Student Name Chamberlain University BIOS-252: Anatomy & Physiology II with Lab Prof. Name Date Week 7 Case Study: Thyroid The thyroid gland plays a vital role in regulating numerous bodily functions. It produces hormones that influence the metabolism of nearly every cell and organ, impacting processes such as heart rate, body temperature, and weight regulation. Imbalances in thyroid hormone levels can lead to significant physiological changes, ranging from fluctuations in body weight to cardiovascular irregularities. One common condition associated with thyroid dysfunction is the formation of a goiter—an abnormal enlargement of the thyroid gland. As the thyroid becomes less efficient in producing adequate hormone levels, the pituitary gland compensates by releasing higher amounts of thyroid-stimulating hormone (TSH). This compensatory mechanism can result in the growth of thyroid tissue, thereby forming a visible or palpable goiter. What condition do you believe the patient has, and why? Based on the symptoms presented, it appears the patient may be experiencing hypothyroidism, which is a condition characterized by an underactive thyroid gland. When the thyroid is unable to produce sufficient amounts of hormones (T3 and T4), the pituitary gland increases the production of TSH to stimulate the thyroid. This prolonged stimulation can result in thyroid gland enlargement, known as a goiter. Additionally, the patient’s sensation of feeling cold could point toward a reduced metabolic rate—a hallmark of hypothyroidism. However, another possibility must also be considered due to her description of heat sensitivity and visual disturbances. Why do you think the patient might have Graves’ disease? While the symptoms of hypothyroidism are prominent, the patient also reports feeling excessively warm in a room that is typically cool. This heat intolerance suggests the possibility of hyperthyroidism, where the thyroid is overactive. Furthermore, her complaints of blurry or double vision are consistent with Graves’ ophthalmopathy, a condition commonly associated with Graves’ disease—a form of autoimmune hyperthyroidism. In Graves’ disease, the immune system mistakenly attacks the thyroid, stimulating it to overproduce hormones. This leads to elevated metabolic activity, including increased body temperature, heart rate, and potential eye complications. The visual symptoms particularly support this diagnosis, as they are less common in other thyroid disorders. Comparison of Hypothyroidism and Graves’ Disease Feature Hypothyroidism Graves’ Disease (Hyperthyroidism) Thyroid Hormone Levels Low High TSH Levels High Low or suppressed Metabolic Rate Decreased Increased Heat SensitivityA Cold intolerance Heat intolerance Weight Changes Weight gain Weight loss Cardiovascular Impact Slowed heart rate Rapid heart rate (tachycardia) Eye Symptoms Rare Common (bulging eyes, double vision) Goiter Common Common Cause Autoimmune or iodine deficiency Autoimmune (TSH receptor antibodies) Both conditions can result in goiter formation due to either hormone deficiency or overproduction. However, the co-occurrence of heat intolerance and vision issues leans more heavily toward Graves’ disease. References MacGill, M. (2020, November 11). Everything you need to know about a goiter. Medical News Today. https://www.medicalnewstoday.com/articles/175274 BIOS 252 Week 7 Case Study: Thyroid

Student Name Chamberlain University BIOS-252: Anatomy & Physiology II with Lab Prof. Name Date BIOS 252 Week 6 Case Study Why was the patient’s diabetic status questioned after assessing level of consciousness and vital signs? After evaluating a patient’s consciousness and vital signs, healthcare professionals often inquire about the individual’s diabetic status—especially when there is a noticeable fruity odor on the patient’s breath. This particular scent may suggest the presence of diabetic ketoacidosis (DKA), a serious complication of uncontrolled diabetes. DKA occurs when the body lacks sufficient insulin to use glucose for energy and begins to break down fat, producing ketone bodies. As ketones accumulate, they can lead to a sweet or fruity breath odor and cause the blood to become acidic, which is a medical emergency (Centers for Disease Control and Prevention [CDC], 2021; Saladin, 2019). Early identification of diabetes or diabetic complications is vital for prompt treatment, especially in emergency settings. DKA can rapidly become life-threatening if not addressed, so establishing whether a patient has diabetes can help guide timely and appropriate intervention. Why might a hypoglycemic patient exhibit decreased consciousness? Hypoglycemia, defined as abnormally low blood glucose levels, can severely affect a patient’s neurological status. Glucose is the brain’s primary energy source, and when levels drop too low, the brain lacks the fuel required for normal function. This can lead to symptoms such as confusion, dizziness, anxiety, excessive hunger, fainting, or even unconsciousness (Mayo Clinic, 2020). In individuals with diabetes, hypoglycemia can result from insulin overuse, missing meals, or engaging in intense physical activity without proper energy intake. Many medications used to control blood sugar, particularly insulin and sulfonylureas, have hypoglycemia as a side effect (Saladin, 2019). Monitoring glucose levels and recognizing signs of hypoglycemia early are critical to prevent deterioration in consciousness. Why might a hyperglycemic patient exhibit decreased consciousness? Hyperglycemia refers to excessively high blood glucose levels and can also impair consciousness, especially in prolonged or severe cases. When blood sugar rises significantly, it causes osmotic diuresis, pulling large amounts of fluid from tissues into the urine. This leads to dehydration and electrolyte imbalances, which may impair cerebral function and result in lethargy or coma (Cleveland Clinic, 2020; Saladin, 2019). If left untreated, hyperglycemia can lead to diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS)—both potentially fatal conditions. Thickened blood, poor circulation, and toxin accumulation further decrease cognitive function, possibly resulting in altered mental status or unconsciousness. What causes fruity breath in diabetic patients, and what condition does it indicate? A fruity-smelling breath in a diabetic patient is a clinical hallmark of diabetic ketoacidosis (DKA). This odor stems from the exhalation of ketone bodies, particularly acetone, which is a byproduct of fat metabolism. When the body lacks insulin and cannot use glucose effectively, it begins breaking down fat for energy. This metabolic shift produces ketones, including acetone, which are acidic and toxic in high concentrations (CDC, 2021). The table below summarizes the link between breath odor and DKA: Cause Resulting Condition Breath Characteristic Explanation Inadequate insulin Diabetic Ketoacidosis Fruity or sweet smell Due to fat metabolism producing ketones like acetone Excessive ketone accumulation Blood acidosis Breath smells like nail polish remover Acetone exhaled from lungs causes characteristic odor High glucose but low cellular uptake Ketosis Potential diabetic coma Ketones build up due to low glucose utilization, raising blood acidity levels DKA requires immediate medical intervention. If ignored, it can lead to coma, organ failure, or death. Monitoring for this breath odor in diabetic patients is a critical diagnostic cue (CDC, 2021). References Centers for Disease Control and Prevention. (2021, March 25). Diabetic ketoacidosis. https://www.cdc.gov/diabetes/basics/diabeticketoacidosis.html Cleveland Clinic. (2020, December 2). Diabetic coma: Causes, risk factors, treatment & prevention. https://my.clevelandclinic.org/health/diseases/16628-diabetic-coma Mayo Foundation for Medical Education and Research. (2020, April 3). Diabetic hypoglycemia. https://www.mayoclinic.org/diseasesconditions/diabetic-hypoglycemia/symptoms-causes/syc-20371525 BIOS 252 Week 6 Case Study Saladin, K. (2019). Anatomy and Physiology: The Unity of Form and Function (9th ed.). McGraw-Hill.

Student Name Chamberlain University BIOS-252: Anatomy & Physiology II with Lab Prof. Name Date Introduction The human body, an intricate and vulnerable system, is susceptible to a range of injuries, particularly in the event of traumatic incidents like explosions. In the case under discussion, the patient sustained multiple trauma-induced injuries resulting from an explosive blast. These injuries are complex and require detailed diagnostic evaluations to determine the extent and severity of damage. A notable concern is the fracture of the cribriform plate, located within the ethmoid bone. This thin, perforated structure contributes to the roof of the nasal cavity and is highly prone to damage from high-impact trauma, including the pressure waves generated by blasts. A fracture in this location significantly increases the risk of cerebrospinal fluid (CSF) leakage, which may lead to secondary complications such as meningitis, infection, or pneumocephalus (Gomez & Pickup, 2022). Immediate and accurate assessment is critical to prevent further deterioration. Injury Assessment and Diagnostic Procedures How are the injuries evaluated and confirmed? The initial step in evaluating the patient’s condition involves conducting a computed tomography (CT) scan, which provides cross-sectional images of the skull and brain structures. Although CT imaging is useful in detecting fractures, it does not always reveal the presence or source of CSF leakage. Therefore, when a CSF leak is suspected, clinicians employ a non-invasive Pledget test. This technique involves inserting small absorbent pads (pledgets) into the nasal cavity. If a ring of clear or yellowish fluid is found around a blood-stained pledget, it is indicative of CSF rhinorrhea. However, the test does not identify the precise origin of the leak. In addition to head trauma, the patient also reports visual disturbances. These symptoms are likely due to intraocular hemorrhage caused by ruptured blood vessels in the vitreous humor. The vitreous body, a gel-like substance within the eye, plays a vital role in maintaining ocular structure and pressure. Disruption in this area can distort vision. To diagnose vitreous hemorrhage, ophthalmologists use fluorescein angiography—a diagnostic procedure involving the injection of a fluorescent dye into the bloodstream. This allows clinicians to detect any leakage or abnormalities in the retinal blood vessels (Saladin, 2020). Bilateral Tympanic Membrane Perforation What is the cause of the ear drum rupture and how is it diagnosed? Another injury sustained involves bilateral rupture of the tympanic membranes, or eardrums. These thin membranes separate the external ear canal from the middle ear and are extremely sensitive to pressure changes. Tympanic membranes typically rupture when exposed to blast pressures exceeding 35 pounds per square inch (Psi) (Baum et al., 2010). Given the explosion’s proximity, it is reasonable to infer that the blast force surpassed this threshold. Furthermore, research indicates that blast forces over 40 Psi can damage hollow internal organs such as the lungs by creating shearing forces that fragment tissues (Jorolemon et al., 2022). Clinical evaluation of the ears confirms the bilateral perforation, with findings supported by knowledge of blast physics and trauma pathology. BIOS 252 Week 5 Case Study Summary Table of Injuries and Diagnostic Measures Injury Description Diagnostic Procedure Cribriform Plate Fracture Fracture at the roof of the nasal cavity; high risk of CSF leak and infection. CT scan for structural imaging, Pledget test for CSF confirmation. Visual Disturbances Caused by ruptured retinal or vitreous blood vessels leading to blurred or distorted vision. Fluorescein angiography (dye test to highlight bleeding or leakage in retinal vessels). Bilateral Tympanic Membrane Rupture Resulting from exposure to high-pressure blast waves exceeding 35 Psi, causing eardrum damage. Clinical otoscopic examination and analysis of blast conditions. Conclusion In summary, the injuries inflicted upon the patient from the blast incident are extensive and demand a multi-disciplinary diagnostic and treatment approach. The cribriform plate fracture poses a grave risk due to its association with CSF leakage and subsequent neurological infections, thus requiring both imaging and Pledget testing for accurate diagnosis. The observed visual symptoms, suspected to be caused by vitreous hemorrhage, are evaluated using fluorescein angiography to detect internal ocular bleeding. Lastly, the bilateral tympanic membrane ruptures—attributed to intense blast wave pressure—require clinical inspection and careful monitoring. These injuries highlight the importance of prompt medical attention and coordinated care strategies to mitigate long-term complications and improve patient outcomes. References Baum, J. D., Rattigan, M. I., Sills, E. S., & Walsh, A. P. (2010). Clinical presentation and conservative management of tympanic membrane perforation during intrapartum. https://doi.org/10.1155/2010/856045 Gomez, J., & Pickup, S. (2022). Cribriform Plate Fractures. StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK562192/ Jorolemon, M. R., Lopez, R. A., & Krywko, D. M. (2022). Blast Injuries. StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK430914/ BIOS 252 Week 5 Case Study Saladin, K. S. (2020). Anatomy & Physiology: The Unity of Form and Function (9th ed.). McGraw-Hill Higher Education (US).

Student Name Chamberlain University BIOS-252: Anatomy & Physiology II with Lab Prof. Name Date Signs and Symptoms of Autonomic Nervous System Activation Looking at the signs and symptoms, you notice that one of the two branches of the autonomic nervous system (ANS) is highly upregulated. Which one is it? Name three signs or symptoms that clued you in on it and why. Based on the clinical presentation, the branch of the autonomic nervous system (ANS) that is significantly upregulated is the parasympathetic nervous system. This branch is primarily responsible for conserving energy and maintaining normal physiological functions. Three key symptoms that indicated parasympathetic overactivity include bradycardia, excessive sweating, and vomiting. Bradycardia, or a slower than normal heart rate, occurs due to increased vagal tone, which is mediated by parasympathetic stimulation. Vomiting is linked to enhanced gastrointestinal motility and secretions, also under parasympathetic control. Although sweating is often associated with sympathetic activation, certain sweat glands, particularly eccrine glands in the palms and soles, are actually stimulated via cholinergic fibers associated with the sympathetic nervous system, but they respond to acetylcholine, a neurotransmitter prominent in the parasympathetic system as well. This overlapping function can sometimes make parasympathetic dominance more complex to interpret (Guy-Evans, 2021). Symptom Linked to Parasympathetic Activation Reason Bradycardia Yes Increased vagal stimulation lowers heart rate. Vomiting Yes Elevated gastrointestinal motility and secretions. Sweating Indirectly Muscarinic activation in eccrine glands via cholinergic fibers. Muscarine and Receptor Binding in the ANS What receptor do you think muscarine binds to in the ANS? What neurotransmitter usually binds to the receptor? Muscarine binds to muscarinic receptors, a subtype of cholinergic receptors located throughout the parasympathetic nervous system. These receptors play a crucial role in mediating the effects of parasympathetic stimulation on various organs. The primary neurotransmitter that naturally activates these receptors is acetylcholine (Kudlak & Tadi, 2021). Muscarinic receptors are categorized into subtypes (M1–M5), each of which is responsible for different physiological responses. For instance, M2 receptors affect cardiac function, while M3 receptors regulate glandular secretions, smooth muscle contraction, and even sweating, which is relevant to this case. Receptor Ligand (Natural) Ligand (Toxin/Drug) Function Muscarinic (M1–M5) Acetylcholine Muscarine Regulates parasympathetic organ functions. Understanding Excessive Sweating At first, it seemed odd that three out of four of your patients were sweating. It makes sense now that you know what they ate. Why? The unusual observation of excessive sweating in three out of four patients can be attributed to the activation of M3 muscarinic receptors, which are present not only in the gastrointestinal tract but also in eccrine sweat glands. These receptors, when stimulated by acetylcholine—whether endogenous or exogenous, such as from muscarine ingestion—lead to increased secretion from sweat glands. The food consumed likely contained muscarine, which mimics acetylcholine and overstimulates the M3 receptors, causing profuse sweating. Though sweating is commonly linked with sympathetic responses, its mechanism is cholinergic, which connects it indirectly to parasympathetic pathways (Guy-Evans, 2021; Kudlak & Tadi, 2021). Treatment and Role of Anticholinergics Treatment for this issue includes the use of atropine. Atropine is anticholinergic. Define anticholinergic and determine why you would use it in this case. Anticholinergic medications are agents that block the action of acetylcholine at muscarinic receptors in the parasympathetic nervous system. This inhibition helps to reduce or completely stop excessive involuntary functions such as glandular secretion, gastrointestinal activity, and muscle spasms. Atropine is a classic anticholinergic drug and is particularly effective in counteracting muscarine poisoning. It works by competitively inhibiting muscarinic receptors, thus preventing acetylcholine from binding and exerting its parasympathetic effects. In this clinical scenario, atropine would help normalize the patient’s heart rate, reduce vomiting, and stop excessive sweating, providing symptomatic relief and preventing further complications (Gal, 2022; National Institute of Diabetes and Digestive and Kidney Diseases, 2012). Drug Type Mechanism of Action Effect in This Case Atropine Anticholinergic Blocks acetylcholine at muscarinic receptors Reduces bradycardia, vomiting, and sweating caused by muscarine. References Gal, K. (2022). Anticholinergic drugs: What to know. https://www.medicalnewstoday.com/articles/323514 Guy-Evans, O. (2021). Peripheral Nervous System. Definition, Parts, and Function. https://www.simplypsychology.org/peripheral-nervous-system.html Kudlak, M., & Tadi, P. (2021). Physiology, Muscarinic Receptor. https://www.ncbi.nlm.nih.gov/books/NBK555909/ BIOS 252 Week 4 Case Study: ANS National Institute of Diabetes and Digestive and Kidney Diseases. (2012). LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. https://www.ncbi.nlm.nih.gov/books/NBK548287/

Student Name Chamberlain University BIOS-252: Anatomy & Physiology II with Lab Prof. Name Date Week 3 Case Study: CNS and PNS Overview 1. What is the term used to describe the inability to voluntarily move the legs? The inability to voluntarily move the legs is medically referred to as paraplegia. This condition results from damage to the spinal cord or brain that disrupts communication between the central nervous system (CNS) and the lower body. Paraplegia specifically affects motor control and often impairs sensory function in the trunk, pelvic organs, and lower limbs. The severity of paraplegia can vary depending on the level and extent of neurological damage. It is most commonly caused by traumatic spinal cord injury, multiple sclerosis, or other diseases that affect the CNS. 2. What are the components of a basic reflex arc? A reflex arc is the simplest neural pathway that mediates a reflex action. It involves a sequence of neural structures working in coordination to produce an involuntary response to stimuli. The basic components are summarized in the table below: Component Description Sensor Sensory receptors in the skin, muscles, or tendons that detect a specific stimulus. Sensory Neuron Afferent neurons that transmit impulses from receptors to the spinal cord or brainstem. Integration Center Located in the gray matter of the spinal cord or brainstem, where the sensory neuron synapses with interneurons or motor neurons. Motor Neuron Efferent neurons that carry commands from the CNS to the effector organ or muscle. Effector The muscle or gland that carries out the response (e.g., contracting or secreting). This process ensures rapid, automatic responses to potentially harmful stimuli, contributing to the body’s defense mechanism (CK-12, 2014). 3. What is Babinski’s sign, and how does it compare to a normal plantar reflex? The plantar reflex is tested by stroking the lateral aspect of the sole of the foot. In healthy adults, this stimulus typically results in plantar flexion of the toes—meaning the big toe points downward. In contrast, Babinski’s sign occurs when the big toe moves upward and the other toes fan outward. This response is normal in infants under 2 years old due to immature nervous systems, but in older children and adults, it suggests pathology in the upper motor neurons or corticospinal tract (Acharya et al., 2022). Reflex Type Hallux Response Clinical Significance Normal Plantar Downward (flexion) Indicates intact corticospinal tract Babinski Sign Upward (extension) Suggests upper motor neuron damage 4. Why might Babinski’s sign appear instead of the normal plantar reflex? Babinski’s sign appears when there is dysfunction or damage in the corticospinal tract (CST)—a crucial descending motor pathway originating in the cerebral cortex and terminating at the spinal cord. Damage to the CST disrupts the normal inhibition of primitive reflexes, such as the Babinski response, leading to their reappearance in adults. Common causes include traumatic spinal cord injury, brain tumors, multiple sclerosis, and stroke. The presence of this abnormal reflex may prompt further diagnostic testing, including MRI, CT scans, and lumbar punctures, to determine the underlying neurological condition (Acharya et al., 2022). 5. Why is this not an issue with a first-order neuron? This condition is not attributed to a first-order neuron issue because the Babinski sign is indicative of upper motor neuron lesions, which involve the central nervous system (CNS) rather than peripheral structures. First-order neurons are part of the peripheral nervous system (PNS) and transmit sensory input to the CNS. Damage to these neurons would more likely cause a loss of reflexes, rather than the pathological reflexes seen with CST disruption. Hence, the Babinski reflex is a valuable tool in localizing CNS pathology and is especially useful in detecting early signs of spinal cord injury or stroke before other symptoms manifest. 6. Where along the spinal cord might a lesion be found in a patient with Babinski’s sign? A lesion associated with Babinski’s sign would typically be located along the corticospinal tract, which runs from the motor cortex, through the brainstem, and down the spinal cord. These fibers synapse with alpha motor neurons in the anterior horn of the spinal cord. Damage anywhere along this descending pathway can lead to an upper motor neuron lesion, resulting in a positive Babinski sign. Location Possible Lesion Sites Brain Primary motor cortex or internal capsule Brainstem Midbrain, pons, or medulla oblongata Spinal Cord Cervical or thoracic spinal cord regions Identification of such lesions through imaging techniques is essential for early intervention and treatment planning. References Acharya AB, Jamil RT, Dewey JJ. (2022, July 25). Babinski Reflex. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519009/ CK-12 Foundation. (2014, November 13). Reflexes: Neurons in Action. Retrieved November 12, 2022, from https://www.ck12.org/book/human-biology-nervous-system/section/5.1/ Wikipedia contributors. (2022, June 12). Reflex arc. Wikipedia. Retrieved November 12, 2022, from https://en.wikipedia.org/w/index.php?title=Reflex_arc\&oldid=1092719613 Wikipedia contributors. (2022, November 4). Plantar reflex. Wikipedia. Retrieved November 12, 2022, from https://en.wikipedia.org/w/index.php?title=Plantar_reflex\&oldid=1119913988 BIOS 252 Week 3 Case Study: CNS-PNS Images retrieved from: https://dr282zn36sxxg.cloudfront.net/datastreams/f-d%3A71953874beb96f8db25c54a2f0770b846802b7343f505555c27e02bf%2BIMAGE_TINY%2BIMAGE_TINY.1 https://upload.wikimedia.org/wikipedia/commons/thumb/9/97/Imgnotraçat_arc_reflex_eng.svg/2560px-Imgnotraçat_arc_reflex_eng.svg.png https://upload.wikimedia.org/wikipedia/commons/thumb/6/69/Lawrence_1960_20.4.png/600px-Lawrence_1960_20.4.png

Student Name Chamberlain University BIOS-252: Anatomy & Physiology II with Lab Prof. Name Date Week 2 Case Study: Multiple Sclerosis Scenario Summary A 30-year-old female patient diagnosed with multiple sclerosis (MS) presents for a routine appointment with her neurologist. Her initial symptoms, which emerged years prior, included a tingling sensation that was mildly bothersome but transient. Over time, this progressed into more severe episodes of tingling and pain, followed by noticeable coordination issues. With each relapse, the patient’s condition deteriorated slightly, and she did not regain full function from the previous flare-ups—indicating a progressive decline in neurological function. Cellular Structures Involved in Multiple Sclerosis What cellular structure is degenerating and rebuilding in MS? In multiple sclerosis, the primary cellular structures undergoing degeneration are the myelin sheath and the oligodendrocytes—the glial cells responsible for producing myelin in the central nervous system (CNS). The immune system erroneously attacks the myelin sheath, leading to demyelination, which in turn hinders the transmission of nerve impulses. Damaged areas are often replaced with hardened scar tissue, or sclerosis, hence the name of the disease (Saladin, 2019). In response to this damage, neural stem cells (NSCs) within the CNS attempt to initiate repair by generating new neurons, astrocytes, and oligodendrocytes. These regenerative processes aim to remyelinate damaged axons and restore some neural function. However, this regenerative capacity is often insufficient to fully reverse neurological deficits, especially in progressive forms of the disease (Myelin, 2022; Saladin, 2019). Symptom Progression and Underlying Pathology Does this explain the progression we see with the signs and symptoms? Explain why. Yes, the ongoing cycle of demyelination and incomplete remyelination explains the progressive nature of MS symptoms. As nerve conduction becomes increasingly impaired, communication between the brain and other parts of the body is disrupted. This leads to a wide range of neurological symptoms, including but not limited to: These manifestations reflect the areas of the CNS where demyelination is occurring. Over time, the cumulative damage results in more persistent and disabling symptoms (Myelin, 2022). The Importance of Eye Examinations in MS When there are issues with neural tissue like this, why do they often look into the eyes? Eye examinations are a crucial diagnostic and monitoring tool for individuals with MS because the optic nerve, which transmits visual information from the eyes to the brain, is part of the CNS. One of the hallmark features of early MS is optic neuritis, an inflammation of the optic nerve. This condition results in: Because these symptoms can be early indicators of MS, an eye exam, particularly with the use of optical coherence tomography (OCT) or visual evoked potentials (VEP), helps clinicians assess the extent of CNS involvement and disease progression (Saladin, 2019). BIOS 252 Week 2 Case Study: Multiple Sclerosis Classification of Early Symptoms Assign the following early symptoms to either the sensory, motor, or autonomic nervous system. Then, describe how MS would cause these symptoms. Early Symptoms Nervous System Involved Explanation of How MS Causes the Symptom Dysarthria Motor (speech production) Dysarthria occurs due to damage in the neural pathways that control the muscles involved in speech. In MS, demyelination of these pathways can cause weakness or lack of coordination in tongue and facial muscles, resulting in slurred or slow speech. Paresthesia Sensory Paresthesia refers to sensations like tingling, burning, or numbness. MS damages sensory pathways through demyelination, disrupting the transmission of sensory input to the brain. This often results in abnormal sensations in the limbs or face. Constipation Autonomic MS may impair the autonomic nervous system’s regulation of bowel function. Demyelination in the spinal cord or brainstem can interfere with the reflexes and muscle coordination needed for regular bowel movements, leading to constipation. References Myelin. (2022). National Multiple Sclerosis Society. Retrieved March 7, 2022, from https://www.nationalmssociety.org/What-is-MS/Definition-of-MS/Myelin BIOS 252 Week 2 Case Study: Multiple Sclerosis Saladin, K. (2019). Anatomy and Physiology: The Unity of Form and Function (9th ed.). McGraw-Hill.

Student Name Chamberlain University BIOS-252: Anatomy & Physiology II with Lab Prof. Name Date Muscles Severed During the Amputation Event 1. Name the muscles severed during the amputation event. In the event of a forearm amputation, several muscles are commonly severed due to their anatomical location and functional role in hand and wrist movement. The following table outlines the key muscles affected: Muscle Name Function Flexor Carpi Ulnaris Flexes and adducts the wrist Extensor Carpi Ulnaris Extends and adducts the wrist Extensor Digiti Minimi Extends the fifth digit (little finger) Extensor Digitorum Extends the medial four digits Extensor Carpi Radialis Brevis Extends and abducts the wrist Extensor Pollicis Brevis Extends the proximal phalanx of the thumb Extensor Pollicis Longus Extends the distal phalanx of the thumb Extensor Indicis Proprius Extends the index finger independently These muscles play critical roles in dexterity, grip strength, and coordinated finger movements. Their severance results in significant functional impairment of the hand and wrist. Impact of Impaired Pronation 2. If the patient were no longer able to properly pronate his arm, which muscle do you think has been compromised? The inability to pronate the forearm—rotating the palm downward—is typically due to damage or dysfunction in the pronator teres and pronator quadratus muscles. These two muscles are chiefly responsible for the pronation movement of the forearm. Injury to either or both of these muscles, or their innervating nerves (particularly the median nerve), can impair this movement. Replantation Time Frame and Tissue Metabolism 3. Why does a severed limb have a smaller window of time for replantation compared to fingers? What does this imply about the metabolic demands of muscles, cartilage, and bone? Severed limbs require more urgent replantation compared to fingers due to the greater metabolic demands and complex tissue composition in larger body parts. Limbs have a higher concentration of vascularized muscle tissue, which is highly sensitive to ischemia (oxygen deprivation). Without oxygen, muscle tissues can begin to undergo necrosis within 6 hours, whereas cartilage and bone are more resilient due to their lower metabolic rate. BIOS 252 Week 1 Case Study: Muscle This suggests the following relative metabolic demands: Tissue Type Metabolic Demand Reason Muscle High Highly vascularized; oxygen-dependent; susceptible to ischemia Cartilage Low Avascular; relies on diffusion; survives longer without oxygen Bone Moderate Vascularized but more durable; less sensitive to ischemia The greater surface area, muscle mass, and complex vascular and neural networks in limbs increase the urgency for successful reattachment. In contrast, fingers contain fewer muscles and less vascular tissue, providing a slightly longer window for replantation. Muscle Healing and Tissue Bridging 4. What tissue type can be found bridging the two halves of the once-severed muscle bellies? Why? Following a muscle severance, connective tissue—particularly scar tissue and fibrous connective tissue—forms a bridge between the separated muscle bellies. While ligaments connect bones to other bones, the actual tissue that helps in muscle repair is fibrous scar tissue that fills in the gap created during trauma. Muscle regeneration occurs through hypertrophy and, to a lesser extent, hyperplasia. In healing, hypertrophy is more typical, with satellite cells (muscle stem cells) activating to repair or replace damaged fibers. However, the bridging tissue itself is often not functional muscle but a combination of collagen-based scar tissue and limited muscle regeneration, affecting long-term function unless surgical intervention (e.g., grafting) is performed. References Leversedge, F. J. (2018, April). Wrist Sprains. OrthoInfo. Retrieved from https://orthoinfo.aaos.org/en/diseases–conditions/wrist-sprains BIOS 252 Week 1 Case Study: Muscle Luna, D. (2021, March 22). Muscle Hypertrophy vs Hyperplasia: The Difference Explained. Inspire Us Foundation. Retrieved from https://www.inspireusafoundation.org/muscle-hypertrophy-vs-hyperplasia/