I. Pathophysiology A. Algorithm: Predisposing Factors: Etiology: Precipitating Factors
I. Pathophysiology A. Algorithm: Predisposing Factors: Etiology: Precipitating Factors
I. Pathophysiology A. Algorithm: Predisposing Factors: Etiology: Precipitating Factors
PATHOPHYSIOLOGY
A. ALGORITHM
Formation of antibody
Proliferation of epithelial
cells lining glomerulus &
cells between
endothelium & epithelium
of capillary
membrane
Swelling capillary
membrane & infiltration
with leukocytes
↑ Permeability of base
Signs and symptoms:
Presence of membrane
Edema
Occlusion of the
capillaries of the
glomeruli vasospasm of
afferent ventricles
↓ Glomerular filtration
rate Signs and symptoms:
Tachycardia Treatment:
Abdominal Penicillin G750,
distension with 000 IV q6 ANST.
Retention of H2O & Na; Paracetamol 160g
abdominal girth of
hypovolemia; 52 cm IV q4 PRN.
circulatory congestion Lung crackles Furosemide 15mg
Tea colored urine IV q8
Captopril 25mg ½
TAB BID
ACUTE
GLOMERULONEPHRITIS
Explanation
Acute Glomerulonephritis is the sudden onset of inflammation of the glomeruli from infections
originating from different parts of the body.
In the patient's case, predisposing and precipitating factors increased his vulnerability to
acquire the disease, such as gender, family history of hypertension and age. AGN mostly affects
boys aged 5-9. The United States has recorded 0.02% of their total population, or 61,422
incidence within a year. That makes 1:4,428 people in the US is affected or had suffered from
AGN..
It is generally accepted that the most common cause of AGN is an infection that is
brought by group-A haemolytic streptococcus. This are infections that commonly misinterpreted
as common sore throat and left unattended. Antigen-antibody circulating immune complexes are
subsequently deposited along the glomerular basement membrane (GBM). Antibodies to
streptoccocus (eg antistreptolysin O) are formed in the circulation. The immune response causes
inflammation of the glomeruli. Scarring on kidney tissues then occurs, leading to the decrease in
ability of the kidney to filter the blood and produce urine. Structurally, cellular proliferation
leads to an increase in the number of cells in the glomerular tuft because of the proliferation of
endothelial, mesangial, and epithelial cells. The proliferation may be endocapillary (ie, within the
confines of the glomerular capillary tufts) or extracapillary (ie, in the Bowman space involving
the epithelial cells). In extracapillary proliferation, proliferation of parietal epithelial cells leads
to the formation of crescents, a feature characteristic of certain forms of rapidly progressive GN.
Leukocyte infiltration is indicated by the presence of neutrophils and monocytes within the
glomerular capillary lumen and often accompanies cellular proliferation. This process increases
glomerular permeability and capillary pressure, causing large molecules, such as proteins, to leak
through the glomerulus. Hence, high protein levels in the urine decrease oncotic pressure,
allowing fluid buildup or edema to happen. When the glomerular filtration rate has severely
decreased, it leads to a decrease in urine output and sodium and water retention. As a result, it
leads to tachycardia, abdominal distension with abdominal girth of 52 cm, a presence of lung
crackle and a tea colored urine. Furthermore, if retention of H2O & Na; hypovolemia; circulatory
congestion will not be cured it can result to a rupture of the kidney. If rupture is to be treated, the
client will need medications. If treatment will be successful, it will lead to wellness of life.