What happens to a baby at birth

Before birth, oxygenated blood from the placenta flows into the child’s inferior vena cava and mixes with blood returning from the lower part of the body. The atria are, in effect, one chamber due to the open foramen ovale; however, laminar blood flow tends to supply the left atrium and ventricle (and hence the upper body) with more placental (oxygenated) blood than the right atrium receives. The ventricles also act as one and pump blood around the body. Blood from the right ventricle bypasses the lungs, flowing through the ductus arteriosus and joining blood from the left ventricle in the descending aorta. A large portion of this blood flow goes to the placenta through the umbilical arteries.

Although the pulmonary vessels are fully developed in the fetus, only a tiny amount of blood (about 5% of cardiac output) flows through them due to intense vasoconstriction of the pulmonary arterioles. The nutritive blood supply to the lungs is from the bronchial arteries that arise from the aorta. The collapsed alveoli (air sacs) are filled with amniotic fluid.

Oxygenated blood is red, de-oxygenated blood is blue, and at the moment of birth, a normal newborn is circulating a mixture of blue and red blood. The color (lips and tongue) of a healthy newborn at birth is a pinkish purple; the child has been this color for nine months and normal placental function (cord pulsating) will maintain this color until the lungs function.

When the lungs are functioning, the umbilical vessels close, the ductus venosis closes, the hepatic portal vein is open, the foramen ovale closes, the heart is two sided, the cardiac output from the right ventricle (blue blood) goes through the lungs and is oxygenated, the left ventricular output (red blood) goes through the body, the ductus arteriosus closes, the pulmonary arterioles are open, the alveoli are full of air and the child turns from purple to pink. All of this complicated process is coordinated and controlled by the child’s reflexes; it usually happens within three or four minutes of birth. What makes it happen?

All babies are born soaking wet, and on meeting the atmosphere, the skin cools; this triggers two reflexes:

The cold crying reflex - cold, wet diapers produce the same result, crying.
The cold pressor reflex - cold skin raises blood pressure.
In order to cry, the child must first take a deep breath, and an inspiratory "gasp" is often the first sign, triggered by cold, that a child is going to cry or breathe. Contraction of the diaphragm and intercostal muscles increase thoracic volume and create negative intra-thoracic pressure. Once air is in the lungs, another reflex is triggered that relaxes the pulmonary arterioles; this causes an enormous increase in pulmonary blood flow.

The cold pressor reflex increases the blood pressure in the aorta, and this may be sufficient to reverse blood flow through the ductus arteriosus causing more blood to flow through the lungs.

The cord is also cooling, and the cord is a well-designed self-refrigerator. It has no skin and blubber to keep it warm like the child. It contains only the cord vessels surrounded by a watery gel, Wharton’s jelly, covered by a single layer of cells, the amnion. Water evaporation cools it rapidly, causing the vessels, especially the muscular arteries, to constrict; this further helps to raise systemic blood pressure and to reverse ductus arteriosus flow.

At the same time, a large transfusion of placental blood is being forced into the child by gravity and/or by uterine contraction, greatly increasing cardiac output and pulmonary blood flow. The net result of these changes is a large amount of blood flowing into the left atrium from the lungs, which raises left atrial pressure and closes the foramen ovale - the heart changes from one-sided to two-sided. The lungs are now oxygenating blood that is pumped round the body by the left ventricle - the child turns pink.

If the child has not taken the first breath, or is depressed and cannot breathe, the massive increase in pulmonary blood flow generated by the placental transfusion may, of itself, initiate ventilation. Jaykka [1,2] showed that the fetal lungs are erectile tissues; by injecting serum through the pulmonary artery of excised animal fetal lungs, the engorged capillaries around the alveoli erected them and caused air to enter through the trachea. With establishment of pulmonary blood flow, the high colloid osmotic pressure of blood causes absorption of amniotic fluid from the alveoli and "dries out" the lungs, filling the "erected" alveoli with air.

Cold will eventually cause the cord vessels to close; however, a high arterial blood oxygen concentration is probably a key factor in umbilical artery closure - they close before the umbilical vein closes; it may also cause ductus arteriosus closure. After umbilical artery closure, the placental transfusion may continue through the cord vein in a very measured and controlled manner.

Information found at: http://whale.to/a/morley4.html

Powerful Picture

Click the title link to view the photo in a larger scale at its original location. This is a five-week-old embryo found in the case of an ectopic pregnancy. Ectopic pregnancies cannot survive and present great danger to the mother's health. The embryo was removed shortly after the photo was taken. The details in the photograph are amazing. At this stage it is difficult to distinguish a human fetus from the fetuses of other animals. Apologies as I reveal the horror movie lover in me, but we do look a bit like alien chestbursters during our earliest stages of development.

Ovarian Follicles

An ovarian follicle consists of a developing oocyte surrounded by one or more layers of cells called follicular cells. At the same time that the oocyte is progressing through meiosis, corresponding changes are taking place in the follicular cells. Primordial follicles, which consist of a primary oocyte surrounded by a single layer of flattened cells, develop in the fetus and are the stage that is present in the ovaries at birth and throughout childhood.
Beginning at puberty follicle-stimulating hormone stimulates changes in the primordial follicles. The follicular cells become cuboidal, the primary oocyte enlarges, and it is now a primary follicle. The follicles continue to grow under the influence of follicle-stimulating hormone, and the follicular cells proliferate to form several layers of granulose cells around the primary oocyte. Most of these primary follicles degenerate along with the primary oocytes within them, but usually one continues to develop each month. The granulosa cells start secreting estrogen and a cavity, or antrum, forms within the follicle. When the antrum starts to develop, the follicle becomes a secondary follicle. The granulose cells also secrete a glycoprotein substance that forms a clear membrane, the zona pellucida, around the oocyte. After about 10 days of growth the follicle is a mature vesicular (graafian) follicle, which forms a "blister" on the surface of the ovary and contains a secondary oocyte ready for ovulation.

Ovulation
Ovulation, prompted by luteinizing hormone from the anterior pituitary, occurs when the mature follicle at the surface of the ovary ruptures and releases the secondary oocyte into the peritoneal cavity. The ovulated secondary oocyte, ready for fertilization is still surrounded by the zona pellucida and a few layers of cells called the corona radiata. If it is not fertilized, the secondary oocyte degenerates in a couple of days. If a sperm passes through the corona radiata and zona pellucida and enters the cytoplasm of the secondary oocyte, the second meiotic division resumes to form a polar body and a mature ovum

After ovulation and in response to luteinizing hormone, the portion of the follicle that remains in the ovary enlarges and is transformed into a corpus luteum. The corpus luteum is a glandular structure that secretes progesterone and some estrogens. Its fate depends on whether fertilization occurs. If fertilization does not take place, the corpus luteum remains functional for about 10 days then it begins to degenerate into a corpus albicans, which is primarily scar tissue, and its hormone output ceases. If fertilization occurs, the corpus luteum persists and continues its hormone functions until the placenta develops sufficiently to secrete the necessary hormones. Again, the corpus luteum ultimately degenerates into corpus albicans, but it remains functional for a longer period of time.

http://training.seer.cancer.gov/module_anatomy/unit12_3_repdt_female1_ovaries.html

Meiosis

Normally, meiosis causes a halving of chromosome material, so that each parent gives 23 chromosomes to a pregnancy

A cool site about meiosis for you to enjoy:
http://www.sciencecases.org/mitosis_meiosis/mitosis_meiosis2.asp

Testes! One, two...three???

We are currently studying the reproductive system in class. Here is some fun trivia about the testes. The information was gathered from Wikipedia.

In land mammals, with the exception of the elephant the testes are located outside of the body, as they are suspended by the spermatic cord and within the scrotum. This is due to the fact that The cremasteric muscle is part of the spermatic cord. When this muscle contracts, the cord is shortened and the testicle is moved closer up toward the body, which provides slightly more warmth to maintain optimal testicular temperature. When cooling is required, the cremasteric muscle relaxes and the testicle is lowered away from the warm body and are able to cool. This phenomenon is known as the cremasteric reflex. It also occurs in response to stress (the testicles rise up toward the body in an effort to protect them in a fight), and there are persistent reports that relaxation indicates approach of orgasm. There is a noticeable tendency to also retract during orgasm.

The testicles can also be lifted voluntarily using the pubococcygeus muscle, which partially activates related muscles. This can sometimes be triggered by tightening or sucking in the stomach or abdomen.

Animals other than mammals do not have externalized testicles. Birds, despite having very high core body temperatures have internal testes: it was once theorized that birds used their air sacs to cool the testes internally, but later studies revealed that birds' testes function at core body temperature.[1] Marine mammals also have internal testes, but it has recently been shown (eg, for dolphins) that they use elaborate vascular networks to provide the necessary temperature lowering for proper operation.

The seminiferous tubules of the testes are the starting point for the process of spermatogenesis, where stem cells adjacent to the inner tubule wall divide in a centripetal direction - beginning at the walls and proceeding into the lumen to produce immature sperm.

What is meant by "my food went down the wrong tube"?

When food is swallowed, it travels down the throat, which is the common conduit for food, drink and air. Midway down the neck, the throat branches. The front branch, the trachea, channels air towards the lungs. At the top of this branch is the larynx. Just behind the larynx is esophagus, which is the tube that directs food to the stomach. As a person swallows, the soft palate closes off the nasal passages so that food doesn't get pushed up into the nose. As the throat squeezes food towards the esophagus, the larynx tips forward to allow the food to pass through, and the epiglottis seals off the airway to prevent food from going down into the trachea. Eating while talking or laughing can sometimes cause the larynx to be slow in sealing off the trachea, allowing a bit of food or drink to head towards the lungs. This triggers a strong coughing reflex to prevent aspiration.

Way Crappy!

For those of you who have never been exposed to the glory of The Poop Report, click the title link to read one of the top funniest stories ever to appear there. They're all funny, but this one's a classic!

A Refreshing Glass...Of Whiz???

There's nothing like being able to take a proper piss. If you can't, your life is made far more difficult. This simple function brings relief several times a day, although as we get older it can be a nuisance at times because it becomes harder to hold your water. For my own part, I'd rather resign myself to wearing Depends than to not be able to go and having to rely on dialysis, which is a wearying and time-consuming procedure.

Much though I enjoy the relief provided by a good leak, I feel no desire to re-consume my pee once it leaves my body. I might do it to save my own life in a situation such as being lost in the desert. However, some folks drink a hearty glass of nature's own "lemonade" by choice. Read all about it here. And fellows, I know this will break your hearts, but you need to know this. Lips that touch piss will never touch mine!

Kidney Anatomy and Physiology

My complete 26-page kidney anatomy and physiology report is available for the asking. It is a good study aid for basic anatomy and physiology from junior high level on up. Just post your request in the comments section along with your email and I will gladly send it to you. I will also be posting it a piece at a time on this site as I get around to it.

And now the irritating disclaimer.

This is intended as a resource for your own studies, not as a tool for plagarism. I enjoy sharing the knowledge I've learned through my studies and if it can make another person's learning process less frustrating, that pleases me. It's ok to take a shortcut to knowledge, but cheating only screws up your karma. Thanks!

Kidney Komponents

More information about kidneys than you ever wanted to know!
Or if you did want to know it, here it is. This is copied from my lab report on the renal system. Click the title link to see some excellent slides of various parts of the kidney along with an in-depth tutorial from the University of Texas cellular biology graduate student program.

Renal Cortex
The renal cortex is the outer portion of the kidney between the renal capsule and the renal medulla. The renal cortex forms a shell around the medulla. Its tissues dip into the medulla between adjacent renal pyramids to form renal columns. It contains renal corpuscles and renal tubules, except for those portions of the loop of Henle which descend into the renal medulla. It also contains blood vessels and cortical collecting ducts. The granular appearance of the cortex is due to the random arrangement of tiny tubules associated with nephrons. The renal cortex is the part of the kidney where ultrafiltration occurs.

Renal Medulla
The renal medulla is the innermost part of the kidney. It is split up into cone-shaped masses of tissue called renal pyramids, whose bases are directed toward the convex surface of the kidney, and the apices of which form the renal papillae. Each pyramid together with the associated overlying cortex forms a renal lobe. The tip of each pyramid, called a papilla, empties into a calyx, and the calices empty into the renal pelvis.
The renal medulla also contains blood vessels. Blood enters into the kidney via the renal artery, which then splits to form the arcuate arterioles. The arcuate arterioles in turn branch into interlobar arterioles, which finally reach the glomeruli.

Renal Pyramids
Renal pyramids, also known as malpighian pyramids, are the cone-shaped masses contained in the renal medulla. The renal medulla is made up of 8 to 18 renal pyramids. The broad base of each pyramid faces the renal cortex. Its apex, or papilla, points internally. The pyramids appear striped because they are formed by straight parallel segments of nephrons.

Bases of Pyramids
The broad outer portion of a renal pyramid that lies next to the cortex. Also known as basis pyramidis renis.

Renal Papilla
The papillae are small conical projections along the wall of the renal sinus. They have openings through which urine passes into the calyces.

Renal Columns
Tissue between the renal pyramids that allows for support of the renal cortex. The columns consist of blood vessels, urinary tubes, and fibrous material.

Renal pelvis
The renal pelvis is the funnel-shaped proximal part of the ureter, located approximately in the center of the kidney. It is the point of convergence of two or three major calyces. Each renal papilla is surrounded by a branch of the renal pelvis called a calyx. The major function of the renal pelvis is to act as a funnel for urine flowing to the ureter.

Calyces
The calyces surround the apex of the renal pyramids. There are minor and major calyces. Urine passes through a papilla at the apex into a minor calyx, then travels into a major calyx before passing through the renal pelvis into the ureter. Peristalsis of the smooth muscle of pace-maker cells in the walls of the calyces propels urine through the renal pelvis.

Glomerulus and Bowman's capsule
The glomerulus is the main filter of the nephron. It is a semipermeable, twisted mass of tiny tubes through which blood passes, allowing water and soluble wastes to pass through and be excreted out of the Bowman's capsule as urine. The filtered blood passes out of the glomerulus into the efferent arteriole to be returned through the medullary plexus to the intralobular vein.
The Bowman's capsule contains the primary glomerulus. Blood is transported into the Bowman's capsule from the afferent arteriole, which branches off of the interlobular artery. Within the capsule, the blood is filtered through the glomerulus and exits via the efferent arteriole. Meanwhile, the filtered water and aqueous wastes are passed from the Bowman's capsule into the proximal convoluted tubule.
Here is the best drawing I've seen of the inside of a glomerulus.

Filtration membrane
The filtration membrane is formed from the endothelial cells of the capillaries, basement membrane, and visceral epithelium of the Bowman’s capsule. It is composed of three layers:
Fenestrated endothelium of the glomerular capillaries
Visceral membrane of the glomerular capsule (podocytes)
Basement membrane composed of fused basal laminae of the other layers

Podocytes
Podocytes are cells of the visceral epithelium in the kidneys. They form a crucial component of the glomerular filtration barrier. Structural features of podocytes indicate a high rate of vesicular traffic. Many coated vesicles and pits can be seen along the basolateral domain of podocytes. Within their cell bodies, podocytes have a well-developed endoplasmic reticulum and a large Golgi apparatus, indicative of a high capacity for protein synthesis and post-translational modifications. There are also a large number of multivesicular bodies and other lysosomal components within the podocytes, indicating high endocytic activity.
Adjacent podocytes interlock to cover the basal lamina of the glomerular capillaries. There are thin filtration slits left between the podocytes. The slits are covered by diaphragms, which are composed of numerous cell-surface proteins, including nephrin, podocalyxin, and P-cadherin. These proteins ensure that large macromolecules such as serum albumin and gamma globulin remain in the bloodstream. Small molecules such as water, glucose, and ionic salts pass through the slit diaphragms and form an ultrafiltrate, which is further processed by the nephron to produce urine.
Disruption of the slit diaphragms or destruction of the podocytes can lead to massive proteinuria, whereby large amounts of protein are lost from the blood. An example of this occurs in Finnish-type Nephrosis, a congenital disorder caused by a mutation in the nephrin gene. This defect causes neonatal proteinuria leading to end-stage renal failure.
Information gathered primarily from http://en.wikipedia.org/wiki/Podocyte

Juxtaglomerular Apparatus
The juxtaglomerular apparatus is a structure consisting of the macula densa, mesangial cells, and juxtaglomerular cells. Juxtaglomerular cells, also known as JG cells, or granular cells, are the site of renin secretion.
JG cells are found in the afferent arterioles of the glomerulus and act as an intra-renal pressure sensor. Lowered pressure leads to secretion of rennin, which increases systemic blood pressure via the renin-angiotensin system.
The macula densa senses fluid flow rate and sodium chloride concentration in the distal tubule of the kidney and secretes paracrine vasopressor, which acts on the adjacent afferent arteriole to decrease glomerular filtration rate.
Mesangial cells regulate blood flow in the glomerulus and monitor sodium and chloride levels in the distal convoluted tubules. These cells communicate with the afferent arteriole and can cause vasoconstriction, decreasing the blood flow and GFR if necessary.

Peritubular Capillaries
Peritubular capillaries are the tiny blood vessels beside the nephrons, allowing reabsorption and secretion between blood and the inner lumen of the nephron. Ions and minerals to remain in the body are reabsorbed into the peritubular capillaries through active transport, secondary active transport, or transcytosis. Ions to be excreted as waste are secreted from the capillaries into the nephron and sent to the bladder. The majority of exchange through the peritublar capillaries occurs because of chemical gradients, osmosis, and Na+ pumps.

Distal Convoluted Tubule
The distal convoluted tubule is the portion of a nephron between the loop of Henle and the collecting duct system. It is partly responsible for the regulation of potassium, sodium, calcium, and pH.
The DCT regulates pH by absorbing bicarbonate and secreting H+ protons into the filtrate. Sodium and potassium levels are controlled by secreting K+ and absorbing Na+.
Sodium absorption by the distal tubule is mediated by the hormone aldosterone. Aldosterone increases sodium reabsorption. Sodium and chlorine reabsorption are also mediated by a group of four kinases called WNK kinases.
The distal convoluted tubule also participates in calcium regulation by absorbing Ca2+ in response to parathyroid hormone.
Histologically, cells of the DCT can be differentiated from cells of the proximal convoluted tubule by looking for these features:
DCT cells do not have an apical brush border
DCT cells are less eosinophilic than proximal cells
DCT cells have less cytoplasm
DCT cells are more likely to have visible nuclei
Information primarily gathered from http://en.wikipedia.org/wiki/Distal_convoluted_tubule

Proximal Convoluted Tubule
The proximal convoluted tubule is the longest (14mm) and widest (60µm) part of the nephron. It is lined with epithelial cells containing microvilli and numerous mitochondria. The most distinctive characteristic of the proximal tubule is its brush border. In the PCT, over 80% of the filtrate is reabsorbed into the tissue fluid and returned to the blood. This ensures that all necessary materials that were filtered out of the blood, such as glucose and amino acids, are now returned.

Thin (descending) Loop of Henle
The descending limb of the Loop of Henle has low permeability to ions and urea, while being highly permeable to water. The ascending limb of the LOH is impermeable to water. The net effect is for sodium chloride to leave the ascending limb and to enter the descending limb, having first passed through the renal medullary interstitium. Water is readily reabsorbed from the descending limb by osmosis, increasing the concentration of the urine. Osmolality can reach up to 1200 mOsmol/kg by the end of the descending limb.

Vasa Recta Capillary
The Vasa recta, or straight vessels, are bundles of thin vessels which carry blood into and out of the medulla. The Vasa recta eventually return blood to arcuate veins.

Thick (ascending) Loop of Henle
The ascending limb of the LOH is impermeable to water. As the fluid passes through the ascending limb, it becomes increasingly dilute as the sodium chloride is removed. Thus, the fluid entering the distal convoluted tubule is hypotonic (150 mmol/l).
Sodium, potassium (K+) and chloride (Cl-) ions are reabsorbed by active transport. K+ is passively transported along its concentration gradient through a K+ channel in the basolateral aspect of the cells, back into the lumen of the ascending limb. This K+ "leak" generates a positive electrochemical potential difference in the lumen. The electrical gradient causes more reabsorption of Na+, as well as other cations such as magnesium (Mg2+) and calcium Ca2+.
Information primarily gathered from http://en.wikipedia.org/wiki/Loop_of_Henle

Collecting Ducts
There are several components of the collecting duct system, which includes the connecting tubules and cortical and medullary collecting ducts. With respect to the renal corpuscle, the connecting tubule is the most proximal part of the collecting duct system. It is adjacent to the distal convoluted tubule, which is the most distal segment of the renal tubule. Connecting tubules from several adjacent nephrons merge to form cortical collecting tubules, and these may join to form cortical collecting ducts. Connecting tubules of some juxtamedullary nephrons may arch upward, forming an arcade.
The cortical collecting ducts receive filtrate from multiple connecting tubules and descend into the renal medulla to form medullary collecting ducts. Medullary collecting ducts are divided into outer and inner segments, the latter reaching deeply into the medulla. The terminal portions of these ducts are the papillary ducts, which end at the renal papilla and empty into a minor calyx.
Each component of the collecting duct system contains two cell types: intercalated cells and a segment-specific cell type. For the connecting tubules, this specific cell type is the connecting tubule cell; for the collecting ducts, it is the principal cell. The inner medullary collecting ducts contain an additional cell type, the inner medullary collecting duct cell.
The principal cell mediates the collecting duct's influence on sodium and potassium balance via sodium and potassium channels located on the cell's apical membrane. Intercalated cells come α and β varieties and participate in acid-base homeostasis. The α-intercalated cells secrete acid via an apical H+-ATPase and H+/K+ exchanger in the form of hydrogen ions and reabsorb bicarbonate via a basolateral Cl-/HCO3- exchanger. Damage to the α-intercalated cell's ability to secrete acid can result in distal renal tubular acidosis.
Similarly, β-intercalated cells secrete bicarbonate via an apical Cl-/HCO3- and reabsorb acid via a basal H+-ATPase. Because of their contribution to acid-base homeostasis, the intercalated cells play important roles in the kidney's response to acidosis and alkalosis.
The collecting duct system plays a role in electrolyte and fluid balance through reabsorption and excretion, which are regulated by the hormones aldosterone and antidiuretic hormone. The collecting duct system is the last component of the kidney to influence the body's electrolyte and fluid balance. It accounts for 4-5% of the kidney's reabsorption of sodium and 5% of reabsorption of water. During extreme dehydration, over 24% of the filtered water may be reabsorbed in the collecting duct system.
The collecting duct system regulates electrolytes, including chloride, potassium, hydrogen ions, and bicarbonate. The variable reabsorption of water and, depending on fluid balances and hormonal influences, the reabsorption or secretion of sodium, potassium, hydrogen, and bicarbonate ion continues here.
The wide variation in water reabsorption levels of the collecting duct system reveals its dependence on hormonal activation. The collecting ducts, particularly the outer medullary and cortical collecting ducts, are largely impermeable to water without the presence of ADH, or vasopressin. In the absence of ADH, excess water in the renal filtrate is allowed to enter the urine, promoting diuresis. When ADH is present, aquaporins allow for the reabsorption of water, inhibiting diuresis.
Information (and copying of unusual alpha-numeric characters) found at http://en.wikipedia.org/wiki/Collecting_duct_system

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.

Phuck Fibromyalgia

I suffer from fibromyalgia. I have a fairly mild case, but sometimes it gets the better of me. I can no longer do heavy physical activity, which is why even though I'm a licensed EMT I don't work on an ambulance. I have also suffered from several lower back injuries and this pain is exacerbated by the fibromyalgia.
There are days when I'm fairly well asymptomatic, especially since I switched to working in a department where the physical demands are far less. Chiropractic treatments tend to help as realigning the muscles and spine means less stress on the muscles and joints. (The type of chiropractic I receive involves manipulation of the muscles which leads to eventual reposition of the vertebrae as opposed to "cracking" the bones. It's far more effective in the long term.) However if I overdo things, whether physically or simply through being under too much stress, my muscles start to ache. Often it radiates down my arms, so that even if I haven't been doing any heavy lifting they feel like I've overdone things at the gym. Currently the pain is mostly in my lower back and my ankles, although there is some pain all over. I consider myself fortunate that I'm not one of those people that has such bad fibromyalgia that I can't bear to be touched. However, experiencing pain all over the body tends to exacerbate the fatigue that I'm already experiencing, and it becomes a vicious cycle. Due to suffering from bipolar disorder as well, the fatigue and resulting frustration can trigger a depressive spiral.
I wonder how closely problems like chronic fatigue or fibromyalgia are tied in with mood disorders.
Here are some basic Fibromyalgia facts:
Fibromyalgia (FM or FMS) is a debilitating chronic syndrome (constellation of signs and symptoms) characterized by diffuse or specific muscle, joint, or bone pain, fatigue, and a wide range of other symptoms. It is not contagious. It affects more females than males, with a ratio of 9:1 by ACR (American College of Rheumatology) criteria[2]. Fibromyalgia is seen in 3% to 6% of the general population, and is most commonly diagnosed in individuals between the ages of 20 and 50. The nature of fibromyalgia is not well understood. There are few, if any, treatments available[3], and there is no cure, but the disease is not life-threatening.
The primary symptom of fibromyalgia is widespread, diffuse pain, often including heightened sensitivity of the skin (Allodynia), tingling of the skin (often needlelike), achiness in the muscle tissues, weakness in the limbs, and nerve pain. Chronic sleep disturbances are also characteristic of fibromyalgia, and some studies suggest that these sleep disturbances are the result of a sleep disorder called alpha wave interrupted sleep pattern, a condition in which deep sleep is frequently interrupted by bursts of brain activity similar to wakefulness.

Many patients experience "brain fog", also known as "fibrofog", which is objectively proven abnormally slow brain waves and objectively proven cognitive deficits[5]. Many experts suspect that "brain fog" is directly related to the sleep disturbances experienced by sufferers of fibromyalgia.

Other symptoms often attributed to fibromyalgia (possibly due to another comorbid disorder) are chronic paresthesia, physical fatigue, irritable bowel syndrome, genitourinary symptoms such as those associated with the chronic bladder condition interstitial cystitis, dermatological disorders, headaches, myoclonic twitches, and symptomatic hypoglycemia. Although it is common in people with fibromyalgia for pain to be widespread, it may also be localized in areas such as the shoulders, neck, back, hips, or other areas. Not all patients have all symptoms.

Fibromyalgia can start as a result of some trauma (such as a traffic accident) or illness, but there is currently no known strong correlation between any specific type of trigger and the subsequent initiation of fibromyalgia. Symptoms can have a slow onset, and many patients have mild symptoms beginning in childhood, such as growing pains. Symptoms are often aggravated by unrelated illness or changes in the weather. They can become more tolerable or less tolerable throughout daily or yearly cycles; however, many people with fibromyalgia find that, at least some of the time, the condition prevents them from performing normal activities such as driving a car or walking up stairs. The syndrome does not cause inflammation as is presented in arthritis, but anti-inflammatory treatments, such as Ibuprofen and Iontophoresis, are known to temporarily reduce pain symptoms.

Variability of Symptoms
The following factors are said to temporarily increase the suffering of patients:
Cold weather, especially when damp
Malnutrition, hunger, or starvation
Physical activity of any kind, including minor tasks such as writing
Lack of deep sleep
Increase of stress
The consumption of alcohol
Some patients have reported a near-complete remission of their symptoms within several weeks of traveling to a warm, or tropical climate, especially with rest and relaxation, and the complete renewal of symptoms upon returning.

Diagnosis
When making a diagnosis of fibromyalgia, a practitioner would take into consideration the patient's case history and the exclusion of other conditions such as endocrine disorders, arthritis, and polymyalgia rheumatica. There are also two criteria established by the American College of Rheumatology for diagnosis:
A history of widespread pain lasting more than three months — widespread as in all four quadrants of the body, i.e., both sides, and above and below the waist.
Tender points — there are 18 designated possible tender points (although a person with the syndrome may feel pain in other areas as well). During diagnosis, four kilograms-force (40 Newtons) of force[3] is exerted at each of the 18 points; the patient must feel pain at 11 or more of these points for fibromyalgia to be considered. Four kilograms of force is about the amount of pressure required to turn fingernails white or to feel pain sensations on the forehead. This technique was developed by the American College of Rheumatology as a means of confirming the diagnosis for clinical studies. It is also used in the United Kingdom. Pressure on nearby areas rarely elicits any reaction. Fibromyalgia patients also have elevated levels of Substance P in the body, which increases the levels of pain and intensity.

Differentials
A number of other disorders can produce essentially the same symptoms as fibromyalgia. Other disorders known to produce similar symptoms are:
Myofascial pain syndrome
Chronic fatigue syndrome
Tendinitis
Gulf War syndrome
Depression
Influenza
Thyroid disease
Vitamin B12 deficiency
Lyme disease
Celiac disease
Mercury toxicity
Lead poisoning
Lupus erythematosus (SLE)
Whiplash-associated disorder

Treatment
As with many other soft tissue and rheumatolgical organic disorders, there is no cure for fibromyalgia, but some treatment options are available. A patient may try many routes of treatment under the guidance of a physician to find relief. Treatments range from symptomatic prescription medication to alternative and complementary medicine.

One experimental treatment is the use of the Guaifenesin Protocol, developed by Dr. R. Paul St. Amand. Because of the large number of patients improving on Guaifenesin, there are now several doctors throughout the U.S. who are using the Guaifenesin protocol in their practices[6].

Conventional analgesics rarely reduce the pain, and even strong narcotics are often not sufficient to entirely eliminate the pain.

Low doses of antidepressants like amitriptyline and trazodone may be used to reduce the sleep disturbances sometimes associated with fibromyalgia and are believed by some practitioners to help correct sleep problems that may exacerbate the symptoms of the condition. Because depression often accompanies chronic illness, these antidepressants have additional psychological benefits for patients suffering from depression. Amitriptyline is often favoured as it can also have the effect of providing relief from neuralgenic or neuropathic pain. Some doctors advise against using narcotic sleep aids ("hypnotics"), since these can actually disrupt deep sleep.

New drugs showing significant efficacy on fibromyalgia pain and other symptoms include milnacipran, gabapentin, meloxicam and possibly pregabalin. Milnacipran belongs to a new series of drugs known as serotonin-norepinephrine reuptake inhibitors (SNRIs), and is currently available in parts of Europe where it has been safely prescribed for other disorders. As of August 2005, Milnacipran is the subject of a Phase III study, and, if ultimately approved by the FDA, will be distributed in the United States.

Muscle relaxants such as Cyclobenzaprine (Flexeril) and Orphenadrine Citrate (Norflex) have also been studied in the treatment of fibromyalgia. Cyclobenzaprine has a tricyclic chemical structure similar to Amitriptyline, yet its anti-depressant effects are minimal. It is used only as a short-term muscle relaxant. In a study of 120 fibromyalgia patients, those receiving Cyclobenzaprine (10 to 40 mg) over a 12 week period had significantly improved quality of sleep and pain score. There was a trend towards improvement in fatigue symptoms but not in duration of morning stiffness. Interestingly, there was also a reduction in the total number of tender points and muscle tightness.

Studies have found gentle exercise, such as warm-water pool therapy, improves fitness and sleep and may reduce pain and fatigue in people with fibromyalgia. Stretching is recommended to allay muscle stiffness and fatigue, as is mild aerobic exercise. Because strenuous activity can exacerbate the muscle pain and fatigue already present, patients are advised to begin slowly and build their activity level gradually to avoid inducing additional pain. Exercise may be poorly tolerated in more severe cases with abnormal post-exertional fatigue.

Cognitive behavioral therapy has been shown to improve quality of life and coping in fibromyalgia patients and other sufferers of chronic pain.

EEG Biofeedback has also shown to provide temporary and long term relief, and as it gains more widespread coverage.

Many patients find temporary relief by applying heat to painful areas. Those with access to physical therapy and/or massage may find them beneficial. Chiropractic care can also help relieve pain due to fibromyalgia.

Treatment for the "brain fog" has not yet been developed, however biofeedback and self-management techniques such as pacing and stress management may be helpful for some patients.

A number of practitioners are attracted to the treatment of fibromyalgia, especially because its cause has yet to be identified, and due to its permanent nature, ongoing treatments can be very profitable. While this interest may promote legitimate medical research, patients should be wary: treatments of dubious validity exist in the meantime.

Living with fibromyalgia
Fibromyalgia can affect every aspect of a person's life. While neither degenerative nor fatal, the chronic pain associated with fibromyalgia is pervasive and persistent. FMS can severely curtail social activity and recreation, and as many as 30% of those diagnosed with fibromyalgia are unable to maintain full-time employment. Like others with disabilities, individuals with FMS often need accommodations to fully participate in their education or remain active in their careers.

In the United States, those who are unable to maintain a full-time job due to the condition may apply for Social Security Disability benefits. Although fibromyalgia has been recognized as a condition, along with chronic fatigue syndrome, by the government, applicants are often denied benefits. However, most are awarded benefits at the state judicial level; the entire process often takes two to four years.

In the United Kingdom, the Department for Work and Pensions recognizes fibromyalgia as a condition for the purpose of claiming benefits and assistance[7].

In India, the position with reference to this condition is unclear. However, where the person is rendered incapable of maintaining a regular life due to any disability, he/she can claim disability benefits. Indian laws guarantee that discrimination against people with disabilities is a violation of their individual rights.

Fibromyalgia is often referred to as an "invisible" illness or disability due to the fact that generally there are no outward indications of the illness or its resulting disabilities. The invisible nature of the illness, as well as its relative rarity and the lack of understanding about its pathology, often has psychosocial complications for those that have the syndrome. Individuals suffering from invisible illnesses in general often face disbelief or accusations of malingering or laziness from others that are unfamiliar with the syndrome.

There are a variety of support groups on the Web that cater to fibromyalgia sufferers. Some are offered at the bottom of this article.

Theories on the cause of fibromyalgia
The cause of fibromyalgia is currently unknown. Over the past few decades, many theories have been presented, and the understanding of the disorder has changed dramatically. Most current theories explain only a few symptoms of the disorder and are thus incomplete.

Sleep disturbance
The sleep disturbance theory postulates that fibromyalgia is related to sleep quality. Electroencephalography (EEG) studies have shown that people with fibromyalgia lose deep sleep[8]. Circumstances that interfere with "stage 4" deep sleep (such as drug use, pain, or anxiety) appear to be able to cause or worsen the condition.

According to the sleep disturbance theory, an event such as a trauma or illness causes sleep disturbance and, possibly, some sort of initial chronic pain. These initiate the disorder. The theory supposes that "stage 4" sleep is critical to the function of the nervous system, as it is during that stage that certain neurochemical processes in the body reset. In particular, pain causes the release of the neuropeptide substance P in the spinal cord, and substance P has the effect of amplifying pain and causing nerves near the initiating ones to become more sensitive to pain. Under normal circumstances, this just causes the area around a wound to become more sensitive to pain, but, if pain becomes chronic and body-wide, then this process can run out of control. The sleep disturbance theory holds that deep sleep is critical in order to reset the substance P mechanism and prevent this out-of-control effect.

An interesting aspect of the sleep disturbance/substance P theory is that it explains "tender points" that are characteristic of fibromyalgia but which are otherwise enigmatic, since their positions don't correspond to any particular set of nerve junctions or other obvious body structures. The theory posits that these locations are more sensitive because the sensory nerves that serve them are positioned in the spinal cord to be most strongly affected by substance P. The theory also explains some of more general neurological features of fibromyalgia, since substance P is active in many other areas of the nervous system.

Critics of the theory argue that it does not explain slow-onset fibromyalgia, fibromyalgia present without tender points, or patients without heightened pain symptoms, and a number of the non-pain symptoms present in the disorder.

Also of interest is a possible connection between this theory and the theory that chronic fatigue syndrome and post-polio syndrome are due, at least in part to damage to the ascending reticular activating system of the reticular formation. This area of the brain, in addition to apparently controlling the sensation of fatigue, is known to control sleep behaviors and is also believed to produce some neuropeptides, and thus injury or imbalance in this area could cause both CFS and sleep-related fibromyalgia, explaining why the two disorders so often occur together.

Deposition disease
Another theory involves phosphate and calcium accumulation in cells that eventually reaches a level to impede the ATP process, possibly caused by a kidney defect or missing enzyme that prevents the removal of excess phosphates from the blood stream. This theory posits that fibromyalgia is an inherited disorder, and that phosphate buildup in cells is gradual (but can be accelerated by trauma or illness). Calcium is required for the excess phosphate to enter the cells. The additional phosphate slows down the ATP process; however the excess calcium prods the cell to continue producing ATP[9].

Diagnosis is made with a specialized technique called mapping, a gentle palpitation of the muscles to detect lumps and areas of spasm that are thought to be caused by an excess of calcium in the cytosol of the cells. This mapping approach is specific to deposition theory, and is not related to the trigger points of myofascial pain syndrome.

While this theory does not identify the causative mechanism in the kidneys, it proposes a treatment known as guaifenesin therapy. This treatment involves administering the drug guaifenesin to a patient's individual dosage, avoiding salicylic acid in medications or on the skin, and, if the patient is also hypoglyemic, a diet designed to keep insulin levels low.

The phosphate build-up theory explains many of the symptoms present in fibromyalgia and proposes an underlying cause. The guaifenesin treatment, based on this theory, has received mixed reviews, with some practitioners claiming many near-universal success and others reporting no success. Only one controlled clinical trial has been conducted to date, and it showed no evidence of the efficacy of this treatment protocol. This study was criticized for not limiting the salicylic acid exposure in patients, and for studying the effectiveness of only guaifenesin, not the entire treatment method. As of 2005, further studies to test the protocol's effectiveness are in the planning stages, with funding for independent studies largely collected from groups which advocate the theory.

Fibromyalgia as severe TMS
Another theory is that fibromyalgia is a severe form of Tension myositis syndrome (TMS) which is a mindbody disorder popularized in the books on healing back, neck, and other limb pain by Dr. John E. Sarno of the Howard A. Rusk Institute of Rehabilitation Medicine. Briefly the theory is that in many cases chronic pain is the result of physical changes (primarily mild oxygen deprivation) caused by the brain through the autonomic nervous system as a strategy for distracting you from painful or dangerous unconscious emotions such as repressed anger. Treatment is through a program of education and attitude change which stops the brain from using that chronic pain strategy. Psychotherapy is suggested in the minority of cases where education alone is not sufficient.

Other theories
Other theories relate to various toxins from the patient's environment, viral causes such as the Epstein-Barr Virus, growth hormone deficiencies, an aberrant immune response to intestinal bacteria,[10][11] neurotransmitter disruptions in the central nervous system, and erosion of the protective chemical coating around sensory nerves. Due to the multi-systemic nature of illnesses such as fibromyalgia and chronic fatigue syndrome (CFS/ME), an emerging branch of medical science called psychoneuroimmunology (PNI) is looking into how the various theories fit together.

Comorbid diseases
Cutting across several of the above theories is a theory that proposes that fibromyalgia is almost always a comorbid disorder, occurring in combination with some other disorder that likely served to "trigger" the fibromyalgia in the first place. This concept fits especially well with the sleep disturbance theory.

By this theory, some other disorder (or trauma) occurs first, and fibromyalgia follows as a result. In some cases, the original disorder abates on its own or is separately treated and cured, but the fibromyalgia remains. In other cases the two disorders coexist. This theory would explain why such a wide variety of symptoms are often ascribed to fibromyalgia, since there are potentially a wide variety of comorbid disorders. It also helps explain why fibromyalgia is so hard to treat, since the fibromyalgia is unlikely to abate while the comorbid condition is untreated.

Commonly proposed comorbid/trigger disorders are:

Spinal disorders
Physical trauma, as from a traffic accident
Post-surgical pain
Chronic fatigue syndrome
Irritable Bowel Syndrome
Myofascial Pain Syndrome
Thyroid disease - for example Hashimoto's thyroiditis; thyroid hormone substitution can be helpful in some cases
Lyme disease
Post-polio syndrome
Hypermobility (including Ehlers-Danlos syndrome)
Restless Leg Syndrome
Clinical depression
Lupus erythematosus (SLE)

Skepticism
Some physicians believe that fibromyalgia is not an actual symptom complex. They claim that the symptoms of fibromyalgia are manifestations of depression, along with symptoms of unrelated diseases such as chronic fatigue syndrome, Epstein-Barr syndrome, interstitial cystitis, irritable bowel syndrome, bacterial infection, and others.

Skeptics point to the following list - some of which is no longer true - to support their skeptical positions:

lack of objective evidence to support patient's claims of suffering (no longer true)
divergent or unrelated symptoms ("syndrome")
the different rates of illness among members of different cultures
a relative lack of evidence-based treatments
a correspondingly large number of "quack" healers providing unproven, incorrect, or ineffective diagnosis and treatment
Some medical authorities who are unaware of the current objective physiological indicators revealed by recent research (such as substance P abnormalities) still believe that depression and psychological factors are the root cause of the syndrome, similar to hypochondria[4][5], despite the fact that as of 2006, there are no known specialist fibromyalgia researchers who agree.

"This isn't a disease, it's merely a description of symptoms... We've taken stress, psychosocial distress and pain and the ordinary life experiences some people have and turned them into something they're not -- a physical illness"
-- Dr. Fred Wolfe, a skeptical Rheumatologist who ironically helped define the disease earlier in his career[12].
However, depression should be expected to accompany any debilitating illness. In other words, depression is not a special trait of fibromyalgia. Interestingly, many victims of fibromyalgia either do not suffer from depression at all, or they did not suffer from it until after its onset.

References
^ Information from the National Fibromyalgia Association
^ Fibromyalgia from WebMD
^ [1] Cough syrup found by University of Florida to reduce fibromaylgia pain "moderately" but not recommended for personal self treatment
^ Fibromyalgia, published by BUPA insurance
^ Fibrofog, Fibromyalgia and Dissociation
^ Recommended Guaifenesin protocol practitioners
^ The Fibromyalgia Association of the UK
^ [2]
^ Are phosphates the hidden enemy? (76.7kb pdf)
^ Kendall SN (May 2004). "Remission of rosacea induced by reduction of gut transit time.". Clin Exp dermatol. 29 (3): 297-9. PMID 15115515.
^ Pimental M, Wallace D, Hallegua D et .al (April 2004). "A link between irritable bowel syndrome and fibromyalgia may be related to findings on lactulose breath testing.". Ann Rheum Dis. 63 (4): 450-2. PMID 15020342.
^ Article from Immune Support
Retrieved from "http://en.wikipedia.org/wiki/Fibromyalgia"

Missing Body Parts

Click the title link. Fun for medical personnel and other sick fucks!

Stem Cell Research

Click the title link. I really need to do more research on this topic myself. As it stands I don't feel qualified to comment. But I'm very interested in learning more.

Online Histology Slides

Study microscopic images of various tissues by clicking the title link!

The Third Degree

Here is a copy of my most recent assignment for my Anatomy and Physiology class. The text is entirely mine. If anyone wishes to quote from it or use the information for their own assignment, or to use the entire essay for teaching purposes, feel free.

COMPLICATIONS AND TREATMENT OF THIRD DEGREE BURNS
The severity of the potential complications posed by third degree burns depends on which part of the body was burned and on the amount of tissue that was damaged. The percentage of damage is calculated using the Rule of Nines. The following is the Rule of Nines measures for an adult: each arm has 9% of the body’s total skin, the head 9%, each leg 18% (two 9’s), the front of the torso 18%, the back of the torso 18%, and the neck 1%. Generally speaking, as the percent of the surface burned increases, morbidity and the probability of mortality increases sharply. Burns which cover 20% or more of the body surface can be fatal without treatment.
The most urgent complication posed by third degree burns is death due to loss of blood plasma, leading to circulatory shock and cardiac arrest. This happens because of fluid being transferred from the bloodstream to replace the fluid lost from the damaged tissue. The result is a decrease in the volume of circulating bloodstream. Another pressing complication comes from the potential for infection in the burned, dead tissue known as eschar. A secondary concern is contracture, or abnormal connective tissue fibrosis as the result of a third degree burn being left to heal on its own without medical intervention. Severe deformities can result from this.
Treatment for third degree burn victims starts with administering intravenous fluid to replace that which has been lost from the damaged tissue. The burn victim must also consume a very high number of calories to make up for protein loss and assist in tissue repair. They will receive supplemental nutrition intravenously or through a gastric tube. They will also receive powerful antibiotics.
The patient is kept in a sterile environment and will receive debridement treatments. The most commonly used method for many years has been mechanical debridement, in which a moist dressing is applied then manually removed. This can be excruciatingly painful for the patient. However, there have been advances in burn treatment and alternative types of debridement such as autolytic debridement are being used in certain cases. Autolytic debridement uses occlusive or semi-occlusive dressings to maintain wound fluid contact with the necrotic tissue. This encourages the body's enzymes and fluids to re-hydrate, soften and finally liquefy hard eschar and slough. Only necrotic tissue is liquefied. This debridement method is virtually painless for the patient but cannot be used in all cases.
After the initial treatment, the patient is likely to require a skin graft. Doctors generally perform an autograft, where skin is taken from another location on the person’s own body, usually the thigh or buttock, and is grafted to the burned area. However, in patients with more extensive burns, surgeons will use an isograft which employs skin from the patient’s close relative, preferably an identical twin. Skin banks also provide skin from cadavers to utilize in homografts. The rejection percentage for homografts is high. Surgeons generally use this measure as a temporary covering for the burned area until the patient is healthy enough to undergo an autograft. Pig skin can also be used in the same way. This method is known as a xenograft. Scientists are also working on developing artificial skin which will provide great advancement in the field of reconstructive treatment for burn patients.
C. Hartley
July 11, 2006

The following text is copied from this website which I utilized in part of my research:
http://www.medicaledu.com/debridhp.htm
Types of Wound Debridement
Autolytic Debridement:
Description:
Autolysis uses the body's own enzymes and moisture to re-hydrate, soften and finally liquefy hard eschar and slough. Autolytic debridement is selective; only necrotic tissue is liquefied. It is also virtually painless for the patient. Autolytic debridement can be achieved with the use of occlusive or semi-occlusive dressings which maintain wound fluid in contact with the necrotic tissue. Autolytic debridement can be achieved with hydrocolloids, hydrogels and transparent films.
Best Uses:
In stage III or IV wounds with light to moderate exudate
Advantages:
Very selective, with no damage to surrounding skin.
The process is safe, using the body's own defense mechanisms to clean the wound of necrotic debris.
Effective, versatile and easy to perform
Little to no pain for the patient
Disadvantages:
Not as rapid as surgical debridement
Wound must be monitored closely for signs of infection
May promote anaerobic growth if an occlusive hydrocolloid is used

Enzymatic Debridement:
Description:
Chemical enzymes are fast acting products that produce slough of necrotic tissue. Some enzymatic debriders are selective, while some are not.
Best Uses:
On any wound with a large amount of necrotic debris.
Eschar formation
Advantages:
Fast acting
Minimal or no damage to healthy tissue with proper application.
Disadvantages:
Expensive
Requires a prescription
Application must be performed carefully only to the necrotic tissue.
May require a specific secondary dressing
Inflammation or discomfort may occur

Mechanical Debridement:
Description:
This technique has been used for decades in wound care. Allowing a dressing to proceed from moist to wet, then manually removing the dressing causes a form of non-selective debridement.
Hydrotherapy is also a type of mechanical debridement. It's benefits vs. risks are of issue.
Best Uses:
Wounds with moderate amounts of necrotic debris
Advantages:
Cost of the actual material (ie. gauze) is low
Disadvantages:
Non-selective and may traumatize healthy or healing tissue
Time consuming
Can be painful to patient
Hydrotherapy can cause tissue maceration. Also, waterborne pathogens may cause contamination or infection. Disinfecting additives may be cytotoxic.

Surgical Debridement:
Description:
Sharp surgical debridement and laser debridement under anesthesia are the fastest methods of debridement.
They are very selective, meaning that the person performing the debridement has complete control over which tissue is removed and which is left behind
Surgical debridement can be performed in the operating room or at bedside, depending on the extent of the necrotic material.
Best Uses:
Wounds with a large amount of necrotic tissue.
In conjunction with infected tissue.
Advantages:
Fast and Selective
Can be extremely effective
Disadvantages:
Painful to patient
Costly, especially if an operating room is required
Requires transport of patient if operating room is required.

Maggots
Click here and scroll down to see the nasty pictures.
These images were supplied by David Janssen, M.D.
Dr. Janssen used to have a very detailed website, but now it's gone.
Other web resources, click here.

Folks, as a trained medical person my stomach is made of fairly strong stuff. During my EMT training we would eat our dinner while viewing slides of gruesome trauma and none of us were fazed. But maggots in a wound, and me knowing they were there? That makes my stomach turn in ways I didn't know it could! Sorry, arm/leg/whatever, but there wouldn't be any saving you if there were maggots involved! Excuse me while I go lose my lunch.

Hopefully the advancements in burn care and reconstruction will continue--without maggots, thanks!

Cie

Marfan Syndrome

What do a former U.S. president and a Swedish heavy metal singer have in common?
Possibly Marfan syndrome.
Marfan syndrome is an autosomal dominant disorder that has been linked to the FBN1 gene on chromosome 15. FBN1 codes for a protein called fibrillin-1, which is essential for the formation of elastic fibers found in connective tissue. Marfan syndrome is also an example of a dominant negative mutation. Marfan syndrome is associated with incomplete penetrance, therefore not all persons carrying the mutation develop the disease.
Without the structural support provided by fibrillin, many connective tissues are weakened, which can have severe consequences on support and stability. The most serious conditions associated with Marfan syndrome primarily involve the cardiovascular system. Marfan syndrome may cause leakage of the mitral or aortic valves that control the flow of blood through the heart. This may produce shortness of breath, an irregular pulse, and undue tiredness. Another complication is aortic aneurysm.
Curvature of the spine (scoliosis) is a common problem, as is abnormal indentation (pectus excavatum) or protrusion (pectus carinatum) of the sternum. These symptoms may in turn cause unusual pressure on the heart and lungs. Other symptoms include; abnormal joint flexibility, high palates, flat feet, stooped shoulders, and dislocation of the optic lens.
Nearsightedness or myopia is a common condition associated with Marfan syndrome. In addition, the weakening of connective tissue often causes detachment of the retina and/or displacement of the lens in one or both eyes.
Quoted from Wikipedia

Marfan syndrome sufferers may grow to larger than normal height, and typically have long, slender limbs and fingers. Their arm span usually exceeds their height. (For instance a person of 6'6" tall would normally have a 6'6" arm span. A person with Marfan Syndrome at this height would likely have a 7' arm span.) Their arms and legs are strikingly long in comparison with the torso.



















Abraham Lincoln was 6'4" tall and weighed around 180 pounds.



















Per Ohlin was 6'4" or 6'5" tall. His weight was likely comparable to that of President Lincoln.

















Persons with Marfan Syndrome sometimes have fingers with a long, thin, spidery appearance known as arachnodactyly.









































































These photos show the markedly angular facial features in both subjects. Both men have a prominent, angular nose with a strikingly broad bridge.

Of course not all tall, slender individuals have Marfan Syndrome. Basketball star Michael Jordan is 6'6" tall and weighs 215 pounds. He exhibits none of the characteristics of Marfan's.

For more information on my models:
Abraham Lincoln (February 12, 1809-April 15, 1865)
Per Ohlin (January 16, 1969-April 8, 1991)

A personal note:
Although not a trait associated with Marfan Syndrome, I find it interesting that both Lincoln and Ohlin suffered from mood disorders, either major depression or possibly Bipolar Type II as both had periods when they described moments of elation or high energy uncharacteristic to their normally melancholy personalities. Lincoln once described himself as being the most miserable man alive. Ohlin committed suicide at the age of 21.
Both of these individuals possessed remarkable qualities far beyond being interesting subjects for scientific observation. They were both highly intelligent. Lincoln was a noble humanitarian and Ohlin a gifted poet and musician. I mention these aspects because I believe in the importance of focusing on a person's soul before their physiology.