ENDOCRINOLOGY BOARDS ABIM EXAM LATEST
VERSION 2024-2025 ACTUAL EXAM 180
QUESTIONS AND CORRECT DETAILED ANSWERS
WITH RATIONALES
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Studied 7 terms
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Terms in this set (140)
Primary - problem with the gland that secretes the
hormone (ie: thyroid doesn't produce thyroid
hormone)
Secondary - problem is the gland that controls the
What are primary,
primary gland (ie. pituitary doesn't produce TSH to
secondary, and tertiary
stimulate the thyroid)
disease?
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 Controls the anterior pituitary via hormones
hypothalamus control the Controls the posterior pituitary via neurohypophysis -
pituitary? direct nerve stimulation
Posterior pituitary Secrete ADH and oxytocin
functions
Anterior pituitary - osmoreceptors to control ADH
release and thirst
Increased release rapidly with elevated osmolarity
Also see increased release with nausea
ADH regulation 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
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
Anterior pituitary - by pulsatile secretion of GnRH from hypothalamus;
hormones and controls (6 Inhibin from ovary & testes decreases FSH (only)
hormones) 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
, 1. Lactotrophs - secrete PRL; tied, most common
macroademona
2. Gonadotrophs -tied, most common
macroademona; presents as mass effect +/- silent or
Pituitary adenoma cell panhypopit or gonadotropin hypersecretion
types 3. Somatotrophs- acromegaly
4. Corticotrophs - cushings
5. Thyrotrophs - hyperthyroidism (least common)
6. Mixed (somatotrophs+lactotrophs) - acromegaly +
hyperPRL
Mass effect sx of pituitary HA, diplopia, visual field defect, seizures; occasionally
mass can get CNS rhinorrhea
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),
Dx of pituitary adenoma
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
Can be misread and be normal
multiparous women in 90% - pituitary compressed by
Empty sella syndrome
CSF, but functions normally
No treatment if no hormone abnormalities
VERSION 2024-2025 ACTUAL EXAM 180
QUESTIONS AND CORRECT DETAILED ANSWERS
WITH RATIONALES
Practice questions for this set
Learn
Studied 7 terms
Nice work, you're crushing it
Continue studying in Learn
Terms in this set (140)
Primary - problem with the gland that secretes the
hormone (ie: thyroid doesn't produce thyroid
hormone)
Secondary - problem is the gland that controls the
What are primary,
primary gland (ie. pituitary doesn't produce TSH to
secondary, and tertiary
stimulate the thyroid)
disease?
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 Controls the anterior pituitary via hormones
hypothalamus control the Controls the posterior pituitary via neurohypophysis -
pituitary? direct nerve stimulation
Posterior pituitary Secrete ADH and oxytocin
functions
Anterior pituitary - osmoreceptors to control ADH
release and thirst
Increased release rapidly with elevated osmolarity
Also see increased release with nausea
ADH regulation 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
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
Anterior pituitary - by pulsatile secretion of GnRH from hypothalamus;
hormones and controls (6 Inhibin from ovary & testes decreases FSH (only)
hormones) 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
, 1. Lactotrophs - secrete PRL; tied, most common
macroademona
2. Gonadotrophs -tied, most common
macroademona; presents as mass effect +/- silent or
Pituitary adenoma cell panhypopit or gonadotropin hypersecretion
types 3. Somatotrophs- acromegaly
4. Corticotrophs - cushings
5. Thyrotrophs - hyperthyroidism (least common)
6. Mixed (somatotrophs+lactotrophs) - acromegaly +
hyperPRL
Mass effect sx of pituitary HA, diplopia, visual field defect, seizures; occasionally
mass can get CNS rhinorrhea
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),
Dx of pituitary adenoma
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
Can be misread and be normal
multiparous women in 90% - pituitary compressed by
Empty sella syndrome
CSF, but functions normally
No treatment if no hormone abnormalities
