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WorksheetsMusculoskeletal system and skin
Total questions: 75
Worksheet time: 38mins
Compared to older children, infectious processes develop more rapidly in the skin of newborns, with various primary and secondary morphological elements of skin rashes appearing. This is due to the following age-related characteristics:
acidic skin pH
a pronounced lipid layer in the skin
thin epidermis, weakly connected to the dermis
low absorption function of the skin
low permeability of the epidermis
Dysfunction of the sebaceous glands, in which increased secretion of defective sebum is observed, is typical for:
mycoses
seborrhea
dermatoses
hidradenitis
common eels
Disruption of the processes of proliferation and keratinization in the epidermis is characteristic of:
seborrhea
vitiligo
psoriasis
pyoderma
hidradenitis
Patient S., 40, has three painful, pear-shaped masses in his left armpit, raised above the skin. One of the masses has two openings in the center, through which thick pus is discharged. Characteristics of this condition include:
purulent inflammation of the eccrine sweat glands
purulent inflammation of the apocrine sweat glands
purulent inflammation of the merocrine sweat glands
development under the influence of herpes simplex viruses
development only in old and senile age
Hyperpigmentation of the skin and mucous membranes in primary chronic adrenal insufficiency is caused by:
excess glucocorticoids
excess mineralocorticoids
excess melanocyte-stimulating hormone
adrenocorticotropic hormone deficiency
beta-lipotropin deficiency
Patient O., 58, has cherry-red skin, blood pressure of 200/110 mmHg, and splenomegaly. Blood tests reveal erythrocytosis, absolute neutrophilia with a hyporegenerative left nuclear shift, thrombocytosis, a slow ESR, and a sharply decreased erythropoietin level. Skin manifestations of this blood disorder include:
dysfunction of the sebaceous glands
disruption of keratinization and inflammation in the dermis
purulent inflammation of the apocrine sweat glands
skin itching, which intensifies after water procedures
increased sensitivity of the skin to ultraviolet radiation
After a manicure, a woman developed a purulent infection on the distal phalanx of her left index finger, which spread from under the nail fold to the nail plate. A complete blood count may reveal the following changes:
absolute lymphocytosis and monocytosis
absolute neutrophilia with a shift in the leukocyte formula to the left
absolute neutropenia with a degenerative shift of the formula to the right
leukemoid reaction of lymphoid type, leukocyte
immune agranulocytosis, hapten form
Diffuse fibrosis, pathological changes in the blood vessels of the skin, joints and internal organs, and pronounced thickening of the skin are characteristic of:
melanoma
toxicoderma
systemic lupus erythematosus
systemic scleroderma
xeroderma pigmentosum
Patient A., 32, complains of pain in the right axillary region. Examination and palpation reveal small, tender, firm, pear-shaped nodules located in the dermis. The skin is hyperemic and has a bluish tint. A necrotic core is absent. The underlying cause of this condition is:
reaginic mechanism of skin damage
purulent inflammation of the apocrine sweat glands
purulent-necrotic lesion of the hair follicle
cell-mediated allergic reaction
disruption of skin keratinization by hyperkeratosis
Dystrophic changes in the nail plate, accompanied by its thinning and concave spoon-shaped deformation, are called:
felon
koilonychia
nail atrophy
nail psoriasis
Watch glass nails
A 28-year-old woman has had hypochromic microcytic anemia for 10 years. Her skin is pale and dry, with flaking. Her hair is dry, thin, and grayish, with increased hair loss. Her nails are spoon-shaped, with pronounced longitudinal striations. These skin derivative changes are caused by a deficiency of:
iron
vitamin B12
folic acid
ascorbic acid
glucose-6-phosphate dehydrogenase
Patient F., 35, complains of joint pain and swelling, along with fever. She has a red, butterfly-shaped erythema on her face, affecting the bridge of her nose and both cheeks. Antinuclear antibodies and LE cells were detected, and she tested positive for lupus anticoagulant. The following factors are important in the pathogenesis of skin lesions in this disease:
decreased activity of B-lymphocytes
decreased activity of T-suppressors
cell-mediated type of tissue damage
violation of histohematic barriers
enhancement of apoptotic mechanisms
Patient S. complains of itching and dandruff on the scalp. Objectively: the hair is greasy and sticky. The scalp is hyperemic, oily, and flaky. Increased sebum secretion is noted on the face. These symptoms are characteristic of:
scabies
seborrhea
psoriasis
pediculosis
hidradenitis
Patient R., 54, with type 2 diabetes mellitus, developed a dense, bright red infiltrate up to 3 cm in diameter on the skin of his thigh, accompanied by a tingling sensation and pain. At the center of the infiltrate is a purulent-necrotic core with a pustule on the surface. The skin lesion develops as a result of a typical pathological process:
ischemia
tumor
allergy
dystrophy
inflammation
Patient F., 17, exhibits increased joint mobility, including dislocations, hyperextensible skin, decreased bone mineral density, and a tendency toward bone fractures. Similar symptoms have been noted in relatives. The underlying cause of connective tissue pathology in the patient is:
vitamin D deficiency
collagen synthesis defect
degenerative joint disease
autoimmune joint inflammation
osteoid mineralization disorder
Patient A., 25, complains of a blistering rash on the skin of her trunk and extremities. The rash is accompanied by itching, sweating, and bronchospasm. She believes the rash is caused by penicillin antibiotics. The key mediators of this disease are:
histamine
serotonin
nitric oxide
oxygen free radicals
components of the complement system
The leading mechanism for the development of acute urticaria is:
reaginic mechanism of injury
cytotoxic mechanism of damage
immune complex mechanism of damage
cell-mediated mechanism of injury
receptor-mediated mechanism of injury
Patient S., 20, complains of itchy skin and a rash on the popliteal and elbow folds. The rash is noted after eating chocolate and oranges. The skin is papular and vesicular. Total immunoglobulin E levels are elevated in the serum. The following factors play a significant role in the pathogenesis of this disease:
activation of beta-adrenergic receptors
cytolytic allergic reactions
decreased production of interleukins 4, 5, 13
imbalance of Th1 and Th2 cells with a predominance of Th2 response
decreased ability of mast cells to release allergy mediators
Hereditary predisposition plays a role in the development of the following skin lesions:
trichophytosis
furunculosis
syphilitic lesion
atopic dermatitis
pyoderma
In atopic dermatitis, disruption of the skin's hydrolipidic layer leads to:
increasing filaggrin production
increased transepidermal water loss
increased production of antimicrobial peptides
reduction of proliferative processes in the epidermis
decreased sensitivity of the skin to various irritants
An important role in the pathogenesis of allergic contact dermatitis is played by:
high production of IgE antibodies
high production of interleukins 4 and 5
increased filaggrin in the stratum corneum of the epidermis
disruption of the epidermal barrier function
mast cell degranulation
Local regulators of bone tissue remodeling that enhance osteoblast replication include:
collagenase
somatotropic hormone
tumor necrosis factor
lysosomal enzymes
transforming growth factor-beta
Systemic factors regulating bone tissue remodeling that stimulate bone formation include:
estrogens
thyroid hormones
glucocorticosteroids
parathyroid hormone
proinflammatory cytokines
The participation of osteoblasts in bone remodeling consists of:
bone tissue nutrition
synthesis of organic matrix proteins
increased activity of mature osteoclasts
destruction of the mineral component of bone tissue
resorption of the organic component of the intercellular substance
A three-year-old child exhibits frequent rib fractures with minor injuries, increased joint mobility, dental changes, and blue sclera. Osteogenesis imperfecta is caused by a defect in the synthesis of:
collagen type I
collagen type II
collagen type III
collagen type IV
collagen type V
In patient N., 68, an X-ray examination of the musculoskeletal system revealed multifocal areas of bone destruction. These changes are associated with increased activity of the following cells:
osteoblasts
osteoclasts
synoviocytes
chondrocytes
With a constant increase in the concentration of parathyroid hormone in the blood, in contrast to its intermittent increase, the following is observed:
stimulation of osteoclast metabolism
increased mineralization of bone matrix
increased functional activity of preosteoblasts
disappearance of the corrugated edge in osteoclasts
inhibition of bone resorption
The most characteristic signs of osteoporosis are:
sclerosis of the subchondral bone
thickening of the cortical layer of bone tissue
increase in bone mineral density
increase in the inorganic matrix of bone tissue
decrease in the number of trabeculae of spongy bone
Primary involutional osteoporosis includes:
iatrogenic osteoporosis
juvenile osteoporosis
alimentary osteoporosis
idiopathic osteoporosis
postmenopausal osteoporosis
A marker fracture in senile osteoporosis is:
femoral neck fracture
vertebral body fracture
fracture of the radius
fracture of the humerus
tibia fracture
In the pathogenesis of postmenopausal osteoporosis, an important role is played by:
OPG overexpression
activation of the Wnt signaling pathway
RANK ligand overexpression
inhibition of RANKL expression by osteoblasts
decrease in the production of interleukins 1-, 6
Senile osteoporosis is characterized by:
A. reduction of osteogenesis
B. enlargement of trabecular plates
C. primarily affecting spongy bones
high intensity of bone metabolism
development of secondary hypoparathyroidism
Patient K., 58, has suffered from chronic kidney disease for 12 years and has been menopausal for nine years. Examination revealed decreased bone mineral density. This may be primarily due to:
25(OH)D3 deficiency
suppression of 1.25(OH)2D3 degradation
expression of vitamin D3 receptors
increase in cholecalciferol
increase in calcitriol
The most important exogenous factors that predispose to the development of osteoporosis and are associated with lifestyle and nutritional disorders include:
excessive exercise, overeating
Itsenko-Cushing's disease, glucocorticoid use
thyrotoxicosis, hyperparathyroidism, rheumatic diseases
excessive consumption of fatty and protein foods, caffeine
smoking, physical inactivity, low calcium and vitamin D intake
In Itsenko-Cushing's disease, the development of osteoporosis is due to the fact that glucocorticosteroids:
suppress RANKL expression
reduce the excretion of calcium in the urine
suppress the expression of OPG (osteoprotegerin)
increase osteoblast activity
enhance osteoclast apoptosis
Postmenopausal osteoporosis, according to the classification of osteoporosis by origin, belongs to the group:
primary osteoporosis
secondary osteoporosis
idiopathic osteoporosis
cortical osteoporosis
senile osteoporosis
Iatrogenic osteoporosis develops when:
bed rest
type 1 diabetes mellitus
malabsorption syndrome
renal failure
long-term treatment with glucocorticoids
A minor injury. She had a history of spinal pain, which worsened with physical activity and walking. Densitometry showed a T-score of -3.0. The following factors play a significant role in the pathogenesis of this disease:
Strengthening of OPG-RANKL interaction
increased synthesis of OPG by osteoblasts
Excessive production of RANKL by osteoblasts
reduction of the synthesis of proinflammatory cytokines
inhibition of RANKL binding to RANK
Overexpression of the gene encoding osteoprotegerin (OPG) results in:
increased bone resorption
increased synthesis of RANKL by preosteoblasts
enhancing the binding of RANKL to its receptor RANK
increase in the number of osteoclasts
increase bone mass
Patient D., 65, has lesions of the cervical, thoracic, and lumbar spine, including osteolytic destruction and osteoporosis. Blood tests revealed moderate anemia, a significantly elevated ESR, hyperproteinemia due to paraproteins, and a high level of M-protein. Urine analysis revealed Bence Jones protein. A myelogram revealed an increase in plasma cells to 48%. Patient D.'s bone damage is associated with the development of:
multiple myeloma
T-cell malignant lymphoma
chronic lymphocytic leukemia
chronic myelocytic leukemia
chronic monocytic leukemia
A 60-year-old woman. Menopause occurred at age 38. She has been taking glucocorticosteroids for the past year. Her body mass index is 17.5 kg/m². Her medical history includes fractures of the distal radius and a thoracic vertebral body, which occurred with minimal trauma. This musculoskeletal disorder is characterized by:
osteophyte formation
degeneration of cartilage tissue
thickening of the cortical bone layer
structural reorganization of the subchondral bone
decrease in the number of trabeculae of spongy bone
In type 2 diabetes mellitus, deterioration of bone tissue quality with subsequent development of osteoporosis is associated with:
decreased parathyroid hormone activity
decreased collagen synthesis by osteoblasts
increased synthesis of alkaline phosphatase by osteoblasts
an increase in active metabolites of vitamin D
In conditions of absolute estrogen deficiency, the imbalance between bone formation and bone resorption leads to:
A. bone loss
B. inhibition of bindingRANKL with RANK
C. increased synthesis of osteoprotegerin (OPG)
D. increasing bone mineral density
E. activation of osteoblastogenesis
Patient N., 50, has primary hyperparathyroidism. Examination revealed fibrocystic bone changes and generalized mixed-origin osteoporosis with compression fractures. A blood biochemistry analysis revealed:
increase in calcium, phosphate ions and alkaline phosphatase
increase in calcium and alkaline phosphatase, decrease in phosphate ions
increase in calcium and phosphate ions, decrease in alkaline phosphatase
decrease in calcium, increase in phosphate ions and alkaline phosphatase
decrease in calcium, alkaline phosphatase and phosphate ions
Patient E., 29, has been taking glucocorticoids for five years for an autoimmune disease. He has a history of recurrent spinal and rib fractures. X-ray examination revealed a significant decrease in bone density in the thoracic and lumbar spine. The mechanism of bone loss in this patient may be related to:
A. inhibition of parathyroid hormone production
B. suppression of osteoblast proliferation
C. increased absorption of calcium in the intestine
D. increased testosterone production
E. increased osteoid formation
Degenerative-dystrophic lesions of articular cartilage with secondary damage to the subchondral bone, synovial membrane, ligaments, capsule and periarticular muscles include:
osteoporosis
osteopathy
osteoarthritis
osteosclerosis
osteomalacia
In osteoarthritis, decreased resistance of articular cartilage occurs due to:
increased catabolic processes in cartilage tissue
increased synthesis of proteoglycans by chondrocytes
increasing growth factors in cartilage tissue
enhancing the shock-absorbing properties of cartilage
increasing the blood supply to the cartilage
BolNuyu Sh., 68, an overweight woman, presents with pain in her right hip joint and difficulty walking. An X-ray revealed a deformed femoral head, a narrowing of the joint space, severe subchondral osteosclerosis, and osteophytes on the edges of the acetabular articular surfaces. The following factors play a significant role in the pathogenesis of this disease:
disappearance of vessels in hyaline cartilage
inactivation of collagenase and phospholipase A2
reduction of proteoglycans of the ground substance of cartilage
increasing the resistance of cartilage to stress
increase in glycosaminoglycans in the matrix
In elderly and senile individuals with type 2 diabetes, the development of osteoarthritis is associated primarily with:
decreased glucose in the ligaments and joint capsule
increased synthetic activity of chondrocytes
accumulation of glycated proteins in articular cartilage
accumulation of interleukins in the joint cavity - 4, 10, 13
accumulation of uric acid crystals in the synovial fluid
In osteoarthritis, the loss of elasticity and strength of articular cartilage is associated with:
high hydrophilicity of proteoglycans
an increase in the size of proteoglycan molecules
excess of proteoglycan aggregates with hyaluronic acid
synthesis of long-chain collagen by chondrocytes
loss of the ability of proteoglycans to retain water
A disease of the musculoskeletal system characterized by slow progression, the presence of mechanical-type joint pain, periodic joint blockade, and predominantly affecting the joints of the legs and distal interphalangeal joints of the hands:
osteoporosis
osteochondrosis
gouty arthritis
rheumatoid arthritis
osteoarthritis
In case of joint defiguration, in contrast to joint deformation, the following is observed:
fusion of the joint space
sclerosis of bone tissue
joint destruction due to immune inflammation
persistent change in the shape of the joints due to the bones that form them
change in the shape of the joints due to effusion and swelling of soft tissues
Reactive arthritis is:
autoimmune joint disease
destructive joint disease
metabolic joint disease
infectious and inflammatory disease of the joints
degenerative joint disease
In patient V., 37 years old, with signs of articular syndrome, an immunological examination revealed increased concentrations of IgM and IgG in the blood to the altered Fc region of IgG. This is characteristic of:
osteoporosis
osteoarthritis
osteomalacia
gouty arthritis
rheumatoid arthritis
In the early stages of rheumatoid arthritis, the synovial membrane is infiltrated by mononuclear cells, among which the following predominate:
B-lymphocytes
CD4+ T cells
CD8+ T cells
mast cells
NK cells
In rheumatoid arthritis, the following are most often affected:
distal interphalangeal joints
proximal interphalangeal joints
joints of the lumbar spine
joints of the thoracic spine
metacarpophalangeal joints of the 1st finger
In rheumatoid arthritis, the proliferation of active fibroblasts and uncontrolled proliferating synoviocytes leads to the formation of:
pannus
tofus
osteophytes
Bouchard's nodes
rheumatoid nodes
Patient G., 45, presents with severe symmetrical pain, swelling, deformities, and limited motion in the proximal interphalangeal joints of the fingers, wrists, and elbows, as well as morning joint stiffness before lunch. Blood tests reveal an elevated ESR of 56 mm/h, an elevated C-reactive protein of 96 mg/ml, and an elevated rheumatoid factor concentration of 120 IU/ml. The following factors are important in the pathogenesis of this disease:
inflammation with pronounced reparation of bone and joint tissue
predominance of local bone formation over bone resorption
modification of arginine to citrulline in intracellular and matrix proteins
inhibition of proliferation and differentiation of mature B-lymphocytes
reduction of matrix metalloproteinases in the synovial intima
In rheumatoid arthritis, pannus formation leads to:
destruction of cartilage
increased angiogenesis
development of osteosclerosis
inhibition of the autoimmune process
suppression of fibroblast proliferation
A significant role in the pathogenesis of synovitis in rheumatoid arthritis belongs to:
inhibition of chemotaxis
inhibition of the complement system
hypoexpression of adhesion molecules
hyperproduction of proinflammatory cytokines
hyperproduction of growth factors
Patient V., 42, complains of pain and swelling in the metacarpophalangeal, wrist, and knee joints. She also reports morning stiffness lasting two hours. Anti-cyclic citrullinated peptide antibodies and elevated rheumatoid factor titers were detected. The following factors play a significant role in the pathogenesis of this disease:
atrophy of the synovial membrane
deficiency of T-suppressor function of lymphocytes
hyperproduction of anti-inflammatory cytokines
hyperproduction of osteoprotegerin by osteoblasts
fragmentation of proteoglycan aggregates
A systemic disease from the group of metabolic osteopathies with excessive accumulation of unmineralized osteoid and a decrease in its mineralization:
osteoporosis
osteoarthritis
osteomalacia
osteosclerosis
osteoarthritis
With an increase in the amount of osteoid, the following is observed:
increase in bone density
hypercalcification of bone structures
increased anabolism in cartilage tissue
abnormal flexibility and deformation of bones
formation of mineralized bone structures
Manifestations of osteomalacia in childhood are:
rickets
osteoarthritis
rheumatoid arthritis
primary hyperparathyroidism
hip dysplasia
An 8-month-old formula-fed child presents with general restlessness, profuse sweating, and poor sleep. The head is square with prominent frontal and parietal ridges. The occiput is flattened and bald, teeth are missing, the chest is compressed at the sides, the ribs are 'rosary beads,' there is kyphosis, generalized muscle hypotonia, and increased joint mobility. The following factors are important in the pathogenesis of this disease:
hypercalcemia
primary hyperparathyroidism
hypofunction of the parathyroid glands
decreased bone resorption
decreased absorption of calcium in the intestine
Decreased bone mineralization in rickets is observed due to:
alkalosis
hypokalemia
hyponatremia
hypophosphatemia
hypercalcemia
Convulsions in children and laryngeal spasm in severe cases of rickets are caused by:
hyperkalemia
hypercalcemia
metabolic alkalosis
hypocalcemia
hypophosphatemia
A 6-month-old child who is formula-fed presents with sweating, restless sleep, and irritability. Tissue turgor and muscle tone are decreased. The head is hydrocephalic. The occiput is flattened. The frontal bossing is prominent. Costal 'rosary' patterns are palpable. Laboratory examination and blood tests may reveal the following changes:
increase in total protein and lipids
hypercalcemia and hyperphosphatemia
decreased parathyroid hormone and citric acid
decrease in the level of 25(OH)D3 and calcitriol
decreased alkaline and acid phosphatase
In the pathogenesis of rachitic "rosary" and "square" head shape in rickets, the following is important:
calcinosis
hypercalcemia
excessive osteoid formation
insufficient osteoid formation
insufficient mineralization of osteoid
Development in Vitamin D-resistant rickets is caused by:
prematurity
insufficient sun exposure of the skin
alimentary deficiency of vitamin D
hereditary tubulopathies
hereditary myopathies
For osteomalacia, in contrast to osteoporosis, the most characteristic feature is:
high bone mineral density
reduction of unmineralized osteoid
discrepancy between bone matrix formation and its mineralization
low alkaline phosphatase levels in the blood
absence of fractures and bone deformities
Patient D., 42, experienced severe pain in the metatarsophalangeal joint of the big toe of his right foot, along with hyperemia of the skin over the joint. His blood showed elevated uric acid levels, which are formed as a result of the following process:
deamination of amino acids
decarboxylation of histidine
amino acid transamination
purine nucleotide catabolism
catabolism of pyrimidine nucleotides
Tophi are:
bony protrusions at the edges of joints
bony protrusions at the site of tendon attachment
a space-occupying lesion caused by the proliferation of connective tissue
a focus of fibrinoid necrosis in the skin, surrounded by macrophages
deposition of uric acid crystals in soft tissues
In gout, the most characteristic kidney damage is:
lupus nephritis
renal amyloidosis
nephrotic syndrome
glomerulonephritis
nephrourolithiasis
To stabilize uric acid levels in the blood, patients with gout are advised to include the following in their diet:
do not eat vegetables
limit your intake of red meat
Do not consume dairy products
increase the amount of animal protein
limit the intake of low-calorie foods
