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
enzymatic pancreatic insufficiency etiology: clinical sign: treatment:
destruction of pancreatic enzymes polyphagia, weight loss replace pancreatic enzymes
26
insulin catabolic/anabolic? mechanisms
anabolic increased storage of glucose, fatty acids and amino acids
27
fastest insulin mechanisms? slowest?
fastest - transport of glucose, aa, K+ into cells slowest - mRNA for lipogenic enzymes
28
glucose catabolic/anabolic? mechanisms
catabolic increased mobilization of glucose, fatty acids, amino acids
29
diabetes mellitus is a ______ disease
metabolic
30
four classic signs of diabetes
polyuria polydipsia polyphagia weight loss
31
how will exercise change the patients insulin requirement
exercise decreases insulin requirement due to more efficient GLUT4 transporters bringing glucose from blood into cells
32
3 ketones of diabetic ketoacidosis
acetoacetate acetone beta-hydroxybutyrate
33
typical findings of a diabetic ketoacidosis patient
anorexia/weight loss lethargic, comatose tachy dehydration vomiting/diarrhea acetone breath hepatomegaly
34
finding in a DKA cat
plantigrade stance
35
finding in a DKA dog
cataracts
36
how does diabetes lead to ketoacidosis and fatty liver
no insulin increased HSL increased lipidemia increased FFA in liver FFA --> ketones
37
stress hormones
epinephrine cortisol growth hormone
38
effect of no insulin and stress on HSL
insulin inhibits HSL, so no insulin = high HSL = fatty liver/ketones stress stimulates HSL = fatty liver/ketones