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IM_Renal and GU > Renal Failure > Flashcards

Renal Failure Flashcards

1
Q

In a nutshell definition of AKI

A

rapid decline in renal function with increase in creatinine (0.5 - 1.0 increase)

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2
Q

acute renal failure vs AKI

A

Acute renal failure is the early stage of AKI when creatinine may be normal despite reduced GFR due to time it takes for creatinine to accumulate in body

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3
Q

3 types of AKI

A

prerenal - due to decreased renal blood flow (MCC)
intrinsic - due to damage to renal parenchyma
postrenal - urinary tract obstruction (least common)

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4
Q

What 3 aspects of kidney function does RIFLE criteria look at?

A

Creatinine increase, GFR decrease, urine output

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5
Q

What does RIFLE stand for?

A 
Risk
Injury
Failure
Loss
ESRD

used to define AKI

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6
Q

Risk

A

1.5x increase creatinine
25% decrease GFR
<0.5 ml/kg/hr UO for 6 hours

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7
Q

Injury

A

2.0x increase in creatinine
50% decrease GFR
<0.5 ml/kg/hr UO for 12 hours

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8
Q

Failure

A

3.0x increase in creatinine
75% decrease GFR
<0.5 ml/kg/hr UO for 24 hours or anuria 12 hours

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9
Q

Loss

A

complete loss of kidney function (requiring HD) for more than 4 weeks

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10
Q

ESRD

A

complete loss of kidney function (requiring HD) for more than 3 months

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11
Q

T/F: AKI always results in oliguria or anuria

A

FALSE. can present with no oliguria (nonoliguric AKI)

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12
Q

Most common findings in AKI patient

A

Weight gain and edema due to positive water and sodium balance

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13
Q

What is azotemia?

A

Elevated BUN and Cr; characterizes AKI

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14
Q

What else causes elevated BUN besides AKI?

A

catabolic drugs like stereoids
GI/soft tissue bleeding
dietary protein intake

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15
Q

What else causes elevated Cr besides kidney problems?

A

baseline Cr depends on muscle mass

so any muscle breakdown can increase Cr…drugs can also increase Cr

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16
Q

Prognosis for AKI

A

80% of patients completely recover…but depends on age of patient and severity of renal failure

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17
Q

Most common causes of death in AKI patients

A

infection followed by cardiorespiratory problems

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18
Q

What mechanisms cause prerenal failure

A

ANYTHING THAT DECREASES BLOOD FLOW TO KIDNEYS

  • decreased CO
  • volume loss / sequestration
  • hypotension

ie hypovolemia, excessive diuretic use, poor fluid intake, vomiting, diarrhea, burns, diarrhea, CHF, renal arterial obstruction, cirrhosis/hepatorenal syndrome, patient on NSAIDs, ACE inhibitors, cyclosporin

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19
Q

What do NSAIDs do to kidneys? and ACE inhibitors?

A

NSAIDs - constrict afferent arterioles

Ace inhibitors - dilate efferent arterioles

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20
Q

Pathophysiology of prerenal AKI

A

DECREASED RENAL BLOOD FLOW leads to LOWER GFR which leads to decreased clearance of metabolites…

however renal parenchyma isn’t damaged so tubular function and CONCENTRATING ABILITY IS PRESERVED.

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21
Q

What clinical features are typically seen in patient with prerenal AKI?

A

SIGNS OF VOLUME LOSS

dry mucous membranes, hypotension, tachycardia, decreased tissue turgor, oliguria/anuria)

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22
Q

What lab findings are seen in AKI

A

OLIGURIA ALWAYS (to preserve volume)
urine with HIGH OSMOLALITY (since kidney retains water) (>500)
urine with LOW Na, (FENa <1%)
Increased urine-plasma Cr ration (>40:1) (filtrate is reabsorbed, but not creatinine)
bland urine sediment

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23
Q

intrinsic renal failure

A

glomerular filtration and tubular function are imparied therefore kidneys CANNOT CONCENTRATE URINE

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24
Q

Causes of intrinsic renal failure

A
  • ATN (Most common - due to ischemia, nephrotoxins
  • glomerular disease (i.e. acute glomerulonephritis)
  • vascular disesase
  • interstitial disease
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25
Q

What kinds of glomerular diseases can cause intrinsic renal failure

A

poststrep glomerulonephritis
Wegner granulomatsosis
goodpasture syndrome
lupus

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26
Q

What kinds of vascular disease can cause intrinsic renal failure

A

TTP
HUS
renal artery occlusion

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27
Q

How does rhabdomyolysis damage kidneys

A

When skeletal muscle breaksdown (either from trauma, crush injuries, or snake bites), skeletal muscles release myoglobin which are toxic to kidneys. In addition, you get hyperkalemia, hyperuricemia, hypocalcemia, and elevated CPK. Treat with IV fluids, mannitol (to drain that bad shit out), and bicarb (to get K back into cells)

28
Q

What causes ischemic AKI

A

ANYTHING THAT LEADS TO SEVERE DECLINE IN RENAL BLOOD FLOW

heart failure, DIC, shock, hemorrhage, sepsis

29
Q

What can cause nephrotoxic AKI

A

any substance that damages renal parenchyma

NSAIDS, antibiotics (aminoglycosides, vanc), radiocontrast agents, NSAIDS (esp in CHF), poisons, myoglobin, hemoglobinuria, chemo (cisplatin), kappa gamma light chains seen in multiple myeloma

30
Q

What recovery usually takes longer, prerenal or intrinsic renal failure?

A

intrinsic

31
Q

Lab findings in intrinsic renal failure

A

DECREASED urine osmolality (kidney cannot concentrate urine)
Increased urine Na (kidney cannot retain Na)
DECREASED urine plasma Cr ratio (kidney cannot reabsorb filtrate)
Decreased BUN/Cr ratio (although both still elevated, kidney cannot reabsorb urea as well as in prerenal)

32
Q

post renal failure

A

least common cause of AKI
obstruction in the urinary tract with intact renal blood supply and parenchyma intact.
Leads to increased GFR (both kidneys must be obstructed for Cr to rise)

33
Q

causes of post renal

A 
urethral obstruction  secondary to BPH (most common cause)
kidney stones
obstructing neoplasm (i.e. bladder, cervical cancer)
34
Q

How to monitor patient with AKI

A
  • daily weight, Is and Os
  • BP
  • Serum electrolytes
  • Hgb/Hct to check for anemia
  • monitor for infection
35
Q

What lab values will usually indicate AKI?

A

elevated BUN and Cr

36
Q

What two types of AKI can cause ATN?

A

ischemic AKI and nephrotoxic AKI (anything that destroys tubular cells)

37
Q

What 3 tests can you do to rule out postrenal failure?

A
  • physical exam (palpate bladder)
  • insert catheter (look for large volume of urine)
  • bladder and kidney U/S to check for obstruction and hydronephrosis
38
Q

What to always obtain in patient with AKI?

A 
U/A
urine chem
serum electrolytes
bladder catheterization to rule out obstruction
renal u/s
39
Q

What do muddy brown cast, RBC casts, fatty casts, and WBC casts indicate on U/A

A

muddy brown casts/renal tubular cells - ATN
RBC casts/ RBCs - glomerular disease
WBC casts/WBCs - pyelonephritis, acute interstitial nephritis
fatty casts - nephrotic syndrome

40
Q

Where would you see increased protein and blood?

A

Acute glomerfulonephritis and acute interstitial nephritis

41
Q

What are some complications of AKI?

A

ECF volume expansion -> pulmonary edema (treat with furosemide)
metabolic/electrolyte disturbances
uremia
infection

42
Q

What electrolyte disturbances can be seen in AKI?

A 
hyperkalemia
metabolic acidosis (increased anion gap) - correct with sodium bicarb
hyperphosphatemia -> hypocalcemia
hyponatremia
hyperuricemia
43
Q

What is a common feared complication of AKI?

A

infection! (ex: pneumonia, UTI, wound infection, and sepsis)

uremia itself is thought to impair immune function; infxn likely multifactorial

44
Q

General measures for AKI treatment

A
  • avoid nephrotoxic meds (i.e. NSAIDS, aminoglycosides, radiocontrasts)
  • adjust medication doses for renal function
  • correct fluid imbalances/electrolyte disturbances
  • optimize cardiac output
  • dialysis if indicated
45
Q

Indications for dialysis

A

symptomatic uremia
intractable metabolic acidosis
hyperkalemia
urgent symptoms of volume overload

46
Q

Definition of chronic kidney disease (CKD)

A

decreased kidney function (GFR<60)

OR

kidney damage (structural/functional abnormalities) for at least 3 months regardless of cause

47
Q

Causes of CKD

A
  • DM (most common)
  • HTN (25% of cases)
  • chronic GN
  • interstitial nephritis, polycystic kidney disease, obstructive uropathy (any AKI left untreated or prolonged)
48
Q

CV features of CKD

A
  • HTN
  • CHF (due to volume overload, HTN, and anemia)
  • pericarditis (from symptomatic uremia)
49
Q

Mechanism behind HTN in CKD

A

decreased GFR stimulates RAAAS system -> BP increase

50
Q

GI features of CKD

A

nausea/vomiting

anorexia

51
Q

Neurologic features of CKD

A

lethargy, somnolence, confusion, confusion, peripheral neuropathy, uremic seizures, weakness, asterexis, hyperreflexia, “restless legs”

these come from hypocalcemia

52
Q

Hematologic features of CKD

A

normocytic normochromic anemia (secondary to EPO deficiency)

bleeding (secondary to platelet dysfunction due to uremia (platelets can’t degranulate in uremic environment)

53
Q

Endocrine/metabolic features of CKD

A
  • hyperphosphatemia -> hypocalcemia
  • can also sometimes have secondary hyperparathyroidism causing hypercalcemia and (calciphylaxis from ppt) and renal osteodystrophy
  • low testosterone in men and amenorrhea/infertility/hyperprolacinemia in women
  • pruitis
54
Q

What tests to run to dx CKD

A
  • urinalysis (sediment)
  • Cr and GFR
  • CBC
  • electrolytes
  • Renal u/s to rule out obstruction
55
Q

What diet to recommend in patient with CKD

A

LOW SALT, LOW PROTEIN

restrict potassium, phosphorus, and magnesium

56
Q

What BP med recommended for CKD patient

A

ACE inhibitors (dilate efferent arteriole) shown to reduce risk of progression to ESRD (BUT WATCH OUT FOR HYPERKALEMIA)

57
Q

How to treat hyperphosphatemia

A

calcium citrate (phosphate binder)

58
Q

What supplements to give to prevent secondary hyperparathyroidism

A

calcium and vit D

59
Q

What intoxications are indications for dialysis?

A

ethylene glycol, lithium, aspirin (salicyclic acid), magnesium containing laxatives

60
Q

Options for HD access?

A
  • central catheter in subclavian or jugular vein
  • tunneled catheter (lowers rate of infxn, can use for up to 6 months)
  • AV fistula (best form; needs surgery, audible bruit)
61
Q

Pros and cons to HD

A

Pro: efficient than PD, can be initiated quickly
Con: less similar to true physiology of kidney, can lead to hypotension during rapid removal and fluid shifts, hypo-osmolality

62
Q

How does peritoneal dialysis work?

A

peritoneum is the dialysis membrane, HYPEROSMOLAR HIGH GLUCOSE solution is used as dialysate fluid and infused into peritoneal cavity which draws up water from blood via osmosis…fluid has to be drained and replaced several times a day

63
Q

Advantages of peritoneal dialysis

A

patient can perform dialysis on their own, mimics true physiology of kidney

64
Q

What are dialysis still prone to despite having the filtration function of the kidney

A

since dialysis only can simulate FILTRATION and NOT SYNTHESIS…patients are still prone to vit D and EPO deficiency

65
Q

Complications of HD

A

hypotension, hypo-osmolality (n/v, headache, seizures), anticoag complications, infection of access site, HD associated amyloidosis of b2 microglobulin in bones and joints

66
Q

Complications of PD

A

peritonitis (accompanied by fever and pain some times, abdominal inguinal hernia, hyperglycemia, protein malnutrition

IM_Renal and GU (10 decks)

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