecal occult blood testing CT,double contrast barium enema

25
Q

bring O2 rich but nutrient poor blood to liver

A

hepatic arteries

26
Q

bring nutrient rich but O2 poor blood to liver

A

hepatic veins

27
Q

vessel in abdominal cavity formed by union of superior mesenteric and splenic veins that channels blood from the GI tract and spleen to capillary beds in the liver

A

hepatic portal vein

28
Q

system of veins comprising the hepatic portal vein and its tributaries

A

hepatic portal system

29
Q

substances absorbed in the ______ ________ travel to the liver for processing before continuing to the ( ) and on to __________ ______

A

small intestine
heart
general circulation

30
Q

blood flows through ______ vein through _______. Blood also flows from branches of the __________ _______ and mixes in the sinusoids. The _________ _____ then drains deoxygenated blood into the ________ ______ _______.

A

portal vein……… sinusoids
hepatic artery
hepatic vein
inferior vena cava

31
Q

role of the liver in terms of carbohydrates, protein and fat metabolism

A

glycogen storage, plasma protein synthesis, & bile production for digestion of lipids, synthesis of albumin-protein that helps balance body fluids

32
Q

Can we survive without a liver?

A

No. No way to compensate for the absence of liver long term

33
Q

causes of jaundice

A

infection, Hepatitis, parasite, drugs, poisons, birth defects, excess bilirubin, or bilirubin can’t be broken down, liver damage, gall stones, gallbladder disorder, blood disorder, pancreatitis, pancreatic CA, bile build-up r/t pregnancy–pressure in abdomen

34
Q

hepato-toxic drugs

A

APAP, NSAIDS, amiodarone, anabolic steroids, erythromycin, OCPs, sulfonamide, phenytoin, carbamazapine, to name a few

35
Q

most common drug-induced liver cell necrosis, injury largely confined to certain area or liver lobule

A

zonal necrosis

36
Q

hepatocellular necrosis with infiltration of inflammatory cells

A

hepatitis

37
Q

liver injury leads to impairment of bile flow and causes inflammation (or sometimes no inflammation), itching and jaundice

A

cholestasis

38
Q

hepatoxicity manifested as triglyceride accumulation: fatty liver

A

steatosis

39
Q

drug induced, associated with other tissue granulomas

A

granuloma

40
Q

injury to the vascular endothelium

A

vascular lesions

41
Q

hepatocellular CA, angiosarcoma, liver adomas

A

neoplasms

42
Q

Hep A - source of infxn, incubation, chronic vs. acute

A

oral/fecal, 15-50 days, no chronic, only acute

43
Q

Hep B - source, incubation, chronic vs. acute

A

blood and bodily fluids, 45-160 days, acute to chronic

44
Q

Hep C - source, incubation, chronic vs. acute

A

blood and bodily fluids, 14-180 days, acute - rare, chronic can lead to cirrhosis

45
Q

Hep D - source, incubation, chronic vs. acute

A

blood and bodily fluids, needs HBV to survive, 3-7 weeks, acute leads to chronic, difficult to treat with HepB

46
Q

Hep E - source, incubation, chronic vs. acute

A

oral/fecal, 3-8 wks, acute unless immunocompromised

47
Q

bile contains too much cholesterol and not enough bile salts, infrequent emptying and contracting of gall bladder & proteins in liver and bile that promote or inhibit cholesterol crystallization

A

causes of formation of gall stones

48
Q

risk factors for pancreatitis

A

ETOH, smoking, gallstones, ERCP, abdominal trauma, carcinoma, drugs, penetrating ulcers, infections, mumps, hepatitis

49
Q

sudden inflammation and edema of the pancreas, leading to necrosis and secondary injury to extrapancreatic organs

A

pancreatitis

50
Q

treatment of pancreatitis

A

NPO, rest pancreas, surgery - remove gall bladder or stones,aggressive fluid rehydration, ICU, surgery

51
Q

gall bladder disease is usually treated by…

A

removing gall bladder

52
Q

deadly CA–abdominal or back pain, jaundice, wt loss, light colored stools, dark urine,

A

pancreatic CA

53
Q

reasons canc of the panc is so deadly…

A

rarely detected early, spreads very quickly, (easy access to nearby organs), recurrence is likely, relatively resistant to chemotherapy

54
Q

diverticular disease occurs in the…

A

large intestine.

Patho Units 7-10 (15 decks)

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