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AAW - Endo/Repro > Test 1 > Flashcards

Test 1 Flashcards

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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
you see colloid | where are you in the pituitary
pars distalis
26
acidophils release what hormones
GH PRL (PRoLactin) acidophiles grow tits
27
the basophils of the pituitary
thyrotrophs - produce TSH gonadotrophs - produce FSH and LH corticotrophs - produce ACTH
28
herring bodies
dilatations of the axon terminals in the pars nervosa that contain stored hormone
29
what type of receptor does growth hormone inhibiting hormone (aka somatostatin) work on
works on Gi (to decrease cAMP and activate K channels) D2 receptor
30
JAK/STAT is downstream of activation of what receptor
tyrosine kinase (example is GH)
31
what produces insulin like growth factor
liver
32
what is more better at make epiphysial plate grow in kid IGF-1 (insulin like growth factor) or GH
IGF-1 ya dingle
33
growth hormone releasing hormone is secreted from where
hypothalamus
34
laron syndrome
autosomal recessive GH *receptor* doesn't work as well imparts resistance to cancer and diabetes and prolongs life span
35
how do assess whether or not the pituitary can release GH
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
36
somatropin
recombinant human growth hormone
37
mecasermin what is it used in what patients
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)
38
pegvisomant
GH receptor antagonist makes you short as a peg
39
Txs for GH hypersecretion | three examples
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
40
prolactin and oxytocin - which causes milk formation? which causes secretion?
prolactin - formation | oxytocin - secretion
41
cabergoline
preferred to other dopamine agonists in use for prolactinoma because it has higher efficacy in normalizing prolactin, and higher frequency of pituitary tumor shrinkage
42
circadian signals from the eye are sent to the _________ nucleus and the ________ganglion
suprachiasmatic nucleus (SCN) and the superior cervical ganglia
43
what cells secrete calcitonin
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)
44
thyroid hormone - amine, protein, or steroid?
amine - tyrosine derivative
45
small, most numerous eosinophilic cells in the parathyroid what do they secrete
chief secrete PTH
46
RANK ligand
secreted from osteoblasts when they are bound with PTH RANK ligand causes osteoclasts to resorb bone
47
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?
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
calcium usually causes exocytosis when does it inhibit is?
inhibits PTH (negative feedback) renin secretion is suppressed by Ca (bizarre tracht fact)
49
T3 and T4 which has longer half life which has more activity
T3 - more activity - | T4 - longer half life - circulates blood mostly as this, gets converted into T3 in cells
50
how is iodide uptaken
symported with sodium (sodium concentration gradient is the driver)
51
thioamides
e.g. propylthiouracil - thyroglobulin peroxidase inhibitor antithyroid used in thyrotoxicosis, graves disease
52
what is responsible for the secretion of melitonin in the brain
pinealocytes
53
where are the following dervied from in the adrenal gland Cortex Medulla
cortex: mesoderm medulla: neural crest
54
the names of the layers of the adrenal cortex in order from outer to inner
zona: glomerulosa - cells in ovoid groups or cords fasciculata reticularis
55
where in the adrenal gland is aldosterone produced?
zona glomerulosa
56
where are most androgens and estrogens made in the adrenal
zona reticularis (but fasiculata also makes some)
57
where in most of the cortisol made in the adrenal
zona fasiculata
58
where is most of the NE made in the adrenal
in the medulla
59
what binds to the mineralocorticoid receptors
aldosterone and cortisol (even though it is a glucocorticoid)
60
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
cortisol is enzymatically converted to cortisone
61
what does licorice do? *tract fact*
prevents the conversion of cortisol to cortisone made his friend gain weight
62
what converts prednisone to prednisolone
liver 11b-hydroxyhydrogenases
63
fludrocortisone
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
metyrapone
inhibits 11 beta hydroxylase in the adrenal gland with the goal of interfering with cortisol production used for cushings
65
does dexamethasone suppress ACTH?
yes in cushing no in ectopic ACTH secretion (e.g. small cell)
66
MODY2
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
what is the major cell amplification signal of insulin binding
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
wtf is CREB
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
wtf is FoxO1
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
mech of metformin
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
drug that can slow the growth of a prolactinoma
dopamine agonist (bromocriptine or cabergoline)
72
what type of nodules in the thyroid are almost always benign
hot nodules AND cold nodules but cold ones are more assc with malignancy (10%)
73
myxedema is assc with what thyroid thing
hypothyroidism
74
you have what looks like an adenoma in the thyroid why do you always take it out
because follicular carcinoma can look just like an adenoma
75
osteitis fibrosa cystica
punched out lesions of bone from hyperparathyroidism
76
most common cause of secondary hyperparathyroidism
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
chvostek sign | trousseau sign
chvostek - tap the facial nerve and it causes facial twitching Trousseau - BP cuff inflation causes arm twitching signs of hypoparathyroidism and low Ca
78
describe a dexamethasone suppression test
**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
what is the super important* way that glucose causes release of insulin from the beta cells *from trachte's prespective
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
bone density scan numbers
>-1 standard deviation, you're fine between -1 and -2.5 standard deviations, you have osteopenia less than -2.5, osteoporosis
81
why don't you give nonselective beta blockers in diabetes
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
why do you get more insulin release if you eat a meal rather than if you give IV glucose
GLP-1 and GIP (glucose dependent insulinotropic peptide (old name is gastric inhibitory peptide))
83
three things that the beta cells secrete
insulin c-peptide amylin
84
what do you give to slow down the progression of diabetic nephropathy two examples
ACEs ARBs
85
give an example of a biguanide
metformin
86
give 3 examples of a second gen sulfonylurea mech?
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
diabetes meds that make people feel full
amylin analogs - pramlintide GLP-1 agonists - Exenatide, Liraglutide
88
what drugs can be used in diabetes that decreases glucose absorption
SGLT2 inhibitors decrease reabsorption of glucose in the PCT also the α-glucosidase inhibitors: Acarbose Miglitol
89
rapid acting insulins
lispro aspart glulisine
90
long acting lisulins
detemir (levemir) | glargine (lantus)
91
what ketone is especially high in DKA
beta-hydroxybutyrate
92
what is the fluid status of someone in DKA usually *on the test*
deficits are typically 100 ml per kg | 70kg would be down 7L
93
initial resuscitation for severe dehydration
15-20ml/kg normal saline also she said "1L, 1L, 1L, then 500ml X 4 hrs"
94
when do you take a person with DKA off of normal saline what do you switch to
when their glucose goes below 250 then switch to D5W/.45% normal saline (half normal saline)
95
cellular mech of GLP-1
stimulates adenylyl cyclase, so that you get more intracellular Ca in the beta cells, so you secrete more insulin
96
what is the relation between alpha2 receptors and insulin
they repress the secretion of insulin
97
GHRH binds what kid of receptor
cAMP
98
what type of receptor does IGF-1 bind to
intrinsic tyrosine kinase (MAP kinase pathway)
99
what type of receptor does TRH bind to
its called TRH receptor its downstream effects are increased IP3
100
GH binds to what type of receptor
receptor associated tyrosine kinase
101
TSH binds what kind of receptor
cAMP
102
glinides mech
same as the sulfonylureas close the potassium channel on the beta cell, which causes the cell to depolarize and release insulin
103
how do the incretins work to secrete insulin (GLP-1)
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
what closes K channels in the beta cells (name two types of drugs)
sulfonylureas (glipizide, glimepiride, glyburide) meglitinides (repaglinide, nateglinide) - not in FA
105
what activates adenylyl cyclase on the beta cell causing insulin release
GLP analogs DPP IV inhibitors
106
thyrotropin releasing hormone acts on what receptors?
Gq (IP3 is downstream) for all the Gqs think GOAT HAG (mneumonic in FA)
107
Corticotropin releasing hormone (CRH) acts of what receptors secreted from where
Gs C in ChAMP hypothalamus (then goes to the pituitary and causes ACTH secretion)
108
ACTH acts on what receptors
Gs A in FLAT
109
Propylthiouracil
Thyroglobulin peroxidase inhibitor - used in graves diesase
110
eplerenone
mineralocorticoid receptor antagonist just like spironolactone (used to treat hyperaldosteronism)

AAW - Endo/Repro (3 decks)

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