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pathology > Inflammation (Acute Inflammation) > Flashcards

Inflammation (Acute Inflammation) Flashcards

1
Q

Define Inflammation ?

A

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

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2
Q

According to …… &…….. , the inflammatory respnse is divided into : ……….. & ………..

A
  1. Defense capacity of the host // Duration
  2. Acute // Chronic
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3
Q

DIFF betw Acute & Chronic inflammation

A

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)

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4
Q

WHAT is Subacute IM ?

A

inflammation betw acute & chronic

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4
Q

A more severe ACUTE inflammation is called ……….

A

Fulminant Acute Inflammation.

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5
Q

What is Acute IM ? Its AIM ?

A

Immediate Rapid response to an injury.
AIM: deliver leucocyte & plasma proteins into site of injury

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5
Q

WHAT is Chronic active IM ?

A

Chronic im. w/ acute exacerbations during the course of the disease.

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6
Q

Causes of Acute IF ?

A
  1. infections
  2. Immune reactions : hypersensitivity reaction.
  3. Physical Agents: heat // cold // mechanical trauma // radiation.
  4. Chemical Agents: acids // alkalies // poisons
  5. Inert material: foerign bodies as sutures & splinters.
  6. Trauma
  7. Tissue necrosis
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7
Q

Acute IF is divided into ………… & ………… events.

A

vascular // cellular

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7
Q

What are vacular changes during Acute IM ?

A

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. **

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7
Q

Vascular events include alterations in ………. //
These alterations include ……….. & ………….

A

microvasculature (Arterioles / cap / venules),
Changes in vascular caliber and flow & increase in vascular permeability.

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8
Q

What are Causes of Increase in vascular permeability during Acute IM ?

A

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

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9
Q

Compare betw Transudate & Exudate

A

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

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10
Q

What are cellular events during Acute IM ?

A
  1. Leucocyte recruitment
  2. Leucocyte Activation
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11
Q

Sequence of events of Leucocyte recruitement

A

**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.

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12
Q

Migration of leucocute through endothelium is mediated by : ……………. & ……………… & ………..

A
  1. Chemotactic factors presented in etravascular tissue.
  2. PECAM-1 : Platelet Endothelial Cell Adhesion Molecule -1, presnted on leucocyte and endothelium surface.
  3. Leucocyte secretes collagenase to cross the basment memeb into the site of infection.
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13
Q

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 ……….

A
  1. age of inflammatory response & type os stimulus.
  2. Neutrophils // monocytes
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14
Q

What’s meant by chemotaxis ?
ex of chemotactic factors ?

A
  • mv of leucocytes to the infection site along w/ a chemical mediator.
  • EX : C5a // soluble bacterial products.
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14
Q

Leucocyte activation can be done by ……… // ………. & ……….

A

microbes // necrotic cells products // mediators.

15
Q

What happen after leucocyte activation ?

A
  1. Phagocytosis : first step of elimination of harmful material.
  2. Production of substances that kill phagocytosed material & remove dead tissues (lysosomal enzymes, reactive O2, nitrogen species)
  3. Production of substances that amplify inflammatory response : cytokines & Arachidonic Acid metabolites.
16
Q

What’s meant by phagocytosis ?

A

it’s the process by w neutrophils & MQ engulf & kill bacteria & foreign particles.

17
Q

Describe steps of Phagocytosis ?

A
  1. Recognition & Attachement : done by specific surface receptors : opsonins forming a coat around MO to be signed to be phagocytosed.
    EX of opsonins : IgG & C3b.
  2. Engulfment : psudopodes extend from MQ & neutrphils froming a coat around microbe => phagocytic vacuole => phagosome.
    phagosome fuse w/ lysosome => phagolysosome.
  3. Killing & Degradation of MO by : ROS (Reactive O2 species) // Reactive Nitrogen Species (esp. NO) // lysosomal enzymes.
18
Q

What is pathogenesis of IM exudate ?

A
  1. Increase vascular Permeability
  2. Arteriolar VD
  3. Increase of osmotic pressure in IF due to breakdown of proteins molecule into smaller ones.
19
Q

IM exudate contains ………. // ………. & …………

A
  1. Plasma / serum rich in fibrinogen
  2. Neutrophils (from emigration)
  3. MQ (from tissue histiocytes or blood monocytes)
20
Q

Functions of IM exudate :

4 functions

A
  1. Dilutes bacterial toxin
  2. 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.
  3. Contains fibrinogen w will change into insoluble fibrin to : form a network on w leucocyte can move to infection site & locate IM area.
  4. Brings Ab to infction site as bacteriolysins, agglutinis & opsonins to kill, fix, and coat MO.
21
Q

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 ……….

A

Cell-derived mediators // Liver // Plasma Protein-derived mediators

22
Q

DIFF betw Cell derived mediators and the plasma protein derived mediators

DEF & EX

A

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

23
Q

What are effects of Histamine ?

A

VD & Increase vascular permeability.

23
Q

What are effects of PGD ?

A

VD // Fever // Pain

24
Q

What are effects of Bradykinin ?

A

Increase vascular permeability // Pain

25
Q

What causes increase in Vascular permeability ?

A

Histamin, PGD, Leukotreines, Bradykinin

26
Q

What causes recruitement of leucocyte ?

A

C5a // C3a // bacterial products

26
Q

What causes fever ?

A

PGD & IL-1 & TNF

27
Q

**

What are responsible for tissue injury ?

A

Lysosomal enzymes & Free radicals

28
Q

What are local signs of IM ?

A
  1. Redness & Hottness : due to VD & Increase BF.
  2. Swelling:: due to IM exudate.
  3. Pain: due to : Realease of PGD & Bradykinin + stretching of Tissue bc of IM exudate irritating nerve endings.
  4. Loss of function: due to Pain & Swelling
29
Q

**

Types of Acute IM ?

A
  1. non suppurative (seroous IM, Fibrinous // catarrhal // pseudomembranous // allergic // haemorrhagic // necrotizing)
  2. Suppurative (localized & diffuse)
30
Q

non suppurative : Serous

  1. Serous IM is ccc by outpouring of ………………. fluid
  2. according to site of injury, fluid comes out from ……… or ………..
  3. EX : ……….
A

1. watery, transparent as protein-poor fluid (transudate)

**2. **serum OR secretion from msothelial cells in serous memb (pleura // pericardium // peritoneum)

  1. **EX **:
    => Skin blisters in burns
    => Herpes simplex in viral infection.
    => pericardial effusion in viral pericarditis.
31
Q

non suppurative : Fibrinous

  1. occurs due to more severe injury resulting in ………………
  2. EX :
  3. Fate :
A
  1. Increase in vascular permeability => passing of large molecules as fibrinogen through endothelial barrier.
  2. EX :
    => Fibrinous in serous memb
    => Lobar pneumonia in lung alevoli.
  3. 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.
32
Q

non suppurative : Fibrinous

Morphologic Features : Grossly & Microscopically

A

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

33
Q

non suppurative : Catarrhal

  1. it’s a mild IM in …………
  2. ccc by ……. secretion
  3. EX : ?
A
  1. MUCUS memeb.
  2. excessive mucus
  3. common cold
34
Q

non suppurative : pseudomembranous

  1. it’s a severe IM in ………..
  2. sites & EX :
  3. pathogenesis ?
A
  1. mucus memb.
  2. 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.
35
Q

non suppurative : pseudomembranous

Morphologic Features : Grossly & Microscopically

A

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

36
Q

non suppurative : Allergic

  1. Cause : ?
  2. EX : ?
  3. CCC BY ?
A
  1. Ag-Ab reaction (type 1 hyper)
  2. eczema // urticaria // bronchial asthma // allergic rhinitis.
    • accumulation of exudate fluid => edema.
    • Increased Eosinophils in tissue & blood.
37
Q

non suppurative : Haemorrhagic

  1. it’s a severe IM ccc by ……… & ………..
  2. EX : ?
A
  1. vascular damage & Haemorrhage
  2. acute haemorrhagic pneumonia
38
Q

non suppurative : necrotizing

  1. it’s IM w/ excessive ………
  2. EX: ?
A
  1. Nerosis
  2. Vincent’s angina (in tonsil)

pathology (4 decks)

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