Renal: vascular and secondary HTN Flashcards

1
Q

list causes of secondary HTN

A
C--> Cushing syndrome 
H--> Hyperaldosteronism aka Conn syndrome 
A-->aorta coarctation 
P--> pheochromocytoma 
S-->stenosis of renal arteries
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2
Q

when do we suspect secondary HTN

A

severe or resistant HTN= pt is tx with 3 antihypertensive drugs (1 of which is a diuretic) and still has persistent HTN

  • pt with perviously stable BP—now suddenly develops acute rise in BP
  • <30 YO with no risk factors for HTN
  • pt with malignant or accelerated HTN with signs of EOD
  • electtolyte or acid-base disordrs + HTN
  • HTN develops befoe puberty
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3
Q

how many grams of salt/day can affect BP

A

> 3 grams/day

***at this level–diuretics stop working

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4
Q

most common causes of resistant HTN (not kidney related)

A
  1. non-comliance with meds
  2. > 3 grams of salt/day
  3. caregievr not aggressive enough with tx
  4. drug induced htn–>NSAIDs****
  5. OSA
  6. primary aldosteronism
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5
Q

consider RAS when the patient:

A
  1. is 50 YO with grade 2 HTN (160/100)
  2. acute creatinine increases >30% AFTER giving ACEI or ARB
  3. HTN resistant to meds (3 meds.. one is a diuretic).
  4. renal or carotid bruits——-abd bruit that lateralizes to one side (40% sensitivity) with 99% specificity
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6
Q

RAS

  • etiologies
  • suspect in who
  • CM
  • DX
  • TX
A

ETIOLOGIES

  • Athersclerosis mc in elderly
  • fibromuscular dysplasia MC cause in women <50 YO

SUSPECT IN:
-pt with HA and HTN <20 YO or >50YO
-severe HTN
-HTN resistent to 3 or more drugs
-abdominal bruits****
-pt develops AKI after initiation of ACEI or ARB (incr in creatinine)
+/- EOD–> fundoscopic changes, hematuira, PU,

DX

  • doppler US
  • CT or MR angiography—> stenosis in 75% in 1 or both arteries
  • DEFINITIVE= renal catheter arteriography

TX

  • MEDS FIRST
    1. ACEI or ARB
  • ->contra for bilateral RAS or if PT with a solitary kidney
    2. Add on tx= thiazides, long acting CCB, mineralcorticoid receptor angatonist
  • SURGICAL
    1. revascularization definitive tx—angioplasty or bypass
    2. can also do a stent
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7
Q

what dye is contraindicated in renal insuff

A

Gadolinium–used in MRAs

*****causes nephrogenic systemic fibrosis

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8
Q

gold standard for dx of RAS

-what is a potential complication

A

renal angiography
+invasive
-done after scnreening test

COMPLICATION
*atheroemboli in 5-10%–>cholesterol emobli in the toes/feet

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9
Q

MC location for RAS

A

proximal 1/3rd or distal region of artery

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10
Q
FIbromuscular Dysplasia 
-define 
-mc in population 
-avg age onset 
-suspect in pts with? 
-
A

stenosis or renal arteries 2nd to muscle hypertrophy–>webbing, dilation and dysplastic
MC in females
-younger PTs
AVG AGE=50

SUSPECT IF:

  • onsten HTN <35 YO ***
  • abd bruit
  • sudden rise in BP from previously stable
  • sig rise in creatinine after ACEi/ARB
  • severe or resist. htn

DX

  • doppler US
  • CT or MR angio–>BEADING OF THE ARTERY

TX

  • MEDS: ACEi or ARB
  • SURGICAL: revascularization via–> angioplasty or surgery
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11
Q

renal vein thrombosis

  • causes
  • CM
  • labs
A

ACUTE CAUSES

  • hypercoaguable state
  • trauma
  • severe dehydration (kids)

CHRONIC CAUSES
-nephrotic syndrome—>membranous nephropathy–> BC loss of protein C, S, antithormbin II, and incr in liver production of more clotting proteins

CM
-severe flank pain

LABS

  • incr LDH
  • UA: hematuria and PU only if nephrotic syndrome present

TX

  • ACUTE= anticoagulation +/- thrombectomy
  • CHRONIC= anticoag or thromblytic therapy
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12
Q

Genetic causes of HTN

A
  1. syndrome of HTN exacerbated in pregnancy–>mutation in mineralcorticoid receptor–>abnormally responds to progesterone and spironolactone
  2. Liddle syndrome–>HTN, hypoK metabolic alkalosis, low renin and aldosterone levels,
    * mutation=unregulated NA reabsorption and volume expansion
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13
Q

Primary Aldosteronism

-when should you suspect this dx

A
  • unexplained HYPOKALEMIA with urinary K+ wasting
  • elevated serum NA
  • drug-resistant HTN
  • HTN with an adrenal incidentaloma
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14
Q

Hyperaldosteronism is assoc with

A
cardiac inflammation 
fibrosis 
pathologic insulin secretion 
metabolic syndrome 
incr mortality
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15
Q

etiology of hyperaldosteronism
MC?
2nd mC?

A
  1. bilateral idiopathic hyperaldosteronism MCC
  2. adrenal tumor–aldosterone prod adenoma 2nd MC
  3. uni or bilateral hyperplasia of zona glomerulosa
  4. incr aldosterone secretion from genetic mutations
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16
Q

Pheochromocytoma

  • what is it
  • patho
  • cm
  • suspect in?
A

RAARE
but an imp cause of HTN

PATHO: cateholamine excess (alpha-receptor vasoconstriction PLUS b1-receptor)= increase cardiac output plus renin release

CM

  • postural hypotension
  • glucose intolerance
  • HTN crisis
  • ->can be precipitated by drugs: TCAs, antidopaminergic agents, metocloproamide, naloxone

SUSPECT IF:
-paroxysmal elevations in BP, pounding HA, palps, and sweating

17
Q

Cushings syndrome

-define

A

HTN is seen in about 80% of pts esp if tumor present

PATHO: excess glucocorticoid—CORTISOL—>mineralcortcioids effects–> NA and water retention->incrs AG2

CM

  • moon facies
  • central obesity
  • proximal muscle wasting
  • ecchymosis

DX
-24 hour urinary free cortisol— low does dexamethasone suppression or late night salivary cortisol tests

18
Q

Coarc of aorta

-cm

A

upper extrem HTN

  • delayed or decr femoral pulses–brachial-femoral or radial-femoral delay)
  • low or unobtainable BP in lower extrems
  • murmurs

+rib nothcing

19
Q

list the thyroid and parathyroid causes of HTN

A
  1. hyPOthyroidism–>elevation in DBP
  2. hyPERthryoidism–>elvation in SBP–>widening pulse pressure
  3. primary hyperparathyroidism–>hypercalcemia–>affect vascular reactivity, cicardian blood pressure rhythm, and renal functon
20
Q

drugs that cause or exacerbate HTN

A

NSAIDS
**
*OCPs
-sympathomimetics
-cocaine
-glucocorticoids
-mineralcorticoids
-cyclosporin
-EPO
-

21
Q

discontinue drugs that affect aldosterone to renin ratio _______ before testing

A

four weeks