Physiology Flashcards

1
Q

How is the heart muscle supplied with blood?

A

Coronary arteries

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2
Q

What is stroke volume?

A

The volume of blood ejected by each ventricle per heartbeat

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3
Q

What does cardiac muscle need to contract?

A

Extracellular calcium ions

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4
Q

What does the plateau phase in ventricular muscle action potential?

A

Calcium ion influx through voltage-gated calcium channels

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5
Q

What does a long refractory period in cardiac muscle prevent?

A

Generation of tetanic contraction (continuous contraction) - protects heart

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6
Q

What happens to the sodium channels in the plateau phase?

A

They are in the depolarised closed state

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7
Q

SV = ?

A

End Diastolic Vol (EDV) - End Systolic Vol (ESV)

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8
Q

How is stroke volume regulated?

A

Intrinsic (within the heart itself) and extrinsic (nervous and hormonal control)

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9
Q

What is cardiac preload?

A

Initial stretching of the cardiac myocytes prior to contraction - indicated by EDV

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10
Q

What is the EDV determined by?

A

Venous return to the heart

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11
Q

What is Starling’s law of the heart?

A

The greater the EDV, the greater the SV

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12
Q

How does stretch affect troponin?

A

Increases it’s affinity for calcium ions

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13
Q

If venous return increases, what happens to EDV and SV?

A

They also increase

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14
Q

What is afterload?

A

Resistance into which the heart is pumping

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15
Q

If there is continuously increased afterload (e.g. untreated hypertension), what happens?

A

Ventricular muscle mass increases (ventricular hypertrophy) to overcome the resistance

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16
Q

Ventricular muscle is supplied by which type of nerve fibres?

A

Sympathetic

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17
Q

What is the neurotransmitter for the sympathetic nerve fibres supplying the ventricle?

A

Noradrenaline

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18
Q

What effect does sympathetic stimulation have on the force of contraction?

A

Increases it

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19
Q

What effect does sympathetic stimulation have on the heart rate?

A

It increase it

20
Q

What does Inotropic refer to?

A

Force of contraction

21
Q

What does chronotropic refer to?

A

Heart rate

22
Q

What does vagal stimulation have a major influence on?

A

Heart rate

23
Q

Why does vagal stimulation have so little effect on force of contraction?

A

There is very little parasympathetic innervation (if any) of the ventricles

24
Q

Where are adrenaline and noradrenaline released from?

A

Adrenal medulla

25
Q

What chronotropic and inotropic effects do noradrenaline and adrenaline have?

A

Minor effects compared with effects of noradrenaline from sympathetic nerves

26
Q

What is cardiac output?

A

The volume of blood pumped by each ventricle per minute

27
Q

CO = ?

28
Q

Describe blood flow across the heart, starting with the right atrium

A

Right atrium -> right ventricle -> pulmonary artery -> lungs -> pulmonary veins -> left atrium -> left ventricle -> aorta -> body tissues -> SVC -> right atrium

29
Q

What is the structure of a lipoprotein?

30
Q

What are the five classifications of lipoproteins?

A

Chylomicrons, Very low-density lipoproteins (VLDL), Intermediate-density lipoproteins (IDL), Low-density lipoproteins (LDL) and High density lipoproteins (HDL)

31
Q

What effect does HDL have on CHD and atherosclerosis?

A

Has a protective effect - the lower the amount of HDL, the higher the risk of CHD

32
Q

What are the normal triglyceride levels?

33
Q

What do statins do and how?

A

Statins reduce amount of cholesterol in body. Act as HMG CoA reductase inhibitors and block the cholesterol synthesis pathway -> acetyl CoA isn’t then made into cholesterol

34
Q

What actions do statins have that aren’t on lipids?

A

Improvement of endothelial dysfunction, increased nitric oxide bioavailability, antioxidant properties, inhibition of inflamm responses, stabilisation of atherosclerotic plaques

35
Q

What are some of the clinical markers of dyslipidaemia?

A

xanthelasms (xanthomas of the eyelids), tendon xanthomas, tuberous xanthomas, eruptive xanthomas, striate palmar xanthomas

36
Q

What effects does hypertension have on the arteries?

A

Can cause widening of the arteries - puts strain on the lining, can cause the artery muscle to thicken - restricts blood flow

37
Q

What are the two types of hypertension?

A

Essential hypertension (no underlying cause) and secondary hypertension (underlying cause)

38
Q

What are the lifestyle modifications to reduce hypertension?

A

Lose weight, limit alcohol intake, increase physical activity, reduce salt intake, stop smoking, limit intake of foods rich in fat and cholesterol

39
Q

What is the system of treatment for a recently diagnosed hypertensive treatment who is 55 years or older or black?

A

STEP 1: calcium-channel blocker or thiazide-type diuretic

STEP 2: Add an ACE inhibitor to initial treatment

STEP 3: All three drugs from above

STEP 4: Add further diuretic therapy or and alpha/beta blocker, consider referral

40
Q

What is the sytem of treatment for a newly diagnosed hypertensive patient who is younger than 55 years old?

A

STEP 1: ACE inhibitor

STEP 2: Add either a calcium-channel blocker or a thiazide-type diuretic

STEP 3: All of the above

STEP 4: Add further diuretic therapy or an alpha/beta blocker

41
Q

What effects does smoking have in relation to cardiovascular disease?

A

Increase blood pressure, decreases HDL, damages arteris and blood cells, increases risk of MI

42
Q

What is the metabolic syndrome?

A

Constellation of major risk factors, life-habit risk factors and emerging risk factors

CLUE: distinctive body type with increased abdominal circumference

43
Q

What risk scoring do we use?

A

The Assign score (assign-score.com)

44
Q

Main therapeutics for tackling ischaemia?

A

Antianginal medications (calcium blockers, nitrates, beta blockers), revascularisation (angioplasty, CABG) and risk factor modification

45
Q

Main therapeutics for tackling atherothrombosis?

A

Aspirin, Statins, beta blocker, ACE inhibitor, exercise, smoking cessation, symptom control (antianginal medications and possibly revascularisation)