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The hard parts of the animal body are collectively known as skeletal system or simply skeleton. The vertebrates possess the hard parts inside the body. It is known as endo skeleton. The endo skeletal structures are formed with cartilages and bones which are the living tissues. The endo skeleton has been divided into:The hard parts of the animal body are collectively known as skeletal system or simply skeleton. The vertebrates possess the hard parts inside the body. It is known as endo skeleton. The endo skeletal structures are formed with cartilages and bones which are the living tissues. The endo skeleton has been divided into:
  1. Axial skeleton - includes the skull and vertebral column.
  2. Appenducular skeleton - includes the girdles and limb bones.
The skull develops in the head of animal body. The skull includes two major parts - 'Cranium' enclosing the brain and the organs of special sense and Visceral arches' which form the jaws and frame work of pharyngeal wall.

The cranium is developed from the mesodermal cells soon after the appearance of the brain. It is also known as brain box. Cranium includes three pairs of capsules for smell, sight and hearing. These are known as olfactory, optic and auditory capsules respectively. The cartilaginous cranium is called chondro cranium and bony cranium is called dermato cranium.

The visceral arches develop around anterior (Pharyngeal) part of the embryonic gut from the cells of neural crests. Mostly seven visceral arches are present. The first one is the largest and highly modified - 'Mandibular arch. It has dorsal & ventral halves. Each side of the dorsal half is termed the palato -pterygoid Quadrate Cartilage. It bears teeth and forms the upper jaw. The ventral half of the mandibular arch is called Meckel's cartilage. It also bears the teeth and form the lower jaw. The wide gap between the two jaws is the mouth. The two jaws articulate their hind ends by hinge joints which enable the mouth to open & close. The second arch is hyoid arch and the remaining five arches are termed bronchial arches. The visceral arches are collectively known as the splanchno cranium. The upper jaw and lower jaw are known as Maxilla and Mandible respectively: See images. 
1. Skull is formed with cartilage tissues. 1. Skull is formed most­ly with bony tissues (but tadpole skull is cartilaginous) 1. Skull is formed most­ly with bony tissues. 1. Skull is formed mostly with bony tissue. 1. Skull is formed with mostly bony tissue.
2. It consists of crani­um, sense capsules and visceral arches. 2. It consists of cran­ium, sense capsules, jaws and hyoid ap­paratus. 2. It consists of crani­um, sense capsules, jaws and hyoid apparatus. 2. Same as in calotes. 2. Same as in calotes.
3. It is the axial portion of the skull. It is more or less a violin box open in front and be­hind with an arched roof and flattened floor. It is divided into occipital, auditory, orbital and ethmoidal regions. 3. It forms the middle hollow part of the skull. It is divided into auditory, olfactory and occipital regions. 3. It forms the median hollow part of the skull. It is divided into occipital, audi­tory, orbital, olfacto­ry and optic regions. 3. It forms the posterior median hollow part of the skull. It is divided into occipital, audito­ry, optic orbital and ol­factory regions. 3. It forms the middle hollow part of the skull. It is divided into occipital auditory, optic orbital & olfac­tory regions.
4. Foramen magnum is posteriorly present. 4. Same. 4. Same. 4. Same. 4. Same.
5. Beneath the foramen magnum a deep concavity is present. On either side of this concavity is a pro­minence - occipital condyle articulates with the first verte­bra, occipital crest is formed. Dicondylic skull. 5. Beneath the foramen magnum there are two occipital con­dyles. On either side of the foramen mag­num dorsolaterally exoccipital bones are present. Dicondylic skull 5. Beneath the fora­men magnum a sin­gle occipital condyle is present.suupraoccipitai, exo occipitals,& basi occipital bones are also present in the occipital region. Monocondylic skull. 5. Beneath the foramen magnum single occip­ital condyle is present. Supra occipital, Exocci pitals & basioccipital bones are also present. Monocondylic skull. 5. Beneath the fora­men magnum two occipital condyles with paroccipital process are present. Supraoccipital, exo-ccipitai, & basio-ccipital bones are also present. Dico­ndylic skull.
6. Auditory region has a mid dorsal depres­sion - parietal fossa. It contain two pairs of apertures. Anteri­orly smaller open­ings of endolymp­hatic ducts and pos­teriorly larger open­ings of perilymphatic spaces are present. 6.— 6.— 6.— 6.—
7. Auditory capsules lie on the poster lat­eral sides of the cranium. Which enclose & protect the ears. Post orbital groove is present on the ven­tral side 7. Auditory capsules enclose the internal ear. Its roof is formed by pro-otic bone, fenestra ovalis, sta­pedial plate and columella auris are present. 7. Each auditory capsule is formed by small, single vertical prootic bone which is lying outside the supra occipital. Epiotic & opisthotic are not differentiat­ed. 7. Each auditory capsule is formed largely by the prooticbone. Fenestra ovalis, fenestra rotun da, columella auris, stapes are also present. 7. Each auditory cap­sule in the adult animal consists only periotic. Flask - like Tympanic bulla bone is significant.
8.— 8. Dorsally the cranium is formed, by frontoparietals, ven­trally by parasphenoid and laterally by sphen ethmoid bones. 8. The dorsal part of the cranium is formed by parietals, frontals interparietal foramen, and ven­trally by basisphenoid, parasphenoid bones. 8. The dorsal part of the cranium is formed by Parietals, frontals a rostum, alisphenoids; ventrally basisphenoid, basitemporal bones. 8. The cranium is formed dorsally by 'Parietals, frontals, inter parietal, and ventrally by basisphenoids, presphenoid bones along with alisphenoids and orbit sphenoids. The cra­nial cavity is closed infront by a narrow vertical bone cibriform plate.
9.  Each orbit lies on the sides of the middle part of the cranium. It is bordered by dor­sal super orbital ridge,anterior preorbital process, posterior post orbital process and ventraily by infra orbital ridge. The orbital region has a large oral cavity anterior fontanelle. 9. On either side of the cranium is large gap - orbit which lodges the eye. 9. In the middle of the cranium laterally two orbits are present. Each orbit is bounded by prefrontal supra orbital, lacri­mal, post frontal and jugal bones. The jugal bone forms the ventral border of the orbit. Supratemporal arch is present. 9. The two orbits are very large cavities present infront of the cranium. Each orbit is bounded dorsally by frontal, antero - dorsally by lac­rimal and posteriorly by the zygomatic process. Orbit is incomplete on the ventral side. The two orbits are separated by inter orbital septum. 9. These are two orbits are large sockets present on the sides of frontal segment of cranium. The orbit is bounded dorsally by frontal, anteriorly by maxilla and lacrimal, posteriorly by squa­mosal and alisp-henoid and external­ly by the zygomatic arch.
10. The olfactory cap­sules lie at the anteri­or side of the cranium. Each capsule possesses a short sic at ethmopalatine ridge. 10. The olfactory cap­sules are separated, from each other by mesethmoid. Each capsule is formed by a large triangular nasal on the dorsal side and a smaller triradiate vomer on the ventral side vomers possess vomerine teeth. 10. Each olfactory capsule is formed by three bones Nasal, septo maxillary and vomer. 10. Each olfactory capsule is formed by two bones - Nasal and vomer. Nasals fuse with frontals and form into super and inferior processes. 10. Each olfactory cap­sule is bounded by dorsally by long na­sal bone and laterally by jaw bones. The two capsules are sep­arated by mesethmoid bone. The lower end of mesethmoid fits into a vomer bone. Vomer is formed by the fusion of a pair of bones.
11. Ethmoidal region tapers anteriorly. It consists of a basal slender barventro-median rostral carti­lage and a pair of similar barsdorso - lateral rostral cartilages aris­en from the roof of ihe olfactory capsules. 11. Absent. 11. Absent. 11. Absent. 11. Absent.
12. Scoliodon has seven visceral arches which are cartilagienous. The first arch forms the jaws and it is catted Mandibular arch the second one is the hyoid arch the remain­ing five arches are called branchial arch­es. 12. Branchial arches are absent.There are upper and lower jaws to support the borders of the mouth. The upper jaw is formed by union of two similar halves. Each half is formed by the Pre-maxilla, maxilla and quadratojugal. The inner set of the jaw has palatine, ptery goid and squamosal bones. The lower consists of two halves and unite an­teriorly by mento-meckelian cartilage. Each half consists of dentary and angio -splenial bones. Just infroni of the articu­lar fact a small coro-nary process is present. Upper jaw alone has teeth. 12. Branchial arches are absent. 12. Branchial arches are absent. 12.   Branchial arches absent.These are upper and lower jaws. Each half of the upper jaw is formed by premax-illa, maxilla jugular, palatine, pterygoid and squamosal.
13. The mandibular arch consists of two halves. Each half of this arch possess an upper paleto-pterygo quadrate cartilage and a lower meckel s cartilage.The pale topterygo Quadrate gives off anteriorly palatine. The two sides of it from the upper jaw with teeth. The two meckel's cartilages united antero medially by lig­ament form the lower jaw with teeth.   13. These are upper and lower jaws. Each half of the upper jaw consists of an outer set of bones - pre maxilla, maxilla, jugal and quadrate and the inner set in­cludes pterygoid, palatine, transp-alatine, epiptery-goid and squamo­sal. Each half of the lower jaw consists of six bones -dentary, angular, supra angular, ar­ticular, splenial and coronoid. Both the jaws possess teeth. 13. These are upper and lower jaws. Each half of the upper jaw is formed by premaxilla, maxilla, quadra tojugal, and jugal bones. The inner ar­cade of the upper jaw forms the roof of bucco pharyngal cav­ity which consists of palatine, pterygoid, and quadrate. Each half of the lower jaw is formed by articu­lar, angular supra an­gular, dentary and splenial. Both the jaws are lacking the teeth. 13. The lower jaw also con­sists of two halves. Each half is formed by a single, large dentary bone. The posterior of the dentary possess con­dylar, coronoid and angular process. Both the jaws pos­sess the codent type of teeth which are having different (Heterodont teeth in mammals) shap­es. Diastema is present in both the jaws because of the absence of canines.
14. Hyostylic jaw suspension. 14. Auto stylic jaw suspension. 14. Auto stylic jaw suspension. 14. Auto stylic jaw suspension. 14. Craniostylic jaw suspension.
Last modified on Tuesday, 11 July 2017 13:22

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    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)
    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
    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.
    • 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.
    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.
    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.
    • 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 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 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
    • 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
    • Uterus
      – Uterine malformations
      – Asherman’s syndrome
      – Tuberculous endometritis
    • Cervix: Sperm antibodies
    • Vagina: Septum
     4. Dysfunction of sexual act: Dyspareunia
    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

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