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Drugs > Drug Properties > Flashcards

Drug Properties Flashcards

1
Q

Uses of UH?

A

Acute coronary syndrome
Prophylaxis/treatment of DVT/PE/AF
Temporary warfarin replacement

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2
Q

What is UH derived from + what is the consequence of this? (MW, PKs)

A

Derived from pig intestinal mucosa/bovine lung
Linear mucopolysaccharide chains + sulphate GAGs
Variable MW 3,000-40,000
Variable bioavailability - binds to endo cells, macrophages, plasma proteins (albumin)
Rapid onset/offset + T1/2 <60min

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3
Q

How is UH administered?

A

IV dosing - negative charge prevents GI absorption
Give loading dose 60units/kg IV bolus over 5min
Maintenance w/ 12units/kg/hr
Check APTT at 4-8hrs + alter doses

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4
Q

What are the SEs of UH? How is it reversed?

A

Bruising/bleeding = GI, intracranial, epistaxis, injection site
Thrombocytopenia (HIT)
Reversed with protamine sulphate

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5
Q

LMWH

  • Name + doses
  • Uses
  • Size + how they are produced
  • only effects ___
A

Enoxaparin = 1mg/kg bd sc (treatment), 20-40mg od sc (prophylaxis)

  • treatment/prophylaxis for DVT/PE, angioplasty/stent, for STEMI/nSTEMI
  • Smaller chains 4-5kDa + produced by enzymatic depolymerisation of UH
  • Unique sequence for Xa inhibition only
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6
Q

What is warfarin derived from?

A

Coumarin

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7
Q

What are the properties of warfarin? What are its uses

A

Long effect T1/2 takes 5-7days to deplete active factors
Inhibits both extrinsic + intrinsic pathways
Synergistic with heparin
1. Treatment = DVT/PE, mural thrombus
2. Prophylaxis = AF, mechanical heart valves

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8
Q

What are the issues and SEs of warfarin?

A

Narrow therapeutic window
Requires regular INR monitoring = 2-3x/wk or LT monthly
Lifetime risk of haemorrhage = 1-5% and intracranial/GI
TERATOGENIC = 1st trimester (osteodysplasia, optic atrophy, microcephaly) and 3rd trimester (intracranial haemorrhage)

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9
Q

Drug Interactions - via which P450 systems?

A

S = CYP2C9 + R = CYP3A4
Potentiated by p450 inhibitors = alcohol, amiodarone, analgesics, allopurinol, anti-fungals/biotic/acid/lipids
Reduced by p450 inducers = alcohol, azathioprine, barbiturates, carbamazepine/phenytoin, OCP, rifampicin

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10
Q

What are the INR targets?

A 
2-3 = treatment of CVT/PE/AF
3-4.5 = prosthetic valves, recurrent thrombosis, anti-phospholipid syndrome, thrombophilia
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11
Q

What does Prothrombinex do?

A

Complex concentrate from plasma derivatives (blood transfusion)
Contains factors II, VII, IX, X, protein C
For immediate reversal of warfarin in life-threatening bleeding

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12
Q

Dabigatran

A

Oral factor IIa inhibitor
Etexilate = prodrug + highly lipophilic increasing absorption in SI mucosa then cleaved by gut/plasma esterases
Substrate for P-GP channels
T1/2 = 12-14hrs
Renal CL - caution in low eGFR
Alternative to warfarin for DVT/PE/AF only
Reversal = idarucizumab

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13
Q

What are the four main effects of ACEi/ARBs? What are they used for?

A

For HTN/CHF

  1. Vasodilation = reduces arterial/venous pressure
  2. Reduced BV = natriuresis/diuresis
  3. Reduced SNA = can effect RBF/GFR, but prevents compensatory tachycardia with rapid loss of BP
  4. Reduced cardiac/vascular hypertrophy
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14
Q

What are the SEs of ACEi/ARBs? When are they contraindicated?

A 
Dry cough, angioedema - worse with ACEi due to effect on bradykinin
Hyperkalaemia
Postural hypotension
Renal Fx deterioration
Contraindicated - pregnancy + BRAS
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15
Q

Why are ACEi contraindicated in pregnancy?

A

Because Ang II is required for fetal renal development (2nd/3rd tri)
Get fetal renal defects, ongoing oligohydroamnios and fetal hypotension

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16
Q

What effect do ACEis have on the GFR + on renal function

A

Ang II causes both an increase in GFR (from constriction of efferent arterioles) and reduction in GFR (from contraction of mesangial cells reducing SA)
Increasing basal efferent tone drives greater filtration due to increased hydrostatic pressures driving into the bowman’s space
In BRAS = compensatory increased SNA increases EFFERENT tone to counteract the increased AFFERENT tone and maintain GFR/perfusion pressures
Blocking SNA = loss of basal efferent tone and more dramatic fall in pressure serverly reducing renal function

17
Q

What are the cardioprotective effects of ACEis?

A

Increasing bradykinin which increases NO/PG synthesis + mediates additional CV benefits e.g. Reducing fibrotic tissue deposition + apoptotic stress

18
Q

How can ACEi prevent new onset diabetes?

A

Ang II = can induce pro-diabetic state

Due to oxidant stress, pro-inflammation, impaired insulin signalling + reduced insulin sensitivity

19
Q

Metoprolol

A

23.75-190mg od
HTN/HF/angina
Lipophilic (hepatic CL + short T1/2)
B1 selective

20
Q

Propanolol

A

Non-selective
Highly lipophilic = crosses BBB at area postrema
Migraine prophylaxis, anxiety
Centrally reduces SNA

21
Q

Carvedilol - used for

A

Non-specific beta + alpha blocker
Anti-oxidant properties = marked reduction in BP
Used in HF

22
Q

What is esmolol used for?

A

For fine BP control/titration in hypertensive crisis.
Very short T1/2 and metabolised by plasma esterases
Given as IV infusion in ICU

23
Q

What effects do beta blockers have on the CVS (to reduce BP)?

A

Unclear MoA
Decrease HR/cardiac work reducing CO
Inhibit renin
Reset baroreceptors for lower set firing rate
Central actions reduce SNA (ameliorate vasomotor centre)
Pre-synaptic reduction in NE/E release = reduce TPR
-ve chronotrope and -ve inotrope (ST) but +ve inotrope (LT)

24
Q

What effect do beta blockers have on the eye?

A

Reduce aqueous humour production

Reduction in IOP

25
Q

What metabolic effect do beta blockers have

A

Reduce glycogenolysis

Can cause hypoglycaemia in patients with diabetes

26
Q

How do beta-blockers treat thyrotoxicosis

A

-ve chronotropes

Reduce conversion of T4 to active T3 which causes symptoms

27
Q

What SEs do beta-blockers have?

A

Fatigue, bradycardia, hypotension
Acute CHF exacerbation - only use for chronic HF
Can cause vasospasm e.g. Raynauds
Impotence, nightmares
Masks hypoglycaemia
Drug withdrawal when suddenly stopped - due to upregulation of B1 receptors and causes sympathetic overdrive

28
Q

What drug interactions are important with beta blockers?

A

Never give with verapamil = potent -ve chronotropes
Diltiazem = monitor dosing
Other BP lowering drugs
Anti-diabetics = can cause marked hypoglycaemia

29
Q

How do beta-blockers treat angina?

A

Reduced HR/cardiac work = reduced CO
Improve O2 delivery balance
Metoprolol = 23.75-190mg
Atenolol = 25-100mg

30
Q

How do b-blockers treat post-MI?

A

Reduce arrhythmias by limiting sympathetic drive
Reduce ventricular rupture by decreasing BP
Increase cardiac remodelling

31
Q

How do beta-blockers treat HF?

A

Reduce cardiac sympathetic tone = increase coronary filling time, reduce O2 consumption
Upregulat beta-1 receptors
Modulation of post-receptor inhibitory proteins
Attenuate apoptosis
Improve baroreceptor function
Improve LV remodelling

Drugs (6 decks)

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