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Introduction to Inflammation all Questions & answers solved 100% accurately with Complete Solution Graded A+ latest version
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Introduction to Inflammation all Questions & answers solved 100% accurately with Complete Solution Graded A+ latest version

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  • July 5, 2024
  • 12
  • 2023/2024
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Introduction to Inflammation
inflammation- ✅✅ local response to tissue injury (exogenous and
endogenous injurious agents)

causes of inflammation- ✅✅ physical agents
chemical substances
microbial infections
tissue necrosis

Celsus signs- ✅✅ heat, swelling, redness, pain, loss of fxn
vascular rxn to inflammation-✅✅ accumulation of fluid in extravascular
space

✅✅ migration and activation of leukocytes
cellular rxn to inflammation-

systemic rxns to inflammation-✅✅ regeneration + scarring

triple response injury-✅✅ flush (cap dilation), flare (arterial dilation) +
wheal (edema)

Phases of inflammation- ✅✅ tissue injury
Vasodilatation and exudation
Proliferative phase

Tissue injury phase- ✅✅ reversible or irreversible lesions upon to a cell, a
tissue or an organ

exogenous causes of tissue injury- ✅✅ mechanical, physical, chemical,
foreign bodies
infectious organisms
exo/endotoxins
immune mechanism

, endogenous causes of tissue injury- ✅✅ tissue necrosis, enzymes
activation
immune-mediated processes
storage of substances

Proteolysis from tissue injury causes- ✅✅metabolite storage, release of
chem mediators, activation of coag. system and self-antigen formation

Storage of metabolites due to tissue injury leads to- ✅✅ acidosis,
hyperionia (K+ ), hyperosmosis


✅✅
release of chemical mediators due to tissue injury from _________,
________ and ___________ leads to :- from neural terminations,
platelets and mast cells vascular reaction

Vasodilatation and exudation stage breaks into 3 parts- ✅✅ vascular rxn
formation of the inflammatory exudate and phagocytosis
migration of neutrophils and bacterial phagocytosis

Vascular rxn of Vasodilatation and exudation stage- ✅✅ arterioles +
arteries - catecolamines cause spasm (vasoconstrict), serotonin releases
-> paralytic dilation
capillaries - stasis -> poststasis all leads to hyperemia and cap congestion

exudate vs. transudate- ✅✅ Exudate
extravascular fluid with high protein content and cellular debris (implies
increased permeability and therefore inflammation)
Transudate
extravascular fluid with low protein content, little to no cellular debris (no
increased permeability and therefore NO inflammation)


✅✅
Formation of the inflammatory exudate of Vasodilatation and exudation
stage- Hyperionia, hyperosmosis, acidosis (h20 exudate) and
Increasing of vascular permeability (serum+plasma exudate and
leukodiapedesis)

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