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Summer FDTN Exam 2 > Pituitary and Hypothalamus I > Flashcards

Pituitary and Hypothalamus I Flashcards

1
Q

Where is the pituitary

A

in the sells turcica of the sphenoid bone

made up of anterior (adenohypophysis) , intermediate, and posterior (neurohypophysis) lobes

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2
Q

What hormones do the pituitary lobes release

A

anterior: FSH, LH, ACTH, TSH, PRL, GH
posterior: Oxytocin, ADH (vasopressin)
Intermediate: Endorphins, MSH (melanocyte stimulating hormone)

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3
Q

What is the function of the hormones released from the hypothalamus

A 
TRH: stim TSH and PRL 
GnRH: stim FSH and LH 
CRH: stim ACTH, MSH, and endorphins 
GHRH: stim GH 
Dopamine: inhibit PRL 
SS: inhibit GH and TSH
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4
Q

What are the different ways you can evaluate hormone levels

A

blood (capillary/finger prick; venipuncture*, arterial)
urine (sample, or 24 hour collection)- clean catch (ex. catecholamines 2/2 pheo)
tissue bx (ex. thyroid tissue bx)

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5
Q

What are the types of urine specimens

A

UA- dipstick, pH, specific gravity, protein, glucose, ketone
Micro- sediment, crystals, casts, WBC, RBC

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6
Q

How do you get a 24 hour urine collection

A

discard first morning void
collect for next 24 hrs
record last void time
keep urine cool

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7
Q

What are different hormone testing levels and how can they be used

A
  • Direct random test: long half life hormone/ not protein bound (TSH)
  • Free/total fraction: protein bound hormone (total T3/T4)
  • Abs against hormone: AI dz (thyroid)
  • Precursor hormone: hyperadrenergic states (ovarian hyperplasia), androstenedione, estrogen, testoterone
  • Hormone ration: FSH:LH (infertility)
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8
Q

How can time make a difference in certain hormone tests

A

some hormones are pulsatile, or have shorter half lives

  • Cortisol: 6-8 AM
  • GH: at night
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9
Q

Everything in endocrine is basically

A

a feedback loop!
Primary: target hormone
Secondary: Pituitary
Tertiary: Hypothalamus

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10
Q

When would you use a suppression test

A

When you suspect HYPERfunctioning of a gland

ex: excess cortisol- Dexamethasone suppression test (normally dexamethasone will suppress adrenals and lower cortisol)

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11
Q

When would you use a stimulation test

A

When you suspect HYPOfunctioning

ex: low cortisol- ACTH stimulation test (when you give ACTH, adrenals should respond positively to it)

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12
Q

What are the disorders of the hypothalamus (tertiary d/o)

A

tumors (craniopharyngioma)
inflammation
infiltration (sarcoidosis)
mets tumor

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13
Q

Tertiary disorders are often associated with

A

loss of posterior pit fxn= central diabetes insipidus

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14
Q

What is the responsibility of the different vasopressin receptors

A

V1a- mediate pressor activity
V1b/V3- modulate ACTH secretion
V2- renal water excretion and Coag factor VIII ation

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15
Q

Give examples of when vasopressin is high and low

A

Alcohol inhibits ADH= you pee all the time

Hypotension/shock= high ADH bc you want to keep water

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16
Q

How do V2 agonists (Desmopressin) work

A

decrease water excretion in central diabetes insipidus and nocturnal enuresis (reduce urine flow)
-improve platelet responsiveness (hemophilia A, VWB dz, uremic coagulopathy)

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17
Q

What happens in diabetes insipidus

A

You have low ADH= massive urine excretion

this is a WATER problem, not a salt problem

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18
Q

What causes central diabetes insipidus

A

*Idiopathic (AI/inflammatory)
Trauma, CNS/pit surgery, anoxic encephalopathy (veterans, NFL players)
Primary tumors
Mets tumors (leukemia, lymphoma)
Granulomatous diseases
Autosomal Dominant
Pregnancy (placenta makes an enzyme that degrades ADH)

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19
Q

How does central Diabetes Insipidus usually present

A

acutely, unremitting thirst, polyuria, cave cold beverages, through day and night

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20
Q

What is the test for diabetes insipidus

A

Water deprivation test: Fluid deprive, and urine osm should be low. give desmopressin, and Uosm should spike

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21
Q

What is nephrogenic diabetes insipidus

A

ADH is produced, but the receptors dont work
No response to desmopressin; plasma ADH will be high before and after dehydration
MCC is chronic lithium use, or, hypercalcemia

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22
Q

What is primary polydipsia

A

Psych d/o in which pt drinks a shit ton of water; Na does not rise
Sna and Sosm are mid-low at start
Thirst does not improve!!

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23
Q

How do you treat neurogenic diabetes insipidus (same as central)

A

Decrease UOP by increasing ADH activity

Replace lost fluids! (avoid hypernatremia)

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24
Q

What is DDAVP

A

Desmopressin! synthetic ADH (makes you keep fluid)
Good Tx to reduce nocturia, provide adequate sleep, control diuresis during day
-Liquid nasal (potent), or tablet (less potent)

25
Q

If desmopressin is not effective in treating diabetes insipidus, what can you give

A

Chlorpropamide: anti-diuretic, promote renal response to ADH- but, high risk HYPOglycemia
Carbamazepine: enhance response to ADH
Clofibrate: increase ADH release
-Carb and clo decrease UOP up to 50%

26
Q

How do you treat nephrogenic DI

A

correct underlying disorder, dc offending drug (stop lithium or normalize calcium)
Thiazide + low salt diet: induce mild volume depletion (hypovolemia)= proximal tubule Na and H2O reabsorption= reduced UOP

27
Q

What is SIADH

A

Inappropriately high ADH= water retention; high urinary sodium loss (with little water loss)- this is a salt problem, not a water problem
Hyponatremia (<135) w/o edema

28
Q

What are the different levels of hyponatremia in SIADH

A

mild: 130-135
mod: 125-129
severe: <125
- Acute= <24 hrs
- chronic= >24 hr

29
Q

What are causes of SIADH

A 
Ectopic production (malignancy) 
Baroreceptor dysregulation (CNS infection, mass, hemorrhage, or MS) (PNA, TB) (Pain, Nausea) 
Multifactorial (antidepressants, narcotics, antipsychotics, cancer, chemo)
30
Q

What are symptoms of hyponatremia (in SIADH)

A

nausea W/O vomiting, confusion, HA

severe: vomiting, somnolence, seizure, GCS <8

31
Q

How do you treat SIADH

A

Restrict fluid intake (bc they are already holding so much fluid)
gently give hypertonic fluids to reverse Sx (sz)
(not common) Demeclocline and lithium (impair renal response to ADH)
(not common) Vasopressin antagonist (block ADH receptor so you pee more)

32
Q

What is a craniopharyngioma

A

MC sellar tumor of childhood- usually suprasellar
arise from rathke’s pouch and extend into diencephalon
can be cystic or full of lipid rick viscous fluid

33
Q

How do craniopharyngiomas present in kids

A

growth retardation
pubertal delay
visual field loss
projectile vomiting (sign of very bad brain tumor)

34
Q

Depending on the size, what anatomic damage can pituitary tumors have

A 
visual field loss
CN injury (VI paralysis= bitemporal hemianopsia) 
hypopituitarism 
CSF leak 
DI (not common)
35
Q

What is hypothalamus/pituitary regulation

A

CNS send signal to hypothalamus
hypothalamus to pituitary
pituitary to target gland
-target gland send negative feedback to pituitary and hypothalamus

36
Q

Explain the different hypothalamic-pituitary tumors and their Sx (overview)

A

Cushing’s: high cortisol, central obesity, striae, hyperglycemia, osteoporosis, hirsutism
TSH Adenoma: thyroid goiter, thyrotoxemia
Acromegaly: acral enlargement, soft tissue swelling, cardiac hypertrophy, HTN, hypergycemia, sleep apnea
Prolactinoma: galactorrhea, amenorrhea, infertility, hypogonadism
Non-fxn adenoma: central effects, hypogonadism, clinically silent

37
Q

What is the MC pituitary adenoma

A

Prolactinoma (40-45%)- secretes prolactin

Sx: galactorrhea, amenorrhea, infertility, hypogonadism

38
Q

What can cause diffuse pituitary hyperplasia

A

pregnancy
prolonged primary hypothyroid/hypogonadism
GhRH secreting tumor
Somatomamatotrophic hyperplasia in Carney complex

39
Q

What is a discrete pituitary tumor

A

monoclonal origin
20-30% are aggressive, invading adjacent structures (bone, sinuses, etc.); but size and extension not signs of aggressive behavioe
true malignancy <1%

40
Q

What is a pituitary incidentaloma

A

found incidentally on MRI or autopsy
no hormonal activity
Track with PRL measurement
-If PRL wnl, <5mm no additional study; 6-9mm repeat MRI in 2 years (per UTD)

41
Q

How do intrasellar pituitary tumors present

A 
HA 
pituitary hypofunction (low GH>LH/FSH>TSH>ACTH)
42
Q

How do suprasellar pituitary tumors manifest

A

impinge optic chiasm (bilateral hemianopsia)

obstruct 3rd ventricle, hydrocephalus, altered sensorium

43
Q

How do lateral extension pituitary tumors present

A

impinge CN III, IV, or VI

LR6, SO4, AO3

44
Q

How do inferior erosion pituitary tumors present

A

spinal fluid leak, meningitis

45
Q

What is the physiologic function of PRL

A 
Milk production 
fat and carb metabolism 
vitamin D metabolism 
fetal development 
**Mammary gland development (puberty) 
**Initiate lactation postpartum
46
Q

How is PRL regulated

A

secreted from lactotrophs of anterior pituitary in pulsatile manner
Inhibited by dopamine
Stimulated by TRH
Increased by chest wall motion and nipple stimulation (sleep, exercise, sex, stress, pregnancy, lactation)

47
Q

What does PRL do

A 
Suppress GnRH (low LH and FSH= altered menses and fertility) 
Stimulate adrenal androgen production= weight gain and hirsutism
48
Q

What are female S/Sx of hyperprolactinemia

A

irregular menses, galactorrhea

infertility, HA, depression, menopause Sx, low libido, weight gain

49
Q

What are male S/Sx of hyperprolactinemia

A

Loss of libido

galactorrhea, infertility, impotence, depression, gynecomastia

50
Q

What is the difference in size oh prolactinomas based on gender

A

Women: Micro because they come in sooner
Men: Macro bc they wait to be seen

51
Q

What are some causes of increased PRL

A

increased lactotroph # (pituitary tumor, pregnancy, hypothyroid/high TRH, chest wall injury)
Decreased PRL disposal (renal failure, Macroprolactinemia)

52
Q

“Increased PRL” is noted on labs as

A 
Diluted 50, stalk effect not prolactinoma (dopamine effects decreased by stalk injury) 
50-10, med cause 
If >100, likely a tumor (100-150) 
40-200**, drugs or stalk compression 
300-500, macroadenomas
53
Q

What is the “hook effect” in hyperprolactinemia

A

Extremely high levels of PRL may read falsely low on undiluted samples- so if you have a large tumor with a very low PRL level, get a diluted sample

54
Q

Who needs a fasting serum PRL level

A

all patients with galactorrhea, gynecomastia, and/or hypogonadism
(then get MRI w/ and w/o)

55
Q

What are pharm causes of hyperprolactinomas

A 
Dopamine antagonist (reglan, 1 gen anti-psych) 
Dopamine depleting (methyldopa, reserpine) 
TCA, Verapamil, estrogens, antiandrogens, opiate, H2 blocker
56
Q

If a woman comes in with galactorrhea and amenorrhea, first thing you get is

A

PREGNANCY TEST!

then get a PRL level

57
Q

Main Tx for prolactinomas

A 
Dopamine agonist (Bromocriptine BID w/ food; Cabergoline) 
\+/- surgical resection if extremely resistant (transsphenoidal resection, radiation) 
(Micro do NOT progress to Macro)
58
Q

What is the difference in bromocriptine and cabergoline

A

Bromo: high success, drug of choice in infertility, but many ADE
Caber: more tolerable, less ADE, biweekly dosing
-High dose cabergoline can cause valvular heart diseae

Summer FDTN Exam 2 (11 decks)

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