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SNAB biology hoe > 1 Heart, CVD, Carbs and Lipids > Flashcards

1 Heart, CVD, Carbs and Lipids Flashcards

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1
Q

explain how dipolar nature of water is essential for living organisms

A
  • water can form H-bonds
  • this holds water together as liquid so can MOVE IN MASS FLOW SYSTEMS
  • has LARGE SPECIFIC HEAT CAPACITY = lots of energy needed to change temp
  • so good as EXTERNAL BUFFER
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2
Q

sucrose

A

ɑ glucose + fructose

condensation reaction forming glycosidic bonds

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3
Q

lactose

A

ɑ glucose + galactose

condensation reaction forming glycosidic bonds

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4
Q

maltose

A

ɑ glucose + ɑ glucose

condensation reaction forming glycosidic bonds

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5
Q

(cellulose)

MORE IN TOPIC 4

A
  • only in plants
  • polymer of long chains of β-glucose joined together by 1,4 glycosidic bonds
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6
Q

systole

A

S uck
C ock

contraction

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7
Q

diastole

A

relaxation

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8
Q

explain how structure of artery wall is adapted both to withstand and to maintain high b.p

A
  • endothelium is ONE CELL THICK and lines lumen of all blood vessels -> v smooth and reduces FRICTION
  • endothelium is HIGHLY FOLDED -> lets it expand under high b.p
  • SMOOTH MUSCLE and ELASTIC TISSUE STRENGTHEN arteries so can withstand high b.p
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9
Q

what is cardiac muscle made up of?

A

cells connected by cytoplasmic bridges
-> enables electrical impulses to pass through tissue

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10
Q

what is the role of valves in the heart?

A
  • prevent back flow of blood
  • maintaining correct pressure in chambers
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11
Q

how are left and right side of heart different and why?

A

LHS is thicker as has to pump blood further and so at HIGHER PRESSURE

RHS is thinner as not at high pressure as might DAMAGE DELICATE LUNG TISSUE

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12
Q

how is cardiac muscle different to skeletal muscle?

A

MYOGENIC -> originating in muscle tissue

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13
Q

describe two blood vessels that bring blood INTO heart

A

VENA CAVA -> brings blood from body (deoxygenated)

PULMONARY VEIN -> brooms blood from lungs (oxygenated)

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14
Q

describe two blood vessels that bring blood AWAY FROM heart

A

PULMONARY ARTERY -> takes blood to lungs (deoxygenated)

AORTA ->takes blood to body (oxygenated)

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15
Q

artery

A
  1. narrow lumen -> maintains high b.p
  2. elastic fibres -> allow stretch and recoil
  3. thicker muscular wall -> contracts and relaxes to CONSTRICT and DILATE BLOOD VESSELS
  4. collagen in walls -> provides strength to withstand high b.p
  5. folded endothelium -> allows EXPANSION -> cope with high b.p
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16
Q

myogenic

A

ability of muscles to make its own electrical impulses at rest (without CNS)

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17
Q

explain how veins are adapted to their function

A
  1. large lumen -> low b.p and minimises resistance
  2. thin layer of elastic tissue -> maintains b.p
  3. valves -> prevent back flow
  4. smooth endothelium -> minimise resistance
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18
Q

capillaries

A

where metabolic exchange occurs
-> subs exchanged between cells and capillaries

  1. network of capillaries -> increase s.a for metabolic exchange
  2. one cell thick walls -> speeds up diffusion of substances (eg. glucose, O₂) in and out of cells
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19
Q

what drugs can be taken to treat CVD?

A
  • antihypertensives
    -> reduces high b.p
  • statins
    -> reduce cholesterol
  • anticoagulants
    -> reduce formation of blood clot
  • platelet inhibitory drugs
    -> reduce formation of blood clot
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20
Q

compare the benefits and risks of STATINS

A

adv.?
- reduce risk of developing CVD

disadv.? -
- muscle/joint pain
- dig system problems
- increases risk diabetes
- nosebleeds, headaches, nausea

21
Q

compare the benefits and risks of ANTIHYPERTENSIVES

A

adv.?
- diff. types of hypertensives work in diff. ways so can be given COMBO.

disadv.?
- palpitations
- abnormal heart rhythms
- fainting
- headaches
- drowsiness

all side effects caused by LOW B.P

22
Q

compare the benefits and risks of ANTICOAGULANTS

A

adv.?
- treat ppl who ALREADY have blood clots / CVD

-> prevent clots growing larger and prevents new clots

disadv.?
- can’t get rid of EXISTING clots
- if patient badly injured -> excessive bleeding
= fainting and death
- osteoporosis
- swelling of tissues
- CAN DAMAGE FEOTUS

23
Q

why are daphnia selected to investigate effect of caffeine on heart rate?

A
  • transluscent bodies so heart rate is more easily observed
  • less developed CNS to humans so reduced awareness of pain
  • very common so no threat to extinction or dependent species (via food chain)
24
Q

how does caffeine work in humans?

A

stimulant that increases heart rate by increasing release of excitatory neurotransmitters

25
Q

(for daphnia practical)

how is control set up?

A

replace caffeine sol with distilled water to measure daphnia heart rate without effect of caffeine

26
Q

what steps should students take to ensure daphnia are ethically treated?

A
  • return to natural habitat after use
  • minimise amount of time exposed to stressful conditions
27
Q

why should cover slip not be used when observing organism?

(daphnia practical)

A

to allow O₂ to reach organism
-> preventing conditions from becoming ANOXIC

28
Q

what is the purpose of placing cotton wool on the slide?

(daphnia practical)

A

to restrict movement of organism so easier to count heart rate

29
Q

outline procedure for investigating the effect of caffeine on heart rate in daphnia

A
  1. dilute caffeine sol to 5 diff conc
  2. place cotton wool on cavity slide and add 1 daphnia -> use filter paper to absorb excess water
  3. use dropping pipette to add few drops DISTILLED WATER to slide
  4. use stopwatch to time a min and record no. of heartbeats (bpm)
  5. repeat experiment -> replacing distilled water with diff caffeine sol
  6. repeats then carried out with 2 OTHER DAPHNIA
30
Q

what reagent is used to test for vitamin C and what is observed?

A

DCPIP
colour change from
blue -> colourless

31
Q

outline procedure to use DCPIP to find vitamin C content of diff samples

A
  1. pipette 1cm³ 1% blue DCPIP sol into conical flask
  2. fill burette with 1% vitamin C sol and note start value
  3. using burette, slowly add vitamin C to DCPIP DROPWISE -> swirl flask
  4. close tap as soon as DCPIP decolourises and note end value
  5. record vol of vitamin C required to change colour of DCPIP
  6. repeat experiment and replace vitamin C sol with fruit juices
32
Q

state a hazard and safety precaution for vitamin C practical

A

DCPIP -> irritant
-> wear goggles and avoid skin contact

33
Q

compare the benefits and risks of PLATELET INHIBITORS

A

adv.?

  • used to treat ppl who ALREADY have blood clots

disadv.?

  • rashes
  • diarrhoea
  • nausea
  • liver function problems
  • excessive bleeding -> especially after serious injury
34
Q

discuss the potential ethical issues of using invertebrates in scientific research

A

AGAINST

  • can’t give consent
  • unethical to cause distress / suffering to ANY organism
    -> eg. subjecting them to extreme temp / depriving them of food

FOR

  • invertebrates have less developed CNS -> feel less/no pain
  • more distantly related to humans that other
    vertebrates
  • daphnia are v common -> no chance of extinction
35
Q

glycogen

A

main energy storage in animals -> animals store excess glucose as glycogen

  • 1,4 and 1,6 glycosidic bonds with LOADS of branches …
  • so stored glucose can be released quickly (important for energy release in animals)
  • also v compact -> so good for storage
  • insol in H₂O so doesn’t cause cells to swell via osmosis
  • large -> so can store LOTS of energy
36
Q

starch

A

main energy store in plants -> plants store excess glucose as starch

(when it needs more energy = breaks down starch to release glucose)

  • insol in H₂O -> doesn’t cause cells to swell via osmosis so good for storage
  • made of 2 polysaccharides of ɑ-glucose…
    -> amylose and amylopectin

AMYLOSE

  • long unbranched chain of ɑ-glucose joined by 1,4 glycosidic bonds
  • coiled = compact -> so good for storage and can fit more into small space

AMYLOPECTIN

  • long branched chain of ɑ-glucose joined by 1,4 and 1,6 glycosidic bonds
  • side branches allow enzymes that break down molecule to get at glycosidic bonds easily
    -> so glucose can be released quickly
37
Q

how do monosaccharides’ and disaccharides’ structure relate to their roles in storing energy?

A

structure makes them sol so can be easily transported and chemical bonds contain lots of energy

  • disaccharide not as sol as mono.
  • disaccharide chemical bonds store more energy
38
Q

how is triglyceride synthesised?

A
  • via condensation reaction (releases H₂O) …
  • between glycerol and 3 fatty acids
  • joined by ester bonds
39
Q

explain why lipids are insol in H₂O

A

triglyceride (kind of lipid) made of glycerol and 3 fatty acid tails

  • fatty acid molecules have long tails of hydrocarbons
  • tails are hydrophobic …
  • so insol in H₂O
40
Q

what is the difference between sat. and unsat. lipids?

A
  • sat. lipids don’t have double C bonds (C=C) in hydrocarbon tails -> each C attached to at least 2 H
  • unsat. lipids have double C=C bonds in hydrocarbon tails

-> causes kink in tail

  • if lipids has 2+ double C bonds -> called polyunsat.
41
Q

body mass index (BMI)

A

body mass (kg)

÷

height ² (m²)

units should be kg m⁻²

42
Q

waist-to-hip ratio

A

waist (cm)

÷

hip (cm)

43
Q

suggest how obesity indicators are used to assess if ppl are obese / overweight and how this relates to CVD

A
  • obesity indicators (waist-to-hip ratio, BMI) used to assess obesity
  • results of these compared to ‘normal’ values in published data table
  • obese ppl more likely to develop CVD
  • these obesity indicators can be used to monitor effects any changes in lifestyle have on person’s weight
44
Q

suggest why people’s perceptions of risks are often diff from actual risks of eg. CVD

A

under/overestimating risks

overestimating risk because …

  • constant media exposure of articles to do with risk makes ppl constantly worry they’ll get eg. CVD
  • personal experience -> eg. known someone who smoked and died of CVD so think if you smoke you must get CVD

underestimating risk because …

  • lack of info making them unaware of factors that contribute to diseases like CVD
45
Q

describe the blood clotting process

(3 marks)

A
  1. thromboplastin (protein) released from damaged blood vessel
  2. thromboplastin + Ca²⁺ (from plasma) trigger conversion of …
    prothrombin (sol protein)->thrombin (enzyme)
  3. thrombin catalyses conversion of …
    fibrinogen (sol protein)->fibrin (solid insol fibres)
  4. fibrin fibres tangle together to form mesh where platelets and RBCs get trapped -> forms blood clot!

CVD can result from blood clots!!!!!!

46
Q

describe the course of events that lead to atherosclerosis

A
  1. damage to endothelium in artery (by eg. high b.p) -> causes inflammatory response -> WBCs move into area
  2. WBCs and lipids from blood clump together under endothelium to form fatty streaks
  3. over time, more WBCs, lipids and connective tissue build up -> form fibrous plaque = atheroma
  4. plaque partially blocks lumen of artery and restricts blood flow -> causes b.p to increase
  5. hardening of arteries caused by atheromas = atherosclerosis
47
Q

explain how the relationship between heart structure and function can be investigated practically

(5 marks)

A

heart dissection

external examination:

  • see 4 main vessels attached to heart
  • feel of vessels used to identify each one -> arteries are thick and rubbery, veins are thinner
  • see RA, LA, RV, LV and coronary arteries

internal examination:

  • LV wall is thicker than RV wall

-> thicker (more muscular) as needs to contract powerfully to pump blood all round body, whereas RV only takes blood to lungs (nearby)

  • atria walls are thinner than ventricle walls
    -> ventricles have to push blood out of heart whereas atria just push blood short distance into ventricles
  • AV valves link atria to ventricles -> stop backflow of blood when ventricles contract
    -> cords attach AV to ventricles to stop them being forced into atria when ventricles contract
  • SL valves link ventricles to pulmonary artery and aorta -> stop backflow blood into heart after ventricles contract
48
Q

outline the cardiac cycle

A

atria systole, ventricular diastole

  • atria contract, ↓ vol chambers and ↑ Pa in chambers
  • pushes blood into ventricles (slight ↑ in ventricular Pa as receives blood)

ventricular systole, atria diastole

  • ventricles contract, ↓ vol chambers and increasing Pa
  • Pa ventricles > Pa atria so AV valves shut to prevent back flow
  • Pa ventricles > Pa aorta / pulmonary artery so SL valves open and blood forced into arteries

cardiac diastole

  • ventricles and atria relax
  • Pa pulmonary artery / aorta > Pa heart so SL valves close to prevent back flow
  • blood returns to heart and atria fill again as Pa pulmonary vein / vena cava > Pa atria
  • this ↑ Pa in atria
  • as ventricles relax … their Pa < Pa atria so AV valves open -> blood passively flows (not pushed by atrial contraction) into ventricles
  • atria contract and repeat

SNAB biology hoe (15 decks)

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