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Renal > care of patients with acute/chronic kidney injury ch 71 > Flashcards

care of patients with acute/chronic kidney injury ch 71 Flashcards

1
Q

onset

difference between acute/chronic

A

acute: sudden (hours to days)
chronic: gradual (months to years)

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2
Q

% of nephrons involved

difference between acute/chronic

A

acute: 50%
chronic: 90-95%

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3
Q

duration of disease

difference between acute/chronic

A

acute: 2-4 weeks, less than 3 months
chronic: permanent

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4
Q

prognosis of disease

difference between acute/chronic

A

acute: good for return of kidney function with supportive care. high mortality in some situations
chronic: fatal without a renal replacement therapy such as dialysis or transplantation

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5
Q

azotemia

A

the retention and buildup of nitrogenous wastes in the blood

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6
Q

When BUN rises faster than the serum creatinine level, the cause is usually related to ____

A

protein breakdown or dehydration

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7
Q

when both the BUN and creatinine levels rise and the ratio between the two remains constant, this indicates ____

A

kidney dysfunction

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8
Q

causes of pre renal AKI

A

any condition that decreases blood flow to the kidneys and leads to ischemia in the nephrons

shock (hypovolemia, hemorrhage, distributive, obstructive)
HF
PE
anaphylaxis
sepsis
pericardial tamponade

most common: shock, HF

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9
Q

causes of intrarenal AKI

A

actual physical, chemical, hypoxic, immunologic image directly to the kidney tissue

usually occurs with damage to glomeruli, interstitial tissue, or tubules

acute interstitial nephritis
exposure to nephrotoxins
acute glomerular nephritis
vasculitis
acute tubular necrosis
renal artery or vein stenosis
renal artery or vein thrombosis
formation of crystals or precipitates in the nephron tubules
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10
Q

normal osmolarity

A

270-300

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11
Q

HCO3 range

A

22-26

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12
Q

PaCO2

A

35-45

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13
Q

early AKI can often be revered by:

A

correcting blood volume
increasing BP
improving cardiac output

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14
Q

drugs that most often cause intrarenal AKI

A 
aminoglycoside antibiotics (gentamicin, neomycin, streptomycin, kanamycin, tobramycin)
NSAIDs
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15
Q

causes of postrenal AKI

A

obstruction of the urine collecting system anywhere from the calyces to the urethral meatus
obstruction must be bilateral to cause post renal failure, unless only 1 kidney is functional

ureter, bladder, urethral cancer
kidney, ureter, bladder stone
bladder atony
prostatic hyperplasia or cancer
urethral stricture
cervical cancer
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16
Q

onset phase of AKI

  • description
  • characteristics
A

begins with precipitating event and continues until oliguria develops

last hours to days

the gradual accumulation of nitrogenous wastes, such as increasing serum creatinine and BUN

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17
Q

oliguric phase of AKI

  • description
  • characteristics
A

characterized by urine output of 100-400 mL/24 hr that does not respond to fluids or diuretics
lasts 1-3 weeks

increasing serum creatinine and BUN
hyperkalemia, metabolic acidosis, hyperphosphatemia, hypocalcemia, hypermagnesemia
sodium retention
urine specific gravity and urine osmolarity do not vary as plasma osmolarity changes

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18
Q

diuretic phase of AKI

  • description
  • characteristics
A

high output phase
often has a sudden onset within 2-6 wk after oliguric stage
urine flow increases rapidly over a period of several days
diuresis can result in an output of 10 L/day of dilute urine

BUN levels start to fall and continues till it reaches normal levels
normal kidney tubular function is re-established

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19
Q

recovery phase of AKI

  • description
  • characteristics
A

patient begins to return to normal levels of activity

complete recover can take up to 12 months

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20
Q

manifestations of volume depletion

yellow box 1541

A 
low urine output
decreased systolic BP
decreased pulse pressure
orthostatic hypotension
thirst
rising blood osmolarity
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21
Q

potential nephrotoxic substances

A 
rifampin
vancomycin
ibuprofen
ketorolac
naproxen
tylenol
captopril
metformin
myoglobin
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22
Q

manifestations of prerenal azotemia AKI

A 
hypotension
tachycardia
decreased cardiac output
decreased central venous pressure 
decreased urine output
lethargy
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23
Q

renal manifestations of intrarenal/postrenal AKI

A

oliguria or anuria

increased urine specific gravity

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24
Q

cardiac manifestations of intrarenal/postrenal AKI

A 
HTN
tachycardia
JVD
increased central venous pressure
tall T waves
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25
Q

respiratory manifestations of intrarenal/postrenal AKI

A 
SOB
orthopnea
crackles
pulmonary edema
friction rub
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26
Q

gastrointestinal manifestations of intrarenal/postrenal AKI

A

anorexia
n/v
flank pain

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27
Q

neurologic manifestations of intrarenal/postrenal AKI

A

lethargy
headache
tremors
confusion

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28
Q

lab values in pt with prerenal azotemia

A 
BUN/creatine ration of greater than 20
sodium often less than 10-20 
urine concentrated
urine sediment (RBCs, RBC casts, tubular cells)
myoglobin, hemoglobin
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29
Q

lab values for intrarenal problem

A

BUN/creatine ration less than 15
urine sodium less than 40
specific gravity less than 1.01

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30
Q

lab values for postrenal problem

A

urine sodium may be normal

specific gravity 1.000-1.010

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31
Q

main problems during the oliguric phase

A

close monitoring for life threatening electrolyte changes and nitrogen retention

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32
Q

problems during the diuretic phase

A

hypovolemia

electrolyte loss

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33
Q

what do calcium channel blockers do in AKI

A

can be given if caused by nephrotoxic acute tubular necrosis
prevent movement of calcium into the kidney cells, maintain kidney cell integrity, improve the GFR by improving kidney blood flow

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34
Q

action/purpose of Digoxin (cardiac glycosides) for kidney disease

A

digoxin (Lanoxin)
used when HF induces kidney injury/disease or makes it worse
Improves ventricular contraction, increasing stroke volume and cardiac output

do not take antacids within 2 hrs

35
Q 
folic acid (Vitamin B9)
-action/purpose
A

when pt is receiving dialysis, many essential vitamins and minerals are removed from the blood. replacement is needed to prevent deficiencies

36
Q

ferrous sulfate

action/purpose

A

when pt is receiving dialysis, many essential vitamins and minerals are removed from the blood. replacement is needed to prevent deficiencies

take with meals, daily stool softeners

37
Q

epoetin alfa (Epogen, Procrit)

-action/purpose

A

synthetic erythropoietin

drug prevents anemia by stimulating RBC growth and maturation in the bone marrow

38
Q

epoetin alfa (Epogen, Procrit)

-nursing interventions

A

teach pt to report any side effects as soon as possible: chest pain, difficulty breathing, high BP, rapid weight gain, seizures, rash, hives, swelling of feet or ankles (drug can induce cardiovascular problems such as an MI)

must have hemoglobin levels monitored weekly

39
Q

two types of synthetic erythropoietin

A

epoetin alfa (Procrit, Epogen)

darbepoeitin alfa (Aranesp)

40
Q

types of phosphate binders

A

aluminum hydroxide gel (Amphojel)

aluminium carbonate gel (Basalijel)

41
Q

purpose of phosphate binders

A

high blood phosphate levels cause hypocalcemia and osteodystrophy. drugs lower serum phosphate levels by binding phosphorus present in food

42
Q

phosphate binders

nursing interventions

A

take with meals (drug binds to phosphate in food)

take digoxin 2 hours before/after

take stool softeners

report muscle weakness, slow or irregular pulse, confusions (manifestations of hypophosphatemia)

43
Q

key features of uremia

1547

A 
metallic taste in mouth
anorexia
n/v
muscle cramps
uremic frost on skin
itching
fatigue
lethargy
hiccups
edema
dyspnea
muscle cramps
paresthesias
44
Q

GFR of >90

-what is stage of CKD

A

stage 1

at risk; normal kidney function
early kidney disease may or may not be present

45
Q

GFR 60-89

-what is stage of CKD

A

stage 2

mild CKD

may be slight elevation of metabolic wastes in the blood. Increased urinary output of dilute urine may occur, and if untreated, can cause dehydration

46
Q

stage 1 CKD

interventions

A 
screen for risk factors:
uncontrolled HTN
DM
chronic kidney or UTI
presence of genetic kidney diseases
exposure to nephrotoxic substances
47
Q

stage 5 CKD

end stage kidney disease

interventions

A

implement renal replacement therapy

kidney transplantation

48
Q

rate of creatinine exception depends on

A

muscle mass
physical activity
diet

49
Q

the method for assessing the GFR is the use of a formula that considers:

A 
serum creatinine level
age
gender
race
body size
50
Q

neurologic manifestations of CKD

A 
lethargy, seizures, coma= uremic encephalopathy
daytime drowsiness
inability to concentrate
slurred speech
asterixis
tremors, twitching, jerky movements
myoclonus
ataxia
paresthesias
51
Q

cardiovascular manifestations of CKD

  • result from:
  • examples:
A

result from fluid overload, HTN, HF, pericarditis, K induced dysrhythmias

cardiomyopathy
HTN
peripheral edema
HF
uremic pericarditis
pericardial effusion
pericardial friction rub
cardiac tamponade
52
Q

respiratory manifestations of CKD

A 
uremic halitosis
tachypnea
deep sighing, yawning
Kussmaul respirations
uremic pneumonitis
SOB
pulmonary edema
pleural effusion
depressed cough reflex
crackles
53
Q

hematologic manifestations of CKD

A

anemia

abnormal bleeding and bruising

54
Q

GI manifestations of CKD

A 
anorexia
n/v
metallic taste in the mouth
change sin taste acuity and sensation
uremic colitis (diarrhea)
constipation
uremic gastritis
possible GI bleeding
breath odor
stomatitis
55
Q

urinary manifestations of CKD

A 
polyuria
nocturia (early)
oliguria 
anuria (late)
proteinuria
hematuria
diluted straw colored appearance (early)
concentrated and cloudy appearance (later)
56
Q

integumentary manifestations of CKD

A 
decreased skin turgor
yellow gray pallor
dry skin
pruritus
ecchymosis
purpura
soft tissue calcifications
uremic forst (late, premorbid)
57
Q

musculoskeletal manifestations of CKD

A

muscle weakness and cramping
bone pain
pathologic fractures
renal osteodystrophy

58
Q

reproductive manifestations of CKD

A

decreased fertility
infrequent or absent menses
decreased libido
impotence

59
Q

priority problems for pts with CKD

A 
fluid overload
potential for pulmonary edema
decreased cardiac output
inadequate nutrition
potential of infection
potential for injury
fatigue
anxiety
60
Q

early s/s of pulmonary edema

A 
restlessness
anxiety
rapid HR
SOB
crackles the begin at base of lungs
frothy pink tinged sputum
61
Q

CKD and pulmonary edema

- nuring interventions

A

furosemide given cautiously
measure urine output q15-30 minutes during acute episode
assess breath sounds q2 hrs
IV morphine to reduce myocardial oxygen demand

62
Q

dietary protein recommendations

-for pt with chronic uremia

A

0.55-0.60 g/kg/day

least amount of protein, compared to other conditions

63
Q

dietary protein recommendations

  • for pt with hemodialysis
A

1-1.5 g/kg/day

64
Q

dietary protein recommendations

  • for pt with peritoneal dialysis
A

1.2-1.5 g/kg/day

slightly higher compared to other 2

65
Q

fluid recommendations

  • for pt with chronic uremia
A

depends on urine output but may be as high as 1500-3000 mL/day

(pt can drink more fluid with this than other two conditions)

66
Q

fluid recommendations

  • for pt with hemodialysis
A

500-700 mL/day plus amount of urine output

67
Q

fluid recommendations

  • for pt with peritoneal dialysis
A

restriction based on fluid weight gain and BP

68
Q

potassium recommendations

  • for pt with chronic uremia
A

60-70 mEq/day

least amount of K+ compared to other conditions

69
Q

potassium recommendations

  • for pt with hemodialysis
70
Q

potassium recommendations

  • for pt with peritoneal dialysis
A

usually no restriction

71
Q

sodium recommendations

  • for pt with chronic uremia
A

1-3 g/day

lowest restriction compared to other conditions

72
Q

sodium recommendations

  • for pt with hemodialysis
73
Q

sodium recommendations

  • for pt with peritoneal dialysis
A

based on fluid wt gain and BP

74
Q

complications of hemodialysis

A 
disequilibrium syndrome
muscle cramps
hemorrhage
air embolus
hypotension
anemia
cardiac dysrhythmias
infection
75
Q

complications of peritoneal dialysis

A 
protein loss
peritonitis 
hyperglycemia
respiratory distress
bowel perforation
infection
76
Q

hemodialysis is started on these patients immediately

A 
fluid overload that doesn't respond to diuretics
pericarditis
uncontrolled HTN
neurologic problems
development of bleeding
77
Q

complications of AV access

A 
thrombosis
stenosis
infection
aneurysm formation
ischemia
HF
78
Q

s/s of disequilibrium syndrome

A 
headache
nausea
vomiting
restlessness
decreased LOC
seizures
coma
death
79
Q

treatment for disequilibrium syndrome

A

anticonvulsants

barbiturates

80
Q

manifestations of peritonitis

A 
cloudy dialysate outflow (earliest sign)
fever
abd tenderness
abd pain
general malaise
n/v
81
Q

post of care following kidney transplant

A

monitor output at least hourly for 48 hours

urine pink/bloody right away, gradually turns normal over several days to weeks

catheter might be used, remove in 3-7 days

mannitol may be prescribed

q2-4 hrs: measure BP, I&O

82
Q

clinical manifestations of hyperacute rejection

A

increased temp
increased BP
pain at transplant site

83
Q

clinical manifestations of acute rejection

A 
oliguria or anuria
temp over 100
increased BP
enlarged tender kidney
lethargy
increased creatinine, BUN, K+
fluid retention

Renal (5 decks)

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