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Pharmacology > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the main diseases of the cardiovascular system?

A 
Hypertension 
Congestive heart failure
Coronary artery disease
MI
Cardiac arrhythmias
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2
Q

What can cause hypertension?

A
  • increased sympathetic activity
  • renal Disease + increased renin-angiotensin-aldosterone activity = high BP + sodium + fluid retention
  • smoking, obesity + increased sodium consumption
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3
Q

What value is high blood pressure treated?

A

Systolic > 160 mmHg +/or diastolic >100 mmHg

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4
Q

What drugs are used to treat hypertension?

A
  • diuretics
  • sympatholytic drugs
  • vasodilator drugs
  • alpha blockers
  • calcium antagonist
  • angiotensin-converting enzyme inhibitor (ACEi)
  • angiotensin receptor blockers (ARBs)
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5
Q

How do thiazide diuretics work in hypertension?

A

Thiazides e.g. bendroflumethiazide, hydrochlorthiazides
Thiazide like diuretics e.g. indapamide, chlortalidone

Thiazides inhibit the Na+/Cl- co-transporter in the distal convoluted tubule of the nephron.
-increased renal excretion of sodium + water = reduces blood volume +
CO + peripheral resistance + cause vasodilation

Sodium + calcium cause muscle contractions (depolarisation = AP). If the sodium is reduced = causes reduction intracellular calcium = therefore muscle becomes less responsive to vascoconstrictors.
= reduces contraction of heart + strength of AP to be reduced.

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6
Q

What are the main side effects of thiazide diuretics?

A
  • hypokalaemia
  • hyperglycaemia due to increased insulin resistance
  • increase LDL-cholesterol + triglycerides
  • hyperuricaemia (raised uric acid) = can cause gout
  • efficacy reduced if taking NSAIDs
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7
Q

How do beta-adrenoceptor antagonists (beta blockers) work in treatment of hypertension?

A

E.g. atenolol, metoprolol and bisoprolol

They block noradrenaline =
-reduces CO by reducing force + rate of cardiac contraction
-reduce renin secretion by kidney (may explain why beta-blockers are
less effective in elderly how have low renin levels).

Most e.g. atenolol are cardioselective = means mostly work on beta 1 receptor = less likely to affect airway resistance or raise serum cholesterol levels.
However, propranolol blocks both receptors

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8
Q

What are the side effects of beta -blockers?

A
  • cold hands + feet
  • bronchospasm
  • bradycardia
  • fatigue
  • heart failure or conductance block
  • reduce HDL cholesterol + increase triglycerides
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9
Q

How do centrally acting antihypertensives work in treatment of hypertension?

A

E.g. methyldopa
It is converted in adrenergic nerve endings to a false transmitter which stimulates alpha 2 receptors in medulla + reduces sympathetic outflow

E.g. clonidine
Works on post synaptic alpha 2 receptors to inhibit activity of adrenergic neurones.
Withdrawal of drug slowly to prevent rebound hypertension

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10
Q

How do vasodilators work in treatment of hypertension?

A

E.g. minoxidil
-opens ATP-sensitive potassium channels in vascular smooth
muscle cells, causing hyperpolarisation + relaxation of smooth muscle
in blood cells = vasodilation
-used alongside other drugs e.g. loop diuretics or beta blockers as
vasodilation is accompanied by increased CO + tachycardia
-causes hirsutism (used for treatment of baldness).

E.g. hydralazine

  • potent vasodilator that acts on arteries + arterioles
  • not used alone as causes fluid retention
  • Given in hypertension associated with eclampsia
  • side effects; reflex tachycardia (may provoke angina, headaches + fluid
    retention) lupus syndrome
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11
Q

How do alpha blockers work in treatment of hypertension?

A

Block alpha 1 adrenoceptor in smooth muscle of blood vessels, prevents constriction = vasodilation + fall in BP

E.g. prazosin, doxazosin + terazosin

Side effects;

  • postural hypotension
  • drowsiness, dizziness, lack of energy
  • exacerbate stress incontinence in women
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12
Q

How do calcium channel blockers (CCBs) work in the treatment of hypertension?

A

-decease calcium entry into vascular + cardiac cells = reducing intracellular calcium concentration = relaxation of arteriolar smooth muscle
= lower contraction, less depolarisation + reduces peripheral resistance = fall in BP

2 groups

  • Dihydropyridines e.g. nifedipine + felodipine
  • non-dihydropyridines e.g. verapamil + diltiazem

Non-dihydropyridines also influence myocardial muscle cells & reduce myocardial contractivity. Should be avoided in heart failure

CCBs are suitable for pts with asthma, angina + peripheral vascular disease

Side effects - caused by excessive vasodilation

  • dizziness
  • hypotension
  • flushing
  • ankle oedema
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13
Q

How do angiotensin-converting enzyme inhibitor (ACEIs) work in treatment of hypertension?

A

E.g. lisinopril, enalapril, cilazapril

Inhibit angiotensin converting enzyme (ACE) that converts angiotensin I to angiotensin II. = reduces formation of angiotensin II = vasodilation + fall in BP

Also prevent renal absorption of sodium by lowering production of aldosterone (diuretic effect, causing sodium loss + potassium retention).

Side effects

  • CANT be used with potassium sparing diuretics because both effect potassium. But can be used with thiazides + loop diuretics
  • dry cough caused by increased bradykinin (metabolised by ACE)
  • angioedema (swelling in lower layer of skin)
  • proteinuria
  • neutropenia
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14
Q

How do angiotensin receptor blockers (ARBs) (sartans) work in the treatment of hypertension?

A

They block the action of angiotensin II on the AT1 receptor (blocks effect of angiotensin II) = vasodilation + fall in BP

E.g. losartan

Produce lower incidence of adverse effects of ACEI

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15
Q

How does the renin-angiotensin-aldosterone system (RASS) work?

A

Liver produces enzyme ANGIOTENSIN
|
When the BP is low, this stimulates the kidney to secrete the enzyme RENSIN.
|
Combination of angiotensin + renin converts to ANGIOTENSIN I
|
Angiotensin converting enzyme is released from the pulmonary endothelium in lungs, converting angiotensin I to ANGIOTENSIN II
|
Angiotensin II acts on the adrenal gland to release ALDOSTERONE (steroid hormone).
|
Aldosterone acts on the collecting ducts of the nephron causing increased Na+ absorbtion, which causes water retention = increases BP

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16
Q

How is a rise in BP controlled?

A

Sensory receptors (baroreceptors) round in arch of aorta + carotid arteries detect change in pressure within arteries, and send impulses to the vasomotor centre (VMC) in the medulla of brain

Rise in BP causes increased impulses from baroreceptors to the VMC
|
Results in inhibition of VMC + decreased stimulation of SNS = peripheral vasodilation of arterioles + veins + fall in BP.
|
Also causes stimulation of PNS, sinoatrial node inhibited = HR + contractile force reduced

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17
Q

How is a fall in BP controlled?

A

A fall in BP leads to stimulation of VMC
|
Causes increased sympathetic vascoconstriction
|
Impulses from cardiac centre lead to increased CO

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18
Q

What hormones in blood stream have an influence on BP?

A

-adrenaline + noradrenaline are released by adrenal gland in
stress + enhance action of SNS = increasing BP
-nitric oxide is secreted by endothelial cells lining blood vessels + is
vasodilator released on stimulation of PNS
-antidiuretic hormone (ADH) increases reabsorbtion of water and by
increasing blood volume = BP
-inflammatory chemicals e.g. histamine are potent vasodilators - there is
fall in BP in anaphylaxis. Also increase capillary permeability leading to
fluid loss from bloodstream
-alcohol causes fall in BP. It inhibits ADH, depresses VMC + promotes
vasodilation

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19
Q

What 2 factors determine BP?

A

Cardiac output + systemic vascular resistance (SVR)

BP = CO x SVR

CO = dependent on stroke volume (amount of blood leaving one ventricle in one contraction) + HR

SVR = dependent on diameter of arterioles

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20
Q

What 2 main systems control BP?

A
  • ANS -neural + chemical

- RAAS

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21
Q

What are the sources of cholesterol?

A

15% of cholesterol is in the diet, the remaining 85% is made in the liver from acetyl CoA (a product of fat metabolism).

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22
Q

Define hyperlipidemia + hypercholesterolaemia

A

Hyperlipidaemia = raised levels of lipids in the bloodstream.

Hypercholesterolaemia = high cholesterol level

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23
Q

How is cholesterol eliminated?

A

-It is broken down by the liver + converted into bile salts to be
eliminated from the body.
-some cholesterol is reabsorbed from the large bowel + transported back
to the liver to be reused. A high fibre diet binds to the bile acids +
promotes excretion of cholesterol by preventing reabsorption.
-sometimes high levels of cholesterol in the bile can crystallise out to
form gall stones.

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24
Q

How are lipids transported in the bloodstream?

A

-lipids are insoluble + transported around body using lipioproteins.
-lipoproteins are mixture of triglycerides, phospholipids +
cholesterol
-LDL carries 70% of cholesterol. it delivers cholesterol from liver to
peripheral tissues
-body cells have LDL receptors on there surface which can autoregulate.
When the cell has enough cholesterol, it will reduce the number of
receptors on its surface. Excess LDL then remains in bloodstream + may
be deposited in arteries.
-HDL is made in liver + small intestine. It picks up excess cholesterol from
the cells + takes it to the liver to be broken down + transported into bile.
20-30% of cholesterol is transported by HDL.
-triglycerides (TG) are secreted into blood as very low density
lipoproteins (VLDL). VLDL transports cholesterol + triglycerides from
liver to blood stream. Enters muscle cells for energy + adipocytes for
storage. Here it is hydrolysed by lipoprotein lipase into fatty acids.

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25
Q

What is the role of LDL in atherosclerosis?

A

Damage to endothelial lining of the blood vessels, esp in areas of turbulence, allows LDL to penetrate the blood vessel wall.
|
LDL is deposited below inner lining (intima) of the blood vessels
|
Oxidation of LDL occurs over time, which attracts WBCs to area. These scavenge LDL, accumulating cholesterol + become foam cells.
|
When WBCs die, their contents becomes deposited as atheroma
|
A collagen cap is formed over the atheroma, as it grows the vessel is narrowed.
|
Over time plaque may become unstable + rupture may occur = aggregation of platelets + blood clot formation = MI

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26
Q

What is secondary hyperlipodaemia?

A

It is the result of another illness e.g. diabetes or hypothyroidism

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27
Q

What are the lipid-lowering drugs?

A
  • statins
  • fibrates
  • anion-exchange resins
  • cholesterol absorption inhibitors
  • nicotinic acid
  • Fish oils
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28
Q

How do statins lower lipids?

A

E.g. atorvastatin, fluvastatin, pravastatin, rosivastatin and simvastatin

-inhibit enzyme HMG CoA reductase (synthesised cholesterols in liver)
= less cholesterol is synthesised = reduces level of cholesterol in blood
-leads to increased LDL receptors on cell surfaces as there is less
cholesterol available for them = further increases removal of LDL from
blood stream
-more effective if given at night when liver synthesises more cholesterol

Side effects
-GI disturbances
-increase anticoagulant effect of warfarin
-elevated creatine kinase (involved in muscle breakdown)
-breakdown of skeletal muscle (rhabdomyolysis)
Lowers LDL and rise in HDL

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29
Q

How do cholesterol-absorbtion inhibitors work in reducing lipid levels?

A

E.g. Ezetimibe

-inhibits intestinal absorption of cholesterol

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30
Q

How do fibrates work in lowering lipid levels?

A

E.g. benzafibrate, ciprofibrate, fenofibrate and gemfibrozil

-reduce triglycerides by stimulating formation of lipoprotein lipase.
Stimulates clearance of LDL from liver

Side effects;

  • GI disturbances
  • myositis esp if renal functions poor
  • modest effect on LDL
  • raise HDL
  • lower TGs
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31
Q

How do anion-exchange resins lower lipid levels?

A

E.g. cholestyramine and colestipol

-bind bile acids in the intestine + prevent there reabsorption
-this promotes the conversion of cholesterol into bile acids in the liver +
increases LDL receptor activity, increasing clearance of LDL from blood

Side effects;

  • Vit K deficiency = bleeding
  • interfere with absorption of fat soluble vitamins
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32
Q

How does nicotinic acid work in reducing lipid levels?

A
  • vitamin which raises HDL cholesterol + reduces triglycerides
  • inhibits triglyceride synthesis in the liver

Side effects;

  • flushing
  • palpitations
  • GI disturbances
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33
Q

How does fish oils work in reducing lipid levels?

A

E.g. omega-3 fatty acids

-lower triglyceride levels and raise HDL

34
Q

How does benecol and other similar margarines lower lipids?

A

-contains plant stanol Ester which helps block uptake of
cholesterol in the gut = less cholesterol enters bloodstream
(normally 50%, benecol reduces it to 30%).

35
Q

What combo of lipid lowering drugs should not be used together?

A

Fibrates + statins

Because it can increase incidence of myopathy

36
Q

What are the different types of angina?

A

stable angina
-angina of effort
-constant narrowing of a coronary artery
-blood supply to heart muscle is sufficient at rest, but when metabolic
demand increases, pain due to lack of oxygen supply to Ischemic
cardiac muscle occurs

Variant angina (prinzmetal)

  • due to spasm of coronary artery + then narrows
  • can occur at any time

Unstable angina (acute coronary syndrome)

  • can come on at rest
  • usually some rupturing of an atheromatous plaque
37
Q

What drugs are used to treat angina?

A
  • beta blocker
  • calcium channel blocker
  • nitrates
  • potassium channel activator
  • sinus node inhibitor
38
Q

How do nitrates work in treatment of angina?

A

E.g. glyceryl trinitrate (GTN), isosorbide mononitrate (ISMN) and isosorbide dinitrate (ISDN)

-relax smooth muscle = vasodilation
-pro drugs, changed into NO which stimulates the secondary messenger
cyclic GMP. This activates protein kinase = smooth muscle relaxation
-vasodilation reduces cardiac oxygen consumption by reducing
workload of heart
-veins are dilated more than arteries, reducing venous return, + work of
left ventricle
-systemic arteries dilate = this also reduces workload of heart
-diseased coronary vessels don’t respond to vasodilation, but nitrates
can divert blood to Ischemic area by dilating collateral circulation
-relaxation of blood vessel wall relieves coronary spasm in variant angina

Side effects;

  • vasomotor flushing, dizziness, headache
  • hypotension
  • reflex tachycardia-can be prevented if taken with beta blockers
39
Q

How do beta blockers work in treatment of angina?

A

E.g. bisoprolol + metoprolol + atenolol

  • slow HR + force of contraction = reduces oxygen demand of the heart
  • slower HR gives more time for coronary perfusion which occurs in cardiac diastole

Side effects;

  • bronchospasm
  • potentiate Peripheral vascular disease
40
Q

How do calcium channel blockers work in treatment of angina?

A

E.g. nifedipine, diltiazem and verapamil

-block calcium channels in smooth muscle + cardiac muscle
causes;
-vasodilation = fall in peripheral + arterial pressure, + reduce arterial
spasm
-slow HR + decrease force of cardiac contraction
-lower oxygen requirements of Ischemic myocardium by reducing BP
-dihydropyridines e.g. nifedipine + amlodipine act on smooth muscle in
blood vessels = arterial vasodilation

Ditiazem + verapamil SHOULD’NT be combined with beta blockers = profound bradycardia or heart failure

Side effects;

  • flushing
  • headache
  • Peripheral oedema
  • constipation
41
Q

How do potassium channel activators work in treatment of angina?

A

E.g. nicorandil

-dilates both arteries + veins due to nitrate generating properties + potassium channel opening properties

Side effects;

  • headache
  • flushing
  • dizziness
  • nausea
42
Q

How do sinus node inhibitors work in treatment of angina?

A

E.g. ivabradine

-inhibits cardiac pacemaker current = reduces rate of depolarisation
within SA node = reduces HR without reducing force of cardiac
contraction

43
Q

What causes arrhythmias?

A

They result from a disturbance in the generation or transmission of these impulses
-can be due to over-excitability of the heart or to defects of the
conduction system
-may be classified according to site of origin
-can be intermediate or continuous
-re-entry mechanism involved - delayed AP re-invade nearby muscle fibres which depolarise again, establishing a loop of depolarisation.

Clinical features;
-palpitations
-dizziness
-feeling faint or LOC 
Caused by reduced blood supply to brain
44
Q

What is class 1 of Vaughan Williams classification of antiarrhymic drugs?

A

Class 1a = lengthen action potential duration + refractory period e.g. quinidine, disopyramide.
-used for supraventricular + ventricular arrhythmias

Class 1b = block sodium channels and shorten repolarisation time e.g. lidocaine
-useful in ventricular arrhythmias

Class 1c =inhibit fast sodium channel. Delay conduction in His-Purkinje System. Minimal effect of repolarisation time. E.g. flecainide + propafenone

45
Q

What is class 2 of Vaughan Williams classification of antiarrhymic drugs?

A

-beta-adrenoceptor antagonists e.g. atenolol, esmolol
-counteract the dysrhythmic effects of catecholamimes + prolong
refractory period of AV node
-useful in super ventricular dysrhythmias, sinus tachycardia

46
Q

What is class 3 of Vaughan Williams classification of antiarrhymic drugs?

A

-increases refractory period by blocking potassium channels e.g.
Amiodarone, bretylium + sotalol
-effective against most cardiac arrhythmias e.g. paroxysmal supraventricular, nodal, VT, AF, atrial flutter + VF

47
Q

What is class 4 (IV) of Vaughan Williams classification of antiarrhymic drugs?

A
  • calcium channel blockers e.g. verapamil, diltiazem
  • shorten the plateau of AP + reduce force of cardiac contraction
  • used in supraventricular tachycardias e.g. AF
  • shouldn’t be used in WPW or ventricular dysrhythmias

Verapamil can’t be used alongside beta blockers or quinidine because of the cumulative negative inotropic effects

48
Q

What drugs are only used in supraventricular arrhythmias?

A

Adenosine
Verapamil (class IV)
Esmolol (class II)
Digoxin

Uses;
SVT, WPW, control of ventricular rate

49
Q

What drugs are used in ventricular arrhythmias?

A

Class 1a = procainamide, disopyramide
Class 1b = lidocaine, mexiletine + flecainide
Class 1c = propafenone
Class 3 = sotalol + Amiodarone

50
Q

What drugs are used in supraventricular + ventricular arrhythmias?

A

Amiodarone, beta blockers, disopyramide, flecainide, propafenone

51
Q

How does adenosine work?

A

-combines with phosphate group to form ATP.
-has important effects on breathing, heart muscle, nervous
conduction & platelets
-increases potassium conductance + inhibits calcium influx
-it hyperpolarises cardiac conducting tissue = slows rate of rise of
pacemaker potential
-used for SVT

52
Q

How does magnesium work in treatment of arrhythmias?

A

-blocks calcium antagonist + inhibits sodium + potassium channels
-magnesium deficiency predisposes to arrhythmias
-used IV to treat torsades de pointes + arrhythmias following digoxin
overdose
-given IV after MI to prevent occupancy of dysthymias
-prevention of recurrent seizures in eclampsia

53
Q

How does potassium work in treatment of arrhythmias?

A

-hypokalaemia predisposes to serious ventricular arrhythmias esp
after MI

54
Q

How does digoxin work?

A

Stimulates vagal activity, causing release of ACh = slows conduction + prolongs refractory period in the AVN + bundle of His.
By delaying atrioventricular conductance, digoxin increases degree of block + slows + strengthens the ventricular beat.

55
Q

What are the adaptive changes that occur in CHF?

A

-activation of SNS + RAAS
-causes elevation of Hr + increase peripheral resistance. The
workload of heart is increased, increasing the need for oxygen + energy
also.
-stimulation of RAAS contributes to sodium + water retention in heart
failure

56
Q

What occurs in acute heart failure (AHF)?

A

-reduced cardiac output, reduced perfusion of the tissues,
increased pressure in the pulmonary circulation + tissue
congestion
-acute pulmonary oedema + breathlessness
-dyspnoea directly related to high left atrial pressure which raises the
pressure in pulmonary circulation + leads to development of pulmonary
oedema

57
Q

What drugs are used in the treatment of acute HF?

A

Main aim is to REDUCE PRELOAD

  • venodilators e.g. GTN. Nitrates relieve pulmonary congestion
  • diuretics e.g. furosemide (loop diuretic)
  • morphine - venodilator, + will dilate arteries
58
Q

What is cardiogenic shock?

A

Tissue hypoperfusion occurring because of HF.

  • there is peripheral vascoconstriction
  • pt cold & sweating with low systolic Bp <90 mmHg
  • confusion

Aim is to reduce the load on the heart, preserve cardiac function + to maintain optimal BP so kidneys receive adequate blood supply.

Inotropic agents that increase force of cardiac contraction may be needed

59
Q

What is congestive heart failure?

A

Combines both right + left heart failure, producing both pulmonary congestion + peripheral oedema

60
Q

What are the causes of heart failure?

A
  • hypertension
  • valvular Disease
  • cardiomyopathy
  • coronary heart disease
61
Q

What drugs are used in chronic heart failure?

A
  • diuretics
  • ACEi
  • digoxin
  • angiotensin blockade
  • beta blockers
  • aldosterone agonists
  • alpha 1 agonists
62
Q

How do diuretics work in treatment of CHF?

A

Used to treat + control fluid retention by reducing circulatory volume + pre-load

  • should be combined with ACEi or beta blocker
  • loop diuretics e.g. furosemide
  • furosemide works by inhibiting sodium + chloride reabsorbtion from ascending loop of Henle + distal renal tubules = increases potassium excretion + plasma volume, promoting excretion of water. This affects pre-load by reducing water + blood.

Adverse effects

  • potassium loss
  • digitalis toxicity may be precipitated by overdiuresis + hypokalaemia
  • metabolic alkalosis

In mild heart failure, thiazides e.g. bendroflumethiazide or metolazone May be used esp if hypertensive

63
Q

How do ACEi work in treatment of CHF?

A

E.g. cilazapril, lisinopril + ramipril

-blocks the RAAS (reduces generation of angiotensin II)
-ACEi vasodilate = gives diuretic effect + causes loss of sodium +
retention of potassium
-decrease cardiac preload + afterload

64
Q

How to beta blockers work in the treatment of CHF?

A

-reduction in HR = improves coronary blood flow + decrease in
force of cardiac contraction = decrease in myocardial oxygen
demand
-reduced automaticity = lessens cardiac arrhythmias
-less renin produced

65
Q

How do aldosterone antagonists work in treatment of CHF?

A

E.g. spironolactone competes with aldosterone for intracellular aldosterone receptors in cells of renal distal tubule = increased sodium loss = water loss

It’s a potassium sparing diuretic, often used in combo with loop diuretics

Side effects;

  • hyperkalemia
  • gunaecomastia
66
Q

How does inotropes work in treatment of CHF?

A

-increase concentration of calcium in cardiac muscle cells
-dobutamine is a sympathomimetic that stimulates the beta 1
receptor = increases formation of cAMP = increases calcium in muscle
cell
-phosphodiesterase inhibitors e.g. milrinone inhibit enzyme that destroys cAMP so it builds up = increasing calcium concentration
-digoxin is a cardiac glycoside. It blocks the Na+/K+/ATPase pump in the
cells membrane = calcium not extruded from cell so builds up =
increasing contractility.

Uses;

  • improve cardiac output + maintain tissue oxygenation (shock)
  • maintain adequate organ perfusion
67
Q

What are the effects of digoxin in treatment of CHF?

A

Inotropic effects

  • increase of calcium in muscle cell
  • increase force of cardiac contractility
  • increases excitability + automaticity of contractile + pacemaker cells - can lead to ectopic beats

Parasympathetic effects

  • sinus bradycardia
  • increased refractory period in AV node = better ventricular filling

Half life = 36-48h (takes a week to obtain stable plasma level).

Side effects;

  • particular or complete AV block
  • excessive bradycardia
  • ventricular extrasystoles
  • N+V
  • abdo pain
68
Q

How does dopamine work in the treatment of CHF?

A

Acts via D1 + D2 receptors via G-protein coupled receptors to lead to increased or decreased levels of cAMP.

Effects;

  • increased cardiac contractility
  • increased HR
  • increased cardiac output
  • increased coronary blood flow
  • fall in renal blood flow
69
Q

What is haemostasis + what are the 3 stages?

A

Haemostasis is the stopping of blood flow from damaged blood vessels.
Stages;
1. Contraction of blood vessels
2. Adhesion + activation of platelets - formation of a platelet plug
3. Formation of fibrin + an insoluble blood clot

70
Q

What 3 classes of drugs are used in the treatment + prevention of thrombosis?

A
  • anticoagulants
  • anti platelets
  • thrombolytics
71
Q

How are anticoagulants used in treatment of thrombosis?

A

E.g. heparin, warfarin

Heparin
-stops formation of fibrin
-heparin combines and activates antithrombin III = neutralises factor Xa
+ inhibits thrombin
-reduces adhesiveness of platelets
-low therapeutic index
-low-molecule weight heparin e.g. dalteparin

Side effects;

  • bleeding. Protamine sulphate is antidote
  • heparin induced thrombocytopenia- severe drop on platelet count
  • osteoporosis
  • hypoaldisteronism + hyperkalemia

Warfarin

  • prevents reduction of vitamin K (needed for clotting process) - inhibits enzyme which reduces vitamin K in liver + interferes with formation of vitamin K clotting factors e.g. prothrombin
  • excess vitamin K + warfarin compete with each other - antidote is vit K
  • takes 2-7 days for onset - heparin used for immediate anticoagulation
  • crosses placenta where heparin doesn’t

Side effects;

  • haemorrhage
  • interaction with food + drugs e.g. green veg has Vit K, antibiotics may suppress action of gut bacteria + reduce Vit K + increase anticoagulation
  • warfarin highly bound to plasma albumin, aspirin + NSAIDs can complete and displace warfarin = increases amount of free warfarin
  • Amiodarone + cranberry juice can metabolise warfarin
72
Q

What anti-platelet drugs are used in treatment of thrombosis?

A

-Aspirin
-dipyridamole
-platelet ADP receptor antagonists
-fibrinolytic drugs
-angioplasty -stent used to hold walls of coronary artery open
-haemostatics e.g. TXA, prevents clot breakdown by inhibiting
fibrinolysis, vasopressin

73
Q

How is aspirin used in treatment of thrombosis?

A

-alters balance between thromboxane, which promotes platelet.
aggregation + prostacyclin, which inhibits it
-inhibits COX - found in platelets + needed for manufacture of
prostaglandins including thromboxane which increases stickiness of
platelets

74
Q

How does dipyridamole work in treatment of thrombosis?

A

Dipyridamole
-inhibits phosphodiesterase (enzyme needed for uptake of adenosine
into platelets + other cells)
-used with warfarin to prevent thrombosis formation on prosthetic heart
valves
-reduces platelet aggregation by increasing cAMP levels

75
Q

How do platelet ADP receptor antagonists work in treatment of thrombosis?

A

Clopidogrel
-inhibits ADP binding to its receptors on platelet surface = helps
prevent platelet binding to fibrin
-inhibits expression of glycoprotein IIb/IIIa receptors

Side effects;

  • bleeding esp if given in combo with aspirin
  • indigestion, abdo discomfort
  • blood disorders

Glycoprotein IIb/IIIa antagonists
-compete with fibrinogen to occupy glycoprotein IIb/IIIa receptor on
platelets = preventing platelet aggregation by blocking binding of
fibrinogen to platelet receptors
-e.g. abciximab

76
Q

How do fibrinolytic drugs work in treatment of thrombosis?

A

Streptokinase

  • converts plasminogen to plasmin = potentiates fibrinolysis
  • can cause allergic reactions
Tissue plasminogen activator (tPA)
-alteplase is a recombinant tPA + mimics endogenous molecule that  
  activates fibrinolytic system 
-used in pts with strep infections 
-increases risk of stroke

Reteplase
-doesn’t cause allergic reactions

77
Q

What is erythropoiseis, and what does it require?

A

It’s the production of WBCs, requires iron, vitamin B & folic acid. Deficiency in any of these causes anaemia.

78
Q

What is the function of iron?

A
  • nucleus of heam is formed by iron
  • deficiency results in small RBCs with insufficient haemoglobin
  • iron administration may be needed in chronic blood loss (heavy periods), pregnancy, gut abnormalities e.g. coeliac Disease and premature births.

-iron preparations contain ferrous salts e.g. ferrous sulphate

Side effects;
-GI upset

79
Q

What is the function of Vitamin B12

A

-essential for DNA synthesis

80
Q

What drug is used to treat haemolytic anaemia?

A

Eculizumab because it reduces red blood cell destruction

Pharmacology (11 decks)

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