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Urinary Systems #2 > Pathophysiology of Tubulointerstitial Disease (Cianciolo) > Flashcards

Pathophysiology of Tubulointerstitial Disease (Cianciolo) Flashcards

1
Q

Cats tend to get ___________

A

Tubulointerstitial disease

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2
Q

Requires knowledge of creatinine or urinalysis etc

A

AKI (Clinical diagnosis)

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3
Q
  • Acute necrosis
  • Acute inflammation
    Describes:
A

Acute Renal Lesions (pathologist)

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4
Q

What are some things that cause acute tubular epithelial injury?

A
  • Ischemic
  • Toxic
  • Obstructive (crystals/ cellular casts/ pigment casts / ureteral blockage etc)
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5
Q

(T/F) Chronic kidney disease may present acutely

A

True

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6
Q

(T/F) Even if animal is acutely azotemic, that doesn’t mean that the lesions will be “acute”

A

True

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7
Q

(T/F) Because significant renal dysfunction occurs with overt necrosis of the tubular epithelial cells, the term has been changed in human medicine to “Acute Tubular Necrosis”

A

False

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8
Q

Epithelial cells don’t reabsorb glucose or amino acids appropriately

A

Fanconi’s Syndrome

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9
Q

(T/F) You can have tubular problems w/o actual evidence of injury

A

True

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10
Q

Glucosuria with normoglycemia and amino aciduria

A
  • Fanconi’s syndrome
  • Jerky treat exposure
    *Proximal tubulopathy is probably the correct term
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11
Q
  • Injured but viable epithelial cell detaches from the tubular basement membrane and exits in urine
  • Very common in kidney
A

Anoikis

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12
Q

The cell starts apoptotic cascade but can’t finish so it undergoes necrosis

A

Necroptosis

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13
Q
  • Controlled, does not incite inflammation
  • Suicide
A

Apoptosis

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14
Q

Cytokine expression of tubular epithelial cells
- __________ induces interstitial fibrosis

A

TGF-beta

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15
Q

Cytokine expression of tubular epithelial cells
- _____________ attenuates fibrosis

A

BMP-7

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16
Q

Cytokine expression of tubular epithelial cells
- Macrophage chemotactic protein (MCP-1) -> attracts ______________________

A

inflammatory cells

17
Q

Cytokine expression of tubular epithelial cells
- Epidermal Growth Factor helps _________ regenerate

A

tubules

18
Q

(T/F) In recovery from ATEI, recovering cells are thought to be more resistant to insult than mature cells

A

True

19
Q
  • Hypovolemic shock
  • Cardiogenic shock
  • Septic shock
  • Disseminated Intravascular Coagulation
  • Straight portion of the proximal tubule (pars recta) is most susceptible (high metabolic demand)
    – Also worry about the thick ascending limb of the Loop of Henle +/- medulla
    ** CANNOT definitively differentiate from nephrotoxic acute tubular injury
    These are causes of ________________
A

Ischemic ATEI / ATN

20
Q
  • Eliminated from the body mostly by glomerular filtration
  • Foals and reptiles are particularly sensitive
  • In animals with decreased GFR, we would be very careful to use this drug
A

Aminoglycosides (antibiotic)
**is a cause of Toxic ATEI

21
Q
  • Grossly, can see papillary necrosis –> obstructs the outflow of urine
  • Medulla and papilla are at increased risk b/c they work hard and have limited blood flow
  • Inhibits Cycloxygenase (COX) -> decreases renal prostaglandin E (PGE2) and PGI2 levels -> afferent arteriolar vasoconstriction -> decreased GFR -> renal ischemia
A

NSAIDs

22
Q
  • Common in dogs and cats (cats more susceptible)
  • Rapidly absorbed from the GI tract -> metabolized in the liver by alcohol dehydrogenase to oxalate (& other compounds)
  • These metabolites are nephrotoxic
  • Calcium oxalate crystals precipitate in tubules
A

Ethylene Glycol (Toxic + obstructive)

23
Q

Other Causes of Oxalate Crystals
Cruciferous vegetables are:

A
  • Rhubarb
  • Spinach
24
Q

(T/F) Can see scattered oxalates in animals with chronic kidney disease because they have lost the ability to process endogenous or dietary oxalates

A

True

25
Q
  • Ruminants and camelids
  • Ingestion of oak leaves, buds, stems or acorns
  • Clinical disease: anorexia, depression, rumen atony, constipation, diarrhea, elevated
  • Acute cases die 1-3 days; chronic cases linger for weeks
  • Gross: swollen pale kidneys with cortical petechiae
  • Can see colitis, perirenal edema, anasarca
A

Oak Nephrotoxicity

26
Q
  • Compounds that crystalize in tubules of small animal kidneys
    – Crystals are yellow-brown
  • Compounds added to pet food in order to increase ammonia content
    – Falsely elevates protein content on the label
A

Melamine / Cyanuric Acid (toxic + obstructive)

27
Q

Other Nephrotoxins in Small Animals
– All parts of the plants are toxic
– Mechanism of toxic action is unknown
– See overt necrosis of entire proximal tubule cross-sections

A

Lilies in cats

28
Q

Other Nephrotoxins in Small Animals
– Seems to be idiosyncratic
– Mechanism of toxic action is unknown

A

Grapes or Raisins in dogs

29
Q
  • RBC lysis -> anemia -> ischemic necrosis
  • And hemoglobin releases -> toxic to tubules
A

Pigmentary Nephropathy (Ischemic + toxic + obstructive)

30
Q

The source of the infectious agent determines the anatomic pattern of inflammation
- Hematogenous:

A

embolic and / or glomerulonephritis

31
Q

The source of the infectious agent determines the anatomic pattern of inflammation
- Urogenous:

A

Pyelonephritis
- Suppurative inflammation centered on the renal pelvis
- Can cause loss of concentrating ability due to renal papillary necrosis

32
Q

The source of the infectious agent determines the anatomic pattern of inflammation
- Interstitial:

A

A generic term used if the source is not apparent or if the inflammation has extended from the original location
** Please note that interstitial inflammation might not be due to infectious process

33
Q

(T/F) Biopsy will help determine if lesion are reversible or irreversible

A

True

34
Q

Chronic Irreversible Lesions
- In between peritubular capillaries and tubules
- Hallmark of chronic disease

A

Interstitial fibrosis

35
Q

Chronic Irreversible Lesions
- Thickened tubular basement membranes and attenuation (reduction) of tubular epithelium
- Likely due to some degree of hypoxia

A

Tubular atrophy

36
Q
  • Glomerulosclerosis (especially global glomerulosclerosis)
  • Arteriosclerosis
    These are:
A

Chronic Irreversible Lesions

37
Q

Molecular Mediators of Fibrosis
* Angiotensin II
* TGF-β
* Connective Tissue Growth Factor
* FGF-23 (might predict the development of azotemia in normal healthy cats)
* Smads (mediate the TGF-β pathway)

A

Promote fibrosis

38
Q

Molecular Mediators of Fibrosis
* BMP-7
* Smads (also mediate BMP-7 pathway)
* HGF
* Some components of the RAAS

A

Slow or inhibit fibrosis

Urinary Systems #2 (9 decks)

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