ii. Cardiovascular System Flashcards
L25: What are the two main risk factors for CVD?
- Smoking;
- Genetics.
L25: Name 3 irreversible risk factors for CVD:
- Age;
- Sex;
- Family history.
L25: Name 3 reversible risk factors for CVD:
- Smoking;
- Obesity;
- Diet;
- Exercise;
- Stress;
- Hypertension;
- Hyperlipidaemia;
- Diabetes.
L25: What is primary prevention for CVD and how can this be achieved?
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.
L25: What is secondary prevention for CVD and how can this be achieved?
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.
L25: Why is primary prevention often difficult to achieve?
It is hard to change the patient’s motivation before anything has happened as they will have an opportunistic approach to it.
L25: What lifestyle changes are included as prevention for CVD?
- Diet, low in saturated fats etc, recommended fibre intake (30g), lower sugar intake;
- Exercise;
- Smoking cessation;
- Reduced alcohol intake.
L25: What medication is used to control total blood cholesterol?
Statins
L25: What is the target to reduce blood cholesterol to?
< 5.0mmol/L or 25%
L25: What is the target to reduce blood pressure to?
<140/85
L25: When are anti platelets (e.g. aspirin) prescribed to prevent CV events?
- When CVD is identified;
- When a pt is HIGH risk but with no identified disease.
L25: What 4 classes of drugs are used to prevent further CVD?
- Anti platelet drugs;
- Lipid lowering drugs;
- Anti-arrhytmics;
- Anticoagulants.
L25: What 5 classes of drugs are used to reduce symptoms of current CVD?
- Diuretics;
- Anti-arrythmics;
- Nitrates;
- Calcium channel blockers;
- ACE inhibitors.
L25: How do antiplatelet drugs work to reduce the risk of a CV event?
- 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).
L25: What is the major consideration/ risk in a dental surgery to anti platelet pts?
Larger risks of bleeding
L25: Give 2 examples of anti platelet drugs:
- Aspirin;
- Clopidogrel.
L25: How do anticoagulant drugs work to reduce the risk of a CV event?
- 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.
L25: How does warfarin work?
- Inhibits synthesis of vitamin K dependent clotting factors;
- 2, 7, 9 and 10;
- Protein C and S.
L25: What is the quick effect warfarin has and how is this counteracted?
- Acts on proteins C and S which initially become hyper coagulating;
- Heparin used concurrently for the first few days.
L25: How long do the effects (for patient to become anticoagulating) of warfarin take to set in?
2-3 days
L25: What are the common suffixes for anti coagulant drug names?
-in, -an
L25: Give 2 examples of anticoagulant drugs:
- Warfarin;
- Rivaroxiban.
L25: How are warfarinised pts monitored?
Use of INR
L25: What does an INR of 2-4 tell you about a pt?
- INR good;
- Warfarin working as wanted.
L25: What does an INR of >4 tell you about a pt?
Pt at risk of bleed
L25: What does an INR of <2 tell you about a pt?
Pt at risk of clot
L25: Why must warfarinised pts be monitored regularly?
- INR susceptible to change;
- Food/ drug interaction.
L25: How do lipid lowering drugs work? (statins)
- Block reductase inhibitors;
- Inhibit cholesterol synthesis in the liver;
- Reduces cholesterol in the blood;
- Prevents further atherosclerosis.
L25: What medications used in dentistry should not be used with statins?
Fluconazole (antifungal)
L25: What are B-blockers used for?
- Reduces heart muscle excitation;
- Prevents increase in heart rate;
- Prevent arrhythmias leading to cardiac arrest (VF).
L25: Which receptors do B-blockers target in the heart?
B1
L25: What is the common suffix for B-blocker drug names?
-olol
L25: Name a selective (B1 only), B-blocker?
Atenolol
L25: Name a non-selective (B1 and B2), B-blocker?
Propanolol
L25: What other receptors can non-selective B-blockers effect?
- B2, lungs (increased risk of asthma!);
- B2, brain (reduces anxiety).
L25: What are diuretics used for in CVD?
- Increase salt and water losses;
- Reduce plasma volume;
- Reduce bp;
- Reduce cardiac workload.
L25: What are the two main types of diuretics used and give examples?
- Thiazide diuretics (bendroflumethiazide);
- Loop diuretics (frusemide).
L25: What are potential side effects of diuretics?
- Can lead to electrolyte imbalance;
- Can lead to dry mouth.
L25: Which part of a nephron do thiazide diuretics work on?
Distal tubule
L25: Which part of a nephron do loop diuretics work on?
Thick ascending limb
L25: What are nitrates used for in CVD?
- Dilate arteries;
- Pressure reduces;
- Reduces cardiac workload;
- Reduces cardiac oxygen consumption;
- Different ones for short or long term relief.
L25: Name a short acting nitrate drug and state what it is used for:
Glycery Trinitrate (GTN) spray, used to relieve angina pain
L25: Name a long acting nitrate drug and state what it is used for:
Isosorbide Mononitrate, prevention of angina pectoris
L25: How are nitrates administered?
- Sublingual;
- Transdermal;
- IV.
(inactivated by first pass metabolism)
L25: What is the common suffix for calcium channel blocker drug names? Give two examples.
- -pine;
- Nifedipine;
- Amlodipine.
L25: How do calcium channel blockers work?
- Block calcium channels in smooth muscle;
- Relaxation and dilation of blood vessels.
L25: Name a calcium channel blocker that is active on heart muscle?
Verapamil, slows conduction of pacing impulses
L25: What is a common dental side effect of calcium channel blockers?
Gingival hyperplasia
L25: What is the common suffix for ACE inhibitor drug names? Give two examples.
- -pril;
- Ramapril;
- Lisonopril.
L25: How do ACE inhibitors work?
- Angiotensin Converting Enzyme inhibitors;
- Inhibit conversion of angiotensin I to II;
- Prevents aldosterone dependent reabsorption of salt and water;
- Reduce bp.
L25: What is a common dental side effect of ACE inhibitors?
- Angio-oedema;
- Lichenoid reaction.
L51: What is infective endocarditis?
- 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.
L51: What is the main microorganism associated with infective endocarditis?
Viridans streptcocci
L51: What is Rheumatic fever?
An autoimmune inflammatory disease, triggered by a throat infection, that can involve the heart, joints, skin, and brain
L51: What is Rheumatic heart disease?
A condition in which the heart valves have been permanently damaged by rheumatic fever (usually a mitral valve)
L51: How does infective endocarditis arise?
- 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.
L51: What are typical signs and symptoms of infective endocarditis?
- 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]
L51: How is infective endocarditis treated?
- IV antibiotics;
- Combination of drugs;
- Permanent valve damage, sometimes need replaces;
- High risk of death (50%).
L51: Who should receive antibiotic prophylaxis, i.e. are considered high-risk (2006 BSAC guidelines)?
- 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!]
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)
- 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.
L51: What advice should be given to reduce risk of IE, day-to-day?
- Attendance for oral care;
- Rapid management of infection;
- Maximal OH and prevention;
- Avoid risk activity: piercings.
L51: What are the current guidelines for antibiotic prophylaxis (SDCEP)?
- 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).
L51: What is the drug regime for AB prophylaxis (SDCEP)?
- 3g oral amoxycillin, 1 hour before procedure, in the dental practice (incase of anaphylaxis);
- IF penicillin allergy: 1.5g clindamycin.
