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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
What are is the action of ACEi?
Limit the conversion of Angiotensin-I to Angiotensin-II by inhibiting circulating and tissue ACE
26
what is ACE and what is its action?
* 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
27
what are the actions of angiotensin II?
• 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
28
What are the effects of ACEi?
• vasodilation (↓ PVR →↓afterload) • reduction in aldosterone release (↑Na + H2O exc.) • reduced vasopressin (ADH) release (↑ H2O exc.) • reduced cell growth and proliferation
29
What ACE independent pathway can produce AngII?
Angiotensin II can be produced by chymases
30
What receptors do ARBs work on?
Angiotensin I receptors
31
What are 2 ACEi?
Lisinopril and ramipril
32
What is the effect of ACEi on bradykinin?
Prevents breakdown of bradykinin, therefore increasing its effects
33
Why does build up of bradykinin cause cough?
sensitisation of airway sensory nerves and an enhancement of the cough reflex
34
What are the possible side effects of ACEi?
- Hypotension! - Dry cough (10-15% - BK association) - hyperkalaemia (low aldosterone ↑ K+) - renal failure - angioedema (BK more common in black population)
35
How may ACEi lead to renal failure?
Prevent formation of AngII, main vasoconstrictor of efferent arteriole, reduce GFR
36
When is ACEi more likely to cause renal failrue?
esp. renal artery stenosis where constriction of efferent arteriole needed
37
What are the warnings/contraindications to ACEi?
• X Renal artery stenosis, AKD, pregnancy, (CKD - caution), idiopathic angioedema
38
What are the important considerations/interactions of ACEi?
- Drugs that increase K+, - NSAIDs (prevent prostaglandin production, prevent AA vasodilation), - other antihypertensive agents
39
What are 2 ARBs?
candesartan | losartan
40
which receptors do ARBs act on ?
AT1 and AT2 receptors - AT1 important in relation to cardiovascular regulation
41
What are the contraindications for ARBs?
- Renal artery stenosis, - AKD, - pregnancy, breastfeeding, - (CKD - caution)
42
What are the important considerations/interactions of ARBs?
- ↑K+ drugs, - NSAIDs, - other antihypertensive agents
43
what is the effect of ARBs on bradykinin?
• no effect on bradykinin - less effective in low-renin hypertensive patients dry cough and angioedema much less likely than with ACEi
44
What are the possible adverse effects of ARBs?
Hypotension! hyperkalaemia (low aldosterone ↑K+) cause or worsen renal failure
45
What may help decide whether to use ACEi or ARBs?
- use ARBs in high chymase levels - ARBs if cough - Less likely to get angioedema with ARBs
46
why are ARBs more effective at inhibiting Ang-II mediated vasoconstriction than ACEi?
Directly targeting AT1 receptors - even block action of angiotensin II produced by chymases which continue to be produced even with ACEi
47
describe the action of L-type calcium channels
* 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
Where are L-type calcium channels located?
Expressed throughout the body - including vascular smooth muscle cells AND cardiac myocytes plus SA and AV nod
49
what do calcium channel blockers target?
s target calcium initiated smooth muscle contraction (in hypertension)
50
On what subunit of the voltage gated calcium channel do the calcium channel blockers act on
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
What are the 2 classes of CCBs?
Dihydropyridines | Non-dihydropyridines
52
Which type of CCBs have selectivity for vasculature?
Dihydropyridines
53
When are CCBs first choice for hypertension?
In low renin patients (typically black people)
54
What are 3 dihydropyridines?
amlodipine nifedipine nimodipine
55
Which CCB has selectivity for cerebral vasculature and when it is used?
Nimodipine | Prevention of ischaemic neurological defects following aneurysmal subarachnoid haemorrhage
56
which dihydropyridine has the longest half life?
Amlodipine
57
What are the adverse effects of dihydripyridines and what are they mostly due to?
Due to vasodilation: • Ankle swelling, flushing, headaches (vasodilation) • Palpitations (compensatory tachycardia), due to vasodilation and hypotension```
58
What are the contraindications to dihydropyridines?
- Unstable angina, | - severe aortic stenosis
59
What are the interactions/considerations of CCB?
- amlodipine + simvastatin (increased effect of statin), | - other antihypertensive agents
60
what dictates which calcium channel blockers are used for hypertension?
dihydropyridines selective for peripheral vasculature, little chronotropic or inotropic effects cerebral vs peripheral selectivity dictates which are used for hypertension
61
What are the 2 classes of non-dihydropyridines?
phenylalkylamines and benzothiazapines
62
What are the effects of the non-dihydropyridines?
* 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
Give an example of phenylalkyamines?
verapamil
64
How do phenylalkylamines work?
``` Prolongs the action potential/effective refractory period - Less peripheral vasodilatation, - negative chronotropic and inotropic effects ```
65
What are phenylalkylamines used for?
Arrhythmia, angina, (hypertension)
66
What are the adverse effects of phenylalkylamines? (4)
- Constipation, - bradycardia (i.v.), - heart block and - cardiac failure
67
What are the contraindication for phenylalkylamines?
- Poor LV function (caution), | - AV nodal conduction delay
68
What are the interactions/considerations of phenylalkylamines?
- β-blockers (cardiologist only), - other antihypertensive and - antiarrhythmic agents
69
Give an example of a Benzothiazapines.
Diltiazem
70
Give an example of a thiazide and a thiazide like diuretic?q
bendroflumethiazide | indapamide (thiazide like)
71
What are the adverse effects of thaizide and thiazide like diuretics?
- Hypokalaemia, - hyponatraemia, - hyperuricemia, - arrhythmia - ↑ glucose (especially with beta-blockers) - ↑ cholesterol and triglyceride
72
WHat are the contraindication to thiazide/thiazide like diuretics?
Hypokalaemia, hyponatraemia, gout
73
WHat are the interactions to thiazide/thiazide like diuretics
NSAIDs, ↓ K+ drugs such as loop diuretics(monitoring)
74
how do thiazides work?
* 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
when are thiazides Useful over CCB?
in oedema
76
What are the stages of treatment for hypertension in 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
77
What are the stages of treatment for hypertension for <55 and not black african?
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
What is the treatment What are the stages of treatment for hypertension for >55 or black african(any age)?
stage 1 CCB stage 2 CCB + ACEi/ARB or thiazide like stage 3 CCB + ACEi/ARB + thiazide like
79
If BP cannot be controlled after step 3, what should be prescribed?
Spironolactone
80
action of spironalactone?
aldosterone (mineralocorticoid) receptor antagonist
81
What are the contraindications and considerations/interactions of spironolactone?
* X Hyperkalaemia, Addison's | * Δ ↑K+ drugs inc. ACEi and ARBs (monitoring), pregnancy
82
what are the adverse effects of spironolactone?
Hyperkalaemia, gynaecomastia
83
If K+ is high, what drugs can be used after step 3?
alpha or beta blockers
84
What beta blocker is used in pregnancy?
Labetalol
85
WHat are 3 beta blockers?
labetalol bisoprolol metoprolol
86
What are the adverse effects of beta blockers?
* Bronchospasm, heart block, Raynaud's (cold hands), lethargy, impotence * Mask tachycardia - sign of insulin induced hypoglycaemia
87
action of beta blocker?
Decrease sympathetic tone by blocking NAd and reducing myocardial contraction resulting in reduced cardiac output ↓ renin secretion β1
88
What are the contraindications to beta blockers?
Asthma, (COPD), haemodynamic instability, hepatic failure (dose monitoring)
89
What are the drug interactions for beta blockers?
non-dihydropyridine CCB - verapamil and diltiazem - asystole!
90
Give an example of an α-adrenoceptor blocker.
doxazosin
91
action of α-adrenoceptor blocker?
* 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
What are the adverse effects of alpha blockers?
Postural hypotension | dizziness, syncope, headache and fatigue
93
What are the contraindications of alpha blockers?
postural hypotension
94
What are the drug interactions of alpha blockers?
dihydropyridine CCBs - oedema
95
What is the "two pronged" approach to ACEi/ARB use in type II diabetics w hypertension?
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
Calcium channel blockers are the primary choice of antihypertensive in what type of patients?
Low renin patients - bcs pointless targeting RAAS (with ACEi) if got a low renin
97
Why do ACEi and ARB precipitate hyperkalaemia?
Prevents the stimulation of RAAS so K+ isn't being excreted, instead reabsorbed

semester 4 - CPT & Prescribing (25 decks)

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