Topic 1 Flashcards

1
Q

Atrial Systole

A
  • atria contract while the ventricles relax.
  • This decreases the volume inside the atria which increases the pressure
  • increased pressure forces the atrioventricular valves open and pushes blood into the ventricles.
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2
Q

Ventricular Systole

A
  • ventricles contract while the atria relaxed
  • This decreases the volume inside the ventricles which increases the pressure
  • this forces the atrioventricular valves closed and causes the semi-lunar valves to open.
  • closure of atrioventricular valves prevents the back-flow of blood into the atria.
  • Blood is forced out of the ventricles and into the arteries (the aorta and the pulmonary artery).
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3
Q

Cardiac Diastole

A
  • atria and ventricles relaxed so the pressure is low in both chambers.
  • pressure is higher in the arteries than in the heart chambers –> semi-lunar valves are forced closed –> prevents blood flowing back into the ventricles
  • Blood is returned to the heart and the atria fill with blood.
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4
Q

Arteries

A
  • thick, muscular, elastic walls to carry blood at high pressure
  • folded endothelium allows for elastic recoil
  • narrow lumen to maintain high blood pressure
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5
Q

Veins

A
  • Valves to prevent the backflow of blood

- wide lumen and thin walls –> blood is at low pressure

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6
Q

Capillaries

A
  • one cell thick for short diffusion pathway

- pores to allow for exchange of substances

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7
Q

How blood clots form

A

blood vessel is damaged –>

protein called thromboplastin is released from damaged blood vessel –>

this triggers the conversion of prothrombin into thrombin (an enzyme) –>

thrombin catalyses conversion of fibrinogen, a soluble protein, into insoluble fibrin fibres –>

fibres tangle together and form a mesh –>

platelets and red blood cells get trapped and form a blood clot

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8
Q

how blood clots cause heart attacks

A

the coronary artery becomes blocked –> blood supply is cut off and no oxygen is received by that area

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9
Q

how blood clots cause strokes

A

artery leading to brain becomes blocked –> reduction in the amount of blood and therefore oxygen that can reach the brain

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10
Q

Atheroma formation

A

endothelium is damaged e.g. by high blood pressure –>

inflammatory response - white blood cells/macrophages move to the area –>

these white blood cells + lipids from the blood clump together under the endothelium to form fatty streaks –>

more white blood cells, lipids and connective tissue build up and harden to form a fibrous plaque called an atheroma –>

this partially restricts the artery, increasing blood flow, increasing blood pressure

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11
Q

atheromas lead to thrombosis by….

A

… breaking through the endothelium and damaging the artery wall –> triggering thrombosis (blood clot formation)

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12
Q

Lifestyle factors that increase risk of CVD

A

lifestyle:
diet- increases blood cholesterol which increases atheroma formation

high bp: risks damage to the artery walls which increases atheroma formation

Smoking: Carbin monoxide reduces the amount of oxygen that is transported in the blood,
if the heart doesn’t receive enough oxygen = heart attack
if the brain doesn’t receive enough oxygen = stroke

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13
Q

Factors beyond your control that increase risk of CVD

A
  • Genetics: such as alleles which make them more likely to have high blood pressure or blood cholesterol
  • Age: Plaques can build up in the arteries very slowly over time
  • Gender
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14
Q

Antihypertesives

strengths, weaknesses and what they are

A
  • beta-blockers: reduce strength of the heartbeat
  • vasodilators: widen blood vessels
  • diuretics: reduce blood volume

ALL REDUCE BLOOD PRESSURE

strengths:
- can be given in combination since all work differently
- blood pressure can be monitored at home so patients can see if they working

weaknesses:
- palpitations, abnormal heart rhythms, fainting and headaches due too low blood pressure

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15
Q

Statins

A

REDUCE BLOOD CHOLESTEROL

  • reduce the amount of LDL cholesterol produced inside the liver
  • which reduces atheroma formation

strengths:
- reduce CVD risk

weaknesses:
- muscle and joint pain, increased risk of diabetes

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16
Q

Anticoagulants

A

REDUCE FORMATION OF BLOOD CLOTS

  • warfarin and heparin
  • less chance of blood vessels becoming blocked

strengths:
- can be used by people who already have CVD or blood clots to reduce any further growth of clots or new clots

weaknesses:
- can cause excessive bleeding if injured and death

17
Q

Platelet inhibitors

A

REDUCE FORMATION OF BLOOD CLOTS

  • prevent platelets from clumping together and forming a blood clot and therefore reduce risk of blood vessel becoming blocked

strengths:
- can be used by people who already have CVD or blood clots to reduce any further growth of clots or new clots

weaknesses:
- can cause excessive bleeding if injured and death

18
Q

Monosaccharides

A
  • monomers
  • 3-7 Carbon atoms
  • examples: alpha and beta glucose, galactose and fructose
  • glucose = monosaccharide with 6 carbon atoms on each molecule
19
Q

Carbohydrates formula

A

(CH2O)n

20
Q

Disaccharides

A
  • two monosaccharides join together with glycosidic bonds through condensation reactions
    (can be reversed through hydrolysis)
  • 1,4 or 1,6 glycosidic bond (numbers refer to which carbons are joined together)
  • sucrose, maltose, lactose
21
Q

Polysaccharides

A
  • more than 2 monosaccharides join together

- amylose, amylopectin, glygogen

22
Q

polysaccharides of starch

A
  • amylose

- amylopectin

23
Q

amylose

A
  • long, unbranched
  • 1,4 glycosidic bonds
  • coiled structure = compact so good storage molecule (more in small space)
  • insoluble - doesn’t swell through osmosis
24
Q

amylopectin

A
  • long, branched
  • 1,4 and 1,6 glycosidic bonds
  • good for energy - branches allow enzymes to break down glycosidic bonds easily so glucose can be released quickly
  • insoluble - doesn’t swell through osmosis
25
Q

Glycogen

A
  • long, large, lots of branches
  • 1.4 and 1,6 glycoside bonds
  • good for fast energy - branches allow enzymes to break down glycosidic bonds easily so glucose can be released quickly
  • compact - good for storage
  • insoluble - doesn’t swell through osmosis
26
Q

Triglyceride structure

A
  • type of lipid - fat
  • 1 glycerol with 3 fatty acids attached to it by ester bonds through condensation reactions
  • fatty acid tails are made of hydrocarbons and are hydrophobic
  • makes triglyceride insoluble in water
27
Q

Triglyceride formation

A
  • condensation reactions
  • 3 fatty acids join 1 glycerol with ester bonds
  • H (hydrogen) on glycerol bonds to OH (hydroxyl) on the fatty acid - releasing water molecule
  • hydrolysis is the opposite water is added to break esher bond
28
Q

Saturated lipids

A
  • animal fats e.g. butter
  • long straight chain
  • no double bonds in hydrocarbon tails
  • every carbon is attached to at least 2 hydrogen atoms –> ‘saturated’ with hydrogen
29
Q

Unsaturated lipids

A
  • plants e.g. olive oil
  • melt faster/at lower temperatures
  • double bonds between carbons in their hydrocarbon tails
  • double bonds cause kinks in chain
  • 2 or more = polyunsaturated
30
Q

HDLs

A
  • mainly protein
  • transport cholesterol from body tissues to the liver to be recycled or excreted
  • function is to reduce blood cholesterol when it is too high
31
Q

LDLs

A
  • mainly lipid
  • transport cholesterol from the liver to the blood where it circulates until needed
  • function is to increase blood cholesterol when it is too high
32
Q

Cholesterol

A
  • some is needed for proper functioning
  • needs to be attached to a protein to move around, uses lipoproteins
  • high blood cholesterol level and high LDL level have been associated with increased risk of CVD
  • because increased cholesterol level is thought to increase atheroma formation