Clin Med/ Pathophys & Diagnostic/Lab methods Flashcards
microcytic iron deficiency anemia etiology
caused by bleeding unless proved otherwise. can be: deficient diet, decreased absorption increased requirements, chronic blood loss, hemoglobinuria , iron sequestration, idiopathic
microcytic iron deficiency anemia signs/sxs
those of anemia itself: fatigue, tachycardia, palpitations, SOB on exertion, smooth tongue, brittle/spooning nails, cheilosis.
microcytic iron deficiency anemia dx workup
low MCV (RBC cell size), low reticulocytes, low ferratin values. Bone marrow bx rarely done. Eval labs and pt’s response to therapeutic trial of iron replacement to determine cause.
microcytic iron deficiency anemia tx
oral/parenteral iron
microcytic iron deficiency anemia complications
long term anemia - heart probs, growth probs, probs during pregnancy
microcytic iron deficiency anemia prevention
take supplements/adequate diet
microcytic thalassemia anemia - major/minor etiology
hereditary disorders characterized by reduction in the synthesis of globin chains. this causes reduced hemoglobin synthesis and thus anemia. 2 types: alpha (caused by gene mutations) and beta (caused by point mutations)
microcytic thalassemia anemia - major/minor signs/sxs
Alpha minor: clinically normal, normal life expectancy, performance status and mild microcytic anemia to pallor/splenomegaly.
Alpha major: no hemoglobin produced. stillborn.
beta minor: clinically insignificant.
beta major: stunted growth bony deformities, HSM, jaundice, cirrhosis, thrombophilia.
microcytic thalassemia anemia - major/minor dx workup
hematocrit, genetic counseling, CBCs, retic count, iron, MCV, blood smears
macrocytic folic acid deficiency anemia etiology
alcohol abuse, anorexia, malnutrition, overcooked foods, concurrent B12 deficiency, decreased absorption of iron (from drugs), increased iron requirement, loss of iron (from dialysis)
macrocytic folic acid deficiency anemia signs and sxs
megaloblastic anemia, glossitis, vague GI disturbances (anorexia, diarrhea)
macrocytic folic acid deficiency anemia dx workup
RBC folic acid level <150ng/mL. B12 can be normal, though.
macrocytic folic acid deficiency anemia tx
folic acid supps
macrocytic B12 deficiency anemia etiology
decreased intrinsic factor production, gastrectomy, dietary deficiency, competition for B12 in gut, decreased absorption, pancreatic insufficiency, H pylori infxn.
macrocytic B12 deficiency anemia signs/sxs
similar to folic acid deficiency + some neuro symptoms. Slow onset anemia such that the sxs might go unnoticed. pallor/mild icterus, glossitis, vague GI issues, neurologic manifestations (peripheral neuropathy, difficulty with position or vibration sensation/balance, dementia).
macrocytic B12 deficiency anemia dx workup
low serum B12 <100.
macrocytic B12 deficiency anemia tx
IM or SubQ inj of B12, PO/sublingual replacements. folic acid replacement, RBC transfusions if severe + diuretics.
macrocytic B12 deficiency anemia complications
altered cerebral fxn, dementia, hypokalemia.
normocytic anemia of chronic disease etiology
associated w chronic diseases: cancer, collagen vascular disease, chronic infections, DM, CAD. caused by low RBC production d/t trapped iron stores in macrophages or reduced uptake in the gut, decreased EPO production, impaired bone marrow response to EPO.
normocytic anemia of chronic disease signs/sxs
mild generalized fatigue, dizziness, mild palpitations, sometimes pallor of palpebral conjunctivae
normocytic anemia of chronic disease dx workup
often diagnosed incidentally by labs: slight Hb decrease (10-11 g/dL), hypo chromic RBCs, MCV normal to low, low absolute retic count, elevated acute phase reactants (ESR, platelets, fibrinogen), reduced transferrin, increased ferritin, low serum iron and total iron binding capacity w normal % saturation
intrinsic defects leading to hemolytic anemias
membrane (hereditary spherocytosis, paroxysmal nocturnal hemoglobulinuria), enzyme systems, hemoglobin (sickle cell, thalassemia)
extrinsic causes leading to hemolytic anemias
immune (autoimmune, lymphoproliferative disease, drug tox), microangiopathic hemolytic anemia (vasculitis), infection of RBCs (malaria, clostridium, lyme dz), hypersplenism, burns.
sickle cell anemia etiology
homozygous mutation in beta Hb chain. Hb molecules w 2 normal and 2 abnormal chains. elongated fibers: sickle cell shaped RBC
sickle cell anemia pathophys
abnormally shaped RBCs occlude capillary beds. sickled cells are prone to hemolysis which leads to a free Hb which attaches a nitric toxic and causes endothelial dysfxn, vascular injury, and pulmonary HTN.
sickle cell anemia epidemiology
genetic: autosomal recessive inheritance; African, Mediterranean, or S Asian heritage; confers resistance to malaria; 30% present symptoms by 1 year, 90% by age 6
sickle cell anemia signs/sxs
acute pain episodes in extremities, abdomen, back, chest. fever, joint swelling, vomitting, tachypnea
sickle cell anemia lab findings
retic count: increased. Hb mild to mod decrease. elevated bilirubin and lactate dehydrogenase. on blood smear: sickling RBCs, Howell-Jolly bodies, target cells. WBC: elevated 12-15K
sickle cell anemia mgmt
hospitalization during attack: hydration and oxygenation, analgesia, antibiotics if infection present. blood transfusions.
sickle cell anemia complications
recurrent acute vasculocclusive crisis. in pregnancy: HTN, infections, preterm birth, fetal growth restrictions, increased maternal mortality.
paroxysmal nocturnal hemaglobulinuria etiology
acquired clonal hematopoietic stem cell disorder. abnormal sensitivity of RBC membranes to lysis by complement. may progress to aplastic anemia, myelodysplasia, or acute leukemia.
paroxysmal nocturnal hemaglobulinuria pathophys
free Hb released into blood scavenges nitric oxide. esophageal spasms, erectile dysfxn, renal damage, thrombocytosis, drop in pH while sleeping facilitates hemolysis.
paroxysmal nocturnal hemaglobulinuria epidemiology
this is genetic.
paroxysmal nocturnal hemaglobulinuria lab findings
mild to very severe anemia (+/- reticulocytosis). hemosiderin due to hemolysis. serum LD: elevated. iron deficiency normo-macrocytic RBCs.
paroxysmal nocturnal hemaglobulinuria mgmt
mild dz: no tx.
severe: RBC transfusions and eculizumab (compliment antibiody), folic acid supps
paroxysmal nocturnal hemaglobulinuria complications
death due to thrombosis
sickle cell trait etiology
heterozygous “carrier” for B-Hb chain mutation
sickle cell trait signs/sxs
if only carrier, most likely none.
sickle cell trait mgmt
no tx necessary. genetic counseling.
sickle cell trait complications
sudden cardiac death, rhabdo during vigorous exercise (esp at altitude), possible increased risk for venothromboembolism, possible increased risk for chronic kidney dz
hereditary spherocytosis etiology
hereditary form of intrinsic hemolytic anemia (i.e. defect involves RBC itself). most commonly an autosomal dominant disorder
hereditary spherocytosis pathophys
microspherocytic shape of RBCs conferred by abnormalities in the cytoskeleton of the cell membrane, decreased pliability leads to increased hemolysis when passing through small capillaries of the spleen.
hereditary spherocytosis signs/sxs
neonatal jaundice, anemia, jaundice, splenomegaly, cholecystitis/cholelithiasis
hereditary spherocytosis lab findings
the peripheral blood smear shows spherocytes w a normal to low MCV and increased MCHC (>36%). diagnosis is established by the osmotic fragility test.
hereditary spherocytosis mgmt
folate therapy and splenectomy may be necessary in severe cases
G6PD deficiency etiology
glucose-6-phosphate dehydrogenase deficiency (enzyme). hereditary enzyme defect causing episodic hemolytic anemia.
G6PD deficiency pathophys
the antioxidant glutathione is unable to be reduced by the defective enzyme G6PD. increased concentration of oxidized glutathione causes denaturing Hb which precipitates out of solution to form Heinz bodies which damage cell membrane of RBC. Damaged membranes lead to premature RBC removal by spleen (extravascular hemolysis)
G6PD deficiency epidemiology
X linked genetic disorder. M>F.
G6PD deficiency signs/sxs
pts usually healthy w/out hemolytic anemia or splenomegaly. hemolysis occurs episodically in response to infection and certain drugs.
G6PD deficiency lab findings
normal labs between episodes. peripheral blood smear may show “bite” cells (look like they’ve had a bite taken out of them) or “blister” cells. Heinz bodies may be visible with stain. G6PD may be measured with specific enzyme assays.
G6PD deficiency mgmt
no tx necessary except to avoid drugs known to trigger acute episodes.
autoimmune hemolytic anemia etiology
acquired hemolytic anemia caused by IgG autoantibody
autoimmune hemolytic anemia pathophys
IgG binds RBC membrane leading to macrophage phagocytosis.
autoimmune hemolytic anemia epidemiology
1/2 of all cases are idiopathic. may be seen in association with SLE.
autoimmune hemolytic anemia signs/sxs
rapid onset of anemia that may be life threatening. fatigue. dyspnea. angina.
autoimmune hemolytic anemia lab findings
Coombs test (agglutination is + indicating presence of IgG)
autoimmune hemolytic anemia mgmt
prednisone is initial tx (PO 1-2mg/kg/d). transfused blood may be subject to hemolysis as well, should consult hematology and blood bank specialists. splenectomy may cure the disorder.
hemochromatosis etiology
an inherited disorder of iron metabolism in which iron absorbed through the intestine results in excess amounts of iron with eventual tissue damage and impaired function in many organs. (Iron overload)
hemochromatosis signs/sxs
most pts are asymptomatic. rarely recognized clinically before the 5th decade of life. early sxs are fatigue, arthralgia. late manifestations are arthropathies, hepatomegaly, hepatic dysfunction, cardiac enlargement, bleeding from esophageal varices, and impotence in men.
hemochromatosis dx workup
usually suspected due to elevated iron saturation or serum ferritin or a family hx. may have abnormal liver tests and a + HFE gene mutation. a CT & MRI will show changes of iron overload in the liver and hepatic iron stores.
hemochromatosis tx
meds: chelating agent deferoxamine; liver transplant for advanced cirrhosis; avoiding food rich in iron; phlebotomies
hemochromatosis complications
increased risk for infections (siderophilic organisms); arthropathy; DM; heart dz; portal HTN; hypopituitarism.
Non Hodgkin Lymphoma (NHL) etiology
most common hematological malignancy. risk factors: exposures (radiation, prior chemo, pesticides/herbicides, petrochems), familial; chronic infections, autoimmune dz, immunodeficiency
Non Hodgkin Lymphoma (NHL) pathophys
tumors originating from lymphoid tissues, mainly of lymph nodes. These tumors may result from chromosomal translocations, infections, environmental factors, immunodeficiency status, and chronic inflamm.
Non Hodgkin Lymphoma (NHL) signs/sxs
lymphadenopathy, fever, wt loss, drenching night sweats, pts w Burkitt lymphoma often note abdominal pain or fullness bc of the predilection of the disease for the abdomen.
Non Hodgkin Lymphoma (NHL) lab findings
dx usually made w lymph node biopsy. PET/CT for staging. the peripheral blood is usually normal even w extensive bone marrow involvement by lymphoma. Bone marrow involvement is manifested as paratrabecular monoclonal lymphoid aggregates.
Non Hodgkin Lymphoma (NHL) mgmt
depends on location and type. observation. immunotherapy (rituximab, R-CHOP), radiation, cytotoxic chemo, targeted agents, hematopoietic stem cell transplant.
multiple myeloma etiology
malignancy of plasma cells. characterized by replacement of bone marrow, bone destruction, and paraprotein formation. the myeloma cells produce abnormal proteins that cause kidney probs instead of producing useful antibodies.
median age of onset for multiple myeloma
65 yrs
multiple myeloma pathophys
the paraprotein is an abnormal immunoglobulin that is produces in excess by an abnormal proliferation of plasma cells. this is what causes probs for the kidney and immune responses overall.
multiple myeloma signs/sxs
bone pain, often in spine/hips/ribs/proximal long bones; anemia symptoms; increased susceptibility to infxn; symptoms of kidney failure; neuropathy or spinal cord compression; pallor/bone tenderness/soft tissue masses
multiple myeloma lab findings
anemia; hypercalcemia; proteinuria; elevated ESR; on peripheral blood smear: plasma cells are rarely visible; paraprotein found on serum or urine protein electrophoreis or immunofixation electrophoresis
multiple myeloma complications
malignant plasma cells can form tumors that may cause spinal cord compression or other soft-tissue probs; light chain component of immunoglobulin often leads to kidney failure; myeloma pts are esp prone to infections with encapsulated organisms (step pneuma, H. flu)
Acute Myeloid Leukemia (AML) etiology
a malignancy of the hematopoietic progenitor cells: the cells proliferate in uncontrolled fashion and replace normal bone marrow elements. heredity, radiation, chem, and other exposures, and drugs may all play a role in causation. Immature cells build up.
Acute Myeloid Leukemia (AML) pathophys
a rapidly progressive neoplasm derived from hematopoietic precursors. Acute leukemias involve bone marrow and usually manifest abnormal circulating leukemia (blast) cells
Acute Myeloid Leukemia (AML) signs/sxs
presents over days to weeks; malaise, fatigue, dyspnea, wt loss, gingival hyperplasia, fever, infections, bleeding/bruising, lymphadenopathy, tumor lysis, leukostasis
Acute Myeloid Leukemia (AML) lab findings
abnormal CBC: high or low WBCs, circulating blasts, anemia, thrombocytopenia. in contrast to mature myeloid cells, leukemic cells have large immature nuclei with open chromatin and prominent nucleoli. Auer Rod, an eosinophilic needle-like inclusion in cytoplasm is pathognomonic.
Acute Myeloid Leukemia (AML) mgmt
initially tx the infections/fever, bleeding, leukostasis (consider when blast count >50K, CNS & pulmonary sxs, emergent aphaeresis), tumor lysis. Than, chemotherapy, bone marrow transplant.
Acute Myeloid Leukemia (AML) complications
a marked increase in the number of circulating blasts can sometimes cause vascular obstruction accompanied by hemorrhage and infarction in the cerebral and pulmonary vascular beds (results in strokes, retinal vein occlusion, pulmonary infarction).
chronic myeloid leukemia etiology
myeloid proliferative isorder characterized by over production of myeloid cells. the cells mature partly but not completely, and they do not fight infection as well as normal RBCs. they survive longer/build up and crowd out the normal cells.
chronic myeloid leukemia pathophys
ass’d with characteristic chromosomal abnormality, the Philadelphia chromosome. the fusion gene bcd/abl produces a novel protein that possess tyrosine kinase activity, leading to leukemia.
chronic myeloid leukemia signs/sxs
fatigue, night sweats, low grade fever, abdominal fullness related to splenomegaly, sternal tenderness. fever in absence of infection. bone pain and splenomegaly mark disease acceleration. bleeding/fatigue/petichiae related to cytopenias.
chronic myeloid leukemia lab findings
elevated WBC count; left shifted myeloid series but low percentage of promyelocytes and blasts; presence of Philadelphia chromosome; platelet count may be normal or elevated; basophilia and eosinophilia may be present
chronic myeloid leukemia complications
the dz may progress from chronic phase to accelerated phase and crisis
chronic myeloid leukemia mgmt
imatinib (targeted therapy for cancer); tyrosine kinase inhibitors now approved including dasatinib, nilotinib, and ponatinib.
Acute Lymphoma Leukemia (ALL) etiology
rapidly progressive neoplasm derived from lymphoblasts (immature lymphocytes) which overtake the bone marrow and can spread to other organs. etiology still unknown. most common acute leukemia in children. occurs in kids (onset 5-6 yrs), and adults (onset around 50)
Acute Lymphoma Leukemia (ALL) pathophys
can sometimes see the Philadelphia chromosome (as described w CML), but plays a different role b/c targeted therapies aren’t ass effective in ALL as in CML.
Acute Lymphoma Leukemia (ALL) signs / sxs
HSM, LAD, bone pain (felt in long bones), anemia, thrombocytopenia, neutropenia, may have fatigue/fever/infection/malaise/dyspnea/wt loss/bleeding/bruising/clots from leukostasis; rapid progression (days to weeks)
Acute Lymphoma Leukemia (ALL) lab findings
nd to do LP at time of dx and later in tx to test for CNS involvement
Acute Lymphoma Leukemia (ALL) mgmt
multiple cycles of complicated combo chemo (can administer intrathecally for CNS prophylaxis/tx)& then maintenance chemo. allogenic hematopoietic stem cell transplant for certain high risk genetic markers.
Chronic Lymphocytic Leukemia (CLL) etiology
A neoplasm of more mature B cells. expansion of a neoplastic clone results in an increased # of small, long-lived lymphocytes that are immunocompetent. results in immunosuppression, bone marrow failure, and organ infiltration w lymphocytes. indolent course. most common leukemia in US.
Chronic Lymphocytic Leukemia (CLL) pathophys
gene mutations. very similar to non-hodgkin lymphoma, but neoplastic cells accumulate in the blood and bone marrow (rather than in the lymph nodes)
Chronic Lymphocytic Leukemia (CLL) signs/sxs
fatigue, fever, wt loss, infections, hemolytic anemia, and/or ITP, abnormal CBC, LAD and/or splenomegaly
Chronic Lymphocytic Leukemia (CLL) lab findings
persistant lymphocytosis >5000/microliter; 75-98% of circulating cells are lymphocytes, CD5(pathognomonic), and CD20&23 B cell immunophenotypes, smear shows SMUDGE cells; may see pseudokyperkalemia bc cells are so fragile they that lyse in the collection tube before lab analyses the same; Hct and platelets are normal
Chronic Lymphocytic Leukemia (CLL)mgmt
no cure. watch and wait until sxs necessitate tx to improve quality of life, then tx w combo chemo; rituximab (targets classic immunophenotypic B cells), cyclophosphamide, doxorubicin, fludarabine, and monoclonal Abs
What does Hemoglobin (HBG) in CBC tell you?
how many red cells are there? gross indicator of tissue oxygenation. appears falsely elevated if pt is dehydrated
what does hematocrit (HCT) in CBC tell you?
how many red cells are there? the % of total blood vol that is d/t RBCs. appears falsely elevated if pt is dehydrated
what does MCV - mean cell vol in CBC tell you?
how big is the RBC? gives an indication of the cause of anemia. normal for this to be high in newborns/infants, so ask the lab if they adjust for age
what does platelet count on CBC tell you?
indication of blood’s clotting ability. majority in circulation, remainder in spleen. increased # trapped in spleen seen in immune-mediated thrombocytopenia
what does MCH - mean cell hemoglobin on CBC tell you?
measures the amount of hemoglobin in one RBC. physically, how dark is the RBC (low Hgb= lighter colored RBC)
what does RDW-red cell distribution width on CBC tell you?
indication of anisocytosis (variation in RBC size). the larger the width percentage, the greater the variation in the size of RBCs. increased in macrocytic anemias. used to differentiate iron-deficient anemia from other thalassemias, but not specific. more sensitive in early stages of anemias
what does WBC count tell you on CBC?
actual count of leukocytes in a given blood vol. elevated by neutrophil demargination w exercise, glucocorticoids, epinephrine. decreased w cold agglutinins.
WBC differential: PMNs
increase during infection. measures amount of margination and subsequent extravasation. also termed “segs” or “polys”
WBC differential: Band neutrophils
increase during infection. appearance of bands indicates a “left shift”, release of immature neutrophils from the bone marrow
WBC differential: lymphocytes
decreased proportionately to increase of PMNs (only exception is lymphocyte decrease w glucocorticoid use). typically not differentiated into T, B, NK cells but can be done via flow cytometry.
WBC differential: monocytes
in circulation for 16-36 hours and enter tissues to become macrophages. important indicators of cell-mediated and humoral immunity.
WBC differential: Eosinophils
increased count indicates parasitic infection, esp with parasite migrating through tissue
MHCH - mean cell hemoglobin concentration
amount of Hgb in terms of % of vol of cell. Hct typically 3x Hgb. iron deficiency anemia only type with routinely low MCHC (but can be low in other Hgb synthesis disorders). RBCs described as hypochromic (pale) in lab reports. can be falsely elevated in hyperlipidemia.
normocytic anemia
RBCs are physically normal, there is just a low # of them. etiology: acute blood loss, hemolytic anemia, or anemia of chronic dz. increase: reticulocyte (blood loss and hemolytic only)
macrocytic anemia
low Hgb value characterized by abnormally enlarged erythrocytes. etiology: iron deficiency anemia. increase: RDW, retic count
microcytic anemia
abnormally small RBCs. etiology: iron deficiency anemia. increase: RDW, retic count
polycythemia
increased hemoglobin (found incidentally on increased RBC or Hct). etiology: overproduction of RBCs, or decrease in plasma.
leukocytosis
high WBC count. order a differential to determine what components are increased/decreased.
leukopenia
decreased WBC count (primarily to absolute decrease in neutrophils). range: <3000-5000/mm3
thrombocytosis (aka thrombocythemia)
elevated platelet count. rnage: 500,000-800,000/uL
thrombocytopenia
decreased platelet count
left shift on CBC
the appearance/increase of band cells (immature neutrophils). happens during an acute infection, usually bacterial.
fresh whole blood
contains RBCs, platelets, plasma.
fresh whole blood indications
cardiac surgery
massive hemorrhage
packed RBCs
used to raise hematocrit. unit = 300mL. 1 unit will increase hematocrit by 3-4%
packed RBCs indications
cardiac surg. repair of hip fraxture. upper GI bleed. hematologic malignancy undergoing chemo.
leukocyte-poor blood
most blood products are leukoreduced.
leukocyte-poor blood indication
reduces incidence of: leukoagglutination rxn, platelet alloimmunization, transfusion-related acute lung injury, CMV exposure
Frozen packed RBCs
can be stored up to 10 yrs. EXPENSIVE. rarely done. has most WBCs and platelets removed.
Frozen packed RBCs indication
used to maintain a supply of rare blood cell types. pt w severe leukoagglutination rxn, or anaphylactic rxn to plasma proteins.
Autologous packed RBCs
using own blood for a transfusion. can be stored up to 35 days before freezing.
autologous packed RBCs indication
used in scheduled, elective surgery, when pt has time to donate blood prior.
potential major complications of blood transfucion
hemolytic transfusion rxn if mismatched.
bacterial contamination.
transmission of infectious dz.
leukoagglutinic rxns (more common in fresh whole blood transfusion).
hypersensitivity rxn.
graft-vs-host dz.
transfusion related acute lung injury.
hemolytic transfusion rxns signs/sxs
severity depends on RBC dose. fever, chills, backache, HA, apprehension, dyspnea, hypotension, vascular collapse, disseminated intravascular coagulation (DIC), acute kidney failure.
hemolytic transfusion rxns mgmt
stop transfusion immediately. check ID of pt and blood (most errors are clerical). return transfusion blood and pts blood to do a retype and cross match. hydrate pt!
anaphylactic rxns to blood transfusion signs/sxs
difficulty breathing, coughing, N/V, hypotension, bronchospasm, loss of consciousness, respiratory arrest, shock.
anaphylactic rxn to blood transfusion mgmt
stop transfusion. maintain vascular access. administer epinephrine, in severe cases glucocorticoids may be required.
indication for Total Iron Binding Capacity (TIBC) test
if iron deficient anemia or anemia of chronic dz is suspected.
clinical usefulness of Total Iron Binding Capacity (TIBC) test
measures transferrin, evaluated w serum iron to determine the amount of iron in circulation, increased as compensation in iron deficiency.
indication for serum ferritin test
if iron-deficiency is suspected
clinical usefulness of serum ferritin test
indirectly measures iron stores, ferritin is the major iron storing protein in the body
indication for a CBC
often ordered if anemia is suspected to determine the extent and what type.
clinical usefulness of CBC
evaluates many elements of blood including RBC morphology which can indicate specific pathology.
indication for Hgb electrophoresis
if sickle cell dz is suspected
clinical usefulness of Hgb electrophoresis
confirms diagnosis of sickle cell hemoglobin, screening test to detect and differentiate variant and abnormal hemoglobin, can differentiate between the sickle cell genotypes.
indication for bone marrow biopsy
needed to complete eval of anemia if an etiology can’t be determined from labs.
clinical usefulness of bone marrow biopsy
eval of iron stores and the ability of the bone marrow to deliver iron to RBCs
indication for test of bilirubin
suspecting hemolytic anemias, spherocytosis, sickle cell anemia, thalassemia, and deficiency of red cell enzymes.
clin usefulness of bilirubin test
a way to determine the extent of hemoglobin breakdown or overproduction of bilirubin
indication for a reticulocyte count
if anemia is suspected, to measure response to iron tx
clin usefulness of reticulocyte count
increased acute blood loss of hemolysis, indicates bone marrow production of RBCs, useful in identifying drug induced bone marrow suppression, used to measure a pt response to iron supplementation, low in iron-deficient anemia
indication for methylmalonic acid (MMA) test
used to distinguish between Vit B12 deficiency and myelpdysplasia or folic acid deficiency.
clin usefulness of methylmalonic acid (MMA) test
Vit B12 deficiency: elevated MMA.
MMA is a good way to determine if tx is working. an elevated homocysteine with normal MMA suggests folate deficiency.
