Unit 3:1 Flashcards

(30 cards)

1
Q

Danger Associated Molecular Patterns (DAMPs)

A

endogenous molecules expressed during times of damage/death; also bind to PRRs

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2
Q

Pathogen Recognition Receptors (PRRs)

A

recognize general pathogenic patterns inducing transcription of cytokines

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3
Q

Types of PRRs

A

Toll-Like Receptors, C Type Lectin Receptors, NOD & NOD Like Receptors, Complement Receptors

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4
Q

Toll-Like Receptors

A

membrane bound receptors that bind various PAMPs and DAMPs to increase inflammation

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5
Q

C Type Lectin Receptors

A

membrane bound receptors that bind carbohydrates of bacteria (MBL) and fungi (dectins)

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6
Q

NOD & NOD-Like Receptors

A

cytoplasmic receptors that recognize G-bacteria and other breakdown products after phagocytosis

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7
Q

Complement Receptors

A

some recognize particles on the surfaces of microbes

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8
Q

Inflammation Goals

A

eliminate cause of injury, remove necrotic tissues, & initiate repair

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9
Q

Inflammation Initiation

A

initiated by IL1, IL6, TNF-alpha acting on hepatocytes or endothelial cells

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10
Q

Inflammation Effects

A

increase vascular diameter (heat & redness), endothelium sprouting cell adhesion molecules causing WBCs to bind endothelium tightly, increase vascular permeability (swelling & pain)

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11
Q

Acute Phase Response

A

response to infection, inflammation, or trauma by changing normal serum proteins called acute phase proteins

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12
Q

Types of Acute Phase Proteins

A

C Reactive Protein, Serum Amyloids, Complement, Alpha Antitrypsin, Fibrinogen, Surfactant

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13
Q

C Reactive Protein

A

recognition molecules that rise withing 4-6 hours of injury of infection; diagnostic tool to identify inflammation show disease management, or healing; mediates apoptosis, complement, phagocytosis

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14
Q

Serum Amyloids

A

serve as opsonins and recruiters of immune cells

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15
Q

Complement

A

lysis, opsonization, & inflammation; includes MBL-opsonin that facilitates the lectin pathway of complement

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16
Q

Alpha 1 Antitrypsin

A

protects self from enzymes secreted from immune cells (emphesyma)

17
Q

Fibrinogen

A

increases with inflammation/tissue destruction to allow generation of clots to prevent spreading of pathogens

18
Q

Surfactant

A

C type lectins that serve as opsonins that facilitate APCs uptake of pathogens and helps bridge innate and adaptive systems and induce direct lysis of microbes

19
Q

Acute Inflammation

A

quick onset; primarily neutrophil response; mild/self limited injury; prominent signs

20
Q

Chronic Inflammation

A

slow onset; primarily monocyte/macrophage response; often severe & progressive; subtle signs

21
Q

Inflammasome

A

is assembled as IL-1 is generated and indicates chronic inflammation

22
Q

Obesity

A

adipocytes secrete inflammatory cytokines (IL1, IL6, TNF-alpha)

23
Q

Metabolic Syndrome

A

combination of glucose intolerance, central obesity, hypertension, & dyslipidemia

24
Q

Eosinophils

A

involved with remodeling of the tissues, fibrosis, due to chronic inflammation

25
Local signs
rubor (erythema), pallor, dolor, & calor in one area
26
Systematic Inflammation
global release of pro-inflammatory cytokines causing: 1. leakage of plasma into tissues, multiple organ failure, & hypotension
27
Type 1 (Alpha & Beta) Interferons
secreted by any virally infected cell: interferes with viral replication, increases expression of ligands for NK receptors, & activates large quantities by plasmacytoid
28
Causes of Fever
Endogenous Pyrogens: secreted from self; IL1, IL6, INE-y, TNF-a Exogenous Pyrogens: secreted from pathogens & induces endogenous pyrogen production
29
Hypothalamus
controls temperature (fever)
30
Benefits of Fever
enhanced leukocyte phagocytosis, increase in leukocyte proliferation endotoxin effects decreased, increased T cell proliferation, enhancement in INF activity & sequestration of iron & zinc