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CCRN > RENAL > Flashcards

RENAL Flashcards

1
Q

if BP falls and renal perfusion is decreased, what do the afferent and efferent arterioles do to compensate?

A

afferent arteriole DILATES to increase flow to the glomerular capillaries and efferent arteriole CONSTRICTS to decrease flow from glomerular capillaries

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2
Q

what are some nephrotoxic substances?

A
  • abx, NSAIDs, ACEIs, ARBs, antineoplastics, contrast, diuretics if overused
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3
Q

what is BUN and what is normal?

A
  • measures amount of nitrogen in blood that comes from the waste product urea (formed in liver)
  • normal 10-23mg/dL
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4
Q

what is creatinine and what is normal?

A
  • non-protein waste product of creatinine phosphate metabolism by skeletal muscle tissue
  • better indicator of renal function than BUN
  • normal males: 0.8-1.4mg/dL; females 0.6-1.1mg/dL
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5
Q

what is the best indicator of glomerular filtration rate (GFR)?

A

24hr urine creatinine clearance

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6
Q

what is GFR?

A
  • volume of plasma filtered from the glomerular capillaries into Bowman’s capsule per minute
  • normal GFR = 125mL/minute, total blood volume filtered ~60x/day
  • normal urine volume is ~1L/day, >99% reabsorption of filtrate
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7
Q

GFR is directly/inversely related to serum creatinine?

A

inversely

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8
Q

finding what in the urine is important in detecting diabetic nephropathy?

A
  • proteinuria
  • normoalbuminuria = <20mg/day
  • microalbuminuria = 30-300mg/day
  • proteinuria = >300mg/day
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9
Q

what is normal urine specific gravity? what is normal spot urine Na?

A

1.010-1.020

40-220

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10
Q

what does low serum albumin indicate? what does extremely high serum CK indicate?

A
  • decrease in oncotic pressure; increased 3rd spacing, decreased vascular volume
  • rhabdomyolysis
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11
Q

what is acute renal failure or acute kidney injury?

A

increase in serum creatinine by >/= 1.5 of baseline within 7 days

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12
Q

what is prerenal failure?

A
  • perfusion reduced to kidneys, but no destruction of tubular basement membranes
  • most common type of acute renal failure, seldom requires HD
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13
Q

what are some causes of prerenal failure?

A
  • impaired cardiac performance - HF, MI, cardiogenic shock, tamponade, dysrhythmias with low CO, pulmonary embolism
  • vasodilation - sepsis, anaphylaxis, drugs, ACEIs
  • vasoconstriction - pressers, compensation
  • intravascular volume depletion - hemorrhage, GI losses, osmotic diuresis, diuretics, burns, pancreatitis, ileus, inadequate volume replacement
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14
Q

how can NSAIDs contribute to prerenal failure?

A
  • block production of prostaglandins in afferent arteriole –> results in afferent arteriole constriction, decreased inflow of blood into glomerulus –> decreased GFR
  • can result with normal doses, especially when associated with other renal risks (HF, sepsis, pre-existing renal insufficiency)
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15
Q

how can ACEIs contribute to prerenal failure?

A
  • prevent production of angiotensin II, efferent arteriole will remain in a dilated state
  • prevents maintenance of adequate glomeruli pressure
  • may cause problems for patients dependent upon efferent arteriole constriction to maintain adequate pressure within glomeruli (HF, hypovolemia)
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16
Q

how would you manage prerenal failure?

A
  • treat cause if able
  • fluids to maintain MAP >70mmHg to improve renal perfusion
  • decrease preload/afterload, improve contractility
  • control vasodilation: pressers, treat sepsis, avoid ACEIs, NSAIDs in high risk populations
  • I&Os with weight correction
  • avoid nephrotoxic drugs, contrast dyes, adjust meds
  • wean pressers if able
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17
Q

what are some causes of infrarenal failure?

A
  • cortical - post infectious (strep, hepatitis, varicella), lupus, vasculitis
  • medullary (ATN) - 1. nephrotoxic - contrast dye, drugs (abx, NSAIDs), rhabdo, organic solvents; 2. ischemic - all causes of prerenal, post renal failure, surgery (CABG, vascular, valve), cardio bypass, hypoTN (sepsis, hypovolemia)
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18
Q

what are some signs of contrast medium nephropathy?

A
  • anuria
  • increased BUN/creatinine
  • fluid overload
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19
Q

how would you treat contrast medium nephropathy?

A
  • diuretics if no response

- treat as intrarenal failure

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20
Q

how would you prevent contrast medium nephropathy?

A
  • NS before procedure and after - increases renal prostaglandins –> improves renal medullary blood flow
  • OR D5W with sodium bicarb before and after
  • avoid offending drugs
  • use iso-osmolar rather than low-osmolar contrast media
    decrease volume of dye given
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21
Q

what are some causes of rhabdo?

A
  • crush injuries, prolonged immobility, compartment syndrome, hyperthermia, DTs
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22
Q

what happens in rhabdo?

A
  • release of myoglobin, creatinine phosphokinase, potassium into extracellular and intravascular spaces due to damaged muscles
  • creatinine kinase and myoglobin obstruct renal tubules
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23
Q

what are the S&S of rhabdo?

A
  • dark, tea colored urine
  • low UO; hypovolemia
  • (+) on dipstick for hgb, but no RBC on UA
  • myoglobin in urine
  • elevated CK > 10,000 U/L
  • muscle cramping
  • arrhythmias
  • hyperkalemia
  • metabolic acidosis
  • acute renal failure
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24
Q

how would you treat rhabdo?

A
  • NS to maintain UO ~300ml/hr, may need up to 500ml/hr to do so
  • bicarb drip to alkalinize urine
  • mannitol
  • monitor and treat hyperkalemia
  • continue to treat until myoglobin clears from urine
25
Q

how would you manage acute infrarenal failure?

A
  • monitor for overload
  • loop diuretics, lasix acts on ascending loop of Henle to decrease Na and H2O reabsorption; often used to “covert” non-oliguric to oliguric renal failure
  • normalize electrolytes; esp hyperkalemia
  • maintain acid-base balance; dialyze for extreme metabolic acidosis
  • prevent uremia: dialyze early
  • prevent infection: highest cause of mortality, poorer immune function
  • address anemia: PRBCs; epogen for chronic
  • prevent bleeding: plt counts normal, but plt function affected by renal failure
  • adjust drug doses: lower
  • prevent malnutrition: don’t restrict protein
  • dialysis prn
26
Q

what makes a pt a candidate for dialysis?

A

any of the AEIOU criteria:

  • Acidemia
  • Electrolyte d/o (hyperkalemia)
  • Intoxication (methanol, ethylene glycol, aspirin, lithium, theophylline)
  • Overload (heart failure)
  • Uremia (elevated BUN with mental status changes)
27
Q

what do the labs look like for prerenal pts?

A
  • BUN:creatinine 20-40:1
  • urine sodium <20 mEq/L
  • urine concentration - concentrated
  • urine osmolality high > 500
  • specific gravity high >1.020
  • urinary sediment normal; hyaline casts
  • fractional excretion of sodium =1%
  • response to lasix >40ml/hr

when renal tubules are still able to function, urine sodium may be low (able to hold onto sodium) and osmolality is high (able to concentrate urine)

28
Q

what do the labs look like for infrarenal pts?

A
  • BUN:creatinine 10-15:1
  • urine sodium >20 mEq/L
  • urine concentration - dilute
  • urine osmolality low <300
  • specific gravity low < 1.010
  • urinary sediment abnormal; cellular casts and debris
  • fractional excretion of sodium >1%
  • response to lasix: none
29
Q

how would you treat post renal failure?

A
  • identify and correct obstruction; may progress to intrarenal failure if not corrected
  • recovery of renal function is directly proportional to the duration of the obstruction
  • easiest renal failure to treat
30
Q

what are some S&S of hypocalcemia?

A
  • anxiety, irritability
  • twitching around mouth
  • laryngospasm
  • sz
  • CHVOSTEK - spasm of lip and cheek when touched
  • TROUSSEAU - carpopedal spasm when BP cuff inflates
  • Torsades VT
31
Q

what causes hypocalcemia?

A
  • acute pancreatitis
  • massive infection of SQ tissues
  • hypoparathyroidism
  • chronic renal failure
  • Vit D deficiency
  • hypoalbuminemia
  • alkalosis; hyperventilation, prolonged vomiting
32
Q

how is hypocalcemia treated?

A
  • IVF, NS
  • calcium gluconate or CaCl, Vit D
  • correct respiratory alkalosis
33
Q

what are some S&S of hypercalcemia?

A
  • lethargy, fatigue, AMS
  • DTRs decreased or absent
  • ab pain, constipation
  • muscle weakness
  • N/V “metallic” taste
  • anorexia, weight loss
  • kidney stones
34
Q

what causes hypercalcemia?

A
  • renal dz
  • hyperparathyroidism
  • prolonged immobilization, bed rest
  • malignancies
35
Q

how is hypercalcemia treated?

A
  • NS to promote diuresis
  • lasix, first r/o hypokalemia
  • glucocorticoids, decrease GI absorption of Ca
  • mithracin IV, calcitonin, or etidronate; decrease Ca release from bones
36
Q

what are some S&S of hyperkalemia?

A
  • muscle weakness; irritability
  • nausea, diarrhea
  • muscle cramps, pain
  • ECG changes: peaked T waves, widening QRS, loss of P waves, bradycardia, PEA
37
Q

what causes hyperkalemia?

A
  • renal failure
  • burns (early)
  • massive crush injuries
  • excessive K intake
  • acidosis, relative
  • adrenal cortical insufficiency
38
Q

how is hyperkalemia treated?

A
  • CaCl of calcium gluconate, sodium bicarb, insulin/glucose, albuterol
  • no K intake
  • correct acidosis
  • kayexalate
  • dialysis
39
Q

what are some S&S of hypokalemia?

A
  • muscle weakness, decreased reflexes
  • n/v
  • paralytic ileus or ab distention/gas
  • shallow respirations
  • mental depression
  • ECG changes; fast, irritable; VT/VF
40
Q

what causes hypokalemia?

A
  • diuretics
  • metabolic alkalosis
  • acute alcoholism
  • uncontrolled diabetes
  • excessive perspiration
  • excess production of aldosterone
  • cirrhosis
41
Q

how is hypokalemia treated?

A
  • KCl
  • correct alkalosis
  • LR
  • correct hypomagnesemia
42
Q

what are some S&S of hypernatremia?

A
  • classic signs of hypovolemic hypernatremia (thirst, tachycardia, orthostasis, and hypotension) may be present, as can dry, sticky mucous membranes
  • restlessness and irritability to obtundation, stupor, coma
43
Q

what causes hypernatremia?

A
  • insensible losses, dehydration
  • osmotic diuresis, mannitol
  • DKA
  • hyperglycemic hyperosmotic syndrome (HHS)
  • DI
44
Q

how is hypernatremia treated?

A
  • identify cause (urine Na will be >20 if hypervolemic, variable with other 2 causes)
  • correct slowly to prevent cerebral edema
  • D5W, 0.45 NS
  • restrict Na
  • vaso for DI
45
Q

what are some S&S of hyponatremia?

A
  • edema
  • fatigue, muscle cramps, weakness
  • ab cramps, diarrhea
  • lethargy, confusion, decreased DTRs
  • sz, coma, brain herniation
46
Q

what causes hyponatremia?

A
  • fluid overload: HF, cirrhosis
  • excessive water ingestion
  • excessive D5W
  • SIADH
47
Q

how is hyponatremia treated?

A
  • if hypervolemic or euvolemic, water restriction
  • loop diuretics
  • dehydration with Na deficits, NS
  • water intoxication: water restriction, avoid hypotonic fluids
  • acute, severe: 3% NS, small amounts
48
Q

what are some S&S of hypermagnesemia?

A
  • decreased DTRs, respiratory depression, arrest
  • bradyarrhythmias, hypotension
  • lethargy, coma
  • n/v
  • flushing
49
Q

what causes hypermagnesemia?

A
  • renal failure
  • mag containing laxative abuse
  • mag containing antacid abuse
  • iatrogenic OD
50
Q

how is hypermagnesemia treated?

A
  • stop mag substances
  • give Ca as for hyperkalemia
  • lasix as for hypercalcemia if renal function ok
  • may need dialysis
51
Q

what are some S&S of hypomagnesemia?

A
  • hyperreflexia (CHVOSTEK, TROUSSEAU)
  • ventricular arrhythmias, PSVT
  • sensitivity to digoxin
  • insulin resistance, hypokalemia, hypocalcemia, hypophosphatemia
  • agitation, confusion
  • impedes correction of low K
52
Q

what causes hypomagnesemia?

A
  • chronic alcoholism - MOST COMMON CAUSE
  • vomiting, diarrhea, NG suction malabsorption
  • post CABG or AMI
  • DKA, HHS, hyperthyroidism
  • nephrotic syndrome
  • drugs: ahminoglycosides, diuretics, EtOH, dig, cisplatin
  • malnutrition, enteral or parenteral feedings
53
Q

how is hypomagnesemia treated?

A
  • MgSO4, max 1g/min
54
Q

what are S&S of hypophosphatemia?

A
  • same as hypercalcemia
  • lethargy, fatigue, AMS
  • DTRs decreased to absent
  • ab pain, peptic ulcers, constipation
  • muscle weakness, hypoventilation
55
Q

what causes hypophosphatemia?

A
  • increased cellular uptake of phos with TPN admin
  • increased glucose admin (TPN)
  • alcoholism
56
Q

how is hypophosphatemia treated?

A
  • replace
57
Q

what are S&S of hyperphosphatemia?

A
  • same as hypocalcemia
  • anxiety, irritability
  • twitching around mouth
  • laryngospasm
  • sz
58
Q

what causes hyperphosphatemia?

A
  • decreased renal excretion, renal failure
59
Q

how is hyperphosphatemia treated?

A
  • phos binders (amphogel), calcium carbonate (Caltrate)

CCRN (10 decks)

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