CHSO 404 EXAM 3 QUESTIONS
WITH ALL CORRECT ANSWERS
common skeletal muscle disorders - Answer--alteration of nerve supply or conduction
-denervation atrophy
-myasthenia gravis
-periodic paralysis
-defect in muscle structure
-muscular dystrophy
-trauma
-myoglobinuria
-energy utilization
-McArdle's disease
myasthenia gravis - Answer--autoimmune disease that causes neuromuscular deficits,
including weakness and fatigue
-caused by antibodies that block the nicotinic receptors in the NMJ and prevent
excitation of muscle fibers
-antibodies prevent acetylcholine from interacting with nicotinic receptors, initiate
inflammatory processes that alter the motor end plate, and compromise nicotinic
receptor availability
-antibody actions
-block nicotinic receptors
-promote destruction of nicotinic receptors
-induce endocytosis to reduce number of receptors on motor end plate
effects of myasthenia gravis - Answer--reduces or blocks excitation-contraction coupling
at NMJ, which compromises ability of skeletal muscle to contract and maintain
contraction
-muscles become fatigued, becoming progressively weaker during contraction and
improving after rest
-muscles that are typically affected control
-eye movement
-chewing, talking, and swallowing
-respiration
-limb movement
,susceptibility to myasthenia gravis - Answer--patients with specific HLA types (B8, DR3,
DR1)
-75% of patients have abnormality of thymus
-10% of patients have a thymoma
-associated autoimmune diseases
-type 1 DM, hashimotos, graves, RA, lupus
treatment of myasthenia gravis - Answer--immunosuppressive agents to reduce
autoimmune response
-acetylcholinesterase inhibitors to block destruction of acetylcholine and make it
available for longer time at the NMJ
-thymectomy to reduce release of T cells that promote production of autoantibodies
primary hyperkalemic periodic paralysis - Answer--hyperkalemia - increased K in blood
-autosomal dominant genetic disorder affecting sodium channels in muscle cells
-affects ability to regular K levels in the blood
-defect in SCN4A gene that encodes voltage-gated sodium channel in the NMJ
-sodium enters voltage-gated channels in NMJ and depolarizes muscle fiber
-mutations result in failure to inactivate channels, which prevents K efflux and
repolarization
-muscle fibers cannot relax; new signals have no effect, resulting in paralysis
-triggers - rest after exercise, K rich foods, stress, fatigue, fasting
-tx - glucose or other carbohydrates, and avoiding unknown triggers
muscular dystrophy - Answer--group of genetically caused myopathies with progressive
degeneration of skeletal muscle fibers
-duchenne muscular dystrophy most common and most severe
-X-linked trait, so affects only males
-gene for dystrophin absent or nonfunctional
-dystrophin protein found within muscle fibers, provides mechanical stabilization and
regulates calcium levels in muscle fiber
-disease begins at birth, apparent by age 3
-calf muscles are enlarged because of fat cell infiltration and degeneration of muscle
fibers
-cardiac failure or pulmonary infection causes death
rhabdomyolysis - Answer--acute muscle destruction often associated with
myoglobinuria
-commonly caused by extensive trauma with crush injuries
-can be life threatening complication of severe trauma
-nontraumatic causes
-increased muscle o2 consumption (heat stroke, severe exercise, seizures)
-decreased muscle energy production (hypokalemia, hypophosphatemia, genetic
enzymatic deficiencies)
-muscle ischemia (arterial insufficiency, drug overdose with coma and muscle
compression)
, -infections (influenza, Legionnaires disease)
-direct toxins (alcohol)
-excessive myoglobin excretion damages renal tubules
-leads to ATN
-can lead to kidney failure
-creatinine kinase levels often elevated
myoglobinuria - Answer--presence of myoglobin in urine, typically associated with
rhabdomyolysis
-molecule in muscle fibers that binds o2
-found in urine after muscle cells damaged
-causes - viral infections, heat stroke, electrolyte disturbances, McArdle's disease,
malignant hyperthermia
fibromyalgia - Answer--poorly characterized chronic disorder associated with -
generalized pain, stiffness, dysfunctional sleep, fatigability
-chronic pain in muscles and surrounding structures
-does not appear to be an inflammatory process
-etiology unknown but believed to involve psychological, genetic, neurobiological, and
environmental factors
-frequent comorbidity of depression, anxiety, PTSD
-tx focuses on alleviating symptoms
-medications include SSRI and paroxetine (Paxil)
glycogen storage disorders - Answer--group of defects in processing, synthesis, or
breakdown of glycogen
-glycogen usually stored in liver and skeletal muscle for energy
-inherited disorders
McArdle's disease - Answer--defect in muscle glycogen phosphorylase
-muscle energy disorder characterized by muscle pain, exercise intolerance,
myoglobinuria, susceptibility to fatigue
Cori disease - Answer--defect in glycogen debranching enzyme
-progressive skeletal weakness and atrophy and/or cardiomyopathy
Von Gierke's disease - Answer--defect in glucose-6-phosphatase
-causes growth failure and lactic acidosis
structure of a long bone - Answer--the diaphysis is the bone shaft providing most of the
length of the bone
-the epiphysis are the ends of the bone
-long bones contain a cavity filled with adipose cells
-called yellow marrow or medullary cavity in adults
-called red marrow or hematopoietic tissue in infants
-red marrow is confined to cavities of spongy bone within flat bones in adults
, -the epiphyseal plate is a flat plate of hyaline cartilage in young growing bone
-it causes lengthwise growth of long bone
-it is replaced by bone at the end of puberty
- adult bone contains epiphyseal line, a remnant of the epiphyseal plate
microscopic anatomy of bone - Answer--osteocytes - mature bone cells located within
lacunae
-osteoblasts - bone building cells
-osteoclasts - bone chewing cells
-lacunae are arranged in concentric circles called lamellae around central Haversian
canals
-each complex consisting of central canal and matrix rings is called an osteon or
Haversian system
bone formation, growth, remodeling - Answer--process controlled by hormones (growth
hormone and sex hormones)
-bone is a dynamic and active tissue
-responds to calcium levels and stress
-low calcium stimulates PTH
-PTH stimulates osteoclasts that break down bone to release calcium into the plasma
joints - Answer--bones form joints (articulations) with other bones
-joints hold bones together and give the rigid skeleton mobility
-structural classification
-fibrous joints are composed of fibrous tissue (collagen)
-cartilaginous joints are composed of cartilage, and bone ends are united by cartilage
-synovial joints are more flexible than other joints and re characterized by articulating
bones, which are separated by a fluid containing joint cavity
synovial joints - Answer--articular (hyaline) cartilage covers the ends of bones, forming
the joint
-joint (synovial) cavity with small amount of synovial fluid
-the articular capsule encloses joint cavity containing synovial fluid
-synovial fluid present within all free spaces within the joint capsule
-reinforcing ligaments strengthen the fibrous capsule
bone fracture - Answer--bone breaks
-types of fracture - simple, compound, comminuted, compression, depressed, impacted,
spiral, greenstick
-treated by reduction - realignment of broken bone ends (closed or open)
-simple fracture can repair in approx 8 weeks
simple fracture - Answer--bone broken cleanly and ends do not penetrate skin
-closed fracture
WITH ALL CORRECT ANSWERS
common skeletal muscle disorders - Answer--alteration of nerve supply or conduction
-denervation atrophy
-myasthenia gravis
-periodic paralysis
-defect in muscle structure
-muscular dystrophy
-trauma
-myoglobinuria
-energy utilization
-McArdle's disease
myasthenia gravis - Answer--autoimmune disease that causes neuromuscular deficits,
including weakness and fatigue
-caused by antibodies that block the nicotinic receptors in the NMJ and prevent
excitation of muscle fibers
-antibodies prevent acetylcholine from interacting with nicotinic receptors, initiate
inflammatory processes that alter the motor end plate, and compromise nicotinic
receptor availability
-antibody actions
-block nicotinic receptors
-promote destruction of nicotinic receptors
-induce endocytosis to reduce number of receptors on motor end plate
effects of myasthenia gravis - Answer--reduces or blocks excitation-contraction coupling
at NMJ, which compromises ability of skeletal muscle to contract and maintain
contraction
-muscles become fatigued, becoming progressively weaker during contraction and
improving after rest
-muscles that are typically affected control
-eye movement
-chewing, talking, and swallowing
-respiration
-limb movement
,susceptibility to myasthenia gravis - Answer--patients with specific HLA types (B8, DR3,
DR1)
-75% of patients have abnormality of thymus
-10% of patients have a thymoma
-associated autoimmune diseases
-type 1 DM, hashimotos, graves, RA, lupus
treatment of myasthenia gravis - Answer--immunosuppressive agents to reduce
autoimmune response
-acetylcholinesterase inhibitors to block destruction of acetylcholine and make it
available for longer time at the NMJ
-thymectomy to reduce release of T cells that promote production of autoantibodies
primary hyperkalemic periodic paralysis - Answer--hyperkalemia - increased K in blood
-autosomal dominant genetic disorder affecting sodium channels in muscle cells
-affects ability to regular K levels in the blood
-defect in SCN4A gene that encodes voltage-gated sodium channel in the NMJ
-sodium enters voltage-gated channels in NMJ and depolarizes muscle fiber
-mutations result in failure to inactivate channels, which prevents K efflux and
repolarization
-muscle fibers cannot relax; new signals have no effect, resulting in paralysis
-triggers - rest after exercise, K rich foods, stress, fatigue, fasting
-tx - glucose or other carbohydrates, and avoiding unknown triggers
muscular dystrophy - Answer--group of genetically caused myopathies with progressive
degeneration of skeletal muscle fibers
-duchenne muscular dystrophy most common and most severe
-X-linked trait, so affects only males
-gene for dystrophin absent or nonfunctional
-dystrophin protein found within muscle fibers, provides mechanical stabilization and
regulates calcium levels in muscle fiber
-disease begins at birth, apparent by age 3
-calf muscles are enlarged because of fat cell infiltration and degeneration of muscle
fibers
-cardiac failure or pulmonary infection causes death
rhabdomyolysis - Answer--acute muscle destruction often associated with
myoglobinuria
-commonly caused by extensive trauma with crush injuries
-can be life threatening complication of severe trauma
-nontraumatic causes
-increased muscle o2 consumption (heat stroke, severe exercise, seizures)
-decreased muscle energy production (hypokalemia, hypophosphatemia, genetic
enzymatic deficiencies)
-muscle ischemia (arterial insufficiency, drug overdose with coma and muscle
compression)
, -infections (influenza, Legionnaires disease)
-direct toxins (alcohol)
-excessive myoglobin excretion damages renal tubules
-leads to ATN
-can lead to kidney failure
-creatinine kinase levels often elevated
myoglobinuria - Answer--presence of myoglobin in urine, typically associated with
rhabdomyolysis
-molecule in muscle fibers that binds o2
-found in urine after muscle cells damaged
-causes - viral infections, heat stroke, electrolyte disturbances, McArdle's disease,
malignant hyperthermia
fibromyalgia - Answer--poorly characterized chronic disorder associated with -
generalized pain, stiffness, dysfunctional sleep, fatigability
-chronic pain in muscles and surrounding structures
-does not appear to be an inflammatory process
-etiology unknown but believed to involve psychological, genetic, neurobiological, and
environmental factors
-frequent comorbidity of depression, anxiety, PTSD
-tx focuses on alleviating symptoms
-medications include SSRI and paroxetine (Paxil)
glycogen storage disorders - Answer--group of defects in processing, synthesis, or
breakdown of glycogen
-glycogen usually stored in liver and skeletal muscle for energy
-inherited disorders
McArdle's disease - Answer--defect in muscle glycogen phosphorylase
-muscle energy disorder characterized by muscle pain, exercise intolerance,
myoglobinuria, susceptibility to fatigue
Cori disease - Answer--defect in glycogen debranching enzyme
-progressive skeletal weakness and atrophy and/or cardiomyopathy
Von Gierke's disease - Answer--defect in glucose-6-phosphatase
-causes growth failure and lactic acidosis
structure of a long bone - Answer--the diaphysis is the bone shaft providing most of the
length of the bone
-the epiphysis are the ends of the bone
-long bones contain a cavity filled with adipose cells
-called yellow marrow or medullary cavity in adults
-called red marrow or hematopoietic tissue in infants
-red marrow is confined to cavities of spongy bone within flat bones in adults
, -the epiphyseal plate is a flat plate of hyaline cartilage in young growing bone
-it causes lengthwise growth of long bone
-it is replaced by bone at the end of puberty
- adult bone contains epiphyseal line, a remnant of the epiphyseal plate
microscopic anatomy of bone - Answer--osteocytes - mature bone cells located within
lacunae
-osteoblasts - bone building cells
-osteoclasts - bone chewing cells
-lacunae are arranged in concentric circles called lamellae around central Haversian
canals
-each complex consisting of central canal and matrix rings is called an osteon or
Haversian system
bone formation, growth, remodeling - Answer--process controlled by hormones (growth
hormone and sex hormones)
-bone is a dynamic and active tissue
-responds to calcium levels and stress
-low calcium stimulates PTH
-PTH stimulates osteoclasts that break down bone to release calcium into the plasma
joints - Answer--bones form joints (articulations) with other bones
-joints hold bones together and give the rigid skeleton mobility
-structural classification
-fibrous joints are composed of fibrous tissue (collagen)
-cartilaginous joints are composed of cartilage, and bone ends are united by cartilage
-synovial joints are more flexible than other joints and re characterized by articulating
bones, which are separated by a fluid containing joint cavity
synovial joints - Answer--articular (hyaline) cartilage covers the ends of bones, forming
the joint
-joint (synovial) cavity with small amount of synovial fluid
-the articular capsule encloses joint cavity containing synovial fluid
-synovial fluid present within all free spaces within the joint capsule
-reinforcing ligaments strengthen the fibrous capsule
bone fracture - Answer--bone breaks
-types of fracture - simple, compound, comminuted, compression, depressed, impacted,
spiral, greenstick
-treated by reduction - realignment of broken bone ends (closed or open)
-simple fracture can repair in approx 8 weeks
simple fracture - Answer--bone broken cleanly and ends do not penetrate skin
-closed fracture
