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
2
Q
what are some nephrotoxic substances?
A
- abx, NSAIDs, ACEIs, ARBs, antineoplastics, contrast, diuretics if overused
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
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
5
Q
what is the best indicator of glomerular filtration rate (GFR)?
A
24hr urine creatinine clearance
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
7
Q
GFR is directly/inversely related to serum creatinine?
A
inversely
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
9
Q
what is normal urine specific gravity? what is normal spot urine Na?
A
1.010-1.020
40-220
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
11
Q
what is acute renal failure or acute kidney injury?
A
increase in serum creatinine by >/= 1.5 of baseline within 7 days
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
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
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)
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)
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
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)
18
Q
what are some signs of contrast medium nephropathy?
A
- anuria
- increased BUN/creatinine
- fluid overload
19
Q
how would you treat contrast medium nephropathy?
A
- diuretics if no response
- treat as intrarenal failure
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
21
Q
what are some causes of rhabdo?
A
- crush injuries, prolonged immobility, compartment syndrome, hyperthermia, DTs
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
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
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
how would you manage acute infrarenal failure?
- 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
what makes a pt a candidate for dialysis?
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
what do the labs look like for prerenal pts?
- 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
what do the labs look like for infrarenal pts?
- 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
how would you treat post renal failure?
- 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
what are some S&S of hypocalcemia?
- 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
what causes hypocalcemia?
- acute pancreatitis
- massive infection of SQ tissues
- hypoparathyroidism
- chronic renal failure
- Vit D deficiency
- hypoalbuminemia
- alkalosis; hyperventilation, prolonged vomiting
32
how is hypocalcemia treated?
- IVF, NS
- calcium gluconate or CaCl, Vit D
- correct respiratory alkalosis
33
what are some S&S of hypercalcemia?
- lethargy, fatigue, AMS
- DTRs decreased or absent
- ab pain, constipation
- muscle weakness
- N/V "metallic" taste
- anorexia, weight loss
- kidney stones
34
what causes hypercalcemia?
- renal dz
- hyperparathyroidism
- prolonged immobilization, bed rest
- malignancies
35
how is hypercalcemia treated?
- 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
what are some S&S of hyperkalemia?
- muscle weakness; irritability
- nausea, diarrhea
- muscle cramps, pain
- ECG changes: peaked T waves, widening QRS, loss of P waves, bradycardia, PEA
37
what causes hyperkalemia?
- renal failure
- burns (early)
- massive crush injuries
- excessive K intake
- acidosis, relative
- adrenal cortical insufficiency
38
how is hyperkalemia treated?
- CaCl of calcium gluconate, sodium bicarb, insulin/glucose, albuterol
- no K intake
- correct acidosis
- kayexalate
- dialysis
39
what are some S&S of hypokalemia?
- muscle weakness, decreased reflexes
- n/v
- paralytic ileus or ab distention/gas
- shallow respirations
- mental depression
- ECG changes; fast, irritable; VT/VF
40
what causes hypokalemia?
- diuretics
- metabolic alkalosis
- acute alcoholism
- uncontrolled diabetes
- excessive perspiration
- excess production of aldosterone
- cirrhosis
41
how is hypokalemia treated?
- KCl
- correct alkalosis
- LR
- correct hypomagnesemia
42
what are some S&S of hypernatremia?
- 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
what causes hypernatremia?
- insensible losses, dehydration
- osmotic diuresis, mannitol
- DKA
- hyperglycemic hyperosmotic syndrome (HHS)
- DI
44
how is hypernatremia treated?
- 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
what are some S&S of hyponatremia?
- edema
- fatigue, muscle cramps, weakness
- ab cramps, diarrhea
- lethargy, confusion, decreased DTRs
- sz, coma, brain herniation
46
what causes hyponatremia?
- fluid overload: HF, cirrhosis
- excessive water ingestion
- excessive D5W
- SIADH
47
how is hyponatremia treated?
- 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
what are some S&S of hypermagnesemia?
- decreased DTRs, respiratory depression, arrest
- bradyarrhythmias, hypotension
- lethargy, coma
- n/v
- flushing
49
what causes hypermagnesemia?
- renal failure
- mag containing laxative abuse
- mag containing antacid abuse
- iatrogenic OD
50
how is hypermagnesemia treated?
- stop mag substances
- give Ca as for hyperkalemia
- lasix as for hypercalcemia if renal function ok
- may need dialysis
51
what are some S&S of hypomagnesemia?
- hyperreflexia (CHVOSTEK, TROUSSEAU)
- ventricular arrhythmias, PSVT
- sensitivity to digoxin
- insulin resistance, hypokalemia, hypocalcemia, hypophosphatemia
- agitation, confusion
- impedes correction of low K
52
what causes hypomagnesemia?
- 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
how is hypomagnesemia treated?
- MgSO4, max 1g/min
54
what are S&S of hypophosphatemia?
- same as hypercalcemia
- lethargy, fatigue, AMS
- DTRs decreased to absent
- ab pain, peptic ulcers, constipation
- muscle weakness, hypoventilation
55
what causes hypophosphatemia?
- increased cellular uptake of phos with TPN admin
- increased glucose admin (TPN)
- alcoholism
56
how is hypophosphatemia treated?
- replace
57
what are S&S of hyperphosphatemia?
- same as hypocalcemia
- anxiety, irritability
- twitching around mouth
- laryngospasm
- sz
58
what causes hyperphosphatemia?
- decreased renal excretion, renal failure
59
how is hyperphosphatemia treated?
- phos binders (amphogel), calcium carbonate (Caltrate)
CCRN
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