Skeletal muscle diseases US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Skeletal muscle diseases. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Skeletal muscle diseases US Medical PG Question 1: A 10-year-old boy is brought to the physician because of recurring episodes of achy muscle pain in his legs. He has a history of poor school performance despite tutoring and has been held back two grades. He is at the 40th percentile for height and 30th percentile for weight. Examination shows ptosis, a high-arched palate, and muscle weakness in the face and hands; muscle strength of the quadriceps and hamstrings is normal. Sensation is intact. Percussion of the thenar eminence causes the thumb to abduct and then relax slowly. Which of the following is the most likely underlying cause?
- A. Defect of voltage-gated sodium channels of the sarcolemmal membrane
- B. CTG trinucleotide expansion in the DMPK gene (Correct Answer)
- C. Complete impairment of the dystrophin protein
- D. Apoptosis of lower motor neurons
- E. Humoral immune attack against the endomysial blood vessels
Skeletal muscle diseases Explanation: ***CTG trinucleotide expansion in the DMPK gene***
- The patient's symptoms, including **myotonia** (evidenced by the slow relaxation after percussion of the thenar eminence), muscle weakness (especially in the face and hands), ptosis, and intellectual disability, are classic features of **myotonic dystrophy type 1 (DM1)**.
- DM1 is caused by a **CTG trinucleotide repeat expansion** in the 3' untranslated region of the **_DMPK_ (dystrophia myotonica protein kinase) gene**.
*Defect of voltage-gated sodium channels of the sarcolemmal membrane*
- This description is characteristic of **nondystrophic myotonias**, such as **paramyotonia congenita** or **potassium-aggravated myotonia**.
- While these present with myotonia, they typically lack the systemic features of DM1, such as the intellectual disability, ptosis, and characteristic facial weakness.
*Complete impairment of the dystrophin protein*
- **Complete impairment of dystrophin** is the underlying cause of **Duchenne muscular dystrophy (DMD)**.
- DMD presents with progressive **proximal muscle weakness**, Gowers' sign, and calf pseudohypertrophy, and typically manifests much earlier with significant motor developmental delays, which are not the primary complaints here.
*Apoptosis of lower motor neurons*
- **Apoptosis of lower motor neurons** is characteristic of conditions like **spinal muscular atrophy (SMA)**.
- SMA causes progressive weakness and atrophy but typically presents as a **flaccid paralysis** and does not involve myotonia, ptosis, or intellectual disability in the same manner as described.
*Humoral immune attack against the endomysial blood vessels*
- A **humoral immune attack against endomysial blood vessels** is the hallmark of **dermatomyositis**, a type of inflammatory myopathy.
- Dermatomyositis presents with **proximal muscle weakness**, characteristic skin rashes (e.g., heliotrope rash, Gottron papules), and systemic inflammation, which are not described in this patient.
Skeletal muscle diseases US Medical PG Question 2: A 33-year-old woman comes to the clinic for a follow-up visit after recently starting high dose corticosteroids for a newly diagnosed autoimmune condition. She was first evaluated a month ago due to fatigue, muscle weakness, and a scaly rash on both hands. On examination, muscle strength was rated 2 out of 5 in the upper extremities. Creatine kinase-MB was elevated, and anti-Jo-1 antibodies were observed. A muscle biopsy later showed perimysial inflammation and treatment was initiated. Today, the patient says that her symptoms have not improved despite treatment with corticosteroids. It is agreed upon to initiate methotrexate with the hopes of achieving better symptom control. Which of the following is most often associated with this patient’s condition?
- A. Ovarian cancer
- B. Arthritis
- C. Lung cancer
- D. Raynaud's phenomenon
- E. Interstitial lung disease (Correct Answer)
Skeletal muscle diseases Explanation: ***Interstitial lung disease***
- The patient's condition, characterized by **fatigue**, **muscle weakness**, **scaly rash** (likely **Gottron's papules** or **heliotrope rash**), **elevated CK-MB**, and **anti-Jo-1 antibodies**, strongly suggests **dermatomyositis**, which is frequently associated with **interstitial lung disease (ILD)**.
- Approximately 70% of patients with **anti-Jo-1 antibodies** develop **ILD**, which can manifest as chronic cough and dyspnea.
*Ovarian cancer*
- While dermatomyositis is associated with an **increased risk of malignancy**, particularly in older patients, **ovarian cancer** is not the *most common* or *most frequently associated* manifestation of the disease overall, especially given the patient's age (33).
- The risk of malignancy is higher in adults with dermatomyositis and polymyositis, with various cancers observed, but no single cancer type predominates as a universal association.
*Arthritis*
- **Arthritis** can occur in dermatomyositis and polymyositis, but it is typically **non-erosive** and **non-deforming**, affecting small and large joints.
- While a possible feature, it is less specific and less frequently highlighted as a major systemic complication compared to interstitial lung disease in the context of anti-Jo-1 antibodies.
*Lung cancer*
- Similar to ovarian cancer, **lung cancer** is a potential malignancy associated with dermatomyositis, especially in older patients and smokers.
- However, for a 33-year-old woman with anti-Jo-1 antibodies, **interstitial lung disease** is a more direct and prevalent associated complication than **lung cancer**.
*Raynaud's phenomenon*
- **Raynaud's phenomenon** (episodic digital ischemia) is observed in a subset of patients with dermatomyositis, often those with features of overlap syndromes.
- While present in some cases, it is not as highly prevalent or as clinically significant as **interstitial lung disease** in patients with anti-Jo-1 antibodies.
Skeletal muscle diseases US Medical PG Question 3: An investigator is examining tissue samples from various muscle tissue throughout the body. She notices that biopsies collected from a specific site have a high concentration of sarcoplasmic reticulum, mitochondria, and myoglobin; they also stain poorly for ATPase. Additionally, the cell surface membranes of the myocytes in the specimen lack voltage-gated calcium channels. These myocytes are found in the greatest concentration at which of the following sites?
- A. Ventricular myocardium
- B. Tunica media
- C. Lateral rectus muscle
- D. Glandular myoepithelium
- E. Semispinalis muscle (Correct Answer)
Skeletal muscle diseases Explanation: ***Semispinalis muscle***
- The described characteristics—**high concentration of sarcoplasmic reticulum, mitochondria, and myoglobin** with **poor ATPase staining**—are hallmarks of **Type I (slow-twitch oxidative) skeletal muscle fibers**.
- Postural muscles like the **semispinalis** (part of the erector spinae group) are predominantly composed of Type I fibers adapted for sustained, aerobic contraction to maintain posture.
- These fibers appear **red** due to high myoglobin content, have abundant mitochondria for aerobic metabolism, and stain **poorly for ATPase** (distinguishing them from Type II fast-twitch fibers).
- While all skeletal muscle does possess voltage-gated calcium channels for excitation-contraction coupling, the overall profile best matches slow-twitch postural muscles.
*Ventricular myocardium*
- While cardiac muscle has high mitochondria, myoglobin, and sarcoplasmic reticulum, it **does possess L-type voltage-gated calcium channels** on the sarcolemma, which are essential for cardiac excitation-contraction coupling.
- Cardiac muscle relies on **both** extracellular Ca²⁺ influx through these channels and calcium-induced calcium release from the SR.
- Cardiac muscle typically stains **strongly for ATPase**, not poorly.
*Tunica media*
- Composed of **vascular smooth muscle** with poorly developed sarcoplasmic reticulum and relatively few mitochondria compared to skeletal or cardiac muscle.
- Smooth muscle relies heavily on **extracellular calcium influx** and the calmodulin pathway for contraction.
- Not characterized by high myoglobin content.
*Lateral rectus muscle*
- This extraocular muscle contains predominantly **Type IIb fast-twitch glycolytic fibers** adapted for rapid, precise eye movements.
- These fibers have **low myoglobin** (white muscle), fewer mitochondria, and stain **strongly for ATPase**.
- Opposite profile from the described tissue.
*Glandular myoepithelium*
- Myoepithelial cells are specialized contractile cells in secretory glands with minimal sarcoplasmic reticulum and mitochondria.
- Function is brief contraction for secretion expulsion, not sustained aerobic work.
- Do not exhibit the high oxidative capacity described.
Skeletal muscle diseases US Medical PG Question 4: A 62-year-old woman is referred to a tertiary care hospital with a history of diplopia and fatigue for the past 3 months. She has also noticed difficulty in climbing the stairs and combing her hair. She confirms a history of 2.3 kg (5.0 lb) weight loss in the past 6 weeks and constipation. Past medical history is significant for type 2 diabetes mellitus. She has a 50-pack-year cigarette smoking history. Physical examination reveals a blood pressure of 135/78 mm Hg supine and 112/65 while standing, a heart rate of 82/min supine and 81/min while standing, and a temperature of 37.0°C (98.6°F). She is oriented to time and space. Her right upper eyelid is slightly drooped. She has difficulty in abducting the right eye. Pupils are bilaterally equal and reactive to light with accommodation. The corneal reflex is intact. Muscle strength is reduced in the proximal muscles of all 4 limbs, and the lower limbs are affected more when compared to the upper limbs. Deep tendon reflexes are bilaterally absent. After 10 minutes of cycling, the reflexes become positive. Sensory examination is normal. Diffuse wheezes are heard on chest auscultation. Which of the following findings is expected?
- A. Thymoma on CT scan of the chest
- B. Incremental pattern on repetitive nerve conduction studies (Correct Answer)
- C. Periventricular plaques on MRI of the brain
- D. Antibodies against muscle-specific kinase
- E. Elevated serum creatine kinase
Skeletal muscle diseases Explanation: ***Incremental pattern on repetitive nerve conduction studies***
- The patient's symptoms (diplopia, fatigue, proximal muscle weakness, absent reflexes that normalize with exercise) are highly suggestive of **Lambert-Eaton myasthenic syndrome (LEMS)**.
- LEMS is characterized by impaired acetylcholine release at the neuromuscular junction, which manifests as an **incremental response** (progressively larger muscle action potentials) during high-frequency repetitive nerve stimulation.
*Thymoma on CT scan of the chest*
- **Thymoma** is strongly associated with **myasthenia gravis**, which typically presents with fluctuating weakness that worsens with activity and improves with rest, unlike the LEMS presentation.
- While LEMS can be paraneoplastic, it is most commonly associated with **small cell lung carcinoma**, not thymoma, making this finding less likely.
*Periventricular plaques on MRI of the brain*
- **Periventricular plaques** are characteristic findings in **multiple sclerosis**, a demyelinating disease of the central nervous system.
- Multiple sclerosis presents with diverse neurological deficits, but not typically with this specific pattern of fluctuating muscle weakness and absent deep tendon reflexes that improve with exercise.
*Antibodies against muscle-specific kinase*
- **Anti-MuSK antibodies** are associated with a specific subtype of **myasthenia gravis**, often presenting with prominent bulbar and respiratory weakness.
- While myasthenic syndromes share some features, the specific clinical picture (especially the improvement of reflexes with exercise) points away from standard myasthenia gravis and towards LEMS.
*Elevated serum creatine kinase*
- **Elevated creatine kinase** is typically seen in **myopathies** (e.g., inflammatory myopathies, muscular dystrophies) where there is direct muscle damage.
- In LEMS, the primary defect is at the neuromuscular junction, not within the muscle itself, so creatine kinase levels are usually normal.
Skeletal muscle diseases US Medical PG Question 5: A 13-year-old girl is brought to the physician by her mother because of a 1-month history of abnormal movements of her muscles that she cannot control. She has a younger brother with cognitive disabilities and epilepsy. Examination shows frequent, brief, involuntary contractions of the muscle groups of the upper arms, legs, and face that can be triggered by touch. An EEG shows generalized epileptiform activity. A trichrome stain of a skeletal muscle biopsy specimen shows muscle fibers with peripheral red inclusions that disrupt the normal fiber contour. Which of the following is the most likely underlying mechanism of the patient's symptoms?
- A. CTG trinucleotide repeat expansion
- B. Mutation of the methyl-CpG binding protein 2 gene
- C. Truncated dystrophin protein
- D. Autoimmune endomysial destruction
- E. Defective oxidative phosphorylation (Correct Answer)
Skeletal muscle diseases Explanation: ***Defective oxidative phosphorylation***
- The constellation of **uncontrolled muscle movements (myoclonus)**, **epilepsy**, and the brother's **cognitive disabilities** strongly suggests a **mitochondrial disorder**.
- **Ragged red fibers** on trichrome stain of skeletal muscle biopsy are pathognomonic for **mitochondrial myopathies**, indicating defective oxidative phosphorylation due to abnormal mitochondrial aggregates.
*CTG trinucleotide repeat expansion*
- This is characteristic of **Myotonic Dystrophy**, which primarily presents with **myotonia** (delayed muscle relaxation), progressive muscle weakness, and often cataracts, rather than prominent myoclonus and seizures.
- While muscle weakness can occur, the specific biopsy findings and prominent myoclonus point away from this diagnosis.
*Mutation of the methyl-CpG binding protein 2 gene*
- A mutation in the **MECP2 gene** causes **Rett Syndrome**, an X-linked dominant disorder seen almost exclusively in girls.
- It involves normal development for 6-18 months followed by regression, loss of purposeful hand movements, **stereotypical hand-wringing**, and microcephaly, which are not described here.
*Truncated dystrophin protein*
- A truncated dystrophin protein causes **Duchenne Muscular Dystrophy**, an X-linked recessive disorder leading to progressive muscle weakness, **Gowers' sign**, and elevated creatine kinase.
- This condition does not typically present with myoclonus or the characteristic ragged red fibers, nor does it typically involve the sibling's intellectual disability and epilepsy in this manner.
*Autoimmune endomysial destruction*
- This mechanism is characteristic of **celiac disease**, which can have neurological symptoms like ataxia or peripheral neuropathy, but not typically the severe myoclonus, epilepsy, or muscle biopsy findings seen here.
- **Inflammatory myopathies** like polymyositis may show endomysial inflammation, but the clinical picture and specific biopsy findings (ragged red fibers) are not consistent.
Skeletal muscle diseases US Medical PG Question 6: A 32-year-old woman presents with diplopia. She says that she has been experiencing drooping of her eyelids and severe muscle weakness. She reports that her symptoms are worse at the end of the day. Which of the following additional findings would most likely be seen in this patient?
- A. Increased acetylcholine receptor antibody (Correct Answer)
- B. Albuminocytological dissociation in the cerebrospinal fluid
- C. Increased calcium channel receptor antibodies
- D. Increased serum creatine kinase levels
- E. Increased antinuclear antibodies
Skeletal muscle diseases Explanation: ***Increased acetylcholine receptor antibody***
- The patient's symptoms of **diplopia**, **ptosis** (drooping eyelids), and severe muscle weakness that worsens with activity (end of the day) are classic manifestations of **myasthenia gravis**.
- **Myasthenia gravis** is an autoimmune disorder characterized by the destruction of **acetylcholine receptors** at the neuromuscular junction, which is confirmed by the presence of **acetylcholine receptor antibodies**.
*Albuminocytological dissociation in the cerebrospinal fluid*
- This finding, characterized by **elevated CSF protein** with a normal white blood cell count, is a hallmark of **Guillain-Barré syndrome**.
- **Guillain-Barré syndrome** typically presents with ascending paralysis and areflexia, which is distinct from the fluctuating, fatigable weakness seen in this patient.
*Increased calcium channel receptor antibodies*
- The presence of **voltage-gated calcium channel (VGCC) antibodies** is characteristic of **Lambert-Eaton Myasthenic Syndrome (LEMS)**.
- While LEMS also causes muscle weakness, it often improves with activity and is frequently associated with **small cell lung cancer**, differentiating it from myasthenia gravis where weakness worsens with activity.
*Increased serum creatine kinase levels*
- Elevated **creatine kinase (CK)** levels are indicative of **muscle damage or inflammation**, as seen in conditions like **myositis** or **muscular dystrophies**.
- Myasthenia gravis is a disorder of neuromuscular transmission, not primary muscle damage, so CK levels are typically normal.
*Increased antinuclear antibodies*
- **Antinuclear antibodies (ANA)** are a common finding in **systemic autoimmune diseases** like **systemic lupus erythematosus (SLE)** or **Sjögren's syndrome**.
- While some autoimmune conditions can have overlapping features, the specific symptom complex presented (diplopia, ptosis, fatigable weakness) strongly points to myasthenia gravis rather than a systemic autoimmune connective tissue disease.
Skeletal muscle diseases US Medical PG Question 7: A 7-year-old boy is brought to his pediatrician by his mother who is worried about his clumsiness. She states that over the past 3 months she has noticed progressive weakness. He used to climb trees and run outside with his cousins, but now he says he gets “too tired.” She’s recently noticed him starting to “walk funny,” despite having “muscular legs.” Upon physical examination, the patient has calf muscle hypertrophy. He uses his arms to rise out of the chair. Labs are obtained that show an elevated creatine kinase. Genetic analysis detects a dystropin gene mutation. A muscle biopsy is performed that reveals reduced dystrophin. Which of the following is the most likely diagnosis?
- A. Fragile X syndrome
- B. Pompe disease
- C. Duchenne muscular dystrophy (Correct Answer)
- D. Spinal muscular atrophy
- E. Becker muscular dystrophy
Skeletal muscle diseases Explanation: ***Duchenne muscular dystrophy***
- This 7-year-old presents with classic features of **Duchenne muscular dystrophy (DMD)**: **progressive proximal muscle weakness**, **calf pseudohypertrophy**, **Gowers' sign** (using arms to rise from a chair), and **markedly elevated creatine kinase**.
- Genetic analysis confirms a **dystrophin gene mutation**, and muscle biopsy shows **reduced dystrophin**, consistent with DMD where dystrophin is absent or severely reduced (<3% of normal).
- The **age of presentation (7 years)** is typical for DMD, as many boys are diagnosed between ages 3-7 when motor delays become apparent in school settings; the recent 3-month history of rapid decline is characteristic of DMD's progressive course.
- Boys with DMD typically lose ambulation by age 12 and require wheelchair assistance, distinguishing it from the milder Becker variant.
*Becker muscular dystrophy*
- While also caused by a **dystrophin gene mutation**, Becker muscular dystrophy (BMD) presents **later** (typically age 8-25) with a **much milder and slower progression**.
- In BMD, dystrophin is **reduced but functional** (3-20% or more of normal, often abnormal in size), not severely deficient as in this case.
- Patients with BMD remain ambulatory into their 20s-30s or beyond, which contrasts with this patient's relatively early onset and rapid 3-month decline.
- The clinical tempo and age of onset in this case are more consistent with Duchenne than Becker.
*Fragile X syndrome*
- This is a genetic disorder primarily characterized by **intellectual disability**, **developmental delays**, **autism spectrum features**, and distinct physical features (long face, large ears, macroorchidism).
- It does not present with **progressive muscle weakness**, **calf pseudohypertrophy**, **elevated CK**, or **dystrophin gene mutations**.
*Pompe disease*
- This is a **lysosomal storage disorder** caused by deficiency of **acid alpha-glucosidase (GAA)**, leading to glycogen accumulation in lysosomes.
- While it can cause **muscle weakness** and elevated CK, infantile-onset Pompe presents with **cardiomyopathy** and **hypotonia** ("floppy infant"), and late-onset Pompe presents with limb-girdle weakness and respiratory failure.
- Pompe does **not involve dystrophin mutations** or **calf pseudohypertrophy**.
*Spinal muscular atrophy*
- This disorder results from **loss of motor neurons** in the spinal cord due to **SMN1 gene mutations**, causing muscle weakness and atrophy.
- SMA presents with **hypotonia**, **areflexia**, and **muscle atrophy** (not hypertrophy), with **fasciculations** of the tongue in some cases.
- It does **not involve dystrophin mutations**, **calf pseudohypertrophy**, or markedly elevated CK levels.
Skeletal muscle diseases US Medical PG Question 8: A 15-year-old boy comes to the physician for the evaluation of progressive difficulty climbing stairs for the last 2 years. During this period, he has also had problems running and standing up from a seated position. He is at the 50th percentile for height and weight. Examination shows enlarged calf muscles bilaterally and a waddling gait. Which of the following is the most likely cause of this patient's condition?
- A. Large deletions (Correct Answer)
- B. Frameshift mutation
- C. Splice site mutation
- D. Missense mutation
- E. Nonsense mutation
Skeletal muscle diseases Explanation: ***Large deletions***
- The presented symptoms (progressive difficulty climbing stairs, running, standing, enlarged calf muscles, waddling gait) are classic for **Duchenne muscular dystrophy (DMD)**.
- **Large deletions** (involving one or more exons) are the **most common cause of DMD**, accounting for approximately **60-70%** of cases.
- These deletions typically cause a **frameshift** that leads to a premature stop codon, resulting in absent or severely truncated **dystrophin protein**.
- The **dystrophin gene** is one of the largest human genes, making it particularly susceptible to deletion mutations.
*Frameshift mutation*
- A **frameshift mutation** (insertion or deletion of nucleotides not in multiples of three) leads to an altered reading frame, resulting in a **premature stop codon** downstream.
- While frameshifts do cause **DMD**, they are typically the **consequence** of deletions or small insertions/duplications, not a primary mutation category.
- The question asks for the underlying genetic cause, which is most commonly a large deletion.
*Splice site mutation*
- **Splice site mutations** affect the splicing of introns and exons, potentially leading to exon skipping or inclusion of intronic sequences.
- These account for a small percentage of **DMD** cases but are much less common than large deletions.
- While they can disrupt the reading frame, they represent a minority of causative mutations.
*Missense mutation*
- A **missense mutation** results in a single amino acid change, producing an altered but full-length protein.
- This type of mutation is more characteristic of **Becker muscular dystrophy (BMD)**, a milder form with later onset and slower progression.
- The severe, early-onset phenotype described here is typical of **DMD**, which requires near-complete absence of functional dystrophin.
*Nonsense mutation*
- A **nonsense mutation** introduces a premature stop codon, leading to a truncated protein.
- While nonsense mutations do cause **DMD**, they account for only about **10-15%** of cases as part of the broader category of point mutations.
- Large deletions remain significantly more common as the causative mutation type.
Skeletal muscle diseases US Medical PG Question 9: You are conducting a lab experiment on skeletal muscle tissue to examine force in different settings. The skeletal muscle tissue is hanging down from a hook. The experiment has 3 different phases. In the first phase, you compress the muscle tissue upwards, making it shorter. In the second phase, you attach a weight of 2.3 kg (5 lb) to its lower vertical end. In the third phase, you do not manipulate the muscle length at all. At the end of the study, you see that the tension is higher in the second phase than in the first one. What is the mechanism underlying this result?
- A. The tension in phase 1 is only active, while in phase 2 it is both active and passive.
- B. Shortening the muscle in phase 1 pulls the actin and myosin filaments apart.
- C. Lengthening of the muscle in phase 2 increases passive tension. (Correct Answer)
- D. There are more actin-myosin cross-bridges attached in phase 2 than in phase 1.
- E. Shortening of the muscle in phase 1 uses up ATP stores.
Skeletal muscle diseases Explanation: ***Lengthening of the muscle in phase 2 increases passive tension.***
- Attaching a weight of 2.3 kg (5 lb) in phase 2 **stretches** the muscle, increasing the **passive tension** generated by elastic components like **titin**.
- This added passive tension, combined with any active tension, results in a **higher total tension** compared to the shortened state in phase 1 where passive tension is minimal.
*The tension in phase 1 is only active, while in phase 2 it is both active and passive.*
- While passive tension is more significant in phase 2 due to stretching, the muscle in phase 1, even when compressed, can still generate some **active tension** if stimulated.
- The key difference contributing to higher tension in phase 2 is the additional **passive component** from stretching, not necessarily the exclusive presence of active tension in one phase.
*Shortening the muscle in phase 1 pulls the actin and myosin filaments apart.*
- Shortening the muscle too much, beyond its optimal resting length, leads to **overlap of actin filaments** and **crumpling of myosin filaments**, reducing the number of available cross-bridge binding sites.
- This **decreases active tension** rather than pulling filaments apart, which would require excessive stretching.
*There are more actin-myofibril cross-bridges attached in phase 2 than in phase 1.*
- Shortening the muscle in phase 1 beyond optimal length **reduces the number of cross-bridges** that can form due to actin filament overlap.
- While lengthening in phase 2 might bring the muscle closer to an **optimal length** for cross-bridge formation (increasing active tension), the primary reason for the higher tension in phase 2 as described is the increase in **passive tension** from stretching, rather than solely increased active cross-bridge formation.
*Shortening of the muscle in phase 1 uses up ATP stores.*
- Muscle contraction, whether shortening or lengthening, requires **ATP hydrolysis** for cross-bridge cycling.
- The act of shortening itself doesn't uniquely "use up" ATP stores more significantly than other contractile actions to explain the observed tension difference; ATP is continuously consumed and regenerated during muscle activity.
Skeletal muscle diseases US Medical PG Question 10: A 25-year-old woman presents to her primary care physician for her yearly physical exam. She has no past medical history and says that she does not currently have any health concerns. On physical exam, she is found to have hyperactive patellar reflexes but says that she has had this finding since she was a child. She asks her physician why this might be the case. Her physician explains that there are certain cells that are responsible for detecting muscle stretch and responding to restore the length of the muscle. Which of the following is most likely a characteristic of these structures?
- A. They inhibit the activity of alpha-motoneurons
- B. They activate inhibitory interneurons
- C. They are in parallel with extrafusal skeletal muscle fibers (Correct Answer)
- D. They are in series with extrafusal skeletal muscle fibers
- E. They are innervated by group Ib afferent neurons
Skeletal muscle diseases Explanation: ***They are in parallel with extrafusal skeletal muscle fibers***
- The structures described are **muscle spindles**, which are **stretch receptors** located within the muscle belly and arranged in parallel with **extrafusal muscle fibers**.
- This parallel arrangement allows them to detect changes in **muscle length** and the rate of change of length, initiating the **stretch reflex**.
*They inhibit the activity of alpha-motoneurons*
- Muscle spindles, primarily through their **Ia afferent fibers**, **excite** alpha-motoneurons, leading to muscle contraction and opposing the stretch.
- **Inhibition** of alpha-motoneurons is typically associated with structures like **Golgi tendon organs**, which respond to muscle tension.
*They activate inhibitory interneurons*
- While muscle spindles do excite **excitatory interneurons** that activate synergistic muscles, their primary action in the monosynaptic stretch reflex is direct excitation of **alpha-motoneurons**.
- **Inhibitory interneurons** are typically involved in mediating **reciprocal inhibition** of antagonistic muscles in response to muscle spindle activation.
*They are in series with extrafusal skeletal muscle fibers*
- Structures arranged in **series** with extrafusal muscle fibers are **Golgi tendon organs**, which are tension receptors.
- Muscle spindles are oriented **in parallel** to detect changes in muscle length.
*They are innervated by group Ib afferent neurons*
- Muscle spindles are primarily innervated by **group Ia (primary) afferent neurons** and **group II (secondary) afferent neurons**, which detect muscle length and rate of change of length.
- **Group Ib afferent neurons** innervate **Golgi tendon organs**, which are sensitive to muscle tension.
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