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 Anatomy and Physiology of the liver  Human liver development begins during the third week of gestation and does not acheive mature architecture until about 15 years of age. It reaches its largest relative size, 10% of fetal weight, around the ninth week. It is about 5% of body weight in the healthy neonate. The liver is about 2% of body weight in the adult. It weighs around 1400gm in an adult female and about 1800gm in the male.  The liver is located in the right upper quadrant of the abdomen, just below the diaphragm. It is almost completely behind the rib cage but the lower edge may be palpated along the right costal margin during inspiration. A connective tissue layer called Glisson's capsule covers the surface of the liver. The capsule extends to invest all but the smallest the vessels within the liver.  The falciform ligament attaches the liver to the abdominal wall and diaphragm and divides the liver into a larger right lobe and a smaller left lobe.  In 1957, the French surgeon Claude Couinaud described 8 liver segments. Since then, radiographic studies describe an average of twenty segments based on distribution of blood supply. Each segment has its own independent vascular and biliary branches. Surgeons utilize these independent segments when performing liver resection for tumor or transplantation. There are at least three reasons why segmental resection is superior to simple wedge resection. First, segmental resection minimizes blood loss because vascular density is reduced at the borders between segments. Second, it results in improved tumor removal for those cancers which are disseminated via intrasegmental branches of the portal vein. Third, segmental resection spares normal liver allowing for repeat partial hepatectomy.  Each segment of the liver is further divided into lobules. Lobules are usually represented as discrete hexagonal aggregations of hepatocytes. The hepatocytes assemble as plates which radiate from a central vein. Lobules are served by arterial, venous and biliary vessels at their periphery. This model is useful for teaching purposes but more closely resembles the adult pig lobule than the human. Human lobules have little connective tissue separating one lobule from another. The paucity of connective tissue makes it more difficult to identify the portal triads and the boundaries of individual lobules. Central veins are easier to identify due to their large lumen and because they lack connective tissue that invests the portal triad vessels.  Lobules consist of hepatocytes and the spaces between them. Sinusoids are the spaces between the plates of hepatocytes. Sinusoids receive blood from the portal triads. About 25% of total cardiac output enters the sinusoids via terminal portal and arterial vessels. Seventy-five percent of the blood flowing into the liver comes through the portal vein; the remaining 25% is oxygenated blood that is carried by the hepatic artery. The blood mixes, passes through the sinusoids, bathes the hepatocytes and drains into the central vein. About 1.5 liters of blood exit the liver every minute.  The liver is central to a multitude of physiologic functions, including: • Clearance of damaged red blood cells & bacteria by phagocytosis • Nutrient management • Synthesis of plasma proteins such as albumin, globulin, protein C, insulin-like growth factor, clotting factors etc. • Biotransformation of toxins, hormones, and drugs • Vitamin & mineral storage  Phagocytosis Red blood cell (RBC) lifespan is about 120 days. Reticuloendothelial (macrophage) cells in the spleen, liver and bone marrow are primarily responsible for clearing pathogens and debris. Kupffer cells are reticuloendothelial cells resident in the liver sinusoids that scavange damaged RBCs and bacteria as they pass through. Hundreds of millions of RBCs are removed by the reticuloendothelial system every minute. Kupffer cells, like other reticuloendothelial macrophages, lyse RBCs into heme and globin. Globin is further catabolized into polypeptide components for reuse. Heme is broken into biliverdin and iron. Biliverdin is converted to bilirubin. Iron is transported by transferrin to the liver and spleen for storage and to the bone for hematopoiesis.  About 85% of bilirubin is derived from lysis of RBCs, the rest comes from the breakdown of other hemoproteins like myoglobin, cytochromes and peroxidases. Kupffer cells like other reticuloendothelial macrophages release bilirubin into the blood. In the blood, bilirubin binds to albumin. The albumin/bilirubin compound is small enough to pass through the endothelial fenestrae and into the space of Disse where it contacts the hepatocyte.  Hepatocytes cleave bilirubin from albumin and absorb the bilirubin. In the hepatocyte cytoplasm, bilirubin is conjugated to glucouronic acid. Bilirubin uridine diphosphate glucuronyl transferase (UDPGT) catalyzes the bonding of glucuronic acid and bilirubin to produce water-soluble bilirubin. Water soluble conjugated bilirubin is secreted into canaliculi along with water, electrolytes, bicarbonate, bile acids, salts, cholesterol and phospholipids. This combination is called bile and serves as a detergent to keep bile soluble in the biliary tract. Bile drains from the canaliculi>canal of Hering>bile ducts>common hepatic duct>gallbladder>common bile duct>ampulla of  vater>duodenum.  In the duodenum, bile salts attach to fat globules forming smaller micelles that collect fatty acids and glycerol. The micelles travel to the jejunum where they deliver their cargo to the intestinal epithelium. Inside the epithelial cells glycerol and fatty acids are rejoined to form triglycerides. Finally triglycerides are joined to cholesterol and proteins are added to the surface; creating a chylomicron.  Lipid management The liver receives a variety of lipid forms including: chylomicrons remnants, very low density lipoproteins (VLDL), low density lipoproteins (LDL), high density lipoproteins (HDL) and fatty acids. Large lipoprotein molecules are broken into smaller units by the lytic action of lipoprotein lipase (LPL) expressed on endothelium of vessels. Circulating lipoproteins small enough to enter the space of Disse attach to receptors on the hepatocyte. These lipoprotein remnants are held near the heptocyte surface and exposed to hepatic lipase compounds. Low Density Lipoprotein receptors transfer the lipoprotein fragments into the hepatocyte by the process of endocytosis.  • Chylomicrons are the product of intestinal packaging of dietary fats. Chylomicrons are produced in the duodenal villi and secreted into the lymph lacteals for delivery to the thoracic duct > subclavian vein > superior vena cava > right ventricle > lungs > Left ventricle > aorta > hepatic artery>sinusoid.Chylomicrons range from 75-1200nm in diameter. They contain 98% lipids and 2% protein. Chylomicrons are degraded in the blood by contact with LPL. Chylomicrons become smaller and more dense as fatty acids are stripped off. Loss of fatty acids results in chylomicron remnants of various sizes and density when they finally reach the liver. Hepatic lipase expressed by the hepatic sinusoidal endothelium and hepatocytes continues the remnant degradation. • Very low density lipoproteins (VLDL) are synthesized primarily in the hepatocyte. VLDLs range from 30-80nm. They contain 90% lipids and 10% protein. Their purpose is to transport triglycerides made in the liver into plasma for use or storage outside the liver. • Low density lipoprotein (LDL) is formed from VLDLs in the plasma by the action of lipase. LDL diameter is about 20nm. They contain 70% lipids and 30% protein. LDLs distribute cholesterol throughout the body. Cholesterol is an important constituent of: VLDL, cell membranes, hormones, bile etc. • High density lipoprotein (HDL) is small lipoprotein particles (5-15nm) formed in the liver and intestine. They range from 5-15nm in diameter. They contain 50% lipids and 50% protein. HDLs collect cholesterol & lipoprotein fragments from the blood and blood vessel plaques and return them to the liver for repurposing. • Fatty acids are linear hydrocarbon chains that are the major constituents of dietary lipoproteins (triglycerides). The liver degrades lipoproteins with hepatic lipase or synthesizes fatty acids from carbohydrate sources. When carbohydrate energy sources are low fatty acids are oxidized for energy.  Carbohydrate management: When energy intake exceeds energy output the body stores the surplus glucose as glycogen or triglyceride. When energy output exceeds energy intake the body reacts by releasing stored energy as glucose and fatty acids.  Glucose is the preferred energy source for most tissues but the body maintains very limited supplies of free circulating glucose. Certain tissues like the brain, RBCs, lens and cornea use glucose almost exclusively. To supply these tissues when blood glucose drops the liver lyses glycogen. Glycogen is a complex molecule composed of thousands of glucose units. Hepatocytes and myocytes store glucose as intracellular glycogen granules. The liver is central to blood glucose management because the liver is the only organ that can store and release glucose into the blood for use by other organs. After a meal the liver removes excess blood glucose and stores up to 8% of its weight as glycogen. Myocytes can store about 1-2% of total muscle mass as glycogen but once glucose enters a myocyte it must be used or stored by that myocyte. Myocytes lack the enzyme necessary to release glucose into the circulation.  The liver uses three metabolic processes to manage carbohydrates and insure adequate blood glucose: • Glycogenesis - excess glucose, fructose, and galactose are converted to glycogen and stored in the liver. • Glycogenolysis - when blood glucose falls, the liver breaks down stored glycogen to raise blood glucose levels • Gluconeogenesis - the liver can synthesize glucose from lactic acid, some amino acids and glycerol. When glucose is low the liver can derive energy from the metabolism of fatty acids which can conserve available glucose.  Protein management: Dietary protein is denatured by stomach acids and digested into amino acids in the small intestine. Amino acids are absorbed by the small intestine and delivered to the liver via the portal circulation. Up to 50% of the livers' energy requirements can be supplied by amino acid oxidation. Oxidative deamination breaks amino acids into keto acid and an ammonia molecule. The keto acid is used in the Kreb's cycle to produce ATP. The liver combines ammonia with CO2 to form urea and H2O.  The liver also uses dietary amino acids and those released during normal tissue breakdown to produce its own proteins and enzymes as well as plasma proteins. Plasma proteins produced by hepatocytes include: albumin, fibrinogen, prothrombin, a-fetoprotein, a2-macroglobin, hemopexin, transferrin, complenent components C3,C6 andC1, a1-antitrypsin, caeruloplasmin.  • Albumin is only produced by the liver and equals about 50% its total protein synthesis. About 12 grams of albumin are synthesized by the normal liver daily. Patients with decompensated cirrhosis produce only about 4 g per day. About 40% of total albumin is intrascular. • a-fetoprotein peaks about 16 weeks gestation and disappears a few weeks after birth. It may reappear in association with chronic hepatitis and a number of carcinomas • a1-antitrypsin deficiency is inherited • a2-macroglobin functions as a protease inhibitor. It is active in the inhibition of thrombin and plasmin. • Hemopexin transports heme in the plasma protecting tissues from the actions of heme. • Transferrin is globulin that transports heme to bone marrow for incorporation into erythroid precursors. • Complement components assist the immune system to raise an immune response. • Caeruloplasmin is the major copper carrying plasma protein. • Biotransformation.  Hepatocytes protect the body from injury by biotransforming toxins and drugs and by deactivating hormones. The liver employs enzymes to make substances more water soluble, so they can be excreted from the body in the urine and feces. In Phase 1 biotransformations the cytochrome P450 enzymes alter the target molecule by adding or exposing functional groups such as -OH or -COOH. Phase 2 biotransformation enzymes add sugars, amino acids, sulfates or acetyl groups to the functional group which makes them more water soluble.  Vitamins The liver also plays an important role in vitamin and mineral (iron & copper) storage. About 80% of the body's vitamin A stores are concentrated in fat droplets within the stellate cells of the liver. In pathological conditions like hepatic fibrosis or liver cirrhosis the stellate cells lose vitamin A, transform into fibroblasts or myofibroblasts and begin producing large amounts of collagen and adhesive glycoproteins. Normal vitamin A reserves are enough to prevent a deficiency for about 10 months. The liver also contains about a year supply of B12. Vitamin D stores equal about 3-4 months. Small amounts of Vitamins E and K and Vitamin C are stored in the liver to facilitate liver functions.



For Direct Consultation
Please Visit

Dr.D.Senthil Kumar, B.H.M.S., M.D(Alt Med)., M.Phil(Psy)
Consulting Homoeopath & Psychologist

Vivekanantha Homoeo Clinic & Psychological Counselling Center
Dr.Senthil Kumar’s Consultation Schedule

Chennai –
Head Office

Wednesday to Saturday:- 10.00am to 1.30pm &
5.00pm to 8.30pm
Sunday: - 11.00am to 03.00pm
(Consultation by Appointment only)
For Appointment
Please call: 09443054168,
82 & 83, 1st floor,
Velachery Railway Station Road,
Annai Indira Nagar,
(Very Next Building To Velachery Railway Station), Velachery
Chennai 600042
Panruti
Branch Office



Monday & Tuesday.
10.00am to 12.45pm &
05.30pm to 8.30pm
(Consultation by Appointment only)
For Appointment
Please call: 09443054168,

126, Chennai Salai,
(Near Raliway Gate, Direct Opposite to Lakshmi Villas Bank ATM), Panruti-607106,
Cuddalore District,
Tamil Nadu, India For
Pondicherry
Branch Office

Every Saturday:
11.00am to 02.00pm
(Consultation by Appointment only)
Appointment
Please call: 09443054168,



NB:-
Ø  We are taking only minimum number of patients per day.
Ø  We are allotting 40 to 5o minutes for new patients & 15 to 20 minutes for follow-ups.
Ø  So be there at time to avoid unwanted waiting
Ø  we concentrate more to patient’s privacy, so we are allotting 40 to 50 minutes/client – “so be there at time”
Ø  We treat Many Diseases, so no one can know for what problem you are taking the treatment – So feel free to talk with Doctor and visit the Clinic.

For Appointment
Please call: 09443054168, 09786901830
Please call the Doctor and explain your problems in short, then SMS your Name – Mobile Number - Problem in Single word - date and day - Place of appointment (Eg: Rajini - 99xxxxxxx0 – Psoriasis – 21st Oct Sunday - Chennai)

You will receive Appointment details through SMS


Get Appointment





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Alopecia Areata





What Is Alopecia Areata?

Alopecia areata is considered an autoimmune disease, in which the immune system, which is designed to protect the body from foreign invaders such as viruses and bacteria, mistakenly attacks the hair follicles, the tiny cup-shaped structures from which hairs grow. This can lead to hair loss on the scalp and elsewhere.


In most cases, hair falls out in small, round patches about the size of a quarter. In many cases, the disease does not extend beyond a few bare patches. In some people, hair loss is more extensive. Although uncommon, the disease can progress to cause total loss of hair on the head (referred to as alopecia areata totalis) or complete loss of hair on the head, face, and body (alopecia areata universalis).


Hair Loss Information

In the contemporary times, people are becoming more and more conscious about their looks. And when it comes to looking good, maintaining shiny smooth hair, undoubtedly, becomes of prime importance. It is here where conditions like baldness, thinning of hair and loss of hair become a cause of concern.


Causes

In alopecia areata, immune system cells called white blood cells attack the rapidly growing cells in the hair follicles that make the hair. The affected hair follicles become small and drastically slow down hair production. Fortunately, the stem cells that continually supply the follicle with new cells do not seem to be targeted. So the follicle always has the potential to re grow hair.


Hair loss symptoms:

· Hair fall on clothes after combing

· Gradual appearance of bald patches

· Receding hairline


Causes of baldness:

· Lack of nutrition

· Mental stress and strain

· Prolonged illness like typhoid, chronic cold etc

· Lack of personal hygiene like unclean conditions of scalp


Hair Loss a Symptom of a Serious Disease?

Alopecia areata is not a life-threatening disease. It does not cause any physical pain, and people with the condition are generally healthy otherwise. But for most people, a disease that unpredictably affects their appearance the way alopecia areata does is a serious matter.


The effects of alopecia areata are primarily socially and emotionally disturbing. In alopecia universalis, however, loss of eyelashes and eyebrows and hair in the nose and ears can make the person more vulnerable to dust, germs, and foreign particles entering the eyes, nose, and ears.

Alopecia areata often occurs in people whose family members have other autoimmune diseases, such as diabetes, rheumatoid arthritis, thyroid disease, systemic lupus erythematosus, pernicious anaemia, or Addison's disease. People who have alopecia areata do not usually have other autoimmune diseases, but they do have a higher occurrence of thyroid disease, Atopic eczema, nasal allergies, and asthma.


Hair Ever Grow Back?

There is every chance that your hair will re grow, but it may also fall out again. No one can predict when it might re grow or fall out. The course of the disease varies from person to person. Some people lose just a few patches of hair, then the hair re grows, and the condition never recurs. Other people continue to lose and re grows hair for many years. A few lose all the hair on their head; some lose all the hair on their head, face, and body. Even in those who lose all their hair, the possibility for full re growth remains.


In some, the initial hair re growth is white, with a gradual return of the original hair colour. In most, the re grown hair is ultimately the same colour and texture as the original hair.


Alopecia Areata Treatment

Conventional Drugs

The following are some commonly used medicines for alopecia areata. Keep in mind that while these treatments may promote hair growth, none of them prevent new patches or actually cure the underlying disease.
Corticosteroids, Minoxidil (5%), Anthralin (Psoriatic), Sulfasalazine, Oral cyclosporine


Homoeopathic Treatment

Homoeopathic medicines acts best in Alopecia Areata

For treatment please click the following link

http://treatmentt.blogspot.com/2009/11/alopecia-areata-treatment.html




For Direct Consultation Please visit


Chennai - Head Office

(Consultation by Appointment only)

Vivekanantha Homeo Clinic & Psychological Counseling Center

B-12, Second Floor, Paramount Park (Dr Plaza) - B Block,

Velachery Main Road,

Direct Opposite to Saravana Stores, Mega mart upstairs,

Near Vijaya nagar Bus Stand,Velachery, Chennai 42,


Panruti – Branch Office

Vivekanantha Homoeo clinic & Psychological Counseling Center

126,Chennai Salai

( Near Railway Gate, Lakshmi Villas Bank ATM Direct Opposite)

Panruti 607106

Cuddalore District

Tamilnadu


For Appointment

Please call: 09443054168, 09786901830


Pondicherry Camp

(Consultation by Appointment only)

Every Saturday:11.00am to 04.00pm


NB:-

Ø We are taking only minimum number of patients per day.

Ø We are allotting 40 to 5o minutes for new patients & 15 to 20 minutes for follow-ups.

Ø So be there at time to avoid unwanted waiting

Ø For Psychological consultation “we concentrate more to client’s privacy, so we are allotting 40 to 50 minutes/client – so be there at time


For Appointment

Please call: 09443054168, 09786901830


For Foreign patients

For more detail and mode of payment

Send mail to consult.ur.dr@gmail.com

Or

Call +91 9443054168, +91 9786901830


http://homeoall.com/

Professional secrecy will be maintained

(Your complaints and other Details should be kept very confidential)




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