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Posterior triangle of the neck What are the borders of the posterior triangle of the neck? Posterior border of sternocleidomastoid Anterior border of trapezius Middle one-third of clavicle Roof of skin medications you cant drink alcohol cheap prasugrel 10mg online, platysma treatment for hemorrhoids generic 10 mg prasugrel with amex, investing layer of deep cervical fascia and external jugular vein Floor of pre-vertebral fascia covering muscles treatment improvement protocol purchase prasugrel us, subclavian artery, trunks of brachial plexus and cervical plexus What are the contents of the posterior triangle? Nerves – Spinal root accessory and branches of cervical plexus Arteries – Superficial (transverse) cervical, suprascapular and occipital Veins – Transverse cervical, suprascapular and external jugular Muscle – Omohyoid with sling Lymph nodes – Level 5 What is the course of the spinal accessory nerve? It has been given the name spinal accessory since it originates from the upper end of the spinal cord (spinal roots, C1–C5). It passes through the foramen magnum and ‘hitches a ride’ with the cranial accessory nerve originating from the nucleus ambiguus. Its function is to supply only two muscles in the neck – the sternocleidomastoid and trapezius muscles. It traverses the posterior triangle of the neck from one-third of the way down the posterior border of the sternocleidomastoid muscle to one-third of the way up the anterior border of trapezius where it terminates (the ‘rule of thirds’). It is vulnerable to iatrogenic injury in procedures that necessitate dissection within the posterior triangle of the neck, such as excision biopsy of a lymph node. In a radical en-bloc lymph node dissection of the neck for malignant disease, the spinal accessory nerve may have to be deliberately sacrificed in order to obtain satisfactory clearance. What are the consequences of injury to the spinal accessory nerve in the posterior triangle of the neck? Damage to the spinal accessory nerve in the posterior triangle of the neck leads to a predictive weakness of the trapezius muscle. This results in an inability to shrug the shoulder on the side in which the spinal accessory nerve is affected and may result in winging of the scapula. The sternocleidomastoid muscle is typically spared as the branch to sternocleidomastoid is given off prior to the spinal accessory nerve entering the posterior triangle of the neck. The trapezius muscle also plays a role in hyperabduction of the arm and so activities such as combing one’s hair would become more difficult. In the long term, the trapezius palsy (with dropping of the shoulder) may result in a chronic, disabling neuralgia. This may occur as a result of pain from neurological denervation, adhesive capsulitis of the shoulder joint, traction radiculitis of the brachial plexus, or more commonly from fatigue. Major salivary glands: Parotid (predominantly serous exocrine secretion) Submandibular (mixed mucinous and serous) Sublingual (mainly mucinous exocrine secretion) Minor salivary glands: Scattered throughout the oral mucosa and submucosa (labial, buccal, palatoglossal, palatal and lingual) What important structures lie within the parotid gland? The retromandibular vein is the commonest culprit in a haematoma following parotidectomy. The facial nerve is the most superficial structure within the parotid gland and hence is extremely vulnerable to injury during parotid surgery. If the retromandibular vein comes into view, the facial nerve has already been severed! A facial nerve monitor should be used throughout and it is important to identify and protect the various branches of the facial nerve, which may be remembered by the mnemonic ‘Ten Zulus Baited My Cat’ (from top to bottom): Ten = Temporal branch Zulus = Zygomatic branch Baited = Buccal branch My = Marginal mandibular branch Cat = Cervical branch the branches of the facial nerve are also likely to be injured by a malignant tumour of the parotid which is usually highly invasive and quickly involves the facial nerve, causing a facial paralysis. The duct opens on the mucous membrane of the cheek opposite to the second upper molar tooth. The secreto-motor supply to the parotid (for secretion of saliva) is by way of parasympathetic fibres of the glossopharyngeal nerve (lesser petrosal nerve), synapsing in the otic ganglion and relaying onwards to the parotid gland through the auriculotemporal nerve. A direct consequence of the innervation of the parotid gland is a phenomenon known as Frey’s syndrome which may occur, not infrequently, following parotid surgery, or penetrating trauma to the parotid gland. It is caused by misdirected reinnervation of the auriculotemporal nerve fibres to the sweat glands in the facial skin following its injury.
Diseases
Overgrowth radial ray defect arthrogryposis
Ciliary dyskinesia-bronchiectasis
M?bius axonal neuropathy hypogonadism
Crow Fukase syndrome
Miller Dieker syndrome
Chromosome 17, trisomy 17p
Chondrodysplasia punctata
Adenoma of the adrenal gland
Van der Woude syndrome
Adenocarcinoma of lung
This agglutinating globulin had the IgG in the serum of normal individuals treatment 4 anti-aging generic prasugrel 10 mg, as well as those peculiar ability to enhance the action of an extremely dilute with a variety of diseases other than rheumatoid arthritis symptoms vomiting diarrhea buy prasugrel 10 mg low price. Agglutinating activating factor was later the Fc region of denatured IgG molecules was found to called rheumatoid factor medicine 4 you pharma pvt ltd generic 10mg prasugrel visa, refecting its association with rheu- be the primary antigen reactive with rheumatoid factor. Rheumatoid factors are natural humoral antibodies whose levels are markedly increased by the etiologic agent or Subsequent studies demonstrated that sera from rheumatoid agents of rheumatoid arthritis and, occasionally, the agents arthritis patients could agglutinate not only certain strepto- of other disease states. Attempts to correlate reac- role of rheumatoid factor in the pathogenesis of rheumatoid tivity against bacteria with the progress of the disease led to arthritis remains an enigma. Further studies of rheumatoid arthritis revealed that anti- the demonstration that rheumatoid factor reacted best with gen–antibody complexes became entrapped on the syn- denatured gammaglobulin led to the concept that it might be ovial surface and in fbrocartilage followed by activation an autoantibody. Franklin and co-workers found both 19S of various biological amplifcation mechanisms, including rheumatoid factor and 7S gammaglobulin as a 22S complex complement, kinins, clotting, fbrinolysis, and phagocyto- when the sera of rheumatoid arthritis patients were studied by sis. Epstein and colleagues showed the abil- found to produce rheumatoid factor and IgG molecules ity of rheumatoid factor and gammaglobulin to give a posi- that were secreted into the joint space, perhaps perpetuat- tive precipitin reaction. The discovery of rheumatoid arthritis in IgG was able to block the interaction of rheumatoid factor, agammaglobulinemic children and the fact that rheuma- and globulin coating-sensitized cells further substantiated toid factor did not produce ill effects following infusion the concept of rheumatoid factor as an autoantibody. Nevertheless, IgM rheumatoid factors were found not to be species restric- immune complexes containing IgG rheumatoid factor and tive, indicating the sharing of active sites on the Fc fragment cryoglobulins were implicated in the pathogenesis of rheu- of human IgG with corresponding structures on immunoglobu- matoid vasculitis. Regrettably, investigation of immune lin molecules of many other mammalian species. Milgrom and complexes was not able to account for joint infammation or Witebsky immunized rabbits with aggregated autologous glob- vasculitis. Abnormal cellular immune phenomena in rheu- ulin and discovered that the rabbits produced antibodies with matoid arthritis were found to include anergy, depressed greater reactivity for human globulin than for rabbit globulin. Possible matoid factors, were conducted by Kunkel and cowork- explanations for the uncontrolled synthesis of rheumatoid ers at the Rockefeller University. Among these individuals factor antibodies against native IgG have included chronic were Franklin and co-workers, Fudenberg and co-workers, antigenic stimulation, enhanced T-helper cell function, or Edelman and colleagues, and a host of others. History of Immunology 45 sj ö g r e n ’s sy n d r o m e further substantiating the autoimmune nature of rabbit anti- rabbit thyroid antibody. This disorder was described as a triad of keratoconjunc- tivitis sicca, xerostomia, and rheumatoid arthritis. In one Following the demonstration by Witebsky and colleagues manifestation the sicca component predominates, whereas in that ammonium sulfate fractionated rabbit thyroglobulin the other the sicca occurs in conjunction with either rheu- incorporated into Freund’s complete adjuvant could elicit matoid arthritis or another disorder. Sjögren’s syndrome has antibodies in the autologous host that were reactive with rab- been associated with the presence of specifc antibodies and bit thyroid extract, Beutner and associates showed by immu- T-lymphocyte sensitization against salivary duct antigens. Anderson and colleagues showed precipitating antibodies reactive with organ extracts Although frst considered to be anatomically isolated in the in the sera of 10 of 29 patients with Sjögren’s syndrome. The follicles of the thyroid gland, and not in contact with immuno- presence of antinuclear antibodies and a positive test for competent cells under normal conditions, relatively low levels rheumatoid factor suggested a resemblance of Sjögren’s syn- of circulating thyroglobulin were subsequently demonstrated. As evidenced T cells were found to be tolerant of low doses of thyroglobulin by lymphoid infltrate of the salivary glands, patients with in the circulation, whereas B cells remained immunocompe- Sjögren’s syndrome were shown to manifest many different tent. In the absence of a signal from the T cell, B cells fail to kinds of lymphoproliferation, most as benign lymphoid infl- mount an autoimmune response against thyroglobulin. Occasional patients developed lymphoproliferation following interaction between serum of Hashimoto thyroiditis leading to lymphoma or Waldenström’s macroglobulinemia. This represented the frst proof that humans with thyroid disease contained cir- culating antibodies reactive with thyroglobulin.
B: One hour later treatment goals and objectives prasugrel 10mg generic, after rapid infusion of fluid medicine 027 generic prasugrel 10 mg line, Kerley A and B-lines are visible symptoms pregnancy purchase prasugrel paypal, with a perihilar predominance. Thickening of the right minor fissure also is visible (arrow) as a result of subpleural edema. Pulmonary edema, the acute respiratory distress syndrome, and radiology in the intensive care unit. B-mode ultrasound lung pattern in a case of advanced pulmonary edema, showing multiple wide B- lines that tend to merge. Real-time lung ultrasound for the diagnosis of alveolar consolidation and interstitial syndrome in the emergency department. The Z-line is also comet tail shaped but can be distinguished from B-lines by the fact that the Z-line (1) quickly fades as it moves away from the bright-line pleural sunset line and never extends all the way to the bottom of the ultrasound image as the B-line does, and (2) does not erase A-lines as the B-line does (Fig. The E-line is another comet tail–shaped artifact that differs from Z- and B-line in that it never arises from the bright-line pleural sunset line, but arises at a point superficial to the pleural line from subcutaneous emphysema or multiple shotgun pellets in the subcutaneous tissue (Figs. Compared with B-lines, they are ill defined, they quickly vanish, after less than 4 cm, and they do not erase the A-line. These comet tails, which spread up to the edge of the screen without fading, do not arise from the pleural line (the rib shadow, which is part of the bat sign, is not visible). The patient has subcutaneous emphysema with extensive collections of gas between anatomic structures—a condition generating E-lines. B: Ill- defined comet-tail artifacts (arrowheads) arise from the pleural line but do not erase the physiologic A-lines (arrows) and quickly vanish without reaching the edge of the screen. Patients suffering from pneumonia will often exhibit the “ragged line” sign which is caused by the reflection of ultrasound waves at the margin of lung consolidation (Figs. Patients suffering from pulmonary embolism will present clinically with shortness of breath, pleuritic chest pain, hemoptysis, and ultrasound scan of the lung demonstrates pleura-based lesions that are most often wedge shaped, although rounded pleura-based defects can be seen in smaller pulmonary infarcts (Figs. Large pleural effusions are easily identified by ultrasound as anechoic areas with well-defined borders. Often the clinician can identify the sharp sign, which has the appearance of the sharp sign used in music or a hashtag or pound sign. The four lines that make of the sharp sign are the upper and lower acoustic shadows of the ribs, the pleural line, and the deep border of the fluid itself (Fig. M-mode ultrasound will help confirm the presence of pleural effusion by demonstration of the “sinusoidal sign” (Fig. The sine wave appearance is caused by the compression of the fluid between the layers of pleura as respiration causes the intrapleural distance to change. Ultrasound can be used not only to identify the presence and location of pleural effusions, but also to quantify their size and impact on the underlying lung (Fig. Ultrasound measurement of the size of effusion pre- and postthoracentesis may also be clinically useful, especially in the setting of recurrent pleural effusions (Fig. The ultrasonic echotexture of the effusion may give the clinician the nature of the effusion, with more echogenic textures suggestive of significant exudate and/or empyema (Fig. Hypoechoic subpleural lesion, with blurred irregular margins and pleura breakdown. Real-time lung ultrasound for the diagnosis of alveolar consolidation and interstitial syndrome in the emergency department.
Specificity is the proportion of people free from disease who react negatively to the test (the higher the specificity the fewer the false positives) medicine abbreviations prasugrel 10mg visa. Alpha-fetoprotein screening is used to detect certain foetal abnormalities in pregnant women treatment 5 shaving lotion order 10mg prasugrel with amex. Cancer screening is an attempt to prevent cancer symptoms 7 days before period buy prasugrel 10 mg low price, or diagnose it in its early stages. For example, the Pap smear is used to detect potentially precancerous lesions and prevent cervical cancer. It provides free breast screening (mammography) every 3 years for all women over 50 years of age. It is a systematic process by which a group of professionals review a current system of practice to identify weakness, make changes and monitor the standard of practice. According to the National Institute for Clinical Excellence, it is ‘a quality improvement process that seeks to improve patient care and outcome through systematic review of care against explicit criteria and the implementation of change’. Standards-based audit – A cycle which involves defining standards, collecting data to measure current practice against those standards and implementing any changes deemed necessary. Peer review – An assessment of the quality of care provided by a clinical team with a view to improving clinical care. Adverse occurrence screening and critical incident monitoring – This is used to peer review cases, which had adverse or unexpected outcomes. A multidisciplinary team discusses individual cases, addresses the way the team functioned and what can be learnt for the future. Patient surveys and focus groups – Allows patients’ views about the quality of care to be heard. The clinical audit cycle is a systematic process of establishing best practice; measuring against criteria, taking action to improve care and monitoring to achieve improvement. Stage 1 – Identify the problem Stage 2 – Define criteria & standards Stage 3 – Data collection Stage 4 – Compare performance with criteria and standards Stage 5 – Implementing change Stage 6 – Re-audit: close the audit loop What is clinical governance? Clinical governance is the term used to describe a systematic approach of maintaining and improving the quality of patient care within a health-care system. There are three key attributes: Maintaining high standards of care Transparent responsibility and accountability for standards Aim for constant improvement What are the seven pillars of clinical governance? A controlled trial is a scientific experiment in which one or more treatments are compared with a control treatment. Randomisation is a method of assigning subjects to an experimental or control arm of a study. In the best randomised controlled trials, neither patient nor researcher is aware of which therapy has been used until after the study has been conducted (double-blinded). It may be complete or incomplete (based on whether both cortices are involved), or open or closed (based on whether the overlying skin is intact). Reactive phase – Fracture and inflammatory phase, followed by granulation tissue formation Reparative phase – Callus formation and lamellar bone deposition Remodelling phase – Remodelling to the original bone contour What classification do you know for proximal femoral fractures? The treatment of bone fractures depends upon the type and location of the fracture and the patient’s age and medical history. However, four phases can be identified (4 R’s): Resuscitation Reduction (open or closed) Restriction (immobilisation) (cast splintage, functional bracing, continuous traction, internal fixation, external fixation) Rehabilitation (Physiotherapy) What are the complications of fractures? Early complications Local: Vascular injury causing haemorrhage (internal or external) Visceral injury causing damage to the surrounding organs (i.
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