Lecture 4: Acute Inflammation Flashcards
What are the 5 cardinal signs of inflammation
- Redness
- Pain
- Swelling
- Heat
- Loss of function
Acute inflammation is dominated by ___
Neutrophils
Fibrinous= ___
Fibrous= ____
Fibrinous= acute
Fibrous=chronic
What is acute inflammation
Vascular response to cell and tissue injury triggered by numerous physical and biological stimuli
What immune system does acute inflammation activate and what is triggered to release
Innate immune system
Releases: Prostaglandins, leukotrienes, cytokines and activates complement
What interleukin results in chemotaxis and activation of neutrophils
IL-8
What cytokines are fever producing
IL-1, TNF, IL-6
What prostaglandins are fever producing
PGE2
What is the mechanism in which fever inducing cytokines and prostaglandins work
Increase vascular permeability
What are the phases of acute inflammation
- Fluidic
- Cellular
- Reparative
What is the fluidic phase of acute inflammation
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
What is the cellular phase of acute inflammation
- Deliver leukocytes into the exudate at site of injury
- Leukocyte adhesion cascade- neutrophils first- kill and eliminate
What is the reparative phase of acute inflammation
- Resolution
- Healing by fibrosis
- Abscess formation
- Chronic inflammation
What do steroids inhibit
Phospholipase
What do NSAIDs inhibit
COX-1 and COX-2
What do leukotriene receptor antagonists inhibit
Bronchospasm and increased vascular permeability
What are the three complement pathways
- Classical
- Mannose binding lectin
- Alternative
What triggers classical pathway
Antibody opsonization
What triggers the alternative pathway
LPS and polysaccharides of fungal cell walls
What are the three outcomes/goals of activated complement
- Formation of C5a and C3a- attracting leukocytes
- Formation of C3b- opsonization of pathogens and phagocytosis
- Formation of MAC complex- puts pore in membrane—> lysis
What do positive acute phase proteins do
Increase inflammation
What do negative acute phase proteins do
Decrease inflammation
Is C-reactive protein a positive or negative acute phase protein
Positive- increase inflammation
Is albumin a positive or negative acute phase protein
Negative- decrease inflammation
Is serum amyloid A a positive or negative acute phase protein
Positive- increase inflammation
What are the endogenous triggers for pyrexia/fever
Phagocytosis, tissue damage, and immune complexes
What endogenous pyrogens cause pyrexia/fever
LPS
What is the pathway leading to pyrexia/fever
- Exogenous pyrogen-LPS
- Endogenous triggers: phagocytosis, tissue destruction, immune complexes
- Activate neutrophils and macrophages
- Release IL-1, IL-6, TNF-alpha and PGE2
- Hypothalamus activated- increase body temp via vasoconstriction in extremities and muscle shivering
What is the ultimate mediator of febrile response
PGE2
Reduction of ___ appears to be key signal to reduce fever
PGE2
What is edema
Excess fluid in tissues
Edema often occurs with ___, but edema does not always indicate ___
Inflammation for both
What is the reason/mechanism in which edema causes swelling with inflammation
Protein rich fluid leaks out of vessels into extracellular space within tissues
What is the Ig that mediates type I hypersensitivity reactions
IgE
What are some examples of type I hypersensitivity disorders
Anaphylaxis, allergies
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
What Ig mediates type II hypersensitivity reactions
IgG and IgM
What are some disorders associated with type II hypersensitivity reactions
IMHA, neonatal isoerythrolysis, MG, transfusion reactions, pemphigus
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
What Ig mediates type III hypersensitivity reactions
IgG and IgM
What are some examples of disorders associated with type III hypersensitivity reactions
Systemic lupus, erythematosus, glomerulonephritis
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
What mediates type IV hypersensitivity reactions
T-lymphocytes
What are some examples of type IV hypersensitivity reactions
Contact dermatitis, transplant rejection, tuberculosis, chronic allergies, Johne’s disease
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
What are immunodeficiency disease
Failure of the immune system to protect the host
Inability of immune system to prevent infections and/or neoplasia
What is a primary immunodeficiency
Congenital or genetic defect in immune system
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
What is a secondary immunodeficiency
Acquired immune defect
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
