WEEK 5 Flashcards
What are the general effects of use of tobacco on health?
Causes cancer, COPD & CVD
- an important cause of morbidity
- on average, cigarette smokers lose 7.5 years of life
To relate one example of Smoking and respiratory disease
(results of a 1 year intensive programme)
Methods: 15 group meetings with 8-10 pts. Met with specialist nurse & researcher
- 38 smokers with COPD/chronic bronchitis & 22 healthy smokers
FOUND: 42% of COPD/CB quit after 1 year & 68% of healthy subjects quit after 1 year
List the principles of Smoking Cessation (4 A’s and 5 R’s)
- ASK about tobacco use
- ADVISE to quit
(ASSESS willingness to make a quit attempt) - ASSIST in quit attempt
- ARRANGE follow-up
- RELEVANCE - ask to identify why quitting might be personally relevant
- RISKS - reiterate benefits for pt & their children
- REWARDS - more oxygen after 1 day, clothes & hair smell better, money, more energy
- ROADBLOCKS - being around smokers, triggers & cravings, -ve moods
- REPETITION
Outline the Stage Model of Behaviour Change (Prochaska and Di Clemente).
PRECONTEMPLATION:
- lack of awareness or lack of intent to change
- strategy = short messages to attract attention, potentially bring up novel & highly relevant facts previously not considered
CONTEMPLATION:
- more awareness of -ve aspects of smoking, intention to quit w/in 6 months
- dispel -ve myths about quitting, reinforce willpower to quit
PREPARATION:
- small behavioural changes to quit are made; intent to quit w/in 1 month
- longer messages, offer concrete tips & methods to help quit
ACTION: implemented plan to stop, still adjusting to change
- offer specific relapse prevention advice for nicotine dependence to include advice on the nicotine patch
MAINTENANCE: long term adjustment as a non-smoker, content with new lifestyle without cigarettes
- congratulate & advise ongoing vigilance to keep off cigarettes
Explain the Vaughan Williams classification of anti-dysrhythmic drugs.
1a: Na Channel Blockers - Disopyramide
1b: Na Channel Blockers - lignocaine
1c: Na Channel Blockers - Flecainide
2: b-adrenoreceptor blockers - Sotalol
3: K channel block - amiodarone
4: Ca channel blockers - Verapamil
Unclassified: adenosine & digoxin
What is the the MoA, of the Class I group of drugs?
- They inhibit AP propagation & reduce the rate of cardiac depol during phase 1
- Being split into a,b & c is based on the properties of the drugs in binding to Na channels in their various states (open, refractory & resting)
- Cardiac myocytes must repolarise to reset the sodium channels back to resting state
- these drugs bind to the open & refractory states of the channels & so are viewed as use-dependent
What is the the clinical uses, of the Class I group of drugs?
CLASS 1A Disopyramide
- ventricular dysrhythmias, prevention of recurrent atrial fibrillation triggered by vagal over activity
CLASS 1B: lignocaine (given by IV)
- treatment & prevention of ventricular tachycardia & fibrillation during & immediately after MI
CLASS 1C: Flecainide
- supresses ventricular ectoptic beats. Prevents paroxysmal AF & recurrent tachycardias associated with abnormal conducting pathways
Define the term ““use-dependent”” block.
They work more effectively if there is high activity & so are more effective against abnormal high frequency activity & not so much against normal beating rates
What is the MoA of the Class II group of drugs?
- they block beta 1 receptors, slowing the heart & decreasing CO
- decreases rate of depolarisation of the pacemaker cells
- reduces the calcium entry in phase 2 of cardiac AP => shorter phase 2
- ## increase refractory period of AVN => prevent recurrent attacks of SVTs
What is the clinical uses of the Class II group of drugs?
Sotalol, bisoporol, atenolol
- reduce mortality followign MI
- prevent recurrence of tachycardias provoked by increased sympathetic activity
What is the mechanism of action of the Class III group of drugs?
Amiodarone
- prolongs the cardiac AP by prolonging the refractory period
What is the uses of the Class III group of drugs?
Amiodarone
- tachycardia associated with WPW (heart condition featuring episodes of abnormally fast HR, can last secs, hrs, or days, may be once/twice a week or just once in a while) The combo of AF & WPW can be life-threatening.
- effective in many other supraventricular & ventricular tachyarrhythmias
Sotalol
- combines class 3 with vlass 2 actions
- used in supraventricular dysrhythmias & suppresses ventricular ectopic beats & short runs of ventricular tachycardia
What is the mechanism of action of the Class IV group of drugs?
VERAPIMIL & DILTIAZEM
- block cardiac V-gated L-type calcium channels
- slow conduction through SAN & AVN where the conduction of AP relies on the slow Ca currents
- they shorten the plateau of the cardiac AP & reduce the force of contraction of the heart
What is the clinical uses of the Class IV group of drugs?
Verapamil = the main drug
- used to prevent recurrence of SVT
- & to reduce the ventricular rate in pts with AF provided they don’t have WPW
- it is ineffective & dangerous in ventricular dysrhythmias
- diltiazem is similar to verapamil but has more effect on smooth muscle Ca channels & has less bradycardia
What are the mechanisms of action, and uses of adenosine?
- produced endogenously with effects on breathing, cardiac & smooth muscle, vagal afferent nerves & platelets
- A1 receptor is responsible for the effect on the AV node
- receptors are linked to the same cardiac K channels that’re activated by ACh =? hyperpolarises cardiac conducting tissue & slos HR. Decreases pacemaker activity
- used to terminate SVTs
What are the mechanisms of action, and uses of digoxin?
Derived from foxglove plant - digitalis purpurea
Increases vagal efferent activity to the heart by an unknown mechanism
- this parasympathomimetic action of digoxin reduces SA firing rate (=> decreasing HR) & reduces conduction velocity of electrical impulses through the AVN
NOTE: toxic concentrations of digoxin can disturb sinus rhythm & this results in inhibition of the Na/K pump causing depolarisation => ectopic beats
