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Pharmacology > Cardiovascular pharmacology > Flashcards

Cardiovascular pharmacology Flashcards

1
Q

Name an example of thrombin-receptor antagonists and explain its mechanism of action.

A

Voripaxar
- prevents activation of PAR-1 receptors on platelets by thrombin. This drug therefore prevents platelet activation (clotting cascade)

No adverse bleeding

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2
Q

What is define as vascular tone? And what determines it?

A

Vascular tone refers to the degree of constriction relative to its maximally dilated state

Determines by vasoconstrictor and vasodilator

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3
Q

What is the definition of blood pressure?

A

Cardiac output x peripheral vascular resistance

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4
Q

Cardiac output depends on two factors which are:

A

Stroke volume

Heart rate

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5
Q

There are two main antithrombotic drugs that target the platelet activation pathway. Name them and state the molecule they target.

Why is a small amount of these drugs effective?

A

Aspirin - targets COX (cyclooxygenase) preventing thromboxane formation. BLOCKS THE PLATELET ACTIVATION PATHWAY

Clopidogrel - P2Y12 receptor antagonists (irreversible blocker). BLOCKS THE ACTIVATED PLATELET PATHWAY

Because platelets have not nucleus and both inhibition are irreversible, therefore inhibition cannot be overcome until new platelets are made. However both can cause problems with bleeding.

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6
Q

Describe the mechanism of action of ezetimibe

A

Inhibition of cholesterol absorption by blocking transport of cholesterol in gut, without affecting the absorption of fat soluble vitamins and triglyceride

Extra: added to statin if response is inadequate alone

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7
Q

There are three hormones released to the vascular system through the stimulation of the sympathetic nervous system what are they? And what effect do they have on the BP?

A

Adrenaline

Ang II

Vasopressin

All are vasoconstrictor which increases BP

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8
Q

Explain the mechanism of K+ channel blockers in treatment of Angina and name an example. Also state its side effects

A
  • opens the K(ATP) channels in smooth muscle which causes vasodilation
  • releases NO
    E.g. nicorandil

Side effects: dizziness, headache, flushing (side effect caused because the drug is NON selective)

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9
Q

How is the name of the enzyme secreted by the kidney when BP is low? And how does this enzyme work to produce its effect on the pre-load and after-load?

A

In response to low pressure, kidney secreted renin
Renin is secreted to the plasma where it catalyse the conversion of angiotensinogen to Ang I

Ang I is converted to Ang II by ACE (angiotensin-converting enzymes)

Ang II directly causes vasoconstriction -> increase PVR -> increase after-load

Ang II also stimulates the release of aldosterone, promoting sodium hence water retention by the kidney -> increase blood volume -> increase pre load

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10
Q

Antithrombotic drugs such as aspirin and clopidogrel often cause bleeding. Name a novel drugs which do not increase bleeding time and explain its mechanism of action.

A

Cangrelor - Reversible P2Y12 receptor antagonists which prevents platelet activation through ADP.

Binding between drugs and receptor is non-covalent hence, there is no need to make new platelets.

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11
Q

What are the three types of treatment of cardiac arrythmias?

A
  1. Cardioversion: electrical resynchronisation to sinus rhythm
  2. Surgery intervention: tissue ablation and replacement with artificial pacemaker
  3. Drug intervention: anti-arrhythmic drugs (along with anti-platelet and coagulant to prevent clotting)
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12
Q

There are three physiological factors that control blood pressure what are they?

A
  • autonomic NS
  • kidney
  • baroreceptors
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13
Q

Describe the formation of fatty streak

A

Endothelial dysfunction -> increase ell permeability -> increase leukocytes adherence -> leukocytes ingest oxidised LDL (due to interaction with oxygen free radicals) -> foam cells formation

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14
Q

What class of drug does spironalactone falls into and what does it affect?

A

Mineralocorticoid receptor antagonists acting on the kidney

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15
Q

What is another name for when the rate of HR is increased (1), decreased (2) and disorganised (3)

A

(1) tachycardia
(2) bradycardia
(3) fibrillination

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16
Q

In the heart, what is the name of the receptor corresponding to sympathetic and para sympathetic stimulation? And how does the sympathetic receptor regulate HR?

A

Sympathetic: beta1 - adrenoreceptors
-> Regulate HR by decreasing the rate of depolarisation of AP

Para: M2 receptors

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17
Q

What is the mechanism of statins?

A

Inhibits the enzyme HMG-CoA reductase
Statins reduce the formation of cholesterol hence LDL and increase LDL receptor expression -> LDL internalised and removed it

Other known benefits of statins:

  • improved endothelial function
  • inhibition of inflammation
  • plaque stabilisation
  • inhibition of thrombus formation
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18
Q

What is meant by venous return?

A

The amount of blood entering ventricle during diastole

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19
Q

What is the name of the enzyme which degrades cGMP?

A

cGMP phosphodiesterase

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20
Q

What is the function of a fibrinolytic clot buster drugs? And explain its mechanism of action. Name an endogenous and exogenous fibrinolytic agents.

A
  • degrades fibrin, remove clot therefore restore blood supply to the heart
  • it degrades fibrin in thrombus by accelerating the conversion of plasminogen to plasmin
  • endogenous fibrinolytic agents: tissue plasminogen activator (tPA)
  • exogenous fibrinolytic agents: streptokinase
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21
Q

Name examples of calcium-channel antagonists and state their mechanism of action.

A

Nifedipine, verapamil and dilthiazem

  • block L-type voltage-gated Ca2+ channels and reduce muscle contraction
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22
Q

What are the two factors causing the activation of platelets?

A

Collagen and thrombin

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23
Q

Name an orally active anti-coagulants which blocks the action of Vitamin K. Describe how is it able to prevent clotting.

A

Warfarin, blocks the enzyme vitamin K epoxide reductase which reactivates vitamin K.
Without vitamin K, active factors VII, IX and X have a reduced ability to form clotting.

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24
Q

What are the symptoms of heart failure? Hint: refer to the vicious cycle of CHF

A
  • myocardial infarction
  • uncontrolled hypertension
  • fluid overload
  • myocarditis
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25
Q

What effect does the sympathetic NS have in the arterioles and veins?

A

Arterioles: increase after load -> increase PVR

Vein: increase pre-load -> increase blood pressure

26
Q

Explain the mechanism of NO in smooth muscle relaxation

A

NO is synthesize in the endothelium through the conversion of L-arginine by the enzyme NO synthase

NO diffuses through the underlying smooth muscle where it stimulates guanylyl cyclase (GC). GC catalyse the conversion of GTP to cGMP. cGMP decreases the [Ca2+]i leading to muscle relaxation

27
Q

What are the three class of drugs used to treat chronic angina?

A
  1. Beta adrenoreceptor antagonists
  2. Ca2+ channel blocker
  3. K+ channel blocker
28
Q

Name a drug which inhibits Factor Xa and which coagulation pathway does it block?
Name another drug which is a direct inhibitor of thrombin (factor II) enzyme activity.

A
  1. Rivaroxaban - blocks both the intrinsic and extrinsic coagulation pathways
  2. Dabigatran - directly inhibits the formation of thrombin through inhibiting the enzyme
29
Q

What causes renin release and activation of the RAAS system?

A

Sympathetic activation mediated by beta-1 adrenoreceptors located in the aortic arch

30
Q

Name three beta-receptor antagonists. Which receptors are they selective for? And how do they help to reduce BP?

A

Propranolol - B1 and B2
Atenolol and metoprolol - B1 selective

  • reduce cardiac output
  • reduce renin release from the kidney -> decrease RAAS activation -> reduce pre-load and after-load
  • action in CNS to reduce BP (parasympathetic stimulation)
31
Q

What causes endothelial dysfunction?

A
  1. Elevated levels of LDL -> hypercholesterolamia
  2. Oxygen free radicals caused by smoking
  3. Infectious microorganism such herpes virus
  4. Physical damage and gene activation cause by high turbulent flow

All of the above cause a common factor - oxidative stress which is an imbalance between reactive oxygen species manifestation and its elimination this ultimately leads to reduction of NO

32
Q

What determines contractility?

A
  • sympathetic nervous system
  • circulating hormones
  • Frank-Starling Mechanism
33
Q

Name one example of nitrates for treatment of acute angina and explain how it helps to treat symptoms.

A

Glyceryl trinitrate

organic nitrates release NO

Therefore it relaxes venous circulation: decreasing venous return hence PRE LOAD -> decrease stroke volume -> decrease cardiac output

Effect on coronary arteries: improves supply if you have a coronary spasm and dilate collaterals and redistribute blood

34
Q

Explain how beta-receptor antagonists able to reduce symptoms of chronic angina.

A

Affecting the sympathetic NS

  • reduce HR therefore O2 demand (sympathetic NS increases HR)
  • decrease pre load (blood volume) therefore O2 demand (sympathetic NS activates the RAAS)
  • increase duration of diastole, increasing O2 supply
35
Q

Name an anti-coagulant drug which activates Antithrombin III. Expand its mechanism of action.

A

Heparin

  • activator of anti-thrombin III through binding of both ATIII and protease
  • accelerates neutralisation of serine protease (XIIa, XIa, IXa, etc)
  • not orally active (need to be injected)
36
Q

What is meant by after load and pre load? And what happens to the BP if both after load and pre load increases?

A

After load is the force/pressure against the chamber of the heart in order to eject blood throughout the body

Pre load is the amount of blood coming back to the heart

After load increases -> increases the resistance (constrict smooth muscle) -> increase blood pressure

Pre load increases -> increase stroke volume -> increase CO hence BP

37
Q

What is the characteristic of a stabilise plaque and what does it cause?

A

Stabilise plaque is define by its thick fibrous cap, a healing response to injury. It is less prone to rupture but it is the cause of angina (chest pain)

38
Q

Explain the mechanism of action of Ca2+ channel blockers in treating Angina. Name an example

A
  • block entry of Ca2+ into cells via L-type Ca channel
  • also known as Ca2+ antagonists
  • reduce force of CONTRACTION and therefore O2 demand

E.g. verapamil

39
Q

What is the difference between primary and secondary hypertension?

A

Primary hypertension has no identifiable cause e.g. could be genetic or environmental

Secondary hypertension, the cause is identifiable e.g. kidney failure (increase Na retention), adrenal disease

40
Q

In cardiac action potential graphs, there is a phase where the slope is close to zero, what is causing this observation?

A

After the rapid closure of NaVGC, the KVGC which immediately followed by the opening of CAVGC. The simultaneous entering of Ca2+ and efflux of K+ causes that part of the graph to be that way.

41
Q

What is the target for the drug sildenafil (viagra) and what is its effect?

A

Inhibition of cGMP phosphodiesterase leading to increase of [cGMP] this causes relaxation due to decrease in Ca2+ conc

42
Q

What is the role of kidney in regulating blood pressure and which cells/group of cells is responsible for detecting the blood pressure?

A

Kidney is important in the LONG TERM control of BP

Pressure is detected in the juxtaglomerular cells near the afferent arterioles

43
Q

What is meant by myocardial infarction and what is the cause?

A

Myocardial infarction is caused by rupturing of plaque leading to thrombosis

MI is the loss of supply of blood to part of the heart caused by blockage in coronary artery. This results in lack of O2 in the heart -> cells die -> cannot transmit contraction signal properly -> heart failure

44
Q

What is the function of glycoproteins on the surface of endothelium?

A

To monitor blood flow

45
Q

What determines the venous return/preload?

A

Capacitance and Na+ and water excretion in the kidney

If capacitance decreases (constricts) venous tone (which reflects venous pressure and resistance) increases
If Na+ and water excretion decreases, blood volume increases (higher venous return/preload)

46
Q

State the definition of Cardiac Arrhythmias

A

The irregular beating of the heart (disturbance in heart beat) due to abnormal pulse generation or abnormal impulse conduction

So two possibilities: either the GENERATION or CONDUCTION of pulse

47
Q

Name 4 mediators release by endothelium.

A

NO
prostacyclin (PGI2)
Endothelin-1
Ang II

48
Q

Describe the ‘vicious’ cycle of congestive heart failure

A

-> vasoconstriction and fluid retention -> increase pre load and after load -> decrease CO due to reduce function of left ventricle -> activation of sympathetic NS (NA) and RAAS pathway ->

49
Q

Two examples of non-pharmacological approach to treating hypertension are weight loss and increase exercise, what are the other two?

A

Reduce dietary salt

Alcohol reduction

50
Q

There are 2 pathway to generate NO, (1) through conversion of L-arginine, so what is the other one?

A

Through nitrate, an enzyme which can release NO to cause relaxation.

We can be desensitised.

51
Q

How does DIURETICS help to regulate high BP?

A

Increase Na+ and water loss, therefore reduces blood volume and PRE-LOAD

SOME have direct effects on arteriole tone therefore decreasing after-load

52
Q

Treatment of Angina uses the principle of reducing demands. There are different treatments for acute angina and chronic. List the treatments for both symptoms.

A

Acute (during attack): rest and organic nitrates

Chronic:

  • beta adrenoreceptor antagonists
  • Ca2+ channel blocker
  • K+ channel activators
53
Q

What are the three structures responsible for the conducting system causing rhythmic contraction in the heart?

A
  1. AV node - pacemaker origin of AP, involuntary firing
  2. SN Node
  3. Bundle of His which proceeds to travel down through the Purkinje fibres.
54
Q

Concerning drugs affecting the RAAS system.

1) Name an example of renin inhibitor.
2) Name examples of ACE inhibitors
3) Name examples of AT1 receptor antagonists

What are the main effects of drug affecting the RAAS system?

A

1) Aliskiren
2) Enalapril and lisinopril
3) Losartan and candesartan

Decrease pre-load and after-load

55
Q

There are two types of diuretics what are they? Name examples of the drugs and their mechanism of action.

A

Thiazides diuretics: bendrofluazide, chlorothiazide

  • inhibit Na+ reabsorption in distal tubule
  • also dilate arterioles

Loop Diuretics: frusemide
- impair Na+ reabsorption in ascending loop of Henle

56
Q

There are four basic mechanisms of cardiac arrythmias, name all of them.

A

(1) heart block - damage to the AV node cause by infarction or fibrosis
(2) abnormal pacemaker activity - where spontaneous pacemaker activity arise in parts of the heart other than the AV node due to catecholamines or Ischemia damage
(3) re-entry - impulse re excites region of myocardium after refractory period (re-entrant conduction). This occurs when there is a damage in myocardium
(4) delayed after depolarisation - additional depolarisation of non-excitable cells before previous depolarisation is complete.

57
Q

What is peripheral vascular resistance? And what does it affect?

A

It is the resistance in the artery and a main contributor affecting after load

58
Q

What determines cardiac contractility?

A
  • sympathetic nervous system
  • circulating hormones
  • Frank-Starling mechanism
59
Q

Describe the mechanism of fibrates such as gemfibrozil and fenofibrate in reducing development of atherosclerosis.

A

Decrease circulating VLDL and triglyceride, increase protective HDL, slightly decrease LDL

Activate PPAR-alpha agonists, increase expression of genes associated with lipid clearance

60
Q

What does a sympatholytic drug does? Name some examples and their mechanism of action.

A

Sympatholytic drugsinhibit the release of NA or block it effects at receptors

  • methyldopa (ganglion blockers)
  • guanethidine (adrenergic neuron blockers)
61
Q

Name two surgery intervention in effort to restore the vessels.

A

Balloon angioplasty and Stenting

62
Q

What is meant by Angina pectoris?

A

Intermittent (occurring at irregular intervals) chest pain cause by a mismatch between oxygen demand by the heart and oxygen supply to the heart.

Pharmacology (8 decks)

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