PATHOLOGY Flashcards
Apoptosis aka
Programmed cell death.
Apoptosis characteristics
cell shrinkage, chromatin condensation, membrane blebbing, and
formation of apoptotic bodies, which are then phagocytosed.
Apoptosis when
embryogenesis, hormone -induction (menstruation), -immune cell– mediated death,
- injurious stimuli (e.g., radiation, hypoxia),
- atrophy.
Enzymatic degradation of a cell resulting from exogenous injury.
Necrosis
Characterized by enzymatic digestion and protein denaturation, with release of
intracellular components.
Necrosis
Necrosis
Different types and there locations
Morphologically occurs as -coagulative (heart, liver, kidney), -liquefactive (brain),
- caseous (tuberculosis),
- fat (pancreas), -fibrinoid, or gangrenous (limbs, GI tract).
Cell injury reversible or irreversible Cellular swelling?
Reversible
Cell injury reversible or irreversible Nuclear chromatin clumping?
Reversible
Cell injury reversible or irreversible Decreased ATP synthesis?
Reversible
Cell injury reversible or irreversible Ribosomal detachment?
Reversible
Cell injury reversible or irreversible Glycogen depletion?
Reversible
Cell injury reversible or irreversible Plasma membrane damage?
Irreversible
Cell injury reversible or irreversible Lysosomal rupture?
Irreversible
Cell injury reversible or irreversible Ca2+ influx → oxidative phosphorylation?
Irreversible
Cell injury reversible or irreversible Nuclear pyknosis, karyolysis, karyorrhexis?
Irreversible
Cell injury reversible or irreversible Mitochondrial permeability?
Irreversible
cells in acute Inflammation
Neutrophil, eosinophil, and antibody mediated
cells in chronic Inflammation
Mononuclear cell mediated:
Phases of Inflammation
Fluid exudation Leukocyte activation Fibrosis Acute Chronic Resolution
Free radical injury what initiates it
Initiated via
radiation exposure, metabolism of drugs (phase I), redox reaction,
nitric oxide,
transition metals, leukocyte oxidative burst.
Inflammation 5 features
Characterized by
- rubor (redness),
- dolor (pain),
- calor (heat),
- tumor (swelling) -functio lassa (loss of function).
cells in acute Inflammation
Neutrophil, eosinophil, and antibody mediated
cells in chronic Inflammation
Mononuclear cell mediated:
Phases of Inflammation
Fluid exudation Leukocyte activation Fibrosis Acute Chronic Resolution
Free radical injury what initiates it
Initiated via
radiation exposure, metabolism of drugs (phase I), redox reaction,
nitric oxide,
transition metals, leukocyte oxidative burst.
Free radical injury when is it a big problem
reperfusion after thrombolytic therapy.
Cytokines involved in acute inflammation
IL-1, IL-6, TNF-alpha
Stages of Leukocyte extravasation
- Rolling
2. Tight binding 3. Diapedesis 4. Migration
Leukocyte extravasation what mediates migration?
chemotactic signals (e.g., cytokines).
Leukocyte extravasation what mediates Tight binding?
ICAM-1 on vascular endothelium binding to LFA-1 on
the leukocyte.
Leukocyte extravasation what mediates Rolling?
E-selectin on vascular endothelium binding to Sialyl-LewisX
on the leukocyte.
What is Diapedisis
––leukocyte travels between endothelial cells and exits blood vessel.
Free radical injury what initiates it
Initiated via
radiation exposure, metabolism of drugs (phase I), redox reaction,
nitric oxide,
transition metals, leukocyte oxidative burst
Free radical injury when is it a big problem
reperfusion after thrombolytic therapy
What happens in different phases of Inflammation?
Fluid exudation
Increased vascular permeability, vasodilation, endothelial injury
What happens in different phases of Inflammation?
Leukocyte activation
Emigration (rolling, tight binding, diapedesis) Chemotaxis (bacterial products, complement, chemokines) Phagocytosis and killing
What happens in different phases of Inflammation?
Chronic
Mononuclear cell mediated: Characterized by persistent destruction and repair Granuloma—nodular collections of macrophages and giant cells
Maintains granulomas
TNF-a
Free radical injury what are the antioxidants
vitamins E and A
