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Nutrition > Final - Disease of GI tract & Pancreas > Flashcards

Final - Disease of GI tract & Pancreas Flashcards

1
Q

what are the functional units for exocrine pancreas

A

acinar cells

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2
Q

what are zymogens

A

inactive forms of enzyzmes
digestive enzymes first produced as zymogens until activated in duodenum

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3
Q

where do digestive enzymes from the pancreas enter the duodenum?

A

major duodenal papilla (major pancreatic duct + common bile duct)
minor duodenal papilla (accessory pancreatic duct)

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4
Q

what duodenal papilla is not found in most cats

A

minor duodenal papilla

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5
Q

what is exocrine pancreatic insufficiency?

A

digestive part of pancreas dysfunctional, common in dogs

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6
Q

what cells and hormones does the pancreas produce

A

alpha cells - glucagon
beta cells - insulin
delta cells - somatostatin

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7
Q

describe intestinal absorption and what allows it to have such high surface area

A

long-lived, self-renewal, multipotency
HSA due to villus, crypts, microvilli (brush border), plica circulariis, mucosa, submucosa

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8
Q

what allows the greatest increase in surface area in the intestine?

A

microvilli (brush border) increases 20x, then villi x10 then plica circularis x3

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9
Q

what cells are located in the villus

A

mature enterocytes for absorption and digestion
goblet cells
enteroendodrine

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10
Q

what cells are located in the crypts

A

young enterocytes for secretions
stem cells (can become various cells = rapid turnover)
paneth cells

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11
Q

Parvovirus attacks what cells in the intestine

A

rapidly dividing cells - thus affecting the crypts
also causes severe villus blunting and atrophy

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12
Q

difference between Metoclopramide and Cisapride

A

Metoclopramide - works in SI to increase peristalsis, but not colon
Cisapride - MOVES CATS COLON

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13
Q

antigens and inflammation in IBD

A

antigens - food, endogenous microbes or pathogens that cause inflammation due to breakdown of the mucosal barrier

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14
Q

GI role in absorption

A

absorbs nutrients, H2O and electrolytes

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15
Q

GI role in immunologic homeostasis

A

recognition, protection, tolerance, response

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16
Q

what cells secrete bicarbonate

A

epithelial cells lining small pancreatic ducts

17
Q

what cells secrete digestive enzymes from pancreas

A

exocrine acinar cells
zymogen cells

18
Q

treatments for IBD

A

no antibiotics
use probiotics, glucocorticoids or other immunosuppressants instead

19
Q

purpose of fiber

A

produced SCFA - acetate, butyrate, propionate which promotes GI mucosa
can cause flatus (gas)

20
Q

most prevalent endocrine disease

A

diabetes mellitus

21
Q

most prevalent exocrine disease

A

pancreatitis

22
Q

diabetes mellitus
etiology:
clinical sign:
treatment:

A

increased glucose
PUPD, polyphagia, weight loss
insulin

23
Q

insulinoma
etiology:
clinical sign:

A

increased insulin
hypoglycemia

24
Q

pancreatitis
etiology:
clinical sign:

A

inflammation
anorexia, vomitting, abdominal pain

25
Q

enzymatic pancreatic insufficiency
etiology:
clinical sign:
treatment:

A

destruction of pancreatic enzymes
polyphagia, weight loss
replace pancreatic enzymes

26
Q

insulin
catabolic/anabolic?
mechanisms

A

anabolic
increased storage of glucose, fatty acids and amino acids

27
Q

fastest insulin mechanisms? slowest?

A

fastest - transport of glucose, aa, K+ into cells
slowest - mRNA for lipogenic enzymes

28
Q

glucose
catabolic/anabolic?
mechanisms

A

catabolic
increased mobilization of glucose, fatty acids, amino acids

29
Q

diabetes mellitus is a ______ disease

A

metabolic

30
Q

four classic signs of diabetes

A

polyuria
polydipsia
polyphagia
weight loss

31
Q

how will exercise change the patients insulin requirement

A

exercise decreases insulin requirement due to more efficient GLUT4 transporters bringing glucose from blood into cells

32
Q

3 ketones of diabetic ketoacidosis

A

acetoacetate
acetone
beta-hydroxybutyrate

33
Q

typical findings of a diabetic ketoacidosis patient

A

anorexia/weight loss
lethargic, comatose
tachy
dehydration
vomiting/diarrhea
acetone breath
hepatomegaly

34
Q

finding in a DKA cat

A

plantigrade stance

35
Q

finding in a DKA dog

A

cataracts

36
Q

how does diabetes lead to ketoacidosis and fatty liver

A

no insulin
increased HSL
increased lipidemia
increased FFA in liver
FFA –> ketones

37
Q

stress hormones

A

epinephrine
cortisol
growth hormone

38
Q

effect of no insulin and stress on HSL

A

insulin inhibits HSL, so no insulin = high HSL = fatty liver/ketones

stress stimulates HSL = fatty liver/ketones

Nutrition (11 decks)

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