ENDO Flashcards

1
Q

which hormones share common beta subunit

A

FSH LH TSH hCG

FLAT HUG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

which ant pit glands are basophilic

A
B-FLAT
FSH 
LH 
ACTH
TSH

Prolactin and GH *(eosinophilic) pig

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

which pancreatic cells produce which hormone and location

A
Beta cells (INSIDE) - insulin
alpha - glucagon (peripheral)
gamma - somatostatin (interspirsed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

preproinsulin syntheiszed where

A

RER…cleavage into “proinsulin” and stored in secretory granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

growth hormone stimulates linear growth and muscle mass through…

A

IGF 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how does growth hormone affect insulin

A

increases insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what hypothalamic hormone does prolactin inhibit

A

GnRH (prvents ovulation and spermatogenesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

GH is strucutrally homologous to…

A

prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

prolactin secretion from ant pit inhibited by…

A

dopamine from tuberoinfundibular pathway hypothal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how does TRH affect prolactin

A

TRH increass prolactin (so can see this in hypthyroid states)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how can antipsychotics cause galacorhea

A

blocking dopamine which disinhibits prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

fertility and puberty emdiated by pulsatile release of what

A

GnRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

treatment acomegaly

A

somatostatin (decrases GH and TSH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

why can you see galactorrhea in hypothyorid

A

increased TRH = increased prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

excess mineral corticoids, dcreated cortisol and sexhormones

A

17ahydroxylaes deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ambiguous genitalia HTN

A

17ahydroxlyase deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

lab value in 17ahydroxylase def

A

lower androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

effects of cortisol

A

A BIG FIB

Appetitei increased
BP increased
Insulin resistance (diabetogenic)
Gluconeogenesis/lipolysis/proteolisis increased (decreased glucose utlization)
Fibroblast activity decasdd (poor wound healing, striae, decreased colagen)
Immune (decreased inflamm and immune response)
Bone (decerased osteoblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

relation between exogenous corticosteroids and TB

A

can cause reactivation TB and candidiasis (blocks IL2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

if steroids decrease immune response and inflammation, why do you see nutrophilia

A

decreaeses WBC adhesion so more is floating around in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

steroids and mast cells

A

blocks histamine relase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

where does pituitary sit

A

sella turcia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

functional vs non functional pit adenoma

A

functional - poduces hormones

non functional doesnt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

MCC pituatry adenoma

A

prolactinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

presentation prolactinoma females

A

galactorrhea, amenorrhea (anovulation due to no FSH, LH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

presentaiton prolactinoma male

A

decrased libido

headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

elvated GH adn IGF1

LACK of gluose suppression

A

growth hormone adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

rx growth hormone excess

A

ocretoide (somatostatin analog) blocks GhRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what tumor in children can result in hypopit

A

craniopharyngioma (can present with bilateral hemianopsia too) big clue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

poor lactation, LOSS OF PUBIC HAIR recently after postpartum bleeding

A

sheehan syndrome (increased susepctiblity of pituitary to uundergo infarction and hypoperfusion during postpartum bleeding, esp since it’s gotten bigger beause of pregnancy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

atrophy or compression of pituitary

A

empty sella

herniation of arachnoid or CSF into sella turcica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

polyuria, polydipsia, hypernatremia and high serum osmoality, low urine osmolality

A

central diabetes inspidus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

specific gravity of urine in diabetes insipidus

A

low (keep losing free water)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

water depriv test in central DI

A

deprivation cauess they to keep peein g(still low urine osmolarity)

give ADH analog and urine osmolaitiy goes up)…able to concetrate urine and keep more water in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

imparied renal responset o ADH

A

nephrogenic DI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

bipolar person keeps peeing

A

lithium can cause nephrogenic DI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

water depriv result nephrogenic DI

A

give ADH analog, no effect on urine osm (urine osm still low)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

DI has what effect on serum osm

A

inncreases it (keeps losing free water)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

SIADH does what to serum osm

A

decreases osm (keeps in too much watere)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Na and serum osmolality in SIADH

A

hyponatremia

low serum osm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what cancer can cause SIADH

A

small cell lung cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

MOA demeclocycline

A

blocks ADH

so this medication causes nephrogenic DI

but treats
SIADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

hyperosmotic volume contraction

A

DI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

why is the body still euvolemic in SIADH

A

bod responds to water retention by increassing ANP and BNP and decreasing aldosterone which will increase Na excretion into urine (hyperosmolar urine)…but further worsens SIADH hyponatremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what chemo drug can cause SIADH

A

cyclophsphamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

transporter that mediates glucose uptake in skeletal muscle cells

A

GLUT4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

TSH function

A

stimulates small amt of T3 and lots of T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

relationship of reverse T3 and T4

A

peripheral T4 floating around gets converted to rt3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how is t4 converted to t3 in peripheral tisssue

A

5’deiodinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what inhibits peripheral t4 to t3 conversion

A

glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

wolff chaikoff effect

A

excess iodine will temporarily inhibit thyroid peroxidase which will decrase iodine organification and deccrease t3/t4 production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what mediates oxidation of I to I2

A

thyroid perioxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

how to form MIT and DIT

A

I2 + thyroglobuiln (tyrosine residues)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what couples DIT and MIT together

A

thyroid perioxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what iodinates thyroglobulin to form MIT and DIT

A

thyroid perioxidase

56
Q

which binds nuclear reeptor at greater affinity t3 or t4

A

t3

57
Q

target PTU and methimazole

A

PTU porpylthiouracil - thyroid peroxidase and 5 deiodinase

methimazole - inhibits thyroid peroxidase only

58
Q

which antithyroid med blocks peripiheral conversion t4-t3

A

PTU Prevents Peripheral conversion

59
Q

teratogen in early pregnancy thyroid med

A

methimazole (meth is a teratogen)

60
Q

adverse affect PTU

A

hepatotoxicity (so use it in later pregnancy instead of meth)

61
Q

anterior neck mass, mobile

A

thyroglossal duct

62
Q

oremnant of thyrglossal duct

A

foramen cecum (remember thyroid starts and tongue andmoves donward)

63
Q

baswe of tongue mass

A

lingual throid

64
Q

how does thyroid icrease basal metabolic rate

A

via increasing Na K ATPase!!!!!! and increasing B1 adrenergic receptors

65
Q

how does thyroid affect cholesterol and glucose

A

hypocholesterolemia
hyperglycemia

thyroid incerases gluconeogenesis and glygogenolysis (icnreased sugar in blood)

66
Q

Igg autantibody TSH receptor (stimualtes

A

Graves disease (increased produciton adn release of TH)

67
Q

hyper thyroid, diffuse goiter, exophtalmos and pretibila myxedma

A

grave disease

68
Q

dough like appearance on shin

A

pretibial myxedema which will increase fibroblast secretion of GLYCOASMINOGLYCANS which will increase osmotic muscle swelling and muscle inflmattion

69
Q

graves hypersensitivity

A

type II

70
Q

HADR3 HLA B8

A

graves disseae

71
Q

how does T4 decrase TSH

A

downregulated TRH on anterior pit so it will not produce as much TSH

72
Q

rx graves

A
5 Ps
propanolol
propylthiouracil
prednsolen (steroids)
potassium iodide
73
Q

“hot” enlarged thyroid gland

A

multinodular goiter (work independently of TSH and increase relase of t3 t4

74
Q

iodine deficient patient who is given iodine causes thyrotoxicosis

A

thyrotoxicosis

75
Q

mental retardation, short stature, coarse facila features
proatruding umblicus
protuberant tomgue

A

cretinism

76
Q

myxedema

A

doughy skin due to increased glycosaminoglycans

77
Q

low thyroid can cause what to choleserol

A

hypercholetolemia

78
Q

HLA DR5

A

hashimotos

79
Q

how does hashiotos present

A

initla hyperthyroidism (as thyroid follicles are destroyed) then ebcomes euthyroid then hypothyroid

low T4 and higher TSH

80
Q

histologic hallmark hashimotos

A

Hurthle cells

lymphoid aggregates with germinal centr

81
Q

lmyphoid aggregates with germinal centers

A

hashimotos

incresaed risk for marginal non hodgkin lymphoma B cell

82
Q

thyroiditis after viral infection with TENDER thyroid

A

subacute gran thyroditis

83
Q

hard as wood non tender thyroid

A

reidel fibrosing thyrodisi

thyroid replaced by fibroid tissue

84
Q

how does thyroid cancer look on iodine radio uptake studies

A

DECREASED UPTAKE (SO DO A Fine needle BIOPSY …IF IT’S COLD)

graves or nodular goiter will have increaesed uptake (hot)

85
Q

fibrous capsul solitary growth thyroid (most are cold) no capsular or vascular invasion

A

thyroid adeoma

benign

86
Q

MCC thyoird cacinoma

A

thyroid carcinoma

87
Q

histologic hallmark papillary thyroid

A

orphan annie eyes

empty nuclei with WHITE CENTRAL CELARING

88
Q

empty uclei with white central celaring

A

papillaryy

89
Q

histologic hall marks of papillary thyroid

A

Papi and Moma adoptee Orphan Annie

papillary
psamomma bodies
orphan annie eys

90
Q

RAS mutation

A

follicular carcinoma

91
Q

invasion of thtroid capsule and vasculature uniform follicles

A

follicular CARCINOMA

92
Q

what thyroid carcinoma likes to spread to blood

A

folicular

93
Q

which carcinomas like to spread to blood

A

follicular
RCC
HCC

94
Q

malignant proliferation of C cells

A

medullary carcinoma

95
Q

hypocalcemia and thyroid mass

A

medullary carcinoma

96
Q

malignant cells in amyloid stroma

A

medulary carcinoma thyroid

97
Q

assocation familial medulary carcinoma

A

MEN 2A 2B

RET oncogene mutations

98
Q

mutation Men 2A and 2B

A

ret mutation oncogene

99
Q

undifferentiated malignant tumor of thyroid

A

anaplastic carcinoma (similar to reidel’s but seen in ELDERLY)

REIDELS SEEN IN YOUNG

100
Q

congo red staining thyroid mass

A

medullary

amyloid has malignant cells in it

101
Q

increasd calcitonin thyroid mass

A

medullary

102
Q

MOA clomiphne

A

estrogen recepo modulation (decreases negative feedback inhibition of hpothalamus) there bincreaseing LH and FSH

103
Q

genital lesion painful ulcer with ragged border and grey exudate with inguinal lymphadenopatyh

A

chancroid H ducreyi *curved gram neg rod)

104
Q

camp signaling hormones

A
FLAT ChAMP
FSH
LH
ACTH
TSH
CRH
hcG
ADH
MSH
PTH
105
Q

how will Mg affect PTH

A

like Ca
low Mg = High PTH
high mg -> low PTH

106
Q

how does PTH affect cAMPin urine

A

high PTH will increase cAMP in urine because it actiavtes kidney cells via Gs mechanism

107
Q

how will PTH affect bone

A

cystic bone spaces with brown fibrous tissue hyper parathyroidsim)

consisting of osteo clasts and hemosierin

108
Q

tourssea sign

A

hypocalcemia
fill bP cuff and get muslces spasms
tap on

109
Q

higher than normal Ca levels required to suppress PTH (excessive renal Ca uptake

A

familial hypocalciuric hypercalcima

due to defective G coupled Ca ensing receptor

110
Q

inflammation islets

A

t1dm

111
Q

ketones

A

by hydroxybutryate and acetoacetate

112
Q

mechanism t2dm

A

decrased numbers of insulin receptors!! = insulin resistance

113
Q

aymloid deposits in islet cells

A

T2DM (islets are overworked)

114
Q

marker t2dm

A

islet amyloid polypeptide deposits

115
Q

elderly comes in with high glucose levels, hypotension and coma ABSENT KETONES

A

HYPEROSMOLAR non ketototic coma

116
Q

how does diabetes cause cardiac complications

A

nonenzymatic gltosylation of larg medium sized vessels leads to athersceloriss in large vessles, leasds to hyaline arterioloscleorisis (kidny)

117
Q

how is peripheral neuropathy caused in diabetes

A

osmotic damge to schwann cells (hyperglycemia increases glucose to SORBITAL metabolism faldose B which can deposit and cause damage)

118
Q

marker insulinoma

A

C peptide

119
Q

marker exogenous insulin

A

high insulin LOW C PEPTIDE

120
Q

achlorhydria, cholelithiasis ans steatorrhea

A
somatostatinoma
no gastric acid
no contration of gallbladder
galls tones
no fat digestion
121
Q

water diarrhea hypokalemia

A

VIPoma

122
Q

abodinal striae cushings mcechaniem

A

cortisol inhibits collagen syntehsis

123
Q

how does cushing cause HTN

A

increase up regulatio nof a1 receptors

124
Q

cortisol inhibits ….

A

il2
histamine
phoslipase a2

125
Q

bilateral adrenal atrophy

A

eogenous corticosteroids (steroids inhibits ACTH which will decrease stimulation of adernals)

126
Q

high cortisol, low acth

A

exogenous glucocorticoids or adrenal tumor

127
Q

high cortisol, high actch, high dose suppresses dex suppresses acth, CRH increass ACTH and cortisol

A

pituitary adeoma (cushing disease)

128
Q

high cortisol high actch, high dose doesn’t dex doesn’t suppress actch, CRH stimulation doesn’t incerase ACTH and cortisol

A

ectopic ACTCH secretion (ct chest abdomen or pelvis)

129
Q

hypernatremia, hypokalemia, metabolic alkaosis HTN

A

hyperaldostronism

HTN

130
Q

secondary hyperaldosteronism causes

A

renovascular hypertension (activates RAAAS system) , renin producing tumors and edma

131
Q

salt wasting and precocious puberty…clitormegaly in females

A

21 hydroxylase ef SHUNTING SEX

decreased cortisol increased ACTH, low aldosterone = HYPOTENSION

132
Q

precocious puberty clitromegaly NO SALT WASTING

A

11 hydroxylase deficiency

133
Q

excess mineralocortoids but no cortisol and sex steroids, ambiguous genitalia and sexual development HTN

A

17a hydroxylase

134
Q

salt wasting

A

hyponatremia, hyperkalemia

due to decreased aldosterone

135
Q

clle type medullary adrenal

A

chromaffin cells

136
Q

brown tumor of adrenla medulla

A

pheochromocytoma

137
Q

what to give before taking out pheochomo

A

pehnoxybenzamine (irreverisble a antagonist) follwoed by b blockers to prevent massive surge of catecholamines and hypertensive crisis