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CCRN > Genitourinary > Flashcards

Genitourinary Flashcards

1
Q

Acute Kidney Injuries (AKI)

A
  • 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
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2
Q

Pre renal AKI

A
  • 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
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3
Q

Urine osmolality

A

500 -1200 mOsm/kg

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4
Q

Acute tubular necrosis (ATN)

A
  • 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

  1. Myoglobin: muscle breakdown products that cause Rhabdomylosis (seen with an elevated CK, reddish/brown urine, muscle pain, weakness, dark urine)
  2. 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

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5
Q

Response to fluid

A
  • 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
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6
Q

Post-renal

A
  • 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
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7
Q

Chronic Kidney Disease (CKD)

A
  • 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
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8
Q

Uremic syndrome

A
  • 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
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9
Q

Dialysis disequilibrium syndrome

A
  • Confusion, restless disorientation, seizures
  • Occurs at the start of dialysis
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10
Q

Continuous Renal Replacement Therapy (CRRT)

A
  • 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
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11
Q

Serum Osmolality

A
  • 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
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12
Q

Sodium

A

135-145 mEq/L
- Regulates total body water
- Transmission of nerve impulses
- Regulation of acid-base balance
- Muscle contraction/cellular depolarization

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13
Q

Hypernatremia

A

> 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
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14
Q

Hyponatremia

A

<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
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15
Q

Potassium

A

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
-

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16
Q

Hyperkalemia

A
  • 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
17
Q

Hypokalemia

A

<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
18
Q

Calcium

A

8.5-10.5mg/dL
Important for regulating contraction of muscle, nerve conduction, and bone building

19
Q

Hypocalcemia

A

<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
20
Q

Phosphate

A

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.

21
Q

Hyperphosphatemia

A

> 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
22
Q

Hypophosphatemia

A

<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

23
Q

Magnesium

A

1.5-2.5 mEq/L
- Neuromuscular transmission, cardiac contraction, cellular metabolism activation and transport

24
Q

Hypermagnesemia

A

> 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

25
Q

Hypomagnesemia

A

<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

26
Q

Contrast-induced nephropathy (CIN)

A
  • 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

CCRN (9 decks)

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