Cell injury, inflammation & repair Flashcards
What is apoptosis?
What is its function?
Programmed cell death which occurs when a cell dies through activation of a tightly regulated internal suicide program.
To eliminate unwanted cells selectively, with minimal disturbance to surrounding cells and the host.
How does apoptosis differ from necrosis?
Apoptosis - cell’s plasma membrane remains intact, but apoptotic cell fragments become target for phagocytosis and dead cell rapidly cleared before contents have leaked out; hence, no inflammatory reaction in the host.
Necrosis - loss of membrane integrity, enzymatic digestion of cells, and often a host reaction (inflammation).
What are the causes of apoptosis?
Physiologic:
Embryogenesis
Hormone-dependent involution of tissues (e.g. endometrium, prostate)
Cell deletion (e.g. intestinal epithelium)
Death of cells that have served their useful purpose (e.g. neutrophils following acute inflammatory response)
Deletion of potentially harmful self-reactive lymphocytes
Pathologic:
DNA damage (e.g. due tp hypoxia, radiation, or cytotoxic drugs)
Accumulation of misfolded proteins (e.g. due to inherited defects or free radical damage)
Cell death in certain viral infections (e.g. hepatitis)
By cytotoxic T cells in tumours and rejection of transplanted tissues
Pathologic atrophy in parenchymal organs after duct obstruction (e.g. pancreas)
What are the 4 types of cellular adaptations and give examples of each?
Hypertrophy - increased cell mass or size. E.g. increased workload (LVH, weight training), compensatory hypertrophy in remaining kidney post nephrectomy.
Hyperplasia - increased cell number. E.g. increased hormone stimulation (endometrial hyperplasia), increase hormone sensitivity (BPH), chronic irritation (skin thickening, bronchial gland hyperplasia, regenerative nodules in cirrhosis), chemical imbalance (hypocalcaemia causing PT gland hyperplasia)
Atrophy - decreased cell mass. E.g. decreased hormone stimulation (hypopituitarism), decreased enervation (ALS), decreased blood flow (atherosclerosis causing cerebral atrophy), increased luminal pressure (hydronephrosis)
Metaplasia - change from one mature cell type to another. E.g. sq to glandular epi in Barret oesophagus, glandular to other glandular epi in HP gastritis, glandular to sq epi in bronchus of smokers.
Describe the 6 intracellular mechanisms of cell injury
Fig 1.2, p8
Describe the sequence of events in reversible and irreversible ischaemic cell injury
Fig 1.3, p11
What is acute inflammation?
Transient, early response to injury
Describe the sequential vascular events in acute inflammation
Vasoconstriction of arterioles Vasodilation of arterioles Increased permeability of venules Swelling of tissue (tumor, oedema) Reduced blood flow
Describe the reactions of leukocytes in acute inflammation
p.26-32
What are the cell-derived mediators of inflammation, their primary sources and actions
p.33
Describe the arachidonic acid pathway and its role in inflammation
Fig 2.3, p.35
Describe the activation and functions of the complement system
Fig 2.5, p. 41
What is chronic inflammation?
What are its morphologic features?
A prolonged process (wks or mths) in which active inflammation, tissue destruction, and healing all proved simultaneously.
Infiltration with mononuclear inflammatory cells (macrophages, lymphocytes and plasma cells)
Tissue destruction, induced by persistent injury and/or inflammation
Attempts at healing by connective tissue replacement, via vascular proliferation (angiogenesis) and fibrosis
What is the role of macrophages in chronic inflammation?
Fig 2.7, p.46
What are the systemic effects of inflammation and their respective mediators?
p. 47
