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| 5179880851 | Macrocytic anemia | 0 | ||
| 5179916977 | Reticulocyte count is an indication of the function of what? | bone marrow | 1 | |
| 5179920302 | Reticulocytosis definition | immature RBC pushed out of bone marrow a few days early | 2 | |
| 5179923291 | Mechanisms causing macrocytic anemia (large RBCs >100 MCV) | - Abnormalities in DNA metabolism - Shift to immature cells - Bone marrow disorder - Lipid abnormalities - Unknown mechanism | 3 | |
| 5179925928 | Macrocytic anemia is defined by what value of MCV? | >100 fl | 4 | |
| 5179926786 | Megaloblastic anemia is defined by what value of MCV? | >115 fl | 5 | |
| 5179926796 | What are some common causes of macrocytic anemia? | - reticulocytosis - alcoholism - liver disease - hypothyroidism - medication effect - aplastic anemia | 6 | |
| 5179929723 | What are some common causes of megaloblastic anemia? | - vitamin B12 deficiency - folic acid deficiency | 7 | |
| 5179937632 | What is the most common anemia found in alcoholics? | Macrocytic anemia - 90% of alcoholics have MCV 100-110 fL | 8 | |
| 5180030323 | Macrocytic anemia can be caused by the effect of what medication therapy? | combination antiretroviral therapy for HIV | 9 | |
| 5180041722 | Myelodysplastic syndromes (MDS) is due to a problem with what? | bone marrow itself (myeloid = bone marrow, dysplasia = ineffective production of all blood cells) | 10 | |
| 5180043984 | MDS results in what reticulocyte response? | inappropriately low reticulocyte response | 11 | |
| 5180044713 | MDS causes what type of anemia | macrocytic anemia | 12 | |
| 5180123568 | Aplastic anemia definition | Bone marrow can't produce any blood components - pancytopenia --- platelets, RBC, and WBC lines are low - it is a type of bone marrow failure, but not all bone marrow failure = aplastic anemia | 13 | |
| 5180131022 | Aplastic anemia is due to an injury to: | *Pluripotent stem cell | 14 | |
| 5180131763 | The mechanism of aplastic anemia is | injury to pluripotent stem cell -> impairs proliferation and differentiation ->*induces T-cell mediated autoimmune response - "idiopathic" | 15 | |
| 5180138901 | Causes of aplastic anemia include what three categories? | Acquired autoimmune congenital | 16 | |
| 5180149794 | Acquired causes of aplastic anemia | - radiation and chemotherapy - *toxins (benzene, solvents, glue vapors) - *viral infections (EBV, hepatitis, HIV, herpes) - *drugs (carbamazepine, phenytoin, sulfonamides, chloramphenicol, indomethacin, methimazole, propylthiouracil, gold - immune disorders - *pregnancy - *anorexia | 17 | |
| 5180150552 | autoimmune causes of aplastic anemia | *idiopathic SLE | 18 | |
| 5180163759 | congenital causes of aplastic anemia | - *Faconi anemia -- defect in DNA repair pathway - dyskeratosis congenita - defect in maintenance of hematopoietic stem cell telomere length maintanence | 19 | |
| 5180167401 | Steps leading up to aplastic anemia: | 1) inciting event 2) aberrant immune response 3) destruction of hematopoietic stem cells 4) clinical disease | 20 | |
| 5180176159 | Clinical presentation of aplastic anemia | - weakness and fatigue - *cardiopulmonary compromise - progressive anemia - mucosal bleeding, skin bleeding, petechiae - infection: --- bacterial, sepsis, pneumonia, UTI --- invasive fungal infection (common cause of death) | 21 | |
| 5180180646 | Most common presentations of aplastic anemia include: | - Recurrent infections d/t profound neutropenia - mucosal hemorrhage d/t thrombocytopenia - increased menstrual flow in premenopausal women | 22 | |
| 5180188472 | Physical exam of aplastic anemia: | generally not helpful - should see pallor, petechiae, purpura - should NOT see: --- hepatosplenomegaly, lymphadenopathy, bone tenderness ^ these are associated with bone cancers. the cells are normal, just very low numbers so won't see hepatosplenomegaly (not recycling defective cells) | 23 | |
| 5180196413 | Aplastic anemia lab studies | CBC: - *PANCYTOPENIA, anemia can be severe Peripheral smear - RBCs normocytic, may be macrocytic - decreased or absent polychromatophilic RBCs - cellular elements -> reduced in number, morphology normal - abnormal cells are NOT present *reticulocyte index/count decreased (d/t stem cell destruction --> decreased production of blood components) | 24 | |
| 5180216489 | Aplastic anemia differential diagnosis criteria: | ***PANCYTOPENIA withOUT prominent splenomegaly - if splenomegaly is present, probably not aplastic anemia | 25 | |
| 5180220605 | Diagnostic criteria for moderate aplastic anemia: | - Bone marrow cellularity <30% - absence of severe pancytopenia - depression of at least two of three blood elements below normal | 26 | |
| 5180229473 | Diagnostic criteria for SEVERE aplastic anemia (SAA): | - bone marrow biopsy showing <25% of normal cellularity OR - bone marrow biopsy showing <50% normal cellularity WITH --- <30% of the cells are hematopoietic (producing blood cells) AND --- at least two of the following are present (1) absolute reticulocyte count <40,000/microL (2) absolute neutrophil count (ANC) <500/microL (3) platelet count <20,000/microL | 27 | |
| 5180251211 | Diagnostic criteria for very severe aplastic anemia (VSAA): | criteria for SAA are met with: - absolute neutrophil count (ANC) <200/micoL | 28 | |
| 5180276409 | Essentials for diagnosis of Aplastic Anemia | - Pancytopenia - no abnormal hematopoietic cells in circulation or in bone marrow - hypocellular bone marrow | 29 | |
| 5180277861 | Aplastic anemia treatment (general) | - treat specific congenital causes or MDS - treat underlying cause - manage cytopenias - infection treatment and prevention - therapy is stratified based on age and disease of severity | 30 | |
| 5180280992 | Treatment of mild-moderate aplastic anemia | - supportive care -erythropoietic growth factors (epoetin or darbepoietin) - myeloid growth factors (filgrastim or sargramostim) - transfusions - antibiotics or antifungals for infection - monitor closely for improvement or decline | 31 | |
| 5180424443 | Treatment of severe aplastic anemia | Allogenic hematopoietic stem cell transplant (HCT) (bone marrow transplant) - treatment of choice in children <20 y/o with HLA matched sibling/donor - Preferred treatment in adults 20-50 y/o with HLA matched donor Immunosuppressive therapy (IST) - adults >50 y/o or no HLA matched donor - consider in adults 20-50 y/o with severe comorbidities overall, if under 50, look at for bone marrow transplant (HCT), if over 50, consider immunsuppressive therapy | 32 | |
| 5180465211 | Immunosuppressive therapy for severe aplastic anemia: | suggested regimen: horse antithymocyte globulin (ATG) plus cyclosporin A (CsA) | 33 | |
| 5180471623 | Prognosis of aplastic anemia | untreated -> 70% 1 year mortality rate SAA = rapidly fatal if untreated survivability rates 80-90% if treated | 34 | |
| 5180480386 | Faconi anemia is the most common cause of | congenital aplastic anemia | 35 | |
| 5180484001 | Faconi anemia is due to | - autosomal recessive disorder - defect in DNA repair pathway | 36 | |
| 5180487307 | Faconi anemia results in | severe congenital abnormalities, progressive bone marrow failure, and increased incidence of malignancies - 60% of children present with a physical abnormality --- Syndaptoli = digits fused, common sign | 37 | |
| 5180494381 | Fanconi anemia management | supportive modalities - androgens (male sex hormone) and hematopoietic growth factors can achieve a transient improvement in hematopoietic fx | 38 | |
| 5180503306 | The only treatment option that can restore normal hematopoiesis in pt with fanconi anemia is | allogeneic hematopoietic cell transplantation (HCT) | 39 | |
| 5180506628 | Megaloblastic anemia include what types of deficiencies? | Vitamin B 12 and Folate deficiencies | 40 | |
| 5180508572 | Megaloblastic anemia classic advanced case presents: | severe anemia macrocytic red cells with or w/o varying neurologic disturbances (seen in vit B12 deficiency, not in folate deficiency) | 41 | |
| 5180513137 | Megaloblastic anemia has MCV of: | >110 fL | 42 | |
| 5180514284 | Megaloblastic anemia RBCs present as | macroovalocytic (oval in shape) | 43 | |
| 5180548978 | Neutrophils in megaloblastic anemia present as | hypersegmented (several nucleus segments in neutrophil [usually 3-4, hypersegmented = 6 or more]) | 44 | |
| 5180517999 | Bone marrow in megaloblastic anemia presents showing | - erythroid hyperplasia (excessive growth of immature RBCs) - megaloblastic morphology | 45 | |
| 5180527274 | Most common cause of megaloblastic anemia are | - faulty preparation of foods (such as vegans, not enough vit B12 in diet) - folate deficiency in pregnancy | 46 | |
| 5180531494 | Clinical history and symptoms of vitamin B12 deficiency | Unexplained neurologic signs and symptoms - dementia or weakness - sensory ataxia (loss of coordination) - paresthesia (pins and needles) | 47 | |
| 5180535011 | Higher risk population of B12 and folate deficiency | - older adults - alcoholics - patients with malnutrition - bariatric surgery pts | 48 | |
| 5180536157 | Lab findings in vitamin B12 and folate deficiency | - macroovalocytes (large oval cells) - MCV > 100 fL with or without anemia - hypersegmented neutrophils (several nucleus segments in neutrophil [usually 3-4, hypersegmented = 6 or more]) - pancytopenia of uncertain cause | 49 | |
| 5180613122 | How long does the body store vitamin B12 (aka cobalamin, Cbl)? | ~3 years, therefore if suffering from vit b12 deficiency, must be chronic or ongoing for a long time | 50 | |
| 5180618452 | Vitamin B12 absoprtion process | Intrinsic factor (IF) produced by *parietal cells in stomach -*IF is required for absortion of B12 - vit B12 and IF complex is absorbed in the *terminal ileum | 51 | |
| 5198080827 | Where is vitamin B12 and IF absorbed? | ** terminal ileum | 52 | |
| 5180629245 | vit B12 and Folic acid function in the body (3): | nucleic acid metabolism myelin synthesis Critical DNA synthesis & regulation - *** DNA synthesis of hematopoietic cells | 53 | |
| 5180635008 | Causes of vitamin B12 deficiency | - dietary deficiency (rare) - inadequate intrinsic factor - pancreatic insufficiency - Ileal disease (crohn's) - competition for vitamin B12 in gut - medications that block absorption | 54 | |
| 5180644781 | Pernicious anemia definition | autoimmune disease where antibodies destroy gastric parietal cells, and binds to and neutralizes IF | 55 | |
| 5180644782 | How does pernicious anemia relate to vitamin B12 deficiency? | Vit B12 absorption requires IF, produced by gastric parietal cells. - pernicious anemia autoimmune dx destroys these needed components, thus decreasing Vit B12 absorption -> megaloblastic anemia, and neurologic symptoms | 56 | |
| 5180654522 | Signs and symptoms of Vit B12 deficiency | - relative to severity of anemia - glossitis (soreness/inflammation of tongue) - vague GI disturbances - *NEUROLOGIC syndrome --- peripheral nerves affected first -> distal/peripheral paresthesia (pins/needles) --- difficulty with balance and proprioception (body awareness in space) --- altered cerebral fxn | 57 | |
| 5180668792 | Physical exam of vit B12 deficiency: | - pale - mildly icteric or sallow (jaundice-like, yellow) - atrophic glossitis - neuro exam: decreased vibration, decreased position sensation (proprioception), memory disturbance | 58 | |
| 5180674074 | Lab findings in vit B12 deficiency** | CBC: - Macrocytic anemia (can be severe) - HCT as low as 10-15% - MCV 110-114 fL - Megaloblastic picture - Pancytopenia (leukopenia and thrombocytopenia in severe cases - low reticulocyte index - serum B12 (cobalamin) level low (<170pg/ml) | 59 | |
| 5180690356 | Schilling test, has limited value, but can be used to test for | testing what is causing vitamin B12 deficiency | 60 | |
| 5180708184 | Schilling test steps | 1) give pt radiolabeled B12 orally + intramuscular unlabeled B12 2) radiolabeled B12 will not be able to bind to liver cuz of saturation by IM B12 3) wait 24-48 hours and measure pts urine for radiolabeled B12 4) if increased radiolabeled B12 in urine, then this means it was ingested, metabolized, and absorbed in GI (normally absorbed, no pathology, therefore dietary deficiency) 5) if decreased radiolabeled B12 in urine, then absorption problem 6) give the patient radiolabeled B12 + intrinsic factor, and two things will happen, either increased in RL B12 or decreased in RL B12 in urine. 7) If increased, then RL B12 was absorbed in GI, and cause is pernicious anemia -> attacks parietal cells -> decrease IF 8) if decreased RL B12 in urine, then there is no dietary deficiency, and no intrinsic factor deficiency | 61 | |
| 5180745541 | Essentials of Diagnosis for Vit B12 deficiency: | macrocytic anemia megaloblastic blood smear - (macro-ovalocytes and hypersegmented neutrophils) Low serum B12 level | 62 | |
| 5180749087 | Treatment of vit B12 deficiency: | parenteral therapy: - vit B12 100mcg SC or IM - daily x1 week, then weekly x 1 month, then monthly for life oral therapy: - methylcoabalamin 1 mg daily - sublingual or oral indefinitely concurrent tx for folic acid deficiency: - folic acid 1 mg PO daily - treat for 1-4 months of vitamin B 12 replacement | 63 | |
| 5180759488 | Expected response with vitamin B12 treatment | - immediate improved sense of well being - hypokalemia possible in first days of therapy - reticulocytosis 5-7 days - hypersegmented neutrophils disappear after 10-14 days - hematologic picture normalizes in 2 months - neurologic symptoms may persist --- only reversible if short duration (<6 months of vit B12 deficiency) CBC starts to turn around at 1-2 weeks, and normalizes at 2 months so do CBC at 1-2 weeks and at 2 months | 64 | |
| 5180777384 | Folic acid (pterolymonoglutamic acid) is found where? | present in most fruits and vegetables | 65 | |
| 5180780515 | Body stores how much of folic acid? | 5 mg, which is equivalent to 2-3 months of regular body requirement | 66 | |
| 5180782786 | Folic acid is absorbed where? | entire GI tract (duodenum and jejunum) | 67 | |
| 5180787977 | Causes of folic acid deficiency | - **MOST COMMON = Inadequate dietary intake - **alcohol abuse - reduced absorption (rare) - increased requirement - excess loss - medications | 68 | |
| 5180797078 | Alcohol abuse and folic acid deficiency: | - alcoholics have lower folic acid stores - decreased serum folate 2-4 days d/t impaired enterohepatic cycle -> inhibiting absorption | 69 | |
| 5180802439 | Signs and symptoms of folic acid deficiency | - Relative to severity of anemia - Glossitis - vague GI disturbances - *NO NEUROLOGIC SYMPTOMS | 70 | |
| 5180806204 | Physical exam of folic acid deficiency | - pale - mildly icteric or sallow (jaundice like) - atrophic glossitis - NEURO EXAM: NORMAL | 71 | |
| 5180808697 | Lab findings of Folic Acid deficiency: | CBC: - macrocytic anemia - can be severe - Hct as low as 10-15% - MCV 110-140 fL - megaloblastic picture - pancytopenia (leukopenia and thrombocytopenia in severe cases) - low reticulocyte index - serum B12 (cobalamin) level NORMAL (>210 pg/ml) - RBC folic acid level low (<150 ng/ml) | 72 | |
| 5180834678 | Essentials of diagnosis for Folic acid deficiency | Macrocytic anemia Megalobalstic blood smear - (macro-ovalocytes and hypersegmented neutrophils) reduced folic acid levels in red blood cells or serum normal vitamin B12 level | 73 | |
| 5180840272 | Treatment of folic acid deficiency: | Folic acid 1 mg PO daily for 1-4 months or hematologic recovery - continue therapy if underlying condition cannot be eradicated (congenital hemolytic anemia) | 74 | |
| 5180843430 | Expected response from treatment of folic acid deficiency: | - Rapid improvement with sense of wellbeing in 5-7 days - reticulocytosis in 5-7 days - normalization of hematologic abnormalities within 2 months - ENSURE no concomitant vitamin B12 deficiency | 75 | |
| 5180852989 | Vitamin B12 and folate overview slide pg 41 notes print | 76 |
