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VETM 442 > Glucose & Lipids > Flashcards

Glucose & Lipids Flashcards

1
Q

what is insuli stimulated by and what does it do

A

stimulated by an increase in blood glucose, as well as an increase in growth hormone, glucagon, or amino acid levels

actions: lowers blood glucose by promoting glucose uptake and use in metabolism, inhibits gluconeogenesis, increases fatty acid and TG stores, promote glycogen synthesis

**pro fat storage and pro glucose usage

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2
Q

glucagon is stimulated by what and does what

A

stimulated by a decrease in blood glucose concntrations

actions: increases blood glucose by stimulating gluconegenesis, help maintain glood glucose under fasting or food deprived states

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3
Q

what do catecholamines do in regards to glucose?

A

net effect is it increases blood glucose concentrations

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4
Q

what does growth hormone do?

A

released from pituitaru during hypoglycemia or epinephrine stim

action: increases glood glucose concentrations by inhibiting glucose update by cells

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5
Q

what do corticosteroids do regarding glucose and lipids?

A

they act to increase blood glucose concentrations, inhibit gucose uptake by cells, and promote storage of glycogen

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6
Q

what happens to glucose cocnentration for each:
- insulin
- glucagon
- catecholamines
- GH
- corticosteroids

A
  • decrease
  • increase
  • increase
  • increase
  • increase
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7
Q

what are the two “types” of hyperglycemia, and birelfy describe them

A
  • physiologic: after eating, excitement or fright
  • pathologic: diabetes mellitus, either beta cell destruction or insulin resistance, could be pancreatitis, or an endocrine disorder???
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8
Q

what is the hallmark of diabetes mellitus

A

persistent fasting hyperglycemia with concurrent glucosuria

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9
Q

what does a fructosamine test tell you

A

it can prove chronicity of high sugars in the blood, reflects the glucose over the past 2-3 weeks

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10
Q

why can you see ketoneuria with diabetes mellitus?

A

because there s diabetic ketoacidosis, because there is lots of fatty acid available for ketone formation and not a lot of glucose getting into cells

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11
Q

up to 40% of diabetes patients have _______

A

a positive culture with an inactive urine sediment

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12
Q

what is acromegaly?

A

happens in cats, excessive GH secretion from a functional somatotropic ademona or hyperplasia of the pituitary gland. you should suspect this when DM is not controlled with climbing insulin doses

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13
Q

list some examples of drugs that can cause hyperglycemia

A

dextrose, steroids, thyroxine, ethylene glycol, xylazine, etc

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14
Q

give 2 examples of a transient hyperglycemia

A
  • sepsis (if acute; chronic will be hypoglycemia)
  • proximal duodenal obstruction like an LDAor RDA in cows
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15
Q

WHAT IS THE NUMBER ONE THING YOU SHOULD RULE OUT WHEN YOU SEE A HYPOGLYCEMIA??????

A

improper handling/how long was that sample sitting on the bocnh before being analyzed–>remember you might also see a hyperkalemia from delayed sampling too

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16
Q

besides improper handling, what are some other reasons you might get a hypoglycemia?

A
  • insulinoma: functional beta pancreatic cells making insulin
  • xylitol toxicity: stimulant for insulin release and happens really fast
  • hypoadrenocorticism: due to no cortisol to tell insulin to stop
  • decreased gluconeogenesis, like if the liver isn’t working, decreased hepatic function
  • lactational, using up all the glucose
17
Q

what is amanita toxicity and what does it cause?

A

essentially an isulin overdose and severe hypoglycemia, from a mushroom usually seen in late summer/fall

18
Q

why does sepsis cause a hypoglycemia?

A

not sure, but it could be the cells are using lots of glucose and glucose is also not being produced. bacteria are NOT eating it

19
Q

what is exocrine pancreatic insufficinecy?

A

pancreas can’t produce and secrete digestive enzymes and bicarbonate, usually due to pancreatic acinar atrophy, most commonly seen in german shepherds

20
Q

what are some clinical signs of EPI?

A

weight loss, polyphagia, loose, pale, frappucino poop

21
Q

how do you diagnose EPI?

A

trypsin like immunoreactivity (TLI)
a low TLI=EPI

22
Q

why would amalyase and lipase be increased?

A
  • decreased GFR
  • pancreatitis
  • medications like steroids
23
Q

why would have you have a hypertriclyceridemia and milk hypercholesterolemia with pancreatitis?

A
  • there is a decrease or defect in lipoprotein lipase activity, which normally catalyzes hydrolysis of triglycerides in the plasma
24
Q

which mineral can be decreased in patients with acute pancreatitis?

A

calcium, due to the saponification of the pancreas

25
Q

the Spec Pli and SNAP Pli tests detect only ____. How should you interpret these tests?

A

pancreatic lipase
increased PLI supports pancreatitis but does not 100% prove it, they are better negative predictors to rule out pancreatitis than to confirm it

26
Q

true or false: you can diagnose pancreatitis based soley on amalyase and lipase elevations

A

FALSE!!!! NEVER DIAGNOSE PANCREATITIS BASED SOLEY ON AMALYASE AND LIPASE ELEVATIONS

27
Q

which causes the milkly appearance of plasma: high triclycerides or high cholesterol

A

high triglycerides!

28
Q

lipoprotein lipase is activated by _____. what does it do?

A

insulin
it converts CM and VLDL to free fatty acids and glycerol for tissue use

29
Q

hormone-sensitive triglyceride lipase is inhibited by ____. what does it do?

A

inhibited by insulin
responsible for lipolysis

30
Q

what are 3 causes of hypertriglyceridemia?

A
  • physiologic, like they just ate
  • iatrogenic: giving steroids
  • pathophysiologic: diabetes, cushings, pancreatits, etc
31
Q

true or false: hypotriglyceridemia is not considered clinically significant

A
32
Q

what are some reasons for a hypercholesterolemia ?

A
  • after eating, diabetes, hypothyroidism, pancreatitis, nephrotic syndrome, cholestasis/obstructive
33
Q

what are some reasons for a hypocholesterolemia?

A
  • decreased hepatic function
  • protein losing enteropathy, esp lymphangiectasia
  • hydroadrenocorticism
  • select neoplasia like lymphoma (rare)
34
Q

a horse with a marked hypertriglyceridemia you are worried about

A

equine hyperlipiemia–>negative energy balance, excessive mobilization of fat from adipose tissue

VETM 442 (18 decks)

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