Final Flashcards
What is azotemia?
an accumulation of nitrogenous waste products (urea, nitrogen, creatinine) in the blood
What is urea? How is it measured? What is the normal value?
BUN
By product of protein
=20
What is creatinine? How is it measured? What is the normal value?
By product of muscle
=1
What are waste products?
Urea
Creatinine
Electrolytes
Acute Kidney Injury (AKI) stage 1
Prerenal = decreased blood flow, decreased blood volume
Prerenal causes of AKI
Hypovolemia
Decreased cardiac output
Decreased vascular resistance
Decreased renovascular blood flow
Hypovolemia (prerenal) causes
- dehydration
- hemorrhage
- GI losses (diarrhea, vomiting)
- excessive diuresis
- hypoalbuminemia
- burns
Decreased CO (prerenal) causes
- dysrhythmias
- cardiogenic shock
- heart failure
- MI
Decreased vascular resistance (prerenal) causes
- anaphylaxis
- neuro injury
- septic shock
Decreased renovascular blood flow (prerenal) causes
- bilateral renal vein thrombosis
- embolism
- hepatorenal syndrome
- renal artery thrombosis
Acute Kidney Injury (AKI) stage 2
Intrarenal = inside the kidney
Intrarenal causes
Nephrotoxic injury
Interstitial nephritis
Other causes
Nephrotoxic injury (intrarenal) causes
- drugs: aminoglycosides (gentamicin), amphotericin B
- contrast media
- hemolytic blood transfusion reaction
- severe crush injury
- chemical exposure: ethylene glycol, lead, arsenic, carbon tetrachloride
Interstitial nephritis (intrarenal) causes
- allergies: antibiotics (sulfonamides, rifampin), NSAIDS, ACE inhibitors
- infections: bacterial (acute pyelonephritis), viral (CMV), funal (candidiasis)
Other causes of intrarenal
- prolonged prerenal ischemia
- acute glomerulonephritis
- thrombotic disorders
- toxemia of pregnancy
- malignant hypertension
- systemic lupus erythematosus
Acute Kidney Injury (AKI) stage 3
Postrenal = blockage in kidney! (back up of urine)
Postrenal causes
- BPH
- bladder or prostate cancer
- calculi formation
- neuromuscular disorders
- spinal cord disease
- strictures
- trauma (back, pelvis, perineum)
AKI phases
Oliguric or nonoliguric
Diuretic
Recovery
Oliguric phase of AKI
*holding onto waste
- decreased urine output <400 mL/day
- hypervolemia
- edema in extremities
- hypertension
- pulmonary edema, crackles, short of breath
- metabolic acidosis
- increased BUN, creatinine, K
- decreased Na
*asterixis-flapping hand motion
Nonoliguric phase of AKI
urine output >400 mL/day
What should be restricted during oliguric phase?
Potassium
Sodium
Protein
If protein is low, give _______.
albumin
Diuretic phase of AKI
(hypo everything!)
- urine output 5L/day
- hypovolemia
- hyponatremia
- hypotension
- hypokalemia
- dehydration
Recovery phase of AKI
- GFR increases
- BUN and creatinine decrease
- casts-tubules sloughing
- dark, concentrated urine
*high protein and calorie diet
Normal GFR
125 mL/min
GFR ________ with injury
decreases
GFR ________ when recovery phase begins in AKI
increases
Chronic Kidney Disease (CKD) is…
progressive and irreversible
CKD manifestations
Psychologic
- anxiety
- depression
CKD manifestations
Cardio
- HTN
- HF
- CAD
- pericarditis
- PAD
CKD manifestations
GI
- anorexia
- N/V
- GI bleeding
- gastritis
CKD manifestations
Endocrine
- hyperparathyroidism
- amenorrhea
- erectile dysfunction
- thyroid abnormalities
CKD manifestations
Metabolic
- carb intolerance
- hyperlipidemia
CKD manifestations
Hematologic
- anemia
- bleeding
- infection
CKD manifestations
Neuro
- fatigue
- headache
- sleep disturbances
- encephalopathy
CKD manifestations
Ocular
-hypertensive retinopathy
CKD manifestations
Pulmonary
- pulmonary edema
- uremic pleuritis
- pneumonia
CKD manifestations
Integumentary
- pruritis
- ecchymosis
- dry, scaly skin
CKD manifestations
Musculoskeletal
- vascular and soft tissue calcifications
- osteomalacia
- osteitis fibrosa
CKD manifestations
Peripheral neuropathy
- parathesias
- RLS
Stage 1 of CKD
GFR >90
manage with diet
control B/P
Stage 2 of CKD
GFR 60-89
manage with diet
control B/P
Stage 3 of CKD
GFR 30-59
Stage 4 of CKD
GFR 15-29
Stage 5 of CKD
GFR <15
Kidney failure
Chronic Renal Failure (CRF)
-diminished renal reserve
(stages 1 and 2 of CKD)
-renal insufficiency
(stages 3 and 4 of CKD)
-end stage renal disease (ESRD)
(stage 5 of CKD)
Diminished renal reserve
stages 1 and 2 of CKD
- GFR >90 mL/min
- control B/P
- kidney damage with normal or increased GFR
- decreased urinary concentration (nocturia)
- treatment of diabetes, hypertension, renal artery stenosis
- 24 hour urine (creatinine)
Renal insufficiency
stages 3 and 4 of CKD
- GFR 30-89 mL/min
- headaches
- decreased ability to concentrate urine
- polyuria to oliguria
- increased BUN, creatinine
- edema
- mild anemia
- increased B/P
- weakness/fatigue
End stage renal disease (ESRD)
stage 5 of CKD
- GFR <15 mL/min
- confusion, weakness, fatigue
- increased B/P, pitting edema, increased CVP, pericarditis
- SOB, suppressed cough, thick sputum
- amonia odor to breath, metallic taste, mouth ulcers, anorexia, N/V
- behavior changes
- anemia (decreased RBC, increased HR)
- dry, flaky skin, pruritis, ecchymosis, pupura
- cramps, renal osteodystrophy, bone pain
Diffusion
urea, creatinine, uric acid and electrolytes move from the blood to the dialysate to lower the concentration in the blood
Osmosis
glucose is added to the dialysate and creates an osmotic gradient across the membrane, pulling excess fluid from the blood
Advantages of peritoneal dialysis (PD)
- immediate initation in most hospitals
- less complicated
- portable system with CAPD
- fewer dietary restrictions
- pts with vascular access problems
- decreased cardio stress
- home dialysis possible
- preferable for diabetes pt
Advantages of hemodialysis (HD)
- rapid fluid removal
- rapid urea and creatinine removal
- potassium removal
- less protein loss
- decreased triglycerides
- temporary access can be placed at bedside
Process for PD
Exchange
3 phases
Phase 1 of PD
Inflow
-2L solution infuses-10 minutes
Phase 2 of PD
Dwell
- diffusion and osmosis between pt’s blood and peritoneal cavity
- 20 or 30 min-8 hours, depending on method
Phase 3 of PD
Drain
- 15-30 minutes
- can be facilitated by gently massaging abdomen or changing position
Process for HD
1 needle pulls blood
1 needle puts blood back into pt
Potential complications of PD
- infections
- pain
- peritonitis
- heart problems
- pulmonary problems (pneumonia, atelectasis, bronchitis)
- protein loss
- carb abnormalities
Potential complications of HD
- hypotension
- muscle cramps
- hepatitis
- infection
- heart disease
Human Leukocyte Antigen (HLA)
- antigens responsible for rejection of genetically unlike tissue
- histocompatibility antigens
- matching organs and tissues for transplants
The more HLA matches =
less likely for rejection
HLA matching for corneas
None needed (avascular)
HLA matching for liver, heart, lungs
some needed
HLA matching for kidneys and bone marrow
EXACT match needed
Positive crossmatch
bad reaction with donor/recipient blood
Negative crossmatch
NO reaction
-organ safe for transplantation
What tests are needed for transplants?
HLA matching
Crossmatch
ABO
Types of rejection
- hyperacute
- acute
- chronic
Hyperacute rejection
- within 24 hours
- blood vessels destroyed rapidly from pre-existing antibodies (positive crossmatch)
- RARE
- No treatment
- transplant organ needs to be removed
Acute rejection
- within 6 months
- recipients lymphocytes activated against donated tissue or antibodies develop after transplant
- common with deceased organs
- REVERSIBLE-treat with immunosuppressants and corticosteroids
Chronic rejection
- over months or years
- repeated acute rejections
- fibrosis and scarring occurs
- IRREVERSIBLE-pt placed on transplant list
- difficult to manage, support therapy needed
Graft vs host disease
occurs when immuno-incompetent pt transfused or transplanted with immuno-competent cells
*donor T cells attack recipient
Graft vs host disease manifestations
ONLY 3
Skin-maculopapular rash to desquamation
Liver-mild jaundice to hepatic coma
GI-diarrhea, GI bleeding, malabsorption, abdominal pain
PCs for organ transplantation
- rejection
- susceptibility to infection
- heart disease
- malignancies
- recurrence of kidney disease
- corticosteroid-related complications
Determines how well pt is oxygenated
PaO2
Determines how well pt is ventilating
PaCO2
3 mechanisms that control acid/base
Kidney-bicarb (HCO3)
Lungs-carbon dioxide (CO2)
Buffer-electrolytes
Normal pH range
7.35-7.45
Normal range for PaCO2
35-45
Normal range for HCO3
22-26
ABG sites
- radial artery (most common)
- brachial artery (avoid in obese pts)
- femoral artery (only used as last resort)
When doing the Allen’s test, which artery do you release pressure?
ULNAR ARTERY!
Blood will _______ into the syringe
pulsate
Blood gas syringes fill by themselves, stopping at ___
2mL
Indications for arterial lines
- Frequent ABG sampling
- Continuous BP monitoring
Indications for continuous BP monitoring
- shock
- infusion of vasoactive drugs
- procedures for coronary interventions
- acute hypo and hypertension
- respiratory failure
- neuro injuries
How often should ABG draws be done if pt is on a vent?
Daily AM
Arterial line complications
- hemorrhage
- infection
- thrombus formation
- neuro impairment
- loss of limb
True or false:
H+, CO2, and K is more acidic
TRUE
Acidosis indicates an ______ of H+, and a _______ of HCO3
excess; deficit
Alkalosis indicates an ______ of HCO3, and a ______ of H+
excess; deficit
pH <7.35
acidosis
pH >7.45
alkalosis
What does high PaCO2 indicate?
Respiratory acidosis
What does low PaCO2 indicate?
Respiratory alkalosis
What does high HCO3 indicate?
Metabolic alkalosis
What does low HCO3 indicate?
Metabolic acidosis
Respiratory acidosis causes
(Hypoventilation)
- COPD
- OD/sedation
- chest trauma
- severe pneumonia
- pulmonary edema
- atelectasis
- respiratory muscle weakness
- mechanical hypoventilation
- phrenic nerve injury (C2)
Respiratory alkalosis causes
- hyperventilation
- stimulated respiratory center
- mechanical hyperventilation
Respiratory alkalosis hyperventilation causes
- hypoxia
- PE
- anxiety
- fear
- pain
- exercise
- fever
- high altitudes
- pregnancy
Respiratory alkalosis stimulated respiratory center causes
- septicemia
- encephalitis
- brain injury
- salicylate poisoning
Metabolic acidosis causes
- DKA
- diarrhea
- renal failure
- shock
- salicylate OD
- sepsis
Metabolic alkalosis causes
- loss of gastric secretions (NG suction, severe vomiting)
- diuretic therapy (K wasting diuretics)
- overuse of antacids
Normal intracranial pressure (ICP)
5-15 mmHg
Normal compensatory adaptations
- changes in CSF volume
- cerebral vasodilation or vasoconstriction
Cerebrospinal fluid =
10%
Intravascular blood =
12%
Brain tissue =
78%
Autoregulation of cerebral blood flow (CBF)
- brain has ability to regulate own blood flow
- ensures adequate blood flow to brain
- influenced by systemic arterial pressure
How much glucose and O2 does brain need?
25% and 20%
Cerebral perfusion pressure (CPP)
pressure needed to ensure blood flow to brain
Normal CPP
60-100 mmHg
How to calculate CPP
MAP-ICP=CPP
CPP <50 mmHg
associated with ischemia and neuronal death`
Compliance
expandibility of the brain
Stage 1 of CBF
- high compliance
- increase of volume in brain does not increase ICP
- autoregulation intact
Stage 2 of CBF
- compliance lessens
- increase of volume in brain increases risk of increasing ICP
Stage 3 of CBF
- decrease compliance
- small addition of volume increases ICP
- loss of autoregulation
- B/P rises to maintain CPP
- decompensation about to happen
- cushing’s triad
Stage 4 of CBF
- ICP at lethal levels with little increase in volume
- herniation of brain