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Renal Exam 1 > Kidney Diseases Glomerulopathies > Flashcards

Kidney Diseases Glomerulopathies Flashcards

1
Q

Glomeruli are responsible for

A

Filtration of blood

Produce ultra-filtrate

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2
Q

Endothelial fenestrae

A

Pores that allow filtration of blood to occur

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3
Q

Kidney is a

A

Bunch of glomeruli and tubules that controls electrolyte balance and acid base balance and produces renin

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4
Q

Define Glomerulonephritis

A

Inflammation

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5
Q

Primary disease =

A

Affects the glomerulus FIRST

Autoimmune

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6
Q

Chronic glomerulonephritis =

A

Most common cause of CKD

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7
Q

Primary Glomerulopathies (high potential to progress to chronic)

A 
Rapidly progressive (crescentic)
Membranous glomerulopathy
Minimal-change disease
Focal segmental glomerulosclerosis
Membranoproliferative
IgA nephropathy
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8
Q

Acute proliferative

A

Associated with infection
Last for a few weeks and then goes away
No serious consequences

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9
Q

Amyloidosis

A

Disease in which you have deposition of certain stage proteins in different parts of the body
Leads to an inflammatory reaction

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10
Q

Systemic disease with glomerular involvement

A

Lupus
DM
Amyloidosis

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11
Q

Glomerulus Pathology

A

Blood enters through afferent arteriole
Blood leaves through the efferent arteriole
Primary ultra-filtrate accumulates in the Bowman’s capsule
When blood leaves it has to pass through endothelial basement membrane and podocytes

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12
Q

Juxtaglomerular cells produce

A

Renin after sensing a change in BP

(Stretch = increase BP –> they act

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13
Q

Kidney filtration barrier

A

Between podocytes there is space which is where the filtrate occurs

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14
Q

Pathogenesis Main

A

Antibody-Mediated Injury (in situ immune complex deposition)

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15
Q

Antibody-Mediated Injury

A

Immune complexes formed inside you leads to circulating antibodies and antigens in the kidney
A lot of immune complexes in the plasma and kidney
Cytotoxic antibodies go and kill certain cells

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16
Q

Complement Pathway

A

T cells go to the kidney and destory some of the kidney structure –> complement is activated –> destroy cells via cell lysis through terminal complement complex which leads to holes in the cytoplasmic membrane

17
Q

Where do antibodies deposit

A

Within the filtration barrier (under the endothelium, within basement membrane, under the epithelium)

18
Q

Testing for Antibody-Mediated Injury

A

Use antibodies to detect antibody complexes

Important bc glomerularnephritis is very harsh

19
Q

Epithelial injury Pathogensis

A

After deposition, destruction of components of the barrier (basement membrane, podocytes) –> process are becoming flat –> podocyte effacement –> barrier is leaky and proteinuria

20
Q

Mediator of Injury Pathogenesis

A

Immune complexes can active classical branch of complement

21
Q

C5b-9

A

Incorporate themselves into the membrane and make holes –> cell lysis

22
Q

C5a

A

Potent inflammatory mediator

Attracts chemokines greatly and causes production of oxidants, cytokines, chemokines

23
Q

What disease progress to chronic glomerulonephritis?

A

Crescentic GN
Focal segmental glomerulosclerosis
Membraneoproliferative GN
Membranous nephropathy

24
Q

Clinical manifestations:

A 
Nephritic syndrome
Rapidly progressive 
Nephrotic syndrome
Chronic Renal Failure
Isolated urinary abnormalities
25
Q

Nephritic syndrome Symptoms

A 
HEMATURIA
Azotemia
Proteninuria
Oliguria
Edema
HTN
26
Q

Nephrotic syndrome Symptoms

A 
PROTEINURIA >3.5 g/d
Hypoalbuminemia
Hyperlipidemia
Lipiduria
Edema
27
Q

Nephritic syndrome Etiology

A 
Primary Glomerular Disease (acute proliferative GN)
Systemic disease (SLE)
28
Q

Nephrotic syndrome Etiology

A

Primary: Membranous GN, minimal change disease (children- given steroids and everything goes back to normal = nephrotic)) and focal segmetnal

29
Q

Nephrotic Syndrome Systemic Disease

A

DM
Amyloidosis
SLE
Malignancy

Renal Exam 1 (8 decks)

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