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132 Cards in this Set
- Front
- Back
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fxns of the hematopoietic system
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Transport:
supply o2 for aerobic metabolism remove waste products host defense system transport nutrients Homeostasis: fluid & electrolyte balance buffer system (acid base balance) temperature regulation. Hematopoiesis & Hemostasis as well. |
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reticulocyte
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immature RBC
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erythropoietin
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hormone synthesized in kidneys, released when O2 decreases, starts erythrogenesis
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monocyte macrophage system
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Their role is to phagocytose (engulf and then digest) cellular debris and pathogens either as stationary or mobile cells, and to stimulate lymphocytes and other immune cells to respond to the pathogen
Monocytes are organ specific and produce macrophages |
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Components of Host Defense System (4)
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1) Phagocytosis by neutrophils & macrophages
2) Monocyte-macrophage system 3) Inflammation 4) Immunity (B and T lymphocytes) |
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B lymphocytes govern _____ immune response while T cells govern ____ ____ immune response
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humoral immune response, cell mediated immune response
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humoral immune response
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the aspect of immunity that is mediated by secreted antibodies produced in the cells of the B lymphocyte lineage (B cell). Secreted antibodies bind to antigens on the surfaces of invading microbes (such as viruses or bacteria), which flags them for destruction.
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cell mediated immune response
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an immune response that does not involve antibodies or complement but rather involves the activation of macrophages, natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen.
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Components of Hemostasis
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1) Endothelial activation causing vasoconstriction ( a cut)
2) platelet activation and aggregation 3)coagulation, fibrin & clot formation, clot retraction (enlargement) 4) fibrinolysis, anticoagulant |
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Components of Assessment of Hematologic system r/t Patient History
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Biographical & demographic data
Current health (cheif complaint, symptoms) Past health history (operations, childhood diseases, meds, allergies) Family health history Psycho social history (occupation, nutrition, habits) |
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Hematologic symptom of pallor =
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anemia
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Hematologic symptom of ruddy skin, pruritis=
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polycythemia
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Hematologic symptom of jaundice=
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hemolytic anemia
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Hematologic symptom of dry brittle nails, concave with longitudinal lines=
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iron deficiency anemia
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Hematologic symptom of petechiae, purpura, ecchymosis=
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thrombocytopenia and bleeding disorders
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Hematologic symptoms of rashes, urticaria, pruritis, dryness=
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allergies
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Hematologic symptom of delayed wound healing=
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dysfunction of hemapoietic system
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RBC lab values
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Men 4.5 - 5.3 million/mm3
Women 4.1 - 5.1 million/mm3 numbers in relation to volume |
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Hemoglobin lab values
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men 13 - 18 g/100ml
women 12 - 16 g/100ml |
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Hematocrit lab value
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packed cell volume
men 37 - 49% women 36 - 46% |
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Red blood cell indices
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Labs that show morphology of RBC's and hemoglobin content. Used to assess anemia. Include MCV, MCH, MCHC and RDW
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MCV
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mean corpuscular volume.
average size of RBC |
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macrocytic
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too big
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microcytic
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too small
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MCH
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mean corpuscular hemoglobin.
amount of hemoglobin present in one cell |
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MCHC
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mean corpuscular hemoglobin concentration.
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RDW
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red cell distribuition width (aka variation range in RBC width)
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Platelet lab values
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150,000 - 450,000/mm3
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Total white cell count in differential definition and %'s
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Total WBC's in a cubic mm. Percentage of types of white cell. The differential always adds to 100%.
neutrophils/segs 55-70% basophils 0.5-1% eosinophils 1 - 4% Monocytes 2-8% (all in organs, not serum) lymphocytes 20-40% |
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Causes of low serum folic acid and in what disorder is it decreased?
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dietary deficiency or malabsorption (e.g. Crohn's disease)
decreased in macrocytic anemia |
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Causes of low Vitmain B12 and in what disorder is it low?
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Dietary deficiency or malabsorption.
Low in pernicious anemia. |
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transferrin vs ferritin
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transferrin is the blood plasma protein for iron ion delivery and ferritin is the iron storage protein (for intracellular storage)
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erythrocyte sedimentation rate (ESR)
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speed RBC's settle in tube.
Very general lab value. Gives you a heads up that something is wrong but doesn't hint towards a specific disease. |
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Erythropoietin assay: increased in ______ and decreased in _______
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most anemias, renal disease
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MCHC
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mean corpuscular hemoglobin concentration
Width of a RBC (Would be way off in sickled cell anemia) |
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RDW
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Red cell distruibuition width
(measure of the variation in RBC width) |
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platelet count lab value
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150000 - 450,000
measure of circulating platelets |
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Total WBC count and differential (definition)
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Total WBC's in a cubic mm.
Precentage of types of white cells (so its just a screening type test) The differential always adds up to 100% |
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WBC lab range
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4,500 - 11,000
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WBC differential ranges
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neutrophils/segs 55 - 70%
basophils 0.5 - 1% eosinophils 1 - 4% monocytes 2 - 8% lymphocytes 20 - 40% |
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DIsorders all WBC's are increased
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bacterial, stress, inflammation, tissue damage
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Different Disorders where each of the different WBCs are increased
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basophils in leukemia, Polycythemia Vera
eosinophils in antigen/antibody, parasitic monocytes in chronic inflammation (not in circulation) lympthocytes in viral, leukemia, mono, TB |
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Serum Folic Acid lab: when is it low and why?
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causes: dietary deficiency, malabsorption (Crohn's disease)
Decreased in macrocytic anemia |
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Vitamin B12 lab: when is it low? why?
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causes decrease: Dietary defieciency, malabsorption
Low in pernicious anemia |
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transferrin
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plasma iron carrier protein
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ferritin
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iron storage protein
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erythrocyte sedimentation rate (ESR)
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tests how fast RBC's settle in a tube
very general screening test. |
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when is the RBC sed rate increased?
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infections, malignant tumors, collagen vascular disease, etc etc.
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Erythropoietin assay: When is it increased and when is it decreased?
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increased in most anemia (outside of renal disease)
decreased in renal disease |
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PT prothrombin time
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(along with INR) is a measure of the extrinsic pathway of coagulation. Its specifically to monitor Coumadin therapy
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Antidote to Coumadin
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Vitamin K, aquaMEPHYTON
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PTT activated partial thromboplastin time
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Lab to monitor intrinsic pathway of coagulation, or more specifically, to monitor heparin.
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Antidote to heparin
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Protamine sulfate (half life is shorter than heparin)
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activated clotting time lab
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measures the time it takes whoel blood to clot
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When are fibrin degradation products produced
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they are a by product of fibrinolysis
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general manifestations of all anemias
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impaired oxygen transport
(tissue hypoxia is underlying cause of most symptoms) pallor (nails, lips, palm lines, conjunctiva) FATIGUE SOB, dyspnea on exertion tachycardia, angina |
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Iron deficiency anemia
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inadequate supply of iron to synthesize hgb
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iron deficiency anemia: causes
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chronic blood loss, insufficient intake, mal absorption (duodenum, jejunum), excessive demands for RBC's
GI bleeding, diarrhea, gastrectomy |
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iron deficiency anemia: symptoms (and what do the RBC's look like, lab values?)
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general symptoms of anemia
microcytic: pale hypo-chromic RBC's Low: hgb, MCV,MCH,MCHC, serum iron level |
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iron deficiency anemia: management
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correct underlying cause
dietary adjustments iron supplement: oral and injectable |
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megaloblastic anemia
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vitamin B12 and folic acid deficiency (or possible DNA synthesis, ineffective cell development cause)
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megaloblastic anemia: symptoms
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general symptoms of anemia
appearance of megaloblasts in blood (large primitive RBC's) leukopenia thrombocytopenia |
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megaloblastic anemia: management
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vitamin B12 and folic acid replacement
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pernicious anemia
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Anemia of older individuals. Vitamin B12 deficiency
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pernicious anemia: symptoms
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progresses over 20-30 yrs (avrg. age 60)
general symptoms of anemia low: hgb, hct, RBC's sallow skin, beefy red tongue **neuro manifestations: neuropathies |
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Schilling test
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Vitamin B12 tagged with cobalt is ingested. Test to see if someone has pernicious anemia
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Why are there neurological symtpoms in perniciosu anemia?
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because B12 deficiency affects myelin sheaths in periphery by decreasing amnt of myelin
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pernicious anemia: management
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vitamin B12 injections, Iron, Folic acid
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Folic acid deficiency anemia: causes
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lack of folic acid in the diet, malnutrition
(green leafy veggies, citrus, liver, yeast) ETOH malabsorption syndromes |
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Folic acid deficiency: symptoms
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Same as Pernicious anemia but without Neuro symptoms
General symptoms of anemia |
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Aplastic anemia: causes
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suppression or failure of bone marrow to produce all types of cells; Pancytopenia
Hereditary or Acquired: chemical, viral, arsenic, chemotherapy, total body irradiation |
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Aplastic anemia: symptoms
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Slow progression or very rapid
1) adaptation over time vs. 2) overwhelming infection/bleeding (e.g. Hiroshima victims) General symptoms of anemia but more SEVERE Infection, bleeding low: hct,hgb,RBC's, platelets, WBC's |
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Aplastic anemia: management
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Transfusion of needed blood products (transfuse whatever is the lowest first)
prevention and Rx of infection and hemorrhage allogenic bone marrow transplant |
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Hemolytic anemia
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premature destruction of RBC's
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Hemolytic anemia: causes
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hyperactive spleen, destruction by macrophages
immune system mediated-blood transfusion reaction toxins, venom (snakebite!) physical hemolysis: burns, radiation, prosthetic heart valve Failure of bone marrow to replace RBC's |
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hemolytic anemia: symptoms
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general symptoms of anemia
renal failure (clogs it) normocytic anemia, increased # reticulocytes (marrow is trying to compensate, pumps out new cells too early) |
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hemolytic anemia: management
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remove causative agent
fluid to flush kidneys (sodium bicarb to alkalize urine so there's less kidney destruction) Spleenectomy if hyperactive spleen is the casue |
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Anemia of chronic disease: causes
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Unknown mechanism.
Chronic diseases cause it: COPD, AIDS, inflammatory diseases, malignancies, bowel diseases, renal failure |
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Anemia of chronic diseases: 3 pathological mechanisms
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1)decreased RBC life span
2) decreased bone marrow response (to RBC need) 3) altered iron metabolism |
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Anemia of chronic disease: symptoms
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general symptoms of anemia- but less severe
low: hgb, hct, RBC's |
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Anemia of chronic disease: management
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treat underlying problem-chronic disease
Erythropoietin (limited success) |
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Post hemorrhagic anemia: causes
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trauma
acute blood loss |
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Post hemorrhagic anemia: symptoms
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loss of blood volume so....
hypotension, decreased venous return loss of hemoglobin so... decreased O2 carrying capacity loss of cells for hemostasis |
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Post hemorrhagic anemia: management
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Pt. shift of fluid and electrolytes from tissues
volume replacement fluids: crystalloids colloids: albumin, hespan Blood and blood components (depends on need): whole blood, PRBC's, FFP, clotting factors Repair of trauma site |
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hespan
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Used as a volume expander, its a starch, metabolized by the liver, larger than albumin (so less likely to leak out of vasculature) shorter life than albumin
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Nursing Diagnosis r/t hematologic disorders
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Activity Intolerance r/t hypoxemia, endurance, pain, metabolic changes, fever, overwhelming illness.
Altered protection r/t infection, coagulation status Altered perfusion r/t decreased tissue perfusion Fatigue Knowledge Defecit (disease process, energy conservation) Pain |
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Spleenectomy: indications
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spleen rupture (severe hemorrhage)
Hypersplenism (destroys excessive # of RBC's) |
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Hypersplenism: symptoms
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anemia, leukopenia, thrombocytopenia
symptoms of anemia, decreased host defense, bleeding increased cell production by the bone marrow |
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Spleenectomy: Patient Post Op Care
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Increased Risk for infection (the spleen is important in phagocytosis of circulating foreign organisms)
children at highest risk of infx. Educate: seek out Rx for any indication of infx. Prophylactic antibiotics (before dental procedures, etc) Routine post surgical care (check for bleeding etc.) |
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Polycythemia
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increase in # RBC's and hct
Absolute (or polycythemia vera)= over production of RBC's, deficiency in the RBC Relative=associated with hemo-concentration (e.g. dehydration) |
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Polycythemia Vera: Pathophysiology
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Excessive bone marrow production of RBC's, WBC's and platelets
Excessive activation of peripotential stem cell (hematopoietic stem cell) |
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Polycthemia Vera: symptoms
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Increased blood viscosity = congestion tissues and organs
Increased total volume X 2-3 ruddy complexion headache, dizziness, visual disturbances pain in the joints HTN CHF, MI, increased clotting-CVA High: RBC's, Hgb (18 - 25), hct 49 - 54%, platelets, uric acid |
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Polycythemia Vera: management
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phlebotomy (bleed patient, give saline)
Decrease bone marrow production: e.g. radioactive phosphorus |
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Thrombocytopenia (different levels)
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low platelets, below 100,000/mm3
below 50,000 = hemorrhage with minor trauma below 10,000 - 15,000 = spontaneous hemorrhage (without trauma): Petichiae, frank bleeding... Less than 10,000 = severe bleeding, fatal |
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Idiopathic Thrombocytopenia Purpura
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aka "No idea why, bruising from low platelets".
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Idiopathic Thrombocytopenia Purpura: Causes
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Autoimmune bleeding disorder
Antibodies to own platelets Phagocytosis: macrophages in the spleen destroy platelets |
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Normal platelets lifespan vs lifespan in Idiopathic Thrombocytopenia
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normal: 8 - 10 days
Thrombocytopenia: 1 - 3 days |
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Idiopathic Thrombocytopenia Purpura: symptoms
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bleeding gums, petechiae (pinpoint bruises), ecchymosis (large bruises), epistaxis (nosebleed)
Severe hemorrhage: nose, cerebral, GI, urinary systems bleed hematoma (collection blood outside blood vessel) pressure on nerves = pain and paralysis |
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Idiopathic Thrombocytopenia Purpura: management
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If cause is macrophage ingestion of platelets-give steroids.
If cause is antibodies against platelets (often is) then plasmapheresis (take out old plateles and whatever crap is on them "antibodies" and put in nice fresh platelets) IV gamma globulin (increase platelets) Spenectomy (60 - 80% permanent remission) |
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Heparin Induced Thrombocytopenia (HIT)
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Occurs in patients with exposure to heparin (may not know they've even been exposed to heparin)
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Heparin Induced Thrombocytopenia: Etiology
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From either an Adverse drug reaction (immune mediated: the more dangerous one) OR
Nonimmune mediated HIT (10-30%): decreased platelets, 1-2 days post exposure, transient, benign, self-limited. If thrombocytes are decreased w/ in |
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Always know this when you start someone on Heparin
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Their baseline thrombocyte level. If it decreases below 50% they should never be touched by heparin again!
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Immune mediated heparin induced thrombocytopenia: pathophysiology
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IgG antibodies activate platelets (process takes about 5 days, so you wont' see antibodies in labs for 5 - 14 days post exposure)
This results in platelet activation and the formation of platelet microparticles, which initiate the formation of blood clots; the platelet count falls as a result |
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Immune Mediated heparin induced thrombocytopenia: labs to look out for
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platelet count less than 150,000/mm3 OR
50% decrease from baseline platelet level |
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How long can thrombosis occur post exposure to heparin in immune mediated HIT?
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up to 30 days
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Immune Mediated Heparin induced thrombocytopenia: symptoms
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limb and organ ischemia (arterial thrombosis: 10% amputation rate, venous thrombosis associated w/ limb gangrene)
If moderate to severe: 10-20% fatality rate! |
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Immune Mediated heparin induced thrombocytopenia: management
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Stop ALL heparin (heparin flushes, dialysate, coated catheters, guide wires)
Treat/Prevent active thrombosis with thrombin inhibitors/anticoagulant: argatroban, lepirudin,, warfarin (BUT can't give Coumadin until platelets are over 100,000/mm3!!!) |
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hypoprothrombinemia
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Decreased amount of prothrombin (factor II)
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Hyporpothrombinemia: causes
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prothrombin synthesis is decreased in the liver (happens with ETOH, hepatitis...etc)
Vitamin K deficiency (malabsorption in intestines) Liver disorders Overdose of Coumadin |
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Hypoprothrombinemia: Symptoms
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increased Prothrombin time
bleeding (vein puncture, GI, ecchymosis, epistaxis) |
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Hypoprothrombinemia: Management
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AquaMEPHYTON (Vitamin K, antidote to Coumadin)
Transfusion of prothrombin factors |
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Disseminated Intravascular Coagulation (DIC)
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Results from overstimulation of clotting/anticlotting processes in response to disease/injury: Clotting (what usually kills this patient) and Hemorrhagge within the same disease
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Medical conditions that increase the risk of getting DIC (disseminated intravascular coagulation)
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shock, sepsis, cirrhosis, glomerulonephritis, acute hepatitis, acute bacterial/viral infections
Conditions that release platelet factor III: snake bite, fat emboli Hemolytic processes: transfusion reaction major trauma: burns, trauma malignancies acute obstetric conditions: abruptio placentae, eclampsia Toxic Shock Syndrome |
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Lab Indicators of Procoagulant Activation in DIC (not on exam)
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Increased D-Dimer lab (the most reliable and specific test for DIC)
D-dimer assess levels of neoantigen (produced by plasmin lysis of fibrin clots) |
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Lab indicator of fibrinolytic activity in DIC (not on exam)
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increased D-dimer
increased Fibrin Degradation products (FDP) lab |
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Lab indicators of inhibitor consumption in DIC (not on exam)
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increased Thrombin-antithrombin (TAT) complex
decreased Antithrombin III (inactivates coagulation) |
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Lab indicators of End Organ Damage in DIC (not on exam)
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Increased lactate dehydrogenase LDH (tissues release when damaged)
increased creatinine (renal failure) decreased pH (lactic acidosis, not enought O2 to cells) decreased paO2 |
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Lab indicators of coagulopathy in DIC (not on exam)
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PT, PTT, Thrombin times prolonged
decreased fibrinogen level (used up) decreased platelet count (used up) |
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Disseminated Intravascular Coagulation: management
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Correct underlying cause
reverse the pathologic clotting Control bleeding and shock Maintain end organ viability (fluid resuscitation, oxygenation, organ support) Administer blood products (washed RBC's removing anticoag. substances, platelets, clotting factors) Anticoagulants to stop microcirculation clotting (Antithrombin III drugs aka Desirudin, Heparin (controversial)) |
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DIC full systems assessment (in brief)
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integumentary: for signs of bleeding
resp: tachypnea, hemoptysis, rales CV: tachycardia, hypotension, shock GI: Abd distention, guaic + stool GU: u/ouput, hematuria, oliguria Neuro: vision changes, headache, irritability, change in mental status |
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Hemophilia
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characterized by prolonged bleedeing
common disorder, hereditary Three types |
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Hemophilia A
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classic hemophilia.
80% of patients have this Factor VIII deficiency |
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Hemophilia B
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Christmas disease
Factor IX deficiency |
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Von Willebrand's disease
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Third type of hemophilia
Factor VIII deficiency Platelet dysfunction |
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Hemophilia: symptoms
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slow persistent bleeding w/ minor trauma
delayed hemorrhage severe hemorrhage from gums after dental work, hard tooth brushing epistaxis after injury (can be fatal) recurrent hematoma formation in deep tissue GI hemorrhage Bleeding into joints-deformity |
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Hemophilia: Management
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Stop bleeding as quickly as possible
mild episode Desmopressin increases factor VIII Raise level of anti-hemophilic factor (factor XIII or IV concentrate, transfuse q 12 hrs until bleeding stops) Prevent complications during procedures |
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Hemophilia: Nursing Management (r/t joints and pt teaching)
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analgesics and corticosteroids reduce joint pain, joint immobilization local chilling
After swelling subsides, ROM, exercises, weight bearing. Pt education: risk of bleeding, contact sports, minor invasive procedures, falls and cuts, early recognition of bleeding episode adn early intervention |
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Symptoms of 10%/500ml "a pint" blood loss
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None
rarely vaso vagal syncope in blood donors |
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Symptoms of 20%/1000ml blood loss
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Postural changes in BP (vitals can be normal when flat lying)
difficult to detect changes at rest |
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Symptoms of 30%/1500ml blood loss
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Neck veins flat supine position
postural hypotension, exercise tachycardia resting VS may still be normal |
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Symptoms of 40%/2000ml blood loss
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decreased CVP, CO, Arterial BP even at rest
Air hunger, rapid thready pulse, cold clammy skin feeling of doom |
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Symptoms of 50%/2500ml blood loss
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Severe shock
lactic acidosis death from hypo perfusion |
