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AS Level > Biology Health and Disease > Flashcards

Biology Health and Disease Flashcards

1
Q

health is..?

disease is..?

A

physical and mental state of well-being

depature of health due to the malfunction of th mind and the body

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2
Q

pathogens are?

parasites are?

A

organism are cause diseaase
lie in or on another living organism (the host)
All pathogens are parasites but not all parasites are pathogens (not all cause disease)

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3
Q

malaris is caused and carreid by?

A

genus plasmodium and carried by female anopheles mosquito

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4
Q

life cycle of malaria?

A

1) If person already has malaria,the mosqito sucks he gametes of the plasmidium into its stomach
2) Gamestes fuse and produce zygotes- infective dstages are formed
3) moved to salivary g;ans
4) The mosqito bites someon>injects salivia>contains infective stages>
5) In human, blood corcualtion carreis it to lungs>multiplies and moves into red blood cells
6) Here, it multiplioes by mitois o produce more gametes

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5
Q

causes of malaria?

A
  • unsterilised needles
  • unscreened blood trasnfusions
    3) pass through placenta into foetus
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6
Q

prevenion methods?

A
  • drain marshalnds when mosqitois lay their eggs
  • spray fetislsiers
  • insect repllent on skin
  • not use chmicals like DDT
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7
Q

global impact?

A

3 million people die/300 million affected per year

-confined to tropical regions (vector mosqito lives)

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8
Q

HIV/AIDS?

A

AIDS disease is caused by HIV virus

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9
Q

Life cycle of HIV

A

1) Virus enters cell
2) Uses reverse trabnscriptaser to convert viral RNA into viral DNA
3) Viral DNA joins wih our DNA
4) Produces mroe RNA>builds up at cell membrane
5) Leaves the cell, damaging it
- Lacks proofreading enzymes to correct errros, therofore ghigh erro rate and shrot life span makes it easy for it to rapidly mutate

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10
Q

Causes of HIV

A

hypodermic needles
unscreeened blood transfusins
unprotected sexual intercourse
breat milk

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11
Q

Prevenion emthods for HIV

A
  • condoms during intercourse
  • screen blood transfusions
  • sterilsie needles
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12
Q

What usally causes people to die from HIV?

global impact of HIV

A
  • HIV virus enters cell- remaisn inactive (HIV +) When it becomes active>it destroys/attacks T helper cells>leaves the body vunerbaket o infection.peoplea re usually killed by opurtunistic diseases
    45 million people living with it at end of 2005/5 people newly infected each year
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13
Q

Why is it hard to find a vaccine for malaria and why are people in poor areas more affected?

A

eukyratoic organism- immune system dinds it hard to recognise>doesn’t stimulate immune response (antigen concelament)
por areas- few resources for medical care/vaccines therefore more die
HIV- less medical cures- antiretorivral drug therapy

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14
Q

TB usually afefcts the?

A

lungs (can eb anywherelse)

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15
Q

Life cyle of TB?

A

1) The bacterium reacht he alvoli in the lungs>the macrophagesenglulf them
2) The enzymes in the amcrophages don’t destroy/damge the bacterium like they shoudl therefore they remain in cells
3) They divide by mitois priducing more bacterium>englulfed by more macrophaes>disease spreads

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16
Q

Causes of TB?

A
  • poor ventilation
  • poor diet
  • overcrowding (slums)
  • droplet infection- passed from laughing/coughing within close prmixity of others
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17
Q

Prevention methods for TB?

A
  • openign irs/windows- ventilaiting air
  • no too many people living in one corwded space
  • balanced diet
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18
Q

global impact of TB?

A
  • 8.8. m affected/1.6 m die
    -2 types- mycobacterium tuberolis and mycorbacterium bovis
    mycobacterium bovis- 30% of people living with it- doesn’t genrally do anything
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19
Q

Why does living in poor areas liek in slums in Rio make ypu at more rsk to all 3 diseases?

A

few medical reosurces fir treatment
poorer areas- more overcroded e.g. livin in slums, blood trasnusions aren’t going to be screrned always, needles aren’t always going to eb sterilsied>more at risk from catching it and dying form it

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20
Q

Non-specifi immune reposnses- e.g. skin?

A

dead cells that act as a barrier to pathogens

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21
Q

mucous membranes?

A
  • air contans harmsul substances
    -gobelt cells secrete mucus which traps pathogens
    cilia- hair-liek extensions waft musucs up back of throat>top of trache. diwn oesphuhus>swallowed>in stomach tis killed by enzymes in stomach
    also in nsoe
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22
Q

defences in eyes/ears/vagina?

A

eyes- tear fluid contins antibiodies

  • ears- wax which traps pathogens
  • vagina- aintinas relatively acidic condtions
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23
Q

Phagocytes- secidnary defence- difference between neutrophils and macrophages?

A

-both manufacured in bone marrow-
neutriopihls are squuezed out of blood in tissue fluid- patrol parts of the body (short-lived)
macrophages- larger and settle in lymph nodes- longer lived so tend to survive after englufing pathogens

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24
Q

Phagocytosis?

A

1) The pathogen ahs foreign markers (antigens) > which is recognised
(own cells have anigens but recognised as our own)
2) The antibody binds to the pathogen.phagocte binds to the antibody (receptr that is a complementary shape to it)
3) englufs the apthogen - folds its membrane inwards
4) Lyosomes release hydrolitic enzymes which digest the pathogen
5) Products priduced are safe nutietns and absorbed into cyutoplasm

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25
Q

hat happens to draw the athogens to the macrophaes in the lymoh nodes?

A

Infected cells secrete chemicals such as histamine which attract neutrophils to the area

  • makes capillaries more leaky which causes more tissue fluid to leak out
  • contains apthogns>brings them to macrphage waiting in the lymph nodes>destroy them
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26
Q

Immune response is?

A

response towards a patghogen by the activation of lyphocytes and the productiobn of antibodies

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27
Q

Antigens?

A

chemical markers on outer membrane

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28
Q

Antibodies?

A

glycoporteins (carbohydate chain)

  • receprtors- detect the foreign antigen
  • variable region binds to it
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29
Q

Streucure of an antibody?

A

4 polypeptide chains- held by disulfide bond
y-shaped molecule-
hinge region- allows flexibilityy fort he arms to attach to more than one pathogen
constant region- same in all pathogens>enables it to bind to phagotic cells (phagocytosis)
varibale region- differnet for all (depends on amino acid sequence)>sahep is complementary to specific antigens

30
Q

Agguliaition of pathogena?

A

attahcing to mroe than one make them clump together> can’t fit into a host cell

31
Q

neutrilisation of apthogens?

A

Binds to binding site >antigen can’t bind to host cell

32
Q

B lyphoctues?

A

-come across an antigen that their receptor is complemetary to ti binds to it.triggers a repsonse
-meet angines in blood or on antigine-presenting cells e.g. macrphages
-divide by mitois (conal expansioon) and produce identical antibodies (have the same receptor to kill that spcific antign)
-antiboies diffenetriate into plasma cells>shrot-lived but produce many antibodies (lots of protein-syntheis equipment)> bind to antigen 9same receptors) and neutrislei them ect
Some cells don’t diffenriate into plasma cells but into memory cells
- Hold memory of that antigen>so if it evr comes abck.quicly prioduce antiboies

33
Q

T lymphoctes?

A

also have recepttor wich binds to specific antigen
onyl meet on antigen-presenting cells like macrophages [ injested antigen thorugh phagoctosis and presnted the ‘foreign amrkers’ to make it easier for antibodies to detect]
didvides by mitosis (clonal expansion]
- diffentriates into T helper cells or T killer cells
T- killer cells- bind to antigen on APC and destroy it
T-helper cells bind to antigen and secrete chemsicals (cytokines)>stimualte other cells to attack the pathogen
e.g. macriphaes, B lymohicytes (helps them to divide)
Others diffentiate into memory cells-long-lived [stay in blood]

34
Q

Problem with perimary resposne?

A

Few lymphoctyes when pathogen first eneters the blood
takes time for them tio bind to antigen>divide by lcoanl expasion (B lympocytes) >secrete enough antiboides to kill pathogen or produce enough T lymphocytes to kill the pathgoen
in this time, pathogens rapidly multiply, release toxins that make the person ill

35
Q

What is the secondary response and why is it better than the primary repsponse?

A

Subsequen invasions past the prmiary defence the secondary defenceis the memory cells that ca produce antibodies at a much faster/efficent rate
Both P and S- require B/T lymphocytes
P- people get ill/S- perosn doesn’t usualyl get ill

36
Q

natural immuntiy is gained though?

A

natural living processes

37
Q

Natural can eb active so??

Natural can be passive so??

A

immune system ahs been stimulated to produce a particualr antiboy (make it quick)
Immune system hasn’t been stimualted- given the antibodies already made

38
Q

Artifical is when?

A

deliberate exposure to antiboides, usually through a vaccine

39
Q

Artifial can be?

A

passsive- given a collection of antibodies like hepatitus B

active- stimulate the body to make it- toxins of tetanus

40
Q

A vaccination is?

A

deliberate exposure to antigens to stimuate the immune system
Body treats it as a real disease and produces lyphocytes like B and T lyphocytes and memorty cells that are long-lived

41
Q

Why are people given a booster or second injection?

A

raise the level/amount of antibodies produced and to make sure it lasts for some time

42
Q

Different ways in which vaccines can be given? [forms]

A 
- weakened strain (measles)
dead strain (typhoid)
collection of antibodeis (epatitus B)
harmeless toxin from pathogen (tetanus)
whole live [less harm,ful] micr-organsim (smallpox)
43
Q

Herd vaccination?

A

vacinate msot of population e.g. 80-85%
prevent spread of disease
even those aren’t vaccinated are unlikely to get it

44
Q

Ring vaccianton?

A

New case is reported- vaccinate everyone in close priximity like town/viallage
used to cotnrol livestock disease

45
Q

Cholesterol is?

A

found in the phosolipid bilayer so its not soluble >converted into lipoporetns>pass though the lipid bilayer (soluble in water)

46
Q

HDL’s?

A

unsaturated fats, proteins, cholesterol
carry body tissues>liver where the choleterol is used to make bile/broken down
The HDL’s have receptors which bind to cholesterol
HDL’s help to reduce blood cholerterol levels and reduce fatty depsotion in artery

47
Q

LDL’s?

A

saturated fats, cholersterol, priotein
take choleterol to body tissue from liver
LDL’s have receptor that bind to the cholersterol
increase blood cholerterol and increase fatty acid depsots

48
Q

Saturated fats…..?

Unsaturated fats..?

A

decrease activity of LDL receptors (so less removed from the blood)
increase actvitiy of HDL receptors (more removed from blood)

49
Q

What is infleunza?

A

killer disease that affects people’s respitary system that is partiularly at risk to >65 year olds, people with other repsitory tract conditons
can result in an epidermic= widespread occurence of an infectious disease

50
Q

What are governements doing to try and stop infleunza epidemic?

A

priogramme to vacciante people more at risk e.g in 2006/07- 74% of people >65 got vaccinated
world health organisation monitors situations, predicts what flu (influenza) strain is more likely to break out
encourage governments to dhare knowledge/statistis
recommend to be prepared e.g stockpiling/developing vaccines

51
Q

New possible sources of medicine?

A

currently most medicine comes from plant species- 3000 plan species are used/70% from tropical rainforests
new expected disoveries are also suppiosed to come from the tropicl rainforest due to its great biodiversity
Scientists ahev always used traditional plan/animal behaviour as a starting point for dicering new medicines
Therefore a lot of new drugs have an origin in traditional medicines
New drugs can be disovered by accident- e.g. Alexander Fleming’s pencillin disovery
new drugs can be found by observing native people in culture’s e.g. acupuncture
In the last 50 years most drugs have come from the study of the bacterium streptomyces

52
Q

Nictoien causes?

A
  • replaces transmitter substances at synapses so makes nervous sytem more sensitive, increasign altertness
  • increasgn breahting rate, heart rate and constircts arteries>reduces 02/blood flow to extremties
  • makes plateltes more sticky, increased chance of a blood clot forming
53
Q

Carbon monxide?

A

hgiher affintiy for oxygen>gets enters red blood cells>combines with haemoglobin to form carboxyhaemoglobin

  • less 02 to tissues
  • damage inner lining of arteries
54
Q

All these changes from nicotine and carbon monoxide?

A

coronary heart disease (CHD)

55
Q

Atherescolosis?

A

Damage to inner lining (CO, LDL penetrating enothilial wall)
causes macrophages to repair this>injest fatty acids.cause depostion of fatty acid (LDL’s) in arterial wall>formation of foam cells
formation of a fatty streak
Depotiis include cholesterol from LDL’s, fibres (causes artery to bulge onwards), platelets
build up of athermoas occurs in wall of artery
hardens to form a plaque which sticks out into the lumen of the artery>narrows it>limits amount of oxygen/blood flow to the tissues/reduced removal of CO2

56
Q

Stroke is?

A

death of part of th brain tissue

  • an artery bursts
  • blood clot forms around plaque>blocks the artery leadung to brain
57
Q

CHD?

A

The coronary arteries>aortra branches off close to heart.carries blood at high pressure [prone to damage]

  • Plaque reduces size of lumen
    1) angina- chest pain -extrend up left arm or neck
    2) heart attack- part of the muscle dies- due to clot of coronary artery
    4) Cardiac arrest- pumping action of the heart fails due to blockage of coronary arteries
58
Q

Factors of CHD?

Risk factors of cardiovascualr disease?

A

smoking, hgih blood pressure, high salt intake, low vitamin intake
excess salt/saturated fats/high cholsterol

59
Q

Epidermology is?
used to show smoking..?
hard to tell it conrtivutes to CHD as..?

A

study of distribution of diseases
epidermiligcial evidance shows smoking greatly increases risk of lung cancer (18 x more liekly to devlop it than a non-smoker))
but hard to tell as it could be other risk factors
world health organisation- whcih ountries may be at greater risk, whcih sex/age-range
help target research at particualr risk factors

60
Q

Experimental evidance shows?

A

studies on dogs- smoking-shows early signs of lung cancer an similair to chronic onstructive pulmonary disorder

61
Q

prevalance of smoking?

A

decline in number of people in western world smoking
Howver more young people are
more people in LEDC’s are which is worrying as symptoms can take years to appear

62
Q

what do cigarettes contain?

A

-nicotine- nervous system
-carbon monoxide- reduces 02 carrying to celld
-tar- contaons carcinogens
particulates- small particles of carbon irrittate airways

63
Q

Effects of smoking on the mammalian gas exchange system?
what happens to the 02/C02?
what does smooth muscle do?

A
  • tar settles in airways and alveloi
  • increases diffusion pathway for 02 into blood and C02 into alevloi (less is given/removed)
  • can cause an allergic reaction- smooth muscle contracts, narrowing the lumen in airway which reduces 02 to blood
64
Q

Effects of smoking- mucus and bacteria build-up?

A

-tar paralyses/destroys cilia, so don’t move to waft it back up throat>down oesphugus
-It enlarges goblet cells and mucus-secreting glands so releases more
bacteria are trapped by mucus but not removed
build-up of mucus and bacteria blocks the brochioles

65
Q

long-term effects?
increased cough?
scar tissue?
smooth muscle?

A

Increased cough to try and clear this bacteria-ladden mucus out of airway (let air in)
cough damages the delciate inner lining of airways and delciate alevoli
The linging will be replaced by scar tissue- less flexible/thicker
smoth muscle that lines brochioles>thickens which permantly reduces lumen>permanetly reduces flow of 02

66
Q

long-term effects of smoking?
infections?
macrophages?
brochioles and alvoli?

A

frequent infections caused by trapped bacteria cause infmalation>destroy inner lining of airway (epithelium layer)
macrophages [WBC] try and destroy pathogens
Try to make their way to the bacteria-ladden muscus>have to release digestive enzymes to get through that destroy part of the lining of the lungs
Damage to elastic tissue
greatest effect is in small brochioles and alveoli>destroy elastic tissue>causes it to become less flexible>during expiration it doesn’t recoil o push air out
Brochioles collapse trapping the air inside the alvoli>increases pressure>cause them to burst

67
Q

Lung cancer?

A

carcinogens (in tar), cause disruption to cell divison process so cause clumps of disorganised cells called a tumour
The turmour usually grows at branching points like when brochi serpeates into brochioles
As this tumour grows, it can block the airways
Symtoms: diffuculuty breathing, chronic ough, bring up blood, lose weight

68
Q

Chronic brochitius?

A

inflammation of airways (pathogens being trapped)- overprduction of mucus (goblet cells) and paralysed cilia cause a bacteria-laden mucus blockage of airways
Symtoms:
irritated lungs
chronic cough
coughing up mucus (filled with bacterua + WBC)

69
Q

Empheysena?

A

reduction in elactsity of alveloi walls>increase in pressure>cause them to burst
Reduced surface arera to allow gasoues exchange- less 02 in/more C02 removed
Symtoms:
shallow/rapid breath
short of breath, espeically during exercise
diffuclty exhaling
fatigue

70
Q

Chronic Obstruvtive Pulmonary disorder?

A

disease caused by a collection of diseases such as chronic brionchtiis, emphysena, asthma- [results in diffuclutes breathing]
Symtoms:
combination of symtoms e.g. chronic cough, diffuckuty exhaling

AS Level (74 decks)

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