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PA- AP > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Indication for clopidogrel

A

For ACS, used in combo with aspirin

To prevent occlusion of coronary artery stents

long term secondary prevention for CVS, cerebrovascular

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2
Q

Contraindication for clopidogrel

A

NOT for people with active bleeding

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3
Q

Patient education for clopidogrel

A

In those who are taking clopidogrel following the insertion of a drug-eluting stent, emphasise the importance of continuing treatment as directed, usually for 12 months, to make sure that the stent stays open and does not block and cause a heart attack.

Report any unusual bleeding

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4
Q

Side effect for clopidogrel (5)

A

Bleeding

Dyspepsia, abdominal pain, diarrhoea,

thrombocytopenia (Rare)

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5
Q

Monitoring for clopidogrel

A

Clinical monitoring for adverse effects is most appropriate.

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6
Q

Key interaction for clopidogrel

A

CYP inhibitor -e.g. omeprazole , ciprofloxacin, erythromycin

Co-prescription with other antiplatelet or anticoagulant

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7
Q

MOA for clopidogrel

A

Thrombotic events occur when platelet-rich thrombus forms in atheromatous arteries and occludes the circulation. These drugs prevent platelet aggregation and reduce the risk of arterial occlusion by binding irreversibly to adenosine diphosphate (ADP) receptors (P2Y12 subtype) on the surface of platelets. As this process is independent of the cyclooxgenase (COX) pathway, its actions are synergistic with those of aspirin.

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8
Q

Indication for aspirin (2)

A

Painkiller, reduce fever or inflammation (antiplatelet drug)

Used to prevent chest pain, Heart attack or stroke

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9
Q

side effects for aspirin

A

Dyspepsia, Haemorrhage , gi irritation

Dyspnoea, Skin reactions

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10
Q

contraindication for aspirin-5

A

Active ulcer, haemophilia, severe cardiac failure

Avoid in children under 16 years and in 3rd trimester

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11
Q

Monitoring for aspirin

A

Enquire about side effect

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12
Q

Patient education for aspirin

A

Advice purpose of low dose aspirin to prevent heart attacks and strokes. Warn to watch out for bleeding symptoms

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13
Q

Key interaction for aspirin-5

A

NSAID, Steroid, Anticoagulant ,SSRI, Alcohol

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14
Q

MOA for aspirin

A

Blocks prostaglandin synthesis. It is a non selective COX-1 COX-2 inhibitor.

COX-1 inhibition→ inhibition of platelet aggregation

COX-2 inhibition→ inhibits production of prostaglandin involved in mediating pain and the inflammatory process

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15
Q

Indication for statins

A

Primary/ secondary prevention of CVD

Primary hyperlipidaemia

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16
Q

side effects for statins

A

Headache, GI disturbances, rise in liver enzymes

Muscle aches to myopathy

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17
Q

contraindication for statins (3)

A

cautious when using with existing hepatic impairment

low dose in people with renal impairment

Not in pregnancy or breastfeeding

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18
Q

Monitoring for statins

A

Lipid profile before treatment & after 3 months → aim

for 40% reduction in non-HDL

For safety check liver enzymes

Intervention required if ALT rises x3 because of statin

Check before treatment after 3 and 12 months

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19
Q

Patient education for statins

A

Explain this lowers cholesterol →reduce HA or stroke

Seek medical attention if experience muscle pain

simvastatin/atorvastatin → avoid grapefruit juice

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20
Q

Key interaction for statins(2)

A

Cytochrome p450 inhibitors e.g amiodarone, diltiazem,

itraconazole, macrolides

Amlodipine

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21
Q

MOA for statins

A

Statins reduce serum cholesterol levels. They inhibit HMG CoA reductase, an enzyme involved in making cholesterol.

They decrease cholesterol production by the liver and increase clearance of low density lipoprotein (LDL)-cholesterol from the blood, reducing LDL-cholesterol levels.

They also indirectly reduce triglycerides and slightly increase high density lipoprotein (HDL)-cholesterol levels

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22
Q

Indication for warfarin (3)

A

prevent venous thromboembolism

1st line for AF associated mechanical heart valve

To prevent arterial embolism in patients with mechanical heart valves even if AF is not present

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23
Q

side effects for warfarin

A

Bleeding

minor over-warfarinsation→ increased risk of bleeding from minor trauma

Severe over-warfarinisation→ spontaneous bleeding

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24
Q

Contraindication for warfarin

A

in patients at immediate risk of haemorrhage e.g. after trauma and in patients in need of surgery

liver disease -lack of metabolise of drug→ overdose

First trimester

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25
Q

Monitoring for warfarin

A

INR Measurement

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26
Q

Patient education for warfarin

A

It is important for patients to understand how food, alcohol and other drugs can affect warfarin treatment.

Patients receive an anticoagulant book (‘Yellow Book’)

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27
Q

Key interaction for warfarin

A

low therapeutic index→ small changes by CYP enzymes can cause change in anticoagulation.

CYP indices like carbamazepine increases warfarin metabolism and risk of clot

CYP inhibitor like macrolides decrease warfarin metabolism and increase bleeding risk

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28
Q

MOA for warfarin

A

Warfarin inhibits hepatic production of vitamin K-dependent coagulation factors (factors II, VII, IX and X, and proteins C and S). It does this by inhibiting vitamin K epoxide reductase, the enzyme responsible for restoring vitamin K to its reduced form, necessary as a co-factor in the synthesis of these clotting factors.

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29
Q

Indication for heparin

A

Primary prevention of VTE

Acute coronary syndrome

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30
Q

Contraindication for heparin

A

avoid in clotting disorders

severe uncontrolled hypertension and recent surgery or trauma

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31
Q

side effects for heparin

A

Haemorrhage, Hyperkalaemia

immune reaction (rare) (HIT)

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32
Q

Monitoring for heparin

A

Does not need constant laboratory monitoring

if prolonged therapy (>4 days) then platelet count and serum K+ concentration monitored

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33
Q

Patient education for heparin

A

Advise patients to avoid activities that may increase their risk of bleeding and to inform healthcare professionals they encounter that they are taking anticoagulants.

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34
Q

Key interaction for heparin

A

other antithrombotic drugs e.g.

antiplatelets, warfarin

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35
Q

MOA for heparin

A

Antithrombin (AT) inactivates clotting factors, particularly factors IIa (thrombin) and Xa,
providing a natural break to the clotting process.

Heparins act by enhancing the anticoagulant effect of AT.

The size of heparin molecules determines their molecular specificity: unfractionated heparin (UFH) (large and small molecules) promotes inactivation of both factors IIa and Xa, whereas LMWH (smaller molecules) is more specific for factor Xa.

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36
Q

Indication for DOACS

A

Venous thromboembolism

Atrial fibrillation (AF)

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37
Q

Side effects for DOACS

A

Bleeding (greater chance of GI bleeding)

Anaemia, GI upset, dizziness and elevated liver enzyme

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38
Q

Contraindication for for DOACS

A

avoid in pt with active bleeding or those with risk factor for major bleeding

Avoid in pregnancy and breastfeeding

contact sprots

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39
Q

Monitoring for DOACS

A

Do not require routine monitoring

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40
Q

Patient education for DOACS

A

Provided with an alert card, contact for prolonged bleeding

They should contact a healthcare professional immediately if they develop prolonged or serious bleeding, or weakness, tiredness or breathlessness that could be signs of anaemia.

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41
Q

Key interaction for DOACS

A

Risk of bleeding with DOACs is increased by concurrent therapy with other
antithrombotic agents

the anticoagulant effect can be increased by
macrolides, protease inhibitors and fluconazole and decreased by rifampicin and phenytoin.

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42
Q

moa for DOACS

A

he DOACs act on the final common pathway of the coagulation cascade, comprising factor X, thrombin and fibrin.

Apixaban, edoxaban and rivaroxaban directly inhibit activated factor X (Xa), preventing
conversion of prothrombin to thrombin.

Dabigatran directly inhibits thrombin, preventing the conversion of fibrinogen to fibrin.

All DOACs therefore inhibit fibrin formation, preventing clot formation or extension in the veins and heart.

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43
Q

example of DOACS

A

apixaban
edoxaban
rivaroxaban
dabigatran

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44
Q

Indication for loop diuretics

A

For relief of breathlessness in acute pulmonary oedema

For symptomatic treatment of fluid overload in chronic heart failure.

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45
Q

Side effects for loop diuretics

A

water loss → dehydration and hypotension

Hearing loss and tinnitus at high doses

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46
Q

Contraindication for loop diuretics

A

Avoid in pt with hypovolemia or dehydration

Can worsen gout as it inhibits excretion of uric acid

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47
Q

Monitoring for loop diuretics

A

In longer- term therapy, you should monitor your patient’s symptoms, signs and body weight

For safety, periodic monitoring of serum sodium, potassium and renal function is also advisable, particularly in the first few weeks of therapy.

48
Q

Patient education for loop diuretics

A

Explain to your patients that their body is overloaded with water. You are therefore offering a treatment to increase urine flow, which will hopefully improve this.

The medicine will inevitably cause them to need to pass water more often. Provided they do not take doses late in the day it shouldnot affect them at night.

49
Q

Key interaction for loop diuretics

A

Loop diuretics have the potential to affect drugs that are excreted by the kidneys. e.g lithium

risk of increased digoxin toxicity, increase the ototoxicity and nephrotoxicity of ▴aminoglycosides.

50
Q

MOA for loop diuretics

A

loop diuretics act principally on the ascending limb of the loop of Henle, where they inhibit the Na+/K+/2Cl− co-transporter

This protein is responsible for transporting sodium, potassium and chloride ions from the tubular lumen into the epithelial cell. Water then follows by osmosis.

ALSO, it can cause dilation of veins so used in acute HF as it reduces preload which puts less strain on the overstretched heart muscles

51
Q

Examples of loop diuretics

A

furosemide, bumetanide

52
Q

Indication for beta blocker

A

Ischaemic heart disease

Chronic heart failure→ bisoprolol used to improve prognosis

Atrial fibrillation (AF): to reduce the ventricular rate and, in
paroxysmal AF, to maintain sinus rhythm.

Supraventricular tachycardia (SVT)

Hypertension→ if other do not work

53
Q

Side effects for beta blocker

A

fatigue,

cold extremities,

headache and

nausea

sleep disturbance

nightmares.

impotence in men.

54
Q

Contraindication for beta blocker

A

Avoid in asthma, choose b1 selective in COPD

Avoid in haemodynamic instability and in Heart block

55
Q

Monitoring for beta blocker

A

Adjust dosage according patients’ symptoms

56
Q

Patient education for beta blocker

A

Discuss side effects, warn for initial deterioration in HF 9seek medical attention if it occurs)

seek attention if breathing difficulty occurs

57
Q

Key interaction for beta blocker

A

β-blockers must not be used with non-dihydropyridine calcium channel blockers (e.g. verapamil, diltiazem), except in specialist practice. This combination can cause heart failure, bradycardia and even asystole.

58
Q

where are beta 1 and beta 2 adrenoreceptors found in the body

A

β1-adrenoreceptors are located mainly in the heart, whereas β2 adrenoreceptors are found mostly in smooth muscle of blood vessels and airways

59
Q

MOA of beta blocker in ischemic heart disease

A

Via the β1receptor, β-blockers reduce force of contraction and speed of conduction in the heart. This relieves myocardial ischaemia by reducing cardiac work and oxygen demand and increasing myocardial perfusion.

60
Q

MOA of beta blocker in chronic HF

A

They improve prognosis in heart failure, probably by ‘protecting’ the heart from chronic sympathetic stimulation

61
Q

MOA of beta blocker in atrial fibrillation and svt

A

They slow the ventricular rate in AF mainly by prolonging the refractory period of the atrioventricular (AV) node. Through the same effect they may terminate SVT if this is due to a self-perpetuating (‘re-entry’) circuit that takes in the AV node.

62
Q

MOA of beta blocker in hypertension

A

β-blockers lower BP through a variety of means, one of which is by reducing renin secretion from the kidney, since this is mediated by β1 receptors.

63
Q

Indication for alpha blocker

A

As a first-line medical option to improve symptoms in benign prostatic enlargement, when lifestyle changes are insufficient.

As an add-on treatment in resistant hypertension when others are insufficient

64
Q

side effects for alpha blocker

A

postural hypotension,

dizziness

syncope.

65
Q

Contraindication for alpha blocker

A

AVOID in patients with existing postural hypotension.

66
Q

Monitoring for alpha blocker

A

For tolerability and safety, adverse effects are identified by symptom enquiry and by measuring their lying and standing BP.

67
Q

Patient education for alpha blocker

A

Advise them to start by taking the medicine at bedtime to minimise the impact of this (warn to rise slowly from bed)

68
Q

examples of beta blocker

A

bisoprolol, atenolol, propranolol,

69
Q

key interaction for alpha blocker

A

combining antihypertensive drugs results in additive BP lowering effects

70
Q

MOA for alpha blocker

A

Although often described using the broad term ‘α-blocker,’ most drugs in this class (including doxazosin, tamsulosin and alfuzosin) are highly selective for the α1-adrenoceptor.

α1 adrenoceptors are found mainly in smooth muscle, including in blood vessels and the urinary tract (the bladder neck and prostate in particular). Stimulation induces contraction; blockade induces relaxation. α1-blockers therefore cause vasodilatation and a fall in blood pressure (BP), and reduced resistance to bladder outflow.

71
Q

examples of alpha blocker

A

tamsulosin, doxazosin, alfuzosin

72
Q

Indication for thiazide like diuretics

A

alternative first-line treatment for hypertension

Add-on treatment for hypertension in patients whose BP is not adequately controlled by a calcium channel blocker plus an ACE inhibitor or angiotensin receptor blocker (ARB).

73
Q

Side effects for thiazide like diuretics

A

hyponatraemia

hypokalaemia → cardiac arrhythmias

impotence in men

74
Q

Contraindication for thiazide like diuretics

A

avoided in patients with hypokalaemia and hyponatraemia. As they reduce uric acid excretion, they may precipitate
acute attacks in patients with gout.

75
Q

Monitoring for thiazide like diuretics

A

The best measure of efficacy is the patient’s BP and, if applicable, the severity of the patient’s oedema. Measure the patient’s serum electrolyte concentrations before starting the drug, at 2–4 weeks into therapy, and after any change in therapy that might alter electrolyte balance.

76
Q

patient education for thiazide like diuretics

A

Enquire whether they have any difficulty getting to the toilet in time
Advise patients that antiinflammatory drugs like ibuprofen, may reduce the effectiveness of diuretics.

At review, ask men directly about the possible side effect of impotence

77
Q

Key interaction for thiazide like diuretics

A

The effectiveness of thiazides may be reduced by NSAIDs

78
Q

MOA for thiazide like diuretics

A

Thiazides inhibit the Na+/Cl− co-transporter in the distal convoluted tubule of the nephron.

This prevents reabsorption of sodium and its osmotically associated water. The resulting diuresis causes an initial fall in extracellular fluid volume.

79
Q

MOA for thiazide like diuretics

A

Thiazides inhibit the Na+/Cl− co-transporter in the distal convoluted tubule of the nephron.

This prevents reabsorption of sodium and its osmotically associated water. The resulting diuresis causes an initial fall in extracellular fluid volume.

80
Q

Examples of thiazide like diuretics

A

bendroflumethiazide, indapamide, chlortalidone

81
Q

Indication for CCB

A

Hypertension

Reduce the risk of stroke and MI

control symptoms in people with stable angina

supraventricular arrhythmias

82
Q

Side effects for CCB

A

Amlodipine →ankle swelling, flushing, headache and palpitations

Verapamil → constipation (common) or bradycardia, heart block and cardiac failure (less common)

83
Q

Contraindication for CCB

A

caution in patients with poor left ventricular function

avoided in people with AV nodal conduction delay

Amlodipine should be avoided in patients with unstable angina

Avoid in severe aortic stenosis,

84
Q

Monitoring for CCB

A

Treatment efficacy can be judged by regular blood pressure monitoring for hypertension, enquiry about chest pain for angina and by pulse rate from examination or ECG. A 24-hour tape can be performed to review arrhythmias.

85
Q

Patient education for CCB

A

discuss other measures to reduce cardiovascular risk, including smoking cessation.

86
Q

key interaction for ccb

A

Non-dihydropyridine calcium channel blockers (verapamil and diltiazem) should not be prescribed with ✗β-blockers except under close specialist
supervision.

87
Q

MOA of CCB

A

Calcium channel blockers decrease calcium ion (Ca2+) entry into vascular and cardiac cells, reducing intracellular calcium concentration. This causes relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure.

In the heart, calcium channel blockers reduce myocardial contractility. They suppress cardiac conduction, particularly across the atrioventricular (AV) node, slowing ventricular rate. Reduced cardiac rate, contractility and afterload reduce myocardial oxygen demand, preventing angina

88
Q

2 classes of ccb

A
  • Dihydropyridines, including amlodipine and nifedipine, are relatively selective for the vasculature
  • Non-dihydropyridines are more selective for the heart. Of the non-dihydropyridines, verapamil is the most cardio selective, whereas diltiazem also has some effects on blood vessels.
89
Q

examples of ccb

A

amlodipine, felodipine, nifedipine, diltiazem, verapamil

90
Q

Indication for acei

A

Hypertension

Chronic HF

Ischemic heart disease

Diabetic nephropathy and (CKD) with proteinuria

91
Q

side effects of acei

A

Hypotension

dry cough

hyperkalaemia

angioedema and other anaphylactoid reactions

92
Q

Contraindication for acei

A

be avoided in patients with renal artery stenosis or
acute kidney injury: in women who are, or could become, pregnant; and those who are breastfeeding

93
Q

Patient education for acei

A

If you get allergic reaction seek medical attention

Explain that it can effect the kidney function thus importance of blood test

Advise to avoid taking over the counter

94
Q

Monitoring for acei

A

Check electrolyte and renal function before starting on med and 1-2 weeks and after increasing the dose

If creatinine conc rises more than 30% and if r GFR falls more than 25%

If k+ conc goes above 5mmol/L stop other potassium elevating drug and if it still remains at 5 then Reduce dosage of ACEi and if it goes Higher than 6 then stop ACEi and seek expert advice

95
Q

key interaction for acei

A

avoid prescribing ACE inhibitors with other potassium-elevating drugs,

NSAID

96
Q

MOA for acei

A

ACE inhibitors block the action of ACE, to prevent the conversion of angiotensin I to angiotensin II. Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion.

Blocking its action reduces peripheral vascular resistance (afterload), which lowers blood pressure (BP).

It particularly dilates the efferent glomerular arteriole, which reduces intraglomerular pressure and slows the progression of CKD. Reducing the aldosterone level promotes sodium and water excretion. This can help to reduce venous return (preload), which has a beneficial effect in heart failure.

97
Q

examples of acei

A

ramipril, lisinopril, perindopril

98
Q

Indication for spironolactone-4

A

Ascites and oedema due to liver cirrhosis

Chronic HF

Primary hyperaldosteronism

End stage of HTN

99
Q

Side effects for spironolactone

A

Hyperkalaemia

Gynaecomastia

Liver impairment and jaundice

Bullish skin eruption

100
Q

Contraindication for spironolactone -4

A

Severe renal impairment

hyperkelaemia

Addison’s disease

Pregnancy and breastfeeding

101
Q

Monitoring for spironolactone

A

Check renal function and potassium levels

102
Q

Patient education for spironolactone

A

warn men about the possibility of growth and tenderness of tissue under the nipples and impotence.

Reinforce importance of blood test monitoring as potassium level can rise

103
Q

Key interaction for spironolactone

A

ACEi and ARB

Potassium supplement

104
Q

MOA of spironolactone

A

Aldosterone is a mineralocorticoid that is produced in the adrenal cortex. It acts on mineralocorticoid receptors in the distal tubules of the kidney to increase the activity of luminal epithelial sodium (Na+) channels (ENaC). This increases the reabsorption of sodium and water, elevating blood pressure, with a corresponding increase in potassium excretion. Aldosterone antagonists inhibit the effect of aldosterone by competitively binding to the aldosterone receptor. This increases sodium and water excretion and potassium retention

105
Q

Indications for nitrates

A

Shirt acting → Acute angina

Long acting → prophylaxis of angina

IV nitrate → pulmonary oedema

106
Q

Side effects for nitrates

A

Flushing

Headache

Light headedness

Sustained use → tolerance

107
Q

Contraindications for nitrates

A

Severe aortic stenosis

Heamodynamic instability e.g hypotension

108
Q

Monitoring for nitrates

A

When doing IV nitrate → monitor BP frequently ensure systolic does not drop below 90

109
Q

Patients education for nitrates

A

Explain may develop headache but normally short lived

Use GTN spray before doing task that brings on the angina

Sit down and rest for 5 minute after taking GTN

110
Q

Key interactions for nitrates

A

AVOID co use with PDE inhibitors like sildenafil

Caution when prescribing with any hypertensive med

111
Q

MOA for nitrates

A

Nitrates are converted to nitric oxide (NO). NO increases cyclic guanosine monophosphate (cGMP) synthesis and reduces intracellular Ca2+ in vascular smooth muscle cells, causing them to relax. This results in venous and, to a lesser extent, arterial vasodilatation. Relaxation of the venous capacitance vessels reduces cardiac preload and left ventricular filling. These effects reduce cardiac work and myocardial oxygen demand, relieving angina and cardiac failure. Nitrates can relieve coronary vasospasm and dilate collateral vessels, improving coronary perfusion. They also relax the systemic arteries, reducing peripheral resistance and afterload. However, most of the antianginal effects are mediated by reduction of preload.

112
Q

Examples of nitrates

A

glyceryl trinitrate, isosorbide mononitrate

113
Q

4 indication of ARB

A

Hypertension
Chronic. Heart failure
Diabetic neuropathy
Ckd with proteinuria

114
Q

MoA of ARB

A

ARB blockes the action of angiotensin II on the angiotensin type 1 receptor. angiotensin II is a vasoconstrictor and stimulates‘ aldosterone secretion.
blocking its action reduces peripheral vascular resistance, which lowers blood pressure, particularly dilates the efferent golmerular arteriol, which reduces intraglomerular pressure and slows the progression of CKD reducing aldosterone promote sodium and water excretion, which help to reduce venous return, which has a beneficial effect in heart failure

115
Q

Side affects of ARB

A

Hypertension
hyperkalaemia
renal failure

116
Q

Contra indications of arb

A

Avoid in renal artery stenosis, and in acute kidney injury and in women who are or could become pregnant, or who are breastfeeding

117
Q

Monitoring for Arb

A

Check electrolytes and renal function before start treatment and repeat this one to 2 weeks into treatment, and after increasing the dose

ARB should generally be stopped if the serum creatinine concentration rises more than 30% or the eGFR falls more than 25%.
If serum potassium rises above 5MMOL/L stop all the potassium, elevating and nephrotoxic drugs, if, despite this, it remains above five, then reduce the Arb dose
if exceed six then stop ARb and seek expert advice.

PA- AP (11 decks)

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