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CDL301 Cardiovascular Pharmacology > Lecture 8 Physiology of the Vasculature II > Flashcards

Lecture 8 Physiology of the Vasculature II Flashcards

1
Q

How does atherosclerosis impact the ability of the endothelium to regulate vascular smooth muscle

A

As atheroma’s develop the endothelial cells become separated and further away from the VSMCs. This means that the artery wall less able to regulate itself hence often leading to hypertension. In addition VSMCs are triggered to proliferate in response to immune cell invasion. This causes them to lose adhesion to each other and no longer contract as effectively

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2
Q

What can happen specifically to the endothelium as a result of a loss of the glycocalyx as a result of oxLDL

A

They can become hyper-responsive and more likely to release contractile mediators

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3
Q

What happens as a result of calcification of the blood vessels in disease

A

The build-up of calcified deposits results in a stiffening of the artery. This makes it less able to contract and relax in a coordinated way

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4
Q

Loss of which extracellular matrix protein in the vessel wall can also play a role in disease

A

Elastin

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5
Q

Hypoxia uncouples eNOS T or F

A

T

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6
Q

What is the evidence for the incidence of hypertension

A

Around 30% of people are affected in England

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7
Q

What risk is massively increased in patients left untreated for hypertension

A

Increased risk of heart attack and stroke

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8
Q

What is the leading risk factor for the overall global burden of disease

A

Hypertension

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9
Q

What are the symptoms of hypertension

A

Breathlessness fatigue fluid retention as cardiac output not adequate to meet metabolic demands

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10
Q

What is the most common cause of hypertension

A

Secondary to atherosclerosis

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11
Q

Heart Failure is where there is an inadequate cardiac output to meet metabolic demand what is the most common cause of heart failure

A

Disease of heart itself secondary to coronary artery disease (atherosclerosis) and/or myocardial infarction

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12
Q

Other than MI and atherosclerosis what else can cause heart failure

A

Severe viral infections kidney failure and sleep apnoea

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13
Q

What is meant by angina

A

Angina is where the oxygen supply to the heart is insufficient upon exertion leading to chest pain

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14
Q

What is the main cause of angina

A

Coronary artery disease

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15
Q

What are the two types of angina and how do they differ

A

Stable angina is where symptoms present during exercise. On the other hand unstable angina is where the angina can occur in the absence of exertion and is often linked to other myocardial syndromes

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16
Q

What is pulmonary hypertension

A

Pulmonary hypertension is where there is a narrowing of the pulmonary arteries. This is caused by proliferation of the vascular smooth muscle and endothelial cells

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17
Q

What are the effects of pulmonary hypertension

A

Increased pressure in the lungs and in the right side of the heart. This often results in right sided heart failure

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18
Q

What is the prognosis for patients with pulmonary hypertension

A

There is an extremely poor prognosis with patients usually surviving only 1-3 after diagnosis

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19
Q

What is Raynaud’s disease

A

This is where there is an inappropriate vasoconstriction of smaller arteries/arterioles. This is most commonly seen in the hand and fingers

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20
Q

How does Raynaud’s disease usually present

A

White then blue fingers when exposed to the cold. Then redness upon warming up (reactive hyperaemia return of blood flow)

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21
Q

What happens in severe cases of Raynaud’s disease

A

It can cause ulceration and gangrene

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22
Q

What are the risk factors for Raynaud’s disease

A

Smoking hereditary component connective tissue disorders

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23
Q

What causes Raynaud’s disease

A

The spasms in the VSMCs of the arteries are due to an overactivation of the sympathetic nervous system

24
Q

Other than avoiding cold and smoking cessation what therapies are often administered to patients with Raynaud’s

A

Vasoactive therapies that promote vasodilation

25
Q

What are the 4 pathways by which the endothelium regulate the VSMCs and what is the effect of each

A

NO – relaxation angiotensin II – constriction prostanoids – constriction and relaxation endothelin – constriction

26
Q

What are the three drugs used to target the NO pathway and trigger vasodilation

A

Glyceryl trinitrate nitroprusside and inhaled NO

27
Q

Which NO donor is commonly used in angina and how does it act

A

Glyceryl trinitrate or nitroglycerine is an NO donor used in angina. It is administered as a rapid acting spray or dissolvable sublingual tablet. Nitroglycerine is rapidly converted to NO by mitochondrial aldehyde dehydrogenase where it can then stimulate guanylate cyclase

28
Q

Which NO donor therapy is often used in severe hypertension and hospital settings where is can be delivered intravenously

A

Nitroprusside

29
Q

Which NO therapy isn’t an NO donor and is used mainly in pulmonary hypertension and in the clinical setting

A

Inhaled NO

30
Q

What is the aim of prostanoid therapy with regard to the individual prostanoids involved

A

Prostanoid therapies try to block the TP-R receptor that is responsible for contraction of the vascular smooth muscle and stimulate the IP-R receptor that is responsible for relaxation

31
Q

What is the mechanism of action of Iloprost

A

Iloprost is a stable analogue of prostaglandin I2 that binds to the IP-R and increases cAMP

32
Q

What is the main indication for iloprost

A

Pulmonary hypertension and Raynaud’s disease

33
Q

What is the mechanism of action of Epoprostenol

A

Epoprostenol is an IP-R agonist that binds to the IP-R and increases cAMP

34
Q

What is the main indication for epoprostenol

A

Pulmonary hypertension

35
Q

What is the effect of corticosteroids on the prsotenoid pathway

A

Corticosteroids decrease COX2 transcription and hence suppresses the formation of prostaglandins. These are used to cause a vasoconstriction

36
Q

Why do we want to target drugs just for the ETA receptor in terms of vascular therapies

A

The endothelin receptor ETA is specific for vascular smooth muscle cells. A drug that was an agonist of this specific receptor wouldn’t have the negative feedback activity of the ETB receptor agonists. This would be able to cause a more substantial vasodilation

37
Q

Give an example of a vasoactive drug that targets the endothelin pathway

A

Bosentan is a drug that non-specifically blocks ETA and ETB receptors and causes vasodilation. It is used in the treatment of pulmonary hypertension

38
Q

When are ACE inhibitors often used in vascular disease

A

In hypertension and heart failure where this has occurred after myocardial infarction

39
Q

What is the mechanism of action of captopril

A

Captopril blocks the active site of the ACE enzyme

40
Q

What are the side effects of ACE inhibitors

A

Hypotension drug cough proteinuria and a change in taste perception

41
Q

What is the benefit of enalapril and lisinopril over captopril

A

These drugs require conversion to an active metabolite. They therefore are much longer acting drugs

42
Q

Give some examples of AT-1 receptor antagonists used in hypertension

A

Losartan valsartan

43
Q

Which enzyme cleaves angiotensinogen to angiotensin I

A

Renin released by the JGA of the kidney

44
Q

Which enzymes converts angiotensin I to angiotensin II

A

ACE

45
Q

Where is ACE specifically expressed

A

In the renal and lung endothelium

46
Q

Where is angiotensinogen produced

A

In the liver

47
Q

As well as targeting the endotheliums’ regulation of VSMCs what other target are there for therapies in vascular disease

A

Targets of the smooth muscle itself

48
Q

What are the opposing effects of adrenoceptor agonists in the vascular system

A

Noradrenaline acting on αARs causes IP3 production and contraction of the muscle. Meanwhile adrenaline acting on βARs stimulates adenylate cyclase and cAMP production causing relaxation

49
Q

Many sympathetic nervous system-acting drugs effective in hypertension now rarely used due to multiple or severe side-effects T or F

A

T

50
Q

Which Ca2+ channel blockers are used in hypertension

A

Nifedipine verapamil and diltiazem

51
Q

Which Ca2+ channel blockers are used in angina

A

Nifedipine and diltiazem

52
Q

Which Ca2+ channel blocker is used in Raynaud’s

A

Nifedipine

53
Q

Give some examples of K+ channel activators used in hypertension

A

Minoxidil diazoxide and nicorandil

54
Q

What is the additional benefit of nicorandil that makes it useful in the treatment of angina

A

As well as it opening K+ channels nicorandil is an NO donor and is therefore quite often used in refractory angina

55
Q

How can PDE be targeted in the treatment of pulmonary hypertension

A

PDE inhibitors can be a valuable therapeutic target in the treatment of vascular disease. Sildenafil the PDE V inhibitor inhibits the breakdown of cAMP and cGMP. This causes relaxation of the smooth muscle. Hence this treatment is used for pulmonary hypertension (as well as ED)

56
Q

What is the major contraindication of PDE inhibitors

A

They should never be used in conjunction with an angina treatment such as NO donors. This could dangerously reduce blood pressure in the patients

CDL301 Cardiovascular Pharmacology (17 decks)

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