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International Islamic University Chittagong
Department of Pharmacy
Assignment Topic-
Course Title: Clinical Pharmacy Lab
Course Code: Pharm-4810
Semester:8th
Student Id. : P171007 (Md. Mahmudul Hasan)
Section: Male
Session: Autumn, 21
Introduction:
Hypertension (HTN or HT), also known as high blood pressure (HBP) is defined as persistent
elevation of systolic BP of 140 mmHg or greater and/or diastolic BP of 90 mmHg or greater. It is
a long term medical condition in which the blood pressure in the arteries is persistently elevated.
Hypertension (HTN) is an increasingly important medical and public health problem.
Hypertension is responsible for 13% of global deaths and three-quarters of the world’s
hypertensive population reside in low- and middle-income countries. Bangladesh is one of those
countries that experiencing an epidemiological transition from communicable to non-
communicable diseases, a nutritional transition from a traditional diet to process and fast food,
and an increase in a sedentary lifestyle, resulting in increased hypertension prevalence.In
Bangladesh, approximately 20% of adult and 40–65% of elderly people suffer from HTN. For
those >30 years old, the prevalence has increased from 42.6% to 43.5%. About 60.6% of total
hypertensive were “undiagnosed” Hence BP should be measured at every opportunity.
Approximately 7.6 million deaths (13 –15% of the total) and 92 million disability- adjusted life
years worldwide (2001). No significant difference between gender was observed. Globally,
cardiovascular diseases (CVDs) lead to one-third of all annual deaths, which is nearly 17 million
total deaths worldwide. Of these deaths due to CVDs, complications of hypertension account for
53% of CVD-related mortality worldwide every year. Although highly preventable, hypertension
is the most prevalent risk factor for CVD. The global prevalence of hypertension is projected to
increase from 26% in 2000 to 29.2% by 2025. Factors attributed to the increase in prevalence of
hypertension include, population growth, ageing of the population, and behavioral risk factors,
such as smoking, poor diet, harmful use of alcohol, low physical activity, and overweight or
obesity. Globally, the observed increasing burden of hypertension is a major public health
concern.
 Pre hypertension: SBP: 120-139 mmHg ; DBP: 80-89 mmHg
 Hypertension stage I: SBP: 140-159 mmHg ; DBP: 90-99 mmHg
 Hypertension stage II: SBP: More or equal to 160 mmHg ; DBP: More or equal to 100
mmHg
 Pregnancy induced HTN: because of increased production of hormones and enzymes
during pregnancy.
High blood pressure can damage our health in many ways. It can seriously hurt important
organs like your heart, brain, kidneys, and eyes.
 Heart Attack and heart disease: High blood pressure can damage our arteries by making
them less elastic, which decreases the flow of blood and oxygen to our heart and leads
to heart disease. In addition, decreased blood flow to the heart can cause:
 Chest pain, also called angina.
 Heart attack, which happens when the blood supply to our heart is blocked and heart
muscle begins to die without enough oxygen. The longer the blood flow is blocked, the
greater the damage to the heart.
 Heart failure, a condition that means our heart can’t pump enough blood and oxygen to
our other organs.
 Stroke and Brain Problems: High blood pressure can cause the arteries that supply blood
and oxygen to the brain to burst or be blocked, causing a stroke. Brain cells die during
a stroke because they do not get enough oxygen. Stroke can cause serious disabilities in
speech, movement, and other basic activities. A stroke can also kill us. Having high
blood pressure, especially in midlife, is linked to having poorer cognitive function and
dementia later in life.
 Kidney Disease: Adults with diabetes, high blood pressure, or both have a higher risk of
developing chronic kidney disease than those without these conditions.
ETIOLOGY /CAUSES
 Essential (90-95 %): Unknown specific cause – multifactorial.
– Environmental factors – Genetic factors – Fetal factors – Humoral mechanisms – Insulin
resistance - Metabolic syndrome
 Secondary: consequence of a specific disease or abnormality leading to sodium
retention and/or peripheral vasoconstriction
Essential hypertension
 Genetic factors
 tends to run in families, by shared environmental influences.
 still largely unidentified genetic component.
 Fetal factors ,– Low birth weight: May be due to fetal adaptation to intrauterine
undernutrition with long-term changes in blood vessel structure • Or the function of
crucial hormonal systems.
 Environmental factors
– Obesity, • Fat people have higher blood pressures than thin people. • Sleep disordered
breathing often seen with obesity may be an additional risk factor
– Alcohol intake, • close relationship between the consumption of alcohol and blood pressure
level. • But small amounts of alcohol seem to be beneficial
– Sodium intake, • Directly proportional • some evidence that a high potassium diet can protect
against the effects of a high sodium intake
– Stress, • Chronic stress – uncertain • acute pain or stress can raise blood pressure
 Humoral mechanisms
– Autonomic nervous system, reninangiotensin system, natriuretic peptide and kallikrein-kinin
system. Short- term changes in blood pressure. But no convincing evidence directly involved in
the maintenance of hypertension.
 Insulin resistance - Metabolic syndrome ,- Hyperinsulinaemia, glucose intolerance,
reduced levels of HDL cholesterol, hypertriglyceridaemia and central obesity with with
hypertension
- Association between diabetes and hypertension has long been recognized
Secondary Hypertension
 Pregnancy (pre-eclampsia)
 Renal disease, Renal vascular disease – Parenchymal renal disease, particularly
glomerulonephritis, Polycystic kidney disease Drugs – Oral contraceptives containing
oestrogens, – Anabolic steroids, Corticosteroids – NSAIDs, carbenoxolone,
Sympathomimetic agents
 Contrarctation of the aorta
 Endocrine diseases
 Phaeochromocytoma - vascular tumor of the adrenal gland
 Cushing’s syndrome – excessive cortisol
 Primary hyperaldosteronism (Conn’s syndrome)
 Glucocorticoid-suppressible hyperaldosteronism
 Hyperparathyroidism
 Acromegaly
 Primary hypothyroidism
 Thyrotoxicosis
 Congenital adrenal hyperplasia due to 11-β-hydroxylase or 17α-hydroxylase
deficiency
 Liddle’s syndrome
 1-β-hydroxysteroid dehydrogenase deficiency.
RISK FACTORS /FREE DISPOSING FACTOR
Moreover,
Hyperglycaemia (15 %)
Complications of Hypertension*
Central nervous system
• Stroke most common complication – Cerebral haemorrhage or infarction
• Subarachnoid haemorrhage
• Hypertensive encephalopathy – rare conditions – High BP
– Neurological symptoms: transient disturbances of speech or vision, paraesthesiae,
disorientation, fits and loss of consciousness.
• Neurological deficit - usually reversible if the hypertension is properly controlled
Retina
• Optic fundi - gradation of changes linked to the severity of hypertension
• Cotton wool exudates – Associated with retinal ischaemia or infarction – Fade in a few weeks
• Hard exudates – Assoicated with diabetic retinopathy – small, white, dense deposits of lipid –
microaneurysms (‘dot’ haemorrhages)
Heart
• Coronary artery disease, – Very high incidence – Ressure load on the heart – may lead to left
ventricular hypertrophy – forceful apex beat and fourth heart sound
• Atrial fibrillation, – diastolic dysfunction caused by left ventricular hypertrophy – Or the
effects of coronary artery disease.
• Left ventricular failure - severe hypertention
– Absence of coronary artery disease – Risk factor: impaired renal function, and therefore
sodium retention.
Kidneys
• Major risk factor for renal injury and end-stage renal disease
• Atherosclerotic, hypertension-related vascular lesions - preglomerular arterioles – Resulting in
ischemic changes in the glomeruli and postglomerular structures – This leads to reduced GFR
and, finally, a reduction in Na and water excretion – activation of the renin-angiotensin system
• May cause proteinuria (>3 g/24 h) or if untreated it may cause Progressive renal failure
CLINICAL FEATURES /SIGN & SYMPTOM
silent killer disease.
Prognosis
• Depends on a number of features: – Level of blood pressure – Presence of target-organ changes
(retinal, renal, cardiac or vascular) – Co-existing risk factors for cardiovascular disease, such as
hyperlipidaemia, diabetes, smoking, obesity, male sex – Age at presentation.
• Several studies have confirmed that the treatment of hypertension, even mild hypertension,
will reduce the risk not only of stroke but of coronary artery disease as well.
DIAGNOSTIC EVALUATIONS
Evaluation of patients with documented hypertension has three objectives: 1. To exclude
secondary causes of hypertension. 2. To ascertain the presence of target organ damage or
complication. 3. To assess lifestyle and identify other CVS factors or co-existing condition that
affect prognosis and guide treatment.
Conventional Diagnosis such as of,
ction and physical examination
-
Investigation: All patients
• Urinalysis for blood, protein and glucose • Blood urea, electrolytes and creatinine • Blood
glucose • Serum total and HDL cholesterol • 12-lead ECG - left ventricular hypertrophy,
coronary artery disease.
Selective Patient Diagnosis such as of,
Investigation: Selected patients
 Chest X-ray: cardiomegaly, heart failure, coarctation of the aorta
 Ambulatory BP recording: assess borderline or ‘white coat’ hypertension
 Echocardiogram: detect or quantify left ventricular hypertrophy • Renal ultrasound: to
detect possible renal disease
 Renal angiography: detect or confirm presence of renal artery stenosis
 Urinary catecholamines: possible phaeochromocytoma
 Urinary cortisol and dexamethasone suppression test: possible Cushing’s syndrome •
Plasma renin activity and aldosterone: possible primary aldosteronism.
MANAGEMENT & TREATMENT
Mainly the management of hypertension is possible by two ways, which include-
-st
LIFE STYLE MODIFICATION
The life-style modification measures mainly includes,
Stress management
 Body weight: Maintain normal body weight (BMI 20– 25 kg/m2)
 Diet – Reduce intake of fat and saturated fat – Reduce salt intake <100 mmol/day (<6 g
NaCl or <2.4 g Na/day) – Limit alcohol to ≤3 units/day men and ≤2 units/day women –
Consume ≥5 portions of fresh fruit and vegetables/day
 Aerobic exercise: Perform ≥30 min brisk walk most days of the week
 Cardiovascular risk reduction: Avoid cigarette smoking and increase oily fish intake.
Pharmocological Management
• Decision to commence specific drug therapy - only after a careful period of assessment with
lifestyle changes, of up to 6 months. – Unless its not having end organ damage or other
hyperetensive complications.
• Aim, plan and side effect of drug treatment - carefully explained to the patient.
• Patient compliance is very essential for efficacy of drugs – long term results.
• Various groups of drugs are used for the treatment of hypertension, collectively these drugs are
called as anti-hypertensive drugs, which includes,
– Alpha-blockers – Aldosterone antagonists – Angiotensin-converting enzyme inhibitors –
Angiotensin II receptor blockers – Beta-blockers – Calcium channel blockers – Centrally acting
– Diuretics – Renin inhibitors – Vasodilators
 Diuretics: it helps the kidneys to inhibit the sodium reabsorption in the distal convoluted
tubules, ascending limb and loop of henle. Eg: chlorothiazide, furosemide
 Beta blockers: These medications reduces the workload of the heart and blood vessal
and causing the heart to beat slowly and with less force. Eg: Atenolol, propanolol
 Alpha blockers: These medications causes the peripheral vasodilation of blood vessals.
Eg: Prazosin
 Vasodilators: These medications acting directly on the muscles in the wall of arteries
and preventing the muscles from tightening and arteries from narrowing. Eg:
reduce the conversion of A-I to A-II and prevents vasoconstriction. Eg: Captopril,
Ramipril
 Calcium channel blockers: These medicines will block the movement of extra cellular
calcium into the cells and causing vasodilation and decreased heart rate. Eg:
Amlodipine, Verapamil
 Alternative therapies which are helpful to regulate blood pressure includes acupuncture,
relaxation techniques and diversional therapies.
Picture-1
Hypertension in Pregnancy
• There are three types of hypertension seen in pregnant women: – Chronic or pre-existing
hypertension – Gestational hypertension – Pre-eclampsia and eclampsia
 1st line therapy: Methyldopa (no adverse effects on the fetus)
 2nd line agents: Nifedipine and labetalol.
The target blood pressure should be <150/100 mmHg
• Gestational hypertension: >140/90 mmHg in the 2nd trimester in a previously normotensive
woman. – risk of developing pre-eclampsia
Pre-eclampsia -
• Multi-system disorder that occurs after 20 weeks’ gestation consisting of:
 Hypertension
 Oedema – Proteinuria (>0.3 g/24 hours).
• These patients should be admitted and treated for hypertension with regular
 BP measurements (4 times daily)
 blood tests 2–3/week.
 close fetal monitoring due to the risks of placental insufficiency and intrauterine growth
retardation.
• Patients who progress to eclampsia (convulsions) and/or HELLP (haemolysis, elevated liver
enzymes, low platelet count) syndrome should be admitted to a critical care unit (CCU)
 intravenous hydralazine, labetalol, and magnesium sulphate (for convulsions)
 Prompt delivery.
Reference:
 www.cdc.com; https://www.cdc.gov/bloodpressure/about.htm
 https://www.nature.com/articles/s41371-018-0087-5
 https://www.slideshare.net/yuyuricci/hypertension-126740125
 https://www.slideshare.net/DeepakKumarGupta2/hypertension-63582065
 https://www.slideshare.net/Ratheeshkrishnakripa/hypertension-
66802042?from_action=save;
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860599/
 https://clinicalhypertension.biomedcentral.com/articles/10.1186/s40885-020-00143-1
Clinical Pharmacy Lab Assignment on Hypertension (HTN

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Clinical Pharmacy Lab Assignment on Hypertension (HTN

  • 1. International Islamic University Chittagong Department of Pharmacy Assignment Topic- Course Title: Clinical Pharmacy Lab Course Code: Pharm-4810 Semester:8th Student Id. : P171007 (Md. Mahmudul Hasan) Section: Male Session: Autumn, 21
  • 2. Introduction: Hypertension (HTN or HT), also known as high blood pressure (HBP) is defined as persistent elevation of systolic BP of 140 mmHg or greater and/or diastolic BP of 90 mmHg or greater. It is a long term medical condition in which the blood pressure in the arteries is persistently elevated. Hypertension (HTN) is an increasingly important medical and public health problem. Hypertension is responsible for 13% of global deaths and three-quarters of the world’s hypertensive population reside in low- and middle-income countries. Bangladesh is one of those countries that experiencing an epidemiological transition from communicable to non- communicable diseases, a nutritional transition from a traditional diet to process and fast food, and an increase in a sedentary lifestyle, resulting in increased hypertension prevalence.In Bangladesh, approximately 20% of adult and 40–65% of elderly people suffer from HTN. For those >30 years old, the prevalence has increased from 42.6% to 43.5%. About 60.6% of total hypertensive were “undiagnosed” Hence BP should be measured at every opportunity. Approximately 7.6 million deaths (13 –15% of the total) and 92 million disability- adjusted life years worldwide (2001). No significant difference between gender was observed. Globally, cardiovascular diseases (CVDs) lead to one-third of all annual deaths, which is nearly 17 million total deaths worldwide. Of these deaths due to CVDs, complications of hypertension account for 53% of CVD-related mortality worldwide every year. Although highly preventable, hypertension is the most prevalent risk factor for CVD. The global prevalence of hypertension is projected to increase from 26% in 2000 to 29.2% by 2025. Factors attributed to the increase in prevalence of hypertension include, population growth, ageing of the population, and behavioral risk factors, such as smoking, poor diet, harmful use of alcohol, low physical activity, and overweight or obesity. Globally, the observed increasing burden of hypertension is a major public health concern.  Pre hypertension: SBP: 120-139 mmHg ; DBP: 80-89 mmHg  Hypertension stage I: SBP: 140-159 mmHg ; DBP: 90-99 mmHg
  • 3.  Hypertension stage II: SBP: More or equal to 160 mmHg ; DBP: More or equal to 100 mmHg  Pregnancy induced HTN: because of increased production of hormones and enzymes during pregnancy. High blood pressure can damage our health in many ways. It can seriously hurt important organs like your heart, brain, kidneys, and eyes.  Heart Attack and heart disease: High blood pressure can damage our arteries by making them less elastic, which decreases the flow of blood and oxygen to our heart and leads to heart disease. In addition, decreased blood flow to the heart can cause:  Chest pain, also called angina.  Heart attack, which happens when the blood supply to our heart is blocked and heart muscle begins to die without enough oxygen. The longer the blood flow is blocked, the greater the damage to the heart.  Heart failure, a condition that means our heart can’t pump enough blood and oxygen to our other organs.  Stroke and Brain Problems: High blood pressure can cause the arteries that supply blood and oxygen to the brain to burst or be blocked, causing a stroke. Brain cells die during a stroke because they do not get enough oxygen. Stroke can cause serious disabilities in speech, movement, and other basic activities. A stroke can also kill us. Having high blood pressure, especially in midlife, is linked to having poorer cognitive function and dementia later in life.  Kidney Disease: Adults with diabetes, high blood pressure, or both have a higher risk of developing chronic kidney disease than those without these conditions. ETIOLOGY /CAUSES  Essential (90-95 %): Unknown specific cause – multifactorial. – Environmental factors – Genetic factors – Fetal factors – Humoral mechanisms – Insulin resistance - Metabolic syndrome  Secondary: consequence of a specific disease or abnormality leading to sodium retention and/or peripheral vasoconstriction Essential hypertension  Genetic factors  tends to run in families, by shared environmental influences.  still largely unidentified genetic component.
  • 4.  Fetal factors ,– Low birth weight: May be due to fetal adaptation to intrauterine undernutrition with long-term changes in blood vessel structure • Or the function of crucial hormonal systems.  Environmental factors – Obesity, • Fat people have higher blood pressures than thin people. • Sleep disordered breathing often seen with obesity may be an additional risk factor – Alcohol intake, • close relationship between the consumption of alcohol and blood pressure level. • But small amounts of alcohol seem to be beneficial – Sodium intake, • Directly proportional • some evidence that a high potassium diet can protect against the effects of a high sodium intake – Stress, • Chronic stress – uncertain • acute pain or stress can raise blood pressure  Humoral mechanisms – Autonomic nervous system, reninangiotensin system, natriuretic peptide and kallikrein-kinin system. Short- term changes in blood pressure. But no convincing evidence directly involved in the maintenance of hypertension.  Insulin resistance - Metabolic syndrome ,- Hyperinsulinaemia, glucose intolerance, reduced levels of HDL cholesterol, hypertriglyceridaemia and central obesity with with hypertension - Association between diabetes and hypertension has long been recognized Secondary Hypertension  Pregnancy (pre-eclampsia)  Renal disease, Renal vascular disease – Parenchymal renal disease, particularly glomerulonephritis, Polycystic kidney disease Drugs – Oral contraceptives containing oestrogens, – Anabolic steroids, Corticosteroids – NSAIDs, carbenoxolone, Sympathomimetic agents  Contrarctation of the aorta  Endocrine diseases  Phaeochromocytoma - vascular tumor of the adrenal gland  Cushing’s syndrome – excessive cortisol  Primary hyperaldosteronism (Conn’s syndrome)  Glucocorticoid-suppressible hyperaldosteronism  Hyperparathyroidism  Acromegaly  Primary hypothyroidism
  • 5.  Thyrotoxicosis  Congenital adrenal hyperplasia due to 11-β-hydroxylase or 17α-hydroxylase deficiency  Liddle’s syndrome  1-β-hydroxysteroid dehydrogenase deficiency. RISK FACTORS /FREE DISPOSING FACTOR Moreover, Hyperglycaemia (15 %)
  • 6. Complications of Hypertension* Central nervous system • Stroke most common complication – Cerebral haemorrhage or infarction • Subarachnoid haemorrhage • Hypertensive encephalopathy – rare conditions – High BP – Neurological symptoms: transient disturbances of speech or vision, paraesthesiae, disorientation, fits and loss of consciousness. • Neurological deficit - usually reversible if the hypertension is properly controlled Retina • Optic fundi - gradation of changes linked to the severity of hypertension • Cotton wool exudates – Associated with retinal ischaemia or infarction – Fade in a few weeks • Hard exudates – Assoicated with diabetic retinopathy – small, white, dense deposits of lipid – microaneurysms (‘dot’ haemorrhages)
  • 7. Heart • Coronary artery disease, – Very high incidence – Ressure load on the heart – may lead to left ventricular hypertrophy – forceful apex beat and fourth heart sound • Atrial fibrillation, – diastolic dysfunction caused by left ventricular hypertrophy – Or the effects of coronary artery disease. • Left ventricular failure - severe hypertention – Absence of coronary artery disease – Risk factor: impaired renal function, and therefore sodium retention. Kidneys • Major risk factor for renal injury and end-stage renal disease • Atherosclerotic, hypertension-related vascular lesions - preglomerular arterioles – Resulting in ischemic changes in the glomeruli and postglomerular structures – This leads to reduced GFR and, finally, a reduction in Na and water excretion – activation of the renin-angiotensin system • May cause proteinuria (>3 g/24 h) or if untreated it may cause Progressive renal failure CLINICAL FEATURES /SIGN & SYMPTOM silent killer disease. Prognosis • Depends on a number of features: – Level of blood pressure – Presence of target-organ changes (retinal, renal, cardiac or vascular) – Co-existing risk factors for cardiovascular disease, such as hyperlipidaemia, diabetes, smoking, obesity, male sex – Age at presentation. • Several studies have confirmed that the treatment of hypertension, even mild hypertension, will reduce the risk not only of stroke but of coronary artery disease as well.
  • 8. DIAGNOSTIC EVALUATIONS Evaluation of patients with documented hypertension has three objectives: 1. To exclude secondary causes of hypertension. 2. To ascertain the presence of target organ damage or complication. 3. To assess lifestyle and identify other CVS factors or co-existing condition that affect prognosis and guide treatment. Conventional Diagnosis such as of, ction and physical examination - Investigation: All patients • Urinalysis for blood, protein and glucose • Blood urea, electrolytes and creatinine • Blood glucose • Serum total and HDL cholesterol • 12-lead ECG - left ventricular hypertrophy, coronary artery disease. Selective Patient Diagnosis such as of, Investigation: Selected patients  Chest X-ray: cardiomegaly, heart failure, coarctation of the aorta  Ambulatory BP recording: assess borderline or ‘white coat’ hypertension  Echocardiogram: detect or quantify left ventricular hypertrophy • Renal ultrasound: to detect possible renal disease  Renal angiography: detect or confirm presence of renal artery stenosis  Urinary catecholamines: possible phaeochromocytoma  Urinary cortisol and dexamethasone suppression test: possible Cushing’s syndrome • Plasma renin activity and aldosterone: possible primary aldosteronism. MANAGEMENT & TREATMENT Mainly the management of hypertension is possible by two ways, which include- -st LIFE STYLE MODIFICATION The life-style modification measures mainly includes, Stress management  Body weight: Maintain normal body weight (BMI 20– 25 kg/m2)
  • 9.  Diet – Reduce intake of fat and saturated fat – Reduce salt intake <100 mmol/day (<6 g NaCl or <2.4 g Na/day) – Limit alcohol to ≤3 units/day men and ≤2 units/day women – Consume ≥5 portions of fresh fruit and vegetables/day  Aerobic exercise: Perform ≥30 min brisk walk most days of the week  Cardiovascular risk reduction: Avoid cigarette smoking and increase oily fish intake. Pharmocological Management • Decision to commence specific drug therapy - only after a careful period of assessment with lifestyle changes, of up to 6 months. – Unless its not having end organ damage or other hyperetensive complications. • Aim, plan and side effect of drug treatment - carefully explained to the patient. • Patient compliance is very essential for efficacy of drugs – long term results. • Various groups of drugs are used for the treatment of hypertension, collectively these drugs are called as anti-hypertensive drugs, which includes, – Alpha-blockers – Aldosterone antagonists – Angiotensin-converting enzyme inhibitors – Angiotensin II receptor blockers – Beta-blockers – Calcium channel blockers – Centrally acting – Diuretics – Renin inhibitors – Vasodilators  Diuretics: it helps the kidneys to inhibit the sodium reabsorption in the distal convoluted tubules, ascending limb and loop of henle. Eg: chlorothiazide, furosemide  Beta blockers: These medications reduces the workload of the heart and blood vessal and causing the heart to beat slowly and with less force. Eg: Atenolol, propanolol  Alpha blockers: These medications causes the peripheral vasodilation of blood vessals. Eg: Prazosin  Vasodilators: These medications acting directly on the muscles in the wall of arteries and preventing the muscles from tightening and arteries from narrowing. Eg: reduce the conversion of A-I to A-II and prevents vasoconstriction. Eg: Captopril, Ramipril  Calcium channel blockers: These medicines will block the movement of extra cellular calcium into the cells and causing vasodilation and decreased heart rate. Eg: Amlodipine, Verapamil  Alternative therapies which are helpful to regulate blood pressure includes acupuncture, relaxation techniques and diversional therapies.
  • 11.
  • 12. Hypertension in Pregnancy • There are three types of hypertension seen in pregnant women: – Chronic or pre-existing hypertension – Gestational hypertension – Pre-eclampsia and eclampsia  1st line therapy: Methyldopa (no adverse effects on the fetus)  2nd line agents: Nifedipine and labetalol. The target blood pressure should be <150/100 mmHg • Gestational hypertension: >140/90 mmHg in the 2nd trimester in a previously normotensive woman. – risk of developing pre-eclampsia Pre-eclampsia - • Multi-system disorder that occurs after 20 weeks’ gestation consisting of:  Hypertension  Oedema – Proteinuria (>0.3 g/24 hours). • These patients should be admitted and treated for hypertension with regular  BP measurements (4 times daily)  blood tests 2–3/week.  close fetal monitoring due to the risks of placental insufficiency and intrauterine growth retardation. • Patients who progress to eclampsia (convulsions) and/or HELLP (haemolysis, elevated liver enzymes, low platelet count) syndrome should be admitted to a critical care unit (CCU)  intravenous hydralazine, labetalol, and magnesium sulphate (for convulsions)  Prompt delivery. Reference:  www.cdc.com; https://www.cdc.gov/bloodpressure/about.htm  https://www.nature.com/articles/s41371-018-0087-5  https://www.slideshare.net/yuyuricci/hypertension-126740125  https://www.slideshare.net/DeepakKumarGupta2/hypertension-63582065  https://www.slideshare.net/Ratheeshkrishnakripa/hypertension- 66802042?from_action=save;  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860599/  https://clinicalhypertension.biomedcentral.com/articles/10.1186/s40885-020-00143-1