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CP Board Review - Chemistry > Endocrinology 1 > Flashcards

Endocrinology 1 Flashcards

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1
Q

Thyroid regulation

A
  • Hypothalamus makes TRH at relatively constant rate
  • Pituitary TSH response to TRH inversely related to cellular T3
  • At least 50% of pituitary T3 produced within cell from T4
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2
Q

Thyroid hormone synthesis

A
  • All steps activated by TSH; normally, TSH rate limiting
  • T4 predominant (90-95%) product
  • When TSH high, iodine rate limiting and progressively more T3 made
  • T3, active hormone, mostly produced in cells using it; circulating T3 mostly from liver
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3
Q

Thyroid PERIPHERAL FATE

A
  • Protein bound in blood (99.97% T4, 99.7% T3); free hormone active, regulated by TSH
  • Protein bound inactive, unregulated
  • Altered T4/T3 levels may be due to changes in production rate or binding protein levels
  • Changes in binding proteins common
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4
Q

Thyroid hormone metabolism

A
  • Most T3 produced peripherally (liver, kidney) by action of monodeiodinases
  • Type 1 3’,5’ monodeiodinase produces T3; enzyme labile, low in very young and old, acute illness, starvation
  • Pituitary type 2 monodeiodinase not affected in these states, so sees normal T3
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5
Q

TSH

A
  • Most important thyroid test; TSH changes logarithmically, even before T4/T3 outside reference range (more sensitive)
  • Almost all disorders are primary in thyroid
  • Test must distinguish low normal from suppressed (usually < 0.05 mIU/L)
  • TRH stimulation no longer used
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6
Q

Total T4, T3

A
  • Still performed by many labs
  • Affected both by thyroid function and binding proteins
  • Normal results (central 75%) effectively rule out thyroid disease
  • Abnormal results require estimation of binding protein levels
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7
Q

TBG ESTIMATION

A
  • Required if total T4 assays used and results outside central 75%
  • Two competing formats: resin uptake and T-uptake
  • Results of each have exactly opposite relation to TBG capacity from the other
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8
Q

T3 Resin Uptake

A

tell the story

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9
Q

FREE THYROXINE

A
  • Measure small amount of FT4 with large amount of protein bound T4
  • Cannot significantly disturb normal equilibrium between bound, free
  • Equilibrium constant considered “gold standard”; falsely high with acute illness
  • Most labs use other FT4 assays; may be falsely low or high with acute illness
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10
Q

Thyroid: AUTOANTIBODIES

A
  • Anti-TPO - seen in Graves’, Hashimoto’s in high titers, other forms of thyroiditis in low levels
  • TSH receptor antibodies found in Graves’ (stimulatory), atrophic thyroiditis (blocking)
  • TSI – measure cAMP production when thyroid cells incubated with IgG fraction; specific for Graves’
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11
Q

THYROGLOBULIN (TG)

A
  • Produced only by thyroid; related to mass, inflammation
  • After removal, used as marker of thyroid tumor metastases (after TSH stimulation, usually)
  • Anti-TG often present, interferes; test for Ab’s with TG assay, don’t report if positive
  • Loss of anti-TG implies lack of antigen; good prognosis
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12
Q

HYPERTHYROIDISM

A
  • Suppressed TSH first finding
  • T3 elevated before T4 (in Graves), free before total; nL T3 suggests other cause
  • Total T4, T3, T3RU all high, T-uptake low
  • With recovery, T4 normalizes first, then T3, TSH last (may take months); persistently low TSH – high risk of recurrence
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13
Q

HYPOTHYROIDISM

A
  • Separated into subclinical (high TSH, Nl FT4, no symptoms), clinical
  • Incidence increases with age (5% at age 60, 20% at age 80)
  • Most with subclinical hypothyroidism progress; controversy about screening, treatment
  • Increased TSH first; usually > 50 mU/L when symptoms begin, lesser degree of elevation in elderly; NL-sl increased with pituitary disease (reduced bioactive TSH)
  • Low free, total T4, low T3RU occur later than high TSH
  • T3 normal in 30-40% (more T3 made by failing thyroid); not helpful
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14
Q

TFT IN OTHER STATES

A
  • Acute illness: decreased T3 (low peripheral conversion), normal total/free T4, TSH
  • High TBG caused by estrogen (pregnancy, OC), phenothiazines, opiates, active liver injury: high total T4 (and T3), low T3RU, normal TSH, free T4
  • Low TBG caused by cirrhosis, nephrotic syndrome, congenital deficiency; low total T4(and T3), high T3RU, normal TSH, free T
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15
Q

ADRENAL FUNDAMENTALS

A
  • Functionally, three distinct glands in one anatomic structure
  • Most adrenal disorders detected by change in function
  • Most functional disorders affect only one hormone class
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16
Q

GLUCOCORTICOID

REGULATION

A
  • Hypothalamic CRH, pituitary ACTH
  • Cyclic production (highest on waking, lowest in early sleep)
  • Stress stimulates (IL-6, serotonin), minimizes cyclic production
  • Cortisol only endogenous steroid inhibiting ACTH production
17
Q

PLASMA CORTISOL

A
  • Simplest to measure, difficult to evaluate because of diurnal changes, stress effects
  • Highest on waking (5-25 g/dL), low early sleep (1-7 g/dL)
  • Some synthetic steroids cross react (not dexamethasone)
  • Protein bound, affected by binding proteins
  • Free cortisol better, not widely used
18
Q

Urinary Free Cortisol

A
  • Normally, little unmetabolized (free) cortisol excreted
  • When binding capacity exceeded, increases exponentially (e.g., recent case, plasma 2x normal, urine 50x normal)
  • Most sensitive direct test of cortisol production
19
Q

URINE METABOLITES

A
  • 17-ketosteroids - measure of androgen production (does not include testosterone)
  • 17-hydroxysteroids - measures cortisol, precursor, and metabolites
  • Colorimetric assays outmoded, non-specific; replaced by assays for specific metabolites in most cases
20
Q

PLASMA ACTH

A
  • Episodic bursts of release make single levels difficult to interpret unless cortisol highly abnormal
  • Unstable; requires special handling to prevent loss
  • Because adrenal dysfunction both primary and central, not as useful as TSH
21
Q

SUPPRESSION TESTS

A
  • Dexamethasone, a potent steroid, should suppress ACTH production
  • Dose required for suppression gives information on state of pituitary ACTH production
  • Used when cortisol excess (Cushing’s syndrome) suspected
22
Q

DEXAMETHASONE SUPPRESSION TESTS

A

TEST DOSE USES EXPECTED RESULTS
OVERNIGHT 1 mg AT 11 p.m.
Screen Plasma cortisol < 2.5 g/dL

LOW DOSE 0.5 mg q6H x 2d
Confirmation of Cushing’s syndrome
Urine cortisol < lower reference limit

HIGH DOSE 2.0 mg q6H x 2d OR 8 mg AT 11 p.m.
Differential diagnosis - Cushing’s disease shows fall in cortisol
Urine cortisol < 20% of basal
Or
Plasma cortisol < 50% of basal

23
Q

CORTROSYN STIMULATION

A
  • Uses synthetic fragment (1-24) of ACTH; has same effects,
  • Typical dose (250 ug) produces equivalent of > 1,000 x normal ACTH levels
  • Lower dose (1 ug) used by some
  • Cortisol should be > 18 ug/dL at 30 min
24
Q

PITUITARY STIMULATION

A
  • Insulin hypoglycemia most sensitive but rarely used; cortisol should be > 18 ug/dL
  • Metyrapone blocks 11-hydroxylase; normal response is for cotrisol to fall, but ACTH and 11-deoxycortisol to rise (the latter by at least 7 ug/dL
  • Less commonly used, but asked on boards
25
Q

CUSHING’S - CLINICAL

A
  • Relatively rare (5/million/yr)
  • Due to excess cortisol/androgens
  • Obesity, hypertension, poor wound healing, hyperglycemia, hypokalemia, alkalosis due to cortisol excess
  • Acne, hirsutism, menstrual problems due to androgen excess
26
Q

CUSHING’S - ETIOLOGY

A
  • Pituitary ACTH overproduction (Cushing’s disease) - 70%
  • Adrenal adenoma or carcinoma - 15%
  • Ectopic ACTH production (usually lung small cell or carcinoid tumors) - 15%
27
Q

EVALUATION FOR CUSHING’S SYNDROME

A

make image of this slide - 1089

28
Q

ADRENAL INSUFFICIENCY -

FEATURES

A
  • Much more common than Cushing’s
  • Mineralocorticoid - dehydration, decreased Na+, elevated
    K+, metabolic acidosis
  • Glucocorticoid - weakness, wt. loss, vomiting, hypoglycemia, decreased Na+ (due to SIADH, not volume depletion)
  • May be due to pituitary, adrenal pathology
29
Q

ADRENAL INSUFFICIENCY -

DIAGNOSIS

A
  • Plasma cortisol inappropriately low for illness; if < 3 ug/dL confirms diagnosis
  • Lack of response in stimulation tests
  • ACTH helpful to distinguish primary from secondary
30
Q

ADRENOGENITAL

SYNDROMES

A
  • Normal genital development:
  • External - female unless androgen present
  • Internal - female unless Y chromosome present
  • Excess or deficient androgen leads to different genetic, apparent sex
  • 21-hydroxylase deficiency causes 95% of congenital adrenal hyperplasia
  • Deficient cortisol, aldosterone; often low normal with high 17-OH progesterone
  • Genetic females have ambiguous genitalia
  • Mild deficiency may present with hirsutism after puberty
31
Q

Stimulate Adrenals

A
  • decreased blood flow
  • decreased urine Na
  • diuretics
  • hyperkalemia
32
Q

Inhibit Adrenals

A
  • ANP / BNP
  • NSAIDS
  • Beta Blockers
  • ACE inhibitors
  • Hypokalemia
  • Heparin
  • Adrenal disease
  • AR Blockers
33
Q

HYPERALDOSTERONISM

A
  • May be up to 5-10 % of hypertension
  • Hypokalemia, metabolic alkalosis; hypokalemia may not be present with low sodium diet
  • Adenoma - unilateral, cured by surgery
  • Hyperplasia - bilateral, not cured by surgery
34
Q

Hyperaldosteronism laboratory test

A
  • Plasma catecholamines - affected by stress, not routinely done
  • Total metanephrines, VMA - metabolites, measure total production
  • Fractionated catecholamines, metanephrines - can detect tumors making only epinephrine
  • HVA - dopamine metabolite
  • Fractionated metanephrines in plasma most sensitive but less specific
35
Q

PHEOCHROMOCYTOMA

A
  • Adult tumor, rare cause of hypertension
  • “10% tumor” - 10% bilateral, familial, extraadrenal, malignant; recent data suggest that up to 1/3 actually have germ line genetic mutations (VHL, RET, SDH2)
  • May cause episodic HTN, sweating, tachycardia, hyperglycemia, feeling of doom
36
Q

NEUROBLASTOMA

A
  • Infantile medulla tumor, Dx as abdominal mass
  • Malignant; spread to certain sites (skin, liver, BM) not associated with worse prognosis
  • N-myc amplification poor prognosis
  • VMA, HVA used to follow Rx
37
Q

INCIDENTAL MASS

A
  • Common finding on imaging
  • If asymptomatic, limited workup usually performed (DST, urine catecholamines or fractionated metanephrines; ? plasma metanephrines)
  • “Subclinical” Cushing’s – some progress, treatment controversial; surgery suggested if > 2-3 cm in diameter, ACTH low, DM/HTN

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