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Path Part Deaux > Mt Notes Kidneys > Flashcards

Mt Notes Kidneys Flashcards

1
Q

3 pathogenic mechanisms of glomerular pathology

A
  • circulating immune complex deposition
  • anti-glomerular basement membrane glomerulonephritis
  • heymanns glomerulonephritis
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2
Q

circulating immune complex deposition

A

⋅ Type III Hypersensitivity reaction
⋅ Formation of antigen-antibody immune complex outside kidney that circulates and deposits in the
subintimal space, between the endothelial cells and the glomerular basement membrane of kidney ⋅ Phagocytes can’t engulf the Ag/Ab complex because they are hidden, so they release enzymes. The
enzymes damage the Ag/Ab complex, the structure of the glomerulus, as well as the vascular walls leading
to vasculitis. Function of the glomerulus is lost due to the damage. ⋅ Eventually develops vasculitis with damage of vascular walls

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3
Q

anti-glomerular basement membrane

A

⋅ Type II Hypersensitivity reaction (complement-dependent), autoimmune ⋅ Antigen forms against GBM, Ag/Ab complex forms in the kidneys (within glomerulus), attract phagocytic
cells causing chemical injury to GBM – can engulf entire glomerulus

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4
Q

heymanns glomerulonephritis

A

⋅ No specific type of hypersensitivity reaction, combination of several types ⋅ Ag/Ab complex forms against the visceral epithelial cells (podocytes) within kidneys. ⋅ Fragments of bacterial walls and dead cells get caught in the space between the glomerular basement
membrane and the podocytes. Viruses like to go to where these fragments are.
-sub epithelial deposits

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5
Q

Mesangial Cells

A

– part of the interstitial tissue within the glomeruli. They are active contractile cells that
produce and release collagen and matrix (mucopolysaccharides).
⋅ Monocytes can also be found in the space between capillaries and mesangial cells
– Located in the space between the capillaries – Contractile – Can produce components of connective tissue and participate in process of proliferation (healing) – Can produce erythropoietin – Can also produce some physiologically active substances
– Interstitial space

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6
Q

Juxtaglomerular Cells “Security”

A

– produce renin (most important), control blood pressure in the afferent
arteriole.
– Immune system of kidney function, control blood pressure in afferent arteriole – Angiotensin II, which functions to increase blood pressure – Decrease of glomerular filtration rate due to decrease BP (At least 50 mL/Hg)

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7
Q

Visceral Epithelial Cells

A

– aka podocytes
● Cover the outermost layer ● Podocytes (foot-like cells) aka foot processes
(pedicels, or pedicles)
● Filtration slits exist between podocytes

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8
Q

Glomerulonephritis

A

-Glomerular cells are extremely permeable to water and absolutely impermeable to proteins like albumins. Protein found in the urine is usually pathological.
⋅ There are two types of Glomerulonephritis – nephritic and nephrotic syndromes.
⋅ Type 3 Hypersensitivity

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9
Q

2 types of nephritic syndromes

A
  • ACUTE PROLIFERATIVE (POST-INFECTOUS-STREPTOCOCCAL) GLOMERULONEPHRITIS
  • RAPIDLY PROGRESSIVE (CRESCENTIC) GLOMERULONEPHRITIS
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10
Q

ACUTE PROLIFERATIVE (POST-INFECTOUS-STREPTOCOCCAL) GLOMERULONEPHRITIS

A
  • Type II Hypersensitivity reaction
  • B-hemolytic streptococcus A bacteria (pyogenes)
    (nephrogenic)
  • molecular mimicry
  • proteinuria and swelling of the eyes in children
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11
Q

3 types of Rapidly progressive a=(aka crescent) glomerulonephritis

A

-TYPE I: ANTI-GLOMERULAR BASEMENT MEMBRANE GLOMERULONEPHRITIS
-TYPE II: IMMUNE COMPLEX DEPOSITION
TYPE III: PAUCI-IMMUNE

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12
Q

TYPE I: ANTI-GLOMERULAR BASEMENT MEMBRANE GLOMERULONEPHRITIS

Type II hypersensitivity

A

Goodpasture’s Syndrome

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13
Q

Goodpasture’s Syndrome

A 
type I: antiglomerular basement membrane glomerulonephritis
-Type II hypersens
-autoimmune
-basement membranes of lung and kidneys
-hemoptysis
treat with plasmapheresis
-exudate in arterioles
-immune complex mediated inflamation
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14
Q

kinds of TYPE II: IMMUNE COMPLEX DEPOSITION

type III hypersensitivity

A
  • Systemic Lupus Erythematosus
  • Post Infectious Glomerulonephritis
  • henoch-Scholein Purpura
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15
Q

Systemic Lupus Erythematosus

A
  • autoimmune against cells and nuclei of cells
  • Antinuclear antibodies ANA and anti-smith antibodies
  • lupus nephritis
  • lung involvement leads to cerebral vasculitis
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16
Q

Antinuclear antibodies ANA

A

-ANA against double strand DNA
-ANA against Anti Smith antigen (antibodies)
-

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17
Q

Henoch-Scholein Purpura

A

-men under 30
-/\ IgA production
attacks 4 major syndromes
1-cutaneous
2-articular
3-abdominal
4- kidney

1,2,3 have 100% survival rate
4- 70% survival

18
Q

IgA deposits where?

A

in the mesangium

19
Q

Henoch-Scholein Purpura Cutaneous syndrome

A

multiple subcutaneous hemorrhages up to 2 cm typically found on the thighs, buttocks and abdomen

20
Q

Henoch-Scholein Purpura articular syndrome

A

arthralgia,

on and off benign pain to joints with NO inflammation

21
Q

Henoch-Scholein Purpura abdominal syndrome

A

gastroduodenitis,

painful inflammation of the stomach and duodenum

sometimes with bleeding

22
Q

Henoch-Scholein Purpura kidney syndrome

A

rapidly progressive glomerulonephritis (crescentic nephritis)

o The more crescents present, the shorter the life span

o Once kidneys reach 80% crescentic, prognosis is very bad

23
Q

TYPE III: PAUCI-IMMUNE

A
  • Wegener’s Granulematosus
  • Polyarteritis Nodosa (aka Periarteritis)
  • Berger’s Disease (aka IgA Nephropathy)
  • Alport Syndrome (aka Hereditary Glomerulonephritis)
24
Q

diseases that are nephritic syndrome

A
  • goodpasture’s syndrome
  • systemic lupus erythematosus
  • post infectious glomerulonephritis
  • henoch-scholein purpura
  • Wegener’s granulematosus
  • polyarteritis nodosa (Periarteritis)
  • berger’s disease (IgA nephropathy)
  • alport syndrome (hereditary glomerulonephritis)
25
Q

diseases that are associated with nephrotic syndrome

A
  • Minimal Change Disease aka Lipoid Nephrosis
  • Membranous Glomerulonephritis
  • Focal Segmental Glomerulonephritis
  • Membranoproliferative Glomerulonephritis
  • diabetes mellitus
  • acute pyelonephritis
  • chronic glomerulonephritis
  • amyloidosis
26
Q

nephritic syndrome

A
  • azotemia
  • oliguria
  • decrease GFR
  • uremia
  • hematuria
  • hypertension
27
Q

nephrotic syndrome

A
  • massive proteinuria (>3.5g/day)
  • hypoalbuminemia
  • generalized edema
  • muehrcke’s lines/nails/leukonychia striata (white stripes)
  • hyperlipidemia
  • cardiac tamponade
  • kidney amyloidosis
28
Q

Wegener’s granulematosus

A

Classified by Necrotic Vasculitis of three major systems:
1. Upper Respiratory Tract – soft tissue and bones decay (facial skull), death occurs within
months, supporative inflammation accompanied with bad smelling person
2. Lower Respiratory Tract – cavities form in the lungs due to vasculitis
o Causes decrease in pressure in the pulmonary artery
3. Rapidly Progressive Glomerulonephritis – crescentic nephritis

29
Q

Polyarteritis Nodosa (aka Periarteritis)

A

– Vasculitis and pouching all over body except the lungs and aortic arch (medium and small)
● Narrowing of the artery lumen caused by swelling of the vascular wall (due to inflammation),
leading to ischemia of the tissue
– Arterial walls become thin, brittle, and distend in pouches (nodes) further weakening wall – Pouching out of the walls of the arteries compress adjacent tissues, causing atrophy of these tissues,
therefore infarctions
– High mortality rate, swelling of soft tissues/loss of soft tissue with no damage to bones
– Autoimmune disease, unknown cause. It may be a genetic predisposition involving antigens.
– Associated with Wet Gangrene

30
Q

Berger’s Disease (aka IgA Nephropathy)

A

– Most common glomerular disease in the world and most common cause of gross hematuria
– Not part of rapidly progressive
– Usually develops in children and young people, particularly boys.
– Gross hematuria (most common) develops within 1-2 days of non-specific respiratory infection (common
cold), lasts for several days and subsides on its own. Occurs again in several months
● (or after urinary or gastrointestinal tract infection, which may be associated with
development of gross hematuria)
– Patient will complain of loin pain (low back, buttocks)
– Increased findings of IgA, which are deposited into mesangium (hallmark of disease)
● Compare to purpura, which is a systemic disease ● If missed, it is not a real big deal. (chronic nephritis)

31
Q

BUERGER DISEASE aka Thromboantitis Obliterans

A
  • autoimmune vasculitis of middle to small sized arteries
  • TIBIAL, RADIAL, ULNAR a.
  • “disease of smoking people”
  • young people 30-35
  • instep claudication
  • reynauds syndrome
  • thrombophlebitis
  • dry gangrene
  • india, japan, israel genetic predisposition
32
Q

Alport syndrome

aka hereditary glomerulonephritis

A
  • boys = 10
  • nerve deafness, lens dislocation, posterior cataracts, corneal dystrophy
  • chronic glomerulonephritis
33
Q

Things that lead to chronic Glomerulonephritis (GN)

A
  • Poststreptococcal GN
  • rapidly progressive (crescent) GN
  • Membranous GN
  • Focal Glomerulosclerosis
  • Membranoprliferative GN
  • bergers IgA nephropathy
34
Q

Amyloidosis

A

– pathologic proteins (Amyloid AA or Amyloid BB) deposit into tissue interstitium and create pressure
atrophy in the kidneys, liver, heart and skin . or brain
-nephrotic syndrome= kidney amyloidosis

35
Q

most likely nephritic syndrome to become chronic GMN

A

rapidly progressive crescent GMN

36
Q

most likely nephrotic syndrome to become GMN

A

Focal segmental GMN

37
Q

gouty GMN

A
  • itching due to urine excretion through the skin

- CNS infection

38
Q

Acute Pyelonephritis

A

– infection of the urinary tract, commonly traveling up the ascending pathway through the
ureter and into the kidney paths and parenchyma
-renal pyramids broke down
-necrotizing papilitis (suppurative)
-assoc w/ diabetes mellitus
-usually e coli or strep, g- rods
-chronic pyelonephritis is #1 cause of female Chronic GMN

39
Q

diabetic nephropathy

A
  • glomerular lesions
  • thickening of basement membrane
    - diffuse glomerulosclerosis
    - nodular glomerulosclerosis
  • renal vascular lesions
  • pyelonephritis
40
Q

Diffuse glomerulosclerosis

A

– diffuse increase of mesangial matrix, mesangial cell proliferation

41
Q

Nodular glomerulosclerosis

A

– characterized by Kimmelstiel-Wilson lesions (ball-like deposits of a
laminated matrix within the mesangium)

42
Q

Chronic GMN presentation

A
  • kidney becomes granulated
  • breath smells like urine (uremia)
  • manifestations of either nephrotic or nephritic syndromes or both

Path Part Deaux (14 decks)

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