Flashcards in 3/8 endo Deck (129)
How does excess cortisol lead to HTN?
-up-regulates alpha-1 receptors on arterioles.
-has slight mineralocorticoid ability.
Dexamethasone suppression test
-low dose suppresses ACTH =
-high dose (8mg) suppresses ACTH =
-no suppression w/high dose (8mg) =
-low dose suppresses ACTH = normal
-high dose suppresses ACTH = pituitary adenoma
-no suppression w/high dose = ectopic ACTH prod.
How does excess cortisol lead to osteoporosis?
-cortisol dec. osteoblastic activity
CRH stimulation test
-differentiate btwn a pituitary adenoma and ectopic source.
-an ectopic source will not increase cortisol production in response to CRH b/c the pituitary is super suppressed by all the negative feedback of the ectopic ACTH.
-the pituitary adenoma will make even more ACTH and thus cortisol in response to CRH b/c its negative feedback mechanism is obviously fucked up which is a key property thats allowing it to pump out all of this ACTH in the first place.
Primary or secondary hyperaldo
-surgery (primary) or spironolactone
Which bug has been known to destroy the adrenals?
-Neisseria meningitidis septicemia, DIC, and endotoxic shock
Resting tone on vasculature?
-hence neurogenic shock - you lose that sympathetic tone.
-originates from what tissue?
-Neural crest cells
-abdominal distension and a firm, irregular mass B that can cross the midline (vs. Wilms tumor, which is smooth and unilateral).
*it does not cause HTN like pheo does.
-what is increased in urine?
-associated w/which oncogene?
-Homovanillic acid (HVA) = breakdown product of dopamine.
Homovanillic acid (HVA)
-inc urinary levels in what disease?
-HVA is breakdown product of what?
-breakdown product of dopamine.
*dopamine = precursor to catecholamines.
-bombesin + or -
-what do you see on histology?
-bombesin + (tumor marker)
-rosettes & classic small, round, blue/purple nuclei.
-arise from what cells?
-what color is it usually?
-neural crest cells
-brown - the adrenal medulla is usually brown.
-rule of 10s
Rule of 10’s:
*More than 70% of cases of pheochromocytomas
are bilateral when familial.
-associated w/which diseases?
-Associated with von Hippel-Lindau disease, MEN 2A and 2B.
Irreversible α-antagonists (phenoxybenzamine) and β-blockers followed by tumor resection.
-α-blockade must be achieved before giving
-β-blockers to avoid a hypertensive crisis.
-diarrhea or constipation?
-inc or dec reflexes?
-whats the skin & hair like?
-hypo or hypercholesterolemia?
-Warm, moist skin; fine hair
-Hypocholesterolemia (due to inc. LDL receptor expression). *you're basically burning more fuel.
-hypercalcemia (inc. burn resorption).
-hyperglycemia (gluconeo & glycogenolysis going on).
dyspnea on exertion
-Sx of hypo or hyperthyroidism
large fontanels & macroglossia in children.
-hypo or hyperthyroidism?
Whats the most common cause of myopathy?
-myoedema will be present (edema of muscle s/p percussion), inc. creatine kinase, + other hypothyroid Sxs like weight gain, fatigue, etc.
-will present w/myalgia, proximal muscle weakness, & cramping.
Abs found in hashimotos thyroiditis
*they do not cause the disease, they are byproducts of the disease.
*Pernicious anemia also associated w/HLA-DR5
-inc risk of what cancer?
-chronic inflammatory states like hashimotos (or sjogrens or h.pylori gastritis) inc. risk of developing a marginal zone lymphoma.
Which hypothyroid states can present w/initial transient hyperthyroid state?
-Subacute thyroiditis (de Quervain)
Long standing hashimoto pt that suddenly has an progressively enlarging thyroid, think what?