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Immune and lymphatic system > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation?

A
  • Response of living tissue to injury/insult, can be physical/chemical/infective/hypersensitive
  • Protective reaction: dilute/destroy/isolate/initiate repair
  • Potentially harmful - componments can injury bystander normal tissue
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2
Q

Two types of inflammation

A

Acute and chronic

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3
Q

Signs of infection

A

Heat/redness/swelling/pain/loss of function

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4
Q

Characteristics of acute inflammation

A

Fast
Mainly neutrophils
Usually mild and self-limited
Prominent symptoms

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5
Q

Characteristics of chronic inflammation

A

Slower
Mainly monocytes/macrophage and lymphocytes
Severe and progressive tissue injury
More subtle symptoms

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6
Q

Vascular response of acute inflammation

A

Vasodilation, leaky capillaries

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7
Q

Cellular response of acute inflammation

A

Margination, adhesion, emigration and activation of neutrophils

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8
Q

Is the complement cascade activated in acute inflammation?

A

Yes

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9
Q

How is vasodilation stimulated?

A

Histamines and NO act on smooth muscle

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10
Q

What is stasis?

A

Shortened blood flow, hyperviscosity

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11
Q

Characteristics of vasodilation

A

Increased permeability of vasculature: formation of early transudate (protein-rich filtrate of plasma) gives rise to exudate (protein rich filtrate) into extracellular tissues

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12
Q

Which molecules cause endothelial cell contact to widen intercellular gaps of venues?

A

Histamines, bradykinins, leukotrienes

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13
Q

Process of vascular leakage

A
  • Histamines, bradykinins, leukotrienes cause endothelial cell contraction that widens intercellular gaps of venules
  • Outpouring of exudate into extracellular tissue leads to reduction of intravascular osmotic pressure and increase in extravascular, interstitial osmotic pressure
  • Increase of interstitial osmotic pressure leads to edema (water and ions)
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14
Q

How can leukocytes leave vasculature?

A

Margination and rolling
Activation and adhesion
Transmigration

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15
Q

How is CRP produced?

A

Interleukins stimulate liver to produce CRP

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16
Q

What impact does TNF have on the heart?

A

Negative - stops it beating as strongly

Increases risk of thrombosis

17
Q

Symptoms of systemic infection

A

Lower blood pressure, change in heart rate, fatigue, depression, fever

18
Q

What happens to [albumin] in inflammation?

A

Goes down

19
Q

Factors impacting would healing

A

Infection/pressure /nutrition/ age/ immunocompromised/diabetes /BMI

20
Q

Factors aiding wound healing

A

Oxygen, maggots, Manuka honey, general good health, antibiotics

21
Q

Symptoms of acute inflammation

A

Malaise, fever, pain, rapid pulse

22
Q

Laboratory investigations for acute inflammation

A

Increased neutrophils, increased erythrocyte sedimentation rate, increased concentration of acute-phase proteins
CRP begins to rise and peak at 36-50 hours after infection
ESR shows slower rise and return to normal than CRP

23
Q

Components of chronic inflammation

A

Lymphocytes, plasma cells, macrophage infiltration

24
Q

How are cells repaired after chronic inflammation?

A

Fibrosis and angiogenesis

25
Q

Through which routes can chronic inflammation occur?

A

May progress from acute inflammation or repeated episodes of acute inflammation or occur ‘de novo’ if the causative agent produces only a mild acute response

26
Q

Chemicals stimulating vasodilation

A

Prostaglandins, NO

27
Q

Chemicals stimulating increased vascular permeability

A

Histamines, serotonin, C3a, C5a, bradykinin, leukotrienes (C4, D4, E4), platelet activating factor

28
Q

Chemicals stimulating chemotaxis and leukocyte activation

A

C5a, leukotriene B4, bacterial products, chemokines (IL-8)

29
Q

Chemicals stimulating fever

A

IL-1, IL-6, TNF, prostaglandins

30
Q

Chemicals stimulating pain

A

Prostaglandins, bradykinin

31
Q

Chemicals stimulating tissue damage

A

Neutrophil and macrophage lysosomal enzymes, oxygen metaboplites, NO

32
Q

Where can chemical mediators arise from?

A

May be derived locally at the site of inflammation or may be derived from circulating inactive precursors that are activated at the inflammation site

33
Q

When are cell-derived mediators created?

A

Normally sequestered in intracellular granules, they are rapidly secreted when activated or are synthesised ‘de novo’ in response to stimulus

34
Q

What are plasma protein-derived mediators?

A

Complement proteins/kinins which circulate in an inactive form and undegro proteolytic cleavage to acquire biologic activities

Immune and lymphatic system (27 decks)

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