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MODA > Dr Henderson - Medics only CVS > Flashcards

Dr Henderson - Medics only CVS Flashcards

0
Q

What does renal artery sclerosis cause?

A

Hypertension

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1
Q

What is phaeochromocytoma?

A

An adrenal-secreting tumour of the chromaffin cells in the adrenal medulla

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2
Q

What happens to the vascular system in chronic hypertension?

A

Chronic smooth muscle contraction may induce thickening of the arteriolar vessel walls = irreversible rise in peripheral resistance

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3
Q

What is Liddle’s syndrome and what cause it?

A

Patients with very high rate of Na+ reabsorption in the presence of very low aldosterone = severe hypertension

Caused by various mutations in ENaC channels in the late distal tubule = overexpression and more frequent opening

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4
Q

What are the drugs used in the treatment of hypertension?

A 
Diuretics
ACE inhibitors
Beta blockers
Alpha 1 antagonists
Centrally acting α1/I1 agonists
KCOs
Ca2+ channel antagonists
Other
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5
Q

What are thought to be the modes of action of beta-blockers?

A

Decrease CO
Decreased plasma rening
CNS action increase plasma NA?

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6
Q

Doxazosin?

A

α1 antagonist used in the treatment of hypertension

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7
Q

How do α1 antagonists block blood pressure?

A

They inhibit the sympathetic control of vasoconstriction = vasodilation and drop in BP

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8
Q

Labetalol?

A

α1, β1 and β2 antagonist

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9
Q

How do Ca2+ channel antagonist cause antihypertensive effects?

A

Act on L-type Ca2+ channels = decreased force of contraction and reduced CO

Also have a mild diuretic effect

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10
Q

Amlodipine?

A

Ca2+ channel blocker used in the treatment of hypertension and angina

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11
Q

How do KCOs help lower BP?

A

Act on ATP-sensitive K+ channels in vascular smooth muscle = hyperpolarisation and relaxation

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12
Q

Moxonidine

A

I1 agonist
Centrally acting hypertensive (fewer side effects than alpha 2 agonists)
Mechanism unknown (maybe involving generation of DAG and aá)

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13
Q

What are the other hypertensive drugs?

A

Guanethidine
Reserpine

Ganglion blockers

Other direct acting vasodilators:
Sodium nitroprusside (metabolised to NO) BUT also gives cyanide
Hydralazine

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14
Q

What is an atheroma?

A

An accumulation of a soft, flaky, yellowish material at the centre of large plaques, composed of macrophages nearest the lumen of the artery

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15
Q

What are the stages of development of an atheroma?

A

Yellow fatty streak -> Lipid plaque -> Fibrous plaque

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16
Q

What can atheroma lead to?

A

If atheroma leads to stenosis and compromises the arterial supply of the heart then this produces angina

Parts of the atheroma can break off = MI/stoke

Chronic under perfusion of the heart can lead to chronic heart failure

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17
Q

What is a lipoprotein composed of?

A

Cholesterol, intercalated in a phospholipid membrane together with cholesteryl esters

Apolipoproteins associated with the lipid particle

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18
Q

What kind of apolipoprotein do HDLs have?

A

ApoA

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19
Q

What kind of apolipoprotein do LDLs have?

A

ApoB

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20
Q

What does the liver use cholesterol for? How does it take it up?

A

To synthesise bile salts

Using LDL receptors

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21
Q

What mechanism does the liver use to take in cholesterol?

A

Receptor mediated endocytosis

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22
Q

What is the enterohepatic circulation?

A

The circulation of bile salts and cholesterol from the liver to the GI tract and back

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23
Q

Draw the mechanism for the synthesis of cholesterol

A 
Acetyl CoA + acetoacetyl CoA + Water
        \/
HMG-CoA
        \/           HMG CoA reductase
Mevalonate
        \/
Cholesterol
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24
Q

How do statins work?

A

Inhibit HMG-CoA reductase (rate limiting enzyme for cholesterol synthesis)

Liver takes up more LDLs from the blood to make cholesterol (achieved by synthesis of more LDL receptors)

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25
Q

Simvastatin?

A

Statin - HMG CoA reductase inhibitor

Prodrug - metabolised in the liver

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26
Q

How is the LDL receptor and therefore [cholesterol] controlled in hepatocytes?

A

When there is low [cholesterol] causes a disinhibition of the protease S1P
S1P then cleaves the inactive ER bound SREBP
S2P then removes the NH2- terminal from SREBP freeing it from the ER and thus activating it
SREBP then enters the nucleus to bind to SRE promoter = increased transcription of LDL receptor gene

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27
Q

Atorvastatin?

A

Long-lasting statin (longer half life)

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28
Q

Rosuvostatin?

A

Long-lasting statin because of its longer half life (HMG CoA inhibitor)

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29
Q

What are the pleiotropic effects of statins?

A

Improves endothelial function
Enhances plaque stability
Decrease in oxidative stress and inflammation
Inhibition of thrombus formation

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30
Q

How do fibrates work?

A

Increase uptake of LDL and increase production of HDLs

Acts as an agonist of PPARα and PPARγ which induce transcription of Liver X Receptors (LXRs)

These act as metabolic sensors for cholesterol action

LXR causes an increase in the transcription of SREBP, causing an increase in LDL uptake, and ABCA1

ABCA1 controls the rate limiting step of HDL synthesis

Also stimulates lipoprotein lipase

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31
Q

What is the role of liver X receptors?

A

Cause increased transcription of SREBP, causing an increase in LDL uptake, and ABCA1

ABCA1 controls the rate limiting step of HDL synthesis

They also stimulate lipoprotein lipase

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32
Q

Clofibrate?

A

Fibrate (PPARα/γ agonist = increase LXR production)

Causes an increase in HDL synthesis and increase in LDL uptake

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33
Q

Bezafibrate?

A

Fibrate (PPARα/γ agonist = increase LXR production)

Causes an increase in HDL synthesis and increase in LDL uptake

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34
Q

Fenofibrate

A

Fibrate (PPARα/γ agonist = increase LXR production)

Causes an increase in HDL synthesis and increase in LDL uptake

35
Q

Rosiglitazone

A

PPARγ agonist = increase LXR production

Causes an increase in HDL synthesis and increase in LDL uptake

Currently in clincal trials

36
Q

Which drugs can be used to inhibit cholesterol absorption?

A

Ezetimibe

Colestyramine

37
Q

Colestyramine

A

Sequesters bile acids thus preventing their uptake

This causes an increase in cholesterol metabolism in order to replace these (and therefore an increased uptake of LDLs)

38
Q

Ezetimibe?

A

Blocks NPLC1L1 channel and therefore uptake of sterols into the intestinal epithelium

Circulate enterohepatically = repeated action

39
Q

ApoA-I Milano?

A

Mutated form of ApoA in which the 173rd amino acid, arginine has been replaced with cysteine = disulphide dimer and subsequent low level of HDLs
Individuals with this mutation have low rates of heart disease

Clinical use as recombinant protein - clinical trials have shown increase cholesterol metabolism and decreased atheromatous lesion in rabbits

40
Q

Niacin?

A

Decreases LDL concentrations and increases HDL concentrations

Believed to act via a GPCR called HM74A

41
Q

Fish oils?

A

Shown to influence blood lipid levels - unknown mechanism

42
Q

What is angina pectoralis?

A

A chest pain as a result of inadequate blood supply to the myocardium

43
Q

Why does sympathetic stimulation tend to predisposes angina sufferers to pain?

A

Increases HR = reduced time in diastole
Increases force of contraction (O2 demand)
Decrease cardiac efficiency

44
Q

What is variant angina? (AKA Prinzmetal’s angina)

A

Angina caused by spontaneous spasm of the coronary arteries

45
Q

What are the three types of angina pectoralis?

A

Stable - symptoms precipitate from activity
Unstable - symptoms at rest/new onset/occurs in crescendos
Variant - Spasms of coronary arteries

46
Q

What are the changes of the vasculature of the heart in angina?

A

Arteries are already fully dilated due to the partial occlusion and therefore cannot dilate further to accommodate increased O2 demand

47
Q

What drugs are used to treat angina?

A

Nitrovasodilators
Beta blockers
Ca2+ blockers
I(f) blockers

48
Q

How do nitrovasodilators work in the treatment of angina?

A

They are converted to NO by eNOS

Main way they work is thought to be by the producing venous dilation (reduced central venous pressure, RAP and thus work done)

49
Q

What is coronary steal?

A

Vasodilator drugs (such as dypiridamole) opens all vessel and diverts the blood away from the ischaemic regions

50
Q

Glyceryl trinitrate

A

Nitrovasodilators used in the treatment of angina

Converted to NO to cause vasodilation of collateral arteries and veins (Reduced RAP/work done)

Administered sublingually as poorly absorbed in the stomach

51
Q

Isosorbide dinitrate

A

Nitrovasodilators used in the treatment of angina

Converted to NO to cause vasodilation of collateral arteries and veins (Reduced RAP/work done)

Converted to isorobide mononitrate in the liver = active form

52
Q

How do β-blockers act in the treatment of angina?

A

Decrease DP and thus work of the heart against resistence (afterload)

Non specific β blockers have unwanted side effects

53
Q

How do Ca2+ channel blockers work in the treatment of angina?

A

Block Ca2+ entry into smooth muscles cells = vasodilation and reduced BP/afterload

54
Q

Why do Ca2+ channel blockers act preferentially on smooth muscles channels as opposed to those in the heart?

A

Vascular smooth muscle has a lower resting potential (-50mV to -60mV) than those of the heart (-80mV to -90mV) and therefore have more inactivated channel (DHPs bind to inactivated channels)

55
Q

How do I(f) current blockers work in angina?

A

Reduces pacemaker activity = slows HR

Only acts on pacemaker

56
Q

Ivabradine?

A

I(f)-blocker

Reduces HR, used in the treatment of angina

57
Q

What is ischaemic reperfusion injury?

A

Reperfusion causes the opening of the mitochondrial permeability transition pore (MPTP), which leads to the rupture of the mitochondria and ultimately apoptosis

58
Q

What causes the MPTP to open?

A

High mitochondrial [Ca2+], ATP depletion, oxidative stress and mitochondrial depolarisation

59
Q

Nicorandil?

A

K(ATP)- opening drug
Used to mimic ischaemic preconditioning - may act through mitoK(ATP)

Also an NO donor - may help preconditioning

60
Q

What is the role of adenosine in ischaemia?

A

Concentration increase in ischaemia and adenosine has negative inotropic and chronotropic effects

61
Q

How might VEGF and FGF be used in the treatment of angina?

A

VEGF/FGF causes the development of new blood vessels at the site of VEGF expression - unregulated expression can cause abnormal angiogenesis though

62
Q

What are the two ways coronary arteries can be revascularised?

A

Coronary artery bypass graft or percutaneous coronary intervention

63
Q

What are drugs eluting stents?

A

Stents coated with a polymer within which are embedded antiproliferative drugs

64
Q

Paclitaxel?

A

Drug eluted from stents which interferes with the normal function of microtubule growth

65
Q

Sirolimus?

A

Drug eluted from stents that acts as an immunosuppressant and anitproliferant

66
Q

What are the types of dysrhithmia?

A

Escape beats and rhythms - extra beats that interrupt the dominant sinus rhythm

Premature beats and extrasystoles - can arise from ectopic foci in the atria, nodal tissue or ventricles

Ectopic tachycardia - A run of three or more extrasystoles

67
Q

What are the types of atrial tachycardia?

A

Atrial paroxysmal tachycardia

Atrial flutter

Atrial fibrillation

68
Q

What causes atrial paroxysmal tachycardia?

A

Ectopic pacemae gives rise to bouts of regular beating at rateos 110-180bpm

Press on the carotid sinus to stop this

69
Q

What cause atrial flutter?

A

An ectopic pacemaker discharges at 250-350bpm

Only half the impulses are converted to ventricular beats

70
Q

What is atrial fibrillation?

A

Continuous uncoordinated atrial activity

Impulses reach the AVN at 500-600 per min

Ventricular activity limited by the ability of the AV conducting system to respond

71
Q

What are the types of ventricular tachycardia?

A

Ventricular paroxysmal tachycardia

Ventricular fibrillation

72
Q

What is ventricular paroxysmal tachycardia?

A

Ectopic pacemaker in the ventricles

Bad if ventricular rate exceeds the atrial rate

73
Q

What is ventricular fibrillation?

A

Uncoordinated contraction of the ventricles

74
Q

What state of the Na+VGCs do Class IA antidyrhythmics have the highest affinity for?

A

Inactivated

75
Q

What kind of dysrhythmias are Class IA antidysrhythmics used for?

A

Atrial and ventricular dysrhythmias

76
Q

Which phase of the cardiac AP do Class IB antidysrhythmics during?

A

Phase 0

77
Q

In what state do Class IB drugs bind to Na+ VGCs?

A

When they are open

78
Q

How do Class IB antidysrhythmics prevent premature beats?

A

When the beat arrives, they are still bound and thus prevent an AP being propagated

79
Q

Why are Class IB antidysrhythmics useful in prevent ventricular dysrhythmias after an MI?

A

They bind to channel in partly depolarised cells which are present in ischaemic regions

80
Q

What was the CAST and what did it show?

A

Cardiac Arrhythmia Suppression Trial

Showed that Class IC antidysrhythmic agents (flecainide) caused an increase in morality (7% compared to 3% in the control group)

81
Q

What are Class IC drugs used for now?

A

Only used for treatment of patients with anomalous conducting pathways

82
Q

What is myocardial salvage? How does it work?

A

Secondary protection of the mycocardium by drugs

Ca2+ channel blockers (eg nifedipine) decrease the Ca2+ loading of damaged tissue

83
Q

What are the antidysrhythmics that do not fit Vaughan Williams Classification?

A

Adenosine

Cardiac glycosides

84
Q

How does adenosine function as an antidysrhythmic?

A

Acts on A1 receptors in the AV node

GPCRs with Gi = decrease in cAMP

Results in activation of I(K-ACh) thus hyperpolarising pacemaker

85
Q

How do cardiac glycosides function as antidysrhythmics?

A

Act by increase vagal activity through an action in the CNS

Leads to inhibition at the AV node (so slowly AV conduction)

Also affects atrial refractory period

86
Q

Anacetrapib

A

A cholesteryl transfer protein (CETP) inhibitor

CETP normally transfers cholesteryl esters from HDL to LDL/VLDL in exchange for triglycerides

Therefore inhibition of this inhibits LDL formation

MODA (8 decks)

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