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ENDOCRINOLOGY BOARDS ABIM EXAM LATEST VERSION ACTUAL EXAM 180 QUESTIONS AND CORRECT DETAILED ANSWERS WITH RATIONALES|ALREADY GRADED A+ $17.99   Add to cart

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

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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 ACTUAL EXAM 180 QUESTIONS AND CORRECT DETAILED ANSWERS WITH RATIONALES|ALREADY GRADED A+

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  • August 11, 2024
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ENDOCRINOLOGY BOARDS ABIM EXAM LATEST
VERSION 2023-2024 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, it's not a
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

GH -> liver -> IGF-1 ->effects



Acromegaly sx - ANSWER-Insidious onset, usually 10+yr to dx

Enlarged hands, feet, coarse facial features, deepened voice, carpal tunnel, acanthosis nigricans, skin
tags; jaw growth causing dental abnormalities

Cardiac - ischemic HD, cardiomyopathy, diastolic HF, HTN, LVH; increased risk of CVA, DM, OSA, colon
polyps, malignancy

Untreated, lifespan reduced 10+ yrs

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