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Patho > Adrenal Secretion Disorders > Flashcards

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?

A

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
Q

T/F Pheochromocytoma can be persistent or intermittent in bursts and is commonly fatal if left untreated

A

T

26
Q

What are the S/S of Pheochromocytoma?

A

-Severe and/or labile HTN; palpitations, pallor, dysrhythmias , flushing
-Episodes triggered by exercise, ↑ tyrosine intake, ↑ caffeine

27
Q

What is the presentation of Pheochromocytoma?

A

Hypertension (90%) extremely elevated, resistant to standard treatments
Headache (80%)
Profuse sweating (70%)
Palpitations (60%)
Anxiety (50%)
Weight loss
Glucose Intolerance
Pallor
Constipation

28
Q

What are the complications of Pheochromocytoma ?

A

Complications due HTN
Cardiac damage
Hypertensive retinopathy
Stroke

29
Q

What are Hyposecretion Disorders?

A
  1. Hypoaldosteronism
  2. Adrenal Insufficiency
    -Addison’s disease
    -Congenital adrenal hyperplasia
30
Q

What is Aldosterone Deficiency?

A

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
Q

What are the causes of primary adrenal failure?

A

Addison’s disease, Autoimmune destruction, TB, adrenal hemorrhage, others

32
Q

What are the secondary causes of adrenal failure?

A

Due to Pituitary Failure (Atrophy, Necrosis, Tumor), rapid withdrawal of exogenous corticosteroids

33
Q

What is addison’s disease and what is it caused by?

A

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
Q

Addison’s disease affects all three adrenocortical hormones which are:

A
  1. Zona fasciculata (cortisol)
  2. Zona glomerulosa (mineralocorticoids)
  3. Zona reticularis (androgens, estrogens)
35
Q

In primary addison’s disease, more than 90% of both adrenal glands are destroyed. What causes this destruction?

A

autoimmune, where autoantibodies attack adrenal tissue, or idiopathic

36
Q

What is addisonian crisis?

A

most serious complication; rapid decline of cortisol and aldosterone

37
Q

Addison’s disease: cortisol insufficiency

A

↓ gluconeogenesis, ↑ insulin sensitivity leading to hypoglycemia

38
Q

Addison’s disease: aldosterone insufficiency

A

↓ sodium retention and increased water loss with potassium retention, leading to arrhythmias, decreased cardiac output, hypovolemia, hypotension

39
Q

In addison’s disease, there is a ____ in ACTH and other hormones 2° to HPA feedback, leading to _________

A

increase, hyperpigmentation

40
Q

In addison’s disease you see a ________ stress response secondary to cortisol deficiency and this leads to patients unable to withstand

A

decreased, surgical stress, trauma, infection

41
Q

Addison’s disease: Androgen deficiency

A

noticeable in women > men, ↓ in axillary/pubic hair

42
Q

What are the clinical findings in addison’s disease?

A

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
Q

What is the clinical presentation of addiosn’s

A

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
Q

What is the prognosis of addison’s disease?

A

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
Q

S/S of adrenal crisis

A

HA (headache)
N/V
Abdominal pain
Hypotension
Fever
Hypoglycemia
Shock

46
Q

What is Congenital Adrenal Hyperplasia?

A

-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

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