Renal Flashcards Preview

Step 1 AB > Renal > Flashcards

Flashcards in Renal Deck (290):
1

What criteria define Nephrotic syndrome?

>3.5g of protein/day
Hypoalbuminemia --> edema
Hyperlipidemia/ Hypercholesterolemia
Hypogammaglobulinemia
Hyper coagulable state --> lose ATIII

2

What criteria define Nephritic syndrome?

Hypertension
Increase BUN and creatinine (Azotemia)
Oliguria (decreased urine volume)
Hematuria
RBC casts in urine

3

What does focal mean?
What does diffuse mean?

< half of glomeruli affected
> half of glomeruli affected

4

What does membranous mean?

Basement membrane is thickened

5

What does proliferation mean?

There are increased number of cells

6

Post-Streptococcal glomerulonephritis
a. Pathophysiology
b. Seen in:
c. Presentation
e. On light microscopy
f. On immunofluorescence
g. On electron microscopy

a. Type III hypersensitivity; immune complexes are deposited in glomerulus. Treating strep with Abx does NOT prevent post-strep GN
b. Children who had strep infection three weeks earlier
c. Peripheral and periorbital edema, cola-colored urine, HTN
e. Glomeruli enlarged and hyper cellular
f. starry sky granular appearance; lumpy bumpy due to IgG, IgM and c3 deposition along GBM and mesangium
g. Subeptihelial immune complex humps


7

IgA nephropathy
a. Pathophysiology
b. Presentation
c. Associated with
d. On LM
e. On IF

a. Increased IgA
b. Hematuria, after URI
c. Henoch Schonlein purpura
d. Mesangial proliferation
e. IgA based IC deposits in mesangium

8

Alport syndrome
a. Pathophysiology
b. Presentation
c. On EM

a. Mutation in type IV collagein --> thinning and splitting of glomerular BM; most commonly X linked
b. Eye problems, glomerulonephritis, sensorineural deafness
c. Basket weave appearance

9

Goodpasture's
a. Pathophysiology
b. Presentation
c. on LM and IF

a. Type II hypersensitivity with Abs to GBM and alveolar basement membrane
b. Hemoptysis, hematuria
c. Crescent moon shape --> crescents consist of fibrin and plasma proteins --> linear pattern

10

What are three types of rapidly progressive glomerulonephritis (Crescentic)

Goodpastures
Wegeners (GPA)
Microscopic polyangiitis

11

Diffuse Proliferative Glomerulonephritis
a. Pathophysiology
b. Presentation
c. on LM
d. on EM

a. Due to SLE or membranoproliferative glomerulonephritis
b. Sometimes presents as nephrotic and nephritic syndrome concurrently (heavy proteinuria)
c. Wire looping of capillaries - makes BM look really pronounced
d. Subendothelial IgG immune complexes with C3 deposition

12

Most common cause of death in SLE

Diffuse proliferative glomerulonephritis

13

Minimal Change Disease
a. Pathophysiology
b. Presentation
c. on LM
d. on EM
e. Treatment

a. idiopathic or triggered by infection/immunization; secondary to lymphoma
b. CHILDREN; proteinuria, edema, hyperlipidemia, hypoalbuminemia
c. NORMAL glomeruli
d. EFFACEMENT (fusion) of foot processes
e. Responds to steroids

14

Focal Segmental Glomeruloscelsosis
a. Pathophysiology
b. Presentation
c. on LM
d. on IF
e. on EM
f. Treatment

a. Idiopathic or secondary to HIV!!!!, sickle cell, heroin abuse, obesity, interferon treatment, chronic kidney disease
b. Adults (african american and hispanics); nephrotic syndrome
c. segmental sclerosis and hyalinosis
d. nonspecific of foot process similar to minimal change disease
e. effacement of foot process similar to minimal change disease
f. Does not respond to steroids

15

Membranous Nephropathy
a. Pathophysiology
b. Presentation
c. on LM
d. on IF
e. on EM

a. Idiopathic or secondary to drugs, HBV, HCV, SLE, tumors
b. Caucasian adults
c. Diffuse capillary and GBM THICKENING
d. granular from immune complex deposition
e. Spike and dome appearance with SUBEPITHELIAL DEPOSITS

16

Membranoproliferative glomerulonephritis
a. Pathophysiology
b. Presenation
c. Type I
d. Type II

a. Nephritis syndrome that co present with nephrotic syndrome
b. Idiopathic or due to HBV/HCV infection, SLE or subacute bacterial endocarditis
c. Subendothelial immune complex deposits with granular IF = TRAM TRACK appearance on PAS stain from GBM splitting
d. Intramembranous IC deposits

17

Diabetic nephropathy
a. Pathophysiology
b. On Biopsy...

a. Non-enzymatic glycosylationg of GBM --> increased permeability and thickening
b. Kimmelstiel Wilson lesions, mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis

18

Linear pattern of IgG deposition on IF

Goodpasture syndrome (anti GBM Abs)

19

Lumpy bumpy deposits of IgG, IgM, C3 in the mesangium

Post-strep glomerulonephritis

20

Deposits of IgA in the mesangium

IgA Nephropathy (Berger disease)

21

Anti-GBM antibodies, hematuria, hemoptysis

Goodpasture's syndrome

22

Nephritis, deafness, cataracts

Alport syndrome

23

Crescent formation in the glomeruli

Rapidly progressive glomerulonephritis

24

Wire loop appearance on LM

Lupus nephritis

25

Most common nephrotic syndrome in children

Minimal change disease

26

Most common nephrotic syndrome in adults

Focal segmental glomerulonephritis

27

Kimmelstiel-Wilson lesions (nodular glomerulosclerosis)

Diabetic nephropathy

28

EM shows effacement of epithelial foot processes

Minimal change disease

29

Nephrotic syndrome associated with Hepatitis B

Membranoproliferative glomerulonephritis

30

Nephrotic syndrome associated with HIV

Focal Segmental Glomerulosclerosis (FSGS)

31

EM: sub endothelial humps and tram-track appearance

Membranoproliferative glomerulonephritis

32

LM: segmental sclerosis and hyalinosis

FSGS

33

Purpura on back or arms/legs, abdominal pain, IgA nephropathy

Henoch Schonlein Purpura

34

EM: spiking of GBM due sub epithelial deposits

Membranous nephropathy (Spike and dome)

35

Nodular hyaline deposits in the glomeruli

Kimmelstiel-Wilson nodules

36

Glomerulonephritis plus pulmonary vasculititis

GPA
Goodpasture

37

RBC casts

Indicate glomerular damage
Glomerulonephritis, malignant HTN
Appear yellowish-brown, cylindrical with ragged edges

38

WBC casts

Indicate acute pyelonephritis
Means damage is ALL the way up in kidney

39

Bacterial casts

Pyelonephritis

40

Epithelial cell cast

ATN, toxic ingestions
Difficult to distinguish from WBC casts

41

Waxy casts

Chronic renal failure
Low urine flow situations

42

Hyaline casts

Most common cast type
Solidified Tam horsefall proteins
Not necessarily pathology
Tend to see them in concentrated urine, dehydration

43

Fatty cast

Nephrotic syndrome

44

Granular cast

From breakdown of cellular casts or aggregates of plasma proteins (albumin, light chains)
Chronic renal disease
ATN (muddy brown cast)

45

Where is common location of kidney stone?

Ureterovesicular junction

46

Radiopaque
Envelope or dumbbell shaped

Calcium kidney stones

47

Risk factors for calcium oxalate stones

Ethylene glycol or Vitamin C abuse, malabsorption

48

Treatment for calcium stones

Hydration, Thiazides, Citrate

49

Hypercalciuria and normocalcemia

Most common kidney stone presentation; calcium stones

50

Radiopaque, coffin lid stones

Struvite (ammonium, Mg, phosphate stones)

51

Cause of Struvite stones

Infection with urease + bugs

52

Urease + bugs

Proteus mirabilis
Staph saphrophyticus
Klebsiella
Pseudomonas
They all hydrolyze urea to ammonia --> causes urine alkalinization

53

Treatment for struvite stones

Eradication of infection, surgical removal of stone

54

Form staghorn calculi (outlines the renal pelvis - looks like a big stag's horn)

Struvite stones

55

RadioLUCENT
Precipitates at Decreased pH

Uric acid stone

56

Uric acid stone

Radiolucent - can't see on plain film but can see on US and CT
Strong association with hyperuricemia (gout); seen in diseases with increased cell turnover like leukemia

57

Treatment of uric acid stones

Allopurinol, alkalinization of urine

58

Risk factors for uric acid stones

Decreased urine volume, arid climates, acidic pH

59

Cystine stones

Seen in patients with Cystinuria (children)
Staghorn calculi
Treated with alkalinization of urine
Hereditary condition where cystine-reabsorbing transporter loses function --> causing cystinuria

60

Paraneoplastic syndromes associated with renal cell carcinoma

Ectopic erythropoietin --> polycythemia
ACTH --> Cushing syndrome
PTHrP --> hypercalcemia
Prolactin --> hypogonadism, galactorrhea

61

Complications of Renal cell carcinoma

Invades inferior vena cava -> spreads hematogenously
Associated with von Hippel Lindau syndrome

62

Most common renal malignancy of children aged 2-4

Wilms tumor

63

Presentation of Wilms tumor

Hematuria
Large flank mass

64

Pathogenesis of Wilms tumor

Deletion of WT1 or WT2 on chromosome 11 (tumor suppressor gene)

65

Beckwith-Wiedemann syndrome

Wilms tumor
Aniridia
Genitourinary malformation
mental Retardation

66

Most common tumor of urinary tract

Transitional cell carcinoma (in renal calcyes, renal pelvis, ureters, bladder)

67

Risk factors for transitional cell carcinoma

Smoking
Aniline dye exposure
Cyclophosphamide

68

Cause of diffuse cortical necrosis

Vasospasm
DIC
Occurs in very sick patients

69

Most common causes of ATN

Ischemia
Nephrotoxic drugs (aminoglycosides, cephalosporins, polymyxins, radio contrast dye)

70

Key finding in ATN

Granular muddy brown casts

71

What is renal papillary necrosis?

Sloughing of necrotic renal papillae that causes gross hematuria and proteinuria

72

What triggers renal papillary necrosis? Associations?

Recent infection or immune stimulus
Associated with sickle cell disease, acute pyelonephritis, NSAIDs, diabetes mellitus

73

Three categories of acute renal failure

Prerenal - not enough blood
Intrinsic
Postrenal - outflow obstruction causing back up

74

Causes of prerenal failure

Hypovolemia
Shock
Hypotension
Renal vasoconstriction with NSAIDS

75

a. BUN/creatinine ratio in pre-renal azotemia
b. FENa
c. urine Na
d. urine osmolality

a. >20
b. < 1%
c. <20
d. 500

76

Causes of intrinsic renal failure

Acute interstitial necrosis
Glomerulonephritis
ATN
DIC
Acute pyelonephritis

77

a. BUN/creatinine ratio in intrinsic renal failure
b. FENa
c. Urine Na
d. Urine osmolality

a. < 15
b. > 2%
c. > 40
d. < 350

78

Causes of post-renal disease

Stones, BPH, neoplasia, congenital anomalies
ONLY happens with bilateral obstruction

79

Post-renal azotemia
a. BUN/creatinine
b. FENa
c. Urine Na
d. Urine osmolality

a. Varies
b. > 1% mild, >2% severe
c. >40
d. < 350

80

Consequences of renal failure
MADHUNGER

Metabolic Acidosis
Dyslipidemia
Hyperkalemia (retain K without normal kidney function)
Uremia (Nausea, anorexia, asterixis)
Na/H20 retention
Growth retardation
Erythropoietin failure (anemia)
Renal osteodystrophy

81

What is renal osteodystrophy?

Failure of vitamin D hydroxylation, hypocalcemia, hyperphosphatemia --> secondary hyperparathyroidism
Causes subperiosteal thinning of bones

82

ADPKD

Adults
Bilateral enlarged kidneys
Flank pain, hematuria, HTN, urinary infection, renal failure

83

ARPKD

Kids

84

Fever, Rash, Eosinophilia, Azotemia

Drug Induced Interstitial Nephritis

85

Changes in metabolic panel of renal failure

Elevated potassium
Decreased calcium
Elevated BUN and Cr

86

Thyroid like appearance of kidney

Chronic pyelonephritis

87

Associated with Hodgkin lymphoma

Minimal Change Disease
(effacement of foot processes from cytokines)

88

Selective proteinuria (loss of albumin but not immunoglobulin)

Minimal Change Disease

89

HIV, heroin use, Sickle cell

FSGS

90

Nephrotic syndromes

Minimal Change Disease
Focal Segmental Glomerulosclerosis
Membranous nephropathy
Membrano-Proliferative Glomerulonephritis
Diabetic Nephropathy
Amyloidosis

91

Nephritic syndromes

Post-Strep Glomerulonephritis
IgA Nephropathy
Rapidly Progressive Glomerulonephritis (Goodpastures, Wegeners, Microscopic polyangiitis)
Alport Syndrome
Diffuse Proliferative Glomerulonephritis

92

Positive sodium cyanide nitroprusside test with kidney stones

Cystinuria - Cyanide converts cystine to cysteine and a purple color is created when nitroprusside binds cysteine

93

POTTER Sequence

Pulmonary hypoplasia
Oligohydramnios
Twisted face (flattened)
Twisted skin
Extremity defects
Renal failure (in utero)
Babies who can't PEE in utero, develop Potter sequence

94

Causes of POTTER sequence

ARPKD
Obstructive uropathy (posterior urethral valves)
Bilateral renal agenesis

95

Which artery traps horseshoe kidney?
What is it associated with?

Inferior Mesenteric Artery
Turner's syndrome

96

Where does ureter lie compared to uterine artery?

Ureter is UNDER Uterine artery
Water under the bridge

97

How much of body water is extracellular fluid?

1/3 of TBW
20% of body weight (1/3 of 60%)

98

How much of TBW is intracellular fluid?

40% (2/3 of TBW)

99

How much of Extracellular fluid is Interstitial fluid?

75% of ECF

100

How much of Extracellular fluid is Plasma?

25% of ECF

101

What are the units of clearance?

Volume/unit time

102

What is the equation for clearance?

UV/P
U = urine concentration of substance
V = urine flow rate (mL/min)
P = plasma concentration

103

What is the excretion rate equation?

Urine concentration of substance (mg/mL) X urine flow rate (mL/min) = mg/min

104

What is measured to calculate GFR?

Inulin is best but not practical
Creatinine - only a small amount is secreted

105

What is normal GFR?

90-135ml/min (100ml/min)

106

What is renal plasma flow?

Blood going to glomeruli AND blood going to tubules
Estimated with PAH (filtered AND secreted in tubule)

U(PAH) x V/P(PAH

107

What is filtration fraction? What is the equation?

The position blood going to the kidney that is filtered through the glomerulus
FF = GFR/RPF (clearance of creatinine/clearance of PAH)
Normally 20%

108

How do NSAIDS affect GFR?

They constrict afferent arterioles
Decrease RBF and GFR --> no change in FF

109

How does Angiotensin II affect kidney?

Constricts efferent arteriole --> congestion of blood in glomerulus --> Renal blood flow decreases but GFR increases --> filtration fraction increases

110

Effect of ACE inhibitors on kidney

Dilate efferent arteriole --> decrease GFR and increase RPF

111

Constriction of afferent arterioles effects

GFR decrease
RBF decrease
FF no change

112

Constriction of efferent arteriole effects

GFR increase
RBF decrease
FF increase

113

Dilation of afferent arteriole effects

GFR increase
RBF increase
FF no change

114

Dilation of efferent arteriole effects

GFR decrease
RBF increase
FF decrease

115

Increase in serum protein effects on GFR, RBF, FF

GFR decrease
RBF no change
FF decrease

116

Ureter stone obstruction

GFR decrease (back up of urine causes increased hydrostatic pressure in the tubules --> favors blood staying in capillaries)
RBF no change
FF decrease

117

ACE inhibitors effect on GFR, RBF, FF

GFR decrease
RBF increase
FF decrease
-This is why serum creatinine goes up initially when patients are started on ACE inhibitors

118

NSAIDS effect on GFR, RBF, FF

GFR decrease
RBF decrease
FF no change

119

What is the filtered load equation?

GFR x the plasma concentration of the substance

120

What is the excretion rate equation?

urine concentration x urine flow rate (U x V)

121

What is threshold for glucosuria?

Plasma glucose of 200mg/dL

122

When are all glucose transporters fully saturated?

Plasma glucose of 375mg/dL

123

What is Hartnup disease?

Deficiency in transporter for neutral amino acids like Tryptophan in proximal renal tubules --> aminoaciduria and decrease absorption from gut --> no tryptophan for conversion to niacin (B3) --> pellagra (diarrhea, dementia, dermatitis)

124

How do you treat Hartnup disease?

High protein diet
Nicotinic acid

125

Where are glucose and amino acids reabsorbed?

ALL in the proximal tubule

126

What kind of absorption takes place in proximal tubule?

Isotonic absorption

127

What does carbonic anhydrase do?

Converts CO2 and H2O into H+ and Bicarb --> bicarb is reabsorbed into the interstitium (blood)

128

Which part of the nephron is impermeable to water?

The thick ascending loop of Henle

129

Which part of the nephron is impermeable to Na?

Thick descending loop of Henle - passively absorbs water (it is a concentrating segment --> makes urine hypertonic)

130

Where is the Na/K/Cl transporter?

Thick ascending loop of Henle

131

Which class of drugs inhibits the Na/2Cl/K symporter in the thick ascending loop of Henle?
What kind of water excretion do these drugs cause?

Loop diuretic
Isotonic water excretion

132

How and where are Ca and Mg reabsorbed in the nephron?

In the thick ascending limb they are absorbed paracellularly through positive lumen potential generated by K+ back leak

133

What is happening in early distal convuluted tubule?

Reabsorbs Na/Cl
Makes urine most dilute (hypotonic)
PTH increases reabsorption of Calcium through Ca/Na exchanger

134

What actions are taking place in collecting tubule?

Reabsorbs Na in exchange for secreting K/H (action of Aldosterone)
Water is reabsorbed - ADH

135

What two types of cells compose the collecting duct and the last segment of the distal tubule? What do they do?

Principal cells - Reabsorb Na, H20 and secrete K
Intercalated cells - Secrete Hydrogen, bicarb and reabsorb K

136

What determines how much water is reabsorbed in collecting tubule?

ADH - acts on V2 receptors on principal cells and tells them to inset Aquaporin water channels

137

What class of diuretics directly affects the principal cells?

K sparing diuretics
Spironolactone/Epleronone = aldosterone antagonists
Inhibit epithelial Na channels - Triamterene, Amiloride

138

What effect does aldosterone have on principal cells and intercalated cells of collecting duct?

Principal cells - Reabsorption of Na and secretion of K
Intercalated cells - Stimulates secretion of H+ ions

139

Site of secretion of organic anions and cations

Proximal tubule

140

Site of isotonic fluid reabsorption

Proximal tubule

141

Site responsible for diluting urine

Thick ascending limb

142

Mechanism of Acetazolamide

Carbonic anhydrase inhibitor --> inhibits formation of H+ and bicarb from CO2/H2O --> causes limited NaHCO3 diuresis and decreased total body bicarbonate stores

143

Uses for Acetazolamide

Glaucoma - (bc Bicarb draws water into the eye to make aqueous humor)
Urinary alkalinization
Metabolic alkalosis
Altitude sickness - (partial pressure of O is lower so you have to breathe faster and deeper --> blow off CO2 --> respiratory alkalosis)
Pseudotumor cerebri

144

S/E of Acetazolamide

Metabolic acidosis
NH3 toxicity
Sulfa allergy!!!

145

What are the sulfa drugs?

Acetazolamide
Furosemide, Bumetanide, Torsemide

146

What is mechanism of Mannitol

Osmotic diuretic that prevents reabsorption of free H20 --> increases urine flow --> decreases intracranial/intraocular pressure

147

What is the use of Mannitol?

Drug overdose
Elevated intracranial/intraocular pressure - with acute glaucoma
Shock

148

S/E of Mannitol

Pulmonary edema
Dehydration - from losing free water
C/I in anuria, HF

149

Furosemide, Bumetanide, Torsemide mechanism

Loop diuretic; inhibits Na/K/2Cl transporter in thick ascending limb; prevent concentration of urine
LOSE CALCIUM (loops lose calcium, thiazides retain calcium)

150

Ethacrynic acid

Loop diuretic that is NOT a sulfonamide
Can be used in patients with Sulfa allergy

151

Use of loop diuretics

Patients with serious edema
CHF
Pulmonary edema
Nephrotic syndrome
Cirrhosis

152

S/E of loop diuretics

Ototoxicity
HYPOkalemia
Dehydration
Nephrotoxicity
Gout - interfere with uric acid secretion
Allergy (SULFA)

153

Chlorthalidone, HCTZ mechanism

Inhibit Na/Cl reabsorption in early DCT --> decrease diluting capacity of nephron
Retain Calcium (decrease Ca excretion)

154

Uses for Thiazide diuretics

HTN
HF
Idiopathic hypercalciuria (normal serocalcemia but dumps a lot in urine --> calcium stones)
Nephrogenic diabetes insipidus

155

S/E of Thiazides

Hyper LIPIDEMIA
hyper GLYCEMIA
hyper CALCEMIA
hyper URICEMIA
Sulfa allergy

156

Uses for K sparing diuretics

Hyperaldosteronism
K depletion
HF (improve mortality)

157

S/E of K sparing diuretics

Hyperkalemia --> arrhythmia
Endocrine effects (gynecomastia, anti-androgen)

158

Mechanism of Tiamterene, Amiloride

Block Na channels in the cortical collecting tubule --> spare K

159

What are kidney endocrine functions?

Make EPO in response to hypoxia
1alpha hydroxylase converts vitamin D into active form (1,25 OH2 D3) when stimulated by PTH
Renin is secreted by JG cells in response to decreased renal arterial pressure and increased renal sympathetic discharge (B1)

160

When is PTH secreted?
What are it's actions?

PTH is secreted in response to low calcium, increased phosphate or low vitamin D
It activates vitamin D, increases Calcium reabsorption and decreases phosphate reabsorption

161

When is ANP secreted?
What are it's actions?

Secreted in response to increased atrial pressure
Causes increased GFR and increases Na filtration with NO compensatory REABSORPTION of Na --> Na, volume loss

162

How does Lithium cause Diabetes Insipidus?

ADH causes aquaporins to be put into luminal cell to reabsorb water --> lithium interferes with this process

163

Signs of hyponatremia

Confusion, altered mental status
Seizures
Stupor
Coma
(messes with resting potential or neurons)

164

Signs of hypercalcemia

Stones
Bones
Groans (abdominal)
Psychiatric overtones (confusion, delirium)

165

Hypocalcemia signs

Tetani (Trousseau sign = Tighten BP cuff, Chvostek sign = cheek)

166

Hypomagnesemia signs

Tetani

167

Hypermagnesemia signs

Depressed reflexes

168

Hypokalemia

Prolongs QT interval --V tach and Torsades
Flattened T waves

169

Hyperkalemia

V tach
PEAKED T waves

170

What kinds of things shift K outside of cells --> hyperkalemia?

Low insulin
Beta blockers
Acidosis - cells trying to correct acidosis by moving H+ ions out of blood (exchange H for K)
Digoxin
Cellular lysis (leukemia)

171

What kinds of things shift K inside to cells?

Insulin
Beta agonist
Alkalosis
Cell formation

172

Three emergency treatments for hypokalemia?

Beta agonist (Albuterol)
IV Insulin
IV Bicarb

173

Treatment for central DI

Desmopressin

174

Treatment for nephrogenic DI

HCTZ
Indomethacin
Amiloride

175

Treatment for Lithium-Induced Nephrogenic DI

Amiloride

176

Causes of hypernatremia

Diuretics
Dehydration
Diabetes Insipidus
Docs (iatrogenic)
Diarrhea
Disease of Kidney

177

Causes of respiratory acidosis

Hypoventilating
Airway obstruction
Air trapping
Lung disease (interstitial especially)
Weak respiratory muscles
Opioids

178

Causes of metabolic acidosis

Adding acid to blood of losing excessive Bicarbonate
Can be classified by high or low metabolic anion gap

179

Increased anion gap metabolic acidosis (MUDPILES)

(ADDING ACID TO BLOOD)
Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets/Isoniazid
Lactic acidosis (shock, not perfusing)
Ethylene glycol
Salicylates (LATE)

180

Normal anion gap metabolic acidosis (HARD-ASS)

(FROM LOSING BICARBONATE)
Hyperalimentation
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion

181

Causes of respiratory alkalosis

Hyperventilating --> blowing off CO2
Psychogenic
High altitude
Acute hypoxemia (PE)
Aspirin toxicity (EARLY) --ASA directly stimulates respiratory center in brain and causes hyperventilation and later you MIGHT see metabolic acidosis

182

Causes of metabolic alkalosis

Losing Hydrogen ions
Excessive vomiting
Diuretics
Hyperaldosteronism (Hypokalemia, hypertension, metabolic alkalosis)

183

Renal Tubular Acidosis

1. Type 1 RTA - distal; alpha intercalated cells can't secrete hydrogen --> metabolic acidosis ---> hypokalemia, urine pH > 5.5, increased bone turnover
2. Type 2 RTA - proximal; defect in PCT Bicarbonate reabsorption
3. Type 4 RTA - from hyperaldosteronism --> causes hyperkalemia --> decreased ammonia synthesis in PCT --> decreased NH4 excretion, urine pH < 5.5; Caused by decreased aldosterone production, aldosterone resistance

184

What is winter's formula?

Pco2 = 1.5 (HCO3) + 8 +/- 2
Not that important for Step1

185

pH 7.4
HCO3 23
pCO2 40

Normal

186

pH 7.5
HCO3 35
pCO2 42

Metabolic alkalosis

187

pH 7.33
HCO3 13
pCO2 28

Metabolic acidosis with respiratory compensation

188

pH 7.42
HCO3 32
pCO2 64

Mixed respiratory acidosis/metabolic alkalosis

189

pH 7.2
HCO3 18
pCO2 40

Metabolic acidosis

190

pH 7.20
HCO3 24
CO2 54

Respiratory acidosis

191

pH 7.52
HCO3 22
CO2 22

Respiratory alkalosis

192

pH 7.66
HCO3 36
pCO2 30

Mixed alkalosis

193

pH 7.47
HCO3 14
PCO2 22

Respiratory alkalosis with metabolic compensation

194

pH 7.46
HCO3 35
PCO2 53

Metabolic alkalosis with respiratory compensation

195

pH 7.39
HCO3 12
PCO2 22

Mixed metabolic acidosis/respiratory alkalosis

196

pH 7.34
HCO3 31
pCO2 62

Respiratory acidosis with metabolic compensation

197

pH 7.10
HCO3 15
pCO2 50

Mixed acidosis

198

a. What is the pronephros?
b. What is the mesonephros?
c. What is the metanephros?

a. The embryonic kidney up until week 4 and then it degenerates
b. Functions as interim kidney for 1st trimester; later contributes to male genital system
c. Permanent; appears in 5th week of gestation; nephrogenesis continues through 32-36 weeks of gestation

199

Which embryologic kidney is permanent?

Metanephros

200

Parts of metanephros?

a. Ureteric bud - derived from caudal end of mesonephric duct; gives rise to ureter, pelvises, calyces, collecting ducts --> entire collecting system
b. Metanephric mesenchyme - ureteric bud interacts with this tissue to induce differentiation and formation of glomerulus through to distal convoluted tubule

201

What can cause several congenital malformations of the kidney during embryogenesis?

If the ureteric bud and metanephric mesenchyme interaction is abnormal

202

What is the last part of the kidney to canalize? Why is this significant?

The ureteropelvic junction; it is the MOST common site of obstruction (hydrophrosis) in fetus

203

Cause of multi cystic dysplastic kidney

Abnormal interaction between ureteric bud and metanephric mesenchyme

204

Cause of duplex collecting system

Bifurcation of ureteric bud before it enters the metanephric blastema creates Y shaped bifid ureter or can occur when two ureteric buds reach and interact with metanephric blastema

205

Associations with duplex collecting system

Vesicoureteral reflux
Ureteral obstruction
Increased risk for UTIs

206

Why if left kidney taken during donor transplantation?

Left renal vein is longer

207

Which vessels are at risk of damage during gynecologic procedures?

If there is ligation of uterine vessels in the cardinal ligament there is a possibility of damaging ureter --> ureteral obstruction or leak

208

What makes up the glomerular filtration barrier?

Fenestrated capillary endothelium (size barrier)
Fused basement membrane with heparin sulfate (negative charge barrier)
Epithelial layer consisting of podocyte foot processes

209

Which part of the glomerular filtration barrier is lost in nephrotic syndrome?

The charge barrier is lost --> albuminuria, hypoproteinemia, generalized edema, hyperlipidemia

210

Equation for RBF

RBF = RPF/(1-Hct)

211

What is the normal filtration fraction?

20%

212

Estimate of GFR?
Estimate of Renal plasma flow?

GFR = creatinine clearance
RPF = PAH clearance (Filtered and secreted = 100% excretion)

213

How does constriction of ureter change GFR, RPF and FF?

Causes decreased GFR, no change in RPF and decreased FF

214

Where is glucose reabsorbed?

100% reabsorbed in proximal tubule by Na/glucose co-transport

215

What happens to glucose regulation in kidney during pregnancy?

It may decrease the ability of PCT to reabsorb glucose and amino acids --> glucosuria and aminoaciduria

216

What is Hartnup disease?

Deficiency of neutral amino acid transporter in proximal renal tubular cells and enterocytes --> neutral aminoaciduria and decreased absorption form the gut --> decreased tryptophan for conversion to niacin --> pellagra (diabetes, dementia, dermatitis)

217

How do you treat Hartnup disease?

High protein diet and nicotinic acid

218

Where does Angiotensin II exert it's effects?

The proximal tubules (Na/H exchanger) --> causes Na, H20 and bicarb reabsorption

219

Where does Parathyroid hormone exert effects in nephron?

1. Inhibits Na/PO4 co-transport in PCT --> causes PO4 excretion
2. Causes increased Ca/Na exchange in early distal convoluted tubule --> increased Ca reabsorption

220

Where does ADH act?

Acts at V2 receptor (Gs receptor) --> insertion of aquaporin H20 channels on apical side --> increased H20 reabsorption

221

Where does Aldosterone act?

a. Acts on mineralcorticoid receptor --> mRNA --> protein synthsis
b. In Principal cells it causes apical K+ conductance, increased activity of Na/K pump, Increased ENaC channels --> lumen negativity --> K+ loss
c. In alpha-intercalated cells --> increased H+ ATPase activity --> HCO3/Cl exchanger activity

222

Generalized reabsorptive defect in PCT
What does it cause?

Fanconi syndrome
Increased excretion of all amino acids, glucose, HCO3, PCO4
May result in metabolic acidosis

223

Reabsorptive defect in thick ascending loop of Henle
Results in what?

Bartter syndrome
Affects Na/K/2Cl co-transporter --> results in hypokalemia and metabolic alkalosis with hypercalciuria

224

Reabsorptive defect of NaCl in DCT
Results?

Gitelman syndrome (less severe than Bartter)
Causes hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria

225

Gain of function mutation --> increased Na reabsorption in collecting tubules

Liddle syndrome

226

Hypertension, hypokalemia, metabolic alkalosis, decreased aldosterone (not deficiency of 11B hydroxysteroid dehydrogenase)

Liddle syndrome (autosomal dominant)

227

Treatment of Liddle syndrome

Amiloride (blocks Na channels in collecting tubule)

228

11B-hydroxysteroid dehydrogenase deficiency

Syndrome of apparent mineralcorticoid excess --> cortisol doesn't get converted to cortisone and excess cortisol acts on mineralocorticoid receptors to cause hypertension, hypokalemia, metabolic alkalosis

229

Acquired 11B-hydroxysteroid dehydrogenase deficiency

From licorice (glycyrrhetic acid)

230

Where does ACE come from?

Lungs and kidney

231

What causes increased production of renin?

1. Decreased BP sensed by JG cells
2. Decreased Na delivery sensed by macula densa
3. Increased sympathetic tone (B1 receptors) (Gs)

232

Where does Angiotensinogen come from?

Liver

233

Effects of AT II
How does it avoid reflex bradycardia?

Acts at angiotensin II receptor on vascular smooth muscle to cause vasoconstriction and increased BP
It affects baroreceptor function and limits reflex bradycardia which would normally accompany pressor effects

234

What does ADH primarily regulate?

Osmolarity (but also responds to low volume state)

235

What dose Aldosterone primarily regulate?

ECF volume and Na content (but also responds to low volume states)

236

What makes up the Juxtaglomerular apparatus?

Mesangial cells
JG cells (modified smooth muscle of afferent arteriole)
Macula densa (NaCl sensor, part of DCT)

237

Function of JG cells?

Secrete renin in response to decreased renal BP and increased sympathetic tone

238

Function of macula densa?

Sense decreased NaCl delivery to DCT --> cause adenosine release --> vasoconstriction

239

How do beta blockers decrease BP through the kidney?

They inhibit B1 receptors of the JGA and cause decreased renin release

240

Kidney endocrine functions (4)

1. EPO is released by interstitial cells in peritubular capillary bed in response to hypoxia
2. PCT cells convert 25-OH vitamin D to 1,25-OH2 Vitamin D via 1alpha hydroxylase
3. JG cells secrete renin in response to decreased renal arterial pressure and increased sympathetic tone
4. Paracrine secretion of prostaglandins vasodilator the afferent arterioles to increase RBF

241

What K+ shift does Digitalis cause?

Shifts K+ out of cells causing hyperkalemia (blocks Na/K ATPase)

242

Things causing Hyperkalemia (6)

Digitalis
Hyperosmolarity
Lysis of cells (crush injury, rhabdomyolysis, cancer)
Acidosis
Beta blocker
High blood sugar (insulin deficiency)

243

Things causing Hypokalemia (4)

Hypo-osmolarity
Alkalosis
Beta adrenergic agonist (increased Na/K ATPase)
Insulin (increased Na/K ATPase; shifts K into cells)

244

Electrolyte disturbance causing tetany, seizures, QT prolongation

HYPOcalcemia

245

Electrolyte disturbance causing stones, bones, groans, thrones, psych overtones

HYPERcalcemia

246

Electrolyte disturbance causing nausea, malaise, stupor, coma seizures

HYPOnatremia

247

Electrolyte disturbance causing U waves on EKG, flattened T waves, arrhythmias, muscle spasm

HYPOkalemia

248

Electrolyte disturbance causing wide QRS and peaked T waves on EKG, arrhythmias, muscle weakness

HYPERkalemia

249

Electrolyte disturbance causing torsade de pointes, tetany, hypokalemia

HYPOmagnesium

250

Causes of respiratory acidosis

Hypoventilation (caused by airway obstruction, acute or chronic lung disease, opioids or sedatives, weakened respiratory muscles)

251

a. Another name for Methanol
b. Another name for Ethylene glycol

a. Formic acid
b. Oxalic acid

252

Cause of Normal anion gap metabolic acidosis (HARDASS)

Hyperalimentation
Addison disease - hypoaldosteronism
Renal tubular acidosis
Diarrhea - losing bicarbonate
Acetazolamide - not reabsorbing bicarbonate
Spironolactone
Saline infusion

253

Flank pain, hematuria, oliguria with high anion gap metabolic acidosis

Ethylene glycol poisoning

254

Cause of distal (type 1) renal tubular acidosis

Defect in ability of alpha intercalated cells to secrete H+ --> can't generate HCO3 --> metabolic acidosis

255

Symptoms of distal (type 1) renal tubular acidosis

Urine pH > 5.5
Hypokalemia
Increased risk for calcium phosphate kidney stones (from increased urine pH and bone turnover)
Normal anion gap metabolic acidosis

256

Cause of Proximal (type 2) renal tubular acidosis

Defect in PCT HCO3 reabsorption --> increased excretion of HCO3 in urine

257

Causes of proximal renal tubular acidosis

Fanconi syndrome
Carbonic anhydrase inhibitors (Acetazolamide)

258

Cause of hyperkalemic (type 4) renal tubular acidosis

Hypoaldosteronism --> hyperkalemia --> decreased NH3 synthesis in PCT --> decreased NH4 excretion

259

Urine pH in hyperkalemic (type 4) renal tubular acidosis

260

Hematuria but no casts

Bladder cancer or kidney stones

261

Pyuria and no casts

Acute cystitis

262

What do presence of casts signify?

Hematuria/pyuria is of glomerular or renal tubular origin

263

Increased anti-DNase B titers, decreased complement levels

Acute post-strep glomerulonephritis

264

What do crescents consist of in Rapidly progressive glomerulonephritis?

Fibrin and plasma proteins (C3b) with glomerular parietal cells, monocytes, macrophages

265

Treatment of rapidly progressive glomerulonephritis

Emergent plasmapheresis

266

MPO-ANCA

p-ANCA --> Microscopic polyangiitis

267

Basket weave appearance on EM

Alport syndrome (mutation in type IV collagen --> thinning and splitting of glomerular basement membrane)

268

Stones that precipitate at
a. increased pH
b. decreased pH

a. Calcium phosphate, Ammonium magnesium phosphate (Struvite)
b. Calcium oxalate, Uric acid, Cystine

269

Causes of calcium oxalate stones

Ethylene glycol (antifreeze) ingestion
Vitamin C abuse
Hypocitraturia
Malabsorption (Crohn's)

270

Treatment for calcium oxalate/phosphate stones

Increased citrate
Thiazide diuretics
Hydration

271

Bugs causing struvite stones

Proteus mirabilis
Staph saprophyticus
Klebsiella
(all urease +)

272

How does renal cell carcinoma spread?

Invades renal vein then IVC --> spreads hematogenously and metastasizes to lung and bone

273

Gene deletion associated with Renal cell carcinoma

Gene deletion on chromosome 3 (sporadic or inherited in von Hippel-Lindau)

274

Paraneoplastic syndromes associated with renal cell carcinoma

Ectopic EPO, ACTH, PTHrP

275

Renal oncocytoma histology

Large eosinophilic cells with abundant mitochondria without perinuclear clearing

276

Painless hematuria without casts

Bladder cancer

277

Associations of transitional cell carcinoma of bladder (P SAC)

Phenacetin, Smoking, Aniline dyes, Cyclphosphamide

278

Risk factors for squamous cell carcinoma of bladder

Schistosoma haematobium
Chronic cystitis
Smoking
Chronic nephrolithiasis

279

Lab findings of acute bacterial cystitis

+ leukocyte esterase
+ nitrites (for gram negative organisms)

280

Urethritis with sterile pyuria and negative urine cultures

Neisseria gonorrhoeae or Chlamydia trachomatis

281

Striated parenchymal enhancement of kidney on CT

Acute pyelonephritis

282

Thyroidization of kidney

Chronic pyelonephritis

283

Drugs causing acute interstitial nephritis

Diuretics
Penicillins
Proton pump inhibitors
Sulonamides
Rifampin
NSAIDS - (months after for this one)

284

Causes of acute tubular necrosis

Ischemic injury or nephrotoxic injury by drugs/crush injury/hemoglobinuria

285

SAAD with papillary necrosis

Sickle cell
Acute pyelonephritis
Analgesics (NSAIDs)
Diabetes mellitus

286

How do the following affect serum Calcium?
a. Hyperphosphateima
b. Decreased Vitamin D

a. Decreased serum Calcium by causing tissue calcifications
b. Decreased intestinal Ca absorption

287

Associations of ADPKD

Berry aneurysms
Mitral valve prolapse
Benign hepatic cysts

288

Associated with congenital hepatic fibrosis

ARPKD

289

Shrunken kidneys on ultrasound
Inability to concentrate urine

Medullary cystic disease

290

What are the types of renal cysts?
Which ones need to be removed?

Simple - very common, clear on US, typically asymptomatic and found incidentally
Complex - septated, enhanced or have solid components on imaging; require follow up or removal due to risk of RCC