MindMap Gallery Leishmaniasis
This is a clear mind map of leishmaniasis, mainly explaining contents such as skin, mucous membranes, skin, and viscera. Each content is further explained on several levels, including the pathogenesis, clinical manifestations, diagnostic methods, and treatment plans for leishmaniasis.
Edited at 2022-12-08 17:01:33This is a clear mind map of leishmaniasis, mainly explaining contents such as skin, mucous membranes, skin, and viscera. Each content is further explained on several levels, including the pathogenesis, clinical manifestations, diagnostic methods, and treatment plans for leishmaniasis.
Clinical neoplasia refers to the manifestation and presentation of cancer in a patient. Neoplasia is the abnormal growth of cells that can form tumors or invade surrounding tissues. Clinical neoplasia involves the observation and assessment of signs and symptoms that indicate the presence of cancer, such as unexplained weight loss, pain, changes in organ function, or the detection of abnormal masses through imaging or physical examination. The clinical evaluation of neoplasia often involves diagnostic tests, such as biopsies or imaging studies, to confirm the presence of cancer and determine its extent. Understanding the clinical aspects of neoplasia is crucial for early detection, accurate diagnosis, and appropriate treatment planning for cancer patients.
Carcinogenesis, the process of cancer development, involves a series of genetic and epigenetic changes that lead to the transformation of normal cells into cancerous ones. This intricate process encompasses multiple stages, including initiation, promotion, and progression, and is influenced by various factors such as genetic predisposition, environmental exposures, and lifestyle choices. In this mind map, we will explore the complexities of carcinogenesis, including the molecular and cellular mechanisms involved in the initiation and progression of cancer. By delving into the intricacies of carcinogenesis, we can gain a deeper understanding of this critical process and its implications for cancer research and patient care.
This is a clear mind map of leishmaniasis, mainly explaining contents such as skin, mucous membranes, skin, and viscera. Each content is further explained on several levels, including the pathogenesis, clinical manifestations, diagnostic methods, and treatment plans for leishmaniasis.
Clinical neoplasia refers to the manifestation and presentation of cancer in a patient. Neoplasia is the abnormal growth of cells that can form tumors or invade surrounding tissues. Clinical neoplasia involves the observation and assessment of signs and symptoms that indicate the presence of cancer, such as unexplained weight loss, pain, changes in organ function, or the detection of abnormal masses through imaging or physical examination. The clinical evaluation of neoplasia often involves diagnostic tests, such as biopsies or imaging studies, to confirm the presence of cancer and determine its extent. Understanding the clinical aspects of neoplasia is crucial for early detection, accurate diagnosis, and appropriate treatment planning for cancer patients.
Carcinogenesis, the process of cancer development, involves a series of genetic and epigenetic changes that lead to the transformation of normal cells into cancerous ones. This intricate process encompasses multiple stages, including initiation, promotion, and progression, and is influenced by various factors such as genetic predisposition, environmental exposures, and lifestyle choices. In this mind map, we will explore the complexities of carcinogenesis, including the molecular and cellular mechanisms involved in the initiation and progression of cancer. By delving into the intricacies of carcinogenesis, we can gain a deeper understanding of this critical process and its implications for cancer research and patient care.
Leishmaniasis
cutaneous
Old world
L.tropica
-Dry sore/urban -incubation: 6months -Host: dog but not reservoir -Vector: Phlebotomus (sand fly)
Leishmania recidivans: -new lesions in the same area -slowly enlarging lesion that heals in center
*L.major
-Wet sore/rural -incubation: few days -Host: desert gerbil (reservoir) -Vector: Phlebotomus Papatasii
Lesions caused by L.tropica & L.major heal spontaneously leaving disfiguirment and long-lasting immunity
L.aethiopica (DCL)
-Diffuse cutaneous L. -Host: hyrax rodent(reservoir) -Vector: Phlebotomus longipes *Defective cell meddiated immune response
Leprosy
new world
*L.mexicana
-rural -Host: rodents (reservoir) -Vector: Phlebotomus Lutzomyia
mucocutaneous
L.braziliensis
-Rural -Host: rodents (reservoir) -Vector: Phlebotomus Lutzomyia
after resolution of primary lesion, recurrence at a distal mucosal site can follow
visceral (kala-azar)
L.donovani (old)
-incubation: 4-10months -Vector: Phelobtomus -other modes: Blood transfusion, person to person transplacental, accidental (laboratory) -affects reticuloendothelial system
clinical picture: Kala- azar: -Fever (remittent/intermittent) -Organomegaly -Cachexia -Pancytopenia -Hypergammaglobulinemia (reversed serum albumin/globulin ratio) -diarrhea/dysentery -earth gray skin colour (dark granulomas)
Post kala-azar Leishmaniasis (PKDL): Leprosy due to incomplete/inappropriate course of treatment
African -During or at the end of treatment -resolve after few months -no further therapy needed
Indian* -insidious or many years after treatment -resolve after few months -no further therapy needed
L.chagasi (new)
Treatment: (CL) Ketoconazole: effective against L.Major,L.Mexicana* Fluconazol/itraconazole: similar to ketoconazole and better tolerated (FIT>Keto) Topical:Aminosidine (applied 2 times daily for 20 days)
Treatment:(VL) Miltefosine: 1st oral drug that is effective against kala-azar
Treatment: (ALL) Pentavalent antimonial(sodium stibogluconate): high toxicity, ineffective in advanced MCL Paromomycin: synergistic with Na stibogluconate Amphotercin B: 1st line drug in india, non toxic, effective in advanced MCL
Diagnosis: 1)Biopsy: -Bone marrow: children: iliac crest/ Adults: sternal puncture (safe but painful),+ve in 70-85% of cases -Spleen: +ve in 95% of cases but its not safe -lymph gland simple but low +ve yield (60% of cases only) -Liver: +ve in 70-85% of cases 2)blood examination:* amastigotes may be seen in blood smears of buffy coat only in indian kala-azar 3)Culture: material from biopsy can be cultured in NNN media where promastigotes can be diagnosed 4)IFAT: specific antibodies appear early and disappear within 6months of treatment (test of choice for VL) 5)ELISA: used for large scale epidemiological studies 6)Leishmanin/ Montenegro test: in VL It becomes +ve only after recovery so it can be used for follow up
Diagnosis: 1) microscopic examination: of material obtained from nodule and staining it with Giemsa stain *Amastigotes are abundant in fresh CL and DCL and few in old CL and MCL 2) Culture: a portion of material from biopsy can be cultured in NNN media where promastigotes can be diagnosed 3) Leishmanin/ Montenegro test: 0.1ml of treated promastigotes are injected intradermally +ve reaction: red indurated circle after 48hrs 4) IFAT: Negative