Pharmacology Flashcards

1
Q

What is Ramipril?

A
  • Anti-hypertensive

- Limits angiotensin-II mediated LV remodelling in CF

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2
Q

What is Furosemide?

A
  • Potent diuretic

- Indicated with CF fluid overload

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3
Q

What is Digoxin?

A
  • Positive inotrope

- Indicated for systolic CF

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4
Q

Why are K levels important to monitor/manage in cardio patients?

A
  • Determine cells membrane potential + electrical excitability (via Na/K ATPase)
  • Hyper/po kalaemia = serious impact on normal cardiac rhythm by disruption of phase 3
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5
Q

What is the MOA of Ramipril?

A

ACE inhibitor - prevents angiotensin II generation

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6
Q

What is the ADR of Ramipril?

A

Hyperkalaemia

  • blocks ang-II/aldosterone-mediated Na re-uptake from urine in CT
  • Na re-uptake normally drives K+ secretion into urine
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7
Q

What is the MOA of Furosemide?

A

Blocks Na/K/Cl symporter in ascending LOH

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8
Q

What is the ADR of Furosemide?

A

Hypokalaemia

- Traps Na+ in urine = drives K+ secretion into urine

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9
Q

What is the MOA of Digoxin?

A

Blocks Na/K/ATPase which increases [Ca] in cardiomyocytes = + inotropy

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10
Q

What is the ADR of Digoxin?

A

Hyperkalaemia

Competes with K+ so prevents it entering into cells = increases serum K

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11
Q

What is the normal serum K?

A

3.7 - 5.2

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12
Q

What is seen on the ECG for Hyperkalaemia?

A
  • Peaked T waves
  • Prolonged QRS
  • Eventual loss of P waves
  • Bradycardia
  • Asystole

Increasied serum K = depressed electrical excitability

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13
Q

How is Hyperkalaemia treated?

A
Ca glutamate 
Insulin 
Glucose 
Salbutamol 
Resonium
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14
Q

What is seen on the ECG for Hypokalaemia?

A
  • Large P waves
  • T wave flattering/inversion
  • ST depression
  • U waves
  • Prolonged PR interval
  • Predisposition to re-entrant arrhythmias

Reduced serum K = hyper electrical excitability

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15
Q

How is Hypokalaemia treated?

A

Oral or IV K

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