Unit 1 biology
- Created by: charlie
- Created on: 15-02-14 18:50
lungs structure
DIAGRAM
ventilation
INSPIRATION (active process requiring ENERGY):
- intercostal + diaphragm muscles contract
- rib cage (UP + OUT) diaphragm (FLATTEN) inc. vol. of THORAX
- vol of THORAX inc, pressure in lungs dec. below atmos. pressure
- air flows in
EXPIRATION (passive process not requiring ENERGY)
- intercostal muscles + diaphragm muscles relax
- rib cage (DOWN + IN) diaphragm (CURVED)
- vol of THORAX dec, pressure in lungs inc. above atmos. pressure
alveoli
air sacs where gas exchange takes occurs - surrounded by network of capillaries
STRUCTURE
- single layer of thin flat cells -ALVEOLAR EPITHELIUM
- capillary walls made from -CAPILLARY EPITHELIUM
- alveoli walls contain elastin (protein) helping return to normal shape after inhaling + exhaling
GAS EXCHANGE
- O2 out across walls into Hb
- CO2 into + breathed out
factors affecting diffusion rate
- thin exchange surface- one cell thick = short DIFFUSION PATHWAY
- large SA - large number = lots of diffusion
- steep concen gradient of O2 + CO2 between alv.+ cap. (maintained by blood flow + ventilation)
measuring lung function
PULMONARY VENTILATION
pulmoary ventilation = tidal volume X ventilation rate
- tidal volume = volume of air in each breathe
- ventilation rate = number of breaths per minute
Spirometer traces
- spirometer is machine used to volume of air breathed in + out
- produces graph called spirometer trace
DIAGRAM
lung diseases
PULMONARY TUBERCULOSIS
INFECTION
- immune system cells build wall around bacteria in lungs
- forms small hard lumps - tubercles
- infected tissue in tubercules dies + gaseous exchange surface damaged (tidal vol. dec.)
- can also cause fibrosis (reduce tidal vol.) bacteria enters blood streams
SYMPTOMS
- coughing up blood + mucus
- chest pain, shortness of breath, fatigue
- ASYMPTOMATIC - infected without symptoms
TRANSMISSION
- DROPLET INFECTION - sneezes or coughs
- TREATED by prevention using BCG vaccine and antiobiotics
Fibrosis
- formation of scar tissue in lungs due to infection of substances (asbestos, dust)
- scar tissue is elastic + thicker so tidal vol. of lungs dec.
- reduces rate of gas exchange in alveoli - diffusion pathway lengthened
- less oxygen - rate of respiration dec.
- fatigue, weakness
- dry cogh, chest pain, shortness of breath
Asthma
- airways inflamed + irritated due to allergic reation (pollen/dust)
- smooth muscle lining in bronchioles contracts = large amounts of mucus produced
- airways constricted - air flow reduced = less O2 received
- wheezing, tight chest, shortness of breath
- muscle relaxant drugs
Emphysema
- lung diease (smoking/air pollution exposure)
- inflammation attracts phagocytes --> produces enzyme --> breaks down elastin --> alveoli cant recoil to expel air + destroys walls (dec. SA)
- tired/ weak as lack of O2
- shortness of breath, wheezing
lung disease data
RISK FACTORS = factors inc. persons chance of getting that disease
CORRELATION = only shows one factor of causing the disease
heart structure
- LV = thicker, muscular walls, contract powerfully (blood to whole body)
- V = thicker walls than A as have to push blood out of heart
- AV valves = stop blood flowing back to A after V contract
- SL valves = stop blood flow back to heart
- cords = attach AV valves to ventricles - stop being forced into A when V contract
- valves = open if higher pressure behind valve (closed if vice versa)
DIAGRAM
control of heart beat
- MYOGENIC - contract + relax without receiving signals from nerves
SAN -
- pacemaker sending electrical waves across A walls (right+left A contract together)
- NON CONDUCTING COLLAGEN TISSUE - prevents direct waves going to V
- electrical activity transferred from SAN to AVN
AVN -
- passing electrical waves to BUNDLE OF HIS
- delay to make sure V contact after A emptied
- BUNDLE OF HIS - muscle fibres responsible for conducting to finer muscle fibres in right + left ventricle walls (PURKYNE FIBRES)
- PURKYNE FIBRES - carry to muscular walls of right+left V (simulataneos contraction from BOTTOM UP)
cardiac output
'volume of blood pumper out by the heart per minute'
CARDIAC OUTPUT = STROKE VOLUME x HEART RATE
- HEART RATE = no. of heartbeats per minute
- STROKE VOLUME = vol. of blood pumped during each heartbeat
cardiac cycle
'ongoing sequence of contractio + relaxation of A + V keeping blood continuously pumping round body'
1. V RELAX + A CONTRACT
- A dec. vol in chamber which inc. pressure
- blood pushed into V
- slight inc. in V pressure + chamber vol. as V received ejected blood from contracting A
2. V CONTRACT + A RELAX
- V dec. vol which inc. pressure
- pressure higher in V than A (AV valves shut)
- V pressure higher in V than aorta + p. artery (SL valves open + blood out)
3. V RELAX + A RELAX
- high pressure in p. arterty + aorta closes SL valves
- blood returns + atria fill due to higher pressure in vena cava and p. vein
- V relax + pressure falls below A (AV valves open) - blood flows passively into V from A
interpreting events of cardiac cycle
DIAGRAM
cardiovascular disease
'diseases associated with heart + blood vessels. Include aneurysms, thrombosis + myocardial infarction; most start with atheroma formation.'
Atheroma formation
- arteries made from - enothelium (smooth inner lining)
- if damage occurs (high BP) white BC (macrophages) + lipids from blood clump together under lining forming fatty streaks
- over time more white BC, lipids + connective tissues build + harden = fibrous plaque (ATHEROMA)
- plaque partially blocks lumen + restricts blood flow = BP inc.
aneurysm + thrombosis
ANEURYSM
'balloon-like swelling of artery'
- starts with formation of atheromas - damages + weakens arteries
- narrow arteries - inc. BP
- blood travels pushing inner layers of artery through outer elastic layers forming (ANEURYSM)
- may burtst = HAEMORRHAGE (bleeding) ]
THROMBOSIS
'formation of blood clot'
- starts with formation of atheromas - ruptures endothelium of artery
- damages wall + leaves rough surface
- platelets + fibrin (protein) accumulate at site of damage + form blood clot (THROMBUS)
- can cause complete blockage of artery OR dislodge + block blood vessel elsewhere
- debris from rupture cause another blood clot
myocardial infarction (heart attack)
- coronary artery blocked (blood clot) + area of heart muscle totally cut off from blood supply (receiving no O2)
- causes MYOCARDIAL INFARCTION
- causes damage + death of heart muscle
- SYMPTOMS = pain in chest + upper body, shortness of breath, sweating
risk factors + CHD
CHD = coronary arteries have lots of atheromas (restricts blood flow to heart) - type of cardivascular disease
RISK FACTORS
- HIGH BP = inc. risk of damage to coronary artery walls (Atheroma) - overweight, no exercise, salt
- HIGH BLOOD CHOLESTROL = main fatty acid deposit in atheromas - saturated fats
- CIGARETTE SMOKING = dec. amount of antioxidants in blood (protect cell damage), also CO recudes O2 in tissues
REDUCING RISK
- MOST within our control - LIFESTYLE CHOICES
- GENETIC PREDISPOSITION - to CHD or high BP
1st STAGE OF IMMUNE RESPONSE - phagocytosis
'process white blood cells phagocytes (e.g. macrophage) engulfs any foreign material entering the body'
STAGES
- phagocyte recognises ANTIGENS on pathogen
- cytoplasm of phagocyte move round pathogen ENGULFING it
- pathogen now conatined in PHAGOCYTIC VACUOLE
- LYSOSOME fuses with it + secretes LYSOSOMAL ENZYMES
- break down pathogen
- phococyte presents pathogens ANTIGENS (sticks on its surface)
- other immune system cells are activated
2nd STAGE OF I.R - T-cell activation
T-CELL = 'another type of white BC'
- PROTEINS on its surface
- BIND TO antigens presented by phagocytes
- ACTIVATES t-cell
- different types respond in different ways
- some RELEASE SUBSTANCES that ACTIVATE B-CELLS
- some ATTACH to ANTIGENS on pathogen and KILL the cell
3rd STAGE OF I.R - B-cell activation + plasma cell
B-CELLS = 'covered with antibodies (proteins bind to antigens forming ANTIGEN-ANTIBODY COMPLEX'
each B-CELL has DIFFENT SHAPED antibody on membrane = so bind to diff. shaped antigens
- antibody meets COMPLEMENTARY SHAPED antigen
- BINDS
- with substances released from T-CELLS this ACTIVATES B-CELL
- then divides to produce many more B-CELLS (PLASMA CELLS)
4th STAGE OF I.R - antibody production
- plasma cells IDENTICAL to b-cells (clones)
- SECRETE loads of antibodies specific to antigen
ANTIBODY FUNCTIONS:
- COATING PATHOGEN makes it easier for PHAGOCYTE TO ENGULF
- COATING PATHOGEN prevent it from ENTERING HOST CELLS
- BINDING TO + NEUTRALISING (inactivating) TOXINS produced by pathogen
antibodies + antigens
ANTIGEN =
- substance (protein/carb) that not normally found in host's body
- outer surface of pathogen recognised as foreign due to many antigens
- antigens stimulate production of complementary antibodies
ANTIBODIES =
- protein made from host's B-cells in response to specific antigen
- antibody combines with antigen + carries out many functions
- 1) coating pathogen - making it easier for phagocyte to engulf
- 2) coating pathogen - prevent from entering host cells
- 3) binding to + neutralising toxins - produced by pathogen
antibody structure
- made up of chains of A.A monomers linked by peptide bonds
- SPECIFITY depends on VARIABLE REGIONS
- each antibody has diff. shaped VARIABLE (diff. A.A sequences) complementary to specific antigen
- CONSTANT REGIONS are same in all antibodies
DIAGRAM
cellular + humoral responses
IMMUNE SYSTEM SPLIT INTO TWO
both responses needed in removing pathogen from the body
CELLULAR (cell-mediated immunity)-
- T-cells (help activate B-cells)
HUMORAL (antibody-mediated immunity)
- B-cells
- production of antibodies
primary + secondary responses
PRIMARY RESPONSE
- pathogen enters body first time activates immune system
- slow because arent many B-cells that can make antibody needed to bind to it
- symptoms are shows till infection overcome
- after exposure B+T-cells produce MEMORY CELLS
- remain in body for years - remember specfic antigen + immidiately bind to it
- person now IMMUNE
SECONDAY RESPONSE
- if same pathogen enters body - quicker, stronger response
- MEMORY B-CELLS divide into plasma cells - produce right complementary antibody
- MEMORY T-CELLS divide into correct typ of T-cells - kill cell carrying antigen
- no symptoms shown
Vaccines
- symptoms are expressed whilst B-cells dividing to build up numbers
- VACCINES help avoid this
- contain antigens that cause body to produce memory cells against particular pathogen - without pathogen causing disease
- immuninty with NO SYMPTOMS
- protect individuals + those not vaccinated as fewer people to catch from (HERD IMMUNITY)
- ANTIGENS may be free or attached to dead / attenuated (weakened) pahogen
- injected or taken orally
- ORALLY - broken down by enzymes in gut / molecules of vaccine too large to be absorbed by blood
- BOOSTER VACCINES given later on - make sure more memory cells are produced
vaccines - ethical issues
- all vaccines tested on animals before humans (cotroversial)
- animal based substances used to produce a vaccine
- testing on humans is risky - might not have worked thinking it had
- side effect risks - but still protected by herd immunity (unfair)
- if epidemic of new disease - rush to receive vaccines - difficult decisions made (e.g. who would be first to receive it)
antigenic variation
- antigens on surface of pathogens acitvate primary response.
- infected second time with same pathogen activated secondary response - dont get ill
'sneaky pathogens change their surface antigens'
- when infected second time, memory cells wont recognise different antigens
- I.S has to carry out primary response again - takes time - get ill again
- makes it difficult to make vaccines for 1 disease - e.g. influenza virus
monoclonal antibodies
'antibodies produced from single group of genetically identical B-cells (plasma cells)'
- very specific shape - binding site unique structure for complementary shape
- make them bind on to anything (e.g. cell antigen or other substance)
ETHICAL ISSUES
- animal rights issues
- animals used to produce the cells from which monoclonal antibodies are produced
validating new knowledge about vaccines + antibodi
- study presents evidence (e.g. that vaccine X has side effects)
- other scientists have to come up with more evidence to validate theory
- may repeat the study / conduct other studies to prove same theory
MAKING DECISIONS
- when info. has been validated by scientists
- society can use info to make informed decisions
Disease
'...is when part of the body doesnt function properly, different diseases have different causes...'
- INFECTIOUS: pathogens
- NON-INFECTIONS: body malfunctioning / environment
DISEASE IF AFFECTED BY LIFESTYLE - increasing the risk...
- CHD - poor diet, smoking, lack of exercise, excessive alcohol
- CANCER - smoking, excessive exposure to sunlight, excessive alcohol
pathogens
types of pathogen - microorganisms + some larger organisms (tape worms)
- bacteria
- fungi
- viruses
ENRTRY TO THE BODY - through organisms surface of contact (interface) with enviro.
- GAS EXCHANGE SYSTEM - breathe in air - become trapped in mucus lining the lung epithelium (have cilia beat + move mucus up trachea to mouth + removed ) - some pathogens still reach alveoli
- SKIN - damaged - pathogens enter bloodstream
- DIGESTIVE SYSTEM - some survive acidic conditions of stomach
HOW THEY CAUSE DISEASE
- PRODUCTION OF TOXINS - harmful molecules
- CELL DAMAGE - physical damage host cells by: rupture to release nutrients / break down nutrients inside / replicating inside cells + bursting
digestive system
DIGESTION
'process of breaking down food into substances that can be used by the body'
DIAGRAM
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