Inflammation I Flashcards

(30 cards)

1
Q

what is inflammation

what are the types

A

a biological reaction to NOXIOUS STIMULUS such as microbes, burns and trauma
- fundamentally PROTECTIVE, but can be harmful if it leads to tissue injury
Types: acute, chronic

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2
Q

what are the 4 cardinal signs of inflammation

what is the 5th one

A
  • Rubor (Redness)
  • Tumor (Swelling)
  • Calor (Heat)
  • Dolor (Pain)

5th sign: Functio Laesa (Loss of function)

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3
Q

describe acute inflammation

A

rapid host response to deliver leukocytes and plasma proteins eg such as ANTIBODIES to the sites of infection or tissue injury

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4
Q

what does acute inflammation protect the body from

A
  • infection
  • trauma (blunt/penetrating)
  • burns/frostbite (thermal/chemical)
  • allergic reaction
  • tissue necrosis
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5
Q

how quickly does acute inflammation last

what does it consist of

A

hours to days

consists of: vascular and cellular reaction

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6
Q

what are the 3 major components of acute inflammation

A

1) VASCULAR DILATION: inc blood flow
2) STRUCTURE CHANGES: in microvasculature to allow plasma proteins and leukocytes to leave circulation
3) EMIGRATION: of leukocytes from microvasculature, their accumulation in the injury site and their activation to eliminate the offending agent

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7
Q

what is the vascular reaction as a result of inflammation

A
  • vessel dilation and INC blood flow
  • leakage of plasma fluid and protein
  • leukocyte EMIGRATION and accumulation in the site of injury
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8
Q

what is the purpose of VESSEL DILATION
what does VESSEL DILATION result in
what is it induced by

A
  • inc blood flow
  • result in HEAT and REDNESS (hyperaemia)
  • induced by: HISTAMINE, BRADYKININ, NO
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9
Q

what is the source and function of histamine as a mediator of vascular reactions

A

source:
mast cells, basophils, platelets
function: arteriole dilatation, inc of venous permeability

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10
Q

what is the source and function of bradykinin as a mediator of vascular reactions

A

source:
Kinin system
function: vasodilatation, inc vascular permeability, PAIN

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11
Q

what is the source and function of nitric oxide as a mediator of vascular reactions

A

source:
endothelial cells
function:
vasodilation

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12
Q

increased vascular permeability is a hallmark of what

A

acute inflammation

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13
Q

what is the purpose of inc vascular permeability

A
  • allows plasma fluid and protein to escape from circulation into extracellular tissue (causes oedema)
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14
Q

what are mechanisms of increasing vascular permeability

A
  • endothelial cell contraction to INC INTRACELLULAR SPACES
  • endothelial cell injury and detachment
  • INC transport of fluid and protein through the endothelial cells
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15
Q

what is extravasation

A

movement of leukocytes from VESSEL LUMEN to interstitial lumen to INTERSTITIAL TISSUE

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16
Q

what are the endothelial adhesion molecules used by leukocytes

A
P-selectin
E-selectin
CD34
ICAM-1 
VCAM-1
17
Q

describe chemotaxis of leukocytes

A

a process in which leukocytes EMIGRATE to the site of injury, driven by substances called CHEMOATTRACTANTS

18
Q

what are the initially phagocytic cells

what do they do

A

neutrophils, followed by monocytes

- produce inflammatroy mediators that maintain the inflammatory response

19
Q

what is chemotaxis

A

process by which leukocytes are attracted by CHEMOTACTIC AGENTS to the site of injury once outside the blood vessel

20
Q

what are the 2 types of chemoattractants

give examples of each

A
endogenous and exogenous 
exogenous: 
- bacterial products 
endogenous:
- complement components 
- cytokines
- products of lipoxygenase pathway (leukotriene B4)
21
Q

what do leukocytes use for recognition

A

LEUKOCYTE RECEPTORS:

  • Toll-like receptors (TLRs) for MICROBIAL PRODUCTS
  • G-protein coupled receptors for SHORT BACTERIAL PEPTIDES CONT N-FORMYLMETHIONYL RESIDUES
  • Opsonin receptors for antibodies, complements, lectins
  • Cytokine receptors
22
Q

what is phagocytosis

A

removal of offending agents

23
Q

what are the stages of phagocytosis

A

1) recognition and attachment
2) engulfment ( engulfed particle fuses with lysosome to form PHAGOLYSOSOME, degranulation)
3) killing (ROS, other lysosomal enzymes)

24
Q

what are the acute inflammatory cytokines

A

TNF-alpha
IL-1
IL-6
chemokines

25
what are the sources of the acute inflammatory cytokines
TNF-alpha: macrophages, mast cells, T-lymphocytes IL-1: macrophages, endotheilial cells, epithelial cells IL-6: macrophages,other cells chemokines: macrophages, endothelial cells, T lymphocytes, mast cells, other cells
26
what is fibrinous inflammation
characterised by FIBRINOUS EXUDATE which can lead to SCAR FORMATION and LIMITATION OF FUNCTION
27
what is purulent inflammation
pus filled fluid consisting of NEUTROPHILS and DEAD CELLS | - typically caused by Staph. infections
28
what is serous inflammation
copious EFFUSION of non-viscous SEROUS FLUID | eg skin blister
29
what is ulcerative inflammation
NECROTIC loss of tissue from the surface, exposing LOWER layers leading to ulcer formation
30
what are the possible outcomes of acute inflammation
- complete resolution (injury is limited/short lived or little tissue damage) - healing by CONNECTIVE TISSUE REPLACEMENT(fibrosis) (if substantial tissue damage, fibroblats grow into area of damage) - progression to CHRONIC inflammation