awinml/medqa-textbooks-chunked · Datasets at Hugging Face

id stringlengths 14 28	file_name stringclasses 18 values	content stringlengths 1 722k
Anatomy_Gray_300	Anatomy_Gray.txt	Fig. 1.31 A. This computed tomogram with contrast, in the axial plane, demonstrates the normal common carotid arteries and internal jugular veins with numerous other nonenhancing nodules that represent lymph nodes in a patient with lymphoma. B. This computed tomogram with contrast, in the axial plane, demonstrates a large anterior soft tissue mediastinal mass that represents a lymphoma.
Anatomy_Gray_301	Anatomy_Gray.txt	Fig. 1.32 CNS and PNS.
Anatomy_Gray_302	Anatomy_Gray.txt	Fig. 1.33 Arrangement of meninges in the cranial cavity.
Anatomy_Gray_303	Anatomy_Gray.txt	Fig. 1.34 Differentiation of somites in a “tubular” embryo.
Anatomy_Gray_304	Anatomy_Gray.txt	Fig. 1.35 Somatic sensory and motor neurons. Blue lines indicate motor nerves and red lines indicate sensory nerves.
Anatomy_Gray_305	Anatomy_Gray.txt	Somatic sensory neurondeveloping from neural crest cellsEpaxial (back) musclesHypaxial musclesAxon of motor neuronprojects to muscle developingfrom dermatomyotomeSomatic motor neuroncell body in anterior regionof neural tube
Anatomy_Gray_306	Anatomy_Gray.txt	Fig. 1.36 Dermatomes.
Anatomy_Gray_307	Anatomy_Gray.txt	C6 segment of spinal cordSpinal ganglionDermatomyotomeAutonomous region(where overlap ofdermatomes isleast likely)of C6 dermatome(pad of thumb)Skin on the lateral side of the forearm and on thethumb is innervated by C6 spinal level (spinal nerve).The dermis of the skin in this region develops from the somiteinitially associated with the C6 level of the developing spinal cordCaudalCranialSomite
Anatomy_Gray_308	Anatomy_Gray.txt	Fig. 1.37 Myotomes.
Anatomy_Gray_309	Anatomy_Gray.txt	C6 segment of spinal cordMuscles that abduct the arm are innervated by C5 and C6 spinal levels (spinal nerves) and develop from somites initially associated with C5 and C6 regions of developing spinal cordC5 segment of spinal cordDermatomyotomeSomite
Anatomy_Gray_310	Anatomy_Gray.txt	Fig. 1.38 Dermatomes. A. Anterior view. B. Posterior view.
Anatomy_Gray_311	Anatomy_Gray.txt	Fig. 1.39 Development of the visceral part of the nervous system.
Anatomy_Gray_312	Anatomy_Gray.txt	Motor nerve endingassociated withblood vessels,sweat glands,arrector pili musclesat peripheryPart of neural crest developinginto spinal gangliaVisceral motor ganglionMotor nerve ending associated with visceraDeveloping gastrointestinal tractSensory nerve endingBody cavity(coelom)Visceral sensory neuron developsfrom neural crest and becomespart of spinal ganglionVisceral motorpreganglionicneuron in lateralregion of CNS(spinal cord)Postganglionic motor neuron is outside CNS.An aggregation of postganglionic neuronal cellbodies forms a peripheral visceral motor ganglion.
Anatomy_Gray_313	Anatomy_Gray.txt	Fig. 1.40 Basic anatomy of a thoracic spinal nerve.
Anatomy_Gray_314	Anatomy_Gray.txt	Fig. 1.41 Parts of the CNS associated with visceral motor components.
Anatomy_Gray_315	Anatomy_Gray.txt	SympatheticT1 to L2spinal segmentsBrainstemcranial nervesIII, VII, IX, XS2 to S4spinal segmentsParasympathetic
Anatomy_Gray_316	Anatomy_Gray.txt	Fig. 1.42 Sympathetic part of the autonomic division of the PNS.
Anatomy_Gray_317	Anatomy_Gray.txt	Abdominal visceraHeartOrgansPeripheralSympathetic nerves followsomatic nerves to periphery(glands, smooth muscle)Pelvic visceraGanglion imparEsophageal plexusPrevertebral plexus
Anatomy_Gray_318	Anatomy_Gray.txt	Fig. 1.43 Course of sympathetic fibers that travel to the periphery in the same spinal nerves in which they travel out of the spinal cord.
Anatomy_Gray_319	Anatomy_Gray.txt	Gray ramus communicansT10 spinal nervePosteriorramusAnteriorramusPeripheral distribution of sympatheticscarried peripherally by terminal cutaneousbranches of spinal nerve T1 to L2Motor nerve to sweat glands,smooth muscle of bloodvessels, and arrector pilimuscles in the part of T10dermatome supplied by theanterior ramusT10 spinal segmentWhite ramus communicans
Anatomy_Gray_320	Anatomy_Gray.txt	Fig. 1.44 Course of sympathetic nerves that travel to the periphery in spinal nerves that are not the ones through which they left the spinal cord.
Anatomy_Gray_321	Anatomy_Gray.txt	Sympathetic paravertebral trunksPeripheral distribution ofascending sympatheticsPeripheral distribution ofdescending sympathetics(C1) C2 to C8T1 to L2L3 to CoWhite ramus communicansGray ramus communicansPosterior rootGray ramus communicansGray ramus communicansAnterior root
Anatomy_Gray_322	Anatomy_Gray.txt	Fig. 1.45 Course of sympathetic nerves traveling to the heart.
Anatomy_Gray_323	Anatomy_Gray.txt	Sympathetic cardiac nervesSympathetic cardiac nervesSympathetic trunkCardiac plexusT1 to T4CervicalWhite ramuscommunicansGray ramuscommunicans
Anatomy_Gray_324	Anatomy_Gray.txt	Fig. 1.46 Course of sympathetic nerves traveling to abdominal and pelvic viscera.
Anatomy_Gray_325	Anatomy_Gray.txt	White ramus communicansGray ramus communicansSacral splanchnic nervesLumbar splanchnic nervesLeast splanchnic nervesLesser splanchnic nervesGreater splanchnic nervesPrevertebral plexusand gangliaParavertebralsympathetic trunkAbdominalandpelvic visceraAortaT5 to T9T12T9 to T10(T10 to T11)L1 to L2
Anatomy_Gray_326	Anatomy_Gray.txt	Fig. 1.47 Parasympathetic part of the autonomic division of the PNS.
Anatomy_Gray_327	Anatomy_Gray.txt	Thoracic visceral plexusPrevertebral plexusAbdominal visceraSynapse with nerve cellsof enteric systemErectile tissues of penisand clitorisS2 to S4Sacral parasympatheticoutflow via pelvicsplanchnic nervesCranial parasympatheticoutflow via cranial nervesHeartSubmandibularganglionPterygopalatineganglionOtic ganglionCiliary ganglion[III][VII][IX][X]Pelvic visceraPupillary constrictionTransition from supply by [X]to pelvic splanchnic nervesSalivary glandsLacrimal glandParotid gland
Anatomy_Gray_328	Anatomy_Gray.txt	Fig. 1.48 Enteric part of the nervous system.
Anatomy_Gray_329	Anatomy_Gray.txt	Fig. 1.49 Nerve plexuses.
Anatomy_Gray_330	Anatomy_Gray.txt	C7C6C5C4C3C2C1T1T2T3T4T5T6T7T8T9T10T11T12L1S1S2S3S4S5L2L3L4L5C8GreaterLeastLesserSOMATIC PLEXUSESVISCERAL PLEXUSESCervical plexusanterior rami C1 to C4Brachial plexusanterior rami C5 to T1Lumbar plexusanterior rami L1 to L4Sacral plexusanterior ramiL4 to S4Parasympathetic [X]S2 to S4 pelvic splanchnic nerves(parasympathetic)Pulmonary branchPulmonary branchesCardiac branchesCardiac plexusThoracic aortic plexusEsophageal plexusPrevertebral plexusVagal trunkGanglion imparSacral splanchnic nervesSplanchnicnervesLumbar splanchnicnerves
Anatomy_Gray_331	Anatomy_Gray.txt	Fig. 1.50 Mechanism for referred pain from an inflamed appendix to the T10 dermatome.
Anatomy_Gray_332	Anatomy_Gray.txt	Table 1.1 The approximate dosage of radiation exposure as an order of magnitude
Anatomy_Gray_333	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_334	Anatomy_Gray.txt	These are extra bones that are not usually found as part of the normal skeleton, but can exist as a normal variant in many people. They are typically found in multiple locations in the wrist and hands, ankles and feet (Fig. 1.13). These should not be mistaken for fractures on imaging.
Anatomy_Gray_335	Anatomy_Gray.txt	Sesamoid bones are embedded within tendons, the largest of which is the patella. There are many other sesamoids in the body particularly in tendons of the hands and feet, and most frequently in flexor tendons of the thumb and big toe.
Anatomy_Gray_336	Anatomy_Gray.txt	Degenerative and inflammatory changes of, as well as mechanical stresses on, the accessory bones and sesamoids can cause pain, which can be treated with physiotherapy and targeted steroid injections, but in some severe cases it may be necessary to surgically remove the bone.
Anatomy_Gray_337	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_338	Anatomy_Gray.txt	Determination of skeletal age
Anatomy_Gray_339	Anatomy_Gray.txt	Throughout life the bones develop in a predictable way to form the skeletally mature adult at the end of puberty. In western countries skeletal maturity tends to occur between the ages of 20 and 25 years. However, this may well vary according to geography and socioeconomic conditions. Skeletal maturity will also be determined by genetic factors and disease states.
Anatomy_Gray_340	Anatomy_Gray.txt	Up until the age of skeletal maturity, bony growth and development follows a typically predictable ordered state, which can be measured through either ultrasound, plain radiographs, or MRI scanning. Typically, the nondominant (left) hand is radiographed, and the radiograph is compared to a series of standard radiographs. From these images the bone age can be determined (Fig. 1.14).
Anatomy_Gray_341	Anatomy_Gray.txt	In certain disease states, such as malnutrition and hypothyroidism, bony maturity may be slow. If the skeletal bone age is significantly reduced from the patient’s true age, treatment may be required.
Anatomy_Gray_342	Anatomy_Gray.txt	In the healthy individual the bone age accurately represents the true age of the patient. This is important in determining the true age of the subject. This may also have medicolegal importance.
Anatomy_Gray_343	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_344	Anatomy_Gray.txt	The bone marrow serves an important function. There are two types of bone marrow, red marrow (otherwise known as myeloid tissue) and yellow marrow. Red blood cells, platelets, and most white blood cells arise from within the red marrow. In the yellow marrow a few white cells are made; however, this marrow is dominated by large fat globules (producing its yellow appearance) (Fig. 1.15).
Anatomy_Gray_345	Anatomy_Gray.txt	From birth most of the body’s marrow is red; however, as the subject ages, more red marrow is converted into yellow marrow within the medulla of the long and flat bones.
Anatomy_Gray_346	Anatomy_Gray.txt	Bone marrow contains two types of stem cells. Hemopoietic stem cells give rise to the white blood cells, red blood cells, and platelets. Mesenchymal stem cells differentiate into structures that form bone, cartilage, and muscle.
Anatomy_Gray_347	Anatomy_Gray.txt	There are a number of diseases that may involve the bone marrow, including infection and malignancy. In patients who develop a bone marrow malignancy (e.g., leukemia) it may be possible to harvest nonmalignant cells from the patient’s bone marrow or cells from another person’s bone marrow. The patient’s own marrow can be destroyed with chemotherapy or radiation and the new cells infused. This treatment is bone marrow transplantation.
Anatomy_Gray_348	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_349	Anatomy_Gray.txt	Fractures occur in normal bone because of abnormal load or stress, in which the bone gives way (Fig. 1.16A). Fractures may also occur in bone that is of poor quality (osteoporosis); in such cases a normal stress is placed upon a bone that is not of sufficient quality to withstand this force and subsequently fractures.
Anatomy_Gray_350	Anatomy_Gray.txt	In children whose bones are still developing, fractures may occur across the growth plate or across the shaft. These shaft fractures typically involve partial cortical disruption, similar to breaking a branch of a young tree; hence they are termed “greenstick” fractures.
Anatomy_Gray_351	Anatomy_Gray.txt	After a fracture has occurred, the natural response is to heal the fracture. Between the fracture margins a blood clot is formed into which new vessels grow. A jelly-like matrix is formed, and further migration of collagen-producing cells occurs. On this soft tissue framework, calcium hydroxyapatite is produced by osteoblasts and forms insoluble crystals, and then bone matrix is laid down. As more bone is produced, a callus can be demonstrated forming across the fracture site.
Anatomy_Gray_352	Anatomy_Gray.txt	Treatment of fractures requires a fracture line reduction. If this cannot be maintained in a plaster of Paris cast, it may require internal or external fixation with screws and metal rods (Fig. 1.16B).
Anatomy_Gray_353	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_354	Anatomy_Gray.txt	Avascular necrosis is cellular death of bone resulting from a temporary or permanent loss of blood supply to that bone. Avascular necrosis may occur in a variety of medical conditions, some of which have an etiology that is less than clear. A typical site for avascular necrosis is a fracture across the femoral neck in an elderly patient. In these patients there is loss of continuity of the cortical medullary blood flow with loss of blood flow deep to the retinacular fibers. This essentially renders the femoral head bloodless; it subsequently undergoes necrosis and collapses (Fig. 1.17). In these patients it is necessary to replace the femoral head with a prosthesis.
Anatomy_Gray_355	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_356	Anatomy_Gray.txt	As the skeleton develops, there are stages of intense growth typically around the ages of 7 to 10 years and later in puberty. These growth spurts are associated with increased cellular activity around the growth plate between the head and shaft of a bone. This increase in activity renders the growth plates more vulnerable to injuries, which may occur from dislocation across a growth plate or fracture through a growth plate. Occasionally an injury may result in growth plate compression, destroying that region of the growth plate, which may result in asymmetrical growth across that joint region. All fractures across the growth plate must be treated with care and expediency, requiring fracture reduction.
Anatomy_Gray_357	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_358	Anatomy_Gray.txt	Degenerative joint disease is commonly known as osteoarthritis or osteoarthrosis. The disorder is related to aging but not caused by aging. Typically there are decreases in water and proteoglycan content within the cartilage. The cartilage becomes more fragile and more susceptible to mechanical disruption (Fig. 1.22). As the cartilage wears, the underlying bone becomes fissured and also thickens. Synovial fluid may be forced into small cracks that appear in the bone’s surface, which produces large cysts. Furthermore, reactive juxta-articular bony nodules are formed (osteophytes) (Fig. 1.23). As these processes occur, there is slight deformation, which alters the biomechanical forces through the joint. This in turn creates abnormal stresses, which further disrupt the joint.
Anatomy_Gray_359	Anatomy_Gray.txt	In the United States, osteoarthritis accounts for up to one-quarter of primary health care visits and is regarded as a significant problem.
Anatomy_Gray_360	Anatomy_Gray.txt	The etiology of osteoarthritis is not clear; however, osteoarthritis can occur secondary to other joint diseases, such as rheumatoid arthritis and infection. Overuse of joints and abnormal strains, such as those experienced by people who play sports, often cause one to be more susceptible to chronic joint osteoarthritis.
Anatomy_Gray_361	Anatomy_Gray.txt	Various treatments are available, including weight reduction, proper exercise, anti-inflammatory drug treatment, and joint replacement (Fig. 1.24).
Anatomy_Gray_362	Anatomy_Gray.txt	Arthroscopy is a technique of visualizing the inside of a joint using a small telescope placed through a tiny incision in the skin. Arthroscopy can be performed in most joints. However, it is most commonly performed in the knee, shoulder, ankle, and hip joints.
Anatomy_Gray_363	Anatomy_Gray.txt	Arthroscopy allows the surgeon to view the inside of the joint and its contents. Notably, in the knee, the menisci and the ligaments are easily seen, and it is possible using separate puncture sites and specific instruments to remove the menisci and replace the cruciate ligaments. The advantages of arthroscopy are that it is performed through small incisions, it enables patients to quickly recover and return to normal activity, and it only requires either a light anesthetic or regional anesthesia during the procedure.
Anatomy_Gray_364	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_365	Anatomy_Gray.txt	Joint replacement is undertaken for a variety of reasons. These predominantly include degenerative joint disease and joint destruction. Joints that have severely degenerated or lack their normal function are painful. In some patients, the pain may be so severe that it prevents them from leaving the house and undertaking even the smallest of activities without discomfort.
Anatomy_Gray_366	Anatomy_Gray.txt	Large joints are commonly affected, including the hip, knee, and shoulder. However, with ongoing developments in joint replacement materials and surgical techniques, even small joints of the fingers can be replaced.
Anatomy_Gray_367	Anatomy_Gray.txt	Typically, both sides of the joint are replaced; in the hip joint the acetabulum will be reamed, and a plastic or metal cup will be introduced. The femoral component will be fitted precisely to the femur and cemented in place (Fig. 1.25).
Anatomy_Gray_368	Anatomy_Gray.txt	Most patients derive significant benefit from joint replacement and continue to lead an active life afterward. In a minority of patients who have been fitted with a metal acetabular cup and metal femoral component, an aseptic lymphocyte-dominated vasculitis-associated lesion (ALVAL) may develop, possibly caused by a hypersensitivity response to the release of metal ions in adjacent tissues. These patients often have chronic pain and might need additional surgery to replace these joint replacements with safer models.
Anatomy_Gray_369	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_370	Anatomy_Gray.txt	The importance of fascias
Anatomy_Gray_371	Anatomy_Gray.txt	A fascia is a thin band of tissue that surrounds muscles, bones, organs, nerves, and blood vessels and often remains uninterrupted as a 3D structure between tissues. It provides important support for tissues and can provide a boundary between structures.
Anatomy_Gray_372	Anatomy_Gray.txt	Clinically, fascias are extremely important because they often limit the spread of infection and malignant disease. When infections or malignant diseases cross a fascial plain, a primary surgical clearance may require a far more extensive dissection to render the area free of tumor or infection.
Anatomy_Gray_373	Anatomy_Gray.txt	A typical example of the clinical importance of a fascial layer would be of that covering the psoas muscle. Infection within an intervertebral body secondary to tuberculosis can pass laterally into the psoas muscle. Pus fills the psoas muscle but is limited from further spread by the psoas fascia, which surrounds the muscle and extends inferiorly into the groin pointing below the inguinal ligament.
Anatomy_Gray_374	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_375	Anatomy_Gray.txt	Placement of skin incisions and scarring
Anatomy_Gray_376	Anatomy_Gray.txt	Surgical skin incisions are ideally placed along or parallel to Langer’s lines, which are lines of skin tension that correspond to the orientation of the dermal collagen fibers. They tend to run in the same direction as the underlying muscle fibers and incisions that are made along these lines tend to heal better with less scarring. In contrast, incisions made perpendicular to Langer’s lines are more likely to heal with a prominent scar and in some severe cases can lead to raised, firm, hypertrophic, or keloid, scars.
Anatomy_Gray_377	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_378	Anatomy_Gray.txt	Muscle paralysis is the inability to move a specific muscle or muscle group and may be associated with other neurological abnormalities, including loss of sensation. Major causes include stroke, trauma, poliomyelitis, and iatrogenic factors. Paralysis may be due to abnormalities in the brain, the spinal cord, and the nerves supplying the muscles.
Anatomy_Gray_379	Anatomy_Gray.txt	In the long term, muscle paralysis will produce secondary muscle wasting and overall atrophy of the region due to disuse.
Anatomy_Gray_380	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_381	Anatomy_Gray.txt	Muscle atrophy is a wasting disorder of muscle. It can be produced by a variety of causes, which include nerve damage to the muscle and disuse.
Anatomy_Gray_382	Anatomy_Gray.txt	Muscle atrophy is an important problem in patients who have undergone long-term rest or disuse, requiring extensive rehabilitation and muscle building exercises to maintain normal activities of daily living.
Anatomy_Gray_383	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_384	Anatomy_Gray.txt	Muscle injuries and strains tend to occur in specific muscle groups and usually are related to a sudden exertion and muscle disruption. They typically occur in athletes.
Anatomy_Gray_385	Anatomy_Gray.txt	Muscle tears may involve a small interstitial injury up to a complete muscle disruption (Fig. 1.26). It is important to identify which muscle groups are affected and the extent of the tear to facilitate treatment and obtain a prognosis, which will determine the length of rehabilitation necessary to return to normal activity.
Anatomy_Gray_386	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_387	Anatomy_Gray.txt	Atherosclerosis is a disease that affects arteries. There is a chronic inflammatory reaction in the walls of the arteries, with deposition of cholesterol and fatty proteins. This may in turn lead to secondary calcification, with reduction in the diameter of the vessels impeding distal flow. The plaque itself may be a site for attraction of platelets that may “fall off” (embolize) distally. Plaque fissuring may occur, which allows fresh clots to form and occlude the vessel.
Anatomy_Gray_388	Anatomy_Gray.txt	The importance of atherosclerosis and its effects depend upon which vessel is affected. If atherosclerosis occurs in the carotid artery, small emboli may form and produce a stroke. In the heart, plaque fissuring may produce an acute vessel thrombosis, producing a myocardial infarction (heart attack). In the legs, chronic narrowing of vessels may limit the ability of the patient to walk and ultimately cause distal ischemia and gangrene of the toes.
Anatomy_Gray_389	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_390	Anatomy_Gray.txt	Varicose veins are tortuous dilated veins that typically occur in the legs, although they may occur in the superficial veins of the arm and in other organs.
Anatomy_Gray_391	Anatomy_Gray.txt	In normal individuals the movement of adjacent leg muscles pumps the blood in the veins to the heart. Blood is also pumped from the superficial veins through the investing layer of fascia of the leg into the deep veins. Valves in these perforating veins may become damaged, allowing blood to pass in the opposite direction. This increased volume and pressure produces dilatation and tortuosity of the superficial veins (Fig. 1.27). Apart from the unsightliness of larger veins, the skin may become pigmented and atrophic with a poor response to tissue trauma. In some patients even small trauma may produce skin ulceration, which requires elevation of the limb and application of pressure bandages to heal.
Anatomy_Gray_392	Anatomy_Gray.txt	Treatment of varicose veins depends on their location, size, and severity. Typically the superficial varicose veins can be excised and stripped, allowing blood only to drain into the deep system.
Anatomy_Gray_393	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_394	Anatomy_Gray.txt	All organs require a blood supply from the arteries and drainage by veins. Within most organs there are multiple ways of perfusing the tissue such that if the main vessel feeding the organ or vein draining the organ is blocked, a series of smaller vessels (collateral vessels) continue to supply and drain the organ.
Anatomy_Gray_395	Anatomy_Gray.txt	In certain circumstances, organs have more than one vessel perfusing them, such as the hand, which is supplied by the radial and ulnar arteries. Loss of either the radial or the ulnar artery may not produce any symptoms of reduced perfusion to the hand.
Anatomy_Gray_396	Anatomy_Gray.txt	There are circumstances in which loss of a vein produces significant venous collateralization. Some of these venous collaterals become susceptible to bleeding. This is a considerable problem in patients who have undergone portal vein thrombosis or occlusion, where venous drainage from the gut bypasses the liver through collateral veins to return to the systemic circulation.
Anatomy_Gray_397	Anatomy_Gray.txt	Normal vascular anastomoses associated with an organ are important. Some organs, such as the duodenum, have a dual blood supply arising from the branches of the celiac trunk and also from the branches of the superior mesenteric artery. Should either of these vessels be damaged, blood supply will be maintained to the organ. The brain has multiple vessels supplying it, dominated by the carotid arteries and the vertebral arteries. Vessels within the brain are end arteries and have a poor collateral circulation; hence any occlusion will produce long-term cerebral damage.
Anatomy_Gray_398	Anatomy_Gray.txt	In the clinic
Anatomy_Gray_399	Anatomy_Gray.txt	Lymph nodes are efficient filters and have an internal honeycomb of reticular connective tissue filled with lymphocytes. These lymphocytes act on bacteria, viruses, and other bodily cells to destroy them. Lymph nodes tend to drain specific areas, and if infection occurs within a drainage area, the lymph node will become active. The rapid cell turnover and production of local inflammatory mediators may cause the node to enlarge and become tender. Similarly, in patients with malignancy the lymphatics may drain metastasizing cells to the lymph nodes. These can become enlarged and inflamed and will need to be removed if clinically symptomatic.

Anatomy_Gray_300

Anatomy_Gray.txt

Fig. 1.31 A. This computed tomogram with contrast, in the axial plane, demonstrates the normal common carotid arteries and internal jugular veins with numerous other nonenhancing nodules that represent lymph nodes in a patient with lymphoma. B. This computed tomogram with contrast, in the axial plane, demonstrates a large anterior soft tissue mediastinal mass that represents a lymphoma.

Anatomy_Gray_301

Anatomy_Gray.txt

Fig. 1.32 CNS and PNS.

Anatomy_Gray_302

Anatomy_Gray.txt

Fig. 1.33 Arrangement of meninges in the cranial cavity.

Anatomy_Gray_303

Anatomy_Gray.txt

Fig. 1.34 Differentiation of somites in a “tubular” embryo.

Anatomy_Gray_304

Anatomy_Gray.txt

Fig. 1.35 Somatic sensory and motor neurons. Blue lines indicate motor nerves and red lines indicate sensory nerves.

Anatomy_Gray_305

Anatomy_Gray.txt

Somatic sensory neurondeveloping from neural crest cellsEpaxial (back) musclesHypaxial musclesAxon of motor neuronprojects to muscle developingfrom dermatomyotomeSomatic motor neuroncell body in anterior regionof neural tube

Anatomy_Gray_306

Anatomy_Gray.txt

Fig. 1.36 Dermatomes.

Anatomy_Gray_307

Anatomy_Gray.txt

C6 segment of spinal cordSpinal ganglionDermatomyotomeAutonomous region(where overlap ofdermatomes isleast likely)of C6 dermatome(pad of thumb)Skin on the lateral side of the forearm and on thethumb is innervated by C6 spinal level (spinal nerve).The dermis of the skin in this region develops from the somiteinitially associated with the C6 level of the developing spinal cordCaudalCranialSomite

Anatomy_Gray_308

Anatomy_Gray.txt

Fig. 1.37 Myotomes.

Anatomy_Gray_309

Anatomy_Gray.txt

C6 segment of spinal cordMuscles that abduct the arm are innervated by C5 and C6 spinal levels (spinal nerves) and develop from somites initially associated with C5 and C6 regions of developing spinal cordC5 segment of spinal cordDermatomyotomeSomite

Anatomy_Gray_310

Anatomy_Gray.txt

Fig. 1.38 Dermatomes. A. Anterior view. B. Posterior view.

Anatomy_Gray_311

Anatomy_Gray.txt

Fig. 1.39 Development of the visceral part of the nervous system.

Anatomy_Gray_312

Anatomy_Gray.txt

Motor nerve endingassociated withblood vessels,sweat glands,arrector pili musclesat peripheryPart of neural crest developinginto spinal gangliaVisceral motor ganglionMotor nerve ending associated with visceraDeveloping gastrointestinal tractSensory nerve endingBody cavity(coelom)Visceral sensory neuron developsfrom neural crest and becomespart of spinal ganglionVisceral motorpreganglionicneuron in lateralregion of CNS(spinal cord)Postganglionic motor neuron is outside CNS.An aggregation of postganglionic neuronal cellbodies forms a peripheral visceral motor ganglion.

Anatomy_Gray_313

Anatomy_Gray.txt

Fig. 1.40 Basic anatomy of a thoracic spinal nerve.

Anatomy_Gray_314

Anatomy_Gray.txt

Fig. 1.41 Parts of the CNS associated with visceral motor components.

Anatomy_Gray_315

Anatomy_Gray.txt

SympatheticT1 to L2spinal segmentsBrainstemcranial nervesIII, VII, IX, XS2 to S4spinal segmentsParasympathetic

Anatomy_Gray_316

Anatomy_Gray.txt

Fig. 1.42 Sympathetic part of the autonomic division of the PNS.

Anatomy_Gray_317

Anatomy_Gray.txt

Abdominal visceraHeartOrgansPeripheralSympathetic nerves followsomatic nerves to periphery(glands, smooth muscle)Pelvic visceraGanglion imparEsophageal plexusPrevertebral plexus

Anatomy_Gray_318

Anatomy_Gray.txt

Fig. 1.43 Course of sympathetic fibers that travel to the periphery in the same spinal nerves in which they travel out of the spinal cord.

Anatomy_Gray_319

Anatomy_Gray.txt

Gray ramus communicansT10 spinal nervePosteriorramusAnteriorramusPeripheral distribution of sympatheticscarried peripherally by terminal cutaneousbranches of spinal nerve T1 to L2Motor nerve to sweat glands,smooth muscle of bloodvessels, and arrector pilimuscles in the part of T10dermatome supplied by theanterior ramusT10 spinal segmentWhite ramus communicans

Anatomy_Gray_320

Anatomy_Gray.txt

Fig. 1.44 Course of sympathetic nerves that travel to the periphery in spinal nerves that are not the ones through which they left the spinal cord.

Anatomy_Gray_321

Anatomy_Gray.txt

Sympathetic paravertebral trunksPeripheral distribution ofascending sympatheticsPeripheral distribution ofdescending sympathetics(C1) C2 to C8T1 to L2L3 to CoWhite ramus communicansGray ramus communicansPosterior rootGray ramus communicansGray ramus communicansAnterior root

Anatomy_Gray_322

Anatomy_Gray.txt

Fig. 1.45 Course of sympathetic nerves traveling to the heart.

Anatomy_Gray_323

Anatomy_Gray.txt

Sympathetic cardiac nervesSympathetic cardiac nervesSympathetic trunkCardiac plexusT1 to T4CervicalWhite ramuscommunicansGray ramuscommunicans

Anatomy_Gray_324

Anatomy_Gray.txt

Fig. 1.46 Course of sympathetic nerves traveling to abdominal and pelvic viscera.

Anatomy_Gray_325

Anatomy_Gray.txt

White ramus communicansGray ramus communicansSacral splanchnic nervesLumbar splanchnic nervesLeast splanchnic nervesLesser splanchnic nervesGreater splanchnic nervesPrevertebral plexusand gangliaParavertebralsympathetic trunkAbdominalandpelvic visceraAortaT5 to T9T12T9 to T10(T10 to T11)L1 to L2

Anatomy_Gray_326

Anatomy_Gray.txt

Fig. 1.47 Parasympathetic part of the autonomic division of the PNS.

Anatomy_Gray_327

Anatomy_Gray.txt

Thoracic visceral plexusPrevertebral plexusAbdominal visceraSynapse with nerve cellsof enteric systemErectile tissues of penisand clitorisS2 to S4Sacral parasympatheticoutflow via pelvicsplanchnic nervesCranial parasympatheticoutflow via cranial nervesHeartSubmandibularganglionPterygopalatineganglionOtic ganglionCiliary ganglion[III][VII][IX][X]Pelvic visceraPupillary constrictionTransition from supply by [X]to pelvic splanchnic nervesSalivary glandsLacrimal glandParotid gland

Anatomy_Gray_328

Anatomy_Gray.txt

Fig. 1.48 Enteric part of the nervous system.

Anatomy_Gray_329

Anatomy_Gray.txt

Fig. 1.49 Nerve plexuses.

Anatomy_Gray_330

Anatomy_Gray.txt

C7C6C5C4C3C2C1T1T2T3T4T5T6T7T8T9T10T11T12L1S1S2S3S4S5L2L3L4L5C8GreaterLeastLesserSOMATIC PLEXUSESVISCERAL PLEXUSESCervical plexusanterior rami C1 to C4Brachial plexusanterior rami C5 to T1Lumbar plexusanterior rami L1 to L4Sacral plexusanterior ramiL4 to S4Parasympathetic [X]S2 to S4 pelvic splanchnic nerves(parasympathetic)Pulmonary branchPulmonary branchesCardiac branchesCardiac plexusThoracic aortic plexusEsophageal plexusPrevertebral plexusVagal trunkGanglion imparSacral splanchnic nervesSplanchnicnervesLumbar splanchnicnerves

Anatomy_Gray_331

Anatomy_Gray.txt

Fig. 1.50 Mechanism for referred pain from an inflamed appendix to the T10 dermatome.

Anatomy_Gray_332

Anatomy_Gray.txt

Table 1.1 The approximate dosage of radiation exposure as an order of magnitude

Anatomy_Gray_333

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_334

Anatomy_Gray.txt

These are extra bones that are not usually found as part of the normal skeleton, but can exist as a normal variant in many people. They are typically found in multiple locations in the wrist and hands, ankles and feet (Fig. 1.13). These should not be mistaken for fractures on imaging.

Anatomy_Gray_335

Anatomy_Gray.txt

Sesamoid bones are embedded within tendons, the largest of which is the patella. There are many other sesamoids in the body particularly in tendons of the hands and feet, and most frequently in flexor tendons of the thumb and big toe.

Anatomy_Gray_336

Anatomy_Gray.txt

Degenerative and inflammatory changes of, as well as mechanical stresses on, the accessory bones and sesamoids can cause pain, which can be treated with physiotherapy and targeted steroid injections, but in some severe cases it may be necessary to surgically remove the bone.

Anatomy_Gray_337

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_338

Anatomy_Gray.txt

Determination of skeletal age

Anatomy_Gray_339

Anatomy_Gray.txt

Throughout life the bones develop in a predictable way to form the skeletally mature adult at the end of puberty. In western countries skeletal maturity tends to occur between the ages of 20 and 25 years. However, this may well vary according to geography and socioeconomic conditions. Skeletal maturity will also be determined by genetic factors and disease states.

Anatomy_Gray_340

Anatomy_Gray.txt

Up until the age of skeletal maturity, bony growth and development follows a typically predictable ordered state, which can be measured through either ultrasound, plain radiographs, or MRI scanning. Typically, the nondominant (left) hand is radiographed, and the radiograph is compared to a series of standard radiographs. From these images the bone age can be determined (Fig. 1.14).

Anatomy_Gray_341

Anatomy_Gray.txt

In certain disease states, such as malnutrition and hypothyroidism, bony maturity may be slow. If the skeletal bone age is significantly reduced from the patient’s true age, treatment may be required.

Anatomy_Gray_342

Anatomy_Gray.txt

In the healthy individual the bone age accurately represents the true age of the patient. This is important in determining the true age of the subject. This may also have medicolegal importance.

Anatomy_Gray_343

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_344

Anatomy_Gray.txt

The bone marrow serves an important function. There are two types of bone marrow, red marrow (otherwise known as myeloid tissue) and yellow marrow. Red blood cells, platelets, and most white blood cells arise from within the red marrow. In the yellow marrow a few white cells are made; however, this marrow is dominated by large fat globules (producing its yellow appearance) (Fig. 1.15).

Anatomy_Gray_345

Anatomy_Gray.txt

From birth most of the body’s marrow is red; however, as the subject ages, more red marrow is converted into yellow marrow within the medulla of the long and flat bones.

Anatomy_Gray_346

Anatomy_Gray.txt

Bone marrow contains two types of stem cells. Hemopoietic stem cells give rise to the white blood cells, red blood cells, and platelets. Mesenchymal stem cells differentiate into structures that form bone, cartilage, and muscle.

Anatomy_Gray_347

Anatomy_Gray.txt

There are a number of diseases that may involve the bone marrow, including infection and malignancy. In patients who develop a bone marrow malignancy (e.g., leukemia) it may be possible to harvest nonmalignant cells from the patient’s bone marrow or cells from another person’s bone marrow. The patient’s own marrow can be destroyed with chemotherapy or radiation and the new cells infused. This treatment is bone marrow transplantation.

Anatomy_Gray_348

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_349

Anatomy_Gray.txt

Fractures occur in normal bone because of abnormal load or stress, in which the bone gives way (Fig. 1.16A). Fractures may also occur in bone that is of poor quality (osteoporosis); in such cases a normal stress is placed upon a bone that is not of sufficient quality to withstand this force and subsequently fractures.

Anatomy_Gray_350

Anatomy_Gray.txt

In children whose bones are still developing, fractures may occur across the growth plate or across the shaft. These shaft fractures typically involve partial cortical disruption, similar to breaking a branch of a young tree; hence they are termed “greenstick” fractures.

Anatomy_Gray_351

Anatomy_Gray.txt

After a fracture has occurred, the natural response is to heal the fracture. Between the fracture margins a blood clot is formed into which new vessels grow. A jelly-like matrix is formed, and further migration of collagen-producing cells occurs. On this soft tissue framework, calcium hydroxyapatite is produced by osteoblasts and forms insoluble crystals, and then bone matrix is laid down. As more bone is produced, a callus can be demonstrated forming across the fracture site.

Anatomy_Gray_352

Anatomy_Gray.txt

Treatment of fractures requires a fracture line reduction. If this cannot be maintained in a plaster of Paris cast, it may require internal or external fixation with screws and metal rods (Fig. 1.16B).

Anatomy_Gray_353

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_354

Anatomy_Gray.txt

Avascular necrosis is cellular death of bone resulting from a temporary or permanent loss of blood supply to that bone. Avascular necrosis may occur in a variety of medical conditions, some of which have an etiology that is less than clear. A typical site for avascular necrosis is a fracture across the femoral neck in an elderly patient. In these patients there is loss of continuity of the cortical medullary blood flow with loss of blood flow deep to the retinacular fibers. This essentially renders the femoral head bloodless; it subsequently undergoes necrosis and collapses (Fig. 1.17). In these patients it is necessary to replace the femoral head with a prosthesis.

Anatomy_Gray_355

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_356

Anatomy_Gray.txt

As the skeleton develops, there are stages of intense growth typically around the ages of 7 to 10 years and later in puberty. These growth spurts are associated with increased cellular activity around the growth plate between the head and shaft of a bone. This increase in activity renders the growth plates more vulnerable to injuries, which may occur from dislocation across a growth plate or fracture through a growth plate. Occasionally an injury may result in growth plate compression, destroying that region of the growth plate, which may result in asymmetrical growth across that joint region. All fractures across the growth plate must be treated with care and expediency, requiring fracture reduction.

Anatomy_Gray_357

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_358

Anatomy_Gray.txt

Degenerative joint disease is commonly known as osteoarthritis or osteoarthrosis. The disorder is related to aging but not caused by aging. Typically there are decreases in water and proteoglycan content within the cartilage. The cartilage becomes more fragile and more susceptible to mechanical disruption (Fig. 1.22). As the cartilage wears, the underlying bone becomes fissured and also thickens. Synovial fluid may be forced into small cracks that appear in the bone’s surface, which produces large cysts. Furthermore, reactive juxta-articular bony nodules are formed (osteophytes) (Fig. 1.23). As these processes occur, there is slight deformation, which alters the biomechanical forces through the joint. This in turn creates abnormal stresses, which further disrupt the joint.

Anatomy_Gray_359

Anatomy_Gray.txt

In the United States, osteoarthritis accounts for up to one-quarter of primary health care visits and is regarded as a significant problem.

Anatomy_Gray_360

Anatomy_Gray.txt

The etiology of osteoarthritis is not clear; however, osteoarthritis can occur secondary to other joint diseases, such as rheumatoid arthritis and infection. Overuse of joints and abnormal strains, such as those experienced by people who play sports, often cause one to be more susceptible to chronic joint osteoarthritis.

Anatomy_Gray_361

Anatomy_Gray.txt

Various treatments are available, including weight reduction, proper exercise, anti-inflammatory drug treatment, and joint replacement (Fig. 1.24).

Anatomy_Gray_362

Anatomy_Gray.txt

Arthroscopy is a technique of visualizing the inside of a joint using a small telescope placed through a tiny incision in the skin. Arthroscopy can be performed in most joints. However, it is most commonly performed in the knee, shoulder, ankle, and hip joints.

Anatomy_Gray_363

Anatomy_Gray.txt

Arthroscopy allows the surgeon to view the inside of the joint and its contents. Notably, in the knee, the menisci and the ligaments are easily seen, and it is possible using separate puncture sites and specific instruments to remove the menisci and replace the cruciate ligaments. The advantages of arthroscopy are that it is performed through small incisions, it enables patients to quickly recover and return to normal activity, and it only requires either a light anesthetic or regional anesthesia during the procedure.

Anatomy_Gray_364

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_365

Anatomy_Gray.txt

Joint replacement is undertaken for a variety of reasons. These predominantly include degenerative joint disease and joint destruction. Joints that have severely degenerated or lack their normal function are painful. In some patients, the pain may be so severe that it prevents them from leaving the house and undertaking even the smallest of activities without discomfort.

Anatomy_Gray_366

Anatomy_Gray.txt

Large joints are commonly affected, including the hip, knee, and shoulder. However, with ongoing developments in joint replacement materials and surgical techniques, even small joints of the fingers can be replaced.

Anatomy_Gray_367

Anatomy_Gray.txt

Typically, both sides of the joint are replaced; in the hip joint the acetabulum will be reamed, and a plastic or metal cup will be introduced. The femoral component will be fitted precisely to the femur and cemented in place (Fig. 1.25).

Anatomy_Gray_368

Anatomy_Gray.txt

Most patients derive significant benefit from joint replacement and continue to lead an active life afterward. In a minority of patients who have been fitted with a metal acetabular cup and metal femoral component, an aseptic lymphocyte-dominated vasculitis-associated lesion (ALVAL) may develop, possibly caused by a hypersensitivity response to the release of metal ions in adjacent tissues. These patients often have chronic pain and might need additional surgery to replace these joint replacements with safer models.

Anatomy_Gray_369

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_370

Anatomy_Gray.txt

The importance of fascias

Anatomy_Gray_371

Anatomy_Gray.txt

A fascia is a thin band of tissue that surrounds muscles, bones, organs, nerves, and blood vessels and often remains uninterrupted as a 3D structure between tissues. It provides important support for tissues and can provide a boundary between structures.

Anatomy_Gray_372

Anatomy_Gray.txt

Clinically, fascias are extremely important because they often limit the spread of infection and malignant disease. When infections or malignant diseases cross a fascial plain, a primary surgical clearance may require a far more extensive dissection to render the area free of tumor or infection.

Anatomy_Gray_373

Anatomy_Gray.txt

A typical example of the clinical importance of a fascial layer would be of that covering the psoas muscle. Infection within an intervertebral body secondary to tuberculosis can pass laterally into the psoas muscle. Pus fills the psoas muscle but is limited from further spread by the psoas fascia, which surrounds the muscle and extends inferiorly into the groin pointing below the inguinal ligament.

Anatomy_Gray_374

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_375

Anatomy_Gray.txt

Placement of skin incisions and scarring

Anatomy_Gray_376

Anatomy_Gray.txt

Surgical skin incisions are ideally placed along or parallel to Langer’s lines, which are lines of skin tension that correspond to the orientation of the dermal collagen fibers. They tend to run in the same direction as the underlying muscle fibers and incisions that are made along these lines tend to heal better with less scarring. In contrast, incisions made perpendicular to Langer’s lines are more likely to heal with a prominent scar and in some severe cases can lead to raised, firm, hypertrophic, or keloid, scars.

Anatomy_Gray_377

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_378

Anatomy_Gray.txt

Muscle paralysis is the inability to move a specific muscle or muscle group and may be associated with other neurological abnormalities, including loss of sensation. Major causes include stroke, trauma, poliomyelitis, and iatrogenic factors. Paralysis may be due to abnormalities in the brain, the spinal cord, and the nerves supplying the muscles.

Anatomy_Gray_379

Anatomy_Gray.txt

In the long term, muscle paralysis will produce secondary muscle wasting and overall atrophy of the region due to disuse.

Anatomy_Gray_380

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_381

Anatomy_Gray.txt

Muscle atrophy is a wasting disorder of muscle. It can be produced by a variety of causes, which include nerve damage to the muscle and disuse.

Anatomy_Gray_382

Anatomy_Gray.txt

Muscle atrophy is an important problem in patients who have undergone long-term rest or disuse, requiring extensive rehabilitation and muscle building exercises to maintain normal activities of daily living.

Anatomy_Gray_383

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_384

Anatomy_Gray.txt

Muscle injuries and strains tend to occur in specific muscle groups and usually are related to a sudden exertion and muscle disruption. They typically occur in athletes.

Anatomy_Gray_385

Anatomy_Gray.txt

Muscle tears may involve a small interstitial injury up to a complete muscle disruption (Fig. 1.26). It is important to identify which muscle groups are affected and the extent of the tear to facilitate treatment and obtain a prognosis, which will determine the length of rehabilitation necessary to return to normal activity.

Anatomy_Gray_386

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_387

Anatomy_Gray.txt

Atherosclerosis is a disease that affects arteries. There is a chronic inflammatory reaction in the walls of the arteries, with deposition of cholesterol and fatty proteins. This may in turn lead to secondary calcification, with reduction in the diameter of the vessels impeding distal flow. The plaque itself may be a site for attraction of platelets that may “fall off” (embolize) distally. Plaque fissuring may occur, which allows fresh clots to form and occlude the vessel.

Anatomy_Gray_388

Anatomy_Gray.txt

The importance of atherosclerosis and its effects depend upon which vessel is affected. If atherosclerosis occurs in the carotid artery, small emboli may form and produce a stroke. In the heart, plaque fissuring may produce an acute vessel thrombosis, producing a myocardial infarction (heart attack). In the legs, chronic narrowing of vessels may limit the ability of the patient to walk and ultimately cause distal ischemia and gangrene of the toes.

Anatomy_Gray_389

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_390

Anatomy_Gray.txt

Varicose veins are tortuous dilated veins that typically occur in the legs, although they may occur in the superficial veins of the arm and in other organs.

Anatomy_Gray_391

Anatomy_Gray.txt

In normal individuals the movement of adjacent leg muscles pumps the blood in the veins to the heart. Blood is also pumped from the superficial veins through the investing layer of fascia of the leg into the deep veins. Valves in these perforating veins may become damaged, allowing blood to pass in the opposite direction. This increased volume and pressure produces dilatation and tortuosity of the superficial veins (Fig. 1.27). Apart from the unsightliness of larger veins, the skin may become pigmented and atrophic with a poor response to tissue trauma. In some patients even small trauma may produce skin ulceration, which requires elevation of the limb and application of pressure bandages to heal.

Anatomy_Gray_392

Anatomy_Gray.txt

Treatment of varicose veins depends on their location, size, and severity. Typically the superficial varicose veins can be excised and stripped, allowing blood only to drain into the deep system.

Anatomy_Gray_393

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_394

Anatomy_Gray.txt

All organs require a blood supply from the arteries and drainage by veins. Within most organs there are multiple ways of perfusing the tissue such that if the main vessel feeding the organ or vein draining the organ is blocked, a series of smaller vessels (collateral vessels) continue to supply and drain the organ.

Anatomy_Gray_395

Anatomy_Gray.txt

In certain circumstances, organs have more than one vessel perfusing them, such as the hand, which is supplied by the radial and ulnar arteries. Loss of either the radial or the ulnar artery may not produce any symptoms of reduced perfusion to the hand.

Anatomy_Gray_396

Anatomy_Gray.txt

There are circumstances in which loss of a vein produces significant venous collateralization. Some of these venous collaterals become susceptible to bleeding. This is a considerable problem in patients who have undergone portal vein thrombosis or occlusion, where venous drainage from the gut bypasses the liver through collateral veins to return to the systemic circulation.

Anatomy_Gray_397

Anatomy_Gray.txt

Normal vascular anastomoses associated with an organ are important. Some organs, such as the duodenum, have a dual blood supply arising from the branches of the celiac trunk and also from the branches of the superior mesenteric artery. Should either of these vessels be damaged, blood supply will be maintained to the organ. The brain has multiple vessels supplying it, dominated by the carotid arteries and the vertebral arteries. Vessels within the brain are end arteries and have a poor collateral circulation; hence any occlusion will produce long-term cerebral damage.

Anatomy_Gray_398

Anatomy_Gray.txt

In the clinic

Anatomy_Gray_399

Anatomy_Gray.txt

Lymph nodes are efficient filters and have an internal honeycomb of reticular connective tissue filled with lymphocytes. These lymphocytes act on bacteria, viruses, and other bodily cells to destroy them. Lymph nodes tend to drain specific areas, and if infection occurs within a drainage area, the lymph node will become active. The rapid cell turnover and production of local inflammatory mediators may cause the node to enlarge and become tender. Similarly, in patients with malignancy the lymphatics may drain metastasizing cells to the lymph nodes. These can become enlarged and inflamed and will need to be removed if clinically symptomatic.