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87 Cards in this Set
- Front
- Back
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what is endocrine htn seen in
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insulin resistance, mc excess, cs, pheo, hyper/hypothyroid, hyperparathryoid and acromegala
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eval htn
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getn plasma renin, and serum aldo with urine na
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if individuals have nl kidneys they
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do not have htn
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renal pressure-natriuresis relationship
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any increase in salt relesed from gi tract causes exponential increase in renal output to ensure nl arterial pressure is maintained
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if chronic htn the problem is
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chronic increases in blood volue based on press= vol/ compliance
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what increases high last
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rass, mc's, av, sns
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htn therapy
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salt restriction, b blockers, vaso veno blockers
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antihypertensive fx of the kidney
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increase anp, decrease avp, (lower volume) decrease raas, decerase sympathetics
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beta blockers htn
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lower hr and sv lowerirng q which lowers Va
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vaso-veno bloacker
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increase complianse and lower arteral resistant increasing q out
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endocrine htn syptoms
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primary aldosteronism, cushings, CAH 17 and 11, apparentminearlocorticoid excess, GC remediable, pseudohyperaldosteronism (liddle) pheo, hyperpara, hyperthryoid, hypothyroid, acromegaly
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agiontensin II actson on
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adrenal cortex (aldo) kidney, intestine, central nervous, peripheral nervous, vascular smooth mucle (constricts) hear (inceas co), + growth factors
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aldo action on distal nephron
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synergizes with effects of angiotensin, binds MR, migrates to nucleus where it induces transcription of mRNA, increases sodium potasium ATPASE protein and activity at basolateral membranes incraseing mitochondrial atp formation and increasing sodium and potassium channels at the luminal membrane
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hyperalodsteronism
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most common adenoma that produces aldosterone si most common, 11B and 17 B
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gc remediable
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dna crossover mutation reuslt in chimeric gnee in which aldosterone prodcution is regulated by adrenocorticotropic hormeon (ACTH), resulting in increase in aldosterone
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liddle syndrome
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excess epithelail sodium channel activity… causes low aldo (low renin and aldo) often with hypokalemia by absorbing na…
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mutation in liddle
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b or gamma subunit.. The channel has 3 subunity a b or y and this is in b or y
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specific problem in liddle
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prolien rich domains in the carboyl terminal region of b or y
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glycyrrhizing acid
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blocks 11 b ohsd
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carbenoxolone
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blocks 11 b oshd
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tx mineralocorticoid excess
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sprionolactione (inhibits MR and is able to block excessive action of cortisol on the MR receptor)
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hemodynamic abnormality underlying essential hypertension
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peripheral vascular resistance… complex array of systemic and locally produced hormoens and factors
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RAS in essential hypertension?
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yes
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is renin profiling used for EH?
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no longer used to be that it was if high renin then you had a vasocnstrictor mechanism
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low renin htn and ras drugs
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responds
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what activates mc receptors
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aldo, doc and cortisol
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what dose MC induse
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SGK
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SGK action
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disengages Nedd 4 from Na chanels… decreasesdecredation
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aldo effects on distal tuble
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increase na cl cotransporter and na k atpase
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aldo effects on collecting tuble
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increase ENaCs and Na-K ATPase
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why hypokalemia in high aldo levels
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Na K atpase
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in high aldo why alkalosis
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K-H exchanger in intercalated cells tries to regain K
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lorsartan
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ANGII agonist
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what blocks aldo effects
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Losartan and spronolaction (aldo antaogist)
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primary hyperaldoseteronism is usually due to
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aldrenal aldo prodcuineg adenoma #2 is bilateral micronodular hyperplasia
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rare cuases of hyperaldosteronism
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familial (gc remdiable) or uniltareral hyperplasia
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unilaterl hyperaldoserism txsurgical while bilateral is medical tell on adrenal vein catherterization
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do you always have hypokalemia in hyperaldosteronism
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no only 50%
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plasma reninin in hyperaldosteronism
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lower hr and sv lowerirng q which lowers Va
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cv effects of aldo
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increased expressoin of at1r in cardiac myocites (+ino) and vascular smooth muclse cells (vasoconsticiton) both of with increase HTN
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when aldo is high do you get edema?
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no.. Escape phenomenon; spontaneious diuresis occurs in response to continued high aldo exposure so no fluid is retained
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HTN in high GC's due to
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doc/cortisol overwhelms 11BHSD and thus they can chronically stim MCR and increase Na retetion---> HTN
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GC other HTN effects
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induction of PMNT (increase epi) and vasoconstricition by inhibition of COMT and decreased expression of Na-Ca exchanger
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HTN in pheo's
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paroxysmal… due to pulsatile natuer of catecholamine release from tumor
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labs in pheo
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hyperglycemia and triglyceriedes since catecholamines make fuels readily available
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case 3 and 4
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clues to adrenal insufficenty
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hypotension (in acute illness or prolonged with DA dependence) prior GC TX, hyponatremia (vol status), eosinophilia and decreased appetite / fatigue
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how to asses adrenal insufficency
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acth stim, plasma acth if low; acth stim, metyrapone if normal and 11 deoxycortisol\
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metyrapone and elevated acth following
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no 2ary since it inhibits cyp11 b1
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metyrapone and nl acth
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or if acth low afer metyrapone then faulty hpa axis
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if cortisol gives normal response after acth stim
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metyrapone
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if cortisole gives low response after acth stim test
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suggests adrenocortical insufficiency; msut look at plasma acth if elevated 1ary, if nl/lwo 2ndary
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rigampin
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inhibits dna dependet rn polymerase in bacteria--> induces P450 to accelearate cortisol breakdown
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ketoconazole
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inhibits CYP cscc and tus lowers cortisol synthesis
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what to r/o is hirsuitism
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cs, cah, androgen secreting neoplasm, polycystic ovary syndrome,
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if hirsutism is idiopathic what do you expect
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no irregular menses
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dhea-s
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lab workup for hirsuitism… tells you how much androgen is coming from adrenals since dhea is only sulfated in adrenals
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cortrosyn
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(acth stim test)if you supect CAH in hirsuitism… 17-00H-progesterone and cortisol should be high
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tx hirsutism
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GC's enough to suprress androgen release but not too much to avoid bad side effects or oral contraceptives (combats androgen and decrease androgen release from ovaries
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enzymes in CAH
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P450scc, 17 alpha, B, 21 hydroxylase, 11 hydroxylase, 3 B HSD, 17, 20 lysase
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most virulizing CAH
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21 and 11 hydroxylase secondary to high testosterone/DHT
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minimal virulization in CAH
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3B HSD second to DHEA's weak androgen ction
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do 17,20 lysase, and 17 alpha hydroxylase cause virulizing
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no feminization in men
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elevated in21 hydroxylase
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17 hyrdoxy progesterone and androsterodine
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21 hydroxylase deficnecy and genital developemnt
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infant firls have ambiguidity
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cortisol in 21 hydoxlase
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low in classic sufficinet in non - classic, why non-classic has late onset
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urogenital sinus
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high androgens before 12 week
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clitoromegally
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after 12 weeks high androgens (labia may fuse and some degree of rugation
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toral disruption in male infants
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fbefore 12 week los androgen
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micropenin
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after 12 weeks low androgens
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classic labs in 21
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hyponatremia, hyopkalemia, acidotic, low glucose
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b/o acne in 5y/o
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non classic 21
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fals positives for 17-oh progestorn
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in low birth weight babies or sample drawn < 24hrs after birth
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false negs in 17-OH prog
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measuing 7-oH will miss 3B HSD and CYP17
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prader scale
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I like F, III ambigious, V most like M
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heel stick levels for 17 OH
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<50 nromal >125 probable
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what comes after >125 17OH
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serum chemistries and renin
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tx 21 CAH
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ABC's; dextrose as necessary for hypoglycemia; abx; stress hydrocorsone replacemne is 75mg/m2 or 4g/kr IV: miantenance hyrdocortisone 15mg/m2 3X per day; fludrocortisone BID, education of risk of adrenal ciris; stress steroids in times of ferever vomiting and truam/surger
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hyperpirgmented in CAH
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yes
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renin in 21
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high androgens before 12 week
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masculinization
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21 or 11B
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low ineralocorticoids
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17 or 21 in 1B DOC is secreted in excess and it is a mineralocorticoid
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adrenal glands in all CAH
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enlarged due to increase ACTH due to low cortisol
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gender ident
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what pt. feelse
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gender role
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what society feels
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gender role behavior
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behoviros or traits exhibited in sex-related variation
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cortisol and aldosterone deficinecy in a infant
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in 21 tx w/ hyrdocortison and fludrocortisone
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