Reactivity and Resistance

Resistance is:
1. The ability of the living system to respond precisely to irritants.
2. The ability of the living system not to respond to irritants.
3. The ability of the living system to oppose irritants.
4. The ability of the living system of self – improvement.
5. 1, 4.
The most precise definition of reactivity is:
1. The ability of the living system to adapt.
2. The response of the living system to irritants.
3. The combination of reactions of the living system.
4. The ability of the living system to change itsliving activity.
5. The continuous adaptive alterability of the organisms.
The external factors, influencing reactivity and resistance are:
1. Environment.
2. Ecology.
3. Nutrition.
4. Gender and age.
5. 1, 2, 3.
6. 1, 3, 4.
The internal factors, influencing reactivity and resistance are:
1. Social conflicts.
2. Psychological factors.
3. Climate and geographic influence.
4. Heredity, gender and age.
5. Lifestyle of the individual.
According to the reaction magnitude, reactivity is classified as:
1. Normergic, hyperergic, hypergic, super-allergic.
2. Normergic, hyperergic, hypergic, anergic.
3. Local, segment, diffuse, generalized.
4. Organelle, cellular, organ, organism.
5. Paralytic, kinetic, tonic.
Natural resistance is:
1. Acquired.
2. Postnatal.
3. Adaptively developed.
4. Neurogenic developed.
5. Genetically pre-programmed.
What type of resistance is acquired by vaccination:
1. Natural, absolute, active.
2. Natural, relative, passive.
3. Acquired, artificial, active.
4. Acquired, artificial, passive.
5. Acquired, natural, active.
6. Acquired, natural, passive.
The type of resistance, acquired by hyperimmune serum therapy:
1. Acquired, artificial, active.
2. Acquired, artificial, passive.
3. Natural, absolute, passive.
4. Natural, relative, active.
5. Acquired, natural, active.
6. Acquired, natural, passive.
What type of resistance is acquired following an infectious disease:
1. Acquired, artificial, active.
2. Acquired, artificial, passive.
3. Natural, absolute.
4. Acquired, natural, active.
5. Acquired, natural, passive.
Allergy is developed by the following mechanisms:
1. Non-immunological mechanisms.
2. Mechanisms of direct injury.
3. Mechanisms of disturbed reflex arc.
4. Immunological mechanisms .
5. 1, 2.
Allergy is:
1. Normergic immunological reactivity.
2. Hyperergic immunological reactivity.
3. Reaction of idiosyncrasy.
4. Explosive cellular – tissue distress.
5. Non – specific hypersensitivity.
The main types of allergic reactions are:
1. Of humoral type.
2. Of neuro – reflex type.
3. Of cellular type.
4. Of neuroendocrine type.
5. 1, 3.
6. 2, 4.
The main types of disturbed immune response are:
1. Immune hypersensitivity.
2. Immune idiosyncrasy.
3. Disturbed auto - tolerance.
4. Immune insufficiency.
5. 1, 3, 4.
6. 1, 2, 3, 4.
Humoral immunity deficiency is characterized:
1. Failure to recognise foreign antigens.
2. Lack of activation of T-helpers.
3. Suppressed proliferation and differentiation of B – Lymphocytes.
4. Disturbed synthesis of specific immunoglobulines.
5. 3, 4.
6. 1, 2, 3, 4.
The alteration of which mechanisms does NOT disturb the immune response:
1. Phagocytosis, processing and presentation of the antigen.
2. Activation of T – helper lymphocytes.
3. Activation of cytotoxic T – cells and B – lymphocytes.
4. Reflex activation of the HPA axis ( hypothalamus – pituitary – adrenal)
5. Binding and clearance of antigens.
Type I hypersensitivity (anaphylaxis) is related to the presence of:
1. Plasma IgG and/or IgM.
2. Cytotoxic Т-Ly.
3. Mast cell / basophil – bound IgE.
4. Epithelium – bound IgA2.
5. Circulating free IgE.
Atopy is:
1. IgE mediated hypersensitivity.
2. IgM mediated hypersensitivity.
3. IgA secretory hypersensitivity.
4. Non-specific hyperreactivity.
5. IgG mediated idiosyncrasy.
In the mechanism of cell-dependent cytotoxicity in allergy are NOT involved:
1. NK- cells.
2. Т-helper lymphocytes.
3. Macrophages.
4. Т- killer lymphocytes.
5. All of the above–mentioned are involved.
Cell-mediated allergic reactions of delayed type are a manifestation of the interactions between:
1. Macrophagesand Т-helper lymphocytes.
2. Memory lymphocytes and idiotype antibodies.
3. Null lymphocytes, complement and antigens.
4. B-sensitized lymphocytes and antigens.
5. T-sensitized lymphocytes and antigens.
6. Activated segments cells.
The Arthus reaction (e.g. Farmer’s Lung) is:
1. Cytotoxic immune reaction.
2. Immunocomplex hypersensitivity with excess of antigens.
3. Granulomatous type of hypersensitivity.
4. Immunocomplex hypersensitivity with excess of antibodies.
5. Atopic allergic effect.
Which of the mechanisms of antigen elimination always has clinical manifestations:
1. Steric antigen elimination.
2. Immune inflammation.
3. Opsonization and phagocytosis.
4. Immune-dependent apoptosis.
5. Macrophageal antigen adhesion.
The disturbed immune memory disrupts:
1. The specificity of the immune response to the antigen.
2. The magnitude and speed of the consequent immune reaction.
3. The combination of humoral and cellular immune responses.
4. The transition of immunological stress into distress.
5. The interaction between immune and neuronal memory.
Autoimmune reaction is:
1. The interrupted tolerance towards own antigens.
2. Embryonic genetic autointolerance.
3. A synonym of autoimmune disease.
4. An attempt for immune-mediated species self-isolation of the individual.
5. A component of the immune autoregulation that cannot be omitted.
Lost autotolerance is a manifestation of :
1. Unveiling sequestered, hidden autoantigens.
2. HPA-axis (hypothalamus-pituitary-adrenal) activation.
3. T–suppressors insufficiency.
4. T-helpers mistake and/or T-effectors or B-lymphocyte direct activation.
5. 1, 2, 3, 4.
6. 1, 3, 4.
Which of the following mechanisms prevents the occurrence of autoimmune reaction:
1. Unveiling sequestered antigens.
2. Autoreactive T-helpers deficiency.
3. Autoreactive T-suppressors activation.
4. Modulation of own antigens – “self plus X”.
5. Direct stimulation of cytotoxic autoreactive cells.
Which of the mechanisms of disturbed autotolerance switches-off T-helper involvement:
1. Flaws in the process of antigen recognition.
2. Contact of sequestered antigens with competent T- and B-cells.
3. Direct activation of the autoreactive T-effectors and/or B-cells.
4. Suppressed T-suppressor activity.
5. Inadequate presentation of own antigens by APC.
Immunodeficient states are a representation of:
1. Specific enzymopathy.
2. Antigen deficiency.
3. Inadequate immune reaction.
4. Hypo-, anergic immune response.
5. Hyperergic immune reaction.
The most common consequences of immunodeficiencies are:
1. Susceptibility to hemorrhagic diathesis.
2. Facilitated development of hypoxia.
3. Increased susceptibility to infections.
4. Starvation (cachexia).
5. Facilitated cancerogenesis.
Non-specific inborn immunodeficit state is present in:
1. Genetic defects of the immunoglobulin synthesis.
2. Thymus embryogenesis disturbances.
3. Genetically determined phagocyte hypofunction.
4. Genetic abnormalities in the complement.
5. 1, 2.
6. 3, 4.
AIDS-related immune deficiency is associated predominantly with the damage of:
1. All types of lymphocytes.
2. Т-helper lymphocytes.
3. B-lymphocytes.
4. Т-suppressor lymphocytes.
5. Null lymphocytes.

Reactivity and Resistance

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