2. Disease
Pathogens enter the body through:
Gas-Exchange system
Digestive system
Skin Damage
Bodily Defenses:
Mucus, produced by goblet cells, catches the pathogens and cilia move the mucus out of the
trachea, then it’s removed
If skin is damaged pathogens can enter bloodstream, blood clots stop most pathogens entering
the body
Enzymes can digest some pathogens
Stomach acid kills pathogens but a few will survive and invade cells causing disease
How they cause disease:
Production of toxins:
Bacteria release these toxins into the body
Cell Damage:
Rupturing them: - This releases the nutrients inside them
Breaking down nutrients inside the cell for pathogens use
Replicating inside the cells and bursting them when they’re released
Pathogen:
Any microorganism that
causes harm
Includes:
Bacteria, Fungi and Viruses
3. Risk of Developing
Diseases
Risk Factors of Coronary Heart Disease:
Poor Diet – High levels of sat. fat or salt
Smoking, Lack of Exercise, Excessive Alcohol:
Leads to high BP, damages heart/vessels
Cancer:
Smoking –mouth, throat and lung cancer
Excessive Sunlight Exposure –skin cancer
Excessive Alcohol Intake –liver cancer
4. Immunity
Non-specific – Phagocytosis & barrier to entry of pathogen
Specific – Cell-mediated involving T lymphocytes & Humoral involving
B lymphocytes
Antigens are proteins found on the surface of a pathogen that trigger
an immune response
Phagocytosis:
Recognises antigens on the pathogen
Phagocyte engulfs pathogen
A membrane is created around the pathogen called a Phagosome
(Phagocytic Vacuole)
Lysosomes fuse with phagosome. They release lytic enzymes
The pathogen is broken down by the enzyme
The phagocyte then presents the antigens on it’s surface to initiate other
immune cells
5. Phagocytosis
Barriers to entry:
Protective covering – skin covers the body
Epithelia covered in mucus - catches the pathogens, cilia move the mucus
out of the trachea, to be swallowed by the stomach
HCl in stomach – enzymes of most enzymes are denatured
Phagocytosis:
Recognises antigens on surface of pathogen
Cytoplasm of phagocyte moves round the pathogen, engulfing it
Pathogen now contained in a vesicle, called a phagosome
Lysosomes fuse with the vacuole – lysosomal enzymes break down the
pathogen
Phagocyte presents pathogen’s antigens on it’s surface – this stimulates
other immune responses
6. Lymphocytes
B–Lymphocytes (B-cells) – are associated with humoral response
T–Lymphocytes (T-cells) – are associated with cell-mediated
response
Both formed from stem cells:
B-cells – mature in Bone marrow
T-cells – mature in Thymus gland
7. Cell-Mediated Immunity
T-lymphocytes – respond to organisms own cells that have been invaded by
foreign material
Can distinguish between normal & invaded cells: (called antigen-presenting
cells)
Phagocytes that have engulfs a pathogen present the antigens on it’s surface
Body cells invaded by viruses can also present viral antigens on it’s surface
Cancer cells also present antigens on their surface
Pathogens invade body cells or take in by phagocytes
Phagocyte presents antigens on surface
Receptors on certain T-helper cells fit exactly onto these antigens
This activates other T-cells to divide by mitosis and form a clone
The cloned T-cells:
Develop into memory cells that enable rapid response if infected by same pathogen
Stimulate phagocytes to engulf pathogens by phagocytosis
Stimulate B-cells to divide
Kill infected cells – by producing a protein that makes holes in the cell-surface membrane
T-cells only respond to
antigens attached a
body cell
This is called Cell-
Mediated
8. B-cells & Humoral
Response
Humoral – involves antibodies that are soluble in blood & tissue fluid (body fluids
called ‘humour’)
Surface antigens of pathogen are taken up by B-cells
B-cells present antigens on their surface
T-helper cells attach to antigens on B-cells, activating B-cells
B-cells divide by mitosis to produce cloned plasma cells
Cloned plasma cells produce antibodies that fit the antigen
Antibodies attach to antigens on pathogen & destroy them (Primary Immune
Response)
Some B-cells develop into memory cells – they can respond more quickly if re-
infected (Secondary Immune Response)
Antigenic Variation:
Influenza viruses and other pathogens have lots of strains, they have constantly
changing antigens. Memory cells produced from previous infection will be defunct,
taking longer to fight of the pathogen.
9. Antibodies
Proteins made by B-cells
They have a specific shape
Made of 4 polypeptide chains
2 light (shorter) & 2 heavy (longer)
chains
Antibody binding site known as a
Antigen – Antibody Complex
The binding site is the variable region
The rest of antibody is constant
10. Producing Monoclonal
Antibodies
Mouse exposed to foreign pathogens
B-cells in the mouse produce a mixture of antibodies, these are extracted from
it’s spleen
B-cells are mixed with cancerous cells that are ready to divide
Detergent is added to break down cell membranes to fuse cells together
Fused cells are separated under a microscope
Each cell is then cultured to form a clone
Any clone producing the required antibody is grown on a large scale
These antibodies come from cloned cells so they’re known as Monoclonal
11. Vaccinations
Passive Immunity:
Introduction of antibodies from an outside source
These antibodies aren’t produced by the patient so they are short-lived as
they aren’t replaced
Active Immunity:
Produced by stimulating the production of antibodies
They are created by the patient so are longer-lasting
They contain antigens that cause your body to produce memory cells
The antigens can be attached to an, attenuated or dead, pathogen or free
Booster vaccines are given to make sure memory cells are produced
12. Enzymes and Digestive
SystemLocation Enzyme Class Hydrolyses Product
Salivary
Glands
Amylase Carbohydrase Starch Maltose
Stomach Pepsin Protease Protein Peptides
Pancreas Amylase Carbohydrase Starch Maltose
Lipase Lipase Lipids 3 Fatty Acid +
Glycerol
Ileum Maltase Carbohydrase Maltose Glucose
Sucrase Carbohydrase Sucrose Glucose + Fructose
Lactase Carbohydrase Lactose Glucose + Galactose
Peptidase Protease Peptides Amino Acids
Oesophagus:
Takes food to stomach by peristalsis. Mucus is secreted by tissues in wall to lubricate foods passage to stomach
Stomach:
Sphincter muscles controls what enters & leaves. Stomach walls produce gastric juice (HCl, Mucus & Pepsin). Peristalsis
in the stomach a produces an acidic fluid called ‘chyme’
Small Intestine:
Two parts duodenum & ileum. Chyme is neutralised and broken down by bile & pancreatic juice
In ileum small, soluble molecules are absorbed by villi
Large Intestine (Colon):
Absorbs water, salts & minerals. Bacteria digest some of the undigested nutrients in the large intestine
Rectum:
Faeces stored in rectum and pass through sphincter muscles at anus during defecation
Amylase, trypsin, chymotrypsin, lipase & NaHCO3
13. Proteins
A dipeptide is joined by a peptide bond
formed in a condensation reaction by
removing water
Primary Structure:
A chain of polypeptides
Secondary Structure:
Chain twisted due to H-bonds forming
between peptides
Tertiary Structure:
When the secondary structure is again
twisted due to disulphide, H & ionic
bonds
Quaternary Structure:
Chains of polypeptides joined together
that sometimes contain a prosthetic
group e.g. Fe in haemoglobin
Amino
Group
Carboxyl
Group
Primary
QuaternaryTertiary
Secondary
Test:
Add equal vols of Biuret & sample
+ve = Purple
-ve = Blue
14. Carbohydrates
Maltose = Glucose + Glucose
Lactose = Glucose + Galactose
Sucrose = Glucose + Fructose
Glucose is a hexose sugar
Condensation joins 2 monosaccharides by removing H2O
Hydrolysis opposite of condensation
Glycosidic bonds link monomer units
Starch:
Made of amylose & amylopectin, a polysaccharide of glucose
Test = Add iodine (dissolved in KI). +ve = brown to black
Reducing Sugars:
All monosaccharides & some disaccharides
Test = add Benedict's Reagent and boil. Red = +ve
Non-reducing Sugars:
Need to broken into monomer units
Test = Boil with HCl then neutralise with NaHCO3. Add Benedict’s and boil. Red = +ve
15. Enzymes
They act as biological catalysts that lower the activation energy
Lock & Key:
Only certain substrates can fit into the active site of the enzyme
Induced Fit:
Enzyme changes shape slightly to accommodate the substrate
This put the substrate under a strain which distorts particular bonds, lowering the
activation energy
Factors affecting rate of enzyme action:
Temperature:
Too high they become denatured, when bonds break into the enzyme, distorts it’s active
site, can no longer form an ESC
pH:
Denatured if too acidic or alkali
16. Enzyme Inhibition
Competitive Inhibitor:
Similar shape to substrate
This means they can fit into the active site of the enzyme.
More inhibitors slows down the rate at which an enzyme can work
Non-Competitive Inhibitor:
Attach themselves to the enzyme but not in the active site
This changes the shape of the active site
So the substrate no longer fits into the active site
Less ESCs form
18. Name Function
Nucleus Controls cell activity & makes ribosomes & mRNA (for Protein
Synthesis)
Mitochondrion Site of aerobic respiration releasing energy
Ribosome Protein synthesis
Smooth
Endoplasmic
Reticulum
Synthesises, stores & transports lipids
Rough
Endoplasmic
Reticulum
Modifies & transports proteins
Golgi Apparatus Modifies lipids and proteins from ER
Vesicle Carry modified protein & lipids to plasma membrane for
secretion
Lysosome Vesicles containing lytic enzymes, digests invading or worn
out cells
Nuclea
r Pore
Chromatin
Nuclear
Envelo
pe
Nucleolu
s Nucleolu
Large
Subunit
Small
Subunit Vesicl
es
Cisternae Ribosome RER
CisternaeSER
Outer
Membran
e
Inner
Membrane
Crista
e
Matrix
19. Microscopy
Magnification = Size of Image/Size of Object
1mm = 1000 micrometres = 1,000,000 nanometres
Resolution:
Ability to distinguish between 2 points that are close together.
Light waves are longer than electron waves
TEM SEM
2D 3D
Cross-section Surface
• Limitations:
• In a vacuum, so dead specimens
• Complex staining
• Image may contain artifacts
• Extremely thin for TEM
20. Separating Cell
Components
Cell Fractionation:
Tissue cut up and kept in col isotonic buffer solution:
Cold – Reduce enzyme activity which might break down organelles
Isotonic – same H2O potential as original tissue, avoid bursting
Buffer – constant pH
Homogenised (blended)
Fluid is filtered removing debris from homogenate
Homogenate spun in ultracentrifuge
Heaviest organelles at bottom forming a pellet, rest of fluid is the
supernatant
Supernatant spun again forcing next heaviest organelles to form a
pellet
21. Lipids
Triglycerides: 3 Fatty Acids & 1 Glycerol
Functions:
Energy source – store twice amount of energy as equivalent carbohydrate
Waterproofing – Insoluble in H2O
Insulation – Poor heat conductor
Protection – Cover delicate organs
Test:
Add 2cm3 of sample & 5cm3 of
Ethanol. Shake. Add 5cm3 water.
Shake. Cloudy white = +ve
Hydrolysis
opposite to
condensation
Saturated Unsaturated
No C=C in ‘R’ group C=C in ‘R’ group
No bend in chain – ‘R’ groups lie
close together
Bend in chain – ‘R’ groups can’t
lie close together
Higher melting point – solid at RTP Lower melting point – liquid at
RTP
Monounsaturated = 1 C=C
Polyunsaturated = many C=C
24. Fluid – Mosaic Model
Fluid:
Individual phospholipids can move creating a
flexible structure
Mosaic:
Protein embedded in bilayer vary in shape, size &
position
Lipid Soluble Molecules:
Dissolve through bilayer, fast
Water Soluble Molecules:
Pass through proteins
Ions – Protein Channels
Uncharged – Protein Carriers
25. Diffusion
Movement of molecules from an area of higher conc to an area of lower
conc
Passive Process (No Energy)
Occurs until dynamic equilibrium occurs
Factors:
Conc Grad – Higher = Faster Diffusion Rate
Surface Area – Larger = Faster Diffusion Rate
Exchange Surface Thickness – Thinner = Faster Diffusion Rate
Size of Molecule Diffusing
Increasing Temp
Composition of plasma membrane e.g. no of pores
Fick’s Law: SA X Conc Grad
Thickness of Exchange Surface
Diffusion Rate =
26. Facilitated Diffusion
Passive
Down conc grad
Only occurs where there are specialised proteins
Only allow certain molecules through
2 Mechanisms:
Ion Channels:
Allow ions that are water soluble
Carrier Proteins:
Allow uncharged molecules through. Binds on one side of membrane and
is release on other side
27. Osmosis
The movement of WATER from a less –ve water potential to a more –
ve water potential through a semi-permeable membrane
Less –ve water potential to more –ve water potential. Pure H2O = 0
Water Potential is pressure created by H2O molecules measured in
KiloPascals (kPa)
Water potential of cells worked out by placing them in different H2O
potentials and seeing when there is no change in mass
Plant Cells (H2O Potential):
In less –ve solution water moves into cell, cell is turgid. Protoplast swells.
In equal solution no water movement, cell is Incipient Plasmolysis.
In more –ve solution water moves out of cell, cell is plasmolysed.
Protoplast shrinks.
28. Active Transport
The movement of molecules or ions from a lower
concentration to higher concentration (against the
concentration gradient) requiring carrier proteins
and energy
Co-Transport Carrier:
e.g. Glucose & Na+ in the intestinal epithelium
Only glucose moves against the conc grad
29. Cholera
Most killed by acidic stomach conditions, but a few survive
Bind to epithelium cells
Release a toxin that causes ion channels to remain open
Chloride ions enter lumen
Water potential more –ve so water moves by osmosis into the lumen
Causing dehydration & diarrhoea
Prokaryotes Eukaryotes
No Nucleus Nucleus
No Nucleolus Nucleolus
No Membrane-Bound
Organelles
Membrane-Bound Organelles
No Chloroplasts Chloroplasts only in Plants/Algae
Ribosomes are Smaller Ribosome are Larger
No ER/Golgi/Lysosome ER/Golgi/Lysosomes
Cell Wall made of In Plants made of Cellulose
• Transmission:
• Impure water
• Sewage enters water
• Contaminated food
• Organisms fed on
sewage then eaten
30. Oral Rehydration Therapy
Needed due to loss of nutrients (e.g. water) due to diarrhoea
Contains:
Water – rehydrates tissues
Sodium – replaces lost ions to increase use of Na+ Glucose Co-transport
Carrier
Glucose – More energy and uptake of Na+
Potassium – Replace lost ions & stimulate appetite
+ Other electrolytes to help prevent electrolyte imbalance
Can’t always be taken orally as patient may vomit it back up. So
sometimes it is fed directly into the blood supply
31. Breathing
Breathing In:
External intercostal muscles contract, Internal relax
Ribs pulled upwards & outwards, increasing the volume of the thorax
Diaphragm contracts, it flattens, so volume of thorax increases
Increased volume of thorax = Decreased pressure
Air moves into the lungs
Breathing out:
External intercostal muscles relax, Internal contract
Ribs move downwards & inwards, decreasing the volume of the thorax
Diaphragm relaxes, it domes, so volume of thorax decreases
Decreased volume of thorax = Increased pressure
Air moves out of the lungs
Pulmonary Ventilation = Tidal Volume x Ventilation Rate
32. Pulmonary Tuberculosis
Leads to persistent cough, tiredness & loss of appetite
Transmission:
Spread in tiny droplets containing the bacterium
Close Contact
Over – Crowding
Infection:
Build up in the lungs
Immune response forms a barrier around the pathogens
This forms hard lumps known as Tubercles
Infected tissue dies, SA decreases, gas exchange is less efficient
Also causes fibrosis
Formation of scar tissue which is thick and less elastic
So lungs can hold less air and expand less
If bacteria enter blood stream they can spread around the body
33. Lung Diseases
Asthma:
Airways become inflamed
Muscle lining contracts
Lots of mucous produced
Causing constriction of airways
Gas Exchange severely reduced
Symptoms:
Wheezing
Tight Chest
Shortness of Breath
Emphysema:
Foreign particles trapped in
lungs
Causes inflammation
Phagocytes produce an enzyme
that breaks down elastin
Alveoli can’t return to normal
shape
Less air expelled from alveoli
Also leads to alveolar
membranes breakdown
Less SA so gas exchange
decreased
Symptoms:
Wheezing
Shortness of Breath
Increasing breathing rate
35. Heart
Heart muscle is ‘Myogenic’ – Contract
& Relax without receiving an impulse
Heart Beat;
SAN – sends out impulse
Right & left atria contract at the same
time
AVN – passes to Bundle of His after
slight delay
Bundle of His contract from bottom
upwards
Cardiac Output = Stroke Volume x Heart Rate
36. Heart Disease
Atheroma:
Fatty deposit within the artery wall
Narrows the diameter of the artery
They increase the risk of thrombosis’
and Aneurysms
Thrombosis:
If an atheroma breaks through the
endothelium it forms a rough surface
This interrupts the flow of blood
This may result in a blood clot,
thrombus
If a clot occurs in coronary artery, it
will stop O2 & glucose reaching the
heart
The heart then dies
Aneurysm:
Atheroma leads to a weaker artery
wall
The weakened points break forming
a balloon like structure
They often burst forming a
haemorrhage
A brain aneurysm is known as a
stroke
Myocardial Infarction:
Known as a heart attack
Reduced supply of O2 to heart
muscle
So heart can’t beat effectively
Heart dies
37. Heart Disease Risk Factors
Smoking:
Carbon Monoxide:
Combines with RBCs to form
carboxyhaemoglobin
Reduces O2 carrying capacity of the
blood
This leads to high blood pressure
Nicotine
Stimulates production of adrenaline
Increases HR & blood pressure
This increases chance of a thrombosis
High Blood Pressure:
Heart must work harder
More prone to failure
More likely to create an aneurysm
To resist the pressure artery walls
thicken, restricting blood flow
Blood Cholesterol:
HDLs:
They help protect arteries from heart
disease
LDLs:
Increase chance of heart disease
Diet:
Lots of salt = high blood pressure
Lots of saturated fats = more LDLs
