Health and Science
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.
Angioplasty is a cutting-edge medical procedure that helps your heart last
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
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.
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
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
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
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
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
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
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.
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
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
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
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
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
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
Although eating foods with a fever is fine, do not force foods.
Potential Drug-Drug Interactions
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
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
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.
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.
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
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
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
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
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.
1. Reducing the strength of treatment (for example reducing from 5% to 2.5%
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
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
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
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
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
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
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
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
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-
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
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
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
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
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.
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
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
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.
The patient with anterior dislocation holds the arm at the side of body in external
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 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
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
Nerve and vascular injury are not common.
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
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
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:
Blue, green, or hazel eyes
Blond or red hair
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"
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
Wear sunglasses that include a warranty stating they provide 99-100% UVA and UVB
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
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
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 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
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 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
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
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
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
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
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
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
Acetylcholine is removed from the
synapse by enzymatic breakdown into
inactive fragments. The enzyme used
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
This is another transmitter substance which
may be in some synapses instead of
acetylcholine, e.g. some human brain
synapses and sympathetic nervous
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.
Strychnine and some nerve gases
inhibit or destroy
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
Mescaline and LSD produce their
hallucinatory effect by interfering
Synapses where acetylcholine is
the neurotransmitter = cholinergic
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 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
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
Maximum dosage: 4 g per 24 hours or 2
g per 24 hours in patients with comorbid
First-line analgesia in noninflammatory
mild OA, LBP, mild PN because of
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
600-800 mg TID PRN for pain
Take with food
Schedule around the clock for
inflammatory condition (eg,
inflammatory OA) or persistent
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
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
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
TCAs and others
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)
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
Consider for neuropathic pain; also as
an adjunct in any type of LBP
unresponsive to acetaminophen and
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),
incoordination; risk of cardiac conduction
abnormalities and overdose at higher
For neuropathic pain, other potential
agents include venlafaxine and
duloxetine; these are inadequately
studied in people with HIV infection or
show limited efficacy
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,
To discontinue, taper over course of ≥7
Pregabalin: sometimes better tolerated
Uncertain efficacy in HIV-related PN
Possible adverse effects include
somnolence, constipation, dizziness,
ataxia, and weight gain
To discontinue, taper over course of ≥7
Lamotrigine: has shown the greatest
efficacy in clinical trials for HIV-SN
Possible adverse effects: rash (including
To discontinue, taper slowly
Drug interactions: LPV/r may decrease
lamotrigine levels; may need to increase
lamotrigine dosage for therapeutic effect
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
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
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
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
In renal insufficiency with CrCl <30,
reduce dose frequency to Q12H, and
maximum dosage to 200 mg/day
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
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
Maximum dosage: 12 tablets per 24
hours; 6 tablets for elderly patients
and those with liver disease
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
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
Adverse effects include oversedation,
hypotension and respiratory depression,
central nervous system stimulation or
somnolence, dizziness, constipation,
Codeine and morphine can cause
urticarial reactions (hives)
For patients with renal and hepatic
impairment, use low dosages and
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
Consult with pharmacist
Hydromorphone 2-4 mg Q4H PRN
12-100 mcg patch Q72H; a small
proportion of patients will need
dosing Q48H to maintain a stable
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:
Chronic opioid therapy should
incorporate an opioid use agreement
that includes functional goals for
outcome, not reduction of pain intensity
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
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.