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80 Cards in this Set
- Front
- Back
Define anemia.
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A reduction in the total number of RBCs, amount of Hb in the circulation, or circulating RBC mass
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General causes of anemia?
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1. decreased RBC production
2. increased RBC destruction or loss |
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What is the physiologic result of anemia?
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Impaired oxygen delivery gives rise to physiologic consequences secondary to tissue hypoxia as well as compensatory mechs to correct anoxia
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Criteria for anemia in adults?
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RBC x 10(12)/L <4.0 <4.5
Hb (g/dl) <12 <14 Hct (%) <37 <40 |
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Compare and contrast normocytic, microcytic, and macrocytic RBCs.
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Based on Mean Corpuscular Volume (MCV) --
normocytic: 80-100fl microcytic: <80fl macrocytic: >100fl |
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What is RDW?
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Red cell distribution width.
-- a measure of RBC size variability, or ANISOCYTOSIS -- anemic d/o's can be classified on the basis of RDW |
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When is RDW more often elevated?
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Iron deficiency anemia
(less likely in thalassemia or anemia of chronic disease) |
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What is RPI? What does it measure?
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Reticulocyte count/Retic productions index
-- percentage of total RBCs that are reticulocytes Measures: bone marrow productivity |
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What are reticulocytes?
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young RBCs, newly produces
-- distinguishable by their gray-pink color on smears -- show a network (reticulum) of blue granules when stained w/ special stains like Methylene Blue |
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Symptoms of slow anemia vs. acute anemia?
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SLOWLY -- few symptoms since the homeostatic mechs provide remarkable adaptation
ACUTE -- weakness, fatigue, palpitations, lightheadedness |
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Blood loss in a "typical" menstrual cycle?
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45-50ml
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What drugs may induce BM suppression? Hemolytic anemia? GI bleeding?
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PREDICTABLE BM SUPPRESSION: cancer chemo drugs
IDIOSYNCRATIC BM SUPPRESSION: chloramphenicol HEMOLYTIC ANEMIA: penicillin GI BLEEDING: ASA, NSAIDs, recreational drugs |
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Name some concurrent illnesses in which pts may experience anemia
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chronic infections
inflamm disease malignancies HIV renal or hepatic failure endocrine d/o's |
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How can eating habits cause anemia?
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1. Folic acid deficiency due to poor dietary intake
-- anorexia assoc w/ cancer -- elderly w/ severe depression -- alcoholics w/ hx of binge drinking 2. post gastrectomy pts w/ achlorhydria -- develop vitamin B12 malabsorption although anemia may take years to develop 3. food picas |
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What are the classic symptoms of anemia? Other indicators?
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weakness
fatigue dyspnea palpitations dizziness -- jaundice and dark urine are indicators of hemolysis -- dysphagia may be sign (esophageal webs) -- gait or balance difficulties may signify the neuro disorder assoc w/ pernicious anemia |
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What are the classic physical finding with anemia?
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pallor (skin, mucous mbrns)
tachycardia postural hypotension palmar creases appear pink in fully opened hand unless Hb is <7gm/dl -- useful guide to presence of severe anemia |
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What skin and mucous mbrn findings w/ anemia?
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IRON DEFICIENCY
-- tongue can be devoid of papillae and sore -- koilonychia (spoon shaped fingernails) PERNICIOUS ANEMIA -- jaundice - "lemon yellow" tint due to simultaneous pallor and jaundice -- can also have tongue completely devoid of papillae that is often also sore ACUTE LEUKEMIA -- gingival hypertrophy LEAD POISONING -- dark line of lead sulfide deposited in gums and at base of teeth |
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CV findings w/ anemia?
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tachycardia
postural hypotension flow murmurs |
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Spleen findings w/ anemia?
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may be enlarged concomitantly w/ anemia due to:
-- primary hematologic disease - lymphoma, leukemia, autoimmune hemolytic anemia -- secondary to infection, inflammation |
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Liver findings w/ anemia?
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Exam liver size and for stigmata of chronic liver disease:
spider angiomata, gynecomastia, palmar erythema, testicular atrophy, caput medusae |
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Neurologic findings w/ anemia?
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Vitamin B12 deficiency impairs:
central olfactory spinal cord peripheral n fxn (especially vibratory and proprioception) Severe chronic deficiency may lead to irreversible neuro dysfxn |
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List causes of hypochromic microcytic anemia.
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MCV < 80fl
iron deficiency thalassemias lead poisoning chronic disease sideroblastic anemia |
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Blood smear cells seen in iron deficiency?
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pencil (cigar) cells
high RDW sometimes thrombocytosis |
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Typical labs of iron deficiency anemia?
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↓ iron
↑ TIBC Fe/TIBC < 10% ↓ ferritin Confirm if necessary w/ BM stores (absent in iron deficiency) |
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Blood smear cells seen with thalassemias?
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target cells
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Typical labs of thalassemias?
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confirm presence of target cells w/ Hb electrophoresis
high A2 ± F hemoglobins for B thalassemias |
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Blood smear cells seen w/ lead poisoning?
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course basophilic stippling
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Typical labs of lead poisoning
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Confirm w/ lead level, free erythrocyte protoporphyrin
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Blood smear cells seen w/ anemia of chronic disease.
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More are normochromic
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Typical labs of anemia from chronic disease?
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↓ Fe
↓ TIBC Fe/TIBC > 15% ↑ ferritin BM iron stores increased and present in RE cells |
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Blood smear cells seen w/ sideroblastic anemia?
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ringed sideroblasts demonstrated by Prussian Blue staining of BM RBC precursors
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Typical labs seen w/ sideroblastic anemia?
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↑ Fe
nl TIBC ↑ Fe/TIBC ↑ ferritin |
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List list causes of macrocytic anemia.
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MCV > 100fl
B2/folic acid deficencies Liver disease Cancer chemotherapy |
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Blood smear of B12/folic acid deficiency would show?
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pancytopenia
macroovalocytes hypersegmented PMNs |
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Typical labs of B12/folic acid deficiency?
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↓ serum B12, RBC folate
↑ indirect bilirubin ↑ LDH ↑ uric acid ↑ serum iron ↑ Fe/TIBC Helpful test to confirm PERNICIOUS anemia is anti-IF antibody -- highly specific but only positive in 75% |
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Treatment of B12/folate deficiency anemia?
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usually responds rapidly and dramatically to B12 or folate
Schilling test best done 6-8 wks after B12 replacement to correct malabsorption due to megaloblastic GI epithelium |
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Blood smear of liver disease would show?
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macrocytosis secondary to abnormal lipid composition in the RBC membrane
round macrocytes (as opposed to oval in B12/folate) may also see target and/or spur cells (acanthocytes) |
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Blood smear of cancer chemo would show?
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many cytotoxic drugs or antimetabolites used in chemo drugs impair DNA synth and produce a defect in hematopoiesis that resembles B12 or folate deficiency
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Polychromasia/polychromatophilia?
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reticulocytes
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Target cells?
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liver disease
hemoglobinopathies post-splenectomy |
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Microspherocytes?
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autoimmune hemolytic anemia
hereditary spherocytosis |
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Shistocytes?
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fragmented RBCs seen in fragmentation hemolysis:
TTP DIC cardiac valve hemolytic anemia malignant HTN massive venous thromboembolism |
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Teardrops?
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bone marrow infiltration:
- tumor - infection (granulomas) - fibrosis |
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Leukoerythroblastic blood smear?
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refers to presence of both immature WBC and nucleated RBCs, often accomp by teardrop-shaped RBCs
-- correlates w/ highly infiltrative process of the bone marrow |
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Howell-Jolly bodies?
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nuclear remnants seen in post-splenectomy patients
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Sickle cells?
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sickle cell anemia
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Rouleaux formation?
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"Rouleaux" are stacked RBCs caused by coating individ cells by charged proteins that neutralize the normally negative charge that by repulsion keeps RBCs from agglutinating
-- multiple myeloma when RBCs become coated by the + charged paraproteins |
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Describe how RPI classifies anemias.
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RPI ≥ 2 favors destruction problem
RPI ≤ 2 favors production problem |
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Laboratory parameters of hemolysis include?
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↑ indirect bilirubin
↑ LDH ↓ haptoglobin **haptoglobin can be low in liver disease where the problem is decreased synth, NOT hemolysis ** ineffective erythropoiesis seen in megaloblastic anemias can produce same chemical abnormalities so one must always have in mind clinical context |
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What does the Coombs test measure?
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Antibodies bound to the RBC surface
-- direct Coombs test is (+) in autoimmune hemolytic anemia and hemolytic transfusion rxns |
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Disorders assoc w/ decreased production of RBCs?
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renal failure
chronic diseases (infection, inflamm, malignant) nutritional deficiencies myelodysplasia ("pre-leukemia") aplastic anemia/pure red cell aplasia endocrine d/o's (thyroid, pituitary) |
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Disorders assoc w/ increased destruction of RBCs?
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hemolytic transfusion rxn
infections immune hemolysis RBC fragmentation Hereditary spherocytosis Hemoglobinopathies Hypersplenism RBC enzyme defects PNH Miscellaneous (burns, drowning) |
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Clinical use of blood transfusions?
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RBC transfusion is always symptomatic and supportive rather than definitive therapy for anemias
-- only use when no definitive trtmt for the underlying cause OR when severity and clinical manifestations deem necessary **signif risks incl allosensitization, transfusion rxns, infection transmission, iron overload |
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Iron deficiency may occur as a result of...?
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inadequate dietary intake
-- almost exclusively problem of infants and children and of pregnancy and lactation malabsorption (duodenal) chronic blood loss OR combination of above |
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In an adult, Fe deficiency is almost always assoc w/...?
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blood loss
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In pregnancy, the avg iron loss totals about...?
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900mg
diversion of Fe to fetus, blood lost at delivery and lactation |
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Preferred mode of iron therapy?
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oral route -- most economical, highest dosage, most safely, in readily assimilated form (ferrous sulfate FeSO4)
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Approp dose of oral iron prep?
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should provide 150-200mg of elemental iron/day
Usually 3-4 tablets per day Ex: one 320mg FeSO4 tablet contains 66mg elemental Fe |
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How soon can we achieve normal RBC parameters after beginning treatment?
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usually after 6 wks (if no concurrent blood loss)
continue therapy for 4-6mos to ensure full replacement of total body iron stores |
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When is parenteral iron indicated?
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rarely indicated
- patients whoh cannot absorb oral iron - patients unable to follow instructions or comply w/ oral therapy **frequency of systemic rxns high |
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Approach to megaloblastic anemia?
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pending definitive dx, empiric B12 and folate therapy can be initiated w/o harm
Once dx established, consider possible etiologies. |
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Etiologies of B12 deficiency?
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Nutritional - vegans
Pernicious anemia Post-gastrectomy Malabsorption -- bacterial overgrowth -- D.latum fish tapeworm -- pancreatic insuff -- tropical/nontropical sprue -- Crohn's, intestinal lymphoma -- transport d/o's -- metabolic d/o's (rare) |
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Etiologies of folate deficiency?
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nutritional causes
-- decreased intake -- increased requirement: pregnancy, lactation, hemolysis malabsorption |
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Describe the B12 treatment.
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1. daily injections of 100μg for 5-7 days THEN
2. weekly injections for 3-4 weeks THEN 3. 1000μg monthly for life Correction is rapid: BM abnormalities corrected w/in 24-72h and reticulocytosis occurs by 4-6d Rapid reversal of ineffective erythropoiesis by B12 causes rapid cellular uptake of K and may result in severe hypokalemia -- monitor levels Reversal of neuro manif is unpredictable and variable; persisting >6mos likely permanent |
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Describe the folate treatment.
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oral folic acid 1mg daily
course of response similar to B12 deficiency duration depends on clinical situation |
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What if pt does not respond to B12 or folate?
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evaluate for concurrent iron deficiency
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What is DIC?
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Disseminated Intravascular Coagulation
-- occurs when coag system is activated by generation of excessive thrombin in the circulation Catastrophic bleeding d/o characterized by: -- depletion of procoag factors -- thrombocytopenia -- activation of fibrinolytic system |
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Causes of DIC?
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obstetrical complications
- retained dead fetus - absorption placentae - amniotic fluid embolism septic shock trauma cancer |
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How is DIC anemia characterized?
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fragmentation hemolysis
-- schistocytes present in circulation |
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DIC Dx?
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Prolonged PT, PTT, and TT
Presence of fragments of cross-linked fibrinogen (d-dimer) in circulation Presence of fibrin/fibrinogen fragments (fibrin degradation products, FDP) in circulation |
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DIC Tx?
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address underlying cause
supportive care of blood, platelets, plasma transfusion |
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What is TTP?
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Thrombotic thrombocytopenic purpura
Characterized by: -- microantiopathic hemolytic anemia (fragmentation hemolysis) -- thrombocytopenia -- fever -- renal manifest -- neuro manifest May present as isolated syndrome or can be assoc w/ infection, malig, meds, vasculitis, preggers, etc. |
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Pathogenesis of TTP?
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related to absence of vWF cleaving protease activity
-- abnormally large vWF multimers in circulation -- platelet hyperaggregability |
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TTP Dx?
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clinical picture
hemolysis w/ plentiful schistocytes coag studies are NORMAL |
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TTP Tx?
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plasma exchange -- removes unusually large vWF multimers and provides missing protease activity
corticosteroids **platelet transfusions CONTRAINDICATED b/c can contribute to disease progression |
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What is AIHA?
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Autoimmune hemolytic anemia
-- may be primary (25%), secondary (60%) or drug induced -- secondary assoc w/ systemic immunologic d/o's like SLE, cancer, or infection |
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Pathogenesis of AIHA?
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binding of autoantibodies ± complement to the RBC surface and destruction of coated RBCs in the spleen
-- 75% of RBC autoantibodies are IgG and react w/ RBC at 37C (warm autoantibodies) -- 25% are IgM and react at temps <37C (cold agglutinins) |
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Characteristic cell of AIHA?
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microspherocyte
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Warm agglutinin AHIA Tx?
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directed toward eradication of autoantibody and/or reduction of RBC rate of destruction
1. corticosteroids (DOC) -- 75% respond, but half relapse when tapered off 2. splenectomy (TOC) for pts who fail (1) -- removes major site RBC destruction and source of autoAb production -- 2/3 have beneficial response to splenectomy 3. Fail to respond to (1) and (2) -- try other immunosuppressive agents, macrophage poisons, RE blockade w/ IV Ig -- use of synth androgen, danazol, may prove useful |
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Cold agglutinin AHIA Tx
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frequently have assoc malignancies or infect diseases
-- direct Tx toward underlying dz **corticosteroids and splenectomy are relatively ineffective **cold avoidance may be addtnl impt aspect of dz management |