Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

NUR 4050 > lecture 9: Renal > Flashcards

lecture 9: Renal Flashcards

(55 cards)

Start Studying
1
Q

pathophysiology review

A

Protein metabolism results in ATP and NH3 (ammonia) -> Liver processes ammonia into Urea -> travels to the kidneys for urinary excretion -> BUN result from PROTEIN metabolism, Cr result from MUSCLE breakdown

BUN: 7-20
Cr: 0.6-1.2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Extra-Renal Causes of Increases in BUN (5)

A

Catabolic states
Steroids
Burns
Tetracycline abx
Low flow states

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Extra-Renal Causes of Increases in Creatinine (2)

A

Increased Muscle mass
Increased Muscle breakdown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Extra-Renal Causes of Decreases in BUN (1)

A

Liver failure
- Can no longer turn ammonia into BUN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Extra-Renal Causes of Decreases in Creatinine (1)

A

Decreased muscle mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Acute Kidney Injury (AKI)

  • AKI occurs in up to ___ to ___ of hospitalized patients and in up to ___ of ICU patients.
  • Mortality rate between ___-___% patients treated with _______ ________ _______.
  • Greater than ____% survivors of severe AKI are _______ of dialysis by discharge.
  • what is the hallmark sign of AKI? term? what is sometimes considered a better marker d/t being relatively unaffected by metabolic factors?
A
  • AKI occurs in up to 15% to 18% of hospitalized patients and in up to 66% of ICU patients.
  • Mortality rate between 50% and 60% patients treated with renal replacement therapy (RRT)
  • Greater than 80% survivors of severe AKI are independent of dialysis by discharge.
  • Hallmark decrease GFR and accumulation of BUN and serum creatinine
    —- Termed “azotemia” (means high levels of nitrogenous compounds)
    —- Serum creatinine is sometimes considered a better marker because relatively unaffected by metabolic factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute Kidney Injury definition (3)

A

Increase in Serum Creatinine of >0.3mg/dl within 48 hours

Increase serum creatinine of >1.5 mg/dL times baseline in 7 days

Urine volume <0.5mL/kg/hr for >6hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

RIFLE Classification: Grades AKI

A

Risk (>1.5mg/dL Cr)
Injury (>2mg/dL Cr)
Failure (>3mg/dL Cr)
Loss (persistent AKF>4weeks)
End-stage kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Urine Output Patterns (3)

what is this NOT?

A

Oliguria (< 400 mL/d)
Nonoliguria (> 400 mL/d)
Anuria (< 100 mL/d)

NOT Diagnostic criteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pre-Renal Kidney injury (2)

A
  • Changes in the blood flow to the kidney
  • Evidence of preserved tubular function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes of Prerenal AKI (2)

A

Hypo perfusion
Renal artery stenosis (Very rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Resulting Pathophysiology of Prerenal AKI

  • what?
  • drugs that interfere with auto-regulation include? (3)
  • what does prerenal AKI change?
A

Disruption in the Renin–angiotensin–aldosterone cascade
- Drugs that interfere with auto-regulation include:
—–NSAIDs
—–ACE inhibitors, ARBs
- Changes urinary composition and volume follow predictable pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pre-renal Labs (3)

A

Concentrated urine
FE Ur (Fractional excretion of Urea)
FE Na (Fractional excretion of Sodium)

What does this mean?: The percentage of Na or Urea in the urine as it relates to the concentrations in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Labs changes during Pre-renal Failure

  • BUN
  • GFR
    -BUN/CR
A

BUN will increase at a higher rate than Creatinine

This indicates a low glomerular filtration rate

Both BUN and Creatinine will not filter out as quickly a result of decreased GFR

BUN, however, once filtered out, will be reabsorbed back into the blood in low flow states

This results in a higher BUN:Cr ratio
- Normal may be 15:1
- May increase to 30:1. (ie. BUN is 60, Creatinine is 4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Intrarenal AKI (4) catergorized according to?

A

Categorized according to anatomical compartment:
- Glomerular
- Vascular
- Interstitial
- Tubular*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Glomerular (2)

A

Acute glomerulonephritis
Immune complex–mediated causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Interstitial (1)

A

Acute allergic interstitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Vascular (2)

A
  • Malignant hypertension
  • Microangiopathic processes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Tubular (Acute tubular necrosis in most cases) (2)

A
  • Obstructive or prolonged ischemia
  • Drug intoxication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Postrenal AKI

  • about ____% of hospital cases
  • caused by?
  • etiologies include: 3
A

About 10% hospital cases

Caused by any obstruction in flow of urine from collecting ducts in kidneys to external urethral orifice

Etiologies include
- Ureteral obstruction (ie, stones)
- Urethral blockage (ie, strictures)
- Extrinsic source (ie, tumor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pathophysiology: Post-renal AKI (5)

A
  • Congestion causes retrograde pressure.
  • Slows tubular fluid flow and lowers GFR
  • Increased reabsorption Na+, water, and urea
  • Dilated collecting ducts that compress nephrons
  • Dysfunction concentrating and diluting mechanism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Acute Tubular Necrosis (2)
what?
____% of AKI cases seen in the ICU

A
  • A type of Intra-renal failure caused by Pre-renal
  • 76% of AKI cases seen in the ICU
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Diagnosis of AKI: History and Physical

1) history that indicates ______

2) history of any disease that affect ______ ______: (3)

3) _____ status

Study These Flashcards
A

1) History that indicates hypoperfusion
2) History of any diseases that affect the renal system:
- Renal artery stenosis
- Lupus or vasculitis
- Abdominal tumors
3) Fluid status

24
Q

ATN phase 1

phase?

onset?

injury ->?

Study These Flashcards
A

Phase: onset phase
- Onset hours to days (treatment aimed at preventing damage)
- Injury -> signs and symptoms

25
ATN phase 2 phase: s/sx (8) interventions (5)
Phase: ATN 1) Signs and Symptoms - <400ml/day, low GFR, BUN/Cr, Neuro changes/confusion, itching, fluid retention, metabolic Acidosis - Electrolyte imbalances, concentrated urine (>1.020) 2) Interventions: - Limit protein consumption, survey for hyperkalemia, BP monitoring, assess lung sounds - Dialysis
26
ATN phase 3 phase:? s/sx: (5) interventions: (2)
Phase: Diuretic phase - lasts 1-3 weeks 1) S/S: - Slight increase in GFR - improved MS - osmotic diuresis (Urine grav <1.020) - hypotension - hypokalemia 2) Interventions: - Track I/O’s - replace fluid and electrolytes
27
ATN phase 4 phase:? s/sx (2) interventions (2)
Phase: Recovery phase - several months to a year 1) S/S: - 1-2L/day urine - labs normalize 2) Interventions: - Track I/O’s - replace fluid and electrolytes
28
Treatment of AKI (13) 1) correct? (4) 2) treat? 3) what is something to consider between? 4) avoid what types of medications? 5) restrict what in anuric patients? 6) monitor? 7) what type of medication does NOT work? 8) what medication has no influence on the outcome of oliguric AKI 9) know the status of? 10) don't overload with what? 11) what needs to be done to keep the patient alive? 12) what 2 factors influence survival and recovery?
1) Correct life-threatening problem - Hypoxemia, hypotension, hyperkalemia, acidosis (malperfusion) 2) Treat underlying cause 3) Fluids vs Diuretics (issues with flow -> CHF -> diuretics) 4) Avoid nephrotoxins- VANCOMYCIN 5) Restrict K+ in anuric patients- 6) I&O, Daily electrolytes and waste products 7) Low dose dopamine doesn’t work 8) Diuretics have no influence on the outcome of oliguric AKI (If it doesn’t work, they won’t respond) 10) Know the volume status- ie. Dry or overloaded? 11) Don’t overload with protein 12) Keep them alive- correct underlying problems 13) Age and co-morbidities influence survival and recover
29
Common Nephrotoxins 1) _______________ -> what type of medications? - 10-20% of patients - onset delayed, 5-10 days after onset treatment - where do you want to keep the MAP? 2) ________ ________ _________ - may not be as big of a problem as we once thought - occurs within ___to__ hours and peaks within __to__ days - ____ _____ patients - how do you reduce risk of developing it? (4)
Aminoglycosides – Gentamycin, Vancomycin - 10% to 20% of patients - Onset delayed, 5 to 10 days after onset treatment - KEEP MAP 65+ Contrast-induced nephropathy (CIN) - May not be as big of a problem as we once thought - Occurs within 24 to 48 hours and peaks within 5 to 7 days - High-risk patients - Reduce risk: fluid administration (1L), using low or iso-osmolar nonionic contrast or CO2, N-acetylcysteine (NAC) - mucomist, alkalinize urine - bicarb to help with metabolic acidosis
30
Contrast Induced Nephropathy (2)
1) Contrast has always been linked to worsening nephropathy 2) Recent studies suggest that this may not be the case - Studies involved retrospective audit of patients with nephropathy who received IV contrast - In practice, most still treat contrast as a nephrotoxic agent
31
Urinary Values (5)
Urine tests helpful in diagnosing etiology Urine sodium, osmolality, and specific gravity Fractional excretion of Na+ Fractional excretion urea nitrogen Sedimentation
32
Diagnostic Studies (3)
1) Renal ultrasonography - R/O obstruction 2) CT and MRI - Evaluate for masses or vascular disorders 3) Renal biopsy
33
Chronic Kidney Failure what (2) leads to? (1)
Slow, progressive, irreversible deterioration of renal function Kidney’s inability to eliminate waste products and maintain fluid and electrolyte balances Leads to end-stage renal disease (ESRD)
34
ESRD (3)
Currently, more than 52,000 dialysis and renal transplant recipients in the United States 24% higher in men than in women Incidence in African American 3.7 times higher than in white population
35
CKD Causes 1) two most common? 2) other common causes (5)
Two most common: 1) Diabetes (54%) - mgmt c/ meds 2) Hypertension (33%) Other common causes include 1) Glomerulonephritis 2) Interstitial nephritis 3) Genetic disorders 4) Hepatorenal syndrome 5) Microangiopathic
36
Pathophysiology of ESRD (3) 1) common morphological features (3) 2) ______ ______ theory (3) 3) possible mediators include (2)
1) Common morphological features - Fibrosis - loss of native renal cells - infiltration 2) Intact nephron theory - Hyperfiltration response non-diseased nephrons - Eventually reach maximal filtration - May accelerate loss of nephrons 3) Possible mediators include - Hypoxia - angiotensin
37
Proteinuria 1) result of (2) 2) _______ _______ ______ is reabsorbed and stored where? - causes? - results in (2) 3) very strong predictor of what?
1) Result of glomerular hypertension and abnormal glomerular permeability 2) Abnormally filtered protein is reabsorbed and stored intracellularly - Causes production of pro-inflammatory cytokines - Results in scarring and fibrosis 3) Very strong predictor of chronic kidney disease progression tip: - should never have protein (can induce damage to nephron) - powerlifters -> normal find
38
Preventing the Progression 1) _______ insults accelerates the loss of? 2) include: (7)
1) Secondary insults accelerate loss of nephrons. 2) Include: - Hypovolemia - Nephrotoxic agents - Urinary obstruction and infections - NSAIDs - Hyperglycemia - Hypertension - Hyperlipidemia
39
Management of Renal Failure (3)
1) Manage fluid balance changes - Treat hypovolemia - Prevent hypervolemia 2) Use diuretics - Furosemide, mannitol, thiazide diuretics 3) Dialysis or ultrafiltration
40
Manage acid–base alterations (2)
- Metabolic acidosis - IV sodium bicarbonate
41
Manage cardiovascular alterations (3)
1) Hypertension - Be aware of risk for Hypotension during dialysis 2) Hyperkalemia 3) Pericarditis
42
Managing pulmonary alterations (4)
- Pulmonary edema - Pleural effusions - pneumonitis - pulmonary infections
43
Managing gastrointestinal alterations (4)
- GI bleeding - Anorexia, nausea and vomiting, diarrhea, GERD - Stomatitis - Constipation
44
Managing neuromuscular alterations (3)
- Sleep disturbances, muscle irritability - Peripheral neuropathies - Seizures
45
Managing hematological alterations (1)
Increased bleeding tendency
46
Management of alterations in drug elimination (1)
Adjust dosages according to GFR
47
Management of skeletal alteration includes loss of bone density and formation of calcium phosphate crystals (4)
- Regulate phosphate. - Maintain calcium levels. - Treat vitamin D deficiency. - Control metabolic acidosis.
48
Managing of integumentary alterations include dryness, pruritus, uremic frost, ecchymosis, and purpura (2)
- Meticulous skin care - Prevent skin breakdown
49
Managing alterations in dietary intake (2)
- Restrict fluid, sodium, potassium, and phosphate - High calorie, moderate protein restrictions
50
Managing alterations in psychosocial functioning
?
51
ECG Changes in Hyper-kalemia (3)
1) Peaked T-waves, prolonged PR interval, depressed ST segment 2) Lost P-waves 3) Widened QRS complex
52
Anemia in ESRD 1) causes include: (4) 2) mgmt: (2)
Causes include: - Erythropoietin deficiency - Decreased RBC survival time - Blood loss - Other Management: - Administer iron and human erythropoietin. - Blood products
53
CAPD- Continuous Ambulatory Peritoneal Dialysis pros: 3 cons: 2
Pro’s Ambulatory Can be done while sleeping Gentle relative to HD Con’s Risk of infection* Requires high level of adherence
54
AKI Management during hemodynamic instability via Continuous Renal Replacement Therapy 1) NEVER? 2) after ESRD reaches stage ____ -> what occurs? - avoid ______ - administer?
1) NEVER draw blood or take blood pressures on a limb with a graft/fistula 2) *After ESRD reaches stage 3- Vein preservation strategies should be employed - Avoid subclavian veins - Administer IV medications appropriately
55
Continuous Renal Replacement Therapy - CRRT 1) requires? 2) what is the process? 3) provides _____ ______ at a rate around ? -> removes more ______ + more gentle if? - slower rates allow? 4) how long does each cartridge last for? 5) removes more _____ than?
1) Requires “leur lock” dialysis access catheter (Quinton/groin or Permacath/subclavian) 2) Uses Diffusion to remove solute - Solutes move across a semipermeable membrane 3) Provides continuous dialysis at a rate around 150ml/min -> removes more solute + more gentle if hemodynamically unstable - Slower rate allows more control over fluid volume 4) Each cartridge lasts 48 hours 5) Removes more solute than conventional dialysis

NUR 4050 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions