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Nursing 2240: Patho > Kidneys: renal failure and UTI's > Flashcards

Kidneys: renal failure and UTI's Flashcards

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1
Q

An abnormal constituent of urine is:

a) creatinine
b) glucose
c) potassium
d) urea

A

B) glucose

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2
Q

With normal daily fluid intake, the anticipated amount to be excreted in the urine is approximately:

a) 0.5 L
b) 1.5 L
c) 2.5 L
d) 4.0 L

A

B) 1.5 L

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3
Q

Increased blood osmolality will result in:

a) ADH stimulation
b) decrease in urine volume
c) diuresis
d) less reabsorption of water

A

A) ADH stimulation and

B) decrease in urine volume

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4
Q

A major, sensitive indicator of kidney disease is the:

a) BUN levels
b) serum creatinine level
c) serum potassium level
d) uric acid level

A

B) serum creatinine

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5
Q

A major manifestation of uremia is:

a) hypophosphatemia
b) polycythemia
c) hypocalcemia
d) hypokalemia

A

c) hypocalcemia

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6
Q

Oliguria is described as urinary output

a) less than 30 ml/hr
b) about 100 ml/hr
c) between 300-500 ml/hr
d) between 500-1000 ml/hr

A

a) < 30 ml/hr

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7
Q

Significant data collected during a nursing assessment relevant to renal function should include information about

a) any voiding disorders
b) client occupation
c) the presence of HTN of DM
d) all of the above

A

D) all of the above

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8
Q

A 24-hr urine collection is scheduled to begin at 0800. The nurse should begin collection

a) after discarding the 0800 specimen
b) at 0800 with or without a specimen
c) with the first specimen voided after 0800
d) start collection with the beginning of the 0700 shift

A

A) after discarding the 0800 specimen

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9
Q

Nursing responsibilities after renal angiography include

a) assessment of peripheral pulses
b) colour and temperature comparisons between the involved and uninvolved extremities
c) examination of the puncture site for swelling and hematoma formation
d) all of the above

A

D) all of the above

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10
Q

Nursing management after a renal biopsy includes

a) assessing for the clinical manifestations of hemorrhage
b) encouraging a fluid intake of 3L q24h
c) obtaining a sample of each voided urine to compare with prebiopsy specimen
d) all of the above

A

D) all of the above

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11
Q

Serum potassium levels can rise in which of the following situations

a) blood transfusions
b) administration of spironolactone
c) diabetic ketoacidosis
d) myocardial infarction

A

all of these

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12
Q

Which of the following findings is consistent with urinary tract infection?

a) hematuria
b) an output of 200-900 mls with each void
c) cloudy urine
d) urine with a specific gravity of 1.005-1.022

A

A) hematuria and

C) cloudy urine

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13
Q

Chronic renal failure clinical manifestations include which of the following?

a) decreased packed cell volume
b) hypercalcemia and hypophosphatemia
c) hypokalemia and elevated bicarbonate
d) metabolic alkalosis

A

A) decreased packed cell volume

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14
Q

Hyperkalemia is a serious electrolyte imbalance that occurs in acute renal failure and results from

a) dietary intake
b) electrolyte shifts in response to metabolic acidosis
c) tissue breakdown
d) all of the above

A

D) all of the above

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15
Q

Potassium intake can be restricted by eliminating high-potassium foods, such as

a) butter
b) citrus fruits
c) cooked white rice
d) bananas

A

B) citrus fruits and

D) bananas

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16
Q

Dietary intervention for renal deterioration includes limiting the intake of

a) carbohydrates
b) fluid
c) protein
d) sodium and potassium
e) all of the above

A

B) fluid and
C) protein and
D) sodium and potassium

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17
Q

Alternatives to aluminum based antacids to lower serum phosphate levels include

a) calcium carbonate
b) sodium bicarbonate
c) kayexalate
d) milk of magnesia

A

A) calcium carbonate

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18
Q

Potential complications of chronic renal failure include which of the following?

a) angina pectoris
b) HTN
c) peripheral neuropathy
d) polycythemia
e) prolonged coagulation

A

A) angina and
B) HTN and
C) peripheral neuropathy and
E) prolonged coagulation

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19
Q

Vital signs consistent with chronic renal failure include which of the following?

a) tachypnea
b) bradycardia
c) hypotension
d) pyrexia

A

A) tachypnea (to compensate for metabolic acidosis)

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20
Q

Emergency interventions in response to hyperkalemia include administration of IV

a) hypotonic glucose solution
b) intermediate insulin
c) calcium gluconate
d) ringer’s lactate
e) sodium bicarbonate

A

C) Calcium gluconate and

E) sodium bicarbonate

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21
Q

At the end of 5 peritoneal exchanges, the client’s fluid loss is 500 mls. This loss equates to approximately

a) 0.5 lbs
b) 1.0 lbs
c) 1.5 lbs
d) 2 lbs

A

B) 1.0 lb (500 mls fluid = 0.5 kg)

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22
Q

Complete the following flowchart:
Hypotension –> kidneys release (A) –> liver manufactures/converts to (B) –> (C) –> adrenals release (D) –> increases sodium retention –> (E) is released from pituitary –> BP rises

A 
A) renin
B) angiotensin I
C) angiotensin II
D) aldosterone
E) ADH
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23
Q

Where do the kidneys rest anatomically?

A

outside the peritoneal cavity (retroperitoneal) at the level of T12 to L3
- Right kidney is lower than left (due to liver)

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24
Q

How much fluid does the kidney process daily?

A

1700 Litres of blood –> becomes 1.5 L of urine

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25
Q

What is the functional unit of the kidney and how many are there approximately?

A

nephron

~ 1,000,000/kidney

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26
Q

How much kidney function can be lost before manifestations?

A

67% can be lost ie. kidney can function with only 33% of nephrons

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27
Q

What are some of the ESSENTIAL functions of the kidney?

A

Excretion of metabolic wastes
Regulate fluid volume
Regulate electrolyte composition
Maintain acid-base balance
Regulation of BP (RAA)
RBC production through EPO
Calcium metabolism through activation of vitamin D
GNG - from amino acids during periods of fasting/stress
Degradation of insulin (30-40%)
Synthesis of prostaglandins (which have vasomotor effect, increase capillary permeability)

28
Q

Briefly describe the development of the kidneys in utero

A

start to develop in 5th week of gestation
start to function at 8 weeks
urine formation begins ~9-12th week gestation

29
Q

What are the effects of aging on kidney function?

A

progressive atrophy –> decreasing function

loss of function begins at 30 yrs at a rate of 1% per year –> by 70 years, renal function is approximately 50%

30
Q

What is the minimum daily urine output for normal kidney function?

A

400 ml/day

31
Q

Differentiate between Acute renal failure (ARF) and chronic renal failure (CRF) re: onset

A

ARF - sudden onset

  • GFR falls but creatinine and BUN rise
  • oliguria (100-400 ml/day) or anuria (< 100 ml/day)

CRF - insidious onset or after unresolved ARF
- irreversible destruction of kidney structures and reduced renal function

32
Q

Describe the different etiologies for ARF

A

PRERENAL = hypoperfusion
- due to decreased CO, decreased blood volume, decreased vascular resistance (due to vasodilation e.g.septic or anaphylactic shock), or renal vascular obstruction
INTRARENAL = damage to renal tissue
- nephrotoxic injury e.g. medications
- hemolytic transfusion reactions (type III hypersensitivity)
- severe crush injuries causing myoglobin
POSTRENAL = mechanical obstruction of urinary outflow
- urine backs up into kidneys –> ARF
- e.g. UTI, BPH, tumors

33
Q

What are the disorders that can result in/cause CRF?

A

HUG PDS
uncontrolled HTN
urinary tract obstruction and infection
hereditary defect of the kidneys (polycystic)
disorders of glomeruli (acute glomerulonephritis)
systemic disorders like diabetes, SLE

34
Q

What is the pathophysiology of ARF?

A

Usually due to acute tubular necrosis

1) Renal ischemia - deterioration of tubular epithelium
2) Nephrotoxic injury - necrosis of tubular epithelial cells slough off and plug tubules

35
Q

Describe the stages (including GFR rates) for CRF

A 
At high risk for chronic kidney disease when GFR is greater or equal to 90 ml/min with CKD risk factors
STAGE 1: GFR equal or greater than 90 ml/min
- kidney damage with normal or high GFR
STAGE 2: GFR 60-89 ml/min
- kidney damage with mild decreased GFR
STAGE 3: GFR 30-59 ml/min
- moderate decrease in GFR
STAGE 4: GFR 15-29 ml/min
- severe decrease in GFR
STAGE 5 = GFR < 15 ml/min
- kidney failure
36
Q

What are the 4 phases of ARF?

A
  1. Onset (hours up to 7 days)
  2. Oliguric-anuric (1-2 to several weeks)
  3. Diuretic (2-6 weeks, until BUN stops rising)
  4. Recovery/convalescent (up to 12 months)
37
Q

Compare the prognosis for ARF vs. CRF

A

ARF prognosis is good ~ 50-60%

  • lowest mortality with nephrotoxic (intrarenal), obstruction and glomerulonephritis
  • the longer the period of olguric-anuric phase, the poorer the prognosis

CRF prognosis has improved in the past 20 years due to dialysis and transplantation

38
Q

What are complications of ARF?

A

End stage renal disease (ESRD) and CRF
Infections
Pericarditis
Encephalopathy

39
Q

What are complications of CRF?

A

Infections
Cardiovascular alterations
Osteodystrophy
CNS encephalopathy

40
Q

What diagnostics are common for ARF?

A

Hx
Urinalysis:
- urine sediment containing abundant cells, casts, or proteins suggests intrarenal disorders
- ATN is associated with abundant urinary casts
- Postrenal may have hematuria, pyuria, and crystals
Scan, biopsy, ultrasound

41
Q

What diagnostics are common with CRF?

A

Identification of reversible renal disease
Renal scan/CT/ultrasound
Biopsy
Hct and Hgb
BUN, serum creatinine, creatinine clearance
serum electrolytes
urinalysis and urine culture

42
Q

Explain the pathophysiology of the electrolyte imbalances that occur with kidney failure.

A

1) Sodium may be normal/decreased with vomiting, diarrhea, or dilution; high late in disease
2) Potassium: high late in disease due to catabolism, medications that contain K+, trauma, blood transfusions, acidosis
3) Calcium: decreased conversion of vitamin D to calcitriol –> decreased GIT absorption of Calcium (phosporus retention due to inverse relationship) –> PTH causes phosphorus excretion and resorption of calcium from bone

43
Q

Explain the pathophysiology of the metabolic changes that occur with kidney failure.

A

1) protein metabolites e.g. high creatinine, urea nitrogen, and uric acid
- BUN levels influenced by protein intake, fever, and catabolic rate
2) carbohydrate intolerance due to impaired insulin production and metabolism
3) elevated triglycerides: likely increased production of lipids by liver in response to elevated blood glucose and insulin
- often aggravated with peritoneal dialysis (glucose dialysate)
4) metabolic acidosis due to inability to excrete H+, decreased absorption of NaHCO3, decreased formation of phosphoric acid and ammonia
5) vitamins - toxicity of fat-soluble vitamins not excreted with renal failure

44
Q

Explain the pathophysiology of the hematologic changes that occur with kidney failure.

A

Anemia: initially due to low EPO
- later due to hemolysis (fragile RBC), GI losses, and clotting abnormalities
Bleeding tendencies: uremic toxins interfere with platelet adhesiveness

45
Q

Explain the pathophysiology of the GI changes that occur with kidney failure.

A

Anorexia, N+V
Stomatitis due to ammonia in saliva
Accumulation of gastrin (abnormal gastric acid) predisposes to GIT ulcers
Constipation due to Phophate binding agents, restriction of fluids, and inactivity

46
Q

Explain the pathophysiology of the immunologic changes that occur with kidney failure.

A

Depression of humoral antibody formation
decreased chemotactic function of WBC
contributing factors include protein malnutrition, hyperglycemia, external trauma (e.g. needles)

47
Q

Explain the pathophysiology of the CV changes that occur with CRF.

A

~50-60% of CRF deaths from CV complications d/t VOLUME OVERLOAD
Anemia, electrolyte imbalance, acidosis, increased atherosclerosis
HTN
DM have added risk for CV complications (HTN, CVA, CHF)

48
Q

Explain the pathophysiology of the respiratory changes that occur with kidney failure.

A

Kussmaul respirations d/t acidosis
Dyspnea d/t pulmonary edema
Pleuritis, pneumonitis, pericarditis d/t uremic toxicity
Predisposition to infection d/t fluid overload, a/o RAA mechanism, a/o electrolyte disturbances, a/o high concentration of urea/creatinine

49
Q

Explain the pathophysiology of the musculoskeletal changes that occur with kidney failure.

A

Affected early and in 90% of CRF
Osteodystrophy d/t kidney-bone-PTH and calcium, phosphate and vitamin D dynamics:
initial hypocalcemia due to low GFR –> PTH causes bone demineralization –> hypercalcemia and Phosphorus excretion
Progressive RF –> vit D conversion fails –> low calcium absorption in GIT and high phophorus retention –> mineralization impaired –> PTH continues –> demineralization continues
Calcification deposits in SC tissue, vascular and visceral tissue –> joint pain, bone deformities and fractures

50
Q

Explain the pathophysiology of the integumentary changes that occur with kidney failure.

A

Pruritus d/t secondary hyperPTH and high calcium deposits in the skin
Dry skin d/t atrophy of sweat glands
Colour changes: purpura with decreased platelet adhesiveness and low calcium
Pallor d/t anemia or orange-green-grey d/t retention of urochronme pigments
Brittle hair that easily falls out, thin and brittle nails

51
Q

Explain the pathophysiology of the neurologic changes that occur with kidney failure.

A

Due to increased nitrogenous waste products, electrolyte imbalances, metabolic acidosis
Also axonal atrophy and demyelination of nerve fibers due to high levels of uremic toxins

52
Q

Explain the pathophysiology of the reproductive changes that occur with kidney failure.

A

Menstrual irregularities, amenorrhea and infertility
Men: impotence, testicular atrophy, low sperm count and motility
Loss of libido in both men and women

Due to decreased sex hormones and anemia, and peripheral neuropathy

53
Q

Explain the pathophysiology of the medication metabolism changes that occur with kidney failure.

A

Risk for medication toxicity due to altered protein binding sites, loss of excretory ability (prolonged half-life)

54
Q

Is the nephropathy that occurs with DM intrarenal or prerenal?

A

renal failure that occurs with DM is chronic, not acute, so it would be neither

55
Q

In what situation is Acute tubular necrosis (ATN) reversible?

A

if basement membrane is not destroyed and necrotic tubular epithelium regenerates

56
Q

How is chronic kidney disease diagnosed/defined?

A

kidney damage (confirmed by imaging) or GFR < 60 ml/min/1.73 m2 for 3 months

57
Q

T/F: Urine output is an indicator of renal function

A

False: urine output is an indicator of renal PERFUSION

58
Q

What are emergency/temporary interventions for electrolyte imbalances in kidney failure?

A
  1. IV Insulin for hyperkalemia with dextrose to prevent hypoglycemia
    - if K+ > 7.0, give with D50W
    - if K+ < 7.0, give with D10W
  2. Sodium bicarbonate to correct acidosis and shift K+ into cells if pH is < 7.2
  3. IV Calcium gluconate for cardiac toxicity of hyperkalemia because calcium raises the threshold for dysrhythmias
59
Q

What are (non-emergency) interventions for K+ imbalance in kidney failure?

A

A) Dialysis to bring K+ levels to normal
B) Kayexalate: K+ exchanged for Na+ in GIT (1 mmol K+ removed per gram of Kayexalate)
- sorbitol is often prescribed concurrently to cause osmotic diarrhea to rid of excess Na+ and water
Dietary restriction of K+

60
Q

What are interventions for the increased creatinine, BUN and uric acid that occur with kidney failure?

A

Reduce dietary protein intake (normal = 80-120 g/day)

May be necessary to administer enteral feeds or TPN when anorexia

61
Q

What causes the carbohydrate intolerance associated with renal failure?

A

impaired insulin production and metabolism due to:

1) peripheral insulin antagonism
2) impaired insulin secretion
3) prolonged insulin half-life directly related to kidney malfunction
4) abnormalities in circulating insulin

62
Q

What precautions should be made when treating constipation related to kidney failure?

A

Caution re: laxatives that are high in K+ or P

  • bulk laxatives may be given but with recommended fluid only
  • use enemas sparingly if required
63
Q

What are interventions for Ca++ imbalance in kidney failure?

A

Limit phosphorus intake
Calcium-based phophate binders (e.g. calcium carbonate = Tums, or calcium acetate) to promote phossphate excretion in feces
Vitamin D analogues (calciferol) promotes bone mineralization by increasing GIT absorption of Calcium and decreasing PTH and phosphate
Occasionally, subtotal parathyroidectomy

64
Q

What are the interventions for Carbohydrate intolerance and elevated triglycerides that occur with kidney failure?

A

Ensure high carbs with low-moderate fat intake to avoid use of stored proteins for energy
Very important to monitor insulin/blood glucose

65
Q

What are interventions for metabolic acidosis that occurs in kidney failure?

A

sodium bicarbonate and same measures as for hyperkalemia

66
Q

What interventions are started for Anemia that occurs in kidney failure?

A

EPO via IV or SC routes or given with dialysis
EPO must be supplemented concurrently with folic acid and iron
Also blood transfusions

Nursing 2240: Patho (12 decks)

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