You are on page 1of 5

Dengue

CAUSE
The dengue flavivirus is a common cause of fever andacute systemic illness in the tropics The principal vector is the mosquito Aedes aegypti, There are four serotypes of dengue virus, all producing a similar clinical syndrome; homotypic immunity after infection with one of the serotypes is life-long, but heterotypic immunity against the other serotypes lasts only a few months after infection.

Clinical features
The incubation period from being bitten by an infected mosquito is usually 2–7 days. Asymptomatic infections are common but the disease is more severe in infants and the elderly. A morbilliform rash, which characteristically blanches under pressure, may occur, often as the fever is settling. A more severe illness, called dengue haemorrhagic fever or dengue shock syndrome There is thrombocytopenia and haemoconcentration. In the most severe form, after 3–4 days of fever, hypotension and circulatory failure develop with pleural effusions, ascites, hypoalbuminaemia and features of acute respiratory distress syndrome

Diagnosis
Leucopenia is usual and thrombocytopenia common. The diagnosis is confirmed by either a fourfold rise in IgG antibody titres, isolation of dengue virus from blood or detection of dengue virus RNA by PCR.

Management and prevention
Treatment is symptomatic. Aspirin should be avoided due to bleeding risk. Volume replacement and blood transfusions may be indicated in patients with shock. Corticosteroids have not been shown to help. No existing antivirals are effective. Breeding places of Aedes mosquitoes should be abolished and the adults destroyed by insecticides. There is no licensed vaccine available.

Multiple myeloma
This is a malignant proliferation of plasma cells. Normal plasma cells are derived from B cells and produce immunoglobulins which contain heavy and light chains. Normal immunoglobulins are polyclonal, which means that a variety of heavy chains are produced and each may be of kappa or lambda light chain type. In myeloma, plasma cells produce immunoglobulin of a single heavy and light chain, a monoclonal protein commonly referred to as a paraprotein. Although a small number of malignant plasma cells are present in the circulation, the majority are present in the bone marrow. The malignant plasma cells produce cytokines which stimulate osteoclasts and result in net bone reabsorption. The resulting lytic lesions cause bone pain, fractures and hypercalcaemia. Marrow involvement can result in anaemia or pancytopenia.

Clinical features and investigations
The clinical features include pancytopenia Renal failure due to: Paraprotein deposition, Hypercalcaemia, Infection, Dehydration, Bruising, bleeding. Diagnosis of myeloma requires two of the following criteria: • increased malignant plasma cells in the bone marrow • serum and/or urinary paraprotein • skeletal lytic lesions.

Management
Immediate support • High fluid intake to treat renal impairment and hypercalcaemia • Analgesia for bone pain. • Bisphosphonates for hypercalcaemia and to delay other skeletal related events • Allopurinol to prevent urate nephropathy. • Plasmapheresis, as necessary, for hyperviscosity. Chemotherapy: Thalidomide is the first line of treatment (not given in pregnancy as it is tertogenic)

Aplastic anaemia
Primary idiopathic acquired aplastic anaemia
The basic problem is failure of the pluripotent stem cells, producing hypoplasia of the bone marrow with a pancytopenia in the blood. The diagnosis rests on exclusion of other causes of secondary aplastic anaemia

Clinical features and investigations
Patients present with symptoms of bone marrow failure, usually anaemia or bleeding, and less commonly infections. An FBC demonstrates pancytopenia, low reticulocytes and often macrocytosis. Bone marrow aspiration and trephine reveal hypocellularity.

Management
All patients will require blood product support and aggressive management of infection. The prognosis of severe aplastic anaemia managed with supportive therapy, allogeneic bone marrow transplantation if there is an available donor. Those with a compatible sibling donor should proceed to transplantation as soon as possible. In older patients, immunosuppressive therapy with ciclosporin and antithymocyte globulin

Secondary aplastic anaemia
• Drugs such as Cytotoxic drugs, Antibiotics—chloramphenicol, sulphonamides, Antithyroid drugs, Anticonvulsants, Immunosuppressives—azathioprine • Radiation • Viral hepatitis • Pregnancy can Cause aplasia. The clinical features and methods of diagnosis are the same as for primary idiopathic aplastic anaemia. An underlying cause should be treated or removed but otherwise management is as for the idiopathic form.

Acute myeloid leukemia
Acute myeloid leukemia (AML), also known as acute myelogenous leukemia or acute nonlymphocytic leukemia (ANLL), is a cancer of the myeloid line of blood cells, characterized by the rapid growth of abnormal white blood cells that accumulate in the bone marrow and interfere with the production of normal blood cells. AML is the most common acute leukemia affecting adults

Clinical Features:
A lack of normal white blood cell production makes the patient susceptible to infections; fatigue, paleness, and shortness of breath. A lack of platelets can lead to easy bruising or bleeding with minor trauma. The early signs of AML are often vague and nonspecific, and may be similar to those of influenza or other common illnesses Enlargement of the spleen may occur in AML.Some patients with AML may experience swelling of the gums because of infiltration of leukemic cells into the gum tissue.

Management:
Chemotherapy   All except M3 are given 7+3 therapy i.e., Cytarabine and daunorubicin In M3 we give ATRA (all trans-retinoic acid)

FAB Classification of AML:
         M0-minimally differentiated acute myeloblastic leukemia M1-acute myeloblastic leukemia, without maturation M2-acute myeloblastic leukemia, with granulocytic maturation M3-promyelocytic, or acute promyelocytic leukemia (APL) M4-acute myelomonocytic leukemia M4eo-myelomonocytic together with bone marrow eosinophilia M5-acute monoblastic leukemia (M5a) or acute monocytic leukemia M6-acute erythroid leukemias, including erythroleukemia (M6a) and very rare pure erythroid leukemia M7-acute megakaryoblastic leukemia

Chronic myeloid leukemia (CML)
Chronic myelogenous (or myeloid) leukemia (CML), also known as chronic granulocytic leukemia (CGL), is a cancer of the white blood cells. It is a form of leukemia characterized by the increased and unregulated growth of predominantly myeloid cells in the bone marrow and the accumulation of these cells in the blood. CML is a clonal bone marrow stem cell disorder in which a proliferation of mature granulocytes (neutrophils, eosinophils and basophils) and their precursors is found. It is a type of myeloproliferative disease associated with a characteristic chromosomal translocation called the Philadelphia chromosome

Clinical Features:
Patients are often asymptomatic at diagnosis, presenting incidentally with an elevated white blood cell count on a routine laboratory test. Symptoms of CML may include: enlarged spleen causing pain on the left side, malaise, joint and/or hip pain, low-grade fever, increased susceptibility to infections, anemia, and thrombocytopenia with easy bruising (although an increased platelet count (thrombocytosis) may also occur in CML).

Treatment or Management:
Previously Hydroxyurea (antimetabolite) was given in CML but now Imatinib is first choice but if patient is resistant then we give Dasatinib and nilotinib