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Unit 4 Study Guide

1. Know Infectious mononucleosis: patho, clinical manifestations, diagnostics, treatment &
complications. It is Epstein-Barr virus.
a. In infectious mononucleosis (IM), what does the Monospot test detect? Immunoglobulin M
(IgM).
b. Which classic clinical manifestations are symptoms of IM? (Select all that apply.) Lymph node
enlargement, Pharyngitis, Fever.
c. What is a notable characteristic of infectious mononucleosis? Presence of atypical lymphocytes.
d. What is the primary transmission route of the virus that causes infectious mononucleosis?
Transfer of saliva through close personal contact.
2. Know the leukemias: patho, clinical manifestations, diagnostics, treatment & complications
a. Early detection of acute leukemia would include which of the following symptoms? (Select all that
apply.) Anorexia, Bruising, Bone pain.
b. Which statements are true regarding leukemias? (Select all that apply.) A single progenitor cell
undergoes a malignant change; Leukemia is a result of uncontrolled cellular proliferation; Bone marrow
becomes overcrowded; Hematopoietic cell production is decreased. Lymphoma usually starts in the
lymph nodes of the stomach or intestines.
c. The two major forms of leukemia, acute and chronic, are classified by which criteria? (Select all that
apply.) Predominant cell type; Rate of progression.
d. What is the significance of hyperdiploidy when diagnosing and treating leukemia? Hyperdiploidy
indicates a good prognosis.
ALL: Individuals with the Philadelphia chromosome carry the worst type of prognosis. This chromosome is
found in 25% to 30% of adults with ALL.
a. Which description is consistent with acute lymphocytic leukemia (ALL)? ALL is a progressive
neoplasm defined by the presence of greater than 30% lymphoblasts in the bone marrow or blood. The
most common leukemia in children is ALL, and it represents 78% of leukemias in children. It often
occurs in the first decade of life.
b. The cell from which ALL most often arises is: B Cell. A bone marrow analysis reveals an abnormally
high number of lymphoblasts. The likely diagnosis is: ALL.
c. Which molecular anomaly with acute lymphoblastic leukemia carries the worst prognosis? Philadelphia
chromosome.
d. Signs and symptoms of acute leukemia include all of the following except: a. splenomegaly. b.
petechiae. c. lymphadenopathy. d. polycythemia. e. pallor? . Pallor.
CML:
a. Which description is consistent with chronic myelogenous leukemia (CML)? The translocation of
genetic material from genes 9 and 22 creates an abnormal, fused protein identified as BCR-ABL1.
b. Chronic myelogenous leukemia is Diagnosed by the Philadelphia chromosome.
c. CML is characterized by: association with presence of hyperuricemia
CLL:
a. Which description is consistent with chronic lymphocytic leukemia (CLL)? B cells fail to mature into
plasma cells that synthesize immunoglobulins.
b. Which molecular anomaly with acute lymphoblastic leukemia carries the worst prognosis? Philadelphia
chromosome.
c. Signs and symptoms of acute leukemia include all of the following except: a. splenomegaly. b.
petechiae. c. lymphadenopathy. d. polycythemia. e. pallor? D. Polycythemia
AML:
a. Symptoms that individuals with acute myelogenous leukemia (AML) may present with include all of the
following except: a. ecchymosis and petechiae. b. fatigue and weakness. c. hypertension and myocardial
hypertrophy. d. recurrent infections; C.
3. Know multiple myeloma: patho, clinical manifestations, diagnostics, treatment, complications,
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electrolyte imbalances. Causes: Bence Jones protein in urine. B cells and plasma cells.
a. Which electrolyte imbalance accompanies multiple myeloma (MM)? Elevated levels of calcium in
the blood (hypercalcemia) characterize the common presentation of MM.
b. Clinical manifestations of multiple myeloma include all of the following except: a. bone pain. b.
decreased serum calcium. c. M protein. d.renal damage. e. pathologic fractures. B. In multiple
myeloma the malignant plasma cells migrate to and accumulate in the bone marrow.
c. Which of the following cells proliferate in multiple myeloma? Plasma cells
4. Know lymphomas: patho, clinical manifestations, diagnostics, treatment and complications
a. Local signs and symptoms of Hodgkin disease-related lymphadenopathy are a result of which of
the following? Pressure and obstruction. The peak incidence of Hodgkin lymphoma occurs
during the early 20s through the 30s and again in the sixth and seventh decades of life. The
incidence is greater in whites, and Japan and Australia have the lowest incidence. An increase in
Reed-Sternberg cells occurs.
b. Burkitt lymphoma is fast growing and primarily involves the jaw and facial bones; it is associated
with Epstein-Barr virus. Burkitt lymphoma is a type of non-Hodgkin lymphoma and most
common in children from east-central Africa and New Guinea, although rare in the United States.
5. What are Reed-Sternberg cells?
a. Reed-Sternberg (RS) cells represent malignant transformation and proliferation of which of the
following? B Cells.
b. Hodgkin disease is characterized by the presence of which. Reed Sternberg cells.
6. Know Burkitt lymphoma: patho, clinical manifestations, diagnostics, treatment and complications.
a. Which virus is associated with Burkitt lymphoma in African children? Epstein-Barr virus.
b. What are the clinical manifestations of advanced non-African Burkitt lymphoma? (Select all that
apply.) Abdominal swelling, Night sweats, Fever
c. Which of the following is a TRUE statement regarding Burkitt lymphoma? It is a fast-growing
tumor of the jaw and facial bones.
7. Know DIC: patho, clinical manifestations, diagnostics, treatment & complications
a. Which disorder is described as an unregulated release of thrombin with subsequent fibrin formation and
accelerated fibrinolysis? Disseminated intravascular coagulation (DIC).
b. In disseminated intravascular coagulation (DIC), what activates the coagulation cascade? Tissue factor
(TF) located in the endothelial layer of blood vessels and subcutaneous tissue.
c. Which proinflammatory cytokines are responsible for the development and maintenance of disseminated
intravascular coagulation (DIC)? Tumor necrosis factor-alpha (TNF-α); IL-1, IL-6, and IL-8; and
platelet-activating factor (PAF).
d. In disseminated intravascular coagulation (DIC), what are the indications of microvascular thrombosis?
Symmetric cyanosis of fingers and toes.
e. What is the most reliable and specific test for diagnosing disseminated intravascular coagulation (DIC)?
D-dimer.
f. What conditions are evidence of disseminated intravascular coagulation (DIC)? (Select all that apply.)
Fibrinolytic activity; Consumption of platelets; End-organ damage; Depletion of clotting factors:
rocoagulant activity (not inhibition), fibrinolytic activity, consumption of platelets, end-organ damage,
and depletion of clotting factors are all evidence for DIC.
g. DIC is associated with: a. endothelial damage. b. the activation of factor X. c. the release of tissue factor.
All are correct.
h. In DIC, plasmin: a. begins to degrade fibrin before a stable clot develops.
8. Genetic abnormalities leading to thrombus formation.
a. Immune thrombocytopenia (ITP) is a(n) _____ condition in adults and a(n) _____ condition in children.
Chronic; acute.
b. Which statement best describes heparin-induced thrombocytopenia (HIT)? Immunoglobulin G immune-
mediated adverse drug reaction that reduces circulating platelets.
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c. What term is used to identify thrombi that occlude arterioles and capillaries and are made up of platelets
with minimal fibrin and erythrocytes? Thrombotic thrombocytopenic purpura (TTP). Which of the
following is characterized by what is referred to as pathognomonic pentad of symptoms? Acute
idiopathic thrombotic thrombocytopenic purpura which is also Mononuclear phagocytes in the spleen
remove antibody-coated platelets from circulation.
d. What are the most significant risk factors for the development of thrombus formation as referred to by
the Virchow triad? (Select all that apply.). Endothelial injury to blood vessels, Turbulent arterial blood
flow, Rapid coagulation of the blood, Stagnant venous blood flow.
e. Which factors can cause the thrombus formation known as Virchow triad? (Select all that apply.) Injury
to endothelium, Hypercoagulability of the blood, Abnormalities of blood flow. The factors that can
cause thrombus formation known as Virchow triad are: (1) vessel wall injury, (2) blood flow
abnormalities, and (3) altered blood constituents leading to hypercoagulability.
9. Know normal/abnormal hematology values in infants
a. During fetal life, the synthesized hemoglobin is composed of two alpha and two beta chains: False.
Although a frequent problem,
b. ABO incompatibility seldom results in significant disease: True.
c. Which blood cell type is elevated at birth but decreases to adult levels during the first year of life? Only
monocyte counts are high in the first year of life and then decrease to adult levels.
d. An infant's hemoglobin must fall below _5_ g/dl before signs of pallor, tachycardia, and systolic
murmurs occur.
10. Know hemolytic disease of the newborn: patho, clinical manifestations, diagnostics,
treatment and complications.
a. What is the cause of polycythemia in the fetus? Erythroblastosis fetalis, also known as
hemolytic disease of the newborn (HDN), is an alloimmune disease in which maternal blood
and fetal blood are antigenically incompatible, causing the mother's immune system to
produce antibodies against fetal erythrocytes. Increased erythropoiesis occurs in response to
the hypoxic intrauterine environment. The hypoxic intrauterine environment stimulates
erythropoietin production in the fetus.
b. How does hemolytic disease of the newborn (HDN) cause acquired congenital hemolytic
anemia? HDN is an alloimmune disease in which the mother's immune system produces
antibodies against fetal erythrocytes, which are recognized as foreign and removed from
circulation.
c. Hemolytic disease of the newborn (HDN) can occur if the mother: Is Rh-negative and the
fetus is Rh-positive.
d. When diagnosed with hemolytic disease of the newborn (HDN), why does the newborn
develop hyperbilirubinemia after birth but not in utero? Excretion of unconjugated bilirubin
through the placenta into the mother's circulation is no longer possible.
11. What is kernicterus?
a. What is the name of the disorder in which levels of bilirubin remain excessively high in the newborn and
are deposited in the brain? Without replacement transfusions, during which the child receives Rh-
negative erythrocytes, the bilirubin is deposited in the brain, a condition called kernicterus.
b. What treatment prevents the development of kernicterus in an infant born with hemolytic disease of the
newborn (HDN). Replacement transfusion of new Rh-positive blood that is not contaminated with anti-
Rh antibodies.
12. Know G-6-PD: patho, inherited pattern, clinical manifestations, diagnostics, treatment and
complications.
a. Glucose 6-phosphate dehydrogenase (G6PD) deficiency is what type of inherited disorder? X-
linked recessive. G6PD deficiency is an inherited, X-linked recessive disorder. This selection is
the only option that accurately identifies the mode of inheritance for the stated disorder.
b. Which statement is true regarding glucose-6-phosphate dehydrogenase (G6PD) deficiency?
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G6PD deficiency is an X-linked recessive disorder most commonly found in males. It is

associated with icterus neonatorum in Asian and Mediterranean infants and results in hemolysis.
Fava beans and the ingestion of certain drugs can cause a reaction.
13. Know sickle cell disease: patho, inherited pattern, clinical manifestations, diagnostics,
treatment and complications May present early as symmetric, painful swelling of the hands and
feet, May result in aplastic crises.
a. Sequestration crisis is a serious complication of sickle cell disease seen only in the young
child. True.
b. Sickle cell disease is autosomal recessive disease.
c. In sickle cell disease, vasoocclusive crisis is the result of: b. the "plugging" of peripheral blood
vessels by "stiff" sickled erythrocytes.
d. Sickle cell disease is classified as a(an): Disorder initiated by hypoxemia and acidosis.
Sickling is an occasional, intermittent phenomenon that can be triggered or sustained by one or
more of the following stressors: decreased oxygen tension (PO2) of the blood (hypoxemia),
increased hydrogen ion concentration in the blood (decreased pH), increased plasma
osmolality, decreased plasma volume, and low temperature.
e. Hemoglobin S (HbS) is formed in sickle cell disease as a result of which process. HbS is
formed by a genetic mutation in which one amino acid (valine) replaces another (glutamic
acid).
f. What is the reason most children diagnosed with sickle cell anemia are not candidates for
either bone marrow or stem cell transplants? Bone marrow or stem cell transplants can cure
sickle cell anemia. However, the only reason these procedures are not currently an option for
most children is because well-matched stem cell donors are often difficult to find.
g. Which manifestations of vasoocclusive crisis are associated with sickle cell disease (SCD) in
infants. Edema of the hands and feet. Symmetric, painful swelling of the hands and feet (hand-
foot syndrome) caused by infarction in the small vessels of the extremities is often the initial
manifestation of SCD in infants.
h. What is the chance with each pregnancy that a child born to two parents with the sickle trait
will have sickle cell disease (SCD). A 25% chance exists with each pregnancy that a child
born to two parents with sickle cell trait will have SCD.
i. Which of the following is a trigger for sickling? (Select all that apply.) A. Hypoxemia C.
Increased plasma osmolality E. Dehydration Hypoxemia is the most common cause of
sickling. Sickling is an occasional, intermittent phenomenon that can be triggered or sustained
by hypoxemia, increased hydrogen ion concentration in the blood (decreased pH), increased
plasma osmolality, decreased plasma volume, and low temperature. HbS, also known as sickle
hemoglobin, reacts to deoxygenation and dehydration by solidifying and stretching the
erythrocyte into an elongated sickle shape.
14. Know the thallasemias: patho, inherited pattern, clinical manifestations, diagnostics,
treatment and complications.
a. Which type of anemia occurs as a result of thalassemia? Microcytic, hypochromic.
b. What is the fundamental defect that results in beta-thalassemia major. A severe uncoupling
of α- and β-chain synthesis occurs. The fundamental defect in beta-thalassemia is the
uncoupling of α- and β-chain synthesis. β-Chain production is moderately depressed in the
heterozygous form—beta-thalassemia minor, and severely depressed in the homozygous
form—beta-thalassemia major (also called Cooley anemia).
c. The alpha- and beta-thalassemias are considered what types of inherited disorder?
Autosomal recessive
15. Know hemophilias/bleeding disorders: patho, inherited pattern, clinical manifestations,
diagnostics, treatment and complications.
a. Hemophilia B is caused by a deficiency of which clotting factor? Only factor IX deficiency
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causes hemophilia B (Christmas disease).

b. Hemophilia A is considered to be what type of inherited disorder? Hemophilia A (classic
hemophilia) is inherited as an X-linked recessive disorder.
c. Which disease is an autosomal dominant inherited hemorrhagic disease? The bleeding
disorder, von Willebrand disease, results only from an inherited autosomal dominant trait.
von Willebrand disease is caused by factor VIII deficiency.
d. Which type of hemophilia affects only men? only hemophilia A (classic hemophilia) is
caused by factor VIII deficiency and is inherited as an X-linked recessive disorder that
affects men and is transmitted by women.
e. Which hemophilia occurs equally in both men and women? only hemophilia C (factor XI
deficiency) occurs as an autosomal recessive disease while occurring equally in men and
women.
16. Know Heparin Induced Thrombocytopenia (HIT): patho, etiology, clinical manifestations,
diagnostics, treatment and complications. Clinically administered heparin or heparin sulfate (on
the surface of endothelial cells) binds to AT-III and induces a conformational change that greatly
enhances its activity. Under normal conditions, the presence of endothelial cell heparin sulfate and
available AT-III in the circulation cooperate to protect the vessels from the effects of spontaneously
activated thrombin.
a. Which statement best describes heparin-induced thrombocytopenia (HIT)? Immunoglobulin G
immune-mediated adverse drug reaction that reduces circulating platelets.
THE HEART
17. Know the heart: circulation (oxygenated and deoxygenated blood), chambers, valves, cardiac
cycle, pressures.
a. Which statement does not accurately describe the pericardium: It is made up of connective tissue
and a surface layer of squamous cells.
b. Which cardiac chamber has the thinnest wall and why? The right and left atria; they are low-
pressure chambers that serve as storage units and conduits for blood. The two atria have the
thinnest walls because they are low-pressure chambers that serve as storage units and conduits for
blood that is emptied into the ventricles.
c. Which chamber of the heart endures the highest pressures? Pressure is greatest in the systemic
circulation, driven by the left ventricle.
d. Regarding the heart's valves, what is a function of the papillary muscles? These muscles prevent
backward expulsion of the atrioventricular valve.
e. During the cardiac cycle, why do the aortic and pulmonic valves close after the ventricles relax?
Blood fills the cusps of the valves and causes the edges to merge, closing the valves.
f. Oxygenated blood flows through which vessel? Only the four pulmonary veins, two from the right
lung and two from the left lung, carry oxygenated blood from the lungs to the left side of the
heart.
g. Pressure in the left ventricle must exceed pressure in which structure before the left ventricle can
eject blood? Aorta.
h. Continuous increases in left ventricular filing pressures result in which disorder? Pressure changes
are important because increased left ventricular filling pressures back up into the pulmonary
circulation, where they force plasma out through vessel walls, causing fluid to accumulate in lung
tissues (pulmonary edema).
i. When the volume of blood in the ventricle at the end of diastole increases, the force of the
myocardial contraction during the next systole will also increase, which is an example of which
law or theory about the heart? This concept is expressed oly in the Frank-Starling law; the cardiac
muscle, like other muscles, increases its strength of contraction when it is stretched.
j. What is the major determinant of the resistance that blood encounters as it flows through the
systemic circulation? Muscle layer of the arterioles
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k. Normal systolic pressure within the left ventricle is in the range of: a. 90 to 140mm Hg.
18. Know the Electrical activity of the heart as displayed on the EKG- ex-what does the QRS
represent, etc.
a. Which phase of the normal myocardial cell depolarization and repolarization correlates with
diastole? Phase 3.
b. The PR interval is a measure of time from the onset of atrial activation to the onset of ventricular
activation; it normally ranges from 0.12 to 0.20 second. The PR interval represents the time
necessary to travel from the sinus node through the atrium, the atrioventricular (AV) node, and the
His-Purkinje system to activate ventricular myocardial cells.
c. Which complex (wave) represents the sum of all ventricular muscle cell depolarizations? Only the
QRS complex represents the sum of all ventricular muscle cell depolarizations.
19. Know coronary artery blood flow and effects of occlusions-which part of the heart is affected by
occlusion in each coronary artery.
a. Occlusion of the left anterior descending artery during a myocardial infarction would interrupt blood
supply to which structures? a. Left and right ventricles and much of the interventricular septum.
b. Occlusion of the circumflex artery during a myocardial infarction would interrupt blood supply to
which area? Left atrium and the lateral wall of the left ventricle.
c. The coronary ostia are located in the: Coronary arteries receive blood through openings in the aorta,
called the coronary ostia.
d. The coronary sinus empties into which cardiac structure? The cardiac veins empty only into the right
atrium through another ostium, the opening of a large vein called the coronary sinus.
e. What is the ratio of coronary capillaries to cardiac muscle cells? The heart has an extensive capillary
network, with approximately 3300 capillaries per square millimeter (ca/mm2) or approximately one
capillary per one muscle cell (muscle fiber). Each cardiac action potential travels from the SA node to
the AV node to the bundle of His (AV bundle), through the bundle branches, and finally to the Purkinje
fibers and the ventricular myocardium, where the impulse is stopped. The refractory period of cells that
have just been polarized prevents the impulse from reversing its path. The refractory period ensures
that diastole (relaxation) will occur, thereby completing the cardiac cycle.
20. Know Beta 1, Beta 2 and Beta 3 receptors of the heart and how catecholamines affect each.
a. What can shorten the conduction time of action potential through the atrioventricular (AV) node?
Catecholamines speed the heart rate, shorten the conduction time through the AV node, and increase
the rhythmicity of the AV pacemaker fibers.
b. What is the effect of epinephrine on B3 receptors on the heart? Prevents overstimulation of the heart
by the sympathetic nervous system. B3 receptors are found in the myocardium and coronary vessels.
In the heart, stimulation of these receptors opposes the effects of B1- and B2-receptor stimulation
and negative inotropic effect. Thus B3 receptors may provide a safety mechanism that decreases
myocardial contractility to prevent overstimulation of the heart by the sympathetic nervous system.
21. Know hypertension: patho, etiology, RAAS system effects, clinical manifestations, diagnostics,
treatment and complications/effects on other organs.
a. Which condition is a complication of hypertension? C. congestive heart failure.
b. Which statements are true regarding hypertension? (Select all that apply.) A. Approximately two
thirds of Americans older than 60 years of age have hypertension. C. Hypertension is defined as a
diastolic pressure higher than 90 mmHg. D. Hypertension is a systolic pressure of 140 mmHg or
higher.
c. Which of the following are risk factors for hypertension? (Select all that apply.) A. Positive family
history for hypertension C. High dietary sodium intake D. Glucose intolerance
22. Know Rheumatic Fever: patho, etiology, clinical manifestations, diagnostics, treatment and
complications CAUSED FROM A DELAYED AUTOIMMUNE RESPONSE TO STREP
INFECTION* inflammatory disease caused by Group A beta-hemoytic Strep; febrile illness; if
untreated progresses to rheumatic heart disease; treatment with antibiotics; may occur following strep
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throat. carditis, polyarthritis, chorea- involuntary CNS movements, erythema marginatum - trunk
rash. If treated with antibiotics then no problem; if untreated may lead to cardiovascular dysfunction
23. Know infective endocarditis: patho, etiology, clinical manifestations, diagnostics, treatment and
complications. inflammation of the endocardium - primarily the cardiac valvitis; lethal disease without
treament; caused by bacteria, viruses, fungi, prosthetic valves; treatment open heart surgery
24. Know heart defects in children. What kind of murmur will you hear and where? How do children
compensate for heart defects?
a. An 8-week-old infant presents to the pediatrician for a well-baby checkup. Physical exam reveals a
murmur, and an echocardiogram confirms a ventricular septal defect. Which genetic disorder is
likely to accompany this diagnosis? Down syndrome is the genetic factor that would most likely
accompany the diagnosis of a congenital heart defect
b. Which statements are true regarding congenital heart defects? (Select all that apply.). A. Congenital
heart disease is the second leading cause of death in infants during the first year of life. B. Incidence
of heart defects is high in stillbirths, low-birth-weight babies, and spontaneous abortions. E. Infants
with trisomy 21 have a high incidence of congenital heart disease.
c. Intrauterine exposure to which factor could be responsible for a diagnosis of congenital heart
disease? One of the identified causes of cardiac defects is an intrauterine viral infection, especially
rubella.
d. A newborn develops a murmur and cyanosis shortly after birth. A diagnosis of pulmonic stenosis
(PS) is made after an echocardiogram revealed narrowing of the pulmonary: Valve
e. What is the most common type of congenital heart defect assessed for in infants? The most common
type of congenital heart defect is a VSD.
f. An infant undergoes an echocardiogram for a suspected heart defect. Tests reveal an opening in the
middle of the atrial septum. What term would the nurse use to describe this defect? An opening in
the middle of the atrial septum is referred to as an ostium secundum ASD.
g. An 8-week-old infant's well-baby check reveals a murmur, and an echocardiogram shows a large
ventricular septal defect. If left untreated, what condition could develop? Pulmonary hypertension.
h. A newborn child is diagnosed with tetralogy of Fallot. What symptoms would the nurse expect to
observe in the child? The child will experience cyanosis and hypoxia.
25. Know function and life span of RBCs (erythrocyte) and platelets.
a. Erythrocytes are solely responsible for tissue oxygenation. Because it cannot undergo mitotic division,
the erythrocyte has a limited life span of approximately 120 days.
b. Reversible deformity enables the erythrocyte to assume a more compact torpedo-like shape, squeeze
through the microcirculation, and return to normal.
c. A platelet circulates for approximately 10 days and ages.
d. Macrophages of the mononuclear phagocyte system, mostly in the spleen, remove platelets.
e. The erythrocyte's size and shape are ideally suited to its function as a gas carrier. A red blood cell
(RBC) is a small disk with two unique properties: (1) a biconcave shape and (2) the capacity to be
reversibly deformed.
26. Know the process of hemoglobin synthesis. What is methemoglobin?
a. Iron and B6 (pyridoxine) are necessary for hemoglobin synthesis (see Table 27-6).
27. Know function of all granulocytes and agranulocytes.
Neutrophils, basophils, and eosinophils are granulocytes. The agranulocytes include monocytes and
macrophages.
28. Know hematopoiesis-the process and where does it occur in the fetus, neonate, child and adult. The
main difference between hematopoiesis and erythropoiesis is that hematopoiesis is the formation of mature
blood cells whereas erythropoiesis is the formation of mature erythrocytes. hemopoiesis, production of blood
cells and platelets occurs in bone marrow). The spleen is the largest of the secondary lymphoid organs and
the site of fetal hematopoiesis.
29. Know erythropoiesis and the iron cycle. What are the nutritional requirements?
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a. Cobalamin and folate are necessary for the synthesis of DNA and for the maturation of erythrocytes.
b. Recycling of iron from erythrocytes is made possible by which of the following? a. Transferrin:
Transferrin is recycled (transferrin cycle) in the following manner: (1) the transferrin-iron complex
binds to a transferring receptor on the erythroblast's plasma membrane; (2) the complex moves into the
cell by receptor-mediated endocytosis; (3) iron is released (dissociated) from transferrin; and (4) the
dissociated transferrin is returned to the bloodstream for reuse.
30. Know the mechanisms of hemostasis: function of the blood vessels, platelets and clotting factors.
Know what regulates hemostasis. What vitamins are needed for normal clotting factor synthesis?
a. Platelet activation involves which processes? (Select all that apply.) A. Adhesion, B. Aggregation,
Platelet activation involves three linked processes: (1) adhesion, (2) activation, and (3) aggregation.
Platelet activation stimuli include epinephrine, thrombin, and collagen. Inhibition is associated with
tissue factor inhibitor and inhibits factor Xa of the clotting cascade. Inactivation of COX-1 decreases
the production of thromboxane A2 (TXA2) and decreases platelet activation. In the clotting process,
collagen provides a particularly strong stimulus to activate platelets.
b. The major regulatory factors that control hemostasis reside where the greatest probability of clotting
would occur—on the endothelial cell surface.
c. The primary anticoagulant mechanisms include thrombin inhibitors (e.g., antithrombin III), tissue
factor inhibitors (e.g., tissue factor pathway inhibitor), and mechanisms for degrading activated
clotting factors (e.g., protein C).
d. Vitamin _____ is required for normal clotting factor synthesis by the _____. K Liver.
31. Know function of the spleen. What happens when a patient has a splenectomy?
a. Splenic absence from any cause (e.g., atrophy, traumatic injury, removal because of disease) has several
secondary effects on the body, among them an increase in morphologically defective blood cells in the
circulation, confirming the spleen's role in removing old or damaged cells. The number of defective
cells in circulation increases.
b. The spleen is the largest of the secondary lymphoid organs and the site of fetal hematopoiesis
(hemopoiesis, production of blood cells and platelets occurs in bone marrow).
32. Know function of lymph nodes. How are they affected by inflammation/infection? Why?
a. Which statements are true regarding lymph nodes? (Select all that apply.) A. Lymph nodes collect
interstitial fluid. B. Lymph nodes are part of the hematologic and immune system. D. Lymph nodes may
enlarge and become tender as a result of infection. Lymph nodes collect interstitial fluid and eventually
return it to circulation via the superior vena cava. Functionally, lymph nodes are part of the hematologic
and immune systems. Infection may result in lymph node enlargement and tenderness (reactive lymph
node). lymphocytes proliferate. Blood flows into the lymph nodes through the lymphatic artery, not the
afferent lymph vessels.
b. During an infection, why do lymph nodes enlarge and become tender? The B lymphocyte proliferation
in response to significant antigen (e.g., during infection) may result in lymph node enlargement and
tenderness (reactive lymph node).
c. Neutrophils are the chief phagocytes of early inflammation.
33. Know all the anemias: patho, etiology, clinical manifestations, diagnostics, treatment,
compensation of the body and complications.
a. The absence of parietal cells would prevent the absorption of an essential nutrient necessary to
prevent pernicious anemia.
b. Anemia refers to deficiency of erythrocytes and hemoglobin.
c. Which of the following symptoms are consistent with aplastic anemia but not with pernicious
anemia? Petechiae and purpura.
d. A 40-year-old white, pregnant woman with four children experienced weakness, loss of
appetite, and pallor. Her CBC revealed the following: Macrocytic RBCs 2.5 x 10^6/mm3
Hematocrit level of 32% Hemoglobin level of 8.7 g/dl She most likely has: Folic acid anemia.
e. The blood disorder of infancy and childhood caused by poor dietary iron intake is: a. a
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microcytic-hypochromic anemia.
f. During childhood, when is dietary iron deficiency commonly diagnosed? Iron deficiency
anemia is the most common blood disorder of infancy and childhood, with the highest incidence
occurring between 6 months and 2 years of age.?
g. True or False The neurologic symptoms in vitamin B12 deficiency anemia are not reversed
even with appropriate treatment. True
h. True or False Considering oral iron therapy, the ferric form is preferred to the ferrous form
because ferric is more readily absorbed. False
i. True or False In hemolytic anemia, the bone marrow is capable of increasing red cell production
because of elevated levels of erythropoietin. True
j. True or False Anemia of chronic disease (ACD) is initially a normochromic and normocytic
anemia, but as the condition progresses, it becomes hypochromic and microcytic. True
k. In some anemias the erythrocytes are present in various sizes, which is referred to as:
a. poikilocytosis.
b. isocytosis.
c. anisocytosis.
d. microcytosis.
l. 1. The major physiologic manifestation of anemia is:
a. hypotension.
b. hyperesthesia.
c. hypoxia.
d. ischemia.
m.
34. How do deficiencies in folate and B12 cause anemia?
a. The cause of macrocytic-normochromic anemia is: deficiency of vitamin B12 and folic acid.
35. Know all about vitamin B12-how is it given, how do you know vitamin B12 administration is
effective?
a. Dietary vitamin B12 is a large molecule that requires a protein secreted by parietal cells into the
stomach (intrinsic factor [IF]) to transport across the ileum. Defects in IF production lead to
decreased B12 absorption and pernicious anemia.
b. An individual who has chronic gastritis and tingling in his or her fingers requires which of the
following for treatment? Vitamin B12 by intramuscular injection.
c. Deficiencies in folate and vitamin B12 alter the synthesis of:
a. RNA.
b. Cell membrane
c. DNA.
d. mitochondria.
d. The underlying disorder of _____ anemia is defective secretion of intrinsic factor, which is
essential for the absorption of vitamin B12.
a. Microcytic
b. Pernicious
c. Hypochromic
d. Hemolytic
e. How is the effectiveness of vitamin B12 therapy measured?
a. Reticulocyte count
b. Serum transferring
c. Hemoglobin
d. Serum vitamin B12
36. Know myeloproliferative RBC disorders: patho, etiology, clinical manifestations, diagnostics,
treatment and complications. Polycythemia vera.
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a. Symptoms of polycythemia vera are mainly the result of:

a. a decreased erythrocyte count.
b. destruction of erythrocytes.
c. increased blood viscosity.
d. neurologic involvement.
b. Treatment for polycythemia vera involves:
a. therapeutic phlebotomy and radioactive phosphorus.
b. restoration of blood volume by plasma expanders.
c. the administration of cyanocobalamin.
d. blood transfusions.
37. What happens to leukocytes during a Type I allergic (hypersensitive) reaction? What change is observed
in leukocytes during an allergic disorder (type I hypersensitivity) often caused by asthma, hay fever, and
drug reactions? Eosinophilia.

38. What is Raynaud phenomenon and disease? Patho?

a. Cyanosis, followed by rubor and paraesthesias in the digits, are associated with which condition?
A. Raynaud phenomenon or disease.
39. How do varicose veins develop? Patho? A varicose vein is a common condition. It is a superficial vein in
which blood has pooled. Varicose veins typically involve the saphenous veins of the legs and are distended,
tortuous, and palpable. Varicose veins are caused by 1) trauma to the saphenous veins that damages one or
more valves, and 2) gradual venous distention caused by the action of gravity on blood in the legs
40. Know consequences of low albumin.
a. Albumin molecules are large and do not freely diffuse through the vascular endothelium, and therefore
maintain the critical colloidal osmotic pressure (or oncotic pressure) that regulates the passage of water
and solutes into the surrounding tissues.
b. Effect of low plasma albumin: In the case of decreased production (e.g., cirrhosis, other diffuse liver
diseases, protein malnutrition) or excessive loss of albumin (e.g., certain kidney diseases, extensive
burns), the reduced oncotic pressure leads to excessive movement of fluid and solutes into the tissues
and decreased blood volume.
c. Low albumim: Osmotic pressure decreases, thus water moves from the capillaries to the interstitium.