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ESA 2 - Pathological Processes > Session 2: Acute Inflammation > Flashcards

Session 2: Acute Inflammation Flashcards

1
Q

When and why does acute inflammation occur?

A
  • Response of living tissue to injury

- Initiated to limit the tissue damage

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2
Q

What are some characteristics of acute inflammation? (4)

A
  1. innate
  2. immediate
  3. stereotyped
  4. Short duration - mins/hrs/few days
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3
Q

What tissue changes are brought about by acute inflammation? (3)

A
  1. Vascular flow
  2. Formation of a fluid exudate
  3. Neutrophil emigration
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4
Q

What are the causes of acute inflammation? (5)

A
  1. Microbial infections
  2. Acute phase hypersensitivity reactions
  3. Physical agents
  4. Chemicals
  5. Tissue necrosis
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5
Q

What are the characteristic clinical signs of acute inflammation? (5)

A
  1. Rubor
  2. Tumour
  3. Calor
  4. Dolor
  5. Loss of function
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6
Q

What are the 3 stages of the vascular phase of acute inflammation?

A
  1. Changes in blood flow
  2. Exudation of fluid into tissues
  3. Infiltration of inflammatory cells
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7
Q

What changes to blood flow occur in the vascular phase? (4)

A
  1. Initial few secs vasoconstriction of arterioles
  2. Vasodilation of arterioles and then capillaries
  3. Increased permeability of blood vessels
  4. Stasis - Concentration of RBCs in small vessels and increased viscosity of blood
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8
Q

What is the effect of increased permeability of blood vessels? (2)

A
  1. Exudation of protein-rich fluid into interstitium

2. Slowing of circulation (swelling)

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9
Q

Which chemical mediator in vessels is involved in the immediate early response?

A

Histamine

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10
Q

Which cells release histamine? (3)

A

Mast cells
Basophils
Platelets

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11
Q

What stimulates the release of histamine? (5)

A
  1. Physical damage
  2. Immunologic reaction
  3. Complement factors C3a and C5a
  4. IL-1
  5. Factors from neutrophils and platelets
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12
Q

What effects does histamine bring about? (3)

A
  1. Vascular dilatation
  2. Transient increase in vascular permeability
  3. Pain
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13
Q

What chemical mediators are involved in the persistent response? (Incompletely understood) (2)

A

Leukotrienes

Bradykinin

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14
Q

What determines fluid loss from vessels? (2)

A
  1. Increased hydrostatic pressure

2. Increased colloid osmotic pressure of interstitium

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15
Q

What causes an increase in hydrostatic pressure resulting in fluid exudation?

A

Arteriolar dilatation

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16
Q

What are the consequences of vascular leakage?

A

Oedema

17
Q

What are the 2 types of fluid that could accumulate in the interstitium in oedema?

A

Transudate or exudate

18
Q

What is transudate?

What is exudate?

A

Transudate - low protein content (fluid loss due to hydrostatic pressure imbalance only)
Exudate - more protein content than plasma (inflammation)

19
Q

How can fluid extracted from pleural effusion help in diagnosis?

A

High protein content (exudate) - inflammation

Low protein content - heart failure or venous outflow obstruction

20
Q

What are the mechanisms of vascular leakage? (5)

A
  1. Endothelial contraction - gaps
  2. Cytoskeletal reorganisation - gaps
  3. Direct injury of vessel walls - toxic burns, chemicals
  4. Leukocyte-dependent injury
  5. Increased transcytosis - channels across endothelial cytoplasm
21
Q

Which chemical mediators are involved in endothelial contraction?

A

Histamine

Leukotrienes

22
Q

Which chemical mediators are involved in cytoskeletal reorganisation?

A

Cytokines

  • IL-1
  • TNF
23
Q

How do leukocytes trigger leukocyte-dependent injury?

A

Toxic oxygen species and enzymes released

24
Q

Which signal protein is responsible for transcytosis?

A

VEGF - vascular endothelial growth factor

25
Q

Which plasma proteins are delivered to area of injury though exudation of fluid? (3)

A
  1. Immunoglobulins
  2. Inflammatory mediators (complement factors)
  3. Fibrinogen
26
Q

Why is fibrinogen delivered to the site of injury?

A
  • gets converted to insoluble fibrin
  • part of the haemostatic cascade
  • localises inflammation - prevents spreading to serosal lining
27
Q

What is the primary type of WBC involved in acute inflammation?

A

Neutrophils

28
Q

What are the four stages of infiltration of neutrophils? What happens in each stage?

A
  1. Margination - stasis causes neutrophils to line up at the edge of blood vessels along endothelium
  2. Rolling - neutrophils roll along endothelium, sticking to it intermittently
  3. Adhesion - cells stick more avidly
  4. Emigration - movement through blood vessel wall
29
Q

What is stasis?

A

Sludging of RS in the middle of the blood vessel due to slower blood flow

ESA 2 - Pathological Processes (4 decks)

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