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nervous system

Total questions: 122

Worksheet time: 1hrs 1mins

Name
Class
Date
1.

A group of hyperactive neurons with weakened inhibitory control is formed when:

a)

blockade of NMDA receptors

b)

sodium channel blockade

c)

severe hypoxic neuronal damage

d)

low calcium content in the cytoplasm of neurons

e)

increased release of aspartate into the synaptic cleft

2.

On the 10th-12th day of complete fasting, neurons in the brain begin to use the following as an oxidation substrate to obtain energy:

a)

glucose

b)

glycogen

c)

triglycerides

d)

ketone bodies

e)

hexose phosphates

3.

One of the consequences of an imbalance of ions and fluid in neurons can be:

a)

persistent depolarization of the neuronal plasma membrane

b)

decrease in osmotic pressure in neurons

c)

inhibition of lipid peroxidation of neuronal membranes

d)

increased activity of neuronal proteosynthesis enzymes

e)

accumulation of K+ ions in the intracellular space

4.

Specific mechanisms of neuronal dysfunction include:

a)

neuronal apoptosis

b)

damage to neuronal membranes

c)

disruption of mediator transport along the axon

d)

disruption of the energy supply to neurons

e)

ion and fluid imbalance due to energy deficiency

5.

In the development of neurodystrophic processes that can occur in peripheral organs and in the nervous system itself, changes in:

a)

synapses

b)

neuroglia

c)

sarcoplasmic reticulum

d)

blood-brain barrier

e)

meninges

6.

The neural pathway for the entry of pathogenic agents into the central nervous system is characteristic of:

a)

pneumococci

b)

tetanus toxin

c)

streptococcal exotoxin

d)

E.coli

e)

influenza viruses

7.

The penetration of viruses and antibodies into the central nervous system is ensured by the work of:

a)

dendrites and their spines

b)

synaptic apparatus of a neuron

c)

fast axonal transport involving microtubules

d)

slow anterograde axonal transport

e)

retrograde axonal transport

8.

Disorders of the integrative activity of neurons consist of a violation of:

a)

post-tetanic potentiation

b)

connections with other neurons through processes

c)

conduction of excitation with the participation of chemical synapses

d)

opening of sodium ion channels on the postsynaptic membrane

e)

summation of all postsynaptic potentials arising on the membrane

9.

The main mechanism of synaptic dysfunction under the influence of botulinum toxin is:

a)

inhibition of glycine secretion into the synaptic cleft

b)

inhibition of acetylcholine secretion into the synaptic cleft

c)

blocking serotonin receptors on the postsynaptic membrane

d)

inhibition of monoamine oxidase activity

e)

inhibition of cholinesterase activity

10.

A characteristic sign of denervation syndrome is:

a)

increased formation of trophogens

b)

excessive electrogenesis of denervation structures

c)

increased excitability and perverted reactivity of neurons

d)

increased entry of K+ into neurons and excessive release of Ca2+

e)

enhancement of GABAergic inhibition of the neuron

11.

Severe denervation syndrome develops as a result of:

a)

sympathectomy

b)

partial decortication

c)

disconnection of the nervous system from organs and tissues

d)

disconnection of the cerebral cortex from the subcortical centers

e)

disconnection of the central and peripheral autonomic nervous system

12.

In the pathogenesis of neurogenic dystrophy of cells of a denervated organ the following is important:

a)

A. increasing the supply of trophogens to cells

b)

B. increasing the excitability threshold of denervated cells

c)

C. increasing the functional activity of the denervated organ

d)

D. absence of neurotransmitter effects on the postsynaptic membrane

e)

E. blockade of sodium channels in the membranes of denervated cells

13.

An altered formation in the central nervous system in the form of a group of hyperactive interconnected neurons and representing a pathological integration at the level of interneuronal relationships:

a)

damage to dendrites

b)

pathological system

c)

pathological dominant

d)

pathological determinant

e)

generator of pathologically increased excitation

14.

When the dorsal roots of the spinal cord are transected, limb movements on the affected side become sprawling and poorly coordinated. This phenomenon is caused by:

a)

activation of inhibitory mechanisms in the spinal cord

b)

increased excitability of deafferented structures

c)

increasing the reactivity of neurons to impulses from different sources

d)

stimulation afferent impulses entering the neurons of the central nervous system

e)

development trophic disorders in the innervation zone

15.

A 45-year-old man, S., is in a general extension position following a massive brainstem infarction (at the level of the midbrain). His head is tilted back, the tone of the extensor muscles of the back and limbs is sharply increased, his hands and fingers are flexed, and his feet are extended. These signs indicate the development of:

a)

pathological parabiosis

b)

pathological determinant

c)

syndrome of deafferentation of nerve structures

d)

decerebrate rigidity

e)

denervation syndrome

16.

With organic lesions of the central nervous system, patients develop Babinski reflexes, grasping, sucking, and other reflexes considered normal in the early postnatal period. Their development in adult patients is a result of:

a)

excessive activity of inhibitory neurons

b)

direct damage to excitation mechanisms

c)

activation of the control function of the cerebral cortex over the spinal cord

d)

disinhibition of the centers of the spinal cord or medulla oblongata

17.

A state of increased general excitability of the central nervous system, arising as a result of prolonged irritation of the afferent nerve and is an example of pathology of systemic relationships in case of damage to the nervous system:

a)

hysteroesis

b)

denervation syndrome

c)

deafferentation syndrome

d)

pathological determinant

e)

pathologically enhanced excitation generator

18.

Pathological dominant, as the functional structure of the central nervous system that is dominant at a certain moment is realized at the level of:

a)

synaptic connections

b)

intersystem relations

c)

intrasystemic relations

d)

intracellular processes

e)

intercellular relationships

19.

Neuropathological syndrome is a clinical expression of the activity of:

a)

anti-systems

b)

pathological system

c)

pathological dominant

d)

damaged nerve cell

e)

focus of pathological parabiosis

20.

To eliminate neurological or psychopathological syndromes, the body develops defense mechanisms aimed at increasing the nervous system's resistance and eliminating the affected areas. These include:

a)

formation of anti-systems

b)

predominance of excitation processes over inhibition

c)

development of generators of pathologically increased excitation

d)

decreased degree of intracellular regeneration of neurons

e)

increased permeability of the blood-brain barrier

21.

Increased resistance of brain neurons to hypoxic damage is observed under the following conditions:

a)

activation of NMDA receptors

b)

glutamatergic denervation

c)

actions of glutamate receptor activators

d)

increasing the activity of NO synthase in neurons

e)

reduction in the density of GABA receptors on the surface of neurons

22.

Metabolic features of the brain that influence the development of ischemia include:

a)

low oxygen consumption

b)

low phosphocreatinine level

c)

the use of free fatty acids as an energy source

d)

low activity of antioxidant enzymes

e)

the presence of large reserves of glucose and glycogen

23.

The independence of the level of blood flow through the brain from changes in systemic arterial pressure is within the range:

a)

from 0 to 180 mmHg

b)

from 40 to 160 mm Hg

c)

from 60 to 180 mm Hg

d)

from 80 to 200 mmHg

e)

from 90 to 220 mmHg

24.

The main factor in the regulation of cerebral circulation is:

a)

myogenic factor

b)

humoral factor

c)

neurogenic factor

d)

metabolic factor

e)

membranogenic factor

25.

Dilation of cerebral arteries occurs when:

a)

hypercapnia

b)

hyperoxemia

c)

increasing pH

d)

increased blood pressure

e)

increasing the tone of precapillary arterioles

26.

Patient F., with a severe traumatic brain injury, developed an increase in intracranial pressure to 32 mmHg with a significant decrease in perfusion volume. In this case, the disruption of cerebral blood flow is due to the fact that intracranial hypertension causes:

a)

increased cerebrospinal fluid resorption

b)

acceleration of venous blood outflow

c)

compression of the veins at the points where they enter the sinuses of the brain

d)

reduction of pressure in the ventricles of the brain

e)

compression of extracranial vessels

27.

In cerebral ischemia, the development of focal necrosis is associated with:

a)

increased activity of neurotrophic factors

b)

activity of the calcium-glutamate cascade

c)

an increase in the level of inhibitory amino acids

d)

NMDA receptor hyporeactivity

e)

A. increased activity of mitochondrial enzymes

28.

Transient ischemic attacks are characterized by:

a)

development of cysts in the brain

b)

development of ischemia only in the white matter

c)

development of white infarcts in the brain

d)

hemorrhagic transformation of cerebral infarction

e)

reversibility of neurological dysfunction within 24 hours

29.

The threshold for the development of irreversible changes in neurons is the level of perfusion:

a)

80 ml/100 g/min-1

b)

50 ml/100 g/min-1

c)

35 ml/100 g/min-1

d)

20 ml/100 g/min-1

e)

10 ml/100 g/min-1 or less

30.

A 70-year-old patient complained of weakness on the right side of his body, difficulty speaking, headache, and nausea. The patient had a history of primary hypertension and coronary artery disease. Examination revealed severe right-sided hemiparesis, hemianesthesia, and a positive pathological Babinski reflex. A CT scan of the brain revealed no signs of an intracerebral hematoma. These abnormalities suggest the patient is developing:

a)

ischemic stroke

b)

hemorrhagic stroke

c)

subarachnoid hemorrhage

d)

arteriovenous malformation

e)

hemorheological occlusion

31.

Uncontrolled (non-modifiable) risk factors for the development of ischemic stroke include:

a)

hypercoagulability

b)

hyperhomocysteinemia

c)

arterial hypertension

d)

type 2 diabetes mellitus

e)

heredity

32.

A 62-year-old man, weighing 115 kg, and a heavy smoker, suddenly developed left-sided paralysis and sensory loss. He died three hours later. Autopsy revealed a grayish, crumbling, irregularly shaped lesion in the right temporoparietal region of the brainDense, round, yellowish-white lesions were found in the arteries, narrowing the lumen by more than 75%. The most likely cause of the patient's typical form of nervous system pathology is:

a)

age

b)

smoking

c)

male gender

d)

atherosclerosis

e)

excess body weight

33.

The most important modifiable risk factor for the development of the cardioembolic subtype of ischemic stroke is:

a)

type 1 diabetes mellitus

b)

arterial hypotension

c)

atrial fibrillation

d)

alcohol abuse

e)

chronic kidney disease

34.

The group of systemic etiological factors in the development of ischemic stroke includes:

a)

compression of cerebral arteries

b)

cerebral artery dissection

c)

thrombus formation in the cerebral vessels

d)

atherosclerosis of cerebral vessels

e)

arterial hypotension

35.

In the pathogenesis of ischemic stroke, an important role is played by:

a)

increased ATP formation

b)

glutamate excitotoxicity

c)

suppression of NMDA receptor activity

d)

increased calcium release from the neuron

e)

increase antioxidants

36.

In stroke, activation of NMDA receptors of postsynaptic cells by glutamate and aspartate is accompanied by:

a)

increased potassium intake into the cell

b)

increased calcium intake into the cell

c)

suppression of lipid peroxidation processes

d)

inhibition of the activity of proteolytic enzymes

e)

suppression of AMPA receptor activity

37.

High local concentration of extracellular glutamate in the ischemic zone and excessive activation of glutamate receptors leads to:

a)

suppression of voltage-dependent calcium channels

b)

neuronal death by apoptosis and necrosis

c)

increasing the activity of ATP-dependent pumps

d)

increased synthesis of neurotrophic factors

e)

A. inhibition of neuronal depolarization

38.

Hyperactivation of ionotropic postsynaptic AMPA receptors in the ischemic brain causes:

a)

osmotic swelling of cells

b)

release of sodium and water from neurons

c)

magnesium blocker of NMDA receptors

d)

closing of calcium ion channels

e)

inhibition of neuronal excitotoxicity mechanisms

39.

In the area of the ischemic penumbra are located:

a)

irreversibly damaged neurons

b)

neurons with a high level of plasticity

c)

irreversibly damaged neuroglial cells

d)

neurons with high bioelectrical activity

e)

functionally unstable but viable neurons

40.

In the pathogenesis of ischemic cerebral edema in stroke, the following is important:

a)

sodium and chlorine release from neurons

b)

decreased permeability of the vascular wall

c)

reduction of hydrostatic pressure in vessels

d)

ATP-dependent sodium pump deficiency

e)

decrease in oncotic pressure in the perivascular space

41.

In ischemic stroke, the development of petechiae and parenchymal hematomas indicates the development of:

a)

ischemic penumbra

b)

ischemic cerebral edema

c)

excessive collateral circulation

d)

hemorrhagic transformation of cerebral infarction

e)

reperfusion injury of brain tissue

42.

Delayed mechanisms of neuronal death in ischemic stroke include the development of:

a)

neuronal hypoperosis

b)

oxidative stress

c)

glutamate excitotoxicity

d)

cytotoxic cerebral edema

e)

lactic acidosis

43.

In the early post-stroke period, the patient's neurological symptoms continued to worsen, despite the restoration of blood flow in the damaged cerebral vessel. The following factors contributed to the worsening of neurological symptoms in the early post-stroke period:

a)

neuronal reperfusion

b)

shrinkage of neurons

c)

calcium release from neurons

d)

decreased osmolarity of neurons

e)

inhibition of glutamate receptors

44.

A 62-year-old man, weighing 115 kg, and a heavy smoker, suddenly developed left-sided paralysis and sensory loss. He died three hours later. Autopsy revealed a grayish, crumbling, irregularly shaped lesion in the right temporoparietal region of the brain. Dense, round, yellowish-white lesions were found in the arteries, narrowing the lumen by more than 75%. The most likely cause of the patient's typical form of nervous system pathology is:

a)

age

b)

smoking

c)

male gender

d)

atherosclerosis

e)

excess body weight

45.

Patient D., 60, was admitted with signs of acute cerebrovascular accident. Her medical history revealed that she had been treated for hypertension for 15 years. Examination revealed lesions up to 10-15 mm in diameter and microangiopathy in the form of lesions of small perforating arteries. These signs suggest the development of:

a)

cryptogenic stroke

b)

hemorrhagic stroke

c)

subarachnoid hemorrhage

d)

atherothrombotic stroke

e)

lacunar stroke

46.

The most significant factors in the development of the atherothrombotic subtype of ischemic stroke include:

a)

atherosclerotic plaque instability

b)

hemorrhagic transformation of cerebral infarction

c)

formation of cavities in the brain filled with cerebrospinal fluid

d)

microangiopathy in the white matter of the brain

e)

angiodystonic disorders in the cerebral vessels

47.

A patient with acute transmural myocardial infarction of the anterior wall of the left ventricle and atrial fibrillation developed ischemic stroke. The main pathogenetic factor for the development of cerebral ischemia in this case is:

a)

increased blood viscosity

b)

increased aggregation of formed blood elements

c)

increased activity of the blood fibrinolytic system

d)

decrease in systemic perfusion pressure

e)

deterioration of blood rheological properties

48.

Occlusion of a deep perforating artery leads to the development of the following pathogenetic subtype of ischemic stroke:

a)

lacunar

b)

cardioembolic

c)

atherothrombotic

d)

hemodynamic

e)

cryptogenic

49.

Patient N., who suffered an ischemic stroke, developed rapid and deep breathing. As a result, his PaCO2 dropped to 29 mmHg, which, in turn, caused changes in cerebral vascular reactivity, such as:

a)

decreased cerebral blood flow

b)

reduction of vascular resistance

c)

increasing the linear velocity of blood flow

d)

increase in volumetric blood flow

e)

dilation of cerebral vessels

50.

A pronounced impairment of vital functions with a disorder of regulation of the respiratory and cardiovascular systems, swallowing disorders, and complete loss of speech are more often observed with a decrease in blood flow in the pool:

a)

carotid system

b)

middle cerebral artery

c)

anterior cerebral artery

d)

internal carotid artery

e)

vertebrobasilar system

51.

In ischemic stroke, the main target of neuroprotection is:

a)

penumbra

b)

infarction core

c)

marginal zone

d)

oligemia zone

e)

necrosis zone

52.

In ischemic stroke, as opposed to hemorrhagic stroke, the following is more often observed:

a)

compression of brain tissue

b)

focal symptoms

c)

internal hydrocephalus

d)

increased intracranial pressure

e)

hemorrhagic transformation of cerebral infarction

53.

Unlike ischemic stroke, this form of acute cerebrovascular accident with hemorrhage into the subarachnoid space of the cerebral membranes is characterized by:

a)

brainstem lesion

b)

low intracranial pressure

c)

significant activation of microglia

d)

aseptic meningitis

e)

visual impairment

54.

The main cause (≈85% of cases) of spontaneous subarachnoid hemorrhage is:

a)

aneurysm rupture

b)

arterial dissection

c)

blood clotting disorder

d)

inflammatory changes in cerebral vessels

e)

rupture of cerebral arteriovenous malformation

55.

Hemorrhagic stroke is anatomically manifested by:

a)

white cerebral infarction

b)

vasogenic cerebral edema

c)

liquefaction necrosis

d)

gray softening of the brain

e)

focal hemorrhagic infiltration of the brain

56.

Factors that determine the more severe course of hemorrhagic stroke compared to ischemic stroke include:

a)

more pronounced compression and swelling of the brain

b)

absence of glutamate excitotoxicity

c)

the influence of vasodilatory substances of the spilled blood

d)

pronounced activation of the antioxidant system

e)

lesser severity of ATP deficiency

57.

Patient V. suffered a hemorrhagic stroke. Post-stroke, the patient experienced pain and tactile disturbances. These symptoms are more typical of damage to the following nerve structure:

a)

thalamus

b)

cerebellum

c)

hippocampus

d)

frontal lobe

e)

occipital lobe

58.

The most common clinical syndrome of stroke is spastic hemiparesis. Its development is associated with damage to:

a)

cerebellum

b)

hypothalamus

c)

pyramidal tracts

d)

extrapyramidal system

e)

anterior horns of the spinal cord

59.

A patient with tetanus experiences prolonged muscle contractions, resulting in the "freezing" of the torso or limbs in various forced positions. This type of rapid hyperkinesias belongs to the group:

a)

clonic seizures

b)

tonic convulsions

c)

athetosis

d)

chorea

e)

ticks

60.

The development of pyramidal hyperkinesis is indicated by the appearance of:

a)

chorea

b)

athetosis

c)

tremors

d)

muscle fibrillation

e)

clonic seizures

61.

The most characteristic manifestations of damage to the pyramidal system are:

a)

ataxia, tics

b)

causalgia, phantom pain

c)

tonic and clonic seizures

d)

paralysis, pathological reflexes

e)

Parkinsonian tremor, asynergy

62.

Complete loss of movement due to a disorder of the motor function of the nervous system is called:

a)

paresis

b)

myotonia

c)

myasthenia

d)

paralysis

e)

hyperesthesia

63.

When the pyramidal tract (the central neuron and its axon) is damaged above the crossing at the border of the brain and spinal cord, the following develops:

a)

opisthotonus

b)

Parkinson's disease

c)

peripheral paralysis on the affected side

d)

spastic paralysis on the side of the lesion

e)

spastic paralysis on the side opposite the lesion

64.

Characteristic signs of central paralysis include:

a)

hyporeflexia

b)

muscle hypotonia

c)

qualitative changes in muscle electrical excitability

d)

increased tendon and periosteal reflexes

e)

fibrillary and fascicular muscle twitching

65.

In central paralysis, due to the release of the segmental reflex apparatus of the spinal cord from cortical influences in the affected limbs, the following is observed:

a)

disappearance of tendon reflexes

b)

increased muscle tone

c)

hypo-, areflexia

d)

muscle atrophy

e)

paresthesia

66.

Patient K. suffered an ischemic stroke. Spastic left-sided paralysis of the upper limb developed. This indicates that the ischemic lesion is located in the following gyrus of the cerebral hemispheres:

a)

inferior frontal

b)

superior temporal

c)

hippocampal

d)

postcentral

e)

precentral

67.

A 15-year-old adolescent was admitted with a spinal cord injury sustained while diving. Physical examination revealed tetraplegia. The injury level in this case was:

a)

sacral region

b)

lumbar region

c)

thoracic and lumbar regions

d)

thoracic region

e)

cervical spine

68.

Monoparesis in humans most often occurs with:

a)

cerebellar damage

b)

brain stem damage

c)

damage to the cerebral cortex

d)

hemorrhage into the internal capsule

e)

damage to the pyramidal tract at the level of the spinal cord

69.

The most common cause of hemiparesis in humans is:

a)

cerebellar damage

b)

damage to the cerebral cortex

c)

damage to the pyramidal tract at the level of the medulla oblongata

d)

damage to the pyramidal tract at the spinal cord level

e)

hemorrhage into the internal capsule

70.

Patient Sh., 75, has no movement in the right upper and right lower extremities, marked hypertonicity, hyperreflexia, and positive Babinski signs on the right. These symptoms indicate the development of the following movement disorder syndrome with a lesion located in:

a)

right-sided flaccid paraplegia, cerebellum

b)

right-sided flaccid paraplegia, internal capsule

c)

right-sided central hemiplegia, internal capsule

d)

right-sided central hemiplegia, substantia nigra

e)

right-sided central hemiplegia, cerebellum

71.

Increased spinal reflexes are observed in:

a)

damage to spinal motor neurons

b)

development of primary neurological coma

c)

functioning of intercalary inhibitory neurons of the spinal cord

d)

rupture of connections between the spinal cord and the higher parts of the central nervous system

e)

transection of the posterior roots of the spinal cord (deafferentation)

72.

The tone of the affected muscles decreases with:

a)

central paralysis

b)

peripheral paralysis

c)

decerebrate rigidity

d)

convulsions

e)

athetosis

73.

Following a severe injury to the posterior left thigh, a patient exhibits severe limitation of active movement in the lower limb, signs of muscle wasting and hypotonia in the left calf, and a decreased Achilles reflex on the left. These symptoms indicate the following type of locomotor dysfunction:

a)

flaccid paralysis

b)

central paralysis

c)

peripheral paresis

d)

spastic paresis

e)

myasthenia

74.

The patient experiences simultaneous increased flexor and extensor tone, decreased motor coordination, and prolonged limb rigidity in a given position. Abnormal reflexes are absent. These disturbances of locomotor function of the nervous system are caused by lesions of the following:

a)

cerebellum

b)

brainstem

c)

pyramidal system

d)

extrapyramidal system

e)

autonomic nervous system

75.

A prolonged increase in the tone of one or more antagonist muscle groups, which is observed with damage to the extrapyramidal system, is characteristic of the following form of hypokinesia:

a)

flaccid

b)

rigid

c)

spastic

d)

myasthenic

e)

peripheral

76.

Muscle hypertonia, a slow pace of active movements, a shuffling, small-step gait, and quiet, monotonous speech are characteristic of damage to:

a)

pyramidal tract

b)

cerebral cortex

c)

pallido-nigral system

d)

anterior horns of the spinal cord

e)

hypothalamic-pituitary region

77.

A 68-year-old female patient presents with head and upper extremity tremors at rest, difficulty walking and unsteadiness, hypomimia, and infrequent blinking. Her gait is shuffling, her posture is hunched, and muscle rigidity is present. Decreases in dopamine and tyrosine hydroxylase levels were detected. This disease (syndrome) is characterized by:

a)

decreased muscle tone

b)

disappearance of Lewy bodies in neurons

c)

degeneration of nigrostriatal neurons

d)

damage to the structures of the pyramidal system

e)

increased dopamine levels in the striatum

78.

Ataxia, muscle hypotonia, intention tremor, nystagmus, and scanned speech are characteristic of damage to:

a)

cerebellum

b)

pallido-nigral system

c)

parietal lobe of the brain

d)

midbrain

e)

pituitary gland

79.

A patient with a cerebellar tumor was admitted to the neurosurgical department. Examination revealed ataxia, characterized by:

a)

increased muscle tone

b)

impaired coordination of movements

c)

weakening of movements in the lower limbs

d)

the appearance of pathological reflexes

e)

loss of voluntary movements

80.

In myasthenia gravis, as a result of the production of autoantibodies to the alpha chain of acetylcholine receptors, which are localized at the site of contact between nerve and muscle cells, the following is observed:

a)

neuromuscular transmission disorder

b)

impaired temperature sensitivity

c)

an increase in the number of cholinergic receptors in neuromuscular synapses

d)

increase in postsynaptic action potential

e)

increased synaptic depolarization

81.

A 42-year-old patient complained of blurred vision, double vision, thirst, and difficulty swallowing. He had eaten homemade pickled mushrooms one day prior to the illness. Examination revealed diplopia, mydriasis, and ptosis. Pharyngeal and palatal reflexes were absent. Tendon reflexes were normal, sensory function was intact, and there were no meningeal symptoms. The neuromuscular dysfunction in this case was due to:

a)

disappearance of acetylcholine reserves

b)

blockade of H-cholinergic receptors of the postsynaptic membrane

c)

blockade of the release of acetylcholine from the endings of motor axons

d)

activation of calcium channels in the presynaptic membrane

e)

activation of calcium-dependent exocytosis of acetylcholine

82.

Signs of peripheral nerve damage:

a)

muscle hypertrophy

b)

sensory disturbance

c)

the appearance of pathological reflexes

d)

strengthening of protective reflexes

83.

In demyelinating neuropathies the following is observed:

a)

primary damage to the extrapyramidal system

b)

primary destruction of the myelin sheath of axons

c)

primary lesion of peripheral nerve axons

d)

normal conduction velocity

e)

acceleration of nerve impulse conduction

84.

In the pathogenesis of peripheral neuropathies in diabetes mellitus, the following is of great importance:

a)

neurofilament damage

b)

disorders of axonal transport of substances

c)

destruction of the myelin sheath of the nerve by antibodies

d)

damage to the peripheral nerve vessels (vasa nervorum)

e)

blockade of acetylcholine release from motor axon terminals

85.

Patient N., 56, with vitamin B-12 deficiency, experiences paresthesia, loss of deep sensation, impaired balance when standing and walking, decreased knee and ankle reflexes, and spastic paresis of the lower extremities. The patient's neurological impairment is associated with the following deficiency:

a)

transcobalamin

b)

methylcobalamin

c)

folic acid

d)

methylmalonic acid

e)

5-deoxyadenosylcobalamin

86.

The formation of a pathologically enhanced excitation generator in the central nervous system after a stroke or as a result of spinal cord injury is characteristic of the development of the following type of pathological pain:

a)

visceral

b)

peripheral

c)

neuropathic

d)

nociceptive

e)

somatic

87.

Patient A., 15, was admitted to the clinic with severe abdominal pain. During an abdominal examination, the surgeon discovered peritoneal hyperemia and edema, along with purulent exudate. The type of pain that developed in this patient with widespread purulent peritonitis:

a)

visceral

b)

parietal

c)

functional

88.

Patient D., 28, developed intense, diffuse, radiating gum pain following the traumatic extraction of his upper incisors. His temperature rose to 37.8°C, and his regional lymph nodes were enlarged. The type of pain he experienced was:

a)

phantom

b)

visceral

c)

projection

d)

primary (epicritic)

e)

secondary (protopathic)

89.

Weakening and disintegration of the natural antinociceptive system is a pathogenetic factor in the development of:

a)

pathological pain

b)

receptor anesthesia

c)

convulsive syndrome

d)

extrapyramidal palsy

e)

meningeal irritation syndrome

90.

Primary (epicritic) pain is characterized by:

a)

diffuse character

b)

high threshold of perception

c)

occurrence immediately after injury

d)

type of conducting fiber - unmyelinated, type C

e)

long duration after removal of the irritant

91.

For afferent thin nociceptive fibers of the A-delta (Aδ) type, the following is characteristic:

a)

absence of myelin sheath

b)

low impulse conduction velocity (< 1 m/s)

c)

blocking the release of substance P from neurons

d)

participation in the development of primary (epicritic) pain

e)

being found only in the autonomic nervous system

92.

Polymodal fibers of type C are characterized by:

a)

Distribution only in the central nervous system

b)

inhibition of NMDA receptors

c)

rapid conduction of nerve impulses

d)

participation in the development of acute, localized (epicritic) pain

e)

stimulation by temperature, mechanical and chemical stimuli

93.

Patient A., suffering from severe spinal pain due to a herniated disc, was prescribed blockades using a local anesthetic whose primary mechanism of action is the closure of Na+ channels in neuronal axons. This results in:

a)

increased excitability of nerve fibers

b)

activation of unmyelinated thin nociceptive C fibers

c)

acceleration of impulse propagation along the nerve fiber

d)

slowing of depolarization and conduction of action potentials

e)

slowing down the processes of hyperpolarization of the neuronal membrane

94.

Following amputation of his left lower limb, a patient began complaining of excruciating, unbearable pain in his missing leg. Pain medications and acupuncture were ineffective in relieving the pain. The underlying mechanism of this type of pain is:

a)

memory of previous life experience

b)

activation of neurogenic mechanisms of the antinociceptive system

c)

increased excitability of deafferented primary neurons

d)

excessive excitation of the endings of regenerating nociceptive fibers

e)

regeneration of nerve fibers of an amputated organ with the formation of a neuroma

95.

Patient M., 48, experienced severe pain in the stump postoperatively following amputation of his left lower limb, along with a sensation of the missing limb. Peripheral mechanisms for this type of pathological pain include:

a)

memory of previous life experience

b)

inhibition of the endings of regenerating nociceptive fibers

c)

increased excitability of deafferented primary neurons

d)

regeneration of nerve fibers of an amputated organ with the formation of a neuroma

e)

excitation of secondary nociceptive neurons in the dorsal horns of the spinal cord

96.

Three weeks after a hip injury with sciatic nerve damage, the patient developed intermittent, intensifying burning pain and a sensation of "boiling water poured over the limb" and "pins being stuck into it." The pain was accompanied by hyperemia and swelling on the injured side. Touching the injured area triggered severe pain. The mechanisms for this type of pain are:

a)

demyelination of the nerve at the site of injury

b)

inhibition of nociceptive fibers by catecholamines

c)

significant reduction of endogenous algogens at the site of injury

d)

excitation of the nociceptive fiber by acetylcholine

e)

excitation of the parasympathetic nervous system

97.

A 36-year-old patient, 10 years after being diagnosed with syphilis, developed difficulty urinating, numbness, crawling, and tingling sensations. Examination revealed decreased tendon reflexes. The patient exhibits a typical form of neurogenic sensory disturbance:

a)

athetosis

b)

atrophy

c)

myasthenia gravis

d)

hypoesthesia

e)

paresthesia

98.

Sensory disturbances and anesthesia in the innervation zone in the form of "gloves" and "stockings" are observed in case of damage to:

a)

hypothalamus

b)

posterior horns of the spinal cord

c)

lateral trunks of the spinal cord

d)

peripheral nerve trunks

e)

cortical projection of pain sensitivity

99.

Dissociation of sensitivity occurs when:

a)

complete transverse spinal cord injury

b)

half-lateral spinal cord injury

c)

pathological processes in the area of the thalamus

d)

damage to the cells of the anterior horns of the spinal cord

e)

damage to the striatum

100.

The most characteristic symptoms of posterior root damage are the following

a)

paralysis

b)

paresthesia

c)

complete analgesia

d)

violation of all types of sensitivity

e)

dissociated sensory disorder

101.

The development of seizures with an increase in the sodium content in the blood to 180 mmol/l may be associated with the occurrence of:

a)

cerebral edema

b)

intracranial hypertension

c)

dehydration of nerve cells

d)

process of hyperpolarization of brain neurons

e)

low-amplitude bioelectrical activity of the brain

102.

The high prevalence of convulsive syndrome in children in the first year of life is explained by the presence at this age of:

a)

high hydrophobicity of neurons

b)

high content of gamma-aminobutyric acid

c)

low levels of neurotransmitters - aspartate and glutamate

d)

low-amplitude electrical activity of the brain

e)

immature inhibitory mechanisms of the brain

103.

The patient developed clonic seizures, twitching of the neck, face, and trunk muscles, with a brief period of apnea. Foamy saliva was observed coming from the mouth. The pupils were dilated and unreactive to light. After the seizure, which lasted two minutes, the muscles relaxed.The basis of this typical form of pathology is:

a)

decreased excitability of neurons

b)

suppression of neuronal discharge generation

c)

destruction of dopamine neurons in the areablue spot

d)

predominance of cholinergic system activity in the striatum

e)

increased neural activity with hypersynchronous discharges

104.

In children, the occurrence of epilepsy is most often associated with:

a)

hippocampal sclerosis

b)

brain tumor processes

c)

drug use

d)

anomalies in the development of the cerebral cortex

e)

damage to the somatosensory cortex of the brain

105.

Epileptic neurons are characterized by:

a)

low excitability

b)

membrane instability

c)

membrane hyperpolarization

d)

low generation of high-frequency discharges

e)

absence of depolarization under the influence of glutamate

106.

Pathogenetic essence of the epileptic focus:

a)

activation of GABAergic receptors

b)

blockade of voltage-dependent Na+ channels

c)

formation of generators of pathologically increased excitation

d)

decreased synaptic transmission of impulses

e)

destruction of the determinant structure

107.

The pathognomonic feature of epileptic neurons is:

a)

progressive increaseseizure threshold

b)

generation of low-amplitude and low-frequency action potentials

c)

paroxysmal depolarization shifts in membrane potential

d)

suppression of acetylcholine receptor activity

e)

suppression of glutamate release

108.

A generalized epileptic seizure differs from a partial seizure by the presence of

a)

hyposalivation

b)

constricted pupils

c)

preserved consciousness

d)

cramps in all limbs

e)

cramps in the facial muscles

109.

Patient V., 20, has been experiencing seizures for the past five years. At the onset of a seizure, the patient experiences a bitter taste in the mouth, then loses consciousness, and then develops generalized tonic-clonic seizures. No focal neurological symptoms or cognitive impairment were detected. From a pathogenetic perspective, the following basic medications are appropriate for the patient:

a)

nootropics

b)

antioxidants

c)

antidepressants

d)

anticonvulsants

e)

immunomodulators

110.

In meningism, unlike meningitis, examination of the cerebrospinal fluid reveals:

a)

absence of glucose in the cerebrospinal fluid

b)

no changes in cerebrospinal fluid

c)

high neutrophil count in cerebrospinal fluid

d)

the appearance of a fibrinous film in the cerebrospinal fluid

e)

elevated protein levels in cerebrospinal fluid

111.

The patient has hyperpyretic fever, severe headaches, nausea, repeated vomiting, and photophobia. His condition is severe. He lies on his side with his head tilted back and his legs bent at the knees and drawn up to his stomach. Petechial rash on the thighs and buttocks. Kernig's and Brudzinski's signs are positive bilaterally. The cerebrospinal fluid is yellow-green and turbid. The portal of entry for this neuroinfection is usuallyare:

a)

tonsils

b)

nasopharynx

c)

genital tract

d)

damaged skin

e)

lower urinary tract

112.

The predominant route of transmission of Neisseria meningitidis is:

a)

alimentary

b)

transmissible

c)

airborne

d)

hematogenous

e)

contact

113.

In meningitis, the etiological factor of which is Neisseria meningitidis, the syndrome of inflammatory changes in the cerebrospinal fluid is manifested by:

a)

low cerebrospinal fluid pressure

b)

low cerebrospinal fluid pressure

c)

. low relative density of cerebrospinal fluid

d)

high levels of glucose in the cerebrospinal fluid

e)

neutrophilic pleocytosis

114.

The main manifestations and severity of the development of meningococcal infection are associated with the following pathogenicity factor of the pathogen:

a)

drank

b)

capsule

c)

endotoxin

d)

hyaluronidase

e)

neuraminidase

115.

The leading pathogenetic factor in the development of meningococcal meningitis is:

a)

hypohydration of neurons

b)

intracranial hypertension

c)

narrowing of the cerebrospinal fluid spaces

d)

reduction in the formation of cerebrospinal fluid

e)

decreased permeability of the blood-brain barrier

116.

The development of meningeal symptoms is indicated by:

a)

rigidity of the long muscles of the trunk and limbs

b)

weakening of muscle contractile function

c)

flaccid paralysis of the limb muscles

d)

tremor of the limbs and trunk

e)

paresis of the trunk muscles

117.

In the cerebrospinal fluid of patients with serous meningitis, the following cells predominate:

a)

neutrophils

b)

eosinophils

c)

lymphocytes

d)

monocytes

e)

basophils

118.

The most unfavorable prognosis for cerebral edema developing with meningitis is the development in patients:

a)

coma

b)

hyperthermia

c)

hemorrhagic rash

d)

clonic-tonic seizures

e)

pathological pyramidal signs

119.

Changes in the body that occur during vagotomy:

a)

development of bronchospasm

b)

increased intestinal peristalsis

c)

decreased secretory function of the stomach

d)

decreased heart rate

e)

stimulation of pancreatic juice production

120.

Disorders of higher nervous activity are primarily indicated by:

a)

instincts

b)

irritability

c)

sensitivity

d)

orienting reflexes

e)

analytical and synthetic activities

121.

A 57-year-old patient had been suffering from gastric ulcers for 10 years. A recent relapse was accompanied by intense abdominal pain, loss of appetite, weight loss, and nausea. All symptoms subsided during treatment, but the patient developed obsessive thoughts about cancer. He became irritable and believed that doctors were concealing his stomach cancer diagnosis. For this typical form of pathology, the vegetative-vascular neuritis (VNV) is a common cause of this condition.also characteristic is the development of:

a)

amnesia

b)

delirium and hallucinations

c)

peripheral paralysis

d)

disorders of autonomic functions

e)

organic changes in the cerebral cortex

122.

Functional diseases of the brain, characterized by disturbances of higher nervous activity and neurovegetative functions, can be pathogenetically associated with the development of the following disease:

a)

viral hepatitis

b)

Itsenko-Cushing's disease

c)

Addison-Biermer disease

d)

diffuse glomerulonephritis

e)

primary arterial hypertension