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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
How do statins work?
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)
25
Simvastatin?
Statin - HMG CoA reductase inhibitor Prodrug - metabolised in the liver
26
How is the LDL receptor and therefore [cholesterol] controlled in hepatocytes?
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
27
Atorvastatin?
Long-lasting statin (longer half life)
28
Rosuvostatin?
Long-lasting statin because of its longer half life (HMG CoA inhibitor)
29
What are the pleiotropic effects of statins?
Improves endothelial function Enhances plaque stability Decrease in oxidative stress and inflammation Inhibition of thrombus formation
30
How do fibrates work?
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
31
What is the role of liver X receptors?
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
32
Clofibrate?
Fibrate (PPARα/γ agonist = increase LXR production) Causes an increase in HDL synthesis and increase in LDL uptake
33
Bezafibrate?
Fibrate (PPARα/γ agonist = increase LXR production) Causes an increase in HDL synthesis and increase in LDL uptake
34
Fenofibrate
Fibrate (PPARα/γ agonist = increase LXR production) Causes an increase in HDL synthesis and increase in LDL uptake
35
Rosiglitazone
PPARγ agonist = increase LXR production Causes an increase in HDL synthesis and increase in LDL uptake Currently in clincal trials
36
Which drugs can be used to inhibit cholesterol absorption?
Ezetimibe | Colestyramine
37
Colestyramine
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
Ezetimibe?
Blocks NPLC1L1 channel and therefore uptake of sterols into the intestinal epithelium Circulate enterohepatically = repeated action
39
ApoA-I Milano?
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
Niacin?
Decreases LDL concentrations and increases HDL concentrations Believed to act via a GPCR called HM74A
41
Fish oils?
Shown to influence blood lipid levels - unknown mechanism
42
What is angina pectoralis?
A chest pain as a result of inadequate blood supply to the myocardium
43
Why does sympathetic stimulation tend to predisposes angina sufferers to pain?
Increases HR = reduced time in diastole Increases force of contraction (O2 demand) Decrease cardiac efficiency
44
What is variant angina? (AKA Prinzmetal's angina)
Angina caused by spontaneous spasm of the coronary arteries
45
What are the three types of angina pectoralis?
Stable - symptoms precipitate from activity Unstable - symptoms at rest/new onset/occurs in crescendos Variant - Spasms of coronary arteries
46
What are the changes of the vasculature of the heart in angina?
Arteries are already fully dilated due to the partial occlusion and therefore cannot dilate further to accommodate increased O2 demand
47
What drugs are used to treat angina?
Nitrovasodilators Beta blockers Ca2+ blockers I(f) blockers
48
How do nitrovasodilators work in the treatment of angina?
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
What is coronary steal?
Vasodilator drugs (such as dypiridamole) opens all vessel and diverts the blood away from the ischaemic regions
50
Glyceryl trinitrate
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
Isosorbide dinitrate
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
How do β-blockers act in the treatment of angina?
Decrease DP and thus work of the heart against resistence (afterload) Non specific β blockers have unwanted side effects
53
How do Ca2+ channel blockers work in the treatment of angina?
Block Ca2+ entry into smooth muscles cells = vasodilation and reduced BP/afterload
54
Why do Ca2+ channel blockers act preferentially on smooth muscles channels as opposed to those in the heart?
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
How do I(f) current blockers work in angina?
Reduces pacemaker activity = slows HR Only acts on pacemaker
56
Ivabradine?
I(f)-blocker Reduces HR, used in the treatment of angina
57
What is ischaemic reperfusion injury?
Reperfusion causes the opening of the mitochondrial permeability transition pore (MPTP), which leads to the rupture of the mitochondria and ultimately apoptosis
58
What causes the MPTP to open?
High mitochondrial [Ca2+], ATP depletion, oxidative stress and mitochondrial depolarisation
59
Nicorandil?
K(ATP)- opening drug Used to mimic ischaemic preconditioning - may act through mitoK(ATP) Also an NO donor - may help preconditioning
60
What is the role of adenosine in ischaemia?
Concentration increase in ischaemia and adenosine has negative inotropic and chronotropic effects
61
How might VEGF and FGF be used in the treatment of angina?
VEGF/FGF causes the development of new blood vessels at the site of VEGF expression - unregulated expression can cause abnormal angiogenesis though
62
What are the two ways coronary arteries can be revascularised?
Coronary artery bypass graft or percutaneous coronary intervention
63
What are drugs eluting stents?
Stents coated with a polymer within which are embedded antiproliferative drugs
64
Paclitaxel?
Drug eluted from stents which interferes with the normal function of microtubule growth
65
Sirolimus?
Drug eluted from stents that acts as an immunosuppressant and anitproliferant
66
What are the types of dysrhithmia?
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
What are the types of atrial tachycardia?
Atrial paroxysmal tachycardia Atrial flutter Atrial fibrillation
68
What causes atrial paroxysmal tachycardia?
Ectopic pacemae gives rise to bouts of regular beating at rateos 110-180bpm Press on the carotid sinus to stop this
69
What cause atrial flutter?
An ectopic pacemaker discharges at 250-350bpm Only half the impulses are converted to ventricular beats
70
What is atrial fibrillation?
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
What are the types of ventricular tachycardia?
Ventricular paroxysmal tachycardia Ventricular fibrillation
72
What is ventricular paroxysmal tachycardia?
Ectopic pacemaker in the ventricles Bad if ventricular rate exceeds the atrial rate
73
What is ventricular fibrillation?
Uncoordinated contraction of the ventricles
74
What state of the Na+VGCs do Class IA antidyrhythmics have the highest affinity for?
Inactivated
75
What kind of dysrhythmias are Class IA antidysrhythmics used for?
Atrial and ventricular dysrhythmias
76
Which phase of the cardiac AP do Class IB antidysrhythmics during?
Phase 0
77
In what state do Class IB drugs bind to Na+ VGCs?
When they are open
78
How do Class IB antidysrhythmics prevent premature beats?
When the beat arrives, they are still bound and thus prevent an AP being propagated
79
Why are Class IB antidysrhythmics useful in prevent ventricular dysrhythmias after an MI?
They bind to channel in partly depolarised cells which are present in ischaemic regions
80
What was the CAST and what did it show?
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
What are Class IC drugs used for now?
Only used for treatment of patients with anomalous conducting pathways
82
What is myocardial salvage? How does it work?
Secondary protection of the mycocardium by drugs Ca2+ channel blockers (eg nifedipine) decrease the Ca2+ loading of damaged tissue
83
What are the antidysrhythmics that do not fit Vaughan Williams Classification?
Adenosine Cardiac glycosides
84
How does adenosine function as an antidysrhythmic?
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
How do cardiac glycosides function as antidysrhythmics?
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
Anacetrapib
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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