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KC Nephro > AKI/CKD > Flashcards

AKI/CKD Flashcards

1
Q

eGFR can be calculated using etither of these 2 equations:

A
  • Cockcroft-Gault equation

- MDRD equation

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2
Q

PCT almost complete reabsorption of: (5)

A 
1- glucose 
2- AA
3- lactate
4- water soluble vitamins
5- electrolytes
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3
Q

What electrolytes are included in the PCT reabsorption: (4)

A

1- sodium
2- potassium
3- bicarb
4- chloride

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4
Q

PCT excretion includes:

A

1- organic cations and anions as end-products of metabolism (oxalate, urate)
2- minimal exogenous organic compounds: ASA, morphine, and penicillin (2/2 bound to proteins and difficulty entering ultrafiltrate)

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5
Q

Taken as a whole the Loop of henle always reabsorbs more of this molecule than water

A

NaCl

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6
Q

Loop of Henle’s major role

A

determining the concentration of urine by establishing a high concentration of osmotically active particles in the renal parenchyma surrounding the medullary collecting tubules where ADH exerts it’s effects

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7
Q

Declining renal function leads to increased levels in these substances in the serum: (4)

A
  • creatinine
  • phosphate
  • urea
  • potassium
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8
Q

Renal clearance is dependent on: (2)

A

1- the ability of the glomeruli to filter the substance

2- the capacity of the renal tubules to reabsorb or secrete it

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9
Q

Kidneys excrete H+ ions in urine for regulating pH via these 3 buffers:

A

1- Ammonia
2- Phosphate
3- Bicarbonate

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10
Q

Increases in urea can be seen in these 3 conditions:

A

1- GI bleed
2- Tissue breakdown
3- increase PRO diet

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11
Q

AKI Dx Criteria: Only need 1

A

1- Increase in serum Cr by 0.3 mg/dL or more in 48 hours
2- Increase in serum Cr by 150% or more in 48 hours
3- Oliguria of less than 0.5 mL/kg/hr for more than 6 hours (in a 150 lb pt. that equal UOP<35 cc/hr)

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12
Q

Two situations in when you cannot rely on Cr levels:

A

1- HD

2- pt is not in a steady state

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13
Q

Nephrotoxins that cause Intrinsic or Renal Azotemia:

A
  • NSAIDs
  • Aminoglycosides
  • contrast
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14
Q

When is imaging with AKI required? (2)

A

1- likely obstructive pathology

2- determine if it is chronic renal failure when no baseline labs are available

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15
Q

early renal bx in AKI dx looks for: (4)

A
  • HUS
  • TTP
  • vasculitis
  • GN
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16
Q

Renal bx in AKI indicated in pts. w/ these sxs: (3)

A

1- clinical situation suggesting vascular pathology
2- oliguria >4 weeks
3- If based on hx, pre-renal and ATN unlikely, and no improvement w/ conservative care

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17
Q

Deadly complications of uremia: (4)

A

1- sz
2- arrhythmias
3- fluid overload (pulmonary edema)
4- metabolic acidosis

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18
Q

Indications for Urgent HD: (4)

A

1- hyperkalemia
2- sxs of uremia (coma, confusion, pericarditis, sz, coagulopathy, n/v, GIB)
3- fluid overload- unresponsive to tx
4- metabolic acidosis

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19
Q

Name the phases in the patho remodeling of ATN: (3)

A

1- initiation
2- management
3- recovery

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20
Q

Etiologies of the Initiation phase in the patho remodeling of ATN: (5)

A

1- loss of ET border of lumen, leading to back-leak of filtrate
2- damage to Na/K ATPase pumps, leading to increased Na and Ca retention and swollen cells
3- sloughing, leading to granular casts
4- decreased vasodilator production (NO, prostacyclin)
5- Increased free radicals and resultant damage

21
Q

Describe the Maintenance phase in the patho remodeling of ATN:

A
  • stable, but very low GFR (lasts 1-2 wks)
22
Q

Describe the Recovery phase in the patho remodeling of ATN:

A
  • some tubular cell regeneration

- abnormal diuresis sometimes occurs resulting in salt and water loss with occasional hypovolemia

23
Q

List the aminoglycosides: (3)

A

1- gentamycin
2- tobramycin
3- neomycin

24
Q

aminoglycosides induced ATN presentation:

A

5-10 days after exposure and is generally mild and non-oliguric

25
Q

Specific NSAID’s that can lead to AIN: (3)

A

1- fenoprofen
2- ibuprofen
3- naproxen

26
Q

Other drugs that can lead to ATN: (8)

A 
1- Antivirals
2- Amph. B
3- Acyclovir
4- ACE/ARB
5- Cephalosporins
6- Cannabinoids (synthetic forms)
7- Foscarnet
8- Vancomycin
27
Q

Rhabdomyolysis can be seen in which pts: (4)

A

1- elderly who fall and cannot get up
2- Statin SE
3- extreme exercise
4- crush injury

28
Q

Sxs/Labs seen with Rhabdomyolysis: (7)

A 
1- dark, brown urine
2- elevated Cr
3- elevated Myoglobin
4- Urine w/ false positive for Hemoglobin
5- hyperphosphatemia
6- hyperuricemia
7- hyperkalemia
29
Q

Two main causes of CKD:

A

HTN and DM

30
Q

SXS of CKD:

A
  • Pts. typically remain asxs until stage 4 or 5
  • General: appears chronically ill w/ fever, malaise, and weakness
  • GI: hiccups, anorexia, n/v, metallic taste in mouth
  • CV: “overload sxs”-> rales, peripheral edema, pericardial friction rub, and cardiomegaly
  • Neuro: asterixis, clonus, cognitive deficits, irritability, difficulty concentrating, RLS, rarely coma
  • Skin: carotinemic color changes, severe itching (secondary to elevated BUN), easy bruising
31
Q

As CKD becomes more severe, pts typically get these sxs: (3)

A

1- fluid overload
2- hyperkalemia
3- metabolic acidosis

32
Q

What medications are nephroprotective? (3)

A

1- ACE
2- ARB
3- CCB (Both DHP and Non-DHP)

33
Q

Criteria for initiating HD: (2)

A

1- GFR 10-15mL/min

2- higher GFR w/ sxs of ESRD

34
Q

MC cause of mortality overall in ESRD

A

CV dz

35
Q

MC cause of sudden death in CKD is due to:

A

hyperkalemia (usually due to non-compliance with diet or missed HD)

36
Q

5 year survival rate of HD pts

A

36%

- but dependent etiology of uremia and on comorbidities and compliance

37
Q

C/I for a kidney transplant: (4)

A

1- active substance abuse
2- active infx
3- chronic illness w/ short life expectancy
4- active malignancy

38
Q

Kidney transplant anti-rejection medications (2)

A

1- cellcept

2- Cyclosporine

39
Q

Nephrogenic systemic fibrosis involves what structures? (5)

A 
1- skin
2- heart
3- muscle
4- fascia
5- lungs
40
Q

Dx for Nephrogenic systemic fibrosis

A

skin biopsy

41
Q

Tx for Nephrogenic systemic fibrosis

A

No known tx

42
Q

Etiology for Nephrogenic systemic fibrosis

A
  • occurs secondary to MRI w/ Gadolinium contrast in renal insufficiency pts.
  • avoid in anyone after stage 3B CKD
43
Q

Skin appearance in Nephrogenic systemic fibrosis:

A

symmetrical, B/L fibrotic indurated papules, plaques, or subQ nodules +/- erythema
- often preced by edema and frequently misdx for cellulitis

44
Q

Types of anemia associated w/ CKD: (3)

A

1- IDA
2- anemia of CKD
3- anemia secondary to erythropoietin deficiency

45
Q

List the phosphate binders used to tx secondary hyperparathyroidism in CKD: (4)

A
  • all given w/ meals
    1- Calcium acetate (PhosLo)- only Ca containing one
    2- Selevamer (Renvela, Renagel)
    3- Fosrenol (Lanthanum)- chewable and crushable
    4- Sucroferric oxyhydroxide (Velphoro)
46
Q

List the Vitamin D substitutes used to tx secondary hyperparathyroidism in CKD: (3)

A

1- Calcitriol (rocaltrol)- active metabolite; QD IJ or after HD; want serum Ca to be 9-10 mg/dL
2- Doxercalciferol (hectoral)- rq. kidney metabolize to active form; takes 10-12 wks. for effects
3- Paricalcitol (zemplar)- synthetic form which binds to and activates Vitamin D receptors in kidney; dosed Q2-4 wks.

47
Q

List the calcimimetic used to tx secondary hyperparathyroidism in CKD: (1)

A
  • Cinacalcet (Sensipar)
48
Q

Tx mild hyperkalemia and asxs:

A
  • phosphate binder

- sodium polysterene sulfonate- kayexelate

49
Q

Tx more severe hyperkalemia and sxs:

A
  • IV calcium gluconate to stabilize cardiac membranes, glucose, and insulin

KC Nephro (9 decks)

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