Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

1 STEP Renal pathology > Acute renal failure 12/13 > Flashcards

Acute renal failure 12/13 Flashcards

1
Q

The hallmark of acute renal failure?

A

Azotemia (increased BUN and creatinine) often with oliguria/anuria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Increased BUN indicates ………

A

Acute renal failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acute renal failure is divided in 3 azotemias, which are based on etiology. Name them.

A

Prerenal, postrenal and intrarenal azotemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Decreased Renal Blood Flow leads to ….

A

hypoperfusion-> Prerenal azotemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Prerenal azotemia mechanism?

A

Decreased RBF (e.g. hypotension due to HF) –> decreased GFR . Body conserve volume –> oliguria. Increased BUN/creatinine ration because urea is absorbed, but creatinine not.
RESULT: Decr. GFR, azotemia, oliguria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

BUN:Cr ratio in acute renal failure?

A

> 15.
Increased BUN/creatinine ratio because urea and fluids are absorbed, but creatinine not.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What causes prerenal azotemia?

A

Decreased renal blood flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What about tubular function in prerenal?

A

Intact. (fractional excretion of sodium (FENa) <1 proc.,
UNa< 20 mEq/, and urine osmolality (osm) > 500 mOsm/kg.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why there is acute tubular necrosis?

A

Due to ischemia or toxins –> injury and necrosis of tubular cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mechanism of intrarenal azotemia?

A

Tubular cell injury and necrosis –> necrotic cells plug tubules –> obstruction –> decreased GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What causes intrarenal azotemia (ischemic and toxic)?

A

Ischemic - dereased blood flow –> necrosis of tubules.
Severe hemorrhage, severe renal vasoconstriction, hypotension, dehydration, shock.

Nephrotoxic –> toxic agents result in necrosis of tubules.
Ethylene glycol (assoc with oxalate crystals in urine),
myoglobinuria (due to crush injury to muscle),
radiograph contrast,
drugs (sulfonamides, methicilin, aminoglyciosides - most common),
heavy metals (eg lead),
organic solvents (methyl alcohol, chloroform, carbon tetrachloride).
urate (due to tumor lysis syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which part of kidney is the most susceptible for ISCHEMIC injury?

A

PCT and ascending thick part of Henle in medulla.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which part of kidney is the most susceptible for toxic injury?

A

PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What ATN is preceded by prerenal failure?

A

Ischemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the most common cause of ARF?

A

Acute tubular necrosis (intrarenal azothemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ATN. What casts?

A

brown, granular casts in the urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is used prior chemotherapy to prevent ATN?

A

Hydration and allopurinol –> decrease risk of urate-induced ATN.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ATN clinical features?

A

Oliguria with brown, granular casts
Decreased BUN and Cr
hyperkalemia (due to decr. renal excretion) with metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ATN is reversible, sometimes need dialisis due to electrolyte imbalances that may be fatal.

A

.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How long can persist oliguria prior recovery? ATN

A

2-3 weeks. tubular cells (stable cells) take time to reenter the cell cycle and regenerate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ATN. Dysfunctional epitelium results in decreased ….

A

decr. reabsorbtion of BUN (serum BUN:Cr ration <15), decreased reabs. of Na (FENa > 2 proc.) and inability to concentrate urine (urine osm < 500 mOsm/kg).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

decr. reabsorbtion of BUN (serum BUN:Cr ration <15), decreased reabs. of Na (FENa > 2 proc.) and inability to concentrate urine (urine osm < 500 mOsm/kg).?

A

ATN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Intact. (fractional excretion of sodium (FENa) <1 proc., and urine osmolality (osm) > 500 mOsm/kg.?

A

Prerenal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Postrenal, decrease outflow results in 3

A

decr. GRG, azotemia, oliguria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Postrenal. due to?

A

obstruction of urinary tract downstream from the kidney eg ureters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Postrenal. Early stage of obstruction? FENa, BUN/Cr

A

Increased tubular pressures ,,forces” BUN into the blood (serum BUN/Cr ratio > 15); tubular function remains intact (FENa < 1 proc. and urine osm>500 mOsm/kg).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Postrenal. Late stage of obstruction? FENa, BUN/Cr

A

with long-standing obstruction, tubular damage ensues, resulting in decreased reabsorption of BUN (serum BUN:Cr ration < 15), decreased reabsorption of sodium FENa > 2 proc., and inability to concentrate urine (urine osm < 500 mOsm/kg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Acute interstitial nephritis. causes? what type of azotemia?

A

Drug-induced hypersensitivity involving the interstitium and tubules.
Results in ARF (intrarenal azotemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Acute interstitial nephritis. Drugs?

A

NSAIDs, penicillin, diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Acute interstitial nephritis. presentation?

A

oliguria, fever, rash days to weeks after starting a drug. eosinophils may be seen in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Acute interstitial nephritis. what cells in the urine?

A

Eosinophils may be seen in the urine

32
Q

Acute interstitial nephritis. when resolves?

A

with cessation of drug

33
Q

Acute interstitial nephritis. may progress to what?

A

renal papillary necrosis

34
Q

Renal papillary necrosis. definition?

A

necrosis of renal papillae.

35
Q

Renal papillary necrosis. presentation?

A

gross hematuria and flank pain

36
Q

Renal papillary necrosis. causes?

A
  1. chronic analgetic abuse (long-term phenacetin or aspirin use)
  2. DM
  3. Sickle cell trait or disease
  4. severe acute pyelonephritis
37
Q

what is difference between prerenal and intrarenal due to decr. blood flow?

A

prerenal - HYPOPERFUSION
intrarenal - HYPOPERFUSION WITH ISCHEMIA

38
Q

liver disease with portal hypertension–> effect on kidney

A

Vasoconstriction -> prerenal azotemia. hepatorenal syndrome

39
Q

intrarenal. what is classification based on the damaged site?

A

tubular (85 proc.)
glomerular - GN
interstitial (interstitial nephritis)

40
Q

Hemolytic intravascular anemia - what ATN?

A

toxic

41
Q

Bence Jones protein light chains - what ATN?

A

toxic

42
Q

Aminoglycosides - effect PCT cells? 3

A

impair lisosomal function, protein synthesis and mitochondrial activity –> ATN.

43
Q

Aminoglycosides - histology of PCT?

A

FOCAL tubular epithelial necrosis with casts that obstruct the tubular lumen –> lead to rupture of the basement membrane.

44
Q

Aminoglycosides -> damage to PCT –> electrolytes?

A

loss of reabsorptive capacity –> electrolyte wasting

45
Q

Aminoglycosides -> damage to PCT. if very severe, what syndrome?

A

Fanconi

46
Q

Aminoglycosides -> if damage to Distal CT occurs–> ?

A

loss of concentration capacity with poliuria (nonoliguric renal failure).

47
Q

Is ethylen glycol toxic to kidney?

A

No, its not toxic.
Toxic are its metabolites.

48
Q

ethylen glycol metabolized to —-> 2?

A

glycolic acid and oxalic acid —> cause toxicity.

49
Q

ethylen glycol what symptoms?

A

as intoxication of alcohol: altered mental status innitially
Renal failure - 24-72h post ingestion (oliguria, flank pain).

50
Q

ethylen glycol. what causes obstruction?

A

glycolic and oxalic acids crystalizes –> obstruction -> ATN

51
Q

ethylen glycol. what crystals on biopsy?

A

oxalate

52
Q

ethylen glycol. histology?

A

proximal tubular ballooning and vacuolar degeneration (cia tiesiog nekrozei budingi pokyciai) with morphologically normal glomeruli.

53
Q

ethylen glycol. What all findings?

A

altered mental status
renal failure
high anion gap metabolic acidosis
increased osmolar gap, calcium oxalate in the urine

54
Q

ethylen glycol. why acidosis and high osmolar gap?

A

elevated anion gap metabolic acidosis - due to acid. metabolite formation.

high osmolar gap - due to uncharged parent alcohol

55
Q

contrast induced pehropathy (CIN). what is damage?

A

direct citotoxicity of intravenous contrast on tubular cells -> diffuse necrosis of PCT cells.

prevention: avoids NSAIDs, give smallest possible volume of contrasts, give periprocedural intravenous saline

56
Q

Hemoglobin. prolonged seizure –> renal injury?

A

prolonged seizure –> rhabdomyolysis –> kindney injury

57
Q

Cristaline induced kidney injury due to ….

A

acyclovir or sulfonamide.
urinalysis - needle shaped or rosette-shaped crystals

58
Q

vancomycin - when injury?

A

after prolonged course (days). single dose would not cause injury. Also, no cristals

59
Q

intrarenal due to GN. mechanism?

A

immune complex deposition –> activation of complement –> attracts iimune cells (macrophages, neutrophils) –> release of LYSOSOMAL ENZYMES – >inflammation and damage to podocytes –> increased membrane permeability -> filtration of huge molecules -> proteinuria and hematuria

60
Q

GN. Damage to podocytes -> fluid leakage –> what result?

A

REDUCED PRESSURE DIFFERENCE –> lower GFR -> oliguria
more fluids in body –> volume overload -> edema and hypertension

less filtration –> azotemia

61
Q

AIN - renal biopsy?

A

inflammatory interstitial infiltrate and edema

cells: lymphocytes, macrophages, eosinophils

62
Q

AIN - what hypersensitivity?

A

type I and IV.

63
Q

AIN - urinalysis?

A

sterile pyuria (EOSINOPHILS), WBC, WBC casts

however, eosinphils are not specific finding - it may be also in prostatitis or transplant rejection

64
Q

renal papillary necrosis.
- analgetic nephropathy - findings?

A

papillary necrosis and tubulointerstitial nephritis

65
Q

renal papillary necrosis.
Why DM?

A

DM -> metabolic abnormalities eg nonenzymatic glycosylation -> changes in vessels -> renal vasculopathy -> subsequent hypoperfusion

66
Q

renal papillary necrosis.
why pyelonephritis/urinary tract obstruction?

A

edematous interstitium of pyelonephric kidney compresses the medullary vasculare -> ischemia.

67
Q

renal papillary necrosis. why gross hematuria?

A

due to sloughed papillae

68
Q

renal papillary necrosis. why flank pain?

A

due to ureteral obstruction

69
Q

renal papillary necrosis. macroscopically?

A

Gray-white or yellow necrosis of the distal two-thirds of the renal pyramids is seen macroscopically

70
Q

what vascular diseases can cause ATN? 5

A

HUS, TTP, Hypertensive emergency, vasculitis or scleroderma renal crisis, renal vein thrombosis/atheroemboli/renal infarction

71
Q

postrenal - what side obstruction?

A

BILATERAL

72
Q

postrenal - causes?

A

ACQUIRED OBSTRUCTIONS:
- BPH
- iatrogenic - catheter-assoc. injuries
- Tumors - bladder, prostate, cervical, metasteases, intraabdominal turmors
- stones
- bleeding with subsequent clot formation

Neurogenic bladder - eg due to multiple sclerosis, spinal cord lesions, peripheral neuropathy

Congenital malformations - posterior urethral valves

73
Q

posterenal. unilateral obstruction. what creatinine?

A

!!!As long as the contralateral kidney remains intact, patients with unilateral ureteral obstruction typically maintain normal serum creatinine levels.

also, if one kidney is okay, GFR ir maintained

74
Q

posternal - UG?

A

distended bladder, high postvoidal residual volumes, bilater hydrophrosis, and/or obstructing stones

75
Q

posternal. If bladder outlet obstruction - what management?

A

urgent relief of UT obstruction: cateterization, suprapubic cateterizatio

76
Q

posternal. If ureteral or renal pelvic obstruction - what management?

A

urgent urology consultation to relieve obstruction
Management: ureteral stenting; percutaneous nephrostomy

1 STEP Renal pathology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions