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Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Describe phase 4 of action potential in cardiac myocytes

A

Outward flux of potassium through Ik1 is dominant. Vm is not exactly Ek as there is a small inward movement of sodium.

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2
Q

During phase 4 how is the concentration gradient maintained?

A

Sodium-potassium pump

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3
Q

Describe phase 0 of action potential in cardiac myocytes

A

sodium channels rapidly open, Ina resulting in an inward flux of sodium

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4
Q

Why is phase 0 only brief?

A

Sodium channels enter an inactivate state which they only recover from after repolarisation

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5
Q

Describe phase 1 of action potential in cardiac myocytes?

A

Rapid inactivation of Ina, activation of transient outward potassium current called Ito

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6
Q

What happens to calcium in phase 2?

A

moves through L type channels relatively slowly to produce a ICaL current

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7
Q

What happens to potassium in phase 2?

A

Ik1 decreases Ito continues but reduced with time as voltage gated rectifier channels open

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8
Q

Describe phase 3 of action potential in cardiac myocytes

A

Outward flux of potassium is dominant as ICaL, calcium channels begin to inactivate white more Ikr and Iks activate

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9
Q

What is the difference between atrial and ventricular cardiac cells?

A

phase 2 is less evident in atrial myocytes as there is an additional ultra rapid potassium rectifier current Ikur

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10
Q

Describe what happens in nodal tissue

A

Depolarisation is caused by opening of L type calcium channels when a threshold is reached. When the potential reaches 10mV delayed rectifier potassium channels open bringing about repolarisation

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11
Q

How is pacemaker potential regulated?

A
  • potassium efflux - calcium influx - HCN response to hyper polarisation by moving sodium into the cell
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12
Q

Define automaticity

A

spontaneously polarise without external stimuli

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13
Q

Describe the funny current

A

hyper polarisation activates ‘hyper-polarisation activated cyclic nucleotide gated channels’ HCN

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14
Q

What drug can be used to block HCN?

A

Ivabradine - used to decrease the pacemaker slope and reduce heart rate in angina.

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15
Q

Describe sympathetic regulation of cardiac rate and force

A

noradrenaline & adrenaline activate beta1 adrenoceptors in nodal and myocardial cells

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16
Q

What is the effect of an activated beta 1 adrenoceptor?

A

coupling through Gs alpha subunit stimulates adenylyl cyclase to increase the intracellular concentration of cAMP producing cellular responses

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17
Q

Name seven cellular responses caused by activation through Gs beta 1 adrenoceptors

A
  • increase SA node action potential frequency & heart rate due to enhanced If and ICaL
  • increase contractility due to increase in calcium influx
  • increase conduction velocity in AV node due to enhance If and ICaL
  • increase automaticity
  • increase activity of sodium potassium pump - increase mass of cardiac muscle
  • decrease in duration of systole
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18
Q

What does activation of cAMP do?

A
  • increases calcium influx by phosphorylation of the channel to enhance contraction
  • increase rate of calcium pump to increase the rate of contraction
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19
Q

Describe parasympathetic regulation of cardiac rate and force

A

acetylcholine activated M2 muscarinic cholinoceptors in nodal cells

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20
Q

What is the effect of activating M2 muscarinic receptors?

A

coupling through Gi protein; - via alpha subunit inhibits adenylyl cyclase & reduces cAMP - via beta/gamma subunit dimer, opens specific potassium channels (GIRKs in SA node)

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21
Q

What does signalling through Gi activation cause?

A
  • decreased SA node action potential and heart rate due to reduced ICaL and If
  • decreased contractility due to decrease in phase 2, decreased calcium
  • decreased conduction in AV node due to decreased calcium channels & hyper polarisation via GIRKs
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22
Q

Name a medical condition parasympathetic stimulation can cause

A

arrhythmias

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23
Q

In six steps briefly describe contraction

A
  1. ventricular action potential
  2. opening of voltage activated calcium channels mainly L type during phase 2
  3. calcium influx into cytoplasm
  4. calcium release from the sarcoplasmic reticulum
  5. calcium binds to troponin C and shifts tropomyosin our of the actin
  6. cross bridge formation between actin and myosin results in contraction via the sliding filament mechanism
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24
Q

Name the channels calcium moves through in calcium induced calcium release

A

Ryanodine type 2 channels

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25
Q

In six steps describe relaxation

A
  1. repolarisation in phase 3/4
  2. voltage activated L type calcium channels return to closed state
  3. calcium influx ceases, calcium efflux occurs by the sodium/calcium exchanger
  4. calcium release from the SR ceases, active removal of calcium from the cytoplasm by the calcium pump
  5. calcium dissociated from troponin C
  6. cross bridges between actin and myosin break causing relaxation
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26
Q

Give three examples of beta agonists

A
  • dobutamine - adrenaline - noradrenaline
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27
Q

What is the effect of beta agonists?

A

enhance the sympathetic system - increase force, rate and cardiac output - decrease efficiency due to increased oxygen consumption

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28
Q

Name two clinical uses of adrenaline

A
  • cardiac arrest - anaphylactic shock
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29
Q

Name one clinical use of dobutamine

A
  • reversible heart failure
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30
Q

What does the effect of beta antagonists depend on?

A

How much the sympathetic system is activated

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31
Q

Name the three types of beta antagonist

A

Non-selective (act on beta 1 and 2 receptors) Selective (act on beta 1 or 2) Partial

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32
Q

Give an example for each type of antagonist

A

non-selective - propranolol selective - atenolol, bisoprolol, metoprolol partial - alprenolol

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33
Q

What are the pharmacodynamic effects of beta blockers?

A

little effect at rest but reduce rate, force and output during exercise. Coronary vessel diameter is reduced

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34
Q

Name four clinical uses of beta blockers

A
  • arrhythmias - angina - heart failure - hypertension
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35
Q

Describe how a beta blocker can be used to treat arrhythmias

A

excess stress can cause tachycardia or spontaneous activation of pacemaker cells. Beta blockers decrease excess sympathetic drive to restore sinus rhythm and delay conduction through the AV node

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36
Q

State six adverse effects of beta blockers

A
  • bronchospasm - aggravation of cardiac failure - bradycardia - hypoglycaemia - fatigue - cold extremities
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37
Q

Give an example of a non-selective muscarinic antagonist

A

atropine

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38
Q

Name the pharmacodynamic effect of atropine

A
  • increase heart rate - no effect on arterial BP or response to exercise
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39
Q

State two clinical uses of atropine

A
  • bradycardia particularly following an MI - anti cholinesterase poisoning
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40
Q

What is digoxin?

A

A cardiac glycoside that increases contractility of the heart

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41
Q

How does heart failure occur?

A

when the cardiac output is insufficient to provide adequate tissue perfusion

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42
Q

Name the class of drugs that enhance contractility

A

inotropic drugs

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43
Q

How do inotropic drugs work?

A
  • inhibit sodium potassium pump
  • increase sodium and reduce Vm
  • decrease sodium/calcium exchange to increase calcium
  • increase storage of calcium in SR
  • increase CICR and increase contractility
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44
Q

What does digoxin bind to? When is it dangerous?

A

alpha subunit of sodium potassium pump in competition with potassium. Dangerous when potassium levels are low

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45
Q

Name three clinical uses of digoxin

A
  • IV in acute heart failure - Orally in chronic heart failure - Atrial fibrillation
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46
Q

State six adverse effects of digoxin

A
  • excessive depression of AV node conduction
  • propensity to cause arrhythmias
  • nausea
  • vomiting
  • diarrhoea
  • disturbances in colour vision
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47
Q

What does levosimendan do?

A
  • Binds to troponin C in cardiac muscle sensitising it to the action of calcium. - Opens Katp channels in vascular smooth muscle causing vasodilatation
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48
Q

Name two indilators

A
  • amrinone - milrinone
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49
Q

What do indilators do?

A
  • Inhibit PDE in cardiac and smooth muscle cells therefore increasing cAMP - increase contractility and decrease peripheral resistance
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50
Q

Name three anti-cholesterol drug classes

A
  • statins - fibrates - PCSK 9 Inhibitors
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51
Q

Name three anti-hypertensive drug classes

A
  • diuretics - beta blockers - vasodilators
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52
Q

Name four anti-anginas drugs

A
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53
Q

State three uses of organic nitrates

A
  1. to treat acute angina 2. prophylaxis for angina 3. to treat pulmonary oedema
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54
Q

State three uses of calcium channel blockers

A
  1. to treat hypertension 2. to treat stable angina 3. to control heart rate in patients with supra ventricular arrhythmias
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55
Q

Define angina

A

pain that occurs when the oxygen supply to the myocardium is insufficient to meet metabolic demands

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56
Q

What are the three types of angina?

A
  • stable - unstable - variant
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57
Q

Describe stable angina

A

fixed narrowing of the coronary vessels as a consequence of atherosclerosis - characterised by pain on exertion

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58
Q

Describe unstable angina

A

due to platelet -fibrin thrombus in association with an atheromatous plaque - characterised by pain to less and less exertion

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59
Q

What is variant angina associated with?

A

coronary artery spasm

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60
Q

What do organic nitrates get converted into?

A

Nitric oxide

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61
Q

What is the result of nitric oxide formation?

A
  • venorelaxation - arteriolar dilatation - increased coronary blood flow - decreased preload, after load & improved perfusion
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62
Q

In patients with angina what are the added benefits of increased blood flow & decreased preload?

A

Increased blood flow - redirected to ischaemic area Decreased preload - decreased myocardial oxygen requirement

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63
Q

Describe how blood can be equally distributed in the myocardium

A

Due to plaques narrowing the arteries untreated CAD will lead to reduced flow to ischamic myocardium. However, nitrates dilate the collateral and therefore allow even distribution to both normal and ischaemic areas

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64
Q

Name two types of nitrate used to treat angina

A
  • Glyceryltrinitrate
  • Isosorbide Mononitrate
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65
Q

Describe GTN

A
  • short acting (30mins) undergoes first pass metabolism
  • administered sublingually as a tablet or spray
  • can be delivered as a transdermal patch for a sustained effect
  • Before exertion in stable angina or IV with aspirin in unstable angina
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66
Q

Describe ISMN

A
  • longer acting, resistant to first pass metabolism
  • administered orally for prophylaxis & sustained effect
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67
Q

What are the side effects of organic nitrates?

A
  • headaches
  • hypotension & fainting
  • reflex tachycardia (prevented by beta blockers)
  • formation of methaemoglobin (oxidation product of haemoglobin which does not carry oxygen)
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68
Q

What is meant by tolerance?

A

Repeated administration may be associated with a diminished effect, most likely to occur in long acting drugs

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69
Q

How do calcium channel blockers work?

A

Physically block or prevent the opening of L type channels in excitable tissues in response to depolarisation & so limit increased calcium

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70
Q

State the three main types of calcium channel blocker

A
  • verapamil (selective for cardiac L type channels, block channels)
  • amlodipine (smooth muscle L type channels, act alosterically to prevent opening)
  • diltiazem (intermediate selectivity)
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71
Q

Name three clinical uses of calcium channel blockers

A
  • hypertension
  • angina
  • dysrhythmias
72
Q

How can calcium channel blockers be used to treat hypertension?

A

reduced calcium entry to vascular smooth muscle causes arteriolar dilatation reducing TPR and MAP.

73
Q

What caclium channel blockers are preferred in treatment of hypertension?

A

Those with a selectivity for smooth muscle L type channels to minimise unwanted effects on cardiac muscle

74
Q

What are the adverse effects of vasodilatation?

A
  • hypotension
  • dizziness
  • flushing
  • swollen ankles
75
Q

How can calcium channel blockers be used to treat angina?

A

Prophylactic treatment in combination with GTN if beta blockers contraindicated. Arteriolar dilatation decreases afterload & oxygen requirement

76
Q

What type of calcium channel blocker has little effect on the heart?

A

Amlodipine

77
Q

What is the effect of diltiazem & verapamil?

A

Negative inotropic effect by activation of baroreceptor reflex in response to vasodilatation & sympathetic activity

78
Q

How can calcium channel blockers be used to treat dysrhthmias?

A

Reduced ventricular rate in rapid AF by supression of conduction through AV node

79
Q

When must verapamil not be used?

A

Heart failure - verapamKILL

80
Q

Name an ACE inhibitor and explain its mode of action

A

Lisinopril - blocks the conversion of angiotensin I to angiotensin II

81
Q

What are the effects of ACE inhibitors?

A
  • cause venous & arterial dilatation
  • reduce the release of aldosterone
  • reuduce growth action of angiotensin IIon the heart and vasculature

All of which decrease blood pressure

82
Q

What are the adverse effects of ACE inhibitors?

A
  • hypotension
  • dry cough
  • hyperkalaemia
  • angioedema
83
Q

How to angiotensin I receptor blockers work?

A

They have similar properties to ACE inhibitors but they do not inhibit bradykinin metabolism. Useful if patients get a dry cough from ACE inhibitors

84
Q

Name two circumstances where ACE and ARB are contraindicated

A
  • Pregnancy
  • Bilateral renal artery stenosis
85
Q

What are the clinical uses of ARBs?

A
  • hypertension
  • cardiac failure
  • following MI
86
Q

Describe the use of beta adrenoceptor antagonists in the treatment of angina

A

Beta blockers can be used to

  • decrease myocardial oxygen requirement
  • counter elevate sympathetic activity associated with ischaemic pain
  • increase time spent in diastole improving perfusion to the left ventricle
87
Q

Describe the use of beta blockers in the treatment of hypertension

A

restore normal blood pressue by reducing cardiac output, renin release & a CNS action to reduce sympathetic activity

88
Q

How can beta blockers be used to treat heart failure?

A

combination with other drugs to suppress adverse effects associated with elevated activity of sympathetic nervous system

89
Q

How do potassium channel openers work?

A

They antagonise intracellular ATP (which closes the channels). This causes hyperpolarisation which switches off the L type channel leading to relaxation

90
Q

Name two potassium channel openers

A
  • minoxidil - severe hypertension
  • nicorandil - angina
91
Q

Why is minoxidil a last resort?

A

It causes reflex tahchycardia (beta blockers can stop) and salt/water retension (diuretics can stop)

92
Q

How do alpha adrenoceptor antagonists work?

A

Blcoks alpha 1 adrenoceptors, reducing sympathetic transmission and MAP by vasodilatation

!! They also decrease sympathetic transmission in benign prostatic hyperplasia

93
Q

Name two examples of alpha adrenoceptor antagonists

A

Prazosin & Doxasin

94
Q

What is the adverse effect of alpha adrenoceptor antagonists?

A

Postural Hypotension

95
Q

Are lipids soluble or insoluble?

A

Insoluble

96
Q

What is the function of lipids?

A
  • energy sources
  • precursors for hormones & signalling molecules
97
Q

How are lipids transported?

A

In the blood within lipoproteins

98
Q

What do lipoproteins consist of?

A
  • a hydrophobic core containing esterified cholesterol & triacylglycerols
  • a hydrophilic coat of amphipathic cholesterol, phospholipids & apoproteins
99
Q

What is the significance of apoproteins?

A

Recognised by receptors in the liver allowing lipoproteins to bind

100
Q

Name the four classes of lipoproteins and state what apoprotein they contain

A

HDL (apoA-I and apoA-II)

LDL(apoB-100)

VLDL (apoB-100)

Chylomicrons (apoB-48)

101
Q

What is the function of apoB lipoproteins?

A

carry TAGs to muscle for ATP biogenesis or adipocytes for storage

102
Q

Describe chylomicrons

A

formed in intestinal cells, transport dietary TAGs - the exogenous pathway

103
Q

Describe VLDL

A

formed in the liver, transport TAGs synthesised by that organ - endogenous pathway

104
Q

Describe the life cycle of apoB lipoproteins

A
  1. Assembly with apoB-100 in the liver & apoB-48 in the intestine
  2. Intravascular metabolism
  3. Receptor mediated clearance
105
Q

How are chylomicrons assembled?

A

Monoglycerides and fatty acids diffuse into enterocytes where they form TAGs.

Cholesterol moves into enterocytes through NPC1L1 where it gets esterificated to form cholesteryl ester

The ribosome produces apoB-48 and MTP adds TAGs to the vesicle. Cholesteryl ester is added to the vesicle and a chylomicron is produced.

106
Q

After being assembled what happens to the chylomicron?

A

It gains an apoA-1 before leaving the enterocyte by exocytosis

107
Q

How is a VLDL assembled?

A

From fatty acids in the liver, apoB-100 is added with additional TAGs and cholesteryl ester.

108
Q

How are chylomicrons and TAGs activated?

A

By the addition of apoC-II from HDL

109
Q

Name the enzyme associated with the endothelium in capillaries

A

Lipoprotein lipase

110
Q

How are apoB lipoproteins metabolised?

A

ApoC-II binds to lipoprotein lipase causing the release of TAGs from the core. This releases glycerol and fatty acids into the tissues.

111
Q

What is left in the remnants?

A

Cholesteryl esters

112
Q

In five steps describe the clearance of apoB lipoproteins

A
  1. Chylomicrons & VLDL rich in cholesteryl ester dissociate from LPL
  2. ApoC-II is exchanged for ApoE from HDL
  3. Remnants return to the liver & are metabolised by hepatic lipase
  4. Chylomicrons & 50% VLDL are cleared by endocytosis into hepatocytes
  5. VLDL remnants loose TAG through hepatic lipase & become smaller & enriched with cholesteryl ester via IDL they become LDL lacking in ApoE
113
Q

What is LDL clearance dependent on?

A

LDL receptor

114
Q

Describe LDL clearance

A
  1. LDL binds to LDL receptors and is endocytosed
  2. In the lysosomes cholesterol is released from cholesteryl ester
115
Q

What does the released cholesterol do?

A
  • inhibits HMG-coA reductase
  • down regulates LDL receptor expression
  • stored or used as a precursor for bile salt synthesis
116
Q

What is the function of HMG coA reductase?

A

Rate limiting factor in the synthesis of new cholesterol

117
Q

Describe the process which makes LDL ‘bad cholesterol’

A
  1. Uptake of LDL from the blood into the intima causes LDL to be oxidised to OXLDL
  2. Migration of monocytes through the endothelium means they become macrophage
  3. Macrophage ingest OXLDL to produce foam cells & form a fatty streak
  4. Release of inflammatory substances from various cell types causes smooth muscle & collagen to move into the intima
  5. Atheromatous plaque of a lipid core & fibrous cap is formed
118
Q

What makes HDL ‘good cholesterol’?

A

HDL removes cholesterol from cells by transporting it to the liver

119
Q

How is HDL formed?

A

In the liver, apoA-I, surface phospholipid & unesterified cholesterol form pre ß HDL

pre ß HDL matures by the surface cholestrol being esterifed and moving to the core to form spherical alpha HDL

120
Q

What are the two methods of reverse cholesterol transport?

A
  • HDL reaching the liver interacts with a receptor that allows transfer of cholesterol & cholersteryl esters into hepatocytes
  • in the plasma cholesteryl transfer protien mediates transfer of cholesteryl esters from HDL to VLDL and LDL
121
Q

Name three drugs used to treat high cholesterol

A
  • statins
  • Fibrates
  • Cholesterol Absorption Inhibitors
122
Q

What is the mode of action of statins?

A

Act as competitive inhibitors of HMG-CoA reductase - a rate limiting step in cholesterol synthesis

123
Q

What does a decrease in cholesterol synthesis result in?

A

Increased LDL expression & enhanced clearance of LDL

124
Q

How are statins administered?

A

Orally at night

125
Q

What are the side effects of statins?

A
  • Myositis (muscle diseases involving inflammation & degenerative changes)
  • Rhabdomyolosis (rapid breakdown of skeletal muscle) - increased if combined with fibrate
126
Q

What is the mode of action of fibrates?

A

Act as agonists of PPARalpha a nuclear receptor to enhance transcription of genes encoding LPL

127
Q

What are the side effects of fibrates?

A

Usually increased incidence compared to statins

  • myositis

!! avoid in alcoholics due to increased risk of rhabdomyolosis & hyperglyceridaemia !!

128
Q

How do cholesterol absorption inhibitors work?

A

Bile acid resins cause the excretion of bile salt resulting in more cholesterol to be converted into bile salts. As a result they cause;

  • decreased TAG absorption
  • increased LDL expression
129
Q

Give an example of a cholesterol absorption inhibitor

A

Ezetimibe

130
Q

Describe Ezetimibe

A

New agent, inhibits NPC1L1 transport protein in enterocytes to reduce cholesterol absorption, decreasing LDL

131
Q

When is ezetimibe administered?

A

When statins alone do not work, administerd orally but have many GI side effects

!! not used in breast feeding females !!

132
Q

When a vessel wall is damaged what is the very first thing to happen?

A

Vasoconstriction

133
Q

How is a platelet acitvated?

A

Collagen bound to vWF binds to the platlet activating it

134
Q

What two things will platelet activation result in?

A
  • platelet extends pseudopodia
  • platelet releases thromboxane A2
135
Q

Describe the pathway by which thromboxane is synthesised

A
136
Q

When thromboxane A2 is released from platelets what two things does it do?

A
  • binds to GPCR TXA2 receptors causign release of 5-HT (serotonin) and ADP
  • binds to vascular smooth muscle to cause vasoconstriction
137
Q

What does thromboxane A2 and ADP go on to do?

A

Binds to purine receptors

138
Q

Name three consequences of binding to purine receptors

A
  • activates further platelets
  • exposes acid phospholipids to initate blood coagulation
  • aggregates platelets into a soft plug
139
Q

How is the soft plug made?

A

Increased expression of GPIIb /IIIa receptors which acitvate fibrinogen

140
Q

Describe the coagulation cascade

A
  1. Tenase (IXa & VIIIa) turn factor X into Xa and Va
  2. Prothrombinase (Xa & Va) turns prothrombin (II) into thrombin (IIa)
  3. Thrombin causes fibrinogen to be converted into fibrin forming a solid clot
141
Q

What drugs are used for arterial thrombus? Where do they usually lodge?

A

Antiplatelets, emboli lodge in carotid (stroke) or coronary (MI)

142
Q

What drugs are used for venous thrombus? Where do emboli usually go?

A

Anticoagulants, emboli lodge in the lungs causing a PE

143
Q

Name four clotting factors that are precursors to active factors

A

II, VII, IX & X are precursors for IXa and Xa

144
Q

How do precursors become active factors?

A

post translational modifications e.g. carboxylation of glutamate residues

145
Q

What does carboxylation require?

A

Vitamin K in its reduced form

146
Q

How does warfarin work?

A

Prevents the production of reduced vit K

  • renders factors IXa and X inactive
  • blocks coagulation
  • takes a few days to work as active factors are removed from the plasma
147
Q

What is the problem with warfarin?

A

low therpaeutic effect that must be monitored using INR, overdosage can be treated with vitamin K

148
Q

In what circumstances is there a higher risk of haemorrhage?

A
  • liver disease
  • high metabolic rate
  • drug interactions
149
Q

In what circumstances is there a higher risk of thrombosis?

A
  • physiological state (pregnant/hypothyroid)
  • Vit K consumption
  • Drug interactions
150
Q

What is antithrombin III?

A

An inhibitor of coagulation by neutralising serine protease factors

151
Q

How does heparin work?

A

Binds to antithrombin, increasing its affinity for clotting factors Xa and IIa increasing their rate of inactivation

152
Q

What is the difference between the binding of IIa and Xa?

A

IIa needs heparin to bind to both IIa and antithrombin III whereas heparin only needs to bind to ATIII in Xa

153
Q

How is heparin administered/eliminated?

A

IV or SC, clotting test is required for optimum dose and is eliminated by zero order

154
Q

How do low molecular weight heparins work?

A

Inhibit Xa but not IIa, preferred except in renal failure

155
Q

Name two low molecular weight heparins

A
  • enoxaparin
  • dalteparin
156
Q

Name two drugs that act in a similar way to LMWHs

A
  • fondaparinux
  • idrabioraparinux
157
Q

How are LMWHs administered/eliminated?

A

SC administration & renal excretion

158
Q

State four adverse effects of heparin & LMWHs

A
  • haemorrage
  • osteoperosis
  • hypoaldosteronism
  • hypersensitivity reactions
159
Q

If a patient is haemorrhaging due to heparin what drug must be given

A

IV protamine sulfate

160
Q

How do orally active inhibitors work?

A

Directly inhibit;

thrombin - dabigatron etexilate

factor Xa - rivaroxaban

161
Q

What is the advantage/disadvantage of orally active inhibitors?

A

Convinent but no agent to reduce haemorrhage - can cause bleeding

162
Q

When are orally active inhibitors used?

A

To prevent venous thrombosis in knee/hip replacements

163
Q

How does aspirin work?

A

blocks COX-1 to prevent TXA2 synthesis

164
Q

What does COX in endothelial cells do? How is this overcome when aspirin is used?

A

Produces prostaglandin I2 an antithrombotic agent. It can synthesise a new COX enzyme when aspirin used

165
Q

When and how is aspirin administered?

A

Orally in patients at high risk of CVD

166
Q

What is the side effect of asprin?

A

GI bleeding & ulcers

167
Q

How do clopidogrel and tricegralor work?

A

Links to purine receptors by a disulphide bond producing reversible inhibition

168
Q

When is clopidogrel used?

A

In patients intolerant to aspirin and can be combined with aspirin as it has a synergistic effect

169
Q
A
170
Q

Describe the fibrinolytic cascade

A
  1. plasminogen gets converted to plasmin by tissue plasminogen activator (tPA)
  2. plasmin causes fibrin to be converted into fibrin fragments
171
Q

How is thrombolysis administered?

A

IV with aspirin - used to reopen occluded arteries

172
Q

Name three thrombolytic drugs

A
  • streptokinase
  • alteplase
  • duteplase
173
Q

Describe streptokinase

A

protein extract from streptococci, reduces mortality in acute MI but is not a long term solution - plasminogen activator

174
Q

What is the problem with streptokinase?

A

Patients who have had a recent infection may suffer an allergic reaction

175
Q

How do alteplase and duteplase work?

A

recombinant tPA, more effective on fibrin than plasma plasmingoen - clot selective

IV infusion with a short half life

176
Q

What is the key risk in all thrombolytic drugs?

A

haemorrhage - can be treated with tranexamic acid

177
Q

Name seven contraindications of thrombolysis

A
  • internal bleeding
  • bleeding diatheses
  • pregnancy
  • haemorrhagic cerebrovascular disease
  • uncontrolled hypertension
  • recent trauma (aggressive CPR)
  • invasice procedures

Cardiovascular (19 decks)

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