1 Heart, CVD, Carbs and Lipids Flashcards
(48 cards)
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
2
Q
sucrose
A
ɑ glucose + fructose
condensation reaction forming glycosidic bonds
3
Q
lactose
A
ɑ glucose + galactose
condensation reaction forming glycosidic bonds
4
Q
maltose
A
ɑ glucose + ɑ glucose
condensation reaction forming glycosidic bonds
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
6
Q
systole
A
S uck
C ock
contraction
7
Q
diastole
A
relaxation
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
9
Q
what is cardiac muscle made up of?
A
cells connected by cytoplasmic bridges
-> enables electrical impulses to pass through tissue
10
Q
what is the role of valves in the heart?
A
- prevent back flow of blood
- maintaining correct pressure in chambers
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
12
Q
how is cardiac muscle different to skeletal muscle?
A
MYOGENIC -> originating in muscle tissue
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)
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)
15
Q
artery
A
- narrow lumen -> maintains high b.p
- elastic fibres -> allow stretch and recoil
- thicker muscular wall -> contracts and relaxes to CONSTRICT and DILATE BLOOD VESSELS
- collagen in walls -> provides strength to withstand high b.p
- folded endothelium -> allows EXPANSION -> cope with high b.p
16
Q
myogenic
A
ability of muscles to make its own electrical impulses at rest (without CNS)
17
Q
explain how veins are adapted to their function
A
- large lumen -> low b.p and minimises resistance
- thin layer of elastic tissue -> maintains b.p
- valves -> prevent back flow
- smooth endothelium -> minimise resistance
18
Q
capillaries
A
where metabolic exchange occurs
-> subs exchanged between cells and capillaries
- network of capillaries -> increase s.a for metabolic exchange
- one cell thick walls -> speeds up diffusion of substances (eg. glucose, O₂) in and out of cells
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
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
(for daphnia practical)
how is control set up?
replace caffeine sol with **distilled water** to measure daphnia heart rate without effect of caffeine
26
what steps should students take to ensure daphnia are ethically treated?
- **return** to **natural habitat** after use
- minimise amount of **time** exposed to **stressful** conditions
27
why should cover slip not be used when observing organism?
(daphnia practical)
to **allow O₂ to reach organism**
-> preventing conditions from becoming ANOXIC
28
what is the purpose of placing cotton wool on the slide?
(daphnia practical)
to **restrict movement** of organism so easier to count heart rate
29
outline procedure for investigating the effect of caffeine on heart rate in daphnia
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
what reagent is used to test for vitamin C and what is observed?
DCPIP
colour change from
blue -> colourless
31
outline procedure to use DCPIP to find vitamin C content of diff samples
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
state a hazard and safety precaution for vitamin C practical
DCPIP -> irritant
-> wear goggles and avoid skin contact
33
compare the benefits and risks of PLATELET INHIBITORS
adv.?
- used to treat ppl who **ALREADY have blood clots**
disadv.?
- rashes
- diarrhoea
- nausea
- liver function problems
- **excessive bleeding** -> especially after serious injury
34
discuss the potential ethical issues of using invertebrates in scientific research
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
glycogen
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
starch
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
how do monosaccharides' and disaccharides' **structure** relate to their **roles** in **storing energy**?
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
how is **triglyceride** synthesised?
- via **condensation** reaction (releases H₂O) ...
- between **glycerol** and **3 fatty acids**
- joined by **ester bonds**
39
explain why **lipids** are **insol** in H₂O
**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
what is the difference between sat. and unsat. lipids?
- 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
body mass index (BMI)
body mass (**kg**)
÷
height **²** (**m²**)
units should be kg m⁻²
42
waist-to-hip ratio
waist (cm)
÷
hip (cm)
43
suggest how obesity indicators are used to assess if ppl are obese / overweight and how this relates to CVD
- 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
suggest why people's **perceptions** of risks are often **diff** from **actual** risks of eg. CVD
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
describe the blood clotting process
(3 marks)
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
describe the course of events that lead to atherosclerosis
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
explain how the relationship between heart structure and function can be investigated practically
(5 marks)
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
outline the cardiac cycle
***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
