Pathology – Dentowesome

https://drive.google.com/open?id=1dow8Kc-EV3SNamk1lFlkj6gttzViwvrN

Link highlights:• Definition• Pathogenesis of Giant cells• Types of giant cells - grossly classified into 2 types. –• The giant cells which exist in normal tissue (physiological) e.g osteoclasts in bones, trophoblasts in placenta, odontoclast, straited muscle.• The giant cells which exist pathological -eg. Foreign body giant cellsLanghan's giant cellsTouton giant cellsAschoff giant cells
Anaplastic cancer giant cells Reed-Sternberg giant cells

Curated by: Dr. Tabassum Sayyad (Dental Intern – MARDC)

Dentowesome 2020✍🏻

Source- textbook of pathology for dental students Ramdas Nayak and pinterest

Source – textbook of pathology for dental students Ramdas Nayak and Google images

Source- textbook of pathology for dental students Ramdas Nayak and Google images

Source – textbook of pathology for dental students Ramdas Nayak and Google images

Leukemias are malignant Neoplasms of the haematopoetic stem cells characterized by diffused replacement of bone marrow by Neoplastic cells with or without involvement of the peripheral blood.

➡️ Chronic leukaemia is a disease of insidious onset, affecting middle aged & young adults (CML)

🔅CLINICAL FEATURES:

1. Gradually developing Anaemia
2. Hepatosplenomegaly (In CML, a massive splenomegaly reaching upto the umblicus) Therefore, acute pain due to splenic infarction
3. Bleeding tendencies
4. Hypermetabolism
5. Bone pain
6. Juvenile CML: Lymph node enlargement, frequent infections, haemorrhagic manifestations & facial rash

🔅LAB. FINDINGS:

• Thick and sticky & shows a wide buffy coat in the haematocrit tube
• Anaemia – Moderate, normocytic normochromic

🔘 1 lakh - 5 lakh/cu.mm

🔘 Differential count reveals more mature forms in Peripheral smear, complete spectrum of granulocytes, myelocytes & band cells (50%)

🔘 Blast cell > 10% of leukocytes

🔘 Phases:

1. Chronic phase:

➡️ Myeloproliferative disorder – excessive proliferation of myeloid cells & mature segmented Neutrophils

➡️ Basophils upto 10% (feature of CML)

2. Accelerated phase:

• ⬆️ Anaemia
• Blast count: 10-20%
• Basophils: 20%
• Platelet: ⬇️ 1 lakh/µl
• Leucocytosis

3. Blastic phase: Myeloid blast crisis in CML resembles AML >20%

1. Cellularity: Hypercellular fat spaces replaced by Myeloid cells.
2. Myeloid cells: ⬆️ M:E ratio
3. Erythropoiesis: Normoblastic
4. Megakaryocytes: Conspicuous, smaller in size
5. Chromosomal abnormalities: The philadelphia chromosome is present in about 90% of the cases of CML

• neutrophil alkaline phosphatase (NAP) activity is markedly reduced in CML

VI. Miscellaneous: Uric acid ⬆️

🔅TREATMENT:

• The standard treatment for chronic phase CML is a tyrosine kinase inhibitor (TKI) like imatinib oral therapy. Imatinib works by reducing the production of abnormal white blood cells.
• Allogenic bone marrow transplants.
• Interferon was once the best treatment for CML, but now, the tyrosine kinase inhibitors are the mainstay of treatment and interferon is rarely used. To treat CML, this drug is most often given as a daily injection (shot) under the skin. It may also be injected into a muscle or vein. It’s given for many years.
• Chemotherapy: Today, chemo may be used to treat CML when the TKIs have stopped working. It’s also used as part of a stem cell transplant.
• Others:

• Splenectomy
• Splenic irradiation
• Leukapheresis

🔘 Splenectomy and splenic irradiation have been used in patients with large and painful spleens, usually in the late phase of CML. This is rarely needed in patients whose disease is well controlled.

🔘 For those patients unable to tolerate chemotherapy, leukapheresis is a viable option.

Dr. Mehnaz Memon🖊

References:

1. Textbook of Pathology, Harsh Mohan; Internet articles
2. Image source: Google

🔹OEDEMA〰️Swelling. Abnormal/excessive accumulation of free fluid in the interstitial tissue spaces & serous cavities.

🔹Accumulation of fluid (abnormally) inside the cell is intracellular edema/hydropic degeneration.

🔹Accumulation in body cavities:

• Peritoneal Cavity – Ascitis
• Pleural Cavity – Hydrothorax (T.B)
• Pericardial cavity – Hydropericardium

TYPES OF OEDEMA👆🏻

🔹PITTING & NON-PITTING EDEMA:

Source: Healthline

➡️ When interstitial fluid volume increases, most of the fluid becomes free that is not bound to proteoglycan meshwork. This type of edema is called pitting edema because when this area is pressed with finger, fluid gets displaced producing depression or a pit as seen in SUBCUTANEOUS TISSUES.

➡️ Edema also develops due to swelling of the cells/clotting of interstitial fluid in the presence of fibrinogen. This is called Non-pitting/solid edema because its hard & a pit is not formed by pressing.

• e.g. – Myxodema
• – Elephantiasis

🔹 Pathogenesis of Edema:

➡️ Causative mechanisms that produce edema are:

1. ⬇️ Plasma oncotic pressure
2. ⬆️ capillary hydrostatic pressure
3. Lymphatic obstruction
4. Sodium & Water retention
5. ⬆️ capillary permeability
6. Tissue factors

These mechanisms interfere with normal fluid balance of plasma, interstitial fluid & lymph flow.

1. Increased Plasma Oncotic Pressure:

• It is exerted by total amount of plasma proteins that tend to draw fluid into the vessels normally.
• A fall in the total plasma protein level (