Nephrology Flashcards

1
Q

Drugs causing a functional decrease in renal perfusion are:

A
NSAIDs, 
ACE-1, 
Cyclosporine, 
Cocaine, 
Contrast used in radiology
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2
Q

Risk factors for CIN (contrast induced nephropathy):

A

GFR

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3
Q

Prevention of CIN

A

Administartion of crystalloid 1-1,5 ml/kg/hour for 8 to 12 hours before this procedure
Administartion of acetylsteine in two 600 mg doses the day along with saline infusion for patients with stable chronic renal insufficiency ( Cr > 2,0 mg/dL)

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4
Q

Predisposing factors for NSAID induced AKI

A
CHF
Liver Cirrhosis
Atherosclerotic disease of renal artery
Nephrotic syndrome
Chronic renal failure
Hypovolemia
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5
Q

Natural clinical course of ATN

A
Initiation Phase (hours to days)
	Continuous ischemic or toxic insult
	Evolving renal injury
	ATN is potentially preventable at this time
Maintenance Phase (typically 1-2 wks)
	Maybe prolonged to 1-12 months
	Established renal injury
	GFR
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6
Q

Increase in creatinine without AKI

A

Inhibition of tubular creatinine secretion
Trimethoprim, Cimetidine, Probenecid

Interference with creatinine assays in the lab (false elevation)
glucose, acetoacetate, ascorbic acid, cefoxitin
flucytosine

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7
Q

Increase in BUN without AKI

A
Increased production
	GI Bleeding
	Catabolic states (Prolonged ICU stay)
	Corticosteroids
	Protein loads (TPN-Albumin infusion)
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8
Q

Prerenal azothemia

A

Intravascular volume depletion
bleeding, GI loss, Renal loss, Skin loss, Third space loss
Decreased cardiac output
CHF
Renal vasoconstriction
Liver Disease, Sepsis, Hypercalcemia
Pharmacologic impairment of autoregulation and GFR in specific settings
ACEi in bilateral RAS, NSAIDS in any renal hypoperfusion setting

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9
Q

Fenoldepam in prevention or treatment of AKI

A

Dopamine-1 receptor agonist, lack of Dopamine-2, and alpha-1 receptor effect, make it a potentially safer drug than Dopamine!

Reduces in hospital mortality and the need for RRT in AKI

Reverses renal hypoperfusion more effectively than renal dose Dopamine

So far so good specially in cardiothoracic ICU patients, awaiting more powered trials in other groups!

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10
Q

When do renal biopsy in AKI

A

Any evidence of glomerular disease

- nephrotic range proteinuria
- sub-nephrotic range proteinuria with hematuria 
- RBC cast

AKI in renal allograft

Determine the prognosis and chance of recovery of renal function in dialysis dependent AKI.

Whenever potential Bx result can change the management or prognosis.

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11
Q

When to initiate RRT in a patient with AKI

A
1) Renal Replacement Therapy:
		Electrolytes imbalances
		Acid-base disturbances
		Uremic complications
			-Encephalopathy
			-Pericarditis
			-Persistant nausea, and food 			 intolerance
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12
Q

Dialysis for removal of toxic agents in overdose

A

3) Removal of toxic agents in overdose
- Ethylene Glycol
- Methanol
- Salicylates
- Lithium
- Theophylline
- Isopropanol

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13
Q

Dialysis in renal/Multiorgan Support Therapy

A

2) Renal/Multiorgan Support Therapy
- Protects other organs by improving overall body milieu (balance of inflammatory mediators)
- Allowing therapies for other organs that pt could not otherwise tolerate
- volume resuscitation
- aggressive nutrition

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14
Q

Physical examination in AKI

A
Skin – new rashes.
Livedo reticularis – atheroemboli, SLE, cryoglobulins.
Petechiae – HSP.
Malar rash – SLE.
Eye
Papilledema – malignant HTN.
Roth’s spots – endocarditis.
CV
Rub – suggestive of uremic pericarditis, lupus.
Gallop – suggesting CHF.
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15
Q

Assessing volume status in AKI

A

Is the patient intravascularly volume depleted?
Neck veins – JVP
Peripheral edema or lack of.
Orthostatic vitals.
Pt. may be edematous (low albumin) or have significant right sided heart disease.

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16
Q

Fractional excretion of sodium in AKI

A
FENa
 2% suggestive of ATN/tubular damage.
Not quite so clear cut – low FENa seen in other causes of renal failure.
Nonoliguric ATN.
Radiocontrast nephropathy.
Acute GN.
Acute interstitial nephritis.
Not as helpful in setting of diuretics.
Can use FEUrea
17
Q

Urine sediment in AKI

A

Don’t forget the urine sediment!
Can be helpful in identifying underlying disease states (proteinuric disease, underlying chronic GN) as well as examining acute insult.

18
Q

Definition of AKI

A

Sudden and sustained loss of renal function over several hours to several days. ARF results in derangements in extracellular fluid, acid base balance, electrolytes and kation regulation.
An increased serum creatinine concentration, accumulation of other nitrogenous waste products and often a decline in urinary output are the hallmarks of ARF.