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Endocrine wk 1 > Pituitary dysfunction > Flashcards

Pituitary dysfunction Flashcards

1
Q

GH

  1. def
  2. excess
  3. assay
A

Acromegaly

GH Deficiency

IGF-1

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2
Q

PRL

  1. def
  2. excess
A

Failed Lactation

Hypogonadism

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3
Q

FSH/LH

  1. def
  2. excess
  3. assay
A

Hypogonadism

Rarely Clinically Evident

Testosterone estradiol

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4
Q

ACTH

  1. def
  2. excess
  3. assay
A

Adrenal Insufficiency

Cushing’s Disease

cortisol and DHEA-S

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5
Q

TSH

  1. def
  2. excess
  3. assay
A

Hypothyroidism

Hyperthyroidism

TSH
free T4
total T3

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6
Q

ADH

  1. def
  2. excess
A

Diabetes Insipidus

SIADH

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7
Q

which hormones can we do dynamic testing on?

A

Growth hormone

ACTH

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8
Q

Growth hormone

-physiology

A

stimulator- GHRH
Inhibitor Somatostatin
-acts on liver to produce IGF-1, which feeds back (-) on pituitary and hypothalamus

-pulsatile

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9
Q

Growth hormone excess

  • disease
  • signs symptoms
  • Tx
A

Gigantism- pre puberty growth hormone excess

Acromegaly- post puberty growth hormone excess

  • acral facil achnages
  • headaches, hyperhidrosis
  • oligo,amenorhea
  • obstructive sleep apnea
  • HTN, dyslipidemia, paratheisas, carpal runnel
  • Impaired glucose tolerance, DM
Tx-Surgery
Medical Therapies
-Somatostatin Analogs
-Growth Hormone Receptor Antagonist
Radiation Therapies
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10
Q

Dx of AoGHD

A
  1. Provocative Testing for GH Reserve
    Limited Reagents
    -Insulin induced hypoglycemia (gold standard).
    ——Contraindications: Elderly, h/o seizure disorder, coronary artery disease or cerebrovascular disease.
    -GHRH-Arginine (second best test), although no longer available in U.S
    -Available tests: Arginine and glucagon stimulation tests
  2. IGF-1 Level -Low (in the setting of multiple other
    pituitary hormone deficiencies). Must be age/gender-matched.
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11
Q

causes of hyperprolactinemia

A 
Physiological 
-Pregnancy, suckling, sleep, stress
Pharmacological
-Estrogens (OCPs)
-Antipsychotics, antidepressants (TCAs), 
    anti-emetics (e.g., Reglan), opiates
Pathological
-Pituitary Stalk Interruption
-Hypothyroidism, chronic renal/liver failure, seizure (cross talk)
-Prolactinoma
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12
Q

Prolactinoma

  • womens manifestations
  • mens manifestations
  • Dx
A

women- often present with microadenomas

  • galactorhea
  • menstrual irregularities
  • infertility
  • (impairs GnRH pulse generator

Men- macroadenomas

  • galactorrhea
  • visual field abnormalities
  • headache
  • impotence
  • EOM paralysis
  • anterior pituitary malfunction

Diagnosis
-Random PRL level (gender-based normative ranges)
-Levels usually correlate with tumor size
>100-150 ng/dl with microadenomas
>200-250 ng/dl with macroadenomas
Pituitary MRI (with/without contrast)

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13
Q

prolactin deficiency

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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14
Q

Cortisol Excess (Hypercortisolism)

  • ACTH dependent causes
  • ACTH independent causes
A

ACTH-Dependent

  • Corticotrope Adenoma (Cushing’s Disease)
  • Ectopic Cushing’s (ACTH/CRH tumors)

ACTH-Independent

  • Adrenal Adenomas
  • Adrenal Carcinoma
  • Nodular Hyperplasia (micro or macro)
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15
Q

no specific manifesatiions Cushings Syndrome

A 
Obesity
Fatigue
Menstrual Irregularities 
Hirsutism 
HTN
Glucose Intolerance/DM 
Dyslipidemia 
Acne
Anxiety/Depression
Peripheral Edema
Metabolic Syndrome
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16
Q

specific signs of cushings syndrome

focus on these

A 
Plethoric/moon facies
Wide (>1 cm), violaceous striae (abdominal, axillary) 
Spontaneous Ecchymoses
Proximal Muscle Weakness
Early/Atypical  Osteoporosis
	(atraumatic rib fx)
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17
Q

screening tests for cushings

A 
Disrupted Circadian Rhythm
-Midnight Salivary or Serum Cortisol
Increased Filtered Cortisol Load 
-24 hr Urine Free Cortisol
Attenuated Negative Feedback
-Low Dose (1 mg) Dexamethasone Suppression -test (11-12 p.m.)
18
Q

Cushings Disease work up

A

ACTH LEVEL
1. Plasma ACTH levels are usually high-normal to mildly elevated in Cushing’s disease

IMAGING
2. Pituitary MRI (~80% microadenomas, 50% identified on MRI)

INFERIOR PETROSAL SINUS SAMPLING
3. For a negative/equivocal MRI

19
Q

Central Adrenal Insufficiency (AI)

-etiology of secondary AI

A

Etiologies of Primary AI-separate lecture

Etiologies of Secondary/Tertiary AI

  1. Suppression of the HPA axis
    - S/p tumor resection for Cushing’s Syndrome (pituitary, ectopic or adrenal)
    - Supraphysiologic exogenous glucocorticoid use (most common) > 5-7.5 mg prednisone (or equivalent glucocorticoid dose) for >1 month
    - Drugs: Opioids and megace
  2. Hypothalamus/Pituitary Diseases and/or their treatments.
  3. Other-Isolated ACTH deficiency (very rare)
20
Q

Central Adrenal Insufficiency 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

21
Q

Central Adrenal Insufficiency work up

A

Basal Testing: Random a.m. cortisol level, 18 ug/dl (excludes AI diagnosis), additional provocative testing required for equivocal results.

Stimulation Tests
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.

22
Q

Hypogonadism Differential Dz
High FSH/LH
Low FSH/LH

A

High FSH/LH

  • Congenital Anorchia
  • Klinefelter’s Syndrome
  • Testicular Injury
  • Autoimmune Testicular Dz
  • Glycoprotein Tumor (rarely)

Low FSH/LH
Hypogonadotropic Hypogonadism Hypothalamic/Pituitarydiseases -Macroadenomas, prolactinomas, XRT
-Isolated GnRH Deficiency (Kallman’s=anosmia vs. Idiopathic)
-Hemochromatosis
“Functional” Deficiency-
Critical Illness, OSA, starvation, Meds-opiates, glucocorticoids

23
Q

Hypogonadism clinical features

  • Men
  • Women
A

Male
Reduced libido
Erectile dysfunction
Oligospermia or azoospermia
Infertility
Decreased muscle mass, testicular atrophy and decreased BMD
Hot flashes with acute and severe onset of hypogonadism

FEMALES
 Anovulatory cycles
oligo/amenorrhea, infertility
 Vagina dryness, dyspareunia
 Hot Flashes
 Decreased libido
 Breast atrophy
 Reduced bone mineral density (BMD)
24
Q

LH/FSH (Gonadotropin) Excess

A 
Clinical Presentation of Gonadotrope Adenomas
The majority of FSH/LH tumors are clinically silent (?inefficient intact LH/FSH hormone synthesis or secretion).
Rare presentation (from functionally-intact FSH/LH molecules) include: ovarian hyper-stimulation syndrome (females) or macro-orchidism (males).
Middle-aged patients (males >females) with macroadenomas and related mass effects (e.g., headaches, vision loss, cranial nerve palsies, and/or pituitary hormone deficiencies).
25
Q

Thyrotropin (TSH) Elevation

A

Secondary

Thyrotropin secreting pituitary tumor-very rare (

26
Q

Central hyperthyroidism

A

Clinical Presentation
Thyrotropinoma (TSHoma)-similar clinical presentation to primary hyperthyroidism (e.g., goitre, tremor, weight loss, heat intolerance, hair loss, diarrhea, irregular menses) but also with associated mass effects (e.g., headaches, vision loss, loss of pituitary gland function) from macroadenoma.

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

27
Q

Central TSH deficiency

  • etiology
  • clinical presentation
A

Etiologies

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

Clinical presentation: similar to primary hypothyroidism (e.g., fatigue, weight gain, cold intolerance, constipation, hair loss, irregular menses). Possible mass effects
Diagnosis: Low Free T4 levels in the setting of a low or normal TSH

28
Q

Hypopit overview

A

Definition: Deficiency of 1 or more pituitary hormones. Panhypopituitarism=loss of all pituitary hormones
Etiologies:
Congenital-Genetic Diseases (transcription factor mutations)
Acquired-Pituitary Lesions and/or their treatments (75%)
Macroadenomas/Pituitary Surgery/Radiation Therapy
Infiltrative/Infectious/Granulomatous diseases
Traumatic Brain Injury/Subarchnoid Hemorrhage
Apoplexy

29
Q

Apoplexy

A

Definition: 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

Diagnosis: Pituitary MRI or CT

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

30
Q

Chronology of hypo pit loss

A

GH, LH/FSH->TSH, ACTH->PRL

31
Q

Hypo pit clinical presentation

A

-similar presentation to target gland hormone deficiency, with some exceptions:
-Primary adrenal insufficiency also presents with hyperkalemia from mineralcorticoid deficiency and hyperpigmentation from ACTH excess.
Diagnosis: Basal and Dynamic Testing

32
Q

Hypo Pit management

A

Treatment of Anterior Pit. Hormone Deficiencies (End Organ Hormone Replacement):
Thyroid – Multiple L-thyroxine formulations available.
Adrenal – Physiologic hydrocortisone or prednisone
Medic Alert Bracelet, Sick day rules for glucocorticoid replacement
No mineralcorticoid replacement needed
Gonadal –
Various formulations-oral/transdermal E2, transdermal/IM Testosterone
Gonadotropin or pulsatile GnRH therapy
Growth Hormone
Various Formulations of subcutaneous shots (not orally active).
Prolactin – SQ formulation, research purposes only.

33
Q

causes of SIADH

A

Malignant Disease- Carcinoma, Lymphoma, Sarcomas
Pulmonary Disorders-Infections, Asthma, Cystic Fibrosis, Positive Pressure Ventilation
CNS Disorders-Infection, Tumors, Trauma, Bleeds
Drugs-Stimulate/Potentiate AVP release/actions
Narcotics, Nicotine, Anti-psychotics, Carbamazepine, Vincristine
Miscellaneous-Nausea, Stress and Pain

34
Q

SIADH clinical presentation

A

Depends on the severity of hyponatremia and the rapidity of development (acute,

35
Q

SIADH DX

A

Criteria

  • Hyponatremia (Na+ 135 mmol/L) (hypotonic plasma (100mOSm/kg)with normal renal fcn
  • Euvolemic Status (no orthostatics hypotension)
  • Exclusion of other potential causes of euvolemic hypo-osmolality
  • —Hypothyroidism
  • —Hypocortisolism
36
Q

SIADH TX

A

Identify and Reverse Underlying Disorder (when possible)

Tx depends on the severity of hyponatremia

Mild-to-Moderate Hyponatremia (Na+ ~120-134 mmol/L)

  • Water Restriction (500-1000L/24hrs)
  • V2 Receptor Antagonists ($$$)
  • Salt tablets, Lasix, Urea (Europe)
Severe  Hyponatremia (usually Na+ = 120mmol/L)
-hypertonic saline
37
Q

Diabetes Insipidus (DI)

A

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

Hallmark-Voluminous (Urine output > 40ml/kg/d) dilute urine

Main Causes:
Central Diabetes Insipidus
Nephrogenic Diabetes Insipidus
Pregnancy-increased ADH metabolism from placental vasopressinase, but is generally not clinically relevant 
Primary Polydipsia

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

38
Q

DI causes

A

Nephrogenic DI
Congenital: X-linked recessive AVP V2 receptor gene mutation; autosomal recessive aquaporin-2 water channel gene mutation
Drugs: demeclocycline, lithium, amphotericin B
Electrolyte abnormalities: hypokalemia and hypercalcemia
Infiltrative kidney diseases: sarcoidosis and amyloidosis
Vascular disease: sickle cell anemia

Neurogenic DI
Neoplasms: craniopharyngioma, metastatic pituitary disease (e.g., colon, breast, lung)
Idiopathic:+AVP Ab
Congenital defects: autosomal dominant AVP neurophysin gene mutation
Inflammatory/Infectious/granuloma pituitary diseases: lymphocytic hypophysitis, histiocytosis, sarcoidosis
Trauma/Vascular event: neurosurgery, TBI/deceleration injury

39
Q

Triphasic response to stalk trauma from pituitary surgery

A

Classic Triphasic 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
Permanent DI-uncommon complication with an experienced neurosurgeon (

40
Q

Outpatient DI DX

A

Confirm polyuria with 24 hr urine volume collection (normalized to creatinine)

Exclude hyperglycemia (osmotic diuresis), renal insufficiency and electrolyte disturbances (K+/Ca 2+)
Assess Urine and Plasma Osmolalities
Consider Water Deprivation Test
Pituitary Imaging (for suspected neurogenic DI)

41
Q

DI treatment

A

DDAVP

Endocrine wk 1 (27 decks)

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