Annette Battersby Flashcards

1
Q

Which type of drug is diamorphine?

A

Opioid agonist - heroin

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2
Q

Is diamorphine lipid soluble?

A

Yes

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3
Q

What are the central actions of diamoprhine?

A
  1. Reduce sympathetic vascular reflexes (vasocontriction)
  2. Veno and arteriolar dilation
  3. Euphoria and sedation
  4. Release histamine (vasodilator)

Preload and afterload reduced and therefore relieve heart failure

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4
Q

Unwanted side effects of diamorphine?

A
  1. Resp depression and sedation
  2. Hypotension
  3. Bronchospasm
  4. Nausea and vomiting
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5
Q

What are the therapeutic effects of loop diuretics in HF?

A
  1. Promotes Na+ & H20 excretion (reduces pre-load)
  2. May promote direct vasodilatation (reduce afterload)
  3. Increase excretion of K+, Mg2+, Ca2+; reduced urate
    excretion

Desired Therapeutic Effects:

  1. Relief of heart failure symptoms (reduce pre-load)
  2. Treatment of Na+ and H2O overload
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6
Q

Unwanted side effects of loop diuretics?

A
  1. Hypovolaemia & hypotension
  2. Hypokalaemia; (Hypo –magnesaemia & -calcaemia)
  3. Hyperuricaemia
  4. Dose-related hearing loss (rarely) because same channels are in the inner ear
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7
Q

What are the functions of nitrates in HF?

A

Examples: Glyceryl trinitrate, Isosorbide mononitrate

Indirect nitric oxide (NO) donors

Activate Guanylate cyclase in vascular smooth
muscle cells → cGMP

Predominantly venoselective

Also inhibit platelet aggregation & endothelial
inflammation

Effect: Veno- and (vaso-) dilatation

Reduce preload and to a lesser extent afterload

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8
Q

What is the use of beta blockers in HF?

A

SA node: Decreases heart rate

Myocardium: Decreases contractility

Renal: Decreases renin release, RAAS activation,
vasoconstriction, fluid retention → Decrease blood
pressure

Saves energy and oxygen demand

Reduces Ca cycling and propensity for arrhythmias

Halts progression of the disease

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9
Q

Side effects of spironolactone?

A
  1. Hypotension
  2. Renal impairement
  3. K+ excess
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10
Q

MOA of digoxin?

A

Digoxin is negatively chronotropic (it reduces the heart rate) and
positively inotropic (it increases the force of contraction). In atrial
fibrillation and flutter its therapeutic effect arises mainly via an indirect
pathway involving increased vagal (parasympathetic) tone. This reduces
conduction at the atrioventricular (AV) node, preventing some impulses
from being transmitted to the ventricles, thereby reducing the ventricular
rate. In heart failure, it has a direct effect on myocytes through
inhibition of Na+/K+-ATPase pumps, causing Na+ to accumulate in
the cell. As cellular extrusion of Ca2+ requires low intracellular Na+
concentrations, elevation of intracellular Na+ causes Ca2+ to accumulate
in the cell, increasing contractile force.

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11
Q

Indications for digoxin

A
  1. In atrial fibrillation (AF) and atrial flutter, digoxin is used to reduce
    the ventricular rate. However, a β-blocker or non-dihydropyridine calcium
    channel blocker is usually more effective.
  2. In severe heart failure, digoxin is used as a third-line treatment in
    patients who are already taking an ACE inhibitor, β-blocker and either an
    aldosterone antagonist or angiotensin receptor blocker. It is used at an earlier stage in patients with co-existing AF.
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12
Q

Compare the indications, mechanism of action and place in therapy of heparin and warfarin and novel oral anticoagulants.

A

See notes in drug book

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13
Q

Is aspirin effective in the prevention of stroke in a fib?

A

No- aspirin is not indicated for stroke prevention in A Fib

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14
Q

What is the care pathway in VTE?

A

Patient admitted to hospital&raquo_space; assess risk of VTE&raquo_space;> assess bleeding risk&raquo_space;> balance risk of VTE and bleeding&raquo_space;> offer VTE prophylaxis if approp. do not offer pharm VTE prophylaxis if pt. has any risk factor for bleeding and risk of bleeding outweighs the risk of VTE&raquo_space;» Reassess risk of VTE and bleeding within 24 hours of admission and whenever clinical situation changes

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15
Q

What are the main differences between UFH and LMWH?

A

UFH: short half life and accelerates inhibition of Xa and thrombin

LMWH: longer half life and accelerates inhibition of Xa more than thrombin

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16
Q

How long do we give anticoagulants for DVT?

A

DVT

Below knee = 3 months

Above knee >/= 6 months

Recurrent with removable risk factor - 6 months or for period of risk

Recurrent unprovoked - long term

Before stopping consider

Provoked or spontaneous event

Past history of VTE

Family history of VTE

Predictors of recurrence

17
Q

How long do we prescribe anticoagulants for PE?

A

3- 6 months

Recurrent with removable risk factor - 6 months or for period of risk

Recurrent unprovoked - long term

18
Q

How long do we give anticoagulants in cardiac abnormalities?

A

Cardiac indications

Indefinitely

  • AF, unless reverts to SR
  • Mechanical heart valves
  • 3 months
    Bioprosthetic valves
  • Variable
    Intracardiac thrombus
19
Q

What is the strength of each anticoagulant

A

Rapid onset and offset of action =UFH

Predictable pharmacokinetics
LMWH

Predictable anticoagulation
LMWH

No food or drug interactions
LMWH/UFH

No off-target effects
LMWH

Safe antidote
UFH/Warfarin

Good compliance
LMWH

Reasonable cost
All