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Diseases of human systems > Cardiovascular conditions > Flashcards

Cardiovascular conditions Flashcards

1
Q

What diseases fall under acute coronary syndrome (ACS)

A
  1. Unstable angina (not stable angina)​
  2. ST-elevation myocardial infarction (STEMI)​
  3. Non-ST-elevation myocardial infarction (NSTEMI)
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2
Q

What causes acute coronary syndromes

A

Supply/demand mismatch of oxygen to the myocardium​
-Blockage of blood flow (narrowing or occlusion of a coronary artery)​
-Increased demand (e.g. arrythmia, during acute illness)​

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3
Q

What are the symptoms of ACS

A

Central, crushing chest pain ***​

Pain radiating to the jaw or arms ​

Nausea and vomiting​

Sweating and clamminess​

A feeling of impending doom​

Shortness of breath​

Palpitations

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4
Q

What is the name of the substance that builds up on vessel walls

A

Atherosclerotic plaque

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5
Q

What does embolise mean

A

Plaque breaks off (or blood clot forms) and travels down the vessel

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6
Q

What is unstable angina

A

Partial occlusion of coronary artery​

Ischaemia ​

No infarction

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7
Q

What is NSTEMI

A

Partial occlusion​

Ischaemia ​

Infarction

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8
Q

What occurs with STEMI

A

Total occlusion​

Infarction

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9
Q

What complications does ACS pose

A

Death (cardiac arrest) – Basic Life Support!​

Arrythmia​

Heart failure ​

Rupture of heart wall​

New valvular disease (papillary muscle infarction)

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10
Q

What tests are used to diagnose ACS

A

ECG
Troponin (blood test)
-high troponin levels are bad as it is released when the heart muscle infarcts (dies)

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11
Q

How is ACS (heart failure) managed

A

Minimise tissue loss from infarction

Re-establish blood flow (reperfusion)
-break up and remove clot/dissolve

Prevent further episodes
-lifestyle management/medication

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12
Q

What is the procedure if a patient have acute onset of chest pain in the dental practice

A

At this point we do not know if stable angina, unstable angina, NSTEMI or STEMI

PHONE AN AMBULANCE AND GET TO HOSPITAL

100% oxygen via non-rebreather mask​

Glyceryl trinitrate spray (GTN), 2 puffs, sublingual​
-Repeated after 3 minutes if no improvement​

Aspirin 300mg oral tablet​
-Chewed​

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13
Q

Why is oxygen given to patients with ACS

A

increase oxygen delivery to the ischemic myocardium and thereby limit infarct size​

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14
Q

What is GTN

A

Glyceryl trinitrate spray

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15
Q

Why is GTN given to patients with chest pain

A

Vasodilator​

Release of nitrous oxide (NO) in vascular smooth muscle​

Dilates veins – reduces preload on heart (less hard work)​

Dilates arteries – increases blood flow through coronary arteries​

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16
Q

What role does aspirin do in releiving chest pain and reducing infarction risk

A

Prevents thrombus enlarging​

Reduces platelet aggregation at clot​

“inhibits COX enzyme, to reduce production of thromboxane A2, thereby reducing platelet aggregation”

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17
Q

What is reperfusion/types

A

Break-up/remove clot by a procedure​
-Percutaneous coronary intervention (PCI)​
-Access via coronary artery from peripheral artery​
-Break-up clot​
-Widen the artery (angioplasty)​
-Place stent to maintain width​
-Within 120 minutes of onset**

Dissolve blood clot​
-“Thrombolysis”​
-Clot-busting drug (alteplase), given IV

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18
Q

What ,medication can be prescribed to prevent ACS

A

Aspirin (75mg)​

Another antiplatelet (e.g. clopidogrel for 12 months)​

Atorvastatin (lipid lowering)​

ACE-inhibitor (blood pressure)​

Atenolol (or another beta blocker like bisoprolol)

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19
Q

Why is adrenaline risky for patients with ACS

A

Supply/demand mismatch of oxygen to the myocardium​

Blockage of blood flow (narrowing or occlusion of a coronary artery)​

Increased demand (e.g. arrythmia, during acute illness)​

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20
Q

What is PAD

A

Peripheral arterial disease

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21
Q

What does PAD refer to

A

PAD refers to narrowing of arteries suppling limbs ​

Commonly legs

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22
Q

What do PAD and ACS have in common

A

Pathophysiology and risk factors

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23
Q

What are the symptoms of PAD

A

Leg, thigh, buttock, calf cramping pain particularly when walking (intermittent claudication)​

Non-healing ulcers on toes, foot, leg​

One leg cooler than the other​

One leg paler than the other​

Hair loss on leg​

Necrosis of skin on digits

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24
Q

How is PAD diagnosed

A

CT angiography of limb

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25
Q

What surgical procedures can be carried out for PAD

A

Angioplasty and stent​

Endartectomy​

Bypass surgery​

Amputation

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26
Q

What dental implications may arise for patients with PAD

A

Shared risk factor with periodontal disease​

Smoking​

​

Antiplatelet medication​

Bleeding risk​

​

Cardiovascular health​

Risk of ACS increased

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27
Q

What is the difference between ACS and PAD

A

ACS is reduction/absence of blood supply to myocardium
PAD is reduction/absence of blood supply to leg tissue

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28
Q

What causes cardiovascular diseases

A

Impairment of any of:
heart
arteries
veins
capillaries

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29
Q

Movement of blood through the heart

A

In via superior vena cava
right atrium
tricuspid valve
right ventricle
pulmonary valve
pulmonary artery
lungs
pulmonary vein
left atrium
mitral
left ventricle
aortic valve
Out via aorta

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30
Q

What is atherosclerosis

A

Refers to the deposition of fatty deposits in the artery walls

Creates “stiffening” of the arteries

Narrowing results in “stenosis”​

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31
Q

What can atherosclerosis cause

A

Myocardial infarction​

Angina​

Stroke / TIA​

Peripheral arterial disease​

Mesenteric ischaemia​

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32
Q

What are the risk factors for cardiovascular diseases

A

Older age​

Male​

Family history​

Ethnicity

Hypertension​

Obesity​

Diabetes​

Lipids​

Smoking​

Alcohol​

Stress​

Poor sleep

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33
Q

How does plaque form in vessel walls

A

Damage to vessel wall (e.g. hypertension and smoking)​

High lipid content of blood (LDL cholesterol)

High circulating glucose (diabetes)​

Immune cells

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34
Q

Why is Atorvastatin prescribed to patients with cardiovascular disease or at risk of infarction

A

It lowers the lipid content (cholesterol) within the blood to reduce plaque build up

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35
Q

What is hypertension

A

High blood pressure

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36
Q

When is hypertension diagnosed

A

With a Bp >140/90

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37
Q

What complications can arise from existing hypertension

A

Atherosclerosis​

Chronic kidney disease​

Heart failure​

Stroke​

Retinopathy​

Vascular dementia

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38
Q

What non-modifiable risk factors exist for hypertension

A

Age​

Gender ​

Ethnicity (black African, black Caribbean)​

Genetic factors (family history)​

Family history

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39
Q

What medications treat hypertension

A

ACE-inhibitors​

Angiotensin-II-receptor blockers​

Beta blockers​

Calcium channel blockers​

Diuretics

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40
Q

What does angina refer to

A

collection of symptoms due to myocardial ischaemia

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41
Q

What is the difference between stable and unstable angina

A

Stable angina – only experienced during exertion

Unstable angina – experienced at rest (see Acute CVS Disease lecture)

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42
Q

How is coronary artery disease managed

A

Lifestyle modifications​
-E.g. weight loss, healthy diet, stop smoking, reduce alcohol…

Immediate symptom management​
-GTN (glyceryl trinitrate) spray​

Long term secondary prevention​
-Covered more in Medications lecture​
-Manage hypertension, lipids, aspirin

Interventional management​
-Widen the narrowed bit of artery​
-Bypass narrowed bit of artery

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43
Q

What is PCI

A

Percutaneous coronary intervention ​
-Inserting a ballon to widen diseased coronary arteries​
-Inserting a stent to maintain the arteries​
-Via the radial or femoral artery

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44
Q

What is a CABG

A

Coronary artery bypass graft

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45
Q

What does a CABG surgery involve

A

Blood flow through damaged coronary artery is by-passed​

Harvest a vessel from elsewhere in body (commonly leg)

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46
Q

What is heart failure

A

where the heart fails to work effectively in its role of pumping blood

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47
Q

What does right or left sided heart failure heart failure indicate

A

right sided-heart cant pump from right ventricle
Left sided-heart cant pump blood from right ventricle

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48
Q

What are some common causes of heart failure

A

Hypertension​

Coronary artery disease (e.g. previous MI)​

Valvular heart disease​

Arrythmias​

Congenital heart defects

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49
Q

What is the result of left or right sided heart failure

A

Left-sided heart failure means congestion of blood from the heart into the pulmonary vein and backing up into the lungs​
**Results in fluid in the lungs (pulmonary oedema)

Right-sided heart failure means congestion of blood from the heart into the vena cava and backing up into the systemic circulation​
**Results in fluid in the abdomen and legs (peripheral oedema)

50
Q

What is orthopnea

A

Shortness of breath when lying flat

51
Q

What are the symptoms of heart failure

A

Shortness of breath (SoB)​

Cough (frothy sputum)​

Orthopnoea – SoB when lying flat​

Paroxysmal nocturnal dyspnoea – suddenly waking at night with SoB​

Peripheral oedema – fluid in the legs, abdomen, sacrum​

Fatigu

52
Q

What are arrythmias

A

Abnormal heart rhythmns

Due to interrupted electrical signals that coordinate heart muscle contraction

53
Q

What is atrial fibrillation

A

Disorganised electrical activity in the atria, resulting in fibrillation (random muscle twitching) and an irregular pulse

54
Q

What is the major health risk with atrial fibrillation

A

Blood clots
Due to the uncoordinated heart muscle activity, blood flow is not smooth through the heart. This makes blood more likely to clot.

Blood clot can travel to brain – 5x higher risk of stroke in AF​

55
Q

Name an arrythmia

A

Atrial fibrillation

56
Q

What devices can be placed into the body to manage arrythmias

A

Pace makers

57
Q

What are the 4 heart valves

A

Aortic
Pulmonary
Tricuspid
Mitral

58
Q

Why is it important to be aware if the patient has a pacemake

A

Can interact with bipolar diathermy (used in oral surgery)

59
Q

What are some diseases of the valves

A

Stenosis – means valve is stiff and does not fully open​

Regurgitation – means the valve does not fully close, and is leaky

60
Q

What can cause valvular disease

A

Aging (aortic stenosis)​

Congenital (bicuspid aortic valve)​

Damage following myocardial infarction​

Rheumatic heart disease​

Infective endocarditis​

61
Q

What is a bicuspid aortic valve

A

3 leaflets instead of 2 – can be stenotic or leaky

Congenital (from birth)

Spectrum of severity​

Management with medications and/or surgery

62
Q

What is the most common valvular pathology

A

Aortic stenosis

63
Q

How does aortic stenosis occur and how is it managed

A

Due to age - narrowing of aortic valve

managed through valve replacement

64
Q

When does valve disease often occur

A

Following myocardial infarction
-infarction of valves leads to disfunction (most commonly mitral valve)

65
Q

How can rheumatic heart disease cause valve disease

A

Damage to heart valves by body’s immune system, following streptococcal throat infection​

​

Group A streptococcus infects throat - untreated​

Bacteria cell wall has M protein antigen​

Immune system produces antibodies against M protein​

However, cardiac valves have proteins which resemble M protein​

Immune system attacks heart valves​

Fibrosis and vegetation forms on valves​

Valves become leaky or stenotic​

Valve replacement required​

66
Q

What conditions lead to valve replaced

A

Severe aortic stenosis​

Rheumatic heart disease​

Papillary muscle rupture​

Congenital valvular disease

67
Q

What are the types of valve replacements and the adv and disadv

A

Bioprosthetic​
-Less likely to have a blood clot, no need for anticoagulation​
-Reduced lifespan​
-Commonly derived from pig tissue

Metallic​
-Longer lifespan​
-Higher risk of blood clot, need anticoagulation with warfarin

68
Q

What is infective endocarditis

A

Infection of the lining of the heart (endocardium), particularly heart valves

69
Q

Why is there a risk of infective endocarditis developing due to dental procedures

A

Invasive dental procedures introduce bacteria to bloodstream

In predisposed patients, this can result in bacteria colonising and infecting the endocardium

Antibiotic prophylaxis (before a procedure) is recommended in some patients

Bacteria – most commonly Staphylococcus aureus.

70
Q

How does infective endocarditis develop

A

Altered heart valve morphology (to provide suitable site for bacterial colonisation)​

Bacteria into the bloodstream (e.g. from dental procedure, IV drug use… )​

Bacteria circulates in blood and deposits on valve​

Formation of vegetation on valve leaflets​

71
Q

What does infective endocarditis cause

A

Impaired heart valve function – heart failure​

Focus of infection - sepsis​

Source of emboli – stroke

72
Q

How is infective endocarditis managed

A

4-6 weeks of IV antibiotics​

Surgery may be required

73
Q

What patients are predisposed to infective endocarditis

A

Patients:
-With a heart valve replacement
-Have previously had infective endocarditis
-Born with a congenital heart defect
-Who currently have valvular heart disease

74
Q

What is the procedure when opperating on patients at risk of infective endocarditis

A

Give antibiotic 60 mins prior to procedure (amoxicillin powder sachet/clindamycin capsules, penicillin alergy)

75
Q

Why is prevention of dental diseases so important in patients with infective endocarditis

A

Reduce risks involved with dental procedures

76
Q

What dental implications does chronic CVS disease have

A

Medications ​
-Anticoagulants in AF and metallic valve replacement​
-Polypharmacy – dry mouth​
-Lichenoid tissue reactions to anti-hypertensive medications

Appointments​
-Stress-inducing – angina (medical emergency)​
-Heart failure – lying patients back (orthopnea)

Infective endocarditis​
-High risk patients / high risk procedures​
-Dental pre-assessment of patients before cardiac surgery***

77
Q

What drugs are anti-hypertensives

A

ACE-inhibitors​

Angiotensin-II-receptor blockers​

Beta blockers​

Calcium channel blockers​

Diuretics

78
Q

What are the types of anti-platelets

A

Aspirin​

Clopidogrel​

Ticagrelor​

Dipyramidole​

79
Q

What are anti-anginals

A

Nitrates​

Nicorandil

80
Q

What are lipid lowering medications classed as

A

Statins

81
Q

What is the equation of blood pressure

A

Cardiac output x total peripheral resistance

82
Q

What increases total peripheral resistance

A

Vasocontriction of peripheral blood vessels

83
Q

How is cardiac output, stroke volume and TPH calculated

A

(Cardiac output = heart rate x stroke volume)​

(Stroke volume = volume of blood being pumped by left ventricle)

(Total Peripheral Resistance = how much vasoconstriction vs. vasodilation is present in peripheral circulation)

84
Q

How is blood pressure reduced

A

by lowering any of:​

Heart rate​

Stroke volume​

Total peripheral resistance

85
Q

Which areas of the body will anti-hypertensives target

A

Heart (reduce heart rate or contractility)​

Blood vessels (vasodilation)​

Kidneys (reduce how much fluid is being reabsorbed into circulation)

86
Q

What do anti-hypertensive drugs do

A

Reduce blood pressure

87
Q

What are some ACE-inhibitors

A

Ramipril, lisinopril, perindopril

88
Q

Why are ACE-inhibitors classed as anti-hypertensives

A

ACE-inhibitors stop the formation of angiotensin-II (by inhibiting Angiotensin Converting Enzyme)(RAAS)

This means that less aldosterone is produced, resulting in less fluid reabsorption in kidneys​

Thereby reducing blood pressure​

89
Q

How do ACE-inhibitors affect the oral cavity

A

Dry mouth
Lichenoid tissue reaction

90
Q

How do ARB’s reduce blood pressure

A

ARBs bind to angiotensin-II receptors on:​

Smooth muscle of blood vessels (prevent vasoconstriction)​

Cortical cells of adrenal gland (prevent aldosterone production)

Thereby reducing blood pressure

91
Q

Name some ARBs

A

Candesartan, losartan, valsartan

92
Q

What receptors are found on the heart, lungs and blood vessels (smooth muscle)

A

Blood vessels - alpha 1
Heart - beta 1
Lungs - beta 2

93
Q

What medications are classed as beta blockers

A

Atenolol, bisoprolol, propranolol, carvedilol

94
Q

What action do beta blockers prevent

A

Increases in heart rate and contractility

95
Q

How do beta blokers reduce hypertension

A

Competitively inhibit beta 1 receptors on cardiac muscle cells

Prevent stimulation by adrenaline which would increase heart rate

96
Q

Why should beta blockers be avoided in patients with asthma

A

Broncho-constriction

97
Q

How do calcium channel blockers affect the cardiovascular system

A
  1. Inhibit calcium channels on smooth muscle around peripheral blood vessels – thereby reducing vasoconstriction, reducing TPR
  2. Inhibit calcium channels at sino-atrial node (pacemaker of the heart) – thereby reducing heart rate
  3. Inhibit calcium channels on cardiac muscle cells – thereby reducing heart contractility
98
Q

Name 3 calcium channel blockers

A

Amlodipine, nifedipine, felodipine

99
Q

What drugs can cause gingival enlargement

A

Nifedipine (calcium channel blocker)​

Ciclosporin (immunosuppressant)​

Phenytoin (anti-convulsant)

100
Q

What drugs are types of diuretics

A

Furosemide, bendroflumethiazide, bumetanide

101
Q

How do diuretics work to reduce blood pressure

A

Work at different parts of the nephron to decrease fluid reabsorption

Increased urination = reduced circulating fluid

Reduced blood pressure​

102
Q

What anti-hypertensive drugs cause dry mouth

A

Diuretics
ACE-inhibitors

103
Q

Why might a patient be presribed anti-platelet drugs

A

Coronary artery disease​

Secondary prevention following MI ​

Peripheral artery disease​

Secondary prevention following stroke/TIA

104
Q

Name 4 anti-platlet drugs

A

Aspirin*​

Clopidogrel​

Ticagrelor​

Dipyramidole

105
Q

How does aspirin work

A
  • inhibits COX-1 enzyme, to reduce production of thromboxane A2, thereby reducing platelet aggregation
106
Q

What dose of aspirin is used for acute MI/stroke

A

300mg

107
Q

What are the dental implications of anti-platelets

A

Patient likely to have prolonged bleeding times​

Patients on DAPT (two anti-platelets) likely to have higher bleeding risk than single drug​

Often only for 12 months – can treatment be delayed?​

No need to stop anti-platelet for dental treatment​

Risk / benefit

108
Q

What drugs are classed as anti-coagulants

A

DOACs – used in atrial fibrillation (stroke prevention)​
-Edoxaban, rivaroaxaban, apixaban​
-Dabigatran​

Warfarin – metallic valve replacement

109
Q

Why is it possible to remain taking DOACs while undergoing dental procedures such as extractions

A

Rapid onset of action and short half lives

110
Q

What is the recomendation for operating on patients taking warfarin

A

Do not delay or miss dose​
-Long half-life and onset of action​

INR checked ideally < 24 hours before dental treatment​
-If stable readings, 72 hours is acceptable

If INR < 4 – can proceed with dental treatment

111
Q

What are the types of cholesterol

A

LDL and HDL cholesterol​

Low-density lipoprotein (“bad”)​

High-density lipoprotein (“good”)

112
Q

Why is LDL cholesterol worse

A

High levels of LDL contribute to atherosclerotic process

113
Q

What is the main lipid-lowering medication

A

Statins

114
Q

What are the names of some statins

A

Atorvastatin, simvastatin, rosuvastatin

115
Q

How do statins work

A

Works by inhibiting enzyme in liver (HMG-CoA reductase), which halts production of LDL cholesterol

116
Q

What dental implications do statins present

A

Interaction with fluconazole, miconazole and clarithromycin to cause rhabdomyolysis (breakdown of skeletal muscle)

117
Q

How do nitrates reduce affects of angina

A

Nitrates relax smooth muscle within coronary vessels, thereby causing vasodilation and improving blood flow​

Also, dilate veins returning to heart, to reduce preload and therefore reduce the work being done by heart

118
Q

What types of nitrates do patients with angina take

A

GTN spray (glycerlyltrinitrate) - taken for acute relief​

Isosorbide mononitrate (ISMN) - taken daily for prevention

119
Q

What is Nicorandil used for

A

Treatment of angina

120
Q

What are the dangers of taking nicorandil

A

Can cause severe oral ulceration (up to 5%)

Heals on withdrawal of medication
Lead by medical team!

121
Q

What is given to patients suffering from side effects of nicorandil

A

Symptomatic relief​

Benzydamine mouthwash​

Diseases of human systems (7 decks)

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