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Body system myasthenia gravis effects
Body system myasthenia gravis effects
Body system myasthenia gravis effects
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oretta Parker
Bios 487
Extra Credit Assignment 2
Based on the apparent symptoms of the elderly patient consisting of muscle weakness and a drooping of the eyelids, it appears that the cause of illness is myasthenia gravis, a condition that weakens the voluntary muscles of the body. The cause of this eyelid drooping, or muscle paralysis in general, is due to a misstep in the flow from the nerve fiber to the muscle fiber. It is known that an action potential in the muscle fiber is required for muscle contraction. However, if the release acetylcholine is blocked, or the number of acetylcholine receptors is reduced, it causes a chain of events that prevent muscle contraction. This prevention of the binding of acetylcholine to the receptor prevents
In the beginning phases of muscle contraction, a “cocked” motor neuron in the spinal cord is activated to form a neuromuscular junction with each muscle fiber when it begins branching out to each cell. An action potential is passed down the nerve, releasing calcium, which simultaneously stimulates the release of acetylcholine onto the sarcolemma. As long as calcium and ATP are present, the contraction will continue. Acetylcholine then initiates the resting potential’s change under the motor end plate, stimulates the action potential, and passes along both directions on the surface of the muscle fiber. Sodium ions rush into the cell through the open channels to depolarize the sarcolemma. The depolarization spreads. The potassium channels open while the sodium channels close off, which repolarizes the entire cell. The action potential is dispersed throughout the cell through the transverse tubule, causing the sarcoplasmic reticulum to release
...st the sacrolemma will depolarized, thus activation potentials along the T-tubules. This signal will transmit from along the T-tubules to sarcroplasmic reticulum's terminal sacs. Next, sarcoplasmic reticulum will release the calcium into the sarcroplasm leading to the next second event called contraction. The released calcium ions will now bind to troponin. This will cause the inhibition of actin and mysoin interaction to be released. The crossbridge of myosin filaments that are attached to the actin filaments, thus causing tension to be exerted and the muscles will shorten by sliding filament mechanism. The last event is called Relaxation. After the sliding of the filament mechanism, the calcium will be slowly pumped back into the scaroplasmic reticulum. The crossbridges will detach from the filaments. The inhibition of the actin and myosin will go back to normal.
"Duchenne Muscular Dystrophy: MedlinePlus Medical Encyclopedia." U.S National Library of Medicine. U.S. National Library of Medicine. Web. 20 May 2014.
As motor neurons degenerate, this obviously means they can no longer send impulses to the muscle fibers that otherwise normally result in muscle movement. Early symptoms of ALS often include increasing muscle weakness, especially involving the arms and legs, speech, swallowing or breathing. When muscles no longer receive the messages from the motor neurons that they require to function, the muscles begin to atrophy (become smaller). Limbs begin to look thinner as muscle tissue atrophies (Choi, 1988).
Imagine you are in a boring lecture and you start to drift to sleep, usually you can manage to force yourself to wake up. This may be common occurrence but try to imagine falling asleep while driving or walking. These situations seem more rare. A narcoleptic’s body doesn’t care what it is doing when it goes into these paralyzed sleeping episodes. The sudden overwhelming feeling drives the narcoleptic person to fall asleep. One type of episode that they experience is called cataplexy, which is usually caused by some stressful situation or other common activities such as laughing or running (6). During these periods the person suffers from muscle weakness and paralysis. Although the person appears to be sleeping, they are still conscious, but unable to move. They can hear and feel but cannot react to stimulation. For this reason narcolepsy is a very dangerous condition to have without receiving treatment because serious vehicle accidents can result as well as an general inability to succeed in school (6).
For some types of MD, medication can help. Guys with Duchenne MD may be helped by a medicine called prednisone, and teens with myotonic MD might use mexilitine to relax muscles.
Bell’s palsy is the name given to a nerve disorder that results in unexpected paralysis of the face due to the facial nerve acting abnormally. Paralysis is commonly found only on one side of the face; however, it can occur on both sides. Bell's palsy is named for Sir Charles Bell, a 19th century Scottish surgeon who first came across the condition. (NINDS Bell's Palsy, sec. 1). In this paper, the pathophysiology, which is a discussion of the mechanism behind Bell’s Palsy will be discussed as well as causes and effects. Also, the clinical manifestations of this condition will be provided in order to pinpoint some key aspects of Bell’s Palsy. Finally, advances in medical management, in terms of prevention, treatment and current research will be discussed.
Bell’s Palsy, named after a Scottish anatomist named Charles Bell, is a form of facial paralysis in which one side of the face suddenly cannot be controlled through the normal facial muscles (1). One thing characteristic of the condition is its suddenness and apparent randomness – as with my mother, it can often come along in the middle of the night. Bell’s Palsy is idiopathic, meaning its general cause is unknown. In fact, another name for the disease is “idiopathic facial paralysis.” (2) (You can imagine my frustration at trying to research the known causes and then realizing that by definition it has none). A great deal of diseases may lead to facial paralysis, among them tumors and strokes, but when no preceding physiological disease or condition can be pinpointed, the diagnosis of Bell’s Palsy is given.
Multiple sclerosis (MS) is an acquired demyelinating disease of the central nervous system (CNS) that typically is diagnosed in the second or third decade of life. Normally, nerves are enclosed in myelin sheaths that help facilitate transmission of nerve impulses within the CNS and the peripheral nervous system throughout the body. In patients with MS, the myelin sheath is damaged and eventually degenerates, causing patches of scar tissue called plaques or lesions to occur anywhere randomly on the myelin sheath (Ruto, 2013). This results in impaired nerve conductivity, which interferes with message transmission between the brain and the other parts of the body. As a result, impulse transmission is altered, distorted, short-circuited, or completely absent. This interference in impulse transmission creates muscle weakness, muscle imbalance, and possibly muscle spasms with partial or complete paralysis. Multiple sclerosis also can result in visual impairment and alteration of cognitive abilities, as well as pain, numbness, or tingling sensations (Ruto, 2013).
As we age, we face a host of age related changes, like hearing impairments, visual changes, increased short-term memory loss, natural bone loss, and decreased mobility. Comorbidities also increase with age such, as arthritis, hypertension, and heart disease. Another prevalent and often disregarding age related occurrence are essential tremors (ET) also referred to as senile tremors, familial tremors, benign tremors, intentional and action tremor. Essential tremors are the most common place neurological disorder in older adults (Louis & Ferreira 2010). It is defined as involuntary rhythmic movements of any body part. Typically affecting the fingers, hands, and forearm, less commonly they may affect the head and legs. Movememnt can be fast or slow visible with rest, action or sustained posture (Abboud & Ahmed, 2011). Though this is a frequently occurring condition, it often misdiagnosed or underdiagnosed due to lack of admission by patient or clinician inability to recognize signs and symptoms.
In regards to business practices, incentives are common tool used in negotiations. With that being said, Intel, a technology conglomerate, gave huge incentives to its customers for using computer-chip. Many would argue that Intel was wrong, while others would say Intel business practices were fair game. Below is a detailed report, discussing Intel actions.
Treatment depends on signs and severity of disease. These treatments include artificial tears, surgery, glucocorticoids, immunomodulators and prisms. Artificial tears can be used for corneal exposure and associated dryness. In severe lid retraction, eyelid surgery can be considered. Orbital congestion and optic neuropathy can be treated by high dose glucocorticoids. Steroid-sparring agents and additional immunomodulators (cyclosporine, azathioprine) are also used. Sometimes, surgical decompression of the orbit is necessary to prevent severe exophthalmos and optic nerve compression. If patients have diplopia secondary to muscle enlargement and fibrosis, prisms and then strabismus surgery are needed after the inflammatory response is controlled. Eyelid surgery is suggested in patients that have severe exposure due to a fibrotic levator
Atropine is a non-selective muscarinic cholinergic antagonist and it functions by directly blocking the M3 receptor (Bhattacharjee et al., 2013). This is an example of pharmacological antagonism whereby atropine competitively inhibits Ach, antagonizing the action of Ach at postganglionic muscarinic sites (Bhattacharjee et al., 2013). The inhibition effect of atropine is concentration-dependent (Wali et al., 1987). In high concentrations, atropine reduces Ach-induced contractions by blocking ion channels present at the postsynaptic membrane of the smooth muscle cells (Wali et al., 1987).
1. What is a motherboard chipset and why is it important? The chipset defines many aspects of the motherboard. Tell me about what they do and what they control?
At Computers and more, we have reviewed almost every kind of product that Corsair offers except for the SSDs lineup. So this time Corsair has been generous enough to provide us with the Corsair Neutron GTX SSD for review. Now here I have the 480Gb variant for review, which is the largest capacity that is being offered by the company in the GTX series.