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Endocrine (F.A.) Flashcards

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1
Q

embryology of thyroid?

A

starts as diverticulum at pharynx floor. descends into neck with origin being foramen cecum, connection being thyroglossal duct

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2
Q

thyroglossal duct cyst

A

midline, moves with tongue movement

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3
Q

thyroid tissue is derived from what type of embryological tissue

A

endoderm

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4
Q

Adrenal gland outside to inside layers

A

capsule-> CORTEX( zona glomerulosa -> zona fasciculata) -> zona reticularis -> medulla

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5
Q

Z. Glomerulosa makes what category of hormone, and specifically?
its regulated by?

A

Mineralocorticoids, Aldosterone

Angiotensin II

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6
Q

Z. fasciculata makes what category of hormone, and specifically?
its regulated by?

A

Glucocorticoids, Cortisol

ACTH, CRH

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7
Q

Z. Reticularis makes what category of hormone, and specifically? its regulated by?

A

Androgens, DHEA

ACTH CRH

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8
Q

MEDULLA of adrenal gland makes? regulated by

A

catecholamines- Epi, NE

sympathetic preganglionic nerves (Ach)

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9
Q

anterior pituitary derived from

A

“Rathke’s Pouch”

Oral Ectoderm

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10
Q

anterior pituitary secretions

A

FLAT PiG= FSH, LH, ACTH, TSH, Prolactin, Growth H

the “FLAT” is basophilic, Prl and GH are acidophilic

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11
Q

what does intermediate lobe secrete

A

MSH

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12
Q

what does posterior lobe secrete

A

Oxytocin, ADH (vasopressin)

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13
Q

neurophysin

A

carrier protein brings Oxy and ADH from hypothalamus to post pit for storage and release

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14
Q

post pit embryology

A

neuroectoderm

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15
Q

islets of Langerhaans morphology

A

pancreatic buds
alpha on the outside- glucagon
B in the middle- insulin
delta- interspersed and few- somatostatin

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16
Q

parafollicular cells (C cells) are derived from what tissue type?

A

NCC

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17
Q

17 alpha OH deficiency symptoms

A

increase in aldosterone (high BP, low K), but decrease in cortisol and sex steroids
so ambiguous genitalia (if male), or late 2ndary sex devpt (if female) with HIGH BP

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18
Q

21 OH deficiency symptoms

A

increase in sex steroids, but decrease in aldosterone (salt wasting) and cortisol production
so hypervirile with LOW BP and HIGH K+

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19
Q

11 Beta OH deficiency symptoms

A

increase in sex steroids and 11 deoxycorticosterone
decrease in aldosterone and cortisol.
so hypervirile, but HIGH BP because 11 deoxy corticosterone results in high BP and K+ LOW

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20
Q

ADH

A

made in: hypothalamus
store and release: post pit
actions: V2 at principle renal cells at CD- increase AQP so increase water reabsorption
actions: V1 for increasing BP

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21
Q

Ghrelin

A

made by: stomach
effects: hunGHRE aka orexigenic and increase GH
ghrelin promoters: sleep deprivation and Prader Willi

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22
Q

Leptin

A

made by: adipose tissue
effects: Satiety “leptin keeps you thin”
leptin is inhibited by: sleep deprivation and starvation state

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23
Q

Growth Hormone

A

pulsatile release by anterior pit
stimulated by GHRH (hypothalamus) and inhibited by Somatostatin (pancreatic delta)
effects: causes increase in IGF1 (somatomedin) release by liver which causes bone and muscle growth

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24
Q

Prolactin

A

released by ant pit
release stimulated by: TRH (from hypothalamus)
release inhibited by: Dopa (from hypothalamus)
effects: milk production in breast, inhibition of GnRH (by hypothalamus) which stops ovulation and spermatogenesis

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25
Prolactin looks like what other hormone ?
Growth Hormone
26
what drug inhibits prolactin secretion
Dopa agonist (bromocriptine)
27
what drugs stimulate prolactin secretion
Dopamine antagonists (antipsychotics) and Estrogens
28
CRH
made by: hypothalamus | effect: increase ACTH (by ant pit), increase MSH, and B-endorophins
29
Dopamine
made by: hypothalamus | effect: inhibit prolactin secretion (ant pit) and inhibit TSH (ant pit)
30
GHRH
made by: hypothalamus | effect: increase GH release by ant pit
31
GnRH
made by: hypothalamus | effect: increase LH, FSH release by ant pit
32
prolactin
made by: ant pit | effect: decrease GnRH
33
SST
made by: pancreatic delta cells | effect: decrease GH and decrease TSH
34
TRH
made by: hypothalamus | effect: increase TSH and Prl
35
Insulin made by?
pancreatic B cells in Islet of Langerhans
36
describe insulin synthesis
preproinsulin made in RER and presignal cleaved. Now the proinsulin will be stored in secretory granules. cleavage of proinsulin causes release of insulin and C-peptide
37
functions of insulin
causes glucose uptake by insulin sensitive cells (GLUT4) increases glycogen, TGs, and protein synthesis decrease lipolysis increase K+ uptake by cells decreases urinary Na+ excretion
38
GLUT 4
adipose and skm
39
GLUT 1
RBC, cornea, brain, and placenta
40
GLUT2
birectional! | pancreatic B cells, liver, kidney, SI
41
GLUT 3
brain and placenta
42
GLUT 5
sperm (fructose)
43
insulin receptor
tyrosine kinase w/ PIP3k and RAS/MAP pathway
44
how does pancreatic B cell respond to glucose
``` GLUT 2- glucose entry glycolysis makes ATP ATP sensitive K+ ch closes- depol causes Ca2+ vgc to open exocytosis of insulin ```
45
oral vs IV glucose
oral glucose causes release of incretins GLP1 and GIP which makes Bcells more sensitive to glucose causing more insulin release
46
Cortisol Actions
A BIG FIB increase in : appeitite, bmr, insulin resistance, gluconeogen/lipolysis/proteolysis a decrease in: fibroblast activity, inflammatory response (IL2), bone formation
47
why should you not give a TB patient glucocorticoids
can cause TB reactivation by inhibiting IL2
48
where is cortisol made?
Zona fasciculata of cortex of adrenal gland
49
what effects cortisol secretion
(1) CRH--> ACTH --> cortisol | (2) stress --> cortisol
50
how is Ca2+ found in the blood
45% free ions **** active! 40% bound to albumin 15% bound to other anions
51
why does pH affect Ca2+ levels
high pH levels/ basic environment will cause albumin (neg charged) to bind Ca2+ more than usual (b/c less H+ floating around to bind to) causing hypocalcemia.
52
tap cheek, facial muscles contract?
Chvostek sign | hypocalcemia
53
where do we get vit D from?
sunlight (D3)- cholecalciferol | diet (D2) - ergocalciferol
54
what happens to the vit D in our body?
chole/ergo calciferol --> 25 OH D (in liver)---> 1,25 OH D(active form) (in kidney via 1 alpha OHlase)
55
what is another name for 1,25 OH2 D
calcitriol
56
what are the actions of calcitriol
increase Ca2+ and PO43- absorption in gut
57
vit D deficiency causes?
bone mineralization problems rickets in children osteomalacia in adults
58
where is PTH made
chief cells of Parathyroid
59
what causes an increase in PTH release?
low Ca2+levels high PO43- levels slightly low Mg2+ levels (very low Mg2+ will cause PTH decrease)
60
what does PTH do
1. ) increases Ca2+ reabsorption in kidney, decreases PO43- reabsorption in kidney 2. ) stimulates kidney 1 alpha OH to make more 1,25 OH2 3. ) stimulates resorption of PO43- and Ca2+ from bone by increasing RANKL on osteoBlasts and osteoCytes making RANK expressing osteoCLasts more active
61
how does cortisol increase BP?
it increases alpha 1 receptors on blood vessels having a "permissive" effect on NE/Epi
62
what is PTHrP?
its released by malignancies (sqccl, rcc) and acts like PTH
63
what is calcitonin
only active when Ca2+ levels are very increased it helps bring them down by decreasing bone resorption of Ca2+
64
what does T3/T4 do?
4B's - brain maturation - increase BMR ( increase Na/K activity, increase glycogenolysis/lipolysis/gluconeogenesis) - helps Bone growth - increases B1 receptors on heart
65
Wolff Chaikoff Effect
Excess Iodine can inhibit thyroid peroxidase activity, decreasing T3/T4 formed temporarily
66
how does TBG levels affect thyroid hormone?
increase TBG causes decrease free T3/T4 bc it binds it!
67
what causes increased TBG levels
OCPs and pregnancy
68
what decreases TBG levels
hepatic failure
69
how does I- enter thyroid cells?
Na+/I- cotransporter
70
what does thyroid peroxidase do?
(1) oxidation of I- to I2 (2) organification of I2- allows it to bind TG making MITs and DITS (3) coupling- allows MITs and DITs to combine to make T3/T4
71
what does 5' deiodinase do?
peripheral conversion of T4 to T3 (more active)
72
what thyroid hormone is produced most by thyroid
T4
73
what thyroid hormone is most active
T3
74
what increases TSH secretion, what inhibits it
TRH (hypothalamus) | SST (delta of langerhans of pancreas)
75
hormones that use cAMP signalling
FLAT ChAMP | FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2), MSH, PTH
76
hormones that use cGMP for signalling
BAD (GRMP) | BNP, ANP, EDRF (NO)
77
hormones that use IP3 for signalling
GOAT HAG | GnRH, Oxy, ADH (v1), TRH, histamine, Ang II, Gastrin
78
hormones that use intracellular receptors for signalling
PET CAT on TV | prolactin, estrogen, testosterone, cortisol, aldosterone, T3/T4, vitamin D
79
hormones that use receptor tyrosine kinase
IGF1, insulin, FGF, PDGF, EGF
80
non-receptor tyrosine kinase
``` GH/JAK STAT cytokines prolactin erythropoeitin, thrombopoetin, G-CSF ```
81
Cushing Syndrome
excess Cortisol
82
most common cause of Cushing's Syndrom
exogenous corticosteroids
83
Cushing Syndrome due to exogenous corticosteroids show:
decreased: ACTH, CRH | the adrenal glands: bilateral atrophy
84
Cushing Syndrome caused by primary adrenal adenoma, hyperplasia or carcinoma will show?
decreased: ACTH, CRH adrenal glands- unilateral atrophy *may be accompanied by pseudohyperaldosteronism
85
Cushing Disease
a tumor of the anterior pituitary producing excess ACTH
86
Cushing disease will show
INCREASED ACTH | adrenal glands- bilateral adrenal hyperplasia
87
what is paraneoplastic acth secretion
ACTH secretion by SCLC or bronchial carcinoids that causes increased ACTH levels and bilateral adrenal hyperplasia and excess Cortisol secretion causing Cushing's Syndrome
88
how do we differentiate between Cushing disease and a paraneoplastic ACTH secreting tumor
(1) high dose Dexamethasone test -- adequate suppression of cortisol in Cushing Disease, but no change in paraneoplastic syndrome (2) CRH stimulation test- increase in ACTH and cortisol in Cushing Disease, no change in paraneoplastic syndrome
89
Adrenal Insufficiency
DECREASED cortisol levels (maybe mineralocorticoid levels)
90
diagnosing cause of adrenal insufficiency
(1) electrolytes and ACTH levels | (2) metyrapone test- blocks last step in cortisol synthesis in adrenal gland.
91
how do you interpret the metyrapone test
normal- increased ACTH, increased 11 deoxycortisol primary adrenal insufficiency- ACTH increases, but 11 deoxycortisol stays low (b/c WHOLE z.fasculata out of whack) 2/3 adrenal insufficiency- both ACTH and 11 deoxy are low
92
clinical signs of primary adrenal insufficiency
``` hyperkalemia (low aldosterone) orthostatic hypotension (low cortisol) hyperpigmentation (high ACTH, causes high MSH) metabolic acidosis weight loss (low cortisol) ```
93
Addison's disease
primary CHRONIC adrenal insufficiency (1) autoimmune cause of adrenal destruction in developed nations (2) TB destruction of adrenal in developing
94
2ndary adrenal insufficiency
decreased ACTH production due to pituitary adenoma. While cortisol levels may lower, aldosterone levels remain the same because of AngII stimulation
95
how do primary and secondary adrenal insufficiency present differently?
primary- hyperkalemia and skin pigmentation | secondary- no hyperkalemia or skin pigmentation
96
tertiary adrenal insufficiency
taking glucocorticoids and suddnely stopping. (note bc glucocorticoids mainly cause atrophy of zf, zr should be fine and aldosterone levels should be ok)
97
Hyperaldosteronism clinical signs
htt, low (or normal) K+, metabolic ALKalosis
98
primary vs secondary hyperaldosteronism
``` primary= Conn's disease (adrenal adenoma or bilateral adrenal hyperplasia) ... renin will by LOW due to feedback secondary= CHF, HTT 2ndary to renovascular causes, JG cell tumor.. renin will be HIGH and thats the cause of the high aldosterone ``` note in primary, you will not see edema due to aldosterone escape (renal pees out the excess sodium/water) but in secondary the edema may be present
99
Neuroblastoma
- NET of adrenal medulla in children under 4 - origin NCC -increased catecholamine production (but note, htt might not be present) -clinical- abdominal distension with irregular abdominal mass. OPSOCLONUS MYOCLONUS !
100
increased HVA and VMA in a kid under 4?
neuroblastoma
101
Homer-Wright Rosette?
classic of neuroblastomaand medulloblastoma
102
Bombeisin and NSE +
neuroblastoma
103
N-myc
neuroblastoma
104
pheochromocytoma
NET of adrenal medulla in adults - increased catecholamines (HTT!!!!!) - spells of "relapsing and remitting" - chromaffin cells- NCC
105
pheochromocytoma genetic associations
VHL, NF1, RET (MEN 2A 2B)
106
metanephrines in urine
pheochromocytoma!
107
why is order of medication in pheo treatment imortant
give alpha 1 blocker and THEN B blocker bc if B blocker given first there might be reflex vasoconstriction making BP WORSE
108
How are cholesterol levels affected by thyroid functioning?
HYPERthyroidism- INCREASE LDLrs causing hypocholesterolemia | HYPOthyroidism - DECREASE LDLrs causing hypercholesterolemia
109
symptoms of HYPOthyroidism
cold intolerance, weight gain, decrease appetite, puffy face, hypoactive, decreased reflexes, CONSTIPATED, hypothyroid myopathy with INCREASED serum CK, dry/cool skin, brittle hair, BRADYCARDIA
110
symptoms of HYPERthyroidism
heat intolerant, decrease weight, increase appetite, increased reflexes, anxious, diarrhea, brisk reflexes, myopathy (w/o CK increase), warm/moist skin w/ fine hair, palpitation, arrhythmia, chest pain

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