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Human Disease > 2) Clinical And Pathological Aspects Of Cardiovascular Disease > Flashcards

2) Clinical And Pathological Aspects Of Cardiovascular Disease Flashcards

1
Q

What is hypertension and how often is it found?

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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2
Q

What is Primary (Essential) Hypertension?
What causes it?

A

• Most common cause of preventable disease in developed world
• Normally detected between 20-50 years of age

Multifactorial Aetiology
• Genetic factors
• Environmental
• Obesity (ensure correct cuff size)
• Alcohol
• Salt intake
• Stress
• Humoral mechanisms
• Insulin resistance – link between diabetes and hypertension

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3
Q

What is Secondary Hypertension due to?

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

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4
Q

How do you diagnose hypertension?

A

• Measurement of blood pressure on at least 3 occasions over 3 month period
• Patients often require a 24 hour monitor

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5
Q

How do you treat primary and secondary hypertensions?

A

• Secondary hypertension – treat cause if possible
• Primary / Essential hypertension General advice (BHS)
Weight loss
Increase exercise
Reduce alcohol
Stop smoking
Reduce salt intake
Increase fruit and vegetable intake

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6
Q

Medical treatment of hypertension?
ABCD

A

• ACE Inhibitors (eg captopril)
• Angiotensin II receptor blockers (eg candesartan)
• B β-blockers (eg atenolol)
• Ca channel blockers (eg nifedipine)
• Diuretics (eg bendroflumethiazide)

ABCD

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7
Q

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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8
Q

What is the dental relevance of hypertension?

A

• Minimise stress and pain to minimise further increase in BP which may precipitate CVA, MI
• No problem with adrenaline in LA (as long as intravascular injection avoided)
• Controlled hypertensive – treat as normotensive
• 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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9
Q

Hypertension - dental relevance
What are the oral manifestations of medical treatment of hypertension?

A

ACE inhibitors
• Loss of taste
• Angioedema
• Lichenoid reactions

β-blockers
• Lichenoid reactions

Ca channel blockers
• Gingival overgrowth

Diuretics
• Xerostomia

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10
Q

What is atherosclerosis dependant on?

A

LDL:HDL cholesterol

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11
Q

What does a normal artery look like?

A
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12
Q

What is intima?
Not on lecture slides

A

Innermost coating of artery

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13
Q

Features of normal intima?

A

<0.1 mm thickness
Loose fibrous tissue
Endothelial later on top

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14
Q

See slide 19

A
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15
Q

PDAY study findings?
How does smoking affect and gender?

A
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16
Q

What is atherosclerosis?

A
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17
Q

Where is the location of Atherosclerosis?

A
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18
Q

What are the stages of atherosclerosis

A

Fatty streak
Fibrous plaque

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19
Q

Complications of atherosclerosis

A
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20
Q

Process of atherosclerosis? (5)

A
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21
Q

Picture for process of atherosclerosis (note foam cell formation)

A
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22
Q

Formation of atherosclerosis diagram

A
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23
Q

What is atheroma / atherosclerosis?

A

It is a build of fibro-fatty material and inflammatory cells (macrophages) within the intimal layer of blood vessels

24
Q

Hyperlipidaemia and LDL:HDL imbalance?

A
25
Q

LDL:HDL ratio?

A
26
Q

HDL - what does it do?

A
27
Q

Link between hypertension and atherosclerosis?

A
28
Q

Advanced atherosclerosis?

A
29
Q

What happens after atherosclerosis?

A
30
Q

What are two conditions that can cause interference with blood flow?

A

Ischaemia
Infarction

31
Q

What is the definition of ischaemia?

A

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

32
Q

What is the definition of infarction?

A

Tissue death caused by a lack of oxygen due to obstruction in blood flow

33
Q

What are the clinical symptoms of ischaemia?

A

Angina (chest pain)

Transient ischaemic attack - TIA

Peripheral vascular disease - “intermittent claudication” (pain in legs /arms)

34
Q

What are the clinical symptoms of infarction?

A

Myocardial infarction

Stroke

Gangrene

35
Q

Whether the result of luminal narrowing is ischaemia or infarction could depend on:

A

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

36
Q

What are the clinical aspects of ischaemic heart disease?

A
37
Q

What are the risk factors of ischaemic heart disease ?

A
38
Q

What is angina?

A
39
Q

What is the dental relevance of angina?

A
40
Q

What are the symptoms and signs of myocardial infarction?

A

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

Signs:

• Grey tinge
• Sweating
• Tachycardia

41
Q

What is the management of myocardial infarction?

A

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

42
Q

What is the dental relevance of myocardial infarction?

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
- β-blockers
– lichenoid reactions
- Nicorandil
– oral ulceration

43
Q

What is the difference between thrombosis and clotting?
What is thrombosis?
What is clotting?

A
44
Q

What is virchows triad?

A

The 3 factors that contribute to thrombosis

1) changes in the surface of the vessel
2) changes in the blood flow
3) changes in the constituents of the blood

45
Q

Virchows triad - changes in the surface of the vessel
What are the ways the vessel surface can be changed?
(The other means slide is less important)

A
  • Atheromatous plaque
  • splitting/fraying/loss of surface endothelial cell layer
  • exposure of sub endothelial tissues (fibrous/fatty plaque) leads to platelet activation
46
Q

Virchows triad- changes in blood flow
What can cause changes in blood flow?
What is the difference in blood flow between arterial and venous thrombosis?

A
  • deep vein thrombosis
    -embolus
  • patients with congestive cardiac failure (venous stagnation)
  • post myocardial infarction
  • atrial fibrillation
  • heart valve disease

Arterial thrombosis has turbulent flow
Venous thrombosis has sluggish flow

47
Q

Virchows triad - changes in the constituents of the blood
What is a hypercogulate state?

What can cause a hypercoagulate state?

A

Hypercoagulate state : haemo’static equilibrium is tilted in the favour of thrombosis
(Ie more likely to form blood clots)

What can cause a hypercoagulate state?
- Increase in procoagulant factors
- Procoagulant factors from malignant tumours
- increased viscosity of the blood
- decrease in anticoagulant factors
- increased platelet count and adhesiveness/aggregatibility

48
Q

What can increased plasma fibrinogen and factor VIIc concentrations be caused by?

A

Increasing age
Obesity
Oral contraceptives
Menopause
Diabetes
Smoking

(Plasma fibrinogen is one of the 13 coagulation factors responsible for normal clotting, so is factor VIIc)

49
Q

Virchows triad

A

(Stasis is stopping of normal flow and hypercoagulability is increased tendency to form a thrombus (blood clot))

50
Q

What is the fate of a thrombus (3)?

A
  • lysis
  • organisation / recanalisation
  • embolisation

(Embolisation, already mentioned, where a piece of thrombus breaks off and travels through the circulation until it meets a vessel that is of the same size as itself, and then lodges.
For arterial emboli, this will be in a more distal vessel, possibly extremities, kidneys, bowel, leading to ischaemia or infarction of that target organ.
Venous, from DVTs, travel through to the right side of the heart, through the pulmonary arteries and into the lungs, eventually lodging in a pulmonary vessel that matches their size, and causing PE (pulmonary embolus) – a possible medical emergency if a sizable vessel has been affected.)

51
Q

What is embolisation?

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

52
Q

What are the types of emboli?

A
  • Thrombus (99%)
  • infective (vegetations of infective endocarditis)
  • gaseous
  • fat
  • foreign material
53
Q

Clinical aspects of heart failure
What is heart failure and why can it occur? (3)

A

Heart failure is when the heart is not able to pump blood at a rate that the bodies requirements

The heart can not fill quickly enough to match demand or where it can not pump the blood out
• Types: left sided, right sided or both

Why?
- 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

54
Q

Heart failure signs and symptoms?

A
55
Q

See summary notes

A
56
Q

B and c only not a and d?????

A

Human Disease (17 decks)

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