Endocrine I Flashcards

1
Q

what are the hormones secreted from the endocrine pancreas and their cells of origin? and % breakdown of cells in islet of langerhans

A

glucagon- alpha cells- 20%
insulin- beta cells- 70%
somatostatin- delta cells- 10%

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2
Q

what does somatostatin do?

A

inhibits insulin, glucagon and GH

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3
Q

how does insulin antagonize glucagons effect?

A

driving glucose uptake and thus decreasing blood sugar

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4
Q

how does glucagon antagonize insulins effect?

A

stimulating hepatic glucose release and increasing blood sugar

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5
Q

what is a normal blood sugar

A

4-6mM = 80-100mg/dL

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6
Q

what is the main regulator of pancreatic hormones?

A

glucose

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7
Q

what things stimulate insulin?

A
glucose (hyper)
amino acids
incretins (GIP, GLP)
glucagon
sulfonylurea drugs
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8
Q

what things inhibit insulin

A

somatostatin
NE/Epi and cortisol
fasting/exercise

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9
Q

what things stimulate glucagon?

A

glucose (hypo)
amino acids
NE/Epi and cortisol
exercise and fasting

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10
Q

what things inhibit glucagon?

A

incretins (GIP, GLP)
insulin
somatostatin

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11
Q

explain the mechanism of action of glucose binding to beta cells?

A
glucose binds GLUT 2 R on pancreatic beta cell
closes the K channel
depolarizes beta cell
opens Ca channel
insulin is released
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12
Q

what do incretins (GIP and GLP) stimulate?

A

they are either broken down quickly by DPP4

OR they go to the pancreas to stimulate insulin secretion and lower glucagon.

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13
Q

what can make incretins work better?

A

DPP4 antagonist

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14
Q

is insulin anabolic or catabolic? and what does it cause in skeletal muscle, liver, and adipose tissue

A

anabolic
AA uptake in skeletal muscle
suppress hepatic glucose production
adipose inhibit lipolysis

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15
Q

is glucagon anabolic or catabolic? and what does it cause in skeletal muscle, liver, and adipose tissue

A

catabolic
no effect skeletal muscle
hepatic glycogen breakdown, sugar formation, ketone formation
adipose lipolysis

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16
Q

what tissue is responsible for type 2 diabetes?

A

skeletal muscle, primary glucose storage

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17
Q

what controls glut4?

A

Atk pathway stimulates GLUT4 vasible to translocate

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18
Q

what is type 1 diabetes?

A

loss of beta cells due to autoimmune distruction

triggered by environmental factor

19
Q

how do we develop type 2 diabetes?

A

insulin resistance (inactivity and genetics)
obesity
beta cell hyperplasia (normal glucose/high insulin)
beta cell fatigue (high glucose/ high insulin)
beta cell failure (high glucose/ low insulin

20
Q

how do we know that insulin resistance (inactivity and genetics) precede obesity for type 2 diabetes?

A

research shows that from just two weeks of inactivity insulin and glucose levels increased

21
Q

what causes someone to develop insulin resistance?

A

JNK binds and phosphorylates the syr molecule in the Atk pathway and GLUT4 vesicles are not translocated
due to oxidative stress

22
Q

what does insulin resistance mean about how much insulin must be released to create the same response as before?

A

more insulin must be released because the curve is shifted to the right

23
Q

OGTT

A

oral glucose tolerance test

24
Q

HbA1C

A

hemoglobin that is covalently bound to hemoglobin and a test for diabetes

25
what does elevated HbA1C increased the risk of
``` mortality CVD/Stroke CKD Cancer retinopathy/neuropathy ```
26
what is a normal HbA1C?
6% >7.6% is poor blood glucose 114
27
what does HbA1C predict preop in non diabetic pts?
mortality | acute kidney injury
28
what is the leading cause of CKD and ESRD?
diabetes
29
DKA
diabetic ketoacidosis ketones (blood acids elevated) sugar elevated dehydration and coma
30
what are the symptoms of someone with insulin resistance?
``` low HDL high triglycerides obesity hypertension NAFLD ```
31
why is GH release pulsatile?
circadian rhythm but also tied to nutrition, metabolism and hormones
32
why is GH surge at night significant?
growth and repair during rest
33
why effect would high carb meal before bed have?
reduced GH pulses, affect growth and repair in adults
34
children what are the thyroid hormones, GH and androgens doing?
high T4, limited GH pulses, limited androgen
35
puberty what are the thyroid hormones, GH and androgens doing?
normal T4, androgens increase GH pulses and increases IGF1
36
aging what are the thyroid hormones, GH and androgens doing?
reduced T4, GH, and androgen effectiveness
37
what does the peak in rate of growth for puberty correspond with?
peak in concentration of IGF-1 in serum
38
what are the three problems that start before puberty? GH
gigantism: GH overexpression pituitary dwarfism: GH deficiency achondroplasia (w/o cartlidge): not related to GH
39
what are the two problems that start after puberty? GH
acromegaly: GH overexpresion, bone growth in face | larons syndrome: GHR insensitivity (no IGF1)
40
what is special about larons syndrome?
they are resistant to cancer and type 2 diabetes
41
the pt has a lesion in the ant pit, elevated IGF1, elevated GH and no GHRH, what does the pt have?
acromegaly
42
why is GH diabetogenic?
it increases insulin resistance
43
when should normal insulin peak and return to baseline?
peak at 30 min | baseline after 3 hr