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Clinical Pharmacology & Intro to Prescribing > Session 3: Hypertension & Heart Failure > Flashcards

Session 3: Hypertension & Heart Failure Flashcards

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1
Q

Explain how activation of beta1-adrenoceptors on the heart cause increase in BP.

A

Increased inotropy in heart -> increased CO -> increased BP

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2
Q

Explain how activation of alpha1 adrenoceptors on smooth muscle lead to increased BP.

A

Increased venous return and increased peripheral resistance via vasoconstriction -> increased BP

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3
Q

Explain how activation of b1 adrenoceptors on kidney lead to increased BP.

A

Increased production of renin -> angiotensin II -> increased peripheral resistance via vasoconstriction -> increased BP

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4
Q

How does radius of blood vessel relate to resistance and mean arterial pressure.

A

A decreased radius leads to increased resistance to flow.

This explains why vasoconstriction causes increased peripheral resistance and increased BP.

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5
Q

NICE guidelines to define hypertension.

A

140/90 mmHg

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6
Q

Explain how to make a clinical diagnosis of hypertension.

A

Sitting relaxed and arm is supported.

Test both arms. If there is a >15 mmHg difference then repeat measurement and use the arm with a higher reading.

Can do measurements over period of visits +/- ABPM/HBPM

Assess CVD risk and end organ damage.

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7
Q

Stage 1 hypertension.

A

140/90 minimum

Subsequent ABPM daytime average or HBPM average BP ranging from 135/85 - 149/94

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8
Q

Stage 2 hypertension.

A

160/100 mg or higher

Subsequent ABPM daytime average or HBPM average BP of 150/95 or higher.

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9
Q

Stage 3/Severe Hypertension

A

Clinic systolic BP of 180 mmHg or higher

or

Clinic diastolic BP of 120 mmHg or higher

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10
Q

What is prehypertension?

A

>120/80<140/90 mmHg

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11
Q

Interventions in prehypertension.

A

Promotion of regular exercise

Diet

Reduction in stress and increased relaxation

Limit alcohol

Limit caffeine

Smoking cessation

Limit dietary sodium

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12
Q

Primary hypertension therapeutic agents

A

Ace inhibitors

Angiotensin receptor blockers (AT1)

Calcium channel blockers (CCBs)

Diuretics (thiazide and thiazide-like)

Other agents

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13
Q

Where can ACE be found?

A

Luminal surface of capillary endothelial cells predominantly in lungs.

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14
Q

Briefly explain how ACE inhibitors work.

A

They inhibit the conversion of angiotensin I to angiotensin II (the active form) by ACE.

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15
Q

What does a reduction in angiotensin-II cause?

A

Vasodilation (lower afterload)

Reduction in aldosterone release (More Na+ and H2O excreted)

Reduced ADH release (More H2O excreted + less vasoconstriction)

Reduced cell growth and proliferation

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16
Q

Can angiotensin I be converted into angiotensin II without ACE?

A

Yes it can, via chymases.

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17
Q

Give example of ACE inhibitors.

A

Lisinopril

Ramipril

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18
Q

Explain ACE inhibitors interaction with bradykinin.

A

ACE inhibitors inhibit the degradation of bradykinin causing an increase in bradykinin.

ACEi therefore potentiates bradykinin.

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19
Q

Functions of bradykinin.

A

Vasodilatory effect via NOS/NO and PGI2

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20
Q

Side-effects of ACEi.

A

Hypotension

Dry cough

Hyperkalaemia (low aldosterone leading to increased K+)

Renal failure

Angioedema

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21
Q

When should you not give ACEi?

A

Renal artery stenosis

Acute kidney injury

Pregnancy

Breastfeeding

CKD

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22
Q

Give examples drugs with important interactions with ACEi and when you should be wary of their effects.

A

K+ sparing drugs

NSAIDs

Other anti-hypertensive agents

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23
Q

Why should you not give ACEi in renal artery stenosis?

A

Because in renal artery stenosis there is a requirement of efferent arteriole to be able to constrict.

ACEi would dilate the efferent arteriole.

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24
Q

In which people should you not give ACEi?

A

Black African population

African-Carribean population

Age >55

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25
Why should you not give ACEi in Black African or African - Carribean population?
Because their are more sensitive to bradykinin so the ACEi will have an increased effect. This can lead to life-threatening **angioedema**.
26
What are angiotensin II receptor blockers also called?
ARBs Angiotensin II blockers AT1-receptor blockers.
27
Give examples of ARBs
Cande**sartan** Lo**sartan**
28
Explain the difference between ARBs and ACEi.
In ARBs you will still have angiotensin II but ARBs **block** AT1 receptors and **inhibit** the action of Ang-II mediated vasoconstriction. There is also no production of bradykinin meaning **no dry cough and angioedema.** It is more effective in **high-renin** hypertensives as Ang-II can still be produced by **chymases**.
29
When should you not give ARBs?
Renal artery stenosis Acute kidney injury Pregnancy Breastfeeding CKD
30
Give examples of drugs with important interactions with ARBs.
K+ sparing drugs NSAIDs Other antihypertensive agents.
31
Explain action and location of L-type calcium channels.
LTCCs allow influx of Ca2+ into cells. They are VOCCs. They can be found throughout the body **including vascular smooth muscle and cardiac myocytes** + SA node and AV node.
32
Give the subclasses of CCBs.
Dihydropyridines Non-dihydropyridines
33
Subclasses of non-dihydropyridines.
Phenylaklylamines Benzothiazapines
34
Explain the action of dihydropyridines.
Selective for **peripheral vasculature** and will not have much of chronotropic and inotropic effect as it does not affect LTCCs on cardiomyocytes, AV node and SA node. They will **block** calcium channel and prevent influx of Ca2+. This leads to inhibition of vasoconstriction and **reduced peripheral resistance**. 3 classes of CC interact with **different** sites on alpha1 subunit of VOCC. This means there is a **selectivity** for vascular smooth muscle or myocardium.
35
Explain the action of phenylalkylamines.
Depresses SA node and slows AV conduction leading to **lower inotropy**. Prolongs the action potential/effective refractory. Less peripheral vasodilation, neg. chronotropic and inotropic.
36
Explain the action of benzothiazapines.
Sits in the middle and blocks both cardiac activity as well as vascular.
37
What is the first line CCB for hypertension?
Dihydropyridines.
38
What is the primary choice of antihypertensive in **low renin patients**?
CCBs
39
Examples of dihydropyridines.
Amlod**ipine** Nifed**ipine** Nimod**ipine**
40
How does amlodipine differ to other dihydropyridine class drugs?
It has a long half life whereas other tned to have a shorter.
41
Selectivity for nimodipine.
For cerebral vasculature meaning it is effective in prevention of subarachnoid haemorrhage.
42
Side effects of dihydropyridines class.
Ankle swelling Flushing Headaches All due to vasodilation Palpitations due to compensatory tachycardia.
43
Diseases when to be wary of dihydropyridines.
Unstable angina Severe aortic stenosis
44
Interactions of dihydropyridines with other drugs.
Amlodipine + simvastatin (causing increased effect of statin) Other anti-hypertensive agents.
45
What are phenylalkyamines used for?
Arrhythmia, angina and hypertension
46
Side effects of phenylalkylamines.
Constipation Bradycardia Heart block Cardiac failure
47
Diseases when to be wary of phenylalkylamines.
Poor LV function AV nodal conduction delay
48
Interactions of phenylalkylamines with other drugs.
Beta blockers Other antihypertensives Other antiarrhythmic agents
49
Example of benzothiazapines.
Diltiazem
50
Example of phenylalkylamines.
Verapamil
51
Action of thiazide and thiazide-like diuretics.
Inihibit Na+/Cl- co-transporter in DCT leading to lower Na+ in blood and H2O (i.e. more excretion)
52
When are thiazide and thiazide-like diuretics preferred instead of CCB.
In oedema
53
Side effects of thiazide and thiazide-like diuretics.
Hypokalaemia Hyponatraemia Hyperuricaemia Arrhythmia Increased glucose Increased cholesterol and triglycerides
54
Diseases when to be wary of thiazide and thiazide-like diuretics.
Hypokalaemia Hyponatraemia Gout
55
Interactions of thiazide and thiazide-like diuretics with other drugs.
NSAIDs K+ wasting drugs
56
Example of thiazide and thiazide-like drugs.
Bendroflumethiazide Indapamide
57
In the case of BP not being controlled after step 3 i.e. resistant hypertension. What is the first thing to consider?
Administering an aldosterone receptor antagonist like spironolactone.
58
Diseases when to be wary of spironolactone.
Hyperkalaemia Addison's
59
Interactions of spironolactone with other drugs.
K+ sparing drugs including ACEi and ARBs
60
If a patient has resistant hypertension and hyperkalaemia. What is given instead of spironolactone?
**Alpha and beta-blockers** Centrally acting drugs like **labetalol** (in pregnancy and hypertensive emergency) to reduce the **sympathetic outflow**
61
Explain the action of beta-blockers.
Decrease sympathetic tone by blocking NAd and reducing myocardial contraction (reduced inotropy). This causes lower CO and decrease in renin secretion as well via beta-1.
62
Side-effects of beta-blockers.
Bronchospasm Heart block Raynaud's Lethargy Impotence Masking of tachycardia as a sign of insulin induced hypoglycaemia.
63
Diseases of when to be wary of beta-blockers.
Asthma and COPD Haemodynamic instability Hepatic failure
64
Interactions of beta-blockers and other drugs.
Non-dihydropyridine CCB like verapamil and diltiazem causing **asystole**
65
Examples of beta blockers.
Labetalol Bisoprolol Metoprolol
66
Action of alpha-blockers.
Selective antagonism of alpha-1 adrenoceptors to reduce peripheral vascular resistance and also has an effect in urinary tract including bladder neck and prostate. They are also relatively safe in renal disease.
67
Explain why alpha1-blockers can be given in BPH
Tamsulosin can be given in BPH to relax IUS and also the muscles of the prostate in order to relieve the urinary retention and increase urine flow
68
Side-effects of alpha-blockers.
Dizziness Syncope Headache Fatigue
69
Diseases of when to be wary of alpha-blockers
Postural hypertension
70
Interactions of alpha-blockers with other drugs.
Dihydropyridine CCBs causing oedema
71
Explain the self perpetuating spiral of heart failure.
Decreased arterial blood pressure as the CO goes down in HF. Baroreceptors respond to the fall in BP and cause increase in sympathetic outflow. Beta will cause increased renin, increased ATII, increased aldosterone, Na+ retention, vasoconstriction via ADH, and therefore more volume of blood and increased **preload**. Alpha will cause vasoconstriction and increased **afterload.** Both lead to an increased myocardial O2 demand and worsening of the **heart failure**.
72
First line treatment of heart failure.
Diuretics such as furosemide
73
Management of heart failure with reduced ejection fraction.
ACEi like lisonopril or ramipril Beta-blocker like bisoprolol Spironolactone If intolerant to ACEi then consider ARBs like candesartan or losartan.
74
Aims of treatment of HFREF.
Reduction in symptoms such as dyspnoea, fatigue and oedema Managed increased in exercise tolerance Address arrhythmias, hyperlipidaemia and diabetes Decreased mortality
75
Non-pharmacological management of HFREF.
Reduce salt intake Liquid reduction
76
What can happen if you give spironolactone.
Refractory hyperaldosteronism that is adjunct to ACEi/ARB + diuretic
77
Why do ACEi and ARB precipitate hyperkalaemia?
Because they block the angiotensin II causing an increase in aldosterone. Aldosterone is potassium wasting and if that doesn't work then potassium will be spared and can cause hyperkalaemia.
78
Explain the two-pronged approach of to ACEi/ARB use in type 2 diabetes with hypertension.
In diabetic nephropathy and CKD with proteinuria there is less dilation of efferent glomerular arteriole. Therefore a two pronged approach is used where ACEi and ARBs cause lower peripheral vascular resistance leading to **lowered BP**. There is also **dilation** of efferent glomerular arteriole to cause **reduced intraglomerular pressure** which is good for T2DM.
79
Why are ACEis more beneficial in low-renin hypertensives than ARBs?
Because ACEis also causes vasodilation via bradykinin and doesn't entirely rely on the RAAS system.
80

Clinical Pharmacology & Intro to Prescribing (24 decks)

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