Physiological Response to Inflammation Flashcards
(28 cards)
Five Cardinal Symptoms of Inflammation and Tissue Damage
Pain Redness Heat Swelling Loss of Function
What is inflammation
Physiological reponse to injury
Haemostasis
The normal response of the vessel to injury by forming a clot that serves to limit haemorrage
Describe events of Inflammation
a) Injury - RBCs leak, platelets rush to clot the area
b) Coagulation - Fibrin accumulates at the wound
c) Early Inflammation (24h) - PMN rush to the site
d) Late Inflammation - Macrophages rush to the wounded area
e) Healing Part
How does microcirculation help in inflammation
- Acute and Intermediate Inflammation
- Oedema formation
- Long Term Inflammatory Conditions
Dilatation
Increased vascularity in an inflamed region
Caused by extravasation (leakage) of coagulating lymph and serum
What does blood flow through tissue normally depend on
Systemic arterial pressue (Function of cardiac output and total peripheral resistance)
Local Vascular resistance (Arteriolar tone)
- Neuronal constrictor and dilator influences
- Endocrine and paracrine hormones (angiotensin II & PGs)
- pO2 & pCO2
Which blood vessels are surrounded by smooth muscle cells and why
All blood vessels except capillaries are surrounded by smooth muscle to alter vessel calibre
This layer surrounds an endothelial cell monolayer
What do mast cells release at inflammation and what does that cause
also by what is it released
Histamines - causes vasodilation and local redness
released by local surrounding tissue
What does bradykinin cause
Direct vasodilation and release of endothelial prostaglandins (PGs); also stimulates nociceptors to cause pain
What are 3 sensory neuropeptides that cause an increase in blood flow during inflammation and thus heat
Substance P
Vasoactive Intestinal Polypeptide
Calcitonin Gene-related peptide
**JESUS CHRIST DONT MEMORISE THIS I HAVE TOO MUCH SYMPATHY FOR YOU
At what level does heat change in injury occur
At the level of microcirculation
What cannot pass through the capillary bed pores
Proteins cannot pass through the pores of the capillary bed
Where does there tend to be an even distribution of contractile proteins and where is there a selective distribution
On the arteriolar side there is an even distribution but on the venular side there is selective distribution around the pores where the two cells come together
Why is the venular site ideal for modification of microvascular permeability
Low hydrostatic pressure
Large surface area
Oedema
Build up of fluid in the body’s tissues making them puffy and swollen
How does oedema occur
Movement of proteins from luminal side into extra-vascular space
factors that modulate contractile state of proteins on venular endothelium has potential to reduce or increase movement of proteins from lumen into extra-vascular space; if they move (as they do in inflammation), the gap between endothelium cells expands so protein can move between them which then causes water to follow
What do factors that increase venular permeability do and 3 examples
Contracting the selectively distributed contractile proteins by elevating Ca2+ in venular endothelia
Expands the gap junction
Histamine
Bradykinin
Leukotriene C4, D4 & Platelet Activating Factor
How do agents that decrease venular permeability work and 2 examples
Relaxing pore proteins by cyclic AMP
B2-adrenoceptor agonists (Salbutamol)
PGl2/Prostacyclins
Triple Response in skin
Biological response to chemical irritant/bee sting/histamine
Flush - Immediate vasodilatation due to histamine coming from outside or as response; capillary vasodilation
They activate sensory nerves causing conscious acknowledgement of injury
Flare - extensive vasodilation in undamaged area surrounding flush; pain and itching. Antidromic activation of sensory nerves releasing inflammatory vasodilators and increasing blood flow
Wheal - Oedema in damaged area but increase in swelling and protein extravasation/vascular permeability in undamaged area (CHECK LAST STEP)
How long are microvascular changes responsible for acute inflammation
Not more than a few hours (approx 2ish?)
Tumour Necrosis Factor (TNFα)
A cytokine/protein released by macrophages that activates complement proteins
Attracts neutrophils to site of action that interact with endothelium, causing them to release other cytokines (IL8) which influences these proteins to allow interactions between neutrophils and endothelium near the site of injury
Only takes place during injury
Cell Adhesion Molecules
Some cells (e.g. neutrophils, monocytes, lumphocytes) will express certain proteins - cell adhesion molecules - that may interact with others on endothelial cell
Level of expression on endothelial and leukocytes determines the type of cell attracted to site of injury
What does release of interleukin 8 (IL8) from activated endothelium cause
Stimulation of neutrophil G protein receptor causing changes in conformation of some cell adhesion molecules on neutrophils which means they interact with the complementary protein on surface of endothelia, attracting the neutrophils to site of injury
