PATHO-- RBC's, anemias, alterations in homeostasis Flashcards
aplastic anemia
stem cell disorder characterized by reduction of hematopoietic tissue in bone marrow and pancytopenia (reduction in WBC, RBC, platelets)
aplastic anemia etiologies
toxic, radiant, or immunologic injury to bone marrow stem cells
aplastic anemia clinical manifestations
late symptoms–fatigue, tachycardia, weakness, lethargy. Pancytopenia
labs of aplastic anemia findings
RBC’s are normocytic and normochromic
aplastic anemia treatment
bone marrow transplant
anemia of chronic renal failure
failure of renal function impairs erythropoietin production and bone marrow compensation
anemia of chronic renal failure labs
decreased RBC count with low HCT and HGB level
anemia of chronic renal failure treatment
dialysis and administration of erythropoietin
RBC appearance in labs anemia of chronic renal failure
normocytic, normochromic
pernicious anemia etiology
lack of intrinsic factor causes vitamin B-12 deficiency due to malabsorption of vitamin b-12
pernicious anemia lab findings
low RBC, WBC, and platelets, increased MCV
RBC appearance in labs pernicious anemia
microcytic
pernicious anemia clinical manifestations
pallor, fatigue, sore tongue, anaorexia, nausea and vomiting, abdominal pain
pernicious anemia neurological manifestations
Paresthesias of hands and feet, reduced vibratory position and sense, muscle weakness, impaired thought process
folate deficiency anemia etiologies
poor dietary intake,
folate deficiency anemia cells
macrocytic, normochromic
iron deficiency anemia etiologies
inadequate diet, malabsorption of iron, blood loss
iron deficiency anemia pathogenesis
body’s Fe+ stores depleted, lack of Fe+ for bone marrow which leads to iron deficient RBC production
iron deficiency anemia clinical manifestations
pallor, fatigue, hypoactivity, pica, glossitis
iron deficiency anemia lab findings
hypochromic and microcytic RBC’s, low MCV, MCH, and MCHC, TIBC increased
iron deficiency anemia treatment
PO ferrous sulfate or IV ferrous gluconate
thalassemia etiology
is a GENETIC DISORDER group associated with presence of mutant genes
thalassemia pathogenesis
increased RBC destruction (hemolysis) results in decreased RBC survival rate
thalassemia lab findings
hypochromic and microcytic RBC’s, MCV, MCH, and MCHC are low, erythroblastic hypoplasia
thalassemia treatment
blood transfusions, splenectomy, bone marrow transplantation, genetic counseling
sickle cell anemia etiology
genetic defect of hemoglobin synthesis, results in hemoglobin instability, autosomal recessive disorder
sickle cell anemia pathogenesis
predisposes RBC’s to early destruction due to abnormalities in structure, sickled cells cause vascular occlusion
lab findings sickle cell anemia
severe anemia, RBC’s of different shapes and sizes
sickle cell anemia treatment
O2, pain management, fluids, stem cell transplant
hemolytic disease of the newborn
fetal RBC’s cross the placenta, stimulate production of maternal antibodies against antigen on fetal RBC’s not inherited by mother, maternal antibodies cross into fetal circulation and destroy fetal cells
complications of hemolytic disease of the newborn for the newborn
anemia, reticulocytosis, nucleated RBC’s in blood of infant
how to prevent hemolytic disease of the newborn
Standard dose of anti-Rh immune globulin (RhoGAM) is given to mother
before or after delivery, in some cases in eutero transfusion or early delivery
acute blood loss
may be from trauma or secondary to a disease process, Symptoms develop with activity at 20% loss of blood volume (tachycardia & postural drop in BP), and increase in severity with
continued blood loss
acute blood loss treatment
blood volume replacement therapy
thrombocytopenia
common cause of general bleeding: has 2 types– ITP and acquired thrombocytopenia
ITP–idiopathic thrombocytopenia purpura
autoimmune, platelets function normally but live only 1-3 days. acute= after viral illness. chronic= women aged 20-40
acquired thrombocytopenia
diminished or defective platelet production, splenic sequestration, medications, platelet dilution
thrombocytopenia pathogenesis
general mechanisms: decreased platelet production, decreased platelet survival, intravascular dilution of circulating platelets
thrombocytopenia lab findings
low platelet count, prolonged bleeding time, abnormal peripheral smear
thrombocytopenia clinical manifestations
platelet count is less than 150,000 (50,000 for spontaneous bleeding from slight trauma, below 20,000 life threatening), bruising (purpura, petechae), internal bleeding.
treatment for thrombocytopenia
based on identified cause
hemophilia
most common inherited genetic disorder; excessive bleeding
hemophilia etiology
x linked recessive disorder (mother to son), 25% due to genetic mutation (not family history)
types of hemophilia
hemophilia A–classic hemophilia, factor VIII deficiency
hemophilia B– Christmas disease, factor 9 deficiency
treatment for hemophilia
patient/family education,
hemophilia A= cryoprecipitate or factor VIII concentrate
hemophilia B= fresh frozen plasma or cryoprecipitate
hemophilia clinical manifestations
hemarthrosis (oozing of blood into soft tissue, muscle, joint capsule). Knee is most common site. Begins with a slight tear and joint expands with blood, leads to degenerative arthritis.
Von willebrand disease
disorder of factor VIII and platelet function, excessive bleeding
etiology of vwd
autosomal dominant inheritance
pathogenesis of vwd
VW factor is needed to stabilize factor VIII and for platelet adherence. Bleeding occurs when VWF is decreased or absent
vwd clinical manifestations
nose bleed, mucosal bleed, bruising, GI hemorrhage, menorrhagia, hemarthrosis (rare)
vwd lab tests
prolonged bleeding time, normal platelet count
vwd treatment
replace VWF
disseminated intravascular coagulation
acquired bleeding syndrome, clotting and bleeding occur simultaneously. NOT a disease itself, develops second to other conditions
etiology of DIC
trauma, burns, shock
pathogenesis of DIC
continued release of thromboplastic material causes abnormal levels of thrombin in plasma–> essential to clot breakdown—> leads to emboli
clinical manifestations of DIC
Bleeding; often from 3 or more sites, Weakness, malaise, fever, CNS bleeding, altered LOC
