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Block 2 > PPT > Flashcards

PPT Flashcards

1
Q

Describe the Strategies for Pharmacology of Asthma

A
  • Promote Bronchodilation directly - beta2-adrenoreceptor agonists, Anti-muscarinics, Methylxanthines
  • Reduce Tissue Inflammation and Allergy Triggers - Corticosteroids, Leukotriene Receptor Antagonists
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2
Q

O SHIT (acronym)

A
  • Useful acronym for Severe Acute Asthma Treatment
  • O - Oxygen
  • S - Salbutamol (beta-2 Agonist Class)
  • H - Hydrocortisone (Corticosteroid)
  • I - Ipratropium (Anti-muscarinic)
  • T - Theophylline (Metyhlxanthine)
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3
Q

Describe Normal Nervous System Involvement in Airway Regulation

A
  • Sympathetic NS - Mostly via adrenergic nerve fibres and noradrenaline - Drives BronchoDILATION
  • Parasympathetic NS - Mostly via cholinergic nerve fibres and acetylcholine - Drives BronchoCONSTRICTION
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4
Q

Define Bronchospasm

A

Tightening of muscles that line the bronchi in the lungs

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5
Q

Describe the Mechanism of Action Of Salbutamol

A
  • Beta-2 agonist
  • Binds to Beta-2 Adrenergic Receptor (normal ligand adrenaline&noradrenaline)
  • Results in activation of cAMP and Increased Concentration within the smooth muscle cell. A small, diffusible intracellular mediator
  • Activates PKA - Protein Kinase A enzyme, phosphorylates target molecules
  • Result: Reduced activity of myosin light chain kinase; Promotes Dephosphorylation of Myosin Light Chain. + Reduced Cytoplasmic calcium (drives into storage vesicles) reduces smooth muscle contraction
  • Overall: Reduces smooth muscle contraction
  • Dilation of the airway
  • More air enters the lung and reduces bronchospasm symptoms
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6
Q

What are the Cellular and Molecular Targets of Beta-2 Adrenoreceptor agonists

A
  • Cellular Target - Bronchiolar Smooth Muscle Cells

- Molecular Target - Stimulation of Beta-2 Adrenergic Receptors

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7
Q

What are the side effects of Beta-2 Adrenoreceptor use?

A
  • Tremor
  • Tachycardia
  • Cardiac Arrythmia
  • Less profound when an inhaler is used
  • As introducing cardiovascular stimulant
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8
Q

What Class of drug does Salbutamol belong to? What is it’s Mechanism of Action

A
  • Short-acting
  • Beta-2 Adrenoreceptor Agonist
  • Stimulation of Beta-2 Adrenergic Receptors on Bronchiolar Smooth Muscle cells
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9
Q

What Class of drug does Terbutaline belong to? What is it’s Mechanism of Action

A
  • Short-acting
  • Beta-2 Adrenoreceptor Agonist
  • Stimulation of Beta-2 Adrenergic Receptors on Bronchiolar Smooth Muscle cells
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10
Q

What Class of drug does Salmeterol belong to? What is it’s Mechanism of Action

A
  • Long-acting
  • Beta-2 Adrenoreceptor Agonist
  • Stimulation of Beta-2 Adrenergic Receptors on Bronchiolar Smooth Muscle cells
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11
Q

What Class of drug does Formoterol belong to? What is it’s Mechanism of Action

A
  • Long-acting
  • Beta-2 Adrenoreceptor Agonist
  • Stimulation of Beta-2 Adrenergic Receptors on Bronchiolar Smooth Muscle cells
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12
Q

Compare the Difference between Short-acting and Long-acting Beta-2 agonists

A
  • Salbutamol (short-acting) binds directly to Beta2 adrenergic receptor
  • Salmeterol (long-acting) enters plasma membrane and interacts with receptor active site via Membrane Translocation - Takes longer
  • Formoterol (long-acting) - Diffuses into membrane proximal to receptor and interacts with active site as a depot
  • Different in timescale and kinetics, precipitates longer or shorter stimulation responses
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13
Q

State the Methylxanthines

A
  • Theophylline

- Aminophylline

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14
Q

What Class of drug does Theophylline belong to? What is it’s Mechanism of Action

A
  • Methylxanthines

- Blockade of Phosphodiesterase (PDE enzymes) on Bronchiolar Smooth Muscle cells

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15
Q

What Class of drug does Aminophylline belong to? What is it’s Mechanism of Action

A
  • Methylxanthines

- Blockade of Phosphodiesterase (PDE enzymes) on Bronchiolar Smooth Muscle cells

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16
Q

Explain the Mechanism of Action of Theophylline

A
  • Methylxanthine
  • Blockade of Phosphodiesterase (PDE) enzymes
  • Subsequently sustains cAMP levels and promoting muscle relaxation (bronchodilation)
  • Oral tablet/IV in Acute Asthma
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17
Q

Explain the Mechanism of Action of Aminophylline

A
  • Methylxanthine
  • Blockade of Phosphodiesterase (PDE) enzymes
  • Subsequently sustains cAMP levels and promoting muscle relaxation (bronchodilation)
  • Oral tablet/IV in Acute Asthma
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18
Q

Explain the Mechanism of Action of Methylxanthines

A
  • Blockade of Phosphodiesterase (PDE) enzymes (usually breaks down cAMP)
  • Subsequently sustains cAMP levels and promoting muscle relaxation (bronchodilation)
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19
Q

What are the side effects of Methylxanthines

A
  • Very toxic cardiac & neurological side effects, monitoring of serum levels required
  • Possible cardiac arrhythmias + seizures
  • Usually used in emergencies
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20
Q

Explain the Mechanism of Action of Anti-Muscarinics

A
  • Ipratropium (short-acting), Tiotropium (long-acting), Glycopyrronium (Long-acting)
  • M3 Muscarinic Acetylcholine Receptor Antagonist on Bronchiolar Smooth Muscle Cells
  • Inhibition of Phospholipase C enzymes (PLC), reducing IP3 Generation, reducing calcium release from intracellular stores into cytoplasm
  • Reduced cytoplasmic calcium reduces smooth muscle contraction I/e promotes bronchodilation by suppressing bronchoconstriction
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21
Q

What are possible side effects of Anti-Muscarinics for Airway Diseases?

A
  • Dry Mouth
  • Constipation
  • Urinary Retention
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22
Q

What are the Cellular and Molecular Targets of Methylxanthines

A
  • Cellular - Bronchiolar Smooth Muscle cells

- Molecular - Phosphodiesterase Enzyme (PDE) Blockade

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23
Q

What are the Cellular and Molecular Targets of Anti-Muscarinics for Airway Diseases

A
  • Cellular - Bronchiolar Smooth Muscle cells

- Molecular - Blockade of M3 Muscarinic Acetylcholine Receptors

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24
Q

What Class of drug does Ipratropium belong to? What is it’s Mechanism of Action

A
  • Short-acting
  • Anti-Muscarinic
  • Blockade of M3 Muscarinic ACh Receptors on Bronchiolar Smooth Muscle Cells
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25
What Class of drug does Tiotropium belong to? What is it's Mechanism of Action
- Long-acting - Anti-Muscarinic - Blockade of M3 Muscarinic ACh Receptors on Bronchiolar Smooth Muscle Cells
26
What Class of drug does Glycopyrronium belong to? What is it's Mechanism of Action
- Long-acting - Anti-Muscarinic - Blockade of M3 Muscarinic ACh Receptors on Bronchiolar Smooth Muscle Cells
27
State the Anti-Muscarinics
- Ipratropium - Short-Acting - Tiotropium - Long-acting - Glycopyrronium - Long-acting
28
What are Leukotrienes (LT)
- Secreted signalling molecules that drive airway inflammation and also bronchospasm via LT-R/CysLT-R - Receptors - Found on Eosinophils within lungs + Bronchiolar smooth muscle cells
29
What are the Cellular and Molecular Targets of Leukotriene Receptor Antagonists
- Montelukast, Zafirlukast - Cellular targets - Predominantly Eosinophils in the lungs (LTs augmenting inflammation); And Bronchiolar Smooth Muscle Cells (LTs driving bronchospasm) - Molecular target - Blockade of CysLT1 Leukotriene Receptors
30
What Class of drug does Montelukast belong to? What is it's Mechanism of Action
- Leukotreine Receptor Antagonist - Cellular targets - Predominantly Eosinophils in the lungs (LTs augmenting inflammation); And Bronchiolar Smooth Muscle Cells (LTs driving bronchospasm) - Molecular target - Blockade of CysLT1 Leukotriene Receptors
31
What Class of drug does Zafirlukast belong to? What is it's Mechanism of Action
- Leukotreine Receptor Antagonist - Cellular targets - Predominantly Eosinophils in the lungs (LTs augmenting inflammation); And Bronchiolar Smooth Muscle Cells (LTs driving bronchospasm) - Molecular target - Blockade of CysLT1 Leukotriene Receptors
32
Explain the Mechanism of Action of Leukotriene Receptor Antagonists
- Montelukast, Zafirlukast - Cellular targets - Predominantly Eosinophils in the lungs (LTs augmenting inflammation); And Bronchiolar Smooth Muscle Cells (LTs driving bronchospasm) - Molecular target - Blockade of CysLT1 Leukotriene Receptors - Reduce inflammatory responses in early & late phases of asthma - Additive effect when used with other drugs e.g. glucocorticoids - No evidence of effect on remodelling (chronic asthma) - Administered as oral tablets - Used as preventer
33
What are possible side effects of Leukotriene Receptor Antagonist use?
- Abdominal pain | - Headache
34
Explain the Mechanism of Action of Corticosteroids in Airway Disease
- Beclomethasone (inhaled), Fluticasone (inhaled), Prednisolone (oral), Hydrocortisone (IV) - Cellular target: Immune cells of the lung, especially macrophages, T-lymphocytes, Eosinophils - Molecular targets: Stimulates Intracellular Glucocorticoid Receptor (GR) - A Transcription Factor - Activated GR interacts with selected DNA sequences and influences expression of many key genes - For inflammation control, mostly via macrophages and T cells: - Suppression of pro-inflammatory mediators, e.g. TH1 cytokines (TNF-alpha, IL-8) - Important and TH2 cytokines IL-3 and IL-5 - Expression of Anti-inflammatory products e.g. Lipcortin-1, Secreted Leukocyte Peptidase Inhibitor SLPI) - Overall - Dual suppression of pro-inflammatory + Stimulation of anti-inflammatory responses.
35
State the Corticosteroids used for Airway Disease
- Beclomethasone - Inhaled - Fluticasone - Inhaled - Prednisolone - Oral - Hydrocortisone - IV - Emergency/Acute Asthma
36
What Class of drug does Beclomethasone and Fluticasone (inhaled) belong to? What is it's Mechanism of Action
- Corticosteroids - Cellular target: Immune cells of the lung, especially macrophages, T-lymphocytes, Eosinophils - Molecular targets: Stimulates Intracellular Glucocorticoid Receptor (GR) - A Transcription Factor
37
What Class of drug does Prednisolone (oral) belong to? What is it's Mechanism of Action
- Corticosteroids - Cellular target: Immune cells of the lung, especially macrophages, T-lymphocytes, Eosinophils - Molecular targets: Stimulates Intracellular Glucocorticoid Receptor (GR) - A Transcription Factor
38
What Class of drug does Hydrocortisone (IV) belong to? What is it's Mechanism of Action
- Corticosteroids - Cellular target: Immune cells of the lung, especially macrophages, T-lymphocytes, Eosinophils - Molecular targets: Stimulates Intracellular Glucocorticoid Receptor (GR) - A Transcription Factor - Used in Emergency/Acute Asthma - Suppression of Pro-inflammatory responses + Stimulation of Anti-inflammatory responses + reduction of bronchospasm
39
What are the possible side effects of Beclomethasone (inhaled), Fluticasone (inhaled), Prednisolone (oral), and Hydrocortisone (IV)?
- Many - Especially long-term oral corticosteroids - Moon face, weight gain, osteoporosis, hyperglycaemia - Poor wound healing, plethoric cheeks
40
What are the possible side effect of corticosteroid use?
- Many - Especially long-term oral corticosteroids | - Moon face, weight gain, osteoporosis, hyperglycaemia
41
Outline Principles of Treatment for Coronary Artery Disease - Stable Angina
- Increase oxygen supply to myocardium - Improve coronary blood flow - Beta-blockers - Reduce oxygen demand of myocardium - Reduce HR and force of heart contraction - Nitrates - Calcium channel blockers can also be used - not first line - increase O2 supply and improve blood flow
42
Outline Principles of Treatment for Acute Coronary Syndromes
- Initial - Morphine for pain relief - Aspirin ASAP - Reduce platelet activity + further thrombus development - Nitrates - Promote blood flow to heart - Once stabilised: Regularly - Beta blocker - Reduce cardiac workload - ACEi or ARB to avoid dysfunctional heart remodelling - Antiplatelet drugs - Aspirin/Clopidogrel - Maintenance dose levels - HMG-CoA Reductase Inhibitor - Atorvastatin - Control cholesterol levels + reduce atherosclerosis progression
43
Outline Principles of Treatment for Chronic Heart Failure
- Manage symptoms: Breathlessness and Oedema - ACEi / ARBs - Balance RAAS activation and reduce cardiac afterload - Diuretics - Promote fluid removal, reduce oedema and breathlessness + Generates more urine and reduces preload
44
Outline Principles of Treatment for Hypertension
- ACE Inhibitors/ ARBs + calcium channel blockers - Vasodilation - Often used together with drugs that affect blood volume - E.g. Diuretics
45
What are key side effects of ACE inhibitors?
Can cause a PERSISTENT Dry Cough
46
Outline the Target of ACE inhibitors used to drive therapeutic cellular events in the heart and blood vessels
- Block conversion of Angiotensin I to Angiotensin II by Angiotensin Converting Enzyme - Ramipril and Lisinopril
47
Outline the Mechanism of Action of ACE inhibitors used to drive therapeutic cellular events in the heart and blood vessels
- Ramipril + Lisinopril - Reduce levels of Angiotensin II - Decreases vasoconstriction in numerous peripheral blood vessels - Reduced Systemic Vascular Resistance and reduced cardiac afterload, lowers blood pressure - Indirectly, aldosterone secretion also reduced leading to increased sodium and water loss - Lowering plasma volume + decreasing cardiac preload
48
Outline the Target of Angiotensin Receptor Blockers used to drive therapeutic cellular events in the heart and blood vessels
- Losartan, Valsartan - Directly block activation of Angiotensin II Receptor on Specialised Vascular Smooth Muscle cells - Reduced Systemic Vascular Resistance and reduced cardiac afterload, lowers blood pressure - Indirectly, aldosterone secretion also reduced leading to increased sodium and water loss - Lowering plasma volume + decreasing cardiac preload
49
Outline the targets of the classes of Calcium Channel Blockers (CCB) used to drive therapeutic cellular events in the heart and blood vessels.
- Amlodipine, Nifedipine - Prevent opening of voltage-gated L-type Calcium Channels - Antagonist /Blocking - Mainly arteries and arterioles, not veins
50
Outline the Mechanisms of Action of the Calcium Channel Blockers (CCB) used to drive therapeutic cellular events of the heart and blood vessels
- Prevents opening of voltage-gated L-type Calcium Channels - Reduce Ca2+ influx into vascular smooth muscle cells - Vasodilator effect in vessels - reduces afterload, reduces BP - Used for hypertension - Drive coronary artery dilation - Improved blood flow to cardiac muscle - Useful in stable angina
51
Outline the Key side effects of Calcium Channel Blockers (CCB) used to drive therapeutic cellular events in the heart and blood vessels
- Ankle swelling | - Palpitations
52
What drugs are Calcium Channel Blockers?
- Amlodipine | - Nifedipine
53
What drugs are Angiotensin Receptor Blockers
- Losartan | - Valsartan
54
What drugs are ACE Inhibitors
- Ramipril | - Lisinopril
55
Which type of immune cells, commonly associated with triggering asthma attacks, are Leukotriene Receptor Antagonists especially effective at targeting?
Eosinophils
56
What is a drug which is a Leukotriene receptor Antagonist
Montelukast
57
A 67 year old woman has stable angina and uses Glyceryl Trinitrate (GTN) to relieve her symptoms. What is the key enzyme in vascular smooth muscle cells that is activated by the action of this Nitrate drug?
- Guanylate Cyclase - Secondary messenger generated to particular stimulus in Vascular Smooth Muscle cell - Nitrate drugs release NO which selectively activate guanylate cyclase
58
A 77 year old man with coronary artery disease is taking Aspirin as part of his secondary prevention treatment programme. Which cell type is primarily targeted by Aspirin in the context of secondary prevention of cardiovascular disease?
Platelets - Inhibits thromboxane A2 in platelets, inhibits platelet activation and reduces risk of thrombus formation, protecting CV system from blood vessel occlusion and acute coronary syndrome
59
A 35 year old woman with chronic asthma uses a Beclometasone inhaler/ Which immune cell is especially targeted by this drug, leading to altered cytokine expression that promotes anti-inflammatory responses?
- Macrophage | - Corticosteroid / Glucocorticoid drugs - interacts with glucocorticoid receptor in immune cells
60
When the Glucocorticoid Receptor binds to Beclometasone where in the macrophage does it become especially active in modifying cell physiology
- Nucleus - Glucocorticoid Receptor - Is a Transcription factor - Upon activation influence upregulation of anti-inflammation genes that reduce tissue damage in the lung
61
An 82 year old man suffering from chronic heart failure is taking a drug hydrochlorothiazide which helps relieve the associated oedema. How else can this drug alleviate heart failure?
- Reduction in blood volume and reduction in cardiac preload - Thiazide diuretic drug - Inhibits sodium reuptake into the blood and promotes urine production - Reduces circulating blood volume which in turn reduces cardiac preload, easing exertion by the heart and managing heart failure symptoms
62
77 year old woman is taking Sacubitril with Valsartan as part of her treatment for heart failure. The Sacubitril component is an inhibitor of the enzyme Neprilysin. Which substance, involved in regulating cardiovascular function is normally broken down by the action of Neprilysin?
- Natriuretic Peptide B | - sacubitril is a neprilysin inhibitor drug. Exerts Sodium reuptake by Kidneys?? Check
63
34 year old man is given intravenous Aminophylline, powerful methylxanthine drug, to treat a severe acute asthma attack. Which key enzyme will this drug directly target in the bronchiolar smooth muscle cells?
Phosphodiesterase
64
What major side effect could occur when using Aminophylline?
- Cardiac Arrhythmia - Methylxanthine - inhibit phosphodiesterase - breaks down cAMP, drives smooth muscle relaxation - Can strongly influence adrenergic responses in other system, including cardiac muscle, can lead to abnormal heart contraction and arrhythmia
65
a 73 year old woman recovering from an acute coronary syndrome is taking Atorvastatin. This drug targets the enzyme HMG-CoA Reductase, present predominantly in which cells? This patients GP also recommends a drug that helps prevent blood clots by blocking the ADP Receptor on platelets. Which drug is this?
- Hepatocytes - Cholesterol synthesis and processing into secreted LDL mostly takes place in liver, within hepatocytes. - Atorvastatin reduces cholesterol synthesis and promote LDL reuptake into hepatocytes - Reducing development of atherosclerotic plaques - Clopidogrel
66
What receptors do Beta-Blockers for the heart work on?
- Beta-1 Adrenergic Receptors - Different and well localised for specific therapeutic effect - Stimulation results in contraction of the heart
67
What drugs are found within the Nitrates Drug class?
- Glyceryl Trinitrate (GTN) | - Isosorbide Mononitrate (ISMN)
68
What is the Mechanism of action of Glyceryl Trinitrate / Nitrates
- Also Isosorbide Mononitrate (ISMN) - Metabolised in body - Releases Nitric Oxide (NO) - Stimulates intracellular Guanylate Cyclase - Increases cGMP in Vascular Smooth Muscle Cells - Drives dephosphorylation of myosin light chains (MLC) via activation of MLS Phosphatase - Inhibits influx of Ca2+ from intracellular stores into cytoplasm - Drives vascular smooth muscle relaxation
69
What are the targets of Nitrates used to drive therapeutic cellular events in the heart and blood vessels
- Passively diffuse into Vascular Smooth muscle cells as NO once metabolised - Stimulates intracellular Guanylate Cyclase - Increases cGMP and drives dephosphorylation of myosin light chains (MLC) via activation of MLC Phosphatase - Inhibits influx of Ca2+ from stores + Drives muscle relaxation
70
What are Key side effects of GTN spray
Headache
71
What are key Side effect of Nitrates - GTN + Isosorbide Mononitrate (ISMN)
Headache
72
What are key Side effect of Nitrates - GTN + Isosorbide Mononitrate (ISMN)
Headache
73
What effects do Nitrate Vasodilator drugs have on the heart?
- Nitrates dilate arteries and veins - Promote venodilation - Reduces cardiac preload (muscle stretch as blood fills heart), which reduces oxygen demand - Promote coronary artery vasodilation - Increases blood and oxygen supply to the myocardium - Promote moderate arteriolar dilation - Helps reduce cardiac afterload
74
How is Beta-adrenergic stimulation of cardiac muscle cells different from that of Beta-adrenergic stimulation of smooth muscle cells?
- Beta-adrenergic stimulation of cardiomyoctes drive cardiac muscle contraction - Beta-adrenergic stimulation of vascular smooth muscle cells drive muscle relaxation - Opposite effects due to cardiomyocytes having different cell physiology
75
Outline the targets of Beta-Blockers used to drive therapeutic cellular events in the heart and blood vessels.
- Competitive inhibitors of adrenaline and noradrenaline at Beta-adrenoreceptor sites - Inhibit sympathetic stimulation of heart muscle - Atenolol, Bisoprolol - Beta-1-antagonists - Selective for heart muscle
76
Outline the mechanisms of action of Beta-Blockers used to drive therapeutic cellular events in the heart and blood vessels
- Atenolol, Bisoprolol - Competitve inhibitors of adrenaline and noradrenaline at beta-adrenoreceptor sites - Inhibit sympathetic stimulation of heart muscle - Negative Chronotrope - Reduces heart rate - Negative Inotrope - Reduce Cardiomyocyte contractility - Reduce workload of the heart - Relieve oxygen demand
77
What are key side effects of beta-blockers used to drive therapeutic cellular events in the heart and blood vessels
- Dizziness | - Constipation
78
Outline the targets of Diuretics used to drive therapeutic cellular events in the heart and blood vessels
- Act in Kidney on renal tubular epithelial cells - Furosemide - Loop Diuretic - Inhibits renal Na+/K+/2Cl- Transporter - Hydrochlorothiazide - Thiazide Diuretic - Inhibits renal Na+/Cl- Symporter - Spironolactone - Potassium-sparing diuretic - Inhibits aldosterone activity
79
Outline the mechanism of action of Diuretics used to drive therapeutic cellular events in the heart and blood vessels
- Furosemide - Loop Diuretic - Inhibits renal Na+/K+/2Cl- Transporter - Hydrochlorothiazide - Thiazide Diuretic - Inhibits renal Na+/Cl- Symporter - Spironolactone - Potassium-sparing diuretic - Inhibits aldosterone activity - Diuretics increase water and sodium output in urine - Reduce blood volume and reduce cardiac preload - Reduce oedema
80
What Diuretic drugs are used to drive therapeutic cellular events in the heart and blood vessels
- Furosemide - Hydrochlorothiazide - Spironolactone
81
Outline the targets of Neprilysin Inhibitors used to drive therapeutic cellular events in the heart and blood vessels.
- Sacubitril | - Inhibit Neprilysin (major enzyme involved in breakdown of Natriuretic peptides)
82
Outline the mechanism of action of Neprilysin Inhibitors used to drive therapeutic cellular events in the heart and blood vessels.
- Sacubitril - Inhibit Neprilysin (major enzyme involved in breakdown of Natriuretic peptides) - Prolongs presence + activity of NPs, which promote water + sodium excretion - Found effective when used together with ARB - Valsartan
83
What class of drug does Sacubitril belong to?
- Neprilysin Inhibitors
84
Outline Acute Cardiac Arrest Treatment with Adrenaline
- Adrenaline - Emergency treatment - Administered Intravenously - Adrenaline is a powerful sympathomimetic + positive inotrope - Binds and stimulates cardiomyocyte B1-adrenergic receptors - Drives heart muscle contraction to restore heart function
85
Outline Atropine use for Acute Heart Block
- Emergency Treatment for Sinus Bradycardia (dangerously slow HR due to disturbance of electrical cardiac activity) Can lead to heart block (Atrioventricular Block) - Atropine IV (anti-muscarinic) - Raises heart rate - Blocks M2 Muscarinic ACh Receptors on cardiomyocytes - Inhibits effects of parasympathetic, cholinergic vagus nerve transmission in the heart, normally exerts negative chronotropy - Atropine accelerates repolarisation rate in cardiac muscle
86
Name the common drugs used in secondary prevention of cardiovascular disease.
- Antiplatelet drugs | - HMG-CoA Reductase Inhibitors (Statins)
87
Outline the pharmacological targets and mechanisms of actions of - COX inhibitors/ Aspirin (Anti-Platelet) drugs in secondary prevention of cardiovascular disease.
- Aspirin - COX inhibitor - Cyclo-oxygenase Inhibitor - Blocks enzyme action of platelet COX enzyme - Required for Thromboxane A2 synthesis (TXA2) - Reduced TXA2 synthesis inhibits platelet activation and thrombus formation - Can be used to treat/prevent cardiovascular disease WITHOUT affecting blood pressure
88
Outline the pharmacological targets and mechanisms of actions of Platelet ADP Receptor Inhibitors/Clopidogrel (Anti-Platelet) drugs in secondary prevention of cardiovascular disease.
- Binds and blocks function of ADP Receptors on platelet surfaces - Inhibits platelet activation and subsequent thrombus formation - Increases threshold for activation
89
Outline the pharmacological targets and mechanisms of actions of HMG-CoA Reductase Inhibitor drugs in secondary prevention of cardiovascular disease.
- Atorvastatin, Simvastatin - Cholesterol reduction - Protection against development of atherosclerosis - Live is main site of cholesterol production - Produced in hepatocytes and secreted in Low Density Lipoprotein (LDL) - Enzyme HMG-CoA Reductase essential, rate-limiting in cholesterol synthetic pathway - Inhibitors reduce circulating cholesterol levels and promote uptake of excess cholesterol from bloodstream into the liver - Used to treat/prevent CVD WITHOUT affecting BP

Block 2 (15 decks)

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