4.1.1 Communicable Diseases, Disease Prevention and the Immune System COMPLETE Flashcards

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1
Q

DEFINITION- Health

A

A state of complete physical, mental and social wellbeing and not merely the absence of disease or infirmity

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2
Q

DEFINITION- Disease

A

Anything that impairs the normal functioning of the body/ mind

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3
Q

Disease Types

A
Infectious- Colds 
Non Infectious- Cancer
Mental- Depression 
Inherited- Cystic Fibrosis 
Deficiency- Anaemia
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4
Q

Parasites

A

An organism that lives on or in a host organism, takes nutrition and causes harm.
ANIMAL- Flea
PLANT- Mistletoe

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5
Q

Pathogens

A

Microorganisms that cause disease, either produce TOXINS
Bacteria- breakdown plasma membrane, inactivate enzymes and prevent mitosis
Fungi- Produce toxins that damage host cell
or DIGEST living cells i.e. fungi and protoctista

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6
Q

DEFINITION- Epidemiology

A

The study of the spread of diseases and the factor affecting it

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7
Q

DEFINITION- Pandemic

A

A Worldwide epidemic

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8
Q

DEFINITION- Mortality

A

The number of people who die each year from a disease

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9
Q

DEFINITION- Prevalence

A

The number of people with a disease at a given time

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10
Q

DEFINITION- Incidence

A

The number of new cases of a disease in a population per year

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11
Q

DEFINITION- Endemic

A

A disease that is always present in the population

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12
Q

DEFINITION- Epidemic

A

A disease that spreads rapidly to a lot of people over a wide area

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13
Q

DEFINITION- Morbidity

A

The number of people with a disease as a proportion of the population

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14
Q

Examples of how health organisations help

A
  • Education programmes
  • Advertisement
  • Screening programmes
  • Vaccination programmes
  • Target research for cures
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15
Q

Disease in Developing Countries

A

Mainly infectious disease, as well as deficiency diseases, accidents and deaths at birth.
CAUSES- poor sanitation, unsafe water, overcrowding, poverty, climate, lack of medical facilities

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16
Q

Disease in Developed Countries

A

Mainly Cardiovascular, cancer or road accidents, also more degenerative diseases.
CAUSES- Improved hygiene and vaccinations, however poor diets, smoking, too much alcohol and longer lives,

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17
Q

Bacteria

A

Belong to the Prokaryote kingdom, reproduce quickly and waste can be toxic.
ANIMAL- Meningitis
PLANT- Ring Rot

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18
Q

Viruses

A

Non living pathogen, also parasites, invade living cells and make copies before cell lyses and releases new viruses, evolve rapidly.
ANIMAL- HIV
PLANT- Tobacco Mosaic Virus

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19
Q

Protoctista

A

Eukaryotes, single celled organisms, sometimes parasites/ pathogens, some need vectors to transport them.
ANIMAL- Malaria
PLANT- Potato Blight

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20
Q

Fungi

A

Devastating for plants, multicellular eukaryotes, many are saprophytes, reproduces quickly releases millions of spores.
ANIMAL- Athletes foot
PLANT- Black Sigatoka

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21
Q

Bacterial Meningitis

A

CAUSE- Bacterial infection
TRANSMISSION- Direct physical contact
DETAILS- Blotchy red rash, causes blood poisoning and rapid death, antibiotics cure if early can get vaccine.

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22
Q

Influenza

A

CAUSE- Viral Infection
TRANSMISSION- Droplet infection
DETAILS- Infects the ciliated epithelium and leaves airway open for second infection, can be fatal

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23
Q

Ringworm

A

CAUSE- Fungal disease
TRANSMISSION- Direct Physical Contact
DETAILS- Causes grey white crusty infections, different fungi for different animal species i.e. Cattle, dogs, cats. Treated with anti fungal cream

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24
Q

Athletes Foot

A

CAUSE- Fungal infection
TRANSMISSION- Direct Physical Contact/Fomites
DETAILS- Digests warm moist skin between toes, causes cracking and itching, treated with anti fungal cream

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25
Q

Malaria

A

CAUSE- Protoctista
TRANSMISSION- Vector via female mosquito
DETAILS- Female sucks blood to make her eggs, plasmodium cells enter the bloodstream and invade RBC causing fevers.

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26
Q

Malaria details

A

SYMPTOMS- Repeated fevers, muscle aches
TREATMENT- Many strains have become resistant
GLOBAL IMPACT- Climate change makes it worse, difficult to vaccinate, increased resistance.

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27
Q

Prevention of Malaria

A

Avoid being bitten- repellant, long sleeves, sleep under nets
Reduce Mosquito Number- Fish ponds, oil on surface preventing larvae breathing, pesticide.

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28
Q

Tuberculosis

A

CAUSE- Bacteria
TRANSMISSION- Droplet infection
DETAILS- Affects the lungs, at greater risk if have HIV, if bacteria reaches the alveoli then macrophages engulf them but they’re not destroyed and instead divide

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29
Q

TB Details

A

SYMPTOMS- weight loss, night sweats, coughing blood.
TREATMENT- 6 month antibiotic course, DOT directly observed therapy.
GLOBAL IMPACT- leading killer of HIV positive people, common in south east Asia and Sahara Africa

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30
Q

HIV/AIDS

A

CAUSE- Virus
TRANSMISSION- Physical Contact, body fluids, sex, dirty needles, blood transfusions
DETAILS- Infects the T Helper cells and destroys them, leads to opportunistic diseases i.e. phneumonia

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31
Q

HIV/AIDS Details

A

TREATMENT- Drugs are available but are expensive, best to prevent using condoms and sterile needles
GLOBAL IMPACT- Major public issue claiming 35 million lives so far, WHO area in Africa most effect

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32
Q

Ring Rot

A

TYPE- Bacteria
AFFECTS- Potatoes, aubergines, Tomatoes
DETAILS- Decay of vascular tissue, causing wilting. Spread via direct contact, dirty water and equipment.

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33
Q

Tobacco Mosaic Virus

A

TYPE- Virus
AFFECTS- Tobacco plants
DETAILS- Causing decolorisation of leaves, only multiply in living cells, survive dormant in dead cells. Spread by workers hands, clothing and tools

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34
Q

Potato Blight

A

TYPE- Protoctist
AFFECTS- Potatoes
DETAILS- microscopic fungus like organism who’s spores break away easily, airborne in high temps, waterborne in lower temps.

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35
Q

Black Sigatoka

A

TYPE- Fungus
AFFECTS- Bananas
DETAILS- Attacks and destroys the leaf, spots result in lower yield, spread by wind, rain and irrigation water. Fungicides spreads using aeroplanes.

36
Q

Transmission between animals

A
  • Direct Contact
  • Ingestion
  • Droplet Infection
  • Inoculation
  • Fomites
  • Vectors
37
Q

Factors Affecting Transmission (Animal)

A
  • Overcrowded living conditions
  • Poor Nutrition
  • Compromised immune system (HIV)
  • Poor waste disposal
  • Climate changes (introducing new vectors)
38
Q

Transmission between plants

A
  • Direct contact between healthy and infected plant

- Indirect contact via vectors (wind, water, animal, human) and soil contamination

39
Q

Factors affecting Transmission (Plants)

A
  • Plant varieties susceptible to disease
  • Overcrowding
  • Poor nutrition lowers resistance
  • Damp warm conditions
  • Climate change
40
Q

Physical Defences in Plants

A
  • Cellulose Cell Wall
  • Lignin is waterproof
  • Bark contains pathogen fighting bacteria
  • Stomata Closure prevents entry
  • No immune system but sacrifice parts, i.e. swelling that blocks xylem.
  • Chemical defences
41
Q

Primary Defences in Animals

A
  • Skin acts as a barrier, also produces sebum that inhibits growth of pathogens
  • Mucus membrane traps pathogens and get wafted up throat by ciliated epithelium.
  • Hydrochloric acid in stomach denatures the pathogen
  • Waxy ear canal traps pathogen
  • Expulsive reflexes
  • Blood clotting
42
Q

Blood clotting

A
  1. Temporary platelet plug forms when the platelets bind to collagen after vessel wall is exposed
  2. Inactive thromboplastin is activated and becomes Thrombin when combined with Ca2+ and Prothrombin. Then combines with Fibrin/ Fibrinogen to produce another plug.
43
Q

Wound Repair

A

Clots prevent the entry of microbes, serotonin also released to trigger vasoconstriction reducing blood flow. The scab shrinks once formed to pull sides together.
Collagen is deposited and stem cells in the epidermis undergo mitosis.
New blood vessels grow

44
Q

The inflammatory response

A

Characterised by pain, heat, swelling.

Presence of microbes detected by mast cells that then release cytokines and histamine

45
Q

Histamine

A

Causes Vasodilation, capillary becomes more permeable to WBC. Increases tissue fluid leading to swelling, this drains into the lymphatic system where lymphocytes are stored, pathogen then meets lymphocyte

46
Q

Cytokines

A

Attract phagocytes that remove pathogens via phagocytosis

47
Q

Fevers

A
  • Cytokines stimulate the hypothalamus to reset bodies thermostat
  • Higher temp will inhibit pathogen, immune system also works faster
48
Q

Neutrophils

A

(phagocytes)

Small and squeeze through capillaries to patrol tissues, short lived

49
Q

Macrophages

A

(phagocytes)

Leave bone marrow as monocytes, settles in an organ and becomes a macrophage, long lived cells.

50
Q

Antigens

A

Protein on cell surface composed of glycoproteins and proteins, allows recognition of foreign pathogens and ‘self cells’

51
Q

Opsonins

A

Chemicals that bind to pathogen to identify them, phagocytes therefore bind onto the antigen on the pathogen

52
Q

Antigen Presentation

A

Antigens on the surface of foreign cells will be recognised by the immune system

53
Q

Phagocytosis- Macrophages

A
  1. Antigen on pathogen attaches to receptor
  2. Pathogen is engulfed by phagocytosis and enclosed in a vesicle
  3. Lysosome fuses with phagosome forming a phagolysosome
  4. Pathogen is partially digested by hydrolytic enzymes
  5. Indigestible material is removed by exocytosis
54
Q

Phagocytosis- Neutrophils

A

Same as with macrophages but pathogen is fully digested and all products absorbed by the cells.

55
Q

T lymphocytes

A

Made in the bone marrow but develop in the Thymus gland. They have specific receptors for a particular antigen but only recognise when with a self protein. This could be a macrophage or a virus infected cell

56
Q

T lymphocytes Activation

A

ANTIGEN PRESENTATION- Macrophage engulfs, processes and presents antigen with self protein
CLONAL SELECTION- When a complimentary receptor binds cytokines are released by macrophages that activate specific T lymphocytes.
CLONAL EXPANSION- Mitosis of the T Lymphocytes forming clones

57
Q

T Helper Lymphocytes

A

Secrete cytokines called interleukins, they bind to receptors and act over short distances.
LEADS- stimulates B lymphocytes, production of other T cells, macrophages ingest pathogen

58
Q

T Killer Lymphocytes

A

Destroys cells that they bind to, produce a chemical called Perforin, creates pores in the membrane so its freely permeable.

59
Q

T Memory Cells

A

Remain in the blood, help body respond more quickly and effectively if same antigen enters again.

60
Q

T Regulator Cells

A

Cells suppress the immune system, once pathogen has been removed, involves autoimmunity

61
Q

B Lymphocyte

A

Made and mature in the bone marrow, have cell surface embedded antibodies which act as receptors. They’re specific for particular antigens. Can become antigen presenting cells b engulfing the pathogen.

62
Q

B Lymphocyte Activation

A

CLONAL SELECTION- Specific B lymphocytes encounters an antigen with complimentary antibody and it becomes activated. T Helper cells also activate them.
CLONAL EXPANSION- Divide many times by mitosis
DIFFERENTIATION- Becomes a protein factory (Plasma Cell) increased number of organelles, Synthesise particular antibody and releases by exocytosis.

63
Q

B Memory Cells

A

Remain in the blood so if same antigen invades they’ll be a quicker response, they develop into plasma cells to produce more antibodies.

64
Q

Immune Response

A

Specific response to antigens on a pathogen, involving lymphocytes and antibodies.

65
Q

Rheumatoid Arthritis

A

Autoimmune Disease

Effects joints especially hands and wrists. No cure but steroids and immunosuppressants

66
Q

Lupus

A

Autoimmune Disease
Attacks organs like the kidneys, affects joints and causes fatigue
No cure but anti inflammatories help

67
Q

Type 1 Diabetes

A

Autoimmune Disease

Affects insulin secreting cells in the pancreas, insulin injections

68
Q

Antibodies

A

Composed of glycoproteins, consist of 4 polypeptide chains and a variable region that binds to specific antigens

69
Q

Variable Region

A

Complimentary to the antigen, composed of varying amino acids

70
Q

Constant region

A

Amino acid sequences are the same, receptors on phagocytes have receptors specific for this region, same on all antibodies

71
Q

Hinge Region

A

Allows flexibility when binding to antigens

72
Q

Disulphide Bridges (Antibodies)

A

Hold the polypeptides together

73
Q

Opsonisation

A

Action of Antibodies

A group of antibodies that can bind to the antigen on a pathogen, also a binding site for phagocytes

74
Q

Agglutination

A

Actions of Antibodies

Large antibodies binding pathogens together, makes bacteria easier to engulf and prevents viruses entering new hosts.

75
Q

Anti toxins

A

Actions of Antibodies

Antibodies can act as antitoxins by binding to the toxin produced by pathogens making them harmless

76
Q

Neutralisation

A

Actions if Antibodies

Antibodies binding to the surface of pathogens can prevent it binding to host cells

77
Q

Primary immune response

A

Clonal Selection and expansion can take up to several days. During this time the pathogen multiplies and the person gets ill. Antibodies are produced slowly and over time kill the pathogen, after this antibody numbers drop

78
Q

Secondary response

A

If the same pathogen invades again memory cells allow a faster response. Antibodies are produced quickly an din large numbers, pathogen is destroyed before any symptoms.

79
Q

Forms of antigenic material in vaccines

A
  • Inactive bacteria/ viruses
  • Attenuated strains of live B/V (Weakened)
  • Toxin molecules that’ve been altered
  • Isolated antigens extracted from the pathogen
  • Genetically engineered antigens
80
Q

Natural Passive Immunity

A

Mothers milk

81
Q

Natural Active Immunity

A

Memory cells

82
Q

Artificial Passive Immunity

A

Extracted and injected directly into bloodstream

83
Q

Artificial Active

A

Immune system stimulated to make its own antibodies, i.e. vaccine

84
Q

Herd Vaccination

A

Significant number of people have been vaccinated so protect those without due to minimal break out chances

85
Q

Ring Vaccination

A

Controls an outbreak by vaccinating and monitoring a ring of people around each infected individual

86
Q

Sources of new medicine

A
  • Accidental Discovery
  • Traditional Remedies
  • Observing wildlife
  • Synthetic biology
87
Q

Why new drugs are needed

A
  • New diseases
  • Many diseases still don’t have treatments
  • Antibiotic resistance