Cardiovascular Flashcards

(125 cards)

1
Q

Furosemide

A

Loop Diuretic

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2
Q

How Loop Diuretics work?

A

Act in thick ascending limb of loop of Henle. Prevents Na+ and K+ reabsorption decreasing water reabsorption

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3
Q

Indications for Loop Diuretics

A

Peripheral oedema, pulmonary oedema and acute renal insufficiency

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4
Q

Contraindications for Loop Diuretics

A
Anuria
Hypokalaemia
Gout
Type II DM
Pregnancy
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5
Q

Side effects of Loop Diuretics

A
Ototoxicity (toxic to ear)
GI disturbance
Hypokalaemia
Gout
Rash
Postural Hypotension
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6
Q

Possible interactions for Loop Diuretics

A
  • ACEi increased risk of first dose hypotension
  • Reduce excretion of lithium causing serum concentrations to rise
  • Digoxin - hypokalaemia increases risk of toxicity from digoxin and antiarrythimic grus
  • Theophylline- risk of hypokalaemia increased
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7
Q

Bendroflumethiazide, Chlortalidone, Metolazone

A

Thiazide Diuretic

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8
Q

Thiazide Diuretics

A

Act in distal convoluted tubule. Inhibits NaX reabsorption so decreases water reabsorption

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9
Q

Indications for Thiazide Diuretics

A

Hypertension
Oedema
Prophylaxis of Ca-containing renal stones
Nephrogenic diabetes insipidus

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10
Q

Contraindications for Thiazide Diuretics

A

Addison’s disease; hypercalcaemia; hyponatraemia; refractory hypokalaemia; symptomatic hyperuricaemia, hypotension, gout, TYype II DM , loop diuretic, pregnancy, poor renal function, breast feeding

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11
Q

Side effects for Thiazide Diuretics

A

Hypomagnesaemia, hypercalcaemia, postura hypotension, gout, hyperuricaemia, hyperlipidaemia, allergic vsculitis, hyperlipidaemia, a, allergic vasculitis, photosensitivity hyperglycaemia, erectile impotence, thrombocytopenia

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12
Q

Possible interactions for Thiazide Diuretics

A

NSAIDs, ACEI, Lithium- increasing plasma concentration, Digoxin, theophyllines

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13
Q

Spironolactone

A

Potassium Sparing Diuretic and Aldosterone Receptor Antagonist

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14
Q

How does Spironolactone work?

A

Competes for receptors in distal convoluted tubule. Inhibits Na+ reabsorption and K+ secretion so decreases water reabsorption. Results in sodium loss and potassium retention

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15
Q

Indications of Spironolactone

A

Ascite and oedema, heart failure, nephrotic syndrome, primary hyperaldosteronism (Conn’s syndrome)

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16
Q

Contra-indications of Spironalactone

A

Renal insufficiency, pregnancy, breast feeding, Addison’s disease

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17
Q

Side-effects of Spironolactone

A

Potassium sparing drugs, ACEi, ciclosporin, NSAIDs, digoxin, lithium

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18
Q

Atenolol

A

Beta-blocker drug

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19
Q

How do beta-blocker drugs work?

A
  • Beta-adrenoreceptors form part of sympathetic pathway causing vasconstriction, increase force, rate, conductance and bronchodilation.
    Blocking these receptors causes vasodilation, decreased force, rate, conductance and bronchoconstriction. They are negatively inotropic ( decreases contraction) and negatively chronotropic (decreases heart rate)
  • Antihypertensive as decreases renin production by kidneys
  • Antiarrhythmic as decreases AP initiation of heart
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20
Q

Stimulation of B1 adrenoreceptors causes what

A

Increase in force, rate and conductance of the heart

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21
Q

Stimulation of B2 adrenorecptors causes what

A

Smooth muscle relaxation, bronchodilation, vasodilation

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22
Q

Stimulation of B3 adrenoreceptors causes what

A

Fat lipolysis

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23
Q

Indication of Beta-blockers

A

Hypertension, Angina, arrhythimas, Heart failure, Migarines, MI, Hyperthyroidism, Aortic Dissection, Pheochromocytoma, Anxiety, Glaucoma, Benign Essential Tremor

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24
Q

Contra-indications of Beta-blockers

A

Asthma, heart block, unstable heart failure, unstable angina, bradycardia, sick sinus syndrome, hypotension, metabolic acidosis, cardiogenic shock, pregnancy

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25
Side effects of Beta Blockers
Bronchoconstriction, heart failure, Raynaud's, sleep distturbances, erectile impotence, liver damage, rash and dry eyes
26
Interactions of Beta-blockers
Verpamil as can increase risk of asystole or catastrophic reduction of cardiac output, antihypertensives, anti-arrhythmic drugs, NSAIDs
27
How are beta- blockers eliminated?
50% urine and 50% faeces
28
Stimulation of Alpha-1 adrenoreceptors causes what
vasoconstriction, relaxes GIT
29
Stimulationof ALpha-2 adrenoreceptors causes what
Platelet aggregation, inhibits NA and Ach release at presynaptic terminals
30
Amlodipine
Calcium Channel Blocker
31
How do Calcium Channel Blockers work?
Blocks L-type voltage-gated calcium channels preventing entry of Ca2+ and depolarisation of tissues. Vasodilates and lowers blood pressure
32
Effect of CCB on myocardial cells
Reduces contractility and anti-dysrhytmic action
33
Effect of CCB on Vascular smooth muscle
Vasodilation Arterial dilation: reduces resistance and pressure Venous dilation: increase in venous pooling, reduced flow to heart, reduces end-diastolic pressure
34
Indications of Amlodipine
Hypertension, Angina, Raynauds, Migraine,
35
Contraindications of Amlodipine
Pregnancy, breast feeding, heart failure, unstable angina, bradycardia,
36
Side effects of Amlodipine
Flushing, headache, peripheral oedema, bradycardia, SA block, palpitations
37
Interactions of CCB
other hypotensives, cyclosporin, digoxin, theophylline, grapefruit juice (except amlodipine)
38
Elimination of CCB
1st pass metabolism
39
Patient information for CCB
Ankle swelling or headache | Stop drinking grapefruit juice
40
Diltiazem
Benzthiazepine Calcium channel blocker
41
L-type Voltage Gated Calcium Channels
responsible for excitation-contraction coupling of skeletal, smooth, and cardiac muscle, hormonesecretion in endocrine cells and conduction of cardiac pacemaker signals
42
Indications for Dilitiazem
Angina, Hypertension, Cardiac Arrhythmias
43
Ramipril
Angiotensin Converting Enzyme Inhibitor (ACEi)
44
How do ACE inhibitors work?
ACE inhibitor inhibits ACE Reduces formation of Angiotensin 2 Reduces vasoconstriction, aldosterone secretion, water retention BP decreases
45
Indications for ACE inhibitors
Hypertension, Symptomatic heart failure, following MI, diabetic nephropathy
46
Contra-indications of ACE inhibitors
Pregnancy, Angioedema, renovascular disease
47
Side effects of ACE inhibitors
Persistent dry cough, hypotension, hypersensitivity, renal impairment, hyperkalaemia
48
Interactions of ACE inhibiotrs
Diuretics- increase risk of hyperkalaemia | NSAIDS- increase risk of renal impairment
49
Patient information for ACE inhibitors
Avoid in pregnancy as may effect fetal BP and renal function | Patients should take 1st dose to avoid 1st dose hypotension
50
Losartan
Angiotensin Receptor Blocker (ARBs)
51
How do ARBs work
ARB inhibits angiotensin II type I receptors Reduces vasoconstriction, aldosterone secretion, H2O retention BP decreases
52
Indication of ARBs
Alternative to ACEi as causes less frequent coughs, hypertension, heart failure, MI, Diabetic nephropathy
53
Contraindications of ARBs
Pregnancy, Angioedema, renovascular disease, fixed cardiac output, peripheral vascular disease, hyperkalaemia
54
Interactions of ARBs
Diuretics, NSAIDs
55
Isosorbide mononitrate
Nitrates/ Nitrovasodilators. Like GTN but slower onset and longer half-time than GTN
56
How do Nitrates work?
Administered as a prodrug. Nitrates undergoes a chemical reduction by enzymes releasing NO. This stimulates guanylate cyclase pathway in smooth muscle cells causing vascular smooth muscle relaxation and vasodilation. This reduces preload and afterload so heart requires less oxygen
57
Indications for Nitrates
Angina Pectoris Short term reduction of BP Pulmonary Oedema Chronic Heart Failure
58
Contraindications for Nitrates
``` Hypovolaemia and Hypotension Cardiac Disease e.g. mitral stenosis, hypertrophic cardiomyopathy Bleeding and haemorrhage Anaemia Close-angle Glaucoma Pregnancy ```
59
Side effects of nitrates
``` Throbbing headache Dizziness Postural hypotension Tachycardia Methaemoglobinaemia ```
60
Interactions of nitrates
Sildenafil (Viagra) - risk of severe hypotension Other antihypertensives Antimuscarinic drugs - cause of dry mouth, reduce absorption of sublingual nitrates PDE5 inhibitors- block deactivation of cGMP whilst nitrates increase cGMP levels, leads to venous pooling
61
Patient Information of Nitrates
Nitrate free period required everyday (min 4-8hours) to prevent nitrate tolerance Tolerance reversed within 18hours of stopping nitrates
62
Digoxin
Cardiac glycoside (digitalis)
63
How does Digoxin work?
Inhibits Na/ K pump so increases intracellular Na concentration. This causes Ca+ to be pumped out of cell increasing force of contraction. Increases vagal activity and decreases AV node conduction so increases stroke volume and decreases heart rate
64
Indications of Digoxin
Rate control for AF | Heart Failure
65
Contra-indications for Digoxin
- Second degree/ Complete Heart Block- slows conduction via AV node - Supraventricular Tachycardia (SVT) associated with Wolff-Parkinson- White syndrome - Hypokalaemia - risk of arrhythmias so give potassium supplements - Pregnancy - Renal Insufficiency
66
Side effects of Digoxin
Cardiac Arrhythmias/ Heart Block HTN Digoxin toxicity: N&V, diarrhoea, abdominal pain, visual disturbances, confusion, delirium, arrhythmias, heart block
67
Possible interactions of Digoxin
- Drugs that impair renal function e.g. NSAIDs, ACEi - Diuretics can cause hypokalaemia resulting in digoxin toxicity without a change in plasma concentration - Antiarrhythmic drugs e.g. beta blockers, amiodarone, verapamil, diltiazem - Amiodarone, quinidine, spironolactone, verpamil
68
Patient information for Digoxin
Effective dose can be close to toxic dose so close monitoring is neeed Pregnancy and breast feeding require small dose
69
Amiodarone
Antiarrhythmic
70
How does Amiodarone work?
Prolongs the action potential and refractory period throughout the heart. Often last drug of choice
71
Indications for Amiodarone
Tachycardia AF and flutter VF or pulseless VT - Emergency
72
Contraindications for Amiodarone
Sinus bradycardia, SA disease, Heart Block Thyroid disease Pregnancy, breast feeding Heart Failure/ Cardiomyopathy bolus IV administration
73
Side effects of Amiodarone
``` Corneal lipofuscin microdeposits (almost 100% of patients will get this) Sunlight sensitivity Pneumonitis Peripheral neuropathy Hypo/Hyperthyroidism Hepatotoxicity Hypersensitivity/ Vasculitis Haemolytic or aplastic anaemia ```
74
Interactions of Amiodarone
- Warfarin- inhibits metabolism increasing effect - Digoxin- reduces excretion increasing effect - Drugs that reduced heart rate: CCB, beta blockers - Drug that prolongs QT interval: antiarrhythmics, co-amoxiclav Erythromycin, antipsychotics, lithium, TCA, Phenytoin
75
Half life of Amiodarone
Very long half life up to 1 month so interactions can occur after stopping drug
76
Patient information for Amiodarone
- Before starting, measure TFT, LFTs, ECG and CXR - Measure TFT and LFT every 6 months - Patients may become more sensitive to the sun so should use SPF
77
Aspirin
Anti-platelet, NSAID
78
How does Aspirin work?
Irreversible COX-inhibitor. Irreversibly inhibits COX-1 and modifies the activity of COX-2
79
Mechanism of Aspirin
Aspirin is a weak acid so is protonated in the stomach and crosses the mucosa, most absorption is in the ileum, hydrolysed by esterase to form salicylate. Salicylate enters active site of COX-1 and 2 and acetylates serine 530, irreversibly activating them. Reduces PGE2 and TXA2 production.
80
Indications of Aspirin
``` Primary and secondary prevention of atherosclerotic diseae Analgesia Anti-Inflammatory Pyrexia Dysmenorrhoea Headaches and Migraine ```
81
Contraindications of Aspirin
``` Haemophilia Active peptic ulceration Uncontrolled hypertension Renal/ Hepatic bleeding Pregnancy Asthma Renal insufficiency G6PD deficiency Children under 16 ```
82
Side effects of aspirin
``` Intracranial bleeding GI disturbance Tinnitus due to salicylism Hypersensitivity Bronchospasm Asthma Nasal Polyps Thrombocytopenia ```
83
Interactions of aspirin
Displaces warfarin from plasma increasing its effect Antagonises effect of diureics and causes fluid retention at higher doses Ibuprofen inhibits anti-platelet action of aspirin Reduces excretion of methotrexate increasing risk of toxicity
84
Elimination of Aspirin
75% metabolised by liver 25% oxidised 25% excreted unchanged
85
Clopidogrel
Anti-platelet
86
How does Clopidogrel work
ADP receptor antagonist | Inhibits ADP receptors on platelets that stimulate platelet aggregation so inhibits thrombus formation
87
Indications for Clopidogrel
Prevention of atherosclerotic disease: MI, angina, storke with aspirin Following Angioplasty with aspirin
88
Contraindication for Clopidogrel
``` Active Bleeding Conditions Haemophillia or other bleeding disorders Active peptic ulceration Renal/hepatic insufficiency Pregnancy ```
89
Side effects of Clopidogrel
``` Increase risk of bleeding Abdominal PAin Nausea Dizziness/Vertigo Paraesthesia Hepatic/biliary damage ```
90
Interactions of Clopidogrel
With aspirin, anti-platelet effect and risk of bleeding increases Caution with warfarin due to increase risk of bleeding
91
Fibrinolytics
Streptokinase Tissue Plasminogen Activator (TPA) Urukinase (UA)
92
Streptokinase drugs
Alteplase, Reteplase, Tenecteplase
93
Mechanism of Streptokinase
Combines with plasminogen to form an active complex which activates plasminogen to plasmin which breaks fibrin down
94
Indications for Streptokinase
``` Elevated ST elevation Acute MI Acute Stroke DVT/PE Unblock venous catheters/thromboses arteriovenous shunts ```
95
Contraindications for Streptokinase
``` Active Bleeding Haemophilia Active Peptic Ulceration Pregnancy Surgery or trauma in last 12 weeks Pericarditis/ Inefective endocarditis Acute pancreatitis ```
96
Side effects of Streptokinase
Bleeding Hypotension in MI Allergic Reaction Nausea and Vomiting
97
When to give Alteplase, Reteplase, Streptokinase, Tenecteplase
Alteplase: within 6-12 hours of symptom onset Reteplase and Streptokinase: within 12 hours of onset Tenecteplase: 6 hours of onset
98
Tinzaparin Enoxaparin Dalteparin
Low Molecular Weight Heparin (LMWH)
99
Mechanism of Unfractionated Heparins (UF)
Activates antithrombin in turn inactivating clotting factor Xa and thrombin
100
Mechanism of LMWH
Inhibits factor Xa
101
Fondaparinux
Inhibits factor Xa only
102
Indications for LMWH/UF
1. Venous Thromboembolism: DVT, PE 2. Acute Coronary Syndrome: LMWH and Fondaparinux are first-line choice 3. Prophylaxis against thromboembolic disease
103
Contraindication for LMWH/UF
Haemophilia | Thrombocytopenia
104
Side effects of LMWH/UF
``` Bruising Haemorrhage Osteoporosis Hypoaldosteronism/ Hyperkalaemia Thrombocytopenia ```
105
Elimination of Heparins
Around 1 hour Eliminated by renal excretion Use UH in renal failure
106
Drug for Heparin overdose or to reverse the effects of Heparin
Protamine Sulphate
107
Warfarin
Oral Anticoagulant
108
Mechanism of Warfarin
Inhibits Vitamin K-dependent coagulation factors and cofactors (1972). Inhibits Vitamin K epoxide reductase preventing reactivation of Vitamin K and coagulation factor synthesis
109
INR ranges for people on Warfarin
2.0-3.0 | For healthy people an INR < 1.1 is normal
110
Indications for Warfarin
Prevention of thromboembolic disease: DVT, PE, AF, prosthetic heart valves, after heart valve replacement
111
Contraindications for Warfarin
``` Haemophilia Thrombocytopenia Active Peptic Ulceration Uncontrolled HPT Renal/ Hepatic insufficiency Pregnancy Following trauma or surgery ```
112
Side effects of Warfarin
``` Haemorrhage Hypersensitivity Alopecia Diarrhoea Hepatic Dysfunction Pancreatitis ```
113
Interactions of Warfarin
Cytochrome P450 inhibitors decrease warfarin metabolism and increase bleeding risk Cytochrome P450 inducers increase warfarin metabolism and risk of clots Antibiotics can increase anticoagulation by killing gut flora that synthesise vitamin K
114
Cytochrome P450 inhibitors
Fluconasole Macrolides Protease Inhibitors
115
Cytochrome P450 inducers
Phenytoin Carbamazepine Rifampicin
116
Dosage of Warfarin
5-10mg OD
117
Rivaroxaban
Anticoagulant. Inhibitor of activated factor Xa.
118
Indications for Rivaroxaban
Prevention of stroke and systemic embolism in patients
119
Contraindicatons for Rivaroxaban
``` Active bleeding Antiphospholipid syndrome Malignant neoplasms Oesophageal varices Following an ACS event ```
120
Simvastatin
Statin - HMG CoA reductase inhibitors
121
Mechanism for Simvastatin
1. Statins reduce serum cholesterol levels by Inhibiting HMG CoA reductase, the enzyme involved in cholesterol synthesis. 2. Indirectly reduce triglycerides
122
Indications for Simvastatin
1. Primary and Secondary prevention of Cardiovascular Disease 2. Hyperlipidaemia
123
Contraindications for Simvastatins
Pregnancy and breast feeding Renal/Hepatic Insufficiency High alcohol intake Risk factors of myopathy/rhabdomyolysis
124
Side effects of Simvastatin
Headache GI disturbances ie Abdominal cramps Myopathy and Rhabdomyolysis Increase liver enzymes
125
Interactions of Simvastatin
Metabolism of Statins reduced by Cytochrome P450 inhibitors | Grapefruit Juice may increase statin levels by inhibiting Cytochrome P450 enzymes involved in metabolism