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

BP = HR X SV X TPR

Question 6

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

3

Answer 6

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

Question 7

what are examples of anti-hypertensive drugs?

Answer 7

• ACE inhibitors
• Angiotensin-II-receptor blockers (ARBs)
• Beta blockers
• Calcium channel blockers
• Diuretics

Question 8

what is the mechanism of action of ACE-inhibitors? 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

ACE inhibitors inhibit the release of ACE from the lungs so angiotensin 2 and aldosterone is not produced
* reduced fluid reabsorption in the kidneys
* reduced blood volume and **blood pressure
**
ramipril, lisinopril, perindopril

Question 9

what are the oral impliations of ACE inhibitors?

2

Answer 9

oral lichenoid tissue reaction and dry mouth

Question 10

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

Answer 10

ARBs bind to angiotensin 2 receptors on
* smooth muscle of blood vessels to prevent vasocontriction
* cortical walls of adrenal gland to prevent aldosterone production

candesartan, losartan, valsartan

Question 11

what is the mechanism of action of beta blockers to reduce blood pressure? give examples

Answer 11

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 12

what are the oral implications for beta blockers?

1

Answer 12

oral lichenoid tissue reaction

Question 13

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

Answer 13

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 14

what are the oral implications of calcium channel blockers?

Answer 14

gingival enlargement

Question 15

what is the mechanism of action of diuretics? give examples

Answer 15

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 16

what are the oral implications of diuretics?

Answer 16

oral lichenoid reactions
dry mouth

Question 17

what do antiplatelets do? what conditions are antiplatelets used for? give examples

Answer 17

reduce platelet aggregation

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

aspirin, clopidogrel, ticagrelor, dipyramidole

Question 18

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

Answer 18

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 19

what is the mechanism of action of dipyramidole?

Answer 19

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

Question 20

what is the mechanism of action for clopidogrel and ticagrelor?

Answer 20

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

Question 21

what are the dental implications of anti-platelets?

3

Answer 21

• 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 22

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

Answer 22

DOCS - used in atril fibrillation (prevents stroke)
warfarin - used with metallic valve replacement

Question 23

what are the mechanisms of action of DOACs? give examples

Answer 23

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

Question 24

what is the mechanism of action of warfarin?

Answer 24

inhibits formation of coagulation factors 2,7,9,10 by inhibiting formation of vitamin K which is needed for their formation

Question 25

what are the dental implications of warfarin?

Answer 25

* requires **INR monitoring** ideally ** less than 24 hours before treatment** * if **INR below 4**, can proceed with treatment * **cannot delay or miss dose** * **interactions** with medications and foods

Question 26

what are the general principles for anticoagulants? | 8

Answer 26

* consult with **GP or senior dentist** if unsure * **delay dental treatment** until anticogulant finishes if planned (DAPT) * plan treatment for **early in the day and week** * **"atraumatic" surgery, staged** * consider **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 27

what are the advantages of DOACs vs. warfarin? | onset, dosing, food effect, drug interactions, monitoring, offset

Answer 27

Question 28

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

Answer 28

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

Question 29

what is the mechanism of action of statins? give examples

Answer 29

inhibits **enzyme** in liver (**HMG-CoA reductase**) which **halts** the production of **LDL cholesterol** atorvastatin, rosvastatin, simvastatin

Question 30

what are the dental implications of statins?

Answer 30

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

Question 31

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

Answer 31

**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 **work done** by heart GTN spray, isosorbide mononitrate (ISMN), nicorandil

Question 32

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

Answer 32

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

Question 33

give the oral implications of ACE-inhibitors, beta blockers, calcium channel blockers and diuretics, anti platelets, anti coagulants, statins and anti anginals

Answer 33

* **ACE-inhibitors**: oral lichenoid tissue reaction, dry mouth * **beta blockers**: oral lichenoid tissue reaction * **calcium channel blockers**: gingival enlargement * **diuretics**: oral lichenoid tissue reaction, dry mouth * **anti-platelets**: increased bleeding times * **anti-coagulants**: increased bleeding risk * **statins**: interactions with fluconazole, miconazole and clarithromycin to cause rhabdomyolysis * **anti-anginals**: severe oral ulceration