Biology AQAModule 1

DiseasePathogens 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

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

ImmunityNon-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

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

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

Cell-Mediated ImmunityT-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 cellThis is called Cell-Mediated

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.

AntibodiesProteins 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

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

VaccinationsPassive 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

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

ProteinsA 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

CarbohydratesMaltose = 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

EnzymesThey 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

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

Animal Cell

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

Nuclear Pore

Chromatin

Nuclear Envelope

NucleolusNucleol

us

Large Subunit

Small Subunit Vesicl

esCisternae

Ribosome

RER

Cisternae

SER

Outer Membrane

Inner Membrane

Cristae

Matrix

MicroscopyMagnification = 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 wavesTEM SEM

2D 3D

Cross-section Surface

• Limitations:• In a vacuum, so dead specimens• Complex staining• Image may contain artifacts• Extremely thin for TEM

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

LipidsTriglycerides: 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=CPolyunsaturated = many C=C

Phospholipids

Hydrophilic Head

Hydrophobic Tail

They’re polar so they arrange themselves in a bilayer

• Cholesterol adds strength

• Glycolipid & Glycoprotein recognition site for chemicals

Cell-Surface MembraneGlycolipid

Cholesterol Extrinsic Protein

Intrinsic Protein (Carrier)

Intrinsic Protein (Channel)

PoreHydrophobic Tail

Glycoprotein

Hydrophilic Head

Fluid – Mosaic ModelFluid:

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

DiffusionMovement 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 =

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

OsmosisThe 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.

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 epitheliumOnly glucose moves against the conc grad

CholeraMost 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 & diarrhoeaProkaryotes 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 Peptidoglycan

In Plants made of Cellulose

• Transmission:• Impure water• Sewage enters

water• Contaminated food• Organisms fed on

sewage then eaten

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

BreathingBreathing 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

Pulmonary TuberculosisLeads 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 fibrosisFormation 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

Lung DiseasesAsthma:

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

Heart

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

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

Heart Disease Risk FactorsSmoking:

Carbon Monoxide:Combines with RBCs to form carboxyhaemoglobin

Reduces O2 carrying capacity of the blood

This leads to high blood pressure

NicotineStimulates 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