Electrolyte imbalance Metabolic: hyperglycemia, hyperlipidemia, hyperuricemia. Erectile dysfunction Not effective in chronic renal disease. More effective in elderly: also in patients with isolated systolic hypertension. Long acting, used once a day No tolerance and no fluid retention Reduce calcium excretion, preferred in osteoporosis (especially older women). Hydrochlorothiazide is one commonly used thiazide and consider as 1st choice. the main problem with thiazide is hypokalemia and this can be avoided by K+ supplementation or using K+ sparing diuretics. However, ACEI/ARBs should not combined with K+ sparing diuretics which cause dangerous hyperkaliemia in some pt. Indications: HT, especially co-existing with:- DM, Nephropathy, Left Ventricular Hypertrophy (LVF), Chronic Heart Failure (CHF), Angina, Post Myocardial Infarction (MI) cases. ADRs: Dry persistent cough, Fetal malformations, granulocytopenia, proteinuria (Rare). Efficacy as monotherapy ~30-40%. Always combined with other drugs Slow onset (1-3 weeks), well sustained action Gradual  in BP in hypertensives only. Mech : Initially, TPR increases due to -blockade Later TPR decreases – resistance vessels adapt to chronically decreased CO Both systolic & diastolic BP reduced. Also, ↓ release of NA from sympathetic nerve endings, ↓ Renin release from kidney (1). Contraindicated in CHF, Pulmonary diseases (Bronchial asthma/COPD), Peripheral vascular disease and Variant angina. Cardioprotective – especially helpful to prevent sudden cardiac death if given Post MI, along with ACEIs. Hypoglycemic episodes – (1 selective less risky) Absence of SEs like Postural Hypotension, GIT effects etc Efficacy as monotherapy ~30-40%. Always combined with other drugs Slow onset (1-3 weeks), well sustained action Gradual  in BP in hypertensives only. Mech : Initially, TPR increases due to -blockade Later TPR decreases – resistance vessels adapt to chronically decreased CO Both systolic & diastolic BP reduced. Also, ↓ release of NA from sympathetic nerve endings, ↓ Renin release from kidney (1). Almost obsolete drugs Reserpine – R.serpentina roots. Indigenous. Inhibits tpt of NA into storage granules  depletion. Slow onset (2-3 wks). Also CA & 5HT depletion in brain  depression, antipsychotic effect & Parkinsonism like symptoms. Not preferred as anti-HT drug now. Guanethidine – Displaces NA from storage granules, release of NA from nerve terminals & NA reuptake inhibited  depletion. Obsolete drug. Latest guidelines (JNC8, NICE 2011): Consider:- Age / Race: Younger patients (↑ renin) respond better to ACEIs/ARBs. Blacks & aged respond better to CCBs. Diuretics alternatives to CCBs. If monotherapy ineffective – ACEIs/ARBs + CCBs/Diuretics. ACEIs/ARBs + CCBs + Diuretics – 3rd step If all fails – resistant HT – add a aldosterone antagonist or beta-blocker with vasodilator action. BP > 140/90 in pregnancy can be risky CKD, Diabetes & Chronic HT are risk factors for Pre-eclampsia Aspirin

2. Advantages Disadvantages
More effective in elderly: also in
patients with isolated systolic
hypertension.
Electrolyte imbalance
Long acting, used once a day Metabolic: hyperglycemia,
hyperlipidemia, hyperuricemia.
No tolerance and no fluid retention Erectile dysfunction
Reduce calcium excretion, preferred
in osteoporosis (especially older
women)
Not effective in chronic renal disease.
DIURETICS

3. Uses-
Hydrochlorothiazide is one commonly used thiazide
and consider as 1st choice.
 the main problem with thiazide is hypokalemia and
this can be avoided by K+ supplementation or using K+
sparing diuretics.
However, ACEI/ARBs should not combined with K+
sparing diuretics which cause dangerous
hyperkaliemia in some pt.

4. • Indications: HT, especially co-existing with:-
• DM,
• Nephropathy,
• Left Ventricular Hypertrophy (LVF),
• Chronic Heart Failure (CHF),
• Angina,
• Post Myocardial Infarction (MI) cases.
ADRs: Dry persistent cough, Fetal malformations, granulocytopenia,
proteinuria (Rare).
4
ACEIs

5. Mechanism of action
Blocking voltage sensitive L-type Ca++ channels (Long lasting current
channels) in Blood Vessels
 Ca++ entry in smooth muscle cells of BVs
Reduced depolarization
Relaxation
 PVR by arteriolar vasodilatation & mild venous dilatation
5
Ca++ CHANNEL BLOCKERS 1st line drugs

6. Advantages Disadvantages
No sedation Short acting
Safe in Bronchial Asthma, Variant
Angina, Peripheral Vascular Disease.
Renal perfusion maintained
Hypertension associated with
ischemic heart diseases and post MI
CCBs not preferred
Male sexual function maintained
No effect on plasma lipids, Uric Acid,
electrolytes,
Hypertension associated with
ischemic heart diseases and post MI
do not improve survival.
No teratogenicity  safely used in
pregnancy [mild tocolytic (+)]
Ca+ channel blockers

7. • Efficacy as monotherapy ~30-40%. Always combined with other drugs
• Slow onset (1-3 weeks), well sustained action
• Gradual  in BP in hypertensives only.
• Mech : Initially, TPR increases due to -blockade
• Later TPR decreases – resistance vessels adapt to chronically decreased
CO
• Both systolic & diastolic BP reduced.
• Also, ↓ release of NA from sympathetic nerve endings, ↓ Renin
release from kidney (1).
7
BETA BLOCKERS

8. Advantages Disadvantages
Absence of SEs like Postural
Hypotension, GIT effects etc
Unfavorable lipid profile (TGs/LDL)
No salt & water retention Decreased work capacity / libido
Cheap; once a day administration Hypoglycemic episodes – (1 selective
less risky)
Cardioprotective – especially helpful
to prevent sudden cardiac death if
given Post MI, along with ACEIs.
Contraindicated in CHF, Pulmonary
diseases (Bronchial asthma/COPD),
Peripheral vascular disease and
Variant angina.
BETA blockers

9. Advantages Disadvantages
Improved carbohydrate metabolism –
suitable for DM except with
neuropathy - high risk of postural
hypotension.
First dose Effect
Improved lipid profile / no alteration
of exercise capacity
blurred vision
Symptomatic relief of co-existing BPH
/ PVDs
ejaculation in males
Palpitations
ALPHA blockers

10. • Almost obsolete drugs
• Reserpine – R.serpentina roots. Indigenous. Inhibits tpt of
NA into storage granules  depletion. Slow onset (2-3 wks).
Also CA & 5HT depletion in brain  depression,
antipsychotic effect & Parkinsonism like symptoms. Not
preferred as anti-HT drug now.
• Guanethidine – Displaces NA from storage granules, release
of NA from nerve terminals & NA reuptake inhibited 
depletion. Obsolete drug.
10
ADR NEURONE BLOCKERS

11. Treating Hypertension : Important clinical
aspects
• Latest guidelines (JNC8, NICE 2011): Consider:-
• Age / Race: Younger patients (↑ renin) respond better to
ACEIs/ARBs. Blacks & aged respond better to CCBs.
Diuretics alternatives to CCBs.
• If monotherapy ineffective – ACEIs/ARBs +
CCBs/Diuretics.
• ACEIs/ARBs + CCBs + Diuretics – 3rd step
• If all fails – resistant HT – add a aldosterone antagonist or
beta-blocker with vasodilator action
11

12. HT in Pregnancy
• BP > 140/90 in pregnancy can be risky
• CKD, Diabetes & Chronic HT are risk factors for Pre-
eclampsia
• Aspirin 80-100mg/d
• Contraindicated drugs: ACEIs, Diuretics, Non-selective
beta-blockers, Nitroprusside
• Drugs permitted: Labetalol (preferred), Nifedipine SR,
Methyldopa, Hydralazine
• Titrate dosage for optimal response
12

13. Hypertensive Emergencies
• Controlled but rapid reduction of BP mandatory
• To be reduced to 160/100 mm Hg initially
• Nicardipine (preferred, 1st line) – in combination with
Labetalol/Esmolol to prevent reflex tachycardia. 5mg/hr
I/v infusion; can be titrated up to 15mg/hr.
• Sod Nitroprusside – 2nd line.
13

14. Hypertensive Emergencies
• Glyceryl trinitrate – mainly useful in severe HT associated
with ACS or MI. Combined with Labetalol/Nicardipine. 5-
20µg/min I/v infusion. Avoided in stroke. Onset: 2-5 mins.
• Esmolol – Short acting β1 blocker. Onset: 1-2 mins;
Duration: 10-20 mins. 0.5mg/kg I/v bolus dose; 50-
200µg/kg/min I/v infusion subsequently, combined with
Nicardipine/Nitroprusside. Preferred in aortic dissection.
14

15. Hypertensive Emergencies
(Oral drugs)
• Labetalol – 100-200 mg BD.
• Amlodipine – 10mg, repeated after 12 hrs.
• Captopril – 25mg. Not preferred
• Clonidine - 100µg every 1-2 hrs. Not preferred.
15

18. Clinical Case Study
A 35 year old multiparous lady, in the 36th week of pregnancy,
complaining of mild to moderate headache with occasional
episodes of breathlessness was found to have a blood pressure of
166/98 mm Hg on repeated recordings. She was treated for
hypertension with pregnancy in her earlier pregnancy too. Though
there was no history of Diabetes in the past, the lady has an altered
glucose tolerance test. There were traces of albumin in the urine,
but no glucose. Blood urea was 20 mg /dl and Serum creatinine
was 0.6 mg/dl. All other lab reports were WNL. Routine ante-natal
exam and USG did not reveal any fetal abnormalities.
How will you manage this case? Which drugs can be used and why?
18

19. Question 1
• Mark the wrong match about antihypertensive drugs and its
mechanism.
a) Clonidine-central α₂ agonist
b) Hydralazine- direct vasodilator
c) Amlodipine- calcium channel blocker
d) Losartan- ace inhibitor

20. Question 2
• Which of the following drug is preferred for treatment of
hypertensive emergency?
a) Nicardipine
b) Enalapril
c) Spironolactone
d) Propranolol

21. Question 3
• Which of the following antihypertensive drug is avoided during
pregnancy?
a) Labetalol
b) α-Methyldopa
c) Lisinopril
d) Nifedipine

22. Question 4
• All of the following drugs are used for pulmonary hypertension Except
a) Sildenafil
b) Fenoldopam
c) Epoprostenol
d) Bosentan

23. Question 5
• Which of the following antihypertensive drug causes sedation?
a) Clonidine
b) Hydralazine
c) Candesartan
d) Amlodipine

24. Question 6
• All of the following statement are correct EXCEPT
a) Hydrochlorothiazide is suitable agent in hypertension in patients
with osteoporosis
b) Lisinopril is considered first line drug in hypertension
c) Prazosin is preferred in hypertension in patients with prostatic
hypertrophy
d) Propranolol is preferred for hypertension in patients with diabetes