Topic 1 Flashcards

(65 cards)

1
Q

Properties of Water

A

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

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2
Q

Mass Transport Systems

A

For Multicellular organism
Carry raw materials from exchange organs
Remove metabolic waste

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3
Q

Cohesion

A

Attraction between molecules of the same type

Helps water to ‘flow’ (great for transport)

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4
Q

Solvency

A

+ve dipole end attracts -ve ion, -ve dipole end attracts +ve ion
Ion totally surrounded by H2O -> dissolves

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5
Q

Right side of the heart

A

Deoxygenated blood -> lungs

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6
Q

Left side of the heart

A

Oxygenated blood -> head and body

Left ventricle = thicker more muscular walls (needs to contract more powerfully)

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7
Q

Ventricles

A

Thicker walls than atria (need to push blood up and out of the heart)

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8
Q

Atria-Ventricular valves

A

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

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9
Q

Semi-Lunar valves

A

Stop blood backflow into the heart

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10
Q

Valves

A

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.

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11
Q

Arteries

A

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)

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12
Q

Veins

A

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)

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13
Q

Capillaries

A

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

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14
Q

Cardiac cycle

A
  1. Ventricular Diastole and Atrial Systole
  2. Ventricular Systole and Atrial Diastole
  3. Cardiac Diastole
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15
Q

Ventricular Diastole/Atrial Systole

A

Ventricles relax
Atria contract -> increased pressure/decreased volume
Blood pushed into ventricles -> slight increase in ventricular pressure + Chamber volume, ventricles receive blood

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16
Q

Ventricular Systole/Atrial Diastole

A

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

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17
Q

Cardiac Diastole

A

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

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18
Q

Cardiac cycle takes?

A

0.8 seconds

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19
Q

Why is pressure greater in the left ventricle?

A

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.

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20
Q

Why is pressure greater in the left ventricle?

A

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.

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21
Q

Atheroma formation

A
  1. Damage to endothelium (e.g. by toxins from smoking)
  2. Inflammatory response (e.g. macrophages) and increased risk of blood clotting
  3. White blood cells + lipids clump together under endothelium -> fatty streaks
  4. With the adition of calcium salts and fibers -> fibrous plaque = atheroma
  5. Partially blocks lumen, restricts blood flow -> blood pressure increased (increased likelihood of endothelial damage)
  6. Arteries harder due to decreased ability to recoil caused by atheroma presence -> atherosclerosis.
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22
Q

Thrombosis

A
  1. Atheroma ruptures the endothelium -> leaves rough surface
  2. Triggers thrombosis -> blood clot forms at rupture
  3. Clot can completely block artery; or dislodge & block elsewhere
  4. Blood flow severely restricted to tissues
  5. Possible cause: Heart attack, Stroke, Deep vein thrombosis
    Note thrombosis = blood clotting
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23
Q

Clotting cascade

A
  1. Platelets form a plug at damage site
  2. Blood vessels + platelets release Thromboplastin (protein)
  3. Thromboplastin + Calcium ions + Vitamin K (from Plasma) allow conversion: Prothrombin (soluble protein) -> Thrombin (enzyme)
  4. Thrombin catalyses soluble Fibrinogen -> insoluble Fibrin
  5. Fibrin fibres tangle together, forming mesh entangling RBC’s and platelets -> clot blood
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24
Q

Heart Attacks

A

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

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25
Coronary heart disease
Lots of atheromas Restricted blood flow Increased thrombosis risk Increase myocardial infraction risk
26
Stroke
Rapid loss of brain function | Thrombosis in brain/related artery (e.g. carotid)
27
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
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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)
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Risk
The chance of something unfavourable happening Statistical chance Supported by scientific research
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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 ```
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Treatment of CVD
1. Antihypertensives - Beta blockers - Calcium Channel Blockers - Diuretics 2. Statins 3. Anticoagulants 4. Platelet Inhibitory drugs
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What are Anti-hypertensives?
Reduce high blood pressure
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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 ```
34
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 ```
35
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
36
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
37
Energy budget
Amount of energy taken in by an organism | (-) the amount of energy used up by the organism
38
Energy imbalance
Weight Change
39
Carbohydrates
Comprised of monosaccharides (single sugar units) -> polysaccharides Cx(H2O)n = general formula
40
Glucose
``` Hexose Sugar Carbon ring (5C in ring) Two forms: α and β Soluable -> easily transported Formula = C6H12O6 ```
41
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
42
Two main types of studies
Cohort | Case-control
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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
44
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
45
Disaccharides
``` Join together via glycosidic bonds Formed in condensation reactions (loss of H2O molecule) Reversed via hydrolysis Less Soluable Bonds have more energy ```
46
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
47
Maltose
Disaccharide 2 x alpha glucose 1-4 glycosidic bond
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Lactose
Disaccharide Beta glucose + galactose 1-4 glycosidic bond
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Sucrose
Disaccharide Alpha glucose + fructose 1-2 glycosidic bond
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Amylose
``` Unbranched Polysaccharide Alpha glucose (1-4 glycosidic bonds) Straight chain -> coils due to hydrogen bonding Compact = good storage Slow energy release ```
51
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)
52
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)
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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
54
Fructose
``` Hexose sugar 5 ring (4 carbons in, two out) ```
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Triglycerides
glycerol + 3 fatty acids Joined by three ester bonds Formed via condesation reactions 3 H2O lost (OH from fatty acid, 3H from glycerol)
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Fatty Acids
Long hydrocarbon tails | Hydrophobic
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Saturated Lipids
``` Animal fats (usually) No double bond between C atoms in hydrocarbon tails Diet high in them increases CVD risk (higher cholestrol level) ```
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Unsaturated Lipids
Plant fats (usually) Melt at lower tempretures Double C bond in tails -> kink in chain Two+ kinks = polyunsaturated
59
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
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Lipoprotein
HDL = High density lipoprotein LDL = Low density lipoprotein High combo = risk High LDL = risk
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HDL
Mainly protein Cholestrol from body tissues transported to liver - recycled - excreted Reduce blood cholestrol when too high (mops up 'bad' LDL)
62
LDL
Mainly lipid Cholestrol from liver -> blood (circulates) Increase blood cholestrol levels when too low Needs to be lower to be considered 'healthy'
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Beta Blockers
ngng
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Calcium Channel Blockers
ngng
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Diuretics
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