Lifespan of erythrocyte
120 days
Key Terms
Lifespan of erythrocyte
120 days
Anisocytosis
Varying sizes
Poikilocytosis
Varying shapes
Erythrocytosis
Polycythemia = ↑ Hematocrit
Reticulocyte
Immature erythrocyte marker of erythroid proliferation
Platelet
Derived from…
What do they contain
Storage
Derived from Megakaryocytes
Dense granules (ADP, Ca) and α granules (vWF, fibrinogen)
1/3 stored in spleen
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| Term | Definition |
|---|---|
Lifespan of erythrocyte | 120 days |
Anisocytosis | Varying sizes |
Poikilocytosis | Varying shapes |
Erythrocytosis | Polycythemia = ↑ Hematocrit |
Reticulocyte | Immature erythrocyte marker of erythroid proliferation |
Platelet Derived from… What do they contain Storage | Derived from Megakaryocytes Dense granules (ADP, Ca) and α granules (vWF, fibrinogen) 1/3 stored in spleen |
Results of Thrombocytopenia or Platelet Dysfunction | Petechiae |
vWF receptor | GpIb |
Fibrinogen receptor | GpIIb/IIIa |
Leukocyte Subtypes Normal range | Granulocytes (Neutrophils, Eosinophils, Basophils) Mononuclear cells (Monocytes, Lymphocytes) 4000-10000 |
WBC differential | "Neutrophils Like Making Everything Better" Neutrophils (60%) Lymphocytes (30%) Monocytes (7%) Eosinophils (2%) Basophils (<1%) |
Neutrophil Increased in what state? Function Histo Granules | Bacterial infection Phagocytic Multilobed nucleus Small numerous specific granules (ALP, Collagenase, Lysozyme, Lactoferrin) Larger less numerous Azurophilic granules are lysosomes (Acid phosphatase, Peroxidase, β-glucuronidase) |
Hypersegmented polys Histo Seen in | 5 or more lobes VitB12/Folate Deficiency |
Increased Band Cells What are they? What do they reflect? | Immature Neutrophils Increased myeloid proliferation (bacterial infection or CML) |
Monocyte Where do they exist? What does it differentiate into? Histo | In blood Macrophages in tissue Large, kidney shaped nucleus with extensive frosted glass cyto |
Macrophage Function Lifespan What activates them? Marker | Phagocytosis, APC via MHCII Long life in tissues Activated by γ-Interferon CD14 |
Eosinophil Function Histo What does it produce? | Defends again helminthic infections. Phagocytic for Ag-Ab complex Bilobate nucleus. Large eosinophilic granules Produce Histaminase and Arylsulfatase to limit reaction following mast cell degranulation |
Causes of eosinophilia | “NAACP” Neoplastic, Asthma, Allergy, Collagen vascular disease, Parasites |
Basophil Function Histo with function | Mediates allergic reactions Basophilic granules with heparin (anticoagulant), Histamine (vasodilator), and Leukotrienes (LTD4) |
Mast Cells Function Histo Physiology Molecules it releases What type of reaction is it involved with? Inhibition? | Allergic reactions in local tissue Resemble basophils Can bind Fc portion of IgE to membrane. IgE cross-links upon Ag binding –> degranulation Releases Histamine, Heparin, Eosinophil chemotactic factors Type I hypersensitivity reaction Cromolyn prevents degranulation |
Dendritic cells Function Role Re Immune systems Expresses... In skin they are called | Phagocytic APC Link between innate and adaptive immune systems MHCII and Fc receptor Langerhans cells in skin |
Lymphocyte Mediates what kind of immunity Subtypes Histo | Adaptive immunity B and T cells Densely stained nucleus with small amount of cytoplasm |
B Lymphocyte What kind of immune response? Where does it arise from? Where does it mature? Where does it migrate to? What does it differentiate into? Function MHC Markers | Humoral response Bone marrow Bone marrow Migrates to peripheral lymphoid tissues (follicles of lymph nodes, white pulp of spleen, unencapsulated lymphoid tissue) When encounters Ag, differentiates into Ab producing plasma cell and memory cells APC via MHCII CD19 and CD20 |
Plasma Cell Function Histo Pathology | Ab production Off center nucleus, clock face chromatin, RER, well developed Golgi Multiple Myeloma |
T Lymphocyte What kind of immune response? Where does it arise from? Where does it mature? What does it differentiate into? Surface marker Percentage of circulating lymphocytes | Cellular immune response Bone marrow Thymus Tc cells (CD8), Th (CD4), Treg (CD28) CD3 80% |
Blood group A | A Ag and B Ab |
Blood group B | B Ag and A Ab |
Blood group AB | A and B Ag. No Abs Universal Recipient of RBCs Universal Donor of Plasma |
Blood group O | No Ag. A and B Abs Universal donor of RBCs Universal Recipient of Plasma |
Rh factor | Ag on RBC surface |
Erythroblastosis Fetalis PathoPhys Treatment | Rh- mother exposed to fetal Rh+ blood. Mother makes anti-Rh IgG that crosses placenta and causes hemolytic disease in the next fetus Rho (D) immune globulin for mother at first delivery to prevent initial sensitization of Rh- mother to Rh Ag |
Blood groups Re crossing placenta | anti A and anti B IgM does not cross placenta | anti Rh IgG does cross the placenta |
Intrinsic Coagulation Pathway | Collagen, Basement membrane, Activated platelets, or HMWK --> XII --> XI --> IX IX + VIII --> X XII --> Kallikrein |
Extrinsic Coagulation Pathway | Thromboplastin (tissue factor) --> VII --> X |
Common Coagulation Pathway | X + V --> II (thrombin) --> Fibrin XIII (fibrin stabilizing factor) helps stabilize fibrin mesh Thrombin also activates V, VIII, XIII |
Kinin Cascade | Kallikrein thurs HMWK into Bradykinin | Bradykinin ↑ Vasodilation, Permeability, and Pain |
Fibrinolytic System | XII --> Kallikrein --> Plasmin --> Fibrin mesh degradation | Plasmin also activates C3 |
Which reactions of the coagulation cascade require Ca and Phospholipids | XIa --> IX VII --> VIIa VIIa and (IXa + VIIIa) activation of X Xa + Va activation of II |
Hemophilia A | Deficiency in VIII |
Hemophilia B | Deficiency of IX |
VitK Pathway | Oxidized VitK --> [epoxide reductase] --> Reduced VitK | Reduced VitK is a cofactor for the maturation of II, VII, IX, X, C, and S |
Warfarin | MoA | Inhibits Epoxide Reductase |
Why are neonates given VitK? | They lack enteric bacteria that produce VitK |
What does vWF do? | Carries/protects VIII |
Anticoagulation cascade | Thrombomodulin on endothelial cells --> Protein C | C + S cleaves and inactivates Va and VIIIa |
What does antithrombin do? | Inhibits activated forms of II, VII, IX, X, XI, XII |
Function of Heparin | Activates Antithrombin |
Factor V Leiden mutation | Classical presentation | Factor V resistant to inhibition by protein C | DVT --> PE |
tPA | Thrombolytic that activates plasmin |
Platelet Plug Formation Schematic | Injury: vWF binds exposed collagen upon endothelial damage Adhesion: Platelets bind vWF via Gp1b and release Ca and ADP. Activation: ADP binding induces GpIIb/ IIIa expression on platelet surface --> aggregation |
How does ADP affect coagulation | Released by platelets. | Helps platelets adhere to endothelium and induces platelets to express GpIIb/IIIa at platelet surface |
Platelet Aggregation Pathway | Fibrinogen binds GpIIb/IIIa and links platelets |
Pro Platelet Aggregation Factors | TXA2 (released by platelets), ↓ blood flow, ↑ platelet aggregation |
Anti Platelet Aggregation Factors | PGI2 and NO (released by endothelial cells) ↑ blood flow ↓ platelet aggregation |
Ticlopidine | Inhibits ADP induced expression of GpIIb/IIIa | Causes Neutropenia, Oral Ulcers, Fever |
Clopidogrel | Inhibits ADP induced expression of GpIIb/IIIa |
Abciximab | Inhibits GpIIb/IIIa directly |
ESR What causes it to increase? ↑ ESR ↓ ESR | Acute phase reactants in plasma (Fibrinogen) cause RBC aggregation and ↑ ESR ↑: Infection, Autoimmune, Malignancy, Pregnancy ↓: "CHaMP" Polycythemia, Sickle Cell Anemia, CHF, Microcytosis, Hypofibrinogenemia |
Acanthocyte | Spur cell indicative of Liver disease or Abetalipoproteinemia (cholesterol dysregulation) |
Basophilic Stippling | "BASte the ox TAiL" | Thalassemias, Anemia of chronic disease, Lead Poisoning |
Bite Cell | G6PD deficiency |
Eliptocyte | Hereditary Elliptocytosis |
Macro-Ovalocyte | Megaloblastic anemia (w/ hypersegmented polys) and Marrow failure |
Ringed Siderblasts | Sideroblastic anemia | Excess Fe in Mito |
Schistocyte | Helmet Cell | DIC, TTP/HUS, Traumatic Hemolysis (metal heart valve prosthesis) |
Sickle Cell | Sickle Cell Anemia |
Spherocyte | Hereditary spherocytosis, Autoimmune hemolysis |
Teardrop cell | "RBC sheds a tear because it has been forced out of its home" Bone marrow infiltration (myelofibrosis) |
Target Cell | "HALT said the hunter to his target" | HbC disease, Asplenia, Liver disease, Thalassemia |
Heinz Bodies Process Associated pathology | Oxidation of sulfhydryl groups leads to denatured Hb precipitation and damage to RBC membrane --> formation of bite cells G6PD deficiency and α-thalassemia |
Howell-Jolly Bodies What is it? How are they normally dealt with? Associated pathology | Basophilic nuclear remnants found in RBCs Normally removed from RBCs by splenic macrophages Functional hyposplenia, asplenia, mothball ingestion (naphthalene) |
Microcytic Anemias | "Find Those Small Plump Cells" | Iron Deficiency, ACD, Thalassemia, Pb poisoning, Sideroblastic anemia |
Nonhemolytic Normocytic Anemias | ACD, Aplastic, Chronic Kidney Disease |
Hemolytic Normocytic Anemias | Intrinsic: "SHEEPS" Spherocytosis, G6PD or PK deficiency, HbC, Sickle Cell Anemia, Paroxysmal Nocturnal Hemoglobinuria Extrinsic: Autoimmune, Microangiopathic, Macroangiopathic, Infections |
Megaloblastic Macrocytic Anemias | Folate deficiency, B12 deficiency, Orotic Aciduria |
NonMegaloblastic Macrocytic Anemias | Liver disease, Alcoholism, Reticulocytosis |
Iron Deficiency Anemia What kind of anemia What causes it? PathoPhys Labs Histo How may it manifest | Microcytic, Hypochromatic ↓ Fe due to chronic bleeding, malnutrition, or pregnancy Impaired final step in heme synthesis ↓ Fe and Ferritin, ↑ TIBC Microcytosis (MCV<80) and hypochromia Plummer Vinson Syndrome |
α Thalassemia What kind of anemia PathoPhys Epidemiology How # of gene mutations re disease | Microcytic, Hypochromatic α globin gene mutation cis deletion in Asians, trans deletions in African 3 deletions: HbH disease. Very little α, excess β forms β4 (HbH) 1-2 gene deletions: no clinical significance |
β Thalassemia What kind of anemia PathoPhys Epidemiology | Microcytic, Hypochromatic Point mutation in splice sites and promoter sequence --> ↓ β Mediterranean populations |
β Thalassemia minor PathoPhys Symptoms Diagnosis | Heterozygote: β chain underproduced Asymptomatic Increased HbA2 on electrophoresis |
β Thalassemia major PathoPhys Symptoms Treatment Complications Presentation Hb | Homozygote: β chain absent Severe anemia Blood transfusions (--> hemochromatosis) Marrow expansion (crew cut on skull XR) --> skeletal deformities. Chipmunk facies HbF (α2γ2) |
Presentation of HbS/β-Thalassemia Heterozygote | Mild to moderate sickle cell disease depending on amount of β globin production |
Lead Poisoning What kind of anemia PathoPhys Presentation Treatment | Microcytic, Hypochromatic Pb --/ ferrochelatase and ALA dehydratase which leads to ↓ heme synthesis Pb --/ rRNA degradation causing RBCs to retain rRNA aggregates (Basophilic Stipling) "LEAD" Lead lines on Gingivae (Burton's Lines) and on metaphysis of long bones Encephalopathy and Erythrocyte basophilic stippling Abdominal colic and sideroblastic Anemia Drops (wrist and foot) Treat with Dimercaprol and EDTA Succimer in children |
Sideroblastic Anemia What kind of anemia PathoPhys What causes it? Histo Labs Treatment | Microcytic, Hypochromatic Defect in Heme synthesis X linked defect in δALA synthase, EtOH, Lead, Isoniazid Ringed sideroblasts (with iron laden mito) ↑ Fe and ferritin, Normal TIBC Treat with VitB6 |
Megaloblastic Anemia Basic Pathology Consequences | Impaired DNA synthesis --> maturation of nucleus delayed relative to cytoplasm Ineffective erythropoiesis --> pancytopenia |
Folate Deficiency What kind of anemia Etiologies Presentation Histo Labs | Megaloblastic Malnutrition (alcoholics), malabsorption, antifolates (methotrexate, trimethoprim, phenytoin), ↑ requirement (hemolytic anemia, pregnancy) Glossitis Hypersegmented neutrophils ↓ Folate, ↑ Homocysteine, normal Methylmalonic acid |
B12 Deficiency What kind of anemia Etiologies Presentation Histo Labs | Megaloblastic Insufficient intake, Malabsorption, Pernicious anemia, Diphyllobothrium latum (fish tapeworm), PPI Glossitis, B12 invovled with FA and myelin synthesis leading to Peripheral neuropathy w/ sensorimotor dysfunction, Posterior column (vibration/propioception), Lateral CST (spasticity), and Dementia Hypersegmented neutrophils ↓ B12, ↑ Homocysteine, ↑ Methylmalonic acid |
Orotic Aciduria What kind of anemia? PathoPhys Presentation Histo Labs Treatment | Megaloblastic Enzyme deficiency impairs conversion of uridine from orotic acid Children with glossitis and megaloblastic anemia that cannot be cured by folate or B12 Hypersegmented neutrophils Orotic acid in urine Uridine monophopshate to bypass mutated enzyme |
NonMegaloblastic Macrocytic Anemia Pathology What causes it? | Macrocytic anemia in which DNA synthesis is unimpaired | Liver disease, Alcoholism, Retculocytosis, Drugs (5FU, AZT, Hydroxyurea) |
Intrinsic Hemolytic Normocytic, Normochromic Anemias Intravascular w/ examples and findings Extravascular w/ examples and findings | Intra: Paroxysmal nocturnal hemoglobinuria or mechanical destruction ↓ haptoglobin, ↑ LDH, hemoglobin in urine Extra: Hereditary spherocytosis Macs in spleen clears RBCs. ↑ LDH + ↑ UCB causes jaundice |
Anemia of Chronic Disease What kind of anemia? PathoPhys Findings What can it become? | Normocytic, Normochromic NonHemolytic Inflammation --> ↑ hepcidin Hepcidin is released by liver binds ferroportin on intestinal mucosal cells and macs thus inhibiting iron transport ↓ release of iron from macs ↓ Fe, ↓ TIBC, ↑ Ferritin Can become microcytic, hypochromic |
Aplastic Anemia What kind of anemia What causes it? | Normocytic, Normochromic NonHemolytic Caused by failure or destruction of myeloid stem cells due to: Radiation and drugs (benzene, chloramphenicol, alkylating agents, antimetabolites), Viral agents (parvovirus B19, EBV, HIV, HCV), Fanconi's Anemia, Idiopathic (immune mediated, stem cell defect, may follow acute hepatitis) |
Aplastic Anemia Labs/Histo Presentation Treatment | Pancytopenia, severe anemia, Leukopenia, Thrombocytopenia, Normal cell morphology, Hypocellular bone marrow with fatty infiltration (dry bone marrow tap) Fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection Withdrawal of offending agent, Immunosuppressive regimens (antithymocyte globulin, cyclosporine), allogeneic bone marrow transplantation, RBC and platelet transfusion, G-CSF or GM-CSF |
How does chronic kidney disease lead to anemia? | What kind of anemia? | ↓ erythropoietin --> ↓ hematopoiesis --> Normocytic, Normochromic NonHemolytic anemia |
Hereditary Spherocytosis What kind of anemia? PathoPhys How do RBCs look? What happens to RBCs Presentation Findings Treatment | Extravascular Intrinsic Hemolytic Normocytic Anemia Defects in proteins interacting with RBC membrane (Ankryn, Band3, Protein4.2, Spectrin) Less membrane causes small and round RBCs with no central pallor (↑ MCHC, ↑ red cell distribution width) Premature removal of RBC by spleen Splenomegaly, Aplastic crisis (Parvovirus B19 infection) osmotic fragility test, normal or ↓ MCV with abundance of cells; Masks microcytia Splenectomy |
G6PD Deficiency What kind of anemia? Inheritance PathoPhys What happens to RBCs? Presentation Histo | Intra/Extra-vascular Intrinsic Hemolytic Normocytic Anemia X linked Defective G6PD --> ↓ Glutathione --> ↑ RBC susceptibility to oxidant stress (sulfa drugs, infections, fava beans) RBCs destroyed extravascularly Back pain followed a few days later by hemoglobinuria Heinz bodies and bite cells |
PK deficiency What kind of anemia Inheritance PathoPhys Presentation | Extravascular Intrinsic Hemolytic Normocytic Anemia AR Defective PK --> ↓ ATP --> rigid RBCs Hemolytic anemia in a newborn |
HbC defect What kind of anemia PathoPhys HbSC vs HbSS | Extravascular Intrinsic Hemolytic Normocytic Anemia Glutamic Acid --> Lysine mutation at reside 6 of β globin HbSC less severe than HbSS |
Paroxysmal Nocturnal Hemoglobinuria What kind of anemia PathoPhys Genetics Presentation Labs Treatment | Intravascular Intrinsic Hemolytic Normocytic Anemia ↑ complement mediated RBC lysis (impaired synthesis of GPI anchor or decay-accelerating factor that protects RBC membrane from complement Acquired mutation in hematopoietic stem cell Hemolytic anemia, Pancytopenia, Venous Thrombosis CD55/59 negative RBCs on flow cytometry Eculizumab |
Sickle Cell Anemia What kind of anemia? Genetics Pathogenesis Newborns Heterozygotes | Extravascular Intrinsic Hemolytic Normocytic Anemia HbS point mutation in β globin at 6th residue (glutamic acid --> val) Low O2 or dehydration precipitates sickling (deoxidized HbS polymerizes) --> anemia and vaso-occlusive disease Newborns are initially asymptomatic b/c of ↑HbF and ↓HbS Hets resistant to malaria |