COORDINATED MOVEMENTS OF THE HAND

COORDINATED MOVEMENTS OF THE HAND

The apparently simple human functions of closing the hand to grasp an object, or opening the palm to release it, are in reality tasks of considerable mechanical complexity, requiring the simultaneous contraction of many individual muscles. The isolated action of a single muscle may be inferred from the positions of its origin and insertion, and the estimated line of action (usually the centre line of the muscle) in relation to the axes of all the joints traversed by the muscle and its tendon. The limb can be regarded as a chain of joints crossed by muscles. If it is known which muscles are active, then the reason why one joint moves and others do not is a matter of simple mechanical relationships.

For example, flexor pollicis longus is considered to have a major role as a flexor of the interphalangeal joint of the thumb. However, the position of its tendon relative to more proximal joints in the limb gives it the potential for producing flexion at the metacarpophalangeal joint and also at the trapeziometacarpal and wrist joints. In the living subject the actual motion that takes place depends on which other muscle groups are acting, and so the potential for movement must be considered for each joint in the chain in turn. Motion at the wrist is generally balanced by wrist extensors. Motion at the trapeziometacarpal joint is balanced by abductor pollicis longus. Flexor pollicis longus will then have an action as a flexor of the metacarpophalangeal and interphalangeal joints only.

The factor that determines whether one or both of two joints will move is the turning moment at each. The greater the perpendicular distance from the line of muscle or tendon pull to the axis of the joint, the stronger is the turning effect of the muscle at the joint, but the smaller the range of joint motion that can be produced. In the case of flexor pollicis longus, the tendon is situated further from the axis of the metacarpophalangeal joint than from the axis of the interphalangeal joint: it will therefore tend to produce flexion preferentially at the metacarpophalangeal joint unless that joint is restrained by extensor pollicis brevis. In this way different postures of the thumb can be produced by the interplay of flexor and extensor forces. These simple guiding principles should provide an understanding of muscle action in the hand that is sufficient for most purposes.

In considering the role of a particular muscle, there is a tendency to concentrate on motion. Indeed, many muscles are named on the basis of the movements that they generate, although others – often those whose actions are the most difficult to interpret – are described according to their morphology or situation. A more important function may be the nature of the force generated. For example, although flexor pollicis longus flexes the thumb (see above), a large range of flexion is actually required in only a few activities, such as certain ripping tasks. In most pinch and manipulative tasks the role of the thumb is to apply isometric force, which it does with such precision that it is possible to pick up an egg and neither crush nor drop it. Thus for much of the time flexor pollicis longus behaves as an extremely sophisticated mechanism for the application of force, in which contraction and proprioception are equally important.

The anatomical position of the hand (palm flat and pointing anteriorly, forearm supinated) is a convenient standard for studying structural relationships. The hand in the relaxed (anaesthetized) position adopts a posture of partial flexion and mid-supination/pronation (the reader can verify this by relaxing completely and observing forearm and hand position).

POLYCYTHEMIA VERA

POLYCYTHEMIA VERA

Polycythemia vera is a disorder in the group of chronic myeloproliferative disorders (MPDs), also refered to as myeloproliferative neoplasms, that includes essential thrombocythemia (ET), primary myelofibrosis (PMF), and chronic myelogenous leukemia (CML). Polycythemia vera is an acquired clonal primary polycythemic disorder. Primary polycythemias result from abnormal intrinsic properties of erythroid progenitors that proliferate independently or excessively in response to extrinsic regulators; low serum erythropoietin is their hallmark. The most common primary polycythemia is polycythemia vera. Polycythemia vera arises from mutations in a multipotential hematopoietic stem cell, which results in an excess production of functionally normal erythrocytes, a variable overproduction of granulocytes and monocytes, and of platelets. It is usually accompanied by splenomegaly. Most patients with polycythemia vera have a somatic mutations of the Janus-type tyrosine kinase-2 gene (JAK2) that is detectable in blood myeloid cells. This mutation, JAK2 V617F, results in constitutive hyperactivity of JAK2 stemming from the loss-of-function of its negative regulatory domain. JAK2 V617F is present in virtually all cases of polycythemia vera; however, ET, MF, and, much less commonly, other hematologic neoplastic disorders are also associated with this mutation, albeit at lower frequency. As with other clonal hematologic disorders, polycythemia vera can undergo a clonal evolution to PMF (typically JAK2 V617-positive) and acute leukemia (often JAK2 V617-negative). In virtually all PV JAK2 V617F-positive patients at least some progenitors exist that became homozygous for the JAK2 V617F mutation by uniparenteral disomy acquired by mitotic recombination and the majority of these account for the erythropoietin-independent erythroid colonies detected in vitro by clonogenic burst-forming unit–erythroid assay (BFU-E). The JAK2 V617F mutation is not a cause of clonal proliferation of these disorders but is preceded by other germ-line and somatic mutation(s) that remain to be identified. Arterial and venous thromboses are the major causes of morbidity and mortality of polycythemia vera. A small proportion of patients develop secondary myelofibrosis (spent phase) and/or an invariably fatal acute leukemic transformation. Myelosuppressive therapy has been an effective mode of therapy, with drugs such as hydroxyurea, busulfan, and radioactive phosphorus useful in controlling proliferation of all blood cell lineages. Myelosuppressive therapy decreases the incidence of thrombotic complications but these drugs have variable leukemogenic potential. Newer, better-tolerated preparations of interferon such as pegylated interferon-alpha may lead to complete hematologic remission and restoration of polyclonal hematopoiesis. Targeted therapy with JAK2 kinase inhibitors is currently being evaluated for effects on splenomegaly and splenomegaly-associated symptoms, hypercoagulability, and control of the polycythemia vera clone.

ACETAMINOPHEN (PARACETAMOL) POISONING

ACETAMINOPHEN (PARACETAMOL) POISONING

Overdosage of acetaminophen is the most common pediatric poisoning and can produce severe hepatotoxicity. The incidence of hepatotoxicity in adults and adolescents has been reported to be 10 times higher than in children younger than age 5 years. In the latter group, fewer than 0.1% develop hepatotoxicity after acetaminophen overdose. In children, toxicity most commonly results from repeated overdosage arising from confusion about the age-appropriate dose, use of multiple products that contain acetaminophen, or use of adult suppositories.

Acetaminophen is normally metabolized in the liver. A small percentage of the drug goes through a pathway leading to a toxic metabolite. Normally, this electrophilic reactant is removed harmlessly by conjugation with glutathione. In overdosage, the supply of glutathione becomes exhausted, and the metabolite may bind covalently to components of liver cells to produce necrosis. Some authors have proposed that therapeutic doses of acetaminophen may be toxic to children with depleted glutathione stores. However, there is no evidence that administration of therapeutic doses can cause toxicity, and only a few inadequate case reports have been made in this regard.

Treatment

Treatment is to administer acetylcysteine. It may be administered either orally or intravenously. Consultation on difficult cases may be obtained from your regional poison control center or the Rocky Mountain Poison and Drug Center. Blood levels should be obtained 4 hours after ingestion or as soon as possible.

The nomogram is used only for acute ingestion, not repeated supratherapeutic ingestions. If the patient has ingested acetaminophen in a liquid preparation, blood levels obtained 2 hours after ingestion will accurately reflect the toxicity to be expected relative to the standard nomogram. Acetylcysteine is administered to patients whose acetaminophen levels plot in the toxic range on the nomogram. Acetylcysteine is effective even when given more than 24 hours after ingestion, although it is most effective when given within 8 hours

The oral (PO) dose of acetylcysteine is 140 mg/kg, diluted to a 5% solution in sweet fruit juice or carbonated soft drink. The primary problems associated with administration are nausea and vomiting. After this loading dose, 70 mg/kg should be administered orally every 4 hours for 72 hours.

For children weighing 40 kg or more, IV acetylcysteine (Acetadote) should be administered as a loading dose of 150 mg/kg administered over 15–60 minutes; followed by a second infusion of 50 mg/kg over 4 hours, and then a third infusion of 100 mg/kg over 16 hours.

For patients weighing less than 40 kg, IV acetylcysteine must have less dilution to avoid hyponatremia.

☆Aspartate aminotransferase (AST–SGOT), alanine aminotransferase (ALT–SGPT), serum bilirubin, and plasma prothrombin time should be followed daily. Significant abnormalities of liver function may not peak until 72–96 hours after ingestion.

☆Repeated miscalculated overdoses given by parents to treat fever are the major source of toxicity in children younger than age 10 years, and parents are often unaware of the significance of symptoms of toxicity, thus delaying its prompt recognition and therapy.

CHOLECYSTOHEPATIC TRIANGLE

Cholecystohepatic triangle or CALOT'S Triangle

Boundaries:

Lateral: Cystic duct and gall bladder.
Medial: Common hepatic duct.
Above: Inferior surface of right lobe of the liver

Contents:

☆Right hepatic artery and its branch, the cystic artery
☆Cystic lymph node of Lund