Lecture notes on Hypertension

Hypertension

Important,  b,cose-

Secondary organ damage and

Reduced life span

Stress, Anxiety, Physical activity, etc can increase BP transiently and acutely

So, Several Estimations Needed to establish the diagnosis

Mechanism

In most cases, (­SBP, ­DBP, or mean BP), basic haemodynamic abnormality is Increased Vascular Resistance at Small Muscular Arteries.

This is due to

1. Ratio of lumen to wall thickness

2. Neural influences

Norepinephrine- vasoconstrictor

Acetylocholine- vasodialator

3. Humeral and Locally acing substances

Angiotensin II- Vasoconstrictor

Prostaglandins and Kinins- Vasodilators

Hypoxia, Acidosis- Vasodilators

Systolic Hypertension

            Mostly in Elderly

            Due mainly to

1.Decreased Compliance of aortic wall due to Atherosclerosis

                           Is a risk factor for atherosclerosis

2. Due to ­ CO - In Thyrotoxicosis, Fever, Anemia, PDA, AV Fistula, 

   AR ctc,

                           Here there is a Wide Pulse pressure( Low Diastolic BP)

Theories of mechanism of Hypertension

            1, Hypertension as a reaction to Deficient Renal Na output

            ¯ Na excretion® ­ Blood Volume, ­ CVP, ­ CO, ­ Systemic Blood Flow

            Tissues react to this overperfusion by increasing local vascular resistance

            So, BP rises, ­ Afterload, ¯ Stroke volume and CO

            ­ Pressure ® ­ Renal flow, ­ Na excretion, ¯ Blood volume, ¯ CVP, ¯ CO

            So, end result is

                        Increased PVR

                        Increased BP

Normal B Volume, Normal CO, Normal CVP, Normal Na excretion

            2. Primary elevation in Peripheral Vascular Resistance

                        May be due to

                                    Increased Activity/Sensitivity of vasoconstrictors

                                    Reduced activity of vasodilators

                                    Change in size arterial smooth muscle

Both the above theories are equally valid and not mutually exclusive

Both may be important in any particular patient

In Hypertension due to Stress, Epinephrine may be the cause of  ­ BP

What is High BP?

            Due consideration needed for both Systolic and Diastolic BP

            150/90 in Men above 45 yrs or

130/90 in Men below 45 yrs

Sustained Hypertension- If Diastolic BP is always above these  levels

Labile Hypertension- They occasionally have BP in the hypertensive range

Malignant Hypertension- BP above 240/140, with Papilloedema

Acclerated Hypertension-

Recent increase in a hypertensive patient along with vascular damage in fundoscopy ,but without Papilloedema

Young Black Males have higher BP and increased incidence of complications

Etiology

            Primary- Essential or Idiopathic- > 90%

            Secondary-

                        Systolic and Diastolic Hypertension

1.      Renal

Ch.Pyelonephritis

Ac and Ch Glomerulonephritis

Polycystic Renal Disease

Diabetic Nephropathy

                                                Renovascular stenosis and Infarction

                                                Renin producing Tumours

2.      Endocrine

Oral contraceptuives

Adrenocortical hyperfunction

            Cushings Disease/Syndrome

            Primary Hyperaldosteronism

            Con/Heriditory Adrenogenital syndromes

Pheochromocytoma

Acromegaly

3.      Neurogenic

Psychogenioc

Familial Dysautonomia

Acute Porphyria,

Lead Poisoning

Increased Intracranial pressure

4.      Miscellaneous

Coarctation of aorta

Excessive transfusion,

Polycythemia

Scleroderma

Polyarteritis Nodosa

Hypercalcemia

5.      Unknown Etiology

Toxemia of Pregnancy

Acute Intermittent Porphyria

Essential Hypertension

            Underlying mechanism not known

            Kidney probably has a central role

            Positive family history often present

            Inheritance is probably multifactorial

            Environmental factors

                        Salt intake, Obesity, Occupation, Family size, Overcrowding

            Modifying factors

                        Age- Younger the patient, greater the reduction in life expectancy

                        Females- fare better than men, But CV complications same

Serum Cholesterol, Smoking, Glucose intolerance, all increase

Atherosclerosis and effect of Hypertension

Obesity- Higher incidence of high BP, but does not affect mortality

            Untreated- Shortens life by 10-20 yrs- due to atherosclerosis and its effects

            Mild disease  with no end organ involvement- Untreated , compli in 7-10 yrs

                        30% will have atherosclerosis

            50% will have end organ damage due to Hypertension-

         Cardiomegaly, CCF, CVA, Renal insufficiency, Retinopathy etc

            Factors indicating Bad prognosis

1.      Young patient

2.      Male

3.      Persistent Diastolic BP above 115

4.      Smoking

5.      DM

6.      Dyslipidemia

7.      Obesity

8.      Evidence of End organ damage

1.      Cardiac

Cardiomegaly

ECG – Ischemia or LV strain

MI

CCF

2.      Eyes

Retinal Exudates, Haemorrhage

Papilloedema

3.      Renal

Impaired Renal function

4.      Nervous system- CVA

Secondary Hypertension

            Cause can be identified only in a small group of patients

            But important b,cose Correction of cause cures Hypertension

■ Renal Hypertension

            Due to either

1.      Deranged renal handling of Na and Fluids® Volume expansion

2.      Altered renal secretion of vasoactive substances® change in arteriolar tone

Subdivisions of Renal Hypertension

1.      Renovascular ( Including pre-eclampsia and Eclampsia)

2.      Renal parenchymal Hypertension

♦Renovascular

There is decreased perfusion of Renal tissue due to Stenosis or Occlusion

Renin- angiotensin system is activated

Angiotensin raises BP by direct vasoconstriction and stimulates adrenergic system

It stimulates Aldosterone which causes Na retention

Angiotensin antagonist Saralasin reduces BP in such patients

Usual causes are Renal artery Stenosis due to Atherosclerosis- More in males, Occurs in advancing age

♦Fibromuscular Dysplasia-

Fibromuscular thickening of Intima, Media and Sub adventitial region

            More in

10 times more in Females,

Often B/L,

Usually in 3^rd decade

Involves Distal part of RA and branches

Does not usually affect Asians and Africans

PTA S is very successful

Investigations

1.      IVP

♦ Small kidney

♦ Delayed appearance of contrast in affected kidney

♦ Hyperconcentration in affected kidney in late films

♦ Filling defects in Pelvis and Ureter due to dilated collateral

   vessels

2.      Ultrasound

3.      Doppler

4.      CT Angiography

5.      MR Angiography

6.      Radionuclide Renogram

7.      Arteriography

8.      Renal vein and Aortic Renin sampling- Atleast 50% increase on affected side

9.      Fall in BP following Saralasin ( atleast by 10 mm Hg)

Renal Parenchymal Hypertension

There is Decreased perfusion of Renal parenchyma due to Inflammatory and Fibrotic changes in multiple small intra renal vessels.

This leads to stimulation of Renin- Angiotensin mechanism

May be other factors are also involved

1.      Damaged tissue produce some vasoconstrictor – other than Renin

2.      They fail to produce vasodilators

3.      They fail to inactivate circulating vasopressors

4.      They are ineffective in disposing Na → Na retention results

This is probably the best explanation

            Renin secreting Tumours

Juxtaglomerular cell tumours and Nephroblastomas may secrete excess Renin

They present like Primary Hyperaldosteronism

But peripheral Renin activity is increased instead of Subnormal

■ Endocrine Hypertension

1.      Adrenal Hypertension

           

            Primary Hyperaldosteronism

                        Leads to Na retention and Hypertension

                        Hypokalemia is a prominent feature(K exchanged for Na)

                        Serum K is a screening test

                        There is Suppression of Renin activity and Aldosterone levels are high

                        May be due to Adrenal tumour or B/L Hyperplasia

                        B/L Hyperplasia is not surgically treatable

            Cushing Syndrome

                        Glucocorticoids Increase Na retention

                        This is Due to production of Renin substrate- Angiotensin

                        Mineralocorticoids may also be increased in Cushings

            Adrenogenital Syndromes

                        C-11 or C-17 Hydroxylase deficiency causes Na retention

                        Renin is suppressed

            Pheochromocytoma

                        Increased Epi and Norepinephrine

                        Peripheral vasoconstriction and Cardiac stimulation

                        Rare tumour- But curable, 0.1% of all hypertensives

                        ♦May be Adrenal or Extra adrenal

( Coeliac plexus, SM ganglia or IMGanglia)

♦May be associated with

-MEN II(Pheochromocytoma, MTC & Parathyroid hyperplasia)

-MEN III(MTC, Pheo & Mucosal neuromas)and

-Von R Disease,

80% Unilteral, 10% B/L 10% Extra adrenal

Right side is favoured

Usually Young Adults affected- Slight Female preponderance

Sustained Hypertension-in 60%.

Half of them have paroxysms of Hypertention and associated signs

40% have High BP only during attacks

Precipitated by any abdominal movement

Paroxysmal attacks-

            Sudden onset, Lasts minutes to hours

            Headache, Profuse sweating, Palpitation, anxiety

            Feeling of Impending death

            Chest or abdominal pain with Nausea and Vomiting

            Pallor and flushing

            High BP and Tachycardia

Diagnosis

            Urinary Catecholamines (Normal 100-150 µg per 24 hrs)

            VMA- ( Normal-7 mg/24 hrs )

            Urinary Metanephrines( Normal- 1.3 mg/24 hrs)

            Acromegaly

            Hypercalcemia

                        High BP due to Nephrocalcinosis and Nephrolithiasis

                        Ca may have  a direct Vasoconstrictive effect

            Oral Contraceptives

                        From Oestrogen containing pills

                        Oestrogen stimulates production of Angiotensinogen from liver

                        Thus Angiotensin II and Aldosterone are produced

                        Not all on OC develop High BP, Why?

                                    ? Increased sensitivity to AngiotensinII

                                    ? Family H/O High BP

                                    ? Mild Renal disease present

                                    ? Obesity

                        May regress after 6 months of stopping OC

            Pre-Eclampsia and Eclampsia

                        Pre eclampsia-

Usually 3^rd trimester

                                    High BP, Oedema, Proteinuria

                        Thickened Glomerular Basement Membrane

                        Due to Increase in cytoplasm of endothelial cells

                        So, Lumen narrowed(Glomerular Endotheliosis)

                       

                        Sub endothelial fibrinoid deposition also may occur

            Scleroderma

                        Narrowing of Intralobular arteries

                        Due to deposition of Fibrin and Mucopolysacchrides

                        Distal occlusion leads to Ischemia and infarction

                        Haemorrhages and wedge shaped cortical infarcts are seen

            Polyarteritis Nodosa

                        Progressive, Recurrent Necrotizing Inflammatory disease of Medium

small sized muscular arteries

Occur at Sites of Branching

Subendothelial and Medial oedema, Fibrinoid necrosis, Infiltration with inflammatory cells, Proliferation of Fibroblasts

During healing, vessel wall replaced by fibrous tissue and lumen narrowed

Renal Insufficiency and Hypertension develops

Approach to patients with High BP

            Symptoms and Signs

            Clinical Evaluation

                        History

                                    Family History

                                    Age- below 35 and above 55, think of Sec.Hypertension

                                    Use of steroids

                                    Repeated UTI

                                    Weight gain

                                    Look for risk factors

                        Physical Exam

                                    Obesity, esp truncal

                                    BP- Rise in Diastoilc on standing Essential Hypertension

                                    Fall In Diastolic- ? Secondary

                                    Fundus

                                                Keith- Wagner- Barker grading

                                                4 grades-

                                    Chest exam- For cardiac disease

                                    Abdominal Bruits

                       

                                    BF Delay, Collaterals on Chest wall

                        Lab Tests

1.      Basic Investigations

Always should be done

            Urine- Protein, Blood, Glucose

            Haematocrit

            Serum K

            Serum Creatinine, Urea

            ECG

Done if cost allows

            Urine microscopy

            WBC Count

            Serum Glucose, Cholesterol, Tg

            Serum Ca, Po4, Uric acid

            Chest X-Ray

2.      Special studies

A.     Renovascular

IVP, Renogram, Arteriogram, Saralasin test

                             B.   Pheochromocytoma

                                    Urine VMA, Metanephrines, Catecholamines

                           C.  Cushing

                                    Overnight Deaxamethasone Suppression test

           

                       

                       

                       

                       

                        

Osteoporosis

Introduction

The word osteoporosis simply means “porous bones”. Bones become porous, or less dense, with age. Bone is a

dynamic living tissue; it is constantly being broken down and rebuilt, a process known as remodelling. As we age,

the mineral rich, internal part of bone breaks down faster than it is rebuilt. It should not be treated as disease unless

you experience one or following multiple symptoms over a period of time:

Bone fracture,

Agradual loss of height.

Arounding of the shoulders.

Guminflammation and loosening of the teeth.

Acute lower backache.

Swelling of a wrist after a minor fall or injury.

Trouble with nail, hair, teeth, gums, joints, or back;

Nocturnal leg cramps,

Rheumatoid arthritis,

Restless behaviour,

Persons with osteoporosis suffer from a loss in bone mass and bone strength at a higher rate than expected with

aging. Their bones become weak and brittle which makes them more prone to fracture. Any bone can be affected

by osteoporosis, but the hips, wrists and spine are the most common sites. Peak bone mass is reached between

the ages of 25 and 35 years. After 35, bone mass is stable until, in women, it starts to drop with menopause. 6-18%

of women between 25-34 years of age have “abnormally low” bone density. Hip-fracture rates for white women in

the US and Britain begin to rise abruptly between the ages of 40-44 much earlier than menopause begins. This

drop occurs more slowly in males.

From Ayurvedic perspective any vata imbalance or disease pattern in the body is indicated by in one of the

symptoms such as stress, anxiety, constipation, dry skin, hypertension, restlessness, insomnia, PMS or many

menstrual disorders, Irritable bowl syndrome and Inability to relax etc.

Some of the behavioural patterns that can create a vata imbalance in the body are: being in stress or reacting to

stress with anxiety; physical exhaustion; mental strain and overwork without giving body a chance to relax and recreate;

addictive patterns; lack of sleep; suffering emotionally from grief, fear or shock; travelling (flying or long car

journeys); stringent diets; eating cold, raw or dry foods frequently; living in a cold, dry and windy weather.

Osteoporosis is one of the natural processes that occur with age, however, vata body type individuals or people in

vata stage of life, are likely to experience loss of bone density at a higher rate. Consequently risk for osteoporosis

will be higher in a person of vata body, old people and women after menopausal age. For women, a regular

menstrual cycle is important for building and maintaining bone strength throughout a woman's reproductive years.

Risk factors

.

Certain risk factors that increase the likelihood of developing and aggravating osteoporosis are:

Being female - women are four times more likely to develop osteoporosis than men. Though most women

start to think of bone loss only at menopause, it often begins years before. 50%of the bone lose over their

lifespan is lost before menopause even begins. The reasons are:

Their bones are generally thinner and lighter.

They live longer than men.

They have rapid bone loss at menopause due to a sharp decline of oestrogen. Natural

menopause before age 40; a hysterectomy which includes removal of both ovaries with no

hormone replacement therapy (HRT); a lack of/or irregular menstrual flow.

Oestrogen/ progesterone deficiency

Having a thin, small framed body.

Heredity and Race - the risk increases if there is a history of osteoporosis and/or bone fractures in your

family. Some races e.g. Caucasians are at a higher risk thanAsians andAfricanAmericans.

Skim and low-fat milks, yogurts and cheeses. Soft-boned fish and shellfish, such as salmon with the

bones, sardines and shrimp. Vegetables e.g. dark green leafy vegetables, broccoli, kale, collards. Beans

and bean sprouts as well as tofu (soy bean curd, if processed with calcium). Calcium-fortified foods such

as some orange juices, apple juices and ready-to-eat cereals and breads.

Lack of physical activity especially activities such as walking, running, tennis and other weight-bearing

exercises.

Lack of calcium and vitamin D, Magnesium and other mineral deficiencies from our modern diet of

processed foods

Cigarette smoking and Excessive Alcohol - Heavy drinkers and smokers often have poor appetite and

poor nutrition.

Taking certain medicines such as corticosteroids (anti-inflammatory drugs used to treat asthma, arthritis,

lupus, etc.) and aluminium containing antacids like Rolaids or Di-Gel., anti-seizure drugs and overuse of

thyroid hormones.

Hyperthyroidism, hyperparathyroidism, and certain forms of bone cancer, anorexia nervosa, scoliosis and

gastrointestinal disease.

Malabsorption of nutrients as a result of antibiotic use

High Fat, high protein diet

Medical management, especially if you are at a high risk of getting the disorder. Doctor may prescribe

hormone replacement therapy (HRT) and/or calcium. These are recommended to prevent fractures from

osteoporosis if taken during or soon after the start of menopause and then on a continual basis. HRT does not

rebuild bone, but it is supposed to prevent further bone loss. New research on HRT is bringing question mark on

this method.

Surgery, such as hip replacement, if necessary.

Dietary and lifestyle measures.

Natural approaches to osteoporosis treatment are to focus on supporting this dynamical, bone rebuilding process

and not on replacing the natural and healthy decline of oestrogen during menopause. To prevent or slow

osteoporosis, take these steps now:

Ahigh-Complex-Carbohydrate, Low-Fat Diet, Relatively low in protein - Limit servings of red meat to lean

cuts no more than three times per week (Red meat is very high in phosphorous, as is soda. High phosphorous

intake extracts calcium from bones to keep calcium/phosphorous levels in balance.) Concentrate on eating dark

green leafy vegetables.

Plan to get enough calcium every day: If our diets were mostly whole grains, greens, beans and

vegetables, our bones would be more apt to stay healthy on relatively less calcium, as long as we also

exercised and got out in the sun for vitamin D. Some high calcium foods are:

Follow a program of regular, weight-bearing exercise at least three or four times a week. Examples

include:Walking, jogging, cycling, weight training, low-impact or non-impact aerobics anything that puts

weight on the bones, twenty minutes five times per week or thirty minutes three times per week.

Do not smoke and limit alcohol consumption.. Smoking makes osteoporosis worse. Smokers, along with

those who consume two or more alcoholic drinks daily, are at highest risk of osteoporosis. Smoking

poisons the ovaries.

Pay attention to your posture. Keep your back straight when you sit, stand and walk.

Take measures to prevent falls and injury to your bones.

No Cola or soda drinks These are too high in phosphate, which directly interferes with calcium absorption.

VitaminC is involved in collagen synthesis and repair and is found in Citrus fruits.

Magnesium It is found in organically grown vegetables, whole grains, seaweed (kelp) and meats such as

Traditional Treatment includes:

Natural Dietary and Lifestyle Measures:

turkey. Over-consumption of processed food (refined grains and too few dark green leafy vegetables) is usually

the culprit in magnesium deficiency.

Boron The minimum dose of boron needed per day is easily met with a daily diet rich in fruit, nuts and

vegetables.

Beta Carotene Vitamin A promotes a healthy intestinal epithelium and promotes strong joints, which is

important for optimal absorption of nutrients. It is found in yellow and orange vegetables e.g. pumpkin,

carrots, leafy vegetables and broccoli.

Ayurvedic Treatment for Osteoporosis:

Ayurveda also focuses on balancing doshas, especially vata, and the dhatus are free of ama, then the body's

homeostatic mechanisms will more efficiently help our metabolism adjust to natural aging process. When the body's

natural healing ability is strengthened, and root imbalances in basic bodily functions are removed, the bone rebuilding

process will be positively influenced.Ayurveda recommends on:

Detoxification and balancing the doshas, especially vata dosha, using Purvakarma and Basti treatments.

The Panchakarma treatment consists of internal oleation, Snehana, Bashpa swedana, Kati basti, and shiro dhara,

followed by purge to remove all the vitiated doshas from the body systems, this followed by basti with herbal oil (vata

shamak or dashmoola) for the vitiated vata dosha.

Food supplements and Rejuvenators like Shatavari (Asparagus racemosus), Ashwagandha

(Withania somnifera) and Bala (Sida cordifolia), Amalaki (Emblica officinalis) should be taken in the

powdered form in the dose of 2-3gmdaily.

Shatavari and vidari mixed in equal parts, or just shatavari taken on regular basis (1/2 tsp twice daily)

with warm milk, help to make up for oestrogen in the metabolic cycle. These herbs are food

precursors of oestrogen and progesterone.

Abhyanga or self massage using sesame oil, for vata pacification.

Ashokarishta Ashoka bark has silica, sodium, potassium, phosphate, magnesium, iron, and

calcium among others. It is used for many uterine disorders and is a good herb for time of

menopause.

Dashamularishta Dashmoola is used for vata pacification. These preparations should be taken after

consulting anAyurvedic consultant.

Daily chewing a handful of sesame seeds in the morning provides at least 1200 mg of natural

calcium. These seeds won't clog arteries, as dependence upon calcium from dairy products may do.

One part black or white sesame seeds, half part shatavari, with ginger and raw sugar added to taste

is good for the bones.

The vata pacifying diet includes warm, heavy moist and slightly oily foods that give you strength.

Frequent small meals, mildly spiced and with only a few different types of foods per meal are

recommended. Don't eat when you are nervous or worried. If possible eat with your friends/ family.

Amalaki is a rasayana for the bones, nourishing the bones, strengthening the teeth, causing hair and

nails to grow. Fivegmpowder in one cup water twice a day is used as a general tonic. Triphala can be

used on regular basis as a tridoshic tonic.

Few diet/ lifestyle things to complement the beneficial effect ofAyurvedic Medicines:

Consume more of calcium-rich foods such as skimmed milk and spinach, avoiding red meat at the

same time.

Nourish yourself with whole, natural foods. Avoid saturated fats such as cheese and butter. Instead

use ghee, low fat butter or unsaturated fat such as sunflower and corn oils.

Make exercise a daily routine (after consulting your doctor) to keep yourself fit

Avoid smoking and drinking alcohol.

Limit your intake of tea or coffee to max. one to two cups daily, avoid completely if possible.
Practise yoga and meditation for calming effect and mind control. If osteoporosis has begun to
develop, yoga exercises should be done gently, with care, as there could be a real danger of
breaking a bone.
Develop positive approach towards menopause and life in general.
Excess Vata (air) may also be reduced to proper levels by having regularity of routine, enough rest to
the body, meditation and using vata pacifying essential oils.