hematological dis in pregnancy Flashcards
(36 cards)
CDC defined anemia in iron-supplemented pregnant women using a cutoff of the 5th percentile — IN 1ST and 3rd trimester, —- in 2nd trimester
—11 g/dL in the first and third trimesters, and 10.5 g/dL in the second trimester
Anemia is associated with several adverse pregnancy
outcomes including
preterm birth, Children born to iron-deficient women and without iron supplementation are
reported to have lower mental development scores
The two most common causes of anemia during pregnancy and the puerperium are
iron deficiency and acute blood loss.
In a typical singleton gestation, the maternal need for iron averages nearly
1000 mg.
Routinely in pregnancy, daily oral supplementation btw
30 to 60 mg of elemental iron and 400 μg of folic acid is recommended
For iron-deficiency anemia, resolution and restitution of iron stores can be accomplished with simple iron salts that provide approximately 200 mg daily of elemental iron.
for parenteral IV iron ferrous sucrose is safer than iron-dextran.
Chronic renal insufficiency is the most common disorder that cause anemia of chronic disease during pregnancy.
In pregnancies complicated by chronic renal insufficiency, recombinant erythropoietin is usually considered when the hematocrit approximates 20 percent
More folic acid daily 4-mg folic acid supplement is given with
Women who previously have had infants with neural-tube defects, multifetal pregnancy, hemolytic anemia, Crohn disease, alcoholism, and inflammatory skin disorders. Women with a family history of congenital heart disease may also benefit from higher doses
Those who have undergone total gastrectomy require — μg of vitamin B12 given intramuscularly each month.
1000 μg of vitamin B12 given intramuscularly each month.
Autoimmune Hemolysis: The cause of aberrant antibody production is unknown. Typically, both the direct and indirect antiglobulin (Coombs) tests are positive. Anemias caused by these factors may be due to warm-active autoantibodies (80 to 90 percent), cold-active antibodies, or a combination.
also may be classified as primary (idiopathic) or secondary due to underlying diseases or other factors. Examples of the latter include lymphomas and leukemias, connective-tissue diseases, infections,
chronic inflammatory diseases, and drug-induced antibodies
Coldagglutinin disease may be induced by
infectious etiologies such as Mycoplasma
pneumoniae or Epstein-Barr viral mononucleosis
Hemolysis and positive antiglobulin test results may be the consequence of either (IgM) or (IgG) antierythrocyte antibodies. When thrombocytopenia is comorbid, it is termed
Evans syndrome
Rituximab, along with prednisone, is first-line treatment
Drug-induced hemolysis is usually chronic and mild to moderate, but occasionally acute hemolysis is severe.
severe Coombs-positive hemolysis stimulated by cefotetan given as prophylaxis for obstetrical procedures. Alpha-methyldopa can cause similar hemolysis
The most fulminant acquired hemolytic anemia encountered during pregnancy is
caused by the exotoxin of Clostridium perfringens or by group A β-hemolytic streptococcus
Diamond-Blackfan anemia
pure red-cell hypoplasia. Approximately 40 percent of cases are familial and have autosomal dominant inheritance
Gaucher disease
autosomally recessive lysosomal enzyme deficiency
characterized by deficient activity of acid β-glucosidase. Affected women have anemia and thrombocytopenia that is usually worsened by pregnancy
Sickle-Cell Hemoglobinopathies
(hemoglobin S) originates from a single β-chain substitution of glutamic acid by valine, which stems from an A-forT substitution at codon 6 of the β-globin gene.
. Hemoglobin C originates from a single β-chain substitution of
glutamic acid by lysine, which stems from a T-for-C
substitution at codon 6 of the β-globin gene.
Chronic and acute changes from sickling include (complications Happened to sicklers)
bony abnormalities such as osteonecrosis of femoral and humeral heads, renal medullary damage, autosplenectomy in homozygous SS patients and splenomegaly in other variants, hepatomegaly, ventricular hypertrophy, pulmonary infarctions, pulmonary HTN, cerebrovascular accidents, leg ulcers, and a propensity for infection and sepsis, cerebrovascular aneurysms and sickle-cell vasculopathy
Treatment OF SCD
- hydroxyurea: which augments Hgb F production and reduces the number of sickling episodes
- crizanlizumab, an antibody against P-selectin, significantly lowered the incidence of adverse events.
Bone marrow transplantation has 5-year survival rates
that exceed 90%. Cord-blood stem-cell transplantation from related donors also shows great promise. Finally, successful gene therapy has been accomplished by lentiviral vector-mediated addition of a B-globin gene into stem cells
in PREGNANT women with sickle-cell syndromes they had a –fold greater incidence of hypertensive disorders— percent; a —–fold higher rate of fetal‑growth restriction— percent; and a –fold increased cesarean delivery rate— percent.
a 1.8-fold greater incidence of hypertensive disorders—19 percent; a 2.9-fold higher rate of FGR —6 percent; and a 1.7-fold increased cesarean delivery rate—45 percent.
Prophylactic Red Cell Transfusions For sicklers During pregnancy
the most dramatic benefit of prophylactic transfusions has been on maternal morbidity rates, Transfusions were given throughout pregnancy to maintain the
hematocrit above 25 volumes percent and the portion of hemoglobin S <60 percent, Maternal morbidity was minimal, and erythropoiesis suppression was not problematic. Their outcomes were compared with historical controls who were not routinely transfused. Overall, morbidity and hospitalization rates were significantly reduced in the transfused group, Still, adverse perinatal outcomes are prevalent
Sickle-Cell Trait carriers could have
occasional hematuria, renal papillary necrosis, and hyposthenuria, which is urine of low specific gravity
The congenital diseases associated with poor platelet function are divided into four types of dysfunction:
(a) adhesion to collagen,
(b) adhesion to subendothelium, e.g. von Willebrand disease, RF, CML
(c) release reaction defects, and
(d) ADP aggregation defects.
