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BDS2: Oral Medicine > CVS > Flashcards

CVS Flashcards

0
Q

What types of drugs reduce the symptoms of cardiovascular disease?

A 
ACE inhibitors
Beta blockers (anti-arrhythmic)
Ca channel blockers
Diuretics
Nitrates
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1
Q

What types of drugs prevent cardiovascular disease?

A

Anti-platelet drugs
Lipid lowering drugs
Anti-arythmics

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2
Q

What are antiplatelet drugs?

A

Drugs that don’t allow the platelets to stick together easily.
Have to reduce dose when tooth is being extracted as they cause prolonged bleeding.
e.g. aspirin, clopidogrel, dipyridamole

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3
Q

What is the function of aspirin?

A

Anti-platelet drug
Inhibits platelet aggregation
Alters the balance between thromboxane A2 and prostacyclin
Irreversible effect on the platelet (lasts 7-10 days)

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4
Q

What is the function of clopidogrel?

A

Inhibits ADP induced platelet aggregation

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5
Q

What is the action of lipid lowering drugs?

A

HMG CoA Reductase Inhibitors (statins)
Inhibit production of cholesterol from cholesterol precursors (cholesterol synthesis takes place in the liver)
As a result they reduce the total cholesterol and LDL cholesterol
e.g. simvastatin, atorvastatin

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6
Q

What is the action of anti-arrhythmic drugs?

A

Slow down heart conduction so the heart remains at a safe level. Prevent unusual heart rhythms which can lead to heart attacks.

a. k.a. Beta blockers
e. g. atenolol, propanolol

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7
Q

What is the downside of using antiarrhythmics?

A

Blocks beta receptors in the lungs - making asthma worse
Blocks renal B1 receptors - release of renin blocked
Reduce heart efficiency - make heart failure worse, reduced contractility

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8
Q

What is the action of atenolol?

A

Beta blocker

Selective B1 only - heart and kidney

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9
Q

What is the action of propanolol?

A

Beta blocker

Non-selective B1 and B2 - lungs, liver, vascular smooth muscle & skeletal muscle

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10
Q

How would you calculate cardiac output?

A

Stroke Volume x Heart Rate

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11
Q

What is meant by total peripheral resistance?

A

The combined resistance of all the systemic blood vessels

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12
Q

What is the action of diuretics?

A

Increase salt and water loss:

  • reduce plasma vol
  • reduce cardiac workload
  • heart copes better as it does less work
    e. g. thiazide diuretics (bendrofluazide), loop diuretics (frusemide)
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13
Q

What are the side effects of diuretics?

A

Can lead to Na+/K+ imbalance if not monitored carefully

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14
Q

What is the action of nitrates?

A

Short acting or long acting
Dilate veins - reduce preload to heart
Dilate resistance arteries - reduce cardiac workload, reduce cardiac oxygen consumption
Dilate collateral coronary artery supply - reduce anginal pain
*Inactivated by first pass metabolism

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15
Q

What methods of administration can be used for nitrates?

A

Sublingual, transdermal, intravenous

Inactivated by first pass metabolism so must enter into the systemic circulation.

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16
Q

What are short acting nitrates?

A 
Glyceryl trinitrate (GTN)
Works in minutes
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17
Q

What are long acting nitrates?

A 
Isosorbide mononitrate (skin patch)
Works for many hours
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18
Q

What are the possible side effects of nitrates?

A

Headache

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19
Q

What is the action of calcium channel blockers?

A

Block calcium channels in smooth muscle.
Some are more active on the heart muscle e.g. verapamil
Some are more active on peripheral blood vessels e.g. nifedipine

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20
Q

What is the action of verapamil?

A

Slows conduction of pacing impulses in the heart (AV node conduction) therefore decreasing the heart rate
Ca channel blocker

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21
Q

What is the action of nifedipine?

A

Relaxation and vasodilation of peripheral blood vessels

Ca Channel blocker

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22
Q

What are the side effects of calcium channel blockers?

A

Those acting on peripheral blood vessels can cause gingival hyperplasia

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23
Q

What is the action of ACE inhibitors?

A

Inhibit conversion of angiotensin I to angiotensin II
Prevents aldosterone dependent reabsorption of salt and water
Reduces blood pressure (due to b.v. dilation & decrease of water)
e.g. analapril, ramapril, lisinopril

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24
Q

What are the possible side effects of using ACE inhibitors?

A

Cough

Hypertension

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25
Q

What problems are caused by blood vessel narrrowing?

A

Inadequate oxygen delivered to tissues
‘cramp’ in affected tissue/muscle
No residual deficit at first

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26
Q

What problems are caused by blood vessel occlusion?

A

No oxygen delivery - results in tissue death
More severe pain
Loss of function of tissue

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27
Q

What is coronary artery disease?

A

When the heart’s blood supply becomes blocked due to build up of fat
Heart is supplied by - right coronary artery, circumflex coronary artery and the left anterior descending coronary artery

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28
Q

What is angina pectoris?

A

Reversible ischaemia of heart muscle - narrowing of one or more coronary arteries.
Classical - worse with exercise
Unstable - rapidly deteriorates

29
Q

What are the symptoms of classical angina?

A 
No pain at rest, only with certain level of exertion
Pain relieved by rest
Gradual deterioration
Often no signs
Occasionally hyperdynamic circulation
30
Q

What investigations can be used for angina?

A 
ECG - resting and exercise
Angiography
Echocardiography
Isotope studies
Elimination of other disease - thyroid, anaemia, valve
31
Q

What is angiography?

A

Medical imaging used to visualise the inside (lumen) of blood vessels and organs of the body with interest in the arteries, veins and heart chambers.

32
Q

What is echocardiography?

A

Sonogram of the heart

33
Q

What are the treatment options for angina?

A

Reduce O2 demands of heart
- reduce afterload and preload (drugs/modifying risk factors)
Increase O2 delivery to the tissues
- dilate blocked/narrowed blood vessels (angioplasty)
- bypass blocked/narrowed vessels (CABG)

34
Q

What non-drug treatments are available for angina?

A

Modifying risk factors

  • stop smoking
  • exercise programme
  • improve diet/control cholesterol
35
Q

What drugs can be used to treat angina?

A

Reduce MI risk - aspirin
Hypertension - diuretics, ca channel blockers, ACE inhibitors, Beta blockers
Reduce preload/dilate coronary b.v. - nitrates (short & long)
Emergency treatment - GTN spray

36
Q

What is a coronary artery bypass graft?

A

A healthy artery/vein from the body is connected/grafted to the blocked coronary artery, bypassing the blocked portion of the coronary artery, creating a new path for oxygen rich blood to flow to the heart muscle.

37
Q

What is atheroma/atherosclerosis?

A

Ulcerated plaques within platelet aggregates that develop on the inside lining of blood vessels.
The cause of many CVD such as angina, MI, stroke and peripheral vascular disease.

38
Q

What is peripheral vascular disease?

A

Reversible ischaemia of the tissues - usually lower limb

39
Q

What are the different types of infarction?

A

Heart - coronary artery atheroma
Limb - femoral & popliteal arteries
Brain - carotid arteries

40
Q

What are the irreversible risk factors for CVD?

A

Age, gender, family history

41
Q

What are the reversible risk factors of CVD?

A 
Smoking
Obesity
Diet (cholesterol)
Exercise
Stress
High blood pressure
Drug and alcohol abuse
Diabetes
42
Q

What is primary prevention?

A

Preventing CVD before it happens through exercise, diet and smoking cessation.

43
Q

What is secondary prevention?

A

Preventing reocurrence of disease after patient has presented with CVD.

44
Q

What is the general approach for preventing CVD?

A

Lifestyle changes - diet, exercise, smoking
Control total cholesterol - statins, diet
Control hypertension - blood thinners, vasodilators
Antiplatelet drugs - e.g. aspirin

45
Q

What is hypertension?

A

Raised blood pressure
Systolic >140mmHg
Diastolic >90mmHg
High risk of CVD

46
Q

What causes hypertension?

A

Common - no cause (essential hypertension)

Rare - renal artery stenosis, endocrine tumours

47
Q

What are the symptoms of hypertension?

A

Usually none

May experience headaches or transient ischaemic attacks

48
Q

What is phaeochromocytoma?

A

Rare benign tumour that develops in cells at the centre of an adrenal gland. Causes the gland to release hormones that cause persistent or episodic high b.p. Requires surgical removal.

49
Q

What is renal artery stenosis?

A

Failure of kidney growth due to blockage. Renal function is normal, however due to the blockage it thinks that b.p. is low (as very little blood gets through the blockage) and it sends the wrong signals around the body.

50
Q

What treatments are available for hypertension?

A

Lower b.p. to <140/90mmHg
Modify risk factors
Drugs - thiazide diuretics, beta blocker, ca channel antagonist, ACE inhibitor

51
Q

What is systolic dysfunction?

A

Ventricles are enlarged.
Enlarged ventricles fill with blood normally. (diastolic)
The ventricles pump out less than 40-50% of the blood. (systolic)

52
Q

What is diastolic dysfunction?

A

Ventricles are stiff and fill with less blood than normal. (diastolic)
The ventricles pump out about 60% of the blood but the amount may be lower than normal. (systolic)

53
Q

What is systole?

A

Ventricle contraction

54
Q

What is diastole?

A

Ventrical relaxation/atrial contraction

55
Q

What are the causes of cardiac failure?

A

Myocardial injury e.g. MI
Increased workload e.g. hypertension, valve disease
Abnormal cardiac rhythm

56
Q

What is cardiac failure?

A

When cardiac function fails to maintain a circulation adequate for the metabolic needs of the body despite an adequate blood volume.

57
Q

What is shock?

A

Widespread hypoperfusion of tissues due to an inadequate effective circulating blood volume. Leads to death if effective treatment is not instituted.

58
Q

What is hypovolaemic shock?

A

Critical reduction in blood or plasma volume

e.g. haemorrhage, fluid loss (diarrhoea, vomiting, large burns)

59
Q

What is cardiogenic shock?

A

Failure of the myocardial pump due to myocardial damage or blood flow obstruction
e.g. MI, cardiac rupture, massive pulmonary thromboembolism

60
Q

What is septic shock?

A

Overwhelming bacterial infection resulting in loss of vascular tone with pooling of blood in peripheral blood vessels - and so diminution in the effective circulating blood volume.

61
Q

What is compensated shock?

A

Pathophysiological stage of shock.
Mild reduction in b.p., increased heart rate, peripheral vasoconstriction producing skin pallor with cold & clammy extremities (except in septic shock when periphery may be warm and flushed due to initial vasodilation).

62
Q

What is decompensated shock?

A

Pathophysiological stage of shock.
If circulatory insufficiency persists, the compensatory methods will fail.
Resulting progressive fall in b.p., increasing HR, systemic tissue hypoxia and worsening tissue damage.

63
Q

What is irreversible shock?

A

Pathophysiological stage of shock.
If the circulatory and metabolic defects are not corrected, progressive significant cell necrosis occurs in vital organs. Leads to coma and death of the organism.

64
Q

What are the effect of shock on the brain, heart, lungs & kidneys?

A

Brain - cortical neuronal necrosis & focal cerebral infarction
Heart - focal myocyte necrosis
Lungs - damage to alveolar lining cells possible leading to adult respiratory distress syndrome and respiratory failure
Kidneys - acute tubular necrosis and resulting renal failure

65
Q

What is infective endocarditis?

A

Colonisation of normal or damaged heart valves by micro-organisms with the formation of friable, infected thrombi (vegetations) on the surface of the valve cusps and resultant valve injury.
They can embolise & spread infection.
Also cause the valves to become severely damaged & dysfunctional.

66
Q

What are the predisposing factors to infective endocarditis?

A

Conditions which cause bacteraemia or septicaemia e.g. dental procedures, sites of infection, major/minor surgery
Abnormalities of the heart valves - congenital or acquired
Immunosuppressed host

67
Q

What are the clinical effects of infective endocarditis?

A

Injury to valves or adjacent myocardium
Embolic events
Fever, malaise and weight loss

68
Q

What are the predisposing factors to thrombosis?

A

Abnormality of the blood vessel wall, particularly the endothelium.
e.g. atheroma, inflammation, trauma, bacterial toxins
Alterations in blood flow - stasis and or turbulence in e.g. atrial fibrillation, varicose veins, aneurysms
Hypercoagulable blood - occurs after surgery, in disseminated cancer, during pregnancy, oral contraceptive pill, genetic deficiency states

69
Q

What are the three fates of thrombi?

A

Removal by fibrinolytic system
Organisation - replacement fibrosis
Embolism - moves elsewhere in the body & blocks a vessel

70
Q

What are the symptoms of atherosclerosis?

A

Asymptomatic until arteries are 70% narrowed.

Ischaemic pain

71
Q

What are the major risk factors for atheroma?

A

Age - atheroma progresses slowly as you get older
Sex - lower incidence in w than m until menopause
Plasma lipids - hyperlipidaemia predisposes atheroma
Hypertension
Cigarette smoking - risk related directly to number of cigarettes smoked
Diabetes mellitus

BDS2: Oral Medicine (7 decks)

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