Notesale: Turn your study into money

Document Preview

Extracts from the notes are below, to see the PDF you'll receive please use the links above

---

Chapter 1
For microorganism to be considered pathogen
- gain entry to host
- colonise tissues of host
- resist defences of host
- cause damage to host tissues
Pathogens affect body in two ways – damaging host tissues, producing toxins
Lifestyle factors that contribute to cancer
- smoking
- diet
- obesity
- little/no physical activity
- sunlight
Lifestyle factors that contribute to coronary heart disease
- smoking
- high blood pressure
- high blood cholesterol levels
- obesity
- diet
- little/no physical activity
Chapter 2
Physical digestion – large pieces broken down into smaller pieces by teeth or muscles in stomach
Chemical digestion – breaks down large, insoluble molecules into smaller, soluble ones carried out by enzymes
Test for reducing sugars
- Benedict’s reagent
- Heat in gently boiling water bath
- If present turns brick red
Glucose + glucose = maltose
Glucose + fructose = sucrose
Glucose + galactose = lactose
Condensation reaction – monosaccharides join, molecule of water removed, glycosidic bond
Hydrolysis – water added to disaccharide
Test for non-reducing sugars
- Benedict’s reagent
- Heat in gently boiling water bath
- Solution remains blue, no reducing sugar
- Dilute hydrochloric acid
- Sodium hydrogencarbonate to neutralise acid
- Test with pH paper to ensure alkaline
- Benedict’s reagent
- Heat in gently boiling water bath
- If non-reducing present, solution now turn brick red
Test for starch
- Potassium iodide solution

-

Shake or stir
If present, blue-black colour

Starch digestion
- Salivary amylase – hydrolyses starch to maltose
- Pancreatic amylase – hydrolyses remaining starch to maltose
- Epithelial cells in lining of intestine – maltose – hydrolyses maltose to α-glucose
Sucrose broken down by sucrase in small intestine
Lactose broken down by lactase in small intestine
Lactose intolerance – undigested lactose reaches large intestine, microorganisms break it down, giving rise to large
volume of gas, results in nausea, diarrhoea and cramps
Structure of amino acid
- Amino group (-NH2)
- Carboxyl group (-COOH)
- Hydrogen atom (-H)
- R group – variety of different chemical groups
Formation of peptide bond – condensation reaction, peptide bond
Primary structure – sequence of amino acids
Secondary structure – shape polypeptide chain forms as result of hydrogen bond
Tertiary structure – due to bending and twisting of polypeptide helix into compact structure, contains disulfide, ionic
and hydrogen bonds
Quaternary structure – combination of number of different polypeptide chains and associated non-protein groups
Test for proteins
- Biuret test
- Sodium hydroxide solution (at room temperature)
- Few drops of very dilute copper (II) sulfate solution
- Mix gently
- Purple colour if peptide bonds and hence protein
- Blue colour if no protein present
Lock and key model of enzyme – active site has rigid shape and cannot change
Induced fit model of enzyme – changes shape slightly to fit shape of substrate, flexible
...

- Loss of ions establishes concentration gradient, water moves by osmosis from blood into intestine
- Loss of water from blood into intestine that causes diarrhoea and dehydration
What causes diarrhoea?
- Damage to epithelial cells lining intestine
- Loss of microvilli due to toxins
- Excessive secretion of water due to toxins
Rehydration solution contains
- Water – rehydrate tissues
- Sodium – replace sodium ions lost from epithelium of intestine
- Glucose – stimulate uptake of sodium ions from intestine and provide energy
- Potassium – replace lost potassium ions and stimulate appetite
- Other electrolyes – such as chloride and citrate ions, help prevent electrolyte imbalance
Chapter 4
Inspiration (breathing in)
- External intercostal muscles contract, internal intercostal muscle relax
- Ribs pulled upwards and outwards, increasing volume of thorax
- Diaphragm muscles contract, causing it to flatten, increasing volume of thorax
- Increased volume of thorax results in reduced pressure in lungs
- Atmosphere pressure higher than pulmonary pressure, air forced into lungs
Expiration (breathing out)
- Internal intercostal muscles contract, external intercostal muscles relax
- Ribs move downwards and inwards, decreasing volume of thorax
- Diaphragm muscles relax, making it return to upwardly domed position, decreasing volume of thorax
- Decreased volume of thorax increases pressure in lungs
- Pulmonary pressure higher than atmosphere, air forced out of lungs
Pulmonary ventilation = tidal volume x ventilation rate
Features of gas exchange surface
- Large surface area to volume ratio
- Very thin
- Partially permeable
- Movement of environmental medium
- Movement of internal medium
Pulmonary tuberculosis (TB)
- Transmitted in droplets
- Engulfed/ingested by phagocytes
- Encased in wall
- Dormant
- If immunosuppressed, bacteria activates
- Bacteria destroys alveoli
- Leads to scar tissue

-

Less surface area/diffusion
Damage allows bacteria to enter blood

Pulmonary fibrosis (scar tissue)
- Shortness of breath, especially when exercising
- Chronic, dry cough
- Pain and discomfort in the chest
- Weakness and fatigue
Asthma
- Difficulty in breathing
- Wheezing sound when breathing
- Tight feeling in the chest
- Coughing
Emphysema (elastin permanently stretched)
- Shortness of breath
- Chronic cough
- Blueish skin coloration
Chapter 5
Aorta – connected to left ventricle, carried oxygenated blood to all parts of body except lungs
Vena cava – connected to right atrium, brings deoxygenated blood back from tissues of body
Pulmonary artery – connected to right ventricle, carried deoxygenated blood to lungs
Pulmonary vein – connected to left atrium, brings deoxygenated blood back from lungs
The cardiac cycle
- Pressure in atria is higher than pressure in ventricles forcing atrioventricular valve open
- Blood flows into ventricles, increasing pressure whilst decreasing pressure in atria
- Forces atrioventricular valve shut and opens the semi-lunar valve open
- Pressure is higher in ventricles than aorta/pulmonary artery so moves into them
- As pressure in ventricles is now lower, semi-lunar valve closes
How is the cardiac cycle controlled?
- SAN sends out wave of electrical impulse which spreads across atria and cause them to contract
- Layer of non-conductive tissue prevents electrical activity moving down through ventricles
- Wave of electrical activity then moves down through AVN
- Short pause to allow ventricles to fill with blood
- Impulse then moves down to the Bundle of His and spreads out across the ventricles
- Ventricles contract from bottom upwards, forcing blood out through semi-lunar valves
Atheroma – fatty deposit that forms in wall of arteries
Thrombosis – atheroma breaks lining of wall, rough surface, blood clots
Aneurysm – atheromas that lead to thrombus also waken artery walls, swell and can burst
Myocardial infarction – blockage of coronary arteries
Chapter 6
Non-specific defence mechanisms – do not distinguish between different types of pathogen, respond to all in same
way
Specific defence mechanisms – distinguish between different pathogens, response less rapid u proved long-lasting
protection

Barriers to entry – protective covering, epithelia covers in mucus, hydrochloric acid in stomach
Phagocytosis
- Phagocyte attracted to pathogen by chemoattractants, moves towards pathogen along concentration
gradient
- Phagocyte bonds to pathogen
- Lysosome within phagocyte migrate towards phagosome formed by engulfing the bacterium
- Lysosomes release lytic enzymes into phagosome, where break down bacterium
- Breakdown products of bacterium area absorbed by phagocyte
B lymphocytes (B cells) – humoral immunity, immunity involving antibodies present in body fluids
T lymphocytes (T cells) – cell-mediated immunity, immunity involving body cells
Cell mediated diffusion
- Pathogens invade body cells or taken in by phagocytes
- Phagocyte places antigens from pathogen on cell-surface membrane
- Receptors on certain T helper cells fit exactly onto antigens
- Activates other T cells to divide rapidly by mitosis and form clones
- Cloned T cells:
 Develop into memory cells that enable rapid response to future infections by same pathogen
 Stimulate phagocytes to engulf pathogens by phagocytosis
 Stimulate B cells to divide
 Kill infected cells
Humoral immunity
- Surface antigens of invading pathogen taken up by B cells
- B cells process antigens and present them on their surface
- T helper cells attach to processed antigens on B cells, activating them
- B cells activated to divide by meiosis to give clone of plasma cells
- Cloned plasma cells produce antibodies that exactly fit antigens on pathogens surface
- Antibodies attach to antigens of pathogen and destroy them (primary immune response)
- Some B cells develop into memory cells, respond to future infections by same pathogen by dividing rapidly
and developing into plasma cells that produce antibodies (secondary immune response)
Antibodies – heavy/light chains, antigen-antibody complex, variable region (binding site), constant region
Monoclonal antibodies have number of useful functions in science/medicine
- Separation of a chemical from a mixture
- Immunoassay
- Cancer treatment
- Transplant surgery



---