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physio > pancreas > Flashcards

pancreas Flashcards

1
Q

what are the main tissues that insulin regulates (3)

A
  • liver» glucose into glycogen
  • muscle> glucose uptake into muscle
  • adipose» glucose into fat to form triglycerides
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2
Q

what is glucagon,what does it oppose, what does it do?

A

-opposing hormone to insulin
- stimulates glycogen breakdown and increases glucose release from the liver

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3
Q

what are the functions of the pancreas
- what is their percentage of pancreatic mass

A

exocrine(98%) and endocrine function (2%)

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4
Q

what part of the pancreas is responsible for endocrine function

A

islets of langerhan

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5
Q

what are the cell types of islets of langerhan , what is their percent make up, and function

A

alpha cells (20%)- secrete glucagon and increase plasma glucose and mobilize glycogen and fat

beta cells (60-75%)- secrete insulin to increase glucose uptake and deposit glycogen and fat

delta cells (<5%)- secrete somatostatin and decreases insulin and glucagon secretinf and decreases excocine gastric secretions

F cells <5% - secreate pancreatic polypeptide to decrease foood absorption

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6
Q

synthesis and structure of insulin

A
  • pre-proinsulin has A, B ,and C Chain with A and b linked by 2 disulfied bond
  • signal sequence is cleaved from pre-proinsulin to form pro-insulin
  • cleavage of the C peptide chain to leave active insulin
  • insulin and C peptide stored in secretory granuels complexed with zinc for storage and release
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7
Q

how does C peptide have a diagnostic use

A

in synthetic insulin there is no C peptide so it can be used to measure how much endogenous peptide is being prodcued

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8
Q

in what cells is insulin synthesized and stored and what is its form when synthesized

A

in beta cells which synthesisezes pre-proinsulin

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9
Q

what is the half life of insulin in circulation

A

5 min

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10
Q

what are the normal glucose levels
- what happens as glucose increases about this range

A
  • 5.5mM ( 1000mg/dL)
  • insulin is stimulated
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11
Q

what is the relationship between glucagon and glucose

A

inverse relationship- when glucose is high glucagon is low and when glucose is low glucagon is high

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12
Q

what is the relation ship between insulin and glucagon

A

as insulin rises glucagon drops

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13
Q

what is the relationship between glucose and insulin

A

when glucose rises insulin rises and when it drops insulin drops

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14
Q

what is the mechanism of insulin secretion

A
  • glucose enters beta-cells by GLUT 2 transporters
  • its phosphorylated and metabolized into pyruvate and further metabolized in the citric acid cycle
  • ATP formed by oxidative phosphorylation inhibits ATP sensitive K channels reducing K efflux
  • THis depolarizes the B cell and increases ca influx which stimulats the release of insulin
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15
Q

insulin secretion is modulated by ____ and ____ signals

A

metabolic and hormonal

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16
Q

what are the stimulators of insulin secretion

A

glucose, glucagon, amino acids, GLP1s

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17
Q

what are the inhibitors of insulin

A

somatostatin and catecholamines ( alpha adrenergic)

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18
Q

mechanism of insulin activated glucose transport

A
  • activation of insulin receptor intiates translocation of GLUT 4 containing endosome into the cell membrane,
  • GLUT 4 then mediates glucose transport into the cell
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19
Q

what are the transporters that transport glucose via active transport and what is their function

A

SGLT 1 and SGLT 2 are involoved in active glucose transport into the the gut and kidney(renal tubules)

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20
Q

what are the facilitated transporters of glucose and what are their function

A

GLUT 2 -12-20 Km - uptkae of glucose into beta cells

GLUT 4 - 5Km- insulin stiumulated glucose uptake in skeletal and cardiac muscle, adipose, and other tissues

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21
Q

Effects of insulin on metabolic fluxes
- what are the effects of insulin on muscles, liver , and adipose tissue ( what does it stimulate and inhibit)

A
  • muscle stimulates glucose and amino acid uptake
    and inhibits amino acid release
  • inhibits glucose release from the liver
  • stimulates glucose uptake into adipose and inhibits relaease from free fatty acids and ketogenesis
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22
Q

what is glucagon synthesized by and when is stimulated

A

synthesized by alpha cells and stiumulated when glucose is low

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23
Q

what is the half life of glucagon and what is it degraded by

A

5-10 min - degraded by the liver

24
Q

what gene is glucagon synthesized by and in what form is produced

A
  • GCG gene produced as a pre-prohormone which is cleaved in alpha cells to yield glucagon
25
Q

what does the GCG gene also give rise to and what is its function

A

GLP-1 glucagon like polypeptide -is it incretin and enhances the secretion of insulin and increases glucose uptake from the blood

26
Q

what are the stimulators of glucagon secretion

A
27
Q

what are the inhibitors of glucagon

A
28
Q

effects of glucagon on metabolic fluxes
- what are the effects of glucagon on the liver and adipose tissue

A
  • stimulates the generation of glucose from glycogen and amino acids in the liver
  • and mobalization of fatty acids in fat
29
Q

by what cells is somatostatin produced by

A

delta cells in tha pancreas

30
Q

what is somatostatin release stimulated by

A

stimulated glucose and amino acids ( same as insulin)

31
Q

what is the affect of somatostatin on the islets and GI

A

inhibts the release of islet hormones such as insulin and glucogon
- in the gi tract it decreases glucose absorption and decreases blood flow

32
Q

how do epinephrine and norepinephrine affect glucose metabolism

A
  • epinephrine stimulates glucose production by increasing gluconeogenesis iin the liver and glycogenolysis in the liver and muscle
  • inibits the action of insulin
  • lipolyisis and ketogenesis are stimulated
    INCREASE BLOOD GLUCOSE
33
Q

what is the major effect of cortisol on metabolism

A

stimulates mobilization of amino acids and their conversion to glucose

34
Q

how does cortisol do to insulin and adipose tissue

A
  • inhibts glucose uptake by insulin and can cause mobilization of fat or facilitate fat storage
35
Q

what is cortisol describes as since it increases glucose

A

hypeglycemic but doesnt stimulate glycogen deposition

36
Q

what is the endocrine hormone of adipose tissue
-what is the amount of secretion proportional to

A

leptin and is secreted propotional to the amount of adipose tissue

37
Q

what is the function of leptin

A

reports the size of adipose mass to the hypothalamus

38
Q

what happens with exxcessive food intake

A

increase adipose mass, leptin increases and leads to a series of behavorial and metabolic changes

39
Q

what are the effects of leptin

A
  • reduced appetite, incresased energy expenditure, thermognesis etc
40
Q

what does mutation of leptin do to the mouse

A

eats too much and gets fat

41
Q
A
42
Q

what is the most common cause of hypoglycemia and convulsions

A

overdose of insulin

43
Q

why is the brain sensitive to hypoglycemia

A
  • it has little stored carbs and depends on glucose for energy
44
Q

what are the symptoms of hypoglycemia

A

cognitive dysfunction
lethargy
coma
convulsions
brain damage

45
Q

what is Diabetes mellitus caused by

A

defieceny in the effects of insulin

46
Q

what is type 1 diabetes
-what is it called
- what is it caused by

A

insulin dependent mellitus - due to primary failure of insulin secretion by the endocrine pancreas

47
Q

what is type 2 diabetes
-what is it called and what is it caused by

A

non insulin dependent diabetes, due to loss of insulin sensitivity of the tissues which is acompannied by reduced inuslin secretion

48
Q

what is DM charecterized by and what is the cause of these effects

A
  • polyuria (excessive urine output),
  • polydipsia (excessive thirst),
  • polyphagia (excessive eating),
  • hyperglycemia,
  • glucosuria (glucose in urine)

The primary cause of these effects are failure of glucose uptake

49
Q

when does type 1 diabetes (IDDM) present and what is the casus
- what is the treatment
- what are the levels of plasma insulin
- what happens to weight

A

presents early in life so called juvenile onset diabetes
- caused by loss of pancreatic beta cells other cells remain intact
- insulin is low
-weight loss
administer insulin

50
Q

when does type 2 diabetes present
- what is the cause
- what are the insulin levels
- weight
- treatment

A

presents later in life >40 adult onset diabetes
- caused by the development of insulin resistance
- may over stimulate beta cells to compensate for low insulin
- insulin can be low or near normal
- cant administer insulin
- patients are generally obese
- Treatments include sulfonylureas, metformin and diet

51
Q

diagnosis diabetes mellitus with the glucose test

A
  • when glucose is given plasma glucose increases greater than normal and doesnt decrease for a ling time
52
Q

how can you measure blood glucose with HbA1c

A
  • measures how much glucose is covalently bound to hemoglobin
  • can measure a 3 month time window and how much glucose was consumed
53
Q

what is a normal and prediabetic,diabetic A1c

A

normal 4.5-5.6
pre- 5.7-6.4
diabetic- >6.5

54
Q
A
55
Q

metabolic syndrome
- what are the metabolic risk factors

A

Abdominal obesity
* High plasma triglycerides
* Low HDL- and high LDL-
cholesterol
* High fasting blood glucose
* Insulin resistance
* Elevated blood pressur

56
Q

what diseases are increased with metabolic syndrome

A
  • Type 2 Diabetes
  • Coronary Artery Disease
  • Stroke

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