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First Aid Express 2013 workbook: RENAL

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Renal
How to Use the Workbook with the Videos
Using this table as a guide, read the Facts in First Aid for the USMLE Step 1 2013,
watch the corresponding First Aid Express 2013 videos, and then answer the workbook
questions.
Facts in First Aid
for the USMLE
Step 1 2013
478.1478.4

Renal Embryology

12

479.1479.2

Renal Anatomy

34

480.1482.2

Renal Physiology part 1

521

483.1487.2

Renal Physiology part 2

2240

487.3488.2

Renal Physiology part 3

4143

489.1492.1

Renal Pathology part 1

4453

493.1496.2

Renal Pathology part 2

5459

496.3498.1

Renal Pathology part 3

58, 6067

499.1502.1

Renal Pharmacology

6874

Corresponding First Aid Express


2013 video

Workbook
questions

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First Aid Express 2013 workbook: RENAL

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Questions
EMBRYOLOGY
1.

Which genetic disease is associated with horseshoe kidney? (p. 478) _______________________

2.

What are the three causes of Potters syndrome?

. (p. 478) ________________________________

ANATOMY
3.

Why is the left kidney harvested for transplantation rather than the right? (p. 479) ______________
______________________________________________________________________________

4.

Ureters pass __________ (over/under) the uterine artery and the ductus deferens. (p. 479)

PHYSIOLOGY
5.

Extracellular fluid consists of __________ (high/low) sodium chloride and __________ (high/low)
potassium, whereas intracellular fluid consists of __________ (high/low) sodium chloride and
__________ (high/low) potassium. (p. 480)

6.

What is the 60-40-20 rule of total body weight? (p. 480) _________________________________
______________________________________________________________________________

7.

The fenestrated capillary endothelium of the glomerular filtration barrier is responsible for the
filtration of plasma by which characteristic: size or charge? (p. 480) _________________________
______________________________________________________________________________

8.

The fused basement membrane of the glomerulus containing heparan sulfate is responsible for the
filtration of plasma molecules by which characteristic, size or charge? (p. 480)
______________________________________________________________________________

9.

The epithelial layer of the glomerular filtration barrier is formed by which cells? (p. 480)
______________________________________________________________________________

10.

What is the formula for calculating the clearance of substance X, the volume of plasma from which
the substance is cleared completely per unit of time? (p. 480) _____________________________
_____________________________________________________________________________

11.

If renal clearance is greater than the glomerular filtration rate (GFR) of substance X, then there is a
net tubular __________ (reabsorption/secretion) of substance X. (p. 480)

12.

Creatinine clearance slightly __________ (overestimates/underestimates) the GFR rate because


creatinine is __________ (secreted/reabsorbed) by the renal tubules. (p. 480)

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13.

What is the formula for estimating renal blood flow if renal plasma flow is known? (p. 480)
______________________________________________________________________________

14.

What are the effects of prostaglandins on the glomerulus? (p. 481) _________________________
______________________________________________________________________________

15.

What are the effects of angiotensin II on the glomerulus? (p. 481) __________________________
______________________________________________________________________________

16.

Decreased plasma protein concentration causes ____________ (decrease/increase/no change) in


renal plasma flow and ____________ (decrease/increase/no change) in GFR, which in turn results
in ____________ (decrease/increase/no change) in the filtration fraction. (p. 481)

17.

Constriction of the afferent arteriole causes ____________ (decrease/increase/no change) in renal


plasma flow and ____________ (decrease/increase/no change) in GFR, which in turn results in
____________ (decrease/increase/no change) in the filtration fraction. (p. 481)

18.

What is the formula for excretion rate? (p. 481) _________________________________________


______________________________________________________________________________

19.

In the nephron, glucose at normal plasma concentrations is reabsorbed in which structure? And by
which transporter? (p. 482) ________________________________________________________

20.

At what plasma glucose concentration is the transport mechanism of the proximal tubule
completely saturated, leading to glucose spilling into the urine? (p. 482) _____________________

21.

________________________develops due to a deficiency of tryptophan, an amino acid that is


normally reabsorbed in the ___________________ of the kidney. (p. 482) ___________________
______________________________________________________________________________

22.

What ion is secreted into the lumen of the early proximal convoluted tubule and acts to reabsorb
bicarbonate? (p. 483) _____________________________________________________________

23.

Which three ions are actively reabsorbed in the thick ascending loop of Henle? (p. 483) ________
______________________________________________________________________________

24.

Which two ions are indirectly reabsorbed in the thick ascending loop of Henle? (p. 483)
______________________________________________________________________________

25.

Which hormone controls the reabsorption of calcium in the early distal convoluted tubule? (p. 483)
______________________________________________________________________________

26.

On which segment of the nephron does the hormone aldosterone act? (p. 483) _______________
______________________________________________________________________________

27.

ADHs effect at V

receptors results in what action? (p. 483) _______________________________

______________________________________________________________________________
28.

The ratio of solute concentration in the tubular fluid versus plasma (TF/P) can indicate the level of
secretion or reabsorption of that solute along the proximal renal tubule. If the TF/P ratio of that
solute is less than that of inulin, there is net ________________ (reabsorption/secretion) along the
proximal tubule. (p.484)

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29.

Along the length of the proximal tubule, does the relative concentration of chloride increase,
decrease, or stay the same? (p. 484) _________________________________________________

30.

Which five actions of angiotensin II serve to increase intravascular volume and blood pressure? (p.
485) __________________________________________________________________________
______________________________________________________________________________

31.

What is the site of action of angiotensin-converting enzyme? (p. 485) _______________________

32.

When blood pressure falls, the kidneys release which proteolytic enzyme? (p. 485) ____________

33.

ADH primarily regulates __________ (osmolarity/blood volume), whereas aldosterone primarily


regulates __________ (osmolarity/blood volume). However, in __________ (low/high) volume
states, both ADH and aldosterone act to protect __________ (osmolarity/blood volume). (p. 485)

34.

What are the effects of aldosterone secretion? (p. 485) __________________________________


______________________________________________________________________________
______________________________________________________________________________

35.

Atrial natriuretic peptide __________ (decreases/increases) renin secretion and _____________


(decreases/increases) the GFR. (p. 485)

36.

Which cells in the kidney secrete renin? (p. 486) _______________________________________

37.

Which hormone is released by the endothelial cells of renal peritubular capillaries in response to
hypoxia? (p. 486) ________________________________________________________________

38.

Which enzyme from the kidney is activated by PTH, and what is the function of that enzyme? (p.
486) __________________________________________________________________________

39.

In the chart below, check the effect that each condition has on the potassium shift. (p. 487)
Effect

Shifts K into Cell


Hypokalemia

Shifts K out of Cell


Hyperkalemia

Acidosis
Alkalosis
-Adrenergic agonists
-Adrenergic antagonists
Cell lysis
Digitalis
Hyperosmolarity
Hypo-osmolarity
Insulin
Insulin deficiency
40.

By what mechanism does insulin cause hypokalemia? (p. 487) __________________________


______________________________________________________________________________

41.

What is the primary electrolyte disturbance in metabolic acidosis? (p. 487) ___________________

____________________________________________________________________________________________________________________
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42.

What is the compensatory respiratory response to metabolic acidosis, and does PCO2 increase or
decrease? (p. 487) _______________________________________________________________

43.

What are the ten causes of increased anion gap metabolic acidosis? (p. 488) _________________
______________________________________________________________________________

PATHOLOGY
44

What glomerular diseases can be considered both nephritic and nephrotic syndromes? (p. 489)
______________________________________________________________________________

45.

What four clinical findings are associated with nephrotic syndrome? (p. 490) __________________
______________________________________________________________________________

46.

Match the nephrotic syndrome with its characteristic findings. (pp. 490-491)
_____ A. Amyloidosis
_____ B. Diabetic glomerulonephropathy
_____ C. Focal segmental glomerulosclerosis
_____ D. Membranous glomerulonephritis
_____ E. Membranoproliferative glomerulonephritis
_____ F. Minimal change disease

47.

1.
2.
3.
4.
5.
6.

Associated with chronic disease


Foot process effacement on EM
Hyalinosis on LM
Kimmelstiel-Wilson lesion on LM
Spike-&-dome appearance on EM
Tram-track appearance on EM

What is the most common cause of nephrotic syndrome in adults? (p. 490) ___________________
______________________________________________________________________________

48.

In diabetic glomerulonephropathy, what causes mesangial expansion? (p. 491) _______________


______________________________________________________________________________

49.

What four clinical findings are associated with nephritic syndrome? (p. 492) __________________
______________________________________________________________________________
______________________________________________________________________________

50.

Match the nephritic syndrome with its characteristic finding on light microscopy. (p. 492)
_____ A.
_____ B.
_____ C.
_____ D.
_____ E.

Acute poststreptococcal glomerulonephritis


Alports syndrome
Diffuse proliferative glomerulonephritis
IgA glomerulopathy
Rapidly progressive glomerulonephritis

1.
2.
3.
4.
5.

Crescent-shaped scars
Immune complexes in mesangium
Lumps and bumps
Split basement membrane
Wire looping of capillaries

51.

A 10-year-old boy presents with swollen ankles and periorbital edema, which were beginning to
resolve without intervention. Electron microscopy of a kidney biopsy specimen shows subepithelial
immune complex humps. Which form of nephritic syndrome does he most likely have? (p. 492)
______________________________________________________________________________

52.

Wegener's granulomatosis is __________ (c-ANCA/p-ANCA) positive, whereas microscopic


polyarteritis is __________ (c-ANCA/p-ANCA) positive. (p. 492)

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53.

For which systemic disease is diffuse proliferative glomerulonephritis the most common cause of
death? (p. 492) __________________________________________________________________

54.

Kidney stones are most commonly composed of what element? (p. 493) _____________________
______________________________________________________________________________

55.

Both antifreeze and vitamin C abuse can result in the formation of which type of crystals? (p. 493)
______________________________________________________________________________

56.

An 80-year-old man with leukemia presents with hematuria and right-sided flank pain. Which type
of kidney stone is he most likely to have? And how would this stone appear on x-ray? (p. 493)
______________________________________________________________________________

57.

Name the four components of the WAGR complex. (p. 494) _______________________________
______________________________________________________________________________

58.

Match the renal pathology with its characteristic findings. (pp 495-497)
_____ A. Acute pyelonephritis
_____ B. Acute tubular necrosis
_____ C. Bladder cancer
_____ D. Chronic pyelonephritis
_____ E. Diffuse cortical necrosis
_____ F. Drug-induced interstitial nephritis
_____ G. Renal cell carcinoma
_____ H. Renal papillary necrosis
_____ I. Transitional cell carcinoma
_____ J. Wilms tumor

59.

1.
2.
3.
4.
5.
6.
7.
8.
9.
10.

Associated with aniline dye exposure


Associated with diabetes
Associated with obstetric catastrophe
Associated with vHL syndrome
Muddy brown casts in urine
Nephroblastoma
Painless hematuria
Pyuria and azotemia
Thyroidization of kidney
WBC casts in urine

What are three causes of acute tubular necrosis? (p.496) ________________________________


______________________________________________________________________________

60.

Which three general types of renal dysfunction can lead to acute renal failure? (p.496)
______________________________________________________________________________

61.

True or False: Unilateral postrenal outflow obstruction can lead to acute renal failure. (p. 496)
______________________________________________________________________________

62.

A patient's urine osmolarity is <350 mOsm/L, urine sodium level is >40 mEq/L, fractional excretion
of sodium is >4%, and BUN/creatinine ratio is >15:1. Is the etiology of the acute renal failure most
likely to be prerenal, renal, or postrenal? (p. 496) _______________________________________

63.

A patients urine osmolarity is >500 mOsm/L, urine sodium level is <10 mEq/L, fractional excretion
of sodium is <1%, and BUN/creatinine ratio is >20:1. Is the etiology of the acute renal failure most
likely to be prerenal, renal, or postrenal? (p. 496) _______________________________________

64.

What are the eight consequences of renal failure? (p. 497) _______________________________
______________________________________________________________________________

65.

Which type of mutation causes autosomal-dominant polycystic kidney disease (formerly adult
polycystic kidney disease)? (p. 498) _________________________________________________

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66.

What are the two major causes of death associated with autosomal-dominant polycystic kidney
disease? (p. 498) ________________________________________________________________

67.

What are the complications of autosomal-recessive polycystic kidney disease in utero and after the
neonatal period? (p. 498) __________________________________________________________

PHARMACOLOGY
68.

What is the mechanism of action of acetazolamide? (p. 500) ______________________________


______________________________________________________________________________

69.

What is the mechanism of action of furosemide? (p.500) _________________________________


______________________________________________________________________________

70.

Which loop diuretic is used for diuresis in patients who are allergic to sulfa drugs? (p. 500) ______
______________________________________________________________________________

71.

What are the effects of hydrochlorothiazide toxicity? (p. 501) ______________________________


______________________________________________________________________________

72.

What is the mechanism of action of spironolactone? (p. 501) ______________________________


______________________________________________________________________________

73.

What is the mechanism by which ACE inhibitors can cause angioedema? (p. 502)
______________________________________________________________________________
______________________________________________________________________________

74.

What are three clinical uses of ACE inhibitors? (p. 502) __________________________________
______________________________________________________________________________

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Answers
EMBRYOLOGY
1.

Turners syndrome.

2.

ARPKD, posterior urethral valves, bilateral renal agenesis.

ANATOMY
3.

Because the left kidney has a longer renal vein.

4.

Under. (Remember: "water [ureters] under the bridge [artery and ductus deferens]").

PHYSIOLOGY
5.

High; low; low; high. (Remember: HIKIN': HIgh K Intracellular.)

6.

60% of total body weight is made up of total body water, 40% is made up of intracellular fluid, and
20% is made up of extracellular fluid.

7.

Size.

8.

Net charge.

9.

Podocyte foot processes.

10.

Renal clearance of X = the urine concentration of X times the urine flow rate, divided by the plasma
concentration of X (Cx = Ux V/Px).

11.

Secretion.

12.

Overestimates; secreted. (The plasma concentration of creatinine is slightly lower than it would be
from filtration alone.)

13.

Renal blood flow = renal plasma flow divided by (1 the hematocrit), or RBF = RPF/(1 Hct). In a
normal individual, renal blood flow will be approximately double the renal plasma flow.

14.

Prostaglandins cause dilation of the afferent arteriole and an increase in the GFR.

15.

Angiotensin II causes constriction of the efferent arteriole and an increase in the GFR.

16.

No change; increase; increase.

17.

Decrease; decrease; no change.

18.

Excretion rate = V Ux; where V is the urine flow rate and Ux is the urine concentration of X.

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19.

Glucose is reabsorbed in the proximal tubule by sodium/glucose cotransport.

20.

350 mg/dL.

21.

Hartnup disease. Proximal tubule. Amino acids are filtered and then reabsorbed from the urine at
the level of the proximal tubule by three distinct sodium-dependent transporters, each with
competitive inhibition.

22.

Hydrogen ions.

23.

Sodium, potassium, and chloride.

24.

Magnesium and calcium.

25.

PTH.

26.

Collecting tubule.

27.

Insertion of aquaporin water channels on the luminal side of the collecting tubules, resulting in
increased water reabsorption.

28.

Reabsorption.

29.

Increase. (Chloride is reabsorbed distally in the nephron.)

30.

Vasoconstriction; stimulation of sodium resorption in the proximal tubule; release of aldosterone


from the adrenal cortex; release of ADH from the posterior pituitary; and simulation of thirst via the
hypothalamus.

31.

Lungs.

32.

Renin.

33.

Osmolarity; blood volume; low; blood volume.

34.

Aldosterone secretion from the adrenal cortex increases sodium channel and sodium/potassium
pump insertion in principal cells and enhances potassium and hydrogen excretion by upregulating
potassium channels in the principal cells and hydrogen ion channels in the intercalated cells. These
actions create a favorable gradient for sodium and water reabsorption.

35.

Decreases; increases.

36.

Juxtaglomerular cells.

37.

Erythropoietin.

38.

1-Hydroxylase, which converts 25-OH vitamin D to 1,25(OH)2 vitamin D.

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39.
+

Shifts K Into Cell


Hypokalemia

Effect
Acidosis
Alkalosis

-Adrenergic agonists

Shifts K Out of Cell


Hyperkalemia

-Adrenergic antagonists

Cell lysis

Digitalis

Hyperosmolarity

Hypo-osmolarity

Insulin

Insulin deficiency

40.

Insulin increases activity of the Na /K /APTase pump. This increases the amount of K pumped
+
+
into the cell in exchange for Na , thus leaving less K outside the cell.

41.

Decreased serum bicarbonate.

42.

Hyperventilation, which causes PCO2 to decrease.

43.

Methanol (formic acid), Uremia, Diabetic ketoacidosis, Paraldehyde or Phenformin, Iron tables or
Isoniazid, Lactic acidosis, Ethylene glycol (oxalic acid), and Salicylates. (Remember: MUDPILES.)

PATHOLOGY
44.

Diffuse proliferative glomerulonephritis and membranoproliferative glomerulonephritis.

45.

Massive proteinuria (>3.5 g/day), edema, fatty casts, and hyperlipidemia.

46.

A-1, B-4, C-3, D-5, E-6, F-2.

47.

Focal segmental glomerular sclerosis.

48.

Nonenzymatic glycosylation of the efferent arterioles, leading to an increased GFR and thus
mesangial expansion.

49.

Azotemia, oliguria, hypertension, and proteinuria <3.5 g/day.

50.

A-3, B-4, C-5, D-2, E-1.

51.

Acute poststreptococcal glomerulonephritis.

52.

c-ANCA; p-ANCA.

53.

Systemic lupus erythematosus.

54.

Calcium in the form of calcium oxalate, calcium phosphate, or both.

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55.

Oxalate crystals.

56.

The patients leukemia (a disease with high cell turnover)


can result in hyperuricemia, so he is at
risk for developing uric acid stones, which are radiolucent and do not appear on x-ray studies.

57.

WAGR complex = Wilms' tumor, Aniridia, Genitourinary malformation, and mental-motor


Retardation.

58.

A-10, B-5, C-7, D-9, E-3, F-8, G-4, H-2, I-1, J-6.

59.

Renal ischemia, crush injury, and toxins.

60.

Prerenal (e.g., hypotension and reduced renal blood flow), intrinsic renal (e.g., tubular necrosis),
and postrenal (outflow obstruction).

61.

False; bilateral (not unilateral) postrenal outflow obstruction leads to acute renal failure.

62.

Postrenal.

63.

Prerenal.

64.

Na /H2O retention, hyperkalemia, metabolic acidosis, uremia, anemia, renal osteodystrophy,


dyslipidemia, and retarded grown and development in children.

65.

An autosomal dominant mutation in the APKD1 or APKD2 gene.

66.

Death usually results from complications of chronic kidney disease or hypertension (due to
increased renin production).

67.

Renal failure in utero, from autosomal recessive polycystic kidney disease, can lead to Potters
syndrome (see page 478). After the neonatal period, potential complications include hypertension,
portal hypertension, and progressive renal insufficiency.

PHARMACOLOGY
68.

Acetazolamide acts as a carbonic anhydrase inhibitor, causing self-limited sodium bicarbonate


diuresis and a reduction in total-body bicarbonate stores.

69.

Furosemide inhibits the Na /K /Cl cotransport system in the thick ascending limb of the loop of
Henle, thereby abolishing the hypertonicity of the medulla and preventing the concentration of
urine.

70.

Ethacrynic acid.

71.

Glucose (hyperGlycemia), lipids (hyperLipidemia), uric acid (hyperUricemia), and calcium


(hyperCalcemia). (Remember: HyperGLUC.)

72.

Spironolactone competitively antagonizes the aldosterone receptor in the cortical collecting tubule.

73.

ACE inhibitors prevent the inactivation of bradykinin, a potent vasodilator. Increased bradykinin
levels can lead to angioedema in susceptible individuals.

74.

To treat hypertension, to treat congestive heart failure, and to slow the progression of diabetic renal
disease.

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