Unit 1 biology

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  • Created by: charlie
  • Created on: 15-02-14 18:50

lungs structure

DIAGRAM 

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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 
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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)
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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 

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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 
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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 
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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 
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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 
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lung disease data

RISK FACTORS = factors inc. persons chance of getting that disease 

CORRELATION = only shows one factor of causing the disease 

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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 

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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) 
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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 
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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 
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interpreting events of cardiac cycle

DIAGRAM 

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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. 
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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 
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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 
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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 
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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 
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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 
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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) 
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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 
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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 
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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 

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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 
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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 
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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 
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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)
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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 
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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 
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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 
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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 
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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 
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digestive system

DIGESTION

'process of breaking down food into substances that can be used by the body' 

DIAGRAM 

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