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#MedSchool > Endocrine > Flashcards

Endocrine Flashcards

1
Q

which adrenergic receptors increase hepatic glucose output

A

beta 2 and 3

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2
Q

alpha 1 receptor works by which second messanger

A

IP3, Ca (Gq)

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3
Q

alpha 2 receptor works by which second messanger

A

Gi : decrease cAMP

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4
Q

beta1 receptor works by which second messanger

A

Gs increase cAMP

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5
Q

beta2 receptor works by which second messanger

A

Gs increase cAMP

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6
Q

alpha 1 prefers which adrenergic ligand

A

NE

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7
Q

alpha 2 prefers which adrenergic ligand

A

NE

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8
Q

which adrenergic receptor inhibits insulin release

A

alpha 2

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9
Q

beta 1 prefers which adrenergic ligand

A

NE=E

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10
Q

beta 2 prefers which adrenergic ligand

A

E

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11
Q

beta 3 prefers which adrenergic ligand

A

NE

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12
Q

where do you find beta 2 receptors

A

GI, urinary, adipose, liver, skeletal muscle, alpha cells in pancreas, bronchiole

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13
Q

where do you find beta 1 receptors

A

heart

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14
Q

where do you find alpha receptors

A

veins, lymph, beta cells in pancreas

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15
Q

beta3 receptor works by which second messanger

A

Gs increase cAMP

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16
Q

disease: high circulating catecholamines causing headache, palpitations, HTN, sweat, tachycardia

A

pheochromocytoma

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17
Q

disease: high cortisol, low ACTH

A

cushing syndrome (spontaneous or drug induced cortisol excess)

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18
Q

disease: high cortisol, high ACTH

A

cushing disease (pituitary adenoma)

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19
Q

how to distinguish cushing disease from syndrome

A

dexamethasone suppression test

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20
Q

osteoporosis, poor wound healing, virilization, HTN, round face, buffalo torso

A

cushing

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21
Q

treatment for cushings

A

ketoconozole, metyrapone

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22
Q

why do we get HTN with high cholesterol

A

alpha 1 stimulation causes vasoconstriction

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23
Q

disease: hypoglycemia, hypotension, hyperkalemia, acidosis, decreased hair and libido, hyperpigmentation

A

addisons

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24
Q

what will cortisol, CRH, ACTH look like in secondary adrenocortical insufficiency

A

low cortisol, high CRH, low ACTH

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25
Q

disease: primary adrenocortical insufficiency

A

addisons

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26
Q

why do we get hyper pigmentation with addisons

A

increased ACTH with alphaMSH can’t stimulate adrenal cortex (cuz its messed up) but the MSH produces discoloration

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27
Q

disease: primary hyperaldosteronism

A

conn syndrome

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28
Q

disease: hypervolemic, hypernatremic, HTN, low K, low H (alkalosis)

A

Conn syndrome

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29
Q

how do you treat conn syndrome

A

spironolactone (aldosterone antagonist)

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30
Q

disease: overproduction of mineral corticoids can occur when we have deficiency in which enzyme

A

17alpha hydroxylase

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31
Q

disease: cannot synthesize gluco or mineral corticoids so we get excess androgens leading to urinary ketosteroids and sterility

A

21 beta hydroxylase deficiency

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32
Q

a deficiency in which enzyme along the steroid hormone synthesis pathway would lead to HTN

A

11 beta hydroxylase

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33
Q

a deficiency in which enzyme along the steroid hormone synthesis pathway would lead to Hypotension

A

21 beta hydroxylase

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34
Q

angiotensin II stimulates what enzyme

A

aldosterone synthase

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35
Q

what regulates secretion of cholesterol desmolase

A

ACTH

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36
Q

what enzyme is needed to convert cortisol to the less active corticosterone after binding mineral corticoid receptors

A

beta hydroxysteroid dehydrogenase

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37
Q

who secretes PTH

A

chief cells

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38
Q

who secretes calcitonin

A

C parafollicular cells

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39
Q

oxytocin and ADH are stored in these enlarged axon terminals

A

herring bodies

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40
Q

glial cells of neurohypophysis

A

pituicytes

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41
Q

pineal gland secretory function is mediated by what type of receptor

A

beta adrenergic

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42
Q

what do F cells in pancreas secrete

A

pancreatic polypeptide

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43
Q

what do delta cells secrete in pancreas

A

somatostatin and gastrin

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44
Q

what do catecholamines and thyroid hormones have in common

A

derived from tyrosine (amine hormones)

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45
Q

POMC neurons make what kind of hormone

A

ACTH, MSH

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46
Q

what stimulates GH release

A

low glucose, GHRH, estrogen, testosterone, exercise, stress, sleep, alpha adrenergic agonist

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47
Q

Somatomedin C is also called

A

IGF1

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48
Q

GH directly affects what organs

A

skeletal muscle, adipose, liver

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49
Q

what does GnRH do

A

stimulates anterior pituitary to make LH and FSH

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50
Q

GH has indirect anabolic affect via what mediator

A

somatomedins made in liver

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51
Q

the hypothalamus releases what product that inhibits GH secretion from anterior pituitary

A

somatostatin

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52
Q

what test is performed to confirm diagnosis of GH excess (acromegaly)

A

administer oral glucose– should suppress GH levels and if they remain high we know there is exogenous GH secretion

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53
Q

how does prolactin suppress ovulation

A

inhibit GnRH

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54
Q

what stimulates prolactin release

A

TRH

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55
Q

what inhibits prolactin release

A

dopamine

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56
Q

3 sources of dopamine which inhibits release of prolactin

A

posterior pituitary, hypothalamus, non lactotroph cells of anterior pituitary

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57
Q

how does ADH increase peripheral resistance

A

binds V1 receptors increasing intracellular ca++ and contraction of SM in arterioles

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58
Q

disease: large volume of dilute urine excreted and high osmolarity of body fluids– fixed with ADH analogue

A

central DI

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59
Q

disease: large volume dilute urine excreted and high osmolarity of body fluids and high ADH

A

nephrogenic DI

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60
Q

MOA for nephrogenic DI

A

V2 defect

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61
Q

nephrogenic DI can occur secondary to what

A

lithium use, polycystic kidney disease, sickle cell anemia

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62
Q

how to treat nephrogenic DI

A

thiazide diuretics: inhibit Na reabsorb from PCT

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63
Q

disease: dilute body fluids, hyponatremia, high concentration of urine

A

SIADH

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64
Q

disease: enlargement of pituitary during pregnancy leads to infarction and hypopituitism

A

sheehan syndrome

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65
Q

what enzyme activates a GPCR by making the GDP GTP

A

GEF

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66
Q

what enzyme deactivates GPCR by hydrolyzing GTP

A

GAP

67
Q

what are the ligands for RTKs

A

growth factors

68
Q

inactive versus active form of insulin

A

hexamer: inactive
monomer: active

69
Q

end result of RAS dependent insulin action

A

upreg glucokinase

70
Q

end result of RAS independent insulin action

A

move GLUT4 to membrane (and activate glycogen synthase)

71
Q

insulin resistance may happen because PKB does not activate to insert GLUT4 into PM’s. this could be because ___ gets phosphorylated at the wrong spot (ser/thr instead of tyr)

A

IRS1 and IRS2

72
Q

epinephrine encourages what pancreatic secretion

A

glucagon (stress can cause DKA because E also inh insulin)

73
Q

when we have no more glycogen, ___ stimulates gluconeogenesis

A

cortisol

74
Q

estrogen binds ___ which is a HAT loosening DNA allowing transcription

A

SRC1

75
Q

estrogen antagonists like ___ are going to activate HDAC to tighten chromatin

A

tamoxifen

76
Q

conversion from T4 to T3 requires what enzyme

A

deiodinase

77
Q

what enzyme hydrolyzes bonds to release MIT and DIT from TG allowing them to combine and form thyroid hormones

A

lysosomal proteases

78
Q

MIT and DIT interact with ___ in the thyroid epithelial cell to produce tyrosine and thyroglobulin

A

intrathyroidal deiodinase

79
Q

deficiency in intrathyroid deiodinase mimics what other condition

A

I- deficiency

80
Q

who does I- get to lumen

A

pendrin + peroxidase

81
Q

drug that blocks NIS

A

perchlorate and thiocynate

82
Q

drug that blocks peroxidase

A

PTU

83
Q

high levels of I- inhibit organification and synthesis of thyroid hormones (peroxidase aint working)

A

wolff chaikoff effect

84
Q

what causes high TBG

A

pregnancy

85
Q

thyroid hormone encourages synthesis of

A

NaK ATPase, beta adrenergic receptors, lysosome enzymes

86
Q

to convert carotene to vitamine A we need what hormone

A

thyroid hormone

87
Q

disease: antibodies destroy or block thyroid hormone synthesis by blocking peroxidase resulting in hypothyroid with goiter

A

autoimmune thyroiditis

88
Q

disease: hypothyroidism in mother during pregnancy leads to this in baby

A

cretinism

89
Q

disease: antibody stimulates TSH receptors

A

graves disease

90
Q

disease: protruding eyeballs, periorbital edema, elevated thyroid hormone, goiter

A

graves

91
Q

disease: impaired synthesis of thyroid hormones due to TG or TPO antibodies

A

hashimoto disease

92
Q

disease: iodide deficiency in developing baby

A

cretinism

93
Q

most common hyperthyroidism cause

A

graves

94
Q

can you have goiter with i deficiency

A

yes- low T3/T4 stimulates TSH release

95
Q

disease: new bones fail to mineralize so we get bending and softening

A

osteomalacia

96
Q

disease: hyperreflexia, muscle twitching, tingling

A

hypocalcemia

97
Q

disease: decrease QT interval, constipation, lack apetite, hyporeflexive, coma

A

hypercalcemia

98
Q

academia leads to what ca++ related condition

A

H displaces Ca from albumin and you get increase in free ionized ca

99
Q

chromic hypomagnesemia in alcoholics inhibits synthesis storage and secretion of what

A

PTH

100
Q

how does vitamin D increase calcium reabsorption in GI tract

A

synthesis of calbindin which increases the absorptive capacity of GI epithelial cells so we can bring more into blood

100
Q

how does PTH increase Pi excretion

A

inhibits NPT (NaPi cotrasport) in PCT

101
Q

whats the job of osteoprotegrin

A

bone formation (inactivate osteoclast)

102
Q

where does ca reabsorption take place in a kidney stimulated by PTH

A

TAL, distal tubule

103
Q

what does estrogen do to [ca]

A

stimulate intestinal and renal absorbtion

105
Q

what regulates activity of 1alpha hydroxylase

A

activated by PTH

inhibited by Ca

105
Q

disease: stones, bones, groans

A

primary hyperparathyroidism

106
Q

what are vitamin D levels like in someone with parathyroid adenoma

A

increased PTH causes lots of vitamin D activation so levels are HIGH

107
Q

disease: renal failure or vitamin D deficiency leads to low ca

A

secondary hyperparathyroidism

108
Q

in secondary hyperparathyroidism what are the Pi levels like

A

DEPENDS on the cause
vitamin D deficient: low Pi levels
renal failure: high Pi levels (cannot excrete)

109
Q

disease: low ca, low vitamin D, high serum Pi, muscle cramping, seizure, poor tooth development, mental deficit, intestinal malabsorbtion

A

hypoparathyroidism

110
Q

disease: autosomal dominant inherited, Gs of PTH-R is broken leading to hypocalcemia and hyperphosphatemia

A

pseudohypoparathyroidism

112
Q

what do glucocorticoids do to [ca]

A

inhibit absorption from kidney and intestine

113
Q

disease: high PTH, low vitamin D, low ca, high Pi

A

pseudohypoparathyroidism

114
Q

disease: PTHrp

A

humoral hypercalcemia of malignancy

115
Q

what are vitamin D levels in humoral hypercalcemia of malignancy

A

low (this is the only difference from hyperparathyroid symptoms)

116
Q

how to treat humoral hypercalcemia of malignancy

A

furosimide (increase ca excretion)

etidronate (inhibit bone resorbtion)

117
Q

disease: autosomal dominant mistake in CaSR

A

hypocalcuric hypercalcemia

118
Q

disease: deficiency in 1alpha hydroxylase

A

rickets type I

119
Q

disease: deficiency in vitamin D receptor

A

rickets type II

120
Q

disease: bone mass decreases

A

osteoporosis

121
Q

treat for osteoporosis

A

PTH, estrogen, calcitonin, RANKL inhibitor

122
Q

treat for rickets/osteomalacia

A

vitamin D, ca, sunlight

123
Q

what brings glucose into beta cell to initiate insulin release

A

GLUT2

124
Q

high levels of ATP in pancreatic beta cell causes what to happen

A

K channels close (depolarization)

125
Q

an increase in intracellular ___ causes clathrin coated vesicles containing insulin to be released from beta cell

A

Ca

126
Q

drugs that promote closure of ATP dependent K channels to increase insulin secretions in T2D

A

sulfonurea (tolbutamide, glyburide)

127
Q

which tissues require insulin for effective glucose uptake (via GLUT4)

A

muscle, adipose, liver

128
Q

insulin activates SREBP1c for what purpose

A

uptake more LDL’s (to build more TAG’s not break them down)

129
Q

what does insulin release do to blood [k]

A

decrease

130
Q

disease: autoimmune destruction of beta cells

A

type I diabetes

131
Q

disease: progressive exhaustion of beta cells leading to insulin resistance

A

type II diabetes

132
Q

medication for type II diabetics that sensitizes them to insulin

A

metformin

133
Q

disease: patient has antibodies to GAD65, IA2, insulin autoantibody

A

type i diabetes

134
Q

disease: patient has antibody that is antagonist against insulin

A

type ii diabetes (blocks insulin at target tissue)

135
Q

while auto Ab’s are found in type i diabetic patients, who is actually doing the most harm to beta cells

A

CTL’s

136
Q

what is the most common genotype mutation in type i diabetes patients

A

HLA: DQ2 or DQ8

DR3 or DR4

137
Q

if you have this genotype you are said to have “protective” factor from developing type i diabetes

A

HLA DR2 DQ6

138
Q

what viruses can cause direct or indirect (via molecular mimicry) development of T1D

A

mumps, rubella, CMV

139
Q

what bacteria can cause harm to beta cells

A

streptozocin, bafilomycin a1

140
Q

cell markers for treg

A

CD4+25+FOXP3+

141
Q

disease: messed up FOXP3

A

IPEX

142
Q

what kind of cell infiltrates adipose tissue in obese patients causing inflammation and eventually leading to insulin resistance

A

M1 macrophages (TNFalpha and IL1beta)

143
Q

excess palmitate induces expression of TLR4 in beta cells which will release cytokines to attract ___ which are cells that cause harm to these cells

A

M1 macrophages

144
Q

what gets released (at normal term birth) in order to stimulate surfactant production in newborn babies– otherwise they get IRDS

A

glucocorticoids

145
Q

enzyme that turns cortisol into cortisone so it doesn’t overstimulate mineral corticoid receptors

A

11 beta hydroxysteroid dehydrogenase

146
Q

why does real licorice give us HTN

A

it blocks 11 beta hydroxysteroid dehydrogenase allowing mineral corticoids AND glucocorticoids to raise BP

147
Q

how does cortisol suppress immune function

A

inhibit NFKB by sequestering it
reduce IL2 synthesis
promote T cell apoptosis

148
Q

enzyme required to make estradiol in the ovaries

A

aromatase

149
Q

estradiol that gets circulated to the brain has what effect

A

down regulation of FSH and LH

150
Q

gives breath a fruity smell in T1D

A

acetoacetate

151
Q

disease: headache, weakness, diarrhea, arrhythmia, increase HR, vomitting, SOB with kussmaul

A

DKA

152
Q

disease: parathyroid, pituitary, pancreas tumors

A

MEN1

153
Q

disease: L dopa decarboxylase deficiency

A

this is in APUD cells – MEN syndromes

154
Q

most common parathyroid abnormality with MEN 1

A

hyper– hyperplasia of all 4 glands

155
Q

most common pancreas abnormality with MEN 1

A

gastrinoma

156
Q

most common pituitary abnormality with MEN 1

A

prolactinoma

157
Q

whats RET

A

protooncogene– MEN2

158
Q

whats menin protein

A

product of MEN1 gene (tumor suppressor)

159
Q

disease: MTC and pheochromocytoma

A

MEN2

160
Q

disease: MTC, pheochromocytoma, hyperparathyroidism

A

MEN 2a

161
Q

what is unique to MEN2a

A

hyperparathyroid, cutaneous lichen amyloidosis

162
Q

what is unique to MEN2b

A

mucosal neuroma, marfanoid habitus

163
Q

disease: high E, high calcitonin, normal PTH

A

MEN 2b

#MedSchool (17 decks)

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