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Nephritic Syndromes Flashcards

1
Q

What is azotemia?

A

Kidney damage and incr BUN and creatinine

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2
Q

Describe Nephritic syndrome in one word.

A

decr GFR

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3
Q

Four outcomes of decr GFR

A

1.** Slight protenuria** (decr. plasma oncotic pressure)—->EDEMA
2. RBC Cast (describe as Coca-cola urine or smoky)
3. Decr. Blood supply to kidneys–>azotemia
4. Faliure to filter Na+ and Cl- –>Incr. Plasma Hydrostatic pressure–>EDEMA+ Hypertension

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4
Q

Presentation in Nephritic syndrome?

A

-<3.5g/day of protein, Dark urine, swelling (periorbital or lower limbs), Fatigue (uremia).

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5
Q

Diagnosis

Dark urine,slight protenuria, fatigue and on auscultation you hear pericardial rub and EKG shows ST segment elevation everywhere..

A

Nephritic syndrome pesenting with** pericarditis **due to uremia (irridates pericardium)–>progress to pericardial effusion.

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6
Q

Where is cast formed in the anatomy of nephron?

A

collecting tubules because urine is mostly concentrated.

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7
Q

Is Hematuria a unike diagnosis of Nephritic syndromes?

A

NO.
-Urethral, ureter,bladder,penile ruptures can all cause bleeding but NOT cast.

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8
Q

Name the 3 divisions of your Nephritic syndromes?

A

1.Type 3 Hypersensitivity(Acute Post-strep Glomerulonephritis/IgA Nephropathy/Diffuse Proliferative Glomerulonephritis)
2.Multiple cause(Membranous Proliferative Glomerulonephritis/Rapidly Progressive Glomerulonephritis/Pauci Immune Vasculitis)
**3.Collagen related **(Alport syndrome)

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9
Q

Diffrent types of Group A Strep skin infections?

A

pharyngitis,cellulitis,impetigo(“honey-crusted”lesions),erysipelas

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10
Q

Diagnosis

Honey-coomb crusted lesion on face in a 6yr old, 1 week later has dark urine with azotemia, 24Hr hour urine test shows 2.5g /day

A

PSGN

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11
Q

Can you get PSGN and Rheumatic Fever at same time?

A

NO, either **M protein **is Nephrogenic or rheumatogenic.

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12
Q

JONES criteria uesed for?
Dukes citeria?

A

-RF
-Endocartitis

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13
Q

What do you see?

PSGN
IF,LM,EM

A

-IF:subEpithelial IgG,C3 deposits IgM(Granular pattern)”starry sky”
-LM:Hypercellular glomeruli**
-EM: **subEpithelial Humps **(usually diagnostic)

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14
Q

Why PSGN and RF takes at least 1-2 to develop?

A

Your body has to create immune response towards M protein.

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15
Q

PSGN has decr C3?

A

Yes, when immune complex deposits subepi it will activate continously complement system,

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16
Q

Diagnosis

DNAse and streptolysin O antibodies on serum with pharyngitis or impetigo

A

Group A Strep

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17
Q

Diagnosis

A

SubEpithelial Humps

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18
Q

prognosis of Children and Adult in PSGN?

A

-children (95% reslove)
-Adults(may progress to renal insufficency), may also be causd by Stap Aureus.

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19
Q
A

RBC cast

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20
Q
A

-Achantosis (Di-morphic RBC)–>squeezing througt nephron (looses shape)
-RBC cast

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21
Q

Two important virulence F for Group A strep

A

M protein, Exotoxin B (ass with the skin infections)

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22
Q

Diffrence between RF and PSGN

A

RF=Type 2 Hypersensitivity
PSGN=Type 3 Hypersensitivity

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23
Q

IgA nephropathy (Berger Dis.) characteristics

A

-Immune deposits in mesangium intraglomerular cell (NOT extraglomerular)–> stimulates cytokine (mediates damage)
-Ass with GI and Resp infections.
-IF: vey specific–>immune complex mesangium. Still considered granular pattern but very diffrent. Involves IgA deposition
-*LM; *mesangial proliferation.

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24
Q
A

-IF; mesangial deposition
-LM;mesangial proliferation

IgA nephropathy

25
Q

Diagnosis

recurrent episodes of hematuria since childhood, episodes following Upper Resp Tract infect, diarrheal illnes, slow renal decline…

A

Iga Nephropathy (Berger dis.)

26
Q

**Diffrence **timeline between IgA nephropathy and PSGN

A

PSGN (1-2 weeks)
IgA nephropathy (1-2 days)

27
Q

Berger disease mechanism?

A

-Abnormal IgA antibodies produced,where your immune system makes IgG against them a promotes deposistion on your mesangial cells–>activates cytokine mediated damage.

28
Q

Diagnosis

decreased glycosylation of O-linked glycans in Hinge region of Ig

A

IgA nephropathy (Berger disease)

29
Q

IgA nephropathy ass confusion?Why?
-PSGN
-IgA vasculitis (Henoc Purpura)

A

-IgA vasculitis can cause Berger disease, but you see palbable purpura rash in lower extremity and buttocks, arthriti.
-IgA nephropathy only causes nephropathy.

30
Q

Diffuse Proliferative Glomerulonephritis (DPGN) highly Ass with….

A

SLE (Lupus Nephritis)

31
Q

Type of deposition

A

**SubEndothelial deposits. **
-“Wire Looping”–hypercellular

32
Q

DPGN,meaning…

A

Diffuse means >50% og glomeruli are affected.

33
Q

Rapidly Progressive Glomerulonephritis (RPGN) Types (3)

A

1.Type 1: Idiopathic or Good Pasture syndrome–>Type 2 Hypersensitivity
2.Type 2 (PSGN or SLE Nephritis)–>Type 3 Hypersensitivity
3.Type 3 (Paucini immune vasculitis)–>NO immune complex formation

34
Q

What ass does Exotoxin B of Group A strep has?

A

Skin infections.

35
Q

IgA nephropathy is ass with GI and Respiratory secretions,Why?

A

-When you get infections of this sites, your immune system secrtes more abnormal IgA.

36
Q

Does IgA nephropathy decr C3?

37
Q

What deposits does IgA nephropathy involve?

38
Q

Prognosis of RPGN (Rapidly progressing Glomerulonephritis)

A

-Poor prognosis, RUPTURE of basement membrane–>rapid decline of kidney function.
- **Fibrinoid necrois. **

39
Q

Diagnosis

Anti-GBM antibodies towards Type 4 collagen in the alpha-3-chain.
1.Type of Hypersensitivity?
2.Presentation
3.Treatment

A

-Good Pasture syndrome (Type 1 RPGN)
1.Type 2 Hypersensitivity
2.Hematuria (kidney damage) and Hemoptysis (alveolar damage)
3.Plasmapheresis

40
Q

Composition?

A

-“Crescent-moon shape”(mainly made up of FIBRIN)
-Seen in **ALL **Rapidly progressing Glomerulonephritis.
-Fibrin (fibrinoid necrosis)+plasma proteins (C3)+monocyte+macrophages+Bowman space parietal cells
-The **expansion of Bowman space is due to parietal cell proliferation **

41
Q

What type of deposit do you see in Type 2 Rapidly Progressive Glomerulonephritis?

A

**Sub-Endothelial **
IM:Granular pattern.

42
Q
A

IF:Linear pattern (deposits in only GBM)
-Good Pastures

44
Q

Types of Paucini immune vasculitis?

A

1.Eosinphilic Granulomatosis
2.Microscopic Granulomatosis
3.Granulomatosis with Polyangitis (Wegner)

45
Q

Diagnosis

Hemoptysis,Hematuria, nasal septal perforation,otitis media, mastotitis,
-C-ANCA/PR3-ANCA
-Non-casseating Granulomas

A

Granulomatosis Polyangitis

46
Q

What does all Pauccini immune vasculitis have in common?

A

-All relate ANCAS’s
-All are** IF NEGATIVE **(NO immune complex is present)
-crecentic moon shape

47
Q

Diagnosis

Hematuria,Hemoptysis
-MPO-ANCA/P-ANCA
-NO granulomas
-Ass with penincillin

A

Microscopic Polyangitis (NO URT association)

48
Q

How do we diagnose Pauccini syndrome since they all are IF negative?

A

-Look for ANCA involvmenet.

49
Q

Celle responsible for Crescent moon shape in RPGN

A

Bowna’s parietal cells

50
Q

DIAGNOSIS

Ass with ANCA

A

Pauccini immune vasculitis

51
Q

Diagnosis

“Can’t see, can’t pee, can’t hear a bee”

A

***Alport syndrome
-Eye problems (retinopathy, ant lenticonus), sensineural deafness, glomerulonephritis.
-Irregular thickening of basement membrane.

52
Q

-Alport syndrome mutation ?
-People mayorly affected

A

X linked Dominant of Type 4 collagen.
-Affects mayorly very youn MALE

53
Q

Diagnosis

A

-Alport syndrome
-EM:Irregular thin areas and thicker areas “basket weave”

54
Q

Patient with some collagen disorder, describe lesion.

A

Alport syndrome (retinopathy)

55
Q

IgA nephropathy is damage mediated by what?

56
Q

Where does IgA Nephroptahy deposist?

A

mesangial cells.

57
Q

Differential diagnosis of hematuria girl following URT infection 1 week ago?

A

-IgA nephropathy and PSGN.

58
Q

Dipstick of 2g per day?and other examples

A

2+
3g=3+
4-20g=4+

RENAL (17 decks)

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