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Internal medicine > SU2M - Renal Failure > Flashcards

SU2M - Renal Failure Flashcards

0
Q

RIFLE Criteria for AKI

A
  1. RISK: 1.5 fold increase in serum creatinine or GFR decreased by 25% or urine output <0.5 mL/kg/hr for 6 hrs
  2. INJURY: Twofold increase in the serum creatinine or GFR decrease by 50% or urine output <0.5 mL/kg/hr for 12 hrs
  3. FAILURE: Three fold increase in serum creatinine or GFR decreased by 75% or urine output <0.5 mL/kg/hr for 24 hours, or anuria for 12 hrs
  4. LOSS: Complete loss of kidney function (requiring dialysis) for more than 4 wks
  5. ESRD: Complete loss of kidney function for more than 3 mnths
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1
Q

Acute Renal Failure: definition?

A
  • AKA Acute Kindey Injury (AKI)
  • rapid decline in renal function
  • with an increase in serum creatinine
  • at first the creatinine can be normal, despite the low GFR, bc it takes time for the creatinine to accumulate in the body
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2
Q

Most common clinical findings in AKI?

A
  1. Weight gain
  2. Edema
    * *due to water and sodium retention
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3
Q

Azotemia: definition?

A

-elevated BUN and Creatinine

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4
Q

What are 3 non-kidney causes of an elevated BUN?

A
  1. Catabolic drugs (ex. Steroids)
  2. GI/soft tissue bleeding
  3. Dietary protein intake
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5
Q

2 non-kidney causes of elevated creatinine?

A
  1. Increased muscle breakdown –> baseline creatinine varies proportionately with muscle mass
  2. Some drugs
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6
Q

3 Categories of AKI?

A
  1. Prerenal
  2. Intrinsic renal failure
  3. Postrenal failure
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7
Q

2 Ssx of prerenal failure?

A
  1. Signs of volume depletion

2. Signs of CHF

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8
Q

Signs of acute interstitial nephritis?

A
  • aka intrinsic renal failure

- signs of an allergic rxn, ex. Rash

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9
Q

3 ssx that suggest post renal failure etiology?

A
  1. Suprapubic mass
  2. BPH
  3. Bladder dysfunction
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10
Q

Pathophysiology of prerenal AKI?

A
  • renal blood flow decreases enough (by whatever cause, CHF, hypovolemia, etc.) to lower GFR –> decreased clearance of metabolites (ex. BUN, creatinine)
  • kidney conserves as much sodium and water as possible –> renal parenchyma is undamaged, tubular function & concentrating ability is preserved!
  • *reversible if blood flow is restored before extensive damage from ischemia occurs
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11
Q

8 Things to monitor in AKI?

A
  1. Daily weights
  2. Intake
  3. Output
  4. BP
  5. Serum electrolytes
  6. Hb –> watch for anemia
  7. Hct –> watch for anemia
  8. Watch for infection
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12
Q

Urine osmolarity: prerenal failure v. ATN?

A
  • prerenal: > 500 –> kidney is still able to resorb water!

- ATN: 250-300mOsm –>water reabsorption is impaired

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13
Q

Urine Na+: prerenal failure v. ATN?

A
  • prerenal failure = < 20 –> because kidney can still resorb Na!
  • ATN = > 40 –> Na is poorly absorbed
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14
Q

Fractional excretion of Na: prerenal failure v. ATN?

A
  • prerenal = <1%

- ATN = > 2-3%

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15
Q

Urine sediment: prerenal failure v. ATN?

A
  • prerenal = scant

- ATN = full brownish pigment, granular casts w/ epithelial casts

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16
Q

BUN/Cr ratio: prerenal v. ATN?

A
  • prerenal = > 20:1 –> kidney can still resorb urea!

- ATN = < 20:1 –> less urea can be absorbed

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17
Q

Intrinsic renal failure: definition?

A
  • kidney tissue is damaged
  • glomerular filtration and tubular function are significantly impaired
  • kidneys are unable to concentrate urine effectively
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18
Q

4 causes of intrinsic renal failure?

A
  1. Tubular disease = ATN, can be caused by ischemia or nephrotoxins
  2. Glomerular disease = acute glomerular nephritis, ex. Goodpastures, Wegener’s, poststreptococcal GN, lupus
  3. Vascular disease –> ex. Renal artery stenosis, etc
  4. Interstitial disease –> ex. Allergic interstitial nephritis (often due to hypersensitivity rxn to a medication)
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19
Q

Rhabdomyolysis: 5 causes

A
  • skeletal muscle breakdown, caused by:
    1. Trauma
    2. Crush injuries
    3. Prolonged immobility
    4. Seizures
    5. Snake bites
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20
Q

Rhabdomyolysis: pathophysiology?

A
  • release of muscle fiber contents (myoglobin) into the blood stream
  • myoglobin is toxic to the kidneys
  • can lead to AKI
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21
Q

Rhabdomyolysis: lab findings?

A
  • markedly elevated creatinine phosphokinase (CPK)
  • hyperkalemia
  • hypocalcemia
  • hyperuricemia
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22
Q

Rhabdomyolysis: tx?

A
  1. IV fluids
  2. Mannitol = osmotic diuretic
  3. Bicarbonate = drives K back into the cells
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23
Q

Ischemic AKI

A
  • cause of ATN
  • secondary to severe decline in renal blood flow –> shock, hemorrhage, sepsis, DIC, heart failure
  • ischemia ==> death of tubular cells
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24
Q

Nephrotoxic AKI

A
  • cause of ATN
  • kidney injury secondary to substances that directly injure renal parenchyma ==> death of cells
  • causes: antibiotics, radiocontrast, NSAIDs (esp w/ CHF), poisons, myoglobinuria (ex from rhabdo), hemoglobinuria, chemotx, and kappa and gamma light chains produced in multiple myeloma
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25
Q

Post renal failure: definition

A
  • obstruction of any segment of the urinary tract (with intact kidneys) –> increased tubular pressure bc the urine produced cant be excreted –> decreased GFR
  • blood supply and renal parencyma are intact
  • *both kidneys must be obstructed for creatinine to rise
  • renal fctn can be restored if obstruction is relieved before the kidneys are damaged
  • can lead to ATN if untreated
26
Q

6 common causes of postrenal failure?

A
  1. Obstruction due to enlarged prostate –> most common cause
  2. Obstruction of one kidney
  3. Nephrolithiasis
  4. Obstructing neoplasm
  5. Retroperitoneal fibrosis
  6. Urethral obstruction –> uncommon, bc must be bilateral to cause renal failure
27
Q

3 basic tests for postrenal failure?

A
  1. Palpate the bladder
  2. Ultrasound –> look for obstruction or hydronephrosis
  3. Catheter –> look for large volume of urine
28
Q

3 phases of ATN?

A
  1. Oliguric phase:
    - azotemia and uremia
    - usually lasts 10-14 days
    - urine output <400-500 mL/day
  2. Diuretic phase:
    - begins when urine outflow is >500 mL/day
    - high urine output due to: fluid overload (excess retained during oliguric phase) osmotic diuresis (due to retained solutes during oliguric phase), tubular cell damage (delayed recovery of epithelial cell function relative to GFR)
  3. Recovery phase:
    - recovery of tubular function
29
Q

What are hyaline casts seen in?

A

-prerenal failure

30
Q

RBC casts seen in?

A

-glomerular disease

31
Q

WBC casts indicate?

A

-indicate renal parenchymal inflammation

32
Q

What do fatty casts indicate?

A

-nephrotic syndrome

33
Q

In early phase of AKI, what are the 2 most deadly complications?

A
  1. Hyperkalemic cardiac arrest

2. Pulmonary edema

34
Q

4 possible complications of Acute Kidney Injuries?

A
  1. ECF volume expansion –> pulmonary edema
  2. Metabolic disturbances –> hyperkalemia (decreased excretion, and K is moving from ICF –> ECF) metabolic acidosis (decreased excretion of H+), hypoCa, hypoNa, hyperphos, hyperuricemia
  3. Uremia –> toxic end products from metabolism accumulate
  4. Infection –> occurs in 50-60% of cases (possibly bc uremia impairs immune fctn)
35
Q

3 tx for prerenal failure?

A
  1. Tx underlying disorder
  2. Give normal saline to maintain euvolemia and restore BP –> do not give with edema or ascites though!
  3. Eliminate any offending agents (ex. ACEi or NSAIDs)
36
Q

3 Tx for intrinsic renal failure?

A
  1. Supportive
  2. Eliminate causal/offending agent
  3. If oliguric –> furosemide to increase urine flow
37
Q

Postrenal tx?

A
  1. Bladder catheter
38
Q

Chronic kidney disease: definition?

A

-decreased kidney function (GFR <60mL/min) or kidney damage (structural or functional) for at least 3 months, regardless of cause

39
Q

5 Causes of Chronic kidney disease?

A
  1. Diabetes –> MOST common! (30%)
  2. HTN –> second most common! (25%)
  3. Chronic glomerular nephritis (15%)
  4. Interstitial nephritis, polycystic kidney disease, obstructive uropathy
  5. Any cause of AKI can lead to CKD
40
Q

At what BUN does uremia typically occur?

A
  • > 60
41
Q

Chronic renal insufficiency?

A
  • when a pts renal function os irreversibly compromised, but NOT failed
  • chronic elevation of serum creatinine to 1.5-3.0mg/dL
42
Q

What is the major cause of mortality in pts with CKD?

A
  • infection

- have increased susceptibility –> uremia inhibits cellular and humoral immunity

43
Q

Why can CKD lead to fragile bones and fractures?

A
  • kidney cant clear phosphate as well –> hyperphosphetemia –> decreased production of 1,25-dihydroxy vitamin D –> hypocalcemia –> hyperparathyroidism –> removes Ca from bones –> bones become weak
  • this is called renal osteodystrophy!
44
Q

Calciphylaxis and CKD

A
  • CKD causes hyperphosphetemia bc the kidney can get rid of phosphate as well
  • hyperphosphetemia can cause phosphate and calcium to precipitate –> vascular calcifications –>necrotic skin leasions
45
Q

In CKD what are the 2 most common complications that require urgent intervention?

A
  1. Symptomatic volume overload

2. Severe hyperkalemia

46
Q

3 life-threatening complications in CKD?

A
  1. Hyperkalemia –> get EKG (but can have hyperK without EKG changes)
  2. Pulmonary edema –> secondary to volume overload, monitor weight
  3. Infection –> ex pneumonia, UTI, sepsis
47
Q

What are the preferred meds in CKD? What should you be cautious about when using them?

A
  • ACEi

- can cause hyperK

48
Q

What can be used to correct hyperphosphetemia? MOA?

A
  • calcium citrate

- MOA: binds phosphate

49
Q

Dialysate

A
  • artificial solution that resembles human plasma used in all forms of dialysis
  • diffusion of fluid and solutes occurs through a semipermieable membrane between the blood and the solution
50
Q

3 Situation in which dialysis can be used?

A
  1. CKD –> to bridge until renal transplant, or as a permanent tx when transplant is not an option
  2. AKI –> until the kidneys heal & renal fctn improves
  3. Overdose if medications or the ingestion of some substances cleared by the kidneys –> some, but not all can be dialyzed
51
Q

5 Absolute indications for dialysis?

A
  1. Acidosis –> significant metabolic acidosis
  2. Electrolytes –> severe, persistent hyperkalemia
  3. Intoxication –> of methanol, ethylene glycol, lithium, aspirin
  4. Overload –> hypervolemia that is not managed by other means
  5. Uremia –> severe, based on CLINICAL presentation, not by labs (**uremic pericarditis is an absolute indication for dialysis!!)
    * *Think “A-E-I-O-U”
52
Q

4 Dialyzable substance?

A
  1. Salicyclic acid
  2. Lithium
  3. Ethylene glycol
  4. Magnesium-containing laxatives
53
Q

What is the usual frequency of hemodyalisis?

A

-3-5 hrs of dialysis for 3 days a week

54
Q

Which arteries are used to make an AV fistula for dialysis? What clinical sign indicates that it is patent?

A
  • radial or brachial arteries are connected to veins in the forearm
  • an audible bruit indicates that the fistula is patent
55
Q

What are 2 advantages to hemodialysis?

A
  1. More efficient than peritoneal dialysis –> high flow rates and efficient dialyzers = shorter time required for dialysis
  2. Can be initiated more quickly in the emergency setting
56
Q

2 Disadvantages to hemodialysis?

A
  1. Less similar to the physiology of the natural kidney than peritoneal dialysis, so the pt is predisposed to:
    a) hypotension - bc of rapid removal of intravascular volume –> rapid fluid shifts from extravascular space into cells
    b) hypo-osmolality - due to solute removal
  2. Requires vascular access
57
Q

Frequency of peritoneal dialysis?

A
  • dialysis fluid is drained and replaced every hour in acute peritoneal dialysis
  • but only needs to be drained and replaced every hour in CAPD ( = continuous ambulatory peritoneal dialysis)
58
Q

2 Advantages of peritoneal dialysis?

A
  1. Patient can learn to perform dialysis on their own

2. Mimics the physiology of the normal kidney more closely than hemodialysis

59
Q

4 Disadvantages to peritoneal dialysis?

A
  1. High glucose load in the solution can lead to hyperglycemia and hypertriglyceridemia
  2. Peritonitis is a significant potential complication
  3. Patient must be highly motivated to self-administer
  4. Cosmetic = the dialysate fluid will increase their abdominal girth
60
Q

Limitations to both forms of dialysis?

A

-dialysis cannot replace the kidneys synthetic functions –> pts are often epo and vit D deficiency

61
Q

6 Complications of hemodialysis?

A
  1. Hypotension - can cause myocardial ischemia, fatigue, etc
  2. Hypo-osmolality - relative to the brain, can cause nausea, vomiting, headache, seizures, or coma
  3. “First-use syndrome” = chest pain, back pain, & anaphylaxis (rare) - can occur immediately after the use of a new machine
  4. Anticoagulation complications - bleeding
  5. Infection of vascular site - can lead to sepsis
  6. Amyloidosis of beta2 microglobulin in bones and joints
62
Q

4 Complications associated with peritoneal dialysis?

A
  1. Peritonitis - ssx: fever and abdominal pain
  2. Abdominal/inguinal hernia - risk is increased bc of increased abdominal P
  3. Hyperglycemia - esp in diabetics
  4. Protein malnutrition

Internal medicine (14 decks)

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