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GenPath > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Mediators of Inflammation

A

Histamine
Prostaglandins
Leukotrienes
Cytokines
Chemokines
Platelet-activating factor
Complement
Kinins

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2
Q

What is inflammation?

A

Response of vascularised tissue to bring cells of host defence from blood circulation to site of inflammation (where foreign bodies are present) to eliminate these pathogens

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3
Q

Differences between acute and chronic inflammation (4)

A
  1. Acute onset is rapid (minutes/hours), chronic onset is slow (days)
  2. Infiltrate of acute inflammation consists of mostly neutrophils, infiltrate of chronic inflammation consists of macrophages and lymphocytes
  3. Cellular injury and fibrosis in acute inflammation is mild and self-limiting, in chronic inflammation it is often severe and progressive
  4. Local and systemic signs of acute inflammation are prominent, in chronic inflammation they are less prominent
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4
Q

Process of acute inflammation (think about the 5 presentations of acute inflammation!)

A
  1. Antigen enters the dermis
  2. Mast cells release histamine and prostaglandins and macrophages release prostaglandins, causing vasodilation of blood vessels, increasing blood flow and causing redness and warmth
  3. During vasodilation, endothelial cells separate, forming gaps, which causes plasma and protein to leak into the tissues, creating exudate, increasing extravascular fluid and causing swelling
  4. Kinins enter the gaps and are activated to form bradykinins. Bradykinins and prostaglandins stimulate nerve endings and send pain signals, causing avoidance of touching or moving and hence a loss of function.
  5. Chemokines are released by inflammatory cells, causing transmigration of neutrophils through endothelial gaps, allowing neutrophils to travel to the site of inflammation to carry out its actions by phagocytosis. Neutrophils have multilobulated nucleus and are comprised of 3 lobes in order to fit through endothelial gaps more easily. Neutrophils are inflammatory cells.
  6. Cytokines (e.g. IL-1, TNF) are released by macrophages that travel to other parts of the body (e.g. brain, hypothalamus), causing fever
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5
Q

Mediators of vasodilation

A

Histamine
Prostaglandins
Nitric Oxide

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6
Q

Mediators of increased vascular permeability

A

Histamine
Serotonin
C3a and C5a
Leukotrienes

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7
Q

Mediators of chemotaxis, leukocyte recruitment and activation

A

IL-1, TNF
Chemokines
C3a and C5a
Leukotrienes

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8
Q

Mediators of fever

A

IL-1, TNF
Prostaglandins

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9
Q

Mediators of pain

A

Prostaglandins
Bradykinins

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10
Q

Mediators of tissue damage

A

Lysosomal enzymes of leukocytes
Reactive oxygen species

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11
Q

Exudate vs Transudate (6)

A
  1. Exudate has higher specific gravity than transudate
  2. Exudate has higher protein concentration than transudate
  3. Exudate is cell rich, with many inflammatory cells, transudate is cell poor
  4. Exudate contains plasma fibrinogen and coagulates easily, transudate does not
  5. Exudate is not clear, transudate is clear
  6. Exudate is unilateral, results from increased vascular permeability or decreased lymphatic drainage. Transudate is bilateral, arises from increased capillary hydrostatic pressure or decreased capillary oncotic pressure.
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12
Q

Fluid in pleural cavity/pleural effusion: transudate or exudate?

A

Can be both!
Transudate: Heart failure
Exudate: Infection in the lungs/pneumonia with possible tumour

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13
Q

Role of lymphatics

A

Carry away exudate and injurious stimuli, then drain into lymph nodes for further deactivation by immune system

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14
Q

5 cardinal signs of acute inflammation

A

Heat
Redness
Swelling
Pain
Loss of function

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15
Q

Outcomes of inflammation

A

Abscess (pus) formation
Chronic inflammation
Resolution
Fibrosis with excessive fibrous layers (scar formation)

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16
Q

Systemic effects of inflammation

A

Fever, lethargy, nausea, weight loss
Swelling of lymph nodes
Haematological effects:
- increased erythrocyte sedimentation rate (RBCs settle faster because they clump faster)
- increased WBC production
- anemia because bone marrow HSCs are producing more WBCs and less RBCs

17
Q

Special patterns of acute inflammation

A

Serous
Fibrinous
Suppurative
Ulcer

18
Q

Serous acute inflammation

A

When exudate is cell poor, and not associated with infection
e.g. blister

19
Q

Fibrinous acute inflammation

A

When there is a lot of fibrinogen in the exudate, and threads of fibrin are formed
e.g. pericarditis

20
Q

Suppurative acute inflammation

A

When there is pus containing neutrophils, necrotic debris, bacteria
When it is localised, an abscess is formed

21
Q

Ulcer acute inflammation

A

When there is a defect in the epithelium
e.g. gastric ulcer

22
Q

What is chronic inflammation?

A

A response of prolonged duration in which inflammation, injury and attempts at repair can occur simultaneously
Can occur following acute inflammation or insidiously (e.g. in autoimmune disease such as rheumatoid arthritis)

23
Q

Causes of chronic inflammation

A

Persistent infections that resist elimination
Hypersensitivity reactions (autoimmune, allergies)
Continuous exposure to toxins (exo, endo)
e.g. Exogenous - silicosis from silica; Endogenous - atheroscleorosi from cholesterol

24
Q

Granulomatous inflammation: a type of chronic inflammation

A

Characterised by formation of granulomas aka aggregates of epithelioid histiocytes (macrophages)
Results in formation of multinucleated giant cells
Often with T lymphocytes, sometimes with central necrosis

25
Q

Causes of granuloma formation

A

Mycobacteria (tuberculosis, leprosy)
Syphilis, fungi, parasites
Sarcoidosis, Crohn’s disease

26
Q

Cells involved in chronic inflammation

A

Mononuclear cells (macrophages, lymphocytes, plasma cells), Eosinophils, Mast cells

27
Q

Why is inflammation not always good?

A

Allergies (inflammation against harmless things)
Autoimmune (inflammation against self tissues)
Acute inflammation that is not resolved can lead to chronic inflammation, abscess formation or fibrosis

28
Q

Benefits of inflammation

A

Dilution of toxin, entry of antibodies
Fibrin formation
Delivery of nutrients and oxygen
Activation of immune response

29
Q

Harms of inflammation

A

Digestion of normal tissue
Swelling
Inappropriate inflammatory response

GenPath (5 decks)

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