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Side Effects of Mixing Bactrim With Alcohol

June 25, 2011 by rfcamat Leave a Comment

Trimethoprim/sulfamethoxazole (Brand name: Bactrim)
Trimethoprim/sulfamethoxazole (Brand name: Bactrim)

Drinking can be the most exciting part of your weekend. You just can’t wait to head to the bar, elbow your way through the crowd waiting to be served. Whether it’s beer, vodka, whisky, gin or rum, a couple of drinks make your life seem content. You express yourself freely to your friends and you have a sense of being powerful enough to achieve anything.

 

However, instead of any positive outcomes, you are soon vomiting, rashes appear on your skin, there is severe pain in your bones and you feel extremely fatigued.

Later, doctors diagnosed you had a dangerous combination of alcohol and Bactrim. You remember taking the medicine for the ear infection you had been having for some time. You are lucky to have been saved because the seemingly innocuous pastime of drinking when on Bactrim can be much more dangerous.

What is Bactrim

Bactrim is a common medicine used to treat bacterial infections but it has various side effects which is why caution is always advised. Bactrim generally contains sulfamethoxazole and trimethoprim and is commonly recommended for cholera, diarrhea, urinary tract infections, ear infections, pneumonia, chronic bronchitis besides prostate and lung infections.

The main task of Bactrim, which has earned its infamy, is to check the bacteria’s ability to use folic acid. Due to its action on folic acid, Bactrim is not recommended to people with lack of folic acid, lactating mothers and infants under two months of age. Pregnant women are advised caution because folic acid is essential for normal development of the fetus.

People allergic to certain drugs including diabetes drugs, thiazide diuretics and sulfa drugs are advised against taking Bactrim because of increased chance of fatal allergic reaction. Those with renal or liver diseases can also be affected because Bactrim can have adverse impact on urine output.

Fever, cough, chills, sensitivity to light, diarrhea, loss of appetite, vomiting, nausea, upset stomach, rash, itching, fatigue, excessive pain, swelling of eyes, coating of the tongue, neurological symptoms and reduced blood counts are some of the adverse effects of taking Bactrim.[ad#co-1]

Mixing Bactrim with Alcohol

Notably, some of the side effects recorded with consumption of Bactrim are also seen after alcohol use which is why side effects of mixing Bactrim with alcohol are much more pronounced. Importantly you don’t need to be on a high to notice the side effects. Even consuming mouthwash containing alcohol and cough medicines can prove to be detrimental resulting in rapid heart rate, shortness of breath, headache, nausea and vomiting which can also lead to dehydration. So it’s better to check the label of these products before using them when you are on Bactrim.

However, alcohol does not reduce the efficacy of Bactrim which is why there is no need to worry about the treatment unless the dose is vomited out.

If you are an alcoholic or don’t have  control over drinking, it’s better to talk to your doctor and substitute Bactrim with some other medicine. However, keep in mind that alcohol does delay your recovery from any disease. In addition, alcohol impacts the liver and may also alter the way drugs, including antibiotics other than Bactrim, are metabolised. This may reduce the impact of these medicines and hence higher doses would be required which may also lead to multi-drug resistance.

So, the best way is to avoid alcohol until you feel fit and hearty again and are totally off medication. This will surely keep the side effects of mixing Bactrim with alcohol at bay.[ad#afterpost]

Filed Under: Health, Medicine

Urinalysis Interpretation: Information on Urinalysis Values

June 22, 2011 by rfcamat Leave a Comment

Sample of urine
Sample of urine (Wikimedia Image)

We have still not been able to understand the human body which seems to be as perplexing as the universe we are a part of. However, with time we have developed certain techniques to dwell into the physiology and get exact reasons for some of the diseases that befall us. Lab tests involving sample of urine cannot only help the doctors diagnose but also observe medical conditions. One of these tests is urinalysis. The urine, which is adjudged by all as a body’s waste, carries important information about what’s going on inside and how things, if gone wrong, can be rectified.

Here’s how you can interpret urinalysis to diagnose various bodily issues.

Color

Color of the urine is the most evident aspect in judging somebody’s help. You must have noticed by yourself that during sickness or when on certain medication, the color of urine changes to dark yellow. The hot weather also can result in yellow color. A red or reddish-brown urine color may occur because of a presence of either hemoglobin after breakdown from the blood, myoglobin from muscle breakdown, a food dye, and consumption of beets or due to intake of a drug.

Clarity

Cloudiness in the urine sample can be due to excessive protein or because of crystallization of salts due to room temperature. People who have undergone bladder surgery often have cloudy urine because of presence of bacteria in the body. Urinary tract infection can also lead to cloudy urine.

Protein

As mentioned earlier, high protein levels in the urine can lead to cloudiness in the sample. However, detection of protein in the urine means kidneys are not functioning properly. Kidneys act as a filter and usually don’t let large molecules like proteins to get into the urine. Another reason for elevated protein levels can be intake of excess meat or urinary tract infection.

Acidity

Our kidneys work overtime to remove the excess acid from our body. The acidity is generally picked up by pH of urine. Normal pH range is from 4.5 to 9.0 and anything beyond that indicates acidity or alkalinity. Low pH level can also affect the detection of other elements including nitrites which don’t show up even if present in the sample. High nitrite values indicate presence of bacteria in the urinary tract.

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Casts

If the urine sample is tested positive for casts, it can be due to several reasons. While white casts can be due to kidney infection, red casts are a result of nephritic syndrome and muddy brown casts can indicate kidney failure.

Specific gravity

Specific gravity is another indicator that can be of great help in diagnosing various conditions. The normal range of specific gravity is 1.002 to 1.035 and any reading above this range indicates contamination or high level of glucose. A patient who receives intravenous dyes for radiography tests also gets a high reading.

Ketones and Glucose

Ketones are compounds that are produced when fatty acids are broken down for energy in the liver or kidney. Excess ketones are produced when the body is under starvation. Type I diabetics can also have excess ketones when the body is deprived of insulin and switches to burning fatty acids. Excess sugar in urine or glycosuria usually indicates diabetes mellitus.

Leukocyte Esterase

This test indicates if there is any infection present in the upper or lower urinary tract or with acute glomerulonephritis. A positive test will indicate presence of white blood cells which defend our bodies against infection. A negative test indicates there is no infection present.

Bacteria

Our genitals normally harbour bacteria because of abundant normal microbial flora of the vagina in females and external urethral meatus in both males and females. This is why only more than 100,000/ml of an individual reflects significant presence of bacteria.

All this knowledge can help you interpret urinalysis in a better way.[ad#afterpost]

Filed Under: Laboratory Tests, Medicine

Is Skin Tanning Cancerous?

June 22, 2011 by rfcamat 1 Comment

Skin tanningSkin color has been the greatest divider in the history of mankind with wars fought, slaves tortured and communities stigmatised because of difference in skin tones. However, things have changed and we have become more acceptable to people of different appearance than others. In fact, there seems to be a reversal of trends. While in many countries people still wish to have fair skin, those with white skin are going crazy over tanning to make their skin appear darker because they feel that it is much sexier.

They are spending hours basking in the sun or sitting in the artificial chambers of ultraviolet (UV) radiations even though their grandparents always thought dark skin is associated with lower class. However, various research studies have shown that skin tanning causes cancer. Read on to know how.

Understanding tanning

Tanning is actually your skin’s response to UV radiation. The melanocytes cells in the skin produce pigment melanin, which darkens the cells of the outer skin as a defence against further damage from UV radiation which is called tanning in common terminology.

However, this protection mechanism can also lead to skin cancer. When the UV rays damage DNA of the outer skin cells, body rushes certain enzymes to do the repairing job but since not every repair is perfect, the leftover DNA damage results in mutations and hence skin cancer.

It’s not that sun rays are always bad for you. In fact, moderate exposure is essential because it triggers the production of vitamin D in your body. Vitamin D has been found beneficial in reducing the risk of many forms of cancers, diabetes, and other diseases but natural food sources of this vitamin are limited. In comparison, just 20 minutes exposure to sunlight can help you maintain the optimal levels.

However, try to restrict this exposure to early morning because the wavelength of sunshine at early hours is most effective. On the other hand, avoid the sun between 11 am and 3 pm because during this time the sunlight is strongest and hence can cause skin burn and tanning, both of which have been linked to development of skin cancer.[ad#co-1]

Ultraviolet radiations

The ultraviolet radiations from sunlight are of different wavelengths are divided into UVA, UVB and UVC. UVC is mostly absorbed by the ozone layer and hence is not deemed a threat while UVB is considered to be the most dangerous of all wavelengths.

UVA is present uniformly throughout the day and throughout the year while the amount of UVB in sunlight varies by season, location and time of the day.
There was doubt about the effect of UVA till some time back as many thought it was not harmful but according to recent studies the wavelength penetrates deeper causing greater genetic damage to the skin cells than UVB and hence being equally if not more carcinogenic. Moreover, sunscreens are more effective in blocking UVB than UVA which can only be barred to some extent by clothing.

Saloon owners have been selling their tanning machines by claiming that the artificial exposure is safer than outdoor tanning because they use UVA rays in a controlled manner. However, as the new studies have shown these machines are as much responsible for causing skin cancer as traditional sunbathing.

The message is simple: Skin tanning causes cancer so better avoid it. Your natural skin color is as good as any other.

Risk factors

Most skin cancers affect the body parts which are frequently exposed to the sun, including head, face, hands, neck, forearms, shoulders, back, chests of men, tips of the ears and lower legs of women.

Caucasians are more likely to get skin cancer because they have light skin which means less melanin to protect against harmful sun radiations. Those with a dark complexion have more melanin in their skin which acts as a sun blocker. Hence, a white skinned man will fall to skin cancer in lesser time than an Asian or an African. Even among fair skinned, those who get sunburns easily are at greater risk. Having a history of skin cancer in the family, having several moles, freckles or birthmarks on the body and being out in the sun a lot during childhood are some other risk factors.

Filed Under: Health, Medicine Tagged With: skin tanning

The 12 Cranial Nerves and Their Functions

June 21, 2011 by rfcamat Leave a Comment

Inferior view of the brain and brain stem showing cranial nerves.
Inferior view of the brain and brain stem showing cranial nerves. (Wikimedia Commons Image)

Cranial nerves in humans consist of twelve pairs of nerves that emerge from the ventral side of the brain. The first two pairs arise from the cerebrum while the other ten pairs emanate from the brainstem. As in the case of spinal nerves which are named based on their origin from the spinal cord, cranial nerves derived their name from their close association with the cranium. The holes or openings in the skull serve as their passage to reach their targets throughout the human body. Some of these nerves send messages from our senses while other cranial nerves control muscle movement, glandular secretions and our internal organs.

A cranial nerve may also be classified as sensory, motor or both according to their mode of signal transmission. Motor nerves carry impulses from the brain to target tissues such as muscles and glandular tissues while sensory nerves transmit impulses from sensory organs to the brain. The table below shows an overview of the cranial nerves, their modality and function.

Table 1.

CRANIAL NERVES MODALITY FUNCTION
I. Olfactory Sensory Smell
II. Optic Sensory Vision
III. Oculomotor Motor Eye movement and pupil constriction
IV. Trochlear Motor Eye movement
V. Trigeminal Both Controls muscles for mastication (motor); somatosensory output from face, head and neck
VI. Abducens Motor Eye movement
VII. Facial Both Controls muscles for facial expression (motor); sensory input from anterior 2/3 of tongue (taste) and ear (tympanic membrane)
VIII. Vestibulocochlear Sensory Hearing and balance
IX. Glossopharyngeal Both Controls some muscle for swallowing (motor); sensory input from posterior 1/3 of tongue, tonsil and pharynx
X. Vagus Both For motor, sensory and autonomic functioning of the viscera (e.g. digestion, glandular secretion, heart rate)
XI. Spinal Accessory Motor Controls muscles used in head movement
XII. Hypoglossal Motor Controls muscles of tongue except palatoglossal

 

I. Olfactory Nerve

This nerve functions primarily for the sense of smell. Its name is derived from the Latin words ‘olfactare’, which means to sniff at, and ‘olfacere’, which means to smell. Among all the cranial nerves, this is the only one capable of self-renewal since it has the property to regenerate continually through adulthood. Also, aside from being the smallest nerve, the olfactory nerve doesn’t branch out into left and right entities. Instead, it consists of a collection of sensory rootlets that extend from the olfactory epithelium to the olfactory bulb as it passes through the numerous openings of the cribriform plate in the ethmoid bone. When a person inhales, molecules of air attach themselves to the sensory parts of the olfactory nerve which are located in the olfactory mucosa at the upper part of the nasal cavity. As these nerve endings become stimulated, electrical activity is generated and is transmitted to the olfactory bulb. The cells in the olfactory bulb in turn relay the electrical signal to the brain through the olfactory tract.

II. Optic Nerve

During embryonic development, the optic nerve arises from the diencephalon, thus considered a part of the central nervous system. As with other CNS components, optic nerves are covered with Myelin sheath rather than Schwann cells and are wrapped by meninges. Unlike the olfactory nerve, optic nerves are incapable of regeneration which increases the risk of permanent blindness when severed.

Optic nerve conveys visual information from the retina to the brain. When light reaches the retina, stimulation of the photoreceptors (rods and cones) occurs which triggers the production of electrical impulses. These are relayed to the bipolar cells which contain the optic nerve endings. The bipolar cells in turn transmit the electrical impulses to the CNS via the optic nerve. The optic nerves enter the CNS at the optic chiasm where they become the optic tract. From there, the electric signal is transduced to the lateral geniculate nucleus of each thalamus before going to the visual centers of the brain for interpretation.

III. Oculomotor Nerve

Oculomotor nerve has two components: 1. Somatic motor or general somatic efferent which controls muscles responsible for precise eye movement for visual tracking and fixation on an object and 2. Visceral motor or general visceral efferent provides parasympathetic innervation of the constrictor pupillae and ciliary muscles of the eye which regulate light accommodation by controlling pupil constriction.

The somatic motor component is further divided into inferior and superior divisions. The inferior division innervates the medial rectus, inferior rectus and inferior oblique muscles while the superior division supplies the levator palpebrae superioris and superior rectus muscle. The table below shows a summary of the function of the eye muscles controlled by the somatic motor component.

Table2.

Eye Muscles Primary action Secondary action Tertiary action
Medial rectus Adduction – —
Inferior oblique Extorsion Elevation Abduction
Inferior rectus Depression Extortion Adduction
Superior rectus Elevation Intortion Adduction
Levator palpebrae superioris Controls movement of the upper eyelid

 

Table adapted from http://www.med.yale.edu/caim/cnerves/cn3/cn3_3.html

The other two eye muscles not included in Table2 are the Superior oblique (Intorsion, Depression, Abduction) and Lateral rectus (Abduction) which are controlled by the Trochlear Nerve (IV) and the Abducens Nerve (VI) respectively.

IV. Trochlear Nerve

This nerve has only a somatic motor component which controls one eye muscle – the Superior oblique. As mentioned above, superior oblique carries out three different functions: intorsion, depression and adbuction.

Though this nerve only supplies one eye muscle, it has several characteristics that distinguish it from the other cranial nerves.

1.This is the only nerve that exit the brain dorsally.

2.This is the only nerve that decussate or cross which makes the nerve fibers supply the superior oblique muscle on the side opposite their origin.

3.This has the longest intracranial route.

4.This has the smallest number of neurons.

V. Trigeminal Nerve

The trigeminal nerve, as the name implies, is consists of three large branches: Ophthalmic and Maxillary which are both sensory, and the Mandibular branch which has both motor and sensory functions. The Ophthalmic branch innervates the forehead and the eye while the Maxillary branch supplies the cheeks. The Mandibular branch on the other hand controls the lower jaw and lower portion of the face. Since this nerve has both sensory and motor functions, it is responsible for sensing facial touch, pain, and temperature and controlling the mandibular muscles during mastication.

The three branches meet in an area called the Gasserion ganglion. The fused branches extends backwards to the brainstem, inserting itself into the pons. Inside the brainstem, the signals that pass through the trigeminal nerve arrive at a structure called trigeminal nerve nucleus. From there, the information is sent to the cerebral cortex where perception of the sensation is achieved.

VI. Abducens

This nerve has only a motor component which innervate the lateral rectus muscle of the eye. To make a lateral movement, inputs from the higher centers of the brain in the form of electrical impulses synapse at the lateral gaze center. From there, the signal travels through the longitudinal fasciculus to reach the abducens nucleus, which then sends the message to the lateral rectus muscle via CN VI , causing the muscle to be abducted.

VII. Facial Nerve

The facial nerve is a mixed nerve having both the sensory and motor components. It has approximately 10,000 neurons in which 70% of these are myelinated and control facial expressions. The other 30% are somatosensory and secretomotor in function. The table below shows the nature and function of the facial nerve.

Table3.

Branchial motor
(special visceral efferent)
The largest component of the facial nerve 

 

Supplies voluntary control of the posterior belly of the digastric, stylohyoid and stapedius muscles as well as muscles involve in facial expression such as the buccinator, occipitalis and platysma muscles

Visceral motor
(general visceral efferent)
Comprise the parasympathetic constituent of CN VII 

 

Provides parasympathetic control over the submandibular, sublingual, and lacrimal glands

 

Innervates the mucous membranes of the nasopharynx and hard and soft palates

Special sensory
(special afferent)
Consists of fibers that transmit sensation of taste from the anterior 2/3 of the tongue as well as from the hard and soft palates
General sensory
(general somatic afferent)
Conveys sensory information from the skin of the concha of the auricle and from a small area of skin behind the ear 

 

Acts as a supplement to the Mandibular component of the Trigeminal Nerve to provide sensation at the wall of the acoustic meatus and the outer surface of the tympanic membrane

 

VIII. Vestibulocochlear Nerve

This is a sensory nerve that consists of two components – vestibular and cochlear. The vestibular nerve detects head and body motion while the cochlear nerve detects sound. Thus, the vestibulocochlear nerve functions for hearing and balance. Balance is achieved by conveying information to the vestibular component of the CN VIII which are done by the semicircular canal and the otolithic organ. The former detects angular acceleration while the latter detects linear acceleration.

For us to hear and recognize the sounds around us, the cochleat component of the CN VIII should be stimulated. This happens when sound waves collected by the outer ear travel through the ear canal and cause vibrations of the ear drum. The vibration of the ear drum moves the bones of the middle ear which in turn pass the vibrations to the fluid-filled cochlea. As the fluid inside the cochlea moves, it causes the cilia to vibrate and stimulate the sensory cochlear nerve. When stimulated, the nerve sends signal to the area of the brain where the signals are processed into the sound we hear.[ad#co-1]

IX. Glossopharyngeal Nerve

As the name implies, CN IX innervates the tongue and the pharynx and has both the motor and sensory components. The functions of each component are summarized in the table below.

Table4.

Branchial motor
(special visceral efferent)
Provides voluntary control of the stylopharyngeus muscle which elevates the pharynx during swallowing and speech
Visceral motor
(general visceral efferent)
Parasympathetic component which innervates the parotid gland and the smooth muscle of the pharynx, larynx, and viscera of the thorax and abdomen
Visceral sensory
(general visceral afferent)
Controls the baroreceptors of the carotid sinus and chemoreceptors of the carotid body
General sensory
(general somatic afferent)
Transmits sensation of pain, temperature, and touch from the skin of the external ear, internal surface of the tympanic membrane, the walls of the upper pharynx, and the posterior 1/3 of the tongue
Special sensory
(special afferent)
Carries sensation of taste from the posterior one-third of the tongue

X. Vagus Nerve

The term ‘Vagus’ is a Latin word which means ‘wandering’. Vagus nerve fits its name since it wanders from the brainstem and extend to organs found in the neck, chest and abdomen. Table 5 summarizes the vagus nerve’s components and their respective functions.

Table5.

Brancial motor
(special visceral efferent)
Supplies voluntary control to the striated muscle of the pharynx and larynx (except for the stylopharyngeus muscle and the tensor veli palatini muscle) as well as the palatoglossus muscle of the tongue
Visceral motor
(general visceral efferent)
Parasympathetic control of the smooth muscle and glands of the pharynx, larynx, and thoracic and abdominal viscera down to the splenic flexure resulting to increased GI tract secretion and motility, higher bronchiolar secretions and bronchoconstriction in the lungs and slower heart rate.
Visceral sensory
(general visceral afferent)
Transmits sensory information from the larynx, esophagus, trachea, abdominal and thoracic viscera, aortic arch and the aortic bodies
General sensory
(general somatic afferent)
Carries sensation of pain, temperature, and touch from from the larynx and pharynx as well as information from the skin of the back of the ear and external auditory meatus, parts of the external surface of the tympanic membrane
Special sensory
(special afferent)
Transmits sensation of taste from the epiglottic region

 

XI. Spinal Accessory Nerve

This is a motor nerve consisting of cranial and spinal parts that control muscles of the neck and shoulders to move the head. The cranial part (special visceral efferent) innervates muscles of the pharynx and larynx while the spinal part (special visceral efferent) controls the trapezius and sternocleidomastoid muscles. The trapezius muscle moves the scapula, acts as a support for the arm, assists in breathing, keeps the head in position and produces bending and rotational head movement. The sternocleidomastoid muscle on the other hand flexes the neck and turns the head obliquely.

XII. Hypoglossal Nerve

As indicated in its name, this nerve innervates the muscles found below (hypo) the tongue hence consists only of the motor component. It provides voluntarily control over the three out of four extrinsic muscles of the tongue which include genioglossus, styloglossus, and hyoglossus. Genioglossus muscle is responsible for protruding (or sticking out) the tongue while styloglossus draws up the sides of the tongue to aid in swallowing. The hyoglossus muscle on the other hand retracts and depresses the tongue for chewing and speech.[ad#afterpost]

Filed Under: Biology, Health, Medicine

Polydactyly: Causes, Symptoms and Treatments

June 21, 2011 by rfcamat Leave a Comment

Polydactyly

Left hand of African woman with postaxial polydactyly.
Left hand of African woman with postaxial polydactyly (Wikimedia Commons Image)

Polydactyly is a congenital physical aberration in which a person has more than five fingers on his/her hand or if his/her foot has more that five toes each. The term is derived from the Greek words ‘polus’ which means ‘many’ and ‘daktulos’ which means ‘fingers’. The extra digit on either hand or toe may be rudimentary or fully formed with or without bones at all. For rudimentary polydactyly, the extra finger or toe is usually a piece of soft tissue. In rare cases, the extra digit may develop fully and become a functional finger or toe.

Polydactyly is one of the most prevalent inborn hand abnormalities which manifests in 1 out of 500 live births. Experts formed a classification for this congenital condition based on its extent and location. Fully formed digits having a complete number of bones and joints are classified as Type A polydactyly while rudimentary fingers or toes are classified as Type B polydactyly. Based on location, polydactyly can be preaxial, central or postaxial. Preaxial when the extra digit occurs near the thumb or big toe; postaxial when it is located near the pinky or near the smallest digit of the foot; and central when the extra digit arises between the  biggest and smallest digits of the limbs. Among Asians, an extra thumb is most likely to arise (preaxial polydactyly) while an extra finger on the small digit side is most common among African-Americans (postaxial polydactyly). Polydactyly may occur as an isolated condition or it may be expressed as a result of an underlying health condition such as Meckel syndrome, trisomy 13  and Grebe type Chondrodysplasia. In most cases however, polydactyly is caused by genetic factors.

Genetic Causes of Polydactyly

The gene that codes for polydactyly is found on one of the short legs of chromosome seven and has an autosomal dominant mode of inheritance. Since it is autosomal, its occurrence among males and females is equal. And because it follows a dominant pattern of inheritance, a child with a polydactyl parent has at least 50% possibility to inherit and show the trait.

One of the genes behind polydactyly is GLI3. It serves its function by providing instructions for making a protein (GLI3 protein) that has the capacity to turn on or to turn off gene expression. During embryonic development, GLI3 protein plays a key role in shaping tissues and organs by interacting with other genes. When a mutation or a change related to the GLI3 gene in chromosome seven occurs, deletion or rearrangement of genetic materials for example, limb development becomes severely affected which can lead to polydactyly at birth.

Another gene that can cause polydactyly is the LMBR1 gene which is also located in chromosome seven. Similar to the case of GLI3 gene, a disruption in the LMBR1 region can alter the expression of a protein called Sonic hedgehog homolog (SHH) which regulates vertebrate organogenesis and growth of digits. Defects in this gene are associated with preaxial polydactyly while abnormalities in GLI3 gene are associated with both preaxial and postaxial polydactyly.[ad#co-1]

Diagnosis

Physical examination after birth is the easiest way to diagnose polydactyly. Diagnosis can also be done before childbirth by looking at family histories and by performing several prenatal tests. One of the most commonly used method during pregnancy is a prenatal ultrasound called a sonogram. If polydactyly is seen in the ultrasound, other medical tests may be conducted to determine if the condition is associated with other genetic disorders. In cases where the result of a sonogram becomes unyielding, a method called embryoscopy is also employed. This test involves the the direct visualization of the embryo by inserting a fiber optic scope through the mother’s abdominal wall and uterus. For a more genetic approach and reliable result, amniocentesis is performed. This requires the analysis of amniotic fluid sampled from the mother’s womb primarily to detect chromosomal abnormalities in the fetus.

Treatment

Treatment for polydactyly depends on the severity of the disorder. X-ray is usually done to determine the extent of polydactyly so as to apply the corresponding treatment for such condition. For isolated cases where no major health consequences are likely to arise, surgery is used to remove the extra digit. For Type B polydactyly, the extra finger or toe can be surgically removed before the newborn is discharged from the hospital. Type A polydactyly on the other hand is more complicated and requires more surgeries compared to the other type and is usually corrected when the child is above one year of age.[ad#afterpost]

References

  • http://www.nlm.nih.gov/medlineplus/ency/article/003176.htm
  • http://www.umm.edu/ency/article/003176.htm
  • http://www.healthline.com/galecontent/polydactyly
  • http://www.childrenshospital.org/az/Site1073/mainpageS1073P1.html
  • http://ghr.nlm.nih.gov/condition/greig-cephalopolysyndactyly-syndrome
  • http://www.brighthub.com/science/genetics/articles/47390.aspx
  • http://answers.yourdictionary.com/medical/what-causes-polydactyly.html
  • http://www.springerlink.com/content/d2t10p466rm502kt/

 

Filed Under: Genetics, Medicine

Understanding the Serum Angiotensin Converting Enzyme Test

June 20, 2011 by rfcamat Leave a Comment

Space-filling models of angiotensin I (left) and II (right).
Space-filling models of angiotensin I (left) and II (right). (Wikimedia Image)

Serum angiotensin converting enzyme test is a test that measures the amount of angiotensin converting enzyme in blood levels. Angiotensin converting enzyme is an enzyme that converts angiotensin I to angiotensin II. These two proteins play a vital role in regulating blood pressure. Angiotensin I is usually inactive, but when acted upon by angiotensin converting enzyme, it becomes angiotensin II.

Angiotensin II is the active form of angiotensin I. Angiotensin II causes the blood vessels to narrow. When there is a decrease in area, fluids (in this case, blood), flows faster, causing a resultant increase in blood pressure. Serum angiotensin converting enzyme test is primarily carried out to test for suspected cases of sarcoidosis, a disease that results in the formation of structures called granulomas in various organs. Granulomas are abnormal aggregations of inflammatory cells that, in some organs, form nodules.

Sarcoidosis may occur in an individual for years without any symptoms. When an organ is affected by sarcoidoisis, several symptoms may appear. These include weight loss, fatigue, arthritis and dry eyes. Skin symptoms may include rashes and lesions particularly on the face, neck and ears. The lymph nodes near the affected area may exhibit swelling (lymphadenophaty).

Sarcoidosis may also cause other symptoms depending on the area where it is located. When sarcoidosis affects the lungs, there would be lessening of the lungs air intake as well as blockages when severity increases. Sarcoidosis is usually asymptomatic, thus it is usually accidentally detected when undertaking mundane tests like x-rays, blood tests, CT scans of the chest area and lung biopsy.

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High angiotensin converting enzyme levels are a sign of sarcoidosis. An individual afflicted with sarcoidosis would have elevated levels of angiotensin converting enzyme. This could be 50% to 80% more than normal. Serum angiotensin levels are also related to the severity of sarcoidosis; rise and fall of the levels signify intensity or improvement of the condition.

Testing for serum angiotensin converting levels requires obtaining blood from the patient. Normal test results would be from 8 to 27 U/ml (units per milliliter). Individuals below the age of twenty have naturally high serum angiotensin converting enzyme levels, which may mask the presence of sarcoidosis.

There are several causes if a serum angiotenesin converting enzyme test results show low level of the enzyme. Low levels of angiotensin converting enzyme may be caused by hypothyroidism, a disorder that signifies a decrease in thyroid production. This disorder is primarily caused by iodine deficiency though other factors like radioactivity, genetics and environment may contribute to the development of the disorder.

Low levels of serum angiotensin converting enzyme may also be caused by the eating disorder anorexia nervosa. Anorexia nervosa is a disorder that generally manifests as a loss of any desire to consume food.

The disorders mentioned above can be very serious. They may escape the notice of several other tests. Undergoing a serum angiotensin converting enzyme test lets one know the possible occurrence of these disorders. This would better help him to take the appropriate steps to facilitate treatment and return to a healthy life.[ad#afterpost]

References

  • James, William D.; Berger, Timothy G.; et al. (2006). Andrews’ Diseases of the Skin: clinical Dermatology. Saunders Elsevier.
  • McGonagle D, McDermott MF (2006) A proposed classification of the immunological diseases. PLoS Med
  • White, E.S.; Lynch Jp, 3rd (2007). Current and emerging strategies for the management of sarcoidosis. Expert Opinion on Pharmacotherapy
  • Kumar MS, Safa AM, Deodhar SD, Schumacher OP (1977). The relationship of thyroid-stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3) in primary thyroid failure.  American Journal of Clinical Pathology

Filed Under: Laboratory Tests, Medicine

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