Renal exam - clinical Flashcards
recommendation for BP in elevated range
nonpharmacologic therapy with reassessment in 3-6 months
recommendation for stage 1 HTN and ASCVD risk < 10%
nonpharmacologic therapy with reassessment
recommendation for stage 1 HTN and ASCVD risk > 10%
start meds
recommendation for stage 2 HTN
start meds
1st line HTN drug categories
thiazides, CCBs, ACEIs, ARBs
thiazide prototype
HCTZ, chlorthalidone
CCB prototypes
amlodipine, clevidipine
ACEI prototype
captopril
ARB prototype
losartan
thiazides mechanism
block Na/Cl cotransporter in DCT
thiazides side effects
hypokalemia, increase in glucose, lipids, uricemia, calcium.
ACEI/ARB side effects
cough (ACE only), angioedema, teratogen, increased creatinine, hyperkalemia, hypotension (CATCHH)
special ACEI/ARB indication
first choice for patients with DM, CKD, CHF
drugs for HTN in pregnancy
Nifedipine, methyldopa, labetalol, hydralazine (new moms love hugs)
drugs for HTN with heart failure
diuretics, ACEIs/ARBs, beta blockers, aldosterone antagonists
drugs for HTN with DM
ACEIs/ARBs, CCBs, thiazides, beta blockers
consideration of BBs in DM
BBs can mask ssx of hypoglycemia
specific drug for HTN with CHF
vaslartan-sacubitril
prototype alpha-1 blocker
prazosin
prototype alpha-2 agonist
clonidine
mechanism of beta blockers
decrease cardiac output and renin release. Also decrease peripheral resistance if combined with vasodilating agent (labetalol)
mechanism of alpha 2 agonists
sensitize brainstem to inhibition by baroreceptor reflexes
hypertensive urgency
asymptomatic, >180/>120
hypertensive emergency
severe HTN associated with end-organ damage
treatment for hypertensive urgency
gradual decrease with oral meds
treatment for hypertensive emergency
IV meds, decrease BP by 25% in 1-2 hours then get to 160/100 within 2-6 hours
AKI definition
increase of Cr of >0.3 mg/dl within 48 hours
2 forces opposing glomerular filtration
oncotic pressure, capsule hydrostatic pressure
1 force driving glomerular filtration
glomerular hydrostatic pressure
most common type of outpatient AKI
prerenal
most common type of inpatient AKI
intrinsic
prerenal AKI mechanism
lack of bloodflow that overwhelms autoregulation (hypovolemia or loss of afferent vasodilation or loss of efferent vasoconstriction)
why do ACEI/ARBs drop GFR
loss of angiotensin II effects means loss of efferent arteriolar vasonstriction leading to reduced GFR
why do NSAIDs drop GFR
loss of prostaglandins leads to loss of afferent arteriole dilation
tests for AKI
BUN/Cr ratio, fractional excretion of Na, fraction excretion of urea
AKI BUN/Cr ratio
> 20
normal BUN/Cr ratio
<10
interfering factors with BUN/Cr ratio
malnutrition can cause lower Cr, GI bleeds can cause higher BUN, low protein intake can cause low BUN
interfering factors with fractional excretion of Na
CHF, cirrhosis, contrast nephropathy can all cause low FENa
causes of prerenal AKI
anything that decreases BP, anything causing afferent arteriole vasoconstriction (hypercalcemia, NSAIDs, pressors) or efferent arteriole vasodilation (ACEI/ARBS)
treatment of prerenal AKI
d/c offending meds, maintain MAP>65
causes of intrarenal AKI
acute tubular necrosis, atheroembolic renal disease, glomerulonephritis, acute interstitial injury
acute tubular necrosis location
proximal tubule
muddy brown cellular casts
acute tubular necrosis
causes of acute tubular necrosis
ischemic injury (shock), exogenous toxin (abx, chemo, contast, etc), endogenous toxin (cytokines, myoglobin, tumor lysis syndrome, bilirubin, etc)
how to differentiate AKI from prerenal
AKI is a severe and prolonged prerenal, with or without superimposed nephrotoxin
why oliguria in acute tubular necrosis
protective mechanism via tubuloglomerular feedback
treatment of acute tubular necrosis
maintain MAP, loop diuretics for fluid overload (but does not fix ATN), may use dialysis for refractory cases
indications for dialysis
Acidosis Electrolyte imbalances (refractory) Intoxication Overload of volume Uremia
uremia ssx
CNS irritation, GI (N/V/anorexia), pericardial effusion, uremic bleeding (platelet dysfunction)
causes of acute interstitial nephritis
Meds (especially abx, PPIs, loop diuretcs), infections (CMV, HIV, EBV), autoimmune, hypercalcemia
what is acute interstitial nephritis
hypersensitivity reaction that spares glomeruli
ssx of AIN
asymptomatic, constitutional symptoms, bilateral flank pain
AIN triad
fever, rash, eosinophilia (only seen in 10%)
AIN urine findings
no proteinuria or hematuria, may find WBCs or casts
how is AIN diagnosed
usually clinical based on new drugs, unexplained Cr rise, findings of urine WBCs and casts
RPGN causes
ANCA vasculitis, lupus nephritis, Goodpasture’s disease
Glomerulonephritis injury from immune complexes damages ____ and leads to _____, with _____ urine findings
capillaries, nephritic syndrome, hematuria
glomerulonephritis injury from autoantibodies damages ____ and leads to ____, with ____ urine findings
podocyte filtration barrier, nephrotic syndrome, proteinuria
nephrotic or nephritic? massive edema
nephrotic
causes of nephrotic syndrome
membranous nephropathy, minimal change disease, diabetic nephropathy
causes of nephritic syndrome
lupus nephritis, ANCA vasculitis, IgA nephropathy
nephrotic or nephritic causes dysmorphic RBCs
nephritic
tests for glomerulonephritis
ANA, complement, hepatitis, HIV, anti-GBM titer
treatment of glomerulonephritis
if mild, ACE/ARB, immunosuppression if nephrotic proteinuria or rapid decline in renal function (for several years)
causes of postrenal AKI
bilateral uretral obstruction, neurogenic bladder, bladder neck obstruction from BPH
diagnosis of postrenal AKI
renal US/CT, bedside bladder scan with post voice residual volume (>100)
treatment of postrenal AKI
relieve obstruction, d/c offending meds - may be reversible if not too prolonged
what is common after postrenal AKI
postobstructive diuresis (due to high BUN/Na+/H2O accumulated during obstruction or decreased Na+ reabsorption capacity)
carbonic anhydrase inhibitor prototype
acetazolamide
osmotic diuretic prototype
mannitol
carbonic anhydrase inhibitor mechanism
inhibition of carbonic anhydrase in proximal convoluted tubule
osmotic diuretic mechanism
high osmolarity prompts fluid shift from ICF to ECF
loop diuretic mechanism
Inhibition of Na/K/2CL symporter in ascending limb of loop of Henle
thiazide diuretic mechanism
inhibition of Na+/Cl- cotransporter in DCT
uses of carbonic anhydrase inhibitors
metabolic alkalosis, mountain sickness
uses of osmotic diuretics
reduce intracranial pressure, acute renal failure
uses of loop diuretics
edematous states, acute renal failure, HTN, hypercalcemia, hyperkalemia
uses of thiazide diuretics
HTN, CHF, nephrolithiasis, diabetes insipidus, osteoporosis
ADH antagonist uses
SIADH, HF, polycystic kidney disease
adverse effects of carbonic anhydrase inhibitors
non AG metabolic acidosis, hypokalemia, sulfa allergy, nephrolithiasis
adverse effects of osmotic diuretics
initial volume expansion with subsequent dehydration
adverse effects of loop diuretics
ototoxicity, hypokalemia, hypocalcemia, hypomagnesemia, alkalosis, hyperglycemia, hyperlipidemia, gout
adverse effects of thaizide diuretics
hyponatremia/kalemia/magnesemia, hyperglycemia, uremia, hyperlipidemia, sulfa allergy, gout
adverse effects of potassium-sparing diuretics
hyperkalemic metabolic acidosis, gynecomastia (spironolactone)
prototype of potassium-sparing diuretics
amiloride, spironolactone
adverse effects of ADH antagonists
nephrogenic diabetes insipidus
most common cause of CKD in US
Diabetic nephropathy
first treatment of hyperkalemia in CKD
calcium gluconate (stabilize cell membrane)
2nd treatment of hyperkalemia in CKD
push K into cells (insulin/glucose, beta agonist, sodium bicarb)
3rd treatment of hyperkalemia in CKD
eliminate K from body (lasix, dialysis)
what is CKD contraindication to metformin
GFR<30
meds associated with hyperkalemia
NSAIDs, metformin, ACEI/ARB, aldosterone antagonists, beta blockers, dig, potassium-sparing diuretics
lab findings in secondary hyperparathyroidism
low-normal Ca, low-high Ph, low vit D, high PTH
phos binder prototypes
sevelamer, calcium carbonate
how to treat elevated PTH in secondary hyperparathyroidism
calcitriol (1,25 vit D-OH)
poorly controlled secondary hyperparathyroidism can lead to
osteitis fibrosa
overtreatment of Vit D analogs or chronic disease can lead to
adynamic bone disease due to low bone turnover (low PTH levels)
what does acute rise in creatinine after ACEI use suggest
bilateral renal artery stenosis
“string of pearls” appearance on renal angiography is suggestive of
fibromuscular dysplasia as cause of renal artery stenosis
what is responsible for voiding bladder
parasympathetics from S2-S3 pelvic nerve
what is responsible for storing urine
sympathetics: hypogastric T11-L2
voluntary control of bladder
pudendal nerve
inhibitory process to parasympathetics at baseline (to keep people from peeing everywhere all the time)
pontine micturition center at baseline
failure to store forms of incontinence
urge/stress
failure to empty forms of incontinence
overflow
causes of urge incontinence
overactive bladder, decreased bladder compliance
causes of stress incontinence
intrinsic sphincter dysfunction, pelvic floor laxity. Childbirth, age, obesity
causes of overflow incontinence
bladder won’t contract, protastatic or urethral obstruction
symptoms of stress incontinence
incontinence with increasing abdominal pressure (sneezing, coughing etc)
cause of overactive bladder
detrusor muscle contracts when it shouldn’t
symptoms of urge incontinence
urgency, frequency, nocturia
total incontinence cause
surgery, neuropathy
symptoms of overflow incontinence
frequency, nocturia, distended bladder on exam, incomplete empyting
medical treatment for urge incontinence
muscarininc antagonists (anticholinergics): oxybutynin
medical treatment for prostate enlargement
alpha antagonists (tamsulosin)
4 most common types of kidney stones
calcium based, uric acid, struvite, cystine
risk factors for calcium based stones
low urine volume, abnormal urine pH, high dietary sodium/animal protein consumption
types of calcium based stones
calcium oxalate and calcium phosphate
causes of calcium oxalate stones
hypercalciuria: increased absorption from intestine, primary hyperparathyroidism, impaired resoprtion of Ca from tubules
treatment of calcium based stones
high fluid intake, adequate Ca, limit Na/animal protein intake, thiazides, potassium citrate
primary cause of uric acid stones
low urinary pH, associated with DM and insulin resistance
treatment of uric acid stones
increase fluid intake, alkalinize the urine with potassium citrate, allopurinol
struvite stones made of
ammonium/magnesium/phosphate
cause of struvite stones
UTI with proteus, klebsiella, staph
treatment of struvite stones
urease inhibitor
cause of cystine stones
autosomal recessive defect in proximal tubule
treatment of cystine stones
decrease sodium intake, alkalinize urine, cystine binder
3 most common types of bladder malignancy
transitional cell, squamous cell, adenocarcinoma
most common type of bladder cancer
transitional cell carcinoma
risk factors of transitional cell carcinoma
smoking, hair dye, cyclophosphamide, industrial solvents
treatment of transitional cell carcinoma
if nonmuscle invasive: transurethral resection
if muscle invasive: radical cystectomy
location of bladder adenocarcinoma
dome of bladder or urachus
squamous cell carcinoma risk factors
chronic inflammatory conditions
autoantibodies seen in SLE
Anti-double stranded DNA, anti-Smith, ANA
post-strep GN is nephrotic or nephritic
nephritic
what is lupus nephritis
glomerulonephritis caused by immune complex deposits
causes of acute pyelonephritis
ascending bacteria from urethra/bladder (more common) - usually E coli, proteus, klebsiella. OR hematogenous spread from bloodstream (less common)
risk factors for acute pyelonephritis
reduced urine flow (obstruction, bladder dysfunction, vesico-ureteral reflux)
acute pyelonephritis urinalysis
neutrophils with white cell casts
complications of acute pyelonephritis
papillary necrosis, pyelonephrosis, perinephric abscess, sepsis, chronic inflammation with scarring
clinical picture of nephrotic syndrome
insidious onset, massive proteinuria, hypoalbuminemia, edema, hyperlipidemia
clinical picture of nephritic syndrome
hematuria, azotemia (increased creatinine and BUN), oliguria, acute onset, HTN
clinical picture of membranoproliferative glomerulonephritis
young people with a slowly progressive nephritic syndrome that is unresponsive to immunosuppressants
secondary MPGN is due to
SLE, hep B, hep C
ANCA disease clinical picture
adult with nephritic syndrome and possible acute renal failure treated with high dose steroids and cyclophosphamide
2nd leading bacteria causing UTI in sexually active women
staph saprophyticus
causes of sterile pyuria that mimics UTI
chlamydia, gonorrhea
why is urine yellow
urobilin
specific gravity < 1.01
hydration
specific gravity >1.03
dehydration
causes of alkaline urine
(with UTI) struvite stone, RTA
what type of casts can be normal in UA
hyaline
what do nitrites in urine indicate
UTI with gram-negative bacteria
red cell casts indicate
glomerular disease
white cell casts indicate
AIN, chronic pyelo
fatty casts indicate
nephrotic syndrome
renal tubular epithelial casts indicate
acute tubular necrosis
granular casts indicate
chronic renal failure
waxy casts indicate
chronic renal failure
most common cause of intrarenal AKI
acute tubular necrosis
what is acute tubular necrosis
damage to tubules due to ischemia or exposure to nephrotoxins
glomerular disease is type of
intrarenal AKI
