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Case Study Dan Nadeau, Kjetil Rossignol, Ben Wyman, Alex Maroun Part I 1.

What vital signs or symptoms does Annie exhibit and can you see any common features in Annies signs and symptoms Annie is showing symptoms of muscle fatigue, and a decline in physical performance !he is experiencing "lurred #ision, eye strain, lac$ of "reath, aching fingers, and constant fatigue that all seem to "e related to s$eletal muscles %er symptoms of eye strain and "lurred #ision could "e attri"uted to optic ner#e damage as the primary sensory ner#e of #ision &'( !. What muscles are responsible for breathing and "hy is Annie having problems breathing )he muscles that are responsi"le for "reathing are the internal intercostals which aid acti#e expiration, the external intercostals which aid in inspiration, and the diaphragm which is the prime mo#er of inspiration )he reason Annie is ha#ing trou"le "reathing is "ecause these s$eletal muscles responsi"le for "reathing are affected "y the disease myasthenia gra#is which compromises their use )his disease in#ol#es a shortage of Ach receptors, which interferes with the process of e#ents at the neuromuscular junction the result is inferiority within the effected muscles as less Ach can "ind to receptors and allow an end plate potential to "e cataly*ed &'( #. In addition to the muscular disorder $yasthenia %ravis& "hat are other possible reasons for Annies condition Annie could "e experiencing pro"lems with her ner#es +f the ner#e impulse is not reaching the neuromuscular junction, acetylcholine &Ach( is not released and cannot "ind

to the sarcolemma to change its permea"ility and change mem"rane potential )he entire process of the neuromuscular junction would fail to initiate causing wea$ness and fatigue in her muscles Without this signal, depolari*ation of the muscle fi"er would not occur and contraction could not happen &'(

Part II 1. What ne"'additional signs or symptoms has Annie described to her doctor Annie now descri"es "eing excessi#ely tired and sleeps for extended periods of time !he has excessi#e shortness of "reath, and tells that her swimming times are getting slower !he complains of ha#ing eye,strain, "lurred #ision, and dou"le #ision, and has drooping eyelids %er hands and fingers get tired when typing on the computer, and has a lac$ of control &she couldn-t hold on to the car $eys( Annie also complains of "eing stressed out "ecause of school

!. (ra" a neuromuscular )unction and include the presynaptic terminal& synaptic cleft and motor end plate& then label all important structures& chemicals& ions and receptors. *Attached Page+ *$arieb& p. !,-+

#. .xplain ho" a decline in muscle function could contribute to eye strain and blurred vision Annie-s eye strain stems from focusing on her computer screen )he muscles responsi"le for focusing the eyes, the ciliary muscles, are relaxed when the eye is focusing on an o"ject off in the distance, and contract when focusing the eye on closer

o"jects less than six meters from the face &'( !ince Annie is ha#ing trou"le controlling her muscles, it would ma$e sense that the muscles of her eye would not "e a"le to contract and focus on the screen, causing Annie to ha#e "lurred #ision

Part III 1. What is a nerve conduction test and "hat do Annies normal results help to rule out A ner#e conduction test is a procedure where the speed of a ner#e.s reaction to an electrical impulse is tested at many different sites of the "ody )o conduct this test electrodes are placed at different points of the "ody and each gi#es off an electrical impulse which stimulates the ner#e at a certain site and this stimulation is recorded "y the other electrodes %er normal results rule out any suspicion of her ha#ing damaged or destroyed ner#es within her "ody +t shows that her ner#es are a"le to pass on stimulus, meaning there is another cause for her wea$ness

!. What is an .$% test and "as Annies s/eletal muscle function normal& and "hy did activity in Annies motor nerves produce a s/eletal muscle response that fatigued during repetitive stimulation An /lectromyography &/M0( is a test where thin needle electrodes are inserted into the muscles, and used to test the electrical acti#ity of one.s muscle When the muscle isn.t flexed there should "e little electrical acti#ity "ut as you contract the muscle harder and harder this acti#ity increases Annie.s s$eletal muscle function seemed fine until they used a repetiti#e stimulus test that showed increasing muscle fatigue as the test

continued Annie.s result is called decrement of the 1ompound Muscle Action 2otential &1MA2(, and this is caused "y too many anti"odies "inding to the muscle end plate mem"rane "loc$ing the "inding of A1h &acetylcholine( which causes the li$eliness of a muscles contraction to decrease

#. 0utline the se1uence of steps involved in the excitation portion of excitation2 contraction coupling of s/eletal muscle beginning "ith a nerve impulse and concluding "ith an action potential traveling do"n the t2tubules on the sarcolemma. )o "egin the se3uence an action potential tra#els down a motor neuron to the neuromuscular junction, which causes a release of A1h )he A1h released "inds to the nicotinic acetylcholine receptors on the opposite side of the junction, creating the depolari*ation of the neuron )he sum of all these minute #oltage changes create the large end 4plate potential which pushes the action potential 5inally the action potential tra#els down the entire muscle mem"rane and down the t tu"ules, which acti#ates the #oltage operated 1alcium channel &6(

3. 4o" ta/e each step in turn and discuss ho" sustained neural activity could create a problem and result in a decrease in muscle response during repetitive motor nerve stimulation *in both a healthy and unhealthy muscle+. +f a ner#e impulse is not released from the "rain it will not create an action potential to mo#e any muscles )he release of A1h is put into the synaptic cleft, without

this part of the process muscle contraction would not "e possi"le "ecause of a lac$ of generating an action potential 1alcium and acetylcholine is fused into the axon terminal

to "e released and open the channels to let in sodium and potassium to cause a muscle contraction +f ner#e impulses cease during this phase, the channels will "e open and muscle twitches may continue without reason otherwise $nown as 2ar$inson.s disease With the channels "eing opened "y A1h, )he swap of sodium in the system and potassium out causes the action potential +f there is no action potential that means there is no muscle twitch at threshold stimulus As the channels open, the sarcolemma

"ecomes less negati#e on the inside as the action potential mo#es down to the ),tu"ule With only little neural acti#ity the muscle will continue to experience small twitches until the acti#ity ceases &'(

Part I5 1.What is the role of the thymus in the body& and briefly& "hat are antibodies and "hat is an antigen )he thymus is in#ol#ed in the immune system function +t is located in the middle region of the chest )he role of the thymus in the "ody is processing a type of white "lood cell $nown as a ),lymphocyte ),lymphocytes control cellular immunity which means they help cells recogni*e and destroy in#ading "acteria, #irus, a"normal cell growth such as cancer, and foreign tissue An antigen is a su"stance that causes your immune system to produce anti"odies against it An antigen can "e a foreign su"stance from the en#ironment such as chemicals, "acteria, #iruses, or pollen An antigen may also "e formed within the "ody, as with "acterial toxins or tissue cells &7( Anti"odies are proteins that are used "y the immune system to identify and neutrali*e foreign o"jects such as "acteria and #iruses &7(

!. %o bac/ to the diagram and predict "here the antibodies in Annies blood could act to decrease synaptic function at the neuromuscular )unction. )he most li$ely scenario is that the anti"odies are at the presynaptic terminal Within the terminal, they are decreasing the rate of calcium "inding to release acetylcholine into the synaptic cleft to cause any type of action potential Multiple sclerosis is the decreased rate of muscular function and to pre#ent muscular mo#ement, you would need to "egin in the central ner#ous system or the axon terminal to pre#ent any channels from opening to release sodium and potassium

#. 4eostigmine is one pharmacological agent that may be prescribed for people "ith myasthenia gravis. 6his drug& li/e the endrophonium chloride in)ection& "ill ma/e Annie feel stronger. 7elated to the flo" diagram& determine ho" these drugs could "or/ to increase synaptic performance. Multiple sclerosis is not as 3ualified in this case as myasthenia gra#is which is the autoimmune disease that is affected in the postsynaptic mem"rane of the neuromuscular junction where acetylcholine isn.t "eing released to cause the channels to open and muscle twitch to happen Neostigmine is used in pediatric anesthesia practice to extend the length of time of action of caudal "loc$ with a local anesthetic agent &8( )hen endrophonium chloride "elongs to the group of medicines called anticholinestrase +t wor$s "y prolonging acetylcholine, which is found naturally in the "ody +t does this "y inhi"iting the action of the en*yme acetylcholinestrase )hese drugs will help at the neuromuscular junction le#el to increase performance "y ha#ing acetylcholine wor$ well

with the #oltage,gated channels and not ha#e any malfunctions within the synaptic cleft &8(

3. In the absence of treatment& "hat has happened to the amplitude of Annies endplate potentials as her disease has progressed 8 and "hat might be the outcome )here would "e decreased rapid firing without surgery to remo#e the tumor )he use of cold compresses such as a rag may help with muscle soreness and help to ha#e synapses fire in that region for a little while longer With Annie swimming for all this time and ignoring the symptoms until just recently, the antigens will attac$ the anti"odies with more precision until Annie will feel no muscle mo#ement and no action potential Acetylcholinestrase has "ound to the endplate of the sarcolemma and cause lac$ of sodium and potassium to go "eyond the gated channels +f Annie follows through with the surgery, she could "e cured and not ha#e to deal with any more of the muscle wea$ness and constant fatigue which will allow her to $eep swimming while hopefully maintaining the scholarship

References &'( Marie", /laine Nicpon 9 %oehn, Katja, &author ( 9 %utchinson, Matt, &author ( Human anatomy & physiology &:th edition( ;!an 5rancisco< 2earson /ducation=Benjamin 1ummings 7>'6 p 7?@,6A>, A:6, 7?B,7?? &7( CAnti"odyD Medline2lus Medical /ncyclopedia C U.S National Library of Medicine E ! National Fi"rary of Medicine, n d We" >7 No# 7>'6 &6( Ke#in !heth Medline 2lus ;Gnline< httpD==www nlm nih go#=medlineplus=ency=article=>>6:7B htm ;@='?=7>''< &A( Da#id 1 Dugdale Medline 2lus ;Gnline< httpD==www nlm nih go#=medlineplus=ency=article=>>6:6B htm ;?=7B=7>'>< &8( Hale !chool of Medicine Neurology ;Gnline< medicine yale edu=neurology=di#isions=neuromuscular=mg aspx ;7>'6< &@( DeiI, M C)reating Multiple !clerosis with Monoclonal Anti"odies C NCBI E ! National Fi"rary of Medicine, n d We" >6 No# 7>'6