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WEEK 7:
Physiological Response to Inflammation:
| Question | Answer |
|---|---|
| inflammation | body's response to physical injury |
| exudate | outpouring of cells and fluid, rich in protein with a gravity greater than 1.02 found within extravascular spaces |
| stimulus for acute inflammation (3) | infections (bacterial or viral), immune reactions (reaction to bee sting), other stimuli (tissue necrosis in acute MI, trauma, radiation, burns, and foreign bodies eg splinter) |
| cardinal signs (5) | rubor (redness), calor (heat), dolar (pain), tumour (swelling), and laesio functae (loss of function) |
| cause of rubor and calor | vasodilation due to histamine mediated vasodilation of arterioles |
| cause of tumour | increased vessel permeability |
| increased vessel permeability can lead tumour (swelling) and | laesio functae (as swelling can make movement more difficult) |
| cause of dolar | tissue stretching due to tumour (swelling) and chemical mediators |
| duration of acute inflammation | short (hour or days) |
| duration of chronic inflammation | long (years) |
| cell derived chemical mediators (products) in acute inflammation (2) | NO and arachidonic acid derivatives (eicosanoids) |
| plasma derived chemical mediators (products) in acute inflammation | kinin system |
| starling forces | how fluid moves out (capillary hydrostatic pressure (and interstitial)) and how fluid moves in (plasma oncotic pressure (and interstitial)) |
| blood enters capillaries at what pressure | 35mmHg |
| blood exits capillaries and enters veins at what pressure | 15mmHg |
| difference between pressure when blood enters capillaries and then enters veins is good because | it drives fluid into interstitium (down a pressure gradient) |
| colloid osmotic pressure/ main force opposing capillary pressure (Pc) is | osmotic pressure created by plasma proteins (protein like albumin stay in blood so retain water with them) |
| average values for oncotic pressure | 25mmHg |
| interstitial fluid pressure is typically between | 0-3mmHg |
| mediators/ factors controlling blood flow (5) | systemic arterial pressure, local vascular resistance, neuronal constrictor and dilator influences, endocrine and paracrine hormones, and pO2 and pCO2 |
| systemic arterial pressure (pressure of blood in arteries) depends on | CO (cardiac output - how much blood the heart pumps), and total peripheral resistance (how narrow blood vessels are) |
| local vascular resistance (arteriolar tone) refers to | how constricted or relaxed arterioles are |
| examples of things which influence neuronal constriction and dilation (2) | sensory nerves and noradrenaline |
| examples of endocrine and paracrine hormones (2) | angiotensin II and prostaglandins |
| diapedesis | WBC move across vessel wall into extravascular compartment |
| transudate | low protein fluid with a specific gravity of less than 1.02 |
| purulent exudate | pus (contains dead/ dying bacteria and neutrophils) |
| consistency of pus depends on | amount of digestion by neutrophil enzymes |
| colour of pus depends on | type of organism and presence of neutrophil derived myeloperoxidase (causing yellow-green colour) |
| types of endothelial linings (and basement membrane) | continuous capillary, fenestrated capillary, discontinuous (sinusoidal) capillary |
| histamine causes endothelial cells to | contract (at post capillary venule) causing fluid and protein to leak out into intravascular space |
| venous vasculature compared to arterial vessels | lower flow rate, thinner walls, and fewer tight junctions than arterial vessels |
| why is contraction at post capillary venule good | their properties eg lower flow rate, ,as well suited for leukocyte trafficking and extravasation (leakage of fluid) |
| events in acute inflammation (AI) | arteriole vasoconstriction -> arteriole vasodilation -> increase blood flow -> mast cells release histamine + high blood flow increase HP in capillaries + venules -> venule increased permeability ->contract exposing BM where transudate flows -> swelling |
| initial vasoconstriction of arterioles is caused by | neurogenic reflex (only lasting a few seconds) |
| arteriole vasodilation during acute inflammation is caused by | histamine and other vasodilators (eg NO) causing vascular smooth muscle to relax |
| movement of leucocytes out blood vessels and role in fighting infection steps (6) | margination, adhesion, emigration, chemotaxis, phagocytosis, and degranulation |
| margination of neutrophils in AI | RBCs aggregate into rouleaux (stack of coins) in venules( due to fibrinogen released from liver) and the rouleau mechanically forces neutrophils out of central axial stream and pushes them to periphery (sides) |
| rolling in of neutrophils in AI | neutrophils roll across venular endothelial cells - occurs in venules due to expression of selectin adhesion molecules on neutrophils and venular endothelial cells |
| why does rolling occur between neutrophils and venular endothelial cells | both express selectin adhesion molecules so can stick to each other and connection is weak/transient so they can bind-detach-bind-detach (roll) along surface |
| selectins | carbohydrate binding adhesion molecules |
| L-selectin | selectin ligand on leukocytes (stimulated by IL-1 and TNF) |
| E-selectin | selectin molecule on endothelial cells |
| P-selectin | derived from Weibel-Palade bodies in endothelial cells (granules in cells) |
| adhesion of neutrophils to venule endothelial cells in AI occurs because | neutrophils express B2-integrins (CD11a:CD18) and venular endothelial cells express integrin adhesion molecules |
| catecholamines and corticosteroids | inactivate neutrophil B2-integrins and produces neutrophilic leucocytosis so marginating pool becomes part of circulating pool |
| enhanced activation of neutrophil B2-integrins causes | total circulating neutrophil count to decrease (neutropenia) |
| neutropenia | decrease in total circulating neutrophils |
| transmigration (diapedesis) of neutrophils in AI | neutrophils moving along venular endothelium dissolve venular basement membrane so exudate can leak in and then neutrophils follow via chemotaxic factors (C5a, LTB4, bacterial products, and IL-8 etc) |
| why is exudate important | dilutes bacterial toxins and brings opsonins like IgG C3b |
| features of chemical mediators | cause vasodilation, increase venular permeability, produce pain, produce fever, promote chemotaxis, and include acute phase reactants |
| examples of acute phase reactants | fibrinogen, ferritin, complement, and C-reactive protein |
| examples of chemical mediators which promote chemotaxis | C5a, LTB4, IL-8 |
| examples of chemical mediators which produce a fever | PGE2, IL-1, TNF |
| examples of chemical mediators which produce pain | PGE2 and bradykinin |
| examples of chemical mediators which increase venular permeability | histamine, bradykinin, LTC4, LTD4, LTE4, C3a, and C5a |
| examples of chemical mediators which cause vasodilation | histamine, NO, PGI |
| histamine | released from mast cells, basophils, and platelets and causes bronchoconstriction, vasodilation of arterioles and increased vessel permeability |
| mast cells are found where | around tissues where vasoactive properties are found |
| when do mast cells degranulate (4) | physical trauma/force/heat/cold, binding antigen, antibody binding fragments of c3a and c5a, and releasing factors from other WBCs eg IL-1/8 |
| triple response | wheal, erythema and flare - classic reaction to abrasion or histamine-releasingstimuli |
| erythema | red spot developed that spreads outward for a few minutes reaching maximal size in 1 minute |
| flare | brighter flush spreads slowly around origin (red halo around wheal) |
| wheal | forms over site of insult (raised bump) |
Created by:
kablooey
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