• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/26

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

26 Cards in this Set

  • Front
  • Back
What is anuria?
Less than 50ml/24 hours
What is oliguria?
50-500ml/24 hours
What is non-oliguric?
More than 500ml/24 hours
How do you classify prerenal AKI
Hypoperfusion to the kidney

Can be caused by systemic hypoperfusion: hemorrhage, volume depletion, drugs, CHF

Urinanalysis will be normal but concentrated

Serum BUN/Scr ratio: >20:1
Low FENa, low urine Na
High urine osmolarity
How do you classify functional AKI
Kidney undamaged, often lumped with prerenal

Caused by reduced glomerular hydrostatic pressure

In general, medication related (cyclosporine, ACEI, NSAIDS) or patients with ineffective bloodflow (CHF, liver dx)

Serum BUN/Scr ratio: >20:1
Low FENa, low urine Na
High urine osmolarity
Intrinsic AKI
Kidney is damaged, but common cause is acute tuberular necrosis

Serum BUN/SCr ratio: 15:1
Urine Na>40, FENA>2
Low urine osmolarity
Postrenal AKI
Kidney is undamaged, bladder outlet obstruction is most common cause

Serum Bun/SCr ratio: 15:1
Urine Na >40meq
FENA>2
Low urine osmolarity
How do you treat established AKI
Prerenal:
- Normal saline if volume depleted
-pressure management
-blood products

Intrinsic:
- Eliominate causative hemodynamic abnormality or toxin, fluid and elyte managemment

Postrenal:
- relieve obstruction
What is the medical therapy for AKI
1) Fenoldopam - may reduce the need for renal RRT
2) Atrial natriuretic peptide: may reduce need for renal RRT
3) Loop diuretics: consider for oliguric and euvolemic or hypervolemic patients
What are the most common causes of acute tubular necrosis
Aminoglycoside, cyclosporine, amphB, diuretics

Radiographic contrast

Cisplatin/carboplatin

AmphoB
How do you prevent radiographic contrast type nephrotoxicity
Hydration, begin 6-12 hours before procedure

Avoid diuretics

Acetylcysteine - antioxidant and vasodilatory

Ascorbic acid: give 3g before procedure and 2gm BID x 2 doses after procedure

Theophilline - potentially preventative
How do you prevent cisplatin/carboplatin nephrotoxicity
Hydration

Amifostine: cisplatin chelating agent
How do you prevent Amphotericin nephrotoxicity
Avoid nephrotoxins

IV hydration

Use liposomal product in high risk patients
Hemodynamically mediated kidney failure causes
Results from a decrease in intraglomerular pressure through the vasoconstriction of afferent arterioles or the vasodilation of efferent arterioles

1) ACEI
2) NSAIDS
3) Cyclosporine/tacrolimus
What NSAIDS can you use that causes less prostaglandin synthesis in the kidney
Sulindac
What is tubulointerstitial disease
Involves the renal tubules and surrounding interstitium

Acute allergic interstitial nephritis (penicillins, NSAIDS,)

Chronic interstitial nephritis (lithium, cyclosporine)
What is obstructive nephropathy
Obstruction of the flow of urine

Renal tubular obstruction causes by precipitation of drugs: sulfonamides, methotexate, acyclovir, uric acid after tumor lysis

Extrarenal urinary tract obstruction caused by anticholinergics worsened BPH or cyclophosphamide caused hemorrhagic cystitis

Nephrolithiasis: triamterene, sulfadiazine, indiniavir`
how do you manage diabetic nephropathy
1) Aggressive BP management, in patients with diabetes and CKD BP target 130/80
ACEI or ARBs are preferred
Most patients need diuretic in combination
CCB (nonDHP) are considered second line to ACEI/ARB

2) Intensive blood glucose control

3) Protein restriction
What are the indications for RRT
A - acidosis
E - electrolyte abnormality
I - intoxication
O - fluid overload
U - uremia
How do you treat anemia in CKD
Do not treat Hgb to >13

Erythropoiesis stimulating agents (REMS program)
- Epoetin, darbepoetin
- goal to 11-12
- dose adjustments made every 4 weeks, 25% intervals
- most common cause of inadequate response is iron deficiency
What are the target levels of ferritin and transferrin in CKD
ferritin - 200 to 500
transferrin is >20%
How do you treat iron deficiency in CKD
Do not use oral agents, use parenteral

Iron Dextran (need test dose)
Ferric gluconate (125mg IV TID during HD)
Iron sucrose
Ferumoxytol
How do you treat hyperphosphatemia
1) Phosphate binders - take with meals
- aluminum binders (aluminum hydroxide, sucrulfate). In general not used
- calcium containing binders (calcium carbonate, acetate). Initial binder of choice for stage 3 and 4 CKD
- Sevelamer. Considered primary therapy in stage 5. Use is calcium levels very high
- lanthasum. Not widely used, can use if high calcium
What are the vitamin D analogs
Suppress PTH synthesis and reduce PTH concentrations

Calcitriol - approved for use in hypocalcemia and prevention of secondary hyperparathyroidism. Dose adjust every 4 weeks. High incidence of hypercalcemia

Paracalcitol - lower incidence of hypercalcemia

Doxercalciferol - vitamin D analog
- lower incidence of hypercalcemia
What is cinacalcet
calcimimetic that attaches to the calcium receptor on the parathyroid gland and increased sensitivity to serum calcium levels reducing PTH

Especially useful in patients with high PTH, high calcium levels and vitamin D analogs cant be used

Caution in seizure disorder
Metabolized by Cyp3A

Can be used whether or not patient on phosphate binders of vitamin D analogs
How do you generally calculate renal adjusted doses
Rowland-Tozer

Q=1-[Fe(1-KF)]

Q= kinetic parameter or drug dose adjustment factor
Fe=fraction of drug excreted unchanged in urine
KF=ratio of patients ClCr to normal (120ml/min)