| Based on the body’s reactivity, inflammation can be: | normoergic; hyperergic; hypoergic; |
| Which of the following pathological manifestations is an inflammation? | hepatitis |
| Local manifestations of the inflammatory process are: | lesions secondary to the action of an inflammatory agent and body’s defensive reactions |
| Inflammation is a component of: | the second line of nonspecific defense of the body |
| The protective reactions of the body that take place during the inflammatory response are grouped into the following categories of processes: | exudative-vascular processes and proliferative processes |
| Rubor is a cardinal sign of inflammation and involves: | redness of the inflamed tissue |
| Calor is a cardinal sign of inflammation and involves: | increasing the temperature of the inflamed tissue |
| Dolor is a cardinal sign of inflammation and involves: | pain sensitivity of the inflamed tissue |
| Tumor is a cardinal sign of inflammation and involves: | the swelling of the inflamed tissue |
| The cardinal signs’ intensity of the inflammatory reactions is higher in: | acute and well localized inflammation |
| Which of the following pathologic manifestations is not an inflammation? | myocardosis |
| In the decompensated shock of gastrointestinal tract (GIT) (organ failure) we can find: | lesions, overlapping infections and toxiemia |
| Which of the following pathologic manifestations is the inflammation of the hepatic capsule: | perihepatitis |
| The vascular stage of the inflammatory reaction entails the successive unfolding of the following phases: | initial vasoconstriction, arterio-capillary vasodilation and increased vascular permeability |
| Based on the nature of the pathogenic factor involved in producing the inflammatory process, inflammation is classified as: | septic and aseptic inflammation |
| What kind of inflammation are those caused by biotic phlogogenic factors: | septic |
| What kind of inflammations are those based on specific hypersensitivity: | immunologic |
| Acute inflammatory reactions are characterized by: | answers a and d obvious manifestation of the cardinal signs of inflammation/ short-term evolution |
| Acute inflammatory reactions are characterized by: | predominance of the vasculo-exudative processes |
| Chronic inflammatory reactions are characterized by: | answers a and c discreet manifestation of the cardinal signs of inflammation/ long-term evolution |
| Chemotaxis is: | the ability of pro-inflammatory cells to move towards the inflammatory center |
| The inflammatory reaction goes through the following stages: | vascular- cellular and tissue repair |
| The first phase of the vascular stage in the inflammatory reaction is characterized by: | arteriocapillary vasoconstriction |
| The manifestations of the first phase of the vascular stage in the inflammatory reaction is due to: | answers a and b thromboxane A2 and serotonin/ catecholamines |
| The second phase of the vascular stage in the inflammatory reaction is characterized by: | arteriocapillary vasodilation accompanied by venous vasoconstriction followed by arteriocapillary vasodilation and venous vasodilation |
| The manifestations of the second phase of the vascular stage in the inflammatory reaction, which are characterized by arteriocapillary vasodilation and venous vasoconstriction (postcapillary), are due to: | some soluble mediators of inflammation |
| The soluble mediators of inflammation that induce the second phase of the vascular stage, which is characterized by arteriocapillary vasodilation and venous vasoconstriction (postcapillary), are: | histamine and PAF |
| The manifestations of the second phase of the vascular stage in the inflammatory reaction, which are characterized by arteriocapillary vasodilation and venous vasodilation (postcapillary), are due to: | some soluble mediators of inflammation |
| Which of the following are soluble mediators of inflammation that are involved in inducing the second phase of the vascular stage, characterized by arteriocapillary and venous (postcapillary) vasodilation: | histamine, bradykinin and I and E prostaglandin |
| Which of the following features does not belong to the soluble mediators of inflammation : | inactivating the adhesion receptors found on the membranes of pro-inflammatory and endothelial cells |
| The second phase of the vascular stage in the inflammatory reaction lasts about: | 24 hours |
| The activation of the complement system takes place during the: | vascular stage of the inflammatory reaction |
| The activation of the coagulase system takes place during the: | vascular stage of the inflammatory reaction |
| The third phase of the vascular stage of the inflammatory reaction is characterized by: | increasing the vascular permeability |
| The third phase of the vascular stage of the inflammatory reaction is induced, among others, by: | hypoxia and consecutive acidosis |
| The third phase of the vascular stage of the inflammatory reaction is induced, among others, by: | histamine and bradykinin |
| The major effect of the third phase of the vascular stage in the inflammatory reaction is characterized by: | plasmexodia |
| Plasmexodia, which follows the third phase of the vascular stage in the inflammation reactions, induces: | intratissular accumulation of inflammatory exudate |
| Vascular stasis (venous congestion) is characterized by a decreased blood flow and the stagnation thereof in the affected area, an occurrence called: | pooling |
| Which of the following clinical signs are not specific to the inflammations: | necrosis |
| Which of the following modifications are not specific to the septic inflammation: | increasing the number of red blood cells |
| The aims of the inflammatory reaction are: | answers a and c healing lesions/ eliminating the pathogenic agent and the negative effects it has produced |
| A morphofunctional structure is formed at the periphery of the inflammatory outbreak; its role is to limit the diffusion, it is called: | fibrin-immuno-leukocyte barrier |
| Which of the following substances do not belong to the second line of soluble mediators of inflammation: | histamine |
| Which of the following belong to the proinflammatory cells: | neutrophilic granulocytes |
| Which of the following also belong to the proinflammatory cells: | macrophages |
| Which of the following are cells that functionally support the proinflammatory cells: | endothelial cells |
| Which of the following cells is specialized in phagocytosis of antigen-antibody complexes? | eosinophil granulocyte |
| The endothelial cells functionally support the proinflammatory cells by: | releasing PAF and prostaglandins |
| Which of the following substances do not belong to the third line of soluble mediators of inflammation: | bradykinin |
| Mast cells and basophiles functionally sustain the proinflamatory cells through: | release of histamine |
| Proinflamatory cells of the tisular compartment act, among others, through: | chemotaxis and chemokinesis |
| Proinflamatory cells of the tissular compartment act, among others, through | phagocytosis |
| Proinflamatory cells of the tissular compartment act, among others, through: | oxygen dependent cytotoxicity |
| Proinflamatory cells of the circulant compartment act, among others, through: | irreversible adherence on the vascular endothelium level |
| Proinflamatory cells of the circulant compartment act, among others, through: | diapedesis |
| First chemotactic wave is characterized by: | duration of aprox 2-4 hours sustained by neutrophils |
| The second chemotactic wave is characterized by: | duration of aprox 36 hours sustained by macrophages |
| The tissular repair stage of the inflamatory reaction is characterized by: | intensification of proliferative phenomena |
| The tissular repair stage of the inflamatory reaction is characterized by: | diminution of vasculo-exudative phenomena |
| The tissular repair stage of the inflamatory reaction is composed of the next succesive phases: | fibroplasia - angiogenesis - specific tissular reconstruction - tissular remodeling |
| One of the two capital shock inducing elements is: | lowering of the tissular perfusion |
| One of the two capital shock inducing elements is: | tissular hipoxia |
| Hypovolemic shock can be induced by: | severe plasmorrhagia |
| Which of the next mechanisms are not activated during the shock with the tendency to restore the circulating blood volume? | increase water ingestion |
| Cardiac shock can be induced by:
a) severe arrhythmias,
b) pulmonary embolism;
c) answers a, d and e;
d) ;
e) | answers a, d and e severe arrhythmias/ valvular insufficiency/ cardiomyopathy |
| Disvolemic (distributive) shock can be induced by: | bacterial endotoxins |
| Disvolemic (distributive) shock can be induced by: | acute intoxication with depressants |
| Obstructive shock can be induced by: | massive pulmonary embolism |
| Obstructive shock can be induced by: | pneumothorax |
| In hypovolemic compensated shock it is noticed: | vasoconstriction induced by the closing of pre- and post-capillary sphincters and opening of arteriolo-venular shunts |
| In hypovolemic compensated shock it is noticed: | mobilization of blood stored in venous deposits |
| In decompensated hypovolemic shock it is noticed: | acidosis and opening of precapillary sphincters |
| In the decompensated stage of hypovolemic shock it is noticed: | blood stasis, that induces relative hypovolemia |
| In the decompensated stage of hypovolemic shock it is noticed: | hyperpermeabilization of the vascular endothelium |
| Consecutively to the increasing of the vascular permeability, in the hypovolemic decompensated shock, it is noticed: | plasma leakage and increased blood viscosity |
| Plasmexodia, consecutively to the increasing of the vascular permeability in the hypovolemic shock, induces: | hypovolemia |
| In the decompensated stage of hypovolemic shock, posthypoxic lesions and increased blood viscosity cause: | Disseminated Intravascular Coagulation (DIC) |
| During the compensatory stage of hypovolemic shock, it is noticed: | an intensification of cardiac activity and an amplification of cardiac output |
| In the decompensated hypovolemic shock it is noticed: | diminution of cardiac output and general hypoperfusion |
| Disorders of carbohydrate metabolism secondary to shock consist in: | early postaggressive hyperglycemia and, during the late stages of shock, hypoglycemia |
| The refractory shock (irreversible) is characterized by: | all above answers are correct |
| Early or initial shock (reversible) corresponds to the immediate imbalance phase of the SRA and is characterized by: | answers a and d low arterial blood pressure/ mitochondrial insufficiency |
| Disorders of lipid metabolism secondary to shock consist in the activation of lipolysis via certain catabolic hormones such as: | answers a and d, noradrenaline and glucocorticoids/ glucagon and iodine thyroid hormones |
| In the decompensated shock it is noticed: | hypoglicemia and fat overload of the liver (hepatocellular failure) |
| In compensated shock it is noticed: | hyperglicemia and activation of lipolysis |
| Which of the following modifications isn’t specific for disorders of protein metabolism secondary to shock: | increased plasma protein levels |
| In renal insuficiency induced by the decompensated shock it is noticed: | anuria |
| In decompensated shock, at the level of hidro-mineral metabolism it is noticed: | water is transferred inside cells due to intracellular accumulation of Na+ |
| In the liver in decompensated shock (organ insufficiency) it is noticed: | diminution of protein synthesis |
| Which of the following modifications are not characteristic for hepatic insufficiency instituted in the decompensated phase of shock. | amplification of protein synthesis |
| In the compensated shock it is noticed: | intracellular transfer of K+ and extracellular transfer of Ca++ |
| In the decompensated shock it is noticed: | answers a and b hyperalkalemia/ calcium intracellular accumulation |
| In decompensated shock, the intracellular accumulation of Ca++ determines: | the activation of endonuclease involved in programmed cell death (apoptosis) |
| In decompensated shock, the extracellular K+ accumulation determines: | cardiac arrhythmias |
| In decompensated shock, intracellullar acummulation of Na+ determines: | cellular edema |
| The cause of cellular edema, specific for decompensated shock is: | functional impairment of Na+/K+ pumps |
| The cause for intracellular Ca++ accumulation, specific for decompensated shock is: | functional blocking of the Ca++ pumps |
| In the decompensated shock at the level of the lung (organ insufficiency) we find: | answers b and c, blockage of the pulmonary microcirculation with formation of thrombi (DIC)/ stasis in the pulmonary microcirculation |
| In the decompensated shock at the level of the liver (organ insufficiency) we find: | answers a and d diminution of the synthesis of coagulation factors/ amplification of fibrinolysis |
