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Adrenal Secretion Disorders Flashcards

1
Q

What is hypercortisolism?

A

Glucocorticoid excess

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2
Q

What are the mechanisms for hypercortisolism?

A
  1. Cushing’s disease: ACTH overproduction by pituitary gland
  2. Cushings syndrome: adrenal glands spontaneous hypersecretion of cortisol
    long term exogenous intake
    Also classified as ACTH dependent vs non ACTH dependent
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3
Q

Cushing’s disease involves manifestations of hypercortisolism due to _____________ by the pituitary gland

A

ACTH hypersecretion

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4
Q

What is cushings disease typically caused by?

A

Benign pituitary adenomas that are typically very small
10% due to non-pituitary neoplasms (small cell lung CA produces ectopic ACTH)

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5
Q

32% of the time Cushings syndrome is due to what?

A

excessive autonomous secretion of cortisol by the adrenals independent of ACTH

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6
Q

What are the two classes of cushings

A
  1. ACTH dependent (secondary) disease
  2. ACTH non-dependent (primary) syndrome
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7
Q

What is characteristic of ACTH dependent (secondary) disease

A
  1. Adrenocortical hyperfunction
  2. Abnormal and excessive secretion of ACTH from pituitary
  3. Ectopic ACTH syndrome
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8
Q

What is characteristic of ACTH non-dependent (primary) syndrome

A
  1. Autonomous adrenocortical hyperplasia
  2. Formation of cortisol-secreting tumors
    *Adenoma
    *Carcinoma
    *+/- exogenous intake
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9
Q

What are the S/S of Cushings

A
  1. central obesity
  2. moon faces
  3. buffalo hump
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10
Q

What are the effects of excess glucocorticoids?

A

Catabolism
Weakening of bone
Skin changes: striae
Blood vessel weakening (ecchymosis)
Adipose buildup
Electrolyte abnormalities
Immunosuppression
Peptic ulcer formation
Psychological changes
↓ inflammation
Changes in blood sugar

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11
Q

What type of tests would you run for hypercortisolism and explain what the results would indicate

A
  1. Dexamethasone Suppression Test
    *If ACTH is high, further evaluate pituitary
    *If ACTCH is low, further evaluate adrenals
  2. 24 hour cortisol and creatinine collection
  3. Midnight Serum or Salivary Cortisol level
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12
Q

Cushings= issues in which gland

A

pituitary

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13
Q

What are the complications of hypercortisolism?

A

untreated= death
HTN, DM
increase risk to infection (superficial skin, opportunistic)
Renal Calculi
Osteoporosis with compression fractures
Avascular Necrosis
Glaucoma
Impaired Wound Healing
Psychosis

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14
Q

What is hyperaldosteronism and what are the two types?

A

Excess production of aldosterone, a mineralcorticoid
Two types:
1. Primary:
Increased aldosterone secretion from hyperplasia or tumor of adrenal cortex
2. Secondary:
↑↑ stimulation of RAAS system due to ↓ arteriolar pressure in glomerulus
Can occur with CHF, renal artery occlusion, cirrhosis of the liver, nephrotic syndrome

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15
Q

In Hyperaldosteronism, what does the increase in sodium and water retention lead to?

A

HTN, hypernatremia, hypokalemia

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16
Q

What are the labs would we run for Hyperaldosteronism and what are the findings?

A

measurement of aldosterone and renin in urine and plasma
Primary: see decreased urinary renin
Secondary: see increased urinary renin

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17
Q

What are the two disorders of androgen excess?

A

Hirtuism and Virilism

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18
Q

What is Hirsutism ?

A

-Excessive growth of body hair on female in characteristic male distribution (e.g. abdomen, chest, face)
-Can lead to male pattern baldness or hairline receding
-Can see associated acne, menstrual abnormalities
-See decreased binding, increased free circulation of testosterone

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19
Q

What is Virilism?

A

-Rare; almost always due to adrenal tumors, ovarian tumors, or adrenal hyperplasia
-Characterized by defeminization (amenorrhea, breast atrophy, loss of body contour) and masculinization (hirsutism, acne, voice deepening, muscular development, sexual organ changes)

20
Q

Which one is worse, Hirsutism or Virilism?

21
Q

What are Etiologies of Androgen Excess Disorders?

A
  1. Adrenocortical origin
    *Cortisol excess (i.e. Cushing’s)
    *Androgen excess (i.e. CAH)
  2. Ovarian origin (i.e. polycystic ovary syndrome)
  3. Simple or idiopathic hirsutism
  4. Miscellaneous states (endocrine versus non-endocrine causes)
22
Q

What is the Hirsute Women Clinical Presentation?

A

-Virilized women: 32% of secreted testosterone is extracted and metabolized by peripheral tissues, not just liver; tissue then becomes more androgenic

-Determine if hirsutism is isolated or in setting of virilism

-If recent, rapid onset: more likely due to toxic nodule or malignancy

-Blood tests to measure androgen levels (DHEA); if Congenital Adrenal Hyperplasia (CAH) suspected, enzyme levels

-In setting of PCOS: alterations of other hormones such as LH, insulin, glucose

-May see changes in vaginal exam, ovarian mass or abdominal fullness if associated with malignancy

23
Q

What is Pheochromocytoma?

A

epi/norepi excess
Catecholamine(epi/norepi) producing tumors of the adrenal gland
Most occur between 30-50 years of age
~80% are solitary & unilateral
10% are Malignant
10% occur in children
10% are familial

24
Q

Pheochromocytoma is a tumor of ____________ that releases excessive amounts of _________

A

adrenal medulla, catecholamines

25
T/F Pheochromocytoma can be persistent or intermittent in bursts and is commonly fatal if left untreated
T
26
What are the S/S of Pheochromocytoma?
-Severe and/or labile HTN; palpitations, pallor, dysrhythmias , flushing -Episodes triggered by exercise, ↑ tyrosine intake, ↑ caffeine
27
What is the presentation of Pheochromocytoma?
Hypertension (90%) extremely elevated, resistant to standard treatments Headache (80%) Profuse sweating (70%) Palpitations (60%) Anxiety (50%) Weight loss Glucose Intolerance Pallor Constipation
28
What are the complications of Pheochromocytoma ?
Complications due HTN Cardiac damage Hypertensive retinopathy Stroke
29
What are Hyposecretion Disorders?
1. Hypoaldosteronism 2. Adrenal Insufficiency -Addison’s disease -Congenital adrenal hyperplasia
30
What is Aldosterone Deficiency?
Aldosterone insufficiency = ↓ sodium retention and increased water loss with potassium retention Decreased plasma volume leads to postural hypotension BP is normal when lying down, but have marked hypotension and tachycardia upon standing for several minutes Postural HTN: SBP/DBP ↓ by 20 mmHg Postural tachycardia: HR ↑ by 20 bpm Severe deficiency can cause hyperkalemia and cardiac toxicity Arrhythmias, decreased cardiac output
31
What are the causes of primary adrenal failure?
Addison’s disease, Autoimmune destruction, TB, adrenal hemorrhage, others
32
What are the secondary causes of adrenal failure?
Due to Pituitary Failure (Atrophy, Necrosis, Tumor), rapid withdrawal of exogenous corticosteroids
33
What is addison's disease and what is it caused by?
Uncommon disorder cause by destruction or dysfunction of the adrenal cortices Rarely decrease of single hormones can occur, but typically affects adrenal cortex globally
34
Addison's disease affects all three adrenocortical hormones which are:
1. Zona fasciculata (cortisol) 2. Zona glomerulosa (mineralocorticoids) 3. Zona reticularis (androgens, estrogens)
35
In primary addison's disease, more than 90% of both adrenal glands are destroyed. What causes this destruction?
autoimmune, where autoantibodies attack adrenal tissue, or idiopathic
36
What is addisonian crisis?
most serious complication; rapid decline of cortisol and aldosterone
37
Addison's disease: cortisol insufficiency
↓ gluconeogenesis, ↑ insulin sensitivity leading to hypoglycemia
38
Addison's disease: aldosterone insufficiency
↓ sodium retention and increased water loss with potassium retention, leading to arrhythmias, decreased cardiac output, hypovolemia, hypotension
39
In addison's disease, there is a ____ in ACTH and other hormones 2° to HPA feedback, leading to _________
increase, hyperpigmentation
40
In addison's disease you see a ________ stress response secondary to cortisol deficiency and this leads to patients unable to withstand
decreased, surgical stress, trauma, infection
41
Addison's disease: Androgen deficiency
noticeable in women > men, ↓ in axillary/pubic hair
42
What are the clinical findings in addison's disease?
Weakness Fatigability Weight Loss Anxiety Mental Irritability Pigmentary Changes Vitiligo Emotional Changes Hyperplasia Lymph Myalgias Arthralgias Fever Anorexia Nausea / Vomiting Hypoglycemia Hypotension Orthostasis Small Heart Scant Axillary / Pubic Hair
43
What is the clinical presentation of addiosn's
CBC: Neutropenia, Lymphocytosis, Eosinophilia Hyponatremia, Hyperkalemia, Hypoglycemia, Hypercalcemia BUN is high Low plasma cortisol (< 3µg/dl diagnostic), esp. elevation of ACTH DHEA is <1000 ng/ml in 100% with Addisons May see nodules in lungs related to malignancy or TB Adrenals will be: -Small, noncalcified adrenals in autoimmune Addison’s disease, -Enlarged in 85% cases of metastatic or granulomatous disease (TB) -Calcification is noted in 35% of cases of TB but also with hemorrhage, fungal infection, pheochromocytoma, and melanoma
44
What is the prognosis of addison's disease?
Normal life expectancy if the adrenal hormones are replaced properly Will be susceptible to infections Watch for Adrenal crisis: May occur during stress Following sudden withdraw of ACTH hormone or exogenous corticosteroids Following adrenalectomy or pituitary gland Adrenal injury With certain medications (etomidate)
45
S/S of adrenal crisis
HA (headache) N/V Abdominal pain Hypotension Fever Hypoglycemia Shock
46
What is Congenital Adrenal Hyperplasia?
-Adrenal insufficiency due to genetic disorder -Absence of an essential enzyme necessary to produce cortisol, aldosterone or both -May have associated excess of androgen, which may lead to male characteristics in girls and precocious puberty in boys -Congenital adrenal hyperplasia can remain undiagnosed for years in those with more mild enzyme deficiency -Severe cases, may present in infancy with ambiguous genitalia, dehydration, vomiting, poor weight gain and growth

Patho (16 decks)

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