HEMODYNAMIC DISORDERS REVIEW
OF PATHOLOGY CH4 ILLUSTRATED
PATHOLOGY QUESTION WITH
CORRECT ANSWERS
D) Petechiae
Note the small punctate 1- to 2-mm petechial hemorrhages on the epicardial surface
shown in the figure. Such hemorrhages most often result from reduced numbers of
platelets or reduced platelet function. It is platelets that plug small vascular defects.
Congestion occurs when there is vascular dilation with pooling of blood within an organ.
A hematoma is a collection of blood in a potential space or within tissue. Purpura
denotes blotchy hemorrhage on skin, serosal surfaces, or muco - Answer-An autopsy
study is performed to correlate patterns of hemorrhage with underlying causes. Patients
with the gross appearance of hemorrhage shown in the figure had minimal blood
volume loss, but an appearance similar to this in many other organs. Which of the
following terms best describes this pattern?
A Congestion
B Ecchymosis
C Hematoma
D Petechiae
E Purpura
E) Vasoconstriction
The initial response to arteriolar injury is vasoconstriction, since there is smooth muscle
in the vessel wall. But this is transient, and the coagulation mechanism must be initiated
to maintain hemostasis. Fibrin polymerization is part of secondary hemostasis after the
vascular injury is initially closed. Neutrophils are not essential to hemostasis. Platelet
aggregation occurs with release of factors such as ADP, but this takes several minutes.
Protein C is involved in anti - Answer-A superficial puncture wound from a needlestick
injury leads to a small amount of bleeding in a healthy person. Sec- onds after this injury
occurs, the bleeding stops. Which of the following mechanisms is most likely to stop
small arteriolar blood loss from this injury?
A Fibrin polymerization
B Neutrophil chemotaxis
C Platelet aggregation
D Protein C activation
E Vasoconstriction
,C) Prostacyclin
Endothelial injury releases glycoprotein tissue factor (factor III) that drives the
coagulation process and activates platelets. Adjacent intact endothelium generates
prostacyclin (PGI2) via arachidonic acid metabolism to inhibit clot propagation beyond
where it is needed. PGI2 and nitric oxide are powerful vasodilators and inhibitors of
plate- let aggregation. This limits thrombus formation just to the area of injury.
Glycoprotein IIb/IIIa, which induces shape change; phospholi - Answer-A 15-year-old
girl incurs a cut to the sole of her foot after stepping on a piece of broken glass. On
examination, a superficial 0.5-cm laceration ceases to bleed within 5 minutes after
application of local pressure. Which of the following substances is released by
endothelium and is most likely to counteract platelet aggregation near this site of injury?
A Glycoprotein IIb/IIIa
B Platelet-activating factor
C Prostacyclin
D Tissue-type plasminogen activator
E Thrombomodulin
F Thromboxane
E) Thrombomodulin
Thrombomodulin is present on intact endothelium and binds thrombin, which then
inhibits coagulation by activating protein C. Normally, thrombin activates factors V, VIII,
and IX, and also stabilizes the secondary hemostatic plug by activating factor XIII, which
cross-links fibrin. Thrombin helps activate platelets. Calcium is a cofactor that assists
clotting in the coagulation cascade (ethylene-diaminetetraacetic acid [EDTA] in some
blood collection tubes binds calcium to prev - Answer-In an experiment, thrombus
formation is studied in areas of vascular damage. The propagation of a thrombus in an
area of vascular injury to adjacent normal arteries is prevented. Which of the following
substances diminishes thrombus propagation by activating protein C?
A Calcium
B Fibrin
C Platelet factor 4
D Prothrombin
E Thrombomodulin
F Tumor necrosis factor (TNF)
B) Platelet adhesion
Von Willebrand factor (vWF) acts like a "glue" between platelets and the exposed
extracellular matrix of the vessel wall after vascular injury. None of the other steps listed
depends upon vWF. Because the patient's prothrombin time (PT) is normal, a lack of
prothrombin or the presence of an inhibitor is unlikely. Because vWF stabilizes factor
VIII, a deficiency of vWF may prolong the partial thromboplastin time (PTT). - Answer-A
,26-year-old woman has a history of frequent nose- bleeds and increased menstrual
blood flow. On physical examination, petechiae and purpura are present on the skin of
her extremities. Laboratory studies show normal partial thromboplastin time (PTT),
prothrombin time (PT), and platelet count, but decreased von Willebrand factor activity.
This patient most likely has a derangement in which of the following steps in
hemostasis?
A Fibrin polymerization
B Platelet adhesion
C Platelet aggregation
D Prothrombin generation
E Prothrombin inhibition
F Vasoconstriction
B Aggregation of platelets
Aspirin blocks the cyclooxygenase pathway of arachidonic acid metabolism and
generation of eicosanoids in platelets, including thromboxane A2, to block
vasoconstriction and inhibit platelet aggregation. Platelet adhesion to extracellular
matrix is mediated by interactions with von Willebrand factor. Tissue factor (factor III),
produced by injured endothelium as well as subendothelial smooth muscle and
fibroblasts, is released with tissue injury and is not platelet dep - Answer-A 59-year-old
woman with a history of diabetes mellitus had a myocardial infarction 3 months ago. Her
BMI is 35. She is now taking a low dose of aspirin to reduce the risk for recur- rent
arterial thrombosis. On which of the following steps in hemostasis does aspirin have its
greatest effect?
A Adhesion of platelets to collagen
B Aggregation of platelets
C Production of tissue factor
D Synthesis of von Willebrand factor
E Synthesis of antithrombin III
A) Adenosine diphosphate
ADP is released from the platelet-dense granules and is a potent stimulator of platelet
aggregation. ADP also stimulates further release of ADP from other platelets. Many
other substances involved in hemostasis, such as fibrinogen, fibronectin, and factors V
and VIII, are stored in the α granules of platelets. Thromboxane A2, another powerful
aggregator of platelets, is synthesized by the cyclooxygenase pathway. Fibronectin
forms part of the extracellular matrix betwee - Answer-In an experiment, platelet
function is analyzed. A sub- stance is obtained from the dense body granules of normal
pooled platelets from healthy blood donors. When this sub- stance is added to platelets
obtained from patients with a bleeding disorder, no platelet aggregation occurs. Adding
the substance to platelets from a normal control group induces platelet aggregation.
Which of the following substances is most likely to produce these effects?
, A Adenosine diphosphate
B Antithrombin III
C Fibronectin
D Fibrinogen
E Plasminogen
F Thromboxane A2
A) Decrease in production of thrombin
He has hemophilia A. Factor VIII, tissue factor (III), and factor V act as cofactors or
reaction accelerators in the clot- ting cascade leading to thrombin production. Factor VIII
acts as a reaction accelerator for the conversion of factor X and factor Xa. The platelet
surface provides phospholipid for assembly of coagulation factors. Platelet aggregation
is promoted by thromboxane A2 and ADP. Thromboxane A2 is released when platelets
are activated during t - Answer-A 12-year-old boy has a 10-year history of multiple soft
tissue hemorrhages and acute upper airway obstruction from hematoma formation in
the neck. On physical examination, he has decreased range of motion of the large
joints, particularly the knees and ankles. He has no petechiae or purpura of the skin.
Laboratory studies show normal prothrombin time, el- evated partial thromboplastin time
(PTT), and normal platelet count, but markedly decreased factor VIII activity. Which of
the following mechanisms best describes the development of his disease?
A Decrease in production of thrombin
B Decrease in membrane phospholipid
C Failure of platelet aggregation
D Failure of fibrin polymerization
E Inability to neutralize antithrombin III
F Inability of platelets to release thromboxane A2
F Vitamin K deficiency
His elevated prothrombin time that corrects with normal plasma points to coagulation
factor deficiency, and factors II, VII, IX, and X are synthesized in the liver and affect this
"extrinsic" in vitro coagulation pathway. They are vitamin K dependent and therefore
may also be affected by warfarin therapy or by parenchymal liver disease.
Antiphospholipid syndrome has an inhibitory effect upon in vitro coagulation tests and
does not correct with addition of normal plasma. T - Answer-A 58-year-old man has had
episodes of prolonged epistaxis in the past 6 months. On examination he has occult
blood detected in his stool. Coagulation studies show that his prothrombin time is
elevated, but his partial thromboplastin time (PTT), platelet count, and platelet function
are all normal. When his plasma is mixed with an equal amount of normal plasma, the
prothrombin time corrects to normal. Which of the following underlying diseases is most
likely to be associated with these findings?
A Antiphospholipid syndrome
OF PATHOLOGY CH4 ILLUSTRATED
PATHOLOGY QUESTION WITH
CORRECT ANSWERS
D) Petechiae
Note the small punctate 1- to 2-mm petechial hemorrhages on the epicardial surface
shown in the figure. Such hemorrhages most often result from reduced numbers of
platelets or reduced platelet function. It is platelets that plug small vascular defects.
Congestion occurs when there is vascular dilation with pooling of blood within an organ.
A hematoma is a collection of blood in a potential space or within tissue. Purpura
denotes blotchy hemorrhage on skin, serosal surfaces, or muco - Answer-An autopsy
study is performed to correlate patterns of hemorrhage with underlying causes. Patients
with the gross appearance of hemorrhage shown in the figure had minimal blood
volume loss, but an appearance similar to this in many other organs. Which of the
following terms best describes this pattern?
A Congestion
B Ecchymosis
C Hematoma
D Petechiae
E Purpura
E) Vasoconstriction
The initial response to arteriolar injury is vasoconstriction, since there is smooth muscle
in the vessel wall. But this is transient, and the coagulation mechanism must be initiated
to maintain hemostasis. Fibrin polymerization is part of secondary hemostasis after the
vascular injury is initially closed. Neutrophils are not essential to hemostasis. Platelet
aggregation occurs with release of factors such as ADP, but this takes several minutes.
Protein C is involved in anti - Answer-A superficial puncture wound from a needlestick
injury leads to a small amount of bleeding in a healthy person. Sec- onds after this injury
occurs, the bleeding stops. Which of the following mechanisms is most likely to stop
small arteriolar blood loss from this injury?
A Fibrin polymerization
B Neutrophil chemotaxis
C Platelet aggregation
D Protein C activation
E Vasoconstriction
,C) Prostacyclin
Endothelial injury releases glycoprotein tissue factor (factor III) that drives the
coagulation process and activates platelets. Adjacent intact endothelium generates
prostacyclin (PGI2) via arachidonic acid metabolism to inhibit clot propagation beyond
where it is needed. PGI2 and nitric oxide are powerful vasodilators and inhibitors of
plate- let aggregation. This limits thrombus formation just to the area of injury.
Glycoprotein IIb/IIIa, which induces shape change; phospholi - Answer-A 15-year-old
girl incurs a cut to the sole of her foot after stepping on a piece of broken glass. On
examination, a superficial 0.5-cm laceration ceases to bleed within 5 minutes after
application of local pressure. Which of the following substances is released by
endothelium and is most likely to counteract platelet aggregation near this site of injury?
A Glycoprotein IIb/IIIa
B Platelet-activating factor
C Prostacyclin
D Tissue-type plasminogen activator
E Thrombomodulin
F Thromboxane
E) Thrombomodulin
Thrombomodulin is present on intact endothelium and binds thrombin, which then
inhibits coagulation by activating protein C. Normally, thrombin activates factors V, VIII,
and IX, and also stabilizes the secondary hemostatic plug by activating factor XIII, which
cross-links fibrin. Thrombin helps activate platelets. Calcium is a cofactor that assists
clotting in the coagulation cascade (ethylene-diaminetetraacetic acid [EDTA] in some
blood collection tubes binds calcium to prev - Answer-In an experiment, thrombus
formation is studied in areas of vascular damage. The propagation of a thrombus in an
area of vascular injury to adjacent normal arteries is prevented. Which of the following
substances diminishes thrombus propagation by activating protein C?
A Calcium
B Fibrin
C Platelet factor 4
D Prothrombin
E Thrombomodulin
F Tumor necrosis factor (TNF)
B) Platelet adhesion
Von Willebrand factor (vWF) acts like a "glue" between platelets and the exposed
extracellular matrix of the vessel wall after vascular injury. None of the other steps listed
depends upon vWF. Because the patient's prothrombin time (PT) is normal, a lack of
prothrombin or the presence of an inhibitor is unlikely. Because vWF stabilizes factor
VIII, a deficiency of vWF may prolong the partial thromboplastin time (PTT). - Answer-A
,26-year-old woman has a history of frequent nose- bleeds and increased menstrual
blood flow. On physical examination, petechiae and purpura are present on the skin of
her extremities. Laboratory studies show normal partial thromboplastin time (PTT),
prothrombin time (PT), and platelet count, but decreased von Willebrand factor activity.
This patient most likely has a derangement in which of the following steps in
hemostasis?
A Fibrin polymerization
B Platelet adhesion
C Platelet aggregation
D Prothrombin generation
E Prothrombin inhibition
F Vasoconstriction
B Aggregation of platelets
Aspirin blocks the cyclooxygenase pathway of arachidonic acid metabolism and
generation of eicosanoids in platelets, including thromboxane A2, to block
vasoconstriction and inhibit platelet aggregation. Platelet adhesion to extracellular
matrix is mediated by interactions with von Willebrand factor. Tissue factor (factor III),
produced by injured endothelium as well as subendothelial smooth muscle and
fibroblasts, is released with tissue injury and is not platelet dep - Answer-A 59-year-old
woman with a history of diabetes mellitus had a myocardial infarction 3 months ago. Her
BMI is 35. She is now taking a low dose of aspirin to reduce the risk for recur- rent
arterial thrombosis. On which of the following steps in hemostasis does aspirin have its
greatest effect?
A Adhesion of platelets to collagen
B Aggregation of platelets
C Production of tissue factor
D Synthesis of von Willebrand factor
E Synthesis of antithrombin III
A) Adenosine diphosphate
ADP is released from the platelet-dense granules and is a potent stimulator of platelet
aggregation. ADP also stimulates further release of ADP from other platelets. Many
other substances involved in hemostasis, such as fibrinogen, fibronectin, and factors V
and VIII, are stored in the α granules of platelets. Thromboxane A2, another powerful
aggregator of platelets, is synthesized by the cyclooxygenase pathway. Fibronectin
forms part of the extracellular matrix betwee - Answer-In an experiment, platelet
function is analyzed. A sub- stance is obtained from the dense body granules of normal
pooled platelets from healthy blood donors. When this sub- stance is added to platelets
obtained from patients with a bleeding disorder, no platelet aggregation occurs. Adding
the substance to platelets from a normal control group induces platelet aggregation.
Which of the following substances is most likely to produce these effects?
, A Adenosine diphosphate
B Antithrombin III
C Fibronectin
D Fibrinogen
E Plasminogen
F Thromboxane A2
A) Decrease in production of thrombin
He has hemophilia A. Factor VIII, tissue factor (III), and factor V act as cofactors or
reaction accelerators in the clot- ting cascade leading to thrombin production. Factor VIII
acts as a reaction accelerator for the conversion of factor X and factor Xa. The platelet
surface provides phospholipid for assembly of coagulation factors. Platelet aggregation
is promoted by thromboxane A2 and ADP. Thromboxane A2 is released when platelets
are activated during t - Answer-A 12-year-old boy has a 10-year history of multiple soft
tissue hemorrhages and acute upper airway obstruction from hematoma formation in
the neck. On physical examination, he has decreased range of motion of the large
joints, particularly the knees and ankles. He has no petechiae or purpura of the skin.
Laboratory studies show normal prothrombin time, el- evated partial thromboplastin time
(PTT), and normal platelet count, but markedly decreased factor VIII activity. Which of
the following mechanisms best describes the development of his disease?
A Decrease in production of thrombin
B Decrease in membrane phospholipid
C Failure of platelet aggregation
D Failure of fibrin polymerization
E Inability to neutralize antithrombin III
F Inability of platelets to release thromboxane A2
F Vitamin K deficiency
His elevated prothrombin time that corrects with normal plasma points to coagulation
factor deficiency, and factors II, VII, IX, and X are synthesized in the liver and affect this
"extrinsic" in vitro coagulation pathway. They are vitamin K dependent and therefore
may also be affected by warfarin therapy or by parenchymal liver disease.
Antiphospholipid syndrome has an inhibitory effect upon in vitro coagulation tests and
does not correct with addition of normal plasma. T - Answer-A 58-year-old man has had
episodes of prolonged epistaxis in the past 6 months. On examination he has occult
blood detected in his stool. Coagulation studies show that his prothrombin time is
elevated, but his partial thromboplastin time (PTT), platelet count, and platelet function
are all normal. When his plasma is mixed with an equal amount of normal plasma, the
prothrombin time corrects to normal. Which of the following underlying diseases is most
likely to be associated with these findings?
A Antiphospholipid syndrome
