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MS1 - Pharmacology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

for the following neurons list what neurotransmitter they release:

  1. pre-ganglionic sympathetic fibbers
  2. post-ganglionic sympathetic fibbers
  3. pre-ganglionic parasympathetic fibers
  4. post-ganglionic parasympathetic fibers
A
  1. pre-ganglionic sympathetic fibers - Ach
  2. post-ganglionic sympathetic fibers - norepinephrine
  3. pre-ganglionic parasympathetic fibers - Ach
  4. post-ganglionic parasympathetic fibers - Ach
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2
Q

list 3 tissues that does NOT get parasympathetic innervation

A
  1. peripheral blood vessels
  2. adrenal medulla
  3. skin
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3
Q

list the 5 steps/molecules at a cholinergic junction that can be pharmacologic targets.

give an example of substance that targets each one

A
  1. choline uptake - hemicholinium (reuptake of choline is the rate limiting step in the synthesis of ACh)
  2. Neurotransmitter storage - vesamicol
  3. Nt release - botulinum toxin
  4. termination of signal - AChE inhibitors
  5. receptors - various agonists and antagonists
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4
Q

what type of receptors can ACh bind to?

A
  1. nicotinic receptors

2. muscarinic receptors

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5
Q

what protein is used for choline reuptake?

what enzyme converts choline to ACh? where does the substrate come from?

A

the Na+/choline co-transporter

choline acetyltransferase uses acetyl-CoA from the mitochondria to make ACh

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6
Q

list the 5 steps/molecules at a adrenergic junction that can be pharmacologic targets.

give an example of substance that targets each one

A
  1. Nt synthesis - metyrosine (inhibits tyrosine to dopa, rate limiting step of catecholamine transmitter synthesis)
  2. Neurotransmitter storage - reserpine (inhibits VMAT)
  3. Nt release - bretylium
  4. reuptake - cocaine, TCA, Ang II (inhibits NET)
  5. receptors - various agonists and antagonists
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7
Q

what AA is the precursor for catecholamines?

list 3 specific catecholamines

A

tyrosine

  1. epinephrine
  2. norepinephrine
  3. dopamine
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8
Q

what protein transfers adrenergic ligands into the cell? which one loads them into vesicles?

A

taken up from synaptic cleft by NET (norepinephrine transporter)

loaded into vesicles by VMAT (vesicular monoamine transporter)

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9
Q

what are sympathomimetics? what are some examples of them?

how do they relate to the adrenergic neuronal junction?

A

they are molecules (drugs) that are capable of binding to adrenaline receptors (however poorly)

  1. tyramine
  2. amphetamine
  3. ephredrine

these are poor agonists for the adrenergic receptors for work great with the reuptake and storage proteins the norpinephrine uses (VMAT and NET). they get taken up and put in vesicles which kicks the norepinephrine out and into the synaptic cleft (via reverse NET transport) thus increasing norepinephrine activity

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10
Q

list the steps of synthesizing norepinephrine starting with free extracellular tyrosine (5)

A
  1. tyrosine uptake via Na+/tyrosine cotransmitter
  2. tyrosine converted to DOPA via tyrosine hydroxylase
  3. DOPA converted to dopamine (DA via dopamine decarboxylase)
  4. DA transported into granules (process can stop here in some neurons)
  5. DA converted to norepinephrine via DA-beta-hydroxylase (in the granule)
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11
Q

what percent of norepinephrine (NE) is reuptaken into the presynapse?

A

70%

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12
Q

list the products of the epinephrine synthesis pathway starting with tyrosine and what (in general) was modified at each step

A
  1. tyrosine
  2. DOPA - OH added to ring
  3. dopamine - COOH removed from chain
  4. NE - OH added to chain
  5. epinephrine - methyl CH3 added to N in chain
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13
Q

list 2 enzymes that metabolize catecholamines. where are they found?

A
  1. COMT - kidney, liver, GI tract (therefore not active orally) and other target organs
  2. MAO - primarily in neural tissue
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14
Q

for the following catacholamine structures, list how modification of the site will affect their activity.

  1. beta carbon
  2. alpha carbon
  3. amine group
  4. aromatic ring and catechol OH groups

what is the purpose of modifying these sites

A
  1. beta carbon - ANY additional group here increases alpha AND beta receptor activity
  2. alpha carbon - ANY additional group here increases the half-life by inhibiting MAO (drug acts as an indirect sympathomimetic)
  3. amine group - methyl group here gives alpha receptor selectivity
  4. aromatic ring and catechol OH groups - depends on what is added and where. 2 OHs needed for max efficiency)

for drug discovery

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15
Q

list 4 important cholinoceptors, where they are typically found and the result of their binding

A
  1. M2 (heart) - Gi expressed (decreased cAMP [inhibits adenyl cyclase])
  2. M3 (exocrine glands [sweat], vessels, iris circular muscle) - Gq expressed (increased IP3 and DAG)
  3. Nn (autonomic ganglia, adrenal medulla) - opens Na and K channels, causes depolarization (therefore excitatory)
  4. Nm (skeletal muscle) - opens Na and K channels, causes depolarization therefore excitatory
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16
Q

list 4 important adrenoceptor, where they are typically found and the result of their binding

A
  1. alpha1 (smooth muscle, iris radial muscle) - Gq (IP3 and DAG)
  2. aplha2 (smooth muscle, presynaptic?) - Gi (decreases cAMP)
  3. beta1 (heart, JGA of renal tubule) - Gs (increases cAMP)
  4. beta2 (lungs, smooth muscle) - Gs (increases cAMP)
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17
Q

differentiate heteroreceptors with autoreceptors

A

heteroreceptors respond to substances released from adjacent neurons/cells of different type

auto receptors respond to substance of the same type

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18
Q

how do alpha2 receptors autoregulate the release of NE?

A

alpha 2 receptors are found on both the post AND presynapse. when NE is released most of it acts on the post synaptic receptors. as the NE concentration goes up in the cleft more and more of it starts to interact with the presynaptic alpha2 receptors. triggering those inhibits the influx of calcium into the presynapse which is needed for vesicle fusion and NE release thus reducing the amount of NE in the cleft.

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19
Q

what is phenoxybenzamine (POB) indicated for?

A

indicated for pheochromocytoma (tumor of the adrenal gland which makes NE and Epi)

POB is an inhibitor of alpha1 and 2 which results in a lowering of blood pressure. (however, inhibiting the negative feedback of aplha2 on NE and Pei release causes a excess to be released which then binds to beta2 receptors and raises blood pressure)

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20
Q

what receptors in the eye control pupil aperture?

A
  1. M3 (cholenergic) - controls iris circular muscles, constricts pupil (miosis)
  2. alpha1 (adrenergic) - controls iris radial muscle, dilates pupil (mydriasis)
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21
Q

what 3 receptors control the action of the ciliary body of the eye? what do they do?

A
  1. beta1 - facilitates aqueus humor secretion (ciliary epithelium)
  2. alpha2 - reduces aqueus humor production
  3. M3 - mediates ciliary muscle contraction, accommodation to focus, opens pored in the trabecular mesh work for aqueous humor outflow (ciliary muscle)
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22
Q

what is one of the causes of glaucoma?

A

glaucoma is caused by increased intraoccular pressure inside the eye. this can be due to too much aqueus humor present inside the eye which usually exits through the canal of schlemm through the trabecular mesh work

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23
Q

how does ACh relate to blood vessels and sweat glands? what affects does it have?

A

it causes vasodialation of vessels but there is no parasympathetic innervation to them

it causes sweat to activate but its released via sympathetic innervation (not parasympathetic)

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24
Q

what type of receptor are muscarinic receptors?

how many subtypes are there? what are they?

how does each propagate its signal?

A

G-protein coupled receptors (Gq, Gi and Go[Gbeta-gamma] are all possible)

Gbeta-gamma works to inactivate Galpha AND by activating secondary messangers by activating inwardly rectifying K channels

  1. M1 - Gq (IP3/DAG)
  2. M2 - Gi (less cAMP) also Gbeta-gamma?
  3. M3 - Gq (IP3/DAG)
  4. M4 - Gi (less cAMP) also Gbeta-gamma?
  5. M5 - Gq (IP3/DAG)
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25
Q

what 2 classes of molecule are muscarinic agonists?

A
  1. alkaloids

2. choline esters

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26
Q

what receptor type does pilocarpine bind to?

A

binds to muscarinic receptors. its well absorbed (due to its tertiary structure rather than quaternary like muscarine) and it acts as a partial agonist

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27
Q

what are choline esters? what is the benefit of using choline esters rather than ACh?

A

they are agents with modified ACh structure which allow for a number of benefiets including:

  1. more muscarinic receptor selectvity
  2. less susceptability to cholinesterase activity (therefore longer half-life)
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28
Q

what structure can be added to a a choline ester to make it more selective for muscarinic receptors?

what can you do to it to make them more resistant to AchE?

what is the reason behind choline esters (and ACh’s) poor CNS penetration

A

add a methyl group to make it more muscarinic selective

do an acetly to carbamol substitution to make it more resistant to AchE

poor CAN penetration because they are all charged thus preventing them from crossing the BBB

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29
Q

list 4 choline esters, how suceptable they are to AChE, and which type of cholinergic receptor they are selective for

A
  1. ACh - high AChE suceptability, selective to both muscarinic AND nicotinic
  2. methacholine - low AChE, only muscarinic
  3. carbachol - no AChE, both muscarinic and nicotinic
  4. bethanechol - no AChE, only muscarinic
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30
Q

what is the effect of direct acting muscarinic agonists on the following heart structures:

  1. SA node
  2. atria
  3. AV node
  4. ventricle

which receptor does it work no? what is the general affect?

A
  1. SA node - decrease in rate
  2. atria - decrease in contractile strength
  3. AV node - decreased conduction velocity
  4. ventricle - small decrease in contractile strength

M2 - increases K current into cell (Gbeta-gamma?) thus hyperpolatizing, reducing action potential duration and contractability of the heart

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31
Q

what is the effect of direct acting muscarinic agonists on blood vessles (2)?

A
  1. dialation in low doses (via NO from endothelium, NO activated guanylyl cyclase which increases cGTP and therefore vasodialation) and…
  2. constriction in high doses (via activation of M3 which produces IP3 which increases incracellular Ca, thus vasoconstriction. NOTE: this is not a parasympathetic effect)
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32
Q

what is the effect of direct acting muscarinic agonists on the following lung structures?

  1. bronchial muscle
  2. bronchial glands

what is the primary receptor?

A
  1. bronchial muscle - bronchoconstriction
  2. bronchial glands - stimulation (secretion)

M3 receptor

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33
Q

what is the effect of direct acting muscarinic agonists on the following GI functions?

  1. motility
  2. sphincters
  3. secretion

what is the primary receptor?

A
  1. motility - increase
  2. sphincters - relax
  3. secretion - stimulation

M3 receptor

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34
Q

what is the effect of direct acting muscarinic agonists on the following urinary bladder structures?

  1. detrusor
  2. trigone and sphincter

what is the primary receptor?

A
  1. detrusor - contraction
  2. trigone and sphincter - relaxation

M2 and M3 receptors

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35
Q

what is the effect of direct acting muscarinic agonists on the following glands?

  1. sweat
  2. salivary
  3. lacrimal
  4. nasopharyngeal

what is the primary receptor?

A

all cause secretion

M3 receptor

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36
Q

what physiology are the following receptors in the CNS associated with?

  1. M1
  2. M2
  3. M3
A
  1. M1 - found in areas associated with cognition
  2. M2 - mediated tremor, hypothermia and antinociception
  3. M3 - found in hypothalamus and reduces appetite and diminishes body fat mass
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37
Q

list 4 choline ester drugs and 1 alkaloid (muscarinic agonists) and what they are indicated for

A

choline esters
1. ACh - miosis induction for eye surgery

  1. methacholine - asthma diagnosis
  2. carbachol - miosis induction for eye surgery and glaucome
  3. bethanechol - urinary retention and increased lower esophagus sphincter tone for patients with reflux esophagitis

alkaloids
1.pilocarpine - claucome and sjogren’s syndrom (zerostomia)

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38
Q

why is methacholine used for asthma diagnosis?

A

in asthma the bronchi are hyperreactive to muscarinics and methacholine can induce exagerated bronchoconstriction

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39
Q

what is sjogren’s syndrome? list 2 drugs that can treat its symptoms

A

a systemic autoimmune disease where immune cells destroy exocrine glands

  1. pilocarpine
  2. cevimeline - new drug. used to treat the dry mouth
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40
Q

list 11 side effects to direct acting muscarinic agonists

A

numonic “DUMMBBELSSS”

  1. diarrhea
  2. urination
  3. miosis
  4. muscle weakness
  5. bronchospasm
  6. bradycardia
  7. excitation (erection?)
  8. lacrimation
  9. salivation
  10. sweating
  11. seizures
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41
Q

list 4 contraindications to direct acting muscarinic agonists

A
  1. coronary insufficiency (reduced blood pressure would exacerbate reduced coronary blood flow)
  2. hyperthyroidism (reduced AV conduction plus the increased heart rate would yield arrhythmias)
  3. asthma (bronchoconstriction)
  4. peptic ulcer disease (increased gastric secretions would be bad)
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42
Q

what is most likely to pass the BBB, tertiary antimuscarinics or quaternary?

A

tertiary are

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43
Q

which receptors can atropine bind, muscarinic, nicotinic or both?

A

both, however its potency for nicotinic receptors is so low its considered an “anti-muscarinic”

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44
Q

list 5 muscarinic antagonists

A
  1. atropine
  2. scopolamine
  3. ipratropium
  4. tiotropium
  5. tolterdine
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45
Q

what is the effect of scopolamine at low doses in the CNS? what about atropine?

what about high doses of scopolamine? atropine?

A
  • low scopolamine - CNS depression (drowsieness and amnesia)
  • low atropine - mild vagal excitation

high scopolamine AND atropine (to a lesser degree) - excitation, agitation, hallucinations, delirium and coma

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46
Q

list 3 effects antimuscarins (muscarinic antagonists) have on the eye

A
  1. unopposed sympathetic dilator activity and mydriasis
  2. weakened contraction of the ciliary muscle (normally controlled by M3) leading to a loss of ability to focus or accommodate the eye
  3. in patients with a narrow anterior chamber angle it can cause acute glaucoma
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47
Q

what is the effect of a high dose of an antimuscarinic in the cardiovascular system

A

tachycardia

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48
Q

list a use of antimuscaric drugs in the respiratory system

A
  1. bronchodialation and reduced secretion (not as usefull as beta-adrenoceptor stimulants though)
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49
Q

what is the effects of antimuscarinic drugs on the GI system?

A

reduced tone and mobility (gastric emptying time is prolonged). the GI “paralysis” usually only lasts 1-3 days. the tract reestablishes some parastalsis

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50
Q

what is the effects of antimuscarinic drugs on the urinary tract?

A

relazed smooth muscles of uriters and bladder which slows the process of voiding

can exacerbate urinary retention in men with prostatic hyperplasia

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51
Q

what is the effects of antimuscarinic drugs on the glands

A

inhibits secretion

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52
Q

list 6 antimuscarinic drugs and their clinical indications

which receptor is it selective for?

A
  1. scopolamine - prophylactic for motion sickness and postoperative nausea and vomiting
  2. atropine (non selective M) - antidote for parasympathomimetic drugs (drugs that mimic the PNS, ex. organophosphates liek seran, VX and tear gas)
  3. ipratropium (non-selective M) - COPD and nasal discharge
  4. tiotropium (M1, M3) - COPD

[NOTE: #3 and 4 are quartionary and therefore cant cross the BBB)

  1. tolterodine (M3) - overactive bladder
  2. dicyclomine (M3) - irratable bowl syndrom
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53
Q

list the side effects of atropine

A

it has a numonic

  • “mad as a hatter” - confusion and delirium
  • “dry as a bone” - dry mucous-, no sweat
  • “blind as a bat” - blurred vision, cycloplegia
  • “red as a beet” - skin flushed
  • “hot as hell” - hyperthermia
  • “heart goes on alone” - tachycardia
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54
Q

list 3 contraindications of antimuscarincs

A
  1. patients with glaucoma (especially angle-closure glaucoma)
  2. elderly men with prostatic hyperplasia
  3. patients with gastric ulcers
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55
Q

list 3 places where you would find nicotinic receptors

A
  1. autonomic ganglia
  2. neuromuscular junction of skeletal muscles
  3. adrenal medulla
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56
Q

what kinds of receptors are nicotinic receptors? what do they do?

how many are there?

A

they are ligand dependent ion channels that allow Na and K to move down their concentration gradient thus causing depolarization)

there are 2 types:

  1. Nn - neuronal type found on autonomic ganglia
  2. Nm - muscular type found on neuromuscular junction
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57
Q

how many subunits do the nicotinic receptors have? which ones bind to the ligand?

A

they have 5.

they bind to the 2 alpha subunits

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58
Q

what is the benefit of using nicotinic choline esters during surgery?

A

they have a high affinity for nicotinic receptors and they are resistant to AChE (therefore longer half-life) so they can be used to paralyze muscles (via over activation of the nicotinic ACh receptors)

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59
Q

describe the depolarizing blockade

A

a nirotinic agonist (succinylcholine for example) can bind the nicotinic receptor and cause depolarization. however, since it is also resistant to AChE it sticks around more and constantly activates the receptor. eventually its remained active so long it becomes less responsive even after the agonist is gone thus paralyzing the muscle

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60
Q

list 3 effects nicotinic receptors have on the CNS

A
  1. the presynaptic nicotinic receptors regulate the release of neurotransmitters (glutamate, serotonin, GABA, dopamine and NE)
  2. high concentrations of nicotine induces tremors, emesis and respiratory center stimulation
  3. even higher levels cause convulsions and can even progress to fatal coma
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61
Q

list 2 nicotinic agonists and their clinical indications

A

not many clinical indications
1. nicotine - smoking cessation

  1. succinylcholine - meuromuscular blockade for surgery, rapid sequence intubation
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62
Q

list 3 side effects of nicotinic agonists

A
  1. central stimulant - convulsions to coma to respiratory arrest
  2. depolarization blockade and respiratory paralysis
  3. hypertension and cardiac arrhythmias
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63
Q

where are ganglion blocking agents more useful; research or clinical? why?

A

they are more important in research because they competitively block nicotinic receptors of both sympathetic AND parasympathetic autonomic ganglia (thus blocking all autonomic outflow).

because of their lack of selectivity they have limited clinical use

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64
Q

list 5 ganglion blocking drugs

A
  1. tetraethylammonium
  2. hexamethonium
  3. decamethonium
  4. mecamylamine
  5. trimethaphan
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65
Q

briefly, what are the effects of ganglion blocking agents for the following systems

  1. CNS
  2. eye
  3. cardiovasuclar
  4. GI tract
  5. genitourinary
A
  1. CNS - sedation, tremor, choreiform movements and mental aberrations (mecamylamine crosses the BBB)
  2. eye - cycloplagia (paralysis of the ciliary muscle of the eye leading to dilation)
  3. cardiovasuclar - decreased arterial and venous tone, but moderate tachycardia
  4. GI tract - constipation
  5. genitourinary - hesitancy, urinary retention and sexual dysfunction
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66
Q

what do indirect-acting cholinomimetic do?

A

they are ChE inhibitors (ChEI). they act by reducing choline metabolism and increasing endogenous choline concentration.

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67
Q

list 5 ChEIs and their duration of action

A
  1. edrophonium - 2 to 10 mins (H-bonds to ChE thus preventing ACh degradation)
  2. neostigmine - 0.5 to 6hrs
  3. pyridostigmine - 0.5 to 6hrs
  4. physostigmine - 0.5 to 6hrs (all bind to the carbamyl group of ChE which takes a while to remove)
  5. echothiophate (organophosphate) - 100s of hrs (covalent binds to ChE, IRREVERSABLE, unlike the others above)
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68
Q

how does ChE cleave ACh?

what are the two parts of the active site of ChE? what do they do?

A

via serine hydrolase activity

  1. anionic site - binds choline (edrophonium binds here)
  2. esteratic site - where the acetyl group is transferred during hydrolysis
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69
Q

in general, what is the result of high concentrations of ChEI in the CNS?

what about the eye? respiratory tract? GI tract? urinary tract?

A

generalized convulsions that can lead to coma and respiratory arrest

eye, respiratory, urinary and GI tract effects are all basically the same as the direct-acting cholinomimetics (this includes both muscarinic and nicotinic agonists). the symptoms are:

  • miosis
  • bronchoconstriction
  • urination
  • GI motility
  • secretion
  • defecation
70
Q

which part of the ANS would ChEIs affect? what would they do?

A

BOTH the sympathetic and parasympathetic NS.

they would increase activity at the ganglia

71
Q

what part of the ANS predominates in the heart? the musculature?

what would be the effect of giving a moderate dose of ChEI to these tissues?

A
  • heart - parasympathetic dominates (moderate dose would reduce heart rate)
  • vasculature - sympathetic dominates because no parasympathetics present (moderate dose causes modest bradycardia and increased vascular tension [therefore increased BP])
72
Q

what are the result of low doses of ChEIs at the skeletal muscles (neuromuscular plate)? what about high doses?

A
  • low - prolonged and intensified actions of ACh (therefore increased strength of contraction [good of myestenia gravis])
  • High - muscle fiber fibrillation (backward firing of APs toward neuron soma)
73
Q

list 5 ChEIs, their duration (in general) and their clinical indications

which can cross the BBB?

A
  1. edrophonium (short acting)
    - diagnosis of myasthenia gravis
    - nondepolarizing reversal of neuromuscular blockade
  2. neostigmine (intermediate acting)
    - myasthenia gravis
    - nondepolarizing reversal of neuromuscular blockade
  3. pyridostigmine (intermediate acting) -myasthenia gravis
    - nondepolarizing reversal of neuromuscular blockade
    - prophalaxis for organophosphate poisoning
  4. physostigmine (intermediate acting, crosses BBB)
    - glaucoma
    - reversal of anticholinergic (antagonists) toxicity
  5. echothiophate (long acting, organophosphate)
    - glaucoma
    - esotropia with accomodative compensation (type of strabsmus where one eye points inward)
74
Q

list 3 pathogenic mechanisms of the autoantibodies in myesthenia gravis.

what are the symptoms of this condition

A
  1. they cross-link nicotinic Ach receptors in the neuromuscular junction causing them to become internalized and degraded
  2. they cause lysis of the post synapse membrane
  3. in also simply binds to and inhibits the nicotinic receptors
    symptoms: ptosis, diplopia, difficulty speaking and swollowing and extremity weakness
75
Q

how can you differentiate whether myesthenia gravis is caused bu the AChR autoantibodies of excessive ChEI?

A

give the patient an IV dose of edrophonium. if it improves muscle strength briefly then its caused by the autoantibodies. it it gets worse than its escessive ChEI

76
Q

aside from acting as a ChEI, what additional action does neostigmine have?

compare and contrase neostigmine with pyridostigmine

A

it also acts as a direct nicotinic agonist

pyridostigmine is an analog of neostigmine and it has:

  • slower onset of action
  • longer duration of action (therefore drug of choice for myesthenia gravis)
  • it also has off label use as an organophosphate prophylactic
77
Q

what are the side effects of ChEIs?

A

muscarinic side effects predominate initially (cognative disturbances, convulsions, coma)

these are followed by nicotinic side effects (depolarizing neuromuscular blockade)

78
Q

list 3 ways people can get cholinergic poisoning

A
  1. some commonly used insecticides are ChEIs
  2. wild mushrooms
  3. chemical warefare (organophosphates) - sarin, VX, soman
79
Q

how do you treat the muscarinic effects of cholinergic poisoning? nicotinic effects?

A

Muscarinic effects - 3 ways
1. atrophine - a tertiary (can cross BBB) amine drug that can treat the CNS effects as well as the organophosphate effects

  1. pralidoxime - has quaternary group (cant cross BBB) therefore cant treat organophosphates
  2. pretreatment with pyridostigmine - to prevent the irreversible organophosphate inhibitor
80
Q

Apply 3 neurotransmitters of the ANS and 5 adrenergic receptors upon which they act to a to a clinically-relevant case scenario.

also list the secondary messenger for each receptor

A

ANS NTs

  1. ACh (not adrenergic)
  2. epinephrine
  3. norepinephrine

adrenergic receptors

  1. alpha-1 (Gq, Gi and Go)
  2. alpha-2 (Gi and Go)
  3. beta-1 (Gs)
  4. beta-2 (Gs)
  5. beta-3 (Gs)
81
Q

Apply the correct adrenergic receptor subtypes to the heart, blood vessels, and lung to a clinically-relevant case scenario.

A

heart - β1, (a1)

blood vessels - a1, (a2)

lungs - β2

ones in ( ) are less important

82
Q

what is the main adrenergic receptor of the heart? what is the effect of its activation on:

  1. SA node
  2. AV node
  3. myocardium
A

β1

  1. SA node - increases heart rate
  2. AV node - increased conduction velocity
  3. myocardium - increased force of contraction

together, these all increase blood pressure

83
Q

by what molecular action do beta adrenergic cause their action?

A
  1. beta agonist binds beta receptor
  2. Gs G-protein is released and it exchanges it GDP for GTP (thus activating it)
  3. Gs activates adenyl cyclase
  4. adenyl cyclase converts ATP to cAMP
  5. cAMP activates a protein kinase
  6. the active protein kinase activates an inwardly rectifying Ca++ channel
84
Q

what effect would a calcium channel blocker have on beta-1 receptors?

A

it would be inhibitory to beta-1 activity and since beta-1 is primarily found on the heart it would act as an anti-hypertensive

85
Q

what is the main adrenergic receptor of the lungs? what is the effect of its activation?@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2

A

β2

β2 receptors on bronchial smooth muscle of the lung results in dialation (therefore selective β2 antagonists are used to alleviate asthma)

86
Q

Apply 3 β1 selective antagonists and the populations they are the preferred drug for to a clinically-relevant case scenario.@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@

A
  1. metoprolol
  2. atenolol
  3. nebivolol

these are prefered (over non-selective blockers) in patients with diabetes and asthma

87
Q

Apply the effect of alpha1-receptor antagonists on vascular smooth muscle to a clinically-relevant case scenario.

A

binding of an agonist to an alpha-1 receptor on vascular smooth muscle causes it to contract. this means that an ANTAGONIST to alpha 1 would cause vasodialation (and therefore lower blood pressure)

88
Q

Apply the action of alpha1 antagonists in the prostate to a clinically-relevant case scenario.

A

the action of alpha1 receptors is to contract smooth muscle, particularly in the prostate and urethra therefore an alpha1 ANTAGONIST will cause them to relax thus alleviating benign prostate hypreplasia

89
Q

Contrast the anti-hypertensive mechanism of alpha1 versus alpha2 antagonists.

list 2 alpha-2 agonists. what are they used for?

A

alpha 2 can act as an autoreceptor and therefore lower blood pressure (vasodialation)

alpha 1 can increased blood pressure by vasoconstriction of the blood vessels

  1. clonidine
  2. guanabenz (not really used anymore)
    these both use the autoreceptor action of alpha2 to treat hypertension (decreases rate, tone and contractility)
90
Q

what receptors does epinephrine have the highest affinity for?

what does it do?

A

higher with beta receptors (especially beta 2) compared with alpha

increases heart rate and contraction force

  • therefore increasing blood flow to muscles
  • also dilates airways
91
Q

what receptors does norepinephrine have the highest affinity for?

what does it do?

A

higher with alpha receptors than beta

it increases peripheral vascular resistance (via vasoconstriction) and increases contractile force of the heart

92
Q

what G-protein are all the beta receptors couples with? what does it do?

A

Gs - increases cAMP (cellular response depends on the tissue)

93
Q

list the general response of agonist stimulation for:

  1. beta 1
  2. beta 2
A
  1. beta 1 - increased cardiac contractile force and increased heart rate
  2. beta 2 - increased bronchial smooth muscle relaxation
94
Q

in general, where would you find the following receptors expressed:

  1. beta 1
  2. beta 2
  3. beta 3
A
  1. beta 1 - heart and kidneys
  2. beta 2 - smooth muscle (including bronchioles), liver and skeletal muscles
  3. beta 3 - adipose tissue
95
Q

list 4 conditions that can be pharmacologically managed with beta receptors

A
  1. asthma
  2. cardiac arrhythmia
  3. angina
  4. COPD
96
Q

for the following dopamine receptors list which G-protein they are coupled with and their effects:

  1. D1
  2. D2
  3. D3
  4. D4
  5. D5
A
  1. D1 - Gs (increase cAMP)
  2. D2 - Gi (decrease cAMP, increase K conductance, decrease Ca influx)
  3. D3 - Gi (decrease cAMP, increase K conductance, decrease Ca influx)
  4. D4 - Gi (decrease cAMP, increase K conductance, decrease Ca influx)
  5. D5 - Gs (increased cAMP)
97
Q

what tissues would you normally find D1 receptors in? what do they do? list a partial agonist for D1.

A

kidneys, mesentery and coronary arteries.

they cause vasodialation (SM relaxation)

fenoldopam

98
Q

list 3 conditions that dopamine receptors are pharmacologicallyy able to treat

A
  1. parkenson’s disease
  2. schizophrenia
  3. shock (caused by low cardiac output)
99
Q

what does activation of beta 1 receptors on the AV and SA node do?

A

stimulation increases the rate and contractile force of the heart

100
Q

list 2 partial non-selective beta antagonistss.

what are they used to treat?

what are the advantages of using these drugs?@@@@@@@@@@(the notes use the words antagonist AND agonists, look up)

A
  1. pindolol
  2. acebutolol
    (equal affinity with B1 and B2)

hypertension and angina

less increase in heart rate, blood pressure and abnormalities in plasma lipids compared with ordinary antagonists

101
Q

list a partial agonist that is selective of beta 1 over beta 2

what are they used to treat?

what are the advantages of using these drugs?@@@@@@@@@@(the notes use the words antagonist AND agonists, look up)

A

acebutolol

hypertension

-produces less bradycardia

102
Q

what is the molecular cascade produced from the activation of an alpha 1 receptor?

A

activates Gq G-protein –> stimulates phospholipase C (PLC) –> PLC cleaves PIP2 to DAG and IP3 –> IP3 causes release of intracellular stores of Ca, DAG activates PKC which phosphorilates target proteins

MAP kinase also gets activated in there somewhere

103
Q

where are alpha 1 receptors expressed?

A

on the post-synaptic terminals in:

  • vascular smooth muscles
  • genitourinary tract smooth muscles
  • prostate
  • heart
  • liver
104
Q

what is the molecular cascade produced from the activation of an alpha 2 receptor?

A

activates Gi G-protein –> inhibits adenyl cyclase –> decreases the amount of cAMP

some also activate inward rectifying K channels and neuronal Ca channels

105
Q

where are alpha 1 receptors expressed?

A

they are epsressed at both:

  • pre-synaptic terminals (auto receptors [regulatory]) AND
  • post-synaptic membranes
106
Q

for the following alpha antagonists, list their indication and specific selectivity (if applicable):

  1. prazosin
  2. terazosin
  3. doxazosin
  4. tamsulosin
A
  1. prazosin - hypertension, dialates both arteries and veins without causing tachycardia (highly selective for alpha1)
  2. terazosin - hypertension and urinary compliations from benign prostatic hyperplasia (alpha 1 selective antagonist)
  3. doxazosin - hyper tension adn BPH, longer half-life than the others
  4. tamsulosin - BPH but causes less orthostatic hypotension than others (selective for a1A and a1D)
107
Q

list 2 mixed alpha-beta antagonists, their indications and their selectivity

list any possible complications with these drugs

A
  1. carvedilol - treats chronic heart failure with decreased systolic function [by inhibiting mitogenesis in vascular smooth muscles and the formation of injurious foam cells] (more potent at beta receptors than alpha)
    - (r)-form has increased drug interaction potential
  2. labetalol - treatment for hypertensive emergencies, like pregnancy induced ones (slightly more selective for alpha1)
    - may induce hepatitis
108
Q

Draw 4 types of ion channels and three receptors and explain how they affect ion influx and interact.

A
  1. voltage gated
  2. ligand gated
  3. membrane delimited metababotrophic (directly activated by cytosolic G-protein)
  4. diffusable second messenger metabotrophic (activated bu a cytosolic secondary messenger)
109
Q

Apply the 4 listed ion channel (differentiated by activation style/ligand) blockers to a clinically-based scenario (what blocks them)

A
  1. voltage gated Na channel - blocked by/antagonized by tetrodotoxin
  2. nicotinic ACh receptor (Na influx?) - alpha-bungarotoxin (from marine snake)
  3. GABAa receptor (conducts Cl) - picrotoxin (south pacific plant)
  4. glycine receptor (conducts Cl) - strychnine (indian plant)
110
Q

list the ligand for for following receptors:

  1. AMPA
  2. NMDA
A
  1. AMPA - glutamate (cation conductance)
  2. NMDA - also glutamate (Ca conductance)

one neurotransmitter can have multiple receptor types

111
Q

list 4 drugs that are inhibitory to GABAa receptors

A
  1. benzodiazepines
  2. flumazenil
  3. zolpidem
  4. barbituates (a sedative)
112
Q

what is the most abundant neurotransmitter in the brain?

A

glutamate

113
Q

what is a new clinical use for ketamine?

A

its testing well as a rapidly acting antidepressant

114
Q

List a nucleus producing norepinephrine.

list the projection sites of NE (3 primary and 4 minor)

A

mostly the locus caeruleus (also a bunnch of nuclei called “A” something)

projection sites:

  1. hypothalamus (paraventricular)
  2. cortex
  3. subiculum (part of the hippocampus)
  4. (olfactory bulb)
  5. (thalamus)
  6. (amygdala)
  7. (midbrain central gray)
115
Q

Apply the order of metabolism of the three catecholamines to a clinically-relevant scenario.

A

tyrosine –> DOPA –> dopamine –> NE –> Epi

116
Q

Apply one drug of abuse acting on norepinephrine systems to a clinically-relevant scenario.

A

cocaine - blocks NE reuptake causing an increased concentration of NE in the synapse

117
Q

list 3 SNRIs, what they are indicated for and how they work

A
  1. desipramine
  2. maprotyline
  3. protryptiline

they are all anti-depressants

they are selective NE reuptake inhibitors (AKA tricyclic antidepressandt).

118
Q

Apply the three dopaminergic pathways and one associated pathology or physiological role for each to a clinically-relevant scenario.

A
  1. Nigrostriatal pathway (dies off in parkinsons disease)
  2. mesolimbic pathway (the reward pathway, related to psychosis)
  3. tuberoinfundibular pathway (regulates prolactin release for anterior pituitary [inhibits it])
119
Q

Apply the precursor of dopamine used for Parkinson’s disease and the enzyme inhibitor that is often combined with it in a single pill to a clinically-relevant scenario.

A

L-DOPA is the precursor for dopamine

Sinmet is a combination drug that contains levodope (L-DOPA) and CARBIDOPA (which is a DOPA carboxylase inhibitor used to inhibit L-DOPAs metabilization so it has time to reach the domenergic receptors (where it gets converted to dopamine)

120
Q

Apply 4 anti-psychotics agent and the receptor it acts on to a clinically-relevant scenario.

A

most anti-psychotics are DA2 antagonists

  1. spiroperidol
  2. pimozide
  3. haloperidol
  4. phenothiazine
121
Q

List the primary nucleus of 5-HT production and 3 sites of projection. Apply the extent of these projections to a clinically-relevant scenario.

A

primary nucleus:
1. raphe magnus

Projection sites:

  1. hypothalamus
  2. cortex
  3. subiculum
122
Q

list the ligand and one of its agonists for the following receptors:

  1. muscarinic receptor
  2. D1 receptor
  3. D2 receptor
  4. GABAa receptor
  5. NMDA receptor
  6. glycine receptor
  7. 5-HT receptor
A
  1. muscarinic receptor - ACh (muscarine)
  2. D1 receptor - dopamine
  3. D2 reeptor - domapine (bromocriptine)
  4. GABAa receptor - GABA (muscimol, barbiturates)
  5. NMDA - glutamate (NMDA)
  6. glycine receptor - glycine (taurine, beta-alanine)
  7. 5-HT receptor - serotonin (LSD)
123
Q

name 2 benzodiazepines

what receptors do these bind to?

A
  1. valium
  2. liprium

GABA agonists (both anti-anxiety drugs)

bind to GABAa receptors

124
Q

list the projection pathways for dopamine in the brain

A
  1. tuberoinfundibular pathway - tuberoinfundibular to the neurohypophysis and median eminence
  2. nigrostriatal pathway - starts at substantia nigra and goes to the caudate nucleus/putamen (thgether they form the dorsal straitum)
  3. mesolimbic pathway - starts at ventral tegmental area (VTA) and the substantia nigra and goes to the nucleus accumbens
125
Q

hoe did the substantia nigra get its name?

A
  • substantia because its large (substantial)

- nigra (black) because when dopamine gets metabolized it turn black

126
Q

what do amphetamines and methamphetamines cause the release of?

A

dopamine

127
Q

list 6 SSRIs

A
  1. fluozetine
  2. escitalopram
  3. fluvoxamine
  4. paroxetine
  5. trazodone
  6. imipramine
128
Q

what is the result of stimulation of a GABA receptor?

A

it hyperpolarizes the cell (therefore acting as a depressant)

129
Q

what receptor do barbiturates bind to? what is the result?

A

GABA receptors, cause increased Cl influx into cell (agonists)

130
Q

what are they 3 major areas of toxicology and 2 specialized areas and what do they entail?

A

MAJOR
1. descriptive tox - tox testing in cells, animals and humans

  1. mechanistic - study of how chemicals cause adverse effects and how the body protects against these effects
  2. regulatory - involves the rules and compliance of use of chemicals (FDA, EPA, OSHA)

SPECIALIZED
1. forensic - use of chemistry and tox for investigations. involves both medical and legal agencies

  1. clinical - the treatment of poisoned patients and the development of new treatments for poisoning
131
Q

what is the best way to distinguish a disease from an adverse effect caused by a drug/toxin?

A

take a history

132
Q

what does a GRADED dose response relationship look at? what about QUANTAL?

A

graded - drug response in an individual

quantal - drug response in a population (most important for toxicology)

133
Q

what would the shape of done-responce curve for a substance that is required for normal physiologic function and survival?

A

it would be a “U” where the two tops of the U are death (one side is sever deficiency and the other overdone) with the middle being the region of homeostasis

134
Q

what is the calculation for the therapeutic index? what about margin of safety?

A

therapeutic index = (TD50 / EF50)

margin of safety = (LD1 / ED99)

135
Q

define to following terms:

  1. toxication

2. detoxication

A
  1. toxication - biotransfermation of molecule to a harmful product
  2. detoxication - biotransformation that causes elimination of the toxin or prevents its formation
136
Q

list the 4 steps for the mechanism of toxicity

A
  1. delivery of the toxin
  2. reaction of toxin with target molecule/biological microenvironment
  3. cellular dysfunction and resultant toxicity
  4. repair (or dysrepair [fibrosis, necrosis, carsinogenesis])
137
Q

what percent of human exposures to toxins is unintentional?

A

80%

138
Q

list 6 strategies for treatment of a poisoned patient

A
  1. clinical stabilization of the patient (make sure they are alive and breathing) [1st priority]
  2. clinical evaluation (history & physical, labs and radiology)
  3. prevention of further toxin absorption
  4. enhancing toxin elimination
  5. administration of antidote
  6. supportive care and clinical follow-up
139
Q

what is the normal anion gap?

what would metabolic acidosis AND a simultaneous elevated anion gap suggest?

A

less than 12

it would suggest toxicity from a limited number of agents (AT MUD PILES):

  • Alcohol
  • Toluene
  • Methanol
  • Uremia
  • Diabetic ketoacidosis
  • Paraldegyde
  • Iron/Isoniazid
  • Lactic acid
  • Ethylene glycol
  • Salicylate
140
Q

what is the osmol gap? what is the normal value?

what does a high osmol gap indicate?

A

the osmol gap is the difference between the measured and calculated serum osmolality

normal is less than 10 mOsm

it indicates the presence of an osmotically active substance present in the serum that is not accounted for by Na, glucose or BUN concentrations

141
Q

what is one of the few toxin related lesions that you can visualize on a CT?

A

CO can cause lesions in the brains consisting of low density areas of the cerebral white matter and basal ganglia

142
Q

what are the 5 pollutants that account for 98% of all air pollution and their respective percentages

A
  1. CO - 52%
  2. sulfur oxides - 14%
  3. nitrogen oxides - 14%
  4. volatile organic compounds - 14%
  5. particulate matter - 4%
143
Q

what are the 2 types of air pollution? give an example of each

A
  1. reducing type - SO2 and smoke from incomplete combustion of coal
  2. oxidizing type - hydrocarbons, nitrogen oxides and photochemical oxidants in areas with bright sunlight
144
Q

by what mechanism is CO toxic (2 ways)?

A
  1. it forms a bond with the Fe in the hemoglobin heme that is much stronger (220X) than than what the oxygen can form therefore hemoglobin cant store and deliver oxygen to tissues as well
  2. it can bind the heme-Fe in any molecule including the cytochromes in respiratory enzymes and the heme in myoglibin which disrupts them as well.
145
Q

list 3 populations/conditions that cause someone to be at increased risk from CO exposure

A
  1. anemic people - since they don’t have as much blood and/or hemoglobin in the first place
  2. increased metabolic rate (children) - they have a higher oxygen demand
  3. fetuses - CO can cross the placenta and damage the brain. particularly at risk from prolonged low level exposure
146
Q

what condition does CO poisoning mimic?

A

hypoxia

147
Q

what is the half-life of CO-Hb association in room air? what about 100% O2? hyperbaric chamber?

A

CO-Hb cannot be excreted without active respiration

  • room air - 320 minutes
  • 100% oxygen - 80 minutes
  • hyperbaric - < 25 minutes
148
Q

what are 4 consequences of prolonged low level exposure to CO

A
  1. a shift from aerobic to anaerobic mechanisms
  2. increased incidence of atherosclerosis
  3. impaired performance on vigilance test
  4. polycythemia (increased number of RBCs)
149
Q

what are the effects of CO on the lungs/airway? what about SO2?

A
  • CO: nothing; its nonirritating, odorless, tasteless and colorless
  • SO2: its a water soluble upper airway irritant that stimulates mucus secretion and bronchoconstriction
150
Q

what population would be particularly at risk from SO2 poisoning?

A

asthmatics because it can can bronchoconstriction

151
Q

what other harmful pollutants can SO2 turn into? what do they do?

A
  1. sulfuric acid (H2SO4)
    - also upper respiratory irritant
    - more bronchoconstriction than SO2.
    - injures phagocytes and causes bronchitis
  2. ammonium sulfate
    - also more bronchoconstriction than SO2
    - associated with increased mortality
152
Q

what triggered the creation of the clean air act in 1970?

A

the donora fog of 1948

153
Q

what are come of the consequences of NO2 inhalation (3)

A
  1. its a deep lung irritant
  2. can produce pulmonary edema in high concentrations
  3. bronchiole inflammation (loss of ciliated cells and secretory granules)
154
Q

what are some sources of NO2 gas (2)

A
  1. liberated from fermenting fresh silage

2. gas stoves in homes

155
Q

how does formaldehyde cause harm? what conditions is it associated with (4)? where might you encounter it?

A

it acts via the sensory fibers in the trigeminal nerve and induces bronchoconstriction through the vagus nerve

associated with:

  • nasopharyngeal cancer
  • leukemia
  • sinonasal cancer
  • a weak allergen

it can be used as a construction material

156
Q

what is pneumoconiosis?

A

a restrictive lung disease caused by inhalation of dust

157
Q

what is silicosis? how long does it take to develop? symptoms?

A

silicosis is disease caused by inhalation of silica (2nd most abundant element)

takes 10 to 25 years to develop (prevalent in gold, iron, coal mining and stonework)

causes shortness of breath and increased risk of infection

158
Q

list the 3 diseases caused by asbestos and what they do

A
  1. asbestosis - causes formation of fibrous pleuritis which causes the pleural membrane to thicken forming a rigid fibrous capsule (causes dyspnea, tachypnea and caugh)
  2. bronchial lung cancer - occurs 2- to 30s after initial exposure
  3. malignant mesothelioma - cancer of the thin cell wall lining the internal organs (25 to 40 years after exposure)
159
Q

list 2 classes of hazardous pesticides

A
  1. organophosphates

2. organochlorine

160
Q

list a hazardous organochlorine. what does it do?

A

chlorophenothane (AKA DDT)

its relatively safe for humans (lipophilic) but it causes thin eggshells in birds

161
Q

list 2 organophosphate pesticides. what do they do? how do you treat poisoning?

A
  1. parathion
  2. malathion

they inhibit cholinesterases through phosphorylation of their esteric site

causes “cholinergic syndrom” (sweating, salavation, bronchiole secretion and constriction, salavation, miosis, increased GI motility, diarrhea, tremors, muscle twitching, and respiratory collapse in sever cases)

treated with atropine IV

162
Q

what are the non-cancerous symptoms of agent orange? what cancers does it cause?

A

non-cancerous: vomiting, burning of the mouth, abdominal pain, hypotension, and potentially coma

cancers: soft-tissue carsinomas, non-hodgkin’s lymphoma, chronic lymphocytic leukemia, hodgkin’s disease and chloacne (not sure if this is cancer)

163
Q

what is paraquat? what does it do?

A

its a toxic herbacide

it basically depletes the amount of radical metabolizing enzymes in the body like:

  • superoxide dismutase
  • peroxynitrite
  • glutathione reductase

symptoms come in 2 stages:
1. loss of alveolar epithelium, alveolar edema (death can occur due to anoxia)

  1. alveolar epithelium tries to repair itself via intensive fibrosis (which can still cause death from loss of lung function)
164
Q

what molecule does capsaicin deplete?

A

neuropeptide P

165
Q

what are ergots? what do they cause?

A

fungal paracites that grow on grain (rye)

cause vasoconstriction in the extremities following by gangrene. can also cause abortion in women

166
Q

what two toxins does the death cap mushroom contain? what do they do?

A
  1. phalloidin - conbines with muscle cell actin to interfere with muscle function (diarrhea)
  2. amatoxins - binds RNA pol II this preventing protein synthesis (liver failure then death)
167
Q

what dangerous chemical is in brachen ferns? what does it do?

A

ptaquiloside

it alkylates adenine and quanines of DNA causing increased incidents of:

  • epithelial tumors
  • bladder tumors
  • esophageal cancer
  • stomach cancer
168
Q

what toxin is in water hemlock? what does it do?

A

cicutoxin

binds GABA-gated CL channels and causes convulsions

169
Q

name 3 non-selective beta-antagonists and 3 beta1 selective antagonists

A

non-selective

  1. propranolol
  2. nadolol
  3. timolol - good for glaucoma?
beta1 selective
1. metoprolol
2. atenolol
3. nebivolol
all these are better for diabetes and asthma patients
170
Q

what does the drug prazosin do?

A

its an alpha 1 antagonist used to treat hypertension. i caused dialation of arteries and veins without causing much tachycardia

171
Q

how does phenoxybenzamine work? what dose it cause?

A

it irreversible blocks alpha1 and 2.

it may increase cardiac output (and reflex tachycardia)

MS1 - Pharmacology (1 decks)

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