TORSION AND DETORSION IN MOLLUSCA

Written by Sunday, 11 February 2018 14:35
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.

PROCESS OF FORMATION OF PEARL IN MOLLUSCS

Written by Tuesday, 06 February 2018 19:42
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
 
 
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.
 

ROLE OF FAMILY SUPPORT IN DIABETES MANAGEMENT

Written by Wednesday, 17 January 2018 19:10
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.

CHOLERA: CAUSES, SYMPTOMS, DIAGNOSIS AND TREATMENT

Written by Tuesday, 09 January 2018 13:31
CHOLERA is a specific infectious disease that affects the lower portion of the intestine and is characterized by violent purging, vomiting, muscular cramp, suppression of urine and rapid collapse. It can a terrifying disease with massive diarrhea. The patient’s fluid losses are enormous every day with severe rapid dehydration, death comes within hours.

ETIOLOGY
 
  • Site: GIT (Gastrointestinal Track)
  • Agent: VIBRIO CHOLERA
 
MORPHOLOGICAL CHARACTER
 
Gram-negative, curved rods, non-capsulated, non-spore, motile by means of flagella (polar) they occur singly.
 
CULTURAL CHARACTER
 
  1. They produce smooth, convex, round, colonies which appear opaque and granular in transmitted light.
  2. They can grow on many kinds of media including enriching media contains bile salt and asparagine.
  3. They particularly grow on TCB agar (Thiosulfate Citrate Bile Salt agar) and produce yellow colonies.
  4. They are readily killed by acid and optimum pH for growth is 8.5-9.5.

BIOCHEMICAL CHARACTER
 
They ferment sucrose and maltose but not arabinose. They are oxidase positive which make them different from enteric Gram-negative rods. Some are halotolerant while others are halophilic require presence of NaCl for their growth.
 
ANTIGENIC CHARACTER
 
  • Vibrio Cholera contains two types of antigen flagellar (H) and somatic (O).
  • Vibrio Cholera contains two types of antigen flagellar (H) and somatic (O).
  • All Vibrios shared a single heat labile H antigen.
  • The O antigen is composed of heat stable polysaccharides and are classified into 6 serogroups and are further classified into 60 serotypes on the basis of O antigen.
  • One serotype of Vibrio Cholera bacilli is responsible for epidemic cholera and is subdivided into two types.
    (1) Classical (2) El Tor
  • El Tor types Vibrios were different from the classical types in their ability to cause lysis of goa or sheep erythrocyte in a test known as Grieg Test.
  • Each of the two biotypes of 01 serotypes of Vibrio is comprised of two or three antigenic factor A, B, and C
  • Factor A and B are found in serotype Ogawa, A and C in serotype Inaba and A, B and C in serotype Hikojima.
 
CHOLERA TOXIN
 
V. Cholera elaborated an enterotoxin that is responsible for the loss of fluid is Cholera, called CHOLERAGEN. It is a polymeric protein with a molecular weight 84,000 daltons containing two major domains. The domain "A" with molecular weight 28,000 daltons, play the key role in the biological activity of the Choleragen. The domain "B" is also known as CHOLERAGENOID with a molecular weight 56,000 daltons bind the toxin to its receptors on host cell surface. it is also the immunologically active region of the toxin.
 
Vibrio Cholera has been shown to produce a second toxin called ZONULA OCCULUDENS TOXIN (ZOT). This toxin disintegrates the tight junction between enterocytes, allowing escape of water and electrolytes.
 
MODE OF ACTION OF TOXIN
 
The toxin subunit "A" and "B" promote the entry of subunit "A" into the cell, "B" subunit is responsible for attachment of toxin to the epithelial cell of the small intestine. This subunit alters the activity of the regulatory protein, that controls the activity of enzyme, Adenylate Cyclase. This enzyme converts the ATP (Adenosine Tri-Phosphate) into CAMP (Cyclic Adenosine 5 Mono Phosphate). This increase in cyclic AMP level causes loss of water, electrolytes and result in diarrhea. This may lead to death because of dehydration and acidosis.

PATHOGENESIS
 
Cholera occurs in epidemic form under the condition of overcrowding, floods, wars, and famine. Humans are the only known natural hosts. A person may have to ingest 108 – 1010 organism to become infected. Vibrio Cholera is transferred from one person to another by ingestion of contaminated water or foodstuff. The contact with the carrier can also contribute to epidemics.
 
The Cholera bacilli find their way into the small intestine where they proliferate and elaborate the Choleragen. The toxin elevates the produces a massive secretion of isotonic fluid into the lumen of the intestine.

CLINICAL FINDING
 
The incubation period is few hours to 4 days. After incubation, there is sudden onset of nausea, vomiting, diarrhea with abdominal cramps, rapid dehydration and loss of fluid electrolytes. Mortality rate without treatment is 25% to 50%.
 
LABORATORY DIAGNOSIS
 
Diagnosis of Cholera patient by physical examination of stool, direct microscopic examination. Culture technique and also by agglutination method.
 
SMEAR
 
Smear made from stool sample is not distinctive however darkfield microscopy or phase contrast microscopy can show motile Vibrios.
 
CULTURE
 
There is rapid growth on peptone agar, TCB’s near pH 9 colony can be picked after 18-24 hours of incubation.
 
AGGLUTINATION
 
Agglutination test using anti O group on serum and also by the biochemical reaction.
 
EPIDEMIOLOGY
 
Man is the only host of Cholera disease and spread of infection is from person to person with contaminated water, food or flies. In many intensive 1% to 5% of exposed susceptible person developed the disease. The carrier state seldom exceeds 3 to 4 weeks.
 
PREVENTION
 
  1. Good water supply. Proper treatment of water should be there before supply to the town.
  2. Proper treatment of sewerage system.
  3. Personal hygiene and proper sanitation.
 
TREATMENT
 
Individual infected with Cholera require rehydration adequately by giving a solution of Oral Rehydration Salts (ORS) containing sodium chloride, sodium bicarbonate, potassium chloride and glucose. During the epidemic, 80-90% of diarrhea patient can be treated by oral rehydration alone but the patient who becomes severely dehydrate must be given intravenous fluid.

HIGH BLOOD PRESSURE AFTER THE GREEN TEA CONSUMPTION

Written by Saturday, 06 January 2018 18:14
Green tea is frequently touted as one of the most beneficial drink alternatives. Similarly, as with different sorts of tea, green tea originates from Camellia sinensis plant clears out. Be that as it may, contrasted and dark tea, green tea brings down in caffeine and has a high epigallocatechin gallate content. Green tea is positively more advantageous than sugary soda pops, yet regardless you hazard symptoms from this refreshment. Such dangers may even incorporate lifted pulse, additionally called hypertension.
 
Caffeine in Green Tea
 
The Center for Science in the general population intrigue evaluates that 8 ounces of green tea contains in the vicinity of 35 and 60 milligrams of caffeine. This is a small amount of some espresso. The exact measure of caffeine differs amongst brands and relying upon to what extent you soak the tea. Caffeine goes about as a stimulant, boosting state of mind and expanding sharpness. While uncommon with green tea, an excessive amount of caffeine can prompt uneasiness, tremors, and expanded heart rate. You may likewise be more inclined to unfavorable impacts in the event that you have caffeine affectability, which differs between people. This happens when the body processes caffeine at an underneath normal rate. As indicated by the European Food Information Council, it takes in the vicinity of two and 10 hours to utilize caffeine, with four hours being normal.
 
Circulatory strain Impacts
 
Advocates of green tea frequently recommend that flavonoids in tea leaves may advance heart wellbeing and even lower circulatory strain. In any case, the caffeine substance may really cause a brief ascent in circulatory strain as a result of the fast rate the body assimilates the substance. An examination distributed in the August 1999 issue of "Journal of Hypertension" announced that tea utilization caused slight increments in circulatory strain among thinking about members. In any case, the increments were not viewed as sufficiently huge to raise genuine wellbeing concerns. What can be earned from this examination is that green tea may not be the most tried and true or most secure technique for circulatory strain direction.
 
Decide Legitimate Tea Utilization
 
Direct utilization of green tea is probably not going to cause a huge increment in circulatory strain. With regards to green tea, MedlinePlus characterizes direct utilization of the drink as a normal of five glasses for each day or an aggregate or in the vicinity of 200 and 300 milligrams of caffeine. The caffeine substance of green tea settles on this drink a superior decision for expanding mental readiness in case you're stressed over higher caffeine sources, for example, dark tea and espresso. There is additionally the additional advantage of the cancer prevention agent epigallocatechin gallate, a catechin that may help keep free radicals from decimating cells that can prompt perpetual ailments. In case you're stressed over general caffeine admission and circulatory strain, it's critical to expend green tea with some restraint.
 
Unique Contemplations for Caffeine 
 
While the caffeine substance of green tea alone may not prompt hypertension, you might need to keep away from the refreshment in the event that you as of now have this wellbeing concern. Youngsters, pregnant ladies, and nursing moms should cease from green tea due to the potential for antagonistic wellbeing impacts. Amid pregnancy, the body uses caffeine at a slower rate, so it remains in the body longer. Caffeine has the likelihood of promoting birth deserts and might be gone through the bosom drain. Uneasiness and hyperactivity can happen in a few kids from caffeine. To stay away from these worries, consider decaffeinated green tea.

TOTAL THYROXINE (T4)

Written by Thursday, 28 September 2017 14:23
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.

DISORDERS OF THYROID

Written by Thursday, 28 September 2017 01:34
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

FEMALE INFERTILITY: CAUSES AND INVESTIGATIONS

Written by Friday, 22 September 2017 13:37
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

MALE INFERTILITY: CAUSES AND INVESTIGATIONS

Written by Friday, 22 September 2017 00:03
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.
 
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