Acute Inflammation Flashcards
Cardinal Signs of Inflammation
Rubor Calor Tumour Dolor Loss of Function
Causes of Acute Inflammation
Micro-organism Mechanical Chemical Physical Necrosis Hypersensitivity
In microcirculation capillary beds are fed by ______ by ______ and ______ by _______
oxygen and arterioles
drained and venules
Starling forces
Control fluid flow across the membrane - Hydrostatic and oncotic pressure
Hydrostatic pressure
Increases filtration of fluid out of capillaries
Oncotic Pressure
Pulls fluid into capillaries and prevents it from leaking
Poiseuille’s Law
Flow is proportional to radius to the power of four
Pathogenesis of Acute inflammation
Changes is vessel radius flow
Changes in permeability
Movement of neutrophils from vessel to extravascular space
TRIPLE RESPONSE
- Red- Vasodilation of capillaries and venules
- Flare- Arteriolar dilation
- Wheal- increased permeability and exudation
Consequences of increased permeability
Imbalance of Starling forces
Exudation = oedema
Fluid loss = increase in viscosity
Decrease in blood flow = decreased in blood pressure
Neutrophil flow in inflammation
Margination –> pavementing –> emigration –> extravascular tissue
Diapedesis
Passage of blood cells through the intact wall of capillaries during inflammation
Benefits of acute inflammation
Non specific response
Neutrophils destroy organism
Plasma protein localises process
Outcomes of acute inflammation
Resolution
Organisation
Chronic Inflammation
Suppuration (pus)
Inflammation of Peritoneal Cavity
Peritonitis
Inflammation of Meninges
Meningitis
Inflammation of Appendix
Appendicitis
Inflammation of Pleural Cavity
Pluerisy
Functions of Neutrophils (8)
Recognise foreign antigens Chemotaxis Adhere to organism Release granules with oxidants and enzymes Release granule contents Phagocyte and destroy Produces pus Extend inflammation to other tissues
Plasma proteins
Fibrinogen
Immunoglobulin
Fibrinogen Function
coagulation factor that forms fibrin and clots exudate
Immunoglobulin Function
Humoral response
Mediators of Acute Inflammation (cells)
Histamine Serotonin Prostaglandin Thromboxane Nitric Oxide Oxygen free radicals
Mediators of Acute Inflammation (endothelial cell surface membranes)
ICAM-1- helps neutrophil stick
Mediators in plasma
Fibrinolysis
Kinin
Complement cascade
Preformed is mast cells besides vessels and released in result of local injury and IgE mediated reaction
Histamine
Preformed in platelets and released when platelets degranulate during coagulation and causes vasoconstriction
Serotonin
Produced from arachidonic acid via cyclo-oxygenase pathway and increases the effect of histamine
Prostaglandin
Promotes platelet aggregation and vasoconstriction
Thromboxane A2
Nitric Oxide
Smooth muscle relaxation
Anti-platelet
Leukocyte recruitment
Released by neutrophils in phagocytosis, amplify other mediators
Oxygen free radicals
Fibronolysis
Breaks down fibrin and prevents blood clots
Kinin system
Bradykinin (pain)
Complement cascade
inflammation-immune system
Molecules inside cells-signalling
PAMP
Danger associated molecular pattern
Intracellular pathways
NF-kB
MAPK
JAK-STAT
Collective effect of mediators
Vasodilation Increased permeability Neutrophi adhesion Chemotaxis Itch and pain
Immediate systemic effects
Pyrexia (pyrogens from WBC)
Fell unwell
Neutrophilia
Longer term effects
Lymphadenopathy
Weight loss
Anaemia
Outcomes of acute inflammation
Granulation
Healing and repair
Fibrosis and formation of scar
Granulation tissue
universal patch forms new capillaries (angiogenesis), fibroblasts, collagen and macrophages
Cardiac output
amount of blood pumped by heart in a minute
Stroke volume
amount of blood pumped by the left ventricle
___ = SV X HR
cardiac output =
_____ = CO X systemic vascular resistance
blood pressure =
Pathogenesis of Septic Shock
mediators lead to vasodilation and and loss of systemic vascular resistance. Results in catecholamine release, increase in HR to compensate
What happens when compensation of increased HR fails to restore SVR
low BP
Reduced perfusion of tissues
Tissue hypoxia- cell death
Causes vasoconstriction
Serotonin
