Cardiovascular disease and pathology Flashcards

1
Q

Why is cardiovascular disease important?

A

*7 million people in the UK living with cardiovascular disease
*Will be a regular feature when taken history in clinics.
*Relevant in dentistry

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2
Q

Statistics on hypertension.

A

Depending on criteria said to be present in 20-30% of the adult population

Persistently raised blood pressure > 140/90 mm Hg

90% No cause found = Primary / Essential hypertension
10% Cause found = Secondary hypertension

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3
Q

What are the causes of Primary (Essential) Hypertension?

A

Most common cause of preventable disease in developed world
Normally detected between 20-50 years of age
Has a Multifactorial Aetiology
There may be Genetic factors

There may be Environmental factors:
o Obesity (ensure correct cuff size)
o Alcohol
o Salt intake
o Stress

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4
Q

What causes secondary hypertension?

A
  • Renal disease – E.g. diabetic nephropathy, chronic glomerulonephritis, adult polycystic disease
  • Pregnancy
  • Endocrine disease –E.g. Conn’s syndrome, adrenal hyperplasia, phaeochromocytoma, Cushing’s syndrome, acromegaly
  • Drugs – E.g. Cortocosteroids, oral contraceptive pill
  • Coarctation of the aorta – there is a narrowed area can lead to high blood pressure
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5
Q

How is hypertension diagnosed?

A
  • Measurement of blood pressure on at least 3 occasions over 3 month period
  • Patients often require a 24 hour monitor so continuous recordings can be analysed.
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6
Q

How is secondary hypertension treated?

A

Secondary hypertension – treat cause if possible

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7
Q

How is primary hypertension treated?

A

Primary / Essential hypertension you would give General advice (BHS):
* Weight loss
* Increase exercise
* Reduce alcohol
* Stop smoking
* Reduce salt intake
* Increase fruit and vegetable intake

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8
Q

How is primary hypertension medically treated?

A

Medical treatment:
* ACE Inhibitors (eg captopril)
* Angiotensin II receptor blockers (eg candesartan)
* B β-blockers (eg atenolol)
* Ca channel blockers (eg nifedipine)
* Diuretics (eg bendroflumethiazide)
Before giving medication must look into the cause of hypertension, age, co-morbidities of the patient.

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9
Q

What are the complications of hypertension?

A
  • Heart failure
  • Stroke – cerebrovascular accident (CVA)
  • Coronary artery disease / Myocardial infarction (MI)
  • Renal failure
  • Peripheral vascular disease
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10
Q

What is the dental relevance of patients with hypertension?

A
  • Minimise stress and pain to minimise further increase in BP which may precipitate cerebral vascular accident (CVA), MI
  • No problem with adrenaline in LA (as long as intravascular injection avoided)
  • Controlled hypertensive – treat as normotensive (treat as normal)
  • Uncontrolled hypertensive (>140/90mmHg) – delay elective treatment. Refer to GP.
  • Severe hypertension (>180/110mmHg) – Refer urgently to GP or hospital
  • Post-operative bleeding more likely
  • Patient likely to be taking aspirin
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11
Q

What are the oral manifestations of hypertension medication?

A

ACE inhibitors:
* Loss of taste
* Angioedema
* Lichenoid reactions
β-blockers: Lichenoid reactions
Ca channel blockers: Gingival overgrowth
Diuretics: Xerostomia

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12
Q

What does a normal artery look like?

A

normal intima:
* <0.1mm thickness
* Loose fibrous tissue
* Endothelial layer on top forms a barrier between blood and vessel wall/

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13
Q

What does an artery look like with Atherosclerosis?

A

Fatty streaks present in 45% of infants dying in the first year of like and these are seen as minimally elevated 1-2mm yellowish dots. It is reversible at this stage.

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14
Q

What is Atherosclerosis?

A

Widely prevalent disease affecting large elastic and muscular arteries.

Thickening of the intima: composed of lipid derived from plasma and deposits of extra connective tissue make calcify overtime.

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15
Q

What are the main sites of Atherosclerosis?

A

Main site of occurrence are:
* Aorta
* Carotid
* coronary arteries
* more peripheral leg of diabetics

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16
Q

How are atheromas formed?

A
  • LDL into intima.
  • Once entered the LDL is Oxidised, sends chemotactic messages to monocytes.
  • Ingestion of LDL by monocytes / macrophages.
  • Macrophages sends growth factor signals which leads to the stimulation of smooth muscle cell migration and connective tissue synthesis.
  • Death of lipid containing macrophages, spillage of lipid and cholesterol

Increased entry of LDL is more likely when there is endothelial damage, this may be due to turbulent blood flow, hypertension and damage to endothelial cells due to toxins in cigarettes.

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17
Q

What causes Hyperlipidaemia and LDL:HDL imbalance?

A

Maybe due to diet but could also be due to:
* Familial hypercholesterolaemia
* Decrease receptors (cells which aid in elimination via liver) for LDL cholesterol
* Increased circulating levels of LDL

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18
Q

What is HDL?

A

Good type of cholesterol
Blocks several process involved in the formation of atheroma:
o Blocks oxidation of LDL
o Actively block attachment of monocytes inhibiting entry
o Blocks growth factors from LDL containing macrophages reducing smooth muscle and fibroblastic proliferation.
o Make platelets aggregation

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19
Q

How is hypertension linked with atheroma?

A

Degree of atherosclerosis has positive correlation with hypertension
Haemodynamic forces which exits in patient with hypertension causes damage to endothelial cell and facilitates passage of LDL intima.

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20
Q

what is advanced atherosclerosis?

A

Sex: primarily a disease of men until 7/8th decade more elderly women are affected as protective effect of female sex hormones are lost.
Cigarette smoking can lead endothelial damage allowing LDL to enter.
Diabetes increased incidence of hyperlipidaemia and microvascular damage.

Regression of plaque could be due to change of diet and positive life style changes.

If no lifestyle change this could lead to:
* Interference with blood flow to target organs (ischaemia/infarction)
* Thrombosis
* Embolisation

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21
Q

What is ischemia?

A

Ischaemia: restriction in supply of blood to the tissues causing a shortage of oxygen and glucose necessary for cellular metabolism.

22
Q

What is an infarction?

A

Infarction: tissue death caused by lack of oxygen due to obstruction in blood flow

23
Q

What are the clinical symptoms of ischaemia?

A
  • Angina
  • Transient ischemic attack
  • Peripheral vascular disease – intermittent claudication
24
Q

What are the clinical symptoms of infarction?

A
  • Myocardial infarction
  • Stroke
  • Gangrene
25
Q

What does it depend on to get ischaemic or infarction?

A
  • Collateral blood supply
  • speed of arterial occlusion
  • metabolic needs of tissue
  • degree of arterial blocking
26
Q

What are the clinical aspects of ischemic heart disease (IHD)?

A
  • Inadequate O2 supply to meet demands of the heart
  • Most common cause of death in Western world accounting for 35% of total mortality.
  • Aetiology – atheromatous plaque within coronary arteries causing constriction to blood flow
  • Risk of plaque rupturing leading to acute thrombus and MI
27
Q

What are the modifiable risk factors of IHD?

A
  • Hyperlipidaemia
  • Smoking
  • Hypertension
  • Diabetes
  • Obesity
  • lack of exercise
  • High alcohol intake
  • Stress
  • Oral contraceptive pill
28
Q

What are the modifiable risk factors of IHD?

A

Unmodifiable:
* Age
* Male gender
* Family history

29
Q

What is angina?

A

ANGINA PECTORIS- reduced O2 perfusion of the cardiac muscle resulting in:
* Strangling feeling in the chest. (Greek ‘Angina’= Strangling, Latin ‘Pecta’ = chest)
* Breathlessness
* Pain radiating to the jaw and the left arm

Pain resolves in minutes following rest and GTN.

30
Q

What is the dental relevance of angina?

A

Polypharmacy:
* Side affects of these medications - how will they affect the patient and what you plan to do to them
* Aspirin - bleeding tendency
* Beta Blockers/Ca channel blockers - mucosal disease,
* Nicorandil - oral ulceration

31
Q

What are the symptoms of Myocardial Infarction (heart attack)?

A
  • Central strangling pain lasting longer than 15 minutes
  • Pain radiates to the neck, jaw and left arm
  • Nausea, vomiting
32
Q

What are the signs of Myocardial Infarction (heart attack)?

A
  • Grey tinge
  • Sweating
  • Tachycardia

Characteristic on an ECG are a ST elevation.

33
Q

How is Myocardial Infarction (heart attack) managed?

A
  • Sit patient up
  • Calm and relaxed approach
  • Dial for an ambulance/crash team
  • Administer O2 and GTN (repeat every 10 minutes)
  • Aspirin 300mg PO crushed or chewed
  • Entonox if available
  • Monitor pulse and oxygen saturation
34
Q

What is the dental relevance of a Myocardial Infarction (heart attack)?

A

Dental treatment may precipitate angina / MI - need to minimise stress and pain
May present as jaw pain
May use GTN prophylactically
Unstable angina – delay elective treatment until controlled
Likely to be taking aspirin

35
Q

What are the oral manifestations of the drugs given to with patients who suffered from Myocardial Infarction?

A

Oral manifestations of drugs
o Ca channel blockers - gingival overgrowth
o β-blockers – lichenoid reactions
o Nicorandil – oral ulceration

36
Q

What is clotting?

A
  • Essential psychological and beneficial activation of clotting cascade when there has been tissue injury.
  • Refers to activation of protein cascade leading to formation of fibrin
37
Q

What is thrombosis?

A
  • Involves activation of both platelets and clotting cascade
  • Haemostasis hoccurring in the wrong place and at the wrong time
  • Harmful
38
Q

What is Virchows triad?

A

Virchow’s triad: Factors promoting thrombosis:
* changes in the surface of the vessel
* changes in the blood flow
* changes in the constituents of the blood

39
Q

What can lead to changes in vessel surface?

A

Changes in the vessel surface can be due to:
* Formation Atheromatous plaque
* Splitting/ fraying/ loss of surface and endothelial cell layer
* Exposure of sub-endothelial tissues (fibrous/ fatty plaque) leads to platelet activation.

40
Q

What are other causes for changes in vessel surface?

A
  • burning/ freezing “frostbite” closest trauma to the endothelium
  • mechanical: indwelling cannulae
  • chemical injury: injectable materials (sometimes deliberate)
  • inflammation “vasculitis”
41
Q

What leads to changes in the pattern of blood flow?

A

Occurs:
* In hypertension
* Presence of plaque
* Thrombosis in lower limbs of immobile individuals (DVT) – use of calve muscle encourages blood flow back to the heart, decreased propulsion due to immobility means accumulated slow flowing blood around the valves when stagnant can under go thrombosis.

42
Q

What are the other causes for changes in the pattern of blood flow?

A

Other alterations in the blood flow
* Patients with congestive cardiac failure (venous stagnation)
* Post myocardial infarction
* Atrial fibrillation
* Heart valve disease
Arterial thrombosis there is usually turbulent flow whereas in venous thrombosis there is sluggish or slow flow or even stagnation of the flow.

43
Q

What leads to the changes in the constituents of the blood?

A

Hypercoagulable state: haemostatic equilibrium is titled in the favour of thrombosis.
* Increase pro- coagulant factors
* Procoagulant factors from malignant tumours
* Decrease in anti- coagulant factors
* Increased platelet count and adhesiveness/ aggregatibility
* Increased viscosity of the blood

44
Q

What factors can increase plasma fibrinogen and factor VIIc concentrations?

A
  • Increasing age
  • Obesity
  • Oral contraceptive
  • Menopause
  • Diabetes
  • Smoking
    When they have developed the atheroma, they have the risk of thrombosis.
45
Q

What does the fate of thrombus depend on?

A
  • Lysis
  • Organisation/recanalization
  • Embolisation
46
Q

What is Embolisation?

A
  • Thrombi detach and travel at high speed through the circulation.
  • Until a vessel is reach whose lumen is smaller that the size of the thrombus.
47
Q

What are the types of emboli?

A
  • Thrombus
  • Infective (vegetation of infective endocarditis)
  • Gaseous
  • Fat
  • Foreign material
48
Q

What are Clinical aspects of heart failure?

A

Heart failure is when the heart is not able to pump blood at a rate that the bodies requirements
The heart cannot fill quickly enough to match demand or where it cannot pump the blood out.

49
Q

What causes heart failure?

A
  • Pump failure eg. heart muscle disease, restricted filling, inadequate heart rate
  • Excessive preload eg. Mitral regurgitation, fluid overload
  • Chronic excessive afterload eg aortic stenosis, hypertension
50
Q

What are the signs and symptoms of left-sided and righ-sided heart failure?

A

look at notes