acute inflammation Flashcards
—– is a reaction of a vasuclarized living tissue to a local injury, protective response intended to eliminate the initial —- and the —- cells , it may be —-
-inflammation
- cause of the cell injury
- necrotic cells
- harmful
inflammation is intimately associated w the — process
repair process
the objectives of inflimination:
1- —— and —– the causative agent
2- —– tissue injury
3- begin the process of —-
- localise and eliminate
- limits
- healing
the causes of inflammation include:
- infectious agents
- physical agents
- chemical agents
- immune reaction
- necrotic tissue
1.acute inflammation lasts —–
2. —— and —— response to injury
3- characterised by —- and —-
4- uses —– cells
- minutes to days
- immediate and early
- fluids and proteins
- neutrophils aka polymorphonuclear cells
- chronic inflammation lasts —– and the cells involved are —–
- weeks to years
- mononuclear cells as: macrophages , lymphocytes , and plasma cells
1-the aim of acute inflammation is to get the —- to the site of —- as fast as possible to eliminate — or clear —–
2- the components of acute inflammation:
- neutrophils
- injury
- pathogens
- clear necrotic debris
- components include:
1- vasodilatation
2- endothelial permeability aka leaking fluids
3- extravasation of neutrophils
the five classical local signs of acute inflammation and were known by the romans are:
- heat aka calor
- loss of function aka fcuntion laesa
- swelling aka tumor
- pain aka dolor
- redness aka rubor
heat and redness are caused by ——
swelling is caused by ——
pain is caused by —–
loss of function is caused by —-
- vasodilatation
- vascular permeability
- mediator release
- pain/odema
the 2 major events of acute inflammation are:
1- vascular response: (micro-vessels )
- vasodilation
- increased in vascular permeability
2- cellular réponse
- extraversion of neutrophils
the vascular responses includes
1- —- which is transient and last few seconds
2-
3- increased —– which leads to exudation of protein rich fluid
4- loss of — which leads to concentration of red cells and increased — which leads to blood stasis
- vasoconstriction
- vasodilation
- vascular permeability
- fluid
- visocity
increased vascular permeability is due to:
1- increase in —– pressure
2- decrease in intravascular —- pressure
3- changes in —– cells which includes:
- retraction of endothelial cells
- endothelial injury
- hydrostatic
- osmotic
- endothelial
vasodilation increases the —- and this leads to an increase in —- pressure
- blood flow
- hydrostatic
true or false:
transudate is an ultra filtrate blood plasma and contains a lot of proteins
false , little proteins
vascular permeability —- osmotic pressure as the intravascular pressure of interstitial fluid —-
the exudate are — in proteins with neutrophils and is a characteristic fluid of acute inflammation
- decreases
- increases
- rich
—– is an extravasular fluid with low protein conencetration , the specific gravity is — 1.012 and its from —- imbalance
- transudate
- lower than
- hydrostatic
—- an extravascular fluid with high protein concentration and the specific gravity is —– 1.020 and its from alteration in —–
- exudate
- higher than
- vascular permeability
the steps of the cellular response include:
1- margination
2- rolling
3- pavementing
4- transmigration
5- migration into interstitial tissue
— is the first step of cellular response by which the leuocytes moving from the centre of the vessel towards the periphery of blood vessel.
- normal flow of rbc and wbc in the centre of the vessel
- a —- plasma is moving adjacent to endothelium
- as blood flow – the wbc collect along the endothelium aka magrination
-magrination
- cell poor
- slow
-endothelial activation :
the underlying stimulus causes the release of — which activate the endothelium causing — and —- to be moved quickly to the surface
-selected + lectins ( sugar ) —>
- which are found in :
- mediators
- selectins and other mediators
- selectins
- found in: endothelial cells as E-selectins , leucocyte as L-selectins and platlets as P-selectins
—- is the 2nd step of the cellular process by which the neutrophils bounce/roll along the endothelial cells and transiently adhere to the endothelial cells , this is mediated by —-
- rolling
- selection as they bind to their receptors
leucocytes firmly adhere to endothelial cells in —– which is mediated by:
- pavemteing aka adhesion
- interns , ICAM-1, VCAM-1
—- refers to the cell crawling aka diapedesis and is mediated by PECAM-1
- transmigration
—- is the movement towards the site of injury aka migration and recognition of —– and —–
—– recongnise components of diff types of microbes responsible for the unregulation of nf-kb
- chemotaxis
- microbes
- dead tissue
- tall like receptors TLRs
in cellular response :
1- activation of —–
2- —– which is the coating of the bacterium or the particle to facilitate phagocytosis includes:
3- —- to eat/ingest and destroy
4- release of —– which leads to
- leucocytes
- opsonisation
- immunoglobin and C3b complement
- phagocytosis
- leococytes
- tissue injury which is why inflammation can be harmful
—- are the main effector cells in acute inflammation
neurophil which is responsible in:
- phagocytosis of micro-organism n tissue debris
- mediate cell injury
- inflammatory mediators
- reactive oxygen metabolites
- lysosomal granule contents
the chemical mediators can be derived from :
1- plasma :
- circulating precursor
- have to be activated
2- cell derived
- sequestered intracellularly
- sythesised de novo
most mediators bind to — on the cells surface but have direct —- or — activity and they are tightly —-
- receptors
- toxic activity or direct enzymatic
- regulated
- vasoactive amines
- plasma proteases
- phospholipid derived products
- cytokines
- nitric oxide
- lysosomal enzymes
- oxygen derived free radicals
are all examples of —–
chemical mediators of inflammation
—– responsible for vascular dilation and leakage and includes:
- vasoactive amines
- histamine and serotonin
1—– are found in mast cells, basophils , and platelets .
2- are released in response to —-
3- promotes arterial —- and venular endothelial —- which results in the — of the inter endothelial cell junctions w the —- vascular permeability
- histamines
- stimuli
- dilation
- contraction
- widening
- increase
—– is a vasoactive amine similar to histamine but are found in platelets and released when platetes aggregate
serotonin
plasma protease consist of:
- complement system
- kinin system
- clotting system
The complemtrary system consists of 2 pathways
1- — pathway which requires antibodies to activate as Ag-Ab complex C1 binds to IgG or IgM that’s bound to an antigen
2- —- pathway which doesnt require antibodies and has a microbial surface
- the complement system has a role in —- and membrane —- complex which bunches — in the membrane
-the complement system has also a role in —– includes C3a and C5a which leads to :
- vascular effect aka :
- cellular effect aka:
- classical
- alternative
- immunity ( c5-9 complex )
- attack ( MAC C5-9)
- holes
- inflammation
-increase vasodilatation and vascular permeability - leocycte activation , adhesion , chemotaxis C5a , phagocytosis c3b
kinin cascade leads to the formation of:
this causes :
and its — lived due to kininases
- bradykinin
- increased vascular permeability , arteriolar dilation , smooth muscle contraction , and pain
- short lived
the key for the activation of the clotting system is factor — aka — and the end result is —
- factor XII ( hangman factor )
- fibrin which acts as a glue
arachidonic acid metabolites and platelet activating factor are —- derived products
phospholipids
arachidonic acid is a component of the —-
- the metabolism of it occurs in 2 major pathways which are:
- cell membrane phosphodiser
1- lipoxygenase —> lecotriene
2- cyclooxyrgenase –> prostagladin and prostacyclin
( check slide 46 important )
-arachadonic acid participates in —– inflammation as its effective —– agents act on AA pathways
as:
- acute
- anti inflammatory
1- aspirin and nsaids , coox inhibitors
20 steroid act , in part , by inhibiting phospholipase A2
the —– induces aggregation of planets as it causes —– and —-
it also enhances ——–
- platelets activating factor PAF
- vasoconstriction and bronchosctriciton
-enhances leucocyte adhesion , chemotaxis , and degranulation
—— are soluble mediator and short lived , produced by many cells , are multifunctional and has systemic effect ( bc they can circulate )
cytokines
the nitric oxide is toxic to —- and causes damage in — and it also causes —–
- bacteria
- tissue
- vasodilation
—– causes eradication of bacteria and tissue damage
lysosomal enzymes
—— causes elimination of bacteria and tissue damage which includes:
- oxygen derived free radicals
-direct injury to endothelial cells - injury to extracellular matrix
- injury to other cell types as tumor cells
- dilution of toxins
- arrival of antibodies to the site of inflammation
- drug transport
- delivery of nutrients and o2
- removal of tissue debris
- firbongen —> fribin aka delays bacterial spread
-destrcution of microbial agents - stimulation of immune response responses
are all —– effects of inflammation
beneficial
-mehcnaical effect as epiglottis
- impaired flow as acute meningitis
- impaired function
- tissue destrcution
are all —–
harmful effects go inflammation
the outcomes of acute inflammation are:
- resolution
- abscess formation
- abscess is walled of collection of pus
- progression to chronic inflammation
- healing and repair
( check slide 50 etc for summary plsss)
