Cardiovascular Drugs Flashcards
1
Q
Who are statins indicated for primary prevention
A
Individuals >40y with a QRISK2 score of >10%
2
Q
What is the MOA of statins
A
Inhibits HMG coA reductase
3
Q
What are the 2 most common side effects of statins
A
Headache
GI disturbances
4
Q
What are 3 serious side effects of statins
A
Myopathy
Rhabdomyolysis
Increase in ALT
5
Q
Why should statins not be prescribed to pregnant and breastfeeding women
A
as cholesterol is required for foetal development
6
Q
What drugs may lead to increased statin in the body
A
CYP450 inhibitors
7
Q
What dose is used for primary prevention with a statin
A
40mg simvastatin
20mg atorvastatin
8
Q
What time of day should statins be taken and why
A
Evening - as cholesterol synthesis is greatest in the morning
9
Q
What monitoring is required with a statin
A
Check liver enzymes at 3 and 12 months
10
Q
Explain the MOA of clopidogrel
A
Binds to ADP receptors on platelets and prevents aggregation preventing arterial occlusion
11
Q
What is the most common adverse effe ct of clopidogrel
A
Bleeding
12
Q
What are two other side effects of clopidogrel
A
GI disturbance
Thrombocytopenia
13
Q
What is an absolute CI of clopidogrel
A
Active bleeding
14
Q
How long before elective surgery should clopidogrel be with-held
A
7d
15
Q
What drugs may clopidogrel interact with
A
CYP450 inhibitors - prevent metabolic, leading to increased concentration of clopidogrel
16
Q
What drugs should clopidogrel be used with caution in
A
Other anti-platelets, increased risk of bleeding
17
Q
What is the MOA of gabapentin
A
Act via pre-synaptic voltage-gated calcium channels to inhibit neurotransmitter release reducing neuronal excitability
18
Q
What are 3 main side effects of gabapentin
A
Drowsiness
Dizziness
Ataxia
19
Q
What is a relative CI of gabapentin
A
Renal impairment - need to reduce dose
20
Q
What drugs may gabapentin interact with
A
Other sedatives - increases sedating effects.
21
Q
What is the indication of aspirin
A
- Treatment ACS
- Treatment of ischaemic stroke
- Secondary prevention of cardiovascular events and stroke
22
Q
What is the mechanism of action of aspirin
A
It is a COX inhibitor. By inhibiting COX, it prevents the production of arachidonic acid from thromboxane A2
23
Q
How long dose the effect of aspirin last and why
A
during the lifespan of a platelet - this is because a platelet does not have a nucleus and therefore is unable to synthesise new COX
24
Q
What is the most common side effect of aspirin
A
GI irritation
25
What side effects may aspirin cause in the gastrointestinal system
Peptic Ulcer
| Gastric Haemorrhage
26
What is another side effect of aspirin
In high-doses aspirin can cause tinnitus
27
What are symptoms of aspirin overdose
- Hyperventilation
- Metabolic acidosis
- Confusion
- Convulsions
- Cardiovascular collapse
- Respiratory arrest
28
What are 3 absolute contraindications to aspirin
- 3rd trimester of pregnancy
- Allergic
- Children under the age of 16
29
Why should aspirin not be given to children under the age of 16
Due to risk of Reye's syndrome
30
What is Reye's syndrome
Rare disorder that causes brain and liver damage
31
What condition is aspirin not routinely contraindicated in
Asthma
32
Why should aspirin not be given in the third trimester
As inhibition of COX causes decreased prostaglandin production that can lead to premature closure of the ductus arteriosus
33
What are two conditions were aspirin is relatively contraindicated
Gout - acute flare
| History of peptic ulcers
34
In what drugs does care need to be taken when giving aspirin
Other anti-coagulants - increases risk of bleed
35
What dose of aspirin is given in ACS
300mg loading dose and 75mg thereafter
36
What dose of aspirin is given for acute ischaemic stroke
300mg for two weeks
37
What dose of aspirin is given for long-term prevention of thrombotic events
75mg
38
What should be prescribed with aspirin
Omeprazole (20mg) if at risk of peptic ulcer
39
When should aspirin be taken to minimise gastric complications
Following food
40
What are 4 indications of morphine
1. Treatment of acute severe pain (eg. ACS)
2. Treatment of chronic pain where other medications are ineffective (WHO analgesia ladder stage 3)
3. Relieve breathlessness in acute pulmonary oedema
4. Relieve breathlessness + pain in palliative care patients
41
Explain the MOA of opioids
- bind to and activate opioid u receptors, which are G protein coupled receptors
- acts to reduce neuronal excitability and pain
- in the medulla they blunt the response to hypoxia and hypercapnia, reducing respiratory drive and breathlessness
- by relieving pain + breathlessness, they reduce sympathetic NS activity
42
What are the side effects of morphine
- Respiratory depression
- Constipation
- Pupil constriction
- Euphoria
- CNS depression in high doses
- Itching, Urticaria
- Tolerance and dependence
43
Why do the pupils constrict when using morphine
As morphine stimulates u-opioid receptors in the edinger-westphal nucleus
44
Why do opioids cause constipation
As increase smooth muscle tone decreasing motility
45
Why do opioids cause itching
Stimulate degranulation of mast cells and histamine release
46
When should doses of opioids be reduced
Liver Failure
Kidney Failure
Elderly
47
What is a relative contraindication to opioid use and why
Biliary colic. Opioids can cause spasm of the sphincter of Oddi which can worsen pain. Therefore, different analgesia should be used.
48
What drugs should morphine not be used with
Other sedative agents (eg. benzodiazepines)
49
What dose of morphine is given in ACS
2-10mg IV
50
What are two indications of heparin/ fondaparinux
1. Fondaparinux indicated in ACS treatment
| 2. Prevention of VTE
51
What is the role of anti-thrombin
Inhibits F2a and F10a of the coagulation cascade
52
How do heparins and fondaparinux function
Enhance action of anti-thrombin to inhibit F2 and F10
53
What is the mechanism of action of unfractioned heparin
Inhibits F10 and F2
54
What is the mechanism of action of LMWH
Inhibits just F10
55
What is the mechanism of action of fondaparinux
Inhibits just F10
56
What is the main risk of heparins
Haemorrhage
57
Does LMWH, UFH or Fondaparinux have the lowest risk of haemorrhage
Fondaparinux
58
What is another side effect of heparin
- Bruising at injection site
| - Hyperkalaemia
59
What is an immune reaction to heparin
Heparin induced thrombocytopenia: characterised by low platelet count and thrombosis
60
Is heparin-induced thrombocytopenia less likely to occur with fondaparinux, UFH or LMWH
- It does NOT occur with fondaparinux
| - It is less likely to occur with LMWH than UFH
61
What is a relative contraindication of heparin
Risk of bleeding:
- clotting disorders
- uncontrolled severe HTN
- recent surgery or trauma
62
What is the heparin regimen surrounding surgery
Stop heparin immediately before and after surgery
63
What heparin should be used in renal impairment and why
Unfractioned heparin as it is less dependent on the kidneys for metabolism
64
What is used to reverse heparin anticoagulation in major bleeding
Protamine
65
What is the effect of protamine on different types of heparin
Protamine most effective against UFH, less against LMWH and not at all against fondaparinux.
66
What is an alternative to protamine for reversing heparin
adexanet
67
What are 3 indications of fibrinolytic drugs
1. Ischaemic stroke - improves chance of living independently in the long-term if given in the first 24h
2. ACS
3. Massive PE w/haemodynamic instability
68
What is the time frame for alteplase in acute ischaemic stroke
4.5h
69
What is the time frame for fibrinolytic drug in STEMI
12h
70
What is the mechanism of action of fibrinolytic drugs
Increases conversion of plasminogen to plasmin which degrades fibrin clots
71
What are 3 common adverse effects of fibrinolytic drugs
1. Hypotension
2. N+V
3. Bruising around the injection site
72
What are 4 serious effects that cause fibrinolytic drugs the be stopped
1. Serious bleed
2. Allergic reaction
3. Cardiogenic shock
4. Cardiac arrest
73
What treatment of haemorrhage whilst on fibrinolytic drugs may be given and why is it often not
Clotting factors and tranexamic acid - often not given due to short half-life of fibrinolytic drugs
74
What can reperfusion of infarcted brain tissue cause
Cerebral oedema
75
What can reperfusion of infarcted cardiac tissue cause
Arrhythmias
76
What are 3 CI to fibrinolytic drugs
1. Bleeding
2. Intracranial haemorrhage
3. Previous streptokinase use - for streptokinase only
77
Why is previous streptokinase treatment a CI to using streptokinase again
as can develop anti-streptokinase antibodies that render the treatment ineffective
78
What drugs increase risk of anaphylactoid reactions with fibrinolytic drugs
ACEi
79
Why is the chance of death following fibrinolytic drugs increased for a week
due to bleeding
80
What are 4 indications of ACEi
1. HTN
2. Long-term management after ACS
3. CKD with proteinuria
4. Chronic HF
81
What is the action of ACEi
Inhibits angiotensin coverting enzyme converting angiotensin I to angiotensin II
82
What is the role of angiotensin II
causes vasoconstriction and stimulates aldosterone release
83
What happens if angiotensin II production is blocked
causes vasodilation enabling decrease in peripheral vascular resistance
84
How does ACEi work in CKD
Inhibits angiotensin II producing causing dilation of the efferent arteriole, reducing hyper filtration and pressure in the glomerulus
85
How does ACEi work in chronic heart failure
Decreases aldosterone secretion, reducing reabsorption of sodium and water, therefore reducing pre-load
86
What are 3 common side effects of ACEi
Dry Cough
Hyperkalaemia
First-dose hypotension
87
When do ACEi particularly cause hypotension
following first-dose
88
Why do ACEI cause a dry persistent cough
as ACE normally degrades bradykinin. Dysfunction in ACE causes accumulation of bradykinin
89
What are 2 absolute CIs to ACEi and why
- Renal artery stenosis - as in this circumstance relies on constriction of the efferent to maintain pressure
- AKI
90
What are two idiosyncratic SE of ACEi
Angioedema
| Anaphylactoid
91
What are 2 relative CI to ACEi
Breast Feeding
| Pregnancy
92
What drugs should ACEi be carefully prescribed with and why
potassium-sparing drugs (eg. potassium sparing diuretics)
93
What drugs when prescribed with ACEi are particularly nephrotoxic
NSAIDs
94
When are ACEi advised to be taken and why
Before bed to reduce risk of hypotension
95
What monitoring should happen on ACEi and why
U+E - to check for hyperkalamia
| BP
96
What should be checked prior to starting ACEi
GFR
97
What are 5 indications of B-blockers
- HTN
- IHD
- CHF
- AF
- SVT
98
What is the MOA of B-blockers
Reduce rate and force of contraction by antagonising B1 adrenoceptors
99
How do B blockers work in AF
Slow conduction through the AV node
100
How do B blockers work in HTN
Promote renin secretion
101
What are side effects of B blockers
```
Fatigue
Cold extremities
Impotence
Headache
GI disturbance
Sleep disturbance
```
102
What are 2 absolute CIs to B blockers
- Asthma
| - HF
103
What are B blockers absolutely CI in asthma
Due to causing bronchoconstriction by acting on B2 receptors
104
What are the B1 selective B-blockers
Metoprolol, Bisoprolol
105
What are the non-selective B-blockers
Carvediol, Propanolol
106
What drug can B-blockers not be prescribed with and why
Non di-hydropyridine calcium channel blockers causes HF, bradycardia and systole.
107
What are two loop diuretics
- Furosemide
| - Bumetanide
108
What are 3 main indications for loop diuretics
1. Acute pulmonary oedema
2. Reduce fluid overload in HF
3. Reduce fluid overload in other conditions (eg. renal failure)
109
What is the mechanism of action of loop diuretics
Inhibit Na+/K+/2Cl- in the ascending loop of henle
110
What are some side effects of loop diuretics
- Hypotension
- Dehydration
- Low electrolyte states: hypokalaemia, hyponatremia, hypocholraemia, hypomagnesaemia, hypocalaemia
111
Why may loop diuretics cause tinnitus at high-doses
Due to similar Na+/K+/2Cl- channel controlling endolymph in the ear
112
What are two absolute CI of loop diuretics
Dehydration
| Hypovolaemia
113
What are 4 relative CI of loop diuretics
Hepatic encephalopathy
Gout
Hypokalaemia
Hyponatremia
114
Why are loop diuretics relatively CI in gout
As they decrease excretion of uric acid and therefore may precipitate acute attacks of gout
115
Why are loop diuretics relative CI in hepatic encephalopathy
Hypokalaemia can worsen hepatic encephalopathy
116
What 3 drugs may loop diuretics increase toxicity of
Digoxin
Lithium
Aminoglycosides
117
what rate should IV furosemide be administered
4mg/ml
118
when should patients be advised to take loop diuretics
in the day to avoid nocturia
119
Explain the MOA of nitrates
- Nitrates are converted to NO
- NO increases cGMP synthesis and reduces intracellular calcium in smooth muscle cells causing relaxation
- This causes venous and lesser extent arterial dilation. Also causes relaxation of venous capacitance vessels
- Relaxation of capacitance vessels reduces pre-load and and left-ventricular filling reducing cardiac work and myocardial demand
120
What are 4 common SE of nitrates due to they vasodilatory effects
Headache
Flushing
Light-Headedness
Hypotension
121
What can sustained use of nitrates cause
Tolerance
122
What are 2 contraindications of nitrates
Severe Aortic stenosis
| Hypotension
123
Why are nitrates CI in aortic stenosis
As the heart cannot increase CO sufficiently through narrowed valve area to maintain pressure in dilated vasculature
124
what drugs must nitrates NOT be used with
phosphodiesterase inhibitors
125
give an example of a phosphodiesterase inhibitor
sidinefil
126
why can nitrates not be used with sidenifil
phosphodiesterase inhibitors prolong hypotensive effects of nitrates
127
What is the half-life of sublingual GTN
5min
128
How is GTN given in ACS
IV
129
How is GTN given in angina
Sublingual
