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Physiology & Science: Immunity Basics > Acute inflammation > Flashcards

Acute inflammation Flashcards

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1
Q

What is acute inflammation?

A
  • Initial response to tissue injury
  • Relatively non-specific
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2
Q

What are triggers of acute inflammation?

A
  • Pathogens/infection: bacteria, viruses, parasites
  • Physical: frost bites, burns, radiation
  • Chemical: chemical burns, irritants
  • Mechanical: trauma, tissue crush
  • Foreign: silica, swallowed bones, dentures, sutures
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3
Q

What is the purpose of acute inflammation?

A
  • Alert the body
  • Limit spread (of infection/injury)
  • Protect injured site from becoming infected
  • Eliminate dead cells + tissue
  • Create conditions required for healing
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4
Q

What are the signs of inflammation?

A
  • Redness (rubor): inc BF to injured area
  • Swelling (tumor): fluid accumulation due to inc vasc perm
  • Heat (calor): inc BF + metabolic activity
  • Pain (dolor): release of pain mediators; inc pressure on nerve ends
  • Loss of function (functio laesa): xs swelling + pain
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5
Q

What agents cause fever?

A

Pyrogens: IL-1, TNF-a

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6
Q

What causes neutrophilia?

A
  • G-CSF stimulation of bone marrow
  • Replenish dead neutrophils
  • Release of immature neutrophils
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7
Q

What are the acute phase reactants?

A
  • CRP, fibrinogen, complement, SAP
  • prod in liver
  • induced by IL-6, IL-1, TNF-a
  • Inc fibrinogen -> roleaux -> higher ESR
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8
Q

What are the 4 vascular events of acute inflammation?

A
  1. Vasodilation: due to histamine, 5HT release from injured cells
  2. Inc BF to injured area: results in influx of WBC, O2, nutrients
  3. Inc vessel perm: endothelial cells contract, results in leakage of fluid + cells in injured tissue
  4. Walling off of injured area: due to formation of fibrinogen clots
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9
Q

What does inflammatory exudate consist of?

A
  • Water
  • Salts
  • Small plasma proteins (fibrinogen)
  • Inflammatory cells
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10
Q

What are the 4 different types of inflammatory exudate?

A
  • Purulent
  • Fibrinous
  • Serous
  • Haemorrhagic
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11
Q

What are the cellular events of acute inflammation?

A
  1. Migration + accumulation of cells
    - > first step - neutrophils
    - > involves a complex process of exit from blood vessels
  2. Removal of pathogens/injured/dead cells
    - > neutrophils phagocytose pathogens + dead tissue
    - > neutrophils live briefly -> dead neutrophils = pus
  3. Migration + accumulation of monocytes
    - > monocytes diferentiate into macrophages
    - > phagocytosis -> clearance of injured site
    - > release factors that promote tissue repair (TGF-B)
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12
Q

RIFTC

What are the 5 steps of neutrophil recruitment?

A
  1. Rolling
  2. Integrin activation by chemokines
  3. Firm adhesion
  4. Transmigration through endothelium into tissue
  5. Chemotaxis to inflammed site
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13
Q

Which molecules are involved in neutrophil recruitment?

A
  • Selectins
  • Integrins
  • Immunoglobulin superfamily cell adhesion molecules (CAMs)
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14
Q

What is the role of selectins?

A
  • Mediate rolling of neutrophils
  • Expressed by activated endothelium
  • Selectins bind to ligands on neutrophils
  • Ligands - carbohydrates
  • Low affinity interaction -> disrupted by flowing blood -> repetetive binding + detaching -> rolling; slow down
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15
Q

What are the two types of selectins?

A
  • P-selectin - preformed granules
  • E-selectin - induced by IL-1 and TNF-a
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16
Q

How does integrin play into neutrophil recruitment?

A
  • Rolling neutrophils express integrins (LFA-1)
  • Integrins in low affinity configuration; no binding to ligands
  • Activated endothelial cells produce chemokines
  • Chemokines bind to receptors on neutrophils
  • -> integrin activation -> high affinity configuration
  • Binding of integrins to ligands on endothelium
  • -> firm adhesion of neutrophils to endothelium
  • Integrin ligands: ICAM-1, VCAM-1
17
Q

Describe neutrophil transmigration

A
  • Neutrophils migrate through interendothelial spaces
  • Neutrophils pass through vessel wall + enter tissue
  • Migrate (chemotaxis) through tissue towards inflammed site
18
Q

Describe neutrophil chemotaxis including examples

A
  • Movement of cells into inflammed sites
  • Guided by chemoattratants:
    • Chemokines (IL-8)
    • Complement components (C5a)
    • Bacterial components (formyl-methionyl petides)

*Note that monocytes use similar mechanisms to leave blood vessels and enter sites of inflammation

19
Q

At the inflammation site, neutrophils clear pathogens. How do they do this?

A
  • Release of granule content
  • Phagocytosis
  • Generation of reactive oxygen species
  • Formation of Neutrophil Extracellular Traps (NETs)
20
Q

What can be phagocytosed?

A
  • Pathogens
  • Damaged cells
  • Dead cells
  • Nutrients
21
Q

What are the roles of phagocytosis?

A
  • Protection from pathogens
  • Disposal of damaged/dying cells
  • Processing + presentation of antigens
    • activation of adaptive immune system
    • links innate + adaptive immunity
22
Q

Name some mediators of acute inflammation

A
  • Inflammatory cytokines: IL-1, TNF-a
  • Histamine, prostaglandins, leukotrienes
  • Chemokines: IL-8
  • Complement (C5a)
23
Q

What are the 3 possible outcomes of acute inflammation?

A
  1. Resolution
  2. Repair
  3. Chronic inflammation
24
Q

What is regeneration?

A
  • Damaging agent removed
  • Injured tissue replaced by cells of same type
  • No change in tissue structure/function
25
Q

What is repair by replacement?

A
  • Injured tissue replaced with connective tissue
  • Scarring -> can alter tissue function
26
Q

What is an abscess?

A
  • Mass of necrotic (dead) tissue
  • Caused by pyogenic (pus-forming) bacteria
  • Can become chronic if not reabsorbed/drained
27
Q

Which tissues have high regeneration ability?

A
  • Epithelial cells
  • Blood cells

Sometimes perfect regeneration, no scarring

28
Q

Which tissues have an intermediate regeneration ability?

A
  • May regenerate when injured
  • Eg. liver, kidney, pancreas
  • If extensive injury -> scarring
29
Q

Which tissues have no/limited regeneration ability?

A
  • Neurons
  • Skeletal muscle
  • Myocardium

Heal with fibrosis, scarring, loss of function

30
Q

What are factors that favour resolution?

A
  • minimal destruction
  • minimal cell death
  • good regenration ability of injured tissue
  • fast clearance of infection
  • quick removal of dead tissue (debris)
31
Q

What factors prevent healing?

A
  • extensive injury
  • poor vascular supply
  • haemorrhage
  • infection
  • poor general health/nutrition; diabetes
  • old age
  • drugs: corticosteroids
32
Q

What is chronic inflammation?

A
  • damaging/infective agent persists
  • persistent inflammation
  • tissue destruction

Physiology & Science: Immunity Basics (6 decks)

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