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STEP 1 > 10a: Renal > Flashcards

10a: Renal Flashcards

1
Q

Embryology: the (X) functions as the interim kidney in developing embryo for the first (Y) weeks

A 
X = mesonephros
Y = 12 (first trimester)
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2
Q

The ureteric bud arises from (X) and eventually gives rise to which part(s) of kidney?

A

X = caudal end of mesonephric duct

Ureter, pelvises, calyces, collecting ducts

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3
Q

Woman taking (X) drugs puts baby at risk for Potter sequences. What are the symptoms/findings?

A

X = ACEi/ARB (causes oligohydramnios, since A-II required for kidney development)

“POTTER” =

  1. Pulmonary hypoplasia (cause of death)
  2. Oligohydramnios
  3. Twisted face (low-set ears, retrognathia, flat nose)
  4. Twisted skin
  5. Extremity defects (club feet)
  6. Renal failure in utero
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4
Q

Patient with Duplex Collecting system is at high risk for:

A

UTIs (strongly associated with vesicoureteral reflux and ureteral obstruction)

Note: Duplex collecting system means two ureters for one kidney

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5
Q

Which amino acid is provided by amniotic fluid and helps in fetal lung development?

A

Proline

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6
Q

List the components of the glomerular filtration barrier, starting from inside Bowman capsule

A
  1. Podocytes (epithelial layer)
  2. Glomerular BM
  3. Fenestrated capillary endothelium
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7
Q

T/F: The mesangial cells of the kidney are located in Bowman capsule

A

False - located near afferent/efferent arterioles in glomerulus

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8
Q

Ureters pass (over/under) which key vessels in males/females?

A

Under (“water under the bridge”)
F: uterine artery
M: vas deferens

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9
Q

Plasma volume, part of (ECF/ICF) can be measured by which method?

A

ECF (25% of it)

Radiolabeling albumin

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10
Q

ECF volume can be measured by which method?

A

Radiolabeling mannitol or inulin

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11
Q

Glomerular filtration barrier is selective based on size and charge of molecules. Which parts of barrier are responsible for these?

A

Size: slit diaphragm (podocyte feet with basement membrane) and fenestrated capillary endothelium

Charge: negatively-charged glycoproteins on all three layers (prevent neg-charged molecules from entering)

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12
Q

Renal clearance equation:

A

(Ux)*(V)/(Px)

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13
Q

T/F: Oncotic pressure of glomerular capillary normally equals zero

A

False - oncotic pressure of Bowman space normally zero

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14
Q

Best estimate of GFR is (X). (Y) is also used, but tends to (over/under)-estimate the value

A

X = inulin clearance
Y = creatinine clearance;
Over-estimates (moderately secreted by tubules)

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15
Q

A reduction of GFR by half will (increase/decrease) serum Cr by which factor?

A

Increase; 2x

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16
Q

Renal (plasma/blood) flow can be estimated using (X) clearance

A 
Plasma flow (RPF)
X = PAH (para-aminohippuric acid)

Note: Renal blood flow can be calculated via RPF/(1-Hct)

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17
Q

Filtration fraction equation:

A

GFR/RPF (normally about 20%)

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18
Q

Filtered load equation:

A

GFR*Px

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19
Q

Prostaglandins (dilate/constrict) (X) arteriole in kidney and Angiotensin II (dilates/constricts) (Y) arteriole. Which of these affects filtration fraction?

A

Dilate;
X = afferent
Constricts
Y = efferent

Angiotensin II (increases FF since increases GFR, decreases RPF)

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20
Q

How does dehydration affect filtration fraction in kidney?

A

Decrease (decrease in GFR, but even greater decrease in RPF)

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21
Q

After certain point, efferent arteriole constriction will actually decrease (GFR/FF).

A

GFR (flow-mediated increase in glomerular cap oncotic P)

Note: FF will ALWAYS be increased with efferent arteriole constriction due to greater decrease in RPF

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22
Q

Glucosuria in normal adult will begin at plasma conc of (X). And at transport rate of (Y) mg/min, all transporters are fully saturated

A 
X = 200 mg/dL
Y = 375
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23
Q

In metabolic (acidosis/alkalosis), renal ammoniagenesis is stimulated. (X) is metabolized to eventually form ammonium and (Y).

A

Acidosis
X = glutamine (to glutamate and then to alpha-KG and then to glucose + CO2)
Y = HCO3 (combines with CO2 and reabsorbed into blood)

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24
Q

Posterior fracture of L 12th rib: which structure likely injured?

A

L kidney

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25
Q

Ureter courses (anterior/posterior) to gonadal vessels and then anterior to (X) key vessel in the true pelvis

A

Posterior

X = internal iliac a

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26
Q

T/F: PCT absorbs the majority of water, regardless of hydration status

A

True (60%)

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27
Q

Which key hormones work on the proximal tubule?

A
  1. A-II: increases Na/H exchange to increase Na, H2O and HCO3 reabsorption
  2. PTH: inhibits Na/PO4 co-transport (increases PO4 excretion)
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28
Q

(X) portion of tubule is the concentrating segment. And (Y) is the diluting segment.

A 
X = thin descending loop of Henle (permeable to water, not solutes)
Y = thick ascending loop of Henle (permeable to solutes, not water)
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29
Q

Thick ascending loop of Henle: which ions are reabsorbed by transporter?

A

Na/K/Cl2 co-transporter

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30
Q

Describe the mechanism behind paracellular transport of (X) ions in (Y) segment of kidney tubules

A 
X = Mg, Ca
Y = Thick ascending limb

K back-leak into lumen gives it positive potential, inducing paracellular reabsorption of Mg, Ca into interstitium

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31
Q

Which key ions are being reabsorbed in DCT of kidney?

A

Na/Cl (cotransporter); Ca (channel)

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32
Q

Which key hormones work on the distal convoluted tubule?

A
  1. PTH: upregulates basolateral Na/Ca antiporter to increase Ca reabsorption (decreasing Ca conc in tubule cell induces more Ca absorption from lumen via apical channel)
  2. A-II (increase Na reabsorption)
  3. ANP (decrease Na reabsorption)
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33
Q

T/F: Aldosterone binds to Collecting tubule transporters to upregulate Na absorption at the expense of H and K.

A

False - binds to mineralocorticoid receptors and upregulates gene expression/protein synthesis of the transporters

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34
Q

Alpha-intercalated cell: H (enters/exits) lumen while (X) (enters/exits).

A

Enters (secreted from alpha-intercalated cell)
X = K exits (reabsorbed into cell)

H/K ATPase; ammonium is generated in lumen

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35
Q

(X) cells in Collecting duct of nephron are responsible for reabsorbing Na from lumen via (Y) channel

A 
X = Principal 
Y = ENaC (apical membrane)
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36
Q

Child presents with hypertension, hypokalemia, and metabolic alkalosis, so you check (X) levels and find they are undetectable. If this is a receptor issue, what’s the likely Dx? Rx?

A

X = aldosterone

Liddle syndrome (hyperactive ENaC); Amiloride

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37
Q

Fanconi syndrome: main defect is…

A

Decreased reabsorption of AA, glucose, HCO3, PO4 in PCT (resulting in Type II renal tubule acidosis)

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38
Q

(X) syndrome is reabsorptive defect in thick ascending loop of Henle, affecting (Y) transporter.

A 
X = Bartter (AR inheritance)
Y = Na/K/Cl2 (presents similarly to chronic loop diuretic use)
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39
Q

(X) syndrome is reabsorptive defect in DCT, affecting (Y) transporter.

A 
X = Gitelman (AR inheritance)
Y = Na/Cl co-transporter (similar to using chronic thiazide diuretics)
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40
Q

Which metabolic abnormalities would you expect to see in Bartter syndrome?

A

Decreased Na/K/Cl2 transport in TAL

Hypokalemia, metabolic alkalosis, Hypocalcemia (hypercalciuria)

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41
Q

Which metabolic abnormalities would you expect to see in Gitelman syndrome?

A

Decreased Na/Cl co-transport in DCT

Hypokalemia, metabolic alkalosis, Hypercalcemia (hypocalciuria), HypoMg-emia

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42
Q

Syndrome of apparent mineralocorticoid excess: what’s the main defect?

A

Deficiency of 11-beta-hydroxysteroid dehydrogenase (typically converts cortisol to cortisone, the latter of which is inactive on mineralocorticoid receptors)

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43
Q

Syndrome of apparent mineralocorticoid excess: what are the main symptoms?

A

Similar to hyperaldosteronism (hypertension, hypokalemia, metabolic alkalosis) but low aldosterone levels since cortisol is activating the mineralocorticoid receptors

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44
Q

Patient eating (X), which is present in licorice, can acquire which syndrome?

A

X = glycyrrhetinic acid

Syndrome of apparent mineralocorticoid excess

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45
Q

Syndrome of apparent mineralocorticoid excess: Rx?

A

Corticosteroids (to decrease endogenous cortisol production)

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46
Q

List the solutes absorbed more quickly than water in the PCT

A

Glucose, AA, HCO3

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47
Q

Along the proximal tubule, tubular inulin (increases/decreases/doesn’t change) in concentration. And in total amount?

A

Increases in concentration, but not amount (due to H2O reabsorption)

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48
Q

In early PCT, Cl reabsorption occurs at (faster/slower/same) rate as Na

A

Slower (then matches Na reabsorption rate more distally)

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49
Q

Angiotensin II has effects on which parts of brain?

A
  1. Post pit (increase ADH secretion)

2. Hypothalamus (increase thirst)

50
Q

ANP and BNP have which effect on GFR?

A

Increase (dilate afferent, constrict efferent; promote natiuresis)

51
Q

List the components of the Juxtaglomerular apparatus

A
  1. Mesangial cells
  2. JG cells = modified smooth muscle (of afferent arteriole)
  3. Macula densa = NaCl sensor (of DCT)
52
Q

Where is 1-alpha hydroxylase found in kidney?

A

PCT cells

53
Q

(X) chatecholamine is secreted by (Y) tubular cells in kidney and works to promote:

A 
X = DA
Y = PCT

Natriuresis (at low doses; vasodilator that increases RBF)

54
Q

(X) (increases/decreases) urea permeability in collecting duct

A

X = ADH

Increases

55
Q

(Acidosis/alkalosis), (hyper/hypo)-osmolarity, and (X) adrenergic (agonists/antagonists) shift K out of cells.

A

Acidosis; hyperosmolarity

X = beta antagonists (decrease Na/K ATPase)

56
Q

Which key drugs shift potassium out of cells (causing hyperkalemia)?

A
  1. Digoxin
  2. BB
  3. Succinylcholine
57
Q

Which electrolyte abnormality causes U waves on EKG?

A

Hypokalemia

58
Q

Muscle weakness is primarily a feature of which electrolyte abnormality?

A

Low or high K

59
Q

Hypercalcemia symptoms

A

“Stones, bones, groans, thrones, pysch overtones”

  1. Renal stones
  2. Bone pain
  3. Abdominal pain
  4. Increased urinary frequency
  5. Anxiety, altered mental status
60
Q

Which electrolyte disturbance can cause Torsades?

A

Hypomagnesemia

Hypocalcemia can cause prolonged QT

61
Q

Osteomalacia/rickets primarily due to which electrolyte disturbance?

A

Low PO4

62
Q

Gap metabolic acidosis differential

A

MUDPILES

  1. MeOH
  2. Uremia
  3. DKA
  4. Propylene glycol (antifreeze)
  5. Isoniazid or Iron tablets
  6. Lactic acidosis
  7. Ethylene glycol (antifreeze)
  8. Salicylates (late)
63
Q

Non-gap metabolic acidosis differential

A

HARDASS

  1. Hyperalimentation (artificial nutrient supply)
  2. Addison’s
  3. Renal tubular acidosis
  4. Diarrhea
  5. Acetazolamide
  6. Spironolactone
  7. Saline infusion
64
Q

Chronic COPD patient will likely have which acid/base abnormality?

A

Respiratory acidosis due to hypercapnia (with compensatory increase in serum HCO3 and near-normal pH)

65
Q

Measuring (X) urine levels helps differentiate between etiologies of metabolic alkalosis. Give examples.

A

X = Cl

  1. Loops (increased urine Cl)
  2. Vomiting (decreased urine Cl)
  3. Hyperaldosteronism (high BP and high urine Cl)
66
Q

Renal tubular acidosis with low urine pH

A

Type 4 (hyperkalemic RTA) and early on in Type 2 (PCT RTA)

67
Q

Heparin can cause Type (X) RTA

A

X = 4 (via inhibiting zona glomerulosa and thus aldosterone production)

68
Q

Amphotericin B toxicity can cause Type (X) RTA

A

X = 1 (at DCT)

69
Q

Multiple myeloma can cause Type (X) RTA

A

X = 2 (PCT; Fanconi)

70
Q

Waxy renal casts seen in:

A

ESRD/chronic renal failure

71
Q

Hyaline renal casts seen in:

A

Normal finding (concentrated urine sample)

72
Q

Classic bladder cancer Sx

A

Gross hematuria (gradually reddening urine)

73
Q

Nephritic syndrome is due to (X) disruption whereas nephrotic is due to (Y) disruption

A 
X = GBM (inflammatory process)
Y = podocyte (massive proteinuria)
74
Q

Post-strep glomerulonephritis EM findings

A

Sub-epithelial electron-dense bumps (immune complex)

75
Q

“Granular” appearance of glomerulus on immunofluorescence signifies which pathogenesis?

A

Immune complex (IgG, IgM, C3 deposition)

76
Q

Renal nephritic/nephrotic syndrome: LM shows mesangial proliferation and EM shows mesangial immune complex deposits. Dx?

A

IgA nephropathy (most common glomerulonephritis)

77
Q

Nephritic presentation of SLE is (X). And nephrotic presentation is (Y).

A 
X = Diffuse proliferative glomerulonephritis (common cause of death in SLE)
Y = Membranous nephropathy
78
Q

“Tram tracking” on PAS/H&E stain of glomeruli

A

Membranoproliferative glomerulonephritis (due to mesangial ingrowth splitting GBM)

79
Q

Glomerulonephritis, sensorineural deafness, and retinopathy/lens dislocation

A

Alport syndrome (mutation in type IV collagen leads to thinning/splitting of basement membrane)

“Can’t see, can’t pee, can’t hear a bee”

80
Q

Glomeruli on EM have “basket weave” appearance

A

Alport syndrome (glomerulonephritis)

81
Q

“Wire-looping” capillaries on LM of glomeruli

A

Diffuse proliferative GN (like SLE)

“Wire Loopus”

82
Q

Nephritic syndrome associated with Hep (B/C) infection

A

B or C

Membranoproliferative GN (Type I)

83
Q

Nephritic syndrome associated with C3 nephritic factor activating complement system

A

Membranoproliferative GN (Type II) aka Dense deposit disease

84
Q

(Nephritic/nephrotic) syndrome are accompanied by (increase/decrease) in serum lipid levels. Why?

A

Nephrotic; increase (hyperlipidemia)

Liver senses low serum proteins and so pumps up protein (including lipoproteins) synthesis

85
Q

(Nephritic/nephrotic) syndrome are accompanied by (hyper/hypo)-coagulability. Why?

A

Nephrotic

Hypercoagulability (increased anti-thrombin III loss in urine)

86
Q

(Nephritic/nephrotic) syndrome are accompanied by increased risk of infection. Why?

A

Nephrotic

Increased loss of Ig in urine

87
Q

(X) disease: selective loss of albumin in urine

A

X = minimal change disease (due to podocyte effacement and decreased anionic properties of BM)

Most common nephrotic syndrome in children

88
Q

Minimal change disease Rx

A

Corticosteroids (excellent response)

89
Q

FSGS can be distinguished from minimal change disease via which ways?

A
  1. Non-selective proteinuria (not just albuminuria)

2. Non-responsive to corticosteroids

90
Q

Most common cause of nephrotic syndrome in AA and Hispanics

A

FSGS

91
Q

Nephrotic syndrome(s) associated with Hepatitis B or C infection

A

FSGS, Membranous nephropathy

92
Q

GBM and mesangial changes in diabetic glomerulonephropathy is the result of which process?

A

Non-enzymatic glycosylation (increases GBM thickness/permeability; hyaline arteriosclerosis of efferent arterioles causes mesangial expansion)

93
Q

“Spike and dome” appearance with subepithelial deposits: (X) nephropathy

A

X = membranous (granular due to immune complex deposition)

94
Q

Most common cause of nephrotic syndrome in Caucasian adults

A

Membranous nephropathy

95
Q

Primary Membranous nephropathy MOA:

A

Ab against phosphlipase A2 receptor (abundant on podocytes)

96
Q

Secondary Membranous nephropathy causes

A

SLE, solid tumors (lung, colon), drugs (NSAIDs, gold, penicillamine), infections (HBV, HCV)

97
Q

Nephrotic syndrome(s) associated with HIV and sickle cell disease

A

FSGS

98
Q

Most common kidney stones are (X) stones with which electrolyte abnormality?

A

X = Ca oxalate
Hypercalciuria despite NORMOcalcemia (maybe due to dehydration or increased Ca gut reabsorption followed by immediate secretion)

99
Q

How do citrate levels affect (X) kidney stone formation?

A

X = Ca

Normally bind Ca (and prevent its precipitation) in tubules; in acidemia, citrate reabsorption increased to bind H+ (increase risk Ca kidney stone formation)

100
Q

Diarrhea increases risk of (X) kidney stone formation

A

X = Ca and uric acid
(Diarrhea causes met acidosis, increasing citrate reabsorption; also met acidosis will increase urinary H secretion, acidifying urine and predisposing to Urate stone formation)

101
Q

High protein diet increases risk of (X) kidney stone formation

A

X = Ca

Causes met acidosis due to protein breakdown, increasing citrate reabsorption

102
Q

Ca kidney stones can form as a result of vitamin (X) deficiency

A

X = C (due to low citrate levels)

103
Q

T/F: Low Ca intake will decrease chance of Ca stone formation

A

False - low Ca intake means more free oxalate to be absorbed in gut and thus excreted in urine (Ca oxalate stone formation risk)

104
Q

Most common kidney stones seen in children

A

Ca- phosphate

105
Q

Hereditary disorder in (X) leads to impaired reabsorption of which amino acids, thus disposing child to (Y) kidney stones

A

X = PCT transporter
For Cystine, Ornithine, Arg, Lys (“COAL”)
Y = cystine

106
Q

Na-cyanide and nitropruside added to urine turns it red-purple. What is this a test for?

A

Cystinuria

107
Q

Renal cell carcinoma: gross and histo appearance.

A

Most commonly “clear cell carcinoma”

Gross: golden-yellow (high lipid content)
Histo: Polygonal clear cells (filled with accumulated lipids/CHO)

108
Q

Renal cell carcinoma: originates from (X) cells and most often spreads via (blood/lymph) to which organs?

A

X = PCT
Blood (renal vein if on left, then IVC)
Lung and bone

109
Q

T/F: Renal cell carcinoma is resistant to chemo and radiation

A

True

110
Q

Renal cell tumor arising from collecting ducts

A

Renal oncocytoma (very rare; benign, well-circumscribed with central scar)

111
Q

Child born with mental retardation and Aniridia (absent iris) likely has which tumor?

A

Wilms/Nephroblastoma (WT1 deletion; WAGR complex)

112
Q

Wilms tumor arises from which cells?

A

Metanephric blastema (hence name nephroblastoma)

113
Q

Wilms tumor, early nephrotic syndrome, and male pseudohermaphroditism triad

A

Denys-Drash (WT1 mutation)

114
Q

Wilms tumor, macroglossia, organomegaly

A

Beckwith-Wiedemann (WT2 mutation)

115
Q

“Overactive bladder” aka detrusor hyperactivity is (X) incontinence

A

X = urge (leakage with urge to void immediately)

116
Q

“Underactive bladder” aka detrusor hypoactivity is one cause of (X) incontinence. What’s another cause?

A

X = overflow (incomplete voiding and leaks with overfilling)

Outlet obstruction (ex: BPH)

117
Q

Patient with Multiple Sclerosis presents with incontinence. What is the most likely etiology?

A

Urge (micturition control centers are compromised)

118
Q

“Thyroidization” of kidney refers to:

A

Eosinophilic casts that form due to chronic pyelonephritis (resemble thyroid tissue)

119
Q

Consequences of renal failure:

A

“MAD HUNGER”

  1. Metabolic Acidosis
  2. Dyslipidemia
  3. Hyperkalemia
  4. Uremia (high BUN)
  5. Na/H2O retention (edema, HF, HT)
  6. Growth retardation/developmental delay
  7. EPO failure (anemia)
  8. Renal osteodystrophy (subperiosteal thinning)
120
Q

T/F: Glomeruli are spared in acute interstitial nephritis

A

True

121
Q

Which metabolic abnormalities are seen in maintenance phase of acute tubular necrosis?

A

Hyperkalemia, metabolic acidosis (H+ and anion retention), uremia; also oliguria leading to V overload

122
Q

Which metabolic abnormalities are seen in recovery phase of acute tubular necrosis?

A

Hypokalemia

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