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*USMLE* > Endocrine > Flashcards

Endocrine Flashcards

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USMLE® Step 1 flashcards
1
Q

Differential: clinical, diagnostic, histo

Subacute granulomatous thyroiditis

vs.

Hashimoto’s

A

de Quervain - after virus, painful, transient hyperthyroid sx; high ESR/CRP; decreased radio-iodine uptake; infiltrate with macros + giant cells

Hashimoto’s - painless, mostly hypothyroid; anti-TPO, variable radio-iodine uptake; lympho infiltrate with germinal centers + Hurthle cells (eosinophilic follicular epithelium with granular cytoplasm/vesicular nucleus)

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2
Q

Papillary thyroid cancer

histo of NORMAL variant

A

branching papillary structures with concentric calcification (Psamomma bodies)

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3
Q

Papillary thyroid cancer

histo of TALL CELL variant, differential

A

follicular hyperplasia lined with tall epithelial cells

Graves can also have follicular hyperplasia, but would have increased radio-iodine uptake (via high TSH stim)

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4
Q

Riedel thyroiditis

histo? clinical?

A

extensive fibrosis extending into surrounding structures

hard + non-tender thyroid

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5
Q

Neonatal complications of diabetes during pregnancy

6

A
  1. premature delivery
  2. macrosomia
  3. malformations - NT, CV and “caudal regression syndrome”
  4. respiratory distress
  5. transient hypoglycemia
  6. polycythemia + hyperviscosity
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6
Q

Why does TRANSIENT HYPOGLYCEMIA occur in neonates born to diabetic mothers with poorly controlled glucose?

A

Glucose passes placenta but insulin does not –> stimulates fetal insulin production –> after birth insulin production is still high but maternal glucose is not being provided

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7
Q

2 mechanisms of diabetic neuropathy

A
  1. NEG - affects endoneural arterioles > thickening, hyalinization and luminal narrowing > ischemia
  2. Intracellular hyperglycemia - glucose converted to fructose and sorbitol by ALDOLASE REDUCTASE > water influx with osmotic damage
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8
Q

3 types of diabetic neuropathy

A
  1. Distal symmetric neuropathy
  2. Autonomic neuropathy
  3. Mononeuropathy
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9
Q

Distal symmetric diabetic polyneuropathy

s/s?

A

Mostly SENSORY with paresthesias, burning pain, loss of pain/temp/vibration/position

Motor comes mostly with sensory sx, not on its own > weakness, atrophy, decreased deep tendon reflexes

symmetric, bilateral, stocking and glove pattern

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10
Q

Autonomic Diabetic Neuropathy

effects by organ system

A

GI - gastroparesis and constipation
CV - orthostatic hypo
Urinary - overflow incontinence, “neurogenic bladder”
Sexual - erectile and ejaculatory issues

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11
Q

Diabetic Mononeuropathy

specific nerves commonly affected

A

Cranial: oculomotor, facial and optic (ischemic optic neuropathy)

Somatic: commonly bilateral, ULNAR, MEDIAN and COMMON PERONEAL

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12
Q

Medullary thyroid cancer

histo, assoc.

A

nests / sheets of polygonal or spindle cells and EC amyloid (calcitonin)

amyloid stains red with CONGO

MEN2A/B

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13
Q

GPCR-mediated control of insulin release

4 stimulators, 2 inhibitors

Overall effect of epinephrine?

A 
Stimulators:
M3 receptor (Gq)
Glucagon (Gq or Gs)
Beta2 (Gs)
GLP-1 (Gs)

Inhibitors:
Alpha2 (Gi)
Somatostatin 2 receptor (Gi)

Epinephrine stimulates B2 and A2, but overall effect is DECREASED insulin release

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14
Q

Diffuse atrophy of thyroid follicles with decreased colloid is seen on histo

Thyroid is small + non-tender and without palpable nodules

What is the cause?

A

Excess exogenous thyroid hormone

Can be either by mis-dosing of a hypothyroid patient or EATING DISORDER patient with access to thyroid meds

Histo shows atrophy without signs of inflammation

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15
Q

Gigantism

cause (TWO hormones involved + where they’re from + molecular pathways they effect)

A

increased GH > GH-R on liver > JAK-STAT activation > increased transcription of IGF-1

IGF-1 binds a receptor tyrosine kinase, affecting mostly bone, cartilage, skeletal muscle + other soft tissues

(note that IGF-1 released by hypothalamus regulates CNS and does not play role in growth)

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16
Q

Gigantism

s/s

A

rapid linear growth

weight gain
excess SWEATING
OILY SKIN
large hands + feet
THICK CALVARIUM
PROGNATHISM (large jaw)
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17
Q

Laron dwarfism

cause? effect? labs?

A

GH-R defect > high GH but low IGF-1

decreased linear growth

18
Q

Androgen insensitivity syndrome

cause? karyotype? phenotype?

A

testosterone receptor defect
46, XY

phenotypically FEMALE adolescent with PRIMARY AMENORRHEA due to ABSENT INTERNAL REPRODUCTIVE TRACT and presence of CRYPTORCHID testes

19
Q

mechanism of infertility in hypothyroidism

A

low T3/4 > TRH release from hypothalamus > there are TRH RECEPTORS ON LACTOTROPHS in the pituitary > PROLACTIN release

Prolactin inhibits GnRH secretion from the hypothalamus > low FHS/LH

pt may also have galactorrhea

20
Q

Which commonly deficient steroid synthesis enzyme is responsible for the “DOWNWARD MOVEMENT” on the chart from PROGESTERONE and 17-OH PROGESTERONE to final products?

what results from deficiency?

A

21 hydroxylase - #1 type of CAH

increased androgens; decreased cortisol + aldosterone

males - normal junk; hyperkalemic/hypotensive
females - male junk; hyperkalemic/hypotensive

21
Q

Which commonly deficient steroid synthesis enzyme is responsible for FURTHER DOWNWARD MOVEMENT on the chart from slightly active intermediates to the final products?

what results from deficiency?

A

11B-hydroxylase

decreased cortisol; increased androgens and weak MCs (11-deoxycorticosterone)

males - normal junk; hypokalemic/hypertensive
females - male junk; hypokalemic/hypertensive

may have low renin levels

22
Q

Which commonly deficient steroid synthesis hormone is responsible for ‘RIGHTWARD MOVEMENT’ on the chart from pregnenolone and progesterone to final products?

what results from deficiency?

A

17alpha-hydroxylase

decreased cortisol + androgens; increased aldosterone

males - feminine junk; hypokalemic/hypertensive

females - normale junk (but delayed menarche); hypokalemic/hypertensive

low renin levels; do not undergo puberty

23
Q

What is the triad for confirming symptomatic hypoglycemia?

A

Whipple’s triad

  1. Symptoms - tremor, sweating, confusion
  2. Low blood glucose
  3. Relief when glucose is admin’d
24
Q

What role do FREE FATTY ACIDS play in type 2 DM?

why are FFAs elevated and what do elevated FFAS affect?

A

increased circulating FFAs are both caused by and contribute to insulin resistance

  1. Insulin resistance > less anti-lipolytic effect on fat cells > release of FFAS
  2. Chronic FFA elevation > IMPAIRS INSULIN-DEPENDENT GLUCOSE UPTAKE and INCREASES GLUCONEOGENESIS
25
Q

McCune Albright Syndrome

mutation + result?

A

a mosaic SOMATIC mutation during embryogenesis of the GNAS gene, encoding ALPHA STIMULATORY SUBUNIT of G protein

constitutive activation of Gs pathway

hormone overproduction etc.

26
Q

McCune Albright Syndrome

first sign; later signs

complications (think of the results of the mutation)

A
  1. Cafe Au Lait Macules - usually UNILATERAL with IRREGULAR borders (melanocyte overstimulation)
  2. POLYOSTOTIC FIBROUS DYSPLASIA - fibroblast proliferation, high IL-6 and osteoclast activation; typically UNILATERAL
  3. PERIPHERAL PRECOCIOUS PUBERTY - before 8 in girls

hormone overproduction can also cause a) ACROMEGALY, b) THYROTOXICOSIS, and c) CUSHING

27
Q

Differentiation of cafe au lait in NF1 and McCune Albright syndrome

A

MAS - large, unilateral, irregular border

NF1 - small, bilateral, smoother border (plus axillary/inguinal freckles, cutaneous neurofibromas; bone involvement can be tibial bowing and pseudoarthrosis)

28
Q

what 3 molecules bind thyroid hormones for transport in blood?

A
  1. THYROXINE-BINDING GLOBULIN - not to be confused with thyroglobulin which is only in the thyroid; binds 70% of bound T hormones
  2. ALBUMIN
  3. TRANSTHYRETIN - binds both T4 and retinol+retinol-binding-protein complexes
29
Q

What effect does INCREASED ESTROGEN have on THYROID HORMONES?

as in pregnancy, oral contraceptives, postmenopausal hormone therapy

A

first - INCREASES THYROXINE-BINDING GLOBULIN

this binds free T4 > transient TSH increase > more T4 produced > T4 binds excess TBG

finally - TOTAL T4 is INCREASED (but fT4 remains same and patient is clinically euthyroid)

30
Q

What effect does TNF-alpha have on carbohydrate metabolism and how?

What other molecules have the same effect via the same mechanism?

A

induces INSULIN RESISTANCE by activating SERINE KINASES that phosphorylate beta subunits of INSULIN RECEPTOR and IRS-1

this inhibits their phosphorylation on Tyr residues by the insulin receptor itself, and thus inhibits downstream signaling

catecholamines, glucocorticoids and glucagon all have same effect

31
Q

Maternal to fetal transfer of what causes thyroid aplasia?

A

T4

32
Q

Endocrine abnormalities in Klinefelter’s (2 + histo picture involved in one of them)

A
  1. SEMINIFEROUS TUBULE DYSGENESIS (don’t see normal lumen in testicular histo) > low inhibin B from Sertolis > HIGH FSH
  2. Abnormal Leydig cell function > low testo > high LH > HIGH ESTROGEN
33
Q

Cushing’s DISEASE adrenal histo

A

cush DISEASE = pituitary ACTH adenoma

increased ACTH causes CORTICAL HYPERPLASIA (not hypertrophy; so number of cells, not size of cells)

34
Q

Very SPECIFIC dermatological finding of Graves

+ its pathophys mech

A

“thyroid dermopathy”

PRETIBIAL MYXEDEMA - induration and thickening of shin skin

stimulation of FIBROBLASTS by anti-TSH-R Ab and activated T-cells > produce GAGs

(similar mech for retro-ocular fibroblasts in Graves ophthalmopathy)

35
Q

2 molecular pathways stim’d by insulin + their effects

A

PI3K - glycogen, lipid + protein synth; GLUT4 translocation

RAS/MAP kinase - cell growth + DNA synth

36
Q

biochem mechanism of opposing actions of glucagon and insulin on glycogen metabolism

A

insulin - activates PROTEIN PHOSPHATASE > DEphosphorylation of glycogen synthase + glycogen phosphorylase promotes glycogen SYNTHESIS

glucagon - activates PKA > PHOSPHORYLATION of glycogen synthase + glycogen phosphorylase promotes glycogenoLYSIS

(glucagon > PKA > glycogen phosphorylase kinase > activated glycogen phosphorylase)

37
Q

SIADH

how does it affect sodium levels and volume and why?

A

“Euvolemic Hyponatremia”

high ADH > water resorption in CDs > transient hypovolemia suppresses RAAS and activates ANP + BNP SECRETION > natriuresis

this compensates for the volume overload, but the hyponatremia remains

38
Q

What is the weak mineralocorticoid that is in excess in one of the forms of CAH?

A

11-deoxycorticosterone

in 11B-hydroxylase deficiency

(results in increased androgens and mineralocorticoid effects)

39
Q

What are endogenous fasting serum insulin levels like in someone with long-standing T2DM treated with insulin?

A

VERY LOW

due to beta cell exhaustion + inhibition of insulin release by control of blood sugar via exogenous insulin

40
Q

Fasting glucose and random glucose values ABOVE WHICH a diabetes diagnosis can be made

A

fasting at least 126 mg/dl

random at least 200 mg/dl

*USMLE* (28 decks)

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