The following quiz provides veterinarian-client-patient relationship (VCPR) questions and answers as it is based on the veterinary care of the pets. If you are a veterinary doctor or want to be one, check out this quiz and see if you know how to take care of diseases, illnesses, and disorders of the animals. A VCPR is essential for the interaction between veterinarians, their clients, and animal patients. Let's check if you know how to diagnose different diseases in animals.
Demyelination of nerve fibers
Regular myelination of nerve fibers
Hyperkalemia
Hypokalemia
Milk fever (hypocalcemia)
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Calcium is the primary component of lipofuscin which is an indicator of canine intelligence
It is necessary for the docking phase of neurotransmitter release
Calcium makes up the bulk of astrocytes which are necessary for cognitive function
Calcium is used by Nissl bodies in the neuron to synthesize acetylcholine
Calcium causes a conformational change of synapsin I releasing the neurotransmitter from the cytoskeleton
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Blocks sodium membrane permeability and decreases action potential
Increases sodium
Increases action potential
Increase calcium
Increase potassium
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Hypocalcemia, decreased calcium levels and increased sodium influx
Hypercalcemia, increased calcium and reduced sodium influx
The cow is just tired and lacks energy reserves (glycogen depletion)
None of the above
All are accurate
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Organophosphates inhibit cholinesterase, an enzyme that breaks down acetylcholine, a neurotransmitter that carries signals between nerves and muscles
Organophosphates increase cholinesterase production, an enzyme that breaks down acetylcholine, a neurotransmitter that carries signals between nerves and muscles
Organophosphates inhibit the release of epinephrine which breaks down acetylcholine, a neurotransmitter that carries signals between nerves and muscles
Organophosphates inhibit the release of epinephrine which breaks down acetylcholine, a molecule that prevents signal transduction between nerves and muscle
Organophosphates inhibit cholinesterase, an enzyme that breaks down acetylcholine, a neurotransmitter that inhibits signal transduction between nerves and muscles
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Sodium Channels on the presynaptic neuron
Potassium Channels on the presynaptic neuron
Calcium Channels on the presynaptic neuron
Nicotinic Receptors on the postsynaptic neuron
Cholinergic Receptorson the postsynaptic neuron
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Hyperoxia leading to an excess supply of oxygen in tissues and organs
Ischemia from blood vessels becoming blocked and reduced blood flow
Rigor Mortis from persistent muscle contractions and failure to relax
Lactate shuttle due to glucose being absorbed in the blood
None of the above
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Absolute refractory period with a consequence of tetany
Relative refractory period with a consequence of a longer absolute refractory period
Absolute refractory period with a consequence of a longer relative refractory period
Relative refractory period with a consequence of a compound action potential
Absolute refractory period with a consequence of a supernormal phase
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The injection of lidocaine and bupivacaine will decrease sodium membrane permeability resulting in a decrease of action potential and causing loss of sensory neuron activity.
Lidocaine and bupivacaine act to block Ach receptors causing loss in muscle fiber sensation.
In order to ensure proper pain management, you give lidocaine and bupivacaine as they are powerful painkillers.
The injection of lidocaine and bupivacaine will increase the sodium membrane permeability resulting in a decrease of action potential and causing loss of sensory neuron activity.
Lidocaine and bupivacaine will increase the calcium membrane permeability resulting in an increase of action potential and causing loss of sensory neuron activity.
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Glutamate, the cell is becoming hyperpolarized, decreasing excitability, leading to no sensory input
Epinephrine, the cell is becoming hyperpolarized, increasing excitability, leading to sensory input
Glutamate, the cell is becoming hyperpolarized, increasing excitability, leading to no sensory input
Norepinephrine, the cell is becoming hyperpolarized, increasing excitability, leading to sensory input
Benzodiazepine, the cell is becoming hyperpolarized, decreasing excitability, leading to no sensory input
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Stimulation of the type A gamma nerve fibers to compete with the arriving afferent information of the needle stick
Stimulation of the type C fibers to compete with the arriving afferent information of the needle stick
Stimulation of the type A alpha fibers to compete with the arriving afferent information of the needle stick
Temporal summation to compete with the arriving afferent information of the needle stick
Nothing, the client is clearly insane
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You explain that this disease increases the resistance to membrane ion inflow and therefore increases the electrocurrent speed.
You explain that this disease increases the resistance to membrane ion inflow and therefore increases the electrocurrent speed.
You explain that this disease decreases the resistance to membrane ion inflow and therefore decreases the electrocurrent speed.
You explain that this disease decreases the resistance to membrane ion inflow and therefore increases the electrocurrent speed.
You explain that this disease doesn’t change the resistance to membrane ion inflow and therefore increases the electrocurrent speed
Cervicosacral
Craniosacral
Lumbosacral
Craniothoracic
Thoracolumbar
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Decreased potassium which makes the axon more hyperpolarized
Decreased potassium which makes the axon more depolarized
Increased potassium which makes the axon more hyperpolarized
Increased potassium which makes the axon more depolarized
None of the above
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