Pa Tho Physiology of Glomerulonephritis
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PATHOPHYSIOLOGY PREDISPOSING FACTORS Age Gender Nationality Heredofamilial PRECIPITATING FACTORS Lifestyle High sodium and protein diet Exposure to Group A Beta Deposition of antigen- antibody complex in glomerulus Leukocytes infiltrate the glomerulus Increased production of epithelial cells lining the glomerulus If not treated Passage of protein in the nephrons Damage nephrons allow the passage of large molecules like RBC hematuria Thickening of the glomerular filtration Renal damage especially the nephrons Antigen-antibody product Antigen Group A Beta Hemolytic streptococcal (Sore throat, impetigo, viral proteinuria Edema or anasarca Decrease osmotic IgG combines with host antibodies Streptococcal neuraminidase may alter host immunoglobulin G Scarring and loss of glomerular filtration membrane Hypertension Renin angiotensin II promotes Decrease of blood flow and affects the Renin- Angiotensin- Decrease in circulating blood volume IgG/anti-IgG immune complex are formed and then collect in the Decreased glomerular filtration rate (GFR) Acute glomerulonephritis Alteration in excretion of sodium Inflammation of glomerular cap If treated MEDICATION: Antibiotic drugs High dose Corticosteroid Immunosuppressant Loop diuretic medications Antihypertensive Progresses towards renal failure Result in kidney death Abnormal urinalysis (microhematuria) PROGNOSIS: With aggressive treatment, patient with rapidly progressive glomerulonephr itis is DIET: Dietary protein and sodium Severe hypertension Encephalopathy Hypertensive retinopathy Hypertensive encephalopathy Rapidly progressive glomerulonephritis Chronic renal failure End-organ damage in the central nervous system and cardiopulmonary Clinical manifestations: Headache Malaise Flank pain Circulatory overload DEATH PROCEDURES: bed rest Plasma exchange (plasmapheresis) Dialysis
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Transcript of Pa Tho Physiology of Glomerulonephritis
PATHOPHYSIOLOGY
-
PREDISPOSING FACTORS
Age
Gender
Nationality
Heredofamilial
PRECIPITATING FACTORS
Lifestyle
High sodium and protein diet
Exposure to Group A Beta Hemolytic streptococcus
Deposition of antigen-antibody complex in glomerulus
Leukocytes infiltrate the glomerulus
Increased production of epithelial cells lining the
glomerulus
If not treated
Passage of protein in the nephrons
Damage nephrons allow the passage of large molecules like
RBC
hematuria
Thickening of the glomerular filtration membrane
Renal damage especially the nephrons
Antigen-antibody product
Antigen
Group A Beta Hemolytic streptococcal
(Sore throat, impetigo, viral infection)
proteinuria
Edema or anasarca
Decrease osmotic pressure
IgG combines with host antibodies
Streptococcal neuraminidase may alter host immunoglobulin
G (IgG)
Scarring and loss of glomerular filtration membrane
Hypertension
Renin angiotensin II promotes vasoconstriction
Decrease of blood flow and affects the Renin-Angiotensin-
aldosterone-system
Decrease in circulating blood volume
IgG/anti-IgG immune complex are formed and then collect in
the glomeruli
Decreased glomerular filtration rate (GFR)
Acute glomerulonephritis
Alteration in excretion of sodium
Inflammation of glomerular cap
If treated
MEDICATION:
Antibiotic drugsHigh dose CorticosteroidImmunosuppressantLoop diuretic medicationsAntihypertensive agentsCytotoxic agents
Progresses towards renal failure
Result in kidney death
Abnormal urinalysis (microhematuria)
PROGNOSIS:
With aggressive treatment,
patient with rapidly
progressive glomerulonephritis is
greatly improved.
DIET:
Dietary protein and sodium restriction
Severe hypertensionEncephalopathyPulmonary edema
Hypertensive retinopathyHypertensive encephalopathyRapidly progressive glomerulonephritisChronic renal failureNephrotic syndrome
End-organ damage in the central nervous system and cardiopulmonary system
Clinical manifestations:
HeadacheMalaiseFlank painCirculatory overloadEngorged neck veinCardiomegaly
DEATH
PROCEDURES:
bed restPlasma exchange (plasmapheresis)Dialysis
