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Cardiology > Lecture 7 - Cardiovascular Pharmacology 1 > Flashcards

Lecture 7 - Cardiovascular Pharmacology 1 Flashcards

1
Q

Which vessels contain smooth muscle?

A

Arteries, arterooles, veins. Venules have some smooth muscle

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2
Q

What is the role of vascular smooth muscle?

A

Control vascular dilation and constriction of blood vessels

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3
Q

What are vascular smooth muscles innervated by?

A

Sympathetic nerves - control contraction

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4
Q

How does vascular smooth muscle regulated vascular tone?

A

Interaction between vascular smooth muscles and endothelial cells - produce Nitric oxide and endothelin

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5
Q

What does the sympathetic nervous system produce

A

Adrenaline and nor adrenaline

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6
Q

What hormones are circulated?

A

Angiotensin 2 and natriuretic peptides

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7
Q

Describe the mechanism of vascular smooth muscle contraction

A
  1. Angiotensin type 2 type 1 receptors or alpha 1 adrenergic receptors stimulated
  2. This leads to activation of phospholipase C which produces seondary messenger inositol triphosphate.
    This stimulates release of Ca2+ from the sarcoplasmic reticulum and an increase in cytosolic conc of Ca2+.
    Raised Ca2+ binds to and activates calmodulin and that activates myosin light chain kinase . This phosphorylates myosi light chain
  3. Phosphorylated myosin light chain interacts with actin to form actin - myosin cross bridges - intiates vascular smooth cell contraction.
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8
Q

How do vasodilators act?

A

act to decrease vascular tone. reduce contractility of actin - myosin complexes in vascular smooth muscles

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9
Q

What do K+ channel openers do

A

Induce vasodilation by opening ATP sensitive K+ channels: results in hyperpolarization of the cell prevents activation of the voltage gated Ca2+ channels necessary for Ca2+ influx

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10
Q

What do Ca2+ channel blockers do?

A

Cause Vasodilation by reducing the entry o extracellular Ca2+ through L-type Ca2+ channels

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11
Q

What do ACE Inhibitors do?

A

Inhibit vasoconstriction by inhibiting formation of angiotensin 2

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12
Q

Angiotensin 2 type 1 receptor anatogonists?

A

Inihibit vasoconstriction by blocking Angiotensin 2 binding to the receptor

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13
Q

Alpha 1 adrenergic receptor antagonists?

A

Inhibit vasoconstriction by blocking the binding of adrenaline and nor adrenaline to the receptor

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14
Q

What is the major role of Renin - angiotensin aldosterone system

A

Vasoconstriction and sodium retention. Maintains tissue perfusion and increase extracellular fluid volume.

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15
Q

What does overstimulation of RAS do?

A

leads to hypertension and cardiac and vascular remodelling

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16
Q

What produces renin?

A

Juxtaglomerular cells of the kidney

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17
Q

What does renin do?

A

It is a protease that cleaves the prohormone angiotensinogen (produced by the liver) to angiotensin 1

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18
Q

What does ACE do?

A

Converts angiotensin 1 to 2

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19
Q

Where is ACE highly expressed?

A

In the endothelium of the lungs and on other endothelial cells.

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20
Q

ACE has a broad substrate specificity

A

includes bradykinin

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21
Q

Which membrane receptors do angiotensin 2 bind to?

A

AT1 and AT2 receptors

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22
Q

What do juxtglomerular cells express and what happens when they are activated?

A

They express AT1 receptors (vasoconstriction) and when they are activated they inhibit renin secretion. - negative feedback loop

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23
Q

What is angiotensin At1 receptor responsible for?

A
  1. Stimulates aldosterone secretion by the adrenal glands - increases NaCl reabsorption
  2. Vasoconstriction of blood vessels
  3. Sympathtic activation of adrenaline and noradrenaline
  4. Stimulation of thirst - ADH secretion
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24
Q

Angiotensin AT2 receptor

A

Appears to have opposite effects to AT1 including vasodilation (through bradykinin and no release)
expression is mostly foetal but appears again following injury or ischaemia

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25
Q

What effect does ACE i on AT receptors?

A

They reduce activation of AT1 and AT2 which has a net effect of vasodilation.

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26
Q

What does reduced circulating levels of Angiotensin 2 lead to?

A

Increase circulation of renin and hence more angiotensin 1 formed

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27
Q

What effect do ACE i have on bradykinin

A

They decrease bradykinin degradation in order to help vasodilation and reduce BP through stimulating nitric oxide production in endothelial cells.

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28
Q

How do ACE i reduce blood pressure

A

Decrease levels of Angiotensin 2 and increase levels of bradykinin.

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29
Q

ACE i therapeutic uses?

A

anti-hypertensive, prevent left ventricular hypertrophy, MI, improve haemodynamics of people with congestive heart failure . protection against diabetic and non-diabetic nephropathy , cervical incompetence

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30
Q

Adverse effects of ACE i

A

Cough and angioedema (build up of fluid in the skin )

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31
Q

Examples of ACE i

A

Ramipril, Lisinopril, Enalapril

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32
Q

What do angiotensin 2 receptor blockers do?

A

Inhibit binding of Ang 2 to the AT1 receptor, promote vasodilation.
Developed for people with reactions to ACE inhibitors.

33
Q

What effect does ARB have on renin

A

increases renin levels and ang 1. this in turn leads to increase in Ang 2. Can also increase activation of AT2 receptors.

34
Q

DIfference between ACE i and ARB’s

A

Block Angiotensin binding to receptor and does not affect bradhykinin degradation whereas ace i decrease degradation.

35
Q

ARB’s therapeutic uses

A

Anti-hypertensives - young and diabetics. Less side -effects
Still need to monitor renal function/potassium levels

36
Q

Examples of ARB’s

A

Losartan, Valsartan, Candesartan

37
Q

Mechanism of vascular smooth muscle relaxation

A

Nitric oxde activates guanylyl cyclase by haem-dependent mechanisms. Activation results in elevated levels of cGMP and forms from guanosine triphosphate (GTP). cGMP activates myosin light chain phosphatase via cGMP-dependent protein kinase (PKG). MLCP dephosphorylates myosin light chains and inhibits interaction between phosphorylated myosin LC and actin. reduces formation of actin -myosin cross bridges and hence causes relaxation.

38
Q

What is the role of Nitric oxide?

A

NO is produced in endothelial cells and plays an important role in vascular tone and platelet aggregation.

39
Q

What factors promote endothelial synthesis of NO?

A

Shear stress, acetylcholine and bradykinin

40
Q

How is NO useful clinically?

A

As vasodilatory agents which release NO - used to treat angina GTN spray, or agents whic inhibit cGMP, phosphodiesterase type 5 (Sildenaphil) - erectile dysfunction

41
Q

What is Glyceryl trinitrate used for

A

is a prodrug - Angina, acute severe hypertension, pulmonary oedema

42
Q

Why is GTN used acutely?

A

High first pass metabolism - rapid inactivation in the liver by nitrate reductase

43
Q

Side effects of GTN

A

Mainly effects venous circulation. Side effects are headaches and hypotension

44
Q

What is nitroprusside

A

powerful vasodilatorm reacts with sulfhydryl groups to give NO. Acts equally on venous and arterial smooth muscle

45
Q

Contra indications of Nitroprusside

A

Protect from light as it turns to cyanide - hypertensive emergency

46
Q

What should GTN not be used with ?

A

Not be used together with vasodilators that combat erectile disfunction like Viagra, Cialis or Levitra. - combination can cause hypotension, circulatory collapse and death.

47
Q

Mechanism of vascular smooth muscle relaxation via stimulation of B2 adrenergic receptors

A

Activates adenylate cyclase which produces cAMP and activates protein kinase which after phosphorylation events

  1. Increase in Sarco endoplasmic reticulum Ca activity - stores Ca in SER
  2. Increases Plasma membrane Ca activity - Ca transported outside the cell.
48
Q

What is the net result of Mechanism of vascular smooth muscle relaxation via stimulation of B2 adrenergic receptors

A

Ca 2+ is transported out of the cytosol and so lowers concentration so there is decreased activation of myosin light chain kinase - relaxation
reduction in MLCK activity - less myosin light chain kinase phosphorylation - vascular smooth muscle relaxation

49
Q

How do most vasodilators work?

A

reducing the contractility of actin-myosin complexes through reducing intracellular Ca2+ or dephosphorylation of myosin LC

50
Q

Arterial and venous thrombosis therapies

A

Percutaneous cornorary intervention ( Angioplasties)

Antiplatelet therapies
COX 1 inhibition
P2Y12 ADP receptor inhibitors
alpha 2b Beta 3 integrin inhibitors

Antithrombotic therapies - Vitamin K antagonists - Warfarin/Phenindione, Heparin

51
Q

What is a complication of DVT

A

Pulmonary embolism

52
Q

What is the primary target for arterial thrombosis

A

Rupture of an atherosclerotic plaque

53
Q

What are the steps of an arterial thrombus formation

A

adhesion, activation, aggregation of platelets and platelet plug formation

54
Q

What is percutaneous coronary intervention

A

Non -surgical widening of the coronary artery, using a balloon catheter to dilate the artery and a metal stent is placed. Anti-platelet therapy is important after. involves arterial access via femoral, radial or brachial branches.Guidewire passed into the coronary artery across the stenosis.

55
Q

What are given in high risk procedures

A

Glycoproein 2b and 2a inhibitors and opiates if angina occurs during angioplasty

56
Q

Types of stents

A

Bare metal stents

Drug - eluting stents - inhibits smooth muscle cell proliferation

57
Q

After procedure care

A

Anti- platelets, aspirin indefinitely to reduce CVD risk

usually aspirin and clopidogrel

58
Q

What happens when a plaque ruptures

A

platelets recruited to site and interact with collagen and von willebrand factor.
Primary activation of platelets through thrombin activation. Integrin complex induces binding to fibrinogen - allows cross linking of platelets - further thrombus development.
Activation of this receptor complex - final common pathway for platelet aggregation.

59
Q

What are the primary targets of antiplatelet therapy?

A

Molecules involves in platelet activation and aggregation - inhibit thrombin activation and fibrinogen.

60
Q

What is clopidogrel

A

an anti-platelet drug

61
Q

What do COX 1 enzymes do?

A

Involved in protecting GI mucosa and in clotting

62
Q

How does Aspirin work?

A

Suppresses the production of thromboxanes due to irreversible inactivation of the COX 1 enzyme by platelets.

63
Q

Platelet ADP - receptors

A

P12Y12 receptors one of the receptors found on the cell surface of platelets involved in irreversible of platelet. Platelet Integrin complex formation for platelet aggregation and is important for cross-linking platelets of fibrin

64
Q

What inhibits P2Y12 ADP receptor inhibition

A

Phioenopyridines
Clopidogrel - most widely used activated by cyt p450 in the liver. irreversibly inhibits P2Y12 ADP receptor. used for patients undergoing PCI

65
Q

What do inhibitors of the glycoprotein 2b/3a receptor complex do?

A

Designed to reduce platelet aggregation
Abciximab - platelet aggregation inhibitor. used during and after procedures like angioplasty so platelets dont stick together
eptifibatide - integrilin
also antiplatelet drug of glycoprotein 2b/3a inhibitor class

66
Q

What are the triggers of a venous thrombosis

A

abnormal blood flow
altered properties of blood itself
alterations in blood vessel wall(endothelium)

67
Q

What are anticoagulants

A

Treat wide variety of conditions like venous and arterial thrombosis.
Main 2 classes - vitamin k antagonists eg. warfarin and heparins - target multiple proteases in cascade

68
Q

What is Vitamin K

A

Fat soluble vitamin

essential for production of clotting factors - 2,7,9 and 10

69
Q

WARFARIN

A

Anticoagulant effective and safe for preventing thrombosis and embolism formation. Has to be monitored closely as some medications and food interact with it.

70
Q

difference between anticoagulants and anti-platelets and thrombolytics

A

Anticoagulants, such as heparin or warfarin (also called Coumadin), work on chemical reactions in your body to lengthen the time it takes to form a blood clot. Antiplatelet drugs, such as aspirin, prevent blood cells called platelets from clumping together to form a clot. Thrombolytics - dissolve clots

71
Q

Mechanism of action of warfarin

A

Warfarin acts by inhibiting the synthesis of vitamin K-dependent clotting factors, which include Factors II, VII, IX, and X, and the anticoagulant proteins C and S

72
Q

What effects dose of warfarin

A

Up to 50% of interindividual variability of warfarin dosing due to CYP2C9 and VKORC1 polymorphisms

73
Q

Actions of heparin

A

Activates antithrombin 3 - serpin
Activation leads to a 1000 fold increase in Antithrombin 3 for thrombin and factor 10a
intravenous or subcutaneous due to high -ve charge.

74
Q

When is unfractionated heparin used?

A

Used in combination with anti-platelet agents in acute coronary events

75
Q

Low molecular weight heparins ?

A

Inactivating factor 10a and are selective. used in prevention and treatment of dvt

76
Q

What are the 2 main types of anti-platelet therapy

A

Inhibitors of activation (target COX 1 and P2Y12 ADP receptor)
Inhibitors of aggregation (target αIIbβ3-integrin complex)

77
Q

What are the anti-thrombotic therapies

A

Warfarin and heparin

78
Q

How does warfarin act

A

inhibits vitamin K epoxide reductase

leads to loss of post-translational carboxylation of four coagulation factors (II,VII, IX and X)

79
Q

How does heparin act

A 
Heparin (inhibition depends on polymer length)
Unfractionated heparins (targets thrombin and Factor Xa)
LMW heparins (Factor Xa specific)

Cardiology (12 decks)

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