Hematology and oncology- Anatomy and physioogy Flashcards
Erythrocytes
- Life span
- Source of energy
- Anisocytosis and poikilocytosis
- Polychormasia
Life span of 120 days. Source of energy is glucose (90% used in glycolysis, 10% used in HMP shunt).
Membranes contain Cl−/HCO3 antiporter
Anisocytosis = varying sizes. Poikilocytosis = varying shapes
Bluish color (polychromasia) on Wright-Giemsa stain of reticulocytes represents residual ribosomal RNA.
Thrombocytes (platelets)
- Life span and amount stored in spleen
- Dense and alfa granules
- vWF and Fibrinogen receptors
Life span of 8–10 days. 1⁄3 of platelet pool is stored in the spleen.
Dense granules (ADP, Ca2+) and α granules (vWF, fibrinogen, fibronectin).
VWF receptor: GpIb.
Fibrinogen receptor: GpIIb/IIIa.
Leukocytes
- WBC differential count
WBC differential count from highest to lowest (normal ranges per USMLE): Neutrophils (~ 60%) Lymphocytes (~ 30%) Monocytes (~ 6%) Eosinophils (~ 3%) Basophils (~ 1%)
Neutrophils
- Hypersegmented
- Band cells
- Chemotactic agents
Hypersegmented neutrophils (nucleus has 6+ lobes) are seen in vitamin B12/ folate deficiency.
band cells (immature neutrophils) reflect states of myeloid proliferation (bacterial infections, CML)
Important neutrophil chemotactic agents: C5a,
IL-8, LTB4, kallikrein, platelet-activating factor.
Monocytes
- Morphology
Large, kidney-shaped nucleus. Extensive “frosted glass” cytoplasm.
Macrophages
- Activated by
- Lipid A
γ-interferon. Can function as antigen-presenting cell via MHC II.
Lipid A from bacterial LPS binds CD14 on macrophages to initiate septic shock.
Eosinophils (*Bilobate nucleus)
- Causes of eosinophilia
PACCMAN: Parasites Asthma Churg-Strauss syndrome Chronic adrenal insufficiency Myeloproliferative disorders Allergic processes Neoplasia (eg, Hodgkin lymphoma)
Basophils
- Basophilia
- Cointainment
is uncommon, but can be a sign of myeloproliferative disease, particularly CML.
contain heparin (anticoagulant) and histamine (vasodilator). Leukotrienes.
Mast cells
- Activated by
- Cromolyn sodium
tissue trauma, C3a and C5a, surface IgE crosslinking by antigen.
prevents mast cell degranulation (used for asthma prophylaxis).
Dendritic cells
Function as link between innate and adaptive immune systems.
Express MHC class II and Fc receptors on surface. Called
Langerhans cell in the skin.
NK cells innate oder Adaptative inmmune response?
are part of the innate immune response
Plasma cells
- Morphoology
- Found in
“Clock-face” chromatin distribution and eccentric nucleus, abundant RER, and well-developed Golgi apparatus.
Found in bone marrow and normally do not circulate in peripheral blood.
Fetal erythropoiesis
Fetal erythropoiesis occurs in: Yolk sac (3–8 weeks) Liver (6 weeks–birth) Spleen (10–28 weeks) Bone marrow (18 weeks to adult)
Hemoglobin development
- Embryonic globins
- Fetal hemoglobin (HbF)
- Adult hemoglobin (HbA1)
- HbA2
ζ and ε
α2γ2
α2β2
α2δ2
- Alpha Always; Gamma Goes, Becomes Beta.
- HbF has higher affinity for O2 due to less avid binding of 2,3-BPG.
Blood groups
Pag. 400
Rh hemolytic disease of the newborn
- Interaction
- Mechanism
- Presentation
- Treatment
Rh ⊝ mothers; Rh ⊕ fetus.
First pregnancy: mother exposed to fetal blood (often during delivery) formation of maternal anti-D IgG.
Jaundice shortly after birth, kernicterus, hydrops fetalis
Prevent by administration of anti-D IgG to Rh ⊝ pregnant women during third trimester and early postpartum period.
ABO hemolytic disease of the newborn
Type O mothers; type A or B fetus.
Pre-existing maternal anti-A and/or anti-B IgG antibodies cross placenta HDN in the fetus.
Mild jaundice in the neonate within 24 hours of
birth. Usually less severe than Rh HDN.
Treat newborn with phototherapy or exchange
transfusion.
Hemoglobin electrophoresis
HbA migrates the farthest, followed by HbF, HbS, and HbC. This is because the missense mutations in HbS and HbC replace glutamic acid ⊝ with valine (neutral) and lysine ⊕
ANTICOAGULANTS: factor Xa
- LMWH (greatest effcacy)
- heparin
- direct Xa inhibitors (apixaban, rivaroxaban)
- fondaparinux
ANTICOAGULANTS: IIa (thrombin)
- heparin (greatest effcacy)
- LMWH (dalteparin, enoxaparin)
- direct thrombin inhibitors (argatroban, bivalirudin, dabigatran)
THROMBOLYTICS:
alteplase, reteplase, streptokinase, tenecteplase
Hemophilia A:
Hemophilia B:
Hemophilia C:
deficiency of factor VIII (XR)
deficiency of factor IX (XR)
deficiency of factor XI (AR)
Vitamin K deficiency
- Factors
- Warfarin mechanism
- Factors Life span
synthesis of factors II, VII, IX, X, protein C, protein S.
Warfarin inhibits vitamin K epoxide reductase.
Factor VII—Shortest half life.
Factor II—Longest half life
Antithrombin
inhibits activated forms of factors II, VII, IX, X, XI, XII. Heparin enhances the activity of antithrombin.
Principal targets of antithrombin: thrombin and factor
Xa.
Platelet plug formation (primary hemostasis)
- Injury
- Exposure
- Adhesion (vWF + GpIb)
- Activation (ADP + P2Y12 induces GpIIb/IIIa)
- Aggregation
Clopidogrel, prasugrel, and ticlopidine
inhibit ADP-induced expression of GpIIb/IIIa by
irreversibly blocking P2Y12 receptor.
Abciximab, eptifibatide, and tirofiban
inhibit GpIIb/IIIa directly.
Ristocetin
activates vWF to bind GpIb. Failure of aggregation with ristocetin assay occurs in von Willebrand disease and Bernard-Soulier syndrome.
Glanzmann thrombasthenia
Bernard- Soulier syndrome
GpIIb/IIIa
GpIb
