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BDS3 Human Disease > Introduction to cardiovascular drugs in dentistry > Flashcards

Introduction to cardiovascular drugs in dentistry Flashcards

1
Q

Angina vs MI?

A

Angina = heart pain usually on exertion and will stop with meds and/or rest

lasts 15-30 mins

MI = more serious and can be spontaneous/not induced by exercise

lasts over 30 mins

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2
Q

Types of Cerebrovascular disease?

A

Transient ischemic attack

Thrombotic stroke

Vascular dementia

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3
Q

Common arrhythmias?

A

Atrial fibrillation

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4
Q

Healing process of healing in atherosclerosis?

A

Activation of platelets

Inflammatory cells - incorporation of cholesterol

Fibrous cap

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5
Q

Therapeutic targets for atherosclerosis?

A

reduce Wall stress (high bp) by targeting high BP

Inhibit platelets

Reduce cholesterol

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6
Q

What does aspirin inhibit?

A

Thromboxane A2

COX- 1

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7
Q

What does clopidogrel target?

A

ADP receptor antagonists

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8
Q

Dose of aspirin for stable angina pts?

A

75mg

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9
Q

Dose of aspirin after stroke or TIA/stroke?

A

300mg first 2 weeks after

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10
Q

If you take a pt of aspirin too early, what could this cause?

A

stent thrombosis

increase chance of MI

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11
Q

Implications of antiplatelts and dental therapy?

A

Interaction with NSAIDs
- potent COX inhibitors

  • Increased bleeding - particularly GI tract
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12
Q

When to use beta blockers?

A

Reduce mortality in IHD and heart failure

Reduce symptoms of angina, AF and SVT

*Antihypertensive (2nd line now)- (multiple mechanisms of action both central and peripheral)

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13
Q

Do you use beta blockers for hypertension?

A

No

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14
Q

Examples of beta blockers?

A

Bisoprolol

Carvediol

Atenolol

Metoprolol

Propranolol

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15
Q

Where are beta I blockers located?

A

Heart - SA, AV nodes and myocardial cels

Kidneys - reduce secretion of renin

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16
Q

Where are beta 2 receptors located?

A

Smooth muscles e.g. airways, peripheral vasculature

Skeletal muscle

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17
Q

Positive effects of beta I blockers?

A

Slows heart rate and conduction

Reduced BP

Protects heart from effects of catecholamines

Increased diastolic time

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18
Q

Positives of beta 2 blockers?

A

Reduces tremors

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19
Q

Negative effect of beta I blockers?

A

Reduces contractility (negatively ionotropic)

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20
Q

BETA I blockers?

A

Bisopolol

Atenolol

Carvediol

Metoprolol

these inhibit beta 2 but not as prfound effect

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21
Q

Beta I and 2 blockers?

A

Propranolol

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22
Q

Implications of beta blockers in dentistry?

A

Protects heart from potentially deleterious effect of adrenaline

Can disguise physiological signs of significant blood loss

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23
Q

What is the first line of defence for hypertension in white/asian patient under 55?

A

ACE inhibitors

ARBS

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24
Q

Positive effect of ACE inhibitors?

A

Reduce blood pressuree

Reduce after load on heart

Prevents aberrant remodelling after mi

Reduces protienuria

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25
Q

Negative effects of ACE inhibitors?

A

Reduces perfusion pressure in glomerulus

  • cough
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26
Q

Examples of ACE inhibitors?

A

Ramipril

Lisinopril

Captopril

Perindopril

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27
Q

Positive effects of ARBS?

A

Reduce BP

Reduce after load on heart

Presets aberrant remodelling and reduce proteinuria

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28
Q

Negative effects of ARBS?

A

Reduces perfusion pressure in glomerulus

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29
Q

What is the role of angiotensin II and what does angiotensin II act upon?

A

Postent vaoconstrictor

  • peripheral vasculature
  • efferent arteriole of the glomerulus
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30
Q

Role of aldosterone?

A

Retention of na (and therefore H20) at the expense of K in the DCT of the kidneys (sweat glands, duct)

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31
Q

Role of calcium channel blockers?

A

Antihypertensive agent

stop calcium from entering the cells of the heart and arteries. Calcium causes the heart and arteries to squeeze more strongly. By blocking calcium, calcium channel blockers allow blood vessels to relax and open.

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32
Q

What can calcium channel blockers reduce the symptoms of?

A

Angina

AF/SVT

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33
Q

2 classes of calcium channel blockers?

A

Non dihydropyridine and dihydropyridine

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34
Q

What does dihydropyridine block?

A

Calcium entry into smooth muscle

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35
Q

What does non-dihydropyridine block?

A

Blocks calcium entry into smooth muscle

Blocks calcium entry in the myocardial pacemaking tissue

  • slow SA node function
  • slow AV conduction
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36
Q

Implications for calcium channel blocker in dentistry?

A

Gingival hypertrophy -

particularly dihydropyridine

poor dental hygiene is a risk factor

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37
Q

What calcium channe blocker causes gingival hypertrophy?

A

Dihydropyridine

38
Q

Types of ischaemic heart disease?

39
Q

Coronary artery disease?

A

symptoms and damage of the heart muscle caused by narrowing of the blood vessels of the heart.

This leads to an imbalance between Oxygen demand and supply.

40
Q

Causes of atherosclerosis?

A

high cholesterol and triglyceride levels, high blood pressure, smoking, diabetes, obesity, physical activity, and eating saturated fats.

41
Q

What is the effect of atherosclerosis?

A

cardiovascular disease

it is central to these pathologies

42
Q

Mode of action of aspirin?

A

Aspirin inhibits cyclooxygenase (mainly COX-1), resulting in a reduction of thromboxane A2, an inducer of platelet aggregation

irreversibly bind

effects lasts 7-10 days

43
Q

What drug inhibits thrombin receptors?

44
Q

What drug is a fibrinogen receptor blocker?

45
Q

What is the main indication for aspirin, primary or secondary prevention?

A

secondary

after CVD diagnosis

46
Q

Dose of aspirin after CABG?

47
Q

When to use clopidogrel?

A

75mg after initial acute phase of tx or with aspirin

48
Q

What should you need to control before the pt leaves the practice after an invasive technique (pt on blood thinners)?

A

haemostasis obtained

49
Q

side effects of antiplatelest?

A

Bleeding
Roughly 0.25 to 1% annual risk of a significant bleed with a single agent,
synergistic effect when multiple agents used
Effect will last for up to 1 week.

50
Q

NSAIDs and cardiovascular implications?

A

increased cardiovascular mortality in high risk patients and sodium retention in HF

51
Q

What is meant by beta I blockers being negatively chronotropic?

A

reduce heart rate

52
Q

Dromotropic (beta I blcokers)

A

increases rate of conduction through AV node

53
Q

Negative effect of beta 2 blockers?

A

potentially lethal bronchospasm in asthmatics, vasoconstriction and PVD

54
Q

The role of ACE inhibitirs and angiotensin receptor antagonsists?

A
  • Antihypertensive- first line in under 55 White/ Asian patient
  • Reduction in mortality and progression of disease in IHD, CVD and renal disease with proteinuria (particularly diabetic nephropathy)
  • Prevent aberrant remodelling following MI
  • Reduction in symptoms in heart failure
55
Q

renin-angiotensin-aldosterone axis?

A

Renin enzyme released by the kidney in response to reduction in perfusion pressure
ACE isEndothelial enzyme found predominantly in the lungs
Aldosterone acts on the Distal Convoluted tubule to retain sodium and excrete potassium

56
Q

Example of ARBS?

A

losartan, candersartan

57
Q

Implications of ACE inhibitors and ARBS in dental practice?

58
Q

Example of aldosterone antagonists?

A

Spironolactone and eplenerone

59
Q

Implication for aldosterone inhibitors?

A

used in heart failure (frequently coprescribed with ACE/ARB).

Spiro sometimes used in hypertension

60
Q

What aldosterone antagonsist is sometimes used in hypertension?

A

Spironolactone

61
Q

What class of drugs should be used with great caution with aldosterone antagonists?

A

NSAIDS should be used with extreme caution- marked hyperkalaemia seen if AKI occurs

61
Q

Effect of aldosterone antagonists?

A

Enhanced diuretic effect
Reduces mortality in IHD and Heart failure

62
Q

What is entresto?

A

Combination of Valsartan and Sacubitril

63
Q

What does sacubitril inhibit?

A

it is an entresto

Neprilysin Inhibitor

64
Q

Effect of entresto?

A
  • inhibits breakdown natriuretic peptides eg. ANP and BNP (and Bradykinins)
  • increase diuresis, natriuresis and vasodilation
65
Q

Indication for entresto?

A
  • indicated in symptomatic chronic HF with reduced ejection fraction
66
Q

What should you not co-prescribe entresto with?

A
  • Do not co prescribe with ACE inhibitor (allow 36 hour washout period) as increased risk of angioedema
67
Q

Key role of calcium in smooth muscle contraction?

A

Calcium key role in smooth muscle contraction- binding to contractile apparatus and activating enzymes
In cardiac muscle movement of calcium into cells contributes to the action potential- particularly important in the Nodal tissue of the AV node. Slow conduction within this tissue and prolongs effective refractory period.

68
Q

dihydropyridine vs non-dihydropyridine?

A

dihydropyridine less effect on heart pace making tissue

non-dyhydropyridine does have effect on heart pace making tissue

  • slow SA node function
  • slow AV conduction
69
Q

example of dihydropyridine and what class of drug is this?

A

Amlodipine, felodipine

calcium channel blocker

70
Q

example of non-dihydropyridine and what class of drug is this?

A

Verapamil and Diltiazem

calcium channel blocker

71
Q

When to use statins?

A

high level LDL (high cholesterol)

already had a heart attack or stroke, or have peripheral arterial disease.

72
Q

When are statins the primary prevention?

A

reduce cardiovascular risk if patients 10 year risk is > 20%

73
Q

When are statins the secondary prevention?

A

after cardiovascular event

74
Q

How do statins work, what do they inhibit?

A

Hydroxy-methyl-glutaryl Coenzyme A (HMGCoA)reductase inhibitor
Rate limiting step in production of cholesterol

75
Q

Examples of statins?

A

Simvastatin, Rosuvastatin and Atorvastatin

76
Q

myositis?

A

condition which makes your immune cells attack your muscles

77
Q

Implication of statins in dental practice?

A

Clarithromycin contraindicated with Simvastatin and increases risk of Myositis

78
Q

Implication of diuretics in the dental practice?

A

Potentially nephrotoxic effect in combination with NSAIDs

79
Q

Effects of diuretics?

A

Antihypertensive effects- Thiazides eg. Indapamide and Bendroflumethizide

Promote Sodium and Water loss in the kidney (also can lead to hypokalaemia)

80
Q

How do thiazide diuretics work and what is their effect?

A

Act by blocking NaCl reabsorption in distal convoluted tubule of the kidney

Mild diuretic effect
Vasodilatory effect

81
Q

Example of thiazide diuretics?

A

Indapamide, Bendroflumethiazide

82
Q

Common side effects of thiazide diuretics?

A
  • Electrolyte disturbance (Low Na and K in particular but also Hypercalcaemia)
  • Hyperuricaemia (causing gout and increased Cardiovascular risk)
  • Hyperglycaemia
  • Dehydration, renal impairment
  • Orthostatic Hypotension
83
Q

How do loop diuretics work and what is their effect?

A

Act by blocking NaCl Reabsorption in the ascending limb of the loop of Henle

Intense diuretic effect

Pronounced vaso and venodilatory effect

84
Q

Example of loop diuretics?

A

furosemide and bumetanide

85
Q

Common side effects of loop diuretics?

A

Electrolyte disturbance (Low K, Na and Mg and Ca)

Dehydration, renal impairment

Orthostatic Hypotension

86
Q

When to use Vit K antagonists eg Warfarin and DOACs?

A

Primary or secondary prevention in CVD associated with AF

Prosthetic valves

Other indications eg. Mural thrombus in severe heart failure

87
Q

Implications of anti-coagulants?

A

Bleeding covered by Dr Khan

Interactions with antibiotics commonly used:

  • Enhanced anticoagulant effect via inhibition cP450 eg. Clarithromycin, Azole anti fungals
  • Reduced anticoagulant effect via induction of cP450 eg. Rifampycin
88
Q

Antianginals?

A

Nitrates long and short acting

Nicorandil- can be associated with ulceration

89
Q

Antihypertensive?

A

alpha blockers eg doxasocin

90
Q

Antiarrythmics?

A

Digoxin

Amiodarone- theoretically reduces the toxic dose of Lignocaine

BDS3 Human Disease (33 decks)

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