Genitourinary Flashcards
Acute Kidney Injuries (AKI)
- A rise in the serum creatinine or a decline in UO that has developed over hours to days
- Accumulation of urea and other waste products - Azotemia - protein catabolism, elevated BUN
- Dysregulation of extra cellular volume - fluid overload
- electrolyte imbalance - retain K, Mg, Ph
- metabolic acidosis
-S/S: edema, HTN, oliguiria, anuria
- 3 different causes: 1. pre-renal; 2. intra renal (ATN); 3. post renal
Pre renal AKI
- R/t hypoperfusion (E.g., sepsis, HF, hypotension, hypovolemia); injuries prior to blood reaching the kidneys
- If hypoperfusion is not corrected, pre-renal progresses to ATN
- Increased BUN/Creat ratio 25:1 (normal 10:1)
- Urine sodium concentration <10 mEq/L or Fractional excretion of sodium (FENa) <1% (injured kidneys first conserve sodium and water before they shut down so urine sodium will be low and oliguric)
- High urine osmolality >500 mOsm/kg (Kidneys conserve sodium and water) and High USG
- Tx: restore perfusion w/ IVF (NS or LR), correct electrolytes
Urine osmolality
500 -1200 mOsm/kg
Acute tubular necrosis (ATN)
- intra-renal damage; direct structural injury to the nephrons and necrosis of the tubular epithelial cells
- Common causes: renal ischemia, sepsis, nephrotoxins
Toxic ATN: caused by nephrotoxins
1. Medications - vancomycin, aminoglycosides, radiocontrast, AmphoB, NSAIDS
- Myoglobin: muscle breakdown products that cause Rhabdomylosis (seen with an elevated CK, reddish/brown urine, muscle pain, weakness, dark urine)
- Toxin ATN: reversible and involves a more rapid recovery <7 days once the underlying problem is resolved or nephrotoxic meds are stopped
Ischemic ATN: prolonged hypoperfusion from pre-renal AKI, tubular cell ischemia, and necrosis causing tubular obstruction by casts and cell debris, longer recovery 7-21 days
Dx:
- Low urine osmolality <400 mOsm/kg
- Elevated BUN & Cr; normal BUN/Cr ratio (10:1)
- Urine sodium >50 mEq/L
- FENA >2% (tubules are injured and can’t conserve sodium)
- 1st 48 hours - oliguric; 7-14 cays - polyuria/diuretic phase; 6mo-2yrs normal UO/recovery
Tx: Optimize volume, prevent acidosis, correct electrolyte and uremia, avoid nephrotoxin, monitor drug therapeutic levels, adequate hydration before proceduresAZ
Response to fluid
- Respond to fluid with an increase in UO and drop in creatinine = Pre-renal
- Does not respond to fluid, suspected ATN, and often requires dialysis
Post-renal
- Caused by inadequate drainage of urine distal to kidneys that cause increased intr-tubular pressure –> decreases GFR
- Causes: BPH, kidney stones, blood clots, neurogenic bladder, cancer
-S/S: bladder distention pain, urinary urgency or hesitancy, nocturia, gross hematuria, HTN, varied UO
- Normal BUN/Cr ratio 10:1 but both elevated; elevated USG; decreased Urine Osmo; urine Na >40
- Dx: US, elevated serum creat
- T: Reverse the cause, bladder cath, percutaneous nephrostomy, lithotripsy, ureteral or rethral stenting
Chronic Kidney Disease (CKD)
- Presence of kidney damage or decreased kidney function for 3 months or more regardless of cause
- Slow, progressive deterioration of renal function: GFR <60, presence of albuminuria >30 mg/day
- Complications: Fluid overload (leads to pulmonary congestion), electrolyte imbalance (hyperkalemia, hypocalcemia, hyperphosphatemia), metabolic acidosis, hormonal dysfunction (renin, erythropoietin, calcitriol –> causes HTN, anemia, bone disease), azotemia (accumulation of Urea, creat, toxins), uremic syndrome
Uremic syndrome
- A group of systemic clinical features caused by uremia
- Uremic encephalopathy: lethargy, fatigue, seizure, coma
- Uremic frost: urea crystals on the skin
- Asterixis: hand tremor
- ECG changes from hyperkalemia
- Pulmonary crackles/edema
- HTN
- Decreased appetite, malnutrition
- Ascites
- Bleeding
- Pericarditis
Dialysis disequilibrium syndrome
- Confusion, restless disorientation, seizures
- Occurs at the start of dialysis
Continuous Renal Replacement Therapy (CRRT)
- For patients with hemodynamic instability who cannot tolerate HD
- Slower HD that is performed >24 hours
- Modes: 1. Slow continuous Ultrafiltration (SCUF) - only removes water; 2. Continuous venovenous hemofiltration (CVVH) - remove fluids and moderate solutes; 3. Continuous venovenous HD (CVVHD) - similar to IDH but for >24hrs; 4. Continuous venovenous hemodiafiltration (CVVHDF) - removes maximal fluid and solutes
Serum Osmolality
- Body’s electrolyte-water balance
- Normal 275-295 mOsm/kg
- higher values = greater concentration of solutes in the serum
- Lower numbers = serum is more dilute
Sodium
135-145 mEq/L
- Regulates total body water
- Transmission of nerve impulses
- Regulation of acid-base balance
- Muscle contraction/cellular depolarization
Hypernatremia
> 145 mEq/L
- Increased intake of sodium from consumption of saline solutions, and/or dehydration
- Increases serum sodium, serum osmolality, urine specific gravity, decreased urine Na+
- Osmotic shift of water out of cells that primarily affects the brain - rapid increase in brain volume can rupture cerebral veins –> ICH & SAH
- Persistent hypernatremia –> ADH release –> thrist mechanism to correct the imbalance
- S/S: lethargy, weakness, irritability
- Tx: reverse the cause, restrict sodium intake, D5W, free water flushes, serial labs to check sodium
- Goal to lower is about 10 mEq/L over 24 hours
Hyponatremia
<135 mEq/L
- Sodium depletion from GI or GU losses, or excess water retention (i.e., SIADH), DKA,
- Low serum osmolality promotes the movement water into the cells –> cerebral edema
- S/S: neuro changes (HA, confusion, seizures), nausea, malaise, abdominal cramps, tachycardia, hypotension
- Tx: prevent a further drop in serum sodium; prevent brain herniation; slow correction of sodium levels (sodium tabs, hypertonic saline); avoid overlay rapid correction in sodium levels to prevent osmotic demyelination syndrome (an irreversible neurologic disorder where pt s become “locked in”)
- Goal: 4-6 mEq/L over 24 hour period
Potassium
3.5-5 mEq/L
- Primarily regulated and excreted by the kidneys; intestines excrete K+
- Transmission of nerve impulses
- Myocardial, skeletal, & smooth muscle contractility
- Acid/base balance
-
Hyperkalemia
- Causes: kidney impairment, burn or trauma, excess ingestion/infusion, drugs (ACE inhibitors, potassium-sparing diuretics); inverse relationship between potassium and pH (H+ ions move into the cell, K+ moves out; acidosis = hyperkalemia)
- S/S: muscle weakness, flaccid paralysis, cardiac conduction abnormalities, arrhythmia (Tall peaked or tented T-waves on the ECG)
- Calcium chloride IVP - stabilize cardiac action potentials, infuse via CL, no effect on K+
- Calcium gluconate - okay for PIV
- IV insulin pushes potassium back into the cells; give 10 units IVP followed by IV dextrose to prevent hypoglycemia
- Nebulized albuterol
-Sodium bicarb to correct acidosis
- Remove excessive potassium from the body - loop diuretics (furosemide); sodium polystyrene sulfate (Kayexalate), HD
Hypokalemia
<3.5 mEq/L
- Causes: GI losses (diarrhea, vomiting), renal losses (loop diuretics), polyuria (i.e., DI), poor daily nutrition, ETOH, magnesium depletion, induced hypothermia, dialysis
- S/S: muscle weakness, cramping or rhabdomyolysis; cardiac arrhythmias (ST depression, inverted T waves, large U waves)
- Tx: potassium replacement, continuous ECG monitoring and labs
Calcium
8.5-10.5mg/dL
Important for regulating contraction of muscle, nerve conduction, and bone building
Hypocalcemia
<8.5mg/dL
-Causes: decreased intake, chronic alcoholism, malabsorption
- S/S: tetany with neuromuscular irritability (numbness, tingling spasms, seizures, laryngospasms)
-
Trosseu sign: BP cuff inflated around the arm and blood occluded for 3 minutes –> absence of blood flow to the hand and forearm will induce muscle spasm
-Chvostek sign: less sensitive test where facial nerve produces a twitch when tapped - QT prolongation
- hypotension
- Tx: rapid correction of calcium with IV calcium gluconate
Phosphate
2.5-4.5 mg/dL
- Inverse relationship with calcium
- Phosphorus is present in every cell in the body and makes up 1% of body weight
- Key energy source (ATP) that is essential for life.
Hyperphosphatemia
> 5 mg/dL
- Symptoms similar to hypocalcemia
- Tx: in the setting of renal impairment - dietary phosphorus restrictions, phosphate binders - calcium acetate or sevelamer; Acetazolamide stimulated urinary PO4 excretion
Hypophosphatemia
<1mg/dL
-Causes: decreased intake, GI problems, increased urinary losses, increased utilization, refeeding syndrome
-S/S: metabolic encephalopathy, impaired myocardial contractility, respiratory failure d/t weakness of the diaphragm
-Tx: increase dietary intake, PO or IV Kphos, Naphos
Magnesium
1.5-2.5 mEq/L
- Neuromuscular transmission, cardiac contraction, cellular metabolism activation and transport
Hypermagnesemia
> 2.5 mEq/L
- very rare and only seen with renal insufficiency or from excessive infusion
- S/S: neuromuscular toxicity: diminished DTR, somnolence, muscle paralysis; >5 - bradycardia and hypotension as it blocks calcium channels & promotes vasorelaxation
-Tx: IVF, diuretics, HD
Hypomagnesemia
<1.5 mEq/L
- Acute pancreatitis; usually have hypocalcemia and hypokalemia
- S/S: tetany, arrhythmias, seizures
- polymorphic ventricular tachycardia/Torsades de pointed, increased risk for digoxin toxicity
Tx: Magnesium sulfate
Contrast-induced nephropathy (CIN)
- Risks: DM, HTN, HF, pre-existing renal insufficiency, dehydrated, concurrent use of nephrotoxic medications (i.e., NSAIDS, some abx), high volume of IV contrast
- Prevention: hydration
- Sodium bicarb infusion 1 hour before & 6 hours after exposure to contrast dye
- N-acetylcysteine (Mucomyst) - day before and day of contrast exposure, thought to prevent toxicity to renal tubules
