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Medicine Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

First pass metabolism

A

Drugs that are swallowed are carried from the gut to the liver by portal circulation, where they undergo variable metabolism by the liver before reaching systemic circulation. Concentration is greatly reduced before the drug reaches systemic circulation

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2
Q

Anti-cholesterol drugs (4)

A

Statins, PCSK9 inhibitors, fibrates, ezetimibe

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3
Q

Statins:

  • What do they do?
  • Examples
  • What are they used in?
  • Side effects
A
  • Blocks HMG coenzyme reductase
  • Simvastatin, atorvastatin, fluvastatin, pravastatin, rosuvastatin
  • Hypercholesterolaemia, diabetes, angina, MI, TIA/stroke
  • Renal failure, myalgia, myopathy
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4
Q

PCSK9 inhibtors:

  • What do they do?
  • Examples
  • What are they used to treat and why?
  • How are they administered?
A
  • Increase number of LDL receptors for LDL to bind to leading to less LDL in the bloodstream and decreased cholesterol
  • Evolucumab, alirocumab
  • Used to treat FH because they are stronger
  • Administered subcutaneously
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5
Q

Fibrates:

  • Example
  • When are they used?
  • Side effects
A
  • Bezafibrate
  • As an alternative to statins - when patients don’t tolerate statins. Also used in hypertriglyceridaemia and low HDL cholesterol
  • Nausea, stomach upset, inflammation of liver
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6
Q

Familial hypercholesterolaemia

A

Inherited condition where there is a naturally occurring high level of cholesterol

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7
Q

Anti-hypertensive drugs (7)

A

Beta-blockers, diuretics, calcium antagonists, ACE inhibitors, angiotensin receptor blockers, alpha blockers, mineralocorticoid antagonists

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8
Q

Diuretics:

  • Mechanism
  • 2 types and examples
  • Side effects
A
  • Blocks sodium reabsorption in kidneys
  • Thiazide diuretics (e.g. bendrofluozide), loop diuretics (e.g. furosemide, not used in hypertension)
  • Hypokalaemia, hyperglycaemia, increased uric acid (gout), impotence
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9
Q

Beta blockers:

  • 2 types
  • Side effects
A
  • Cardioselective and non-selective

- Worsen asthma, tiredness, cold peripheries

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10
Q

Cardioselective beta blockers:

  • What do they block?
  • Examples
  • What are they generally used in?
A
  • Only beta-1 receptors
  • Atenolol, bisoprolol
  • Angina, acute coronary syndrome, MI, hypertension and heart failure
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11
Q

Non-selective beta blockers:

  • What do they block?
  • Examples
  • When are they used?
A
  • Beta-1 and beta-2 receptors
  • Propanolol, carvedilol
  • Thyrotoxicosis, migraines
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12
Q

Calcium antagonists:

  • What do they do?
  • 2 types
  • They shouldn’t be given in combination with which drug?
A
  • Act on AV node to slow heart rate
  • Rate limiting calcium antagonists, dihydropyridines
  • Beta blockers
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13
Q

Rate limiting calcium antagonists:

  • Examples
  • When are they used?
A
  • Verapamil, diltiazem

- Hypertension, angina, supraventricular arrhythmias

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14
Q

Dihydropyridines:

  • Example
  • What are they used in?
  • Common side effect
A
  • Amlodipine
  • Hypertension and angina
  • Ankle oedema
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15
Q

ACE inhibitors:

  • How do they work?
  • Example
  • When are they used?
  • When should they not be used?
  • Side effects
A
  • Stop angiotensin I converting to angiotensin II
  • Lisinopril
  • Used in hypertension and heart failure
  • Never use in pregnancy
  • Dry cough, renal dysfunction, angioneurotic oedema
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16
Q

Angiotensin receptor blockers:

  • How do they work?
  • Example
  • When are they used?
  • When should they not be used?
  • Side effects
A
  • Block angiotensin II receptors
  • Losartan
  • Hypertension and heart failure, often when ACE inhibitors can’t be used
  • Never use in pregnancy
  • Renal dysfunction
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17
Q

Alpha blockers:

  • What do they do?
  • Example
  • What can it be used to treat?
  • Side effect
A
  • Block alpha adrenoreceptors causing vasodilatation
  • Doxazosin
  • Hypertension and prostatic hypertrophy
  • Postural hypotension
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18
Q

Mineralcorticoid Antagonists:

  • What do they do?
  • Examples
  • When are they used?
  • Side effects
A
  • Block aldosterone receptors
  • Spironolactone, eplerenone
  • Used in heart failure and resistant hypertension
  • Gynaecomastia, hyperkalaemia, renal impairment
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19
Q

Anti-anginal drugs (6)

A

Nitrates, nicorandil, calcium antagonists, beta blocker, ivabradine, metabolic modulator

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20
Q

Nitrates:

  • What do they act as?
  • Administration
  • Example
  • What are they used in?
  • Side effects
A
  • Venodilators
  • Sublingually either as GTN spray or GTN tablet
  • Isosorbide mononitrate
  • Used in angina and heart failure
  • Headache, syncope, nausea
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21
Q

Nicorandil:

  • What is it?
  • Side effects
A
  • K ATP channel opener

- Headache, mouth ulcers

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22
Q

Ivabradine:

  • What does it do?
  • When does it work/not work
  • Side effects
A
  • Slows heart rate by acting on funny current
  • Works in the SA node and only works in sinus rhythm, doesn’t work in atrial fibrillation
  • Altered visual disturbances
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23
Q

Metabolic modulator:

  • Example
  • What does it do?
  • Side effects
A
  • Ranolazine
  • Decreases calcium load on heart
  • Dry mouth, pre-syncope, nausea
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24
Q

Drugs used in plaque rupture and MI (4)

A

Anti-thrombotics, anti-platelets, anti-coagulants, fibrinolytics

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25
Q

Anti-platelet drugs:

  • Examples
  • What do they do?
  • What are they used to treat?
  • Side effects
A
  • Aspirin, clopidogrel, ticagrelor, prasugrel
  • Prevent new thrombosis
  • Angina, acute MI, patients at high risk of TIA/stroke
  • Haemorrhage, peptic ulcer leading to haemorrhage, aspirin sensitivity leading to asthma
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26
Q

Anticoagulants:

  • Examples
  • What do they do?
  • What are they used to treat?
  • Side effects
  • What are they reversed by?
A
  • Heparin (IV only), warfarin (oral use only), rivaroxaban, dabigatran
  • Block clotting factors (2, 7, 9, 10)
  • DVT, PE, NSTEMI, atrial fibrillation
  • Haemorrhage
  • Vitamin K
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27
Q

Fibrinolytic drugs:

  • Examples
  • What do they do?
  • What are they used to treat?
  • Side effects
  • When should they be avoided?
A
  • Steptokinase and tissue plasminogen activator
  • Dissolve a formed clot
  • STEMI, select cases of PE, select cases of CVA
  • Serious risk of haemorrhage
  • Recent haemorrhage, trauma, bleeding tendencies, severe diabetic retinopathy, peptic ulcer
28
Q

Atrial fibrillation:

  • Drugs to control rate
  • Drugs to chemically cardiovert
A
  • Beta blockers, digoxin, rate limiting calcium channel blockers
  • Amiodarone
29
Q

Drugs used in the treatment of heart failure (7)

A

ACE inhibitors, ARBs, Beta-blockers, mineral corticosteroid antagonists, neprilysin inhibitors, diuretics, digoxin

30
Q

Digoxin I:

  • What does it do?
  • What is it good in?
  • Why is it bad in excess?
A
  • Blocks AV conduction, produces a degree of AV conduction delay
  • Good in atrial fibrillation
  • Heart rate falls too much giving bradycardia and heart block
31
Q

Why is digoxin II bad?

A

Increases ventricular irritability producing ventricular arrhythmias and has a very narrow therapeutic index

32
Q

Signs and symptoms of digoxin toxicity

A

Nausea and vomiting, yellow vision, bradycardia, heart block, ventricular arrhythmias

33
Q

Neprilysin inhibitors:

  • Example
  • What does it do?
  • Side effects
A
  • Salcubitril valsartan
  • ARB and endopeptidase inhibitor
  • Hypotension, renal impairment, hyperkalaemia, angioneurotic oedema
34
Q

Haemostasis

A

Arrest of blood loss from a damaged vessel

35
Q

Sequence of events in haemostasis

A
  • Vascular wall damage exposing collagen and tissue factor
  • Primary haemostasis - forms a soft plug
  • Activation of blood clotting (coagulation) and the formation of a stable clot by fibrin enmeshing platelets – forms a solid clot
36
Q

Events in primary haemostasis to form a soft plug

A

Local vasoconstriction
Platelet adhesion, activation and aggregation of fibrinogen
Platelets are held together loosely by fibrinogen forming a soft plug

37
Q

How is a soft plug converted into a solid clot

A
  • Inactive factor X is converted by tenase to the active factor Xa by IXa and VIIIa
  • Inactive factor II (prothrombin) is converted by prothrombinase (Xa and Va) to the active factor IIa (thrombin)
  • Thrombin converts fibrinogen to fibrin which forms a solid clot
38
Q

Thrombosis

A

A haematological plug in the absence of bleeding

39
Q

Arterial thrombus:

  • Describe colour and structure
  • If it detaches where does the embolus usually lodge?
  • Treatment
A
  • White thrombus: mainly platelets held together in a fibrin mesh
  • Embolus usually lodges in an artery in the brain or other organ
  • Treated with antiplatelets
40
Q

Venous thrombus:

  • Describe colour and structure
  • If it detaches where does the embolus usually lodge?
  • Treatment
A
  • Red thrombus: white head, jelly-like red tail, fibrin rich
  • Embolus usually lodges in the lungs
  • Treated with anticoagulants
41
Q

What does warfarin block?

A

A modification of factors X and II (prothrombin) essential for their function

42
Q

What does rivaroxaban inhibit?

A

Directly inhibits factor Xa (prothrombinase)

43
Q

What do heparin, LMWHs and fondaparinux inactivate?

A

Factor Xa (prothrombinase) via antithrombin III

44
Q

What does dabigatran inhibit?

A

Directly inhibits factor IIa (thrombin)

45
Q

Another thing that heparin inactivates

A

Factor IIa (thrombin) via antirhombin III

46
Q

Role of vitamin K reductase

A

Allows vitamin K to go from epoxide, to quinone and then hydroquinone

47
Q

Which drug blocks vitamin K reductase?

A

Warfarin

48
Q

Important side effect of anticoagulants

A

Significant risk of haemorrhage

49
Q

What factors does warfarin render inactive?

A

Factors II, VII, IX, X

50
Q

Administration of warfarin

A

Orally

51
Q

Is the onset of warfarin slow or fast?

A

Slow (2-3 days), whilst inactive factors replace active gamma-carboxylated factors that are slowly cleared from the plasma

52
Q

Half-life of warfarin

A

About 40 hours

53
Q

Therapeutic index for warfarin

A

Very low therapeutic index

54
Q

Treatment of warfarin overdose

A

Administration of vitamin K1 as phytomenanadione

55
Q

Factors that can increase the risk of haemorrhage whilst on warfarin

A

Liver disease (decreased clotting factors), high metabolic rate (increased removal of clotting factors), drug interactions

56
Q

Drug interactions that can increase the risk of haemorrhage with warfarin

A

Agents that inhibit hepatic metabolism of warfarin by CYP2C9, drugs that inhibit platelet function, drugs that inhibit reduction, or decreased availability of, vitamin K

57
Q

Factors that can increase the risk of thrombus with warfarin

A

Physiological state (e.g. pregnancy, hypothyroidism), vitamin K consumption, drug interactions

58
Q

Role of antithrombin III

A

Inhibitor of coagulation by neutralising the enzymatic activity of thrombin

59
Q

What is heparin?

A

Heparin is a naturally occurring sulphated glycosaminoglycan of variable molecular size

60
Q

Examples of low molecular weight heparins

A

Enoxaparin and dalteparin

61
Q

Administration of heparin and LMWHs

A

Heparin - IV (immediate onset) or SC (delayed onset by 1 hour)
LMWHs - SC

62
Q

What is required to determine optimum dosage of heparin?

A

In vitro clotting test

63
Q

Elimination of heparin vs LMWHs

A

Heparin - zero order

LMWHs - first order, excreted by kidneys

64
Q

What inactivates heparin

A

Sulfate - given as IV

65
Q

Adverse effects of heparin and LMWHs

A

Haemorrhage, osteoporosis, hypoaldosteronism, hypersensitivity reactions

66
Q

When are orally active inhibitors used to prevent thrombosis?

A

In patients undergoing hip and knee replacements

Medicine Cardiovascular (24 decks)

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