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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
Q

Secondary aldosteronism is dependent on what?

A

renin

26
Q

What inhibits synthesis of steroids?

A

Ketoconazole
Metyrapone
Mitotatane (kills adrenal cortical cells)

27
Q

What are the effects of growth hormone?

A

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
Q

What are the effects of Insulin?

A

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
Q

What is the GH Axis?

A

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
Q

What does IGF1 do?

A

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
Q

What are the different causes of increased GH production?

A

pituitary adenoma
ectopic tumor producing GH (lymphoma)
ectopic tumor producing GHRH (small cell carcinoma)

32
Q

What labs would you expects to see with someone who has a pituitary adenoma?

A

high GH
possibly high PL
low every other hormone from the anterior pituitary

33
Q

What is the difference between adults and children with excessive GH?

A

children - giantism

adults - acromegaly

both end up with type 2 DM d/t increase insulin and glucose and insulin resistance

34
Q

What will you see in people with GH deficiency?

A

kids - dwarfism

adults -
fatigue, obesity, decrease in muscle mass, increase in LDL, decrease in heart function

35
Q

How do you dx insulin deficiency?

A

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
Q

How do you measure GH level?

A

better to measure it indirectly via IGF1 since GH fluctuates throughout the day

37
Q

How do the cells in islets of langerhan communicate?

A

gap junctions

38
Q

What do alpha cells in the pancreas produce?

A

glucagon

39
Q

Where is insulin produced?

A

beta cells in pancreas

40
Q

What do delta cells in the pancreas produce?

A

somatostatin

41
Q

Why is glucose control so important?

A

damage cells if too high

42
Q

How does insulin get released?

A

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
Q

What are stimulants of insulin release?

A 
glucose 
fatty acids
hormones (incretins, secretin) 
parasympathetic stimulation 
B2 agonist
44
Q

Incretins

A

released from intestine cells to stimulate pancreas to release insulin

45
Q

What are inhibitors of insulin?

A

sympathetic stimulation (although it stimulates beta 2 receptors it inhibits alpha receptors causing an overall inhibitory effect)
somatostatin
insulin (neg feedback)
beta antagonists

46
Q

GLUT4

A

insulin promotes relocation of this transported to the membrane of muscle and fat cells

47
Q

What happens when you have chronic insulin activation?

A

receptor internalization and down regulation of response

48
Q

What is insulins effect?

A

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
Q

What stimulates glucagon?

A

hypoglycemia
epinephrine
vagal stimulation

50
Q

What inhibits glucagon?

A

hyperglycemia

somatostatin

51
Q

What do catecholamines do to glucose and insulin?

A

increase blood glucose

inhibit insulin secretion

52
Q

What do glucocorticoids and GH do to glucose and insulin?

A

increase blood glucose

decrease insulin sensitivity

53
Q

What stimulates somatostatin?

A

glucose
AA
fatty acids

54
Q

Where in the body is the bulk of glucose taken up?

A

skeletal muscle

55
Q

Adipokines

A

adipose tissues release this hormone to aide in insulin’s effect

56
Q

Leptin

A

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
Q

How can excessive exercise in a DM pt precipitate hypoglycemia?

A

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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