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RENAL Pathology > Acute Renal Failure > Flashcards

Acute Renal Failure Flashcards

1
Q

The degree of acute renal failure is named by the acronym ?

A

RIFLE: Risk, Injury, Failure, Loss, End stage renal disease.

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2
Q

Acute tubulointerstitial nephritis is often a drug hypersensitivity (1) are a common cause) in which numerous (2) are present in the urine as well as in the tissues.

A
  1. penicillins 2. eosinophils
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3
Q

Serum IgE levels increase, and IgE-containing plasma cells and basophils (Type I)

A

Drug hypersensitivity–>Acute tubulointerstitial nephritis

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4
Q

Maintenance phase of AKI:Urine output ____, ____ overload, rising BUN concentrations, ___kalemia, and metabolic acidosis

A

1) 40- 400 mL/day (oliguria); salt and water;hyper

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5
Q

Acute tubular necrosis: The cells are then sloughed into the tubule, forming (1) which obstruct it, causing back pressure as well as tubuloglomerular feedback, which causes (2).

A
  1. casts 2. afferent arteriolar vasoconstriction and decreased filtration
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6
Q
  1. ___ is induced experimentally by mixture of aspirin and phenacetin,
  2. Analgesic nephropathy may lead to ___
A

Papillary necrosis;

transitional papillary carcinoma of the renal pelvis

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7
Q

AKI begins with an initiation phase over the first 36 hours with a decline in (1) and increased (2)

A
  1. urine output 2. BUN
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8
Q

(1) can cause what is termed post-renal azotemia which has (2) BUN/creatinine ratio.

A
  1. Obstruction to the urinary tract 2. intermediate level
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9
Q

(1) can cause pre-renal azotemia, which is generally found with (2) BUN/creatinine ratio.

A
  1. Decreased renal blood flow 2. elevated
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10
Q

This is not as accurate as a creatinine clearance, and is intended as a screening method for estimating GFR without a timed urine collection.

A

Cockcroft-Gault estimate of GFR

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11
Q

Acute renal failure can be a consequence of problems with ?

A

blood vessels, glomeruli, tubules, or the interstitium.

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12
Q

Patients with acute tubulointerstitial nephritis may also have (1)

A
  1. fever, peripheral eosinophila, hematuria, and proteinuria.
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13
Q

Acute Tubulointerstitial Nephritis

15 days after drug exposure–> fever, ___, maculopapular rash, hematuria, mild proteinuria, and leukocyturia (often including ___ in urine)

A

eosinophilia; eosinophils

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14
Q

Other causes of AKI include direct toxic injury to tubules such as can occur with (1) and (2)

A
  1. radiocontrast dyes 2. acute tubulointerstitial nephritis
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15
Q

(1) is a fusion of the two kidneys which don’t separate completely during development. This occurs in about 1: 500 individuals, and rarely leads to obstruction. The kidney is usually fused at the (2).

A
  1. Horseshoe kidney 2. lower pole
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16
Q

Estimates of ___: Cockcroft‐Gault
[(140‐Age) * Mass] \ [72 * Serum creatinine}

if female, multiply above by 0.85

(whatever above means according to Holt; what a dumbass)

A

GFR

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17
Q 
radiographic contrast agents
 heavy metals (mercury)
 organic solvents (carbon tetrachloride).
A

Nephrotoxic AKI

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18
Q

gentamicin and other antibiotics

A

Nephrotoxic AKI

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19
Q

Histologically the kidney has a fetal appearance with immature (1) and abundant (2) surrounding (3)

A
  1. glomeruli 2. cartilage 3. mesenchyme. refers to multicystic renal dysplasia
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20
Q

In bilateral agenesis, the absence of urine prevents the development of (1) and the subsequent pressure needed for (2) development (this disorder is called (3): they have strange facial development as well, from the loss of amniotic fluid pressure).

A
  1. amniotic fluid 2. lung 3. Potter’s syndrome
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21
Q

Multicystic renal dysplasia is usually a consequence of an obstruction: either (1).

A
  1. ureteropelvic obstruction or ureteral atresia
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22
Q

Bilateral agenesis is a fairly common lethal congenital abnormality which leads to stillborn infants who are born with (1)

A
  1. hypoplastic lungs.
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23
Q

___ most frequently occurs with synthetic penicillins
(methicillin, ampicillin), other synthetic antibiotics (rifampin), diuretics (thiazides),
NSAIDs, and miscellaneous drugs (allopurinol, cimetidine).

A

Acute tubulointerstitial nephritis

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24
Q

Acute tubular necrosis: There can also be fluid leakage and inflammation within the (1)

A
  1. interstititum between tubules.
25
Q

About half of AKI patients have (1) AKI with increased (2) but decreased (3)

A
  1. non-oliguric 2. urine volumes 3. glomerular filtration rate (GFR).
26
Q

what do these cause?

  1. gentamicin and other antibiotics
  2. radiographic contrast agents
  3. heavy metals (mercury)
  4. organic solvents (carbon tetrachloride).
  5. mismatched blood transfusions and other hemolysis causing hemoglobinuria
  6. skeletal muscle injuries causing myoglobinuria
    characteristic intratubular hemoglobin or myoglobin casts
    toxic iron content of these globin molecules contributes to the AKI
A

B. Nephrotoxic AKI

27
Q

GFR formula

A

(urine creatinine X urine volume)/ serum creatinine

28
Q

Recovery phase AKI

1) in urine volume that may reach up to 3 L/day;

Loss of 2) ;

Hypokalemia, rather than hyperkalemia; ALSO increased risk of 3)

A

1) Increase;
2) H20, Na, and K
3) INFECTION

29
Q

Most patients recover from AKI unless the cause is fatal such as in ?

A

infections or burns.

30
Q

Ischemic acute tubular necrosis; type of necrosis? Inflammation present or absent?

A

Coagulative with LACK of inflammation

31
Q

Acute renal failure due to carbon tetrachloride poisoning can show (1) histologically.

A

fatty change followed by necrosis

32
Q

This may be at least in part a (1) hypersensitivity reaction since (2) levels increase and (3) are found.

A
  1. Type I 2. IgE 3. basophils Refers to acute tubulointerstitial nephritis
33
Q

If the cause of AKI is reversed or eliminated, then there is a (1) recovery phase, which can have (2)

A
  1. diuretic (high urine output) 2. ery high urine outputs.
34
Q

more commonly unilateral defect in children.

A

Renal Hypoplasia

35
Q

Ischemic changes

A. reversible injury–> signs?
B. lethal injury–> necrosis and apoptosis

A

cellular swelling, loss of brush border & polarity, blebbing, cell detachment

36
Q

Acute tubular necrosis: decreased (1) to the (2) produces necrosis of the (3)

A
  1. blood flow or oxygen delivery 2. proximal tubules 3. proximal tubule cells.
37
Q

Acute renal failure due to ethylene glycol (antifreeze) poisoning produces (1) histologically

A
  1. hydropic degeneration of the proximal convoluted tubules.
38
Q

Activated tubular cells will express molecules which activate cytokines leading to (1) which will further damage the tubules.

A
  1. interstitial fibrosis
39
Q

The most common cause of AKI is a pathologic entity known as (1).

A
  1. acute tubular necrosis
40
Q

AKI findings:

  1. __ casts, ____ casts in distal tubules and collecting ducts
  2. ____ protein (urinary glycoprotein secreted by thick limb and distal tubules)
  3. ____ edema
  4. ___within dilated vasa recta
  5. Epithelial regeneration
A

Hyaline; pigmented granular;

2) Tamm-Horsfall
3) Interstitial
4) Leukocytes

41
Q

A maintenance phase follows the initiation phase of AKI with ?

A

oliguria, rising BUN, hyperkalemia, and metabolic acidosis (from inability to excrete urea, potassium and acid).

42
Q

Importance of Tubular Damage1) predicts decrease renal function more than glomerular2) causes direct injury to and activation of tubular cells Activated tubular cells express 3) which cause interstitial fibrosisFiltered 4) and other proteins damage tubules(also transferrin Fe, Ig, and lipids).

A

1) Tubulointerstitial fibrosis2)Proteinuria 3) adhesion molecules cytokines4) cytokines, complement

43
Q

Acute renal failure most commonly presents with ?

A

anuria (complete absence of urine) or oliguria (decreased urine flow), and azotemia (elevated BUN).

44
Q

Although pathologists enjoy looking at glomeruli, we must remind ourselves that (1) can be equally as, or potentially more, important in acute renal failure.

A
  1. tubular defects
45
Q

Another congenital abnormality is multicystic renal dysplasia, which is a defect in the development of the (1). This leads to persistence of (2), undifferentiated mesenchyme and abnormal (3).

A
  1. metanephric kidney 2. cartilage 3. collecting ducts
46
Q

Unilateral agenesis can also occur and generally produces a compensatory (1) of the opposite kidney which can lead to (2)

A
  1. hypertrophy 2. focal segmental glomerulosclerosis
47
Q

Because the flow rate is slow, most of the BUN can be reabsorbed, explaining the high ratio (more than 20fold) relative to the creatinine.

A

Pre-renal azotemia

48
Q

(2) tends to affect the BUN reabsorption and the creatinine filtration to the same extent so it has a (1) BUN/creatinine ratio.

A
  1. Intrarenal disease 1. decreased
49
Q

Grossly: kidneys have pale cortex and hyperemic medullary regions

A

acute tubular necrosis

50
Q

Renal tubular defects can initially present with ?

A

polyuria, nocturia, or electrolyte disorders like hyperkalemia.

51
Q

Ischemic AKI etiology:

Severe ___ and ____

Decreased blood flow accompanied by __ and ____

A

trauma; acute pancreatitis;

marked hypotension and shock

52
Q

Tubules can be damaged by ?

A

protein, cytokines, complement, iron, or lipids.

53
Q

3 reasons why tubular cell injury occurs:

  1. vast charged surface for ___
  2. active transport systems for ions and organic acids
  3. high ____
A

tubular reabsorption;

metabolic rate and oxygen consumption requirement

54
Q

Nephrotoxic AKI

Skeletal muscle injuries causing ___
characteristic ____ casts
toxic iron content of these globin molecules contributes to the ___

A

myoglobinuria; intratubular hemoglobin or myoglobin;

AKI

55
Q

Glomerular filtration rate can be calculated by determining the (1) clearance, which is equal to (2)

A
  1. creatinine 2. urine creatinine concentration x urine volume, divided by the serum creatinine concentration (UV/P)
56
Q

a slight decline in urine output with a rise in BUN

A

Initiation phase (36 hours) of AKI

57
Q

Biochemical changes in ischemia:

  1. depletion of ___
  2. accumulation of ___
  3. activation of proteases (calpain) which cause ____
  4. activation of phospholipases, which damage ___
  5. generation of reactive oxygen species
  6. activation of caspases, which induce apoptotic cell death
A

ATP;

2) intracellular calcium
3) cytoskeletal disruption
4) membranes

58
Q

Histologically, in acute renal failure, one sees (1) casts of the (2) in (3) as well as (4)

A
  1. hyaline 2. Tamm-Horfstall urinary glycoprotein 3. distal tubules and collecting ducts 4. interstitial edema and leukocytes

RENAL Pathology (21 decks)

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