Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Internal Medicine > Part 13 - Nephrology > Flashcards

Part 13 - Nephrology Flashcards

1
Q

True or false: AKI is a clinical diagnosis

A

True

p. 1799

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the most common form of AKI?

A

Prerenal

p. 1799

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What type of AKI is due to inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal GFR?

A

Prerenal

p. 1799)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the most common conditions/causes associated with prerenal azotemia?

A

Hypovolemia
Decreased cardiac output
Medications (NSAIDS, inhibitors of angiotensin II)
(p. 1800)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

True or false: prerenal azotemia involves no parenchymal damage to the kidney

A

True

p. 1800

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

True or false: Prerenal azotemia is rapidly reversible once hemodynamics are restored

A

True

p. 1800

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Renal blood flow accounts for how many percent of the cardiac output?

A

20%

p. 1800

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Homeostatic responses occur in response to prerenal azotemia. Mediators of this response include?

A

Angiotensin II
Norepinephrine
Vasopressin
(p. 1800)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the myogenic reflex?

A

Dilation of the afferent arteriole in the setting of low perfusion pressure to maintain glomerular perfusion
(p. 1800)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the compensatory mechanisms involved in prerenal azotemia?

A

1) Homeostatic responses
2) Myogenic reflex
3) Tubuloglomerular feedback
(p. 1800)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Vasodilators that increase in response to low renal perfusion pressure (in prerenal azotemia)

A

Prostaglandins (prostacyclin, prostaglandin E2)
Kallikrein and kinins
Nitric oxide
(p. 1800)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the tubuloglomerular feedback?

A

Decreases in solute delivery to the macula dense elicit dilation of the afferent arteriole to maintain glomerular perfusion
(p. 1800)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Renal autoregulation usually fails once the systolic blood pressure falls below ____.

A

80 mmHg

p. 1800

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is macula densa?

A

Specialized cells within the distal tubule

p. 1800

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What do you call the dilation of afferent arteriole in response to decreased solute delivery to the macula densa?

A

Tubuloglomerular feedback

p. 1800

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Effect of NSAIDs to the kidney

A

Limits renal prostaglandin production –> limit renal afferent vasodilation
(p. 1800)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Effect of ACE-I and ARBs to the kidney

A

Limit renal efferent vasocontriction

p. 1800

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which type of hepatorenal syndrome has the poorer prognosis?

A

Hepatorenal syndrome Type 1

p. 1800

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Type of hepatorenal syndrome wherein AKI is seen without an alternate cause persisting despite volume administrate and withholding of diuretics

A

Hepatorenal syndrome Type 1

p. 1800

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Type of hepatorenal syndrome which is characterized mainly by refractory ascites

A

Hepatorenal syndrome Type 2

p. 1800

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

True or false: Decreases in GFR with sepsis can occur even in the absence of overt hypotension

A

True

p. 1801

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Segment of the proximal tubule that is metabolically very active

A

S3 segment

p. 1802

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What procedures are most commonly associated with AKI?

A

Cardiac surgery with cardiopulmonary bypass
Vascular procedures with aortic cross clamping
Intraperitoneal procedures
(p. 1802)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are common risk factors for postoperative AKI?

A 
Underlying CKD
Older age
Diabetes Mellitus
Congestive heart failure
Emergency procedures
Longer duration of cardiopulmonary bypass
(p. 1802)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does cardiopulmonary bypass cause AKI (mechanisms)?

A

1) Extracorporeal circuit activation of leukocytes and inflammatory processes
2) Hemolysis with resultant pigment nephropathy
3) Aortic injury with resultant atheroemboli
(p. 1803)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the abdominal compartment syndrome?

A

Markedly elevated intraabdominal pressures (usually > 20 mmHg) leading to renal vein compression and reduced GFR
(p. 1803)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What do you call markedly elevated intraabdominal pressures (usually above 20 mmHg) that lead to renal vein compression and reduced GFR?

A

Abdominal compartment syndrome

p. 1803

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Microvascular causes of AKI

A

Thrombotic microangiopathies (APAS, radiation nephritis, malignant nephrosclerosis, TTP-HUS)
Scleroderma
Atheroembolic disease
(p. 1803)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Large vessel diseases associated with AKI

A 
Renal artery dissection
Thromboembolism
Thrombosis
Renal vein compression or thrombosis
(p. 1803)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Risk factors for nephrotoxicity

A 
Older age
CKD
Prerenal azotemia
Hypoalbuminemia
(p. 1803)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

In contrast-induced nephropathy, when does creatinine begin to rise?

A

24-48 hours after exposure

p. 1803

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

In contrast-induced nephropathy, creatinine peaks within ____ day/s.

A

3-5 days

p. 1803

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Contrast-induced nephropathy resolves within how many days?

A

1 week

p. 1803

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Mechanisms involved in contrast-induced nephropathy

A

1) Hypoxia in the renal outer medulla due to perturbations in renal microcirculation and occlusion of small vessels
2) cytotoxic damage to the tubules directly or via the generation of oxygen free radicals
3) transient tubule obstruction with precipitated contrast material
(p. 1803)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

AKI secondary to aminoglycosides typically manifest after how many days of therapy?

A

5-7 days

p. 1803

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

True or false: AKI secondary to aminoglycosides can present even after the drug has been discontinued.

A

True

p. 1803

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What electrolyte abnormality is a common finding in AKI secondary to aminoglycoside use?

A

Hypomagnesemia

p. 1803

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

True or false: Nephrotoxicity from Amphotericin B is dose and duration dependent.

A

True

p. 1803

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Metabolic/electrolyte abnormalities found in AKI secondary to Amphotericin B use

A

Hypomagnesemia
Hypocalcemia
Non-gap metabolic acidosis
(p. 1803)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

AKI secondary to acute interstitial nephritis can occur as a consequence of exposure to what medications?

A 
Penicillins
Cephalosporins
Quinolones
Sulfonamides
Rifampin
(p. 1804)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the renal adverse effects of Ifosfamide?

A 
Hemorrhagic cystitis
Type II RTA (Fanconi's syndrome)
Hypokalemia
Modest decline in GFR
(p. 1804)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the renal adverse effect of bevacizumab?

A

Proteinuria
Hypertension via injury to the glomerular microvasculature (thrombotic microangiopathy)
(p. 1804)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Cause of “Chinese herb nephropathy” and “Balkan nephropathy”

A

Aristolochic acid

p. 1804

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the most common protein in urine which is produced in the thick ascending limb of the loop of Henle?

A

Uromodulin

p. 1804

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What serum level of uric acid leads to precipitation of uric acid in the renal tubules and AKI?

A

> 15 mg/dL

p. 1804

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Definition of AKI (according to Harrison’s)

A

1) Rise from the baseline of at least 0.3 mg/dL within 48 hours OR
2) At least 50% higher than baseline within 1 week OR
3) Reduction in urine output to less than 0.5 ml/kg per hour for longer than 6 hours
(p. 1805)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Characteristic urine sediment findings in AKI secondary to ATN

A

1) Pigmented “muddy brown” granular casts
2) Tubular epithelial cell casts
(p. 1805)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Finding of oxalate crystals in AKI should prompt an evaluation for _____ toxicity.

A

Ethylene glycol

p. 1805

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

True or false: Anemia is common in AKI.

A

True

p. 1807

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the fractional excretion of sodium (FeNa) in prerenal azotemia?

A

<1%

Pp. 1806-1807

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the fractional excretion of sodium (FeNa) in ischemic AKI?

A

Frequently above 1%

p. 1807

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Why is fractional excretion of sodium (FeNa) in ischemic AKI frequently above 1%?

A

Because of tubular injury and resultant inability to reabsorb sodium
(p. 1807)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Ischemia and nephrotoxin-associated AKI that can present with FeNa < 1%

A

Sepsis (often early in the course)
Rhabdomyolysis
Contrast nephropathy
(p. 1807)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Causes of RBC or RBC casts in urine

A 
Glomerulonephritis
Vasculitis
Malignant hypertension
Thrombotic microangiopathy
(p. 1807, Figure 334-6)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Causes of WBCs or WBC casts in urine

A 
Interstitial nephritis
Glomerulonephritis
Pyelonephritis
Allograft rejection
Malignant infiltration of the kidney
(p. 1807, Figure 334-6)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Causes of renal tubular epithelial cells (RTE), RTE casts, or pigmented casts in the urine

A 
Acute tubular necrosis
Tubulointerstitial nephritis
Acute cellular allograft rejection
Myoglobinuria
Hemoglobinuria
(p. 1807, Figure 334-6)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Causes of granular casts in the urine

A 
Acute tubular necrosis
Glomerulonephritis
Vasculitis
Tubulointerstitial nephritis
(p. 1807, Figure 334-6)
58
Q

Causes of eosinophiluria

A 
Allergic interstitial nephritis
Atheroembolic disease
Pyelonephritis
Cystitis
Glomerulonephritis
(p. 1807, Figure 334-6)
59
Q

Causes of crystalluria

A

Acute uric acid nephropathy
Calcium oxalate (ethylene glycol intoxication)
Drugs or toxins (acyclovir, indinavir, sulfadiazine, amoxicillin)
(p. 1807, Figure 334-6)

60
Q

True or false: Enlarged kidneys in a patient with AKI suggests the possibility of acute interstitial nephritis

A

True

p. 1808

61
Q

Biomarker for AKI that is a type 1 transmembrane protein abundantly expressed in proximal tubular cells injured by ischemia or nephrotoxins

A

Kidney injury molecule-1 (KIM-1)

p. 1808

62
Q

Biomarker for AKI with the role of conferring phagocytic properties to tubular cells, enabling them to clear debris from tubular lumen after injury

A

Kidney injury molecule-1 (KIM-1)

p. 1808

63
Q

Biomarker for AKI which is also known as lipocalin-2 or siderocalin

A

Neutrophil gelatinase associatied lipocalin (NGAL)

p. 1808

64
Q

Biomarker for AKI which can bind to iron siderophore complexes and may have tissue-protective effects in the proximal tubule

A

Neutrophil gelatinase associated lipocalin (NGAL)

p. 1808

65
Q

Biomarker for AKI which can be detected in the plasma and urine within 2 hours of cardiopulmonary bypass-associated AKI

A

Neutrophil gelatinase associated lipocalin (NGAL)

p. 1808

66
Q

Biomarker for AKI that may mediate ischemic proximal tubular injury and L-type fatty acid binding protein

A

Interleukin-18

p. 1808)

67
Q

Fluid solution that is contraindicated in AKI secondary to prerenal azotemia

A

Hydroxyethyl starch solutions

p. 1809

68
Q

True or false: Albumin may prevent AKI in those treated with antibiotics for spontaneous bacterial peritonitis

A

True

p. 1810

69
Q

Definitive treatment of the hepatorenal syndrome

A

Orthotopic liver transplantation

p. 1810

70
Q

Treatment for AKI due to scleroderma (scleroderma renal crisis)

A

ACE-inhibitors

p. 1810

71
Q

Treatment for idiopathic TTP-HUS

A 
Plasma exchange
(p. 1810)
72
Q

Initial fluid resuscitation requirement for rhabdomyolysis

A

10 liters of fluid per day

p. 1810

73
Q

True or false: In decompensated heart failure, stepped diuretic therapy is superior to ultrafiltration in preserving renal function

A

True

p. 1810

74
Q

According to KDIGO guidelines, patients with AKI should achieve a total energy intake of ____.

A

20-30 kcal/kg/day

p. 1810

75
Q

According to KDIGO guidelines for patients with AKI, what is the protein intake requirement per day in non-catabolic AKI without the need for dialysis?

A
  1. 8-1 g/kg/day

p. 1810

76
Q

According to KDIGO guidelines for patients with AKI, what is the protein intake requirement per day in patients on dialysis?

A

1 - 1.5 g/kg/day

p. 1810

77
Q

According to KDIGO guidelines for patients with AKI, what is the protein intake requirement per day if hypercatabolic and receiving continuous renal replacement therapy (CRRT)?

A

Up to a maximum of 1.7 g/kg/day

p. 1810

78
Q

True or false: Anemia seen in AKI is improved by erythropoiesis-stimulating agents

A

False

p. 1810

79
Q

Why is erythropoiesis-stimulating agents not helpful for anemia in AKI patients?

A

1) Delayed onset of action
2) Presence of bone marrow resistance in critically ill patients
(p. 1810)

80
Q

Uremic bleeding may respond to what medications?

A

Desmopressin or estrogens

p. 1810

81
Q

Risk factors for CKD

A

1) Small for gestational age birth weight
2) Childhood obesity
3) Hypertension
4) Diabetes mellitus
5) Autoimmune disease
6) Advanced age
7) African ancestry
8) Family history of kidney disease
9) Previous episode of AKI
10) Presence of proteinuria, abnormal urinary sediment, or structural abnormalities of the urinary tract
(p. 1811)

82
Q

Allelic versions of what gene contribute to the several-fold higher frequency of certain common etiologies of non-diabetic CKD?

A

APOL1

p. 1811

83
Q

True or false: Mean GFR is lower in women than in men

A

True

p. 1812

84
Q

What is the normal annual mean decline in GFR with age?

A

~1 ml/min per year per 1.73 m2

p. 1812

85
Q

True or false: Microalbuminuria is a good screening test for early detection of renal disease

A

True

p. 1813

86
Q

True or false: Albuminuria is a major risk factor for cardiovascular disease

A

True

p. 1813

87
Q

Leading cause of CKD

A

Diabetic nephropathy

p. 1813

88
Q

What is the pathophysiology of the uremic syndrome?

A

1) accumulation of toxins
2) loss of other kidney functions
3) progressive systemic inflammation and its vascular and nutritional consequences
(p. 1814)

89
Q

True or false: Hyponatremia is not commonly seen in CKD patients

A

True

p. 1814

90
Q

What is the mechanism of action of metolazone?

A

Inhibits the sodium chloride co-transporter of the distal convoluted tubule
(p. 1814)

91
Q

How does metabolic acidosis occur in CKD?

A

Patients produce less ammonia thus cannot excrete the normal quantity of protons
(p. 1814)

92
Q

Acid-base abnormality found in early CKD (specific)

A

Non-anion gap metabolic acidosis

p. 1814

93
Q

Acid-base abnormality seen in late stages of CKD (specific)

A

Anion-gap metabolic acidosis

p. 1814

94
Q

Alkali supplementation for CKD patients is recommended when the serum bicarbonate concentration falls below what level?

A

20-23 mmol/L

p. 1814

95
Q

What is the classic lesion of secondary hyperparathyroidism?

A

Osteitis fibrosis cystica

p. 1815

96
Q

Bone changes in CKD start to occur when the GFR falls below what level?

A

60 ml/min

p. 1815

97
Q

In CKD, how does FGF-23 defend normal serum phosphorus levels?

A

1) increased renal phosphate excretion
2) stimulation of PTH –> increases renal phosphate excretion
3) suppression of the formation of 1,25(OF)2D3 –> diminished phosphorus absorption from the GI tract
(p. 1815)

98
Q

True or false: high levels of FGF-23 is an independent risk factor for LVH and mortality in CKD, dialysis, and renal transplant patients.

A

True

p. 1815

99
Q

Osteitis fibrosa cystica is also known as what?

A

Brown tumor

p. 1815

100
Q

What disorder seen in CKD is associated with high bone turnover with increased PTH levels?

A

Osteitis fibrosa cystica

p. 1815

101
Q

What disorder/s seen in CKD is associated with low bone turnover with low or normal PTH levels?

A

Adynamic bone disease
Osteomalacia
(p. 1815)

102
Q

What is “tumoral calcinosis”?

A

When calcium precipitate in the soft tissues into large concretions
(p. 1815)

103
Q

True or false: There is a strong association between hyperphosphatemia and increased cardiovascular mortality rate in patients with CKD

A

True

p. 1815

104
Q

What condition seen almost exclusively in patients with advanced CKD is heralded by livedo reticularis and then advance to patches of ischemic necrosis?

A

Calciphylaxis

p. 1816

105
Q

True or false: Warfarin treatment is a risk factor for calciphylaxis

A

True

p. 1816

106
Q

What is the optimal management of secondary hyperparathyroidism and osteitis fibrosa cystica?

A

Prevention

p. 1816

107
Q

According to KDOQI, the recommended target PTH level is ____.

A

Between 150 and 300 pg/ml

p. 1816

108
Q

What is the leading cause of morbidity and mortality in patients at every stage of CKD?

A

Cardiovascular disease

p. 1816

109
Q

What are the CKD-related risk factors for ischemic vascular disease?

A 
Anemia
Hyperphosphatemia
Hyperparathyroidism
Increased FGF-23
Sleep apnea
Generalized inflammation
(p. 1816)
110
Q

True or false: Cardiac troponin levels are frequently elevated in CKD without evidence of acute ischemia

A

True

p. 1817

111
Q

True or false: Consistently elevated levels of cardiac troponin is an independent prognostic factor for adverse cardiovascular events in CKD patients

A

True

p. 1817

112
Q

True or false: The absence of hypertension in CKD patients may signify poor left ventricular function

A

True

p. 1817

113
Q

True or false: In dialysis patients, low blood pressure has worse prognosis than those with high blood pressure

A

True

p. 1817

114
Q

Goal BP in CKD patients with diabetes or proteinuria > 1 g per 24 hours (according to Harrison’s)

A

130/80

p. 1817

115
Q

Classic ECG abnormalities seen in pericarditis

A

PR interval depression
Diffuse ST segment elevation
(p. 1817)

116
Q

Anemia is universal at what stage of CKD?

A

Stage 4

p. 1818

117
Q

What is the primary cause of anemia in CKD patients?

A

Insufficient production of EPO

p. 1818

118
Q

True or false: The susceptibility to bacterial infections is increased in CKD patients on IV iron therapy

A

True

p. 1818

119
Q

What is the target hemoglobin concentration in CKD patients (according to Harrison’s)?

A

100-115 g/L

p. 1818

120
Q

Subtle clinical manifestations of uremic neuromuscular disease usually become evident at what stage of CKD?

A

Stage 3

p. 1818

121
Q

Peripheral neuropathy usually become clinically evident by what stage of CKD?

A

Stage 4

p. 1819

122
Q

What is the pattern of peripheral neuropathy in CKD?

A

Sensory > Motor
Lower extremities > Upper extremities
Distal > Proximal
(p. 1819)

123
Q

What is the “restless leg syndrome” seen in CKD?

A

Ill-defined sensations/debilitating discomfort in the legs and feet relieved by frequent leg movement
(p. 1819)

124
Q

True or false: In CKD patients, evidence of peripheral neuropathy without another cause (ex. Diabetes mellitus) is an indication for starting renal replacement therapy

A

True

p. 1819

125
Q

Assessment of protein-energy malnutrition should begin by what stage of CKD?

A

Stage 3

p. 1819

126
Q

Imaging/diagnostic test that is widely used to estimate lean body mass versus extracellular fluid volume (ECFV)

A

Dual-energy X-ray absorptiometry

p. 1819

127
Q

Pregnancy is associated with a high rate of spontaneous abortion when the GFR has declined to what level?

A

~40 ml/min

p. 1819

128
Q

True or false: Pregnancy may hasten the progression of CKD

A

True

p. 1819

129
Q

What is nephrogenic fibrosing dermopathy?

A

Progressive subcutaneous induration (especially on the arms and legs) seen in CKD patients who have been exposed to gadolinium contrast
(p. 1819)

130
Q

What is the skin condition seen in CKD patients who have been exposed to gadolinium contrast?

A

Nephrogenic fibrosing dermopathy

p. 1819

131
Q

True or false: Liver disease is a risk factor for nephrogenic fibrosing dermopathy

A

True

p. 1819

132
Q

What is the most useful imaging study for CKD?

A

Renal ultrasound

p. 1820

133
Q

Etiologies of CKD which may present as normal to large-sized kidneys

A 
Diabetes mellitus
Amyloidosis
HIV nephropathy
Polycystic kidney disease
(p. 1820)
134
Q

What diagnostic/imaging test can be done if reflux nephropathy is suspected in CKD patients?

A

Voiding cystogram

p. 1820

135
Q

What are contraindications to renal biopsy?

A

1) Bilaterally small kidneys
2) Uncontrolled hypertension
3) Active UTI
4) Bleeding diathesis
5) Severe obesity
(p. 1820)

136
Q

Why is renal biopsy contraindicated in patients with bilaterally small kidneys?

A

1) Technically difficult and has greater likelihood of causing bleeding
2) So much scarring that the underlying disease may not be apparent
3) Window of opportunity to render disease-specific therapy has passed
(p. 1820)

137
Q

The renoprotective effect of antihypertensive medications is gauged through what laboratory finding?

A

Proteinuria

p. 1820

138
Q

What is the effect of ACE inhibitors and ARBs in the renal vasculature?

A

Inhibits the angiotensin-induced vasoconstriction of the efferent arterioles
(p. 1821)

139
Q

True or false: ACE inhibitors and ARBs are effective in slowing the progression of renal failure in patients with advanced stages of BOTH diabetic and nondiabetic CKD

A

True

p. 1821

140
Q

Which calcium channel blockers exhibit superior anti-proteinuric and renoprotective effects?

A

Diltiazem
Verapamil
(p. 1821)

Internal Medicine (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions