Drugs that don't fit in the Vaughn-Williams classification system Flashcards

1
Q

Nifedipine
Drug class
Use

A

Blocks L-type Calcium channels
but not used for dysrhythmias
Use: Hypertension, angina

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2
Q

Ziconotide

Pros

A

treats severe, chronic pain
No significant respiratory depression or loss of motor coordination
No euphoria associated with opioid analgesics
No development of tolerance
No withdrawal symptoms
Not addictive

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3
Q

Ziconotide

Cons

A

-intrathecal delivery
narrow therapeutic window
severe but reversible psychiatric symptoms - cognitive impairment, hallucinations, changes in mood+consciousness

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4
Q

Digoxin groups and what they’re like

A
  • Aglycone group - determines pharmacodynamic properties
  • Lactone group - intermediate solubility
  • steroid nucleus - lipid soluble
  • sugar resides: water soluble and determine pharamacokinetic properties
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5
Q

How digoxin works

A

Blocks Na+/K+ ATPase

-positive inotropic effect i.e. ↑Heart rate

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6
Q

Digoxin for whom and how it may help

A

Patients in sinus rhythm that remain symptomatic despite taking an ACE inhibitor and a diuretic

  • ↑exercise tolerance
  • helps symptoms
  • ↓need for hospitalisation
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7
Q

Digoxin effects on cardiac rate and rhythm

at therapeutic doses

A

↑vagus nerve activity:

  • Slows SA node firing rate
  • Slows AV node conduction velocity
  • improves filling and pumping
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8
Q

Digoxin effects on cardiac rate and rhythm at toxic doses

A

Dysrhymias
↑sympathetic tone
Inhibition of Na+/K+ ATPase causes membrane to be closer to threshold for depolarisation, so more APs firing, more ectopic beats and more after-depolarisations

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9
Q

Signs of digoxin toxicity

A

Nausea and vomiting
sight disturbances
ventricular tachyarrhythmias

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10
Q

Treatment of digoxin toxicity

4 steps

A
  • Stop digoxin
  • Correct hypokalaemia via giving KCl and/or NaCl or KCl and glucose IV infusion
  • Propranolol or phenytoin to control arrhymias
  • digoxin-specific antibody fragments IV infusion
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11
Q

Uses of adenosine

A

suppression of:

  • PSVT
  • Ventricular tachycardia associated with Wolff-Parkinson-White syndrome
  • supraventricular tachyarrthymias that may occur during general anaesthesia
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12
Q

Adenosine method of actions

A

Activates (GPCR) A1-purinoceptors on cardiac myocytes
-oepns K+Ach channel causing hyperpolarisation
This inhibits VSCC from opening so ↓AP duration, ↓slope of pacemaker potentials
-lower discharge rate of SA node
-lower conduction
-↑refractory period in AV note
decreased excitability

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13
Q

Physiochemical properties of Adenosine

A
purine nucleoside (+neurotransmitter) 
half life= 10 secs hence not oral
effects of rapid bolus dose last 20-30 secs
Rapid uptake and metabolism by RBCs-beneficial for treatment of SVT
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14
Q

Adenosine unwanted effects

when to avoid

A
  • Bradycardia - hence avoid in sick sinus syndrome and heart block
  • facial flushing
  • chest pain
  • bronchoconstriction - avoid in asthma
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