the tissue, located in the anterior chamber of the eye at the angle between the cornea and iris, that consists of a group of tiny canals through which aqueous fluid drains into *Schlemm’s canal and exits the anterior chamber.
Position and size The spleen lies behind the stomach, high up on the left side of the abdomen, and corresponds to the position of the ninth, tenth and 11th ribs, from which it is separated by the diaphragm. It is a soft, highly vascular, plum-coloured organ, and has a smooth surface. It is usually about 12·5–15 cm (5–6 inches) in length, and weighs about 170 grams or more. In diseased conditions the organ may reach a weight of 8–9 kg.
Structure The spleen is enveloped by peritoneal membrane beneath which is a strong elastic tunic, composed partly of ?brous tissue
containing many elastic ?bres, and partly of unstriped muscle. This elastic coat allows of the free expansion and contraction of the organ according to the varying amount of blood present in it. From the inner surface of the membrane, ?brous partitions known as trabeculae run down into the substance and form a network in which the dark spleen pulp is contained. The pulp consists of delicate connective-tissue ?bres passing between the various trabeculae, and of white and red blood cells lying in this meshwork. The spleen is very vascular and venous blood leaves by the splenic vein and then enters the portal vein from the liver. There are also numerous lymphatics in the organ, which run in the trabeculae or surround the veins.
Functions The organ produces lymphocytes (see LYMPHOCYTE) and acts as a reservoir of red blood cells for use in emergencies. It is also one of the sites for the manufacture of red blood cells in the fetus, but not after birth. Useless or worn-out red and white blood cells and blood PLATELETS are broken up by this organ. This results in the production of BILIRUBIN, which is conveyed to the liver, and of iron, which is used in the bone marrow for the production of new red blood cells.... spleen
for the muscles and protects certain body organs. Bone consists of several layers: a thin outer covering (the periosteum), which contains blood vessels and nerves; an inner shell of hard (compact or cortical) bone composed of columns of bone cells (osteoclasts and osteoblasts), each with a central hollow (haversian canal) that is important for the nutrition, growth, and repair of the bone; and a central, mesh-like structure (known as spongy, cancellous, or trabecular bone). The cavity in the centre of some bones, and the spaces in spongy bone, contain bone marrow.
Bone is continuously reabsorbed by osteoclasts and replaced by osteoblasts. Osteoblasts encourage deposition of calcium phosphate on the protein framework of the bone, and osteoclasts remove it. The actions of these cells are controlled by hormones, which also maintain the calcium level in the blood.
At birth, many bones consist mainly of cartilage, which ossifies later (see ossification).
The epiphyses (growing ends of the long bones) are separated from the bone shaft (diaphysis) by the epiphyseal plate.
Some bones, such as certain skull bones, do not develop from cartilage and are known as membranous bones.... bone
Bone fractures These occur when there is a break in the continuity of the bone. This happens either as a result of violence or because the bone is unhealthy and unable to withstand normal stresses.
SIMPLE FRACTURES Fractures where the skin remains intact or merely grazed. COMPOUND FRACTURES have at least one wound which is in communication with the fracture, meaning that bacteria can enter the fracture site and cause infection. A compound fracture is also more serious than a simple fracture because there is greater potential for blood loss. Compound fractures usually need hospital admission, antibiotics and careful reduction of the fracture. Debridement (cleaning and excising dead tissue) in a sterile theatre may also be necessary.
The type of fracture depends on the force which has caused it. Direct violence occurs when an object hits the bone, often causing a transverse break – which means the break runs horizontally across the bone. Indirect violence occurs when a twisting injury to the ankle, for example, breaks the calf-bone (the tibia) higher up. The break may be more oblique. A fall on the outstretched hand may cause a break at the wrist, in the humerus or at the collar-bone depending on the force of impact and age of the person. FATIGUE FRACTURES These occur after the bone has been under recurrent stress. A typical example is the march fracture of the second toe, from which army recruits suffer after long marches. PATHOLOGICAL FRACTURES These occur in bone which is already diseased – for example, by osteoporosis (see below) in post-menopausal women. Such fractures are typically crush fractures of the vertebrae, fractures of the neck of the femur, and COLLES’ FRACTURE (of the wrist). Pathological fractures also occur in bone which has secondary-tumour deposits. GREENSTICK FRACTURES These occur in young children whose bones are soft and bend, rather than break, in response to stress. The bone tends to buckle on the side opposite to the force. Greenstick fractures heal quickly but still need any deformity corrected and plaster of Paris to maintain the correction. COMPLICATED FRACTURES These involve damage to important soft tissue such as nerves, blood vessels or internal organs. In these cases the soft-tissue damage needs as much attention as the fracture site. COMMINUTED FRACTURES A fracture with more than two fragments. It usually means that the injury was more violent and that there is more risk of damage to vessels and nerves. These fractures are unstable and take longer to unite. Rehabilitation tends to be protracted. DEPRESSED FRACTURES Most commonly found in skull fractures. A fragment of bone is forced inwards so that it lies lower than the level of the bone surrounding it. It may damage the brain beneath it.
HAIR-LINE FRACTURES These occur when the bone is broken but the force has not been severe enough to cause visible displacement. These fractures may be easily missed. Symptoms and signs The fracture site is usually painful, swollen and deformed. There is asymmetry of contour between limbs. The limb is held uselessly. If the fracture is in the upper
limb, the arm is usually supported by the patient; if it is in the lower limb then the patient is not able to bear weight on it. The limb may appear short because of muscle spasm.
Examination may reveal crepitus – a bony grating – at the fracture site. The diagnosis is con?rmed by radiography.
Treatment Healing of fractures (union) begins with the bruise around the fracture being resorbed and new bone-producing cells and blood vessels migrating into the area. Within a couple of days they form a bridge of primitive bone across the fracture. This is called callus.
The callus is replaced by woven bone which gradually matures as the new bone remodels itself. Treatment of fractures is designed to ensure that this process occurs with minimal residual deformity to the bone involved.
Treatment is initially to relieve pain and may involve temporary splinting of the fracture site. Reducing the fracture means restoring the bones to their normal position; this is particularly important at the site of joints where any small displacement may limit movement considerably.
with plaster of Paris. If closed traction does not work, then open reduction of the fracture may
be needed. This may involve ?xing the fracture with internal-?xation methods, using metal plates, wires or screws to hold the fracture site in a rigid position with the two ends closely opposed. This allows early mobilisation after fractures and speeds return to normal use.
External ?xators are usually metal devices applied to the outside of the limb to support the fracture site. They are useful in compound fractures where internal ?xators are at risk of becoming infected.
Consolidation of a fracture means that repair is complete. The time taken for this depends on the age of the patient, the bone and the type of fracture. A wrist fracture may take six weeks, a femoral fracture three to six months in an adult.
Complications of fractures are fairly common. In non-union, the fracture does not unite
– usually because there has been too much mobility around the fracture site. Treatment may involve internal ?xation (see above). Malunion means that the bone has healed with a persistent deformity and the adjacent joint may then develop early osteoarthritis.
Myositis ossi?cans may occur at the elbow after a fracture. A big mass of calci?ed material develops around the fracture site which restricts elbow movements. Late surgical removal (after 6–12 months) is recommended.
Fractured neck of FEMUR typically affects elderly women after a trivial injury. The bone is usually osteoporotic. The leg appears short and is rotated outwards. Usually the patient is unable to put any weight on the affected leg and is in extreme pain. The fractures are classi?ed according to where they occur:
subcapital where the neck joins the head of the femur.
intertrochanteric through the trochanter.
subtrochanteric transversely through the upper end of the femur (rare). Most of these fractures of the neck of femur
need ?xing by metal plates or hip replacements, as immobility in this age group has a mortality of nearly 100 per cent. Fractures of the femur shaft are usually the result of severe trauma such as a road accident. Treatment may be conservative or operative.
In fractures of the SPINAL COLUMN, mere damage to the bone – as in the case of the so-called compression fracture, in which there is no damage to the spinal cord – is not necessarily serious. If, however, the spinal cord is damaged, as in the so-called fracture dislocation, the accident may be a very serious one, the usual result being paralysis of the parts of the body below the level of the injury. Therefore the higher up the spine is fractured, the more serious the consequences. The injured person should not be moved until skilled assistance is at hand; or, if he or she must be removed, this should be done on a rigid shutter or door, not on a canvas stretcher or rug, and there should be no lifting which necessitates bending of the back. In such an injury an operation designed to remove a displaced piece of bone and free the spinal cord from pressure is often necessary and successful in relieving the paralysis. DISLOCATIONS or SUBLUXATION of the spine are not uncommon in certain sports, particularly rugby. Anyone who has had such an injury in the cervical spine (i.e. in the neck) should be strongly advised not to return to any form of body-contact or vehicular sport.
Simple ?ssured fractures and depressed fractures of the skull often follow blows or falls on the head, and may not be serious, though there is always a risk of damage which is potentially serious to the brain at the same time.
Compound fractures may result in infection within the skull, and if the skull is extensively broken and depressed, surgery is usually required to check any intercranial bleeding or to relieve pressure on the brain.
The lower jaw is often fractured by a blow on the face. There is generally bleeding from the mouth, the gum being torn. Also there are pain and grating sensations on chewing, and unevenness in the line of the teeth. The treatment is simple, the line of teeth in the upper jaw forming a splint against which the lower jaw is bound, with the mouth closed.
Congenital diseases These are rare but may produce certain types of dwar?sm or a susceptibility to fractures (osteogenesis imperfecta).
Infection of bone (osteomyelitis) may occur after an open fracture, or in newborn babies with SEPTICAEMIA. Once established it is very di?cult to eradicate. The bacteria appear capable of lying dormant in the bone and are not easily destroyed with antibiotics so that prolonged treatment is required, as might be surgical drainage, exploration or removal of dead bone. The infection may become chronic or recur.
Osteomalacia (rickets) is the loss of mineralisation of the bone rather than simple loss of bone mass. It is caused by vitamin D de?ciency and is probably the most important bone disease in the developing world. In sunlight the skin can synthesise vitamin D (see APPENDIX 5: VITAMINS), but normally rickets is caused by a poor diet, or by a failure to absorb food normally (malabsorbtion). In rare cases vitamin D cannot be converted to its active state due to the congenital lack of the speci?c enzymes and the rickets will fail to respond to treatment with vitamin D. Malfunction of the parathyroid gland or of the kidneys can disturb the dynamic equilibrium of calcium and phosphate in the body and severely deplete the bone of its stores of both calcium and phosphate.
Osteoporosis A metabolic bone disease resulting from low bone mass (osteopenia) due to excessive bone resorption. Su?erers are prone to bone fractures from relatively minor trauma. With bone densitometry it is now possible to determine individuals’ risk of osteoporosis and monitor their response to treatment.
By the age of 90 one in two women and one in six men are likely to sustain an osteoporosis-related fracture. The incidence of fractures is increasing more than would be expected from the ageing of the population, which may re?ect changing patterns of exercise or diet.
Osteoporosis may be classi?ed as primary or secondary. Primary consists of type 1 osteoporosis, due to accelerated trabecular bone loss, probably as a result of OESTROGENS de?ciency. This typically leads to crush fractures of vertebral bodies and fractures of the distal forearm in women in their 60s and 70s. Type 2 osteoporosis, by contrast, results from the slower age-related cortical and travecular bone loss that occurs in both sexes. It typically leads to fractures of the proximal femur in elderly people.
Secondary osteoporosis accounts for about 20 per cent of cases in women and 40 per cent of cases in men. Subgroups include endocrine (thyrotoxicosis – see under THYROID GLAND, DISEASES OF, primary HYPERPARATHYROIDISM, CUSHING’S SYNDROME and HYPOGONADISM); gastrointestinal (malabsorption syndrome, e.g. COELIAC DISEASE, or liver disease, e.g. primary biliary CIRRHOSIS); rheumatological (RHEUMATOID ARTHRITIS or ANKYLOSING SPONDYLITIS); malignancy (multiple MYELOMA or metastatic CARCINOMA); and drugs (CORTICOSTEROIDS, HEPARIN). Additional risk factors for osteoporosis include smoking, high alcohol intake, physical inactivity, thin body-type and heredity.
Individuals at risk of osteopenia, or with an osteoporosis-related fracture, need investigation with spinal radiography and bone densitometry. A small fall in bone density results in a large increase in the risk of fracture, which has important implications for preventing and treating osteoporosis.
Treatment Antiresorptive drugs: hormone replacement therapy – also valuable in treating menopausal symptoms; treatment for at least ?ve years is necessary, and prolonged use may increase risk of breast cancer. Cyclical oral administration of disodium etidronate – one of the bisphosphonate group of drugs – with calcium carbonate is also used (poor absorption means the etidronate must be taken on an empty stomach). Calcitonin – currently available as a subcutaneous injection; a nasal preparation with better tolerance is being developed. Calcium (1,000 mg daily) seems useful in older patients, although probably ine?ective in perimenopausal women, and it is a safe preparation. Vitamin D and calcium – recent evidence suggests value for elderly patients. Anabolic steroids, though androgenic side-effects (masculinisation) make these unacceptable for most women.
With established osteoporosis, the aim of treatment is to relieve pain (with analgesics and physical measures, e.g. lumbar support) and reduce the risk of further fractures: improvement of bone mass, the prevention of falls, and general physiotherapy, encouraging a healthier lifestyle with more daily exercise.
Further information is available from the National Osteoporosis Society.
Paget’s disease (see also separate entry) is a common disease of bone in the elderly, caused by overactivity of the osteoclasts (cells concerned with removal of old bone, before new bone is laid down by osteoblasts). The bone affected thickens and bows and may become painful. Treatment with calcitonin and bisphosphonates may slow down the osteoclasts, and so hinder the course of the disease, but there is no cure.
If bone loses its blood supply (avascular necrosis) it eventually fractures or collapses. If the blood supply does not return, bone’s normal capacity for healing is severely impaired.
For the following diseases see separate articles: RICKETS; ACROMEGALY; OSTEOMALACIA; OSTEOGENESIS IMPERFECTA.
Tumours of bone These can be benign (non-cancerous) or malignant (cancerous). Primary bone tumours are rare, but secondaries from carcinoma of the breast, prostate and kidneys are relatively common. They may form cavities in a bone, weakening it until it breaks under normal load (a pathological fracture). The bone eroded away by the tumour may also cause problems by causing high levels of calcium in the plasma.
EWING’S TUMOUR is a malignant growth affecting long bones, particularly the tibia (calfbone). The presenting symptoms are a throbbing pain in the limb and a high temperature. Treatment is combined surgery, radiotherapy and chemotherapy.
MYELOMA is a generalised malignant disease of blood cells which produces tumours in bones which have red bone marrow, such as the skull and trunk bones. These tumours can cause pathological fractures.
OSTEOID OSTEOMA is a harmless small growth which can occur in any bone. Its pain is typically removed by aspirin.
OSTEOSARCOMA is a malignant tumour of bone with a peak incidence between the ages of ten and 20. It typically involves the knees, causing a warm tender swelling. Removal of the growth with bone conservation techniques can often replace amputation as the de?nitive treatment. Chemotherapy can improve long-term survival.... bone, disorders of
The three-stage process of coagulation is complex, involving many di?erent substances. There are two cascading pathways of biochemical reactions for activating coagulation of blood. The extrinsic pathway is the main physiological mechanism, which is triggered when blood vessels are damaged, usually by trauma or surgery. The intrinsic pathway is activated by internal disruption of the wall of a blood vessel. The basic pattern is broadly the same for both and is summarised simply as follows:
prothrombin + calcium + thromboplastin
thrombin + ?brinogen
?brin
Prothrombin and calcium are normally present in the blood. Thromboplastin is an enzyme which is normally found in the blood platelets and in tissue cells. When bleeding occurs from a blood vessel, there is always some damage to tissue cells and to the blood platelets. As a result of this damage, thromboplastin is released and comes into contact with the prothrombin and calcium in the blood. In the presence of thromboplastin and calcium, prothrombin is converted into thrombin, which in turn interacts with ?brinogen – a protein always present in the blood – to form ?brin. Fibrin consists of needle-shaped crystals which, with the assistance of the blood platelets, form a ?ne network in which the blood corpuscles become enmeshed. This meshwork, or CLOT as it is known, gradually retracts until it forms a tight mass which, unless the tissue injury is very severe or a major artery has been damaged, prevents any further bleeding. It will thus be seen that clotting, or coagulation, does not occur in the healthy blood vessel because there is no thromboplastin present. There is now evidence suggesting that there is an anti-thrombin substance present in the blood in small amounts, and that this substance antagonises any small amounts of thrombin that may be formed as a result of small amounts of thromboplastin being released.
The clotting or coagulation time is the time taken for blood to clot and can be measured under controlled conditions to ensure that it is normal (3–8 minutes). In certain diseases – HAEMOPHILIA, for example – clotting time is greatly extended and the danger of serious haemorrhage enhanced.... coagulation
The outer coat consists of the sclera and the cornea; their junction is called the limbus. SCLERA This is white, opaque, and constitutes the posterior ?ve-sixths of the outer coat. It is made of dense ?brous tissue. The sclera is visible anteriorly, between the eyelids, as the ‘white of the eye’. Posteriorly and anteriorly it is covered by Tenons capsule, which in turn is covered by transparent conjunctiva. There is a hole in the sclera through which nerve ?bres from the retina leave the eye in the optic nerve. Other smaller nerve ?bres and blood vessels also pass through the sclera at di?erent points. CORNEA This constitutes the transparent, colourless anterior one-sixth of the eye. It is transparent in order to allow light into the eye and is more steeply curved than the sclera. Viewed from in front, the cornea is roughly circular. Most of the focusing power of the eye is provided by the cornea (the lens acts as the ‘?ne adjustment’). It has an outer epithelium, a central stroma and an inner endothelium. The cornea is supplied with very ?ne nerve ?bres which make it exquisitely sensitive to pain. The central cornea has no blood supply – it relies mainly on aqueous humour for nutrition. Blood vessels and large nerve ?bres in the cornea would prevent light from entering the eye. LIMBUS is the junction between cornea and sclera. It contains the trabecular meshwork, a sieve-like structure through which aqueous humour leaves the eye.
The middle coat (uveal tract) consists of the choroid, ciliary body and iris. CHOROID A highly vascular sheet of tissue lining the posterior two-thirds of the sclera. The network of vessels provides the blood supply for the outer half of the retina. The blood supply of the choroid is derived from numerous ciliary vessels which pierce the sclera in front and behind. CILIARY BODY A ring of tissue extending 6 mm back from the anterior limitation of the sclera. The various muscles of the ciliary body by their contractions and relaxations are responsible for changing the shape of the lens during ACCOMMODATION. The ciliary body is lined by cells that secrete aqueous humour. Posteriorly, the ciliary body is continuous with the choroid; anteriorly it is continuous with the iris. IRIS A ?attened muscular diaphragm that is attached at its periphery to the ciliary body, and has a round central opening – the pupil. By contraction and relaxation of the muscles of the iris, the pupil can be dilated or constricted (dilated in the dark or when aroused; constricted in bright light and for close work). The iris forms a partial division between the anterior chamber and the posterior chamber of the eye. It lies in front of the lens and forms the back wall of the anterior chamber. The iris is visible from in front, through the transparent cornea, as the ‘coloured part of the eye’. The amount and distribution of iris pigment determine the colour of the iris. The pupil is merely a hole in the centre of the iris and appears black.
The inner layer The retina is a multilayered tissue (ten layers in all) which extends from the edges of the optic nerve to line the inner surface of the choroid up to the junction of ciliary body and choroid. Here the true retina ends at the ora serrata. The retina contains light-sensitive cells of two types: (i) cones – cells that operate at high and medium levels of illumination; they subserve ?ne discrimination of vision and colour vision; (ii) rods – cells that function best at low light intensity and subserve black-and-white vision.
The retina contains about 6 million cones and about 100 million rods. Information from them is conveyed by the nerve ?bres which are in the inner part of the retina, and leave the eye in the optic nerve. There are no photoreceptors at the optic disc (the point where the optic nerve leaves the eye) and therefore there is no light perception from this small area. The optic disc thus produces a physiological blind spot in the visual ?eld.
The retina can be subdivided into several areas: PERIPHERAL RETINA contains mainly rods and a few scattered cones. Visual acuity from this area is fairly coarse. MACULA LUTEA So-called because histologically it looks like a yellow spot. It occupies an area 4·5 mm in diameter lateral to the optic disc. This area of specialised retina can produce a high level of visual acuity. Cones are abundant here but there are few rods. FOVEA CENTRALIS A small central depression at the centre of the macula. Here the cones are tightly packed; rods are absent. It is responsible for the highest levels of visual acuity.
The chambers of the eye There are three: the anterior and posterior chambers, and the vitreous cavity. ANTERIOR CHAMBER Limited in front by the inner surface of the cornea, behind by the iris and pupil. It contains a transparent clear watery ?uid, the aqueous humour. This is constantly being produced by cells of the ciliary body and constantly drained away through the trabecular meshwork. The trabecular meshwork lies in the angle between the iris and inner surface of the cornea. POSTERIOR CHAMBER A narrow space between the iris and pupil in front and the lens behind. It too contains aqueous humour in transit from the ciliary epithelium to the anterior chamber, via the pupil. VITREOUS CAVITY The largest cavity of the eye. In front it is bounded by the lens and behind by the retina. It contains vitreous humour.
Lens Transparent, elastic and biconvex in cross-section, it lies behind the iris and in front of the vitreous cavity. Viewed from the front it is roughly circular and about 10 mm in diameter. The diameter and thickness of the lens vary with its accommodative state. The lens consists of: CAPSULE A thin transparent membrane surrounding the cortex and nucleus. CORTEX This comprises newly made lens ?bres that are relatively soft. It separates the capsule on the outside from the nucleus at the centre of the lens. NUCLEUS The dense central area of old lens ?bres that have become compacted by new lens ?bres laid down over them. ZONULE Numerous radially arranged ?bres attached between the ciliary body and the lens around its circumference. Tension in these zonular ?bres can be adjusted by the muscles of the ciliary body, thus changing the shape of the lens and altering its power of accommodation. VITREOUS HUMOUR A transparent jelly-like structure made up of a network of collagen ?bres suspended in a viscid ?uid. Its shape conforms to that of the vitreous cavity within which it is contained: that is, it is spherical except for a shallow concave depression on its anterior surface. The lens lies in this depression.
Eyelids These are multilayered curtains of tissue whose functions include spreading of the tear ?lm over the front of the eye to prevent desiccation; protection from injury or external irritation; and to some extent the control of light entering the eye. Each eye has an upper and lower lid which form an elliptical opening (the palpebral ?ssure) when the eyes are open. The lids meet at the medial canthus and lateral canthus respectively. The inner medial canthus is ?xed; the lateral canthus more mobile. An epicanthus is a fold of skin which covers the medial canthus in oriental races.
Each lid consists of several layers. From front to back they are: very thin skin; a sheet of muscle (orbicularis oculi, whose ?bres are concentric around the palpebral ?ssure and which produce closure of the eyelids); the orbital septum (modi?ed near the lid margin to form the tarsal plates); and ?nally, lining the back surface of the lid, the conjunctiva (known here as tarsal conjunctiva). At the free margin of each lid are the eyelashes, the openings of tear glands which lie within the lid, and the lacrimal punctum. Toward the medial edge of each lid is an elevation known as the papilla: the lacrimal punctum opens into this papilla. The punctum forms the open end of the cannaliculus, part of the tear-drainage mechanism.
Orbit The bony cavity within which the eye is held. The orbits lie one on either side of the nose, on the front of the skull. They a?ord considerable protection for the eye. Each is roughly pyramidal in shape, with the apex pointing backwards and the base forming the open anterior part of the orbit. The bone of the anterior orbital margin is thickened to protect the eye from injury. There are various openings into the posterior part of the orbit – namely the optic canal, which allows the optic nerve to leave the orbit en route for the brain, and the superior orbital and inferior orbital ?ssures, which allow passage of nerves and blood vessels to and from the orbit. The most important structures holding the eye within the orbit are the extra-ocular muscles, a suspensory ligament of connective tissue that forms a hammock on which the eye rests and which is slung between the medial and lateral walls of the orbit. Finally, the orbital septum, a sheet of connective tissue extending from the anterior margin of the orbit into the lids, helps keep the eye in place. A pad of fat ?lls in the orbit behind the eye and acts as a cushion for the eye.
Conjunctiva A transparent mucous membrane that extends from the limbus over the anterior sclera or ‘white of the eye’. This is the bulbar conjunctiva. The conjunctiva does not cover the cornea. Conjunctiva passes from the eye on to the inner surface of the eyelid at the fornices and is continuous with the tarsal conjunctiva. The semilunar fold is the vertical crescent of conjunctiva at the medial aspect of the palpebral ?ssure. The caruncle is a piece of modi?ed skin just within the inner canthus.
Eye muscles The extra-ocular muscles. There are six in all, the four rectus muscles (superior, inferior, medial and lateral rectus muscles) and two oblique muscles (superior and inferior oblique muscles). The muscles are attached at various points between the bony orbit and the eyeball. By their combined action they move the eye in horizontal and vertical gaze. They also produce torsional movement of the eye (i.e. clockwise or anticlockwise movements when viewed from the front).
Lacrimal apparatus There are two components: a tear-production system, namely the lacrimal gland and accessory lacrimal glands; and a drainage system.
Tears keep the front of the eye moist; they also contain nutrients and various components to protect the eye from infection. Crying results from excess tear production. The drainage system cannot cope with the excess and therefore tears over?ow on to the face. Newborn babies do not produce tears for the ?rst three months of life. LACRIMAL GLAND Located below a small depression in the bony roof of the orbit. Numerous tear ducts open from it into predominantly the upper lid. Accessory lacrimal glands are found in the conjunctiva and within the eyelids: the former open directly on to the surface of the conjunctiva; the latter on to the eyelid margin. LACRIMAL DRAINAGE SYSTEM This consists of: PUNCTUM An elevated opening toward the medial aspect of each lid. Each punctum opens into a canaliculus. CANALICULUS A ?ne tube-like structure run-ning within the lid, parallel to the lid margin. The canaliculi from upper and lower lid join to form a common canaliculus which opens into the lacrimal sac. LACRIMAL SAC A small sac on the side of the nose which opens into the nasolacrimal duct. During blinking, the sac sucks tears into itself from the canaliculus. Tears then drain by gravity down the nasolacrimal duct. NASOLACRIMAL DUCT A tubular structure which runs down through the wall of the nose and opens into the nasal cavity.
Visual pathway Light stimulates the rods and cones of the retina. Electrochemical messages are then passed to nerve ?bres in the retina and then via the optic nerve to the optic chiasm. Here information from the temporal (outer) half of each retina continues to the same side of the brain. Information from the nasal (inner) half of each retina crosses to the other side within the optic chiasm. The rearranged nerve ?bres then pass through the optic tract to the lateral geniculate body, then the optic radiation to reach the visual cortex in the occipital lobe of the brain.... eye
Individuals most at risk have a family history of GLAUCOMA (especially among siblings), are myopic (short-sighted), or have diabetic or thyroid eye disease. People with a strong family history of the disease should have regular eye checks, including tonometry, from the age of 35 years.
Glaucoma is usually classi?ed as being either open-angle glaucoma or narrow-angle glaucoma.
Open-angle glaucoma is a chronic, slowly progressive, usually bilateral disorder. It occurs in one in 200 of people over 40 and accounts for 20 per cent of those registered blind in Great Britain. Symptoms are virtually non-existent until well into the disease, when the patient may experience visual problems. It is not painful. The characteristic ?ndings are that the intraocular pressure is raised (normal pressure is up to 21 mm Hg) causing cupping of the optic disc and a glaucomatous visual-?eld loss. The angle between the iris and the cornea remains open. Treatment is aimed at decreasing the intraocular pressure initially by drops, tablets and intravenous drug administration. Surgery may be required later. A trabeculectomy is an operation to create a channel through which ?uid can drain from the eye in a controlled fashion in order to bring the pressure down.
Narrow-angle glaucoma affects one in 1,000 people over 40 years of age and is more common in women. Symptoms may start with coloured haloes around street lights at night. These may then be followed by rapid onset of severe pain in and around the eye accompanied by a rapid fall in vision. One eye is usually affected ?rst; this alerts the surgeon so that action can be taken to prevent a similar attack in the other eye. Treatment must be started as an emergency with a topical beta blocker (see BETA-ADRENOCEPTOR-BLOCKING DRUGS) in eye drops with other drugs such as ADRENALINE or pilocarpine added as necessary. Dorzolamide, a topical anhydrase inhibitor, can also be used. ACETAZOLAMIDE, also an anhydrase inhibitor, can be given by mouth. In an emergency before surgery, MANNITOL can be given through an intravenous infusion; this is followed by surgery to prevent recurrence. Acute narrow-angle glaucoma occurs because the peripheral iris is pushed against the back of the cornea. This closes o? the angle between iris and cornea through which aqueous humour drains out of the eye. Since the aqueous humour cannot drain away, it builds up inside the eye causing a rapid increase in pressure.
Various types of LASER treatment – trabeculoplasty (‘burning’ the trabecular network); iridotomy (cutting holes to relieve pressure); and ciliary-body ablation by ‘burning’ – are sometimes used in preference to surgery.... glaucoma
When a blood vessel is damaged, it constricts immediately to reduce blood flow to the area. The damage sets off a series of chemical reactions that lead to the formation of a clot to seal the injury. First, platelets around the injury site are activated, becoming sticky and adhering to the blood-vessel wall. Then, the activated platelets release chemicals, which, in turn, activate blood clotting factors. These factors, together with vitamin K, act on fibrinogen and convert it to fibrin. Strands of fibrin form a meshwork, which traps red blood cells to form a clot.
There are several anticlotting mechanisms to prevent the formation of unwanted clots. These include prostacyclin (a prostaglandin), which prevents platelet aggregation, and plasmin, which breaks down fibrin (see fibrinolysis). Blood flow washes away active coagulation factors; and the liver deactivates excess coagulation factors.
Defects in blood clotting may result in bleeding disorders.
Excessive clotting (thrombosis) may be due to an inherited increase or defect in a coagulation factor (see factor V), the use of oral contraceptives, a decrease in the level of enzymes that inhibit coagulation, or sluggish blood flow through a particular area.
Treatment is usually with anticoagulant drugs such as heparin or warfarin.... blood clotting
—trabecular adj.... trabecula
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