Diseases Flashcards

(36 cards)

1
Q

Defined as a sudden decline in kidney function causing disturbances in fluid, electrolytes and acid-base balance due to a loss of small solute clearance and
decreased GFR

A

acute kidney injury

Increased mortality even if renal function returns to normal**

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2
Q

AKI is defined as

A

Reduction of renal function within 48 hrs as defined by:
Absolute increase in serum creatinine > or equal to 0.3 mg/dl
Percentage increase in serum creatinine > or equal to 50%
Reduction in urinary output, with documented oliguria of less than 0.5 ml/kg per hour for more than 6 hours

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3
Q

stages of AKI

A

Stage 1-Inc. in Serum Cr >.3 or 150-200% from baseline, along with oliguria for
>6 hrs

Stage 2-Inc. in Serum Cr 200-300% from baseline, along with oliguria for >12 hrs

Stage 3-Inc. in Serum Cr >300% from baseline, need for RRT, and/or oliguria for 24 hrs/anuria > 12 hrs

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4
Q

An adaptive response to severe volume depletion and hypotension, with structurally intact nephrons
**Most common form of AKI, accounts for 55% AKI

A

pre-renal

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5
Q

what can cause prerenal failure

A
  • volume depletion
  • decreased CO
  • arteriole vasoconstriction
  • systemic vasodilation
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6
Q

M/C caused by acute tubular injury (ATN), either ischemic or cytotoxic

A

intrinsic

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7
Q

what can cause intrinsic renal failure

A
  • drugs
  • vascular
  • AI
  • tubular
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8
Q

Mechanical obstruction of urinary collecting system resulting in obstructive uropathy

A

postrenal

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9
Q

S/S chronic renal failure

A

fatigue, weight loss, anorexia, nocturia, and pruritis

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10
Q

acute tubular necrosis casts

A

granular, muddy brown

epitheleal

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11
Q

glomerulonephritis casts

A

RBC, tea colored

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12
Q

prerenal failure will have a FENa of

A

< 1%

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13
Q

how to tx AKI

A

volume expansion

decrease potassium intake, insulin & glucose, albuterol, kayexelate, lasix, IV calcium (cardiac instability)

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14
Q

when is dialysis indicated

A

volume expansion that cannot be controlled by diuretics Hyperkalemia refractory to medication
Severe acid-base imbalances refractory to medication Severe azotemia (BUN > 80-100), uremia,

Seizure/coma

CC <10 and serum Cr >9

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15
Q

how long after AKI is a pt dx with chronic renal failure

A

no improvement after 6-8 weeks

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16
Q

Accounts for 85% of Intrinsic AKI

Death of tubular cells that form the tubule that
transports urine to the ureters while reabsorbing 99% of the water (and highly concentrating the salts and
metabolic byproducts)

17
Q

ischemic ATN shows

A

skip lesions through tubules

18
Q

toxic ATN

A

Characterized by proximal tubular epithelium necrosis due to a toxic substance, necrotic cells fall into the tubule lumen, obliterating it
BM intact, so regen is possible

19
Q

MC drug causing toxicity

A

aminogylcosides

20
Q

acute interstitial nephritis usually caused by

A

acute allergic reaction to a medication, including antibiotics and nonsteroidal anti-inflammatory drugs (NSAIDs)

Also linked to infections, diseases, and transplant rejection

21
Q

Clinical presentation hallmark:

Fever, Rash, Eosinophilia **
Also arthralgias, proteinuria, hematuria, and Sterile pyuria

22
Q

AGN

A

Acute glomerular Nephritis always have some urinary
protein, hematuria with RBC casts, and sometimes pyuria with WBC casts….this is known as nephritic or active urine. Dark tea colored urine

23
Q

CGN

A

Chronic Glomerular Nephritis is noted for heavy

proteinuria and urine fat (oval fat bodies)….this is known as nephrotic urine.

24
Q

low vs normal complement for AGN

A

low-Post infectious, SLE, MPGN

normal-Iga nephropathy, Good pastures,

25
Young men > women (6 X ) Hemoptysis , SOB, anemia, reddish urine High bun/creat. , high anti serum anti GMB Often have pulmonary & renal symptoms
Goodpasture's Syndrome | tx w/plasmapharesis and steorids
26
Patients tend to be s/p pharyngitis, impetigo, sub acute endocarditis…. Group A beta hemolytic streptococcal infections 1-3 weeks after infection Patient becomes lethargic slight edema,oligiuric, HTN, red urine “cola colored”.
post infectious GN
27
Most common form of Acute GN Children and young adults, M>W Occurs 1-3 days af ter throat infection with reddish “cola” urine.
IgA Nephropathy (Berger's dx)
28
MCC Cryoglobulin Associated GN (Necrotizing skin lesions, Arthralgias, Fever, Hepatosplenomegaly, Low complement levels)
Hep B/C
29
Effects the basement membrane becomes thickened due to immune deposition and mesangial proliferation. BM “double layer” appearance
membranoproliferative GN type one is more nephrotic type two is more nephritic
30
``` Heavy proteinuria (>3.5gr./24hr) Hypoalbuminemia (<3gr./dl) ``` Fat bodies in urine (“maltase cross”)
nephrotic syndrome
31
MC cause of N.S. in kids (<10 y/o) and can follow a viral URI Loss / fusion of epithelial cell foot processes In adults its MC associated NSAIDS, and less commonly associated with Hodgkin's Dx. Proteinuria with no hematuria
minimal change disease (nil's)
32
M.C. primary Cause of N.S. in adults, 5-6th decade of life
membranous nephropathy
33
Characterized by scaring of mesangial cells on microscopy and is diagnostic May see decreased renal function at time of diagnosis in 30-50% of patients
Focal Segmented Glomerulur Sclerosis
34
MCC end stage renal disease
Diabetic nephropathy
35
chronic renal failure
GFR will increase to nl as a result of hyper filtration of remaining nephrons… this eventually leads to scaring and progressive rapid loss of GFR broad waxy casts
36
when should diabetics start dialysis
GFR is 15 or serum Cr. Is