Dr Anupam Priyad
About Me
Dr Anupam Priyad
MBBS
Hematologists
10 Years Experience
Biography
My Clinic
OPD Hours
| Monday | Morning | 10:00 AM | - | 02:00 PM |
| Evening | 06:00 PM | - | 09:00 PM | |
| Tuesday | Morning | 10:00 AM | - | 02:00 PM |
| Evening | 06:00 PM | - | 09:00 PM | |
| Wednesday | Morning | 10:00 AM | - | 02:00 PM |
| Evening | 06:00 PM | - | 09:00 PM | |
| Thursday | Morning | 10:00 AM | - | 02:00 PM |
| Evening | 06:00 PM | - | 09:00 PM | |
| Friday | Morning | 10:00 AM | - | 02:00 PM |
| Evening | 06:00 PM | - | 09:00 PM | |
| Saturday | Morning | 10:00 AM | - | 02:00 PM |
| Evening | 06:00 PM | - | 09:00 PM | |
| Sunday | Morning | 10:00 AM | - | 02:00 PM |
| Evening | 06:00 PM | - | 09:00 PM |
Treatments
Specialised care and treatments offered
IDIOPATHIC THROMBOCYTOPENIC PURPURA (ITP)
An immune-mediated disorder marked by low platelet counts causing increased bleeding tendencies. ITP commonly presents sudden onset bruises and petechiae without apparent injury especially among young adults but also across ages worldwide.
- Signs include unexplained easy bruising/bleeding gums along with tiny red dots under the skin known as petechiae resulting from deficient platelets responsible for clotting.
- Root cause entails autoantibodies targeting platelet surface proteins triggering their premature destruction predominantly in spleen.
- Diagnosis utilizes complete blood count highlighting thrombocytopenia alongside exclusion tests ruling out other causes through bone marrow biopsy when uncertain.
- Treatment modalities vary according to severity: corticosteroids reduce immune attack initially whereas intravenous immunoglobulin boosts platelet counts rapidly during bleeding episodes; refractory cases might require splenectomy.
- The outlook is generally favorable though some experience chronic low platelets necessitating ongoing hematology follow-up.
This condition highlights importance of immune regulation maintenance plus prompt intervention aiming symptom relief preserving platelet functionality crucial for hemostasis.
HEMOLYTIC ANEMIA
This condition arises when red blood cells are destroyed faster than they can be produced. Recognizing hemolytic anemia early allows proper treatment aimed at stopping excessive breakdown of red cells while addressing underlying causes.
- range between inherited defects such as enzyme disorders or membrane abnormalities versus acquired issues including autoimmune diseases , infections , certain drugs , or toxins . / li > ; lt ;span > strong > Diagnosis / strong > requires comprehensive lab evaluations like peripheral smear showing abnormal red cells features , elevated reticulocyte counts indicating bone marrow compensation , Coombs test for autoimmune involvement , along with bilirubin levels . / li> strong > Treatment / strong > depends on cause but often includes immunosuppressants for autoimmune types , removal of offending agents , folate supplementation , transfusions when needed , sometimes splenectomy plays a role . / li > ; lt span > ; strong > Prognosis / strong & gt ; varies widely based on etiology severity yet many respond well following tailored interventions ensuring improved hemoglobin stability . / li>& # 60; / ul >< p > Effective management minimizes symptoms impact preventing complications secondary anemia entails maximizing patient wellbeing through individualized hematologic care .
SICKLE CELL CRISIS MANAGEMENT
Sickle cell crisis is a painful episode resulting from blockage of blood flow by abnormally shaped red cells. Prompt relief measures are vital for patient comfort and preventing complications.
- The sudden onset severe pain, often in bones or abdomen, characterizes these crises along with possible swelling or fever indicating infection risk.
- Crisis episodes arise due to red cell sickling triggered by dehydration, infection, low oxygen levels, or stress on the body’s system.
- A detailed history alongside complete blood count helps establish presence of sickle cell disease contributing to recurrent crises as part of diagnosis confirmation.
- Efficacious treatments include vigorous hydration, pain control through analgesics including opioids if needed, oxygen supplementation where hypoxia exists, and managing precipitating factors like infections promptly with antibiotics.
- Avoidance strategies such as regular checkups and preventive medications reduce frequency; emergencies need hospitalization for severe attacks supportively managed by healthcare professionals skilled in hematology care.
This condition requires both acute interventions during attacks and ongoing management strategies targeting overall disease control for quality of life improvement.
DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
DIC is an acute condition marked by widespread activation of clotting pathways that paradoxically causes both clot formation and bleeding. It often complicates severe infections or trauma.
- Clinical signs include abnormal bleeding from multiple sites, skin bruises, organ dysfunction due to microthrombi, and shock symptoms in severe cases.
- The disease mechanism involves excessive consumption of coagulation factors leading to imbalance between clotting and fibrinolysis systems.
- A combination of laboratory tests such as prolonged clotting times, decreased platelets, elevated D-dimer levels confirm the diagnosis.
- Treatment primarily focuses on managing the underlying trigger like infection while supporting coagulation with transfusions if necessary; anticoagulants are used cautiously based on bleeding risk.
- The course varies widely but rapid recognition with multidisciplinary care improves survival in this life-threatening state.
DIC represents a critical hematological emergency requiring intensive monitoring and tailored interventions for best results.
THROMBOTIC THROMBOCYTOPENIC PURPURA (TTP)
This rare but serious disorder causes small blood clots throughout the body’s small vessels. It demands urgent diagnosis and management to prevent organ damage from impaired circulation.
- TTP typically presents with symptoms such as purplish skin spots (purpura), fatigue, confusion, or fever due to reduced platelet counts and anemia.
- The underlying cause involves deficiency of an enzyme called ADAMTS13 leading to uncontrolled clot formation in capillaries.
- An accurate diagnosis requires blood smears showing fragmented red cells (schistocytes), low platelets, and specialized enzyme activity assays.
- Main treatment consists of plasma exchange therapy combined with immunosuppressive medications to stop autoantibody production against ADAMTS13.
- The outlook improves greatly with prompt therapy; untreated TTP can be fatal due to multi-organ failure caused by microthrombi.
A swift clinical approach enhances survival chances and minimizes long-term complications in affected patients.
ACUTE LEUKEMIA
Acute leukemia is a rapidly progressing cancer of the blood and bone marrow. It requires immediate medical attention to manage the fast multiplication of abnormal white blood cells that impair normal blood function.
- Symptoms often include fatigue, fever, frequent infections, easy bruising or bleeding, and bone pain.
- Causes may involve genetic mutations or exposure to certain chemicals and radiation.
- Diagnosis is usually confirmed by blood tests showing immature white cells and bone marrow biopsy examining cell morphology.
- Treatment relies heavily on chemotherapy to eradicate leukemic cells, sometimes supported by targeted therapies or stem cell transplantation in suitable candidates.
- Prognosis depends on factors such as age, subtype of leukemia, and response to therapy; early intervention improves outcomes significantly.
Caring for individuals with acute leukemia involves close monitoring due to the disease’s aggressive nature and potential complications during treatment.