2. JESSEN GEORGE K
M PHARM PART 1
PHARMACY PRACTICE
CPS, MEDICAL COLLEGE
TVM
HYPERTENSI
ON
3. CONTENTS
INTRODUCTION
EPIDEMIOLOGY
TYPES OF HYPERTENSION
ETIOLOGY
PATHOPHYSIOLOGY
CLINICAL PRESENTATION & DIAGNOSIS
MANAGEMENT OF HYPERTENSION
SPECIAL POPULATION
PATIENT COUNSELLING
REFERENCES
4. INTRODUCTION
Hypertension is defined by persistently elevated
arterial blood pressure.
Elevated systolic and diastolic blood pressure -
(≥ 140/90 mm of Hg).
In diabetic patient (≥ 130/80 mm of Hg).
5. Classification Systolic Blood Pressure
(mm Hg)
Diastolic Blood Pressure
(mm Hg)
Normal <120 <80
Pre hypertension 120-139 80-89
Stage1 HT 140-159 90-99
Stage 2 HT Greater than or equal to160 Greater than or equal or100
JNC 7 Classification of blood pressure in adults
6. EPIDEMIOLOGY
Prevalence of HT increases with age & greater among
African Americans than Caucasians.
In US, 68% of adults have HT, only 53% are on
treatment & only 27% have achieved control of BP.
Prevalence of HT in India is about 26.2% in men &
23.6% in women.
Hypertension is similar between men and women of the
same race.
7. TYPES OF HYPERTENSION
Essential hypertension.
Secondary hypertension.
White coat hypertension.
Isolated systolic hypertension.
Gestational hypertension.
Hypertensive crisis.
a) Hypertensive urgencies.
b) Hypertensive emergencies.
8. ETIOLOGY
Essential or Primary hypertension
- 90 % .
- sedentary lifestyle - smoking, alcohol intake, stress,
obesity.
- inherited genetic mutation, ageing etc.
- cannot be cured, but can be controlled.
9. Secondary hypertension.
- 10 % .
- Due to either a co morbid disease or a drug.
- Diseases : chronic kidney disease, cushing's
syndrome, coarctation of aorta, pheochromocytoma,
primary aldosteronism, thyroid disease etc.
- Drugs :Oral contraceptives, phenylpropanolamine,
cyclosporine, corticosteroids, MAO inhibitors,
antidepressants etc.
13. POTENTIAL MECHANISMS OF PATHOGENESIS
1 ) Humoral mechanisms.
a) RAAS system
b) Natriuretic hormone
c) Hyperinsulinemia
2) Neuronal regulation.
3) Peripheral autoregulatory components.
4) Vascular endothelial mechanism.
5) Electrolytes and other chemicals.
14.
15.
16. b) Natriuretic Hormone :
inhibit sodium and potassium ATPase block
the active transport of sodium increase
intracellular conc of Na.
c) Hyperinsulinemia :
Increased insulin concentration elevate BP by,
- increased renal Na retention.
- enhanced sympathetic NS activity.
- increased intracelllar Ca increase
vascular resistance.
17. 2) Neuronal mechanisms :
- Stimulation of α1 (arterioles and venules) :
vasoconstrictions.
- Stimulation of α2 : decrease sympathetic outflow.
- Stimulation of β1 (heart, JG cells in kidney) :
increase in heart rate and contractility, renin release.
- Stimulation of β2 (lungs, liver, arteriolar smooth
muscles, pancreas) : vasodilation, bronchodilation.
- Baroreceptor reflex system
BR: nerve endings lying in the walls of large
arteries, especially in carotid arteries and aortic arch.
Transmit impulse through 9 th cranial nerve
and vagus nerves.
18.
19.
20.
21. 3) Peripheral autoregulatory components
- Kidney : maintain normal BP
- BP drops --- kidney increase retention of Na --- PV
expansion --- BP increases (viceversa)
4) Vascular endothelial mechanism
- Deficiency in local synthesis of vasodilating
substances (eg : prostacyclin and bradykinin)
- Excess vasoconstricting substances (eg : angiotensin
2 and endothelin 2 )
- Deficiency in NO release (from endothelium )
5) Electrolytes and other chemicals
- Excess sodium Intake
- Potassium depletion --- increase peripheral VR.
22.
23. CLINICAL PRESENTATION & DIAGNOSIS
HT is usually asymptomatic.
BP measured using sphygmomanometer.
HT is confirmed when the average of two or more DBP
measurements is 90mm Hg or higher & average of two
or more SBP measurements is consistently greater than
140 mm Hg.
24. Initial assessment include a complete history and
physical examination.
If hypertension seems reasonable, tests as
echocardiogram and electrocardiogram should be
done to measure the electrical activity of heart.
Laboratory tests can also be performed to identify
possible causes of secondary hypertension.
(Eg : serum creatinine, fasting blood glucose, serum
potassium, urinalysis etc)
25. SIGNS AND SYMPTOMS
Mild to moderate essential hypertension
- asymptomatic
Secondary hypertension
- Hyperthyroidism : weight loss, tremors, heart rate
abnormalities, reddening of the palms and increased
sweating.
- Hyperaldosteronism : numbness, excessive
urination, excessive sweating, electrolytes imbalance ,
dehydration and elevated blood alkalinity.
26. In pregnancy
- Pre Eclampsia, Eclampsia.
In newborns and neonates
- Failure to thrive, seizures, irritability, lack of
energy and difficulty breathing.
In children
- Headache, fatigue, blurred vision, nosebleeds, and
facial paralysis.
28. KEY MODIFICATIONS RECOMMENDED ACTIONS Approximate BP
reduction
Physical activity → Get at least 30 minutes of
moderate to vigorous activity (such
as brisk walk) at least 4days/week
4-9mm of Hg
Healthy diet (Adopt
DASH eating plan )
→ Eat plenty of fruit and vegetables
, low fat dairy products with a
reduced content of saturated and
total fat, ,whole grains,fish. lean
poultry and nuts.
→Reduce sodium Intake (≤ 2.4
gm/day)
→maintain adequate dietary
potassium
8-14 mm of Hg
Weight reduction Maintain normal body weight (body
mass index,18.5-24.9 kg/m2 )
5-20 mm of Hg per 10
kg weight loss.
Life style modifications
29. PHARMACOTHERAPY
A) PRIMARY ANTIHYPERTENSIVES
1) DIURETICS
a) Thiazides - eg : chlorthalidone, indapamide (lozol),
hydrochlorothiazide (esidrix ).
b) Loops - eg : furosemide (Lasix), torasemide.
c) Potassium sparing
(1) Inhibitors of renal epithelial Na channel -
eg : amiloride, triamterene.
(2) Aldosterone antagonist - eg : spironolactone,
(aldactone).
33. 1) DIURETICS :
Reduces plasma volume and stroke volume & thus CO
& BP is reduced.
Thiazides most prefered. ( also se TPR )
loop prefered in patients with decreased renal
function, in cardiac failure & in elderly
ADR : hypokalemia, hyperglycemia, hyperuricemia,
dyslipidemia.
DOSE - hydrochlorothiazide 25-50mg daily
- furosemide 40- 80mg daily
- spironolactone 25-50mg daily
- low dose or combine with K sparing diuretics .
34. 2) ACE INHIBITORS
Blocks the conversion of Ang I to Ang II.
Also stimulate the synthesis of vasodilating
substances (prostaglandin E2 and prostacyclin)
Contraindicated in bilateral artery stenosis also in
pregnancy.
ADR : renal failure, dry cough, hypotension,
angioedema, dysgeusia, foetopathic, hyperkalaemia.
DOSE : captopril initially 12.5 mg bid, max 50mg tid
enalapril initially 5mg at bedtime.
35. 3) ANGIOTENSIN RECEPTOR BLOCKERS
ARB directly block angiotensin type I receptor (AT 1)
which mediates the effect of angiotensin II.
Stimulation of AT II– vasodilation
Angiotensin II from RAAS and an alternative
pathway through the enzyme chymase.
ADR : edema, headache, renal failure
DOSE : losartan K 50-100mg in two divided doses,
telmesartan 40 mg OD, max 80 mg/day
36. 4) β-BLOCKERS
Decrease CO through –ve chronotropic & inotropic
effect.
Patient with asthma, COPD, and diabetes :
cardioselective safer than non selective β-blockers.
Abrupt cessation may cause rebound HT
ADR- bradycardia, conduction abnormalities,
broncospasm, dizziness, drowsiness.
DOSE : atenolol 25-100 mg OD
propranolol 160- 480 mg b.i.d
37. 5) CALCIUM CHANNEL BLOCKERS
Blocks voltage sensitive Ca channels & cause
relaxation of cardiac & smooth muscles
vasodilation & fall in BP.
a) Dihydropyridines
ADR : flushing, edema, headache
DOSE : amlodipine 5mg OD
nifedipine 10-40 mg bid
b) Non dihydropyridines
ADR : bradycardia, heart block, constipation
DOSE : verapamil 240 mg daily in 2-3 div doses
diltiazem 60-120 mg bid.
38. 1) α-1 BLOCKERS
- prevent noradrenaline induced vasoconstriction
se TPR & BP.
ADR : edema, postural hypotension, depression
DOSE : terazosin 2-10mg OD
2) CENTRAL α2 AGONIST
- stimulation of α2 adrenergic receptors in brain
reduce sympathetic outflow from vasomotor
centre increase in vagal tone.
ADR : depression, sedation , drymouth
DOSE : methyl dopa -initially 250 mg bid/tid
clonidine 50-100 mcg tid.
39. 3) PERIPHERAL ADRENERGIC ANTAGONIST
Depletes norepinephrine from sympathetic nerve
endings & blocks transport of NE into storage
granules
ADR : mental depression, nasal conjestion, headache
DOSE : 250 mcg daily
4) DIRECT ARTERIAL VASODILATORS
Direct arterial smooth muscle relaxation
Hydralazine ADR : dermatitis, headache
DOSE : 20-100 mg/day
Minoxidil ADR : reversible hypertrichosis on
face,arms etc
40.
41. SITES OF ACTION OF MAJOR
ANTIHYPERTENSIVE AGENTS
1) ACE inhibitors
2) ARB
3) β-blockers
4) CCB
5) Diuretics
6) Aldosterone antagonist
7) Renin inhibitors
42.
43. SPECIAL POPULATION
HT IN ELDERLY :
Treatment initiated with a small dose of diuretic
hydrochlorothiazide 12.5 mg & increased gradually
then an ACE inhibitor added in small dose &
gradually increased.
HT IN PULMONARY DISEASES
Non selective β blockers should be avoided in
asthma ,COPD
44. HT IN PREGNANCY :
- methyldopa - drug of choice.
- β-blockers,labetalol and CCB - other alternatives
- ACE inhibitors and ARB - contraindicated.
HT with DYSLIPIDEMIA
- Thiazides, β blockers without ISA : affect serum
lipids (raise triglyceride level and LDL/HDL ratio)
- ACE inhibitors, CCBs prefered.
45.
46. PATIENT COUNSELLING
Silent killer.
Should advice the importance of taking medications
regularly at the same time.
Advice the patient not to stop medication abruptly
Should monitor the side effects & give necessary
advices
Should council the patient regarding
-life style modifications
-regular exercise
-reducing weight
47. - sodium & calorie restriction
- restriction of saturated fats
- increased intake of dietary fibres
- restriction of alcohol
- smoking cessation
- avoid stress
- caution while using cold remedies
containing sympathomimetics
48. METHODS TO IMPROVE ADHERENCE TO
DRUG THERAPY
- simplifying the drug regimen
- avoid side effects by starting with low doses
- schedule drug doses once/twice daily
- label prescriptions clearly & indicate the purpose of
drug
- provide written schedules/ pill box for patients taking
multiple drug
- encourage the use of calenders to remind the patient to
take medication
49. REFERENCES
Clinical pharmacy and Therapeutics- Eric T Herfindal
7th edition page no.401-425
Pharmacotherapy. A pathophysiologic approach- 6th
edition ,Joseph T Dipiro page no.157-181
Essentials of medical pharmacology – K D Tripathi page
no. 539 – 554.
Clinical pharmacy and Therapeutics-Rojer wallker page
no.295-309
All data were collected from various sources
Only for educational purpose.
