cram.firstaid.renal Flashcards

1
Q

ureters pass under ___ or ___

A

uterine a.

vas deferens

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2
Q

___ of total bodyweight is water

A

60%

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3
Q

2 compartments of total body water

A

ICF

ECF

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4
Q

ICF is ___ of total body water

A

3-Feb

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5
Q

2 parts of ECF

A

interstitial fluid

plasma

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6
Q

interstitial fluid is ___ of ECF

A

4-Mar

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7
Q

plasma volume is measured via ___ (2)

A

radiolabeled albumin

evans blue

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8
Q

ECF is measured via ___ (2)

A

inulin

mannitol

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9
Q

negative charge of glomerular BM is from ___

this is lost in ___

A

heparan sulfate

nephrotic syndrome

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10
Q

formula for clearance of substance X

A
C_x = U_xV/P_x
where C_x = clearance of x, 
U_x = urinary concentration of x, 
V = urine flow rate,
P_x = plasma concentration of x
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11
Q

if C_x < GFR, then ___

A

x is reabsorbed

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12
Q

if C_x > GFR, then ___

A

x is secreted

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13
Q

because ____, ____ (2) can estimate GFR

A

they are neither reabsorbed nor secreted
inulin clearance
creatinine clearance (slightly secreted though)

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14
Q

starling forces equation for GFR

A

GFR = K_f[(P_GC - P_BS) - (Pi_GC - Pi_BS)]

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15
Q

renal plasma flow may be estimated by ___

this is because ___

A

CL_PAH

it is primarily secreted and only slightly filtered

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16
Q

RPF in terms of RBF

A

RPF = RBF(1-HCT)

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17
Q

estimated RPF (from PAH) over/underestimates RPF

A

underestimates

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18
Q

definition of filtration fraction (FF)

normal value of FF

A

FF = GFR/RPF

20%

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19
Q

Ang II works on ___ arteriole
effect is ___
effect is blocked by ___

A

efferent
constriction
ACEI or ARB

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20
Q

PGs work on ___ arteriole
effect is ___
effect is blocked by ___

A

afferent
dilation
NSAIDs

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21
Q

afferent arteriole constriction does
___ to RPF
___ to GFR
___ to FF

A

lowers
lowers
no change

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22
Q

efferent arteriole constriction does
___ to RPF
___ to GFR
___ to FF

A

lowers
raises
raises

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23
Q

plasma protein concentration increase does
___ to RPF
___ to GFR
___ to FF

A

no change
lowers
lowers

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24
Q

ureter constriction does
___ to RPF
___ to GFR
___ to FF

A

no change
lowers
lowers

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25
Q

definition of free water clearance

A

C_H2O = V - C_osm
where V = urine flow rate,
C_osm = clearance of osmoles = U_osmV/P_osm
i.e. C_H2O = V(1 - U_osm/P_osm)

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26
Q

when ADH is present, C_H2O is ___

otherwise, it’s ___

A

0

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27
Q

quantity of x excreted in terms of GFR (filtered load)

A

filtered load = (GFR)(P_x)

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28
Q

2 related measures of urinary transit of substance x

A

filtered load

excretion rate

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29
Q

filtered load is product of ___ (2)

A

GFR

P_x

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30
Q

excretion rate is product of ___ (2)

A

V

U_x

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31
Q

(excretion rate)_x = (filtered load)_x if ___

A

x is neither reabsorbed nor filtered

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32
Q

glucosuria occurs at plasma glucose levels above ___ mg%

A

160

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33
Q

___ happens above plasma glucose of 350mg%

A

saturation of Glc transporters

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34
Q

2 disease resulting from deficient PT AA transporters

A

Hartnup

cystinuria

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35
Q

descending limb of LOH is ___ for water

ascending limb is ___

A

permeable (water efflux from urine)

impermeable (electrolyte efflux)

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36
Q

5 substances with secretion > reabsorption

on plot of [TF]/[P] vs. distance along PT, this is represented as ___

A
PAH
inulin
creatinine
urea
Cl-
slope > 1
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37
Q

4 substances with reabsorption > secretion

A

Glc
AAs
HCO3-
P_i

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38
Q

2 parts of juxtaglomerular apparatus

A

JG cells

macula densa

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39
Q

JG cells are ___ cells in ___

A

smooth muscle

afferent arteriole

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40
Q

macula densa cells are ___ cells in ___

A

epithelial

early DCT

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41
Q

renin is secreted by ___

in response to ___ (3)

A

JG cells
hypoTN
reduced Na+ at macula densa
NE (beta_1 R)

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42
Q

renin acts via ___

A

converting angiotensinogen -> Ang I

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43
Q

EPO is made by ___ cells of ___

A

endothelial

peritubular capillaries

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44
Q

2nd hydroxylation of D3 is done by ___ cells
enzyme is ___
it is induced by ___

A

proximal tubule
1alpha hydroxylase
PTH

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45
Q

3 physiologic states which cause K+ shift OUT of cell

A

acidosis
severe exercise
hyperosmolarity

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46
Q

2 drugs which cause K+ shift OUT of cell

mechanism of both is ___

A

beta blocker
digoxin
Na+/K+ ATPase inhibition

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47
Q

acidosis causes hyperkalemia because ___

A

H+/K+ exchanger swaps extracellular H+ for intracellular K+

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48
Q

2 drugs which cause K+ shift INTO cell

mechanism is ___

A

insulin
beta agonists
Na+/K+ ATPase activation

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49
Q

2 kinds of acidosis

A

respiratory

metabolic

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50
Q

2 defining lab values for respiratory acidosis

A

pH40 mmHg

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51
Q

2 defining lab values for metabolic acidosis

A

pH<40 mmHg

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52
Q

2 kinds of metabolic acidosis

A

anion gap high

anion gap normal

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53
Q

anion gap definition

A

AG = Na+ - (Cl- + HCO3-)

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54
Q

anion gap is comprised of ___ (4)

A

anionic protein
P_i
citrate
sulfate

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55
Q

elevated anion gap metabolic acidisis means ___ (2)

A

HCO3- was lost

the unmeasured anions have increased to take its place

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56
Q

non-elevated anion gap metabolic acidosis means ___ (2)

A

HCO3- was lost

Cl- has increased to take its place

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57
Q

4 causes of non-anion gap metabolic acidosis

A

diarrhea
glue sniffing
RTA
hyperchloremia

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58
Q

normal anion gap

A

8-12 mEq/L

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59
Q

2 kinds of alkalosis

A

metabolic

respiratory

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60
Q

2 lab values for metabolic alkalosis

A

pH>7.4

PCO2>40 mmHg

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61
Q

2 required lab values for respiratory alkalosis

A

pH>7.4

PCO2<40 mmHg

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62
Q

4 causes of metabolic alkalosis

A

diuretics
vomiting
antacids
hyperaldosteronism

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63
Q

2 causes of respiratory alkalosis

A
hyperventilation
aspirin intoxication (early)
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64
Q

3 types of RTA

A

1
2
4

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65
Q

type 1 RTA is caused by ___ in ___

A

deficient H+ excretion

collecting tubule

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66
Q

type 1 RTA is associated with ___ (2)

A

hypokalemia

Ca2+ stones

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67
Q

type 2 RTA is caused by ___ in ___

A

deficient HCO3- reabsorption

proximal tubule

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68
Q

type 2 RTA is associated with ___ (2)

A

hypokalemia

hypophasphatemic rickets

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69
Q

type 4 RTA is caused by ___ (2)

A

hypoaldosteronism

aldosterone insensitivity

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70
Q

type 4 RTA is associated with ___

A

hyperkalemia

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71
Q

hyperkalemia in type 4 RTA causes ___ in PT

this causes ___

A

reduced NH3 excretion

aciduria

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72
Q

dd of RBC casts (3)

A

GN
ischemia
malignant HTN

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73
Q

dd of WBC casts (3)

A

tubulointerstitial inflammation
acute pyelonephritis
transplant rejection

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74
Q

cause of granular casts

A

ATN

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75
Q

cause of waxy casts

A

RF (main chronic)

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76
Q

presence of casts means urinary complaint is ___

A

of renal origin

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77
Q

3 kinds of causes of RPGN

A

anti-GBM disease
immune complex vasculitis
pauci-immune vasculitis

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78
Q

___ causes anti-GBM RPGN

A

Goodpasture’s disease

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79
Q

5 immune complex causes of RPGN

of these ___ (2) also cause plain GN

A
essential cryoglobulinemic
HSP
cutaneous leukocytoclastic
SLE
PAN
HSP
SLE
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80
Q

GN causes ___ (2) in urine

A

hematuria

RBC casts

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81
Q

GN causes ___ (4) derangements of renal function

A

azotemia
oliguria
HTN
proteinuria

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82
Q

proteinuria in GN is ___

A

<3.5g/day

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83
Q

post-strep GN has ___ (2) on LM,
___ on EM, and
___ on IF

A

hypercellular glomeruli (proliferative)
neutrophilic infiltrate
subepithelial deposits
lumpy-bumpy pattern

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84
Q

post-strep GN happens mostly in ___
end-point is ___
causative strep species is ___

A

kids
spontaneous resolution
S. pyogenes

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85
Q

immune complexes in post-strep GN consist of ___ (3)

A

IgG
IgM
C3

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86
Q

2 lab values for post-strep GN

A

high ASO

low C3

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87
Q

4 components of RPGN cresents

A

glomerular parietal epitheilum
fibrin
plasma protein
MQs

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88
Q

fibrin, plasma protein and MQs of RPGN crescents are located in ___

A

urinary (Bowman’s) space

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89
Q

2 causes of diffuse proliferative GN

A

SLE

MPGN

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90
Q

diffuse proliferative GN has ___ on EM, and

___ on IF

A

subendothelial deposits

lumpy-bumpy pattern

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91
Q

diffuse proliferative GN represents WHO class ___ SLE renal disease

A

4

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92
Q

class I SLE renal disease

A

no changes

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93
Q

class II SLE renal disease

A

mesangial GN

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94
Q

class III SLE renal disease

A

focal proliferative GN

95
Q

class V SLE renal disease

A

diffuse membranous GN

96
Q

most common form of SLE renal disease

A

class IV

97
Q

on LM, DPGN has ___ aka ___
on EM it has ___
on IF it has ___

A

capillary wall thickening
wire looping
subendothelial deposits
lumpy bumpy pattern

98
Q

IgA nephropathy GN has ___ on LM

it commonly occurs after ___ (2)

A

mesangial IC deposits
URI
gastroeneteritis

99
Q

___ is the MCC of nephrotic syndrome in adults

it is caused by ___ (4)

A
diffuse membranous GN (DMGN)
SLE (class V)
drugs
infections
solid tumors
100
Q

on LM, DMGN has ___ (2)

on EM it has ___

A

capillary wall thickening
GBM thickening
subepithelial deposits

101
Q

DMGN subepithelial deposits have ___ appearance

A

spike and dome

102
Q

___ is MCC of nephrotic syndrome in kids

A

minimal change disease (MCD)

103
Q

on LM, MCD has ___

on EM it has ___

A

minimal change

foot process effacement

104
Q

MCD patients lose ___ but not ___

A

albumin

globulins

105
Q

MCD tx

A

CS

106
Q

most common glomerular disease in HIV patients

A

FSGS

107
Q

T/F: FSGS is usually secondary to systemic disease

A

false: usually idiopathic

108
Q

idiopathic FSGS is more common in ___ (2 ethnicities)

A

hispanic

black

109
Q

___% of FSGS reach end-stage disease within 10 years

A

50

110
Q

in FSGS, IF identifies ___ (2) deposits. these are not ___s.

A

IgM
C3
ICs

111
Q

in FSGS, ____ is visible on EM in non-sclerotic areas

A

foot-process effacement

112
Q

idiopathic FSGS is caused by defect in ___. for example, ____ (3 proteins).

A

filtration slit
nephrin
podocin
alpha-actinin

113
Q

in membranous nephropathy complement causes capillary damage directly via ___ and indirectly via ____ from ____ (2)

A

MAC
MAC-triggered ROS and protease release
epithelial cells
mesangial cells

114
Q

2 kinds of MPGN are ___. ___ is much more common than the other.

A

immune complex MPGN
dense deposit disease
immune complex MPGN

115
Q

in both kinds of MPGN, ____ cells try to phagocytose ____, after which they ___.
in response ____ cells secrete more ____, which causes loss of ____.

A
mesangial
subendothelial deposits
proliferate
endothelial
GBM
capillary lumen
116
Q

deposits in IC MPGN are ___ (4)

A

IgG
C3
C4
C1

117
Q

deposits in dense deposit disease are ___ (2)

A

C3

properdin

118
Q

in MPGN serum C3 is high/low

A

low

119
Q

amyloidosis deposits accumulate in ___ (2)

A

mesangium

subendothelium

120
Q

3 GBM changes in DM

A

thickening
more collagen IV
less proteoglycans

121
Q

___ is a useful early test in DM

A

microalbuminuria

122
Q

2 DM risk factors for DM nephropathy

A

uncontrolled DM

HTN

123
Q

___ are essential drugs for arresting DM nephropathy

A

ACEIs

124
Q

all DM has ___. this is caused by ___.

some patients progress to ___ and others to ___.

A

diffuse GBM thickening
non-enzymatic glycation
diffuse GS
nodular GS

125
Q

nodular GS has ____ surrounded by ___. nodular GS is aka ___

A

PAS + nodules
dilated capillaries
Kimmelstiel-Wilson disease

126
Q

microalbuminuria is ____/day

macroproteinuria is ___/day

A

> 30mg

>300mg

127
Q

in addition to GS, ____ (2) are DM associated nephropathies

A

hyaline arteriolosclerosis

pyelonephritis

128
Q

exposure to ___ such as in ___ (occupation) is a risk factor for Goodpasture

A

volatile hydrocarbons

gasoline workers

129
Q

3 problems in Alport’s syndrome

A

nephritis
deafness
ophthalmic disorders

130
Q

2 inheritance patterns for Alport’s. the more common is ___.

A

XLR
AR
XLR

131
Q

Alport’s is caused by mutations in ___.

A

collagen IV

132
Q

Alport’s appears as ___ on EM

A

lamellation of GBM

133
Q

in nephrotic syndrome ANP is high/low

A

low

134
Q

2 complications of nephrotic syndrome

A

infection

thrombosis

135
Q

infection in nephrotic syndrome is because of ___

thrombosis in nephrotic syndrome is because of ___

A

loss of Igs

loss of anticoagulants

136
Q

IgA nephropathy is aka ___. it is caused by accumulation of ___ (2) in ___. this activates ___.

A
Berger's disease
IgA
C3
mesangium
alternate complement pathway
137
Q

IgA nephropathy may appear via LM as ___ (3)

A

normal
focal GN
mesangial cell proliferation

138
Q

IgA nephropathy is associated with ___ (2).

A

celiac

liver disease

139
Q

IgA nephropathy is a mild/severe disease.

A

mild

140
Q

T/F: in MCD renal function is normal.

A

TRUE

141
Q

MCD is occasionally associated with ___ and rarely with ___ (3)

A

nephrin deficiency
HLy
NSAIDs
atopy

142
Q

3 systemic diseases causing nephrotic syndrome

A

SLE
amyloidosis
DM

143
Q

2 complications of kidney stones

A

hydronephrosis

pyelonephritis

144
Q

___ is most common kind of kidney stone

A

Ca2+

145
Q

2 kinds of Ca2+ kidney stone

A

Ca2+ oxalate

Ca2+ phosphate

146
Q

Ca2+ stones are radio-___

A

opaque

147
Q

Ca2+ stone crystal shape

A

rectangular with X

148
Q

4 causes of Ca2+ stones

A

hyper-PTH
hypervitaminosis D
cancer
milk-alkali syndrome

149
Q

2 causes of Ca2+ oxalate crystals

A

ethylene glycol poisoning (antifreeze)

vitamin C abuse

150
Q

2nd most common kidney stone

A

struvite (15%)

151
Q

struvite is either ___ or ___

A

NH4MgSO4

NH4Mg(PO3)3

152
Q

struvite stones can cause ___

A

staghorn calculi

153
Q

staghorn calculi can cause ___

A

UTI

154
Q

struvite stones are radio-___

A

opaque

155
Q

struvite stones are caused by ___

A

urease + bacteria

156
Q

5 urease + bugs

A
Proteus vulgaris
Klebsiella
HP
Ureaplasma
Staph
157
Q

struvite crystal shape

A

rectangular

158
Q

3rd most common kidney stone

A

urate (5%)

159
Q

urate crystals are associated with ___ (2)

A

leukemia
MPD
(high cell turnorver rate)

160
Q

urate crystals are radio-___

A

lucent

161
Q

4th most common kidney stone

A

cystine (1%)

162
Q

main cause of cystine stones

A

cystinuria

163
Q

cystine crystals shape

A

hexagonal

164
Q

cystine crystals can cause ___

A

staghorn calculi

165
Q

cystine crystals are radio-___

A

opaque (faintly)

166
Q

4 ectopic hormones associated with RCC

A

EPO
ACTH
PTHrP
PRL

167
Q

RCC is associated with ___

A

VHL

168
Q

___ is most common renal malignancy in kids

A

Wilms’

169
Q

Wilms’ tumor contains ___

A

embryonic glomeruli

170
Q

growth disorder associated with Wilms’ tumor

A

hemihypertrophy

171
Q

___ on chromosome ___ is a gene linked to Wilms’ tumor

it is a ___ gene

A

WT1
11
tumor-suppressor

172
Q

complex including Wilms’ tumor

A
Wilms' tumor
Aniridia
Genitourinary malformation
mental-motor Retardation
(WAGR)
173
Q

symptom suggestive of transitional cell ca

A

painless hematuria

174
Q

TCC is associated with ___ (4)

A
Phenacetin (analgesic)
Smoking
Aniline dyes
CTX
(Pee SAC)
175
Q

pyelonephritis primarily affects ___ of kidney

A

cortex

176
Q

pyelonephritis has ___ casts in ___

this is called ___

A

eosinophilic
tubules
thyroidization

177
Q

2 causes of diffuse cortical necrosis

A

obstetric catastrophe

septic shock

178
Q

2 mechanisms of diffuse cortical necrosis

A

DIC

vasospasm

179
Q

___ is reversible but requires ___ to prevent death

A

ATN

supportive dialysis

180
Q

ATN is associated with ___ (3)

A

shock
crush injury (myoglobinuria)
toxins

181
Q

ATN has ___ phase followed by ___ occurring at ___

A

oliguric
recovery
2–3 weeks

182
Q

death from ATN occurs in ___ phase

A

oliguric

183
Q

prerenal azotemia is caused by ___

A

reduced RBF

184
Q

postrenal azotemia is caused by ___

A

BILATERAL outflow obstruction

185
Q
prerenal ARF has 
\_\_\_ urine osmolality
\_\_\_ urine Na+
\_\_\_ FENa
and \_\_\_ BUN/Cr ratio
A

high (>500)

low (20

186
Q
renal ARF has 
\_\_\_ urine osmolality
\_\_\_ urine Na+
\_\_\_ FENa
and \_\_\_ BUN/Cr ratio
A

low (20)
>2%
<15

187
Q
postrenal ARF has 
\_\_\_ urine osmolality
\_\_\_ urine Na+
\_\_\_ FeNa
and \_\_\_ BUN/Cr ratio
A

low (40)
>4%
>15

188
Q

electrolyte disorder in RF

A

hyperkalemia

189
Q

acid-base disorder in RF

A

metabolic acidosis

190
Q

uremia syndrome includes ___ (5)

A
nausea
pericaditis
encephalopathy
platelet dysfunction
asterixis
191
Q

skeletal disorder in RF

cause is ___

A

renal osteodystrophy

deficient 1,25-OHD

192
Q

metabolic disorder in RF

A

dyslipidemia (hyper-TAG)

193
Q

Fanconi’s syndrome is deficient ___ in ___

A

metabolite transport

PT

194
Q

4 metabolites lost in Fanconi’s syndrome

A

Glc
AAs
phosphate
uric acid

195
Q

2 kinds of Fanconi’s syndrome

A

congenital

acquired

196
Q

3 kinds of causes of Fanconi’s

A

Wilson’s
glycogen storage disease
drugs

197
Q

2 drugs causing Fanconi’s

A

cisplatin

expired tetracycline

198
Q

simple renal cysts are located in ___

they are benign/symptomatic

A

cortex

benign

199
Q

medullary renal cysts pw ___ (2)

prognosis is good/bad

A

concentrating defect
small kidney on US
bad

200
Q

4 sx of hyponatremia

A

disorientation
stupor
coma
seizure

201
Q

3 sx of hypernatremia

A

irritability
delirium
coma

202
Q

hypochloremia is associated with ___ (4)

A

metabolic alkalosis
hyperaldosteronism
hypokalemia
hypovolemia

203
Q

hyperchloremia is associated wtih ___

A

non-anion gap metabolic acidosis

204
Q

2 sx of hypokalemia

A

paralysis

arrhythmia

205
Q

2 EKG signs of hypokalemia

A

U wave

flattened T wave

206
Q

U wave is ___
it has same polarity as ___
it is caused by ___

A

small deflection after T wave
T wave
septal repolarization

207
Q

T/F: u wave is pathological

A

false: present in 50% of normal EKG

208
Q

sx of hyperkalemia

A

arrhythmia

209
Q

2 EKG signs of hyperkalemia

A

peaked T wave

wide QRS

210
Q

2 sx of hypocalcemia

A

tetany

neuromuscular irritability

211
Q

T/F: hypercalcemia can occur without hypercalciuria

A

TRUE

212
Q

2 sx of hypomagnesemia

A

neuromuscular irritability

arrhythmia

213
Q

3 sx of hypermagnesemia

A

delirium
decreased DTRs
cardiopulmonary arrest

214
Q

2 sx of hypophosphatemia

A

bone loss

osteomalacia

215
Q

2 sx of hyperphosphatemia

A

kidney stones

metastatic calcification

216
Q

4 indications for mannitol

A

high ICP
high intraocular pressure
drug OD
shock

217
Q

2 mannitol SEs

A

pulmonary edema

dehydration

218
Q

mannitol is contraindicated in ___ (2)

A

CHF

anuria

219
Q

acetazolamide mechanism

A

CA inhibition

220
Q

CA does ___

A

H2O + CO2 H2CO3

221
Q

in PT, filtered ___ combines with secreted ___ to make ___

A

HCO3-
H+
H2CO3

222
Q

normally, CA facilitates ___
therefore, inhibition causes ___
this causes ___

A

HCO3- reabsorption
HCO3- excretion
metabolic acidosis

223
Q

6 indications for acetazolamide

A
open angle glaucoma
pseudotumor cerebri
cystinuria
altitude sickness
metabolic alkalosis
dural ectasia
224
Q

furosemide causes increased ___ excretion

A

Ca2+

225
Q

6 furosemide SEs

A
Ototoxicity
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout
226
Q

___ is a non-sulfonamide loop diuretic

it can be used in the presence of ___

A

ethacrynic acid

gout

227
Q

4 indications for thiazide

A

HTN
CHF
idiopathic hypercalciuria
nephrogenic DI

228
Q

7 thiazide SEs

A
hypokalemic metabolic alkalosis
hyponatremia
hyperGlycemia
hyperLipidemia
hyperUricemia
hyperCalcemia
sulfa allergy
229
Q

triamterene acts at same channel as ___

A

amiloride

230
Q

___ diuretics cause acidemia

___ (2) cause alkalemia

A

acetazolamide
loop diuretics
thiazide

231
Q

___ diuretics cause hypercalciuria

___ cause hypocalciuria

A

loop diuretics

thiazide

232
Q

10 ACEI SEs

A
Cough
Angioedema
Proteinuria
Taste changes
hypOtension
Pregnancy problems
Rash
Increased renin
Lower Ang II
hyperkalemia
233
Q

ACEIs are contraindicated in ___

because ___

A

bilateral renal artery stenosis

they lower GFR