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Total leucocyte counts are commonly increased in infections and when considered along with the differential leucocyte count can be indicators as to whether the infecting agent is bacterial or viral generic diclofenac gel 20gm without a prescription. Red Cell Count Although red cell counts are of diagnostic value in only a minority of patients suffering from blood diseases purchase diclofenac gel 20gm free shipping, the advent of electronic cell counters has enormously increased the practicability of such counts discount diclofenac gel 20 gm overnight delivery. Their value, too, has been increased now that they can be done with a degree of accuracy and reproducibility comparable to that for hemoglobin estimation. Although clearly an 104 Hematology obsolete method (because the combined error of dilution and enumeration is high), visual counting will still has to be undertaken for some years to come in the smaller laboratories. Principle A sample of blood is diluted with a diluent that maintains (preserves) the disc-like shape of the red cells and prevents agglutination and the cells are counted in a Neubauer or Burker counting chamber. Diluting Fluid 1% formal citrate Dilution Thomma Red Cell Pipette Take a well mixed blood or blood from a freely flowing capillary puncture to the “0. Tube Dilution Take 20µl blood with sahli pipette and mix it with 4ml diluent in a small tube to give a final dilution of 1:201 105 Hematology Counting and Calculation After the suspension is charged into the chamber and the cells allowed to settle, cells should be counted using the 40× objective and 10× eyepiece in 5 small squares of the central 1mm2 area of the improved Neubauer counting chamber (4 corner and 1 central squares each with an area of 0. It is important to count as many cells as possible for the accuracy of the count is increased thereby; 500 cells should be considered as the absolute minimum. Platelet counts are also performed when patients are being treated with cytotoxic drugs or other drugs which may cause thrombocytopenia. Method using formal-citrate red cell diluent Diluent should be prepared using thoroughly clean glassware and fresh distilled water. To prevent drying of the fluid, place the chamber in a petri dish or plastic container on dampened tissue or blotting paper and cover with a lid. Count the number of platelets which will appear as small refractile bodies in the central 1mm2 area with the condenser racked down. Not more than 500ml should be prepared at a time using thoroughly clean glassware and fresh distilled water. The preparation is mixed, the chamber filled and the cells allowed to settle in a similar fashion as Method 1. The cells are counted in 5 small squares in the central 1mm2 of the improved Neubauer counting chamber. Rough estimation of platelet number from a stained blood film Normally there are 10-20 platelets per oil immersion field. Special care must be taken when counting platelets: • To check there are not clots in the blood sample. Platelet counts from capillary blood are usually 111 Hematology lower than from venous blood and are not as reproducible. Thrombocytosis Causes of an increase in platelet numbers include: • Chronic myeloproliferative disease e. Principle Blood is diluted with a fluid that causes lysis of erythrocytes and stains eosinophils rendering them readily visible. Diluting Fluid Hinkleman’s fluid It has the advantage of keeping well at room temperature and not needing filtering before use. Method Make dilution of blood using thomma pipette or tube dilution as described for the white cell count. Reference range 40 - 440 × 106/l Interpretation of eosinophil counts Eosinophilia is common in allergic conditions (e. How do you calculate the number of cells per unit volume of blood after you count the cells in a sample of diluted blood? The count is usually performed by visual examination of blood films which are prepared on slides by the wedge technique. For a reliable differential 117 Hematology count the film must not be too thin and the tail of the film should be smooth. This should result in a film in which there is some overlap of the red cells diminishing to separation near the tail and in which the white cells on the body of the film are not too badly shrunken. If the film is too thin or if a rough-edged spreader is used, 50% of the white cells accumulate at the edges and in the tail and gross qualitative irregularity in distribution will be the rule. The polymorphonuclear leucocytes and monocytes predominate at the edges while much of smaller lymphocytes are found in the middle. The problem is to overcome the differences in distribution of the various classes of cells which are probably always present to a small extent even in well made films. Of the three methods indicated underneath for doing the differential count, the lateral strip method appears to be the method of choice because it averages out almost all of the disadvantages of the two other methods. The Longitudinal Strip Method The cells are counted using the X40 dry or X100 oil immersion objectives in a strip running the whole length of the film until 100 cells are counted. If all the cells are counted in such a strip, the differential totals will approximate closely to the true differential count.

Trigeminal receptors in the inflamed perineural tissues can be stimulated by muscle activity and globe palpation generic diclofenac gel 20 gm line. Slide 20 Anterior ischemic optic neuropathy is accompanied by sudden buy diclofenac gel 20gm free shipping, painless visual loss due to infarction of the optic disc buy diclofenac gel 20gm online. Pallid disc swelling evolves into atrophy 4-6 weeks later, a time course typically consistent with ganglion cell soma death following axon damage (Wallerian degeneration). Idiopathic anterior ischemic optic neuropathy is associated with an anatomically crowded optic disc. Slide 21 Giant cell arteritis is an important cause of one of the few ophthalmic emergencies, sudden painless visual loss, because it is treatable, not necessarily to regain the vision in the affected eye but to preserve vision in the other eye. It is a subacute, granulomatous disease affecting the arteries in several organ systems. Visual loss usually occurs from central retinal artery or ophthalmic artery obstruction. Knowledge of the early non-ophthalmic symptoms as well as the emergent nature of sudden painless visual loss is important for any physician who cares for the elderly. Giant cell arteritis is also called temporal arteritis because the temporal artery is often exquisitely tender when involved and is the most common artery biopsied to confirm the presence of this systemic disease. Neuropathologic signs are panarteritis, intimal 148 hyperplasia, and fragmentation of the internal elastic lamina associated with multinucleated giant cells. Slide 22 Compressive optic neuropathy such as due to meningioma is usually accompanied by insidiously slow, painless visual loss with progressive enlargement of scotomas. Slides 23-24 Inflammatory optic neuropathy is usually associated with optic nerve demyelination and pain exacerbated by eye movements. Subacute visual loss can range from subtle symptomatic loss of central vision (acuity) or asymptomatic loss of peripheral vision to no light perception. These people initially have normal appearing optic discs, hence the statement, “Optic neuritis is a disease when the patient sees nothing and the internist sees nothing. Slide 25 Optic atrophy is a common end sign of many diseases purely ocular as well as systemic. As we have seen, sometimes the pattern of atrophy and visual loss can suggest a diagnosis or localize the lesion. However a diagnosis is best considered by all of the “company” a sign does or doesn’t keep. Slide 26 Glaucoma describes many different diseases characterized by elevated intraocular pressure and optic atrophy associated with saucerization of the optic disc. Acute pain, red eye, and visual change associated with corneal edema producing halos around lights characterizes acute angle closure glaucoma, an ophthalmic emergency. The most common type of glaucoma, chronic open angle glaucoma, is a leading cause of blindness. Elevated intraocular pressure creates an “intraocular compressive optic neuropathy” with initial loss of axons usually predominantly entering the optic disc at its superior and inferior poles resulting in vertical elongation and saucerization of the optic disc cup. The usual pattern of early visual loss is therefore arcuate scotoma reflecting damage to these axon bundles that branch around the fovea. Retinal vascular narrowing is the earliest sign of this disturbance of outer retinal layer or retinal pigment epithelium function. Also known as pigmentary retinopathy, retinal degeneration is accompanied by release of pigment from damaged retinal pigment epithelial cells that can migrate into the retina, appearing as focal pigment aggregates or larger “bone spicules. Slide 28 Obstruction of the central retinal artery, usually due to embolic or inflammatory disease, causes sudden complete loss of vision and infarction of the inner retina. The outer retina receives its oxygen supply from the underlying choroid by passive 149 diffusion and survives. The retinal pallor surrounds residual hyperemia beneath the fovea where only cones and glial Muller cells, components of outer retina, survive. Recanalization of the obstructed vessel often occurs, leaving a fundus with ghost vessels, vascular narrowing, and optic atrophy. Causes of elevated intracranial pressure include structural, neoplastic, inflammatory, hemorrhagic, thrombotic, and infectious disorders. The earliest sign of papilledema is increased hyperemia of the optic disc and obliteration of the optic disc cup. Slide 30 Papilledema develops when increased intracranial pressure causes distension of the subarachnoid space leading to centripetal rotation of the meninges and scleral canal, effectively choking the optic disc. Slide 31 Swelling of the optic disc with hemorrhages, exudates, and vascular distension can be marked as in this obese 12-year-old boy with idiopathic intracranial hypertension. Slide 32 In addition to elevated intracranial pressure, swelling of the optic discs occurs in the presence of inflammatory, ischemic, thrombotic, infiltrative, and hypertensive diseases.

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The chemical bond between the second and third phosphate groups buy diclofenac gel 20gm line, termed a high-energy bond cheap diclofenac gel 20gm without prescription, represents the greatest source of energy in a cell 20 gm diclofenac gel amex. Of the four major macromolecular groups (carbohydrates, lipids, proteins, and nucleic acids) that are processed by digestion, carbohydrates are considered the most common source of energy to fuel the body. They take the form of either complex carbohydrates, polysaccharides like starch and glycogen, or simple sugars (monosaccharides) like glucose and fructose. Excess glucose is either stored as an energy reserve in the liver and skeletal muscles as the complex polymer glycogen, or it is converted into fat (triglyceride) in adipose cells (adipocytes). Among the lipids (fats), triglycerides are most often used for energy via a metabolic process called β-oxidation. About one- half of excess fat is stored in adipocytes that accumulate in the subcutaneous tissue under the skin, whereas the rest is stored in adipocytes in other tissues and organs. When one is chronically starving, this use of amino acids for energy production can lead to a wasting away of the body, as more and more proteins are broken down. These nucleotides are readily absorbed and transported throughout the body to be used by individual cells during nucleic acid metabolism. Anabolic reactions combine monosaccharides to form polysaccharides, fatty acids to form triglycerides, amino acids to form proteins, and nucleotides to form nucleic acids. Anabolic reactions, also called biosynthesis reactions, create new molecules that form new cells and tissues, and revitalize organs. Hormonal Regulation of Metabolism Catabolic and anabolic hormones in the body help regulate metabolic processes. Anabolic hormones are required for the synthesis of molecules and include growth hormone, insulin-like growth factor, insulin, testosterone, and estrogen. Catabolic Hormones Hormone Function Released from the adrenal gland in response to stress; its main role is to increase blood Cortisol glucose levels by gluconeogenesis (breaking down fats and proteins) Released from alpha cells in the pancreas either when starving or when the body needs to generate additional energy; it stimulates the breakdown of glycogen in the liver to increase Glucagon blood glucose levels; its effect is the opposite of insulin; glucagon and insulin are a part of a negative-feedback system that stabilizes blood glucose levels Released in response to the activation of the sympathetic nervous system; increases heart rate Adrenaline/ and heart contractility, constricts blood vessels, is a bronchodilator that opens (dilates) the epinephrine bronchi of the lungs to increase air volume in the lungs, and stimulates gluconeogenesis Table 24. Metabolic diseases are most commonly the result of malfunctioning proteins or enzymes that are critical to one or more metabolic pathways. However, normally functioning proteins and enzymes can also have deleterious effects if their availability is not appropriately matched with metabolic need. Clinically, Cushing syndrome is characterized by rapid weight gain, especially in the trunk and face region, depression, and anxiety. Patients with Cushing syndrome can exhibit high blood glucose levels and are at an increased risk of becoming obese. They also show slow growth, accumulation of fat between the shoulders, weak muscles, bone pain (because cortisol causes proteins to be broken down to make glucose via gluconeogenesis), and fatigue. Other symptoms include excessive sweating (hyperhidrosis), capillary dilation, and thinning of the skin, which can lead to easy bruising. Depending on the cause of the excess, treatment may be as simple as discontinuing the use of cortisol ointments. Where surgery is inappropriate, radiation therapy can be used to reduce the size of a tumor or ablate portions of the adrenal cortex. Adrenal insufficiency, or Addison’s disease, is characterized by the reduced production of cortisol from the adrenal gland. Patients with Addison’s disease may have low blood pressure, paleness, extreme weakness, fatigue, slow or sluggish movements, lightheadedness, and salt cravings due to the loss of sodium and high blood potassium levels (hyperkalemia). Victims also may suffer from loss of appetite, chronic diarrhea, vomiting, mouth lesions, and patchy skin color. Oxidation-Reduction Reactions The chemical reactions underlying metabolism involve the transfer of electrons from one compound to another by processes catalyzed by enzymes. The electrons in these reactions commonly come from hydrogen atoms, which consist of an electron + and a proton. A molecule gives up a hydrogen atom, in the form of a hydrogen ion (H ) and an electron, breaking the molecule into smaller parts. The loss of an electron, or oxidation, releases a small amount of energy; both the electron and the energy are then passed to another molecule in the process of reduction, or the gaining of an electron. These two reactions always happen together in an oxidation-reduction reaction (also called a redox reaction)—when an electron is passed between molecules, the donor is oxidized and the recipient is reduced. Oxidation-reduction reactions often happen in a series, so that a molecule that is reduced is subsequently oxidized, passing on not only the electron it just received but also the energy it received. Glucose and fructose are examples of simple sugars, and starch, glycogen, and cellulose are all examples of complex sugars. During digestion, carbohydrates are broken down into simple, soluble sugars that can be transported across the intestinal wall into the circulatory system to be transported throughout the body. Carbohydrate digestion begins in the mouth with the action of salivary amylase on starches and ends with monosaccharides being absorbed across the epithelium of the small intestine.

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Slowing of blood flow and clumping of erythrocytes (rouleaux formation) forces leukocytes to the periphery (margination) order 20 gm diclofenac gel free shipping. Loss of central flow also allows contact between neutrophils buy 20 gm diclofenac gel mastercard, platelets and the endothelium purchase 20gm diclofenac gel with mastercard. Expression of adhesion molecules between leukocytes and the endothelium occurs (pavementing). Cell adhesion molecules facilitate leukocyte adhesion by binding to a single cell surface glycoprotein found on activated monocytes, fibroblasts and vascular endothelial cells. Chemotaxis – directional movement of phagocytic cells, mediated by a series of chemical messengers a. Diapedesis – passive escape of erythrocytes – may be facilitated by chemotactic leukocyte migration. Monocytes and macrophages appear after 4 hours and peak 16-24 hours after injury occurs. They have greater killing potential and have a role in preparing the tissue for healing and repair. Adherence between the phagocyte and unwanted material is the first step in the process of phagocytosis. Opsonins, which facilitate adherence of opsonin coated substances to receptors on phagocytes. Specific surface receptors are present on phagocytes for immunoglobulin molecules, C3b and fibronectins – note that not all bacteria bind fibronectins and adhere to phagocytes through non-specific mechanisms. Antibody-mediated opsonization can be enhanced by activation of complement, and is critical if non-specific opsonization is not effective. Activated macrophages are larger, have more mitochondria and Lysosomes, and a greater amount of hydrolytic chemicals. Coagulation factors (factor V and thromboplastin) Note that some bacteria still survive – e. Microbicidal function - chronic granulomatous disease of childhood Clinical manifestations of acute inflammation: 1. Redness caused by arteriolar dilatation and increased vascularity – congestion may progress to stasis leading to reduction of haemoglobin 2. Heat due to increase blood flow – central body temperature may also be elevated 3. Processes contained within rigid structures may not swell, but can occlude structures. Pain due to physical tension and swelling, as well as the release of bradykinin 5. Note that deliberate motion and function may promote the spread of the injurous process through tissue planes and lymphatics. Endocrine change – an increase in glucocorticoid steroid hormone production due to stress • Chronic Inflammation Chronic inflammation is a prolonged process in which destruction and inflammation are proceeding at the same time as attempts at healing. After repeated bouts of acute inflammation with intervals of healing – gall bladder, kidney and large intestine 3. Immune reactions Mononuclear cells are the characteristic features of chronic inflammation: 1. Activated macrophages, which are motile, capable of phagocytosis, stimulate fibroblasts to divide and are hardy and long lived. B and T lymphocytes may be involved also, along with plasma cells, eosinophils and fibroblasts The histological hallmarks of chronic inflammation are: 1. Hyperplasia of mononuclear/phagocytic cells in lymph nodes, spleen, liver and bone marrow b. Non-specific complaints include fatigue, anorexia, low grade fever A granulomata is a focal chronic inflammatory reaction, with macrophages and epithelioid cells in compact masses surrounded by lymphocytes. Modified macrophages are characteristic: Epithelioid cells are specialised for secretion over phagocytosis – seen in tuberculosis and sarcoidosis Multinucleate giant cells are formed by fusion of macrophages or epithelioid cells – they may be seen in chronic inflammation without granulomatas. Non-immune – foreign body may attract macrophages without epithelioid cells or cell-mediated immune response. Inhalation/ingestion of organisms Æ acute reaction Æ organism survives (waxy coat) 2. Immune status change Æ reactivation of dormant bacteria Pathogenesis of syphilis: 1. Bone and skin – gumma necrosis (extensive, few giant cells) • Healing by Regeneration and Repair Regeneration is the replacement of lost cells by those of the same type – the capacity of tissues for regeneration depends on the presence of stem cells: 1. Axons of peripheral nerve cells may regenerate slowly if the nerve sheath is not damaged – a displaced sheath may produce a traumatic neuroma. Satellite cells at the basement membrane of skeletal muscle cells can differentiate into myocytes to replace those that have necrosed. The cells are also stimulated to migrate and proliferate until contact is restored with neighbouring cells of the same time (‘contact inhibition’). Repair is the regeneration of vascular, fibrous connective tissue – it is characterised by the proliferation and maturation of this tissue to: 1.