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Drugs for Ischaemic Heart Disease Flashcards

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1
Q

How many mitochondria are in each cardiomyocyte?

A

5000

Generate ATP- far more than any other organ of the body

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2
Q

What is preload?

A

Volume of blood in the ventricles at the end of diastole

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3
Q

What is preload determined by?

A

Blood volume

Venous tone, capacity of the venous circulation to hold blood (constriction= more return)

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4
Q

What is preload increased by?

A

Sympathetic NS activation
Renal failure
Heart failure

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5
Q

What is afterload?

A

Resistance the heart must overcome to circulate blood

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6
Q

What is afterload determined by?

A

Tone in arterial circulation

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7
Q

What is afterload increased by?

A

SNS activation

Hypertension

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8
Q

What causes narrowing of the coronary arteries?

A

Atheroma
Coronary artery spasm (smooth muscle spontaneously constrict)
leads to ischaemic heart disease

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9
Q

What do stable plaques lead to?

A

Lack of oxygen and chest pain (angina)

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10
Q

What leads to myocardial infarction?

A

Unstable plaque and thrombus

MINOCA= myocardial infarction non obstructed coronary artery

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11
Q

What does vascular endothelium regulate?

A

Blood vessel tone
Permeability
Leukocyte adhesion, platelet aggregation and tendency for thrombus formation

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12
Q

What occurs to lead to lesion formation?

A

Changes in endothelial function

Leukocyte adhesion and migration as endothelial permeability increases

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13
Q

What are the causes of endothelial dysfunction?

A
  • Elevated and modified low density lipoprotein (in familial hypercholesterolaemia)
  • Oxygen free radicals (smoking, hypertension, activated inflammatory cells)
  • Infectious microorganisms (herpes virus, chlamydia pneumoniae, h. pylori)
  • physical damage and gene activation by turbulent flow, high blood pressure
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14
Q

What are the risk factors for endothelial dysfunction?

A

Diabetes, ageing, male (females after menopause)

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15
Q

What are foam cells?

A

Macrophages that take up low density lipoprotein oxidised by interaction with oxygen free radicals

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16
Q

Describe the formation of a fatty streak

A 
Inflammatory cell activation
Smooth muscle migration
Foam cell formation
T cell activation
Adherence and aggregation of platelets
Adherence and entry of leukocytes
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17
Q

Describe the formation of advanced complex lesion

A

Macrophage accumulation
Formation of necrotic core
Fibrous cap formation- stability key to prognosis
Healing response to injury

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18
Q

What is the difference in outcome between unstable and stable angina?

A 
Stable= chest pain
Unstable= cap rupture or erosion= thrombus= heart attack/MI, stroke
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19
Q

Which drug lowers cholesterol and low density lipoprotein?

A

Statins

simvastatin

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20
Q

How is LDL formed?

A

HMG CoA into mevalonate via HMG CoA reductase (rate determining step in liver)
Mevalonate precursor for cholesterol, then LDL
binds to LDL receptors for clearance

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21
Q

What is the mechanism of statin drug action?

A

statins are inhibitors of HMG CoA reductase

Increase expression of LDL receptors (so more clearance)

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22
Q

What are the other effects of statins (pleiotropic)?

A 
Improved endothelial function
Inhibition of inflammation
Plaque stabilisation
Inhibition of thrombus formation
(mevalonate compounds involved in intracellular signal transduction)
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23
Q

What other lipid lowering drugs are used with or as an alternative to statins?

Study These Flashcards
A

Fibrates (bezafibrate, gemfibrozil, fenofibrate)

ezetimibe

24
Q

Describe fibrates

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A

Activate intracellular PPARa (peroxisome proliferator receptor a)
Decrease circulating very low density lipoprotein and triglyceride, only very small effect on LDL but also increase protective high density lipoprotein

25
Describe ezetimibe
Lowers cholesterol absorption from small intestine vis action in epithelial cells
26
What is angina pectoris?
Intermittent chest pain caused by mismatch between demand of oxygen by the heart and supply of oxygen to the heart (stimulates chemoreceptors- chest pain)
27
What is oxygen supply decreased by?
Coronary artery disease | Anaemia
28
What is oxygen demand increased by?
Exercise Tachycardia Hypertension
29
What is the aim of angina treatment?
Reduce demand or increase supply | Reduce demand by reduce heart rate/ force of contraction/ preload/ afterload
30
Describe acute angina treatment
Rest | Rapid acting organic nitrate (glyceryl trinitrate)
31
Describe prophylactic angina treatment
Targets blood vessels- longer lasting nitrate/ K (ATP) channel opener Targets heart- beta adrenoreceptor antagonist/ calcium antagonist/ funny channel blocker
32
How do nitrates affect the blood vessels?
NO in endothelial cells into smooth muscle cell- guanylate cyclase converts GTP into cGMP= relaxation (reduces availability for Ca 2 for contraction) Veins more than arteries
33
What are the effects of nitrates on venous circulation?
Dilate veins, decrease venous return and preload on heart, reduce oxygen demand
34
What are the effects of nitrates on arterioles and coronary arteries?
Dilate and reduce afterload on heart therefore reduce oxygen demand Coronary= improves supply (coronary spasm)
35
What are examples of nitrates?
- Glyceryl trinitrate- acute (sub-lingual or spray), chronic use leads to tolerance (loss of responsiveness) rapid action - Isosorbide dinitrate- slow release patch/ oral, can be prophylactic, nitrate free periods required, longer acting
36
What are the effects of nicorandil?
Reduces preload and afterload on heart and therefore oxygen demand Dilates coronary arteries and can increase oxygen supply in coronary spasm
37
What are the mechanisms of nicorandil?
``` Causes blood vessel dilation by opening ATP sensitive K+ channels in smooth muscle cells Nitrate moiety (releases NO) in structure therefore additional vasodilator action ```
38
What are the mechanisms and effects of beta adrenoreceptor antagonists (like atenolol)?
- Blocks cardiac beta 1 adrenoreceptor= reduce heart rate and therefore oxygen demand - Blocks renal beta 1 adrenoreceptor= reduce blood volume by reducing renin release and activation of RAAS, reduce preload and therefore oxygen demand
39
What does RAAS stand for?
Renin Angiotensin Aldosterone System
40
What are the mechanisms and effect of ivabradine?
Blocks 'funny current' in sino-atrial node cells= reduces rate of spontaneous depolarisation during action potential generation- reduce heart rate so oxygen demand (Less side effects than beta blockers)
41
What are the mechanisms and effects of calcium antagonists?
nifedipine, diltiazem Prevent opening of voltage dependent Ca 2 channels= prevents Ca 2 entry into cardiac muscle cells from extracellular space= reduce availability to contractile apparatus= reduce force of contraction and therefore oxygen demand
42
Describe thrombus formation
Endothelial cells produce anti-thrombotic mediators, damage= collagen exposure= platelet activation (change shape and stick together)= coagulation cascade= fibrin
43
What are anti-thrombotic drugs?
Taken prophylactically to reduce risk of thrombus if atherosclerotic plaque ruptures, in patients at high risk or already had MI - Anti-platelet (aspirin, clopidogrel, vorapaxar) - Anti-coagulant (warfarin, rivaroxaban)
44
Describe platelet activation
Stimulus (collagen)- thrombin activates coagulation cascade- Arachidonic acid via phospholipaseA2- cyclic endoperoxidases via cyclooxygenase (COX)- TxA2 prostaglandin via Tx synthetase- TxA2 receptor= increase in iCa 2+ so activation of platelet
45
What is the mechanism of anti-platelet drugs?
Thrombin antagonist | COX inhibitor
46
How do platelets further increase activation?
Activated platelets change shape and release contents of granules- adenosine diphosphate (ADP)
47
How do activated platelets stabilise the thrombus?
Platelets express glycoprotein 2b/3a receptors for attachment of fibrin, from coagulation cascade
48
What other mechanisms of anti-platelet drugs have directly on the platelet?
``` P2Y12 receptor antagonists to block ADP so less platelet aggregation abciximab antibody (IV)- blocks fibrin binding to gp2b/3a ```
49
What are the overall mechanisms of anti-platelet drugs?
- COX inhibitor- aspirin- irreversible inhibition of COX, prevents formation of TxA2 and platelet activation - P2Y12 inhibitor- clopidogrel, ticagrelor- blocks effect of ADP and prevents platelet activation - Thrombin-receptor antagonist- vorapaxar- prevent activation of PAR-1 receptors on platelets
50
What are the risks of anti-platelet drugs?
Bleeding | Newer drugs shorter acting or reversible
51
What are anti-coagulant drugs and what are the types?
Prevent the formation of fibrin to stabilise platelet plug - Intravenous= heparin - Orally active= warfarin, rivaroxaban
52
What is the action of heparin?
Binds to Anti-thrombin 3- released by endothelial cells naturally in response Promotes action, reduces coagulation cascade
53
What is the action of warfarin?
Reduces the action of enzyme reductase so less oxidised Vitamin K is converted into hydroquinone Vitamin K so less Glu converted into Glu-COOH which is involved in active factors 2,7,9,10 (prevents cofactors forming)
54
What are the common indications of warfarin?
AF, artificial heart valves, DVT, pulmonary embolism, occasionally after MI
55
What are the cons of warfarin?
Narrow optimal range, high risk of bleeding Broken down in liver, enzymes induced by other drugs, environmental influences Blood levels must be checked regularly
56
What is the action of rivaroxaban?
Inhibits action of Xa in thrombin formation

Cardiovascular (52 decks)

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