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3rd Year Drugs > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

1
Q

Name loop diuretics

A

Furosemide, bumetanide

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2
Q

When to use loop diuretics

A

1) Acute pulm. oedema
2) Chornic heart failure
3) Symptomatic fluid overload

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3
Q

How do loop diuretics work?

A

Inhibits the Na+/K+/2CL- transporter in the ascending loop of Henle
Also dilate capicatance veins –> reduces preload and improves contractile function of heart in acute heart failure

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4
Q

Side effects of loop diureits

A

Dehydration + hypotension
Increased loss of sodium and potassium –> also indirectly causes the excretion of Mg, Ca and H+
Hearing loss and tinnitus at high doses –> this is because there is a similar transporter in the ear

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5
Q

Contraindications of loop diuretics

A

Severe kypokalaeamia

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6
Q

Caution of loop diuretics

A

Hepatic encephalopathy ( as low potassium can cause/worse coma)
Hypokalaemia/natraemia
Gout (as they inhibit the excretion of uric acid)

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7
Q

Interactions of loop diurectics

A

1) Lithium increased (due to reduced excretion)
2) Increased risk of digoxin toxicity due to possible hypokalaemia
3) Increased risk of ototoxicity and nephrotoxicity with aminoglycosides!

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8
Q

Name potassium sparing diuretics

A

Amiloride

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9
Q

How does amiloride work

A

Weak dirutetic alone
Inhibits Na reabsorption via ENaC channels in the distal convoluted tubule
Causes sodium and water excretion

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10
Q

How is amiloride normally prescribed

A

As combination e.g.

Co-amilofruse or co-amilozide

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11
Q

Adverse effects of amiloride

A

GI Upset

Hypotension and urinary symptoms

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12
Q

Contrainidcations of amiloride

A

Severe renal impairment

Hyperkaelaemia

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13
Q

Do not start amiloride if??

A

Hypokalaemia as effects on potassium are unpredictable

Severe volume depretion

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14
Q

What drugs do most diuretics effect

A

Most diuretics effect the renal clearance of digoxin and lithium increasing there dose so monitor this!!

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15
Q

Name an aldosterone antagonist

A

Spirinolactone, eplerone (only for heart failure)

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16
Q

Indications for aldosterone antagonists

A

1) Ascites and oedema due to liver cirrhosis –> first line
2) Chronic heart failure: usually with ACEi and beta blocekr
3) Primary hyperaldosteronism

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17
Q

How does aldosterone antagonists work

A

Normally aldosterone produced by the adrenal cortex –> Increase ENaC activity causing Na and water reabsorption
BUT these block this

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18
Q

Adverse effects of aldosterone antagonists

A

Gynacomastia
Hyperkalaemia –> muscle weakness, arrhytmias
Liver impairment and jauncide
Steven Johnsons Syndrome

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19
Q

Contraindications of aldosterone antagonists

A 
Severe renal impairment and hyperkalaemia
Addisons disease (aldosterone deficient)
Avoid in pregnant or lactating women
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20
Q

Interactions of aldosterone antagonists

A

1) Other potassium elevating drugs e.g. ACEi and ARB)

Don’t combine with potassium supplements

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21
Q

Name Beta blockers

A

Bisoprolol, atenolol, metoprolol (beta 1 selective)

Propanolol (non-selective)

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22
Q

Indications of beta blockers

A

1) IHD –> 1st line to improve angina & ACS
2) CHD –> 1st line to improve prognosis
3) AF –> 1st line to ventricular rate and in paroxysmal AF to maintain sinus rhythm
4) SVT –> 1st line
5) Hypertension –> not for initial therapy, use 4th line; after ACEi, ARBs, Ca2+ channel blockers, thiazide diuretics

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23
Q

Where are the different types of beta receptors

A

B1 receptors - mainly heart

B2 receptors - smooth muscle in vessels and airways

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24
Q

How do beta blocker work

A

Via B1 receptors reduce the force of contraction and speed of condution in the heart

This decreases oxygen demand to relieve ischaemia and increase myocardial perfusion
Also protects the heart from chronic sympathetic stimulation

Prolongs the refractory period of the AV node
Breaks self-perpetuating circuits of SVT
Reduce renin secretion from the kidney –> as this is mediated by B1 receptors

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25
Adverse effects of beta blockers
``` Fatigue Cold extremities Headache GI disturbance Impotence Sleep distrubance ```
26
Contradindications of beta blockers
Asthma Heart failure --> can use but start slow dose as initially decreases cardiac function Haemodynamic instability Hear block Avoid with verapamil and diltiazem (non-DHP calcium channel blockers ) --> can cause HF, bradycardia and asystole!
27
Name thiazide diuretics
Bendroflumethiazide
28
Indications of thiazide diuretics
1) Alternative 1st line for hypertension (where Ca blockers otherwise unsuitable e.g. oedema or features of heart failure) 2) Add on tratment for hypertension --> in patients who bp isnt controlled by ACEi or Ca channel blockers
29
How do thiazide diuretics work
Inhibit the Na+/Cl- transported in the distal convoluted tubulue Diuresis causes fall in extracellular volume --> overtime compensatory changes this (due to RAS activation) Long term anti-hypertesnive effect is due to vascodilatation
30
Adverse of effects of thiazide diurtetics
Hyponatraemia Hypokalaemia (as increase Na delivery to distal tubulae, is exchanged for K+) Increased glucsoe --> may unmask type 2 DM Increase LDL triglycerids Impotence in men
31
Contraindications of thiazide diuretics
Hypokalaemia Hyponatraemia Gout (decreases uric acid excretion_
32
Interactions of thiazide diurietics
NSAIDS --> reduce their efffect | Avoid combo with other drugs that lower potassium
33
Name cardiac glycosides
Digoxin
34
Indications for digoxin
1) AF or atrial flutter --> 3rd line | 2) Severe HF --> 3rd line after ACEi and beta blocker
35
Actions of digoxin
Negatively chronotropic and positively inotropic (decreaeses HR and increases force of contraction) Increaese parasympathetic tone --> slow conduction at the AV node Inhibits the Na/K ATPase pump --> sodium accumulates in the cell
36
Adverse effects of digoxin
``` Bradycardia GI disturbance Dizziness Visual distubance Rash Proarrhythmic --> Low therapeutic index ```
37
Contraindications of digoxin
2nd degree heart block | ventricular arrhytmias
38
Caution of digoxin in
Renal failure --> as eliminated by kidneys Electrolyte disturbance --> potassim is the most important as digoxin competes with K+ at the Na/K pump, hence low potassium enhance the effects of digoxin
39
Interactions of digoxin
Loop and thiazide diuretics --> these decrease potassium | Amiodarone, calicum channel blockers, spirinolactone, quinine --> all increase the risk of digoxin toxicity
40
Name an anti-dysrhythmic
Amiadorane
41
How does amiodarone work?
Blockade of the Na, Ca and K channels Antagonism of the alpha and beta adrenergic receptors --> this reduces spontaneous depoaliration, slows conduction velocity, increases refractoriness, affects the AV node Breaks the self-perpetuating circle in SVT Treats VT and refractoy VF by suppressing spontaneous depolaristations
42
Indications for amiodaroneq
Wide range of tachyarrhytmias | e.g. SVT, AF, refractory VF, ventricular tachycardia
43
Adverse effects of amiodarone
Hypotension if IV Chronic side effects: pneumonitis, hepatitis, bradycardia, skin photosensitivity and grey discolouration, thyroid abnormalaties
44
Why does amiodarone cause thyroid abnormalities
As it has a similar structural similarties to thyroid hormones
45
Warnings of using amiodarone
Avoid in severe hypotension Heart block Active thyroid disease
46
Incteractions of amiodarone
Increases the plasma conc of digoxin, dilitazem and verpalmil This may incrases the risk of bradycardia, AV block and heart fialure therefore doses of these drugs should be halved if amiodarone is started
47
Name calcium antagonists
Amlodipine, nifedipine | Verapamil, diltiazem
48
Indications of calcium antagonsis
1) Hypertension --> 1st line 2) stable angina --> use all calcium channel blockers 3) Supraventricular arrhytmias -> use diltiazem and verapamil
49
Action of calcium antagnosis
Decreases Ca2+ entry into vasculr and cardiac cells Causes relaxation and dilatation of arterial smooth mucle reduces myocardial contractility Suppresses cardiac conduction --> particularly across the AV node
50
What are the 2 classes of calcium antagonists
1) Dihydropyridines: Amlodipine and nifedipine --> relatively selective for vessels 2) Non-DHP: Verampil and diltiazem. Relatively cardioselective, diltiazem some action on vessels
51
Side effects of calcium antagonists
Dihydropyridies: Ankle swelling, flushing, headaches, palpitations Non- DHP: Constiption, bradycardias, hert block, F
52
Contraindications of calicum antagonists
Poor LV function Avoid in AV nodal delay Unstable angina --> as vasodilatation causes reflex increase in contractility and tachycardia increases o2 demand Severe aortic stenosis
53
Interactions of calcium antagonists
Avoid non-DHP and beta blockers unless close supervision: Both drugs are -vely chronotropic and negatively inotropic --> together might cause HF, bradycardia and even asytole
54
Name nitrates
GLyceryl trinatrate | Isosorbine mononitrate
55
Indications of nitrates
1) acute angina/ACS 2) angina prohylaxis 3) Pulm oedema --> with O2 and furosemide
56
How do nitrates work
Converted to NO--> increases intracellular cGMP and decreases intracellular calcium Causes venous and arterial vasodilatation (arterial lesser) Relaxation of cappacitance veins --> decreases preload and LVF filling --> this reduces cardiac work and myocardial demand hence relieving angina and AF IT IS REDUCING PRELOAD THAT RPEVENT MOST ANDINA It also relieves coronary vasospasm and dilates collateral vessels to increase coronary perfusion
57
Adverse effets of nitrates
Vasodilatory effects: headache, flushing, light-headedness, hypotension Sustained use can cause tolerance
58
Contraindications of nitrates
Severe aortic stenosis Haemodynamic instability Hypotension
59
Interactions of nitrates
1) DO NOT USE WITH PHOSPHODIESTERASE INHIBITOS --> these enhance and prolong the effects of nitrates 2) Caution with anti0-hypertensives
60
Name some statins
Simvastatin, atorvastatin, rosuvastatin, pravastatin
61
Indications for statins
1) Primary preventin of CV Disease 2) Secondary prevention of CV disease 3) Primary hyperlipidaemia
62
Action of statins
Inhibit HMG CoA Reductase --> Decreases cholesterol production by the liver and also increases clearance of LDL cholesterol Indirectly also reduces triglycerides and slightly increases HDL levels
63
Adverse effects of statins
Headaches and GI disturbances Sumple aches to more serious myopathy and rhabdomyolysis Can cause a rise in liver enzymes (ALT)
64
Contraindications of statins
Pregnancy | Breastfeeding
65
Caution of statins in
Heptic | Renal impairment
66
What should you avoid grapefruit juice when taking?
Statins | As grapfruit juive is a CP450 inhibitor, enzymes whcih eliminate simvastatin and atorvastatin
67
Interactions of statins
Metabolism reduced by CP450 inhibitos Amlodipine --> has a similar interaction to CP450 inhibitors
68
Name some CP450 inhibitors
Amiodarome, diltiazem, itraconazide, macrolides, protease inhibtors, grapefruit juice
69
When should you take statins
at night as they have greater effect when dietary intake is at its lowest
70
Uses of heparins
1) VTE 2) ACS --> use LMWH and fondaparinux as first line to impve revascularisation and prevent intracoronary trombus progression
71
How does UFH work
Activates antithrombin --> inturn inactivates FXa and thrombin
72
How does LMWH work?
Similar action to UFH but preferentially inhibits FXa
73
How does fondaparinux work?
It is a synthetic ocmpound that only inhibits FXa
74
Adverse effects of heparins
Bleeding Injection site reactions Heparin induced thrombocytpenia --> stop drug immediately if this occurs
75
Caution of heparis
1) Increased bleeding risk 2) renal impairment --> as can accumulate 3) AVOID AROUND TIME OF INVASIVE PROCEDURES
76
Interactions of heparins
Avoid combining with other antithrombotics except 1) when initiating warfarin 2) antiplateletls with fondaparinux/LMWH in ACS
77
What reverses heparin
Protamine --> doesnt work for fondaparinux
78
How do we give heparins?
SC injection
79
How do we measure UFH effect
APTT
80
How do we measure LMWH and fondaprinux's effect
FXa activity --> rarely requires monitoring
81
Name TPAs
Alteplase, Reteplase, tenetplase
82
Uses of TPAs
1) Acute MI 2) Fibrinolytic treatment of acute ischaemic stroke 3) Acute massive PE with haemodynamic instability
83
How do TPA's work
Convert plasminogen to plasmin | Plasmin then breaks down the clots
84
Adverse effects of TPAs
1) Haemorrhages --> intracererbal and haeamatomas are common 2) Hypersensitivity 3) Cardiac disorders --> ischaemia/angina and hypotension and heart failure are common
85
Contrainidications of TPAs
1) Hypersensitivity to the drug OR gentamicin | 2) High risk of haemorrhage
86
What shoudl we avoid the use of when taking TPAs
Rigid catheters
87
Interactions of TPAs
1) ACEi --> enhanced risk of anaphylactoid reactions | 2) anticoagulants --> enhances risk of haemorrhage
88
What is the short life of TPAs
4-5 minutes hence quickly eliminated
89
What are the infications for warfarin?
1) VTE --> 3-6 months if single episode, life long if recurrent 2) AF 3) Heart valve replacement --> short term if tissue replacement, lifelong in mechanical
90
What should we not use warfarin to prevent
Do not use to prevent arterial thrombosis as they are primarily driven by platelet aggregation
91
How does warfarin work
VKOR Inhibitor | This prevents oxidised vitamin K being reactivated which is needed for coagulation factors
92
Adverse effects of warfarin
Bleedigin
93
Contraindicatinos fo warfarin
1) immediate risk of bleeding
94
Cautions of warfarin
1) Liver disease --> less able to metabolise drug and can be over-anticoagulated 2) Avoid in first trimester as teratogenic and avoid in the last trimester as associate with maternal haemorrhage
95
Interactions of warfarin
1) CP450 inhibitors can cause increased bleeding risk (e.g. fluconazole, macrolides and protease inhibitors 2) CP450 induces increase the clot risk (e.g. carbamzepine, rifampicin, phenytoin) 3) Antibiotics increase anticoagulation as they kill gut flora that synthesis vitamin K
96
What time shoudl you take warfarin?
18:00
97
What is the INR target in AF & VTE
2-3
98
Indications of NOACs
AF VTE DVT + PE (Apixiban only)
99
Mechanisms of NOACs
Riovoraxiban and Apixiban = FXa inhibitors | Dabigatran = Direct thrombin inhibitor
100
ADVERSE EFFECTS OF NOACS
Bleeding | GI Upset
101
Contraindications of NOACS
ACtive pathological bleeding Hypersensitvity Mechanical/prosthetic heart valves
102
Interactions of NOACs
Antiplatelets/NSAIDS | CP450 Inhibitors --> increases the bleeding risk
103
How are NOACS eliminated
Dabigatran --> primarily renally eliinitaed Rivoroxciban --> 1/3 eliminated by the liver unchanged, the rest is by hepatic CP450 enzymes

3rd Year Drugs (10 decks)

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