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2.2.2 (Chapter 11) –
Health and Disease
Lesson Objectives:
To define the terms ‘health’ and ‘disease’
To discuss different categories of disease
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So what is ‘health’?
What do we mean by ‘health’?
What are the characteristics of health?
Health a person’s physical, mental and social condition
World Health Organisation (WHO):
‘a state of complete physical, mental and social well-being and
not merely the absence of disease and infirmity’
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Health a person’s physical, mental and social condition
Good
PoorHappiness
Fulfilling life
More than just the absence of disease!
Positive outlook
Well adjusted to society
Can undertake physical and mental tasks without difficulty
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EVERYONE is born with the genetic potential for growth and development … they need good health to grow and realise their potential both as humans and within society.
World Health Organisation (WHO; an agency of the UN):
“Good health is a fundamental human right”
What do we NEED for good health?
-Shelter
-Nutrition
-Exercise
-Sleep and rest
-Good hygiene
-Access to medical and social care
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So what is ‘disease’?
What do we mean by ‘disease’?
Disease a disorder or malfunction of the mind or body
which leads to a departure from good health
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Disease a disorder or malfunction of the mind or body which leads to a departure from good health
What are the causes of disease?
How do you know if you have a disease? (what are the characteristics?)
Single cause eg: malaria
Multifactorial eg: heart disease
Signs (symptoms) – physical and/or mental
ACUTE eg: influenza CHRONIC eg: TB
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The 9 categories (types) of disease
‘Miss D. Pind’MISS
D
P
IND
ental
nfectious
hysical
on-infectious
ocial
elf-inflicted
eficiency
egenerative
nherited
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Name this infection.
The infection is….
….. a cold or flu
This infection is caused by….
…..a virus
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Name this infection.
The infection is….
…..athletes foot
This infection is caused by….
…..a fungus
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Name this infection.
The infection is….
…..warts
This infection is caused by….
…..a virus
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Name this infection.
The infection is….
…..chicken pox
This infection is caused by….
…..a virus
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Name this infection.
The infection is….
…..food poisoning
This infection is caused by….
…..bacteria
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Name this infection.
The infection is….
…..measles
This infection is caused by….
…..a virus
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Name this infection.
The infection is….
…..fungal nail infection
This infection is caused by….
…..obviously a fungus
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Name this infection.
The infection is….
…..impetigo
This infection is caused by….
…..bacteria
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Name this infection.
The infection is….
…..oral thrush
This infection is caused by….
…..a fungus
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Single celled
organisms
Types of pathogenic organisms …
Bacteria
Virus
Fungi
Protozoa
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= An organism that causes a disease= a kind of parasite (an organism that lives in a very close relationship with another organism, the host, and does it harm … a well adapted pathogen will not kill its host)
Pathogen
Pathogens can enter the body in a number of ways ...
…or other natural openings…
They can be breathed in through the mouth or nose
They can enter through cuts or bites in the skin
HOST
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So how are diseases spread?
Vectors (eg: insects)
Contaminated food/water
Air
Contaminated needles
Direct contact
Indirect contact
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So how are diseases spread?
Vectors (eg: insects)
Contaminated food/water
Air
Contaminated needles
Direct contact
Indirect contact
Micropredator that actively delivers the parasite to the next host
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What have you learnt today?
Define ‘health’ Define ‘disease’
What is the WHO? What do we need for good health?
What are the 9 categories of disease?
a person’s physical, mental and social condition
a disorder or malfunction of the mind or body which leads to a departure from good health
Shelter, nutrition, exercise, sleep and rest, health and social care, good hygiene
World Health Organisation
MISS D PIND
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Homework
Go to WHO website:1.Write a brief description of what the WHO is and it’s remit.2.Then choose one disease of your choice to research, write a 200 word review of the information on that website on your chosen disease.
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Lesson Objectives:
To describe the causes & means of transmission of TB
To assess the worldwide importance of this disease
To describe the roles of different factors in the prevention and control of TB
Tuberculosis
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STARTER – Read the fact sheet from the WHO about TB
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KEY WORDS
Incidence
Prevalence
Mortality
Endemic
Epidemic
Pandemic
The number of NEW cases in a population occurring in a given time period
The number of people in a population with a disease within a given time period
The number of people who have died of a certain disease in a given time period
An infectious disease that is always present in a population
When a disease suddenly spreads rapidly to affect many people (eg: influenza)
When a disease spreads over a very large area (eg: a continent or the whole world; we are having pandemics of AIDS and TB at present)
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What do you already know?
Cause?
Prevalence?
Treatment?Prevention?
Impact?TB
Symptoms?
http://www.youtube.com/watch?v=JtyX694ubio Basic Summaryhttp://www.nhs.uk/conditions/Tuberculosis/Pages/Introduction.aspx Better!!
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TB – symptoms
Some people become infected and develop TB quite quickly whilst others harbour the bacteria for many years …
… it may become active when the immune system is weakened eg: malnutrition, HIV/AIDS
persistent cough
coughing up blood
fever
loss of appetite
emaciation
tiredness
night sweats
(caused by release of hormone-like compounds)
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TB – treatment
Antibiotic – Streptomycin (1940s) has been used to decrease incidence of TB
Samples of sputum (pus and mucus) taken from lungs for analysis – identified using a microscope
Chest x-rays (fibrosis, calcification, pneumonia)
Skin tests
Sufferers isolated for most infectious stage (2-4 weeks)
Treated for 9 months to a year with antibiotics – bacteria are slow growing and not sensitive to the drugs
Drug resistance – found after 1950s
READ p167-168 on TB
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TB – treatment http://www.youtube.com/watch?v=XvxCs8IlyQk
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TB – the cause
Two bacteria:
Mycobacterium tuberculosis
Mycobacterium bovis
Live inside human cells, particularly the lungs, though can spread through the entire body (even bone tissue)
Also occurs in cattle – spreads to humans through meat and milk
first isolated in 1882 by a German physician named Robert Koch who received the Nobel prize for this discovery
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SECONDARY TB
TB – the cause
Cough, sneeze, talk, spit
Bacilli in air in tiny droplets of liquid
Inhaled
Infectious stage: 2-4 weeks
Taken into the lungs
Macrophages (phagocytic WBCs) coat the TB bacilli in thick waxy coat (‘walled off’)
Local lung infection (pneumonia)
Lymph nodes become enlarged
Leads to scar tissue forming (fibrosis)
PRIMARY TB
Kidneys
Bone
Lining of the brain
Spinal cord
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TB – impact
Quite hard to catch - spreads most rapidly when there is overcrowding, especially if people are:
Homeless
Living in poor, substandard housing
Prisoners
Have low immunity eg: malnutrition, HIV positive
IV drug users, alcoholics or have diabetes
‘The biggest killer of women in the world’ - WHO Deaths in women aged 15-44 years:
9% TB, 3% war, 3% HIV, 3% heart disease
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Estimated that 30% of the world’s population is infected with TB (~1.8 billion)
8-10 million people infected per year
2-3 million die per year (eg: in 2002 - 2 million deaths due to TB)
~1 person per second contracts TB
By 2020 nearly 1 billion will be newly infected, of which 70 million will die (WHO)
M. bovis – spread from cattle to humans:
1850-1950 ~800,000 deaths in the UK
Now very few in developed countries
TB – prevalence
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TB – prevalence
The leading cause of death of HIV positive people.
Has been prevalent for thousands of years …
evidence in 4000 year old Egyptian mummies
Found primarily in: eastern Europe (250,000 cases/year)
Asia (3 million cases/year)
Africa (28% of all cases)
A worldwide pandemic
Those with HIV are 100x more likely to develop TB than other members of the population
Bangladesh, China, India, Indonesia, Pakistan, Philippines
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TB – prevalence
Incidence in the UK decreased BEFORE introduction of the vaccine (1950s) due to improvement in housing and diet … showing a resurgence now
Resistant strains
HIV/AIDS pandemic
Poor housing in inner cities
Rising homelessness
Breakdown of TB control programmes (partial treatment)
Migration
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TB – prevention
Prevention Break the lifecycle!
Isolation of infected people
Address social issues such as overcrowding
Better treatment
(maybe not antibiotics?)
Vaccinations
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TB – prevention
Vaccinations – Injected:
BCG Bacille Calmette Guérin – some protection
Vaccinations update:
2004 Contains 2 TB proteins that stimulate a strong immune response in humans
(taken from naturally immune individuals)
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So what do we know now?
Cause?
Prevalence?
Treatment?Prevention?
Impact?TB
Symptoms?
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Think, Pair, Share
How can we prevent TB, now and in the future?
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Lesson Objectives:
To describe the causes & means of transmission of HIV/AIDS
To assess the worldwide importance of this disease
To describe the roles of different factors in the prevention and control of HIV/AIDS
HIV/AIDS
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What’s the difference?
• HIV means human immunodeficiency virus – so it’s the name of the pathogen that causes the disease
• AIDS means Acquired immune deficiency syndrome – so it’s the name of the disease
• http://www.nhs.uk/conditions/HIV/Pages/Introduction.aspx Basic SUMMARY
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The nature of HIV• Viruses are very small!• HIV is a ball of protein and lipid
around RNA and reverse transcriptase (an enzyme). It’s a member of the group of viruses called retroviruses
• Once inside a cell the enzyme makes a ‘DNA version’ of the virus’s RNA
• The infected cell then follows the code on the ‘new’ DNA to make new viruses.
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HIV – the cause
HIV only reproduce when inside a host cell.
HIV infects T lymphocytes.
Dr Robert Gallow, National Cancer Institute, 1984 – isolated HTLVIII
which causes AIDS
AIDS is not a disease – it is a collection of opportunistic diseases associated with acquired immunodeficiency
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HIV – symptoms
Later symptoms:
Lack of energy
Weight loss
Frequent fevers and sweats
Yeast infections (oral or vaginal)
Skin rashes or flaky skin
Pelvic inflammatory disease in women
Short-term memory loss
Shingles
Children grow slowly or are sick frequently
Initial infection:Flu-like symptomsFeverHeadacheTirednessEnlarged lymph nodes
Months to years after infection
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HIV – symptomsAIDS:
Coughing and shortness of breath
Seizures and lack of coordination
Difficult/painful swallowing
Forgetfulness
Confusion
Diarrhoea
Fever
Vision loss
Nausea, abdominal cramps and vomiting
Weight loss and extreme fatigue
Severe headaches
Coma
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HIV – symptoms
HIV develops into AIDS due to opportunistic infections such as:
oral thrush (Candida albicans)
pneumonia (Pneumocystis carinii) – an unusual form of pneumonia
Leads to collapse of the immune system, meaning the body cannot detect and deal with:
cancer (eg: Kaposi’s sarcoma – a rare skin cancer caused by a herpes-like virus)
dementias
TB
malaria
malnutrition
TB + HIV: A dual Epidemic
http://www.youtube.com/watch?v=MnvdYfgb2DA
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HIV – the cause
Spread by intimate human contact:
direct exchange of bodily fluids (eg: sexual intercourse, blood donation, sharing of needles, over the placenta)
may pass through breast milk – viral particles and infected lymphocytes are found in breast milk
high risk individuals – haemophiliacs treated with Factor VIII from many donors
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HIV – impact
Affects economic development of countries as it affects primarily 20-30 year olds (potentially the most economically productive)
Drugs expensive eg: major impact on the growth of some African states
HIV leaving a cell
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HIV – prevalence
Pandemic in early 1980s
47 million infected with HIV by 1998 of which 14 million had already died
980,000 cases reported in USA since 1981
1 million Americans may be infected, ¼ of whom don’t know
Leading killer of 25-22 year old African-American males
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HIV – prevalence
Initial epidemic in North America (first reported in 1981) in male homosexuals that practised anal intercourse with many partners (high risk as the mucous lining of the rectum is not as thick as that of the vagina and less natural lubrication … virus can pass from semen into blood)
Transmission through heterosexual intercourse on the rise especially in Africa
Endemic in: sub-Saharan Africa
USA
Europe
Asia
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HIV – treatment
No cure as yet and no vaccine
Anti-HIV drugs eg: zidovudine (AZT) works by blocking the viral reverse transcriptase
Not sure if 100% of HIV positive patients will develop AIDS – some appear to be symptomless carriers
Antiretroviral drug therapy slows onset of AIDS but have side-effects:
rashes
headaches
diarrhoea
nerve damage
abnormal fat distribution
Mild and temporary
Severe and permanent
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HIV – treatment
AIDS = advanced HIV infection with significant loss of CD4 cells,
weakening the immune system to a point where the body is at risk of ‘AIDS-defining’ illnesses (ones that mark the onset of AIDS)
= CD4 count below 200 cells per cubic mm of blood
CD4 cells are the host cells that aid HIV in replication.
Test identifies presence of antibodies to HIV – several weeks after the initial infection
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HIV – prevention
Prevention Education
Spread of AIDS difficult to control – long latent stage means that carriers may not know that they have HIV
Virus changes its surface proteins making it hard to detect and the production of a vaccine difficult
Protection Condoms,
femidoms and dental dams, screen blood
Clean needles
Testing people –
cheap but does it infringe your
rights?
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Microbicides protecting against HIV
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• http://www.bbc.co.uk/iplayer/episode/b011r4gs/Queen_Days_of_Our_Lives_Episode_2/
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Lesson Objectives:
To explore the causes, transmission and effects of Malaria
http://www.nhs.uk/Conditions/Malaria/Pages/Introduction.aspx Summary
Malaria
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STARTER – quick recap
1. What type of pathogen causes TB and HIV/AIDS?
2. What is the means of transmission of TB and HIV?
3. What is the leading cause of death of HIV+ patients?
4. What is the main cause of a resurgence of TB in the last 20 years?
5. Define the following:
a)Pathogen
b)Incidence
c) Mortality
d)Endemic
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Malaria – symptoms
Fever
Anaemia
Nausea
Headaches
Muscle pain
Shivering
Sweating
Enlarged spleen
Symptoms in cycles – related to the asexual cycle of Plasmodium in RBCs – periodically burst open and reinfect RBCs
Causes the RBCs to become sticky – obstruct blood vessels
World Malaria Day (25th April)http://www.youtube.com/watch?v=O0Fsw-0_ldM
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Malaria – the cause
Protozoan parasite Plasmodium:
Plasmodium falciparum
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
Eukaryote (RBC) bursting after
infection
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Malaria – method of transmission
Vector = female Anopheles mosquitoes feeding on human blood (to get protein to develop their eggs!)
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Heineman Text Page 162
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Step by Step Life Cycle
1. If the host already has malaria, the mosquito will such the parasite gametes into it’s stomach.
2. Gametes fuse, zygotes develop in mosquito's stomach.
3. Infective stages are formed move to mosquito’s salivary glands.
4. Mosquito bites another person, saliva injected as anti-coagulant.
5. Infective stage of parasite transmitted, travels to liver, multiplies and enters blood.
6. In blood they enter RBCs, gametes produced.
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Malaria – impact
A widespread and dehabilitating disease for the human population over thousands of years leaving a mark on our genome.
One of the world’s biggest threats to health – over 40% of the population live in areas where there is risk of Malaria.
Accounts for 1 in 10 deaths of children in the developing world.
Recent resurgence of the disease in sub-Saharan Africa.
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Malaria – prevalence
1/3 of the global population are at risk from malaria (~2 billion)
Incidence = 400-500 million per year
Causes 1.5-2.7 million deaths per year (3,000 in the under 5s)
5 people per minute die of Malaria
Endemic in – South AmericaAfricaIndonesia
90% of clinical malaria cases
India, Brazil, Sri Lanka, Vietnam, Colombia, Solomon Islands
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Think, Pair, Share
How can we prevent the spread of malaria?
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Malaria – prevention
Plasmodium still retains a ‘relict’ chloroplast (fatty acid biosynthesis) complete with a genome – a possible target for anti-malarial drugs?
CONTROL
Reduce number of vectors Avoid
being bitten
Use drugs to prevent infection
Better testing?
Vaccines
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Malaria – anti-malaria drugs – more information!
Prophylactics (preventative drugs – stops infection if you are bitten by an infected mosquito)
1.Chloroquinine – inhibits protein synthesis and prevents the parasite from spreading within the body – problems with resistance to this drug
2.Proguanil – also inhibits sexual reproduction of Plasmodium inside the mosquito
3.Mefloquine – a newer drug. Expensive and sometimes causes side effects such as restlessness, vomiting, dizziness and disturbed sleep
Read p172 on anti-malaria drugs (prophylactics) and make your own
notes
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Malaria – immunity
Sickle Cell Anaemia
A disease that alters the shape of red blood cells (into a sickle shape), thereby reducing their oxygen capacity, causing weakness, cramps, organ damage and anaemia especially during high activity.
CAUSE – single point mutation in the Hb gene, recessive disease
Typically in black Africans/Afro-Americans
Homozygous HbS - lethal
Heterozygous - selective advantage
Continuous Reinfection-Become immune to malaria if they survive the first 5 years of life
-Immunity only lasts for as long as you are in contact with the disease
Sickle Cell Anaemia
A disease that alters the shape of red blood cells (into a sickle shape), thereby reducing their oxygen capacity, causing weakness, cramps, organ damage and anaemia especially during high activity.
CAUSE – single point mutation in the Hb gene, recessive disease
Typically in black Africans/Afro-Americans
Homozygous HbS - lethal
Heterozygous - selective advantage
Sickle Cell Anaemia
A disease that alters the shape of red blood cells (into a sickle shape), thereby reducing their oxygen capacity, causing weakness, cramps, organ damage and anaemia especially during high activity.
CAUSE – single point mutation in the Hb gene, recessive disease
Typically in black Africans/Afro-Americans
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Summary –
copy and complete the following table (from
memory!)
Pathogen
Vector (Definitive host)
Main stages of development
Intermediate host
Features
Incidence
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Key word Bingo!
PathogenPlasmodium
Vector
Transmission
Liver
RBCsSCA
Immunity
Definitive
Intermediate
Gametes
Sexual
Asexual
Anticoagulant
Sporozoite
Erythrocyte
SalivaSymptoms
Endemic
Malaria
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Lesson Objectives:
To be able to name and give the functions of the different parts of blood
To describe the lines of defence against disease in humans
Blood and the immune system
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Where are blood cells made?
-From blood stem cells
-In bone marrow in various places around the body
How much blood?
How much blood is found in the
average human?
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What is blood made up of?
55% plasma =
water
proteins
other chemicals
45% cells =
RBCs
WBCs
PlateletsWhat is the structure and function of each of these
cells?
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Blood cellsRed Blood Cells
-Erythrocytes (‘red cells’)
-Contains haem groups (Fe)
-Transport oxygen
Platelets
-Thrombocytes
-Anuclear in mammals
-Functions – blood clotting, cell adhesion, signalling
White Blood Cells
- Leukocytes
-Immune response
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Defending ourselves against pathogens
First line of defence
(non-specific)
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What is the body’s first line of defence?
Skin (sebum)
Nasal hairs
Tears, saliva (lysozymes and salt)
Lungs (cilia & mucus)
Stomach - HCl
The virus that causes warts can pass through unbroken
skin!
Staphylococcus aureus
The skin harbours a ‘flora’ of bacteria – most pathogenic
bacteria cannot survive there
Blood clotting
Helps to seal wounds rapidly until more permanent repair by mitosis
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Oh no! A cut!
Damaged cells produce Thrombokinase
This stops a chemical called Heparin from working
… which allows Thrombin to work …
Fibrinogen Fibrin + Platelets
BLOOD CLOTS!
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Heparin
Thrombokinase
ProthrombinThrombin
Fibrinogen Fibrin + Platelets
BLOOD CLOTS!
What happens when you get cut
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Heparin
Thrombokinase
ProthrombinThrombin
Fibrinogen Fibrin + Platelets
‘Normal’ (non-cut!) cells
NO BLOOD CLOTS!
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What happens if a pathogen gets past the first line of
defence?
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White blood cells – fight disease
Phagocytes Lymphocytes
SECOND LINE of defence - engulf and digest microbes
THIRD LINE of defence – recognise invaders and make antibodies and anti-toxins
Neutrophils Macrophages
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PhagocytosisBody recognises invaders and releases chemicals eg: HISTAMINE
NEUTROPHILS move towards the pathogen (chemotaxis)
Release digestive enzymes (lysosomes) … afterwards the neutrophils die
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What is pus?
White blood cells (neutrophils) and dead bacteria!
Inflammation?
Areas become red and hot due to extra blood being taken there … extra white blood cells and the higher temperature also help to kill microbes (second line of defence!)
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White blood cells – fight disease
Phagocytes Lymphocytes
SECOND LINE of defence - engulf and digest microbes
THIRD LINE of defence – recognise invaders and make antibodies and anti-toxins
Neutrophils Macrophages
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Lymphocytes
Key points:
Smaller than phagocytes
A large nucleus
2 types, both produced before birth in the bone marrow
Contain receptor proteins which bind to antigens
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White blood cells – fight disease
Phagocytes Lymphocytes
T cells
Recognise antigens,
stimulate B cells
B cells
Make antibodies
Memory B cells
‘remember’ antigens
(immunity)
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T cells
Recognise antigens,
stimulate B cells
B cells
Make antibodies
Lymphocytes
Mature in the bone marrow
Concentrate in lymph nodes and spleen
Mature in the bone marrow
Collect in the thymus (in the chest just below the sternum)
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Write down all the key words you
have met in today’s lesson –
with a brief definition!
Lymphocytes
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Lesson Objectives:
To work independently
To find out more detail about leukocytes (white blood cells)
Leukocytes
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YOUR TASK
Get into 8 groups (maximum 3 students per group)
Select a theme from below (maximum 2 groups per theme)
1. B cells and memory cells
2. T helper cells and killer cells
3. Primary and secondary response and its role in immunisation
4. Active and passive immunity
YOUR TASK – using the questions set on the next slide as prompt, produce a 5 minute overview of your theme suitable for the rest of the class to make notes from. You may produce handouts if needed (including diagrams or slides etc. – maximum 1 side of A4 paper)
You have the rest of the lesson and homework to prepare this – due in NEXT LESSON
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Your task …1. B cells and memory
cellsWhere do they develop? How do
they respond to antigens? Why do they clone themselves? What is the difference between plasma and memory cells?
2. T helper cells and killer cells
Where do they develop? What do they respond to? What is the difference between helper and killer cells? How do they work?
3. Primary and secondary response and its role in immunisation
What is this? How does immunity develop? What is the difference between the two responses? Show diagrams detailing both.
4. Active and passive immunity
What is this? How do you get both active and passive immunity? Where is it important? How does it work? How long do both types last for?
An OUTSTANDING presentation will address AT LEAST these questions and will involve background reading (ie: reading the text
book is NOT ENOUGH!)
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Lesson Objectives:
To give our presentations
To recap our learning from this chapter so far!
Mini review
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YOUR TASK - what is lurking on your skin?!
1 agar plate per person
Split into 4 sections by drawing lines on the back
Place a finger gently onto a section
Now run your hand under my desks (yuck!) and place a finger in another section
Now wash your hands and place a (‘clean’) finger on another section
What about my door handle? Or your text book?!
Label the sections and write on your name. Tape the top on (2 pieces of sellotape only). Put in the tray at the front …
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Lesson Objectives:
To summarise our learning from the previous lessons
To look at our agar plates
Immunity
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YOUR TASK
In your notes:
1. Define the terms immune response, antigen and antibody
2. Describe (with diagrams) the structure and mode of function of phagocytes
3. Describe (with diagrams) the structure and mode of action of T lymphocytes and B lymphocytes including the significance of cell signalling and the role of memory cells
4. Compare and contrast the primary and secondary immune responses
EXTENSION:
Complete SAQ 5 and 6 from page 180
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Answers …
1. Definitions:
a) Immune response the way in which lymphocytes respond to infection by pathogens
b)Antigen a molecule or cell that is recognised as
foreign by the immune system
c) Antibody A small protein secreted by B lymphocytes in
response to a particular antigen
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2. PhagocytosisBody recognises invaders and releases chemicals eg: HISTAMINE
NEUTROPHILS move towards the pathogen (chemotaxis)
Release digestive enzymes (lysosomes) … afterwards the neutrophils die . ‘Waste’ material egested.
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3. Lymphocytes
Stimulated when they detect ANTIGENS (‘free’ or as part of a cell wall for example).
Lymphocytes detect SPECIFIC antigens only – so we have many different types in our blood.
As they mature, lymphocytes produce ANTIBODIES (small globular glycoproteins) which are specific to an antigen.
They are placed into the plasma membrane of the lymphocyte – act as receptors for an antigen.
If bacteria enters the body it is detected and the immune response is triggered!
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3. Lymphocytes – B lymphocytes
Triggered into action when an antigen binds to a receptor (could be found on a macrophage – an antigen presenting cell, APC, which might be in the lymph nodes)
-Divides by mitosis (clones are formed)
-Some clones DIFFERENTIATE into plasma cells (short lived) which develop extra ER, ribosomes and golgi apparatus to make loads of antibodies to be released by exocytosis (up to 2000 molecules per second!)
-Antibodies secreted into the blood – bind with antigens on bacteria
-Some clones do not secrete antibodies – they remain as MEMORY CELLS (long lived, circulate, secondary response!)
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3. Lymphocytes – T lymphocytes
Triggered by binding of an antigen to glycoproteins on the plasma membrane ONLY when this is found in the plasma membrane of another cell (eg: APC or virus particles found on the outside of an invaded body cell)
T helper cells with complementary receptors bind to the antigen then divides. The clones secrete CYTOKINES which stimulate other cells (eg: macrophages, B lymphocytes, T killer cells)
T killer cells destroy the cell (including infected body cells) using chemicals such as hydrogen peroxide
Some cells remain as MEMORY CELLS
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The ways in which lymphocytes work …
1.Antibodies make microbes stick together in clumps … then phagocytes ingest them!
2.Some antibodies stick to microbes to make it easier for phagocytes to find them
3.Some even stick to TOXINs produced by the microbes and make them harmless (ANTI-TOXINs!)
4.Antibodies stick to microbes and make them burst open
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4. Primary and Secondary Response
Only a few lymphocytes with receptors that fit the antigen in the body – takes time to form clones and produce antibodies – delay when pathogen can divide and damage body tissues
Memory cells remain in the blood – a faster response when the pathogen invades again preventing any illness (immunity!)
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Lesson Objectives:
To discuss immunity
To find out about antibiotics and antibodies
Antibiotics and
preventing illness
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STARTER
Grab a mini whiteboard, pen and rubber and sketch the following:
1.A graph showing the primary and secondary immune response (with explanations)
2.Phagocytosis
Compare your pictures with your partner!
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Active Immunity
Your immune system is stimulated to make a particular type of antibody – fast secondary response
1. Due to first infection
2. By vaccination
Natural immunity
Artificial immunity
Herd immunity (80-85%)
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Passive Immunity:
Short lived immunity
Natural immunity - Babies get antibodies via the placenta and breast milk, giving them immunity to the same diseases as their mother.
Only present during growth in the womb and when breast feeding.
Artificial immunity – injections of antitoxins eg: in A&E against tetanus after a cut
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Antibiotics – what are they?
Drugs used to treat/cure infections
Show selective toxicity
A wide variety available to treat bacterial and fungal and infections
Only a few available to treat viral infections
Sir Alexander Fleming 1928
PenicillinAmoxicillin
Streptomycin Erythromycin
Neomycin Vancomycin
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Penicillin works by destroying
bacteria's ability to maintain the rigidity
of their cell wall.
Antibiotics – where do we get them from?
Derived from living organisms
Can be synthetic (eg: isoniazid)
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Antibiotics – how do they work?
Broad spectrum effective against a wide range of bacteria
Narrow spectrum active against a few
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Antibiotics – how do they work?
What it does Examples Effect on bacteria
Inhibits cell wall synthesis
Penicillin, cephalosporin, vancomycin
Bactericidal
Inhibits transcription
Rifampicin Bactericidal
Inhibits protein synthesis
Chloramphenicol, tetracyclineErythromycin, streptomycin
Bacteriostatic
Bactericidal
Interferes with metabolic reactions
Sulpha drugs Bacteriostatic
Inhibits membrane functions
Polymyxin Bactericidal
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Antibodies
Glycoproteins – amino acid chain with sugar units
Also known as IMMUNOGLOBULINS – different types eg: IgG and IgA
The ways they work:
Antibodies make microbes stick together in clumps … then phagocytes ingest them!
Some antibodies stick to microbes to make it easier for phagocytes to find
them Some even stick to TOXINs produced
by the microbes and make them harmless (ANTI-TOXINs!)
Antibodies stick to microbes and make them burst open
Some may stop pathogens from attaching to cells or tissues
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Lesson Objectives:
To recap HIV/AIDS, TB and Malaria
To discuss the response to the threat of new strains of influenza each year
New diseases, and old
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SUMMARY OF DISEASES
Malaria TB HIV
Cause
Symptoms
Treatment
Prevention
Prevalence
Impact
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SARS
Severe acute respiratory syndrome (SARS)
Caused by a virus
Respiratory disease in humans
One near pandemic (Nov 2002 – July 2003; 8,096 known cases, 774 deaths (9.6% fatality))
Started in China and rapidly spread
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An RNA virus which constantly mutates (antigenic drift) meaning that if you are immune to it one year, you may not be immune the next year
Spreads easily and rapidly
Peak outbreaks in winter months (ie: twice a year across the globe due to seasonal differences – one per hemisphere)
Typically 3-5 million severe cases per year with 500,000 deaths worldwide
A pandemic every 10-20 years
Pandemic in 1918 – if a similar strain emerged today it would kill 50-80 million people
Influenza (flu)
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Influenza (flu) – H5N1
Easily transmissible between birds
Enzootic in many bird populations esp. Southeast Asia
Epizootic (epidemic in nonhumans)
Panzootic (affecting many birds of different species over a wide area)
Transmitted through saliva, nasal secretions, faeces and blood
Lasts in the environment (without a host) for weeks
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New hope?
Few drugs work against viruses
Antibiotic resistance
Sponges
One of the earliest multicellular animals on Earth (up to 600 million years old)
Found in seas over the world
Animals – no cell walls, fixed permanently to sea bed or coral reef
Absorb food across cells with flagella which beat rhythmically creating currents
Contain specialised cells but no true tissues or organs
Interest from pharmaceutical companies – they have evolved a defence mechanism to deter predators
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Our changing attitudes to smoking …
With all of the information that we now have about the effects of smoking on our health, is it a good idea to smoke?
Used since 500 AD
1565 - First introduced in England
1875
1921
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Cigarettes
NicotineAddictive
Affects the brain, nervous system and the cardiovascular system
TarCarcinogenic
Carbon monoxideProduced by incomplete oxidation which reduces oxygen carrying capacity of the blood
ParticulatesTiny particles (eg: C) which irritate lungs and airways
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Nicotine-A neurotoxin (chemical that damages the nervous system)
-Used as an INSECTICIDE (!)
-Addictive
-Relatively small molecules which move into every part of the body including the brain
-Increases amount of dopamine (feeling of pleasure)
-Causes the release of adrenaline into the blood (increased heart rate, breathing rate and blood pressure)
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Carbon monoxide
-Diffuses into capillaries from alveoli
-Forms carboxyhaemoglobin
-Hb has a very high affinity for CO
-Less Hb available to transport oxygen
-SMOKING REDUCES THE AMOUNT OF OXYGEN DELIVERED TO TISSUES (including heart tissue)
-Less energy available to muscles during exercise
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Knock on effects
Increased blood pressure (nicotine)
Atherosclerosis and CHD
Blood clots/blood vessel bursts = stroke
Left hemisphere – language skills, memory
Right hemisphere – movement, spacial awareness, memory
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Lung diseases associated with smoking
1.COPD – Chronic obstructive pulmonary disease (includes emphysema)
2.Lung cancer
3.Infectious organisms
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Lesson Objectives:
To think about the effects of smoking on health
To review Chapter 11
Finishing off the unit!
Sir Richard Doll (1912-2006)
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Smoking and lung cancer … the results
Why the difference between males and females?
Why is there a time lag between the peaks?
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Smoking and lung cancer
Cells in the lungs divide uncontrollably and form a tumour
Mortality rate in England and Wales: ~35,000/year (30% of smoking related deaths)
Smokers are almost 20x as likely to die from lung cancer than non-smokers
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Smoking and lung cancer
Cigarette smoke contains CARCINOGENS
A lump of disorganised cells (tumour) forms
This tumour can be almost anywhere in the gas exchange system (most often where bronchi begin or at other branching points)
The tumour will displace other tissues as it grows – leading to blockage of airways or part of the lungs
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Other lung illnesses
Tuberculosis
Bronchitis
Cause: Inflammation of the trachea and bronchi due to infection (or other causes)
Tobacco smoke has been linked to acute bronchitis
Smoking has been shown to increase risk of infection, risk of progression from infection to disease and risk of death
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COPD – Chronic Obstructive Pulmonary Disease
Airflow into and out of the lungs gradually and progressively becomes more obstructed
~600 million worldwide suffer from COPD
Mortality rate: 300 million/year
Approx. 80-90% caused by smoking
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Some chemicals from cigarette smoking stimulate NEUTROPHILS
They come to the lungs and CAUSE illness by secreting NEUTROPHIL ELASTASE (a protease that breaks down elastin; forms the elastic fibres in tissues of the airways)
Inhibitors prevent enzyme from doing too much harm – in smokers the balance between inhibitor and enzyme tips towards the enzyme (bad!)
Proteases gradually break down the elastin tissues in the lungs – irreversible damage esp. to alveoli
COPD – Chronic Obstructive Pulmonary Disease
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COPD – Chronic Obstructive Pulmonary Disease
Emphysema
Bronchitis
Beta antagonists widen airways
Severe cases – use oxygen cylinders
Pathology of lung showing centrilobular emphysema characteristic of smoking. Closeup of fixed, cut surface shows multiple cavities lined by heavy black carbon deposits. (CDC/Dr. Edwin P. Ewing, Jr., 1973)