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Chapter chapter 13 pathophysiology-fifth edition

NURS 2112 Chapter Notes - Chapter chapter 13 pathophysiology-fifth edition: Disseminated Intravascular Coagulation, Hemolytic Anemia, Central Venous Pressure

Course Code
NURS 2112
Joseph Usiji
chapter 13 pathophysiology-fifth edition

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Blood loss acute:
Blood loss anemia presents after a trauma or secondary to a disease process
Rapid decrease in the overall blood volume and impairs oxygen delivery to the body
Clinical manifestations; 10% of blood loss usually does not cause clinical presentation,
usually only occasional vasovagal syncope
20% blood loss shows as tachycardia with exercise, and a slight postural drop in blood
pressure occurs
30% loss usually presents with flat neck veins when supine, postural hypotension, and
exercise tachycardia
40% loss causes the central venous pressure, cardiac output, and arterial blood
pressure to fall below normal while the patient is supine and at rest with associated air
hunger, tachycardia, and cold, clammy skin
50% loss of total blood volume often causes shock and death
Blood volume replacement therapy with crystalloid solutions, colloid solutions ( plasma
protein, albumin, or dextran), and fresh whole blood is essential in the early
management of acute hemorrhage whole blood is essential in early management of
acute hemorrhage to restore blood volume and prevent shock.
Hemolytic disease of the newborn
When fetal red cells cross the placenta, they may stimulate the production of maternal
antibodies against antigens on the fetal red cell not inherited from the mother.
Maternal antibodies cross into the fetal circulation and cause destruction of fetal cells.
Fetal-maternal ABO incompatibility is the most common cause
Rh incompatibility is clinically more important because of the severity of the hemolytic
disease in the fetus
With introduction of Rh treatment, the total incidence of HDNB in Rh negative women
has been greatly reduced
Clinical manifestations.
Hemolytic anemia, extramedullary erythropoiesis, and hyperbilirubinemia, jaundice,
petechial hemorrhages, hepatomegaly, splenomegaly, heart failure, ( with edema,
pleural effusions, ascites, and edema) kernicterus ( a condition in the newborn marked
by severe neural symptoms, associated with high levels of bilirubin in the blood), and
diffuse intravascular coagulation are seen in these infants. Many die in utero
Standard dose of anti-Rh immunoglobulin is given to the mother before and after
delivery, immunoglobulin destroys the infant’s RBCs before they can sensitize the
In utero transfusion may be done depending on the severity of the case and also early
delivery have been performed on fetuses with severe erythroblastosis
Phototherapy and phenobarbital are used to lower the bilirubin level
Group of diseases associated with the presence of mutant genes that suppress the rate
of synthesis of globin chains
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Imbalanced rate of production of the globin chain of adult hemoglobin
Because of the lack of hemoglobin, the anemia is severe, and the peripheral cells are
microcytic and hypochromic
The disruption of the globin balance causes the normal chains to accumulate and
precipitate within the cytoplasm. This damages the cell membranes, which leads to
premature cell destruction.
Clinical manifestations
Untreated patients with thalassemia major have
skull bone deformities from intramedullary and extramedullary bone
marrow expansion, mongoloid facies, bowing and rarefaction of long
bones, extension of bone marrow into paraspinal or intra abdominal
tumors, icterus, hepatomegaly, splenomegaly, and cardiac failure or
endocrinopathies, such as diabetes mellitus and hypogonadism from
excessive intestinal iron absorption. Patients with thalassemia intermedia
show fewer effects of iron overload, growth retardation, marrow
expansion, and splenomegaly; however, deforming bone and joint disease,
chronic leg ulceration, and infection are common in this form of
thalassemia. Thalassemia minor is usually relatively asymptomatic.
Bone marrow transplant only way in which it can be cured
Symptomatic management is based on regular blood transfusions, iron chelation
therapy, and the judicious use of splenectomy
Sickle cell
Genetically determined defect of hemoglobin synthesis
Production of abnormal hemoglobin called sickle hemoglobin
Sickle red cells have a decreased survival time, which causes anemia, and sickle cells
cause vascular occlusion, which results in capillary stasis, venous thrombosis, and
arterial emboli, the most dangerous feature of sickle cell anemia is the occurrence of
acute episodes of “ crisis” which can be hemolytic or vascular
Clinical manifestations
Recurrent painful episodes, acute and chronic organ dysfunction particularly of the
spleen, bones, brain, kidneys, lungs, skin, and heart are the cardinal features of sickle
cell anemia.
Red cell life span is already shortened by the sickling and may precipitate a hemolytic
crisis with jaundice
Sudden massive pooling of red cells, particular in the spleen, can create a sequestration
crisis, which is thought to result in the deaths that occur in the first years of life
Stem cell transplantation is curative and the treatment of choice
Currently there are no safe, effective antisickling agents, and treatment is primarily
To avoid precipitation of a vaso-occlusive crisis, it is important to prevent dehydration,
infection, fever acidosis, hypoxia, and cold exposure
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