Pathology II Flashcards
What is the pathophysiology associated with secondary hyperaldosteronism?
Renal perception of low intravascular volume. This results in an overactive renin-angiotensin system (p.296)
Name five causes of secondary hyperaldosteronism.
Renal artery stenosis, chronic renal failure, CHF, cirrhosis, nephrotic syndrome (p.296)
What lab finding is characteristic of secondary hyperaldosteronism?
Elevated plasma renin (p.296)
What is the treatment for secondary hyperaldosteronism?
Spironolactone (p.296)
What is Addison’s disease?
Chronic primary adrenal insufficiency due to adrenal atrophy or destruction by disease (p.297)
Name three types of disease states that can cause chronic primary adrenal insufficiency.
Autoimmune, Infection (TB), metastasis (p.297)
What endocrine hormones are deficient in primary adrenal insufficiency?
Aldosterone and cortisol (p.297)
What are the typical clinical findings in a patient with primary adrenal insufficiency?
Hypotension (hyponatremic volume contraction due to lack of aldosterone), hyperkalemia, acidosis, skin hyperpigmentation (due to MSH, a by-product of increased ACTH production from POMC) (p.297)
What endocrine hormone is elevated in primary adrenal insufficiency?
ACTH (p.297)
What characterizes primary adrenal insufficiency?
Adrenal atrophy and absence of hormone production from all three cortical divisions. Medulla is spared (p.297)
What lab finding distinguishes primary adrenal insufficiency from secondary adrenal insufficiency?
High ACTH in primary adrenal insufficiency; decreased pituitary ACTH production in secondary adrenal insufficiency (p.297)
What clinical features distinguish primary adrenal insufficiency from secondary adrenal insufficiency?
Secondary adrenal insufficiency has no hyperpigmentation and no hyperkalemia (p.297)
What is Waterhouse- Friderichsen syndrome?
Acute primary adrenal insufficiency due to adrenal hemorrhage (p.297)
What four pathologies are associated with Waterhouse Friderichsen syndrome?
Neisseria meningitidis, septicemia, DIC, and endotoxic shock(p.297)
What is a pheochromocytoma?
The most common tumor of the adrenal medulla in adults. Symptoms occur in spells and are relapsing/remitting (p.297)
From what cells are pheochromocytomas derived?
Chromaffin cells (which arise from neural crest) (p.297)
Where do chromaffin cells arise from?
Neural crest (p.297)
What is most commonly secreted by pheochromocytomas?
Epinephrine, Norepinephrine, dopamine (p.297)
What symptoms are associated with pheochromocytomas?
Episodic hyperadrenergic symptoms- pressuire (elevated BP), Pain (headache), Perspiration, Palpitations (tachycardia), Pallor (p.297)
What lab findings are consistent with a diagnosis of pheochromocytoma?
Urinary VMA and plasma catecholamines are elevated (p.297)
What is Vanillylmandelic acid?
A breakdown product of norepinephrine and epinephrine. Elevated in the urine with pheochromocytoma (p.297)
What three conditions are pheochromocytomas associated with?
MEN 2A, MEN 2B, Neurofibromatosis type 1 (p.297)
What is the treatment for pheochromocytoma?
Surgical removal after effective a-and b-blockade is achieved (p.297)
What treatment is required before a patient can undergo surgery to remove a pheochromocytoma?
Before surgery, irreversible a-antagonists (phenoxybenzamine) must be given to avoid a hypertensive crisis. B-blockers are then given to slow heart rate (p.297)
What is the rule of 10s associated with pheochromocytoma?
10% are: malignant, bilateral, extra-adrenal, calcified, in children (p.297)
Outline the pathway of epinephrine production.
Phenylalanine –> Tyrosine –> L-Dopa –> Dopamine –> Norepinephrine –> Epinephrine (p.297)
