Cardiovascular Disease Flashcards

1
Q

What happens to your BP with Hypertension

A
  • sustained elevation of resting systolic BP (>140mmHg), diastolic BP (>90mmHg)
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2
Q

What are the 2 types of hypertension

A

Primary (essential, idiopathic)

Secondary

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3
Q

Describe the features of primary hypertension (how common, risk factors, mechanism)

A
  • Most common - 85-95%
  • Many factors, hereditary is a predisposing factor
  • Environmental factor plays a role in genetically susceptible people
  • Mechanism is largely unclear
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4
Q

What can cause Secondary Hypertension

A
  • Renal Disease (80% of cases)
  • Endocrine Disease
  • Coarctation of the aorta
  • Excessive alcohol intake
  • Drugs
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5
Q

What renal diseases can cause secondary hypertension

A
  • Renal parenchymal disease - chronic glomerulonephritis, pyelonephritis, polycystic renal disease and post transplant
  • Reno-vascular diseases
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6
Q

What Endocrine diseases can cause secondary hypertension

A
  • Hyperaldosteronism
  • Pheochromocytoma
  • Cushing’s Syndrome
  • Congenital adrenal hyperplasia
  • Hyperthyroidism
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7
Q

Use of what kinds of drugs can cause secondary hypertension

A
  • Oral contraceptives

- Sympathomimetics, NSAIDs, corticosteroids, cocaine

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8
Q

What are the clinical features of Hypertension

A
  • Usually asymptomatic until complications develop in target organs
  • Dizziness
  • Facial flushing
  • Headache
  • Fatigue
  • Epistaxis
  • Nervousness
  • Retinal changes
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9
Q

What does severe/prolonged hypertension increase the risk of

A
  • Coronary artery disease and myocardial infarction
  • Heart failure
  • Stroke (particularly haemorrhagic)
  • Renal failure
  • Death
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10
Q

What are some of the complications associated with Hypertension

A
  • Generalised arteriolosclerosis = small arterioles (eyes and kidneys)
  • Kidney = narrow arteriolar lumen = increase total peripheral resistance = worsening hypertension
  • Increased afterload = left ventricular hypertrophy = dilated cardiomyopathy = heart failure
  • Thoracic aortic dissection
  • Abdominal aortic aneurysms
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11
Q

What are some special investigations that can be done for hypertension

A
  • Multiple readings of BP using a sphygmomanometers
  • Urinalysis and urinary albumin/creatinine ratio
  • Blood tests
  • ECG
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12
Q

When is ambulatory BP monitoring needed

A

If clinic BP > 140/90 mmHg

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13
Q

What blood tests are taken for hypertension

A
Fasting blood glucose
Lipid profile
Creatinine
Potassium
Sodium
Thyroid fxn test
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14
Q

What can be done for the management of hypertension

A
  • Weight loss and exercise
  • Smoking cessation
  • Dietary changes
  • Medication (only if unresponsive to lifestyle changes)
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15
Q

What dietary changes are made for the management of hypertension

A
  • Increases fruits and vegetables, decrease salt, limit alcohol
  • Low-fat dairy products with reduced saturated and total fat content
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16
Q

Name some types of Antihypertensive drugs

A
  • Alpha adrenergic blockers
  • ACE inhibitors
  • AT II receptor blockers
  • Beta adrenergic blockers
  • Calcium channel blockers
  • Diuretics
  • Sympatholythics
  • Vasodilators
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17
Q

Name some Alpha adrenergic blockers and ACE inhibitors

A

Alpha adrenergic = Doxazosin, Prazosin, Indoramin

ACE inhibitor = Captopril, enalapril, lisinopril, ramipril

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18
Q

Name some ATII receptor blockers and beta adrenergic blockers

A

ATII ting - Candesartan, Iosartan, Irbestatan

Beta adrenergic - Atenolol, Propanolol, Bisoprolol

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19
Q

Name some calcium-channel blockers and diuretics

A

Calcium Channel ting - Amlodipine, nifedipine, verapamil, diltiazem

Diuretics - Furosemide, spironolactone, indapamide

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20
Q

Name some sympatholythics for hypertension and vasodilators

A

Sympath ting - methyldopa, clonidine

Vasodilators - Minoxidil, hydralazine

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21
Q

What is the dental relevance of hypertension

A
  • Patient with stable hypertension may receive dental care in short, minimally stressful appointments
  • Hypertensive drugs can impact oral health
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22
Q

What is a common side effect amongst antihypertensive drugs

A

Xerostemia

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23
Q

What are some potential oral side effects of ACE inhibitors

A
  • Ulceration/ Burning Sensation/ Loss of Taste
  • Angioedema
  • Lichenoid lesion
  • Xerostemia
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24
Q

What are some potential oral side effects of vasodilators

A

Ulceration

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25
Q

What are some potential oral side effects of Diuretics

A
  • Erythema Multiformis
  • Xerostemia
  • Lichenoid Lesion
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26
Q

What are some potential oral side effects of CCBs

A
  • Gingival hyperplasia
  • Salivation
  • Angioedema
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27
Q

What are some potential oral side effects of ATII receptor blockers

A
  • Facial Flushing
  • Taste disturbance
  • Gag reflex
  • Xerostemia
  • Lupoid reaction
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28
Q

What are some potential oral side effects of Beta- adrenergic blockers

A
  • Xerostemia
  • Lichenoid lesion
  • Paraaesthesia
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29
Q

What causes the problems associated with atherosclerosis

A
  • Patchy intimal plaques (atheroma) = encroach on the lumen of medium-sized and large arteries
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30
Q

What does the plaque in atherosclerosis consist of

A

Lipids
Inflammatory cells
Smooth muscle cells
Connective tissue

31
Q

What initiates plaque formation and atherosclerosis

A

Endothelial injury

32
Q

What are some risk factors for atherosclerosis

A
  • Hyperlipidemia
  • Diabetes
  • Cigarette smoking
  • Family history
  • Sedentary lifestyle
  • Obesity
  • Hypertension
33
Q

What kinds of plaque can form in atherosclerosis

A

Stable

Unstable

34
Q

Describe the characteristics of a stable plaque in atherosclerosis

A
  • Regresses
  • Remains static or grows slowly
  • Leads to stenosis or occlusion
35
Q

What is stenosis

A

a narrowing of a blood vessel or some shit

36
Q

Why are unstable plaques more dangerous than stable ones

A

They are vulnerable to spontaneous rupture, erosion of fissuring and can easily lead to acute thrombosis due to the plaque content

37
Q

What can the acute thrombosis from unstable plaques from atherosclerosis lead to

A
  • Thrombus becomes organised and incorporated into existing plaques
  • Thrombus rapidly occludes the vascular lumen = acute ischaemic event
  • Thrombus may embolise
  • Plaque may fill with blood , balloon out and occlude the artery
  • Plaque contents (rather than thrombus) may embolise, occluding vessels downstream
38
Q

What are the clinical features of atherosclerosis

A
  • Initially asymptomatic, often for decades
  • Stable plaque grows = reduce arterial lumen by >70%
  • Unstable plaque ruptures = acutely occludes major artery
  • Sudden death without preceding stable/unstable angina
  • Aneurysms and arterial dissection
39
Q

What complications arise from stable plaques occluding arterial lumen by >70%

A
  • Stable exertional angina
  • Transient ischaemic attacks
  • intermittent claudication
40
Q

What complications arise from unstable plaques occluding arterial lumen

A
  • Unstable angina
  • Myocardial infarction
  • Ischaemic stroke
  • Rest pain in limbs (blood flow is impeded)
41
Q

What are some special investigations that can be done for atherosclerosis

A
  • CT angiography
  • Blood tests - fasting lipid profile, plasma glucose and HbA(1C) levels
  • Catheter based imaging - Angioscopy, intravascular ultrasonography, plaque thermography
42
Q

What management options are there for atherosclerosis

A
  • Diet changes - less saturated and trans fats, more fruit, vegetables and fibre
  • Stop smoking and start exercising
  • Drugs to treat diagnosed risk factors
43
Q

What drugs can be administered for atherosclerosis to treat which diagnosed risk factors

A
  • Hyperlipidaemia - Statins
  • Hypertension - ACE inhibitors, Beta blockers
  • Diabetes - Metformin, Glicazide
  • Antiplatelet drugs - Aspirin, clopidogrel, prasugrel
44
Q

Describe angina pectoris and describe the causes of it

A

Clinical syndrome of precordial discomfort or pressure due to transient myocardial ischaemia without infarction

Cardiac workload and myocardial oxygen demand exceed supply of oxygenated blood via narrow coronary arteries

Narrowed coronary arteries due to atherosclerosis, spasm, embolism

45
Q

Describe the onset of unstable angina

A

Chest pain at rest, increase frequency/intensity of episode

46
Q

What are the clinical features of angina pectoris

A
  • Triggered by exertion or strong emotion
  • Persists for no more than a few minutes and subsides with rest
  • Described as a discomfort beneath the sternum
  • Can radiate to left shoulder, inside of left arm, back, throat, jaw and teeth
  • Atypical angina = abdominal distress, gas, bloating, indigestion
  • Nocturnal angina
47
Q

What are some special investigations that can be done for angina pectoris

A
  • ECG
  • Stress testing with ECG or echocardiography
  • Coronary artery angiography
  • Intravascular ultrasonography
48
Q

What treatment goals and drugs are used for angina pectoris

A
  • Relieve acute symptoms - sublingual nitroglycerin
  • Prevent or reduce ischaemia - antiplatelet, Beta blockers
  • Prevent future ischaemic events - CCBs and long acting nitrates
49
Q

What are myocardial infarctions caused by

A

Myocardial necrosis resulting from acute obstruction of a coronary artery

50
Q

What are the clinical features of myocardial infarctions

A
  • Similar pain to angina pectoris
  • More severe, long lasting and associated with dyspnoea, diaphoresis, nausea and vomiting
  • Relieved little or only temporary by rest or nitroglycerin
  • Pale clammy skin
  • Cyanosis
  • Thready pulse
  • Syncope
51
Q

What are some special investigations that can be done for Myocardial infarctions

A
  • Initial and serial ECGs = STEMI/NSTEMI
  • Serial cardiac markers (troponin I or troponin T and CK)
  • Coronary angiography
52
Q

What pre-hospital care can be used to treat myocardial infarctions

A
Oxygen
Nitrates
Aspirin
\+/- opioids for pain
Triage to medical centre
53
Q

What drug treatment can be used for myocardial infarctions

A
Antiplatelet drugs
Antianginal drugs
Anticoagulants
ACE inhibitors
Statins
Beta blockers
54
Q

What is reperfusion therapy for myocardial infarction

A

Fibrinolytics or angiography with percutaneous coronary intervention or coronary artery bypass surgery

55
Q

After discharge from a myocardial infarction what management of future MIs can be used

A

Change in lifestyle - regular exercise, diet modification, weight loss, smoking cessation

Drugs - Continuation of antiplatelet drugs, beta blockers, ACE inhibitors and statins

56
Q

Briefly describe infective endocarditis

A

Rare condition associated with microbial infection of the endocardial surface of the heart esp heart valves

Potentially life-threatening

57
Q

What might infective endocarditis occur after

A

After bacteraemia in patient with pre-disposing cardiac lesion

58
Q

What predisposing factors place patients at the highest risk of infective endocarditis

A
  • Prosthetic heart valves
  • Previous infective endocarditis
  • Acquired valvular heart disease with stenosis or regurgitation
  • Congenital defect e.g. tetralogy of fallot
59
Q

Describe the characteristics of acute bacterial endocarditis

A
  • Aggressive (within 7 days of bacteraemia)
  • Common in elderly and IV drug users
  • Staphylococcus aureus is the most common offending organism
60
Q

Describe the characteristics of sub-acute bacterial endocarditis

A
  • Insidious onset (2-3 weeks of suspected bacteraemia)

- Streptococcus viridian’s is the most common offending organism

61
Q

What are some symptoms/complications associated with infective endocarditis

A
  • Flu like symptoms
  • Fever
  • Anorexia
  • Malaise
  • Weight loss
  • Night sweats
  • Embolic phenomena-stroke
  • Haematuria
62
Q

Why is prophylaxis not used before dental treatment in patients at risk of infective endocarditis anymore

A
  • Efficacy of antibiotic prophylaxis in humans is difficult to investigate
  • Bacteraemia arise from tooth brushing and chewing
  • No strong association between IE episodes and preceding interventional procedures
  • Adverse reactions, like anaphylaxis, to antimicrobials are possible
  • Cost-effectiveness of prophylaxis is questionable
  • Increased risk of resistant bacteria in society
63
Q

Instead of giving patients at risk of Infective endocarditis prophylaxis, what alternatives are recommended

A
  • Receive intensive preventative oral healthcare to minimise the need for dental intervention
  • Achieve and maintain high standards of oral health
  • Are informed of the benefits and risk of antibiotic prophylaxis
  • Informed of risk associated with undergoing non-medical procedures e.g. piercings and tattoos
  • Recognise symptoms that may indicate IE and when to seek medical advice
64
Q

What is heart failure

A

Syndrome of left and/or right ventricular dysfunction

65
Q

What are some of the causes of left ventricular heart failure

A
  • Coronary heart disease
  • Diabetes mellitus
  • Hypertension
  • Obesity
  • Valvular heart disease
  • Hyperthyroid disease
  • Substance abuse
66
Q

Describe the pathogenesis of left ventricular failure

A
  1. Decreased cardiac output
  2. Triggers compensatory mechanisms (Symp. nervous and Renin-angiotensin-aldosterone systems)
  3. Increased afterload
  4. Further myocardial deterioration and worsening myocardial contractility
  5. Vicious cycle of above steps
  6. Worsening of cardiac failure
67
Q

ERRRRR sooooooo describe the other pathogenesis of left ventricular failure

A
  1. Pulmonary venous pressure increases
  2. Pulmonary capillary pressure exceeds the oncotic pressure of plasma proteins
  3. Fluid extravasates from the capillaries into the interstitial space and alveoli (pulmonary oedema and crackles)
  4. Reduced pulmonary compliance and increasing the work of breathing (shortness of breath and dyspnoea)
  5. Decreased systemic arterial oxygenation
  6. Myocardial deterioration
68
Q

What are the clinical features of left ventricular failure

A
  • Pulmonary Oedema
  • Tachycardia
  • Fatigue
  • Confusion
  • Cough
  • Wheezes
  • Restlessness
    Many more
69
Q

What are some of the causes of Right Ventricular Failure

A
  • Previous LV failure - increase pulmonary venous pressure leads to pulmonary arterial hypertension thus overloading the RV
  • Severe lung disorder -> cor-pulmonale
  • Multiple pulmonary emboli and RV infarction etc
70
Q

Describe the pathogenesis of right ventricular failure

A
  1. Right ventricular dysfunction
  2. Systemic venous pressure increases
  3. Fluid extravasation and oedema, primarily in dependent tissues and abdominal viscera
  4. Fluid accumulation in the peritoneal cavity
71
Q

What are the clinical features of right ventricular failure

A
  • Hepatomegaly
  • Splenomegaly
  • Abdominal distension
  • Elevated jugular venous pressure
  • Nausea and vomiting
  • Chronic venous congestion in the viscera = anorexia, malabsorption of nutrients
  • Dependent (peripheral) oedema
  • Nocturnal diuresis
  • Swelling of fingers and hands
72
Q

What are some of the special investigations that can be done for heart failure

A
  • FBC
  • Electrolyte and urea
  • Thyroid function test
  • ECG
  • Chest radiography
  • Echocardiography
  • Coronary angiography
  • Cardiac MRI
73
Q

What treatment can help to relieve the symptoms of heart failure

A
  • Diuretics - loop diuretic (furosemide)
  • Nitrates - isosorbide nitrate
  • Digoxin
74
Q

What drugs types can help the long term management and improved survival of heart failure give examples as well

A
  • ACE inhibitors - Ramipril, captopril
  • Beta-blockers - atenolol, bisoprolol
  • Aldosterone antagonists - spironolactone
  • ATII receptor blockers - Losaratan