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72 Cards in this Set
- Front
- Back
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what patient history makes you think anemia? |
- dietary habits that are low in iron - medication: drugs - possible exposure to chemicals and/or toxins - descriptions and duration of symptoms blood loss (acute or chronic), malignancies, chronic diseases, hemolysis |
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what are the clinical symptoms of anemia? |
- tiredness - muscle fatigue and weakness - headache and vertigo (dizziness) - dyspnea (difficult or labored breathing) from exertion - GI problems - overt signs of blood loss such as hematuria (blood in urine) or black stools |
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what will you find on physical exam of a patient with anemia? |
- hepato or splenomegaly - heart abnormalities - skin pallor |
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what specific findings on physical exam may help establish the underlying cause? |
- in vitamin B12 deficiency there may be signs of malnutrition and neurological changes - in iron deficiency there may be severe pallor, smooth tongue, esophageal webs
- hemolytic anemias there may be jaundice due to increased levels of bilirubin from increased RBC destruction |
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if you suspect hemolytic anemia, what is the most obvious physical sign you'd except? which labs would you check? what are a few differential diagnoses you may suspect?
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jaundice labs: - increased bilirubin - increased LDH - increased reticulocyte count - coombs test positive (+ means antibodies are bound to surface of RBCs)
differential diagnoses: babeiosis (blood parasite) if coombs test is positive --> warm antibody hemolytic anemia potential due to hemolysis |
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what history of medical problems could cause anemia? |
- sickle cell disease - thalassemia - renal disease |
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how are anemias classified? |
classified morphologically based on the average size of the cells and hemoglobin concentration - macrocytic - normochromic, normocytic - hypochromic, microcytic |
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microcytic |
MCV < 80
iron deficiency- high RDW (red cell distribution with) - thalassemia minor - normal RDW - thalassemia major - rare, sideroblastic anemia - metal poisoning esp lead or aluminum - occasional hemoglobinopathies
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microcytic hypochromic anemia diagnosis mild- which diseases are associated? severe- which diseases are associated |
mild (MCV > 70 fl) - iron deficiency - thalassemia - lead toxicity - sideroblastic anemia - anemia of chronic disease
severe (MCV <70 fl) - iron deficiency - thalassemia |
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hypochromic- microcytic anemia |
low MCV (smaller volume than normal) and low MCH (less hemoglobin per RBC than normal) - values vary by age - Fe deficiency (95%) - lead poisoning - parasites: roundworm, hookworm - anemia of chronic disease - thalassemia - GI: gastritis (ulcer), colon cancer ALWAYS r/o colon cancer in patients >50 years old (hemoccult/FOB &/or colonoscopy) |
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anemia due to thalassemia 1) what is it? 2) patho 3) what does the smear show? |
1) microcytic anemia 2) defects in either the alpha or beta chains of hemoglobin, leading to ineffective erythropoiesis and hemolysis alpha thalssemia: prevalent in africa, mediterranean, middle east, asia beta thalassemia: prevelent in mediterranean, south east asia, india and pakistan 3) smear shows microcytosis with target cells |
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macrocytic anemia Provide two MCVs for macrocytic anemia what are the two most frequent causes? there are two forms of macrocytic anemia. what are they and how do you tell the difference?
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MCV >100 if MCV 100- 110 fl look for other causes of macrocytosis
if MCV > 110 almost always folate or cobalamin (chemical form of vit b12) deficiency
megloblastic and nonmegaloblastic the peripheral smear will show you what kind of cells there are.
this is not on test: megaloblastic means that the nucleus of the cell has not developed to the same extent as the cytoplasm. |
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macrocytic anemia megaloblastic what is the most common cause? |
B12 and/or follate deficiency present in most
- concomitant measure of serum B12 and folate required to determine true dificienc vs spurious elevation - more common if hx of GI surgery/malabsorption, poor nutrition/vegetarianism, ETOH, pregnancy |
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macrocytic anemia nonmegalobasltic, you look at the reticulocyte count. if it is: high: evaluate for? low: evaluate for? |
reticulocyte count (reticulocytes are immature RBCs that mature for 3 days in the bone marrow then one day in circulation)
- high: evaluate for hemolysis or hemorrhage because the body is trying to compensate for blood loss - low: evaluate for hypothyroidism, liver disease or alcoholism because they interfere with reticulocyte production |
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hyperchromic, macrocytic anemia what are the three most frequent causes? |
high MCH (more hemoglobin per RBC than normal) AND high MCV (larger volume than normal)
1) folate deficiency (from lack of nutrition or malabsorption in GI tract) 2) B12 deficiency from chronic alcoholism 3) early post bleed (high reticulocytes to compensate from blood loss) |
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normochromic, normocytic anemia what lab value do you look at? extrinsic? intrinsic? |
normal MCH (normal amount of hemoglobin per RBC) AND MCV (normal RBC volume) look at the reticulocyte count - low = anemia of underproduction (there's something wrong with the production of reticulocytes and you're going to look for the cause) - high = anemia of blood loss (trying to compensate for blood loss somewhere and you're going to look for the cause)
extrinsic (problem is outside the cells) - autoimmune - infection: malaria - trauma: burns, DIC
intrinsic (problem is in the cell itself) - hemoglobinopathies: sickle cell - enzyme deficiencies: G6PD - membrane defects: spherocytosis |
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what will the reticulocyte count tell you? what's normal (without anemia)? |
level of the bone marrow activity (done by staining a peripheral blood smear with new methylene blue to help visualize remaining ribosomes and ER.
(# reticulocytes)/ (1000 RBC) is counted and reported as %
at birth normal is 1.8-8% adult normal is 0.5- 1.5% in anemia, reticulocyte count is elevated above normal values |
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why correct reticulocyte count? RPI? as anemia gets more severe, what happens? |
a reticulocyte count is a percentage of [reticulocytes (immature RBC)] / [total RBC]
patients with anemia may have a falsely elevated percentage of reticulocytes in RBCs because their mature RBCs are depleted due to various potential causes. we correct the value by using the reticulocyte production index (RPI):
RPI formula [patient's HCT*]/ [(0.45 (normal HCT) x reticulocyte count or an absolute count (% reticulocytes x RBC count)]
as anemia gets more severe, younger cells that take longer than 24 hours to mature are thrown out into the peripheral blood (shift reticulocyte). could be corrected to give retriculocyte production index (RPI) which is a truer indication of the renal bone marrow activity
things to remember: HCT is the amount of RBC in the blood 0.45 (45%) is the normal value for HCT in a healthy patient |
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1) wright's or giema stain 2) what does it aim to identify? 3) what are erythrocyte inclusions? |
1) blood smear exam 2) poikilocytosis: describes variation in the shape of RBCs, normal to have some variation in shape but some shapes are characteristic of a hematologic disorder or malignancy 3) RBCs in the peripheral smear should be examined for the presence of inclusions* or variation in erythrocyte distribution
not on test: *inclusions are nuclear or cytoplasmic aggregates of sustainable sources, most often proteins. you can see them when you stain blood and usually are the hallmark of genetic disease. |
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anisocytosis - if there's an increased % of reticulocytes, what color would the stain be? |
variation in size and classified as - normocytic - microcytic - macrocytic
variation in hemoglobin concentration (color) should be noted and the cells should be identified as - normochromic - hypochromic - hyperchromic - polychromasia (pinkish- blue color due to an increased % of reticulocytes) should be noted - variation in shape should be noted (poikilocytosis) and different shapes found should be indicated - variation in RBC distribution should be noted (agglutination or rouleaux formation) |
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peripheral smear shows abnormalities in leukocytes or platelets. what do you most often find?
what other lab investigation may be helpful when tests are inconclusive |
abnormal findings are clues to correct type if anemia - nutritional deficiencies - stem cell disorders - bone marrow abnormalities will affect production, function, and/or morphology of platelets and/or granulocytes
bone marrow smear and biopsy (used when other tests are not conclusive) |
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why would you evaluate RBC enzymes and metabolic pathways? what kind of anemia is associated? |
enzyme deficiencies in carbohydrate metabolic pathways are associated with hemolytic anemia |
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why would you evaluate erythropoetin levels? |
determine if a proper bone marrow response is occurring
low levels of RBCs could be due to a bone marrow problem or lack of erythropoetin production |
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why check bone marrow cultures? |
viability of stem cells |
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how are anemias classified functionally? |
- hypoproliferative: proliferation defect - ineffective: maturation defect - hemolytic: survival defect |
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why check serum iron? |
iron binding capacity & % saturation to diagnose iron deficiency anemias |
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iron deficiency anemia chronic and acute causes |
chronic: GI or menstrual acute/ hemodynamically significant: - GI - retroperitoneal (space in the abdominal cavity behind the peritoneum, lining of the abdominal cavity) |
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causes of absolute iron deficiency anemia |
iron deficiency is a symptom, not a disease 1) increased requirements - GI, retroperitoneal, GI tract, blood donation - pregnancy and lacation
2) inadequate iron supply - insufficient dietary iron - impaired iron absorption gastric (bariatric) srugery, atrophic gastritis, celiac disease, G. pylori infection, intestinal malabsorption from decreased absorption in celiac disease, inflammatory bowel disease |
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neurologic syndromes associated with iron deficiency
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- pica: complusive ingestion of non food substance - phagophagia: ice eating more common in women than men 25% of patients with iron deficiency anemia from any cause
restless leg syndrome - common neurologic disorder criteria for dx: 1) urge to move legs accompanied by uncomfortable sensation 2) sensation begins or worsens during periods of rest 3) sensations relieved by movement 4) worse in the evening/night occurs in10% of cases of iron deficiency anemia |
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iron deficiency anemia kolionychia |
nail spooning |
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what's the best laboratory marker for iron deficiency? what are typical lab findings? |
ferritin - serum iron: low <60 micrograms/dL - total iron binding capacity (TIBC) HIGH > 360 micrograms/ dL - serum ferritin LOW (<20 nanograms/ mL) can be falsely normal in inflammatory states |
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body iron distribution and storage where are the three places iron is used/stored? how is iron lost? |
dietary iron is taken into the duodenum (1-2 mg/day) then continues on to plasma transferrin
plasma transferrin is utilized in three places: 1) muscle (myoglobin) 2) sent and stored in the liver (the liver can send it back to the duodenum too) 3) bone marrow --> circulating erythrocytes (hemoglobin) and reticuloendothelial macrophages --> plasma transferrin
iron is lost: 1) sloughed mucosal cells 2) desquamation/menstruation contributes to iron loss |
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iron intake what's the mean iron intake per day? |
mean iron intake 10-15 mg/ day historically the main source of iron intake has been meat not a marker of overall nutrition |
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major iron compartments |
metabolic - hemoglobin (1800-2500 mg) - myglobin (300- 500 mg) storage 0-100 mg transit - serum iron 3 mg
total: 3000-4000 mg |
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treatment with iron: principles which salt is absorbed best? what does ascorbic acid to? when is iron absorbed best? how often does reticulocytosis occur? what's the max iron dose?
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- ferrous salts are absorbed better than ferric salts. all ferrous salts are absorbed to the same extent - ascorbic acid increases absorption and toxicity - iron is absorbed best on an empty stomach; not given with antacids - prescription iron generally better tolerated than iron salts - reticulocytosis occurs <7 days; increase in hgb 2-3 weeks - max iron dose is 200 mg/day |
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what can cause inadequate response to oral iron? |
- intolerance/ noncompliance - persistent blood loss - decreased iron absroption - chronic inflammation or bone marrow damage - chronic kidney disease |
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what are the three parenteral iron fomulations? |
- iron dextran (InFed) efficient high dose single day reatment risk of allergy and anaphylaxis - iron sucros (venofer) treatment spaced over weeks little risk of allergy pregnancy category B - ferumoxytol (feraheme) rapid infusion of intermediate doses of iron little risk of allergy |
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serious IV iron reactions what are the three syndromes? |
1) anaphylaxis or anaphylactoid reaction 2) labile iron reaction 3) intolerance reaction |
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anaphylaxis or anaphylactoid reaction |
sensitivity reaction marked by allergic manifestations hypotension with dyspnea, chest pain, angioedema, or urticaria
immediate, sudden, severe, usually with test dose or 1st dose |
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labile iron reaction |
crampy pain, hypotension non-allergic, commonly dose related |
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intolerance reaction |
- presumed sensitivity reaction of any kind, may not be anaphylactic, taste disturbance, flushing - incidence of adverse reactions increases with underlying autoimmune disease or infection |
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anemia of chronic disease |
normocytic, normochromic, common - can become hypochromic, microcytic over time - occurs in people with inflammatory conditions such as collage vascular disease, malignancy, or chronic infection - develops over 1-2 months - iron replacement is not necessary - may benefit from erythropoietin supplementation - non-profressive - WBC, platelets normal or increased |
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anemia of chronic disease: pathophysiology |
- cytokine effects - retriculocytopenia - anemia - DNA & RNA iron response elements DECREASE - erythropoietin responsiveness (& production) - transferrin synthesis - iron mobilization from macrophages - iron reutilizationin erythropoiesis - serum iron despite adequate stores
INCREASE in serum ferritin
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anemia of chronic disease: causes |
- thyroid disease - collagen vascular disease: rheumatoid arthritis, lupus, polymyositis, polyarteritis nodosa - inflammatory bowel disease: ulcerative colitis, crohn's disease - malignancy - chronic infectious diseases: osteomyelitis, tuberculosis - familial mediterranean fever - renal failure |
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characteristics of anemia of chronic disease |
- immune driven by inflammatory cytokines - diversion of iron into RE system and decreased iron absorption - blunted erythropoietin response |
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typical labs for anemia of chronic disease ** ask parameter, anemia of chronic disease response, iron deficiency anemia
serum iron TIBC % saturation ferritin |
serum iron: reduced in both TIBC: chronic reduced to normal, iron increased % saturation: reduced in both ferritin: chronic normal- increased, iron is reduced |
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anemia of chronic disease from underlying kidney disease |
- normochromic, nomocytic - low reticulocyte count - frequently the peripheral smear in uremic patients show "burr cells" or echinocytes - target hemoglobin for patients on dialysis is 11-12 administer erythropoietin or darbopoietin weekly good iron stores must be maintained |
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treatment options for anemia of chronic disease and kidney disease |
- RBC transfusions - erythroid stimulating agents (ESA) erythropoietin alpha darbepoetin - iron supplementation |
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adverse events associated with ESAs* is this important? |
CKD: increased risk of death, serious cardiac events, stroke with target Hgb cancer: anemia with chemo: shortened overall survival and/or increased risk of tumor progression and recurrence increased serious cardiac events MI, stroke, CHF, vascular access thrombosis |
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causes of B12/folate anemia (pernicious anemia) * how much detail? |
inadequate intake, rare impaired absorption intraluminal consumption in the small intestine increased demand drugs |
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Anemia due to cobalamin (vit b12) deficiency what kind of anemia? common lab values patho? what does a smear show? |
vit b12 water soluble vitamin, is needed for DNA synthesis - macrolytic anemia lab values: - cobalamin level <200 pg/mL, tx before 350 - elevated serum methylmonic acid - elevated serum homocystein binds to intrinsic factor in the small bowel to be absorbed- pernicious anemia: antibodies to instrinstic factor, dx by checking antibody levels (rather than schilling test)
deficiency can result in neuropsychiatric symptoms: spastic ataxia, psychosis, dementia
smear shows macrocytosis w/ hypersegmentaition of polymorphonuclear cells, possible basophilic strippling |
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what is needed for cobalamin absorption? |
intrinsic factor |
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what are the causes of cobalamin deficiency |
- GI mucosa not screting IF - GI surgery > loss of IF secreting gastric mucosal cells - long term use of h2 histamine receptor blockers cause atrophy or loss of gastic mucosa - nutritional deficiency - hereditary defects of cobalamine utilization |
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clinical manifestations |
- general symptoms of anemia - sore tongue -anorexia - weakness - parathesias of feet and hands - altered thought processes, confusion >> dementia |
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treatment of Vit B12 deficiency |
vt B12 - 1000 micrograms IM monthly vit B12 100-200 micrograms PO daily |
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folate deficiency what kind of anemia common lab values |
macrocytic anemia lab values - low folate - increased serum homocystine - normal methylmalonic acid |
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folate deficiency when does it often occur? what does the smear show? |
decreased oral intake, increased utilization or impaired absorption of folate
- folate is absorbed in the duodenum and proximal jejunum, deficiency is found in celiac disease, regional enteritis, amyloidosis - defiency in alcoholics bc enzyme required for deglutamation of folate is inhibited by alcohol - deficiency often found in pregnant women, persons with desquamating skin disorders, patients with sickle cell anemia (and other conditions associated with rapid cell division and turnover)
smear shows macrocytosis with hypersegmented neutrophils |
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folic acid deficiency clinical manifestations |
similar to cobalamin deficiency insidious onset: progress slowly
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folic acid deficiency treatment |
encourage pt to eat foods with large amounts of folic acid - leafy green veggies - liver - mushrooms -peanut butter - red beans
treat with folate replacement therapy 1-5 mg po daily |
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comparison of features of Vit B12 and folic acid deficiency states
1) nutritional deficiency 2) onset 3) absorption 4) neurological lesions |
1) nutritional deficiency common in folate, not in cobalamin 2) onset slow for cobalamin and weeks in folate deficiency 3) drug related in folate deficiency (anti convulsant therapy, anti metabolities) but never in cobalamin 4) frequent neurological lesions in cobalamin b12 but none in folate |
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anemia due to destruction of red blood cells what are the top 3 big causes? |
- hemoglobinopathies (sickle cell anemia) - aplastic anemia: decrease in all lines of cells - hemolytic anemia hemoglobin hematocrit WBC platelets parvovirus B19, EBV, CMV acquired aplastic anemia
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sickle cell disease |
inherited, lifelong condition of the red blood cells that can effect every organ system in the body and result in early mortality - variable clinical severity/phenotype
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sickle cell clinical findings |
- pallor of mucus membrane - fatigue - decreased exercise tolerance - jaundice - gallstone formation - leg ulcer - priapism - repeated episodes of pulmonary infarction - pulmonary hypertension - stroke - seizures - heart failure |
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sickle cell lab findings |
- mild to moderate anemia - reticulcytosis - elevated total bilirubin - elevated serum lactate dehydrogenas - low serum haptoglobin - peripheral blood smear will show sickled red cells, polychromasia indiciative of reticulocytisis, howell-jolly bodies |
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sickle cell management |
infection control and prophylaxis routine treatments and evals - hydroxyurea - hydration - pain management: inpatient and outpatient - transfusion therapy Hgb< 7 g/dL - new study: viagra |
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aplastic anemia characterized by? |
characterized by panocytopenia decrease of all blood cell types, RBCs, WBCs, platelets hypocellular bone marrow |
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aplastic anemia etiology |
- congenital: chromosomal alterations - acquired: results from exposure to ionizing radiation, chemical agents, viral and bacterial infections - manageable with erythropoietin or blood transfusion 0 can be critical: hemorrhage, sepsis |
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aplastic anemia clinical manifestations |
gradual development symptoms caused by suppression of any or all bone marrow elements - general manifestations of anemia |
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aplastic anemia diagnosis |
blood tests: CBC bone marrow biopsy |
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aplastic anemia treatment |
identify cause blood transfusion antibiotics immunosuppressants (neoral, sandimmune) corticosteroids (medrol, solumedrol) bone marrow stimulants filgrastim, epoetin alfa bone marrow transplantation |
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hemolytic anemia |
hereditary spherocytosis glucose 6 phosphate dehydrogenase (G6PD) thrombotic thrombocytopenic purpura hemolytic uremic syndrome autoummune hemolytic anemia infections trauma |
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hemolytic anemia lab analysis |
- increased indirect bilirubin - increased LDH - increased reticulocyte count (normal 0.5-1.5%) >3% sign of increased reticulocyte production, suggestive of hemolysis - reduced or absent haptoglobin <25 mg/dL suggest hemolysis |
