Nephritic Syndromes- GK Flashcards

1
Q

Define Segmental

A

A portion of a glomerulus is involved

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2
Q

Define Global

A

All of a glomerulus is involved

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3
Q

Define Focal

A

Some of the glomeruli are involved

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4
Q

Define Diffuse

A

All or almost all of the glomeruli are involved

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5
Q

-itis

A

inflammation

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6
Q

-tic

A

pertaining to

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7
Q

What are podocytes?

A

Cells of the renal system

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8
Q

What is the four things does the kidney control?

A
  • H20
  • RBC production
  • acidity
  • BP
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9
Q

The kidney filters ______ and passes the _______ to the bladder for _______ as urine.

A

blood, waste, excretion

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10
Q

What is the average urine physiologic excretion in adults?

A

80mg/day

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11
Q

Pathologic proteinuria is equal to _____mg or greater over 24 hrs.

A

150

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12
Q

______ is the smallest plasma protein.

A

Albumin

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13
Q
  • comprises 20-40% of physiologic proteinuria (16-32mg/day)
  • Filtered more than other plasma proteins

What is this?

A

Albumin

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14
Q

T/F: microalbuminuria occurs before clinical proteinuria becomes evident and can therefore be used as an early diagnostic tool for early intervention in diabetic patients.

A

True

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15
Q

Microalbuminuria is defined as excretion of _____ to ______mg/day of albumin

A

30-300mg/day

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16
Q

Daily excretion of more than 3.5g of protein is called what?

A

nephrotic range proteinuria

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17
Q

What is the most common cause of proteinuria?

A

glomerular disease

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18
Q

What is the pathophys of Glomerular disease?

A

alteration of glomerular permeability –> injury to podocytes (renal cells), basement membrane, capillary endothelium or the mesangium.

Initially there is excess albumin w/eventual progression to larger proteins

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19
Q

What are 3 causes of proteinuria?

A
  1. Glomerular Disease MC
  2. Overflow proteinuria
  3. Tubular Proteinuria
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20
Q

What is this?

overproduction of smaller proteins overwhelming the reabsorptive ability of proximal tubule.

A

Overflow proteinuria

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21
Q

What is this?

Tubulointerstitial dz leads to diminshed reabsorptive capacity of the proximal tubule.

A

Tubular proteinuria

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22
Q

Glomerular Disease is classified into 2 classes. What are these two classes?

A

NephrITIC vs. NephrOTIC

Primary vs Secondary

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23
Q

Regardless of the classification, both types of Glomerular Dz cause what 3 things?

A
  • glomerular damage
  • hypoalbuminemia (low albumin in the blood since you have proteinuria)
  • Biopsy = gold standard = definitive diagnosis
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24
Q

What dz?

inflammatory process w/associated immunologic response that leads to renal glomeruli damage.

*allows blood cell passage*

A

NephrITIC** syndrome**

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25
Q

Overall Clinical Px of NephrITIC syndrome

A

“PHAROH”

P—Proteinuria (<3.5g/day)

H—Hematuria (coca-cola urine)

A—Azotemia (inc. creatinine & uria)

R—RBC casts

O—Oliguria

H–HTN (secondary to urine retention= edema is distal extremities LE>UE)

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26
Q

Facial Clinical Px of NephrITIC syndrome

A

Periorbital edema

Puffy, pale face

Swollen lips

27
Q

What do RBC casts in the urine signify?

A

severe inflammation

28
Q

Describe the nephritic spectrum.

A

Asymptomatic Glomerular Hematuria –> Nephritic Syndrome –> Rapidly progressive glomerular nephritis –> chronic glomerular disease

29
Q

What dz is this?

  • glomerular capillary wall, glomerular basement membrane (GBM), and Bowman’s capsule are severely injured
  • most severe & clinically urgent end of the nephritic syndrome
  • progression to renal failure in weeks-months, resulting in kidney transplants or dialysis
A

Rapidly Progressive Glomerulonephritis (RPGN)

30
Q

What are the 5 types of PRIMARY Nephritic Syndromes?

A
  1. Post-Inf Glomerulonephritis
  2. IgA nephropathy
  3. Henoch-Schonlein Purpura
  4. Pauci-immune glomerulonephritis (ANCA associated)
  5. Anti-Glomerular Basement Membrane Glomerulonephritis (Goodpasture Syndrome)

PIPHA

31
Q

Pathophys of what dz?

Group-A Beta Hemolytic strept

Immune mediated injury: circulating immune complexes with strept antigen deposit.

A

Post Infectious Glomerulonephritis

32
Q

Clinical Px of Post Infectious Glomerulonephritis

A
  • occurs 1-3 wks after GABHS infection like pharyngitis or impetigo
  • Oliguria
  • Edema
  • +/- HTN
33
Q

Dx of Post-infectious GN

A

Coca cola urine

UA: RBCs, red cell casts, proteinuria

ASO (antistreptolysin) titers high _** unless immune response blunted by ABX tx**_

34
Q

Tx of post-inf GN

A

supportive:

  • anti-hypertensives (ACE-I, ARBs)
  • restrict salt
  • diuretics (loop/furosemide/thiazide)
35
Q

Do steroids help with post-inf GN?

A

NO

36
Q

What is the main tx for post-inf GN?

A

treat the underlying infection!!

37
Q

What is the prognosis of post-inf GN in children?

A

GOOD

38
Q

What is the prognosis of Post-inf GN in adults?

A

less favorable: more prone to develop CKD or RPGN

39
Q

Also known as Berger’s disease….

A

IgA nephropathy

“I, GArima like burgers”

40
Q

Pathophys of which dz?

IgA deposition in the glomerular magnesium

same lesion is seen in Henoch-Schonlein Purpura

A

IgA Nephropathy

41
Q

IgA nephropathy is most common in _____(gender) and _______(population)

A

Male

children & young adults

I, gArima am not a male but I do love children & young adults

sorry, i know it was super corny lol

42
Q

Clinical Px of IgA Nephropathy

A
  • follows a URI or GI infection

- coca-cola urine 1-3 days after infection (unlike 1-3 weeks like in post-inf GN)

43
Q

Dx of IgA Neuropathy

A

Labs:

  • Hematuria
  • Proteinuria

Serum:

Inc. IgA levels, complement levels normal

44
Q

What is the prognosis of IgA Nephropathy?

A

1/3 of pts = spontaneous clinical remission

20-40% = CKD

Most imp: *Remaining* = chronic microscopic hematuria, stable serum creatinine.

45
Q

What is the most unfavorable prognostic indicator of IgA Nephropathy?

A

Proteinuria > 1g/d

46
Q

When are corticosteroids helpful in IgA Nephropathy?

A

proteinuria 1-3.5 g/d

47
Q

Tx of IgA Nephropathy

A

ACE-I or ARB if severe proteinuria

48
Q

What is the target BP of IgA Nephropathy?

A

<130/80

49
Q

Pathophys of what dz?

systemic small-vessel vasculitis w/IgA deposition in vessel walls

  • associated with an inciting infection: group A strept
A

Henoch-Schonlein Purpura (HSP)

50
Q

Clinical Px of Henoch-Schonlein Purpura

A
  • palpable purpura in buttocks & LE
  • arthralgias & abd sx (nausea, colic, melena)

melena = dark starry stool w or w/o blood.

  • dec. GFR (if inc, damage = nephrOTIC px)

“PAAG”

51
Q

Tx of Henoch-Schonlein Purpura

A

no definitive tx

case studies: plasmaphoresis (plasma exchange) & DMARD (dz modifying anti-rheumatic drugs)

52
Q

Pathophys of which dz?

  • seen with small vessel vasculitis
  • granulomatosis w/polyangiitis (Wegener’s granulomatosis)
  • eosinophillic granulomatosis w/polyangiitis (Churg-Strauss syndrome)
    • microscopic polyangiitis
A

Pauci-immune glomerulonephritis (ANCA associated)

53
Q

Clinical Px of Pauci-immune GN (ANCA associated)

A

look like a systemic inflammatory dz

  • fever, malaise, weight loss
  • purpura
  • if pt has granu w/poly, they will have resp tract sx with bleeding nodular lesions
54
Q

Dx for Pauci Immune GN (ANCA associated)

A
  • ANCA ++ (antineutrophil cytoplasmic antibodies)
  • UA: heamturia &proteinuria
55
Q

Tx for Pauci-Immune GN (ANCA associated)

A
  • high dose corticosteroids

- DMARDS

56
Q

What is the prognosis of Pauci-immune GN (ANCA Associated)

A

w/tx = 75% complete remission

w/o tx= poor prognosis

57
Q

Pathophys of which dz?

Glomerulonephritis + pulm hemorrhage

basement membrane injured from anti-GBM antibodies

A

Goodpasture syndrome

AKA

anti-glomerular basement membrane glomerulonephritis

58
Q

T/F: 1/3rd of pts with anti-GBM glomerulonephritis (Goodpasture syndrome) have no lung injury.

A

TRUE

59
Q

When is the peak incidence of Goodpasture syndrome (Anti-Glomerular Basement Membrane Glomerulonephritis)

A

20-30

60-70

60
Q

Clinical Px of Goodpasture syndrome (Anti-Glomerular Basement Membrane Glomerulonephritis)

A
  • preceded by URI
  • Hemoptysis, dyspnea
  • RPGN
61
Q

Dx of Goodpasture syndrome (Anti-Glomerular Basement Membrane Glomerulonephritis)

A

sputum: hemosiderin-laden macrophages

anti-GBM antibodies

CXR: pulm infiltrates

62
Q

Tx of Goodpasture syndrome (Anti-Glomerular Basement Membrane Glomerulonephritis)?

A

Plasmapheresis

corticosteroids

DMARDs

63
Q
A