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HHAD: Human Disease > Clinical and pathological aspects of cardiovascular disease > Flashcards

Clinical and pathological aspects of cardiovascular disease Flashcards

1
Q

How many people in the UK are living with CV disease?

A

approx 7 million

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2
Q

Primary (essential) hypertension has multifactorial aetiology - name the 4 examples

A
  • Genetic factors
  • Environmental (e.g. obesity, alcohol, salt intake, stress)
  • Humoral mechanisms
  • Insulin resistance
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3
Q

What percentage of hypertension cases are primary hypertension (i.e. no cause found)?

A

90%.

Remaining 10% is secondary hypertension (i.e. cause found)

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4
Q

What value would be considered to be raised blood pressure?

A

> 140/90 mm Hg

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5
Q

Between what age is primary hypertension normally detected?

A

20-50 years of age

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6
Q

What could cause secondary hypertension? (5)

A

Renal disease

Pregnancy

Endocrine disease

Drugs (e.g. pill, corticosteroids)

Coarctation of the aorta (birth defect where part of aorta is narrower)

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7
Q

How would you diagnose hypertension?

A

Measure blood pressure on at least 3 occasions over 3 month period.

Patients often require 24 hr monitor

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8
Q

How would you treat secondary hypertension?

A

You would treat the cause if possible, as it is secondary

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9
Q

How would you treat primary/essential hypertension?

  1. General advice (6)
  2. Medical treatment (5)
A 
1. 
Weight loss
Increase exercise 
Reduce alcohol 
Stop smoking 
Reduce salt intake 
Increase fruit and veg intake
  1. (AABCD)
    ACE inhibitors (e.g. captopril)
    Angiotensin II receptor blockers (e.g. candesartan)
    Beta blockers (e.g. atenolol)
    Calcium channel blockers (e.g. nifedipine)
    Diuretics (e.g. Bendroflumethiazide)
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10
Q

What are the complications of hypertension? (5)

A 
Heart failure 
Stroke (cerebrovascular accident CVA)
Coronary artery disease/myocardial infarction 
Renal failure 
Peripheral vascular disease
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11
Q

Outline the dental relevance of hypertension (7)

A
  1. Know to minimise stress and pain in order to minimise a further increase in BP (as this could then lead to CVA or MI)
  2. Can have LA with adrenaline (as long as IV injection avoided)
  3. Controlled hypertensive - treated as normotensive
  4. Uncontrolled hypertensive - delay elective treatment and refer to GP
  5. Severe hypertension - refer urgently to GP or hospital
  6. Post-operative bleeding more likely
  7. Patient likely to be taking aspirin
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12
Q

What measurements indicate uncontrolled hypertension?

A

> 140/90mmHg

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13
Q

What measurements indicate severe hypertension?

A

> 180/110 mmHg

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14
Q

Dental relevance of hypertension: what oral manifestations may arise if your patient is taking ACE inhibitors? (3)

A

Loss of taste
Angioedema
Lichenoid reactions

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15
Q

Dental relevance of hypertension: what oral manifestations may arise if your patient is taking beta blockers? (1)

A

Lichenoid reactions

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16
Q

Dental relevance of hypertension: what oral manifestations may arise if your patient is taking calcium channel blockers? (1)

A

Gingival overgrowth

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17
Q

Dental relevance of hypertension: what oral manifestations may arise if your patient is taking diuretics? (1)

A

Xerostomia

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18
Q

What is an intima/tunica intima?

A

It is the innermost layer of an artery or vein

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19
Q

Describe a normal intima (3)

A

<0.1 mm thick
Loose fibrous tissue
Endothelial layer on top

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20
Q

What is atherosclerosis?

A

It is a prevalent disease affecting large elastic and muscular arteries.
Intima thickens - composed of lipid derived from plasma and deposits of extra connective tissue
May calcify over time

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21
Q

Outline the possible locations of atherosclerosis (4)

A

Aorta
Carotid
Coronary arteries

More peripheral (e.g. legs of diabetics)

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22
Q

What are the possible complications of atherosclerosis? (7)

A 
Rupture 
Ulceration 
Thrombosis
Haemorrhage 
Calcification 
Aneurysm 
Embolus
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23
Q

Outline the stages of atherosclerosis (5)

A
  1. Endothelial dysfunction
  2. Formation of lipid layer or fatty streak within intima
  3. migration of leukocytes and smooth muscle cells into the vessel wall
  4. Foam cell formation
  5. Degradation of extracellular matrix (ECM)
24
Q

Outline the progressive stages of endothelial dysfunction (6)

A
  1. Initial lesion: histologically normal, macrophage infiltration, isolated foam cells
  2. Fatty streak: mainly intracellular lipid accumulation
  3. Intermediate lesion: intracellular lipid accumulation, small extracellular lipid pools
  4. Atheroma: intracellular lipid accumulation, core extracellular lipid
  5. Fibroatheroma: single or multiple lipid cores, fibrotic/calcific layers
  6. Complicated lesion: surface defect, haematoma-haemorrhage, thrombosis
25
Q

What are the consequences of familial hypercholesterolaemia on the levels of LDLs?

A

Increased levels of circulating LDL, due to the decreased receptors for LDL cholesterol (these cells aid in elimination via the liver)

26
Q

LDL:HDL ratio - ideally, you never want this ratio to be above what level?

A

3-4:1

27
Q

What is the purpose of HDL cholesterol in the blood?

A

It absorbs cholesterol and carries it back to the liver, where it is then eliminated from the body. High levels of HDL can lower risk of heart disease and stroke

28
Q

Does the degree of atherosclerosis have a positive or negative correlation with hypertension?

A

Positive correlation

29
Q

What happens in hypertension? (3)

A

Haemodynamic forces
Damage to endothelial cells and facilitating passage of LDL into intima
Coarctation (narrowing of aorta) of aorta findings

30
Q

Outline the 3 factors that may contribute to advanced atherosclerosis

A
  1. Sex: mainly affects males until 7/8th decade, when protective effect of female sex hormone is lost
  2. Cigarettes: endothelial cell damage
  3. Diabetes: increased incidence of hyperlipidaemia and microvascular damage
31
Q

What could happen in the event of advanced atherosclerosis? (4)

A
  1. Regression (improve the condition) - HDL, antioxidants
  2. Interference with blood flow to target organ (ischaemia/infarction)
  3. Thrombosis
  4. Embolisation
32
Q

What is ischaemia?

A

Restriction in supply of blood to the tissues causing a shortage of oxygen and glucose necessary for cellular metabolism

33
Q

What is infarction?

A

It is tissue death caused by a lack of oxygen due to obstruction in blood flow

34
Q

What are the clinical symptoms of ischaemia? (3)

A

Angina
Transient ischaemic attack (TIA)
Peripheral vascular disease (Intermittent claudication) - pain in thigh, calf or bum when you walk i.e. reduced blood flow to your legs

35
Q

What are the clinical symptoms of infarction? (3)

A

Myocardial infarction
Stroke
Gangrene

36
Q

What 4 things are important to consider in atherosclerosis?

A

Collateral blood supply
Speed of arterial occlusion
Metabolic needs of tissue
Degree of arterial blocking

37
Q

Outline the clinical aspects of IHD (ischemic heart disease i.e. angina, MI) (3)

A

Inadequate oxygen supply to meet demands of heart

Atheromatous plaque within coronary arteries causing constriction to blood flow
Risk of plaque rupturing leading to acute thrombus and MI

38
Q

What are the unmodifiable risk factors of Ischemic heart disease? (3)

A

Age
Male gender
Family history

39
Q

What are the modifiable risk factors of Ischemic heart disease? (9)

A 
Hyperlipidaemia
Smoking 
Hypertension
Diabetes
Obesity
Lack of exercise
High alcohol intake 
Stress
OCP (oral contraceptive pill)
40
Q

What is angina and what are the signs?

A

Angina is reduced oxygen perfusion of cardiac muscle

Strangling feeling in chest, breathlessness, pain radiating to jaw and left arm (pain resolves in minutes following rest and GTN)

41
Q

What do you need to consider with angina - what is the dental relevance? Give examples (3)

A

Polypharmacy: Side effects of these meds - how they affect the patient and what you plan to do to them.

Aspirin - tendency to bleed
Beta blockers/calcium channel blockers - mucosal disease
Nicorandil - oral ulceration

42
Q

What are the symptoms of myocardial infarction? (3)

A

Central strangling pain lasting longer than 15 minutes
Pain radiates to neck, jaw and left arm
Nausea, vomiting

43
Q

What are the signs of MI? (3)

A

Grey tinge
Sweating
Tachycardia

44
Q

What steps do you take to manage myocardial infarction? (7)

A
  1. Sit patient up
  2. Stay calm and relaxed
  3. Dial for an ambulance
  4. Administer oxygen and GTN (repeat every 10 minutes)
  5. Aspirin 300mg PO crushed or chewed
  6. Entonox if available
  7. Monitor pulse and oxygen saturation
45
Q

In what ways may myocardial infarction be relevant in a dental scenario? (6)

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
  • Oral manifestations of drugs - Ca channel blockers (gingival overgrowth), beta-blockers (lichenoid reactions), nicorandil (oral ulceration)
46
Q

What is the main, important difference between clotting and thrombosis?

A

Clotting occurs when there has been tissue injury, whereas, thrombosis occurs at the wrong time and wrong place, so it is harmful

47
Q

Outline clotting

A

Essential, physiological and beneficial activation of clotting cascade when there has been tissue injury.

Refers to activation of protein cascade leading to formation of fibrin

48
Q

Outline thrombosis:

  1. what is activated?
  2. what happens?
A

Involves activation of both platelets and clotting cascade

Haemostasis occurs in the wrong place at the wrong time. This is harmful.

49
Q

What are the 3 factors involved in Virchow’s triad? (factors that promote thrombosis)

A
  1. Changes in surface of blood vessel (endothelial injury)
  2. Changes in blood flow (stasis of blood flow)
  3. Changes in constituents of blood (hypercoagulability)
50
Q

Describe how the blood vessel surface may change in Virchows triad (7)

A
  1. Atheromatous plaque
  2. Splitting/fraying/loss of surface endothelial cell layer
  3. Exposure of sub-endothelial tissues (fibrous/fatty plaque) leads to platelet activation
  4. burning/freezing “frostbite” causes trauma to the endothelium
  5. Mechanical: indwelling cannulae
  6. Chemical injury: injectable materials (sometimes deliberate)
  7. Inflammation “vasculitis”
51
Q

Outline how the pattern of blood flow can change in Virchow’s triad

A

DVT (deep vein thrombosis)
Embolus (when part of clot breaks off and travels)

Congestive heart failure (venous stagnation) 
Post myocardial infarction 
Atrial fibrillation 
Heart valve disease
Arterial vs. venous thrombosis 
Turbulence vs.  speed
52
Q

Outline the changes in the blood constituents in Virchow’s triad

A

Hypercoagulable state: haemostatic equilibrium is tilted in favour of thrombosis:

  • Increase pro-coagulant factors
  • Pro-coagulant factors from malignant tumours
  • Decrease in anti-coagulant factors
  • Increased platelet count and adhesiveness/aggregability
  • Increased viscosity of the blood
53
Q

Name groups of patients that are said to have increased fibrinogen and factor VIIc concentrations? (6)

A 
Increasing age
Obesity
Oral contraceptives 
Menopause 
Diabetes
Smoking
54
Q

Name the 3 possible fates of a thrombus

A

Lysis
Organisation/recanalisation
Embolisation

55
Q

What is embolisation? (2)

A

Thrombi detach and travel at high speed through the circulation

Until a vessel is reached whose lumen is smaller than the size of the thrombus

56
Q

What are the 5 types of emboli - which one is most common?

A 
Thrombus (99%)
Infective (vegetations of infective endocarditis) 
Gaseous 
Fat
Foreign material
57
Q

What are the clinical aspects of heart failure?

A

Pump failure e.g. heart muscle disease, restricted filling, inadequate heart rate

Excessive preload e.g. mitral regurgitation, fluid overload

Chronic excessive afterload e.g aortic stenosis (narrowing of valve), hypertension.

HHAD: Human Disease (20 decks)

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