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Yr 3 - Pharmacology > Drugs - CVS > Flashcards

Drugs - CVS Flashcards

1
Q

Give some examples of ACE inhibitors

A

Ramipril, lisinopril etc

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2
Q

Indications of ACE inhibitors?

A
  • Hypertension - 1st line in patients <55 and NOT of black african or african-caribbean origin OR all patients with type 2 diabetes
  • LV failure
  • Symptomatic heart failure
  • Prophylaxis post MI in patients with evidence of heart failure
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3
Q

Mechanism of ACE inhibitors?

A
  1. Blocks conversion of angiotensin I to II by ACE
  2. This blocks vasoconstrictive effects of angiotensin II, causing blood vessels to relax and widen which reduces O2 demand on heart
  3. Blocking of angiotensin II also prevents release of aldosterone - this increases excretion of salt and water which lowers BP further
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4
Q

What are the most common side effects of ACE inhibitors?

A
  • Dry cough (as ACE inhibitors prevent breakdown of bradykinin)
  • Low blood pressure
  • Headaches
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5
Q

Contraindications for ACE inhibitors?

A
  • Hypotension
  • Hypersensitivity
  • Angioedema
  • Renal artery stenosis
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6
Q

What class of drug are azilartan, candesartan and losartan?

A

Angiotensin receptor blockers (ARBs)

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7
Q

Indications of ARBs?

A
  • Hypertension (if ACEi contraindicated)
  • Heart failure
  • Post MI
  • CKD
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8
Q

Mechanism of ARBs?

A

Block the action of angiotensin II at the receptor

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9
Q

Contraindications of ARBs?

A
  • If patient is already taking ACE inhibitor
  • Pregnancy
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10
Q

How do ACEi and ARBs affect potassium levels?

A

ACE inhibitors and ARBs reduce proteinuria by lowering the intraglomerular pressure, reducing hyperfiltration. These drugs tend to raise the serum potassium level** and **reduce the glomerular filtration rate (GFR).

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11
Q

Why can ACEi and ARBs not be taken together?

A

Risk of hyperkalaemia and AKI (as both drugs increase potassium levels)

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12
Q

What other medications should ARBs NOT be taken with?

A

Any other medications that increase potassium levels e.g. ibuprofen, potassium-sparing diuretics

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13
Q

Main side effects of ARBs?

A

Dizziness

Headache

Fainting

Fatigue

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14
Q

What class of drugs are atenolol and bisoprolol?

A

Beta blockers (b2 antagonists)

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15
Q

Indications for beta blockers?

A
  • Tachycardia
  • Angina
  • Atrial fibrillation
  • Hypertension
  • Post MI
  • Congestive heart failure
  • CAD
  • Arrhythmias
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16
Q

Mechanism of beta blockers?

A

Block the effects of catecholamines at B1 adrenergic receptors which decreases the sympathetic activity of the heart (by decreasing conduction through the AV node).

Also reduces renin secretion which blocks the formation of angiotensin II.

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17
Q

Contraindications of beta blockers?

A
  • Bradycardia
  • Hypotension
  • Wolf-Parkinson-White syndrome
  • Asthma → likely to exacerbate bronchoconstriction
  • 2nd/3rd degree AV block
  • Peripheral vascular disease (i.e. poor circulation)
  • Diabetes
  • Hypersensitivity
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18
Q

Why is atenolol contraindicated in diabetes?

A

As atenolol may mask signs of hypoglycaemia e.g. increased HR

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19
Q

Main side effects of beta blockers?

A
  • GI disorder; diarrhoea, constipation, N&V
  • Dizziness, syncope, confusion (bradycardia)
  • Rash → concern
  • Cold fingers and toes
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20
Q

Why must beta blockers be prescribed with caution in the elderly?

A

Consider other medications, bradycardia, heart block, diabetes, asthma, obstructive respiratory diseases

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21
Q

Why should you avoid abrupt withdrawal of beta blockers?

A
  • Avoid abrupt withdrawal, especially in heart disease patients as may cause rebound worsening of myocardial ischaemia
  • Encourage gradual reduction
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22
Q

Why are patients encouraged to initially take beta blockers before bed?

A

May feel dizzy after first dose so take at bedtime, then can take in morning if you do not feel dizzy

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23
Q

What are the 3 major classes of diuretics?

A
  1. thiazide
  2. loop
  3. potassium-sparing
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24
Q

Give the site of action of each of the 3 classes of diuretics

A
  • Thiazide → distal convoluted tubule & connecting segment
  • Loop → ascending loop of Henle
  • Potassium sparing → cortical collecting duct
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25
Q

Give one example of a thiazide diuretic

A

Bendroflumethiazide

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26
Q

Mechanism of bendroflumethiazide?

A

Inhibits the sodium/chloride transporter (Na+ Cl- carrier) in the distal convoluted tubule of the nephron.

This inhibits sodium uptake and increases the excretion of sodium and water.

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27
Q

Indications for bendroflumethiazide

A
  • Oedema due to chronic heart failure
  • Hypertension (lower doses)
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28
Q

Contraindications of bendroflumethiazide?

A
  • Addison’s disease (adrenal insufficiency - decreased cortisol and aldosterone)
  • Hyponatraemia
  • Hypokalaemia
  • Hypercalcaemia
  • Symptomatic hyperuricaemia (gout)
  • Hypersensitivity
  • Liver failure
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29
Q

How do diuretics affect potassium levels?

A

Have potassium depleting effects - can cause hypokalaemia

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30
Q

Which drugs can enhance the potassium-depleting effects of diuretics?

A

Steroids

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31
Q

Side effects of bendroflumethiazide?

A
  • Needing to urinate more often
  • Dehydration (feeling thirsty with dry mouth)
  • Electrolyte imbalances (e.g. hypokalaemia)
  • Hyperuricaemia
  • Constipation/diarrhoea
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32
Q

What class of diuretic are bumetanide and furosemide?

A

Loop diuretics

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33
Q

Indications for loop diuretics?

A

Pulmonary oedema due to LVF

Chronic heart failure

Hypertension

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34
Q

Mechanism of loop diuretics?

A
  • Inhibits the Na+/K+/2Cl co-transporter in the loop of Henle (in the kidney) which reduces the Na & K reabsorption
  • This leads to increase Na (& water) excretion
  • Less fluid in bloodstream → eases symptoms of oedema
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35
Q

Contraindications of loop diuretics?

A
  • Anuria
  • Hypokalaemia/hyponatraemia
  • Hypotension
  • Hypersensitivity
  • Liver disease
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36
Q

Side effects of loop diuretics?

A
  • Urinating more frequently
  • Symptoms of dehydration: feeling thirsty and dry mouth
  • Weight loss (as body loses water)
  • Headaches
  • Confusion/dizziness
  • Muscle cramps/weakness
  • Electrolyte imbalance
  • Hypotension
  • Serious side effects (consult doctor):
    • Ringing in ears (tinnitus) or loss of hearing
    • Unexplained bruising or bleeding
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37
Q

Give an example of a potassium sparing diuretic

A

Spironolactone

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38
Q

Which diuretic is also an aldosterone antagonist?

A

Spironolactone

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39
Q

Which diuretic is also an anti-androgen?

A

Spironolactone

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40
Q

Why would spironolactone be given alongside thiazide/loop diuretics?

A
  1. Only works as weak diuretic if used alone
  2. Causes retention of potassium (thiazide/loops cause potassium loss) and are more effective alternative to potassium supplements
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41
Q

Indications for potassium sparing diuretics?

A
  • Resistant hypertension
  • Oedema & ascites (caused by liver cirrhosis)
  • Oedema in CHF
  • 1ary hyperaldosteronism (Conn’s syndrome)
  • Nephrotic syndrome
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42
Q

Mechanism of spironolactone?

A
  • Resembles aldosterone (adrenocorticoid hormone) so competitively inhibits aldosterone which normally acts on the distal renal tubule
  • This increases Na and H20 excretion** and **reduces K excretion (potassium sparing) → urinate more often
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43
Q

Contraindications of spironolactone?

A
  • Addison’s disease (adrenal insufficiency e.g. low aldosterone)
  • Anuria
  • Hyperkalaemia (due to K+ sparing)
  • Hypersensitivity
  • Hypercalcaemia, hypernatraemia
  • Hypotension
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44
Q

Side effects of spironolactone?

A
  • Hyperkalaemia (discontinue)
  • Gynaecomastia
  • GI upset
  • Breast tenderness
  • Irregular periods
  • Low BP
  • Increased urination
  • Dizziness
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45
Q

What class of drug are amlodipine and felodipine?

A

Calcium channel blocker

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46
Q

What class of drug is diltiazem?

A

Calcium channel blocker

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47
Q

What class of drug is verapamil?

A

Calcium channel blocker

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48
Q

Indications for calcium channel blockers?

A
  • Hypertension → 1st line in patients >/= 55 y/o (without type 2 diabetes) or patients of any age of Black African or African-Caribbean origin (without type 2 diabetes)
  • Angina
  • Arrhythmias
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49
Q

Mechanism of calcium channel blockers?

A
  1. Prevents calcium from entering the cells of the heart and arteries → this decreases conduction through the AV node
  2. This causes the heart to contract less strongly (as SA and AV node AP upstroke is Ca2+ dependent)
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50
Q

Side effects of CCBs?

A
  • Ankle swelling
  • Constipation
  • Headache
  • Flushing
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51
Q

Contraindications of CCBs?

A
  • Heart failure
  • Severe bradycardia
  • Hypotension
  • Atrial flutter or fibrillation due to accessory conducting pathways (e.g. Wolff-Parkinson-White syndrome)
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52
Q

Give an example of a nitrate

A

Isosorbide mononitrate

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53
Q

Indications for nitrates?

A

Stable angina → relieve symptoms or used to prevent angina just before activities that may bring it on

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54
Q

Mechanism of nitrates?

A
  1. Causes vasodilation of coronary vessels which increases the oxygen supply to the myocardium
  2. Dilation of peripheral veins/arteries also reduces preload and afterload → this lowers myocardial oxygen consumption (and stress of heart)
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55
Q

Cause of angina?

A

narrowing/blockage/spasms of coronary arteries which reduces oxygenated blood reaching heart

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56
Q

In what form are nitrates typically taken?

A

GTN spray (sublingual)

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57
Q

Side effects of nitrates?

A
  • Hypotension (don’t use spray repeatedly!)
  • Headaches (common)
  • Dizziness, light-headed, flushing
58
Q

What is the most commonly prescribed class of drug in the UK?

A

Statins

59
Q

Give 2 examples of statins

A

Atorvastain, Simvastatin

60
Q

What class of drugs are statins?

A

HMG co-reductase inhibitors

61
Q

Indications for statins?

A
  • Hypercholesterolaemia
  • Coronary heart disease
  • Stroke
  • Prevent MI
62
Q

Mechanism of statins?

A
  1. Inhibit HMG CoA reductase which blocks the pathway synthesising cholesterol in the liver (most circulating cholesterol comes from internal synthesis NOT diet)
  2. Liver senses reduced cholesterol → increased expression of LDL receptors → increased uptake of cholesterol from blood → less circulating LDLs
  3. Also enhances stability of atherosclerotic plaques → reduces risk of blood clots
63
Q

Most common side effect of statins?

A

Muscle aches

64
Q

Link between statins and Alzheimer’s?

A

Alzheimer’s prevalence 70% lower in people taking statins BUT does not slow development in symptomatic Alzheimer’s patients.

65
Q

Statins should be stopped temporarily if patients are started on which antibiotic? Why?

A

Clarithromcyin → due to greater risk of muscle pain/damage

66
Q

How does grapefruit affect statins?

A

Grapefruit is an inhibitor → slows liver metabolism of statins

67
Q

Give 3 examples of antiplatelets

A
  1. Aspirin
  2. Clopidogrel
  3. Ticagrelor
68
Q

Indication for aspirin?

A

Post MI (dual antiplatelet therapy)

N.B. antiplatelets should not be prescribed for the primary prevention of CVS disease

69
Q

What class of drug is aspirin?

A

NSAID

70
Q

Mechanism of aspirin?

A

COX inhibitor → prevents formation of thromboxane A2 and prostaglandins from arachidonic acid (which is released from activated platelets)

Thromboxane is a potent vasoconstrictor and platelet aggregant

71
Q

Reversal agent for aspirin?

A

No reversal agents – irreversible effect (lasts 4-5 days).

72
Q

Contraindications for aspirin?

A
  • Age <16
  • Hypersensitivity
  • Peptic ulceration
  • Haemophilia
  • Reye’s syndrome
  • Thrombocytopenia
73
Q

Side effects of aspirin?

A
  • GI upset: N&V
  • Heartburn
  • Bleeding
  • Bruising
  • Ulcers
74
Q

What class of drug are ticagrelor & clopidogrel?

A

P2Y12 receptor antagonist

75
Q

Indications for clopidogrel/ticagrelor?

A

Post MI (dual antiplatelet therapy)

  • Prevent atherothrombotic events in patients with acute coronary syndrome (in combination with aspirin)
  • Prevention of atherothrombotic events in patients with history of MI and high risk of atherothrombotic event (in combination with aspirin)
76
Q

Contraindications for ticagrelor/clopidogrel?

A
  • Active bleeding
  • Intracranial haemorrhage
  • Liver failure
77
Q

Mechanism of P2Y12 receptor antagonists (clopidogrel/ticagrelor)?

A

Prevents ADP-mediated P2Y12 dependent platelet activation and aggregation by irreversibly binding to P2Y12 class of ADP receptor on platelets

78
Q

Main side effect of clopdiogrel/ticagrelor?

A

Bleeding - nosebleeds, bruising, gum bleeding, heavy periods

79
Q

What class of drug is warfarin?

A

Anticoagulant (vitamin K antagonist)

80
Q

What is the most commonly prescribed anticoagulant?

A

Warfarin

81
Q

Why is the preference for warfarin slowly decreasing?

A
  • Extensive drug and diet interactions
  • Higher incidence of major bleeding
  • Need for laboratory monitoring compared to DOACs
82
Q

Warfarin is the anticoagulant of choice in patients with which 3 conditions?

A
  1. Mechanical heart valves
  2. Valvular AF
  3. End stage renal failure
83
Q

Mechanism of warfarin?

A

Antagonises vitamin K which is responsible for synthesising vitamin K dependent clotting factors

84
Q

What are the vitamin K dependent clotting factors?

A

10, 9, 7, 2 (and protein C and protein S)

85
Q

DOACs inhibit a single clotting factor. Which clotting factor does Dabigatran inhibit?

A

Thrombin

86
Q

DOACs inhibit a single clotting factor. Which clotting factor does Rivoraxaban, apixaban and edoxaban inhibit?

A

Factor Xa

87
Q

Give 6 indications for warfarin

A
  1. Treatment of VTE (DVT/PE) → 2nd line after DOACs
  2. Atrial fibrillation → 2nd line after DOACs
  3. Rheumatic heart disease
  4. Mitral valve disease
  5. Mechanical valve disease
  6. Inherited, symptomatic thrombophilia

It is used for a) treatment or b) prophylaxis of systemic embolisation

88
Q

Contraindications for warfarin?

A
  • Cancer/malignancy
  • Hypersensitivity
  • Low vitamin K levels
  • Haemorrhagic stroke
  • Active bleeding (e.g. peptic ulcer, oesophageal varices)
  • Pregnancy
  • Drugs with which there is significantly increased risk of bleeding (e.g. antiplatelet drugs, NSAIDs and enzyme inhibitors)
89
Q

Why is warfarin contraindicated in pregnancy?

A

Teratogenic

90
Q

In malignancy, what should be used instead of warfarin?

A

Heparin or DOAC

91
Q

Treatment targets for warfarin are referred to in the terms of what?

A

International normalised ratio (INR).

92
Q

What is the INR? What does a high/low INR mean?

A

A standardised version of the prothrombin time (the time taken for blood to clot via the extrinsic pathway)

Higher INR → Blood clots more slowly (risk of bleeding)

Lower INR → Blood clots more quickly (risk of clotting)

93
Q

INR target for treatment of VTE, atrial fibrillation, mitral valve disease and inherited symptomatic thrombophilia?

A

2-3

94
Q

INR target for mechanical heart valves?

A

2.5-3.5

95
Q

How long may warfarin take to achieve an INR within the therapeutic range?

A

5 days

96
Q

Warfarin may initially induce a hypercoaguable state. Why?

A

Suppression of protein C (vit K dependent) occurs much more quickly than that of the coagulation factors (10, 9, 7, 2) due to protein C having a short half life → cannot degrade coagulation factors

97
Q

What can be considered as concurrent treatment during this ‘hypercoaguable’ state induced by warfarin initially?

A

If patient develops an acute VTE and is at high risk of further thrombosis → consider concurrent administration of heparin for at least 5 days until INR is within therapeutic range

98
Q

Side effects of warfarin?

A
  • Haemorrhage (most common) → can be life threatening or not
  • Coumarin induced skin necrosis
99
Q

What is coumarin induced skin necrosis? Why does it occur?

A

Skin and subcutaneous tissue necrosis occur due to acquired protein C deficiency following treatment with vitamin K anticoagulant

100
Q

What is administered concurrently for four to five days after warfarin initiation?

A

Heparin

101
Q

Give some P450 enzyme inhibitors

A

Amiodarone, ciprofloxacin, clarithromycin, erythromycin, oral contraceptives, St John’s Wort

102
Q

Give some P450 enzyme inducers

A

Carbamazepine

Phenytoin

Alcohol

Allopurinol

Paracetamol

SSRIs

103
Q

An advantage of warfarin over DOACs is its ability to be rapidly reversed. Give 2 scenarios where warfarin might need to be reversed?

A
  1. Prior to surgery
  2. INR is supratherapeutic (clots too quickly → bleeding)
104
Q

Give 3 main options for reversing warfarin

A
  1. Withholding warfarin
  2. Vitamin K (oral or IV)
  3. Prothrombin complex concentrate (PCC)
105
Q

Why would PCC be given for reversing warfarin?

A

Contains vitamin K dependent clotting factors (10, 9, 2, 2)

106
Q

If PCC is unavailable, what can be given instead to reverse warfarin?

A

Fresh frozen plasma → contains normal levels of all coagulation factors

107
Q

How do inducers of the P450 system affect warfarin?

A

Induce enzymes → warfarin metabolised more quickly → efficiency of warfarin decreases → blood clots more slowly (decreased INR → tendency to clot)

108
Q

How do inhibitors of the P450 system affect warfarin?

A

Inhibit enzymes → warfarin metabolised more slowly → blood warfarin levels rise → blood clots more quickly (higher INR → risk of bleeding)

109
Q

How do cranberries affect warfarin?

A

Inhibitor → increases warfarin potency

110
Q

What type of drug are Tinzaparin and Enoxaparin examples of?

A

Heparin (Enoxaparin is a LMWH)

111
Q

What class of drug is heparin?

A

Anticoagulant

112
Q

Why is heparin more often used in LMWH form?

A

as this has a lower risk of HIT (heparin induced thrombocytopenia)

113
Q

What is HIT (heparin induced thrombocytopenia)?

A

Occurs when heparin dependent IgG antibodies bind to heparin/platelet factor 4 complexes to activate platelets and produce a hypercoagulable state

114
Q

Indications for heparin?

A
  • Used alongside warfarin to prevent hypercoaguable state
  • PE
  • Unstable angina
  • Prophylaxis for thrombosis
115
Q

Mechanism of heparin vs LMWH?

A

Heparin → Enhances action of antithrombin by binding to it; has equal effect in inhibiting both thrombin and FXa BUT will not be effective in inhibiting effects of thrombin bound to clot that already exists.

LMWH → Binds to antithrombin but has much greater effect on FXa than thrombin (FIIa) so functions more as inhibitor of FXa than as inhibitor of thrombin

116
Q

Administration of heparin?

A

Subcutaneous injection (not orally)

117
Q

How is dosage of heparin adjusted?

A

Body weight

118
Q

Are DOACs used for prevention of thrombus formation or extension in the venous or arterial circulation? Why?

A

venous → fibrin rich (and affects clotting cascade which ends with a fibrin mesh)

119
Q

Do venous or arterial thrombi contain lots of fibrin?

A

Venous

120
Q

Indications for DOACs?

A
  • AF
  • VTE treatment (DVT/PE)
121
Q

Which DOAC inhibits FIIa (thrombin)?

A

Dabigatran

122
Q

Which DOACs inhibit FXa?

A

Rivaroxaban, apixaban, edoxaban

123
Q

What class of drug is digoxin?

A

Digitalis glycoside

124
Q

Indications for digoxin?

A

1) For the treatment of mild to moderate heart failure in adult patients
2) To increase myocardial contraction in children diagnosed with heart failure
3) To maintain control ventricular rate in adult patients diagnosed with chronic atrial fibrillation.

125
Q

Contraindications of digoxin?

A
  • Acute myocardial infarction.
  • Severe renal failure
  • Hypersensitivity.
  • Ventricular fibrillation.
  • Myocarditis.
  • Hypomagnesemia.
  • Hypokalemia.
  • Wolf-Parkinson-White syndrome.
  • Patient on other HR lowering drugs → bradycardia
126
Q

Mechanism of digoxin?

A

Digoxin lowers the heart rate by enhancing vagal tone, which leads to slowing of SA and AV nodal conduction and thereby a reduction in heart rate.

(Inhibits Na+/K+ ATPase)

127
Q

Side effects of digoxin?

A
  • D&V
  • Diarrhoea
  • Fatigue
  • Fainting
  • Palpitations
  • Visual disturbances
  • Digoxin toxicity → delirium
128
Q

Why is digoxin contraindicated in severe renal failure?

A

Digoxin is excreted by the kidneys without metabolism by the liver → In kidney failure, the body is unable to eliminate digoxin, causing levels to accumulate (digoxin toxicity)

129
Q

What class of drug is amiodarone?

A

Class III Anti-arrhythmic

130
Q

Indications for amiodarone?

A
  1. Recurrent ventricular fibrillation (VF)
  2. Recurrent hemodynamically unstable ventricular tachycardia (VT).
131
Q

Mechanism of amiodarone?

A
  1. Blocks potassium currents that cause repolarisation of heart during 3rd phase of action potential → increases duration of action potential
  2. Cardiac muscle cell excitability is reduced → preventing and treating abnormal heart rhythms
132
Q

Why is a loading dose of amiodarone often required?

A

58 days half life

133
Q

Contraindications of amiodarone?

A
  • Thyroid dysfunction → hyper/hypo, thyrotoxicosis
  • Hypokalaemia
  • Hypomagnesaemia
  • Severe conduction disturbances (unless pacemaker fitted)
  • Sinus node disease (unless pacemaker fitted)
134
Q

Side effects of amiodarone?

A
  • Arrythmias
  • Hyper/hypothyroidism
  • N&V
  • Constipation
135
Q

Why is amiodarone contraindicated in thyroid disorders?

A

As amiodarone contains iodine so can cause disorders of thyroid function

136
Q

What class of drug is adenosine?

A

Class V Anti-arrhythmic

137
Q

Indications for adenosine?

A

emergent treatment of supraventricular tachycardia

138
Q

Calcium channel blockers should be avoided in heart failure as they can further depress cardiac function and exacerbate symptoms. Which CCB is the one exception to this?

A

Amlodipine

139
Q

Why are CCBs contraindicated in Wolff-Parkinson-White syndrome?

A

In patients with WPW and atrial fibrillation, the erratic atrial action potentials can conduct through the accessory pathway very quickly (faster than through the AV node). Therefore, WPW patients who develop atrial fibrillation have higher ventricular rates than those without WPW.

If an AV blocking agent is given, fewer atrial action potentials will pass through the AV node and more will pass through the accessory pathway, paradoxically increasing the ventricular rate potentially causing ventricular fibrillation (fatal).

140
Q

Which 3 classes of drugs block the AV node?

A
  1. Beta blockers
  2. Calcium channel blockers
  3. Digoxin
141
Q

Name 3 classes of drugs contraindicated in Wolff-Parkinson-White syndrome. Why?

A
  1. Beta blockers
  2. Calcium channel blockers
  3. Digoxin

As block AV node, causing ventricular tachycardia

Yr 3 - Pharmacology (18 decks)

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