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Endocrinology Exam 3 > Adrenal Disorders > Flashcards

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
Q

ACTH (cosyntropin) test

A
  1. Baseline plasma cortisol measured
  2. IV administration of 250 mcg of ACTH
  3. Plasma cortisol measured again after 30-60 minutes
26
Q

If we know the patient has adrenal insufficiency, how do we know if it’s
Addison’s or from a secondary cause?

A

Order plasma ACTH
○ Elevated à Primary adrenal insufficiency (Addison’s Disease)
○ Decreased à Secondary adrenal insufficiency

27
Q

Management for Adrenal Insufficiency

A

○ Glucocorticoids: Prednisone, Dexamethasone, Hydrocortisone
○ Mineralcorticoid: Fludrocortisone (9-alpha-fluorohydrocortisone)

28
Q

Main problem with adrenal insufficiency treatment

A

Overtreating with glucocorticoids & undertreatment with mineralocorticoids

29
Q

Acute Adrenal Crisis

A

acute stress event combined with chronic adrenal suppression, & the body is unable to respond. Leads to multi-system failure

30
Q

Adrenal Crisis Clinical Presentation

A

○ Volume depletion (primary)
○ Hypotension
○ Weakness (99%)
○ Pigmentation of skin (98%)
○ Weight loss (97%)

31
Q

Management of adrenal crisis

A

● 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
Q

Cushing’s syndrome =

A

a constellation of clinical
abnormalities caused by chronic high blood levels
of cortisol or related corticosteroids

33
Q

Cushings syndrome can be

A

● 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
Q

Cushing disease is Cushing syndrome that results from
_____

A

excess pituitary production of adrenocorticotropic hormone
(ACTH), generally secondary to a pituitary adenoma

35
Q

Cushing’s DISEASE accounts for ____% of ACTH-dependent Cushing’s
SYNDROME

A

80

36
Q

Ectopic source of ACTH most commonly seen in patients with ____

A

small cell
lung carcinoma (Usually older, hx of smoking, with signs & symptoms of
lung cancer)

37
Q

Pheochromocytoma

A

● 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
Q

Dexamethasone Suppression Test normal physiology

A

HPA axis should be suppressed and cortisol levels should decrease

39
Q

Classic triad of pheochromocytoma

A

episodic headache, sweating, tachycardia
Patients may have some or all of those symptoms

40
Q

Treatment for PHEOCHROMOCYTOMA

A

● 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

Endocrinology Exam 3 (6 decks)

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