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CRRAB II- Week 2 > Warren- Diseases of Tubules and Interstitium > Flashcards

Warren- Diseases of Tubules and Interstitium Flashcards

1
Q

What does ischemic or toxic inury to tubules lead to?

A

ATN (acute tubular necrosis)

or

ATI (acute tubular injury)

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2
Q

What does INFLAMMATORY rxt of the tubules and interstitium lead to?

A

TIN (tubulointerstitial nephritis)

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3
Q

What is acute tubular necrosis?

A

Destruction of TUBULAR EPITHELIAL CELLS which presents as acute loss of renal function

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4
Q

What is the MCC of acute renal failure?

A

ATN

50% of ARF in hospitalized pts

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5
Q

What causes ischemic ATN?

A

hypotension/shock>

Inadequate blood flow to kidneys

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6
Q

What causes nephrotoxic ATN?

A

drugs
heavy metals
organic solvents
contrast dye

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7
Q

What is the pathogenesis of ATN?

A
  1. tubular epithelial cell injury (reverisble: cell swelling, loss of polarity; lethal: necrosis and apoptosis)
  2. Disturbances in blood flow (intrarenal vsoconstriction)
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8
Q

What causes tubule cell injury?

A 
1. DEPLETION OF ATP>
increased intracellular Ca>
redistribution of membrane proteins>
abnormal ion transport>
increased Na/Cl to DT>
tubuloglomerular feedback and vasoconstriction
  1. INJURED CELLS RECRUIT WBCS
  2. LUMINAL TUBULE OBSTRUCTION BY DETACHED CELLS> increased intratubular pressure and decreased GFR
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9
Q

How do disturbances in renal blood flow relate to tubular injury?

A
  1. intrarenal vsoconstriction> decreased glomerular plasma flow/oxygen to TAL and the PT
  2. Vasoconstrictor pathways>
    RAS>
    endothelin released by damaged endothelial cells decreases NO
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10
Q

Can you recover from ATN?

A

Yes!

Reversibly injured epithelial cells proliferate and differentiate d/t GFs like EGF

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11
Q

What is the pathology of ATN?

A
  1. Tubular epithelial necrosis
  2. SLOUGHING of tubular cells into lumen
  3. Hyaline/granular CASTS
  4. interstitial edema and increased lymphocytes
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12
Q

What specific changes are associated w/ toxic ATN specifically ethylene glycol poisoning?

A

Ca oxalate crystals in the tubular lumen

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13
Q

Describe the clinical course of ATN.

A
  1. initiation- decreased urine output and increased BUN (36 hrs)
  2. Maintenance- oliguria, increased BUN, hyperkalemia, met. acidosis (requires dialysis)
  3. Recovery (steady increase in urine volume), hypokalemia d/t loss of K
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14
Q

HOw do you differentiate acute and chronic forms of tubulointersitital nephritis?

A

acute PMN/Eos, edema

Chronic- fibrosis/tubular atrophy

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15
Q

What are the clinical sxs of tubulointerstitial nephritis?

A

Polyuria
nocturia
metabolic acidosis

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16
Q

What are causes of TIN?

A 
Infections
toxins
Metabolic disease
Neoplasms- MM
Physical factors
Immunologic rxns
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17
Q

What causes acute pyelonephritis?

A

bacterial infection

18
Q

What causes chronic pyelonephritis?

A

Bacterial infection
reflux
obstruction

19
Q

What accounts for >85% of casses of pyelonephritis?

A

Gram - bacilli from GI tract

E. COLI
proteus
klebsiella

20
Q

What is the pathogenesis of pyelonephritis?

A

Colonization of urethra>
organisms into bladder>
multiplication d/t decreased urine flow (obstruction/neurogenic bladder)

21
Q

What is vesicoureteral reflux? What commonly causes it?

A

INCOMPETENCE of the vesicoureteral valve>
allows bacteria to enter ureter/renal pelvis

Congenital shortening of intravesicle portion of the ureter

22
Q

What is intrarenal reflux?

A

Occurs via the ducts at the tips of papillae

another cause of pyelonephritis

23
Q

What is the morphology of Acute Pyelonephritis?

A

Intersitital inflammation by PMN

Intratubular aggregates of NEUTROPHILS>
tubular necrosis>
heals by scarring>
tubular atrophy w/ interstitial fibrosis w/ lymphocytes

24
Q

What part of the kidney is most commonly affect with acute pyelonephritis?

A

Upper and lower poles

easier to have reflux through these papillae

25
Q

What are complications of acute pyelonephritis?

A
  1. papillary necrosis–> yellow necrosis of papillary tips seen in pts w/ obstruction (diabetics)
  2. pyonephrosis (kidney full of pus)
  3. Perinephric abscess (suppurative inflammation extends through capsule to adjacent tissue
26
Q

What is seen in chronic pyelonephritis?

A

chronic reflux/chronic obstruction>
Pelvocalyceal damage >
important cause of END STAGE RENAL DISEASE

27
Q

What morphology it typical of chronic pyelonephritis?

A

Irregular scarred kidney surface

Blunt calyces

cortex filled w/ THYROIDIZATION- tubules w/ colloid casts

May see glomeruli normal or secondarily affected by FSGS

28
Q

Describe the onset of chronic pyelonephritis.

A

SILENT

or

associated w/ recurrent acute pyelonephritis

29
Q

How do pts with chronic pyelonephritis present?

A

Late in disease w/ HTN or renal insufficiency

FSGS and proteinuria

30
Q

What are three ways that drugs can induce injury?

A
  1. Interstitial immunologic rxn (methicillin)
  2. Cause acute tubular injury/ARF
  3. Slow injury to tubules over many years (analgesic abuse nephropathy)
31
Q

Describe the course of acute DRUG induced interstitial nephritis.

A 
Take drug>
onset 15 d after exposure>
fever, rash, renal abnormalities (hematuria, proteinuria, white cells)>
EOSINOPHILIA>
Stop the offending drug>
full recovery

*50% develop ARF (elderly)

32
Q

What do you see microscopically with Acute Drug induced interstitial nephritis?

A
  1. Eosinophils and PMNs
  2. Granulomas and giant cells
  3. Lymphocytes infiltrate tubular epithelium> tubular necrosis
  4. Gomeruli NORMAL
  5. Interstitial edema, MACROPHAGES AND LYMPHOCYTES

*NO neutrohpils in lumen of tubules just inflammation in interstitium

33
Q

What is the pathogenesis of Acute Drug induced interstitial nephritis? How long does it take to progress to sxs?

A

Idiosyncratic IR

Drug (hapten)>
covalently bind to cytoplasmic/extracellular component of tubular cells>
Mix:
Type I (IgE- eosinophilia)
Type IV (delayed)

2 wks

34
Q

How can NSAIDS effect the kidney?

A
  1. ARF
  2. Acute hypersensitivity
  3. Acute interstitial nephritis and MCD
  4. Membranous glomerulonephritis
35
Q

How do NSAIDS cause ARF?

A

Nsaid>
inhibition of PG>
lose vasodilation/local vasoconstriction>
decreased blood volume

36
Q

What causes tubulointerstitial disease?

A

Urate nephropathy

Hypercalcemia and nephrocalcinosis (Ca stones and deposition of Ca)

37
Q

What is Urate nephropathy?

A

ACUTE UA nephropathy> precipitation of UA crystals in tubules>
obstruction>
ARF

Chronic UA nephropathy>
gout

38
Q

What is acute UA nephropathy associated with?

A

CHEMO

Chemo>
tumor cells killed>
release urate>
clogs up kidney tubules>
obstructs flow>
ARF
39
Q

What is Multiple myeloma?

A

plasma cell neoplasm

40
Q

What causes MM?

A

Occurs in HALF of all MM pts

Bence jones proteins (kappa/lambda light chains)>
combine w/ Tamm horsfall protein>
large tubular casts>
obstruction/peritubular inflammation

CRRAB II- Week 2 (9 decks)

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