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Cardiovascular, Renal & Peripheral Nervous System Pharmacology > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

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1
Q

What are the P wave, QRS complex and T wave representations on the ECG for?

A

P wave = Depolarisation of the Atria
QRS complex = Depolarisation of the ventricles
T wave = Repolarisation of the ventricles

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2
Q

In a Ventricular Action Potential there are 5 phases (0-4). What are they? (Contractile Myocytes)

A 
0 = Depolarisation
1 = Rapid Repolarisation
2 = Plateau
3 = Repolarisation 
4 = Baseline Potential
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3
Q

Pacemaker cells have a different Action Potential sequence to contractile myocytes. Highlight the action potential they go through.

A

0 = depolarisation
3 = repolarisation
4 = baseline potential
repeat

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4
Q

Membrane depolarisation and repolarisation is a results of ion flows across the membrane of the cell. What ion channels are responsible for depolarisation and repolarisation?

A

Depolarisation:
Sodium INFLUX, Calcium INFLUX

Repolarisation:
Potassium EFFLUX, Active Na+-K+-ATPase

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5
Q 
What do the following in the ECG represent?
PR Segment
PR Interval
ST Segment
QT Interval
A

PR Segment = AV Delay
PR Interval = Atrial Systole
ST Segment = Ventricular Plateau
QT Interval = Ventricular Depolarisation & Repolarisation

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6
Q

What are the ion mechanisms for a contractile myocyte action potential? Describe with the 5 phases (0-4)

A 
0 = Rapid Na+ influx via Voltage Activated Sodium Channels (iNa)
1 = Transient K+ efflux (iTO1)
2 = Ca2+ influx via L-Type Voltage Activated Calcium Channels (iCa(L))
3 = K+ efflux via: slow (iKs) & rapid (iKe) delayed rectifier potassium channels, also via iK1
4 = K+ efflux via iK1
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7
Q

What is absolute/effective refractory period?

A

The refractory period when the generation of the next action potential is not even possible at the strongest stimulus.

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8
Q

What is relative refractory period?

A

When the generation of the next action potential is possible, but requires a stronger stimulus.

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9
Q

Describe the mechanism of refractoriness

A
  1. Depolarisation stimulus opens Voltage Gated Sodium Channels
  2. They are rapidly INACTIVATED. If depolarisation is maintained (plateau), channels cannot be reopened until…
  3. Repolarisation below the threshold voltage (-65mV) recovers Na+ channels from inactivation moving them into the closed state.
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10
Q

Why does prolonging refractoriness in the heart a problem?

A

Causes a long QT interval which can promote cardiac dysrhythmias.

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11
Q

Describe the ion mechanisms that occur in a Pacemaker Potential.

A 
4 = Pacemaker current
4 = Voltage gated T-type Calcium influx, iCa(T)
0 = Voltage Activated L-Type Calcium influx, iCa(L)
3 = Voltage Activated K+ Channels efflux, iK
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12
Q

What 2 ways activate iF (funny current)?

A 
Membrane repolarisation (hyperpolarisation)
Directly by cAMP (kinase dependent phosphorylation)
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13
Q

How is the iF current modulated by the Peripheral Nervous System?

A

Sympathetic: STIMULATION via β1 adrenoceptors; increases current.
Parasympathetic: INHIBITION via Muscarinic M2 receptors; decreases current

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14
Q

What functions does the iF current have?

A

Cardiac Automaticity

Heart Rate control by the PNS and Adrenaline

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15
Q

What drug will inhibit the iF current?

A

Ivabradine

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16
Q

Describe the Ion Mechanisms for the modulation of the Pacemaker potential via the Peripheral Nervous System.

A 
Sympathetic: 
1) β1 Adrenoceptor is stimulated 
2) Increase Adenylyl Cyclase
3) Increase Cellular cAMP
4) Increase iF current
5) Increase the rate of pacemaker depolarisation
6) Increase conduction velocity 
RESULT: INCREASED HEART RATE

Parasympathetic:
1) M2 receptor is stimulated 
2) Decrease Adenylyl Cyclase
3) Decrease Cellular cAMP
4) Decrease iF current
5) Decrease the rate of pacemaker depolarisation
6) Decrease conduction velocity 
RESULT: DECREASED HEART RATE
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17
Q

What are the 3 major pathways and 1 minor pathway of contraction through calcium entry and release?

A

MAJOR PATHWAYS:

1) Activation of L-VACC (Voltage Activated Calcium Channels) - responsible for phase 2 plateau - provides the influx of Ca++ ions.
2) Activation of RyRs on the Sarcoplasmic Reticulum (SR)
3) Calcium-Induced Calcium release from the Sarcoplasmic Reticulum

MINOR PATHWAY:
4) Ca++ influx via Ca++/Na+ Exchanger (NCX)

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18
Q

What are the activators and inhibitors of RyR2 (cardiac Ryanodine Receptors)?

A

Activators:
Ca++ ions
Ryanodine (at nanomolar concs)

Inhibitors:
Ryanodine (At micromolar concs)

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19
Q

What are the sensitisers for RyR2?

A

Caffeine
Halothane
CATECHOLAMINES

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20
Q

What are the MAJOR and MINOR calcium pathways for cardiac muscle relaxation?

A
  1. Ca++ REUPTAKE into the Sarcoplasmic Reticulum via SERCA (Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase) (70-80%)
  2. Ca++ extrusion by Na+-Ca++ exchanger (NCX) (20-30%)
  3. Ca++ extrusion by Ca++-ATPase (Ca++-pump) ~1% Ca++ removal
  4. Ca++ uptake into mitochondria via mitochondrial Ca++ uniporter (~1% Ca++ removal)
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21
Q

What regulates the Cardiac Isoform of SERCA (SERCA2a)?

A

Phospholamban (PLB)

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22
Q

How does PLB regulate Ca++ reuptake?

A

RE-UPTAKE

1) β1 adrenoceptors are stimulated from catecholamines
2) PKA is activated.
3) PKA promotes the phosphorylation of PLB
4) Phosphorylated-PLB promotes faster re-uptake and therefore faster relaxation

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23
Q

The Sodium-Calcium Exchanger (NCX) has two different modes. What are they and how do they work?

A

1) Forward (Normal) Mode - Responsible for repolarisation in phase 3 of AP.

Activated by a build up of cytosolic Ca++ during the cardiac AP
Extrude 1 Ca++ ion in exchange for 3 Na+ ions.

2) Reverse Mode - Responsible for the depolarisation in phase 0 of AP

Activated by a build up of cytosolic Na+
Exclude 3Na+ ions for 1 Ca++ ion

Increase in cytosolic [Ca++] (MINOR ROLE)

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24
Q

Sympathetic stimulation has the effects of both increasing AND decreasing the concentration of cytosolic Calcium. Why?

A

Increase in [Ca++]:

1) increase in calcium influx via L-voltage activated calcium channels activation
2) Increase in calcium release via RyR2 activation
3) Increase in calcium sensitisation via Tropinin I phosphorylation

Decrease in [Ca++]:
1) Increase in calcium reuptake via increase in SERCA activity (PLB-mediated)

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25
What drug binds to the Ca++-TNC complex to prolong systole action?
Levosimendan
26
Describe the ion mechanism in cardiac glycosides (eg. Digoxin)
Digoxin will inhibit the Na+/K+-ATPase by binding to the extracellular K+ binding site of the ATPase. There will be an indirect activation of the REVERSE MODE of the NCX as a result of the accumulation of the intracellular Na+, thus resulting in an increase in cytosolic Ca++.
27
What is digoxin used for?
Congestive Heart Failure | Antidysrhythmic: Atrial Fibrillation & Atrial Flutter
28
In terms of coronary circulation, what are the roles of the left and right coronary artery?
Left Coronary Artery: supplies the left and right sides of th heart (about 85% of CBF) Right Coronary Artery: Supplies the SA node, AV node and right side of the heart
29
What cardiac metabolites will cause vasodilation of the coronary arteries?
Adenosine Potassium Hypoxia (decreased tissue partial oxygen)
30
In an emergency with heart block, what drugs are used?
Atropine (IV), or Isoprenaline (IV)
31
There are several mechanisms behind tachydysrhythmias, what are they?
Automaticity: Enhanced (Sympathetic overreactivity) Abnormal (Ectopic pacemaker) Triggered: Early after depolarisation (EAD) - TORSADES DE POINTES Delayed After Depolarisation (DAD) Reentry
32
There are three types of Re-entry. What are they?
``` AV Node and Atria (AVNRT) Purkinje Fibres (VT) Accessory Pathways (AVRT) ```
33
Re-entry causes what on an ECG?
An atrial echo
34
What is the common cause of Atrial Fibrillation?
Random ectopic activity from the pulmonary vein in the left atrium
35
Classify antidyrhythmic drugs according to the Vuaghan-Williams Classification
Class I: Na+ Channel Blockers Class II: β-Blockers Class III: Drugs that prolong the action potential duration Class IV: Calcium Channel Blockers
36
What is the main mechanism of Class I antidysrhythmics?
Blockage of FAST voltage activated Na+ Channels
37
Class I antidysrhythmics are classified based on their dissociation rate and are therefore classified into three sub-types. What are they?
Class Ia: Intermediate Dissociation Rate Class Ib: Fast Dissociation Rate Class Ic: Slow Dissociation Rate
38
What are the drugs in each subtype of Class I Antidysrhythmics?
Ia: Disopyramide, Procainamide, Quinidine Ib: Lignocaine, Mexilitine Ic: Flecainide, Propafenone, Moricizine
39
Class Ia drugs have what effects on the Cardiac Action Potential and what effects on the ECG?
Cardiac Action Potential: decreases Vmax, increases duration | ECG: increases QRS duration, increases QT interval
40
Class Ib drugs have what effects on the Cardiac Action Potential and what effects on the ECG?
Cardiac Action Potential: No effect on Vmax, Decrease in duration ECG: QRS duration unchanged, but a modest decrease in the QT interval NB Blocks extra heart beats
41
Class Ic drugs have what effects on the Cardiac Action Potential and what effects on the ECG?
Cardiac Action Potential: Decrease in Vmax, Small increase/no effect on Action Potential ECG: Increase in QRS duration modest increase in QT interval
42
From each Class I antidysrhythmic subtypes, list the most relevant drug, and its therapeutic use.
``` Class Ia: Disopyramide - Atrial Fibrillation - Ventricular Tachycardia Class Ib: Lidocaine -Ventricular Tachycardia & Ventricular Fibrillation Class Ic: Flecainide -Paroxysmal Supraventricular Tachycardia (due to AVNRT) -Atrial Fib. & Flutter -WPW syndrome ```
43
What are the clinical uses of Class II Antidysrhythmics (β-Blockers)?
Rate control in Supraventricular Tachycardias (due to increased sympathetic activity) Rate and rhythm control in Atrial Fibrillation & Flutter Ventricular Fibrillation
44
What are the drugs that are classified under Class III antidysrhythmics?
Amiodarone, Sotalol, Bretylium
45
What is the common mechanism behind Class III antidysrhythmics?
Blocking voltage-activated K+ channels & prolonging the repolarisation (phase 3)
46
What are the side effects of Amiodarone?
``` Dysrhythmias Thyroid Abnormalities Corneal Deposits Pulmonary Disorders Skin Pigmentation ```
47
What are the drugs under the Class IV antidysrhythmics?
Verapamil, Diltiazem
48
What is the mechanism Class IV antidysrhythmics undergo?
They block voltage-activated L-type Calcium channels
49
What is the main effect of a Class IV antidysrhythmic?
Slows down conduction at the Atrio-Ventricular node
50
What are they main side-effects of a Class IV antidysrhythmic?
Bradycardia Negative inotropic effect Constipation (Verapamil) Hypotension (more with Diltiazem)
51
What main drug interaction does Verapamil have with, and what is it?
with Digoxin, and it increases Digoxin toxicity.
52
There are certain antidysrhythmic drugs that fall out of the Vaughan-Williams classification. What are they and what are their therapeutic indications?
-Atropine (IV route) for Sinus Bradycardia (β-Blocker overdose) -Isoprenaline (IV route) for heart block -Adrenaline for cardiac arrest Adenosine (IV route) for PSVT (Paroxysmal Supraventricular Tachycardia) -Digoxin for rapid Atrial Fibrillation (rate controlling)
53
What is the blood pressure equation?
Blood Pressure = Cardiac Output x Total Peripheral Resistance (Cardiac Output = Heart Rate x Stroke Volume)
54
What factors affect contractile activity?
1) Spontaneous electrical activity in the plasma membrane of the muscle fibre 2) Neurotransmitters released by automatic neurons 3) Hormones 4) Locally induced charges in the chemical composition of the extracellular fluid surrounding the fibre 5) Stretch
55
How does a SMOOTH muscle contract?
1) Increase in cytosolic Ca++ 2) Ca++ binds to calmodulin in cytosol 3) Ca++-Calmodulin complex binds to myosin light chain kinase (MLCK) 4) MLCK uses ATP to phosphorylate myosin cross bridges 5) Phosphorylated cross-bridges bind to actin filaments 6) Cross bridge cycle produces tension & shortening This is a SLOW process
56
How does a SKELETAL muscle contract?
1) Increase in cytosolic Ca++ 2) Ca++ binds to tropinin on thin filaments 3) Conformational change in tropinin moves tropomyosin out of position 4) Myosin cross bridges bind to actin 5) Cross-bridge cycle produces tension and shortening. This is a FAST process
57
What are the main mechanisms in increasing cytosolic Ca++ in Smooth Muscle?
1) Agonist-induced IP3-mediated intracellular Ca++ release from the Sarcoplasmic-Reticulum (SR) 2) Extracellular Ca++ influx via vascular voltage-gated L-type calcium channels
58
How can we facilitate the relaxation of smooth muscle?
1) Inhibition of MLCK | 2) Activation of MLCP
59
What are the two main vasodilators produced by endothelial cells?
1) Nitric Oxide (NO) or Endothelium-Dervied Relaxation Factor EDRF) 2) Prostaglandin I2 (PGI2)
60
There are three isoforms of Nitric Oxide Synthase. What are they, and where are they found (respectively)?
1) Endothelial NOS (eNOS) - abundant in endothelial cells 2) Neuronal NOS (nNOS) - in neurons (NANC transmitter) 3) Inducible NOS (iNOS) - upregulated in inflammation in macrophages
61
What are the typical symptoms of Angina Pectoris?
Chest in the front of the chest, often radiated to the neck, jaw, shoulders or arms
62
What are the first line treatments of Angina?
β-blockers - Atenolol, Acebutolol, Pindolol, Propanolol, Labetolol Ca++ Channel Blockers - Nifedipine, Amlodipine, Diltaziem, Verapamil
63
What treatments are used as a 2nd line treatment in angina? (or when CCBs/β-blockers are contraindicated)
Organic Nitrate Vasodilators Ivabradine (iF current inhibitor) Nicorandil Ranolazine
64
Isosorbide Mononitrate, Isosorbide Dinitrate, Glyceryl Trinitrate & Sodium Nitroprusside are example of what type of drugs?
Nitric Oxide Donors
65
How do Organic Nitrates work?
Dilation of collateral vessels which increases oxygen supply to ischaemic myocardium Systemic Vasodilation dramatically decreases preload and slightly decreases afterload which ultimately decreases the cardiac oxygen demand
66
In stable angina, what are the treatments for: acute pain, and prevention?
Acute Pain: Short lasting GTN sublingual spray | Prevention: Long lasting isosorbides (orally)
67
What is the first line treatment in unstable angina?
GTN IV infusion
68
What is the first line treatment for variant angina?
Nitrate Vasodilator + Calcium channel blocker
69
What are the side effects or Ivabradine?
Blurred vision Bradycardia AV Block Arrythmias
70
What the mechanisms behind the drug "Nicorandil"?
Activates vascular ATP-sensitive K+ channels | Release NO => increases cGMP
71
How does Ranozaline work?
Inhibits late Na+ channels
72
What are the therapeutic uses for Ranozaline?
In unstable angina | Protects cardiac muscles from ischaemic damage
73
What characterises a STEMI?
ST elevation on the ECG
74
There are two types of NSTEMI, what are they?
ST-depression | T-inversion
75
There are prophylaxis for unstable angina. What are they?
Aspirin: 300mg loading dose, and continue indefinitely Fondaparinux: patients who do not have a high bleeding risk Unfractioned heparin: if angiography is likely within 24 hours
76
What are the antiplatelet agents and what are their mechanism of action?
Aspirin: COX-1 Inhibitor Clopidogrel: ADP Receptor antagonsist Dipyramidole: Phosphodiesterase Inhibitors ABCIXIMAB, Eptifibatide, Tirofiban: Glycoprotein IIb/IIIa inhibitors
77
What are the therapeutic indications of Aspirin?
Primary prevention of Acute Coronary Syndrome (ACS) In unstable angina (300mg loading dose) Secondary prevention of Myocardial Infarction
78
What is the mechanism for Clopidogrel?
Irreversible block of Gi-coupled P2Y12 receptors
79
How does Dipyramidole work?
Decreased platelet activation and aggregation. | Vasodilation
80
What are the different anticoagulants?
``` Heparin and LMWHs Fondaparinux Rivaroxaban Huridin Dabigatran Etexilate Warfarin ```
81
What are the side effects of Heparin?
Bleeding Immune Thrombocytopenia Osteoporosis Hypersensitivity
82
What is the antidote for Heparin?
Protamine Sulfate
83
What is Fondaparinux used for?
Acute Coronary Syndromes (eg. STEMI, NSTEMI, Unstable Angina) Stroke Deep Vein Thrombosis Pulmonary Embolism Used as a prophylaxis of venous thromboembolism
84
How does Rivaroxaban work?
Selective factor Xa inhibitor
85
What are the direct thrombin inhibitors?
Huridin Dabigatran Etexilate
86
What therapeutic uses do direct thrombin inhibitors have?
Prevention of stroke and embolism | Prophylaxis of venous thromboembolism
87
How to Warfarin work?
Inhibits Vitamin K reductase which prevents clotting.
88
What is the antidote to Warfarin
Vitamin K
89
What are the drugs used to lower lipid concentrations in the body?
``` Statins Ezetimibe Fibrates Bile Acid Binding resins Nicotinic Acid ```
90
What are the NET effects of statins?
Significantly reduce LDLs | Increases HDLs
91
Give three example of statins.
Simvastatin Atorvastatin Pravastatin
92
How does Ezetimibe work?
Decreases cholesterol absorption
93
What are the NET effects of Fibrates?
Increase in lipoprotein lipase activity Increased in HDL synthesis Increase in β-oxidation of fatty acids
94
Give two examples of Fibrates.
Fenofibrate | Gemfibrozil
95
What are the bile acid binding resins?
Colestyramine | Cholesterol
96
What are the benefits and drawbacks of bile acid binding resins?
Benefit: Decrease LDL Drawbacks: No increase in HDL Increase in triglycerides
97
What are the effects of nicotinic acid?
Decrease LDL | Increase HDL
98
What are the three stages of clinic blood pressure?
Stage 1: 140/90 mmHg Stage 2: 160/100 mmHg Stage 3: 180/110 mmHg
99
According to the NICE Hypertension guidelines, what is the first line treatment for a non-black, younger than 55 year old person suffering from hypertension?
ACE Inhibitor
100
According to the NICE Hypertension guidelines, what is the first line treatment for a black OR older than 55 year old person suffering from hypertension?
Calcium Channel Blocker
101
Activation of the Renin-Angiotensinogen-Angiotensin-System (RAAS) causes what physical changes in the body?
``` Vasoconstriction Salt Retention (Increased Aldosterone = Increased Na+ Absorption) ```
102
Give two examples of ACE Inhibitors
Captopril and Enalapril
103
What is the most common ADR from taking ACE Inhibitors?
Dry Cough
104
Give two examples of Angiotensin Receptor (AT1) Blockers
Losartan | Candesartan
105
Give an example of a Renin Inhibitor
Aliskiren
106
What are the selectivities of the Calcium Channel Blockers?
Nifedipine & Amlodipine - VASCULAR Verapimil - CARDIAC Diltaziem - INTERMEDIATE
107
Thiazides used alongside ACE Inhibitors and Calcium Channel Blockers are used as second-line treatment for what?
Hypertension (according to the NICE guidelines)
108
How do β-blockers act to treat hypertension?
Reduces the sympathetic drive to the heart which lowers the heart rate Blocks juxtaglomerular β-adrenoceptors which reduces renin secretion
109
What is different about Nebivolol in comparison to the other β-blockers?
Uniquely stimulates Nitrous Oxide in the endothelium
110
How do α-adrenoceptor antagonists act to treat hypertension?
Dilates the arteries which causes the reduction in total peripheral resistance Dilates the venous capacitance vessels which ultimately decreases preload
111
How do the 'Directly-Acting Vasodilators': Minoxidil and Diazoxide work?
They activate the ATP-sensitive K+ channels This causes membrane hyperpolarisation which will close off the L-VDCCs. Closure of said channels causes vasorelaxation and thus a decrease in Total Peripheral Resistance meaning a lower blood pressure.

Cardiovascular, Renal & Peripheral Nervous System Pharmacology (3 decks)

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