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MD3001 > Week 5 > Flashcards

Week 5 Flashcards

1
Q

To describe the general effects of use of tobacco on health

A
  1. Principal fatal diseases caused by smoking are cancer, COPD and CVD
  2. Morbidity
  3. Risks for dose and duration dependent
  4. Lose of 7.5yrs of life
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2
Q

4 A’s approach to smoking cessation

A

ASK about tobacco use
ADVISE to quit (Clear, strong and personalized)
(Assess willingness to make quit attempt)
ASSSIST in quit attempt (are they willing?)
ARRANGE follow up

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3
Q

Characteristics and strategy of the pre-contemplation stage in quitting smoking?

A

Characteristics: Lack of Awareness or lack of intent to change

Strategy: Short messages to attract attention, bring up otentially novel and highly relevant facts previously not considered

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4
Q

Characteristics and strategy of the contemplation stage in quitting smoking?

A

Characteristics: Increased awareness of negative aspects of smoking. Has intention
to quit within 6 months.
Strategy: Dispel Negative myths about quitting smoking; reinforce willpower to quit

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5
Q

Characteristics and strategy of the preparation stage in quitting smoking?

A

Characteristics: Some small behavioral changes to quit have been made; intent to quit within 1 month (can set a “quit date”)
Strategy: Longer messages, offer concrete tips and methods to help quit smoking

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6
Q

Characteristics and strategy of the action stage in quitting smoking?

A

Characteristics: Individual has implemented plan to stop, still adjusting to the change
Strategy: Offer specific relapse prevention advice for nicotine dependence to include advice on the nicotine patch

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7
Q

Characteristics and strategy of the maintenance stage in quitting smoking?

A

Characteristics: Long term adjustment as a non-smoker, content with new lifestyle without cigarettes
•Strategy: Congratulate and advise ongoing vigilance to keep off cigarettes

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8
Q

What approach is used to treat patients who decline to quit smoking? (5 R’s)

A

Relevance: What is their motive for quitting?
Risks to health: What do they already know?
Rewards to health
Roadblocks: E.g. negative moods, being around smokers, triggers, cravings, time pressures
Repetition

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9
Q

Health benefits of smoking cessation (6)

A
  1. Increased longevity
  2. Stabilisation of lung cancer risk
  3. Heart disease risk decline toward non-smoker level over 10yrs
  4. Accelerated decline in lung function reduced
  5. Improved reproductive health: Women who stop smoking before pregnancy, there are no adverse effect on infant
  6. Improved recovery from surgery: Fewer wound-related complications, reduced CV complications and secondary surgery
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10
Q

What are the psychological pathways to quitting smoking?

A

Transtheoretical Model of Behaviour Change (Prochaska and DiClemente)

Pre-contemplation –> Contemplation –> Preparation –> Action Maintenance –> relapse –> (back to pre-c)

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11
Q

What are 2 strategies to overcoming the following roadblocks when quitting smoking:

  1. Negative moods
  2. Other smokers
  3. Triggers and cravings
  4. Time pressures
A

Negative moods: Physical activity, relax
Other smokers: Quit with a friend, remove yourself from smoking environment
Triggers and cravings: Change routine, prepare for triggers and substitute smoking
Time pressures: Increase physical activity, reduce stress

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12
Q

7 negative beliefs held by GPs about smoking cessation

A
  1. Discussions too time consuming
  2. Ineffective
  3. Lacked confidence in cessation advice
  4. Discussions unpleasant
  5. Lacked confidence in knowledge
  6. Cessation considered outside professional duty
  7. Inappropriate
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13
Q

Where do the intercostal arteries arise from?

A

1-2 pairs: From a branch of corresponding subclavian artery

3-11 pairs: From descending thoracic aorta

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14
Q

What drains the right and left posterior thoracic wall?

A

Right: Intercostal veins drain directly into azygos vein
Left:
-Intercostal veins 4-8 drain into accessory hemiazygos vein.
-Intercostal veins 9-11 drain into hemiazygos veins.

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15
Q

What position do the vessels lie in the neurovascular bundle in the intercostal space?

A

(sup.) VAN (inf.)
Posterior intercostal vein
Posterior intercostal artery
Intercostal nerve

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16
Q

What structures pass through the diaphragm at T10?

A

Oesophagus

Vagal trunks

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17
Q

What structures pass through aortic hiatus at T12?

A

Descending thoracic aorta
Thoracic duct
Azygos vein

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18
Q

What ganglions fused to form the stellate ganglion?

A

T1 ganglion

Inferior cervical ganglion

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19
Q

The splanchnic nerves arise from the _______ trunk and pass inferomedially. These comprise preganglionic sympathetic fibres that pass into the abdomen to supply ______ _______

A

The splanchnic nerves arise from the SYMPATHETIC trunk and pass inferomedially. These comprise preganglionic sympathetic fibres that pass into the abdomen to supply ABDOMINAL VISCERA

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20
Q

What connects the ganglia of the sympathetic trunk to their adjacent innercostal nerve?

A

Rami communicantes

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21
Q

The spontaneious electrical discharge of the SAN is from the combined effect of:

A
  1. Decrease in K outflow
  2. “funny” Na current
  3. Slow inward Ca current
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22
Q

Define dysrhythmia?
Name 3 possible causes?
Classifications?

A

Dysrythmia describes conditions where the co-ordinated sequence of electrical activity in the heart is disrupted.

Could be due to:

  1. Changes in the heart cells
  2. Changes in the conduction of the impulse through the heart
  3. Combinations of these

Classifications:

  • Atrial (supraventricular)
  • Junctional (associated with AV node)
  • Ventricular
  • Tachycardia/bradycardia
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23
Q

What is the general classification based on the event?

A
  • Ectopic pacemaker activity
  • Delayed after-depolarization
  • Circus re-entry
  • Heart block
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24
Q 
Name an example of a antidysrhythmic drug under each of the following Vaughan Williams classes:
• 1a (Sodium channel blockers)
• 1b (Sodium channel blockers)
• 1c (Sodium channel blockers)
• 2 (b-adrenoreceptor blockers)
• 3 (Potassium channel block)
• 4 (Calcium channel blockers)
• Unclassified
A
  • 1a: -Sodium channel blockers, disopyramide
  • 1b: -Sodium channel blockers, lignocaine
  • 1c: -Sodium channel blockers, flecainide
  • 2: -b-adrenoreceptor blockers, sotalol
  • 3: -Potassium channel block, amiodarone
  • 4: -Calcium channel blockers, verapamil
  • Unclassified: adenosine and digoxin
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25
Q

How do Class 1 antidysrhythmic drugs act?

A

Inhibit action potential propagation and they reduce the rate of cardiac depolarization during phase 1.
Drugs bind to open and refractory states of the channels and so are viewed as use-dependent i.e. work most effectively against abnormal high frequency activity.

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26
Q

Clinical uses of class 1 antidysrhythmic drugs:

  • Class 1a
  • Class 1b
  • Class 1c
A

Class 1a:

  • E.g. Disopryramide
  • Ventricular dysrhythmias, prevention of recurrent atrial fibrillation triggered by vagal over activity

Class 1b:

  • E.g. Lignocaine
  • Treatment and prevention of ventricular tachycardia and fibrillation during and immediately after MI

Class 1c:

  • E.g. Flecainide
  • Suppresses ventricular ectopic beats. Presents paroxysmal atrial fibrillation and recurrent tachycardias associated with abnormal conducting pathways
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27
Q

How do Class 2 antidysrhythmic drugs act? 2

What is the action of the beta-1 receptors? 2

A

Action of Beta-blockers

  • Slows the heart
  • Decreases CO
  • Increase the refractory period of the AV node so prevents recurrent attacks of the supraventricular tachycardias

Action of Beta-1 receptors:

  • Increases rate of depolarization of the pacemaker cells
  • Enhances calcium entry to phase 2 of the cardiac action potential
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28
Q 
3 examples of class 2 drugs?
Clinical uses of class 2 antidysrythmic drugs?
A

B-blockers
E.g. Sotalol, bisoprolol, atenolol
Clinical use: Clinical uses are to reduce mortality following MI and to prevent recurrence to tachycardias provoked by increased sympathetic activity

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29
Q

Class 3 antidysrhythmic drug action?

Examples (2)

A

Action: Prolongs the cardiac action potential by prolonging the refractory period via potassium channel blockage.
Examples: Amiodarone, sotalol

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30
Q

Clinical uses of class 3 antidyrhymic drugs Amiodarone and Sotalol?

A

Amiodarone:

  • Tachycardia associate with the Wolff-Parkinson-White syndrome
  • Effective in other supraventricular and ventricular tachyarrhythmias

Sotalol:
-Combines class 3 with class 2 actions
-Used in supraventricular dysrhythmias
-Suppresses ventricular ectopic beats and short runs of ventricular tachycardia
(WPW syndrome: Conduction by-passes the AV node leading to rapid uncontrolled contractions)

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31
Q

Class 4 antidysrythmic drugs:

  • Action?
  • 2 example?
A

Action:

  • Blocks cardiac voltage-gated L-type calcium channels
  • Slows conduction through the SA and AV nodes where the conduction of the action potential relies on the slow calcium currents
  • Shorten the plateau of the cardiac cells and reduce the force of contraction

Examples: Verapamil and diltazem

32
Q

Clinical uses of verapamil and diltiazem in treating dysarhymias?

A

Class 4 drugs = Calcium channel blockers
Verapamil:
-Main drug
-Used to prevent recurrence of supraventricular tachycardias (SVTs)
-To reduce the ventricular rate in patients with atrial fibrillation provided they do not have Wolff-Parkinson-White syndrome
-Ineffective and dangerous in ventricular dysrhythmias

Diltiazem:

  • Similar to above
  • More of an effect on smooth muscle calcium channels
  • Has less bradycardia
33
Q

What part of the action potential is affect by the different classes of antidysrythmic drugs?

A

Class 1: Inhibits rapid depolarization by Na channel inhibits
Class 2: Inhibits beta-receptors by blocked beta-1 receptors
Class 3: Inhibits repolarization by blocking K channels
Class 4: Inhibits the plateau by blocking Ca channels

34
Q

Why is adenosine used to treat dysrhythmias?

Which dyarhythmias?

A

Acts of A1 receptors which effect the AV node. These receptors are linked to the cardiac potassium channels hence hyperpolarized cardiac conducting tissue and slows the HR. Also decreases pacemaker activity.

Used to terminate SVTs

(Potassium channels also activated by ACh, so adenosine has same affect of PS innervation)

35
Q

How is digoxin used to treat dysrhythmias?

Side effect?

A

Increase vagal efferent to the heart
This parasympathomimetic action of digoxin reduces sinoatrial firing rate and reduces conduction velocity of electrical impulses through the AV node.

Side effect: Toxic concentrations disturb sinus rhythm. Due to inhibition of Na/K pump causes depolarization- ectopic beats

36
Q

What is the systematic approach to epidemiology of CVD?

A

Describe the health status of a population: Descriptive studies (time, place, person)

Understand the natural history of a condition: Longitudinal studies

Identify causes of medical problems: Observational studies (cohort/case-control)

Evaluate medical and health promoting interventions:
-Monitor (routine data, observational studies) -Intervene (experimental studies)

37
Q

Define public health

A

The science and art of preventing disease, prolonging life, and promoting health through the organized efforts of society

38
Q

During the epidemiology of CVD, discuss how the health status of a population is described?

A

Descriptive studies (time, place, person)

Time: Mortality of the population over time
Place: Death rates by CVD by local authorities
Person: Age, sex, genetic factors, health conditions, lifestyle, wider environemnt

39
Q

During the epidemiology of CVD, how is the natural history of a condition understood?

A

Longitudinal studies: observational research method in which data is gathered for the same subjects repeatedly over a period of time.

40
Q

During the epidemiology of CVD, how are underlying causes identified?

A

Observational studies:

  • Cohort studies: Look at factors that contribute to CVD and follow development over time
  • Case/control studies
41
Q

What is the difference between the pathogenic, salutogenic and interactive risk factors?

A

Pathogenic: Linked to disease state e.g. cholesterol
Salutogenic: Linked to health e.g. physical activity
Interactive: Together increase risk e.g. smoking and asbestos

42
Q

What are 3 different types of risk factor?

A

Marker of risk: Associated with the probability of disease by not causal
Causal risk factor: Associated and causal
Modifiable: Causal and can be modified by intervention

43
Q

What is the relevance of Geoffrey Rose in epidemiology of CHD?

A

The population based approach to reducing risk
Population approach = Decreases overall risk
Targeted approach = Only affects the group of people at high risk

44
Q

During the epidemiology of CVD, how are medical and health promoting interventions evaluated?

A

Either:

  • Service level: Monitors performance.
  • Academic study: Epidemiological research

Performance monitoring:

  • Includes prevention, treatment and rehabilitation
  • Evaluation should be systematic and look at structure, process and outcome
  • Epidemiological information that can be used for performance monitoring includes: Quality outcomes framework, data from smoking cessations services, Lifestyles surveys, data about the outcomes for individual clinicians
45
Q

Risk factor:
Aspect of?
Which on the basis of epidemiological evidence…

A

Risk factor is an aspect of :

  • Personal behavior
  • Life style
  • Environmental exposure
  • Genetic trait

On the basis of epidemiological evidence:

  • Is associated with a health-related condition
  • Considered important to prevention
46
Q

What are the different risk factors included in the Framingham study fro CVD?

A

TC: HDL (cholesterol ratio)
Systolic BP

Used for patients without pre-existing CVD or diabetes

47
Q

To identify the four phases of traditional cardiac rehabilitation

A 
Phase 1: Hospital stay
Phase 2: Recovery at home
-Titrate medication
-Review 
-Emotional
-Physical and practical support from cardiac nurses
Phase 3: Exercise component 
-Overlap with phase 2
-Circuit class
-Ongoing support 
Phase 4: Gym based
48
Q

Cardiac misconceptions in recovery from myocardial infarction:

3 common cardiac misconceptions?
Result of misconceptions?

A

Common cardiac misconceptions:

  1. If you’ve had a heart attack, you’ll die prematurely of heart disease
  2. Any shock or excitement could kill me
  3. Rest restores the heart

Results of misconceptions:

  • Feel safe at home
  • Anxious at work
  • Phobic avoidance e.g. exercise, work
  • Health anxiety by paying too much attention to body
  • Emotional distress
  • Slower recovery
  • Poor attendance of cardiac rehab
49
Q

3 main components of cardiac rehab?

EEE

A

Exercise
Education
Emotional

50
Q

What is the new approach to cardiac rehab?

Hint: Stages 0-6

A

Stage 0: Identify and refer patient
Stage 1: Manage referral and recruit to rehab
programme
Stage 2: Assess patient for cardiac rehab
Stage 3: Develop patient care plan
Stage 4: Deliver comprehensive cardiac rehab
programme
Stage 5: Conduct final assessment
Stage 6: Discharge and transition to long-term
management

51
Q

What does the Heart Manual comprise of?

A

Part 1: Your Heart Attack (the facts), recovering from hospital

Part 2: The weekly programme

  • Week 1: Getting home
  • Week 2: Feeling better?
  • Week 3: Making progress
  • Week 4: Getting better all the time
  • Week 5: Feeling more yourself?
  • Week 6: The end…. and the beginning

Part 3: Facts and advice to help recovery

52
Q

Name 4 pieces of information contained within the Heart Manual?

A
  1. Explanation of what has happened to the heart
  2. Relaxation and stress management programme
  3. Quizzes to trap misconceptions
  4. Home based exercise programme
53
Q

What are the independent risk factors for CHD?

A

Depression
Social isolation
Emotional distress after catastrophic event

[Not chronic life stress, unless depression makes you stressed]

54
Q

How to challenge cardiac misconceptions?

A
  1. Patients not aware of their misconception
  2. Direct challenge not always the best way
  3. Re-framing their beliefs
  4. Socratic questioning (use questions to lead someone to a different conclusion about their beliefs)
  5. Base discussion on the patients own values and experiences
  6. Watch out for flippant comments e.g. “Take it easy!”
55
Q

Define quality of life and its measurement in heart disease

A

QOL: The presence of a reasonable amount of measureable, successful and meaningful experience
HRQOL/Health Related QOL: Quality of life relative to one’s health or disease sate

Measurement:

  • SF 36: Widely used, generic measure, 36 items (8 domains)
  • SAQ: Seattle Angina Questionnaire. Disease specific, self administers, 19 item instrument
56
Q

Describe the determinants of quality of life in heart disease

A

Physical functioning:

Psychological functioning: Poor quality of life, impacts disease process and treatment adherence, impact behavioural and cognitive functioning

Social functioning: Anxiety

Occupational functioning

Perception of health status: Influenced by life experiences

57
Q

Describe the relationship between depression/anxiety and heart disease

A

Previous heart disease can cause onset of anxiety/depression. This leads to the following…

Strategies to cope with anxiety/depression can be used to help cognitive function

Adrenaline release in anxiety:

  • Physical effects: dizziness, dry mouth, shortness of breath, heart racing, butterflies in stomach
  • Cognitive effects: Racing thoughts, anxious thoughts, preoccupation with bodily sensations
58
Q

Define reliability

A

Reliability: extent to which a measure provides similar values for individuals with a similar underlying QOL

59
Q

Define validity

A

Validity: extent to which it measures what it purports to measure

60
Q

Define responsiveness

A

Responsiveness: extent to which changes in HRQOL measures correlate with true changes in QOL

61
Q

Define sensitivity

A

Sensitivity: the extent to which a measure can detect meaningful changes in QOL

62
Q

Define SIRS

A

Systemic Inflammatory Response Syndrome (SIRS)

Infection (or other cause of systemic inflammatory response) which produces:

  • Widespread endothelial damage with vasodilation
  • Arterio-venous shunting
  • Microvascular occlusion
  • Capillary leak
  • Tissue oedema
63
Q

What is sepsis?

A 
Infection 
PLUS systemic inflammatory response e.g. 
-Fever, tachycardia
-Tachypnea
-Increase WBC
-Altered mental state 
-Hyperglycaemia
64
Q

What is severe sepsis?

A 
Sepsis 
PLUS organ dysfunction e.g.
-Hypotension
-Hypoxaemia
-Oliguria
-Metabolic acidosis
65
Q

What is septic shock?

A 
Severe sepsis 
PLUS hypotension (despite fluid resus)
66
Q

The presence of which vitals defines SIRS

A

Presence of 2 or more of:

  • Resp rate >20/min
  • HR >90/min
  • WBC > 12 x 109/L or <4 x 109/L
  • 36C>Temp>38C
  • PaCo2 < 4.3kPa or ventilated
67
Q

What 2 conditions are indicators of severe infection?

A

Hypothermia

Septic neutropenia

68
Q

What 2 conditions are indicators of severe infection?

A

Hypothermia

Septic neutropenia

69
Q

5 clinical features of SIRS

A
  • Warm peripheries
  • Bounding pulses and features of high cardiac output (to maintain TPR)
  • Peripheral vasodilation leading to decreased diastolic BP
  • Decreased afterload, therefore stroke volume and systolic BP is maintained
  • Large difference between DBP and SBP

As sepsis advances, systolic BP decreases and the peripheries become cool due to hypovolaemia associated with capillary leak

70
Q

Main risk factors for sepsis (10)

A
  1. Immunosuppression
  2. Asplenics
  3. Diabetics
  4. Pregnancy
  5. Cancer patients
  6. Prosthetic devices
  7. Mechanical ventilation
  8. Severe wounds/burns
  9. Post-surgery
  10. Extremes of age
71
Q

Factors affecting signs and symptoms of sepsis

A
  1. Virulence of pathogen
    - Gram negative/positive endotoxin
    - Streptococcus pyogenes
  2. Bioburden
    - Bioburden is normally defined as the number of bacteria living on a surface that has not been sterilized
    - Bioburden quantification is expressed in colony forming unit (CFU).
    - Salmonella typhimurium
  3. Portal of entry
    - Different portals of entry dictate symptoms
    - Klebsiella pneumoniae
  4. Host susceptibility
    - In general elderly people have a more susceptible immune system
    - People that are immune deficient e.g. AIDS/HIV
    - Steptococcus pneumoniae
  5. Temporal evolution
    - Change of state due to passage of time
    - Neisseria meningitides
72
Q

What is your host innate immunity?
What makes up host cell immunity?
Initiates production of which inflammatory markers?

A

Host innate immunity: First line of defence against pathogenic insult

Comprises many immune molecules/cells/receptors e.g.

  • Complement
  • Mannose-binding lectin (MBL)
  • Phagocytes
  • Toll-like receptors (TLRs)
  • Nucleoside-binding oligmerisation domain receptors

These initiate the production of inflammatory markers e.g.

  • Interleukins (IL)
  • Tumour necrosis factor alpha (TNF-alpha)
  • Reactive oxygen species (ROS)
73
Q

What is the effect of TNF-alpha and IL-1 on the body?

A

Acute phase response:

  • Fever
  • Hypotension
  • Increased HR
  • Corticosteroid and ACTH release
  • Release of neutrophils
  • Generalized vasodilation (NO)
  • Increased vascular permeability
  • Intravascular fluid loss
  • Myocardial depression (tissue hypoxia)
  • Circulatory shock
74
Q

What is the Sepsis Six?

A

A series of interventions/test:

  1. Administer high flow oxygen
  2. Take blood cultures
  3. Give broad spectrium antibiotics
  4. Give IV fluid challenges
  5. Measure serum lactate and haemoglobin
  6. Measure accurate hourly urine output
75
Q

How are each of the following affected during sepsis:

  • Stroke volume (CO)?
  • Peripheral resistance?
A

Stroke volume:

  • Decrease in myocardial contractility due to tissue hypoxia
  • Decrease in venous return due to leaky capillaries

Peripheral resistance: No vasodilation

76
Q

How are the affects of sepsis on the following treated:

  • Stroke volume (CO)?
  • Peripheral resistance?
A

Stroke volume:
- Dobutamine to increase contractility of the heart

Peripheral resistance: Noradrenalin to cause vasoconstriction

77
Q

ST elevation MI requires prompt treatment with….

A

reperfusion therapy; PCI if available promptly, if not

IV thrombolytic therapy

MD3001 (12 decks)

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