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CVPR > Renal exam - clinical > Flashcards

Renal exam - clinical Flashcards

1
Q

recommendation for BP in elevated range

A

nonpharmacologic therapy with reassessment in 3-6 months

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2
Q

recommendation for stage 1 HTN and ASCVD risk < 10%

A

nonpharmacologic therapy with reassessment

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3
Q

recommendation for stage 1 HTN and ASCVD risk > 10%

A

start meds

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4
Q

recommendation for stage 2 HTN

A

start meds

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5
Q

1st line HTN drug categories

A

thiazides, CCBs, ACEIs, ARBs

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6
Q

thiazide prototype

A

HCTZ, chlorthalidone

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7
Q

CCB prototypes

A

amlodipine, clevidipine

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8
Q

ACEI prototype

A

captopril

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9
Q

ARB prototype

A

losartan

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10
Q

thiazides mechanism

A

block Na/Cl cotransporter in DCT

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11
Q

thiazides side effects

A

hypokalemia, increase in glucose, lipids, uricemia, calcium.

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12
Q

ACEI/ARB side effects

A

cough (ACE only), angioedema, teratogen, increased creatinine, hyperkalemia, hypotension (CATCHH)

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13
Q

special ACEI/ARB indication

A

first choice for patients with DM, CKD, CHF

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14
Q

drugs for HTN in pregnancy

A

Nifedipine, methyldopa, labetalol, hydralazine (new moms love hugs)

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15
Q

drugs for HTN with heart failure

A

diuretics, ACEIs/ARBs, beta blockers, aldosterone antagonists

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16
Q

drugs for HTN with DM

A

ACEIs/ARBs, CCBs, thiazides, beta blockers

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17
Q

consideration of BBs in DM

A

BBs can mask ssx of hypoglycemia

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18
Q

specific drug for HTN with CHF

A

vaslartan-sacubitril

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19
Q

prototype alpha-1 blocker

A

prazosin

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20
Q

prototype alpha-2 agonist

A

clonidine

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21
Q

mechanism of beta blockers

A

decrease cardiac output and renin release. Also decrease peripheral resistance if combined with vasodilating agent (labetalol)

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22
Q

mechanism of alpha 2 agonists

A

sensitize brainstem to inhibition by baroreceptor reflexes

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23
Q

hypertensive urgency

A

asymptomatic, >180/>120

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24
Q

hypertensive emergency

A

severe HTN associated with end-organ damage

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25
Q

treatment for hypertensive urgency

A

gradual decrease with oral meds

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26
Q

treatment for hypertensive emergency

A

IV meds, decrease BP by 25% in 1-2 hours then get to 160/100 within 2-6 hours

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27
Q

AKI definition

A

increase of Cr of >0.3 mg/dl within 48 hours

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28
Q

2 forces opposing glomerular filtration

A

oncotic pressure, capsule hydrostatic pressure

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29
Q

1 force driving glomerular filtration

A

glomerular hydrostatic pressure

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30
Q

most common type of outpatient AKI

A

prerenal

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31
Q

most common type of inpatient AKI

A

intrinsic

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32
Q

prerenal AKI mechanism

A

lack of bloodflow that overwhelms autoregulation (hypovolemia or loss of afferent vasodilation or loss of efferent vasoconstriction)

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33
Q

why do ACEI/ARBs drop GFR

A

loss of angiotensin II effects means loss of efferent arteriolar vasonstriction leading to reduced GFR

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34
Q

why do NSAIDs drop GFR

A

loss of prostaglandins leads to loss of afferent arteriole dilation

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35
Q

tests for AKI

A

BUN/Cr ratio, fractional excretion of Na, fraction excretion of urea

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36
Q

AKI BUN/Cr ratio

A

> 20

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37
Q

normal BUN/Cr ratio

A

<10

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38
Q

interfering factors with BUN/Cr ratio

A

malnutrition can cause lower Cr, GI bleeds can cause higher BUN, low protein intake can cause low BUN

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39
Q

interfering factors with fractional excretion of Na

A

CHF, cirrhosis, contrast nephropathy can all cause low FENa

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40
Q

causes of prerenal AKI

A

anything that decreases BP, anything causing afferent arteriole vasoconstriction (hypercalcemia, NSAIDs, pressors) or efferent arteriole vasodilation (ACEI/ARBS)

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41
Q

treatment of prerenal AKI

A

d/c offending meds, maintain MAP>65

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42
Q

causes of intrarenal AKI

A

acute tubular necrosis, atheroembolic renal disease, glomerulonephritis, acute interstitial injury

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43
Q

acute tubular necrosis location

A

proximal tubule

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44
Q

muddy brown cellular casts

A

acute tubular necrosis

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45
Q

causes of acute tubular necrosis

A

ischemic injury (shock), exogenous toxin (abx, chemo, contast, etc), endogenous toxin (cytokines, myoglobin, tumor lysis syndrome, bilirubin, etc)

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46
Q

how to differentiate AKI from prerenal

A

AKI is a severe and prolonged prerenal, with or without superimposed nephrotoxin

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47
Q

why oliguria in acute tubular necrosis

A

protective mechanism via tubuloglomerular feedback

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48
Q

treatment of acute tubular necrosis

A

maintain MAP, loop diuretics for fluid overload (but does not fix ATN), may use dialysis for refractory cases

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49
Q

indications for dialysis

A 
Acidosis
Electrolyte imbalances (refractory)
Intoxication
Overload of volume
Uremia
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50
Q

uremia ssx

A

CNS irritation, GI (N/V/anorexia), pericardial effusion, uremic bleeding (platelet dysfunction)

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51
Q

causes of acute interstitial nephritis

A

Meds (especially abx, PPIs, loop diuretcs), infections (CMV, HIV, EBV), autoimmune, hypercalcemia

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52
Q

what is acute interstitial nephritis

A

hypersensitivity reaction that spares glomeruli

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53
Q

ssx of AIN

A

asymptomatic, constitutional symptoms, bilateral flank pain

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54
Q

AIN triad

A

fever, rash, eosinophilia (only seen in 10%)

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55
Q

AIN urine findings

A

no proteinuria or hematuria, may find WBCs or casts

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56
Q

how is AIN diagnosed

A

usually clinical based on new drugs, unexplained Cr rise, findings of urine WBCs and casts

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57
Q

RPGN causes

A

ANCA vasculitis, lupus nephritis, Goodpasture’s disease

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58
Q

Glomerulonephritis injury from immune complexes damages ____ and leads to _____, with _____ urine findings

A

capillaries, nephritic syndrome, hematuria

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59
Q

glomerulonephritis injury from autoantibodies damages ____ and leads to ____, with ____ urine findings

A

podocyte filtration barrier, nephrotic syndrome, proteinuria

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60
Q

nephrotic or nephritic? massive edema

A

nephrotic

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61
Q

causes of nephrotic syndrome

A

membranous nephropathy, minimal change disease, diabetic nephropathy

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62
Q

causes of nephritic syndrome

A

lupus nephritis, ANCA vasculitis, IgA nephropathy

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63
Q

nephrotic or nephritic causes dysmorphic RBCs

A

nephritic

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64
Q

tests for glomerulonephritis

A

ANA, complement, hepatitis, HIV, anti-GBM titer

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65
Q

treatment of glomerulonephritis

A

if mild, ACE/ARB, immunosuppression if nephrotic proteinuria or rapid decline in renal function (for several years)

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66
Q

causes of postrenal AKI

A

bilateral uretral obstruction, neurogenic bladder, bladder neck obstruction from BPH

67
Q

diagnosis of postrenal AKI

A

renal US/CT, bedside bladder scan with post voice residual volume (>100)

68
Q

treatment of postrenal AKI

A

relieve obstruction, d/c offending meds - may be reversible if not too prolonged

69
Q

what is common after postrenal AKI

A

postobstructive diuresis (due to high BUN/Na+/H2O accumulated during obstruction or decreased Na+ reabsorption capacity)

70
Q

carbonic anhydrase inhibitor prototype

A

acetazolamide

71
Q

osmotic diuretic prototype

A

mannitol

72
Q

carbonic anhydrase inhibitor mechanism

A

inhibition of carbonic anhydrase in proximal convoluted tubule

73
Q

osmotic diuretic mechanism

A

high osmolarity prompts fluid shift from ICF to ECF

74
Q

loop diuretic mechanism

A

Inhibition of Na/K/2CL symporter in ascending limb of loop of Henle

75
Q

thiazide diuretic mechanism

A

inhibition of Na+/Cl- cotransporter in DCT

76
Q

uses of carbonic anhydrase inhibitors

A

metabolic alkalosis, mountain sickness

77
Q

uses of osmotic diuretics

A

reduce intracranial pressure, acute renal failure

78
Q

uses of loop diuretics

A

edematous states, acute renal failure, HTN, hypercalcemia, hyperkalemia

79
Q

uses of thiazide diuretics

A

HTN, CHF, nephrolithiasis, diabetes insipidus, osteoporosis

80
Q

ADH antagonist uses

A

SIADH, HF, polycystic kidney disease

81
Q

adverse effects of carbonic anhydrase inhibitors

A

non AG metabolic acidosis, hypokalemia, sulfa allergy, nephrolithiasis

82
Q

adverse effects of osmotic diuretics

A

initial volume expansion with subsequent dehydration

83
Q

adverse effects of loop diuretics

A

ototoxicity, hypokalemia, hypocalcemia, hypomagnesemia, alkalosis, hyperglycemia, hyperlipidemia, gout

84
Q

adverse effects of thaizide diuretics

A

hyponatremia/kalemia/magnesemia, hyperglycemia, uremia, hyperlipidemia, sulfa allergy, gout

85
Q

adverse effects of potassium-sparing diuretics

A

hyperkalemic metabolic acidosis, gynecomastia (spironolactone)

86
Q

prototype of potassium-sparing diuretics

A

amiloride, spironolactone

87
Q

adverse effects of ADH antagonists

A

nephrogenic diabetes insipidus

88
Q

most common cause of CKD in US

A

Diabetic nephropathy

89
Q

first treatment of hyperkalemia in CKD

A

calcium gluconate (stabilize cell membrane)

90
Q

2nd treatment of hyperkalemia in CKD

A

push K into cells (insulin/glucose, beta agonist, sodium bicarb)

91
Q

3rd treatment of hyperkalemia in CKD

A

eliminate K from body (lasix, dialysis)

92
Q

what is CKD contraindication to metformin

A

GFR<30

93
Q

meds associated with hyperkalemia

A

NSAIDs, metformin, ACEI/ARB, aldosterone antagonists, beta blockers, dig, potassium-sparing diuretics

94
Q

lab findings in secondary hyperparathyroidism

A

low-normal Ca, low-high Ph, low vit D, high PTH

95
Q

phos binder prototypes

A

sevelamer, calcium carbonate

96
Q

how to treat elevated PTH in secondary hyperparathyroidism

A

calcitriol (1,25 vit D-OH)

97
Q

poorly controlled secondary hyperparathyroidism can lead to

A

osteitis fibrosa

98
Q

overtreatment of Vit D analogs or chronic disease can lead to

A

adynamic bone disease due to low bone turnover (low PTH levels)

99
Q

what does acute rise in creatinine after ACEI use suggest

A

bilateral renal artery stenosis

100
Q

“string of pearls” appearance on renal angiography is suggestive of

A

fibromuscular dysplasia as cause of renal artery stenosis

101
Q

what is responsible for voiding bladder

A

parasympathetics from S2-S3 pelvic nerve

102
Q

what is responsible for storing urine

A

sympathetics: hypogastric T11-L2

103
Q

voluntary control of bladder

A

pudendal nerve

104
Q

inhibitory process to parasympathetics at baseline (to keep people from peeing everywhere all the time)

A

pontine micturition center at baseline

105
Q

failure to store forms of incontinence

A

urge/stress

106
Q

failure to empty forms of incontinence

A

overflow

107
Q

causes of urge incontinence

A

overactive bladder, decreased bladder compliance

108
Q

causes of stress incontinence

A

intrinsic sphincter dysfunction, pelvic floor laxity. Childbirth, age, obesity

109
Q

causes of overflow incontinence

A

bladder won’t contract, protastatic or urethral obstruction

110
Q

symptoms of stress incontinence

A

incontinence with increasing abdominal pressure (sneezing, coughing etc)

111
Q

cause of overactive bladder

A

detrusor muscle contracts when it shouldn’t

112
Q

symptoms of urge incontinence

A

urgency, frequency, nocturia

113
Q

total incontinence cause

A

surgery, neuropathy

114
Q

symptoms of overflow incontinence

A

frequency, nocturia, distended bladder on exam, incomplete empyting

115
Q

medical treatment for urge incontinence

A

muscarininc antagonists (anticholinergics): oxybutynin

116
Q

medical treatment for prostate enlargement

A

alpha antagonists (tamsulosin)

117
Q

4 most common types of kidney stones

A

calcium based, uric acid, struvite, cystine

118
Q

risk factors for calcium based stones

A

low urine volume, abnormal urine pH, high dietary sodium/animal protein consumption

119
Q

types of calcium based stones

A

calcium oxalate and calcium phosphate

120
Q

causes of calcium oxalate stones

A

hypercalciuria: increased absorption from intestine, primary hyperparathyroidism, impaired resoprtion of Ca from tubules

121
Q

treatment of calcium based stones

A

high fluid intake, adequate Ca, limit Na/animal protein intake, thiazides, potassium citrate

122
Q

primary cause of uric acid stones

A

low urinary pH, associated with DM and insulin resistance

123
Q

treatment of uric acid stones

A

increase fluid intake, alkalinize the urine with potassium citrate, allopurinol

124
Q

struvite stones made of

A

ammonium/magnesium/phosphate

125
Q

cause of struvite stones

A

UTI with proteus, klebsiella, staph

126
Q

treatment of struvite stones

A

urease inhibitor

127
Q

cause of cystine stones

A

autosomal recessive defect in proximal tubule

128
Q

treatment of cystine stones

A

decrease sodium intake, alkalinize urine, cystine binder

129
Q

3 most common types of bladder malignancy

A

transitional cell, squamous cell, adenocarcinoma

130
Q

most common type of bladder cancer

A

transitional cell carcinoma

131
Q

risk factors of transitional cell carcinoma

A

smoking, hair dye, cyclophosphamide, industrial solvents

132
Q

treatment of transitional cell carcinoma

A

if nonmuscle invasive: transurethral resection

if muscle invasive: radical cystectomy

133
Q

location of bladder adenocarcinoma

A

dome of bladder or urachus

134
Q

squamous cell carcinoma risk factors

A

chronic inflammatory conditions

135
Q

autoantibodies seen in SLE

A

Anti-double stranded DNA, anti-Smith, ANA

136
Q

post-strep GN is nephrotic or nephritic

A

nephritic

137
Q

what is lupus nephritis

A

glomerulonephritis caused by immune complex deposits

138
Q

causes of acute pyelonephritis

A

ascending bacteria from urethra/bladder (more common) - usually E coli, proteus, klebsiella. OR hematogenous spread from bloodstream (less common)

139
Q

risk factors for acute pyelonephritis

A

reduced urine flow (obstruction, bladder dysfunction, vesico-ureteral reflux)

140
Q

acute pyelonephritis urinalysis

A

neutrophils with white cell casts

141
Q

complications of acute pyelonephritis

A

papillary necrosis, pyelonephrosis, perinephric abscess, sepsis, chronic inflammation with scarring

142
Q

clinical picture of nephrotic syndrome

A

insidious onset, massive proteinuria, hypoalbuminemia, edema, hyperlipidemia

143
Q

clinical picture of nephritic syndrome

A

hematuria, azotemia (increased creatinine and BUN), oliguria, acute onset, HTN

144
Q

clinical picture of membranoproliferative glomerulonephritis

A

young people with a slowly progressive nephritic syndrome that is unresponsive to immunosuppressants

145
Q

secondary MPGN is due to

A

SLE, hep B, hep C

146
Q

ANCA disease clinical picture

A

adult with nephritic syndrome and possible acute renal failure treated with high dose steroids and cyclophosphamide

147
Q

2nd leading bacteria causing UTI in sexually active women

A

staph saprophyticus

148
Q

causes of sterile pyuria that mimics UTI

A

chlamydia, gonorrhea

149
Q

why is urine yellow

A

urobilin

150
Q

specific gravity < 1.01

A

hydration

151
Q

specific gravity >1.03

A

dehydration

152
Q

causes of alkaline urine

A

(with UTI) struvite stone, RTA

153
Q

what type of casts can be normal in UA

A

hyaline

154
Q

what do nitrites in urine indicate

A

UTI with gram-negative bacteria

155
Q

red cell casts indicate

A

glomerular disease

156
Q

white cell casts indicate

A

AIN, chronic pyelo

157
Q

fatty casts indicate

A

nephrotic syndrome

158
Q

renal tubular epithelial casts indicate

A

acute tubular necrosis

159
Q

granular casts indicate

A

chronic renal failure

160
Q

waxy casts indicate

A

chronic renal failure

161
Q

most common cause of intrarenal AKI

A

acute tubular necrosis

162
Q

what is acute tubular necrosis

A

damage to tubules due to ischemia or exposure to nephrotoxins

163
Q

glomerular disease is type of

A

intrarenal AKI

CVPR (5 decks)

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