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DEMS IV > hypothalamic pituitary dysfunction > Flashcards

hypothalamic pituitary dysfunction Flashcards

1
Q

List factors which stimulate release of GH

A

sleep, stress, ghrelin, arginine, hypoglycemia

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2
Q

List factors which inhibit release of GH

A

Obesity/FFA, glucocorticoids, leptin, hyperglycemia

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3
Q

clinical signs of GH excess and deficiency. How do you assess?

A

excess: acromegaly (large body tissues). Deficiency: GH deficiency. Check GH and IGF( liver)

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4
Q

clinical signs of PRL excess and deficiency. How do you assess?

A

excess: hypogonadism. Deficiency: failed lactation. Check PRL and breast

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5
Q

clinical signs of FSH/LH excess and deficiency. How do you assess?

A

excess; rare. Deficiency: hypogonadism. Check LHFSH and testosterone or estradiol (gonads)

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6
Q

clinical signs of ACTH excess and deficiency. How do you assess?

A

excess: cushings. Deficiency: adrenal insufficiency. Check ACTH and cortisol/ DHEA-S (adrenal gland)

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7
Q

clinical signs of TSH excess and deficiency. How do you assess?

A

excess: hyperthyroidism. Deficiency: hypothyroidism. Check TSH and T4/T3 (thyroid)

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8
Q

clinical signs of ADH excess and deficiency

A

excess: SIADH. Deficiency: diabetes insipidus

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9
Q

Levels of Hypothalamic-Pituitary- Target Organ Defect

A

Tertiary disorders: hypothalamus. Secondary: pituitary. Primary: target organ

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10
Q

what is dynamic pituitary testing and give examples for GH and ACTH

A

Utilizes Known Physiologic Stimulators and Suppressors of Pituitary Hormone Release. Hormone Excess is assessed by a Suppression Test (e.g., Oral glucose tolerance test for GH suppression to confirm acromegaly). Hormone Deficiency is assessed by a Stimulation Test (e.g., insulin tolerance test to evaluate pituitary (ACTH and GH) reserves.

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11
Q

Dynamic test for ACTH deficiency

A

cosyntropin stimulating test- hypoglycemia using insulin, metryapone

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12
Q

dynamic test for GH deficiency

A

Stimulating tests: glucagon or Arginine, ITT

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13
Q

GH regulation

A

GH stimulates release of IGF-1 from liver, which inhibits pituitary release of GH and hypothalamus release of GHRH. Also, GH directly inhibits pituitary and hypothalamus

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14
Q

List actions of GH

A
  1. increases blood glucose (via IGF-1). 2. increases bone and cartilage mass/growth. 3. increases protein synthesis and muscle mass. 4. increases fat breakdown and TGA levels. 5. increases salt/H20
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15
Q

compare GH excess before and after puberty

A

GIGANTISM-Growth hormone excess before puberty (before closure of the growth plates) results in very tall stature. ACROMEGALY-GH excess after puberty (after completion of linear growth) results in large body tissues but not height.

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16
Q

clinical presentation of acromegaly

A

facial changes, headaches, hyperhidrosis, amenorrhea, sleep apnea, HTN, dyslipidemia, parasthesias, carpal tunnl, impaired glucose tolerance/diabetes

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17
Q

Diagnosis of GH excess

A

Elevated IGF-1 is best screening test due to long half life and integrated 24 hr secretion. Note that GH levels fluctuate widely over 24 hrs and normal values can overlap with GH-secreting tumors. Check OGTT/GH for equivocal cases. Pituitary MRI. Also clinical features

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18
Q

primary cause of GH excess

A

pituitary macroademonas- 80%

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19
Q

acromegaly treatment

A

surgery, somatostatin analogs, GH receptor antagonists, radiation therapy

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20
Q

clinical presentation of GH deficiency

A
  1. body composition: increased fat, decreased muscle mass and strength. 2. bone strength: bone loss and fracture risk. 3. Metabolic/cardiovascular: increased cholesterol and C-RP. 4. psychological: impaired energy and modd, decreased quality of life
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21
Q

GH deficiency treatment

A

GH replacement therapy is controversial in adult onset. Modest benefits in body comp, metabolic parameters and QoL

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22
Q

diagnosis of adult onset GH deficiency

A
  1. insulin induced hypoglycemia (gold standard). 2. GHRH-arginine (second best) no longer available in US. 3. arginine and glucagon stimulation tests. 4. IGF-1 level is low
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23
Q

causes of hyperprolactinemia

A
  1. Physiological :Pregnancy, suckling, sleep, stress. 2. Pharmacological: Estrogens (OCPs), Antipsychotics, antidepressants (TCAs), antiemetics (reglan), Opiates. 3. Pathological: Pituitary Stalk Interruption, Hypothyroidism, chronic renal/liver failure, seizure
    Prolactinoma1. Physiological :Pregnancy, suckling, sleep, stress. 2. Pharmacological: Estrogens (OCPs), Antipsychotics, antidepressants (TCAs), antiemetics (reglan), Opiates. 3. Pathological: Pituitary Stalk Interruption, Hypothyroidism, chronic renal/liver failure, seizure
    Prolactinoma1. Physiological :Pregnancy, suckling, sleep, stress. 2. Pharmacological: Estrogens (OCPs), Antipsychotics, antidepressants (TCAs), antiemetics (reglan), Opiates. 3. Pathological: Pituitary Stalk Interruption, Hypothyroidism, chronic renal/liver failure, seizure
    Prolactinoma1. Physiological :Pregnancy, suckling, sleep, stress. 2. Pharmacological: Estrogens (OCPs), Antipsychotics, antidepressants (TCAs), antiemetics (reglan), Opiates. 3. Pathological: Pituitary Stalk Interruption, Hypothyroidism, chronic renal/liver failure, seizure
    Prolactinoma
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24
Q

Compare prolactinomas in women vs men

A

10:1 female to male. Females: microadenomas- galactorrhoea in 30-80%, menstrual irregularity, infertility, impairs GnRH pulse generator. Males: macroadenomas- galactorrhoea in <30%, visual field abnormalities, headache, impotence, EOM paralysis, antieror pituitary malfunction

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25
Q

prolactinoma diagnosis

A
  1. random PRL level. 100-150ng/dl correlates with microadenoma. 200-250ng/dl correlates with macroadenoma. 2. pituitary MRI
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26
Q

Prolactin deficiency causes, presentation and diagnosis

A

Etiology: Severe pituitary (lactotrope) destruction from any cause (e.g., pituitary tumors, infiltrative diseases, infectious diseases, infarction, neurosurgery or radiation). Clinical Presentation: Failed lactation in post-partum females, no known effect in males. Diagnosis: low basal PRL level

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27
Q

Cortisol functions

A

Gluconeogenesis, Breakdown of Fat and Protein for Glucose Production, Control Inflammatory Reactions

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28
Q

Clinical presentation of chronic cortisol excess

A
  1. changes in carb, protein and fat metabolism: wasting of fat/muscle, central obesity, osteoporosis, diabetes, elevated TG. 2. Changes in sex hormones: amenorrhea, excess hair, impotence. 3. salt and water retention: HTN, edema. 4. impaired immunity. 5. neurocognitive changes
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29
Q

ACTH dependent and independent causes of hypercortisolism

A

Dependent (75%): Corticotrope Adenoma (Cushing’s Disease), Ectopic Cushing’s (ACTH/CRH tumors). Independent (30%): Adrenal Adenomas, Adrenal Carcinoma, Nodular Hyperplasia (micro or macro)

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30
Q

screening guidlelines for Cushings syndrome

A

Screening indicated in patients with multiple and progressive “high-discriminatory” features of Cushing’s Syndrome

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31
Q

Clinical signs of Cushing syndrome

A

Plethoric/moon facies, wide violaceous striae (abdominal, axillary), Spontaneous Ecchymoses (bruising), Proximal Muscle Weakness, early osteoporosis

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32
Q

cortisol rhythms

A

Episodic- Major ACTH/cortisol burst in the early morning (before awakening). Cortisol drops lowest at 11-12pm

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33
Q

Cortisol binding

A

Most cortisol is bound to transcortin (cortisol binding globulin-CBG).10-15% bound to albumin (less tightly). 5% Unbound (Free cortisol)

34
Q

Screening tests for Cushings

A
  1. Disrupted Circadian Rhythm- Midnight Salivary or Serum Cortisol. 2. Increased Filtered Cortisol Load - 24 hr Urine Free Cortisol. 3. Attenuated Negative Feedback- Low Dose (1 mg) Dexamethasone Suppression test (11-12 p.m.)
35
Q

Pseudo-cushings

A

Overactivation of the HPA axis without tumorous cortisol hypersecretion. Severe Depression/ Anxiety/OCD, Severe Obstructive Sleep Apnea, Alcoholism, Poorly-controlled DM, Physical Stress (acute illness, surgery, pain)

36
Q

Cushings workup

A
  1. Midly elevated plasma ACTH. 2. MRI of pituitary: ~80% microadenomas, 50% identified on MRI). 3. Sampling of inferior petrosal sinus if MRI negative
37
Q

Etiology of central adrenal insufficiency

A

secondary causes: Tumor resection for Cushings (pituitary, ectopic or adrenal), Supraphysiologic exogenous glucocorticoid use (most common), opioids and megace

38
Q

Clinical Presentation of secondary/tertiary adrenal insufficiency (AI)

A

Fatigue, Anorexia, nausea/vomiting and weight loss , Generalized malaise/aches, Scant Axillary/Pubic hair (DHEA-S dependent in females), Hyponatremia and Hypoglycemia

39
Q

Diagnosis of central adrenal insufficiency

A
  1. basal testing: random am cortisol18, excludes AI). 2. stimulation: Insulin-induced hypoglycemia (gold standard)–assesses entire hypothalamic-pituitary-adrenal axis. Cosyntropin (synthetic ACTH 1-24) stimulation test-valid for assessing HPA axis only if prolonged (several weeks-months) loss of pituitary signaling and resulting adrenal atrophy.
40
Q

Hypogonadism differential dx

A
  1. Hypergonadotropic (High FSH/LH): Congenital, Klinefelters, testicular injury, autoimmune testicular dz, glycoprotein tumor. 2. Hypogonadotropic (Low FSH/LH): Hypothalamic/pituitary dz (macroadenomas, prolactinomas, XRT, GnRH deficiency, hemochromatosis) or functional deficiency (critical illness, OSA, starvation, meds)
41
Q

compare clinical features of hypogonadism in females vs males

A

females: amenorrhea, infertility, vagina dryness, hot flashes, decreased libido, breast atrophy, reduced bone mineral density. Males: reduced libido, ED, oligospermia, infertility, decreased muscle mass, testicular atrophy, hot flashes with acute/severe onset

42
Q

Clinical presentation of gonadotropin excess

A

Most FSH/LH tumors are silent. Rare presentation include: ovarian hyper-stimulation syndrome (females) or macro-orchidism (males). Middle-aged patients (males >females) with macroadenomas and related mass effects (i.e., headaches, vision loss, cranial nerve palsies, and/or pituitary hormone deficiencies).

43
Q

gonadotropinoma diagnosis

A

Low serum FSH/LH, low serum testosterone or estrogen, pituitary MRI, immunohistochemical staining of tumor for FSH, LH or ASU

44
Q

Secondary Etiologies of thyrotropin (TSH) elevation

A

Thyrotropin secreting pituitary tumor-very rare (<1% of pituitary tumors). Thyroid hormone resistance (generalized or pituitary-specific, rare conditions)

45
Q

Clinical presentation of thyrotropinoma

A

Similar clinical presentation to primary hyperthyroidism (i.e., goitre, tremor, weight loss, heat intolerance, hair loss, diarrhea, irregular menses) but also with associated mass effects (i.e., headaches, vision loss, loss of pituitary gland function) from macroadenoma.

46
Q

Thyrotropinoma diagnosis

A

Elevated Free T4 and a non-suppressed TSH. Pituitary MRI (>80% macroadenomas)

47
Q

Secondary causes of TSH deficiency

A

Pituitary/Hypothalamic Diseases and/or their treatments, Critical Illness/Starvation-Euthyroid Sick Syndrome, Congenital defects (TSH-beta mutations, PROP1, POUF1 mutations), Drug induced-supraphysiologic steroids, dopamine, rexinoids.

48
Q

TSH deficiency presentation

A

Similar to primary hypothyroidism (e.g., fatigue, weight gain, cold intolerance, constipation, hair loss, irregular menses). Possible mass effects

49
Q

TSH deficiency diagnosis

A

Low Free T4 levels in the setting of a low or normal TSH.

50
Q

Hypopituitarism

A

Deficiency of 1 or more pituitary hormones

51
Q

Panhypopituitarism

A

loss of all pituitary hormones

52
Q

Etiologies of hypopituitarism

A

Congenital (trxn factor mutations) Or acquired -75% (macroadenomas/pituitary surgery or radiation, infiltrative/infectious/granulomatous, TBI, subarachnoid hemorrhage, apoplexy)

53
Q

define apoplexy

A

Clinical syndrome of headache, vision changes, ophthalmoplegia and altered mental status caused by the sudden hemorrhage or infarction of the pituitary gland. Occurs in ~10-15% of pituitary adenomas; sub-clinical disease is more common

54
Q

Diagnosis of apoplexy

A

pituitary MRI or CT

55
Q

apoplexy treatment

A

Emergent surgery is indicated for evidence of severe vision loss, rapid clinical deterioration, or mental status changes. Stress dose steroids for adrenal insufficiency

56
Q

Causes of ADH deficiency

A

common with metastatic tumors (i.e., breast, lung or GI) or craniopharyngiomas, but not pituitary adenomas

57
Q

describe the progression of loss of anterior pituitary hormones in hypopituitarism

A

GH=FSH/LH > TSH= ACTH > PRL

58
Q

Diagnosis of hypopituitarism

A

basal and dynamic testing of hormones

59
Q

Treatment of hypopituitarism

A

Replace end organ hormone: 1. thyroid: L-thyroxine. 2. adrenal: hydrocortisone or prednisone. 3. gonadal: estrogen, test, gonadotropin or GnRH. 4. GH: subQ shots. 5. PRL: SQ formulation, research only

60
Q

What are bio-identical hormones

A

hormones made by pharmacies that are supposedly individually tailored based on saliva. Exaggerated and unproven claims of safety and efficacy relative to other FDA-approved products

61
Q

clinical syndromes of posterior pituitary

A

primarily associated with disorders of AVP (aka arginine vasopressin aka ADH)

62
Q

Regulation of ADH release

A

Hyperosmolar state and hypovolemia (baroreceptors)

63
Q

ADH MOA

A

vascular vasoconstriction and water reabsorption in kidneys (via aquaporin channels)

64
Q

SIADH

A

A syndrome of inappropriate AVP release/action in the absence of physiologic osmotic or hypovolemic stimulus

65
Q

SIADH presentation

A

Hallmark is the excretion of inappropriately concentrated urine in the setting of hypo-osmolality and hyponatremia. SIADH is one of the most frequent causes of hyponatremia. Neurological sx from osmotic fluid shifts and brain edema

66
Q

SIADH etiologies

A
  1. Malignant Disease- Carcinoma, Lymphoma, Sarcomas. 2. Pulmonary Disorders-Infections, Asthma, Cystic Fibrosis, Positive Pressure Ventilation. 3. CNS Disorders-Infection, Tumors, Trauma, Bleeds. 4. Drugs-Stimulate/Potentiate AVP release/actions Narcotics, Nicotine, Anti-psychotics, Carbamazepine, Vincristine. 5. Misc.-Nausea, Stress and Pain
67
Q

SIADH criteria

A
  1. Hyponatremia (Na+ 100 mOSm/kg) with normal renal function. 3. Euvolemic Status (no orthostatics hypotension)
68
Q

SIADH treatment

A

Mild-moderate hyponatremia (120-124mmol/L): Water restriction (500-1000ml/24hrs), V2 receptor antagonists, salt tablets, lasix, urea (europe). Severe hyponatremia (<120mmol/L): hypertonic saline (3%) if pt is symptomatic (delirium, seizure,coma)

69
Q

consequence of correcting hyponatremia too fast

A

osmotic demyelination syndrome

70
Q

Features of osmotic demyelination syndrome

A

mutism/dyarthria, lethargy, behavioral changes, confusion, movmement difficulty, muscle contraction, dysphagia

71
Q

How to reduce risk of demyelination syndrome

A

If chronic hyponatremia: limit correction to <48hrs): no limitations

72
Q

Diabetes insipidus

A

DI is a syndrome of hypotonic polyuria as a result of either: Inadequate ADH secretion OR Inadequate renal response to ADH

73
Q

main Causes of diabetes insipidus

A

Central diabetes insipidus, nephrogenic DI, pregnancy (increased ADH metabolism from placental vasopressinase), psychogenic polydipsia.

74
Q

significance of DI

A

§Can lead to severe dehydration if thirst mechanisms are impaired, or if the patient has limited access to water.

75
Q

compare nephrogenic vs neurogenic causes of DI

A

nephrogenic: congenital mutation in aquaporin, drugs (lithium, amphotericin B), electrolyte abnormalities, infiltrative kidney dz, vascular dz. Neurogenic: neoplasms, idiopathic (AVP Ab), congential mutation in AVP, inflammatory/infectious, trauma

76
Q

Post operative DI

A

Triphase response: 1° phase– DI-polyuric phase due to axonal shock/decreased AVP release (days 1-5). 2° phase – SIADH from degenerating neurons/excessive AVP release (days 6-11). 3° phase-Permanent DI after depleted ADH stores and if >80% AVP neuronal cell death. Can also have an isolated second SIADH phase which is more common

77
Q

DI diagnosis

A
  1. 24 hr urine volume collection (normalized to creatinine). 2. urine and plasma osmolalities. 3. water deprivation test. 4. pituitary imaging
78
Q

What is a water deprivation test

A

Restrict fluids to stimulate ADH release, then measure urine and plasma osmolality, serum Na and urine output.

79
Q

compare water deprivation test results for neurogenic, nephrogenic and psychogenic DI

A

neurogenic: no change in urine osmolarity or plasma ADH. Nephrogenic: no change in urine osmolarity and increase in plasma ADH. Psychogenic: increased urine osmolarity and plasma ADH

80
Q

DI treatment

A

First line: dDAVP - no vasopressor effect second line: ADH

DEMS IV (26 decks)

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