π©πΎβπ- Renal & Crisis Test Flashcards
Two functions of the kidney
Regulatory- controls fluid/electrolyte & acid/base balance
Hormonal- RBC formation, BP regulation, vitamin D activation
Normal renal function values
BUN, creatinine, Uric acid, GFR, urine output
BUN- 8 to 25 mg/dL
Creatinine- 0.6 to 1.3 mg/dL
Uric Acid- 2.5 to 8.0 mg/dL
GFR- 125 ml/min
Urine output- 1 to 3 L/day
Hormones in kidney function
ADH- antidiuretic hormone regulates osmolarity
RAAS- renin angiotensin aldosterone System regulates BP and volume
ANF- atrial natriuretic factor regulates BP and volume
Decreased GFR will cause which hormone to be secreted
Renin
3 most common causes of kidney disease
Diabetes
Hypertension
Glomerulonephritis
Types of drugs that are nephrotoxic
Example of each
NSAIDS - ibuprofen, naproxen, ketorolac
Chemo- cisplatin, methotrexate, cyclophosphamide
Antibiotics- vancomycin, gentamicin, amphotericin B, methicillin
Acute kidney injury vs chronic kidney disease
AKI- sudden onset, about 50% kidney function, usually last a few weeks but no more than 3 months, with treatment function resolved to original state
CKD- gradual onset, permanent, less than 10% function is present, fatal with renal replacement therapy
Three causes/subcategories of AKI
Prerenal- outside the kidney, caused by decreased intravascular volume, sepsis, dehydration and obstruction
Intrarenal- actual damage to renal parenchyma, causes by tubular necrosis, prolonged prerenal ischemia, infection and nephrotoxicity
Postrenal- obstruction of urinary outflow from the collecting ducts in the kidney to the external urethral orifice, causes renal stones, bladder tumors, prostate cancer, blood clots
4 phases of acute kidney injury
Onset phase- begins with precipitating event
Oliguric phase- urine output below 400mL/day. HIGH electrolyte levels. Requires supportive measures (no nephrotoxic drugs, decrease BP and possible dialysis). β¬οΈ gfr, hyperkalemia, hypocalcemia
Diuretic phase- occurs when cause of AKI has been corrected. Urine output from 3-5L/day. LOW electrolyte levels.
Recovery phase- NORMAL electrolyte levels. β¬οΈ gfr, complete recovery may take 1-2yrs. Memory improves
How is AKI diagnosed
X-ray (kub)
Renal ultrasound
Serum labs (CBC, bun/creatinine, electrolytes)
Urine labs (24hr collection, u/a, specific gravity)
CT scans/MRI
Nuclear imaging
Cystoscopy
Renal biopsy
Clinical manifestations of hypovolemia or reduced CO
Prerenal azotemia
Hypotension
Tachycardia
Decreased Central Venous Pressure
Decreased urine output
Weakness/fatigue
S&S of volume overload
Intrarenal or postrenal azotemia
Hypertension
Tachycardia
Increased central venous pressure
Increased jugular vein distention
SOB, crackles, pulmonary edema
Weight gain/ edema
Azotemia
S&S
Inability to secrete waste, elevated BUN
S&S- n/v, anorexia, headache, confusion, weakness/fatigue
Lab changes during an AKI
β¬οΈ BUN
β¬οΈ creatinine
β¬οΈ K, Ph, Mg, PaCO2
β¬οΈ Ca, HCO3
βοΈ Na is variable
βοΈ H&H are usually stable unless patient is hemorrhaging
Normal lab values
Bun, creatinine, k, ph, Mg, Ca, Na, hemoglobin, hematocrit, HCO3, PaCO2
Bun: 10-20 mg/dL
Creatinine: 0.5-1.1 mg/dL
K: 3.5-5 mEq/L
Phosphorus: 3-4.5 mg/dL
Mg: 1.3-2.1 mEq/L
Ca: 9-10.5 mg/dL
Na: 135-145 mEq/L
Hemoglobin: 12-17 mmol/L
Hematocrit: 38-50%
HCO3: 22-26 mEq/L
PaCO2: 35-45 mmHg
What is the most serious electrolyte disorder in kidney injury
Hyperkalemia
How is hyperkalemia treated
IV insulin
IV glucose (push k back in cell. Glucose to prevent hypoglycemia)
IV Ca gluconate (β¬οΈ threshold β€οΈ arrhythmia)
Sodium polystyrene sulfonate (kayexelate)
Lasix, sodium bicarb, albuterol nebs
Emergent hemodialysis
Under what conditions should kayexelate NOT be given
Hypoactive bowels
Common causes of chronic kidney disease
Diabetes
Hypertension
Glomerulonephritis (lupus, wegeners, hiv, amyloidosis)
Interstitial nephritis (allergic or pvelo)
Microangiopathic vascular disease (scleroderma)
Cogenital
Genetic disease (pkd)
Neoplasm or tumor
Transplant rejection
Hepatorenal syndrome
Hepatorenal syndrome
Life-threatening medical condition that consists of rapid deterioration in kidney function in individuals with cirrhosis or liver failure
List the 5 phases of chronic kidney disease
Stage I- gfr > 90ml/min. (Screen)
Stage II- gfr 60-89ml/min (Reduce risk factors)
Stage III- gfr 30-59ml/min (Slow progression)
Stage IV- gfr 15-29ml/min (Manage/rrt)
Stage V- gfr < 15ml/min (Rrt/transplant)
Ca has an adverse relationship with which other electrolyte
β¬οΈ Ca = β¬οΈ phosphate
Lab changes in CKD
Bun & creatinine gradual increase to very high levels
Na initial decrease, later maybe increased or βnormalβ
K & Ph rise quickly
Ca decreased
Metabolic acidosis due hydrogen ions not being excreted and unable to bind to HCO3
β¬οΈ iron, folic acid. β¬οΈ cholesterol
People with CKD are more prone to which 3 conditions
Metabolic acidosis , β€οΈ problems and bleeding
Cardiovascular changes in CKD
At risk for ?
Hypertension
Fluid overload
Heart failure (results from htn, hypervolemia, anemia and ultimately causes LV enlargement)
Risk for- CAD, pericarditis, pericardial effusion
Pulmonary changes in CKD
Dyspnea/tachypnea (watch for kussmauls)
Crackles
Pulmonary effusions
Pulmonary edema
Pneumonitis
Kussmauls breathing indicates what
Severe acidosis
Associated with CKD
Neurological changes in CKD
Untreated?
Lethargy
Decreased alertness/cloudy mentation
Poor concentration
Neuropathy
If untreated can cause seizures, coma
Integument changes in CKD
Yellow or darkening of skin
Pruritus
Uremic frost (uremia seeping from pores)
Urinary changes in CKD
Initially May appear βnormalβ
Oliguric
Anuric (may occur once crrt is initiated)