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CARDIO/RESP > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are the classes of antiarrhythmic drugs?

A 
I: Sodium channel blockers
II: beta-adrenergic blockers
III: prolong ERP
IV: calcium channel blockers
Adenosine
Digoxin
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2
Q

What are tachyarrhythmias?

A

Increased HR due to:

(1) ***re-entry/retrograde
(2) enhanced automaticity in non-pacemaker cells
(3) after potentials

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3
Q

What are the main actions (and classes) of antiarrythmic drugs?

A
  • Suppress enhanced automaticity – classes 2 + 4
  • Prolong effective refractory period – class 3
  • Slow conduction in tissue – class 1 + 2
  • Depress resting membrane potential – adenosine
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4
Q

How do sodium channel blockers affect the myocardial action potential? What are the adverse affects?

A

Delays the time taken to raise the membrane potential to threshold (conduction time delayed) so myocardial contraction rate is slower
Adverse affects: enhanced risk of arrhythmia as conduction in latent circus is slowed so timing falls into critical range

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5
Q

How do beta1-adrenoceptor blockers work?

A

Affects the beta-AR linked sodium and calcium channels - reducing HR and slows contraction

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6
Q

What is commonly used to treat angina, heart failure, HTN and risk of sudden death after MI? what are some examples?

A

Beta1-AR blockers

  • metoprolol
  • atenolol
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7
Q

How do the classIII drugs prolong AP duration and ERP?

A

Prolong AP: by blocking K+ channels and prolonging repolarisation and preventing re-entrant arrhythmias

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8
Q

How does adenosine affect the myocardial AP?

A

Adenosine opens the K+ channels which decreases the resting membrane potential so the stimulus cannot raise the potential to threshold - ectopic impulses cannot conduct
Adenosine receptors are on the atrial and AV conducting tissue

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9
Q

What are the strategies of anti-hypertensive drugs?

A

(1) Reduce cardiac output - beta-AR blockers, Ca2+ blockers
(2) Dilate resistance vessels - Ca2+ blockers, RAS blockers, alpha-AR blockers, nitrates
(3) Reduce vascular volume - diuretics , RAS blockers

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10
Q

How does the renin-angiotensin system work?

A
  • Drop in blood pressure
  • Renin released from kidney
  • Renin converts forms angiotensin 1 from angiotensinogen
  • ACE from the lungs converts AT1 to AT2
  • AT2 causes vasconstriction and stimulates kidney to release aldosterone (increases reabsorption)
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11
Q

How does ACE-inhibitors decrease BP?

A

Inhibit the conversion of AT1 to AT2, preventing vasoconstriction and reabsorption

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12
Q

How do Beta-AR and Alpha-AR blockers work to reduce blood pressure?

A

Beta-AR: Reducde HR and contractility

Alpha-AR: suppress vasconstriction and decrease peripheral vascular resistance

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13
Q

What are the main types of calcium channel blockers?

A

(1) cardioselective - verapamil
(2) vascular smooth muscle selective - dihydropyridines
- - both: diltiazem

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14
Q

How do thiazides work?

A

They are diuretics that prevent sodium reabsorption in the loop and DCT - e.g. amiloride

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15
Q

What are some K+ sparing diuretics and how do they work?

A
  • aldosterone antagonist, spironolactone, eplerenone

- they allow the kidney to reabsorb potassium but still excrete more fluid

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16
Q

Drugs acting early in the tubule ____ more Na+ reabsorption than those acting later

A

Prevent

17
Q

What is the clinical use of antihypertensives?

A
  • Thiazide diuretic or ACEI or AT1 blocker
  • Both thiazide diuretic and ACEI or AT1 blocker
  • Add calcium channel blocker
  • Add alpha1 adrenoceptor blocker or beta blocker
18
Q

What are the drug strategies for managing heart failure?

A

ACE-I or AT1 blocker - reduce PVR/aldosterone driven remodelling
Aldosterone antagonists
Beta-adrenoceptor blocker - counter affects of symp stim
Loop diuretic - counter aldosterone driven Na retention
Digoxin - increase cardiac contractility
Nitrates
Oxygen

19
Q

How does digoxin work?

A
  • Competes with K+, thereby blocking Na+/K+ATPase
  • Less efficient calcium exchange = increased IC Ca2+ and more efficient myocyte contraction
  • decreases HR and increases contractility
20
Q

What are the signs of digoxin toxicity?

A

Cardiac: serious arrhythmias
Neurological: nausea, confusion, visual

21
Q

What is the consequence of digoxin in hypokalaemic patients?

A

If there is low K+ then digoxin occupies more ATPase sites

This reduces sodium and potassium exchange - leading to increased arrhythmias

22
Q

How is angina treated?

A

Reduce HR and contractility - beta-AR blockers and calcium channel blockers
Dilate resistance vessels - calcium channel blockers and nitrates (GTN)

23
Q

What are anti-platelet drugs used for? and what are some examples?

A

All coronary artery diseases

- aspirin, clopidogrel, prasugral and ticagrelor, LMW heparin

24
Q

What is used for early management for acute coronary syndromes?

A
  • Antiplatelet/anti-coag therapy
  • Beta-AR blockade
  • ACE inhibition
25
Q

What is the longterm management of CAD?

A

• Anti-platelet agents
• Anticoagulants
• Risk factor management
• Beta adrenergic blockade
• ACE inhibition or ARB
• Specific interventions – revascularization, rhythm etc
Risk management: diabetes, BP, lipids, smoking

26
Q

In asthma, what is the airway narrowing due to?

A

(1) Thickness of airway wall increased
(2) Increased mucous in lumen
(3) constriction of airway smooth muscle

27
Q

What are the therapeutic goals in asthma?

A
  1. Preventing/relieving bronchoconstriction (eg beta-2-adrenoceptor agonists)
  2. Suppressing inflammation – controllers such as inhaled corticosteroids (ICS)
  3. Inhibiting mucous hypersecretion
28
Q

What beta2-AR agonists are used in asthma and how do they work? (reliever)

A
  • Salbutamol and terbutaline
  • stimulate beta2-AR on airway smooth muscle to induce relaxation
    Onset: 5-10mins
    short acting: 4-6 hours
29
Q

What are some longer acting beta2-AR agonists? (reliever) and what are they often conjugated with?

A 
Eformoterol and salmeterol 
- actions last 12-24 hours 
EF onset: 5-10mins
SA onset: 15-20mins
- often used in conjunction with inhaled corticosteroids
30
Q

What is the frontline therapy in maintenance of mild, moderates and severe asthma? (controller)

A

Inhaled corticosteroids:

  • inhalation
  • regulate gene transcription of proteins like cytokines, chemokines
  • must be taken prophylactically
  • beclomethasone, budenoside
31
Q

How do leukotriene receptor antagonists work in asthma?

A

LT mediate inflammation by binding to LT receptors in airways and inducing airway narrowing and promotes secretion of mucous, blood leakage and eosinophil influx (this is inhibited)

32
Q

How to anti-IgE antibodies manage asthma?

A

Omalizumab - binds free IgE

- used to treat moderate to severe allergic asthma in patients with raised IgE and who are on ICS

33
Q

How do statins work?

A

They inhibit HMG CoA reductase

34
Q

What is the relevance of PCSK9 in cholesterol levels?

A

Mutations in PCSK9 can cause high or low cholesterol in people though gain of function (high) or loss function (low) so it is a target for treatment

CARDIO/RESP (5 decks)

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