Endocrinology Thyroid and Adrenal Flashcards

1
Q

Where is TRH made?

TSH release is related to?

Thyroid makes T3 or T4 in higher amounts?

Most T3 made under normal conditions?

A

Hypothalamus at relatively constant rate

Concentration of cellular T3; at least 50% of pituitary T3 produced in cell from T3

T4 and when TSH high iodine rate limiting causing more T3 to be made

Liver

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2
Q

In non-thyroidal illness what are the T3 and T4 and TSH levels?

Most important test of thyroid function?

How is TSH measured, pitfall in pituitary disease?

A

Low T3, normal T4 and TSH

TSH; changed in logarytmicall with T4/T3; must destinguish from low normal from supressed (<0.05 mIU/L)

Immunoassay; pituitary makes abnormal TSH with reducted bio activity but enhanced Immunoassy; TSH ~15% high normalized with T4 administration

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3
Q

Is total T4, T3 still used?

TBG estimation?

A

Yes, normal rules out thyroid disease; need to estimate total binding protein by TBG estimation

Look at residen uptake vs T-uptage: Add excess T3 and fills are the binding protein sites–> add resing ot bind all the residual T3–> wash–> count resin and see how much is on resin

Less on resin=more free protein

More on Resin= less free protein

If change in same direction, thyroid problem, if change in opposite problem in TBG

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4
Q

Gold standard for Free T4 measurement?

False results in what patient states?

Anti-TPO seen in?

TSH receptor antibody seen in?

TSI is a test for?

A

Equilibrium dialysis; hard to measure free T4 due to small amount free

Acute illness and pregnancy

Anti-TPO; Graves’ and Hashimoto’s

TSH receptor antibody: Graves (stimulatory), atrophic thyroditis (blocking)

TSI: Graves, measure cAMP when thyroid cells incubated with patients IgG

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5
Q

When is Thyroglobulin tested for?

What is Anti-TG, lack of TG implies?

A

After cancer removal for residual disease (post TSH stimulation)

Anti-Thyroglobulin; interferars with immunoassay; so test for Ab’s when testing for TG!!

Lack of anti-TG implies lack of TG (no tumor)

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6
Q

First lab finding in hyperthyroidism?

What goes up first T3 or T4?

T4, T3, T3RU?

What normalizes first?

A

Low TSH; “Hot nodule”

T3 before T4

All high!

T4 normalizes first then T3 TSH may takes months before coming back up

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7
Q

What lab goes up 1st in hypothyroidism?

T3, T4, T3 RU, total?

Most common cause, other causes?

A

TSH!

All low; 30-40% have normal T3

Not having a thyroid (surgery, post radioiodine) Hashimotos; check Anti-TPO and Anti-TSH receptors in adults

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8
Q

Acute illness effects thyroid tests how?

Pregnancy/OC effects thyroid tests how?

Other causes of high TBG?

Causes of low TBG, labs?

A

Acute illness: low T3 (low peripheral conversion), normal Total/FreeT4 and TSH

Estrogen increases TBG: High total T4 and T3, low T3RU (most sites filled), normal TSH and Free T4
Opiates, active liver injury, pregnancy and OC pills

Cirrhosis/nephrotic syndrome, congenital deficiency, low total T3/T4, high T3RU (due to lwo TBG), normal TSH and Free T4

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9
Q

What regulated the Glucororticoids?

Highest production when?

What causes an increases?

What drug inhibits?

A

Hypothalamic CRH and pituitary ACTH

Morning

Stress, IL-6, serotonin

Cortisol only endogenous steroid inhibiting ACTH

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10
Q

What makes measuring Cortisol hard?

What is urine free cortisol?

A

Diurnal changes, highest (5-25 ug/dL) in morning and low (1-7 ug) early sleep

Some synthetic steroids cross react

Protein bound; free measurements not commonly used

Urine free: When binding capcity exceeded increases exponentially in urine, most sensitive direct test of cortisol production; HARD, needs 24 hour collection

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11
Q

What is a better way to measure cortisol since urine sucks?

When to check?

Why not used much?

A

Saliva measurements: proportional to plasma free

Easy to collect and best to be checked at bed time

Only available at reference labs

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12
Q

Problems with measuring ACTH?

What are suppression tests for ACTH?

Low vs high suppression tells us?

A

Released in bursts; unstable; difficult to interpert

Supression: Give dexamethasone (should supress ACTH and cortisol)

Look at dose to decrease plasma cortisol; Low dose supression= Cushings syndrome (high cortisol)

High dose suppresion= Cushings Dx (ACTH increase from pituitary adenoma)

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13
Q

What does Cortrysun stimulation test for?

How does insulin hyperglycemia test work?
How does Metyrapone test work (boards love this)?

A

See if patient can respond to ACTH; use synthetic fragment ACTH; see if cortisol goes up

No response means adrenal is no longer functional

Pituitary: Insulin hypoglycemia: most sensitive, rarely used, normal cortisol response >18 ug/dL

Metyrapone: Blocks 11-hydroxylase (last step in cortosol production) normal response is cortisol falling but ACTH and 11-deoxycortisole rise (at least 7ug/dL)

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14
Q

What causes Cushing’s?

Symptoms?

Most common cause?

Other causes

A

Increased cortisol/androgen

Obesity, hypertension, poor would healing, hypokalemia (some mineral activity), alkalosis, acne, hirsutism, etc.

Pituitary ACTH overproduction (Cushing dx); 70%

Adreanal adenoma/carcionoma: 15%

Ectopic ACTH (Small cell lung and carcinoid and thymoma): 15%

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15
Q

New gold standard test for ACTH/Cushing Dx measurement?

A

Inferior petrosal sinus sampling of ACTH after CRH administration: better than high dose DST

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16
Q

Symptoms of adrenal insufficency?

Mineralcorticoids vs glucorticoid deficencies?

A

More common than Cushings

Mineralcorticoid issues: Dehydration, Low sodium, High potassium, metabolic acidosis

Glucocorticoid- weakness, wt loss, vomiting, hypoglycemia, low sodium (SIADH, not volume depletion)

17
Q

1st lab test to dx adrenal insufficiency?

What does ACTH stimulation tell you?

A

Plasma cortisol; if <3 ug/dL confirms

ACTH stimulation tests to see if they respond; if they do ACTH and pituitary are issue

18
Q

Renin-Angiotensin-Aldosteron pathway?

Aldosterone does what?

Hyperaldosteronism symptoms?

Adenoma vs hyperplasia?

A

Renin cleaves angiotensinogen to AT1 to AT2 (by ACE in lung) which stimulates adrenal to make Aldosterone

Aldosterone: Pushs K+ into urine, absorbs sodium, Also pushed H+ into urine and absorbs K+

Hypokalemia, metabolic alkalosis, hypokalemia (may not show up in low sodium)

Adenoma- one sided, cured by surgery

Hyperplasia- not cured by surgery

19
Q

If Renin high and aldosterone high, think?

Renin low and aldosterone high think?

If both low?

A

Kidney making to much renin

Primary production in kidney

Not hyperaldosterone

20
Q

Norepinepherine made where?
Epinepherine?

What do you see in urine of patients with pheo, why not plasma?

Most sensitive test for pheo?

What is HVA?

A

Brain and adrenal

Adrenal medulla; if put epinepherine tumor=more likely to die vs NE and Epi tumor

Urine catecolamines!; plasma levels affected by stress

Fractionated metanepherines in plasma (sen not spec)

HVA: Dompamine metabolite

21
Q

Rules of 10%’s in pheos, germ lines?

A

10% bilateral, familial, extraaadrenal, malignant; 1/2 are germline (VHL, RET, SDH)