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semester 4 - CPT & Prescribing > 3. Hypertension > Flashcards

3. Hypertension Flashcards

1
Q

What is BP?

A
  • Driving force to perfuse organs with blood (force per unit area acting on vessels)
  • Is not uniform throughout the body
  • Commonly measure and report systolic (SBP) and diastolic (DBP)
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2
Q

equation for Mean Arterial Pressure

A
  • Mean Arterial Pressure = cardiac output X total peripheral resistance
  • MAP = DBP + (SBP-DBP)/3)
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3
Q

what is the effect of sympathetic activity when blood pressure is low?

A
  • activation of B1 adrenoceptors on the heart –> ↑ cardiac output
  • activation of a1 adrenoceptors on smooth muscle –> ↑ increased venous return
  • activation of B1 adrenoceptors on kidney –> renin release
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4
Q

What is the effect of renin?

A

• converts angiotensinogen to angiotensin I which is converted to angiotensin II by ACE in lungs
• angiotensin II:
- increases sympathetic activity
- increase Na, Cl and water reabsorption and K+ excretion
- increases aldosterone secretion so increased Na, Cl and water reabsorption and K+ excretion
- causes arteriole vasoconstriction
- increases ADH secretion
• all increase blood pressure

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5
Q

What is the effect of vasoconstriction?

A

↑peripheral resistance requires ↑ BP to drive blood through the systemic circulation

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6
Q

Original

WHat vascular changes does hypertension cause?

A

Remodelling, thickening and hypertrophy

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7
Q

what substances are increased due to hypertension?

A

Increased vasoactive substances including ET-1, NAd, angII

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8
Q

effects of Hyperinsulinemia and hyperglycaemia?

A

lead to endothelial dysfunction and increased reactive oxygen species - NO signalling reduced

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9
Q

what are the combined effects of hypertension?

A

• permanent and maintained medial hypertrophy of vasculature with ↑↑TPR and ↓compliance
of vessels
• End organ damage (renal, peripheral vascular disease, aneurysm, vascular dementia, retinal
disease)
• “Hypertensive heart disease” LVH → dilated cardiac failure
• Increased morbidity and mortality

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10
Q

what factors make defining hypertension difficult?

A

• Labile, age, sex and population differences

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11
Q

define hypertension

A

“An elevation in blood pressure that is associated with an increase in risk of some harm”

• NICE say 140/90 mmHg = hypertension ≥ 40% population of England

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12
Q

causes of hypertension

A

Essential/primary/idiopathic hypertension – 90% of cases
The rest:
secondary hypertension – to other pathology
pre hypertension
isolated systolic/diastolic hypertension
white coat/clinic - real phenomenon

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13
Q

How should the patient be when taking BP?

A

Seated, relaxed, arms supported

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14
Q

Which arm should be measured?

A

Both

  • if more than 15 mmHg difference repeat
  • use arm with higher reading
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15
Q

How often should BP be taken?

A

Measurements over period of visits +/- ABPM/HBPM

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16
Q

When is emergency treatment required?

A

BP > 180/120 + clinical signs

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17
Q

What should be the target BP for different hypertension patients?

A
  • 140/90 < 80 years old inc. type II diabetes
  • 150/90 > 80 years old
  • 135/85 type 1 diabetes
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18
Q

what is the desired bp?

A

120/80 mmHg

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19
Q

What is stage 1 hypertension?

A

Clinic blood pressure ranging from 140/90 mmHg to 159/99 mmHg and subsequent ABPM daytime average or HBPM average blood pressure ranging from 135/85 mmHg to 149/94 mmHg.

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20
Q

What is stage 2 hypertension?

A

Clinic blood pressure of 160/100 mmHg or higher but less than 180/120 mmHg and subsequent ABPM daytime average or HBPM average blood pressure of 150/95 mmHg or highe

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21
Q

What is stage 3 hypertension?

A

Clinic systolic blood pressure of 180 mmHg or higher or clinic diastolic blood pressure of 120 mmHg or higher

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22
Q

What is prehypertension?

A

120/80 - 140/90

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23
Q

What advice should be given to prehypertension/hypertension patients?

A
  • Promotion of regular exercise
  • Modified healthy/balanced diet
  • Reduction in stress and increased relaxation
  • Limited/reduced alcohol intake
  • Discourage excessive caffeine consumption
  • Smoking cessation
  • Reduction in dietary sodium

All contribute to cardiovascular disease risk reduction

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24
Q

what are the Primary hypertension therapeutic agents?

A
  • Angiotensin converting enzyme (ACE) inhibitors (ACEi)
  • Angiotensin (AT1)receptor blockers (ARBs)
  • Calcium channel blockers (CCBs)
  • Diuretics – thiazide and thiazide-like
  • “Other agents”
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25
Q

What are is the action of ACEi?

A

Limit the conversion of Angiotensin-I to Angiotensin-II by inhibiting circulating and tissue ACE

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26
Q

what is ACE and what is its action?

A
  • ACE found on luminal surface of capillary endothelial cells, predominantly in the lungs
  • ACE catalyses conversion of angiotensin-I to potent, active vasoconstrictor - angiotensin-II
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27
Q

what are the actions of angiotensin II?

A

• Angiotensin-II affords action through AT1 (and AT2 receptors)
• AT1 receptor subtype typical of classic angiotensin-II actions
- vasoconstriction
- stimulation of aldosterone which acts at distal renal tubule
- cardiac and vascular muscle cell growth
- vasopressin (ADH) release from posterior pituitary

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28
Q

What are the effects of ACEi?

A

• vasodilation (↓ PVR →↓afterload)
• reduction in aldosterone release (↑Na + H2O exc.)
• reduced vasopressin (ADH) release (↑ H2O
exc.)
• reduced cell growth and proliferation

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29
Q

What ACE independent pathway can produce AngII?

A

Angiotensin II can be produced by chymases

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30
Q

What receptors do ARBs work on?

A

Angiotensin I receptors

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31
Q

What are 2 ACEi?

A

Lisinopril and ramipril

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32
Q

What is the effect of ACEi on bradykinin?

A

Prevents breakdown of bradykinin, therefore increasing its effects

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33
Q

Why does build up of bradykinin cause cough?

A

sensitisation of airway sensory nerves and an enhancement of the cough reflex

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34
Q

What are the possible side effects of ACEi?

A
  • Hypotension!
  • Dry cough (10-15% - BK association)
  • hyperkalaemia (low aldosterone ↑ K+)
  • renal failure
  • angioedema (BK more common in black population)
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35
Q

How may ACEi lead to renal failure?

A

Prevent formation of AngII, main vasoconstrictor of efferent arteriole, reduce GFR

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36
Q

When is ACEi more likely to cause renal failrue?

A

esp. renal artery stenosis where constriction of efferent arteriole needed

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37
Q

What are the warnings/contraindications to ACEi?

A

• X Renal artery stenosis, AKD, pregnancy, (CKD - caution), idiopathic angioedema

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38
Q

What are the important considerations/interactions of ACEi?

A
  • Drugs that increase K+,
  • NSAIDs (prevent prostaglandin production, prevent AA vasodilation),
  • other antihypertensive agents
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39
Q

What are 2 ARBs?

A

candesartan

losartan

40
Q

which receptors do ARBs act on ?

A

AT1 and AT2 receptors - AT1 important in relation to cardiovascular regulation

41
Q

What are the contraindications for ARBs?

A
  • Renal artery stenosis,
  • AKD,
  • pregnancy, breastfeeding,
  • (CKD - caution)
42
Q

What are the important considerations/interactions of ARBs?

A
  • ↑K+ drugs,
  • NSAIDs,
  • other antihypertensive agents
43
Q

what is the effect of ARBs on bradykinin?

A

• no effect on bradykinin - less effective in low-renin hypertensive patients dry cough and angioedema much less likely than with ACEi

44
Q

What are the possible adverse effects of ARBs?

A

Hypotension!
hyperkalaemia (low aldosterone ↑K+)
cause or worsen renal failure

45
Q

What may help decide whether to use ACEi or ARBs?

A
  • use ARBs in high chymase levels
  • ARBs if cough
  • Less likely to get angioedema with ARBs
46
Q

why are ARBs more effective at inhibiting Ang-II mediated vasoconstriction than ACEi?

A

Directly targeting AT1 receptors - even block action of angiotensin II produced by chymases which continue to be produced even with ACEi

47
Q

describe the action of L-type calcium channels

A
  • LTCCs allow inward Ca2+ flux into cells – voltage operated calcium channel (VOCC)
  • influx of Ca2+ stimulates calcium induced calcium release from sarcoplasmic reticulum
  • build up of calcium causes contraction
48
Q

Where are L-type calcium channels located?

A

Expressed throughout the body - including vascular smooth muscle cells AND cardiac myocytes plus SA and AV nod

49
Q

what do calcium channel blockers target?

A

s target calcium initiated smooth muscle contraction (in hypertension)

50
Q

On what subunit of the voltage gated calcium channel do the calcium channel blockers act on

A

Alpha 1 subunit, but on different sites of alpha 1 subunit
• 3 classes of CCB interact with different sites on (α1)subunit of VOCC - they have different selectivity for vascular smooth muscle or myocardium

51
Q

What are the 2 classes of CCBs?

A

Dihydropyridines

Non-dihydropyridines

52
Q

Which type of CCBs have selectivity for vasculature?

A

Dihydropyridines

53
Q

When are CCBs first choice for hypertension?

A

In low renin patients (typically black people)

54
Q

What are 3 dihydropyridines?

A

amlodipine
nifedipine
nimodipine

55
Q

Which CCB has selectivity for cerebral vasculature and when it is used?

A

Nimodipine

Prevention of ischaemic neurological defects following aneurysmal subarachnoid haemorrhage

56
Q

which dihydropyridine has the longest half life?

A

Amlodipine

57
Q

What are the adverse effects of dihydripyridines and what are they mostly due to?

A

Due to vasodilation:
• Ankle swelling, flushing, headaches (vasodilation)
• Palpitations (compensatory tachycardia), due to vasodilation and hypotension```

58
Q

What are the contraindications to dihydropyridines?

A
  • Unstable angina,

- severe aortic stenosis

59
Q

What are the interactions/considerations of CCB?

A
  • amlodipine + simvastatin (increased effect of statin),

- other antihypertensive agents

60
Q

what dictates which calcium channel blockers are used for hypertension?

A

dihydropyridines selective for peripheral vasculature, little chronotropic or inotropic effects cerebral vs peripheral selectivity dictates which are used for hypertension

61
Q

What are the 2 classes of non-dihydropyridines?

A

phenylalkylamines and benzothiazapines

62
Q

What are the effects of the non-dihydropyridines?

A
  • Phenylalkyamine depresses SA node and slows AV conduction, negative inotropy
  • Benzothiazapines sit in the middle between phenylalkylamines and dihydripyridines - some action on vasculature and some on SA AV nodes
63
Q

Give an example of phenylalkyamines?

64
Q

How do phenylalkylamines work?

A 
Prolongs the action potential/effective
refractory period
- Less peripheral vasodilatation,
- negative chronotropic and inotropic
effects
65
Q

What are phenylalkylamines used for?

A

Arrhythmia, angina, (hypertension)

66
Q

What are the adverse effects of phenylalkylamines? (4)

A
  • Constipation,
  • bradycardia (i.v.),
  • heart block and
  • cardiac failure
67
Q

What are the contraindication for phenylalkylamines?

A
  • Poor LV function (caution),

- AV nodal conduction delay

68
Q

What are the interactions/considerations of phenylalkylamines?

A
  • β-blockers (cardiologist only),
  • other antihypertensive and
  • antiarrhythmic agents
69
Q

Give an example of a Benzothiazapines.

70
Q

Give an example of a thiazide and a thiazide like diuretic?q

A

bendroflumethiazide

indapamide (thiazide like)

71
Q

What are the adverse effects of thaizide and thiazide like diuretics?

A
  • Hypokalaemia,
  • hyponatraemia,
  • hyperuricemia,
  • arrhythmia
  • ↑ glucose (especially with beta-blockers)
  • ↑ cholesterol and triglyceride
72
Q

WHat are the contraindication to thiazide/thiazide like diuretics?

A

Hypokalaemia, hyponatraemia, gout

73
Q

WHat are the interactions to thiazide/thiazide like diuretics

A

NSAIDs, ↓ K+ drugs such as loop diuretics(monitoring)

74
Q

how do thiazides work?

A
  • Inhibit N+/Cl- co-transporter in distal convoluted tubule ↓Na+ and H2O reabsorption (RAAS compensates with time)
  • Long term effects mediated by sensitivity of vascular smooth muscle to vasoconstrictors Ca2+/NAd
75
Q

when are thiazides Useful over CCB?

76
Q

What are the stages of treatment for hypertension in type II diabetes?

A

stage 1 ACEi or ARB
stage 2 ACEi or ARB + CCB or thiazide-like
stage 3 ACEi or ARB + CCB + thiazide-like

77
Q

What are the stages of treatment for hypertension for <55 and not black african?

A

Same as type II diabetes:
stage 1 ACEi or ARB
stage 2 ACEi or ARB + CCB or thiazide-like
stage 3 ACEi or ARB + CCB + thiazide-like

78
Q

What is the treatment What are the stages of treatment for hypertension for >55 or black african(any age)?

A

stage 1 CCB
stage 2 CCB + ACEi/ARB or thiazide like
stage 3 CCB + ACEi/ARB + thiazide like

79
Q

If BP cannot be controlled after step 3, what should be prescribed?

A

Spironolactone

80
Q

action of spironalactone?

A

aldosterone (mineralocorticoid) receptor antagonist

81
Q

What are the contraindications and considerations/interactions of spironolactone?

A
  • X Hyperkalaemia, Addison’s

* Δ ↑K+ drugs inc. ACEi and ARBs (monitoring), pregnancy

82
Q

what are the adverse effects of spironolactone?

A

Hyperkalaemia, gynaecomastia

83
Q

If K+ is high, what drugs can be used after step 3?

A

alpha or beta blockers

84
Q

What beta blocker is used in pregnancy?

85
Q

WHat are 3 beta blockers?

A

labetalol
bisoprolol
metoprolol

86
Q

What are the adverse effects of beta blockers?

A
  • Bronchospasm, heart block, Raynaud’s (cold hands), lethargy, impotence
  • Mask tachycardia - sign of insulin induced hypoglycaemia
87
Q

action of beta blocker?

A

Decrease sympathetic tone by blocking NAd and reducing myocardial contraction resulting in reduced cardiac output
↓ renin secretion β1

88
Q

What are the contraindications to beta blockers?

A

Asthma, (COPD), haemodynamic instability, hepatic failure (dose monitoring)

89
Q

What are the drug interactions for beta blockers?

A

non-dihydropyridine CCB - verapamil and diltiazem - asystole!

90
Q

Give an example of an α-adrenoceptor blocker.

91
Q

action of α-adrenoceptor blocker?

A
  • Selective antagonism of α-1 adrenoceptors
  • Reduce peripheral vascular resistance
  • Urinary tract including bladder neck and prostate – benign prostatic hyperplasia (tamsulosin)
  • Relatively safe in renal disease
92
Q

What are the adverse effects of alpha blockers?

A

Postural hypotension

dizziness, syncope, headache and fatigue

93
Q

What are the contraindications of alpha blockers?

A

postural hypotension

94
Q

What are the drug interactions of alpha blockers?

A

dihydropyridine CCBs - oedema

95
Q

What is the “two pronged” approach to ACEi/ARB use in type II diabetics w hypertension?

A

Giving them ACEi/ARB bcs :

1) ↓peripheral vascular resistance →
2) ↓BP and dilation of efferent glomerular arteriole → reduced intraglomerular pressure – good for type II diabetes

Hence it reduces diabetic nephropathy + CKD w proteinuria by dilatation of efferent glomerular arteriole and ACEi have an anti-proteinuric effect.

96
Q

Calcium channel blockers are the primary choice of antihypertensive in what type of patients?

A

Low renin patients - bcs pointless targeting RAAS (with ACEi) if got a low renin

97
Q

Why do ACEi and ARB precipitate hyperkalaemia?

A

Prevents the stimulation of RAAS so K+ isn’t being excreted, instead reabsorbed

semester 4 - CPT & Prescribing (25 decks)

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