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1. Mechanisms of Hemostasis. See page 623, Understanding
hemostasis, three stages
Answer 1. Vessel vasoconstriction
Injury to a blood vessel causes vascular smooth muscle in the vessel wall to contract. This
instantaneously reduces the flow of blood from the vessel rupture. Both local nervous reflexes and
local humoral factors such as TXA2, which is released from platelets, contribute to the vasoconstriction.
2. Formation of the platelet plug
econds after vessel injury, vWF, released from the endothelium, binds to platelet receptors, causing
adhesion of the platelets to the exposed collagen fibers (inset). As the platelets adhere to the collagen
fibers on the damaged vessel wall, they become activated and release ADP and TXA2. The ADP and TXA2
attract additional platelets, leading to platelet aggregation.
3. Development of a blood clot as a result of the coagulation process
Blood coagulation is a complex process involving the sequential activation of various factors in the
blood. There are two coagulation pathways: (1) the intrinsic pathway begins in the circulation and is initiated
by activation of circulating factor XII and (2) the extrinsic pathway, which is activated by a cellular
lipoprotein called tissue factor that becomes exposed when tissues are injured. Both pathways lead to
the activation of factor X, the conversion of prothrombin to thrombin, and conversion of fibrinogen to
the insoluble fibrin threads that hold the clot together.
Additionally, the two following processes occur which allow for dissolution of the newly formed clot.
,clot retraction
clot dissolution/lysis
2. Bleeding Disorders: Bleeding Associated with Platelet Disorders
Answer Bleeding be-cause of platelet disorders reflects a decrease in platelet number because
of decreased production, increased destruction, or impaired function of platelets. Spontaneous bleeding
from platelet disorders most often involves small vessels of the mucous membranes and skin. Common
sites of bleeding are the mucous membranes of the nose, mouth, gastrointestinal tract, and uterine
cavity. Cutaneous bleeding is seen as pinpoint hemorrhages (petechiae) and purple areas of bruising
(purpura) in dependent areas where the capillary pressure is higher (Fig. 22.3). Petechiae are seen
almost exclusively in conditions of platelet deficiency and not platelet dysfunction. Bleeding of the
intracranial vessels is a rare danger with severe platelet depletion.
thrombocytopenia- A reduction in platelet number, also referred to as thrombocytopenia, is an important
cause
of generalized bleeding. Thrombocytopenia usually refers to a decrease in the number of circulating
platelets to a level less than 150,000/μL.19 The greater the decrease in the platelet count, the
greater the risk of bleeding. Thrombocytopenia can result from a decrease in platelet production,
increased sequestration of platelets in the spleen, or decreased platelet survival.
3. Anemia: Red blood cell characteristics seen in different types
anemias
Answer char-acteristic of iron deficiency anemia; (B) macrocytic and misshaped red blood cells,
characteristic of megaloblastic anemia;
,(C) abnormally shaped red blood cells seen in sickle cell disease; and
(D) normocytic and normochromic red blood cells, as a comparison
Blood loss anemia is characterized by loss of iron-containing red blood cells from the body; hemolytic
anemia involves destruction of red blood cells in the body with iron being retained in the body.
4. Anemias of Deficient Red Cell Production. Iron deficiency
anemia (IDA). Compare causes of IDA in adults and children. What
are the most common causes in each group
Answer Iron deficiency is a common worldwide cause of anemia affecting people of all
ages. The anemia results from dietary deficiency, loss of iron through bleeding, or increased demands.5
Because iron is a component of heme, a deficiency leads to decreased hemoglobin synthesis and
consequent impairment of oxygen delivery.
The usual reason for iron deficiency in adults in the western world is chronic blood loss because there
is inadequate iron available for recycling. In men and postmenopausal women, blood loss may occur
from gastrointestinal bleeding because of peptic ulcer, vascular lesions, intestinal polyps, hemorrhoids, or
cancer.5 In women of child-bearing age, iron demand is increased because of losses from menstruation.
Additionally, in pregnant women, fetal development increases iron requirements for erythropoiesis.5
The manifestations of iron deficiency anemia are related to impaired oxygen transport and lack of
hemoglobin. Depending on the severity of the anemia, fatigability, palpitations, dyspnea, angina, and
tachycardia may occur. Pica, a craving for substances lacking nutritional value such as clay or ice, may
develop. Other clinical manifestations can include a spoon-shaped deformity of the fingernails called
koilonychia, smooth tongue, sores in the corners of the mouth, and sometimes dysphagia.5
, Diagnosis and Treatment.
Low hemoglobin and hematocrit, decreased iron stores, and low serum iron and ferritin characterize iron
deficiency anemia. The red cells are decreased in number and are microcytic and hypochromic (see
Fig. 23.7). Poikilocytosis
(irregular shape) and anisocytosis (irregular size) are also present. Laboratory values indicate reduced
MCHC and MCV.
Prevention of iron deficiency is a primary concern in infants and children. Avoidance of cow's milk, iron
supplemen-tation at 4 to 6 months of age in breast-fed infants, and use of iron-fortified formulas and
cereals are recommended for infants younger than 1 year of age.17 In the 2nd year, a diet rich in iron-
containing foods and use of iron-fortified vitamins will help prevent iron deficiency.
The treatment of iron deficiency anemia in children and adults is directed toward controlling chronic
blood loss, increasing dietary intake of iron,
5. Nonneoplastic Disorders of White Blood Cells: Infectious
Mononucleosis. Clinical course, most common complication, and
laboratory diagnostics
Answer Infec-tious mononucleosis is a self-limiting lymphoproliferative disorder. Eighty-five
percent of the time it is caused by
the Epstein-Barr virus (EBV), a member of the herpesvirus family (Fig. 24.6).13 Epstein-Barr virus is
responsible for approximately 90% of all cases of infectious mononucleosis, with cytomegalovirus
(CMV) accounting for the remainder.14 Approximately 35% to 50% of infections with EBV result in
infectious mononucleosis, most often in adolescents and young adults.13 Once an individual is
infected, the virus will remain present in the B lymphocytes for a lifetime.13
Clinical Course