THE FIRST MIDTERM

Question 1

What is another name for cell body?

Answer 1

Perikaryon

Question 2

What is the definition of a direct action of neurotransmitters?

Answer 2

The neurotransmitter binds to and opens ion channels, which promotes rapid responses by altering the membrane potential.

Question 3

What is the definition of an indirect action of neurotransmitters?

Answer 3

The neurotransmitter acts through intracellular second messengers, usually G-protein pathways, which ends up having broader and longer-lasting effects.

Question 4

How does a voltage-gated channel work?

Answer 4

A channel that opens and closes in response to voltage changes across the membrane, or changes in the membrane potential in the cell. An example is a voltage -gated sodium channel, lidocaine.

Question 5

How does a ligand-gated ion channel work? And what is another name for these types of channels?

Answer 5

A hormone, drug, or transmitter binds to the protein and the channel opens up. Action is immediate and brief, some are excitatory and open channels for small cations, some are inhibitory and allow Cl- influx or K+ efflux to cause hyperpolarization. Examples include glutamate (AMPA) and nicotinic ACh receptors and GABA-A. They are also called Ionotropic.

Question 6

How do Metabotropic receptors work?

Answer 6

These are seven-transmembrane G protein-coupled receptors. The binding of neurotransmitter to this type of receptor does not result in the direct gating of a channel. Rather, binding to the receptor engages a G protein, which results in the production of second messengers that modulate voltage-gated channels and change the excitability of the neuron, thus they are not directly linked to ion channels. Metabotropic receptors initiate biochemical processes that mediate more long-term effects (tens of seconds to minutes) and modify the responsiveness of the neuron.

Question 7

What are the two types of Metabotropic receptors?

Answer 7

Membrane-delimited and Diffusible second messengers

Question 8

With which type of Metabotropic receptor does the G-protein subunit interact direct with the voltage-gated ion channel?

Answer 8

Membrane-delimited

Question 9

Which two types of voltage-gated ion channels are the targets of Membrane-delimited signaling?

Answer 9

Calcium channels and potassium channels

Question 10

With membrane-delimited receptors, what happens when G-proteins interact with calcium channels?

Answer 10

They inhibit channel function. This mechanism accounts for the presynaptic inhibition that occurs when presynaptic metabotropic receptors are activated.

Question 11

With membrane-delimited receptors, what happens when G-proteins interact with potassium channels?

Answer 11

They activate channel function and with potassium, they will be postsynaptic, resulting in a slow postsynaptic inhibition.

Question 12

How does a diffusible second messenger metabotropic receptor work?

Answer 12

A classic example of this type of action is provided by the β adrenoceptor, which generates cAMP via the activation of adenylyl cyclase. Whereas membrane-delimited actions occur within microdomains in the membrane, second messenger-mediated effects can occur over considerable distances.

Question 13

What is the definition of an autoreceptor?

Answer 13

It is a receptor on an axon terminal through which the neuron’s own neurotransmitter can influence the function of the terminal, and this is almost always inhibitory. The D2 receptor is an example.

Question 14

What is the definition of a heteroreceptor?

Answer 14

It is a receptor on an axon terminal through which neurotransmitters from other neuronal types can influence the function of the terminal, and they are almost always inhibitory.

Question 15

What are the three main catecholamines?

Answer 15

Dopamine, Norepinephrine, and Epinephrine

Question 16

What is name of the neurotransmitter that looks very similar to catecholamines, but isn’t?

Answer 16

Amphetamine. A lot of times the way drugs exert their effect is by mimicking the neurotransmitter, and if the structure is similar, it is easier.

Question 17

What is the precursor amino acid for catecholamines?

Answer 17

Tyrosine

Question 18

What are the four main monoamine neurotransmitters?

Answer 18

Dopamine, Epinephrine, Norepinephrine, and Serotonin. Histamine is also a monoamine. But remember, serotonin is not a catecholamine like the first three are.

Question 19

What are the two main classes of fibers/receptors of the autonomic nervous system?

Answer 19

Cholinergic (Muscarinic and Nicotinic) and Adrenergic

Question 20

What is the process of Dopamine entering at the adrenergic junction?

Answer 20

Tyrosine is transported into the noradrenergic ending or varicosity by a sodium-dependent carrier. Tyrosine is converted to DOPA (Dihydroxyphenylalanine) by tyrosine hydroxylase, and dopa is converted to dopamine by aromatic amino acid decarboxylase, and transported into the vesicle by the vesicular monoamine transporter (VMAT). Physiologic release of transmitter occurs when an action potential opens voltage-sensitive calcium channels and increases intracellular calcium. Fusion of vesicles with the surface membrane results in expulsion and dopamine can enter the synaptic cleft and do one of the following three things: 1) Bind to a post-synaptic receptor (there are 5, D1-D5), 2) Bind to the D2 autoreceptor (which would shut down tyrosine hydroxylase, so dopamine cannot be made nor released, and 3) Re-enter the neuron through a dopamine transporter. Once it does so, dopamine can be metabolized by MAO, Monoamine Oxidase, which converts dopamine into DOPAC.

Question 21

What is the process of NE entering the synaptic cleft of an adrenergic junction and when does it happen?

Answer 21

For this to happen, it all starts with Tyrosine again, which is converted to Dopamine and Dopamine’s same process takes place but once it enters the synaptic vesicle via VMAT, Dopamine is then converted to NE by Dopamine Beta Hydroxylase, DBH. NE can then enter the synaptic cleft and have the same three options as Dopamine does. However, instead of binding to D1-D5 post-synaptic receptors, NE binds to alpha and beta receptors. And there is no D2 pre-synaptic receptor, it is an alpha-2 receptor.

Question 22

Where is Epinephrine usually found? And what converts NE to Epinephrine?

Answer 22

It is mainly found in adrenal medullary cells, although it is also found in some CNS neurons. It is converted from NE by PNMT, phenylethanolamine-N-methyltransferase.

Question 23

What is another name for Serotonin?

Answer 23

5-HT, 5-hydroxytryptamine. It is associated with sleep, depression, and migraines.

Question 24

What is the amino acid precursor for Serotonin?

Answer 24

Tryptophan

Question 25

What is the process of Serotonin entering at the synaptic cleft?

Answer 25

Tryptophan enters the neuron, is then converted by Tryptophan Hydroxylase to 5-HTP, and 5-HTP is then converted by AAD to 5-HT (Serotonin). 5-HT then enters the synaptic vesicle via VMAT, and eventually makes its way to the synaptic cleft where it can do the usual 3 things, bind to post-synaptic receptor, bind to autoreceptor (5-HT 1A and 1B), or re-enter through a Serotonin Transporter. And because Serotonin is a monoamine, it can also be metabolized by MAO.

Question 26

What is the process of choline at the cholinergic junction?

Answer 26

Choline is transported into the presynaptic nerve terminal by a sodium-dependent choline transporter (CHT). In the cytoplasm, acetylcholine is synthesized from choline and acetyl-CoA (AcCoA) by the enzyme choline acetyltransferase (ChAT). Acetylcholine is then transported into the storage vesicle by a second carrier, the vesicular acetycholine transporter (VAT). Release of ACh occurs when voltage-sensitive calcium channels in the terminal membrane are opened, allowing an influx of calcium. The resulting increase in intracellular calcium causes fusion of vesicles with the surface membrane and exocytotic expulsion of acetylcholine and cotransmitters into the junctional cleft. Acetylcholine’s action is terminated by metabolism by the enzyme acetylcholinesterase, which breaks it down into choline, which can then re-enter the presynaptic nerve terminal, but it doesn’t do so through a acetylcholine transporter, but through a choline transporter, and the lack of this transporter is what makes this process a little different. ACh can also bind to post-synaptic nicotinic or muscarinic receptors, or it can bind to an autoreceptor, which is usually a Muscarinic Receptor (It shuts down the synthesis of ACh and shuts down its release, like an auto receptor does).

Question 27

What are the two main neurotransmitters that are amino acids?

Answer 27

GABA (inhibitory) and Glutamate (excitatory)

Question 28

What is the process of glutamate at the glutamatergic junction?

Answer 28

Alpha-ketoglutarate is the precursor to glutamate. It enters and is converted by amino transferase to Glutamate. It then enters a storage vesicle through a vesicular glutamate transporter. When it enters the synaptic cleft, glutamate can do 1 of 4 things. 1)It can re-enter the neuron through a glutamate transporter, however MAO does not metabolize it here because glutamate is not a monoamine. 2) It can bind to a post-synaptic receptor like AMPA, or NMDA. 3) It can bind to an autoreceptor. 4) It can enter an astrocyte, be converted to glutamine by glutamine synthetase, and by converting to glutamine, it serves as a storage buffer to be taken back up and be converted back to glutamate.

Question 29

What is the process of GABA at the gabaergic junction?

Answer 29

Glutamate is the precursor, it enters and is converted to GABA by glutamate decarboxylase. It then enters a storage vesicle through the vesicular GABA transporter. When GABA enters the synaptic cleft, it can do 1 of 4 things. 1)It can re-enter the neuron through a GABA transporter, however MAO does not metabolize it here because GABA is not a monoamine. 2) It can bind to a post-synaptic receptor like GABA-A or GABA-B, usually just one or the other. 3) It can bind to a GABA-B autoreceptor. 4) It can enter an astrocyte and can be degraded by GABA-transaminase.

Question 30

What are the five “other” neurotransmitters mentioned in class?

Answer 30

1. Histamine 2. Endorphins 3. Neuropeptides 4. Endocannabinoids 5. Nitric Oxide

Question 31

How many main histamine receptors are there, and what does H3 do?

Answer 31

There are 3, H1-H3, and H3 functions as an inhibitory heteroreceptor. So activation of brain H3 receptors decreases the release of ACh, dopamine, NE, serotonin, and certain peptides.

Question 32

What type of receptors do endorphins act on?

Answer 32

u opioid receptors

Question 33

How do opioid receptors modulate the release of neurotransmitters?

Answer 33

If endorphins bind to opioid receptors, it decreases the release of GABA (because opioid receptors are found on GABA neurons), which in turn will increase release of dopamine, because the dopamine neuron relies on a GABA receptor with GABA occupied in it in order to slow down release of dopamine.

Question 34

What are some of the neuropeptides that we need to know

Answer 34

Neurotensin, somatostatin, cholecystokinin, substance P, neuropeptide Y.

Question 35

What does neurotensin do and where is it found?

Answer 35

It regulates dopaminergic systems, inhibitory feedback, and it is found in the G.I. tract and inhibits G.I. motility and causes vasodilation.

Question 36

What is the main endocannabinoid neurotransmitter and to what receptor does it bind?

Answer 36

Anandamide, and it binds to CB1 cannabinoid receptors, and by doing so, causes dopamine release. Endocannabinoids are main ingredient in marijuana.

Question 37

What is nitric oxide and what does it do?

Answer 37

It is a gaseous signaling molecule that relaxes vascular smooth muscle.

Question 38

What are Kainate receptors?

Answer 38

They are a receptor subtype for Glutamate, permeable to Na+ and K+, and are expressed in brain and spinal cord.

Question 39

What does glutamate decarboxylase do?

Answer 39

It is an enzyme that catalyzes the decarboxylation of Glutamate to GABA and CO2.

Question 40

What is the definition of a ganglion?

Answer 40

A collection of cell bodies

Question 41

What two nervous systems is the Peripheral Nervous System made up of?

Answer 41

Somatic and Autonomic Nervous Systems

Question 42

Most organs are innervated by either the parasympathetic or the sympathetic nervous system, but not both. True or False?

Answer 42

False. Most are dually innervated, each having separate effects.

Question 43

Where are the cell bodies of the parasympathetic nervous system?

Answer 43

Craniosacral regions

Question 44

What is the pre-ganglionic neurotransmitter for both parasympathetic and sympathetic and what type of receptor is found where the pre meets the post-ganglionic?

Answer 44

Acetylcholine (ACh)…….Nicotinic (which is a type of cholinergic receptor)

Question 45

What is the post-ganglionic neurotransmitter, receptor, and target site of the parasympathetic nervous system?

Answer 45

ACh, Muscarinic receptor, and cardiac and smooth muscle, gland cells, and nerve terminals.

Question 46

What is the post-ganglionic neurotransmitter and receptor for the sympathetic pathway innervating sweat glands?

Answer 46

ACh, Muscarinic receptor

Question 47

What is the post-ganglionic neurotransmitter and receptor for the sympathetic pathway innervating cardiac and smooth muscle, gland cells, and nerve terminals?

Answer 47

NE, and alpha and beta receptors

Question 48

What is the post-ganglionic neurotransmitter and receptor for the sympathetic pathway innervating renal vascular smooth muscle?

Answer 48

Dopamine, D1 receptor

Question 49

Where are the cell bodies of the sympathetic nervous system?

Answer 49

Thoracolumbar region

Question 50

How does innervation of the adrenal medulla work, and is it parasympathetic or sympathetic?

Answer 50

It is sympathetic, and the pre-ganglionic goes all the way to the adrenal medulla, and at the junction is ACh with a nicotinic receptor, and the adrenal medulla then release NE and epinephrine into the bloodstream.

Question 51

What type of neurotransmitter and receptor are found at the junction of somatic motor nerves?

Answer 51

ACh and nicotinic receptors. These innervate skeletal muscle. The movement is voluntary.

Question 52

Are sympathetic pre-ganglionic axons short or long?

Answer 52

They are short, they extend to para- and pre-vertebral ganglia. The post-ganglionic extend to effector organ and are longer. These are all coming out of the thoracolumbar region.

Question 53

Are parasympathetic pre-ganglionic axons short or long?

Answer 53

They are long, they extend to ganglia near effector organs, so the post-ganglionic are short. These are all coming out of the craniosacaral region.

Question 54

If a drug inhibits the release of ACh, will it effect the parasympathetic or sympathetic pathway?

Answer 54

It will affect both.

Question 55

What type of receptor does ACh released from pre-ganglionic neurons act on, and where are these receptors found?

Answer 55

It acts on nicotinic receptors found on post-ganglionic fibers.

Question 56

On which type of receptor do motor neurons innervating skeletal muscle act?

Answer 56

Nicotinic receptors

Question 57

What are the three different neurotransmitters that post-ganglionic sympathetic fibers release?

Answer 57

Dopamine, NE, and Epinephrine. Most use NE.

Question 58

What are the main two types of adrenergic receptors that NE and epinephrine act on?

Answer 58

Alpha and Beta

Question 59

What are the three types of receptors that dopamine activates?

Answer 59

D1, alpha, and beta

Question 60

What neurotransmitter does post-ganglionic parasypathetic fibers release?

Answer 60

ACh

Question 61

What type of receptor does ACh act on for post-ganglionic parasympathetic fibers?

Answer 61

Acts on muscarinic receptors in most effector tissues.

Question 62

What percent of epilepsy patients are therapy-resistant?

Answer 62

25-40%

Question 63

What is the definition of a seizure?

Answer 63

A finite clinical manifestation of abnormal & excessive excitation of a population of cortical neurons.

Question 64

What is the definition of epilepsy?

Answer 64

A syndrome characterized by chronic, recurrent seizures unprovoked by systemic or neurologic insults.

Question 65

How do you get a diagnosis of epilepsy from seizures?

Answer 65

You have to have three or more non-provoked seizure events to be considered Epilepsy.

Question 66

What is the definition of epileptogenesis?

Answer 66

A sequence of events that converts a normal neuronal network into a hyperexcitable network.

Question 67

What is the lifetime prevalence of seizures for a person?

Answer 67

9-10%

Question 68

What is the prevalence of epilepsy in world population vs US?

Answer 68

1% and 1 in 26

Question 69

In terms of the etiology of epilepsy, what is the biggest factor, and is it inherited or acquired?

Answer 69

Ion channels, and they are inherited.

Question 70

What are the main nine precipitants (causes) of seizures

Answer 70

• Metabolic and/or Electrolyte Imbalance (People’s blood glucose too high or too low, too low sodium, calcium, magnesium, potassium too high) • Stimulant or other pro-convulsant intoxication • Sedative or ethanol withdrawal • Sleep deprivation • Reduction or inadequate ASD treatment • Hormonal variations • Stress • Fever or systemic infection (HSV can be linked) • Concussion and/or closed head injury

Question 71

At what ages is epilepsy most prevalent?

Answer 71

Very young and very old

Question 72

What are the main causative factors for epilepsy at a young age?

Answer 72

Genes, status epilepticus (a continuous seizure activity lasting more than 3 minutes), CNS infection, trauma

Question 73

What are the main causative factors for epilepsy at a middle age?

Answer 73

Trauma, status epilepticus

Question 74

What are the main causative factors for epilepsy at an older age?

Answer 74

Cancer, CVA, neurodegenerative disorders, trauma, status epilepticus

Question 75

What are the three types of partial seizures?

Answer 75

1. Simple partial (single focus that doesn’t spread) 2. Complex partial 3. Initial onset of secondarily generalized

Question 76

What are the five types of generalized (affecting the whole brain) seizures?

Answer 76

1. Tonic-clonic (grand mal) 2. Absence (petit mal) 3. Atonic 4. Myoclonic 5. Tonic

Question 77

What are the three things you need to maintain the characteristic of a simple partial?

Answer 77

1. Normal awareness 2. Memory 3. Consciousness (All throughout entire seizure)

Question 78

How long do simple partial seizures usually last?

Answer 78

60-90 seconds

Question 79

What are the four classes of symptoms that classify simple partial seizures based on cortical involvement?

Answer 79

1. Motor 2. Somatosensory 3. Autonomic 4. Psychic (“aura”)

Question 80

What are the characteristics of a complex partial seizure and how long do they usually last?

Answer 80

Localized onset, spreads bilaterally usually, either awareness, memory, or consciousness is lost during seizures, and they usually last 15 sec to 3 minutes.

Question 81

What are the characteristics of secondary generalized seizures?

Answer 81

They begin as simple or complex partial seizures, and when it continues to spread, it becomes generalized. Has tonic (stiffening) and clonic (jerking) phases once it becomes generalized. And all of this is finishes with a postictal phase.

Question 82

What is a postictal phase?

Answer 82

It is a confusion, somnolence ,with or without transient focal deficit that can lasts minutes-hours. Happens with tonic-clonic activity.

Question 83

What do all generalized seizures include?

Answer 83

Loss of responsiveness or lack of awareness.

Question 84

What is probably the cause of absence seizures and how long do they usually last?

Answer 84

Probably represent abnormal interactions between cortical and thalamic transmissions. 2-15 seconds.

Question 85

What is the main difference between tonic-clonic actions happening with secondary generalized seizures and generalized tonic-clonic seizures? And how long does tonic-clonic usually last?

Answer 85

The two are synchronized with generalized tonic-glonic seizures. Lasts 1-2 minutes.

Question 86

What are some properties of the “ideal” Anti-Seizure Drug (ASD)?

Answer 86

Effective for the specific seizure type Wide therapeutic index No toxicity No drug-drug interactions Long half-life No protein binding (if binds, not active) Water soluble No active metabolites

Question 87

What ratio of patients with epilepsy remain refractory to all pharmacological treatments for seizure symptoms?

Answer 87

1/3 of patients

Question 88

How many generations of ASD’s are there?

Answer 88

3

Question 89

What are the main reasons why the newer ASD’s are safer than the old ones?

Answer 89

The newer drugs are safer because they have fewer reactions with liver enzymes and fewer drug-to-drug interactions.

Question 90

What is the issue with having to give more than one ASD to a patient?

Answer 90

If you’re lucky, the patient will be controlled with a single drug, but if you are not getting good control, you will have to give another drug, which will be an inhibitor or an inducer of the other drug. If the second drug is an inducer of that enzyme, then the first drug will get chewed up and its levels will go down, and same applies the other way. If drug has a broad therapuetic index, you don’t need to worry as much about their interactions.

Question 91

What are the main three mechanisms of ASD’s?

Answer 91

1. Enhancement of GABA-mediated inhibition 2. Reduction of excitatory (usually Glutamatergic) transmission 3. Modification of ionic conductances, and modifying these channels with either accomplish #1 or #2.

Question 92

Carbamezepine

Answer 92

Used for all Partial seizures as well as Tonic-Clonic seizures. Although rare, Steven-Johnsons Syndrome is a side effect. This drug may also activate spike-wave seizures. It is also associated with toxic levels when patients drink grapefruit juice. It is a great drug for epilepsy but the potential for a drug-to-drug interaction is high. It’s MOA is it blocks Na+ channels to inhibit repetitive firing from neurons.

Question 93

What is Steven-Johnsons syndrome? Who are most at risk? And with which drug is it a side effect?

Answer 93

It is a milder form of toxic epidermal necrolysis. You get fever, sore throat, painful red lesions all over body. The most at-risk patients are those that are slow acetylators, immunocompromised, and patients on combination ASD’s. Carbamezepine.

Question 94

Which drug is associated with toxic levels if taken with grapefruit juice?

Answer 94

Carbamezepine. Grapefruit juice inhibits CYP3A4 enzyme in liver, so when patients take drug, the liver doesn’t metabolize the drug as it normally does and you can get toxic levels of the drug.

Question 95

Ethosuximide

Answer 95

Used for uncomplicated absence seizures. Has a very narrow clinical spectrum. It’s MOA is reduces T-type Ca+ channel currents in thalamic pacemaker neurons to quiet rhythmic discharges.

Question 96

What do barbiturates do?

Answer 96

They increase the duration of opening time of GABA channels.

Question 97

Phenobarbital

Answer 97

Used for all Partial seizures as well as Tonic-Clonic seizures. Has long-term cognitive memory and behavioral side effects. This drug is also the BIG TIME INDUCER, interact with almost every drug out there. Can precipitate spike-wave seizures in patients with absence seizures. Used mainly because of low cost and broad spectrum but not great option because of side effects.

Question 98

Phenytoin

Answer 98

Used for all Partial seizures as well as Tonic-Clonic seizures. It masculinizes (hirsuitism) and causes severe gingival hyperplasia, osteopenia, anemia, acne. This drug is special because it has zero-order kinetics at high doses. Most drugs have first-order kinetics. So with this, as you give Phenytoin to patients, it overcomes the metabolize enzymes in the liver, so with even the smallest increase in dose, you get an upshoot increase and can become highly toxic. You have to constantly monitor the levels in your patient. It’s MOA is that it blocks sustained high frequency of action potentials by blocking Na+ channels during repetitive firing.

Question 99

Topiramate

Answer 99

Used for all Partial seizures as well as Tonic-Clonic and Lennox-Gastaut syndrome seizures. This drug is unique because it is the only one that causes weight loss. Decreases word-finding ability as well. One of its side effects is that it metabolizes estrogen which will lower the efficacy of birth control. It’s MOA is that it blocks repetitive firing of Na+ channels, inhibits Ca+ channels, inhibits AMPA/Kainate receptors, and potentiates GABA currents. Know that this drug is broad spectrum and causes weight loss.

Question 100

Valproic Acid

Answer 100

Used for all Partial seizures as well as uncomplicated absence seizures, atypical absence seizures, primary tonic-clonic seizures, and myoclonic epilepsy. Very broad spectrum similar to Topiramate. Associated with weight gain however. As well as Reye-like syndrome and hepatic failure. It is strictly contraindicated with people who have liver problems. It also has an increased risk of spina bifida, category D pregnancy risk. It’s MOA is it blocks Na+ channels, reduces NMDA currents, and increases GABA at high doses.

Question 101

What are the common dose-related ASD adverse effects?

Answer 101

Dizziness, fatigue, ataxia, diplopia, irritability, word-finding difficulty, weight loss, weight gain.

Question 102

Is it better to use fixed or removable prostheses for patients with epilepsy?

Answer 102

Fixed

Question 103

What are some recommendations if a patient has a seizure in the dental chair?

Answer 103

Do not restrain patient and do not put anything in mouth. Place patient on their side and give them oxygen and call 911 if patient is cyanotic or seizure lasts for more than 3 minutes. Administer 10mg diazepem.

Question 104

What is the neurotransmitter, agonists, and antagonists that act on Muscarinic receptors?

Answer 104

Ach Agonists: Bethanechol and Pilocarpine Antagonists: Atropine and Scopalamine

Question 105

What are some of the tissue effects that agonists have on Muscarinic receptors?

Answer 105

Increase stomach acid secretion Decrease heart rate via SA node Decrease contractions via ventricles, atrium, and AV node Increase GI smooth muscle contractions (except sphincters) Increase secretory gland secretions

Question 106

What are the two types of Nicotinic receptors, and what tissues do they act on?

Answer 106

N-m (Neuromsucular - neuromuscular junctions) and N-n (Neuronal - ganglia, adrenal medulla, CNS)

Question 107

What are the two main antagonistic drugs of Nm receptors?

Answer 107

Succinylcholine and d-tubocurarine

Question 108

How does Succinylcholine work as a neuromuscular blocker?

Answer 108

It is depolarizing and non-competitive, it depolarizes/desensitizes the neuromuscular endplate; it opens the NIC channels and keeps these “open” such that the neuron is depolarized and unresponsive to another ACh challenge

Question 109

How does d-tubocurarine work as a neuromuscular blocker?

Answer 109

It is non-depolarizing and competitive. It competes with ACh at nicotinic receptors.

Question 110

What is Sarin and what does it do to the body?

Answer 110

Sarin is nerve gas, an acetylcholinesterase inhibitor, so it allows ACh to accumulate at the cleft and interact with cholinergic receptors to cause too much stimulation. You get a very slow heart rate, diarrhea, cramping, gland secretions, twitching, suffocation, blurred vision, sweating. Soldiers carry around Atropine as a nerve gas antidote, which will block muscarinic receptors to stop all these side effects. Atropine was originally derived from this plant on the left. And blocking these receptors would cause pupils to dilate I think.

Question 111

What are the three main cholinesterase inhibitors and how do they work?

Answer 111

1. Sarin - irreversible; long duration of action, nerve gas 2. Phsyostigmine - short duration of action, used for glaucoma, antidote for atropine 3. Donepezil - extended duration of action, used to treat Alzheimer’s

Question 112

What does botulinum toxin do?

Answer 112

It prevents the release of ACh. It relaxes intraocular muscles, treats muscle dystonia (spasms), removes wrinkles.

Question 113

What are the two main drugs to treat xerostomia and how do they work?

Answer 113

1. Cevimeline (Evoxac) - used for Sjogren’s syndrome 2. Pilocarpine (Sialagen) - used for radiotherapy

Question 114

Which neurotransmitter has a greater affinity for alpha1, alpha2, beta1, and beta2 receptors, Epinephrine or NE?

Answer 114

Epinephrine does. Except for Beta1 receptors, they have the same affinity here.

Question 115

How does phenylephrine work?

Answer 115

It serves as an agonist to alpha1 receptors and it causes vasoconstriction to sinus vessels in order to act as a decongestant. Also causes a decreased heart rate from baroreceptor reflex essentially.

Question 116

Which tissues do alpha1 agonists act on and what do they do?

Answer 116

Radial muscle of iris - constriction (dilation) Genitourinary and GI sphincters - constrict Vasculature - constrict

Question 117

What does Prazosin and Terazosin do?

Answer 117

They are alpha1 blocker/antagonisst so they help treat hypertension.

Question 118

Which tissues do alpha2 agonists act on and what do they do?

Answer 118

Vasculature - constriction NE terminals - decrease NE release Brainstem - decrease NE release

Question 119

What happens to blood pressure when you act on alpha2 autoreceptors?

Answer 119

You can lower blood pressure by acting on these, because it will decrease the release of NE and you will get less vasoconstriction.

Question 120

What does Clonidine act on and what is it used for?

Answer 120

Alpha2 receptor agonist, helps treat hypertension and ADHD

Question 121

What does Guanfacine act on and what is it used for?

Answer 121

Alpha2 receptor agonist, helps treat hypertension and ADHD

Question 122

What does it mean if a drug ends in the letters -OL?

Answer 122

They are most likely a beta blocker.

Question 123

Which tissues do beta1 agonists act on and what do they do?

Answer 123

Increase heart rate via SA node Increase conduction velocity via atrium, AV node, purkinje system, and ventricles

Question 124

Which tissues do beta2 agonists act on and what do they do?

Answer 124

Act on ciliary muscle to relax them for far vision They relax vasculature, especially skeletal muscle for vasodilation They relax lungs, specifically brachial smooth muscle They relax urinary bladder and uterine wall

Question 125

How do beta blockers work to treat hypertension?

Answer 125

By slowing down the heart rate. They are used by athletes and banned by most sports.

Question 126

What does Isoproterenol act on?

Answer 126

Beta1 and Beta2 receptor agonist

Question 127

What does Propranolol act on?

Answer 127

Beta1 and Beta2 receptor antagonist (beta blocker)

Question 128

What does Albuterol act on?

Answer 128

Beta2 agonist (for asthma)

Question 129

What does Terbutaline act on?

Answer 129

Beta2 agonist

Question 130

Where are Beta3 receptors found and do they have a greater affinity for NE or epinephrine?

Answer 130

NE (only one with NE being greater)

Question 131

What are the pathway effects and receptors on iris circular muscle?

Answer 131

Parasympathetic pathway contracts via M receptors

Question 132

What are the pathway effects and receptors on iris radial muscle?

Answer 132

Sympathetic pathway contracts via alpha1 receptors

Question 133

What are the pathway effects and receptors on heart conduction and contractility?

Answer 133

Sympathetic pathway accelerates and increases via beta receptors, and parasympathetic pathway decelerates and decreases via M receptors

Question 134

What are the pathway effects and receptors on skin splanchnic vessels?

Answer 134

Sympathetic pathway contracts via alpha receptors

Question 135

What are the pathway effects and receptors on skeletal muscle vessels?

Answer 135

Sympathetic pathway relaxes via beta2 receptors

Question 136

What are the pathway effects and receptors on bronchial smooth muscle?

Answer 136

Sympathetic pathway relaxes via beta2 receptors and parasympathetic contracts via M receptors

Question 137

What are the pathway effects and receptors on walls of GI tract?

Answer 137

Sympathetic pathway relaxes via alpha2 and beta2 receptors and parasympathetic contracts via M receptors

Question 138

What are the pathway effects and receptors on GI and GU sphincters?

Answer 138

Sympathetic pathway contracts via alpha1 receptors and parasympathetic pathway relaxes via M receptors

Question 139

What are the pathway effects and receptors on GI secretion?

Answer 139

Parsympathetic pathway increases via M receptors

Question 140

What are the pathway effects and receptors on bladder wall?

Answer 140

Sympathetic pathway relaxes via beta2 receptors and parasympathetic pathway contracts via M receptors

Question 141

What are the pathway effects and receptors on the pregnant uterus?

Answer 141

Sympathetic pathway relaxes via beta2 receptors and constricts via alpha receptors while the parasympathetic pathway contracts via M receptors

Question 142

What are the pathway effects and receptors on the penis?

Answer 142

Sympathetic pathway ejaculates via alpha receptors and parasympathetic pathway helps form erection via M receptors

Question 143

What are the pathway effects and receptors on eccrine glands?

Answer 143

Sympathetic pathway increases via M receptors?

Question 144

What are the pathway effects and receptors on Apocrine glands?

Answer 144

Sympathetic pathway increases via alpha receptors

Question 145

What are the pathway effects and receptors on the liver?

Answer 145

Sympathetic pathway increases gluconeogenesis and glycogenolysis via alpha and beta2 receptors

Question 146

What are the pathway effects and receptors on fat cells?

Answer 146

Sympathetic pathway increases lipolysis via beta3 receptors

Question 147

What are the pathway effects and receptors on the kidney?

Answer 147

Sympathetic pathway increases renin release via beta1 receptors

Question 148

From what type of terminals is dopamine released in the kidney?

Answer 148

From sympathetic nerve terminals

Question 149

Which tissue types and what effect does Dopamine have on D1 receptors?

Answer 149

Increases renal blood flow, GFR, and sodium secretion in Kidney Vasodilation in renal, cerebral, and cardiac vasculature CNS effect

Question 150

What are the two agonists to D1 receptors?

Answer 150

Dopamine and Fenoldapam

Question 151

Which tissue types and what effect does Dopamine have on D2 receptors?

Answer 151

It decreases neurotransmitter release in post-ganglionic sympathetic nerve terminals It causes nausea and vomiting in the chemoreceptor trigger zone CNS effect

Question 152

Will Baroreceptor charge, Sympathetic pathway, and Parasympathetic pathway each increase or decrease if you get a drop in mean arterial pressure?

Answer 152

Decrease baroreceptor charge Increase sympathetic pathway, increase in vasoconstriction and total peripheral resistance Decrease parasympathetic pathway, heart rate goes up and cardiac output goes up

Question 153

Does NE favor alpha or beta receptors more in general?

Answer 153

Beta

Question 154

What is the difference with injection epinephrine systemically at low doses compared to high doses?

Answer 154

At a low dose, you may see decrease TPR and diastolic pressure. At higher doses, you may see increased TPR and blood pressure. But you are increasing systolic with both (ventricle contraction with epinephrine). So in the end, at low doses, you don’t have a huge change in mean arterial pressure if you do this slow because systolic and diastolic are counteracting each other. Whereas with high, you have an increased systolic and a flat diastolic so an overall increase in blood pressure and peripheral resistance.

Question 155

What is the definition of the pupils dilating?

Answer 155

Mydriasis

Question 156

What does epinephrine do to the aqueous humor of the eye and what does this help treat?

Answer 156

It increases outflow of aqueous humor and is important for treating glaucoma.

Question 157

What are the five main therapeutic uses of epinephrine?

Answer 157

1. Bronchospasm 2. Anaphylaxis 3. Restore function in cardiac arrest 4. Treat glaucome 5. Prolong action of local anesthetics because it is a vasoconstrictor

Question 158

What are the three main side effects of epinephrine?

Answer 158

1. Cardiac – increased heart rate, palpitaKons, arrhythmias, anginal pain 2. Vascular – increased TPR leading to pallor and increased BP 3. Respiratory – increased TRP can lead to pulmonary edema

Question 159

What is the definition of sympatholytic?

Answer 159

A drug that will block the action of the sympathetic nervous system.

Question 160

Why administer epinephrine with caution if a patient is taking a beta blocker or has heart disease?

Answer 160

Epinephrine still has effects on alpha receptor which would vasocontstrict, increases pressure, which would decrease HR

Question 161

Why administer epinephrine with caution if a patient is taking tricyclic antidepressants?

Answer 161

–Tricyclics work with either 5-HT or NE nerve terminals, which are released, taken back up through their transporters, but these drugs block their re-uptake -So you would have synergistic effects and frankly too much adrenaline going around

Question 162

Why administer epinephrine with caution if a patient is pregnant?

Answer 162

-You would vasoconstrict and would worry about blood flow to the placenta

Question 163

Why administer epinephrine with caution if a patient is diabetic?

Answer 163

It can alter sugar balance in these individuals and it would increase gluconeogenesis and glycogenolysis via alpha and beta 2 receptors

Question 164

Why administer epinephrine with caution if a patient is hyperthyroid?

Answer 164

Has nothing to do with autonomics directly, but if you have too much thyroid hormone in general, you will have increased HR already and putting epinephrine into the mix, you can exacerbate it.

Question 165

How does Pilocarpine work for glaucoma (it also works for xerostomia)?

Answer 165

It acts on muscarinic receptors on iris sphincter muscle, causing the muscle to contract - resulting in pupil contraction (miosis). Pilocarpine also acts on the ciliary muscle and causes it to contract. When the ciliary muscle contracts, it opens the trabecular meshwork through increased tension. This action facilitates aqueous humor leaving the eye to decrease intraocular pressure.

Question 166

To which receptor does NE have the least affinity?

Answer 166

Beta2

Question 167

What is the double-edged sword aspect of NE?

Answer 167

-Because NE doesn’t have much effect on Beta-2, we don’t get much dilation to compensate and we are already getting vasoconstriction so it is a double-edged sword, and when blood pressure increases, the baroreceptors will kick in and the heart rate will slow down to compensate.

Question 168

What is the main therapeutic use of administering NE?

Answer 168

Shock

Question 169

What are the main side effects of administering NE?

Answer 169

Slow heartbeat if BP increased (baroreceptors); forceful beat (β1); vasoconstrict (decreased blood flow to vital organs; α1)

Question 170

What is the administering of Dopamine used for?

Answer 170

Used to treat shock and heart failure (at high doses, increased BP and TPR (α1); increased HR (β1); increased organ perfusion (D1))

Question 171

What does ephedrine do? And what is it used for?

Answer 171

It releases NE, also some direct action on α and β receptors. Used for decongestion and dietary supplements. Side effects: increase HR, vasoconstriction, dilate airways, stimulant (if penetrates CNS)

Question 172

What does amphetamine do?

Answer 172

It helps dopamine be released

Question 173

What does cocaine do?

Answer 173

It blocks the reuptake of dopamine

Question 174

What does methylphenidate do?

Answer 174

It blocks the reuptake of dopamine

Question 175

What does an NRI do?

Answer 175

Blocks reuptake of NE

Question 176

What do TCA’s (Tri-Cyclic Anti-depressants) do?

Answer 176

They increase dopamine levels

Question 177

What is Tyramine’s role with the sympathetic nervous system?

Answer 177

Tyramine is a naturally occurring monoamine compound that serves as a catecholamine releasing agent, in other words, it helps activate the sympathetic pathways. It can displace NE once Tyramine finds its way into nerve terminals. However, tyramine is found in high amounts in certain foods like cheddar cheese and pistachios and if you are taking Monoamine oxidase inhibitors, because MAO is needed in order to break this down and metabolize it.

Question 178

What are the main two non-selective alpha receptor antagonist drugs?

Answer 178

Phenoxybenzamine and Phentolamine. Uses of non-selective α antagonists include treatment of pheochromocytoma (catecholamine secreting tumor), hypertensive emergencies. Effects: - Decreased TPR (α1) and thus decreased BP - Increased HR (baroreceptor response to decreased BP)

Question 179

What are the two main side effects of Phenoxybenzamine and Phentolamine, non-selective alpha receptor antagonists?

Answer 179

1. Orthostatic hypertension (Getting up in a hurry, you don’t have the baroreceptor working appropriately and people can fall down) 2. Nasal stuffiness

Question 180

What are the two main alpha1 antagonists and what do they do?

Answer 180

Prazosin and Terazosin, they help block vasoconstriction so essentially cause vasodilation and are used to treat hypertension as well as benign prostatic hypertrophy (Tamsulosin - flomax). The side effects here are also Orthostatic hypertension and nasal stuffiness.

Question 181

What are the two selective beta1 receptor blockers? And what do they do?

Answer 181

Atenolol and Metoprolol. Uses of β blockers include treatment of hypertension, angina, open- angle glaucoma.

Question 182

What effect do beta blockers have on the heart?

Answer 182

decreased HR and contractility (impair exercise tolerance)

Question 183

What effect do beta blockers have on vasculature?

Answer 183

Increased TPR (blockade of β2 in skeletal muscle) (??Which doesn’t make sense to me?)

Question 184

What effect do beta blockers have on the kidney?

Answer 184

Decreased renin (which would raise BP) release

Question 185

What effect do beta blockers have on the lungs?

Answer 185

Bronchial constriction

Question 186

What effect do beta blockers have on metabolism and the liver?

Answer 186

Decreased glycogenolysis in response to hypoglycemia

Question 187

What things are cholinergic agonists used to treat?

Answer 187

Uses include treatment of myasthenia gravis, glaucoma, Alzheimer’s disease, smoking cessation

Question 188

What are the two main antimuscarinic drugs and what are they used for?

Answer 188

Atropine and Scopolamine. Used for Parkinson’s disease (adjunctive therapy), motion sickness, COPD, urinary urgency……

Question 189

What are the five side effects that should scream anti-cholinergic?

Answer 189

1. Dry mouth 2. Constipation 3. Blurred vision 4. Sedation 5. Urinary retention

Question 190

What are the eight main mechanisms involved with CNS degenerative diseases?

Answer 190

1. Hypoxia 2. Excitatory Amino Acids 3. Ion Fluxes 4. Free Radicals 5. Immune Responses 6. Infections 7. Apoptosis 8. Protein Aggregation

Question 191

What is the mechanism behind hypoxia triggering CNS degenerative diseases?

Answer 191

-These will be cardiovascular in nature, and when you deprive the brain of oxygen you end up with strokes.

Question 192

What is the mechanism behind excitatory amino acids triggering CNS degenerative diseases?

Answer 192

-Glutamate….NMDA/non-NMDA receptors. These are Ionotropic receptors -Too much Ca2+ in cell messes up everything and can kill cells.

Question 193

What is the mechanism behind ion fluxes triggering CNS degenerative diseases?

Answer 193

-Ca2+/Mg2+ can kill neurons and result in degenerative disorders

Question 194

What is the mechanism behind free radicals triggering CNS degenerative diseases?

Answer 194

-Free radicals are usually not good things and the body like to keep these things controlled. -They are reactive electrons that cause a cascade of protein damage and interfere with gene expression -The two places most likely to do this are the catecholamines, especially dopamine, and the other source of free radicals is glutamate, which generates nitric oxide -e.g., catecholamines [quinones] and glutamate [NO

Question 195

What is the mechanism behind immune responses triggering CNS degenerative diseases?

Answer 195

-Autoimmune disorders

Question 196

What is the mechanism behind infections triggering CNS degenerative diseases?

Answer 196

-Viral/bacterial trigger immune systems -Infections can trigger autoimmune responses -Viruses are more common with brain infections because bacteria have a harder time getting across blood-brain barrier

Question 197

What is the mechanism behind apoptosis triggering CNS degenerative diseases?

Answer 197

-Programmed cell death, is part of natural development, healthy when done within certain framework, and uncontrolled cell death is bad. You have more glutamate neurons when you are young than when you are old. Once the area of our brain is developed we don’t need that stimulation anymore so a lot of glutamate goes under apoptosis.

Question 198

What is the mechanism behind protein aggregation triggering CNS degenerative diseases?

Answer 198

-Proteins by nature are very sticky because of negative and positive charged sides. -They are also abnormally sticky because of a protein alteration because of genetics, trauma. -These can elicit an inflammatory response, which can then compromise function, and this is all associated with Beta-amyloid (which is known with Alzheimers)

Question 199

What are lewy bodies?

Answer 199

They are abnormal aggregates of protein that develop inside nerve cells in Parkinson’s disease (PD), Lewy body dementia, and some other disorders. The primary structural component of which is alpha-synuclein. These are associated with Genetics.

Question 200

What are the five main clinical manifestations of Parkinson’s Disease?

Answer 200

1. Tremor/rigidity/bradykinesia 2. Postural abnormalities (-Stooped, they shuffle feet) 3. Autonomic and neuroendocrine (-Increased salivation, can give an anticholinergic like Atropine to help -Speech is slurred as it progresses, they get frustrated -Dysphagia - they can’t swallow very well -They also get altered taste, and that can be an early indication that Parkinson’s is starting) 4. Late symptoms (-Depression, about 60-70% of patients get significant depression, new studies are showing that depression throughout life can make you 4X more likely to get Parkinson’s. ADHD is also linked and Ritalin) 5. Oral status (-They usually come in with a lot of root canals because it is hard for them to take care of their mouths-They salivate more but the saliva isn’t normal, it is very thick and ropy and doesn’t clean and they get cervical caries)

Question 201

What are the characteristics of Stage I of Parkinson’s Disease?

Answer 201

Mild/Early Disease - Only one side of the body is affected, so tremor in just one limb for example, and usually with minimal or no functional impairment

Question 202

What are the characteristics of Stage II of Parkinson’s Disease?

Answer 202

Both sides of the body are affected but posture and balance remain normal

Question 203

What are the characteristics of Stage III of Parkinson’s Disease?

Answer 203

Moderate Disease - Both sides of the body are affected, and there is mild imbalance when standing or walking; however, the person remains independent

Question 204

What are the characteristics of Stage IV of Parkinson’s Disease?

Answer 204

Advanced Disease - Both sides of the body are affected, and there is disabling instability while standing or walking; the person in this stage requires substantial help and cannot live alone

Question 205

What are the characteristics of Stage V of Parkinson’s Disease?

Answer 205

Severe, fully developed disease is present; the person often is cachectic, restricted to bed or wheelchair unless aided

Question 206

What percentage of the general population has Parkinson’s?

Answer 206

0.3%

Question 207

If you are older than 85, what percent chance do you have of getting Parkinson’s?

Answer 207

50%

Question 208

If you are older than 60, what percent chance do you have of getting Parkinson’s?

Answer 208

1%

Question 209

What is the pathophysiology of Parkinson’s Disease?

Answer 209

It is associated with the Nigro striatal Dopamine pathway. It is only the dopamine neurons that get damaged. It is progressive, nothing you can do to stop and halt the disease. When the dopamine neurons get damaged and we lose dopamine and D2 (which is usually inhibitory), GABA and ACh become overactive, so we try and increase dopamine or block ACh, but we would never block GABA. You can also try and activate D2 receptors to help out.

Question 210

What are some common environmental factors that might induce Parkinson’s Disease?

Answer 210

Mg and Hg, Pesticides (farmers are more likely), Trauma (quinones)

Question 211

What are the six main drugs used to treat Parkinson’s Disease?

Answer 211

1. L-dopa + Carbidopa 2. Benztropine 3. Trihexyphenidyl 4. Selegiline 5. Entacapone 6. Pramipexole

Question 212

L-dopa + Carbidopa

Answer 212

Used for Parkinson’s Disease. L-dopa gets across blood-brain barrier much better than dopamine, and Carbidopa blocks the metabolism of L-dopa and dopamine so it can last longer. Some drugs are used in combination with carbidopa-levodopa to either inhibit dopamine breakdown by the body or to improve the effectiveness of carbidopa-levodopa. Azilect inhibits dopamine breakdown while Entacapone improves the effect of Carbidopa-levodopa by inhibiting COMT, Catecholamine Methyl Transferase, which metabolizes neurotransmitters like MAO does.

Question 213

Benztropine

Answer 213

Used for Parkinson’s Disease. This is an anticholinergic medication that helps with tremors, and is effective because it counteracts the cholinergic sensitivity that arises in response to dopamine depletion. It helps dry sialorrhea from PD patients as well. It can give you confusion, blurred vision, urinary retention.

Question 214

Trihexyphenidyl

Answer 214

Used for Parkinson’s Disease. Anticholinergic medication. Everything almost identical to Benztropine.

Question 215

Seligiline

Answer 215

This is used for Parkinson’s Disease. This is an MAO inhibitor, blocking monoamine oxidase B from metabolizing dopamine in the brain, so prolonging the effects of levodopa. Side effects include cardiac dysrhythmias.

Question 216

Entacapone

Answer 216

Used for Parkinson’s Disease. It inhibits COMT, Catecholamine methyl transferase, which metabolizes like MAO does. So works similar to Seligiline, in the sense that they are both inhibiting metabolizing agents.

Question 217

Pramipexole

Answer 217

This is a dopamine agonist, a D2 agonist, which bypasses the depleted neurons int he substantia nigra and provides long-lasting direct stimulation of dopamine receptors. Side effects include orthostatic hypertension, nausea, vomiting, confusion.

Question 218

How does administration of local anesthetic change with Parkinson’s Disease patients?

Answer 218

For patients receiving levodopa and/or entacapone, limit administration to three cartridges of 2 percent lido with 1:100,000 epi per 30 minute period to avoid hypertension and tachycardia. For patients on selegiline, do not administer agents containing epinephrine because of result of severe hypertension.

Question 219

For initiation of treatment on PD patients, how long after PD meds should treatment start?

Answer 219

Should begin 90 minutes after PD meds, and appointments should be shorter than 45 minutes.

Question 220

What are seven tips for maintaining and improving dental health with PD?

Answer 220

1. Use an electric toothbrush 2. Try one handed strategies 3. Apply stannous fluoride gel 4. Visit dentist in the morning 5. Take levodopa 60-90 minutes before visit 6. Try non-alcohol based mouthwash 7. Plan several shorter dentist visits

Question 221

What are the main two clinical manifestations of Huntington’s Disease?

Answer 221

1. Abnormal moves (These moves are eruptive, unpredicted, twisting, turning, grimmacing, facial contortions. We have excess dopamine activity going on here) 2. Progressive intellectual dysfunction (Early on with this disease, they have poor judgment, withdraw from people, get severely depressed. Later on, they become psychotic (Schiz), they get paranoid, compulsive about doing things certain ways)

Question 222

How many have Huntington’s Disease? How long do you live once you’ve been diagnosed on average? What is the name of the gene involved?

Answer 222

0.01% 5-10 years once diagnosed Hunting gene, if you have it, you will get Huntington’s Disease

Question 223

What is the pathophysiology of Huntington’s Disease?

Answer 223

Increase in dopamine and a decrease in GABA because the cell bodies in GABA die. Patients have lost most of the cell bodies because the caudate has been lost, which sits right next to the ventricles on the outside. The hunting gene seems to alter NMDA/AMPA receptors for Glutamate, and you end up killing these receptors from over-excitation of the glutamate system. The hunting gene is found in the GABA neurons.

Question 224

How do you treat Huntington’s Disease?

Answer 224

Do genetic screening. And you use a dopamine antagonist (antipsychotics), usually a D2 antagonist, and Dopamine depletion for choreiform movement, and antidepressants. The D2s are going to be on GABA, but we have lost GABA, then we don’t have a lot of it and we need whatever we can get so we shut down the inhibitory D2 so we can salvage as much GABA as we can to fight the excess dopamine.

Question 225

What are the clinical manifestations, stages, and brain regions affected in Alzheimer’s disease?

Answer 225

-Most common, anywhere from 3-4 million people have it at any given time -Once diagnosed, 10-20 years usually they live -It is broken down into three stages, and all of this relates to eliminating extra capacity of the brain -The brain determines what kind of capacity it will have later on when we are children and adolescents. Brain regions involved are frontal cortex, which is intelligence, judgement, and behavior, memory in the temporal lobe, and language right behind it in the parietal lobe. -Early stage is annoying stage, they have memory lapses and forget names, don’t like change -Moderate stage is when they have problems functioning, normal routine is disrupted -Late stage the motor system gets disrupted, they get less mobile, no judgment, immobile and stop eating.

Question 226

If you are above 85, what is the percentage of you getting Alzheimer’s?

Answer 226

40-50% chance

Question 227

What is the pathophysiology of Alzheimer’s Disease?

Answer 227

Has a lot to do with old age and genetics. It affects the hippocampus, cortex, and nucleus basalis, and is associated with degeneration of cholinergic systems, ACh neurons.

Question 228

What are the histological components of Alzheimer’s?

Answer 228

-Senile plaques (they are inside of the neuron), associated with the B-amyloid plaques -Neurofibrillary tangles, associated with a tau protein -Protein aggregates precipitate and cause inflammation and kills cells. Diminish capacity of brain, not able to do multiple tasks concurrently.

Question 229

What are the main genetic components of Alzheimer’s?

Answer 229

Certain apolipoprotein that has relevance, as well as abnormal APP (amyloid precursor protein) to beta amyloid

Question 230

How do we go about treating Alzheimer’s? What about treating symptoms of Alzheimer’s?

Answer 230

-We try and increase ACh activity -We largely use Cholinesterase inhibitors -The main drug to know is Donepezil -Anti-inflammatories also help -For treating symptoms of Alzheimer’s, antipsychotics/antidepressants and other drugs. -They say you can help prevent it with exercise.

Question 231

What is the main drug in treating Alzheimer’s Disease and what does it do?

Answer 231

Donepezil, it is a cholinesterase inhibitor, targeting the cognitive and functional decline symptoms.

Question 232

What are four tips for managing dental needs in Alzheimer’s Disease?

Answer 232

1. Provide short simple instructions. 2. Use a “watch me” technique 3. Monitor daily oral care 4. Keep up with regular dental visits as long as possible

Question 233

What are the clinical manifestations of Multiple Sclerosis?

Answer 233

Symptoms are highly diverse because they correspond to where the damage is happening in the brain. You can have optic, hearing, sensory, autonomic, cognition, mood, fatigue, muscle weakness and heat tends to worsen everything.

Question 234

What is the incidence of multiple sclerosis?

Answer 234

Less than, 1,000,000

Question 235

What is the group of people must susceptible to multiple sclerosis? More males or females?

Answer 235

Scandinavians have a high incidence, Japan has low. 2:1 ratio from male to female.

Question 236

What is the pathophysiology of Multiple Sclerosis?

Answer 236

It all comes down to oligodendrocytes getting damaged and the myelin is then lost, which results in abnormal or missing conduction. They believe that a virus might trigger it causing acute inflammation and an auto-immune response.

Question 237

What are the four classifications of Multiple Sclerosis?

Answer 237

1. Benign 2. Relapsing remission (symptoms are more severe and you are likely to be diagnosed, episodes typically don’t worsen) 3. Relapsing progressive (cycle, and symptoms worsen) 4. Chronic progression (there is no relapse, and the symptoms progressively get worse, most likely to be fatal, and represents about 10% of all types)

Question 238

How is Multiple Sclerosis best diagnosed?

Answer 238

There are no definitive tests but MRI’s are used often to get a way to feel good about diagnosis. -MRI measures blood perfusion, and these white spots show that there is tissue damage, inflammation, cell death, and could indicate MS, you need 2 or more of these lesions to have a definitive diagnosis that it is multiple sclerosis -These white areas could also be a tumor, stroke scar, cancer -And you combine all this with increased symptoms

Question 239

What are the main treatment options for Multiple Sclerosis?

Answer 239

Prednisone is most common, it is a steroid used for anti-inflammation. Interferons are more extreme, as well as methyltrexate, which are both anti-cancer treatments.

Question 240

What are the main side effects to Prednisone for Multiple Sclerosis?

Answer 240

Bladder dysfunctions, bowel dysfunction, depression, fatigue, pain, tremors.

Question 241

How much does “pain” cost the US each year?

Answer 241

Around $635 billion

Question 242

What is a definition of pain?

Answer 242

An unpleasant sensory and emotional experience associated with actual or potential tissue damage.

Question 243

What are the three components of pain?

Answer 243

1. Sensory-discriminative 2. Cognitive 3. Emotional/affective

Question 244

What is the definition of nociception?

Answer 244

The physiological process by which information on actual/potential tissue damage is conveyed to the CNS

Question 245

What is the definition of nociceptors?

Answer 245

Specialized ion channels on sensory nerve endings that respond to noxious stimuli. There are 4 or 5 different nociceptors that we will be talking about

Question 246

What is the definition of nociceptive pain?

Answer 246

Pain resulting from activation of nociceptors as a result of actual or potential tissue damage and processing by the CNS (Somatic/visceral/inflammatory)

Question 247

What is the definition of neuropathic/neurogenic pain?

Answer 247

A pathophysiological process resulting from abnormal sensory processing, which does not signal actual or potential tissue damage, does not promote healing or repair, and may be considered a disease. Fibromyalgia is an example of neuropathic pain.

Question 248

What is the definition of somatic pain?

Answer 248

Pain associated with musculo-skeletal system and skin - it is well defined. We will see mostly somatic pain in the dental office.

Question 249

What is the definition of visceral pain?

Answer 249

Pain associated with internal organs and associated tissues - it is dull, burning, poorly defined.

Question 250

What is the difference between analgesia and anesthesia?

Answer 250

Analgesia is a selective reduction of pain perception. Anesthesia is the absence of any sensation due to suppression of CNS function.

Question 251

What are the four basic physiologic processes in nociception? And where do they take place?

Answer 251

Transduction, transmission, modulation, and perception. Transduction happens in primary afferent nociceptor, then transmission happens when action potential passes through dorsal root ganglia to actual spinal cord, where modulation takes place, crosses the midline, and goes up spinothalamic tract to the thalamus, and then into the cortex where pain perception takes place.

Question 252

What does TRP stand for and what is it?

Answer 252

TRP stands for transient receptor potential. They are a group of ion channels located mostly on the plasma membrane of numerous animal cell types. They are indirect mediators of pain, making things more or less sensitive. They are involved with transduction.

Question 253

What are the four different subtypes of specific ion channels on free nerve endings that respond to actual or potential tissue damage?

Answer 253

1. Mechanical 2. Chemical 3. Thermal 4. Polymodal

Question 254

What is Capsaicin used for and which nociceptor does it activate primarily?

Answer 254

It is used as a topical pain reliever that activates the TRPV1 directly and indirectly to make them less sensitive.

Question 255

How does secondary activation of nociceptor nerves work?

Answer 255

Chemical messengers released from activated nociceptor nerve endings act locally to release messengers that further activate the nociceptors. This is positive feedback. Action potentials propagate toward the cell body in the dorsal root ganglia and then enter the spinal cord.

Question 256

What is sensitization when it comes to pain?

Answer 256

It is increased sensitivity and response to stimuli in and near the injured area. It is produced by chemical messengers that do not directly activate nociceptors but which sensitize them, making them more excitable and more likely to be activated by stimuli and produce enhanced discharge frequencies.

Question 257

What is hyperalgesia?

Answer 257

It is an increased perception of pain in response to painful stimuli. On same line as allodynia.

Question 258

What is allodynia?

Answer 258

It is pain evoked by normally non-painful stimuli. On same line as hyperalgesia.

Question 259

Why is pain sensitization so important?

Answer 259

It is important for protection of damaged area, and because it promotes healing.

Question 260

What are the two major candidates for pain sensitization?

Answer 260

Substance P (SP) from nerve endings and Prostaglandins from damaged cells

Question 261

What happens when prostaglandin receptors are stimulated?

Answer 261

It results in activation of specific Na+ channels, making the nociceptive nerve ending more excitable, so it is increasing pain sensitization of nociceptors. If you block PG’s or don’t let them form, it doesn’t end up letting sodium come in, which doesn’t activate the TRPV1 nociceptor, and we don’t feel as much pain.

Question 262

Are COX-1 and COX-2 constitutive or induced?

Answer 262

COX-1 is constitutive, meaning it is always there under normal conditions in many tissues. COX-2 is induced by hormones, growth factors, and inflammatory mediators, and isn’t always present.

Question 263

What does COX-1 normally help out with?

Answer 263

GI protection, platelet aggregation, renal activities.

Question 264

What does COX-2 normally help out with?

Answer 264

Cardiovascular protection, renal activities, pain, fever, inflammation. The pain, fever, and inflammation are the inducible activities of COX-2, while the others are constitutive.

Question 265

What is the primary function of NSAIDS?

Answer 265

They inhibit synthesis of prostaglandins that are involved in sensitizing the nociceptor nerve ending.

Question 266

What kind of stimulation usually takes place with nociceptors in the viscera?

Answer 266

Mechanical stimulation, like distention, contractions, and may even be “referred” to somatic sites (like a brain freeze)

Question 267

What are the main two types of sensory nerve fibers than transmit pain?

Answer 267

A delta and C fibers. They carry nociceptive transmission to the spinal cord.

Question 268

What is the difference between A delta and C fibers.

Answer 268

A delta fibers are small, myelinated, fast conducting, associated with mechanical, thermal nociceptors, and they transmit “first” or “fast” pain, diameter of 1-6 mm, sharp localized pain when dentin is first exposed, and more associated with a reflex than C fibers. C fibers are small, unmyelinated, slow conduting, associated with polymodal nociceptors, and they transmit “slow” or “second” pain, diameter of 2 mm, associated with conduction of dull, difuse pain.

Question 269

What is the name of the plexus of nerves in the pulp called? And what two groups of fibers does it consist of?

Answer 269

The Plexus of Raschkow, or Sub-Odontoblastic Plexus. It consists of sensory afferents of the trigeminal nerve and sympathetic branches from the superior cervical ganglion.

Question 270

What do nociceptive fibers synapse with in the dorsal horn?

Answer 270

With “projection” neurons, because they are projecting up, and this is called modulation.

Question 271

What are the two important pain neurotransmitters that are released from A delta and C fibers in order to excite the projection neurons to go up into the thalamus from the dorsal horn?

Answer 271

Glutamate and Substance P

Question 272

What is the pathway of pain transmission starting at the injury?

Answer 272

Starts at injury, the noxious stimuli activate the sensitive peripheral ending of the primary afferent nociceptor by the process of transduction. The message is then transmitted over the peripheral nerve to the spinal cord, projection neurons send axons across the midline, where it synapses with cells of origin of the major ascending pain pathway, the spinothalamic tract. The message is relayed in the thalamus to the somatosensory cortex 1 and 2.

Question 273

What is the name of the nucleus that inputs the information to the thalamus?

Answer 273

Trigeminal nucleus

Question 274

What kind of modulation takes place at the dorsal horn, facilitatory or inhibitory?

Answer 274

Nociceptive input is heavily modulated at the dorsal horn by both facilitatory and inhibitory influences, there are transmitters at all of the levels that will do either one of these.

Question 275

What is central sensitization?

Answer 275

It is when dorsal horn projection neurons become sensitized and hyper-responsive to nociceptive input, which contributes to hyperalgesia, and to touch input, which contributes to allodynia. Prostaglandins released from neurons and/or glia in the dorsal horn in response to neural input and inflammatory mediators are probably involved in central sensitization as well. And NSAIDS can inhibit the synthesis of prostaglandins in the dorsal horn that participate in central sensitization, this is considered a second mechanism for the anti-nociceptive action of NSAIDS.

Question 276

The dorsal horn is also a major site of action for what?

Answer 276

The action for analgesic drugs, including opioids.

Question 277

What is the “gate control” theory of pain? What fibers converge for this?

Answer 277

The gate control theory of pain asserts that non-painful input closes the “gates” to painful input, which prevents pain sensation from traveling to the central nervous system. Therefore, stimulation by non-noxious input is able to suppress pain. So an example is putting pressure on palate to attempt to inhibit nociception from the injection. Gate control is inhibition of pain by touch. There is a convergence of inputs from A-beta and A-delta fibers, competing for same train tracks.

Question 278

What happens during “referred pain?”

Answer 278

Visceral afferent nociceptors converge on the same pain-projection neurons as the afferents from the somatic structures in which the pain is perceived, and the brain cannot distinguish the origin. An example is sinusitis and dental pain.

Question 279

Why is nociceptive pain important to feel and how is it usually terminated?

Answer 279

It is important in signaling actual or potential tissue damage, and is normally terminated by the healing and repair process. However, too much pain can also be maladaptive.

Question 280

What is the periacqueductal gray?

Answer 280

It is the primary control center for descending pain modulation. It has enkephalin-producing cells that suppress pain. The ascending pain and temperature fibers of the spinothalamic tract send information to the PAG via the spinomesencephalic tract (so-named because the fibers originate in the spine and terminate in the PAG, in the mesencephalon or midbrain).

Question 281

What is the key locus in the endogenous pain suppressant neural system? And what are the primary opioid mediators of these pain modulation systems?

Answer 281

Periacqueductal gray, although there are multiple stations in which modulation of pain can occur. Enkephalins.

Question 282

What is another name for the endogenous opioid peptides? And what do they do?

Answer 282

The Endorphins. They play a key role in inhibitory feedback and other physiological processes. They activate various opioid receptors, which are also receptors for opioid analgesic drugs (Mu, delta, and kappa)

Question 283

What are the three main classes of opioid receptors and what are the three endogenous opioid peptides that interact with them?

Answer 283

Mu, Delta, and Kappa. Enkephalin, Beta-Endorphin, and Dynorphin.

Question 284

What are the characteristics of enkephalins?

Answer 284

Act on Delta and Mu receptors. 5 amino acids long. Made up of Methionine and Leucine.

Question 285

What are the characteristics of beta-endrophins?

Answer 285

Act on Delta and Mu receptors. 91 amino acids long. -You can’t give a Beta-endorphin therapeutically, it would be proteased too quickly, but we have drugs that have opioid agonist properties that have a number of naturally occurring narcotics that have selective activities that act on mu or delta receptors.

Question 286

What are the characteristics of dynorphins?

Answer 286

Act on Kappa receptors. 17 amino acids long. There are A and B Dynorphins, they are inhibitory, they tend to block a lot of the typical reward functions. The kappa receptors are antagonistic to mew and delta, but they still have analgesic properties.

Question 287

What kind of effects do drugs that enhance the action of NE and 5HT in the CNS have?

Answer 287

Antinociceptive effects. They don’t give you much of a sensation other than the pain goes away.

Question 288

In what two areas do opioid analgesics primarily act on?

Answer 288

The Periacqueductal Gray (PAG) and the Dorsal Horn.

Question 289

Why would combining an opioid agonist (something that mimics enkephalin) with a substance P antagonist?

Answer 289

You would get synergism and additivity, and it would enhance the drug, and you wouldn’t have to use as much opioid agonist so you could reduce the side effects caused by opioids.

Question 290

How can you get analgesic effects in the dorsal horn of the spinal cord?

Answer 290

Any influence that reduces the release of glutamate and substance P from the primary afferent are analgesic.

Question 291

What is the definition of neuropathic pain?

Answer 291

Pain sensations that may be continuous or periodic, but occur without activation of nociceptors by actual or potential tissue damage. Hyperalgesia and allodynia are common and dramatic here. May result form abnormal activity in nociceptive fibers that have been damaged, but after injury has healed, or from abnormal activity in central pain pathways. There is no protective function and it does not terminate with healing. Triggers can initiate. Involves continuous deep burning, aching, or periodic shock, and is characterized by 1 or more peripheral nerves caused by damage to the nerve.

Question 292

What are five common examples of neuropathic pain?

Answer 292

1. Phantom Limb 2. Shingles 3. Fibromyalgia (9 common points of pain) 4. Diabetes Neuropathies 5. Trigeminal Neuralgia (tic douloureux)

Question 293

Does neuropathic pain respond to NSAIDS, opioids, or antidepressants, anticonvulsants, corticosteroids?

Answer 293

Never to NSAIDS, inconsistently to opioids, and some responses to antidepressants, anticonvulsants, and corticosteroids.

Question 294

What is the name of the antidepressant used for neuropathic pain?

Answer 294

Cymbalta

Question 295

What is the name of the two anticonvulsants used for neuropathic pain?

Answer 295

Lyrica and Gabapentin

Question 296

What are the four main possible mechanisms for neuropathic pain?

Answer 296

1. The peripheral sensitization process may persist rather than subside 2. Damaged nociceptive nerves may fire spontaneously (without activation of nociceptors by usual stimuli) 3. Prolonged input from hyperexcitable nociceptive fibers 4. Decreased activity of endogenous pain-suppressant neural system

Question 297

What is the role of placebos and pain?

Answer 297

They may have an endogenous analgesia effect, most likely caused by release of endorphins, and there might be a connection with acupuncture.

Question 298

What are the three different types of pain that will factor in to which analgesic we choose?

Answer 298

1. Musculoskeletal 2. Inflammatory 3. Visceral Pain

Question 299

What three groups of pain medications work at the Brain level?

Answer 299

1. Opioid narcotics 2. Glutamate, GABA (Tramadol) 3. Antidepressants (5HT/NE) (Maybe 10% of dentists prescribe antidepressants for pain, usually when the person can’t use the common drugs like NSAIDS because of ulcers and GI side effects and stuff)

Question 300

What two groups of pain medications work at the Descending Modulation level?

Answer 300

1. Serotonin drugs 2. Neuropeptides

Question 301

What three groups of pain medications work at the Dorsal Horn (modulation sites) level?

Answer 301

1. Local Anesthetic 2. Opioids 3. NSAIDS

Question 302

What four groups of pain medications work at the Peripheral Nociceptor (transduction site) level?

Answer 302

1. Local Anesthetic 2. NSAIDS, COX-2 inhibitors 3. Acetaminophen 4. Capsaicin (works on TRPV and also releases substance P)

Question 303

What two compounds does COX-1 produce, and what are their four roles in the body?

Answer 303

1. Prostaglandins E2 2. Thromboxane A2 1. Gastric mucosal barrier 2. Renal function 3. Platelet aggregation 4. Vasoconstriction

Question 304

What two compounds does COX-2 produce, and what are their three roles in the body?

Answer 304

1. Prostaglandins 2. Prostacyclin 1. Pain, inflammation, fever 2. Renal function 3. Vasodilation

Question 305

Which COX inhibitor (1 or 2) is more associated with cardiovascular issues?

Answer 305

COX-2 inhibitors are more inclined to cause cardiovascular issues, because you are getting a block of vasodilation and getting vasoconstriction and have a coronary issue than you could have a stroke or myocardial infarction.

Question 306

Which COX inhibitor (1 or 2) is more associated with GI issues and bleeeding?

Answer 306

COX-1 inhibitors. Wouldn’t want to use Cox-1 inhibitor on a bleeding ulcer because it is an anticoagulant and causes GI problems.

Question 307

Which drug is notorious to avoid for anyone with liver damage/alcohol dependencies?

Answer 307

Acetaminophen

Question 308

What are the “anti-“ properties of COX-1 and COX-2 inhibitors?

Answer 308

They are both analgesic, anti-pyretic, and anti-inflammatory.

Question 309

What is acetaminophen’s mechanism?

Answer 309

It is a Non-NSAID, Non-COX 1 or 2 inhibitor—perhaps blocks a COX 3 and/or works on 5HT. It is non-anti-inflammatory, has good anti-pyretic and some good analgesia. So does not help with inflammation, but can help with pain caused by inflammation.

Question 310

What should you avoid if you have kidney disease?

Answer 310

COX-1 and COX-2 inhibitors

Question 311

What are salicylates?

Answer 311

They are non-selective COX-1 and COX-2 inhibitors, ibuprofen-like, so they are NSAIDS.

Question 312

What is Celebrex?

Answer 312

It is a COX-2 inhibitor

Question 313

In general, does it usually take a higher dose to relieve pain or inflammation?

Answer 313

Inflammation

Question 314

What three compounds is Excedrin made up of?

Answer 314

Aspirin, Acetaminophen, and Caffeine

Question 315

What are the dose requirements and characteristics of Salicylates?

Answer 315

COX-1 and COX-2 inhibitor. Analgesia is 600 mg Anti-inflammation is 1 gm Antipyretic is 300-600 mg Duration is 4h -Causes GI irriation, anti-clotting (-You are permanently damaging the platelet when you take these, and you have to regrow platelets, and this anti-clotting can happen with less than 100 mg of salicylates. Don’t prescribe salicylates when you are doing surgery on patients. -When the acetyl group breaks off, this turns into an acid. It has direct and indirect effects on this.), ringing in ears, and Reyes Syndrome in children (With Reyes- You can have permanent damage done to the brain, that is why aspirin-containing products are forbidden in children)

Question 316

What are the dose requirements and characteristics of Ibuprofen-type NSAIDs?

Answer 316

COX-1 and COX-2 inhibitor Analgesia is 400 mg Anti-inflammation is 800 mg Antipyretic is 400 mg Duration is 4 hours Often a little better pain relief than aspirin -Causes GI ulcers, anti-clotting (-Only indirectly affects platelets unlike salicylic acid, but indirectly through prostaglandins), cardiovascular effects.

Question 317

What are the names of the two Ibuprofen-like NSAIDS?

Answer 317

Ketoprofen and Naproxen. Ketoprofen is same properties, but more potent; 50 mg is recommended analgesic dose. Naproxen is longer-lasting and slower-acting (Aleve)

Question 318

What is the main COX-2 selective antagonist?

Answer 318

Celecoxib (Celebrex). • Prescription only • Same analgesia as ibuprofen • Lacks GI and anti-clotting action • Warning about cardiovascular side effects

Question 319

What are the three “other” NSAID agents that are all prescription only?

Answer 319

1. Indomethacin - potent non-selective NSAID/ due to side effects not a common analgesic 2. Meloxicam - preferentially inhibits Cox-2 over Cox-1/ means less GI problems 3. Diflunisal - Related to salicylates- supposed to be good for bone pain

Question 320

What are the analgesic uses of NSAIDS?

Answer 320

Dental pain, headaches, muscle/joint/bone pain, earaches. All NSAIDS have a plateau at the mild to moderate pain reliever level

Question 321

What are the main NSAID contraindications?

Answer 321

1. Coumadin 2. Joint replacement 3. Heart attack/stroke 4. Major surgery 5. Atrial fibrillation 6. Frequent Upset stomach 7. Bleeding in stools 8. Takes antacids 9. Takes H2 blockers (Tagamet) 10. Hemophiliac 11. Already taking high doses (ex. arthritis) 12. Child or adolescent 13. History of allergies

Question 322

What are the main three therapeutic uses for opioid narcotics?

Answer 322

1. Analgesia (somatic and visceral) 2. Antitussive 3. Antidiarrheal

Question 323

What is the most potent opioid narcotic and what is it’s equipotent IM dose?

Answer 323

Fentanyl at 0.1 mg

Question 324

What is the order of equipotent IM doses of opioid narcotics?

Answer 324

Fentanyl at 0.1 mg Oxymorphone at 1 mg Hydromorphone at 1.5 mg Morphine at 10 mg Oxycodone at 20 mg Hydrocodone at 30 mg Codeine at 200 mg

Question 325

What are the four “other” opioid narcotics?

Answer 325

1. Meperidine (for moderate pain, demerol) 2. Pentazocine (It is unique because of its interaction with the kappa receptor, so makes it less likely that people will abuse this, it has a mixed agonist/antagonist effect) 3. Methadone (If an opioid addict is going to methadone clinics, then chart that and know that you don’t need to give them more pain coverage, also used to treat opioid addiction) 4. Buprenorphine (As they go to higher doses it turns into an antagonist, shuts everything off, and kicks them into withdrawals, so harder to get addicted to, similar to two above)

Question 326

What are the four major opioid agonist side effects, and on which receptor do they primarily take place?

Answer 326

1. Respiratory depression/decreased pulmonary reflex 2. Constipation/slow bowel movement 3. Sedation/additive or synergistic with other CNS depressants (e.g., alcohol, antianxiety, sleep aids and natural sleep 4. Euphoria/dependence, addiciton -Mostly Mu opioid receptor mediated

Question 327

How are opioid narcotic overdoses treated?

Answer 327

Inject the Mu antagonist - naloxone (Narcan). Although it may precipitate withdrawals, and it will block the endorphins (endogenous opioid systems), and if you take these alone, you will get anxiety, stress, or hypersensitivity to pain

Question 328

What are the four main contraindications to opioid narcotics?

Answer 328

1. History of substance abuse (alcohol, opioids, etc) 2. Severe constipation and upset stomach 3. Respiratory problems (emphysema or asthma) 4. Use of other CNS depressants (sedative/sleep aids/muscle relaxants)

Question 329

What are the two main suggestions for use of analgesics with dental pain>

Answer 329

1. Use prior to dental procedure, may reduce post-operative pain and inflammation 2. Start with NSAIDS- if not sufficient, start opioid drugs at low dose and go slow (prescribe only a few at a time)

Question 330

What is the first-line drug treatment (3 of them, and they are all FDA approved) to manage neuropathic pain like Trigeminal neuralgia?

Answer 330

1. Gabapentin (antiseizure 2. Duloxetine (antidepressant) 3. Nortriptyline (antidepressant)

Question 331

What is the “next-line” of drug treatment for neuropathic pain like Trigeminal neuralgia?

Answer 331

Tramadol (Ultram). It is a schedule 4 drug. Low drug abuse potential, but some minor opioid action.

Question 332

What is the definition of drug use?

Answer 332

Prescribed and clinically appropriate

Question 333

What is the definition of drug misuse?

Answer 333

Either not prescribed or clinically inappropriate

Question 334

What is the definition of drug dependence?

Answer 334

Persistent use resulting in adaptations typically accompanied by accommodation or tolerance (causing compensatory escalation) and withdrawal (e.g., aches, diarrhea, depression and cravings)

Question 335

What is the definition of drug addiction?

Answer 335

Compulsive drug use that consists of repetition to satisfy intense urges, despite severely negative consequences

Question 336

What drug schedule are most opioid drugs?

Answer 336

Schedule II. Schedule I is strongest.

Question 337

What is the six-step addiction cycle for prescription drugs?

Answer 337

1. Relieve medical condition 2. Causes reinforcing effects (increased dopamine in brain) 3. Induces physical dependence 4. Often there is a tolerance and withdrawal issue 5. Patients often have substance abuse risk before treatment (mental risk/pre-existing problem) 6. Patient uses various strategies to maintain drug supply

Question 338

How many million Americans use prescription drugs at least once a year for “non-medical” reasons?

Answer 338

9 million

Question 339

Where do abused prescription drugs come from primarily?

Answer 339

Friend or Relative (66%) Buy the drugs (21%) Doctor’s prescription (19%) Took/stole the drugs (12% Dealer (8%)

Question 340

How many hours of CE credit on drug abuse issues in Utah do you have to take a year if you want to maintain your license?

Answer 340

2 hours of CE credit

Question 341

What is SBIRT?

Answer 341

It stands for Screening, Brief interview, Intervention, Referral, & Treatment. It is how we assess and monitor drug prescriptions and abuse.

Question 342

What is DOPL?

Answer 342

It stands for Division of Occupational and Professional Licensing. It monitors and regulates the prescriptions of drug prescribers, like Dentists. It also establishes qualifications and requires training for licensing and certifications.

Question 343

How can you best manage high-risk patients for drug prescription abuse?

Answer 343

Medication management agreements, tight control on prescription drug numbers and routine accountability, and drug screens with associated consequences.

Question 344

What does DSM-5 stand for? And what does it do?

Answer 344

Diagnostic and Statistics Manual of Mental Disorders. It organizes each psychiatric diagnosis into five dimensions (axes) relating to different aspects of disorder or disability.

Question 345

What does Axis I through V cover?

Answer 345

Axis I - All psychological diagnostic categories except mental retardation and personality disorder Axis II - Personality disorders and mental retardation Axis III - General medical condition; acute medical conditions and physical disorders (Meningitis, which means I have inflammation, a fever, cause symptoms that look like psychiatric disorders) Axis IV - Psychosocial and environmental factors contributing to the disorder (e.g. stress) Axis V - Global Assessment of Functioning or Children􏰃s Global Assessment Scale for children and teens under the age of 18

Question 346

What are some disorders found in Axis I?

Answer 346

Depression, anxiety disorders, bipolar disorder, ADHD, autism spectrum disorders, anorexia nervosa, bulimia nervosa, schizophrenia and drug dependence (usually).

Question 347

What are some disorders found in Axis II?

Answer 347

Personality disorders: paranoid personality disorder, schizoid personality disorder, antisocial personality disorder, narcissistic personality disorder, dependent personality disorder, obsessive-compulsive personality disorder; and intellectual disabilities.

Question 348

What are some disorders found in Axis III?

Answer 348

Brain injuries and other medical/physical disorders which may aggravate existing diseases or present symptoms similar to other disorders, (sometimes drug abuse?). (-So if you get schizophrenia from a brain injury from a car crash, it is axis III, If you have schizophrenia coming from drug abuse, it is also axis III)

Question 349

What is MSE and how is it collected?

Answer 349

Mental Status Examination. The data are collected through a combination of direct and indirect means: unstructured observation while obtaining the biographical and social information, focused questions about current symptoms, and formalized psychological tests.

Question 350

In regards to the MSE, what is mood?

Answer 350

Types and extreme

Question 351

In regards to the MSE, what is affect?

Answer 351

Appearances, how do you carry yourself, communicate

Question 352

In regards to the MSE, what is thought, and its three categories?

Answer 352

Thought process (organization, able to organize a reasonable answer to a question, needs to be consistent and sequential Thought content (relevant, insightful) Thought perception (understanding, interpretation of what is happening in the environment)

Question 353

In regards to the MSE, what is appearance?

Answer 353

-Relevant attire in certain situations -Hygiene is important -Aware of the environment -Motivation to take things seriously and dress appropriately

Question 354

In regards to the MSE, what is cognitive function, and what are the means of assessing?

Answer 354

It is information processes, decision-making, planning and implementing. The assessment takes place with orientation (-Relate to environment, do you know who you are, question after concussion), concentration (-Can they focus -Can they stay on task), memory (-Short, intermediate, long-term memory? The first one to dissapear for Alzheimer’s is short), fund of knowledge (-Do you have a wealth of knowledge, well-informed, read the newspaper), abstraction (-Going obvious to subtle -Taking basic instruction, extrapolate to real-life case), judgment (-Appropriate reactions to situations like someone telling you your zipper is down), and insight (-Subtle-Intuitive-Schizophrenics are horrible at reading facial expressions)

Question 355

Besides the Mental Status Examination (MSE), what are the two other tests used?

Answer 355

Electroencephalogram and Brain imaging. Electroencephalograms measure the surface electrical activity of the brain. They don’t diagnose this from that but they can indicate reliable diagnostic patterns. Brain imaging involves a CT, MRI, and PET.

Question 356

How would an MRI help with mental status examination?

Answer 356

It measures the amount of oxygen in blood in brain, BOLD - Blood Oxygen Level Dependancy.

Question 357

How would a PET help with mental status examination?

Answer 357

It will tell us where our metabolism of a certain sugar occurred. For a depressed patients, it won’t light up in many places.

Question 358

What is psychosis? What is schizophrenia? And what are the demographics?

Answer 358

Psychosis -They are not able to perceive what is real, they have an impaired sense of reality -They have an altered cognition and emotion -This is a symptom, like hypertension Schizophrenia -is most commonly recognized -This is referred to as the cancer of mental illness -This costs us about $40 billion a year in the US -1% of people in the United States are schizophrenics -Poor urban U.S, because that’s where they end up

Question 359

What are the symptoms of schizophrenia?

Answer 359

-There are many types -There are remissions -They will do better than have a relapse, it is a cycle -They have withdrawn -Their thinking and speech is abnormal -Usually anhedonic, they don’t get pleasure out of life, not rewarding -Often thinking about and occasionally implement suicide -Personal appearance is abnormal -Tends to be worse in men -For men, late teen to 20’s, more aggressive and faster in mens -For women, late 20s to 30s -Their thinking has loose connections -They are dillusional (your sensory input is ok, but the way you interpret that input doesn’t relate to reality) -They have hallucinations (sensory input has been corrupted) -Emotions - flat affect -Difficulty in filtering sensory input, get distracted easy -Lack of pre-pulse inhibition (they get a heightened startle reflex and their brain cannot tone it down)

Question 360

What is the DSM-5 criteria for schizophrenia?

Answer 360

-They need to persist for longer than 6 months -You have deteriorating functions, can’t take care of family or self -Active psychosis, not relating to reality -A differential diagnosis is that there are no drugs or trauma

Question 361

What are the four subtypes of schizophrenia and their features?

Answer 361

1. Disorganized type - -Blunted affect, nothing to read about facial expressions -They are incoherent, don’t make sense -Not particularly dellusional -Bizarre mannerisms 2. Catatonic type - -Nonresponsive, but aware of what is going on -Rigid/bizarre posture 3. Paranoid type - -Positive symptoms, so they are ofen delusional, halllucinations -Aggressive and uncooperative -You would actually want this type if you were a doctor giving medications because of the positive symptoms, most likely to respond 4. Residual type - -Negative symptoms, so no delusions, socially withdrawn -Flat affect -Later stages is when these all get worse -This type is most difficult to treat

Question 362

What is the prognosis of schizophrenia?

Answer 362

1. Chronic equals poor 2. Residual = poor prognosis 3. Institutionalized a lot, that is indication of severity, not a good sign 4. Life expectancy is shortened = 10% suicide, not taking care of selves 5. Best prognosis = temporary, cause-related, principally positive symptoms, If onset is later than 30 years, if person is female, and if there is no family history

Question 363

What is the biology such as the neurochemical basis and genetic elements of schizophrenia?

Answer 363

-No organic measure -But there are hints, Increase in ventricular size suggests that brain damage has occurred, and because only one of the identical twins had brain damage, this says that environmental factors play a role. You get a decrease in corpus callosum, which is the pathway between the cortex, there is a decrease in frontal cortex blood (MRI), these folks don’t yawn, altered startle and accomodation -Dopamine mechanism, D2 receptor in excess, and early anti-psychotics are D2 antagonists -But the more we study, 5HT may also contribute as well as glutamate, especially to the negative symptoms, and dopamine is more associated with the positive symptoms. -There is also a genetic predisposition

Question 364

What is the mechanisms of drugs treating schizophrenia?

Answer 364

-All of them block D2 (-Both pre and post synaptic receptors, you can’t have selective D2 blockers) receptors, but also have other effects that likely contribute. (e.g., 􏰂atypical􏰄 antipsychotics also block 5HT2 (-Also an autoreceptor, and sits on dopamine neurons) receptors)-correlates with antipsychotic actions. -A side effect is excessive D1 activity because everything else is blocked

Question 365

What are the two extrapyramidal side effects that drugs that target D2 and 5HT2 receptors have?

Answer 365

1. Tardive dyskinesias - -These tend to be D1 mediated, because dopamine isn’t acting on D2 with the D2 blockers, it is going to D1, and causing these problems, and this is a bizarre motor behavior, and this can become permanent if you leave them on these drugs for too long. 2. Parkinson’s like-tremors - Same thing, because of anti-dopamine activity. And people don’t want these medications because of side effects so there is a problem with compliance, and they end up on the streets.

Question 366

What causes the sleepiness side effect in anti-psychotic drugs?

Answer 366

It is due to the anticholinergic actions in the drugs, which are added in order to reduce excess ACh activity that is taking place because we are blocking all the dopamine, which would normally regulate the amount of ACh. These anti-psychotics can also cause restlessness, dysrupt endocrine, and pseudodepression and some weight gain.

Question 367

What are the two main classes of anti-psychotic drugs?

Answer 367

1. Phenothiazines - Least expensive, older, more sedation and weight gain, less extrapyramidal side effects, antiemetic action. Anticholinergics mask the effects of tardive dyskinesias but the damage is still being done. Anticholinergics are also used to treat Parkinson’s Disease. 2. Butyrophenones - High extrapyramidal side effects, lacks anticholinergic action

Question 368

What are the two main Phenothiazines (anti-psychotic drugs)?

Answer 368

Chlorpromazine and Thioridizine

Question 369

What is the main Butyrophenone drug?

Answer 369

Haloperidol

Question 370

What are the characteristics of atypical anti-psychotic drugs?

Answer 370

They are newer, and along with D2 antagonism, these are also good 5HT2A antagonists. They have little extrapyramidal side effects, and are most effective against the “negative” symptoms of schizophrenia.

Question 371

What are the main three atypical anti-psychotic drugs?

Answer 371

1. Clozapine (Can cause serious agranulocytosis, wiping out WBC’s) 2. Quetiapine 3. Olanzepine

Question 372

What are the two “other” schizophrenia types?

Answer 372

1. Acute psychotic disorder (-Stress-related/maybe delusions, and maybe halucinations. There is a fast recovery, and once you can resolve the stress, the psychosis goes away) 2. Schizoaffective (-Poorly defined, You have severe depression and bouts of schizophrenia, Looks a lot like bipolar)

Question 373

What are the two minor affective disorders (which are mood disorders)?

Answer 373

1. Depression-dysthymia (-Dysthymia is minor depression, DSM5 qualification requires: longer than two years, lowered mood/anhedonia, incidence is about 6% at any one time females are more likely) 2. Cyclothymia (-Cycles of dysthymia to minor state of mania-minor bipolar-longer than two years-no gender bias -No drugs for these usually, some of our most brilliant people like Einstein entered this manic part of cyclothymia and was productive

Question 374

What are the two subtypes of major mood depression?

Answer 374

1. Post-partum (1-4 weeks, usually second or third child) 2. SADS (Seasonal affective disorder, prolonged darkness, no light)

Question 375

What are the common features to anti-depressants?

Answer 375

Delayed onset, 4-8 weeks sometimes before they kick in, about 70% effective, side effect profile differ

Question 376

What are the three main categories of anti-depressants?

Answer 376

1. Monoamine Oxidase Inhibitors (MAOI) 2. Tricyclic Anti-depressants 3. Monoamine uptake blockers

Question 377

What are the characteristics of Monoamine Oxidase Inhibitors?

Answer 377

They block the metabolizing enzyme for monoamines (serotonin, dopamine, epinephrine, NE), so they increase these neurotransmitters. Side effects include altered autonomic system activity, orthostatic hypertension, weight gain, may interact with foods that have tyra mine, people have died from eating these foods and taking an MAOI inhibitor, remember these will enhance the nervous system, so when we provide local anesthetic with epinephrine, it could cause cardiovascular problems

Question 378

What are the two main drugs that are Monoamine Oxidase Inhibitors?

Answer 378

1. Phenelzine (MAO A/MAO B inhibitor) 2. Selegiline (MAO B inhibitor)

Question 379

What are the characteristics of Tricyclic Anti-depressants?

Answer 379

Have long half-life, single daily lose, they block the uptake of NE and varying affinity for 5HT transporters. They give dry mouth pretty bad, H1 blockade (H1 blockers are decongestants, used for reactions to allergies, look like traditional anti-histamine drugs, H2 blockers are used to treat GI problems, diminishing gastric secretions), some orthostatic hypertension, withdrawal with abrupt discontinuation and subsequent diarrhea because you are taking away anticholinergic effect.

Question 380

What are the three main drugs that are Tricyclic Anti-Depressants?

Answer 380

1. Amytriptyline 2. Desipramine 3. Doxepin

Question 381

What are the characteristics of Monoamine Uptake Blockers?

Answer 381

They block 5HT, NE, doppamine receptors. They have minimal withdrawal because of less or no anti-cholinergic activity, so less xerostomia, constipation, etc. There are two main kinds: Selective Serotonin Reuptake Blockers (SSRI’s) and NE or Mixed transport blockers.

Question 382

What are the two main SSRI’s?

Answer 382

1. Fluoxetine 2. Sertraline -They are popular but can give GI upset, sexual dysfunction, and depression in adolescents. They have no anti-cholinergic activity, so you don’t get dry mouth.

Question 383

What are the two main NE or mixed transport blocker drugs?

Answer 383

1. Venlafaxine 2. Duloxetine -They have no anti-cholinergic properties, so no dry mouth, unlike Tri-cyclics, have more CVS side effects due to increased NE/sympathetic activity, and are moderately a CNS stimulant (insomnia, anxiety)

Question 384

What are the main two types of Bipolar?

Answer 384

1. Cyclothymia (minor bipolar, not treated with meds) 2. Major Manic/Depressive (-When they are manic, they have episodes of grandiosity that might not be realistic -During manic episodes they can’t sleep, they are unrealistic, divorce is common-They get lost for days -They look schizophrenic)

Question 385

What are the two main classes of drugs to treat Bipolar Disorder?

Answer 385

1. Lithium Carbonate 2. Anti-epileptic agents

Question 386

What are the characteristics of Lithium Carbonate for treating Bipolar Disorder?

Answer 386

Slow onset, likely works by altering 2nd messenger systems such as those involving adenylyl cyclase and G proteins, often combined with anti-depressants, still among the most potent mood stabilizers, has many side effects, requires monitoring blood levels (narrow therapeutic window), tremors are common, kidney damage, weight gain, edema, high rate of compliance problems.

Question 387

What are the characteristics of Anti-epileptic agents for treating Bipolar Disorder?

Answer 387

These have fewer side effects, better compliance, more expensive, usually for maintenance after lithium starts, GABA/Glutamate pathways might be responsible for some of the bipolar cycling, depression and manic staging, and that is why antiepileptic agents work.

Question 388

What are the three main anti-epileptic drugs used for Bipolar Disorder?

Answer 388

1. Valproic Acid 2. Carbamazepine 3. Lamotrigene

Question 389

What are the biological theories of mood disorders?

Answer 389

The catecholamine theory. Somehow this on the right (neural junction) has been disrupted at some level and they are not functioning at a smooth well coordinated way, and you end up with the bottom line below, or a combination of all of those. And the bottom line is an imbalance of dopamine, NE, or 5HT activity.

Question 390

What is the background to, and the different types of Anxiety disorders?

Answer 390

It is a natural response but in excess. Involves adrenaline and the sympathetic nervous system 1. Chronic, mild anxiety - -Constant frequent times of irritation, you don’t have patience, you can’t focus -Linked to environment, there is a cause, you can say this happened and then I got anxiety. Usually don’t need drugs, just relax, take a trip 2. Chronic, moderately severe –Anxiety feelings persist for longer than 6 months, and while they may be coming and going, it is there, and it is genetic, and there is no obvious stressor. Anxiolytics, sedatives, psychotherapy, relaxation, exercise.

Question 391

What are the three main classes of sedative/hypnotic drugs used for anxiety disorders?

Answer 391

1. Benzodiazepines 2. Barbiturates 3. Bupropion

Question 392

What are the characteristics of Benzodiazepines?

Answer 392

They are agonists on BDZ receptors (allosteric modulators of GABA A receptors). BDZ doesn’t directly activate the GABA receptor, isn’t an agonist, but it indirectly regulates the sensitivity of the receptor so making it more or less receptive to GABA. These have little effect on respiration, most popular CNS depressants, anxiolytic, helps with alcohol withdrawal, treats insomnia (is short-acting, so they don’t sleep the whole day). Tolerance is common with long-term use, interacts synergistically with other depressants, drowsiness, motor impairment, kids can have paradoxical reaction, don’t use with people with intellectual disability to avoid suicide.

Question 393

What are the two “sedative” benzodiazepine drugs used to treat anxiety disorder?

Answer 393

1. Diazepam 2. Alprazolam -Sedative are longer-lasting (8-12 hours), while hypnotic are shorter lasting (2-4 hours).

Question 394

What are the characteristics of Barbiturates?

Answer 394

They enhance GABA, has short-acting for anesthesia induction, and long-term for seizures. This one is a major depressor of respiration and tolerance (careful with the airway). Not frequently used, narrow margin of safety, major interactions with liver.

Question 395

What are the two main barbiturates for treating anxiety disorders?

Answer 395

1. Pentobarbital (short-acting, helps with anesthesia induction) 2. Phenobarbital (longer-acting, for seizures)

Question 396

What does Bupropion treat, and what are its characteristics?

Answer 396

It is used to treat anxiety disorders, and it is a non-sedating sedative, not a depressant, but still has anxiolytic activity. We use it for everyday stress and anxiety. Usually for short-term use. Not very addicting, can interact with MAO inhibitors or anti-seizure medicines.

Question 397

What is a severe acute anxiety-panic attack?

Answer 397

It is a dramatic acute outburst, peak in 10 minutes-Self-limiting-Autonomic outburst-Sense of dread and impending doom, confusion-Sometimes associated with depression

Question 398

How do you treat a severe acute anxiety-panic attack?

Answer 398

Treat them with an SSRI, like Paxil or anti-depressants that have mixed effects, like Venlafaxin.

Question 399

What are phobic disorders and how do we usually treat them?

Answer 399

They are irrational fears, we know what the cause is unlike anxiety sometimes, but it’s not rational. Symptoms are not always precipitated (meaning all of the sudden it overcomes you, it can happen that way), and they are illogical. We treat them with SSRI’s like Sertraline.

Question 400

What are the two “hypnotic” benzodiazepine drugs used to treat anxiety disorder?

Answer 400

1. Lorazepam 2. Triazolam -Sedative are longer-lasting (8-12 hours), while hypnotic are shorter lasting (2-4 hours).

Question 401

What are the main three characteristics associated with Autism?

Answer 401

1. Problem with social interactions
2. Verbal or non-verbal communication problems
3. Problems with repetivie behavior

Question 402

What is the main cause for autism?

Answer 402

Genetics and environment. It tends to associate with certain medical conditions, like Fragile X syndrome, congenital rubella syndrome, PKU. They are also more vulnerable to toxins because they can’t metabolize them as well.

Question 403

Who is autism most prevalent in?

Answer 403

White boys. 1 in 42 boys, and 1 in 189 girls.

Question 404

What are the drugs that might help with autism psychotic, aggressive or repetitive behaviors, but don’t help with the progression of the disease?

Answer 404

Atypical antipsychotics or SSRI’s

Question 405

What are some symptoms of Anorexia Nervosa?

Answer 405

Restriction of eating, osteoporosis, dry yellow skin, muscle wasting, damage to heart, infertility

Question 406

What are some symptoms of Bulimia?

Answer 406

Frequent binging and purging, usually normal weight, damage to esophagus. Tooth damage, acid reflux, dehydration.

Question 407

What are the main drugs used to treat bulimia or anorexia?

Answer 407

Fluoxetine and other antidepressants. The compulsiveness is more involved with Bulimia than with Anorexia, at least the treatment shows more improvement with Bulimia

Question 408

What is the definition of drug abuse?

Answer 408

The use of a drug in a manner not medically or socially approved.

Question 409

What is the definition of drug dependence?

Answer 409

Persistent use resulting in adaptations typically accompanied by accommodation or tolerance causing compensatory escalation and withdrawal (e.g. depression and cravings)

Question 410

What is SUD and what does it stand for?

Answer 410

Substance Use Disorder, it is the correct jargon for drug dependence

Question 411

What is the definition of drug addiction?

Answer 411

A disorder of pathologic decision making, expression of compulsive destructive behavior despite extreme negative consequences.

Question 412

What do most abused substances do to the brain?

Answer 412

They enhance dopamine activity in the nucleus accumbens (particularly reltaed to pleasure, motor, and cognitive function). Glutamate and GABA are other pathways also involved.

Question 413

What is the nucleus accumbens?

Answer 413

It is a region in the basal forebrain rostral to the preoptic area of the hypothalamus. Each cerebral hemisphere has its own nucleus accumbens. The nucleus accumbens, being one part of the reward system, plays an important role in processing rewarding stimuli, reinforcing stimuli (e.g., food and water), and those which are both rewarding and reinforcing (addictive drugs, sex, and exercise). The nucleus accumbens is selectively activated during the perception of pleasant, emotionally arousing pictures and during mental imagery of pleasant, emotional scenes.

Question 414

What are the main functions of the dopamine pathway? And where in the brain does it go?

Answer 414

Reward, pleasure, motor function, compulsion, perserveration, decision-making. It starts in the Substantia nigra, gets dropped off in the nucleus accumbens, the hippocampus, the striatum, and the frontal cortex.

Question 415

What is the function of serotonin in the brain and what is its pathway?

Answer 415

Mood, memory processing, sleep cognition, and it starts in the dorsal raphe in the brainstem and gets dropped off in the nucleus accumbens, frontal cortex, hippocampus, and striatum, just like the dopamine pathway.

Question 416

All drugs of addiction increase release of dopamine where in the brain?

Answer 416

The Nucleus Accumbens

Question 417

How do opioid narcotics cause dopamine release?

Answer 417

They activate opioid receptors

Question 418

How dooes nicotine cause dopamine release?

Answer 418

It activates nicotinic receptors

Question 419

How does marijuana cause dopamine release?

Answer 419

It activates cannabinoid receptors

Question 420

How does caffeine cause dopamine release?

Answer 420

It activates adenosine receptors

Question 421

How does alcohol and sedative/hypnotics cause dopamine release?

Answer 421

They activate GABA receptors; an inhibitory transmitter

Question 422

How does Cocaine and ritalin work in regards to dopamine?

Answer 422

They sit on the dopamine transporter so dopamine cannot be picked up back into the neuron, so they are reuptake blockers.

Question 423

Is the D1 or D2 receptor more involved with pleasure?

Answer 423

-D2 receptor is more involved with the pleasure than D1, and if you activate these too much, it could start to look like Schizophrenia (to treat Schizophrenia you use a D2 antagonist)

Question 424

What are the four amphetamine-related drugs?

Answer 424

1. Methamphetamine
2. MDMA (Ecstasy
3. Ephedrine
4. “bath salts”

Question 425

How does amphetamines work in regards to dopamine release?

Answer 425

They release dopamine from vesicles and then they pump them in reverse out of the dopamine transporter so they can be in the synaptic cleft and activate dopamine receptors.

Question 426

Which drug causes the highest activity of dopamine release in the nucleus accumbens?

Answer 426

Amphetamines, by far, so it causes the greatest amount of neurotixicity. 1000 for meth and 350 for cocaine.

Question 427

Which part of the brain integrates CNS information to make complex decisions and select appropriate behaviors, GO-NO Go system?

Answer 427

-Prefrontal cortex,

Question 428

Which part of the brain is involved with being the impulsivity center, rapidly selects behaviors based on dominance, rewards, and pereceived immediate emotional needs?

Answer 428

Amygdala/nucleus accumbens.

Question 429

Which part of the brain establishes priorities and motivation to assist Pre-frontal cortex in decision making?

Answer 429

Orbitofrontal cortex

Question 430

What happens to the pre-frontal cortex, orbitofrrontal cortex, and amygdala/nucleus accumbens during drug addiction?

Answer 430

1. You damage the prefrontal cortex
2. You foul up saliency
3. And you lose control of impulsivity and reward systems

Question 431

What does amphetamines do th dendrites and synaptic connections?

Answer 431

They alter dendrites and increase synaptic connections and the influence of an axon is dependent on how many connections are made from one cell to another so Meth makes reward become a more potent driver with these increased synaptic connections.

Question 432

What does meth do to the expression of the dopamine transporter?

Answer 432

It suppresses its expression. You are very more likely to get Parkinson’s disease with substance use disorders or addictions.

Question 433

What happens to post-synaptic D2 receptors after long-time drug addictions?

Answer 433

The ability to experience rewards is damage, the receptors are not as receptive or plentiful because the body is trying to get rid of them because of the increased synapses that have been taking place bcause of the drug addiction. If their D2 receptors are not receptive, they are not getting the same high from something that we might be getting high from.

Question 434

What is the percentage chance that someone has of inheriting genes that might affect their chance of abusing drugs?

Answer 434

40-60%. The process if polygenic and complex. And there might be genes that express variant receptors that are development sensitive or age sensitive, and that is why crap starts in the teens. This was shown using nicotine receptors as an example, 5X more likely if smoking began before 17 years of age, and recent studies have shown alpha 5 subunits linked to reward of nicotine.

Question 435

What percentage of smokers want and try to quit? What percentage of long-term smokers began before 18 years old?

Answer 435

75% and 92%

Question 436

Most people entering drug treatment have additional mental health problems. What type of mental disorders are YOUTH more likely to have, in comparison with OLDER ADULTS?

Answer 436

Youth are more likely to have conduct disorders while older adults are more likely to be depressed or have anxiety.

Question 437

What is SSRT and what does it mean?

Answer 437

It stands for stop-signal reaction time, and it relates to the ability for this pathway, the slower the connector is from the amygdala, the poorer the reaction time, and the more likely that the person will have problems controlling impulsiviity.

Question 438

What part of the brain do cognitive therapies help out with?

Answer 438

Frontal Cortex

Question 439

What part of the brain do motivational enhancement therapies help out with?

Answer 439

The Orbital Frontal Cortex, where your saliency or your priority list is kept

Question 440

What part of the brain do contingency management therapies help out with?

Answer 440

The cortial-amygdala region, this is saying, if you stay drug-free, I am going to give you a reward.

Question 441

Methylphenidate

Answer 441

Indirect adrenergic agent, similar to amphetamine, cocaine, SNRI’s and TCA’s. This drug blocks DA reuptake. It is Ritalin, is used for ADHD, it is a stimulant.

Question 442

Phenobarbital

Answer 442

Used for all Partial seizures as well as Tonic-Clonic seizures. Has long-term cognitive memory and behavioral side effects. This drug is also the BIG TIME INDUCER, interact with almost every drug out there. Can precipitate spike-wave seizures in patients with absence seizures. Used mainly because of low cost and broad spectrum but not great option because of side effects.

Question 443

Ethosuximide

Answer 443

Used for uncomplicated absence seizures. Has a very narrow clinical spectrum. It’s MOA is it reduces T-type Ca+ channel currents in thalamic pacemaker neurons to quiet rhythmic discharges.

Question 444

Phenoxybenzamine

Answer 444

Non-selective alpha antagonist. Treatment of pheochromocytoma, hypertensive emergencies. Helps you get decreased TPR through blocking alpha-1 and thus decreased BP, and an increased HR through baroreceptor response to decreased BP. Major side effects are orthostatic hypertension and nasal stuffiness.

Question 445

Phentolamine

Answer 445

Non-selective alpha antagonist. Treatment of pheochromocytoma, hypertensive emergencies. Helps you get decreased TPR through blocking alpha-1 and thus decreased BP, and an increased HR through baroreceptor response to decreased BP. Major side effects are orthostatic hypertension and nasal stuffiness.

Question 446

Botulinum toxin

Answer 446

It prevents the release of ACh. It relaxes intraocular muscles, treats muscle dystonia (spasms), removes wrinkles.

Question 447

Bethanechol

Answer 447

It is a muscarinic receptor agonist. Specifically, is a cholinesterase inhibitor.

Question 448

Pilocarpine

Answer 448

Muscarinic receptor agonist. Used for radiation therapy xerostomia, glaucoma, myasthenia gravis. It acts on muscarinic receptors on iris sphincter muscle, causing the muscle to contract - resulting in pupil contraction (miosis). Pilocarpine also acts on the ciliary muscle and causes it to contract. When the ciliary muscle contracts, it opens the trabecular meshwork through increased tension. This action facilitates aqueous humor leaving the eye to decrease intraocular pressure.

Question 449

Atropine

Answer 449

Muscarinic receptor antagonist. Sarin is nerve gas, an acetylcholinesterase inhibitor, so it allows ACh to accumulate at the cleft and interact with cholinergic receptors to cause too much stimulation. You get a very slow heart rate, diarrhea, cramping, gland secretions, twitching, suffocation, blurred vision, sweating. Soldiers carry around Atropine as a nerve gas antidote, which will block muscarinic receptors to stop all these side effects. Atropine was originally derived from this plant on the left. And blocking these receptors would cause pupils to dilate I think. Also helps with Parkinson’s disease, motion sickness, COPD. But causes dry mouth, constipation, blurred vision, sedation, urinary retention.

Question 450

Scopalamine

Answer 450

Muscarinic Receptor Antagonist. Along with Atropine, Also helps with Parkinson’s disease, motion sickness, COPD. But causes dry mouth, constipation, blurred vision, sedation, urinary retention.

Question 451

Clonidine

Answer 451

Alpha-2 receptor agonist, helps treat hypertension and ADHD.

Question 452

Carbamezepine

Answer 452

Used for all Partial seizures as well as Tonic-Clonic seizures. Although rare, Steven-Johnsons Syndrome is a side effect. This drug may also activate spike-wave seizures. It is also associated with toxic levels when patients drink grapefruit juice. It is a great drug for epilepsy but the potential for a drug-to-drug interaction is high. It’s MOA is it blocks Na+ channels to inhibit repetitive firing from neurons. Also used for Bipolar Disorder.

Question 453

Atenolol

Answer 453

Selective beta-1 blocker. Uses of β blockers include treatment of hypertension, angina, open- angle glaucoma.

Question 454

Metoprolol

Answer 454

Selective beta-1 blocker. Uses of β blockers include treatment of hypertension, angina, open- angle glaucoma.

Question 455

Isoproterenol

Answer 455

Beta-1 and Beta-2 receptor agonist

Question 456

Propranolol

Answer 456

Beta-1 and Beta-2 receptor antagonist (beta blocker)

Question 457

Physostigmine

Answer 457

Cholinesterase inhibitor. Short duration of action, used for glaucoma, antidote for atropine

Question 458

Sarin

Answer 458

Cholinesterase inhibitor. Irreversible; long duration of action, nerve gas

Question 459

Donepezil

Answer 459

Cholinesterase inhibitor. Used to treat Alzheimer’s.

Question 460

Cocaine

Answer 460

Blocks the reuptake of dopamine

Question 461

Cevimeline

Answer 461

Cholinergic agonist used to treat xerostomia in Sjogren’s Syndrome

Question 462

Terbutaline

Answer 462

Beta-2 agonist

Question 463

Topiramate

Answer 463

Used for all Partial seizures as well as Tonic-Clonic and Lennox-Gastaut syndrome seizures. This drug is unique because it is the only one that causes weight loss. Decreases word-finding ability as well. One of its side effects is that it metabolizes estrogen which will lower the efficacy of birth control. It’s MOA is that it blocks repetitive firing of Na+ channels, inhibits Ca+ channels, inhibits AMPA/Kainate receptors, and potentiates GABA currents. Know that this drug is broad spectrum and causes weight loss.

Question 464

Endocannabinoids

Answer 464

Anandamide is the main endocannabinoid neurotransmitter, and it binds to CB1 cannabinoid receptors, and by doing so, causes dopamine release. Endocannabinoids are main ingredient in marijuana.

Question 465

Phenytoin

Answer 465

Used for all Partial seizures as well as Tonic-Clonic seizures. It masculinizes (hirsuitism) and causes severe gingival hyperplasia, osteopenia, anemia, acne. This drug is special because it has zero-order kinetics at high doses. Most drugs have first-order kinetics. So with this, as you give Phenytoin to patients, it overcomes the metabolize enzymes in the liver, so with even the smallest increase in dose, you get an upshoot increase and can become highly toxic. You have to constantly monitor the levels in your patient. It’s MOA is that it blocks sustained high frequency of action potentials by blocking Na+ channels during repetitive firing.

Question 466

Dopamine

Answer 466

The adminestering of Dopamine itself is used to treat shock and heart failure (at high doses, increased BP and TPR (α1); increased HR (β1); increased organ perfusion (D1))

Question 467

Prazosin

Answer 467

Alpha-1 antagonist, used to treat hypertension. It helps block vasoconstriction so essentially cause vasodilation and are used to treat hypertension as well as benign prostatic hypertrophy (Tamsulosin - flomax). The side effects here are also Orthostatic hypertension and nasal stuffiness.

Question 468

Terazosin

Answer 468

Alpha-1 antagonist, used to treat hypertension. It helps block vasoconstriction so essentially cause vasodilation and are used to treat hypertension as well as benign prostatic hypertrophy (Tamsulosin - flomax). The side effects here are also orthostatic hypertension and nasal stuffiness.

Question 469

Guanfacine

Answer 469

Alpha-2 receptor agonist, helps treat hypertension and ADHD

Question 470

D-tubocurarine

Answer 470

Nicotinic (muscle) antagonist. It is non-depolarizing and competitive. It competes with ACh at nicotinic receptors.

Question 471

Albuterol

Answer 471

Beta-2 agonist

Question 472

Amphetamine

Answer 472

Helps dopamine be released. Adderall is an example, used to treat ADHD. It is a stimulant.

Question 473

Phenylephrine

Answer 473

Alpha-1 receptor agonist and it causes vasoconstriction to sinus vessels in order to act as a decongestant, helps with mydriasis for eye exams. Also causes a decreased heart rate from baroreceptor reflex essentially.

Question 474

Fenoldapam

Answer 474

D1 receptor agonist, along with dopamine

Question 475

Ephedrine

Answer 475

It releases NE, also some direct action on α and β receptors. Used for decongestion and dietary supplements. Side effects: increase HR, vasoconstriction, dilate airways, stimulant (if penetrates CNS)

Question 476

Succinylcholine

Answer 476

It is a Nicotinic (muscular) antagonist. It is depolarizing and non-competitive, it depolarizes/desensitizes the neuromuscular endplate; it opens the NIC channels and keeps these “open” such that the neuron is depolarized and unresponsive to another ACh challenge.

Question 477

Valproic Acid

Answer 477

Used for all Partial seizures as well as uncomplicated absence seizures, atypical absence seizures, primary tonic-clonic seizures, and myoclonic epilepsy. Very broad spectrum similar to Topiramate. Associated with weight gain however. As well as Reye-like syndrome and hepatic failure. It is strictly contraindicated with people who have liver problems. It also has an increased risk of spina bifida, category D pregnancy risk. It’s MOA is it blocks Na+ channels, reduces NMDA currents, and increases GABA at high doses. Also used for Bipolar Disorder.

Question 478

Selegiline

Answer 478

This is used for Parkinson’s Disease. This is an MAO inhibitor, blocking monoamine oxidase B from metabolizing dopamine in the brain, so prolonging the effects of levodopa. Side effects include cardiac dysrhythmias. They block the metabolizing enzyme for monoamines (serotonin, dopamine, epinephrine, NE), so they increase these neurotransmitters. Side effects include altered autonomic system activity, orthostatic hypertension, weight gain, may interact with foods that have tyra mine, people have died from eating these foods and taking an MAOI inhibitor, remember these will enhance the nervous system, so when we provide local anesthetic with epinephrine, it could cause cardiovascular problems

Question 479

Enkephalins

Answer 479

Act on Delta and Mu receptors. 5 amino acids long. Made up of Methionine and Leucine.

Question 480

Barbiturates

Answer 480

They enhance GABA, has short-acting for anesthesia induction (Pentobarbital), and long-term for seizures (Phenobarbital). This one is a major depressor of respiration and tolerance (careful with the airway). Not frequently used, narrow margin of safety, major interactions with liver.

Question 481

Pramipexole

Answer 481

This is a dopamine agonist, a D2 agonist, which bypasses the depleted neurons int he substantia nigra and provides long-lasting direct stimulation of dopamine receptors. Side effects include orthostatic hypertension, nausea, vomiting, confusion. Used to treat Parkinson’s Disease.

Question 482

Clozapine

Answer 482

Atypical anti-psychotic drug. Can cause serious agranulocytosis. Besides D2 antagonism, these typically are also good 5HT2A antagonists. Little extrapyramidal side effects. Most effective against the 􏰂negative􏰄 symptoms in some forms of schizophrenia.

Question 483

Quetiapine

Answer 483

Atypical anti-psychotic drug. Besides D2 antagonism, these typically are also good 5HT2A antagonists. Little extrapyramidal side effects. Most effective against the 􏰂negative􏰄 symptoms in some forms of schizophrenia.

Question 484

Olanzepine

Answer 484

Atypical anti-psychotic drug. Besides D2 antagonism, these typically are also good 5HT2A antagonists. Little extrapyramidal side effects. Most effective against the 􏰂negative􏰄 symptoms in some forms of schizophrenia.

Question 485

Celecoxib

Answer 485

Celebrex. Cox-2 selective antagonist. • Prescription only • Same analgesia as ibuprofen • Lacks GI and anti-clotting action • Warning about cardiovascular side effects

Question 486

Trihexyphenidyl

Answer 486

Used for Parkinson’s Disease. Anticholinergic medication. Everything almost identical to Benztropine.

Question 487

Acetaminophen

Answer 487

Tylenol. It is a Non-NSAID, Non-COX 1 or 2 inhibitor—perhaps blocks a COX 3 and/or works on 5HT. It is non-anti-inflammatory, has good anti-pyretic and some good analgesia. So does not help with inflammation, but can help with pain caused by inflammation.

Question 488

Lyrica

Answer 488

Anticonvulsant used for neuropathic pain

Question 489

Gabapentin

Answer 489

Anticonvulsant used for neuropathic pain

Question 490

Capsaicin

Answer 490

It is used as a topical pain reliever that activates the TRPV1 directly and indirectly to make them less sensitive.

Question 491

Lorazepam

Answer 491

Hypnotic benzodiazepine drug used to treat anxiety disorder

Question 492

Triazolam

Answer 492

Hypnotic benzodiazepine drug used to treat anxiety disorder

Question 493

Tramadol

Answer 493

(Ultram). It is a schedule 4 drug. Low drug abuse potential, but some minor opioid action. Works at brain level. Is the “next-line” of drug treatment for neuropathic pain like Trigeminal neuralgia.

Question 494

Lamotrigene

Answer 494

Anti-epileptic drugs used for Bipolar Disorder

Question 495

Amytryptiline

Answer 495

Tri-cyclic anti-depressant. Have long half-life, single daily lose, they block the uptake of NE and varying affinity for 5HT transporters. They give dry mouth pretty bad, H1 blockade (H1 blockers are decongestants, used for reactions to allergies, look like traditional anti-histamine drugs, H2 blockers are used to treat GI problems, diminishing gastric secretions), some orthostatic hypertension, withdrawal with abrupt discontinuation and subsequent diarrhea because you are taking away anticholinergic effect.

Question 496

Desipramine

Answer 496

Tri-cyclic anti-depressant. Have long half-life, single daily lose, they block the uptake of NE and varying affinity for 5HT transporters. They give dry mouth pretty bad, H1 blockade (H1 blockers are decongestants, used for reactions to allergies, look like traditional anti-histamine drugs, H2 blockers are used to treat GI problems, diminishing gastric secretions), some orthostatic hypertension, withdrawal with abrupt discontinuation and subsequent diarrhea because you are taking away anticholinergic effect.

Question 497

Doxepin

Answer 497

Tri-cyclic anti-depressant. Have long half-life, single daily lose, they block the uptake of NE and varying affinity for 5HT transporters. They give dry mouth pretty bad, H1 blockade (H1 blockers are decongestants, used for reactions to allergies, look like traditional anti-histamine drugs, H2 blockers are used to treat GI problems, diminishing gastric secretions), some orthostatic hypertension, withdrawal with abrupt discontinuation and subsequent diarrhea because you are taking away anticholinergic effect.

Question 498

L-dopa + Carbidopa

Answer 498

Used for Parkinson’s Disease. L-dopa gets across blood-brain barrier much better than dopamine, and Carbidopa blocks the metabolism of L-dopa and dopamine so it can last longer. Some drugs are used in combination with carbidopa-levodopa to either inhibit dopamine breakdown by the body or to improve the effectiveness of carbidopa-levodopa. Azilect inhibits dopamine breakdown while Entacapone improves the effect of Carbidopa-levodopa by inhibiting COMT, Catecholamine Methyl Transferase, which metabolizes neurotransmitters like MAO does.

Question 499

Dynorphins

Answer 499

Endogenous peptides. Act on Kappa receptors. 17 amino acids long. There are A and B Dynorphins, they are inhibitory, they tend to block a lot of the typical reward functions. The kappa receptors are antagonistic to mew and delta, but they still have analgesic properties.

Question 500

Benztropine

Answer 500

Used for Parkinson’s Disease. This is an anticholinergic medication that helps with tremors, and is effective because it counteracts the cholinergic sensitivity that arises in response to dopamine depletion. It helps dry sialorrhea from PD patients as well. It can give you confusion, blurred vision, urinary retention.

Question 501

Beta-endorphins

Answer 501

Endogenous peptides. Act on Delta and Mu receptors. 91 amino acids long. -You can’t give a Beta-endorphin therapeutically, it would be proteased too quickly, but we have drugs that have opioid agonist properties that have a number of naturally occurring narcotics that have selective activities that act on mu or delta receptors.

Question 502

Phenelzine

Answer 502

MAO A/MAO B inhibitor. They block the metabolizing enzyme for monoamines (serotonin, dopamine, epinephrine, NE), so they increase these neurotransmitters. Side effects include altered autonomic system activity, orthostatic hypertension, weight gain, may interact with foods that have tyramine, people have died from eating these foods and taking an MAOI inhibitor, remember these will enhance the nervous system, so when we provide local anesthetic with epinephrine, it could cause cardiovascular problems

Question 503

Entacapone

Answer 503

Used for Parkinson’s Disease. It inhibits COMT, Catecholamine methyl transferase, which metabolizes like MAO does. So works similar to Selegiline, in the sense that they are both inhibiting metabolizing agents.

Question 504

Venlaxafine

Answer 504

NE or mixed transport blocker drug. They have no anti-cholinergic properties, so no dry mouth, unlike Tri-cyclics, have more CVS side effects due to increased NE/sympathetic activity, and are moderately a CNS stimulant (insomnia, anxiety).

Question 505

Duloxetine

Answer 505

NE or mixed transport blocker drug. They have no anti-cholinergic properties, so no dry mouth, unlike Tri-cyclics, have more CVS side effects due to increased NE/sympathetic activity, and are moderately a CNS stimulant (insomnia, anxiety).

Question 506

Prednisone

Answer 506

Drug that treats Multiple Sclerosis. Bladder dysfunctions, bowel dysfunction, depression, fatigue, pain, tremors.

Question 507

Naloxone

Answer 507

Mu antagonist, used to treat opioid narcotic overdoses - naloxone (Narcan). Although it may precipitate withdrawals, and it will block the endorphins (endogenous opioid systems), and if you take these alone, you will get anxiety, stress, or hypersensitivity to pain

Question 508

Meperidine

Answer 508

“Other” opioid narcotics, for moderate pain.

Question 509

Pentazocine

Answer 509

“Other” opioid narcotic. It is unique because of its interaction with the kappa receptor, so makes it less likely that people will abuse this, it has a mixed agonist/antagonist effect.

Question 510

Methadone

Answer 510

“Other” opioid narcotic. (If an opioid addict is going to methadone clinics, then chart that and know that you don’t need to give them more pain coverage, also used to treat opioid addiction)

Question 511

Buprenorphine

Answer 511

“Other opioid narcotic.” (As they go to higher doses it turns into an antagonist, shuts everything off, and kicks them into withdrawals, so harder to get addicted to, similar to two above)

Question 512

Lithium Carbonate

Answer 512

Used for Bipolar Disorder. Slow onset, likely works by altering 2nd messenger systems such as those involving adenylyl cyclase and G proteins, often combined with anti-depressants, still among the most potent mood stabilizers, has many side effects, requires monitoring blood levels (narrow therapeutic window), tremors are common, kidney damage, weight gain, edema, high rate of compliance problems.

Question 513

Salicylates

Answer 513

They are non-selective COX-1 and COX-2 inhibitors, ibuprofen-like, so they are NSAIDS.

Question 514

Ketoprofen

Answer 514

Ibuprofen-like. Ketoprofen is same properties, but more potent. Remember that NSAIDS negate the effects of anti-hypertension medications.

Question 515

Naproxen

Answer 515

Ibuprofen-like. Naproxen is longer-lasting and slower-acting (Aleve).

Question 516

Chlorpromazine

Answer 516

Phenothiazine, anti-psychotic drug. Least expensive, older, more sedation and weight gain, less extrapyramidal side effects, antiemetic action. Anticholinergics mask the effects of tardive dyskinesias but the damage is still being done. Anticholinergics are also used to treat Parkinson’s Disease

Question 517

Thioridizine

Answer 517

Phenothiazine, anti-psychotic drug. Least expensive, older, more sedation and weight gain, less extrapyramidal side effects, antiemetic action. Anticholinergics mask the effects of tardive dyskinesias but the damage is still being done. Anticholinergics are also used to treat Parkinson’s Disease

Question 518

Fluoxetine

Answer 518

SSRI. They are popular but can give GI upset, sexual dysfunction, and depression in adolescents. They have no anti-cholinergic activity, so you don’t get dry mouth.

Question 519

Sertraline

Answer 519

SSRI. They are popular but can give GI upset, sexual dysfunction, and depression in adolescents. They have no anti-cholinergic activity, so you don’t get dry mouth.

Question 520

Haloperidol

Answer 520

It is a butyrophenone that is used to treat Psychotic disorders. High extrapyramidal side effects, lacks anticholinergic action

Question 521

Indomethacin

Answer 521

“Other” NSAID agent. Indomethacin - potent non-selective NSAID/ due to side effects not a common analgesic

Question 522

Meloxicam

Answer 522

“Other NSAID agent.” Meloxicam - preferentially inhibits Cox-2 over Cox-1/ means less GI problems

Question 523

Diflusinal

Answer 523

“Other NSAID agent.” Diflunisal - Related to salicylates- supposed to be good for bone pain

Question 524

Diazepam

Answer 524

Sedative benzodiazipene drug used to treat anxiety disorder.

Question 525

Alprazolam

Answer 525

Sedative benzodiazipene drug used to treat anxiety disorder.

Question 526

Bupropion

Answer 526

It is used to treat anxiety disorders, and it is a non-sedating sedative, not a depressant, but still has anxiolytic activity. We use it for everyday stress and anxiety. Usually for short-term use. Not very addicting, can interact with MAO inhibitors or anti-seizure medicines.

Question 527

Nortryptiline

Answer 527

First-line drug treatment (3 of them, along with Gabapentin, Duloxetine, and they are all FDA approved) to manage neuropathic pain like Trigeminal neuralgia.

Question 528

Modafinil

Answer 528

It is a minor stimulant, or non-stimulant, to treat ADHD, called the “smart drug.” Has few side effects, biggest complaint is that it alters sleep patterns, and it is also used for narcolepsy.

Question 529

Mecamylaline

Answer 529

Nicotinic (neuronal) antagonist