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41 Cards in this Set

  • Front
  • Back
Hypertrophy
↑ size of a cell
Physiological or pathological stimuli → ↑expression of genes encoding cellular proteins → ↑cell size
Hyperplasia
↑ in number of cells usually resulting in ↑ volume of an organ or tissue
may be due to hormones, functional demand or persistent cell injury → changes in gene expression → proliferation of target cells
Atrophy
↓ in cell size and cell number (involution)
caused by ↓ functional demand, inadequate supply of oxygen or nutrients, interrupted trophic signal (menopause), aging
Metaplasia
Conversion from one cell type to another
Usually reversible but has ↑ susceptibility to cancerous transformations
Dysplasia
Alteration in size, shape and organisation of the cellular components of a tissue
Often reversible, can be due to environmental insult
Necessary stage in cancerous transformation
necrosis
loss of calcium gradient causing activation of nucleases, mitochondrial dysfunction, proteolysis (causes plasma membrane blebbing)
what is a main difference in the outcome of necrosis compared to apoptosis
Apoptosis doesn’t invoke inflammatory response but necrosis does
Apoptosis
Genetically determined ‘self destruct’ mechanism of cells
-Seen in foetal development, normal turnover, deletion of self-reactive lymphocytes, neoplasia, mild environmental stressors
-Two pathways: intrinsic and Extrinsic but both lead to activation of effector capases which are enzymes that break down specific proteins
-characteristics : shrinkage, membrane blebbing, fragmentation
what are the main components of all homeostatic control mechanisms
1)the receptor
2)control center
3)the effector
steady state
normal homeostatic state
set point
desired point in a homeostatic system. Can be influenced by modulators
what is the mechanism of fever
cytokine interleukin 1b triggers prostoglandin production which acts on the hypothalamus to increase temp
how is plasma osmoality regulated
release of antidiuretic hormone causes drop in water loss, sweating and an increased thirst
Oedema
accumulation of fluid extra-vascularly in tissues
Exudate
oedema fluid with high protein content resulting from increased endothelial permeability to plasma proteins in inflammation
Pus
Inflammatory exudate containg viable and dead neutrophils, cell debris, viable and dead micro-organisms, protein, lipid DNA, etc
suppuration
formation of pus
acute inflammation
Rapid, short lived, stereotypic response characterised by the movement of polymorphonuclear leukocytes (mostly neutrophils) and fluid into the affected tissue
Four steps of healing
1)Haemostasis
2)inflammation
3)proliferation
3)remodelling
Differences between healing by first intention and healing by second intention
1st = marins can attach, are sutured and there is no infection
2nd = margins not ready to attach, are bruised and necrotic. Infection is present
What cells are involved in healing
C.T = macrophages, mast cells and fibroblasts
Vascular cells = endothelium and circulating cells
C.T matrix = collagen, elastin, protoglycans
Cytokines - signaling cells
What is involved in the Haemostsis stage of healing
- arteriole: vasoconstriction
- blood clots: platelets, fibrin
what is involved in the inflammation stage of healing (1st intention)
- Fibrin & Platelet scab
- WBC migrate from capillaries in response to cytokine signals
- Dead tissue & debris cleared
- More cytokines released
what is involved in the proliferation stage of healing
- Fibroblasts & endothelial cells enter wound site
- Begin to proliferate
-Endothelial cells form new blood vessels
-Fibroblasts lay down collagen cells
What is involved in the remodelling stage of healing
- Fibroblasts transform into myofibroblasts, this is stimulated by TGF-β, PDGF
- Collagen synthesis and degradation is controlled by metalloproteinase’s (produced by macrophages, epidermal cells, endothelial cells and fibroblast
- Re-epithelialisation & Organisation  wound strength

- Inflammatory cells & fibroblasts disappear from scar
- Matrix & blood vessel formation shuts down
- Collagen is reorganised
What is granulation tissue and what is it made up of
perfuse, fibrous connective tissue that replaces a fibrin clot in healing wounds. macrophages, epithelial cells (migrate to the edges), endothelial cells (angiogenesis), fibroblasts (ECM)
How is exudate formed
fluid, salts, neutrophils, complement, and antibodies move into affected tissue
Why is fluid important in exudate
dilutes toxins and increases flow into lymphatics
Chronic Inflammation
Active inflammation in which tissue destruction and repair are proceeding simultaneously over a prolonged period
Types of chronic inflammation
suppurative - abscess
granulomatous - tuberculosis
mixed characteristics- arthritis
Main characteristics of all chronic inflammatory lesions
- Persistence
- Cellular infiltration
- Destruction of normal tissue
- formation of fibrous connective tissue
abscess
circumscribed collection of pus within solid tissue
Ulcer
local defect or excavation on the surface of an organ or tissue produced by the sloughing off of necrotic inflammatory tissue
Chronic suppurative inflammation
-pus
-usually caused by pyogenic bacteria
-fibrotic repair
-may be acute or chronic
Pilonidal sinus
chronic suppurative inflammation seen in hairdresses when hair shafts become embedded in the skin
Granuloma
nodular inflammatory lesion containing predominantly macrophages, lymphocytes and fibroblasts. Forms in response of a persistant irritant, such as a microorganism or foreign body
Granulation tissue
newly formed tissueconsisting of macrophages, blood vessels and fibroblasts that is involved in healing damaged tissues through fibrosis
Immune type chronic granulomatous inflammation
- often caused by invasion of a microorganism that can survive inside a “resting” normal macrophage. Go on the form giant cells
- example is: Mycobacterium Leprae and Mycobacterium tuberculosis
sarcoidosis
an immune system disorder characterised by non-caseating granulomas. Most common in young adults. Unknown cause. Virtually any organ can be affected; however, granulomas most often appear in the lungs or the lymph nodes
what is chronic mixed type inflammation
Involves both neutrophils and macrophages / lymphocytes over protracted period
Initiating agent often unknown eg rheumatoid arthritis
how is a granuloma formed
inability of phagocytes to kill/digest inciting agent causes cell-mediated response and sequestration with tissue macrophages causing the recruitment of monocytes. monocytes then differentiate into macrophages or 'epithelioid cells'. fusion of these epithelioid cells form 'giant cells' this leads to the recruitment of fibroblasts which form a fibrous tissue around the giant cells