Final 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.
AKI
What is most common cause
What is most common cause of death?
Acute tubular necrosis
Infection
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
What are urinary casts?
Clumps of cells and blood cells found in urine when kidneys are not working.
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 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
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
Complications of Dialysis 8
Hypotension, MM cramps Loss of blood hepatitis Steal syndrome- ischemia distal to fistula Tachycardia vision changes nausea mental changes
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.
Drugs that are hard on the kidneys 10
Aminoglycocides-(CIN), Antibiotics, Contrast, NSAIDS, Ibprophen, ACE inhibitors (pril) Hemoglobin and myoglobin- from damaged cells. Metformin, Dig, Opioids.
- What medication is commonly used as a phosphate binder in CKD
- What medication is commonly used as a phosphate binder in CKD
- What are the advantages of an AVF compared to compared to an AVG
Less likely to clot and less likely to become infected. Hear a bruit (whooshing) and feel a thrill.
Below list 5 complications of MG as a result of the muscle weakness in specific muscle groups.
What crisis and what are the s/s?
- ptosis/facial drooping
- difficulty with speech
- issues with chewing food
- problems with swallowing
- difficulty breathing (increased risk for aspiration and infections).
Other complications: fatigue, risk of falls/injury
These complications are associated with the lack of Ach and subsequent progressive muscle weakness. Muscle weakness in the face, neck and chest are especially concerning because they are vital for eating/swallowing/breathing.
Myasthenic Crisis-Exacerbation, worsening of mm weak like swallowing and breathing
RA
Rheumatoid arthritis is a systemic autoimmune disease that is characterized by inflammation of connective tissue in diarthrodial (synovial) joints. The person will have fever, fatigue and potentially organ involvement. Joint stiffness is a common symptom and can last several hours. There is a genetic predisposition associated with RA. Unlike osteoarthritis, those with RA experience periods of remission and exacerbation.
You are doing patient teaching on the treatments used in RA. Explain in layman’s terms to the patient the types of drug therapy used in RA, how they work and any side effects of the drug therapy.
DMARDs (Disease Modifying Antirheumatic Drugs) are the main treatment for slowing the disease progression and decreasing the risk for joint erosion or deformity. Methotrexate is the preferred DMARD. Methotrexate side effects include bone marrow suppression and hepatoxicity. Lab monitoring must take place -therapeutic levels can be reached in 4-6 weeks.
These are for life
Use Aggressively
Cross Match and what do results mean
Used to determine existence of antibodies agains donor mix r serum with d lymphocytes
negative is safe
positive is not safe and means cytotoxic antibodies to the donor
CD4 levels
Normal
Healthy
AIDS
800-1200
>500
<200