NUR 529 EXAM 2 BLUEPRINT QUESTIONS AND
ANSWERS WITH COMPLETE SOLUTIONS | NEW
UPDATE 2026
Hemostasis - ANSWERS Orderly, stepwise process for stopping bleeding that
involves vasospasm, formation of platelet plug, triggering of the coagulation
cascade, and the development of a fibrin clot.
Vascular Spasm - ANSWERS within 30 minutes of damage/trauma to the blood
vessels vascular spasm ensues. It constricts the vessel and reduces blood flow. It is
a transient event that usually lasts minutes or hours.
Formation of the Platelet Plug - ANSWERS 1. Platelets are attracted to
damaged vessel wall. 2. Activation by sub-endothelial tissue. 3. Change from
smooth disks to spiny spheres. 4. Exposing glycoprotein receptors on their
surfaces. (This step requires a protein molecule called von Willebrand factor that
leaks into the injured tissue from the plasma).
Coagulation Cascade - ANSWERS Blood coagulation or development of an
insoluble fibrin clot: stabilization of the plug occurs as the coagulation pathway is
activated on the platelet surface, and fibrinogen is converted to fibrin.
Clot retraction - ANSWERS The consolidation or tightening of the fibrin clot
pulls the edges of the damaged vessel close together, allowing for repair of the
vessel lining.
Clot dissolution - ANSWERS Fibrinolysis occurs through conversion of
plasminogen to plasmin by tissue plasminogen activator (tPA), which is released
,from damaged endothelial cells. This conversion results in digestion of fibrin fibers
within the clot and he production of fibrin degradation production... Clot
dissolves.
Thrombocytopenia - ANSWERS reduction in platelet number. Can result from a
decrease in platelet production, increased sequestration of platelets in the spleen,
destruction of platelets by antibodies, depletion of platelets due to thrombi,
dilution of blood through multiple transfusions, or decreased platelet survival.
Drug Induced Thrombocytopenia - ANSWERS caused by some drugs, such as
aspirin, atorvastatin, and some antibiotics. These drugs induce an antigen-
antibody response and formation of immune complexes that cause platelet
destruction by complement-mediated lysis. In these patients, there is a rapid fall
in the platelet count within 2-3 days of resuming a drug or 77 or more days after
starting a drug for the first time. The platelet count rises rapidly after the drug is
discontinued.
Heparin Induced Thrombocytopenia - ANSWERS caused by an immune
reaction directed against a complex of heparin and platelet factor 4, a normal
component of platelet granules that binds tightly to heparin. The binding of
antibody to platelet factor 4 produces immune complexes that activate the
remaining platelets, leading to thrombosis. Treatment requires immediate
discontinuation of heparin therapy and the use of alternative anticoagulants to
prevent thrombosis recurrence.
Immune Thrombocytopenia Purpura - ANSWERS i. isolated thrombocytopenia
with a platelet count of less than 100,000mL. A purpuric rash along with normal
white blood cells and a normal hemoglobin are found. ITP results in platelet
antibody formation and excess destruction of platelets. Manifestations include a
history of bruising, bleeding from the gums, epistaxis, melena, and abnormal
menstrual bleeding in those with moderately reduced platelet counts. ITP is the
, most common thrombocytopenic disorder among children and often follows an
upper respiratory infection. Treatment is based on the platelet count and the
degree of bleeding. Many people do well without treatment. Corticosteroids are
usually used as initial therapy. Other effective initial treatments include IVIG
(expensive and beneficial effects only last 1-2 weeks).
Thrombotic Thrombocytopenia Purpura - ANSWERS i. familia form, is an
autosomal recessive inheritance. Occurring in late childhood or into adulthood.
Caused by a deficiency of ADAMTS13, which is responsible for severing large WF
multimeters. The unchecked platelet aggregation results in microvascular
occlusions leading to end-organ failure. Clinical manifestations include purpura,
petechia, jaundice, fatigue, tachycardia, bloody urine, and neurologic symptoms
ranging from headache to seizures and altered consciousness. Emergency
treatment includes plasmapheresis.
Iron deficiency anemia RBC characteristics - ANSWERS microcytic and
hypochromic red cells
Megaloblastic anemia RBC characteristics - ANSWERS macrocytic and
misshaped red blood cells.
Sickle cell disease RBC characteristics - ANSWERS abnormally shaped red
blood cells.
Normal RBC characteristics - ANSWERS normocytic and normochromic RBC
Causes of IDA in Adults - ANSWERS chronic blood loss resulting in inadequate
iron available for recycling. In males and postmenopausal females, blood loss may
ANSWERS WITH COMPLETE SOLUTIONS | NEW
UPDATE 2026
Hemostasis - ANSWERS Orderly, stepwise process for stopping bleeding that
involves vasospasm, formation of platelet plug, triggering of the coagulation
cascade, and the development of a fibrin clot.
Vascular Spasm - ANSWERS within 30 minutes of damage/trauma to the blood
vessels vascular spasm ensues. It constricts the vessel and reduces blood flow. It is
a transient event that usually lasts minutes or hours.
Formation of the Platelet Plug - ANSWERS 1. Platelets are attracted to
damaged vessel wall. 2. Activation by sub-endothelial tissue. 3. Change from
smooth disks to spiny spheres. 4. Exposing glycoprotein receptors on their
surfaces. (This step requires a protein molecule called von Willebrand factor that
leaks into the injured tissue from the plasma).
Coagulation Cascade - ANSWERS Blood coagulation or development of an
insoluble fibrin clot: stabilization of the plug occurs as the coagulation pathway is
activated on the platelet surface, and fibrinogen is converted to fibrin.
Clot retraction - ANSWERS The consolidation or tightening of the fibrin clot
pulls the edges of the damaged vessel close together, allowing for repair of the
vessel lining.
Clot dissolution - ANSWERS Fibrinolysis occurs through conversion of
plasminogen to plasmin by tissue plasminogen activator (tPA), which is released
,from damaged endothelial cells. This conversion results in digestion of fibrin fibers
within the clot and he production of fibrin degradation production... Clot
dissolves.
Thrombocytopenia - ANSWERS reduction in platelet number. Can result from a
decrease in platelet production, increased sequestration of platelets in the spleen,
destruction of platelets by antibodies, depletion of platelets due to thrombi,
dilution of blood through multiple transfusions, or decreased platelet survival.
Drug Induced Thrombocytopenia - ANSWERS caused by some drugs, such as
aspirin, atorvastatin, and some antibiotics. These drugs induce an antigen-
antibody response and formation of immune complexes that cause platelet
destruction by complement-mediated lysis. In these patients, there is a rapid fall
in the platelet count within 2-3 days of resuming a drug or 77 or more days after
starting a drug for the first time. The platelet count rises rapidly after the drug is
discontinued.
Heparin Induced Thrombocytopenia - ANSWERS caused by an immune
reaction directed against a complex of heparin and platelet factor 4, a normal
component of platelet granules that binds tightly to heparin. The binding of
antibody to platelet factor 4 produces immune complexes that activate the
remaining platelets, leading to thrombosis. Treatment requires immediate
discontinuation of heparin therapy and the use of alternative anticoagulants to
prevent thrombosis recurrence.
Immune Thrombocytopenia Purpura - ANSWERS i. isolated thrombocytopenia
with a platelet count of less than 100,000mL. A purpuric rash along with normal
white blood cells and a normal hemoglobin are found. ITP results in platelet
antibody formation and excess destruction of platelets. Manifestations include a
history of bruising, bleeding from the gums, epistaxis, melena, and abnormal
menstrual bleeding in those with moderately reduced platelet counts. ITP is the
, most common thrombocytopenic disorder among children and often follows an
upper respiratory infection. Treatment is based on the platelet count and the
degree of bleeding. Many people do well without treatment. Corticosteroids are
usually used as initial therapy. Other effective initial treatments include IVIG
(expensive and beneficial effects only last 1-2 weeks).
Thrombotic Thrombocytopenia Purpura - ANSWERS i. familia form, is an
autosomal recessive inheritance. Occurring in late childhood or into adulthood.
Caused by a deficiency of ADAMTS13, which is responsible for severing large WF
multimeters. The unchecked platelet aggregation results in microvascular
occlusions leading to end-organ failure. Clinical manifestations include purpura,
petechia, jaundice, fatigue, tachycardia, bloody urine, and neurologic symptoms
ranging from headache to seizures and altered consciousness. Emergency
treatment includes plasmapheresis.
Iron deficiency anemia RBC characteristics - ANSWERS microcytic and
hypochromic red cells
Megaloblastic anemia RBC characteristics - ANSWERS macrocytic and
misshaped red blood cells.
Sickle cell disease RBC characteristics - ANSWERS abnormally shaped red
blood cells.
Normal RBC characteristics - ANSWERS normocytic and normochromic RBC
Causes of IDA in Adults - ANSWERS chronic blood loss resulting in inadequate
iron available for recycling. In males and postmenopausal females, blood loss may
