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Y3 DRUGS PROFILES > CARDIOVASCULAR DRUGS > Flashcards

CARDIOVASCULAR DRUGS Flashcards

1
Q

give an example of a loop diuretic

A

furosemide

bumetanide

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2
Q

which organ do loop diuretics act on?

A

kidneys

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3
Q

which part of the kidneys do loop diuretics work on?

A

ascending limb of loop of henle

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4
Q

how do loop diuretics act to inhibit reabsorption?

A

compete for chlorine binding sites by acting on sodium/potassium/chlorine co-transporters

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5
Q

how do loop diuretics cause more urine to be produced?

A

inhibits reabsorption of electrolytes, less osmosis, more urine produced

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6
Q

give 2 instances that loop diuretics are used

A 
pulmonary oedema (LVF)
heart failure
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7
Q

what is the difference between IV and oral administration of loop diuretics?

A

IV fast acting

oral slow acting, lasts six hours, so twice daily

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8
Q

name 2 circulatory instances that contraindicate use of loop diuretics

A

hypovolaemia

hypotension

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9
Q

loop diuretics can cause hyperglycaemia. name 2 conditions that can be exacerbated by this

A

diabetes

gout

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10
Q

what electrolyte imbalances can be caused by use of loop diuretics?

A

hypokalaemia/hyponatraemia

lead to hepatic encephalopathy/coma

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11
Q

what is the risk of taking loop diuretics whilst pregnant?

A

maternal hypovolaemia

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12
Q

name 2 serious GI side effects of loop diuretics

A

pancreatitis

hepatic encephalopathy

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13
Q

name 3 other side effects of loop diuretics

A 
hypersensitivity
visual disturbances
tinnitus
deafness
BM suppression
Urinary retention 
 Metabolic alkalosis
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14
Q

how can loop & thiazide diuretics potentiate digoxin toxicity?

A

hypokalaemia

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15
Q

how do NSAIDs interact with loop and thiazide diuretics?

A

reduce efficacy (COX inhibitors)

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16
Q

why shouldn’t loop and thiazide diuretics be taken with corticosteroids?

A

enhance hypokalaemia

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17
Q

give an example of a thiazide diuretic

A

bendroflumethiazide
metolazone
Chlortalidone

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18
Q

where in the kidneys do thiazide diuretics act?

A

distal convoluted tubule

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19
Q

how do thiazide diuretics inhibit reabsorption?

A

inhibiting Na reabsorption from DCT by inhibiting Na/Cl co-transporter

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20
Q

how does reabsorption inhibition cause more urine to be produced in thiazide diuretics?

A

less osmotic force so less water reabsorbed

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21
Q

name 2 conditions that thiazide diuretics are used in

A

Chronic heart failure

First line treatment or additional treatment for hypertension

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22
Q

at what time in the day should thiazide diuretics be administered?

A

morning so don’t interfere w sleep

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23
Q

name 2 conditions that can be exacerbated by thiazide diuretics

A

diabetes
gout= reduce uric acid secretion
SLE

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24
Q

why are thiazide diuretics a risk in pregnancy?

A

neonatal thrombocytopenia, BM suppression, jaundice , hypoglycemia

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25
Q

what electrolyte imbalances can be caused by thiazide diuretics/

A

hypo-disorders

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26
Q

name 3 other side effects of thiazide diuretics

A 
bone marrow depression
visual disturbances
tinnitus
deafness
hypersensitivity
Impotency in men
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27
Q

name 2 potassium sparing diuretics

A

spironolactone

amiloride

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28
Q

how does spironolactone work?

A

aldosterone antagonist= binds to aldosterone receptor

It blocks the effects of aldosterone which is promotes sodium and water retention and excretion of pottasium

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29
Q

how does amiloride work?

A

interferes with sodium and potassium exchange at the DCT. Promotes excretion of sodium and water and retnation of pottasium
Relatively week diuretic

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30
Q

name 4 conditions where potassium sparing diuretics are used

A 
Chronic heart failure 
Ascited and oedema in liver cirrhosis
Nephrotic syndrome
primary hyperaldosteronism
Hypokalaemia= amiloride
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31
Q

what is an electrolyte imbalance that contraindicates use of potassium sparing diuretics?

A

hyperkalaemia

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32
Q

what is a hormone imbalance syndrome that contraindicates use of potassium sparing diuretics?

A

addison’s

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33
Q

why shouldn’t potassium sparing diuretics be used in pregnancy?

A

feminisation of the male foetus

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34
Q

why shouldn’t potassium sparing diuretics be used in conjunction with ACE inhibitors?

A

potentiate hyperkalaemia

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35
Q

why should NSAIDs be used in conjunction with potassium sparing diuretics?

A

COX inhibitors- reduce efficacy

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36
Q

give an example of a beta blocker

A

atenolol

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37
Q

how do beta blockers work?

A

block beta-adrenoreceptors in the heart, peripheral vasculature, bronchi, pancreas and liver
block action of sympathetic nervous system
slows the heart rate (can be vasodilatory)

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38
Q

give 4 when beta blockers used?

A 
angina/MI
heart failure
hypertension
arrhythmia= AF and SVT
thyrotoxicosis
migraines
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39
Q

why are beta blockers contraindicated with asthma?

A

triggers exacerbation of attacks

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40
Q

why are beta blockers contraindicated in pregnancy?

A

can cause intrauterine growth

can cause neonatal hypoglycaemia

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41
Q

why should beta blockers be used in caution with patients with diabetes?

A

can dull signs of a hypo

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42
Q

name 2 circulatory side effects of beta blockers

A

syncope
bradycardia
cold peripheries

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43
Q

why shouldn’t beta blockers be used with anti-arrhythmias?

A

slow heart rate

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44
Q

why shouldn’t beta blockers be used with anti-hypertensives?

A

lower blood pressure

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45
Q

why shouldn’t antipsychotics be used with beta blockers?

A

can increase risk of arrhythmias

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46
Q

why shouldn’t beta blockers or calcium antagonists be used with clonidine alpha blocker?

A

can cause rebound hypertension

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47
Q

give 2 examples of a calcium antagonist

A

amlodipine
verapamil
diltiazem

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48
Q

how do calcium antagonists work?

A

reduce calcium ion movement through cell membranes into vascular and cardiac cells

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49
Q

how do calcium antagonists affect myocardial contractility, oxygen demand and electrical impulse formation? what is the outcome of this?

A

In the hear reduce myocardial contractility.
They suppress cardiac conduction,= reduce ventricular rate
Reduced cardiac rate, contractility and afterload reduce myocardial oxygen demand, preventing angina

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50
Q

how do calcium antagonists affect coronary vascular tone?

A

Relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure

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51
Q

when are calcium antagonists used?

A

Stable angina
hypertension
Diltiazem and verpamil are used in SVT, atiral flutter and AF

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52
Q

in which type of angina are calcium antagonists not effective against and can worsen the symptoms?

A

unstable

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53
Q

What are the side effects of verapamil?

A 
Commonly= constipation
Rare= bradycardia, heart block and cardiac failure
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54
Q

name common side effects of amlodipine?

A

Ankle swelling
Palpitations
Flushing
Headache

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55
Q

What heart condition should verapmil and diltiazem be used with caution?

A

Patient with left ventricle hypertrophy as it can preciptate or worse the cardiac failure

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56
Q

Patient with what conduction problem should avoid diltiazem and verapmil?

A

With increase AV node conduction delay as it can lead to heart block

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57
Q

What condition predisposes the patient do collapse if taking amlodopine?

A

Severe aortic stenosis

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58
Q

give an example of ACE inihibitors

A

ramipril

lisinopril

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59
Q

give 2 conditions where ACE inhibitors are used

A

Hypertension
chronic heart failure
IHD to prevent MI and stroke
Diabetic nephropathy and CKD with proteinuria

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60
Q

which organ insufficiency is contraindicated in administration of ACE inhibitors or AT1 blockers?

A

Renal artery stenosis or acute kidney injury

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61
Q

what heart abnormality is contraindicated in administration of ACE inhibitors?

A

aortic stenosis

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62
Q

name a circulatory insufficiency contraindicated in administration of ACE inhibitors

A

hypovolaemia

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63
Q

Should ACE inhibitors or AT1 blockers be used in pregnancy and breast feeding?

A

no

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64
Q

What are the common side effects of ACE inhibitor?

A

Hypotension espeially after first dose
Dry cough due elevated levels of bradykinin
Hyperkalaemia due to reduced levels of aldosterone so pottasium retention

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65
Q

how do ACE inhibitors results in vasodilation and reduce BP.

A

Inhibits the renin-angiotensin systemless
Inhibition of the angiotensin-converting enzyme, less angiotensin II.
Angiotensin 2 causes vasoconstriction and aldosterone production= reduced PV resistance and afterload.
Also promotes sodium and water excretion due to reduction in aldosterone and helps with HF

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66
Q

What is the severe interaction of NSAIDS and ACE inihibitors or AT1 blockers?

A

Potentiate the risk of renal failure

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67
Q

what serious allergic reaction can occur with ACE inhibitors?

A

angioedema due to bradykinin release

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68
Q

what electrolyte imbalance can be caused by ACE inhibitors?

A

hyperkalaemia

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69
Q

why shouldn’t ACE inhibitors or AT1 blockers be used with potassium supplements or pottasium sparing diuretics?

A

can cause hyperkalaemia

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70
Q

give an example of an angiotensin-1 blocker and why is it used?

A

losartan and alternative to ACE inhibitor due to dry cough

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71
Q

how do AT1 blockers work?

A

competitive inhibition of angiotensin 2 and bocks the AT1 receptor
Slow renin angiotensin system

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72
Q

which of these processes is not mediated by AT1 blockers?

a) vasoconstriction
b) aldosterone release
c) thermoregulation
d) renal sodium reabsorbtion
e) vasopressin secretion

A

c) thermoregulation

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73
Q

give 3 conditions where AT1 blockers are used

A

Hypertension
chronic heart failure
IHD to prevent MI and stroke
Diabetic nephropathy and CKD with proteinuria:

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74
Q

which one of these is not a contraindication for AT1 blockers?

a) pregnancy
b) renal artery stenosis
c) hyperkalaemia
d) depression

A

d) depression

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75
Q

what serious muscle condition is a side effect of AT1 blockers?

A

rhabdomyolysis

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76
Q

What are the possible side effects of AT1 blocker?

A

Hyerkalamia
Renal failure
Hypotension = particularly after first dose

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77
Q

what effect do rifampicin & fluconazole have on AT1 blockers?r

A

reduce effect

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78
Q

Give example of a short and long acting nitrate?

A

a) short nitrate= glyceryl trinitrate

b) long nirate = isosorbide mononitrate

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79
Q

how do nitrates work?

A

Nitrates converted to NO which prevents Ca from moving in vascular smooth muscles
Direct relaxant of smooth vascular muscle in mainly veins and arteries.
Causes reduction in venous return and left ventricle filling

80
Q

What affect does nitrates have on preload?

A

Reduces caridac preload therefore reduce cardiac work and myocardial oxygen demand relieving the symptoms of angina and caridac failure

81
Q

What 3 conditions are nitrates are used for

A

Short nirate for acute agina and ACS
Long nitrate for prophylaxis of angina
IV for pulmonary oedema with furosemide and oxygen

82
Q

give 2 contraindications of nitrates

A

pregnancy
hypotension
Severe aortic stenosis = cause collapse

83
Q

What are the common side effects of nitrates?

A

hypotension
Flushing
Headache
Light headedeness

84
Q

why should nitrates not be used with alcohol or viagra?

A

also vasodilators - increase risk of serious hypotension

85
Q

Interaction of nitrate with phospodiesterase inhibitor (sildenafil) will cause what?

A

It will increaes and prolong the hypotensive effects of nitrates

86
Q

give an example of a cardiac glycoside

A

digoxin

87
Q

how does digoxin cause intracellular calcium to rise and therefore treat heart failure?

A

Inhibits Na/K- ATPase pumps causing rise in intracellular Na, which inhibits Ca ion pump out of cell, so Ca retained which increases contractile forces

88
Q

What affect does digoxin have on parasympathetic tone and therefore use for AF?

A

Increase in vagal (parasympathetic tone) which causes a reduction in conduction of AV node which means a reduction in ventricle rate

89
Q

what does greater intracellular calcium mean in terms of myocytes in digoxin?

A

increased uptake - more powerful/automatic contraction

90
Q

how does digoxin affect heart rate and force of heart contraction?

A

Decreases heart rate ( negative chronotropic)

Increases force of contraction ( positive inotropic)

91
Q

give 2 conditions where cardiac glycosides are used

A

arrhythmia= AF and atrial flutter ( reduce ventricle rate)

congestive heart failure (severe)= 3rd line treatment

92
Q

give a 3 heart conditions which contraindicates use of digoxin

A

2nd degreee Heart block
Intermittent heart block
Ventricle arrhythmias

93
Q

What is the risk of giving digoxin when patient has electrolyte abnormalitiy? give examples

A

Can lead to digoxin toxicity
hypokalaemia = greatest risk as it competes with pottassium for binding to the pump
Hypomagnesaemia
Hypercalcaemia

94
Q

what is digoxin a substrate of?

A

p-glycoprotein

95
Q

a) Name two drugs that cause hypokalaemia and therefore digoxin toxicity?
b) Name 7 drugs that can increase the plasma concentration of digoxin and therefore risk of toxicity?

A

a) Loop diuretic and thiazide diuretic

b) amiodarone, quinine, spirolactone, verapamil, CA channel blocker, gentimicin and Itraconazole

96
Q

Give an example of class 1 sodium channel blocker anti-dysrhythmics

A

quinidine

lidocaine

97
Q

what are class 2 anti-dysrhythmics?

A

beta blockers

98
Q

give an example of potassium channel blocker class 3 anti-dysrhythmics?

A

amiodarone

99
Q

what are class 4 anti-dysrhythmics?

A

calcium channel blockers

100
Q

give an example of class 5 anti-dysrthmics (unknown mechanism)

A

digoxin

adenosine

101
Q

give 3 examples of when amiodarone is used for?

A 
Ventricular arrhythmias
AF
Atrial flutter 
SVT
ventricular tachycardia
Wolfs-parkinson-white syndrome
102
Q

what is wolfs-parkinson-white syndrome?

A

abnormal electrical conduction pathway between atria and ventricles causing ventricles to contract prematurely

103
Q

why are pregnancy and breastfeeding contraindicated in amiodarone?

A

similar structure to thyroxine can cause foetal thyroid issues

104
Q

What are the potential side effects of chronic use of amiodarone?

A 
Lung= pneumonitis
Heart= AV block and bradycardia
Skin= Photosensitivtiy and great colourisation 
Liver= Hepatitis  and jaundice
105
Q

Amiodarone has similar strucutre to thyroid hormone what effect does this have on the patient potentially?

A

Lead to hypo or hyperthyroidism

106
Q

why shouldn’t amiodarone be used with benzyl-alcohol formulations in neonates?

A

cause gasping syndrome

107
Q

Which patients should use of amiodarone be avoided in?

A

Severe hypotension
Heart block
Active thyroid disease

108
Q

Interaction of amiodarone with what drugs can cause bradycardia, heart failure and Av block. Therefore have there dose halved?

A

Verapamil
Diltiazem
Digoxin

109
Q

What is the interaction of amiodarone and cytochrome p450?

A

Metabolised and inhibits cytochrome p450

110
Q

how does amiodarone affect serum digoxin?

A

increases

111
Q

give 2 examples of anti-platelet agents

A

aspirin

clopidogrel

112
Q

how do anti-platelets inhibit thrombus formation?

A

inhibit platelet aggregation

113
Q

in which circulation system are anti-platelets most effective?

A

arterial

114
Q

how does aspirin block thromboxane formation? Leading to reduction in platelet aggregation and arterial occlusion

A

COX inhibitor= blocks cox 1 formation

115
Q

how does clopidogrel work as an anti-platelet?

A

competitive inhibition of ADP receptors on surface of platelet cell membrane= prevent platalet aggregation

116
Q

What are the most common adverse effect of aspirin and clopidogrel?

A

GI irritation leading to ulceration and bleeding.

117
Q

Give the use of anti-platelet agents

A

ACS
Thromoblytic therapy for, Pe, cerebral infarctiona nd MI
Af to prevent stroke
Mild to moderate pain and fever = aspirin
Prevent occlusion of coronary artery stents= clopidogrel

118
Q

why are anti-platelets contraindicated in haemophilia and dengue fever, peptic ulcers and hypertension?

A

high risk of bleeding

119
Q

which anti platelet is contraindicated in the case of salicylate allergy? Causing potential bronchospasm

A

aspirin

120
Q

why is aspirin contraindicated in hyperuricaemia and gout?

A

inhibits kidney excretion of uric acid

121
Q

what is Reye’s syndrome and which anti-platelet is it associated with?

A

Liver encephalopathy after acute viral illness (influenza, varicella) in under 16 and associated with aspirin

122
Q

Large doses of apsirin can cause what and why?

A

Tinnitus due to large doses of salicylate

123
Q

how does alcohol interact with aspirin?

A

enhances activity

124
Q

how is clopidogrel metabolised?

A

It is a pro drug and is metabolised by cytochrome p450 to its active form

125
Q

which GI drug reduces the effect of clopidogrel?

A

omeprazole therefore use other PPI for GI protection

126
Q

how might SSRIs and anti-platelets interact?

A

increase risk of bleeding

127
Q

how might NSAIDs and warfarin interact with anti-platelets?

A

increase risk of bleeding

128
Q

what is streptokinase (alteplase) and tissue plasminogen activator an example of?

A

thrombolytics

129
Q

how is streptokinase produced?

A

Produced by strep bacilli

130
Q

how do thrombolytics work?

A

Catalyse the conversion of plasminogen to plasmin which breaks down clots=

131
Q

give 3 examples when thrombolytics are used

A

MI with ST elevation = in the first 12 hours with antiplatelet and anticoagulants.
Acute ischaemic stroke
Large PE
arterial occlusion

132
Q

what type of stroke are thrombolytics contraindicated in?

A

haemorrhagic= CT scan before administration for acute stroke

133
Q

What are the main contradications to use of thromblytics?

A

Factors that increase risk of bleeding such as

Recent trauma and surgery, severe hypertension, peptic ulcers and recent haemorrhage and bleeding disorders

134
Q

what aortic abnormality contraindicates use of thrombolytics?

A

aortic dissection

135
Q

What is the time framce for alteplase after a acute ischaemic stroke?

A

Be given within 4.5 hours of the stroke to have maximal effect

136
Q

What is the risk of reperfusion of infarcted brain or heart tissue?

A

Causes cerebral oedema or arrhythmia respectively

137
Q

what is common side effect of thrombolytics?

A

Nausea, vomiting and brusing around the Iv sight

With hypotension

138
Q

give an example of a heparin

A

enoxaparin

139
Q

where are heparins producedf?

A

basophils

mast cells

140
Q 
What is the mechanism of 
a)UF
b)LMWH?
c)Fondaparinux 
to prevent clot formation?
A

a) bind to and activate antithrombin III which inactivates thrombin and factor Xa
b) Direct inhibition of thrombin and factor Xa
c) inhibits factor Xa

141
Q

What is the main adverse affects of heparin?

A

Bleeding and injection sight reaction

142
Q

give 4 examples of when heparin is used

A

ACS
AF
DVT/PE
indwelling venous cannulas

143
Q

why are IM injections of heparins avoided?

A

high risk of haematoma= disabling bruisingof the arm

144
Q

What is a rare but serious side effect of heparin?

A

Heparin induced thrombocytopenia= leading to low levels of platetlet and thrombosis (blood clot formation)
Complications are DVT and PE formation

145
Q

what 2 products in heparin formulations are allergens?

A

pork

benzyl alcohol

146
Q

What contra indications are there for heparin?

A

Heparin should be used with caution for patients with increased risk of bleeding:
Severe uncontrolled hypertension, clotting disorders, recent trauma and surgery

147
Q

What is the risk of giving heparin to a patient that has renal impairment?

A

Reduced excertion and causes accumulation of LMWH and fondaparinux= reduce the dose or use UF

148
Q

give 2 examples of oral anticoagulants

A

warfarin

rivaroxaban

149
Q

how does warfarin work? which clotting factors and proteins does it inhibit production of

A

Inhibits vitamin K epoxide reductase which inhibits vitamin K activation which stimulates synthesis of clotting factors 2, 7, 9, 10 and proteins C, S, Z

150
Q

how dies rivaroxaban work?

which pathways does it interrupt

A

inhibits factor 10a

intrinsic and extrinsic pathways

151
Q

What is the use of oral anticoagulant?

A

Treatment of PE and DVT
Prophylaxis of VTE ( recurrent DVT and PE)
Prevent stroke (embolic event) from AF
Short term use for prevention of embolic event from tissue valve replacement
Long term use for prevention of embolic event from metal valve replacement

152
Q

give 2 conditions which would contraindicate use of oral anticoagulants

A

Risk of bleeding:
thrombocytopenia
ulcerative disease
active haemorrhage

153
Q

what is the major side effect of anti-coagulants?

A

haemorrhage

154
Q

what is purple toe syndrome?

what can it be a side effect of?

A

emboli and bruises in feet due to cholesterol deposits

side effect of oral anticoagulants

155
Q

what is warfarin necrosis?

A

sudden drop in protein C causing rebound coagulation &massive thrombosis. Causing skin and limb necrosis (gangrene)

156
Q

Why is it contradictive to giving oral anticoagulant to patient with liver impairment?

A

Reduced metabolism and therefore greater chance of bleeding

157
Q

Why should you not give warfarin

a) 1st trimester of pregnancy
b) just before delivery?

A

a) neonatal malformations such as cardiac and cranial malformatuons
b) Materal haemorrhage during delivering

158
Q

how are warfarin and rivaroxaban metabolised?

A

cytochrome p450

159
Q

give an example of a statin

A

sinvastatin

atorvostatin

160
Q

how do statins work?

A

HMG-CoA reductase inhibitors so interrupts cholesterol production chain.
Liver produces less cholesterol and more LDL clearance from the blood
Increase in HDL levels

161
Q

give an example of primary statin therapy

A

prevent cardiovascular disease in those with high cholesterol and risk of cardiovascular event

162
Q

give an example of secondary statin therapy

A

decrease mortality and further events in those who have evidence cardiovascular disease

163
Q

give a hereditary condition where statins are used

A

familial hypercholesterolaemia (primary hyperlipidaemia)

164
Q

are statins contraindicated in pregnancy and breast feeding?

Explain

A

yes as cholesterol is essential for the growth of neonate

165
Q

Caution should be used with statin when the patient has impairment of what organs?

A

Liver (metabolism)

Renal (excretion)

166
Q

What is are the rare MSK side effectes of statin?

A

Can cause muscle ache to myopathy and even rhabdomylsis

167
Q

how are statins metabolised?

A

cytochrome p450

168
Q

How does Thiazide increase renal blood flow?

A

By increasing the renal synthesis of prostagladins

169
Q

What is the fatal outcome of using thiazide diuretic with a patient with severe liver disease?

A

Hypokalamia can lead to coma

170
Q

What circulatory side effects are there of Thiazide Diuretics?

A

Postural HT

Cardiac Arrhythmias

171
Q

What is the interaction between B blockers and Thiazide Diruetcs?

A

Potentiate hyperglycemia/ lipidaemia

172
Q

What is the process of elimination of all 3 types of diuretics?

A

Renal with small contribution from liver

173
Q

Should you give potassium sparing diuretics to someone with renal dysfunction?

A

no

174
Q

What are the blood S/E of spirolactone?

A

Leucopenia, agranulocytosis and thrombocytopenia

175
Q

Which of the diuretics have a possible side effect of gynaecomastia, impotence and sexual dysfunction and Steven Johnson syndrome?

A

PSD

176
Q

Where are B1- adrenoreceptors and B2 adrenoreceptors found?

A

B1 found in the heart

B2 found mainly in the smooth muscles of blood vessels and airways

177
Q

Which adrenoreceptors does beta blockers affect and what affect does that have?

A

β1-receptor,–> reduce force of contraction and speed of conduction in the heart.

178
Q

How does beta blockers relieve MI symptoms?

A

Reduce cardiac work and oxygen demand and increase myocardial perfusion

179
Q

How do beta blockers help to improve prognosis of heart failure?

A

By protecting the heart from chronic sympathetic stimulation

180
Q

What affect does beta blockers have on the kidney to low BP?

A

Act on the kidney and cause a reduction in renin secretion

181
Q

How does beta blockers treat Af?

A

By increasing the refractory period of AV node so reduction in venctricle contraction

182
Q

Which two calcium channel blockers are used to treat supraventricular arrhythmias ?

A

Diltiazem and verapamil control cardiac rate

183
Q

Give examples of supraventricular arrhythmias ?

A

Supraventricular tachycardia, Af and atrial flutter

184
Q

Why is LMWH prefered over UF?

A

Low molecular weight heparins have a more
predictable effect and, unlike UFH, do not usually require laboratory
monitoring.

185
Q

What is the interaction of B blocker and Verapamil/ diltiazem?

A

Can cause severe reduction in the force of contraction (inotrophic) and rate of the heart (chronotropic)
Causing potential bradycardia, heart block and even asystole

186
Q

What affect does nitrates have on afterload and coronary perfusion?

A

Reduce afterload

Improve coronary perfusion by reducing coronary vasospasm and dilation of collateral vessels

187
Q

What are the side effects of digoxin?

A 
bradycardia
GI disturbances
Rash
Dizziness
Visual disturbances
188
Q

What is the dose changes requirement for clopidogrel and aspirin before surgery?

A

Aspirin can be carried on taken throughout surgery

Have to stop clopidogrel 7 days before hand

189
Q

What is the possible risk of giving thromboylsis with anticoagulants and antiplatelets for treatment of stroke?

A

Increase risk of haemorrahage

190
Q

Is the risk of heparin induced thrombocytopenia greater with LMWH?

A

No reduced risk

Greater risk with Uf

191
Q

For bleeding assoicated with heparin what is the antidote?

A

protamine = reverses the anticoagulation

192
Q

What is the limitation of protamine?

A

Effective for UF
Reduced effectiveness to stop bleeding for LMWH
Not effective against fondaparinux

193
Q

What is the interacation of aspirin and heparin?

A

Increase anticoagulation effects of heparin

194
Q

What is a antidote for bleeding due to warfarin use?

A

Iv vitamin K= direct antidote
Or
Prothrombin complex concentrate

195
Q

What is the pro and con of rivaroxaban?

A 
Pro= no need to measure INR
Con= no antidote for bleeding
196
Q

Why is warfarin not used for arterial thrombosis (MI)?

A

This is due to platelet formation which is affected by antiplatetels agents such as aspirin and clopidogrel

Y3 DRUGS PROFILES (9 decks)

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