AKI/CKD Flashcards
what are nitrogenous wastes a biproduct of
protein metabolism
what do kidneys excrete
nitrogenous wastes: drugs and toxins
how do kidneys keep acid base balance
excrete h+ ions
reabsorb bicarb
what hormones are released by kidneys
erthropoietin
renin
calcitriol (vit d3)
what does calcitriol do
absorbs calcium from intestines
what is normal gfr
> 60
what is gfr
mL of blood filtered per minute through glomeruli
what happens when kidneys fail
decreased gfr
accumulation of nitrogenous comounds
oliguria
what happens when there is an accumulation of nitrogenous comounds
Azotemia- Elevated BUN/Creatinine
* Uremia- syndrome of ESRF: increased urea/creatinine, fatigue, metallic taste in mouth, anorexia, N/V, pruritis, confusion; can progress to coma and death
what is oliguria
decreased urine ouput
< 400mL in 24 hours
* <0.5mL/kg/hr for at least 6 hours
what is normal urine output
30 ml/hr
what is the gold standard marker
creatinine
what is aki
sudden
full recovery possible
mortality higher if rrt needed, age increased, comorbidities increased
Decreased GFR/Creatinine
Clearance
* Fluid, electrolyte, acid-
base imbalances
* Treatment focused on
managing fluid,
electrolyte, acid base
imbalances + drug
treatment depending on
cause
what is ckd
gradual
progressive and permanent
treatment can slow progression
managing underlying conditions also slows progression
eskd fatal without rrt
lifespan reduced
complex med regimen
more susceptible to aki
what is prerenal in aki
perfusion problem
drop in bp or interuption of blood flow to kidneys
hypovolemia
what is intrarenal in aki
damage to kidney itself
direct damage to kidneys by infalmmation, toxins, drugs, infection or reduced blood supply, injury
-Acute tubular necrosis (ischemia,
nephrotoxic drugs)
-Inflammation (infections, autoimmune,
diabetes, nephrotoxic drugs, hypersensitivity
reaction)
-Other: Rhabdo, hemolysis
what is postrenal in aki
obstruction of urine flow
sudden obstruction of urine flow d/t enlarged prostate, kidney stones, bladder tumor or injury
extra or intrarenal
increased liklihood of aki if bilateral ureters or urethra obstructed
what do you look for with prerenal
Vomiting, diarrhea, diaphoresis,
hemorrhage/trauma, surgery, infection, diuretic use, heart
failure
s/s of hypovolemia
Dizziness, thirst
* Hypotension (including orthostatic hypotension)
* Tachycardia
* Decreased urine output
* Decreased cardiac output
* Decreased CVP
* **BUT: CVP ↑ in HF
* Lethargy
s/s of postrenal aki
Oliguria or Intermittent anuria
* Hydronephrosis
* Changes in urine stream
* Difficulty urinating
* Hematuria (kidney stone) or particles in urine
* Leads to s/s uremia
* Lethargy, etc
s/s of intrarenal
- Oliguria or anuria
- HTN results
- JVD, crackles, SOB, edema
- RBC, protein, casts in urine
- Lethargy, Change in LOC (azotemia)
what causes extrarenal post renal aki
compression by tumor or prostate (BPH),
neurogenic bladder
what causes intrarenal post renal aki
kidney stone, blood clot, tumor, blocked Foley
increased or decreased gfr with post renal aki
decreased
caused by renal tubule pressure increase
what is initiation phase of aki
Begins with initial insult and ends when oliguria develops
what is oliguric phase aki
Begins within a day post hypotensive/nephrotoxic event.
Glomerular dysfunction & less urine production.
* Serum BUN & Creatinine increase
* May have fluid overload, pulmonary edema, hypernatremia
what is diurectic phase aki
When perfusion returns, previously damaged glomeruli
not functioning up to par and cannot concentrate the urine
Can have extreme loss of Na, K, fluid during this phase
what is recovery phase of aki
Can take up to 3 months to fully return to normal GFR
and creatinine
diagonostics for aki
Renal US
* CT scan (w/o contrast)
* Renal biopsy
labs for aki
increase in both BUN/Cr
* decrease Creatinine Clearance/GFR
* Abnormal electrolytes- K, Na,
phosphorus, magnesium
* pH- metabolic acidosis
* Anemia may be present
* Urine Studies
* Sediment- cells, casts,
crystals
* Sodium
* Protein
* RBCs
aki treatment/management
Treat/eliminate cause
* Hypotension/hypovolemia
* Nephrotoxins
* Obstruction
* Maintain fluid balance
* IV fluid challenge/blood transfusion
* Loop diuretics
* Closely monitor I&O
* Correct electrolyte/acid-base imbalances
* Nutritional support- high catabolism
* Diet- low sodium, potassium, phosphorus; high calorie and carbohydrate
* Renal replacement therapy- continuous (CRRT) vs. intermittent HD
aki prevention
Dehydration
* Infection
* Hypoperfusion
* Toxic drug effects
* Close monitoring and assessment + early intervention
* I & O
* Renal function labs
* Urine characteristics
* Daily weights
* Catch decreased urine output early (report if oliguria persists more than 2 hours)
what is aeiou
acid base
electrolyte
intoxication
overload
uremic complications
ckd gfr rate
<60 for greater than 3 mo
is ckd reverable
no
what are the top 2 cuases of ckd
DM and HTN
other causes of ckd
Other causes: unresolved AKI, chronic inflammation (glomerulonephritis, pyelonephritis),
lupus, polycystic kidney disease
stage 1 ckd
> 90 ml/min gfr
At risk, normal kidney function.
Kidney disease may or may not be
present
stage 2 ckd
60-89
mild ckd
stage 3 ckd
30-59
moderate ckd
see azotemia, proteinuria
stage 4 ckd
15-29
severe ckd
consider or initiate dialysis
stage 5 ckd
<15
ESKD
cannot survive w/out dialysis or transplant
functioning nephrons comensate for which stages
1, 2 ,3
early ckd
glomerular compensation, increased output of dilute
urine, hyponatremia
* Monitor for dehydration
later stage ckd
disruption of RAAS, oliguria, hypernatremia
* HTN
* Heart failure, JVD, peripheral edema
* Pulmonary edema
* Management- monitor respiratory status, daily weights, and I&O; loop
diuretics (ineffective for ESKD); fluid restriction (dependent on urine output);
sodium restriction; antihypertensives, dialysis
hyperkalemia assessment
vitals-dysrhythmias
cardiac/ekg monitoring
treatment hyperkalemia
iv insulin and dextrose
sodium polystyrene sulfonate (kayexalate)
management/prevention of hyperkalemia
k+ restriction
dialysis
buildup of nitrogenous wastes- manifestations
uremia
what is uremia
azotemia with symptoms; Uremic syndrome = lab and clinical
manifestations of ESKD
cardiac sy,ptoms of uremia
pericarditis (friction rub), tamponade
hemotologic symptoms uremia
reduced WBC (increased infection risk), platelet dysfunction &
fragile capillaries (abnormal bleeding, bruising)
gi symptoms uremia
halitosis, metallic taste in mouth, mouth ulcerations, anorexia, N/V, abd
pain/cramping peptic ulcers, colitis, GI bleeding
* Inability to ingest, digest, or absorb food/nutrients leads to weight loss
neuro uremia symptoms
lethargy, inability to focus, asterixis, peripheral neuropathy/paresthesia,
ataxia, seizures/coma (uremic encephalopathy)
skin uremia symptoms
sallow (yellow-gray) pigmentation, pruritis, dry skin, ecchymosis, purpura,
uremic frost (late sign)
sexual dysfunction uremia symptoms
impotence, infertility, amenorrhea
managemet for buildup of nitrogenous wastes
dialysis
protein restriciton
prevent bleeding and infection
psychosocial support
symptom specific
management of anemia
Epoetin alfa (Epogen)
* PO/IV iron
* Folic acid
* Conserve energy, balance activity and rest
what causes anemia in ckd
decreased erythropoitin production
acid base imbalance of ckd
metabolic acidosis- hydrogen ions NOT excreted, bicarb not reabsorbed
if chronic- skeletal bone buffering
management of ckd acid base imbalance
oral sodium bicarb
dialysis
effect of calcium in ckd
Decreased production
of calcitriol by kidneys
= decreased active
vitamin D = decreased
absorption of calcium
from GI tract
decreased serum calcium
effect of phosphate in ckd
phosphate retention (hyperphophatemia)
binding of phosphate with calcium
decreased serum calcium
effect of phosphate and calcium in ckd
release of pth by parathyroid glands
release of calcium stored in bones (bone demineralization and bone density loss)
increased serum calcium
binding of phosphate with calcium (further metastatic calcification)
hyperparathyroidism
what is renal osteodystrophy
weakening of bones
what is osteomalacia
bone softening
management of renal osteodytroohy
Safety- prevent injury/fracture
* Phosphate restriction
* Phosphate binders with every meal
* Calcium acetate (PhosLo), calcium carbonate (Caltrate), sevelamer (Renvela)
ckd diagnostics
Bone x-rays- osteodystrophy
* US or CT- small kidney size
ckd labs
Urine
* Serum Sodium
* Hyponatremia - early
vs. Hypernatremia -
later
* Magnesium increased
* Potassium increased
* Metabolic acidosis
* Ca++ decreased /Phos increased
* Hgb/Hct decreased
ckd treatment
Fluid restriction
* Pharmacological
* BP control
* Hemodialysis
* CRRT
* Peritoneal dialysis
* Renal transplant
who recives rrt
AKI (Acute Kidney Injury)
* ESRD (End Stage Renal Disease)
* Post Transplant
* Failed Transplant
* Toxicology cases
* Young, old and everyone in between
what is hemodyalysis
typically 3 days a week approx. 3-6 hours per
treatment
what is peritoneal dialysis
CCPD, CAPD- typically completed every night
while the patient is sleeping
no extreme fluid and electrolyte shifts
what is plasmapheresis
Dependent on the cause for need
what is crrt
used for clients too
unstable for traditional hemodialysis
what is home hemodyalysis
typically 5 days per week (can be more or less
depending on the patient and physician’s orders
types of dialysis access
avf- preffered, connection btwn artery and vein
avg
cvc- risk for infection
pd cath
what do you feel and listen for with avf
thrill and bruit
care for avf
No venipunctures, blood pressures
* Limb alert band/sleeve
* Client education- no heavy lifting/sleeping on side of fistula
nsg responsibilities for dialysis
Assessing patients for signs or symptoms of fluid overload or electrolyte
imbalances, signs or symptoms of infection or need for dry weight
adjustment.
* Accessing CVC or AVF for treatment as needed.
* Monitoring vital signs throughout treatment.
* Administer medications.
* Communicate with physician findings that are abnormal.
* Draw lab work, monitor results for abnormalities.
* Adjust medications per algorithms.
* Hold pressure on sites following completion of treatment.
before treatment assessment for dialysis
ital signs, lung sounds, signs or symptoms of
fluid overload, NVD, bleeding, cramping, falls, injuries or bleeding, fluid
goal, access site for signs or symptoms of infection or functionality
during treatment assessment for dialysis
ssessment of vital signs, presence of bleeding at access
site, level of consciousness, machine settings, arterial and venous
pressures every 30 minutes.
post reatment assessment for dialysis
Vital signs, post treatment weight, hemostasis, patient
response to fluid removal
which has less diatary and fluid restrictions hemo or perit
peritoneal
complications of hemodialysis
disequilibrium syndrome
muscle cramps and back pain
headache
itching
hemodynamic and cardiac adverse events
infection
increased risk for subdural and intracranial hemmorrhage
complications for peritoneal
protein loss
peritonitis
hyperglycemia
resp distress
bowel perforation
infection
wt gain
contraindications of hemodialysis
hemodynamic intability or severe cardiac disease
severe vascular disease affecting access
bleeding disorders
uncontrolled diabetes
contraindications peritoneal
extrensive peritoneal adhesions, fibrosis, or active inflammatory gi disease
ascities or massive central obesity
recent abd surgery
nsg interventions ckd
Head to toe assessment
* VS, O2 sats
* EKG monitoring
* Strict I & O
* Fluid/dietary restriction
* Daily weights
* Phosphate binders with
meals, calcium & iron
supplements
* Monitor vascular access
site
* Monitor labs (esp K+, Ca,
& Phos, ABG)
* Stools occult blood
* Good skin and oral care
* Emotional support
* Energy conservation
* Safety- fractures, bleeding,
meds (renal dosing, avoid
nephrotoxins)
* Patient education
ckd nutrional considerations
Typically restricted:
* Sodium, potassium, phosphorus, magnesium
* Fluid intake
* May have protein restriction
* Generally high calorie, moderate fat
