Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cardiovascular System > Pharmacology of the CVS > Flashcards

Pharmacology of the CVS Flashcards

1
Q

Quantitatively describe the effects of angina pectoris

A
  • 2 million sufferers in the UK
  • annual risk of death (usually MI) of 4 - 6%
  • Quality of life impacted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes angina pectoris?

A

Caused by local myocardial Ischaemia

  • when oxygen demand exceeds supply
  • often precipitated by exertion; reversible at rest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Outline the symptoms of Angina Pectoris

A
  • Crushing chest pain (or in jaw, shoulders ,arms)
  • Ischaemic products (H+, lactate)
    -> stimulate nociceptive afferents
  • may be associated with shortness of breath, sweating
    and nausea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the risk of angina increased by?

A

Increased Systolic BP (afterload)
Increased sympathetic nerve activity
Increased Contractility
Increased vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Explain how increased afterload increases risk of angina

A

Heart has to work harder to eject blood; requires more oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does increased sympathetic activity cause angina?

A

Less diastolic time

Less coronary artery perfusion which only occurs in systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What causes increased contractility?

A

exercise
emotion
stress
aortic valve stenosis

=> all increase Oxygen demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give an example of how increased vasoconstriction trigger angina?

A

e. g.
- Redistribution of blood flow in cold weather
- During large meal blood diverted to GI
etc.

=> vasoconstriction in coronary circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the different types of angina?

A

Stable Angina
Unstable Angina
Variant (prinzmetal) Angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the pathology of Stable angina

A

most common form
- exercise induced: predictable can work out how much
exertion induces symptoms

  • not able to meet increased oxygen demand due to
    atheroma in coronary arteries
  • relieved by rest and medications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe unstable angina

A
  • induced due to minimal exertion; unpredictable
  • rest and medications may not relieve symptoms
  • may indicate thrombosis / plaque rupture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Outline the features of Variant (prinzmetal) angina

A
  • symptoms at rest
  • decreased oxygen supply due to vasospasm
    (uncontrolled vasoconstriction decreasing blood flow)
    downstream of occlusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are the different forms of angina detected?

A

All linked to acute coronary syndrome (coronary thrombosis)

- ECG will show STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the effect of stable angina during normal activity

A

In exercise, metabolic vasodilation of arterioles reduces resistance to increase blood flow to meet increased oxygen demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the effects of stable angina during exercise

A

Stenosis in coronary arteries increases resistance
at rest metabolic vasodilation occurs as normal

However/
during exercise arterioles may attempt further dilation but TPR is still too high - Oxygen demand can’t be met; angina develops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the aims of angina treatment?

A

Improve prognosis

  • prevent MI + death
  • reduce plaque progression - stabilise it
  • prevent thrombosis

Minimise symptoms
- improve quality of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the approaches to angina treatment?

A

Vasodilators: Nitrates
Cardiac depressants: Beta Blockers
Both: Ca2+ blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Explain how ꞵ Blockers aid angina treatment

A

Reduce action of sympathetic activity (NA and adrenaline) on ꞵ₁ adrenoceptors in the heart causing:

  • Slow HR and AV conduction
  • Reduced force of Contractility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the effect of slowed HR and AV conduction?

A

Increased diastolic time - increases coronary artery perfusion
Both of these factors mean more energy is required and ∴ a greater oxygen demand

20
Q

What is the effect of a reduced force of contractility?

A

Reduces myocardial work and oxygen consumption

21
Q

Name an example of a ꞵ-blocker drug used to treat high BP

A

Atenolol

more ꞵ₁ selective - ꞵ₂ found in vasculature & airways

22
Q

Describe the side effects of using atenolol

A

Bronchospasm
Fatigue
Postural hypotension

23
Q

Evaluate the use of ꞵ₁ selective drugs

A

Advantage:
ꞵ₁ selective is better as reduces side effects of ꞵ₂ e.g. bronchospasm (but is still not perfect)

Disadvantage:
Blocking ꞵ₁ causes fatigue as heart rate / force of contraction can’t be increased

24
Q

When is the use of ꞵ blockers such as Atenolol contraindicated?

A

Asthma
- don’t want to block ꞵ₁ as will cause bronchospasm

Heart blockage:

  • already poor perfusion between atria and ventricles
  • don’t want to block AV conduction further via AV node
25
Explain how Ca2+ channel blockers provide anti-anginal effects
Reduces contractility by reducing Ca2+ entry into cardiac myocytes / vascular smooth muscle cells
26
Describe the effects on the CVS of Ca2+ channel blockers
Direct coronary vasodilation ∴ more coronary blood flow Reduced TPR/BP/afterload ∴ heart works less hard to eject blood Reduced force of contraction ∴less oxygen consumption
27
What are the 3 different sub types of Ca2+ channel blockers?
Vascular - dihydropyridines e.g; amplodipine, nifedipine Cardiac - Benzothiazepines e.g; Verapamil Both - Diphenylalkyamines e.g; Diltiazem
28
What are the side effects of dihydropyridines?
lower limb oedema due to increased Pc Flushing and headaches due to vasodilation Reflex tachycardia
29
How do dihydropyridines cause reflex tachycardia?
Dihydropyridine induced vasodilation causes increased sympathetic activity (baroreflex) HR/Contractility - negative in angina
30
What is a major caution of using Ca2+ channel blockers in the heart?
Blocking Ca2+ channels in the heart may alter electrical conduction and contractility
31
How is NO produced / donated in the body?
1. ENOS - endothelium NO synthesis - conversion of L-arginine -> NO 2. NO donors cause dilation of smooth muscles 3. NO -> cGMP -> PKG / GMP via PDE5
32
What is NO production / donation stimulated?
Shear stress ACh Histamine Bradykinin
33
Describe some essential features of NO gas
Lipophilic, soluble gas Continually produced and released Diffusible endothelium -> surrounding vascular smooth myocytes
34
What is the effect of Protein Kinase G (PKG) produced from NO on CVS?
PKG reduces smooth muscle tone: - via myosin light chain dephosphorylation - increased Ca2+ uptake by SR, decreasing cytoplasmic levels - activates K+ channel s causing hyperpolarisation -> closing VGCCs
35
Where does vasodilation occur?
Coronary artery and veins
36
What is the effect of coronary artery dilation?
Coronary artery dilation: - reduces TPR - decreasing afterload - increases collateral arteriole dilation - shunts blood from areas of good perfusion
37
What is the effect of venodilation?
Decreases intraventricular pressure to decrease cardiac preload
38
Give examples of drugs used to cause vasodilation
GTN (glyceryl trinitrate) - spray, sublingual tablets Isosorbide mononitrate - oral, longer acting - high oral dose (1st pass metabolism by liver)
39
Name other anti-anginal drugs
Nicorandil Ivabradine Ranolazine
40
Explain the effects of Nicorandil
K+ channel activator causes hyperpolarisation; decreased VGCCs and Ca2+ entry -> coronary vasodilation Has nitrate moiety ∴ has venodilation action via NO production
41
Describe the effects of Ivabradine
Specific If current inhibitor in SAN - slows HR - Decreases pacemaker potential frequency - Decreases HR reducing myocardial oxygen demand
42
Explain the effects of anti-anginal drug, Ranolazine
``` Late Na+ current inhibitor reduces Ca2+ in ischaemic myocardiocytes reduces Oxygen demand reduces compression of small intra-myocardial vessels -> improves myocardial perfusion ```
43
Name some prophylactic angina drugs
Aspirin Clopidogrel Statins
44
Explain the effects of Aspirin on Angina
Inhibits COX | Decreases Thromboxane A2 and platelet aggregation (GpIIb/IIIa) expression
45
How does Clopidogrel prevent angina?
Inhibits ADP receptor on platelets, reducing aggregation
46
Why are Aspirin and Clopidogrel often used together?
Both reduce thrombosis and can be used together as they have entirely different mechanisms
47
What is the effect of Statins?
HMG-CoA Reductase inhibitor - decreases cholesterol levels

Cardiovascular System (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions