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ESA 2 Mech Of Disease > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

0
Q

What is acute inflammation’s primary role?

A
  • Initiated to limit tissue damage
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1
Q

What is the definition of acute inflammation?

A
  • Response of living tissue to injury
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2
Q

Want are the main features of acute inflammation?

A
  • Innate
  • Immediate
  • Stereotyped (always the same response)
  • Short duration (mins/hrs/days)
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3
Q

How is acute inflammation controlled?

A
  • Variety of chemical mediators derived from plasma cells
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4
Q

What are the two main features of inflammation that would be seen on a histological slide?

A
  • Exudate

- Neutrophils

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5
Q

What are the main causes of acute inflammation?

A
  • Microbial infections
  • Hypersensitivity reactions
  • Physical and chemical agents
  • Tissue necrosis
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6
Q

Why can’t we tell the cause by the response?

A
  • Stereotyped, so all reactions are the same
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7
Q

What are the main clinical signs of inflammation?

A
  • Rubor: redness
  • Tumor: swelling
  • Calor: heat
  • Dolor: pain
  • (Loss of function)
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8
Q

What are the main changes in tissues that are undergoing acute inflammation?

A
  • Change in blood flow (more vasodilation hence redness)
  • Exudation of fluid into tissues
  • Infiltration of inflammatory cells
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9
Q

Outline why there’s a change in blood flow during acute inflammation.

A
  • Vasodilation of blood vessels hence heat and redness.
  • Increased permeability of blood vessels:
    Exudation of fluid into tissues
    Slowing of circulation (swelling)
  • Conc of RBCs in small vessels and increase in viscosity of blood leading to stasis
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10
Q

What are the characteristic of the chemical mediators used in acute inflammation?

A
  • Immediate early response (½ hr)
  • Histamine release in response to stimuli e.g physical damage
  • Persistent response: many and varied mediators interlinked
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11
Q

From what is histamine released and what does histamine cause?

A
  • Released from: mast cells, basophils and platelets

- Causes: vascular dilation, increased vascular permeability, pain

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12
Q

Why is pain caused?

A
  • Possibly a response by the body to try and cause rest so no further damage is caused.
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13
Q

What is Starling’s law?

A
  • Fluid flow across vessel walls determined by hydrostatic and colloid osmotic pressure.
  • Increased hydrostatic pressure -> increased fluid flow out of vessels
  • Increased colloid osmotic pressure of interstitium -> increased fluid flow out of vessels.
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14
Q

How do oedemas form due to acute inflammation?

A
  • Arteriole dilation -> increased hydrostatic pressure -> increased permeability of vessel walls -> loss of protein into interstitium -> leakage -> oedema (excess fluid in interstitium)
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15
Q

What is an exudate?

A
  • High protein content fluid loss
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16
Q

What is a transudate?

A
  • Fluid loss due to hydrostatic pressure imbalance only

- Low protein content

17
Q

What are the different mechanisms for vascular leakage?

A
  • Endothelial contraction leads to gaps
  • Cytoskeletal reorganisation leads to gaps
  • Direct injury
  • Leukocyte dependent injury (toxic O2 species and enzymes from leukocytes)
  • Increased transcytosis (channels across endothelial cytoplasm)
18
Q

What are neutrophils and what are they also known as?

A
  • Primary type of WBC involved in inflammation
  • Type of granulocyte
  • Polymorphs
19
Q

How do neutrophils infiltrate the inflamed tissue?

A
  • Stasis causes neutrophils to line up at edge of bv along endothelium, (MARGINATION)
  • Neutrophils roll along endothelium sticking intermittently (ROLLING)
  • Sticking more avidly (ADHESION)
  • Followed by EMIGRATION of neutrophils through bv wall
20
Q

How does emigration occur?

A
  • Relaxation of inter-endothelial cell junctions
  • Digestion of vascular basement membrane
  • Movement
21
Q

How do neutrophils move?

A
  • Emigration and diapedesis (migration)
  • Chemotoxis: movement along conc gradient of chemoattractants
  • e.g of chemotoxins: C5a, LTB4, bacterial peptides
  • Receptor-ligand binding
  • Rearrangement of cytoskeleton
  • Production of pseudopod (arms to engulf during phagocytosis)
22
Q

What is the main role of neutrophils?

A
  • Phagocytosis
  • Contact, recognition, internalisation
  • (Phagosomes fuse with lysosomes to produce secondary lysosomes)
23
Q

What are the killing mechanisms for neutrophils?

A
  • O2 dependent: Super oxide radicals, H2O2, HOCl
  • O2 independent: Lysozyme and hydrolyases, bactericidal permeability increasing protein (BPI), cationic proteins (defensins)
24
Q

What are the chemical mediators of acute inflammation?

A 
- Proteases (plasma proteins produced in liver) 
Kinins 
Complement system
Coagulation
- Prostaglandins/Leukotrienes 
Metabolites of arachidanic acid
- Cytokines (produced by WBC)
- Increased blood flow
- Vascular permeability
- Neutrophil chemotoxis 
- Phagocytosis
25
Q

What are the responses to a combat injury?

A
  • Exudation of fluid
  • Infiltration of cells (removes pathogenic organisms and necrotic debris)
  • Vasodilation (increases delivery and temperature)
  • Pain and loss of function
26
Q

What is the role of exudation of fluid?

A
  • Delivers plasma proteins to injury area
  • Immunoglobulins
  • Inflammatory mediators
  • Fibrinogen
  • Dilutes toxins
  • Increases lymphatic drainage (delivers microorganisms to phagocytes and antigens)
27
Q

Give examples of local complications of acute inflammation.

A
  • Swelling: blockage of tubes (e.g. Bile duct/intestine)
  • Exudate: compression, serositis
  • Fluid loss: burns
  • Pain and loss of function
28
Q

What is serositis?

A
  • Inflammation of serous tissue

- E.g: pleura, pericardium

29
Q

Give examples of systemic effects of acute inflammation

A
  • Fever, endogenous pyrogens
  • Leukocytosis
  • Acute phase response
  • Spread of microorganisms and toxins
  • Shock (lack of O2 to major organs)
30
Q

What is Leukocytosis?

A
  • IL-1 and TNF alpha cause accelerated released of WBC from marrow
  • Macrophages and T lymphocytes produced
  • Can be due to bacterial infections
31
Q

What is acute phase response?

A
  • Change in plasma conc of acute phase proteins

- Leukocytes/neutrophils produce more cytokines -> more phase proteins produced by the liver

32
Q

What are the possible sequelae of acute inflammation?

A
  • Complete resolution
  • Continued acute inflammation leading to chronic and abscesses
  • Chronic inflammation and fibrous repair -> scarring
  • Death
33
Q

What is the main mechanism of resolution?

A
  • Morphology: changes gradually reverse

- Vascular changes stop: neutrophils no longer marginate, vessel permeability and calibre returns to normal.

34
Q

What are the changes that occur during recovery from inflammation?

A
  • Exudate drains to lymphocytes
  • Fibrin degraded by plasmin (proteases)
  • Neutrophils die and break up - carried away/phagocytosed
  • Damaged tissues MAY repair
35
Q

How are acute inflammation mediators removed?

A
  • Short half life
  • May be inactivated by degeneration
  • Instability
  • Diluted in exudate
  • Binding of inhibitors
36
Q

What is lobar pneumonia?

A
  • Strep. Pneumonia
  • Alveoli filling with exudate not air
  • Fever, hypoxanaemia, dry cough, breathlessness
37
Q

How do skin blisters form?

A
  • Causes: heat, sunlight, chemical
  • Pain and profuse exudate
  • Collection of fluid strips off epithelium
  • Inflamed cells
  • Resolution: scarring
38
Q

What are abscesses?

A
  • Solid tissues
  • Inflamed exudate forces tissues apart
  • Liquefactive necrosis in centre
  • May cause high pressure leading to pain
  • May cause tissue damage and squash adjacent structures
39
Q

What are the symptoms of acute phase response?

A
  • Decreased appetite
  • Increased pulse rate
  • Altered sleep patterns

ESA 2 Mech Of Disease (11 decks)

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