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NUR4630 > Week 4: Kidney injury, renal failure > Flashcards

Week 4: Kidney injury, renal failure Flashcards

1
Q

Role of Kidneys

A
  • Production and excretion of urine.
  • Excretion of urea (this is a by product of protein metabolism).
  • The kidneys maintain the pH balance (acid and base) throughout the body.
  • Regulation of the amount of water that is retained and excreted by the body.
  • Assistance with fluid and electrolyte balance throughout the body.
  • Production of Erythropoietin hormone (which has a role in the production of red blood cells).
  • Compensatory functions (such as assistance with increased/decreased blood pressure).
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2
Q

Na+, K+, Cl-, Ca2+, Phosphorus, Magnesium Norms?

A

Electrolyte
Normal Range

Sodium (Na+) 135-145 mEq/L
Potassium (K+) 3.5-5 mEq/L
Chloride (Cl-) 100-110 mEq/L
Calcium (Ca2+) 8.5-10.0 (total) mg/dL
Phosphorus (Po4-) 2.5-4.5 mg/dL
Magnesium (Mg2+) 1.8-2.5 mEq/L

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3
Q

proximal convoluted tubule

A

reabsorption of sodium potassium calcium and glucose, uses active transport

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4
Q

thick descending

A

absorption of na through active transport but get water as well

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5
Q

thick ascending

A

sodium chloride and bicarb being reabsorbed

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6
Q

distal tubule

A

phos

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7
Q

collective tubule

A

selectively allow water reabsorption based on adh, it’s the last ditch effort to maintain ph. Bicarb and hydrogen and K+ reabsorbed

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8
Q

Antidiuretic Hormone

A
  • Increases the permeability of collecting tubule cells to water.
  • Increases water, but not electrolyte reabsorption
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9
Q

Renin

A
  • Converts angiotensin into angiotensin I which is then converted to angiotensin II
  • Angiotensin II causes vasoconstriction and the release of aldosterone (important for na+ reabsorption in the distal tubules)
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10
Q

Aldosterone

A
  • Promotes sodium reabsorption in the distal tubules
  • Leads to increase water absorption
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11
Q
  • Urinalysis
  • Volume
  • pH
  • Protein
  • Glucose/ketones
  • Sediment
  • Osmolality
  • Sodium concentration
  • Fractional Excretion of Sodium Test

What do each of these tests help identify

A
  • Urinalysis
  • Volume: less than 30, they are anuric
  • pH: between 5 & 6.5. High = UTI. Low= acidodic states in the body
  • Protein: never normal in urine. Check it with 24 hour urine collection
  • Glucose/ketones: present when high glucose serum. Spillage above 200. Ketones present for fat metabolism
  • Sediment: some time of cellular breakdown. Not normal. Good indicator for pre-renal failure
  • Osmolality: 300-900. Specific gravity 1.001-1.022. If specific gravity high= sediment and renal damage.
  • Sodium concentration: less than 10 is normal. If elevated, think of renal failure.
  • *Fractional Excretion of Sodium Test*: compares serum sodium to urine sodium. Greater than 1%= intrarenal failure. 1% or less= pre-renal failure
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12
Q

Blood Studies for renal failure

A

Creatinine/ Creatinine Clearance
Estimated Creatinine Clearance formula
(140-age) X weight in kg/ (Plasma Creatinine mg/dL) X 72

Blood Urea Nitrogen: increases in renal failure, GI bleed, dehydration, trauma.
8-20 mg/dL (normal)

BUN/Creatinine ratio:
Based on serum creatinine
BUN:Creatinine – 10:1 (normal)

  • when ratio goes down: liver failure, fluid volume overload,
  • ratio up: dehydration, catabolic states or high protein diets

Osmolality: Up= kidneys not filtering properly
Normally 280-290

Uric Acid: elevated=kidneys not filtering uric acid properly
2-8.5 mg/dL

Hemoglobin & Hematocrit: decrease shows renal problems
Men 13.5-17.5 g/dL & 40-52%
Women 12-16 g/dL & 37-48%

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13
Q

Increased Anion Gap

A

Increased anions: much more common than decreased
Metabolic acidosis
Lactic acidosis
Ketoacidosis
Uremic acidosis

Ingestion of chemicals
Ethylene glycol
Methanol
Paraldehyde
Salicylates
Penicillin
Carbenicillin

Hyperalbuminemia

Decreased cations
Hypokalemia
Hypocalcemia
Hypomagnesemia

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14
Q

Anion Gap

A

Provides insight into the chemical neutrality of the blood
Na+ + (Cl- + HCO3-)
Normal is 12 mEq/L

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15
Q

Decreased Anion gap

A

Decreased Anion Gap

  • I_ncreased cations_: Hypercalcemia, Hyperkalemia, Hypermagnesemia
  • Lithium
  • Myeloma
  • Decreased anions: hypoalbuminemia
    *
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16
Q

Risk Factors for Excessive Fluid Loss

A
  • Fever
  • Environmental
  • Hyperventilation
  • Gastrointestinal loss
  • Third Spacing
  • Burns
  • Renal Loss
  • Surgical Blood Loss
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17
Q

1 liter of fluid =?kgs

A

1 liter of fluid = 1kg

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18
Q

Oliguria in a child

A

an output of less than 0.5 mL/Kg/hour

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19
Q

Acute Kidney Injury

A
  • Classified as: Sudden loss of renal function resulting in impairment in fluid/ electrolyte and/or acid-base balance.
  • 5% of all hospitalized patients develop AKI
  • 20% of ICU patients develop AKIMortality associated with ARF remains 40-70%
  • Of those who survive, 45% will have return of renal function
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20
Q

Types of kidney failure

A
  • Pre-Renal: occurs before you get to the kidneys. Hypovolemia, blockages. Can lead to Intra-Renal.
  • Intra-Renal: Occurs inside the kidney. Metabolites collecting and causing damage, trauma, toxicity, etc.
  • Post-Renal: Involves ureters, prostate, and bladder.
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21
Q

Risk Factors for AKI/ ARF

A
  • Diabetes (Type I or II)
  • Chronic renal insufficiency
  • Heart disease (heart failure)
  • Hypertension
  • Advanced age
  • Sepsis
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22
Q

Contributing Factors in the Development of AKI/ARF Pre-renal

A
  • Hypotention
  • Hypovolemia
  • Decrease CO
  • Dehydration
  • Vascular Disease
  • Renal Vein Thrombosis
  • DM
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23
Q

Contributing Factors in the Development of AKI/ARF Intrarenal

A
  • Nephrotoxic episodes
  • Infection
  • Systemic inflammation
  • Injured red blood cells
  • Hemolytic blood transfusion reactions
  • Glomerular diseases (systemic lupus, glomerulonephritits)
  • Rhabdomylolysis
24
Q

Contributing Factors in the Development of AKI/ARF postrenal

A
  • Medication that interferes with normal bladder emptying.
  • Benign prostatic hypertrophy (BPH)
  • Prostate cancer
  • Ovarian cancer
  • Obstruction of a urinary catheter
  • Renal calculi
  • Bladder/pelvic neoplasms
  • Urethral strictures
25
Q

Pharmacological Causes and Agravators of AKI/ ARF

A

Causes:
Contrast media
Diuretics (Furosemide)
Heavy metals (mercury, gold lead)
Ibuprofen
Organic chemicals or solvents
Nephrotoxic antibiotics (Gentamycin/Piperacillin)
ACE Inhibitors

Aggravators:
Amiloride
Any medication containing magnesium tetracycline
Cisplatin
Aspirin
Lithium
Nonsteriodal anti-inflammatory agents
Spironolactone

26
Q

Clinical Manifestations of AKI/ ARF

A
  • Decreased urine output (urine may be pink or reddish in color)
  • Edema (face, arms, legs, feet eyes)
  • Flank pain/Pelvic pain
  • Poor appetite (nausea, vomiting)
  • Bitter or metallic taste in mouth
  • Dry itchy skin
  • Easy bruising
  • Fatigue
  • Seizures/LOC
  • Shortness of breath
  • Arrhythmias
  • Sudden weight gain
27
Q

The Four Phases of AKI/ARF

A

Onset Phase: from hours to a day

  • Renal flow at 25% of normal
  • Oxygenation to the tissue at 25% of normal
  • Urine output at 30 ml (or less) per hour
  • Urine sodium excretion greater than 40 mEq/L.

Oliguric Phase: lasts 8-14 days. Tubular wall damage

  • Significant decrease in GFR
  • Increase BUN/Creatinine
  • Electrolyte Imbalance
  • Metabolic Acidosis

Diuretic Phase: Occurs if problem corrected. Lasts 7-14 days.

  • Increase in GFR
  • Urine output as high as 2-4 L/day
  • Renal cells that cannot concentrate urine

Recovery Phase: lasts months to a year. Cells start having some recovery and generation

  • GFR returns to70-80% Baseline
  • Renal Tubules begin to function
  • Fluid/ electrolyte balance returns
28
Q

Diagnostic Imaging Studies in AKI/ARF

A
  • Creatinine Clearance Test:
  • Ultrasound: look to see if there’s a mass or obstruction
  • Doppler Studies: look at vascular and arterial flow
  • Nuclear Studies: looking for a tumor or mass
  • Renal Biopsy: looking for cancer causing or some sort of systemic autoimmune disorder
29
Q

Laboratory Findings for Prerenal vs. Intrarenal Failure

urine osmolality

urine sodium

casts/sediments

FENA

A

See table

30
Q

Medical Management of AKI/ARF

A
  • Address underlying cause
  • Maintain intravascular volume: monitoring how much output and dialyzing them or giving diuretics to get the volume out
  • Maintain MAP: want it above 70. For elderly person, 90-100.
  • Discontinue nephrotoxic agents
  • Correct Acidosis
  • Correct hemolytic issues
  • Correct electrolyte imbalances
  • Strict I & O’s and daily weights
  • Fluid and diet restrictions
    *
31
Q

a loop diuretic that can be used to increase urinary flow with the intent of flushing out cellular debris that may be causing an obstruction.

A

Furosemide (Lasix)

32
Q

an osmotic diuretic that can be used to dilate renal arteries by increasing the synthesis of prostaglandins (resulting in restored renal flow).

A

Mannitol

33
Q

at low doses (1-5 mcg/kg/min), dopamine dilates renal arterioles and increases renal blood flow and glomerular filtration. Because dopamine (even at low doses) can cause tachycardia, myocardial ischemia and arrhythmias it use should be considered carefully.

A

Dopamine

34
Q

this medication can help reverse acute renal failure when the cause is thought to be from a nephrotoxic source.

A

N-acetylcysteine (Mucomyst)

35
Q

Extracorporeal Therapies in AKI/ARF

A

Hemodialysis

Peritoneal dialysis: Not used in ARF
Hemodialysis. Good for quick removal of water and toxins

CRRT

Less likely to cause hypotension: Hemodynamic stability
Correction of metabolic acidosis. Quicker kidney recovery time. Correction of malnutrition. Solute removal

36
Q

Three types of dialysis access

A

Venous Catheters: used for dialysis. Heparinized. Cannot use for blood draw. Used with short and long term dialysis.

Arteriovenous catheters (fistula): From artery and the vein. more for long term dialysis. (wait 1-3 months

Synthestic Grafts: Similar, but connects from a synthetic graft that connects aretery and vein. Has more complications than AV fistula (wait 2-4 weeks)

37
Q

Nursing Care of the AV Fistula

A
  • Cleanse with Soap and water daily
  • Limit contact with site
  • Assess for signs of infection
  • No BP or needle sticks to arm
  • Assess site for Thrill/bruit
  • Patient teaching to avoid pressure to site
38
Q

Risk for increased clotting during dialysis. What is the reversal agent?

A

Protamine

39
Q

HIT acronym

A

heparin induced thrombocytopenia

40
Q

Diffusion

A

high concentration to low concentration. Not great for person in renal failure, but good for fluid volume overload

41
Q

osmosis

A

from high concentration to low concentration. Plasma is low, dialysate is high

42
Q

convection

A

based on hydrostatic pressure. Positive in the blood, negative in the dialysate, allows both water, small, and moderate sized molecules to transfer over.

43
Q

Types of Continuous Renal Replacement

A
  • Slow Continuous Ultrafiltration (SCUF): 100-300 ml taken off every hour. Good for removing fluid, but not good for uremia.
  • Continuous Venovenous Hemofiltration (CVVH): 7-30 liters removed every 24 hours. Can be used for convection.
  • Continuous Venovenous Hemodialysis (CVVHD): Used a lot. Good at getting fluid off, but not the moderate sized molecules
  • Continuous Venovenous Hemodiafiltration (CVVHDF): Good for small and moderate sized molecules. Run continuously, low rate, over 24 hours. Best type for acute renal failure pt.
44
Q

Assessment and management pre, during, and post proceedure dialysis pt.

A

Assessment & Management:

Pre-procedure: Vital Signs, Dry Weight, Electrolytes
Procedure: Dialyzers, Dialysate, Hemodynamic stability
Post Procedure: Fluid volume, Dysrhythmias, Muscle cramps, Dialysis Disequilibrium

45
Q

Advantages and disadvantages for intermittent therapy vs. continuous therapy

A

see table

46
Q

t waves peaked

A

k+ 5-6.5

47
Q

prolonged PR interval

A

6-6.5 k+

48
Q

wide qrs no p wave

A

7.5-8.0

49
Q

Overview of Hyperkalemia Treatment table insulin, calcium gluconate/carbonate, salbutamol, ion exchange resin, haemodialysis

A

see table

50
Q

Most common colloids given

A
  • albumin 5%: giving volume
  • Albumin 25%: more hypertonic, fluid shift from extravascular to intravascular
  • Has high molecular weight, so it doesn’t cross dialysate membrane well. Helps keep fluid inside pt. easier
51
Q

Severe Metabolic Acidosis common in AKI ph?

A

pH less than7.2

52
Q

treatment of acidosis common in AKI

A

Treatment
Alkaline Medications
Sodium bicarbonate tablets)

Sodium bicarbonate???
Used in severe acidosis. Many complications. Now try to not give this bc increases sodium levels and osmolarity.

Hemodialysis

53
Q

Things that can occur that cause acute renal failure that are outside the norm

A
  1. Rapidly progressive glomerulonephritis: seen with autoimmune disorders. Confirm diagnosis with renal biopsy.
  2. Haemolytic‐uraemic syndrome: Pt has ecolli. Do plasma exchange to get ecoli out of the system
  3. Tubulointerstitial nephritis: Drug induced by steroids. Removal of steroids and then therapeutic support
  4. Contrast nephropathy: Contrast dye being given. Nac given day before and day of to help ward it off
  5. Rhabdomyolysis: Muscle breakdown, endotoxin cascade, leads to renal vasoconstriction and ischemia. Decreased vascular volume to kidneys Leads to acute tubular necrosis. Push fluids to get out myoglobin toxins and promote 200ml an hour urine output
  6. Liver disease—hepatorenal syndrome: Less than 10% of people will live from this. Standard treatment is liver transplant. Kidneys have shut down.
54
Q

Nursing Diagnosis for ARF

A
  • Alteration in urinary elimination
  • Fluid volume deficit
  • Fluid volume overload
  • Altered nutrition (less than bodily requirement)
  • Potential for impaired skin integrity
  • Decreased cardiac output
  • Activity intolerance
55
Q

How to prevent ARF?

A
  • Recognize that patients with pre‐existing renal impairment are at higher risk of developing further renal insufficiency—treat and monitor accordingly
  • Temporarily withhold nephrotoxic (especially ACE‐I, ARBs, NSAIDs) and diuretics (to prevent dehydration) when patients become unwell—either in the community or in hospital
  • Ensure that patients remain adequately hydrated, to maintain renal perfusion
  • Remember to monitor renal function after starting, or increasing the dose, of ACE‐I or ARBs (check one to two weeks later)
  • Where necessary, adjust drug doses in patients with renal impairment
  • Monitor drug levels when using aminoglycoside (gentamicin) and/or glycopeptide (vancomycin) antibiotics—and adjust dose accordingly
  • Hydrate the patient and consider using N‐acetyl cysteine before procedures entailing radiological contrast media

NUR4630 (34 decks)

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