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Endocrine (F.A.) Flashcards

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
Q

Prolactin looks like what other hormone ?

A

Growth Hormone

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26
Q

what drug inhibits prolactin secretion

A

Dopa agonist (bromocriptine)

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27
Q

what drugs stimulate prolactin secretion

A

Dopamine antagonists (antipsychotics) and Estrogens

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28
Q

CRH

A

made by: hypothalamus

effect: increase ACTH (by ant pit), increase MSH, and B-endorophins

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29
Q

Dopamine

A

made by: hypothalamus

effect: inhibit prolactin secretion (ant pit) and inhibit TSH (ant pit)

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30
Q

GHRH

A

made by: hypothalamus

effect: increase GH release by ant pit

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31
Q

GnRH

A

made by: hypothalamus

effect: increase LH, FSH release by ant pit

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32
Q

prolactin

A

made by: ant pit

effect: decrease GnRH

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33
Q

SST

A

made by: pancreatic delta cells

effect: decrease GH and decrease TSH

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34
Q

TRH

A

made by: hypothalamus

effect: increase TSH and Prl

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35
Q

Insulin made by?

A

pancreatic B cells in Islet of Langerhans

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36
Q

describe insulin synthesis

A

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

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37
Q

functions of insulin

A

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

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38
Q

GLUT 4

A

adipose and skm

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39
Q

GLUT 1

A

RBC, cornea, brain, and placenta

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40
Q

GLUT2

A

birectional!

pancreatic B cells, liver, kidney, SI

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41
Q

GLUT 3

A

brain and placenta

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42
Q

GLUT 5

A

sperm (fructose)

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43
Q

insulin receptor

A

tyrosine kinase w/ PIP3k and RAS/MAP pathway

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44
Q

how does pancreatic B cell respond to glucose

A 
GLUT 2- glucose entry 
glycolysis makes ATP 
ATP sensitive K+ ch closes- depol 
causes Ca2+ vgc to open 
exocytosis of insulin
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45
Q

oral vs IV glucose

A

oral glucose causes release of incretins GLP1 and GIP which makes Bcells more sensitive to glucose causing more insulin release

46
Q

Cortisol Actions

A

A BIG FIB
increase in : appeitite, bmr, insulin resistance, gluconeogen/lipolysis/proteolysis

a decrease in: fibroblast activity, inflammatory response (IL2), bone formation

47
Q

why should you not give a TB patient glucocorticoids

A

can cause TB reactivation by inhibiting IL2

48
Q

where is cortisol made?

A

Zona fasciculata of cortex of adrenal gland

49
Q

what effects cortisol secretion

A

(1) CRH–> ACTH –> cortisol

(2) stress –> cortisol

50
Q

how is Ca2+ found in the blood

A

45% free ions ** active!
40% bound to albumin
15% bound to other anions

51
Q

why does pH affect Ca2+ levels

A

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
Q

tap cheek, facial muscles contract?

A

Chvostek sign

hypocalcemia

53
Q

where do we get vit D from?

A

sunlight (D3)- cholecalciferol

diet (D2) - ergocalciferol

54
Q

what happens to the vit D in our body?

A

chole/ergo calciferol –> 25 OH D (in liver)—> 1,25 OH D(active form) (in kidney via 1 alpha OHlase)

55
Q

what is another name for 1,25 OH2 D

A

calcitriol

56
Q

what are the actions of calcitriol

A

increase Ca2+ and PO43- absorption in gut

57
Q

vit D deficiency causes?

A

bone mineralization problems
rickets in children
osteomalacia in adults

58
Q

where is PTH made

A

chief cells of Parathyroid

59
Q

what causes an increase in PTH release?

A

low Ca2+levels
high PO43- levels
slightly low Mg2+ levels (very low Mg2+ will cause PTH decrease)

60
Q

what does PTH do

A
  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
Q

how does cortisol increase BP?

A

it increases alpha 1 receptors on blood vessels having a “permissive” effect on NE/Epi

62
Q

what is PTHrP?

A

its released by malignancies (sqccl, rcc) and acts like PTH

63
Q

what is calcitonin

A

only active when Ca2+ levels are very increased it helps bring them down by decreasing bone resorption of Ca2+

64
Q

what does T3/T4 do?

A

4B’s

  • brain maturation
  • increase BMR ( increase Na/K activity, increase glycogenolysis/lipolysis/gluconeogenesis)
  • helps Bone growth
  • increases B1 receptors on heart
65
Q

Wolff Chaikoff Effect

A

Excess Iodine can inhibit thyroid peroxidase activity, decreasing T3/T4 formed temporarily

66
Q

how does TBG levels affect thyroid hormone?

A

increase TBG causes decrease free T3/T4 bc it binds it!

67
Q

what causes increased TBG levels

A

OCPs and pregnancy

68
Q

what decreases TBG levels

A

hepatic failure

69
Q

how does I- enter thyroid cells?

A

Na+/I- cotransporter

70
Q

what does thyroid peroxidase do?

A

(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
Q

what does 5’ deiodinase do?

A

peripheral conversion of T4 to T3 (more active)

72
Q

what thyroid hormone is produced most by thyroid

73
Q

what thyroid hormone is most active

74
Q

what increases TSH secretion, what inhibits it

A

TRH (hypothalamus)

SST (delta of langerhans of pancreas)

75
Q

hormones that use cAMP signalling

A

FLAT ChAMP

FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2), MSH, PTH

76
Q

hormones that use cGMP for signalling

A

BAD (GRMP)

BNP, ANP, EDRF (NO)

77
Q

hormones that use IP3 for signalling

A

GOAT HAG

GnRH, Oxy, ADH (v1), TRH, histamine, Ang II, Gastrin

78
Q

hormones that use intracellular receptors for signalling

A

PET CAT on TV

prolactin, estrogen, testosterone, cortisol, aldosterone, T3/T4, vitamin D

79
Q

hormones that use receptor tyrosine kinase

A

IGF1, insulin, FGF, PDGF, EGF

80
Q

non-receptor tyrosine kinase

A 
GH/JAK STAT
cytokines
prolactin
erythropoeitin, thrombopoetin, 
G-CSF
81
Q

Cushing Syndrome

A

excess Cortisol

82
Q

most common cause of Cushing’s Syndrom

A

exogenous corticosteroids

83
Q

Cushing Syndrome due to exogenous corticosteroids show:

A

decreased: ACTH, CRH

the adrenal glands: bilateral atrophy

84
Q

Cushing Syndrome caused by primary adrenal adenoma, hyperplasia or carcinoma will show?

A

decreased: ACTH, CRH
adrenal glands- unilateral atrophy

*may be accompanied by pseudohyperaldosteronism

85
Q

Cushing Disease

A

a tumor of the anterior pituitary producing excess ACTH

86
Q

Cushing disease will show

A

INCREASED ACTH

adrenal glands- bilateral adrenal hyperplasia

87
Q

what is paraneoplastic acth secretion

A

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
Q

how do we differentiate between Cushing disease and a paraneoplastic ACTH secreting tumor

A

(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
Q

Adrenal Insufficiency

A

DECREASED cortisol levels (maybe mineralocorticoid levels)

90
Q

diagnosing cause of adrenal insufficiency

A

(1) electrolytes and ACTH levels

(2) metyrapone test- blocks last step in cortisol synthesis in adrenal gland.

91
Q

how do you interpret the metyrapone test

A

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
Q

clinical signs of primary adrenal insufficiency

A 
hyperkalemia (low aldosterone)
orthostatic hypotension (low cortisol) 
hyperpigmentation (high ACTH, causes high MSH) 
metabolic acidosis 
weight loss (low cortisol)
93
Q

Addison’s disease

A

primary CHRONIC adrenal insufficiency

(1) autoimmune cause of adrenal destruction in developed nations
(2) TB destruction of adrenal in developing

94
Q

2ndary adrenal insufficiency

A

decreased ACTH production due to pituitary adenoma. While cortisol levels may lower, aldosterone levels remain the same because of AngII stimulation

95
Q

how do primary and secondary adrenal insufficiency present differently?

A

primary- hyperkalemia and skin pigmentation

secondary- no hyperkalemia or skin pigmentation

96
Q

tertiary adrenal insufficiency

A

taking glucocorticoids and suddnely stopping. (note bc glucocorticoids mainly cause atrophy of zf, zr should be fine and aldosterone levels should be ok)

97
Q

Hyperaldosteronism clinical signs

A

htt, low (or normal) K+, metabolic ALKalosis

98
Q

primary vs secondary hyperaldosteronism

A 
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
Q

Neuroblastoma

A
  • 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
Q

increased HVA and VMA in a kid under 4?

A

neuroblastoma

101
Q

Homer-Wright Rosette?

A

classic of neuroblastomaand medulloblastoma

102
Q

Bombeisin and NSE +

A

neuroblastoma

103
Q

N-myc

A

neuroblastoma

104
Q

pheochromocytoma

A

NET of adrenal medulla in adults

  • increased catecholamines (HTT!!!!!)
  • spells of “relapsing and remitting”
  • chromaffin cells- NCC
105
Q

pheochromocytoma genetic associations

A

VHL, NF1, RET (MEN 2A 2B)

106
Q

metanephrines in urine

A

pheochromocytoma!

107
Q

why is order of medication in pheo treatment imortant

A

give alpha 1 blocker and THEN B blocker bc if B blocker given first there might be reflex vasoconstriction making BP WORSE

108
Q

How are cholesterol levels affected by thyroid functioning?

A

HYPERthyroidism- INCREASE LDLrs causing hypocholesterolemia

HYPOthyroidism - DECREASE LDLrs causing hypercholesterolemia

109
Q

symptoms of HYPOthyroidism

A

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
Q

symptoms of HYPERthyroidism

A

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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