Chapter 2 - CV Flashcards
1
Q
Possible causes of hypertension?
A
Renal disease
Endocrine disorders
2
Q
Lifestyle advice for hypertension?
A
Reducing / stopping smoking Weight loss Reducing caffeine / alcohol (unit guidelines per week) Reducing salt Reducing total / saturated fat Increasing exercise Increase fruit / vegetables
3
Q
What is stage 1 hypertension?
A
Clinic bp of 140/90 mmHg + AND ambulatory daytime avg or home bp of 135/85 +
4
Q
When do you treat stage 1 hypertension?
A
Stage 1 &: Target organ damage (LVH, CKD, hypertensive retinopathy) CVD Diabetes Renal disease CV 10yr risk >/= 20%
5
Q
What is stage 2 hypertension?
A
Clinic bp 160/100+ AND ambulatory daytime avg or home bp 150/95+
6
Q
What is severe HT?
A
Clinic systolic bp >= 180
Clinic diastolic bp >=110
7
Q
Target bp in under 80s?
A
Below 140/90 clinic bp
Home / ambulatory below 135 / 85
8
Q
Target bp in 80yrs + ?
A
Clinic bp < 150/90
Ambulatory / home bp <145/85
9
Q
Target bp for diabetics with kidney/eye/CBV Disease and those with establish atherosclerotic CVD?
A
Under 130/80 mmHg
10
Q
Drug treatment for HT in under 55:
A
- ACEi / ATIIRA
- ACEi / ATIIRA & CCB / Thiazide diuretic (if not tolerated)
- ACEi / ATIIRA & CCB & Thiazide diuretic (if not tolerated)
- Seek specialist advise & ~ Spironolactone / high dose thiazides (latter if potassium above 4.5 mmol/L)
11
Q
What other medicines are used to reduce CVD risk?
A
Statins
Aspirin in ESTABLISHED CVD (unproven benefit in primary)
12
Q
What is the difference in treatment of HT for those over 55 or African / Caribbean origin compared to under 55?
A
First two steps different:
- CCB / thiazides
- CCB or thiazide and ACEi / ATIIRA
3 and 4. Same as under 55yrs
13
Q
What is a positive inotropic effect?
A
Increased contraction force
14
Q
What is a positive chronotropic effect?
A
Increased heart rate
15
Q
What is angina ?
A
Lack of oxygen to myocardium resulting in pain.
16
Q
Types of angina?
A
Stable (exertion causes predictable heart pain)
Unstable (pain with less and less exertion until eventually at rest)
Variant
17
Q
What is the biochemical marker to assess myocardial injury?
A
Troponin
18
Q
What can be used to treat SVT in children?
A
Adenosine via rapid IV injection
If not effective; Amiodarone Flecainide Esmolol Verapamil (if child over 1 yr)
19
Q
What can be used to treat Torsade de pointes in children?
A
IV magnesium sulfate.
20
Q
Why is Verapamil C/I in children under 1 yr?
A
Can cause severe haemodynamic compromise (refractory hypotension and cardiac arrest)
21
Q
Dose adjustment needed for children on Flecainide and Amiodarone?
A
Halve Flecainide dose
22
Q
Optimal Flecainide plasma conc. in children?
Same as for adults?
A
200 - 800 micrograms / L
23
Q
Can Flecainide be taken with food in children?
A
Liquid to be given 30 minutes before or after due to local anaesthetic effect
If give by mouth - Milk/ dairy, infant formula may reduce absorption so separate from feeds
24
Q
What warning symptoms should patients on Amiodarone look out for?
A
Vision impairment / optic neuritis or neuropathy - Stop treatment, see specialist.
Hypo / hyperthyroidism due to containing iodine. Withdraw (maybe temporarily) for thyrotoxicosis or Carbimazole. Treat hypo with thyroxine but can keep on Amiodarone if necessary.
Liver disease signs/ liver function abnormalities - Discontinue
SoB / cough - investigate for Pneumonitis
Peripheral neuropathy symptoms.
25
Treatment for ectopic beats (extra / early beats due to non pacemaker cell excitation) ?
If spontaneous and normal heartbeat rarely needed but beta blocker if troublesome
26
What is used for AF risk assessment?
Stroke risk - CHA2DS2VASc
Thromboembolism
Bleeding risk - HASBLED
27
How often should stroke / thromboembolism and bleeding risk be reviewed in AF patients?
Annually
28
How can AF be managed ?
Control ventricular rate (rate control)
Restore / maintain sinus rhythm (rhythm control)
29
AF; option if drug treatment failure?
Ablation
30
How does treatment in AF differ if presenting with haemodynamic instability or not?
If life threatening instability electrical cardioversion with no delay for anticoagulation
If arrhythmia onset < 48 hrs : rate or rhythm
If onset > 48 hrs: rate control
31
What pharmacological cardioversion preferred in structural heart disease?
Amiodarone > Flecainide
32
AF; Urgent rate control options?
IV beta blocker
Or
IV Verapamil
33
When is electrical cardioversion preferred?
If AF onset over 48 hrs ago ( after 3 weeks of anticoagulation)
34
AF; When is rate control not 1st line?
```
New onset AF
HF secondary to AF
Atrial flutter suitable for ablation
AF with reversible cause
If rhythm more suitable (clinically)
```
35
What is cardiac ablation?
Surgical scaring / destroying of tissue causing abnormal heart rhythm normally via catheters
36
Drugs for AF rate control?
Beta blocker
Rate limiting Ca channel blockers - Verapamil, Diltiazem.
Digoxin (for sedentary non paroxysmal AF)
* can combine if needed.
37
What rate control would you use in reduced ventricular function?
Beta blocker
And
Digoxin
38
What drug to use in AF with congestive heart failure?
Digoxin
39
If standard beta blocker not appropriate what rhythm control options are available?
```
Sotalol
Flecainide
Amiodarone
Propafenone
Drone drone (for persistent / paroxysmal AF)
```
40
When should Flecainide / Propafenone NOT be used?
Known ischaemic / structural heart disease
41
What drug to consider for LV impairment or HF?
Amiodarone
42
Treatment options for paroxysmal AF?
Beta blocker
Amiodarone
Dronadone / Sotalol
“Pill in pocket” Flecainide / Propafenone
43
What oral anticoagulation for stroke prevention in AF?
Vitamin K antagonist
Apixaban *
Dabigatran *
Rivaroxaban *
*For non valvular AF
44
Why not aspirin for stroke prevention?
Less effective than Warfarin at preventing emboli and benefit offset by bleeding
45
What are the treatment options for paroxysmal SVT?
Reflex vagal stimulation (valsalva manoeuvre, face ice cold immersion, carotid sinus massage)
If severe issues caused:
IV Adenosine
IV Verapamil (avoid in recent beta blocker users)
Catheter ablation
Flecainide
Propafenone
Diltiazem / Sotalol / Verapamil to prevent recurrent episodes
46
What is the dose adjustment for a patient using Flecainide and Amiodarone?
Half Flecainide dose
47
What side effects warrant discontinuing Propafenone?
Liver failure - If 2 consecutive AAT are 3X normal or ab pain, anorexia, N&V, malaise, dark urine, jaundice, itching
Left ventricular systolic dysfunction - Weight gain, oedema, dyspnoea.
48
Why correct hypokalaemia / hypomagnesia before / during Sotalol use?
Life threatening ventricular arrhythmias could develop due to increase QT interval
Correct before / during and be wary of diarrhoea.
49
Normal potassium plasma value?
4.5 mmol / L
50
IM Magnesium sulfate is used to treat magnesium deficit, what value is classed as a deficit?
0.5 - 1 mmol / kg
51
What to try in Digoxin toxicity before Digoxin Specific Antibody?
Atropine sulfate
Digoxin withdrawal
Electrolyte corrections
52
How would you change Digoxin dose if another cardiac glycoside given within the last two weeks?
Reduce it
53
How would you change Digoxin dose if changing from IV to oral?
Increase 20-33% to maintain plasma concentration.
54
Why is Digoxin not appropriate for rapid heart rate control?
Takes hours to work even via IV
55
What plasma range increases risk of toxicity
1.5 microgram / L to 3 microgram / L
Although this alone can not indicate toxicity
56
What is the minimum heart rate on digoxin treatment?
It should not be allowed to fall below 60 bpm
57
How could you change Digoxin dose frequency to avoid nausea?
From OD to BD
58
How would you adjust Digoxin dose if patient also on Amiodarone, Dronedarone or Quinine?
Half (manufacturers advise)
59
What increases risk of Digitalis toxicity?
```
Elderly
Hypercalcaemia
Hypokalaemia
Hypomagnesaemia
Hypoxia
Renal impairment
```
60
What is the target Digoxin plasma concentration in children?
0.8 - 2 micrograms / L
61
Counselling for Digoxin use in children?
Do not dilute solution and how to use pipette
Digitalis toxicity (fatigue, malaise, visual disturbances, nausea, vomiting,
62
Why do you need to be wary about the side effects of Digoxin?
Digitalis toxicity (anorexia, nausea, vomiting, confusion, visual effects) is similar to clinical deterioration
63
How does the pharmacology of Digoxin relate to its cautions and interactions?
Increases intercellular calcium indirectly via sodium potassium pump inhibition, this increases contractibility (can lead to tachycardia) hence CI in wolfe Parkinson white syndrome
Eliminated mainly via renal therefore renal impairment = prolonged elimination (also with lower body weight) and longer half life
Also eliminated via p-glycoproteins therefore drugs which inhibit this increases serum concentration (e.g Amiodarone, Verapamil, Macrolides, Cyclosporin, Azole antifungals.
64
What needs monitoring in Digoxin?
```
Renal function
Electrolytes
Plasma level (6 hours after last dose due to time to distribute to tissues) - Needed for digoxin specific antibody calculation
```
65
How should venous thromboembolism be prevented?
Risk assessment - To work out risk from mobility and if they are likely to bleed
Mechanical prophylaxis
Pharmacological (LMWH, Fondaparinux, Apixaban, Dabigatran, Rivaroxaban)
-Continue for 5-7 days or sufficient mobility (28 days if major surgery involving abdomen or the pelvis)
66
How to treat venous thromboembolism?
LMWH or unfractionated Heparin - For 5 days and for INR to be 2 or over for 24 hrs+
+
Oral anticoagulation (usually warfarin)
67
What is used to monitor unfractionated heparin levels?
Activated partial thromboplastin time (aPTT), usually daily.
68
Why is LMWH preferred in pregnancy over unfractionated?
Although both do not cross the placenta, LMWH Dalteparin, Enoxaparin, Tinzapatin) have:
reduced chance of osteoporosis
Reduced chance of heparin induced cytopenia (platelet drop 30%, thrombosis, skin allergy)
Eliminated more rapidly (in pregnancy - so can be stopped at labour onset if required)
Longer duration of action
69
What are the cautions for the Heparins?
Bleeding (can withdraw drug but if severe can use protamine sulfate but this only partially reverse LMWH)
Heparin induced thrombocytopenia ( immune mediated usually after 5 - 10 days resulting in 30% platelet drop, thrombosis, or skin allergies - STOP and Change to alternative like Danaparoid) monitor platelets counts before treatment and regularly if over 4 days treatment.
Elderly
Hyperkalaemia (Inhibits aldosterone secretion so patients with DM, chronic renal failure, acidosis, on potassium sparing diuretics, have increased plasma potassium) this risk increases with therapy duration so monitor before (and regularly if over 7 days)
No multi dose vials in pregnancy as it contain benzyl alcohol - e.g hence Fragmin prescribed.
Renal impairment can increase bleeding risk - May need to reduce dose or change to unfractionated
70
How does the pharmacology of ACEi relate to the S/Es and cautions?
Increased bradykinin (reduced breakdown) a potent vasodilator acting via eNO to hyperpolarise vascular smooth muscle - causes dry cough, which requires a class change if intolerable and potentially angioedema, in which it should be discontinued.
Angiotensin 2 binds to the AT1 receptor to cause Aldosterone release from the adrenal cortex so ACE inhibition inhibits this release to cause reduce potassium levels (and sodium levels) this risk is increased in DM, if patient over 70, if on potassium sparing diuretic or dehydrated. Monitor electrolytes.
Angiotensin 2 selectively constricts efferent arterioles (away from kidney) to maintain glomerular filtration so inhibition of this in patients with bilateral renal artery stenosis, Reno vascular disease, generalised peripheral vascular disease and atherosclerosis could precipitate renal failure by reducing GFR. Monitor renal function and be cautious avoid the renin inhibitor Alikskiren. It is contra indicated in the 2nd / 3rd trimesters of pregnancy due to neonatal toxicity resulting in renal failure, hypotension, hyperkalaemia) as well as skull retardation.
Any marked liver enzyme elevation (bilirubin, ATT, ALT, alkaline phosphatase, albumin) or jaundice symptoms (lethargy, itching, malaise, abnormal bleeding, abdominal pain, dark urine) means treatment should be stopped, be particularly wary of pro drug ACEi (perindopril, enalopril, ramipril, quinapril.
Reduced NA release
Hypotension could result in headache
Angiotensin sensitive vascular beds are kidney, heart and brain.
71
What are the major Ramipril interactions?
Aliskeren - Avoid or use in caution as may increase renal impairment risk
Allopurinol = increase sensitivity / haematological reactions
Azathioprine = increase anaemia / leucopenia risk
Lithium = monitor and adjust dose
Sodium aurothiomalate = increased sensitivity risk
72
Can you supply Viagra connect if a patient says yes that they do have BP problems?
No do not supply and refer to doctor
73
Why would an ACEi cause a large BP drop in patients on Furosemide?
Patients on diuretics have enhanced renin secretion already (highly activated) so downstream effects such as vasoconstriction (from direct and NA release) and salt retention (from aldosterone secretion and tubular Na+ reabsorption)
74
Why are patients who are over 70 / have DM / on K+ sparing diuretics / dehydrated at risk of hyperkalaemia ?
Already have reduced aldosterone production
75
Why are ACEi not recommended in bilateral renal stenosis?
Angiotensin 2 maintains glomerular filtration by selective construction of efferent arterioles. If the ACEi stops this production it can lead to renal failure
76
Why would you need to counsel a patient started on Ramipril with : low salt diet, on dialysis, dehydrated, has heart failure) ?
Increased risk of first dose hypotension, so recommend first dose at night.
77
Why would you avoid ACEi in a patient on dialysis or before wasp/ bee venom sensitisation?
Increased risk of anaphylaxis reactions
78
Why would you be more concerned with targeting Angiotensin 2 over NA?
It is 40x more active as a vasoconstrictor than noradrenaline.
79
Why should you ask a patient with a dry cough if they are taking an ACEI?
ACEi increase the amount of bradykinin (reduced breakdown) leading vasodilation to cause dry cough (and increase angioedema risk)
80
Why are ACEi not used in pregnancy and what are the alternatives?
Not recommended in 1st trimester
```
Contraindicated in 2nd and 3rd as can induce:
foetatoxicity (decreased renal function, oligohydramnios, skull ossification retardation)
Neonatal toxicity (renal failure, hypotension, hyperkalaemia)
```
```
Can change to:
methyldopa
Labetalol
MR Nifedipine (after week 20)
```
81
A patient on treatment with direct acting antivirals for Hep C presents with a prescription for warfarin, why might you be concerned and how do you proceed?
Direct acting antivirals ex. Daclatasvir, Sofosbuvir, Simeprevir, Dasabuvir) can affect the efficacy of vitamin k antagonists (Acenocoumarol, Phenindione and Warfarin) Advise patient of this and to monitor INR closely
82
When is Digoxin preferred in arrhythmias?
Sedentary with non paroxysmal AF patients
In a combination with beta blockers or Diltiazem if single drug failure
In diminished ventricular function with a beta blocker
When AF presents with heart failure
83
At what point would you consider the use of Sotalol/ Flecainide/ Propafenone/ Amiodarone / Dronedarone?
Rhythm control when a standard beta blocker has failed or not appropriate.
Dronedarone if persistent or paroxysmal.
84
Why would you use inotropic sympathomimetics over vasoconstrictor sympathomimetics?
They can reduce perfusion to organs such as kidneys (so for example be wary in renal stenosis) and the peripheral vasoconstriction mediated by alpha adrenergic activation can worsen tissue ischaemia and myocardial performance in cardiogenic shock, therefore the inotropes adrenaline, dopamine or dobutamine would be used preferentially over noradrenaline or Metaraminol.
85
When would noradrenaline by preferable to both Metaraminol / phenylephrine in acute hypotension?
When a shorter duration of action is required in patient groups that may be predisposed to excessive vasopressor action and subsequent hypertension.
86
What is the treatment pathway for heart failure?
1. ACEi / AIIRB + Beta blocker ( Bisoprolol / Carvedilol / Nebivolol)
2. Add in Spironolactone or Eplenerone (if not tolerated) or add in Hydralazine together with isosorbide dinitrate
3. Add in Digoxin
4. Add in diuretics in cases of fluid overload
87
Describe the symptoms of Digitalis toxicity that can occur within the therapeutic range of 0.7 - 2 ng / mL?
```
Nausea
Confusion
Anorexia
Arrhythmias
Visual disturbances
```
88
What factors can predispose a patient to digitalis toxicity ?
Lowered renal function
Decreased potassium
Thyroid function
Altered electrolytes
89
What is the normal blood potassium level?
4.5 mmol / L
90
Normal Na plasma level?
142mmol / L
91
Normal plasma calcium level?
2.5 mmol / L
92
Normal Cl plasma level?
103 mmol / L
93
Normal bicarbonate level?
26 mmol / L
94
Why would a patient taking a loop diuretic and Digoxin be at risk of digoxin toxicity?
Loop diuretics can cause electrolyte disturbances, in this case hypokalaemia or reduced potassium from target value of 4.5 mmol / L.
We could use an adjunct potassium sparing diuretic such as Amiloride or Spironolactone or add in a potassium supplement instead of the diuretic.
95
A patient on Furosemide asks for foods high in potassium to offset any side effects he may have, what do suggest eating?
```
Banana
Sweet potato / potato
Avocado
Spinach
Dried apricot
Pomegranate
Milk
Yogurt
Broccoli
Beef
```
96
A HF patient currently taking Ramipril is prescribed Spironolactone 100 mg daily for recent ascites, why might you be concerned?
ACEi can cause hyperkalaemia plus a potassium sparing diuretic can increase the risk
97
Why would you recommend Furosemide be taken at least 6 hours before bed?
Diuretic effect lasts from 1 - 6 hours so taking it this early will prevent sleep disturbances
98
At what point would you introduce diuretics in simple gravitational oedema?
Second line after recommending increasing exercise, raising legs and utilising support stockings, it would also only be for a few days only.
99
What diseases can thiazides and related diuretics worsen?
Gout
Diabetes
Lupus
100
Why is the half life of Amiodarone a concern when it comes to interactions?
The half life can last from 20 - 100 days due to patient variation and consequently certain drugs like macrolides can increase QT interval and increase risk of arrhythmias.
101
A patient receiving bisoprolol complains about nightmares, what can you change him to?
CANS
Celiprolol
Atenolol
Nadolol
Sotalol
These are water soluble so less likely to enter brain and cause CNS effects such as sleep disturbances
102
Why do the beta blockers oxprenolol, pindolol, acebutolol and Celiprolol cause less bradycardia and extremity coldness?
They have partial agonist activity so stimulate AND block
103
A patient prescribed Ramipril starts exhibiting nausea, muscle weakness and irregular heart beat, what is likely to be the problem?
Hyperkalaemia
104
Why would a pregnant woman be prescribed 75mg aspirin OD from Week 12 of pregnancy?
To prevent pre- eclampsia
105
Why specify brand for Diltiazem MR over 60mg ?
Different brands have different bioavailabilities and release times Sonya not achieve the same clinical affect.
106
When would it be appropriate to use unfractionated heparin over LMWH?
In patients with high bleeding risk, this is because unfractionated heparin has a short duration of action so the infusion can be stopped and if necessary protamine sulfate (1mg neutralises 80-100 units IV heparin if given within 15 mins, less if later due to rapid heparin excretion.
107
What situations would it be preferable to use LMWH (Dalteparin / Enoxaparin / Tinzaparin) over unfractionated heparin?
In pregnancy (although use is unlicensed and multi dose vials should be avoided) as they do not cross into the placenta
For patients with issues of adherence and do like injections - LMWH for once daily administration due to longer duration of action.
Reduced risk of thrombocytopenia (thrombosis, skin allergy, 30% reduction in platelet count) although platelet counts should still be monitored before treatment start and regularly if over 4 days duration.
Reduced risk of osteoporosis (so patient on alendronic acid or menopausal it would be more appropriate)
No rebound hyperlipidaemia like with unfractionated heparin withdrawal
108
Why would you advise against a long duration of therapy of heparins especially with Diabetics?
DM, as well as those on potassium sparing diuretics, potassium supplements, chronic renal failure, with acidosis are at increased risk of hyperkalaemia (low potassium causing tiredness, N + V, tingling, arrhythmias, etc) and increasing duration of therapy also does this.
109
When is Danaparoid not contraindicated in thrombocytopenia?
In cases of heparin induced thrombocytopenia (30% platelet reduction, thrombosis, skin allergy), although caution warranted of heparin antibodies developed as this itself may cause it.
110
A patient is admitted with hypotensive crisis displaying bleeding from the eyes (other symptoms include papilloedema, in in presence of ACS, acute coronary dissection, acute pulmonary oedema, acute cerebral infarction, intracerebral / subarachnoid haemorrage, eclampsia or rapidly progressive renal failure), what are the therapeutic options?
```
For emergencies (organ damage) Reducing blood pressure 20-25% with the first few minutes to 2 hours with use of:
Sodium nitroprusside
Nicardipine
Labetalol
Glycerol trinitrate
Hydralazine
Esmolol
```
```
For urgencies (no organ damage but BP over 180/110:
Reduce over 24 - 48 hours with use of :
Labetalol
Felodipine
Amlodipine
```
111
Why is use of the renin inhibitor Aliskiren with not recommended in patients receiving ACEi or ARB?
Increased risk of:
Hyperkalaemia (especially in DM)
Renal failure
Hypotension
112
In what situations a cardio selective beta blockers preferred? (Ex. Atenolol, Bisoprolol, Metoprolol, Cebivolol, Acebutolol)
Asthma / COPD to reduce risk of bronchospasm
DM to reduce hypoglycaemia / hyperglycaemia and to reduce metabolic / autonomic interference's in hypoglycaemia (such as reduced tachycardia
113
Why would phaemochromocytoma need to be controlled with Phenoxybenzamine HCL before introduction of a beta blocker such as Propanolol (which is also used in thyrotoxic issues)?
The beta blocker on its own without the alpha blockade can result in hypertensive crisis.
114
What medication could you use to counter excessive bradycardia from beta blockers?
Atropine
115
What are the features of calcium channel blocker poisoning?
```
Nausea and vomiting
Dizziness
Agitation
Confusion
Coma
Metabolic acidosis
Hyperglycaemia
```
116
Why would you avoid the calium channel blockers Verapamil and Diltiazem in HF?
Verapamil is cardio-selective and diltizem is intermediate between peripheral / arterial blood vessels and the heart, use in heart failure can therefore depress cardiac function and cause deterioration.
117
Why should Verapamil be avoided with beta blockers?
Verapamil is highly negatively inotropic, reducing cardiac output/ heart rate and may impair AV conduction. This makes it good for angina and arrythmias but when combined with beta blockers can exarcerbate heat failure, cause conduction disorders,, bradycardia and hypotension.
118
Why would you use Amlodipine/ Felodipine as a Calcium channel blocker in heart failure?
These are calcium channel blockers that act predominantly on vascular smooth muscle to dilate coronary and peripheral arteries, rarely causing negative inotropic effects (which would be offset by reduce left ventricular work anyway), these are also longer acting than Nifedipine and Nicardipine.
119
Why would you use thiazide diuretics with caution in the following groups:
Lupus sufferers
Gout sufferers
DM sufferers
Elderly
Hepatic failure
Hypokalaemia
Thiazide diuretics can make lupus, gout and DM worse.
In the elderly, side effects, particularly hypokalaemia can be made worse and this is particularly dangerous in CVD / patients being treated with Digoxin as it increases the chance of QT elongation or torsade de pointes.
Hypokalaemia is also dangeorus in hepatic failure as it may lead to encephalopathy and eventually coma. If the patient has alcoholic cirrhosis as the cause this can also cause hypomagnesaemia.
Hypokalaemia can cause disturbances in heart rhythm.
120
Why do you need to monitor liver function in patients with hepatic impairment taking Enalapril, Imidapril, Fosinopril, Moexipril, Perindopril, Quinapril, Ramipril, Trandolapril?
What ACEi could you use that isn't a prodrug?
These are all prodrugs and therefore hepatic impairment could impede metabolism and therefore therapeutic effect could be diminished
Lininopril
121
A prescriber gives an Rx for Ambrisentan to a female patient for pulmonary arterial hypertension, upon questioning you find out she is trying for a baby, what should you do?
The endothelin receptor antagonists (including Bosentan) are teratogenic in animals so avoid in pregnancy, would advise patient / GP to use Iloprost (prostaglandin)
122
Why would you not use Noradrenaline in cardiogenic shock?
Peripheral resistance is already high so increasing it may worsen myocardial performance and increase tissue ischemia. Should use adrenaline, dobutamine or dopamine as these are cardiac inotropes so increase cardiac output
123
Why would you use a maximum dose of 25mg Eplenerone if a patient is already taking Amiodarone?
Amiodarone is a CYP3A4 inhibitor, so it and others will potentially increase levels resulting in increased side effects (hypotension, hyperkalaemia, dizziness, nausea, increased renal impairment)
124
A patient can't tolerate a statin and triglyceride is over 10mmol/L, they are prescribed a fibrate. Why do you need to take special care in patients with renal impairment or disease who are taking Fibrates (Bezafribrate, Ciprofibrate, Fenofibrate, Gemfibrozil) ?
Although effective at reducing serum triglycerides, these can cause myotoxicity in patient with increasing creatinine levels causing rhabdomyolysis, this should be monitored alongside CK and discontinued if necessary
125
Why would you be concerned if a Digoxin patient has a potassium level under 4.5 mmol / L ?
Hypokalaemia predisposes digoxin patients to digitalis toxicity resulting in arryhthmias, bradycardia, nausea, confusion, anorexia and blurred vision.
Other factors include renal function, the plasma concentration itself should be under 2 ng / L although toxicity can occur in the therapeutic range of 0.7 - 2.
126
Why would you be a Hepatitis C patient require further questioning if started on Amiodarone?
Nuceloeside analogues combined with HCC blockers are associated with heart block and bradycardia when taken with Amiodarone. If another anti-arrhythmic cannot be given, careful monitoring is required for 48 hours after initiation. Patient to be aware of signs of heart block including SoB, light-headedness, palpitations, fainting, tiredness and chest pain.
127
Why would you counsel an Amiodarone patient on the following:
Visual disturbances
Signs of hypothyroidism / hyperthyroidism
Jaundice and liver issues
SoB
Nerve pain
Light sensitivity
Amiodarone is associated with corneal micro deposits leading to visual disturbances and night glare
It also contains iodine and so can cause either hypo / hyperthyroidism - full thyroid test at start and every 6 months.
Signs of jaundice, abdominal pain, nausea and vomiting, pruritis can be due to hepatotoxicity and LFTs needed before treatment and every 6 months.
Pulmonary toxicity can arise from Amiodarone so a chest x ray before treatment and patient to be aware of breath shortness and cough development.
Nerve pain (tingling, burning, numb sensations) can be a sign of peripheral neuropathy.
Suncream to be used due to phototoxic reactions.
128
How would you treat simple gravitational oedema?
Advising patient to increasing movement, raising their legs and to prescribe support stockings
Diuretics to be limited to a few days only.
129
What conditions can loop and thiazides worsen?
Gout
Lupus
Diabetes
130
Why would you give Amiloride alongside Furosemide?
In severe heart failure or hypertension Amiloride will be used to preserve potassium (off set the potassium loss caused by loop diuretics)
131
What tests are conduction on an Amiodarone patient?
Eye tests
LFTs
Chest x Ray
Thyroid - T4, T3, TSH
132
Why would you still use caution in a patient who used to take Amiodarone but recently stopped and has been prescribed a QT prolonging drug?
QT prolonging drugs such as the macrolides, clarithromycin, multiple antipsychotics can lead to ventricular arrhythmias when combined with Amiodarone which has a very long half life that varies considerably from patient to patient (20 - 100 days)
133
When would you recommend lowering a diabetics bp target to 130/80?
When presenting with CVD, kidney, eye disease.
134
Why use ACEi and A2RB?
As well as being anti hypertensive they also delay microalbuminuria to nephropathy in DM
135
Why would you report a patient with lip / facial swelling on ACEi to the GP? What if they reported nausea, muscle weakness and irregular heart beat?
Could potentially be signs of angioedema.
The latter are signs of hyperkalaemia and also require referral.
136
Why are pregnant mothers at risk of hypertension recommended aspirin?
Aspirin at 75mg every day from week 12 of pregnancy is to reduce the risk of pre-eclampsia.
137
What strengths of MR Diltiazem and Nifedipine require brand specificity?
Any MR Diltiazem over 60mg and any MR Nifedipine.
138
What is the ideal value for total serum cholesterol?
Under 5 mmol/ L
139
At what point would you add in Digoxin in HF?
1st line: ACEi and Beta blocker
2: Spironolactone
3 add in Digoxin.
Loop diuretics for congestive symptoms and fluid retention.
140
Why would you use Amlodipine in HF?
As a long acting calcium channel blocker (short acting / Diltiazem / Verapamil not appropriate) for comorbid HT / angina.
141
Treatment for post MI?
ACEi / A2RB
Dual antiplatelet
B blocker
Statin
142
What can cause AF?
```
HT
HF
Valvular heart disease
Ischaemic heart disease
Chest infections
Pulmonary embolism
Lung cancer
Excessive alcohol intake
Hyperthyroidism
Infections
DM
```
143
What is assessed in the CHA2DS2VASc?
```
Congestive heart failure
Hypertension
Age over 75
DM
Stroke / TIA/ thromboembolism
Vascular disease
Age between 65 - 74
Female
```
Age and stroke are worth 2 each
144
How do you assess bleeding risk?
HASBLED
```
Hypertension
Abnormal liver / renal function
Stroke
Bleeding
Labile INRs
Elderly
Drugs - antiplatelets / NSAIDs
```
145
Why counsel a warfarin patient on diet?
Bit K is present in green leafy vegetables and can antagonise the effects of warfarin
Alcohol can affect coagulation control as an enzyme inducer
Pomegranate can increase the INR
146
What is the target INR for AF?
2.5
147
Why would a painful rash on Warfarin require referral?
Could potentially be calciphylaxis.
148
What to monitor for Propafenone?
Liver failure and signs of jaundice and hepatotoxicity.
149
Why would you be concerned if a patient on Sotalol had prolonged / severe diarrhoea ?
Anything leading to hypokalaemia or hypomagnesia could increase the QT interval leading to life threatening ventricular arrhythmias and should be corrected before treatment initiation.
150
How would you adjust Digoxin dose when switching from IV to oral?
Increase 20-33%.
151
How long to continue thromboembolism prophylaxis post surgery?
5 - 7 days (or sufficient mobility)
Increased to 28 days for major surgery.
152
When would you stop treatment for venous thromboembolism?
After 5 days and for when INR is under 2
153
Why use heparins and specifically LMWH in pregnancy?
These don’t cross the placenta and LMWH have decreased risk of osteoporosis and heparin induced thrombocytopenia (drop of 30% in platelets, thrombosis, skin allergy).
You would stop at labour onset then continue post birth (bleeding risk)
154
What are the ISA beta blockers? POCA
Pindolol
Oxprenolol
Celiprolol
Acebutol
155
Why might you recommend a beta blocker patient to be changed to Pindolol, oxtenolol, Celiprolol, Acebutolol?
These have intrinsic sympathomimetic activity and therefore offset side effects such as cold hands and bradycardia.
156
Why might you use a cardioselective beta blocker? Examples are Atenolol, Bisoprolol, Metoprolol, Nebivolol.
To reduce risk of bronchospasm in asthmatics
To reduce blood glucose disturbances in DM
157
Why might you reduce Atenolol and Nadolol in renal impairment?
These are 2 of 4 water soluble Beta blockers and will have reduced excretion in renal impairment.
158
How might you adjust dosing for ACE in renal impairment?
Due to increased risk of hyperkalaemia a lower dose may be required and renal and electrolyte monitoring will be needed.
159
Why might you be concerned if an ACEi patient who is also diabetic complains of shaking, tremors?
ACEi May affect blood glucose control and potentiate affects of antidiabetic drugs leading to hypoglycaemia (shaking, tremors, sweating, pins and needles, hunger, palpitation, headache, double vision, difficulty concentration, slurred speech, confusion,behaviour change, convulsions, coma.
*If also on beta blocker, this may hide signs including tremor.
160
Why would the renin inhibitor Aliskiren not be given at same time as ACEi or ARB?
Can increase renal impairment, hyperkalaemia and hypotension.
161
Why is first dose hypotension pronounced in patients on low salt didn’t on 80mg Furosemide when given an ACEi?
The renin system is also highly activated so causes a massive inhibition and large hypertensive effect so would advise first dose at night.
162
Why counsel ACEi patient on signs of jaundice, yellowing, itching?
Reports of cholestatic jaundice, hepatitis, hepatic failure.
