L58 + 59 Flashcards

1
Q

If you saw a hypercellular glomerulus, what would be happening in what you see?

A

Prolif of intracap glomerular cells

Crescents = prolif of extracap glomerular cells

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2
Q

What happens to get sclerosis in the kidney?

A

GBM collapse + mesangial expansion
Damage to segmental structure
Get scar due to collagen deposition

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3
Q

What happens to get hyalinosis in the kidney?

A

Accum protein in sclerotic areas in BV walls

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4
Q

What disease process thickens the GBM itself?

A

Diabetes (vs immune complex deposition thickening)

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5
Q

What is global vs segmental glomerulus damage?

A

Global - entire thing involved

Segmental - part of tuft involved w/ other part patent

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6
Q

Use the name: what is focal segmental glomerulo-sclerosis?

A

Focal - dotted throughout kidney

Segmental - only part glomerulus affected

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7
Q

Which cells are mediators of injury to the glomerulus?

A

Impt ones: neutrophils + mesangial cells

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8
Q

What are the 3 soluble mediators of injury at the glomerulus?

A

Complement
Fibrinogen
TGF beta

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9
Q

Clinical presentation nephritic syndromes

A
Hematuria - RBC casts
Mild proteinuria 
Periorbital edema 
Azotemia
Oliguria
HTN + edema
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10
Q

Pathogenesis of post-infectious glomerular nephritis?

A

Strep pyogenes infection: impetigo > pharyngitis

Immune complex pathogenesis

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11
Q

Post-infectious GN LM, IF, EM

A

LM: hypercellular (nephrotic)
GN: granular
EM: sub-epi humps of Ig

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12
Q

What other labs will indicate post-strep GN

A

+ ASO

↓C3

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13
Q

What is rapidly progressive GN? What are the categories of disease?

A
Crescent 
Renal failure progressing in wks/mos
Diseases may RESULT in RPGN
1. Immune complex mediated = granular IF
2. Anti-GBM = linear IF
3. Pauci-immune = nothing on IF
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14
Q

Treat post-strep GN; what is the complication if not treated?

A

Will resolve on own if treat 1ary infection in kids

Can progress to RPGN

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15
Q

What disease has anti-GBM antibodies?

A

Goodpature’s: T2 HST rxn

Linear IF

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16
Q

What diseases have granular IF and can progress to RPGN?

A

Immune complex disorders

  1. Post-strep GN
  2. SLE (IgG)
17
Q

What disease are RPGN pauci-immune?

A
  1. Wegener’s: c-ANCA
  2. Microscopic polyarteritis (small vessel vasculitis) p-ANCA
  3. Polyarteritis nodosa
  4. Churg Strauss
18
Q

Which diseases that can result in RPGN are reno-pulmonary diseases?

A

Goodpastures
Wegener’s
Microscopic polyangitis

19
Q

What is ANCA?

A

Anti-neurtophilic cytoplasmic autoantibodies
c-ANCA = cytoplasmic staining
p-ANCA = perinuclear staining

20
Q

What is the ANCA in Goodpastures?

A

Confounder - doesn’t matter!

21
Q

Treat Goodpasture’s

A

Plasmapheresis + steroids + cytotox drug

22
Q

Treat RPGN

A

Steroids + cytotoxic drugs

23
Q

What are the characteristics of nephrotic syndrome?

A

Proteinuria > 3.5 g/d
Hypoalbumin
Hyperlipidemia
Edema

24
Q

What is the most common cause of nephrotic syndrome in kids?

A

1ary

Minimal change disease

25
Q

What is membranous glomerulopathy?

A

1ary nephropathy- long onset
Ig @ sub-epi
Diffuse thickening of glomerular capillary walls
Idiopathic

26
Q

Membranous glomerulopathy LM, EM, IF

A

LM: diffuse thickening
EM: sub-epi spike and dome

27
Q

What is minimal change disease? LM, IF, EM

A

Kids: response to steroids
Lose negative change in GBM
ONLY see on EM: effacement of podocytes

28
Q

Presentation of minimal change disease

A

Selective proteinuria: lose albumin but not globulins

29
Q

What might minimal change disease progress to?

A

Focal seg glomerulo-sclerosis

30
Q

Clinico-pathological definition of focal-seg GS

A

Proteinuria (nephrotic) non-selective
FSGS
- Focal makes biopies hard
Effacement of foot processes

31
Q

Usually FSGS is primary and idiopathic. What are 3 secondary causes?

A
Focal scarring from another GN
Reflux nephropathy
Disproportion body:renal mass
HIV
Drug induced: heroin
32
Q

Treat FSGS

A

Not gonna - poor steroid response
Likely progress renal failure
High recurrence in transplant pts

33
Q

What is IgA nephropathy?

A

Nephrotic - recurrent hematuria

IgA deposits in mesangium -> alternative complement

34
Q

What is a systemic IgA disease that can cause IgA nephropathy, vasculitis, and skin purpura?

A

Henoch-Schoenlein purpura

35
Q

Presentation Alport’s

A

Males
Nephritis - hematuria w/ RBC casts
Deafness

36
Q

Pathogenesis Alport’s

A

T4 collagen mutation - don’t see any of this collagen on skin biopsy
X GBM synthesis

37
Q

What is thin membrane disease?

A

Asymptom hematuria

EM: diffuse thinning of GBM

38
Q

Is membrano-proliferative glomerulo-nephritis nephrotic or nephritic? Types

A

Mixed - kids/young adults

  1. Immune complex mediated - Hep C/B, SLE
  2. Complement - mutations or Abs vs complement regulating proteins
  3. W/ thrombotic microangiopathy
39
Q

Does SLE cause nephritis or nephrotic?

A

Nephritis

IF: look for all Ig, complement components