MBBS question bank

INFECTIVE ENDOCARDITIS (IE) It is the colonisation of the heart valves with microbiological organisms, leading to the formation of friable, infected vegetations and frequently valve injury. Types ACUTE INFECTIVE ENDOCARDITIS : caused by highly virulent organisms mainly Staphylococcus Aureus (20-30%), seeding a previously normal valve. SUBACUTE INFECTIVE ENDOCARDITIS : caused by organisms of moderate or low virulence mainly STREPTOCOCCI (60-70%), seeding an abnormal or previously injured valve. ENDOCARDITIS OCCURING IN I/V DRUG ABUSERS : caused predominantly by organisms found on the skin (S. aureus, Candida) and affecting the valves on the right side of the heart. PROSTHETIC VALVE ENDOCARDITIS : This may be early ( symptoms appearing within 60 days of valve insertion ), due to intraoperative infection of the valve or insertion of an infected valve or late ( after 60 days of valve insertion), due to late bacteremia. Predisposing factors to developement of IE Congenital cardiac anoma

Pulmonary hypertension When the mean pulmonary artery pressure is at least 25mmHg at rest, as measured at right heart catheterisation. Causes Respiratory failure due to intrinsic pulmonary disease is the most common cause. Complication of connective tissue disease like systemic sclerosis. Or as result of chronic thromboembolic events. Pathological features There occurs hypertrophy of both the media and the intima of the blood vessel wall and there occurs clonal expansion of endothelial cells which take on the appearance of plexiform lesions. There is marked narrowing of the vessel lumen, this leads to an increase in pulmonary vascular resistance and therefore pulmonary hypertension occurs. Clinical features Breathlessness, chest pain, fatigue, palpitation and syncope. Signs: Elevation of the jugular venous pulse, with prominent 'a' wave if in sinus rhythm. Parasternal heave in right ventricular hypertrophy. Accentuation of the pulmonary component of the second heart sound and a

Non-Hodgkin's Lymphoma (NHL) There is a malignant monoclonal proliferation of lymphoid cells ( majority of B-cells and minority of T-cells ). Working classification Three grades ( low, intermediate, high ). Staging by Ann-Arbor classification Stage 1 Involvement of a single lymph node region or a single extra - lymphatic origin or site. Stage 2 Involvement of 2 or more lymph node regions on the same side of diaphragm.  Stage 3 Involvement of lymph node regions on both sides of the diaphragm. Stage 4 Diffuse or disseminated involvement of one or more extra - lymphatic organs. Stage 5 Localised, solitary involvement of extralymphatic tissue excluding liver and bone marrow. Clinical features Patients present with lymph node enlargement, which may be associated with systemic upset: weight loss, sweats, fever and itching. Hepatosplenomegaly may be present. Site of extranodal involvement include the bone marrow, gut, thyroid, lung, skin, testis  and brain. Compression syndromes may occur

Hodgkin's Lymphoma This is progressive, painless enlargement of lymphoid tissues throughout the body. EB virus involvement is thought to be one of the aetiologies. Pathological classification Lymphocyte predominant Nodular sclerosis Mixed cellularity Lymphocyte depleted Characteristically, cells with mirror image nuclei (REED-STERNBERG CELLS) are seen. Clinical features Patient present with enlarged, painless lymph nodes, alcohol induced pain pain over the enlarged nodes, and features due to the mass effect of the node. 25% have constitutional symptoms like fever, weight loss, night sweats and pruritus. Hepatosplenomegaly may also be present. Investigations Lymph node biopsy  Bone marrow biopsy Liver biopsy Lymphopenia indicates bad prognosis. Moderate eosinophilia may occur in 10 to 15% of the patients. Clinical staging (Ann-Arbor Classification) Stage 1 Involvement of a single lymph node region (1) or extra-lymphatic site (E) Stage 2 Involvement of two or more lymph node regions

• This is the abnormality of red blood cells. • This is usually inherited as an AUTOSOMAL DOMINANT condition. • The most common abnormalities are deficiencies of BETA SPECTRIN or ANKYRIN. • Most cases are associated with an asymptomatic compensated chronic haemolytic state with spherocutes present on the blood film, a reticulocytosis and mild hyperbilirubinaemia. • Pigment GALLSTONES are present in up to 50% of patients and may cause chlolecystitis. The clinical course may be complicated by crisis : • A HAEMOLYTIC CRISIS occurs when the severity of haemolysis increases. • A MEGALOBLASTIC CRISIS follows the development of folate deficiency. • An APLASTIC CRISIS occurs in association with PARVOVIRUS B19 infection. Investigations • The blood film will show spherocytes but the direct Coombs test is negative, excluding immune haemolysis. • An OSMOTIC FRAGILITY TEST may show increased sensitivity to lysis in hypotonic saline solutions but is limited by lack of sensitivity and specificity. •

1. Primary idiopathic acquired aplastic anaemia  2. Secondary aplastic anaemia Primary idiopathoc acquired aplastic anaemia The basic problem is failure of pluripotent stem cells, producing hypoplasia of the bone marrow with a pancytopenia in the blood. Clinical features and investigations • Patients present with symptoms of bone marrow failure, usually anaemia or bleeding and less commonly infections. • FBC shows 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 curative treatment is allogeneic HSCT if there is available donor. In older patients, immunosuppressive therapy with CICLOSPORIN and ANTITHYMOCYTE GLOBULIN gives 5-year survival rates of 75%. Secondary aplastic anaemia Clinical features and methods of diagnosis are same as for primary idiopathic aplastic anaemia. Causes • Drugs Cytotoxic drugs Antibiotics - ch

Introduction 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, but in myeloma plasma cells produce immunoglobulin of a single heavy and light chain, a MONOCLONAL protein called as paraprotein.  In some cases only light chain is produced and this appears in the urine as BENCE JONES PROTEINURIA. The malignant plasma cells produce cytokines, which stimulates osteoclasts and result in net bone reabsorption which causes bone pain, fractures and hypercalcaemia. Clinical features and investigations Bone pain/ fractures Lytic lesions  Nephrotic syndrome, carpal tunnel syndrome  Panda eyes Renal failure due to paraprotein deposition, hypercalcaemia, infection, NSAIDs, amyloid. Spinal cord compression Retinal bleeds Bruising Heart failure Cerebral ischaemia Diagnosis of myeloma requires two of the following criteria: 1. Increase malignant plasma c

Iron deficiency anaemia Blood loss Most common cause is gastrointestinal blood loss result from occult gastric or colorectal malignancy, diverticulitis, polyps, gastritis, peptic ulceration, inflammatory bowel disease and angiodysplastic lesions. Other causes : schistostomiasis, hookworm, aspirin, NSAIDS. Very rarely chronic haemoptysis or haematuria. Malabsorption Achlorhydria (that is lack of gastric acid secretion) in the elderly or due to drugs such as proton pump inhibitors may contribute to the lack of iron availability from the diet. Physiological demands At the time of rapid growth, such as in infancy and puberty In pregnancy, iron is diverted to the fetus. Investigations  Confirmation of iron deficiency  Single best test to detect iron deficiency is measure of plasma ferritin level in blood. Others are plasma iron and total iron binding capacity (TIBC)  Investigation of the cause It depends upon age, sex, underlying disease such as GI bleeding. Endoscopy, radiological studies.