Kidney Failure and Dialysis

If a person's kidneys fail to function properly, the only way to prevent toxic buildup in the body is to undergo dialysis.
There are two types of dialysis: hemodialysis and peritoneal dialysis. The most commonly recognized form of dialysis is hemodialysis. About 90 percent of dialysis patients receive hemodialysis. In this procedure, the blood is circulated from the body into a machine before being returned to the patient.
In order for hemodialysis to be performed, a doctor must make an access into the patient's blood vessels. This is done by minor surgery in the leg, arm or sometimes neck. The best access for most patients is called a fistula, wherein minor surgery is performed to join an artery to a vein under the skin to make a larger vessel.
If no vessels are suitable for a fistula, the doctor uses a soft plastic tube called a vascular graft to join the artery and vein.
Once the access is made and healed, two needles are inserted in the fistula or graft, one on the artery side and one on the vein side.
For temporary dialysis in the hospital, a patient might require a catheter implanted into a large vein in the neck.
A dialysis machine is composed of two parts: one side for blood and one for a fluid called dialysate. A thin, semipermeable membrane separates the two sides. Particles of waste from the blood pass through microscopic holes in the membrane and are washed away in the dialysate. Blood cells are too large to go through the membrane and are returned to the body.
The benefits of hemodialysis are that the patient requires no special training, and he or she is monitored regularly by someone trained in providing dialysis.
The other type of treatment, Continuous Ambulatory Peritoneal Dialysis (CAPD) uses the patient's own peritoneal membrane as a filter. This membrane, like the membrane in the dialysis machine, is semipermeable. Waste particles can pass through it, but larger blood cells cannot.
The patient has a peritoneal catheter surgically implanted into the belly. He or she slowly empties about two quarts of dialysate fluid through the catheter into the abdomen. As the patient's blood is exposed to the dialysate through the peritoneal membrane, impurities are drawn through the membrane walls into the dialysate. The patient drains out the dialysate after three or four hours and pours in fresh fluid. The draining takes about half an hour and must be repeated about five times a day.
The main benefit of CAPD is freedom. The patient doesn't have to be at a dialysis clinic for several hours a day, three times a week. The dialysate can be exchanged in any well-lit, clean place, and the process is not painful. The drawback to this treatment is that there is a risk of infection of the peritoneal lining, and the process may not work well on very large people.
Pediatric patients often do a similar type of dialysis called Continuous Cycling Peritoneal Dialysis (CCPD). Their treatments can be done at night while they sleep. A machine warms and meters dialysate in and out of their abdomens for 10 hours continuously. In this way, they are free from treatments during the day.
This information was gathered from http://www.fda.gov/fdac/features/1998/198_dial.html

The toll on a person who must endure dialysis can be quite high both physically and mentally. Persons with kidney failure often feel ill and tired in spite of dialysis. Hemodialysis is time-consuming and leaves the patient with little freedom to enjoy other activities. Often the patient with kidney failure doesn't feel well enough to consider other activities, even if hemodialysis weren't so time consuming. In spite of the blood-cleaning function of dialysis, the body's toxins still have an effect. People with kidney failure are often flushed or sweating.
I knew a young man in high school whose father had been undergoing dialysis for a number of years. He was in constant pain and eventually committed suicide to escape from the pain and hopelessness of his situation.
A gentleman who was a patient in a long-term care facility where I worked had himself admitted so that we could perform hospice care on him. He had voluntarily ceased his dialysis treatments and knew that he was going to die. His blood pressure was often so high that it was impossible to measure. His appetite was very poor and his skin was usually clammy. He was constantly nauseated and sometimes in terrible pain. He died within a week. I have always remembered him for his gentle personality and friendly attitude in the face of his illness and impending death.
A man in another long-term care facility where I worked had been dialysis for many years. His skin eventually began breaking down and in spite of our best efforts, he developed severe bed sores because he was constantly oozing B.M. and the acidic quality of the stool ate away at his skin. He had been a doctor and my mother, who was a nurse at the facility, conferred with him. Between his medical knowledge and their frank discussion, he made the decision to discontinue his dialysis treatments. After two days he slipped into a coma and was dead within five days.
There are several causes for kidney failure. This website sums them up with simple, easily understandable terminology.
http://www.kidneypatientguide.org.uk/site/fail.php

The Nasal Conchae

What is the purpose of the conchae? How do they increase turbulance of air flow and why would this be useful?
The conchae, or turbinates, are long curled bones protruding into the nasal passages. They divide the nasal airway into three groove-like air passages –and are responsible for forcing inhaled air to flow in a steady, regular pattern around the largest possible surface of cilia and climate controlling tissue. They are lined with pseudo-stratified columnar ciliated respiratory epithelium. The turbinates comprise most of the mucosal tissue of the nose. They contain many airflow pressure and temperature sensing nerve receptors, which are linked to the trigeminal, or fifth cranial nerve.
As a whole, the turbinates are responsible for filtration, heating and humidification of air inhaled through the nose. As air passes over the turbinate tissues it is heated to body temperature, humidified (up to 98% water saturation) and filtered.
There are three turbinates. The inferior turbinates are the largest. They are responsible for airflow direction, humidification, heating, and filtering of air inhaled through the nose.
The smaller middle turbinates project downwards over the openings of the maxillary and ethmoid sinuses, and act as buffers to protect the sinuses from coming in direct contact with pressurized nasal airflow. Some areas of the middle turbinates are also innervated by the olfactory bulb. Most inhaled airflow travels between the inferior turbinate and middle turbinate.
The superior turbinates are smaller still. They are connected to the middle turbinates by nerve endings, and serve to protect the olfactory bulb. The superior turbinates also protect the nerve axons which come through the cribriform plate into the nose.
The respiratory epithelium which covers the Lamina propria of the turbinates is part of the body’s first line of immunological defense. The respiratory epithelium is partially comprised of mucus producing goblet cells. This secreted mucus covers the nasal cavities, and serves as a filter, by trapping air-borne particles larger than 2 to 3 micrometers. The respiratory epithelium also serves as a means of access for the lymphatic system which protects the body from being infected by viruses or bacteria.
The turbinates provide necessary humidity to the delicate olfactory epithelium. If this epithelial layer becomes too dry or irritated, its function will be impaired. By directing and deflecting airflow across the mucosal surface of the inner nose, the turbinates are able to propel the inspired air. This, coupled with the humidity and filtration provided by the turbinates, helps to carry more scent molecules towards the high, narrow regions of the nasal airways, where olfaction nerve receptors are located.
If the turbinates become swollen, it leads to blockage of nasal breathing. Allergies, exposure to environmental irritants, persistent inflammation within the sinuses, or deformity or deviation of the nasal septum can lead to turbinate swelling.
Most information gathered from http://en.wikipedia.org/wiki/Turbinate

Cool Site

Click the title link to see some images of the respiratory system. Contains concise descriptions.

Damn shame...

That they couldn't get funding for the website you'll find if you click the title link.

My Respiratory Anatomy Paper

I know you will be just thrilled to read my descriptions of the respiratory anatomy!

1. Pharynx

a. Nasopharynx

The external nares, or nostrils, lead to the nasopharynx. The nasopharynx lies between the internal nares, or choanae, and the soft palate. On the lateral walls of the nasopharynx are the triangular pharyngeal ostia of the auditory tubes. These are bounded behind by the torus or cushion, a firm prominence formed by the medial end of the cartilage of the tube which elevates the mucous membrane. A vertical fold of mucous membrane, the salpingopharyngeal fold, stretches from the lower part of the torus; it contains the Salpingopharyngeus muscle. A second and smaller fold, the salpingopalatine fold, stretches from the upper part of the torus to the palate. Behind the ostium of the auditory tube is the pharyngeal recess, or fossa of Rosenmüller. The pharyngeal tonsils, or adenoids, are found on the posterior wall. Above the pharyngeal tonsil, the pharyngeal bursa forms an irregular flask-shaped depression which sometimes extends up as far as the basilar process of the occipital bone. The surface of the nasopharynx is covered by pseudostratified columnar epithelium. Goblet cells secrete mucus, which cleans, warms and moistens incoming air before it moved deeper into the respiratory tract. Blood vessels are seen at the base of the epithelium.

b. Oropharynx

The Oropharynx reaches from the soft palate to the epiglottis and hyoid bone. It opens anteriorly, through the isthmus faucium, into the mouth. In its lateral wall, between the two palatine arches, is the palatine tonsil.

c. Laryngopharynx
The Laryngopharynx, or hypopharynx, is the bottom part of the pharynx. It extends from the epiglottis to the cricoid cartilage of the larynx.
Along the oropharynx and the laryngopharynx, the epithelium changes to nonkeritinizing stratified squamous epithelium. The basement membrane varies in thickness and contains blood vessels as well.

2. Larynx
The larynx is a 1.5 inch long tube that is located in the throat below the base of the hyoid bone and tongue and anterior to the esophagus. Its walls are made up of nine rings of supportive cartilages supported by interconnecting ligaments, intrinsic and extrinsic muscles, and lined with mucosa. At the front is the thyroid cartilage, which creates the Adam's apple. The inferior horns of the thyroid cartilage rest on the ring-shaped cricoid cartilage which connects the larynx to the trachea. The cricoid cartilage is narrow in front and broader in back. The arytenoid cartilages are pyramid shaped. They sit on top of the back plate of the cricoid cartilage. At the superior tip of each arytenoid cartilage is a corniculate cartilage. They are shaped like small triangles. The cuneiform cartilages support the soft tissues of the aryepiglottic folds, which connect the arytenoid cartilages to the epiglottis. During swallowing, the cartilages close the entrance to the larynx so food and liquids cannot enter. The larynx also houses the vocal folds and ligaments. The vocal folds consist of connective tissues, muscles, and the vocal ligament which vibrates to produce the vocal sounds. The surfaces of the vocal folds are covered by stratified squamous epithelium. Directly above the vocal folds are the vestibular, or false folds. They are formed by a thick layer of respiratory mucosa and a vestibular ligament. The vestibular folds lubricate and protect the vocal folds. The glottis forms the entryway to the vocal folds. It opens to allow for sounds.

3. Trachea
The trachea is 4 to 5 inches long. It runs through the lower neck and chest. It lies just anterior to the esophagus. It conducts air between the larynx and the primary bronchi. It is composed of 16-20 hyaline cartilage rings.
The tracheal wall is composed of four layers of tissue. The luminal surface is lined by respiratory mucosa. Its epithelium contains goblet cells to produce mucus which warms, moistens and removes foreign particles from air flowing to the trachea.
The submucosa consists mostly of loose connective tissue. It contains seromucous glands, which secrete water and mucus to the luminal surface of the trachea through narrow ducts.
The cartilage rings compose the next layer of the trachea. The outermost layer is the adventitia. It is a band of loose connective tissue which holds the trachea in place in the chest cavity.

4. Bronchi
The primary bronchi split off from the trachea and one enters each lung. The secondary bronchi, also known as lobular bronchi, each enter one lobe of the lungs. The tertiary bronchi branch off from the secondary bronchi. They conduct air to and from the ten bronchopulmonary segments in the right lung and eight in the left lung. The bronchi also have a layer of respiratory mucosa on their luminal surface with mucus-secreting goblet cells. The next layer is a broken ring of smooth muscle fibers which contract during exhalation and relax during inhalation. There are plates of hyaline cartilage which supports the tissue. In the micrograph of the bronchus wall, the alveoli can be seen. The mucosa of the bronchus wall is stained deep pink. The cartilage plates are light blue.

5. Lungs
The lungs are relatively cone-shaped sacs. They lie behind the rib cage. The lungs of mammals have a spongy texture and are honeycombed with epithelium having a much larger surface area in total than the outer surface area of the lung itself. A healthy lung is pink. The base of the lungs rests on the diaphragm muscle. The right lung is slightly larger and has three lobes while the left has only two. The lungs contain the bronchi and alveoli. The lungs are enveloped by plurae. The visceral pleura adheres to the outer surface of the lung. The parietal pleura is an extension of the visceral pleura. The pleurae are serous membranes. They secrete a thin layer of pleural fluid into the cavity that separates them.

6. Bronchial Tree
The bronchial tree is composed of the branches from the main bronchi that penetrate the lungs to deliver air to the alveoli. It is called the bronchial tree because it has the appearance of an inverted tree with the trachea as the trunk, branching into the primary bronchi, which then branch into the secondary bronchi, which branch into the tertiary bronchi, which terminate in the alveoli. The alveoli are the “leaves” of the tree.

7. Alveoli
The alveoli are the spherical outcroppings of the respiratory bronchioles. They resemble clusters of grapes in their appearance. They have radii of about 0.1 mm and wall thicknesses of about 0.2 µm. They are the primary sites of gas exchange in the lungs. Alveoli have an epithelial layer and an extracellular matrix surrounded by capillaries. In some alveolar walls, there are pores between alveoli. There are two major pneumocytes in the alveolar wall: Type I cells that form the structure of an alveolar wall and type II cells that secrete surfactant to lower the surface tension of water The alveoli have an innate tendency to collapse because of their spherical shape, small size, and surface tension due to water vapor. Phospholipids and pores help to equalize pressures and prevent collapse.
Bordering the lumen of the alveoli are wandering cells called alveolar phagocytes, or macrophages. These cells engulf dust, bacteria and other inhaled particles that are trapped in the pulmonary surfactant. After they become filled with debris, the macrophages migrate to the bronchioles, where they then get carried by ciliary action to the pharynx where they get swallowed. Alternatively, they may also migrate into the interstitium where they are then removed via the lymphatic vessels.
Information gathered from http://en.wikipedia.org/wiki/Alveoli and http://www.bioeng.auckland.ac.nz/physiome/ontologies/respiratory/cells.php

8. Type I and II alveolar cells
Type I alveolar cells cover about 95% of the alveolar surface. Type I alveolar cells are extremely thin. They occupy most of the alveolar surface area. Their external surfaces are covered with capillaries. Both their thinness and the capillaries surrounding them make these ideal cells for the diffusion of gases. They form a thin barrier through which gas exchange occurs. The basement membranes of the alveolar I cells and the capillary endothelium are actually fused together. Thus the exchange surface consists of the alveolar I cell membrane, the endothelial cell membrane, and the fused basement membranes. Type I alveolar cells do not divide.
Type II alveolar cells are cuboidal in shape with short microvilli along their apical surface. Their primary function is the secretion of surfactant.
Information primarily found at http://www.mededsys.com/courses_online/302/index.html

Intake this!

A few fun breathing facts from my current biology lab.

1. What are the structural adaptations of the nasal cavity that allow it to carry out its functions?
Nasal hairs act as a filter to keep dust and dirt out of the nasal passages. Loss of nasal hair due to alopecia areata has been linked to increased severity of asthma, seasonal allergy and atopic dermatitis.
In humans, as with most mammals, the nose is the primary organ for smelling. The air flows over structures called turbinates in the nasal cavity. The turbulence caused by this disruption slows the air and directs it toward the olfactory epithelium. At the surface of the olfactory epithelium, odor molecules carried by the air contact olfactory receptor neurons which translate the features of the odor molecule into electrical impulses in the brain.
The shape of the nose is determined by the ethmoid bone and the nasal septum. The septum consists mostly of cartilage. It separates the nostrils.
The ethmoid bone is a cubical bone in the skull that separates the nasal cavity from the brain. It is located at the roof of the nose, between the two orbits. It is lightweight due to its spongy construction. The ethmoid bone consists of four parts: the horizontal Cribriform plate or lamina cribrosa, the vertical Perpendicular plate or lamina perpendicularis, which is part of the nasal septum, and the two lateral masses or labyrinths.
The ethmoid bone is very delicate and is easily injured by a sharp upward blow to the nose. The force of such a blow can drive bone fragments through the cribiform plate into the meninges or brain tissue. Such injuries cause leakage of cerebrospinal fluid into the nasal cavity and the brain. Blows to the head can also shear off the olfactory nerves that pass though the ethmoid bone and cause anosmia, an irreversible loss of the sense of smell. This not only eliminates certain aesthetic pleasures, but can also be dangerous. A person who cannot smell would be unable to detect smoke, gas, or spoiled food.
The nasal septum separates the left and right airways in the nose, dividing the two nostrils. It is composed of the ethmoid bone, vomer bone and the quadrangular.
A turbinate, or nasal conchae, is a long, narrow and curled bone shelf shaped like an elongated sea-shell which protrudes into the breathing passage of the nose. Turbinate bone refers to any of the scrolled spongy bones of the nasal passages in humans and other vertebrates. The turbinates divide the nasal airway into three groove-like air passages, and are responsible for forcing inhaled air to flow in a steady, regular pattern around the largest possible surface of cilia and climate controlling tissue.
The turbinates are located laterally in the nasal cavities. They curl medially and downwards into the nasal airway. Each pair is comprised of one turbinate in either side of the nasal cavity, divided by the septum.
The inferior turbinates are the largest turbinates. They are approximately three inches long, and are responsible for the majority of airflow direction, humidification, heating, and filtering of air inhaled through the nose.

The middle turbinates are usually around 2.5 inches long. They project downwards over the openings of the maxillary and ethmoid sinuses, and act as buffers to protect the sinuses from coming in direct contact with pressurized nasal airflow. Most inhaled air travels between the inferior turbinate and the middle turbinate.
The superior turbinates are smaller structures, connected to the middle turbinates by nerve endings. They protect the olfactory bulb.
The turbinates comprise most of the mucosal tissue of the nose. They are enriched with airflow pressure and temperature sensing nerve receptors linked to the trigeminal nerve route. They are responsible for filtration, heating and humidification of air inhaled through the nose. As air passes over the turbinate tissues it is heated to body temperature, humidified by up to 98% water saturation, and filtered.
The respiratory epithelium which covers the Lamina propria of the turbinates is part of the body’s first line of immunological defense. The respiratory epithelium is partially comprised of mucus producing goblet cells. This secreted mucus covers the nasal cavities and traps air-borne particles larger than 2 to 3 micrometers. The respiratory epithelium also serves as a means of access to the lymphatic system.
Information primarily gathered from http://www.wikipedia.org
2. What are the structural adaptations of the larynx that allow it to carry out its functions?
The larynx is mainly composed of cartilage bound by ligaments and muscle. At the front is the thyroid cartilage. This cartilage forms the Adam's apple. The inferior horns of the thyroid cartilage rest on the ring-shaped cricoid cartilage which connects the larynx to the trachea. Above the larynx is the hyoid bone, by which the larynx is connected to the jaw and skull. These muscles move the larynx during swallowing. The epiglottis consists of cartilage extending upwards behind the back of the tongue and projects down through the hyoid bone. It connects to the thyroid cartilage just beneath the thyroid notch. The space defined by these main cartilages is divided into the supraglottis and the glottis.
The glottis is defined as the space between the vocal cords, which are located at the upper rim of the cricoid cartilage. They attach to the thyroid cartilage at the front, and to the Arytenoid cartilages at the back. These are two roughly tetrahedral cartilages responsible for adduction and abduction of the vocal cords. The vocal cords are muscular masses coated with a mucous membrane which protects much of the respiratory tract from foreign particles. Their inner edges contain the vocal ligament.
The supraglottis is the portion of the pharynx above the glottis. It contains the ventricle of the larynx or laryngeal sinus, the ventricular folds or false vocal cords, the epiglottis, and the aryepiglottal folds. These are two folds of connective tissue that connect the epiglottis to the arytenoid cartilages. Muscles in the aryepiglottal folds have the ability to pull the epiglottis down, sealing the larynx and protecting the trachea below from foreign objects.
3. What are the structural adaptations of the trachea that allow it to carry out its functions?
The trachea, or windpipe, is a tube extending from the larynx to the bronchi, carrying air to the lungs. It is lined with ciliated cells which push particles out, and cartilage rings which reinforce the trachea and prevent it from collapsing on itself during breathing. These numerous cartilaginous half-rings, located one above the other along the trachea, have open ends adjacent to the esophagus. The rings are connected by muscular and fibrous tissue, and they are lined inside with a ciliated mucous membrane.
4. What are the structural adaptations of the alveoli that allow it to carry out its functions?
The alveoli consist of an epithelial layer and extracellular matrix surrounded by capillaries. In some alveolar walls, there are pores between alveoli. The alveoli are composed of Type I cells that form the structure of an alveolar wall, and Type II cells that secrete surfactant to lower the surface tension of water. The lungs contain about 300 million alveoli, each wrapped in a fine mesh of capillaries.
5. Compare the function of the conducting and respiratory zones.
The Conducting zone consists of the mouth, nose, pharynx, larynx, trachea, bronchi
The Respiratory zone consists of the respiratory bronchioles and alveoli.
The conducting zone warms the incoming air and removes pathogens and debris from it before it enters the respiratory zone. In the respiratory zone, oxygen is uploaded into the erythrocytes from the alveoli and transported throughout the body. Erythrocytes which have traveled through the body return to download carbon dioxide, which is then expelled from the body via the conducting zones.

Cystic Fibrosis

This information about cystic fibrosis is an answer to a question that was posed on an upcoming lab for my biology class.

What is Cystic Fibrosis and what specific tissues in the lung does it affect?

CF is caused by a mutation in a gene called the cystic fibrosis transmembrane conductance regulator (CFTR). This gene helps create sweat, digestive juices, and mucus. Although most people without CF have two working copies of the CFTR gene, only one is needed to prevent cystic fibrosis. CF develops when neither gene works normally. Therefore, CF is considered an autosomal recessive disease. The name cystic fibrosis refers to the characteristic scarring (fibrosis) and cyst formation within the pancreas.
The symptoms of cystic fibrosis depend on the age of the individual, the extent to which the disease affects specific organs, and the types of infections experienced. Cystic fibrosis affects the entire body and impacts growth, breathing, digestion, and reproduction. The newborn period may be marked by poor weight gain and intestinal blockage caused by thick feces. Other symptoms of CF appear during growth and early adulthood. These include continued problems with growth, the onset of lung disease, and increasing difficulties with poor absorption of vitamins and nutrients by the gastrointestinal tract.
Lung disease results from clogging of the smaller airways with thick mucus. Inflammation and infection damage the lungs and the resulting damage leads to a variety of symptoms. In the early stages, incessant coughing, copious phlegm production, and decreased tolerance of exertion are common. Sometimes bacteria that normally inhabit the thick mucus grow out of control and cause pneumonia. In later stages of CF, changes in the architecture of the lung further exacerbate chronic respiratory difficulties. Other symptoms include coughing up blood, changes in the major airways in the lungs, known as bronchiectasis, pulmonary hypertension, heart failure, hypoxia, and respiratory failure requiring support with breathing masks such as bilevel positive airway pressure machines or ventilators.
In addition to typical bacterial infections, people with CF more commonly develop other types of lung disease. The lungs of individuals with cystic fibrosis are colonized and infected by bacteria from an early age. These bacteria, which often spread amongst individuals with CF, thrive in the altered mucus, which collects in the small airways of the lungs. This mucus encourages the development of bacterial microenvironments (biofilms) that are difficult for immune cells and antibiotics to penetrate. The lungs respond to repeated damage by thick secretions and chronic infections by gradually remodeling the lower airways (bronchiectasis), making infection even more difficult to eradicate.
Over time, both the types of bacteria and their individual characteristics change in individuals with CF. Initially, common bacteria such as Staphylococcus aureus and Hemophilus influenzae colonize and infect the lungs. Eventually, however, Pseudomonas aeruginosa and sometimes Burkholderia cepacia dominate. Once within the lungs, these bacteria adapt to the environment and develop resistance to commonly used antibiotics. Pseudomonas can develop special characteristics which allows the formation of large colonies. These strains are known as "mucoid" Pseudomonas and are rarely seen in people who do not have CF. Among these are allergic bronchopulmonary aspergillosis, in which the body's response to the common fungus Aspergillus fumigatus causes worsening of breathing problems. Another is infection with mycobacterium avium complex (MAC), a group of bacteria related to tuberculosis which can cause further lung damage. MAC does not respond to common antibiotics.
Mucus in the paranasal sinuses is equally thick and may cause blockage of the sinus passages, leading to infection. This may cause facial pain, fever, nasal drainage, and headaches. Individuals with CF may develop nasal polyps due to inflammation from chronic sinus infections. Such polyps can block the nasal passages and increase breathing difficulties.
Most information gathered from Wikipedia at http://www.wikipedia.org/wiki/Cystic_Fibrosis

Many people with cystic fibrosis do not live beyond their early 20's. Norma far surpassed that. She is 45 years old and has created a website with extensive information on the disease. Click the title link to visit this interesting and informative resource.

Antibodies

In mammals there are five types of antibody: IgA, IgD, IgE, IgG, and IgM, with 4 IgG and 2 IgA subtypes present in humans. (Ig stands for immunoglobulin, which is another name for antibody). These are classified according to differences in their heavy chain constant domains (see below for more information regarding the structural features of antibodies). Each immunoglobulin class differs in its biological properties and has evolved to deal with different antigens. IgA can be found in areas containing mucus (e.g. in the gut, in the respiratory tract or in the urinogenital tract) and prevents the colonization of mucosal areas by pathogens. IgD functions mainly as an antigen receptor on B cells. IgE binds to allergens and triggers histamine release from mast cells (the underlying mechanism of allergy) and also provides protection against helminths (worms). IgG (in its four forms) provides the majority of antibody-based immunity against invading pathogens. IgM is expressed on the surface of B cells and also in a secreted form with very high affinity for eliminating pathogens in the early stages of B cell mediated immunity (i.e. before there is sufficient IgG to do the job).
Immature B cells express only IgM on their cell surface (this is the surface bound form not the secreted form of immunoglobulin). Once the naive B cell reaches maturity, it can express both IgM and IgD on its surface - it is the co-expression of both these immunoglobulin isotypes that renders the B cell 'mature' and ready to respond to antigen. Following an engagement of the immunoglobulin molecule with an antigen, the B cell becomes activated, and begins to divide and differentiate into an antibody producing cell (sometimes called a plasma cell). In this activated form, the B cell will produce its immunoglobulin in a secreted form rather than a membrane-bound form. Some of the daughter cells of the activated B cells will undergo isotype switching, a mechanism by which the B cell begins to express the other heavy chains and thus produce IgD, IgA or (more commonly) IgG.

Influenza

This is a mini-report that I wrote for my biology course.

From the Stanford Website:
"Microbes, bacteria in particular, are the oldest and most abundant form of life — predating humans by about 3.5 billion years. Most microbes are benign or beneficial to humans, but the portion of the microbial world that is pathogenic (capable of producing disease) has periodically wreaked havoc on human populations. Epidemics (localized outbreaks of disease) and pandemics (global outbreaks) have occurred throughout human history."

In 1918, the influenza pandemic killed between 20 and 40 million people worldwide. The virus followed the paths of shipping lines to affect global population. This particular strain was most deadly for people ages 20 to 40. This pattern of morbidity was unusual for influenza, which is usually a killer of the very young and the elderly. This influenza strain had a profound virulence, with a mortality rate at 2.5% compared to the previous influenza epidemics, which were less than 0.1%. The death rate for 15 to 34-year-olds of influenza and pneumonia were 20 times higher in 1918 than in previous years. People who contracted the illness died rapidly.
One physician writes that patients with seemingly ordinary influenza would rapidly "develop the most viscous type of pneumonia that has ever been seen" and later when cyanosis appeared in the patients, "it is simply a struggle for air until they suffocate." Another physician recalls that the influenza patients "died struggling to clear their airways of a blood-tinged froth that sometimes gushed from their nose and mouth.
The origins of this influenza variant is not precisely known. It is thought to have originated in China in a rare genetic shift of the influenza virus. Recently the virus has been reconstructed from the tissue of a dead soldier and is now being genetically characterized.
The loss of life from even a particularly virulent strain of influenza would likely not be as great in modern times due to the ability to vaccinate readily. However, if the population were taken unawares by a drastic infectious agent of this nature, there could very likely be a shortage of the vaccine. Persons living in underprivileged circumstances would likely be deprived of the vaccine and of medical techniques that might save their lives. Persons in positions that involved high public contact, such as health care workers, would have a high degree of exposure to the disease.
Although scientists understand much more than they once did about influenza, the virus mutates and a highly virulent strain could still take a number of lives globally in spite of our more advanced medical technologies. Viruses are still the most difficult of all the infectious agents to combat. Unlike bacteria or parasites, they do not specifically "live." They are not subject to the effects of antibiotics. The only force that can combat them is an organism's immune system, possibly with the help of vaccines.