Professional Documents
Culture Documents
Renal
Questions
ANATOMY
1. Why is the left kidney harvested for transplantation rather than the right? (p. 458) _____________
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2. Ureters pass __________ (over/under) the uterine artery and the ductus deferens. (p. 458)
PHYSIOLOGY
3. 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. 459)
4. What is the 60-40-20 rule of total body weight? (p. 459) __________________________________
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5. The fenestrated capillary endothelium of the glomerular filtration barrier is responsible for the
filtration of plasma by which characteristic: size or charge? (p. 459) _________________________
6. 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. 459) ________________
7. The epithelial layer of the glomerular filtration barrier is formed by which cells? (p. 459) _________
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8. 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. 459) _____________________________
9. 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. 459)
10. Creatinine clearance slightly __________ (overestimates/underestimates) the GFR rate because
creatinine is __________ (secreted/reabsorbed) by the renal tubules. (p. 459)
11. What is the formula for estimating renal blood flow if renal plasma flow is known? (p. 459) ______
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12. What are the effects of prostaglandins on the glomerulus? (p. 460) ________________________
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13. What are the effects of angiotensin II on the glomerulus? (p. 460) __________________________
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15. 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. 460)
16. What is the formula for excretion rate? (p. 460) _________________________________________
17. In the nephron, glucose at normal plasma concentrations is reabsorbed in which structure? And by
which transporter? (p. 460) ________________________________________________________
18. At what plasma glucose concentration is the transport mechanism of the proximal tubule
completely saturated, leading to glucose spilling into the urine? (p. 460) _____________________
19. How and where are amino acids reabsorbed in the kidney? (p. 460) ________________________
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20. What substance is secreted into the lumen of the early proximal convoluted tubule and acts as a
buffer for hydrogen ions? (p. 461) ___________________________________________________
21. Which two ions are actively reabsorbed in the thick ascending loop of Henle? (p. 461) _________
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22. Which three ions are indirectly reabsorbed in the thick ascending loop of Henle? (p. 461) ________
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23. Which hormone controls the reabsorption of calcium in the early distal convoluted tubule? (p. 461)
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24. On which segment of the nephron does the hormone aldosterone act? (p. 461) _______________
25. ADHs effect at V2 receptors results in what action? (p. 461) _______________________________
26. 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. 462)
27. Along the length of the proximal tubule, does the relative concentration of chloride increase,
decrease, or stay the same? (p. 462) _________________________________________________
28. Which five actions of angiotensin II serve to increase intravascular volume and blood pressure? (p.
462) __________________________________________________________________________
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29. What is the site of action of angiotensin-converting enzyme? (p. 462) _______________________
30. When blood pressure falls, the kidneys release which proteolytic enzyme? (p. 462) ____________
31. 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. 462)
32. What are the effects of aldosterone secretion? (p. 462) __________________________________
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33. Atrial natriuretic peptide __________ (decreases/increases) renin secretion and __________
(decreases/increases) the GFR. (p. 462)
34. Which cells produce renin in the kidney? (p. 463) _______________________________________
35. Which hormone is released by the endothelial cells of renal peritubular capillaries in response to
hypoxia? (p. 463) ________________________________________________________________
36. Which enzyme from the kidney is activated by PTH, and what is the function of that enzyme? (p.
463) __________________________________________________________________________
37. In the chart below, checkmark the effect that each condition has on the potassium shift. (p. 464)
+ +
Shifts K Into Cell Shifts K Out of Cell
Effect
Hypokalemia Hyperkalemia
Acidosis
Alkalosis
-Adrenergic agonists
-Adrenergic antagonists
Cell lysis
Digitalis
Hyperosmolarity
Hypo-osmolarity
Insulin
Insulin deficiency
38. By which mechanism does digitalis cause hyperkalemia? (p. 464) __________________________
39. What is the primary electrolyte disturbance in metabolic acidosis? (p. 465) ___________________
40. What is the compensatory respiratory response to metabolic acidosis, and does PCO2 increase or
decrease? (p. 465) _______________________________________________________________
41. What are the ten causes of increased anion gap metabolic acidosis? (p. 465) ________________
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PATHOLOGY
42. What four clinical findings are associated with nephritic syndrome? (p. 467) __________________
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43. Match the nephritic syndrome with its characteristic finding on light microscopy. (p. 467)
_____ A. Acute poststreptococcal glomerulonephritis 1. Crescent-shaped scars
_____ B. Alports syndrome 2. Immune complexes in mesangium
_____ C. Diffuse proliferative glomerulonephritis 3. Lumps and bumps
_____ D. IgA glomerulopathy 4. Split basement membrane
_____ E. Rapidly progressive glomerulonephritis 5. Wire looping of capillaries
44. 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. 467) ___
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46. For which systemic disease is diffuse proliferative glomerulonephritis the most common cause of
death? (p. 467) __________________________________________________________________
47. What four clinical findings are associated with nephrotic syndrome? (p. 468) __________________
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48. Match the nephrotic syndrome with its characteristic findings. (p. 468)
_____ A. Amyloidosis 1. Associated with chronic disease
_____ B. Diabetic glomerulonephropathy 2. Foot process effacement on EM
_____ C. Focal segmental glomerulosclerosis 3. Hyalinosis on LM
_____ D. Membranous glomerulonephritis 4. Kimmelstiel-Wilson lesion on LM
_____ E. Membranoproliferative glomerulonephritis 5. Spike-and-dome appearance on EM
_____ F. Minimal change disease 6. Tram-track appearance on EM
49. What is the most common glomerular disease seen in patients with HIV? (p. 468) ______________
50. In diabetic glomerulonephropathy, what causes mesangial expansion? (p. 468) _______________
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51. Kidney stones are most commonly composed of what element? (p. 469) _____________________
52. Both antifreeze and vitamin C abuse can result in the formation of which type of crystals? (p. 469) _
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53. 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. 469)
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54. Name the four components of the WAGR complex. (p. 469) _______________________________
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55. Match the renal pathology with its characteristic findings. (pp. 469-472)
_____ A. Acute pyelonephritis 1. Associated with aniline dye exposure
_____ B. Acute tubular necrosis 2. Associated with diabetes
_____ C. Bladder cancer 3. Associated with obstetric catastrophe
_____ D. Chronic pyelonephritis 4. Associated with vHL syndrome
_____ E. Diffuse cortical necrosis 5. Muddy brown casts in urine
_____ F. Drug-induced interstitial nephritis 6. Nephroblastoma
_____ G. Renal cell carcinoma 7. Painless hematuria
_____ H. Renal papillary necrosis 8. Pyuria and azotemia
_____ I. Transitional cell carcinoma 9. Thyroidization of kidney
_____ J. Wilms tumor 10. WBC casts in urine
56. What are three causes of acute tubular necrosis? (p. 470) ________________________________
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57. Which three general types of renal dysfunction can lead to acute renal failure? (p. 471) _________
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58. True or False: Unilateral postrenal outflow obstruction can lead to acute renal failure. (p. 471) ____
59. 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. 471) _______________________________________
60. 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. 471) _______________________________________
61. What are the eight consequences of renal failure? (p. 471) ________________________________
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62. Which type of mutation causes autosomal-dominant polycystic kidney disease (formerly adult
polycystic kidney disease)? (p. 472) _________________________________________________
63. What are the two major causes of death associated with autosomal-dominant polycystic kidney
disease? (p. 472) ________________________________________________________________
64. What are the complications of autosomal-recessive polycystic kidney disease in utero and after the
neonatal period? (p. 472) __________________________________________________________
PHARMACOLOGY
65. What is the mechanism of action of acetazolamide? (p. 474) ______________________________
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67. Which loop diuretic is used for diuresis of patients who are allergic to sulfa drugs? (p. 474) ______
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68. What are the effects of hydrochlorothiazide toxicity? (p. 474) _____________________________
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70. What is the mechanism by which ACE inhibitors can cause angioedema? (p. 475) _____________
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71. What are three clinical uses of ACE inhibitors? (p. 475) __________________________________
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Answers
ANATOMY
1. Because the left kidney has a longer renal vein.
2. Under. (Remember: "water [ureters] under the bridge [artery and ductus deferens]")
PHYSIOLOGY
3. High; low; low; high. (Remember: HIKIN': HIgh K Intracellular.)
4. 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.
5. Size.
6. Net charge.
8. 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).
9. Secretion.
10. Overestimates; secreted. (The plasma concentration of creatinine is slightly lower than it would be
from filtration alone.)
11. 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.
12. Prostaglandins cause dilation of the afferent arteriole and an increase in the GFR.
13. Angiotensin II causes constriction of the efferent arteriole and an increase in the GFR.
16. Excretion rate = V Ux; where V is the urine flow rate and Ux is the urine concentration of X.
19. 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.
20. Ammonia.
23. PTH.
25. Insertion of aquaporin water channels on the luminal side of the collecting tubules, resulting in
increased water reabsorption.
26. Reabsorption.
28. 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.
29. Lungs.
30. Renin.
32. 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. Erythropoietin.
37.
+ +
Shifts K Into Cell Shifts K Out of Cell
Effect
Hypokalemia Hyperkalemia
Acidosis
Alkalosis
-Adrenergic agonists
-Adrenergic antagonists
Cell lysis
Digitalis
Hyperosmolarity
Hypo-osmolarity
Insulin
Insulin deficiency
+ + + +
38. Digitalis blocks the Na /K /APTase pump from pumping K into the cell in exchange for Na , thus
+
leaving the K outside the cell.
41. Methanol (formic acid), Uremia, Diabetic ketoacidosis, Paraldehyde or Phenformin, Iron tables or
Isoniazid, Lactic acidosis, Ethylene glycol (oxalic acid), and Salicylates. (Remember: MUDPILES.)
PATHOLOGY
42. Azotemia, oliguria, hypertension, and proteinuria <3.5 g/day.
47. Massive proteinuria (>3.5 g/day), edema, fatty casts, and hyperlipidemia.
50. Nonenzymatic glycosylation of the efferent arterioles, leading to an increased GFR and thus
mesangial expansion.
53. Because of the patients leukemia (a disease with high cell turnover), he is at risk for developing
uric acid stones due to hyperuricemia, which are radiolucent and do not appear on x-ray studies.
54. WAGR complex = Wilms' tumor, Aniridia, Genitourinary malformation, and mental-motor
Retardation.
55. A-10, B-5, C-7, D-9, E-3, F-8, G-4, H-2, I-1, J-6.
57. Prerenal (e.g., hypotension and reduced renal blood flow), intrinsic renal (e.g., tubular necrosis),
and postrenal (outflow obstruction).
58. False; bilateral (not unilateral) postrenal outflow obstruction leads to acute renal failure.
59. Postrenal.
60. Prerenal.
+
61. Na /H2O retention, hyperkalemia, metabolic acidosis, uremia, anemia, renal osteodystrophy,
dyslipidemia, and retarded grown and development in children.
63. Death usually results from complications of chronic kidney disease or hypertension (due to
increased renin production).
64. Renal failure in utero, from autosomal recessive polycystic kidney disease, can lead to Potters
syndrome (see page 132). After the neonatal period, potential complications include hypertension,
portal hypertension, and progressive renal insufficiency.
PHARMACOLOGY
65. Acetazolamide acts as a carbonic anhydrase inhibitor, causing self-limited sodium bicarbonate
diuresis and a reduction in total-body bicarbonate stores.
+ + -
66. 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.
68. Glucose (hyperGlycemia), lipids (hyperLipidemia), uric acid (hyperUricemia), and calcium
(hyperCalcemia). (Remember: HyperGLUC.)
69. Spironolactone competitively antagonizes the aldosterone receptor in the cortical collecting tubule.
70. ACE inhibitors prevent the inactivation of bradykinin, a potent vasodilator. Increased bradykinin
levels can lead to angioedema in susceptible individuals.
71. To treat hypertension, to treat congestive heart failure, and to slow the progression of diabetic renal
disease.
Notes
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