Renal: vascular and secondary HTN Flashcards
list causes of secondary HTN
C--> Cushing syndrome H--> Hyperaldosteronism aka Conn syndrome A-->aorta coarctation P--> pheochromocytoma S-->stenosis of renal arteries
when do we suspect secondary HTN
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
how many grams of salt/day can affect BP
> 3 grams/day
***at this level–diuretics stop working
most common causes of resistant HTN (not kidney related)
- non-comliance with meds
- > 3 grams of salt/day
- caregievr not aggressive enough with tx
- drug induced htn–>NSAIDs****
- OSA
- primary aldosteronism
consider RAS when the patient:
- is 50 YO with grade 2 HTN (160/100)
- acute creatinine increases >30% AFTER giving ACEI or ARB
- HTN resistant to meds (3 meds.. one is a diuretic).
- renal or carotid bruits——-abd bruit that lateralizes to one side (40% sensitivity) with 99% specificity
RAS
- etiologies
- suspect in who
- CM
- DX
- TX
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
what dye is contraindicated in renal insuff
Gadolinium–used in MRAs
*****causes nephrogenic systemic fibrosis
gold standard for dx of RAS
-what is a potential complication
renal angiography
+invasive
-done after scnreening test
COMPLICATION
*atheroemboli in 5-10%–>cholesterol emobli in the toes/feet
MC location for RAS
proximal 1/3rd or distal region of artery
FIbromuscular Dysplasia -define -mc in population -avg age onset -suspect in pts with? -
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
renal vein thrombosis
- causes
- CM
- labs
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
Genetic causes of HTN
- syndrome of HTN exacerbated in pregnancy–>mutation in mineralcorticoid receptor–>abnormally responds to progesterone and spironolactone
- Liddle syndrome–>HTN, hypoK metabolic alkalosis, low renin and aldosterone levels,
* mutation=unregulated NA reabsorption and volume expansion
Primary Aldosteronism
-when should you suspect this dx
- unexplained HYPOKALEMIA with urinary K+ wasting
- elevated serum NA
- drug-resistant HTN
- HTN with an adrenal incidentaloma
Hyperaldosteronism is assoc with
cardiac inflammation fibrosis pathologic insulin secretion metabolic syndrome incr mortality
etiology of hyperaldosteronism
MC?
2nd mC?
- bilateral idiopathic hyperaldosteronism MCC
- adrenal tumor–aldosterone prod adenoma 2nd MC
- uni or bilateral hyperplasia of zona glomerulosa
- incr aldosterone secretion from genetic mutations