Lecture 2 Flashcards

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1
Q

Define homeostasis

A

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.

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2
Q

Define atrophy

A

Decrease in cell size. If enough cells in an organ atrophy the entire organ will decrease in size.

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3
Q

Where might atrophy occur?

A

Tissues and organs especially susceptible to atrophy include skeletal muscle, cardiac muscle, secondary sex organs, and the brain.

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4
Q

Define hypertrophy

A

Increase in cell size

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5
Q

Where might hypertrophy occur?

A

The heart and kidney have increased susceptibility to hypertrophy

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6
Q

Define hyperplasia

A

Increase in the number of cells. Result of increased cell mitosis or division. (Two types - compensatory and hormonal)

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7
Q

Where might hyperplasia occur?

A

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)

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8
Q

Define Dysplasia

A

Abnormal changes in cellular shape, size and/or organisation. Sometimes called ‘atypical hyperplasia’

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9
Q

Where might dysplasia occur?

A

Tissues prone to dysplasia include cervical and respiratory epithelium - strongly associated with development of cancer.

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10
Q

Define metaplasia

A

When a differentiated cell or a certain type is replaced by another cell type, which may be less differentiated.

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11
Q

Where might metaplasia occur?

A

The respiratory tract in response to inhalation of irritants - most common example is Barrett’s eosphagus.

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12
Q

Define neoplasia

A

New growth

Abnormal growth of tissue, that may result in a tumour.

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13
Q

Define anaplasia

A

Structural differentiation loss within a cell or group of cells

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14
Q

Where might anaplasia occur?

A

In malignant neoplasms

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15
Q

Describe the clinical features of inflammation

A
  1. Injury
  2. Chemical mediator release
  3. Vasodilation of arterioles (red and heat)
  4. Capillary permeability (leaky capillaries - swelling and pain)
  5. Leukocyte migration
  6. Phagocytosis

(Immobility may be a feature if joints are involved)

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16
Q

Define chronic inflammation

A

Prolong inflammation where active inflammation, tissue injury and healing proceed together

17
Q

Three phases of deep wound healing

A
  • Inflammatory phase
  • Proliferation phase
  • Remodelling phase
18
Q

Outline the inflammatory phase in deep wound healing

A
  • 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
19
Q

Outline the proliferation phase in deep wound healing

A
  • Fibroblasts deposit more fibers and cells
  • Multiplication of the cells
  • Fibroblasts release growth factors
  • Final stage of proliferative phase is epithelialisation
20
Q

Outline the remodelling phase in deep wound healing

A
  • 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
21
Q

Factors that can promote/delay healing

A

nutrition, circulation, age, infection, hygiene, medications, genetics

22
Q

Three drugs for treatment of inflammation and their actions

A

Aspirin (anti-inflammatory, anti-pyretic, analgesic)

NSAID’s (anti-inflammatory, analgesic)

Glucocorticoids (anti-inflammatory).

23
Q

Causes of chronic inflammation

A
  • Ineffective eradication of cause by the acute inflammatory response
  • Specific bacteria
  • Prolonged irritation (chemicals)
  • Long term abnormal immune responses
24
Q

Acute or chronic inflammation, which characteristically has more oedema

A

Acute

25
Q

Acute vs chronic inflammation - Which has more lymphocytes, macrophages and fibroblasts

A

Chronic

26
Q

Acute vs chronic - which has more collage production resulting in more fibrous scar tissue formation

A

Chronic

27
Q

Acute vs chronic inflammation - which generally has more tissue destruction

A

Chronic

28
Q

Chemical mediators in acute inflammation

A

Complement, kinins, prostaglandins, leukotriens, cytokines (interleukin 1, interleukin 6) from various immune cells, interferon-gamma from T cells

29
Q

Chemical mediators in chronic inflammation

A

Cytokines from macrophages and T lymphocytes

30
Q

Possible lesions in acute inflammation

A

Rash, pus, abscess

31
Q

Possible lesions in chronic inflammation

A

Rash, fibrosis, granuloma

32
Q

Cells involved in acute inflammation

A

Infection: Neutrophils
Allergy: eosinophils, mast cells

33
Q

Cells involved in chronic inflammation

A

Macrophases, lymphocytes

34
Q

Clinical example of acute inflammation

A

Abscesses (brain;skin), allergic reaction (anaphylaxis)

35
Q

Clinical example of chronic inflammation

A

Autoimmune conditions (lupus; Rheumatoid arthritis), cystic fibrosis