Buy online Keflex cheap no RX - Safe Keflex

Buy online Keflex cheap no RX - Safe Keflex

Andrews University. Q. Xardas, MD: "Buy online Keflex cheap no RX - Safe Keflex".

Areas of production in the respiratory and intestinal mucosa are associated with the presence of tissue mast cells (18) generic 500mg keflex mastercard infection 6 weeks after wisdom tooth removal. With the development of techniques to measure total IgE in the blood and the availability of purified IgE protein buy discount keflex 250mg on line antibiotic resistance animal agriculture, investigators were able to study the metabolic properties of this immunoglobulin in normal individuals ( 19) buy discount keflex 250 mg on line infection in stomach. It had been known for several years that the half-life of reaginic antibody in human skin as determined by passive transfer studies was about 14 days buy keflex cheap antibiotics for sinus infection safe during pregnancy. This was reconfirmed with studies that investigated the disappearance of radiolabeled IgE in human skin. The basophil and mast cell-bound IgE pool needs to be investigated thoroughly, but it has been estimated that only 1% of the total IgE is cell bound. Tada (21) studied the production of IgE antibody in rats and found that IgE antibody production is regulated by cooperation between T lymphocytes (T cells) and B lymphocytes (B cells). The T cells provide the helper function, and the B cells are the producers of IgE antibody. In human systems, it became clear that IgE production from B cells required T-cell signals that were unique to the IgE system ( 22). This leads to T-cell B-cell interaction, mutual exchange of cytokine and cell contact signals, and enhanced allergen-specific IgE production. They found that cord serum contained 13 to 202 ng/mL and that the concentration of IgE in the cord serum did not correlate with the serum IgE concentration of the mother, which confirmed that IgE does not cross the placenta. In children, IgE levels increase steadily and peak between 10 and 15 years of age. Johansson and Foucard illustrate well the selection of population groups for determining the normal level of serum IgE. Studies of healthy Swedish and Ethiopian children showed a marked difference in mean IgE levels: Swedish children had a mean of 160 ng/mL, and Ethiopian children had a mean of 860 ng/mL ( 30). Barbee and coworkers (31) studied the IgE levels in atopic and nonatopic people 6 to 75 years of age in Tucson. IgE levels peaked in those aged 6 to 14 years and gradually declined with advancing age; male subjects had higher levels of IgE than female subjects ( Fig. Geometric means and upper 95% confidence intervals are plotted against age for males and females with positive and negative results from skin tests. Double cross-hatched area represents overlap of total IgE levels between the two groups of subjects. The presence of IgE antibody on mast cells in the tissues that contain heparin and histamine points to a role for IgE in controlling the microcirculation, and a role for the mast cell as a sentinel or first line of defense against microorganisms has been advanced. The hypothesis is that IgE antibody specific for bacterial or viral antigens could have a part in localizing high concentrations of protective antibody at the site of tissue invasion ( 32,33). The role of IgE antibody has been studied extensively in an experimental infection of rats with the parasite Nippostrongylus brasiliensis. IgE antibody on the surface of mast cells in the gut may be responsible for triggering histamine release and helping the animal to reduce the worm burden ( 34). In experimental Schistosoma mansoni infection in the rat, IgE is produced at high levels to schistosome antigens. IgE complexed to these antigens has a role in antibody-dependent cell-mediated cytotoxicity, whereas eosinophils, macrophages, and platelets are effector cells that damage the parasite ( 35). These observations in animals have relevance to human populations, where the IgE inflammatory cascade may protect against helminth infections ( 35). These cytokine pathways are under complex genetic control that defines the atopic phenotype. High serum IgE levels have been shown to be under the control of a recessive gene, and specific allergen responses are associated with human leukocyte antigens (41). The chromosomal location and identification of these genes are under intense investigation ( 42). These observations may add to the role of IgE in several diseases in which no definable allergen is present. Measurement of Total IgE Several early studies evaluated the role of IgE in patients with a variety of allergic diseases ( 29,30 and 31). Adults and children with allergic rhinitis and extrinsic asthma tend to have higher total serum IgE concentrations. About half of such patients have total IgE concentrations that are two standard deviations above the mean of a normal control group. Significant overlap of total serum IgE concentrations in normal subjects and in patients with allergic asthma and hay fever has been demonstrated (Fig. Therefore, the total serum IgE concentration is neither a specific nor sensitive diagnostic test for the presence of these disorders. Total serum IgE has been found to be markedly elevated in atopic dermatitis, with the serum IgE concentration correlating with the severity of the eczema and with the presence of allergic rhinitis, asthma, or both. Patients with atopic dermatitis without severe skin disease or accompanying asthma or hay fever may have normal IgE concentrations (45). Total IgE concentrations have been found to be markedly elevated in allergic bronchopulmonary aspergillosis. Measurement of Specific IgE Since the discovery of IgE in 1967, it is possible not only to measure total IgE in the serum but also to measure IgE antibody against complex as well as purified allergens. After a period of incubation, the specific IgE present binds firmly to the solid phase. The solid phase is then washed extensively, and the last reagent added is radiolabeled anti-IgE antibody. However, individuals with the same level of specific IgE antibody to ragweed allergen may vary 100-fold in their skin reactivity to that allergen ( 47). It is possible to estimate the absolute quantity of specific IgE antibody per milliliter of serum against complex and purified allergens ( 48,49). Using one of these methods to measure IgE antibody against ragweed allergens, Gleich and coworkers ( 48) defined the natural rise and fall of ragweed-specific IgE over a 1-year period. In this population of ragweed-sensitive individuals, the IgE antibody specific for ragweed allergens varied from 10 to 1,000 ng/mL. A marked rise of specific IgE level occurred after the pollen season, with a peak in October followed by a gradual decrease. Specific IgE level reached a low point just before the next ragweed season in August (Fig. It is also possible to measure basophil-bound, total, and specific IgE against ragweed antigen E. There are between 100,000 and 500,000 molecules of total IgE per basophil (50) and between 2500 and 50,000 molecules of specific IgE per basophil ( 20). Levels and changes of IgE antibodies to ragweed allergens in 40 untreated allergy patients. Measurement of the absolute levels of IgE antibodies in patients with ragweed hay fever.

The use of in vitro tests for IgE antibody in the specific diagnosis of IgE mediated disorders and in the formulation of allergen immunotherapy purchase cheap keflex online home antibiotics for sinus infection. Nasal immunotherapy to prietaria: evidence of reduction of local allergic inflammation discount keflex 750mg antibiotics youtube. The effects of sodium cromoglycate on the antigen induced nasal reaction in allergic rhinitis as measured by rhinomanometry and symptomology order keflex 250 mg amex alternative antibiotics for sinus infection. Low dose sublingual therapy in patients with allergic rhinitis due to house dust mite buy keflex online pills antibiotics used for acne. A double- blind, placebo-controlled evaluation of sublingual immunotherapy with standardized cat extract. Potential effect of the administration of substance P and allergen therapy on immunoglobulin E-mediated allergic reactions in human subjects. Comparisons of alum- precipitated and unprecipitated aqueous ragweed pollen extracts in the treatment of hayfever. A double-blind placebo-controlled trial of polymerized whole ragweed for immunotherapy of ragweed allergy. Several other conditions mimic allergic disease and should be considered in any patient presenting with conjunctivitis. In addition to the systematic discussion of these diseases, because the chapter is written for the nonophthalmologist, an anatomic sketch of the eye ( Fig. When the causative agent has contact with the conjunctiva and the lid, a dermatoconjunctivitis occurs. Clinical Presentation Contact dermatitis and dermatoconjunctivitis affect women more commonly than men because women use cosmetics more frequently. Causative Agents Contact dermatitis and dermatoconjunctivitis can be caused by agents directly applied to the lid or conjunctiva, aerosolized or airborne agents contacted by chance, and cosmetics applied to other areas of the body. In addition to agents applied directly only to the eye, soaps and face creams can also produce a selective dermatitis of the lid because of the thin skin in this area. Therefore, a cosmetic previously used without ill effect can become a sensitizing agent. Any medication applied to the eye can produce a contact dermatitis or dermatoconjunctivitis. Today, neomycin and idoxuridine are probably the major cause of iatrogenic contact dermatoconjunctivitis. Several other topically applied medications, however, have been shown to cause dermatoconjunctivitis. Of increasing importance is the conjunctivitis associated with the wearing of contact lenses, especially soft lenses. Reactions can occur to the lenses themselves or to the chemicals used to treat them. Thimerosal, a preservative used in contact lens solutions, has been shown to produce classic, cell-medicated contact dermatitis ( 2). With the increasing use of disposable contact lenses, the incidence of contact allergy to lenses and their cleansing agents appears to be declining. Dermatitis of the lid and conjunctiva can also result from exposure to airborne agents. Hair spray, volatile substances contacted at work, and the oleoresin moieties of airborne pollens have all been reported to produce contact dermatitis and dermatoconjunctivitis. Hair preparations and nail enamel frequently cause problems around the eye while sparing the scalp and the hands. Finally, Rhus dermatitis can affect the eye, producing unilateral periorbital edema, which can be confused with angioedema. Diagnosis and Identification of Causative Agents The differential diagnosis includes seborrheic dermatitis and blepharitis, infectious eczematous dermatitis (especially chronic staphylococcal blepharitis), and rosacea. Seborrheic dermatitis usually can be differentiated from contact dermatitis on the basis of seborrheic lesions elsewhere and the lack or pruritus. This is usually the case in dermatitis caused by the application of topical medications. However, many cases present as chronic dermatitis, and the cause is not readily apparent. In such instances, an elimination-provocation procedure and patch tests can identify the offending substance. The elimination-provocation procedure requires that the patient remove all substances under suspicion from the environment. This is often difficult because it requires the complete removal of all cosmetics, hair sprays, spray deodorants, and any other topically applied substances. It should also include the cessation of visits to hair stylists and day spas during the course of the elimination procedure. In recalcitrant cases, the detergent used to wash the pillowcases should also be changed. The elimination phase of the procedure should continue until the dermatitis subsides, or for a maximum of 1 month. When the illness has cleared, cosmetics and other substances can be returned at a rate of one every week. On occasion, the offending substances can be identified by the recurrence of symptoms upon the reintroduction of the substance in question. However, the skin of the lid is markedly different from that of the back and forearm, and drugs repeatedly applied to the conjunctival sac concentrate there, producing high local concentrations of the drug. In addition to the cosmetics themselves, tests can be performed to applying agents, such as sponges and brushes. Fisher describes a simple test consisting of rubbing the substances into the forearm three times daily for 4 to 5 days, and then examining the sites. Because of the difficulty involved in establishing the etiologic agent with standard patch test kits, an ophthalmic patch test tray ( Table 11. Suggested ophthalmic tray for patch testing Therapy The treatment of choice is removal of the offending agent. An example of this is the switch from chemically preserved to heat-sterilized systems in patients with contact lens associated contact conjunctivitis. The offending agent, however, frequently cannot be identified, regardless of the diagnostic procedures applied. In these instances, chronic symptomatic therapy, possibly in conjunction with an ophthalmologist, is all that can be offered to the patient. Symptomatic relief can be obtained with topical corticosteroid creams, ointments, and drops. Corticosteroid drops should be employed only under the direction of the ophthalmologist. Acute Allergic Conjunctivitis Pathophysiology Acute allergic conjunctivitis is the most common form of allergic eye disease ( 4). Patients with allergic conjunctivitis have elevated amounts of total IgE in their tears ( 8,9 and 10), and tear fluid also contains IgE specific for seasonal allergens ( 11). These eosinophils are activated, releasing contents such as eosinophil cationic protein from their granules.

order generic keflex line

This pattern forms the primary r Inthelung discount 750mg keflex antibiotic resistance lesson plan,thebacteriahaveapreferencefortheapices complex with infection at the periphery of the lung (higher pO2) buy discount keflex 250 mg line virus 68 affecting children, and form an apical lung lesion known and enlarged peribronchial lymph nodes buy discount keflex 500mg on line antimicrobial activity. It begins as a small caseating r The outcome of the primary infection depends on the tuberculous granuloma cheap 250mg keflex with amex antimicrobial guide, histologically similar to the balance between the virulence of the organism and Ghon focus, with destruction of lung tissue and cavi- the strength of the host response (see Table 3. T cells are re-induced by the secondary infec- the host can mount an active cell mediated immune tion, with activation of macrophages, and exactly as response the infection may be completely cleared. Collagen is healing of the apical region with collagen de- is deposited around these, often becoming calcied. This is called a progres- tissue, thinning of the collagen wall and increasing sive primary infection. Coughing disperses these bacilli into the at- Poor immune system eg Good immune response, e. This disease is sometimes Use of appropriate antibiotics called galloping consumption. By that time there may be no evidence of tu- comesinfectedbymiliarydisseminationwithmultiple berculosis elsewhere. The hypersensitivity reaction may produce patient mounts a good immune response, organisms atransient pleural effusion or erythema nodosum. Microscopy Formal culture of material is the only way of accu- The characteristic lesion, the tubercle (granuloma) con- rately determining virulence and antibiotic sensitivity sists of a central area of caseous tissue necrosis within and should be attempted in every case, results may which are viable mycobacteria. It relies on the hypersensitivity reaction, usually heals spontaneously but occasionally may per- and is rarely helpful in the diagnosis of tuberculosis: sist giving rise to bronchiectasis particularly of the i The Tine test and Heaf test are for screening: 4/6 middle lobe (Brock s Syndrome). If the spots are conuent, logicalfractures,particularlyofthespinetogetherwith the test is positive, indicating exposure. The reaction is read at Investigations 48 72 hours and is said to be positive if the indura- r An abnormal chest X-ray is often found incidentally tion is 10 mm or more in diameter, negative if less in the absence of symptoms, but it is very rare for a than 5 mm. The X-ray shows puried protein derivative this can indicate active patchy or nodular shadowing in the upper zone with infection requiring treatment. In an immunocom- brosis and loss of volume; calcication and cavita- promised host (such as chronic renal failure, lym- tion may also be present. Human immunity depends largely on the haemag- niazid, ethambutol and pyrazinamide, and a further glutinin (H) antigen and the neuraminidase (N) antigen 4months of rifampicin and isoniazid alone. Major shifts in these antigenic re- taken 30 minutes before breakfast to aid absorption. Thesecancauseapandemic,whereasantigenicdrift organism is sensitive for a full 6 months to avoid de- causes the milder annual epidemics. Other upper and lower respiratory symptoms to6weeks after birth (without prior skin testing) in ar- may develop. Individuals are infective for 1 day prior to eas with a high incidence of tuberculosis. Less commonly, secondary Five per cent of patients do not respond to therapy, only Staph. Inuenza A causes worldwide annual epidemics and is Retrospective diagnosis can be made by a rise in spe- infamous for the much rarer pandemics, the most seri- ciccomplement-xingantibodyorhaemagglutininan- ous of which occurred in 1918 when 40 million people tibody measured 2 weeks apart, but this is usually un- died worldwide. Spread is by respiratory r Bed rest, antipyretics such as paracetamol for symp- droplets. Clinical features They are particularly indicated in the elderly, those Patients present with worsening features of pneumonia, with underlying respiratory disease such as chronic usually with a swinging pyrexia, and can be severely ill. Some are manufactured in strates one or more round opacities often with a uid chickembryosandtheseshouldnotbegiventoanyone level. Echocardiogram should be considered to look for infec- These predications depend on global surveillance or- tive endocarditis. This surveillance depends on viruses being cultured Complication and therefore on nose/throat swabs being taken and Breach of the pleura results in an empyema. Management Lung abscess Posturaldrainage,physiotherapyandaprolongedcourse of appropriate antibiotics to cover both aerobic and Denition anaerobic organisms will resolve most smaller ab- Localisedinfectionanddestructionoflungtissueleading scesses. Largerabscessesmayrequirerepeatedaspiration, to acollection of pus within the lung. Organismswhichcausecav- Denition itation and hence lung abscess include Staphylococcus Thereareessentiallythreepatternsof lungdiseasecaused and Klebsiella. Pathophysiology Aetiology The abscess may form during the course of an acute It is a lamentous fungus, the spores (5 mindiame- pneumonia, or chronically in partially treated pneu- ter) are ubiquitously present in the atmosphere. This results from Aspergillus growing within an area of previously damaged lung such as an old tuberculous Allergic bronchopulmonary aspergillosis cavity (sometimes called a mycetoma). Seen on X-ray as a round lesion with an air halo above i Initially it causes bronchospasm which commonly it. In immunosuppressed individuals with a low granulo- iii Chronic infection and inammation leads to irre- cyte count, the organism may proliferate causing a severe versible dilatation of the bronchi (classically proximal pneumonia, causing necrosis and infarction of the lung. The organisms are present as masses of hyphae invad- iv If left untreated progressive pulmonary brosis may ing lung tissue and often involving vessel walls. Investigation Theperipheralbloodeosinophilcountisraised,andspu- Management tum may show eosinophilia and mycelia. Eosinophilic Invasive aspergillosis is treated with intravenous am- pneumonia causes transient lung shadows on chest X- photericin B (often requiring liposomal preparations ray. Itraconazole and voriconazole have been used more re- Lung function testing conrms reversible obstruction in cently but current studies comparing efcacy with am- all cases, and may show reduced lung volumes in cases photericin B have yet to prove denitive. Management Obstructive lung disorders Generally it is not possible to eradicate the fungus. Itra- conazole has been shown to modify the immunologic Asthma activation and improves clinical outcome, at least over the period of 16 weeks. Oral corticosteroids are used to Denition suppress inammation until clinically and radiograph- A disease with airways obstruction (which is reversible ically returned to normal. Maintenance steroid therapy spontaneously or with treatment), airway inammation may be required subsequently. The asthmatic compo- and increased airway responsiveness to a number of nent is treated as per asthma guidelines. With time this repeated stimula- Can present at any age, predominantly in children. They secrete mediators of acute and 2 Intrinsic asthma tends to present later in life. There is chronic inammation including enzymes and oxygen no identiable allergic precipitant. Patients with occupational asthma from the listed causes are entitled to compensation under in- inammation recruiting and activating broblasts dustrial injuries legislation in the United Kingdom. The pattern of airway reaction following inhalation of an allergen: i An acute reaction occurring within minutes, peaking Table3. Non IgE related Isocyanates, colophony fumes (from ii A late reaction occurring 4 8 hours after inhalation solder), hardwood dust, complex (the chronic inammatory response). If there is diagnostic difculty in patients with mild symp- Mild moderate Life-threatening attack Severe attack attack toms or just cough, exercise tests or peak ow diary card r r r recordings as above. Occasionally, a trial of oral corti- Speech normal Unable to Silent chest costeroids for 2 weeks can be used.

buy 250mg keflex with mastercard

In the able to swallow cheap keflex 500 mg without prescription antibiotic x-206, is vomiting or has impaired con- gametocyte stage there is genetic recombination causing sciousness intravenous quinine is used purchase keflex online antibiotics for sinus infection and birth control. Treatment should be considered in patients with Clinical features features of severe malaria even if the initial blood Most patients have a history of recent travel to an en- tests are negative discount keflex 500mg bacteria lqp-79. The classical description of paroxysmal chills vere cases intensive care may be required generic 250mg keflex amex antibiotics stomach. Examination may reveal tachycardia, pyrexia, subsequent treatment with primaquine to eradicate hypotension, pallor and in chronic cases splenomegaly. In general where there is no chloroquine resistance Complications weeklychloroquineisused. It may also lead to severe intravascular haemol- endemic area (in order to detect establish tolerance) ysis causing dark brown/black urine (blackwater fever) and should continue for 4 weeks after leaving the en- particularly after treatment with quinine. Investigations Diagnosis is by identication of parasites on thick and thin blood lms. Although the rst specimen is positive in 95% of cases at least three negative samples are re- Myelodysplastic and quired to exclude the diagnosis. The thick lm is more myeloproliferative disorders sensitive for diagnosis and the thin lm is used to dif- ferentiate the parasites and quantify the percentage of Myelodysplastic syndromes parasite infected cells. Supportive therapy includes red blood cell and platelet transfusions and the use of antibiotics for infections. Al- Incidence logeneic stem cell transplantation is potentially curative 20 per 100,000 per year over the age of 70 years. These conditions have some common features: r Refractory cytopenia with multilineage dysplasia and r Extramedullary haemopoesis in the spleen and liver. Pathophysiology There may be transformation from one condition to an- The disorder arises from a single abnormal stem cell. Clinical features Patients with myelodysplastic syndrome typically present with symptoms of anaemia, thrombocytopenia Incidence (spontaneous bruising and petechiae or mucosal bleed- 1per 100,000 per year. Investigations Bone marrow aspirate examination shows normal or in- creased cellularity with megaloblastic cells and some- Sex times ring sideroblasts and abnormal myeloblasts. Almost all patients have the Philadelphia chromosome, a Cytogenetic remission is achieved in 70% of patients. Initiallythereisachronicindolentphase lasting3 5years,followedbyanacceleratedphaselasting Polycythaemia vera 6 to 18 months. Myeloid precursors and megakaryocytes may is often found from an incidental full blood count. Investigations Age r Full blood count and blood lm reveal a high neu- Most commonly presents over the age of 50 years. There may also be an increase in other gran- Sex ulocytes (basophils and eosinophils), thrombocytosis M>F and anaemia. In the chronic phase blast cells account for <10% of peripheral white blood cells. Idiopathicdisorder,althoughgeneticandenvironmental r Bone marrow aspirate shows a hypercellular marrow factors have been suggested. Polycythemia results in increased Management blood viscosity increasing the risk of arterial or venous r Hydroxyurea can induce a haematologic remission thrombosis. Platelet function is often disrupted risking and decrease splenomegaly but does not treat the un- bleeding. Patients may complain r Imatinib, a competitive inhibitor of the Bcr-Abl ty- of pruritus especially after a hot bath or shower. Hy- rosine kinase, is recommended for Philadelphia- perviscosity may result in headache or blurred vision. Abnormalities in platelet function can lead to epis- taxis, bruising and mucosal bleeding (including pep- tic ulcer disease) although severe bleeding is unusual. Prevalence r Increased blood cell turnover can lead to hyper- 2per 1,000,000 population. Investigations Fullbloodcountshowsanincreasedredbloodcellcount, Sex haemoglobin and packed cell volume. Polycythaemia vera can be distinguished from other Aetiology causes of polycythaemia by an increase in white cell Increased risk following exposure to benzene or radi- count, platelets and a high neutrophil alkaline phos- ation. On examina- hydroxyurea has been considered safe for long-term tion there is massive splenomegaly. Symptoms and signs maintenance it is also associated with increased risk of marrow failure (anaemia, recurrent infections and of development of leukaemia in comparison with ve- bleeding) may be present. Amyeloproliferative disorder characterised by increased platelets due to clonal proliferation of megakaryocytes Age in the bone marrow. Pathophysiology Platelets although increased in number have disrupted Sex function causing them to clump intravascularly lead- M = F ing to thrombosis, and to fail to aggregate causing bleeding. Risk factors include exposure to excessive ra- bleeding and cerebrovascular symptoms. Pathophysiology In acute leukaemias there is replacement of the normal Investigations bone marrow progenitor cells by blast cells, resulting in The blood lm shows increased numbers of platelets and marrow failure. Bone marrow aspiration demonstrates from the lymphoid side of the haemopoetic system (see increased megakaryocytes. Patients with life-threatening haem- orrhagic or thrombotic events should be treated with Clinical features thrombocytopheresis in addition to hydroxyurea. An- Often there is an insidious onset of anorexia, malaise grelide is occasionally used. There is often a history of recurrent infections and/or easy bruising and mucosal Prognosis bleeding. Other presentations include lymph node en- Essential thrombocythaemia may eventually transform largement, bone and joint pain and symptoms of raised to myelobrosis or acute leukaemia but the disease may intra cranial pressure. Phase 2 involves in- travenous chemotherapy (cyclophosphamide and cy- tosine) with oral 6-mercaptopurine. Lymphoid Stem Cell r Intensication: This involves intravenous metho- trexate and folinic acid, with intramuscular L- asparginase. Lymphoblast r Consolidation: This involves several cycles of chemotherapy at lower doses. Supportive treatment: Cytotoxic therapy and the leukaemia itself depresses normal bone marrow func- T Cell B Cell tion and causes a pancytopenia with resulting infection, anaemia and bleeding. Microscopy Prognosis The normal marrow is replaced by abnormal Prognosisisrelatedtoage,subtypeandinverselypropor- monotonous leukaemic cells of the lymphoid cell line. Over90%ofchildren The leukaemia is typed by cytochemical staining and respond to treatment, the rarer cases occurring in adults monoclonal antibodies to look for cell surface mark- carry a worse prognosis. Full Most common in the middle aged and elderly blood count shows a low haemoglobin, variable white count,lowplateletcount. Bonemarrowaspirationshows Sex increased cellularity with a high percentage of blast cells. On examination there Proerythroblast Myeloid Stem cell Megakaryoblast may be pallor, bruising, hepatosplenomegaly and lym- phadenopathy. Myeloblast Erythrocyte Platelet Microscopy Monoblast Promyelocyte Abnormal leukaemic cells of the myeloid cell line replace the normal marrow. Monocyte Myelocyte The leukaemia is typed by cytochemical staining and Granulocyte monoclonal antibodies to look for cell surface markers.