6.3 Disease Defences Flashcards
1
Q
How is the skin in the first line of defence? (3)
A
- dry, thick and tough region composed of dead cells
- biochemical defence agents (sebaceous gland secrete chemicals ans enzymes which inhibit microbial growth)
- skin secretes lactic acids and fatty acids to lower pH
2
Q
what are the functions of mucous barriers? (4)
A
- protects internal structures (trachea, oesophagus, urethra)
- thin regions of living surface cells that release fluids to wash away pathogens (mucus, saliva, tears)
- contains biochemical defence agents (lysozyme, destroy cell walls and cause lysis)
- mucous membrane are ciliated to aid removal of pathogens
3
Q
what happens to the coagulation cascade? (6)
A
- clotting factors cause platelets to become sticky and adhere to damaged region to form solid plug
- factors initiate localised vasoconstriction to reduce blood flow through damaged region
- clotting factors trigger the conversion of inactive zymogen prothrombin into activated enzyme thrombin
- thrombin catalyses the conversion of soluble fibrinogen into insoluble fibrin
- fibrin forms a mesh of fibres around the platelet plug and traps blood cells to form a temporary clot
- when damaged region is repaired, plasmin (enzyme) is activated to dissolve clot
4
Q
What is the process of the coagulation cascade? (5)
A
- clotting factors cause platelets to become sticky plugs and adhere to the damaged region to form a solid plug
- factors also initiate localised vasoconstriction to reduce blood flow to damaged region
- factors trigger conversion of inactive zymotechnies prothrombin into active enzyme thrombin
- thrombin catalyses conversion of soluble plasma protein fibrinogen to insoluble fibrous form fibrin
- fibrin stands form mesh of fibres around the platelet plug and traps blood cells to from temporary clot
- when damaged region is repaired plasmin (enzyme) is activated to dissolve plug
5
Q
What is the process of coronary thrombosis? (6)
A
- a thermos (fat deposits) develop and reduce diameter of lumen (stenosis)
- restricted blood flow increases pressure in artery and damage arterial wall
- damaged region repaired with fibrous tissue which reduces elasticity of vessel wall
- smooth lining of artery is progressively degraded and lesions of atherosclerotic plaque form
- if plaque ruptures blood clotting is triggered and forms thrombus that restrict blood flow
- if thrombus is dislodged it becomes an embolus and cause a blockage in smaller artériole
6
Q
What is the second line of defence?
A
Non-specific response
- white blood cells
- inflammation, fever and anti microbial chemicals
7
Q
What is the process of phagocytosis? (When solid material are ingested by cell) (5)
A
- phagocytes leukocytes circulate blood and move into body (extravasation) in response to infection
- damaged tissue release chemicals (eg.histamine) drawing white blood cells to site of infection (chemotaxis)
- pathogens are engulfed when pseudopodia (cellular extensions) surround pathogen and fuse to form internal vesicle
- vesicles fuse to a lysosome (forms phagolysosome) and pathogen is digested
- antigen (pathogen fragments) may be presented ont te surface of the phagocyte to stimulate 3rd line of defence
8
Q
What is the 3rd line of defence?
A
Specific
- differentiate between pathogens and respond rapidly upon re-exposure
9
Q
What are B lymphocytes?
A
Antibody producing cells that recognise and target pathogen fragments
Helper T lymphocytes are regulator cells that release cytokines to active B lymphocytes
10
Q
What is the process of 3rd line of defence? (5)
A
- dendritic cells (antigen-presenting cell) migrate toi the lymph node and activate specific helper T lymphocytes
- helper T cells release cytokines to activate B cells capable of producing antibodies specific to antigen
- activated B cella divide and differentiate to form short-lived plasma cells hat produce high amounts of specific antibody
- antibodies will target specific antigen, enhancing capacity of immune system to recognise and destroy pathogen
- a small proportion fo activated B cells (and. T cells) will develop into memory cells to provide long-lasting immunity
11
Q
What are antibodies?
A
- made of 4 polypeptide chains joined together by disulphide bond (Y shaped)
- end of arms -> antigen bind (variable region differ between antibodies)
- rest of molecules is same for all antibodies and acts as recognition site for immunise system
- each antibody recognises a unique antigen (specific)
12
Q
What are prokaryotic metabolic features which are targeted?
A
- enzymes, 70S ribosomes and components of cell wall
(Eukaryotic cells dont have these features so are not targeted) (virus’s dont have metabolism)
13
Q
How is antibiotic resistance increasing? (2)
A
- over-prescribed or misused
- many antibiotics are available without prescribing and included in livestock feed
(Common in hospitals)
14
Q
who discovered penicillin?
A
alexander fleming
15
Q
how was the medical experiment of penicillum conducted? (3)
A
- Florey tested penicillum on infeced mice
- the mice were injected with hemolytic strepococci and four mice were injected with penicillum
- untreated mice died due to bacterial infection and treated ones survived (showed antibiotic potential)
