Topic 1 Flashcards
Properties of Water
Solvent
Cohesive
Good transport medium
Dipole molecule with ability to dissolve ionic bonds
Hydrogen bonds between H2O molecules
H2O joined by shared electrons
Shared hydrogen e-‘s pulled to oxygen
Other side of hydrogen has (slight) +ve charge
Unshared oxygen electrons (slight) -ve charge
Mass Transport Systems
For Multicellular organism
Carry raw materials from exchange organs
Remove metabolic waste
Cohesion
Attraction between molecules of the same type
Helps water to ‘flow’ (great for transport)
Solvency
+ve dipole end attracts -ve ion, -ve dipole end attracts +ve ion
Ion totally surrounded by H2O -> dissolves
Right side of the heart
Deoxygenated blood -> lungs
Left side of the heart
Oxygenated blood -> head and body
Left ventricle = thicker more muscular walls (needs to contract more powerfully)
Ventricles
Thicker walls than atria (need to push blood up and out of the heart)
Atria-Ventricular valves
Stop blood flowing back into atria
Cords attach them to the ventricles to prevent them being forced up into the atria when the ventricles contract
Semi-Lunar valves
Stop blood backflow into the heart
Valves
Help blood flow in one direction
Present in the heart and veins
Pressure behind a valve -> forces it open
Pressure in front of a valve (greater than behind) -> forced shut.
Arteries
Thick muscular wall -> high pressure maintenance and recoil
Thick elastic wall -> allows for recoil (pulse of blood)
Endothelum layer (folded) -> smooths blood flow (reduces friction); helps artery expansion
Narrow lumen -> high blood pressure
Takes oxygenated blood away from the heart (except with pulmonary artery)
Veins
Little elastic/muscle tissue -> no pulse to blood and lower pressure
Blood flow aided by musco-skeletal contractions
Valves prevent blood backflow
Wide lumen allow for a blood resevoir
Takes deoxygenated blood back to the heart (except for pulmonary veins)
Capillaries
Single endothelium layer (1 cell thick)
Metabolic exchange surface (cells capillaries)
Networks in tissues (capillary beds)
Increased surface area
Faster diffusion pathway
Steep concentration gradient provided for exchange
Cardiac cycle
- Ventricular Diastole and Atrial Systole
- Ventricular Systole and Atrial Diastole
- Cardiac Diastole
Ventricular Diastole/Atrial Systole
Ventricles relax
Atria contract -> increased pressure/decreased volume
Blood pushed into ventricles -> slight increase in ventricular pressure + Chamber volume, ventricles receive blood
Ventricular Systole/Atrial Diastole
Atria relax
Ventricles contract -> increase pressure/decreased volume
Pressure higher in ventricles than atria and aorta/pulmonary veins -> forces AV valves to shut (lub noise) + opens SL valves
Cardiac Diastole
Ventricles + Atria relax
Higher pressure in Aorta and Pulmonary Arteries -> shuts SL Valves (dub noise)
Atria fill again -> increased atrial pressure
Ventricles continue to relax -> falls below atrial pressure
AV valves open -> passive blood flow into ventricles
Atria contract
Cardiac cycle takes?
0.8 seconds
Why is pressure greater in the left ventricle?
More muscle on the left side of the heart
Blood has to be pumped all around the body
Right ventricle pumps blood to the lungs -> requires less pressure to prevent damage
Subsequently Aortic pressure is higher than pressure in the Pulmonary Artery.
Why is pressure greater in the left ventricle?
More muscle on the left side of the heart
Blood has to be pumped all around the body
Right ventricle pumps blood to the lungs -> requires less pressure to prevent damage
Subsequently Aortic pressure is higher than pressure in the Pulmonary Artery.
Atheroma formation
- Damage to endothelium (e.g. by toxins from smoking)
- Inflammatory response (e.g. macrophages) and increased risk of blood clotting
- White blood cells + lipids clump together under endothelium -> fatty streaks
- With the adition of calcium salts and fibers -> fibrous plaque = atheroma
- Partially blocks lumen, restricts blood flow -> blood pressure increased (increased likelihood of endothelial damage)
- Arteries harder due to decreased ability to recoil caused by atheroma presence -> atherosclerosis.
Thrombosis
- Atheroma ruptures the endothelium -> leaves rough surface
- Triggers thrombosis -> blood clot forms at rupture
- Clot can completely block artery; or dislodge & block elsewhere
- Blood flow severely restricted to tissues
- Possible cause: Heart attack, Stroke, Deep vein thrombosis
Note thrombosis = blood clotting
Clotting cascade
- Platelets form a plug at damage site
- Blood vessels + platelets release Thromboplastin (protein)
- Thromboplastin + Calcium ions + Vitamin K (from Plasma) allow conversion: Prothrombin (soluble protein) -> Thrombin (enzyme)
- Thrombin catalyses soluble Fibrinogen -> insoluble Fibrin
- Fibrin fibres tangle together, forming mesh entangling RBC’s and platelets -> clot blood
Heart Attacks
Blood to heart = coronary arteries
Blood clot -> area cut of; oxygen starved
Myocardial Infarction:
-damage/death to heart muscle
-pain in chest + upper body, shortness of breath, sweating
-large areas -> complete heart failure
Coronary heart disease
Lots of atheromas
Restricted blood flow
Increased thrombosis risk
Increase myocardial infraction risk
Stroke
Rapid loss of brain function
Thrombosis in brain/related artery (e.g. carotid)
Deep vein thrombosis
Blood clot deep inside the body (e.g. leg veins)
Caused by prolonged inactivity (e.g. long haul flights)
Risk increases with age
CVD lifestyle factors
Diet:
- high saturated fats (increased LDL cholesterol)
- high in salt (blood pressure increase)
High blood pressure (over 140/90mmHg):
- damage to artery walls
- endothelium/oxidative stress caused by alcohol consumption
Smoking:
- [CO] combines with haemoglobin, reducing O2 transport -> depletes availability
- Nicotine -> sticky platelets & increased thrombosis risk
- decreases amount of antioxidants (protect cells from damage)
Inactivity/Lack of Exercise:
- increased blood pressure (heart pumps with more strain)
Genetics: particular alleles
Age:
- decreased lumen
- plaque more readily builds up (+ longtime build up)
Gender:
- Men (x3) more likely than pre-menstrual women (Oestrogen increases levels of good cholesterol)
Risk
The chance of something unfavourable happening
Statistical chance
Supported by scientific research
Risk Perception vs Actual Risk
Overestimate due to constant Exposure Unfamiliar Involuntary Unfair Underestimate (lack of information) Reliance on own experience vs facts Hard to perceive
Treatment of CVD
- Antihypertensives
- Beta blockers
- Calcium Channel Blockers
- Diuretics - Statins
- Anticoagulants
- Platelet Inhibitory drugs
What are Anti-hypertensives?
Reduce high blood pressure
Anti-hypertensives: Benefits vs Risks
B: Combo different ones - home monitoring R: Palpatations - abnormal heart rhythm - fainting - headaches - drowsiness -> blood pressure becomes too low - depression - allergic reactions
Statins
Reduce amount of LDL cholestrol produced inside the liver by inhibiting an enzyme involved in its production B: Reduce atheroma formation R: Muscle + joint pain - digestive system issues - increased risk of diabetes - nosebleeds, headaches, nausea
Anticoagulants
Reduce blood clotting by reducing platelet ‘stickiness’
e.g. Warfarin and Heparin
B: Treat those who already have clots or CVD -> prevent existing clots from growing larger & new ones forming (cannot remove them)
R: excessive bleeding
- osteoporosis
- swelling of tissue
- fetal damage
Platelet Inhibitory Drugs
Anticoagulant that reduces platelet clumping and thrombosis
e.g. aspirin (acetylsalicylic acid)
B: Reduce thrombosis -> lessen onset of CVD
R: Rashes
-Diarrhea
- Liver failure
- Excessive bleeding
Energy budget
Amount of energy taken in by an organism
(-) the amount of energy used up by the organism
Energy imbalance
Weight Change
Carbohydrates
Comprised of monosaccharides (single sugar units) -> polysaccharides
Cx(H2O)n = general formula
Glucose
Hexose Sugar Carbon ring (5C in ring) Two forms: α and β Soluable -> easily transported Formula = C6H12O6
Possible effects of an atheroma
Increased blood pressure - causes damage to kidneys, retina, + can cause strokes
Aneurysm - Increase bp caused by atheroma can lead to bursting of artery + internal bleeding
Angina - Chest pain felt during excerise. Caused by reduced blood flow to heart due to narrowing of coronary arteries
Heart attack - Blockage of coronary artery, usually by a clot, causing part of the heart to become starved of oxygen + die
Stroke - Interruption to blood supply of brain which can cause paralysis or death
Two main types of studies
Cohort
Case-control
Features of a case-control study
A group with the condition (cases) is compared to a group without it (control)
Past histories of the two groups are investigated
The study will only have validity if the two groups are matched for other factors such as age and sex
Features of a cohort study
Follow a large number of people over an extended period of time
Subjects are monitored to see if they develop the condition
Cohort then divided into groups - those with + without condition
Subjects interviewed to assess their risk factors
Correlation between risk factors + development of condition looked for
Disaccharides
Join together via glycosidic bonds Formed in condensation reactions (loss of H2O molecule) Reversed via hydrolysis Less Soluable Bonds have more energy
Galactose
Is a monosaccaride hexose sugar as it contains 6 carbons
Has the formula C6H12O6
Has almost the same structure of glucose except the -H and -OH on the 5th carbon are swapped
Maltose
Disaccharide
2 x alpha glucose
1-4 glycosidic bond
Lactose
Disaccharide
Beta glucose + galactose
1-4 glycosidic bond
Sucrose
Disaccharide
Alpha glucose + fructose
1-2 glycosidic bond
Amylose
Unbranched Polysaccharide Alpha glucose (1-4 glycosidic bonds) Straight chain -> coils due to hydrogen bonding Compact = good storage Slow energy release
Amylopectin
Branched polysaccharide
Alpha glucose (1-4 & 1-6 glycosidic bonds)
1-6 glycosidic bonds cause side branches
Side branches -> quicker energy release (easier enzyme access)
Glycogen
Essentially amylopectin but even more side branches
Insoluable in water (does not impact osmotic potential/cause cell swelling)
Animal glucose store
Very compact (but large molecule -> lots of glucose)
Starch
Amylose + Amylopectin
Plant glucose store
Coiled structure -> compact store (lots of glucose)
Two energy release speeds due to combined polysaccharides
Insoluable -> does not impact cell osmotic potential
Fructose
Hexose sugar 5 ring (4 carbons in, two out)
Triglycerides
glycerol + 3 fatty acids
Joined by three ester bonds
Formed via condesation reactions
3 H2O lost (OH from fatty acid, 3H from glycerol)
Fatty Acids
Long hydrocarbon tails
Hydrophobic
Saturated Lipids
Animal fats (usually) No double bond between C atoms in hydrocarbon tails Diet high in them increases CVD risk (higher cholestrol level)
Unsaturated Lipids
Plant fats (usually)
Melt at lower tempretures
Double C bond in tails -> kink in chain
Two+ kinks = polyunsaturated
High blood cholestrol
Increases CVD risk
Cholestrol = lipid made in the body (liver)
Some recquired for cell function (used in membrane)
Attaches to protein to move = Lipoprotein
Lipoprotein
HDL = High density lipoprotein
LDL = Low density lipoprotein
High combo = risk
High LDL = risk
HDL
Mainly protein
Cholestrol from body tissues transported to liver
- recycled
- excreted
Reduce blood cholestrol when too high (mops up ‘bad’ LDL)
LDL
Mainly lipid
Cholestrol from liver -> blood (circulates)
Increase blood cholestrol levels when too low
Needs to be lower to be considered ‘healthy’
Beta Blockers
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Calcium Channel Blockers
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Diuretics
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