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Pharmacology 3 > L15: Cardiovascular Pharmacology - Pathophysiology (Coronary Heart Disease) > Flashcards

L15: Cardiovascular Pharmacology - Pathophysiology (Coronary Heart Disease) Flashcards

1
Q

What is coronary heart disease?

A

Common but serious condition where the blood vessels supplying the heart are narrowed or blocked by build up of fatty acids.

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2
Q

What is atherosclerosis?

A

Thickening or hardening of the arteries

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3
Q

What can be an outcome of coronary heart disease?

A

Lack of oxygen and chest pain (angina) OR myocardial infarction

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4
Q

What does healthy vascular endothelium regulate?

A
  • vessel tone
  • leukocyte adhesion
  • platelet aggregation
  • tendency for thrombus formation
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5
Q

What do changes in vascular endothelium result in?

A

Changes in endothelial function precede lesion formation

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6
Q

What are the causes of endothelial dysfunction?

A
  • elevated and modified low density lipoprotein (high cholesterol levels)
  • oxygen free radicals caused by smoking, hypertension, activated inflammatory cells
  • infectious microorganisms: herpes virus, chlamydia pneuomoniae, H. pylori
  • physical damage and gene activation by turbulent flow, high blood pressure (increases the damage of endothelia)
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7
Q

How does a fatty streak in vessels form?

A

Fatty streaks appear when the presence of foam cells at the site of plaque formation expands. Foam cells: macrophages take up low density lipoprotein oxidised by interaction with oxygen free radicals.

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8
Q

How does advanced complex lesion form?

A
  • After foam cells formation.
  • Macrophages accumulate, smooth muscle cell proliferation and migration.
  • Fibrous-cap forms as a healing response to injury.
  • Necrotic core forms - leukocytes, lipid and cell debris from apoptosis, necrosis and proteolysis.
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9
Q

What are the risk factors for Coronary Heart Disease?

A

Risk factors:
- high lipid, low anti-oxidants diet
- genetic
- smoking
- hyperlipidaemia (elevated level of lipids in plasma)
- hypertension
- diabetes
- being a male

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10
Q

What is the difference in the outcome of stable/unstable cap formation in vessels?

A

Stable cap results in angina; unstable cap results in myocardial infarction / stroke.

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11
Q

What are the pharmacological tools for treatment of coronary heart disease?

A
  • Development reducing: lipid-lowering drugs - statins, fibrates, ezetemibe
  • treat symptoms: stable angina
  • prevent thrombosis
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12
Q

What is the surgical intervetion for treatment of coronary heart disease?

A
  • stent placement
  • balloon angioplasty for plaque removal
  • coronary artery bypass grafting
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13
Q

What are statins?

A

Lipid lowering drugs for prevention of coronary heart disease. They are HMG-CoA reductase inhibitors

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14
Q

How do statins lower lipid formation? What is the mechanism of LDL formation and clearance?

A
  • HMG CoA is converted to mevalonate by HMG CoA reductase, which is converted to cholesterol and finally to LDL.
  • LDL acts on LDL receptors, which induce clearance from circulation.
  • When HMG CoA reductase is inhibited, LDL receptors expression is increased, thus increased clearance from circulation.
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15
Q

What are the pleiotropic effects of statins?

A
  • improved endothelial function
  • inhibition of inflammation
  • plaque stabilisation
  • inhibition of thrombus formation
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16
Q

What are the side effects of statins?

A
  • muscle pain
  • increased risk of diabetes
  • liver damage
17
Q

How do fibrates decrease LDL in plasma?

A

Decrease circulating LDL and triglyceride, only small effect on LDL, but also increase ‘protective’ high density lipoprotein (HDL).
Activate peroxisome proliferator-activated receptors (PPAR-alpha) and increase expression of genes associated with lipid clearance, e.g. lipoprotein lipase.

18
Q

How does ezetimibe reduce LDL levels in plasma?

A

Blocks transport of cholesterol in gut, withour affecting absorption of fat soluble vitamins, triglycerides or bile acids.
Added to statin where response is inadequate alone

19
Q

What is thrombosis?

A

Inappropriate platelet activation and coagulation. Can be arterial and deep vein thrombosis.

20
Q

What is the result of arterial thrombosis?

A
  • Heart attacks (MI)
  • Stroke
  • peripheral vascular disease
21
Q

What is the deep vein thrombosis?

A
  • ‘economy class syndrome’
  • oral contraceptives
22
Q

What is myocardial infarction?

A

Loss of supply to part of heart caused by blockage in coronary artery. Acute: pain or fatal arrythmias. Also injury and chronic heart failure.

23
Q

What is the effect of anti-thrombotic drugs on myocardial infarction?

A

They can reduce the risk of clot formation on a ruptured atherosclerotic plaque.

24
Q

What are platelets?

A

Platelets (thrombocytes) are small, colorless cell fragments that form clots and stop or prevent bleeding. Made in bone marrow.

25
How **endothelial cells** prevent clot formation in healthy blood vessel?
Endothelial cells produce agents that prevent platelet activation and coagulations.
26
How does a **clot form** in a vessel?
- Damage to the **endothelial cells** allows bleeding and exposes platelets to **collagen** in the vessel wall. - Platelets are activated and aggregate to prevent blood loss, endothelial cells reduce secretion of anti-aggregant. - **Fibrin** is formed by the coagulation cascade to stabilize the platelet plug For summary see L15, slide 46
27
What is the precise **mechanism of platelets activation**?
For diagramm see L15, slide 49 - stimulus (collagen, thrombin) gets converted to **arachidonic acid** by **phospholipase A2**. - arachidonic acid gets converted to **cyclic endoperoxidases** by **COX** - then cyclic endoperoxidases are converted to **thromboxane A2** by **Tx synthase** - thromboxane A2 acts on **TxA2 receptor**, which induces release of **calcium ions**, which activate the platelets
28
What are the drugs of **anti-platelet** formation? What is their mechanism?
1. **COX inhibitor**: aspirin; irreversibly inhibits cyclooxygenase to prevent thromboxane formation 2. **P2Y12 receptor antagonists**: clopidogrel, irreversibly block the receptor.
29
What is the **drawback** of **anti-platelet** drugs?
As platelets have no nucleus, these platelet activation pathways **cannot be overcome until new platelets** are made, can increase **problems with bleeding**.
30
What are the **2nd generation reversible anti-platelet drugs**?
**reversible P2Y12 antagonists**, cangrelor, ticagrelor; non-covalent binding, no need for new platelets
31
How do the **Thrombin-receptor antagonists** work?
Prevent activation of **PAR-1 receptors** on platelets by **thrombin**. Potential for use in place of, or in addition to existing **anti-platelet**, effective in reducing risk of ischaemia but risk of intracranial bleeding so not suitable for all patients.
32
Describe precise **coagulation mechanism**
Series of **clotting factors** (serine proteases) get activated by one another. When blood vessel gets damaged, last **factor gets activated**. It induces formation of **prothrombin** to **thrombin**. **Thrombin** acts on **fibrinogen** conversion to **fibrin**. Last factor stabilises **fibrin**.
33
What is **Antithrombin III (ATIII)**? How does it act?
It's a protease, which inhibits coagulation by acting on clotting factors. **ATIII** is activated by **Heparin**.
34
What is the importance of **heparin** in blood clotting?
It's an activator of **antithrombin II** through binding to both ATIII and a protease. Accelarates neutralisation of serine proteases (clotting factors). NOT active orally.
35
What are the **orally active anti-coagulants**?
- **Factor Xa** inhibitor. Blocks intrinsic and extrinsic coagulation pathways. - **Direct inhibitor of thrombin (factor II) enzyme activity**, bleeding risk
36
What are **clot-busting** fibrinolytic drugs?
- effective at reducing mortality if given immediately after MI or stroke - act to **accelerate conversion of plasminogen to plasmin**, which **degrades fibrin in thrombus**

Pharmacology 3 (21 decks)

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