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20 Cards in this Set
- Front
- Back
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Anemia
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decrease in O2 capacity of RBC
-reduction in RBC, hemoglobin, pact cell volume sign of underlying disease rapid changes in PCV worse then slow changes -rapid loss of 30% of blood more severe then slow loss of 50% blood **could be hemoglobin problem as well** |
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Manifestations of Anemia
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1. UNDERLYING CAUSES: decrease in erythropoeisis (production of RBC) or increase in destruction (destroyed RBC faster then produced)
2. decrease RBC, decreased hemoglobin= decreased O2 carrying capacity 3. tissue hypoxia = liver, CNS, respiratory, pallor, weakness, ischemia (cramping of muscle) all happen 4. Compensatory mechanisms= increase DPG (helps unload O2 off of hemoglobin), renal (renin-aldosterone--> salt retention), cardiovascular (increase in heart rate and stroke volume), increase in O2 demand (angina can happen=chest pain, increase erythropoetin--> stimulate bone marrow) 5. hyperdynamic circulation --> cardiac murmurs (increase viscosity of blood) or high output cardiac failure **kidneys resolve problem if erythropoetin is released and renin-aldosterone work** |
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Signs of anemia
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pallor--> mucous, nail beds
tachycardia with heart murmur angina on exertion (myocardial ischemia) dyspnea--> shortness of breath headache, dizziness, tinnitus (ringing of ears), GI disruption --> CNS dysfunction |
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Classification by morphology
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normocytic, normochromic
-normal cells, normal color, normal hemoglobin, not enough produced -caused by massive bleeding, kidney failure, disease macrocytic, normochromic -large cells, normal color, normal hemoglobin, fewer cells -causes DNA problems--> B12 deficiency, folic acid deficiency -cancer chemotherapeutic drugs |
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microcytic, hypochromic anemia
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small cells, low color, low hemoglobin
-inadequate heme synthesis or globin synthesis iron deficiency (vegetarians), chronic blood loss (ulcer) |
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Classification by etiology (what caused problem)
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increased cell loss by bleeding or destruction (hemolysis)
-hemolysis--> RBC damaged -inherited hemoglobin problems, enzyme and membrane defects --> sickle cell anemia -autoimmune disease -parasitic--> malaria or babesia (nantucket fever--> caused by tick carrying lime disease) -hypersplenism--> enlarged spleen trap and removes more RBC then produced -artificial heart valves (plastic)--> damages RBC |
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Decreased of defective RBC production
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leukemia, lymphoma, myeloma--> crowd out cells
exposure to toxic chemicals--> mitosis interference radiation renal disease--> no erythropoetin dietary deficiencies |
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Specific Anemia --> reticulocyte count to determine regenerative or not
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reticulocyte--> immature RBC
regenerative anemia--> reticulocyte count up with anemia, bone marrow kicking out RBC for more O2=good non-regenerative anemia--> count does not go up, problem with bone marrow=BAD **can start as regenerative then move to non-regenerative --> exhaust bone marrow** |
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Aplastic anemia--> normocytic, normochromic
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lack of formation of RBC, ones produced are normal
life threatening idiopathic, congenital, secondary to toxic chemicals deficient in all types of blood cells reticulocyte count is nonexistant or low--> bone marrow shuts down |
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Signs and Symptoms
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fatigue, dyspnea, weakness, pale mucous membranes--> anemia
brusing or petechial hemorrage, internal bleeding --> lack of platelets increased incidence of infections--> WBC CBC/Differential shows decrease in all blood cells infection and bleeding are major causes of death --> kept alive with blood transfusion |
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Iron deficiency anemia
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microcytic, hypochromic --> small, low color, low HgB
major form in world, especially menstrual age women -chronic blood loss removes Fe faster then can produce -chronic bleeding from parasites, ulcers, other problems diet deficient in iron --> vegetarians, alcoholics, drug addicts |
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Signs and Symptoms
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fatigue, dyspnea, weakness, pale mucous membranes
brittle, fine hair; thin nails atrophy of papillae on tongue, stomatitis --> inflammed mouth low serum iron levels, low Hgb |
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Megaloblastic anemia
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big cells, normal color, normal HgB
lack of B12/ folic acid = disrupted DNA synthesis -cells dont mature/divide correctly pernicious anemia --> lack of intrinsic factor in stomach = lack of absorption of B12 -gastric bypass surgery, stomach removal -need B12 through injection |
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Sickle cell anemia (disease)
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inherited (autosomal recessive) change of one amino acid (beta chain) in globin
-most common in western sub-saharan Africa and Mediterranean -hemolytic anemia --> cells break down rapidly plasma O2 decreases = HgS deforms = RBC elongates and sickles normal size, color, HgB level abnormal cells take longer to get through capillaries, leads to tissue ischemia stick to vascular endothelium--> occulsion reduced RBC life span puts work on bone marrow -can run out of erythrocyte precursor **homozygous person --> shorter life, no survival benefit, have two bad copies of gene ** |
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Signs and Symptoms
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could be normal, then go through sickle cell crisis
vary depending on tissue being damaged children --> failure to thrive (abnormal weight gain and muscle development), increased incidence of bacterial infections enlarged spleen (removes sickle RBC), spleen atrophy from being overworked -can impair immune function swollen, painful, inflamed hands/feet recurring crisis of ischemia, chronic leg ulcers -increased risk of stroke, heart attack, kidney failure |
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Sickle cell trait
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**heterozygote person--> will not get sickle cell disease, also have survival trait = no malaria **
one normal gene, one sickle cell gene = carrier signs/symptoms brought on by strenuous exercise, especially at high altitudes asymptomatic in most people -most states test neonates and NCAA wants to tests athletes |
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Thalassemias
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wide variety of recessive hemoglobin mutations
alpha or beta chain may be affected -alpha controlled by 4 genes -beta controlled by 2 genes **homozygous recessive shows signs/symptoms** |
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Signs/Symptoms of thalassemias
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mild--> asymptomatic
moderate--> enlarged spleen, slow growth, delayed puberty, expanded bone marrow severe--> jaundice, dark urine, enlarged heart, Fe overload from transfusions, increased infections |
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Polycythemia
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increased number of RBC = increased viscosity
myeloproliferative disorder--> myeloid stem cell problem, can be malignant erythropoetin low because increased RBC level polycythemia vera --> middle aged, mostly men - too many RBC's for no reason **different from physiological polycythemia--> marathon runners need more O2 to tissue** |
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Signs and symptoms
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brick red complexion, blood shot eyes
non-specific symptoms progressive enlargement of liver and spleen marrow may overwork and become aplastic or develop acute granulocytic leukemia PCV greater then 60, HgB greater then 18 thrombosis major cause of death **donate blood every 8 weeks to keep hematocrit normal** |
