Adrenal Disorders Flashcards

1
Q

Adrenal insufficiency, of which there are two forms:

A

○ Primary adrenal insufficiency (Addison’s disease): Results from destruction or dysfunction of the adrenal cortex
○ Secondary adrenal insufficiency: Results from inadequate stimulation of adrenal cortex by ACTH

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2
Q

Glucocorticoid

A

General classification of adrenal cortical steroid hormones that are primarily active in protecting against stress & in affecting protein & carbohydrate metabolism

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3
Q

Mineralocorticoid

A

Steroid hormone regulating the retention & excretion of fluids & electrolytes
(especially Na & K) by the kidneys

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4
Q

Adrenal Medulla releases

A

Catecholamines
○ Epinephrine
○ Norepinephrine

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5
Q

BP =

A

CO x TPR

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6
Q

What is cardiac output (CO) determined by?

A

Stroke volume & heart rate

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7
Q

Epinephrine & Norepinephrine CV actions

A

● Strengthens heart contractility
○ β1 action (inotropic, increases muscle contraction)
● Increases heart rate of contraction
○ β1 action (chronotropic, affects the rhythm/rate)
● Constricts arterioles in the skin ( 𝛂 1 action)
● Dilates blood vessels to liver & skeletal muscle ( β2 action)

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8
Q

Epinephrine & Norepinephrine respiratory actions

A

Powerful bronchodilation by acting directly on bronchial smooth muscle (β2 action)

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9
Q

Epinephrine & Norepinephrine other actions

A

● Raises blood sugar
○ Increases release of glucagon
○ Increases glycogenolysis
○ Increases lipolysis

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10
Q

Secretion of aldosterone is mainly dictated by changes in _____

A

blood pressure

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11
Q

What lab results and symptoms would you see with a small tumor of the zona glomerulosa cells

A

● Primary aldosteronism = sodium conservation and potassium excretion
○ Hypernatremia ➔ increased volume ➔ Hypertension
○ Hypokalemia ➔ if severe enough can cause muscle paralysis

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12
Q

Cascade for the release of cortisol initiated at the hypothalamus in response to _____

A

infection, pain, hypoglycemia, trauma, hemorrhage, sleep
*all associated with stress except for sleep

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13
Q

Cortisol

A

● Stimulates glucose production by the liver (gluconeogenesis increases blood sugar)
(Anabolism)
● Promotes protein breakdown (Catabolism)
● Mobilization of fatty acids
● Immunologic & anti-inflammatory effects

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14
Q

Some MAJOR adverse effects of excess glucocorticoid (cortisol)

A

○ Elevated glucose levels (hyperglycemia)
○ Suppression of the immune system
○ Decreased bone density
○ Central nervous system & mental status effects (anxiety/depression, seizures…)
○ Elevation of blood pressure
○ Stimulates gastric acid & pepsin production

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15
Q

Androgens

A

● Zona Reticularis
● Dehydroepiandrosterone (DHEA),
Androstenedione

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16
Q

Results from destruction or dysfunction of the adrenal cortex

A

Primary adrenal insufficiency (Addison’s disease)

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17
Q

Results from inadequate stimulation of adrenal cortex by adrenocorticotropin hormone (ACTH)

A

Secondary adrenal insufficiency

18
Q

Primary adrenal insufficiency (Addison’s disease) pathophysiology

A

○ Usually results from autoimmune destruction of the adrenal glands
○ BOTH glucocorticoid AND mineralocorticoid secretion diminished in this condition
○ If untreated may be fatal
○ Adrenal medulla function usually spared

19
Q

Secondary adrenal insufficiency (uncommon) pathophysiology

A

○ Usually occurs after discontinuation of exogenous steroids after prolonged use
and prolonged suppression of the HPA (Hypothalamic-pituitary-adrenal) axis
○ Endogenous steroids (ie, tumor)
○ Hypothalamic-pituitary disease

20
Q

Adrenal Insufficiency clinical presentation

A

● Hypotension
● Weight loss
● Increasing fatigue
● Vomiting
● Diarrhea
● Anorexia
● Muscle & joint pain
● Abdominal pain
● Postural dizziness

21
Q

_____ are only seen with primary adrenal insufficiency (Addison’s Disease)

A

Hyperpigmentation & salt craving

22
Q

Hyperpigmentation pathophysiology in Adrenal insufficiency

A

○ ↓ levels of cortisol means less inhibition of HPA axis
○ ↑ proopiomelanocortin (POMC) synthesis, a precursor for ACTH.
■ POMC molecule contains melanocyte-stimulating hormone (MSH) fragments
■ When POMC levels ↑, so are levels of MSH, → ↑ pigmentation of the skin

23
Q

Salt craving pathophysiology in Adrenal insufficiency

A

○ Primary adrenal insufficiency (Addison’s disease) is a disease of the adrenal gland itself
○ Low secretion of aldosterone → hyponatremia & salt craving

24
Q

Lab Considerations in Adrenal Insufficiency

A

● AM plasma cortisol level
○ Low plasma cortisol (<3-5 ug/dL) → strong evidence for diagnosis of adrenal
insufficiency
○ Higher levels of plasma cortisol (>20ug/dL) → strong evidence against diagnosis
of adrenal insufficiency

25
ACTH (cosyntropin) test
1. Baseline plasma cortisol measured 2. IV administration of 250 mcg of ACTH 3. Plasma cortisol measured again after 30-60 minutes
26
If we know the patient has adrenal insufficiency, how do we know if it’s Addison’s or from a secondary cause?
Order plasma ACTH ○ Elevated à Primary adrenal insufficiency (Addison’s Disease) ○ Decreased à Secondary adrenal insufficiency
27
Management for Adrenal Insufficiency
○ Glucocorticoids: Prednisone, Dexamethasone, Hydrocortisone ○ Mineralcorticoid: Fludrocortisone (9-alpha-fluorohydrocortisone)
28
Main problem with adrenal insufficiency treatment
Overtreating with glucocorticoids & undertreatment with mineralocorticoids
29
Acute Adrenal Crisis
acute stress event combined with chronic adrenal suppression, & the body is unable to respond. Leads to multi-system failure
30
Adrenal Crisis Clinical Presentation
○ Volume depletion (primary) ○ Hypotension ○ Weakness (99%) ○ Pigmentation of skin (98%) ○ Weight loss (97%)
31
Management of adrenal crisis
● Aggressive volume replacement therapy ● Hydrocortisone ● Maintain ABCs ● Dextrose 50% prn for hypoglycemia ● Correct electrolyte abnormalities ● Determine underlying cause ● Once stabilized, reduce corticosteroid dose, then taper ● Oral maintenance can usually be achieved by day 4 or 5
32
Cushing’s syndrome =
a constellation of clinical abnormalities caused by chronic high blood levels of cortisol or related corticosteroids
33
Cushings syndrome can be
● ACTH dependent: Excess production of ACTH from the pituitary gland = Cushing’s disease, Ectopic sources of ACTH (usually small cell lung cancer) ● ACTH independen: Excess cortisol produced by adrenal adenomas or carcinomas. Excessive exogenous steroid administration
34
Cushing disease is Cushing syndrome that results from _____
excess pituitary production of adrenocorticotropic hormone (ACTH), generally secondary to a pituitary adenoma
35
Cushing’s DISEASE accounts for ____% of ACTH-dependent Cushing’s SYNDROME
80
36
Ectopic source of ACTH most commonly seen in patients with ____
small cell lung carcinoma (Usually older, hx of smoking, with signs & symptoms of lung cancer)
37
Pheochromocytoma
● Rare type of adrenal tumor ● Responsible for about 0.1-2% of all cases of hypertension ● Tumor releases catecholamines causing episodic (typically) OR sustained signs and symptoms ● A surgically correctable form of HTN!
38
Dexamethasone Suppression Test normal physiology
HPA axis should be suppressed and cortisol levels should decrease
39
Classic triad of pheochromocytoma
episodic headache, sweating, tachycardia Patients may have some or all of those symptoms
40
Treatment for PHEOCHROMOCYTOMA
● Tumor excision (usually curative) ● Biopsy to rule out malignancy (10%) ● Must control BP prior to surgery ● Do not use beta-blockers as INITIAL treatment for HTN as this will cause unopposed alpha-adrenergic stimulation. ● Start with alpha blocker, then may add beta blocker several days later