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Human Diseases & Therapeutics > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q

What are the three types of receptors that dopamine activates?

A

D1, alpha, and beta

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2
Q

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

A

Decreased glycogenolysis in response to hypoglycemia

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3
Q

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

A

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

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4
Q

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

A

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.

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5
Q

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

A
  1. Normal awareness 2. Memory 3. Consciousness (All throughout entire seizure)
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6
Q

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

A

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.

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7
Q

What is another name for cell body?

A

Perikaryon

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8
Q

What does Propranolol act on?

A

Beta1 and Beta2 receptor antagonist (beta blocker)

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9
Q

What does an NRI do?

A

Blocks reuptake of NE

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10
Q

What is the definition of a direct action of neurotransmitters?

A

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

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11
Q

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

A

Membrane-delimited

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12
Q

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

A

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.

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13
Q

What are the pathway effects and receptors on eccrine glands?

A

Sympathetic pathway increases via M receptors?

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14
Q

What are the main nine precipitants (causes) of seizures

A

• 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

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15
Q

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

A

Trauma, status epilepticus

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16
Q

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

A

Cholinergic (Muscarinic and Nicotinic) and Adrenergic

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17
Q

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

A

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.

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18
Q

What effect do beta blockers have on vasculature?

A

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

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19
Q

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

A

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

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20
Q

What are the five main therapeutic uses of epinephrine?

A
  1. Bronchospasm 2. Anaphylaxis 3. Restore function in cardiac arrest 4. Treat glaucome 5. Prolong action of local anesthetics because it is a vasoconstrictor
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21
Q

What are the three types of partial seizures?

A
  1. Simple partial (single focus that doesn’t spread) 2. Complex partial 3. Initial onset of secondarily generalized
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22
Q

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

A

Sympathetic pathway contracts via alpha receptors

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23
Q

How does phenylephrine work?

A

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.

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24
Q

What do barbiturates do?

A

They increase the duration of opening time of GABA channels.

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25
Q

What is the definition of the pupils dilating?

A

Mydriasis

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26
Q

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

A

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

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27
Q

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

A

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

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28
Q

What does botulinum toxin do?

A

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

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29
Q

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

A

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

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30
Q

What does Isoproterenol act on?

A

Beta1 and Beta2 receptor agonist

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31
Q

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

A

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.

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32
Q

Where are the cell bodies of the parasympathetic nervous system?

A

Craniosacral regions

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33
Q

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

A

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.

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34
Q

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

A

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.

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35
Q

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

A

Ach Agonists: Bethanechol and Pilocarpine Antagonists: Atropine and Scopalamine

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36
Q

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

A
  1. Motor 2. Somatosensory 3. Autonomic 4. Psychic (“aura”)
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37
Q

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

A

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.

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38
Q

What is the definition of a heteroreceptor?

A

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.

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39
Q

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

A

Alpha and Beta

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40
Q

Where are the cell bodies of the sympathetic nervous system?

A

Thoracolumbar region

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41
Q

How do opioid receptors modulate the release of neurotransmitters?

A

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.

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42
Q

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

A

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.

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43
Q

Phenytoin

A

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.

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44
Q

What are the pathway effects and receptors on fat cells?

A

Sympathetic pathway increases lipolysis via beta3 receptors

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45
Q

What are the two types of Metabotropic receptors?

A

Membrane-delimited and Diffusible second messengers

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46
Q

What does methylphenidate do?

A

It blocks the reuptake of dopamine

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47
Q

What are the three main side effects of epinephrine?

A
  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
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48
Q

What is the process of glutamate at the glutamatergic junction?

A

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.

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49
Q

What does Albuterol act on?

A

Beta2 agonist (for asthma)

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50
Q

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

A

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

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51
Q

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

A

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

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52
Q

What are the two main neurotransmitters that are amino acids?

A

GABA (inhibitory) and Glutamate (excitatory)

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53
Q

What are the pathway effects and receptors on bladder wall?

A

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

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54
Q

What is a postictal phase?

A

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

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55
Q

What things are cholinergic agonists used to treat?

A

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

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56
Q

Carbamezepine

A

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.

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57
Q

What does Prazosin and Terazosin do?

A

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

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58
Q

Why administer epinephrine with caution if a patient is diabetic?

A

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

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59
Q

Are parasympathetic pre-ganglionic axons short or long?

A

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.

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60
Q

What is the definition of epileptogenesis?

A

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

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61
Q

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

A

Calcium channels and potassium channels

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62
Q

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

A

Acts on muscarinic receptors in most effector tissues.

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63
Q

What are the common dose-related ASD adverse effects?

A

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

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64
Q

What are the characteristics of secondary generalized seizures?

A

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.

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65
Q

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

A
  1. Histamine 2. Endorphins 3. Neuropeptides 4. Endocannabinoids 5. Nitric Oxide
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66
Q

What are the pathway effects and receptors on the penis?

A

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

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67
Q

What is the double-edged sword aspect of NE?

A

-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.

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68
Q

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

A

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.

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69
Q

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

A

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.

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70
Q

What effect do beta blockers have on the kidney?

A

Decreased renin (which would raise BP) release

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71
Q

How do beta blockers work to treat hypertension?

A

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

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72
Q

At what ages is epilepsy most prevalent?

A

Very young and very old

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73
Q

What are the pathway effects and receptors on Apocrine glands?

A

Sympathetic pathway increases via alpha receptors

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74
Q

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

A

1/3 of patients

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75
Q

What does cocaine do?

A

It blocks the reuptake of dopamine

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76
Q

What do all generalized seizures include?

A

Loss of responsiveness or lack of awareness.

77
Q

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

A

Alpha2 receptor agonist, helps treat hypertension and ADHD

78
Q

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

A

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)

79
Q

What are the main three mechanisms of ASD’s?

A
  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.
80
Q

What does amphetamine do?

A

It helps dopamine be released

81
Q

What are the pathway effects and receptors on the kidney?

A

Sympathetic pathway increases renin release via beta1 receptors

82
Q

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

A

ACh, Muscarinic receptor

83
Q

What are the pathway effects and receptors on the liver?

A

Sympathetic pathway increases gluconeogenesis and glycogenolysis via alpha and beta2 receptors

84
Q

What effect do beta blockers have on the heart?

A

decreased HR and contractility (impair exercise tolerance)

85
Q

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

A

Dopamine, NE, and Epinephrine. Most use NE.

86
Q

What are the three main catecholamines?

A

Dopamine, Norepinephrine, and Epinephrine

87
Q

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

A

Alpha2 receptor agonist, helps treat hypertension and ADHD

88
Q

What is the definition of sympatholytic?

A

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

89
Q

What effect do beta blockers have on the lungs?

A

Bronchial constriction

90
Q

What percent of epilepsy patients are therapy-resistant?

A

25-40%

91
Q

What is another name for Serotonin?

A

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

92
Q

What is the precursor amino acid for catecholamines?

A

Tyrosine

93
Q

What is the lifetime prevalence of seizures for a person?

A

9-10%

94
Q

How does a voltage-gated channel work?

A

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.

95
Q

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

A

NE, and alpha and beta receptors

96
Q

What are some of the neuropeptides that we need to know

A

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

97
Q

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

A

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

98
Q

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

A

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

99
Q

Topiramate

A

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.

100
Q

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

A

Ion channels, and they are inherited.

101
Q

What type of receptors do endorphins act on?

A

u opioid receptors

102
Q

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

A

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

103
Q

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

A

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

104
Q

How do you get a diagnosis of epilepsy from seizures?

A

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

105
Q

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

A

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

106
Q

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

A

Sympathetic pathway relaxes via beta2 receptors

107
Q

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

A
  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
108
Q

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

A

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.

109
Q

What neurotransmitter does post-ganglionic parasypathetic fibers release?

A

ACh

110
Q

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

A

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.

111
Q

What is the process of GABA at the gabaergic junction?

A

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.

112
Q

What does Terbutaline act on?

A

Beta2 agonist

113
Q

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

A

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

114
Q

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

A

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

115
Q

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

A

Nicotinic receptors

116
Q

What does glutamate decarboxylase do?

A

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

117
Q

What are the two main antagonistic drugs of Nm receptors?

A

Succinylcholine and d-tubocurarine

118
Q

What is the amino acid precursor for Serotonin?

A

Tryptophan

119
Q

What are Kainate receptors?

A

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

120
Q

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

A

NE (only one with NE being greater)

121
Q

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

A

Fixed

122
Q

What is the definition of a seizure?

A

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

123
Q

How do Metabotropic receptors work?

A

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.

124
Q

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

A

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

125
Q

What are the two agonists to D1 receptors?

A

Dopamine and Fenoldapam

126
Q

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

A

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.

127
Q

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

A

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

128
Q

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

A

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

129
Q

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

A

Somatic and Autonomic Nervous Systems

130
Q

What are the pathway effects and receptors on GI secretion?

A

Parsympathetic pathway increases via M receptors

131
Q

Why administer epinephrine with caution if a patient is hyperthyroid?

A

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.

132
Q

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

A

1% and 1 in 26

133
Q

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

A
  1. Cevimeline (Evoxac) - used for Sjogren’s syndrome 2. Pilocarpine (Sialagen) - used for radiotherapy
134
Q

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

A
  1. Tonic-clonic (grand mal) 2. Absence (petit mal) 3. Atonic 4. Myoclonic 5. Tonic
135
Q

How many generations of ASD’s are there?

A

3

136
Q

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

A

They increase dopamine levels

137
Q

What is nitric oxide and what does it do?

A

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

138
Q

What does neurotensin do and where is it found?

A

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

139
Q

What is the definition of an autoreceptor?

A

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.

140
Q

What are the main side effects of administering NE?

A

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

141
Q

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

A

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

142
Q

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

A

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

143
Q

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

A

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

144
Q

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

A

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

145
Q

What are the four main monoamine neurotransmitters?

A

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

146
Q

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

A

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.

147
Q

How does Succinylcholine work as a neuromuscular blocker?

A

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

148
Q

What is the definition of an indirect action of neurotransmitters?

A

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

149
Q

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

A

It will affect both.

150
Q

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

A

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

151
Q

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

A
  1. Orthostatic hypertension (Getting up in a hurry, you don’t have the baroreceptor working appropriately and people can fall down) 2. Nasal stuffiness
152
Q

What is the definition of a ganglion?

A

A collection of cell bodies

153
Q

Ethosuximide

A

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.

154
Q

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

A

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

155
Q

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

A

They are most likely a beta blocker.

156
Q

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

A

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

157
Q

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

A

From sympathetic nerve terminals

158
Q

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?

A

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

159
Q

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

A

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

160
Q

To which receptor does NE have the least affinity?

A

Beta2

161
Q

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?

A

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

162
Q

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

A

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

163
Q

What is the main therapeutic use of administering NE?

A

Shock

164
Q

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

A

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

165
Q

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

A

Dopamine, D1 receptor

166
Q

Are sympathetic pre-ganglionic axons short or long?

A

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.

167
Q

How does d-tubocurarine work as a neuromuscular blocker?

A

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

168
Q

Does NE favor alpha or beta receptors more in general?

A

Beta

169
Q

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

A

–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

170
Q

What is the definition of epilepsy?

A

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

171
Q

Valproic Acid

A

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.

172
Q

What is the administering of Dopamine used for?

A

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

173
Q

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

A

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

174
Q

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

A
  1. Dry mouth 2. Constipation 3. Blurred vision 4. Sedation 5. Urinary retention
175
Q

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

A

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.

176
Q

Why administer epinephrine with caution if a patient is pregnant?

A

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

177
Q

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

A

Parasympathetic pathway contracts via M receptors

178
Q

Phenobarbital

A

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.

179
Q

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

A

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

180
Q

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

A

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

181
Q

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

A

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)

182
Q

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

A

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

183
Q

What is the process of choline at the cholinergic junction?

A

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).

184
Q

How does a diffusible second messenger metabotropic receptor work?

A

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.

185
Q

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

A

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.

186
Q

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

A

Sympathetic pathway contracts via alpha1 receptors

187
Q

How long do simple partial seizures usually last?

A

60-90 seconds

188
Q

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

A

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

189
Q

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

A

Cancer, CVA, neurodegenerative disorders, trauma, status epilepticus

Human Diseases & Therapeutics (16 decks)

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