Brainscape's Knowledge GenomeTM

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


See full index

HST.110 Renal Pathophysiology > 15_HST110 Introduction to Renal Disease I - AKI 2017 > Flashcards

15_HST110 Introduction to Renal Disease I - AKI 2017 Flashcards

1
Q

What is definition of acute kidney injury (AKI)?

A

Sudden, often temporary, loss in kidney function (hours to days). An abrupt decrease in renal function

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

What is the definition of chronic kidney disease (CKD)?

A

Structural or functional kidney abnormalities with or without decreased GFR for > 3 months

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

What is the definition of end stage renal disease (ESRD)?

A

Total and permanent kidney failure

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

AKI encompasses both (X) injury to the kidney and acute (Y). Etiology of AKI can be from within the kidney or from external stresses to the kidney

A 
X = direct
Y = impairment of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

AKI can be defined as any of the following:

Increase in Cr by ≥ (X) mg/dL within 48 hours
Increase in Cr by ≥ 1.5 times the baseline within the prior (Y) days
Urine volume < (Z) mL/kg/hour for 6 hours

A 
X = 0.3
Y = 7
Z = 0.5
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What percent of hospital admissions are due to AKI?

A

5-13%

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

What percent of ICU patients have AKI?

A

1-25%

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

What is the mortality of AKI in ICU patients (in %)?

A

15-60%

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

Recovery potential: Animal studies show permanent damage following experimentally-induced AKI, including what 2 conditions?

A

tubulointerstitial fibrosis

damage to microvasculature

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

Multiple human studies show an increased risk of (X) and (Z) even after recovery from AKI

A 
X = CKD
Y = ESRD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define Azotemia

A

Abnormally high levels of nitrogen-containing compounds (e.g., urea, creatinine) in the blood

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

Define Oliguria

A

Low urine output
< 400 mL/day but >100 mL/day
Also defined as < 0.5 mL/kg/hour in adults

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

Define Anuria

A

Absence of urine

<100 mL/day

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

What are the 3 causes of AKI, based on location in the urinary system?

A

1) Prerenal (“before the kidney”)
2) Intrinsic Renal (“inside the kidney”)
3) Postrenal (“After the kidney”)

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

Postrenal AKI is typically caused by an (X) to urinary flow, occuring at any level of the urinary tract (kidney, ureters, bladder, or urethra)

A

X = obstruction

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

Why is all AKI considered postrenal until proven otherwise?

A

Early diagnosis and prompt correction of obstruction can result in minimal permanent kidney damage

Uncorrected obstruction can lead to irreversible renal failure

~10% of AKI is postrenal. Not most common, but direct intervention is possible so you want to be able to rule it out early on

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

Name 3 causes of kidney-localized postrenal AKI

A

Stones
Cancer
Sloughed papilla

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

Name 8 causes of ureter-localized postrenal AKI

A 
Stones
Cancer
Sloughed papilla
Extrinsic tumors
Retroperitoneal fibrosis
Infection
Blood clot
Trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Name 4 causes of bladder-localized postrenal AKI

A

Cancer
Blood clot
Edema/inflammation
Posterior urethral valves

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

Name 3 causes of urethra-localized postrenal AKI

A

Prostate enlargement
Stones
Strictures

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

How does postrenal AKI cause reduction in GFR? Use a formulaic argument

A

GFR decreases as a result of an increase in P_BS

GFR = Kf * {P_GC - (P_BS + (PI)_GC)]

Obstruction to urinary flow increases tubular pressure throughout the kidney

Increase in tubular pressure is transmitted back to the Bowman’s space and increases the hydrostatic pressure of Bowman’s space

Therefore, the forces favoring filtration will be decreased, and GFR will fall

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

What abnormal anatomical features are common in a postrenal urinary obstruction?

A

Distended structures (renal calyces, renal pelvis), stones or other obstruction present, blocked ureter

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

Under ultrasound, an obstruction results in what condition or appearance in the kidney, characterized by increased water retention?

A

Hydronephrosis. Dark regions were water is accumulating are evident. Thinning of the cortex is also seen

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

Under CT, hydronephrosis appears as a (X) mass

A

X = bulbous, distended

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Name 3 treatment options for postrenal AKI in order of increasing severity and ascending location of obstruction

A

1) Urethra level: Foley catheter
2) Ureter level: Ureteral stent
3) Kidney level (complete bypass): Percutaneous nephrostomy tubes

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

Prerenal AKI is instigated by a decrease in renal perfucion. Name 2 conditions this can result from

A

Decreased ECV

Hypotension

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

Why does prerenal AKI not represent true “kidney injury?”

A

No intrinsic abnormality to the renal parenchyma is seen

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

How can prerenal AKI be corrected?

A

With restoration of volume and circulatory deficits

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

Name 5 causes of prerenal AKI due to ECV depletion (with DECREASED ECF)

A 
Blood loss
GI losses
Renal losses
Skin losses
Third spacing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Name 3 causes of prerenal AKI due to ECV depletion (with INCREASED ECF)

A

CHF
Cirrhosis
Nephrotic syndrom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Stenosis of what blood vessel can cause prerenal AKI?

A

Renal artery

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

Name 6 drugs that can cause prerenal AKI

A 
NSAIDs
ACE inhibitors
ARBs
Cyclosporine
Tacrolimus
IV contrast
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How does prerenal AKI cause reduction in GFR? Use a formulaic argument

A

GFR decreases as a result of an decrease in P_GC

GFR = Kf * {P_GC - (P_BS + (PI)_GC)]

Significant reduction in renal perfusion results in a decrease in capillary hydrostatic pressure

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

What 3 drugs can cause direct afferent vasoconstriction resulting in prerenal AKI?

A

Cyclosporine
Tacrolimus
IV contrast

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

NSAIDs inhibit afferent vasodilation, inhibiting the autoregulatory role of (X), leading to prerenal AKI

A

X = prostaglandins

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

ACE inhibitors and ARBs block the efferent vasoconstrictive effects of (X), leading to prerenal AKI

A

X = angiotensin II

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

Intrinsic Renal AKI can accur at what 4 levels?

A

Glomerular
Tubular
Interstitial
Vascular

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

Name 1 example of intrinsic renal AKI at each of its 4 levels

A

Glomerular: Acute glomerulonephritis

Interstitial: Acute interstitial nephritis

Tubular: Acute tubular necrosis

Vascular: Vasculitis

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

What is acute tubular necrosis (ATN), one of the most common causes of AKI, characterized by?

A

Death of tubular epithelial cells

40
Q

What are the 2 major types of ATN?

A

Ischemic (prolonged hypoperfusion of tubules)

Nephrotoxic (direct toxic injury to tubules)

41
Q

Name 5 common causes of ischemic ATN

A 
Major surgery
Trauma
Severe hypovolemia
Sepsis
Burns
42
Q

Name 4 major categories of the common toxic causes of ATN

A

Antimicrobials (Aminoglycosides, Amphotericin B)
Chemotherapy (Cisplatin, Ifosfamide)
Radiocontrast agents
Heme pigments (Hemolysis, Rhabdomyolysis)

43
Q

Tubular injuries due to ATN affect the (X) and (Y) the most since both are in the outer medulla (relatively hypoxic)

A 
X = Proximal tubule (pars recta or S3 segment) 
Y = TAL of LOH

PT is in charge of secretion of toxins. They can accumulate them as well

44
Q

What is a common morphological change seen in tubular epithelial cells in ATN before necrosis and luminal obstruction set in?

A

Loss of polarity following ischemia and reperfusion

45
Q

Under histological evaluation, ATN appears with what striking features?

A

Dilated, cystic tubules
Loss of brush border
Debris in tubular lumen

46
Q

How does ATN cause reduction in GFR? Use a formulaic argument

A

GFR decreases as a result of an increase in P_BS

GFR = Kf * {P_GC - (P_BS + (PI)_GC)]

Occlusion of the tubular lumens by cellular debris and casts and, with hemolysis or rhabdomyolysis, by precipitation of heme pigments

Elevated intraluminal tubular pressure can disrupt epithelial cell tight junctions and cause backleak of tubular fluid into the circulation

47
Q

What are the 3 phases of ATN and their timeframes?

A

Initiation (hours to days)
Maintenance (1-2 weeks)
Recovery (variable)

48
Q

The “initiation” phase of ATN is characterized by exposure to (X). The injury is evolving but not established. ATN potentially (Y)

A 
X = ischemia or toxin
Y = preventable
49
Q

In the “maintenance” phase of ATN, (X) injury is established. This stage may be prolonged for as long as (Y) months

A 
X = parenchymal
Y = 1-12
50
Q

In the “recovery” phase of ATN, repair and regeneration of tubules is evident. Increase in urine output (“(X)”) and fall in (Y) are typical

A 
X = post-ATN diuresis
Y = creatinine
51
Q

Acute interstitial nephritis (AIN), a common cause of AKI, is characterized by what condition?

A

Acute inflammation of the interstitium

52
Q

What is AIN more commonly caused by?

A

Drugs that cause hypersensitivity-type reactions. Also associated with infections (bacterial, viral, fungal, mycobacterial) and autoimmune disease (SLE, Sjögren’s)

53
Q

Name 4 common antibiotics associated with AIN

A

β-lactam antibiotics (penicillins, cephalosporins)
Sulfonamides
Rifampin
Ciprofloxacin

54
Q

Name 3 non-antibiotic drugs associated with AIN

A

NSAIDs
Diuretics (furosemide, thiazides)
Proton-pump inhibitors

55
Q

AIN presents with a rise in (X) 1-2 weeks after exposure to offending drug. Can be as short as (Y) day(s) (if pre-exposed to drug) or as long as months (e.g. (Z))

A 
X = creatinine
Y = 1
Z = NSAIDs
56
Q

What are the 4 classic signs of drug-associated AIN?

A

Fever (36%)
Arthralgias (45%)
Skin rash (22%)
Eosinophilia (35%)

57
Q

The classic triad of fever, skin rash, and eosinophilia for AIN is seen in less that what % of patients?

A

10-15%

58
Q

Under histolopathological evaluation, AIN presents with what features?

A

Interstitial infiltration (lymphocytes, eosinophils)
Interstitial edema
Tubulitis
Glomeruli and vessels normal

59
Q

How does AIN cause reduction in GFR? Use a formulaic argument

A

GFR decreases as a result of a combined increase in P_BS and a decrease in P_GC

GFR = Kf * {P_GC - (P_BS + (PI)_GC)]

Interstitial inflammation and edema leads to compression of tubules and vasculature

Occlusion of the tubular lumens elevates intraluminal tubular pressure and hydrostatic pressure in

Bowman’s space
Vascular occlusion reduces perfusion and capillary hydrostatic pressure

60
Q

Treatment of AIN involves discontinuation of the offending drug. Often leads to (X) of AKI. Recovery can take weeks to months
Oral (Y) may have benefit if administered early (<14 days) after diagnosis

A 
X = complete resolution
Y = corticosteroids
61
Q

Define Acute Glomerulonephritis (GN)

A

Inflammation and proliferation of glomerular tissue

62
Q

GN can result in damage to what 3 structures?

A

GBM, mesangium, and capillary endothelium

63
Q

What 4 conditions is GN characterized by?

A

Hematuria with or without RBC casts
Proteinuria
Hypertension
Renal impairment

64
Q

Spectrum of GN ranges from asymptomatic (X) to (Y) syndrome

A 
X = hematuria
Y = nephritic
65
Q

Under histolopathological evaluation, Acute GN (Diffuse proliferative GN) presents with what feature?

A

Glomerular hypercellularity (lymphocytes and neutrophils)

66
Q

Name 3 types of vascular acute kidney disease

A

Benign or malignant hypertensive nephrosclerosis

Systemic vasculitis

Thrombotic microangiopathy (Hemolytic uremic syndrome (HUS), Thrombotic thrombocytopenic purpura (TTP), Scleroderma)

67
Q

What is the first “Rule of 3’s” related to the categories of AKI?

A

Postrenal
Prerenal
Intrinsic renal

68
Q

What is the second “Rule of 3’s” related to noninvasive diagnostic tools?

A

History and physical exam

Urinalysis with urinary electrolytes

Ultrasound

69
Q

What is the third “Rule of 3’s” related to the clinical maxims?

A

AKI is considered obstructive until proven otherwise

Eliminate postrenal and prerenal causes prior to pursuing intrinsic renal causes

Examine a fresh urine specimen whenever possible!

70
Q

Name examples of important information to acquire in the History and Exam for renal diseases

A 
Time of onset?
History of volume depletion?
Difficulty voiding?
Other symptoms?
Medications?
Recent events?
(Recent eating/drinking habits and events, recent accidents)
71
Q

Name examples of useful physical exam findings in the History and Exam for renal diseases

A

Fever?
Blood pressure (hypertension? hypotension?)
Volume status?
Other findings (e.g. rashes)?

72
Q

What is the time frame for appropriate urinalysis?

A

30-60 minutes after voiding

73
Q

How does one prevent contamination in specimen acquisition for urinalysis?

A

Midstream voiding and collection. For women, noting stage of menstrual cycle

74
Q

Name 6 of the important tests on a urinalysis dipstick

A

“Leukocyte esterase” detects urinary WBCs

“Nitrate” detects bacteria in the urine

“Protein” detects only albumin in the urine

“pH” reflects degree of acidification of urine

“Blood” detects heme from RBCs or free hemoglobin or myoglobin

“Specific gravity” provides estimate of urine osmolality

75
Q

Urine sediment is collected and evaluated using what technique?

A

Centrifugation of urine sample and resuspension for light microscopy review

76
Q

What are normal values for urine sediment cellular counts?

RBC
WBC

A

RBC: 0-2/hpf

WBC 0-5/hpf

77
Q

Name 4 examples of cells found in urine sediment

A

RBC, WBC, Tubular Epithelial Cells, Squamous Epithelial Cells (skin)

78
Q

What do dysmorphic RBC look like and what causes this condition?

A

Blebbed, mishapen cells

Indicates glomerular filtration barrier damage . Deformation of RBC membranes as they squeeze through the podocyte filtration slits or other barriers causes issues with shape and membrane integrity

79
Q

What is the interpretation of seeing dysmosphic RBCs in a urine sediment?

A

Acute GN
Infection
Stones
Malignancy

80
Q

What is the interpretation of seeing WBCs in a urine sediment?

A

Infection
Acute interstitial nephritis
Acute glomerulonephritis
Contamination

81
Q

Where do the cylindrical casts seen in the urine sediment form?

A

Distal tubule and collecting ducts

82
Q

What is the primary constituent of urine sediment casts?

A

Tamm-Horsfall protein

83
Q

What other general classes of substances can be trapped in the tubular lumen during the formation of casts?

A

Granules and cells

84
Q

Hyaline casts can be see in most renal diseases and contain only (X)

A

X = Tamm-Horsfall protein

85
Q

What non-renal disease-based conditions can result in hyaline casts?

A

Dehydration, fever, and post-physical exercise

86
Q

Granular casts are thought to represent filtered proteins trapped in (X) or cellular degeneration (Y)

A 
X = lysosomes (fine)
Y = coarse
87
Q

“Muddy Brown” granular casts are pathognomonic for what condition?

A

ATN

88
Q

RBC casts are a marker of bleeding within the (X). The RBCs usually originate from a damaged (Y). This condition can be seen in (Z)

A 
X = renal parenchyma
Y = parenchyma
Z = acute glomerulonephritis
89
Q

WBC casts have (X) trapped within a cast matrix and are a marker of intense inflammation within the kidneys. These WBCs can originate from a damaged (Y) or from inflammed (Z)

A 
X = leukocytes
Y = glomerulus
Z = interstitium
90
Q

What 2 AKI conditions can WBC casts be seen in?

A

Acute interstitial nephritis

Acute glumerulonephritis

91
Q

Fractional excretion of sodium can suggest prerenal or ATN AKI based on the cutoff. What are these values?

A

FENa < 1% suggests prerenal

FENa >2% suggests ATN

92
Q

What is the equation for the fractional excretion of sodium using Creatinine to measure GFR?

A 
FENa
= Clearance(Na)/Clearance(Cr)
= [(U_Na)/(P_Na)]/[U_Cr)/(P_Cr)]
Valid only in oliguric AKI 
low FENa is NOT specific for prerenal AKI
93
Q

What is the preferred imaging test to evaluate urinary obstruction

A

Renal ultrasound

94
Q

What do small kidneys suggest on a renal ultrasound?

A

Chronic process (damage or lack of use/atrophy)

95
Q

What does hydronephrosis on renal ultrasound suggest?

A

Dilation of the collecting system in one or both kidneys consistent with obstruction

96
Q

What complications of AKI are common?

A

Water balance: Hard to predict depending on specific site of injury
Sodium/Volume balance: Edema common
Acid-base balance: Metabolic acidosis common
Calcium/Phosphorus Homeostasis: Hyperphosphatemia with low calcium levels common (Ca-P complex takes up free calcium)

HST.110 Renal Pathophysiology (17 decks)

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