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Clin Med - Endocrine > Lecture 1 - 3: Physiology (Also Pharm Lectures) > Flashcards

Lecture 1 - 3: Physiology (Also Pharm Lectures) Flashcards

1
Q

Endocrine communication

A

release of a chemical transmitter (hormone) by specialized cells; carried to a distant site of activation via the blood

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2
Q

Neuroendocrine communication

A

hybrid of neural and endocrine communication; release of “neurohormone”; carried to a distant site of action via blood

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3
Q

Paracrine communication

A

cells secrete chemical transmitters locally; the target cells are near “neighbors” and are reached by diffusion of the hormone

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4
Q

Autocrine

A

cell regulates itself by release of a chemical messenger

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5
Q

Protein/Peptide hormones

A

largest group
post-translationally processed to active hormone
released via exocytosis from secretory granules

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6
Q

Steroid hormones

A

derived from cholesterol
synthesized by adrenal cortex, testes/ovaries, placenta
lipid-soluble, travel bound to binding proteins
bind to cytosolic or nuclear receptors

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7
Q

Amines/Amino acid derivative hormones

A

derived from tyrosine

norepi, epi, dopamine, thyroid hormones

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8
Q

What are hormones made out of?

A

Proteins/peptides
steroids
amines/amino acid derivatives

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9
Q

Peptide hormones

A 
water soluble 
does NOT use carrier protein in plasma 
stored in vesicles prior to secretion 
mainly secondary messengers 
FAST onset but short acting response 
receptors on the plasma membrane
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10
Q

Steroid Hormones

A 
not water soluble 
need carrier protein in plasma 
not stored in vesicles 
intracellular receptors 
mainly altered gene expression 
slow onset but long-lasting responses
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11
Q

Which type of hormones have the longest acting response?

A

Steroid

slower onset

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12
Q

Which type of hormone class is water soluble?

A

peptide

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13
Q

Which type of hormone class is stored in vesicles?

A

peptide

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14
Q

Corticotropic-releasing hormone (CRH)

A

hypothalamus
peptide hormone
stimulates adrenocorticotropic hormone (ACTH)

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15
Q

ACTH

A

secreted from anterior pituitary
peptide hormone
trophic to adrenal cortex
stimulates synthesis and secretion of cortisol, aldosterone, and androgens

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16
Q

How can you have an abnormal function of hormones?

A
  • excess of deficiency of hormone (genetics, agonists, antagonists)
  • decreased receptor number (genetics, downregulation)
  • decreased receptor function (genetics, pathophysiologial)
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17
Q

What affects the half life of hormones?

A

protein binding can increase half life and delay onset of action

metabolism
number or receptors available
clearance

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18
Q

The plasma free hormone concentration is affected by:

A

rate of secretion
rate of elimination (excretion + metabolism)
extent of hormone binding to plasma proteins

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19
Q

Hormone release may oscillate relative to:

A

circadian rhythms
in response to timing of meals
as regulated by other pattern generators

you can’t take a snapshot of hormone levels –have to watch it overtime

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20
Q

Why do we have growth hormone?

A

linear growth in growing ages
maintain lean body mass in adult

highest in puberty but still present in adulthood

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21
Q

What hormones are produced in the adrenal cortex?

A

corticosteroids
mineralocorticoids
androgens

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22
Q

What hormones are produced in the adrenal medulla?

A

epi

norepi

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23
Q

Where is cortisol secreted?

A

in the zona fascilculata in the adrenal cortex

24
Q

Conn syndrome

A

primary aldosteronism

excess secretion of aldosterone due to adrenal disease

K+ depletion
Na+ retention
HTN

25
Secondary aldosteronism is dependent on what?
renin
26
What inhibits synthesis of steroids?
Ketoconazole Metyrapone Mitotatane (kills adrenal cortical cells)
27
What are the effects of growth hormone?
1) uses fat (increase in free fatty acid uptake by cells via increases LDL receptors, so cells use fatty acid for energy) 2) saves glucose for brain (hyperglycemia d/t no glucose being absorbed by cells) 3) builds muscle (decrease plasma AA)
28
What are the effects of Insulin?
STORAGE 1) increase fat storage by increasing VLDL in liver 2) decrease plasma glucose (increase glycolysis and glycogen production) 3) builds muscle (decrease plasma AA)
29
What is the GH Axis?
hypothalamus releases GHRH which stimulates the pituitary which releases GH which stimulates many things including the liver which produces IGF1 which negatively feeds back to the pituitary
30
What does IGF1 do?
used in fetal production (as well as normally in adulthood) - stores fat - decreases plasma glucose - builds muscle (builds muscle better when with GH) causes growth proliferation and apoptosis suppression in visceral organs, cartilage, bone, skin, and muscles (risk of tumor production)q
31
What are the different causes of increased GH production?
pituitary adenoma ectopic tumor producing GH (lymphoma) ectopic tumor producing GHRH (small cell carcinoma)
32
What labs would you expects to see with someone who has a pituitary adenoma?
high GH possibly high PL low every other hormone from the anterior pituitary
33
What is the difference between adults and children with excessive GH?
children - giantism adults - acromegaly both end up with type 2 DM d/t increase insulin and glucose and insulin resistance
34
What will you see in people with GH deficiency?
kids - dwarfism adults - fatigue, obesity, decrease in muscle mass, increase in LDL, decrease in heart function
35
How do you dx insulin deficiency?
in a non DM pt -- given insulin and then check GH --- a normal person would have increase GH in response to decrease in glucose in a DM pt - give GHRF and arginine IV expect to see GH increase in normal person
36
How do you measure GH level?
better to measure it indirectly via IGF1 since GH fluctuates throughout the day
37
How do the cells in islets of langerhan communicate?
gap junctions
38
What do alpha cells in the pancreas produce?
glucagon
39
Where is insulin produced?
beta cells in pancreas
40
What do delta cells in the pancreas produce?
somatostatin
41
Why is glucose control so important?
damage cells if too high
42
How does insulin get released?
via GLUT2 transporter glycolysis produces ATP that blocks K+ channels, depolarizing the membrane and causing an influx of Ca2+ which stimulates insulin release (Ca2+ stimulated exocytosis)
43
What are stimulants of insulin release?
``` glucose fatty acids hormones (incretins, secretin) parasympathetic stimulation B2 agonist ```
44
Incretins
released from intestine cells to stimulate pancreas to release insulin
45
What are inhibitors of insulin?
sympathetic stimulation (although it stimulates beta 2 receptors it inhibits alpha receptors causing an overall inhibitory effect) somatostatin insulin (neg feedback) beta antagonists
46
GLUT4
insulin promotes relocation of this transported to the membrane of muscle and fat cells
47
What happens when you have chronic insulin activation?
receptor internalization and down regulation of response
48
What is insulins effect?
Seconds: - AA uptake - glucose uptake Minutes: - activation of glycolytic enzymes, glycogen synthase, lipid signaling - inhibits glycogen phosporylase and glyconeogenesis Hours: - gene transcription - cell growth differentiation
49
What stimulates glucagon?
hypoglycemia epinephrine vagal stimulation
50
What inhibits glucagon?
hyperglycemia | somatostatin
51
What do catecholamines do to glucose and insulin?
increase blood glucose | inhibit insulin secretion
52
What do glucocorticoids and GH do to glucose and insulin?
increase blood glucose | decrease insulin sensitivity
53
What stimulates somatostatin?
glucose AA fatty acids
54
Where in the body is the bulk of glucose taken up?
skeletal muscle
55
Adipokines
adipose tissues release this hormone to aide in insulin's effect
56
Leptin
made in fat (levels vary based on how much fat a person has) works in the brain to decrease appetite the body becomes desensitized to leptin once you become too fat
57
How can excessive exercise in a DM pt precipitate hypoglycemia?
exercise increases the # of GLUT4 transporters on the skeletal muscle cells increasing the about of insulin that can bind and allow glucose into the cells

Clin Med - Endocrine (13 decks)

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