Lecture 4: Acute Inflammation Flashcards

(50 cards)

1
Q

What are the 5 cardinal signs of inflammation

A
  1. Redness
  2. Pain
  3. Swelling
  4. Heat
  5. Loss of function
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2
Q

Acute inflammation is dominated by ___

A

Neutrophils

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3
Q

Fibrinous= ___
Fibrous= ____

A

Fibrinous= acute
Fibrous=chronic

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4
Q

What is acute inflammation

A

Vascular response to cell and tissue injury triggered by numerous physical and biological stimuli

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5
Q

What immune system does acute inflammation activate and what is triggered to release

A

Innate immune system
Releases: Prostaglandins, leukotrienes, cytokines and activates complement

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6
Q

What interleukin results in chemotaxis and activation of neutrophils

A

IL-8

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7
Q

What cytokines are fever producing

A

IL-1, TNF, IL-6

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8
Q

What prostaglandins are fever producing

A

PGE2

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9
Q

What is the mechanism in which fever inducing cytokines and prostaglandins work

A

Increase vascular permeability

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10
Q

What are the phases of acute inflammation

A
  1. Fluidic
  2. Cellular
  3. Reparative
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11
Q

What is the fluidic phase of acute inflammation

A

Dilute and localize inciting substance
1. Hyperemia or increase BF from mediators most notably HISTAMINE
2. Leaky vessels/ permability of capillaries and post capillary venules
3. Emigration of leukocytes

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12
Q

What is the cellular phase of acute inflammation

A
  1. Deliver leukocytes into the exudate at site of injury
  2. Leukocyte adhesion cascade- neutrophils first- kill and eliminate
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13
Q

What is the reparative phase of acute inflammation

A
  1. Resolution
  2. Healing by fibrosis
  3. Abscess formation
  4. Chronic inflammation
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14
Q

What do steroids inhibit

A

Phospholipase

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15
Q

What do NSAIDs inhibit

A

COX-1 and COX-2

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16
Q

What do leukotriene receptor antagonists inhibit

A

Bronchospasm and increased vascular permeability

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17
Q

What are the three complement pathways

A
  1. Classical
  2. Mannose binding lectin
  3. Alternative
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18
Q

What triggers classical pathway

A

Antibody opsonization

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19
Q

What triggers the alternative pathway

A

LPS and polysaccharides of fungal cell walls

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20
Q

What are the three outcomes/goals of activated complement

A
  1. Formation of C5a and C3a- attracting leukocytes
  2. Formation of C3b- opsonization of pathogens and phagocytosis
  3. Formation of MAC complex- puts pore in membrane—> lysis
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21
Q

What do positive acute phase proteins do

A

Increase inflammation

22
Q

What do negative acute phase proteins do

A

Decrease inflammation

23
Q

Is C-reactive protein a positive or negative acute phase protein

A

Positive- increase inflammation

24
Q

Is albumin a positive or negative acute phase protein

A

Negative- decrease inflammation

25
Is serum amyloid A a positive or negative acute phase protein
Positive- increase inflammation
26
What are the endogenous triggers for pyrexia/fever
Phagocytosis, tissue damage, and immune complexes
27
What endogenous pyrogens cause pyrexia/fever
LPS
28
What is the pathway leading to pyrexia/fever
1. Exogenous pyrogen-LPS 2. Endogenous triggers: phagocytosis, tissue destruction, immune complexes 3. Activate neutrophils and macrophages 4. Release IL-1, IL-6, TNF-alpha and PGE2 5. Hypothalamus activated- increase body temp via vasoconstriction in extremities and muscle shivering
29
What is the ultimate mediator of febrile response
PGE2
30
Reduction of ___ appears to be key signal to reduce fever
PGE2
31
What is edema
Excess fluid in tissues
32
Edema often occurs with ___, but edema does not always indicate ___
Inflammation for both
33
What is the reason/mechanism in which edema causes swelling with inflammation
Protein rich fluid leaks out of vessels into extracellular space within tissues
34
What is the Ig that mediates type I hypersensitivity reactions
IgE
35
What are some examples of type I hypersensitivity disorders
Anaphylaxis, allergies
36
What is the immune mechanism of type I hypersensitivity reactions
IgE produced mast cells release vasoactive amines and other mediates to recruit inflammatory cells resulting in vascular dilation, edema, smooth muscle spams, mucus production and inflammation
37
What Ig mediates type II hypersensitivity reactions
IgG and IgM
38
What are some disorders associated with type II hypersensitivity reactions
IMHA, neonatal isoerythrolysis, MG, transfusion reactions, pemphigus
39
What is the mechanism for type II hypersensitivity reactions
IgG and IgM bind to antigen—> phagocytosis or lysis via complement of Fc receptor, recruitment of leukocytes—> results in cell lysis, inflammation
40
What Ig mediates type III hypersensitivity reactions
IgG and IgM
41
What are some examples of disorders associated with type III hypersensitivity reactions
Systemic lupus, erythematosus, glomerulonephritis
42
What is the mechanism for type III hypersensitivity reactions
Ag-Ab complex deposition—> activate complement—> leukocyte recruitment, release of enzymes and toxic molecules Results in necrotizing vasculitis
43
What mediates type IV hypersensitivity reactions
T-lymphocytes
44
What are some examples of type IV hypersensitivity reactions
Contact dermatitis, transplant rejection, tuberculosis, chronic allergies, Johne’s disease
45
What is the mechanism for type IV hypersensitivity reactions
Activate T cells—> release cytokines and macrophages—> T lymphocyte mediated cytotoxicity Peri vascular cell infiltrates, edema, cell destruction, granuloma formation
46
What are immunodeficiency disease
Failure of the immune system to protect the host Inability of immune system to prevent infections and/or neoplasia
47
What is a primary immunodeficiency
Congenital or genetic defect in immune system
48
What is an example of a primary immunodeficiency and mechanism
Severe combined immunodeficiency syndrome (SCID)- ineffective humoral and cell mediated deficiencies in humans, mice horses, and dogs
49
What is a secondary immunodeficiency
Acquired immune defect
50
What is an example of a secondary (acquired) immunodeficiency and mechanism
Feline acquired immunodeficiency syndrome- lentiviral induced death of CD4 T cells leading to immunosuppression