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Human Disease And Therapeutics > Week 1 > Flashcards

Week 1 Flashcards

1
Q

There are excitatory and inhibitory neuron terminals. Name one excitatory NT, two inhibitory NTs, and three NTs that can be excitatory or inhibitory

A

Excitatory: Glutamate

Inhibitory: dopamine, GABA

Both: Acetylcholine, serotonin, norepinephrine

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2
Q

What is the difference between the direct and indirect actions of NTs?

A

Direct action - neurotransmitters bind to and open ion channels. Promotes rapid responses by altering membrane potential.

Indirect action - neurotransmitter acts through intracellular second messengers, usually G protein pathways. Broader, longer-lasting effects

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3
Q

What are the two types of membrane channels? Describe them.

A

Voltage-gated: opens and closes in response to voltage changes across the membrane (voltage gated sodium channels; lidocaine)

Ligand-gated (ionotropic): a hormone, drug, or NT binds to the protein and the channel opens up (glutamate and ACh receptors)

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4
Q

What are the two different types of receptors on neurons? Describe them.

A

Ligand gated (ionotropic) - 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.

Metabotropic - Not directly linked to ion channels. Initiates biochemical processes (G-protein mechanisms) that mediate more long-term effects and modify the responsiveness of the neuron. NT acts as the first messengers which activates a second messenger that in turn changes the excitability of a neuron.

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5
Q

What are the two types of metabotropic receptors? Describe them.

A

Membrane-delimited: occur entirely in plane of membrane. When G-proteins interact with Ca++ channels, they inhibit channel function (presynaptic inhibition). When G-proteins interact with K+ channels, they open (activate) channels causing postsynaptic inhibition.

Diffusible second messengers: beta-adrenergic receptors and cAMP . (This takes a lot more time to cause an effect than membrane-delimited)

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6
Q

What’s the difference between an autoreceptor and a heteroreceptor?

A

Autoreceptor - receptors on an axon terminal through which the neuron’s own NT can influence the function of the terminal (usually inhibitory) (such as D2)

Heteroreceptor - receptors on an axon terminal through which NTs from other neuronal types can influence the function of the terminal.

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7
Q

What does the chemical structure look like for dopamine, norepinephrine, and amphetamines?

A

Dopamine is a catecholamine that has an ethylamine group

Norepinephrine is a catecholamine with an ethyl group with a hydroxyl group and a terminal amine group

Amphetamine is a catecholamine with a site group with three carbons, one hydroxyl group, and a nonterminal amine group

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8
Q

Dopamine is synthesized from what amino acid precursor?

A

tyrosine

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9
Q

In order to produce dopamine.. once tyrosine is in the neuron, it is first converted to ___ by ____

A

DOPA (dihydroxyphenylalanine)

Tyrosine hydroxylase

Note that DOPA can be used to treat Parkinson’s

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10
Q

Once DOPA is produced it is converted to ____ by ____

A

DA (dopamine)

AAD (aromatic amino acid decarboxylase)

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11
Q

What happens once DA is produced in the neuron?

A

It is transported into vesicles via VMAT (vesicular monoamine transporter). It then can be released from the neuron

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12
Q

Once DA is released from the terminal, what are three fates of DA?

A

Bind to autoreceptor D2 - this will lead to decreased release of DA and decreased activity of tyrosine hydroxylase

Bind to post synaptic neuron receptors (heteroreceptors)

Be reuptaken into the presynaptic neuron via DAT (dopamine transporter)

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13
Q

What other molecules can go through the DAT?

A

Amphetamines can go through DAT. In this case, amphetamines enter the neuron while pumping out DA

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14
Q

Once DA is reuptaken into the presynaptic neuron via DAT, DA is metabolized into DOPAC by what enzyme?

A

Monoamine oxidase (MAO)

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15
Q

Describe the production of NE (norepinephrine)

A

Similar to production of DA. Once DA is produced and pumped into vesicles via VMAT, it is converted to NE by an intravesicular enzyme called DBH (dopamine beta hydroxylase)

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16
Q

Once NE is released from the presynaptic neuron, it has three similar fates to DA. It can bind to its autoreceptor ___, it can bind to ___ or ___ heteroreceptors on other neurons, or it can be pumped back into the presynaptic neuron via ____. _____ metabolizes NE in the neuron (similar to DA).

A

Alpha 2

Alpha or beta

NET (norepinephrine transporter)

Monoamine oxidase

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17
Q

What enzyme converts norepinephrine to epinephrine?

A

(PNMT) Phenylethenolamine-N-methyltransferase

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18
Q

What is a chatechol? What is a catecholamine?

A

A catechol is a benzene ring with two hydroxyl groups on adjacent carbons

A catecholamine is a catechol with a side chain with an amine group in it.

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19
Q

What cells mainly use epinephrine?

A

Adrenal medullary cells

Some CNS neurons

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20
Q

What does the structure of serotonin look like? Is it a catecholamine?

A

Two rings (one 6 carbon ring, one 5 carbon ring) with one hydroxyl group, and two amine groups

It is NOT a catecholamine

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21
Q

Serotonin is derived from what amino acid?

A

Tryptophan

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22
Q

In order to synthesize serotonin, the amino acid precursor ___ is converted to ____ by _____. Then, it is converted to ____ by ____

A

Tryptophan

5-hydroxyltryptophan (5HTP)

Tryptophan hydroxylase

Serotonin (5-hydroxyltryptamine)

AADC (amino acid decarboxylase)

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23
Q

What is the other name for serotonin?

A

5HT (5-hydroxyltryptamine)

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24
Q

What happens once serotonin is produced in the neuron?

A

It is pumped into vesicles via VMAT (vesicular monoamine transporter). Then the vesicles fuse with the membrane for release of the NT.

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25
Q

Similar to other NTs, serotonin can bind to an autoreceptor (___), bind to heteroreceptors, or be pumped back into the neuron (by ____)

A

5HT/1B

SERT (serotonin transporter)

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26
Q

What are SSRIs?

A

Selective serotonin receptor inhibitors. These drugs work on SERTs (serotonin transporters)

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27
Q

What is the function of dopamine beta hydroxylase?

A

Converts DA to NE in vesicles

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28
Q

___ +___ will yield ACh through the action of what enzyme?

A

Choline

Acetyl coA

ChAT (choline acetyl transferase)

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29
Q

Once ACh is produced in the neuron it is stored into vesicles through what transporter?

A

Vesicular ACh transporter

Note that it isn’t VMAT

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30
Q

Once ACh is released from the neuron it is quickly metabolized by ___ back to choline.

A

Acetylcholinesterase

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31
Q

True or false… there is a plasma ACh transporter in neurons

A

False! Just a choline transporter to pump choline back into the neuron

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32
Q

ACh can bind to what kinds of post synaptic receptors?

A

Muscarinic and nicotinic

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33
Q

How does the botulinum toxin work?

A

It prevents the release of ACh from neurons

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34
Q

Once ACh is released from the neuron, it may bind to what autoreceptor to decrease the release of ACh?

A

A muscarinic autoreceptor

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35
Q

GABA is an inhibitory NT whereas glutamate is an excitatory NT. How are their molecular structures similar?

A

Both have four carbons and a carboxyl group, and amine group

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36
Q

What is the precursor for producing glutamate?

A

Alpha keto gluterate (from citric acid cycle)

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37
Q

Alpha keto gluterate is converted to glutamate by the action of the ___ enzyme

A

Aminotransferase

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38
Q

Once glutamate is produced in the neuron, it is transported into vesicles by ___

A

Vesicular glutamate transporter

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39
Q

Once glutamate is released from the neuron, it may re-enter the neuron by the ___ transporter

A

Glutamate transporter

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40
Q

Once released from the neuron, glutamate binds to ____ (autoreceptor )

A

Metabotropic glutamate

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41
Q

Name two post synaptic receptors that glutamate binds to

A

AMPA/kainate

NMDA

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42
Q

Glutamate enters astrocytes through the glutamate transporter. Once in the astrocytes, glutamate is converted to ___ via the action of ____.

A

Glutamine

Glutamine synthetase

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43
Q

Once glutamine is produced in astrocytes, glutamine may enter the neuron and be converted to ___ through the action of ___.

A

Glutamate

Glutaminase

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44
Q

In order to produce GABA, ___ must first be produced

A

Glutamate

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45
Q

In the production of GABA, glutamate is converted to ___ through the action of ___

A

GABA

GAD (glutamate decarboxylase)

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46
Q

Once GABA is produced in the neuron, how does it enter vesicles?

A

Vesicular GABA transporter

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47
Q

Once GABA is released from neurons, it may renter the neuron through ____. Or it may bind to ___ and ___ post synaptic receptors. Or it may bind to its autoreceptor ___. Or it may enter ___.

A

GABA transporter

GABA-A or GABA-B

GABA-B

Astrocytes

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48
Q

Which postsynaptic GABA receptor is involved with chloride channels?

A

GABA-B

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49
Q

Once GABA enters astrocytes, it is converted to ___ through the action of ____

A

Succinate

GABA transaminase

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50
Q

What is an endocannabinoid? Give an example

A

Anandamide (binds to CB1 receptors)

They are natural endogenous NTs

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51
Q

True or false… nitric oxide doesn’t bind to receptors

A

True

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52
Q

Which histamine receptor is thought to function as an inhibitory heteroreceptor? Thus, activation of these receptors decreases the release of ACh, DA, NE, SER, and certain peptides?

A

H3

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53
Q

Endorphins bind to ___ receptors, causing a decrease in the release of ___. This mechanism can cause you to be happy.

A

Muscarinic

GABA

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54
Q

Name 7 neuropeptides

A

Neurotensin

Substance P

Somatostatin

Cholecystokinin

Vasoactive

Intestinal polypeptide

Neuropeptide Y

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55
Q

What does neurotensin do?

A

Acts as endogenous neuroleptic; regulates DA systems (inhibitory feedback)

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56
Q

What is nitric oxide? What does it do to vascular smooth muscle?

A

It is a gaseous signaling molecule

Relaxes vascular smooth muscle

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57
Q

In the autonomic nervous system, ACh binds to what kind of receptor on post ganglionic neurons

A

Nicotinic

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58
Q

True or false… ACh is used by both the sympathetic and parasympathetic pre-ganglionic fibers

A

True

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59
Q

True or false… drugs that alter ACh levels affect BOTH the sympathetic and parasympathetic systems

A

True

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60
Q

What other neurons act via nicotinic receptors?

A

Motor neurons innervating skeletal muscle

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61
Q

What types of NTs do post ganglionic sympathetic neurons use?

A

DA, NE, and EPI.

Most use NE

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62
Q

NE and EPI act on __ and __ receptors. What about DA?

A

Alpha and beta

DA activates D1, alpha, and beta

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63
Q

What NTs do post-ganglionic parasympathetic neruons use?

A

ACh

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64
Q

What receptors does ACh (released from post-ganglionic parasympathetic) neruons bind to?

A

Muscarinic receptors in most effector tissues

Nicotinic in somatic muscles

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65
Q

Name 5 specific receptors that the parasympathetic nervous system acts on.

A

M1
M2
M3

Nm
Nn

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66
Q

Describe where each of the following parasympathetic receptors are found.

M1
M2
M3
Nm 
Nn
A

M1 - Stomach
M2 - Heart (SA node, AV node, atria, ventricles)
M3 - GI tract (GI smooth muscle, secretory glands)

Nm- muscle (neuromuscular junction)
Nn - Neuronal (autonomic ganglia, adrenal medulla)

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67
Q

Name three agonists for parasympathetic muscarinic receptors

A

ACh

Bethanechol

Pilocarpine

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68
Q

If parasympathetic M1 receptors are activated by an agonist, what happens?

A

Acid secretion in the stomach increases

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69
Q

If M2 receptors are activated by an agonist, what happens?

A

SA node -> decrease HR

AV node -> decrease in conduction velocity

Atria -> decrease AP duration and contractility

Ventricles -> decrease in contractility

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70
Q

If M3 receptors are activated by an agonist, what happens?

A

GI smooth muscle - increase contractions (usually; except sphincters)

Secretory gland - increase secretions

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71
Q

Name two antagonists of the muscarinic receptors

A

Atropine

Scopolamine

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72
Q

Name two antagonists of Nm receptors

A

Succinylcholine***

D-tubocurarine

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73
Q

Name two antagonists of Nn receptors

A

Mecamylamine**

Trimethaphan

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74
Q

What are the two classes of neuromuscular blockers ? Describe them and give an example of each

A

Depolarizing (succinylcholine) - non-competitive. Acts as a nicotinic agonist and depolarizes/desensitizes the deuromuscualr endplate by opening up the NIC channels and keeps them open so that the neuron is depolarizer and unresponsive to another ACh challenge.

Non-depolarizing (tubucurare) - competitive. Competes with ACh at nicotinic receptors

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75
Q

What 3 things happen with the blockage of AChE? (Acetylcholinesterase)

A

Affects both sympathetic and parasympathetic systems

Affects tissues innervated by post ganglionic fibers

Affects signaling at the neuromuscular junction

76
Q

Give an example of a cholinesterase inhibitor

A

Sarin

77
Q

What may happen if you block AChE?

A

ACh will build up extraneuronally. This will lead to a decrease heart rate, stimulation of skeletal muscles to cause tetanus (prevents breathing), drooling, watery eyes, blurred vision, sweating, diarrhea.

78
Q

What drug is used to counter the effects of Sarin?

A

Atropine because it is a muscarinic antagonist (competes with excess ACh)

79
Q

Name three cholinesterase inhibitors and what they do.

A

Physostigmine - short duration of action, used for glaucoma, antidote for atropine

Donepezil (aricept)- extended duration of action, used to treat Alzheimer’s

Sarin - irreversible, long duration of action, biological weapon nerve gas

80
Q

how does botulinum toxin work? What does it do?

A

Prevents release of ACh

Relaxes intraocular muscles

Treats muscle dystonia (spasms)

Removes wrinkles

81
Q

Name two cholinergic agents (cholinomemetics) used in dentistry and what they are used for

A

Cevimeline (Evoxac) - cholinergic agonist used to treat xerostomia in SS

Pilocarpine (salagen) - cholinergic agonist used to treat xerostomia after radiation therapy. (Mouthwash available)

82
Q

What is a cholinomimetic?

A

An agent that mimics ACh

83
Q

What is curare (tubocurarine) and how does it work? What is its antidote?

A

Used in poison darts. It competitively and reversibly inhibits nicotinic ACh receptors. This causes skeletal muscle weakness and even death by diaphragm paralysis.

Antidote - Acetylcholinesterase inhibitor

84
Q

True or false… nicotine is a cholinesterase inhibitor

A

True

85
Q

What is the indication for the use of bethanechol (urecholine)?

A

Increase urinary output to treat urinary retention

86
Q

What is the indication for the use of pilocarpine?

A

Increases saliva secretion and treats glaucoma**

87
Q

What is the indication for the use of succinylcholine?

A

It is an antagonist. Used in surgeries to relax muscles

88
Q

The sphincter muscle in the iris has ___ receptors

A

Muscarinic

89
Q

What is closed angle glaucoma?

A

Narrow angle between iris and cornea leads to fluid build up in the vitreous humor (increases intraocular pressure).

Develops very quickly and requires immediate medical attention

Signs and symptoms very noticeable

90
Q

What do you use to treat angle closure glaucoma?

A

Pilocarpine to contract and pull iris to open trabecular meshwork

91
Q

Name two anti muscarinic agents and some uses of them

A

Atropine (antidote for sarin gas)

Scopolamine (used for motion sickness)

Also can be used to treat Parkinson’s, COPD, urinary urgency

92
Q

What are the side effects of anti muscarinic agents? (5)

A

Anticholenergic effects…

Dry mouth
Constipation
Blurred vision
Sedation
Urinary retention
93
Q

What is pralidoxime used to treat? How does it work?

A

Treats organophosphate poisoning

Organophosphates bind to acetylcholinesterase. Pralidoxime binds to acetylcholinesterase to kick of the organophosphates

94
Q

Name two important synthetic anticholinergic agents. What are they used to treat?

A

Propantheline bromide (pro-banthine) - treats travelers diarrhea

Trihyxphenidyl HCl (artane) - anti-parkinsonism

95
Q

Describe where the following sympathetic receptors are found…

Alpha 1
Alpha 2
Beta 1
Beta 2 
Beta 3
A

Alpha 1 - radial muscle of iris, genitourinary sphincters

Alpha 2 - vasculature, NE terminals, brain stem

Beta 1 - heart

Beta 2 - ciliary muscle, vasculature, lungs, urinary bladder

Beta 3 - adipose tissue

96
Q

Name two agonists of alpha 1 receptors

A

Epinephrine > NE

Phenylephrine

97
Q

What happens to the radial muscle of the iris when alpha one receptors are activated by an agonist?

A

Contract. (Opens up pupil to cause dilation)

98
Q

What happens to the genitourinary and GI sphincters when alpha 1 receptors are activated by an agonist?

A

Constrict (leads to retention)

99
Q

Name two antagonists of alpha 1 receptors

A

Prazosin

Terazosin

100
Q

True or false… phenylephrine is used as a decongestant because it causes vasoconstriction of the nasal passages

A

True

101
Q

Name three agonists of alpha 2 receptors

A

Epi>NE

Clonidine

Guanfacine

102
Q

What happens to the vasculature when an alpha 2 receptor is activated by an agonist?

A

Constricts (increases BP)

103
Q

What happens to NE terminals when an alpha 2 receptor is activated by an agonist?

A

Decrease NE release. (Remember that alpha 2 is an autoreceptor in NE terminals)

104
Q

What is the response of the brain stem when alpha 2 receptors are activated by an agonist?

A

The brain stem will decrease NE release (this will cause a reduction of BP)

105
Q

What is guanfacine used to treat?

A

Treats ADD. It’s mechanims are central.

The central signals will trump the peripheral signals to cause vasodilation leading to decease of BP.

106
Q

What is an antagonist of alpha 2 receptors? (This antagonist isn’t used for anything)

A

Yohimbine

107
Q

Name two agonists of beta 1 receptors

A

Epi = NE

Isoproterenol
Dobutamine

108
Q

What tissues are Beta 1 receptors found in?

A

Cardiac tissue (SA node, AV node, Atria, ventricles, His-purkinje system)

109
Q

What happens when the following tissues are Beta 1 activated by their agonist?

SA node
AV node
Atria
Ventricles
His-purkinje system
A

SA node - increase HR
AV node - increase automaticity and conduction velocity
Atria - increase conduction velocity and contractitliy
Ventricles - increase automaticity, conduction velocity and contractility
His-purknje system - increase automaticity and conduction velocity

110
Q

Name one antagonist of beta 1 receptors. What are they used to treat?

A

PropranOLOL

(Also atenolol, metoprolol)

Betablockers are used to treat hypertension.

111
Q

What types of tissues are beta 2 receptors found in?

A

Ciliary muscle

Vasculature

Lungs (tracheal and bronchial smooth muscle)

Urinary bladder, uterine wall

112
Q

Name 4 beta2 agonists. Which is better epi or NE?

A

Epi»>NE***

Isoproterenol

Albuterol

Terbutaline

113
Q

What happens to the following tissues when beta 2 receptors are activated by an agonist?

Ciliary muscle

Vasculature

Lungs (trancheal/bronchial smooth muscle)

Urinary bladder/uterine wall

A

Ciliary muscle - relaxation (for far vision)

Vasculature - relaxation, especially in skeletal muscle (vasodilation)

Smooth muscle in lungs - relaxation for opening of airways

Urinary bladder - relaxation

Uterine wall - relaxation

114
Q

In adipose tissue, are beta 3 receptors activated more easily by NE or EPI?

A

NE

115
Q

When B1 receptors are stimulated in the heart, the increase in HR is a positive ___ effect. The increase strength of ventricular contraction is a positive ___ effect.

A

Chronotropic

Ionotropic

116
Q

When epinephrine binds to alpha 1 receptors of the bladder sphincter, what happens? What about when epi binds to Beta 2 receptors of the muscle of the urinary bladder?

A

Constricts

Relaxes

*this leads to urinary retention

117
Q

Name 5 therapeutic uses of epinephrine

A

Broncospasm

Anaphylaxis

Restore function in cardiac arrest

Treat open-angle glaucoma

Prolong action of local anesthetics

118
Q

Describe open-angle glaucoma

A

Most common type of glaucoma

Imbalance in the production and drainage of aqueous humor that fills the anterior chamber (leading to build up of fluid)

Wide angle between iris and cornea

Develops over lifetime

119
Q

How do you treat open-angle glaucoma?

A

Treat with epinephrine to decrease production of aqueous humor

120
Q

Name three side-effects of epinephrine

A

Cardiac - increased HR, palpitations, arrhythmias, angina

Vascular - increased TPR (total peripheral resistance ) leading to increased BP and pallor (pale face due to less blood flow in face due to vasoconstriction)

Respiratory - increased TPR can lead to pulmonary edema

121
Q

True or false. Epinephrine easily crosses the BBB

A

False. CNS effects are negligible

122
Q

What receptors does NE bind to?

A

Alpha and beta

B1&raquo_space;> B2

123
Q

What are some physiological effects of NE?

A

Vasoconstriction, increased TPR, increased BP. (Things get complicated with baroreceptor involvement)

124
Q

What is a therapeutic use for NE?

A

Shock

125
Q

What are some side effects of NE?

A

Slow heartbeat if BP increased (due to baroreceptors), forceful beat (B1), vasoconstriction (decrease blood flow to vital organs; alpha 1)

126
Q

Which, epi or NE is used as an emergency hormone secreted in response to stress?

A

Epinephrine

Note that A1=A2, B1=B2 in regards to affinity

127
Q

Is this a description of epinephrine or NE?

Increases HR

Redistributes blood to skeletal muscles by dilating pre-capillary resistance vessels in skeletal muscles (B2)

If “high and fast” -> increased TPR (alpha-1)

A

Epinephrine

128
Q

Is this a description of epi or NE?

Increases HR if released by cardiac neurons (beta1) however, decreases HR when infused because vagaries stimulation overrides beta-1 mediated increase in HR

Maintains peripheral resistance by constricting pre-capillary resistance vesicles (alpha-1; alpha-1 trump beta 2)

A

NE

129
Q

Name in order, the affinity of receptors that DA binds to

A

DA > beta > alpha

Primarily alpha 1 and beta 1

130
Q

What is a therapeutic use for DA?

A

Used to treat shock and heart failure (at high doses, increased BP and TPR (alpha 1), increased HR (B1), increased organ perfusion (D1)

131
Q

Name some effects of alpha 1 agonists such as phenylephrine

A

Vasoconstriction and increased TPR (used as nasal decongestant (PE))

Change in HR

Constricts sphincter muscle of bladder

132
Q

What are some effects and uses of alpha 2 agonists?

A

Effects: Bradycardia, dry mouth

Used to treat HTN and ADHD (stimulation of CNS alpha2 receptors decreases sympathetic output

133
Q

What are some uses of B agonists?

A

Asthma

Bronchospasm

COPD

OBGYN (relaxes smooth muscle of uterus during labor to slow contractions)

134
Q

True or false… Isoproterenol is non selective for beta 1 or beta 2. However albuterol and terbutaline are Beta 2 selective

A

True

135
Q

What are some mixed agonists? (Act on alpha and beta, but also cause release of NE)

A

Ephedrine

Ephedra

Pseudophedrine

136
Q

What are some uses of mixed agonists? What are some side effects?

A

Decongestant, dietary supplements

Side effects: increase HR, vasoconstriction, dilation of airways, stimulant (if penetrates CNS)

137
Q

Name 5 other “indirect” adrenergic agents (not sympathemimics)

A

Amphetamine

Cocaine

Methylphenidate

NNRIs

TCAs

138
Q

How does cocaine work?

A

Blocks the reuptake of DA, NE, and Seratonin reuptake

139
Q

What are NNRIs?

A

NE reuptake inhibitors

140
Q

Tyramine is an indirect agonist with the action of a monoamine oxidase inhibitor. Describe its mechanism.

A

Tyramine is usually metabolized by MAO. If taking a MAOI, tyramine concentrations will increase. When neuron terminal vesicles fill with tyramine, NE goes out so you end up with a lot more NE.

141
Q

Name two examples of non-selective alpha antagonists

A

Phenoxybenzamine

Phentolamine

142
Q

What are the uses, effects, and side effects of non-selective alpha antagonists?

A

Uses: treatment of pheochromaocytoma (NE secreting tumor), hypertensive emergencies

Effects - decreased TPR (alpha 1) and decreased BP. Increased HR (baroreceptor response to decreased BP)

Side effects: orthostatic hypotension, nasal stuffiness

143
Q

Name two examples of alpha 1 antagonists. What are their uses, effects, and side effects.

A

Prazosin
Terazosin

Uses: treat hypertension, benign prostatic hypertrophy (tamsulosin)

Effects - vasodilation and thus decreased TPR and decreased BP

Side effects: orthostatic hypotension, nasal congestion

144
Q

What drug is used to treat benign prostatic hypertrophy?

A

Tamsulosin

145
Q

Name four beta antagonists

What are the uses of beta blockers?

A

Propranolol (beta 1 and beta 2)

Atenolol (beta 1)

Metoprolol (beta 1)

Treatment of HTN, angina, open-angle glaucoma

146
Q

What are the effects that beta antagonists have on the following tissues?

Cardiac
Vascular
Renal
Respiratory
Metabolic
Eyes
A

Cardiac: decreased HR and contractility

Vascular: increased TPR (blockade of B2 in skeletal muscle)

Renal: decreased renin release

Respiratory: bronchial constriction

Metabolic: decreased glycogenolysis in response to hypoglycemia

Eyes: decreased aqueous humor production

147
Q

Epilepsy is a neurological disorder affecting __% of the population. __-__% of patients with epilepsy are therapy-resistant

A

1.2

25-40

148
Q

What is the difference between a seizure and epilepsy?

A

Seizure = a finite clinical manifestation of abnormal and excessive excitation of a population of cortical neurons.

Epilepsy = a syndrome characterized by 2 or more* recurrent seizures that are unprovoked* by systemic or neurological insults

149
Q

What is epileptogenesis?

A

A sequence of events that convert normal neuronal networks into a hyperexcitable network

150
Q

What is status epilepticus (SE)?

A

Continuous seizure lasting more than 30 minutes or 2 or more seizures without full recovery of consciousness between them.

  • any seizure lasting >5 minutes is treated clinically as SE due to the high risk of morbidity and mortality
  • most patients in status epilepticus for 30 minutes will die
151
Q

What percentage of the population will have at least one seizure in their lifetime?

A

10%

152
Q

Over a lifetime, 1 in ___ people will be diagnosed with epilepsy

A

1/26

153
Q

What is the main inherited etiology factor for epilepsy

A

Mutations in ion channels

154
Q

What are some common seizure precipitants?

A 
Metabolic imbalance
Stimulate intoxication
Depressant withdrawal 
Sleep deprivation
Reduction of ASD treatment
Hormonal variations
Stress
Hypoxia
High fever
CNS infection 
Concussion and/or closed head injury
155
Q

What are the different seizure classifications?

A

Partial seizures: simple partial, complex partial, secondarily generalized

Generalized seizures: tonic-clonic, absence, atonic

156
Q

What is a simple partial seizure?

A

Single focus

Patient is fully aware and responsive

Shortest duration (<90s)

Phenotype depends on areas of focal cortical involvement. (Focus is confirmed via EEG).

157
Q

What is a complex partial seizure?

A

Focal onset with local spread.

Initially aware and responsive, but may develop some memory impairment if limbic system involved.

A complex partial seizure does not fully generalize, if it does it is considered a secondarily generalized seizure

Clinical manifestations vary with site of origin and degree of spread

Slightly longer duration (<120s)

158
Q

What is a secondarily generalized seizure?

A

May begin as either simple or as complex partial seizures

Seizure activity fully generalizes with variable symmetry, intensity, and duration before evolving to tonic and/or clonic phases

Usually lasts <240s

159
Q

What is the postictal phase of generalized seizures?

A

Confusion, somnolence, with or without transient focal deficit can last minutes - hours

160
Q

What are generalized absence seizures?

A

Impaired awareness and responsiveness for 2-15 seconds. Patient stares off into space

161
Q

Generalized absence seizures represent abnormal interactions between what parts of the brain?

A

Abnormal interactions between cortical and thalamic transmissions

The spike and wave pattern is a hallmark of absence epilepsy

162
Q

Describe generalized tonic-clonic seizures

A

Progresses from tonic (rigid) to clonic (movement). Patient may scream as lungs constrict.

Then the patient enters the postictal phase where the patient is lethargic and confused.

163
Q

What is the problem with ASD (anti seizure disorder) medication?

A

Approximately 1/3rd of all patients with epilepsy remain refractory to all treatments

164
Q

What is the therapeutic (protective) index?

A

Safety margin between the effective dose and toxic dose. Calculated as…

Toxic dose/efficacious dose

Larger the number the better

165
Q

What are three mechanisms of action for most commonly used ASDs?

A

1) enhancement of GABA-mediated inhibition
2) reduction of excitatory transmission (i.e. Glutamate)
3) modification of ionic conductance (i.e. sodium, calcium, potassium ions)

166
Q

Carbamazepine

A

Indicated in partial simple or partial complex, and generalized tonic-clonic seizures

Common side effects: impaired vision, cognitive impairment.
Rare side effects: Stevens-Johnson syndrome

AVOID IN ABSENCE!! (May aggravate spike wave seizures)

Active metabolite
Potent CYP3A4 inducer

167
Q

True or false.. carbamazepine is a great drug for partial epilepsy but the potential for drug-drug interactions is high.

A

True

168
Q

What is the mechanism of carbamazepine?

A

Blocks voltage gated Na+ channels to inhibit repetitive firing neurons (this blocks the onset and spread of seizures)

169
Q

What is Stevens-Johnson syndrome?

A

Toxic epidermal necrolysis - Skin becomes inflamed and sloughes off.

Symptoms: fever, sore throat, fatigue, painful mucosal lesions.

Patients on sodium channel blocker ASDs are at most risk

170
Q

True or false… carbamazepine inhibits CYP3A4 enzyme in gut/liver, decreasing carbamazepine’ metabolism and increases its plasma levels.

A

True.. note that grapefruit juice also raises CBZ plasma levels by inhibiting its breakdown by CYP3A4

171
Q

What drug is used to treat uncomplicated absence only?

A

Ethosuximide

172
Q

What are the indications, common side effects, and other special comments of ethosuximide?

A

Indication: uncomplicated absence only

Common side effects: drowsiness, dizziness, headache, minor weight loss,….**may worsen partial and tonic-clonic seizures

Special comments: narrow clinical spectrum (for absence only). *very long half life (40 hours)

173
Q

What is the mechanism of ethosuximide?

A

Reduces T-type calcium channel currents in thalamic pacemaker neurons

174
Q

What are the indications, common side effects and special comments of phenytoin?

A

Indication: partial simple or complex. Generalized tonic-clonic

Common side effects: nystagmus, cognitive impairment, fetal drug effects
Non-dose related: ***gingival hyperplasia

Special comments: **contraindicated for absence seizures (may aggravate absence spike-wave seizures. Zero-ordered kinetics at high doses; must check plasma levels often and titrate dose as needed

175
Q

What is the mechanism of phenytoin?

A

Blockade of sodium channels during repetitive firing

176
Q

Which ASD causes severe gingival hyperplasia?

A

Phenytoin

177
Q

Why must you monitor plasma levels often and titrate the dosage of phenytoin?

A

Because it has zero order elimination kinetics

178
Q

What are the indications, common side effects, and special comments of topiramate?

A

Indications: simple and complex partial. Generalized tonic-clonic and Lennox-gastuat syndrome

Common side effects: somnolence, **word recall problems, weight loss. (Rare but may also cause open-angle glaucoma)

Special comments: weight loss can be an advantage. Increases metabolism of estrogen so can reduce oral contraceptive efficacy (must use secondary means of birth control)

179
Q

What is the mechanims of topiramate?

A

Broad spectrum

Blocks repetitive firing of voltage gated sodium channels, inhibits calcium currents, inhibits AMPA/kainate recpetors and potentials GABA currents

180
Q

What are the indications, common side effects, and special comments for valproic acid?

A

Indications: atypical absence, absence, myoclonic, tonic-clonic. Partial simple and partial complex

Common side effects: weight gain. Toxic doses may cause reye-like syndrome and hepatic failure

Special comments: **contraindicated in patients with hepatic disease or significant hepatic dysfunction. Increased teratogenicity and neural tube defects such as spina bifida

181
Q

What is the mechanism of valproic acid?

A

Broad spectrum

Blocks voltage gated sodium channels (main mechanism), reduces NMDA currents, increases GABA-mediated chloride currents

182
Q

Why do you want to avoid valproate (valproic acid) during pregnancy?

A

Category D risk for birth defects including spinal bifida and other birth defects

183
Q

What are the drugs of choice for partial seizures?

A

Carbamazepine

Phenytoin

Topiramate (if secondarily generalized)

184
Q

What are the drugs of choice for generalized onset tonic-clonic seizures?

A

Valproate (valproic acid)

Topiramate

185
Q

What are the drugs of choice for absence seizures?

A

Ethosuximide (uncomplicated)

Valproate (complicated)

186
Q

What are the four principles of ASD treatment?

A

Match appropriate ASD to the seizure type confirmed by EEG

Try mono therapy first

Monitor plasma levels of drugs

Tailor therapy to individual patient

Human Disease And Therapeutics (13 decks)

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