Lecture 1 Flashcards
General Pathology
Common reaction of cells and tissue to injury
•acute inflammation in response to an infection
Systemic Pathology
Examines alterations and underlying mechanisms in organ-specific diseases
•Ischemic heart disease
Etiology
The cause of the disease.
Genetic or acquired
Pathogenesis
Biochemical and molecular mechanisms of its development
Morphological changes
Structural alterations induced in the cells, tissues, and organs of the body
Clinical manifestations
Functional consequences which lead to clinical symptoms and signs of
Pyknosis
Condensation of chromatin
Karyorrhexis
Fragmentation into smaller particles: “nuclear dust”
Karyolysis
Dissolution of nuclear structure and lysis of chromatin by enzymes (DNase and RNase)
Post perfusion injury
Over supply of oxygen after removal of obstruction can lead to damage by oxygen radicals and reactive oxygen species.
- Hydrogen peroxide H2O2
- Superoxide O2-
Hydroxyl radicals OH*
Atrophy
Decrease in size of cell, tissue, organ, or entire body
Hypertrophy
Increase in size of cell, tissue, organ or entire body
(Such as the heart during hypertension and the skeletal muscles of body builders)
Hyperplasia
Increased number of cells found within a tissue or organ
(BPH in men, calluses)
Metaplasia
Change of once cell type into another
Coagulative necrosis
Most common form of necrosis
- Often caused by anoxia
- Characterized by rapid inactivation of cytoplasmic hydrolytic enzymes, preventing the lysis of tissue, which retain their original form
-Typically involves solid internal organs, such as the heart, liver and kidney
Liquefactive necrosis
- Dissolution of tissues
- Become soft and diffluent
- Most common in the brain, where cells lose their contours and are “liquefied” (Semifluid mush)
- Typically due to brain infarcts
- Consequence of leukocytes releasing lytic enzymes which turn solid tissue into liquid pus
Caseous necrosis
Special form of coagulative necrosis with limited liquefaction
- Center of a tuberculosis granuloma becomes necrotic (mycobacteria)
- Tissue is yellow-white and appears as a “cheesy” consistency
- Also common in fungal infections (histoplasmosis)
Enzymatic fat necrosis
Special form of liquefactive necrosis caused by the action of lipolytic enzymes
- Limited to fat tissue, usually around the pancreas
- Pancreatic enzymes degrade adjacent fat tissue into glycerol and free fatty acids (FFA)
- FFA bind calcium forming calcium soaps
- Liquified necrosis with calcium soap
Dystrophic calcification
Secondary changes.
Necrotic tissue attract calcium salts in the absence of systemic mineral imbalances
Necrosis
Cause: Exogenous
Mechanism: Vital processes inhibited
Multiple cells affected
Swollen, ruptured cell morphology
Cell membrane is ruptured
Outcome: phagocytosis by neutrophils
Apoptosis
Cause: exogenous or endogenous
Mechanism: energy dependent, vital processes active
A single cell affected
Cells are rounded up and fragmented into apoptotic bodies
Cell membrane isn’t functionally intact
Outcome: phagocytosis by macrophages and non-professional macrophages
