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NURS 470 > Advanced concepts in fluid and electrolyte disturbances in high acuity settings (AKI/CKD) > Flashcards

Advanced concepts in fluid and electrolyte disturbances in high acuity settings (AKI/CKD) Flashcards

1
Q

metabolic and endocrine functions of kidneys

A

BP regulation
EPO production
insulin degradation
prostaglandin synthesis
vitamin D metabolism
acid/base balance

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2
Q

acute kidney injury

A

partial or complete impairment of kidney function
abrupt decrease in kidney function
results in an inability to excrete metabolic waste products and water from the body
rapid onset and ranges from a slight deterioration in kidney function to severe impairment
potentially reversible

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3
Q

definition of AKI

A

rise in serum Cr of 0.3 mg/dL or more over 48 hrs or >50% in 7 days

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4
Q

AKI urine output criteria

A

< 0.5 mL/kg/hour for >6hrs

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5
Q

3 types of AKI

A

prerenal
intrarenal
postrenal

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6
Q

prerenal AKI

A

related to factors that are external to the kidneys
a reduction in systemic circulation reduces BP to the kidneys
can lead to intrarenal disease if impaired perfusion to the kidneys is prolonged

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7
Q

prerenal AKI causes

A

excessive fluid loss
decreased renal perfusion
vascular obstructions
drugs

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8
Q

intrarenal AKI

A

injury caused by direct damage to the kidney tissue, which results in impaired nephron function

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9
Q

conditions that predispose to intrarenal injury

A

infection
tumor growth
diabetes
DI
renal vasculitis

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10
Q

intrarenal AKI causes

A

prolonged ischemia
nephrotoxins
acute tubular necrosis
endogenous: rhabdomyolysis, TLS, HRS
antimicrobials: aminoglycosides
immunosuppressants: cyclosporin, tacrolimus
chemotherapy
NSAIDs
street drugs
contrast

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11
Q

acute tubular necrosis

A

most common intrarenal AKI cause
tissue destruction, causing permanent renal damage

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12
Q

causes of acute tubular necrosis

A

decreased perfusion
shock
sepsis
anaphylaxis
contrast

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13
Q

contrast induced nephropathy

A

renal vasoconstriction, free radical generation
usually resolves within 1-3 weeks
risk fx: CKD, DM, HF, high contrast doses
tx: supportive care

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14
Q

fractional excretion of sodium (FeNa)

A

<1 = prerenal
>2 = ATN

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15
Q

postrenal AKI

A

when the flow of urine is obstructed and urine backs up into the renal pelvis and impairs kidney function
can lead to hydronephrosis (distension and dilation of the kidney)

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16
Q

causes of postrenal AKI

A

blood clots
tumors
calculi
urethral strictures
neurogenic bladder
BPH
trauma
ureteral obstruction
bladder dysfunction
urethral obstruction

17
Q

glomerulonephritis

A

inflammation of glomeruli
acute or chronic

18
Q

causes of glomerulonephritis

A

infections
immune diseases
vasculitis
hypertension
diabetic nephropathy

19
Q

chronic glomerulonephritis

A

end stage of glomerular inflammatory disease
characterized by proteinuria, hematuria, development of uremia
tx is supportive and symptomatic
lab tests: urine, serum, dx

20
Q

RIFLE

A

classification/staging criteria based on GFR, Cr, and UO over time
Risk
Injury
Failure
Loss
ESKD

21
Q

manifestations of AKI

A

oliguria
elevated BUN and Cr
uremia
decline in GFR: anuria, oliguria, azotemia
S3, S4
crackles, DOE, weight gain, edema, fluid overload

22
Q

lab manifestations of inability to excrete waste and maintain homeostasis

A

increasing BUN
increasing Cr
hyperkalemia
hyponatremia
metabolic acidosis
hyperphosphatemia/hypocalcemia
anemia

hemodilution and inability to excrete

23
Q

labs and diagnostic testing for the kidneys

A

BUN and Cr
GFR
urinalysis
ABG
renal US
CT
renal biopsy

24
Q

prerenal treatments

A

restore adequate circulation to kidneys:
monitor I/O
sx of FVE
VS
administer crystalloid or colloid fluids
vasopressors

25
Q

intrarenal treatments

A

minimize nephrotoxic substances and treat underlying cause:
fluid restriction
dietary restrictions of Na and K
lower K levels with NaHCO3, glucose & insulin, kayexalate
decrease transfusions for anemia
prevent infection: abx but monitor levels
decrease serum Cr

26
Q

postrenal treatments

A

treat outlet obstruction:
monitor I/O
pain assessment
monitor lytes during diuresis
IV fluids

27
Q

AKI collaborative treatment

A

avoid nephrotoxic drugs (NSAIDs and ACEs, IV contrast)
monitor for drug toxicity
hypovolemia, & d/t blood loss
inflammation
maintain nutritional status

28
Q

AKI dietary management

A

provide adequate calories to prevent catabolism:
protein restriction
Na restriction
K restriction
phosphorus restriction
vitamin supplements
fluid restriction

29
Q

stages of AKI resolution

A

diuretic stage
recovery stage

30
Q

diuretic stage

A

waste products now being filtered but unable to concentrate urine
up to 5L/day of UP
monitor for hypo Na and K, dehydration, hypotension
lasts 1-3 weeks

31
Q

recovery stage

A

GF increases causing BUN/Cr to decrease
major improvements in 1-2 weeks
can take up to 1yr for full recovery

32
Q

AKI NANDAs

A

fluid volume deficit or excess
imbalanced nutrition
anxiety

33
Q

chronic kidney disease

A

progressive and irreversible
5 progressive stages

34
Q

5 stages of CKD

A

Stage 1: diminished renal reserve
Stage 2: renal insufficiency
Stage 3: moderate renal failure
Stage 4: severe renal failure
Stage 5: End-stage renal disease (ESRD)

35
Q

diagnosis of CKD

A

history
labs
presenting s/s
Cr and BUN

36
Q

clinical signs of CKD

A

uremia
anemia
CHF
HTN
dysrhythmias
edema
pericarditis
pulmonary edema
infection
altered glucose control
N/V
fatigue
seizures
delayed wound healing
metabolic acidosis

37
Q

CKD treatment

A

dialysis
BP control (K sparing diuretics, ACE inhibitors)
EPO/iron/folic acid/B12
normal/high protein diet (if on dialysis)
low Na/K/Phos
calcium supplements

38
Q

CKD NANDAs

A

fluid volume excess
altered fluid and electrolyte imbalance
altered nutrition
infection
bleeding

NURS 470 (28 decks)

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