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146 Cards in this Set
- Front
- Back
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myeloid tissue
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bone marrow/cells derived from in
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lymphoid tissue
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thymus, lymph nodes, spleen
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red cell disorders that result from the formation of autoAb signifying a primary disorder of lymphocytes
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hemolytic anemias
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time frame blood cells first appear/location/derived
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third week of fetal embryonic development in yolk sac; from stem cell population restricted to production of myeloid cells
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time frame in which stem cells from the AGM/yolk sac migrate to the liver
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third month fetal embryonic development
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primary site of blood cell formation until just before birth
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the liver
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time frame in which stem cells migrate to the bone marrow for hematopoiesis
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4th month of fetal embryonic development
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bones of hematopoiesis in adults
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vertebrae, ribs, sternum, skull, pelvis, and proximal epiphyseal regions of the humerus and femur
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sole source of all forms of blood cells at birth
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bone marrow
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precursors common lymphoid stem cell gives rise to
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T cells, B cells, and NK cells
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common myeloid stem cell gives rise to
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three types committed stem cell: erythroid/megakaryocytic eosinophilic, granulocyte/macrophage pathways
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growth factors that act on very early stem cells
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c-KIT ligand adn FLT-3 ligand
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growth factors currently being used to stimulate hematopoieisis
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GM-CSF, G-CSF, and thrombopoietin
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reason hematopoiesis occurs in bone marrow
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specialized environment fosters stem cell homing, survival, differentiation; stem cells are not restricted to this site
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estimate of bone marrow activity
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ratio of fat cells to hematopoietic elements; normally 1:1
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disorders in which bone marrow fat cells is greater than hematopoietic elements
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marrow hypoplasia
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disorders in which hematopoietc elements are greater than fat cells
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hemolytic anemias
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disorders that induce local marrow fibrosis
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metastatic cancer and granulomatous disease
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reduction below normal limits of total circulation of red cell mass
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anemia
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average volume of a RBC expressed in femtoliters
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mean cell volume
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average content of hemoglobin per RBC expressed in picograms
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mean cell hemoglobin
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average concentration of hemoglobin in a given volume of packed RBC expressed in grams per deciliter
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mean cell hemoglobin concentration
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coefficient of variation of RBC volume
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RBC distribution width
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dyspnea on mild exertion; nails can become brittle, lose usual convexity, and assume a concave spoon shape (koilonychia)
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symptoms of anemia caused by reduced oxygen content in the blood
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fatty change in the liver, myocardium, and kidney; cardiac failure can occur
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symptoms of anemia caused by anoxia
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headache, dimness of vision, and faintness
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symptoms of anemia caused by hypoxia
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anemia in which effects are due to loss of intravascular volume which leads cardiovascular collapse, shock, and death; volume restored by water shift
increased production of erythropoietin; leukocytosis; increased reticulocyte count, thrombocytosis |
acute blood loss anemia
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acute blood loss anemia in which iron from hemoglobin is recovered
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internal
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acute blood loss anemia in which iron from hemoglobin is lost
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external
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blood loss anemia induced only when rate of loss exceeds the regenerative capacity of marrow or when iron reserves are depleted
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chronic blood loss anemia
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shortened red cell life span, elevated erythropoietin levels/increased erythropoiesis in marrow and other sites, accumulation of the products of hemoglobin catabolism due to an increased rate of RBC destruction
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hemolytic anemia
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location of physiologic destruction of senescent RBC
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mononuclear phagocytic cells of the spleen
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red cell destruction caused by injury, complement fixation, infection by intracellular parasites, or exogenous toxic factors
hemoglobinemia, hemoglobinuria, jaundice, and hemosiderinuria decreased serum haptoglobin-> red brown urine |
intravascular hemolytic anemia
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agent free hemoglobin binds to that causes its clearance by mononuclear phagocytic cells, preventing excretion into the urine
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alpha 2 globulin (haptoglobin)
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red cells are rendered foreign or become less deformable
splenic sequestration and phagocytosis anemia and jaundice; no hemoglobinemia or hemoglobinuria decrease in haptoglobin work hyperplasia of the mononuclear phagocytic system often leads to splenomegaly |
extravascular hemolytic anemia
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increased production of erythropoietin, increased numbers of erythroid precursors in the marrow
extramedullary hematopoiesis may appear in the liver, spleen, and lymph nodes prominent reticulocytosis in the peripheral blood formation of gallstones due to elevated bilirubin excretion; hemosideerosis confined to the mononuclear phagocyte system |
hemolytic anemia
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inherited disorder caused by intrinsic defects in the RBC membrane that render cells spheroid
RBC are vulnerable to spenic sequestration and destruction Northern Europe |
Hereditary Spherocytosis
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chief protein component of the specialized RBC membrane skeleton
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spectrin composed of alpha and beta flexible heterodimers
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most common cause of hereditary spherocytosis
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mutation of red cell ankyrin
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loss of membrane relative to cytoplasm forces the cell to assume the smallest possible diameter for the given volume
spleen becomes a villain because it is causes a condition that is like an "obese man attempting to bend at the waist"; RBC become trapped/phagocytosed lactic acid accumulates, pH falls inhibiting glycolysis; inability to generate ATP prevents extrusion of sodium leading to osmotic injury |
hereditary spherocytosis
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abnormally small, dark-staining (hyperchromic) red cells lackign the normal central zone pallor
reticulocytosis, marrow hyperplasia due to increased erythropoiesis, hemosiderosis, and mild jaundice cholelithiasis, moderate splenic enlargement |
hereditary spherocytosis
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anemia, splenomegaly, jaundice
compensatory changes are outpaced producing a chronic hemolytic anemia aplastic crisis may occur inthe setting of acute parvovirus infection increased mean hemoglobin concentration |
hereditary spherocytosis
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reduces NADP to NADPH necessary for conversion of oxidized glutathione to reduced glutathione which protects against oxidant injury
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function of G6PD
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G6PD genetic variants
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GP6D A- and G6PD Mediterranean (more abnormal);
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G6PD genetic variants cause
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destabilization of the enzyme, misfolded protein
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hemolytic anemia that is inherited in a recessive X-linked manner
hemolysis is after exposure to oxidant stress: drugs, infection, favism |
GP6D deficiency
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hemolytic anemia that presents as episodic intravascular and extravascular hemolysis
oxidation of reactive sulfhydryl groups on globin chains which become denatured and form membrane boun precipitates known as Heinz bodies: can damage teh membrane sufficiently to cause intravascular hemolysis Bite cells are formed by RBC going through the spleen |
GP6D
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chronic hemolysis, increased formation of bilirubin, and small vessel stasis and thrombosis;
bone marrow is hyperplastic because of compensatory hyperplasia of erythroid progenitors; expansion of marrow leads to bone resorption adn secondary new bone formation resulting in prominent cheek bones and changes in the skull that resemble a crew cut on xray in children: enlarged spleen (congestive); autosplenectomy vascular occlusion may cause infarction in many tissues; pigment gallstones, hyperbilirubinemia |
sickle cell
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episodes of hypoxic injury adn infarction associated with sevre pain in the affected region
infection, dehydration, and acidosis may trigger |
vaso-occlusive crises/pain crisis
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sickle cell crises that frequently manifests as the hand foot syndrome, a dactylitis of bones of the hands or feet or both
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painful bone crisis
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vaso-occlusive crises involving the lungs that presents with fever, cough, chest pain, and pulmonary infiltrate
blood flow becomes sluggish |
acute chest syndrome/ sickle cell disease
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transient cessation of bone marrow erythropoiesis due to an acute infection of erythroid progenitor cells by parvovirus B19
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aplastic crisis
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massive sequestration of sickled red cells leads to rapid splenic enlargement, hypovolemia, and sometimes shock
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sequestration crisis
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diminished synthesis of structurally normal beta globin chains coupled with unimpaired synthesis of alpha chains
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Beta thalessemia
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Beta 0 thalassemia
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Total loss of Beta chains in homozygous state
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Beta + thalassemia
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reduced but detectable beta globin synthesis in the homozygous state
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most common cause of beta thalassemia
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mutation leading to aberrant splicing; mostly affects introns
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deficit in HbA synthesis produces under hemoglobinized hypochromic, microcyti RBC with subnormal oxygen transport capacity
free alpha chains precipitate within the normoblasts, forming insoluble inclusions causing cell membrane damage; ineffective erythropoiesis inclusion bearing red cells are prone to splenic sequestration and destruction due to cell mambrane damage and decreased deformability |
beta thalassemia
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complications of severe beta thalassemia
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massive erythroid hyperplasia in the marrow and sites of extramedullary hematopoiesis
extraosseous masses in thorax, abdomen, pelvis excessive absorption of dietary iron |
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homozygous beta thalassemia genes
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severe, transfusion-dependent anemia
beta thalassemia major |
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heterozygous beta thalassemia genes
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mild microcytic anemia that causes no symptoms
beta thalassemia minor |
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genetically heterogeneous beta thalassemia
milder variants of beta+/beta+ or beta+/beta0 and unusually severe variants of heterozygous beta thalassemia |
beta thalassemia intermedia
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beta thalassemia mst common in mediterranean countries and parts of Africa and Southeast Asia
anemia manifests 6-9 months after birth as hemoglobin synth switches from HbF to HbA marked anisocytosis and poikilocytosis, microcytosis, hypochromia; target cells reticulocyte count is elevated but lower than expected for severity of anemia |
beta thalassemia major
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striking expansionn of hematopoietically active marrow, particularly in facial bones
crew cut appearance on xrays mononuclear phagocytic cell hyperplasia and extramedullary hematopoiesis-> enlargement of the spleen hemosiderosis and secondary hemochromatosis (iron overload); damage to heart liver, pancreas growth retardation |
beta thalassemia major
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more common of the beta thalassemias
heterozygous carriers of beta 0 or beta + some red cell abnormalities: hypochromia, microcytosis, basophilic stippling, target cells; mild erythroid hyperplasia in bone marrow HbF may be normal or slightly increased |
beta thalassemia minor
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reduced or absent synthesis of alpha globin (normally 4)
lack adequate hemoglobin/excess unpaired non alpha chains hemolysis/ineffective erythropoiesis (usually not severe) deletion of alpha globin genes |
alpha thalassemias
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single alpha gene is deleted; barely detectable reduction in alpha globin
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silent carrier of alpha thalassemia
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deletion of 2 alpha globin genes
may be from same chromosome (Asian) or one alpha globin from each of 2 chromosomes (African) only matings between individuals missing 2 gene copies from same chromosome at risk for producing severely affected offspring minimal or no anemia |
alpha thalassemia trait
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deletion of three alpha globin genes
most common in Asian populations synthesis of alpha globin is markedly reduced; tetramers of excess beta globin (HbH) HbH has extremely high affinity for oxygen-> hypoxia disproportion to Hb level HbH is prone to oxidation-> intracellular inclusions moderately severe anemia |
hemoglobin H disease (alpha thalassemia)
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Most severe alpha thalassemia caused by deletion of all four alpha globin genes
in fetus excess gamma globin chains form tetramers (Barts); have high affinity for O2 so almost no O2 delivered to tissue fetal distress by third trimester |
hydrops fetalis
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acquired mutation in phosphatidylinositol glycan A-> essential for synthesis of GPI anchor
X linked; blood unusually susceptible to lysis by complement (CD59) hemosiderinuria eventually leads to iron deficiency; episodic venous thrombosis often involving hepatic, portal or cerebral veins increased risk myelogenous leukemia often arises in setting of primary bone marrow failure |
paroxysmal nocturnal hemoglobinuria
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anemia caused by extracorpuscular mechanisms
immune reaction sometimes initiated by drug ingestion diagnosis requires detection of antibodies and/or complement on patient red cells -> Coombs antiglobulin test |
immunohemolytic anemias
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most common immunohemolytic anemia
most causative antibodies are IgG destruction is extravascular; IgG coated RBC bind Fc on monocytes and splenic macrophages; loss of RBC during partial phagocytosis |
warm antibody immunohemolytic anemia
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model of warm Ab immunohemolytic anemia in wich drugs act as haptens by binding RBC membrane
large IV doses of Ab; occurs 1-2 weeks after onset Tx destruction may be intravascular or extravascular |
Hapten model
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model of warm antibody immunohemolytic anemia in which drugs initiate the production of Ab directed against intrinsic RBC; in particular Rh antigens
alpha methyldopa |
Autoantibody model
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anemia in which IgM antibodies bind and agglutinate RBC avidly at low temperatures
antibodies appear acutely after recovery phase of infectious disorders clinical symptoms from IgM binding to RBC at sites exposed (fingers, toes, etc); C3b opsonization |
Cold agglutinin immunohemolytic anemia
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autoantibodies cause paroxysmal cold hemoglinuria-> intermittent massive intravascular hemolysis, frequently with hemoglobinuria after exposure to cold temperatures
least common of the immunohemolytic anemias autoantibodies are IgG's that bind to P blood group at low temps complement mediated intravascular lysis doesn't occur until cells recirculate to warm central regions follows infections |
cold hemolysin hemolytic anemia
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peripheral blood examination usually reveals pancytopenia; marked variation in size/shape of RBC (anisocytosis); normochromic
RBC are macrocytic and oval with mean corpuscular volume above 100 fl most lack central pallor of normal RBC/appear hyperchromic neutrophils are larger than normal and hyper segmented marrow is hypercellular due to increased number myeloid precursors; nucleus remains large and immature giant metamyelocytes and band forms increased levels of GF; most myeloid precursors undergo apoptosis in marrow RBC hemolysis in the periphery |
megaloblastic anemias
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specific form of megaloblastic anemia caused by atrophic gastritis/attendant failure of intrinsic factor production
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Pernicious anemia
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proteins B12 associates with in saliva
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cobalophilin/R-binder
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protein B12 associates with in the duodenum
complex transported to the ileum and endocytosed by ileal receptors |
intrinsic factor
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carrier protein B12 associates with in the enterocytes
delivers B12 to the liver |
Transcobalamin II
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essential cofactor for methionine synthase; enzyme involved conversion of homocysteine to methionine
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methylcobalamin (B12)
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required as a prosthetic group on the enzyme methyl malonyl-coenzyme A mutase in the isomerization of methylmalonyl coenzyme A to succinyl coenzyme A
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adenosylcobalamin (B12)
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tongue is shiny, glazed, and beefy; diffuse chronic gastritis, atrophy of fundic glands, virtual absence of parietal cells, intestinalization
cells and nuclei may increase in size to 2x normal size degeneration of myelin in the dorsal and lateral tracts of the spinal cord; sometimes followed by loss of axons; spastic paraparesis, sensory ataxia, severe paresthesias in lower limbs |
pernicious anemia
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anemia of insidous onset
serum homocysteine and methylmalonic acid are increased; increased risk sclerosis and thrombosis; increased risk of gastric cancer |
pernicious anemia
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most important metabolic processes dependent on one carbon transfers (FH4)
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purine synthesis, conversion of homocysteine to methionine, deoxythymidylate monophosphate synthesis
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Folate deficiency most frequently encountered in
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chronic alcoholic, elderly, indigent
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diagnosis of folate deficiency anemia
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identical to B12 deficiency anemia; diagnosis can only be made my demonstrating decreased folate levels in the serum or RBC
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protein iron complex found in all tissues but particularly in the liver, spleen, bone marrow,
found mainly in mononuclear phagocytic cells or liver parenchymal cells iron storage pool |
ferritin
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partially degraded protein shells of ferritin aggregate
in normal iron stores only trace amounts found |
hemosiderin
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ferritin below 12 micrograms per liter
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iron deficiency anemia
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iron binding glycoprotein taht transports iron in the plasma
delivers iron to cells |
transferrin
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most iron absorbed in
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iron
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iron that travels the apical adn basolateral membranes of villus enterocytes through the action of DMT1
influenced by substrates in the diet that inhibit or enhance uptake |
nonheme pathway
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substrates in the diet that inhibit nonheme uptake
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phytates, tannates, phosphates
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substrates in the diet that enhance nonheme uptake
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ascorbic acid and amino acids
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small liver derived plasma peptide
inhibits iron uptake in duodenum and iron release from macrophages concentration falls as stores become depleted |
hepcidin
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method in which gastrectomy impairs iron absorption
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decrease hydrochloric acid and transit time through duodenum
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most common cause of iron deficiency in the western world
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chronic blood loss
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hypochromic microcytic anemia
koilonychia, alopecia, atrophic changes in the tongue and gastric mucosa and intestinal malabsorption mild to moderate increase in erythroid progenitors in the bone marrow zone of pallor is enlarged hemoglobin and hematocrit are depressed; serum iron and ferritin are low; total plasma binding capacity is high; transferrin saturation levels are low; hepcidin synthesis is inhibited elevation of free erythrocyte protoporphyrin |
iron deficiency anemia
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microcytic hypochromic anemia, atrophic glossitis, esophageal webs
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plummer vinson syndrome
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low serum ion, reduced total iron binding capacity in association with abundant stored iron in the mononuclear phagocytic cells
erythropoietin levels are inappropriately low for the degree of anemia mild anemia with increased hepcidin synthesis; increased storage iron in marrow macrophages, high serum ferritin level, reduced total iron binding capacity |
anemia of chronic disease
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suppression or disappearance of multipotent stem cells
markedly hypocellular bone marrow is largely devoid o hematopoietic cells; often only fat, fibrous stroma, and scattered/clustered foci of lymphocytes/plasma cells remain granulocytopenia, thrombocytopenia, mucocutaneous infection, abnormal bleeding insidious onset; progressive weakness, pallor, dyspnea; petichiae adn ecchymosis; splenomegaly is characteristically absent normocytic/normochromic red cells; reticulocytopenia |
aplastic anemia
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meylotoxins
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benzene, chloramphenicol, alkylating agents, antimetabolites, whole body irradiation
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rare autosomal recessive disorder caused by defects in a component of the multiprotein complex required for DNA repair
marrow hypofunction early in life, hypoplasia of the kidney and spleen, hypoplastic changes of the bones |
fanconi anemia
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rare form of marrow failure characterized by a marked hypoplasia of marrow erythroid elements in the setting of normal granulopoiesis and thrombopoiesis
associated with thymoma |
pure red cell aplasia
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autoimmune disorder in which platelet destruction results from the formation of antiplatelet autoantibodies
settting of SLE, AIDS, viral infection, complication of drug therapy chronic= formation of autoAb against platelet membrane glycoproteins (IIb-IIa or Ib-IX); usually of the IgG class; spleen is the major site of platelet removal |
immune thrombocytopenic purpura
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spleen is normal size; congestion of sinusoids and hyperactivity/enlargement of teh splenic follicles
marrow reveals modestly increased number of megakaryocytes; accelerated thrombopoiesis most commonly adult women younger than 40; cutaneous bleeding seen in the form of pinpoint hemorrhages wehre capillary pressure is higher; petechiae may give rise to ecchymoses easy bruising, nosebleeds, bleeding from gums; melena, hematuria, excessive menstrual flow; splenomegaly/lymphadonopathy are uncommon megathrombocytes detected on blood smear; prolonged bleeding time, normal PT/PTT |
chronic immune thrombocytopenic purpura
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condition caused by antiplatelet autoantibodies
disease of childhood occurring with equal frequency amongst both genders usually preceded by viral illness resolves spontaneously within 6 months |
acute immune thrombocytopenic purpura
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thrombocytopenia is the most common hematologic manifestation; impaired platelet production and increased destruction
infected megakaryocytes are prone to apoptosis and are impaird in terms of platelet production Hyperplasia and dysregulation of B cells which predispose to the development of immune mediated thrombocytopenia Ab against IIb-III, sometimes cross react with gp120-> act as opsonins/promote phagocytosis premature destruction of the mononuclear phagocyte system |
HIV associated thrombocytopenia
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fever, thrombocytopenia, microangiopathic hemolytic anemia, transient neuro deficits, renal failure
widespread formation of hyaline thrombi, compreised primarily of platelet aggregates in the microcirculation PT/PTT are usually normal |
microangiopathies: TTP and HUS
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symptomatic patients are deficient in ADAMTS 13 (vWF metalloprotease)
very high molecular weight multimers of vWF accumulate in plasma and may promote platelet microaggregate formation throughout microcirculation |
TTP
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Normal levels of vWF
associated with E.Coli 0157:H7 present with bloody diarrhea; irreversible renal damage and death can occur in severe cases |
HUS
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inherited deficiency of platelet membrane glycoprotein complex Ib-IX-> receptor for vWF essential for normal platelet adhesion
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Bernard-Soulier Syndrome
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bleeding due to defective platelet aggregation
autosomal recessive; deficiency or dysfunction of glycoprotein IIb-IIIa that forms bridges between platelets/binding fibrinogen and vWF |
Glanzmann's thrombasthenia
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acquired defects of platelet function
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ingestion of aspirin and uremia
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factor which does not cause bleeding if deficient
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XII
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factors affected in Vitamin K deficiency
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II, VII, IX, X, protein C
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VWF receptor
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Ib-IX; binding promotes platelet adhesion to subendothelial matrix
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vWF carrier function
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carries factor VIII
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spontaneous bleeding from mucous membranes, excessive bleeding from wounds, menorrhagia, and prolonged bleeding time in the presence of a normal platelet count
usually autosomal recessive prolonged bleeding time despite normal platelet count, reduced vWF; secondary decrease factor VIII; prolonged PTT |
von Willebrand disease
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von Willebrand disease associated with reduced quantity of circulating vWF
some of the bleeding characteristics resemble those seen in hemophilia |
Type 1 and 3
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von willebrand disease characterized by qualitative defects in vWF; subtype 2A is most common
autosomal dominant; defective multimer assembly |
Type 2
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most common hereditary disease associated with bleeding
reduction in the amount or activity of factor VIII; X linked recessive trait tendency toward easy bruising and massive hemorrhage after trauma or operative procedures; spontaneous hemorrhages frequently occur in regions of the body normally subject to trauma, particularly in joints; petechiae are characteristically absent normall bleeding time, platelet count, PT; prolonged PTT fibrin depostition is inadequate to achieve hemostasis; inadequate coagulation and inappropriate clot removal |
Hemophilia A
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severe factor IX deficiency; clinically indistinguishable from factor VIII deficiency
X linked recessive; PTT is prolonged, PT is normal, bleeding time is normal |
Hemophilia B/Christmas disease
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Acute, subacute, or chronic thrombohemorrhagic disorder occurring as a secondary complication
activation of teh coagulaion sequence that leads to formation of the microthrombi throughout the microcirculation of teh body; often uneven distribution may present with signs/symptoms of hypoxia/infarction |
DIC
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clotting pathway triggered by release of tissue factor
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extrinsic
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clotting pathway triggered by activation of XII by surface contact with collagen or other negatively charged substances
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intrinsic
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release of tissue factor or thromboplastic substances int the circulation
widespread injury to teh endothelial cells |
DIC
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disorders DIC is most likely to follow
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obstetric complications, malignant neoplasia, sepsis, major trauma
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clotting inhibiting factors
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activation fibrinolyssis by plasmin and clearance of activating factors by mononuclear phagocyte system and the liver
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protein intact on endothelial cellswhich binds thrombin that causes thrombin to become capable of activating protein C
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thrombomodulin
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wide spread deposition of fibrin within the microcirculation that can lead to ischemia of the more severely affected or more vulnerable organs
hemolytic anemia resulting from the fragmentation of RBC as they squeeze through the narrowed microvasculature hemorrhagic diathesis/hemostatic failure |
consequences of DIC
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DIC dominated by bleeding diathesis
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acute
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DIC that presents with thrombotic complications
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Chronics
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space occupying lesion destroys a significant amount of bone marrow or disturbs marrow architecture depressing its productive capacity
all formed blood elements are affected; most common cause is metastatic cancer |
myelophthisic anemia
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abnormally high concentration of RBC usually corresponding with increase in hemoglobin
relative if due to decreased plasma volume, absolute if increase in total cell mass primary if due to intrinsic abnormality of the myeloid stem cells; secondary if in response to erythropoietin |
polycythemia
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time taken for a standardized skin puncture to stop bleeding
assessment of platelet response prolongation= defect in platelet number or function |
bleeding time
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assay that tests extrinsic and common coagulation pathways
prolonged: deficiency/dysfunction of factor V, VII, X, prothrombin, or fibrinogen |
PT
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assay that tests the intrinsic and common clotting pathways
prolongation= dysfunction/deficiency of factor V, VIII, IX, X, XI, XII, prothrombin, fibrinogen |
PTT
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relatively common bleeding disorders that do not usually cause serious bleeding
induce small hemorrhages in the skin or mucous mebranes platelet count, bleeding time, PT/PTT normal infections, drug reactions (Ab med), Scurvy/ehlers-danlos, henoch schonlein, hereditary hemorrhagic telangectasia, amyloid infiltration |
non thrombocytopenic purpuras
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systemic hypersensitivity disease of unknown cause characterized by purpuric rash, colicky abdominal pain, polyarthralgia, acute glomerulonephritis
deposition of circulating immune complexes with in the vessels throughout the body |
henoch-schonlein purpura
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autosomal dominant disorder characterized by dilated tortuous blood vessels with thin walls that bleed readily
most common in the mucous membranes of teh nose, tongue, mouth, and eyes, throughout GI |
hereditary hemorrhagic telangiectasia
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platelet count below 100,000/microliters
prolonged bleeding time, normal PT/PTT spontaneous bleeding that most often involves small vessels |
thrombocytopenia
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major causes of thrombocytopenia
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decreased production of platelets, decreased platelet survival(immunologic and nonimmunologic), sequestration (splenomegaly), dilutional (blood transfusion after 24+ hours storage)
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