CA Lung with metastasis

Dear Friends, Fever of unknown origin is a very important clinical condition in our day to day practice.. I thought to have an UPDATE on this The subject needs longer discussions.. So will be presented in two parts Let's have the initial one… Fever of unknown origin (FUO) in adults is defined as a (1)Temperature higher than 38.3 C (100.9 F) (2)Lasts for more than three weeks (3)With no obvious source despite appropriate investigations. COMMON ETIOLOGIES OF FEVER OF UNKNOWN ORIGIN.. INFECTIONS Tuberculosis (especially extrapulmonary) Abdominal abscesses Pelvic abscesses Dental abscesses Endocarditis Osteomyelitis Sinusitis Cytomegalovirus Epstein-Barr virus Human immunodeficiency virus Lyme disease Prostatitis Sinusitis MALIGNANCIES Chronic leukemia Lymphoma Metastatic cancers Renal cell carcinoma Colon carcinoma Hepatoma Myelodysplastic syndromes Pancreatic carcinoma Sarcomas AUTOIMMUNE CONDITIONS Adult Still's disease Polymyalgia rheumatica Temporal arteritis Rheumatoid arthritis Rheumatoid fever Inflammatory bowel disease Reiter's syndrome Systemic lupus erythematosus Vasculitides MISCELLANEOUS Complications from cirrhosis Factitious fever Hepatitis (alcoholic, granulomatous, or lupoid) Deep venous thrombosis Sarcoidosis Drug-induced fever DRUGS COMMONLY ASSOCIATED WITH DRUG -INDUCED FEVER.. Allopurinol Captopril Cimetidine Clofibrate Erythromycin Heparin Hydralazine Hydrochlorothiazide Isoniazid Meperidine Methyldopa Nifedipine Nitrofurantoin Penicillin Phenytoin Procainamide Quinidine The approach to diagnose the patient and investigations needed ...will be covered in the second and concluding part if HELPFUL to you Thanks Dr K N Poddar

age 34 year female, she is suffering from multiple joint pain , on & off fever, night sweats, breathing difficulties since 3months association with generalised weakness and rapid weight loss.adv diag&treatment

A 48 y/o M came with complaints of progressive abd discomfort and wt loss since 3 months. Labs: Total bilirubin=3.3 AST 141 IU, ALT 100 IU, ALP 436 IU, ESR 78 mm. CT revealed a well-marginated cystic lesion in head of the pancreas, the rest being unremarkable. Endoscopic ultrasound-guided FNA of the lesion was done; histology revealed epithelioid granulomas. A possible case of pancreatic tuberculosis?

Comments on X-ray.. D/D.. Management. A male aged 55 years, having cough, fever , Dyspnoea and weakness since one year. CT chest report is attached . Sputum for AFB is negative.

LYMPHADENOPATHY &SPLEENOMEGALY. IN SYSTEMIC LUPUS ERYTHEMATOSUS. Lymph nodes,in conjunction with the spleen, tonsils,adenoids and peyer patches are highly organized centres of immune cells that filter antigen from the extracellular fluid. STRUCTURE OF LYMPH NODE. Each lymph node is surrounded by a FIBROUS CAPSULE .Directly interior to the fibrous capsule is the SUBCAPSULAR SINUS..This sinus allows lymph ,an ultrafiltrate of blood ,to traverse from the afferent lymph vessels through the sinuses ,and out the efferent vessels. Interior to the subcapsular sinus is the CORTEX.,which contains primary follicles, secondary follicles and interfollicular zone. FOLLICLES : Major sites of B-cell proliferation. INTERFOLLICULAR ZONE : is the site of antigen dependant T-cell differentiation and proliferation. The deepest structure is MEDULLA. :which consists of cords of plasma cells and small B-lymphocytes that facilitate immunoglobulin secretion into the exiting lymph. Lymphadenopathy results ftom reticuloendothelial proliferation secondary to inflammation ,infection or malignancy. LUPUS LYMPHADENOPATHY is a nonspecific finding .Biopsy shows Reactive follicular hyperplasia,with or without atypical cells. Coagulative necrosis with hematoxylin bodies typical findings in SLE ,is rarely seen. IMMUNOPATHOGENESIS OF SLE : The immunopathogenesis of SLE is associated with 1.genetically determined loss of self-tolerance and 2.cellular activation dependant of non-genetic factors ,such as environmental, hormonal and infectious.Activation of - T- lymphocytes by gamma-interferon stimulates the sequence of progressive and persistent expansion of apoptosis - resistant polyclonal B-lymphocytes ,which produce auto-antibodies charateristic of the disease. Lupus Lymphadenopathy mainly involves the cervical and axillary regions .The lymph nodes are soft,mobile,painful and non-adherant to deep planes. Lupus Lymphadenopathy shows Reactive follicular hyperplasia (RFH) on histology. Atypical histological characteristics are also identified which are classified as 1.RFH with gaint follicles.irregular follicles, increased in size with hyperplastic germinal centre and cytolysis. 2.Similar to castleman's disease.(CD). plasmocytosis and interfollicular vascular proliferation is seen. 3.Atypical paracortical hyperplasia with lymphoid follicles. 4.Atypical immunoblastic and lymphoplasma- cytic proliferation. DIFFERENTIAL DIAGNOSIS OOF LYMPHADENOPATHY. 1. INFECTIOUS : CMMV. EBV. HIV. TOXOPLASMOSIS. TUBERCULOSIS. 2.DRUGS. Captopril. Penicillamine. Hydralazine. Phenytoin. Gold salts. 3.INFLAMMATORY. DISESES.: Sarcoidosis. Still's disease. SLE. Rheumatoid arthritis. Kikuchi-Fujimoto disease. 4.NEOPLASIA. Lymphoma. SPLEENOMEGALY.: Spleenomegaly is also seen. Both Lymphadenopathy and spleenomegaly are seen in various diseases.Therefore you have to approach a patient systematically by proper examination,physical examination, laboratory tests and specialised tests.