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
Specific NSAID's that can lead to AIN: (3)
1- fenoprofen 2- ibuprofen 3- naproxen
26
Other drugs that can lead to ATN: (8)
``` 1- Antivirals 2- Amph. B 3- Acyclovir 4- ACE/ARB 5- Cephalosporins 6- Cannabinoids (synthetic forms) 7- Foscarnet 8- Vancomycin ```
27
Rhabdomyolysis can be seen in which pts: (4)
1- elderly who fall and cannot get up 2- Statin SE 3- extreme exercise 4- crush injury
28
Sxs/Labs seen with Rhabdomyolysis: (7)
``` 1- dark, brown urine 2- elevated Cr 3- elevated Myoglobin 4- Urine w/ false positive for Hemoglobin 5- hyperphosphatemia 6- hyperuricemia 7- hyperkalemia ```
29
Two main causes of CKD:
HTN and DM
30
SXS of CKD:
- 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
As CKD becomes more severe, pts typically get these sxs: (3)
1- fluid overload 2- hyperkalemia 3- metabolic acidosis
32
What medications are nephroprotective? (3)
1- ACE 2- ARB 3- CCB (Both DHP and Non-DHP)
33
Criteria for initiating HD: (2)
1- GFR 10-15mL/min | 2- higher GFR w/ sxs of ESRD
34
MC cause of mortality overall in ESRD
CV dz
35
MC cause of sudden death in CKD is due to:
hyperkalemia (usually due to non-compliance with diet or missed HD)
36
5 year survival rate of HD pts
36% | - but dependent etiology of uremia and on comorbidities and compliance
37
C/I for a kidney transplant: (4)
1- active substance abuse 2- active infx 3- chronic illness w/ short life expectancy 4- active malignancy
38
Kidney transplant anti-rejection medications (2)
1- cellcept | 2- Cyclosporine
39
Nephrogenic systemic fibrosis involves what structures? (5)
``` 1- skin 2- heart 3- muscle 4- fascia 5- lungs ```
40
Dx for Nephrogenic systemic fibrosis
skin biopsy
41
Tx for Nephrogenic systemic fibrosis
No known tx
42
Etiology for Nephrogenic systemic fibrosis
- occurs secondary to MRI w/ Gadolinium contrast in renal insufficiency pts. - avoid in anyone after stage 3B CKD
43
Skin appearance in Nephrogenic systemic fibrosis:
symmetrical, B/L fibrotic indurated papules, plaques, or subQ nodules +/- erythema - often preced by edema and frequently misdx for cellulitis
44
Types of anemia associated w/ CKD: (3)
1- IDA 2- anemia of CKD 3- anemia secondary to erythropoietin deficiency
45
List the phosphate binders used to tx secondary hyperparathyroidism in CKD: (4)
- 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
List the Vitamin D substitutes used to tx secondary hyperparathyroidism in CKD: (3)
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
List the calcimimetic used to tx secondary hyperparathyroidism in CKD: (1)
- Cinacalcet (Sensipar)
48
Tx mild hyperkalemia and asxs:
- phosphate binder | - sodium polysterene sulfonate- kayexelate
49
Tx more severe hyperkalemia and sxs:
- IV calcium gluconate to stabilize cardiac membranes, glucose, and insulin