Gani’s Health 1ST EDITION 2014

Health and Science

Babygani Babybuletgani@gmail.com https://www.facebook.com/BabyGani

Editor’s Note

In my free time, I browse often and read news and articles especially about health because

of my proffesion. So one day I thought about collecting it, in case of “I think I’ve read about

it”. You know the feeling of knowing something but it was a blur because its been awhile. For

that reason I make this magazine, for fun and education. Magazine format is neat and good

looking so I go with magazine. There will be another magazine with different theme other

than health, but for now, happy reading and enjoy.

Babygani

Angioplasty is a cutting-edge medical procedure that helps your heart last longer

Your heart pumps blood-rich oxygen to your body’s tissues – but the heart muscle needs oxygen itself. The coronary arteries are small vessels lining your heart’s surface that do this job perfectly, in exact synchronisation with the beats of the heart. However, they can become blocked. A lack of exercise, smoking, poor diet and unlucky genes can all lead to plaques of fatty tissue, called atheroma, blocking these vital arteries. Then, if your heart needs to pump harder, such as during exercise, the reduced blood flow cannot supply enough oxygen. This leads to pain – angina – which is an early warning sign that the heart muscle is dying. Previously, the only way to cure advanced cases was to go under the surgeon’s knife. However, cardiac surgery is a risky procedure. Then along came angioplasty. Via a small artery in the patient’s groin or wrist, doctors insert a guide wire directly into the coronary arteries of the heart. This is tricky, and so they use real-time X-ray images to guide them to exactly the right place. They feed a tiny, thin, flexible hollow tube over this wire (a catheter). Injecting dye into these arteries (via the hollow catheters) and looking carefully at the result shows them exactly where the blockages are. Next, they inflate tiny balloons attached to the end of these long catheters at the exact spot of the blockage. In some cases, this is enough. In others, to prevent the artery closing again, a stent can be placed through the affected area. These are clever stents and can contain drugs that prevent them blocking. A final check X-ray completes the angioplasty process. Angioplasties like this can also be performed on blocked arteries in the legs, where the principle is exactly the same. But no matter where the blockage is, this procedure requires a steady hand and a doctor who can think fast and think in real-time 3D while looking at 2D blackand- white images.

   

Balloon catheter

The balloon catheter is one of the key pieces of the angioplasty doctor’s equipment. Once the guidewire is inserted, the catheter is fed over it and floated into exactly the right place. Through this catheter, special dyes that can be seen on X-ray images (radio-opaque contrast dye) can be injected through the hollow catheter to confirm its position and then confirm the location of the blockages. At the tip of the catheter is a balloon. Using water, this balloon can be inflated from outside to precise pressures. When this is done from the centre of the blockage, the atheromatous plaque is expanded to allow more blood flow. There are many different sizes of catheter and widths of balloons, allowing exact tailoring to the patient’s needs. Sometimes the doctor will start with a small balloon when the blockage is very narrow, and then sequentially insert larger balloons to allow for the maximum effect. However, care is needed – too large a balloon or too much pressure and the vessel can rupture, which is a life-threatening complication. Experience, care and control of the pressures prevent this.

Usually, you will stay in bed for six hours after your angioplasty. During this time, your vascular surgeon and the hospital staff closely monitor you for any complications. If your physician inserted the catheters through an artery in

your groin, you may have to hold your leg straight for several hours. Similarly, if your arm was used, then you will need to hold it still to minimize the risk of bleeding.

If you notice any unusual symptoms after your procedure, you should tell your vascular surgeon immediately. These symptoms include leg pain that lingers or gets worse, a fever, shortness of breath, an arm or a leg that turns blue or feels cold, and problems around your access site, such as bleeding, swelling, pain, or numbness.

After you return home, your vascular surgeon will give you instructions about everyday tasks. For example, you should not lift more than about 10 pounds for the first few days after your procedure. You should drink plenty of water for 2 days to help flush the contrast dye out of your body. You can usually shower 24 hours after your procedure, but you should avoid baths for a few days.

Your physician may prescribe aspirin or other medications that thin your blood. These medications will help prevent clots from forming on your stent. Your physician may also ask you to follow an easy exercise program, like walking.

You will be asked to schedule a time to see your physician after the procedure. At this appointment, your physician may check your blood to make sure your medications are at the right dosage. He or she may also use tests to see how blood is flowing through your treated artery.

   

Are cell mutations troublesome?

A mutation is a change in the genetic material of an organism. We’re made from trillions of cells, each with a nucleus composed of DNA – a set of instructions that tells the cell what to do. Cells copy themselves with astonishing accuracy, but every now and then a piece of code is copied incorrectly. This is largely due to natural radiation interacting with our DNA. This incorrect piece of code can become a permanent change in the DNA. Mutations are rarely harmful though. Indeed, most mutations go unnoticed, as the body has mechanisms to stop a cell copying itself. Sometimes mutations can benefit organisms. When a mutation allows an organism to cope better with an environmental stress, it will be passed on to future generations through natural selection.

 

Evolution works through mutation. Mutation is the source of all new genes and subsequently all new traits; evolution is the process by which the gene pool changes as a result of natural selection. The reason there is variation for natural selection to "select" from is that there are mutations producing new genes and new traits. The eye is a famous example of an organ that had to evolve through many, many steps of mutation. Scientists think the eye probably started out as just a spot of light-sensitive pigment; then at some point it was formed into a cup, a lens formed over the mouth of that cup, etc., and eventually we ended up with they types of eyes we have today. Interestingly, eyes have developed two separate ways on Earth: the compound eyes of insects function on fundamentally different principles than the single gelatinous eyes of vertebrates.

It is true that mutations are almost always damaging. This is because genes and their protein products are so complicated; if you change something randomly, it will very likely stop the gene or protein from working right. But, rarely, a random change will actually -improve- the functioning of the gene or protein product. Then, instead of being eliminated from the gene pool because it causes death or disease, the gene's carrier survives and the gene spreads throughout the gene pool over many generations. Many of these small, beneficial mutations accumulate over millions of years to produce whole new species.

   

Why is this invisible and odourless gas so deadly?

Carbon monoxide poisoning is the most common form of fatal air poisoning. Colourless, odourless and tasteless, carbon monoxide is so deadly as it is adept at binding with haemoglobin in the blood. On doing this it produces carboxyhaemoglobin, which – unlike haemoglobin – is completely ineffective in carrying oxygen to bodily tissues. While carbon monoxide is itself difficult to detect, carbon monoxide poisoning in humans can be seen through the colouration of the skin and lips. This is because carboxyhaemoglobin has a characteristic cherry-red colour and, in large concentrations, causes pigmentation in the skin. Other indications of carbon monoxide poisoning include headaches, dizziness and a weak pulse. One of the biggest contributors of carbon monoxide to the environment is exhaust fumes from combustion engines.

The key to confirming the diagnosis is measuring the patient’s carboxyhemoglobin (COHb) level. Carbon Monoxide levels can be tested either in whole blood or exhaled air. It is important to know how much time has elapsed since the patient has left the toxic environment, because that will impact the COHb level. If the patient has been breathing normal room air for several hours, COHb testing may be less useful. The most common technology available in hospital laboratories for analyzing the blood is the multiple wavelength spectrophotometer, also known as a CO-oximeter. Venous or arterial blood may be used for testing. A fingertip pulse CO-oximeter can be used to measure heart rate and oxygen saturation, and COHb levels. The conventional two-wavelength pulse oximeter is not accurate when COHb is present. An elevated COHb level of 2% for non-smokers and >9% COHb level for smokers strongly supports a diagnosis of CO poisoning.

Other testing, such as a fingerstick blood sugar, alcohol and toxicology screen, head CT scan or lumbar puncture may be needed to exclude other causes of altered mental status when the diagnosis of carbon monoxide poisoning is inconclusive. Carbon monoxide can be produced endogenously as a byproduct of heme metabolism. Patients with sickle cell disease can have an elevated COHb level as a result of hemolytic anemia or hemolysis.

Guidance for Management of Confirmed or Suspected CO Poisoning Administer 100% oxygen until the patient is symptom-free, usually about 4-5

hours. Serial neurologic exams should be performed to assess progress, and to detect the signs of developing cerebral edema.

Consider hyperbaric oxygen therapy (HBO) therapy when the patient has a COHb level of more than 25- 30%, there is evidence of cardiac involvement, severe acidosis, transient or prolonged unconsciousness, neurological impairment, abnormal neuropsychiatric testing, or the patient is ≥36 years in age. HBO is also administered at lower COHb(<25%) levels if suggested by clinical condition and/history of exposure.

Hyperbaric oxygenis the treatment of choice for pregnant women, even if they are less severely poisoned. Hyperbaric oxygen is safe to administer and international consensus favors it as part of a more aggressive role in treating pregnant women.

Other Considerations Cardiac injury during poisoning increases risk of mortality over 10

years following poisoning, so in patients with severe CO poisoning, it may be important to perform an EKG and measurement of troponin and cardiac enzymes.

Chest radiography is recommended for seriously poisoned patients, especially those with loss of consciousness or cardiopulmonary signs and symptoms. Brain computed tomography or MRI is also recommended in these cases; these tests may show signs of cerebral infarction secondary to hypoxia or ischemia.

All discharged patients should be warned of possible delayed neurological complications and given instructions on what to do if these occur. Follow-up should include a repeat medical and neurological exam in 2 weeks.

How does Thermometers reveal the temperature?

   

Traditional thermometers contained mercury, which expands with rising temperatures. Most households now have digital thermometers, as they’re safer, easier to read, and work faster. Digital thermometers contain an electric resistor, also known as a thermistor, which is temperaturesensitive. When the temperature rises, the thermistor becomes more conductive. This happens at about 37°C (99°F). A microcomputer pinpoints the temperature by measuring the conductivity, and displays it on an LCD screen. Originally, Anders Celsius pegged his scale with the boiling point of water at 0 degrees and the freezing point of ice at 100 degrees, based on the water’s behavior under pressure, but Carl Linnaeus swapped these after his death. Daniel Gabriel Fahrenheit first based his scale on three states of brine, which were stable, freezing and boiling. Later his scale was adjusted so there were 180 intervals between the freezing point of ice (32°F) and boiling point of water (212°F). The scales intersect at -40 degrees.  

Fever is the temporary increase in the body's temperature in response to some disease or illness. A child has a fever when the temperature is at or above one of these levels:

100.4 °F (38 °C) measured in the bottom (rectally) 99.5 °F(37.5 °C) measured in the mouth (orally) 99 °F (37.2 °C) measured under the arm (axillary)

An adult probably has a fever when the temperature is above 99 - 99.5 °F (37.2 - 37.5 °C), depending on the time of day.

Infections such as pneumonia, bone infections (osteomyelitis), appendicitis, tuberculosis, skin infections or cellulitis, and meningitis. Respiratory infections such as colds or flu -like illnesses, sore throats, ear infections, sinus infections, infectious mononucleosis, and bronchitis

Urinary tract infections such as Viral gastroenteritis and bacterial gastroenteritis. Children may have a low-grade fever for 1 or 2 days after some immunizations.

Teething may cause a slight increase in a child's temperature, but not higher than 100 °F.

Autoimmune or inflammatory disorders may also cause fevers. Some examples are: Arthritis or connective tissue illnesses such as rheumatoid arthritis and systemic lupus erythematosus. Ulcerative colitis and Crohn's disease. Vasculitis or periarteritis nodosa. The first symptom of a cancer may be a fever. This is especially true of Hodgkin's disease, non-Hodgkin's lymphoma, and leukemia.

Other possible causes of fever include: Blood clots or thrombophlebitis. Medications, such as some antibiotics, antihistamines, and seizure medicines

A simple cold or other viral infection can sometimes cause a high fever (102 - 104 °F, or 38.9 - 40 °C). This does not usually mean you or your child have a serious problem. Some serious infections may cause no fever or even a very low body temperature, especially in infants. If the fever is mild and you have no other problems, you do not need treatment. Drink fluids and rest. The illness is probably not serious if your child:

Is still interested in playing Is eating and drinking well Is alert and smiling at you Has a normal skin color Looks well when their temperature comes down

Take steps to lower a fever if you or your child is uncomfortable, vomiting, dried out (dehydrated), or not sleeping well. Remember, the goal is to lower, not eliminate, the fever. When trying to lower a fever:

Do NOT bundle up someone who has the chills. Remove excess clothing or blankets. The room should be comfortable, not too

hot or cool. Try one layer of lightweight clothing, and one lightweight blanket for sleep. If the room is hot or stuffy, a fan may help.

A lukewarm bath or sponge bath may help cool someone with a fever. This is especially effective after medication is given -- otherwise the temperature might bounce right back up.

Do NOT use cold baths, ice, or alcohol rubs. These cool the skin, but often make the situation worse by causing shivering, which raises the core body temperature.

Here are some guidelines for taking medicine to lower a fever:

Take acetaminophen every 4 - 6 hours. It works by turning down the brain's thermostat.

Take ibuprofen every 6 - 8 hours. DO NOT use ibuprofen in children younger than 6 months old.

Greater than 6 months to 12 years: 5 mg/kg/dose for temperature less than 102.5 degrees F (39.2 degrees C) orally every 6 to 8 hours as needed. 10 mg/kg/dose for temperature greater than or equal to 102.5 degrees F (39.2 degrees C) orally every 6 to 8 hours as needed. The recommended maximum daily dose is 40 mg/kg. OTC pediatric labeling (analgesic, antipyretic): 6 months to 11 years: 7.5 mg/kg/dose every 6 to 8 hours; Maximum daily dose: 30 mg/kg

Aspirin is very effective for treating fever in adults. DO NOT give aspirin to a child unless your child's doctor tells you to.

Know how much you or your child weighs, and then always check the instructions on the package.

In children under age 3 months, call your doctor first before giving medicines.

Eating and drinking with a fever:

Everyone, especially children, should drink plenty of fluids. Water, popsicles, soup, and gelatin are all good choices.

Do not give too much fruit or apple juice and avoid sports drinks in younger children.

Although eating foods with a fever is fine, do not force foods.

Potential Drug-Drug Interactions

Alcohol The package label for adult TYLENOL® acetaminophen products contains an alcohol warning that states, "If you consume 3 or more alcoholic drinks every day, ask your doctor whether you should take acetaminophen or other pain relievers/fever reducers. Acetaminophen may cause liver damage." Chronic heavy alcohol abusers may be at increased risk of liver toxicity from excessive acetaminophen use, although reports of this event are rare. Although some authors suggest that alcoholics may be at increased risk from therapeutic doses, reports usually involve cases of severe chronic alcoholics and the dosages of acetaminophen most often exceed recommended doses and often involve substantial overdose.Studies evaluating the metabolism of doses up to 20 mg/kg of acetaminophen in chronic alcohol abusers and a study evaluating the effects of 2 days of acetaminophen dosing at 4000 mg daily in chronic alcoholics undergoing detoxification do not support an increased risk of hepatotoxicity with recommended doses of acetaminophen. Healthcare professionals should alert their patients who regularly consume large amounts of alcohol not to exceed recommended doses of acetaminophen.

Anticonvulsants Some reports have suggested that patients taking long-term anticonvulsants, who overdose on acetaminophen, may be at increased risk of hepatotoxicity because of accelerated metabolism of acetaminophen. Available data are conflicting. A 7-year retrospective study of acetaminophen overdose admissions indicates that the overall mortality rate was not significantly different for patients taking concomitant anticonvulsant medications.

Hydantoins At usual oral therapeutic doses of acetaminophen and hydantoins, no special dosage adjustment or monitoring is generally required. Pharmacokinetic studies indicate that phenytoin primarily induces the glucuronidation pathway, whereas glutathione-derived metabolites are not increased in patients on chronic phenytoin therapy.Additionally, recent data demonstrate that phenytoin is metabolized primarily by CYP2C9 and CYP2C19,whereas acetaminophen is primarily metabolized by CYP2E1. These data indicate that there is no increased risk from an acetaminophen overdose in patients on chronic hydantoin therapy. Carbamazepine At usual oral therapeutic doses of acetaminophen and carbamazepine, no special dosage adjustment is generally required. Carbamazepine is primarily metabolized by CYP3A4, whereas acetaminophen is metabolized primarily via CYP2E1. It is not

known whether there is increased risk from an acetaminophen overdose in patients on chronic carbamazepine therapy. Diflunisal Professional literature from the manufacturer of diflunisal cautions that concomitant administration with acetaminophen produces an approximate 50% increase in plasma levels of acetaminophen in normal volunteers. Acetaminophen had no effect on diflunisal plasma levels. The clinical significance of these findings has not been established. However, caution should be used with concomitant administration of diflunisal and acetaminophen and patients should be monitored carefully. Isoniazid Some reports suggest that patients on chronic isoniazid therapy may be at risk for developing hepatotoxicity from an acetaminophen overdose at doses that would not have been expected to produce toxicity.Since patients on isoniazid therapy may develop hepatic effects from isoniazid alone, data from individual case reports are unclear as to whether chronic administration of isoniazid may increase the risk of acetaminophen toxicity. Volunteer studies demonstrate that isoniazid inhibits the formation of the toxic metabolite of acetaminophen when taken concurrently, indicating that isoniazid could actually protect against hepatotoxicity from an acetaminophen overdose. However, it also appears that isoniazid acetylation genotype may play a role in the activity of CYP2E1,and based on acetylation genotype, inhibition or induction may be present following discontinuation of isoniazid therapy. In two studies of induction, any evidence suggesting increase of activity was only seen during a brief period from 12 to 48 hours after discontinuation of isoniazid.

Oral Anticoagulants Many factors, including diet, medications, and environmental and physical states, may affect how a patient responds to anticoagulant therapy.There have been several reports that suggest that acetaminophen may produce hypoprothrombinemia (elevated international normalized ratio [INR] or prothrombin time) when administered with coumarin derivatives. In other studies, prothrombin time did not change. Reported changes have been generally of limited clinical significance, however, periodic evaluation of prothrombin time should be performed when these agents are administered concurrently. In the period immediately following discharge from the hospital or whenever other medications are initiated, discontinued, or taken regularly, it is important to monitor patient response to anticoagulation therapy with additional prothrombin time or INR determinations.

Find out what causes pimples to form on the surface of human skin

Pimples are caused by sensitivity to the testosterone hormone present in both males and females, which can trigger the overproduction of an oily substance called sebum. Sebum, which is produced by sebaceous glands attached to hair follicles in the dermis, helps keep hair and skin waterproof. Your skin is constantly renewing itself, and while new cells are produced in the lower layers of skin, the old dead cells are sloughed away from the surface. This, together with excessive sebum production, can lead to acne and pimples. Sebum normally travels through the hair follicle to the surface of the skin. However, if a pore becomes blocked by a few dead skin cells that haven’t been shed properly, the sebum builds up inside the hair follicle. This oily buildup is a breeding ground for bacteria, which then accumulate and multiply around the area, making the skin inflamed and infected. This results in the pimple. Whiteheads and blackheads are types of acne pimples known as comedones. Blackheads are open comedones, which means the blockage of sebum is exposed to the air, causing oxidation of the sebum (like when an apple browns). Whiteheads, on the other hand, are closed comedones and are not exposed to air as they’re covered by a layer of skin.

In mild acne, open and closed comedones (blackheads and whiteheads)

predominate but papules and pustules may also be present. Although the physical

severity of the condition is limited and scarring is unlikely, the psychosocial impact

may be disproportionate in some people, which is an indication for more aggressive

treatment.

Prescribe a single topical treatment.

1. Topical Retinoid (tretinoin, isotretinoin, or adapalene) or Benzoylperoxide

(especially if papules and pustules are present) as first-line treatment.

2. Azelaic acid if both topical retinoids and benzoyl peroxide are poorly tolerated.

3. Combined treatment is rarely necessary for mild acne.

Consider prescribing a standard combined oral contraceptive in women who require

contraception, particularly if the acne is having a negative psychosocial impact.

Arrange follow up after about 6–8 weeks to review the effectiveness and tolerability

of treatment,and the person's compliance with the treatment. If no improvement is

seen after 6–8 weeks, check adherence to treatment:

If adherence is poor, this may be because the treatment is poorly tolerated.

Consider:

1. Reducing the strength of treatment (for example reducing from 5% to 2.5%

benzoyl peroxide).

2. Switching to an alternative topical drug that causes less irritation (for example

a topical antibiotic or azelaic acid).

3. Using a different formulation of drug (for example a cream instead of a drug

with an alcoholic base).

If adherence is adequate, consider:

1. Increasing the drug strength and/or frequency of application.

2. Combining different topical products.

A Topical AB combined with benzoyl peroxide or a topical retinoid is the

preferred regimen, as it is proven to be effective and may limit the development

of bacterial resistance. Where possible, a topical antibiotic course should be

limited to a maximum of 12 weeks. A topical retinoid combined with benzoyl

peroxide is an alternative, but this may be poorly tolerated.

Find out why the tiny yeast cell is essential for making bread, beer and wine

Yeasts are unicellular organisms that are members of the fungus family. There are thousands of different yeast organisms, but only a fraction of them have been studied in any detail. They thrive on oxygen and carbohydrates, such as sugar, which causes them to produce ethyl alcohol and carbon dioxide. These processes are known as fermentation and anaerobic respiration. Yeast cells are a type of eukaryotic cell that mainly multiply through the process of budding. A daughter cell forms on the side of the mother cell and in 20 minutes it swells and separates. During this process, the daughter cell can multiply in the same manner – even as it is still growing.

The saccharomyces cerevisiae strain of yeast is used for brewing and baking. In wine making, yeast converts the sugar in grapes into alcohol. In bread making, as yeast is mixed with the ingredients it is starved of oxygen and its reproduction is reduced, which then causes it to convert sugars in the dough into alcohol and carbon dioxide. This makes the bread dough rise and provides it with flavour. Yeast is also used in the biotechnology industry to convert the sugars in cereal grains, sugar cane, paper and wood chippings into alcohol that can be used as a fuel instead of petrol or diesel.

After the ingredients for bread are mixed together, fermentation occurs when the

yeast cells break down large starch molecules into sugars for energy. They use this

energy for survival and reproduction. The sugars digested by the yeast “burp out”

carbon dioxide and ethyl alcohol into existing air bubbles in the dough. And this

causes the dough to rise.

In the meantime, while you’re working with the dough these bubbles of carbon

dioxide and alcohol burst, allowing for two proteins in the flour, glutenin and

gliadin, to glom onto water particles. As they tango they become an elastic-like

mass of molecules known as gluten. And the more gluten, the stronger your bread

becomes, and the more it can act as a dome to keep in the symphony of organic

chemicals that cause the dough to exponentially rise. All of which results in the

delightful crater-like terrain of the finished product.

When the dough is left to rest it gives the gluten bonds a chance to relax, and,

presumably, reflect on their journey ahead. Byproducts like organic acids and

amino acids, along with sugar, salt and bacteria contribute to the developing

flavor profile of the bread.

During the early stages of baking alcohol evaporates to a gas and helps to leaven

the dough. The end result is a mouth-watering aroma wafting off the crust.

How can scientists synthetically replicate the taste of real food?

Artificial flavourings are used to improve the taste of food or to chemically re-create a flavour that cannot be achieved through conventional production. Artificial flavours can be produced cheaper than their natural counterparts and they can also be so concentrated that much less of them is required to generate the same taste, making them very cost-effective. To chemically re-create the taste of a naturally occurring flavour, specialist flavour chefs first obtain the essential chemicals from the foodstuff they’re trying to emulate. These chemicals are leeched out of the food through either boiling, roasting or some other refining process. This leaves a concentrate (the natural flavouring), which can be further vaporised or liquefied to obtain an even more concentrated version. By looking at the substance through a chromatograph (an instrument that enables the separation of complex mixtures) flavour scientists can establish how the molecules in the concentrate are arranged, and then replicate the chemicals to create a man-made equivalent of the original flavour. Differing combinations of the same molecules can lead to a whole host of different flavours.  

Foods  and  beverages  with  artificial  ingredients  can  cause  an  array  of  health  problems, 

especially when  used  frequently.  Artificial  flavors  have  been  known  to  cause  chest  pain, 

headaches,  fatigue,  nervous  system  depression,  allergies,  and  even  brain  damage. 

Unfortunately,  this  is  only  the  beginning  of  the  list. Other  symptoms  including  seizures, 

nausea, dizziness, and many more. 

With over three thousand artificial flavoring ingredients currently in production, any number 

of these side effects could be swarming your meals on a daily basis, along with additional 

consequences. One of  the more common artificial  flavorings, caramel, has been known  to 

cause vitamin B6 deficiencies, genetic defects, as well as cancer. Saccharin, another popular 

flavor ingredient, can bring on allergic or toxic reactions, tumors, and bladder cancer. 

Some food and beverage companies are attacking the current “health trend” from a whole 

new angle. Rather than cutting out sodium, sugars, and MSG, they’re  implementing a new 

product altogether, one that shuts off your taste buds. Some of these big names are using 

bitter‐tasting alternatives to sodium and sugars, and then removing the bad taste with a new, 

mystery substance that prevents tongues from detecting their flavors. 

Legally though, this “generally safe” item doesn’t have to be listed on the ingredients label. 

Because  of  the  FDA’s  definitions  and  standards,  it  simply  falls  into  the  “artificial  flavors” 

category,  leaving most customers unawares. Companies have also declined to share which 

products currently contain the new taste‐altering substance,  leaving us even further  in the 

dark. 

Unfortunately this and other artificial flavor  ingredients are placed  into most pre‐packaged 

foods and beverages. The best way to avoid them  is to read  labels carefully  (and with the 

understanding  that  “artificial  flavors”  can  be much more  dangerous  than  it  reads),  and 

avoiding such substances. 

 

7 Reasons to Hate Artificial Food Dyes 

1. They are made in a lab with chemicals derived from petroleum, a crude oil product, which 

also happens to be used in gasoline, diesel fuel, asphalt, and tar. 

2. They’ve been linked to long‐term health problems such as cancer. If you’re a child of the 

‘80s, do you remember that rumor about red M&Ms causing cancer? Maybe it wasn’t just a 

rumor after all. 

3. Did you know that food products containing artificial dye are required to have a warning 

label in the U.K.? The label states that the food “may have an adverse effect on activity and 

attention in children.” So speaking of M&Ms, they aren’t so brightly colored in some countries 

outside of the U.S. because manufacturers would rather do away with the artificial dye than 

have to put a warning label on their products. 

4. Synthetic food dyes have been shown to cause an increase in hyperactivity in children as 

well as a negative impact on their ability to learn. 

5. They add absolutely no value to the foods we are eating, but do in‐fact pose quite a few 

serious risks. 

6. They trick your senses…just like other artificial additives including sweeteners. 

7. They are contributing to the obesity epidemic by attracting children (and adults) to highly 

processed food, which in many cases is being eaten instead of fresh whole foods. 

How do hair regrowth products work?

Male and female pattern baldness is caused by hair follicles reacting to the testosterone hormone. Alopecia areata damages hair follicles due to imbalances in the immune system caused by stress, disease, infection, chemotherapy or genetic predisposition. For male pattern baldness, finasteride can be used to block the impact of testosterone on hair follicles and can restore some of the hair lost. Minoxidil lotion can be used for male and female pattern baldness and can reduce or stop hair loss in the long term. Corticosteroid injections into the scalp or topical corticosteroid creams and ointments can be used to deal with alopecia areata, as they suppress the immune system from attacking hair follicles. Immunotherapy involves the application of diphencyprone (DPCP) solution onto the scalp, and ultraviolet light therapy involves shining UVA or UVB rays on the scalp. These all have variable results and side effects. Often alopecia areata can be a temporary form of hair loss that does not require treatment. If it’s permanent and does not respond to these treatments, then hair can be surgically implanted into the scalp. Minoxidil works well for men who don't want to take a pill and who want to stall or prevent hair loss, there's little downside to it, other than having to use it twice a day indefinitely. You don't even need a prescription. Minoxidil seems to enlarge hair follicles and stimulate hair growth, up to 7 in 10 men who take minoxidil say they regrow some hair. Men who try it need to be patient because sometimes results can take four months. Those with very sensitive scalps may have problems with even a foam formulation and might want to try finasteride.

Finasteride blocks the enzyme that converts testosterone to dihydrotestosterone (DHT), a hormone considered the major culprit in male pattern baldness. DHT thins the hair of men who have inherited a baldness gene because it shrinks genetically

sensitive hair follicles until those follicles can no longer grow hair. Finasteride slows hair loss in as many as 90% of men, and most men who take it regrow some hair.

You can use minoxidil and finasteride together, often for better results. Whether you use one or both, you must stick to that treatment. The moment you stop, you start losing hair again, sometimes faster than before.

How do trampolines make us jump high in the air? Trampolines provide a perfect example of both Newton’s laws of motion and Hooke’s law of elasticity. The three key elements are the jumper’s weight, the springs and the fabric, which provide the trampolinist with all they need to get in the air. The total energy of the system (namely, the person jumping on the trampoline) remains constant, so their kinetic and potential energy must increase and decrease relatively to ensure energy conservation. This transfer of energy is made possible thanks to Hooke’s law, which relates to elasticity. A trampoline is basically an elastic disc connected to several springs. When a person lands on the trampoline they stretch both the springs and the fabric surface. Hooke’s law states that stretched springs will always try to return to their original shape. Therefore, the springs, and so the surface, push against the person’s weight, equal to the force they exert downwards, launching them upwards into the air. All moving objects are said to have kinetic energy. While jumping on a trampoline a person’s kinetic energy will change depending on their velocity. Maximum kinetic energy is achieved at the moment just after leaving the trampoline and just before returning to it, when velocity is at its greatest. The minimum occurs at the top of the jump and when at rest on the trampoline, just before the springs propel them up again. The potential energy is determined by the jumper’s mass as well as their height from the ground; the higher the trampolinist is from the ground, the greater the potential energy. This changes inversely to kinetic energy under the laws of the conservation of energy, where total energy is kinetic plus potential. In other words, as the individual leaves the trampoline and rises, their speed decreases and thus so does their kinetic energy, but in contrast their potential energy increases. As they reach the top of the jump and begin to fall, the opposite is true as potential gives way to kinetic, and the process repeats.

 

 

How Superbugs work 

   

Antibiotics are, without question, the miracle drugs of the 20th Century. Penicillin, the first widely produced antibiotic, saved more soldiers’ lives during the Second World War than the Sherman tank. Since the Forties, researchers have discovered newer, more powerful strains of antibiotics to treat everything from the common ear infection to the most exotic tropical disease. When a young mother takes her sick child to the doctor, complaining of high fevers, green mucus and listlessness, she doesn’t want to hear the speech about drinking lots of liquids and getting plenty of rest – she wants something that will alleviate the symptoms almost instantly. She wants antibiotics. And sadly, many doctors are more than happy to prescribe them, whether patients need them or not.

Antibiotics are wrongfully administered in almost 50 per cent of cases. On an individual level, there’s no real harm in unnecessarily taking an antibiotic, but widespread abuse of antibiotics has a potentially catastrophic effect on society as a whole. The more antibiotics that humans (and the animals we eat) take, the quicker bacteria evolve and the stronger they become. And what happens when bacteria evolve so significantly that our beloved antibiotics no longer have any effect on them?.

Antibiotic resistance is one of the world’s most serious health threats. We are already witnessing the rise of socalled ‘superbugs’, pathogenic bacteria that are immune to traditional antibiotic treatment. The best-known superbug is MRSA, short for methicillin-resistant Staphylococcus aureus. Like several other drug-resistant bugs, MRSA spreads quickly through hospitals on the unwashed hands of health workers and patients. Staph infections are nasty enough. If allowed to enter the body, they can target the lungs (pneumonia), the heart (endocarditis) and even the bloodstream (bacteraemia). MRSA is staph on steroids, because it has evolved to be resistant to the most effective antibiotics for curing the infection. Imagine going into the hospital with a sprained ankle and leaving with a drugresistant case of pneumonia. So how do common bacteria like S aureas and E coli evolve so quickly from a curable annoyance to a potential pandemic? Let’s start by dusting off our Darwin. Evolution by natural selection requires three things: reproduction, variety and selective pressure. Bacteria are masters of reproduction. Under the right conditions, a bacterial colony will double in size every ten minutes. They do this through binary fission. Essentially, the bacterium makes a copy of its own DNA, then splits in two. With so much copying and splitting, some mistakes (mutations) are going to be made. These genetic mutations increase the variety of traits that the bacteria can express. Variety is not only the spice of life, but also the engine of evolution. When a doctor administers an antibiotic to kill off an infection of S aureas, this applies a selective pressure to the bacterial colony.

Bacteria that express beneficial traits – such as the ability to pump antibiotics out of their system – will survive, while the others will be wiped out. The surviving bacteria will then repopulate the colony, and the next time the antibiotic is applied, it will be completely useless.

Bacteria are not only evolutionarily efficient, but they are also cheaters. Through a process called conjugation, two bacteria can share slices of genetic material that carry beneficial traits, skipping the randomness of natural selection altogether. By this method, some bacteria have developed techniques for disguising themselves to antibiotics, blocking the entrance to the cell wall, and even tricking the body’s own immune system to release toxic levels of proteins. The best weapon against the spread of superbugs is to reduce our overall consumption of antibiotics – including the beef, pork and dairy industries, which are responsible for administering 70 per cent of the antibiotics in America – and to improve hygiene and sanitation at hospitals, where these infections thrive and spread. Inside an MRSA bacterium MRSA is a drug-resistant strain of Staphylococcus aureus, one of the most virulent and violent bacteria we know. Staph infections come in all flavours, from diarrhoea-inducing food poisoning, to skin lesions, to potentially fatal cases of toxic shock syndrome. MRSA is a staph bacterium that has mutated or otherwise acquired genetic traits that defend it against attacks from antibiotics.

Why antibiotics don’t work

Bacteria exist in our bodies by the billions. Up to 1,000 different species live in the human gut alone. With such a large and thriving population, it’s easy to understand how a few bacteria might randomly acquire traits that make them more resistant to ‘killer’ drugs like antibiotics. Through Darwinian evolution, the strongest, most resistant bacteria survive. Bacteria acquire these resistant traits through two mechanisms: genetic mutations or by genetic transfer from other organisms. These new traits effectively block antibiotic particles from reaching their target enzymes inside the bacterial cell wall.

Superbugs and hospitals

For bacteria, a hospital is like an evolutionary experiment gone mad. Think about how many antibiotics are prescribed in a hospital. And think about the broad range of pathogenic bacteria that walk through the door on the skin and in the mouths, noses, ears and open wounds of patients. Even after we bomb these bacteria with drugs, a few hardy mutants will survive. These germs pass easily from patient to patient on unwashed hands and contaminated surfaces. A healthy patient might come in for a couple of stitches and leave with a raging, drug-resistant infection.

10 TIPS TO PREVENT THE SPREAD OF SUPERBUGS 1 Recognise that the overuse or misuse of antibiotics is a major cause of increasing antibiotic resistance, and be conscious of this. 2 Understand that antibiotics can only cure bacterial infections, and not viral infections such as common colds or the flu. 3 Never take leftover antibiotics that you find in your house. 4 When prescribed antibiotics, follow your doctor’s instructions and take the full course, which is usually the entire bottle. 5 Never take antibiotics prescribed to a friend just because you have the same symptoms as them. 6 Unless your symptoms are extremely severe, make sure that you take the time out to have tests taken in order to determine the exact bacterial pathogen that is affecting you. This will consequently allow your doctor to prescribe a targeted antibiotic rather than a wider spectrum treatment that is unlikely to be as effective. 7 Even if you and your doctor feel that you probably have an infection, ask about alternative treatments and remedies that might resolve the infection before resorting to the use of antibiotics. 8 Try to support farms and dairies that do not use prophylactic antibiotic treatments in order to stave off infections among their animals. Overuse of agricultural antibiotics is, in fact, one of the greatest causes of antibiotic resistance.

9 Don’t use low-level antibiotics to resolve chronic acne. Try other methods instead. 10 Health-care professionals and hospital visitors must be vigilant about hand washing and overall sanitation, particularly when around patients who are immuno-compromised.

How the body manages to keep track of its energy reserves

In order to know how much food to eat, the human body needs a way of assessing how much energy it currently has in storage. Leptin – more commonly known as the ‘fat hormone’ – essentially acts as our internal fuel gauge. It is made by fat cells and tells the brain how much fat the body contains, and whether the supplies are increasing or being used up. Food intake is regulated by a small region of the brain called the hypothalamus, which manages many of our hormones. When fat stores run low and leptin levels drop, the hypothalamus stimulates appetite in an attempt to increase food intake and regain lost energy. When leptin levels are high, appetite is suppressed, reducing food intake and encouraging the body to burn up fuel. It was originally thought that leptin could be used as a treatment for obesity. However, although it is an important regulator of food intake, our appetite is affected by many other factors, from how full the stomach is to an individual’s emotional state or food preferences. For this reason, it’s possible to override the leptin message and gain weight even when fat stores are sufficient.

 

Keep In Mind! Living a healthy life after all will require a few changes to your lifestyle!

No. 1: Never Eat After Dinner

(Eat 3 Hours Before Going To Sleep)

No. 2: Eat Three Meals A Day

(Maintain 3-6 Hours Between These Without Snacking)

No. 3: Do Not Eat Large Meals

(Eat Them Slowly)

No. 4: Eat A Breakfast Containing Protein

(Ingesting 25 & More Grams Will Reduce Your Cravings To Minimum)

No. 5: Reduce The Amount Of Carbohydrates Eaten

(Do Not Cut Them Out Completely, But Their Reduction Is Necessary)

 

How we see

When you take good care of your eyes, you take good care of yourself.  

   

The eye is often compared to a basic camera, and indeed the very first camera was designed with the concept of the eye in mind. We can reduce the complex process that occurs to process light into vision within the eye to a relatively basic sequence of events. First, light passes hrough the cornea, which refracts the light so that it enters the eye in the right direction, and aqueous humour, into the main body of the eye through the pupil. The iris contracts to control pupil size and this limits the amount of light that is let through into the eye so that light-sensitive parts of the eye are not damaged. The pupil can vary in size between 2mm and 8mm, increasing to allow up to 30 times more light in than the minimum. The light is then passed through the lens, which further refracts the light, which then travels through the vitreous humour to the back of the eye and is reflected onto the retina, the centre point of which is the macula. The retina is where the rods and cones are situated, rods being responsible for vision when low levels of light are present and cones being responsible for colour vision and specific detail. All the light information that has been received by the eye is then converted into electrical impulses by a chemical in the retina called rhodopsin, also known as purple visual, and the impulses are then transmitted through the optic nerve to the brain where they are perceived as ‘vision’. The eye moves to allow a range of vision of approximately 180 degrees and to do this it has four primary muscles which control the movement of the eyeball. These allow the eye to move up and down and across, while restricting movement so that the eye does not rotate back into the socket.  

 

Rods and Cones Rods are the light-sensitive cells in our eyes that aid our vision in low levels of light. Rods are blind to colour and only transmit information mainly in black and white to the brain. They are far more numerous with around 120 million rods present in every human eye compared to around 7 million cones. Cones are responsible for perceiving colour and specific detail. Cones are primarily focused in the fovea, the central area of the macula whereas rods mainly surround the outside of the retina. Cones work much better in daylight as light is needed to perceive colour and detail.

When light enters the eye, it first passes through the cornea, then the aqueous humor, lens and vitreous humor. Ultimately it reaches the retina, which is the light-sensing structure of the eye. The retina contains two types of cells, called rods and cones. Rods handle vision in low light, and cones handle color vision and detail. When light contacts these two types of cells, a series of complex chemical reactions occurs. The chemical that is formed (activated rhodopsin) creates electrical impulses in the optic nerve. Generally, the outer segment of rods are long and thin, whereas the outer segment of cones are more, well, cone shaped. Below is an example of a rod and a cone:

The outer segment of a rod or a cone contains the photosensitive chemicals. In rods, this chemical is calledrhodopsin; in cones, these chemicals are called color pigments. The retina contains 100 million rods and 7 million cones. The retina is lined with black pigment called melanin -- just as the inside of a camera is black -- to lessen the amount of reflection. The retina has a central area, called the macula, that contains a high concentration of only cones. This area is responsible for sharp, detailed vision.

When light enters the eye, it comes in contact with the photosensitive chemical rhodopsin (also called visual purple). Rhodopsin is a mixture of a protein called scotopsin and 11-cis-retinal -- the latter is derived from vitamin A (which is why a lack of vitamin A causes vision problems). Rhodopsin decomposes when it is exposed to light because light causes a physical change in the 11-cis-retinal portion of the rhodopsin, changing it to all-trans retinal. This first reaction takes only a few trillionths of a second. The 11-cis-retinal is an angulated molecule, while all-trans retinal is a straight molecule. This makes the chemical unstable. Rhodopsin breaks down into several intermediate compounds, but eventually (in less than a second) forms metarhodopsin II (activated rhodopsin). This chemical causes electrical impulses that are transmitted to the brain and interpreted as light. Here is a diagram of the chemical reaction.

Activated rhodopsin causes electrical impulses in the following way:

1. The cell membrane (outer layer) of a rod cell has an electric charge. When light activates rhodopsin, it causes a reduction in cyclic GMP, which causes this electric charge to increase. This produces an electric current along the cell. When more light is detected, more rhodopsin is activated and more electric current is produced.

2. This electric impulse eventually reaches a ganglion cell, and then the optic nerve.

3. The nerves reach the optic chasm, where the nerve fibers from the inside half of each retina cross to the other side of the brain, but the nerve fibers from the outside half of the retina stay on the same side of the brain.

4. These fibers eventually reach the back of the brain (occipital lobe). This is where vision is interpreted and is called the primary visual cortex. Some of the visual fibers go to other parts of the brain to help to control eye movements, response of the pupils and iris, and behavior.

Eventually, rhodopsin needs to be re-formed so that the process can recur. The all-trans retinal is converted to 11-cis-retinal, which then recombines with scotopsin to form rhodopsin to begin the process again when exposed to light.

Seeing colour 

 

Colour is not actually inherent in any object. We only see colour because objects absorb some colour from light, and refl ect others. It is the reflected ones that we see and that give an object a set ‘colour’. Therefore, for example, grass is not green, it purely absorbs all other colours in light and refl ects back green. If an object refl ects all colours we will see it as white, if it absorbs all colours we see it as black. We use cones to perceive colour as rods are blind to colour.  

 

Ishihara based his test on pseudo-isochromaticism, but with the intention of delivering results that were more easily interpreted and thus more reliable. Almost nine decades on from its first edition, the Ishihara test remains widely used, able to quickly screen for colour vision defects that other, more exacting tests can then elucidate in detail. The Ishihara test can only detect the more common red-green

colour vision deficiencies (not the rarer blue ones), and then with only limited precision. A mild form of red-green deficiency occurs when either the red or green sensitive photopigment in the retina has an altered response to colour; this results in reduced discrimination between the colours red and green. A more severe deficiency occurs when either the red or green photopigment is missing entirely.

Normal colour vision uses all three types of light cones correctly and is known as trichromacy. People with normal colour vision are known as trichromats.

The different anomalous conditions are protanomaly, which is a reduced sensitivity to red light, deuteranomalywhich is a reduced sensitivity to green light and is the most common form of colour blindness and tritanomaly which is a reduced sensitivity to blue light and is extremely rare.

People with deuteranomaly and protanomaly are collectively known as red-green colour blind and they generally have difficulty distinguishing between reds, greens, browns and oranges. They also commonly confuse different types of blue and purple hues.

People with reduced blue sensitivity have difficulty identifying differences between blue and yellow, violet and red and blue and green. To these people the world appears as generally red, pink, black, white, grey and turquoise.

People with monochromatic vision can see no colour at all and their world consists of different shades of grey ranging from black to white, rather like only seeing the world on an old black and white television set. Achromatopsia is extremely rare, occuring only in approximately 1 person in 33,000 and its symptoms can make life very difficult. Usually someone with achromatopsia will need to wear dark glasses inside in normal light conditions.

 

 

 

 

Why does your leg kick out when the doctor taps just below your knee?

Doctors often test the knee-jerk, or patellar reflex, to look for potential neurological problems. Lightly tapping your patellar tendon just below the kneecap stretches the femoral nerve located in your thigh, which in turn causes your thigh muscle (quadriceps) to contract and the lower leg to extend. When struck, impulses travel along a pathway in the dorsal root ganglion, a bundle of nerves in the L4 level of the spinal cord. Reflex actions are performed independently of the brain. This allows them to happen almost instantaneously – in about 50 milliseconds in the case of the knee-jerk reflex. This reflex helps you to maintain balance and posture when you walk, without having to think about every step you take.

The knee-jerk reflex is what's known as a mono-synaptic response. The impulse only has to jump from one nerve to another once. There aren't many variables to be dealt with, so it's its own little controlled experiment. If there is no response to the knee tap, it indicates nerve damage that needs to be dealt with. Continual jerks after the tap can indicate cerebellar disease.

Either problem can lead to huge problems. Without the quick activation of muscles in response to a stretch, any unanticipated weight on the legs would cause them to collapse. Even walking would take concentration. A knee-jerk response is a good thing, as long as its not in debate.

 

Learn the principles that make Boomerangs come back

A boomerang is basically a singlewinged aircraft propelled through the air by hand. Boomerangs have two ‘wings’ joined in a V-shape. Both wings have an airfoil-shaped cross-section just like an aircraft wing. An airfoil is flat on one side but curved on the other with one edge thicker than the other – this helps the boomerang stay in the air due to lift. Lift is generated as the air flowing up over the curved side of the wing has further to travel than the air flowing past the flat side. The air moving over the curved surface must therefore travel quicker in order to reach the other edge of the wing. Because the two sides of a boomerang have different air speeds flowing over them, as it spins the aerodynamic forces acting upon it are uneven. This causes the section of the boomerang moving in the same direction as the direction of forward motion to move faster through the air than the section moving in the opposite direction. These uneven forces make the boomerang start to turn in and follow a circular route, eventually heading back to the thrower.

 

Bones and muscles work in perfect harmony to enable the wide range of movement our arms enjoy

Bones are like levers: this was the conclusion drawn by Italian physician, Giovanni Alfonso Borelli, when he was studying the human skeleton to see how it worked in the 17th century. He applied mechanical principles, showing that bones and joints work as levers, powered by muscles. Today, we have a much more detailed understanding of how the body works, and the shoulder joint is a particularly interesting and complex arrangement, comprising the upper arm bone (humerus), the shoulder blade (scapula) and the collar bone (clavicle) – the last two of which form the roof of the shoulder.

The shoulder has three joints that work together to allow arm movement; the main one is the glenohumeral joint, a synovial ball and socket type. The rounded head of one bone fits into the cup-like cavity of another. This allows the greatest range of movement of any joint in the human body. The others are called the scapulothoracic joint (between the shoulder blade and ribs), and the acromioclavicular joint (between the shoulder blade and the collar bone).

Raising the arm above the head requires all three of these to work in unison. Meanwhile, the deltoid muscle, which covers the shoulder joint, plays an important role in raising the upper arm. Nerve impulses cause the fibres in the anterior and posterior parts of the muscle to balance, while the fibres in the middle contract to draw the arm upwards. A group of four muscles pull the humerus into the shoulder blade. Together, they are called the rotator cuff, and they stabilize the joint and aid arm rotation. The subscapularis muscle is a part of the rotator cuff and enables your arm to turn inwards. Within the joint, the ends of the bones are covered by articular cartilage, which cushions them as they move and generally acts as a shock absorber. The whole joint is encased in a fibrous capsule which helps to provide structural integrity. The capsule contains the synovial membrane, a soft tissue that secretes thick synovial fluid into the joint, to nourish the cartilage and keep it slippery.

Presentation

Anterior dislocation

The patient with anterior dislocation holds the arm at the side of body in external

rotation.

The shoulder loses its usual roundness. An anterior bulge may be seen in thinner

patients. The humeral head is palpable anteriorly.

Abduction and internal rotation are resisted.

Check the radial pulse to assess for vascular injury.

Check sensation in the regimental badge area on the lateral aspect of the shoulder over

the deltoid muscle. This tests for axillary nerve damage. Contraction of the deltoid

during attempted abduction can also be palpated.

Assess radial nerve function: test for thumb, wrist and elbow weakness on extension as

well as reduced sensation on the dorsum of the hand.

The rotator cuff is frequently damaged and should be examined after reduction.

Posterior dislocation

Posterior dislocation is much less obvious on examination and can easily be missed.

Patients may sometimes present with a long-standing posterior dislocation.

The patient usually presents with the arm adducted and internally rotated.

A posterior bulge may be present and the humeral head may be palpable below the

acromion process

Attempted abduction and external rotation are painful.

The arm cannot be externally rotated to a neutral position.

There is inability to supinate.

Examination may resemble a frozen shoulder, especially with a chronic, unreduced

dislocation.

Nerve and vascular injury are not common.  

 

 

 

 

Management

Muscle spasm tends to occur soon after dislocation and makes reduction more difficult.

In recurrent dislocations, some patients learn to reduce their own shoulders and do so

before seeing a doctor.

A fracture dislocation will probably require surgery.

Without a fracture, closed reduction is usually adequate.

Many techniques have been described for shoulder reduction. The technique used is

often chosen because of clinician experience or preference.

Adequate analgesia and relaxation are usually essential. Sedation with an opiate and

benzodiazepine may be used. Emergency departments should have their own protocols.

The patient may need to be managed before reaching hospital, or before X-ray and

reduction.  

 

Getting a tan without exposure to the Sun’s harmful UV rays

Today, the majority of sunless tanning lotions, mousses, sprays and gels contain a safe sugar molecule called dihydroxyacetone (DHA), which darkens skin tone with no side effects. The concentration of the DHA determines the darkness of the fake tan. DHA reacts with the amino acids present in dead cells on the surface of the skin to alter their colour, producing a yellow/brown tanned appearance. The colour doesn’t come through straight away, however; it develops over a number of hours and often keeps getting darker for 24 hours. Further application of the tanning lotion over a number of days will create a darker tone. Because the tan only affects the already-dead surface skin cells, the colour will of course fade and wear off as the skin is eventually shed.  

People of all races and skin colors can develop skin cancer, but some are more susceptible than others. If you have one or more of the following risk factors, you should be especially vigilant about reducing your UV exposure: Fair skin Blue, green, or hazel eyes Blond or red hair Freckles Moles (especially 50 or more) Family or personal history of skin cancer When and where is the sun most dangerous?

UV radiation from the sun is especially damaging under certain conditions, including the following:

from 10 a.m. to 4 p.m. from mid-Spring through mid-Fall at latitudes nearer the equator (for example, Florida) at higher altitudes when there is no thick cloud cover (and clouds only block 20% of UV rays) near water, snow, or other highly reflective surfaces

Sun damage accumulates over time, so if you find yourself in these conditions often, consistent protection is a must. Remember that besides skin cancer, the sun can also cause cataracts and other eye problems, a weakened immune system, unsightly skin spots, wrinkles, and "leathery" skin.

What is the most effective way to protect myself?

If you answered “sunscreen”, you're wrong. The most effective way actually is to simply stay out of the summer sun in the middle of the day. If that's not possible, wearing dark, tightly-woven clothing and a wide-brimmed hat also works. Only then comes sunscreen, which isn't a panacea and shouldn't be exclusively relied upon. Here are some more tips to protect yourself: Wear sunglasses that include a warranty stating they provide 99-100% UVA and UVB

(broad-spectrum) protection. Apply one ounce (a palm full) of sunscreen to all exposed skin 15 minutes before venturing

outdoors. The sunscreen container should specify a sun protection factor (SPF) rating of 15 or above and should state that it provides broad-spectrum (UVA and UVB) protection. Lotion- or cream-based sunscreens tend to adhere to the skin longer, thus providing better protection.

PABA-free sunscreens are recommended for persons with sensitive skin. Susceptible individuals may also want to avoid oxybenzone and dioxbenzone. Products that contain avobenzone (Parsol 1789), ecamsule, zinc oxide, or titanium dioxide are considered broad spectrum sunscreens and are thus offer protection against UVB and most UVA rays, as well as help reduce the development of wrinkles and skin aging.

Depending on your activity (swimming, sweating), sunscreen should be re-applied at least every two hours.

The SPF number on the sunscreen indicates how many times longer, under ideal conditions, a person can stay out in the sun without beginning to turn red in comparison with the amount of time totally unprotected skin would start to burn. Research indicates these numbers are sometimes overstated.

Avoid tanning salons, beds, and sunlamps.

Do children need extra protection?

Yes. Up to 50% of an individual's lifetime contact with sunshine occurs before adulthood. Studies also show that the more incidents of sunburn kids have, the higher likelihood that they will develop skin cancer decades later. So it is especially critical to protect them from the sun. Here are a few tips: Babies 6 months of age or younger should be kept completely out of the direct sun at all

times. In addition, sunscreen shouldn't be applied to babies this age. For children over 6 months, apply sunscreen every time they go outside. Children's swimsuits made from sun-protective fabric and designed to cover the child from

the neck to the knees are popular in Australia.

Are tanning salons healthier than the sun?

No. Tanning lamps give out UVA and frequently UVB rays as well and so can cause serious long-term skin damage and contribute to skin cancer. Remember, tanning is a sign of skin damage and does nothing to protect the skin from further injury. Experts recommend that you prioritize your health over vanity and avoid tanning salons altogether.

The sun causes an estimated 90% of skin cancer cases. Reducing your exposure to UV radiation now is a simple, easy, and effective way to prevent a potentially devastating cancer later.

 

UVA Rays

UVA rays are constantly present, no matter the season or the weather. If you think you can't get sun damage on a cloudy day, tell that to the UVA rays. They are so powerful that they also penetrate some clothing and even glass. (When was the last time you applied sunscreen before getting behind the wheel?). UVA rays used to be considered relatively safe, in terms of the sun's rays, and that's why tanning beds, which use UVA rays, took center stage. But we now know that using tanning beds before the age of 30 can actually increase your risk of skin cancer by 75%!

Also UVA rays are the rays responsible for the signs of aging because they are able to penetrate much deeper into the surface of the skin, damaging the cells beneath. While people think their skin looks younger because it's tan, the reality each, each tan is giving your skin irreversible damage, and you will see it's damage later in life. When you think of UVA rays, think sun spots, leathery skin and wrinkles. UVB Rays

UVB Rays are the rays you can blame when you get a sunburn. Unlike UVA rays, these rays aren't always the same strength year round - They're more prevalent in the summer months, however they are able to reflect off of water or snow, so it's always important to protect yourself year-round. UVB rays are responsible for causing most skin cancers. While large doses of UVA rays can contribute to cancer, it's the UVB rays that are commonly to blame.

If you've heard the advice to stay out of the sun though the mid day hours, it's the UVB rays you're trying to avoid. They are most prevalent mid day, so if you must be out at that time, protect your skin. When you think of UVB rays, think sun burn and cancer.

How to Protect Your Skin

All sunscreens protect against UVB rays, but it wasn't until recent years that sunscreen started including UVA protection. And in fact, not all sunscreens do. Look for one that specifically says UVA/UVB or "broad spectrum coverage" on the bottle.

Use a minimum of SPF 15 and reapply every hour or two at the very most. To see how long your sunscreen will last under perfect conditions, take the number of SPF and multiply it by 10. That is the length of time you'd be safe from the sun's rays. (In perfect conditions - No water or sweating taken into account here.) For example: SPF 20 x 10 = 200 minutes of sun protection.

Don't forget, sunscreen doesn't last forever! You should be using approximately a full ounce on your body and about 1 teaspoon on your face each time you apply.

Don't let a cloudy day affect your decision to protect your skin from the sun's damaging rays. The less you protect your skin, the more prone you are to sunburn, cancer and aging signs.

Tendons and ligaments

While both tendons and ligaments are made of collagen cells, that’s where the similarity ends. Ligaments are the tough connective tissues that link bone to bone by a joint and provide shock absorbency. They are strong and flexible bands of tissue but cannot be stretched. An overstretched ligament results in a sprain as experienced during whiplash. Tendons, meanwhile, are the whitish fibrous cords that link one end of a muscle to a bone or other structure. Tendons look white as, unlike muscles, they don’t contain many blood vessels. A damaged ligament can often be surgically reattached to a joint bone, with mobility returning relatively quickly. A tendon, however, is part of the neuromuscular system and so electrical signals must be able to pass across the tendon to reach a muscle in order for it to react. Treatment typically involves a rest period, with a support, and then a gradual return to exercise. It can be very difficult to be able to distinguish between a ligament and tendon injury and sometimes the only way to do this is X-ray and also rule out any other complications. The most important thing is to make sure you do not leave any injury untreated to prevent further damage. This can be done through a variety of different products available on the market such as supports, braces, taping, strapping, and cold therapy treatments as well as taking other measures such as re-evaluating your warm-up and cool down techniques and working with a physiotherapist with rehabilitation.

Trillions of neurons carry messages around the body, but how do they pass them on?

The nervous system involves a complex collection of nerve cells called neurons. Nerve messages can travel along individual neurons as electrical nerve impulses caused by the movement of lots of electrically charged ion particles. In order to cross the minuscule gaps between two neurons, the nerve message must be converted into a chemical message capable of jumping the gap. These tiny gaps between neurons are called synapses, forming the main contact zone between two neurons. Each neuron consists of a cell body and branching structures known as axons and dendrites. Dendrites are responsible for taking information in via receptors, while axons transmit information away by passing electrical signals across the synapse from one neuron to another.

1. At the end of the pre-synaptic neurone there are voltage-gated calcium channels.

When an action potential reaches the synapse these channels open, causing

calcium ions to flow into the cell.

2. These calcium ions cause the synaptic vesicles to fuse with the cell membrane,

releasing their contents (the neurotransmitter chemicals) by exocytosis.

3. The neurotransmitters diffuse across the synaptic cleft.

4. The neurotransmitter binds to the neuroreceptors in the post-synaptic membrane,

causing the channels to open. In the example shown these are sodium channels,

so sodium ions flow in.

5. This causes a depolarisation of the post-synaptic cell membrane, which may initiate

an action potential, if the threshold is reached.

6. The neurotransmitter is broken down by a specific enzyme in the synaptic cleft; for

example the enzyme acetylcholinesterase breaks down the

neurotransmitter acetylcholine. The breakdown products are absorbed by the pre-

synaptic neurone by endocytosis and used to re-synthesise more neurotransmitter,

using energy from the mitochondria. This stops the synapse being permanently on.

The human nervous system uses a number of different neurotransmitter and

neuroreceptors, and they don’t all work in the same way. We can group synapses into

5 types:

1. Excitatory Ion Channel Synapses.

These synapses have neuroreceptors that are sodium channels. When the

channels open, positive ions flow in, causing a local depolarisation and making an

action potential more likely. This was the kind of synapse described above. Typical

neurotransmitters are acetylcholine, glutamate or aspartate.

2. Inhibitory Ion Channel Synapses.

These synapses have neuroreceptors that are chloride channels. When the

channels open, negative ions flow in causing a local hyperpolarisation and making

an action potential less likely. So with these synapses an impulse in one neurone

can inhibit an impulse in the next. Typical neurotransmitters are glycine or GABA.

3. Non Channel Synapses.

These synapses have neuroreceptors that are not channels at all, but instead are

membrane-bound enzymes. When activated by the neurotransmitter, they catalyse

the production of a “messenger chemical” inside the cell, which in turn can affect

many aspects of the cell’s metabolism. In particular they can alter the number and

sensitivity of the ion channel receptors in the same cell. These synapses are

involved in slow and long-lasting responses like learning and memory. Typical

neurotransmitters are adrenaline, noradrenaline (NB adrenaline is called

epinephrine in America), dopamine, serotonin, endorphin, angiotensin, and

acetylcholine.

4. Neuromuscular Junctions.

These are the synapses formed between motor neurones and muscle cells. They

always use the neurotransmitter acetylcholine, and are always excitatory. We shall

look at these when we do muscles. Motor neurones also form specialised synapses

with secretory cells.

5. Electrical Synapses.

In these synapses the membranes of the two cells actually touch, and they share

proteins. This allows the action potential to pass directly from one membrane to the

next. They are very fast, but are quite rare, found only in the heart and the eye.

Why have gaps in the nerves?

1. They make sure that the flow of impulses is in one direction only. This is because the vesicles containing the transmitter are only in the presynaptic membrane and the receptor molecules are only on the postsynaptic membrane.

2. They allow integration, e.g. an impulse travelling down a neurone may reach a synapse which has several post synaptic neurones, all going to different locations. The impulse can thus be dispersed. This can also work in reverse, where several impulses can converge at a synapse.

3. They allow ‘summation’ to occur. Synapses require the release of sufficient transmitter into the cleft in order for enough of the transmitter to bind to the postsynaptic receptors and the impulse to be generated in the postsynaptic neurone. In spatial summation, several presynaptic neurones converge at a synapse with a single post synaptic neurone. In temporal summation there is only one presynaptic and one postsynaptic neurone but the frequency of impulses reaching the synapse is important. Both types of summation allow for ‘grading’ of nervous response – if the stimulation affects too few presynaptic neurones or the frequency of stimulation is too low, the impulse is not transmitted across the cleft.

4. They allow the ‘filtering out’ of continual unnecessary or unimportant background stimuli. If a neurone is constantly stimulated (e.g. clothes touching the skin) the synapse will not be able to renew its supply of transmitter fast enough to continue passing the impulse across the cleft. This ‘fatigue’ places un upper limit on the frequency of depolarisation.

You only need to know about two main neurotransmitters

Acetylcholine (Ach) Noradrenaline

Widely used at synapses in the

peripheral nervous system. Released

at the terminals of:

All motor neurones

activating skeletal muscle

Many neurones of

the autonomic nervous

system especially those in

the parasympathetic branch

Some synapses in the central

nervous system

Acetylcholine is removed from the

synapse by enzymatic breakdown into

inactive fragments. The enzyme used

is acetylcholinesterase.

Nerve gases used in warfare (e.g.

sarin) and the organophosphate

insecticides (e.g. parathion) achieve

their effects by inhibiting

acetylcholinesterase thus allowing

ACh to remain active. In the

presence of such inhibitors

ACh keeps stimulating the

postsynaptic membranes and the

nervous system soon goes wild,

causing contraction of the muscles in

uncontrollable spasms and eventually

death. Atropine is used as an

antidote because it blocks ACh

receptors.

This is another transmitter substance which

may be in some synapses instead of

acetylcholine, e.g. some human brain

synapses and sympathetic nervous

system synapses.

Synapses result in an appreciable delay,

up to one millisec. Therefore slows down

the transmission in nervous system.

Synapses are highly susceptible to drugs

and fatigue e.g.

Curare (poison used by S. American

Indians) and atropine stops

Acetylcholine from depolarising the

post-synaptic membrane, i.e.

become paralysed.

Strychnine and some nerve gases

inhibit or destroy

acetylcholinesterase

formation. Prolongs and enhances

any stimulus, i.e. leads to

convulsions, contraction of muscles

upon the slightest stimulus.

Cocaine, morphine, alcohol, ether

and chloroform anaesthetise nerve

fibres.

Mescaline and LSD produce their

hallucinatory effect by interfering

with nor-adrenaline.

Synapses where acetylcholine is the neurotransmitter = cholinergic

synapses

Synapses where noradrenaline is the neurotransmitter = adrenergic synapses

Drugs that stimulate a nervous system are called agonists, and those that inhibit a

system are called antagonists. By designing drugs to affect specific neurotransmitters

or neuroreceptors, drugs can be targeted at different parts of the nervous system. The

following paragraph describe the action of some common drugs. You do not need to

know any of this, but you should be able to understand how they work.. By designing

drugs to affect specific neurotransmitters or neuroreceptors, drugs can be targeted at

different parts of the nervous system. The following paragraph describe the action of

some common drugs. You do not need to know any of this, but you should be able to

understand how they work.

1. Drugs acting on the central nervous system

In the reticular activating system (RAS) in the brain stem noradrenaline receptors

are excitatory and cause wakefulness, while GABA receptors are inhibitory and

cause drowsiness. Caffeine (in coffee, cocoa and cola), theophylline (in tea),

amphetamines, ecstasy (MDMA) and cocaine all promote the release of

noradrenaline in RAS, so are stimulants. Antidepressant drugs, such as the

tricyclics, inhibit the breakdown and absorption of noradrenaline, so extending its

effect. Alcohol, benzodiazepines (e.g. mogadon, valium, librium), barbiturates, and

marijuana all activate GABA receptors, causing more inhibition of RAS and so are

tranquillisers, sedatives and depressants. The narcotics or opioid group of drugs,

which include morphine, codeine, opium, methadone and diamorphine (heroin), all

block opiate receptors, blocking transmission of pain signals in the brain and spinal

chord. The brain’s natural endorphins appear to have a similar action.

The brain neurotransmitter dopamine has a number of roles, including muscle

control, pain inhibition and general stimulation. Some psychosis disorders such as

schizophrenia and manic depression are caused by an excess of dopamine, and

antipsychotic drugs are used to block the dopamine receptors and so reduce its

effects. Parkinson’s disease (shaking of head and limbs) is caused by too little

dopamine compared to acetylcholine production in the midbrain. The balance can

be restored with levodopa, which mimics dopamine, or with anticholinergic drugs

(such as procyclidine), which block the muscarinic acetylcholine receptors.

Tetrodotoxin (from the Japanese puffer fish) blocks voltage-gated sodium channels,

while tetraethylamonium blocks the voltage-gated potassium channel. Both are

powerful nerve poisons. General anaesthetics temporarily inhibit the sodium

channels. Strychnine blocks glycine receptors in the brain, causing muscle

convulsions and death.

2. Drugs acting on the somatic nervous system

Curare and bungarotoxin (both snake venoms) block the nicotinic acetylcholine

receptors in the somatic nervous system, and so relax skeletal muscle. Myasthenia

gravis (a weakening of the muscles in the face and throat caused by inactive

nicotinic acetylcholine receptors) is treated by the drug neostigmine, which inhibits

acetylcholinesterase, so increasing the amount of acetylcholine at the

neuromuscular junction. Nerve gas and organophosphate insecticides (DDT) inhibit

acetylcholinesterase, so nicotinic acetylcholine receptors are always active, causing

muscle spasms and death. Damaged tissues release prostaglandins, which

stimulate pain neurones (amongst other things). The non-narcotic analgesics such

as aspirin, paracetamol and ibuprofen block prostaglandin production at source of

pain, while paracetamol has a similar effect in the brain. Local anaesthetics such as

procaine block all sensory and motor synapses at the site of application.

3. Drugs acting on the autonomic nervous system

Sympathetic agonists like salbutamol and isoprenaline, activate the adrenergic

receptors in the sympathetic system, encouraging smooth muscle relaxation, and

are used as bronchodilators in the treatment of asthma. Sympathetic antagonists

like the beta blockers block the noradrenaline receptors in the sympathetic nervous

system. They cause dilation of blood vessels in the treatment of high blood pressure

and migraines, and reduce heartbeat rate in the treatment of angina and abnormal

heart rhythms. Parasympathetic antagonists like atropine (from the deadly

nightshade belladonna) inhibit the muscarinic acetylcholine receptors in

parasympathetic system, and are used as eye drops to relax the ciliary muscles in

the eye.

The science behind the pills that manage pain

We all feel pain differently, depending on the severity of the injury or ache, as well as our health and our pain threshold. When you are in pain, nerve endings transmit the pain signal to the brain via the spinal cord. The brain then interprets the level of pain. There are two key types of painkillers that are commonly used. The first include ibuprofen and paracetamol, which block the body’s ‘prostaglandins’ (chemicals that produce swelling and pain) at the source of the pain, reducing swelling in the area and reducing the intensity of pain. These ‘aspirin medicines’ are used frequently for mild to moderate pain, but they can only work up to a certain intensity of pain. There are different types of painkillers within this group, such as anti-inflammatory medicines, like ibuprofen, which are commonly used to treat arthritis, sprains and strains. Aspirin is used to help lower the risk of blood clots when used in a low dosage, as they thin the blood. Paracetamol is what’s known as an analgesic, which is used for reducing pain and lowering a temperature. The second type of painkillers include morphine and codeine (narcotic medicines), which block the pain messages in the spinal cord and the brain. This is for much more severe pain. As both types of painkillers use slightly different methods to treat pain, they can be combined, such as in co-codamol, which blends codeine and paracetamol.

Pain Medications: Dosage and Indications MEDICATION STANDARD DOSAGE COMMENTS

Abbreviations: CrCl = creatinine clearance; GI = gastrointestinal; HIV-SN = HIV sensory neuropathy; LBP = low back pain; OA = osteoarthritis; PN = peripheral neuropathy; TCAs = tricyclic antidepressants

Acetaminophen 1 g Q6H PRN or 650 mg Q4H PRN Maximum dosage: 4 g per 24 hours or 2 g per 24 hours in patients with comorbid liver disease

First-line analgesia in noninflammatory

mild OA, LBP, mild PN because of

safety profile

Possible adverse effects: hepatotoxicity

(especially if taken with alcohol),

nephrotoxicity (with chronic overdose):

monitor liver and renal function when

using maximal dosages

Use caution and consider reducing total

dosage for patients with comorbid liver

disease or excessive alcohol intake

NSAIDs Ibuprofen

600-800 mg TID PRN for pain

Take with food

Schedule around the clock for

inflammatory condition (eg,

inflammatory OA) or persistent

symptoms

Can titrate up as tolerated and

based on risks to 800 mg TID

Maximum dosage: 3,200 mg/day in

divided doses or 1,800 mg/day for

patients at increased risk of adverse

effects Alternative NSAIDs Naproxen: 250-500 mg BID Sulindac: 150-200 mg BID Celecoxib: 200 mg QD Meloxicam: 7.5 mg QD For chronic pain, use for 2 weeks at initial dosage and reevaluate efficacy; titrate up as needed and if safe; if not effective after a 4-week trial, consider changing NSAID, or adding or changing to another intervention

For persistent noninflammatory and

inflammatory OA, LBP, mild PN

Possible adverse effects: GI bleeding,

abdominal pain, rash and

hypersensitivity, renal and hepatic

impairment, platelet aggregation

abnormalities

Avoid use in patients with peptic ulcer

disease or cirrhosis

Avoid ibuprofen in patients with history

of aspirin-induced asthma

Increased bleeding risk with concurrent

warfarin; if used, monitor closely

Increased risk of renal impairment in

patients on diuretics and those with

baseline renal dysfunction, congestive

heart failure, or cirrhosis

To minimize risks, use the lowest

effective dosage and try to use for short

periods of time

COX-2 inhibitors, such as celecoxib,

have higher risk of cardiovascular events

MEDICATION STANDARD DOSAGE COMMENTS

but fewer GI side effects than

nonselective COX inhibitors

Indomethacin is associated with

increased joint destruction; avoid using

for OA or LBP

Antidepressants: TCAs and others

Amitriptyline Start at 10-25 mg QHS; titrate upward every 3 days by 25 mg to achieve symptom relief, if tolerated; maximum daily dosage is 150 mg (use lower dosages for older patients) Nortriptyline Start at 10-25 mg QHS; titrate upward every 3 days by 25 mg to achieve symptom relief, if tolerated; maximum daily dosage is 150 mg (use lower dosages for older patients)

Consider for patients with comorbid

depression

Consider for neuropathic pain; also as

an adjunct in any type of LBP

unresponsive to acetaminophen and

NSAIDs

Small studies of PN have shown limited

or negative results with antidepressants

Drug interactions: RTV and other PIs

may increase the level of TCAs; start at

low dosage, increase slowly

Monitor serum TCA levels to avoid

cardiotoxicity at higher dosage levels

Possible TCA adverse effects:

anticholinergic (dry mouth, dizziness,

constipation, urinary retention, blurred

vision, orthostatic hypotension),

extrapyramidal symptoms,

incoordination; risk of cardiac conduction

abnormalities and overdose at higher

dosages

For neuropathic pain, other potential

agents include venlafaxine and

duloxetine; these are inadequately

studied in people with HIV infection or

show limited efficacy

Anticonvulsants Gabapentin: start at 300 mg QHS;

may increase every few days, as

tolerated, to achieve symptom relief;

first increase to BID, then TID, then

Consider for PN

Gabapentin: considered first-line for HIV-

SN (SeePeripheral Neuropathy)

Common adverse effects include

nausea, constipation, fatigue,

MEDICATION STANDARD DOSAGE COMMENTS

increase by 300 mg per dose to

maximum of 1,200 mg TID

Pregabalin: start at 25-50 mg TID;

may increase by 25-50 mg per dose

every few days as tolerated to

achieve symptom relief; maximum

dosage: 200 mg TID

Lamotrigine: start at 25 mg every

other day; titrate slowly to 200 mg

BID over the course of 6-8 weeks

somnolence, dizziness, truncal ataxia,

weight gain

To discontinue, taper over course of ≥7

days

Pregabalin: sometimes better tolerated

than gabapentin

Uncertain efficacy in HIV-related PN

Possible adverse effects include

somnolence, constipation, dizziness,

ataxia, and weight gain

To discontinue, taper over course of ≥7

days

Lamotrigine: has shown the greatest

efficacy in clinical trials for HIV-SN

Possible adverse effects: rash (including

Stevens-Johnson syndrome),

cytopenias, dizziness

To discontinue, taper slowly

Drug interactions: LPV/r may decrease

lamotrigine levels; may need to increase

lamotrigine dosage for therapeutic effect

Muscle relaxants (nonbenzo- diazepines)

Cyclobenzaprine (Flexeril) 5-10 mg TID; start with 5 mg doses for elderly patients and those with hepatic impairment; maximum dosage is 30 mg per 24 hours Baclofen 5-10 mg TID or QID; start with 5 mg doses for elderly patients and those with renal impairment; maximum dosage is 80 mg QD in divided doses

May be useful as adjunctive therapy for

acute back pain but not recommended

for chronic or subacute back pain

Common adverse effects include

drowsiness, dry mouth, and dizziness

Severe adverse effects include

arrhythmias, altered mental status, and

seizures

Opiate analgesics Options include: Tramadol (not a typical opiate; exact mechanism of action is unknown; acts in part as a central opioid agonist) Start with 50 mg QAM PRN pain, titrate upward by 50 mg/day every 3 days to 50 mg Q6H Maximum dosage: 400 mg/day, or 300 mg/day if >70 years of age; to

Use opioids for patients who have

severe pain refractory to other

interventions (pharmacologic or

nonpharmacologic) or who cannot

receive those interventions

MEDICATION STANDARD DOSAGE COMMENTS

discontinue, taper dosage in the same way In renal insufficiency with CrCl <30, reduce dose frequency to Q12H, and maximum dosage to 200 mg/day Weak opioids

Codeine

15-30 mg every 4-6 hours; titrate up

by 15 mg every 2-3 days to achieve

pain relief, if tolerated

Maximum dose: 60 mg; take with

food

Hydrocodone + acetaminophen

5 mg/500 mg fixed-dose tablet, 1-2

tablets Q6H PRN pain

Maximum dosage: 12 tablets per 24

hours; 6 tablets for elderly patients

and those with liver disease

Oxycodone + acetaminophen

5 mg/325 mg fixed-dose tablet (other

dosages available), 1-2 tablets Q6H

PRN pain

Maximum dosage: 12 tablets per 24

hours; 6 tablets for elderly patients

and those with liver disease Strong opioids

Morphine (immediate release)

10-30 mg every 3-4 hours PRN pain

Morphine (sustained release)

15-30 mg Q12H as scheduled

Start with weak opioids, assess safety,

efficacy, and usage; titrate up and move

to stronger opioids as needed

Use the lowest effective dosage

Use opioids cautiously in elderly patients

If needed for acute flares, try to limit use

to a designated short period of time

If needed for chronic pain, try to use a

sustained-release opioid (eg, sustained-

release morphine) around the clock, plus

shorteracting opioids (eg, hydrocodone)

for breakthrough pain as needed

Opioid therapy for chronic pain should

use a fixed-dose schedule, not PRN

dosing

Methadone may have utility for

neuropathic pain owing to its action on

NMDA receptors; start at low dosage

and titrate slowly because of its long

half-life; consult with pharmacist

Risk of dependence, overdose

(accidental or deliberate); monitor

closely

Adverse effects include oversedation,

hypotension and respiratory depression,

central nervous system stimulation or

somnolence, dizziness, constipation,

nausea, pruritus

Codeine and morphine can cause

urticarial reactions (hives)

For patients with renal and hepatic

impairment, use low dosages and

monitor carefully

When prescribing opioids, remember to

also give treatment for constipation

(docusate and senna)

MEDICATION STANDARD DOSAGE COMMENTS

doses; if pain control is inadequate,

consider dosing Q8H; may titrate up

by 15-30 mg PRN pain

Oxycodone (immediate release)

5-30 mg Q4H PRN pain

Oxycodone (sustained release)

10 mg Q12H as scheduled doses;

titrate up by 10-20 mg PRN; monitor

carefully

Methadone

Consult with pharmacist

Hydromorphone 2-4 mg Q4H PRN

Fentanyl transdermal

12-100 mcg patch Q72H; a small

proportion of patients will need

dosing Q48H to maintain a stable

blood level

Appropriate only for patients already

on stable dosage of other opiates;

start at equianalgesic (or lower)

dosage; consult with pharmacist;

use for chronic severe pain

Note that tramadol 37.5 mg +

acetaminophen 325 mg has shown pain

relief equivalent to codeine 30 mg +

acetaminophen 325 mg but with fewer

adverse effects (major adverse effect:

headache)

Chronic opioid therapy should

incorporate an opioid use agreement

that includes functional goals for

outcome, not reduction of pain intensity

alone

What causes stiffness and pain in our muscles for days after exercise

Normally, when our muscles contract they shorten and bulge, much like a bodybuilder’s biceps. But if the muscle happens to be stretched as it contracts it can cause microscopic damage. The quadriceps muscle group located on the front of the thigh is involved in extending the knee joint, and usually contracts and shortens to straighten the leg. However, when walking down a steep slope, the quadriceps contract to support your body weight as you step forward, but as the knee bends, the muscles are pulled in the opposite direction. This tension results in tiny tears in the muscle and this is the reason that downhill running causes so much delayed-onset pain. A muscle is made up of billions of stacked sarcomeres, containing molecular ratchets that pull against one another to generate mechanical force. If the muscle is taut as it tries to contract, the sarcomeres get pulled out of line, causing microscopic damage. The muscle gets inflamed and fills with fluid, causing stiffness and pain.

 

The idea behind resistance training is that you're basically tearing something and creating a micro trauma in the muscle. When the muscle recovers, it's going to recover stronger and denser than it was before. The soreness you feel the day after an upper-body workout—when you're hauling groceries into your car and you can hardly lift your arms is good.

Just make sure what you're suffering from is DOMS and not an injury. A good way to tell the difference is if the pain is bilateral. Having one very sore shoulder after you've worked both shoulders could spell injury.

 

What causes us to become flushed and red-faced?

Blushing occurs when you are in a state of excitement, anger or embarrassment. Children and young people are more prone to blushing and some people easily and frequently blush when they are confronted by stressful situations. Unfortunately, the fear of blushing (erythrophobia) causes even more embarrassment and blushing. Blushing is not under your voluntary control as it is caused by the autonomic nervous system that controls the muscles of the blood vessels of your face. In an embarrassing situation your body releases adrenaline as part of the fight or flight response. This hormone triggers the blood vessels to dilate, and the increased blood flow in your cheeks makes your face red. Besides our emotional state, high temperatures, alcohol and certain illnesses and medications can also cause us to have flushed faces.

   

 

There is no definitive method for preventing flushing. However, there are some things you can do to reduce the risk of these episodes. You can:

limit your alcohol consumption. People who have an inactive enzyme that helps break down alcohol are more prone to redness and warmth on the skin after drinking an alcoholic beverage.

limit your handling and eating of spicy foods, especially those derived from the Capsicum species.

try to avoid extreme temperatures and excessive bright sunlight.

limit your niacin intake to the daily recommended allowance of 16 milligrams for men and 14 milligrams for women, unless your doctor tells you differently. Consuming more than 50 milligrams of niacin can cause flushing.

employ coping skills to regulate extreme emotions, such as anxiety. Helpful skills include relaxation techniques and cognitive behavioral skills. Also, hypnosis may be effective in treating some emotional issues that produce flushing.

seek immediate medical care for unusual symptoms of flushing.  

 

What happens to the human body as we age

The whys of ageing, at its most basic level, seem simple: over the course of our lives, our bodies simply wear out. Or that’s what we’ve been led to believe, anyway. Scientists who study gerontology, or the process of ageing, don’t yet have a definitive answer as to why we age. There are two schools of thought. The wear-and-tear concept – meaning our cells are used up over time – that many subscribe to is just one example of an error theory. Proponents of the error theory believe that random external events cause damage that builds up in our bodies over the course of our lifetime until our cells can no longer function. Free radicals – unstable oxygen molecules that are a natural by-product of cell function – can build up and bond to other cells. As a result, DNA can be damaged. They may also result in protein cross-linking, or glycosylation, a phenomenon by which protein molecules in our bodies inappropriately bond together. They aren’t as elastic and don’t move or break down like they’re supposed to. Evidence for this theory is wrinkles, for example, caused by a breakdown of collagen, a type of protein found in the skin. Protein cross-linking may also be responsible for a lot of infirmities associated with ageing that have to do with stiffening or hardening of tissues, such as atherosclerosis. Cells can also mutate on a genetic level due to environmental or other factors. Problems with mitochondria, structures that provide energy inside cells, can cause cells to die as well as diseases associated with old age such as Alzheimer’s disease. Another group of theories puts forth the idea that our life spans are predetermined or programmed. One scenario suggests that the biological clock is ‘set’ by both our neuroendocrine system, which produces hormones, and our immune system. The hypothalamus in the brain sends messages via hormones to the pituitary gland, which in turn stimulates or restricts hormone secretions by the thyroid, adrenal glands, ovaries and testicles.

Over time this complex system does not function as efficiently, leading to everything from problems sleeping to menopause (which is a normal part of ageing for women, but can in fact lead to additional health problems). Different types of cells in the immune system decline in number as we age and do not function as well. Some scientists point to the fact that the overall risk of contracting cancers goes up as we get older; younger, more effi cient immune systems may have been able to fend them off.

Or it could all simply be genetic. That is, our DNA tells our bodies when life is at an end. There does seem to be a genetic component to ageing among most animals – they have predictable life spans. Women also tend to live a little longer than men. If your parents lived for a long time, you are more likely to do so yourself. One group of genes, known as the longevity assurance gene, have been determined to influence life span. If you inherit the ‘helpful’ version then you are more likely to have a longer life.

Although our genes play a part in our life span, obviously they can be infl uenced or changed. Otherwise, we’d still be living to the ripe old age of 30 instead of 80 (the average life span in developed countries). Most researchers believe that ageing is a complex process that no single theory can explain – it’s a combination of our genes, our biological functions and environmental factors.

We tend to focus more on the visible signs of ageing at first, like wrinkles and grey hairs, and these changes are prime examples of how complicated the process can be. We’ve already talked a bit about the cause of wrinkles: the connective tissues collagen and elastin, that keep skin looking smooth, both break down over time. Without the fi rm connections underneath, the skin sags. Many people lose fat deposits in their faces, and the skin’s oil production decreases. Many of these things have a genetic component, but outside factors such as exposure to ultraviolet radiation and smoking both cause wrinkles and sags faster. The Sun’s rays break down connective tissues, while smoking causes blood vessels to contract.

Grey hair is caused by a loss of melanin, the pigment that is responsible for our hair colour. Only recently have scientists learned that melanin production gets interrupted when hydrogen peroxide levels in the body increase over time. Other proteins found in hair cells that are responsible for regrowth diminish over time too. Unlike with wrinkles, however, there isn’t much you can do to avoid going grey other than dye your hair. Genetics do seem to play a part, though. If your parents went grey at a young age, you likely will too. The internal signs of ageing are more serious, health-wise, than the external ones. When and how they occur are also based on a wide variety of factors. Some gerontologists like to generalise that some parts of the body get harder as we age, while others get softer, but everything is interconnected. As we mentioned before, arteries get harder due to a buildup of plaque. The heart builds up pressure because it has to work more to pump blood through the harder, narrower blood vessels, which results in high blood pressure. Other muscles, like the lungs, get harder due to calcium deposits. These can be caused by hormonal changes or from having serious infections such as tuberculosis. Meanwhile, hormonal changes cause calcium to leech from the bones, making them soft and brittle and reducing their density. Known as osteoporosis, this loss means that we’re at a greater risk of breaking bones. Sarcopenia, or loss of muscle mass, is another ‘soft’ sign of ageing. Muscles contain special cells called satellites, a form of stem cell. These cells are responsible for muscle growth as well as regeneration when there’s some form of damage. These cells gradually become less proficient over time, possibly due to a corresponding decrease in growth factors (hormones or proteins that stimulate cell growth). Loss of tone in muscles such as the anal sphincter and the bladder can cause one of the most embarrassing signs of ageing for many people: incontinence. The ageing brain is still very mysterious compared with what we know about the rest of the body. It was once thought that age-related issues such as memory loss had to do with a decrease in neurons. Now, however, researchers believe that unless you have a specific disease that damages neurons, complex chemical processes are more likely to blame. For example, the brains of people with Alzheimer’s disease tend to have deposits of fibrous proteins called amyloids. The exact cause is unknown, although one theory is that the amyloids manage to get into the brain because the system that regulates the exchange of blood in the brain, known as the blood-brain barrier, malfunctions. What’s most fascinating about the ageing process is that it’s different for everyone and it is unpredictable in so many ways. Thanks to the advances being made in medicine, we’re learning more every day about not only what causes the most unpleasant signs of ageing, but also what we are able to do in order to counteract them.

 

 

 

 

Slowing down the ageing process Although ageing itself is inevitable (at least currently), there’s a lot that we can do to slow down the ageing process. Visible signs of ageing like wrinkles can be diminished by avoiding Sun exposure and other risk factors like smoking. Internal signs of ageing can all be combated to some extent by lifestyle changes. Weightbearing exercises such as weight-lifting, for example, have been shown to help maintain bone density and stave off osteoporosis. Aerobic exercise like walking or cycling can prevent weight gain – which leads to numerous diseases and conditions that age us – as well as improve cardiovascular health. Diet also plays a part in ageing – a balanced one can not only reduce the risk of diseases like type two diabetes but also keep our immune systems operating at their peak for longer. Some researchers treat ageing like a disease. To that end, stem-cell treatments and even cryogenics are looked to as a potential cure. But at what cost? Others feel that we weren’t meant to live forever and should focus on ways to age comfortably.

 

 

What makes us Sneeze? 

When we breathe in, the inhaled air can contain dust, chemicals and other irritants that can be 

harmful to the body, particularly to organs in the respiratory system like the lungs. While the tiny 

hairs inside the nostrils (cilia) trap many of these particles, some will often get through. To help you 

out, your body reacts to try and forcibly expel the offending particles via the sneeze reflex arc. 

There are a number of other reasons why we sneeze, including to clear the nasal passages when you 

have a cold, to expel allergens if you are allergic to something, and even bright sunlight can cause 

some people to sneeze. 

When a stimuli is detected by the nerve endings in the nose, impulses are sent to the brain, which 

initiates a chain of physiological events that enable the body to rid itself of the unwelcome item. 

Over‐the‐counter antihistamines such as chlorpheniramine and diphenhydramine block this process 

and can relieve the symptoms. They can also make you sleepy and dry out your eyes, nose, and 

mouth. 

 

For chlorpheniramine : 

o  Adults and teenagers—4 milligrams (mg) every four to six hours as needed. 

o  Children 6 to 12 years of age—2 mg three or four times a day as needed. 

o  Children 4 to 6 years of age—Use and dose must be determined by your doctor. 

o  Children and infants up to 4 years of age—Use is not recommended . 

 

For diphenhydramine : 

o  Adults and teenagers—25 to 50 milligrams (mg) every four to six hours as needed. 

o  Children 6 to 12 years of age—12.5 to 25 mg every four to six hours. 

o  Children 4 to 6 years of age—6.25 to 12.5 mg every four to six hours. 

o  Children and infants up to 4 years of age—Use is not recommended . 

 

For loratadine : 

o  Adults and children 6 years of age and older—10 milligrams (mg) once a day. 

o  Children 4 to 5 years of age—5 mg once a day. 

o  Children and infants up to 4 years of age—Use is not recommended . 

 

For cetirizine : 

o  Adults—5 to 10 milligrams (mg) once a day. 

o  Children 6 years of age and older—5 to 10 mg once a day. 

o  Children 4 to 6 years of age—2.5 mg once a day, up to a maximum of 5 mg. 

o  Children and infants up to 4 years of age—Use is not recommended . 

   

Whiplash Injuries Guidelines 

 

Whiplash is a widespread term used to describe a number of injuries caused when the neck is suddenly and quickly forced to move back and then forth, or forward then back, or even from side to side. Such movement is often the result of a traffic collision, or following a blow to the head or fall during a contact sport. The bones of the human spine serve to protect the fragile spinal cord which is located within. Of the 33 vertebrae of the human spine, whiplash aff ects the seven cervical vertebrae found at the top. Vertebrae are connected to one another by bands of fi brous connective tissue called ligaments. They are also connected to the surrounding muscles by tendons. In the event of an incident, damage can be done to both of these tissues in the vicinity of the neck. During an incident where a vehicle has struck the victim from behind, the head will be forced very quickly back and then forwards, but likewise if the sudden neck movement is due to very abrupt deceleration, the head will instead be jerked in the other direction – ie first forward and then back. Both types can result in whiplash injuries ranging from neck stiff ness and loss of movement to back and shoulder pain, headaches and even numbness that can radiate down the shoulders, arms and hands. It should be noted that although whiplash is considered a fairly minor injury, any head or neck trauma should be checked out by a medical professional. However, most muscle and tissue injuries do not show up on X-rays, so sometimes it can be difficult to diagnose.

Early management of Whiplash Associated Disorders