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Pharmacology (Semester 6) > 6.1 Hypertension and heart failure > Flashcards

6.1 Hypertension and heart failure Flashcards

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1
Q

Give the equation for cardiac output and blood pressure

A

CO = HR x SV

BP = CO x TPR

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2
Q

What are the 2 receptor types (SNS and PNS) found on the heart

A

SNS: β1 adreno

PNS: M2 muscarinic

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3
Q

What are the 2 receptor types found on blood vessels

A

α1 adreno and β2 adreno

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4
Q

Which variable from our equations is changed in heart failure?

A

Inadequate CO

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5
Q

Which variable from our equations is changed in hypertension?

A

persistently high BP

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6
Q

What are the 3 physiological mechanisms which control BP

A

1) ANS
2) RAAS
3) vasoactive agents (metabolites, bradykinin, NO, ANP/BNP)

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7
Q

Give 5 pharamacological treatments for hypertension/ heart failure

(incl the suffix of each class)

A
  1. Diuretics
  2. ACE inhibitors ➞ _prils
  3. Angiotensin II Receptor Blockers ➞ _sartans
  4. Calcium Channel Blockers ➞ _dipines
  5. β blockers ➞ _olols
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8
Q

Give 3 diuretics which can be used to treat hypertension/ heart failure

(incl the suffix of each class)

A

Loop ➞ _semide and _tanides

Thiazide ➞ _thiazides

K+ sparing (aldosterone antagonists) ➞ spironolactone and _renones

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9
Q

What BP is defined as hypertension

A

140/90mmHg or above in clinic measurement

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10
Q

As a clinician why is lowering BP in a patient with hypertention important

A

lowering diastolic BP by 10mmHg is associated with significant reductions in stroke and coronary artery disease

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11
Q

Describe the mechanism underlying hypertension and how this leads to CV mortality and morbidity

A
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12
Q

Compare primary vs secondary hypertension

A

Primary/ Essential ➞ high BP without any evident cause (90% of cases)

Secondary ➞ high BP with a discrete, identifiable underlying cause (eg. renal/ endocrine problems)

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13
Q

Give 5 treatments/considerations we must make for a patient with Hyptertension

A

1) Identify + treat underlying cause if present
2) Identify + treat other CV risk factors/ co-morbidities
3) Lifestyle advice/ non-pharmacological therapy
4) Pharmacological therapy (current NICE guidelines)
5) Calculate a patient’s ‘QRISK’

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14
Q

What is “QRISK”

A

Used in patients with hypertension and estimates their % chance of having CVD in the next 10 years

QRISK results can influence primary prevention strategies

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15
Q

If a patients QRISK >10% what does NICE reccomend?

A

Start a statin

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16
Q

Give the 3 stages of hypertension

A
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17
Q

What is persistant hypertension?

A

Hypertension stage before it is classified as stage 1, defined as high BP at repeated clinical encounters

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18
Q

Give 4 pieces of lifestyle therapy which can be offered to a patient with hypertension

A

Patient education is KEY

1) maintain normal body weight (BMI 20-25 kg/m2)
2) keep dietry sodium low + ⬇ intake of saturated fat
3) limit alcohol consumption and/or smoking cessation
4) engage in regular aerobic physical exercise

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19
Q

Give 4 pharmacological treatments for hypertension

A

1) Angiotensin Converting Enzyme (ACE) inhibitors
2) Angiotensin II Receptor Blockers (ARB)
3) Calcium channel blockers
4) Diuretics

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20
Q

Explain how the RAAS system responds to low BP

A
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21
Q

ACE Inhibitors are _____ inhibitors of the ACE enzyme

A

Competitive

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22
Q

Give 4 actions of ACE inhibitors

A

1) reduce formation of angiotensin II
2) arteriolar vasodilation + some venodilation
3) reduce circulating aldosterone
4) potentiate the action of bradykinin

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23
Q

Give 2 examples of ACE inhibitors

A

lisinopril, ramipril, enalapril

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24
Q

How are ACE inhibitors administered and what is their bioavailability?

A

Oral, once daily titrate dose (according to BNF)

Variable bioavalability

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25
What is special about ramipril and enalapril
These are prodrugs which are metabolised in the liver to \_\_\_\_prilats, the active metabolite
26
What is the MAIN side effect of ACE inhibitors + 3 others which MUST be considered
Main side effect ➞ dry cough Important other side effects: 1. **Angio-oedema** (rare, but more common in black population) 2. **Renal failure** (incl renal artery stenosis) 3. **Hyperkalaemia**
27
Give 2 contraindications for ACE inhibitors
pregnancy and renal artery stenosis
28
Give 2 examples of Angiotensin Receptor Blockers (ARBs)
losartan and valsartan
29
Which receptors do angiotensin receptor blockers bind?
Angiotensin II type 1 (AT1) receptor
30
Give 2 actions of ARBs
1) Inhibit vasoconstriction 2) Inhibit aldosterone stimulation by angiotensin II
31
How are ARBs administered?
Oral once daily, titrate dose as required
32
ARBs have a _____ bioavailability and _____ protein binding
Low bioavailability high protein binding
33
Give 2 important side effects of ARBs
1) Renal failure 2) Hyperkalaemia
34
Give 2 contraindications for ARBs
pregnancy and renal artery stenosis
35
Where do Ca2+ Channel Blockers (CCBs) bind? How does binding effect Ca2+
To specific alpha subunit of L-type calcium channel Binding reduces cellular calcium entry
36
Give the 3 main groups of CCBs and how do they differ? Incl an example of each
1) **Dihydropyridines** ➞ target BV's ➞ Amlodipine (HT) 2) Benzothiazepines ➞ antiarrhythmics ➞ Diltiazem 3) Phenylalkylamines ➞ antiarrhythmics ➞ Verapamil
37
What is the administration, absorption and protein binding of CCBs
* Oral administration * Good oral absorption * Highly protein bound \> 90%
38
Give 4 adverse effects of CCBs
1) SNS activation ➞ tachycardia + palpitations 2) Flushing, sweating 3) Throbbing headache 4) Oedema 5) Gingival hyperplasia (rare)
39
What is the main action of CCBs (dihydropyridines)
Vasodilates peripheral, coronary and pulmonary arteries (no significant effect on veins) Reduces SVR!!
40
Give an example of a diuretic which can be used in each part of the nephron
41
Give an example of a Thiazide and a thiazide-like diuretic (TLD)
Thiazide ➞ Bendroflumethiazide Thiazide-like ➞ Metolazone
42
Give the MoA of Thiazide and TLDs
1) Reduce distal tubular sodium reabsorption (initial decrease in BV) 2) Later effects which aid in decreasing TPR
43
Thiazide and TLDs are ______ acting and hence require only one tablet per day. The effects of thiazide diuretics are NOT \_\_\_\_\_\_, hence the 'dose-blood pressure response curve' is flat
Long, dose dependant
44
Give 4 adverse effects of Bendroflumethiazide
1) Hypokalaemia 2) Increased urea and uric acid levels 3) Impaired glucose tolerance (esp with β-blockers) 4) cholesterol and triglyceride levels increased 5) activation of RAAS
45
Compare antihypertensive drug treatment for: A patient \< 55 years old A patient \> 55 years **OR** black person of african or caribbean family origin of any age
46
Give 4 other anti-hypertensive drugs
47
Define Hypertensive urgency
Very high BP \> 220/120 mmHg Hypertensive Emergency!
48
What is Malignant hypertension?
Very high BP associated with acute complications: Pulmonary oedema, renal failure, aortic dissection, papilloedema etc... Hypertensive Emergency
49
What BP must we aim to achieve in a hypertensive emergency? How do we do this?
Reduction in BP by ~20% OR to 100 mmHg diastolic within 1-2 hours Done through IV use of GTN and/or sodium nitroprusside (powerful rapid onset and offset)
50
Explain the use of Sodium Nitroprusside in the treatment of hypertensive emergencies What must we be careful of?
Releases **NO** (potent vasodilator of arterioles and venules) which lowers BP Caution must be taken in liver disease because it breakdowns into cyanide (avoid prolonged use \>72 hours)
51
Explain the use of Glyceryl Trinitrate in the treatment of hypertensive emergencies What must we be careful of?
Exogenous source of Nitric oxide (venous and arteriolar vasodilator) Side effects incl headaches and hypotension BUT the main problem is tachyphylaxis b/c of reduced efficacy due to tolerance after ~48 hrs
52
Define heart failure?
Reduced cardiac output and/or elevated intra-cardiac pressures
53
Give 3 symptoms and 3 signs of heart failure
Symptoms: breathlessness, ankle swelling, fatigue Signs: tachycardia, tachypnoea, ⬆ JVP, pulmonary crackles, pleural effusion, peripheral oedema, hepatomegaly
54
Give 4 pieces of evidence that would indicate structural/functional abnormality of the heart
1. Cardiomegaly 2. 3rd heart sound 3. Cardiac murmurs 4. ECG abnormalities 5. Raised ANP
55
Give 4 potential causes of L sided heart failure
1. Coronary Heart Disease (IHD) 2. Hypertension (HTN) 3. Cardiomyopathy 4. Mitral and aortic valve disease
56
Give 4 potential causes of R sided heart failure
1. Left heart failure 2. Pulmonary Embolus (PE) 3. Chronic lung disease (cor pulmonale) 4. Shunts (ASD/VSD)
57
How can we distinguish systolic vs diastolic heart failure?
Systolic ➞ reduced ejection fraction (less than 45%) Diastolic ➞ preserved ejection fraction (more than 50%) (Note: EF = SV/EDV)
58
Explain the 'vicious cycle of heart failure'
62
What are the 3 main aims of treatment in patients with heart failure?
1. Treat symptoms and signs (ie oedema) + improve quality of life 2. Prevent hospital admissions 3. Reduce mortality
63
Compare the management of systolic vs diastolic HF
Systolic 1. symptom relief 2. optimal management of comorbidities 3. disease modifying therapies Diastolic 1. symptom relief 2. optimal management of comorbidities
64
Give 2 diuretics precribed to improve symptoms of HF (not disease modifying)
Furosemide (most potent) Bumetanide (alternative to furosemide)
65
Give 4 ADRs of diuretics
1. hyponatraemia and hypokalaemia 2. postural hypotension 3. syncope 4. hyperuricaemia/gout 5. ototoxicity 6. diabetogenic
66
In which type of heart failure are disease modifying therapies available
Systolic Heart Failure
67
Give 3 treatments of systolic heart failure (ABBA)
1) ACE Inhibitors OR ARBs (if intolerant to ACEi) 2) Aldosterone antagonist 3) β-blockers (May improve prognosis)
68
Give 2 examples of ACE inhibitors
Rampril, Enalapril, Lisinopril
69
Give 2 examples of angiotensin receptor blockers
Candesartan, Valsartan, Losartan
70
What is aldosterone "escape" and what is the effect of this? How do we prevent/manage this?
The inability of of ACEi / ARB therapy to reliably suppress aldosterone release. After long time use aldosterone concentration returns to normal in circulation Aldosterone can stimulate fibroblasts ➞ endothelial dysfunction ➞ myocardial fibrosis To prevent/manage this we often prescribe an aldosterone antagonist alongside other treatments to prevent myocardial fibrosis
71
Give 2 examples of aldosterone antagonists
Spironolactone and Eplerenone
72
Give 2 other agents which can be prescribed for heart failure and briefly explain each
73
Give 4 physiological effects of β-blockers
1) reduce HR and negative inotropic effect (β1 = ⬇ CO ) 2) reduce BP (b/c of ⬇ CO) ➞ less afterload on heart _1+2 ➞ Reduce myocardial oxygen demand_ 3) reduce mobilisation of glycogen 4) negate unwanted effects of catecholamines
74
Give 3 examples of β-blockers recommended in BNF
1) Bisoprolol (high β1 selectivity) 2) Carvedilol 3) Nebivolol (β1 selective at low doses + NO potentiating ➞ vasodilator)
75
What is the general rule of prescribing β-blockers and how is this done?
"start low, go slow" As failing myocardium is dependent on HR, we must initiate at a low dose and titrate up to the maximum possible dose slowly. + may have to alter concomitant medication (e.g. diuretic) Impt to monitor HR, renal function and BP when uptitrating
77
Give the 3 aims of disease modifying therapies
1) Improve symptoms and quality of life 2) Improve ventricular function 3) Reduce hospital admissions and death
78
Give 4 ways in which we can promote self management in a patient with HF
1) rehabilitate or prescribe exercise 2) daily weight (gain can mean impending problem) 3) adherence with meds and diet 4) Investigate whether they can self-titrate diuretics?

Pharmacology (Semester 6) (17 decks)

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