Health and Disease Flashcards

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0
Q

Disease

A

A departure from good health caused by a malfunction of the mind or body

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1
Q

Health

A

State of mental, physical and social wellbeing, not just the absence of disease

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2
Q

Parasite

A

An organism that lives in or on another living thing, causing harm to its host

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3
Q

Pathogen

A

An organism that causes disease

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4
Q

Transmission of malaria

A
  • caused by eukaryotic organism from genus Plasmodium
  • spread by a vector: female Anopheles mosquito
  • someone with malaria had Plasmodium gametes in their blood
  • mosquito feeds on blood
  • gametes develop in mosquito stomach and migrate to salivary glands of mosquito
  • an uninfected person is bitten, being injected with saliva as an anticoagulant
  • Plasmodium migrates to liver to multiply
  • Plasmodium migrates to blood, entering red blood cells
  • cycle starts again!!
  • can also be transmitted through placenta or use of unsterilised needles
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5
Q

Transmission of HIV/AIDS

A
  • HIV virus may remain inactive
  • once active, attacks and destroys T helper cells
  • ability to resist infection is reduced - the diseases you can’t fight kill you
  • can be transmitted by:
  • exchange of bodily fluids (blood to blood contact)
  • unprotected sex
  • unscreened blood transfusions
  • use of unsterile surgical equipment
  • sharing hypodermic needles
  • across placenta/during childbirth
  • from mother to baby in breast feeding
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6
Q

Transmission of tuberculosis

A
  • caused by Mycobacterium tuberculosis and M. bovis
  • transmitted by droplet infection: bacteria contained in tiny droplets that are released in coughing, sneezing, laughing or talking
  • not easy to contract TB: need to be in close contact
  • overcrowding, poor ventilation, poor health (e.g. Has HIV/AIDS), poor diet, homelessness and living/working with people from areas where TB is more common make it more likely for you to contract TB
  • can also be contracted from milk/meat of cattle
  • thought that up to 30% of world have TB, but is controlled by immune system/inactive
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7
Q

Impact of malaria

A
  • kills 3 million people a year
  • 300 million are infected
  • only in areas where vector mosquito can survive: tropical regions
  • 90% of people with malaria on sub-Saharan Africa
  • global warming might mean mosquito can survive further north, and malaria may spread to Europe
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8
Q

Impact of HIV/AIDS

A
  • world wide disease, spreading in pandemic proportions
  • 45 million+ people living with HIV at end of 2005
  • more than half these are in sub-Saharan Africa
  • spreading through Russia and china
  • many people with HIV in china
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9
Q

Impact of tuberculosis

A
  • 1% of population newly infected each year
  • 10-15% of these develop TB
  • 1.6 million died in 2005
  • 30% of world infected with bacteria
  • common in South-east Asia and sub-Saharan Africa
  • risk from new strains of bacteria that are resistant to drugs used to treat it
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10
Q

Antigens

A

Molecules that stimulate an immune response

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11
Q

Antibodies

A

Protein molecules that can identify and neutralise antigens

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12
Q

Immune response

A

The specific response to a pathogen, which involves the action of lymphocytes and the production of antibodies

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13
Q

Primary defences

A
  • skin has a layer of dead cells filled with keratin. They act as a barrier to pathogens
  • mucus membranes protect those areas of body exposed to infection such as air passages and digestive system. Goblet cells secrete mucus, trapping pathogens; cilia waft mucus up trachea into oesophagus. Most pathogens are destroyed in stomach by the pH 1-2, denaturing enzymes
  • eyes protected by antibodies and macrophages in tear fluid
  • ear canal lined by wax, trapping pathogens
  • vagina protected by maintaining acidic conditions
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14
Q

Structure of phagocytes

A
  • neutrophils have a multilobed nucleus, are manufactured in the bone marrow and have an extensive cytoskeleton. Released in large numbers upon infection
  • macrophages are larger, made in bone marrow and travel in blood as monocytes. Settle in organs, particularly lymph nodes
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15
Q

Action of neutrophils

A
  • antibodies have already been released, and have bound to antigens on pathogen’s surface
  • receptors on phagocyte binds to antibodies, potentially assisted by proteins called opsonins
  • phagocyte engulfs pathogen by unfolding of its membrane
  • pathogen trapped inside phagocyte in a vesicles called a phagosome
  • lysosomes fuse with phagosome, releasing digestive enzymes, digesting the bacteria
  • end products are nutrients are harmlessly absorbed into cytoplasm
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16
Q

Action of macrophages

A
  • infected cells release histamine, attracting neutrophils and making capillaries more leaky.
  • Infected area becomes swollen and red
  • more tissue fluid is released, passing into the lymphatic system, leading pathogens to waiting macrophages in lymph nodes
  • macrophages help initiate specific response - immune response by activating lymphocytes
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17
Q

Structure of antibodies

A
  • Y shaped
  • 4 polypeptide chains, held together with disqualified bridges
  • constant region, same for all antibodies. Phagocytic cells attach here, helps in process of phagocytosis
  • variable region has a specific shape and differs from one type of antibody to another
  • result of primary structure, ensures antibody can only attach to correct antigen. Variable region has a complementary shape
  • hinge regions allow flexibility, so branches of Y shaped molecule can move further apart so can attach to more than 1 antigen
18
Q

Action of antibodies

A
  • antibodies attach to pathogens on antigens. These antigens may have a different purpose for the pathogen, e.g. A binding site to the host cell
  • antibody blocks binding site, so pathogen can’t join to host cell. This is called neutralisation
  • some antibodies have many branches, and so bind to many antigens on many pathogens. This is called agglutination - when pathogens are stuck together, they can’t enter host cells
19
Q

Cell signalling

A

The communication between cells that allows effective coordination of a response

20
Q

T lymphocytes

A
  • originate in bone marrow
  • develop in thymus
  • the receptors on their surface are complementary to a specific antigen
  • once the antigen has been detected by the correct T lymphocyte, the immune response begins
  • correct lymphocytes divide by mitosis, called clonal expansion, this way, the correct cells are selected - clonal selection
  • differentiate into T helper cells, T killer cells and T memory cells
  • T helper cells release cytokines, stimulating B cells to develop and stimulate phagocytosis by the phagocytes
  • T killer cells attack and kill infected body cells by injecting with hydrogen peroxide
  • T memory cells remain in blood, and stimulate the production of plasma cells and antibodies quickly upon a second infection
21
Q

B lymphocytes

A
  • originate in bone marrow
  • the receptors on their surface are complementary to a specific antigen
  • once the antigen has been detected by the correct B lymphocyte, the immune response begins
  • correct lymphocytes divide by mitosis, called clonal expansion, this way, the correct cells are selected - clonal selection
  • differentiate into plasma cells and B memory cells
  • plasma cells flow around in blood, manufacturing and releasing antibodies
  • B memory cells remain in body for a number of years and act as the immunological memory’s
22
Q

Where are antigens found?

A
  • cells attacked by a pathogen display antigens on their surface
  • macrophages in lymph system become antigen presenting cells
  • on pathogen’s surface
23
Q

Communication in immune response

A
  • pathogen has antigens that label it as foreign
  • infected body cells attempt to destroy pathogens with lysosomes, displaying removed antigens on surface, acting as a distress signal so detected by immune system cells and a marker to show it is infected so T killer cells will destroy it
  • macrophages display antigens from pathogens they digest on surface, becoming antigen-presenting cells
  • cytokines are released by cells, acting over a short distance:
  • macrophages release monokines to attract neutrophils
  • macrophages release monokines to stimulate B cells to differentiate and release antibodies
  • T cells, B cells and macrophages release interleukins, stimulating proliferation and differentiation of B and T cells
  • many cells can release interferon, inhibiting virus replication and stimulate activity of T killer cells
24
Q

Primary and secondary immune response

A
  • primary: takes a few days to select correct lymphocytes, allow them to divide and differentiate into plasma cells, then start producing antibodies. Takes a few days for antibody concentration to rise. Once they are no longer needed, they go away
  • secondary: memory cells stimulate production of plasma cells and antibodies much more quickly, at greater concentration. Starts sooner and is more rapid
25
Q

Active immunity

A

Achieved by activation of the immune system. Lymphocytes manufacture antibodies, and immunity can last for many years/a lifetime

26
Q

Passive immunity

A

Provided by antibodies that have not been manufactured by stimulating immune system. Antibodies may have been provided across placenta/via breast milk/by intravenous injection. Often short lived

27
Q

Natural immunity

A

Gained in normal course of living processes, e.g. as a result of an infection that stimulates an immune response/via placenta or breast milk

28
Q

Artificial immunity

A

Gained by deliberate exposure to antibodies or antigens. By injection of antibodies/a weakened, dead or similar pathogen that stimulates the immune system response

29
Q

Vaccination

A

Provides active, artificial immunity to specific diseases. Immune system attacks a weakened/dead/similar pathogen or the antigens or a toxin as if it were a real disease, developing memory cells

30
Q

Vaccinating against influenza

A
  • as the flu virus has many strains, different strains are used each year, following research into which ones are most likely to spread
  • people over 65 and people with respiratory tract conditions are most at risk, so they are targeted by the vaccination program
31
Q

Chronic bronchitis

A

Inflammation of the lining of the airways, accompanied by damage to the cilia and overproduction of mucus, so that mucus collects in the lungs. Symptoms are irritation in the lungs, continual coughing and coughing up mucus that is often filled with bacteria and white blood cells. Increased risk of lung infection

32
Q

Emphysema

A

Loss of elasticity in alveoli, causing them to burst. Lungs have reduced surface area to exchange gases on. Symptoms include shortness of breath, especially during exercise. In serious cases, breathing rate increases, and fatigue occurs as blood is less oxygenated

33
Q

Chronic obstructive pulmonary disease (COPD)

A

Combination of diseases, including chronic bronchitis, emphysema and asthma.

34
Q

Lung cancer

A

Symptoms include continual coughing and shortness of breath, pain in chest and blood coughed up in the sputum.

35
Q

Short-term effects of tar

A
  • settles on alveoli walls, increasing diffusion distance
  • cause allergic reaction: contraction of smooth muscles, restricting the airway
  • paralyses and destroys cilia, as well as increasing mucus production from goblet cells. Mucus collects in the airway
  • bacteria and mucus aren’t removed, and can block bronchioles
  • lungs are more susceptible to infection
36
Q

Long-term effects of tar

A
  • smokers cough to shift mucus and irritation of airways
  • cough damages airway and alveoli lining, replaced by thicker, less flexible scar tissue
  • layer of smooth muscle thickens, reducing lumen
  • infections inflame lining of airways, in particular epithelium
  • white blood cells come to fight off infection, and digest parts of wall to get there. Elastic tissue is lost, so air is not exhaled from alveoli. Bronchioles collapse, trapping air and causing alveoli to burst
37
Q

Nicotine

A
  • causes addiction
  • mimics action of neurotransmitters at synapses, making smoker feel more alert and nervous system more sensitive
  • causes adrenaline to be released, raising heart and breathing rate, constricting arterioles raising blood pressure
  • causes constriction of arterioles, reducing blood flow to extremities
  • makes platelets sticky, increasing risks of blood clots or a thrombus
38
Q

Carbon monoxide

A
  • combines with haemoglobin in red blood cells more readily than oxygen (forms carboxyhaemoglobin)
  • reduces oxygen carrying capacity of blood. Smokers feel this when they exercise
  • damages lining of the arteries
39
Q

Atherosclerosis

A
  • carbon monoxide damages endothelium of arteries (damaged increased by high blood pressure)
  • phagocytes repair by encouraging growth of smooth muscle and deposition of fatty substances: cholesterol and LDPs
  • Deposits are called atheromas, and may also contain dead cells, fibres and platelets
  • process of deposition is atherosclerosis
  • occurs under endothelium wall
  • atheroma may break through artery wall, forming a plaque sticking out into the lumen
  • plaque makes artery wall less flexible and reduces size of the lumen
40
Q

Coronary heart disease

A
  • coronary arteries carry blood at high pressure, so are prone to damage and atherosclerosis
  • if lumen is narrowed, there is less oxygen for respiration, leading to CHD, which takes 3 forms:
  • angina: severe pain in chest and down left arm/up to neck
  • heart attack or myocardial infarction: death of part of heart muscle, caused by a clot
  • heart failure: when heart can’t sustain pumping action, e.g. blockage of major coronary artery
42
Q

Stroke

A

death of part of brain tissue, caused by loss of blood flow. 2 causes:

  • blood clot (throumbus) floating around blocks a small artery leading to part of brain
  • an artery leading to the brain bursts (haemorrhage)
43
Q

How are drugs discovered?

A
  • by accident, e.g. penicillin
  • by looking at traditional medicines
  • by observing how animals self-medicate
  • by finding drugs in plants and microorganisms, so need to maintain biodiversity, as could be destroying future life saving medicines