Biology
12th Edition
ISBN: 9780134813448
Author: Audesirk, Teresa, Gerald, Byers, Bruce E.
Publisher: Pearson,
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Chapter 41, Problem 2AC
Summary Introduction
To predict:
The symptoms of myasthenia gravis.
Introduction:
Myasthenia gravis is a neuromuscular disorder which causes weakness of skeletal muscle. It commonly affects muscles of eyes, face, and so on. This disorder occurs in a body when signals transmitted from nerve to muscle fiber are disrupted.
Summary Introduction
To explain: How neostigmine could help alleviate myasthenia gravis.
Introduction:
Myasthenia gravis is a neuromuscular disorder which causes weakness of skeletal muscle. It is a type of autoimmune disorder in which the immune system detects its own body cells as foreign cells and destroy them.
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A nerve conduction velocity test measures nerve conduction velocity. In this test, an electrical stimulus is applied to a peripheral nerve and the length of time it takes for the corresponding muscle to contract is measured. Because the length of the nerve from stimulus point to muscle and the time it takes for the muscle to contract are both known, NCV can be calculated.
This test result is helpful in distinguishing between different types of pathologies. For example, a patient with muscle weakness is being tested by a physician. There are three possible sources of the weakness:
Disease of the muscle itself such as muscular dystrophy. In this condition, normal muscle tissue is replaced by adipose tissue and the muscle becomes incapable of contraction.
Disease at the neuromuscular junction (NMJ) such as myasthenia gravis. This condition is described in the Skeletal Muscle Histology exercise and results from damage to the acetylcholine receptors on the muscle end plate.
Disease…
one treatment for myasthenia gravis is a medication that blocks the activity of acetylcholinesteras. suggest why this might be a succesful treatment
One treatment for myasthenia gravis is a medication that blocks the activity of acetylcholinesterase. Suggest why this might be a successful treatment.
Chapter 41 Solutions
Biology
Ch. 41.1 - Prob. 1TCCh. 41.1 - Prob. 2TCCh. 41.1 - Prob. 1CSCCh. 41.1 - White meat or dark? It seems almost everyone has a...Ch. 41.1 - Prob. 1CYLCh. 41.1 - Prob. 2CYLCh. 41.1 - Prob. 3CYLCh. 41.1 - explain how the nervous system causes contraction...Ch. 41.2 - describe the similarities and differences between...Ch. 41.2 - compare cardiac and smooth muscle to skeletal...
Ch. 41.3 - Why are thick, armor like exoskeletons found...Ch. 41.3 - Prob. 2TCCh. 41.3 - Prob. 3TCCh. 41.3 - Prob. 1CSCCh. 41.3 - Prob. 1CTCh. 41.3 - Prob. 1CYLCh. 41.3 - Prob. 2CYLCh. 41.3 - list and describe the functions of the different...Ch. 41.3 - explain how a bone fracture is repaired and how...Ch. 41.3 - Prob. 5CYLCh. 41 - Prob. 1MCCh. 41 - Prob. 2MCCh. 41 - Prob. 3MCCh. 41 - Prob. 4MCCh. 41 - Prob. 5MCCh. 41 - The three types of skeletal systems found in...Ch. 41 - Prob. 2FIBCh. 41 - A skeletal muscle cells is called a(n)__________....Ch. 41 - Prob. 4FIBCh. 41 - Prob. 5FIBCh. 41 - Prob. 6FIBCh. 41 - Prob. 7FIBCh. 41 - Sketch a relaxed muscle fiber containing a...Ch. 41 - Describe the process of skeletal muscle...Ch. 41 - Explain the following two statements: Muscles can...Ch. 41 - What are the three types of skeletons found in...Ch. 41 - Compare the structures of the following pairs:...Ch. 41 - Explain the functions of osteoblasts and...Ch. 41 - Describe a hinge joint and how it is moved by...Ch. 41 - Discuss some of the problems that would result. If...Ch. 41 - Prob. 2AC
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- One tretment for myasthenia gravis is a medication that blocks the activity of acetylcholinesterase. Why is this a successful treatment?arrow_forwardIn the rare neuromuscular disorder Myasthenia Gravis, autoantibodies are produced which inhibit acetylcholine receptor (nicotinic receptor) activity. Explain how inhibition of acetylcholine receptor activity at the neuromuscular junction will affect the sequence of events in muscular excitation and contraction in response to stimuli, and muscle function? (Mention the effects on all the significant events involved in excitation and contraction of muscles, and how it would affect muscle function).arrow_forwardWhen the neurotransmitter acetylcholine (ACh) binds the acetylcholine receptor (a GPCR) on muscle cells, it causes them to contract. ZIGGY, a chemical analog of ACh, also binds to the same acetylcholine receptor on muscle cells, but instead causes the muscle cells to relax. For this reason, it is sometimes prescribed as a muscle relaxer. Explain in 3-4 sentences how ZIGGY could cause muscle relaxation. How can both ZIGGY and ACh bind the same GPCR? And then how can they have different effects on the cells, despite binding to the same receptor on the same cells?arrow_forward
- Why do antibodies contribute to the symptoms of myasthenia gravis?arrow_forwardExplain why a person with myasthenia gravis might prefera soft diet. List several potential complications of acontinued soft diet.arrow_forwardOutline the pathogenesis of Myasthenia gravis and the consequential effects from the disruption at the neuromuscular junction. Is Myasthenia gravis considered an upper or lower motor neuron disorder?arrow_forward
- A patient has been exposed to the organophosphate pesticide malathion,which inactivates acetylcholinesterase. Which of the following symptoms would you predict: blurring of vision, excess tear formation, frequent or involuntary urination, pallor (pale skin), muscle twitching, orcramps? Would atropine be an effective drug to treat the symptoms?(See Clinical Impact 16.2 for the action of atropine.) Explain.arrow_forwardA chemical synapse is a type of synapse that occurs between two neurons and between a motor neuron and skeletal muscle fibers (i.e. at a Neuromuscular junction, NMJ). Compare and contrast the specific events that occur at chemical synapses at these two sites. Describe clearly how they are similar and how they are different, starting at the arrival of a nerve impulse at the pre-synaptic neuron and ending up with the changes observed at the postsynaptic membranes.arrow_forwardare these True or False? Receptors on the post-synaptic cell membrane that bind the acetylcholine are voltage-gated channels (channels that open in response to a change in the electrical charge of the membrane). When a muscle cell is not contracting its cell membrane is negative on the inner surface. The effect of a neurotransmitter on the muscle cell membrane is to modify its ion permeability properties temporarily.arrow_forward
- A drug belonging to the class of monoamine oxidase inhibitors has the following function: Group of answer options Increases the permeability of calcium Increases the breakdown of acetylcholine in the synaptic cleft Increases the level of acetylcholine in the synaptic cleft Increases the level of norepinephrine in the synaptic cleft Increases the breakdown of norepinephrine in the synaptic cleftarrow_forwardWhich of the following statements regarding the motor end plate in the somatic motor division of the nervous system is true? After the activation of voltage-gated calcium channels, the neuron releases ACh onto the muscarinic receptors on the surface of the highly folded area of the muscle fibre. The preganglionic nerve fibre releases ACh onto the postganglionic nerve fibre, which then releases ACh onto the cholinergic receptors of the motor end plate. Chemically gated monovalent cation channels on the motor end plate are activated once the motor neuron releases ACh onto the nicotinic receptors on the surface of the muscle cell. The AChE enzyme enhances the amount of ACh released into the neuromuscular junctionarrow_forwardA researcher is investigating the effects of a toxin, isolated from the skin of a South American tree frog. The researcher is exploring the effect of that toxin on synaptic transmission at the mammalian skeletal neuromuscular junction. Their previous studies established that the toxin had no direct effect upon skeletal muscle contractility, but it did block muscle contractility elicited indirectly via electrical stimulation of the motor nerve. To establish how the toxin influenced synaptic transmission, in vitro studies were performed using the mouse phrenic nerve hemidiaphragm skeletal muscle preparation, bathed in a buffered saline solution containing a raised magnesium and lowered calcium concentration. Under these conditions intracellular recording determined the effect of the toxin on the amplitude (in mV) of miniature endplate potentials (mepps) and endplate potentials (epps) – see Table 1. Mean mepp amplitude Mean epp amplitude Control 0.5 mV 8 mV Toxin 0.5 mV 2 mV Table 1: Mean…arrow_forward
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