Worksheetsnervous system
Total questions: 122
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A group of hyperactive neurons with weakened inhibitory control is formed when:
blockade of NMDA receptors
sodium channel blockade
severe hypoxic neuronal damage
low calcium content in the cytoplasm of neurons
increased release of aspartate into the synaptic cleft
On the 10th-12th day of complete fasting, neurons in the brain begin to use the following as an oxidation substrate to obtain energy:
glucose
glycogen
triglycerides
ketone bodies
hexose phosphates
One of the consequences of an imbalance of ions and fluid in neurons can be:
persistent depolarization of the neuronal plasma membrane
decrease in osmotic pressure in neurons
inhibition of lipid peroxidation of neuronal membranes
increased activity of neuronal proteosynthesis enzymes
accumulation of K+ ions in the intracellular space
Specific mechanisms of neuronal dysfunction include:
neuronal apoptosis
damage to neuronal membranes
disruption of mediator transport along the axon
disruption of the energy supply to neurons
ion and fluid imbalance due to energy deficiency
In the development of neurodystrophic processes that can occur in peripheral organs and in the nervous system itself, changes in:
synapses
neuroglia
sarcoplasmic reticulum
blood-brain barrier
meninges
The neural pathway for the entry of pathogenic agents into the central nervous system is characteristic of:
pneumococci
tetanus toxin
streptococcal exotoxin
E.coli
influenza viruses
The penetration of viruses and antibodies into the central nervous system is ensured by the work of:
dendrites and their spines
synaptic apparatus of a neuron
fast axonal transport involving microtubules
slow anterograde axonal transport
retrograde axonal transport
Disorders of the integrative activity of neurons consist of a violation of:
post-tetanic potentiation
connections with other neurons through processes
conduction of excitation with the participation of chemical synapses
opening of sodium ion channels on the postsynaptic membrane
summation of all postsynaptic potentials arising on the membrane
The main mechanism of synaptic dysfunction under the influence of botulinum toxin is:
inhibition of glycine secretion into the synaptic cleft
inhibition of acetylcholine secretion into the synaptic cleft
blocking serotonin receptors on the postsynaptic membrane
inhibition of monoamine oxidase activity
inhibition of cholinesterase activity
A characteristic sign of denervation syndrome is:
increased formation of trophogens
excessive electrogenesis of denervation structures
increased excitability and perverted reactivity of neurons
increased entry of K+ into neurons and excessive release of Ca2+
enhancement of GABAergic inhibition of the neuron
Severe denervation syndrome develops as a result of:
sympathectomy
partial decortication
disconnection of the nervous system from organs and tissues
disconnection of the cerebral cortex from the subcortical centers
disconnection of the central and peripheral autonomic nervous system
In the pathogenesis of neurogenic dystrophy of cells of a denervated organ the following is important:
A. increasing the supply of trophogens to cells
B. increasing the excitability threshold of denervated cells
C. increasing the functional activity of the denervated organ
D. absence of neurotransmitter effects on the postsynaptic membrane
E. blockade of sodium channels in the membranes of denervated cells
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:
damage to dendrites
pathological system
pathological dominant
pathological determinant
generator of pathologically increased excitation
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:
activation of inhibitory mechanisms in the spinal cord
increased excitability of deafferented structures
increasing the reactivity of neurons to impulses from different sources
stimulation afferent impulses entering the neurons of the central nervous system
development trophic disorders in the innervation zone
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:
pathological parabiosis
pathological determinant
syndrome of deafferentation of nerve structures
decerebrate rigidity
denervation syndrome
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:
excessive activity of inhibitory neurons
direct damage to excitation mechanisms
activation of the control function of the cerebral cortex over the spinal cord
disinhibition of the centers of the spinal cord or medulla oblongata
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:
hysteroesis
denervation syndrome
deafferentation syndrome
pathological determinant
pathologically enhanced excitation generator
Pathological dominant, as the functional structure of the central nervous system that is dominant at a certain moment is realized at the level of:
synaptic connections
intersystem relations
intrasystemic relations
intracellular processes
intercellular relationships
Neuropathological syndrome is a clinical expression of the activity of:
anti-systems
pathological system
pathological dominant
damaged nerve cell
focus of pathological parabiosis
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:
formation of anti-systems
predominance of excitation processes over inhibition
development of generators of pathologically increased excitation
decreased degree of intracellular regeneration of neurons
increased permeability of the blood-brain barrier
Increased resistance of brain neurons to hypoxic damage is observed under the following conditions:
activation of NMDA receptors
glutamatergic denervation
actions of glutamate receptor activators
increasing the activity of NO synthase in neurons
reduction in the density of GABA receptors on the surface of neurons
Metabolic features of the brain that influence the development of ischemia include:
low oxygen consumption
low phosphocreatinine level
the use of free fatty acids as an energy source
low activity of antioxidant enzymes
the presence of large reserves of glucose and glycogen
The independence of the level of blood flow through the brain from changes in systemic arterial pressure is within the range:
from 0 to 180 mmHg
from 40 to 160 mm Hg
from 60 to 180 mm Hg
from 80 to 200 mmHg
from 90 to 220 mmHg
The main factor in the regulation of cerebral circulation is:
myogenic factor
humoral factor
neurogenic factor
metabolic factor
membranogenic factor
Dilation of cerebral arteries occurs when:
hypercapnia
hyperoxemia
increasing pH
increased blood pressure
increasing the tone of precapillary arterioles
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:
increased cerebrospinal fluid resorption
acceleration of venous blood outflow
compression of the veins at the points where they enter the sinuses of the brain
reduction of pressure in the ventricles of the brain
compression of extracranial vessels
In cerebral ischemia, the development of focal necrosis is associated with:
increased activity of neurotrophic factors
activity of the calcium-glutamate cascade
an increase in the level of inhibitory amino acids
NMDA receptor hyporeactivity
A. increased activity of mitochondrial enzymes
Transient ischemic attacks are characterized by:
development of cysts in the brain
development of ischemia only in the white matter
development of white infarcts in the brain
hemorrhagic transformation of cerebral infarction
reversibility of neurological dysfunction within 24 hours
The threshold for the development of irreversible changes in neurons is the level of perfusion:
80 ml/100 g/min-1
50 ml/100 g/min-1
35 ml/100 g/min-1
20 ml/100 g/min-1
10 ml/100 g/min-1 or less
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:
ischemic stroke
hemorrhagic stroke
subarachnoid hemorrhage
arteriovenous malformation
hemorheological occlusion
Uncontrolled (non-modifiable) risk factors for the development of ischemic stroke include:
hypercoagulability
hyperhomocysteinemia
arterial hypertension
type 2 diabetes mellitus
heredity
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:
age
smoking
male gender
atherosclerosis
excess body weight
The most important modifiable risk factor for the development of the cardioembolic subtype of ischemic stroke is:
type 1 diabetes mellitus
arterial hypotension
atrial fibrillation
alcohol abuse
chronic kidney disease
The group of systemic etiological factors in the development of ischemic stroke includes:
compression of cerebral arteries
cerebral artery dissection
thrombus formation in the cerebral vessels
atherosclerosis of cerebral vessels
arterial hypotension
In the pathogenesis of ischemic stroke, an important role is played by:
increased ATP formation
glutamate excitotoxicity
suppression of NMDA receptor activity
increased calcium release from the neuron
increase antioxidants
In stroke, activation of NMDA receptors of postsynaptic cells by glutamate and aspartate is accompanied by:
increased potassium intake into the cell
increased calcium intake into the cell
suppression of lipid peroxidation processes
inhibition of the activity of proteolytic enzymes
suppression of AMPA receptor activity
High local concentration of extracellular glutamate in the ischemic zone and excessive activation of glutamate receptors leads to:
suppression of voltage-dependent calcium channels
neuronal death by apoptosis and necrosis
increasing the activity of ATP-dependent pumps
increased synthesis of neurotrophic factors
A. inhibition of neuronal depolarization
Hyperactivation of ionotropic postsynaptic AMPA receptors in the ischemic brain causes:
osmotic swelling of cells
release of sodium and water from neurons
magnesium blocker of NMDA receptors
closing of calcium ion channels
inhibition of neuronal excitotoxicity mechanisms
In the area of the ischemic penumbra are located:
irreversibly damaged neurons
neurons with a high level of plasticity
irreversibly damaged neuroglial cells
neurons with high bioelectrical activity
functionally unstable but viable neurons
In the pathogenesis of ischemic cerebral edema in stroke, the following is important:
sodium and chlorine release from neurons
decreased permeability of the vascular wall
reduction of hydrostatic pressure in vessels
ATP-dependent sodium pump deficiency
decrease in oncotic pressure in the perivascular space
In ischemic stroke, the development of petechiae and parenchymal hematomas indicates the development of:
ischemic penumbra
ischemic cerebral edema
excessive collateral circulation
hemorrhagic transformation of cerebral infarction
reperfusion injury of brain tissue
Delayed mechanisms of neuronal death in ischemic stroke include the development of:
neuronal hypoperosis
oxidative stress
glutamate excitotoxicity
cytotoxic cerebral edema
lactic acidosis
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:
neuronal reperfusion
shrinkage of neurons
calcium release from neurons
decreased osmolarity of neurons
inhibition of glutamate receptors
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:
age
smoking
male gender
atherosclerosis
excess body weight
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:
cryptogenic stroke
hemorrhagic stroke
subarachnoid hemorrhage
atherothrombotic stroke
lacunar stroke
The most significant factors in the development of the atherothrombotic subtype of ischemic stroke include:
atherosclerotic plaque instability
hemorrhagic transformation of cerebral infarction
formation of cavities in the brain filled with cerebrospinal fluid
microangiopathy in the white matter of the brain
angiodystonic disorders in the cerebral vessels
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:
increased blood viscosity
increased aggregation of formed blood elements
increased activity of the blood fibrinolytic system
decrease in systemic perfusion pressure
deterioration of blood rheological properties
Occlusion of a deep perforating artery leads to the development of the following pathogenetic subtype of ischemic stroke:
lacunar
cardioembolic
atherothrombotic
hemodynamic
cryptogenic
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:
decreased cerebral blood flow
reduction of vascular resistance
increasing the linear velocity of blood flow
increase in volumetric blood flow
dilation of cerebral vessels
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:
carotid system
middle cerebral artery
anterior cerebral artery
internal carotid artery
vertebrobasilar system
In ischemic stroke, the main target of neuroprotection is:
penumbra
infarction core
marginal zone
oligemia zone
necrosis zone
In ischemic stroke, as opposed to hemorrhagic stroke, the following is more often observed:
compression of brain tissue
focal symptoms
internal hydrocephalus
increased intracranial pressure
hemorrhagic transformation of cerebral infarction
Unlike ischemic stroke, this form of acute cerebrovascular accident with hemorrhage into the subarachnoid space of the cerebral membranes is characterized by:
brainstem lesion
low intracranial pressure
significant activation of microglia
aseptic meningitis
visual impairment
The main cause (≈85% of cases) of spontaneous subarachnoid hemorrhage is:
aneurysm rupture
arterial dissection
blood clotting disorder
inflammatory changes in cerebral vessels
rupture of cerebral arteriovenous malformation
Hemorrhagic stroke is anatomically manifested by:
white cerebral infarction
vasogenic cerebral edema
liquefaction necrosis
gray softening of the brain
focal hemorrhagic infiltration of the brain
Factors that determine the more severe course of hemorrhagic stroke compared to ischemic stroke include:
more pronounced compression and swelling of the brain
absence of glutamate excitotoxicity
the influence of vasodilatory substances of the spilled blood
pronounced activation of the antioxidant system
lesser severity of ATP deficiency
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:
thalamus
cerebellum
hippocampus
frontal lobe
occipital lobe
The most common clinical syndrome of stroke is spastic hemiparesis. Its development is associated with damage to:
cerebellum
hypothalamus
pyramidal tracts
extrapyramidal system
anterior horns of the spinal cord
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:
clonic seizures
tonic convulsions
athetosis
chorea
ticks
The development of pyramidal hyperkinesis is indicated by the appearance of:
chorea
athetosis
tremors
muscle fibrillation
clonic seizures
The most characteristic manifestations of damage to the pyramidal system are:
ataxia, tics
causalgia, phantom pain
tonic and clonic seizures
paralysis, pathological reflexes
Parkinsonian tremor, asynergy
Complete loss of movement due to a disorder of the motor function of the nervous system is called:
paresis
myotonia
myasthenia
paralysis
hyperesthesia
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:
opisthotonus
Parkinson's disease
peripheral paralysis on the affected side
spastic paralysis on the side of the lesion
spastic paralysis on the side opposite the lesion
Characteristic signs of central paralysis include:
hyporeflexia
muscle hypotonia
qualitative changes in muscle electrical excitability
increased tendon and periosteal reflexes
fibrillary and fascicular muscle twitching
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:
disappearance of tendon reflexes
increased muscle tone
hypo-, areflexia
muscle atrophy
paresthesia
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:
inferior frontal
superior temporal
hippocampal
postcentral
precentral
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:
sacral region
lumbar region
thoracic and lumbar regions
thoracic region
cervical spine
Monoparesis in humans most often occurs with:
cerebellar damage
brain stem damage
damage to the cerebral cortex
hemorrhage into the internal capsule
damage to the pyramidal tract at the level of the spinal cord
The most common cause of hemiparesis in humans is:
cerebellar damage
damage to the cerebral cortex
damage to the pyramidal tract at the level of the medulla oblongata
damage to the pyramidal tract at the spinal cord level
hemorrhage into the internal capsule
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:
right-sided flaccid paraplegia, cerebellum
right-sided flaccid paraplegia, internal capsule
right-sided central hemiplegia, internal capsule
right-sided central hemiplegia, substantia nigra
right-sided central hemiplegia, cerebellum
Increased spinal reflexes are observed in:
damage to spinal motor neurons
development of primary neurological coma
functioning of intercalary inhibitory neurons of the spinal cord
rupture of connections between the spinal cord and the higher parts of the central nervous system
transection of the posterior roots of the spinal cord (deafferentation)
The tone of the affected muscles decreases with:
central paralysis
peripheral paralysis
decerebrate rigidity
convulsions
athetosis
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:
flaccid paralysis
central paralysis
peripheral paresis
spastic paresis
myasthenia
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:
cerebellum
brainstem
pyramidal system
extrapyramidal system
autonomic nervous system
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:
flaccid
rigid
spastic
myasthenic
peripheral
Muscle hypertonia, a slow pace of active movements, a shuffling, small-step gait, and quiet, monotonous speech are characteristic of damage to:
pyramidal tract
cerebral cortex
pallido-nigral system
anterior horns of the spinal cord
hypothalamic-pituitary region
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:
decreased muscle tone
disappearance of Lewy bodies in neurons
degeneration of nigrostriatal neurons
damage to the structures of the pyramidal system
increased dopamine levels in the striatum
Ataxia, muscle hypotonia, intention tremor, nystagmus, and scanned speech are characteristic of damage to:
cerebellum
pallido-nigral system
parietal lobe of the brain
midbrain
pituitary gland
A patient with a cerebellar tumor was admitted to the neurosurgical department. Examination revealed ataxia, characterized by:
increased muscle tone
impaired coordination of movements
weakening of movements in the lower limbs
the appearance of pathological reflexes
loss of voluntary movements
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:
neuromuscular transmission disorder
impaired temperature sensitivity
an increase in the number of cholinergic receptors in neuromuscular synapses
increase in postsynaptic action potential
increased synaptic depolarization
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:
disappearance of acetylcholine reserves
blockade of H-cholinergic receptors of the postsynaptic membrane
blockade of the release of acetylcholine from the endings of motor axons
activation of calcium channels in the presynaptic membrane
activation of calcium-dependent exocytosis of acetylcholine
Signs of peripheral nerve damage:
muscle hypertrophy
sensory disturbance
the appearance of pathological reflexes
strengthening of protective reflexes
In demyelinating neuropathies the following is observed:
primary damage to the extrapyramidal system
primary destruction of the myelin sheath of axons
primary lesion of peripheral nerve axons
normal conduction velocity
acceleration of nerve impulse conduction
In the pathogenesis of peripheral neuropathies in diabetes mellitus, the following is of great importance:
neurofilament damage
disorders of axonal transport of substances
destruction of the myelin sheath of the nerve by antibodies
damage to the peripheral nerve vessels (vasa nervorum)
blockade of acetylcholine release from motor axon terminals
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:
transcobalamin
methylcobalamin
folic acid
methylmalonic acid
5-deoxyadenosylcobalamin
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:
visceral
peripheral
neuropathic
nociceptive
somatic
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:
visceral
parietal
functional
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:
phantom
visceral
projection
primary (epicritic)
secondary (protopathic)
Weakening and disintegration of the natural antinociceptive system is a pathogenetic factor in the development of:
pathological pain
receptor anesthesia
convulsive syndrome
extrapyramidal palsy
meningeal irritation syndrome
Primary (epicritic) pain is characterized by:
diffuse character
high threshold of perception
occurrence immediately after injury
type of conducting fiber - unmyelinated, type C
long duration after removal of the irritant
For afferent thin nociceptive fibers of the A-delta (Aδ) type, the following is characteristic:
absence of myelin sheath
low impulse conduction velocity (< 1 m/s)
blocking the release of substance P from neurons
participation in the development of primary (epicritic) pain
being found only in the autonomic nervous system
Polymodal fibers of type C are characterized by:
Distribution only in the central nervous system
inhibition of NMDA receptors
rapid conduction of nerve impulses
participation in the development of acute, localized (epicritic) pain
stimulation by temperature, mechanical and chemical stimuli
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:
increased excitability of nerve fibers
activation of unmyelinated thin nociceptive C fibers
acceleration of impulse propagation along the nerve fiber
slowing of depolarization and conduction of action potentials
slowing down the processes of hyperpolarization of the neuronal membrane
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:
memory of previous life experience
activation of neurogenic mechanisms of the antinociceptive system
increased excitability of deafferented primary neurons
excessive excitation of the endings of regenerating nociceptive fibers
regeneration of nerve fibers of an amputated organ with the formation of a neuroma
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:
memory of previous life experience
inhibition of the endings of regenerating nociceptive fibers
increased excitability of deafferented primary neurons
regeneration of nerve fibers of an amputated organ with the formation of a neuroma
excitation of secondary nociceptive neurons in the dorsal horns of the spinal cord
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:
demyelination of the nerve at the site of injury
inhibition of nociceptive fibers by catecholamines
significant reduction of endogenous algogens at the site of injury
excitation of the nociceptive fiber by acetylcholine
excitation of the parasympathetic nervous system
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:
athetosis
atrophy
myasthenia gravis
hypoesthesia
paresthesia
Sensory disturbances and anesthesia in the innervation zone in the form of "gloves" and "stockings" are observed in case of damage to:
hypothalamus
posterior horns of the spinal cord
lateral trunks of the spinal cord
peripheral nerve trunks
cortical projection of pain sensitivity
Dissociation of sensitivity occurs when:
complete transverse spinal cord injury
half-lateral spinal cord injury
pathological processes in the area of the thalamus
damage to the cells of the anterior horns of the spinal cord
damage to the striatum
The most characteristic symptoms of posterior root damage are the following
paralysis
paresthesia
complete analgesia
violation of all types of sensitivity
dissociated sensory disorder
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:
cerebral edema
intracranial hypertension
dehydration of nerve cells
process of hyperpolarization of brain neurons
low-amplitude bioelectrical activity of the brain
The high prevalence of convulsive syndrome in children in the first year of life is explained by the presence at this age of:
high hydrophobicity of neurons
high content of gamma-aminobutyric acid
low levels of neurotransmitters - aspartate and glutamate
low-amplitude electrical activity of the brain
immature inhibitory mechanisms of the brain
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:
decreased excitability of neurons
suppression of neuronal discharge generation
destruction of dopamine neurons in the areablue spot
predominance of cholinergic system activity in the striatum
increased neural activity with hypersynchronous discharges
In children, the occurrence of epilepsy is most often associated with:
hippocampal sclerosis
brain tumor processes
drug use
anomalies in the development of the cerebral cortex
damage to the somatosensory cortex of the brain
Epileptic neurons are characterized by:
low excitability
membrane instability
membrane hyperpolarization
low generation of high-frequency discharges
absence of depolarization under the influence of glutamate
Pathogenetic essence of the epileptic focus:
activation of GABAergic receptors
blockade of voltage-dependent Na+ channels
formation of generators of pathologically increased excitation
decreased synaptic transmission of impulses
destruction of the determinant structure
The pathognomonic feature of epileptic neurons is:
progressive increaseseizure threshold
generation of low-amplitude and low-frequency action potentials
paroxysmal depolarization shifts in membrane potential
suppression of acetylcholine receptor activity
suppression of glutamate release
A generalized epileptic seizure differs from a partial seizure by the presence of
hyposalivation
constricted pupils
preserved consciousness
cramps in all limbs
cramps in the facial muscles
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:
nootropics
antioxidants
antidepressants
anticonvulsants
immunomodulators
In meningism, unlike meningitis, examination of the cerebrospinal fluid reveals:
absence of glucose in the cerebrospinal fluid
no changes in cerebrospinal fluid
high neutrophil count in cerebrospinal fluid
the appearance of a fibrinous film in the cerebrospinal fluid
elevated protein levels in cerebrospinal fluid
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:
tonsils
nasopharynx
genital tract
damaged skin
lower urinary tract
The predominant route of transmission of Neisseria meningitidis is:
alimentary
transmissible
airborne
hematogenous
contact
In meningitis, the etiological factor of which is Neisseria meningitidis, the syndrome of inflammatory changes in the cerebrospinal fluid is manifested by:
low cerebrospinal fluid pressure
low cerebrospinal fluid pressure
. low relative density of cerebrospinal fluid
high levels of glucose in the cerebrospinal fluid
neutrophilic pleocytosis
The main manifestations and severity of the development of meningococcal infection are associated with the following pathogenicity factor of the pathogen:
drank
capsule
endotoxin
hyaluronidase
neuraminidase
The leading pathogenetic factor in the development of meningococcal meningitis is:
hypohydration of neurons
intracranial hypertension
narrowing of the cerebrospinal fluid spaces
reduction in the formation of cerebrospinal fluid
decreased permeability of the blood-brain barrier
The development of meningeal symptoms is indicated by:
rigidity of the long muscles of the trunk and limbs
weakening of muscle contractile function
flaccid paralysis of the limb muscles
tremor of the limbs and trunk
paresis of the trunk muscles
In the cerebrospinal fluid of patients with serous meningitis, the following cells predominate:
neutrophils
eosinophils
lymphocytes
monocytes
basophils
The most unfavorable prognosis for cerebral edema developing with meningitis is the development in patients:
coma
hyperthermia
hemorrhagic rash
clonic-tonic seizures
pathological pyramidal signs
Changes in the body that occur during vagotomy:
development of bronchospasm
increased intestinal peristalsis
decreased secretory function of the stomach
decreased heart rate
stimulation of pancreatic juice production
Disorders of higher nervous activity are primarily indicated by:
instincts
irritability
sensitivity
orienting reflexes
analytical and synthetic activities
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:
amnesia
delirium and hallucinations
peripheral paralysis
disorders of autonomic functions
organic changes in the cerebral cortex
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:
viral hepatitis
Itsenko-Cushing's disease
Addison-Biermer disease
diffuse glomerulonephritis
primary arterial hypertension
