Acute Inflammation Flashcards by Holly Hindson

Q

what’s an infectious inflammatory disease?

A

inflammation caused by an infectious disease

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Q

what’s a sterile infectious disease?

A

inflammation without an infectious cause

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Q

what’s the overarching aim of inflammation?

A

to remove damaged tissue/pathogen in order to allow repair

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Q

which immune system plays a central role in inflammatory line of defense?

A

Innate Immune system

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Q

What is acute inflammation?

A

rapid inflammatory response to infection/injury

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Q

how long does acute inflammation last?

A

hours-days

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Q

what are the 6 causes of acute inflammation?

A

microbial infections
hypersensitivity reactions- e.g. nickel allergy
chemical injury- e.g. burn
physical injury
tissue necrosis-e.g. during/after a stroke
autoimmune diseases- directed against a self-antigen

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Q

when does acute inflammation cease?

A

once the cause has been removed (pathogen/damaged tissue)

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Q

what is suppurative (purulent) inflammation?

A

macroscopic appearance of inflammation
large amounts of pus containing dying/dead neutrophils, microorganisms and oedema fluid. (may be walled off by tissue causes abscess)

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Q

what is fibrinous inflammation?

A

macroscopic appearance of inflammation

lots of fibrinogen which polymerises to form a thick fibrin coating

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Q

what’s pseudomembranous inflammation?

A

macroscopic appearance of inflammation

growth of surface layer made of disrupted mucosa, fibrin, mucus and inflammatory cells (often caused by antibiotics)

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Q

what is serous inflammation?

A

macroscopic appearance of inflammation

lots of protein-rich fluid exudate

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Q

what is cattarhal inflammation?

A

macroscopic appearance of inflammation

hypersecretion/ inflammation of mucous membrane

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Q

what’s hemorrhagic inflammation?

A

macroscopic appearance of inflammation

inflammation caused by severe vascular injury

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Q

what’s membranous inflammation?

A

macroscopic appearance of inflammation

epitheilium coated with fibrin, desquamated epithelial cells and inflammatory cells

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Q

what’s necrotising inflammation?

A

macroscopic appearance of inflammation
high tissue pressure (from oedema) leads to vascular occlusion and thrombosis, leading to widespread septic necrosis of affected organ

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Q

what are the vascular (on site) characteristics of inflammation? (5) (more prevalent in acute inflammation)

A

heat
soreness
redness
swelling
loss of function

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Q

What are the systemic characteristics of inflammation? (tend to be more prominent in chronic inflammation)

A

fever
lethargy
loss of appetite
leukocytosis (increased leukocytes)

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Q

what’s the overall process of acute inflammation?

A

recognition of damaged tissue/ pathogens
release of chemical mediators
recruitment of leukocytes and plasma proteins
increased blood flow and permeability allow them to reach site
they enter tissues and release chemical mediatiators (e.g. phagocytes) to eliminate pathogen/ necrotic tissue
tissue can then repair

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Q

what are PRRs?

A

Pattern Recognition Receptors

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Q

What to PRRs recognise?

A

PAMPs and DAMPs

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Q

What are PAMPs?

A

Pathogen Associated Molecular Patterns

- highly conserved structures in bacteria, fungus and viruses

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Q

What are DAMPs?

A

Danger/ Damage associated Molecular Patterns

- released by necrotic cells

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Q

what are TLRs?

A

Toll Like Receptors

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Where are TLRs found?

cell/ endosome membranes

what do TLRs detect?

both DAMPs and PAMPs

which PAMPs do TLRs detect?

microbial RNA/DNA, flagellin and LPS

what is LPS?

Lipopolysaccharides - a major component of gram-negative bacteria

which DAMPs do TLRs detect?

heat shock proteins, ECM components, oxidised LDL

What is Pentaxin?

A PRR

where is Pentaxin found?

extracullularly (in blood stream)

What does Pentaxin detect?

PAMPs- phosphocholine in microbial membranes

How many TLR types are there?

13

How many TLRs are there in humans?

10

Are TLRs membrane spanning?

yes

what do TLRs do after detecting PAMPs/DAMPs?

induce inflammatory genes

What does the extracellular region of TLRs contain?

leucine-rich repeats to form a ligand bidning domain (horseshoe shaped) which dimerises upon ligand binding

what do endothelial cells secrete in acute inflammation?

NO (nitric oxide)

what does NO do?

vasodilation

what does vasodilation do?

increases delivery of plasma and blood cells to site of inflammation

which cells enter the site first in acute inflammation?

neutrophils

which immune cells are the most numerous in the blood stream?

neutrophils

which immune cells are fastest to respond to chemokine release?

neutrophils

how do neutrophils attach to endothelial cells?

using adhesion molecules

what do neutrophils generate?

reactive oxygen and nitrogen species

what's the difference between monocytes and macrophages?

they're monocytes when in blood stream | they're macrophages in the tissue

what's the main, immune property of macrophages?

they're phagocytic

what do macrophages generate?

cytokines | reactive oxygen species

what do mast cells produce?

histamine and other enzymes involved in allergies

what does histamine do?

causes dilation and permeability of BVs

what do platelets do in an inflammatory response?

blood clotting | synthesise serotonin

what is meant by a vasoactive chemical mediator?

chemical that's active on blood vessels

give 4 examples of vasoactive chemical mediators

histamine serotonin lomoms eicosanoids

generally, what are eicosanoids?

signaling molecules

what are the 2 main examples of eicosanoids?

Prostaglandins (PGs) | Leukotrienes (LTs)

what produces prostaglandins?

mast cells, macrophages, endothelial cells

which parts of inflammation are prostaglandins involved in?

systemic and vascular reactions

what secretes leukotrienes?

leukocytes

what are leukotrienes made from?

12- lipoxygenase

what's the difference between lipoxins and leukotrienes?

lipoxins are anti-inflammatory | leukotrienes are inflammatory

where at PGs and LTs derived from?

phospholipid bilayer

what are cytokines?

protein/polypeptide mediators synthesised and released by cells of the immune system during inflammation they aid in the coordination of the inflammatory response act locally by autocrine or paracrine mechanisms

what are chemokines?

a type of cytokine that control the migration of leukocytes and mediate their activity by binding to GPCRs

what are the 2 important chemokines to remember?

TNF-a and IL-1B

what are TNF-a and IL-1B?

interleukins

other than chemokines, what receptors do most cytokines act on?

kinase-linked receptors

what vascular inflammatory actions do TNF and IL-1 have? (5)

- increase leukocyte adhesion molecules - increase pro-coagulant activity - reduce anti-coagulant activity - activate leukocytes - produce other cytokines

what repair actions do TNF and IL-1 have?

- increase fibroblast proliferation | - increase collagen synthesis

what systemic inflammatory actions do TNF and IL-1 have?

- fever - leukocytosis - increase acute phase proteins - reduce appetite - increase sleep

what makes phagocytosis more effiecient?

opsonization

how are complement proteins activated?

by proteolytic cleavage when they leave blood plasma

what's the critical step of the complement cascade?

cleavage of C3

how many pathways can cause cleavage of C3?

3

what are the 3 pathways that cause cleavage of C3?

classical lectin alternative

what happens in the classical pathway?

fixation of C1 to antibody combined with antigen

what happens in the lectin pathway?

triggered by binding of mannose lectin

what happens in the alternative pathway?

triggered by microbial surface particles

what's the general process/ order of complement proteins?

C3 (activated)--> C3a --> C3b --> C5a--> C 5,6,7,8,9 (membrane attack complex)

what are reactive oxygen species involved in?

phagocytosis

what are 2 important reactive oxygen species?

super oxide | hydrogen peroxide

what is Nitric Oxide (NO)?

soluble gas produced from arginine by the action of NOS

What's NOS?

Nitric Oxide Synthase

how many isoforms of NOS?

3

what are the 3 isoforms of NOS?

nNOS, eNOS, iNOS

what is nNOS?

localised primarily in CNS+ PNS | acts as neurotransmitter

where's eNOS found?

endothelial cells, epithelial cells etc.

What's iNOS?

the only calcium independent NOS | controls vascular tone

what inflammatory responses do histamine and serotonin give? (2)

vasodilation | vascular permeability

what inflammatory responses do prostaglandins give? (3)

vasodilation fever pain

what inflammatory responses does NO give? (1)

vasodilation

what inflammatory response do complement proteins give? (3)

vascular permeability chemotaxis leukocyte recruitment/activation

what inflammatory response do leukotrienes give? (3)

vascular permeability chemotaxis leukocyte recruitment/activation

what inflammatory response do interleukins give? (3)

- chemotaxis - leukocyte recruitment/activation - fever

what inflammatory response do chemokines give? (2)

chemotaxis | leukocyte recruitment/activation

what inflammatory response do leukotrienes give? (2)

chemotaxis | leukocyte recruitment/activation

what inflammatory response do bradykinins give? (1)

fever

what inflammatory response do lysosomal enzymes give? (1)

tissue damage

what inflammatory response do ROSes give? (1)

tissue damage

what inflammatory response does LTB4 give? (1)

tissue damage

give a very general summary of acute inflammation (4 steps)

recognise PAMPs/DAMPs vascular changes- increased BF and permeability attracting phagocytes and leukocytes wide range of chemical mediators