Quiz
Inflammation and Wound Healing - L6-7
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1How do you describe an organ that is inflamed?
[blank_start]Tissue affected + 'itis'[blank_end] = inflammation of that tissue- ATissue affected + 'itis'
2Acute Inflammation
- Amediated by Interleukin-1 and other cytokines
- BSystemic response to severe injury or inflammation
- CTo over come the cause of Inflammation (occurring after the other type of inflammation fails)
- DWalls off area with fibrous connective tissue
3Chronic Inflammation
- AWalls off the area with fibrous connective tissue
- BMediated by Interleukin-1 and other cytokines
- CSystemic response to severe injury or inflammation
- DTo over come the cause of Inflammation (occurring after the other type of inflammation fails)
4What are the five classical signs associated with Inflammation?
1. [blank_start]Heat[blank_end]
2. [blank_start]Redness[blank_end]
3. [blank_start]Swelling[blank_end]
4. [blank_start]Pain[blank_end]
5. [blank_start]Loss of function[blank_end]- AHeat
- BRedness
- CSwelling
- DPain
- ELoss of function
5Changes occurring during the vascular phase of acute inflammation
1. [blank_start]Vasodilation of arterioles[blank_end]
Capillary beds [blank_start]distend with blood[blank_end]
Signs associated: [blank_start]Heat[blank_end] and [blank_start]Redness[blank_end]
2. [blank_start]Contraction of endothelial cells[blank_end]
Chemical mediators are released [blank_start]causing contraction of endothelial cells[blank_end]
Fluid flows through the [blank_start]gaps into the extracellular space[blank_end]
Signs associated: [blank_start]Swelling[blank_end]
3. [blank_start]Leakage of Fluid[blank_end]
Blood is more [blank_start]viscous[blank_end] - [blank_start]Slows[blank_end] the flow
Increase in [blank_start]RBC[blank_end] and [blank_start]WBC[blank_end] in the area- AVasodilation of arterioles
- BContraction of endothelial cells
- CLeakage of Fluid
- Dviscous
- EHeat
- FRedness
- Ggaps into the extracellular space
- HSwelling
- ISlows
- JRBC
- KWBC
- Lcausing contraction of endothelial cells
- Mdistend with blood
6Functions of the vascular phase
1. [blank_start]Dilution of toxic substances[blank_end]
2. [blank_start]Delivery of antibody[blank_end]
3. [blank_start]Provision on nutrients to WBC[blank_end]
4. [blank_start]Provides fibrinogen[blank_end]- ADilution of toxic substances
- BDelivery of antibody
- CProvision on nutrients to WBC
- DProvides fibrinogen
7Changes occurring during the cellular phase of inflammation
1. [blank_start]Margination[blank_end]
Slowing of blood during the vascular phase - leukocytes contact endothelial cells
2. [blank_start]Emigration[blank_end]
2a. [blank_start]Tethering[blank_end]
2b. [blank_start]Rolling[blank_end]
2c. [blank_start]Activation[blank_end] and [blank_start]firm adhesion[blank_end]
2d. [blank_start]Transmigration[blank_end]
2e. [blank_start]Chemotaxis[blank_end]- AMargination
- BEmigration
- CTethering
- DRolling
- EActivation
- Ffirm adhesion
- GTransmigration
- HChemotaxis
8Functions of the cellular phase
1. [blank_start]Prevent spread of bacteria[blank_end]
2. [blank_start]Destroy bacteria[blank_end]
3. [blank_start]Produce cytokines and chemokines[blank_end] to [blank_start]remove necrotic debris[blank_end]
4. [blank_start]liquefy clotted fibrin to aid in repair[blank_end]- APrevent spread of bacteria
- BDestroy bacteria
- CProduce cytokines and chemokines
- Dremove necrotic debris
- Eliquefy clotted fibrin to aid in repair
9What are the Leukocytes associated with inflammation?
1. [blank_start]Mast cells[blank_end]
2. [blank_start]Eosinophils[blank_end]
3. [blank_start]Lymphocytes[blank_end]- ALymphocytes
- BEosinophils
- CMast cells
10What are the four different inflammatory exudates?
1. [blank_start]Serous[blank_end] exudate
[blank_start]Watery fluid[blank_end], low in [blank_start]protein[blank_end]
2. [blank_start]Fibrinous[blank_end] Inflammation
Fibrinogen --> [blank_start]clots[blank_end]
[blank_start]Neutrophils[blank_end] present
3. [blank_start]Catarrhal[blank_end] Inflammation
Mucus
Due to inflammation of [blank_start]mucous membranes[blank_end]
4. [blank_start]Suppurative[blank_end] or [blank_start]Purulent[blank_end] Inflammation
[blank_start]Pus[blank_end]
Lot of [blank_start]neutrophils[blank_end], [blank_start]necrotic debris[blank_end] and [blank_start]fluid[blank_end]- ASerous
- BWatery fluid
- Cprotein
- Dclots
- ENeutrophils
- FCatarrhal
- Gmucous membranes
- HSuppurative
- IPurulent
- JPus
- Kneutrophils
- Lfluid
- Mnecrotic debris
- NFibrinous
11What is the purpose of inflammatory mediators?
Be the [blank_start]messengers[blank_end] that [blank_start]stimulate[blank_end], [blank_start]amplify[blank_end] or [blank_start]inhibit[blank_end] inflammation- Amessengers
- Bstimulate
- Camplify
- Dinhibit
12Demolition Phase
What: The [blank_start]breakdown and removal of necrotic tissue[blank_end] after the fluid and cellular phases
Processes occurring: [blank_start]Liquefaction[blank_end] and [blank_start]Phagocytosis[blank_end]
Processes function: To [blank_start]prepare for repair and regeneration[blank_end]- Abreakdown and removal of necrotic tissue
- BLiquefaction
- CPhagocytosis
- Dprepare for repair and regeneration
13What are the outcomes of acute inflammation?
1. [blank_start]Complete resolution[blank_end]
If injury is [blank_start]short lived[blank_end] and there is [blank_start]little tissue destruction[blank_end]
Damage is [blank_start]repaired[blank_end] or [blank_start]regenerates[blank_end]
2. [blank_start]Healing by connective tissue replacement[blank_end]
[blank_start]Scarring[blank_end] OR [blank_start]Fibrosis[blank_end] occurs when there is lots of tissue destruction or they cant regenerate
3. [blank_start]Progression to chronic inflammation[blank_end]
If the cause of [blank_start]acute inflammation is not resolved[blank_end] OR
Something [blank_start]interferes with normal healing[blank_end]- AComplete resolution
- BHealing by connective tissue replacement
- CProgression to chronic inflammation
- Dshort lived
- Elittle tissue destruction
- Frepaired
- Gregenerates
- HScarring
- IFibrosis
- Jacute inflammation is not resolved
- Kinterferes with normal healing
14Four phases of wound healing
1. [blank_start]Homeostasis[blank_end]
AIM: [blank_start]To prevent further bleeding[blank_end] [blank_start]by blood clotting[blank_end]
[blank_start]Vessel constriction[blank_end] --> [blank_start]Platelet plug[blank_end] --> [blank_start]Fibrin plug[blank_end]
2. [blank_start]Acute Inflammation[blank_end]
[blank_start]Classical signs of inflammation[blank_end] present
[blank_start]Neutrophils and Macrophages[blank_end] remove [blank_start]debris from injury[blank_end]
3. [blank_start]Granulation tissue formation[blank_end] & [blank_start]replacement of epithelial tissue cells[blank_end]
AIM: [blank_start]Fill in gap of damaged tissue[blank_end]
[blank_start]macrophages[blank_end] produce [blank_start]growth factors[blank_end] --> [blank_start]proliferation[blank_end] of epi. cells and fibroblasts
Granulation tissue = [blank_start]fibrous connective tissue + capillaries[blank_end]
4. [blank_start]Wound maturation and Remodeling[blank_end]
Once inflammation finished & new tissue forms - [blank_start]granulation tissue is replaced by mature[blank_end] [blank_start]connective tissue[blank_end]- AHomeostasis
- BAcute Inflammation
- CGranulation tissue formation
- Dreplacement of epithelial tissue cells
- EWound maturation and Remodeling
- FTo prevent further bleeding
- Gby blood clotting
- HVessel constriction
- IPlatelet plug
- JFibrin plug
- KClassical signs of inflammation
- LNeutrophils and Macrophages
- Mdebris from injury
- NFill in gap of damaged tissue
- Ofibrous connective tissue + capillaries
- Pgranulation tissue is replaced by mature
- Qconnective tissue
- Rmacrophages
- Sgrowth factors
- Tproliferation
15Healing by First Intention
[blank_start]Minimal tissue damage[blank_end] + [blank_start]closely apposed wound edges[blank_end]
Occurs if:
Minimal [blank_start]tissue injury and necrosis[blank_end]
Minimal [blank_start]haemorrhage[blank_end]
[blank_start]No bacterial infection[blank_end]
[blank_start]Wound edges closely apposed[blank_end]- AMinimal tissue damage
- Bclosely apposed wound edges
- Ctissue injury and necrosis
- Dhaemorrhage
- ENo bacterial infection
- FWound edges closely apposed
16Healing by second intention
[blank_start]Larger amounts of tissue[blank_end] - [blank_start]traumatic[blank_end], [blank_start]un-sutured[blank_end], [blank_start]infected[blank_end]
Occurs when:
Greater [blank_start]amount of necrosis[blank_end]
[blank_start]Bacterial infection[blank_end]
Wound edges [blank_start]NOT close together[blank_end]
[blank_start]Large defect[blank_end] present- ALarger amounts of tissue
- Btraumatic
- Cun-sutured
- Dinfected
- Eamount of necrosis
- FBacterial infection
- GNOT close together
- HLarge defect
17Process of wound contraction
Feature of [blank_start]2nd Intention[blank_end]
Wound margins [blank_start]grow towards each other[blank_end]
- [blank_start]Myofibroblasts at edges contract[blank_end] [blank_start]bringing edges together[blank_end]
- [blank_start]Makes smaller wound to fill with[blank_end] [blank_start]granulation tissue and epithelial cells[blank_end]
- Continues [blank_start]after re-epithelialisation[blank_end]- A2nd Intention
- Bgrow towards each other
- CMyofibroblasts at edges contract
- Dbringing edges together
- EMakes smaller wound to fill with
- Fgranulation tissue and epithelial cells
- Gafter re-epithelialisation
18Factors affecting wound healing
1. [blank_start]Age[blank_end]
2. [blank_start]Nutrition[blank_end]
3. [blank_start]Concurrent disease[blank_end]
4. [blank_start]Foreign materials[blank_end]
5. [blank_start]Infection[blank_end]
6. [blank_start]Blood Supply[blank_end]- AAge
- BNutrition
- CInfection
- DBlood Supply
- EForeign materials
- FConcurrent disease
19What are the events involved in fracture repair?
1. [blank_start]Formation of a haematoma[blank_end]
2. [blank_start]Mesenchymal cell proliferation[blank_end]
3. [blank_start]Early callus[blank_end]
4. [blank_start]Advanced callus[blank_end]- AFormation of a haematoma
- BMesenchymal cell proliferation
- CEarly callus
- DAdvanced callus
20What are the factors that affect fracture healing?
1. [blank_start]Inadequate blood supply[blank_end]
2. [blank_start]Infection[blank_end]
3. [blank_start]Instability[blank_end]- AInadequate blood supply
- BInfection
- CInstability
21Antigen:
substance that [blank_start]promotes production of antibodies[blank_end] or [blank_start]includes an immune response[blank_end]
Antibody:
[blank_start]Proteins manufactured[blank_end] in response to [blank_start]foreign material[blank_end] or [blank_start]antigenic stimulation[blank_end]- Apromotes production of antibodies
- Bincludes an immune response
- CProteins manufactured
- Dforeign material
- Eantigenic stimulation
22Hypersensitivity reactions P1
Type I = [blank_start]Immediate[blank_end] Hypersensitivity
Due to [blank_start]IgE antibodies[blank_end]
Occurs within [blank_start]minutes of repeat exposure[blank_end]
Reactions directed against [blank_start]antigens from enviro & parasites[blank_end]
activation of [blank_start]mast cells[blank_end], [blank_start]basophils[blank_end] & [blank_start]eosinophils[blank_end]
Mediators that cause: [blank_start]smooth muscle spasm[blank_end], [blank_start]oedema[blank_end] --> [blank_start]swelling[blank_end], [blank_start]excessive mucus secretion[blank_end]
E.g [blank_start]Allergic Rhinitis[blank_end] (Hay fever)- AImmediate
- BIgE antibodies
- Cminutes of repeat exposure
- Dseconds of repeat exposure
- Eantigens from enviro & parasites
- Fmast cells
- Gbasophils
- Heosinophils
- Ismooth muscle spasm
- Joedema
- Kswelling
- Lexcessive mucus secretion
- MAllergic Rhinitis
- NRhinitis Allergic
23Hypersensitivity reactions P2
Type II = [blank_start]Antibody mediated[blank_end] hypersensitivity
Formation of [blank_start]antibodies directed against antigens[blank_end] of the [blank_start]surface of a cell or tissue[blank_end]
Leads to the [blank_start]cell being destroyed[blank_end]
E.g. [blank_start]Immune mediated haemolytic anaemia[blank_end]
Type III = [blank_start]Immune complex[blank_end] hypersensitiviity
Occurs due to [blank_start]formation of antigen-antibody complexes[blank_end] [blank_start]in bloodstream[blank_end]
These [blank_start]get stuck in capillaries[blank_end]
Neutrophils release [blank_start]toxic free radicals and enzymes[blank_end] into tissue - damage tissue
commonly occurs in the [blank_start]joints[blank_end], [blank_start]glomeruli[blank_end], [blank_start]eye[blank_end] and [blank_start]blood vessels[blank_end]
E.g. [blank_start]Lupus[blank_end] (SLE)- AAntibody mediated
- BImmune complex
- CImmune mediated haemolytic anaemia
- DLupus
- Eantibodies directed against antigens
- Fsurface of a cell or tissue
- Gcell being destroyed
- Hformation of antigen-antibody complexes
- Iin bloodstream
- Jget stuck in capillaries
- Ktoxic free radicals and enzymes
- Ljoints
- Mglomeruli
- Neye
- Oblood vessels
24Immunological Test
Measures [blank_start]immunoglobulin[blank_end] - checks the [blank_start]passive transfer of antigens[blank_end] [blank_start]from colostrum[blank_end]
E.g. [blank_start]ELISA - SNAP Test[blank_end]
Serological Test
Based on the ability to detect reactions [blank_start]between antibody and antigen[blank_end] from the [blank_start]animal in a serum[blank_end]
E.g. S[blank_start]NAP tests - FIV/FeLV[blank_end]
- ANAP tests - FIV/FeLV
- BELISA - SNAP Test
- Cimmunoglobulin
- Dpassive transfer of antigens
- Efrom colostrum
- Fbetween antibody and antigen
- Ganimal in a serum
Informationen
- Beschreibung
- Der Nutzer hat seine Fachbereichs-Information gelöscht. Quiz am Inflammation and Wound Healing - L6-7, erstellt von Gelöschter Nutzer am 13/02/2020.
- Autor
- Gelöschter Nutzer
- Sprache
- English
- Aufrufe
- 25
- Verlauf
- Erstellt am 13 Feb 2020 · aktualisiert am 16 Feb 2020
- Schlagwörter
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