NUR 529 ADVANCED PATHO EXAM 2 STUDY
GUIDE WITH COMPLETE SOLUTIONS | NEW
UPDATE 2026
Mechanisms of Hemostasis. See page 623, Understanding hemostasis, three
stages. - ANSWERS 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
Bleeding Disorders: Bleeding Associated with Platelet Disorders. - ANSWERS
Bleeding because 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.
Anemia: Red blood cell characteristics seen in different types anemias. -
ANSWERS characteristic 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.
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? - ANSWERS 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 supplementation at 4 to 6 months of age in
Nonneoplastic Disorders of White Blood Cells: Infectious Mononucleosis.
Clinical course, most common complication, and laboratory diagnostics. -
ANSWERS Infectious 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
The onset of infectious mononucleosis usually is insidious. The incubation period
lasts 4 to 6 weeks.14 A prodromal period, which lasts for several days, follows and
is characterized by malaise, anorexia, and chills. The prodromal period precedes
the onset of fever, pharyngitis, and lymphadenopathy. Occasionally, the disorder
comes on abruptly with a high fever. Most people seek medical attention for
severe pharyngitis, which usually is most severe on days 5 to 7 and persists for 7
to 14 days. The lymph nodes are typically enlarged throughout the body,
particularly in the cervical, axillary, and groin areas. Palatal petechiae may be
present in those with sore throat and lymphadenopathy.15
A maculopapular generalized rash has been reported in 3% to 15% of people. The
rash often follows treatment with beta-lactam antibiotics.16
Complications
GUIDE WITH COMPLETE SOLUTIONS | NEW
UPDATE 2026
Mechanisms of Hemostasis. See page 623, Understanding hemostasis, three
stages. - ANSWERS 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
Bleeding Disorders: Bleeding Associated with Platelet Disorders. - ANSWERS
Bleeding because 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.
Anemia: Red blood cell characteristics seen in different types anemias. -
ANSWERS characteristic 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.
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? - ANSWERS 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 supplementation at 4 to 6 months of age in
Nonneoplastic Disorders of White Blood Cells: Infectious Mononucleosis.
Clinical course, most common complication, and laboratory diagnostics. -
ANSWERS Infectious 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
The onset of infectious mononucleosis usually is insidious. The incubation period
lasts 4 to 6 weeks.14 A prodromal period, which lasts for several days, follows and
is characterized by malaise, anorexia, and chills. The prodromal period precedes
the onset of fever, pharyngitis, and lymphadenopathy. Occasionally, the disorder
comes on abruptly with a high fever. Most people seek medical attention for
severe pharyngitis, which usually is most severe on days 5 to 7 and persists for 7
to 14 days. The lymph nodes are typically enlarged throughout the body,
particularly in the cervical, axillary, and groin areas. Palatal petechiae may be
present in those with sore throat and lymphadenopathy.15
A maculopapular generalized rash has been reported in 3% to 15% of people. The
rash often follows treatment with beta-lactam antibiotics.16
Complications
