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BDS2; CHHD > Cardiovascular diseases > Flashcards

Cardiovascular diseases Flashcards

1. Overview of the cardiovascular system 2. Knowledge of the pathogenesis of: - hypertension - atherosclerosis - angine - myocardial infarction - infective endocarditis - heart failure 3. Knowledge of their clinical features and management 4. Knowledge of the relevance to dental care and management of patients 5. Recognise and carry out emergency management of cardiac emergencies including angina, MI, cardiac arrest in dental care

1
Q

What is cardiovascular disease

A

Disease of the heart and circulation

Incidence is increasing due to higher prevalence of obesity

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2
Q

What is hypertension

A

Sustained elevation of resting systolic and diastolic BP; >140/90mmHg and this can be primary or secondary

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3
Q

What is primary hypertension

A

Most common type due to multiple factors including hereditary; environment plays a factor in genetically susceptible people

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4
Q

What is secondary hypertension

A

It is less common and associated with renal and endocrine diseases

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5
Q

What renal diseases are associated with secondary hypertension

A
  • renal parenchymal disease (chronic glomerulonephritis, pyelonephritis, polycystic renal disease and post transplant)
  • renovascular diseases
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6
Q

What endocrine diseases are associated with secondary hypertension

A
  • hyperaldosteronism
  • pheochromocytoma
  • cushings syndrome
  • congenital adrenal hyperplasia
  • hyperthyroidism
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7
Q

What can cause secondary hypertension

A
  1. Contraction of the aorta (stricture)
  2. Excessive alcohol intake
  3. Drugs; oral contraceptives, sympathomimetics, NSAIDs, corticosteroids, cocaine
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8
Q

Outline the clinical features of hypertension

A
  • Asymptomatic until developed in cardiovascular system, brain and kidneys
  • Dizziness, facial flushing, headache, fatigue, epistaxis, nervousness, retinal changes
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9
Q

What can severe/prolonged hypertension increase the risk of

A
  1. Coronary artery disease or myocardial infarction
  2. Heart failure
  3. Stroke (haemorrhagic)
  4. Renal failure
  5. Death
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10
Q

Outline the complications that can occur with hypertension

A
  • Generalised arteriosclerosis (arterioles in eye and kidney)
  • Reduced kidney lumen increased total peripheral resistance
  • Increased after load causing left ventricular hypertrophy and dilated cardiomyopathy leading to heart failure
  • Thoracic aortic dissection (layers of aorta become torn)
  • Abdominal aortic aneurysms
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11
Q

What is an abdominal aortic aneurysm

A

When the aorta bulges out and so stagnant blood will collect leading to instant death

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12
Q

What special investigations are taken for hypertension

A

Multiple BP readings using a sphygmomanometer

  • ambulatory BP monitoring needed if higher than 140/90mmHg (14 readings over 24hrs to ensure it is not caused by white coat syndrome)
  • urinalysis and urinary albumin/creatine ratio
  • blood tests; fasting glucose, lipid profile, creatine, potassium, sodium, thyroid function
  • ECG
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13
Q

How is hypertension managed

A
  1. Weight loss and exercise
  2. Smoking cessation
  3. Diet; more fruit and veg, less salt and alcohol
  4. Medication
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14
Q

List the types of antihypertensive agents given

A
  1. Alpha-adrenergic blockers
  2. Angiotensin-converting enzyme inhibitors
  3. Angiotensin II receptor blockers
  4. Beta-adrenergic blockers
  5. Calcium-channel blockers
  6. Diuretics
  7. Sympatolythics
  8. Vasodilatory
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15
Q

Give examples of alpha-adrenergic blockers and what is the dental relevance

A

Doxazosin
Prazosin
Indoramin

Xerostomia

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16
Q

Give examples of ACE inhibitors and what is the dental relevance

A

Captopril
Enalapril
Iisinopril
Ramipril

  • burning sensation/ulceration/loss of taste
  • angioedema
  • xerostomia
  • lichenoid lesion
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17
Q

Give examples of ARBs and what is the dental relevance

A

Candesartan
Iosartan
Irbestatan

  • facial flushing, taste disturbance, gag reflex
  • xerostomia
  • lupoid reaction
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18
Q

Give examples of beta-adrenergic blockers and what is the dental relevance

A

Atenolol
Propranolol
Bisoprolol

  • xerostomia
  • lichenoid lesion
  • paraesthesia
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19
Q

Give examples of calcium channel blockers and what is the dental relevance

A

Amlodipine
Nifedipine
Verapamil
Diltiazem

  • gingival hyperplasia (with nifedipine)
  • salivation (with nicardipine)
  • angioedema
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20
Q

Give examples of diuretics and what is the dental relevance

A 
Bendroflumethiazide 
Amiloride
Furosemide
Indapamide
Spironolactone
  • xerostomia
  • erythema multiformis
  • lichenoid lesion
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21
Q

Give examples of sympatolytics

A

Methyldopa

Clonidine

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22
Q

Give examples of vasodilators and what is the dental relevance

A

Minoxidil
Hydralazine

  • ulceration
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23
Q

What is atherosclerosis

A

Patchy intimal plaques encroaching on the lumen of arteries - these contain lipids, inflammatory cells, smooth muscle cells and connective tissue and is initiated by endothelial injury

24
Q

What are the risk factors of atherosclerosis

A

hyperlipidemia, diabetes, cigarette smoking, family history, sedentary lifestyle, obesity, hypertension

25
Q

What is a stable plaque

A

One which regresses, remains static or grows slowly

When slow growing this can causes stenosis or occlusion

26
Q

What is an unstable plaque

A

These are vulnerable to spontaneous rupture, erosion or fissuring and the plaque content triggers acute thrombosis

27
Q

What does acute thrombosis of an unstable plaque lead to

A
  • thrombus becomes incorporated into existing plaques
  • thrombus rapidly occludes vascular lumen
  • thrombus may embolise (detach)
  • plaque may fill with blood, balloon out and occlude artery
  • plaque contents may embolise, occluding vessels downstream
28
Q

What are the clinical features of atherosclerosis

A
  • initially asymptomatic
  • stable plaque reduces arterial lumen causing stable exertionl anginga, TIAs, intermittent claudication
  • unstable plaque ruptures and acutely occludes major arteries causing unstable angina, MI, ischaemic stroke and rest pain in limbs
  • sudden death without preceding angina, aneurysms and arterial dissection
29
Q

What special investigations are done for atherosclerosis

A 
CT angiography 
Blood tests; lipid profile, plasma glucose, HbA1c
Catheter based imaging testing 
- intravascular ultrasonography 
- angiography 
- plaque thermography 
- optical coherence tomography 
- elastography/immunoscintigraphy
30
Q

How can atherosclerosis be managed

A

Lifestyle changes

  • diet = less sat/trans fat, more fruit and veg, more fibre
  • smoking cessation, regular exercise

Drugs

  • hyperlipidaemia = statins
  • hypertension = ACE inhibitors and beta-blockers
  • diabetes = metformin, glicazide
  • antiplatelet drugs = aspirin, clopidogrel, prasugrel
31
Q

What is angina pectoris

A

Precordial discomfort or pressure due to transient myocardial ischaemia without infarction

The cardiac workload and myocardial oxygen demand exceeds supply of oxygenated blood via narrow coronary arteries (due to atherosclerosis, spasm, embolism)

32
Q

What is stable angina

A

Predictable, increased workload leads to ischaemia

33
Q

What is unstable angina

A

Chest pain at rest, increase frequency/intensity of episode

34
Q

What are the clinical features of angina pectoris

A
  • triggered by strong exertion or emotion
  • persists for more than a few minutes and subsides with rest
  • discomfort beneath the sternum
  • radiates to left shoulder, inside arm, back, throat, jaw and teeth
  • atypical angina causes abdominal distress, gas, bloating, indigestion
  • nocturnal angina
35
Q

What are the special investigations for angina

A
  • ECG
  • stress testing with ECG or echocardiograph
  • coronary artery angiography
  • intravascular ultrasonography
36
Q

What drug treatments are used for angina pectoris

A

Relieve acute symptoms = sublingual nitroglycerin
Prevent ischaemia = anti platelets, beta-blockers
Prevent future ischaemic events = Ca channel blockers and nitrates

37
Q

What is myocardial infarction

A

Myocardial necrosis resulting from acute obstruction of a coronary artery characterised by pain similar to angina pectoris but more severe and long-lasting with dyspnoea, diaphoresis, nausea and vomiting

Other features = pale clammy skin, cyanosis, thready pulse, syncope

It is only temporarily relieved by nitroglycerine (unlike angina)

38
Q

What are the special investigations for MI

A

Initial and serial ECGs = STEMI/NSTEMI
Serial cardiac markers = troponin I/ troponin T and CK
Coronary angiography

39
Q

What treatments are given for patients with MI

A

Prehospital = oxygen, nitrates, aspirin, opioids

Drug treatment = anti platelets, antianginal, anticoagulants, ACE inhibitors, statins, beta-blockers

Reperfusion therapy = fribrinolytics, angiography with percutaneous coronary intervention or coronary artery bypass

Post discharge rehabilitation = exercise, diet, weight loss, stop smoking; Drugs - anti platelet, beta-blockers, ACEi and statins

40
Q

What is infective endocarditis

A

Rare condition associated with microbial infection of the endocardial surface of the heart occurring after bacteraemia in patients with predisposing cardiac lesions

41
Q

Which patients are at high risk of IE

A

Those with

  • prosthetic heart valves
  • proviso IE
  • acquired valvular heart disease with stenosis or regurgitation
  • congenital heart defect
42
Q

What is acute bacterial endocarditis

A

Aggressive within 7 days of bacteraemia

  • common in elderly and IV drug users
  • Staphylococcus aureus is most common offending organism
43
Q

What is sub-acute bacterial endocarditis

A

Insidious onset within 2-3 weeks of bacteraemia

- Streptococcus viridian’s is most common offending organism

44
Q

What are the clinical symptoms of IE

A

Flu-like symptoms, fever, anorexia, malaise, weight loss, night sweats, embolic phenomena, stroke, haematuria

Splinter haemorrhages (underneath nails), conjunctival petechiae, Osler’s nodes, Janeway’s lesions

45
Q

What are Osler’s nodes

A

Tender, subcutaneous nodules in the pulp of the digits

46
Q

What are Janeway’s lesions

A

Nontender, erythematous, hemorrhagic, pustular lesions on the soles or palms

47
Q

Why is there no prophylaxis for IE

A

Because there is no evidence that antibiotics prevent IE and there could be adverse reactions from drugs given as well as increasing bacterial resistance

48
Q

What are the causes of left ventricular heart failure

A
  • Coronary artery disease
  • DM and obesity
  • Hypertension
  • Valvular heart disease
  • Hyperthyroid disease
  • Substance abuse
49
Q

Outline the pathogenesis of left ventricular failure

A

Decreased cardiac output triggers compensatory mechanisms (SNS and RAAS) which increases after load leading to further myocardial deterioration and worsening of myocardial contractility

Pulmonary venous pressure increases so pulmonary capillary pressure exceeds oncotic pressure of plasma proteins so fluid extravasates from capillaries into interstitial space and alveoli affecting gaseous exchange

This means there is less pulmonary compliance and increased workload of breathing and decreased systemic arterial oxygenation causing myocardial deterioration

50
Q

What are the clinical features of left ventricular failure

A
  1. Restlessness, confusion and fatigue
  2. Orthopnea
  3. Tachycardia, cyanosis
  4. Exertional dyspnea, paroxysmal nocturnal dyspnea
  5. Elevated pulmonary capillary wedge pressure
  6. Pulmonary congestion; cough, crackle, wheeze, tachypnea, bloody-sputum
51
Q

What are the causes of right ventricular failure

A

Previous LV failure, severe lung disorder (cor-pulmonale), multiple pulmonary emboli and RV infarction

52
Q

What is the pathogenesis of RV failure

A

RV dysfunction causes systemic venous pressure increase so fluid extravasation and oedema in dependant tissues and abdominal viscera causing fluid accumulation in the peritoneal cavity

53
Q

What are the clinical features of RV failure

A
  1. Heaptomegaly, splenomegaly
  2. Abdominal distension (acites) and weight gain
  3. Elevated jugular venous pressure
  4. Nausea, vomiting and fatigue
  5. Chronic venous congestion in the viscera (anorexia and malabsorption of nutrients)
  6. Dependant peripheral oedema
  7. Nocturnal diuresis
  8. Swellings of fingers and hands
  9. Anorexia and complains of GI distress
54
Q

What are the special investigations for heart failure

A

FBC, electrolyte and urea, thyroid function test, ECG, chest radiography, echocardiography, coronary angiography, cardiac MRI

55
Q

Outline the treatments for heart failure

A

Symptomatic relief

  • Diuretics; loop diuretics = furosemide
  • Nitrates; isosorbide nitrate (dilates blood vessels)
  • Digoxin

Long term management

  • ACE inhibitors; ramipril, catopril
  • Beta-blockers; atenolol, bisoprolol
  • Aldosterone antagonists; spironolactone
  • Angiotensin II receptor blockers; losartan

BDS2; CHHD (32 decks)

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