Hypothyroidism

is a condition in which the thyroid gland does not make enough thyroid hormone.
See also:
Chronic thryoiditis (Hashimoto's disease)
Subacute thyroiditis
Silent thyroiditis
Neonatal hypothyroidism
Symptoms
Early symptoms:
Being more sensitive to cold
Constipation
Depression
Fatigue or feeling slowed down
Heavier menstrual periods
Joint or muscle pain
Paleness or dry skin
Thin, brittle hair or fingernails
Weakness
Weight gain (unintentional)
Late symptoms, if left untreated:
Decreased taste and smell
Hoarseness
Puffy face, hands, and feet
Slow speech
Thickening of the skin
Thinning of eyebrows
Treatment
The purpose of treatment is to replace the thyroid hormone that is lacking. Levothyroxine is the most commonly used medication. Doctors will prescribe the lowest dose that effectively relieves symptoms and brings the TSH level to a normal range. If you have heart disease or you are older, your doctor may start with a very small dose.
Lifelong therapy is required unless you have a condition called transient viral thyroiditis.
You must continue taking your medication even when your symptoms go away. When starting your medication, your doctor may check your hormone levels every 2 - 3 months. After that, your thyroid hormone levels should be monitored at least every year.
Important things to remember when you are taking thyroid hormone are:
Do NOT stop taking the medication when you feel better. Continue taking the medication exactly as directed by your doctor.
If you change brands of thyroid medicine, let your doctor know. Your levels may need to be checked.
Some dietary changes can change the way your body absorbs the thryoid medicine. Talk with your doctor if you are eating a lot of soy products or a high-fiber diet.
Thryoid medicine works best on an empty stomach and when taken 1 hour before any other medications. Do NOT take thyroid hormone with calcium, iron, multivitamins, alumin hydroxide antacids, colestipol, or other medicines that bind bile acids, or fiber supplements.
After you start taking replacement therapy, tell your doctor if you have any symptoms of increased thyroid activity (hyperthyroidism) such as:
Rapid weight loss
Restlessness or shakiness
Sweating
Myxedema coma is a medical emergency that occurs when the body's level of thyroid hormones becomes extremely low. It is treated with intravenous thyroid hormone replacement and steroid medications. Some patients may need supportive therapy (oxygen, breathing assistance, fluid replacement) and intensive-care nursing.
Causes
The thyroid gland is located in the front of the neck just below the voice box (larynx). It releases hormones that control metabolism.
The most common cause of hypothyroidism is inflammation of the thyroid gland, which damages the gland's cells. Autoimmune or Hashimoto's thyroiditis, in which the immune system attacks the thyroid gland, is the most common example of this. Some women develop hypothyroidism after pregancy (often referred to as "postpartum throiditis").
Other common causes of hypothyroidism include:
Congenital (birth) defects
Radiation treatments to the neck to treat different cancers, which may also damage the thyroid gland
Radioactive iodine used to treat an overactive thyroid (hyperthyroidism)
Surgical removal of part or all of the thyroid gland, done to treat other thyroid problems
Viral thyroiditis, which may case hyperthyroidism and is often followed by temporary or permanent hypothyroidism
Certain drugs can cause hyperthyroidism, including:
Amiodarone
Drugs used for hyperthyroidism (overactive thyroid), such as propylthiouracil (PTU) and methimazole
Lithium
Radiation to the brain
Sheehan syndrome, a condition that may occur in a woman who bleeds severely during pregnancy or childbirth and causes destruction of the pituitary gland
Risk factors include:
Age over 50 years
Being female
Tests & diagnosis
A physical examination may reveal a smaller-than-normal thyroid gland, although sometimes the gland is normal size or even enlarged (goiter). The examination may also reveal:
Brittle nails
Coarse facial features
Pale or dry skin, which may be cool to the touch
Swelling of the arms and legs
Thin and brittle hair
A chest x-ray may show an enlarged heart.
Laboratory tests to determine thyroid function include:
Serum TSH
T4 test
Lab tests may also reveal:
Anemia on a complete blood count (CBC)
Increased cholesterol levels
Increased liver enzymes
Increased prolactin
Low sodium
Prognosis
In most cases, thyroid levels return to with proper treatment. However, thyroid hormone replacement must be taken for the rest of your life.
Myxedema coma can result in death.
Prevention
There is no prevention for hypothyroidism.
Screening tests in newborns can detect hypothyroidism that is present from birth (congenital hypothyroidism).
Complications
Myxedema coma, the most severe form of hypothyroidism, is rare. It may be caused by an infection, illness, exposure to cold, or certain medications in people with untreated hypothyroidism.
Symptoms and signs of myxedema coma include:
Below normal temperature
Decreased breathing
Low blood pressure
Low blood sugar
Unresponsiveness
Other complications are:
Heart disease
Increased risk of infection
Infertility
Miscarriage
People with untreated hypothyroidism are at increased risk for:
Giving birth to a baby with birth defects
Heart disease because of higher levels of LDL ("bad") cholesterol
Heart failure
People treated with too much thyroid hormone are at risk for angina or heart attack, as well as osteoporosis (thinning of the bones).
When to contact a doctor
Call your health care provider if you have symptoms of hypothyroidism (or myxedema).
If you are being treated for hypothyroidism, call your doctor if:
You develop chest pain or rapid heartbeat
You have an infection
Your symptoms get worse or do not improve with treatment
You develop new symptoms



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Dr.M M ADNAN
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Diseases of the Thyroid

Hyperthyroidism

Most effects of hyperthyroidism are obvious from the preceding discussion of the various physiologic effects of thyroid hormone. However, some specific effects should be mentioned in connection especially with the development, diagnosis, and treatment of hyperthyroidism.Causes of Hyperthyroidism (Toxic Goiter, Thyrotoxicosis, Graves’Disease).

In most patients with hyperthyroidism, the thyroid gland is increased to two to three times normal size, with tremendous hyperplasia and infolding of the follicular cell lining into the follicles, so that the number of cells is increased greatly. Also, each cell increases its rate of secretion severalfold; radioactive iodine uptake studies indicate that some of these hyperplastic glands secrete thyroid hormone at rates 5 to 15 times normal.The changes in the thyroid gland in most instances are similar to those caused by excessive TSH. However,plasma TSH concentrations are less than normal rather than enhanced in almost all patients and often are essentially zero. However, other substances that have actions similar to those of TSH are found inthe blood of almost all these patients. These substancesare immunoglobulin antibodies that bind with the same membrane receptors that bind TSH. They induce continual activation of the cAMP system of the cells,with resultant development of hyperthyroidism.
These antibodies are called thyroid-stimulating immunoglobulin and are designated TSI.They have a prolonged stimulating effect on the thyroid gland, lasting for as long as 12 hours, in contrast to a little over 1 hour for TSH.
The high level of thyroid hormone secretion caused by TSI in turn suppresses anterior pituitary formation of TSH.
The antibodies that cause hyperthyroidism almost certainly occur as the result of autoimmunity that has developed against thyroid tissue. Presumably, at some time in the history of the person, an excess of thyroid cell antigens was released from the thyroid cells, and this has resulted in the formation of antibodies against the thyroid gland itself.
Thyroid Adenoma. Hyperthyroidism occasionally results from a localized adenoma (a tumor) that develops in the thyroid tissue and secretes large quantities of thyroid hormone. This is different from the more usual type of hyperthyroidism, in that it usually is not associated with evidence of any autoimmune disease. An interesting effect of the adenoma is that as long as it continues to secrete large quantities of thyroid hormone, secretory function in the remainder of the thyroid gland is almost totally inhibited because the thyroid hormone from the adenoma depresses the production of TSH by the pituitary gland.

Symptoms of Hyperthyroidism

The symptoms of hyperthyroidism are obvious from thepreceding discussion of the physiology of the thyroidhormones:
(1)a high state of excitability,
(2)intolerance to heat,
(3)increased sweating,
(4)mild to extreme weight loss (sometimes as much as 100 pounds),
(5)varying degrees of diarrhea,
(6)muscle weakness,
(7)nervousness or other psychic disorders,
(8)extreme fatigue but inability to sleep, and
(9)tremor of the hands.

Exophthalmos.

Most people with hyperthyroidism develop some degree of protrusion of the eyeballs. This condition is called exophthalmos.A major degree of exophthalmos occurs in about one third of hyperthyroid patients, and the condition sometimes becomes so severe that the eyeball protrusion stretches the optic nerve enough to damage vision. Much more often, the eyes are damaged because the eyelids do not close completely when the person blinks or is asleep. As a result, the epithelial surfaces of the eyes become dry and irritated and often infected, resulting in ulceration of the cornea. The cause of the protruding eyes is edematous swelling of the retro-orbital tissues and degenerative changes in the extraocular muscles.

In most patients,immunoglobulins can be found in the blood that react with the eye muscles. Furthermore, the concentration of these immunoglobulins is usually highest in patients who have high concentrations of TSIs.

Therefore, there is much reason to believe that exophthalmos, like hyperthyroidism itself, is an autoimmune process.The exophthalmos usually is greatly ameliorated with treatment of the hyperthyroidism.



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Piles (haemorrhoids)

About piles

Piles are round swellings on the inside of the anal canal - the short, muscular tube that connects your rectum (back passage) with your anus - in areas known as the anal cushions.
Many people with piles don't consult a GP so it's difficult to know exactly how many people in the UK get them. However, estimates range from between four and 25 in 100 people.

Types of piles

Although piles develop from inside your anal canal, they can hang down out of your rectum. They are graded as follows.

• First degree piles are swellings on the inside lining of your anal canal. They may bleed but can't be seen from outside the anus.
• Second degree piles are larger and stick out (prolapse) from the anus when you have a bowel movement, but return on their own afterwards.
• Third degree piles are similar, but hang out from your anus and only return inside when pushed back in.
• Fourth degree piles permanently hang down from your anus and you can't push them back inside. They may become extremely swollen and painful if the blood in them clots.
• External piles are swellings that develop from below the anal cushions. They can be more painful than the other types of piles.

Other causes of lumps around the anus can include a sentinel pile, which is the painless skin tag that develops when a crack in the anus (an anal fissure) heals up.

Symptoms of piles

Common symptoms of piles include:

• painless bleeding from your anus, which you may notice in the toilet bowl or when you use toilet paper, or from soiled underwear
• a lump on your anus
• a slimy discharge of mucus
• a feeling that your bowels haven't emptied completely
• itchy skin around your anus
• swelling around your anus
• pain and discomfort after a bowel movement if you have external piles

These symptoms may be caused by problems other than piles. You should visit your GP for advice.

Causes of piles

The exact cause of piles isn't known.
One theory is that piles are a result of a weakness of the tissue that connects the anal cushions to the muscle layers underneath. In combination with frequently straining while passing hard bowel movements, this can cause the anal cushions to slide out of their usual place and down the rectum.
You're more likely to develop piles:

• if you eat a low-fibre diet
• if you strain to empty your bowels (for example, if you have constipation)
• as you age because the support structures in your rectum weaken
• if you're pregnant
• if you're born with a weakness in your rectum or have a family history of piles

Diagnosis of piles

Visit your GP if you notice any signs of bleeding from your rectum.
Your GP will ask about your symptoms and examine you. This may involve a rectal examination, where he or she will gently insert a gloved finger into your rectum. Your GP may also ask you about your medical history.
Your GP may use a proctoscope to look inside your rectum. A proctoscope is a narrow, tube-like telescopic camera. Air can be blown through the tube to open up the bowel so it can be seen more clearly. This test can help to rule out problems in your rectum.
Alternatively, your GP may refer you for a flexible sigmoidoscopy or colonoscopy test that will need to be done in hospital. This allows your doctor to look inside your large bowel. These tests are sometimes done to check that your condition isn't caused by something more serious.

Treatment of piles

There are a number of treatments that can help relieve the symptoms of piles, but there isn't a cure.

Self-help

Regular warm baths may relieve irritation and help to keep the anal area clean. It's important not to strain your bowels during a bowel movement. If you have daily bowel movements that are solid but soft, you won't need to strain as faeces will pass easily and won't put pressure on the blood vessels in your anal area.

Medicines

There are a range of medicines that can help relieve the symptoms of piles.

• If you're passing hard or infrequent faeces, you could try a fibre supplement such as ispaghula husk (eg Fybogel) or mild laxatives such as lactulose, which will soften your faeces. Don't use laxatives that stimulate the bowel, such as senna, unless your doctor advises you to.
• Soothing creams, ointments and suppositories may ease any pain and itchiness. There are many different products available. Some contain a local anaesthetic such as lidocaine.
• Products containing corticosteroids, such as Anugesic-HC and Proctosedyl, may reduce inflammation and pain.

Always read the patient information leaflet that comes with your medicine and if you have any questions, ask your doctor or pharmacist for advice.
If these self-help measures and medicines don't work, or you have a higher grade of piles, you may need to go into hospital for one of the following procedures.

Non-surgical treatments

These are treatments that you can have in hospital, but you won't need to stay overnight.

Banding

This is used mostly to treat second degree piles, but you can also have it with first degree piles if medicines haven't worked for you.
This procedure needs to be done using an endoscope. Your doctor will place a small elastic band just above the pile. This will cut off the blood supply to the pile, causing it to die and fall off after a few days. The area left behind will heal up naturally.

Sclerotherapy

In sclerotherapy your piles will be injected with an oily solution, which makes them shrivel up. It's used for first or second degree piles.
Other treatments include:

• infrared coagulation or laser, where infrared light is used to seal the veins above the pile causing it to shrink
• cryosurgery, which destroys the pile by freezing it - the pile will later shrink and fall off
• bipolar diathermy and direct current electrotherapy, where an electrical current is used to burn the pile off

However, there is little scientific evidence to support the use of these treatments. More research is needed.

Surgery

There are various surgical treatments for piles.

Conventional haemorrhoidectomy

This is the surgical removal of piles and is only used if you have severe piles and other treatments - such as banding and sclerotherapy - haven't worked.
Conventional haemorrhoidectomy is done under general anaesthetic. This means you will be asleep during the operation. Your surgeon will cut the pile away from the muscle underneath and tie off the blood vessels to prevent bleeding. The exposed wound area will then heal naturally. Your surgeon may use stitches to close the wound.

Stapled haemorrhoidopexy

This is an alternative surgical technique that uses a specially-designed circular stapler. The stapler is inserted into the rectum and used to remove a doughnut-shaped piece of tissue above the piles. This pulls the haemorrhoids back up the anal canal and also reduces the blood supply to the piles, which shrink as a result. Recently a review of the value of this operation showed that compared with conventional haemorrhoidopexy, stapled haemorrhoidopexy led to less pain afterwards, a shorter stay in hospital and a shorter recovery time. However, there was a greater risk of piles returning and hanging down from your anus.

Haemorrhoidal artery ligation

In this procedure the small arteries that supply blood to the piles are tied with sutures. This causes the piles to shrink. It's sometimes referred to as HALO (haemorrhoidal artery ligation operation).

Special considerations

Piles are common in pregnant women. However, surgery is rarely considered an appropriate treatment since piles should get better after giving birth.
If you're pregnant, it's important to modify your diet to include more fibre as this will help to soften your bowel movements. If this doesn't help, ask your GP about mild creams and ointments.

Prevention of piles

You can reduce your risk of developing piles. If you have daily bowel movements that are solid but soft, and you don't need to strain, faeces will pass easily and won't put pressure on the blood vessels in your anal area.
To keep your bowel movements soft try to:

• eat plenty of fibre-rich foods such as fruit, vegetables and wholegrain cereals (for example, brown rice, wholemeal bread and wholemeal pasta)
• drink plenty of fluids

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Dr.M M ADNAN
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Eye Diseases

Eye Diseases
Some eye problems are minor and fleeting. But some lead to a permanent loss of vision. Common eye problems include
Cataracts - clouded lenses
Glaucoma - damage to the optic nerve from too much pressure in the eye
Retinal disorders - problems with the nerve layer at the back of the eye
Conjunctivitis - an infection also known as pinkeye

Your best defense is to have regular checkups, because eye diseases do not always have symptoms. Early detection and treatment could prevent vision loss. See an eye care professional right away if you have a sudden change in vision or everything looks dim or if you see flashes of light. Other symptoms that need quick attention are pain, double vision, fluid coming from the eye and inflammation.


At the age of 6, one child out of three has ametropia. This word refers to well-known disorders such as long-sightedness, astigmatism and short-sightedness. They can affect one eye or both of them. These disorders are easily corrected ! Besides, some can disappear as we get older, such as long-sightedness.



Long-sightedness :
The eye is too short : the image which is received gets impressed behind the retina and not on it. The eye needs to compensate by permanent accommodation which tires it.


Short-sightedness :
The eye is too long : the image which is received gets impressed in front of the retina and not on it. The distance between the retina and the cornea is too big and the eyes cannot focus on distant objects.
Astigmatism : The curvature of the cornea is very irregular. Instead of being round, it is oval, like a rugby ball ! In some rarer cases astigmatism is due to a fault in the crystalline lens. In both cases the objects appear distorted.

Maintaining Good Eyesight

Good eyesight plays an important role in your mobility and the enjoyment of life, so it's important to follow these basic steps to keep your eyes seeing clearly.

Visit Your Eye Doctor
You should visit your eye doctor for an eye exam at least once every one to two years to help maintain good eyesight. See your ophthalmologist if you experience eye infections or symptoms of disease like loss of or blurred vision, light flashes, eye pain, redness, itching, swelling and irritation around the eye or eyelid.

Practice Disease Prevention
Disease of the eye is the number one cause of blindness. Most diseases that cause blindness, like glaucoma and diabetes, can be treated or their progression slowed down with the proper diagnosis and management. While there is no cure for some eye conditions, there have been major medical advances for age-related macular degeneration, glaucoma, and cataracts. By visiting your eye doctor on a regular basis, you can catch any eye problems in their early stage when they are easier to treat.

Protect Your Eyes From the Sun's Harmful Rays
Constant exposure to ultraviolet light can damage your eyes. Too much exposure increases pigmentation in the eye, causing a discoloration known as "brown" or "sunshine" cataracts. Some eye diseases, such as macular degeneration, have been linked to UV exposure.

Wear Protective Gear and Eyewear During Work and Sporting Events
Wearing safety glasses and protective goggles while playing sports or working with hazardous and air-born materials lowers your risk for eye injury, impaired vision and complete loss of sight.

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Protein synthesis

is the process in which cells build proteins. The term is sometimes used to refer only to protein translation but more often it refers to a multi-step process, beginning with amino acid synthesis and transcription of nuclear DNA into messenger RNA which is then used as input to translation.

The cistron DNA is transcribed into a variety of RNA intermediates. The last version is used as a template in synthesis of a polypeptide chain. Proteins can often be synthesized directly from genes by translating mRNA. When a protein is harmful and needs to be available on short notice or in large quantities, a protein precursor is produced. A proprotein is an inactive protein containing one or more inhibitory peptides that can be activated when the inhibitory sequence is removed by proteolysis during posttranslational modification. A preprotein is a form that contains a signal sequence (an N-terminal signal peptide) that specifies its insertion into or through membranes; i.e., targets them for secretion. The signal peptide is cleaved off in the endoplasmic reticulum.. Preproproteins have both sequences (inhibitory and signal) still present.

For synthesis of protein, a succession of tRNA molecules charged with appropriate amino acids have to be brought together with an mRNA molecule and matched up by base-pairing through their anti-codons with each of its successive codons. The amino acids then have to be linked together to extend the growing protein chain, and the tRNAs, relieved of their burdens, have to be released. This whole complex of processes is carried out by a giant multimolecular machine, the ribosome, formed of two main chains of RNA, called ribosomal RNA (rRNA), and more than 50 different proteins. This molecular juggernaut latches onto the end of an mRNA molecule and then trundles along it, capturing loaded tRNA molecules and stitching together the amino acids they carry to form a new protein chain.

Protein biosynthesis, although very similar, is different for prokaryotes and eukaryotes.

Amino acids
Amino acids are the monomers which are polymerized to produce proteins. Amino acid synthesis is the set of biochemical processes (metabolic pathways) which build the amino acids from carbon sources like glucose.

Many organisms have the ability to synthesize only a subset of the amino acids they need. Adult humans, for example, need to obtain 8 of the 20 amino acids from their food.





Transcription

Simple diagram of transcription elongationIn transcription an mRNA chain is generated, with one strand of the DNA double helix in the genome as template. This strand is called the template strand. Transcription can be divided into 3 stages: Initiation, Elongation and Termination, each regulated by a large number of proteins such as transcription factors and coactivators that ensure the correct gene is transcribed.

The DNA strand is read in the 3' to 5' direction and the mRNA is transcribed in the 5' to 3' direction by the RNA polymerase.

Transcription occurs in the cell nucleus, where the DNA is held. The DNA structure is two helixes made up of sugar and phosphate held together by the bases. The sugar and the phosphate are joined together by covalent bond. The DNA is "unzipped" by the enzyme helicase, leaving the single nucleotide chain open to be copied. RNA polymerase reads the DNA strand from 3 prime (3') end to the 5 prime (5') end, while it synthsizes a single strand of messenger RNA in the 5' to 3' direction. The general RNA structure is very similar to the DNA structure, but in RNA the nucleotide uracil takes the place that thymine occupies in DNA. The single strand of mRNA leaves the nucleus through nuclear pores, and migrates into the cytoplasm.

The first product of transcription differs in prokaryotic cells from that of eukaryotic cells, as in prokaryotic cells the product is mRNA, which needs no post-transcriptional modification, while in eukaryotic cells, the first product is called primary transcript, that needs post-transcriptional modification (capping with 7 methyl guanosine, tailing with a poly A tail) to give hnRNA (heterophil nuclear RNA). hnRNA then undergoes splicing of introns (non coding parts of the gene) via spliceosomes to produce the final mRNA.


Translation

The synthesis of proteins is known as translation. Translation occurs in the cytoplasm where the ribosomes are located. Ribosomes are made of a small and large subunit which surrounds the mRNA. In translation, messenger RNA (mRNA) is decoded to produce a specific polypeptide according to the rules specified by the trinucleotide genetic code. This uses an mRNA sequence as a template to guide the synthesis of a chain of amino acids that form a protein. Translation proceeds in four phases: activation, initiation, elongation and termination (all describing the growth of the amino acid chain, or polypeptide that is the product of translation).

In activation, the correct amino acid (AA) is joined to the correct transfer RNA (tRNA). While this is not technically a step in translation, it is required for translation to proceed. The AA is joined by its carboxyl group to the 3' OH of the tRNA by an ester bond. When the tRNA has an amino acid linked to it, it is termed "charged". Initiation involves the small subunit of the ribosome binding to 5' end of mRNA with the help of initiation factors (IF), other proteins that assist the process. Elongation occurs when the next aminoacyl-tRNA (charged tRNA) in line binds to the ribosome along with GTP and an elongation factor. Termination of the polypeptide happens when the A site of the ribosome faces a stop codon (UAA, UAG, or UGA). When this happens, no tRNA can recognize it, but releasing factor can recognize nonsense codons and causes the release of the polypeptide chain. The capacity of disabling or inhibiting translation in protein biosynthesis is used by antibiotics such as: anisomycin, cycloheximide, chloramphenicol, tetracycline, streptomycin, erythromycin, puromycin etc.

Translation the process of converting the mRNA codon sequences into an amino acid polypeptide chain.

1.Initiation - A ribosome attaches to the mRNA and starts to code at the FMet codon (usually AUG, sometimes GUG or UUG).
2.Elongation - tRNA brings the corresponding amino acid (which has an anticodon that identifies the amino acid as the corresponding molecule to a codon) to each codon as the ribosome moves down the mRNA strand.
3.Termination - Reading of the final mRNA codon (aka the STOP codon), which ends the synthesis of the peptide chain and releases it.

Events following protein translation

The events following biosynthesis include post-translational modification and protein folding. During and after synthesis, polypeptide chains often fold to assume, so called, native secondary and tertiary structures. This is known as protein folding.

Many proteins undergo post-translational modification. This may include the formation of disulfide bridges or attachment of any of a number of biochemical functional groups, such as acetate, phosphate, various lipids and carbohydrates. Enzymes may also remove one or more amino acids from the leading (amino) end of the polypeptide chain, leaving a protein consisting of two polypeptide chains connected by disulfide bonds.