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AAW - Endo/Repro > Test 1 > Flashcards

Test 1 Flashcards

1
Q

Look at “first aid in brainscape AAW - Endo/Repro”

A

:) - there is a lot of stuff on there that isn’t covered in class, but the drug stuff on there was and it is important!

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2
Q

if you cut off circulation to the pituitary, what hormone actually goes up in the body?

A

prolactin

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3
Q

main prolactin inhibitory factor

A

Dopamine acting on D2 receptors

dopamine agonists (bromocriptine, cabergoline) are the Tx for prolactin secreting tumors

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4
Q

two main posterior pituitary hormones

A

ADH, Oxytocin

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5
Q

patient has endocrine problems and darkened skin

what do you have not enough of? too much of?

A

Too little cortisol

Too much ACTH (in attempt to stimulate cortisol) and MSH

increase ACTH hormone release can cause melanocyte stimulating hormone release

can see this is addison disease, a deficiency of aldosterone and cortisol (

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6
Q

rate limiting step in catecholamine synthesis

A

tyrosine hydroxylase converts tyrosine into DOPA

DOPA goes on to be converted to dopamine via DOPA decarboxylase and vit B6

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7
Q

do you want a constant flow of estrogen when you are on birth control?

A

no, you need it in pulses do you don’t desensitize the receptors

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8
Q

insulin, growth hormone and prolactin all have what in common with their receptors

A

they are tyrosine kinase receptors

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9
Q

tumor secreting cortisol

what low levels of other things are you going to see

A

ACTH and CRH

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10
Q

two disease states that can cause increased ACTH

A

addisons (compensating for low cortisol)

cushing’s (pituitary tumor)

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11
Q

do endocrine glands have ducts?

A

na

they are very vascular

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12
Q

cells that are mesodermally derived produce what types of hormones

endo or ectoderm?

A

mesoderm - steroid hormones

endo, ectoderm - amino acid derivatives (pituitary, thyroid, parathyroids, pancreatic islets)

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13
Q

thyroid hormones - where is the receptor - intracellular or cell surface?

A

intracellular, just like steroids

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14
Q

anterior lobe of the pituitary derived from what? posterior?

A

anterior - oropharynx (from pouch of rathke)

posterior - neuroectoderm

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15
Q

where do these areas of the pituitary come from:

Pars tuberalis
Pars nervosa
Pars distalis
Pars intermedia

A

everything besides Pars nervosa is derived from the ectoderm of the oropharynx (rathke’s pouch)

Pars nervosa derived from neuroectoderm (posterior)

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16
Q

infundibulum is derived form what part of the pituitary

A

the neural ectoderm

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17
Q

the hypophyseal portal system of veins delivers neurosecretory hormones from the primary capillary plexus of the median eminence to the secondary capillary plexus of what part of the pituitary

A

pars distalis

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18
Q

mammotropes
secrete what
acidophilic or basophilic?

A

secrete prolactin
acidophilic
increase during pregnancy and lactation

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19
Q

gonadotropes

in what part of the pituitary
secrete what
acidophilic or basophilic?

A

largest cells in the adenohypophysis

secrete follicle stimulating hormone and lutenizing hormone (LH) in females or interstitial stimulating hormone (ICSH) in male

Basophilic

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20
Q

corticotropes
secrete?
acidophilic or basophilic?

A

ACTH
MSH

basophilic

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21
Q

pars intermedia - what does it release

A

MSH

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22
Q

pituicytes

A

specialized neuroglial cells found throughout posterior lobe of pituitary

“supportive” cells

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23
Q

somatotropes produce what hormone

acidophilic or basophilic?

A

GH

acidophilic

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24
Q

cell bodies of the posterior pituitary lie where

A

supraoptic nuclei

paraventricular nuclei

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25
Q

you see colloid

where are you in the pituitary

A

pars distalis

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26
Q

acidophils release what hormones

A

GH
PRL (PRoLactin)

acidophiles grow tits

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27
Q

the basophils of the pituitary

A

thyrotrophs - produce TSH
gonadotrophs - produce FSH and LH
corticotrophs - produce ACTH

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28
Q

herring bodies

A

dilatations of the axon terminals in the pars nervosa that contain stored hormone

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29
Q

what type of receptor does growth hormone inhibiting hormone (aka somatostatin) work on

A

works on Gi (to decrease cAMP and activate K channels)

D2 receptor

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30
Q

JAK/STAT is downstream of activation of what receptor

A

tyrosine kinase (example is GH)

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31
Q

what produces insulin like growth factor

A

liver

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32
Q

what is more better at make epiphysial plate grow in kid

IGF-1 (insulin like growth factor) or GH

A

IGF-1 ya dingle

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33
Q

growth hormone releasing hormone is secreted from where

A

hypothalamus

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34
Q

laron syndrome

A

autosomal recessive GH receptor doesn’t work as well

imparts resistance to cancer and diabetes and prolongs life span

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35
Q

how do assess whether or not the pituitary can release GH

A

inject arginine over 30 min IV
then inject GHRH 1mcg over 1 min

watch serum growth hormone levels

OR

give them an insulin tolerance test - insulin will cause a more sharp decrease in serum glucose

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36
Q

somatropin

A

recombinant human growth hormone

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37
Q

mecasermin

what is it
used in what patients

A

recombinant human IGF-1

not as effective as GH in children who can respond to growth hormone (so you can give it to someone who has Laron syndrome)

can cause hypoglycemia (because it is insulin like) (GH would cause hyperglycemia)

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38
Q

pegvisomant

A

GH receptor antagonist

makes you short as a peg

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39
Q

Txs for GH hypersecretion

three examples

A

dopamine agonists (bromocriptine (ergot), pramipexole, ropinirole (non-ergot) (also used for parkinsons)

OR

somatostatin analogs (octreotide)

OR

newer tx include GH receptor antagonists like pegvisomant

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40
Q

prolactin and oxytocin - which causes milk formation? which causes secretion?

A

prolactin - formation

oxytocin - secretion

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41
Q

cabergoline

A

preferred to other dopamine agonists in use for prolactinoma because it has higher efficacy in normalizing prolactin, and higher frequency of pituitary tumor shrinkage

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42
Q

circadian signals from the eye are sent to the _________ nucleus and the ________ganglion

A

suprachiasmatic nucleus (SCN) and the superior cervical ganglia

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43
Q

what cells secrete calcitonin

A

parafollicular cells (c-cells) in the thyroid

new research shows that they are derived from pharyngeal endoderm, not neural crest (same with cells in the parathyroid)

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44
Q

thyroid hormone - amine, protein, or steroid?

A

amine - tyrosine derivative

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45
Q

small, most numerous eosinophilic cells in the parathyroid

what do they secrete

A

chief

secrete PTH

46
Q

RANK ligand

A

secreted from osteoblasts when they are bound with PTH

RANK ligand causes osteoclasts to resorb bone

47
Q

what does thyrotropin releasing hormone do and what is the cascade? what cells?

what does thyroid stimulating hormone do and what is THAT cascade? what cells?

A

TRH: causes release and synthesis of thyroid stimulating hormone (TSH) through a PLC IP3 pathway (Gq) in thyrotroph cells of the anterior pituitary

TSH: binds Gs, increasing cAMP. release of T3 and T4 in the follicular cells

48
Q

calcium usually causes exocytosis

when does it inhibit is?

A

inhibits PTH (negative feedback)

renin secretion is suppressed by Ca (bizarre tracht fact)

49
Q

T3 and T4

which has longer half life
which has more activity

A

T3 - more activity -

T4 - longer half life - circulates blood mostly as this, gets converted into T3 in cells

50
Q

how is iodide uptaken

A

symported with sodium (sodium concentration gradient is the driver)

51
Q

thioamides

A

e.g. propylthiouracil - thyroglobulin peroxidase inhibitor

antithyroid

used in thyrotoxicosis, graves disease

52
Q

what is responsible for the secretion of melitonin in the brain

A

pinealocytes

53
Q

where are the following dervied from in the adrenal gland

Cortex
Medulla

A

cortex: mesoderm
medulla: neural crest

54
Q

the names of the layers of the adrenal cortex in order from outer to inner

A

zona:

glomerulosa - cells in ovoid groups or cords
fasciculata
reticularis

55
Q

where in the adrenal gland is aldosterone produced?

A

zona glomerulosa

56
Q

where are most androgens and estrogens made in the adrenal

A

zona reticularis (but fasiculata also makes some)

57
Q

where in most of the cortisol made in the adrenal

A

zona fasiculata

58
Q

where is most of the NE made in the adrenal

A

in the medulla

59
Q

what binds to the mineralocorticoid receptors

A

aldosterone and cortisol (even though it is a glucocorticoid)

60
Q

what makes some receptors in the body responsive to aldosterone and not cortisol, even though they act on the same receptor and there is a hell of a lot more cortisol in circulation

A

cortisol is enzymatically converted to cortisone

61
Q

what does licorice do? tract fact

A

prevents the conversion of cortisol to cortisone

made his friend gain weight

62
Q

what converts prednisone to prednisolone

A

liver 11b-hydroxyhydrogenases

63
Q

fludrocortisone

A

replacement therapy for adrenal insufficiency

glucocorticoid that is also a mineralcorticoid, so it is used if destruction of the adrenal gland includes the cortex

64
Q

metyrapone

A

inhibits 11 beta hydroxylase in the adrenal gland with the goal of interfering with cortisol production

used for cushings

65
Q

does dexamethasone suppress ACTH?

A

yes in cushing

no in ectopic ACTH secretion (e.g. small cell)

66
Q

MODY2

A

Maturity onset diabetes of the young type 2

mutations in glucokinase in the Beta cells make it so they cannot generate ATP to power the potassium channels (which pump out potassium, leading to Ca influx and insulin release)

67
Q

what is the major cell amplification signal of insulin binding

A

PKB –> (P)-glycogen synthase kinase (inactive) –x–| glycogen synthase

it also phosphorylates protein phosphatase-1, which dephosphorylates glycogen synthase.

basically insulin means you get no phosphorylation of glycogen synthase, so glycogen synthase is active!

B for Beta cell

68
Q

wtf is CREB

A

active in fasted state

something that is phosphorylated by PKA (in, for example glucagon binding to a receptor)

it activates PGC1alpha, a transcriptional coactivator

69
Q

wtf is FoxO1

A

something that is phosphorylated when insulin binds. when it is phosphorylated, it is held in the cytoplasm, so it can’t go into the nucleus and cause PEPCK activation

this process stops gluconeogenesis

70
Q

mech of metformin

A

AMP mimetic

activates LKB1, which phosphorylates and activates AMPK. AMPK phosphorylates TORC2, preventing its nuclear localization, which prevents release of glucose from the liver

71
Q

drug that can slow the growth of a prolactinoma

A

dopamine agonist (bromocriptine or cabergoline)

72
Q

what type of nodules in the thyroid are almost always benign

A

hot nodules AND cold nodules

but cold ones are more assc with malignancy (10%)

73
Q

myxedema is assc with what thyroid thing

A

hypothyroidism

74
Q

you have what looks like an adenoma in the thyroid

why do you always take it out

A

because follicular carcinoma can look just like an adenoma

75
Q

osteitis fibrosa cystica

A

punched out lesions of bone from hyperparathyroidism

76
Q

most common cause of secondary hyperparathyroidism

A

renal failure (you can’t excrete phosphate, which makes your calcium levels chronically low, which causes high PTH)

also poor diets in calcium or vit D def.

77
Q

chvostek sign

trousseau sign

A

chvostek - tap the facial nerve and it causes facial twitching

Trousseau - BP cuff inflation causes arm twitching

signs of hypoparathyroidism and low Ca

78
Q

describe a dexamethasone suppression test

A

**If cortisol is suppressed by only high doses: cushings desease (pituitary adenoma)

give low dose dexamethasone, if their cortisol levels do not decrease and:

they have low ACTH: primary hypercortisolism is likely (cushing syndrome)

they have ACTH in the hundreds: ectopic ACTH syndrome (cushing disease) (something is secreting too much ACTH, like small cell lung cancer) (the ATCH in this case is “fake”)

(measure the ACTH first)

79
Q

what is the super important* way that glucose causes release of insulin from the beta cells

*from trachte’s prespective

A

glucose binds to the pancreatic beta cell, which causes ATP to be secreted from the mitochondria, which inhibits a potassium channel, depolarizing the cell

this causes an influx of Ca and a release of insulin

(the reason that thiazides cause hyperglycemia is because they keep this channel K channel open)

80
Q

bone density scan numbers

A

> -1 standard deviation, you’re fine

between -1 and -2.5 standard deviations, you have osteopenia

less than -2.5, osteoporosis

81
Q

why don’t you give nonselective beta blockers in diabetes

A

because it blocks the persons ability to crank up their glucose levels

(strongest stimulus for glycogenolysis in the muscle cells in epinephrine acting through beta 2 receptors)

82
Q

why do you get more insulin release if you eat a meal rather than if you give IV glucose

A

GLP-1

and

GIP (glucose dependent insulinotropic peptide (old name is gastric inhibitory peptide))

83
Q

three things that the beta cells secrete

A

insulin
c-peptide
amylin

84
Q

what do you give to slow down the progression of diabetic nephropathy

two examples

A

ACEs ARBs

85
Q

give an example of a biguanide

A

metformin

86
Q

give 3 examples of a second gen sulfonylurea

mech?

A

glipizide, glimepiride, glyburide

bind to the ATP K channel in beta cells, closing it and causing a depolarization, which causes insulin release

for mechs of all the drugs that we talked about that are also in first aid, go look at First Aid in Brainscape :)

87
Q

diabetes meds that make people feel full

A

amylin analogs - pramlintide

GLP-1 agonists - Exenatide, Liraglutide

88
Q

what drugs can be used in diabetes that decreases glucose absorption

A

SGLT2 inhibitors decrease reabsorption of glucose in the PCT

also the α-glucosidase inhibitors:
Acarbose
Miglitol

89
Q

rapid acting insulins

A

lispro
aspart
glulisine

90
Q

long acting lisulins

A

detemir (levemir)

glargine (lantus)

91
Q

what ketone is especially high in DKA

A

beta-hydroxybutyrate

92
Q

what is the fluid status of someone in DKA usually on the test

A

deficits are typically 100 ml per kg

70kg would be down 7L

93
Q

initial resuscitation for severe dehydration

A

15-20ml/kg normal saline

also she said “1L, 1L, 1L, then 500ml X 4 hrs”

94
Q

when do you take a person with DKA off of normal saline

what do you switch to

A

when their glucose goes below 250

then switch to D5W/.45% normal saline (half normal saline)

95
Q

cellular mech of GLP-1

A

stimulates adenylyl cyclase, so that you get more intracellular Ca in the beta cells, so you secrete more insulin

96
Q

what is the relation between alpha2 receptors and insulin

A

they repress the secretion of insulin

97
Q

GHRH binds what kid of receptor

A

cAMP

98
Q

what type of receptor does IGF-1 bind to

A

intrinsic tyrosine kinase (MAP kinase pathway)

99
Q

what type of receptor does TRH bind to

A

its called TRH receptor

its downstream effects are increased IP3

100
Q

GH binds to what type of receptor

A

receptor associated tyrosine kinase

101
Q

TSH binds what kind of receptor

A

cAMP

102
Q

glinides mech

A

same as the sulfonylureas

close the potassium channel on the beta cell, which causes the cell to depolarize and release insulin

103
Q

how do the incretins work to secrete insulin (GLP-1)

A

increase cAMP in the beta cell

(remember that the DPP-4 inhibitors stop the breakdown of this crap)

its one thing he talked about that isn’t in first aid under what increases cAMP (FLAT ChAMP)

104
Q

what closes K channels in the beta cells (name two types of drugs)

A

sulfonylureas (glipizide, glimepiride, glyburide)

meglitinides (repaglinide, nateglinide) - not in FA

105
Q

what activates adenylyl cyclase on the beta cell causing insulin release

A

GLP analogs

DPP IV inhibitors

106
Q

thyrotropin releasing hormone acts on what receptors?

A

Gq (IP3 is downstream)

for all the Gqs think GOAT HAG (mneumonic in FA)

107
Q

Corticotropin releasing hormone (CRH) acts of what receptors

secreted from where

A

Gs

C in ChAMP

hypothalamus (then goes to the pituitary and causes ACTH secretion)

108
Q

ACTH acts on what receptors

A

Gs

A in FLAT

109
Q

Propylthiouracil

A

Thyroglobulin peroxidase inhibitor - used in graves diesase

110
Q

eplerenone

A

mineralocorticoid receptor antagonist just like spironolactone (used to treat hyperaldosteronism)

AAW - Endo/Repro (3 decks)

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