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01 Renal Respiratory > 6 Glomerular disease > Flashcards

6 Glomerular disease Flashcards

0
Q

Nephrotic syndrome

A
  • Proteinuria >3.5g/day
  • Hypoalbuminemia
  • Edema from loss of plasma oncotic pressure
  • Hyperlipidemia

(lipiduria and hypocoaguability from C and S loss)

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1
Q

3 different kinds of immune kidney disease

A

1) Immune complex deposition between endothelum and BM as well as deposition in BM and subepithelium.
2) Antibodies to BM or to glomerular antigens
3) Cytokines created by inflammatory cells

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2
Q

Nephritic

A
  • Mild proteinuria
  • Hematuria- RBCs, RBC casts, and dysmorphic RBCs
  • HTN
  • Edema
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3
Q

Acute Glomerulonephritis causes

A
  • IgA Nephropathy
  • post infectious GN
  • Anti GBM disease/ Goodpasteure’s
  • Small vessel Vasculitis
  • Lupis Nephritis
  • Membranoproliferative glomerulonephritis
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4
Q

IgA Nephropathy Clinical presentation

A

Nephrotic and Nephritic

1) Hematuria (frequently with URI)
* 50-60% episodic gross hematuria
* 30% persistant microhematuria
* 10% acute GN or nephrotic syndrome
2) Proteinuria
3) Dysuria and loin pain
4) HTN in advanced patients

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5
Q

IgA Nephropathy Histo

A
  • Mesangial hypercellularity
  • IF: mesangial IgA deposition
  • EM: Electron dense deposits
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6
Q

IgA nephropathy course and management

A
  • 40% will develop CKD
  • Fish oil may low progression
  • ACEi for BP control
  • Corticosteroids may be helpful for progressive disease
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7
Q

Henoch-Schoenlein Purpura Presenation

A
  • Small vessel vasculitis
  • IgA Deposition in skin and many organs
  • Lower body nonblanching purpura
  • Arthralgias
  • ABD pain, vomiting, melena, hematochzia
  • hematuria, proteinuria, Rare RF
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8
Q

Post- infectious GN

A

Nephritic

  • HTN, azotemia, oliguria, cola/tea colored urine
    • low c3
    • anti streptolysin O
    • RBC casts
    • Mild proteinuria
  • follows GAS- 7-14d post pharyngitis, 14-28 post skin infection
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9
Q

Post-infectious GN histo

A
  • Enlarged hypercellular glomeruli
    • diffuse proliferation of mesangial, endocapillary, and neutrophils
    • sometimes crescenteric
  • IF: granular capillary wall and IgG and C3 in mesangium
  • EM: Mesangial and sub epithelial HUMP LIKE DEPOSITS
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10
Q

Post strep GN treatment and course

A

95% children- conservative management
*1% KF
60% of adults recover promptly

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11
Q

Rapidly progressing progressive GN Causes

A

Nephritic syndrome

  • Crescenteric
  • Rapid progression to RF

1) Anti GBM- Goodpastures
2) Immune complex GN
* Lupis
* Post- infectious
* Cryoglobulinemia
3) Anca Assocaited GN (pauci immune)

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12
Q

Rapid progressive GN Histo

A

Segmental necrosis early in the disease

Cellular crescent

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13
Q

Anti GBM/Goodpasteure’s Signs/causes

A

Nephritic

  • M>F
  • Hemoptysis
  • Pulmonary infiltrates
  • GN

Caused by circulating anti GBM
* a3 chain of collagen IV

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14
Q

Goodpastures diagnosis/treatment

A
  • anti GBM antibody test
  • Linear IgG and C3 on IF
  • crescenteric

Treatment

  • Plasmapheresis
  • prednison
  • Cytoxan
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15
Q

Pauci-immune GN

A

Nephritic
* Idopathic, Microscopic polyangitis, Wegeners Granulomatosis, Churg-strauss syndrome

Histo

  • little immune deposition on IF
  • Crescenteric
  • ealy segmental necrosis
16
Q

Wegener’s Granulomatosis

A

Nephritic

  • c-ANCA pos in 80%
  • UR smptoms - sinusitis, nasal lesions, hemoptysis
  • purpura
  • Nephritis

Biopsy-
Pauci-immune crescenteric GN

17
Q

Nephrotic Syndrome

A

Primary

  • Membranous nephropathy
  • Focal Segmental Glomerulosclerosis
  • Minimal Change Disease (80% of kiddos with nephrotic)

Secondary:

  • Diabetes, SLE, Amyloidosis
  • HIV, Hep B and C, Syphilis
  • NSAIDs, gold, penicillamine
18
Q

Nephrotic syndrome treatments

A
  • ACE or ARB to reduce proteinuria
  • Statin to decrease lipids
  • Diuretics and salt restriction
19
Q

Minimal change disease course and presentation

A

Nephrotic

  • 2-6 yo.
  • 5% ESRD progression
  • spontaneous remissionscan occur
  • Steroid treatment induces remission but 75% relapse
  • less relapses after puberty
20
Q

Minimal change disease causes in adults

A

NSAIDs
Neoplasms HODGKINS
Syphilis/HIV

21
Q

Minimal change histo

A

Appears normal on LM
IF negative or IgM positive
EM: PODOCYTE FOOT PROCESS EFFACEMENT

22
Q

Minimal change treat

A

Corticosteroids (may need longer treatments in adults)

23
Q

Membranous Nephropathy

A

Nephrotic

  • Heavy proteinuria
  • later Azotemia and HTN
  • Hypercoagulability and renal vein thrombosis.

*Most common caucasian adult nephrotic disease
20% cause by secondary causes
*HBV, SLE, Neoplasm- lumg, colon, stomach, breast, non hodgkins, drugs

24
Q

Membranous nephropathy histo

A

LM: GBM spikes and diffuse thickening,
IF: IgG granular deposits on GBM (Granular BM staining)
EM: Subepithelial dposits

25
Q

Membranous neuropathy course

A

1/3 spontaneous remission
1/3 partial stable remission
1/3 slow progression

Treat: if no poor prognositc factors

  • Sometimes ACEi or ARBs
  • Steroids/immunosuppressants
26
Q

FSGS (foccal sgmental glomerulosclerosis) overview

A 
Nephrotic (most common AA idopathic nephrosis)
Agressive:
*HTN/HEmaturia
*Renal dysfunction
* ESRD 5-20 years later
27
Q

FSGS Types (3)

A

Primary (Acute onset nephrotic syndrome)
Secondary (slow increasing proteinuria and renal insufficiency)
Hereditary ( Slight diaphragm mutations)

28
Q

FSGS causes

A
  • HIV
  • NSAIDs/Heroin
  • Massive obesity
  • Previous glomerular disease
  • loss of functional renal mass
29
Q

FSGS histo

A

LM: focal and segmental glomerular sclerosis:
*Capillary Collapse, Hyaline and lipid deposition (adhesion to bowmans capsule

IF: Negative or IgM and C3 in mesangium or scars

E: Podocyte effacement and

30
Q

FSGS Treatment

A
  • ACEi to decrease proteinuria
  • corticosteroids may induce remission
  • immunosuppresives for relapsing and Steroid refractory
  • 50% ESRD at 10 yrs.
31
Q

Mixed nephrotic nephritic

A
  • Membranoproliferative GN

* SLE

32
Q

MPGN (membranoproliferative GN)

A

Nephrotic or nephritic

  • Proteinuria and Hematuria
  • HTN in 33% patients
  • LOW C3
33
Q

Secondary MPGN causes

A

SLE
Cryoglobulinemia
HCV, HBV, endocarditis, abscesses
Neoplasm

34
Q

MPGN histo

A
  • LM: Hypercellular glomeruli, endocapillary proliferation, LOBULAR GLOMERULI
  • IF: Granular C3 deposition
  • EM: Subendothelial deposits
35
Q

SLE

A
  • Can cause many different renal diseases- Commonly diffuse and proliferative GN
  • Lupis with HTN is frequently GN
36
Q

SLE nephritis Histo

A

LM: lotts of immune cells
EM: Subendothelial deposits

37
Q

SLE Nephritis treatment

A

*BP control
*Lipid control
* Extrarenal treatments
ClassIV: 25% renal failure by 5-10 yrs

01 Renal Respiratory (34 decks)

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