Diseases Flashcards

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)

A

ATN

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

A

AIN

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
Q

Young men > women (6 X )
Hemoptysis , SOB, anemia, reddish urine
High bun/creat. , high anti serum anti GMB
Often have pulmonary & renal symptoms

A

Goodpasture’s Syndrome

tx w/plasmapharesis and steorids

26
Q

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”.

A

post infectious GN

27
Q

Most common form of Acute GN
Children and young adults, M>W

Occurs 1-3 days af ter throat infection with reddish
“cola” urine.

A

IgA Nephropathy (Berger’s dx)

28
Q

MCC Cryoglobulin Associated GN (Necrotizing skin lesions, Arthralgias, Fever, Hepatosplenomegaly, Low complement levels)

A

Hep B/C

29
Q

Effects the basement membrane becomes thickened due to immune deposition and mesangial proliferation.
BM “double layer” appearance

A

membranoproliferative GN
type one is more nephrotic
type two is more nephritic

30
Q
Heavy proteinuria (>3.5gr./24hr)
Hypoalbuminemia (<3gr./dl)

Fat bodies in urine (“maltase cross”)

A

nephrotic syndrome

31
Q

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

A

minimal change disease (nil’s)

32
Q

M.C. primary Cause of N.S. in adults, 5-6th decade of life

A

membranous nephropathy

33
Q

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

A

Focal Segmented Glomerulur Sclerosis

34
Q

MCC end stage renal disease

A

Diabetic nephropathy

35
Q

chronic renal failure

A

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
Q

when should diabetics start dialysis

A

GFR is 15 or serum Cr. Is