90% of time: no cause is found- primary hypertension
10% of time: cause found- secondary hypertension
What could be possible causes of secondary hypertension?
Renal disease
Pregnancy
Drugs e.g corticosteroids
Endocrine disease
Coarctation of aorta
How do you diagnose hypertension?
Measurements of BP on at least 3 occasions over 3 month period & patients often require a 24 hr monitor
How do you treat primary & secondary hypertension?
Secondary:
Treat cause if possible
Primary:
General advice (weight loss, reduce alcohol, exercise more etc.)
Medical treatment (ACE inhibitors, angiotensin II receptor blockers, beta blockers, Ca channel blockers, diuretics)
What are potential complications of hypertension if left untreated?
Heart failure
Stroke- cerebrovascular accident (CVA)
Coronary artery disease/MI
Renal failure
Peripheral vascular disease
What is the dental relevance of hypertension?
-Patient may be taking aspirin
-post-operative bleeding is more likely
-Minimise stress and pain to minimise further increase in BP which may lead to stroke or myocardial infarction
What is the dental relevance of medications being taken for hypertension?
ACE inhibitors:
Loss of taste, angioedema (swelling of blood vessels), lichenoid reactions
Beta blockers:
Lichenoid reactions
Ca channel blockers:
Gingival overgrowth
Diuretics:
Xerostomia
What is the 'good' and 'bad' cholesterol?
Good: HDL (protective and stops oxidation of LDL)
Bad: LDL (low in protein, high in fat)
What is atherosclerosis and what happens?
Widely prevalent disease affecting large elastic & muscular arteries
Thickenings of the intima: composed of lipid derived from plasma and deposits of extra connective tissue
May calcify over time
Atherosclerosis
condition in which fatty deposits called plaque build up on the inner walls of the arteries
Where are the common sites for atheromas?
Aorta
Carotid
Coronary arteries
How does an atheroma form?
1. LDL into intima layer
2. Oxidised and sends chemotactic messages to monocytes
3. Macrophages enter intima and ingest LDL By binding through scavenger receptors
4.This signals the stimulation of smooth muscle cell migration and connective tissue synthesis
5.Death of lipid containing macrophages which causes spillage of lipid and cholesterol into the plaque
Describe the sequence in progression from atheroma to atherosclerosis.
What is hyperlipidaemia?
Too many lipids in the blood
What is familial hypercholesterolaemia?
Inherited disorder of high LDL that can't be removed from circulation because of a decreased level of receptors (cells which aid in elimination via liver) for LDL cholesterol
Heterozygotes have 50% reduction in receptors: disease development in 40s
Homozygotes: disease development in 20s
What are some risk factors for atherosclerosis?
Sex: primarily a disease of men and older women
Cigarette smoking: endothelial cell damage
Diabetes: increased incidence of hyperlipidaemia & microvascular damage
What happens after you have a substantial atherosclerotic plaque?
Could be regression: change in lifestyle, HDL increase, antioxidants
If no regression then:
Interference with blood flow to target organ (ischaemia/infarction)
Thrombosis: could lead to total occlusion
Embolisation
What is ischaemia?
Restriction in supply of blood to the tissues causing a shortage of oxygen & glucose necessary for cellular metabolism
What is an infarction?
Tissue death caused by a lack of oxygen due to obstruction in blood flow
What are clinical symptoms of ischaemia & infarction?
What are some factors that will affect the chances of you getting ischaemia or an infarction from a significant atherosclerotic plaque?
Collateral blood supply to that organ
Speed of arterial occlusion
Metabolic needs of tissue
Degree of arterial blocking
What is ischaemic heart disease (IHD) & what is the aetiology?
Inadequate oxygen supply to meet the demands of the heart
Aetiology: atheromatous plaque within coronary arteries causing constriction to blood flow
What are the modifiable & unmodifiable risk factors for IHD?
Unmodifiable: age, male gender, family history
Modifiable: hyperlipidaemia, smoking, hypertension, diabetes, obesity, lack of exercise, high alcohol intake, stress, OCP
What is angina pectoris?
Reduced oxygen perfusion of the cardiac muscle resulting in strangling feeling in the chest, breathlessness, pain radiating to the jaw & left arm
Central strangling pain lasting longer than 15 minutes
Pain radiates to the neck, jaw & left arm
Nausea, vomiting
Signs:
Grey tinge
Sweating
Tachycardia (fast heart rate)
How do you manage a MI?
Sit patient up
Calm & relaxed approach
Dial for ambulance/crash team
Administer oxygen & GTN (repeat every 10 mins)
Aspirin 300mg PO crushed or chewed
Entonox if available
Monitor pulse & oxygen saturation
What is the dental relevance of a MI?
What is the difference between clotting & thrombosis?
Clotting :-essential and beneficial activation of clotting cascade when there has been tissue injury-refers to activation of protein cascade leading to formation of fibrin
Thrombosis:-Involves activation of both platelets and clotting cascade.-Haemostasis occurring at wrong place and time
What is Virchow's triad?
Factors that promote thrombosis
1. Changes in the surface of the vessel
2. Changes in the blood flow - stasis
3. Changes in the constituents of the blood - hypercoagulation
How can the vessel surface be changed and how does this promote thrombosis?
-Splitting/fraying/ loss of surface endothelial cell layer
-exposure of sub-endothelial tissues lead to platelet activation (promoting thrombosis)
-Atheromatous plaque
Surface can also be changed by burning/freezing: "frostbite" causes trauma to endothelium
Chemical injury - injectable materials
Inflammation (vasculitis)
How could the blood flow change?
DVT- deep vein thrombosis
Patients with congestive cardiac failure (venous stagnation)
Post myocardial infarction
Atrial fibrillation
Heart valve disease
Where are arterial & venous thromboses more likely to occur?
Arterial thrombosis in places where there's more turbulent flow
Venous thrombosis in places where there's more sluggish/slow flow
Why might the blood constituency change?
Hypercoaguable state: haemostatic equilibrium is tilted in the favour of thrombosis
What factors might result in increased plasma fibrinogen & factor VIIc concentrations?
Increasing age
Obesity
Oral contraceptives
Menopause
Diabetes
Smoking
What 3 possible things could happen to a thrombus?
Lysis
Organisation/recanalisation
Embolisation
What is embolisation of a thrombus?
Thrombi detach & travel at high speed through the circulation until a vessel is reached whose lumen is smaller than the size of the thrombus.
This causes ischaemia or infarction at that site
How does a pulmonary embolism occur?
Venous thrombi will travel through vessels of increasing size through the right side of the heart and then sit in the lungs (in a pulmonary vessel)
What are the types of emboli?
Thrombus (99%)
Infective (vegetations of infective endocarditis)
Gaseous
Fat
Foreign material
What is heart failure?
The inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients