communicable diseases Flashcards

(19 cards)

1
Q

blood clotting and inflammation

A

damage to vessel walls exposes collagen fibres
exposed collagen fibres activate platelets which release thromboplastin
with ca2+ and k+ ions thromboplastin activates prothrombin and turns it into thrombin
thrombin turns soluble fibrogen into insoluble fibrin
fibres form a mesh and with platelets and RBCs forms a clot-dries to a scar

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2
Q

non-specific defences

A

-expulsive responses-vomiting, sneezing, coughing, diarrhoea
-skin- oily sebum layer-slightly acidic to stop growth of bacteria - produced by sebaceous glands
-layer of dead skin cells- pathogen cant penetrate
-covered in microorganisms prevent bacteria growth by fighting for resources
-mucus membrane- lines the trachea secretes mucus that traps pathogens that are then killed by phagocytosis
-enzyme lysosome - kills bacteria by digesting cell wall
-hydrochloric acid - in stomach kills pathogens

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3
Q

phagocytosis

A

-opsonins detect foreign chemical and by attaching to it mark it as foreign
-phagocytes attach to opsonins and engulf it via pseudopodia
-pathogen in phagosome, lysosome fuses with it to form phagolysosome
-lysosomal enzymes break down pathogen and destroy it
-neutrophils stop here
-macrophages do antigen presentation
-glycoproteins already in the cytoplasm move to phagolysosome and bind to antigen molecule
-now a MHC antigen complex
-now moves to exterior of cell and presents antigens to lymphocytes

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4
Q

inflammation

A

tissue damage activates mast cells
-mast cells release histamines which cause :
-nearby blood vessels to widen- vasodilation, increasing blood flow causing it to appear red and hot
-heat prevents antigens reproducing
-vessel walls become more permeable, increase in tissue fluid
-releases cytokinin’s- attract phagocytes
-travel to hypothalamus to increase heat

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5
Q

bacteria

A

-prokaryotic cell
-genetic material not membrane bound
-cannot reproduce outside host cells to do so uses host cells enzymes t copy itself, then can leave and infect new host cell
-TB - tuberculosis mycobacterium

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6
Q

Protoctista

A

-eukaryotic cell
-act as parasites that are pathogens in human body
malaria- vector anopheles mosquito, carry it in the gametes
-migrate to human liver + reproduce + burst out of RBC + multiply quickly

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7
Q

fungi

A

-eukaryotic, multicellular
-obtain nutrients by releasing enzymes and digesting the material around them, products then reabsorbed back into fungal cells
-when reproduce create spores so can spread widely
-athletes foot
-ringworm
-thrus- candida albicans

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8
Q

viruses

A

-smaller than bacteria
-non-living, no cellular structure
-contain genetic material wrapped in protein structure- caspid
-have attachment proteins to allow it to attach to host cells
-hiv aids
-covid

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9
Q

plant diseases

A

-ring rot-bacteria
-tobacco mosaic virus
-black sigatoka -fungal
-blight- Protoctista

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10
Q

transmission

A

-direct, leaves touching
-vectors- beetles, gardening tool
-spores from fungi- water, wind
factors affecting it
-susceptibility- plant health
-climate change
-over crowing

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11
Q

physical defences

A

-waxy cuticle-impermeable waterproof barrier
-cellulose+ lignin -cell wall
-guard cells - ability to close stomata
-thick bark
-callose- polysaccharide forms a sticky glue like substance that can enforce cell walls, block plasmodesmata + sieve tube elements
tyloses- balloon like swelling that can impede or block xylem tubes

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12
Q

plant - chemical/ active responses

A

-contain a verity of chemicals that are anti parthenogenic
-as production requires allot of energy many are not produced until a pathogen is detected - active defences
~phenols- deactivate digestive enzymes so insects eventually die
~hydrolytic enzymes- include lysosomes and chitase break down chitin found in fungal cell wall
~alkaloids- morphine, caffeine, nicotine -taste bitter and affect neuronal transmissions
~terpines- deactivate digestive enzymes
~defensins - destroy bacteria surface membrane

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13
Q

specific immune response

A

-phagocytosis
-t helper cell activation
-clonal expansion
-interleukins released
-clonal expansion
-b lymphocyte activation
-antibody production

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14
Q

antibodies can act as

A

-opsonins
-agglutinins
-anti-toxins

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15
Q

t lymphocytes production

A

-produced in bone marrow
-then migrate to thymus gland in chest were it matures
-then released inro blood

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16
Q

B lymphocyte production

A

-made and mature in bone marrow before being released into the blood
-have antigen receptors that are membrane bound

17
Q

primary immune response

A

-T-helper cells bump into pathogen or antigen presenting cell it matches the response is kickstarted
-pathogen engulfed by specific B-lymphocytes - antigens now presented by MHC complex on surface
clonal selection
-B-lymphocytes acting as antigen presenting cell
-activated T-helper cells use receptors to attach to antigen on B-lymphocyte surface
clonal expansion
-T-helper cells now produce interleukins which activate the B-lymphocyte
-activated B-lymphocytes undergo mitosis to produce plasma cells and B-memory cells
-clones of plasma cells now produce identical antibodies

18
Q

secondary immune response

A

-B-memory cells remain in blood waiting for second infection
-when happens, rapidly turn into plasma cells and release antigens
-as it produces higher amount of antigens and is rapid
-can kill pathogen before symptoms show

19
Q

T-cells

A

T-killer cells - find matching pathogen on infected cell, bind to membrane and inject perforins into cell + peroxides are released which destroy target
T-memory cells- stay in your blood stream for years after infection in large numbers (immunity + vaccination)
T-suppressor cells recognise pathogen has been delt with and calms down immune system