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Pathophysio

A detailed illustration of the human body highlighting the inflammatory process and shock reactions, with visual indicators for inflammation, increased blood flow, and pathophysiological changes.

Pathophysiology Understanding Quiz

Test your knowledge of pathophysiology with our comprehensive quiz! This quiz is designed for students, professionals, and anyone interested in understanding the intricacies of inflammation and shock reactions in the body.

99 carefully crafted questions
Multiple-choice format
Scores calculated in real-time

99 Questions25 MinutesCreated by AnalyzingCell32

1.Increased ESR in inflammation is the consequence of:

A.decrease in albumin;

B.decrease in alpha-globulins;

C.leukopenia;

D.increased red blood cell count.

2.Early increase of permeability in the inflammatory focus is achieved under the action of:

A.prostaglandins and serotonin;

B.bioactive lipids;

C.interleukin-1.

D.histamines.

3.Mediators with a vasodilator role in the inflammatory focus are the following:

A.histamine and serotonin.

B.adrenaline;

C.noradrenaline;

D. snakes

4.Activation of membrane phospholipase A2 in phagocytes results in the following reactions:

A.limiting the release of lysophospholipids;

B.decreased prostaglandin synthesis;

C.limitation of vasculo-exudative and chemotactic phenomena;

D. Increased bioactive lipids with vasculo-exudation.

5.Amplification of vasculo-exudative phenomena in the inflammatory focus are the result of the following interventions:

A.increased glucocorticoid concentration;

B.decreased concentration of kinins and prostaglandins;

C.increased concentration of bioactive lipids;

D.decrease in histamine.

6.Blocking the cyclooxygenase pathway results in:

A. Decrease in vasculo-exudative and chemotactic phenomena;

B.pro-inflammatory effect;

C.increased permeability in the microcirculation;

D.increase in vasculo-exudative and chemotactic phenomena.

7.Active hyperemia in the first phase of acute inflammation explains:

A.hyperemia, heat, pulsatile sensation;

B.hyperemia, heat, pain, leukopenia;

C.hyperemia, heat, edema, anemia;

D.hypovolaemia.

8. Generally at the inflammatory focus the chemical mediators of inflammation produce:

A.increased vascular permeability;

B.decreased blood flow;

C.decreased blood flow and vascular permeability;

D. Increased hydrostatic pressure.

9. General reactions in inflammation are as follows:

A.hypothermia;

B.decreased hepatic glycoprotein secretion;

C.leukocytosis;

D.decreased synthesis of proteases and serpins.

10.In the inflammatory focus the activation of factor XII Hageman determines:

A.release of prostaglandins;

B.activation of arachidonic acid metabolites;

C.activation of the complementary cascade, coagulation and fibrinolysis systems, plasma kinin system

D.cytokin release.

11.Interleukin 1, also called granulocyte pyrogen, is involved in inflammation by:

A.increased hepatic glycoprotein secretion;

B.increased secretion of serpins;

C.decreased leukocyte production;

D.inhibition of hypothalamus function and hypothermia;

12.The inflammatory (phlogistic) focus is characterized by:

A. Ischemia and stasis;

B. neutrophilia.

C. alterative, vasculoexudative and proliferative phenomena;

D.alteration of its own proteins, vasodilation and increased permeability.

13.The causes of inflammation are represented:

A. Only by the action of biotic, exogenous factors;

B. Only by the action of abiotic, exogenous and endogenous factors;

C. All biotic and abiotic factors causing tissue damage;

D. All exogenous and endogenous factors that cause tissue damage.

14.In acute septic or aseptic inflammation, the following reactions occur:

A.increased acute phase proteins of hepatic origin

B. Leukocytosis with neutrophilia

C.leukopenia with lymphocytosis

D. VSH growth.

15.Pain in inflammation is the result of the action of the following mediators:

A.histamines;

B.serotonin;

C.bradikinin;

D. Bioactive lipids.

16.In the inflammatory phase:

A.inflammatory exudate is formed;

B.it prepares the ground for the formation of inflammatory exudate;

C.maximum phagocyte diapedesis occurs;

D.vasculoexudation is triggered.

17.The first cells activated in inflammation are:

A. histamine-releasing mast cells;

B.serotonin-releasing platelets;

C. neutrophils, the cells of the attack phase;

D. lymphocytes, antigen-presenting cells.

18.In inflammation of allergic nature is found:

A. Increase in eosinophils;

B. eosinophilia;

C. neutrophilia;

D.lymphocytopenia.

19.Among the consequences of the inflammatory phase are:

A.an active hyperemia produced predominantly by nervous mechanism;

B.an active congestion produced predominantly by nervous mechanism;

C.an active hyperemia initiated by the intervention of mediators of lipid origin;

D.ischemia and stasis.

20.The onset phase of inflammation is characterized by:

A.release of serotonin and arachidonic acid;

B.degranulation of mast cells and release of bioactive lipids;

C.alteration of their own proteins, increase in the caliber and permeability of small vessels, release of histamine and serotonin;

D. Alteration of their own proteins, vasculoexudation.

1. The shock is:

A. A disease;

B. A syndrome;

C. A serious disorder of the whole body;

D. An adaptive change.

2. From a pathophysiological point of view shock is:

A.a disorder of the uniform distribution of blood in the body;

B.o hypervolemia;

C.o hyperperfusion;

D.a predominantly anabolic reaction.

3.Among the definite causes of shock are:

A.all polyglobulias;

B.severe trauma;

C. anaemia;

D.small haemorrhages.

4 The central pathophysiological element of any form of shock is:

A.decrease in effective circulating blood volume;

B.increased effective circulating blood volume;

C.decrease in total blood volume;

D.true hypervolemia.

5. Depending on the mechanism the shock can be:

A. hemorrhagic, anaphylactic, cardiac;

B. hypovolemic, vasogenic, cardiogenic;

C. reversible, irreversible.

D. toxic, neurogenic.

6.Adaptive-compensatory reactions in shock are aimed at the following:

A.increased blood volume, vasoconstriction, increased cardiac output;

B.autotransfusion dependent on predominantly vagal reaction;

C.vasodilation, hypotension, hypoperfusion;

D.increased diuresis by osmotic mechanism.

7. In all types of shock the starting point of decompensation is:

A. Disorders of the vasomotor centre with apparent hypovolaemia;

B. Microcirculation disorders;

C. Ph increase

D. Hyperkalemia secondary to lactic acidosis;

8. Microcirculation disturbance in shock is the consequence:

A.vasodilator action of catecholamines;

B.disturbance of the activity of the vasomotor centres;

C.hemodynamic and metabolic disorders that are interrelated;

D. Increasing the water balance.

9.In shock cell perfusion is most faithfully mirrored by:

A.pH and plasma lactic acid concentration;

B.blood pressure value;

C.extracellular potassium concentration.

D.natremia value.

10.The following humoral changes occur as a result of metabolic disorders in shock:

A.hyperglycemia, hyperlactacidemia, hypolipemia, hypernatremia;

B.hypoglycemia, hyperlipidemia, hyperlactacidemia, hyponatremia, hyperpotassemia;

C.hypoglycemia, hypolipidemia, hypolactacidemia, hypernatremia, hyperpotassemia;

D.hyperglycemia, hyperlipidemia, hypolactacidemia.

11.The shock is:

A.a disease;

B.a syndrome,

C.a serious disorder of the whole body;

D. A serious alteration of all levels of integration of the body.

12.The definite causes of shock are the following:

A.all polyglobulias;

B.severe trauma;

C.extensive burns, large hemorrhages;

D.small haemorrhages.

13.Hyperlactacidaemia in shock represents:

A.a treatment modification index;

B.an irreversibility factor of the shock;

C.an index directly proportional to the severity of the shock;

D. Is an indicator of the restoration of balance.

14.The irreversible shock phase is characterized by the following changes:

A.collapse of blood pressure;

B.alkalosis phenomena;

C.activation of lysosomal enzymes and autodigestion;

D.increased vascular tone.

15. All types of shock start with a:

A. Severe metabolic disorder with alkalosis;

B. Serious hemodynamic alteration;

C.serious circulatory impairment

D.serious disorder of the vasomotor centres.

16.The pathophysiological mechanism in shock is:

A.altered blood pooling in all types of hypovolaemia;

B altered blood distribution only in true hypovolemia;

C.altered blood distribution in both true and apparent hypovolemia.

D. Altered blood distribution secondary to hypervolemia.

17.Changes in protidic metabolism in shock are as follows:

A.amino acid growth;

B.ammonia increase;

C.decrease in albumin.

D.dysproteinemia.

18.In shock cell perfusion is most faithfully mirrored by:

A.pH level;

B.plasma concentration of lactic acid;

C.blood pressure value;

D.extracellular potassium concentration.

19.In shock, hemodynamic disturbances in the microcirculation are dependent on:

A.total blood volume;

B.activity of vasomotor centres;

C.local acidosis;

D.increased acid production.

20.The consequences of metabolic acidosis in shock include the following:

A.stimulation of interleukin release, worsening hemodynamics;

B.increased tendency to disseminated intravascular coagulation;

C.decreased myocardial contractile force;

D.release of lysosomal enzymes.

1.The febrile reaction is:

A.a general non-specific adaptation-defence reaction of the body;

B.a disturbance of the thermogenesis-thermolysis balance by increasing heat production;

C.a derangement of the heat balance due to inefficient thermolysis;

D. A disturbance of the thermogenesis-thermolysis balance due to increased thermogenesis.

2.The following factors have a pyretogenic effect:

A.histamine;

B.bacteria, fungi;

C.kinins;

D.catabolic hormones.

3.The origin of endogenous pyrogen is:

A.leukocyte;

B.erythrocyte;

C.hypothalamic;

D.sanguine.

4.The febrile reaction is triggered by:

A.overheated and humid environment;

B.action of pyretogenic factors;

C.catabolic hormone discharges.

D.protease action.

5.For the state period of the febrile reaction are characteristic:

A.decrease in thermolysis;

B.restoring the thermogenesis-thermolysis balance;

C.intensification of thermogenesis;

D.increased thermogenesis.

6.The temperature rise phase of the febrile reaction is characterized by:

A.vasoconstriction, horipilation, squatting, shivering;

B.preservation of thermoregulation capacity;

C.adaptation reactions to the warm environment;

D.decreased thermogenesis and increased thermolysis.

7.The mechanism of overheating is represented by:

A.functional restructuring of the thermoregulation centre;

B.decrease in thermolysis;

C.amplification of thermogenesis;

D. Decreased thermogenesis and increased thermolysis.

8. In the phase of rising temperature in the febrile reaction occurs:

A.increased thermolysis;

B.increased thermogenesis and decreased thermolysis;

C.peripheral vasodilation.

D. Peripheral vasoconstriction.

9.In hypothermia the thermogenesis-thermolysis imbalance has the following causes:

A.excessive drop in ambient temperature;

B.decreased function of catabolic hormones;

C.increased anabolic activity;

D.increased function of catabolic hormones.

10.The adaptive reactions in overheating are:

A. Stimulating thermolysis;

B. Stimulating thermogenesis;

C. Peripheral vasodilation.

D. Decrease in heat loss.

11.Peripheral vasodilation as an adaptive mechanism in hyperthermia has the following consequences:

A. Hemoconcentration with hypovolemia;

B. Dehydration and haemoconcentration;

C. Dyserythropoietic anemia;

D.negative water balance.

12.The etiology of febrile reaction is represented:

A.only by the action of biotic factors;

B.from the action of biotic and abiotic factors that cause alteration of their own proteins;

C.all factors that produce tissue alteration and inflammation;

D.only by the action of abiotic factors.

13. At the origin of fever from inflammation are:

A. Interleukins released mainly by macrophages;

B. Glucocorticoids secondary to hypothalamic-pituitary-adrenal stimulation;

C. Pyretogenic cytokines;

D. Histamine action.

14.Mild to moderate increases in temperature in the febrile reaction are:

A. Unfavourable because it overloads the activity of some systems;

B. Favourable because they stimulate the body's adaptive capacity;

C. Favourable because they decrease digestive activity;

D.favourable by stimulating non-specific and specific defence mechanisms.

15. Pyrogenic cytokines act:

A.in the medullary adrenals with increased adrenaline concentration;

B.directly on bacteria and viruses, which it inactivates;

C.at the level of the heat centers in the hypothalamus by changing the set-point;

D.in the hypothalamic thermostat producing a functional restructuring.

1.Hyperglycemia may be the result of the following changes:

A.increased activity of hyperglycaemic systems;

B.increased activity of hypoglycaemic systems;

C. Increased insulin concentration;

D. Decreased glycogenolysis.

2.The etiopathogenesis of chronic hyperglycemia in insulin-dependent diabetes mellitus is represented by :

A.pancreatic beta cell alteration;

B.alterations of the liver synthases;

C.increased insulin concentration;

D.cellular insulin receptor disorders.

3.The etiopathogenesis of chronic hyperglycemia in insulin-dependent diabetes mellitus is represented by :

A.pancreatic beta cell alteration;

B.alterations of the liver synthases;

C.increased insulin concentration;

D.cellular insulin receptor disorders.

4.Insulin deficiency in insulin-dependent diabetes mellitus may be the result:

A.Insufficient insulin signal;

B.alterations of pancreatic alpha cells;

C. Disorders of the liver synthases;

D.all situations.

5.Insulin resistance of peripheral tissues can occur by:

A.disorders in insulin-receptor interaction;

B.disorders of the liver synthases;

C.anaerobic glycolysis disorders;

D.all situations.

6.Acute complications of chronic hyperglycemia in diabetes are:

A.ketoacidosis, osmotic polyuria, extracellular dehydration;

B.Metabolic Alkalosis;

C.global hyperhydration;

D.oligoanuria.

7.Hypoglycaemia can result from the following actions:

A.increased insulin;

B.decrease in the amount of insulin;

C. Use of low proportions of glucose post-stressively;

D.all situations.

8.Hypoglycemia can be the consequence:

A. Decrease in glycogenolysis;

B. Increased neoglucogenesis

C. Increased glycogenolysis;

D. Increased glycogenolysis and neoglucogenesis;

9.The etiopathogenesis of chronic hyperglycemia in insulin-dependent diabetes mellitus is represented by :

A.pancreatic beta cell alteration;

B.alterations of the liver synthases;

C.lower insulin concentration;

D.cellular insulin receptor disorders.

10.The etiopathogenesis of chronic hyperglycemia in insulin-dependent diabetes mellitus is represented by :

A. Insulin deficiency;

B.inability of peripheral tissues to respond to insulin;

C.increased insulin concentration;

D.cellular insulin receptor disorders.

11.Insulin resistance of peripheral tissues can occur by:

A.disorders in insulin-receptor interaction;

B.glucose transporter disorders;

C.disorders in the enzyme machinery involved in glucose utilization;

D.active congestion.

12.Insulin deficiency in insulin-dependent diabetes mellitus may be the result:

A.Insufficient insulin signal;

B.insulin secretion modified quantitatively and qualitatively;

C.insulin binding with some proteins;

D.true hypovolemia.

13.Acute complications of chronic hyperglycemia in diabetes are:

A.ketoacidosis;

B.osmotic polyuria;

C.hypertonic extracellular dehydration

D.Metabolic Alkalosis;

14.Hypoglycaemia can result from the following actions:

A.increased insulin;

B.decrease in the amount of insulin;

C.increased use of glucose, post-meal;

D. Increased secretion of insulin-like horman.

15.Hypoglycemia can be the consequence:

A.decrease in glycogenolysis;

B.decrease in neoglucogenesis

C.increased glycogenolysis;

D.decreased glycogenolysis and neoglucogenesis;

1. Dehydration is the result:

A. An insufficient supply or significant losses at the hydro-electrolytic level;

B. A positive water balance;

C. Significant erythropoietic disorders;

D.hyperaldosteronism.

2.Increase in hematocrit, plasma protein, intracellular compartment concomitant with decrease in plasma volume means:

A.isotonic dehydration;

B.hypotonic dehydration;

C.hypertonic dehydration;

D.global hyperhydration.

3.Decrease in hematocrit, plasma proteins, intracellular compartment concomitant with increase in plasma volume means:

A.hypotonic hyperhydration;

B.hypertonic dehydration;

C.hypertonic hyperhydration;

D. Hypotonic dehydration.

4.Lack of thirst is specific to the following water-electrolyte balance disorder:

A.isotonic extracellular dehydration;

B.hypertonic and hypotonic extracellular dehydration;

C.hypotonic extracellular dehydration;

D.cellular dehydration.

5.Compensatory mechanisms in isotonic dehydration are:

A.vasoconstriction, increased blood volume, increased heart activity;

B.vasodilation, increased parasympathetic activity;

C.hyposecretion of ADH and aldosterone;

D.increased diuresis.

6. Mechanisms of oedema include:

A.increased intravascular hydrostatic pressure;

B.increased intravascular oncotic pressure;

C.increased oncotic pressure in hyperalbuminemia;

D.decrease in hydrostatic pressure.

7. The consequences of hypotonic hyperhydration are:

A.global hyperhydration;

B.cellular dehydration;

C.extracellular hyperhydration and cellular dehydration;

D.dyshidria.

8. The consequences of hypocalcaemia on the body are:

A.increased neuromuscular excitability;

B.decrease in clotting time,

C.soft tissue calcifications.

D.decreased excitability.

9.The consequences of hyperkalemia on the body are:

A.metabolic disorders translated by metabolic alkalosis;

B.digestive disorders;

C.arrhythmias;

D. True hypovolemia.

10. Consequences of hyperphosphatemia on the body:

A.tetanic contractions secondary to hypocalcaemia;

B.haematological changes characterised by a disorder of the structure and function of erythrocytes;

C.metabolic changes translated by metabolic acidosis;

D. hypercalcaemia.

11.Among the coping mechanisms in hypovolemia are:

A. Increased secretion and release of ADH;

B. Stimulation of the renin-angiotensin-aldosterone system;

C. Decreased renal reabsorption;

D. Decreased cardiac activity.

12.General mechanisms of oedema include:

A. Increased vascular permeability and hydrostatic pressure;

B. hypoalbuminemia;

C. Actual hypovolaemia;

D. Relative hypovolaemia.

13. The consequences of hypocalcaemia on the body are:

A.increased neuromuscular excitability;

B.blood clotting disorders;

C.soft tissue calcifications.

D.decreased excitability.

14. Consequences of hyperphosphatemia on the body:

A.tetanic contractions secondary to hypocalcaemia;

B.haematological changes characterised by a disorder of the structure and function of erythrocytes;

C.metabolic changes translated by metabolic acidosis;

D. hypocalcaemia.

15. The consequences of hypotonic hyperhydration are:

A.global hyperhydration;

B.cellular dehydration;

C.extracellular and cellular hyperhydration;

D.dyshidria.

1.Acid-base balance disorders can be:

A.respiratory and metabolic;

B.only of respiratory origin;

C. Of metabolic origin only;

D.of diverse origin.

2.Respiratory acidosis is the consequence:

A.increased ventilatory function;

B.decrease in ventilatory function;

C.increased production of non-volatile acids;

D.decrease in base production.

3.Causes of respiratory acidosis include:

A.blood marrow disorders;

B. Disorders of the thoraco-pulmonary system;

C. Stimulation of catabolism;

D.some nephropathies.

4.Hypercapnia from respiratory acidosis may be accompanied by :

A.onset of hypoxemia;

B.the onset of renal acidosis;

C. The onset of a metabolic alkalosis;

D.decrease in red blood cell count.

5.Respiratory alkalosis is the consequence:

A.increase in base production;

B.decrease in the production of non-volatile acids;

C.hyperventilation;

D.hypoventilation.

6.Causes of respiratory alkalosis are:

A.hypothalamus stimulation in hyperthermia;

B.stimulation of the erythrocyte system;

C.inhibition of respiratory centers;

D.increased oxygen pressure in the atmospheric air.

7.Metabolic acidosis is the result of:

A.digestive disorders;

B.blood disorders;

C.pulmonary congestion;

D.respiratory disorders.

8.The mechanisms of metabolic acidosis are:

A.increased production of non-volatile acids;

B.increased production of bases;

C.increased elimination of acids at the renal level;

D.decrease in carbon dioxide concentration.

9.The primary element in metabolic alkalosis is:

A.increase in bicarbonates;

B.decrease in hydrogen ion concentration;

C.decrease in bicarbonates;

D.increased hydrogen ion concentration.

10.Causes of respiratory acidosis can be:

A. Lesions in the respiratory centres;

B.disorders of the thoraco-pulmonary apparatus;

C.stimulation of catabolism;

D.some nephropathies.

11.Hypercapnia from respiratory acidosis may be accompanied by :

A.onset of hypoxemia;

B.the onset of lactic acidosis;

C. The onset of a metabolic alkalosis;

D.decrease in red blood cell count.

12.Causes of respiratory alkalosis are:

A.hypothalamus stimulation in hyperthermia;

B.stimulation of the limbic system;

C.stimulation of respiratory centres;

D.decrease in oxygen pressure in the atmospheric air.

13.Metabolic acidosis is the result of:

A.digestive disorders;

B.renal disorders;

C.tissue hypoxia;

D.respiratory disorders.

14.The mechanisms of metabolic acidosis are:

A.increased production of non-volatile acids;

B.increased loss of bases;

C.decreased elimination of acids at the renal level;

D.decrease in carbon dioxide concentration.

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