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MD3001 > Week 5 > Flashcards

Week 5 Flashcards

1
Q

What are the principal fatal diseases caused by smoking?

A
  • Cancer, COPD and CVD

- On average cigarette smokers lose 7.5 years of life

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2
Q

What are the effects of quitting smoking?

A

20 mins: BP and pulse rate back to normal
8 hours: Blood nicotine and CO halved, oxygen back to normal
24 hours: CO eliminated, lungs start to clear mucus
48 hours: nicotine eliminated, sense of taste and smell improve
72 hours: breathing is easier, bronchial tubes relax
2-12 weeks: circulation improves
3-9 months: lung function increased by <10%, coughs decrease
5 years: risk of heart attack halved
10 years: risk of lung cancer halved compared to continued smoking

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3
Q

What disease risks are decreased due to smoking cessation?

A
  • Minimised risk of bone loss, hip fracture and periodontal disease
  • Rheumatoid arthritis risk reduced
  • Cataract risk reduced
  • Aortic aneurysm
  • Peripheral arterial disease
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4
Q

What is the stage model of behaviour change?

A

Pre-contemplation -> Contemplation -> Preparation -> Action -> Maintenance -> Relapse ->

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5
Q

What is pre-contemplation?

A

Lack of awareness or lack of intent to change

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6
Q

What is contemplation?

A

Increased awareness of negative aspects of smoking. Has intention to quit within 6 months

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7
Q

What is preparation?

A

Some small behavioural changes to quit have been made: intent to quit within 1 month

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8
Q

What is action?

A

Individual has implemented plan to stop, still adjusting to change

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9
Q

What is maintenance?

A

Long term adjustment as a non smoker, content with new lifestyle without cigarettes

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10
Q

What are the 4 As to Approach Smoking Cessation?

A
  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
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11
Q

What are the 5 Rs?

A
  1. Relevance
  2. Risks
  3. Rewards
  4. Roadblocks
  5. Repetition
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12
Q

What is relevance of cessation of smoking?

A

Ask patient to identify why quitting might be relevant such as:

  • children
  • need for money
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13
Q

What is risks of smoking?

A

Reiterate benefits for patient and his/her children after you’ve asked what they know about smoking

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14
Q

What are the rewards of cessation of smoking?

A 
Get more oxygen
Clothes and hair smell better
Have more money
Food will taste better
Will have more energy
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15
Q

What are the roadblocks of cessation of smoking?

A

Negative moods
Being around other smokers
Triggers and cravings
Time pressures

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16
Q

What is a dysrythmmia?

A

Where coordinated electrical sequences in the heart are disrupted

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17
Q

What 3 things could Dysrhythmias be due to?

A
  1. Changes in the heart cells
  2. Changes in the conduction of the impulses through the heart
  3. Combination of these
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18
Q

How are Dysrhythmias Classified?

A
  • Atrial (supraventricular)
  • Junctional (Associated with AV node)
  • Ventricular
  • Tachycardia/Bradycardia
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19
Q

What are the 4 categories of events which can cause Dysrhythmias?

A
  1. Ectopic pacemaker activity
  2. Delayed after-depolarisations
  3. Circus re-entry
  4. Heart block
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20
Q

How are arrythmias identified clinically?

A

ECG

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21
Q

What system is used to classify antiarrythmic drugs?

A

Vaughan Williams System

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22
Q

What are class 1 antiarrythmics?

A

Sodium channel blockers

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23
Q

What are class 2 antiarrythmics?

A

Beta blockers

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24
Q

What are class 3 antiarrythmics?

A

Potassium channel blockers

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25
Q

What are class 4 antiarrythmics?

A

Calcium channel blockers

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26
Q

What are the class 1 sodium channel blockers?

A

Disopyramide
Lignocaine
Flecainide

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27
Q

What types of dysrhythmmias are class 1 drugs used to treat?

A

Ventricular ectopic beats

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28
Q

What is the 1a drug?

A

DISOPYRAMIDE

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29
Q

Whats is the 1b drug?

A

LIGNOCAINE

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30
Q

What is the 1c drug?

A

FLECAINIDE

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31
Q

What is class 1a used to treat?

A

Ventricular dysrhythmmias, prevention of atrial fibrillation

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32
Q

What is class 1b used to treat?

A

Prevention of ventricular tachycardia and fibrillation during/after MI

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33
Q

What is class 1c used to treat?

A

Supress ventricular ectopic beats, prevents paroxymsmal atrial fibrillation and recurrent tachycardias

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34
Q

What are the effects of beta blockers?

A

Slow heart rate and decrease cardiac output

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35
Q

What are the beta blockers used in the treatment of dysrhythmmias?

A

SOTOLOL
BISOPROLOL
ATENOLOL

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36
Q

What is the class 3 potassium channel blocker used in the treatment of dysrhythmmias?

A

AMIODARONE

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37
Q

What effect do potassium channel blockers have?

A

Prolong the cardiac action potential by prolonging the refractory period. Altering the excitability of the cell

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38
Q

What condition and named condition specifially does amiodarone treat?

A

Re-entry tachycardia as found in wolff-parkinson white syndrome

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39
Q

Which kinds of arrythmias can be treated wiith amiodarone?

A

Supraventricular and ventricular tachycardias

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40
Q

Which type of calcium channel is targetted by class 4 drugs?

A

Voltage gated L type calcium channels

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41
Q

what affect do class 4 drugs have on the heart?

A
  • Slows conduction as slows calcium entry in cell through the nodes.
  • Shorten plateau of depolarisation caused by slow L type channels, shortening contraction.
  • Also less forceful contraction as less calcium influx to activate ryanodine receptors
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42
Q

Which class 4 drugs usually used to treat dysrhtymmias?

A

Verapamil- prevents recurrence of supraventricular tachycardias and reduces ventricular rate in patients with AF if they don’t have WPW.

Diltiazem- more effect on smooth muscle

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43
Q

Which syndrome would you NOT use calcium blockers?

A

Wolff-parkinson white syndrome

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44
Q

What are the 2 unclassified drugs?

A
  1. Adenosine

2. Digoxin

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45
Q

How does adenosine work?

A
  • Gi protein coupled receptor inhibits adenylate cyclase, reducing cAMP, reducing amount of protein kinase A able to phosphorylate calcium channels, reducing their activity and thus calcium entry.
  • Calcium drives conduction velocity in AVN thus slows HR
46
Q

What is adenosine used to treat?

A

Supraventricular tachycardias

47
Q

How does Digoxin work?

A

Reduces SAN firing rate reduces conduction velocity, reducing heart rate

48
Q

What is epidemiology?

A

The study of the distribution and determinants of health-related states or events in specified populations and the application of this study to the control of health problems

49
Q

What are the 4 epidemiological approaches?

A
  1. DESCRIBE health status of a population (time, place, person)
  2. UNDERSTAND natural history of a condition (longitudional studies)
  3. IDENTIFY causes of medical problems (observational studies)
  4. ACT / EVALUATE medical and health promoting interventions (monitor or intervene)
50
Q

What 5 steps should doctors take to get the ‘diagnosis’ right?

A
  1. Define the NUMERATOR: clinical condition
  2. Define the DENOMINATOR: who makes up the ‘population at risk’
  3. Dig out good sources of info:
  4. Describe what the data shows in table or graph.
  5. Describe by TIME (over what time), PLACE (who, where, out of how many), PERSON (person related attributes, modifiable and unmodifiable).
51
Q

What is a longitudinal study?

A

Observational research method in which data is gathered for the same subjects repeatedly over a period of time.

52
Q

What is a risk factor? (Framingham Study Definition)

A 
Aspect of :
-Personal behaviour
-Life style
-Environmental exposure
-Genetic trait
Which on the basis of epidemiological evidence: 
-is associated with a health-related condition
-considered important to prevention
53
Q

What does pathogenic mean?

A

Linked to disease state eg cholesterol

54
Q

What does salutogenic mean?

A

Linked to health promoting state eg physical activity

55
Q

What does interactive mean?

A

Together increase risk eg smoking and asbestos

56
Q

What is the Framingham study?

A
  • Objective was to identify common factors or characteristics that contribute to CVD.
  • Risk factors included fruit and veg consumption
57
Q

What is performance monitoring?

A
  • GPs and hospital doctors should know whether they provide safe and effective treatment. Includes prevention, treatment, rehabilitation.
  • Evaluation should be systemic and look at structure, process and outcome.
  • Use QUALITY OUTCOMES FRAMEWORK data (primary care focus on long term conditions)
  • Date from smoking cessation services
  • Lifestyle surveys
  • Data about outcomes for individual clinicians (audit, league tables)
58
Q

What is the interheart study?

A

It shows that 9 potentially modifiable risk factors account for >90% of AMI risk.
Smoking, hypertension, lipids, obesity, diabetes, fruit and veg, alcohol, exercise, psychosocial

59
Q

What is the biomedical model?

A

Physical Damage –> Illness

60
Q

What is the classification of functioning, disability and health (WHO)?

A

It is a framework that measures health and disability at both the individual and population levels

61
Q

What is the biopsychosocial model?

A

General model/approach stating that biological, psychological and social factors all play a significant role in human functioning in context of disease and illness

62
Q

What are the common cardiac misconceptions?

A
  • Once the damage is done you can’t turn the clock back!
  • If you’ve had a heart attack, you will die prematurely of heart disease
  • Any shock or excitement could kill me
  • There is a dead part in my heart that could burst if it was to be put under too much pressure
  • Rest restores the heart
  • Now I’ve had the revascularisation I’m fixed
63
Q

Where do these misconceptions come from?

A
  • Media
  • Family and friend
  • GP etc.
64
Q

Why are psychological factors important in heart disease?

A
  • Can have an impact on disease processes
  • Impact on treatment adherence
  • Prolonged stres
  • Impact on taking in information
  • Create problems in relation to social support and relationships with health professionals
  • Create psychological distress which is a predictor of hospitilisation
65
Q

What happens with psychological distress following MI/ CABG?

A
  • Early mortality
  • Low return to work
  • Low quality of life
  • Lifestyle changes
  • Adherence with medical care
  • More use of health services
  • PTSD and readmission to hospital
66
Q

What are some of the psychological challenges of cardiac disease?

A
  • Fear/reduced life expectancy
  • Loss of control
  • Loss of independence/ financial status
  • Denial
  • Anxiety
  • Hopelessness
  • Being treated differently by others
  • Making lifestyle changes, diet, smoking
67
Q

What is cognitive function?

A

Learning memory, executive function (decision-making), focused attention, psychomotor, processing speed

68
Q

What is the relation between cognitive function and distress?

A
  • Often the result of coronary artery disease where cognitive function is impaired
  • Patients after CABG may need to refer to the heart manual more often because of poorer concentration.
  • Distress can be expressed as complaints about mild memory loss and poorer cognitive function so strategies to cope with anxiety and depression can also be used to help cognitive function
69
Q

What is the definition of quality of life?

A

The presence of a reasonable amount of pleasurable, successful and meaningful experiences

70
Q

What are the 8 domains of the generic SF-36 measurement for quality of life?

A
  1. Physical functioning
  2. Physical role functioning
  3. Bodily pain
  4. General health
  5. Vitality (state of being strong and active)
  6. Social role functioning
  7. Emotional role functioning
  8. Mental health
71
Q

What are the main determinants for quality of life?

A

Depression & anxiety

72
Q

What are the biological features of depression?

A

Changes in sleep (over or under tired), mood (diurnal variation), changes in appetite (reduced or increased) and reduced activity

73
Q

What are the psychological indicators of depression?

A

Loss self-esteem, loss of confidence, flat effect, concentration difficulties, negative thinking, suicidal ideation/self-harm, feelings of uselessness/worthlessness/hopeless/inadequate

74
Q

What are the feelings of loss that you get in depression?

A

Loss of health, self-confidence/sense of purpose, loss of independence/relationships, sense of worthlessness/useless

75
Q

What are the psychological indicators of anxiety?

A

Fear of losing control, impeding doom, fear or terror, hopelessness, sense of dread

76
Q

What are the behavioral indicators of anxiety?

A

Fidgeting, hesitating, shaking, always rushing, avoidance

77
Q

What are the cognitive indicators of anxiety?

A

Apprehension, difficulties concentrating, memory problems, catastrophic thinking

78
Q

What may cause a cardiac patient to become anxious?

A

CAD diagnoses, being in hospital/ treatment/ health professionals, being away from partner and familiar surroundings, chest sensations, return to the situation of the MI (shock, panic, anxious), return to activities (work, marital strain, arguments)

79
Q

What is the hospital anxiety and depression scale?

A

Brief self-report screening assessment of anxiety and depression which is less confounded by somatic symptoms of concurrent physical problems than some other psychological assessments. 7 anxiety and 7 depression items which is administered at discharge and then 6-12 weeks after (not diagnostic but can help)

80
Q

What is the role of adrenaline in anxiety?

A

Worrying thoughts can produce adrenaline. When there is no danger to run away from, physical effects of the adrenaline produced are dizziness, shortness of breath, dry mouth, heart racing, butterflies in stomach and hyperventilation. Cognitive effects are racing thoughts, anxious thoughts, preoccupation with and catastrophising about bodily sensations. Outcome is feling ill, scared, worried, panic

81
Q

What happens with the denial/avoidance strategy in specific patients?

A

Some patients may use this as a coping strategy. 12-20% of patients refuse to accept diagnosis so ‘tempt fate’ by behavior. Coping by avoidance can be good in short term but long term can lead to more anxiety and depression, reduces physical functioning and more discomfort. You should discourage use of avoidance coping

82
Q

What is illness behavior?

A

Process of evaluating symptoms, seeking medical help to bring relief and seeking support from family. Defines a social role with expectations for both the sick and the healer. Often brings secondary gains, rewards or benefits obtained through the sick role (increased sympathy and attention, special favors, being waited on, no school/work/duties)

83
Q

Describe relationship between depression and heart disease?

A

People with heart disease more likely to suffer from depression than otherwise healthy people. Angina and heart attacks closely linked with depression. Some symptoms of depression may decrease overall physical and mental health increasing risk for heart disease or making symptoms worse. Fatigue and feelings of worthlessness may cause you to ignore medication plan and avoid treatment foe heart disease. Having depression increases risk of death after heart attack

84
Q

What is the relationship between erectile dysfunction and risk of CVD?

A
  • Problems with erectile functioning preceded to CVD especially in younger patients that have no relevant cardiac history
  • Erection problems and CVD have same risk factors (diabetes, obesity, hypertension, hypercholesterolemia)
85
Q

What are the most common causes of erectile difficulties?

A

Vascular problems

86
Q

What are some of the causes of sexual difficulties in heart conditions?

A

Sexual drive and performance due to CAD, sexual drive and performance prior to CVD, anxiety, depression, feelings of failure/ guilt, stress cardiovascular damage, medication, avoidance, negative thoughts

87
Q

What should you tell the erectile dysfunction patients when treating them?

A

Inform them that sexual activity is no more strenuous on the heart than other activities such as lifting and carrying objects/ playing golf. Say that is is a reasonable problem and that it is common and treatable

88
Q

What are the effective treatments for erection problems?

A

Sex therapy/counselling, oral tablets, injection therapy, transurethtral therapy, vacuum devices and surgery and implants

89
Q

What are the guiding principles for care for cardiac patients to improve quality of life?

A

Cardiac care should pay particular attention to the patient’s understanding of their illness, patient’s behavior, coping measures they adopt, emotional status, influence of friends and family. Need to also use a biopsychosocial model to help understand the relationship between psychological distress and impact on heart disease

90
Q

What is Sepsis?

A

SIRS + documented infection site (ie positive cultures for organisms from that site)

91
Q

What is Colonisation?

A

Presence of a microbe in the human body that does not cause infection or a specific immune response

92
Q

What is an Infection?

A

Occurrence of inflammation due to the presence of a microbe

93
Q

What is a Bacteraemia?

A

Presence of viable bacteria in the blood.

94
Q

What does “SIRS” stand for?

A

Systemic Inflammatory Response Syndrome

95
Q

What is Severe sepsis?

A

Sepsis plus organ dysfunction (hypotension, hyperaemia, oliguria)

96
Q

What is Septic Shock?

A

Severe Sepsis plus hypotension, despite fluid resuscitation

97
Q

Epidemiology of Sepsis

A
  • In top 10 causes of mortality.
  • Affects all ages
  • Common scenario
98
Q

Risk Factors for Sepsis

A
  • Diabetes
  • Asplenic patients
  • Cancer
  • Immunosuppression
  • Severe wounds/ burns
  • Prosthetic devices
  • Post-surgery
  • Pregnancy
  • Extremes of age
99
Q

Common causative pathogens for Sepsis?

A
  • Staphylococcus aureus (including MRSA)
  • Neisseria meningitidis (e.g. Group A Strep)
  • Streptococcus pneumoniae
  • Streptococcus pyogenes
  • Gram negative bacilli
  • Candida species
100
Q

What is the Sepsis 6?

A

THINK BUFALO!

  1. Administer high flow oxygen.
  2. Take blood cultures
  3. Give broad spectrum antibiotics
  4. Give intravenous fluid challenges
  5. Measure serum lactate and haemoglobin
  6. Measure accurate hourly urine output
101
Q

How do you Diagnose infection?

A

Blood tests- WCC, CRP, platelets, clotting
Microbiology- Blood culture, stool, urine, wound, tissue cultures, CSF, sputum
Serological blood tests for antibodies
Viral studies e.g. PCR, NAAT

102
Q

What does SIRS produce?

A
  • Widespread endothelial damage with vasodilation
  • Aterio-venous shunting
  • Microvascular occlusion
  • Capillary leak
  • Tissue Oedema
103
Q

How can SIRS be diagnosed?

A

The presence of 2 or more of:

  • Respiratory Rate >20/min
  • Heart rate >90/min
  • WBC >12x109/L or <4x109/L
  • Temperature >38oC or <36oC
  • PaCO2 <4.3kPa or ventilated
104
Q

What are the clinical features of SIRS?

A
  • Warm peripheries
  • Bounding pulses and features of high cardiac output
  • Peripheral vasodilation leading to decrease diastolic BP
  • Decreased after load, therefore stroke volume and systolic BP is maintained
  • Large difference between DBP and SBP
105
Q

What are the clinical features as sepsis advances?

A

Systolic BP decreases and the peripheries becomes cool due to hypovolaemia associated with capillary leak

106
Q

What are the factors affecting the signs and symptoms of sepsis?

A
  • Virulence of pathogen
  • Bioburden
  • Portal of entry
  • Host susceptibility
  • Temporal evolution
107
Q

What are the immune and inflammatory pathways in response to pathogen?

A
  • Host innate immunity (1st line response)
  • Comprises many immune molecules/cells/receptors etc
  • These may initiate production of inflammatory markers
108
Q

Give examples of some Immune molecules/cells/receptors produced in innate immunity?

A
  • Complement
  • Mannose-binding lectin (MBL)
  • Phagocytes
  • Toll-like receptors (TLRs)
  • Nucleotide-binding oligomerisation domain receptors (NLRs)
109
Q

Give examples of some inflammatory markers?

A
  • Interleukins (ILs)
  • Tumour necrosis factor alpha (TNFalpha)
  • Reactive oxygen species (ROS)
110
Q

What are the effects of TNFalphs and IL-1 on the body?

A
  • Fever
  • Hypotension
  • Increased HR
  • Corticosteroid and ACTH release
  • Release of neutrophils
111
Q

What are the effects of TNFalpha and IL-1 on the CVS?

A
  • Generalised vasodilation (NO)
  • Increased vascular permeability (activated leukocytes)
  • Intravascular fluid loss
  • Myocardial depression (tissue hypoxia)
  • Circulatory shock

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