Renal Flashcards Preview

Random boards stuff > Renal > Flashcards

Flashcards in Renal Deck (250):
1

What are the three effects of Angiotensin II?

1. systemic vasoconstriction
2. constriction of efferent arteriole
3. Increased aldosterone synthesis

2

Concentration of tubular fluid in proximal tubule

isotonic with plasma (300 mosm/L)

3

Concentration of tubular fluid in descending loop of henle

Increasing (water permeable)
400-1200mOsm/L

4

Concentration of tubular fluid in ascending loop of henle

Decreasing (salt permeable)
1200-200mOsm/L

5

Lowest osmolality site in nephron, assuming low ADH

Distal convoluted tubule. Impermeable, so fluid stays hypotonic with increased reabsorption of solutes

6

When does ARPKD present?

At birth. In contrast, dominant form comes years later.

7

Urea acts on which segment of the collecting duct?

medullary segement to increase urea and water reabsorption

8

When does the pronephros degenerate?

4 weeks

9

Mesonephros

Functions as kidney for the first trimester

10

Metanephros appears wheN?

5th week of gestation. It becomes the permanent kidney

11

Ureteric bud comes from

caudal end of mesonephros

12

Ureteric bud gives rise to:

ureter, pelvises, calyces, collecting ducts

13

what interaction needed to form normal kidney

ureteric bud pokes the metanephric tissue
--induces metanephric tissue to format glomerulus to distal tubule

14

most common site of obstruction in fetus

ureteropelvic junction

15

Potter's syndrome

Oligohydramnios-->
limb deformities
facial deformities
pulmonary hypoplasia

16

Causes of Potter's

ARPKD
posterior urethral valves
bilateral renal agenesis

IF YOU CAN"T PEE in utero, you get potters

17

Horseshoe kidney assoc'd with

Turner syndrome

18

Nonfunctional kidney with cysts and connective tissue in utero. What caused this?

abnormal interaction btw ureteric bud and metanephros

19

Describe path of blood into the kidney

renal artery
segmental artery
interlobal artery
arcuate artery
interlobular artery

20

Which kidney do you harvest for donation?

Left kidney=it has a longer renal vein

21

ureters pass over/under the ductus deferens/uterine artery?

under

22

60-40-20 rule

60% weight is TBW
40% ICF
20% ECF

23

measure plasma volume

radiolabeled albumin

24

measure extracellular volume

inulin

25

what gives negative charge in GFR?

heparan sulfate

26

clearance eq:

C=UV/P
U=urine concenctration
V=urine flow rate
P=plasma concentration

27

how to calc GFR

clearance of inulin or creatinine

28

When is creatinine clearance not accurate for GFR?

When GFR is very low. will have higher concentration of creatinine in urine

29

Calculation for effective renal plasma flow (ERPF)

clearance of PAH

PAH=filtered AND secreted into the proximal tubule. all that enters the kidney is excreted

30

RBF=

RPF/(1-Hct)

--ERPF underestimates true RPF by 10%

31

Filtered load=

GFR*plasma concentration

32

NSAIDs

constrict afferent arteriole

33

ACE-I

dilate efferent arteriole

34

prostaglandins

dilate afferent arteriole

35

angiotensin II

constricts efferent arteriole

36

increased plasma protein

decrease GFR
decrease FF

37

constriction of ureter

decrease GFR
decrease FF

38

Hartnup's disease

deficiency of tryptophan(neutral amino acid) transporter in proximal tubule. neutral AA excreted in urine.

results in pellagra

39

blood glucose level when glucosuria starts? max saturation?

160 mg/DL
350mg/DL

40

which part of nephron generates ammonia?

Prox tubule

41

PTH and ATII on prox tubule

PTH: inhibits Na/Phosphate cotransport
ATII: stimulates Na/H exchange=contraction alkalosis. Holding onto sodium at expense of alkalosis

42

What % Na absorbed at each nephron segment?

1. Prox tubule=65-80%
2. L of H=10-20
3. DCT=5-10%
4. 3-5%

43

Thick loop of henle

Na/K/2Cl resorption
--paracellular resorption of Mg2+ and Ca2+
--dilution of urine as it passes

44

What allows paracellular resorption in thick ascending limb?

potassium backleak.

45

DCT transporter

Na/Cl apical cotransporter
--urine becomes hypotonic

46

PTH effect on DCT

Stimulates Ca/Na Xchange on basolateral surface increasing Ca resorption

47

Thiazide mechanism

Blocks Na/Cl apical cotransporter
-->indirectly blocks Na/Ca2+ exchanger

48

Mechanism of amiloride/triamterene

Blocks ENaC channel in principal cell of CT

49

[Tubular Fluid]/[Plasma] ratio

If >1, solute is reabsorbed less quickly than water
If <1, solute reabsorbed more quickly than water

50

very high TF/P

PAH/creatinine/inulin

51

moderate TF/P

urea/Cl

52

TF/P=1

K/Na

53

TF/P <1

phosphorus
bicarb

54

TF/P <<1

amino acids and glucose (virtually completely reabsorbed

55

Tx: hypovolemic hyponatremia

NS

56

tx: hypervolemic hyponatremia

Salt and fluid restriction, furosemide

57

Euvolemic hyponatremia

free water restriction (NOT hypertonic saline--otherwise will fluid overload them)

58

SIADH hyponatremia

do NOT give normal saline! will excrete sodium and retain water. Give convaptan and water restrict

59

when should you give hypertonic saline?

hyponatremia with NEURO deficits or seizures

60

Six effects of angiotensin II

1. Vascular smooth muscle
2. constricts efferent arteriole
3. aldosterone
4. ADH
5. Increased prox tubule Na/H
6. Stimulates hypothalamus

61

ADH regulates

osmolarity (except in extreme low blood volume)

62

Aldo regulates

blood volume

63

How do beta blockers decrease BP?

inhibiting B1 receptors on the JGA

64

How much K is reabsorbed along the nephron?

65% PCT
30% ascending L of H
5-100% at DCT

65

How does ANP work?

Increases Na filtration and GFR at PCT with no compensatory Na resorption distally.
-->Na and H2O loss

66

PTH effect on kidney

Increased Ca resorption (DCT)
Decreased PO4 resorption (PCT)
Increased activation of vitamin D

67

Causee of hyperkalemia

digitalis
hyperosmolarity
insulin deficiency
cell lysis
acidosis
Beta adrenergic antagonist

68

Hyponatremia Sx

nausea, malaise
stupor coma

69

hypernatremia sx

irritability
stupor coma

70

hypokalemia sx

arrhythmias, muscle weakness

71

-U wave on ECG, flattened T waves

hypokalemia

72

hypocalcemia sx

tetany and seizures
--decreases threshold potential

73

Hypomagnesia

tetany and arrhythmias

74

hypermagnesia

cardiac arrest
hypocalcemia
decreased DTRs
bradycardia
hypotension

75

hypophosphatemia

osteomalacia

76

Hyperphosphatemia

renal stones
metastatic calcifications
hypocalcemia

77

How to tell if there is a mixed disorder (acid base)?

pCO2 and HCO3 move in opposite directions
OR
pCO2 predicted is very different

78

predicted pCO2=

(1.5 HCO3 + 8) +/-2

79

Henderson-Hasselbach

pH=6.1+log [HCO3]/(0.03*pCO2)

80

When do you check anion gap

metabolic acidosis present

81

Eq for anion gap

Na-Cl-HCO3
--Over 12 is abnormal

82

Increase anion gap metabolic acidosis

Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron/INH
Lactic acidosis
Ethylene glycol
Salicylic acid

83

Causes of normal anion gap acidosis

Hyperalimentation
Addison's disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion

84

Causes of primary metabolic alkalosis

loop diuretics
vomiting
antacid use
hyperaldosteronism

85

Type 1 RTA

CT cannot excrete H+

86

Type 2 RTA

Cannot resorb bicarb

87

Type 4 RTA

lack of aldosterone effect

88

RTA: pt with urine pH > 5.5 and is hypokalemic

Type 1

89

RTA: Pt has a urine pH < 5.5 and is hypokalemic

Type 2 RTA

90

RTA: hyperkalemic patient with low urine pH and low BP

Type 4 RTA

91

Increased urine pH puts you at risk for

calcium phosphate stones

92

Type 2 RTA associated with

Fanconi's syndrome

93

WBC caste:

tubulointerstitial inflammation
acute pyelonephritis
transplant rejection

94

fatty casts or oval fat bodies

nephrotic syndrome

95

granular muddy brown casts

acute tubular necrosis

96

Waxy casts

advanced renal disease

97

Hyaline casts

normal

98

Nephrotic syndromes

Minimal change disease
Membranous nephropathy
Focal segmental glomerulosclerosis
Amyloidosis
Diabetic glomerulonephropathy

99

Nephritic syndromes

Acute poststreptococcal GN
Rapidly progressive GN
Berger's IgA GN
Alport

100

Combined Nephritic and Nephrotic syndromes

Diffuse proliferative GN
Membranous GN

101

Sx of nephrotic syndrome

proteinuria
hyperlipidemia
fatty casts
edema

102

Why are pts with nephrotic syndrome at risk for thromboembolism and infection?

AT III is lost in urine
Loss of IgG

103

Most common cause of nephrotic syndrome in adults

FSGS

104

LM: segmental sclerosis and hylinosis
EM: effacement of foot proceses

FSGS

105

LM: GBM thickening
EM: spike and dome with subepithelial deposits
IF: granular

membranous

106

causes of FSGS

HIV, kidney disease, heroin, obesity, interferon

107

causes of membranous

SLE< drugs, infection

108

LM: normal
EM: foot process effacement

minimal change

109

Tx of minimal change

corticosteroids

110

cause of minimal change

loss of polyanion in GBM causing ONLY albumin loss

111

LM: congo red stain with apple-green birefirencence

amyloidosis.

assoc'd with multiple myeloma, TB, RA

112

Subendothelial deposits with tram track appearance
IF: granular

type I MPGN

113

LM: Intramembranous dense deposits

MPGN

114

Type I MPGN associated with

HBV, HCV

115

Type II MPGN associated with

C3 nephritic factor

116

nephritic sx:

azotemia
oliguria
hypertension
proteinuria <3.5 g/day

117

LM: lumpy bumpy glomeruli
EM: subepithelial immune complexes
IF: granular C3, IgG, IgM

acute post strep GN. occurs a few weeks after infection

118

LM: crescent shape made of fibrin and C3b proteins

rapidly progressive GN

119

causes of rapidly progressive GN

1. goodpasture's syndrome
2. Wegener's granulomatosis
3. Microscopic polyangiitis

120

LM: wire looping of capillaries
EM: subendothelial IgG with C3
IF: granular

Diffuse proliferative glomerulonephritis

121

LM: mesangial proliferation
EM: mesangial IC deposits
IF: IgA deposits in mesangium

Berger's disease. occurs a few days after infection

122

Split basement membrane with GN, deafness, and eye problems

Alport syndrome

123

What's mutate in alport syndrome?

type IV collagen.

124

alport inheritance

X linked

125

Which kidney stones can you NOT see on an Xray?

Uric acid stones

126

octahedron kidney stones

calcium oxalate

127

which stones precipitate at a high pH?

struvite
calcium phosphate

128

Most common kidney stone presentation

calcium oxalate stone in a pt with hypercalciuria and normalcalcemia

129

Treatment for calcium stones

thiazides and citrate

130

Causes of oxalate stones

ethylene glycol and vitamin C overdose

131

staghorn calculi

struvite stones (ammonium magnesium phosphate)

132

Tx for calcium stones

thiazides and citrate

133

Cause of struvite stones

urease positive bugs:
1. proteus
2. staph
3. klebsiella

134

hexagonal crystals

cysteinuria

135

coffin lid stones

struvite

136

rhombus red brown stones

uric acid

137

renal cell carcinoma histology

clear limid filled cells

138

RCC associated with a gene deletion on

chromosome 3

139

RCC produces

EPO
ACTH
PTHrP

140

PPresentation of RCC

hematuria
flank mass
polycythemia

141

Tx: RCC

Resection. Resistant to conventional chemo and radiation

142

WWilm's tumor (nephroblastoma) histology

embryonic glomerular structures. Child 2-4 has flank mass and hematuria

143

Wilm's tumor deltion

WT1 tumor suppressor on chromosome 11

144

WAGR complex

wilm's
aniridia
genitourinary malformation
mental retardation

145

biopsy of kidney: papillary growth lined by transitional epithelium with mild nuclear atypia

transitional cell carcinoma

146

Transitional cell carcinoma associated with

PeeSAC
phenacetin
Smoking
aniline dyes
cyclophosphamide

147

ppainless hematuria suggests

bladderr canceer

148

Where can transitional cell carcinoma occur?

calyces, pelvis, ureters, bladder

149

acute pyelonephritis affects which part of kidneys?

Cortex. glomeruli and vessels are spared

150

Cause of chronic pyelonephritis

vesicoureteral reflux or chronic kidney stones. Normal person shouldn't get recurrent UTIs-->chronic pyelonephritis

151

WWhich parts affected in chronic pyelonephritis?

Corticomedullary scarring with blunted calyces. Tubules have eosinophilic casts

152

HIstology of chronic pyelonephritis

Lymphocytic invasion with fibrosis

153

presentation of drug induced interstitial nephritis

eosinophilic pyuria
azotemia

154

How long after drug will drug TIN happenn?

After 1-2 weeks..

Can be months with NSAIDs

155

Which drugs cause TIN (allergic reaction to drug)

penicillin
diuretics
sulfonamides
rifampin

156

Diffuse cortical necrosis caused by

Vasospasm and DIC. Associated with obstetric catastrophes and septic shock

157

maintenance phase of acute tubular necrosis

oliguric for 1-3 weeks. Risk of hyperkalemia

158

Recovery phase of acute tubular necrosis

polyuric. Risk of hypokalemiia

159

Causes of toxic ATN

Aminoglycosides
heavy metals
myglobinuria
ethylene glycol-->oxalate crystals
radiocontrast dye
urate

160

Renal papillary necrosis caused by

diabetes
acute pyelonephritis
chronic phenacetin (acetaminophen)
sickle cell

161

Difference in handling of BUN vs creatinine

BUN is reabsorbed
Creatinine is NOT reabsorbed

162

Acute renal failure: prerenal azotemia

BUN: Cr is increased >20
-urea retained by kidney to conserve volume

163

Intrinnsic renal failure

BUN: Cr ratio decreased <15
-caused by ATN/ischemia/toxins/crescentic GN
-granular casts
-Tubules filled with debris
-decreased BUN reabsorption

164

PPostrenal azotemia

BUN: Cr >15
-Caused by outflow obstruction (bilateral)

165

Urine osm: >500
Urine Na < 1%

prerenal

166

Urine osm: 40
FeNa >2%

Intrinsic or post-renal. Differentiate these by looking at the BUN: Cr ratio

167

Consequences of renal failure

Fluid/sodium retention (CHF)
hyperkalemia
metabolic acidosis
anemia
increased triglycerides

168

Side effect of increased BUN and Cr

Nausea
asterixis
pericarditis
encephalopathy
platelet dysfunction

169

Renal osteodystrophy

Failure of vitamin D hydroxylation
hypocalcemia
hyperphosphatemiia
-->2ndary hyper PTH

170

WWHy does hyperphosphatemia worsen renal osteodystrophy?

Tissue calcifications occur within tissues-->calcium phosphate instead of being excreted

171

Why do pts with ADPKD get hypertension?

Increased renin production

172

ADPKD associated with

berry aneurysms
mitral valve prolapse
benign hepatic cysts

173

AARPKD

presents in infant, often as potter's syndrome

174

AARPKD associated with

congenital hepatic fibrosis. After birth, will have HTN, portal HTN, progressive renal insufficiency

175

Medullary cystic disease

tubulointerstitial fibrosis and renal insufficiency-->cannot concentrate urine.

Inherited with shrunken kidneys seen on ultrasound

176

where does mannitol affect the nephron?

The thin descending limb

177

where does acetazolamide work its effect?

Proximal tubule

178

mmannitol indications

Drug overdose
elevated ICP

179

Mannitol toxicity

pulmonary edema

180

when is mannitol contraindicated

CHF and anuria

181

iindications acetazolamide

urinary alkalization
altitude sickness
glaucoma
metabolic alkalosis

182

acetazolamide toxicity

metabolic acidosis
NH3 tox
sulfa allergy

183

calcium wasting diuretic

loop diuretics

184

furosemide indications

CHF, cirrhosis, nephrotic syndrome, pulmonary edema (too much fluid)

hypertension, hypercalcemia

185

Toxicity of loops

ototoxicity
hypokalemia
dehydration
allergy (sulfa)
nephritis
Gout

186

Ethacrynic acid

Non sulfonamide loop diuretic. Virtually the same, can also cause gout

187

indications for hCTZ

HTN CHF
hypercalciuria
nephrogenic diabetes insipidus

188

Name the K sparing diuretics

Spironolactone
Triamterene
Amiloride

189

Mehcanism: spironolactone and eplerenone

Competitive aldosterone antagonists.

190

mmechanism triamterene and amiloride

Block ENaC at cortical collecting duct

191

IIndications for spironolactone

hyperaldosteronism
K depletion
CHF

192

side effects of spironolactone

Hyperkalemia
Antiandrogenic effects--man boobs

193

WWhich diuretics cause acidemia?

carbonic anhydrase inhibitors--decrease HCO3 reabsorption

aldosterone--blocks K/H secretion. Also, hyperkalemia increases H leak from cells

194

Which diuretics cause alkalemia?

loop and thiazide diuretics
--Contractiion alkalosis
--hypokalemia worsens alkalosis

195

Urine calcium increases with

loops

196

Why are ARBs better than ACE-Is?

they don't increase bradykinin
-->no cough or angioedema. ACE is still able to break down bradykinin

197

What do ACEI do to GFR?

Decrease GFR, b/c efferent arterioles are opened

198

Why is ACE good for CHF?

prevents remodeling

199

ACE-I toxicity

Cough
angioedema
Teratogen
decrease GFR
Hyperkalemia
hypotension

200

When are ACE inhibitors contraindicated?

bilateral renal artery stenosis

201

dysplastic kidney--how is it inherited?

Not inherited. COngenital malformation of renal parenchyma characterized by cysts and abnormal tissue, especially CARTILAGE. NOT BILATERAL LIKE ADPKD

202

baby with portal htn

ARPKD

203

berry aneurysm

ADPKD. cysts in the liver, kidney, and brain.

204

mitral valve prolapse

ADPKD association

205

how is medullary cystic kidney disease inherited?

autosomal dominant with SHRUNKEN kidneys

206

IF Fena is <1% this tells you

tubular function is intact=can resorb sodium. this happens in prerenal ATN

207

why is BUN:cr <15 in intrarenal renal failure

epithelial cells are not working, cannot resorb BUN, so it is excreted through the kidneys

208

Why is BUN:Cr>20 in pre-renal failure?

Kidneys reabsorb as much fluid as possible and BUN follows

209

Why is BUN:Cr>15 in post-renal failure?

High pressure in ureters "pushes" BUN and fluid back into the body from tubular fluid

210

If pre-renal failure doesn't resolve...

becomes ischemic acute tubular necrosis. Prox tubule and medullary thick ascending limb are susceptible

211

What are consequences of ATN?

hyperkalemia with metabolic acidosis. Can't excrete potassium or organic anions (lactic acid)

212

hyperlipidemia seen in

nephrotic syndrome

213

minimal change associated with

hodgkin's lymphoma

214

most common cause of nephrotic syndrome in hispanics and A-As

FSGS

215

FSGS associated with

HIV
heroin
SCD

216

Minimal change and FSGS immunofluorexcence

None. Also poor response to tx/steroids. will progress to renal failure

217

Pt with lupus gets nephrotic syndrome

membranous nephropathy

218

Membranous nephropathy also associated with

Hep B/C

219

nephritic syndrome in lupus pt

DIffuse proliferative GN

220

granular immunofluorescence

immune complex deposition
-membranous
-membranoproliferative

221

type I membranoproliferative

subendothelial
HBV/HCV
more likely to have tram track

222

what determines if GAS can cause nephritic syndrome?

presence of M proteins

223

In adults with post-strep GN

more likely to present to crescent rapidly progressive GN

224

lupus patient with rapidly progressive glomerulonephritis

diffuse proliferative GN

225

Negative IF rapidly progressive nephritis

wegener, churg-strauss,

226

pt with rapidly progressive GN, hemoptysis, hematuria, and sinus infections

Perform cANCA--could be wegeners not goodpasteur's (classic)

227

most common cause of nephritis world wide

Berger's igA. Usually after mucosal infection, episodic.

228

churg strauss features not present in microscopic polyangiitis

Asthma
granulomatous inflammation
eosinophilia

229

tests for UTI

leukocyte esterase and nitrites
>10 WBC/hpf
culture: >100K CFU

230

sterile pyuria

chlamydia and n. gonorrhea

231

Most common pathogens for pyelonephritis

E. Coli
Klebsiella
Enterococcus

232

"thyroidization" of kidney

Chronic pyelonephritis

233

problem with staghorn calculi

can serve as a nidus for additional UTIs

234

what produces EPO

renal peritubular interstitial cells

235

why are crohn's pts more likely to make calcium oxalate stones?

Not able to absorb calcium necessary to bind oxalate

236

shrunken kidneys with cysts

Dialysis patients. Pts at increased risk for RCC

237

Triad of RCC

hematuria
palapable mass
flank pain

238

Cause of RCC

loss of VHL
-increased IGF-1
-Increased HIF=VEGF PDGF

239

wilms tumor cell

blastema

240

beckwith-Wiedemann

wilms tumor
neonatal hypoglycemia
muscular hemihypertrophy
organomegaly (tongue)

241

Serum lab levels of calcium, phoshorus, and PTH in chronic kidney disease

1. Phosphate retention
2. Low calcium from low vitamin D
3. Increased PTH

242

loop diuretics act on

thick ascending loop of henle. Decrease medullary concentration gradient

243

osmotic diuretics act on

thin descending loop

244

when do you see states of hypercalcemia and hypercalciuria?

Hyper PTH and sarcoidosis

245

Situations with hyperoxaluria

excesive intake
low calcium diets (less calcium in gut to bind oxalate for excretion)

246

VHL deletion

chromosome 3P

247

Upper part of ureter is supplied by

The renal artery

248

Explain what happens with hypoaldosteronism to Na, K, HCO3 and Cl

Low Na
High K
acidosis=Low bicarb (H+ATP pump)
High chloride to balance out HCO3-

249

Thiazide tox

Hyperuricemia
Hypercalcemia
Hyperglycemia
Hyperlipidemia

Hypokalemia and hypotension

250

how to treat post GN glomerulonephritis

loop diuretics and vasodilators.
--Kids recover well. Adults do not