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CHAPTER 46 MED SURG QUIZLET for 27. Guillain-Barre Syndrome
CHAPTER 46 MED SURG QUIZLET for 27. Guillain-Barre Syndrome
CHAPTER 46 MED SURG QUIZLET for 27. Guillain-Barre Syndrome
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The syndrome was named after Georges Guillain and Jean Alexandre Barre in 1916, Guillain-Barre Syndrome is an autoimmune disease, activated by an infection, or surgery that causes the immune system to attack the lower motor neurons in the peripheral nervous system, but will gradually work its way distally to more proximal. “This syndrome can affect people in any age group and occurs in 1 in 100,000 of the population.” (Lescher, 2011). Guillain Barre Syndrome typically occurs following an infection. It is believed that respiratory, stomach, and intestinal infections are most likely to be a trigger for Guillain-Barre, such as, pneumonia, food poisoning, flu like symptoms, and in some circumstances can be caused after surgery. Although there …show more content…
seems to be a good understanding of Guillain-Barre, its cause is still widely unknown, but there are theories. One of the theories is that the immune system is tricked into attacking its own myelin sheath in the peripheral nervous system, which can cause disruption to the muscles contracting (Lescher, 2011). “Since GBS specifically attacks myelin, Guillain-Barre syndrome is characterized as an acute inflammatory demyelinating polyneuropathy (AIDP).” (Cameron, 2011) There are different types of Guillain-Barre Syndrome, but all occur with acute or subacute dysfunction in the peripheral nervous system. At about 4 weeks, the symptoms will be at their maximum deficit. (Cameron, 2011). While Guillain-Barre syndrome is a rapidly developing disease that can completely alter someone's life in a matter of days, a person suffering from Guillain-Barre is at their most vulnerable condition approximately three weeks after the onset of symptoms. Typically Guillain-Barre will affect the more distal limbs first, such as, the hands and feet and gradually work its way to the rest of the body. One of the first common signs is numbness, and shortly after tendon reflexes will be lost as well. Naturally this will result in paralysis of all the affected limbs, and can potentially lead to death if it reaches the lungs or the heart muscles (Schenkman, M. L., 2013). The etiology of Guillain-Barre is relatively unknown, and is similar to other demyelination diseases which makes diagnosing this syndrome complicated; however, the rapid onset of symptoms can be a good indicator to the disease.
A good test for confirming Guillain-Barre is the nerve conduction test. If there is a sign of demyelination this test will show that the nerve impulse will take a longer time to contract the muscle. Another test for confirming Guillain-Barre would be testing the blood for cortisol. It has shown that patients with Guillain-Barre will have higher levels of cortisol in their plasma (Lescher, 2011). Efferent paralysis is more prevalent than afferent loss; however, in most variations of Guillain-Barre, sensory deficits will occur on both sides, symmetrically. As stated before, it is more severe in hands and feet; this is commonly stated as, glove-and-stocking sensory loss. “This distal pattern of sensory loss is caused by axonal transport, or the dying-back phenomenon, wherein the parts of the axon most affected are those most remote from the cell bodies in the dorsal root ganglia." (Schenkman, M. L., …show more content…
2013). Although there are no known cures for Guillain-Barre, treatment will be more focused on the symptoms to recover. Some of the medical procedures that can be done include plasmapheresis, supportive care, and intravenous immunoglobulin. The medical procedure plasmapheresis is where the blood it taken out of the patient, plasma is removed and the blood is then returned to the patient, the body will produce more plasma to make up for the discrepancy. Another procedure is intravenous immunoglobulin. Intravenous Therapy normally is the favored method for treatment; this process is done by injecting antibodies that help stabilize the patient’s autoantibody. (Bowyer, H. R. & Glover, M, 2010) Physical Therapy with Guillain-Barre Syndrome is substantial and is one of the key reasons why patients will recover quicker after symptoms have subsided. While these interventions will not treat the syndrome itself, it will help the patient to become more comfortable and is more focused in supportive care. Patients will generally work through passive and active range of motion exercises, as this will also help recuperation time once symptoms begin to withdraw (Lescher, 2011). If Guillain-Barre reaches the respiratory system, it will be imperative for respiratory physical therapy, and monitoring lung function and strength. In certain circumstances an autonomic dysfunction can occur, it will be essential to monitor basic vital signs (Bowyer, H. R., & Glover, M., 2010). In such a case, mechanical ventilation may be required. (Dennis, D., & Mullins, R., 2013). Because of the motor loss and paralyzing affects of Guillain-Barre it will be critical to instruct family and health care providers on checking the skin for sores and pressure ulcers. Having the patient do range of motion exercises, as well as weight shifting techniques, will help limit the chance of pressure ulcers and help avert any type of joint contracture that may occur. Typically Rehabilitation and physical therapy can greatly affect the improvement of muscle strength and recovery after symptoms have subsided. "One study showed rapid increase in muscle strength during the first 6 months after onset, with continuing gradual improvement of strength even after 12 months. Intensive therapy after discharge from an acute care facility is essential for improving function." (Bowyer, H. R., & Glover, M., 2010). Working on ADL’s will also be key contributor to successful rehabilitation, working on fine motor skills and being able to do everyday tasks will help with recovery time. Another form of therapy that has been shown to be advantageous is Hydrotherapy, because of the zero gravity; patients will be able to improve their range of motion and muscle strength, without much impact and energy expenditure. Limiting energy expenditure will be a key factor with physical therapy. Fatigue with Guillain-Barre is unrelated to age, how long it has occurred, or even how sever the symptoms are, approximately 80% will suffer from sever fatigue. (Sharma, V., Kaur, H., Malhotra, L. K., & Sairam, N., 2015). In such circumstances, physical therapy would also include education on assistive devices. Depending on how affected they are some of the education and training could be on proper gait techniques with walkers, canes or crutches, and utilization of a wheelchair. In such instances patients would progress through treatment, slowly making balance and gait training more complex until they return to normal function. Prognosis is typically good; although some of the symptoms can be very severe the recovery period may be as little as a few weeks, or as long as a few years. A small amount of patients will experience a relapse of muscle weakness and tingling (NINDS). It will also depend on the severity of the affected limbs, and if it has reached respiratory, or cardiac muscles. Overall, Guillain-Barre Syndrome is a very scary disease because of the rapid onset of symptoms, taking anywhere from a few days to a week, attacking the LMN and working its way distally to more proximally.
While Guillain-Barre etiology is rather unknown, scientist are looking for answers on why and how Guillain-Barre occurs as well as focusing on finding new treatments and further developing the existing treatments. “The fact that so many cases of Guillain-Barre begin after a viral or bacterial infection suggests that certain characteristics of some viruses and bacteria may activate the immune system inappropriately.” (NINDS). Proper treatment is done so by plasmapheresis, or intravenous immunoglobulin, and after symptoms begin to subside, medical and physical therapy interventions have shown to greatly aid in recovery, and with proper supportive care, typically in about a year, patients will be able to return to a normal
life.
It was the beginning of February when my grandfather was going in to receive his second knee replacement. Being his second time, we were optimistic that the surgery would go well and that he would recover without any issues. My grandfather made it through surgery and accordingly, had to stay for observation. During this time everything appeared to be normal, and knowing that my grandfather hates to be in hospitals, wouldn’t have said otherwise. When he was finally discharged, we took him home and the next day he appeared to have a stroke. The left side of his face had drooped down and he began feeling numbness and tingling on both sides of his body. We immediately rushed him to the hospital and at first it was assumed it was a stroke, but as his illness progressed it was apparent it was not. The numbness soon led to the loss of muscle control beginning at his legs and rapidly spreading up. My grandfather was able to specifically describe what he was experiencing and the doctor was able to diagnose him with Guillain- Barré syndrome.
Andrew Suy Professor Owens History 1302 13 April 2016 Polio: An American Story Polio, formerly known as poliomyelitis, an infectious viral disease that affects the central nervous system and can cause temporary or permanent paralysis. A debilitating disease that was once the affliction of our very own republic. David Oshinsky’s Polio: An American Story chronicles polio’s progression in the United States, a feat it does quite well throughout the course of the novel.
Flaccid dysarthria results from damage to the lower motor neurons (LMN) or the peripheral nervous system (Hageman, 1997). The characteristics of flaccid dysarthria generally reflect damage to cranial nerves with motor speech functions (e.g., cranial nerves IX, X, XI and XII) (Seikel, King & Drumright, 2010). Lower motor neurons connect the central nervous system to the muscle fibers; from the brainstem to the cranial nerves with motor function, or from the anterior horns of grey matter to the spinal nerves (Murdoch, 1998). If there are lesions to spinal nerves and the cranial nerves with motor speech functions, it is indicative of a lower motor neuron lesion and flaccid dysarthria. Damage to lower motor neurons that supply the speech muscles is also known as bulbar palsy (Pena-Brooks & Hedge, 2007). Potential etiologies of flaccid dysarthria include spinal cord injury, cerebrovascular accidents, tumors or traumatic brain injury (Pena-Brooks & Hedge, 2007). Possible congenital etiologies of flaccid dysarthria include Moebius syndrome and cerebral palsy. Flaccid dysarthria can also arise from infections such as polio, herpes zoster, and secondary infections to AIDS (Pena-Brooks & Hedge, 2007). Additionally, demyelinating diseases such as Guilian-Barre syndrome and myotonic muscular dystrophy can also lead to flaccid dysarthria (Pena-Brookes & Hedge, 2007). The lower motor neuron lesion results in loss of voluntary muscle control, and an inability to maintain muscle tone. Fasciculations, or twitching movements, may occur if the cell body is involved in the lesion (Seikel et. al., 2010). The primary speech characteristics of flaccid dysarthria include imprecise consonant production, hypernasal resonance, breathiness, and harsh voice (...
Lou Gehrig's disease is often referred to as Amyotrophic lateral sclerosis (ALS), this is a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord. Motor neurons come from the brain to the spinal cord and from the spinal cord to the muscles throughout the entire body. The progressive degeneration of the motor neurons in ALS would eventually leads to their death. When the motor neurons die, the ability of the brain to initiate and control muscle movement is also lost. With voluntary muscle action progressively affected, for this reason patients in the later stages of the disease may become totally paralyzed (Choi, 1988).
Poliomyelitis was the term used by doctors to describe the condition in which the gray (polios) anterior matter of the spinal chord (myelos) was inflamed (-itis). Until a cure was discovered, no one had the slightest idea where "polio" had come from or why it paralyzed so many children. People learned later that, oddly enough, it was the improved sanitary conditions which caused children to be attacked by the virus. Since people were no longer in contact with open sewers and other unsanitary conditions which had exposed them to small amounts of the polio virus as infants, when paralysis is rare, the dis...
Most cases of mono resolve without complication, but some rarely occur. Complications are tonsillar enlargement, which can cause respiratory obstruction; rupture of spleen; encephalitis, an infection of the brain tissue; Galen-Barer syndrome, a progressive and sequential worsening syndrome of weakness and paralysis; hemolytic anemia, the red blood cells are destroyed; uvetis, an eye involvement; myocarditis, an inflammation of heart muscle; pneumonia; hephritis, a kidney infection; and Reye’s syndrome; a severe neurological syndrome.
(Marieb, 2016). Myelin is the protective coat surrounding and insulating the nerve fibers of CNS. Myelin is fatty tissue substance that if attacked by immune cells causing a short-circuits in the current so that the successive gaps are excited more and more slowly, and eventually impulse conduction ceases which resulted in various forms of symptoms (Marieb, 2016). The degradation could either be “by inflammation, stroke, immune disorder, metabolic disorders, or nutritional deficiencies” (Slomski, 2005). The target that immune cells are sensitized to attack remains
... damaged neurons. (Mayo clinic, 2014). This is called neuroplasticity, the ability for the nerves to compensate for damage caused by some outside force. Because of neuroplasticity physical training works to cure some of the paralysis left by the virus and allows us to walk again after the legs or another appendage is deformed or damaged.
It is also estimated that approximately two and half million people are living with the disease... The name multiple sclerosis refers to the scars that are present in the brain and spinal cord is seen on an MRI. An autoimmune disorder is where a person’s immune system mistakes its own white blood cells as invaders and begins to attack itself damaging healthy body tissue. In these types of disorders, the immune system cannot tell the difference between healthy cells and antigens, which are foreign invaders like bacteria and viruses. Because of the damage, it does to the nerve cells; nerve signals can either slow down or stop completely. Inflammation, or the body’s reaction to infection, is what causes this nerve damage to happen. Multiple sclerosis is most commonly seen in the brain, optic nerve, and spinal cord and often leads to physical and cognitive
Multiple sclerosis was first discovered in 1868 by a neurologist by the name of Jean Martin- Charcot. Multiple sclerosis receives its name from the distinctive areas of scar tissue with the formation of damaged myelin sheaths. Multiple Sclerosis is referred to as an immune- mediated response that targets the central nervous system, including the spinal cord, the brain, and other parts of the body. The central nervous system is usually targeted by an abnormal response to the human body’s immune system causing an attack on the myelin coated fibers around nerve fibers. Generally, this occurs due to inflammation of myelin in the brain, causing lesions or plaques to form. Since myelin sheaths in the nervous system are there to increase nerve impulses,
Guillain- Barre Syndrome (GBS) is a rare, but very fatal auto- immune disease that specifically focuses on attacking the myelin sheath that surrounds the peripheral nerves in the human body. There are many different severities of this disease, but without treatment it can not only affect the entire nervous system but eventually shut down the rest of the body.
The most common type is Peripheral Neuropathy. It is also referred to as distal symmetric neuropathy or sensorimotor neuropathy. In this type, the legs, feet, toes, arms, and hands experience pain and loss of sensation. Typically, the lower extremities are involved before the upper extremities and a loss of reflexes is common. It is with this type of neuropathy that ulcers, wounds, infections, and in severe cases, amputation is most common (Dyck, Feldmen, & Vinick).
Paramedics are frequently presented with neurological emergencies in the pre-hospital environment. Neurological emergencies include conditions such as, strokes, head or spinal injuries. To ensure the effective management of neurological emergencies an appropriate and timely neurological assessment is essential. Several factors are associated with the effectiveness and appropriateness of neurological assessments within the pre-hospital setting. Some examples include, variable clinical presentations, difficulty undertaking investigations, and the requirement for rapid management and transportation decisions (Lima & Maranhão-Filho, 2012; Middleton et al., 2012; Minardi & Crocco, 2009; Stocchetti et al., 2004; Yanagawa & Miyawaki, 2012). Through a review of current literature, the applicability and transferability of a neurological assessment within the pre-hospital clinical environment is critiqued. Blumenfeld (2010) describes the neurological assessment as an important analytical tool that evaluates the functionality of an individual’s nervous system. Blumenfeld (2010) dissected and evaluated the neurological assessment into six functional components, mental status, cranial nerves, motor exam, reflexes, co-ordination and gait, and a sensory examination.
This is a neurodegenerative disease, meaning it results in progressive loss or death of neurons. It often starts off with effecting simple motor skills like writing and holding things, after a few months usually patients start losing the ability to walk, talk, or move any of their limbs. Although the brain trauma is what causes it, ALS has little-no-effect on the brain. This fatal disease is typically diagnosed around age 60 and most patients are given about 3-5 years to live after being diagnosed. It has been found that 10% of cases are shown as genetic. It was brought to attention that athletes were beginning to get diagnosed with ALS at a younger age than most. After extensive research in the early 2000’s, Brain Analyst, Dr. Mckee ran tests and finally came to the conclusion that the toxic proteins in the brains of ALS patients were coming from repeated blows to the head. It was then made evident why so many athletes in contact sports such as football, soccer, boxing, etc… were being diagnosed at such a young age and more frequently than
The patient has experienced fever, chills on body, headaches and anorexia as well as sweating especially during the night. The patient has also been feeling fatigued, muscle aches and nausea as well as vomiting especially after eating (WHO, 2010, p. 117). These symptoms started forty eight hours ago, and the patient has not taken any medication except for some aspirin.