The Human Body

This site is all about human body. From basics to higher levels. It is equally useful to children as well as professionals.

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TREATMENT OF PEPTIC ULCER

Posted by Prakash
Saturday, September 17, 2011
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Peptic ulcer is defined as mucosal erosion equal to or greater than 0.5cm. It is the commonest ulcer in the gastrointestinal tract. Although the pathogenesis of peptic ulcer disease is not fully understood, three major causative factors are recognized: 1) Infection with gram negative Helicobacter pylori, 2) increased hydrochloric acid secretion and 3) inadequate mucosal defense against gastric acid. Treatment approaches include:
  • Eradicating the H. pylori infection
  • Reducing secretion of gastric acid or neutralizing the acid after it is released, and/or
  • Providing agents that protect the gastric mucosa from damage.

 Above figure summarizes drugs that are effective in treating peptic ulcer disease.

INTRAMUSCULAR INJECTION SITES

Posted by Prakash
Saturday, September 10, 2011
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Intramuscular injections are used when rapid absorption is needed, because muscle has a good blood supply. Common sites are the buttock (gluteus medius), the lateral thigh (vastus lateralis), and the shoulder (deltoid).Since these muscles contain major muscles of the body, great care should be taken while giving the injection so that the nerves are not injured. These sites are shown in the given figure.

MUSCLES OF HIP AND LEGS

Posted by Prakash
Tuesday, September 6, 2011
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The hip muscles that move the thigh are anchored to the pelvic bone and cross the hip joint to the femur. Among these are the gluteus maximus (extension), gluteus medius (abduction), and iliopsoas (flexion). The muscles that form the thigh include the quadriceps group anteriorly and the hamstring group posteriorly. For most people, the quadriceps is stronger than the hamstrings, which is why athletes more often have a “pulled hamstring” rather than a “pulled quadriceps.” Movement of the knee joint depends on thigh muscles and lower leg muscles. Movement of the foot depends on lower leg muscles such as the gastrocnemius (dorsiflexion or flexion) and the tibialis anterior (plantar flexion or extension). See table 4 for details.

MUSCLES OF SHOULDER AND ARMS

Posted by Prakash
Sunday, September 4, 2011
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The triangular deltoid muscle covers the point of the shoulder like a cap, and can pull the humerus to the side (abduction), forward (flexion), or backward (extension). You already know the functions of the biceps brachii and triceps brachii, the muscles that form the bulk of the upper arm. Other muscles partially in the upper arm help bend the elbow (flexion). The muscles that form the bulk of the forearm are the flexors and extensors of the hand and fingers. You can demonstrate this yourself by clasping the middle of your right forearm with your left hand, then moving your right hand at the wrist and closing and opening a fist; you can both feel and see the hand and finger muscles at work. See table 3 for details.






MAJOR MUSCLES OF THE TRUNK

Posted by Prakash
Friday, September 2, 2011
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The muscles of the trunk cannot be described with one or two general functions. Some form the wall of the trunk and bend the trunk, such as the rectus abdominis (flexion) and the sacrospinalis group (extension). The trapezius (both together form the shape of a trapezoid) is a large muscle that can raise (shrug) the shoulder or pull it back, and can help extend the head. Other muscles found on the trunk help move the arm at the shoulder. The pectoralis major is a large muscle of the chest that pulls the arm across the chest (flexion and adduction). On the posterior side of the trunk, the latissimus dorsi pulls the arm downward and behind the back (extension and adduction). These muscles have their origins on the bones of the trunk, the sternum, the or vertebrae, which are strong, stable anchors. Another set of muscles forms the pelvic floor, where the muscles support the pelvic organs and assist with urination and defecation. Yet another category is the muscles that are concerned with breathing. These are the intercostal muscles between the ribs and the diaphragm that separates the thoracic and abdominal cavities. See table 2 for details.


MAJOR MUSCLES OF HEAD AND NECK

Posted by Prakash
Thursday, September 1, 2011
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Three general groups of muscles are found in the head and neck: those that move the head or neck, the muscles of facial expression, and the muscles for chewing. The muscles that turn or bend the head, such as the sternocleidomastoids (flexion) and the pair of splenius capitis muscles (extension), are anchored to the skull and to the clavicle and sternum anteriorly or the vertebrae posteriorly. The muscles for smiling or frowning or raising our eyebrows in disbelief are anchored to the bones of the head or to the undersurface of the skin of the face. The masseter is an important chewing muscle in that it raises the mandible (closes the jaw).See table 1 for details of muscles of head and neck.


TYPES OF NEURON

Posted by Prakash
Wednesday, August 31, 2011
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Neurons may be classified into three groups: sensory neurons, motor neurons, and interneurons.

Sensory neurons (or afferent neurons) carry impulses from receptors to the central nervous system. Receptors detect external or internal changes and send the information to the CNS in the form of impulses by way of the afferent neurons. The central nervous system interprets these impulses as a sensation. Sensory neurons from receptors in skin, skeletal muscles, and joints are called somatic; those from receptors in internal organs are called visceral sensory neurons.

Motor neurons (or efferent neurons) carry impulses from the central nervous system to effectors. The two types of effectors are muscles and glands. In response to impulses, muscles contract or relax and glands secrete. Motor neurons linked to skeletal muscle are called somatic; those to smooth muscle, cardiac muscle, and glands are called visceral. Sensory and motor neurons make up the peripheral nervous system. Visceral motor neurons form the autonomic nervous system, a specialized subdivision of the PNS that will be discussed later in this chapter.

Interneurons are found entirely within the central nervous system. They are arranged so as to carry only sensory or motor impulses, or to integrate these functions. Some interneurons in the brain are concerned with thinking, learning, and memory. A neuron carries impulses in only one direction. This is the result of the neuron’s structure and location, as well as its physical arrangement with other neurons and the resulting pattern of synapses. The functioning nervous system, therefore, is an enormous network of “one-way streets,” and there is no danger of impulses running into and canceling one another out.

FACTORS AFFECTING BONE GROWTH

Posted by Prakash
Tuesday, August 30, 2011
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1. Heredity—each person has a genetic potential for height, that is, a maximum height, with genes inherited from both parents. Many genes are involved, and their interactions are not well understood. Some of these genes are probably those for the enzymes involved in cartilage and bone production, for this is how bones grow.

2. Nutrition—nutrients are the raw materials of which bones are made. Calcium, phosphorus, and protein become part of the bone matrix itself. Vitamin D is needed for the efficient absorption of calcium and phosphorus by the small intestine. Vitamins A and C do not become part of bone but are necessary for the process of bone matrix formation (ossification). Without these and other nutrients, bones cannot grow properly. Children who are malnourished grow very slowly and may not reach their genetic potential for height.

3. Hormones—endocrine glands produce hormones that stimulate specific effects in certain cells. Several hormones make important contributions to bone growth and maintenance. These include growth hormone, thyroxine, parathyroid hormone, and insulin, which help regulate cell division, protein synthesis, calcium metabolism, and energy production. The sex hormones estrogen or testosterone help bring about the cessation of bone growth. The hormones and their specific functions are listed in Table.

4. Exercise or “stress”—for bones, exercise means bearing weight, which is just what bones are specialized to do. Without this stress (which is normal), bones will lose calcium faster than it is replaced. Exercise need not be strenuous; it can be as simple as the walking involved in everyday activities. Bones that do not get this exercise, such as those of patients confined to bed, will become thinner and more fragile.

EMBRYONIC GROWTH OF BONES

Posted by Prakash
Saturday, August 27, 2011
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During embryonic development, the skeleton is first made of cartilage and fibrous connective tissue, which are gradually replaced by bone. Bone matrix is produced by cells called osteoblasts (a blast cell is a “growing” or “producing” cell, and osteo means “bone”). In the embryonic model of the skeleton, osteoblasts differentiate from the fibroblasts that are present. The production of bone matrix, called ossification, begins in a center of ossification in each bone.

The cranial and facial bones are first made of fibrous connective tissue. In the third month of fetal development, fibroblasts (spindle-shaped connective tissue cells) become more specialized and differentiate into osteoblasts, which produce bone matrix. From each center of ossification, bone growth radiates outward as calcium salts are deposited in the collagen of the model of the bone. This process is not complete at birth; a baby has areas of fibrous connective tissue remaining between the bones of the skull. These are called fontanels, which permit compression of the baby’s head during birth without breaking the still thin cranial bones. The fontanels also permit the growth of the brain after birth. You may have heard fontanels referred to as “soft spots,” and indeed they are. A baby’s skull is quite fragile and must be protected from trauma. By the age of 2 years, all the fontanels have become ossified, and the skull becomes a more effective protective covering for the brain.

The rest of the embryonic skeleton is first made of cartilage, and ossification begins in the third month of gestation in the long bones. Osteoblasts produce bone matrix in the center of the diaphyses of the long bones and in the center of short, flat, and irregular bones. Bone matrix gradually replaces the original cartilage.

The long bones also develop centers of ossification in their epiphyses. At birth, ossification is not yet complete and continues throughout childhood. In long bones, growth occurs in the epiphyseal discs at the junction of the diaphysis with each epiphysis. An epiphyseal disc is still cartilage, and the bone grows in length as more cartilage is produced on the epiphysis side. On the diaphysis side, osteoblasts produce bone matrix to replace the cartilage. Between the ages of 16 and 25 years (influenced by estrogen or testosterone), all of the cartilage of the epiphyseal discs is replaced by bone. This is called closure of the epiphyseal discs (or we say the discs are closed), and the bone lengthening process stops.

Also in bones are specialized cells called osteoclasts (a clast cell is a “destroying” cell), which are able to dissolve and reabsorb the minerals of bone matrix, a process called resorption. Osteoclasts are very active in embryonic long bones, and they reabsorb bone matrix in the center of the diaphysis to form the marrow canal. Blood vessels grow into the marrow canals of embryonic long bones, and red bone marrow is established. After birth, the red bone marrow is replaced by yellow bone marrow. Red bone marrow remains in the spongy bone of short, flat, and irregular bones. For other functions of osteoclasts and osteoblasts, 

CANCER- ABNORMAL CELLULAR FUNCTIONING

Posted by Prakash
Thursday, August 25, 2011
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There are more than 200 different types of cancer, all of which are characterized by abnormal cellular functioning. Normally, our cells undergo mitosis only when necessary and stop when appropriate. A cut in the skin, for example, is repaired by mitosis, usually without formation of excess tissue. The new cells fill in the damaged area, and mitosis slows when the cells make contact with surrounding cells. This is called contact inhibition, which limits the new tissue to just what is needed. Malignant (cancer) cells, however, are characterized by uncontrolled cell division. Our cells are genetically programmed to have particular life spans and to divide or die. One gene is known to act as a brake on cell division; another gene enables cells to live indefinitely, beyond their normal life span, and to keep dividing. Any imbalance in the activity of these genes may lead to abnormal cell division. Such cells are not inhibited by contact with other cells, keep dividing, and tend to spread.

A malignant tumor begins in a primary site such as the colon, then may spread or metastasize. Often the malignant cells are carried by the lymph or blood to other organs such as the liver, where secondary tumors develop. Metastasis is characteristic only of malignant cells; benign tumors do not metastasize but remain localized in their primary site.

What causes normal cells to become malignant? At present, we have only partial answers. A malignant cell is created by a mutation, a genetic change that brings about abnormal cell functions or responses and often leads to a series of mutations. Environmental substances that cause mutations are called carcinogens. One example is the tar found in cigarette smoke, which is definitely a cause of lung cancer. Ultraviolet light may also cause mutations, especially in skin that is overexposed to sunlight. For a few specific kinds of cancer, the trigger is believed to be infection with certain viruses that cause cellular mutations. Carriers of hepatitis B virus, for example, are more likely to develop primary liver cancer than are people who have never been exposed to this virus. Research has discovered two genes, one on chromosome 2 and the other on chromosome 3, that contribute to a certain form of colon cancer. Both of these genes are the codes for proteins that correct the “mistakes” that may occur when the new DNA is synthesized. When these repair proteins do not function properly, the mistakes (mutations) in the DNA lead to the synthesis of yet other faulty proteins that impair the functioning of the cell and predispose it to becoming malignant.

Once cells have become malignant, their functioning cannot return to normal, and though the immune system will often destroy such cells, sometimes it does not, especially as we get older. Therefore, the treatments for cancer are directed at removing or destroying the abnormal cells. Surgery to remove tumors, radiation to destroy cells, and chemotherapy to stop cell division or interfere with other aspects of cell metabolism are all aspects of cancer treatment.

New chemotherapy drugs are becoming more specific, with very precise targets. For example, the cells of several types of solid-tumor cancers have been found to have mutations in the gene for the cell membrane receptor for a natural growth factor (epidermal growth factor receptor, or EGFR). These altered receptors, when triggered by their usual growth factor, then cause the cell to divide uncontrollably, an abnormal response. Medications that target only these altered receptors have already been developed for some forms of lung cancer and breast cancer. Not only do they show promise in treating the cancer, they do not have the side effects of other forms of chemotherapy.

AGING

Posted by Prakash
Wednesday, August 24, 2011
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Multicellular organisms, including people, age and eventually die; our cells do not have infinite life spans. It has been proposed that some cells capable of mitosis are limited to a certain number of divisions; that is, every division is sort of a tick-tock off a biological clock. We do not yet know exactly what this cellular biological clock is. There is evidence that the ends of chromosomes, called telomeres, may be an aspect of it. With each cell division, part of the telomeres is lost (rather like a piece of rope fraying at both ends), and eventually the telomeres are gone. With the next division, the ends of the chromosomes, actual genes, begin to be lost. This may be one signal that a cell’s life span has come to an end (there are probably many different kinds of signals).

Cellular aging also involves the inevitable deterioration of membranes and cell organelles. Just as the parts of a car break down in time, so too will cells. Unlike cars or machines, however, cells can often repair themselves, but they do  have limits. As cells  age, structural proteins  break down  and  are not
replaced, or necessary enzymes are not synthesized. Proteins called chaperones, which are responsible for the  proper folding of many other proteins and for the repair or disposal of damaged  proteins, no
longer function as well as cells age. Without chaperones, damaged proteins accumulate within cells and
disrupt normal cellular processes. Clinical manifestations of impaired chaperones include cataracts and neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease.

Much about the chemistry of the aging process remains a mystery, though we can describe what happens to organs and to the body as a whole. Keep in mind that a system is the sum of its cells, in tissues and organs, and that all aging is ultimately at the cellular level.

ANEMIA

Posted by Prakash
Tuesday, August 23, 2011
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Anemia is a deficiency of red blood cells, or insufficient hemoglobin within the red blood cells. There are many different types of anemia.

 Iron-deficiency anemia is caused by a lack of dietary iron, and there is not enough of this mineral to form sufficient hemoglobin. A person with this type of anemia may have a normal RBC count and a normal hematocrit, but the hemoglobin level will be below normal.

A deficiency of vitamin B12, which is found only in animal foods, leads to pernicious anemia, in which the RBCs are large, misshapen, and fragile. Another cause of this form of anemia is lack of the intrinsic factor due to autoimmune destruction of the parietal cells of the stomach lining.

Sickle-cell anemia has already been discussed in previous post. It is a genetic disorder of hemoglobin, which causes RBCs to sickle, clog capillaries, and rupture.

Aplastic anemia is suppression of the red bone marrow, with decreased production of RBCs, WBCs, and platelets. This is a very serious disorder that may be caused by exposure to radiation, certain chemicals such as benzene, or some medications. There are several antibiotics that must be used with caution since they may have this potentially fatal side effect.

Hemolytic anemia is any disorder that causes rupture of RBCs before the end of their normal life span. Sickle-cell anemia and Rh disease of the newborn are examples. Another example is malaria, in which a protozoan parasite reproduces in RBCs and destroys them. Hemolytic anemias are often characterized by jaundice because of the increased production of bilirubin.


Apart from the above mentioned anemias, there are few others like megaloblastic anemia, sideroblastic anemia etc. These are somehow related to the above mentioned anemias. No matter whatever the cause of anemia be its signs and symptoms are similar. Cause is basically needed for the proper treatment of the disease.

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