Unit 2 Case Study and Homework
Unit 2 Case Study and Homework PSL 310
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Date Created: 10/11/15
Fall 2015 Hybrid PSL 310 Study Guide for the Case Studies for Unit 2 Any of the material on this Study Guide is fair game for the Unit 2 Exam First draw in the space below the neurons transmitters effectors and receptors for somatic motor neurons and autonomic neurons both sympathetic and parasympathetic Then we ll go through it it will organize your thinking for the Case Studies and will help you prepare for the exam In the sketch below transmitters are in red receptors are in green and effectors are in brown Somatic motor neurons make up the Somatic Nervous System 0 7 w xb Adm NM Autonomic Nervous System sympathetic and parasympathetic neurons Effector is muscle V in Effectors are muscle lt muscle f39 atollMMth MdNS Ad NN aw KlL Parasympathetic l AW D 09 u 39 39 WC gitsu NN Y SWVMC Effectors are in muscle muscle and Terms you may need reminding of Agonist stimulates the receptor and causes a response like the natural chemical Antagonist or Blocker blocks the receptor and prevents the natural chemical from causing a response MAKE SURE YOUR NAME AND PID ARE FILLED OUT CORRECTLY ON THE SCANTRON VERY IMPORTANT NOTE YOU SHOULD USE THE RESOURCES LISTED AFTER THE STEM OF THE QUESTIONS TO HELP YOU THEY SHOULD SAVE YOU LOTS OF TIME AND PREVENT CONFUSION If you don39t use the Resources listed as I have seen many students do you will struggle with the questions 1 Answer all of these questions before your Case Study session However don39t fill the Case Study answers on the FULL PAGE scantron that you used for your Homework answers until after class discussion instead just circle or write your answers on these pages you print and bring to the Case Study session First Case the big one This case may be challenging but it has been constructed by Dr Denison to integrate your knowledge about the ANS and the neuromuscular junction of skeletal muscle It shows how what you are learning about neurotransmitters and receptors is extremely important in health care and neuroscience for our students in that major It also demonstrates how complicated and interesting these cases can be You are working your first shift in the emergency room when Jeremy enters with his wife Deloris They both look about 70 years old Jeremy has difficulty breathing and is not able to speak well His wife tells you that he was out in the orchard working She thinks he may have been spraying fruit trees because she found the insecticide sprayer outside near the trees nearly empty Deloris admits that Jeremy is beginning to suffer from dementia and that his decisions are becoming less and less rational Deloris wonders if Jeremy exposed himself to insecticide and blames herself for not watching him closer You realize that organophosphate insecticides could have been used on fruit trees and protective gear should have been worn by Jeremy You ask Deloris if Jeremy was wearing any protective clothing and eye protection She says no You ask whether she thinks he used malathion less toxic or parathion more toxic She says she does not know what kind of insecticides they have but knows some of them are very old If Jeremy had significant exposure to organophosphate insecticide you may need to act quickly to save his life You notice he is looking worse he vomits and bends over in what looks like severe pain A grandson calls Deloris and verifies that a container of organophosphate insecticide is outside the garden shed and powder is around the container that is it looks like it was recently opened and used The grandson says the front label is too old to read and he can t see which speci c type of organophosphate it is Jeremy s heart rate and arterial blood pressure are recorded The values for both are lower than normal Hints Notice Jeremy s symptoms eg decreased HR increased gut movements dif culty breathing maybe airway constriction Dr Sage the emergency department director and your supervisor enters the room and you report the entire case to her She recommends that Jeremy be given atropine immediately she believes this is a severe case of organophosphate poisoning 21 What is the effect of organophosphate insecticide in the body Resources Course Pack pages 113 and 163 and Readings Appendix page 255 A decreases ACh release B blocks ACh receptors C causes destruction of ACh D inhibits the enzyme that breaks down ACh E causes antibodies to be produced to ACh receptors This question should have been easy to find the answer However it s important It reminds you of different ways interference in transmission at the neuromuscular junction of skeletal muscle can occur Botulism toxin decreases ACh release choice A curare blocks ACh receptors choice B acetylcholinesterase or AChase destroys ACh choice C and organophosphate insecticides would cause decreased AChase activity which would decrease the destruction of ACh so choice C is not right myasthenia gravis is an autoimmune disease in which antibodies are produced against a person s own ACh receptors and makes them nonfunctional choice E Organophosphate insecticides inhibit the enzyme that breaks down ACh that is inhibits acetylcholinesterase or AChase Answer is D 22 Could ACh at the synapse or in the synaptic cleft increase due to organophosphate poisoning Resource Course Pack pages 113 Could ACh increase in the CNS due to organophosphate poisoning Resources Course Pack page 113 near Objective 2 and the top of page 114 Could ACh increase in autonomic ganglia due to organophosphate poisoning Resources Course Pack page 139 and Fig 72 on page 138 of the Course Pack or the larger Figure on page 136 of the Course Pack A yes yes yes B no no no C yes no yes D yes no no If organophosphate insecticides inhibit the enzyme that breaks down ACh that is inhibits acetylcholinesterase or AChase then ACh levels would increase in the synaptic cleft due to decreased breakdown Look on page 113 of the Course Pack to see that ACh is listed as a transmitter in the CNS is the transmitter released at skeletal muscle and is a transmitter in the autonomic nervous system At the top of page 114 of the Course Pack there is a description of ACh pathways in the brain that are important in learning and memory In fact AChase inhibitors different chemicals than the organophosphate insecticides in the Case Study are used clinically at a therapeutic or helpful dose to increase the amount of ACh in the brain in patients with Alzheimer s disease Alzheimer s disease patients have ACh levels that are lower than normal ACh is the transmitter released by preganglionic neurons that is is the transmitter released by preganglionic parasympathetic and preganglionic sympathetic neurons at autonomic ganglia If organophosphate insecticides inhibit acetylcholinesterase or AChase then ACh would increase in the synaptic cleft due to decreased breakdown of the synapses in autonomic ganglia Answer is A 23 Does giving Jeremy atropine make sense Resource Jeremy s symptoms and Course Pack page 147 and Fig 72 on page 138 or larger the Figure on page 136 of the Course Pack A no B yes Course Pack page 147 describes that atropine blocks muscarinic receptors on ANS effector membranes ACh is released by postganglionic parasympathetic fibers to stimulate muscarinic receptors Due to the organophosphate poisoning ACh would be increased at muscarinic receptors since AChase is inhibited and there would be an overstimulation of those receptors Blocking these receptors with atropine does make sense it would help because it would cause a decreased stimulation of the overstimulated muscarinic receptors Answer is B 24 Would ACh increase at the neuromuscular junction in skeletal muscle due to organophosphate poisoning Resources Course Pack pages 146 and 160163 A yes B no there is no ACh at the neuromuscular junction This question is easy but important ACh is released by the somatic motor neuron to cause skeletal muscle contraction On page 161162 of the Course Pack it describes that AChase at the neuromuscular junction breaks down ACh On page 163 of the Course Pack there is a description of AChase inhibitors including organophosphate insecticides If ACh is not broken down due to inhibition of AChase then it will increase at the neuromuscular junction The effect would be similar to black widow spider venom also page 163 of the Course Pack which also causes increased ACh at the neuromuscular junction but the spider venom increases ACh release Answer is A 25 Should atropine have an effect at neuromuscular junction receptors in skeletal muscle Resources Course Pack pages 146147 A yes it should does block receptors there B no it should not does not block receptors there Receptors on the skeletal muscle cell membrane are nicotinic see Course Pack page 146 Atropine blocks muscarinic not nicotinic receptors see Course Pack page 147 Therefore atropine will not have an effect will not block ACh receptors on skeletal muscle cells Answer is B Jeremy s lower than normal heart rate when he rst comes to the emergency department is due to stimulation of receptors on the heart Resources Course Pack pages 145146 and the Table on page 143 WRITE THE ANSWER IN THE BLANK ABOVE BUT IT DOES NOT GO ON THE SCANTRON Since ACh is not being broken down by AChase due to inhibition of the enzyme by the organophosphate insecticide ACh will increase at muscarinic receptors and can increase stimulation of those receptors including at the heart and will decrease heart rate Stimulating adrenergic beta1 receptors on the heart would igcrease heart rate Answer is MUSCARINIC but it does not go on the scantron Now it gets complicated It should eventually make sense to you that potentially there could be an increase in heart rate in a patient poisoned by an acetylcholinesterase inhibitor This is tricky Stimulation of nicotinic receptors at autonomic ganglia due to increased ACh at the ganglia could cause decreased heart rate if parasympathetic neuron activity increased or could cause increased heart rate if sympathetic neuron Mvitv increzLed Look at Fig 7 2 on page 136 of the Course Pack and think about ACh stimulating sympathetic ganglia neurons or ACh stimulating the adrenal medulla It seems that sometimes with poisoning due an AChase inhibitor patients can present with heart rate increased above normal There are reports that some Japanese poisoned by an organophosphate nerve gas military nerve gases are also AChase inhibitors by terrorists in a subway in Tokyo had heart rates increased above normal More often with organophosphate poisoning heart rate is lower than normal One of the main functions of bringing this complicated idea up is to remind you of how complex the body is Another reason for bringing it up is that you might have thought of this and it could have confused you One of Jeremy s symptoms is skeletal muscle weakness and difficulty breathing Dr Sage states that these cases are rare in the United States but the most common cause of death of organophosphate poisoning is respiratory failure She recommends monitoring Jeremy s arterial oxygen level She says that this patient may need mechanical ventilation 26 Does Jeremy s muscle weakness make sense Resources Course Pack page 163 also Readings Appendix page 255 and MAKE SURE TO READ ABOUT depolarization block on page 254 of the Readings Appendix under the topic Black Widow Spider Venom Causes Explosive Release of ACh A no B yes Continued depolarization at the skeletal muscle cell membrane causes the paralysis This should remind you of hyperkalemia in our first case study session in which continual depolarization of the nerve cell membrane caused Na channels of neurons to remain inactivated which caused decreased neuron excitability which could therefore cause inability to move or paralysis Here we also have continual depolarization but now it s of the skeletal muscle cell membrane at the motor end plate In the Readings Appendix on page 254 Sherwood describes depolarization block with increased ACh release due to black widow spider venom If AChase is inhibited due to organophosphate poisoning ACh at skeletal muscle cell membranes will increase similar to what occurs with black widow spider venom and depolarization block can occur in organophosphate poisoning too Depolarization block that Sherwood uses is a good term and she says the voltage gated Na channels are trapped in their inactivated state that is they remain in their closed and not capable of opening conformation That means that the Na channels can t reset for a new action potential because the membrane does not repolarize to resting membrane potential when the Na channels would reset instead the membrane remains depolarized Answer is B 27 Does endotracheal intubation of the patient and mechanical ventilation make sense That is could the patient have an inability to contract the diaphragm Hint the diaphragm is a skeletal muscle and the most important muscle for breathing Resource Course Pack page 162 near the middle of the page A yes B no In the answer to the question directly above the skeletal muscle cell membrane is described as continually depolarized which causes depolarization block and prevents a new action potential and a new contraction If the diaphragm cannot contract the patient cannot breathe and will need mechanical ventilation to keep arterial blood oxygenated and to get rid of the carbon dioxide in blood Answer is A 28 Hint answer this question as if no atropine is given or is not yet an effective dose Could the patient have a problem breathing and getting fresh air to the lungs because of increased airway or bronchial secretions This is rather difficult but Resource see page 147 of the Course Pack near the middle of the page for a hint A yes B no As mentioned in the question this is rather difficult but on page 147 there is a hint that the parasympathetic system causes respiratory secretions which is one reason why atropine is routinely given to patients before surgery to decrease respiratory secretions by blocking muscarinic receptors With organophosphate poisoning the patient can have bronchorrhea excessive secretions in the airways Excessive airway secretions is another reason besides paralysis of the diaphragm that respiratory failure can occur Answer is A Dr Sage says that a drug named pralidoxime 2pyridine aldoxime methyl chloride or 2PAM and called a cholinesterase reactivator should be administered to the patient and that it needs to be given before aging of the acetylcholinesterase enzyme Some resourcesor other help 0 Aging means the enzyme is permanently inactivated and 2PAM can no longer reactivate the enzyme 0 2 PAM regenerates acetylcholinesterase by removing a phosphate group from the enzyme which inhibited the enzyme 0 2PAM should be given within a certain number of hours of organophosphate poisoning since it is not effective after the enzyme has aged 0 2PAM does not cross the blood brain barrier to have central effects that is in the CNS but atropine does cross the blood brain barrier to have central effects 0 2PAM is given with atropine we will cover the blood brain barrier later right now think of it as special blood vessels in the brain which only allow certain substances into the brain 29 Assuming aging of the acetylcholinesterase enzyme has not yet occurred could 2PAM reverse the paralysis of respiratory muscles A yes B no 2PAM reactivates the enzyme that breaks down ACh The problem was an inhibition of the enzyme If now the enzyme is reactivated now ACh can be broken down and now the membrane can repolarize The treatment with 2PAM should reverse the depolarization block and skeletal muscle paralysis including respiratory muscle paralysis Note there has been some controversy about the use of 2PAM in organophosphate poisoning It seems the controversy is now focused on the dose and timing of 2PAM that is most useful Answer is A Another type of drug that is used in organophosphate poisoning is benzodiazepines these drugs increase the effects of GABA Dr Sage reminds you that seizures can occur with organophosphate poisoning 30 Answer this question in a general way Knowing what you know about GABA could a drug that increases the effects of GABA make sense to use in this patient with organophosphate poisoning to prevent seizures Resource Course Pack page 117 A no B yes The drugs called benzodiazepines Valium is one that enhance or increase the effects of GABA are used to prevent seizures GABA is an inhibitory transmitter If the drug increases the action of GABA it could increase inhibition increase inhibitory postsynaptic potentials in the CNS Answer is B Overall statements about the rst case above and organophosphate poisoning Though organophosphate poisoning is not common in the United States many people think knowledge of organophosphate toxicity and treatment is important because nerve gases also organophosphates and cause inhibition of AChase could be used wars eg in Iraq and Syria and in terrorist attacks eg occurred in Japan in a subway described in one of the answers above Also in the developing world poisoning with organophosphate insecticides is more common M importantly this case helps you understand ACh how important it is as a neuro smitter in the bodv and helps you understand the receptors for ACh and why you need to know those receptors This case also shows very well how complicated the treatment of a patient can be NOTE the symptoms vary with the type of organophosphate it was left vague on purpose and how the person was exposed to the toxin eg absorbed through the skin inhaled or ingested The effects organophosphate poisoning are of 3 types muscarinic nicotinic and CNS muscarinic which include decreased heart rate contraction of muscle of the airways and airway constriction increased respiratory secretions bronchorrhea increased salivation increased GI movements and diarrhea urinary incontinence constriction of the pupil nicotinic skeletal muscle contractions would rst occur followed by weakness with depolarization block failure of the diaphragm and other skeletal muscles to contract and respiratory failure note increased respiratory secretions would contribute to respiratory failure Also described in an answer to a question above is that stimulation of nicotinic receptors at sympathetic ganglia could cause symptoms of increased sympathetic activity including increased heart rate CNS that is an effect on the central nervous system via muscarinic and nicotinic receptors confusion tremors seizures coma Some students may want access to the Figure shown during the case study session If you re interested you can use the following link note this is optional the document is somewhat dated but is still very good httpwwwatsdrcdcgovcsemcholinesterasedocscholinesterasepdf The Figure is on page 26 of the document Second Case a little one You have 25 year old female patient with the following symptoms eyelid droop double vision and muscle weakness in the arms and legs The patient has a series of tests that confirm this patient has the disease myasthenia gravis 31 Your patient wants to know how they are different from a normal healthy person You correctly tell the patient that compared to a normal person a person with myasthenia gravis has at the neuromuscular junction Resources Course Pack page 163 and Challenge Questions 15 and 13 A larger amplitude more depolarization end plate potentials B more inhibitory end plate potentials more hyperpolarization at the motor end plate C less functioning ACh receptors than normal on skeletal muscle cells D smaller amplitude less depolarization end plate potentials E C and D Myasthenia gravis is an autoimmune disease in which receptors for ACh at skeletal muscle nicotinic receptors are destroyed by antibodies Choice A is not correct If receptors are gone at the motor end plate then less not more depolarization will occur in response to ACh release ACh can t nd a receptor before it s broken down so it has less effect on the membrane which would cause less depolarization which means Choice D is correct Choice B is wrong because there is no hyperpolarization at the motor end plate all end plate potentials are a depolarization as Challenge Question 13 describes Answer is E 32 One test used to help confirm a diagnosis of myasthenia gravis is an anticholinesterase test In this test the patient is given a drug that inhibits acetylcholinesterase it is a short acting acetylcholinesterase inhibitor Which result would indicate the patient has myasthenia gravis Resource Course Pack page 163 A increased muscle weakness during the anticholinesterase test B decreased muscle weakness during the anticholinesterase test The acetylcholinesterase inhibitor will allow ACh molecules to increase at the neuromuscular junction to stimulate the decreased number of ACh receptors at the patient s motor end plate and will act to decrease muscle weakness In the Course Pack it states that A treatment for the disease is the drug neostigmine or a drug like it which is an acetylcholinesterase inhibitor The acetylcholinesterase inhibitor prevents ACh from being broken down before it can find a receptor During the anticholinesterase test a different acetylcholinesterase inhibitor is used but the idea is the same Answer is B 33 You prescribe the drug neostigmine for this patient with myasthenia gravis Could a side effect of neostigmine treatment be overactivity of muscarinic receptors causing increased gut motility diarrhea and excess salivation Resources the First Case above and Course Page 163 which describes neostigmine A yes it makes sense B no it does not make sense It does make sense that overactivity of muscarinic receptors with neostigmine treatment can occur it can be a side effect or an unwanted effect that occurs with treatment with the drug Neostigmine is an acetylcholinesterase inhibitor and ACh can also increase at muscarinic receptors and could overstimulate those receptors and cause the symptoms listed Answer is A Third Case a little one One of your patients comes into your office and is complaining of a symptom of their hyperthyroidism This patient s thyroid hormones are higher than normal in the blood The patient is scheduled for radioactive iodine treatment later for her hyperthyroidism but is having a hard time coping with the symptom of a very high heart rate a racing heart now 34 Being a competent health care provider you tell the patient that you could successfully treat decrease her faster than normal heart rate with which of the following Resource Course Pack page 145 l46 and first page of this document that describes agonist and antagonist A betal agonist B beta2 agonist C betal antagonist D beta2 antagonist E alphal agonist A beta1 agonist would stimulate beta1 receptors on the heart and would increase heart rate A beta2 agonist would stimulate beta2 receptors The beta2 receptors we discussed in PSL 310 are on the airway smooth muscle and activation of beta2 receptors by an agonist would cause airway dilation A beta2 antagonist would block lung airway dilation An alpha1 agonist would stimulate alpha1 receptors The alpha1 receptors we discussed in PSL 310 are on the blood vessel smooth muscle and activation of alpha1 receptors by an agonist would cause blood vessel constriction From the choices above if you want to decrease the patient s heart rate you should prescribe a beta1 antagonist Answer is C This same patient asks you what is in her asthma inhaler that helps her breathe She says her mom used to have an inhaler with epinephrine in it but she wants to know what the medicine is that is in her inhaler 35 You correctly tell the patient that epinephrine dilate the lung airways but her inhaler has a more selective drug than epinephrine The more selective drug in her inhaler is a Resource Course Pack pages 143 and 145146 and first page of this document that describes agonist and antagonist A would betal agonist B would not beta2 agonist C would betal antagonist D would not beta2 antagonist B would beta2 agonist Epinephrine would dilate airways see page 143 of the Course Pack but epinephrine does more than dilate airways it would stimulate adrenergic receptors in other locations in addition to those on the lungs For a more selective action and to stimulate the adrenergic receptors on the airways but not adrenergic receptors on the heart a beta2 agonist can be used Answer is E The following question is not related to a case but is related to current events the use of nerve gas in war It helps you understand that what you are learning about organophosphate poisoning relates to poisoning by organophosphate military nerve gas 36 The military nerve gas sarin has been used during military con icts Sarin causes inhibition of the enzyme that breaks down ACh Assuming that stimulation of muscarinic receptors in the eyes including in the iris occurs with sarin what should you expect pupils to look like in a victim of sarin poisoning no Resources on this one the previous questions should help A constricted B dilated Stimulation of muscarinic receptors in the eyes including in the iris by organophosphate military nerve gas would cause constriction of the pupils Actually the United Nations workers in Syria looking for evidence of use of nerve gas were looking for this effect that is constriction of pupils Answer is A NOTE the procedure of how to turn in written answers for 3740 will be gone through during class A patient with pheochromocytoma Questions 3740 A patient comes into the emergency department suffering from symptoms you suspect to be caused by a pheochromocytoma A pheochromocytoma is a tumor of adrenal medulla cells that secretes large amounts of the hormones normally made by the adrenal medulla After measuring elevated levels of metabolites of these suspected hormones in the blood you get a CT scan of the patient s abdomen and con rm the presence of a pheochromocytoma it rarely occurs in other places that we will ignore 37 and 38 2 points What are the two main or two most important hormones released from the adrenal medulla Hint you should answer the two hormones that are released by the adrenal medulla in the largest amounts normally and would be released from this adrenal medulla tumor You must label this Question 37 and Question 38 and clearly print your answer of the names of the two hormones next to the Question numbers 39 and 40 2 points Until the patient has surgery to remove the tumor the patient needs to be treated to reduce their symptoms What two types of receptors should you block that is with drugs called antagonists to relieve the symptoms in the patient caused by the hormones from the adrenal medulla excessively stimulating their receptors that is the receptors that the hormones bind to Hint you should assume that blockers or antagonists exist for the receptors that the adrenal medulla hormones stimulate Another hint you should only block the receptors that adrenal medulla hormones bind to and not other receptors You must label this Question 39 and Question 40 and clearly print your answer of the names of the two types of blockers or antagonists next to the Question numbers You may turn in your answers as part of your group by your group recorder clearly listing your name on the group scantron or you may turn in your answers separately if you don t agree with the group answers on your own scantron if you wish Any unreadable or misspelled answers will be marked wrong Also you can t split your answers either all your answers are with the group answers or all your answers are on your own Peochromocytoma is rare tumor of the adrenal medulla or much more rarely can arise at other sites including sympathetic ganglia When it occurs these tumor cells secrete large amounts of norepinephrine and epinephrine into the bloodstream Norepinephrine and epinephrine can bind to alpha 1 and beta 3 adrenergic receptors causing increased sympathetic responses in the patients with the tumor The typical symptoms of patients with peochromocytoma are headaches palpitations and hypertension which can be severe which are caused directly or indirectly by overstimulation of adrenergic receptors that is both alpha and beta receptors Therefore blocking both alpha and beta receptors would relieve symptoms caused by increased norepinephrine and epinephrine levels in the patient ANSWERS 37 norepinephrine 38 epinephrine in either order 39 alpha 40 beta in either order Note about 39 and 40 there was a little confusion about whether you should list the receptors or a specific drug name Once we read through the answers we ll let you know how 39 and 40 will be graded Important physiology learned from this case study session First Case organophosphate poisoning 0 You learned or were reminded that organophosphates inhibit the enzyme that breaks down ACh 0 You learned that ACh is a very important transmitter in the body and that when AChase the enzyme that breaks down ACh is inhibited ACh will increase in the body 0 You learned that when AChase is inhibited ACh will increase at the synapses that release ACh 0 You learned that when AChase is inhibited ACh will increase in the central nervous system CNS 0 You learned that when AChase is inhibited ACh will increase at the synapses of autonomic ganglia 0 You learned that blocking muscarinic receptors makes sense and is a treatment for organophosphate poisoning since it would block decrease the stimulation of the overstimulated muscarinic receptors 0 You learned that stimulation of nicotinic receptors at autonomic ganglia due to increased ACh at the ganglia could cause decreased heart rate if parasympathetic neuron activity increased or could cause increased heart rate if sympathetic neuron activity increased Therefore you learned how complicated clinical cases can be 0 You learned or were reminded that ACh is released at the neuromuscular junction to cause skeletal muscle contraction 0 You learned or were reminded that ACh released at the neuromuscular junction stimulates nicotinic receptors on skeletal muscle 10 You learned that continued depolarization at the skeletal muscle cell membrane with increased ACh due to inhibition of AChase can cause paralysis because continual depolarization of the membrane this would be at the motor end plate where the ACh receptors are causes Na channels to remain inactivated this would be in the area where action potentials occur near but not part of the motor end plate You learned the term depolarization block from the Readings Appendix example with increased ACh release due to black widow spider venom and that depolarization block describes what can occur in organophosphate poisoning which causes paralysis of skeletal muscle You learned that paralysis of diaphragm the most important muscle in breathing which is skeletal muscle means the patient is unable to breathe on their own and needs mechanical ventilation needs a respirator You learned that the patient with organophosphate poisoning could have bronchorrhea excessive secretions in the airways and that excessive airway secretion is another reason besides paralysis of the diaphragm that respiratory failure can occur You learned that 2PAM reactivates AChase and treatment with 2PAM could reverse the depolarization block and skeletal muscle paralysis You learned that 2PAM should be given within a certain number of hours of organophosphate poisoning since it is not effective after the AChase enzyme has aged You learned that effects organophosphate poisoning are of 3 types MUSCARINIC NICOTINIC and CNS MUSCARINIC which include decreased heart rate contraction of muscle of the airways and airway constriction increased respiratory secretions increased salivation increased GI movements and diarrhea urinary incontinence and constriction of the pupil NICOTINIC skeletal muscle contractions would first occur followed by weakness with depolarization block failure of the diaphragm and other skeletal muscles to contract and respiratory failure note increased respiratory secretions would contribute to respiratory failure Also described is that stimulation of nicotinic receptors at autonomic ganglia could cause symptoms of increased sympathetic activity including increased heart rate CNS that is an effect on the central nervous system via nicotinic and muscarinic receptors confusion tremors seizures coma can occur You learned that atropine which blocks muscarinic receptors is used in the treatment of organophosphate poisoning You learned that 2PAM which reactivates the enzyme that breaks down ACh if given before the enzyme ages is used in the treatment of organophosphate poisoning You learned that drugs that enhance the action of GABA called benzodiazepines including Valium are used in the treatment of organophosphate poisoning to prevent seizures Second Case myasthenia gravis You learned or were reminded that the disease myasthenia gravis is an autoimmune disease in which receptors for ACh at skeletal muscle nicotinic receptors are destroyed by antibodies You learned or were reminded that if ACh receptors are decreased compared to normal at the motor end plate then less depolarization will occur in response to ACh release ACh can t nd a receptor before it s broken down so it has less effect on the membrane which would cause less depolarization You learned or were reminded that there is no hyperpolarization at the motor end plate all end plate potentials are a depolarization You learned or were reminded that treatment of a myasthenia gravis patient with an acetylcholinesterase inhibitor will allow ACh molecules to increase at the neuromuscular 11 junction to stimulate the decreased number of ACh receptors there and can decrease skeletal muscle weakness 0 You learned or were reminded that a treatment for the disease myasthenia gravis is the drug neostigmine or a drug like it which is an acetylcholinesterase inhibitor 0 You learned that overactivity of muscarinic receptors with neostigmine treatment can occur it can be a side effect or an unwanted effect that occurs with treatment with the drug and can cause the symptoms of increased gut motility diarrhea and excess salivation Third Case hyperthyroidism 0 You learned or were reminded that to decrease a patient s heart rate the patient with too much thyroid hormone secretion a beta1 antagonist could be used as a treatment 0 You learned or were reminded that epinephrine would dilate airways but for a more selective action to stimulate the adrenergic receptors on the airways but not adrenergic receptors on the heart a beta2 agonist can be used In the News not a Case 0 You learned that if victims poisoned by sarin an organophosphate nerve gas were having muscarinic effects on the eyes the pupils would be constricted Pheochromocytoma case 0 You learned that in pheochromocytoma large amounts of the adrenal medulla hormones are secreted 0 You learned or were reminded that the adrenal medulla secretes the hormones epinephrine and norepinephrine 0 You learned that to block the effects of epinephrine and norepinephrine on effector organs alpha and beta antagonists are used 12 Fall 2015 Use a full page scantron see 1St paragraph PSL 310 Homework for Unit 2 HOMEWORK ANSWERS ARE NOT ACCEPTED UNLESS THE STUDENT ATTENDS THEIR CASE STUDY SESSION You should print this and record your answers on this document since the correct answers will be posted by Thursday night before the exam and that will be the only way you know whether you got questions right or not before the exam the Homework will not be graded until after the exam Note the answers to this Homework will be turned in at the end of your Case Study meeting using the FULL PAGE scantron that you got at our first Case Study session We will continue using the Homework scantron for the Case Study answers To get a scantron if you are missing yours students can do either 1 or 2 below 1 Pick up a scantron outside the Physiology main office 2201 Biomedical and Physical Sciences Building If you face Room 2201 and look on the right wall you will see a sign PSL 310 SCANTRONS with the scantrons in a slot below the sign You only need one scantron 2 Bring their answers clearly listed on this Homework document and transfer their answers to a scantron available in the classroom before the Case Study session begins Students who chose this option must carefully fill out the scantron before the Case Study session starts Preparation for doing this Homework You should finish all the Lecture Recordings from Synapses through and including Muscle all Learning Objectives and all the Practice Questions for those Lecture topics The main function of this Homework is 1 encouraging you to keep up with the class and to give you credit for working through and understanding the Lecture Objective and the Practice Questions and 2 to get you prepared to learn the most you can during the Case Study session Remember the Practice Questions include the Comprehension Checks answered in Videos posted on D2L the Study Questions in the Course Pack the Extra Study Questions in the Appendix of the Course Pack and the Challenge Questions and Reading Questions and the Answers to those questions in the Appendix of the Course Pack If you do that work ahead of this Homework you should a learn a lot b get credit for going through all the Practice Questions and c will be prepared to understand the Case Studies well This means you will be learning the right way If you do not prepare in the way I am encouraging you you will not understand the material well because you will be rushing at the end of the unit to get done and you will struggle through the Case Study session Don t forget to do the Learning Objectives which allow you to understand the practice questions These Homework Questions are based on the Objectives too For all questions select the single BEST answer based on the Learning Objectives and the Practice Questions First set of questions the function is to help you keep up with the material 1 Which of the following is the very next step after an action potential occurs in a synaptic knob Hint you should select the event that is closest in time and is immediately after an action potential occurs in a synaptic knob Another hint assume only one action potential occurs in the synaptic knob A transmitter release into synaptic cleft B postsynaptic potential in postsynaptic cell C binding of transmitter to receptors on subsynaptic membrane D opening of Ca channels E opening of chemically gated ion channels Answer is D This is Synapses Study Question I changed the steps are on page 112 of the Course Pack and in Challenge Question 1 2 Hint This question is related to 1 above and is Challenge Question 2 slightly changed this question is to remind you to do those questions and to give you credit for working through those questions DO THIS QUESTION FIRST BEFORE LOOKING AT THE ANSWER in the Challenge Questions Imagine you are able to keep nerve cells in a uid bath that is exactly like extracellular uid except that it contains no Ca contains no calcium ions Assume that the nerve cells in this bath are healthy and undamaged Assume also that you are set up to stimulate depolarize the nerve cells to cause action potentials and that you can add unlimited neurotransmitters to the nerve cell bath you can add any neurotransmitter that exists What would the lack of Ca in the bath prevent Hint page 112 and 115 of the Course Pack will help A action potentials B binding of neurotransmitter to chemically gated ion channels C opening of chemically gated ion channels after neurotransmitter binds D EPSPs or IPSPs E presynaptic knob neurotransmitter release Answer is E The following is part of the Answer to Challenge Question 2 For this question realize that opening of voltage gated Ca channels in the synaptic knob allows Ca to enter the synaptic knob which causes the release of transmitter from the synaptic knob No Ca to move into the synaptic knob no transmitter release You could still have action potentials and could still have neurotransmitter binding to receptors causing opening of chemically gated ion channels and causing EPSPs or IPSPs those neurotransmitters you are adding to the bath you have an unlimited supply remember See Challenge Question 2 and the Answer to that question 3 Neurotransmitter molecules are released into the synaptic cleft by exocytosis A True B False Answer is A See Extra Study Questions for Synapses 3 4 Hint Challenge Question 14 this question is to remind you to do those questions and to give you credit for working through those questions BUT DO THIS QUESTION FIRST BEFORE LOOKING AT THE ANSWER Imagine you are able to keep skeletal muscle cells in a uid bath that is exactly like extracellular uid except that it contains no Ca contains no calcium ions Assume that the muscle cells in this bath are healthy and undamaged Assume also that you are set up to stimulate depolarize the skeletal muscle cells to cause action potentials in the muscle cell membrane Which below could occur is possible when you depolarize the muscle cell membrane Hint page 176177 of the Course Pack should help A action potentials but no contractions B action potentials and contractions C contractions but no action potentials Answer is B This Question is Challenge Question 14 As it states in the Answer to Challenge Question 14 This question may have been challenging It should help you sort out that action potentials and contractions in skeletal muscle can occur without Ca in the uid outside the cell If you were stimulating a nerve to cause contraction then this would not work that is the transmitter would not be released from the nerve cells to cause contraction you need movement of Ca into the axon ending for exocytosis of transmitter see question 2 above However since you are stimulating the muscle cell directly you can cause action potentials which travel down the sarcolemma then down the T tubules which then causes Ca release from the SR which causes contraction Ca binds to troponin which pulls tropomyosin away from its blocking position and cross bridges of myosin attach to actin and contraction occurs You can see these steps on page 176177 of the Course Pack The purpose of this question was to make you clearly think about what happens after an action potential occurs in the skeletal muscle cell and that the Ca that triggers contraction comes from the SR inside the cell 5 Hint the Challenge Questions Assume for this question that the synapse involved is the typical chemical synapse described in Lecture and on page 111 of the Course Pack that is the typical synapse between the synaptic knob of the presynaptic neuron and the dendrites or cell body of the postsynaptic neuron and assume no other synapses besides the ones described in this question exist Neuron A releases a neurotransmitter transmitter X that causes postsynaptic potentials in neuron B Neuron B releases a neurotransmitter transmitter Y that causes postsynaptic potentials in neuron C Transmitter X opens chemically gated ion channels that are permeable to Na and K Transmitter Y opens chemically gated ion channels that are permeable only to K Select the letter choice that lists ALL the numbers of the INCORRECT statements USE CHALLENGE QUESTION 3 TO HELP YOU ANSWER THIS BUT WORK THROUGH IT BEFORE CHECKING THE ANSWER 1 At the synapse between neuron A and neuron B neuron A is the presynaptic neuron and neuron B is the postsynaptic neuron 2 At the synapse between neuron B and neuron C neuron C is the presynaptic neuron and neuron B is the postsynaptic neuron 3 Action potentials in neuron B will cause excitatory postsynaptic potentials in neuron A 4 Action potentials in neuron A could or will cause excitatory postsynaptic potentials in neuron B 5 Action potentials in neuron A will cause opening of voltage gated channels in the synaptic knob of neuron A 6 Action potentials in neuron A will likely cause inhibitory postsynaptic potentials in neuron B 7 A logical assumption is that transmitter X is GABA gammaaminobutyric acid 8 Action potentials in neuron B could or will cause inhibitory postsynaptic potentials in neuron C 9 Action potentials in neuron B will likely cause excitatory postsynaptic potentials in neuron C 10 Temporal summation in neuron B can occur when neuron A fires action potentials repeatedly 11 Spatial summation in neuron C will occur when neuron B fires action potentials repeatedly 12 Excitatory postsynaptic potentials in neuron B would likely cause excitatory postsynaptic potentials in neuron C 13 Action potentials in neuron B will likely cause opening of voltage gated channels in the synaptic knob of neuron C note think about this one A 2 3 6 7 8 9 10 11 12 13 B 2 3 4 5 6 7 9 11 12 13 C 2 3 6 7 9 11 12 13 D 1 2 3 6 7 9 11 12 13 Answer is C See Challenge Question 3 and the Answer to that Question Hint the Challenge Questions The purpose of this question is to have you think about the anatomy of the somatic and autonomic nervous systems which helps you understand their functions Which of the following is NOT or is LEAST correctly matched Hint pages 135 138 of the Course Pack will help A cell body in the brain axon ends in a ganglion a parasympathetic preganglionic neuron B cell body in thoracic segment of spinal cord axon ends in a ganglion a sympathetic preganglionic neuron C cell body in an autonomic ganglion axon ends on skeletal muscle a somatic motor neuron Answer is C This Question was Challenge Question 6 slightly changed somatic motor neuron cell bodies are in the CNS not in autonomic ganglia 7 Select the match which is LEAST or NOT correct A H zone remains the same size does not shorten or narrow when the sarcomere shortens B A band remains the same size does not shorten or narrow when the sarcomere shortens C I band shortens or gets narrower when the sarcomere shortens D myofilaments do not shorten when a skeletal muscle fiber shortens contracts E Z lines distance between the Z lines decreases when a skeletal muscle fiber shortens contracts Answer is A This is Muscles Study Question 3 and 39 changed 8 Hint Extra Study Questions and Comprehension Checks The end plate potential is an potential that occurs in the that A graded axon terminal is usually but not always a depolarization is usually excitatory B action skeletal muscle fiber membrane travels both ways down the cell membrane and into T tubules C graded skeletal muscle fiber membrane below the axon terminal is always a depolarization or excitatory D graded skeletal muscle fiber membrane below the axon terminal is usually but not always a depolarization is usually excitatory E graded skeletal muscle fiber membrane below the axon terminal is sometimes a hyperpolarization is sometimes inhibitory and is sometimes a depolarization is sometimes excitatory Answer is C This is Comprehension Check for Muscles l and Extra Study Question for Muscles l4 changed The function of the Question was for students to clearly think about what the end plate potential is 9 Consider the following numbered events from 1 to 13 Which 2 events are in the wrong order Hint the rest of the events are in the right order Another Hint pg 161162 and 176177 of the Course Pack you should use this question to help you understand the correct order of the events Another Hint review the Extra Study Questions for Muscles some events may be missing 1 Action potential in somatic motorneuron 2 Opening of Ca channels in somatic motor neuron axon terminal 3 Release of acetylcholine from axon terminal 4 Diffusion of acetylcholine across cleft of neuromuscular junction 5 Binding of acetylcholine to receptors on motor end plate 6 End plate potential 7 Opening of voltage gated Na channels 8 Action potential in sarcolemma 9 Action potential in T tubules 10 Movement of tropomyosin 11 Binding of Ca to troponin 12 Binding of myosin cross bridges to actin 13 Power stroke A 6 and 7 B 5 and 6 C 7 and 8 D 8 and 9 E 10 and 11 Answer is E This question was 21 of the Extra Study Questions for Muscles changed Ca binding to troponin causes the movement of tropomyosin The rest of the events are in the right order and as the question states you should use this question to help you understand the correct order of the events 10 11 12 The sarcoplasmic reticulum of muscle cells contains Ca in higher concentration than the concentration in the cytosol of the cell Hint Extra Study Questions for Muscle but think about What it means A True B False Answer is A This is Extra Study Question for Muscle 4 changed Hint the video of Comprehension Check 8 but answer this first before you check the video Binding of ATP to myosin causes A relaxation of the muscle B detachment of myosin from actin Answer is B Students miss this binding of ATP to myosin allows detachment of the cross bridge and cross bridge cycling to continue For relaxation Ca must decrease in the cytosol due to the Ca pump on the SR Fast glycolytic fibers have B more mitochondria myofibrils Answer is E See the Extra Study Questions for Muscles 2230 than slow oxidative fibers A more capillaries C less glycogen D more myoglobin E more Second set of questions the function is to get the wheels greasedquot in your head so you understand and get the most out of the Case Studies 13 14 15 16 17 18 Which of the following release acetylcholine as a transmitter Hint see Course Pack page 139 A sympathetic preganglionic neurons B parasympathetic preganglionic neurons C a few sympathetic postganglionic neurons D parasympathetic postganglionic neurons E A B C and D or all of the choices listed Answer is E This was Re exes and Autonomic Nervous System Study Question 57 changed Acetylcholine is released from somatic motor neuron axon terminals Answer is A This is Extra Study Question for Muscle 19 changed A True B False Acetylcholinesterase inhibitors used to treat Alzheimer s disease because they cause an acetylcholine in the brain Hint Synapses Lecture Notes A are decrease B are not decrease C are increase D are not increase Answer is C see Course Pack page 114 Which of the following was identified in Lecture as an important inhibitory transmitter A acetylcholine B serotonin C dopamine D norepinephrine E gammaaminobutyric acid Answer is E This question Extra Study Question for Synapses 6 Which receptor type is located at the autonomic ganglia and on skeletal muscle A muscarinic B 32 beta2 C 31 beta1 D a1 alpha1 E nicotinic Answer is E This is Study Question for Re exes and ANS 10 slightly changed Hint the Extra Study Questions Which of the following is NOT a parasympathetic effect or is NOT caused by increased activity in parasympathetic neurons A salivary glands secrete a watery saliva with enzymes C constriction the pupil D constriction of blood vessels muscle of the wall of the urinary bladder Answer is D See Extra Questions for Re exes and ANS B adjustment for near vision E contraction of the 5 19 As a clinician you gave atropine to a patient before his surgery Which of the effects listed would be likely or could occur in the patient after administration of atropine Hint think about what receptors atropine blocks page 146147 of the Course Pack helps and what blockage of those receptors will cause that is it blocks effects which will cause which below Hint use the Challenge Questions to answer this A decreased saliva B dilation of the pupil C decreased GI motility D dilation of lung airways E all of the choices listed Answer is E This Question was Challenge Question 11 changed 20 Which of the following is LEAST or is NOT correctly matched A Adrenergic receptor found on lung airways beta2 B Stimulation of these receptors causes blood vessel constriction alphal C Cholinergic receptor on the cell membranes of smooth muscle cardiac muscle and glands muscarinic D These receptors are blocked by atropine nicotinic E Cholinergic receptor on dendrites and cell bodies of postganglionic neurons nicotinic Answer is D See the Extra Questions for Re exes and ANS 3140 The rest of the scantron to Question 40 will be used for answers filled in during your Case Study Session
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