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
Q

what does elevated HbA1C increased the risk of

A
mortality
CVD/Stroke
CKD
Cancer
retinopathy/neuropathy
26
Q

what is a normal HbA1C?

A

6%
>7.6% is poor
blood glucose 114

27
Q

what does HbA1C predict preop in non diabetic pts?

A

mortality

acute kidney injury

28
Q

what is the leading cause of CKD and ESRD?

A

diabetes

29
Q

DKA

A

diabetic ketoacidosis
ketones (blood acids elevated)
sugar elevated
dehydration and coma

30
Q

what are the symptoms of someone with insulin resistance?

A
low HDL
high triglycerides
obesity
hypertension
NAFLD
31
Q

why is GH release pulsatile?

A

circadian rhythm but also tied to nutrition, metabolism and hormones

32
Q

why is GH surge at night significant?

A

growth and repair during rest

33
Q

why effect would high carb meal before bed have?

A

reduced GH pulses, affect growth and repair in adults

34
Q

children what are the thyroid hormones, GH and androgens doing?

A

high T4, limited GH pulses, limited androgen

35
Q

puberty what are the thyroid hormones, GH and androgens doing?

A

normal T4, androgens increase GH pulses and increases IGF1

36
Q

aging what are the thyroid hormones, GH and androgens doing?

A

reduced T4, GH, and androgen effectiveness

37
Q

what does the peak in rate of growth for puberty correspond with?

A

peak in concentration of IGF-1 in serum

38
Q

what are the three problems that start before puberty? GH

A

gigantism: GH overexpression
pituitary dwarfism: GH deficiency
achondroplasia (w/o cartlidge): not related to GH

39
Q

what are the two problems that start after puberty? GH

A

acromegaly: GH overexpresion, bone growth in face

larons syndrome: GHR insensitivity (no IGF1)

40
Q

what is special about larons syndrome?

A

they are resistant to cancer and type 2 diabetes

41
Q

the pt has a lesion in the ant pit, elevated IGF1, elevated GH and no GHRH, what does the pt have?

A

acromegaly

42
Q

why is GH diabetogenic?

A

it increases insulin resistance

43
Q

when should normal insulin peak and return to baseline?

A

peak at 30 min

baseline after 3 hr