MOD2 Flashcards
5 causes for acute inflammation
- physical agents
- chemicals
- microbial infections
- hypersensitivity reactions
- anything causing tissue necrosis
3 Key features + some characteristics
- Vascular and cellular Rxns: accumulation of fluid exudate and neutrophils
- Controlled by a variety of chemical mediators
- Meant to be protective but it can lead to complications and systemic effects
-short-acting, innate, stereotyped
Clinical features - 5 cardinal signs
Rubor, tumor, calor, functio laeso, dolor
Steps of the vascular phase
- transient vasoconstriction
- vasodilation (tumor and calor) increasing blood flow
- increased permeability due to a balance of hydrostatic (forcing things out due to relative pressure) and oncotic pressures (Net flow of protein-rich fluid going into the spaces - leads to an edema)
What is starling’s law
Movement of fluid across a vessel wall governed by the balance between hydrostatic and osmotic pressure between intra and extravascular space
Name the mechanisms of vascular leakage
- endothelial cell contraction - causing a gap mediated by histamine, C5a and NO
- endothelial cell injury: direct (trauma, chemicals, toxins) and indirect (ROS, proteolytic enzymes)
- structural reorganization: being transported from one side to the other. Mediated by interleukin 1 and TNF
- Transcytosis: VEGF induces angiogenesis, increasing the channels in endothelial cells
How does vascular stasis occur and what does it help?
Losing fluid leads to increased concentration of RBCs, resulting in decreased velocity and stasis
Aids neutrophil margination
What is transudate and where/why would you see it
Lower protein content:
In heart failure, you would have a back up of blood in the venule end - increasing hydrostatic pressure and causing more plasma to leak out - edema
Name the types of exudate and what is exudate
High protein content
- purulent (full of pus) would see in meningitis and TB
- Hemorrhagic
- serous (blister-like, fluid strips overlying epithelium, pain and profuse exudate, few inflamm. cells make it clear unless there’s a bacterial infection
- fibrinous: fibrin leaking out gives a bread and butter appearance. e.g; surface of the heart
Primary leukocyte in acute inflammation? How many hours is it active for
Neutrophils, 6-24 hours
What aids rolling of neutrophils
Selectins are expressed by endothelial cells and bind to carbohydrate ligands called Slex on neutrophils
Aided by IG-1 and TNF
What aids adhesion?
Integrins - expressed by neutrophils bind to integrin ligand on the endothelium, aided by C5a, leukotriene B4, IL-1 TNF
What aids diapedesis and what is it?
Neutrophils emigrating through the endothelium
Chemotaxins (e.g; C5a, leukotriene B4, endogenous cytokines, exogenous bacterial products, clotted blood)
Stimulate neutrophils to migrate through the inter-endothelial cell junction
Receptor ligand binding through selectins and integrins
What is chemotaxis
movement along concentration gradients of chemoattractions and chemotaxins
3 steps in how Neutrophils escape from the vessels (not diapedesis)
- relaxation of inter endothelial cell junction
- digestion of BM
- movement
What is opsonization? Name 3 common opsonins and 4 receptors they can bind to
Marking an antibody for ingestion of phagocytes (e.g; neutrophils and macrophages)
C3b, plasma proteins, IgG
Toll-like receptors, G-protein coupled receptors, opsonin receptors, cytokine receptors
Explain the two killing mechanisms of the phagolysosome
- Oxygen-dependent: free radicals released into the phagosome, superoxide converted to hydrogen peroxide through myeloperoxidase from neutrophil granules
- Oxygen Independent: uses enzymes; lysozyme, protease, nuclease and phospholipase to perforate holes in the microbial membrane
Where do endogenous chemical mediators come from
plasma proteins, leukocytes and local tissues
Where do exogenous chemical mediators come from
gram (-) bacteria
Name the 2 vasoactive amines and what produces them
Histamine - increases permeability and vasodilation, platelets, basophils and MAST cells
Serotonin: immediate-early response to injurious stimuli - causes dilation, permeability and pain. Platelets
Name a vasoactive peptide, what it does and where it comes from
Bradykinin; from the plasma precursors kininogen (in the kinin system)
Pain permeability and dilation
Where do prostaglandins come from and what do they do?
Name 2 ‘Other’ chemical mediators
From arachidonic acid metabolites from membrane phospholipids, vasodilation, fever pain and itching
NO, leukotrienes
What does the coagulation/fibrinolytic cascade form and activate?
Form thrombin and fibrin, and activates the kinin and complement systems
What is a byproduct of the kinin system
Gram (-) bacteria
