CDL 301 Flashcards

1
Q

Anti-arrhythmic drugs (Vaughan Williams classification)

Class I: sodium channel blockers …

A

Ia - Disopyramide
Ib - Ligocaine
Ic - Flecainide

Sodium channel blockers have ‘loose dependence’ - I can bind to na+ channel in a certain state in its cycle e.g inactivated

Resting channels are unaffected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Anti-arrhythmic drugs (Vaughan Williams classification)

Class II: Beta adrenoreceptor antagonsists …

A

(non-selective) - Propranolol

(b1 Selective) - Bisoprolol, Metaprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Anti-arrhythmic drugs (Vaughan Williams classification)

Class III: Prolong the Action potential

A

Act to prolong the refractory period (therefore the heart isn’t susceptible to incoming AP’s)

Amiodarone, Sotalol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Anti-arrhythmic drugs (Vaughan Williams classification)

Class IV: Calcium channel blockers

A
  • Verapamil

- Diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Anti-arrhythmic drug that doesnt fall into this classification …

A

Digoxin

  • comes from a group of drugs called cardiac glycosides
  • inhitis na+/k+ ATPase = decrease in na+ gradient = decrese na+/ca2+ pump activity= increase [ca2+]i (because it cant be pumped out) = INCREASE IN FORCE OF CONTRACTION
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Another arrhythmic drug used in A-fib

(has narrow therapeutic window) and is commonly used for Severe HF

A

Digoxin

  • causes bradycardia (increased vagal tone)
  • causes slowing of av conduction

however too high dose = ectopic activy (pro-arrhythmi) and force of contraction = all due to increase ca2+

therefore narrow therapeutic range

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

very effective anti-arrhythmic drug that increased Q-T interval but has many side effects and risk of polymorphic ventricular tachycardia from increasing Q-T interval too much

A

Amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what would you treat a patient with HF with so ensure their LVEDP isnt too high and their CO isnt too low

A
  • Diuretic e.g furosemide, to shift them left (.e decrease LVEDP
  • ACE inhibtior (e.g captopril, enalopril) to therefore vasodilation = decrease afterload for same EDP therfore increase in CO
    -digoxin may be used to increase contractility to therefore increase CO
    -
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ACE inhibitors

A

-Captopril. enalopril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

humoral control of coronary blood flow, heart also secreted them in response to HF

A

Cardiac Natriuretic peptides

  • atrial natriuretic peptide (ANP)
  • Brain natriuretic peptide (BNP)

both released by stretching of the atrial and ventricular muscle cells of the heart caused by:

  • increase in atrial or ventricular pressure
  • volume overload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What metabolises cardiac natriuretic peptides

A

Neutral endopeptidase (NEP) e.g Neprilysin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is entrestro and why is it used for HF

A

combination of both:

  • Sacubitril (Neprilysin inhibitor= therefore increase in Cardiac natriuretic peptides)
  • Valsartan (ANGII blocker = prevents angII from contributing to HF through vasocontriction etc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

4 classes of diuretics

A
  • Thaizides (bendroflumethiazide)
  • Loop Diuretics ( furosemide, bumetanide)-
  • K+ sparing diuretics ( Spironolactone)
  • Aldosterone antagonists (Spironolactone- inhibits RAAS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Personalised medicine examples

A
  • Warfarin dosage via genetic testins of VKOR and CYP29 genes
  • Isosorbide Dintatres as part of vasodilator therapy in HF - more effective in afro-caribbean patients
  • Stent size shape length etc for in Percutaneous coronory intervention for STEMI patients
  • Specific coagulation factors for hameophillia patietns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

2 drugs that make up ‘vasoldilator therapy’ in HF

A
  • Hydralazine (arterial dilator) = decrease afterload

- Isosorbide dinitrate (venous dilator) = decreased pre-load by increasing the storage capacity of veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Overall Treatment options for HF

A
  • ACE inhibtiors
  • Digoxin
  • Vasodilator therapy
  • Diuretics
  • Cardiac natriueritc peptides (naturally released from heart)
  • Entresto (sacubitril, valsartan)
  • Ivabradine (used in angina and HF in patients with HR over 70 that cant have b-blocker - show significant benefit to HF patients)
17
Q

Treatments to inhibti RAAS/symp.NS system that acts to exaccerbate HF

A
  • B-blockers
  • ACE inhibtior (ramipril)
  • AngII antagonist blocker (ARB)
  • Vasodilator
  • Aldosterone antagonist
  • Diuretic
18
Q

Immediate treatment for acute heart failure

A
  • Oxygen
  • Diamorphine
  • Nitrates (isosorbide dinitrate - venous dilator used in vasodilator therapy for Chronic HF)
  • Loop diuretics e.g furosemide
  • Inotropes (adrenergic agonists, PDEIII inhibtiors-increase cAMP)
19
Q

Different types of adrenergic receptors and their action

A

a1- in periphery and cause vasoconstriction
b1- in heart and cause posiive inotropic effects (increase F.O.C)
b2 - mainly in skeletal muscle and cause vasodilation

inocontrictors (norepinephrine) and inodilators (isoproterenol) are the two main groups of adrenergic agoists

  • ino = because act on b1 ionotropic receptors
  • constrictors = act on a1
  • dilators = act on b2

both Given I.V

20
Q

What is the mainstay treatment of HF

A

Triple therapy

  • ACE inhibitor (ramipril)
  • Beta-adrenoreceptor blocker (bisoprolol - b1 specific, propranolol - on selective)
  • Aldosterone antagonist (Spironolactone) = diuretic
21
Q

Name the different types of NO donor therapies

A
  • Nitroglycerine (treat angina)
  • Sodium nitroprusside (treat emergency hypertension in A+E)
  • Inhaled NO - (treats severe pulmonary hypertension)
22
Q

Name the different prostanoid therapies

A
  • Iloprost (PGI2 stable analogue, activates PGI2 causing vasoidlation) - treats pulmonary hypertension, raynauds
  • Epoprostenol (IP-R agonist, causing vasodilation) - treats pulmonary hypertension
  • Corticosteroids (acts on cox1/2 to supress formation of prostanoids) =prevents shock (hypotension)
23
Q

Endothelin therapies

A
  • Bosentan (ETA/B antagonist) = vasodilation =treats pulmnary hypertension
  • ECE inhibitor - phosporamidon
24
Q

AngiotensinII /ACE therapies

A

ACE inhibtiors

AT1- receptor antagonists (Sartans e.g valsartan)

25
Q

k+ channel activators (to treat hypertension)

A
  • Minoxidil

- Diazoxide

26
Q

PDE inhibtior

A

Sildenafil (PDE-V inhibitor) - treats PAH and Raynauds

27
Q

alpha blocker in RAAS

A

-Doxazosin - also used in begin prostatic hypertrophy with alfuzosin and tamsulosin

28
Q

centrally acting anti-hypertensive (prevents release of noradrenaline)

A

methyldopa

- can be used in pregnancy

29
Q

Direct Renin Inhibtior

A

Aliskiren

30
Q

example of an anti-emetric (stops vomitings) used with morphine/opites

A

metclopramide

31
Q

Endothelin receptor antagonists

A
  • Macitentan, bosentan
32
Q

NO stimulants

A
  • NO , Riociguat
33
Q

PGI2

A

Iloprost, treprostinil, selxipag

34
Q

inhibtior of aromatase in PAH

A

anastrazole