16: Renal disease, HTN, and renal a. stenosis - Thompson Flashcards
what might happen when kidneys fail?
- Electrolyte imbalances (phos gets high, potassium high, calcium low)
- -Anemia
- Blood pressure irregularities
- Meds hang around
renal disease ________ HTN
goes both ways - both can lead to each other
normal Cr
.6-1.2
dialysis level — 5!
JNC8 Recommendations for BP **
greater than 60
150/90
less than 60
140/90
greater than 18 with CKD
140/90
greater than 18 with DM
140/90
risk factors for HTN
Age Smoking DM High lipids Inactivity/weight Family history Race
secondary causes HTN
- Sleep apnea
- Primary hyperaldosteronism (low K, htn resistant)
- CRF
- Thyroid
- Renal vascular disease
- Pheochromocytoma
- Cushings or steroid therapy
Diagnose with a high aldosterone/renin ratio – their K will often be low
Primary Hyperaldosteronism
Consider in patients with resistant hypertension and a low potassium
basic work up for HTN
EKG UA BMP TSH H&H Ca Cholesterol
problems with beta blockers
Dizzy/syncope Fatigue Low HR Impotence Makes working out difficult
use for ACE inhibitors
Used in DM (regardless of BP) CHF and post MI – many beneficial effects
- Decreases all CV causes of death in DM II
- Think increases flexibility of vessels
- Causes cardiac remodeling (repair)
side effects of ACEi
– Increases K
– Angioedema (.2%)
Asians/Blacks 3-4X more likely
– Cough
> 8%
– Increase Cr
Can increase 30% before stop or big w/u
Small increase means intraglomular pressure has been reduced
inhibits NaCl reabsorption
Thiazides
- K/Na reduction
- Renal damage
- Increased glu, Ca
JNC8 recommendations for nonblack v. black population
nonblack: thiazides, CCB, ACEi, or ARB
black: thiazide or CCB
tx CKD
include ACEi or ARB
up-titrate or add therapy after ________ if BP goal not achieved
1 mo
don’t use ACEi and ARB together
if greater than 3 dugs needed, refer to HTN specialist
if _____ to start, just start 2 meds
greater than 160/100
take aways
- Beta Blockers are NOT first line (unless post MI)
- Whites – start almost anything else (Thiazides, ACE/ARB, CCB)
- – Blacks – avoid ACE (why)
- Diabetics/CRF – ACE
- Post MI/CVA – beta blocker/ACE
- CHF – Beta Blocker + ACE, plus thiazide plus spiranolactone
Any increase in BP that results in acute end organ damage
malignant hypertension
still want to lower the BP slowly
> 180 or >110
No symptoms or vague symptoms
Hypertensive urgency
mechanism of renal a. stenosis
When renal arteries are constricted to the point that the kidneys have a decreased blood flow.
Kidney thinks body is hypovolemic and secretes renin which increases BP
Doesn’t respond to treatment Intermittent claudication Sudden worsening of htn Image abnormality ACE leads to worsening creatinine
suspect RAS
caused by atherosclerosis older of fibromuscular dysplasia (younger)
risk factors are: HTN Obesity Vascular disease of any kind Age Smoking
what happen to kidneys if BP uncontrolled?
Affected kidney gets small, ischemic
Ischemic nephropathy
Other kidney gets injured from the increased BP
Hypertensive nephrosclerosis
describe fibromuscular dysplasia
“string of pearls on imaging”
Angiopathy of medium sized vessels; mainly seen in women of childbearing age.
Seems to increase just before menopause
Genetic link as well
Symptoms occur where artery occluded (brain, periphery – kidneys mainly)
Rare – less than 1% of population