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Step 1 > Renal > Flashcards

Renal Flashcards

1
Q

pronephros exists

A

until week 4

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2
Q

mesonephros

A

interim kidney for first trimester

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3
Q

metanephros

A

permanent

appears in 5th week

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4
Q

Where is the ureteric bud derived from?

What does it become?

A

caudal end of mesonephric duct

ureter, pelvises, calyces, collecting ducts

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5
Q

when is the ureteric bud fully developed?

A

week 10

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6
Q

what forms the glomeruli –> distal converluted tubule?

A

metanephric mesenchyme

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7
Q

what is the last area of the kidney to canalise?

A

ureteropelvic junction

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8
Q

most common site of hydronephrosis in fetus

A

ureteropelvic junction

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9
Q

Potter syndrome caused by

A

Oligohydrimonas

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10
Q

What are the signs of potter syndrome?

A 
Pulmonary hypoplasia
Oligohydramnios
Twistsed face
Twisted skin
Extremity deformity
Renal failure in utero
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11
Q

Where does a horseshoe kidney get trapped?

A

inferior mesenteric artery

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12
Q

associations with horseshoe kidney

A

hydronephrosis, renal stones, infection, chromosomal aneuploidy syndromes, renal cancer

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13
Q

unilateral renal agenesis

A

ureteric bud fails to develop - absense of kidney and ureter

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14
Q

multicystic dysplastic kidney

A

ureteric bud doesn’t differentiate metanephric mesenchyme

non-function kidney with cysts and connective tissue

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15
Q

duplex collecting system associated with

A

vesicoureteral reflux, urethral obstruction, UTIs

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16
Q

Left kidney

A

Higher, and has longer renal vein

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17
Q

renal blood flow

A

renal artery –> segmental artery –> interlobar –> arcuate –> interlobular –> afferent –> glomerulus –> efferent –> vasarecta/peritubular capillaries –> venous outflow

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18
Q

interstitial fluide =

A

75% extracellular volume

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19
Q

water weight rule

A

60-40-20
60% water
40% ICF
20% ECF

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20
Q

how can you measure plasma volume?

A

radiolabel albumin

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21
Q

how can you measure extracellular volume?

A

inulin/ mannitol

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22
Q

What is normal blood Osm?

A

285-295 mOsm/kg H2O

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23
Q

what are the three layers of the glomerulus?

A 
capillary endothelium
basement membrane
epithelial layer (podocytes)
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24
Q

what does the basement membrane contain?

A

heperan sulfate

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25
Q

what is special about the basement membrane?

A

negatively charged

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26
Q

renal clearance =

A

(urine concentration x urine flow rate)/

plasma concentration

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27
Q

If clearance is less than GFR

A

net tubular reabsorption of substance

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28
Q

what can be used to measure GFR?

A

inulin clearance

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29
Q

GFR =

A

(urine concentration x urine flow rate)/

plasma concentration

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30
Q

how does Createnine clearance estimate GFR and why?

A

overestimate

moderately secreted by renal tubules

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31
Q

effective renal plasma flow can be estimated using

A

para-aminohippuric acid (PAH) clearance

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32
Q

renal blood flow =

A

RPF/ (1-Hct)

1-Hct = plasma

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33
Q

how does eRPF measure against the true value?

A

slightly underestimates

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34
Q

Filtration fraction =

A

GFR/RPF

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35
Q

what is the normal filtration fraction?

A

20%

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36
Q

what is the filtered load?

A

GFR x plasma concentration

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37
Q

effect of prostaglandins on kidney

A

dilate afferent arteriole

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38
Q

Net filtration pressure =

A

(P-gc + Pi-bs) - (P-bs + Pi-gc)

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39
Q

what preferentially constricts the efferent arteriole?

A

AT II

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40
Q

what does constricting the efferent arteriole do?

A

decreases RPF, increases GFR, increases FF

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41
Q

how does ureter constriction affect GFR?

A

decreases it

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42
Q

Where is glucose reabsorbed?

A

proximal converluted tubule

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43
Q

what is the level of renal glucose to see glucosuria?

A

200 mg/dL

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44
Q

When is Tm for glucose transporters?

A

375 mg/min

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45
Q

Thin descending loop

A

water only

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46
Q

what is reabsorbed and secreted in the proximal converluted tubule?

A

reabsorbed - glucose, a.a, HCO3, Na, Cl, PO4, K, H2O, uric acid
secreted NH3

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47
Q

purpose of NH3 in urine

A

buffer for H+

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48
Q

What does PTH do in the kidney and where does it act?

A 
inhibits Na/PO4 cotransport
PO4 excretion
increases Ca/Na exchange
Ca reabsorbtion
proximal converluted tubule, distal converluted tubule
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49
Q

What does ATII do in the kidney and where does it act?

A

stimulates Na/H, increases Na, H2O and HCO3- reabsorbtion

proximal converluted tubule

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50
Q

What is reabsorbed in the thick ascending loop?

A

Na, K, Cl

IMPERMEABLE to water

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51
Q

what is reabsorbed in the distal converluted tubule?

A

Na, Cl

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52
Q

What is the exchanger for sodium in the collecting duct?

A

Na/K orH

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53
Q

what is the regulation of the collecting duct?

A

aldosterone increases ENaC
secretes K+
H secretion from lumen negativety

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54
Q

How does ADH work?

A

inserts aquaporin

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55
Q

Fanconi syndrome

what does it cause?

A

proximal tubule - excretes substrates

proximal renal tubular acidosis

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56
Q

what can cause Fanconi syndrome?

A 
Leave When It Gets Too Metabolic
lead poisoning
wilson's disease
ischemia
glycogen storage disease
tyrosinemia
multiple myeloma
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57
Q

what drugs can cause Fanconi syndrome?

A 
Thats the TICET
Tenofovir
Ifosfamide
Cisplatin
Expired Tetracyclines
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58
Q

resorptive defect in thick ascending loop of Henle

A

Bartter syndrome (AR)

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59
Q

What is affected in Bartter syndrome?

A

Na/K/2Cl

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60
Q

What will Bartter syndrome look like?

A

chronic loop diuretic use

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61
Q

metabolic changes seen in Bartter’s

A

hypokalemia, metabolic acidosis, hypercalcuria

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62
Q

Gitelman syndrome

A

NaCl resorptive defect in distal converluted tubule

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63
Q

what will Gitelman syndrome look like?

A

lifelong use of thiazides

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64
Q

metabolic changes in Gitelman’s

A

hypokalaemia, hypomagnesia, metabolic acidosis, hypocalciuria

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65
Q

Liddle syndrome

A

increased Na reabsorption in collecting tubules

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66
Q

condition presenting like hyperaldosteronism, but low aldosterone

A

Liddle syndrome

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67
Q

htn, hypokalemia, metabolic acidosis, low aldosterone

A

Liddle syndrome

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68
Q

Rx Liddle syndrome

A

Amiloride

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69
Q

low aldosterone, htn, hypokalemia, metabolic acidosis, deficiency in 11B-hydroxysteroid dehydrogenase

A

syndrome of apparent mineralocorticoid excess

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70
Q

11B-hydroxysteroid dehydrogenase deficiency Rx

A

corticosteroids (decreases endogenous production and receptor activation)

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71
Q

what breaks down ACE?

A

Bradykinin

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72
Q

Renin is linked to what receptor? and responds to what?

A

B1

decreased renal arterial pressure

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73
Q

role of ATII

A

limits reflex bradycardia, maintains blood volume and pressure

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74
Q

function of ATII

A

vasoconstriction, constricts efferent arteriole of glomerulus, stimulates ADH, Na, HCO3, H2O reabsorption in proximale tube, stimulates thirst

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75
Q

function of AMP

A

relaxes s.m via cGMP, dilates afferent arteriole, constricts efferent arteriole

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76
Q

purpose of ADH

A

regulates Osm

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77
Q

action of aldosterone

A

increases Na channel reabsorbtion

enhances K and H secretion

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78
Q

what cells are found in the juxtaglomerular apparatus?

A

mesangial cells

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79
Q

what is the macula dense?

A

NaCl sensor in distal tubule

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80
Q

what releases erythropoeitin?

A

interstitial cells in peritubular capillary bed

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81
Q

what cells are used in calcium metabolism?

A

PCT cells

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82
Q

what do PCT cells do?

A

convert 25-OH D3 –> 1,25-(OH)2 D3

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83
Q

what is secreted by PCT cells?

A

dopamine

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84
Q

what effect does dopamine have on the kidney?

A

promotes naturesis, dilates arteries, increases RBF

in high doses it is a vasoconstrictor

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85
Q

Drugs causing hyperkalaemia

A 
DO LABS
Digitalis
hyperOsmolarity
Lysis
Acidosis
B blockers
Sugar (high)
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86
Q

Drugs causing hypokalaemia

A 
opposite of hyperkalaemia:
DO LABS
Digitalis
hyperOsmolarity
Lysis
Acidosis
B blockers
Sugar (high)
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87
Q

nausea, malaise, stupor, coma, seizure

A

hyponatremia

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88
Q

irritable, stupor, coma

A

hypernatremia

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89
Q

muscle cramps, spasm, weakness, U waves, flat T waves, arrhythmia

A

hypokalemia

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90
Q

muscle weakness, arrhythmia, wide QRS, peaked T waves

A

hyperkalemia

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91
Q

tetany, seizure, long QT, twitching, spasm

A

hypocalcemia

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92
Q

hypercalcemia

A

stones, bones, groans, thrones, psychiatric moans

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93
Q

tetany, torsades de pointes, hypokalemia

A

hypomagnesia

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94
Q

lethargy, bradycardia, hOtn, cardiac arrest, hypocalcemia, low tendon reflexes

A

hypermagnesia

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95
Q

Henderson-Hasselbalch equation

A

pH = 6.1 + log ([HCO3]/0.03 PCO2)

96
Q

how to calculate predicted respiratory compensation in metabolic acidosis

A

PCO2 = 1.5[HCO3-] + 8 +- 2

97
Q

If measured PCO2 is more than predicted PCO2

A

respiratory acidosis on top of metabolic acidosis

98
Q

causes of metabolic alkalosis

A

loop diuretics, vomiting, antacid use, hyperaldosteronism

99
Q

respiratory alkalosis causes

A

hysteria, hypoxemia, salicylates, tumour, PE

100
Q

increased anion gap metabolic acidosis

A 
MUDPILES
Methanol
Uremia
DKA
Propylene glycol
Iron tablets
Lactic acidosis
Ethylene glycol
Salicylates
101
Q

Normal anion gap metabolic acidosis

A 
HARDASS
Hyperalimentation - diarrhoea
Addison's
Renal tubular acidosis
Diarrhoea
Acetazolamide
Spironolactone
Saline infusion
102
Q

renal tubular acidosis type 1 and 2

A

distal

proximal

103
Q

distan renal tubular acidosis urine

A

urine pH >5.5

104
Q

what happens in distal renal tubular acidosis?

A

alpha intercalated cells can’t secrete H+

no new HCO3- is generated

105
Q

what is renal tubular acidosis associated with?

A

hypokalemia

106
Q

what causes distal renal tubular acidosis?

A

ABC
Analgesic nephropathy
amphotericin B toxicity
Congenital abnormalities

107
Q

what happens in proximal renal tubular acidosis?

A

defect in PCT HCO3 reabsorption

108
Q

what is the urine like in proximal renal tubular acidosis?

A

pH <5.5

109
Q

what causes proximal renal tubular acidosis?

A

Fanconi syndrome, carbonic anhydrase inhibitors

110
Q

what does proximal renal tubular acidosis increase the risk of?

A

hypophosphatemic rickets

111
Q

urine pH <5.5, hyperkalemia

A

hyperkalaemic renal tubular acidosis

112
Q

what happens in hyperkalaemic renal tubular acidosis?

A

hyperaldosteronism
decrease NH3 synthesis in proximal tubule
decreased NH4+ secretion

113
Q

causes of hyperkalemic renal tubular acidosis

A

decreased/resistance to aldosterone

114
Q

what causes a decrease in aldosterone?

A 
HCA DAAN
heparin
cyclosporine
adrenal insufficiency
diabetic hyporeninism
ACE inhibitors
ARBs
NSAIDs
115
Q

what causes aldosterone resistance?

A

K sparing diuretics, nephropathy from obstruction, TMP/SMX

116
Q

casts in urine

A

glomerular or renal tubular origin

117
Q

RBC casts

A

glomerulonephritis, malignant htn

118
Q

WBC casts

A

tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

119
Q

Fatty casts

A

nephrotic syndrome

120
Q

granular casts

A

acute tubular necrosis

121
Q

waxy casts

A

end stage renal disease

122
Q

hyaline casts

A

can be normal

123
Q

focal segmental glomerulosclerosis

A

<50% glomeruli

124
Q

membranoproplferative glomerulonephritis

A

hypercellular glomeruli

125
Q

thickening of glomerular basement membrane

A

membranous nephropathy

126
Q

primary disease of kidney impacting glomeruli

A

minimal change disease

127
Q

proteinuria, hypoalbuminemia, edema

A

nephrotic syndrome

128
Q

what causes nephrotic syndrome?

A

podocyte disruption

129
Q

causes of nephritis syndrome

A 
focal segmental glomerulosclerosis
minimal change disease
membranous nephropathy
amyloidosis
diabetic
130
Q

causes of nephritic syndrome

A

IgA, Alport syndrome, rapidly progressive glomerulonephritis, post strep, goodpastures, wegner’s

131
Q

Berger disease

A

IgA nephropathy

132
Q

what causes nephritic syndrome?

A

GMB disruption

133
Q

htn, raised Cr, oliguria, hematuria

A

nephritic syndrome

134
Q

nephritic-nephrotic picture

A

diffuse proliferative glomerulonephritis

membranoproliferative glomerulonephritis

135
Q

starry sky nephritic syndrome

A

acute poststrep

136
Q

what is deposited in acute poststrep glomerulonephritis?

A

IgG, IgM, C3

137
Q

what type of hypersensitivity is acute poststrep glomerulonephritis?

A

III

138
Q

coke coloured urine, edema, htn

A

acute poststrep glomerulonephritis

139
Q

crescent moon shape on microscopy

A

rapidly progressive glomerulonephritis

140
Q

what are the crescents made out of?

A

fibrin, plasma proteins, glomerular parietal cells, monocytes, mpgs

141
Q

Goodpastures

A

antibodies to GBM

type II hypersensitivity

142
Q

immune association with rapidly progressive glomerulonephritis

A

PR2-ANCA/c-ANCA

MPO-ANCA/p-ANCA

143
Q

granular, C3 deposition, wire looping of capillaries

A

diffuse proliferative glomerulonephritis

144
Q

SLE kidneys

A

diffuse proliferative glomerulonephritis

145
Q

Alport syndrome

A

IV collagen mutation

can’t see, can’t pee, can’t hear a bee

146
Q

kidney disease linked with Hepatitis B/C

A

membrano-proliferative glomeruloephritis

147
Q

tram-track PAS stain

A

membranoproliferative glomerulonephritis

148
Q

EM effacement of foot processes

A

minimal change disease

149
Q

Rx minimal change disease

A

steroids

150
Q

most common cause of nephrotic syndrome in African Americans and hispanics

A

focal segmental glomerulosclerosis

151
Q

conditions resulting in focal segmental glomerulosclerosis

A

HIV, sickle cell, heroin abuse, obesity, interferon Rx, CKD from congenital malformation

152
Q

segmental sclerosis and hyalinosis, potential immune deposits, effacment of foot processes

A

focal segmental glomerulosclerosis

153
Q

most common cause of primary nephrotic syndrome in caucasian adults

A

membranous nephropathy

154
Q

capillary an GBM thickening, granular, immune complex deposition
spike and dome

A

membranous nephropathy

155
Q

what is a primary cause of membranous nephropathy?

A

phospholipase A2 receptor antibodies

156
Q

what are secondary causes of membranous nephropathy?

A

NSAIDs, penicillamine, HB/CV, SLE, solid tumours

157
Q

congo red stain shows apple-green birefringence under polarised light

A

amyloidosis

158
Q

where do you get amyloid deposits?

A

mesangium

159
Q

mesangial expansion, GBM thickening, eosinophilic nodular

A

diabeic glomerulonephritis

160
Q

Kimmelstiel-Wilson lesions

A

eosinophilic nodular glomerulosclerosis

161
Q

envelope shaped urine crystals

A

calcium oxalate stones

162
Q

most common kidney stones

A

calcium oxalate

163
Q

hypocitrateuria

A

decreased urine pH

164
Q

Rx hypocitrateuria

A

thiazides, citrate, low sodium diet

165
Q

wedge shaped prism crystals

A

calcium phosphate

166
Q

Rx Ca phosphate stones

A

thiazides

167
Q

coffin lid crystals

A

ammonium magnesium phosphate

168
Q

stones from urase positive organisms

A

ammonium magnesium phosphate

169
Q

urease positive organisms

A

proteus mirabilis, staph saphrophyticus, kelbsiella

170
Q

what is the likely cause of a staghorm calculi?

A

ammonium magnesium phosphate

171
Q

rhomboid/rosette crystals

A

uric acid

172
Q

RF for uric acid stones

Rx

A

low urine volume, arid climates, acidic pH, gout

alkalisation of urine, allopurinol

173
Q

hexagonal crystals

A

cystine stones

174
Q

sodium cyanide nitroprusside positive

A

cystine stones

175
Q

what causes cystine stones?

Rx

A

can’t reabsorb cystine in proximal tubule
or ornithine, lysine or arginine
COLA
low sodium, alkalinisation of urine, chelating agents

176
Q

hydronephrosis

A

distension/dilation of the renal pelvis

177
Q

most common renal malignancy

A

renal cell carcinoma

178
Q

where does renal cell carcinoma originate?

A

PCT cells –> polygonal clear cells

179
Q

golden yellow cells in PCT mean, because

A

renal cell carcinoma

high lipid content

180
Q

spread of renal cell carcinoma

A

hemetogenous through renal vein and IVC

181
Q

Rx renal cell carcinoma

A

aldesleukin, resection

182
Q

gene deletion of chr. 3

A

renal cell carcinoma

183
Q

renal oncocytoma

A

benign epithelial tumour from collecting ducts

184
Q

large eosinophilic cells with lots of mt

no perinuclear clearing

A

renal oncocytoma

185
Q

Wilms tumour

A

nephroblastoma

186
Q

Wilms tumour genetics

A

WT1 or 2 gene on chr.11

187
Q

WT1 causes

A

Wilms tumour, aniridia, genitourinary malformation, mental retardation

188
Q

Denys-Drash

A

Wilms tumour, early onset nephrotic syndrome, male pseudohermaphroditism, WT1 mutation

189
Q

Beckwith-Wiedemann

A

wilms tumour, macroglossia, organomegaly, hemihyertrophy, WT2 mutation

190
Q

RF transitional cell carcinoma

A

phenacetin
smoking
aniline dyes
cyclophosphamide

191
Q

RF squamous cell carcinoma of bladder

A

schistosoma haematobium, chronic cystitis, smoking, chronic nephrolithiasis

192
Q

squamous cell carcinoma of bladder caused by

A

chronic irriration of bladder

193
Q

urge incontinance Rx

A

oxybutanin (antimuscarinic)

194
Q

causes of UTI

A

E coli
Staph saphrophyticus (sexually active young women)
kelbsiella
p. mirabilis

195
Q

urine smells like ammonia

A

proteus mirabilis

196
Q

striated parenchymal enhancement

A

acute pyelonephritis

197
Q

RF acute pyelonephritis

A

UTI, catheter, vesicoureteral reflux, DM, pregnancy

198
Q

complications of acute pyelonephritis

A

chronic, renal papillary necrosis, perinephric abscess

199
Q

asymmetric corticomedullary scarring, blunted calyx

A

chronic pyelonephritis

200
Q

thyrodization of kidney

A

eosinophili casts

chronic pyelonephritis

201
Q

xanthogranulomatous pyelonephritis

A

granulomatous tissue containing foamy mpgs

202
Q

diffuse cortical necrosis

A

cortical infarction of both kidneys

vasospasm + DIC

203
Q

renal osteodystrophy

A

failure of vitamin D hydroxylation due to CKD

204
Q

which AKI has the highest urine Osm?

A

pre-renal

means urine is concentrated

205
Q

AKI with high urine Na

A

renal or post renal

206
Q

effects of high BUN

A

nausea, anorexia, pericarditis, asterixis, encephalopathy, plt dysfunction

207
Q

causes of acute interstitial nephritis

A

diuretics, penicillin, PPIs, sulfonamides, rifampicin, NSAIDs, Sjogren’s syndrome, SLE, sarcoidosis, mycoplasma

208
Q

causes of acute tubular necrosis

risks

A

ischemic - decreased renal blood flow
nephrotoxic - toxic substances, crush injury, hemoglobinurea
risks - hyperkalaemia followed by hypokalaemia in recovery

209
Q

nephrotoxic substances

A

aminoglycosides, radiocontrast, lead, cisplatin

210
Q

gross hematuria and proteinuria and recent infection

A

renal papillary necrosis

211
Q

RF renal papillary necrosis

A

sickle cell, acute pyelonephritis, analgesics, DM

212
Q

PKD1

PKD2

A

85% chr.16

15% chr.4

213
Q

cystic dilation of collecting ducts, seen in infants

Rx

A

AR PKD

ACE inhibitors or ARBs

214
Q

what is associated with AR PKD?

A

congenital hepatic fibrosis

215
Q

medullary cyctic disease

A

tubulointerstitial fibrosis, can’t concentrate urine, shrunken kidneys

216
Q

simple renal cyst

A

ultrafiltrate

217
Q

complex renal cyst

A

septated, enhanced, solid components

218
Q

mannitol
use
s.e.

A

osmotic diuretic PCT
drug overdose, elevated ICP
pulmonary edema, dehydration

219
Q

acetazolamide
use
s.e.

A

NaHCO3 diuresis
glauoma, urinary alkalinization, metabolic alkalosis, pseudotumour cerebri
proximal renal tubular acidosis, parasthesias, NH3 toxicity, sulfa allergy

220
Q

Mechanism loop diuretics

use

A

inhibit Na/K/2Cl in thick ascending limb
stimulate PGE release
edema, htn, hypercalcemia

221
Q

what inhibits loop diuretics?

don’t give loop diuretics to

A

NSAIDs

OP - you loose Ca

222
Q

s.e. loop diuretics

A 
OH DANG
ototoxicity
hypokalaemia
dehydration
allergy
metabolic alkalosis
nephritis
gout
223
Q

ethacrynic acid

s.e.

A

nonsulfonamide loop diuretic

ototoxic

224
Q

thiazides mechanism
use
s.e.

A

inhibit NaCl reabsorption in DCT, decrease Ca excretion
htn, HF, hypercalciuria, nephrogenic diabetes insipidus, OP
hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy

225
Q

K sparing diuretics
use
s.e.

A

spironolactone, amiloride
hyperaldosteronism, K depletion, HF, hepatic ascites, nephrogenic DI
hyperkalaemia, endocrine effects from spironolactone (gynecomastia, antiandrogen)

226
Q

mechanism spironolactone

A

competitive aldosterone receptor antagonist

227
Q

mechanism amiloride/ triamterene

A

block Na channels in collecting duct

228
Q

diuretics increasing urinary NaCl

A

all of them

229
Q

diuretics causing acidemia

A

carbonic anhydrase inhibitors

230
Q

diuretics causing alkalemia

A

loop, thiazide

231
Q

use ACE inhibitors

s.e.

A

htn, HF, proteinuria, diabetic nephropathy

cough, angioedema, teratogenic, decrease GFR, hyperkalemia, hOtn

232
Q

difference between ACE inhibitors and ARBs

A

ARBs do not increase bradykinin

233
Q

use ARBs

s.e.

A

htn, HF, priteinuria, diabetic nephropathy

hyperkalemia, decrease GFR, hOtn, teratogen

234
Q

aliskiren

A

renin inhibitor

235
Q

use aliskiren

s.e.

A

htn

hyperkalaemia, decrease GFR, hOtn, don’t use in combination with other htn drugs

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