D. Glomerular Diseases Flashcards
(1)
(D. Glomerular Diseases)
1-3. Glomerular filtration barrier composed of what three things?
- foot processes form what?
- what kinds of filtration possible?
- pedicles (foot processes) of podocytes (viscearl epi of Bowman’s capsule)
- basal lamina (epi + endo)
- fenestrated epithelium of glomerular capillaries
- filtration slits
- charge and size
(2)
(D. Glomerular Diseases)
(Primary Glomerulonephritis)
- inflammatory/immune-mediated condition in which what is primary site of injury?
- cause ARF or CRF?
with or w/o nephrotic syndrome?
- renal glomerulus
- either
either
(3)
(D. Glomerular Diseases)
(Primary Glomerulonephritis)
(Pathogenesis)
(Immune/Inflammatory Mechanisms)
- In Situ immune complex formation - antibodies react directly with what?
- Circulating immune complex deposition… what happens here?
why do they accumulate?
- Cytotoxic Antibodies - may be directed at what?
- normal antigens of glomerular basement membrane (GBM) (Goodpasture’s) or with antigens planted in GBM (endo or exo)
- antigen-antibody (type III) complexes are filtered by GBM
physiochemical properties/hemodynamic factors
(serum sickness and SLE = system lupus erythmatosus)
- mesangial cells, endo cells, podocytes
(4)
(D. Glomerular Diseases)
(Primary Glomerulonephritis)
(Pathogenesis)
(Immune/Inflammatory Mechanisms - cont)
- Cell-mediated injury - what type?
- Activation of alternate complement pathway - reduced serum levels of what?
what deposited in glomeruli?
n the alternate complement pathway, C3 is directly cleaved to C3b by the interaction of C3 with bacterial polysaccharides, endotoxin, or aggregates of IgA in the presence of factors B and D and magnesium. This leads to the formation of what?
Individuals with this type of GN have a serum factor that does what?
- type IV (limited evidence of this in natural disease)
- factor B, properdin, C3
C3 and properdin (but no IgG)
C3bBb (alternate pathway convertase)
stabilizes the convertase (factor appears to be an Ig)
(5)
(D. Glomerular Diseases)
(Primary Glomerulonephritis)
(Mediators of Immunologic Injury)
1-6. what six?
- neutrophils
- C5b-9
- monocytes and macrophages
- platelets
- glomerular cels
- coagulation system
(6)
(D. Glomerular Diseases)
(Primary Glomerulonephritis)
(Mediators of Immunologic Injury)
- Neutrophils - infiltrate due to activation of what?
release what which degrade GBM?
- C5b-9 - the terminal membrane attack complex can directly damage what/stimulate what?
- Monocytes and macrophages - often seen where?
release what?
- platelets - cann aggregate in glomerulus when?
release what?
- glomerular cells - mesangial cells can produce what?
- coagulation system - fibrin is often present in the glomeruli in GN and may leak into what?
doing what?
- complement
lyctic enzymes and reactive oxygen
(release arachidonic acid metabolites which may participate in reducing GFR.)
- damage cells
stimulate mesangial cells to produce various chemical mediators (proteases, oxygen free radicals, interleukins)
- glomeruli with GN
chemical mediators
- during immune-mediated injury
arachidonic acid metabolites and growth factors
- many chemical mediators of inflammation
- Bowman’s space
stimluates proliferation of parietal epithelial cells and migration of macrophages
(7)
(D. Glomerular Diseases)
(Primary Glomerulonephritis)
(Some known causes of immune complex GN in animals (persistent antigenemia):)
- Dog - what five?
- Cat - what two?
- canine adenovirus 1
bacterial pyometra
dirofilariasis (heartworm)
systemic lupus erythematosus (SLE)
Lyme Disease (Borrelia Burgdorferi)
- Feline leukemia virus (Retro)
Feline infectious peritonitis (mutated Corona)
(8)
(D. Glomerular Diseases)
(Primary Glomerulonephritis)
(Some known causes of immune complex GN in animals (persistent antigenemia):)
- pig - what two?
- bovine - what one?
- horse - what one?
- hog cholera (classic swine fever; pestivirus)
African swine fever (asfivirus)
- bovine viral diarrhea virus (BVD; pestivirus)
- equine infectious anemia (EIA; retrovirus)
(9)
(D. Glomerular Diseases)
(Primary Glomerulonephritis)
(Consequences of Glomerular Injury)
(1. Changes in Renal Plasma flow (RPF) and glomerular filtartion rate (GFR))
1. RPF and GFR initially increased or decreased?
as compensatory mechs fail and damage progresses?
- damage to glomeruli results in ischemia to tubules that are dependent on their blood supply from affected glomeruli - leading to what?
- loss of nephrons and reduced GFR in remaining glomeruli may cause development of what?
- can be increased/decreased/or normal
will decrease
- atrophy and/or necrosis and loss of renal tubules with scarring
- renal failure
(10)
(D. Glomerular Diseases)
(Primary Glomerulonephritis)
(Consequences of Glomerular Injury)
((2) Sodium and fluid retention)
- Consistent features of acute GN - often accompanied by what?
acute GN may result in what?
- Na retention may occur due to what?
- In nephrotic syndrome, Na retetnion may be further increased by what?
- hypertension and edema
ARF
- reduced GFR or enchanced resportion is distal nephron
- low plasma volume stimulating renin-angiotensin-aldosterone system
(11)
(D. Glomerular Diseases)
(Primary Glomerulonephritis)
(Consequences of Glomerular Injury)
(3. Proteinuria)
1. damage to filtration barrier most importantl affects perm to what?
2. in dog, perm at what level?
3. in early damage thre is high perm to what?
what happens as gets worse?
- proteins
- btwn albumin (69,000) and hemoglobin (68,000)
in norma - hemoglobin passes but albumin retained
- albumin (but IgG impermabiilty)
size selectivity lost - all protein can escape
(12)
(D. Glomerular Diseases)
(SYNDROME: Nephtrotic Syndrome)
1-4. comprised of what four principal findings?
- proetinuria
- hypoalbuminemia
- generalized edema
- hyperlipidemia
(13)
(D. Glomerular Diseases)
(SYNDROME: Nephtrotic Syndrome)
(four principal findings)
- proteinuria - how bad?
- hypoalbuminemia - due to what?
- generalized edema - occurs due to what?
loss of plasma volume into tissue stimulates what?
- hyperlipidemia - low serum albumin results in increased synth of what?
reduced what?
changes in what?
- severe
( losses in excess of 200-300 mg/kg/day (normal dog < 30 mg/kg/day; normal cat < 20 mg/kg/day).)
- loss or protein in urine (exceed livers ability to synth)
- reduced plasma oncotic pressure
renin-angiotensin-aldosterone system to retain Na (and H2o)
(hypertension may contribute to edema)
- cholestoral rich LDL and VLDL
catabolism
transport of these lipids
(14)
(D. Glomerular Diseases)
(SYNDROME: Nephtrotic Syndrome)
- Thrombotic Diathesis - mainly due to loss of what in the urine?
also contributing to this are increases in what?
- antithrombin III
clotting factors V, VII, VII and fibrinogen as well as thrombocytosis
(15)
(D. Glomerular Diseases)
(Amyloidosis)
- amyloid is what?
- insoluble fibrillar protein with beta-pleated sheet conformation