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Yr 2 Sem 2 CPT > 4.2 Hypertension and Heart Failure > Flashcards

4.2 Hypertension and Heart Failure Flashcards

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1
Q

What is the consequence of higher blood pressure causing increased arterial thickening?

A

Smooth muscle cell hypertrophy

Accumulation of vascular matrix

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2
Q

What BP defines hypertension?

A

140/90mmHg

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3
Q

What is primary/essential hypertension?

A

High BP without any single evident cause

90% patients

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4
Q

What is secondary hypertension?

A

High BP with a discrete, identifiable underlying cause

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5
Q

What is grade 1 hypertension?

A

140/90

Mild

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6
Q

What is grade 2 hypertension?

A

160/100

Moderate

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7
Q

What is grade 3 hypertension?

A

180/110

Severe

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8
Q

Lifestyle therapy for hypertension

A 
Patient education 
Maintain normal body weight (BMI 20-25)
Reduce salt intake <6g/day
Limit alcohol 
Exercise
Fruit and veg 
Eat less fat
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9
Q

What is the first line pharmacological therapy for hypertension?

A

ACE inhibitor/Angiotensin receptor blocker
Calcium channel blocker
Diuretics

A C D

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10
Q

How do ACE inhibitors work?

A

Prevent generation of AngII
Potentiates action of bradykinin

Less vasoconstriction, less aldosterone release so less salt and water retention, less sympathetic activity

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11
Q

Name some ACE inhibitors

A

lisinopril

ramipril

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12
Q

What is the main side effect of ACE inhibitors? Why?

A

Dry cough

Bradykinin accumulates in the lung causing irritation

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13
Q

What are some important but less common side effects of ACE inhibitors?

A

Angio-oedema
Renal failure incl renal artery stenosis
Hyperkalaemia

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14
Q

Name two angiotensin receptor blockers

A

Losartan

Candesartan

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15
Q

How do angiotensin receptor blockers work?

A

Bind to angiotensin AT1 receptor (blocking effects of AngII)

Inhibits vasoconstriction and aldosterone stimulation caused by AngII

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16
Q

What is the difference between angiotensin receptor blockers and ACE inhibitors in terms of side effects?

A

No effect on bradykinin

Well tolerated with few side effects because doesn’t cause a cough

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17
Q

What are some important side effects of angiotensin receptor blockers?

A

Renal failure

Hyperkalaemia

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18
Q

How do calcium channel blockers work?

A

Bind to specific alpha subunit of L-type calcium channel

Reduces cellular calcium entry

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19
Q

What are the three main groups of calcium channel blockers?

A

Dihydropyridines - nifedipine, amlodipine
Benzotthiazepines - diltiazem
Phenylalkylamines - verapamil

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20
Q

What do calcium channel blockers do?

A

Vasodilate peripheral, coronary and pulmonary arteries

No significant effect on veins

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21
Q

What does verapamil do?

A

Depresses SAN and slows AV conduction

22
Q

What are some properties of calcium channel blockers dihydropyridines? e.g. amlodipine

A

Good oral absorption
Protein bound >90%
Metabolised by the liver
Few have active metabolites

23
Q

What are some side effects of dihydropyridines?

A

Sympathetic nervous system activation leading to tachycardia and palpitations
Flushing, sweating, throbbing headache
Oedema e.g. ankle swelling
Gingival hyperplasia

24
Q

What are some properties of phenylalkylamines? e.g. verapamil

A

Impedes calcium transport across the myocardial and vascular smooth muscle cell membrane
Class IV prolongs AP and RP
Peripheral vasodilation
Reduction in cardiac preload and myocardial contractility

25
Q

Adverse effects of phenylalkylamines?

A

Constipation
Bradycardia
Reduce myocrdial contractility as negative inotrope which can worsen HF

26
Q

What are some properties of benzothiazepines? e.g. diltiazem

A

Impedes calcium transport across myocardial and vascular SM cell membrane
Prolonges AP and RP
Peripheral vasodilation and reduction in preload and contractility

27
Q

Adverse effects of benzothiazepines

A

Bradycardia

Less negative inotropic effect than verapamil

28
Q

Would you give diltiazem or verapamil to a patient with angina or heart failure?

A

Diltiazem

Less negative inotropic effect

29
Q

What do thiazides/thiazide like diuretics do?

A

Reduce distal tubular sodium reabsorption

30
Q

What is the mechanism of blood pressure reduction when using thiazides?

A

Complex
Initial blood volume decrease
Later TPR falls

31
Q

What does the dose-blood pressure response curve look like for thiazides?

A

Flat

32
Q

What are some adverse effects of thiazides?

A 
Hypokalaemia
Increased urea/uric acid 
Impaired glucose tolerance 
Increased cholesterol an TG 
Activates RAAS

Dirty drug

33
Q

Name an alpha blocker

A

Doxazosin

34
Q

Name some properties of alpha blockers

A

Selective antagonists at post synaptic a1 adrenoceptors
Antagonise the contractile effects of NA on vascular SM
= reduce peripheral vascular resistance

35
Q

What are some adverse effects of alpha blockers?

A

Postural hypotension (more effect in upright position)
Headache and fatigue
Oedema

36
Q

Why are beta blockers useful for high blood pressure?

A

Reduce HR and CO

Inhibit renin release (less RAAS)

37
Q

What are some adverse effects of beta blockers?

A 
Lethargy, impaired concentration 
Reduced exercise tolerance
Bradycardia
Raynauds 
Impaired glucose tolerance
38
Q

What is a contraindication for beta blockers?

A

Asthma

But is safe for COPD

39
Q

What is aliskiren?

A

Direct renin inhibitor

40
Q

What does aliskiren do?

A

Binds to a pocket in renin which blocks the cleavage of angiotensinogen to Ang I

(Prevents breakdown of angiotensinogen)

41
Q

How does aliskiren work to lower BP?

A

Reduces plasma renin activity
Vasodilatory
BP reduction

42
Q

How do centrally acting agents lower blood pressure?

methyldopa, clonidine, moxonidine

A

Reduce sympathetic output

43
Q

When is methldopa commonly used?

A

To treat hypertension in pregnancy

44
Q

Name some side effects on centrally acting agents to lower BP? Why do they cause these effects?

A

Tiredness/lethargy
Depression
Because work in the brain

45
Q

What is a contraindication for thiazides?

A

Gout

46
Q

What is a contraindication for ACE inhibitors and ARBs?

A

Pregnancy

Renovascular hypertension

47
Q

What is the aetiology of HF?

A

Ischaemic Heart Disease
Hypertension
Cardiomyopathies (alcohol, chemo, iron overload)
Valve disease

48
Q

What is prognosis after MI related to?

A

Inversely related to amount of LV damage/dysfunction

49
Q

What lifestyle modifications can be made to manage HF?

A

Reduce salt
Decrease alcohol
Increase aerobic exercise
Decrease BP

50
Q

What drugs could be prescribed to treat HF?

A 
ACE inhibitor/ARB
Beta blocker 
Spironolactone 
Ivabradine (Funny channel receptor causing bradycardia)
Sacubitril (increases natriuresis)

nitratesm digoxin, inotropes, phosphodiesterase inhibitors)

51
Q

What are the physiological effects of beta blockers?

A 
Reduce HR 
Reduce BP due to reduced CO 
Reduces myocardial O2 demand
Reduced mobilisation of glycogen 
Negate unwanted effects of catecholamines
52
Q

Why must you be careful with giving b blockers in HF?

A

The failing myocardium may be dependent on HR

Yr 2 Sem 2 CPT (9 decks)

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