Cardiovascular drugs

Question 1

blood pressure equation

Answer 1

blood pressure = cardiac output x total peripheral resistance

Question 2

cardiac output equation

Answer 2

cardiac output = heart rate x stroke volume

Question 3

stroke volume definition

Answer 3

volume of blood being pumped by the left ventricle

Question 4

total peripheral resistance definition

Answer 4

how much vasoconstriciton vs. vasodilation is present in peripheral circulation
* as peripheral blood vessels constrict, TPR increases

Question 5

what can you lower to reduce blood pressure?

3

Answer 5

heart rate
stroke volume
total peripheral resistance

Question 5

how do anti-hypertensives work on different parts of the body?

3

Answer 5

heart: reduce heart rate or comtractability
blood vessels: vasodilation
kidneys: reduce amount of fluid reabsorbed

Question 6

what is the mechanism of action of ACE-inhibitors? give examples

Answer 6

when BP is low, the Renin-Angiotensin-Aldosterone System (RAAS) increases BP
* renin produced in the kidney nephron converts angiotensinogen in the liver to angiotensin 1
* angiotensin 1 is converted to angiotensin 2 by ACE produced in the lungs and can release aldosterone in the adrenal gland
ACE inhibitors inhibit the release of ACE from the lungs so angiotensin 2 and aldosterone is not produced
* reduced fluid reabsorption in the kidneys
* increased blood volume and blood pressure

ramipril, lisinopril, perindopril

Question 7

what are the oral impliations of ACE inhibitors?

2

Answer 7

lichenoid tissue reaction

Question 8

what is the mechanism of action of angiotensin-||-receptor blockers (ARBs)? give examples

Answer 8

when BP is low, the Renin-Angiotensin-Aldosterone System (RAAS) increases BP
* renin produced in the kidney nephron converts angiotensinogen in the liver to angiotensin 1
* angiotensin 1 is converted to angiotensin 2 by ACE produced in the lungs and can release aldosterone in the adrenal gland
ARBs bind to angiotensin 2 receptors on
* smooth muscle of blood vessels to prevent vasocontriction
* coortical walls of adrenal gland to prevent aldosterone production
increased blood pressure

candesartan, losartan, valsartan

Question 9

what is the mechanism of action of beta blockers? give examples

Answer 9

adrenergic receptors throughout the body:
* alpha 1 - blood vessel smooth muscle
* beta 1 - heart
* beta 2 - smooth muscle in bronchi and bronchioles
* beta blockers can be selective or non-selective for different subtypes of adrenergic receptors
beta blockers competitively inhibit beta 1 receptors on cardiac muscle cells and prevent stimulation by adrenaline
* prevent increase heart rate and contractability

atenolol, bisoprolol, propranolol, carvediol

Question 10

what are the oral implications for beta blockers?

1

Answer 10

oral lichenoid tissue reaction

Question 11

what is the mechanism of action of calcium channel blockers? give examples

Answer 11

1. inhibit calcium channels on smooth muscle around peripheral blood vessels - reduce vascoconstriction and TPR
2. inhibit calcium channels at sino-atrial node - reduce HR
3. inhibit calcium channels on cardiac muscle cells - reduce heart contractability

amlodipine, nifedipine, felodipine

Question 12

what are the oral implications of calcium channel blockers?

Answer 12

gingival enlargement

Question 13

what is the mechanism of action of diuretics? give examples

Answer 13

work at different parts of the nephron to decrease fluid reabsorption (DCT and CD)
* increased urination = reduced blood volume = reduced blood pressure

furosemide, bendroflumethazide, bumetanide

Question 14

what are the oral implications of diuretics?

Answer 14

oral lichenoid reactions
dry mouth

Question 14

what are antiplatelets used for? give examples

Answer 14

coronary heart disease
secondary prevention following MI
peripheral artery disease
secondary prevention following stroke/TIA

aspirin, clopidogrel, ticagrelor, dipyramidole

Question 14

what is the mechanism of action for aspirin? what are the possible dosages?

Answer 14

inhibits COX-1 enzyme to reduce production of thromboxane A2, reducing platelet aggregation and preventing thrombus formation
* 75mg a day (secondary prevention)
* 300mg (acute MI/stroke)

Question 15

what is the mechanism of action of dipyramidole?

Answer 15

inhibits phosphodiesterase in platelets
prevents breakdown of cAMP
blocks release of arachidonic acid

Question 15

what is the mechanism of action for clopidogrel and ticagrelor?

Answer 15

binds to P2Y12 receptors on platelets
prevents ADP binding
stops activation of platelet aggregation

Question 16

what are the dental implications of anti-platelets?

3

Answer 16

• likely prolonged bleeding time
• pts on DAPT (two anti-platelets) likely to have higher bleeding risk than on one drug
• no need to stop anti-platelet fro dental treatment

Question 17

what are the two types of anticoagulants? when are they used?

Answer 17

DOCS - used in atril fibrillation
warfarin - used with metallic valve replacement

Question 18

what are the mechanisms of action of DOACs? give examples

Answer 18

Dabigatran: A selective inhibitor of thrombin (Factor IIa)
Rivaroxaban, apixaban, and edoxaban: Selective inhibitors of activated Factor X (FXa)

Question 19

what is the mechanism of action of warfarin?

Answer 19

inhibits formation of coagulation factors 2,7,9,10

Question 20

what are the dental implications of warfarin?

Answer 20

• requires INR monitoring ideally <24 hours before treatment
• if INR <4, can proceed with treatment
• cannot delay or miss dose
• interactions with medications and foods

Question 21

what are the general principles for anticoagulants?

8

Answer 21

• consult with GP or senior dentist if unsure
• delay dental treatment until anticogulant finishes if planned
• plan treatment for early in the day and week
• “atraumatic” surgery, staged
• consuder packing and suturing
• ensure bleeding has stopped
• give post-operative instructions
• advise pt to take paracetamol, unless contraindicated, for pain relief rather than NSAIDs e.g. aspirin, ibuprofen

Question 22

what are the advantages of DOACs vs. warfarin?

onset, dosing, food effect, drug interactions, monitoring, offset

Answer 22

Question 23

what do lipid lowering medications do and what is the name of the medication group?

Answer 23

lower levels of cholesterol
LDL - low density lipoprotein (bad) - contribute to atherosclerosis process
HDL - high density lipoprotein (ok)
statins

Question 24

what is the mechanism of action of statins? give examples

Answer 24

inhibits enzyme in liver (HMG-CoA reductase) which halts the production of LDL cholesterol

atorvastatin, rosvastatin, simvastatin

Question 25

what are the dental implications of statins?

Answer 25

interaction with fluconazole, miconazole and clarithromycin to cause rhabdomyolysis (breakdown of muscle)

Question 25

what is the mechanism of action of anti-anginal medications? give examples

what

Answer 25

angina = narrowing of coronary arteries - chest pain
nitrates relax smooth muscle within coronary vessels, causing vasodilation and improved blood flow
dilates blood vessels returning to heart to reduce preload and reduce work done by heart

GTN spray, isosorbide mononitrate (ISMN), nicorandil

Question 26

what are the oral implications of anti-anginal medication? how can it be relieved?

Answer 26

nicorandil is a second-line agent in management of angina
can cause severe oral ulceration
heals on withdrawal of medication and relieved with denzydamine mouthwash