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PCM 3 exam 1- MARIYA > HYHO Acute Kidney Injury > Flashcards

HYHO Acute Kidney Injury Flashcards

1
Q

Acute Kidney Injury is characterized by an increase in what (diagnostic criteria)?

A

increase in serum creatinine of > or = to 0.3 mg/dL within 48 hrs or within 7 days

OR

urine output of <0.5 mL/kg/hour for >6 hours

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2
Q

Cardiorenal syndrome is a condition in which:

A

therapy to relieve congestive symptoms of HF is limited by a decline in renal function (as seen bc of the low GFR)

there is a bidirectional intx bw heart and kidneys!

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3
Q

What data would show signs of AKI (this is based on the case?)?

A

increase in BUN/CR

Normal EF on Echo

declining BNP from admission levels

improvement of findings on chest xray

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4
Q

What would you expect to see on renal US in a pt with chronic kidney dz?

A

decreased size of kidneys and/or cortical thinning;

It is important to identify underlying dz such as cystic kidneys

You can also identify hydronephrosis easily by US

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5
Q

What does a lack of hydronephrosis mean on US?

A

it eliminates any obstructive causes of kidney injury

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6
Q

What urine sodium value is expected with HF?

A

<25 meq/L

Extra info on it: renal perfusion is reduced with associated activation of RAAS and SNS, both of which promote sodium retention; however urine sodium are higher with concurrent diuretic therapy

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7
Q

What do you expect to see in lab values when exposed to IV contrasts?

A

typical increase in serum creatinine (25-50%) within 48 hrs after administration

(why its impt to take hx)

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8
Q

Undrlying kidney dz may have significant:

A

proteinuria, active urine sediment (hematuria +/- pyuria or casts) or small kidneys

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9
Q

is prerenal or postrenal azotemia more common in HF?

A

prerenal azoetemia (BUN/Cr>20)

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10
Q

What causes prerenal AKI?

A

hypovolemia, decreased CO, decreased effective circulating volume (CHF, liver failure,), impaired renal autoregulation (NSAIDS, ACE-i/ARBs, cyclosporine)

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11
Q

What causes intrinsic AKI?

A

Acute GN

damage to the tubules and interstitium (ischemia, sepsis/infection, nephrotoxins)

vascular causes (vasculitis, malignant HTN, TTP-HUS)

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12
Q

What nephrotoxins can cause intrinsic AKI?

A

exogenous: iodinated contrast, aminoglycosides, cisplatin, amphotericin B, PPis, NSAIDs
endogenous: hemolysis, rhabdomylosis, myeloma, intratubular crystals

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13
Q

What causes postrenal AKI?

A

bladder outlet obstruction, bilateral pelvoureteral obstruction (or unilateral obstruction of a solitary functioning kidneY)

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14
Q

PE finding of blue toes may indicate:

A

possible choelsterol emboli

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15
Q

PE finding of appearance of drug rash may indicate:

A

Acute interstitial nephritis (AIN)

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16
Q

PE finding of signs of volume contraction (tachy, skin tenting, dry oral mucosa, etc.) may indicate:

A

dehydration

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17
Q

PE finding of signs of volume overload AND heart failure signs may indicate:

A

cardiorenal syndrome

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18
Q

PE finding of jaundice + ascites may indicate:

A

liver dz with portal HTN

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19
Q

Signs + syx of AKI include:

A

decreased urine output

worsening dyspnea @ rest, orthopnea and/or PND

worsening edema moving from dependent edema to anasarca and/or ascites

TACHY, S3

hypotension

JVD

liver distention and/or tenderness w/ palpation

-distended abdomen: fluid wave, and/or puddle sign to assess for ascites

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20
Q

Skin tenting is best evaluated by:

A

pinching skin of forehead; skin of dehydrated pt will remain elevated rather than springing back to it’s original position

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21
Q

Signs of respiratory distress include:

A

tachypnea, hypoxia, increased work of breathing (retractions and tripod position)

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22
Q

What is PND and what can mimic it?

A

dyspnea and orthopnea that awakens pts from sleep prompting pt to sit up /stand up

May be associated with wheezing and coughing;

may be mimicked by nocturnal asthma attacks

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23
Q

What is anasarca?

A

severe generalized edema, extends from LE proximally

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24
Q

What can anasarca cause and what is it associated with?

A

can cause ascites as well as subq edema

It is commonly associated with HF, cirrhosis, severe malnutrition, and renal failure

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25
Q

What does fluid wave detect? What does a positive finding rule in?

A

large volumes of free intrabdominal fluid

+ rules in ascites (highly specific- 80-90%)

But 50% sensitivity so it does NOT exclude ascites (volume dependent)

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26
Q

How do you perform a fluid wave test?

A
  1. pt places ulnar surface of their hand along abdominal vertebral midline
  2. operator places on ehand on one flank and taps gently on the other flank

+ sign = when operator feels moderate to strong fluid wave emanating into the contralateral side

27
Q

What is a puddle sign? What is a + sign?

A
  1. Auscultatory percussion sign that requires the pt to support themselves on hands/knees for 5 mins
  2. Operator then listens with the diaphragm while flicking finger over localized flank area of abdomen starting at lowest point and moving over to opposite flank

sudden + sign = when sudden increase in intensity and clarity of sound, signaling that the steth has passed edge of peritoneal fluid

28
Q

What is the sensitivity of a puddle sign?

A

Sensitivity: 40-50% (especially of small amt of ascites)–>positioning of pt makes it very difficult to evaluate

29
Q

OSE Kidney sympathetics:

A

T10-11

30
Q

OSE Kidneys parasympathetic:

A

Vagus nerve

31
Q

OSE Upper ureter sympathetics:

A

T10-11

32
Q

OSE Upper ureter parasympathetics:

A

vagus n.

33
Q

OSE lower ureter sympathetics

A

T12-L2

34
Q

OSE lower ureter parasympathetics

A

pelvic splanchnic n.

35
Q

OSE bladder sympathetics:

A

T12-L2

36
Q

OSE bladder parasympathetics:

A

pelvic splanchnic n.

37
Q

OSE Anterior kidney chapmans point

A

one inch lateral and one inch superior to umbilicus

38
Q

OSE Posterior kidney chapmans point

A

between the transverse process of T12 and L1 (on ipsilateral side)

39
Q

5 model approach: biomechanical

A

SD of OA, AA

SD of thoracic spine @ viscerosomatic levels (T10-T11)

SD of psoas muscles

40
Q

5 model approach: Resp/Circulatory

A

O2 via mask/nasal canula

Lymphatics:

  • thoracic inlet MFR
  • thoracic area: pectoral traction, doming diaphragm, thoracic pump
  • abdominal area: abdominal pump, sacral rocking, pelvic diaphragm
  • extremities: effleurage, petrissage, pedal pump
  • rib raising
41
Q

5 model approach: Neuro

A

review OSE (sympathetics/PS for kidney, ureters, and bladder), chapman points, rib raising tx

42
Q

5 model approach: metabolic/energetic/immune

A
  • loop diuretics
  • fluid restriction
  • remove offending agents like NSAIDs, PPI, -adjust meds based on renal fxn
  • monitor I/O’s, weights
43
Q

5 model approach: Behavioral

A

exercise, diet (restrict fluids), avoid offending agents, better management of CHF (inciting cause)

44
Q

What are the possible mechanisms to account for AKI in conjuctino with AHF?

A

neurohumeral adaptations, reduced renal perfussion, increased renal venous pressure, associations with HFpEF

45
Q

Describe neurohumeral adaptations:

low yield maybe?

A

hemodynamic derangements trigger activation of SNS and RAAS and increases in ADH + endothelin-1 release, which promote salt and water retention and systemic VC; this leads to disproportionate reabsorption of urea compared with that of creatinine

they also overwhelm vasodilatory and natriuretic effects of natriuretic peptides, NO, PGs, and bradykinin

systemic VC increases cardiac afterload which reduces CO, and can further reduce renal perfusion

46
Q

Describe how increased renal venous pressure is involved with AKI in conjunction with AHF?

(low yield maybe?)

A

increases in intra-abdominal/central venous pressure, which should increase renal venous pressure, reduces GFR

(aka inverse relationship bw central venous pressure and GFR)

47
Q

How is HFpEF associated w/ AKI?

low yield maybe?

A

renal dysfxn can lead to metabolic derangements resulting in systemic inflammation and microvascular dysfunction, which can cause cardiomyocyte stiffening , hypertrophy, and interstitial fibrosis

48
Q

What is the first treatment you should do for AKI and cardiorenal syndrome?

A
  1. remove offending agents: NSAIDS, PPI
49
Q

After removing offending agents(1), what should you do for AKI/ cardiorenal syndrome (steps 2-9)?

A
  1. judicious use of loop diuretics (furosemide)
  2. adjust medication dosing on renal fxn
  3. supporative care: oxygen
  4. Monitor weight, I’s + O’s
  5. Fluid restriction (oral and IV)
  6. Monitor electrolytes (Ca, Na, K, Mg, etc.)
  7. Case management/manager
  8. Dietary consult
50
Q

What is the mainstay of treatment for AKI?

A

loop diuretics (furosemide)

51
Q

Can normal urine output be maintained even in face of low GFR?

A

yes;

ability for diuretic use to improve output = good prognosis

52
Q

Which diuretics should you avoid in AKI/HF?

A

avoid K+ sparing diuretics (spironolactone) as they will complicate K+ management

53
Q

Why is it important to monitor electrolytes in an AKI/cardiorenal syndrome pt?

A

electrolyte abnormalities can lead to arrhythmias which will have deleterious affect for both cardiac and renal fxn (monitor electrolytes, Mg and phosphate, and BUN/Cr as well)

54
Q

When should a case manager especially get involved in patient care?

A

should be involved early when there are new complications or signs of deterioration

Advanced directives, Code status, DPAHC, etc. become impt and must be addressed early in hospitalization

55
Q

What Long-term management is important in an AKI/cardiorenal syndrome pt?

A
  1. discussion with pt regarding personal wishes regarding dialysis (ST and LT), as well as other end-of-life matters such as Living Will and DPAHC
  2. Avoid nephrotoxic drugs, including OTC preparations such as NSAIDs, PPI, etc.
  3. Regular monitoring of electrolytes, pt weight, fluid status, etc.
56
Q

What are complications of AKI? What can be initiated for it?

A

progression to oliguria or anuria

Dialysis (renal replacement therapy RRT) may be initiated emergently when life-threatening changes in fluid, electrolyte, and acid-base balance exist per KDIGO guidelines

57
Q

How long should RRT be continued if life-threatening changes occur in AKI pts?

A

continued until renal fxn is recovered or bc continued provision of renal support is no longer consistent with the overall goals of care for the pt

58
Q

Why is Durable healthcare power of attorney important in the care of the patient?

A

DPAHC authorize another person (or surrogate) to make decisions on the pts behalf

59
Q

Why is Living Will (LW) important in the care of the patient?

A

It summarizes choices about future medical care; typically addresses resuscitation and life support, but may include other preferences about treatment (feeding tube, dialysis, intubation/ventilator support)

60
Q

If a patient has elected some restriction (do not resuscitate/intubate) in their living will, the physician:

A

MUST document the order appropriately

The presence of the LW alone does not prevent resuscitation

61
Q

What characterizes stage 1 of KDIGO criteria?

A

increase in serum creatinine > or equal to 0.3 mg/dL or 50-99%

OR

urine output of <0.5 ml/kg/hour for 6 - 12 hours

62
Q

What characterizes stage 2 of KDIGO criteria?

A

increase in serum creatinine of 100-199%

OR

urine output of <0.5 ml/kg/hour for 12-14 hours

63
Q

What characterizes stage 3 of KDIGO criteria?

A

increases in serum creatinine of > or = to 200%

OR

Increase in serum creatinine of > or = to 0.3 mg/dL to > or = to 4.0 mg/dL

OR

urine output of <0.3 mL/kg/hr for > or = to 24 hrs or anuria for > or = to 12 hrs

OR

initiation of renal replacement therapy

64
Q

What are we gonna get on this exam?

A

an AAAAAAAAA

PCM 3 exam 1- MARIYA (6 decks)

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