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55 > CKD-AKI > Flashcards

CKD-AKI Flashcards

1
Q

Definition of AKI

A
  • Abrupt decline in GFR occurring over hours to days/weeks
  • Associated with accumulation of waste products (urea and creatinine)
  • Inability to maintain and regulate fluid, electrolyte and acid-base balance

  • Increase in SCr by ≥ 26.5 μmol/L within 48 h, or
  • Increase in SCr to ≥ 1.5x baseline, within 7 days, or
  • Urine vol < 0.5 ml/kg/h for ≥ 6 h
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2
Q

risk factors for AKI

A
  • > 60yo
  • Female
  • Acute infection
  • Pre-existing chronic respiratory or CVS disease
  • Dehydration/volume depletion
  • Pre-existing CKD -> AoCKD
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3
Q

levels of urine output

normal, non oliguria, oliguria, anuria

A
  • Normal urine output ≥ 1200 ml/day
  • Non-oliguria: Urine output > 500 ml/day
  • Oliguria: Urine output < 500 ml/day
  • Anuria: Urine output < 50 ml/day
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4
Q

Clinical presentation of AKI

A
  • Reduced urine output
  • Peripheral edema (due to fluid accumulation)
  • Flank pain
  • Lab abnormalities:
    a. Elevated SCr, BUN, K
    b. Metabolic acidosis (Low CO2)
    c. Urinalysis -> presence of casts, cells, crystals, WBC, RBC protein or abnormal specific gravity, fractional excretion of Na, urine osmolality
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5
Q

types of AKI

A
  • pre renal (from decreased prefusion to kidneys)
  • intrinsic (from structural damage of kidneys)
  • post renal (obstruction of urine flow after kidneys)
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6
Q

Causes of pre renal AKI

abnormality and what causes the abnormalities

A
  • volume depletion –> hemorrage, GI losses
  • reduced cardiac output –> CHF/MI
  • renal hypoperfusion –> thrombosis, emboli, drug induced (!!)

result in dec afferent arteriole pressure

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7
Q

diagnosis and evaluation of pre renal AKI

clinical presentation and urine lab abnormalities

A
  • Pt history (GI loss, diuresis)
  • Physical Exam (orthostatic hypotension, tachycardia, poor skin turgor)
  • Central venous pressure
  • pt will have highly concentrated urine, low in Na, high SG (specific gravity), oliguria
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8
Q

what drugs can cause pre renal AKI

A
  • NSAIDs
  • ACEi/ARB

PG inhibitor prevents afferent arteriole from dilating –> prevents increased RBF
ACEi prevents constriction of efferenct arteriole due to Ang II –> decrease pressure

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9
Q

management of pre renal AKI

A
  • no specific treatment
  • Reverse of etiologic factors (treat pre-renal causes)
  • Use of vasopressors with fluids in pts with vasomotor shock
  • Supportive care
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10
Q

types of intrinsic AKI

A
  • Acute tubular necrosis (need to know)
  • Acute interstitial nephritis (need to know)
  • Glomerular damage
  • vascular damage
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11
Q

causes of ATN

A

drugs (radiocontrast, aminoglycoside, amphoterin B) / injury

  • Injury causes tubule epithelial cell necrosis/apoptosis; hypoxia and inflammatory response; damaged tubular cells sloughed off
  • Result: Loss of ability to concentrate urine, defective sodium reabsorption and reduction in GFR
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12
Q

4 phases of ATN

A
  • Initiating – ischemia/injury
  • Oliguric – cant excrete waste
  • Diuretic – increase urine, renal blood flow and GFR (reabsorb Na and concentrate urea)
  • Recovery – return to normal

  • Oliguria occurs in 70-80% of patients with ATN
  • Volume is lower than necessary to excrete body waste products
  • Anuria is less common
  • Duration of oliguric phase is 1-2 weeks
  • The longer the duration, the greater the risk of complications and the worse the outcome and prognosis
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13
Q

management of ATN oliguric phase

A
  • Diuretics (mostly loop like furosemide)
  • CCB
  • Water, Na, K, P acid-base balance
  • Nutrition, drug dosage adjustment, dialysis

  • CCB– Reverse renovascular constriction, increase renal blood flow, GFR
  • Role is to increase urine output, fluid management
  • Diuretic resistance is common –needs aggressive Na restriction, Combination diuretic therapy, IV dosing or continuous infusion of loop diuretics
  • Avoid overdiuresis or use of diuretics in pre-renal AKI
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14
Q

how does radiocontrast cause ATN?

A
  • Mechanism: alter renal hemodynamics, cause renal ischemia, direct toxicity
  • Progressive increase in SCr within 24-48h after contrast administration, usually peaks within 5 days

Increased risk for death or prolonged hospitalization

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15
Q

risk factors for radiocontrast induced ATN

A
  • preexisting CKD, DM, HTN, CHF, metabolic syndrome, hyperuricemia
  • age
  • volume depletion
  • concomitant administration of nephrotoxins, use high volume/ionic high osmolar contrast media

  • nephtoxins: discontinue NSAIDs, AG, ampho B, high dose loop diuretics (prevent over diuresis), antivirals, metformin (prevent lactic acidosis)
  • use isotonic/non ionic/low osmolar contrast
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16
Q

prevention of CIN

A
  • Use lowest possible dose in pts at risk
  • Use iso- or low osmolar contrast media rather than high osmolar agents
  • IV Hydration is key
  • N-acetylcysteine (NAC)

  • IV hydration:
    • Normal saline, Hypotonic saline (0.45% NaCl), Sodium bicarbonate
    • Start at least 1 h before and continue for 3-6 h after
  • NAC: prevent nephropathy
    • Antioxidant effects
    • More recent trials do not show consistent benefit (< commonly used now)
17
Q

how does aminoglycoside induce ATN

A
  • AG include Amikacin, gentamicin, tobramycin
  • Accumulates in renal cortex causing tubular epithelial cell damage and obstruction
  • Onset: 5-7 days
18
Q

risk factors for AG induced ATN

A
  • Elderly
  • CKD, DM
  • Volume depletion/hypotension, sepsis, shock
  • Concomitant administration of nephrotoxins
  • AG therapy > 3 days, multiple dosing, high serum conc (gentamicin > 2 mcg/mL)
19
Q

How to prevent AG induced ATN

A
  • use less nephroxic drugs
  • use extended interval dosing (od instead of bd etc)
  • prolong dosing interval

  • use concentration dependent killing for antibiotics for post antibiotic effects and minimise time dependent toxicity
20
Q

How prevent amphoterin B induced ATN

A
  • Continuous infusion
  • Alternate-day dosing rather than daily
  • Use lipid formulations
  • use other antifungals eg azoles
21
Q

Difference in urine in pre renal and intrinsic AKI

urine sediment, SG, osmolarity, urine to plasma osmolarity, Na, urea to sCr, FeNa

A
  • Pre renal vs intrinsic
  • urine sediment: normal, numerous casts
  • specific gravity: >1.015, < 1.010
  • urine osmolarity: >500, < 350
  • urine to plama osmolarity: >1.5, < 1.2
  • urine Na (mEq/L): < 20, >40
  • urea to sCr ratio: > 40:1, < 20:1
  • FeNa(%): < 1, > 2
22
Q

Causes of post renal urine obstruction

A
  • bladder obstruction (prostatic hypertrophy, infection, cancer, improperly placed catheter)
  • Ureteral (cancer with abdominal mass)
  • Nephrolithiatis (stones from oxalate/uric acid)
23
Q

Treatment of postrenal AKI

A
  • relief of obstruction
  • alpha blockers for passage or kidney stones
24
Q

General management of AKI

A
  • hemodynamic support, volume replacement
  • remove underlying cause
  • maintain water and Na and electrolyte and acid base balance
  • drug dosage adjustment

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