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Clinical Pharmacology > Hypertension and Heart Failure > Flashcards

Hypertension and Heart Failure Flashcards

1
Q

How do you calculate MAP?

A

MAP = CO x TPR

(CO= SV x HR)

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2
Q

What are the 2 key drivers to increase blood pressure when blood pressure drops?

A

Increased sympathetic activity and activation of RAAS

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3
Q

What end organ damage can result from hypetension?

A
  • Renal
  • Peripheral Vascular Resistance
  • Aneurysm
  • Vascular Dementia
  • Retinal Disease
  • Hypertensive heart disease → LVH causing cardiac failure
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4
Q

Why treat hypertension if it asymptomatic?

A

Early management slows down/ prevents progression to CVD

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5
Q

What is the NICE definition of hypertension?

A

Hypertension = 140/ 90 mmHg

(>40% of UK population)

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6
Q

What are the 2 main types of hypertension and what are their respective incidences?

A

1) Essential/ primary/ idiopathic - 90%
2) Secondary - related to other pathology (disease/ tumours)

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7
Q

What is the white coat/ clinic effect?

A

Elevated blood pressure when measured in the clinic vs a home

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8
Q

What is best practice for measuring BP?

A
  • Measure with patient sitting, arm supported and relaxed
  • Measure both arms - >15 mmHg difference repeat the measurement and use arm with highest reading
  • +/- ABPM / HBPM
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9
Q

what blood pressure would be considered a hypertensive emergency?

A

> 180 /120 mmHg

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10
Q

Define the stages of hypertension

A

Stage 1: 140/90 mmHg - 159/99 mmHg

Stage 2: 160/100 mmHg >

Stage 3: systolic blood pressure of 180mmHg or higher or diastolic 120mmHg or higher

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11
Q

What BP is defined as pre-hypertension?

A

>120/80 but <140/90 mmHg

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12
Q

What advice would you give to someone who is pre-hypertensive?

A
  • Promote regular exercise
  • Modified healthy/ balance diet
  • Reduction in stress and increased relaxation
  • Limit/ reduce alcohol intake
  • Discourage excessive caffeine consumption
  • Smoking cessation
  • Reduce dietary NaCl
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13
Q

What are the main actions of Angiotensin II?

A
  • Increase sympathetic activity
  • Tubular Na+/ Cl- reabsorption and K+ excretion → H2O retention
  • Aldosterone secretion from the adrenal gland
  • Increase arteriolar vasoconstriction
  • ADH secretion from pituitary → H2O absorption
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14
Q

Which receptor type does Angiotension II primarily exert its actions via?

A

AT1

(There are AT1 and AT2 receptors)

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15
Q

How does a reduction in Angiotensin II effects cause a reduced BP?

A
  • vasodilation
  • reduction in aldosterone release → increased Na+ and H2O excretion
  • reduced ADH release → increased H2O excretion
  • reduced cell growth and proliferation (vascular smooth muscle)
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16
Q

How is Angiotension II produced independently of ACE?

A

Chymases can convert angiotensin I → angiontensin II

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17
Q

What are the 2 major ACEi?

A

Lisinopril

Ramipril

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18
Q

What are the main side effects of ACEi?

A
  • hypotension
  • Dry cough
  • Hyperkalaemia (low aldosterone increases K+)
  • Renal failure (esp. in renal artery stenosis)
  • Angiodema (more common in black population)
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19
Q

Why do ACEi cause dry cough?

A

Bradykinin is a substrate for ACE too

Inhibiting ACE therefore builds up bradykinin which causes cough and vasodilation by NOS/NO and PGI2

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20
Q

In which patients are ACEi contraindicated in?

A
  • Renal Artery Stenosis
  • AKD
  • Pregnancy
  • Breastfeeding
  • CKD
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21
Q

In which patients should ACEi be prescribed with caution?

A
  • Other drugs that increase K+
  • NSAIDs
  • Other anti-hypertensives
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22
Q

Which receptor to Angiotensin II receptor blockers (ARBs) target?

A

AT1 receptor

More effective at inhibiting Ang II mediation vasoconstriction via chymase production

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23
Q

What are the 2 major ARBs used to treat hypertension?

A

Candesartan

Losartan

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24
Q

What are the benefits of ARBs over ACEi?

A

No effect on bradykinin so no dry cough and less angiodema

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25
In which patients are ARBs contraindicated in?
* Renal artery stenosis * AKD * Pregnancy * Breastfeeding * CKD
26
In which patients should ARBs be used with caution?
* Other drugs that increase K+ * NSAIDs * Other anti-hypertensives
27
What is the normal function of calcium channels?
* L type calcium channels found throughout the body (vascular smooth muscle and cardiac myocytes, AV/ SA node) * Allow **inward Ca2+ influx** into cells * Stimulates CICR from internal Ca2+ stores * Ca2+ release causes **contraction**
28
Where do calcium channel blockers target VOCC?
3 classes of VOCC target different sites on the alpha 1 unit of VOCC Selective for **vascular smooth muscle/ myocardium**
29
What are the 3 classes of CCBs?
1. Dihydropyridines 2. Phenylalkylamines 3. Benzothiazapines
30
How do Dihydropyradines work?
Selectively target Calcium channels in **peripheral vasculature** (little chronotropic or inotropic effect) **1st line CCB for hypertension**
31
How do Phenylaklyamines work?
Target Calcium channels depressing SA and AV node → slow conduction → negative inotropy
32
How do benzothiazapines?
act on both myocardium and vascular smooth muscle (sit in between benzothiazapines)
33
In which patient groups are CCBs the primary choice of antihypertensive?
Patients with **low renin** e.g. black african patients
34
What are the main dihydropyridines?
* **Amlodipine** - long half life * **Nifedipine** * **Nimodipine** - selective for cerebral vasculature (useful in subarachnoid haemorrhage)
35
What are some of the side effects of dihydropyridines?
* Ankle swelling * Flushing * Headaches (due to vasodilatoin) * Palpitations (compensatory tachycardia)
36
In which patients are dihydropyradines contraindicated in?
* Unstable angina * Severe aortic stenosis
37
In which patients should you use dihydropyradines with caution?
* Amlodipine and simvastatin * Other anti-hypertensives
38
What is the main phenylalkylamine?
**Verapamil**
39
How do CCBs phenylalkylamines work? Which patients are they used to treat?
Class IV **anti-arrhythmic agent** prolongs the action potential / effective refractive period Less peripheral vasodilation, negative chronotrophic and ionotropic effects Used to treat: **Arrhythmia, angina** and hypertension
40
What are some of the side effects of phenylalkylamines?
* constipation * bradycardia * heart block * cardiac failure
41
In which patients are phenylalkylamines contraindicated in?
* Poor LV function * AV nodal conduction delay
42
Which patients are phenylalkylamines to be used with caution?
* Patients on Beta blockers * Other anti-hypertensives and antiarrhythmics
43
What is the name of the main benzothiazapine?
**Diltiazem**
44
What is the MoA of Thiazide and thiazide like diuretics?
Inhibit the N+/ Cl- co transporter in the **distal convoluted tubule** **Effect:** increased Na+ and H2O excretion
45
What are the 2 main thiazide and thiazide like diuretics?
Bendroflumethiazide Indapamide
46
What are some of the side effects of thiazide/ thiazide like diuretics?
* Hypokalaemia * Hyponatraemia * Hyperuricemia * Arrhythmia * Increased glucose (esp. with beta blockers) * Increased cholesterol and triglyceride
47
What patients should thiazide/ thiazide-like diuretics not be prescribed to?
* Hypokalaemia * Hyponatraemia * Gout
48
In what patients should thiazide/ thiazide like diuretics be used with caution?
* NSAIDs * Other drugs that decrease K+
49
Why are type II diabetics oftered ACEi/ ARB first line?
2 pronged approach * Decreased Peripheral Vascular Resistance which decreased BP * AND dilates the efferent glomerular arteriole→ decreased intraglomerular pressure
50
If BP is not controlled after the 3rd step of treatment what can you add to the patients treatment? Explain the MoA?
**Spironolactone** → aldosterone receptor antagonist
51
Which patients should spironolactone be contraindicated / used with caution?
**Contraindicated** - hyperkalaemia, addison's **Use with caution**- other drugs that increase K+ , ACEi and ARBs
52
Which drugs can you use to lower BP in pregnancy?
**Labetalol** (B blocker)
53
How do Beta blockers work?
* Block Beta adrenoreceptors * Decrease **sympathetic tone** by blocking action of NA and reducing **myocardial contraction** → decreased CO * Decreased renin secretion by B1 * B1 are selective for the heart * B2 are selective for the lungs
54
What are some of the side effects of Beta blockers?
* Bronchospasm * Heart Block * Raynaud's * Lethargy * Impotence * Can mask tachycardia
55
Name 3 Beta blockers
* Labetalol * Bisoprolol * Metoprolol
56
Which patients should beta blockers not be prescribed to/ prescibred with caution?
**Contraindicated**: asthmatics, COPD, Haemodynamic instability, hepatic failure **Use with caution**: non-dihydropyridine CCB (Verapamil and Diltiazem) can cause asystole
57
Explain the MoA of alpha adrenoreceptors blockers
* selective antagonist for **alpha 1** adrenoreceptors * reduce peripheral vascular resistance
58
What are some of the side effects of alpha adrenoreceptor blockers?
* postural hypotension * dizziness * syncope * headache * fatigue
59
Name 2 alpha adrenoreceptor blockers
* Doxazosin * Tamsulosin (used to treat urinary tract problems: bladder, neck and prostate BPH)
60
When should alpha adrenoreceptors be used with caution/ not used?
**Contraindicated:** Postural hypotension **Use with caution:** dihydropyridine CCBs (can cause oedema)
61
What are the aims when treating a patient with heart failure? (mechanism on the body)
Aim: * Dilate capacitance veins * Decrease preload * Reduced Sympathetic stimulation * Reduce blood volume
62
What non-pharmacological methods can be used to manage heart failure?
* reduce salt intake * reduce liquid intake ~1.5L
63
What are the goals when treating heart failure?
* reduce symptoms * manage increase in exercise tolerance * address arrhytmia, hyperlipidaemia, diabetes * decreased mortality

Clinical Pharmacology (25 decks)

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