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Pharmacology > Hypertension and HF > Flashcards

Hypertension and HF Flashcards

(59 cards)

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1
Q

What are the ranges for the different grades of hypertension?

A

Grade I: 140-159/90-99

Grade II: 160-179/100-109

Grade III: >180/>110

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2
Q

What are some drugs that can cause hypertension?

A

OCP
Corticosteroids
NSAIDs

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3
Q

Problems and complications of hypertension?

A 
Increased arterial thickening
Smooth muscle cell hypertrophy
Accumulation of vascular matrix
Loss of arterial compliance
Target organ damage such as heart, kidneys, brain, eyes
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4
Q

Endocrine causes of secondary hypertension?

A 
Conn's syndrome
Congenital adrenal hyperplasia
Cushing's
Phaeochromocytoma
Thyroid disease
Acromegaly
Hyperparathyroidism
Carcinoid
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5
Q

Renal causes of hypertension?

A 
Renovascular hypertension
Chronic pyelonephritis
Diabetic renal disease
Renal parenchymal disease
Liddle's syndrome
Gordon's syndrome
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6
Q

What is phaeochromocytoma?

A

Adrenal catecholamine-secreting tumour - produces large amounts of adrenaline and NA

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7
Q

How is phaeochromocytoma treated?

A

Non-selective alpha-adrenoreceptor antagonists

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8
Q

What is Conn’s syndrome?

A

An aldosterone-secreting adenoma causing fluid reabsorption

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9
Q

How is Conn’s syndrome treated?

A

Aldosterone antagonists eg spironolactone

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10
Q

How is mild (grade I) hypertension treated?

A

Normally a non-pharmacological therapy (lifestyle changes)

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11
Q

What is isolated systolic hypertension and what is it due to?

A

A low diastolic BP and a high systolic BP (>140mmHg)

Common with increasing age due to loss of compliance of arteries

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12
Q

What are some non-pharmacological interventions?

A

Maintain normal body weight
Reduce salt intake
Consume 5+ portions of fruit and veg a day
Limit alcohol
Regular exercise
Reduce total and saturated fat
Stop smoking (just reduces CV risk, not BP)

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13
Q

When is blood pressure treated pharmacologically?

A

When it is above 160/100mmHg

Above 140/90mmHg in diabetics

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14
Q

What is someone under 55 initially treated for hypertension with?

A

ACE inhibitors

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15
Q

What is someone over 55 or black of any age initially treated with?

A

Calcium channel blockers

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16
Q

If there is no response in someone with hypertension with initial treatment, what is done?

A

Combine ACE inhibitors and Ca channel blockers

Then add diuretics

Then add alpha-blockers, beta-blockers, centrally acting drugs or vasodilators

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17
Q

Name some ACE-i

A

Lisinopril

Ramipril

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18
Q

What is the mechanism of action of ACE-i?

A

Competitively inhibits ACE activity

  • reducing formation of angiotensin II
  • preventing degradation of bradykinin
  • minimising production of aldosterone
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19
Q

What are the overall effects of ACE-i?

A

Reduce effect of RAAS

  • reduce Na and water reabsorption
  • reduce peripheral vasoconstriction
  • some venodilation action
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20
Q

ADRs of ACE-i?

A 
HARD
Hyperkalaemia
Angioedema
Renal problems/failure
Dry cough
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21
Q

Name some angiotensin-II receptor blockers (ARBs)

A

Losartan

Valsartan

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22
Q

ADRs of ARBs?

A

Renal failure

Hyperkalaemia

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23
Q

Indications for ARBs?

A

For individuals who cannot tolerate adverse effects of ACE-i

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24
Q

Mechanism of action of calcium-channel blockers?

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A

Bind to the alpha-subunit of L-type calcium channels, reducing calcium entry
Causes vasodilation of peripheral, coronary and pulmonary arteries by smooth muscle relaxation

25
What are the main groups of calcium channel blockers? Name a drug in each group
Dihydropyridines - nifedipine, amlodipine Phenylalkylamines - verapamil Benzothiazepines - dilitiazem
26
Absorption, distribution and metabolism of dihydropyridines?
Good oral absorption 90% protein bound Metabolised by liver
27
ADRs of dihydropyridines?
``` Baroreflex-mediated tachycardia SNS activation - tachycardia and papitations Flushing and sweating Ankle oedema Throbbing headache ``` However normally well-tolerated
28
Mechanism of action of phenylalkylamines eg verapamil and overall effects?
Act on myocardial and smooth muscle cell membrane calcium transport - leads to vasodilation, reducing cardiac preload and myocardial contractility Class IV anti-arrhythmic - prolongs action potential/effective refractory period
29
ADRs of phenylalkylamines?
Constipation Bradycardia Negative inotropy
30
DDIs of phenylalkylamines?
Cannot be given with beta-blockers as they cause bradycardia
31
Effects of benzothiazepines?
Peripheral vasodilation and reduced myocardial contractility | Prolongs action potential/effective refractory period
32
ADRs of benzothiazepines?
Bradycardia | Negative inotropy
33
What are benzothizaepines mostly used for?
Angina rather than hypertension
34
Overall effects of thiazide diuretics?
Act on Na-Cl symport in DCT Reduced sodium and water absorption, reduced blood volume Long-term, reduces TPR
35
ADRs of thiazides?
Hypokalaemia Increased urea and uric acid Impaired glucose tolerance Raised cholesterol and triglyceride levels
36
Name an alpha blocker
Doxazosin
37
Mechanism of action of alpha blockers?
Antagonise alpha-1 adrenoreceptors and antagonises contractile effects of NA, reducing TPR
38
ADRs of alpha-blockers?
Postural hypotension Dizziness Headache and fatigue Oedema
39
Mechanism of action of beta blockers?
Antagonise beta-1 adrenoceptors on ventricular myocardium, reducing HR and CO Inhibit renin release Rarely used as anti-hypertensive as have little significant effect
40
Why are beta-blockers good for angina?
Slow heart rate, increasing diastolic filling of coronary arteries
41
ADRs of beta-blockers?
``` Lethargy Impaired concentration Reduced exercise tolerance Bradycardia Raynaud's Impaired glucose tolerance ```
42
Contra-indications of beta-blockers?
Asthma
43
How do direct renin inhibitors work?
Bind to the renin molecule, preventing cleavage of angiotensinogen to angiotensin I
44
Name a renin inhibitor
Aliskiren
45
Bioavailability and excretion of aliskiren?
Low bioavailability Eliminated unchanged in faeces 1% renally excreted
46
In which patients must care be taken in prescribing renin inhibitors?
Patients at risk of hyperkalaemia, sodium and volume-depleted patients, patients with HF, severe renal impairment, renal stenosis
47
Examples of centrally acting agents?
Methyldopa - alpha-2 adrenoceptor agonist Clonidine - pre-synaptic alpha-2 agonist Monoxidine - alpha-2 agonist
48
Effects of centrally acting agents?
Reduce sympathetic outflow which reduces blood pressure
49
Benefits of centrally acting agents?
Good response | Safe in pregnancy
50
ADRs of centrally acting agents?
Tiredness and lethargy | Depression
51
What can happen in withdrawal of clonidine?
Rebound hypertension - due to NA release leading to desensitisation of alpha 2 receptors and super-sensitivity of post-synaptic alpha-1 receptors
52
What is a hypertensive emergency?
Very high BP of >220/120
53
What can happen in a hypertensive emergency if BP is not reduced by around 20% within 1-2 hours?
Pulmonary oedema Renal failure Aortic dissection
54
Treatment of hypertensive emergencies?
Sodium nitroprusside - acts as an endogenous nitrous oxude causing vasodilation and rapid onset of reduction of BP
55
What are the goals in HF treatment?
Symptomatic improvement Delay progression Reduce mortality Treat complications/associated conditions/CVS risk factors
56
What are the drugs used in HF?
ACE inhibitors and ARBs Aldosterone antagonists Diuretics (loop and thiazide)
57
What can aldosterone do/cause in HF?
Can return to normal even with ACE-i/ARB therapy Endothelial dysfunction leading to myocardiac fibrosis and acute coronary events Potassium and magnesium leading to arrhytmias Myocardiac fibrosis leading to arrhythmias All of these increase risk of sudden cardiac death
58
Why are beta-blockers good in HF?
Reduce myocardial oxygen demand - reduce heart rate via beta receptors - reduce BP, reducing CO Reduce metabolism of glycogen Negate unwanted effects of catecholamines
59
Why do beta-blockers need to be prescribed with care in HF?
A failing myocardium is dependent on HR

Pharmacology (23 decks)

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