Blood pathophysiology Flashcards
1) What is leukemia?
2) Types of leukemias
3) Differences
1) Malignant neoplasms in the blood/bone marrow
2) AML (Acute myeloid), ALL (Acute lymphoblastic), CML, CLL
3) AML/ALL: Cells do not mature
CML/CLL: Cells partially mature
1) Etiology of AML and ALL
2) Pathogenesis and related symptoms
3) Disease progression
1)
AML: Genetic abnormalities, adults
ALL: T-ALL or B-ALL: Translocation of chromosomes
- Children (12-21), good prognosis
- Adults (9-22), bad prognosis
2) Suppression of bone marrow function due to blast cells
- Fatigue (Anemia), bleeding (Decreased platelets)
Bone pain, spleno- or hepatomegaly
3) Abrupt onset
1) Etiology of CML and CLL
2) Pathogenesis of CML and CLL
3) Phases of CML
4) Symptoms
1) Chromosomal abnormalities. CML: BCR/ABL gene
2)
CML: Increased proliferation of granulocytes + other
CLL: B-cells do not die (enlarged LM + decreased antibodies)
3) Chronic -> accelerated -> Terminal blast crisis
4) Weight-loss, fatigue, susceptibility to infections (CLL)
1) Definition of Lymphoma
2) Cell origin of Hodgkin- and Non-Hodgkin lymphoma
3) Differences between the 2 types
4) Clinical manifestations
1) Solid tumor of lymphoid tissue
2)
Non-Hodgkin: B, T or NK-cells. B-cells are most common; different locations and different stages
Hodgkin: B-cells. Reed-Sternberg cells are present
3)
Non-Hodgkin: Extranodal, Non-continuous spread, no Reed-Sternberg cells
Hodgkin: Origin in 1 node, Continuous spread, Reed-Sternberg cells
4) Enlarged LNs
Immunological defect -> Increased risk of infections
Non-Hodgkin: Since it is extranodal -> manifestation + tumors in other parts of body
1) Definition of anemia
2) 4 primary causes of anemia
3) 3 categories of effects
4) General clinical manifestations
5) 3 characteristics of hemolytic anemia
6) What deficiencies can result in anemia and why?
1) Low number of RBCs OR Low level of hemoglobin OR both
2) Loss of RBCs from bleeding, destruction of RBCs, defective RBC production, inadequate RBC production
3) Decreased oxygen transport, Decreased RBCs and hemoglobin, Symptoms from disease causing the anemia
4) Tissue hypoxia -> Fatigue, weakness. Hypoxia of brain -> Headache, visual disturbances. Pallor of skin. Tachycardia (compensation). Hemolytic anemia: Jaundice
5) Premature destruction, iron retention in body, increased RBC production
6) Iron Needed in hemoglobin to transport O2. Vitamin B12 Needed for DNA synthesis (Inhibition of DNA synthesis in RBCs -> No division -> Enlarged RBCs) Folic Acid Needed for DNA synthesis + RBC maturation
1) What is leuko-/neutropenia?
2) What are the main causes (etiology)?
3) Mention types of congenital neutropenia
4) Mention types of acquired neutropenia
1) Decreased count in absolut number of leukocytes / neutrophiles
2) Causes: Decreased production, Increased destruction or Shift from blood to tissue
3) Severe (permanent - genetic mutations) or cyclic (oscillations)
4) Autoimmune, infection related (HIV) or drug related (cancer treatment)
1) What is polycythemia?
2) Difference between absolute and relative
3) Patogenesis + symptoms of primary
4) Secondary etiology + pathogenesis
1) Abnormal high amount of RBCs
2) Relative: Due to loss of plasma volume -> Dehydration
Absolut: Increased RBCs
3) Increased pluripotent cells -> Increased RBCs, WBCs and platelets + Increased blood viscosity
Hypertension, headache, dizziness, itching of fingers
4) Kidney disease, EPO secreting neoplasm (Increased EPO -> Increased RBCs (mechanism against hypoxia))
1) What is mononucleosis?
2) Symptoms
3) Most common age group
4) Progression pace
1) Self-limiting infection caused by Epstein-Barr virus
2) Malaise, anorexia, fever, pain in LNs, pharyngitis. Possible splenomegaly
3) Adolescents + young adults
4) 4-6 weeks incubation, slow onset
1) What is hypercoagulability?
2) What is Factor V Leiden thrombophilia?
3) Mention 3 things that can lead to stasis of blood flow
4) Mention 2 risk factors for acquired disorders
5) Why is stasis of blood flow a problem?
1) Increased thrombus formation -> vessel occlusion
2) Inherited hypercoagulability -> resistance to a clot formation inhibitors
3) Bedrest, heart failure and hyperviscosity
4) Smoking, cancer, immobility, oral contraceptives
5) It makes accumulation of clotting factors posible and it decreased interactions with inhibitors
1) What is Von Willebrand disease?
2) If present, what are the clinical manifestations?
3) What is hemophilia A?
4) Mention 2 acquired blood coagulation deficiencies
1) Inherited blood coagulation disorder with decreased or defect vWF. Type 1 and 2 are mild, 3 is severe
2) Bleeding from nose and mouth. Joint pains due to synovium inflammation
3) X-linked disorder, primary males. Decreased FVIII or deficient FVIII -> bleeding in soft tissue
4) Liver diseases, vitamin K deficiency, hypocalcemia
1) What is thrombocytosis?
2) Pathogenesis of primary (essential)
3) Pathogenesis of secondary (reactive)
4) Clinical manifestations of primary
1) Elevations in platelet count
2) Disorder of hematopoietic stem cells. Normal thrombopoietin -> abnormal receptor or increased binding to platelets
3) Disease with increased thrombopoietin
- Cancer, chronic inflammation, tissue damage
4) Thrombosis (pulmonary, DVT), Hemorrhage
1) What is thrombocytopenia?
2) What are the 3 main causes?
3) Mention 2 possible pathologies for decreased platelet production
4) Mention 2 subtypes of thrombocytopenia
1) Reduction in platelet count
2) Decreased platelet production, Platelet sequestration in spleen (stuck), Decreased platelet survival
3) Aplastic anemia (loss of bone marrow function), Leukemia
4) Drug-induced, immune thrombocytopenic purpura, heparin-induced, thrombotic thrombocytopenic purpura
1) What is disseminated intravascular coagulation (DIC)?
2) Simplified pathogenesis
3) Main cause
4) Manifestations
1) Widespread coagulation and bleeding (Complication to other diseases)
2) Via intrinsic or extrinsic pathway thrombin are generated. This leads to:
- Unregulated intravascular coagulation -> Fibrin formation + anticoagulants -> Bleeding
- Fibrin -> occlusion -> Ischemic damage
3) Inflammation
4) Petechiae, purpura
