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Test Bank for Robbins and Cotran Pathologic Basis of Disease 9th Edition Kumar | Chapter 2 - 29 | Guide 2024
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Test Bank for Robbins and Cotran Pathologic Basis of Disease 9th Edition Kumar | Chapter 2 - 29 | Guide 2024

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  • August 9, 2024
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Test Bank for Robbins and Cotran Pathologic
Basis of Disease 9th Edition Kumar | Chapter 2
- 29 | Guide 2024




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 between cells that "glues" them together.
Plasminogen is activated to promote thrombolysis. Platelet aggregation requires active
platelet metabolism; platelet stimulation by agonists such as ADP, thrombin, collagen,
or epinephrine; the presence of calcium or magnesium ions and specific plasma
proteins such as fibrinogen or von Willebrand factor (vWF); and a plate- let receptor, the
glycoprotein IIb/IIIa (GPIIb/IIIa) complex. Platelet - 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 the process of platelet adhesion. Fibrin polymerization is promoted
by factor XIII. Antithrom- bin III inhibits thrombin to prolong the prothrombin time. - 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. The factor V Leiden mutation leads to
difficulty inactivating factor V by the action of protein C, thus causing thrombosis, not
bleeding. Hemophilia A results from loss of factor VIII function and affects just the partial
thromboplastin time (PTT). Scurvy from vitamin C deficiency affects vascular integrity,
not coagulation factors. Gram-negative sepsis releases lipopolysaccharide that
activates coagulation on a wide scale, con - 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
B Factor V Leiden mutation
C Hemophilia A
D Scurvy
E Sepsis with Escherichia coli
F Vitamin K deficiency

D) Tissue plasminogen activator

,Tissue plasminogen activator (t-PA) is a thrombolytic agent that promotes generation of
plasmin, which cleaves fibrin to dissolve clots. Aspirin prevents formation of new
thrombi by inhibiting platelet aggregation and works best as preventive therapy. Heparin
prevents thrombosis by activating antithrombin III. Nitric oxide is a vasodilator. Vitamin
K is required for synthesis of clotting factors II, VII, IX, and X and facilitates the ability to
form clots. - A 66-year-old woman has the sudden onset of chest pain that radiates to
her neck and left arm. On examination 30 minutes later, she is diaphoretic and
hypotensive. Her serum troponin I level is elevated. Which of the following drugs is most
likely to be administered emergently as thrombolytic therapy for this woman?

A Acetylsalicylic acid (aspirin)
B Low-molecular-weight heparin
C Nitric oxide
D Tissue plasminogen activator
E Vitamin K

B) Damage to endothelium

Atherosclerotic damage to vascular endothelium is the most common cause of arterial
thrombosis; this damage accumulates almost imperceptibly over many years. Diabetes
mellitus types I and II accelerate atherosclerosis. Inhibitors to coagulation, such as
antiphospholipid antibodies, typically prolong the partial thromboplastin time (PTT), the
prothrombin time (PT), or both. Decreased levels of antithrombin III and mutation in the
factor V gene are inherited causes of hypercoagulability; they are far less common than
atherosclerosis of coronary vessels. Decreased production of tissue plasminogen
activator from intact endothelial cells may occur in anoxia of the endothelial cells in
veins with sluggish circulation. Stasis of blood flow is important in thrombosis within the
low-pressure venous circulation. - A 60-year-old woman with a history of diabetes
mellitus has had left-sided chest pain radiating to the arm for the past 5 hours. Serial
measurements of serum creatine kinase-MB levels show an elevated level 24 hours
after the onset of pain. Par- tial thromboplastin time (PTT) and prothrombin time (PT)
are normal. Coronary angiography shows occlusion of the left anterior descending
artery. Which of the following mechanisms is the most likely cause of thrombosis in this
patient?


A Antibody inhibitor to coagulation
B Damage to endothelium
C Decreased antithrombin III level
D Decreased tissue plasminogen activator
E Mutation in factor V gene
F Stasis of blood flow

B) Factor V mutation

, Recurrent thrombotic episodes at such a young age strongly suggest an inherited
coagulopathy. The factor V (Leiden) mutation affects 2% to 15% of the population, and
more than half of all individuals with a history of recurrent deep venous thrombosis have
such a defect. Inherited deficiencies of the anticoagulant proteins antithrombin III and
protein C can cause hypercoagulable states, but these are much less common than
factor V mutation. Hyperhomocysteinemia is a less common cause of inherited risk of
thrombosis than is factor V mutation. It also is a risk factor for atherosclerosis that
predisposes to arterial thrombosis. Although some cancers elaborate factors that
promote thrombosis, this patient is unlikely to have cancer at such a young age; a 10-
year history of thrombosis is unlikely to occur in a patient with cancer. Oral
contraceptive usage contributes to risk for thrombosis, but mainl - A 21-year-old woman
has had multiple episodes of deep venous thrombosis during the past 10 years and one
episode of pulmonary thromboembolism during the past year. Laboratory tests show
that her prothrombin time (PT), partial thromboplastin time (PTT), platelet count, and
platelet function studies all are normal. Which of the following risk factors is the most
common cause for such a coagulopathy?

A Antithrombin III deficiency
B Factor V mutation
C Hyperhomocysteinemia
D Mutation in protein C
E Occult malignancy
F Oral contraceptive use
G Smoking cigarettes

C) Increased hydrostatic pressure

The hydrostatic pressure exerted from standing upright leads to edema in dependent
parts of the body. In a healthy patient, normal renal function would be sufficient to clear
free water ingested orally. Hypoalbuminemia leads to more generalized edema,
although the effect is more pro- nounced in dependent areas. Lymphatic obstruction
from infection or tumor can lead to lymphedema, but this is a chronic process.
Secondary aldosteronism results from con- gestive heart failure and renal
hypoperfusion, but this is a generalized process. - A 45-year-old woman who works
while standing for long periods notices at the end of her 8-hour shift that her lower legs
and feet are swollen, although there was no swelling at the beginning of the day. There
is no pain or erythema associated with this swelling. She is otherwise healthy and takes
no medications; laboratory testing reveals normal liver and renal function. Which of the
following mechanisms best explains this phenomenon?

A Excessive free water intake
B Hypoalbuminemia
C Increased hydrostatic pressure
D Lymphatic obstruction
E Secondary aldosteronism

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