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Med-Surg Exam 2 > Renal II > Flashcards

Renal II Flashcards

1
Q

what are the types of congenital renal malformation?

A

-agenesis/hypoplasia
-alterations in kidney position
-horseshoe kidney
polycystic kidneys

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2
Q

what is agenesis/hypoplasia?

A

small, or complete absence of both kidneys

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3
Q

what is potters syndrome?

A

The kidneys fail to develop properly as the baby is growing in the womb.
-fatal if bilaterally

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4
Q

what are some precautions of renal agenesis/hypoplasia?

A

-No aminoglycosides
-no sports
-no IV contrast-things (could harm the one kidney if you have unilateral)

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5
Q

what do alterations in kidney position effect in the body?

A

Can affect ureters and urine flow, resulting in UTIs, stones.

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6
Q

what is a horseshoe kidney?

A

One horseshoe shaped kidney with 2 ureters

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7
Q

what are some precautions to take with an horseshoe kidney?

A

-Educate patient to avoid dehydration, use good hygiene to avoid UTIs
-Avoid sports-damage to kidney

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8
Q

what is polycystic kidney?

A

Fluid-filled cyst formation develop in nephrons of kidney r/t abnormal cell division. Renal blood vessels and nephrons are compressed and obstructed.

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9
Q

when do s/s of polycystic kidney dominant form develop?

A

-slow progression
-Symptoms usually develop by 30-50 years of age

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10
Q
A
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11
Q

what are the s/s of polycystic kidney?

A

hematuria
proteinuria
HTN (r/t kidney ischemia)
UTIs
renal injury->chronic renal failure

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12
Q

what is the most common cause of pre-renal azotemia?

A

perfusion reduction, or decreased cardiac output
-hemorrhage, shock, MI

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13
Q

what is azotemia?

A

the retention and buildup of nitrogenous wastes in the blood.

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14
Q

is pre-renal azotemia reversible?

A

yes, rapidly reversible when blood flow is restored

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15
Q

what is the cause of intrinsic (intra-renal) injury?

A

Damage is within the kidney (damage to the glomeruli, nephrons or tubules).

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16
Q

what ways can the kidney be damaged and lead to intrinsic failure?

A

-Nephrotoxins (certain chemotherapies, antibiotics, contrast media)
-Glomerulonephritis, pyelonephritis, lupus, scleroderma
-Rhabdomyolysis (rapid breakdown of skeletal muscle tissue due to “crush” injury->myoglobin released into bloodstream->clogs tubules=Acute Tubular Necrosis)
-Infection(sepsis) & chronic pyelonephritis
-Major trauma or surgery,

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17
Q

what causes post-renal azotemia? What is the most common cause?

A

Problem occurs after the kidney:
-obstruction of ureter, bladder, etc., reducing urine flow.
-BPH most common cause!
* Kidney stones, neurogenic bladder, certain cancers, blood clots

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18
Q

Is AKI reversable?

A

often if treated early

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19
Q

what are the common s/s of AKI?

A

*Decreased urine output (oliguria)
*Fluid volume overload
*Labs: Increased K and Phos, decreased Na and Ca, anemia, increased BUN and Creatinine
*N/V, azotemia
*Metabolic acidosis

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20
Q

what occurs in the initiation or onset phase of oliguric AKI?

A

*A decrease in UO with high specific gravity can be observed.
*If AKI is identified now and pre-renal condition corrected, prognosis is best to prevent renal dysfunction.
*Compensatory mechanisms like aldosterone, ADH, etc. will respond.

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21
Q

what happens during the oliguric phase of oliguric AKI?

A

*U/O = 100-400ml/day
*Elevated BUN/Creatinine
*Electrolyte imbalances; fluid volume overload can occur
*Metabolic acidosis d/t impaired renal hydrogen ion elimination

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22
Q

what happens during the diuretic phase of oliguric AKI?

A

*Often sudden onset. Occurs when cause of AKI has been corrected.
*Osmotic diuresis occurs from high urea levels. UO = 1-5 L/day
*Risk for dehydration from severe fluid loss

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23
Q

what happens during the recovery phase of oliguric AKI?

A

*Kidney begins to return to regular function with increased GFR.
*Fluid and electrolyte balance stabilize.

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24
Q

what is the most important renal lab value and the range?

A

creatinine (0.6-1.2)

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25
Q

what lab value is related to nutrition, protein, and hydration? what is the range of this lab value?

A

BUN (6-20)

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26
Q

what are some phosphate binders?

A

-calcium carbonate (tums)
-calcium acetate (phoslo)
-sevelamer HCL (renvela)

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27
Q

co2 in a chem panel relates actually to what value and what is the range?

A

bicarb (22-26)

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28
Q

what is the range for Ca?

A

-who do you call (9-1-1)
9-11

29
Q

what happens during AKI or CRF to serum creatine? what diet implication should be used?

A

-increased
-low protein diet

30
Q

what happens during AKI or CRF to GFR?

A

it would decrease

31
Q

what is the normal range for GFR?

A

120-125

32
Q

what happens during AKI or CRF to sodium? what diet implication should be implemented?

A

-increased, decreased, or normal
-low sodium diet, fluid restriction

33
Q

what happens during AKI or CRF to potassium? what diet implication should be used?

A

-increased
-low potassium diet

34
Q

what happens during AKI or CRF to phosphorus? what diet implication should be used?

A

-increased phosphorus (no Ca)
-low phosphorus diet, admin a phosphate binder

35
Q

what happens during AKI or CRF to calcium?

A

it would be decreased (low activated vitamin D)

36
Q

what happens during AKI or CRF to magnesium?

A

it would be high or low

37
Q

what happens during AKI or CRF to hemoglobin and hematocrit?

A

they would be decreased (low EPO)

38
Q

what happens during AKI or CRF to your ABG? pH?

A

-metabolic acidosis
-pH would be low
-HCO3 would be low

39
Q

what would happen to a EKG when someone has hyperkalemia?

A

-peak (extra) T wave

40
Q

What ways do you treat hyperkalemia?

A

-Ca gluconate, or furosemide (calms the heart)
-insulin and D50

41
Q

why do you give dextrose when admin insulin?

A

dextrose makes the cells more permeable to insulin

42
Q

what is a K binder example med? what does this medication do?

A

sodium polystyrene sulfonate (kayexalate)
-excretes K in the stool, slower than admin through an IV

43
Q

how does albuterol effect K?

A

makes K move into the cell

44
Q

how does spirolactone effect K?

A

-K sparing
-do NOT give to someone with hyperkalemia

45
Q

what is the primary complication of peritoneal dialysis? how is it prevented?

A

peritonitis (cloudy fluid)
-sterility is important
-infection prevention

46
Q

what is the secondary complication of peritoneal dialysis? how is this monitored/prevented?

A

occlusion
-monitor dialysate outflow, last bowel movement (avoid constipation
-monitor for respiratory distress (retained fluid creates more pressure in the diaphram)

47
Q

what is the best way to prevent a dialysis complication? what is the #1 complication?

A

hypotension
-check BP!!!!!!!

48
Q

how do you prevent occlusion of AV fistula/catheter?

A

-avoid tight clothing
-avoid labs/bp on affected side
-assessment signs:
*absent of bruit (no whoosh)
*absent of thrill (feel the thrill)
*decreased cap refill
*coolness of extremity

49
Q

how would you tell if there was an infection at the dialysis site?

A

redness/swelling at the shunt site

50
Q

what is the major concern when doing a kidney biopsy if the cause of AKI is unclear?

A

bleeding!
-needs monitored

51
Q

what is the major concern when treated AKI with diuretics?

A

-balance of bp
Aggressive hypertension treatment with avoidance of hypotension

52
Q

what is an very early finding sign for AKI?

A

specific gravity

53
Q

what is the most dangerous electrolyte imbalance associated with renal failure?

A

hyperkalemia

54
Q

what are other common electrolyte imbalances in renal failure?

A

hypocalcemia
hyperphosphatemia
hypermagnesemia.

55
Q

what are some general characteristics for CKD?

A

*Generally slow and gradual onset
*Nephron damage is irreversible
*Normal function of the kidney is disrupted: decreasing filtration, decreasing resorption, decreasing erythropoietin production

56
Q

what are some common causes of CKD?

A

*Diabetes (44%)
*HTN (16%)
*Glomerulonephritis (17%),
*Recurrent kidney infections
*Others- polycystic disease, SLE, HF

57
Q

what are the stages of CKD?

A
  1. at risk/ decreasing renal reserve
  2. mild CD
  3. moderate CKD
  4. severe CKD
  5. ESRD/ESKD
58
Q

what are the characteristics of stage 1 CKD?

A

*GFR WNL (>90 ml/min per your book, 120ml/min per other sources)
*Decreased renal function without waste build-up
*Undamaged nephrons overwork to compensate

59
Q

what are the characteristics of stage 2 CKD?

A

*GFR 60-89
*Not enough healthy nephrons remain to completely compensate
*Slight elevations of metabolic wastes; sometimes large amounts of dilute urine produced
*careful medical management can prevent further damage and slow progression

60
Q

what are the characteristics of stage 3 CKD?

A

*GFR 30-59
*Remaining nephrons can’t keep up
*Fluid overload (crackles in lungs, SOB), electrolyte imbalances, metabolic waste build-up (IMPORTANT)
*Dietary restrictions of fluid, proteins, electrolytes and other strategies are needed to slow disease progression

61
Q

what are the characteristics of stage 4 CKD?

A

*GFR (15-29)
*Severe fluid, electrolyte, acid/base imbalance; manage complications

62
Q

what are the characteristics of stage 5 CKD?

A

*GFR (<15)
*Replacement therapy or kidney transplant is needed for life to continue

63
Q

what are some medical management concerns of a pt with CKD?

A

1- fluid volume status

#2- Na levels risk for hypo (hyper in late)
–wt and bp (indicate fluid and Na)

64
Q

what are potassium containing foods?

A

citrus, tomatoes, potatoes, and salt substitutes are big offenders.

65
Q

dialysis will not increase what lab level of a patient?

A

hemoglobin concentrations

66
Q

what is hemodialysis?

A

Involves shunting patient’s blood from the body, through a dialyzer (artificial kidney) which filters the blood, and returns the blood to the patient with use of dialysate tailored to the client’s needs and a semipermeable membrane filter (artificial kidney).

67
Q

1 aftercare for dialysis?

A

check bp as soon as they return to the floor

68
Q

what is one CV complication about kidney transplant? how can this be prevented?

A

HTN and increased risk of stroke and MI (monitor blood pressure frequently post-op)

69
Q

what is the most serious complication or kidney transplant

A

-rejection

Med-Surg Exam 2 (4 decks)

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