NEPHROLOGY Flashcards
WHAT IS GLOMERULONEPHRITIS?
Inflammation of nephrons and glomerulus due to an infection where the antigen-antibody complexes attack the nephrons.
> can be sudden (acute) / gradually (chronic)
WHAT IS NEPHRITIS?
LEAK OF RED BLOOD CELLS + MILD PROTEINS > hematuria > oligouria > less urine volume > azotemia - elevation in blood urea nitrogen + serum creatinine levels > arterial hypertension
WHAT IS NEPHROSIS?
> HEAVY PROTEINURIA > 3.5g/day
hypoalbuminemia
hyperlipidemia
edema
OUTLINE MORPHOLOGICAL PHASES OF GLOMERULAR INJURY?
> EXUDATIVE PHASE
PROLIFERATIVE PHASE
SCLEROTIC PHASE OF INFLAMMATORY PROCESS
OUTLINE INJURY MECHANISM FOR GLOMERULONEPHRITIS?
- IMMUNE COMPLEX ASSOCIATED INJURY
2. INJURY ASSOCIATED WITH ANTIBODY TO GLOMERULAR BASEMENT MEMBRANE
DESCRIBE IMMUNE COMPLEX ASSOCIATED INJURY TO NEPHRONS?
> presence of antigen-antibody complexes
circulating in blood or in situ of glomerulus
in situ complexes formed when Ab directed at glomerular Ag or foreign bodies + get trapped in glomerulus»_space; SLE
Ag-Ab complexes entrapped + precipitates in glomerular basement membrane
DESCRIBE INJURY ASSOCIATED WITH ANTIBODY TO GLOMERULAR BASEMENT MEMBRANE
> Ab directed against Ag of basement membrane
Ab reacts with Ag
this is seen with immunofluroscent staining for IgG
Ab + Ag reaction > activates inflammatory mediators
inflammation > glomerular injury
godpasteurs syndrome
WHAT IS GODPASTEURS SYNDROME
> group of acute illnesses affecting lungs + kidneys
autoimmune disorder
immune system > antibodies attack lungs + kidneys
GLOMERULONEPHRITIS
PULMONARY HEMORRHAGES
ANTIGENS ATTACKING ALVEOLAR BASEMENT MEMB.
OUTLINE MEDIATORS OF GLOMERULAR DAMAGE?
1. COMPLEMENT > role of inflammatory process > activated by immune complexes > attract neutrophil polymorph > increase vascular permeability > membrane damage
- POLYMORPHONUCLEAR LEUKOCYTES
> attracted by C5a
> bind to complexes by C3 + FC receptors
> release lysosomes in response to trapped complexes
> further increase damage to glomerular basement memb
3. CLOTTING FACTORS > mediate glomerular damage > fibrin - entraps platelets due to C3 + FC receptors > micro thrombi formation > degranulation > release of vasoactive peptides > increase vascular permeability
OUTLINE MORPHOLOGICAL DIAGNOSTICS FOR GLOMERULONEPHRITIS
- Ab tagged with fluorochrome
- localise immuinoreactants in glomerulus - Ultrastructural studies
- position of immune complexes
- basement membrane reactions
- epithelial changes - Renal biopsy
- light microscopy > 20 glomeruli
- immunofluorescence > 5 glomeruli
- electron microscopy > 2 glomeruli - Glomerular hypercellularity
- Podocytes
- intracapillary > mesangium + endothelium
- intercapillary > mesangium
- extracapillary > bowmans capsule - Thickening of glomerular capillary loops
- deposition of immune complexes
- increase GBM material
- infiltrate abnormal materials - amyloid - Basement membrane immune deposition
- sub epithelial
- intramembranous
- sub endothelial - Hyalinosis
- Sclerosis/ Collagenous scarring
- irreversible damage due to chronic process
WHAT POST-STREPTOCOCCAL GLOMERULONEPHRITIS
> 10-14 days after upper respiratory infection w/ nephritic strains of beta hemolytic streptococci.
DESCRBINE PATHOGENISIS OF POST-STREPTOCOCCAL GN?
> immune complexes of strept. Ag-Ab > circulate in blood > deposit in glomeruli OR > immune complexes formed in situ from bacterial Ag that are trapped in glomeruli
OUTLINE CLINICAL MANIFESTATIONS OF POST-STREPTOCOCCAL GN?
> most common in children > proteinuria > hematouria > hypoalbuminemia > edema > hypertension > renal failure >> leading to slow progression of chronic glomerulonephritis or rapid progression of progressive glomerulonephritis
DESCRIBE MICRO OF POST-STREPTOCOCCAL GN?
> diffuse + inflammation of glomeruli
enlarged + hypercellular glomeruli
> due to proliferation of mesengial cells + inflammatory inflitration of neutrophils + macrophages
DESCRIBE ELECTRON MICROSCOPY OF POST-STREPTOCOCCAL GN?
> inflammatory cells appear in capillaries attached to basement membrane
osmophilic dense deposits of immune complexes
> form large humps on subepithelium