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STEP1 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Dopamineprolactin

A

Dopamine inhibitsprolactin
Low dopamine= lactogenésis

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2
Q

Arterial supply pituitary

A

Superior and inferior hypophyseal arteries

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3
Q

Thyroid surgery nerve risk

A

Protect recurrent laryngeal nerve when lighting inferior thyroid a
Superior laryngeal - superior thyroid a

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4
Q

Congenital hypothyroidism

A

Course facial features, short stature, mental impairment
“Pot belly” protruding umbilicus
Puffy face, protruding tongue
Pale skin

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5
Q

Thyroid peroxidase

A

Iodide → iodine
Adds to tyrosine residues on thyroglobulin
Combines MIT + dit or dit x2 to make t3 or t4

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6
Q

Thyroglobulin

A

Large protein, many tyrosines
Tyrosines → MIT, dit → t3/4
Found in follicular cell lumen
When ready endocytosed into cell and cleave d by proteases

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7
Q

5’ deiodinase

A

At tissues
T4 → active t3

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8
Q

Wolff chaikoff effect

A

Excess iodide inhibits TPO

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9
Q

Thyroid binding globulin

A

Transports almost all t3 and t4 in blood
Inactive whenbound
Increased during pregnancy and with OCPs - bound elevated, free normal
Decreasedhepatic failure, steroids-bound low, free normal

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10
Q

Thyrotoxic crisis

A

Thyroid storm
Triggered acute physiologic stressors
Agitation, delirium
Fever
Diarrhea
Tachyarrythmia - high output heart failure- A fib
Coma

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11
Q

Antithyroid antibodies graves

A

Anti tsh-r

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12
Q

Tx hyperthyroid

A

Propranolol for tachycardia
Antithyroid propylthiouracil or * methimazole - PTU in first tri preg
Prednisone for exophthalmos if present

If failed:
Radioactive ablation
Thyroidectomy

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13
Q

Irregularly enlarged thyroid

A

Multinodular goiter

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14
Q

Antibodies hashimotos

A

Anti-tpo, thyroglobulin, microsomal ig G

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15
Q

Hla hashimotos

A

DR 3/5

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16
Q

Atrophic thyroiditis

A

Blocking-anti.TSH-R
Absent goiter
Middle age to elderly

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17
Q

Drug induced hypothyroidism

A

Amiodarone- antiarrythmic
Lithium
Aspirin
Sulfonamide

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18
Q

Myxedema coma

A

Diminished mental status
Low temp
Hypoglycemia
Hyponatremia
Hypoxia
Hypoventilation
Bradycardia
Hypercapnia

Often neither myxedema nor coma…

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19
Q

Calcitonin tumor marker

A

Medullary thyroid cancer

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20
Q

Thyroglobulin tumor marker

A

Papillary or follicular thyroid cancer

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21
Q

CEA tumor marker

A

Carcinoembryoniz antigen
Medullary thyroid, colon, pancreas, lung, breast

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22
Q

Biopsy hashimotos

A

Lymphocytes and hurthle cells

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23
Q

Painful enlarged thyroid low thyroid

A

Subacute granulomatous / de quervain thyroiditis,
Usually precipitated by acute viral infection

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24
Q

Thyroiditishyperthyroid

A

Silent lymphocytic - May also be asymptomatic - often self- limita and mild- may progress to mild hypothyroid
De quervain thyroiditis
Or transient in ear h ly disease course hashimotos

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25
Q

Riedel thyroiditis

A

Fibrosis due tochronic inflammation
Low or euthyroid
Painless goiter
Local compressive sx

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26
Q

Methimazole

A

Preferredantithyroid drug except in pregnancy
Inhibits iodine → tyrosine and iodotyrosine coupling

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27
Q

Propylthiouracil

A

2nd choiceantithyroid
Preferred inpregnancy first tri
Similar Mx to methimazole
Plus 5’ deiodlinase inhibition of t4→t3

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28
Q

Antithyroid Æs

A

Agranulocytosis
Liver damage
Anca - antineutrophö cytoplasmic ab
Vasculitis with glomerular injury

More common ptu

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29
Q

Thyroid adenomas

A

Generally benign
Most nonfunctional, some secretory
No tumor capsule invasion or blood vessel invasion

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30
Q

Papillarythyroid carcinoma

A

Most commonmalignancy of thyroid
Great prognosis
Likely t4 secretory

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31
Q

Papillary thyroid carcinoma mutations

A

Ret or braf
Or childhood radiation

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32
Q

Oxytocin production

A

Mostly PVN of ht

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33
Q

Oxytocin storage

A

Posterior pituitary

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34
Q

Prolactin sex hormones

A

Reduces GnRH
Thus _ low T and E
Implicated in infertility

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35
Q

Sheehan syndrome

A

Postpartum hemmorhage- → pituitary infarction → low prolactin → lactation failure, menstrual irregularities

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36
Q

Thyroid andprolactin

A

TRH, - → TSH and prolactin
Primary hyperthyroid eg graves or secondary hypothyroid → low prolactin

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37
Q

Pituitary stalk compression prolactin

A

Hyper prolactinemia
Interrupts inhibitory dopamine signal

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38
Q

Hyper prolactin causes

A

Dopamine blockers eg. Antipsychotics
Prolactinomas
Pituitary stalk compression
Pregnancy
Primary hypothyroid dt TRH increase
End stage renal disease unknown why

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39
Q

Estrogen prolactin

A

Directly increases

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40
Q

Progesterone prolactin

A

Inhibits milk production effects eg pregnancy

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41
Q

G H starvation

A

-increased t o stabilize blood sugar
By ghrelin

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42
Q

Congenital gh deficiency

A

Poor linear growth after first few months
Delayed motor muscle Devi

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43
Q

Laron syndrome

A

Similar to manifestations ofcongenital gh deficiency but gh not → IGF
So high gh low IGF

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44
Q

Childhood gh deficiency

A

Short stature, doll-like or infantile facial features
Check IGF levels ( more consistent than_gh), bone Age
Ro causes of failure

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45
Q

Testinggigantism

A

Oral glucose boles would normally decrease gh but not in true gigantism
Dd: marfan, precocious puberty, normal genes

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46
Q

Acromegaly

A

Adult high gh
Joint pain, muscle aches, gradualoftenunnoticable while happening hand and foot growth c coarse facies
Diabetes, atherosclerosis dt glucose and lipid fx
Causes:
- tumor
- mccune Albright
- men-1
- carney complex
- x linked acrogigantism

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47
Q

Tx Gh excess

A

Octreotide - somatostatin analog

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48
Q

Somatostatin

A

Secreted by ht to decrease gh

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49
Q

Hyper prolactin Tx

A

Cabergoline
Bromocriptine
Note these ore also implicated in hypo when taken for other reasons eg. Pd

Or removal - based on severity. of visual field defects

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50
Q

ACTH deficiency

A

Mild: postural hypotension and pots
Severe: weight loss, fatigue, low libido, hypoglycemia
Extra bad: fatal vascular collapse - shock

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51
Q

ADH deficiency

A

Central di
High volume dilute urine
Dehydration, thirst, dizziness

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52
Q

Pituitary apoplexy

A

Sudden pituitary hemorrhage
Trauma, aneurysm
Emergency
Low ACTH → shock
Sudden excruciating headache, diploma, progressive hypopituitarism

Immediate tx: stabilize bp with fluids and cortisol
Also Tx hypoglycemia

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53
Q

PTH

A

Increased blood calcium
Low bone density
Low phosphate -renal exchange

Gut uptake, urine reuptake, vitamin D production i bone breakdown

54
Q

Hyper calcemia sx

A

Asymptomatic at first

Then:
Fatigue
Irritability
Depression
Memory problems
Decreased bone density if dt high PTH

Then:
Shortened qt_interval
Arrhythmia
Fractures
Kidney stones
Acute pancreatitis
Ulcers
Ab pain, constipation
Stupor, confusion
Seizures,
coma

55
Q

Men1 and men 2 both cause

A

High PTH

56
Q

Men- 1 Gene

A

Men 1

57
Q

Men 2a Gene

A

Ret

58
Q

High PTH sx

A

Hypercalcemia
Pain Bones, kidney stones, ab groans, psych moans

59
Q

Osteitis fibrosis cystica

A

High PTH → cystic bone lesions
Brown color tumors dt hemorrhage → hemosiderin deposits
Rank-l expression on osteoblasts, rank on osteoclasts

60
Q

Secondary hyper PTH

A

Dt chronically * low calcium
Most common CKD dt low vitamin D conversion to active form in renal tubules by 1-a-hydroxylase
Other causes _ malabsorption, vitamin D deficiency

61
Q

Primary hyperPTH tx

A

Bisphosphanates eg alendronate decrease bone loss
Cinacalcet mimics ca to turn off PTH

Surgery possible but often fails, tricky

62
Q

Polyuria calcium

A

High Ca → polyuria via inhibition of action of ADH in renal tubules = nephrogenic di

Also potentially type I renal tubular acidosis, AKI

63
Q

Acute hypercalcemia

A

Most often dt cancer dt:
- pthrp production
- metastasis bone
- ectopic1-a-hydroxylas e→ excess calcitrol vitamin D

64
Q

Causes hypercalcemia

A

Parathyroid
Cancer
Granuloma- 1 alpha hydroxylse production
Meds:
-Lithium
- thiazide diuretics
- excess Ca or vit Dsupplement
-Familial hypocalcuric hypercalcemia - defects in ca receptors inparathyroid and kidney

65
Q

Calcium action potential

A

Blocks sodium channels
Raises threshold
Weakness

66
Q

Calcium heart

A

ReCduced Na movement de Ca blocking channels
Less depolarization → shorter depolarization
Shortened q T interval

Later arrhythmia, St changes
Cv. calcium deposits → valve stenosis, HTN, cardiomyopathy

67
Q

Loop diuretics ca

A

Decrease

Loops lose ca
Used in symptomatic hypercalcemia t x

68
Q

Acute symptomatic hyper Ca Tx

A

1 fluids

  1. Loop diuretics
  2. Bisphosphanates

Calcitonin if severe but resistance if long term
Cancer: denosumab anti-rank-l
High pth: cinacalcet
Granulomatous and lymphoma: prednisone

69
Q

Resorption

A

Breakdown of bone

70
Q

Pancreatitis calcium

A

Acute pancreatitis can cause low Ca dt deposits forming

High Ca can cause pancreatitis - one of the “groans”

71
Q

Drugs causing hypocalcemia

A

Loop diuretics eg furosemide
Bisphosphonates
Cinacalcet
Foscarnet_antiviral

72
Q

Loop diuretics target

A

Na-k-2cl transporter thick ascending loop of henle

73
Q

Chvostek sign,

A

Hypocalcemia
Tap facial nerve → twitching

74
Q

Trousseausign

A

Hypocalcemia
Inflate bp cuff 3 min → hand twitching and contracture

75
Q

Severe hypocalcomia st

A

Laryngospasm
Bronchospasm
Seizures
Life threatening

76
Q

Hypocalcemia reflexes

A

Hyperreflexia

77
Q

Hypocalcemia st

A

Irritability of nerves, muscles, heart

M sk:
Numb/tingle
Twit ching
Hyperreflexia
Tetany

PsyCch:
Anxiety
Depression
Psychosis
Am s
.chronic: Parkinsonism
, dementia, cataracts

Heart
Prolonged qt interval
Torsdades de pointes- potentially fatal

78
Q

Albumin Ca

A

Transports
Standard Ca lab is total including albumin bound but only free is active
Free isphysiollogically important
So low albumin means total Ca will be low or normal even if free is normal or high

79
Q

Acute symptomatic hypocalcemia Tx

A

Iv calcium gluconate then transition to oral Ca with vit D
Underlying cause

80
Q

Bisphosphonattes

A

Prevent bone resorption
Lower serum Ca
Induce apoptosis in osteoclasts

  • dronate

AES:
-N/v
- esophageal erosions
- iv: jaw osteonecrosis

81
Q

Denosumab

A

Hyper - Ca of malignancy
Prevents resorption
Decreases serum Ca
Anti-rank-l
Blocks osteoclast maturation

82
Q

Hypo-mg

A

Causes hypo-ca
Reduces PTH release
Poor diet, alcohol

83
Q

Sevelamar

A

Gut phosphate binder
For hyper. Phosphate → hypo-ca of CKD

84
Q

Calcium acetate

A
  • Gut phosphate binder
    Good if Ca supplement also needed but use caution in CKD
85
Q

Zone glomerulosa adrenal

A

Outermost
Mineralocorticoid’S

86
Q

Zone fasciculat a

A

Middle layer of cortex
Less staining due to high lipid content
Glucocorticoids

87
Q

Zone reticularis

A

Innermost oadvenal cortex
Androgens

88
Q

Chromaffin cells

A

Adrenal medulla
Catecholamine’S

89
Q

ACTH cellular targets

A

Upregulate StAR - steroidogenic acute regulatory protein - rate limiting incortisol formation - transferscholesterol into mitochondria

StimulatesCholesterol desmolase - convertscholesterol to pregnenolone

90
Q

CBG

A

Cortisol binding globulin
Transports most of cortisol in blood, prolongs t 1/2

91
Q

Cortisoltarget

A

Intracellular gr-glucocorticoid receptor
Complex directly binds glucocorticoid response element of gene

92
Q

Cortisol bone

A

Decreases osteoblast ‘ activity
excess → less new bone generation i i weaker bones

93
Q

Cortisol neutrophils

A

Demargination
Artificially increases count but decreases function

94
Q

Cushing disease

A

Cushing syndrome caused by an ACTH- secreting pituitary adenoma
Syndrome: all cause

95
Q

Bp cushings

A

Diastolic htn

96
Q

Bilateraladrenal_hyperplasia_tx

A

Cortisol synthesis inhibitors
Metyrapone
Ketoconazale
Mitotane

97
Q

Hyperaldosterone acid base

A

Metabolic alkalosis- excess H+ loss

98
Q

Conn syndrome

A

Benign aldosterone-secreting adenoma of adrenal gland

99
Q

Hypokalemia EKG

A

T wave inversion
Prominent U waves

100
Q

Main test to distinguish primary from secondary hyper-aldosteronis m

A

Plasma renin
Renin →aldosterone
So elevated in secondary and low in primary

101
Q

Hyper-aldosterone Tx

A

Underlying cause
K sparing diuretics - spironolactone and eplerenone

102
Q

Spironolactore

A

Competitive aldosterone receptor antagonist
Cortical collecting duct
K sparing diuretic

AES - androgen t progesterone - gynecomastia

103
Q

Eplerenone

A

More specific aldosterone receptor antagonist
K sparing diuretic
Alternative to spironolactone
No gynecomastia

104
Q

Causes of secondary hyperaldosteronism

A

Renal artery stenosis - impaired read blood flow
J G cell tumors
Liver cirrhosis
Hear t failure
Nephrotic syndrome

105
Q

Usually first presenting sign hyper aldosterone

A

Refractory hypertension
Labs then show hypokalemia and metabolic alkalosis

106
Q

Congenital adrenal hyperplasia

A

Autosomal recessive
Usually low cortisol and aldosterone but high sex steroids
Generally masculinizing - external genital ambiguity in female

107
Q

Most commonenzyme deficient cah

A

21 -hydroxylase

108
Q

Classic vs. nonclassic CAH

A

Classic - salt-wasting, dehydration, adrenal crisis - most common.

Non-classic- non-salt wasting - partial enzyme fx makes aldosterone but still no cortisol
→ less severe
→ may be silent till puberty
→ generally nogenital ambiguity but will have precocious virilizing puberty

Simple virilizing -cortisol andaldosterone present but high DHEA i

109
Q

Pheochromocytoma MEN

A

Types 2a and 2b

110
Q

Neuroblastoma

A

Abdominaltumor arising from neuralcrest cells
Generally along sympathetic chain or in adrenal medulla
Usually kids <4
Rapid growth

Hypertension from renal artery compression or catecholamine secretion
Rapid involuntary eye movements
Muscle twitchin
Abdominal distention
Palpable mass

111
Q

Neuroblastoma gene

A

Usually MYCN Amplification
If present isassociated with more aggressive course with 50%mortality
Without mutation better px with chance of spontaneous regression

112
Q

Biopsy neuroblastoma

A

Homer-wright rosettes
Small, round blue cells in circular patterns

Eosinophilic neuropil
IHC bombesin

113
Q

Suppression testing pheochromocyta

A

ClonidineSuppression testing if 24 h urine catacholemine and metarephrines is indeterminate

114
Q

Octreotide

A

Inhibits insulin and gh release
Chronic hypoglycemia
Acromegaly
Esophageal bleed
Hepatorenal syndrome

115
Q

HLA T1DM

A

Dr3 and dr4

116
Q

Hs type TIDM

A

. Type 4

117
Q

Mechanism of microvascular damage in diabetes

A

Mostly non-enzymatic glycosylation of various cellular proteins. - ages

In eye and Schwann cells - osmotic and oxidative injury from glucose → sorbitol

118
Q

Rapid insulins

A

Lispro, aspart, glulisine

119
Q

Intermediate acting insulin

A

NPH “

120
Q

Long acting insulins

A

detemir, glargine

121
Q

Metformin

A

Class: biguanide
Mx: glut 4 phosphorylation → glucose uptake
Also reduced gluconeogenesis and reduced gutreabsorption.
Ae: lactic acidosis. Gi
Ci: renal failure, CHF, hypoxia

122
Q

-glitazone

A

Class: thiazolidinediones
Mx: ppar- gamma activation → fatty acid storage → insulin sensitivity

Ae: fluid retention, liver damage, weight gain, low bone density
Ci: CHF

123
Q

Gly-/gli-

A

Class: sulfonylureas
Mx: stimulate pancreatic insulin release by closing atp-sensitive k channels

Ae: hypoglycemia, weight gain
Ci: sulfa allergy

124
Q

_Glinide

A

Class: meglitinides
Mx:similar tosulfornylureas
Ok in sulfa allergy

125
Q
  • Gliflozin
A

Class: sglt-2 inhibitors
Mx: inhibit renal glucose reabsorption
Æ: UTI, dehydration, fatigue

126
Q

Pramlintide

A

Class: amyline-anoloague
Mx: slow gastric emptying, promote fullness
Use: prevent hyper and hypoglycemia, weight loss, also T1DM

127
Q

-Tide

A

Class; GLP -1 agonist
Mx: endogenous incretin mimic
- Increasedpostprandial insulin
-Less glucagon
- delayed gastric emptying
-Fullness
- weight loss
Route: sub Q
A E: gi upset, acute pancreatitis

128
Q

_Gliptin

A

Class: Dpp4 inhibitor
Mx: inhibits degradation of glp-1
Similar fx to glp-1 agonists
Route: oral

129
Q

Hormones inducing insulin release

A

Glp- 1 and GIP

130
Q

Glucagonoma

A

Diabetes
Depression
Declining weight
DVT
Dermatitis - migratory necrolyticerethema

131
Q

Vip-oma

A

“Pancreatic cholera”

STEP1 (15 decks)

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