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Renal Module > Tubulointerstitial Diseases > Flashcards

Tubulointerstitial Diseases Flashcards

1
Q

What is Acute kidney injury?

A

An abrupt impairment in renal function manifest by increased creatinine, increased BUN and oliguria

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2
Q

In extrememe cases of AKI what results?

A

Irreversible anuric renal failure with increasesed creatinine and potassium as well as acidosis. Fatality in a matter of days or sooner if hyperkalemia triggers cardiac arrhythmia

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3
Q

What is the most common cause of AKI?

A

Ischemia.

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4
Q

What is the most common histopathologic counterpart to AKI?

A

Acute Tubular necrosis

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5
Q

What is the most common cause of acute tubular necrosis?

A

Systemic disease affecting the kidney or multi-organ disease affecting the kidney.

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6
Q

What is the most common cause of the ischemia resulting in Acute Tubular Necrosis?

A

Shock….especially septic shock.

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7
Q

What is the second most common cause of ATN?

A

Nephrotoxins.

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8
Q

What is the most common nephrotoxin which causes ATN?

A

Radiologic contrast dye.

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9
Q

What anatomical structure does renal ischemia usually spare?

A

The Glomeruli!

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10
Q

What is the name of the type of Ischemia that affects the Glomeruli?

A

Cortical Necrosis.

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11
Q

What is the difference between tubular necrosis and Glomerular necrosis?

A

Tubular necrosis is reversible.

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12
Q

How is Tubular necrosis reversible?

A

The epithelial tubular cells die but the Basement membrane is still intact and there are stem cells there that can regenerate and replace the lost epithelial cells.

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13
Q

What is the standard time for tubular regeneration?

A

1-3 weeks but may take up to 6 weeks.

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14
Q

What feature of the renal medulla makes it even more susceptible to ischemia?

A

The epithelial cells are incapable of anaerobic metabolism

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15
Q

What portion of the medulla is most prone to ischemia?

A

The outer medulla is a major target of hypoxic injury because of regional hypoxia and metabolic oxygen demand of the portions of the tubules there

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16
Q

What are the portions of the tubule in the Outer medulla?

A
  1. Straight portion of the Proximal tubule

2. Thick ascending limbs of the loop of Henle

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17
Q

What molecules would be found in increased amounts arterioles in post ischemic kidney?

A
  1. Endothelin 1
  2. Angiotensin II
  3. Thromboxane A2
  4. PGH2
  5. Leukotriene C4
  6. Leukotriene D4
  7. Adenosine
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18
Q

What would post ischemia arterioles of the outter medulla show?

A

Reduced vasodilation in response to acetylcholine, bradykinin and NO

19
Q

What are the cytokines which play a role during ischemia?

A
  1. I-1-beta
  2. IL-6
  3. IL-12
  4. IL-15
  5. IL-18
  6. IL-32
  7. TNF-alpha
  8. endothelin
20
Q

How is the tubular epithelium actively involved in the inflammatory response during ischemia?

A

Injured tubular epithelial cells produce proinflammator chemotactic cytokines such as:

  1. TNF-alpha
  2. IL-1-beta
  3. TGF beta
  4. IL-6
  5. IL-8
  6. MCP-1
  7. RANTES
  8. ENA-78 (endothelial neutrophil activating protein 78)
21
Q

What happens to kidneys with ATN?

A
  1. Usually become enlarged up to 30%
  2. Pale cortex
  3. Congested Medulla (especially in the region near the corticomedullary junction.
22
Q

What is one of the early findings in ATN on light microscopy?

A

Loss of brush border and Bleb formation in its place.

23
Q

What are some other early signs of ATN?

A
  1. Diffuse tubular epithelial cell edema

2. Vacuolization of the cytoplasm

24
Q

What else has some of the same signs as early ATN?

A
  1. Calcineurin toxicity

2. Osmotic Diuresis (hetastarch, mannitol)

25
Q

What morphological changes occur in the epithelial cells?

A

Normally are cuboidal become Flat

26
Q

What form of necrosis occurs in the renal tubular epithelial cells in ATN?

A

Coagulative necrosis

27
Q

What forms in the tubules during ATN?

A

Casts from cells that have sloughed off and mixed with proteinacious debris.

28
Q

In rhabdomyolysis (necrosis of skeletal muscle) what forms the casts?

A

Rhabdomyolysis releases myoglobin which precipitates in renal tubules creating myoglbin casts which contribute to ATN

29
Q

How are myoglobin casts different from the ones generated from the casts generated in ATN from ischemia?

A

Myoglobin casts are denser, more acellular and more intensly and darkly eosinophilic. (Can also use stains to show presence of myoglobin in tissue)

30
Q

What are the signs of acute tubular necrosis from Ethylene Glycol consumption?

A

Acute tubular necrosis with prominent cytoplasmic vacuoles and formation of Oxalate crystals in the tubular lumen.

31
Q

What is the morphology of the Oxalate crystals from Ethylene Glycol induced ATN?

A

These are translucent, rounded and fragment into wedge shapes with tissue sectioning.

32
Q

What is the morphology of cells in the recovery phase of ATN?

A

Initial replacement cells are very flat like squamous cells and mitoses can be sometimes found.

33
Q

What are the symptoms of ATN?

A
  1. Anorexia progressing through nausea to vomiting
  2. Pruritis
  3. Confusion
  4. Lethargy
  5. G.I hemorrhage
  6. Epistaxis
  7. Dysfunctional platelets
34
Q

What do patients with ATN frequently suffer from hypotension?

A

This is because patients suffering with ATN usually are suffering from shock.

35
Q

What is the effect of ATN on urine output.

A

Low urine output is a manifestation of ATN.

36
Q

What are 2 staple features of ATN?

A
  1. Hyperkalemia

2. Metabolic acidosis

37
Q

What lab test can help make a specific diagnosis?

A

Urinanalysis

38
Q

What are the type of casts present in ATN?

A

Granular Muddy brown casts

39
Q

What are the values of urine sodium in ATN?

A

High

40
Q

What is the treatment for ATN?

A

Dialysis if the patient can tolerate it

41
Q

What is a key determinant for whether a patient needs dialysis in ATN?

A

Potassium

42
Q

What is the consequence of hyperkalemia?

A

Cardiac Arrhythmia

43
Q

What is a major concern during the recovery phase of ATN?

A

Hypokalemia

Renal Module (29 decks)

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