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A_First Aid Random Memorizing > renal > Flashcards

renal Flashcards

1
Q

parts of developing kidny

A

pronephors, degen at 4 weeksmesonephros (interim kdiney)

metanephros (permanent)

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2
Q

when does metanephros appear

A

5th week

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3
Q

how does glomerulus through to DCT form

A

utereric bud interacts with metanephric mesenchyme which induces differentaiton

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4
Q

last part of uro system to canalize

A

ureteropelvic junction MOST COMMON SITE OBSTRUCTION

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5
Q

potter sequence etiology

A

anything that causes OLIGOhydramnios

ARPKD, obstructive uropathy (posterior urethral valves), bilateral renal agensis

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6
Q

cause of death in potter sequence

A

pulmonary hypoplasia

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7
Q

symptoms of potter sequence

A 
all compression related
POTTER
Pulmonary hypoplasia
oligohydramnios
twisted face
twisted skin
extremity deformities
renal failure in urtero
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8
Q

etiology horsehoe kidney

A

abnormal fusion of inferior poles of both kidneys

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9
Q

what does the horshoe kidney get stuck under as it ascends from pelvis during dvlpmt

A

IMA

thats why they remain low in abdomen

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10
Q

complications of horshoe kidney

A

kidney function NORMAL but

can develop hyronephrosis (uteropelvic junction), renal stones, infection,

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11
Q

unilateral renal ageneiss vs multicystic dysplastic kidney

A

unilateral - complete absence of kidney and ureter
multicystic - nonfunctional kidney is just a bunch of cysts and connective tissue

BOTH INVOLVE FAILURE OF URETERIC BUD TO INDUCE DIFFERENTIATION WITH METANEPHRIC MESENCHYME

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12
Q

y shaped bifid ureter

A

duplex collecting system

assocaitd with vesicoureteral reflux or ureteral obsrution

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13
Q

MCC cause of bladder outlet obstruction in male infants

A

posterior urethral valvues

presents with hydronephrosis

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14
Q

ureters travel under what structures

A

female - uterine artery
male - vas deferens

water under bridge

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15
Q

renal blood flow from renal artery to venous outflow

A 
renal artery
segmental artery
interlobar artery
arcuate artery
interlobular artery
afferent arteriole
glomerulus
efferent arteriole
vasa recta/peritubular capillaries
venous outflow
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16
Q

GFR barrier composed of….

A

fenestrated capillary endothelium
basement membrane with type IV collagen
epithelial layer of PODOCYTES

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17
Q

which is a better filter fenestrated capillary epithelium or podycyte foot processes

A

podocyte foot processes forms slit diaphragm chich presvents 50-60 nm molecules
fenestrated capillary prevenst greater than 100

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18
Q

charge of GFR barier

A

negatively charge glycoproteins (prevent postiive charged molecule entry)

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19
Q

where does AT II target on nephron

A

PCT - stimulates Na/H exchange (inrease Na reabsorption, h20, and hc03 reabs) permitting contraction alkalosis

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20
Q

how does angiotensin II affect RBF

A

constricts efferent arteriole

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21
Q

ANP stimulated by what

A

increases in atrial pressure…will increasee GFR and NA filtration with no reabsorption…Na loss and water loss (brake on RAAAS system)`

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22
Q

how is EPO released

A

releasd by intertitial cells in peritubular cap bed in response to hypoxia

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23
Q

formula correlating RBF and RPF

A

RBF = RPF/1-Hct

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24
Q

every time GFR halves serum creatinine will

A

double (creatinine not a sensitive indicator of kidney function when GFR is normal)

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25
Q

which part of nephron is impermeabl to water despite adh

A

thick ascending loop

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26
Q

winters formula

A

predicted Pco2 =( hco3x1.5) + 8 +/-2

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27
Q

what part of nephron is Mg and Ca reabsorbed

A

Thick ascending loop

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28
Q

distal RTA type 1

A

distal tubule cannot acidify urine (urine ph high) assocaited with hypokalemia
low bicarb

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29
Q

assocaited symptoms of distal RTA type 1

A

alkalinized urine increases risk for calcium phosphae kidney stones

an rickets

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30
Q

how to calculate URINE anion gap

A

Na + K - Cl

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31
Q

what is the Cl in urine anion gap a good approx for?

A

Nh4 (Nh4 leaves with Cl)

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32
Q

Urine anion gap in setting of GI acidosis like diarrhea

A

UAG becomes negative (more chlorine leaving and NH4)

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33
Q

Urine anion gap in setting of distal RTA?

A

since urine can’t be acidified, it does not become negative despite acidosis

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34
Q

when given ammonia “challenge” (acid load of NH4Cl) what will RTA urine ph be

A

would still be greater than 5.3

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35
Q

negative UAG in acidosis vs psoitive UAG in acidosis

A

negative UAG = GI acidosis

postivie UAG - RTA

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36
Q

autoimmune disease (srogens or RA) presents with bilateral recurrent kidney stones, with high urine pH, hypokalemia, positive UAG

A

distal RTA

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37
Q

urine pH high or low ins type II proximal RTA

A

low as it should be

since DCT can still excrete H+

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38
Q

loss of HCO3 resportion in PCT

A

proximal rta type II

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39
Q

why is proximal rta type II assocaited with hypokalemia

A

low bi carb, low volume, increase in aldosterone, HYPOKALEMIA

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40
Q

assocaited with fanconi syndrome

A

type II proximal RTA

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41
Q

hypophosphatemic rickets BUT NO KIDNEY STONES

A

type II proximal RTA

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42
Q

only RTA with hyperkalemia

A

type 4 RTA

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43
Q

dysfuction of aldosterone channels

A

type 4 rta (distal)

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44
Q

dysfunction of distal H/K exchanger

A

type 1 RTA distal

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45
Q

dysfunction of proximal bicarb channels HCO3

A

type 2 rta

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46
Q

noninherited cysts in kidnys

A

dysplastic kidney

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47
Q

inherited defect, BILATERAL enlarged kidneys with cysts in renal cortex AND medulla

A

Polycystic kidney disease

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48
Q

infant PKD

A

autosomall recessive

renal failure HTN

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49
Q

ARPKD assocaited with what complications

A

cysts in kidney- so bad you can get oligohydram-> potter

cysts in LIVER also -> PORTAL HTN -> hepatic fibrosis

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50
Q

ADPKD presents what age

A

young adults

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51
Q

mutation ADPKD

A

APKD1 APKD2, cysts develop GRADUALLY over time

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52
Q

why do ADPKD present wiht HTN

A

can have dysfunctional release of renin

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53
Q

CNS complication of ADPKD

A

berry aneurysm

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54
Q

cardiac complication ADPKD

A

MVP

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55
Q

inherited defect ONLY IN MEDULLARY COLLECTING DUCTS

A

medullary cystic kidney disase (kidneys are SHRUNKEN)

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56
Q

shrunken kidneys

A

medullary cystic kidney disease

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57
Q

prerenal Bun:cr ratio and FeNa, urine osm

A

BunCr>15
FeNa < 1 (tubules still able to resorb Na)
urine osm > 500 (high)

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58
Q

key finding ATN

A

granular “muddy brown “ casts in urine

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59
Q

Bun cr, FeNa, Urin osm in intrinsic renal

A

Buncr low
Fe na High
urine osm low

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60
Q

part of nephron most suseptible to injury during renal failure

A

PCT and thick ascending limb

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61
Q

agents that can cause nephrotoxic injury

A 
aminoglycosies
heavy meatlas
myoglobinuria (crush injiry)
urate (TLS)
radiocontrast!
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62
Q

how does ATN afect acidase status and potassium status

A

metabolic acidosis

hyperkalemia

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63
Q

how long can oliguria persist in ATN

A

2-3 weeks before recovery (tuublar cells are stable cells)

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64
Q

drug induced hypersensivitiy reaction of intersitium

A

acute interstitial nephritis

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65
Q

oligura, fever, RASH, hematuria with Eosinophils

A

aute interstitial neph

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66
Q

key finding in urine in AIN

A

eosinophils

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67
Q

drugs tha can induce AIN

A 
P's
Pee (diuretics)
Pain free (NSAIDS)
Penicillins
PPi
rifamPin
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68
Q

long term aspirin use or phenacitin can cause

A

acute papillary necrosis

69
Q

etiologie renal papillary necrosis

A 
SAAD papa with papillary necrosis
Sickle cell
acute pyelo
analgesics (NSAIDS)
DM
70
Q

what is lost in nephrotic syndrome

A

albumin (3.5 day)
gammaglobulin (incrased infxn
anti thrombin III (hypercoag)

also associated with hyperlipidiema and hypercholesterol

71
Q

minimal change assocaited with what cancer

A

hodgkin lymphoma

72
Q

key findings in minimal change

A

NORMAL GLOMERULI on Hand E stain
but EFFACEMENT OF FOOT PROCESSES on electron microscopy
NOTHING IMMUNOSTAINS

73
Q

how does hodgkin lymphoma cause amage to kidney

A

overproduction of CYTOKINEs can efface foot processes

74
Q

nephrotic syndrome with HIV!?!?!

75
Q

nephrotic syndrom ein heroin user

76
Q

nephrotic syndorme in sickle cell

77
Q

key findings in FSGS

A

look for local sclerosis of SEGMENTS

effacement of foot processesalso

78
Q

nephrotic syndomr with Hep B/C

A

membranous nephropathy

79
Q

nephrotic syndrome in SLE patient

A

membranous nephropathy

80
Q

two hep B renal complications

A 
membranoproliferative glomerulonephritis (nephritic)
membranous nephropathy (nephrotic)
81
Q

THICKening of membrane on Hand E

A

membranous nephropathy

82
Q

any time you see “membran” in front of glomerulo it usually due to

A

imune complex deposition

so positiev immnofluresent

83
Q

granular IF

A

membranous nephropathy

84
Q

spike and dome appearance on EM

A

membranous nephropathy

85
Q

“tram track” appearance

A

membranoproliferative glomerulonephritis (due to (proliferation of membranes splits )

86
Q

two types of membranoproliferative

A
  1. subendothelial (HBV/HCV)

2. basement membrane

87
Q

c3 nephritic factor

A

type 2 membranoproliferative

88
Q

function of C3 nephritic factor

A

IgG antibody that stabilizes c3 convertase which will elad to persistent coplement acivaiotn and lowered C3 levels

89
Q

first chagneseen inkdiney in DM

A

high blood glucose caues nonenzymatic gycosylation of vascular basement ;membrane (vessels more permeable and laeky) resulting in hyaline arteriosclerosis which will increse GFR (backup)causing thickening of mesangial cells

90
Q

key finding in DM glomerfulonephropatyh

A 
esoinophilic nodular glomerulsclerosis
MESANGIA EXPAINSION (krimmelsteil wilson lesions
91
Q

apple green biferingence in congo stain

A

systemic amyloidosis

92
Q

where does systemic amyloidosis affectkidney

93
Q

nephritic syndrme presents with what

A

RBC casts
htn and salt retntion
perioberital edema
limited proteinuria

HALL MARK IS GLOMERULAR BLEEDING

94
Q

what bateria can ca;use nephritic snydorme

A

GABHS (acute post streptococcal glomerulnephritis)

95
Q

virulence factor of GABHS causing nephritic

96
Q

subepithelial hump on EM, immune complx deposition

A

acute post strep glomerulnephritis

97
Q

nephritic syndorme that progresses to RENAL FAILURE in weeks to month

A

rapidly progressing glomeruloneph (crescentic)

98
Q

biopsy in rapidly progressive glomer

A

creseceent in bowman Space Hand E

99
Q

what makes up “crescent” in crescentic glomerfulnephritis

A

FIBRIN AND MACROPHAGES

100
Q 
crescentic glom
LINEAR immunofluoresence (antiboddy to basement membraen)
A

goodpasture syndrome (hematuria and hemoptysis)

101
Q

granular IF pattern

A

immuncomplex deposition

PSGN or diffuse proliferative glom

102
Q

MCC disease that damages kidney in SLE

A

diffuse proliferative glomerulonephritis

103
Q

negative IF neph *pauci immune)

A

check ANCA

104
Q

patient comes in with hemoptysis, hx of sinus infections hematuria,

A

Wegner’s gran

c-ANCA

105
Q

how to differentiate goodpastureu and wegner’s

A

wegners - negative IF, nasopharynx involvement

goodpasture - positive IF (linear IF)

106
Q

microscopic polyangitis vs. churgstrauss

A

BOTH have p-anca

but only churg strauss has granulomas, asthma, and eosinophils

107
Q

where does IgA nephropathy deposoit

108
Q

EPISODIC HEMATURIA, rbc casts, following mucosal infection i childhood

A

IgA nephropathy (granular IF) due to immune complexes

109
Q

isoalted hematuria, sensory hearing loss, ocular disturbances

A

alport syndrome (in a faimily)

110
Q

dysuria, urinary frequency, urgency, suprapubic pain…NO FEVER OR MALAISE

111
Q

UTI with alkaline urine and ammonia scent

112
Q

pyuria with urine culture

A

urethritis

chlamydia, neisseria

113
Q

wbc casts

114
Q

structural abnoramlity which increses risk UTI

A

vesiculourethral reflux

115
Q

cortial scarring blunted calyces (thyroidization) thyroid follicles (eosinophilic protenacious material)

A

chronic pyelo

116
Q

IBD assocaited with which kidney stone

A

calcium oxalate (decreased absorption of oxlate)

117
Q

how to treat calcium oxalate stones

A

ca sparin gdiuretic

thiazide

118
Q

staghorn calculi renal calyces ADULT

A

ammonium mag phosphate (struvite) coffin) kebseilla or pretus

119
Q

which stones aren’t seen on xray

120
Q

which stones precipitate in low pH acidic urine

A

uric acid stones (esp in DCT)

121
Q

staghorn calculi in child

A

cytinuria (treat by alkalinzing urine)

122
Q

only stone asasociatd with ialkaine urine

A

ammonioum magneuim phosphate stone

123
Q

cardiac complication uremia

A

periccarditis

124
Q

where is EPO produced

A

renal peritubular interstitial cells

125
Q

ESRD chagnes calcium an dphosphate how

A

hypocalcemia
hyperphosphatemia’
failure of vitD hydroxylation

126
Q

renal osteodystrophy pathogenesis

A

bad kidney = hypocalcemia = increased PTH = increasd bone turnover

127
Q

acid base ESRD

A

metabolic acidosis with uremia

128
Q

Esrd kidneys will get bigger or shrink

A

shrink (increased risk of RCC)

129
Q

angiomyolioma assocaited with what

A

tuberous sclerosis

130
Q

hematuria PALPABLE MASS and flank pain

131
Q

paraneoplastic syndromes associated with RCC

A

EPO - secondary polycythemia
renin- HTN
ACTH - cushings
PTHrp - hypercalcemia

132
Q

testicular complciation RCC

A

left sided varicocele

133
Q

MCC histologic presentaiotn RCC

A 
clear cytoplasm (clear cell carcinoma)
polyganla clear cells
134
Q

RCC tumors color and filled with what

A

yellow illed with lipids

135
Q

risk factor sporadic RCC

136
Q

hereditary syndrome RCC

A

VHL on chromosome 3p (AD) inactivation of VHL gene (deletion)

137
Q

VHL increased risk of what cancers

A

RCC and HEMANGIOBLASTOMA

138
Q

RCC likes to spread where

A

invades IVC to invade lung and bone

retroperitoneal lymph nodes

139
Q

kidney mass child

A

wilm’s tumor (nephroblastoma)

140
Q

child large unilateral flank mass and HTN

A

wilms tumor

141
Q

wilms tumor mutation

A

loss of function of tumor suppressor WT1 WT2 onchormosome 11

142
Q

wilms tumor syndrome

A 
WAGR
wilms tumor
aninirida (absence of risi)
genitourinary malformations
Retardation (mental (WT1)
143
Q

wilms tumor assocaited with what other genetic syndrome

A

beckwith wiedemann

144
Q

wilms tumor, macroglossia, organomegaly…HALF OF MUSCLES ON ONE SIDE OF BODY BIGGER THAN OTHER (HEMIHYPERPLASIA)

A

beckwith wiedemann (WT2 loss of function tumor suppressor)

145
Q

MCC lower urinary tract

A

transitional cell (urothelial)

146
Q

number oen risk factor TCC

A

SMOKING
also increased with dye use, pehnacitin
cyclophosphamide

147
Q

painless hematuria

A

transitional cell carcinoma

148
Q

risk factors of SCC bladder

A

chronic INFLAMATION

schistosoma hemaboium

149
Q

middle eastern male presents with painless hematuria

A

squamous cell carcinoma of bladder from schistosoma haebotulum

150
Q

which diuretic causes acidosis

A

acetazoalmide (carbonic anhydrase inhibitor) (cannot secrete bicarb) similar to type 2 proximal RTA

151
Q

what part of loop does furosemide, bumetanide, torsemide worke

A

thick ASCENDING limb

152
Q

which transporter do loop diuretics inhibit

A

Na K 2 cl cotrasnport

cannot concentrate urine

153
Q

which diuretics increase excretion of calcium

A

loop diuretics

154
Q

adverse affects of loop diuretics

A 
OHH DAANG
oto toxicicity
hypokalemia
hypomag
dehdyration
allergy *sulfa)
alkalosis
gout
155
Q

where to thiazide diuretics target

A

DCT inhibit Na Cl reabsorption (decreaseing Ca exrcretion ) Ca sparin diuretic

156
Q

diuretics which increase urinary Ca and decrese urinary Ca

A

increase urinary Ca - loop

decrease - thiazide

157
Q

adverse effects thiazides

A 
hyperGLUC
hypergly
hyperlipid
hyperuriciema
hypercalc
158
Q

diuretics to treat hypraldosterone

A

spironlactone, eplerenon, trimaterine, amiloride

159
Q

target K sparing diurecics

A

cortical collectin tubule (aldosterone antoagnoists)

160
Q

which diuretics make you acidotic and alkalotic

A 
acidotic - ccetoazoamide (cabonic anyhdrase)
potassioum sparking (spirono, amilordie, triamteren, eplenrone)
alkaloti c- loop and thiazide diretics
161
Q

teratogenic effect ace inhibitor

A

fetal malofmraiotn

162
Q

ace inhibitors do what to GFR

A

constrict efferent ateroiel ACE decreasing egf

increases renin

163
Q

adverse renal side effect acylovir

A

crystla nephropathy GIVE WITH AGGRESSIVE IV HYDRATION

164
Q

which di;uretic assocaited with gyneco mastia (antiandorgen effect

A

sprionolactone

165
Q

causes metalk

A

vomiting/nasogastric suctioning
thiazie loop diuretics
mineralcorticoid excess (primary hyperaldosteron) saline UNRESPONSIVE (HTN and high urine Cl

166
Q

what to values to evaluate metalk

A

urinary Cl and volume status

167
Q

why do distal RTA increase risk for ca stones

A

decerased CITRATE

168
Q

how is digoxin cleared

A_First Aid Random Memorizing (17 decks)

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