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Anal sex refers to the activity in which penis is inserted into the anus. Some people found anal sex more joyful, but the fact is that the practice has the downside and it contains so many health risks.

It is prohibited in various cultures especially with regard to religious prohibition. It is a criminal offense in some countries and punishable by corporal or capital punishments. By disparity, people regard it a valid and natural form of sexual activity.

Is Anal Sex Safe?

There are so many health risks associated with the anal sex and anal intercourse, for both partners. Some of the health risks which may affect both homosexual and heterosexual couples are listed below.

Risk of bacterial infection: E. coli is a Gram-negative, facultative anaerobic bacteria, that is commonly found in the lower intestine. Anal sex increases the risk of transmission of E. coli bacteria from anal to your penis, which may cause a severe type of urinary tract infection.

E. coli may cause many bacterial infections, including, urinary tract infection (UTI), meningitis, cholecystitis, cholangitis, bacteremia, and pneumonia.

Hepatitis A Virus (HAV): Hepatitis A Virus can transmit by the oral sex (anal licking). HAV causes jaundice. It is usually not a life-threatening virus but may cause illness.

Hepatitis C Virus (HCV): It may be transmitted through the anal intercourse. Hepatitis C Virus is the cause of fetal liver chronic disease. It is a life-threatening virus and may lead to death.

Human Papilloma Virus (HPV): It may be transmitted through the anal intercourse and may cause to the anal wart. A research showed that some of the strain of HPV have carcinogenic potential. Some strains of HPV cause cancer of the cervix in women and also cause cancer of the throat.

Human immunodeficiency virus (HIV): There is a greater risk of transmission of HIV through anal intercourse. It is a life-threatening virus and leads to death.

Weakening of the anal sphincter: The anal anus is enclosed by the ring-like muscle, called the anal sphincter. The main function of anal sphincter is to hold the feces until you get to the toilet. After the excretion of feces, it tightens. Penetration of something like a penis inside the anal can be difficult and painful. Anal intercourse may lead to the weakening of the sphincter muscles, and make it hard to hold the feces.

Lack of natural lubrication: Naturally, the anal is not made for sex. The anal has lack of lubricant as vagina have, which makes the penetration harder and painful. Penetration can tear the tissues inside the anal and cause the wound, allowing viruses and bacteria to easily enter the bloodstream. Somehow, usage of oil or other lubricants can help in preventing the tearing of tissues inside the anal but doesn't completely.

A research showed that risk of transmission of HIV and HPV is much higher in anal sex and compared to the vaginal sex.

How to Prevent Anal Sex Problems

There is no way to completely eliminate the risk factors of anal sex until you avoid the anal sex. However, you can reduce the risk by the following tips.

  1. Always use a condom during anal sex.
  2. Do not enter penis into the mouth after inserting it into the anal.
  3. Use a sufficient amount of lubricants when penetrating into the anal to reduce the risk of tissue tear. Always use water-based lubricants with condoms.
  4. Do not lick the anal as it may cause the transmission of bacteria and viruses.
  5. Take a warm bath before anal sex.
  6. Lying on your stomach will make the insertion easier.
  7. Stop if you feel so much pain during anal sex.
  8. Stop if you experience bleeding or discharge coming from it, go to the hospital as soon as possible.

The Middle East respiratory syndrome (MERS) caused by coronavirus which has a large family of virus. This viral disease first identified in September 2012 in Saudi Arabia. This virus can cause disease ranging from common cold to Severe Acute Respiratory Disease (SARS).

This deadly virus may originate from bats and categorize as a zoonotic virus. Which mean a virus that transmitted from animal to human by direct or indirect contact. Especially dromedary camel which is a reservoir host for this virus.

Which Country Infected By MERS-CoV

Saudi Arabia is the leading country. About 80% of cases have reported. The United Arab Emirates and the Republic of Korea come in second. But specific antibodies that can found in previously infected animal have been identified in Middle East, Africa, and South Asia

*According to WHO, since 2012, 27 countries have reported cases of MERS including Algeria, Austria, Bahrain, China, Egypt, France, Germany, Greece, Islamic Republic of Iran, Italy, Jordan, Kuwait, Lebanon, Malaysia, the Netherlands, Oman, Philippines, Qatar, Republic of Korea, Kingdom of Saudi Arabia, Thailand, Tunisia, Turkey, United Arab Emirates, United Kingdom, United State, and Yemen.

How MERS-Cov virus Spread or Transmitted?

From animal to human. Taking care of infected animal without proper precaution can transmit the virus easily. Eating raw meat or milk without proper preparation can also infect the human.

Secondly, they spread by human to close human contact. For example, unprotected care to a patient in health-care facilities. The facilities provided inadequate prevention and didn’t separate MERS patient with another patient. Traveller whose have infected. Traveling to another country and spread the virus.

However, the exact route is still unknown.

What Are The Symptoms of MERS-CoV

Typical symptoms that infected patient presented are the common cold, cough, and shortness of breath. These are the common/mild symptoms. Pneumonia(not always present), and severe acute respiratory disease which leads to respiratory failure. The patient needs to use mechanical ventilation in intensive care unit (ICU).

Gastrointestinal symptoms also present for example diarrhea. Some of the patients might be asymptomatic meaning absent from clinical symptoms. But they are positive for MERS proved by a laboratory test.

Is There A Possibility For Me To Get Infected?

High-risk people: eating raw contaminated milk and meat. Older people. Low immunity person. Chronic disease patient such as renal disease, cancer, lung disease and diabetes. This person should avoid direct contact with camel, drinking raw camel milk or urine and eating raw meat.

*According to WHO, 750 death related to MERS-Cov since 2012. But there are still patient with mild cases that might miss due to ignorance about the disease. This disease has high mortality rates of 35%.

How Can We Treat MERS-CoV Disease?

Unfortunately, there is no vaccine, or specific treatment is currently available. However, according to WHO, three vaccines currently under development. One vaccine to prevent transmission from animal to human. While the other two for outbreaks of this disease and protection for high-risk people). As for now, we can only treat clinical symptoms and supportive treatment.

What Can We Do To Avoid The Virus?

We can take some precaution. For examples in the farms, market, and barns. The home where dromedary camel and other animals live; we should practice general hygiene measures. Washing hand before and after contact with the animal and avoid visiting sick animal. In health-care facilities, the worker should know or educated in the prevention of disease and applied it. Fortunately, according to WHO, a disease outbreak in healthcare facilities have significant drop compared to previous year.

MERS-CoV is still a threatening virus, and WHO reports the recent case. A male patient 74 years old lives in Batinah, Omani. The disease transmitted when he is taking care of his sick camel. Laboratory confirmed that it is a case of MERS-Cov disease. Take care of ourselves better. Educate yourself and take alert of what happens in our world. The world is getting sicker day by day, and we can change it. Little by little.

What Is Yellow Fever? 
 
Yellow fever refers to jaundice that presents in a patient infected with the virus by getting a bite from a mosquito carrying the virus. The virus is arbovirus of the flavivirus genus. And the species of the mosquito is Aedes and Hemogogus. 
 
The disease endemic in tropical areas of Africa, Central, and South America especially Brazil. Circulate in the highest concentrated population with a high density of mosquito. An area that yellow fever vaccination not previously recommended. 
 
*According to WHO, between 1 July 2017 and 28 February 2018, 723 confirmed human cases of yellow fever had reported in Brazil, including 237 deaths. This number increase since 2015/2016. 
 
What Are The Symptoms Of Yellow Fever? 
 
Symptoms include fever, headache, jaundice, muscle pain with prominent back pain, loss of appetite, nausea, vomiting, and fatigue. Most cases are asymptomatic for few days after bitten by a mosquito. Some symptoms disappear after 3 to 4 days. 
 
Severe symptoms or toxic phase just within 24 hours after initial symptoms disappear may occur. By high fever and affected several systems such as liver and kidney. The patient will develop jaundice, dark urine and abdominal pain with vomiting. Bleeding can occur from patient’s mouth, nose, ear or stomach. Within 7 – 10 days, half of the patient may die. 
 
Misleadingly yellow fever symptoms can be confused with severe malaria, leptospirosis, viral hepatitis, other hemorrhagic diseases, and poisoning. But testing Polymerase chain reaction (PCR) in blood and urine can help detect the disease in early stage
 
Do I Have Possibility Getting Yellow Fever? 
 
High-risk people are people who live in an endemic area in Africa and Central South America. Travelers who visit the yellow fever area may spread the disease in another country. Old people over 60 years old or patients with severe immunodeficiency can easily get infected. 
 
How Can Yellow Fever Transmit? 
 
Three ways can transmit the disease. First, a worker who’s working in the jungle or brave traveler roaming in the forest is bitten by a mosquito. The mosquito transfer the virus in monkeys which is a reservoir host for the virus by biting them. 
 
The second way is the mosquito infected both monkey and human. The mosquito roaming in the jungle and household. Increase contact from both of species will lead to outbreaks even in neighborhood village at the same time. In Africa, the second way is the most common way to cause an outbreak of yellow fever disease. 
 
The third way is when infected people bring the disease in an area with high density of mosquito and lack of vaccination. Plus this people usually have low immunity and easily to be infected. In this case, the disease transmitted from people to people. 
 
Do We Have Treatment For Yellow Fever? 
 
Treatment is supportive treatment from the hospital. The specific drug for yellow fever is still under development. Treating the symptoms present such as liver or kidney failure and fever may improve the outcomes. 
 
However! 
 
We can prevent it! 
 
By highly effective vaccine which is safe and affordable. A single dose is sufficient to prevent the disease and prolong the lifespan. Plus a booster dose is not needed. Within 30 days the vaccine provided effective immunity for the person vaccinated. 
 
Prevention by vaccination is the most important step in battling against this disease. At least 80% of the population in an endemic area should be vaccinated to prevent the outbreak. Don’t forget the traveler who is going to visit the endemic area need to confirm whether they are vaccinated or not. Many countries require the traveler to prove that they have been vaccinated for yellow fever before issue visa, especially in endemic countries. 
 
But! 
 
Some people excluded from vaccination. Please pay attention to this to avoid other problems.
 
  • Infants aged less than nine months. But if the infants live in the endemic area, they are required to be vaccinated.
  • Pregnant woman except during outbreak of disease.
  • People with severe allergies to egg protein.
  • People with low immunity due to HIV/AIDs and thymus disorder
 
Other prevention is mosquito control. Eliminate potential breeding sites by applying larvicides to prevent breeding of mosquito larva. We can put the larvicides in water container or places where water is collected.
 
Doing surveillance on Aedes or Hemogogus species by knowing which area have a high density of them can prevent further outbreak. We can apply vector control as early as possible. We also can prevent it by minimizing exposure of ourselves to avoid mosquito bite.
 
The Eliminate Yellow fever Epidemics (EYE) Strategy launched in 2017. An initiative to prevent, detect and respond to suspected case and outbreaks. With an objective to protect, prevent and contain outbreak as soon as possible. Many strategies have implied such as promoting vaccination, increase surveillance on mosquito and expanding partnership with different countries. Hopefully by 2026 more than 1 billion people will be protected against the disease.

The medical term for an infection in the vagina is vaginitis. The infection caused by any pathogenic organism such as streptococcus, staphylococcus, Trichomonasvaginalis or maybe Candida. It can happen in a child of age one to five years old, adults and old women.

But How Do You Get Infected?

The organism can transmit from a child or adult by hands or clothes. Sometimes a foreign body such as a pin is inserted by the child into the vagina can cause infection. Wiping your butt from your anus to vagina may transfer organism to the vagina.

A child with a near infection or tonsillitis can transmit bacteria by hand to her genital area as she is touching it.

Sexual abuse is leading to any sexually transmitted disease as gonorrhea.

Or nylon underclothes and harsh soap may cause the infection in your vagina.

So What Are The Symptoms Of Vagina Infection?

  1. Vaginal discharge. Purulent (pus discharge), blood stained if there is a foreign body or cervical polyp (growth that appear on the cervix look like bulbs on thin stems).
  2. Irritation, pain, and soreness due to discharge.
  3. Severe itching of the skin area around genital.
  4. Pain during peeing like burning sensation and the frequency of peeing is an increase.

How Does Your Genital Look Like If Infected?

The vulva is inflamed, red, tender, sometimes oedematous and bathed in discharge. The labia minora might stick together but can be separated apart leaving inflamed red surfaces.

What Treatment Will You Get?

You need to get proper treatment in the hospital to avoid further infection.

A specific antibiotic is given according to the nature of the organism. For non-specific vaginitis, estrogen cream is applied to the vulva each night for about two weeks. It increases local resistance to infection and relieves soreness.

Any foreign body must be removed. Local washes with warm water and boiling of the underclothes which should be cotton. If one of your child infected, you must isolate from other children to prevent cross infection.

Take extra precaution in sexual activity to avoid sexually transmitted disease which can cause infection to your vagina.

Monitor your daughter during her play time or any changes happen to her. Since prevention is better than cure isn’t it?.

Reviewed by Dr. Nida Hayat Khan
Editor @ BioScience.pk

Menopause is a phase when you stop getting your period. It marks the end of your menstrual cycles. You stop getting your period for at least six months or one year and confirm with your gynecologist. Woman between 40s to 50s is the age of getting menopause, but in the United States, the average age is 51 years old.

Which Types of Menopause You Could Get?

  1. Normal or Natural menopause: occurring between the age of 40 and 55 with an average of 50 years
  2. Premature menopause: Period stop before you hit 40. About 1% of women have menopause below the age of 40
  3. Delayed menopause: you still have your period until the age of 55
  4. Artificial menopause: caused by surgical removal of both ovaries or destruction of ovaries by exposure to irradiation

How Menopause Started?

Maybe preceded by the infrequent period, scanty or decrease the amount of your usual period (less than 30ml). Or the length of your period becomes less to two days. A period of dysfunctional uterine bleeding or suddenly your period stop and never return. About 10% of women suddenly their period stop.

What Changes Happen To You During Menopause?

General Changes:

  1. Your breast might become smaller due to tissue in your breast atrophied or larger due to increase fat deposition
  2. Your appetite may be decreased or increase which leading to obesity. Constipation and gases accumulate (Fart! Fart! Fart!)
  3. The tendency to develop menstrual hypertension as the amount of estrogen decrease. Oestrogen can protect you from atherosclerosis
  4. You gradually have a high risk of coronary heart disease because the level of cholesterol and triglycerides is increased
  5. Liability to osteoporosis (bone disease which resulted in bone become weak easy to break)
  6. Mild hirsutism (increase amount of hair in the manly pattern, e.g., in an area where men typically grow hair)
  7. Psychological changes for examples headaches, irritability and depression

Local Changes:

  1. The pubic hair becomes scanty, grey or white
  2. The vagina becomes narrow, and the pH becomes neutral or alkaline. This condition will predispose to infection
  3. The uterus becomes small and atrophic. Senile endometritis may occur (inflammation of uterus)
  4. The ovaries become small, fibrotic (excess fibrous of connective tissue) and containing no follicles (no egg)
  5. Bladder becomes small. The condition may lead to going to the bathroom a lot (you pee a lot), inflammation of your bladder and urethra

Symptoms You Might Get With Menopause

Palpitation, hot flushes (sensation of heat felt in the chest, neck, face, head or spread to all over body) and night sweats. About 75% of postmenopausal women have hot flushes. Usually, hot flushes disappear after one or two years even without treatment from a doctor.

The hot flush lasts for seconds, minutes, and rarely for one hour but usually 3 minutes. One or two in 24 hours to one every 15-30 minutes in a day.

However, about 25% of cases will continue to have hot flushes for more than five years.

Lack of concentration, poor memory and insomnia (difficult in sleeping/staying asleep). Insomnia is usually the result of night sweats

Joint pain and backache due to loose ligament and muscle become weak

What Can You Do With Menopause?

Well, menopause is a change in life and not the end of life. You can avoid factors which can cause hot flushes as hot weather, hot bath, nervousness, excessive intake of coffee or tea, excessive blanket and covering during sleep.

Control of diet with less fat to avoid obesity. Increase intake of calcium, i.e., dairy product, green leafy vegetables, nuts or fish where you eat the bones-sardine and pilchards.

However!

There are some treatment or therapy to help you in menopause.

Treatment for symptoms such as depression and palpitation

Estrogen therapy: for a woman without a uterus

Given to women if the symptoms such as hot flushes, senile vaginitis (inflammation of vagina), increase the frequency of peeing and psychological disturbances. Treatment is given for at least one year to prevent recurrence of symptoms

This therapy also is given to premature menopause as this condition predisposes to osteoporosis (bone break easily). Treatment is given at least until the age of 50 years. The treatment reduces the risk of osteoporosis by 50% to 60%

Combined estrogen-progesterone therapy: for a woman with a uterus

To protect against endometrial hyperplasia (womb cancer).

Progesterone alone is given to control hot flushes. Although progesterone less effective than estrogen but it causes a less side effect.

Menopause happens to every woman on earth. It differs in every woman of how it started, the changes in your body, the symptom might present in you and the suitable treatment you can do. Consult your gynecologist for explanation and reassurance of the changes in your life.

Medically reviewed by Dr. Nida Hayat Khan
Editor @ BioScience.pk

Have you ever listened about the “Second Brain”?

Yes, you have! whenever you are told to trust your gut instinct. This brain and gut connection is not just metaphorical. An extraordinarily extensive network of neurons (more than 100 million neurons) lines our gut that scientists have named it the Second Brain.

What about the inhabitants of gut including good and bad microbial flora?

Gut microbiota weighs up to 2kg containing trillions of micro-organisms. One-third of these microbiotas is common to all people while others are specific to every individual’s gut depending on the type of diet they take in and their lifestyle.

“Gut flora is a complex community of organisms that inhabit human and animal digestive system”. Relation between humans and gut flora is mutualistic. Bacteria in the digestive system assist in nutrient metabolism, vitamin production, and waste processing. They also aid in the host's immune system response to pathogenic bacteria.

Healthy Microbiota & Healthy Brain

The gut has a bidirectional relationship with the central nervous system referred to as the “gut-brain axis”. Introduction of good bacterial strain reduces anxiety and stress level. Gut-brain axis is used by bacteria to affect the brain function. The most significant factor related to the health of microbiome -- thus, brain – is healthy food. Following are the positive influencing microbiota Lactobacillus that produce lactic acid are found in yogurt. Taking in yogurt will boost mental capacity and relieve stress, it also aids in digestion and relieves constipation. But make sure yogurt is live culture (probiotic). Bifidobacteria feast on chocolate and ferment it causing positive effects on our health and body. Dark chocolate is also very beneficial for the heart because bacteria (Bifidobacterium, LAB, yeast) ferment it into healthful anti-oxidants. Prebiotic foods including raw garlic, raw, and cooked onions allow the healthy microbiota to grow and thrive while inhibits the growth of non-healthy microbiota. Environmental toxins can disturb microbiome and have adverse effects on brain health to save ourselves from these effects, use of home filtered water should be made compulsory. Such filters should be used that remove harmful toxins like chlorine. Fermented foods like pickles, kefir, kimchi etc. are the source of Lactobacillus lactis species and defend against leaky gut. These were some healthy microbial flora and their sources having a positive effect on your body and brain.

Non-Healthy Microbiota & Whacky Gut

There are bidirectional links between stress and microbiota. Irritable Bowel Syndrome (IBS) and Chronic Fatigue Syndrome (CSF) are also related to the gut microbiota. In CSF patients there is an alteration in normal microbiota resulting in symptoms as depression, neurocognitive impairment, pain and sleep disturbance. While IBS is considered as a gut-brain disorder which is worsened by stress. Researchers are investigating whether these unhealthy microbiota resulting in IBS are also the cause of mood disorders. No bacteria can be inherited as bad, when our body is out of balance it takes advantage and proliferates. Some bacteria having a bad reputation are given below Microbial imbalance as a high level of Lactobacillus can also cause mood disturbance and sleep disturbances. Staphylococcus can cause food poisoning, it can be found in unpasteurized milk and can affect when hygiene is poor. Higher levels of the bad clostridium bacteria can cause fatigue by using bidirectional gut-brain axis. By eating junk food firmicutes and bifidobacteria level falls and there is a rise in the level of bacteroidetes causing the lethargic behavior to upshot and immunity problems set in.

Healthy Gut of a Baby

It is believed that when babies are born their guts are sterile, as soon as they encounter the genitourinary tract and mother’s skin, they are exposed to microbial flora. Microbial flora is important to develop in infants or babies for normal functioning. This healthy microbial flora to a baby is also provided by mother through breastfeeding. Milk is a cocktail of healthy microbiota and immunoglobulins causing development and growth of microbial flora in infant’s gut. So it is necessary for mothers to take healthy balanced diets rich in probiotic, prebiotic and fermented foods.

Due to the increased demand for fruits and vegetables, portals like Selly.pk offer a much feasible way of shopping. It takes a lot less effort to buy fruits and vegetables online.

Selly.pk is a welcome initiative if you ask me because the streets and roads are already piling up with fruit & vegetable vendors. More people should realize similar ideas. However, this can be depressing for those conventional vendors if the people start buying online sabzi in Lahore. The status quo always works against change but because this is a good change, we should all work together to make it a successful prospect.

Selly.pk Doing Business with Morals

Fruit market Lahore receives new rates of fruits & veggies daily. In order to comply with a standardized rate, Selly.pk is in touch with fruit officials who know this industry on fingertips. This only gives it an upper hand over the common vendors who are more interested in earning high profits rather than being civil and selling products at a decent price.

In the fruit & vegetable market, the Jin of inflation is still under control but as soon as those items reach private vendors in different localities, the price starts touching the skies. Fruit price in Pakistan should have checks & balances so the vendors can’t get greedy.

Your Online Partner

Selly.pk is one of a kind online fruit shop in Lahore. There are not many online fruit shops in Pakistan, therefore, this is a healthy and productive initiative. Where to order fresh vegetables online? How many of us haven’t thought about this question? It is time, a serious response came through and it has in the form of Selly.pk.

Price Comparable to the Average Market Price

It is a pioneering name regarding online fruit and vegetable shopping. Moreover, one would think the price would be higher because it is online. No, not at all. I do most of my shopping from Selly.pk and the online vegetable rates are lower than most vendors out there.

Every household has a need for a fresh supply of fruits and vegetables daily. Online vegetable shopping is much more time-saving because lives are getting busier every day. It is not easy to stop the car on your way back home from work and buy fruits or vegetables.

Fixed Reasonable Rates – Bargaining Not Required

There is no need to overexert yourself anymore with Selly.pk in town. Online vegetable shopping is simpler rather than spending your brains in bargaining with the vendor at the end of the street. Moreover, the call representatives taking your call are very well-behaved, often stating the list of items to make the selection process easier for you. As soon as you place an order for fresh vegetables online, the processing starts and they promise you to reach within 45 minutes. In my case, they have always been on time. They have met my expectations so far delivering high-quality fruits and vegetables to my doorstep.

Buying Fresh Fruits and Vegetables Online Through Selly.pk

Call at your Convenience

Some of us may have trouble ordering through the website due to the fact some of us aren’t technical enough. But you can always call on 0304-111-7355 to place your order.

How Can We Pay?

Cash on delivery is encouraged because we can’t pay by debit or credit cards on the website. Neither is there a card reader with the rider to swipe those cards. These two procedures are something that is lacking in the current order of things.

The riders delivering the goods speak to you in a polite tone without being aggressive or suddenly getting rude.

Return Policy

They have openly declared their return policy. We can instantly return stale fruits or vegetables at the time of delivery and no questions, whatsoever, will be asked.

Fruit and vegetable grocery list – it doesn’t matter how long the list is, Selly.pk is always up for the task delivering them on time. Fresh fruit for sale online, especially in winters is more like a blessing because it’s too cold to go out for shopping anyway. Buy vegetables online easily through Selly.pk because the website is superb. Just keep on tapping the items you want to buy and keep adding them to cart until you are ready to check out.

Elite Packaging

Fresh vegetables for sale at this website are packed in a luxurious way, unlike those cheap plastic bags we normally see at shops, with a symbol or monogram of Selly.pk attached to each packet.

The Gist of the Matter

Selly.pk provides fresh vegetables near you if you are in Lahore. However, one can consider it as a fresh vegetable market nearby with so many choices to choose from. You only need a working smartphone with an active Wi-Fi connection or mobile data connection. Type in Selly.pk in your browser and you are good to go. Fresh fruits and vegetables delivered to your doorstep in a matter of minutes. Shopping was never so convenient before!

TORSION
 
Torsion is a process in which the viscero-pallium rotates anti-clockwise through 180° from its initial position during larval development. So that the mantle cavity, with its pallial complex, is brought to the front of the body in the adult.
 
How Torsion Occurs
 
Torsion is not an evolutionary hypothesis. Its occurrence can be seen during embryogeny of living gastropods. Before torsion the larva is quite symmetrical, the mantle cavity is backward and downward, the alimentary canal is straight and anus opens posteriorly in the middle line. The shell and visceral mass originally saucer-shaped, which is first cone-shaped and then spirally coiled. When the shell lies dorsally and forms a coil anterior side then the shell is called exogastric.
 
The ventral flexure is followed by a lateral torsion, so that the dorsal or exogastric shell becomes a ventral or endogastric shell. The entire process takes 2 to 3 minutes as in Acmaea.
 
Torsion is actually effected due to the contraction of the larval retractor muscles, in which only the narrow neck of the larva is actually twisted. So the everything between the head and the anus undergoes an anti-clockwise rotation at the angle of 180°.
 
Thomson (1958) described five ways by which the torsion can be brought about.
 
  1. In Archaeogastropods, the Acmaea, the torsion takes place by muscles contraction alone.
  2. The rotation of 180° is completed in two stages, the first movement takes place by the contraction of larval retractor muscle and second rotation is slower by different growth. It is very common as in Patella, Haliotis etc.
  3. The rotation of 180° takes place by only differential growth processes like Vivapara.
  4. Rotation by differential growth processes, with anus coming to a position appropriate to the adult state like Aplysia.
  5. Torsion is no longer recognizable as a movement of viscera-pallium, the organs in the post-torsional position from their first appearance as in Adalaria.
 
Effects of Torsion
 
The effect of torsion first time indicated by Spengel in 1881. The effects are not equally examined in all the gastropods by the general effects are described as follows:
 
  1. Displacement of mantle cavity: The mantle cavity was primarily present on the posterior side. The elongation of the ventral foot which was primarily very small. After torsion, the mantle cavity opens just behind the head and its associated parts are shifted forwards.
  2. Changes in relative position: Before torsion, the anus, ctenidia and excretory opening were placed on the posterior side and the auricles were placed behind the ventricle but after torsion the anus, ctenidia and excretory opening become anterior and the auricles lie in front of the ventricle. The original posterior face of the visceral sac becomes the anterior face so that the visceral organs morphologically of the original right side change into the left side.
  3. Looping of alimentary canal: The alimentary canal which was originally straight from mouth to anus, after torsion, it changes into a loop.
  4. Chiastoneury: The long, uncoiled pleuro-visceral nerve connectives become a figure of "8" after twisting. The right connective with its ganglion passes over the intestine to form the supra-intestinal connective, while the next connective pass under the intestine to form the infra-intestinal connective.
  5. Endogastric coil: The coil of visceral sac and shell, which was primarily dorsal or exogastric become ventral and endogastric after torsion.
  6. Loss of Symmetry of Atrophy: The anus changes their original position towards the right side of the pallial cavity so that the original symmetrical condition disturbed.
 
DETORSION
 
The torsion is reversible in Eu-thy-neura and its reversal is known as detorsion by which animal become untwisted and symmetrical.
The “pearl” is literally formed by the mantle epithelium, which becomes deposit around any external body or particles, these external particle or body invade in between the shell and mantle in any way.

Pearl is secreted by the mantle as a means of protection against a small external particle. When an external particle or body, such as a grain of sand or a small parasite invades in between the mantle and the shell it becomes enclosed in a sac of mantle epithelium which produces irritation. The irritation stimulates the mantle epithelium to secrete thin concentric layers of mother of pearl around the foreign body. The amount of deposition is in direct proportion to the degree of irritation. After several years, a pearl will be formed, usually, it requires 3 to 4 years to produce a pearl of considerable size but a large pearl requires about 7 years. The foreign particles in the pearl are called nucleus whereas the thin nacre layers are concentric and called the mother of pearl.
 
Pearls are formed by various clams and oysters, but those produced by the marine pearl oysters, Meleagrina of Eastern Asia are the most valuable.
 
Formation of Pearl
 
 
Blackheads are the most common problem in the majority of people. This problem arises when the oily secretion of the sebaceous glands forms a blockage in your skin pores. When the oil is exposed to air, it oxidizes and turns into black and forms blackhead. So the question is that how you can remove blackheads from your skin.
 
Removing of blackheads from your skin is very simple and you can do this at home, all you need to do is remove the entire blockage from your skin pores.
 
In order to remove the blockage from your skin pores, you need the following material.
 
  1. Towel or soft cloth
  2. Blackhead removal strips or pads
  3. Salicylic acid (C7H6O3)
 
Step 1
 
Wash your skin with the slightly hot water, and gently compress your skin pores with the help of towel or soft cloth. The warmth will open the pores of your skin and make it easier to remove the blockage caused by secretion of the sebaceous glands and to get rid of blackheads. Follow this step upto 5 times.
 
Step 2
 
Apply a blackhead elimination strip or pad to your face while your skin pores are still moist from the compress done in step 1. The moisture to your pores and skin will help the blackhead removal strip cohere on your skin and blackheads. Allow 10 to 15 minutes for the blackhead removal strip to stick itself.
 
After 10 to 15 minutes, pull the strip off. It should remove the blockage and blackheads from your skin pores in a different level of success. But in some cases, it removes the entire blockage and blackheads; in other situations, only the head of the blockage is ripped from the pores of the skin.
 
Step 3
 
With the help of your fingertips, squeeze your skin gently to remove the blackheads from your skin. Note that fingernails should not be used for that purpose as it may harm your skin. If they do not pop out effortlessly, do not squeeze harder as it may harm your skin. Rather, try making use of warmth compress and squeezing another time straight away after removing the warm compress.
 
If the blackheads do not pop out by this method, they probably cannot be removed adequately with your fingers.
 
Step 4
 
Salicylic acid (C7H6O3) is a medication most commonly used for the skin treatment. It removes the outer layer of the skin and most commonly used for the treatment of calluses, dandruff, acne, ringworm, warts, psoriasis and ichthyosis.
 
Apply a thin layer of salicylic acid liquid or paste onto your skin and leave it for a minute. After the use of salicylic acid, do another hot compress and try to squeeze out the remaining extra blackheads.
 
MODE OF ACTION: When you apply the layer of salicylic acid liquid onto your skin, it breaks down the sebum oil and can get deep into your skin pores where your fingers cannot.
You can compare the deionized water vs distilled water, however, to mention that the distilled water is that the same as deionized water may be a mistake. The terms “distilled water” and “deionized water” are usually misunderstood. during this article, you'll notice the reason to grasp the variations and similarities of those 2 completely different water cleanup technologies.
 
DISTILLED WATER
 
The oldest technique for production of pure water is that the thermal technique or distillation – water evaporation from the surface and condensation. the premise of the method is that the transfer of water within the vapor section with its later condensation. the most downside of this technique is that the terribly high maintenance prices of the electricity required to convert the water into the steam. additionally, within the method of steam formation in conjunction with water molecules, alternative solutes will enter the steam in keeping with their volatility. Evaporation is achieved in varied ways: the vacuum on top of the water, heating, etc.
 
Let’s contemplate the distillation. What’s happening within the method of distillation? The water molecules have the boiling purpose of 100°C or 212° F. alternative substances have completely different boiling points. The substance that boils at a lower temperature evaporates initial. The boiling purpose of assorted impurities is higher, and, in theory, they're going to begin to evaporate, once the water has already cooked out. The substance that boils at a lower temperature evaporates initial. because of this distinction the water is separated.
 
As a result, in theory when the distillation the fully pure water is obtained. Actually, organic substances, that have the similar boiling purpose than that of water will supply the water. let's say if the water contains the oil drops they will be found additionally within the liquid. There area unit much no salts within the water, as a result of the salt boils at a far higher temperature. To eliminate the matter of organic substances, the water distillers have pre- and post water filters.
 
The absolute advantage of the water is that the complete absence of harmful substances.
 
REVERSE OSMOSIS (RO) WATER
 
The latest various to the thermal technique for getting of water may be a two-stage reverse diffusion. The technology relies on the double passage of raw water through a tissue layer beneath the pressure. As a result, water is split into 2 streams: the filtrate (purified water) and concentrate (a targeted resolution of impurities). The two-stage reverse diffusion system will considerably cut back operational prices and improve the standard of obtained water. The reverse diffusion water treatment technology is that the most typically employed in households and within the trade for preparation of drinkable.
 
DEIONIZED (DI) WATER
 
Deionized water is deeply demineralized, ultrapure water with the impedance on the point of eighteen megohm-cm. it's employed in electronics, computer circuit boards, instrument manufacture, pharmacy, laundry liquids, etc.
 
In order to get the top quality pure deionized water, a multi-stage water purification method is used. when pre-cleaning, the water is equipped with the reverse diffusion membrane, so the water is filtered through a special deionization medium, that removes the remainder of the ions from the water. The purity of deionized water will exceed the purity of water.
 
SIMILARITIES AND DIFFERENCES: DISTILLED WATER Vs RO WATER Vs  DEIONIZED WATER 
 
 DISTILLED WATER REVERSE OSMOSIS (RO) WATER DEIONIZED (DI) WATER
Distillation is employed in the main in laboratories and factories, wherever it's required. Reverse diffusion is widely employed in water treatment plants, each reception and for the manufacture of assorted drinks, drinking water, etc.
  • RO water is additional saturated with salts and atomic number 8 then the water and DI water.
  • Reverse osmosis and deionization are more cost-effective than the distillation.
DI water is as pure because the water or maybe purer

 

Distillation, RO and deionization processes are supposed to purify the water of the contaminants: mercury, lead, strontium, nitrates, phosphates, manganese, in addition, pesticides.
 
Diabetes is epidemic; there is barely any family left that does not have a member diagnosed with diabetes. In urban areas, almost one-tenth of people have diabetes, and at least one-third are at risk of developing it soon if they do not do something about it. That means if not diabetic, every family surely has someone with prediabetes.
 
Diabetes is primarily caused by faulty lifestyle, followed for years, wrong kind of diet, absolute lack of exercise, and chronic stress, and low interaction between family members are all contributors to it.
 
Diabetes differs from all the other diseases in a way that it is infectious by lifestyle instead of microbes. Meaning a particular kind of lifestyle seems to prevail within the family. Finding an only single obese person in a family is rare. Similarly, if one is not doing exercise in the family, probably none is doing it.
 
The family is intended to function as a single entity, but not in negative direction, thus by changing the course of lifestyle by motivating and helping each other, whole family can benefit.
 
However, it seems that families are not discussing much diabetes, exercise, stress, and emotional problems.
 
“They say they care, but they rarely help, participate or motivate, they do not seem to understand me” is the most common complaint of people about their family members and close friends. In fact, some research shows that often friends are helping and providing more emotional support than the family members.
 
Although we all expect greater emotional support from family members, lack of such support may have reasons like little time or other lifestyle issues.
 
Can family support indeed make a difference?
 
At least all the research, hundreds of them, seems to support the idea that family support can make a huge difference. As we already mentioned that particular kind of lifestyle is prevalent in the whole family.
 
Whether it is a preference for specific type of food items, going out, meeting friends, doing exercise, spending leisure time, everything needs to be changed in diabetes, and perhaps everyone in the family has to change a bit. Wouldn’t it be best to work as a team? Instead of individual efforts. Sharing experience, motivating, has indeed shown to make efforts more successful.
 
Research has shown that adherence to exercise and medications are much better when done with the family support. Married people usually have higher compliance rate, though that cannot always be said about the lifestyle changes. People with families may exercise less as compared to those living alone.
 
Isn’t a family all about emotional support, love, help? Principally it must be the case, though in reality things often differ.
 
Thus for better diabetes management, prevention, it is vital that the whole family participates, and the process does not have to be boring. Supporting each other should be converted into a game, a fun, something to be enjoyed, something that brings emotional happiness to all the participants.
 
Iron sharpens iron; humans are not made to be left alone. They always psychologically feel better when they are continually communicating, when they are loved and praised. Modern technology has made us busier than ever; we are spending more time in unnecessary communication at the cost of neglecting the necessary one.
 
Thus the solution to the problem created by the technology should also be sought in technological advancement itself.
 
Why not start using an app that is made explicitly for members of the family, instead of social apps that are more open, and less focused on interaction at the family level.
 
An app called CricleCare is explicitly made to fulfill that gap. It is a fun way to keep you close friends and family members motivated. It is different in a way that it has been created to improve the communication between the small and closed circles. It has all the tools to make that conversation more relaxed and fun. So you can exchange messages, send stickers. Most importantly, you can encourage the family members by giving batches. Thus you can provide batches to kids for being good at home, doing all the tasks. Give batches for keeping up with exercise, reminding to take medicine, and much more. It has many features of health app like counting steps, providing information about burnt calories. However, unlike the traditional health apps, it is also about the involvement of the whole family. It merges the benefits of health app and family support platform.
Total serum thyroxine includes both free and protein-bound thyroxine and is usually measured by competitive immunoassay. Normal level in adults is 5.0-12.0 μg/dl.
 
Test for total thyroxine or free thyroxine is usually combined with TSH measurement and together they give the best assessment of thyroid function.
 
Causes of Increased Total T4
 
  1. Hyperthyroidism: Elevation of both T4 and T3 values along with decrease of TSH are indicative of primary hyperthyroidism.
  2. Increased thyroxine-binding globulin: If concentration of TBG increases, free hormone level falls, release of TSH from pituitary is stimulated, and free hormone concentration is restored to normal. Reverse occurs if concentration of binding proteins falls. In either case, level of free hormones remains normal, while concentration of total hormone is altered. Therefore, estimation of only total T4 concentration can cause misinterpretation of results in situations that alter concentration of TBG.
  3. Factitious hyperthyroidism
  4. Pituitary TSH-secreting tumor.
 
Causes of Decreased Total T4
 
  1. Primary hypothyroidism: The combination of decreased T4 and elevated TSH are indicative of primary hypothyroidism.
  2. Secondary or pituitary hypothyroidism
  3. Tertiary or hypothalamic hypothyroidism
  4. Hypoproteinaemia, e.g. nephrotic syndrome
  5. Drugs: oestrogen, danazol
  6. Severe non-thyroidal illness.
 
Free Thyroxine (FT4)
 
FT4 comprises of only a small fraction of total T4, is unbound to proteins, and is the metabolically active form of the hormone. It constitutes about 0.05% of total T4. Normal range is 0.7 to 1.9 ng/dl. Free hormone concentrations (FT4 and FT3) correlate better with metabolic state than total hormone levels (since they are not affected by changes in TBG concentrations).
 
Measurement of FT4 is helpful in those situations in which total T4 level is likely to be altered due to alteration in TBG level (e.g. pregnancy, oral contraceptives, nephrotic syndrome).
 
Total and Free Triiodothyronine (T3)
 
Uses
 
  1. Diagnosis of T3 thyrotoxicosis: Hyperthyroidism with low TSH and elevated T3, and normal T4/FT4 is termed T3 thyrotoxicosis.
  2. Early diagnosis of hyperthyroidism: In early stage of hyperthyroidism, total T4 and free T4 levels are normal, but T3 is elevated.
 
A low T3 level is not useful for diagnosis of hypothyroidism since it is observed in about 25% of normal individuals.
 
For routine assessment of thyroid function, TSH and T4 are measured. T3 is not routinely estimated because normal plasma levels are very low.
 
Normal T3 level is 80-180 ng/dl.
 
Free T3: Measurement of free T3 gives true values in patients with altered serum protein levels (like pregnancy, intake of estrogens or oral contraceptives, and nephrotic syndrome). It represents 0.5% of total T3.
 
Thyrotropin Releasing Hormone (TRH) Stimulation Test
 
Uses
 
  1. Confirmation of diagnosis of secondary hypothyroidism
  2. Evaluation of suspected hypothalamic disease
  3. Suspected hyperthyroidism
 
This test is not much used nowadays due to the availability of sensitive TSH assays.
 
Procedure
 
  • A baseline blood sample is collected for estimation of basal serum TSH level.
  • TRH is injected intravenously (200 or 500 μg) followed by measurement of serum TSH at 20 and 60 minutes.
 
Interpretation
 
  1. Normal response: A rise of TSH > 2 mU/L at 20 minutes, and a small decline at 60 minutes.
  2. Exaggerated response: A further significant rise in already elevated TSH level at 20 minutes followed by a slight decrease at 60 minutes; occurs in primary hypothyroidism.
  3. Flat response: There is no response; occurs in secondary (pituitary) hypothyroidism.
  4. Delayed response: TSH is higher at 60 minutes as compared to its level at 20 minutes; seen in tertiary (hypothalamic) hypothyroidism.
 
Antithyroid Antibodies
 
Box 864.1 Thyroid autoantibodies
 
  • Useful for diagnosis and monitoring of autoimmune thyroid diseases.
  • Antimicrosomal or antithyroid peroxidase antibodies: Hashimoto’s thyroiditis
  • Anti-TSH receptor antibodies: Graves’ disease
Various autoantibodies (TSH receptor, antimicrosomal, and antithyroglobulin) are detected in thyroid disorders like Hashimoto’s thyroiditis and Graves’ disease. Antimicrosomal (also called as thyroid peroxidase) and anti-thyroglobulin antibodies are observed in almost all patients with Hashimoto’s disease. TSH receptor antibodies (TRAb) are mainly tested in Graves’ disease to predict the outcome after treatment (Box 864.1).
 
Radioactive Iodine Uptake (RAIU) Test
 
This is a direct test that assesses the trapping of iodide by thyroid gland (through the iodine symporters or pumps in follicular cells) for thyroid hormone synthesis. Patient is administered a tracer dose of radioactive iodine (131I or 123I) orally. This is followed by measurement of amount of radioactivity over the thyroid gland at 2 to 6 hours and again at 24 hours. RAIU correlates directly with the functional activity of the thyroid gland. Normal RAIU is about 10-30% of administered dose at 24 hours, but varies according to the geographic location due to differences in dietary intake.
 
Causes of Increased Uptake
 
  • Hyperthyroidism due to Graves’ disease, toxic multinodular goiter, toxic adenoma, TSH-secreting tumor.
 
Causes of Decreased Uptake
 
  • Hyperthyroidism due to administration of thyroid hormone, factitious hyperthyroidism, subacute thyroiditis.
 
Uses
 
RAIU is most helpful in differential diagnosis of hyperthyroidism by separating causes into those due to increased uptake and due to decreased uptake.
 
Thyroid Scintiscanning
 
An isotope (99mTc-pertechnetate) is administered and a gamma counter assesses its distribution within the thyroid gland.
 
Interpretation
 
  • Differential diagnosis of high RAIU thyrotoxicosis:
    – Graves’ disease: Uniform or diffuse increase in uptake
    – Toxic multinodular goiter: Multiple discrete areas of increased uptake
    – Adenoma: Single area of increased uptake
  • Evaluation of a solitary thyroid nodule:
    – ‘Hot’ nodule: Hyperfunctioning
    – ‘Cold’ nodule: Non-functioning; about 20% cases are malignant.
 
Interpretation of thyroid function tests is shown in Table 164.1.
 
Table 864.1 Interpretation of thyroid function tests
Test results Interpretations
1. TSH Normal, FT4 Normal Euthyroid
2. Low TSH, Low FT4 Secondary hypothyroidism
3. High TSH, Normal FT4 Subclinical hypothyroidism
4. High TSH, Low FT4 Primary hypothyroidism
5. Low TSH, Normal FT4, Normal FT3 Subclinical hyperthyroidism
6. Low TSH, Normal FT4, High FT3 T3 toxicosis
7. Low TSH, High FT4 Primary hyperthyroidism
 
Neonatal Screening for Hypothyroidism
 
Thyroid hormone deficiency during neonatal period can cause severe mental retardation (cretinism) that can be prevented by early detection and treatment. Estimation of TSH is done on dry blood spots on filter paper or cord serum between 3rd to 5th days of life. Elevated TSH is diagnostic of hypothyroidism. In infants with confirmed hypothyroidism, RAIU (123I) scan should be done to distinguish between thyroid agenesis and dyshormonogenesis.
Box 863.1 Terminology in thyroid disorders
  • Primary hyper-/hypothyroidism: Increased or decreased function of thyroid gland due to disease of thyroid itself and not due to increased or decreased levels of TRH or TSH.
  • Secondary hyper-/hypothyroidism: Increased or decreased function of thyroid gland due to increased or decreased levels of TSH.
  • Tertiary hypothyroidism: Decreased function of thyroid gland due to decreased function of hypothalamus.
  • Subclinical thyroid disease: A condition with abnormality of thyroid hormone levels in blood but without specific clinical manifestations of thyroid disease and without any history of thyroid dysfunction or therapy.
  • Subclinical hyperthyroidism: A condition with normal thyroid hormone levels but with low or undetectable TSH level.
  • Subclinical hypothyroidism: A condition with normal thyroxine and triiodothyronine level along with mildly elevated TSH level.
Among the endocrine disorders, disorders of thyroid are common and are only next in frequency to diabetes mellitus. They are more common in women than in men. Functional thyroid disorders can be divided into two types depending on activity of the thyroid gland: hypothyroidism (low thyroid hormones), and hyperthyroidism (excess thyroid hormones). Any enlargement of thyroid gland is called as a goiter. Terminology related to thyroid disorders is shown in Box 863.1.
 
Hyperthyroidism
 
Hyperthyroidism is a condition caused by excessive secretion of thyroid hormone. Causes of hyperthyroidism are listed in Table 863.1.
 
Table 863.1 Causes of hyperthyroidism
  1. Graves’ disease (Diffuse toxic goiter)
  2. Toxicity in multinodular goiter
  3. Toxicity in adenoma
  4. Subacute thyroiditis
  5. TSH-secreting pituitary adenoma (secondary hyperthyroidism)
  6. Trophoblastic tumours that secrete TSH-like hormone: choriocarcinoma, hydatidiform mole
  7. Factitious hyperthyroidism
 
Clinical Characteristics
 
Clinical characteristics of hyperthyroidism are nervousness, anxiety, irritability, insomnia, fine tremors; weight loss despite normal or increased appetite; heat intolerance; increased sweating; dyspnea on exertion; amenorrhea and infertility; palpitations, tachycardia, cardiac arrhythmias, heart failure (especially in elderly); and muscle weakness, proximal myopathy, and osteoporosis (especially in elderly).
 
The triad of Graves’ disease consists of hyperthyroidism, ophthalmopathy (exophthalmos, lid retraction, lid lag, corneal ulceration, impaired eye muscle function), and dermopathy (pretibial myxoedema).
 
Box 863.2 Thyroid function tests in hyperthyroidism
  • Thyrotoxicosis:
    Serum TSH low or undetectable
    – Raised total T4 and free T4.
  • T3 toxicosis:
    – Serum TSH undetectable
    – Normal total T4 and free T4
    – Raised T3
Laboratory Features
 
In most patients, free serum T3 and T4 are elevated. In T3 thyrotoxicosis (5% cases of thyrotoxicosis), serum T4 levels are normal while T3 is elevated. Serum TSH is low or undetectable (< 0.1 mU/L) (Box 863.2).
 
Undetectable or low serum TSH along with normal levels of T3 and T4 is called as subclinical hyperthyroidism; subtle signs and symptoms of thyrotoxicosis may or may not be present. Subclinical hyperthyroidism is associated with risk of atrial fibrillation, osteoporosis, and progression to overt thyroid disease.
 
Features of primary and secondary hyperthyroidism are compared in Table 863.2.
 
Table 863.2 Differences between primary and secondary hyperthyroidism
Parameter Primary hyperthyroidism Secondary hyperthyroidism
1. Serum TSH Low Normal or high
2. Serum free thyroxine High High
3. TSH receptor antibodies May be positive Negative
4. Causes Graves’ disease, toxic multinodular goiter, toxic adenoma Pituitary adenoma
 
Evaluation of hyperthyroidism is presented in Figure 863.1.
 
Figure 863.1 Evaluation of hyperthyroidism
Figure 863.1 Evaluation of hyperthyroidism. TSH: thyroid stimulating hormone; FT4: free T4; FT3: free T3; TRAb: TSH receptor antibody; TRH: Thyrotropin releasing hormone
 
Hypothyroidism
 
Hypothyroidism is a condition caused by deficiency of thyroid hormones. Causes of hypothyroidism are listed in Table 863.3. Primary hypothyroidism results from deficient thyroid hormone biosynthesis that is not due to disorders of hypothalamus or pituitary. Secondary hypothyroidism results from deficient secretion of TSH from pituitary. Deficient or loss of secretion of thyro-tropin releasing hormone from hypothalamus results in tertiary hypothyroidism. Secondary and tertiary hypothyroidism are much less common than primary. Plasma TSH is high in primary and low in secondary and tertiary hypothyroidism. Differences between primary and secondary hypothyroidism are shown in Table 863.4.
 
Table 863.3 Causes of hypothyroidism 
  1. Primary hypothyroidism (Increased TSH)
    • Iodine deficiency
    • Hashimoto’s thyroiditis
    Exogenous goitrogens
    • Iatrogenic: surgery, drugs, radiation
  2. Secondary hypothyroidism (Low TSH): Diseases of pituitary
  3. Tertiary hypothyroidism (Low TSH, Low TRH): Diseases of hypothalamus
 
Table 863.4 Differences between primary and secondary hypothyroidism
Parameter Primary hypothyroidism Secondary hypothyroidism
1. Cause Hashimoto’s thyroiditis Pituitary disease
2. Serum TSH High Low
3. Thyrotropin releasing hormone stimulation test Exaggerated response No response
4. Antimicrosomal antibodies Present Absent
 
Box 863.3 Thyroid function tests in hypothyroidism
  • Primary hypothyroidism
    – Serum TSH: Increased (proportional to degree of hypofunction)
    – Free T4: Decreased
    – TRH stimulation test: Exaggerated response
  • Secondary hypothyroidism
    – Serum TSH: Decreased
    – Free T4: Decreased
    – TRH stimulation test: Absent response
  • Tertiary hypothyroidism
    – Serum TSH: Decreased
    – FT4: Decreased
    – TRH stimulation test: Delayed response
Clinical features of primary hypothyroidism are: lethargy, mild depression, disturbances in menstruation, weight gain, cold intolerance, dry skin, myopathy, constipation, and firm and lobulated thyroid gland (in Hashimoto’s thyroiditis).
 
In severe cases, myxoedema coma (an advanced stage with stupor, hypoventilation, and hypothermia) can occur.
 
Laboratory Features
 
Laboratory features in hypothyroidism are shown in Box 863.3.
 
Normal serum thyroxine (T4 and FT4) coupled with a moderately raised TSH (>10 mU/L) is referred to as subclinical hypothyroidism. It is associated with bad obstetrical outcome, poor cognitive development in children, and high risk of hypercholesterolemia and progression to overt hypothyroidism.
 
Evaluation of hypothyroidism is presented in Figure 863.2
 
Figure 863.2 Evaluation of hypothyroidism
Figure 863.2 Evaluation of hypothyroidism. TSH: thyroid stimulating hormone; FT4: free T4; TRH: Thyrotropin releasing hormone
The ovaries are the sites of production of female gametes or ova by the process of oogenesis. The ova are released by the process of ovulation in a cyclical manner at regular intervals. Ovary contains numerous follicles that contain ova in various stages of development. During each menstrual cycle, up to 20 primordial follicles are activated for maturation; however, only one follicle becomes fully mature; this dominant follicle ruptures to release the secondary oocyte from the ovary. Maturation of the follicle is stimulated by follicle stimulating hormone (FSH) secreted by anterior pituitary (Figure 862.1). Maturing follicle secretes estrogen that causes proliferation of endometrium of the uterus (proliferative phase). Follicular cells also secrete inhibin which regulates release of FSH by the anterior pituitary. Fall in FSH level is followed by secretion of luteinizing hormone (LH) by the anterior pituitary (LH surge). This causes follicle to rupture and the ovum is expelled into the peritoneal cavity near the fimbrial end of the fallopian tube. The fallopian tubes conduct ova from the ovaries to the uterus. Fertilization of ovum by the sperm occurs in the fallopian tube.
 
Figure 862.1 The hypothalamus pituitary ovarian axis
Figure 862.1 The hypothalamus-pituitary-ovarian axis 
 
The ovum consists of the secondary oocyte, zona pellucida and corona radiata. The ruptured follicle in the ovary collapses and fills with blood clot (corpus luteum). LH converts granulose cells in the follicle to lutein cells which begin to secrete progesterone. Progesterone stimulates secretion from the endometrial glands (secretory phase) that were earlier under the influence of estrogen. Rising progesterone levels inhibit LH production from the anterior pituitary. Without LH, the corpus luteum regresses and becomes functionless corpus albicans. After regression of corpus luteum, production of estrogen and progesterone stops and endometrium collapses, causing onset of menstruation. If the ovum is fertilized and implanted in the uterine wall, human chorionic gonadotropin (hCG) is secreted by the developing placenta into the maternal circulation. Human chorionic gonadotropin maintains the corpus luteum for secetion of estrogen and progesterone till 12th week of pregnancy. After 12th week, corpus luteum regresses to corpus albicans and the function of synthesis of estrogen and progesterone is taken over by placenta till parturition.
 
The average duration of the normal menstrual cycle is 28 days. Ovulation occurs around 14th day of the cycle. The time interval between ovulation and menstruation is called as luteal phase and is fairly constant (14 days) (Figure 862.2).
 
Figure 862.2 Normal menstrual cycle
Figure 862.2 Normal menstrual cycle
 
Causes of Female Infertility
 
Causes of female infertility are shown in Table 862.1.
 
Table 862.1 Causes of female infertility
1. Hypothalamic-pituitary dysfunction:
  • Hypothalamic causes
    – Excessive exercise
    – Excess stress
    – Low weight
    – Kallman’s syndrome
    Idiopathic
  • Pituitary causes
    – Hyperprolactinemia
    Hypopituitarism (Sheehan’s syndrome, Simmond’s disease)
    – Craniopharyngioma
    – Cerebral irradiation
 2. Ovarian dysfunction:
  • Polycystic ovarian disease (Stein-Leventhal syndrome)
  • Luteinized unruptured follicle
  • Turner’s syndrome
  • Radiation or chemotherapy
  • Surgical removal of ovaries
  • Idiopathic
 3. Dysfunction in passages:
  • Fallopian tubes
    Infections: Tuberculosis, gonorrhea, Chlamydia
    – Previous surgery (e.g. laparotomy)
    – Tubectomy
    Congenital hypoplasia, non-canalization
    Endometriosis
  • Uterus
    – Uterine malformations
    – Asherman’s syndrome
    – Tuberculous endometritis
    Fibroid
  • Cervix: Sperm antibodies
  • Vagina: Septum
 4. Dysfunction of sexual act: Dyspareunia
 
Investigations
 
Evaluation of female infertility is shown in Figure 862.3.
 
Figure 862.3 Evaluation of female infertility
Figure 862.3 Evaluation of female infertility. FSH: Follicle stimulating hormone; LH: Luteinizing hormone; DHEA-S: Dihydroepiandrosterone; TSH: Thyroid stimulating hormone; ↑ : Increased; ↓ : Decreased
 
Tests for Ovulation
 
Most common cause of female infertility is anovulation.
 
  1. Regular cycles, mastalgia, and laparoscopic direct visualization of corpus luteum indicate ovulatory cycles. Anovulatory cycles are clinically characterized by amenorrhea, oligomenorrhea, or irregular menstruation. However, apparently regular cycles may be associated with anovulation.
  2. Endometrial biopsy: Endometrial biopsy is done during premenstrual period (21st-23rd day of the cycle). The secretory endometrium during the later half of the cycle is an evidence of ovulation.
  3. Ultrasonography (USG): Serial ultrasonography is done from 10th day of the cycle and the size of the dominant follicle is measured. Size >18 mm is indicative of imminent ovulation. Collapse of the follicle with presence of few ml of fluid in the pouch of Douglas is suggestive of ovulation. USG also is helpful for treatment (i.e. timing of coitus or of intrauterine insemination) and diagnosis of luteinized unruptured follicle (absence of collapse of dominant follicle). Transvaginal USG is more sensitive than abdominal USG.
  4. Basal body temperature (BBT): Patient takes her oral temperature at the same time every morning before arising. BBT falls by about 0.5°F at the time of ovulation. During the second (progestational) half of the cycle, temperature is slightly raised above the preovulatory level (rise of 0.5° to 1°F). This is due to the slight pyrogenic action of progesterone and is therefore presumptive evidence of functional corpus luteum.
  5. Cervical mucus study:
    Fern test: During estrogenic phase, a characteristic pattern of fern formation is seen when cervical mucus is spread on a glass slide (Figure 862.4). This ferning disappears after the 21st day of the cycle. If previously observed, its disappearance is presumptive evidence of corpus luteum activity.
    Spinnbarkeit test: Cervical mucus is elastic and withstands stretching upto a distance of over 10 cm. This phenomenon is called Spinnbarkeit or the thread test for the estrogen activity. During the secretory phase, viscosity of the cervical mucus increases and it gets fractured when stretched. This change in cervical mucus is evidence of ovulation.
  6. Vaginal cytology: Karyopyknotic index (KI) is high during estrogenic phase, while it becomes low in secretory phase. This refers to percentage of super-ficial squamous cells with pyknotic nuclei to all mature squamous cells in a lateral vaginal wall smear. Usually minimum of 300 cells are evaluated. The peak KI usually corresponds with time of ovulation and may reach upto 50 to 85.
  7. Estimation of progesterone in mid-luteal phase (day 21 or 7 days before expected menstruation): Progesterone level > 10 nmol/L is a reliable evidence of ovulation if cycles are regular (Figure 862.5). A mistimed sample is a common cause of abnormal result.
 
Figure 862.4 Ferning of cervical mucosa
Figure 862.4 Ferning of cervical mucosa
 
Figure 862.5 Serum progesterone during normal menstrual cycle
Figure 862.5 Serum progesterone during normal menstrual cycle
 
Tests to Determine the Cause of Anovulation
 
  1. Measurement of LH, FSH, and estradiol during days 2 to 6: All values are low in hypogonadotropic hypogonadism (hypothalamic or pituitary failure).
  2. Measurement of TSH, prolactin, and testosterone if cycles are irregular or absent:
    Increased TSH: Hypothyroidism
    Increased prolactin: Pituitary adenoma
    Increased testosterone: Polycystic ovarian disease (PCOD), congenital adrenal hyperplasia (To differentiate PCOD from congenital adrenal hyperplasia, ultrasound and estimation of dihydroepiandrosterone or DHEA are done).
  3. Transvaginal ultrasonography: This is done for detection of PCOD.
 
Investigations to Assess Tubal and Uterine Status
 
  1. Infectious disease: These tests include endometrial biopsy for tuberculosis and test for chlamydial IgG antibodies for tubal factor in infertility.
  2. Hysterosalpingography (HSG): HSG is a radiological contrast study for investigation of the shape of the uterine cavity and for blockage of fallopian tubes (Figure 862.6). A catheter is introduced into the cervical canal and a radiocontrast dye is injected into the uterine cavity. A real time X-ray imaging is carried out to observe the flow of the dye into the uterine cavity, tubes, and spillage into the uterine cavity.
  3. Hysterosalpingo-contrast sonography: A catheter is introduced into the cervical canal and an echocontrast fluid is introduced into the uterine cavity. Shape of the uterine cavity, filling of fallopian tubes, and spillage of contrast fluid are noted. In addition, ultrasound scan of the pelvis provides information about any fibroids or polycystic ovarian disease.
  4. Laparoscopy and dye hydrotubation test with hysteroscopy: In this test, a cannula is inserted into the cervix and methylene blue dye is introduced into the uterine cavity. If tubes are patent, spillage of the dye is observed from the ends of both tubes. This technique also allows visualization of pelvic organs, endometriosis, and pelvic adhesions. If required, endometriosis and tubal blockage can be treated during the procedure.
 
Possible pregnancy and active pelvic or vaginal infection are contraindications to tubal patency tests.
 
Figure 862.6 Hysterosalpingography
Figure 862.6 Hysterosalpingography
The male reproductive system consists of testes (paired organs located in the scrotal sac that produce spermatozoa and secrete testosterone), a paired system of ducts comprising of epididymis, vasa deferentia, and ejaculatory ducts (collect, store, and conduct spermatozoa), paired seminal vesicles and a single prostate gland (produce nutritive and lubricating seminal fluid), bulbourethral glands of Cowper (secrete lubricating mucus), and penis (organ of copulation).
 
The hypothalamus secretes gonadotropin releasing hormone (GnRH) that regulates the secretion of the two gonadotropins from the anterior pituitary: luteinizing hormone (LH) and follicle stimulating hormone (FSH) (Figure 861.1). Luteinizing hormone primarily stimulates the production and secretion of testosterone from Leydig cells located in the interstitial tissue of the testes. Testosterone stimulates spermatogenesis, and plays a role in the development of secondary sexual characters. Testosterone needs to be converted to an important steroidal metabolite, dihydrotestosterone within cells to perform most of its androgenic functions. Testosterone inhibits LH secretion by negative feedback. Follicle stimulating hormone acts on Sertoli cells of seminiferous tubules to regulate the normal maturation of the sperms. Sertoli cells produce inhibin that controls FSH secretion by negative feedback.
 
Figure 861.1 Hypothalamus-pituitary-testis axis. + indicates stimulation; – indicates negative feedback
Figure 861.1 Hypothalamus-pituitary-testis axis. + indicates stimulation; – indicates negative feedback
 
During sexual intercourse, semen is deposited into the vagina. Liquefaction of semen occurs within 20-30 minutes due to proteolytic enzymes of prostatic fluid. For fertilization to occur in vivo, the sperm must undergo capacitation and acrosome reaction. Capacitation refers to physiologic changes in sperms that occur during their passage through the cervix of the female genital tract. With capacitation, the sperm acquires (i) ability to undergo acrosome reaction, (ii) ability to bind to zona pellucida, and (iii) hypermotility. Sperm then travels through the cervix and uterus up to the fallopian tube. Binding of sperm to zona pellucida induces acrosomal reaction (breakdown of outer plasma membrane by enzymes of acrosome and its fusion with outer acrosomal membrane, i.e. loss of acrosome). This is necessary for fusion of sperm and oocyte membranes. Acrosomal reaction and binding of sperm and ovum surface proteins is followed by penetration of zona pellucida of ovum by the sperm. Following penetration by sperm, hardening of zona pellucida occurs that inhibits penetration by additional sperms. A sperm penetrates and fertilizes the egg in the ampullary portion of the fallopian tube (Figure 861.2).
 
Figure 861.2 Steps before and after fertilization of ovum
Figure 861.2 Steps before and after fertilization of ovum
 
Causes of Male Infertility
 
Causes of male infertility are listed in Table 861.1.
 
Table 861.1 Causes of male infertility 
2. Hypothalamic-pituitary dysfunction (hypogonadotropic hypogonadism)
3. Testicular dysfunction:
  • Radiation, cytotoxic drugs, antihypertensives, antidepressants
  • General factors like stress, emotional factors, drugs like marijuana, anabolic steroids, and cocaine, alcoholism, heavy smoking, undernutrition
  • Mumps orchitis after puberty
  • Varicocele (dilatation of pampiniform plexus of scrotal veins)
  • Undescended testes (cryptorchidism)
  • Endocrine disorders like diabetes mellitus, thyroid dysfunction
  • Genetic disorders: Klinefelter’s syndrome, microdeletions in Y chromosome, autosomal Robertsonian translocation, immotile cilia syndrome (Kartagener’s syndrome), cystic fibrosis, androgen receptor gene defect
4. Dysfunction of passages and accessory sex glands:
 5. Dysfunction of sexual act:
  • Defects in ejaculation: retrograde (semen is pumped backwards in to the bladder), premature, or absent
  • Hypospadias
 
Investigations of Male Infertility
 
  1. History: This includes type of lifestyle (heavy smoking, alcoholism), sexual practice, erectile dysfunction, ejaculation, sexually transmitted diseases, surgery in genital area, drugs, and any systemic illness.
  2. Physical examination: Examination of reproductive system should includes testicular size, undescended testes, hypospadias, scrotal abnormalities (like varicocele), body hair, and facial hair. Varicocele can occur bilaterally and is the most common surgically removable abnormality causing male infertility.
  3. Semen analysis: See article Semen Analysis. Evaluation of azoospermia is shown in Figure 861.3. Evaluation of low semen volume is shown in Figure 861.4.
  4. Chromosomal analysis: This can reveal Klinefelter’s syndrome (e.g. XXY karyotype) (Figure 861.5), deletion in Y chromosome, and autosomal Robertsonian translocation. It is necessary to screen for cystic fibrosis carrier state if bilateral congenital absence of vas deferens is present.
  5. Hormonal studies: This includes measurement of FSH, LH, and testosterone to detect hormonal abnormalities causing testicular failure (Table 861.2).
  6. Testicular biopsy: Testicular biopsy is indicated when differentiation between obstructive and non-obstructive azoospermia is not evident (i.e. normal FSH and normal testicular volume).
 
Table 861.2 Interpretation of hormonal studies in male infertility 
Follicle stimulating hormone Luteinizing hormone Testosterone Interpretation
Low Low Low Hypogonadotropic hypogonadism (Hypothalamic or pituitary disorder)
High High Low Hypergonadotropic hypogonadism (Testicular disorder)
Normal Normal Normal Obstruction of passages, dysfunction of accessory glands
 
Figure 861.3 Evaluation of azoospermia
Figure 861.3 Evaluation of azoospermia. FSH: Follicle stimulating hormone; LH: Luteinizing hormone
 
Figure 861.4 Evaluation of low semen volume
Figure 861.4 Evaluation of low semen volume
 
Figure 861.5 Karyotype in Klinefelter's Syndrome
 Figure 861.5 Karyotype in Klinefelter’s syndrome (47, XXY)
 
Common initial investigations for diagnosis of cause of infertility are listed below.
 
Anatomically, stomach is divided into four parts: cardia, fundus, body, and pyloric part. Cardia is the upper part surrounding the entrance of the esophagus and is lined by the mucus-secreting epithelium. The epithelium of the fundus and the body of the stomach is composed of different cell types including: (i) mucus-secreting cells which protect gastric mucosa from self-digestion by forming an overlying thick layer of mucus, (ii) parietal cells which secrete hydrochloric acid and intrinsic factor, and (iii) peptic cells or chief cells which secrete the proteolytic enzyme pepsinogen. Pyloric part is divided into pyloric antrum and pyloric canal. It is lined by mucus-secreting cells and gastrin-secreting neuroendocrine cells (G cells) (Figure 859.1).
 
Figure 859.1 Parts of stomach and their lining cells
Figure 859.1 Parts of stomach and their lining cells 
 
In the stomach, ingested food is mechanically and chemically broken down to form semi-digested liquid called chyme. Following relaxation of pyloric sphincter, chyme passes into the duodenum.
 
There are three phases of gastric acid secretion: cephalic, gastric, and intestinal.
 
  • Cephalic or neurogenic phase: This phase is initiated by the sight, smell, taste, or thought of food that causes stimulation of vagal nuclei in the brain. Vagus nerve directly stimulates parietal cells to secrete acid; in addition, it also stimulates antral G cells to secrete gastrin in blood (which is also a potent stimulus for gastric acid secretion) (Figure 859.2). Cephalic phase is abolished by vagotomy.
  • Gastric phase: Entry of swallowed food into the stomach causes gastric distension and induces gastric phase. Distension of antrum and increase in pH due to neutralization of acid by food stimulate antral G cells to secrete gastrin into the circulation. Gastrin, in turn, causes release of hydrochloric acid from parietal cells.
  • Intestinal phase: Entry of digested proteins into the duodenum causes an increase in acid output from the stomach. It is thought that certain hormones and absorbed amino acids stimulate parietal cells to secrete acid.
 
The secretion from the stomach is called as gastric juice. The chief constituents of the gastric juice are:
 
  • Hydrochloric acid (HCl): This is secreted by the parietal cells of the fundus and the body of the stomach. HCl provides the high acidic pH necessary for activation of pepsinogen to pepsin. Gastric acid secretion is stimulated by histamine, acetylcholine, and gastrin (Figure 859.2). HCl kills most microorganisms entering the stomach and also denatures proteins (breaks hydrogen bonds making polypeptide chains to unfold). Its secretion is inhibited by somatostatin (secreted by D cells in pancreas and by mucosa of intestine), gastric inhibitory peptide (secreted by K cells in duodenum and jejunum), prostaglandin, and secretin (secreted by S cells in duodenum).
  • Pepsin: Pepsin is secreted by chief cells in stomach. Pepsin causes partial digestion of proteins leading to the formation of large polypeptide molecules (optimal function at pH 1.0 to 3.0). Its secretion is enhanced by vagal stimulation.
  • Mucus
  • Intrinsic factor (IF): IF is necessary for absorption of vitamin B12 in the terminal ileum. It is secreted by parietal cells of stomach.
 
Figure 859.2 Stimulation of gastric acid secretion
Figure 859.2 Stimulation of gastric acid secretion. Three receptors on parietal cells stimulate acid secretion: histamine (H2) receptor, acetylcholine or cholinergic receptor, and gastrin/CCK-B receptor. Histamine is released by enterochromaffin-like cells in lamina propria. Acetylcholine is released from nerve endings. Gastrin is released from G cells in antrum (in response to amino acids in food, antral distention, and gastrin-releasing peptide). After binding to receptors, H+ is secreted in exchange for K+ by proton pump
  • Gastric intubation for gastric analysis is contraindicated in esophageal stricture or varices, active nasopharyngeal disease, diverticula, malignancy, recent history of severe gastric hemorrhage, hypertension, aortic aneurysm, cardiac arrhythmias, congestive cardiac failure, or non-cooperative patient.
  • Pyloric stenosis: Obstruction of gastric outlet can elevate gastric acid output due to raised gastrin (following antral distension).
  • Pentagastrin stimulation is contraindicated in cases with allergy to pentagastrin, and recent severe gastric hemorrhge due to peptic ulcer disease.
 
Gastric analysis is not a commonly performed procedure because of following reasons:
 
  • It is an invasive and cumbersome technique that is traumatic and unpleasant for the patient.
  • Information obtained is not diagnostic in itself.
  • Availability of better tests for diagnosis such as endoscopy and radiology (for suspected peptic ulcer or malignancy); serum gastrin estimation (for ZE syndrome); vitamin assays, Schilling test, and antiparietal cell antibodies (for pernicious anemia); and tests for Helicobacter pylori infection (in duodenal or gastric ulcer).
  • Availability of better medical line of treatment that obviates need for surgery in many patients.
  1. Hollander’s test (Insulin hypoglycemia test): In the past, this test was used for confirmation of completeness of vagotomy (done for duodenal ulcer).

    Hypoglycemia is a potent stimulus for gastric acid secretion and is mediated by vagus nerve. This response is abolished by vagotomy.

    In this test, after determining BAO, insulin is administered intravenously (0.15-0.2 units/kg) and acid output is estimated every 15 minutes for 2 hours (8 post-stimulation samples). Vagotomy is considered as complete if, after insulin-induced hypoglycemia (blood glucose < 45 mg/dl), no acid output is observed within 45 minutres.

    The test gives reliable results only if blood glucose level falls below 50 mg/dl at some time following insulin injection. It is best carried out after 3-6 months of vagotomy.

    The test is no longer recommended because of the risk associated with hypoglycemia. Myocardial infarction, shock, and death have also been reported.

  2. Fractional test meal: In the past, test meals (e.g. oat meal gruel, alcohol) were administered orally to stimulate gastric secretion and determine MAO or PAO. Currently, parenteral pentagastrin is the gastric stimulant of choice.

  3. Tubeless gastric analysis: This is an indirect and rapid method for determining output of free hydrochloric acid in gastric juice. In this test, a cationexchange resin tagged to a dye (azure A) is orally administered. In the stomach, the dye is displaced from the resin by the free hydrogen ions of the hydrochloric acid. The displaced azure A is absorbed in the small intestine, enters the bloodstream, and is excreted in urine. Urinary concentration of the dye is measured photometrically or by visual comparison with known color standards. The quantity of the dye excreted is proportional to the gastric acid output. However, if kidney or liver function is impaired, false results may be obtained. The test is no longer in use.

  4. Spot check of gastric pH: According to some investigators, spot determination of pH of fasting gastric juice (obtained by nasogastric intubation) can detect the presence of hypochlorhydria (if pH>5.0 in men or >7.0 in women).

  5. Congo red test during esophagogastroduodenoscopy: This test is done to determine the completeness of vagotomy. Congo red dye is sprayed into the stomach during esophagogastroduodenoscopy; if it turns red, it indicates presence of functional parietal cells in stomach with capacity of producing acid.
 
REFERENCE RANGES
 
  • Volume of gastric juice: 20-100 ml
  • Appearance: Clear
  • pH: 1.5 to 3.5
  • Basal acid output: Up to 5 mEq/hour
  • Peak acid output: 1 to 20 mEq/hour
  • Ratio of basal acid output to peak acid output: <0.20 or < 20%
In gastric analysis, amount of acid secreted by the stomach is determined on aspirated gastric juice sample. Gastric acid output is estimated before and after stimulation of parietal cells (i.e. basal and peak acid output). This test was introduced in the past mainly for the evaluation of peptic ulcer disease (to assess the need for operative intervention). However, diminishing frequency of peptic ulcer disease and availability of safe and effective medical treatment have markedly reduced the role of surgery.
 
  1. To determine the cause of recurrent peptic ulcer disease:
    To detect Zollinger-Ellison (ZE) syndrome: ZE syndrome is a rare disorder in which multiple mucosal ulcers develop in the stomach, duodenum, and upper jejunum due to gross hypersecretion of acid in the stomach. The cause of excess secretion of acid is a gastrin-producing tumor of pancreas. Gastric analysis is done to detect markedly increased basal and pentagastrinstimulated gastric acid output for diagnosis of ZE syndrome (and also to determine response to acidsuppressant therapy). However, a more sensitive and specific test for diagnosis of ZE syndrome is measurement of serum gastrin (fasting and secretin-stimulated).
    To decide about completeness of vagotomy following surgery for peptic ulcer disease: See Hollander’s test.
  2. To determine the cause of raised fasting serum gastrin level: Hypergastrinemia can occur in achlorhydria, Zollinger-Ellison syndrome, and antral G cell hyperplasia.
  3. To support the diagnosis of pernicious anemia (PA): Pernicious anemia is caused by defective absorption of vitamin B12 due to failure of synthesis of intrinsic factor secondary to gastric mucosal atrophy. There is also absence of hydrochloric acid in the gastric juice (achlorhydria). Gastric analysis is done for demonstration of achlorhydria if facilities for vitamin assays and Schilling’s test are not available (Achlorhydria by itself is insufficient for diagnosis of PA).
  4. To distinguish between benign and malignant ulcer: Hypersecretion of acid is a feature of duodenal peptic ulcer, while failure of acid secretion (achlorhydria) occurs in gastric carcinoma. However, anacidity occurs only in a small proportion of cases with advanced gastric cancer. Also, not all patients with duodenal ulcer show increased acid output.
  5. To measure the amount of acid secreted in a patient with symptoms of peptic ulcer dyspepsia but normal X-ray findings: Excess acid secretion in such cases is indicative of duodenal ulcer. However, hypersecretion of acid does not always occur in duodenal ulcer.
  6. To decide the type of surgery to be performed in a patient with peptic ulcer: Raised basal as well as peak acid outputs indicate increased parietal cell mass and need for gastrectomy. Raised basal acid output with normal peak output is an indication for vagotomy.
To assess gastric acid secretion, acid output from the stomach is measured in a fasting state and after injection of a drug which stimulates gastric acid secretion.
 
Basal acid output (BAO) is the amount of hydrochloric acid (HCl) secreted in the absence of any external stimuli (visual, olfactory, or auditory).
 
Maximum acid output (MAO) is the amount of hydrochloric acid secreted by the stomach following stimulation by pentagastrin. MAO is calculated from the first four 15-minute samples after stimulation.
 
Peak acid output (PAO) is calculated from the two highest consecutive 15-minute samples. It indicates greatest possible acid secretory capacity and is preferred over MAO as it is more reproducible.
 
Acidity is estimated by titration.
 
Collection of Sample
 
All drugs that affect gastric acid secretion (e.g. antacids, anticholinergics, cholinergics, H2-receptor antagonists, antihistamines, tranquilizers, antidepressants, and carbonic anhydrase inhibitors) should be withheld for 24 hours before the test. Proton pump inhibitors should be discontinued 5 days prior to the test. Patient should be relaxed and free from all sources of sensory stimulation.
 
Patient should drink or eat nothing after midnight.
 
Gastric juice can be aspirated through an oral or nasogastric tube (polyvinyl chloride, silicone, or polyurethane) or during endoscopy.
 
Oral or nasogastric tube (Figure 855.1) is commonly used. It is a flexible tube having a small diameter and a bulbous end that is made heavy by a small weight of lead. The end is perforated with small holes to allow entry of gastric juice into the tube. As the end is radiopaque, the tube can be positioned in the most dependent part of the stomach under fluoroscopic or X-ray guidance. The tube is lubricated and can be introduced either through the mouth or the nose. The patient is either sitting or reclining on left side. The tube has three or four markings on its outer surface that correspond with distance of the tip of the tube from the teeth, i.e. 40 cm (tip to cardioesophageal junction), 50 cm (body of stomach), 57 cm (pyloric antrum), and 65 cm (duodenum). The position of the tube can be verified either by fluoroscope or by ‘water recovery test’. In the latter test, 50 ml of water is introduced through the tube and aspirated again; recovery of > 90% of water is indicative of proper placement. The tube is usually positioned in the antrum. A syringe is attached to the outer end of the tube for the aspiration of gastric juice.
 
Figure 855.1 Oral or nasogastric Ryles tube
Figure 855.1 Oral or nasogastric Ryle’s tube. The tube is marked at 40, 50, 57, and 65 cm with radiopaque lines for accurate placement. The tip is bulbous and contains a small weight of lead to assist the passage during intubation and to know the position under fluoroscopy or X-ray guidance. There are four perforations or eyes to aspirate contents from the stomach through a syringe attached to the base
 
For estimation of BAO, sample is collected in the morning after 12-hour overnight fast. Gastric secretion that has accumulated overnight is aspirated and discarded. This is followed by aspiration of gastric secretions at 15-minute intervals for 1 hour (i.e. total 4 consecutive samples are collected). All the samples are centrifuged to remove any particulate matter. Each 15-minute sample is analyzed for volume, pH, and acidity. The acid output in the four samples is totaled and the result is expressed as concentration of acid in milliequivalents per hour or in mmol per hour.
 
After the collection of gastric juice for determination of BAO, patient is given a subcutaneous or intramuscular injection of pentagastrin (6 μg/kg of body weight), and immediately afterwards, gastric secretions are aspirated at 15-minute intervals for 1 hour (for estimation of MAO or PAO). MAO is calculated from the first four 15-minute samples after stimulation. PAO is calculated from two consecutive 15-minute samples showing highest acidity.
 
Titration
 
Box 855.1 Determination of basal acid output, maximum acid output, and peak acid output
 
  • Basal acid output (BAO)= Total acid content in all four 15-minute basal samples in mEq/L
  • Maximum acid output (MAO) = Total acid content in all four 15-minute post-pentagastrin samples in mEq/L
  • Peak acid output (PAO) = Sum of two consecutive 15-minute post-pentagastrin samples showing highest acidity ×2 (mEq/L)
Gastric acidity is estimated by titration, with the end point being determined either by noting the change in color of the indicator solution or till the desired pH is reached.
 
In titration, a solution of alkali (0.1 N sodium hydroxide) is added from a graduated vessel (burette) to a known volume of acid (i.e. gastric juice) till the end point or equivalence point of reaction is reached. The concentration of acid is then determined from the concentration and volume of alkali required to neutralize the particular volume of gastric juice. Concentration of acid is expressed in terms of milliequivalents per liter or mmol per liter.
 
Free acidity refers to the concentration of HCl present in a free, uncombined form in a solution. The volume of alkali added to the gastric juice till the Topfer’s reagent (an indicator added earlier to the gastric juice) changes color or when the pH (as measured by the pH meter) reaches 3.5 is a measure of free acidity. A screening test can be carried out for the presence of free HCl in the gastric juice. If red color develops after addition of a drop of Topfer’s reagent to an aliquot of gastric juice, free HCl is present and the diagnosis of pernicious anaemia (achlorhydria) can be excluded.
 
Combined acidity refers to the amount of HCl combined with proteins and mucin and also includes small amount of weak acids present in gastric juice.
 
Total acidity is the sum of free and combined acidity. The amount of alkali added to the gastric juice till phenolphthalein indicator (added earlier to the gastric juice) changes color is a measure of total acidity (Box 855.1).
 
Interpretation of Results
 
  1. Volume: Normal total volume is 20-100 ml (usually < 50 ml). Causes of increased volume of gastric juice are—
    • Delayed emptying of stomach: pyloric stenosis
    • Increased gastric secretion: duodenal ulcer, Zollinger-Ellison syndrome.
  2. Color: Normal gastric secretion is colorless, with a faintly pungent odor. Fresh blood (due to trauma, or recent bleeding from ulcer or cancer) is red in color. Old hemorrhage produces a brown, coffee-ground like appearance (due to formation of acid hematin). Bile regurgitation produces a yellow or green color.
  3. pH: Normal pH is 1.5 to 3.5. In pernicious anemia, pH is greater than 7.0 due to absence of HCl.
  4. Basal acid output:
    • Normal: Up to 5 mEq/hour.
    • Duodenal ulcer: 5-15 mEq/hour.
    • Zollinger-Ellison syndrome: >20 mEq/hour.
    Normal BAO is seen in gastric ulcer and in some patients with duodenal ulcer.
  5. Peak acid output:
    • Normal: 1-20 mEq/hour.
    • Duodenal ulcer: 20-60 mEq/hour.
    • Zollinger-Ellison syndrome: > 60 mEq/hour.
    • Achlorhydria: 0 mEq/hour.
    Normal PAO is seen in gastric ulcer and gastric carcinoma. Values up to 60 mEq/hour can occur in some normal individuals and in some patients with Zollinger-Ellison syndrome.
    In pernicious anemia, there is no acid output due to gastric mucosal atrophy. Achlorhydria should be diagnosed only if there is no free HCl even after maximum stimulation.
  6. Ratio of basal acid output to peak acid output (BAO/PAO):
    • Normal: < 0.20 (or < 20%).
    • Gastric or duodenal ulcer: 0.20-0.40 (20-40%).
    • Duodenal ulcer: 0.40-0.60 (40-60%).
    • Zollinger-Ellison syndrome: > 0.60 (> 60%).
    Normal values occur in gastric ulcer or gastric carcinoma.
 
Conditions associated with change in gastric acid output are listed in Table 855.1.
 
It is to be noted that values of acid output are not diagnostic by themselves and should be correlated with clinical, radiological, and endoscopic features.
 
Table 855.1 Causes of alterations in gastric acid output
Increased gastric acid output Decreased gastric acid output
• Duodenal ulcer Chronic atrophic gastritis
• Zollinger-Ellison syndrome     1. Pernicious anemia
Hyperplasia of antral G cells     2. Rheumatoid arthritis
Systemic mastocytosis     3. Thyrotoxicosis
• Basophilic leukemia • Gastric ulcer
  • Gastric carcinoma
  • Chronic renal failure
  • Post-vagotomy
  • Post-antrectomy

Bioethics

  • 04 Sep 2017
Bioethics is the study of the ethical issues emerging from advances in biology and medicine. It is also moral discernment as it relates to medical policy and practice. Bioethicists are concerned with the ethical questions that arise in the relationships among life sciences, biotechnology, medicine, politics, law, and philosophy. It includes the study of values ("the ethics of the ordinary") relating to primary care and other branches of medicine.
Animal biotechnology is a branch of biotechnology in which molecular biology techniques are used to genetically engineer (i.e. modify the genome of) animals in order to improve their suitability for pharmaceutical, agricultural or industrial applications. Animal biotechnology has been used to produce genetically modified animals that synthesize therapeutic proteins, have improved growth rates or are resistant to disease.

Biophysics

  • 04 Sep 2017
Biophysics or biological physics is an interdisciplinary science that applies the approaches and methods of physics to study biological systems. Biophysics covers all scales of biological organization, from molecular to organismic and populations. Biophysical research shares significant overlap with biochemistry, physical chemistry, nanotechnology, bioengineering, computational biology, biomechanics and systems biology.
 
The term biophysics was originally introduced by Karl Pearson in 1892.

Histopathology

  • 04 Sep 2017
Histopathology (compound of three Greek words: ἱστός histos "tissue", πάθος pathos "suffering", and -λογία -logia"study of") refers to the microscopic examination of tissue in order to study the manifestations of disease. Specifically, in clinical medicine, histopathology refers to the examination of a biopsy or surgical specimen by a pathologist, after the specimen has been processed and histological sections have been placed onto glass slides. In contrast, cytopathology examines (1) free cells or (2) tissue micro-fragments (as "cell blocks").

Physiology

  • 04 Sep 2017
Physiology (/ˌfɪziˈɒləi/; from Ancient Greek φύσις (physis), meaning 'nature, origin', and -λογία (-logia), meaning 'study of') is the scientific study of normal mechanisms, and their interactions, which works within a living system. A sub-discipline of biology, its focus is in how organisms, organ systems, organs, cells, and biomolecules carry out the chemical or physical functions that exist in a living system. Given the size of the field, it is divided into, among others, animal physiology (including that of humans), plant physiology, cellular physiology, microbial physiology (microbial metabolism), bacterial physiology, and viral physiology.
 
Central to an understanding of physiological functioning is its integrated nature with other disciplines such as chemistry and physics, coordinated homeostatic control mechanisms, and continuous communication between cells.
 
The Nobel Prize in Physiology or Medicine is awarded to those who make significant achievements in this discipline by the Royal Swedish Academy of Sciences. In medicine, a physiologic state is one occurring from normal body function, rather than pathologically, which is centered on the abnormalities that occur in animal diseases, including humans.

Food Science

  • 04 Sep 2017
Food science is the applied science devoted to the study of food. The Institute of Food Technologists defines food science as "the discipline in which the engineering, biological, and physical sciences are used to study the nature of foods, the causes of deterioration, the principles underlying food processing, and the improvement of foods for the consuming public". The textbook Food Science defines food science in simpler terms as "the application of basic sciences and engineering to study the physical, chemical, and biochemical nature of foods and the principles of food processing".

Ecology

  • 04 Sep 2017
Ecology (from Greek: οἶκος, "house", or "environment"; -λογία, "study of") is the scientific analysis and study of interactions among organisms and their environment. It is an interdisciplinary field that includes biology, geography, and Earth science. Ecology includes the study of interactions that organisms have with each other, other organisms, and with abiotic components of their environment. Topics of interest to ecologists include the diversity, distribution, amount (biomass), and number (population) of particular organisms, as well as cooperation and competition between organisms, both within and among ecosystems. Ecosystems are composed of dynamically interacting parts including organisms, the communities they make up, and the non-living components of their environment. Ecosystem processes, such as primary production, pedogenesis, nutrient cycling, and various niche construction activities, regulate the flux of energy and matter through an environment. These processes are sustained by organisms with specific life history traits, and the variety of organisms is called biodiversity. Biodiversity, which refers to the varieties of species, genes, and ecosystems, enhances certain ecosystem services.
 
Ecology is not synonymous with environment, environmentalism, natural history, or environmental science. It is closely related to evolutionary biology, genetics, and ethology. An important focus for ecologists is to improve the understanding of how biodiversity affects ecological function. Ecologists seek to explain:
 
  • Life processes, interactions, and adaptations
  • The movement of materials and energy through living communities
  • The successional development of ecosystems
  • The abundance and distribution of organisms and biodiversity in the context of the environment.
 
There are many practical applications of ecology in conservation biology, wetland management, natural resource management(agroecology, agriculture, forestry, agroforestry, fisheries), city planning (urban ecology), community health, economics, basic and applied science, and human social interaction (human ecology). For example, the Circles of Sustainability approach treats ecology as more than the environment 'out there'. It is not treated as separate from humans. Organisms (including humans) and resources compose ecosystems which, in turn, maintain biophysical feedback mechanisms that moderate processes acting on living (biotic) and non-living (abiotic) components of the planet. Ecosystems sustain life-supporting functions and produce natural capital like biomass production (food, fuel, fiber, and medicine), the regulation of climate, global biogeochemical cycles, water filtration, soil formation, erosion control, flood protection, and many other natural features of scientific, historical, economic, or intrinsic value.
 
The word "ecology" ("Ökologie") was coined in 1866 by the German scientist Ernst Haeckel (1834–1919). Ecological thought is derivative of established currents in philosophy, particularly from ethics and politics. Ancient Greek philosophers such as Hippocrates and Aristotle laid the foundations of ecology in their studies on natural history. Modern ecology became a much more rigorous science in the late 19th century. Evolutionary concepts relating to adaptation and natural selection became the cornerstones of modern ecological theory.

Forensic Science

  • 04 Sep 2017
Forensic science is the application of science to criminal and civil laws, mainly—on the criminal side—during criminal investigation, as governed by the legal standards of admissible evidence and criminal procedure.
 
Forensic scientists collect, preserve, and analyze scientific evidence during the course of an investigation. While some forensic scientists travel to the scene of the crime to collect the evidence themselves, others occupy a laboratory role, performing analysis on objects brought to them by other individuals.
 
In addition to their laboratory role, forensic scientists testify as expert witnesses in both criminal and civil cases and can work for either the prosecution or the defense. While any field could technically be forensic, certain sections have developed over time to encompass the majority of forensically related cases.

Microscopic examinations done on fecal sample are shown in Figure 846.1.

Collection of Specimen for Parasites

A random specimen of stool (at least 4 ml or 4 cm³) is collected in a clean, dry, container with a tightly fitting lid (a tin box, plastic box, glass jar, or waxed cardboard box) and transported immediately to the laboratory (this is because trophozoites of Entameba histolytica rapidly degenerate and alter in morphology). About 20-40 grams of formed stool or 5-6 tablespoons of watery stool should be collected. Stool should not be contaminated with urine, water, soil, or menstrual blood. Urine and water destroy trophozoites; soil will introduce extraneous organisms and also hinder proper examination. Parasites are best detected in warm, freshly passed stools and therefore stools should be examined as early as possible after receipt in the laboratory (preferably within 1 hour of collection). If delay in examination is anticipated, sample may be refrigerated. A fixative containing 10% formalin (for preservation of eggs, larvae, and cysts) or polyvinyl alcohol (for preservation of trophozoites and cysts, and for permanent staining) may be used if specimen is to be transported to a distant laboratory.

Figure 846.1 Microscopic examinations carried out on fecal sample
Figure 846.1 Microscopic examinations carried out on fecal sample

One negative report for ova and parasites does not exclude the possibility of infection. Three separate samples, collected at 3-day intervals, have been recommended to detect all parasite infections.

Patient should not be receiving oily laxatives, antidiarrheal medications, bismuth, antibiotics like tetracycline, or antacids for 7 days before stool examination. Patient should not have undergone a barium swallow examination.

In the laboratory, macroscopic examination is done for consistency (watery, loose, soft or formed) (Figure 846.2), color, odor, and presence of blood, mucus, adult worms or segments of tapeworms.

Figure 846.2 Consistency of feces
Figure 846.2 Consistency of feces

Trophozoites are most likely to be found in loose or watery stools or in stools containing blood and mucus, while cysts are likely to be found in formed stools. Trophozoites die soon after being passed and therefore such stools should be examined within 1 hour of passing. Examination of formed stools can be delayed but should be completed on the same day.

Color/Appearance of Fecal Specimens

  • Brown: Normal
  • Black: Bleeding in upper gastrointestinal tract (proximal to cecum), Drugs (iron salts, bismuth salts, charcoal)
  • Red: Bleeeding in large intestine, undigested tomatoes or beets
  • Clay-colored (gray-white): Biliary obstruction
  • Silvery: Carcinoma of ampulla of Vater
  • Watery: Certain strains of Escherichia coli, Rotavirus enteritis, cryptosporidiosis
  • Rice water: Cholera
  • Unformed with blood and mucus: Amebiasis, inflammatory bowel disease
  • Unformed with blood, mucus, and pus: Bacillary dysentery
  • Unformed, frothy, foul smelling, which float on water: Steatorrhea.

Preparation of Slides

After receipt in the laboratory, saline and iodine wet mounts of the sample are prepared (Figure 846.3).

Figure 846.3 Saline and iodine wet mounts of fecal sample
Figure 846.3 Saline and iodine wet mounts of fecal sample

A drop of normal saline is placed near one end of a glass slide and a drop of Lugol iodine solution is placed near the other end. A small amount of feces (about the size of a match-head) is mixed with a drop each of saline and iodine using a wire loop, and a cover slip is placed over each preparation separately. If the specimen contains blood or mucus, that portion should be included for examination (trophozoites are more readily found in mucus). If the stools are liquid, select the portion from the surface for examination.

Saline wet mount is used for demonstration of eggs and larvae of helminths, and trophozoites and cysts of protozoa. It can also detect red cells and white cells. Iodine stains glycogen and nuclei of the cysts. The iodine wet mount is useful for identification of protozoal cysts. Trophozoites become non-motile in iodine mounts. A liquid, diarrheal stool can be examined directly without adding saline.

Concentration Procedure

Concentration of fecal specimen is useful if very small numbers of parasites are present. However, in concentrated specimens, amebic trophozoites can no longer be detected since they are destroyed. If wet mount examination is negative and there is clinical suspicion of parasitic infection, fecal concentration is indicated. It is used for detection of ova, cysts, and larvae of parasites.

Various concentration methods are available; the choice depends on the nature of parasites to be identified and the equipment/reagent available in a particular laboratory. Concentration techniques are of two main types:

  • Sedimentation techniques: Ova and cysts settle at the bottom. However, excessive fecal debris may make the detection of parasites difficult. Example: Formolethyl acetate sedimentation procedure.
  • Floatation techniques: Ova and cysts float on surface. However, some ova and cysts do not float at the top in this procedure. Examples: Saturated salt floatation technique and zinc sulphate concentration technique.

The most commonly used sedimentation method is formol-ethyl acetate concentration method since: (i) it can detect eggs and larvae of almost all helminths, and cysts of protozoa, (ii) it preserves their morphology well, (iii) it is rapid, and (iv) risk of infection to the laboratory worker is minimal because pathogens are killed by formalin.

In this method, fecal suspension is prepared in 10% formalin (10 ml formalin + 1 gram feces). This suspension is then passed through a gauze filter till 7 ml of filtered material is obtained. To this, ethyl acetate (3 ml) is added and the mixture is centrifuged for 1 minute. Eggs, larvae, and cysts sediment at the bottom of the centrifuge tube (Figure 846.4). Above this deposit, there are layers of formalin, fecal debris, and ether. Fecal debris is loosened with an applicator stick and the supernatant is poured off. One drop of sediment is placed on one end of a glass slide and one drop is placed at the other end. One of the drops is stained with iodine, cover slips are placed, and the preparation is examined under the microscope.

Figure 846.4 Formol ethyl acetate concentration technique
Figure 846.4 Formol-ethyl acetate concentration technique

Classification of Intestinal Parasites of Humans

Intestinal parasites of humans are classified into two main kingdoms: protozoa and metazoa (helminths) (Figure 846.5).

Figure 846.5 Classification of intestinal parasites of humans
Figure 846.5 Classification of intestinal parasites of humans
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