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Human Diseases Yr3 > Cardiovascular Disease > Flashcards

Cardiovascular Disease Flashcards

1
Q

On an ECG what does each of the following show?

a) P wave
b) PR interval
c) QRS complex
d) T wave

A

a) Atria depolarising and physically contracting
b) Gap where bundle of His creating a pause
c) Ventricles contracting
d) Ventricles repolarising

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2
Q

What are the 3 main sites of atherosclerosis?

A
  • Coronary arteries = ischaemic heart disease (angina, MI, heart failure)
  • Cerebral circulation and carotids = stroke
  • Legs = peripheral vascular disease (gangrene), small bowel ischaemia
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3
Q

What is an aneurysm and what can they look like?

A

Weakening of blood vessel wall resulting in ballooning

  • Sacular aneurysm on side of artery
  • Fusiform aneurysm whole artery dilates
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4
Q

What are the a) reversible and b) non-reversible risk factors for atherosclerosis?

A

a) Diabetes, smoking, hypertension, hyperlipidaemia (raised LDLs), obesity
b) Age, male sex, post menopausal, family history

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5
Q

Where is a a) pulmonary embolus b) peripheral embolus usually from?

A

a) DVT

b) Aorta e.g. abdominal aneurysm down into leg

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6
Q

What are the different causes of heart failure?

A
  • Valve stenosis or regurgitation
  • Ischaemic heart disease (damage from MI)
  • Sustained arrhythmia
  • Hypertension causing damage to heart muscle
  • Cardiomyopathy
  • COPD - cor pulmonale (RHS HF from pulmonary hypertension)
  • Excessive demand e.g. anaemia, hyperthyroidism
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7
Q

What is the definition of generalised atheroma?

A

Many lesions in arteriole walls become fibrotic and calcified with deposition of Ca salts - a sclerotic process causing hardening

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8
Q

How does atherosclerosis form?

A

1) Fatty streak
2) Fibrolipid plaque
3) Complicated lesion

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9
Q

What is the difference between a muscular artery and an elastic artery?

A

In muscular, tunica media has smooth muscle cells, elastic tissue found throughout wall in elastic

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10
Q

How does a fatty streak form?

A

1) Endothelial damage
2) Permeability - lipids enter intima
3) Monocyte adhesion to endothelium (precursors of macrophages)
4) Entry of LDLs and smooth muscle cells come through internal elastic lamina
5) Foamy macrophages take up LDLs but cant digest it, forming a fatty streak

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11
Q

How does a fibrolipid plaque form?

A

1) Smooth muscle cells migrate to surface along with fibroblasts
2) Cell proliferation
3) Lipid uptake
4) Production of collagen - part of the repair process but causes damage
5) Macrophage breakdown and forms a lipid lake. Can see cholesterol crystallising out

Endothelial lining still intact!

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12
Q

How does a complicated lesion form?

A

1) Impaction of platelets onto the surface
2) Fibrolipid plaque becomes ulcerated
3) Clotting cascade causes thrombus formation on surface of plaque
4) This sits over the lipid lake and calcification of tissue occurs creating a mass
5) Further fibrosis weakens artery wall, fissure breaches plaque which can rupture into luman
6) Can occlude whole artery
7) Thrombus can break off and cause embolism
8) Weakened wall can form aneurysm

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13
Q

How what features show that the atheroma is a stabilized plaque?

A
  • Small lipid pool
  • Fibrous cap
  • Preserved lumen
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14
Q

How is atherosclerosis managed medically?

A
  • Beta blockers (reduce BP)
  • Angiotensin-converting enzyme (ACE Inhibitors)
  • Diuretics
  • Anti-platelet meds
  • Cholesterol meds (reduce LDL levels)
  • Fibrinolysins (dissolve thrombi)
  • Calcium channel blockers
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15
Q

How is atherosclerosis managed surgically?

A
  • Angioplasty (surgical modification of arteries)
  • Bypass
  • Stent
  • Endarterectomy (internal lining with plaque removed)
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16
Q

In Virchow’s Triad, what are the 3 things that may result in thrombosis?

A

1) Changes to the intimal surface of a vessel e.g. atherosclerosis
2) Changes to the pattern of blood flow e.g. venous stasis or injury to blood vessel
3) Changes in blood constituents e.g. hypercoagulable blood

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17
Q

What is the appearance of arterial thrombosis histologically?

A

Lines of Zahn

Pale = platelets and thrombin, Dark = RBCs

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18
Q

What are the risk factors for venous thrombosis?

A
  • Burns and trauma
  • Surgery
  • Cardiac failure
  • Pregnancy
  • Immobility
  • Long haul flight
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19
Q

What is the definition of

a) Thrombophlebitis
b) Phlebothrombosis

A

a) Inflammation of the deep vein

b) Stasis with no inflammation from platelets

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20
Q

Why might

a) Atrial thrombosis occur?
b) Valvular thrombosis occur?
c) Ventricular thrombosis occur?

A

a) - Mitral stenosis
- Atrial fibrillation

b) - Endocarditis
- Rheumatic fever

c) Following MI as dead heart muscle disrupts endothelium

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21
Q

What are the 4 fates of thrombi?

A

1) Lysis and resolution - given fibrinolysin
2) Retraction and recanalization (relinied with endothelium)
3) Organisation and scarring
4) Embolism (breaks off)

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22
Q

In a pulmonary embolism

a) Where is the embolus originally from?
b) What happens if it blocks entire pulmonary artery?
c) What happens if it blocks branch of pulmonary artery?
d) What happens if it blocks small arteries?

A

a) DVT or pelvic veins
b) Sudden death
c) Chest pain and breathlessness, wedged shaped ischaemia
d) Pulmonary hypertension

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23
Q

Where is a systemic embolism originally from?

A

Arterial side i.e. thrombosis on LHS heart or thrombi formed on atheromatous plaques

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24
Q

What are the causes of infarction?

A
  • Atheroma
  • Hyperviscosity
  • Compression (tumour or injury)
  • Embolism
  • Thrombosis
  • Vasculitis (inflammation vessel wall)
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25
Q

What happens to tissue after infarction and what occurs to the cellular material?

A
  • Autolysis
  • Enzymes released dissolve cellular material
  • Nucleus breaks up = karyorexis
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26
Q

In a myocardial infarction, what is seen in the heart muscle at:

a) Less than 6 hours
b) 24-48 hours
c) Several days
d) Several weeks

A

a) Only ECG changes
b) Pallor with red rim
c) Pallor with red rim and softened
d) Grey and fibrotic

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27
Q

What is the definition of

a) False aneurysm
b) Dissecting aneurysm
c) Mycotic aneurysm

A

a) Blood filled space due to vasculature rupture (Haematoma)
b) Damage to intima of vessels, blood dissecting layers of wall apart
c) Related to infection

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28
Q

Why is the jugular venous pressure raised in heart failure?

A

Backlog of blood making right side of heart under pressure

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29
Q

How is angina managed?

A
  • GTN spray to shorten attack

- Anti-anginal drugs: beta-blockers, nitrates, CCB, nicorandil, aspirin etc

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30
Q

Give examples of cardiac investigations

A
  • ECG
  • Chest Xray
  • Echocardiogram
  • Stress tests
  • Coronary angiogram (invasive)
  • CT/MRI
  • Troponin levels
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31
Q

What are the common valve problems:

a) AS
b) MR
c) TR
d) MS

A

a) Aortic stenosis (narrowing with age)
b) Mitral Regurgitation
c) Tricuspid regurgitation (from heart failure or chronic lung disease)
d) Mitral Stenosis (usually from rheumatic inflammation)

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32
Q

What are the pulse and blood pressure like in

a) Atrial regurgitation
b) Atrial stenosis

A

a) BP high, pulse increased volume

b) BP low, pulse slow rising/ collapsing pulse

33
Q

What are the treatments for valvular heart disease?

A
  • Surgical valve replacement (mechanical needs anticoagulants)
  • Mitral valve clip for regurgitation
  • TAVI for a AS
34
Q

What are the signs of heart disease?

A
  • Premature archus senalis (white ring cholesterol deposition around eye)
  • Tendon xanphomas (cholesterol deposition in tendons)
  • Pitting oedema
  • Raised JVP
  • Finger clubbing
  • Splinter haemorrhages in fingernails (infective endocarditis)
  • General appearance, breathlessness, pallor, sweating, cyanosis
35
Q

What is bicuspid valve disease?

A

3 cusps lost and replaced by 2 cusps - distorted and undergo calcified degeneration

36
Q

What is rheumatic fever?

A

Occurs after a streptococcal URTI infection, antibodies cross react with cardiac antigens

37
Q

What do repeated episodes of rheumatic fever do to the heart?

A
  • Fibrosis of endocardium and valves
  • Vegetations on heart valve leaflets0
  • Fusion of heart valve leaflets
  • Calcifications of heart valves
  • Myocarditis ( Aschcoff bodies in heart muscle)
  • Endocarditis (lining of heart inflamed)
38
Q

Which valve is affected more with rheumatic fever?

A

Mitral valve more than aortic valve (stenosis and incompetence)

39
Q

What are the 3 main sites of infective endocarditis?

A
  • Heart valve (Left more often than right-only IV drug abusers and immunosuppressed)
  • Mural endocardium (especially if previous MI)
  • Congenital defect
40
Q

What bacteria from the oropharynx can cause infective endocarditis when doing dental procedures?

A
  • Streptococci
  • Strep. viridans
    Acute IE most often caused by Staphylococcus aureus
    HACEK
41
Q

What disorders predispose to infective endocarditis?

A
  • Acquired valvular heart disease
  • Hypertrophic cardiomyopathy
  • Previous IE
  • Structural congenital heart disease
  • Valve replacement
42
Q

What is the pathogenesis of infective endocarditis?

A
  • Abnormal endocardium
  • Platelet and fibrin deposition (vegetation) creates a site for bacteria / fungi to colonise
  • Has to be bacteraemia (circulation of organisms)
  • Bacteria colonise and blanket of platelet and fibrins forms
  • Bacteria proliferate and vegetation grows from small nodules to large friable masses.
43
Q

What are the a) local and b) systemic effects of infective endocarditis?

A

a) - Valve incompetence
- Rupture of chordae tendineae
- Myocarditis
- Embolism to coronary vessels
- Perforation of valve leaflets

b) - Fever, weight loss, malaise
- Splenomegaly
- Embolism

44
Q

What are the signs of infective endocarditis?

A
  • Splinter haemorrhages
  • Blisters in extremities from septic embolisms in the digits
  • Finger clubbing
  • Osler nodes
  • Skin (purpura)
  • Janeway lesions
  • Retinal haemorrhages
  • Pyrexia and sweats
  • Malaise and weight loss
  • Splenomegaly
  • Arrhythmia, changing murmurs, heart failure
  • Septic emboli
45
Q

What is essential hypertension?

A

High BP due to environmental factors e.g. obesity, salt intake etc and genetics
90% of cases and diagnosis of exclusion

46
Q

What are the comment causes of secondary hypertension?

A
  • Renal artery stenosis
  • Coarctation (narrowing of aorta as it comes out of heart)
  • Endocrine causes e.g. Conn’s syndrome (adrenal tumours) or Cushing’s syndrome (tumour secreting ACTH or prolonged therapeutic steroid)
  • Intrinsic renal disease e.g. glomerular nephritis
47
Q

What effects does elevated BP have on other parts of the body?

A
  • Increases risk of heart disease from left ventricular hypertrophy
  • Aortic aneurysm
  • Peripheral vascular disease - atherosclerosis
  • Increased risk of stoke
  • Hypertensive encephalopathy (coma and seizures)
  • Retinal haemorrhages
48
Q

What are the risk factors for a stroke?

A
  • Hypertension
  • Diabetes
  • TIA
  • Vascular disease
  • Smoking
  • Atrial fibrillation
49
Q

What are the forms of stroke prevention?

A
  • Treat raised BP
  • Lower cholesterol
  • Aspirin and anti-platelets
  • Warfarin
  • Surgery for pts with narrow carotid arteries (endarterectomy)
50
Q

What drugs increase BP?

A
  • Amphetamines
  • Oestrogens
  • Cocaine
  • Ciclosporin
  • Sympathomimetic amines
  • Erythropoietic (for making RBCs in anaemia)
51
Q

What are the overall effects of the renin-angiotensin system?

A
  • Peripheral vasoconstriction
  • Aldosterone secretion
  • Activated sympathetic NS (increase HR and BP)
  • Stimulates kidneys to retain NA which also increases BP
  • Oedema
52
Q

What is the criteria for giving patients lifestyle advice and treatment for hypertension?

A
  • BP more than 140/90mmHg

- Vascular risk more than 20% in 10years

53
Q

What fungi causes IE?

A

Candida, Aspergillus - higher mortality

54
Q

What are the criteria for diagnosing IE?

A

Dukes criteria: Major and minor

55
Q

What is claudication?

A

Pain in the leg on walking due to blocked/narrowed arteries (anaerobic metabolism and lactic acid). Ankle brachial pressure index less than 9.

56
Q

How is claudication treated?

A
  • BP control
  • ACE inhibitors
  • Lipid control - statins
  • Antiplatelets - clopidogrel/aspirin
  • Control diabetes
  • Lifestyle modification
57
Q

How is critical ischaemia treated?

A

Balloon angioplasty, stenting, bypass

58
Q

What are the 5 P’s of acute ischaemia of the leg?

A 
Pain in leg 
Pale/cold leg
Pulseless
Paralysis
Paraethesia/numbness
59
Q

When are aortic aneurysms treated? How are they treated?

A

When above 5.5cm diameter

Open AAA surgery, Endovascular aortic aneurysm repair EVAR with sent graft

60
Q

What does internal carotid stenosis cause?

A

TIA and strokes by embolization or restriction of flow. Mini stroke resolving in 24 hrs

61
Q

What are the prevention/treatment options for atherosclerosis arterial and venous thrombosis in preventing clots?

A
  • Antiplatelet therapy
  • Anticoagulant therapy
  • Thrombolytic therapy
62
Q

What is the process of normal haemostasis?

A

1) Constriction of damaged vessels
2) Mechanical blockage of hole by platelet plug:
- Thromboxane A2
- Aggregation stimulated by ADP and thromboxane
- Fibrinogen links adjacent platelets
3) Coagulation cascade
4) Thrombolysis (fibrin mesh prevented from increasing and dissolved by enzyme plasmin)

63
Q

What are the 3 types of antiplatelet drugs?

A

Cyclooxygenase inhibitors e.g. Aspirin
ADP receptor antagonists e.g. Clopidogrel
Adenosine reuptake inhibitors e.g. Dipyridamole

64
Q

What are the 2 anti-coagulant drugs and what is their main MOA?

A
  • Heparin (Vit K antagonist) = enhances activity of antithrombin III and inactivates prothrombin
  • Warfarin (Vit K antagonist) = Inhibits vit K dependent clotting factors
65
Q

What does warfarin interact with?

A
  • Aspirin
  • Fluconazole
  • Miconazole
  • Erythromycin
  • Metronidazole
66
Q

What is warfarin used for?

A
  • Preventing DVT
  • Prevent emboli on prosthetic heart valves
  • Treatment of pulmonary embolism
  • Prevent emboli in atrial fibrillation
67
Q

What dental procedures are considered a) Low risk and b) High risk with DOACs

A

a) -Incision and drainage
- RSI
- Simple XLA
- Detailed perio examination
- Restorations with subgingival margins

b) - Complex/adjacent XLA
- Gingival recontouring
- Biopsies
- Flap raising procedures

68
Q

In acute heart failure, what signs/symptoms are seen more predominantly with

a) Right sided HF
b) Left sided HF

A

a) Peripheral oedema and raised JVP

b) Raised pulmonary venous pressure and pulmonary oedema

69
Q

What are the different phases of cardiac potential?

A

Phase 0 = fast Na entry
Phase 1 = Inactivation of sodium channels
Phase 2 = slow calcium influx
Phase 3 = Efflux of K+
Phase 4 = spontaneous diastolic drift towards threshold potential

70
Q

Which class of drugs

a) Alter the conduction velocity thus interfere with reentry?
b) Reduce intrinsic pacemaker rates?
c) Prolong effective refractory period?

A

a) Class I and IV
b) Class II and IV
c) Class Ib and III

71
Q

What are the dental complications of anti-hypertensive treatment?

A
  • Xerostomia
  • Orthostatic hypertension (lying flat)
  • Postural hypertension (standing up)
  • Lichenoid reactions
  • Gingival overgrowth
  • Drug interactions
72
Q

What should you do regarding dental treatments for

a) Acute MI patients
b) Cardiac failure patients
c) Cardiac surgery patients

A

a) Postpone for 3-6 months later
b) Don’t lie flat as they get breathless
c) Avoid immediate post op period as potential for bacterial infection - post 6 months will have epithelialised

73
Q

What cardiac drug causes gingival hyperplasia?

A

CCBs

74
Q

What cardiac drug causes persistent oral ulcerations?

A

Nicorandil

75
Q

What cardiac drug causes angioedema

A

ACE inhibitors

76
Q

How can a septic emboli result from IE?

A

Fungi/bacteria form on heart valve and cause infection

77
Q

What are the signs and symptoms of heart disease?

A

Chest pain (ischaemia)
Breathlessness (HF)
Swollen ankles (HF)
Peripheral oedema pitting on pressure
Palpitations
Faintness
Pallor, sweating, cyanosis
Jugular venous pressure raised

78
Q

What drug causes lichenoid reactions and increased tooth demineralisation?

A

Beta blockers

79
Q

What are the contraindications for aspirin?

A

Active peptic ulcer
Bleeding disorders
Severe liver disease
Less than 12 = reyes syndrome
Allergy

Human Diseases Yr3 (6 decks)

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