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
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Slide1
Basic Pathology
Slide2Phase 2a Revision Session
Sara Howells & Katie Edwards
6th march
Basic Pathology
The Peer Teaching Society is not liable for false or misleading information…
Slide3Process of inflammation
Thrombus and infarction
Growth, cell death and neoplasia
The Peer Teaching Society is not liable for false or misleading information…
Outline
:
Slide4What 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.
Slide5Effects of inflammation
Benefits:
Destruction if invading microbes
Can also have harmful effects Digestion of normal tissues Swelling Inappropriate inflammatory response
Slide62 main types of inflammation
Acute v Chronic
What is the difference?
Duration Cells involved Cause
Slide7What 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
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
Slide9Examples of inflammation
Septic Arthritis
Cellulitis
Appendicitis Acne Asthma
Slide10What 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
Slide11Slide12Chemical 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
Slide13What 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
Slide15Outcomes 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
Slide16Slide17Chronic 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
Slide18What 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
Slide19What 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.
Slide20What 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
Slide21Define 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.
Slide22Thrombosis and Infarction
Slide23What 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
Slide24What are the 3 factors affecting the formation of a thrombus
Slide25Venous 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)
Slide26Atherosclerosis
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
Slide27Endothelial 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)
Slide28Complications
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
Slide29What 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
Slide30What 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