Past Years (2006 & 2007) Questions And Answers Compilation.
Please note that some questions are not being answered by us.
Credit to: RCSIan ‘08
2006
Q1. A 70 year old woman’s blood pressure is found to be elevated on two separate
occasions (180/105). Describe the mechanisms of action and the possible adverse
effects of two drug classes that you would consider using to lower blood pressure in
this woman.
Antihypertensive Drugs: ABCD AVAC
•ACE-Inhibitors
•Beta-blockers
•Calcium-channel blockers
•Diuretics
•Angiotensin II antagonists
•Alpha-blockers
•Vasodilators
•Central sympathophlegics
ThiazideDiuretics
•Ex.Hydrochlorthiazide
•MOA:.Inhibition of NaCl reabsorption in early distal tubule of renal nephron, decrease
water reabsorption, decrease in blood volume.
•S.E.s Fatigue
Hypokalaemia
Impotance
Glucose intolerance
Dyslipidaemia
Hyperuricaemia
Beta-blockers
Examples
Non-selective; Propranolol,
β1 selective; Atenolol
With vasodilatation; Pindolol(β1 selective antagonist and partial agonist at B2
adrenoceptors)
Carvidalol (non-selective β-blocker but also α1 blocker)
Nebivolol (releases NO)
Mechanisms of action: decrease HR, and decrease CO
Inhibition of rennin secretion
- S.Es:
Bronchospasm(non-selective)
Worsening of peripheral vascular disease (non-selective)
,Glucose intolerance
Dyslipidaemia
Negative inotrophy
Impotance
Fatigue
CNS effects, nightmares
Q2. A 10 year old girl with asthma is still suffering recurrent moderately severe
attacks of asthma despite treatment with an inhaled beta-2 adrenoceptor agonist.
Discuss the mechanisms of action and side effects of two classes of drugs you would
consider adding to her treatment regimen, so as to reduce frequency and severity of
attacks.
Bronchodilators
• B2 adrenoreceptor agonists
• Muscarinic (M3) antagonists
• Xanthines
Anti-inflammatory Drugs
• Glucocorticoids
• Cromones
• Leukotriene synthesis inhibitors & receptor antagonists
1. MUSCARINIC ANTAGONISTS
Ipratropium Bromide - derivative of N-isopropylatropine
Tiotropium bromide - Newer long-acting :
Administration
Given by inhalation –
not well absorbed -little systemic effects.
Mechanism of action
Inhibition of the action of acetyl choline at M1, M2,
and M3 muscarinic receptors. thus producing
bronchodilation and reducing mucous secretion.
Slower acting than B2 agonists.
2. XANTHINES
Caffeine
Theophylline
Oral.
Short T1/2.
Sustained release preparations available
Aminophylline
IV.
MOA: Relax bronchial smooth muscle (bronchodilation)
by inhibiting phosphodiesterase resulting in increased
cAMP and cGMP.
,Also anti-inflammatory actions (inhibit the late phase)
? inhibition of phosphodiesterase present in
inflammatory cells.
Selective PD4 inhibitors (Roflumilast, Cilomilast)
may be particularly beneficial in COAD)
Side Effects
Narrow therapeutic range (27-80mmol/l)
Side effects likely with concentrations >110mmol/l
® gastrointestinal: nausea / anorexia
® cardiovascular: arrhythmias can be fatal
® CNS: nervousness, tremor, seizures
Pharmacokinetics
Metabolised in the liver
T1/2 increased by liver disease, heart failure and decreased by
smoking and heavy drinking
NB Drug interactions
Pharmacokinetic Drug Interactions occur with Theophylline because of extensive
Metabolism by Cytochrome P450 Enzymes
Cytochrome P450 1A2 is the main isoform responsible for the metabolism of
theophylline
Erythromicin and Cimetidine are also metabolised by this isoform – hence competitive
inhibition can occur when co-administered
Enzyme inducers such as; Phenytoin, Carbamazepine, Rifampicin, Barbiturates, Alcohol
result in reduced plasma concentrations and decreased effects of drugs (such as
theophylline) which are extensively metabolised by Cytochrome P450 enzymes
Note: Delayed onset (2-3 weeks) as enzyme induction requires synthesis of new protein.
Note: Pharmacokinetic drug interactions are most important for drugs, such as
theophilline, that have a low therapeutic index
Q3. Describe the treatment of arrhythmias, giving special attention to the Vaughan
Williams classification and side effects of two classes of anti-arrhythmic drugs.
, There are five main classes in the Vaughan Williams classification of antiarrhythmic
agents:
Class I agents interfere with the sodium (Na+) channel.
Class II agents are anti-sympathetic nervous system agents. All agents in this
class are beta blockers.
Class III agents affect potassium (K+) efflux.
Class IV agents affect the AV node.
Class V agents work by other or unknown mechanisms.
Class IV ( Verapmil Block the L-type of Ca channel. -Reduce cardia
Ca Diltaizem Shorten phase 2 (plateau) contractility.
channel Reduce contractility of heart. -Bradycardia
blockers) Act on AV node
Treat SVT
Class V Digoxin Increases vagal activity via its central -Hypokalaemia
(Digitalis) action on the central nervous system. -Nausea &
Thus, decreasing the conduction of vomiting.
electrical impulses through the AV
node.
Positive inotropic effect
Q4. The levels of plasma lipoproteins in human subjects are used diagnostically to
evaluate cardiovascular risk. Name the two lipoproteins mainly responsible for
cholesterol transport and state FOUR of the properties by which these two may be
distinguished.
Low density lipoprotein (LDL)
Lower density, larger
Contain a larger proportion of cholesterol than HDL
Move cholesterol around to/from liver and peripheral tissues in the circulatory
system
As a result, cholesterol may be deposited in the walls of blood vessels and cause
cardiovascular diseases such as atherosclerosis
High density lipoprotein (HDL)
Higher density, smaller
Carry least amount of cholesterol
Carry cholesterol back to liver for elimination from body
As a result, accelerate the removal of cholesterol from blood, reducing the
likelihood of cholesterol becoming deposited in arterial walls provide
protection from cardiovascular diseases
Please note that some questions are not being answered by us.
Credit to: RCSIan ‘08
2006
Q1. A 70 year old woman’s blood pressure is found to be elevated on two separate
occasions (180/105). Describe the mechanisms of action and the possible adverse
effects of two drug classes that you would consider using to lower blood pressure in
this woman.
Antihypertensive Drugs: ABCD AVAC
•ACE-Inhibitors
•Beta-blockers
•Calcium-channel blockers
•Diuretics
•Angiotensin II antagonists
•Alpha-blockers
•Vasodilators
•Central sympathophlegics
ThiazideDiuretics
•Ex.Hydrochlorthiazide
•MOA:.Inhibition of NaCl reabsorption in early distal tubule of renal nephron, decrease
water reabsorption, decrease in blood volume.
•S.E.s Fatigue
Hypokalaemia
Impotance
Glucose intolerance
Dyslipidaemia
Hyperuricaemia
Beta-blockers
Examples
Non-selective; Propranolol,
β1 selective; Atenolol
With vasodilatation; Pindolol(β1 selective antagonist and partial agonist at B2
adrenoceptors)
Carvidalol (non-selective β-blocker but also α1 blocker)
Nebivolol (releases NO)
Mechanisms of action: decrease HR, and decrease CO
Inhibition of rennin secretion
- S.Es:
Bronchospasm(non-selective)
Worsening of peripheral vascular disease (non-selective)
,Glucose intolerance
Dyslipidaemia
Negative inotrophy
Impotance
Fatigue
CNS effects, nightmares
Q2. A 10 year old girl with asthma is still suffering recurrent moderately severe
attacks of asthma despite treatment with an inhaled beta-2 adrenoceptor agonist.
Discuss the mechanisms of action and side effects of two classes of drugs you would
consider adding to her treatment regimen, so as to reduce frequency and severity of
attacks.
Bronchodilators
• B2 adrenoreceptor agonists
• Muscarinic (M3) antagonists
• Xanthines
Anti-inflammatory Drugs
• Glucocorticoids
• Cromones
• Leukotriene synthesis inhibitors & receptor antagonists
1. MUSCARINIC ANTAGONISTS
Ipratropium Bromide - derivative of N-isopropylatropine
Tiotropium bromide - Newer long-acting :
Administration
Given by inhalation –
not well absorbed -little systemic effects.
Mechanism of action
Inhibition of the action of acetyl choline at M1, M2,
and M3 muscarinic receptors. thus producing
bronchodilation and reducing mucous secretion.
Slower acting than B2 agonists.
2. XANTHINES
Caffeine
Theophylline
Oral.
Short T1/2.
Sustained release preparations available
Aminophylline
IV.
MOA: Relax bronchial smooth muscle (bronchodilation)
by inhibiting phosphodiesterase resulting in increased
cAMP and cGMP.
,Also anti-inflammatory actions (inhibit the late phase)
? inhibition of phosphodiesterase present in
inflammatory cells.
Selective PD4 inhibitors (Roflumilast, Cilomilast)
may be particularly beneficial in COAD)
Side Effects
Narrow therapeutic range (27-80mmol/l)
Side effects likely with concentrations >110mmol/l
® gastrointestinal: nausea / anorexia
® cardiovascular: arrhythmias can be fatal
® CNS: nervousness, tremor, seizures
Pharmacokinetics
Metabolised in the liver
T1/2 increased by liver disease, heart failure and decreased by
smoking and heavy drinking
NB Drug interactions
Pharmacokinetic Drug Interactions occur with Theophylline because of extensive
Metabolism by Cytochrome P450 Enzymes
Cytochrome P450 1A2 is the main isoform responsible for the metabolism of
theophylline
Erythromicin and Cimetidine are also metabolised by this isoform – hence competitive
inhibition can occur when co-administered
Enzyme inducers such as; Phenytoin, Carbamazepine, Rifampicin, Barbiturates, Alcohol
result in reduced plasma concentrations and decreased effects of drugs (such as
theophylline) which are extensively metabolised by Cytochrome P450 enzymes
Note: Delayed onset (2-3 weeks) as enzyme induction requires synthesis of new protein.
Note: Pharmacokinetic drug interactions are most important for drugs, such as
theophilline, that have a low therapeutic index
Q3. Describe the treatment of arrhythmias, giving special attention to the Vaughan
Williams classification and side effects of two classes of anti-arrhythmic drugs.
, There are five main classes in the Vaughan Williams classification of antiarrhythmic
agents:
Class I agents interfere with the sodium (Na+) channel.
Class II agents are anti-sympathetic nervous system agents. All agents in this
class are beta blockers.
Class III agents affect potassium (K+) efflux.
Class IV agents affect the AV node.
Class V agents work by other or unknown mechanisms.
Class IV ( Verapmil Block the L-type of Ca channel. -Reduce cardia
Ca Diltaizem Shorten phase 2 (plateau) contractility.
channel Reduce contractility of heart. -Bradycardia
blockers) Act on AV node
Treat SVT
Class V Digoxin Increases vagal activity via its central -Hypokalaemia
(Digitalis) action on the central nervous system. -Nausea &
Thus, decreasing the conduction of vomiting.
electrical impulses through the AV
node.
Positive inotropic effect
Q4. The levels of plasma lipoproteins in human subjects are used diagnostically to
evaluate cardiovascular risk. Name the two lipoproteins mainly responsible for
cholesterol transport and state FOUR of the properties by which these two may be
distinguished.
Low density lipoprotein (LDL)
Lower density, larger
Contain a larger proportion of cholesterol than HDL
Move cholesterol around to/from liver and peripheral tissues in the circulatory
system
As a result, cholesterol may be deposited in the walls of blood vessels and cause
cardiovascular diseases such as atherosclerosis
High density lipoprotein (HDL)
Higher density, smaller
Carry least amount of cholesterol
Carry cholesterol back to liver for elimination from body
As a result, accelerate the removal of cholesterol from blood, reducing the
likelihood of cholesterol becoming deposited in arterial walls provide
protection from cardiovascular diseases
