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100
What clinical presentation leads you to believe that Mr. Hernandez has a neurological related problem? (Be more specific that listing out symptoms)
Diarreha, Nausea, salivary gland overstimulation, specifically multisystem issues are seen which is important because autonomic nervous system is involved in multiple body systems
100
Why did the bandana not work?
it is respiratory!
100
What are ways to avoid and educate farmers on how to prevent organophosphate poisoning?
Education, using masks (not bandanas), emphasizing effective hygenic practices, etc.
100
What is the difference between parasympathetic and sympathetic nervous system?
Para-chillaxin system (Opposite of Sympathetic)
Sympathetic-eyyo time to stress mode system (increase heart rate, decrease activity of GI, dilated pupil, heart beats faster, BP go up)
100
How can you diagnose organophosphate toxicity via testing?
Measure plasma level acetycholinesterase activity, which would be decreased a LOT
200
What exactly is affected by organophosphate poisoning?
Acetycholinesterase is irreverisbly inactivated
200
What are some neuropsychiatric symptoms seen from organophosphate poisoning even after recovery?
Psychosis, confusion, impairment in memory, irritability
200
What is the Department State of Health services?
HHS works with federally qualified health clinics, medical associations, community partners and local governments to help clients find the health care they need. Aging and Disability Resource Centers can help Texans find personal care, nursing care, help at home and other long-term care services.
200
How does the red blood cell acetycholinesterase test work?
During a cholinesterase test, a needle is inserted into a vein and blood is collected in an air-tight vial or a syringe. The sample is taken to the laboratory for evaluation. The lab evaluates the enzymes acetylcholinesterase and pseudocholinesterase, which act to break down acetylcholine. Looks at choline levels in blood
200
What are risk factors of organophosphate poisoning?
Location (rural), foods (certain foods), job
300
How do organophosphates inhibit acetycholinesterase activity?
The organophosphate insecticide inactivates AChE by phosphorylating the serine hydroxyl group on the enzyme. This is followed by the accumulation of acetylcholine which then overstimulates the nicotinic and muscarinic receptors.
300
What are big differences in the structure in terms of how neurons are organized in somatic versus autonomic nervous system?
Upper and Lower Motor Neurons versus preganglionic/post-ganglionic neurons
300
Atropine is useful in the treatment of organophosphate toxicosis because it
antagonizes all of the following effects EXCEPT:
a. Miosis
b. excessive salivation
c. bradycardia
d. muscle fasciculation
e. GI hypermotility
D!
300
A 35-year-old woman is brought to the emergency department due to difficulty breathing. The patient is a farmer and developed symptoms while working in the fields. Past medical history is significant for major depressive disorder and two prior suicide attempts. Temperature is 36.7°C (98.1°F), pulse is 53/min, respirations are 32/min, and blood pressure is 90/65 mmHg. Oxygen saturation is 87% on ambient air. Physical examination reveals a lethargic and diaphoretic adult female with bilateral pinpoint pupils and watering from the eyes. The patient’s body and clothes are soiled in vomit and feces. Lung auscultation reveals diffuse wheezing with rhonchi. Which of the following agents most likely precipitated this patient's symptoms?
A. Atropine
B. Organophosphate
C. Amitriptyline
D. Caustic substances
E. Amphetamine
B
300
Where is acetycholinesterase found?
Postsynaptic neuromuscular junctions where it hydrolyzes acetycholine to acetic acid and choline
400
how do you differentiate acute versus chronic organophosphate poisoning
More long term neurological changes is a good indication of chronic organophosphate poisoning such as memory loss, loss of concentration, mood changes, and hallucinations (psychosis)
400
Why can testing for high amylase levels and hyperglycemia be useful for knowing if the patient has organophosphate poisoning.
heavily increased digestive activity since amylase breaks down carbs, means that the parasympathetic nervous system is super active; leads to high insulin production (parasympathetic nervous system) since the levels are kinda low
400
What are some examples of organophosphates?
- Chlorpyrifos
- Diazinon
- Dursban
- Fenthion
- Malathion
- Parathion
400
What are the three ways of taking in organophosphates?
- Inhalation
- Skin contact
- Ingestion (eating or drinking)
400
What are the differences between musarinic and nicotinic receptors? How are these receptors affected by organophosphates and list a type of symptom that you could see, as it relates to both receptors and why this would happen.
Musarinic generally have to do more with visceral organs, whereas nicotonic is mainly skeletal muscle based. Also musarinic receptors are seen in BOTH CNS and PNS. Nicotonic is mainly seen in neuromuscular junction and CNS! Organophosphates can lead to overstimulation of these receptors and lead to problems like muscle tremors, nausea, diarreha, or pupil constriction.
500
How does G-protein coupled receptor influence heart reate increase and decrease (sympathetic and parasympathetic) activity?
Gs leads to an increase in cAMP which leads to an increase in ATP and MLCK working together to lead to contraction of the smooth muscle, Gi does the opposite
500
What common sympathetic response is affected by the organophosphate poisoning, and why would you expect this?
Sweating! The reason is because sympathetic nervous system still uses acetycholine at the preganglionic synapse! Additionally, nicotonic receptors (which are generally found on preganglionic synapse) are seen on adrenal glands which stimulate sweat
500
A farmer comes in with a diagnosis of organophosphate poisoning. Why does the physician give the patient both atropine to increase the heart rate of the patient, how does atropine do this and why is pralidoxime also given with atropine?
Atropine is a muscarinic receptor antagonist, meaning that it would reduce the activity of the receptor. Less of this receptor means more visceral organ activity since the parasympathetic nervous system is "relaxed." This would lead to an increase in acetycholine that is not being using leading to a toxic amount. That is why pralidoxime is given with it to dephosphorylate the acetycholinesterase so that not it is active to degrade the high amounts of acetycholine
500
Draw out what is happening at the neuromuscular junction!
500
Could long-term smoking affect organophosphate poisoning symptoms? (Theory-based question)
Nicotine binds to nicotinic receptors that acetycholine normally binds too, and can lead to a further increased level in acetycholine since nicotine takes its place and the excess cannot be broken down so symptoms might be worse. Nicotine adds increased stress of the parasympathetic nervous system