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Basic Pathology        Phase 2a Revision Session Basic Pathology        Phase 2a Revision Session

Basic Pathology Phase 2a Revision Session - PowerPoint Presentation

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Basic Pathology Phase 2a Revision Session - PPT Presentation

Sara Howells amp Katie Edwards 6 th march Basic Pathology The Peer Teaching Society is not liable for false or misleading information Process of inflammation Thrombus and infarction ID: 934146

cells inflammation blood acute inflammation cells acute blood tissue formation thrombus chronic inflammatory due response site process modifiable lymphocytes

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Slide1

Basic Pathology

Slide2

Phase 2a Revision Session

Sara Howells & Katie Edwards

6th march

Basic Pathology

The Peer Teaching Society is not liable for false or misleading information…

Slide3

Process of inflammation

Thrombus and infarction

Growth, cell death and neoplasia

The Peer Teaching Society is not liable for false or misleading information…

Outline

:

Slide4

What is inflammation?

Inflammation is the

local physiological response to tissue injury

. Why does inflammation occur? Occurs to bring all the essential cells for healing to the area of tissue damage.

Slide5

Effects of inflammation

Benefits:

Destruction if invading microbes

Can also have harmful effects Digestion of normal tissues Swelling Inappropriate inflammatory response

Slide6

2 main types of inflammation

Acute v Chronic

What is the difference?

Duration Cells involved Cause

Slide7

What causes inflammation ?

ACUTE

CHRONIC

Tissue Necrosis

Transplant rejection

Microbial Infections

Persistent infection (recurrent acute inflammation)Hypersensitivity reactions e.g. hay feverAutoimmunity -immune responses of an organism against its own cells and tissuesPhysical agents e.g. radiation

Progression from acute inflammation e.g. supprative if an abscess is formed

Chemicals e.g. acid

 

Slide8

5 cardinal sign of Acute Inflammation

Swelling

Due to oedema – accumulation of fluid in the extravascular space Redness Due to dilation of small blood vessels within the damaged area

HeatDue to increased blood flow (hyperaemia) PainDue to stretching and distribution of the tissues to inflammatory oedema

Loss of function

Slide9

Examples of inflammation

Septic Arthritis

Cellulitis

Appendicitis Acne Asthma

Slide10

What are the key cells involved in acute inflammation?

Neutrophil polymorphs

= hallmark of inflammation

Phagocytose pathogens Phagocytosis: pathogens ingested to form phagosome, lysosomes released from neutrophils to kill pathogens, and then expelled from phagolysosomeMacrophages – secrete chemical mediators essential for chemotaxis

Slide11

Slide12

Chemical Mediators of Acute Inflammation

Spread the acute inflammatory response following the injury of a small area

Histamine and Thrombin – cause neutrophil adhesion to endothelial surface

Slide13

What are the 3 main stages of acute inflammation?

1. Changes in vessel calibre

– vasodilation brings blood and cells into the site of inflammation

2. Fluid exudate - the vasodilation and chemical mediators (e.g. histamine, bradykinin, NO, C5a) make vessels more permeable.

Slide14

… continued

Cellular exudate

– accumulation of

neutrophil polymorphs into the extracellular space Later stages of Acute inflammation: Chemotaxis – attraction of cells to site through release of chemicals: process by which neutrophils move to inflammation site, attracted to inflammatory mediators released

Chemotaxis

Slide15

Outcomes of Acute inflammation

Resolution

complete restoration of the tissues to normal Suppuration formation of pus Organisation When tissue is replaced with granulation tissue as part of the healing process Progression

to chronic inflammation

Slide16

Slide17

Chronic Inflammation

Not ideal – it’s an unnecessary when your body cannot turn of the immune response.

Unresolved acute inflammation = chronic inflammation

e.g. ulcers, pulmonary fibrosis etc

Slide18

What causes chronic inflammation?

Primary:

Agent resistant to phagocytosis, e.g. TB, leprosy

Agent indigestible, i.e. fat, bone, asbestos, silicaAutoimmune diseases Crohn’s disease/ulcerative colitisTransplant rejection

Slide19

What cells are involved?

Lymphocytes, plasma cells and macrophages

Less swelling than acute (less exudate formation)

Inflammation and repair is occurring at the same time Fibrosis (scar tissue formation) = key feature.

Slide20

What are the role of each of these cells?

Plasma Cells:

What do they do and where are they derived from?

derive from B lymphocytes, produce antibodiesB-lymphocytes – differentiate into plasma cells to make antibodiesT-lymphocytes – cell-mediated immunity

Slide21

Define Granuloma?

AGGREGATE OF EPITHELIOID HISTIOCYTES

These cells excrete

ACE, which therefore is a blood marker if someone has systemic granulomatosis disease Can you name 4 examples.

Slide22

Thrombosis and Infarction

Slide23

What is a thrombus?

Solid mass of blood constituents

Not necessarily a bad things – essential part of healing and repair.

Physiological - as part of haemostasis (to prevent bleeding outside vessels)Pathological - when there is an imbalance in the blood coagulation system

Slide24

What are the 3 factors affecting the formation of a thrombus

Slide25

Venous and Arterial

ARTERIAL THROMBOSIS

VENOUS THROMBOSIS

Most

commonly superimposed on an atheromaMost commonly due to stasis

HIGH pressureLOW pressureMade up mainly of platelets – WHITE THROMBUS

Made up of mainly coagulation factors (RBC) – RED THROMBUSCan lead to MI/StrokeCan lead to DVT/PETreatment – ANTI-PLATELETS e.g. Aspirin, Clopidogerel Treatment – ANTI-COAGULANTS e.g. Warfarin, Heparin, NOACs (Rivaroxaban)

Slide26

Atherosclerosis

What vessels does it effect?

Name 5 Risk factors for atherosclerosis – try to split them into non modifiable and modifiable

Large and Medium Risk factors:Modifiable - Smoking, hypertension, hyperlipidaemia, diabetes

Non-Modifiable - Age, male sex, post menopausal, family history

Slide27

Endothelial cell dysfunction (lots of cholesterol damages wall

)

High levels of LDL in the blood will begin to accumulate in the arterial wall Macrophages are attracted to the site of damage and take up lipid to form foam cells (inflammatory response)

Formation of a fatty streak (earliest stage of plaque)

The activated macrophages will release lots of their own products - cytokines and growth factorsSmooth muscle proliferation (to intima) around the lipid core and formation of a fibrous cap (collagen)

Slide28

Complications

Thrombus formation if the unstable cap of the plaque ruptures and partially occludes the vessel. Causing ischaemia of tissue

Embolism:

If the thrombus is dislodgedPlaques can weaken wall of arteries and lead to aneurysm AAA – DD central abdominal pain

esp in Males >55

Slide29

What is infarction?

Tissue death due to lack of blood supply to the affected area.

Normally due to a disruption in the blood flow

e.g fibrous plaque

Slide30

What is an embolism?

Process of a mass in the blood being carried through the circulation to the place where it gets stuck

Can also include air, fat or foreign body e.g.

vegetations of bacteria

Slide31