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

6.1 Hypertension and heart failure Flashcards

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
Q

What is special about ramipril and enalapril

A

These are prodrugs which are metabolised in the liver to ____prilats, the active metabolite

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26
Q

What is the MAIN side effect of ACE inhibitors + 3 others which MUST be considered

A

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
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27
Q

Give 2 contraindications for ACE inhibitors

A

pregnancy and renal artery stenosis

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28
Q

Give 2 examples of Angiotensin Receptor Blockers (ARBs)

A

losartan and valsartan

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29
Q

Which receptors do angiotensin receptor blockers bind?

A

Angiotensin II type 1 (AT1) receptor

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30
Q

Give 2 actions of ARBs

A

1) Inhibit vasoconstriction
2) Inhibit aldosterone stimulation by angiotensin II

31
Q

How are ARBs administered?

A

Oral once daily, titrate dose as required

32
Q

ARBs have a _____ bioavailability and _____ protein binding

A

Low bioavailability

high protein binding

33
Q

Give 2 important side effects of ARBs

A

1) Renal failure
2) Hyperkalaemia

34
Q

Give 2 contraindications for ARBs

A

pregnancy and renal artery stenosis

35
Q

Where do Ca2+ Channel Blockers (CCBs) bind?

How does binding effect Ca2+

A

To specific alpha subunit of L-type calcium channel

Binding reduces cellular calcium entry

36
Q

Give the 3 main groups of CCBs and how do they differ?

Incl an example of each

A

1) Dihydropyridines ➞ target BV’s ➞ Amlodipine (HT)
2) Benzothiazepines ➞ antiarrhythmics ➞ Diltiazem
3) Phenylalkylamines ➞ antiarrhythmics ➞ Verapamil

37
Q

What is the administration, absorption and protein binding of CCBs

A
  • Oral administration
  • Good oral absorption
  • Highly protein bound > 90%
38
Q

Give 4 adverse effects of CCBs

A

1) SNS activation ➞ tachycardia + palpitations
2) Flushing, sweating
3) Throbbing headache
4) Oedema
5) Gingival hyperplasia (rare)

39
Q

What is the main action of CCBs (dihydropyridines)

A

Vasodilates peripheral, coronary and pulmonary arteries (no significant effect on veins)

Reduces SVR!!

40
Q

Give an example of a diuretic which can be used in each part of the nephron

A
41
Q

Give an example of a Thiazide and a thiazide-like diuretic (TLD)

A

Thiazide ➞ Bendroflumethiazide

Thiazide-like ➞ Metolazone

42
Q

Give the MoA of Thiazide and TLDs

A

1) Reduce distal tubular sodium reabsorption (initial decrease in BV)
2) Later effects which aid in decreasing TPR

43
Q

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

A

Long, dose dependant

44
Q

Give 4 adverse effects of Bendroflumethiazide

A

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
Q

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

A
46
Q

Give 4 other anti-hypertensive drugs

A
47
Q

Define Hypertensive urgency

A

Very high BP > 220/120 mmHg

Hypertensive Emergency!

48
Q

What is Malignant hypertension?

A

Very high BP associated with acute complications:

Pulmonary oedema, renal failure, aortic dissection, papilloedema etc…

Hypertensive Emergency

49
Q

What BP must we aim to achieve in a hypertensive emergency?

How do we do this?

A

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
Q

Explain the use of Sodium Nitroprusside in the treatment of hypertensive emergencies

What must we be careful of?

A

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
Q

Explain the use of Glyceryl Trinitrate in the treatment of hypertensive emergencies

What must we be careful of?

A

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
Q

Define heart failure?

A

Reduced cardiac output and/or elevated intra-cardiac pressures

53
Q

Give 3 symptoms and 3 signs of heart failure

A

Symptoms: breathlessness, ankle swelling, fatigue

Signs: tachycardia, tachypnoea, ⬆ JVP, pulmonary crackles, pleural effusion, peripheral oedema, hepatomegaly

54
Q

Give 4 pieces of evidence that would indicate structural/functional abnormality of the heart

A
  1. Cardiomegaly
  2. 3rd heart sound
  3. Cardiac murmurs
  4. ECG abnormalities
  5. Raised ANP
55
Q

Give 4 potential causes of L sided heart failure

A
  1. Coronary Heart Disease (IHD)
  2. Hypertension (HTN)
  3. Cardiomyopathy
  4. Mitral and aortic valve disease
56
Q

Give 4 potential causes of R sided heart failure

A
  1. Left heart failure
  2. Pulmonary Embolus (PE)
  3. Chronic lung disease (cor pulmonale)
  4. Shunts (ASD/VSD)
57
Q

How can we distinguish systolic vs diastolic heart failure?

A

Systolic ➞ reduced ejection fraction (less than 45%)

Diastolic ➞ preserved ejection fraction (more than 50%)

(Note: EF = SV/EDV)

58
Q

Explain the ‘vicious cycle of heart failure’

A
62
Q

What are the 3 main aims of treatment in patients with heart failure?

A
  1. Treat symptoms and signs (ie oedema) + improve quality of life
  2. Prevent hospital admissions
  3. Reduce mortality
63
Q

Compare the management of systolic vs diastolic HF

A

Systolic

  1. symptom relief
  2. optimal management of comorbidities
  3. disease modifying therapies

Diastolic

  1. symptom relief
  2. optimal management of comorbidities
64
Q

Give 2 diuretics precribed to improve symptoms of HF (not disease modifying)

A

Furosemide (most potent)

Bumetanide (alternative to furosemide)

65
Q

Give 4 ADRs of diuretics

A
  1. hyponatraemia and hypokalaemia
  2. postural hypotension
  3. syncope
  4. hyperuricaemia/gout
  5. ototoxicity
  6. diabetogenic
66
Q

In which type of heart failure are disease modifying therapies available

A

Systolic Heart Failure

67
Q

Give 3 treatments of systolic heart failure

(ABBA)

A

1) ACE Inhibitors OR ARBs (if intolerant to ACEi)
2) Aldosterone antagonist
3) β-blockers

(May improve prognosis)

68
Q

Give 2 examples of ACE inhibitors

A

Rampril, Enalapril, Lisinopril

69
Q

Give 2 examples of angiotensin receptor blockers

A

Candesartan, Valsartan, Losartan

70
Q

What is aldosterone “escape” and what is the effect of this?

How do we prevent/manage this?

A

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
Q

Give 2 examples of aldosterone antagonists

A

Spironolactone and Eplerenone

72
Q

Give 2 other agents which can be prescribed for heart failure and briefly explain each

A
73
Q

Give 4 physiological effects of β-blockers

A

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
Q

Give 3 examples of β-blockers recommended in BNF

A

1) Bisoprolol (high β1 selectivity)
2) Carvedilol
3) Nebivolol (β1 selective at low doses + NO potentiating ➞ vasodilator)

75
Q

What is the general rule of prescribing β-blockers and how is this done?

A

“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
Q

Give the 3 aims of disease modifying therapies

A

1) Improve symptoms and quality of life
2) Improve ventricular function
3) Reduce hospital admissions and death

78
Q

Give 4 ways in which we can promote self management in a patient with HF

A

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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