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Pathology I > Lecture 4: Acute Inflammation > Flashcards

Lecture 4: Acute Inflammation Flashcards

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
Q

Is serum amyloid A a positive or negative acute phase protein

A

Positive- increase inflammation

26
Q

What are the endogenous triggers for pyrexia/fever

A

Phagocytosis, tissue damage, and immune complexes

27
Q

What endogenous pyrogens cause pyrexia/fever

A

LPS

28
Q

What is the pathway leading to pyrexia/fever

A
  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
Q

What is the ultimate mediator of febrile response

A

PGE2

30
Q

Reduction of ___ appears to be key signal to reduce fever

A

PGE2

31
Q

What is edema

A

Excess fluid in tissues

32
Q

Edema often occurs with ___, but edema does not always indicate ___

A

Inflammation for both

33
Q

What is the reason/mechanism in which edema causes swelling with inflammation

A

Protein rich fluid leaks out of vessels into extracellular space within tissues

34
Q

What is the Ig that mediates type I hypersensitivity reactions

A

IgE

35
Q

What are some examples of type I hypersensitivity disorders

A

Anaphylaxis, allergies

36
Q

What is the immune mechanism of type I hypersensitivity reactions

A

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
Q

What Ig mediates type II hypersensitivity reactions

A

IgG and IgM

38
Q

What are some disorders associated with type II hypersensitivity reactions

A

IMHA, neonatal isoerythrolysis, MG, transfusion reactions, pemphigus

39
Q

What is the mechanism for type II hypersensitivity reactions

A

IgG and IgM bind to antigen—> phagocytosis or lysis via complement of Fc receptor, recruitment of leukocytes—> results in cell lysis, inflammation

40
Q

What Ig mediates type III hypersensitivity reactions

A

IgG and IgM

41
Q

What are some examples of disorders associated with type III hypersensitivity reactions

A

Systemic lupus, erythematosus, glomerulonephritis

42
Q

What is the mechanism for type III hypersensitivity reactions

A

Ag-Ab complex deposition—> activate complement—> leukocyte recruitment, release of enzymes and toxic molecules

Results in necrotizing vasculitis

43
Q

What mediates type IV hypersensitivity reactions

A

T-lymphocytes

44
Q

What are some examples of type IV hypersensitivity reactions

A

Contact dermatitis, transplant rejection, tuberculosis, chronic allergies, Johne’s disease

45
Q

What is the mechanism for type IV hypersensitivity reactions

A

Activate T cells—> release cytokines and macrophages—> T lymphocyte mediated cytotoxicity

Peri vascular cell infiltrates, edema, cell destruction, granuloma formation

46
Q

What are immunodeficiency disease

A

Failure of the immune system to protect the host

Inability of immune system to prevent infections and/or neoplasia

47
Q

What is a primary immunodeficiency

A

Congenital or genetic defect in immune system

48
Q

What is an example of a primary immunodeficiency and mechanism

A

Severe combined immunodeficiency syndrome (SCID)- ineffective humoral and cell mediated deficiencies in humans, mice horses, and dogs

49
Q

What is a secondary immunodeficiency

A

Acquired immune defect

50
Q

What is an example of a secondary (acquired) immunodeficiency and mechanism

A

Feline acquired immunodeficiency syndrome- lentiviral induced death of CD4 T cells leading to immunosuppression

Pathology I (11 decks)

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