Lecture 2 Flashcards
Define homeostasis
The balance achieved when the physiological needs of the body are met.
Disease will occur when the body can no longer adapt to its internal or external environment.
Define atrophy
Decrease in cell size. If enough cells in an organ atrophy the entire organ will decrease in size.
Where might atrophy occur?
Tissues and organs especially susceptible to atrophy include skeletal muscle, cardiac muscle, secondary sex organs, and the brain.
Define hypertrophy
Increase in cell size
Where might hypertrophy occur?
The heart and kidney have increased susceptibility to hypertrophy
Define hyperplasia
Increase in the number of cells. Result of increased cell mitosis or division. (Two types - compensatory and hormonal)
Where might hyperplasia occur?
Common in epithelial cells of epidermis and intestine, liver hepatocytes, bone marrow cells, and fibroblasts.
(A common pathologic hyperplasia in women occurs in the endometrium - endometriosis)
Define Dysplasia
Abnormal changes in cellular shape, size and/or organisation. Sometimes called ‘atypical hyperplasia’
Where might dysplasia occur?
Tissues prone to dysplasia include cervical and respiratory epithelium - strongly associated with development of cancer.
Define metaplasia
When a differentiated cell or a certain type is replaced by another cell type, which may be less differentiated.
Where might metaplasia occur?
The respiratory tract in response to inhalation of irritants - most common example is Barrett’s eosphagus.
Define neoplasia
New growth
Abnormal growth of tissue, that may result in a tumour.
Define anaplasia
Structural differentiation loss within a cell or group of cells
Where might anaplasia occur?
In malignant neoplasms
Describe the clinical features of inflammation
- Injury
- Chemical mediator release
- Vasodilation of arterioles (red and heat)
- Capillary permeability (leaky capillaries - swelling and pain)
- Leukocyte migration
- Phagocytosis
(Immobility may be a feature if joints are involved)
Define chronic inflammation
Prolong inflammation where active inflammation, tissue injury and healing proceed together
Three phases of deep wound healing
- Inflammatory phase
- Proliferation phase
- Remodelling phase
Outline the inflammatory phase in deep wound healing
- Brief vasoconstriction followed by vasodilation
- Fluid moves out into the tissue spaces
- Flow of blood to the tissue reduces –> blood clots
- WBCs enter the site and cause phagocytosis
- Release of chemical mediators
Outline the proliferation phase in deep wound healing
- Fibroblasts deposit more fibers and cells
- Multiplication of the cells
- Fibroblasts release growth factors
- Final stage of proliferative phase is epithelialisation
Outline the remodelling phase in deep wound healing
- New tissue is formed to fill the wound
- Scar tissue development
- It is formed from the fibroblasts and epithelial cells. It contains new blood vessels.
- The tissue is soft and pink
- This stage begins about 3 weeks
Factors that can promote/delay healing
nutrition, circulation, age, infection, hygiene, medications, genetics
Three drugs for treatment of inflammation and their actions
Aspirin (anti-inflammatory, anti-pyretic, analgesic)
NSAID’s (anti-inflammatory, analgesic)
Glucocorticoids (anti-inflammatory).
Causes of chronic inflammation
- Ineffective eradication of cause by the acute inflammatory response
- Specific bacteria
- Prolonged irritation (chemicals)
- Long term abnormal immune responses
Acute or chronic inflammation, which characteristically has more oedema
Acute
Acute vs chronic inflammation - Which has more lymphocytes, macrophages and fibroblasts
Chronic
Acute vs chronic - which has more collage production resulting in more fibrous scar tissue formation
Chronic
Acute vs chronic inflammation - which generally has more tissue destruction
Chronic
Chemical mediators in acute inflammation
Complement, kinins, prostaglandins, leukotriens, cytokines (interleukin 1, interleukin 6) from various immune cells, interferon-gamma from T cells
Chemical mediators in chronic inflammation
Cytokines from macrophages and T lymphocytes
Possible lesions in acute inflammation
Rash, pus, abscess
Possible lesions in chronic inflammation
Rash, fibrosis, granuloma
Cells involved in acute inflammation
Infection: Neutrophils
Allergy: eosinophils, mast cells
Cells involved in chronic inflammation
Macrophases, lymphocytes
Clinical example of acute inflammation
Abscesses (brain;skin), allergic reaction (anaphylaxis)
Clinical example of chronic inflammation
Autoimmune conditions (lupus; Rheumatoid arthritis), cystic fibrosis
