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Pathophysiology Chapter 10,11

Terms in this set (56)

includes total RBCs, WBCs, and platelets
Complete blood count (CBC)
Associated with inflammation or infection
Leukocytosis (increased WBCs)
Associated with drug reactions; radiation and chemotherapy
Leukopenia (decrease in WBCs)
Differential blood count for WBCs includes:
Morphology- observed with blood smears
Hematocrit - packed cell volume (PCV)- normally 45%
Hemoglobin
Assessment of rate of formation of RBCs by the bone marrow- normal 1.5%-how many of them are reticulocytes; the rate of formation
Reticulocyte count
Bleeding time measures
platelet function
Prothrombin Time (PT) measures
extrinsic pathway
partial thromboplastin time (PTT)- measures
intrinsic pathway
cause a reduction in oxygen transport.
Anemias
Oxygen deficit leads to:
-Less energy production in all cells- decreased cell regeneration
-Compensation mechanisms- tachycardia and peripheral vasoconstriction
General clinical features of anemia:
fatigue, pallor (pale face), dyspnea, tachycardia (compensatory mechanisms)
Severe anemia may lead to
angina or CHF
A decreased regeneration of epithelial cells can lead to:
stomatitis, dysphagia, degenerative changes in hair and skin
Insufficient iron impairs ____
hemoglobin synthesis
Etiology of iron deficiency anemia:
-Dietary intake of iron below minimum requirement
-Chronic blood loss
*Bleeding, peptic ulcer, hemorrhoids, colon cancer, menorrhagia etc.
-Impaired duodenal absorption of iron
*In many disorders - malabsorption syndromes
-Severe liver disease
*May affect iron absorption as well as storage
Clinical features of iron deficiency anemia:
-Pallor of skin and mucous membranes
-Fatigue, lethargy, cold intolerance
-Degenerative changes- spooning of nails
-Stomatitis and glossitis
-Menstrual irregularities
-Delayed healing
-Tachycardia, heart palpitations, dyspnea, syncope
Diagnostic tests for iron deficiency anemia:
-Low Hb, HCT, MCV, MCHC,
Low serum ferritin, serum iron
microcytic, hypochromic RBCs
Treatment for iron deficiency anemia:
-Treat the cause
-Iron supplements
Insufficient iron impedes the synthesis of hemoglobin, thereby reducing the amount of oxygen transported in the blood. This results in ____ and _____
microcytic hypochromic
micro (small)
hypochromic (less color)-erythrocytes owing to a low concentration of hemoglobin in each cell
Etiology of pernicious anemia-Vit B12 deficiency:
malabsorption of vitamin B12 due to lack of intrinsic factor, caused by chronic autoimmune gastritis
Intrinsic factor is secreted by gastric mucosa and is required for intestinal absorption of B12
Chronic autoimmune gastritis
Other causes of Vit B12 deficiencies:
regional ileitis, resection of ileum, gastrectomy
Vitamin B12 deficiency leads to impaired maturation of
RBCs- have a shorter lifespan- anemia
Vitamin B12 deficiency also causes
demyelination of nerves
Vit B12 deficiency is characterized by:
-very large, immature, erythrocytes
-Shorter lifespan
-hypersegmented neutrophils
Manifestations of pernicious anemia-Vit B12 deficiency:
-Digestive discomfort, often with nausea
-"Pins and needles," tingling in limbs
Diagnostic tests for pernicious anemia-Vit B12 deficiency:
-Macrocytic erythrocytes
-Bone marrow exam (hyperactive)
-B12 serum levels below normal
-Presence of gastric atrophy-->presence of hypochlorhydria or achlorhydria confirms
Treatment for pernicious anemia-Vit B12 deficiency:
-Injectable vitamin B12 supplements
Impairment or failure of bone marrow
May be temporary or permanent
aplastic anemia
Etiology of aplastic anemia:
-Most often idiopathic
-Myelotoxins (bone marrow suppressants)
*Radiation, chemotherapy, drugs
When diagnosing aplastic anemia, blood counts indicate
pancytopenia
Manifestations of aplastic anemia include:
Low RBC count, leukopenia, thrombocytopenia- manifest as anemia, recurrent infections, pinpoint hemorrhages
In aplastic anemia, a bone marrow biopsy shows
mostly fatty marrow. (Lower reticulocyte count)
In aplastic anemia, identification of cause and prompt treatment needed for bone marrow recovery
Removal of any bone marrow suppressants. This includes:
-Blood transfusions may be needed
-Bone marrow transplantation is an option
-Failure to identify cause and treat effectively is LIFE-THREATENING
Hemolytic anemias result from
excessive & premature destruction of RBCs
-hereditary anemia
-Substitution of amino acid valine instead of glutamic acid in one ß globin chain
sickle cell anemia
-Anemia occurs in homozygous recessive.
-Diagnostic testing is available.
-More common in individuals of African ancestry- I in 10 African Americans is heterozygous for trait, 1 in 600 have sickle cell anemia
sickle cell anemia
Characteristics of sickle cell anemia:
-Abnormal hemoglobin (HbS)
-HbS crystallizes when Hb is deoxygenated- RBC become sickle shaped
Sickling is at first reversible- then irreversible due to:
-These cells are prematurely destroyed (life span 20 days)
-Sickle-shaped cells log jam in the microcirculation, these obstructions leads to multiple infarctions and areas of necrosis in brain, bones, spleen other organs
-Due to high rate of hemolysis: Hyperbilirubinemia, jaundice, gallstones are other effects
Clinical features of sickle cell anemia:
(Clinical signs do not usually appear until the child is about 12 months old)
-Pallor, weakness, tachycardia, dyspnea
-Hyperbilirubinemia - jaundice
-Spleen splenomegaly in children, later small fibrotic
-Sickling crises - severe pain due to ischemia of tissues and infarction
-Vascular occlusions and infarctions- bones, stroke, skin ulcerations, hand-foot syndrome
-In lungs- acute chest syndrome due to occlusion & infection
-Frequent infections - due to damaged spleen- pneumonia common cause of death
Diagnostic tests for sickle cell anemia:
-Hemoglobin electrophoresis for HbS
-Prenatal DNA analysis
-Sickle cells in blood smear
-Bone marrow hyperplastic,
high reticulocyte count in the blood
Treatment for sickle cell anemia:
-Hydroxyurea has reduced frequency of crisis
-Prevention of infections, dehydration
-Immunization in children against pneumonia, influenza, meningitis
-Blood transfusions
-Bone marrow transplant
An increased production of erythrocytes and other cells in the one marrow; it is considered a neoplastic disorder; serum erythropoietin
primary polycythemia AKA polycythemia vera
Increase in RBCs in response to prolonged hypoxia
Hypoxia causes increased erythropoietin secretion
A compensation mechanism to provide increased oxygen transport
E.g. in respiratory disorders, high altitudes
Secondary polycythemia AKA erythrocytosis
Clinical features of polycythemia:
-Increased blood pressure: headaches
-Sluggish blood flow due to high viscosity- thrombosis & infarctions; heart, kidney, brain
-Congestive heart failure- due to increased work load on heart
Diagnostic tests for polycythemia:
-Increased red blood cell count
-Increased hematocrit
-Hypercellular bone marrow
Treatment for polycythemia:
-Identify cause
-Drugs or radiation to suppress bone marrow
-Periodic phlebotomy
Indications of blood clotting disorders:
-Bleeding from gums, epistaxis
-Petechiae- pinpoint red spots on skin and mucous membrane
-Purpura and ecchymosis- larger
-More than normal bleeding in trauma
-Bleeding into joints - hemarthroses- swollen, painful
-Hemoptysis
-Hematemesis
-Coarse brown particles ("coffee grounds" emesis)
-Blood in feces
-Black or occult
-Follows acute viral infections in children- resolves
-Chronic Immune thrombocytopenic purpura: In young women caused by antibodies to platelets
-Can be due to bone marrow suppression
Thrombocytopenia
in uremia & ingestion of aspirin
defective platelet function
decrease in clotting factors
Vit K deficiency; chronic liver disease
Examples of bleeding disorders:
thrombocytopenia, defective platelet function, Vit K deficiency, chronic liver disease and inherited deficiencies of clotting factors
Classic hemophilia caused by
inherited deficiency of factor VIII
Most common inherited clotting disorder causing major bleeding
X-linked recessive trait
Manifested in men, women mostly carriers
Varying degrees of severity depending on the factor VIII activity present
Mild- prolonged bleeding after minor tissue trauma
Severe- spontaneous bleeding into joints in those with less than 1% factor VIII activity
Possible hematuria or blood in feces
Hemophilia A
Diagnostic tests for hemophilia A
-Bleeding time and PT normal
-PTT( intrinsic pathway affected) prolonged
-Serum levels of factor VIII are low.
Treatment for hemophilia A
-Replacement therapy for factor VIII
-Desmopressin may raise factor VIII levels
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