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Flashcards in Pituitary 3 Deck (44)
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1
Q

5 physiologic functions of PRL (prolactin)

A
  1. Milk production
  2. Steroidogensis in adrenals
  3. Metabolism of fats/carbs
  4. Vit D metabolism
  5. Fetal development
2
Q

2 main functions of PRL?

A
  • Mammary gland development (puberty)
  • Initiation of lactation post-partum (pregnancy)
3
Q

PRL is secreted by what?

Where are they secreted?

What is the manner?

A
  • Lactotrophs
  • Anterior pituitary
  • Pulsatile
4
Q

PRL is inhibited by what??

A

Prolactin Inhibitory Factor

(Dopamine)

5
Q

PRL is stimulated by what??

A

High Thyrotropin Releasing Hormone

6
Q

PRL is increased by what 2 things?

Smaller increases occur w/ what 6 things?

A
  • CW motion & nipple stimulation
  1. After sleep
  2. Exercise
  3. Intercourse
  4. Stress
  5. Pregnancy
  6. Lactation
7
Q

PRL suppresses which 3 hormones?

Suppression of this hormone leads to what sxs?

A
  • Gonadotropin Releasing Hormone (GnRH)
  • LH and FSH are lowered too as result
  • –> altered menses & fertility
8
Q

PRL stimulates adrenal androgen production leading to what 2 sxs?

A
  • Weight gain
  • Hirsuitism (esp women)
9
Q

What are 4 S/S of Hyperprolactinemia in ONLY women?

A

◦Irregular menstruation

◦Menopausal symptoms

◦Weight gain

◦Signs of increased androgens (hirsuitism)

10
Q

What are 2 S/S of Hyperprolactinemia in ONLY men?

A

◦Impotence

◦Gynecomastia

11
Q

What are S/S of Hyperprolactinemia in BOTH men/women?

A
  • Infertility
  • HA
  • Loss of libido
  • Peripheral Vision Problems
  • Moods changes/ depression
  • Galactorrhea
12
Q

What 2 sxs are indicative of MACROadenoma when PRL levels are elevated?

A
  • HA & Vision Changes
13
Q

Fasting Serum Prolactin Levels should be measured in ALL pts w/ what 3 sxs?

A
  • galactorrhea
  • gynecomastia
  • hypogonadism
14
Q

What does “further work up” for Hyperprolactinemia entail?

A

MRI (with or without contrast)

15
Q

What are some causes of Hyperprolactinemia?

A

}Prolactinoma (autonomous production)

}Other pituitary tumors (GH, ACTH)

}Hypothalamic disease

}Chronic Kidney Failure (decreased clearance by kidneys)

}Cirrhosis or Liver Disease

}Spinal cord damage

}Chest wall injury (such as in herpes zoster or surgery)

}Severe Primary Hypothyroidism (high TRH)

}Anti-psychotic medications

}Radiation, Surgery

}Idiopathic

16
Q

1st and 2nd MC cause of Pituitary Adenomas?

Least common?

A
  1. PRL (40-45%)
  2. GH (20%)

LC: TSH (1-2%)

17
Q

What type of PRL level if above 200 is HIGHY suggestive of a PRL secreting adenoma?

A

Basal (fasting serum) PRL level

18
Q

What types of adenomas are MC in men vs women?

A

Women: MICROadenomas

Men: MACROadenomas

(Women are smaller than men)

19
Q

90% of women w/ hyperprolactinemia have what 3 sxs?

A
  • Amenorrhea
  • Glactorrhea
  • Infertility

(GIA)

20
Q

Men c/o what 5 sxs most commonly w/ hyperprolactinemia?

A
  • dec. libido
  • HA
  • vision changes
  • impotence
  • infertility

(men need an ID to get HIV checked)

21
Q
  • Medications may cause hyperprolactinemia w/ PRL levels at what range?
  • Which drugs? (try to remember 7)
A
  • ≤50-100 ng/mL
  • Dopamine-receptor “antagonists” (1st gen. anti-psychotics and Reglan)

Dopamine-”depleting” agents (methyldopa, reserpine)

Others (INH, danazol, tricyclic antidepressants, verapamil, estrogens, antiandrogens, cyproheptadine, opiates, H2-blockers)

22
Q

Work up for Hyperprolactinemia:

  • H&P
  • identify autonomous prolactinoma / other etiologies
  • Serum assays (which 8?)
  • MRI of which 2 structures?
  • Visual field exam (if mass suspected)
  • Neuro testing (if mass effect suspected)
A
  1. Fasting PRL
  2. FSH
  3. LH
  4. Estradiol
  5. Tesosterone
  6. TSH
  7. Renal/Hepatic
  8. HCG (in females)
  • Pituitary & Brain MRI
23
Q

T/F

  • MOST microadenomas DO NOT progress to macroadenomas
A

True

24
Q

T/F

  • Most macroprolactinomas DO NOT require therapy?
A

False,

  • Dopamine agonists: Bromocriptine twice daily w/ food
  • +/- surgical resection
25
Q

3 tx options for Prolactinemia & Prolactinoma

A
  • Transsphenoidal resection
  • Surgical resection
  • Radiation therapy
26
Q

Definition:

  • Inability to lactate
A

Hypoprolactinemia

27
Q

Hypoprolactinemia

  • Lactotrophs are at risk for what 2 things (esp w/ what comorbidity)
A

Infarction & Necrosis (HTN)

28
Q

Hypoprolactinemia

  • What is post-partum hemorrhage called?
  • Pts w/ which comorbidity are more susceptivle to Post-partum pituitary infarction?
A
  • Sheehan’s Syndrome
  • Diabetics
29
Q

What is the Autoimmune Destruction associated w/ Hypoprolactinemia?

A
  • Lymphocytic Hypophysitis
30
Q

What test is used for Hypoprolactinemia?

What are the results which would be +?

A

Stimulation test:

◦Administration of TRH (chlorpromazine and others)

◦Rise in PRL levels <200% = Hypoprolactinemia

31
Q

Functions of ADH

  • Synthesized where?
  • Secreted by what?
  • Increase in serum osmolarity or a decrease in intravascular volume
A
  • Hypothalamus
  • Posterior Pituitary Gland
32
Q

Abnormalities in ADH

  • Absent/too little/receptor issues w/ ADH leads to what?
  • Too much ADH leads to what?
A
  • Too little: Diabetes Insipidus
  • Too much: SIADH
33
Q

2 types of DI?

A
  • Central / Neurogenic (rare)
  • Nephrogenic
34
Q

MC etiology of Neurogenic/Central DI?

A

Idiopathic (30%)

35
Q

2nd MC etiology of Neurogenic/Central DI?

A

Tumors (25%)

◦Primary (gliomas, craniopharyngiomas)

◦Secondary (lung cancer, breast cancer, leukemia or lymphoma)

◦Pituitary or Hypothalamus

36
Q

3 lesser common etiologies of Neurogenic/Central DI from greates to least?

A
  1. Neurosurgery
  2. Trauma
  3. Familial disease (defect in gene that codes for ADH precursor)
37
Q

MC cause of Nephrogenic DI?

A

Lithium (20%)

38
Q

Which 2 etiologies of Nephrogenic DI block the action of ADH?

A

}Hypercalcemia and/or hypokalemia

39
Q

Which etiology of Nephrogenic DI?

◦Defective expression of ADH receptors or aquaporin-2

A

Congenital / Hereditary

40
Q

3 diseases which cause Nephrogenic DI?

A

Sickle cell disease,

PCKD,

pyelonephritis

41
Q

Nephrogenic or Neuro/Central DI?

  • relatively common
  • Almost all patients: elderly, sick,
A

Nephro

42
Q

Both Nephro and Neuro DI have what sxs?

A

◦*New onset nocturia in the absence of drinking before sleep or prostatic enlargement (in men over age 50)

43
Q

S/S of DI

  • Frequent passage of large volumes of dilute urine
  • Excessive/intense thirst (predilection for cold or iced drinks)
    • Increased fluid ingestion
  • 24 hour urine volumes range from ___ to ___ L
A

2.5 - 20 L!!!

44
Q

Clinical Manifestations of DI

  • Water balance maintained IF thirst intact & adequate ingestion of fluid
  • IF access to water is interrupted, the pt may develop what??
A

Hypertonic volume depletion:

  • CNS manifestations:
    • irritability
    • mental dullness
    • coma