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S6 > Pharmacology S9 > Flashcards

Pharmacology S9 Flashcards

1
Q

1 st Line Pharmacological Therapy of hypertension

A

Angiotensin Converting Enzyme (ACE)

inhibitors/ Angiotensin Receptor Blockers (ARB)

§ Calcium channel blockers

§ Diuretics

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2
Q

ACE Inhibitors give examples

A

E.g. lisinopril, ramipril,captopril

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3
Q

ACE Inhibitors
Main side effects

Important side effects

A

Main side effect – dry cough (10-15%)

  • Important side effects
  • Angio-oedema (rare, but more common in black pop.)
  • Renal failure (incl. renal artery stenosis)
  • Hyperkalaemia
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4
Q

Angiotensin Receptor Blockers give examples

A

Eg. Losartan, Valsartan

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5
Q

Angiotensin Receptor Blockers Important side effects

A

Well tolerated few side effects

• Important side effects

  • Renal failure
  • Hyperkalaemia
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6
Q

Calcium Channel Blockers

Three main groups:

A

Dihydropyridines (Nifedipine, Amlodipine)

  • Benzothiazepines (Diltiazem)
  • Phenylalkylamines (Verapamil)
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7
Q

Dihydropyridine Calcium Channel Blockers

Properties

A

Good oral absorption

  • Protein bound > 90%
  • Metabolised by the liver
  • Few have active metabolite
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8
Q

Dihydropyridine Calcium Channel Blockers

Adverse effects:

A

Sympathetic nervous system activation – tachycardia and palpitations

  • Flushing, sweating, throbbing headache
  • Oedema
  • Gingival hyperplasia (rare)
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9
Q

Phenylalkylamines - Verapamil

Properties

A

Impedes calcium transport across the myocardial and vascular smooth muscle cell membrane

  • Class IV anti-arrhythmic agent/prolongs the action potential/effective refractory period
  • Peripheral vasodilatation and a reduction in cardiac preload and myocardial contractility
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10
Q

Phenylalkylamines - Verapamil

Side effects

A

Constipation

  • Risk of bradycardia
  • Reduce myocardial contractility (negative inotrope) can worsen heart failure
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11
Q

Benzothiazepines - Diltiazem

Properties

A

Impedes calcium transport across the myocardial and vascular smooth muscle cell membrane

  • Prolongs the action potential/effective refractory period
  • Peripheral vasodilatation and a reduction in cardiac preload and myocardial contractility
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12
Q

Benzothiazepines - Diltiazem

Adverse effects:

A

Risk of bradycardia

• Less negative inotropic effect than verapamil – can worsen heart failure

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13
Q

Thiazide/Thiazide Like Diuretics

Give examples of

A

Bendroflumethiazide

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14
Q

Bendroflumethiazide: Adverse Effects

A
  • Hypokalaemia
  • Increased urea and uric acid levels
  • Impaired glucose tolerance (especially with beta-blockers)
  • Cholesterol and triglyceride levels increased
  • Actives renin angiotensin system

So we use ACE inhibitors

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15
Q

Alpha Blockers

Give examples

A

Doxazosin

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16
Q

Alpha Blockers

Properties

A

Selective antagonism at post-synaptic a-1 adrenoceptors and antagonise the contractile effects of noradrenaline on vascular smooth muscle

  • Reduce peripheral vascular resistance
  • More effect in upright position
  • Benign effect on plasma lipids / glucose
  • Safe in renal disease
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17
Q

Alpha Blockers (Doxazosin)

Adverse effects:

A

Postural hypotension

  • Dizziness
  • Headache and fatigue
  • Oedema (especially if combined with dihydropyridines)
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18
Q

Beta Blockers

Give examples

A

E.g. Atenolol, bisoprolol, nebivolol

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19
Q

b

-Blockers Adverse Effects

A
  • Lethargy, impaired concentration
  • Reduced exercise tolerance
  • Bradycardia
  • Cold hands – Raynaud’s
  • Impaired glucose tolerance
  • Contraindication - asthma
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20
Q

b

-Blockers
CI

A

Contraindication - asthma

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21
Q

Direct Renin Inhibitor

Give examples

A

Aliskiren

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22
Q

Aliskiren Pharmacokinetics

Main elimination route:

A

Mainly eliminated as unchanged compound in faeces (78%) o Less than 1% is renal excreted o NOT metabolised via cytochrome P450 o Caution in patients at risk of hyperkalaemia, sodium and volumedepleted patients, patients with HF, severe renal impairment and renal stenosis

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23
Q

Aliskiren cautions
Contra indication

significant drug interaction

A

Caution in patients at risk of hyperkalaemia, sodium and volumedepleted patients, patients with HF, severe renal impairment and renal stenosis

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24
Q

Aliskiren Pharmacokinetics

A

Bioavailability ~2.6%

  • t 1/2 ~ 40 hours (range 25-45) - supports once-daily dosing
  • Steady state takes 5-8 days
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25
Q

Centrally acting Agents

Give examples

A

Methydopa

Clonidine

Moxonidine

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26
Q

Classification of Hypertension

Isolated Systolic Hypertension

Grade 1
Grade 2

A

Systolic BP (mmHg)

140-159/ diastolic blood pressure
<90
Grade 2 
Systolic >160 
Diastolic <90
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27
Q

Classification of Hypertension
Optimal
Normal
High normal

A 
Systolic <120
Diastolic <80
Normal
Systolic <130
Diastolic <85
High normal 
Systolic 130-139
Diastolic 85-89
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28
Q

Classification of Hypertension

Hypertension
Grade one mild
Grade 2 moderate
Grade 3 severe

A

Grade 1 (mild)
Systolic 140-159
Diastolic 90-99

Grade 2 (moderate)
Systolic 160-179
Diastolic 100-109

Grade 3 (severe)
Systolic >180
Diastolic >110

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29
Q

Methydopa mechanism of action

A

converted to a-methyl-noradrenaline a potent a2-adrenoceptor agonist

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30
Q

Clonidine mechanism of action

A

direct pre-synaptic a2-adrenoceptor agonist

Centrally acting Agents

31
Q

can be used to treat hypertension in pregnancy

A

a-Methyldopa

32
Q

Moxonidine mechanism of action

A

imidazoline I 1receptor agonist and some a2 agonist effect

Centrally acting Agents

33
Q

Centrally acting Agents

Side effects restrict use:

A

Tiredness/lethargy

– Depression

34
Q

Prognosis may be improved HF

A

RAS antagonism:

  • ACE I / ARB
  • Aldosterone blockade
  • Beta-blocker
35
Q

b-blockers: Physiological effects in HF

A
  1. Reduce heart rate (cardiac beta receptor)
  2. Reduce BP (Reduced CO)

1+2 Þ Reduced myocardial oxygen demand

  1. Reduce mobilisation of glycogen
  2. Negate unwanted effects of catecholamines
36
Q

Minoxidil mechanism of action

A

Direct Acting Vasodilators

Minoxidil – Open ATP-modulated potassium channels thus inhibits influx of Ca++

  • Usually needs to be accompanied by a diuretic and bblocker to reduce effects of tachycardia and fluid retention
  • Other main side-effect is hirsutism
37
Q

Direct Acting Vasodilators

Give examples

A

Minoxidil

Hydralazine

38
Q

Minoxidil side effects

A

tachycardia and fluid retention

• Other main side-effect is hirsutism

39
Q

Hydralazine – mechanism?

A

Hydralazine – mechanism unclear (?similar to minoxidil)

  • Oral or IV
  • Main ADRs: flushing, tachycardia and mild fluid retention
  • A lupus-like syndrome may occur
40
Q

Hydralazine side effects

A

Main ADRs: flushing, tachycardia and mild fluid retention

• A lupus-like syndrome may occur

41
Q

Which drug may lead to lupus like symptoms

A

Hydralazine direct acting vasodilators

42
Q

What is Phaeochromoctyoma

A

Adrenal catecholamine-secreting tumour

  • Adrenaline / Noradrenaline / (dopamine)
  • Paroxysmal symptoms v. sustained high BP
  • Diagnosed: urinary catecholamines / Imaging
  • 10% Rule
43
Q

How to treat Phaeochromoctyoma

A

Treat with non-selective alpha blockers: Direct effect on a1 and a-2 adrenoceptors preventing the action of released noradrenaline

Phenoxybenzamine – oral non competitive Phentolamine – IV competitive for use in hypertensive crisis b-blockers are given AFTER a-blockade

44
Q

non-selective alpha blockers give examples

A

Phenoxybenzamine – oral non competitive Phentolamine – IV competitive for use in hypertensive crisis b-blockers are given AFTER a-blockade

45
Q

Primary Hyperaldosteronism

Causes

A

Causes hypertension

• Includes:

o Conn’s syndrome o Bilateral adrenal hyperplasia

  • Excess secretion of aldosterone
  • Plasma renin suppressed
46
Q

Primary Hyperaldosteronism how to treat

A

Treat with aldosterone antagonists

  • Spironolactone
  • Eplerenone
  • Alternative: high dose amiloride
47
Q

aldosterone antagonists give examples

A

Spironolactone

• Eplerenone

48
Q

Sodium Nitroprusside: mechanism of action when it use

A

Mimics the action of endogenous

nitric oxide on vascular smooth muscle, acting as a potent vasodilator

• Intravenous use with powerful rapid onset and offset

• Breakdown to cyanide – caution in liver disease, but renal excretion. Avoid prolonged use (>72 hours).
Used in Hypertensive Emergencies

49
Q

Hypertensive Emergencies define

A

Very high BP (often over 220/120 mmHg)

  • Associated with acute complications – pulmonary oedema, renal failure, aortic dissection etc
  • Need to reduce BP by ~20% or to 100 mmHg diastolic within 1-2 hours
50
Q

Warfarin: Action

A

Vit K reductase enzyme inhibitors

51
Q

PKs of warfarin

A

Good GI Absorption: Give PO

Preferred choice for long term AC

Slow onset of action:

Heparin cover

Slow offset: t1/2 48 hrs but variable!

Need to stop 3 days before surger

Time to synthesize new clotting factors

Heavily Protein Bound

Caution with drugs that displace it

Hepatic Metabolism: MFO p450 System

Caution with Liver Disease

Caution if used with drugs that affect p450 system

Crosses Placenta:

Do not give in 1 st Trimester: Teratogenic

Do not give in 3 rd Trimester: Brain Haem

If Female patient on warfarin advise re pregnancy

52
Q

Monitoring Warfarin

A

Extrinsic Pathway Factors Prothrombin Time

I.N.R=International Normalised Ratio

53
Q

Drugs potentiating Warfarin

A

3 Ways are Clinically Significant 1. Inhibit Hepatic Metabolism

• Amiodarone, Quinolone, Metronidazole, Cimetidine, ingesting alcohol

  1. Inhibit Platelet function

• Aspirin

  1. Reduce Vitamin K from gut bacteria

• Cephalosporin Antibiotics Albumin Displacement (NSAIDS) & drugs that

decrease GI absorption of Vit K have lesser effect

INR will increase

if you start one de novo

54
Q

Drugs inhibiting Warfarin

A

Antiepileptics (except Na valproate) Rifampicin St Johns Wort

Most work by inducing hepatic enzymes thereby increasing metabolism of warfarin

INR decreased

55
Q

Main Uses of Warfarin

A

DVT (3-6 months) PE (6 Months) Atrial fibrillation (Until Risk > Benefit)

2.0–3.0

Mechanical prosthetic valves (high risk) 2.5–4.5 Patients with recurrent thromboses on Warfarin Thrombosis associated with inherited thrombophilia conditions

Other Uses: Cardiac Thrombus, CVA esp with AF, cardiomyopathy

56
Q

Adverse Effects of warfarin

A

Bleeding / bruising at sites : intracranial epistaksis injection GI loss

Teratogenic at first T
Brain Haem an second T

57
Q

Heparin Molecules

A

Unfractionated Heparin (intravenous, continuous, occasionally, subcutaneous for prophylaxis) 20 kDa

Low Molecular Weight Heparins (subcutaneous) 3-4 kDa

58
Q

Unfractionated Heparin

Mechanism of action

A

Unique pentasaccharide sequence which binds to ANTI-THROMBIN III n This causes conformational change and increased AT III activity n AT III inactivates thrombin (IIa) and factor Xa: but also V,VII,IX,XI

59
Q

Selective factor Xa inhibitors

A

Fondaparinux, idaparinux, rivaroxaban, apixaban, edoxaban

60
Q

Direct thrombin inhibitors

A

Bivalirudin, desirudin, lepirudin, argatroban, dabigatran

No effect on Xa

61
Q

Low Molecular Weight Heparins (LMWH)

Mechanism of action

A

Like UH, have unique sequence to bind to ANTI-THROMBIN III Unlike UH, they do not inactivate thrombin (IIa) Affects Factor Xa specifically. No monitoring required usually. Cleared by Kidneys, care in Renal Failure Less likely to cause thrombocytopenia

62
Q

Pharmacokinetics of UFH & LMWH

A

Must be given parenterally as poor GI absorption

•Rapid onset and offset of action

UFH

LMWH

Dose-response

Non-linearity

Predictable

Bio-availability

Variable

(unpredictable binding to cells and proteins)

Predictable (less

binding to macrophages and endothelium)

Action

Variable

Monitor with APTT test

No monitoring

Little affect on APTT

Administration

IV

SC (Not IM!)

Initiation

Bolus then IVI

OD/BD

63
Q

Uses of UFH & LMWH

A

Prevention of Thrombo-embolism
Peri-operative: LMWH low dose

Immobility: CCF, frail or unwell patient

Used to cover for risk of thrombosis around times of operation in those normally on warfarin but who have stopped it for the surgery, as quick offset time allows its cessation if bleeding

Treatment

n

DVT/PE and AF

n

n

Administered prior to warfarin-quick onset to cover patient whilst warfarin loading is achieved LMWH often used unless fine control required

Acute Coronary Syndromes

Reduces recurrence/extension of coronary artery thrombosis MI, unstable angina

Pregnancy

Can be used cautiously in pregnancy in place of warfarin

64
Q

Adverse Effects of heparin ttt

A

Bruising/bleeding Sites
Intracranial

Injection sites Gastrointestinal loss Epistaxis

Thrombocytopenia (HIT)

Autoimmune phenomenon (usually 1-2 weeks of Rx) May bleed or get serious thromboses Heparin and PF4 on platelet surface are immunogenic – immune complexes activate more platelets, release more PF4, forms more IgG and complexes, leads to depletion of platelets, thrombosis Platelets <100 (or a 50% reduction) Lab assay for these antibodies Stop heparin, add hirudin

Osteoporosis

65
Q

Mechanism of action of hirudin

A

Inhibit factor 2 ( thrombin )

66
Q

Reversal of Therapy of heparin

A

Protamine sulphate
Dissociates heparin from anti-thrombin III Irreversible binding to heparin Allergy/Anaphylaxis

Stop Heparin If actively bleeding, give Protamine Monitor APTT if unfractionated

67
Q

Anti-platelet Drugs

Give examples

A

Aspirin n COX-1 inhibition

Dipyridamole
Phosphodiesterase Inhibitors

Clopidogrel n ADP antagonists

Glycoprotein IIb / IIIa Inhibitors

68
Q

Phosphodiesterase Inhibitors give examples

A

Dipyridamole

69
Q

ADP antagonists antagonist

A

Clopidogrel

70
Q

G IIb / IIIa Inhibitors

Give examples & mechanism of action

A

Abciximab, tirofiban, eptifibatide

Decreases platelet crosslinking by fibrinogen

71
Q

P2Y12 antagonist

Give examples

A

Clopidogrel, prasugrel, ticagrelor blocks P2Y12

P2Y12 receptor decreases cAMP via Gi

72
Q

What is the effect of PGI 2 increases

A

PGI 2 increases cAMP reduces aggregation

73
Q

Glycoprotein IIb/IIIa Receptor Antagonists

Uses

A

High risk ACS

Post PCI (Increases bleeding complications but decreases acute thrombosis and restenosis

S6 (20 decks)

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