It is reasonable to accept that valvular regurgitation may not always be detected by routine clinical auscultation 60caps lasuna sale cholesterol medication safe in pregnancy. This suggests that carditis was missed by clinical examination purchase lasuna 60caps on-line cholesterol definition chemistry, even in the golden era of clinical auscultation buy 60caps lasuna amex cholesterol in eggs myth. A second advantage of echocardiography is that it should allow the valve structure to be detected, as well as nonrheumatic causes of valvular dysfunction (e. This could be ascribed either to the high sensitivity of Doppler echocardiography for diagnosing valvular regurgitation, or to the overdiagnosis of physiological valvular regurgitation as an organic dysfunction, or to both. But in many developing countries, it is unreasonable to expect that previous echocardiograms or records will be available for comparison. Transesophageal echocardiography: technique, anatomic correlations, implementation, and clinical applications. Role of echocardiography in the diagnosis and follow-up evaluation of rheumatic carditis. Directions for the use of intracardiac high-frequency ultrasound scanning for monitoring pediatric interventional catheterization procedures. Three-dimensional and four-dimensional transesophageal echocardiographic imaging of the heart and aorta in humans using a computed tomographic imaging probe. Prevalence of rheumatic fever and rheumatic heart disease in school children of Kathmandu city. The prevalence of valvular regurgitation in children with structurally normal hearts: a colour Doppler echocardiographic study. Is continuous wave Doppler too sensitive in diagnosing pathologic valvular regurgitation? Evidence against a myocardial factor as the cause of left ventricular dilation in active rheumatic carditis. Echocardiographic evaluation of patients with acute rheumatic fever and rheumatic carditis. Inﬂammatory valvular prolapse produced by acute rheumatic carditis: echocardiographic analysis of 66 cases of acute rheumatic carditis. Quantitative assessment of mitral regurgitation by Doppler colour ﬂow imaging: angiographic and hemodynamic correlations. Semiquantitative assessment of mitral regurgitation by Doppler colour ﬂow imaging in patients aged <20 years. Noninvasive estimation of left ventricular end-diastolic pressure using transthoracic Doppler-determined pulmonary venous atrial ﬂow reversal. American Heart Association guidelines for the diagnosis of rheumatic fever: Jones criteria, 1992 update. Long-term outcome of patients with rheumatic fever receiving benzathine penicillin G prophylaxis every three weeks versus every four weeks. Three-versus four-week administration of benzathine penicillin G: effects on incidence of streptococcal infections and recurrences of rheumatic fever. Role of echocardiography in the timing of surgical intervention for chronic mitral and aortic regurgitation. Doppler echocardiographic ﬁndings of mitral and aortic valvular regurgitation in children manifesting only rheumatic arthritis. Echocardiographic diagnosis of subclinical carditis in acute rheumatic fever (editorial). Usefulness of echocardiography in detection of subclinical carditis in acute rheumatic polyarthritis and rheumatic chorea. Advocacy for echocardiography in Jones criteria for the diagnosis of rheumatic fever. Manila, Philippine Foundation for the Prevention and Control of Rheumatic Fever and Rheumatic Heart Disease, 2001:27–33. Prospective comparison of clinical and echocardiographic diagnosis of rheumatic carditis: long term follow up of patients with subclinical disease. Intravenous immunoglobulin in acute rheumatic fever: a randomized controlled trial. Occurrence of valvular heart disease in acute rheumatic fever without evident carditis: colour ﬂow Doppler identiﬁcation. A common colour ﬂow Doppler ﬁnding in the mitral regurgitation of acute rheumatic fever. Doppler echocardiography distinguishes between physiologic and pathologic “silent” mitral regurgitation in patients with rheumatic fever. Persistence of acute rheumatic fever in the intermountain area of the United States. The value of echocardiography in the diagnosis and follow up of rheumatic carditis in children and adolescents: a 2 years prospective study. Echocardiographic evaluation of patients with acute rheumatic fever and rheumatic carditis. American Heart Association guidelines for the diagnosis of rheumatic fever: Jones criteria, updated 1992. A long-term epidemiologic study of subsequent prophylaxis, streptococcal infections, and clinical sequelae. Relation of the rheumatic fever recurrence rate per streptococcal infection to preexisting clinical features of the patients. A long- term epidemiologic study of subsequent prophylaxis, streptococcal infections, and clinical sequelae. The teaching and practice of cardiac auscultation during internal medicine and cardiology training. The microbiol- ogy laboratory plays an important role in ensuring that the documen- tation of group A streptococcal infections is accurate. It does so by using scientiﬁc methods both to determine whether group A strepto- cocci (Streptococcus pyogenes) are present on swabs from suspected streptococcal throat infections, and to measure streptococcal serum antibody titres for documenting previous infection. The conventional methods and procedures for serologically identifying group A strep- tococcal infections are described elsewhere (3). Diagnosis of streptococcal infection Group A streptococci can be subdivided into more than 130 distinct types, based upon a characterization of the M protein of the cell wall, opacity factors antigens produced by the organism, and by molecular sequencing of the emm gene that codes for M protein. A less-speciﬁc method is to determine the T-antigen pattern, but similar T antigens may be shared by several different M types (4–7). Nevertheless, all group A streptococci produce hemolysis on blood agar, and have an optimum growth temperature in the range 35–37°C. The gold standard for detecting Streptococcus pyogenes remains a throat swab cultured on blood agar, although it takes 24–48 hours to produce a result, with the consequent delay in starting antibiotic therapy. If possible, throat swabs should be examined for all patients with clinically suspected streptococcal upper respiratory tract infec- tion. The correct procedure for taking a throat swab is to directly observe the tonsillar-pharyngeal area while vigorously swabbing the tonsils or tonsillar crypts and the posterior pharyngeal wall (2, 4, 8–10).
Types of Suture Materials Suture materials can generally be classified as absorbable and non absorbable buy cheap lasuna 60 caps line cholesterol cell membrane. Catgut (natural or biologic type) Vicryl (Synthetic) Non absorbable: This is a type of suture material that remains unabsorbed by the tissue generic lasuna 60 caps free shipping cholesterol test blood donation. Figure 2: Continuous Sutures Useful Tips: • Place a single suture and ligate but only cut the short end of the suture buy lasuna on line cholesterol definition for biology. Figure 3: Mattress Sutures Fig 3 a: Horizontal Fig 3 b: Vertical Mattress sutures may be either vertical or horizontal. Small bites of the subcuticular tissues on alternate sides of the wound are taken and then pulled carefully together. Introduction Successful wound management with rapid and complete healing and minimal complication depends on understanding the basic principles of assessment, bacteriology and application of the general principles of wound care. The primary goal of wound management is to aid the natural body process to produce optimal functional and cosmetic result. This requires an understanding of the basic principles of wound care and the process of healing. Failure to do this may result in delay of healing and unwanted secondary complications which may be distressing to the physician, patient and family and may lead to greater economic loss. It is caused by a transfer of any form of energy into the body which can be either to an externally visible structure like the skin or deeper structures like muscles, tendons or internal organs. There are integrated sequences of events leading to cellular proliferation and remodeling. It is characterized by vaso-constriction, clot formation and release of platelets and other substances necessary for healing and help as a bridge between the two edges. It is characterized by classical inflammatory response, vasodilatation and pouring out of fluids, migration of inflammatory cells and leukocytes and rapid epithelial growth. It is characterized by fibroblast, epithelial and endothelial proliferation, Collagen synthesis, and ground substance and blood vessel production. Equilibrium between protein synthesis and degradation occurs during this phase with cross linking of collagen bundles leading to slow and continuous increase in tissue strength of the wound to return to normal. Clinical types of healing Traditionally, wound healing can be classified into three clinical types: Healing by first, second and third intention. Healing by first intention: This is a type of healing of clean wound closed primarily to approximate the ends. Healing by Second intention: This occurs in wide, contaminated wounds, which are not primarily closed. Healing takes place by granulation tissue formation, tissue contraction and epithelialization. Healing by third intention: This occurs in wounds which are left open initially for various reasons and closed later (delayed primary closure) 48 Factors affecting healing Healing of a wound can be affected by various conditions. In the history, one has to answer the following principal questions: • How the wound was caused and what caused it? General inspection and specific tests have to be done to assess the following conditions: • Extent of skin loss • Degree of circulation • Damage to nerves, tendons, bone and other structures (deep under) the skin • The degree of contamination • Presence of foreign body and tissue necrosis 49 Classification of wounds Once wound is carefully assessed, it is necessary to classify into a specific type in order to plan a proper management scheme. Closed wounds: These are wound types, which have an intact epithelial surface, and skin cover not completely breeched. Example: Contusion, Bruise, Hematoma Open wounds: These are wounds caused by injury which leads to a complete breakt of the epithelial protective surface. Example: Abrasion, Laceration, Puncture, Missile injuries, Bites… The following method is the traditional surgical wound classification scheme that was introduced in 1964. This method classifies wounds according to the likelihood or rate of wound infection. Clean: Non-traumatic, non-infected wound, no break in sterility technique, the respiratory, gastrointestinal or genitourinary tracts not entered. Clean-contaminated: Minor break in technique, oropharynx entered, gastrointestinal or respiratory tracts entered without significant spillage, genitourinary or biliary tracts entered in absence of infected urine or bile. If other serious conditions exist, which endanger the patient’s life, the wound should be covered with sterile gauze and priorities attended to. However, the goal in all cases is to establish a good environment to assist wound healing and prevent infection. Proper wound care includes the following measures: • Adequate hemostasis locally to stop bleeding. However, general guidelines that can be followed are: • Clean wounds should be closed primarily • Clean-contaminated wounds can be primarily closed if they can be converted, into clean wounds • Untidy, contaminated wounds which cannot be converted to tidy wounds should not be closed primarily • All missile wounds, animal and human bites should never be primarily closed unless strongly indicated Primary closure Primary closure is effective in wounds presenting within 6-8 hours and can accurately be debrided. It provides a reliable drainage and opportunity for repeated inspection and debridement as necessary. There is no specific management needed except local compress and analgesics if pain is severe. Management: - It usually gets absorbed spontaneously and should be left - Local compress to alleviate pain - Aseptic evacuation or aspiration only if very large (expanding) or over a cosmetic area or leading to compression of vital structures. Management: - Cleanse using scrubbing brushes - Use antiseptic or lean tap water and soap - Analgesic Punctures These may be compound wounds which involve deeper structures. Management: - Careful inspection - Adequate cleansing - Closure, if feasible, under appropriate anesthesia - Proper wound debridement if needed - Appropriate antibiotic prophylaxis - Tetanus Prophylaxis - Analgesics as needed Crush and avulsion wounds These are compound complicated wounds. They are usually associated with systemic involvement and have more extensive damage than may appear. Management: - Correct associated life threatening conditions - Proper wound debridement - Early skin cover if possible or late graft, wound left open if contaminated - Appropriate antibiotics - Tetanus Prophylaxis - Analgesics as needed Missile injuries These are type of wounds which are compound and complicated. They usually present with severe life threatening conditions and should be carefully managed. Human bites These are relatively rare but more heavily contaminated than those of most animalss due to polymicrobial nature including anaerobic organisms as a normal oral flora. To avoid this complication the animal must be kept for observation for at least 10 days. Management should include: First aid measures: - Local wound irrigation - Apply pressure bandage proximally to avoid or reduce venom spread with caution on the blood supply - Immobilize the limb to minimize venom absorption - Transport patient immediately to nearby hospital Hospital Measures: - Identify the species - Conduct necessary laboratory investigations like hemoglobin, renal function. Local: Local complications may manifest as one or more of the following conditions- - Hematoma - Seroma 55 - Infection - Dehiscence - Granuloma formation - Scar formation - Contracture leading to loss of joint function etc Systemic: - Death may occur if un controlled sepsis or hemorrhage - Systemic manifestations of hemorrhagic shock due to massive bleeding - Bacteremia and sepsis from a source of locally infected wound 56 Review Questions 1. A) Duration of injury B) The circumstance of wounding C) The mechanism of injury D) Local appearance of the wound E) All of the above 2. A) Bullet wound of one hour duration B) Human bite of 30 minutes duration C) Glass laceration of five hours duration D) Crush injury of the leg following car accident E) None of the above 3. A proper wound care includes all measures except A) Removing all devitalized tissue B) Removing foreign bodies impregnated to the wound C) Wound inspection following primary management D) Inadequate hemostasis of a bleeding artery E) Decision to close a wound primarily 4. A) Forearm laceration from a knife B) Dog bite to the calf of one hour duration C) Blast wound to the thigh of two hours duration D) Stick wound to the scalp of four hours E) B and C are correct 5. In a contaminated wound left open to heal without closure, healing is effected by A) First intention B) Second intention C) Third intention D) Purely by epithelialization E) All of the above 7. A) Presence of foreign body B) Systemic illness C) Sex of the patient D) Poor patient nutritional state E) Presence of infection 58 Key to the Review Questions 1.
Specificity: Each cell possesses protein specified to transport a specific substance or few closely-related chemical compounds amino acid cannot bind to glucose carrier purchase lasuna 60 caps online cholesterol vs fatty acid, but similar amino acids may use the same carrier purchase generic lasuna canada cholesterol test kit tesco. A number of inherited disorders involve defects in transport system for a particular substance buy 60caps lasuna with mastercard cholesterol test ottawa. Saturation: In a given time only a limited amount of a substance can be transported via a carrier; limited number of carrier site are available within a particular plasma membrane for a specific molecule. The substance’s rate of transport across the membrane are directly related to its concentration. When the Tm is reached, the carrier is saturated, and the rate of transport is maximum. Further increase in the substance concentration is not accompanied by corresponding increase in the rate of transport. Saturation of carrier is a critical rate-limiting factor to the transport of selected substances across the plasma membrane in kidney and the intestine. Competition: Several closely related compounds may compete for ride across the plasma membrane on the same carrier. Primary active transport process Facilitated Diffusion Facilitated diffusion uses a carrier protein to facilitate the transfer of a particular substance across the membrane “downhill” from higher to lower concentration. This process is passive and does not require energy because movement occurs naturally down a concentration gradient. Active transport, on the other hand, requires the carrier to expend energy to transfer its passenger “uphill” against a concentration gradient from an area of lower concentration to an area of higher concentration. Active transport requires protein carrier to transfer a specific substance across the membrane, transporting against concentration gradient. Phosphorylation and binding of particle on the low concentration side induces a conformational change in the carrier protein so that passenger is now exposed to the high concentration side of the membrane. Removal of phosphate reduces the affinity of the binding site for the passenger, so the passenger is released on the high concentration side. It establishes sodium and potassium concentration gradients across the plasma membrane of all cells; these gradients are important in the nerve and muscle to generate electrical signals. It helps regulate cell volume by controlling the concentration of solutes inside the cell and thus minimizing osmotic effects that would induce swelling or shrinking of the cell. The energy used to run the pump also indirectly serves as the energy source for the co-transport of glucose and amino acids across the membrane (intestine and kidney cell). Vesicular Transport The special cell membrane transport system selectively transports ions and small polar molecules. But large polar molecules and even multimolecular material may leave or enter the cell, such as hormone secretion or ingestion of invading microbe by leukocytes. This process of transport into or out of the cell in a membrane-enclosed vesicle is - vesicular transport. Transport into the cell is termed endocytosis, whereas transport out of the cell is called exocytosis. In endocytosis, the transported material is wrapped in a piece of the plasma membrane, thus gaining entrance to the interior of the 30 cell. Endocytosis of fluid is called pinocytosis cell (drinking), whereas endocytosis of large multimolecular particle is known as phagocytosis (cell eating). In some cells, endocytic vesicle bypasses the lysosome and travels to the opposite side of the cell, where it releases its contents by exocytosis. Some materials are transferred through the thin capillary walls cells, between the blood and surrounding tissue fluid. Exocytosis is the reverse of endocytosis, in which a membrane- enclosed vesicle formed within the cell fuses with the plasma membrane, then opens up and releases its contents to the exterior. Such materials are packaged for export by the endoplasmic reticulum and Golgi complex. It is a mechanism for secreting large polar molecules, such as protein molecules and enzymes that cannot cross the plasma membrane. The Vesicular contents are highly specific and are released only upon receipt of appropriate signals. It enables the cell to add specific components to the plasma membrane, such as carrier, channels, or receptors depending on the cell’s need The rate of endocytosis and exocytosis is maintained in balance to maintain a constant membrane surface area and cell volume. More than 100% of the plasma membrane may be used in an hour to wrap internalized vesicles in a cell actively involved in endocytosis, needing rapid replacement of surface membrane by exocytosis. In some cases of endocytosis, receptor sites on the surface membrane recognize and bind with specific molecule in the environment of the cell. Antibodies attach to the bacteria forming a coat that can be recognized by the specific receptor sites in the plasma membrane of the phagocytic leukocyte. A specific neural or hormonal stimuli initiates opening of calcium channels in the membranes of secretory cell. Calcium influx increases cytosolic calcium levels triggering fusion of the exocytic vescicle with plasma membrane and subsequent release of its secretory products. The process of exocytosis 32 Caveolae Role in membrane transport and signal transduction: the outer surface of the plasma membrane is not smooth; it has tiny, cave-like indentations known as caveolae (tiny caves). Coordination of diverse activities to maintain homeostasis requires the cells to communicate with each other. The most intimate communication is through gap junctions, which are minute tunnels that bridge the cytoplasm of nearby cells. Gaps are important in permitting spread of electrical signals from one cell to the next in cardiac and smooth muscle. The presence of signaling molecules on the surface membrane of some cells gives them ability to directly link up and interact with certain other cells in a special way. Thus phagocytic cells recognize and selectively destroy only undesirable cell, such as invading microbes while sparing the body’s own cell. Intercellular chemical messenger is the commonest means by which cells communicate with each other. These chemicals messengers are paracrines, neurotransmitters, hormones, and neurohormones. Various ways of cell-to-cell communicaton 34 Signal Transduction Binding on chemical messenger to membrane receptors brings about a wide range of responses in different cells through only a few similar pathways used. Dispersed within the outer surface on the plasma membrane of cell (muscle/ nerve/ gland) are specialized protein receptors that bind with the selected chemical messenger - neurotransmitter, hormone, or neuro-hormone, that are delivered by the blood or a neurotransmitter released from the neuron. The chemical messenger binds with receptor triggering a sequence of intracellular events that ultimately influence/control a particular cellular activity important in the maintenance of homeostasis, such as membrane transport, secretion, metabolism, or contraction. There are wide ranging responses, but there are mainly two ways by which binding of the receptor with extracellular chemical messenger bring about the desired effects. By opening or closing of specific channels in the membrane regulating a particular ion to move in or move out of the cell, or 2. By transferring the signal to an intracellular chemical messenger (the second messenger), which is turn triggers a preprogrammed series of biochemical events within the cell.
Moreover purchase 60 caps lasuna free shipping cholesterol levels life insurance, plasmin escaping from the fibrin surface is almost instantaneously neutralized by 2- antiplasmin cheap lasuna 60 caps amex cholesterol medication kidney failure. Their severe tissue bleeding after trivial injury establishes 2-antiplasmin as a key regulator of normal fibrinolysis buy lasuna online from canada cholesterol med chart. An occasional patient with decompensated chronic liver disease may bleed uncontrollably because of excessive fibrinolysis thought to partially stem from acquired severe 2-antiplasmin deficiency (secondary to diminished hepatocellular synthesis plus increased consumption caused by excessive plasminogen activator activity). Screening tests measure combined effects of factors that influence a particular phase of coagulation (eg, bleeding time). Additional tests may measure a product or effect of pathologic in vivo activation of platelets, coagulation, or fibrinolysis (eg, level of fibrin degradation products). Screening test results and knowledge of the clinical disorder guide the selection of more specific diagnostic tests. A disposable, spring-loaded bleeding time device is used to make a 6-mm × 1-mm incision on the volar aspect of the forearm. Plasma is incubated for 3 min with a reagent supplying procoagulant phospholipid and a surface-active powder (eg, micronized silica). Because the test is independent of the reactions that generate thrombin, it is used to screen specifically for abnormalities affecting the thrombin-fibrinogen reaction: heparin, large fibrin degradation products, and qualitative abnormalities of fibrinogen. It is particularly useful in establishing whether a plasma sample contains heparin (eg, residual heparin not neutralized after an extracorporeal bypass procedure or contaminated plasma obtained from blood drawn from a line kept open with heparin flushes). In plasma that contains heparin, the thrombin time will be prolonged, but a repeat test will be normal if the reagent batroxobin (a snake venom enzyme insensitive to heparin that directly converts fibrinogen to fibrin) is substituted for thrombin. A normal result does not rule out a milder yet potentially 368 Hematology clinically significant abnormality of fibrinolysis (eg, a reduced plasma 2-antiplasmin level in the 10 to 30% of normal range). One-tenth volume of 1% protamine sulfate is mixed with plasma, which, after a brief incubation at 37° C (98. A false-positive result may be caused by difficulty with venipuncture or by inadequate anticoagulation of a blood sample. In the D-dimer test, undiluted test plasma and diluted test plasma as necessary are mixed with latex particles coated with monoclonal antibodies that react exclusively with derivatives of fibrin that contain D-dimer, which are formed when plasmin degrades cross-linked fibrin. The antibodies will not react with fibrinogen itself, which is why the test can be performed on plasma, nor with fibrinogen degradation products because these are not cross-linked. Agglutination with a 1:20 dilution of serum indicates increased amounts (>= 40 µg/mL) of fibrin degradation products. A euglobulin lysis time is also often part of screening if increased fibrinolytic activity is suspected. The euglobulin fraction, which is relatively free of inhibitors of fibrinolysis, is clotted with thrombin, and the time for the clot to dissolve is measured. Normal lysis is > 90 min; a shorter time indicates increased plasma plasminogen activator activity (eg, in some patients with advanced liver disease). A reduced plasma fibrinogen concentration, by yielding a smaller clot to be dissolved, may also result in a shorter time. Disorders of hemostasis Excessive bleeding may occur as a result of an abnormality of blood vessels, platelets, or coagulation factors. Vascular disorders In vascular bleeding disorders, tests of hemostasis are 370 Hematology usually normal. Purpura Simplex (Easy Bruising) The most common vascular bleeding disorder, manifested by increased bruising and representing increased vascular fragility. No drug prevents the bruising; the patient is often advised to avoid aspirin and aspirin-containing drugs, but there is no evidence that bruising is related to their use. Senile Purpura A disorder affecting older patients, particularly those who have had excessive sun exposure, in whom dark purple ecchymoses, characteristically confined to the extensor surfaces of the hands and forearms, persist for a long time. Lesions slowly resolve over several days, leaving a brownish discoloration caused by deposits of hemosiderin; this discoloration may clear over weeks to months. Hereditary Hemorrhagic Telangiectasia (Rendu- Osler-Weber Disease) A hereditary disease of vascular malformation transmitted as an autosomal dominant trait affecting men and women. Diagnosis is made on physical examination by the discovery of characteristic small, red-to-violet telangiectatic lesions on the face, lips, oral and nasal mucosa, and tips of the fingers and toes. These fistulas may produce significant right-to-left shunts, which can result in dyspnea, fatigue, cyanosis, or polycythemia. However, the first sign of their presence may be a brain abscess, transient ischemic attack, or stroke, as a result of infected or noninfected emboli. Cerebral or spinal arteriovenous malformations occur in some families and may cause subarachnoid hemorrhage, seizures, or paraplegia. Biopsy of an acute skin lesion reveals an aseptic vasculitis with fibrinoid necrosis of vessel walls and perivascular cuffing of vessels with polymorphonuclear leukocytes. Granular deposits of immunoglobulin reactive for IgA and of complement components may be seen on immunofluorescent study. Therefore, deposition of IgA-containing immune complexes with consequent activation of complement is 374 Hematology thought to represent the pathogenetic mechanism for the vasculitis. The disease begins with the sudden appearance of a purpuric skin rash that typically involves the extensor surfaces of the feet, legs, and arms and a strip across the buttocks. Most patients also have fever and polyarthralgia with associated periarticular tenderness and swelling of the ankles, knees, hips, wrists, and elbows. The disease usually remits after about 4 wk but often recurs at least once after a disease-free interval of several weeks. In most patients, the disorder subsides without serious sequelae; however, some patients develop chronic renal failure. The presence of diffuse glomerular involvement or of crescentic changes in most glomeruli predicts progressive renal failure. Vascular Purpura Caused By Dysproteinemias Hypergammaglobulinemic purpura is a syndrome that primarily affects women. It is characterized by a polyclonal increase in IgG (broad-based or diffuse hypergammaglobulinemia on serum protein electrophoresis) and recurrent crops of small, palpable purpuric lesions on the lower legs. Cryoglobulinemia is characterized by the presence of immunoglobulins that precipitate when plasma is cooled (ie, cryoglobulins) while flowing through the skin and subcutaneous tissues of the extremities. In amyloidosis, deposits of amyloid within vessels in the skin and subcutaneous tissues produce increased vascular fragility and purpura. Periorbital purpura or a purpuric rash that develops in a nonthrombocytopenic patient after gentle stroking of the skin should arouse suspicion of amyloidosis. In some patients a coagulation disorder develops, apparently the result of adsorption of factor X by amyloid. Leukocytoclastic Vasculitis A necrotizing vasculitis accompanied by extravasation and fragmentation of granulocytes. Causes include hypersensitivity to drugs, viral infections (eg, hepatitis), and collagen vascular disorders. The most common clinical manifestation is palpable purpura, often associated with systemic symptoms, such as polyarthralgia and fever. Autoerythrocyte Sensitization (Gardner-Diamond Syndrome) An uncommon disorder of women, characterized by local pain and burning preceding painful ecchymoses that occur primarily on the extremities. However, most patients also have associated severe psychoneurotic symptoms, and psychogenic factors, such as self-induced purpura, seem related to the pathogenesis of the syndrome in some patients. Platelet disorders Platelet disorders may cause defective formation of hemostatic plugs and bleeding because of decreased platelet numbers (thrombocytopenia) or because of decreased function despite adequate platelet numbers (platelet dysfunction).
Definition: - inadequate tissue perfusion to supply oxygen and nutrients to meet the metabolic demands of the body - three major types include hypovolemic buy cheap lasuna 60 caps online ideal cholesterol hdl ratio, distributive and cardiogenic - hypovolemic shock is the most common form cheap lasuna online american express cholesterol levels conversion, and is due to an absolute loss of volume from the vasculature (blood loss (hemorrhage) buy generic lasuna 60caps on-line cholesterol & shrimp levels, body water loss (dehydration) or loss of plasma) - distributive shock results when total circulating volume has been redistributed and a functional hypovolemic state results (seen in sepsis, Neutrogena shock and anaphylaxis) - cardiogenic shock occurs when the heart is unable to maintain cardiac output (may be intrinsic i. Evaluation: rapid evaluation of airway, breathing and circulation Clinical history - underlying disease, recent infection or illness, trauma, surgery, etc. Treatment: - establish a patent airway, ensure adequate oxygenation and ventilation (support cervical spine if trauma suspected) - establish intravascular access - fluid resuscitation (crystalloids i. While the hand skills necessary for performing intubation do take a certain amount of practice, the decision of when to intubate and the choice of technique is of at least equal importance, and is often ignored. While you may not acquire significant “hands on” training in intubating non-neonates during your pediatric residency, you will have the opportunity to learn how to decide when someone should be intubated, as well as the potential complications and problems that may be encountered. Indications for intubation--Thinking about the indications will help you decide on a technique. Requirement for positive pressure ventilation due to pulmonary disease (ie, hypoxia or hypercarbia) C. Paralysis relaxes the pharyngeal muscles, which may obscure landmarks in the difficult airway, and may make bag-mask ventilation difficult. Patients with primary cardiac disease, however, generally do not tolerate unsedated intubations, and carefully titrated anesthesia is warranted. Bag-mask ventilation with cricoid pressure and intubation can generally be accomplished without difficulty. These patients should be intubated “awake” to preserve airway protective reflexes, or by rapid sequence induction with cricoid pressure. Head injury-laryngoscopy and intubation may lead to increased intracranial pressure in the unanesthetized patient with an evolving head injury. Nebulized lidocaine (2cc 1% lidocaine in nebulizer) will decrease the laryngospasm and bronchospasm with intubation. Laryngoscopy and intubation should proceed firmly but gently, with attention to the teeth and tongue if the child is struggling V. Lung disease with moderate to high O2 requirement (may desaturate during period of apnea necessary for rapid sequence intubation) B. Co-administration of a small dose of benzodiazepine will reduce emergence phenomena. Gentle ventilatory assistance through cricoid pressure is sometimes necessary in extremely hypoxic or unstable patients. Common theme-Desire to blunt undesirable physiologic response to intubation-hypertension, tachycardia, bronchospasm, increased intracranial pressure. Technique-rapid sequence refers to rapid infusion of medications, followed by a brief period where airway protective reflexes are lost, followed by ideal intubating conditions. During the period after medications are given, cricoid pressure is applied and positive pressure ventilation is avoided. This is a long time if you can’t get the airway or bag mask ventilate the patient. Cardiovascular-succinylcholine stimulates the vagus nerve and sympathetic ganglia leading to bradycardia, hypertension, or hypotension. Hyperkalemia-With depolarization there is opening of acetylcholine receptor channels, allowing efflux of potassium from the cell through receptors in the muscle end plate and extra-junctional receptors. In certain disease processes, there is an upregulation of acetylcholine receptors, and hence, a massive increase in serum potassium with the administration of - 39 - succinylcholine. These include: burns (3 days to 6 months after injury), spinal cord injury (3 days to 1 year after injury), tetanus, severe intra-abdominal infections, Guillain-Barre syndrome, Duchenne’s Muscular Dystrophy, Myotonic Dystrophy, multiple sclerosis, many progressive neuromuscular diseases. Risk factors include positive family history, Duchene’s Muscular Dystrophy, and certain myopathies. Increased intracranial pressure-blunted by pretreatment with adequate sedation and a defasciculating dose of pancuronium. Equipment For any and all intubations, have available: •Large suction catheter “Yankauer” and reliable suction. If there is no leak, there may be increased risk of stridor and airway obstruction due to tracheal edema. Indications: Need for central venous pressure monitoring, need for reliable venous access. Decide on site: subclavian vein, internal jugular vein (contraindicated in patients with increased intracranial pressure), femoral vein (contraindicated in patients with severe abdominal trauma). Internal jugular: place patient in 15-20° angle Trendelenburg position, hyperextend the neck and turn head away from site of line placement, palate sternal and clavicular heads of the muscle and enter at the apex of the triangle formed, insert needle at 30° angle to skin and aim toward ipsilateral nipple b. Subclavian vein: place patient in Trendelenburg position, hyperextend back with towel roll under thoracic spine, aim needle from distal third of clavicle toward sternal notch c. Femoral vein: flex and abduct hip, locate femoral pulse just distal to inguinal crease, place finger on femoral artery to locate, insert needle at 30° angle to skin medial to pulse which should be 2-3cm distal to inguinal ligament, aim for umbilicus 4. When blood return occurs, remove syringe and insert guidewire through needle 1/2 to 3/4 the length of the wire. If you need an additional wire, it must be at least twice the length of the catheter including the hub. Slip catheter (preflushed with sterile saline) over wire into vein with a twisting motion until hub is at the skin. Indications: Need for emergency venous access, for infusion of fluids or medications. If they are on a spontaneous mode of ventilation, change to a controlled mode for the procedure and sedation. Insert the needle at the L3-4 or L4-5 intervertebral space advancing until there is a decrease in resistance or the feeling of a pop as the dura is penetrated 8. Collect about 1cc per tube and send tubes for 1) culture and gram stain 2) glucose and protein 3) cell count and differential 4) hold. Locate the 3 to 5 intercostals space in the mid to anterior axillary line avoiding breast tissue 4. Anesthetize skin, subcutaneous tissue, periosteum of rib, chest-wall muscles and pleura with 1% lidocaine 6. Make sterile incision one intercostal space below target and bluntly dissect with hemostat until superior portion of rib is reached (Remember nerve-artery-vein run along the inferior side of the rib! Push hemostat over tope of rib, through pleura and into pleural space—don’t go deeper than 1 cm into pleural space 8. Spread open hemostat and place chest tube in clamp, then guide to desired distance 9. Placement: pneumothorax—insert tube anteriorly toward apex, pleural effusion— insert tube inferiorly and posteriorly 10. Secure tube with purse-string sutures: suture first tied to skin, then wrapped around tube once and tied at the tube 11. Locate the 3 to 5 intercostals space in the mid to anterior axillary line avoiding breast tissue 4. Anesthetize skin, subcutaneous tissue, periosteum of rib, chest-wall muscles and pleura with 1% lidocaine 6. Secure tube: suture first tied to skin, then wrapped around tube once and tied at the tube 14. Indications: Need for minute to minute blood pressure monitoring, need for arterial blood gas monitoring, need for frequent labs in the absence of a functioning central venous line.
Nerve cells grow 2 types of processes from their cell bodies - axons and dendrites cheap lasuna 60 caps otc cholesterol levels in shrimp. Dendrites: are those processes that are concerned with reception of stimuli from environment purchase cheap lasuna on-line cholesterol levels of athletes. Axons: are those processes that are concerned with conduction and transmission of the stimuli-signal to another cell or cells order lasuna us q steps biometer cholesterol test strips. Glial cells or Neuroglial cells The various functions of glial cells are: • Mechanical supportive elements of neurons • Insulator of neuron • Phagocytic defense mechanism • Secretory • Modifiers of electrical activity in neuron • Regulation of metabolism in neuron • Development assistance in neuronal circuitry • Producers of myelin sheath Glial cells retain the ability to divide throughout life. A receptor is a biologic transducer which picks up one form of energy or stimulus and transforms it into another form of energy. Exteroreceptors: Localized in the body surface; recieve information from the external environment • Sight, hearing, smell • Pick up distant stimuli (teleoreceptors) • Touch, pressure, temperature • Stimulation by contact 2. Interoreceptors (visceroreceptors) Visceral activity (digestion, excretion, circulation) Located in Viscera and blood vessels Free nerve endings: Most free nerve endings arborize between the tissue cells; other surround the hair follicles. Depending on the presence or absence of myelin, the fibers are classified as myelinated or 65 nonmyelinated. Within each bundle, between the fibers, collagen fibers and a few fibroblasts are situated. Through chemical means neurons pass messages to muscles and glands through intricate pathways from neuron to neuron. Characteristics of Graded potential • Graded potential change: magnitude varies with the magnitude of triggering event • Decremental conduction: magnitude diminishes with distance from initial site • Passive spread to nearby inactive areas of membrane • No refractory period • Can be summed (temporal and spatial) • Can be depolarized or hyperpolarized • Triggered by stimulus, by combination of neurotransmitter with receptor or by spontaneous shift in leak-pump cycle. As soon as the critical level of depolarized, the threshold is reached, any further increase in the strength of the applied current do not affect size of the potential. The action potential crosses the zero line it is moving from -80 to +30 mV inside the membrane. The action potential is propagated along the whole length of the fiber membrane with a constant speed and amplitude. When one electrode is kept inside and the other is outside, potential changes across the membrane can be measured and if properly amplified and electrodes connected to a cathode ray oscilloscope, they can be recorded as the monophasic action potentials. After potentials • Depolarization after potentials: The membrane potential for a brief period becomes more positive than the resting membrane potential and the cell, therefore, is slightly more excitable than normal. Action potentials for nerves are very brief, lasting only about 2-3 milliseconds, and the nerve cell is almost instantly ready again to conduct the next potential. Ionic basis of the action potential The different phases of the action potential are correlated with the following changes in ionic influxes: (See figure 22 & 23). Consequently, the increase in potassium conductance / permeability starts a little later and lasts longer. The outward flow of the potassium ions slows the rise of the potential, then causes it to fall to its initial level by negative feedback mechanism, the membrane regains its original permeability and is ready to conduct another impulse. During this time the nerve fiber is unresponsive to a depolarizing current and, therefore, cannot conduct an impulse. This interval is very brief (2 millisecond) and the nerve fibers can carry very fast frequency of impulses. The absolute refractory period is followed by a recovery of excitability 71 during which time the threshold of the nerve is higher than normal, and so only stimuli of very great strength can evoke a propagated impulse, which is it self smaller and slower. There exists self regenerative sodium conductance of the stimulated membrane, which changes the initial depolarization to the all or none full-sized action potential that is propagated without loss of amplitude along the entire length of the fiber. Unmyelinated fibers are thin, slow conducting nerves often called "C" fibers on the basis of their diameter of less than 1 micron. The addition of myelin sheath allows an enormous increase in conduction velocity with a relatively small increase in fiber diameter. Saltatory conduction Inefficient electrical characteristic are compensated by the wrapping of the axon in concentric layers of myelin, which acts as insulating sheath that increases the resistance and greatly lowers the capacitance of the surface and by nodes of Ranvier at 1 mm distance that lifts the attenuated signals( see fig. Shows propagation of Nerve impulse in myelinated nerve fibers 74 The stimulus A stimulus is any change that can alter the energy state of a tissue sufficiently to depolarize the membrane. A nerve can be stimulated by mechanical, thermal, chemical, osmotic or electrical stimulation. These various stimuli are converted or transduced by the nerve to an electrical response, i. Excitability Excitability may be defined as the ability of a cell to respond to a stimulus with an action potential. Excitability and parameters of the stimulus A stimulus must fulfill to evoke response. Neuromuscular junction / synapse The neuromuscular junction is the specialized region of contact between nerve and muscle. Each skeletal muscle fiber receives only one of the many terminal branches of the nerve fiber. All movements are composites of contraction of muscle unit, the motor neuron, its axon, and all the muscle fibers it innervates. The resulting contraction of each muscle fiber of the motor unit is all –or- nothing. Increase in the strength of muscle contractions are obtained through the recruitment of greater number of motor units. Motor unit: is the motor nerve and all the muscle(s) innervated by the nerve Functional anatomy of neuromuscular Junction Presynaptic Structure The axon terminals in knobs on the membrane surface do not fuse with it. There are active zones of the presynaptic membrane, where transmitter 75 release occurs. The presynaptic membranes have selective ionic gates, voltage gated ++ Ca channels The synaptic Cleft: The cleft is a gap of about 40 mm separating the axon terminal and the muscle membrane. Postsynaptic Structure At the junction area, there is an enlargement of the sarcoplasm of the muscle fiber, known as the end plate. The postsynaptic membrane is both structurally and physiologically different from the rest of the muscle membrane. The region of the muscle surface membrane under the nerve terminal is sensitive to acetylcholine. Recycling of vesicles: The disrupted vesicles are modified and same vesicles are pinched off and filled. The Ach receptor is a protein; its conformation changes when Ach binds to it, resulting in the opening of the ionic gates and a change in permeability. Curare also binds to receptor protein but alters it to an inactive form, which does not result in depolarization. Snake venom containing bungarotoxin binds very tightly and specifically to Ach receptor. The receptor 7 4 density is very high (3x 10 ) per end plate, which is enough for the 10 quanta of Ach released. Inactivation of acetylcholine The concentration of Ach at the end plate remains high briefly for it is hydrolyzed rapidly by the enzyme AchE into choline and acetate. Synapse and neuronal integration A neurotransmitter transmits the signal across a synapse. Classically, a neuron to neuron synapse is a junction between an axon terminal of one neuron and the dendrites or cell body of a second neuron.
Cerebral Hypoxia Head trauma is frequently accompanied by episodes of hypotension or hypoxia purchase lasuna no prescription cholesterol lowering foods diet, due either to the head injury itself or to concurrent injuries to the rest of the body generic lasuna 60 caps cholesterol levels in cheese. Alone or in combination with raised intracranial pressure lasuna 60 caps with visa cholesterolosis, such episodes often result in hypoxic damage to the brain. It is most common in young infants, with the majority of cases occurring before 6 months. Since the 1970’s, this syndrome has been attributed to violent shaking of the infant, whose large head and weak neck muscles allow a whiplash-like effect. These findings may be accompanied by rib fractures (from grabbing the thorax) and by metaphyseal fractures of the long bones, from flailing of the limbs. At autopsy, the subdural hemorrhage is rarely of sufficient volume to cause a significant mass effect, yet the brain is commonly swollen. Axonal spheroids are often seen, especially if immunohistochemical staining for amyloid precursor protein is performed to demonstrate them. The pathophysiology of this disorder is extraordinarily controversial and has given rise to some of the most passionate letters to editors imaginable about a neuropathological topic. One issue is whether the forces generated by shaking are sufficient to cause axonal shearing. Some authors have claimed that this is impossible, that most cases are accompanied by some evidence of impact, and that when this is lacking, there still must have been impact, albeit 163 against an object, such as a cushion, that prevented injury to the scalp or skull. Others have claimed that the only axonal injury directly caused by the shaking is at the junction of the medulla and cervical spinal cord, which leads to apnea, and that any further axonal injury is due to hypoxia and increased intracranial pressure; which they claim produce patterns of axonal injury that can be distinguished from those produced by trauma. They have also proposed that the subdural and retinal hemorrhages are the result of increased intracranial pressure, rather than the direct effect of trauma. Thus, they conclude that the entire syndrome can result from hypoxia without trauma. Related controversies, also with important implications in the prosecution of alleged baby-shaking, involve the reversibility of axonal damage and the question of whether infants can experience a lucent interval between trauma and loss of consciousness. These issues are difficult to resolve because of the absence of disinterested witnesses to the handling of the infants. However, from cases without scalp injury and with a confessed shaking, it seems clear that whatever the mechanism, shaking alone can give rise to subdural and retinal hemorrhages with loss of consciousness and axonal injury. On the other hand, if evidence of direct impact to the head is present, it is probably impossible to tell whether there was shaking or not. Anatomic Considerations The spinal canal becomes narrower when flexed or extended. This is particularly true in the presence of traumatic instability, when the vertebrae or the pieces of fractured vertebrae may be properly aligned when the spine is straight but displaced into the canal with motion. Therefore, it must always be remembered that in the presence of injury to the bony spine, movement of the spine can cause serious compression injury to the spinal cord, even if no such injury occurred initially. The spinal canal is narrowest in its cervical portion, the spine is weakest at this level, and violent motion of the head can place the cervical spine under tremendous stress. Traumatic spinal injuries are thus most commonly cervical, and cervical spine injuries must be ruled out in the presence of violent injuries to the head or face. Cranial or facial trauma can result in tearing of the ligaments that hold the odontoid process in place. If the spinal cord is injured, the level of cord injury will often differ from that of spinal injury. Posterior stab wounds are therefore likely to affect one side more than the other. Direct Injuries to the Spine These are caused by stab wounds or by bullets or other high velocity projectiles. As mentioned above, stab wounds are likely to involve one side more than the other, causing a complete or partial Brown-Sequard syndrome (ipsilateral paralysis and loss of vibratory and positional sensation with contralateral loss of pain and temperature sensation). Stab wounds tend to cause localized damage to the spinal cord with little intraparenchymal hemorrhage. Ascending and descending degeneration occur in a pattern predictable from the anatomy of the severed tracts. As in the brain, the damage from gunshot wounds extends beyond the region penetrated, for similar reasons The injuries tend to extend for several segments in either direction and to be fairly hemorrhagic. Gunshot wounds to the vertebrae can injure the spinal cord without penetrating it, by virtue of transferred energy alone. Bullets frequently become trapped in the spinal canal, and in the early stages of injury they can move. Eventually, whether epidurally or intraparenchymally located, they become encased in fibrous tissue. The adjacent spinal cord loses its normal structure and becomes a mixed glial-mesenchymal scar, poorly demarcated from the meninges to which it had become adherent. Indirect Injuries to the Spinal Cord These are blunt force or compressive injuries secondary to spinal trauma. While they occasionally result from temporary spinal deformities, they are more commonly the result of spinal fracture or subluxation. It should be borne in mind that spinal instability may result in temporary deformity that is not appreciated at the time of examination but that has already caused injury to the cord. Injury to the cervical spine is generally the result of cranial or facial injuries, commonly the result of motor vehicle accidents or falls. Motorcycle and diving accidents are particularly likely to result in such injuries. Thoracic spine fractures are more commonly the result of industrial accidents, such as mining cave-ins or collapsed roofs, in which weight falls on the victim. The immediate effects of spinal cord compression are necrosis, hemorrhage, edema, and inflammation. The edema resolves after two or three weeks, and the necrotic foci become infiltrated by phagocytes. During this period the blood becomes resorbed, which can result in the formation of a syrinx (cystic space within the spinal cord). In less severely damaged areas, the astrocytic component predominates, while in the most severely damaged areas the scar is entirely fibroblastic, the glia having been lost with the other elements of the cord. Eventually, the injured portion of the cord is reduced to scar tissue, which is adherent to, and indistinct from, the surrounding meninges. Victims become bedridden or wheelchair-bound, with all the attendant problems, and they frequently require urethral catheterization. Common long-term sequelae include infected decubitis ulcers and urinary tract infections, and such infections often result in death years after the injury. Occasionally, a syrinx that forms during the resolution of a cord injury may enlarge years after the injury.