Pharmacology Flashcards
(141 cards)
1
Q
What cells use the fast response?
A
atrial and ventricular muscle cells and Purkinje fibres
2
Q
What cells use the slow response?
A
SA node and AV node cells
3
Q
What ion is the fast response dependent on?
A
sodium
4
Q
What ion is the slow response dependent on?
A
calcium
5
Q
What are changes in the duration and phases of action potentials due to?
A
hormones, cardiac disease, pH and drugs
6
Q
What is resting potential in ventricular cardiac muscle cells?
A
-90mV which is close to potassium’s equilibrium potential due to outward Ik1 but not exactly due to inward Na+ movement
7
Q
What is dominant movement in Phase 4 in atrial and ventricular myocytes?
A
outward flux of K+
8
Q
What is dominant movement in Phase 0 in atrial and ventricular myocytes?
A
inwards lux of Na+
9
Q
What happens in Phase 0 of atrial and ventricular myocytes?
A
- triggered by impulses from SA node
- rapid activation of Na+ channels do inward, depolarising, Na+ current
- inactivation of channels
10
Q
What is the dominant movement in Phase 1 of atrial and ventricular myocytes?
A
outward movement of K+
11
Q
What happens in Phase 1 of atrial and ventricular myocytes?
A
- brief
- rapid inactivation of Na channels
- activation of Ito so outward K+ current
12
Q
What is the dominant movement in Phase 2 of atrial and ventricular myocytes?
A
inward flux of Ca2+ which is roughly balanced by outward flux of K+
13
Q
What happens in Phase 2 of atrial and ventricular myocytes?
A
- balance of conductances
- inward depolarising of Ca2+ and outward depolarising of K+
- Ca2+ is voltage-activated Ca2+ channels (L-type) which inactivate slowly producing long lasting Ca2+ current crucial to cardiac muscle contraction
- Ik1 and Ito reduce and delayed rectifier potassium channels open to give Ik
14
Q
What factor determines how long plateau persists for?
A
as long as inward Ca2+ balances the outward K+
15
Q
What drugs reduce plateau?
A
drugs that reduce Ica,l (calcium channel blockers)
16
Q
What drugs increase duration of ventricular action potential and what is this called?
A
drugs that block certain potassium channels
an acquired long QT syndrome
17
Q
What is the dominant movement in Phase 3 for atrial and ventricular myocytes?
A
outward flux of K+ is dominant
18
Q
What happens in Phase 3 of atrial and ventricular myocytes?
A
- outward K+ exceeds inward Ica,l
- Ica,l decreases due to inactivation of L-type Ca2+ channels
19
Q
What is the difference in conductance between atrial and ventricular myocytes?
A
- phase 2 is less evident due to extra Ikur channel so final repolarisarion occurs more rapidly
20
Q
How does the slow response (in SA and AV tissue) differ from the fast response?
A
- Vm between action potentials gradually shifts up which is the pacemaker potential
- the upstroke is less steep as Ica,l channels open not voltage-gated ones
- no distinct plateau phase but a gradual repolarising by delayed rectifier channels
21
Q
What is the dominant movement of ions in Phase 4 of SA and AV node tissue?
A
outward flux of K+ is reduced and inward flux of Ca2+ and Na+ is increased generating the pacemaker potential
22
Q
What three conductances does pacemaker potential in SA and AV node tissues rely on?
A
- decrease in outward Ik causing depolarisation
- increase in inward Ica,l causing depolarisation
- HCN channels edit cation conductance in response to hyper polarisation triggering the funny current so Na+ ions move in causing depolarisation
23
Q
Which cells do sympathetic adrenaline and noradrenaline activate beta 1 adrenoceptors in?
A
nodal cells and myocardial cells
24
Q
How is cAMP concentration increased?
A
coupling though Gs protein aloha subunit means adenyl cyclase increases the intracellular concentration of cAMP from ATP
25
What does sympathetic signalling through Gs beta 1 adrenoceptors cause?
- increased SA node action (+ chronotropic effect) with increased slope of Phase 4 and reduced threshold
- increased contractility (+ inotropic effect)
- increased conduction velocity in AV node
- increased automacity
- decreased duration of systole
- increased activity of sodium-potassium pump
- increased mass of cardiac muscle
26
How does acetylcholine produce a parasympathetic impulse in regulation of cardiac rate and force?
ACh acitvate m2 muscarinic cholinoceptors in nodal cells, coupling through a Gi protein
inhibition of adenylyl cyclase and reduction in cAMP
opening of specific potassium channels in the SA node (GIRKs)
27
What does ACh signalling in the autonomic regulation of rate and force cause?
- decreased SA node frequency (- chronotropic effect) with decreased in Phase 4 slope, increase in threshold and hyperpolarisation during Phase 4 via GIRKs
- deceased contractility due to decrease in Phase 2 and decreased Ca2+
- decreased conduction in AV node due to decreased Ca2+ activity
- possible arrhythmias occurring in the atria
28
What is the funny current activated by?
hyperpolarisation and cAMP
29
What effect will block of HCN channels have?
decreased slope of the pacemaker potential and reduced heart rate
30
What does ivabradine do?
selective blocker of HCN channels that is used to slow heart rate in angina and therefore reduces oxygen consumption
31
How does a muscle contract?
- ventricular action potential
- opening of voltage- activated Ca2+ channels during Phase 2
- Ca2+ influx into cytoplasm
- Ca2+ release from SR
- cross bridge formation between A and M
32
How does a muscle relax?
- repolarisation in phase 3 to 4
- voltage-activated L-type Ca2+ channels return to closed state
- Ca2+ influx ceases and Ca2+ efflux occurs by Ca2+/Na+ exchanger
- Ca2+ release from SR stops and SERCA actively moves Ca2+ from the cytoplasm
- cross bridges between A and M break
33
What are examples of beta adrenoceptor agonists and what effect do they have on the heart?
- dobutamine, adrenaline and noradrenaline
- increased force, rate and CO and O2 consumption
- decreased cardiac efficiency
- disturbance in rhythm
34
What are the clinical uses of adrenaline?
- in cardiac arrest causing positive ionotropic and chronotropic actions, redistribution of blood flow and dilation of coronary arteries
- anaphylactic shock
35
What are the clinical uses of dobutamine?
- acute heart failure
36
What is an example of beta adrenoceptor antagonist that non-selectively blocks beta adrenoceptors?
propranolol
37
What is an example of beta adrenoceptor antagonist that selectively blocks beta adrenoceptors?
atenolol, bisoprolol and metoprolol
38
What are the pharmacodynamic effects of non-selective beta adrenoceptor antagonists?
- little effect on rate force or CO
- reduction maximal exercise tolerance
- coronary vessel diameter marginally reduced but myocardial oxygen requirement falls
39
What are the clinical uses of beta adrenoceptor antagonists?
- treatment of disturbances of cardiac rhythm (tachycardia or a-fib)
- treatment of angina
- treatment of heart failure
- treatment of hypertension
40
What are the adverse effects of beta-blockers?
- bronchospasm
- aggravation of cardiac failure (decompensated.. it is still used in compensated)
- bradycardia
- hypoglycaemia
- fatigue
- cold extremities
41
What are the pharmacodynamic effects of atropine?
- increase in HR
- no effect upon arterial BP
- no effect on response to exercise
42
What are the clinical uses for atropine?
- first line in treatment of bradycardia, esp following MI
| - im anti cholinesterase poisoning
43
What is digoxin used for?
- heart failure
- to increase contractility of the heart
- heart failure with a-fib
44
What do inotropes do to the ventricular function curve of SV against EDP?
upward and leftward shift so SV increases any given EDP
45
What is the biochemical effect of digoxin?
- inhibits sodium-potassium pump
- increases Na concentration inside and reduced Vm
- decreases sodium calcium exchange and increase inside calcium ion concentration
- increased storage of calcium ions in SR
- increases CICR and contractility
46
What are digoxin's effects on electrical activity?
indirect- increased vagal activity so slows SA node discharge and slows AV node conduction to increase refractory period
direct- shortens action potential and refractory period in atrial and ventricular myocytes but a toxic concentration causes oscillatory afterpotentials
47
What are the most serious cardiac effects of digoxin?
- excessive depressions of AV node conduction (heart block)
| - propensity to cause arrythmias
48
What are some other adverse non-cardiac effects of digoxin?
- nausea
- vomiting
- diarrhoea
- disturbances of colour vision
49
What is an example of a calcium-sensitiser drug and how does it work?
Levosimendan
- binds to troponin C in cardiac muscle sensitising it to the action of Ca2+
- opens Katp channels in vascular smooth muscle causing vasodilation
- used in acute decompensated heart failure
50
What are examples of inodilators and how do they work?
Amrinone and Milrinone
- inhibit PDE in cardiac and smooth muscle cells and increase cAMP concentration
- increases contractility, decrease peripheral resistance but worsen survival
- used for IV administration in acute heart failure
51
What are organic nitrates used to treat?
- acute angina and chest pain with associated with acute coronary syndrome
- prevention of angina
- treatment of pulmonary oedema
52
What are calcium channel blocker used to treat?
- hypertension
- treatment of stable angina
- control HR in patients with supraventricular arrhythmias
53
What is angina?
a pain that occurs when the oxygen supply to the myocardium is insufficient to meet its metabolic demands
54
What are the three types of angina?
- Stable angina- due to a fixed narrowing of coronary vessels as a consequence of atherosclerosis
- Unstable angina- due to platelet-fibrin thrombus in association with an atheromatous plaque
- Variant angina- associated with coronary artery spasm
55
How does cyclic GMP-dependent PKG cause smooth muscle relaxation?
- stimulating myosin phosphatase
- stimulating plasma membrane Ca2+ ATPase
- stimulating sarcoplasmic reticulum Ca2+ ATPase
- activating K+ channels that cause hyperpolarization
- inactivating Ca2+ channels
56
What do small doses of organic nitrates do?
cause venorelaxation with a decrease CVP/preload but CO is maintained by the increased heart rate
57
What do large doses of organic nitrates do?
increased arteriolar dilation
58
What is the effect of organic nitrates?
decreased myocardial oxygen requirements by...
- decreased preload
- decreased afterload
- improved perfusion of the ischaemic zone
59
How do organic nitrates increase perfusion to the ischaemic zone?
they dilate the collateral vessels so the blood flow to ischaemic myocardium is increased so blood can still get to the ischaemic myocardium despite a plaque blocking the main vessel
60
What are the main types of organic nitrates and what are they used to treat?
Organic nitrates are used in all types of angina
The main examples are glycerylnitrate (GTN) and isosorbide mononitrate (ISMN) which are both metabolised to nitric oxide
61
How is GTN administered and how long does it act for?
Glyceryltrinitrate is short-acting (30 mins), administered sublinguinally or as a spray (stable angina) or IV with aspirin (unstable angina)
GTN never reaches in the veins from the liver because it is so metabolised by the liver (first-pass metabolism). Therefore, GTN is not effective if swallowed.
62
What is first-pass metabolism?
First-pass metabolism is that after a drug is swallowed and enters the intestines, it enters the portal circulation between the intestines and the liver
63
What is isosorbide mononitrate used for and how is it administered?
Isosorbide mononitrate (ISMN) is resistant to first-pass metabolism and is administered orally for angina prophylaxis and has a more sustained effect than GTN
64
What are the adverse side-effects of organic nitrates?
headaches, hypotension/ fainting, reflex tachycardia (prevented by adding a beta blocker) and formation of methaemoglobin (can be used with amyl nitrate to treat cyanide poisoning)
65
How is tolerance of organic nitrates avoided?
there can be a diminished effect which can be avoided by only taking the drug at breakfast and lunch
66
How are calcium channel blockers used to treat hypertension?
reduced calcium ion entry into vascular smooth muscle which causes arteriolar dilation
reducing total peripheral resistance and mean arterial blood pressure
drugs with selectivity for smooth muscle L-type channels are preferred to minimise effects on cardiac muscle, they can be used for patients with both angina and hypertension and for isolated systolic hypertension
67
How are calcium channel blockers used to treat angina?
prophylactic treatment, used with GTN if beta-blockers are contraindicated
they cause peripheral arteriolar dilation decreasing afterload and myocardial oxygen requirement and they produce coronary vasodilation (useful in variant angina)
68
What are some examples of calcium channel blockers used for angina?
Examples are amlodipine (little effect on heart and long-acting) and diltiazem and verapamil (negative inotropic effects)
69
How are calcium channel blockers used to treat dysrhythmias and what particular drug is used?
suppression of conduction through AV node
| verapamil is used but avoid in heart failure particularly with a beta-blocker
70
What are the adverse effects of calcium channel blockers?
from excessive vasodilation so hypotension, dizziness and swollen ankles
71
What so calcium channel blockers do?
block or prevent the opening of L-type channels in tissues that depolarise and hence limits an increase in intracellular calcium ions
72
Where do calcium channel blockers act?
L-type calcium channels in the heart, smooth muscle or in other locations
73
What do L-type calcium channels mediate and how do antagonists affect this?
upstroke of AP in SA and AV nodes (calcium ion antagonists can reduce rate and conduction through AVN) and phase 2 of the ventricular AP (calcium ion antagonists can reduce the force of contraction by reducing the amount of calcium)
74
What are the roles of angiotensin 2?
- Increases sympathetic nerve activity causing vasoconstriction and increasing BP
- Increases ADH release so increases water reabsorption so there is more water in the circulation so increases blood volume
- Increases thirst
- Increases sodium ion reabsorption from the kidney
75
What do ACE inhibitors block and what is an example?
the conversion of angiotensin 1 to angiotensin 2 eg Lisinopril
76
What do AT1 receptor antagonists block and what is an example?
the agonist action of angiotensin 2 at AT1 receptors in a competitive manner eg Losartan
77
What do ACE inhibitors cause?
- venous dilation (decreased preload) and arteriolar dilation (decreased afterload) which decreases ABP and cardiac load
- no effect on cardiac contractility
- reduce the release of aldosterone
- small fall in MAP (larger fall in hypertensive patients)
- reduce growth action of angiotensin 2 upon the heart and vasculature
78
What are the adverse effects of ACE inhibitors?
hypotension, dry cough, hyperkalemia and angioedema
79
What are AT1 receptor blocker useful for?
useful for patients who find dry cough by ACE intolerable
80
When should ACE inhibitors and AT1 receptor blockers never be used?
pregnancy and bilateral renal artery stenosis
81
What are the uses of ACEIs and AT1 receptor blockers?
- hypertension (reduced TPR and MABP)
- cardiac failure (improving perfusion, increassing excretion of Na+ and H2O and causing regression of left ventricular hypertrophy)
- following MI
82
What are the clinical uses of beta-adrenoceptors?
- Angina pectoris- they decrease myocardial oxygen requirement, counter elevated sympathetic activity associated with ischaemic pain and they increase diastole)
- Hypertension- reducing cardiac output, reducing renin release from the kidney and reducing sympathetic activity
- Heart failure- suppress adverse effects associated with increased sympathetic activity and RAAS
83
How do Katp channels act?
- antagonising intracellular ATP
- cause hyperpolarisation which switches off L-type Ca2+ channel
- act potently and primarily upon arterial smooth muscle
84
What is an example of a Katp channel opener?
E.g. Minoxidil used in severe hypertension (causes adverse reflex tachycardia and salt and water retention) or Nicorandil used in angina
85
What effect do alpha blockers have?
Alpha 1 adrenoceptor antagonists cause vasodilation and reduced sympathetic transmission resulting in decrease MAP
They can also relieve benign prostatic hyperplasia
86
What is the adverse effect of alpha blockers?
postural hypotension
87
What is a cardiac arrhythmia?
a disturbance of rate or rhythm that may be caused by changes in impulse formation or impulse conduction
88
How can cardiac arrhythmias be described?
in terms of rate so bradycardia and tachycardia or by site of origin so supraventricular (atria and AV node) or ventricular
89
What do alterations in impulse formation involve?
changes in automaticity or triggered activity
90
How does automacity usually work in normal cells?
- SA node is the normal pacemaker but all components in the cardiac conduction system demonstrate a slower phase 4 depolarisation and thus possess automaticity
- SA node pacemaker is normally highest and is dominant over other latent pacemakers such as the AV node and Purkinje fibres which is known as overdrive suppression
- SA node must discharge APs at a higher, regular frequency than any other structure in the heart
91
What are the two types of altered autemacity?
physiological or pathophysiological (when SA node is taken over by another latent pacemaker as a result of loss of overdrive suppression)
92
When does overdrive suppression occur?
- if SA node firing frequency is pathologically lower or if conduction of impulse from SA node is impaired then a latent pacemaker will initiate an escape beat
- if latent pacemaker fires at an intrinsic rate faster than the SA node rate: latent pacemaker makes ectopic beat
- in response to tissue damage even non-pacemaker cells may assume spontaneous activity
93
What can an ectopic beat result from?
ischemia, hypokalaemia, increased sympathetic activity or fibre stretch
94
What are afterdepolisations?
a normal AP may trigger abnormal oscillations in membrane potential termed afterdepolarizations, ADs of amplitude sufficient to reach threshold cause premature AP and beats
95
What are EADs?
early afterdepolaisations occur during the inciting of AP within phase 2 (ca2+ channels) and phase 3 (Na+ channels)
96
When are EADs most likely?
- when HR is slow
- often occur in Purkinje fibres
- are associated with prolongation of the action potential and drugs prolonging the QT interval
- when sustained can lead to life-threatening arrhythmia called ‘torsades de pointes’
97
When do DADs occur and what are they caused by?
- occur after complete repolarization
- caused by large increases in Ca2+ concentration
- result in release of Ca2+ from SR and a transient inward current of Na+ that occurs in phase 4
98
When are DADs most likely to occur?
- when the heart rate is fast
- are affected by drugs that change the length of APs
- may be triggered by drugs that increase Ca2+ influx or release from SR
99
What do abnormalities in impulse conduction arise from?
- re-entry
- conduction block
- accessory tracts
100
How does re-entry cause an impulse conduction abnormality?
- self sustaining electrical circuit stimulates an area of myocardium repeatedly
- requires unidirectional block (anterograde conduction prohibited and retrograde conduction allowed) and slowed retrograde conduction velocity
- two APs from two columns collide they extinguish each other but when there is unidirectional block then only one AP gets down so it is not extinguished
101
What are the types of partial conduction block (through AV node)?
- slowed conduction (first degree AV block)
- intermittent block (second degree AV block)
- complete block
102
What are the types of intermittent AV partial conduction block?
- Mobitz type 1 (PR interval gradually increases until it fails completely an beat is missed); treat with atropine
- Mobitz type 2 (PR interval is constant but every nth depolarization is missing); don't treat with atropine
103
What is complete block?
- no impulses are conducted through the affected area eg third degree AV block
- atria and ventricles beat independently
- ventricular pacemaker is now purkinje fibres
104
What are the ways that accessory tract pathways can cause arrhythmias?
bundle of Kent is another electrical pathway that is in parallel to the AV node and it conducts more quickly than through the AV node so ventricles receive two signals so there can be tachyarrhythmias
105
What do class IA target?
Voltage-activated Na+ channels (moderate rate association/dissociation from Na+ channels, they slow rate of rise of AP and prolong refractory period)
106
What do class IB target?
Voltage-activated Na+ channels (rapid association and dissociation and prevent premature beats)
107
What do class IC target?
Voltage-activated Na+ channels (slow association/dissociation and depress conduction)
108
What do class II target?
Beta-adrenoceptor (decrease rate of depolarisation in SA and AV nodes)
109
What do class III target?
Voltage-activated K+ channels (prolong AP duration increasing refractory period)
110
What do class IV target?
Voltage-activated Ca2+ channels (slow conduction in SA and AV node, decrease force of cardiac contraction)
111
How do Class I agents work?
Class I agents bind and target areas of the myocardium where firing frequency is highest so they block the open state and stabilise the inactivated state.
Class I agents dissociate from the Na+ channel when it is at rest so if HR increases there is less time for dissociation so steady state block increases
112
What changes for Class I agents in ischaemic myocaridum?
- the APs are longer so the inactivated state of the Na+ channel is available to the blockers for longer and the rate of recovery is decreased
- the higher affinity of channel blockers for the open and inactivated states allows them to act on ischaemic tissue and block arrhythmias at the source
113
What are the features of lipids?
insoluble
essential for membrane biogenesis and integrity
energy source
precursors for hormones and signalling molecules
114
What are examples of non-polar lipids?
cholesterol esters and triglycerides
115
How are non-polar lipids transported?
in the blood
116
What are lipoproteins made up of?
- Lipoproteins have a hydrophobic core containing esterified cholesterol and triglyceride
- They have a hydrophilic coat comprising of a monolayer of amphipathic cholesterol, phospholipids and one or more apoproteins
117
What are the major lipoproteins and what apoproteins are they associated with?
HDL (apoA1 and apoA2)
LDL (apoB-100)
VLDL (apoB-100)
chylomicrons (apoB-48)
118
What do apo-B lipoproteins do?
deliver triglycerides to muscle for ATP biogenesis and adipocytes for storage
119
What pathway do chylomicrons form?
exogenous pathway
120
Where are VLDL particles synthesised and what do they do?
synthesised in the liver and transport the TAGs synthesised by that organ which is the endogenous pathway
121
What is the outline of the life-cycle of an app-B containing liposome?
- assembly
- intravascular metabolism (hydrolysis of TAG core)
- receptor mediated clearance
122
How are chylomicrons assembled?
- cholesteryl ester and TAGs are in cytoplasm
- apoprotein is synthesised in the enterocyte
- vesicle grows and cholesteryl ester is added to make a chylomicron
- moves out of the enterocyte by exocytosis and enters the lymphatic system
123
How are VLDLs assembled?
assembled in liver hepatocytes from free fatty acids and are derived from adipose tissue and de novo synthesis
124
How are chylomicrons and VLDL particles activated?
activated by the transfer of apoC2 from HDL particles
once apoC2 has been added to the LDL
it allows the particles to interact with an enzyme of the surface of capillary cells called LPL
the enzyme can then digest the core to give three fatty acids and a glycerol which can use simple diffusion to cross the capillary wall into the tissues
125
How are chylomicrons cleared?
- depleted core
- triglycerides removes
- dissociation from LPL
- apoC2 returned to the HDL particles and poE is given to partially digested particles
- remnants are sent to the liver and enter by receptor-mediated endocytosis
- metabolism by hepatic lipase
- LDL receptor needed to internalise LDL into liver cell
- released cholesterol causes inhibition of HMG-CoA reductase
- down regulation of LDL receptor expression
- storage of cholesterol as cholesterol ester
126
What do stains block?
competitively block HMG-CoA reductase so increases cell surface expression of LDL receptor so more LDL into the liver cells so increased LDL clearance from the blood
127
Why is LDL bad?
- Uptake of LDL into intima and is oxidised to oxidised LDL
- Migration of monocytes into intima where they become macrophages
- Uptake of OXLDL by macrophages so they become cholesterol-laden foam cells and form a fatty streak
- Release of inflammatory substances and proliferation of smooth muscle cells into the intima and deposition of collagen
- Atheromatous plaque formation involving a lipid core and a fibrous cap
128
Why is HDL good?
- HDL removes excess cholesterol by transporting it into the liver
- HDL is formed in the liver initially as ApoA1
- Can accept excess cholesterol onto its surface and is stored in the core as esterified cholesterol
- It then delivers the cholesterol to the liver by reverse cholesterol transport
129
What is primary dyslipidemia?
occurs through a combination of diet and genetics
130
What is secondary dyslipidameia?
a consequence of other diseases
131
What are the other benefits of statins?
decreased inflammation, reversal of endothelial dysfunction, decreased thrombosis and stabilization of atherosclerotic plaques
132
What do fibrates do?
Used to decrease TAGs and small decreases in LDL and HD
| It increases activity of LPL by binding to PPARalpha as a competitive agonist
133
What do bile acid binding resins do?
bile acid binding resins cause excretion of bile salts resulting in more cholesterol to be converted to bile salts by interrupting enterohepatic recycling
134
What does Ezetimibe do?
Inhibits NPC1L1 transport protein in enterocytes which reduces the absorption of cholesterol in the duodenum
This causes a decrease in LDL but little change in HD
L
135
What is the treatment for an MI acutely?
- morphine and anti-emetic
- oxygen (if needed)
- nitroglycerin
- aspirin 300mg
- clopidogrel
136
What is the treatment of a STEMI in hospital?
- beta-blocker orally if no heart failure, no low output state, no increased risk cardiogenic shock and no contraindications
- anti-coagulation with fondaparinux
137
What is the time limit for PCI before fibrinolytic are used?
90 mins
138
What are the contraindications for thrombolysis?
- recent surgery
- recent trauma or head injury
- bleeding diatheses
- coma
- active peptic ulcer
- recent stroke
- suspected aortic dissection
- traumatic resuscitation attempt
- allergy to streptokinase
- severe hypertension – control the blood pressure first eg with GTN then proceed.
139
What are the side-effects of opiates?
sedation, hypoventilation and nausea
140
What are the side-effects of beta-blockers?
bradycardia, cardiac failure, bronchospasm in asthma & chronic bronchitis, hypotension
141
What drugs reduce the effects of anti-hypertensive ACEIs?
NSAIDs so ibuprofen
