Hyperemia & Congestion

Hyperemia = increased blood flow to tissue due to dilation of arteries.

Erythema = redness of tissues due to increased oxygen delivery

Congestion = reduced drainage of blood from tissues that can occur systemically (e.g. heart failure) or locally (e.g. venous obstruction). Remember, reduced venous drainage causes back up of blood and increased hydrostatic pressure within capillaries which leads to edema. Also, because blood can not be drained from the tissues, new blood can not be effectively sent to the tissues either, leading to hypoxia which can lead to ischemia, injury, etc. If the pressure from the increased hydrostatic pressure is too much, the capillaries may rupture leading to hemorrhage, as red blood cells enter the interstitium.

cyanosis = blue-red color of tissues due to hypoxia e.g. deoxygenated hemoglobin in the red-blood cells.
acute pulmonary congestion = fluid accumulates in alveolar septa, and fluid along with red blood cells (due to capillary rupture) often accumulate in alveoli.
chronic pulmonary congestion = alveoli contain heart failure cells and alveolar septa become thick and fibrotic.

heart failure cells (microscopic) = aka hemosiderin-laden macrophages. Macrophages ingest the red blood cells that were scattered into the interstitium when the capillaries ruptured. Hemosiderin is the iron-storage complex in the red blood cells.

acute hepatic congestion = periportal hepatocytes survive longer due to blood supply from hepatic arteries, whereas, centrilobular hepatocytes die sooner because they are further away from the hepatic arteries.
chronic hepatic congestion = as the centrilobular hepatocytes die, these regions become, darker and more defined compared to the periportal regions, creating a "nutmeg liver" pattern.

nutmeg liver (microscopic, gross) = due to hemosiderin-laden macrophages. Macrophages in the centrilobular region ingest red blood cells (from ruptured capillaries), and the mixture of dead hepatocytes, red cells, and hemosiderin-laden macrophages give the region a red-brown color which contrasts against the mostly normal periportal regions.

Comments

Chronic Myeloid Leukemia (CML)

Quick Review Patient is often older, and can no symptoms or have B symptoms (night sweats, etc), fatigue, and weight loss (caused by early satiety due to enlarged spleen). On physical exam, an enlarged spleen can be palpated. CBC shows very high WBC count (typically >100,000) with elevated basophils on differential. Peripheral smear shows early, immature neutrophil precursors (myelocytes, metamyelocytes) as well as many basophils. It is important for CML to know the details of the genetic abnormality because it relates to the treatment. CML is due to a translocation of BCR and ABL on chromosomes 9 and 22 resulting a fusion BCR-ABL gene that produces a tyrosine kinase that is always active. The treatment of choice is a tyrosine kinase inhibitor e.g. imatinib. They work to suppress the tyrosine kinase and can induce disease remission. Relevant Images Immature neutrophil precursors on peripheral smear BCR-ABL translocation

Chemotherapy

Terminology Adjuvant therapy - given in addition to standard therapy Consolidation therapy - given after induction therapy with multidrug regimens to further reduce tumor burden Induction therapy - initial dose of treatment to rapidly kill tumor cells and send the patient into remission Maintenance therapy - given after induction and consolidation therapies or after the initial standard therapy to kill any residual tumor cells and keep the patient in remission Neoadjuvant therapy - given before the standard therapy for a particular disease Remission - less than 5% tumor burden Salvage therapy - given when standard therapy fails Adjuvant therapies in various cancers Metastasis to bone - bisphosphonates (e.g. zoledronic acid) are given to prevent lytic lesions and pathologic fractures as well as malignant hypercalcemia. Bisphosphonates work by inhibiting osteoclasts and thereby preventing bone breakdown. Breast cancer Tamoxifen , a selective estrogen recep

Acute Myeloid Leukemia (AML)

Quick Review Patient is an adult (usually older, but can also be younger) with fatigue (due to anemia) and bleeding (due to thrombocytopenia) and on CBC there is decreased hemoglobin, decreased platelets, and WBC varies (can be normal, increased or decreased). LDH will be elevated. The most important form of AML to know is acute promyelocytic leukemia (APML). On peripheral smear, AML presents with myeloblasts with Auer rods. Bone marrow biopsy will show myeloid blasts, for APML this would be atypical promyelocytes. In AML, the bone marrow is crowded with immature myeloid cells ("blasts") preventing development of other cell types (platelets, RBCs, normal WBCs). These myeloblasts are also present in the peripheral blood in large numbers. This is why patients have fatigue (anemia), bleeding/ bruising (thrombocytopenia), increased infections (granulocytopenia). APML can present with DIC (disseminated intravascular coagulation) which results in elevated PT and aPTT and re

pathology

Search This Blog