Cell Pathology 3

Question 1

Causes of inflammation

Answer 1

• Mechanical injury
• Bacteria, viruses, parasites • Ischaemia
• Chemical injury
• Temperature
• Radiation
• Immune mechanism • Foreign body

Question 2

Inflammation symptoms

Answer 2

Note s

Question 3

Inflammatory Process

Answer 3

• Microvasculature changes
• Vasodilation → Redness & heat •  Permeability → Swelling
• Inflammatory exudate • Fluid
• Cells → Chemical mediators

Question 4

Immediate-transient response

Answer 4

• Peaking at 5-10 minutes
• Lasts 15-30 minutes
• Produced by chemical mediators
• Nettle stings or insect bits

Question 5

Immediate-persistent response

Answer 5

• Direct endothelial damage
• Peaking at around 1h
• Lasts until thrombus plugs vessel
• Severe direct injury e.g. burns

Question 6

Delayed-persistent response

Answer 6

• Subtle endothelial damage
• Leakage starts 18-24hr later
• Last 36h or more
Causes include;
• Sunburn
• Radiotherapy
• Bacterial toxins

Question 7

Cellular events in inflammation

Answer 7

• ChangesinBloodflow
• White cells fall to edge of
vessels
• Adhesion molecules allow attachments between endothelial cell and leukocyte
Emigration
• Pseudopodiaform
• Push between endothelial cells
• Proteasesreleased
• Digestbasementmembrane

• Leukocytemigratesbetween endothelial cells
• Basementmembraneseals behind them
• Cellsmovetowardschemical signal
• Towardsinflammatory mediator

Question 8

Phagocytosis

Answer 8

-Phagosome engulfs foreign material
-kill foreign material
-damage to surrounding tissue

Question 9

Leukocytes order in blood

Answer 9

Neutrophils > lymphocytes>monocytes>eosinophils >basophils

Question 10

Neutrophils

Answer 10

• Mediatesmajorityofacuteinflammatoryeffects
• Granulecontentsincreasevascularpermeability
• Migrate to damaged area by chemotaxis
• Phagocytic

Question 11

Granulocytes

Answer 11

> Eosinophils
• Allergic/parasitic conditions
• Granules include major basic protein
Basophils
• Give rise to mast cells
• Granules include histamine

Question 12

Macrophage

Answer 12

• Derived from monocytes
• Migrate to damaged area (later than neutrophils)
• Low numbers which increase with time
• Survive much longer than neutrophils

Question 13

Lymphocytes

Answer 13

> TCells
- Antigen recognition and presentation
• Cell killing
•>Bcells
• Give rise to plasma cells
• Synthesize immunoglobulin’s

Question 14

Chemical mediators;cell derived

Answer 14

• Vasoactive amines (histamine and serotonin)
• Arachidonic acid derivatives (prostaglandin and leukotrienes) • Cytokines (interleukins, interferons, chemokines and GFs)
• Platelet activating factor
• Nitric oxide
• Lysosomal conten

Question 15

Chemical mediators; Plasma-derived

Answer 15

• Kinin system (bradykinin)
• Coagulation and fibrinolytic system (plasmin/fibrin degradation products)
• Complement system (C3a and C5a)

Question 16

Systemic effects of inflammation

Answer 16

• Systemic effects
• Leukocyte production
• Fever
• Tachycardia
• lower Blood pressure • lossofappetite
• vomiting
• skeletalweakness • aching

Question 17

Acute Inflammation

Answer 17

• Short duration
• Minutes to days
• Sequential process
• Neutrophil and macrophage driven
• Protective and reparative mechanism
• Sometimes inflammatory response more harmful than initial
tissue damage/infection

Question 18

Chronic Inflammation

Answer 18

• Persistent (months or years)
• Defined by type of cell present (Lymphocyte,
macrophage and plasma cell)
• Necrotic cell debris
• Tissue granulation
• Fibrosis
• Balance between repair and continues tissue damage

Macrophage are the main effector cells in chronic inflammation:
• Antigen presentation (to lymphocytes)
• Scavenging
• Phagocytosis
• Giant cell formation
• Harbouring of organisms
• Secretion
• Reactive oxygen metabolites
• Proteases
• Arachidonic acid metabolites
• Cytokines
• Growth factors

Question 19

Nonspecific chronic inflammation

Answer 19

➢Occurs following infection
➢Lymphocyte and plasma cell

Question 20

Chronic suppurative chronic inflammation

Answer 20

➢Continued neutrophil production and recruitment
➢Surrounded by fibrous tissue & poorly vascularized
➢Eosinophil-rich

Question 21

Granulomatus chronic inflammation

Answer 21

➢Agents difficult to destroy using lysosomal enzymes

Question 22

Granulomatous Inflammation

Answer 22

• Collection of macrophages frequently surrounded by lymphocytes
• Macrophagefuseforming multi-nucleated giant cell or epitheliod cell
• Micro-organismswhichexcite an immune response eg mycobacteria
• Non-living foreign material

Question 23

Tuberculosis

Answer 23

• Primary
• Never affected before
• Produce lesions
• Neutrophil inflammatory response → macrophage influx
• Macrophage ingest bacilli → present antigen to lymphocytes
• Proliferation of specific T lymphocytes → attract macrophage → Granuloma
• Caseating necrosis

• Secondary
• Patients previously sensitized
• Largely due to reactivation of latent mycobacteria
• More common in immune compromised e.g. steroid treatment, HIV/AIDS
• Miliary
• Extensive caseous necrosis
• Tissue destruction
• Bacilli may enter bloodstream • Granulomas appear in other
organs

Question 24

Crohn’s Disease

Answer 24

• Chronic inflammation
• Affectsalllayersofthebowelwall

• Unknownaetiology
• Non-caseatinggranulomas

Question 25

Wound Healing

Answer 25

Four stages in process
1. Haemostasis
2. Inflammation (removal)
3. Cell proliferation (regeneration)
4. Remodelling (replacement)

Question 26

Last 5 slides

Answer 26

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