Advanced Pathophysiology HESI
review
Acute Bronchitis patho - ANS-contamination or irritation of the bronchi. In more than 90% of
individuals, this is a self-restricting disease resulting from viruses.
Will not have high fevers and will have only scattered coarse wheezes on examination without
proof of pulmonary consolidation.
Chest X-ray exam is typically regular.
Acute chest syndrome in sickle cell disorder - ANS-ACS in SCD is described because the
presence of fever and/or new respiratory signs accompanied by using the presence of a new
pulmonary infiltrate on chest X-ray.
Scientific manifestations:
-mild respiration contamination
-acute respiration misery syndrome.
-presence of excessive hypoxemia is a useful predictor of severity and outcome.
Etiology:
- improved adhesion of sickle pink cells to pulmonary microvasculature within the presence of
hypoxia.
-contamination,
-pulmonary fats embolism,
- infarction.
Acute pertussis patho - ANS-gram poor bacterium Bordetella pertussis that produces mutiple
antigenic and biologically energetic products:
Pertussis toxin
Filamentous hemagglutinin (FHA)
Agglutinogens
Adenylate cyclase
Pertactin
Tracheal cytotoxin
Pathogenesis:
normally a toxin-mediated ailment. The bacteria connect to the cilia of the breathing epithelial
cells, produce pollution that paralyze the cilia, and purpose irritation of the respiration tract,
which interferes with the clearing of pulmonary secretions.
, Acute poststreptococcal glomerulonephritis - ANS-Cloudy tea coloured urine
Decreased output
Irritability
Ill look
Lethargy
Anorexia
Discomfort-headache, ab ache, dysuria
Periorbital edema
Facial edema in morning
Ab edema in nighttime
Mild to intense hypertension
Throats subculture
Urinalysis-proteinuria
Renal-BUN and creatine
ASO titer- nice for the presence of strept antibodies
AHase and ADNase-B
Serum complement (C3)
Chest x ray
Acute poststreptococcal glomerulonephritis patho - ANS--organization A streptococcal
contamination results in antibodies to form immune complexes which might be deposited inside
the glomerular capillaries.
-Complement, polymorphonucleocytes (neutrophils), and monocytes are activated.
-Inflammatory cytokines and poisonous oxygen radicals also are launched.
-altered permeability leads to proteinuria & hematuria
-Coagulation gadget activated and deposition of fibrin results in scarring
atherosclerosis pathophysiology - ANS--Inflammatory response
-Injury to endothelial lining
-LDL penetrates vessel wall
-inflammation/macrophage adhesion
-cytokines released
-release enzymes & oxygen radicals that oxidize LDL
-foam cells arise that form fatty streak
-collagen deposits & makes company plaque
CAD threat factors pathological - ANS-Major:
Advanced age
Gender (men > girls earlier than age fifty five, girls > men after age fifty five)
Dyslipidemia
Hypertension
review
Acute Bronchitis patho - ANS-contamination or irritation of the bronchi. In more than 90% of
individuals, this is a self-restricting disease resulting from viruses.
Will not have high fevers and will have only scattered coarse wheezes on examination without
proof of pulmonary consolidation.
Chest X-ray exam is typically regular.
Acute chest syndrome in sickle cell disorder - ANS-ACS in SCD is described because the
presence of fever and/or new respiratory signs accompanied by using the presence of a new
pulmonary infiltrate on chest X-ray.
Scientific manifestations:
-mild respiration contamination
-acute respiration misery syndrome.
-presence of excessive hypoxemia is a useful predictor of severity and outcome.
Etiology:
- improved adhesion of sickle pink cells to pulmonary microvasculature within the presence of
hypoxia.
-contamination,
-pulmonary fats embolism,
- infarction.
Acute pertussis patho - ANS-gram poor bacterium Bordetella pertussis that produces mutiple
antigenic and biologically energetic products:
Pertussis toxin
Filamentous hemagglutinin (FHA)
Agglutinogens
Adenylate cyclase
Pertactin
Tracheal cytotoxin
Pathogenesis:
normally a toxin-mediated ailment. The bacteria connect to the cilia of the breathing epithelial
cells, produce pollution that paralyze the cilia, and purpose irritation of the respiration tract,
which interferes with the clearing of pulmonary secretions.
, Acute poststreptococcal glomerulonephritis - ANS-Cloudy tea coloured urine
Decreased output
Irritability
Ill look
Lethargy
Anorexia
Discomfort-headache, ab ache, dysuria
Periorbital edema
Facial edema in morning
Ab edema in nighttime
Mild to intense hypertension
Throats subculture
Urinalysis-proteinuria
Renal-BUN and creatine
ASO titer- nice for the presence of strept antibodies
AHase and ADNase-B
Serum complement (C3)
Chest x ray
Acute poststreptococcal glomerulonephritis patho - ANS--organization A streptococcal
contamination results in antibodies to form immune complexes which might be deposited inside
the glomerular capillaries.
-Complement, polymorphonucleocytes (neutrophils), and monocytes are activated.
-Inflammatory cytokines and poisonous oxygen radicals also are launched.
-altered permeability leads to proteinuria & hematuria
-Coagulation gadget activated and deposition of fibrin results in scarring
atherosclerosis pathophysiology - ANS--Inflammatory response
-Injury to endothelial lining
-LDL penetrates vessel wall
-inflammation/macrophage adhesion
-cytokines released
-release enzymes & oxygen radicals that oxidize LDL
-foam cells arise that form fatty streak
-collagen deposits & makes company plaque
CAD threat factors pathological - ANS-Major:
Advanced age
Gender (men > girls earlier than age fifty five, girls > men after age fifty five)
Dyslipidemia
Hypertension
