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RENAL > Nephrotic syndromes > Flashcards

Nephrotic syndromes Flashcards

1
Q

Nephrotic characteristics?

A

1.RBC barrier mantained (NO RBC cast and NO HEMATURIA). No Glomerular endothelium inflamation.
2.Protein Barrier ruptured–>podocytes( >3.5 g/day )in a 24HR. urine test
3.Hyperlipedemia (increase liver activity)–>Fatty cast (oval bodies) or Maltose cross (polarized light)
4.DECR albumin
5.Edema (decr plasma oncotic pressure)
6.Decr Ig (incr risk infections)
7.Hypercoaguble state (decr, Anti-Thrombin3)

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2
Q

Nephrotic table….

A
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3
Q

Types of nephrotic syndromes

A

Primary (direct sclerosis and inflam to podocytes)
1.Minimal change, 2. Focal segmental, 3. Membranous Nephropathy
Secondary (Indirect)
1.Diabetic Nephropathy
2. Systemic amyloidosis

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4
Q

Light Microscopy (LM) and Immunoflorascense unchanged (IF)

A

Minimal change disease
(EFFACEMENT)=flatten out podocytes.

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5
Q

What type of Nephropathy present with SELECTIVE PROTENURIA?

A

MINIMAL CHANGE DISEASE (only damages the foot processes of podocytes and nothing else).

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6
Q

4 I’s Nephropathy + (Minimal Change disease)

A

**Idiopathic
recent Immnunization
**recent Infection
* Immune stimulus (Bee sting)

Hodkins Lymphomas; rel. of anbormal cytokines by reedsternberg cells. –>T cell cytokines rel

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7
Q

Hodkin Lymphoma cells and markers

A

CD 15+ and CD 30+ with 2 owls eye.

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8
Q

Minimal change disease other name

A

Lipoid nephrosis

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9
Q

Diagnosis

Child treated with corticosteroids with recent history of immunization that presented with: edema, >300mg cholesterol, >3.5g/ day protein and negative IF and LM.

A

Minimal change disease
-Ass. children most commonly
-Adults can have it
-Corticosteroid treatment is effective.

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10
Q

Why corticosteroids work in Minimal change disease?

A

Inhb. NF-KB (transcripton factor for potent cytokines like TNF alpha), Minimal change being related to cytokine release, greatly supress it.

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11
Q

Effacement child

A

Lipoid nephrosis

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12
Q

Histological Diag.

  • <50% of biopsy glomerulus affected, only segments affected (not entirley) and thickening of glomerulus
  • -Hyaline and effacement presentt.
A

(FSGS)Focal Segmental Glomerulosclerosis.

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13
Q

non-selective protenuria in Nephrotic syndromes

A

-Focal segmental glomerulosclerosis
-Membranous nephropathy

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14
Q

FSGS 1* and 2* associations.

A

1* Idiopathic.
2* Heroin, HIV infect, Congenital malformations, sickle cell, interferon tretament (Hepatitis B and C), obesity

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15
Q

mutations of nephrin and porocin protein located on slit diamphragm

A

1* FSGS association

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16
Q

1.LM:sclerosis + Hyalinosis
2.Pinkage color, what stain?

A

1.FSGS
2.PAS stain

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17
Q
A

FSGS
-Sgmental Focal thickening (protein deposits)+ Hyalinosis (PAS stain)

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18
Q

Prognosis od FSGS

A

within 10 yrs 50% develop ENRF

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19
Q

Membranous nephropathy other name

A

Membrane glomerulonephritis

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20
Q

Membranous glomerulonephritis 1*

A

Antibodies (IgG) towards phospholipase A2 (M TYPE),present serum
-phospholipase A2 are present in podocytes.

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21
Q

Where are phospholipase A2 recep located?

A

membrane of podocytes

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22
Q

Membranous nepgropathy 2*

A

-Drugs (NSAIDS, penincillamine, Gold–.R.A)
-Infection (Hepatitis B and C and syphylis)
-SLE
-Solid tumors (COLON most comm, lung , melanoma)

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23
Q

Membrabous Glomerulonephritis

A

Silver stain

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24
Q

Describe

A

Membranous Nephropathy
-Diffuse capillaries, GBM thickening (Complex deposition)+ NO HYPERCELLULARITY

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25
Q

SUB-EPITHELIAL DEPOSITS (imm complex) + spike and dome app

A

Membranous nephropathy

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26
Q

Membranous Nephropathy Prognosis

A

slow onset progression (many yr). Normal creatine .
-Exception is in Thrombosis (more quickly lose of function; ELEVATED creatinine)

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27
Q

site of thrombosis in Membranous Nephropathy

A

RENAL VEIN (quick onset of depression)

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28
Q

Membranous nephropathy response to corticosteroids

A

POOR

29
Q

DIAGNOSIS

A

Systemic Amyloidosis
-Most common side of aggregation is kidney
-LM: Congo red stain (PINK AMYLOID DEPOSITS)
-Polorized ligth:apple green
-Locolized in mesangium

30
Q

Most common cause of End stage renal disease in US

A

Diabetic Glomerulonephritis

31
Q

Cause of Diabetic glomerulonephritis

A

Non-enzymatic glycation

32
Q

Diagnosis

A

Wilson nodules+mesangial expansion+Glomerular basement membrane thickening.

33
Q

Diagnosis

Obtrs. efferent arterioles due to non enzymatic glycation–> afferent arteriole dilation , Further incr pressure->INCR GFR (Hyperfiltration)–>mesangial cell expansion

A

Diabetic Glomerulonephritis

34
Q

Beta 2 microglobulin deposition

A

Amyloidosis

35
Q

Ass syndrome with amyloidosis

A

Carpal Tunnel synddrome

36
Q

Pathophysiology of carpal tunnel syndrome

A

-entrapment of median nerve–>parasthesia, but sensory is spared due to cutaneous branch enters hand external to carpal tunnel.
-Thenar muscle atrophy .

37
Q

What related secondary nephroticc syndrome (Diabetic and Amyloidosis)

A

Both are associated with mesangium.

38
Q

Tram Track app in silver stain

A

Membranous Glomerulonephritis.

39
Q

Where do you see also Maltose cross?

A

Babbesia and Minimal change disease

40
Q

Effacemnet do you see it where

A

Membronous nephropathy (Hyaline) and Minimal change.

41
Q

Crecent shape of RPGN made up off what and what cell proliferates?

A

Made primarly of Fibrin but parietal cells over grow

42
Q

Lumpy-bumby pattern on sliver stain

A

Focal segmental glomerulonephritis, most likely** HIV Nephropathy** telated FSGS

43
Q

Lung-Hepatitis-Rheumatid Arthritis

A

Membranous Nephropathy 2*

44
Q

Nephrin Factor nephropathy

A

Membranous Proliferative Type 2

45
Q

What does your nephritic factor do?

A

Overactivates C3 convertase–>depletion of C3 in serum.

46
Q

Diagnosis

Intramembronous deposition of a ribonlike homogenous extremly electron dense material of unknown material.

A

Membranous Proliferative Glomerulonephritis Type 2

47
Q

MPGN ass…

A

Hepatitis C and B.

48
Q

Pathogenesis of Type 1 MPGN..

A

-Chronic infection will promote formation of immune complexes causing deposition sub-Endothelial–>mesangial ingrowth “interposition”–>TRAM-TRACK app
-Activates classical and alternate pathways.
-All due to chronic localization of immune complex.

49
Q

Pattern of deposition in Type 1 MPGN..

A

Sub-Endothelial with mesangial interposition, cretaing TRAM-TRACK app.

50
Q
A

-Sub-Endothelial deposits with interposed mesangial cells cretaing TRAM-TRACK app.

51
Q
A

-Homogenous dense electron deposits of unkonwn material
-MPGN Type 2

52
Q

Mixed cryoglobulinic vasculitis ass with what nephritic syndrome?

A

MPGN Type 1

53
Q

Diagnosis

Triad of weakness, arhthralgia, palbable purpura
-Biospy you see TRAM TRACK app.

A

Mixed Cryoglobulinic Vasculitis(ass with Hepatitis C)

54
Q

Pathogenesis of Mixed Cryoglobulinic Purpura

A

Abn IgG antibodies that agglutinate RBC in cold temp–> small clot formation that may lead to skin cotting (palbable purpura), kidney clotting (glomerulonephritis), joint clotting (arthritis).

55
Q

Pathogenesis of diabetus…

A
56
Q

How does Uncontrolled Diabetus Mellitus cause Hyperfiltration.

A

-non ezymatic glycation of efferent arterioles cause narrow lumen–>decr blood supply to kidney–>afferent arteriole dilation–>combination of both leads to HYPERFILTRATION –>incr glomerular pressure–>glomerulat hyperthrophy+incr capillary surface area

57
Q

What does sorbitol to Fructose consumes and effect?

A

NADPH.
-NO Gluthaione is reduced–>Incr ROS

58
Q

How does INCR ROS cause damage?

A

Lipid peroxidation, Protein oxidative modfification,DNA damage.

59
Q

How does hyperglycemia cause Retinpathy?

A

-by your Advanced Glycated products promoting release of VEGF –>leads to retinopathy.

60
Q

How does hyperglycemia accelerate atherogenesis?

A

By** LDL trapping** (in your endothelial cells)

61
Q

What product does hyperglycemia form?

A

-Advanced Glycated Products.
-via **Non-enzymatic Glycation. **

62
Q

What product does hyperglycemia form?

A

-Advanced Glycated Products.
-via **Non-enzymatic Glycation. **

63
Q

1.First onset of Diabetic kidney disease is what?
2.Timeline from diagnosis of Diabetus

A

1.micro-albuminuria (30-299mg/day).
2.5-10yr.

64
Q

-Clinical diabetic kidney?
-Timeline from micro-albuminuria?

A

Clinical albiminuria (>300mg/day)
-5-10yrs from onset of micro-albuminuria.

65
Q

What the role of angiotensin 2 in kidney?

A

-constricts efferent arterioles.

66
Q

What drugs can we give to slow down progression from micro-albuminuria to clinical albuminuria?Why?

A

-ACE inhb. and ARB–>dilate efferent arterioles (reduce Hyperfiltration)

67
Q

Diagnosis

Broad masses of eosinophilic acellular material in the glomerulus

A

Amyloidosis (NO basement membrane thickening)

68
Q

Diagnosis

Chronic Hemodyalisis ass with signs of tingling in hands…

A

AMYLOIDOSIS (ass with Carpal Tunnel Syndrome)

RENAL (17 decks)

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