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DT3-Exam 3 > Interstitial Disease--Melissa > Flashcards

Interstitial Disease--Melissa Flashcards

1
Q

What type of tumors come from metanephric blastema derivatives? In general, what does the blastema give rise to?

A
  • Tubule and interstitial tumors–> Renal cell Ca.

- Gives rise to proximal portion of the nephrons (glomerulus –> distal convoluted tubule) and the interstitium

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2
Q

What type of tumors come from ureteric bud derivatives?

A

Tumors of the collecting ducts–> Uretal Tumors

*“uroepithelial/ ureteral is the same thing as “transitional”.

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3
Q

Describe generally the kidney’s location:
Who has larger kidneys boys or girls?
How many major and minor calyces per kidney?

A

Retroperitoneal at the level of T12-L3 with rt lower than lt

  • Larger in males than females
  • Each kidney has 12 Minor calyces–> 2-3 Major calyces
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4
Q

Most important structure in the renal cortex?

A

Glomeruli!

*This is where be biopsy for nephropathy

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5
Q

Most important structure in the renal medulla?

A

Tubules! Especially the loops of henle and the collecting ducts

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6
Q

Where are the pyramids and the column located and what do we call the location at the tip of each pyramid?

A

Pyramids are in the medulla and the columns are between the pyramids– the tip of a pyramid is referred to as a papilla

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7
Q

What is the fascia that encases the kidneys and the adrenals called?
List the layers of connective tissue/ fat surrounding the kidneys and adrenals from outside in:

A

From outside in:
*Gerota’s fascia–> perirenal fat (contains adrenals)–> renal capsule–> kidney

Important for staging of tumors.

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8
Q

By when does a developing fetus form a functional kidney?

A

25 weeks

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9
Q

Compare and contrast a proximal and distal convoluted tubule histology:

A

Distal: smaller simple cuboidal epi with crisp boarders
Proximal: larger simple cuboidal epi cells with cilia; more eosinophilic.

*This is important because the PT cilia can be injured with disease

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10
Q

What is acute renal failure?

What are the three types?

A

Sudden decrease in renal function:

  • (#1) Intrinsic: Kidney organ damage
  • Prerenal: Hypovolemia***, metabolic derangement, sepsis
  • Post renal: Obstruction (tumor, BPH, clots)
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11
Q

What do oliguria and anuria mean?

A

Oliguria: UNDER 500ml/24 hrs urine produced
- Decrease in urine production

Anuria: ~100ml/24hrs urine produced
- Absent or near absent during production

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12
Q

What are the 4 causes if intrinsic acute renal failure?

Which is the most common?

A

1 ACUTE KIDNEY INJURY (AKI)

  • Acute interstitial nephritis
  • Glomerulonephritis
  • Thromboembolism
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13
Q

What are the two causes of AKI?

A
  • Ischemia

- Nephrotoxicity (#1)

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14
Q

Explain how Ischemia causes AKI

In what two ways does it differ histologically from nephrotoxic AKI?

A

Ischemia–> Vasoconstriction –> tubular injury–> DECREASE GFR

  • Most necrosis in PT with SKIPPED areas
  • Tubulorrhexis PRESENT (BM ruptured)
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15
Q

Explain how Nephrotoxicity causes AKI

In what 3 ways does it differ histologically from ischemic AKI?

A 
Nephrotoxic Substance--> 
Direct tubular injury--> DECREASE GFR
-Necrosis of 100% PT 
-NO SKIPPING
-NO Tubulorrhexis
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16
Q

What is the #1 cause of AKI

A

Nephrotoxicity

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17
Q

Histo features of mercury tox related AKI

A

Eosinophillic inclusions; ^ Ca++ deposits

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18
Q

Histo features of carbon tetrachloride related AKI

A

Lipid inclusions

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19
Q

Three histo features of Ethylene Glycol nephrotoxicity:

A
  • Hydropic/ Vacuolar change
  • Birefringent Oxalate crystals
  • ^ Ca++ deposits
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20
Q

Two histo features of Lead nephrotoxicity:

A

-Large acidophilic nuclear inclusions

w/o Ca++ or Crystals

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21
Q

Describe the gross path associated with all AKI:

A
  • Enlarged kidney (edematous)

- Hyperemic medulla + Anemic cortex–>Sharp demarcation of corticomedullary junction

22
Q

What are the three phases used to identify the micro path and clinical features associated with AKI? Which phase is most assc with mortality?

Describe each of the three phases in one to two words.

A

Initiation (Hrs-Days; reversible damage)–>
Maintenance (5-7days; cell death)–>
Recovery (1-2 weeks; cell regeneration)

*Maintenance phase most dangerous (2/3 deaths): cells die in this phase. So do people.

23
Q

What are 4 histo features associated with the initiation phase of AKI?

A
  • Interstitial Edema + tubular Dilation
  • Lose PAS+ Brush Boarder
  • Leukocytes in Vasa Recta
24
Q

What are 2 histo features associated with the maintenance phase of AKI? What type of casts are seen?

A

Necrosis + apoptosis–> cell sloughing–> Eosinophilic hyaline casts

(Summary of this phase: dying cells –> dying people; note- casts are basically dead cells in urine.)

25
Q

What are 3 features associated with the recovery phase of AKI?

A
  • Flat cells
  • Hyperchromatic nucleoli
  • mitosis
    (summary: cells regenerate)
26
Q

Clinical features associated with initiation phase of AKI?

A

-Brief Azotemia

27
Q

Clinical features associated with maintenance phase of AKI? (3)

A
  • Oliguria
  • Dialysis Required
  • 2/3 people DIE
28
Q

Clinical features associated with recovery phase of AKI? Is this disease reversible? (2)

A
  • Profuse diuresis w/ replacement of losses
  • Most susceptible to infection
  • Often reversible
29
Q

Which organisms cause ACUTE bacterial pyelonephritis? (4)

Who is at especially high risk of recurrent bacteria infections?

A 
#1: E. coli; PEK bugs; Strep faecalis; Staph 
Patients with vesicoureteral reflex commonly have recurrent infections; common in boys.
30
Q

What are the 3 viruses that can cause ACUTE pyelonephritis and in which patients do we see this?

A

Immunocompromised:

Polyloma (JC), CMV, Adenovirus

31
Q

Gross path changes associated with acute pyelonephritis? (4)

A
  • Cortical thinning
  • Gray-white inflammatory areas
  • Subcapsular abcesses

*If supurrative look for white streaks in medulla and blotches in cortex

32
Q

Micro path changes associated with acute pyelonephritis?

A

Neutrophillic throughout kidney

33
Q

What are 5 predisposing risks for acute pyelonephtiris?

A

Previous UTI, Reflux, DM, Preggos, any obstruction or cath

34
Q

How does Acute pyelonephritis present? (3)

A
  • Systemic signs of infection
  • Costovertebral angle tenderness
  • WBC CASTS; distinguishes from cystitis or lower UTI
35
Q

3 complications that may result from acute pyelonephritis?

A

Papillary necrosis, pyonephrosis, perinephric abscesses

36
Q

How does one get chronic pyelonephritis?

A

ALWAYS associated with anatomic abnormality: Reflux or obstruction

37
Q

What are two gross path changes associated with chronic pyeloneprhtis from BOTH reflux and obstruction?

A
  • Asymmetric scars; calyx mutation

- Shrunken kidney (contraction)

38
Q

What are the differences in gross path between reflux and obstructive chronic pyelonephritis?

A

Reflux:
Polar scarring & blunted calyces

Obstruction:
Diffuse scarring

39
Q

Describe three micro path changes associated with chronic pyelonephritis:

A
  • THYROIDIZATION*** (tubular atrophy and dilation)
  • chronic inflammatory cells infiltrate
  • Interstitial fibrosis
40
Q

Who typically gets chronic pyelonephritis?

A

Little kids with reflux –> polar scars!

41
Q

List 5 types of drugs that can cause drug induced interstitial nephritis:

A

Synthetic Penicillins, Rifampin, Diuretics, NSAIDS, Anesthetics

42
Q

Describe micro path changes associated with ALL forms of drug induced interstitial nephritis

A
  • Lymph and EOS infiltrate (EOS mostly around tubules)
  • EOS casts (You see this –> you know the answer.)
  • Patchy interstitial inflammation at CM jxn.
43
Q

What are two distinctive micro path changes associated with phenacetin induced interstitial nephritis?

A

Gross papillary necrosis w/ little inflammation

44
Q

Describe the Clinical prognosis, onset and features associated with all types of drug induced interstitial nephritis:

A
  • Treatable w/ early Dx.
  • Onset 15 days after exposure
  • EOS in urine
45
Q

Describe the cause and progression of urate nephropathy:

A

Gout/Chemo/Metabolic disease–>
Uric acid crystal deposition in nephron–>
Tophi (giant cells + UA crystals)–>
~Stone formation

*Had 2 Rx questions on chemo drug (doesn’t matter which really) –> cell death –> uric acid release –> stones;; give these guys allopurinol

46
Q

Describe the cause and progression of Nephrocalcinosis nephropathy:

A

CaPO4 deposition in tubules–>
Calcification of tubular BM + interstitial fibrosis
–> ~renal infarct

47
Q

What is a cause of light chain cast nephropathy and how can we diagnose

A
  • Multiple myeloma: (punched out lesions on radiograph) –> CAUSES Primary Amyloidosis.
  • Kidney biopsy will stain Congo red w/ green birefringent crystals

Rx question.

48
Q

Describe how multiple myeloma can cause light chain nephropathy:

A

^^^IgG, IgA; Light chains get dumped in urine

Bence Jones Proteinuria!!!

49
Q

Two histo features of light chain nephropathy:

A
  • Light chain casts surrounded by inflammation w giant cells

- Nephrocalcinosis

50
Q

Xanthogranulomatous Pyelonephritis must be distinguished from what disease?

A

Renal cell ca. !!

51
Q

Describe how Xanthogranulomatous Pyelonephritis occurs:

A

PROTEUS infection + Obstruction–>

FOAMY HISTIOCYTES–> Benign inflammatory disease

DT3-Exam 3 (9 decks)

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