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2a. BDS2 BAMS > ii. Cardiovascular System > Flashcards

ii. Cardiovascular System Flashcards

1
Q

L25: What are the two main risk factors for CVD?

A
  • Smoking;

- Genetics.

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2
Q

L25: Name 3 irreversible risk factors for CVD:

A
  • Age;
  • Sex;
  • Family history.
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3
Q

L25: Name 3 reversible risk factors for CVD:

A
  • Smoking;
  • Obesity;
  • Diet;
  • Exercise;
  • Stress;
  • Hypertension;
  • Hyperlipidaemia;
  • Diabetes.
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4
Q

L25: What is primary prevention for CVD and how can this be achieved?

A

Primary prevention is a patient centred and controlled approach to prevent CVD before it becomes a problem.

This largely involves the patient’s motivation with doctor’s guidance but if they are high risk, medication will also be used.

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5
Q

L25: What is secondary prevention for CVD and how can this be achieved?

A

Secondary prevention is applied after a CV event has occurred. This still involves the methods used in primary prevention but medication will always be advised.

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6
Q

L25: Why is primary prevention often difficult to achieve?

A

It is hard to change the patient’s motivation before anything has happened as they will have an opportunistic approach to it.

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7
Q

L25: What lifestyle changes are included as prevention for CVD?

A
  • Diet, low in saturated fats etc, recommended fibre intake (30g), lower sugar intake;
  • Exercise;
  • Smoking cessation;
  • Reduced alcohol intake.
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8
Q

L25: What medication is used to control total blood cholesterol?

A

Statins

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9
Q

L25: What is the target to reduce blood cholesterol to?

A

< 5.0mmol/L or 25%

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10
Q

L25: What is the target to reduce blood pressure to?

A

<140/85

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11
Q

L25: When are anti platelets (e.g. aspirin) prescribed to prevent CV events?

A
  • When CVD is identified;

- When a pt is HIGH risk but with no identified disease.

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12
Q

L25: What 4 classes of drugs are used to prevent further CVD?

A
  • Anti platelet drugs;
  • Lipid lowering drugs;
  • Anti-arrhytmics;
  • Anticoagulants.
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13
Q

L25: What 5 classes of drugs are used to reduce symptoms of current CVD?

A
  • Diuretics;
  • Anti-arrythmics;
  • Nitrates;
  • Calcium channel blockers;
  • ACE inhibitors.
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14
Q

L25: How do antiplatelet drugs work to reduce the risk of a CV event?

A
  • Prevent platelets from aggregating/ sticking to artery walls;
  • Irreversible effect so will work on platelets whilst in circulation, until they are replaced;
  • Effects are additive (e.g. aspirin and clopidogrel are more effective than aspirin alone).
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15
Q

L25: What is the major consideration/ risk in a dental surgery to anti platelet pts?

A

Larger risks of bleeding

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16
Q

L25: Give 2 examples of anti platelet drugs:

A
  • Aspirin;

- Clopidogrel.

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17
Q

L25: How do anticoagulant drugs work to reduce the risk of a CV event?

A
  • Reduce the efficiency of the coagulation cascade, i.e. reduce clot formation;
  • Prevent embolisms (clot in leg, thrombosis, being fired up to lungs or heart.
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18
Q

L25: How does warfarin work?

A
  • Inhibits synthesis of vitamin K dependent clotting factors;
  • 2, 7, 9 and 10;
  • Protein C and S.
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19
Q

L25: What is the quick effect warfarin has and how is this counteracted?

A
  • Acts on proteins C and S which initially become hyper coagulating;
  • Heparin used concurrently for the first few days.
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20
Q

L25: How long do the effects (for patient to become anticoagulating) of warfarin take to set in?

A

2-3 days

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21
Q

L25: What are the common suffixes for anti coagulant drug names?

A

-in, -an

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22
Q

L25: Give 2 examples of anticoagulant drugs:

A
  • Warfarin;

- Rivaroxiban.

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23
Q

L25: How are warfarinised pts monitored?

A

Use of INR

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24
Q

L25: What does an INR of 2-4 tell you about a pt?

A
  • INR good;

- Warfarin working as wanted.

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25
Q

L25: What does an INR of >4 tell you about a pt?

A

Pt at risk of bleed

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26
Q

L25: What does an INR of <2 tell you about a pt?

A

Pt at risk of clot

27
Q

L25: Why must warfarinised pts be monitored regularly?

A
  • INR susceptible to change;

- Food/ drug interaction.

28
Q

L25: How do lipid lowering drugs work? (statins)

A
  • Block reductase inhibitors;
  • Inhibit cholesterol synthesis in the liver;
  • Reduces cholesterol in the blood;
  • Prevents further atherosclerosis.
29
Q

L25: What medications used in dentistry should not be used with statins?

A

Fluconazole (antifungal)

30
Q

L25: What are B-blockers used for?

A
  • Reduces heart muscle excitation;
  • Prevents increase in heart rate;
  • Prevent arrhythmias leading to cardiac arrest (VF).
31
Q

L25: Which receptors do B-blockers target in the heart?

A

B1

32
Q

L25: What is the common suffix for B-blocker drug names?

A

-olol

33
Q

L25: Name a selective (B1 only), B-blocker?

A

Atenolol

34
Q

L25: Name a non-selective (B1 and B2), B-blocker?

A

Propanolol

35
Q

L25: What other receptors can non-selective B-blockers effect?

A
  • B2, lungs (increased risk of asthma!);

- B2, brain (reduces anxiety).

36
Q

L25: What are diuretics used for in CVD?

A
  • Increase salt and water losses;
  • Reduce plasma volume;
  • Reduce bp;
  • Reduce cardiac workload.
37
Q

L25: What are the two main types of diuretics used and give examples?

A
  • Thiazide diuretics (bendroflumethiazide);

- Loop diuretics (frusemide).

38
Q

L25: What are potential side effects of diuretics?

A
  • Can lead to electrolyte imbalance;

- Can lead to dry mouth.

39
Q

L25: Which part of a nephron do thiazide diuretics work on?

A

Distal tubule

40
Q

L25: Which part of a nephron do loop diuretics work on?

A

Thick ascending limb

41
Q

L25: What are nitrates used for in CVD?

A
  • Dilate arteries;
  • Pressure reduces;
  • Reduces cardiac workload;
  • Reduces cardiac oxygen consumption;
  • Different ones for short or long term relief.
42
Q

L25: Name a short acting nitrate drug and state what it is used for:

A

Glycery Trinitrate (GTN) spray, used to relieve angina pain

43
Q

L25: Name a long acting nitrate drug and state what it is used for:

A

Isosorbide Mononitrate, prevention of angina pectoris

44
Q

L25: How are nitrates administered?

A
  • Sublingual;
  • Transdermal;
  • IV.

(inactivated by first pass metabolism)

45
Q

L25: What is the common suffix for calcium channel blocker drug names? Give two examples.

A
  • -pine;
  • Nifedipine;
  • Amlodipine.
46
Q

L25: How do calcium channel blockers work?

A
  • Block calcium channels in smooth muscle;

- Relaxation and dilation of blood vessels.

47
Q

L25: Name a calcium channel blocker that is active on heart muscle?

A

Verapamil, slows conduction of pacing impulses

48
Q

L25: What is a common dental side effect of calcium channel blockers?

A

Gingival hyperplasia

49
Q

L25: What is the common suffix for ACE inhibitor drug names? Give two examples.

A
  • -pril;
  • Ramapril;
  • Lisonopril.
50
Q

L25: How do ACE inhibitors work?

A
  • Angiotensin Converting Enzyme inhibitors;
  • Inhibit conversion of angiotensin I to II;
  • Prevents aldosterone dependent reabsorption of salt and water;
  • Reduce bp.
51
Q

L25: What is a common dental side effect of ACE inhibitors?

A
  • Angio-oedema;

- Lichenoid reaction.

52
Q

L51: What is infective endocarditis?

A
  • Infection of the endocardium (inner most layer of tissue of the heart, lines the chambers);
  • Microbial colonisation of thrombi on endocardial surface abnormalities;
  • Bacteria from bloodstream (often oral origin);
  • Usually originates (and causes most damage to) on the valves.
53
Q

L51: What is the main microorganism associated with infective endocarditis?

A

Viridans streptcocci

54
Q

L51: What is Rheumatic fever?

A

An autoimmune inflammatory disease, triggered by a throat infection, that can involve the heart, joints, skin, and brain

55
Q

L51: What is Rheumatic heart disease?

A

A condition in which the heart valves have been permanently damaged by rheumatic fever (usually a mitral valve)

56
Q

L51: How does infective endocarditis arise?

A
  • Surface abnormalities on valves/ endocardium;
  • Lead to haemodynamic changes (change in flow);
  • Turbulence;
  • This causes platelet/ fibrin deposition (thrombus);
  • Thrombus could then become colonised by bacteria from the blood stream, leading to a vegetation;
  • This can enlarge and cause damage to the tissue, bacteria can spread to endocardium.
57
Q

L51: What are typical signs and symptoms of infective endocarditis?

A
  • Many experience ‘flu-like’ symptoms;
  • Fever;
  • Heart murmur;
  • Splinter hemorrhages (under finger nails);
  • Splenomegaly.

[can take up to six weeks to develop - hard to link to dentistry sometimes]

58
Q

L51: How is infective endocarditis treated?

A
  • IV antibiotics;
  • Combination of drugs;
  • Permanent valve damage, sometimes need replaces;
  • High risk of death (50%).
59
Q

L51: Who should receive antibiotic prophylaxis, i.e. are considered high-risk (2006 BSAC guidelines)?

A
  • Valve replacement patients;
  • Patients who have pulmonary shunts/ congenital heart problem;
  • Patients who have previously had infective endocarditis.

[receiving any dental tx involving the dento-gingival junction, bacteraemia!]

60
Q

L51: Why did NICE guidelines (2008) suggest that AB prophylaxis was not necessary for any patients? (still v similar but with ‘routinely’ added to guidelines)

A
  • Not enough sufficient evidence of its benefit;
  • Bacteraemia load should be minimised where possible (to reduce IE risk), to keep bacterial load similar to that of what enters the blood after brushing/ eating etc.;
  • Risks of adverse antibiotic reaction.
61
Q

L51: What advice should be given to reduce risk of IE, day-to-day?

A
  • Attendance for oral care;
  • Rapid management of infection;
  • Maximal OH and prevention;
  • Avoid risk activity: piercings.
62
Q

L51: What are the current guidelines for antibiotic prophylaxis (SDCEP)?

A
  • Risk assessed by dentist via patient’s medical history;
  • Decision made by patient and physician, communicated to dentist in writing;
  • Patients must be aware of risks of allergy v IE;
  • AB prophylaxis will be given for procedures likey to produce a significant bacteraemia (manipulation of dents-gingival junction).
63
Q

L51: What is the drug regime for AB prophylaxis (SDCEP)?

A
  • 3g oral amoxycillin, 1 hour before procedure, in the dental practice (incase of anaphylaxis);
  • IF penicillin allergy: 1.5g clindamycin.

2a. BDS2 BAMS (10 decks)

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