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ENDOCRINOLOGY BOARDS ABIM EXAM LATEST VERSION ACTUAL EXAM 180 QUESTIONS AND CORRECT DETAILED ANSWERS WITH RATIONALES|ALREADY GRADED A+

EXAMS AND CERTIFICATIONS Oct 4, 2024
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ENDOCRINOLOGY BOARDS ABIM EXAM LATEST VERSION ACTUAL EXAM 180 QUESTIONS AND CORRECT DETAILED ANSWERS WITH RATIONALES|ALREADY GRADED A+

ENDOCRINOLOGY BOARDS ABIM EXAM LATEST VERSION

2026-2027 ACTUAL EXAM 180 QUESTIONS AND CORRECT

DETAILED ANSWERS WITH RATIONALES|ALREADY

GRADED A+

What are primary, secondary, and tertiary disease? - ANSWER- Primary

- problem with the gland that secretes the hormone (ie: thyroid doesn't

produce thyroid hormone)

Secondary - problem is the gland that controls the primary gland (ie.

pituitary doesn't produce TSH to stimulate the thyroid)

Tertiary - problem with the gland that controls the secondary gland that

controls the primary gland (ie. hypothalamus not producing TRH ->no

TSH from pituitary -> no T3/T4 from thyroid)

How does the hypothalamus control the pituitary? - ANSWER- Controls

the anterior pituitary via hormones

Controls the posterior pituitary via neurohypophysis - direct nerve

stimulation

Posterior pituitary functions - ANSWER- Secrete ADH and oxytocin

ADH regulation - ANSWER- Anterior pituitary - osmoreceptors to

control ADH release and thirst

Increased release rapidly with elevated osmolarity

Also see increased release with nausea


ADH osmolar release set point is affected by:

Lower set point (release at lower osm) with pregnancy and pre-menses

Higher set point with chronic hypovolemia, acute HTN, corticosteroids

Anterior pituitary - hormones and controls (6 hormones) - ANSWER- 1.

ACTH - peak 3-4 am, nadir 10-11pm; stimulates corticosteroids and

androgens from adrenals; increase with corticotropin releasing hormone,

physical/psych stress

2. Growth hormone - GHRH increases, somatastatin decreases, both

from hypothalamus

3. LH & FSH - produced by gonadotrophs; increased by pulsatile

secretion of GnRH from hypothalamus; Inhibin from ovary & testes

decreases FSH (only) production

4. PRL - tonic inhibition from hypothalamic dopamine; increase with

sleep, stress, lactation, nipple stimulation; Metaclopramine,

phenothiazines (decrease dopamine) increase PRL; Hypothyroid

modestly increases PRL

5. TSH - stim by TRH from hypothalamus, inhibited by T3, T4,

somatastatin

Pituitary adenoma cell types - ANSWER- 1. Lactotrophs - secrete PRL;

tied, most common macroademona

2. Gonadotrophs -tied, most common macroademona; presents as mass

effect +/- silent or panhypopit or gonadotropin hypersecretion

3. Somatotrophs- acromegaly

4. Corticotrophs - cushings

5. Thyrotrophs - hyperthyroidism (least common)


6. Mixed (somatotrophs+lactotrophs) - acromegaly + hyperPRL

Mass effect sx of pituitary mass - ANSWER- HA, diplopia, visual field

defect, seizures; occasionally can get CNS rhinorrhea

Dx of pituitary adenoma - ANSWER- Sx first

Check MRI

Labs - PRL, IGF-1 (for acromegaly), 24 hr urine free cortisol or 1mg

overnight dexamethasone suppression test (for excess) or ACTH stim

test (for deficiency), TSH, FT4, alpha subunit of FSH, LH (confirms

pituitary origin)

If mass on MRI, but all labs normal, likely a non-pituitary tumor -

craniopharyngioma, meningioma, eosinophilic granuloma, histiocytosis

X, pituitary mets

Empty sella syndrome - ANSWER- Can be misread and be normal

multiparous women in 90% - pituitary compressed by CSF, but

functions normally

No treatment if no hormone abnormalities

Symptoms and labs in prolactinoma - ANSWER- Most common

functional tumors; usually microadenomas, can be space occupying

lesions

Elevated PRL->decreased release of GnRH->decreased LH/FSH->

decreased libido, ED in men, amennorhea and hirsutism in females;

Increased size=increased PRL, so if > 1cm and PRL<100>

prolactinoma


Men present later->only decreased libido, so present as space occupying

lesion (visual field defects)

Can cause galactorrhea in women, decreased bone mineralization

Causes of increased PRL - ANSWER- Prolactinoma, phenothiazines,

amitriptyline, metaclopramide (all decreased dopamine), estrogen

(inhibits dopamine->elevated PRL in pregnancy), hypothyroidism

Treatment for prolactinoma - ANSWER- Begin treatment when neuro sx

from size or sx of hypogonadism

Medical - dopamine agonists: Cabergoline and bromocriptine

Cabergoline -better tolerated, less nausea, 2x/wk dosing; increased valve

dz if high doses, contraindicated with valve dz, known lung dz,

retroperitoneal fibrosis

Surgery - is can't tolerate meds; trtanssphenoidal; ofter rucurs

Radiation- to eradicate residual tumor post-surgery

Treating prolactinoma in pregnancy - ANSWER- Stop meds

Observe for sx, do visual field testing

1/3 enlarge in pregnancy - if enlarges enough to cause sx, restart

bromocriptine (safe in pregnancy)

Growth hormone regulation - ANSWER- Suppressed - hyperglycemia,

somatastatin, chronic steroids

Stimulated by - hypoglycemia, estrogens








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