Nephrology Flashcards

1
Q

Site of erythropoietin (EPO) production

A

Interstitial cells of the peritubular capillaries

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2
Q

Active form of Vitamin D

A

1,25-dihydroxycholecalciferol (calcitriol)

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3
Q

Contains vasa recta and has longer loops of Henle

A

Juxtamedullary nephrons (less common than cortical nephrons)

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4
Q

Components of the juxtaglomerular apparatus

A

Macula densa (walls of the dital tubule; detects changes in BP)

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5
Q

Physiologic function of renin

A

None (merely converts angiotensinogen from the liver to angiotensin I)

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6
Q

Physiologic function of angiotensin I

A

None (merely converted to angiotensin II due to ACE in the lungs)

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7
Q

Physiologic functions of angiotensin II

A

Vasoconstricts afferent and efferent arteriole (efferent > afferent)

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8
Q

Site of aldosterone production

A

Zona glomerulosa of the adrenal cortex

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9
Q

Aldosterone actions

A

Increases Na+ reabsorption, K+ secretion, H+ secretion

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10
Q

ADH actions

A

Insertion of aquaporins (AQP-2) in the collecting ducts

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11
Q

Triggers for ADH secretion

A

Increased plasma osmolarity

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12
Q

Increases GFR

A

Afferent arteriolar vasodilation

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13
Q

Decreases GFR

A

Afferent arteriolar vasoconstriction

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14
Q

Principal cells

A

Absorb Na+ and H20 and secrete K+

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15
Q

Intercalated cells

A

Absorb K+ and secrete H+

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16
Q

Tubuloglomerular feedback

A

Macula densa feedback

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17
Q

Glomerulotubular balanca

A

“Percentage of solute reabsorbed is held constant”

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18
Q

Substances with no transport maximum and renal threshold

A

Sodium and all passively transported solutes

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19
Q

Ascending limb of the Loop of Henle is permeable to

A

Solutes (Mnemonic: asin-ding limb is permeable to solutes)

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20
Q

Descending limb of the Loop of Henle is permeable to

A

Water

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21
Q

Normal pH in various fluid sites

A

Arterial blood: 7.4

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22
Q

Acid-base abnormalities caused by diuretics

A

Metabolic acidosis: acetazolamide (Mnemonic: acid-azolamide)

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23
Q

Intact Nephron Hypothesis by Neil Bricker

A

Decreases in the number of functioning nephrons causes remaining nephrons to carry a larger burden of transport, synthetic function and regulatory function

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24
Q

Bricker’s Trade-Off Hypothesis

A

Some physiologic adaptations to nephron loss also produce unintended clinical consequences

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25
Q

Hyperfiltration Hypothesis by Barry Brenner

A

Some adaptations accelerate the deterioration of residual nephrons

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26
Q

Standard test for measurement of albuminuria

A

Accurate 24-hour urine collection

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27
Q

Most useful renal imaging study

A

Renal ultrasound

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28
Q

The only test to establish etiology in early-stage CKD in the absence of a clinical diagnosis

A

Renal biopsy

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29
Q

Most sensitive test for renal vein thrombosis (RVT)

A

CT angiography

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30
Q

Imaging test for diagnosis of nephrolithiasis

A

Helical computed tomography (CT) scanning without radiocontrast enhancement

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31
Q

Most common form of renal replacement therapy for AKI

A

Hemodialysis

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32
Q

Clear indications for initiation of renal replacement therapy in patients with CKD

A
  1. Uremic pericarditis
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33
Q

Best potential for complete renal rehabilitation

A

Kidney transplantation

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34
Q

Educational programs should be commenced

A

No later than stage 4 CKD

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35
Q

Most common therapeutic modality for end-stage renal disease (ESRD)

A

Hemodialysis

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36
Q

Leading cause of ESRD

A

Diabetes mellitus

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37
Q

Dialysis access with highest long-term patency rate

A

Fistula

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38
Q

Most important complication of arteriovenous grafts

A

Thrombosis of the graft and graft failure

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39
Q

Most common acute complication of hemodialysis, particularly among DM patients

A

Hypotension

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40
Q

Preferred buffer in peritoneal dialysis solutions

A

Lactate

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41
Q

Most common additives to peritoneal dialysis solutions

A

Heparin

42
Q

Most common organisms in peritoneal dialysis-related peritonitis

A

Gram-positive cocci including Staphylococcus (reflecting the origin from the skin)

43
Q

Absolute indication for the urgent initiation of or intensification of dialysis prescription

A

Uremic pericarditis

44
Q

Definition of AKI (Acute Kidney Injury)

A

A rise of at least 0.3 mg/dL within 48h or 50% higher than baseline within 1 week; or reduction in urine output to <0.5 mL/kg/h for >6 hours

45
Q

Definition of oliguria

A

<400 mL/24h

46
Q

Associated with multiple myeloma

A

Renal amyloidosis

47
Q

Most common cause of Acute Renal Failure (ARF)

A

Acute Tubular Necrosis (ATN)

48
Q

Most common form of AKI

A

Prerenal Azotemia (from Harrison’s IM)

49
Q

Patchy necrosis, PCT & LH affected, relatively short lengths of tubules affected

A

Ischemic-type ATN (e.g. in hypovolemia)

50
Q

Extensive necrosis, PCT and DT affected, relatively longer lengths of tubules

A

Toxic-type ATN (e.g. in use of aminoglycosides, radiocontrast dyes)

51
Q

Three broad categories of AKI

A

Prerenal Azotemia

52
Q

Most common clinical conditions associated with prerenal azotemia

A

Hypovolemia

53
Q

Most common causes of intrinsic AKI

A

Sepsis, ischemia, and nephrotoxins

54
Q

Most common clinical course of contrast nephropathy

A

A rise in SCr beginning 24-48 hours following exposure

55
Q

Most common protein in urine and produced in the thick ascending limb of the loop of Henle

A

Uromodulin/ Tamm-Horsfall Protein

56
Q

Hallmark of AKI

A

Buildup of nitrogenous waste products, manifested as an elevated BUN concentration

57
Q

Causes of large kidneys observed in CKD

A

Diabetic nephropathy

58
Q

Can provide definitive diagnostic and prognostic information about CKD

A

Kidney biopsy

59
Q

Definitive treatment of the hepatorenal syndrome

A

Liver transplantation

60
Q

Cerebral edema

A

Severe hemodynamic instability

61
Q

Continuous Renal Replacement Therapy is often preferred in patients with

A

Significant volume overload

62
Q

Chronic renal failure typically corresponds to

A

Stage 3-5 CKD

63
Q

ESRD refers to

A

Stage 5 CKD (<15% GFR)

64
Q

Screening test for early detection of renal disease

A

Microalbuminuria (especially in DM)

65
Q

Major side effect of calcium-based phosphate binders

A

Total-body calcium accumulation and hypercalcemia

66
Q

Leading cause of morbidity and mortality in patients at every stage of CKD

A

Cardiovascular disease (CVD)

67
Q

Major risk factor for ischemic CVD

A

Presence of any stage of CKD

68
Q

Among the strongest risk factors for cardiovascular morbidity and mortality in CKD

A

Left ventricular hypertrophy and dilated cardiomyopathy

69
Q

Absence of hypertension in CKD may signify

A

Salt-wasting form of renal disease

70
Q

Stage of CKD where normocytic, normochromic anemia appears

A

As early as Stage 3 CKD

71
Q

Primary cause of anemia

A

Insufficient production of EPO by the diseased kidneys

72
Q

Target hemoglobin concentration in CKD

A

100-115 g/L

73
Q

Stage of CKD where peripheral neuropathy usually becomes clinically evident

A

Stage 4 CKD

74
Q

Stage of CKD where assessment for protein-energy malnutrition should begin

A

Stage 3 CKD

75
Q

Indication for therapy with ACE inhibitors for ARBs

A

Protein excretion >300 mg

76
Q

Derives from the breakdown of urea to ammonia in saliva and is often associated with an unpleasant metallic taste (dysgeusia)

A

Uremic fetor

77
Q

Most important initial diagnostic step in the evaluation of a patient presenting with elevated serum creatinine

A

To distinguish newly diagnosed CKD from acute or subacute renal failure

78
Q

Classic lesion of secondary hyperparathyroidism; high bone turnover with increased PTH levels

A

Osteitis fibrosa cystica

79
Q

Low bone turnover with low or normal PTH levels

A

Adynamic bone disease and Osteomalacia

80
Q

Devastating condition seen almost exclusively in patients with advanced CKD

A

Calciphylaxis (Calcific uremic arteriolopathy)

81
Q

Seen in patients with CKD who have been exposed to gadolinium

A

Nephrogenic fibrosing dermopathy

82
Q

“Thyroidization” (appearance similar to thyroid follicles) of the kidney

A

Chronic glomerulonephritis (GN)

83
Q

RBC casts or dysmorphic RBCs seen in the sediment

A

GN

84
Q

Most common causes of glomerulonephritis throughout the world (save for subacute bacterial endocarditis in the Western hemisphere)

A

Malaria and schistosomiasis (closely followed by: HIV, chronic hepatitis B and C)

85
Q

Prototypical for acute endocapillary proliferative GN

A

Poststreptococcal GN (PSGN)

86
Q

Streptococcal strains associated with impetigo

A

M types 47, 49, 55, 2, 60, and 57

87
Q

Streptococcal strains associated with pharyngitis

A

M types 1, 2, 4, 3, 25, 49, and 12

88
Q

Kidneys have subcapsular hemorrhages with a “flea-bitten” appearance

A

Endocarditis-associated GN

89
Q

Primary treatment for endocarditis-associated GN

A

Eradication of the infection with 4-6 weeks of antibiotics

90
Q

May produce nephrotic or nephritic signs and symptoms

A

Membranoproliferative GN (MPGN)

91
Q

Type I MPGN characteristics

A

Presence of subendothelial deposits; low C3

92
Q

Type II MPGN characteristics

A

Intramembranous deposits, ribbon-like pattern, IgG autoantibody; low C3

93
Q

Most proliferative of the three types of MPGN

A

Type I MPGN

94
Q

Pathologic changes of FSGS are most prominent in

A

Glomeruli located at the corticomedullary junction (if the renal biopsy specimen is from superficial tissue, the lesions can be missed, leading to a misdiagnosis of MCD)

95
Q

Has the highest reported incidences of renal vein thrombosis, pulmonary embolism, and deep vein thrombosis

A

Membranous Nephropathy (MGN)

96
Q

Sensitive indicator for the presence of diabetes but correlates poorly with the presence or absence of clinically significant nephropathy

A

Thickening of the GBM

97
Q

Earliest manifestation in ~40% of patients with diabetes who develop diabetic nephropathy

A

Increase in albuminuria detected by sensitive radioimmunoassay

98
Q

Potent risk factor for cardiovascular events and death in patients with type 2 diabetes

A

Microalbuminuria

99
Q

Most renal amyloidosis is the result of

A

Fibrillar deposits of immunoglobulin light chains

100
Q

Lesion in HIV-associated nephropathy

A

FSGS