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level: Physiopathology

Questions and Answers List

level questions: Physiopathology

QuestionAnswer
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, throughphagocytosis
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