Pathological Basis of Disease 8th Edition By Kumar Abbas -Test Bank

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Pathological Basis of Disease 8th Edition By Kumar Abbas -Test Bank



Pathological Basis of Disease 8th Edition By Kumar Abbas -Test Bank

Kumar: Robbins and Cotran Pathologic Basis of Disease, 8th Edition


Chapter 02: Acute and Chronic Inflammation


Test Bank




  1. Transmembrane adhesive heterodimeric proteins, composed of an a and a chain, are expressed on activated leukocytes during inflammation. They bind primarily to intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), both of which belong to the family of proteins known as
a. selectins
b. integrins
c. immunoglobulins
d. lectins
e. growth factors


ANS: C, Surface proteins expressed on activated leukocytes are integrins, and they bind to intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), which belong to the immunoglobulin family of proteins.


  1. Which of the following mediators of inflammation has chemotactic properties and is increased in persons taking aspirin?
a. Thromboxane A2
b. Prostaglandin E2
c. Platelet-activating factor
d. Leukotriene B4
e. Interleukin-1


ANS: D, Leukotriene B4 is chemotactic. It is increased in persons who take aspirin, because aspirin inhibits the cyclooxygenase pathway, thus shunting more arachidonic acid early derivatives into the lipoxygenase pathway. This promotes the synthesis of leukotrienes.


  1. A 2-year-old child known to suffer from recurrent bacterial infections and poor wound healing was found to have leukocyte adhesion molecule deficiency 1 (LAD-1). The leukocytes of this patient do not express CD18, a molecule classified as belonging to the family of
a. selectins
b. integrins
c. lectin type of vascular adhesion molecules
d. aminotransferases
e. glycosidases



ANS: B, LAD-1 is characterized by a deficiency of CD18, a cell surface molecule that is a 2 integrin. The infections occur because the defective leukocytes cannot adhere to endothelial cells, cannot spread and attach, and cannot phagocytose bacteria. PBD7 62


  1. Bradykinin is produced from a high-molecular weight kininogen circulating in the blood. This reaction is mediated by
a. coagulation factor X
b. kallikrein
c. Hageman factor
d. complement C3
e. protein C


ANS: B, Kallikrein promotes the formation of bradykinin from the high-molecular weight kininogen. PBD7 67


  1. Nitric oxide synthesis is augmented in endothelial cells by a calmodulin-mediated influx of which element?
a. Calcium
b. Sodium
c. Potassium
d. Oxygen
e. Nitrate


ANS: A, Endothelial cell nitric oxide synthase is constitutively expressed at low levels, but it can be increased by a calmodulin-mediated influx of calcium into the endothelial cells. PBD7 72


  1. Which of the following mediators of inflammation causes pain?
a. Nitric oxide
b. Complement C3a
c. Bradykinin
d. Leukotriene B4
e. Interleukin-1


ANS: C, Bradykinin causes pain. Other pain-causing substances are substance P and prostaglandin E2. PBD7 65


  1. Aspirin lowers the body temperature by inhibiting the synthesis of which regulator of the central thermostat in the hypothalamus?
a. Leukotriene B4
b. Lipoxin
c. Thromboxane A2
d. Prostacyclin
e. Prostaglandin E2


ANS: E, Aspirin inhibits the action of cyclooxygenase, and thus inhibits the synthesis of thromboxane A2, prostacyclin, and prostaglandin E2. However, only prostaglandin E2 is involved in thermoregulation. The synthesis of lipoxin and leukotrienes is not inhibited by aspirin. PBD7 70


  1. C-reactive protein binds to the surface of microbes in tissues acting as a(n)
a. caspase
b. peroxidase
c. opsonin
d. anaphylatoxin
e. membrane attack protein


ANS: C, C-reactive protein, an acute phase protein produced by the liver in acute and chronic inflammation, binds to microbes acting as an opsonin. Opsonization of bacteria facilitates phagocytosis.



Kumar: Robbins and Cotran Pathologic Basis of Disease, 8th Edition


Chapter 04: Hemodynamic Disorders, Thromboembolic Disease, and Shock


Test Bank




  1. A 60-year-old man had congestive heart failure and sodium retention. Pitting edema of the lower extremities in this patient is most likely associated with an increased blood level of
a. albumin
b. globulin
c. aldosterone
d. troponin
e. plasminogen


ANS: C, Renal hypoperfusion due to heart failure leads to secondary hyperaldosteronism and consequent retention of sodium and water.


  1. A 60-year-old woman had a mastectomy for advanced cancer in her left breast, followed by chemotherapy and radiation therapy. She developed edema of the left arm. This edema is caused by
a. obstruction of the lymph flow
b. arterial thrombosis
c. venous thrombosis
d. spread of cancer into the soft tissue of the arm
e. hypoalbuminemia secondary to liver injury caused by hepatic metastases


ANS: A, Arm edema following a mastectomy is a complication of breast cancer treatment caused by an obstruction of the lymphatics in the axilla. This obstruction of lymphatics is a consequence of radiation injury or scarring associated with surgery.


  1. A 63-year-old woman died 2 days after the onset of severe myocardial ischemia caused by coronary thrombosis. At autopsy, the lungs were heavy. Upon sectioning of the lungs, frothy fluid was seen oozing from the cut surface of the parenchyma. Which of the following is the most likely diagnosis?
a. Pulmonary embolism
b. Pulmonary infarction
c. Pulmonary edema
d. Atelectasis
e. Lobar pneumonia


ANS: C, Lungs that are heavy and on cross section show oozing of frothy fluid are filled with edema fluid. In this case, edema developed due to left-sided heart failure.


  1. A 60-year-old man who had longstanding congestive heart failure complained of pain under the right costal margin. He died of worsening heart failure. At autopsy, the liver appeared enlarged and congested, showing a nutmeg pattern on cross section. Histologically this liver will show
a. atrophy of bile ducts
b. dilatation of bile ducts
c. intralobular cholestasis
d. centrolobular necrosis and loss of hepatocytes
e. fibrosis of the Glisson capsule


ANS: D, Chronic passive congestion of the liver caused by heart failure leads to accumulation of blood in the terminal hepatic venule and the centrolobular sinusoids. Aggravation of the heart failure expands the blood-containing spaces, causing centrolobular liver cell necrosis.


  1. Which form of hemorrhage is most typical of defective platelet function seen in uremia (end stage kidney failure)?
a. Multiple petechiae
b. Multiple ecchymoses
c. Solitary ecchymoses
d. Hematoma
e. Hemarthrosis


ANS: A, Defective platelet function in uremia is typically associated with multiple petechiae in the skin and on mucosal surfaces.


  1. Which of the following substances is an anticoagulant secreted by endothelial cells?
a. Von Willebrand factor
b. Prothrombin
c. Inhibitor of plasminogen activator
d. Thrombomodulin
e. Tissue factor


ANS: D, Thrombomodulin is an anticoagulant that acts by binding to thrombin and converting it from a procoagulant to an anticoagulant capable of activating protein C.


  1. Bernard-Soulier syndrome is a bleeding disorder caused by a defect of glycoprotein Ib (GpIb) on platelets. Platelets lacking GpIb cannot adhere to the wall of the damaged blood vessels, because GpIb is the receptor for which essential coagulation protein?
a. Hageman factor (factor XII)
b. Von Willebrand factor
c. Fibrinogen
d. Factor VIII
e. Thrombin


ANS: B, GpIb, a platelet cell membrane glycoprotein, is the receptor for the von Willebrand factor (vWF), which mediates the adhesion of platelets to the damaged vascular wall. Congenital deficiency of GpIb, as seen in Bernard-Soulier syndrome, is similar to the deficiency of vWF in von Willebrand disease and results in a bleeding disorder.


  1. The most common form of congenital coagulopathy, factor V mutation (Leyden mutation), causes the altered coagulation factor V to be resistant to the action of which enzyme?
a. Protein C
b. Protein S
c. Antithrombin III
d. Plasmin
e. Thrombin


ANS: A, Leyden mutation of factor V makes this factor resistant to the action protein C. Under normal circumstances, protein C inactivates factor V, and the mutation eliminates this very important anticoagulant control mechanism. As a result of these changes, there is uncontrollable activation of factor V, which promotes thrombosis.


  1. In the antiphospholipid syndrome of systemic lupus erythematosus, arterial thrombi occur most often in the arteries of the
a. brain
b. heart
c. kidneys
d. intestines
e. bronchi


ANS: A, Antiphospholipid syndrome is characterized by widespread venous and arterial thrombi. Venous thrombi are found most often in the veins of the lower extremities, whereas the arterial thrombi are most often found in the cerebral arteries.


  1. Which of the following is the most common site for arteriolar thromboembolization?
a. Brain
b. Heart
c. Kidneys
d. Lower extremities
e. Eyes


ANS: D, The lower extremities are the major site of arteriolar thromboemboli. This site is involved in 75% of all cases.


  1. A 30-year-old woman fractured her leg, and a few days later developed a diffuse petechial rash in the nondependent areas of the body. She was short of breath and had minor neurologic symptoms. Laboratory studies showed thrombocytopenia. These findings are most consistent with
a. air embolism
b. bone marrow embolism
c. fat embolism
d. talc embolism
e. cholesterol crystal embolism


ANS: C, Rash in nondependent areas of the body following fracture of major bones, especially if associated with thrombocytopenia, is suggestive of fat embolism. Shortness of breath is indicative of pulmonary embolization, and neurologic symptoms suggest that the emboli have passed through the lungs and entered the cerebral vessels.


  1. Most cases of septic shock are caused by endotoxin-producing bacteria, which are classified as
a. pyogenic
b. gram-positive
c. gram-negative
d. encapsulated
e. acid fast


ANS: C, Most cases of septic shock (70%) are caused by endotoxin-producing gram-negative bacteria. Endotoxins produced by gram-negative bacteria are lipopolysaccharides that bind to leukocytes, stimulating the release of cytokine, which in turn acts on vessels and other cells, propagating the development of shock.


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