ACUTE RENAL Flashcards

1
Q

Are the kidneys normally palpable? Which sits lower?

A

No (if palpable, could indicate enlargement)

Right –> therefore easier to detect

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2
Q

Where would tenderness be seen with renal dysfunction?

A

Possibly over the costovertebral angle (angle formed by lower border of 12th [bottom] rib and spine

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3
Q

Renal failure results when …

What occurs generally ?

A

kidneys cannot remove body’s metabolic wastes or perf regulatory fx
• Substances accumulate, affect endocrine + metb fx, fluid, electrolyte, acid-base balance

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4
Q

What is ARF?
What is the widely accepted criterion for ARF? (characteristic changes)
Other changes that occur?

A

Rapid loss of kidney function (less than 48 hours) - Secondary to damage of the kidneys

Criterion = Dec GFR
Accum of BUN + creatinine
….other changes in ARF = azotemia, fluid + electrolyte imbalance (such as hyperkalemia), a/b imbalance (metb acidosis)

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5
Q

Possibly reversible causes of ARF

A

hypovolemia, hoTN, dec CO + HF, obstruction of kidney or lower urinary tract (tumour, blood clot, kidney stone), or bilateral obstruction of renal arteries or veins

o These reduce blood flow + reduce kidney fx

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6
Q

Functions of the kidneys?

A

1) Excretion of wastes
2) Reabsorption of vital nutrients
3) Acid-base homeostasis
4) Osmolality regulation
5) Blood pressure regulation
6) Hormone secretion

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7
Q

Define:

1) Oliguria

2) Anuria

A

urine output

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8
Q

What term describes accum of nitrogenous wastes in the blood?

A

Azotemia

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9
Q

What is uremia?

A

Azotemia with toxic symptoms

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10
Q

Are acute and chronic kidney disease reversible?

A

acute = possible reversible

Chronic = irreversible

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11
Q

3 categories of acute renal injury based on cause?

A

Prerenal
Intrarenal
Postrenal

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12
Q

Prerenal ARF?
How common?
Causes?

A

= Hypoperfusion
– 70% of cases
Causes: volume depletion (hemorrhage, renal loses, GI losses), impaired cardiac efficiency (d/t MI, HF, cardiogenic shock), vasodilation (d/t sepsis, anaphylaxis, antihypertensive meds)

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13
Q

Intrarenal ARF?

A

parenchymal damage to glomeruli or kidney tubules)
Causes: prolonged renal ischemia, nephrotoxic agents (d/t nephroxic drugs (such as NSAIDS, vancomycin, contrast dyes for CT, chemo drugs), infectious processes

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14
Q

What is the most common type of intrarenal ARF? What is it? Causes?

A

Acute tubular necrosis = intratubular obstruction, tubular back leak (abnormal reabsorption of filtrate + dec urine flow through tubule), vasoconstriction + changes in glomerular perm → result in dec GFR, azotemia, fluid + electrolyte imbalance

Causes of ATN are CKD, diabetes, HF, HTN, cirrhosis

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15
Q

What hormones are produced by the kidneys?

A

Erythropoeitin
Calcitriol = active vit D3
(Calcitriol stimulates release of calcium from bone by its action on osteoblasts)

The hormones parathyroid hormone (PTH) and calcitonin help regulate blood calcium levels.

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16
Q

What enzyme is produced by the kidneys

A

Renin

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17
Q

Outline the RAA system

A

When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the prorenin already present in the blood into renin and secrete it directly into the circulation –> this then carries out the conversion of angiotensinogen released by the liver to angiotensin I. Angiotensin I is subsequently converted to angiotensin II by ACE found in the lungs. Angiotensin II is a potent vasoconstrictor, + stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone causes the tubules of the kidneys to increase the reabsorption of sodium and water into the blood, while at the same time causing the excretion of potassium (to maintain electrochemical balance). This increases the volume of extracellular fluid in the body, which also increases blood pressure.

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18
Q

What is a normal eGFR value?

A

Teacher said 90-120…different from VIHA.

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19
Q

What protective measure is used for kidneys when going in for CT?

A

B/c of possible damage from contrast dye…

Will always take kidney fx tests before any CT procedure…if see to be low, acetylcysteine used as protective measure for CT (given before + after procedure)

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20
Q

Postrenal ARF?
What is it
Causes
How is it treated

A

Sudden obstruction to urine flow

Causes: tumour, BPH (benign prostatic hypertrophy), kidney stones, strictures, clots

**Note: For acute renal failure to occur, will be having bilateral damage!

From class:
• Will put in nephrostomy tube to bypass obstruction + drain kidney; lithrotripsy (break up large stones surgically), or will put in stent
• Flomax commonly given → dilates ureters so can allow obstruction to pass; tell patient will cause inc in urine stream

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21
Q

What is the normal ration of BUN to creatinine?

A

20:1
BUN:creatinine

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22
Q

Comparing Clinical Characteristics of Acute Renal Failure (Table 45-12, p. 1413)

A

Not sure if we’re expected to know this detail?

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23
Q

What are the phases of renal failure?

A

1) Initiation
2) Oliguria
3) Diuresis
4) Recovery

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24
Q

Initiation phase

A

initial insult until when oliguria develops

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25
Q

Oligura phase

A

Output

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26
Q

What is an important consideration regarding the oliguria phase in kidney failure? Is this phase always seen?

A

Some forms of kidney failure are “non-oliguric” meaning have accum of N wastes but still producing normal amounts of urine (2L or more)

mainly in people exposed to nephrotoxic drugs + burns

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27
Q

Diuresis period in kidney failure:
What occurs?
What is an important role of the nurse during this phase?

A
  • gradual inc in urine output
  • signs that filtration has begun to recover
  • lab values stabilize + dec
  • output increases but still may be sig kidney abnormalities
  • nurse to watch carefully for signs of dehydration (will inc uremic symptoms)
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28
Q

How long does the recovery period take?

What occurs?

A

may take 3-12 months

improvement in renal fx; lab values return to normal

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29
Q

Manifestations of ARF?

Including complications

A
  • Almost every system affected
  • Critically ill, lethargic
  • Skin + mucous membranes dry d/t dehydration
  • CNS: Drowsiness, muscle weakness, twitching
Complications:
Hypertension & Fluid Overload
Azotemia --> Uremia 
Hyperkalemia
Anemia 
Hyperphosphatemia & Hypocalcemia
Metabolic Acidosis
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30
Q

WHat kind of assessments for ARF?

A
All systems!!
History 
Vital Signs 
Weight
CNS
CVS
Respiratory 
GI
Fluid balance
     -FVE 
     -FVD 
Integumentary
31
Q

How would urine characteristics change in ARF?

A

Urine output varies from scanty to normal, possible hematuria, urine w low specific gravity

32
Q

What kind of diagnostic measure is essential for detecting changes?

A

U/S critical – renal sonogram, CT, MRI show changes

33
Q

What does anemia result in ARF?

A

result of dec erythropoietin production, uremic GI lesions, reduced RBC life span, blood loss

34
Q

Why do you see hyperkalemia in ARF?

A

•High risk of hyperkalemia w dec GFR, oliguria, anuria; protein metb results in release of K+

35
Q

Why inc phosphate + dec Ca2+ levels with ARF?

A

• Possible inc in phosphate levels
- dec in Ca levels d/t dec absorption in GI tract, and as compensatory mech for inc P in blood; Ca2+ also excreted when acidosis occurs

From class: HyperP can affect thyroid, also factor in metb acidosis

36
Q

Outline the lab values that would be seen in ARF

A

Elevated BUN
Elevated Serum Creatinine
GFR

37
Q

WHat is a complication of ARF r/t heart (not dysrhythmias)

A

Pericarditis

Protein bound uremic toxins

38
Q

Prevention of ARF?

A
  • Careful hx to detect nephrotoxic agents + meds
  • Those taking nephrotoxic meds (gentamicin, aminoglycosides, vancomycin, etc) monitored carefully for change in renal fx – BUN + creatinine baseline, 24hrs after inititiating tx and twice weekly after
39
Q

What is RIN?

What is the best prevention method for this?

A

• Radiocontrast-introduced nephropathy (RIN) major cause of hospital-acquired ARF

hydration most effective prevention of this

40
Q

Why are elderly at particular risk of ARF?

A
  • ½ of those with ARF during hospitalization >50yrs
  • Etiology of ARF in elderly incl dehydration, nephrotoxic agents (meds, contrast agents), complications of major sx
  • Further dehydration d/t lack of thirst, confusion, enforced bed rest, lack of access to drinking H2O
41
Q

Do kidneys recover from damage well?

A

Yes, remarkably well!

42
Q

What are the objective of managing kidney failure?

A

restore normal chemical balance, prevent complications until repair of renal tissue and restoration of renal fx can occur
• Eliminate cause, maintain fluid balance (avoid excess), provide renal replacement tx
• Shock + infection treated prompty if present

43
Q

Which type of ARF will most likely recieve fluids + blood products?

A

Prerenal (hypoperfusion)

44
Q

Nursing priorities for ARF?

A

1) Understand and ensure Cause treated
2) Monitor Fluid/electrolyte: Daily weights, Ins/outs, Strict care with fluid restrictions, possible dialysis/CRRT
3) Vital signs: know FVE and FVD
4) Lab values: K+,BUN, Cr, GFR
5) Dec metb rate:bed rest, tx fever + infection promptyl
6) Promote pulm fx – assist to turn, take deep breaths, cough
7) Skin Care
8) Nutrition
9) Support: Psychological and hemodynamic
10) Catheter Care
11) Short term dialysis if treatment unsuccessful?
12) Education to prevent CKD

45
Q

What is the most life threatening fluid + electrolyte changes in kidney failure? What might you see?

A

Hyperkalemia
- pt monitored for serum K, ECG changes, changes in clinical status.

May see irritability, cramping, diarrhea, paresthesia, generalized muscle weakness (slurred speech, difficulty breathing, etc.)

46
Q

What does dialysis do for the patient?

A

will correct biochemical abn, allow liberalization of fluid, protein and sodium intake, diminishes bleeding tendencies + promotes healing

47
Q

What are CRRT’s

A

Continuous Replacement Therapies

= used to replace normal kidney fx by circulating blood through hemofilter

48
Q

How is hyperkalemia treated?

A

o Treated w cation-exchange resins orally or retention enema: Kayexalate (works by exchanging sodium for potassium ions in GI tract
o Colon is major site of K+ exchange (why use enema)
o Sorbitol in combo with this to induce diarrhea
o If hemodynamically unstable, may give IV dextrose 50%, insulin + calcium replacement to shift K+ back into cells
o Salbuamol sulfate (Ventolin HFA) by neb can lower plasma K+
o Temporary changes, so need dialysis on emergent basis

49
Q

What other pharm interventions are seen in ARF besides tx of hyperkalemia?

A
  • Must adjust drugs as hard on kidneys, esp aminoglycosides, digoxin, ACE inhibitors, etc
  • Diuretics often used for fluid balance but not shown to improve recovery from ARF
  • ABGs and serum bicarbonate monitored for severe acidosis – might need sodium bicarbonate tx or dialysis
  • Resp support measures if necessary
  • Phosphate-binding agents to control serum phosphate levels
50
Q

Why do dietary imbalances occur in kidney failure?

A

nausea + vomiting, impaired glucose use + protein synthesis, inc tissue catabolism

51
Q

nutritional tx in acute renal failure

A
  • Exact therapy depends on cause, comorbidities, nutritional status, etc
  • Replacement of dietary proteins individualized to min uremic symptoms
  • High calories to promote protein sparing
  • Foods + fluids containing K+ and P minimized
  • Following diuretic phase, pt placed on high calorie, high protein diet to resume activities gradually
52
Q

What hesitation might you see in family of pt and how should this be responded to? (to promote psychological support)

A

family may be hesitant to touch + talk to pt during dialysis, PD, CRRT but should be encouraged to do so

53
Q

Why skin care for ARF?

Strategies?

A

may be dry d/t edema, itchy + excoriation d/t deposit of irritating toxins in tissues → can bath in cool water, turn frequent, keep skin clean + moisturized, fingernails traimmed to avoid excoriation

54
Q

Psychological Considerations for pt receiving urologic testing?

A
  • Pt’s undergoing urologic testing are often apprehensive – can be embarrassing
  • Voiding in presence of others causes guarding = natural reflex that inhibits voiding with situational anxiety
  • Nurse can help by providing privacy + thorough explanation of procedure
55
Q

WHy is urinalysis used in ARF?

A
  • Provides info on kidney function and helps diagnose conditions like DM
  • Determines bacteria, strains, and concentration – can determine what antibiotics to follow with
56
Q

What is looked at in urinalysis?

A
o	Colour
o	Clarity and odour
o	Urine pH and specific gravity
o	Proteins 
o	Glucose
o	Ketone bodies
o	Microscopic exam for: hematuria, pyuria (WBC’s in urine), cylinduria (casts), crystals (crystalluria), and bacteria (bacteriuria)
57
Q

Why would hematuria possibly be seen in urinalysis?

A

Hematuria d/t acute infection (cystitis, urethritis, prostatitis), renal calculi and neoplasm, bleeding disorders, malignant lesions, meds such as warfarin + heparin

58
Q
Urine specific gravity
What is it?
Normal range?
How is affected by hydration level?
How do changes in this occur in renal disease/injury?
A
  • Measures density of solution compared with density of water, which is 1.000
  • Altered by presence of blood, proteins, casts
  • Normal range = 1.010 to 1.025
  • Dehydration will raise specific gravity
  • Those with kidney disease have “fixed” sg = sg doesn’t change with fluid intake
  • Disorders causing decreased: diabetes insipidous, glomerulonephritis, sever renal damge
  • Disorders causing inc: DM, nephritis, fluid deficit
59
Q

Osmolality
What does this measure?
How is this assessed?
Normal values?

A
  • Most accurate measure of kidney’s ability to dilute + concentrate urine
  • = # of solute particles in kg of H2O
  • Serum + urine osmolality measured simultaneously to assess fluid status
  • Normal serum = ~300 mmol/L
  • Normal urine = ~300-1100 mmol/kg
60
Q

What is creatinine?

A

end product of muscle energy metabolism. In normal, level of creatinine which is regulated by kidneys, will remain relatively constant

61
Q

BUN?

What affects this?

A

urea is nitrogenous end product of protein metabolism. Test values affected by protein intake, tissue breakdown, and fluid volume changes

62
Q

What ratio can be used to assess hydration status?

A

BUN to creatinine ratio

63
Q

Creatinine clearance?

A

detects and evals progression of renal disease. Test measures volume of blood cleared of endogenous creatinine in 1 min, which provides approx of GFR. Sensitive indicator of renal diseae used to follow progression of renal disease

64
Q

What diagnostic imaging is used

A

1) Kidney, Ureter, and Bladder Studies (KUB)
• X ray of abdomen or kidneys, ureter + bladder (KUB) may be performed to delineate size, shape, position
2) General Ultrasonography
• Sound waves used to detect abnormalities: fluid accum, masses, congenital malformations, changes in organ size, obstructions
• Requires full bladder
• Is sensitive test – has replaced many others as initial diagnostic procedure
3) Bladder U/S
• Used to measure urine vol
4) CT + MRI
And many more….

65
Q

What is hemodialysis?
Short or long term tx?
What is the contraption called that’s used?

A
  • Most common method of dialysis
  • Used as short-term, long-term or permanent form of therapy
  • Dialyzer = artificial kidney
  • Serves as a synthetic semi-permeable membrane
66
Q

What is peritoneal dialysis?

A

x

67
Q

What sort of issues are you assessing for in ARF with regard to:

1) CNS
2) CVS
3) Resp
4) GI

A

1) seizures, confusion
2) Shock, arrhythmias
3) compensation (for acidosis). fluid overload/pulmonary edema? JVD?
4) Cost-vertebral angle (CVA) tenderness

68
Q

WHat are casts?

A

Particles found during routine U+A (urinalysis) or R+M (routine + microscopic), whole bunch of different types; muddy brown casts are indication of ATN

69
Q

What will we do for someone with pulm edema (as complicaiton of ARF)?
2 meds included in this tx?

A

Want to treat underlying cause but first want to: inc head of bed, put on O2, give meds
o Mannitol. Is osmotic diuretic – inhibits reabsorption of sodium and water; works by expanding plasma volume and inc blood flow to kidney
• Is safer because less of effect on electrolytes (confirm this?) – will use this if very worried about electrolytes
o Lasix is loop diuretic, acts on ascending loop of henle; can inc BUN + creatinine levels + cause potassium shifts so more risky for lyte imbalances (but generally used more than mannitol)

70
Q

What will we see with pulm edema?

A

Inc resp rate, dec sats, cyanosis, anxiety, crackles, venous distension

71
Q

What are 3 main drugs used to manage hyperkalemia?

A

1) Kayexalate
2) Dextrose/Insulin/Calcium
3) Ventolin

72
Q

Kayexalate

A

gets rid of potassium; causes diarrhea for days; not first line defense for those who are really sick

73
Q

How does dextrose, insulin + calcium help hyperkalemia?

A

can use CaCl or Ca gluconate to inc threshold potential…restores normal threshold potential, onset 3-5min, lasts 30-60min, given IV
o 50ml D50 first (to prevent hypoglycemia)
o Then insulin, which will lead to shift of K+ ions into the cells; takes a few hours so may need to be repeated

74
Q

Why ventolin for pt with hyperkalemia?

Possible side effect?

A

lowers blood levels of K+ in serum my promoting uptake into cells; can cause side effect of inc HR, which is concen for pt with hyperkalemia!