Pulselessness (Cyanosis Petechial hemorrhages Congestion ) Hanging Strangulation | Autopsy findings in hanging | Suffocation | Traumatic Asphyxia | Drowning | Hydrocution | Immersion syndrome | Postmortem findings in drowning | Tests in drowning death #mbbs #forensicmedicine #medicos

Decomposition of human body , mummification, embalming of human corpse, Thanatopraxia , Forensic entomology #mbbs #forensicmedicine #medicos

Forensic medicine : Early postmortem changes : Eye changes , skin changes , Rigor mortis , Algor mortis , Livor mortis .

Autopsy procedures for forensic medicine students who are perusing there MBBS and right now want to revise forensic medicine. #Forensicmedicine #autopsy #mbbs #medicos

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Rheumatoid Arthritis , Gout , Osteoarthritis, Psudogout . Robbins Pathology Book Podcast. Bone Pathology

Many diseases are caused or influenced by environmental factors. Broadly defined, the term ambient environment encompasses the various outdoor, indoor, and occupa- tional settings in which humans live and work. In each of these settings, the air people breathe, the food and water they consume, and the toxic agents they are exposed to are major determinants of health. Other environmental factors pertain to the individual (“personal environment”) and include tobacco use, alcohol ingestion, therapeutic and “recreational” drug consumption, diet, and the like. It is generally believed that factors in the personal environment have a larger effect on human health than that of the ambient environment, but new threats related to global warming (described later) may change this equation. The term environmental disease refers to disorders caused by exposure to chemical or physical agents in the ambient, workplace, and personal environments, includ- ing diseases of nutritional origin. Environmental diseases are surprisingly common. The International Labor Organi- zation has estimated that work-related injuries and ill- nesses kill more people per year globally than do road accidents and wars combined. Most of these work-related problems are caused by illnesses rather than accidents. The burden of disease in the general population created by nonoccupational exposures to toxic agents is much more difficult to estimate, mostly because of the diversity of agents and the difficulties in measuring the dose and dura- tion of exposures. Whatever the precise numbers, environ- mental diseases are major causes of disability and suffering and constitute a heavy financial burden, particularly in developing countries. Environmental diseases are sometimes the consequence of major disasters, such as the methyl mercury contamina- tion of Minamata Bay in Japan in the 1960s, the leakage of methyl isocyanate gas in Bhopal, India, in 1984, the Cher- nobyl nuclear accident in 1986, the Fukushima nuclear meltdown following the tsunami in 2011, and lead poison- ing resulting from contaminated drinking water in the city of Flint in the United States in 2016. Fortunately, these are unusual and infrequent occurrences. Less dramatic, but much more common, are diseases and injury produced by chronic exposure to relatively low levels of contaminants. It should be noted that a host of factors, including complex interactions between pollutants producing multiplicative effects, as well as the age, genetic predisposition, and dif- ferent tissue sensitivities of exposed persons, create wide variations in individual sensitivity. Disease related to mal- nutrition is even more pervasive. In 2010, it was estimated that 925 million people were malnourished—one in every seven persons worldwide. Children are disproportionately affected by undernutrition, which accounts for more than 50% of childhood mortality worldwide. In this chapter, we first consider the emerging problem of the health effects of climate change. We then discuss the mechanisms of toxicity of chemical and physical agents, and address specific environmental disorders, including those of nutritional origin.

Pathology : Robbins & Cotran : Adaptations of cellular growth & differentiation Hypertrophy| Hyperplasia| Atrophy | Metaplasia Hypertrophy Hypertrophy is an increase in the size of cells resulting in an increase in the size of the organ. In contrast, hyper- plasia (discussed next) is an increase in cell number. Stated another way, in pure hypertrophy there are no new cells, just bigger cells containing increased amounts of structural proteins and organelles. Hyperplasia is an adaptive response in cells capable of replication, whereas hypertro- phy occurs when cells have a limited capacity to divide. Hypertrophy and hyperplasia also can occur together, and obviously both result in an enlarged organ. Hypertrophy can be physiologic or pathologic and is caused either by increased functional demand or by growth factor or hormonal stimulation. Hyperplasia Hyperplasia is an increase in the number of cells in an organ that stems from increased proliferation, either of differentiated cells or, in some instances, less differenti- ated progenitor cells. As discussed earlier, hyperplasia takes place if the tissue contains cell populations capable of replication; it may occur concurrently with hypertrophy and often in response to the same stimuli. Hyperplasia can be physiologic or pathologic; in both situations, cellular proliferation is stimulated by growth factors that are produced by a variety of cell types.Metaplasia Metaplasia is a change in which one adult cell type (epi- thelial or mesenchymal) is replaced by another adult cell type. In this type of cellular adaptation, a cell type sensitive to a particular stress is replaced by another cell type better able to withstand the adverse environment. Metaplasia is thought to arise by the reprogramming of stem cells.Atrophy Atrophy is shrinkage in the size of cells by the loss of cell substance. When a sufficient number of cells are involved, the entire tissue or organ is reduced in size, or atrophic Although atrophic cells may have diminished function, they are not dead. Causes of atrophy include a decreased workload (e.g., immobilization of a limb to permit healing of a fracture), loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, and aging (senile atrophy). Although some of these stimuli are physiologic (e.g., the loss of hormone stimulation in menopause) and others are pathologic (e.g., denervation), the fundamental cellular changes are similar. They represent a retreat by the cell to a smaller size at which survival is still possible; a new equilibrium is achieved between cell size and dimin- ished blood supply, nutrition, or trophic stimulation. Cellular atrophy results from a combination of decreased protein synthesis and increased protein degradation. • Protein synthesis decreases because of reduced meta- bolic activity. • The degradation of cellular proteins occurs mainly by the ubiquitin-proteasome pathway. Nutrient deficiency and disuse may activate ubiquitin ligases, which attach multiple copies of the small peptide ubiquitin to cellular proteins and target them for degradation in protea- somes. This pathway is also thought to be responsible for the accelerated proteolysis seen in a variety of cata- bolic conditions, including the cachexia associated with cancer. • In many situations, atrophy also is associated with autophagy, with resulting increases in the number of autophagic vacuoles. As discussed previously, autoph- agy is the process in which the starved cell eats its own organelles in an attempt to survive.

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The hollow tube inside the neck that starts behind the nose and ends at the top of the trachea (windpipe) and esophagus (the tube that goes to the stomach). The pharynx is about 5 inches long, depending on body size.The pharynx, more commonly known as the throat, is a five cm long tube extending behind the nasal and oral cavities until the voice box (larynx) and the esophagus. Essentially, it forms a continuous muscular passage for air, food, and liquids to travel down from your nose and mouth to your lungs and stomach.Most sensory innervation of the pharynx is derived from the glossopharyngeal nerve, specifically the pharyngeal and tonsillar branches (cranial nerve IX), except for the anterior part of the nasopharynx, which is innervated by a branch of the maxillary nerve (cranial nerve V2) called the pharyngeal nerve.The pharynx is composed of mucous membrane, submucosal connective tissue, glands, lymphoid tissue, muscle and an outermost adventitial coating. The mucous membrane does not possess a muscular layer.The oropharynx and pharynx proper are lined by largely non-keratinizing stratified squamous epithelium. The nasopharynx is mainly lined by ciliated columnar epithelium but stratified squamous epithelium occurs at its lower end where it joins the oropharynx.

The Mendel's laws of inheritance include law of dominance, law of segregation and law of independent assortment. The law of segregation states that every individual possesses two alleles and only one allele is passed on to the offspring.The Mendel's four postulates and laws of inheritance are: (1) Principles of Paired Factors (2) Principle of Dominance(3) Law of Segregation or Law of Purity of Gametes (Mendel's First Law of Inheritance) and (4) Law of Independent Assortment (Mendel's Second Law of Inheritance).

R.H. Whittaker (1969) proposed a Five Kingdom Classification. The kingdoms defined by him were named Monera, Protista, Fungi, Plantae and Animalia. The main criteria for classification used by him include cell structure, body organisation, mode of nutrition, reproduction and phylogenetic relationships. Table 2.1 gives a comparative account of different characteristics of the five kingdoms. The three-domain system has also been proposed that divides the Kingdom Monera into two domains, leaving the remaining eukaryotic kingdoms in the third domain and thereby a six kingdom classification. You will learn about this system in detail at higher classes. Let us look at this five kingdom classification.KINGDOM MONERA Bacteria are the sole members of the Kingdom Monera. They are the most abundant micro-organisms. Bacteria occur almost everywhere. Hundreds of bacteria are present in a handful of soil. They also live in extreme habitats such as hot springs, deserts, snow and deep oceans where very few other life forms can survive. Many of them live in or on other organisms as parasites. Bacteria are grouped under four categories based on their shape: the spherical Coccus (pl.: cocci), the rod-shaped Bacillus (pl.: bacilli), the comma-shaped Vibrium (pl.: vibrio) and the spiral Spirillum (pl.: spirilla).KINGDOM PROTISTA All single-celled eukaryotes are placed under Protista, but the boundaries of this kingdom are not well defined. What may be ‘a photosynthetic protistan’ to one biologist may be ‘a plant’ to another. In this book we include Chrysophytes, Dinoflagellates, Euglenoids, Slime moulds and Protozoans under Protista. Members of Protista are primarily aquatic. This kingdom forms a link with the others dealing with plants, animals and fungi. Being eukaryotes, the protistan cell body contains a well defined nucleus and other membrane-bound organelles. Some have flagella or cilia. Protists reproduce asexually and sexually by a process involving cell fusion and zygote formation. Amoeboid protozoans: These organisms live in fresh water, sea water or moist soil. They move and capture their prey by putting out pseudopodia (false feet) as in Amoeba. Marine forms have silica shells on their surface. Some of them such as Entamoeba are parasites. Flagellated protozoans: The members of this group are either free-living or parasitic. They have flagella. The parasitic forms cause diaseases such as sleeping sickness. Example: Trypanosoma. Ciliated protozoans: These are aquatic, actively moving organisms because of the presence of thousands of cilia. They have a cavity (gullet) that opens to the outside of the cell surface. The coordinated movement of rows of cilia causes the water laden with food to be steered into the gullet. Example: Paramoecium (Figure 2.4d). Sporozoans: This includes diverse organisms that have an infectious spore-like stage in their life cycle. The most notorious is Plasmodium (malarial parasite) which causes malaria, a disease which has a staggering effect on human population. KINGDOM FUNGI The fungi constitute a unique kingdom of heterotrophic organisms. They show a great diversity in morphology and habitat. You must have seen fungi on a moist bread and rotten fruits. The common mushroom you eat and toadstools are also fungi. White spots seen on mustard leaves are due to a parasitic fungus. Some unicellular fungi, e.g., yeast are used to make bread and beer. Other fungi cause diseases in plants and animals; wheat rust-causing Puccinia is an important example. Some are the source of antibiotics, e.g., Penicillium. Fungi are cosmopolitan and occur in air, water, soil and on animals and plants. They prefer to grow in warm and humid places. Have you ever wondered why we keep food in the refrigerator ? Yes, it is to prevent food from going bad due to bacterial or fungal infections. With the exception of yeasts which are unicellular, fungi are filamentous.Virus.

Blood groups and genetic linkage Red cell groups act as markers (inherited characteristics) for genes present on chromosomes, which are responsible for their expression. The site of a particular genetic system on a chromosome is called a locus. Each locus may be the site of several alleles (alternative genes). In an ordinary cell of the human body, there are 46 chromosomes arranged in 23 pairs, 22 pairs of which are autosomes (chromosomes other than sex chromosomes), with the remaining pair being the sex chromosomes, designated XX in females and XY in males. The loci of the blood group systems are on the autosomes, except for Xg, which is unique among the blood groups in being located on the X chromosome. Genes carried by the X chromosome are said to be sex-linked. Since the blood groups are inherited in a regular fashion, they can be used as genetic markers in family studies to investigate whether any two particular loci are sited on the same chromosome—i.e., are linked. The genes sited at loci on the same chromosome travel together from parent to child, and, if the loci are close together, the genes will rarely be separated. Loci that are farther apart can be separated by recombination. This happens when material is exchanged between homologous chromosomes (pair of chromosomes) by crossing over during the process of cell division (mitosis). The reproductive cells contain half the number of chromosomes of the rest of the body; ova carry an X chromosome and spermatozoa an X or a Y. The characteristic number of 46 chromosomes is restored at fertilization. In a classical pedigree linkage study, all the members of a family are examined for a test character and for evidence of the nonindependent segregation of pairs of characters. The results must be assessed statistically to determine linkage. Individual chromosomes are identified by the banding patterns revealed by different staining techniques. Segments of chromosomes or chromosomes that are aberrant in number and morphology may be precisely identified. Other methods for localizing markers on chromosomes include somatic cell hybridization (cell culture with alignment of single strands of RNA and DNA) and use of DNA probes (strands of radiolabeled DNA). These methods are useful in classical linkage studies to locate blood group loci. The loci for many red cell groups have been found on chromosomes and in many cases have been further localized on a particular chromosome.In some of the blood group systems, the amount of antigen produced depends on the genetic constitution. The ABO blood group gene codes for a specific carbohydrate transferase enzyme that catalyzes the addition of specific sugars onto a precursor substance. As a new sugar is added, a new antigen is produced. Antigens in the MNSs blood system are the products of genes that control terminal amino acid sequence. The amount of antigen present may depend on the amount of gene product inherited or on the activity of the gene product (i.e., transferase). The red cells of a person whose genotype is MM show more M antigen than do MN red cells. In the case of ABO, the same mechanism may also play a role in antigen expression, but specific activity of the inherited transferase may be more important. The amount of antigen produced can also be influenced by the position of the genes. Such effects within a genetic complex can be due to determinants on the same chromosome—they are then said to be cis—or to determinants on the opposite chromosome of a chromosome pair—trans. In the Rh combination cdE/cde, more E antigen is produced than in the combination cDE/cde. This may be due to the suppressor effect of D on E. An example of suppression in the trans situation is that more C antigen is detectable on the red cells from CDe/cde donors than on those of CDe/cDE people. The inheritance of the Rh system probably depends on the existence of operator genes, which turn the activity of closely linked structural genes on or off.

ANTERIOR TRIANGLE OF THE NECK The anterior triangle of the neck is bounded anteriorly by the median line of the neck and posteriorly by the anterior margin of sternocleidomastoid. Its base is the inferior border of the mandible and its projection to the mastoid process, and its apex is at the manubrium sterni. It can be subdivided into suprahyoid and infrahyoid areas above and below the hyoid bone, and into digastric, submental, muscular and carotid triangles by the passage of digastric and omohyoid across the anterior triangle (see Fig. 29.5). Digastric triangle The digastric triangle is bordered above by the lower border of the mandible and its projection to the mastoid process, posteroinferiorly by the posterior belly of digastric and by stylohyoid, and anteroinferiorly by the anterior belly of digastric. It is covered by the skin, superficial fascia, platysma and deep fascia, which contain branches of the facial and transverse cutaneous cervical nerves. Its floor is formed by mylohyoid and hyoglossus. The anterior region of the digastric triangle contains the submandibular gland, which has the facial vein superficial to it and the facial artery deep to it. The submental and mylohyoid arteries and nerves lie on mylohyoid. The submandibular lymph nodes are variably related to the submandibular gland. The posterior region of the digastric triangle contains the lower part of the parotid gland. The external carotid artery, passing deep to stylohyoid, curves above the muscle, and overlaps its superficial surface as it ascends deep to the parotid gland before entering it. The internal carotid artery, internal jugular vein and vagus nerve lie deeper and are separated from the external carotid artery by styloglossus,stylopharyngeus and the glossopharyngeal nerve.Submental triangle The single submental triangle is demarcated by the anterior bellies of both digastric muscles. Its apex is at the chin, its base is the body of the hyoid bone and its floor is formed by both mylohyoid muscles. It contains lymph nodes and small veins that unite to form the anterior jugular vein. The structures within the digastric and submental triangles are described in more detail with the floor of the mouth. Muscular triangle The muscular triangle is bounded anteriorly by the median line of the neck from the hyoid bone to the sternum, inferoposteriorly by the anterior margin of sternocleidomastoid and posterosuperiorly by the superior belly of omohyoid. The triangle contains omohyoid, sternohyoid, sternothyroid and thyrohyoid. Carotid triangle The carotid triangle is limited posteriorly by sternocleidomastoid, anteroinferiorly by the superior belly of omohyoid and superiorly by stylohyoid and the posterior belly of digastric. In the living (except the obese), the triangle is usually a small visible triangular depression, sometimes best seen with the head and cervical vertebral column slightly extended and the head contralaterally rotated. The carotid triangle is covered by the skin, superficial fascia, platysma and deep fascia containing branches of the facial and cutaneous cervical nerves. The hyoid bone forms its anterior angle and adjacent floor; it can be located on simple inspection and verified by palpation. Parts of thyrohyoid, hyoglossus and inferior and middle pharyngeal constrictor muscles form its floor. The carotid triangle contains the upper part of the common carotid artery and its division into external and internal carotid arteries. Overlapped by the anterior margin of sternocleidomastoid, the external carotid artery is first anteromedial, then anterior to the internal carotid artery. Branches of the external carotid artery are encountered in the carotid triangle. Thus the superior thyroid artery runs anteroinferiorly, the lingual artery anteriorly with a characteristic upward loop, facial anterosuperiorly,occipital,post.auricular,maxillary.

anteriorly in the lower neck, level with the fifth cervical to the first thoracic vertebrae (see Fig. 29.17). It is ensheathed by the pretracheal layer of deep cervical fascia and consists of right and left lobes connected by a narrow, median isthmus. It usually weighs 25 g but this varies. The gland is slightly heavier in females and enlarges during menstruation and pregnancy. Estimation of the size of the thyroid gland is clinically important in the evaluation and management of thyroid disorders and can be achieved non-invasively by means of diagnostic ultrasound. Mean thyroid volume increases with age (Chanoine et al 1991). No significant difference in thyroid gland volume has been observed between males and females from 8 months to 15 years. The lobes of the thyroid gland are approximately conical. Their ascending apices diverge laterally to the level of the oblique lines on the laminae of the thyroid cartilage, and their bases are level with the fourth or fifth tracheal cartilages. Each lobe is usually 5 cm long, its greatest transverse and anteroposterior extents being 3 cm and 2 cm, respectively. The posteromedial aspects of the lobes are attached to the side of the cricoid cartilage by a lateral thyroid ligament (Berry’s ligament). The isthmus connects the lower parts of the two lobes, although occasionally it may be absent. It measures 1.25 cm transversely and vertically, and is usually anterior to the second and third tracheal cartilages, although it can be higher or even sometimes lower because its site and size vary greatly. A conical pyramidal lobe often ascends towards the hyoid bone from the isthmus or the adjacent part of either lobe (more often the left). It is occasionally detached or in two or more parts. A fibrous or fibromuscular band, the levator of the thyroid gland, musculus levator glandulae thyroideae, sometimes descends from the body of the hyoid to the isthmus or pyramidal lobe. For further reading, see Mohebati and Shaha (2012). Ectopic thyroid tissue is rare but may be found around the course of the thyroglossal duct or laterally in the neck, as well as in distant places such as the tongue (lingual thyroid), mediastinum and the subdiaphragmatic organs (Noussios et al 2011). The most frequent location of ectopic thyroid tissue is at the base of the tongue, in particular at the region of the foramen caecum; often it is the only thyroid tissue present. Small, detached masses of thyroid tissue may occur above the lobes or isthmus as accessory thyroid glands. Vestiges of the thyroglossal duct may persist between the isthmus and the foramen caecum of the tongue, sometimes as accessory nodules or cysts of thyroid tissue near the midline or even in the tongue, where they are called thyroglossal duct cyst.PARATHYROID GLANDS The parathyroid glands are small, yellowish-brown, ovoid or lentiform structures, usually lying between the posterior lobar borders of the thyroid gland and its capsule. They are commonly 6 mm long, 3–4 mm Neck 472SECTION 4 across and 1–2 mm from back to front, each weighing about 50 mg. Typically, there are two on each side, superior and inferior, but there may be more or there may be only three or many minute parathyroid islands scattered in connective tissue near the usual sites. Very occasionally, an occult gland may follow a blood vessel into a groove on the surface of the thyroid. Normally, the inferior parathyroids migrate only to the inferior thyroid poles, but they may descend with the thymus into the thorax or they may be sessile and remain above their normal level near the carotid bifurcation. The anastomotic connection between the superior and inferior thyroid arteries that occurs along the posterior border of the thyroid gland usually passes very close to the parathyroids, and is a useful aid to their identification. The superior parathyroid glands are more constant.

External acoustic meatus The temporal bone contains the bony (osseous) part of the external acoustic meatus. Ossification The four temporal components ossify independently (Fig. 37.2). The squamous part is ossified in a sheet of condensed mesenchyme from a single centre near the zygomatic roots, which appears in the seventh or eighth week in utero. The petromastoid part has several centres that appear in the cartilaginous otic capsule during the fifth month; as many as 14 have been described. These centres vary in order of appearance. Several are small and inconstant, soon fusing with others. The otic capsule is almost fully ossified by the end of the sixth month. The tympanic part is also ossified in mesenchyme from a centre identifiable about the third month; at birth, it is an incomplete tympanic ring, deficient above, its concavity grooved by a tympanic sulcus for the tympanic membrane. The malleolar sulcus for the anterior malleolar process, chorda tympani and anterior tympanic artery inclines obliquely downwards and forwards across the medial aspect of the anterior part The superior border of the mastoid part is thick and serrated for articulation with the mastoid angle of the parietal bone. The posterior border is also serrated and articulates with the inferior border of the occipital bone between its lateral angle and jugular process. The mastoid element is fused with the descending process of the squamous part; below, it appears in the posterior wall of the tympanic cavity. Petrous part The petrous part is a mass of bone that is wedged between the sphenoid and occipital bones in the cranial base; it contains the labyrinth. It is inclined superiorly and anteromedially, and has a base, apex, three surfaces (anterior, posterior and inferior) and three borders (superior, posterior and anterior). The base would correspond to the part that lies on the base of the skull and is separated from the squamous part by a suture. However, this suture disappears soon after birth. The subsequent development of the mastoid processes means that the precise boundaries of the base are no longer identifiable. The apex, blunt and irregular, is angled between the posterior border of the greater wing of the sphenoid and the basilar part of the occipital bone. It contains the anterior opening of the carotid canal and limits the foramen lacerum posterolaterally. The anterior surface contributes to the floor of the middle cranial fossa (Ch. 28) and is continuous with the cerebral surface of the squamous part (although the petrosquamosal suture often persists late in life). The whole surface is adapted to the inferior temporal gyrus. Behind the apex is a trigeminal impression for the trigeminal ganglion. Bone anterolateral to this impression roofs the anterior part of the carotid canal but is often deficient. A ridge separates the trigeminal impression from another hollow behind, which partly roofs the internal acoustic meatus and cochlea. This, in turn, is limited behind by the arcuate eminence, which is raised by the superior (anterior) semicircular canal but is not necessarily directly over it. Laterally, the anterior surface roofs the vestibule and, partly, the facial canal. Between the squamous part laterally and the arcuate eminence and the hollows just described medially, the anterior surface is formed by the tegmen tympani, a thin plate of bone that forms the roof of the mastoid antrum, and extends forwards above the tympanic cavity and the canal for tensor tympani. The lateral margin of the tegmen tympani meets the squamous part at the petrosquamosal suture, turning down in front as the lateral wall of the canal for tensor tympani and the osseous part of the pharyngotympanic tube; its lower edge is in the squamotympanic fissure. Anteriorly, the tegmen bears a narrow groove related to the greater petrosal nerve (which passes pos.

SCLERA The sclera accounts for approximately 93% of the outer coat of the eye. Anteriorly, it is continuous with the cornea at the corneoscleral junction (see Fig. 42.1). It is punctured by a number of foramina containing nerves and blood vessels, most notably the optic foramen, which lies 3 mm medial to the midline and 1 mm below the horizontal, and houses the optic nerve. Smaller openings contain anterior ciliary arteries that penetrate anteriorly, vortex veins that cross the sclera equatorially, and the long and short ciliary nerves and arteries that enter posteriorly. There is considerable individual variation in scleral dimensions. The sclera is thickest at the posterior pole (approximately 1 mm) and decreases anteriorly, reaching a minimum equatorially at about half this thickness. It also thins approaching the optic nerve. The sclera is thinner when the eye is elongated in myopia. The external surface of the sclera is covered by a delicate episcleral lamina of loose fibrovascular tissue, which contains sparse blood vessels and is in contact with the inner surface of the fascial sheath of the eyeball. Anteriorly, the external scleral surface is covered by conjunctiva, which is reflected on to it from the posterior surfaces of the eyelids. The scleral internal surface adjacent to the choroid is attached to it by a delicate fibrous layer, the suprachoroid lamina, which contains numerous fibroblasts and melanocytes. Anteriorly, the inner sclera is attached to the ciliary body by the lamina supraciliaris. Posteriorly, the sclera is pierced by the optic nerve. Here, the outer half of the sclera turns back to become continuous with the dura mater, while the inner half is modified to form a perforated plate, the lamina cribrosa sclerae. The optic nerve fascicles pass through these minute orifices, while the central retinal artery and vein pass through a larger, central aperture. The lamina cribrosa sclerae is the weakest part of the sclera and bulges outwards (a cupped disc) when intraocular pressure is raised chronically, as in glaucoma. Like the cornea, the scleral stroma is composed mainly of densely packed collagen embedded in a matrix of proteoglycans, which are mixed with occasional elastic fibres and fibroblasts. However, in contrast to the cornea, scleral collagen fibrils show a large variation in diameter and spacing, and the lamellae branch and interlace extensively. This arrangement of fibres results in increased light scatter, which is responsible for the opaque, dull-white appearance of the sclera, and also imparts a high tensile strength to the sclera to resist the pull of the extraocular muscles and contain the intraocular pressure. Collagen fibre bundles are arranged circumferentially around the optic disc and the orifices of the lamina cribrosa. The fibres of the tendons of the recti intersect scleral fibres at right angles at their attachments, and then interlace deeper in the sclera. Collagen fibres of the scleral spur are orientated in a circular fashion, and there is an increased incidence of elastic fibres here (Figs 42.2–42.3A). Although the sclera acts as a conduit for blood vessels, scleral vessels are few and mainly disposed in the episcleral lamina, especially close to the limbus. Its nerve supply is surprisingly rich, accounting for the intense pain associated with scleral inflammation (Watson and Young 2004). Scleral development is under active regulation to ensure an eye of the correct axial length to produce a focused image (Wallman and Winawer 2004). Filtration angle and aqueous drainage Aqueous humour is produced by the ciliary epithelium; it passes through the pupil and circulates within the anterior chamber, supplying the avascular cornea and lens with nutrients and removing metabolic waste products. It drains from the eye mainly through the trabecular meshwork into the canal of Schlemm.

Horner’s syndrome Any condition or injury that destroys the sympathetic trunk ascending from the thorax through the neck into the face results in Horner’s syndrome, characterized by a drooping eyelid (ptosis), sunken globe (enophthalmos), narrow palpebral fissure, contracted pupil (meiosis), vasodilation and lack of thermal sweating (anhydrosis) on the affected side. Classically, this is seen in patients with bronchial carcinomas that have invaded the sympathetic trunk and is also a recognized complication of cervical sympathectomy or a radical neck dissection. Avulsion of the first thoracic nerve from the spinal cord may be diagnosed by development of the syndrome after closed traction lesion of the supraclavicular brachial plexus. Congenital Horner’s syndrome has been reported in association with ipsilateral internal carotid artery agenesis (Fons et al 2009). Special features of congenital Horner’s syndrome are iris heterochromia, a difference in colour between the two eyes that results from interference with melanocyte pigmentation of the iris by a lack of sympathetic stimulation during development, and unilateral straight hair.