Inflammation (Acute Inflammation) Flashcards
Define Inflammation ?
protective Response of the cell to eliminate the cause of the cell injury as well as the necrotic cells & tissues resuling from that injury.
Thsi response helps is neutralizing microorganims & toxines
According to …… &…….. , the inflammatory respnse is divided into : ……….. & ………..
- Defense capacity of the host // Duration
- Acute // Chronic
DIFF betw Acute & Chronic inflammation
Onset:
A: early & rapid
C: more gradual.
Duration:
A: Short (mins - days)
C: Long (weeks - years)
CCC by
A : Fluid & plasma protein accumulation w/ recruitment of leucocyte as Neutrophils.
C : Accumulation of lymphocyte, MQ, plasma cells w/ vascular proliferation & fibrosis (scarring)
WHAT is Subacute IM ?
inflammation betw acute & chronic
A more severe ACUTE inflammation is called ……….
Fulminant Acute Inflammation.
What is Acute IM ? Its AIM ?
Immediate Rapid response to an injury.
AIM: deliver leucocyte & plasma proteins into site of injury
WHAT is Chronic active IM ?
Chronic im. w/ acute exacerbations during the course of the disease.
Causes of Acute IF ?
- infections
- Immune reactions : hypersensitivity reaction.
- Physical Agents: heat // cold // mechanical trauma // radiation.
- Chemical Agents: acids // alkalies // poisons
- Inert material: foerign bodies as sutures & splinters.
- Trauma
- Tissue necrosis
Acute IF is divided into ………… & ………… events.
vascular // cellular
What are vacular changes during Acute IM ?
1. Changes in vascular caliber & flow by : **
=> Transient vasoconstriction in arterioles irrespectible to the type of injury.
=> Persistent progressive vasodilatation mainly in arterioles but less in cap & venules.
=> This vasodilatation causes :
- Erythema (redness) & warmth in site of IM.
- Increase in local intrvascular hydrostatic pressure => flow of fluid from Cap to extracellular space. FLuids in calles Transudate consisitng of blood plasma w/ few plasma proteins.
** 2. Increase in vascular permeability
this event allows the mv of proetin rich fluid and cells (exudate) into interstitum causing :
- Decrease in osmotic pressure in intravascular space & increasing osmotic pressure in interstitial fluid => mv of water & salts into interstitial fluid => edema (swelling) in sit if acute IM.
- RBCs conc => increase Blood viscosity => stasis (lower blood circulation). Prolonges stasis will result in accumulation of neutrophils on vascular endothelium surface : a process called **margination. **
Vascular events include alterations in ………. //
These alterations include ……….. & ………….
microvasculature (Arterioles / cap / venules),
Changes in vascular caliber and flow & increase in vascular permeability.
What are Causes of Increase in vascular permeability during Acute IM ?
1.** Endothelium Contraction **
- Most common cause.
- leads to intercellular gabs in postcapillary venules.
- Reversible
- Mediated by Histamine, Bradykinin, some chemical mediators.
2. Endothelium Retraction
- Caused by vhanges in cytoskeleton of the cell.
-Affects venules
- Reversible
- Mediated by some cytokines as TNF & IL-1
3. Endothelium injury
By direct injury as burns or infection // or by activation of leucocyte
Compare betw Transudate & Exudate
Transudate:
- Fluid consisitng of blood plasma w/ low plasma proteins.
- Accumulate as a result in increase local intravascular Hydrostatic pressure due to vasodilatation.
**Exudate: **
- Protein rich fluid & cells
- Accumulate as a result of increase vascular permeability
What are cellular events during Acute IM ?
- Leucocyte recruitment
- Leucocyte Activation
Sequence of events of Leucocyte recruitement
**1. Margination & Rolling. **
- Prolonged stasis => accumulation of neutrophils at periphery of vessel => MARGINATION
- Transient & weak adhesion betw leucocyte & endothelium to stick along the way => ROLLING
- This weak adhesion is formed by selectin family (receptors expressed on endothelium & leucocyte).
2. Adhesion:
- Firm adhesion is fromed betw leucocyte & endothelial surfaces by integrins expressed on leucocyte cell surface binding to their ligand on endothelial cell surface.
3. Transmiguration:
- Arrested on endothelial surface => leucocyte migrate through vessel wall by squeezing betw endothelial cells at intervellular junctions => Diapedesis, occurs mainly in venules.
Migration of leucocute through endothelium is mediated by : ……………. & ……………… & ………..
- Chemotactic factors presented in etravascular tissue.
- PECAM-1 : Platelet Endothelial Cell Adhesion Molecule -1, presnted on leucocyte and endothelium surface.
- Leucocyte secretes collagenase to cross the basment memeb into the site of infection.
1- The type of emigrating leucocyte depends on …………. &…………
2- The predominant leucocyte migrating in the 6 - 24 h are …………..
from 24 - 48 h, predominant leucocytes are ……….
- age of inflammatory response & type os stimulus.
- Neutrophils // monocytes
What’s meant by chemotaxis ?
ex of chemotactic factors ?
- mv of leucocytes to the infection site along w/ a chemical mediator.
- EX : C5a // soluble bacterial products.
Leucocyte activation can be done by ……… // ………. & ……….
microbes // necrotic cells products // mediators.
What happen after leucocyte activation ?
- Phagocytosis : first step of elimination of harmful material.
- Production of substances that kill phagocytosed material & remove dead tissues (lysosomal enzymes, reactive O2, nitrogen species)
- Production of substances that amplify inflammatory response : cytokines & Arachidonic Acid metabolites.
What’s meant by phagocytosis ?
it’s the process by w neutrophils & MQ engulf & kill bacteria & foreign particles.
Describe steps of Phagocytosis ?
-
Recognition & Attachement : done by specific surface receptors : opsonins forming a coat around MO to be signed to be phagocytosed.
EX of opsonins : IgG & C3b. -
Engulfment : psudopodes extend from MQ & neutrphils froming a coat around microbe => phagocytic vacuole => phagosome.
phagosome fuse w/ lysosome => phagolysosome. - Killing & Degradation of MO by : ROS (Reactive O2 species) // Reactive Nitrogen Species (esp. NO) // lysosomal enzymes.
What is pathogenesis of IM exudate ?
- Increase vascular Permeability
- Arteriolar VD
- Increase of osmotic pressure in IF due to breakdown of proteins molecule into smaller ones.
IM exudate contains ………. // ………. & …………
- Plasma / serum rich in fibrinogen
- Neutrophils (from emigration)
- MQ (from tissue histiocytes or blood monocytes)
Functions of IM exudate :
4 functions
- Dilutes bacterial toxin
- Contain neutrophils to kill MO, if Neutrophils are destroyed/ they will be chenged into Pus cell => secrete proteolytic enzymes => liquiefy nectrotic debris & prepare area for repair.
- Contains fibrinogen w will change into insoluble fibrin to : form a network on w leucocyte can move to infection site & locate IM area.
- Brings Ab to infction site as bacteriolysins, agglutinis & opsonins to kill, fix, and coat MO.
Mediators may be produced locally by cell in IM site w are called ……….. OR circulating in plasma, synthsized by ………. , as inactive precursors w will be activated as IM site, w are called ……….
Cell-derived mediators // Liver // Plasma Protein-derived mediators
DIFF betw Cell derived mediators and the plasma protein derived mediators
DEF & EX
DEF:
Cell: They are mediators produced locally at site of inflammation in response to stimulus
Plasma: They are mediators circulating in the plasma synthesized by the liver, in inactive precursors form which will be activated at the site of inflammation
EX:
Cell :
- Vasoactive amines: histamine // serotonin // neuropeptides as substance P
- Cytokines: il-1 // TNF-alpha & beta // IFN-gamma
- Arachidonic acid metabolites: prostaglandin // Leukotreines.
- Free radicals : ROS & NO.
- PAF (Platlet Activating Factor)
- Lysosomal components
Plasma:
- Kinin System (Bradykinin)
- clotting system & fibrinolytic system.
- Complement : C5a // C3a // C3b
What are effects of Histamine ?
VD & Increase vascular permeability.
What are effects of PGD ?
VD // Fever // Pain
What are effects of Bradykinin ?
Increase vascular permeability // Pain
What causes increase in Vascular permeability ?
Histamin, PGD, Leukotreines, Bradykinin
What causes recruitement of leucocyte ?
C5a // C3a // bacterial products
What causes fever ?
PGD & IL-1 & TNF
**
What are responsible for tissue injury ?
Lysosomal enzymes & Free radicals
What are local signs of IM ?
- Redness & Hottness : due to VD & Increase BF.
- Swelling:: due to IM exudate.
- Pain: due to : Realease of PGD & Bradykinin + stretching of Tissue bc of IM exudate irritating nerve endings.
- Loss of function: due to Pain & Swelling
**
Types of Acute IM ?
- non suppurative (seroous IM, Fibrinous // catarrhal // pseudomembranous // allergic // haemorrhagic // necrotizing)
- Suppurative (localized & diffuse)
non suppurative : Serous
- Serous IM is ccc by outpouring of ………………. fluid
- according to site of injury, fluid comes out from ……… or ………..
- EX : ……….
1. watery, transparent as protein-poor fluid (transudate)
**2. **serum OR secretion from msothelial cells in serous memb (pleura // pericardium // peritoneum)
- **EX **:
=> Skin blisters in burns
=> Herpes simplex in viral infection.
=> pericardial effusion in viral pericarditis.
non suppurative : Fibrinous
- occurs due to more severe injury resulting in ………………
- EX :
- Fate :
- Increase in vascular permeability => passing of large molecules as fibrinogen through endothelial barrier.
- EX :
=> Fibrinous in serous memb
=> Lobar pneumonia in lung alevoli. -
Resolution: degradation of fibrin by fibrinolysis and removal of debris by MQ => regain the normal tissue structure.
Organization: failure to complete remove fibrin => ingrowth of fibroblasts & BV => opaque dense scarring. if in pericardium => district the mv of heart.
non suppurative : Fibrinous
Morphologic Features : Grossly & Microscopically
Grossly :
=> fibrin precepitated in inner surface of parital memb & outer surface of visceral memb.
=> Opaque // dense // bread & butter appearance.
**Microscopically: **
=> fibrin precipitation appears as eosinophilic meshwork of threads OR as an amourphous coagulum
non suppurative : Catarrhal
- it’s a mild IM in …………
- ccc by ……. secretion
- EX : ?
- MUCUS memeb.
- excessive mucus
- common cold
non suppurative : pseudomembranous
- it’s a severe IM in ………..
- sites & EX :
- pathogenesis ?
- mucus memb.
- EX :
=> Oral & upper Respiratory tract in Diphteria.
=> large intestine in Bacillary dysentry (ccc by bloody mucoid diarrhea) - Bacteria Attached to mucosal surface => produce its exotoxine xasuing patchy necrosis.
- Exotoxin diffuse in submucosal surface casuing acute IM releasing exudate rich in fibrin w will mixes up w/ nectrotic mucosa fromin pseudomembrane.
- Exotoxin reaches the blood => severe toxaemia.
non suppurative : pseudomembranous
Morphologic Features : Grossly & Microscopically
Grossly :
=> grayish white, dirty, loosly attached to underlying tissue.
=> can easily be removed causing bleeding ulcer.
**Microscopically: ** pseudomembrane contains :
=> causative organism.
=> necrotic mucosa
=> fibrin threads.
=> neutrophils (dead or alive) & MQ
non suppurative : Allergic
- Cause : ?
- EX : ?
- CCC BY ?
- Ag-Ab reaction (type 1 hyper)
- eczema // urticaria // bronchial asthma // allergic rhinitis.
- accumulation of exudate fluid => edema.
- Increased Eosinophils in tissue & blood.
non suppurative : Haemorrhagic
- it’s a severe IM ccc by ……… & ………..
- EX : ?
- vascular damage & Haemorrhage
- acute haemorrhagic pneumonia
non suppurative : necrotizing
- it’s IM w/ excessive ………
- EX: ?
- Nerosis
- Vincent’s angina (in tonsil)
