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Pharmacotherapeutics > AKI (exam 3) > Flashcards

AKI (exam 3) Flashcards

(100 cards)

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1
Q

Acute Kidney Injury

A

Abrupt reduction in kidney function within past 7 days
Retention of waste products

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2
Q

Acute kidney disease

A

Kidney injury > 7 days

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2
Q

Chronic kidney disease

A

Kidney injury > 90 days

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3
Q

One of the following must be present for AKI diagnosis

A

increase SCr by > 0.3 in 48 hrs
increase SCr by > 1.5 times baseline in past 7 days
urine output < 0.5 for 6 hrs

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3
Q

Classification of AKI

A

RIFLE Criteria
AKIN Criteria
KDIGO Criteria

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4
Q

RIFLE

A

Risk
Injury
Failure
Loss
End-Stage

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5
Q

AKIN

A

Acute Kidney Injury Network

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6
Q

KDIGO

A

Kidney Disease Improving Global Outcomes

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7
Q

KDIGO Stage 1

A

SCr increase >0.3 OR 1.5-1.9 times baseline
Urine output <0.5 for 6-12 hours

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8
Q

KDIGO Stage 2

A

SCr increases 2-2.9 times baseline
Urine output <0.5 for > 12 hrs

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9
Q

KDIGO Stage 3

A

SCr increases 3 times baseline OR >4 OR need RRT OR eGFR <35 in children
Urine output <0.3 for >24 hrs OR anuria >12 hrs

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10
Q

Which criteria takes into account GFR?

A

RIFLE

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11
Q

Urine output classifications

A

Anuria
Oliguric
Nonoliguric

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12
Q

Anuric

A

No urine
<50 mL/24 hrs

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13
Q

Oliguric

A

Reduced urine
50-500 mL/24 hrs

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14
Q

Nonoliguric

A

Normal urine
>500 mL/ 24 hrs

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15
Q

Why is there a delay in AKI diagnosis?

A

increase in SCr occurs 1-2 days after onset

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16
Q

What is an inconsistent measure of kidney function?
Why?

A

Urine output (UOP)

Not always affected and varies with volume status, diuretic use, and obstruction

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17
Q

Functional unit of kidneys

A

Nephron

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18
Q

Nephron contains

A

Glomerulus
Bowman’s Capsule
Tubules and long tubular portion

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19
Q

Afferent arteriole

A

vessel bringing blood to glomerulus

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20
Q

Efferent arteriole

A

vessel bringing blood away from glomerulus

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21
Q

Prerenal AKI

A

Before blood reaches kidney
Decreases perfusion

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22
Q

Intrinsic AKI

A

Damage IN kidneys
Structural damage

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23
Postrenal AKI
Obstruction of urine flow downstream
24
Kidneys receive _____ of cardiac output
20-25%
25
In prerenal AKI, patients can develop reduced perfusion....
decreased intravascular volume decreased circulating BV Bilateral renal artery occlusion
26
Medications that interfere with compensatory processes
ACEIs/ARBs NSAIDs Cyclosporine Tacrolimus
27
Kidney compensatory mechanisms
Increased vasodilatory prostaglandins Increased angiotensin II
28
Increased vasodilatory prostaglandins
Dilation of AFFERENT arterioles
29
Increased angiotensin II
Constriction of EFFERENT arterioles
30
Result of compensatory mechanisms
maintenance of GFR
31
How do NSAIDs affect compensatory mechanisms?
Inhibit prostaglandin production --> constriction of AFFERENT
32
How do ACEIs/ARBs affect compensatory mechanisms?
Decrease angiotenesin II --> vasodilation of EFFERENT
33
Types of Intrinsic AKI
Renal vasculature Glomeruli Renal Tubules Interstitium
34
Renal Vascular Damage
blood clots block larger vessels
35
Glomerular damage
Damage to capillary system
36
Interstitial Damage
Acute Interstitial Nephritis (AIN) Hypersensitivity reaction
37
AIN presentation
fever, rash, eosinophilia, hematuria, proteinuria
38
AIN is commonly caused by ____
drugs
39
Tubular damage
Acute Tubular Necrosis (ATN) Caused by direct tubule toxins and renal ischemia
40
Direct tubule toxins
Aminoglycosides Contrast agents uric acid, hemoglobin, myoglobin
41
Postrenal AKI is blockage of ____ or ____
Ureters Urethra
42
Ureters can be blocked due to
Nephrolithiasis or blood clots
43
Urethra can be blocked due to
prostate issues or improperly placed urinary catheter
44
History/Clinical presentation of Prerenal AKI
Volume depletion CHF NSAIDs, ACE/ARB, cyclospor, tacro
45
History/Clinical presentation of Intrinsic AKI
Nephrotoxic drugs Hypoperfusion
46
History/Clinical presentation of Postrenal AKI
Kidney stones BPH Cancers
47
Physical Exam of Prerenal AKI
Hypotension Dehydration Ascites
48
Physical Exam of Intrinsic AKI
Rash (AIN) Fever (AIN)
49
Physical Exam of Postrenal AKI
Distended bladder Enlarged prostate
50
Anuria from complete urinary obstruction
Postrenal
51
Anuria from catastrophic event
Prerenal
52
Oliguria from decreased perfusion to kidneys
Prerenal
53
Nonoliguria from incomplete obstruction
Postrenal
54
Nonoliguria from interference with quality but not volume
Intrinsic
55
Unilateral flank pain
Postrenal
56
Bilateral flank pain
Intrinsic
57
Fever, rash, arthralgia
Intrinsic
58
Blood in urine
Intrinsic
59
High urine specific gravity or osmolarity
Prerenal
60
Low urine specific gravity or osmolarity
Intrinsic
61
RBCs in urine
Intrinsic
62
WBCs in urine
Intrinsic (AIN)
63
Presence of crystals
Postrenal
64
Presence of hyaline casts
Prerenal
65
Presence of granular casts
Intrinsic
66
Low FENa (<1%)
Prerenal
67
FENa 1-2%
Prerenal or Intrinsic
68
High FENa (>2%)
Intrinsic
69
Low UNa (<20)
Prerenal
70
High UNa (>40)
Instrinsic
71
Signs of volume depletion or dehydration
increased BUN and BUN/SCr
72
BUN/SCr >20:1
Prerenal
73
Prevention of AKI
Avoid nephrotoxic meds Aggressive hydration (2L/day)
74
IV Fluids for prevention
Crystalloids: balanced solutions or NS Colloids: Albumin or HES
75
What is preferred IV fluid for AKI
Balanced solutions: LR, hartmann's, plasmaLyte
76
Why is normal saline not preferred?
Increased risk of hyperchloremic acidosis
77
When to use vasopressors for AKI prevention?
With fluids in patients with hypotension not responsive to fluids
78
Vasopressor examples
Norepinephrine Dopamine Vasopressin
79
Therapies NOT recommended for prevention of AKI
Diuretics Renal replacement therapy (RRT)
80
AKI treatment focus
Removing causative factors Supportive care
81
Supportive care includes
Hemodynamic support Maintain fluid balance Maintain acid-base balance Maintain electrolyte homeostasis
82
AKI Treatments
Hydration Diuretics Electrolyte management Relieve obstruction Renal replacement therapy
83
Goal of hydration/perfusion
UOP >0.5 during initial use
84
Indications for IV fluids
hypoperfusion and hypovolemia prerenal or intrinsic AKI
85
Albumin is primarily used for
fluid resuscitation
86
Limit albumin use to patients with
hypoalbuminemia and resistance to crystalloid therapy
87
Patients with blood loss leading to AKI
RBC transfusion
88
Critically ill patients with vasodilatory shock
fluids + vasopressors
89
Electrolyte abnormalities in AKI
Hyperkalemia Hypernatremia Hyperphosphatemia Hypermagnesemia
90
Indications for RRT
Acid-base abnormalities Electrolyte imbalances Intoxications Overload of fluid Uremia
91
Types of RRT
Intermittent HD Continuous Renal Replacement Therapy (CRRT) Hybrid Dialysis Therapies
92
Indication of diuretic use in AKI
Fluid overload
93
Preferred diuretics in AKI
Loops: Furosemide Torsemide Bumetanide Ethacrynic Acid
94
Diuretics efficacy in edema depends on
Filtered Na reabsorbed Na reabsorbed distal to site of action Adequate drug delivery Na reaching site of action
95
Why are loop diuretics preferred?
Increase FENa from <1% to 20-25%
96
Loop diuretic ADRs
Decreased Ca, Mg, K Hearing loss, tinnitus Hypersensitivity
97
Causes of diuretic resistance
excessive Na intake decreased # of functioning nephrons proteinuria intestinal edema
98
Management of diuretic resistance
increase dose give two different classes: loop + metolazone give loop via continuous infusion

Pharmacotherapeutics (28 decks)

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