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#US PCM III MO > HYHO AKI > Flashcards

HYHO AKI Flashcards

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1
Q

Clinically, what defines AKI?

A

increase in serum creatine of > .3mg/dL within 48hrs or > 50% within 7 days

OR

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

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2
Q

What is it called when treatment for HF is limited by a decline in renal function? How is this decline noticed?

A

Cardiorenal syndrome is a condition in which therapy to relieve congestive symptoms of HF is limited by a decline in renal function as manifested by reduction in GFR.

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3
Q

Pre-renal azotemia is more common in what pts?

A

HF

(BUN/Cr > 20)

*30-60% of HF pts develop severe kidney probs

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4
Q

What phyiscal changes of the kidneys are seen in CKD?

A
  • decrease size
  • cortical thinning

(others include cystic kidneys –> look for underlying disease)

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5
Q

What can be used to rule out obstructive cause of KI?

A

US –> +/- hydropnephrosis

(if -, rules out obstruction)

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6
Q

What should you expect of Na+ levels in HF pts? Why?

A
  • <25meg/L
  • due to reduced renal perfusion –> inc RAAS/SNS –> promote Na+ retention

*urine Na+ inc with diuretics

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7
Q

What are causes of prerenal AKI?

A
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8
Q

What are the causes of intrinsic AKI?

A
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9
Q

What are causes of postrenal AKI?

A
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10
Q

When I say ___, you think:

a. Blue toes
b. ‘Drug Rash’
c. Volume contraction
d. Volume overload/HF
e. Jaundice/ascites

A

a. cholesterol emboli
b. acute interstitial nephritis
c. dehydration
d. cardiorenal syndrome
e. liver disease with portal HTN

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11
Q

What are common sx of AKI?

A
  • oliguria
  • edema (dependent –> anasarca –> ascites)
  • dyspnea (orthopnea, PND, rest)
  • tachycardia (S3)
  • JVD
  • hypotension
  • liver distenstion/tenderness
  • distended abdomen (+puddle sign)
  • skin tenting
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12
Q

What is the best way to measure skin tenting?

A
  • pinching skin of the forehead
  • if dehydrated, skin will remain elevated
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13
Q

What can mimic PND?

A

nocturnal asthma attacks

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14
Q

What is anasarca?

A
  • severe generalized edema that extends from LE proximally
  • can cause ascites and subcutaneous edema

*associated with HF, cirrhosis, severe malnutrition, RF

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15
Q

How is a fluid wave test performed? what does it tell us?

A

a. pt. places ulnar surface of their hand along midline; operator places one hand on one flank and taps gently on the opposite flank –> + when the operator feels a moderate to strong fluid wave emanating into the contralateral side
b. if +, rules in ascites; if -, cannot rule out ascites

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16
Q

Describe a puddle sign

A
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17
Q

What are the sympathetic/parasympathetic levels of the kidney?

A

S: T10-11

P: vagus n.

18
Q

What are the sympathetic/parasympathetic levels of the ureters upper? lower?

A

upper: S - T10-11; P - vagus n.
lower: S - T12-L2; P - pelvic splanchnic n.

19
Q

What are the sympathetic/parasympathetic levels of the bladder?

A

S - T12-L2

P - pelvic splanchnic n.

20
Q

What are the ant/post chapman points of the kidney?

A
  • Anterior: one inch lateral and one inch superior to the umbilicus
  • Posterior: between the transverse process of T12 and L1 (on the ipsilateral side)
21
Q

What is included in the biomechanical approach of AKI?

A
  • SD of OA, AA
  • SD of thoracic spine at viscerosomatic levels (T10-11)
  • SD of the psoas muscles
22
Q

What is included in the lymphatic approach of AKI?

A
  • O2 via mask/nasal canula
  • Lymphatics
o Thoracic inlet MFR
o Diaphragms (thoracolumbar, pelvic)
o Thoracic area: pectoral traction, doming the diaphragm, thoracic pump

o Abdominal area: abdominal pump, sacral rocking, pelvic diaphragm
o Extremities: effleurage, petrissage, pedal pump
o Rib raising

23
Q

What is included in the neurologic approach of AKI?

A

all the related sympathetics/parasympathetics/chapmans points and rib raising

24
Q

What is included in metabolic/energetic/immune approach?

A
  • Loop diuretics
  • Fluid restriction
  • Remove offending agents like NSAIDs, PPI
  • Adjust meds based on renal function
  • Monitor I/O’s, weights
25
Q

What is included in behavioral approach?

A
  • Exercise
  • Diet – restrict fluids
  • Avoid offending agents
  • Better management of CHF (inciting cause)
26
Q

What happens with increased vasopressin and endothelin 1?

A
  • salt and water retention
  • systemic vasoconstriction
27
Q

The SNS and RAAS lead to what changes in reabsorption?

A
  • disproportionate reabsorption of urea to creatine
  • overwhelm VD and natriuretic effects of natriuretic peptides, NO, PGs, and BK
    • systemic VC leads to increased cardiac afterload –> recduces CO –> further dec renal perfusion
28
Q

There is an inverse relationship between central venous pressure and what?

A

GFR

*Increases in intra-abdominal or central venous pressure, which should increase renal venous pressure, reduces GFR.

29
Q

How can renal dysfunction cause cardiomyocyte stiffening, hypertrophy, and interstitial fibrosis?

A

via metabolic derangements resulting in systemic inflammation and microvascular dysfunction

30
Q

What are the treatments (9) of AKI?

A
  1. Remove offending agents: NSAIDS, PPI, etc.
  2. Judicious use of loop diuretics (furosemide)
  3. Adjust medication dosing based on renal function
  4. Supportive care: oxygen
  5. Monitor weight, I’s & O’s
  6. Fluid restriction
  7. Monitor electrolytes (Na+, K+, Ca+, Mg+, etc.)
  8. Case management/manager
  9. Dietary consult
31
Q

What diuretic is the mainstay of tx?

A

Furosdemide (loop)

*avoid use of K sparing diuretics Ithey complicate K+ management)

32
Q

What is included in fluid restriction?

A

oral and IV fluids

*helps to minimize overload and preverse cardiac function

*daily weight monitoring helps with fluid status ID

33
Q

Why is monitoring of electrolytes important?

A
  • abnormalities can lead to arrhythmias

*monitor: Mg, Phophate, BUN/Cr

34
Q

Who must be involved early in pt care?

A

- Case managers - especially when there are new complications or signs of deterioration. Advanced directives, Code status, DPAHC, etc. become important and must be addressed early in the hospitalization

-Dieticians to address protein needs based on patient condition (nephrotic vs non- nephrotic), electrolytes as well as calorie requirements in an acute illness.

35
Q

What is important in long term management of AKI pts?

A
  1. Discussion on dialysis, living will, DPAHC
  2. Avoid nephrotoxic drugs (ex. NSAIDs)
  3. Regular monitoring (electrolyte, weight, fluid status…)
36
Q

Pt. presents with oliguria. They have had declining renal function for a few years, but this is a new sx. What is the best next step to tx?

A
  • Dialysis (Renal Replacement Therapy)

*RRT should be continued until renal function is recovered or if continued provision of renal support is not longer consistent with tx goals

37
Q

Define Living will and Durable Power of Attorney

A
  • Living Will: summarizes choices about future medical care (resuscitation, life support; may include feeding tube, dialysis, intubation/ventilator support)
  • Durable Power of Attorney for Healthcare (DPAHC) authorizes another person (or surrogate) to make decisions on the patient’s behalf.
38
Q

Pt. in ESRF requests a visit from advance care planning in order to plan their next steps with their family. They ask if you will be there as their long time physician: how do you respond?

During the session, they say they do not want to be resuscitated when the times come. It is the doctor’s job to do what with this infomration?

A
  1. yes –> doc’s role is to provide info about prognosis and tx option
  2. Document appropriately becuase the presence of a LW alone will not prevent their resuscitation
39
Q

What is the KDIGO diagnostic criteria for AKI?

A
40
Q

What is Stage 1 of AKI on KDIGO criteria?

A

Risk Phase

41
Q

What is Stage 2 of AKI on the KDIGO criteria?

A

Injury Phase

42
Q

What is Stage 3 of AKI on the KDIGO criteria?

A

Failure stage

#US PCM III MO (25 decks)

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