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Flashcards in WEEK 5 Deck (40):

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)

1. ASK about tobacco use
2. ADVISE to quit
(ASSESS willingness to make a quit attempt)
3. ASSIST in quit attempt
4. ARRANGE follow-up

1. RELEVANCE - ask to identify why quitting might be personally relevant
2. RISKS - reiterate benefits for pt & their children
3. REWARDS - more oxygen after 1 day, clothes & hair smell better, money, more energy
4. ROADBLOCKS - being around smokers, triggers & cravings, -ve moods


Outline the Stage Model of Behaviour Change (Prochaska and Di Clemente).

- 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
- more awareness of -ve aspects of smoking, intention to quit w/in 6 months
- dispel -ve myths about quitting, reinforce willpower to quit
- 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?

- prolongs the cardiac AP by prolonging the refractory period


What is the uses of the Class III group of drugs?

- 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
- 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?

- 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


What are the basics of an epidemiological approach?

1. DESCRIBE the health status of a population
- descriptive studies (time, place & person)
2. UNDERSTAND the natural history of a condition
- longitudinal studies
3. IDENTIFY underlying causes of medical problems
- observational studies (cohort or case-control)
4. ACT/EVALUATE medical & health promoting interventions
- monitor (routine data, observational studies) or intervene (experimental studies)


What is the Framingham Heart Study?

Objective of the study was to identify the common factors/characteristics that contribute to CVD by following its development over a long period of time in a large group of participants who had not yet developed overt symptoms of CVD or suffered a heart attack or stroke


Define (i) pathogenic (ii) salutogenic (iii) interactive.

(i) linked to disease state
(ii) linked to health e.g. physical activity
(iii) together increase risk


What are the 3 types of 'risk factor'?

1. MARKER of risk
- associated with the probability of disease but not causal
2. CAUSAL risk factor (determinant)
- associated & causal
3. MODIFIABLE risk factor
- causal & can be modified by intervention


What are the four phases of cardiac rehabilitation?

Phase 1: hospital stay
Phase 2: recovery at home
- titrate medication, review, emotional, physical & practical support provided by cardiac nurses
Phase 3: exercise component
- overlaps with phase 2, circuit class, ongoing support
Phase 4: gym based


What are the implications of cardiac misconceptions in recovery from myocardial infarction? (HINT: there's 7 points)

1. Higher level of emotional distress & invalidism
2. Slower recovery
3. Reduced rate of return to work
4. Increased hospitalisations
5. Poor attendance at cardiac rehab
6. Angina pts are more likely to be anxious, depressed and/or physically limited
7. Angina misconceptions are a significant predictor of pts physical limitations at 1 yr follow up


What is the role of the Heart Manual in cardiac rehabilitation? (HINT: there's 10 points)

1. Explanation of what has happened to the heart
2. Undermines damaging & upsetting beliefs
3. Home based exercise programme
4. Advice on goal setting & pacing
5. Relaxation & stress management programme
6. Recovering pts vignettes
7. Quizzes to trap misconceptions
8. CD for partner & family advising how to best help
9. Short questionnaires to determine adjustment e.g. anxiety, sexual relations, panic attacks
10. Answers what most people want


What is quality of life?

The presence of a reasonable amount of pleasurable, successful & meaningful experience


What are the 2 example scales used to measure the QoL? (HINT: one is a general survey & one is CV specific)

1. SF-36
- widely used genetic measure. 36 items, 8 domains
2. Seattle Angina Questionnaire (SAQ)
- disease specific, self-administers, 19 item instrument


What are the determinants of quality of life in heart disease

1. PHYSICAL functioning
2. PSYCHOLOGICAL functioning
3. SOCIAL functioning
4. OCCUPATIONAL functioning
5. Perception of HEALTH STATUS


What does the QoL measure?

The illness experience
(as opposed to the disease)


What is a biopsychosocial model used to help understand?

the relationship between psychological distress & impact on heart disease


Describe the relationship between depression and heart disease

Estimated 15-45% pts in depression after MI
Predictive of:
- poor mortality, social & functional outcomes
- depression = most common feature of QoL
- a major risk factor for relapse in cardiac pts


What should cardiac care include attention to?

1. The pts understanding of their illness
2. Pts behaviour
3. Coping measures they adopt
4. Emotional status
5. Influence of friends & family


Define (i) SIRS (ii) sepsis (iii) septic shock.

(i) infection or other cause of systemic inflammatory response which produces:
- widespread endothelial damage with vasodilation
- arterio-venous shunting
- microvascular occlusion
- capillary leak
- tissue oedema
(ii) suspected or proven infection PLUS systemic inflammatory response (e.g. fever, tachycardia, tachypnea, increased WBC, altered mental state, hyperglycaemia in absence of diabetes)
(iii) Severe sepsis plus hypotension, despite fluid resuscitation


What are the clinical features of SIRS?

1. warm peripheries
2. bounding pulses & features of high CO
3. peripheral vasodilation leading to decreased diastolic BP
4. decreased afterload, therefore stroke volume & systolic BP is maintained
5. Large difference between systolic & diastolic BP (e.g. 115/42mmHg)
- as sepsis advances, systolic BP decreases & peripheries become cool due to hypovolaemia associated with capillary leak


What is the sepsis six? List them.

A series of interventions/tests
1. Administer high flow oxygen
2. Take blood cultures
3. Give broad spectrum antibiotics
4. Give IV fluid challenges
5. Measure serum lactate & Hb
6. Measure accurately urine output


What are the main risk factors for sepsis? (HINT: theres 10 factors)

1. Immunosuppression
2. Asplenics
3. Diabetics
4. Pregnancy
5. Cancer pts
6. Prosthetic devices
7. Mechanical ventilation
8. Severe wounds/burns
9. Post surgery
10. Extremes of age


What are the 5 factors affecting signs & symptoms of sepsis?

1. Virulence of pathogen
e.g. streptococcus pyogenes
2. Bioburden
e.g. salmonella typhimurium
3. Portal of entry
e.g. klebsiella pneumoniae
4. Host susceptibility
e.g. streptococcus pneumoniae
5. Temporal evolution
e.g. neisseria meningitidis


Host innate immunity is the first line of defence against pathogenic insult. What is it comprised of? What do these initiate the production of?

Complement, mannose binding lectin, phagocytes, toll-like receptors, nucleoside-binding oligomerisation domain receptors.
- these initiate the production of inflammatory markers (e.g. ILs, TNFalpha, ROS-reactive oxygen species)


What are the effects of TNFalpha & IL-1 on the BODY?

- fever, hypotension, increased HR, corticosteroid & ACTH release, release of neutrophils


What are the effects of TNFalpha & IL-1 on the CVS? (HINT: there's 5 effects)

Generalised vasodilation (primary driver = NO)
Increased vascular permeability (activated leukocytes)
Intravascular fluid loss
Myocardial depression (tissue hypoxia)
Circulatory shock


During sepsis, what happens to the peripheral resistance?

Vasodilation by nitric oxide


During sepsis, what 2 things happen to the stroke volume? They occur as a result of what?

1. Decreased myocardial activity due to tissue hypoxia
2. Decreased vascular volume due to increased vascular permeability