Cardiovascular Flashcards
(117 cards)
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
2
Q
Contraindication for clopidogrel
A
NOT for people with active bleeding
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
4
Q
Side effect for clopidogrel (5)
A
Bleeding
Dyspepsia, abdominal pain, diarrhoea,
thrombocytopenia (Rare)
5
Q
Monitoring for clopidogrel
A
Clinical monitoring for adverse effects is most appropriate.
6
Q
Key interaction for clopidogrel
A
CYP inhibitor -e.g. omeprazole , ciprofloxacin, erythromycin
Co-prescription with other antiplatelet or anticoagulant
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.
8
Q
Indication for aspirin (2)
A
Painkiller, reduce fever or inflammation (antiplatelet drug)
Used to prevent chest pain, Heart attack or stroke
9
Q
side effects for aspirin
A
Dyspepsia, Haemorrhage , gi irritation
Dyspnoea, Skin reactions
10
Q
contraindication for aspirin-5
A
Active ulcer, haemophilia, severe cardiac failure
Avoid in children under 16 years and in 3rd trimester
11
Q
Monitoring for aspirin
A
Enquire about side effect
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
13
Q
Key interaction for aspirin-5
A
NSAID, Steroid, Anticoagulant ,SSRI, Alcohol
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
15
Q
Indication for statins
A
Primary/ secondary prevention of CVD
Primary hyperlipidaemia
16
Q
side effects for statins
A
Headache, GI disturbances, rise in liver enzymes
Muscle aches to myopathy
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
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
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
20
Q
Key interaction for statins(2)
A
Cytochrome p450 inhibitors e.g amiodarone, diltiazem,
itraconazole, macrolides
Amlodipine
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
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
23
Q
side effects for warfarin
A
Bleeding
minor over-warfarinsation→ increased risk of bleeding from minor trauma
Severe over-warfarinisation→ spontaneous bleeding
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
25
Monitoring for warfarin
INR Measurement
26
Patient education for warfarin
It is important for patients to understand how food, alcohol and other drugs can affect warfarin treatment.
Patients receive an anticoagulant book (‘Yellow Book’)
27
Key interaction for warfarin
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
28
MOA for warfarin
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.
29
Indication for heparin
Primary prevention of VTE
Acute coronary syndrome
30
Contraindication for heparin
avoid in clotting disorders
severe uncontrolled hypertension and recent surgery or trauma
31
side effects for heparin
Haemorrhage, Hyperkalaemia
immune reaction (rare) (HIT)
32
Monitoring for heparin
Does not need constant laboratory monitoring
if prolonged therapy (>4 days) then platelet count and serum K+ concentration monitored
33
Patient education for heparin
Advise patients to avoid activities that may increase their risk of bleeding and to inform healthcare professionals they encounter that they are taking anticoagulants.
34
Key interaction for heparin
other antithrombotic drugs e.g.
antiplatelets, warfarin
35
MOA for heparin
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.
36
Indication for DOACS
Venous thromboembolism
Atrial fibrillation (AF)
37
Side effects for DOACS
Bleeding (greater chance of GI bleeding)
Anaemia, GI upset, dizziness and elevated liver enzyme
38
Contraindication for for DOACS
avoid in pt with active bleeding or those with risk factor for major bleeding
Avoid in pregnancy and breastfeeding
contact sprots
39
Monitoring for DOACS
Do not require routine monitoring
40
Patient education for DOACS
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.
41
Key interaction for DOACS
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.
42
moa for DOACS
he DOACs act on the final common pathway of the coagulation cascade, comprising factor X, thrombin and fibrin.
Api**xa**ban, edo**xa**ban and rivaro**xa**ban 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.
43
example of DOACS
apixaban
edoxaban
rivaroxaban
dabigatran
44
Indication for loop diuretics
For relief of breathlessness in acute pulmonary oedema
For symptomatic treatment of fluid overload in chronic heart failure.
45
Side effects for loop diuretics
water loss → dehydration and hypotension
Hearing loss and tinnitus at high doses
46
Contraindication for loop diuretics
Avoid in pt with hypovolemia or dehydration
Can worsen gout as it inhibits excretion of uric acid
47
Monitoring for loop diuretics
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
Patient education for loop diuretics
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
Key interaction for loop diuretics
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
MOA for loop diuretics
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
Examples of loop diuretics
furosemide, bumetanide
52
Indication for beta blocker
**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
Side effects for beta blocker
fatigue,
cold extremities,
headache and
nausea
sleep disturbance
nightmares.
impotence in men.
54
Contraindication for beta blocker
Avoid in asthma, choose b1 selective in COPD
Avoid in haemodynamic instability and in Heart block
55
Monitoring for beta blocker
Adjust dosage according patients’ symptoms
56
Patient education for beta blocker
Discuss side effects, warn for initial deterioration in HF 9seek medical attention if it occurs)
seek attention if breathing difficulty occurs
57
Key interaction for beta blocker
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
where are beta 1 and beta 2 adrenoreceptors found in the body
β1-adrenoreceptors are located mainly in the heart, whereas β2 adrenoreceptors are found mostly in smooth muscle of blood vessels and airways
59
MOA of beta blocker in ischemic heart disease
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
MOA of beta blocker in chronic HF
They improve prognosis in heart failure, probably by ‘protecting’ the heart from chronic sympathetic stimulation
61
MOA of beta blocker in atrial fibrillation and svt
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
MOA of beta blocker in hypertension
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
Indication for alpha blocker
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
side effects for alpha blocker
postural hypotension,
dizziness
syncope.
65
Contraindication for alpha blocker
AVOID in patients with existing postural hypotension.
66
Monitoring for alpha blocker
For tolerability and safety, adverse effects are identified by symptom enquiry and by measuring their lying and standing BP.
67
Patient education for alpha blocker
Advise them to start by taking the medicine at bedtime to minimise the impact of this (warn to rise slowly from bed)
68
examples of beta blocker
bisoprolol, atenolol, propranolol,
69
key interaction for alpha blocker
combining antihypertensive drugs results in additive BP lowering effects
70
MOA for alpha blocker
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
examples of alpha blocker
tamsulosin, doxazosin, alfuzosin
72
Indication for thiazide like diuretics
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
Side effects for thiazide like diuretics
hyponatraemia
hypokalaemia → cardiac arrhythmias
impotence in men
74
Contraindication for thiazide like diuretics
avoided in patients with hypokalaemia and hyponatraemia. As they reduce uric acid excretion, they may precipitate
acute attacks in patients with gout.
75
Monitoring for thiazide like diuretics
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
patient education for thiazide like diuretics
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
Key interaction for thiazide like diuretics
The effectiveness of thiazides may be reduced by NSAIDs
78
MOA for thiazide like diuretics
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
MOA for thiazide like diuretics
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
Examples of thiazide like diuretics
bendroflumethiazide, indapamide, chlortalidone
81
Indication for CCB
Hypertension
Reduce the risk of stroke and MI
control symptoms in people with stable angina
supraventricular arrhythmias
82
Side effects for CCB
Amlodipine →ankle swelling, flushing, headache and palpitations
Verapamil → constipation (common) or bradycardia, heart block and cardiac failure (less common)
83
Contraindication for CCB
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
Monitoring for CCB
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
Patient education for CCB
discuss other measures to reduce cardiovascular risk, including smoking cessation.
86
key interaction for ccb
Non-dihydropyridine calcium channel blockers (verapamil and diltiazem) should not be prescribed with ✗β-blockers except under close specialist
supervision.
87
MOA of CCB
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
2 classes of ccb
- 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
examples of ccb
amlodipine, felodipine, nifedipine, diltiazem, verapamil
90
Indication for acei
Hypertension
Chronic HF
Ischemic heart disease
Diabetic nephropathy and (CKD) with proteinuria
91
side effects of acei
Hypotension
dry cough
hyperkalaemia
angioedema and other anaphylactoid reactions
92
Contraindication for acei
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
Patient education for acei
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
Monitoring for acei
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
key interaction for acei
avoid prescribing ACE inhibitors with other potassium-elevating drugs,
NSAID
96
MOA for acei
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
examples of acei
ramipril, lisinopril, perindopril
98
Indication for spironolactone-4
Ascites and oedema due to liver cirrhosis
Chronic HF
Primary hyperaldosteronism
End stage of HTN
99
Side effects for spironolactone
Hyperkalaemia
Gynaecomastia
Liver impairment and jaundice
Bullish skin eruption
100
Contraindication for spironolactone -4
Severe renal impairment
hyperkelaemia
Addison’s disease
Pregnancy and breastfeeding
101
Monitoring for spironolactone
Check renal function and potassium levels
102
Patient education for spironolactone
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
Key interaction for spironolactone
ACEi and ARB
Potassium supplement
104
MOA of spironolactone
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
Indications for nitrates
Shirt acting → Acute angina
Long acting → prophylaxis of angina
IV nitrate → pulmonary oedema
106
Side effects for nitrates
Flushing
Headache
Light headedness
Sustained use → tolerance
107
Contraindications for nitrates
Severe aortic stenosis
Heamodynamic instability e.g hypotension
108
Monitoring for nitrates
When doing IV nitrate → monitor BP frequently ensure systolic does not drop below 90
109
Patients education for nitrates
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
Key interactions for nitrates
AVOID co use with PDE inhibitors like sildenafil
Caution when prescribing with any hypertensive med
111
MOA for nitrates
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
Examples of nitrates
glyceryl trinitrate, isosorbide mononitrate
113
4 indication of ARB
Hypertension
Chronic. Heart failure
Diabetic neuropathy
Ckd with proteinuria
114
MoA of ARB
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
Side affects of ARB
Hypertension
hyperkalaemia
renal failure
116
Contra indications of arb
Avoid in renal artery stenosis, and in acute kidney injury and in women who are or could become pregnant, or who are breastfeeding
117
Monitoring for Arb
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.
