Summer Patho Flashcards
Etiology
is the origin of disease, underlying causes and modifying factors. -WHY a disease develops)
Pathogenesis
refers to the steps of in the development of the disease -( HOW a disease develops)
Morphology
Changes in gross or microscopic appearance of cells and tissues and biochemical alterations in body fluids (blood and urine).
Adaptation
achieving a new steady state and preserving viability and function.
Principal adaptive responses are;
hypertrophy, hyperplasia, atrophy, metaplasia
Causes of cell death:
Ischemia, infections, toxins, and immune reactions.
CELL DEATH
is a normal and essential process in embryogenesis, the development of organs, and the maintenance of homeostasis.
Hypertrophy
(an increase in the size of the individual cells & ultimately the entire heart)- Myocardium subjected to persistent increased load, as in hypertension or with a narrowed stenotic valve adapts by undergoing hypertrophy.
3 processes that affect cells and tissues:
intracellular accumulations, pathological calcification, and cell aging.
Adaptations
are reversible changes in the number, size, phenotype, metabolic activity, or functions of cells in response to changes in their environment.
Physiologic adaptation
represent responses of cells to normal stimulation by hormones or endogenous chemical mediators (ex.- the hormone-induced enlargement of the breast and uterus during pregnancy).
Pathologic adaptations
responses to stress that allow cells to modulate their structure and function and thus escape injury.
Hypertrophy
increase in the size of cells resulting in an increase size of the organ. NO NEW CELLS JUST BIGGER CELLS. -can be physiologic or pathologic.
Hyperplasia
an adaptive response in cells capable of replication. Increase # of cells - increased organ size.
Mechanisms driving cardiac hypertrophy;
mechanical triggers-stretch
trophic triggers- soluble mediators that stimulate cell growth, such as adrenergic hormones.
Hyperplasia
Can be physiologic (1.hormonal hyperplasia-proliferation of the glandular epithelium of the female breast 2. Compensatory hyperplasia- residual tissue grows after removal or loss of part of an organ)
and pathologic.
Pathologic hyperplasia
caused by excessive hormonal or growth factor stimulation.
Atrophy
Shrinkage in the size of the cell by the loss of cell substance. Cells decrease in size, therefore organ size diminishes. Diminished function but are not dead. Decreased workload, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, and aging.
Mechanisms of atrophy
consist of a combination of decreased protein synthesis and increased protein degradation in cells.
Metaplasia
a reversible change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult type.
Reversible cell injury
If the damaging stimulus is removed, the injury has typically not progressed to severe membrane damage and nuclear dissolution.
Cell death
Continuing damage, the injury becomes irreversible, the cell cannot recover and it dies.
2 types of cell death
- Necrosis- damage to membranes is severe, enzymes leak out lysosomes, enter the cytoplasm, and digest the cell.
- Apoptosis - When a cell is deprived of growth factors or the cell’s DNA or protein are damaged beyond repair, the cell kills itself.
Causes of cell injury:
Oxygen deprivation, chemical agents, infectious agents, immunologic reactions, genetic factors, nutritional imbalances, physical agents, aging.
Fibrinoid necrosis
Only detected by histological examination
Coagulative necrosis
Affected tissues become firm, the injury denatures structural proteins and enzymes. It is also a characteristic of INFARCTS (areas of ischemia necrosis) in all of the solid organs except the brain.
Liquefactive necrosis
seen in focal bacteria, fungal infections, because microbes stimulate the accumulation of inflammatory cells and enzymes of leukocytes digest (liquefy) the tissue. Tissue liquefied due to hydrolytic enzymes from tissue and/or PMNs
See in abscesses and CNS tissue
Gangrenous necrosis
Condition of the limb, that has lost its blood supply and has undergone coagulative necrosis involving multiple tissue layers.
Caseous (“cheese-like”) necrosis
often in foci of tuberculous infection. Yellow white appearance of the area of necrosis.ype of necrosis which is a collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border.
Fat necrosis
refers to focal areas of fat destruction, resulting from the release of activated pancreatic lipase’s into the substance of the pancreas and the peritoneal cavity.
types of fat necrosis (3)
Enzymatic necrosis (pancreatic necrosis of fat)Traumatic necrosisNecrosis of abdominal fat of cattle.
Fibrinoid necrosis
Bright pink and amorphous ‘hyaline’ deposits of immune complexes (Ags + Abs), complements with leaked out fibrin in the walls of arteries; not a true type of necrosis
