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OCR A-level Biology Module 4: Disease, Biodiversities and Evolution > Communicable Diseases > Flashcards

Communicable Diseases Flashcards

the scary diseases that ANY of us can contract, and WHY...!

1
Q

What is a pathogen?

A
  • This is a microorganism that can causes diseases in other organisms, acting as the host
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2
Q

Explain the bacteria that causes disease…

A

Undergoes binary fission by means of reproduction, damaging cells through toxins released.
* PROKARYOTES
* Reletivly large, compared to the virus

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3
Q

Explain the fungi that causes disease

A
  • Grows into structures of micellium as main-body structures, that may grow into mushrooms.
  • Produces reproductive hyphae, releases spores in the atmosphere to reproduce across environment
  • Hyphae = releases extracellular digestive enzymes (cellulase) causing additional decay
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4
Q

Explain the Viruses that causes disease

A
  • Invade organism cells, using genetic machinery to manufacture more copies of same virus
  • Host cell will burst, cusing cell damage, relasesing many more viruses to invade further cells
  • NON-LIVING, according to M.R.S G.R.E.N

Movement, Respiration, Sensitivity, Growth, Reproduction, Excretion and Nutrition.

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5
Q

Explain the Protists that causes disease

A
  • These enter host’s cell, and will feed with the available nutrition to grow and reproduce
  • Normally carried with vectors, and transfered through fluids/contact

e.g Plasmodium via Mosquitoes…….

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6
Q

How does Ring Rot come about?

A
  1. Occurs in PLANTS
  2. Caused by BACTERIA
  3. Ring of decay around vascular tissues in potatoes/tomatoes, alongside leaf wilting
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7
Q

How does Tobacco Mosaic Virus come about?

A
  1. Occurs in PLANTS
  2. Caused by VIRUSES
  3. Leaf discolouration in mosaic-like pattern in many plants.
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8
Q

How does Blight come about?

A
  1. Occurs in PLANTS
  2. Caused by PROTISTS
  3. Chlorosis and browning of plant tissues in potatoe tubers, alongside leaf wilting
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9
Q

How does Black Sigatoka come about?

A
  1. Occurs in PLANTS (bananas mostly)
  2. Caused by FUNGI
  3. causing leafing spots on bananas, significantly reducing yeilds
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10
Q

How does Athlete’s Foot come about?

A
  1. Occurs in ANIMALS (human mostly)
  2. Caused by FUNGI
  3. Redness, Itching and flaking of growth between toes in feet.
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11
Q

How does Ring Worm come about?

A
  1. Occurs in ANIMALS
  2. Caused by FUNGI
  3. Ring-shaped growth with spores erupting through the skin, causing rashes in mammals
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12
Q

How does Influenza come about?

A
  1. Occurs in ANIMALS
  2. Caused by VIRUS
  3. attacking respiratory system, causes muscle pains and headache in humans
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13
Q

How does Bacterial Meningitis come about?

A
  1. Occurs in ANIMALS
  2. Caused by BACTERIA
  3. infection of the meninges, being membranes surrounding brain and nerves , may become inflamed/swollen
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14
Q

How does HIV come about?

A
  1. Occurs in ANIMALS
  2. Caused by VIRUS
  3. **destroys the immune system by attacking WBCs, compromising immune response ** in humans
  4. Becomes AIDS when developed for a while, becoming much more susceptible to many other diseases
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15
Q

What makes HIV a more unique virus to many?

A
  1. This is a RETROVIRUS!
  2. Will contain RNA rather than DNA, like a regular virus
  3. Will have enzyme Reverse Transriptase, to convert single stranded RNA genome to DNA when injected into host cell’s machinery
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16
Q

Why would Bacteria and Fungi thrive more in vascular tissue, in a plant?

A
  1. Abundant supplyof water (xylem) and sugar+nutrients (phloem)
  2. Will MASSIVLEY aid for optimal growth in these organisms
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17
Q

How does Malaria come about?

A
  1. A parasite in the bloodstream that can cause headaches and repeating episodes of fever - comas and even DEATH
  2. Protist = Plasmodium Falciparum
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18
Q

How does Tuberculosis (TB) come about?

A
  1. Occurs in ANIMALS
  2. Caused by BACTERIA
  3. Killing cells in the entire body, mainly affecting respiratory systems (lungs…)
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19
Q

Give and explain the methods of Direct Transmissions of disease

A
  1. Physical Contact: direct touching involved my ANY means; stopped by Condoms, Disinfectant, Sterilising equipments
  2. Feacal/Oral: Consuming anything with pathogens; stopped by Sewage Treatment, Cooked and Washed meats
  3. Droplets: Pathogens carried in air via drops; stopped by “Catch it - Kill it -Bin it”, tissues when sneezing
  4. Spore Transmission: Fungal/pathogenic spores carried in air; stopped by masks when needed, wash skin after soil contact
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20
Q

Give and explain the methods of Indirect Transmissions of disease

A
  1. Vector Transmission: another organism used to gain entry into primary host, without harming this organism; stopped byKilling potential vector organisms, vaccinations, sterilising vectors
  2. Fungal Spores: airborne transission carried in the air; stopped by Condoms, Disinfectant, Sterilising equipments
  3. Leaf Distribution: Infected leaf shedding falls to soil, able to reproduce, and infect other plants ; stopped by Incinerating infected leaves/entire plant before shedding
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21
Q

How does Malaria infect an individual?

A
  1. A female anopheles mosquito will suck blood of infected person
  2. Will also pick up gammetes of plasmodiumin the bloodstream
  3. Plasmodium will be nurtured and develop in mosquitotes salivary glands
  4. Another person is bitten
  5. Inside the liver, the parasites invade liver cells and multiply asexually to form more parasites.
  6. After maturing, the liver cells burst, releasing many parasites back into the bloodstream.
  7. The parasites (plasmodium falciparium) then invade erythrocytes, where they continue to multiply and cause the symptoms of malaria.
    and cycle starts over!!
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22
Q

What are Passive Defences in organsims?

A
  • These are defences in place BEFORE a pathogen infection has taken place, preventing initial entry of said pathogen!!
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23
Q

What are Active Defences in organisms?

A
  • These are defences in place AFTER a pathogen infection has taken place, preventing internal speading of said pathogen, using ENERGY, and CHEMICALS (mostly….)
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24
Q

What is a way to remeber Plant Physical Defences?

A
  1. LST CW BC = Lost Cow Back!

= Ligin, Stomata, Tylose, Cellulose, Waxy Cuticle, Bark, CALLOSE,

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25
Q

How can we describe CALLOSE and TYLOSE?

A
  1. CALLOSE = Large polysaccharide, blocking sieve end-wall plates, as such polymers will block pathogen = spread decrease!
  2. TYLOSE = Baloon-Like swelling of toxic chemicals, filling/blocking xylem cavity, containing Terpenes, also toxic to pathogens
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26
Q

What is a way to remeber Plant Chemical Defences?

A
  1. P.A.T.H.O.D. = say how it is read

= Phenols (tanins that kill insects), Alkeniods (caffine, cocaine = bitter taste!), Terpeniods (antibacterial oils) , Hydrolictic Enzymes (degrading pathogen cell wall), Defensive Proteins (inhibiting ion channel transport), Oxidative Reagents (highly reactive oxygen molecules damaging pathogens)

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27
Q

Another means of Active defence? (plants…)

A

NECROSIS!

Another programmed cell death, due to untreatable site of infection

Killings infected cells = Stoppping pathogen spead through stopping water/nutrient access to reproduce

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28
Q

Define what is meant by parasite

A

This is an organism that lives inside a host organism, feeding and using nutrients from this organism, while harming this host organism

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29
Q

Suggest reasons for possible rapid spread of pathogens (e.g. Fungi)?

A
  1. Vectors/Infected individuals moving over a large geographical area
  2. Lack of resistance/Immunity from the pathogen
  3. Overpopulation/Overcrowding in a small area
  4. Fungal spores / larger distances
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30
Q

Why would protsist Plasmodium use erythrocytes as part of life cycle?

A
  1. To avoid any foreign recognition from the immune system
  2. To complete its life cycle
  3. Provides a source of nutrients to grow and nourish
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31
Q

What chemical processes will take place during Blood Clotting?

A
  1. Abrasion to skin will cause opening to pathogens!
  2. Exposed Collagen will bind to platelets, to release 12 Clotting Factors + Ca2 ions
  3. Inactive Thrombokinase will become Active Thrombokinase = important enzyme for next step
  4. THEN Prothrombin becomes Active Thrombin = another enzyme inportant for next step
  5. THENN Soluable Fibrinogen becomes Insoluable Fibrin = big player in “fish netting” of RBCs.
  6. THENNN RBCs and Platelets are all trapped in a fat clump, drying up and becoming solid…….

Thrombin becomes active when certain amino acids are removed from the active site: REALLY COOL!

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32
Q

Outline the Skin’s details on primary defence….

A
  • Upper Layer = Epidermis Layer, with layer of cells underneath
  • Most cells are Keratinocytes, produced by mitosis from base-layer Multipotent Adult Stem Cells
  • As such cells approach surface, they undergo Keratinisation = Cytpolasm slowly replaced by Keratin Protien, drying out…..
  • Keratinised DEAD CELL SURFACE LAYER becomes very surface of skin!
    HENCE, BEING MAIN PRIMARY DEFENCE OF HUMANS!
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33
Q

What makes the skin surface a good primary defence

A

Keratin-Tough Epidermis= Keratinocyes provide a very tough outer barrier to pathogens to penetrate
Non-Living cells = no cyloplasm; no chemical reactions; less susceptible to pathogenic infection on skin!

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34
Q

What is an Enzyme Cascade?

A
  • An enzymatic cascade is a sequence of successive activation reactions involving enzymes, characterized by a series stemming from an initial stimulus.
  • The product of each preceding reaction catalyzes and is consumed in the next reaction, and so forth……
35
Q

WHERE and WHY are the Mucus Membranes found?

A
  1. Found in: Ears, Lungs, Genitals and Digestive System
  2. These all have very thin membranes that means pathogens can enter much more easily, into the body
  3. Hence, at airways, epithelial tissue has GOBLET CELLS that secretes the mucus, to TRAP said pathogens
  4. At epithelial tissue, we also have Ciliated cells, that have Cilia, to waft bands of mucus away from the lungs!!
36
Q

How does Inflammation Response take place?

A
  • Pathogen enters via wound site!
  • Mast Cells will detect and recognise foreign pathogens invading tissue, releasing Histamines in response
  • Histamines will cause VASODILATION in nearby blood vessels, causing neutrophils and erythrocytes to leak out
  • ERYTHROCYTES = causes the redness and swelling, due to more concentrated in a smaller location
  • MACROPHAGES = Releases cytokines to initiate tissue repair

(can be paired with specific immune response….)

37
Q

How does the Lymphatic Sytem help with Inflammation?

A
  • Main Role: Drains away waste fluids from site of injuries!
  • Such fluid will drain to nearby Lymph Nodes, containing Lymphocytes (can haveLymph Node Swelling during sudden surge of lymphocyes activity and numbers!!)
38
Q

What does Lymph Fluid consist of?

A
  • Contains fluid that CAN NOT be absorbed back into the cappileries!!!
  • Consists of Fats, Protiens, Damaged/Cancerous cells, Pathogens and Lymphocytes
39
Q

What are some other secret primary defences?

A
  1. TEARS: Contains enzymes, providing killing of some pathogens in the eyes
  2. WAX: At ear canal, ca trap entering pathogens
  3. REPRODUCTIVE: Mucus plug walls in the cervix, also trapping pathogens!
40
Q

Some expulsive forces to remove pathogens by Reflex Actions?

A
  • SNEEZING!
  • COUGHING!
  • VOMITING!

All are methods to urgently remove disturbances/toxins/irritation inflicted by PATHOGENS!!

41
Q

What are Secondary Non-Specific Defences?

A
  • These are defences that are used when a pathogen has already entered the bloodstream
  • These still remain as NOT SPECIFIC to antigens, but forigen pathogens as a whole…
42
Q

What are Antigens?

A
  • These are protiens on plasma membrane that are chemical markers for immune system to recognise if self or foriegn cell
43
Q

What are Opsonins?

BE SURE TO CHECK THIS LIL BIT OUT!!!!!

A
  1. These are protien molecule that attach to antigens on pathogen surface
  2. Type of UNIVERSAL ANTIBODY that is NON-SPECIFIC, allowing a phagocytic cell to easily bind, engulf and digest the pathogen.
  3. Hence, are able to bind to a RANGE of antigens of differing pathogens, (but not ALL…)

RELEASED BY PHAGOCYTES!!!!!!!!!!!!!!

44
Q

What is Opsoninisation?

A

The act of Opsonins binding to antigens on the pathogen surfaces…….

45
Q

What are some activity differences between Neutrophils and Macrophages?

A
  1. Macrophages: Engulfs pathogens, but not FULLY digesting
    Antigens on digested pathogens are conserevd, and used for protien complex on plasma membrane
    Becomes antigen presenting cell, presenting antigens for antibody production in Lymphocytes
  2. Neutrophils: 100% killing , undergoes the good and proper engulfing and digesting of pathogens, containing lysosomes of hydrolyctic enzymes to do so!
46
Q

What are some physical differences between Neutrophils and Macrophages?

A
  1. Macrophages: Larger in size, lasts for 3 months, irregular outer membrane shape, engulfs up to 100 pathogens
  2. Neutrophils: Smaller in size, Multi-Lobed nucleus, smoother outer membrane shape, lasting for a few days with consumption of up to 20 pathogens.
47
Q

What is a Monocyte and a Phagosome?

A
  1. Monocyte = This is the IMMATURE VERSION of a Macrophage, as it travels inactive in the bloodstream (more adolecscent in the life cycle)
  2. Phagosome = The large vauole/vesicle that surrounds pathogens when engulfed
48
Q

How do Neutrophils engulf and digest pathogens?

A
  • They contain many Lysosomes, that contain Hydrolyctic Enzymes, that will break down the structure of the pathogen, destroying it
  • Waste products will be expelled via excocytosis
49
Q

Why does the macrophages also antigen-presetning cells, and not neutrophils?

and WHY ANTIGEN PRESENTING, and not just ANTIGEN….

A
  • This is because macrophages are larger in size, with a much longer lifespan than neutrophils (despite both phagocytes)
  • This will mean that they will be able to carry antigen-presetning much longer, for the lymphocytes to produce antibodies for same antigen!

If a sole antigen, macrophage will be recognised by immune response as foreign, and will be attacked, and we do NOT want thia to happen

50
Q

4 Main ways Phagocytes are adapted to their function!

A
  1. Well Developed Cytoskeleton = Easily changes shape to engulf and digest pathogens + important lysosome transportation network
  2. Many mitochondria = ATP releases energy for cell movements + endo/exocytosis
  3. Multi-LObed Nucleus (neutrophils specific) = Able to squeeze through cell layers in tissue to reach infected locations
  4. Many Ribossomes = Efficient protiensynthesis to make lysozyme enzymes + antigen-presenting!
51
Q

Where are the phagocytes made??

A

IN THE BONE MARROW!!!!

52
Q

What are Hydrolyctic Enzymes?

A

Enzymes using water molecules to break down most chemical bonds in biological structues (ester/peptide/Hydrogen….)

53
Q

Describe how a Neutrophil can undergo phagocytosis!

A
  • Chemicals released by pathogens as well as chemicals released by the body cells under attack attract neurtophills via chemotaxis to the site where the pathogen are located
  • Neutrophills move towards pathogens, Which may have antibodies attached to their surface antigens
  • Neutrophills have receptor molecules on their surface that recognise antibody molecule and attatch to them
  • Once attached to the pathogen the cell surface membrane of the neurtophill extends out engulfing the pathogen and trapping the pathogen with a phagosome
  • This part of the process is known as endocytosis
  • The neutrophill releases digestive enzymes into the vacuole, becoming phagolysosome to occur
  • These enzymes destroy the pathogens structure
  • After killing and digesting the pathogens the neutrophill die (eventually)
54
Q

What is a Lymphocyte?

A
  • This is a WBC with a round, whole nucleus, found mostly in the lymphatic nodes/vessels
  • Undergoes SPECIFIC IMMUNE RESPONSE, capable of recognising specific antigens!
55
Q

What are Cytokines?

A
  1. These are cell-signalling chemicals heavily involved in immune response (but not quite hormones)
  2. Use to signall to other WBCs, to carry out certain immune responses
56
Q

What are the different types of Cytokines?

A
  1. Monokines: Released by macrophages, attracting neutrophils to stimulate B lymphocytes to differentiate and relase specific antibodies
  2. Interleukins: Released by T Cells and macrophages Stimulates clonal expansion and differentiation of B lymphocytes
  3. Interferons: Inhibiting virus replication, by stimulating T Killer Cell activity!
57
Q

What is Clonal Expansion?

A

This is a method of mitosis to rapidly produce lymphocytes in a shorter given time period

58
Q

What are B lymphocytes Plasma+Memory Cells?

A
  • B PLASMA CELLS: These will produce the specific, complamentary antibodies via exocytosis, at very very large quantities
  • B MEMORY CELLS: Cells that remain in the bloodstream for a very long period, providing immunity from encountered pathogens and a much faster secondary immune response
59
Q

How would B Lymphocytes respond to antigen exposure?

A
  1. B lymphocytes encounters anitgen via pathogen or macrophage antigen-presenting cell
  2. Interleukins released from T Cells and macrophages will cause CLONAL EXPANSION.
  3. Monokines released from macrophages will cause CELL DIFFERENTIATION, into plasma and memory cells
  4. Plasma cells die in days due to ATP energy all used for mass-producing antibodies, while Memory cells remain for YEARS!

CLONAL EXPANSION = PROLIFERATION!! (hit a 4 if u forget…..)

60
Q

What are T Helper+Killer+Memory+Regulator cells

A
  1. T Helper Cells: Secretes cytokines to stimulate colonal expansion and differentiation of B Cells
  2. T Killer Cells: Destroys cells infected with viruses, by injecting H2O2, causing cell lysis (killing away cell+virus)
  3. T Memory Cells: Remains in the blood, casugin a much faster secondary response upon second encounter!
61
Q

What do T Regulator Cells even do?

A
  • They are responsible for shutting down immune activity following removal of pathogen
  • Preventing AUTOIMMUNITY!
62
Q

Mention and state why do we need the 3 lines of Defences?

A

These are PRIMARY NON-SPECIFIC, SECONDARY NON-SPECIFIC AND SPECIFIC DEFENCES
1. = Prevents initial pathogen entry into body/bloodstream
2. = Short-Term response that can remove pathogen, but NOT lead to longer-term immunity
3. = Immune response that remains SPECIFIC to PARTICULAR ANTIGEN, leading to life-long immunity via B Memory Cells!

63
Q

What is a immunoglobin?

A
  • Complex protiens produced by B Plasma Cells, released in response to an infection!
  • Antibodies can be classified as immunoglobins!
64
Q

How can we describe the structure of an Antibody?

A
  1. Consists of Light polypeptide (top region) and Heavy polypeptide chains (lower region)
  2. CONSTANT REGION: Universal region for overall body of the antibody and providing easy binding site for phagocytes!
  3. VARIABLE REGION: Has specific shape to anigen, different for ALL antibodies, and will bind to the antigen
  4. HINGE REGION: Region that allows antibody flexibility, can bind to more than one antigen per antibody!
  5. DISULFIDE BRIDGES: Holding polpeptides together in antibody
65
Q

What are the main types of Antibodies?

A
  1. Opsonins: Binds to pathogen antigens;binding sites for phagocytic cells, allowing easly phagocytosis!
  2. Agglutinins: Each antibody has 2 binding sites; will use each “arm” to bind to 2 pathogens each, clumping together (easily engulfednd digested) > agglutination!!
  3. Antitoxins: will bind to toxic chemicals with antibodies produced by pathogens, cancelling out toxic effect in the body!
66
Q

What are Primary and Secondary responses?

A
  1. PRIMARY: This is the first encounter with pathogen, where plasma cells first start producing the specific antibodies for specific pathogen (SLOWER RESPONSE ,FEWER ANTIBODIES PRODUCED)
  2. SECONDARY: This is the second encounter with same pathogen, but B and T memory cells with recognise pathogens, stimulating cytokines to plasma cels to produce many antibodies (RAPID RESPONSE, HUGE AMOUNT OF ANTIBODIES)
67
Q

What is vaccination?

A
  • A method of stimulating an immune response to achieve immunity!
68
Q

What can be contained in vaccines?

A
  1. Whole, live microorganisms with similar antigens (copox vs smallpox)
  2. Weakened versions of the pathogens
  3. Dead version of pathogen
  4. Antigens only only!
  5. Harmless version of toxin!
69
Q

How can vaccines prevent disease spread?

A
  • Herd Vaccination: almost all population are given vaccine, where disease spread to non-immune hosts is very unlikey (herd immunity acheived)
  • Ring Vaccination: Vaccinating people, mostly towns, villages and homes, in the IMMIDIATE VICINITY of new cases or possible occurences of infection with pathogen (Smallpox…)
70
Q

How can we combat an ever-mutating virus like influenza?

A
  1. High-mutation rate: constant change of virus antigens
  2. In order to decrease chance to develop a pandemic of particular strain, most vulnerable people are vaccinated (65+, respiratory issues, weak immune systems)
71
Q

What are 4 types of immunity achieved?

What are

A
  1. Natural = Acheived through natural, biological processes (Natural body infection/Placenta and Breastfeeding in newborns)
  2. Artificial = Acheived through medical interventions (Dead-Pathogen Vaccination/Antibody antigens)
  3. Active = immune system activated and making own antibodies
  4. Passive = antibodies made supplied by another source
72
Q

Why some diseases have vaccines over others??

A
  1. Humans being the main host
  2. Pathogen mutates very slow
  3. Easy to identify symptoms
  4. Pathogen not concelased in other cell in life cycle!
72
Q

Why do we need to research for new medicines

A
  • New diseases emerging always
  • Non-effective treatments of some disease
  • Antibiotics less effective!
73
Q

Main sources of finding new medicines?

A
  1. Accidental findings = Penicillin discovery
  2. Traditional, herbal medicine = Poppy Seeds for morphine
  3. Observing Wildlife = Elephant+Parrot clay eating for toxin treatment
  4. Using plant sources = Foxgloves = Digitalis and Willow tree = Aspirin
74
Q

Why should we sustainably farm rainforests?

A
  1. As plants are used for medicine, we must ensure to not allow species to be extinct, by removing them!
  2. Species are potential sources for new medicines!
75
Q

What are personalised medicines?

A
  • Where we sequence the genes of specific individuals, and use them to create specific, tailored medicine treatment to the same patient!!
76
Q

How has the Human Genome Project helped with personalised medicine?

A
  • Access to a full genetic sequence can help identify faulty genes in individual, that may give rise to certain diseases!
77
Q

What is Synthetic Biology?

A

This is the production of new molecules that mimic natural processes, or the use of natural molecules to produce new biological systems, that DO NOT EXIST IN NATURE!!!!

78
Q

Examples of Synthetic Biology taking place!

A
  • Tomatoes with anthocyanin pigment, being antioxidants against CHD
  • Goldent Rice, a GM Crop, producing beta-carotene, used to produce vitamin A to combat blindless in children
79
Q

How antibiotics kill bacteria?

and SOMETIMES WILL NOT!

A
  • They are chemicals that inhibits the growth of the bacteria, allowing them to be managed and killed via immune response!
  • BUT, antibiotic resistance is a real deal, so must COMPLETE COURSES and PRESCRIBE WHEN NECESSARY to reduce this!
80
Q

Describe the shape of Primary Response curve!

A
  1. Lag time = time needed for clonal selection and expansion of B Lymphocytes
  2. Rise = B Plasma cells rapidly divide, producing specific antibodies to pathies
  3. Fall = Plasma cells eventually die, and infection is overcome
  4. Rapid Increase+Shorter timespan = B memory cells remain in blood, giving faster secondary response
81
Q

Why no symptoms felt in upon second infection in Primary Response curve?

A
  • Second immune response is much faster, with much larger quantity of antibodies produced!
82
Q

How do vaccines lead into Memory Cells?

A
  1. Vaccines inject antigens, where APC presents to T helper cells
  2. Antigen will bind to T Helper, releases cytokines
  3. B Lymphocytes for clonal selection and expansion, forming B memory cells after differnetiation!!
83
Q
A

OCR A-level Biology Module 4: Disease, Biodiversities and Evolution (2 decks)

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