Kidneys unit one Flashcards
Lab value for serum creatinine and what kind of test is it?
What is creatinine
How does it compare to BUN
What do different levels mean?
0.6-1.3mg/dl blood test
A waste product from mm and protein. It is not reabsorbed in the kidneys and is there for a reliable indicator of kidney function.
It is more accurate than BUN
Increase=inflammation or infection, kidney damage
Decrease=malnutrition
BUN level and what type of test
What is BUN
What are the non renal factors that can increase it-7
10-20mg/dl Blood
Blood urea nitrogen
Infections, GI bleeds, Trauma, Athletic activity, mm breakdown, dehydration, steroids.
What is GFR normal value and what kind of test?
What does it say about kidney function?
How accurate is it?
> 90ml/min It is based on creatinine, age, sex, and race and it estimates the GFR.
If it is decreased then we have decreased kidney function
It is very accurate because it measures GFR and that is the best indicator of kidney function.
Creatinine clearance normal value and what kind of test?
How does the test work?
What about accuracy?
24 hour urine test that compares serum creatinine to creatinine in urine. It approximates GFR most accurate indicator of kidney function but
It takes time
AKI
What is most common cause
What is most common cause of death?
Acute tubular necrosis
Infection
What is Azotemia?
Accumulation of nitrogenous waste (Urea nitrogen Creatinine) in blood. AKI
What are the types of AKI with examples
prerenal- From lack of blood flow
Intrarenal-From damage to the kidneys
Postrenal- From blockage below the kidneys
What is parenchyma
soft tissue of the kidneys
Prerenal AKI
What is oliguria from?
What is happening in the kidney?
What do we treat?
What can it lead to?
Decreased volume of blood not damage to parenchyma
Because of low BP kidneys are trying to raise BP by saving NA+ and H2O RAAS
Fix cause and hydrate
Intrarenal AKI
Drugs that are hard on the kidneys 9
Aminoglycocides-(CIN), Antibiotics, Contrast, NSAIDS, ACE inhibitors (pril) Hemoglobin and myoglobin- from damaged cells. Metformin, Dig, Opioids.
What is the most common cause of intrarenal AKI
Acute tubular nephrosis from sepsis or nephrotoxins most common
others-Major surg, hypovolemia, shock, blood transfusion, mm injury
What other things can cause AKI besides drugs?
Glomerular nephrosis, systemic lupis erythmatosus
Intrarenal AKI
Reversible?
one manifestation
Yes-if basement membranes are still intact
Casts in urine
What are urinary casts?
Clumps of cells and blood cells found in urine when kidneys are not working.
Post Renal AKI Common causes
One complication
Recovery
Tx
BPH, Prostate cancer, cancer, Stones, trauma, tumors.
Bilateral urine obstruction leads to dilation (hydronephrosis)
If relieved in 48 hours or less=total recovery if prolonged-Tubular atrophy and irreversible fibrosis.
Remove obstruction
What are the stages of AKI 4
Initiation, Oliguric, Diuretic, recovery
RIFLE STAGING AKI
RIsk SC increases X1.5 or GFR Dec by 25% UOP-<0.5ml/kg/hr for 6 hours
Injury SC up X2 or GFR Down by 50% uop <0.5ml/kg//hr for 12 hours
Failure SC up X3 or >4mg/dl with acute rise of >/= 0.5 or GFR down by 75%
UP- <0.3 ml/kg/hr for 24 hours or anuria for 12 hours
Loss- Persistant acute kidney fail complete loss of function >4 weeks UOP same as fail
End- Complete loss of kidney function > 3months
Value for oliguric
<400ml/day
What defines oliguric stage value
When does it happen-3
How long does it last
Prognosis?
A reduction of urine output of less than 400ml a day. Usually happens within 1-7 days of injury but if ischemia is present than 24 hours. If from drugs it might be a week.
10-14 days up to months
Longer=poor prognosis
Oliguric phase in prerenal looks like
Low perfusion to the kidneys activates RAAS- Na+ and H2O retention =Low urine Na+ and High Specific gravity.
Describe Oliguric phase in Intrarenral
Damage to the kidneys makes Na+ spill out so increase Na+ and fixed specific gravity. Urine will have WBC, RBC, casts and prot in urine if their is glom dysfunction.
Relationship between K+ and acidosis
Hydrogen ions will push K+ out and cause more hyperk+
What are nitrogenous wastes?
From prots- Ammonia,urea, uric acid, creatinine.
Describe diuretic phase of AKI
UOP
WHy?
One thing
How long
Two more things
UOP- 1-3 lt sometimes 5 or more. It is from osmotic diuresis from high urea concentration. Kidneys can excrete waste but cant concentrate it. Can last 1-3 weeks. BUN and creatine start to stabilize.
Hypoeverything
Recovery phase of AKI
starts when?
What does recovery look like 4
Starts when GFR starts to increase and BUN and c start to decrease Major improvement in first 1-2 weeks. Full recovery can take 2 months.
Older adults less likely to recover, can progress to CKD
What are the diagnostics for AKI
Urine output and creatinine can be late (50% kid loss) but are diagnostic
Urine-Cells, cats, prots for intra renal
CT/MRI
Renal Biopsy
Care for AKI 10
eliminate cause-drugs dose blockage
Nutrtion-add cal increase carbs decrease fat and prot
Possible restrictions in electrolytes
loop diuretics- zides
fluids-replace what was lost- Daily output plus 600m
Dialysis- can help with hyperk+
Weights, IO,
Prevent infection
Skin checks
mouth care
drug for AKI
drugs tx for Hyperk
Loops-lasix zides, manitol, Na+ bicarb
Ca+ gluconate
Glucose
Insulin
Kayexalate- If these fail or there are neuro s/s dialyze
Glomerulonephritis path history
Inflammation of the glomerulus bl kidneys can be chronic or acute can cause Vascular scarring. can be sudden, temporary, or reversible chronic is slow and leads to irreversible renal failure
Infections, drugs, problems with immune system and disease
causes of glomerulonephritis
Diabetic neuropathy, HTN, goodpasture syndrome, Immunogloba ne. scleroderma, systemic lupus erthematosus, Infective carditis, post strep, virusus, pollyarth,
GLomerulonephritis history check includes 4
Infection, sore throat, upper respiratory infection, diabetes
Acute post streptococcal glomerulonephritis patho/history
Cause, when, how
Most common cause of aute GN developes 1-2 weeks after strep A infection or impetigo, injury from antibody antigen complex that deposits in glomeruli.
s/s of APSG 8
Periorbital edema early sign, HTN, hematuria, protein in urin, Oliguria, ab/flank pain, can be asympotmatic,
Diagnosis of APSG 8
History and examination, titers, renal biopsy, dipstick, urine microscope-RBC, casts, Proteins,. BUN and creatinine GFR
Tx for APSG 6
Most recover fine. Rest,
Na+ and fluid restrictions
Antihypertensives
Decrease prot if BUN is up
Antiiotics only is strep is present
PREVENTION
Chronic glomerularnephritis Patho history 4
Syndrome of permanent and progressive renal failure can progress to ESRD Acute can lead to chronic, Slow and over time, can be unaware until kidneys start to fail.
CGN show up in 3
Increased BP, abnormal urine, or increased creatinine
S/s of cgn 6
Tx
Protein urea, hematuuria, casts, Increased BUN, increased Creatinine, asymp
manage CKD and symptoms
Goodpasture syndrome patho and history 4
Autoimmune disorder characterized by antibodies attacking glomerular and aveolar basement membranes. Rare seen in older children and adults 30-60
Goodpasture syndrome Manifestations
Lungs- Cough, dyspnea, hemoptysis, crackles, pulmonary insuficiency, flu like
Renal- hematuria, weakness, pallor, anemia,.
Can quickly go into renal fail but usually lungs kill.
Goodpasture tx 5
Immunosuppressants, Corticosteroids, plasmapheresis, dialysis, renal transplant.
Rapidly progressive GN Patho/ history
Rapid and progressive loss of kidney function over days-weeks
can be idopathic, acute, or chornic, has glomerular cresscent formation, Cacn be from infections, ASPGN, goodpasture or SLE
manifestations of RPGN 5
txn 4 and one more thing
HYpertn, Edema, Protur, Hematuria, Casts
Corticosteroids, immunosuppressants, plasmaphereisi, dialysis, transplant if ESRD
can reoccur in transplants
Nephrotic syndrome Patho history 4
Glom is perm to prot=prot in urine=low plasma albumin and tissue edema.
SLE and diabetes are common.
Manifestations of Nephrotic syndrome 8
Massive proteinuria, Generalized edema, HTN, Hyperlip, Hypoalbum, Impaired immune, Hypo ca+, Hypercoagulability
Nursing considerations for Nephrotic syndrome 7
Control primary disease, tx s/s, Corts, ARBS ACE, Low Na+ and mod prot diet measure-Weights, IO, Edema
Chronic KIdney disease. Patho/ history 7
Progressive, irreversible damage to kidneys. More common than AKI, Getting more prevanlent, defined as koidney damage- GFR <60ml/min for longer than 3 moths.
high mortality rate
disability
Staging for CKD
Stage GFR
1 > or equal to 90.
2 60-89
3a 45-59
3b 30-44
4 15-29
5 <15 need Dialysis or transplant
CKD Manifestations most common cause of death
Cardiovascular
cardio stuff, pericarditis, GI bleeding, Hyperparithyroid, thyroid abn, amenorrhea, ED, increase in Rennin, hyperlip, Acidosis, anemia, bleeding, encephalopathy, sleep issues, HTN, retinopathy, Pleuris, pneomia, eccymosis, dry scaley skin, calcifications, osteofibrosa, osteomalacia, paresthesia, RLS
CKD Manifestations most common cause of death
Cardiovascular
cardio stuff, pericarditis, GI bleeding, Hyperparithyroid, thyroid abn, amenorrhea, ED, increase in Rennin, hyperlip, Acidosis, anemia, bleeding, encephalopathy, sleep issues, HTN, retinopathy, Pleuris, pneomia, eccymosis, dry scaley skin, calcifications, osteofibrosa, osteomalacia, paresthesia, RLS
Electrolyte imbalances CKD
Hyperk+, Na+ up or down, Hypermag, Hyperphosphate,
Diagnosis of CKD 4
Prot in urine is first indication
UA can detect RBC WBC Prots, Casts, Glucose
ultrasound
Lab
Treatment for CKD 5
Preserve kid function, decrease risk for cardiac event. prevent complications, Recognition and diagnosis for hyperk, weights and measurements.
Drugs CKD 6ish
Ca+ supplements, phosphate binders, AntiHTN- Ace-pril ARBs -statrtan
Erythropo
lipid decrease- statins
Adust other drugs,
Iron, EPO, blood transfusions.
Nutrition for CKD
Normal not high prot
Don’t usually restrict H2o but if UOP low previous day + 600ml
use diuretics
Na+ 2-4g/day
K+ 2,000-3,000mg a day
Phosphate-not restrict use meds
When do we start dialysis?
GFR <15ml/min
Mortality with Peritoneal dialysis
Higher similar for two years then higher
Cycle of Peritoneal Dialysis
How often?
two things
Exchange=Fill, dwell, drain
four that last 1-2 hours each or continuous
Aseptic technique to prevent peritonitis
may still need dialysis
complications of peritoneal d 6
Peritonitis-more perm for prot loss
Catheter site infection
Hernias
Low back pain
Pulmonary complications-from decreased lung expansion
prot loss
What are CI in low kidney function
Central lines, blood draws, BP, aeseptic
oliguria and value
Low urine output less than .5ml/kg/h
Anuria and value
No urine output less than 50ml/day
Normal urine value
0.5-1.0ml/kg/hr
Chloride level
97-107 mEq/L
Potassium level
3.5-4.5mEq/L
Calcium level
8.6-10.2 mg/dl
phosphate level
2.4-4.4g/dl
One thing about peri vs hemo dy
peri may need more prot due to loss
what does hemodialysis contain
3
2 lg bore needles 14-16 G
Heparin
Assess fluid status before -difference between last post d weight and current weight is how much to pull off
Complications of Dialysis 4
Hypotension, MM cramps
Loss of blood
hepatitis
Steal syndrome- ischemia distal to fistula
Tachycardia
vision changes
nausea
mental changes
What is continuous renal replacement therapy
Double luman cath in large vein
slow and continuous
can be continued for 40 days
For when they can handle it being pulled off they are sick and in the ICU
Transplant info
How many ger?
Wait time?
<4%
2-5 yrs
What are the contraindications for Transplant 5
Advanced cancer, Untreated cardiac disease., chronic respiratory fail. extensive cardiovascular disease, nonadherence to medical reg.
Complication of transplant
Rejection, infection, CVD, Cancer, Recurrence
Ophase e-
Pre-rass low Na+ high SG
Intra-Na+ spills out Fixed SG
