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Prescribing > Cardiac conditions And Meds > Flashcards

Cardiac conditions And Meds Flashcards

1
Q

What are the stages of SYSTOLIC HTN

A

< 120 - Normotensive

120-140- pre HTN

140-159 Stage 1

160- 180 Stage2

180 + stage 3

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2
Q

What are the stages of DIASTOLIC HTN

A

< 80 - Normotensive

80 -90- pre HTN

90-99 Stage 1

100-120 - stage 2

120+ stage 3

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3
Q

Nitrates- name common uses and mechanism of action

A

Relief of angina- GTN spray and sublingual/buccal tablets- rapid acting

Prevention of angina- ISMN, GTN patch- long acting

Mechanisms:

Peripheral vasodilation – reduces preload – reduces myocardial oxygen demand

Coronary artery vasodilation - improves endocardial blood flow – increases myocardial oxygen supply

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4
Q

Calcium channel Blockers- name indication and mechanism of action of Non Rate limiting CCB

A

Non Rate limiting CCB- Indication- hypertension

Mechanism: block calcium channels of smooth muscle

Arterial dilation reduces systemic vascular resistance and myocardial oxygen demand

non cardiac specific

amlodipine, felodipine, nifedipine

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5
Q

Calcium channel Blockers- name indication and mechanism of action of Rate limiting CCB

A

Rate limiting CCB- Indication- hypertension, angina, arrhythmias

Mechanism: block calcium channels of smooth muscle
and reduce myocardial contractility- reduced myocardial oxygen consumption

Slow sinus node and AV node conduction
Reduced HR = reduced myocardial oxygen demand

caution with other selective rate controlling drugs e.g. bisoprolol.

– verapamil and diltiazem

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6
Q

Nicorandil- what is its indication and mechanisms

A

prophylaxis and treatment of stable angina

Mechanisms: Dual mechanisms

Potassium channel opening action to provide vasodilation

Nitrate component promotes venous dilation

dual mode of action avoids some of tolerance seen with long term nitrates.

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7
Q

Aspirin- indications and mechanisms

A

Stops platelet aggregation and clot formation

Mechanism: A non-selective cyclo-oxygenase (COX) inhibitor- Inhibits thromboxane A2 (TA2) formation

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8
Q

Clopidigrel- indications and mechanisms

A

Stops platelet aggregation and clot formation

Used in dual antiplatelet therapy with aspirin e.g post MI

Mechanism: Antagonist at adenosine diphosphate (ADP) receptors- blocking it reduces aggregation

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9
Q

ticagrelor- indications and mechanisms

A

Stops platelet aggregation and clot formation

Used in dual antiplatelet therapy with aspirin e.g post MI

Mechanism: stops the action of ADP

Ticagrelor vs clopidogrel

not a prodrug

faster onset

more potent inhibition of platelet aggregation

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10
Q

name 3 common antiplatelets drugs

A

Aspirin

Ticagrelor

Clopidogrel

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11
Q

which common class of drugs are used to lower cholestrol?

A

STATINS

Simvastatin

Atorvastatin

Rosuvastatin

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12
Q

Statins- indications and mechanisms

A

Decreases cholesterol production and increases LDL clearance

Other actions:

Stabilises plaque

Improves endothelial function

Prevents thrombus formation

mechanism- Inhibit hydroxy-methylglutaryl-coenzyme A reductase (HMG-CoA)

HMG coenzyme a is an essential cholesterol precursor

Primary prevention - Atorvastatin 20mg nocte
Post myocardial infarction (MI) - Atorvastatin 80mg nocte

Atorvastatin and pravastatin can be given AM due long action of onset in cases of poor adherence nocte.

many interaction- avoid grapefruit juice

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13
Q

Beta-(adrenoreceptor) blockers- indication and mechanisms

A

Indications- hypertension, Angina, MI (secondary prevention), aryhthmias e.g. AF

Mechanism: antagonist to Beta 1 receptor

Decrease myocardial oxygen requirements by:

slowing heart rate

reduce force of contraction

reduce blood pressure

caution with other rate control drugs

caution in Severe asthma- can block beta 2 receptors

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14
Q

what is the role of the Renin angiotensin Aldosterone system (RAAS) ?

A

RAAS plays a role in regulating blood pressure/volume, maintaining sodium concentration and the right amount of water in the blood

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15
Q

how does the RAAS moderate BP?

A

A reduction in blood pressure is detected by the kidneys

Renin - released by the kidneys, stimulates the formation of angiotensin I in the liver - this inconverted to Angiotensin II in lungs by angiotensin converting enzyme

Angiotensin II - stimulates the release of aldosterone from the adrenal cortex and causes direct vasoconstriction- increase in BP

Aldosterone - stimulates reabsorption of sodium and water- increase BP

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16
Q

Which two classes of drugs act on RAAS to lower BP ?

A

ANGIOTENSIN – CONVERTING ENZYME (ACE) INHIBITORS

e.g. Ramipril, Captopril, Enalapril, Lisinopril, Perindopril

ANGIOTENSIN RECEPTOR BLOCKERS (ARBs)

e.g. Candesartan, Eprosartan, Irbesartan, Olmesartan, Valsartan

THESE TWO DRUGS SHOULD NOT BE USED TOGETHER !

17
Q

how do ACE inhibtors lower BP?

A

they inhibit ACE in the lungs and thus Angiotensin II formation.

18
Q

how do ARBs lower BP?

A

they block receptors and are angiotensin II receptor antagonists.

19
Q

Management HTN “with” T2DM any age/origin

management HTN “without” T2DM < 55yrs - not black African/African-Caribbean.

A

step 1 ACE/ARB

Step 2 in addition to ACE/ARB add CCB or thiazide diuretic (THD)- in HF offer THD

step 3 ACE/ARB + CCB + THD

Step 4 consider adherence, specialist help

consider spironolactone- K < 4.5mmol

consider alpha/beta blocker - k >4.5 mmol

20
Q

Management HTN “without” T2DM > 55yrs

Or all age black African/African-Caribbean “without” T2DM

A

step 1 CCB

Step 2 in addition CCB add ACE/ARB or thiazide diuretic (THD)

step 3 ACE/ARB + CCB + THD

Step 4 consider adherence, specialist help

consider spironolactone- K < 4.5mmol

consider alpha/beta blocker - K >4.5 mmol

21
Q

Which oral anticoagulants are vitamin k antagonist

A

Warfarin - most common

Inhibits Vitamin K Reductase

Prevents degradation of vitamin K to its active form- stops phase of clotting cascade.

older generation -Acenocoumarol and Phenindione

22
Q

which are the common direct oral anticoagulants (DOACs)

A

Rivaroxaban, Apixaban and Edoxaban– Factor Xa inhibitor

Dabigatran – direct thrombin inhibitor

All have rapid onset and offset of action, so adherence is paramount

23
Q

What are drawbacks when using warfarin ?

A

Narrow therapeutic range- can be condition specific

Slow onset of action- 3 -5 days before therapeutic

Long elimination half-life

Multiple drug and dietary interactions- including herbal and over counter preparations

Monitoring required- INR regularly

Difficult to manage peri-operatively- long half life.

Inconvenient and/or unsuitable for some patients

Large commitment of resources in primary and secondary care

24
Q

What are drawbacks of DOACs ?

A

Specific contraindications and cautions for DOACs

Renal impairment- renally excreted

Extreme body weight eg. Apixaban only in BMI < 40, < 120 kg

Pregnancy - animal studies showed crossed placenta.
Advice re: contraception in women of child-bearing age

Adherence- short halve life - can soon be non therapeutic

Specialist indications- not suitable in mechanical valves, sinus venous thrombosis and cancer, antiphospholipid syndrome

Peri-operative management

25
Q

Important patient education whom are taking

any oral anticoagulation

A

Importance of regular administration

Always seek medical advice when starting new treatments or any new diet regimes

Work by stopping blood clotting formation- Report any signs or symptoms of Bruising or Bleeding

If you miss a dose, do not double up !!!!

Carry patient alert card

26
Q

When to anti coagulate - CHA2DS2VASc Score

A

CHA2DS2-VASC >1 anti-coagulate for women or > 2 for men

CHA2DS2-VASC ≤1no treatment

Must consider a risk of bleeding assessment such as the by calculating the HAS-BLED score

27
Q

Consider HASBLED score when anticoagulating

A

Bleeding risk classification:

0-1 low risk

2 intermediate risk

≥ 3 high risk

NOTE: A score of 3 or more is not a contraindication to oral anticoagulation but these patients require extra care

Prescribing (18 decks)

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