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HD&T > Exam 1 study guide for final > Flashcards

Exam 1 study guide for final Flashcards

1
Q 
Which of the following is not a monoamine?
a: serotonin
b : dopamine
c : histamine
d : acetylcholine
A

Acetylcholine

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2
Q

Serotonin

A

-tryptophan comes into the neuron-> tryptophan hydroxalase turns it into 5HTP-> AAD turns it into 5HT (Serotonin)-> VMAT-> into vesicle package-&raquo_space;> gets released to many postsynaptic receptors, 5HT1A postsynaptic autoreceptor, or back in through serotonin transporter where it gets degraded by Monoamine Oxidase into 5 hydroxyacetic acid

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3
Q

Dopamine

A

-Tyrosine is precursos-> tyorsoin hydroxylase turn it into DOPA-> AAD turns that into dopamine-> goes into VMAT-> packaged into vesicle-»> goes to postsynaptic receptor d1-d5, or autoreceptor D2, or back in through dopamine transporter where it is broken down by MO

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4
Q

Histamine

A

-is a monoamine

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5
Q

Acetylcholine

A

-Choline precursor -> choline + acetylcoa-> choline acetyltransferase turns that into Ach-> goes into VAT -> into vesicle package-»> to muscarinic or nicotinic post synap receptor, muscarinic auto receptor , or EXTRANEURONALLY METABOLIZED by ACH-ESTERASE

  • Ach has no ach transporter to get back into neuron
  • Uses VAT (vesicular ach transporter)
  • Is metabolizes extraneuronally.
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6
Q

Severe orthostatic hypotenison is a consequence of which of the following?

a. dopamine beta hydroxylase insufficiency
b. tryptophan hydroxylase insufficiency
c. pheochromocytoma
d. propanolol administration

A

dopamine beta hydroxylase insufficiency

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7
Q

What are monoamines?

A

Catecholamines, serotonin and histamine are monamines

*but serotonin is NOT a catecholamine

**But catecholamines which are monoamines include: DA, NE, Epi

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8
Q

Describe dopamine protocol

A

Tyrosonie -> tyr hydroxylase->DOPA-> AAD-> Dopamine-> packages inside vesicle-> goes through VMAT-> inside vesicle now DA

Could be taken back up via dopamine transporter or binds to post synpatic dopamine receptors/ D2 receptors

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9
Q

Tyrosine hydroxylase

A

turns Tyrosine into DOPA (dopamine precursor)

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10
Q

Tryptophan hydroxylase

A

turns tryptophan to 5HTP (serotonin phosphate)

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11
Q

Serotonin decarboxylase

A

decarboxylizes serotonin

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12
Q

monoamine oxidase

A

the pacman of them all, they degrade dopamine, serotonin, NE,

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13
Q 
A farm work is poisoned by a pesticide and presents in an emergency room with symptoms such as blurred vision, excess salivation, twitiching and decreased heart rate, he or she would most likely be treated with 
an acetylcholiesterase inhibitor
a muscariin antagonist
a sympathomimietic
an acetylcholine transporter inhibitor
A

a muscaranic antagonist

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14
Q

a acetylcholinesterase inhibitor

A

prevents the breakdown of acetylcholine, causing an increase in acetylcholine. This is especially helpful in overriding the stimulation or tubocurare.

Non-depolarizing: Tubocurare - competes with ACh at nicotinic receptors…..
Question….. What is effect of acetylcholinesterase inhibitor (neostigmine, physostigmine)?
(they outcompete the tubocurare so that acetylcholine ends up binding back on its appropriate receptors)

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15
Q

a muscarinic antagonist

A

atropine and scopalamine
does opposite of the muscarics
m one : moan (increase in gastric secretion)
m2 (m and m’s in your heart) decreases heart rate, contractility, heart conduction etc.
M3 : everything else : increases secretions, and Gi sphincters

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16
Q

Sympathomimetic

A

– mimics action of symp nervous system (meth, epinephrine, NE)

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17
Q

Sympatholytic

A

Drugs that block action of something from sympathetic nervous system

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18
Q

Acetylcholine transporter inhibitor

A

Acetylcholine doesnt have its own acetylcholine transporter

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19
Q

Dopamine beta hydroxylase

A

turns dopamine to NE. So without it you don’t get NE. NE causes increase in blood pressure, so without dopamine beta hydroxylase you get severe orthostatic hypotension.

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20
Q

Propanolol

A

class 2 beta blcking drugs. Remember B1 = Bone hitting the heart and the kidney (raises blood pressure and renin release), B2 is expansion (increases secretions, increases camp causing smooth muscle relax, increases blod flow, expand glucagon, and lysis, increases insulin releae, expands uterues to maintain bbaby, expand proteinsecretion)

So if you have a beta blocker you essentially stop all these things from happening. (decreases lipolysis, heart rate, secretions, NE, insulin secretions etc.)

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21
Q

phenoxybenzamine and phentolamine

A

non selective alpha antagonists
Uses of non-selective α antagonists include treatment of pheochromocytoma (rare catecholamine secreting tumor), hypertensive emergencies

Effects:

  • Decreased TPR (α1) and thus decreased BP
  • Increased HR (baroreceptor response to decreased BP)

Side Effects:

Orthostatic hypotension – getting out
Of dental chair

2) Nasal stuffiness- blocking alpha receptors in sinus so no normal vasoconstrction

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22
Q

Select the correct statement

a. preganglionic sympathetic neurons are craniosacral in origin
b. sympathetic preganglionic neurons act upon nicotininc receptors in adrenal medulla
c. motor neurons innervating skeletal muscles act via nicotininc receptors
d. postganglionic symptathic neurons can release dopamine

A

B,C,D

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23
Q

Preganlionic sympathic neurons are craniosacral in origin true or false?

A

FALSE. Preganglionic PARAsympathetics are craniosacral

But preganglionic sympathetics are THORACOLUMBAR T1-L2 in origin.

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24
Q

Sympathetic preganglionic neurons act upon nicotinic receptors in adrenal medulla

A

true. they use nicotinic receptors to bind Ach to.

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25
Q

Motor neurons innervating skeletal muscle act via nicotinic receptors

A

true

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26
Q

Post ganglionic sympathetic neurons innervating sweat glands release what and act via what receptors

A

Ach->muscarinic

*Ach also used for cardiovascular, smooth muscle parasympathetc effects from post ganglionic PARASYMPATHATIC activating muscarinic receptors.

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27
Q

Sympathetic postganliconic neurons can release what?

A

Ach - acts on muscarinic receptors (For sweat glands)
NE- acts on alpha/beta receptors
DA- acts on dopamine receptors

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28
Q

Preganglionic sympathic and parasympathetic fibers release ____, postganglionic sympathetic fibers release ____, (for adrenergic receptors), and postganglionic parasmpathetic fiberes release ____for muscarnic cholinergice receptors

A

ACh
NE
Ach

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29
Q

Bethanechol

A

-is a muscaranic agonist
Being such is activates :
m1 (moan) increases Gi secretions
M2 ( decreases heart rate, conduction, contractility,)
M3 (does everything else parasympathatic-> increases saliva, relaxes sphincters,inc gi motility, releases gas, point (in point and shoot), induces nausea, constricts the lungs)

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30
Q 
Bethanacol administration causes :
increased gastric acid secretion
increased heart rate
urinary retention
dry mouth
A

Increased gastric acid secretion

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31
Q

Muscarinic agonists are_____

antagonists ____?

A

Ach, bethanacol, pilocarpine (A Bench Press HELPS(AGONIST) build Muscles (m for muscarinic)

Atropine, scopalmine,
Atroop of soldiers SCOOPed some icrecream, thats BAD (ANTAGONIST) for their Muscles(muscarinic receptors)

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32
Q

The cardiovascular effects of epinephrine in a person treate with propanolol and prazosin will most likely resemble the response after the admin of

a. pilocarpine
b. phenelephrine
c. clonidine
d. isoprotenerol

A

C

propanolol is a beta blocker

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33
Q

Pilocarpine

A

Pilocarpine is a muscarnic agonist

• Pilocarpine: cholinomimetic-contract ciliary muscle and increases outflow of aqueous humor.

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34
Q

Phenylephrine

A 
Phenylephrine is an alpha 1 agonist
alpha 1 (one alpha fish in tank)
causes: 
vascoconstriction
constricts: blood vessles, sphinctersm GI,GU, Uterus (pushed baby out), shoots (in point and shoot), pupil DILATION by constricting radial muscles

Epi>NE for alpha 1

Antagonist to this is prazosin

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35
Q

Clonidine

A

Alpha 2 agonist
with Guanafacine too
Epi>NE

Alpha with 2 eyes eats all the betas
(so its reverse of the Beta effects):
decreases: lipolysis, insulin release, NE secretion, heart rate, CO, salivary secretion, platelet aggregate

Antag:yohimbe

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36
Q

Isoproteerenol

A

Beta 1 agonist/Beta 2 agonist (nonselective)
EPI=NE

B1:: increases heart rate, CO, contractility, renin release
B2:: Expansion: increases cAMP (smooth muscle relaxed), releaxes and expand bronchioles, increases flow of blood, expand glucagon and glycogenolysis, insulin release increase, expand uterus to help lady maintain baby, expands protein secretion.

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37
Q

Beta 2 specific drugs

A

albuterol

terbutaline

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38
Q

Beta blockers always end with

A

-olol

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39
Q

Which is the most likely used to treat asthma

a. epinephrine
b. albuterol
c. phentolamine
d. atenolol

A

b

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40
Q

Epinephrine

A

stimulates both the alpha and beta receptors. Greater affect on B2 than NE though.

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41
Q

Albuterol

A

B2 agonist, will relax smooth muscle and bronchiole and lungs. Great for chronic asthma

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42
Q

Phentolamine

A

phentolamine /phenoxybenzamine (α1 and 2- nonselective)

therefore:
constrcts radial eye muscles- pupil dilation
constricts blood vessel, sphingters, GI/GU, uterus, shoots

Decreases:::lipolysis, insulin release, NE secretion, heart rate, CO, salivary secretion, platelet aggregate

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43
Q

atenolol

A

B1 antagonist only
B1 = Bone

decreases heart rate, decreases renin release
decreases contractility and conduction

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44
Q

Most effective decogenestant is which

a. alpha 1 agonist
b. alpha 1 antagonist
c. beta 1 agonst
d. muscarinic agonist

A

a

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45
Q

Alpha 1 agonist

A

Constricts everything. Because of this its great for decongestants. Because we get runny noses, this will CONSTRICT those channels causing the runny nose to stop

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46
Q

Alpha 1 antagonist

A

causes a dilation of things
like
:blood vessels, sphincters, GI/GU, uterues, pupil constrictio instead of dilation

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47
Q

Beta 1 agonist

A

Increases heart rate and renin release

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48
Q

Muscarinic agonist

A

will be used for
m1 = moan :: increase gastric secretions
m2 = m&m in hearts= decreased heart rate, contractility and CO.
m3= everything else parasymp:: releases gas, increases GI motility, relax sphincters, releaxes urethra, vascular smooth muscle relax, increases saliva, point in point and shoot, constricts lungs, induces nausea

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49
Q

Which of the following are most likely to be used by an opthamologist for a retinal exam

a. a beta 1 agonist or a muscarinic agonist
b. an alpha 1 antagonist or a muscarinic agonist
c. an alpha 1 agonist or a muscrainic agonist
d. an alpha 1 agonist or a muscarinic antagonist

A

d

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50
Q

An alpha 1 agonist or muscarnic antagoist via opthamologist?

A

If you use a alpha 1 agonist you are going to start stimulating more alpha 1 that gives constriciton.
Remember the alpha 1 fish

he has 1 eye. That eye gets dilated
why though? It’s because his radial eye muscles get CONSTRICTED

If you use a muscarninc antagonist you will not get a more parasympthatic response but a more sympathetic one like the eye dilation

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51
Q

beta 1 agonist or muscarinic antagonist via opthamologist?

A

sure the muscarinic antagonist will cause less parasymp and more symp leading to pupil dilation due to constriction of radial eye muscles

but the beta 1 agonist is focused more on the heart so itsnot used by opthamologist

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52
Q

alpha 1 agonist or muscarinic agonist via opthamologist?

A

Alpha 1 agonist yes, the radial eye muscle gets constricted and that leads to pupil dilation. Which is done by eye doctor.

Muscarinic agonist is a no though. Its more parasympathetic and would cause pupil constriction, not likly used by eye doctor (they need to see you pupil dilated to dx)

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53
Q

Which antiseizure drug if FDA APPROVED as a monotherapy for generalized tonic clonic seizures, but also has indication for uncomplicated absence seizures, atypical absence seizures, simple and complex partial seizures?

a. ethosuximide
b. perampanel
c. carbamezepine
d. valproic acid

A

d

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54
Q

Valproic acid

A

used for partial, generalized and abscence seizures.

causes weight gain, reye likesyndomre, contraindicated in hepatic disease,

Reduced NMDA glutamtate channels
Increases GABA

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55
Q

Ethosuximide

A

Used ONLY for ABSCENE seizures

Blocks t type calcium channel currents in thalmic pacemaker neurons to quiet ryhmic discharges

anorexia side effect

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56
Q

Perampanel

A

3rd gen ASD anti seizure drug

has less drug interaction and side affects

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57
Q

Carbamezepine

A

used for all partial seizures, and ONLY tonic clonic generalized seizures

Can cause steven johnsons syndrome

Great drug for partial epilepsy but potential for drug-drug interactions is high.

: similar to phenytoin, blocks use-dependent voltage-gated Na+ channels to inhibit repetitive firing in neurons.

*Grapefruit inhibits metabolism of carbamezpine, so if you eat alot of that you can get toxic levels
CBZ plasma levels increased (CYP3A4 inhibition of ASD metabolism in gut / liver) if patients consumes GFJ while on CBZ

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58
Q

Steven johnson syndrome

A

milder form of toxic epidermal necrolysis (TEN)

MOST AT RISK PATIENTS: slow acetylators,- chinese, immunocompromised,

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59
Q

This type of seizure is characteized by a localized focus, minimal spread, a short duration, and mintenance of normal awareness, consciousness, and memory of the seizure event by patient

a. complex partial
b. generalized abscence
c. generalzied tonic clonic
d. simple partial

A

D

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60
Q

Simple partial seizure

A

Localized focus
minimal spread- but can spread over time/stays in one cortex

NORMAL memory, awarness, and consciousness throught
short duration

Lose any of these normalities and you get a complex partial!

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61
Q

Complex partial

A

localized onset, spread bilaterally

involves limbic system

*awarenss, memory, or consciounsess are LOST DURING SEIZURE

semi long duration 15sec-3min

Presence of aura (dejavu)

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62
Q

Generalized absence

A

usually detected by teachers
brief, looks to b daydreaiming

simultaneous genearlized bilat seizure activity

involves loss of awarness or lack of responsiveness

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63
Q

Generalized tonic clonics

A

simult. bilat corticol seizure activity, tonus and clnus jerking of limb phase

duration of greater than 5 minutes is defined as status epilepticus

loss of awarness or responsiveness during this

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64
Q

Status epilepticus

A

(SE) is an epileptic seizure of greater than five minutes or more than one seizure within a five-minute period without the person returning to normal between them

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65
Q

Which of the following drugs is LEAST likely to be persribed to tx symptoms of parkinsons?

a. Ldopa+carbidopa
b. Slegiline
c. Haloperidol
d. Pramipexole

A

C

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66
Q

Haloperidol

tx’s parkinsons (no DOPamine in the park)

A

antipsychotic - butyrophenones (Haloperidol-causes tardive dyskinesias)->more d1 action
-high extrapyramidal side effects, TD dykensia, lack anticholinergic action and assoc side effects

Blocks D2 receptors leaving more dopamine out to flow.

BUT LEAST LIKELY USED TO TX PARKINSONS BECAUSE IT CAUSED TARDRIVE DYKENISIA

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67
Q

Selegiline

A

MAO inhibitor (blocks dopamine metabolism in brain)

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68
Q

Pramipexole

A

D2 agonist

Well in parkinsons you have a lack of dopamine, so obviously a D2 agonist is needed to promote more dopamine activity. Pramipexole is your guy. For bradykinesia and rigidity

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69
Q

Ldopa

A

used for parkinsons disease,crosses BBB and turns into dopamine later (which is what parkinsons lack)

can be used with entacapone, carbidopa, benztropine

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70
Q

Carbidopa

A

for parkinson

drug that inhibits L-dopa metabolism and allows it to get into brain and become dopamine

eventually the area where dopamine conversion takes place will be gone and L-dopa will have no affect

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71
Q

Which of the following processes is LEAST LIKELY to cause a degenerative CNS disorder?

a. enhanced GABA receptor activity
b. enhanced NMDA receptor activity
c. Abnormal intracellular protein aggregation
d. exceesive calcium influxes into neuron

A

a

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72
Q

Enhanced GABA receptor activity

A

Gaba is excitatory, stimulation, too much of this wont lead to a degn cns disease most likely

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73
Q

Excessive calcium influxes into neuron

A

Metabolic and Electrolyte Imbalance
Low (less often, high) blood glucose, Low sodium, Low calcium, Low magnesium

leads to degen disease common seizure precipitant

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74
Q

Enhanced NMDA receptor activity

A

leads to degen disease huningtons

Pathophysiology (striatal cell bodies affected—AMPA/NMDA glutamate systems)-> caudate is destroyed because of the overexcitation of the ampa/nmda receptors due to Huntington gene in gaba neurons (feedback issue and at the end of the day gaba is wiped “we aren’t getting anything from gaba so lets turn up glutamate even more”

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75
Q

Abnormal intracellular protein aggregation

A

leads to degen disease alzheimers

(plaque/tangels accumulate in brain and kill brain cells)

b. Early stage: lose short term memory and skill sets
c. Moderate stage: problem functioning, routine is disrupted. Hard time getting dressed.
d. Late stage: less movement, stops eating, no judgement can run own life.

• Histological effects (e.g., amyloid precursor protein [APP] to beta amyloid plaques-senile plaques; neurofibrillary tangles-tau protein)

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76
Q

This antiseizure drug is associated with a non dose dependet risk of gingival hyperplasia as an adverse side effect and it has been demonstrated to have azero order kinetics at higher doses.

a. carbamezpine
b. phenytoin
c. tiagabine
d. ethosuximid

A

B

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77
Q

Phenytoin

A

Phenytoin
Zero order kinetics
Hirsutisum
Gingival HYPERPLASIA

As you give phenytoin it overcomes the metabolic enzymes in liver(shutting down its own) so increase in dose you get upshoot In serum concetration potentially reaching highly toxic levels.

Gotta see how indiv patients react to the drug

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78
Q

Tiagabine

A
  • Fewer drug interactions
  • Less complex pharmacokinetics
  • Much more expensive

Newer drug

79
Q

Ethosuximide

A

Only used for absence seizure

  • Slow clearance (T1/2 often >12 hours) 􏰅 Complex pharmacokinetics
  • Side effects very common
  • Drug interactions very common
80
Q

Which of the following is NOT a generalized seizure

a. Tonic clonic sizure grnad mal
b. absence seizure petit mal
c. complex partial seizure
d. myclonic seizure

A

C

81
Q

Tonic clonic seizure grand mal

A

Grand mal tonic clonic -> tonus then clonus jerking

generalized seizure

82
Q

Absence seizure petit mal

A

Petitt mal – absence (involve whole brain)

All involve loss of awareness or lack of responsiveness:

Happens in children , dx by school teachers
Brief
Looks lke daydreaming

83
Q

Complex partial seizure

A

Complex Partial – whole brain

Awareness, memory, and/or consciousness are lost during seizure.

partial seizure NOT a generalized seizure

84
Q

Myoclonic seizure

A

Myoclonic “Jerking” seizures
Symptom of a number of other non-epileptic conditions and toxicities
If confirmed with EEG, always treat primary seizure phenotype.

generalized seizure

85
Q

Which of the following is NOT a common seizure precipitant

a. sedative or ethanol withdrawl
b. metabolic or electrolyte imbalance
c. sleep
d. concussion and or head injury

A

sleep

*but sleep deprivation does start it

86
Q

Common seizure precipitants

A

Metabolic and/or
Electrolyte Imbalance

Stimulant or other pro-

convulsant intoxication

Sedative or ethanol withdrawal

Sleep deprivation

Reduction or inadequate

ASD treatment

Hormonal variations

Stress

Fever or systemic infection

Concussion and/or closed head injury

87
Q

This type of seizure has a sudden onset cessation and is characterized by a loss of attention, vacant stare, and blinking or rolling eyes in the patient during the seizure. It is most often first reported in children by their teachers. The patient will have impaired awareness and no memory of the event afterward. Duringthis seizure the patients EEG has a characteristic 3hz generalzied spike wave discharge pattern, MOST LIKELY representing simultaneous bilateral abnormal seizure activity involving borth cortex and thalamus

a. simple partial
b. complex partial
c. generalized absence
d. generalized tonic clonic

A

c

88
Q

simple partial

A

Localized focus

Minimal spread- can over time, but typically stays in one cortex

Normal awareness, memory, and consciousness throughout seizure.

89
Q

complex partial

A

Awareness, memory, and/or consciousness ARE LOST during seizure.

90
Q

generalized absence

A

Happens in children ,

dx by school teachers
Brief
Looks like daydreaming

All involve loss of awareness or lack of responsiveness:

91
Q

Generalized Tonic Clonic Seizure

A

Complete simulatenous bilateral
Prolonged posttical period

> 5 minutes is defined as status epilepticus

92
Q

Which of the following disorders is MOST LIKELEY to be associated with excessive dopamine and diminished GABA activity in the striatum?

a. multiple sclerosis
b. hunintos disease
c. bipolar disorder
d. major anxiety disorder

A

B

93
Q

Multiple scleroris

A

lesion of brain

94
Q

Huntingtons disease

A

Pathophysiology (striatal cell bodies affected—AMPA/NMDA glutamate systems)-> caudate is destroyed because of the overexcitation of the ampa/nmda receptors due to Huntington gene in gaba neurons (feedback issue and at the end of the day gaba is wiped “we aren’t getting anything from gaba so lets turn up glutamate even more”

  • affects GABA and cholinergic striatal cells- there is decreased GABA in cell bodies.
  • excessive dopamine activity
95
Q

Bipolar disorder

A

(2) Bipolar (manic/Depressive)
• Types (know symptoms and treatment approaches)
-cyclothymic-mild type) -> cyclothmia mood swings
-Major manic/depressive- > episodes of grandiosity (cant sleep, unrealistic, lost for days, looks schizo)

• Medications (know properties, side effects and uses)
(a) Lithium carbonate

96
Q

lithium carbonate

A

slow onset, likely work by altering 2nd messenger systems such as those involving adenylyl cyclase and g proteins. Combined with antidepressents, still potent, but MANY side effects
side effects: req monitor blood flow-narrow therapeutic window, tremors, potential kidney damage, edema, weight gain of 40-05lb

97
Q

Major anxiety disorder

A

Anxiety: self defense mechanism, about fight or lfight activation of sympathetic nervous system.

  • Mediated by adrenal glands and steroids
  • > increase in sympathetic nervous system, adrenaline etc.
  • > In excess: its out of proportion, feel anxious all the time, debilitating,

Types:
Chronic mild anxiety: constant or ffrequent time of irrtation, don’t have patience, distracted,
->linked to environments
-> distinct cause
-> no drugs, tx via relaxion, trips, let system get back into balance and subside

Chronic moderalte severe:
-> tricks of relaxation according to DMSV if anxeiety persists for longer than 6 months while there is coming and going its there and its connected with genetics
-> no obvious stressor : ppl wake up and feel anxious
Drugs:
Anxiolytics-> or sedatives , some have depressent effect in higher doses put you into sleep.
Psycho therapy neded-> relaxation, exercise, engage in fun stuff

98
Q

Which of the following is NOT ASSOCIATED with Alzheimers disease?

a. abrnomal amyloid precursor protein
b. beta amyloid plaques
c. neurofribrillary tangles
d. alpha synucleain lewy bodies

A

d

99
Q

Abnormal amyloid precursor protein

A

AAP
• Anatomical effects (hippocampus, cortex, nucleus basalis-site of cholinergic neurons→ these areas are getting destroyed due to plaque/tangles)
• Histological effects (e.g., amyloid precursor protein [APP] to beta amyloid plaques-senile plaques; neurofibrillary tangles-tau protein), causes and consequences

Causes Alzheiemers..kills brain cells.

100
Q

Beta amyloid plaques

A

C. Alzheimer’s disease (plaque/tangels accumulate in brain and kill brain cells)

AAP become beta amyloid.

101
Q

Neurofib tangles

A

cause damage to brain cells - Alzheimers

102
Q

Which of the following psychiatric conditions is LEAST LIKELY to have a significant impact on dental care/managment

a. Schizophrenia
b. bipolar disorder
c. cyclothymia
d. autism spectrum disorder

A

c

103
Q

Schizophrenia

A
  1. Clinical -symptoms and manifestations- most commonly known and appreciated of the psycho disorders, (not hard to recognize, they don’t sort out reality really well, cause of mental illness)
104
Q

bipolar disorder

A

Bipolars are manics and depressives
Cyclothymia: not treated with meds, kinda gloomy, in dysthmic phase sometimes or mania. Not always a bad thing
Bipolars have major depressive disorders associated. Spend 70% of time in depressive side.

105
Q

Cyclothymia

A

Cyclothymia
Go between dythymia and minor stage of manica. Minor bipolar. They have DSMV if longer than 2 years
No gender bias
No drugs needed
Very productive though. (Thomas Edison was good in manic part)

106
Q

Autism spectrum disorder

A

autistic children and people have a hard time keeping up with dental hygiene typically

107
Q

A patient experiencing major psychosis caused by an automobile accident is MOST LIKELY to be classified in which of the following psychiatric dimensional axis?

a. axis 1
b. axis 2
c. axis 3
d. axis 4

A

Axis III: General medical condition;
acute medical conditions and
PHYSICAL disorders

108
Q

Axis 1

A

Axis I: All psychological diagnostic
categories except mental retardation and
personality disorder

Common Axis I disorders include depression, anxiety disorders, bipolar disorder, ADHD, autism spectrum disorders, anorexia nervosa, bulimia nervosa, schizophrenia and drug dependence

109
Q

Axis 2

A

Axis II: Personality disorders and mental retardation

Common Axis II disorders include personality disorders/mental retardation: paranoid personality disorder, schizoid personality disorder, antisocial personality disorder

110
Q

Axis 3

A

Axis III: General medical condition;
acute medical conditions and
physical disorders

Common Axis III disorders include brain injuries and other medical/physical disorders which may aggravate existing diseases or present symptoms similar to other disorders, (sometimes drug
abuse?).

111
Q

Axis 4

A

Axis IV: Psychosocial and environmental factors contributing to the disorder (e.g. stress)

112
Q

Which of the follwing combinations of symptoms has the best prognosis for schizophrenia?

a. male : dx at 20 years of age, father with a history of schizo has anegative symptoms
b. female: dx at 20 years of age, mother with history of schizo, has negative sympt
c. male dx at 30 yrs, neither parent has history of schizo, has positive symptoms
d. female dx at 30 years, neither parent has history of schizo, has positive symptoms

A

D

113
Q

. female dx at 30 years, neither parent has history of schizo, has positive symptoms

A

Best prognosis: temporary and is cause related (Something triggered it) principly positive symptoms.
Later the onset better the prognosis, and if female or no fam history that’s a good sign.
No organic measure, but some things are hints.

more time spent in residual state is bad!

114
Q

a. male : dx at 20 years of age, father with a history of schizo has anegative symptoms
b. female: dx at 20 years of age, mother with history of schizo, has negative sympt
c. male dx at 30 yrs, neither parent has history of schizo, has positive symptoms

A

a : male so worst prognosis
b female so thats good..but has a family history so thats bad
c : male so worst prognosis

115
Q

Parkinsons disease

drug used to help/description

A 
entacapone - COMT inhibitor
Blocks COMT (catechol o methy transferase).

COMT will typically break down dopamine precursor L-dopa, so its an inhibitor of COMT to prevent that from happening since low dopamine is apparent.s given with levodopa/carbidopa to treat symptoms of Parkinson’s disease, such as tremors, stiffness, slow movement, and problems with balance.

116
Q

Schizophrenia

drug used to help/description

A
  • **Chlorpromazine - phenothiazine (D2 antagonist)
  • typical antipsychotic, blocks D2 receptors
  • you block dopamine activity/anticholinergic action

***Clozapine - Atypical D2 and 5HT2A antagonist

  • atypical antipsychotics, D2 antagonism AND 5HT2A antagonism
  • you block dopamine activity, and dopamine synthesis
  • most effective against negative symptoms, can cause serious agranulocytosis wiping out blood cells
117
Q

Bulimia

drug used to help/description

A

Fluoxetine (Prozac)
SSRI drug

  • Monoamine(catecholamine) uptake BLOCKERS
  • depression in adolescents, no anticholinergic activity, minmal withdrawl, wide margin of safety / would get rid of ropey saliva.
  • SSRI
  • SSRIs are believed to increase the extracellular level of the neurotransmitter serotonin by limiting its reabsorption into the presynaptic cell, increasing the level of serotonin in the synaptic cleft available to bind to the postsynaptic receptor.
118
Q

MS

drug used to help/description

A

Prednisone

antiinflammatory steroids

no cure for MS so you use steroids to treat symptoms

119
Q

Bipolar mania

drug used to help/description

A

*Carbamezepine - antiseizure med

  • similar to phenytoin, blocks use-dependent voltage-gated Na+ channels to inhibit repetitive firing in neurons.
  • Stevens-Johnson syndrome, grapefruit inhibits metabolism of drug causing toxicity

*Lithimum carbonate- element that alters g proteins

  • alters 2nd messenger systems, potent
  • slow onset, combine with antidepressent, a ton of side affects->can cause like parkinsons tremor
  • req watch blood flow like a hawk, narrow therapeutic window, weight gain of 100lbs! Edema, kidney disease,
120
Q

Severe anxiety

drug used to help/description

A

bupropion (buspar) - non addiciting subsitute for sedatives
-short term use, for everyday anxiety, very expensive

Alprazolam (Xanax) -agonsit at benzodiazepine receptor

  • agonist of BDZ receptors stimulate pro gaba A
  • little effect on respiraton, most popular CNS depressant, anxiolytic, treate seizure, alcohol withdrawl, insomnia, muscle relaxation
  • you stimulate gaba helping you relax
121
Q

ADHD

drug used to help/description

A

Modafinil -DAT or NET blocker but mostly a NON stimulant

inhibits reuptake of DA so is a way

122
Q

Alzheimers

drug used to help/description

A

Donepezil - cholinesterase inhibitor
keeps the Ach from being degraded because its helps activate neurons since afterall those are being destroyed.

123
Q

Sertraline

A
  • Monoamine(catecholamine) uptake BLOCKERS
  • for major depression
  • ssri
  • depression in adolescents, no anticholinergic activity, minmal withdrawl, wide margin of safety
  • mood stabilizer
124
Q

Benztropine

A

For parkinson

  • Anticholinergic drug. Used to stop drooling. Like atropine (but ‘nicer’)
  • Because dopamine is lacking, there is most aCH action to compensate (reciprical relationship)-> causes siallorhea (drooling), hence an anticholinergic is used
125
Q

Ibuprofen

A

• COX-1 inhibitor (salicylates, ibuprofen-types are non-selective)-blocks production of prostaglandins

  • side effects:- Reduce gastric mucosal protective barrier
    - Compromise renal function
    - Interfere with platelet aggregation
    - Reduce vasoconstriction
  1. Ibuprofen-type NSAIDs
    • Somewhat more COX 2 than COX 1
    • Plateau for analgesia=400 mg
    • Plateau for antiinflammation= 800 mg
    • Mild to moderate pain relief—somewhat more effective than salicylates
    • Warning for cardiovascular side effects
    • Other related NSAIDs:
    -ketoprofen (same properties, but more potent; 50 mg is recommended analgesic dose)
    -naprosyn (Naproxen or Alleve)- longer lasting and slower acting
126
Q

Vitamins OTC

A

a vitamin

127
Q

Aspirin (Anacin)

A
  1. Salicylates
    • Plateau for analgesia= 600mg
    • Plateau for anti-inflammatory= 1 gm
    • Effective against mild to moderate pain
    • Often combined with acetaminophen, opioid analgesics and or caffeine
    • Anticlotting is due to acetylation of platelets, effect lasts up to 1-2 weeks (must replace the cells to restore full function)
    • High doses can cause tinnitus
  • Reye’s syndrome: salicylates in children/adolescents “saly raeye Jensen”
  • Liver damage for acetaminophen “live acetomen”

cox1/2 inhibitor so:

Reduce gastric mucosal protective barrier

- Compromise renal function

	- Interfere with platelet aggregation
	- Reduce vasoconstriction

and heart related issues potential as well.

128
Q

Of the following which is LEAST LIKELY to cause a problem for dental mgt in patient?

a. xerostomia
b. patient endurance
c. stage of disease
d. use of sertraline

A

d

129
Q

Using sertraline bad for dental stuff?

A

Not really, just stabilizes moods.

130
Q

xerostomia bad for dental work?

A

Yes it causes dry mouth and increased risk for caries

131
Q

Stage of disease bad for dental work?

A

Of course, it needs to be controled

132
Q

Patient endurance bd for dental work?

A

Something to be considered, espeically if they cant stay n the chair or keep their mouths open long enough.

133
Q

Which of the following is most likely responsible for worsening of patients memory?

a. sertraline
b. benztropine
c. ibuprofen
d. vitamins

A

b: because benztropine is like atropine but nicer. benztropine is an anticholinergic, and because the patient on the test question has already been dx with alzheimers (which is a degen disease where ach is dropping and neurons are being destroyed by plaques etc.) the benztropine is definetly not helping the situation and accelerating it.

134
Q

What is the MOST LIKELY mechanism for your benztropine worseining a patients memory that has been prev dx with alzheimers?

a. overdose of ca and vit c
b. agitation
c. anticholinergic activity
d. antiinflamm

A

c

135
Q

Which of the following drugs of abuse is most likely to be neurotoxic because of its ability to DRAMATICALLY alter the intracellular and extracellular release patterns of dopamine?

a. heroin
b. nicoitine
c. methylphenidate
d. methamphetamine

A

d

Methamphetamie, emphetamine, MDMA ectasy, ephedrine, bath salts -> increase DA (sympathomimetic) = they cause release of vesicels and reverse the DAT transporter!

136
Q

nicotine

A

nicotine (activate nicotinic receptors)

increases dopamine release

137
Q

methylphenidate

A

Dopamine reuptake blocker

for ADHD

138
Q

Which of the following behavarioal therapy for treating drug addiciton most likely affects the frontal cortex?

a. motivational enhancement
b. adverse therapy
c. urine drug checks
d. cognitive therapy

A

d

139
Q

Cognitive therapy

A

affects (Frontal Cortex)

strengtehn prefrontal cortex

140
Q

Motivational Enhancement therapy-

A

affects orbital frontal cortex

orbital frontal cortex (let drug priority go down and other better priorities up)

141
Q

Contingency Management

A

(inhibition
control-cortical-amygdala function)

(if you stay drug free ill give you a reward (inhibits control of corticol-amygdala function)
*giving motivation to not suppress amygdala and have control over impulsiviity.

142
Q

Which of the following has been sohwn to MOST LIKELY be a genetic explanation for elevated risk of becoming addicited to cocaine?

a. elevated activity of GABA receptors
b. diminished activity of D2 receptors
c. diminshed activity of d1 receptors
d. ekevated activity of NMDA receptors

A

B…less activity means more of the drug is needed to reach the same high.

143
Q

methamphetamine

A

Much greater
Activity than any
Other drug of abuse
-causes neurotoxicity

144
Q

. diminished activity of D2 receptors has been linked to a genetic explanation for elevated risk of becomging addicted to cocaine

A

D2 receptor study

Looked at alcohol, metha, cocaine, food can all cause excess release of dopamine causing a higher pleasure baseline.

Receptors of D2 are altered in some fashion, diminished requiring more stimulation of dopamine to fix that underlying deficit.

D2 receptors are underfunctionsing so you need a higher rate of dopamine to get that ‘fix’

Quinones don’t form extracellulary and therefore don’t destroy a d2 receptor.

145
Q

what acts through D1 receptors

A

Huntingtons

146
Q

Elevated NMDA receptor activity

A

characteristic of huntingtons

-> caudate is destroyed because of the overexcitation of the ampa/nmda receptors due to Huntington gene in gaba neurons (feedback issue and at the end of the day gaba is wiped “we aren’t getting anything from gaba so lets turn up glutamate even more”

147
Q

elevated activity of GABA receptors

A

typically a sign that pain is present somewhere and you are using a drug to elevate the activity of Gaba to help calm the system down.

148
Q

Insulin injections

A

help for type 2 diabetes (getting glucose back into body instead of just @ bloodstream)

149
Q

Lyrica (gabapentin)

A

Managing Neuropathic pain (e.g., trigeminal neuralgia)
A. FDA-approved:

• Gabapentin (antiseizure/anticonvulsant)- Lyrica : affects GABA/glutamate systems

also FDA approved..
• Duloxetin (antidepressant)- blocks NE/5HT uptake
• Nortriptyline (antidepressant)- blocks NE uptake

150
Q

tylenol

A

• Acetaminophen: Non-NSAID, Non-COX 1 or 2 inhibitor

—perhaps blocks a COX 3 and/or works on 5HT

  • ***-NON-antiinflammatory
  • has good antipyretic
  • has analgesic effects that are somewhat less than the antiiflammatory analgesics

stable in solution,no gi issues , no anticlotting, no reyes , small antiinflamm action, contrandicated in ppl with bad livers!!

151
Q

Is it ok to do careful plaque removal and root planing to reduce dental discomfort for a patient if he has perio issues and is taking 3 aspirins, gabapentin, and has type 2 diabetes?

A

Yes if CAREFULLY done.

152
Q

Which of these would most likely be associated with stomach discomfort/issues and bleeding?

a. Lyrica
b. Insulin
c. OTC antacids
d. Aspirin

A

D aspirin because:

cox1/2 inhibitor so:

Reduce GASTRIC mucosal protective barrier (gets ulcers)

- Compromise renal function

	- Interfere with platelet aggregation (thins blood)
	- Reduce vasoconstriction

and heart related issues potential as well.

153
Q

Which of the following would MOST LIKELY be used to help a diabetic with foot pain?

a. Lyrica
b. Aspirin
c. OTC antacids
d. none

“Patient has severe pain associated with his faeet which his doctor describes as a neuropathic pain”

A

A..Lyrica

Its for Managing Neuropathic pain (e.g., trigeminal neuralgia)
A. FDA-approved:

• Gabapentin (antiseizure/anticonvulsant)- Lyrica : affects GABA/glutamate systems

*aspirin wouldnt help with this because not used for “neuropathic pain”

154
Q

After checking with patients physician you decide its appropriate to do extensive periodontal surgery, which of the following WOULD BE THE BEST Tx for post surgical pain of patient?

a. increase dose of Anacin up to 4 tablets
b. Replace Anacin with 2 tablets of ibuprofen
c. Prescribe indomethacin
d. Perscribe celexob (celebrex)

A

D

if you perscribed more A = more aspirin = more bleeding not good./more gastric issues

B= replacing aspirin with ibuprofen would not really cause a large effect

C= potent NSAID. potent non-selective …not used regularly due to ALOT of side effects

D= Celexoib would work since its a cox 2 inhibitor and takes out pain without causing more bleeding/damage to GI tract (that patient is already experiencing in the test question)
-interferes with renal function, higher incidence of heart attack and stroke, lacks GI and anticlotting action!!!

155
Q

Celecoxib

what does it NOT cause?

A

interferes with renal function, higher incidence of heart attack and stroke, LACKS GI and anticlotting action!!!

156
Q

ibuprofen

A

COX1 and 2 inhibitor, blocks production of prostaglandins

analgesic, antiinflamm, antipyretic

more cox 2 than 1, CV effects
(so more Heart issue potentially, but still affects GI ulcers, and thins out blood so more bleeding)

*referring to After checking with patients physician you decide its appropriate to do extensive periodontal surgery, which of the following WOULD BE THE BEST Tx for post surgical pain of patient? (dont change aspirin for ibuprofen…just lessens the effects but celexocib is better since it eleminates Gi and bleeding problem completely)

157
Q

Which of the following is considered to be a “modulating receptor” on the free endsings of sensory nerve terminals?

a. prostaglandin receptors
b. thermo nociceptrs
c. chemo nociceptors
d. mechanical nociceptors

A

a

158
Q

neuropathic pain is

A

May result from abnormal activity in nociceptive fibers that have been damaged, but after injury has healed, and/or:
From abnormal activity in central pain pathways
Mechanisms poorly understood
No protective function; does not terminate with healing

phantom pain

159
Q

prostaglandin receptors

A

• MODULATION receptors on nerve endings (TRP V, prostaglandin/purino and pyrimidine-receptor types)->

160
Q

b. thermo nociceptrs
c. chemo nociceptors
d. mechanical nociceptors

A

• Nociceptors (know types-thermo, chemical, mechanical, polymodal) → specialized ion channels on sensory nerve endings that respond to noxious stimuli.

Polymodal subtype: in extremes a thermal receptor can turn into a mechanical receptor (capacity to sense other modalities) but requries a ton of stimulation to do so.

These nociceptors are equipped with a range of receptors that render them sensitive to thermal, mechanical and some chemical stimuli

161
Q

Select the INCORRECT statement concerning pain types

a. neuropathic pain occurs without activation of recetors on the free endings of sensory nerve terminals
b. somatic pain typically responds to NSAId analgesics
c. Visceral pain usually reponds to opioid narotic anaglesics
d. Allodynia refers to a reduction in pain sensistitivty to sensory stimuli

A

d

162
Q

allodynia

A

Allodynia: pain evoked by normally nonpainful stimuli

Allodynia : takes non painful stimuli to painful stimuli (neutral but now painful)

163
Q

Hyperalgesia

A
  • You sensitized perception of pain in repsonse to painful stimuli (less stimulation to get same response)
164
Q

a. neuropathic pain occurs without activation of recetors on the free endings of sensory nerve terminals T/F?

A

True
Pain sensations may be continuous (esp. burning, aching) or periodic (lancing, electric), but occur WITHOUT activation of nociceptors by actual or potential tissue damage

Hyperalgesia and allodynia are common and dramatic.

165
Q

somatic pain typically responds to NSAId analgesics

T/F?

A

True

Nociceptive pain: pain resulting from activation of nociceptors as a result of actual or potential tissue damage and processing by the CNS
somatic/visceral/inflammatory (3 major areas of pain)

Somatic pain- well defined (you know right where it is)
(assoc w/ skin and musculo skeletal system) we know NSAIDS help with this

166
Q

Visceral pain usually reponds to opioid narotic anaglesics

A

True (since its typically a referred pain)

Visceral: pain associated with internal organs and associated tissues-dull, burning, poorly defined, diffuse

In viscera its more mechanical – more stretching/burning sensations

  1. Therapeutic uses for opioid narcotics: mild to sever pain
    • Analgesia- mild to severe somatic or visceral types of pain
    • Causes drug dependence in everyone with ~1 month of use leading to withdrawal
    • Antitussive : no cough
    • Antidiarrheal : constipation
167
Q

Select the INCORRECT statement concerning pain fibers

a. plexus of rashkow is assoc wit dental pulp of tooth
b. Alpha delta fibers are small and myelinated and assoc with sharp llocalized pain
c. C fibers are small and nonmyelinated and assoc with dull diffuse pain
d. c fibers conduct pain impulses ata faster rate than A delta fibers

A

D

168
Q

c fibers conduct pain impulses ata faster rate than A delta fibers t/f

A

FALSE

2) C- fibers: unmyelinated, slower conducting and smaller in diameter (2mm); associated with conduction of dull diffuse pain.

slower than A delta fibers

169
Q

C fibers are small and nonmyelinated and assoc with dull diffuse pain t/f

A

True

170
Q

Alpha delta fibers are small and myelinated and assoc with sharp llocalized pain t/f

A

True

1) A-delta fibers: myelinated, fast conducting fibers of diameter 1-6mm; associated with conduction of sharp, localized pain when the dentin is
first exposed.

171
Q

a. plexus of rashkow is assoc wit dental pulp of tooth

t/f

A

true

Plexus of nerves in tooth called the
Sub-Odontoblastic plexus or
plexus of Raschkow.

172
Q

Nociceptors on free endings of sensory nerve terminals are DIRECTLY ASSOCiated with which of the processes in nocicept?

a. transmission
b. modulation
c. transduction
d. perception

A

C

173
Q

transduction

A

Specific ion channels on free nerve endings that respond to actual or potential tissue trauma
are involved in:

174
Q

Transmission

A

action potentials) : you feel a burner, it releases a signal to a thermal tryp receptor located on a nocicepther neuron, depolarizes then is transmitted to dorsal root ganglia…ex: capsaicin activates tryp1

175
Q

Modulation

A

• Modulation (multi-levels; including dorsal lateral horn of spinal cord [i.e., facilitatory and inhibitory influences], Periaqueductal grey area, thalamus, sensory cortex)

176
Q

Perception

A

• Perception (cortex)

177
Q

Which of the following are naturally occuring opioid peptides that primarily activate kappa opiid receptors?

a. enkephalin
b. dynorphin
c. b endorphin
d. subtance p

A

Dynorphins A & B (primarily κ, but some of the others)- 17 amino acids

178
Q

Enkephalns activate

A
  1. Enkephalins (opioid receptor types- υ and δ)- 5 amino acids : part of modulation.
179
Q

B endorphin activate

A
  1. β-endorphins (υ and δ receptors)- 91 amino acids
180
Q

F. Endogenous opioid peptide

A

(AKA, the endorphins)-> activate opioid receptors like muew, kappa and delta and provide an inhibitory feedback to pain “gunshot wound during war” prob wont hurt as bad as during walking. (body natural painkillers)

  1. Enkephalins (opioid receptor types- υ and δ)- 5 amino acids : part of modulation.
  2. β-endorphins (υ and δ receptors)- 91 amino acids
  3. Dynorphins A & B (primarily κ, but some of the others)- 17 amino acids
  4. Key role is inhibitory feedback, especially for pain transmission—although it also has other function such as mitigates stress responses.
181
Q

Substance P

A

ncluding substance P (SP). Substance P causes vasodilation and neurogenic edema with further accumulation of bradykinin (BK). Substance P also causes the release of histamine (H) from mast cells and serotonin (5HT) from platelets.

usualy use opioids to decrease this effect since this is what causes pain like sensations

182
Q

Which of the following is NOT an NSAID analgesic

a. indomethacin
b. diflunisal
c. naprosyn
d. meperedine

A

D

183
Q

Indomethacin

A

a. Indomethacin:

• Potent, non-selective NSAID- major side effects so not used for regular pain management…more for arthritis

184
Q

Diflunisal (Dolobid):

A

• Related to salicylates-supposed to be good for bone pain

NSAID

185
Q

Naprosyn

A

-naprosyn (Naproxen or Alleve)- longer lasting and slower acting

ibuprofen type nsaid

186
Q

Meperidine

A

• Meperidine (Demerol)-for moderate pain

narcotic analgesic

187
Q

Other narcotic analgesic

A

b. Other narcotic analgesics
• Meperidine (Demerol)-for moderate pain
• Pentazocine (Talwin)- for moderate pain; it is a mixed agonist/antagonist narcotic-discourages abuse
• Methadone- moderate to strong analgesic-used to treat opioid dependence and addiction and sometimes as an analgesic
• Buprenorphine- moderate analgesia-also a agonist and antagonist, txs opioid addiciton

188
Q

Which of the following is the most potenent narcotic analgesic

a. morphine
b. fentanyl
c. hydrocodone
d. tramadol

A

B

189
Q

tramadol

A
  • Tramadol (Ultram)- non-opioid
  • It is Schedule 4- low drug abuse potential, but some minor opioid action
  • Works for some, but not all, stressful for the liver.

for neuropathic pain

190
Q

Basic narcotic analgesics and doses

A
  1. Types of narcotic analgesics
    a. Equipotent IM doses:
  • Morphine (10 mg), hydromophone (1.5 mg), oxymorphone (1 mg)
  • Codeine (200 mg), hydrocodone (30 mg), oxycodone (20 mg)

• Most potent is fentanyl (0.1 mg)

191
Q

More info on narcotic analgesics

A

Codeine and morphine are natural
Looks fairly similar : codein can actually be converted to morphine in body.
Side change same in all 3 codone groups
Morphone alll have same hydroxy side chain though
Increased potency as you get stronger.

20mg oxycodone is same as 200 mg codeine

Try to combine to use less of narcotic and more of the analgesic from acetometaphin

Fentanyl requires .1mg VERY POTENT
Fentanyl patch for chronic pain
Cancer type of tx
They don’t need analgesic since fentayl used

Give fentayl drop.

192
Q

Which of the follwing is LEAST LIKELY to be a side effect of a potentn narcotic analgesic

a. diarrhea
b. reduced pulmonary reflex
c. additive / syngeric interaction with other cns depressents
d. euphoria

A

c. Major side effects (mostly υ opioid mew receptor mediated):
• Respiratory depression (reduced pulmonary reflex linked to detection of elevated CO2 and reduced O2)-most common cause of death
• Constipation- slows bowel movement
• Sedation/additive/synergistic with other CNS depressants (e.g, alcohol, antianxiety-anxiolytics, sleep aids-hypnotics and natural sleep)
• Euphoria/dependence/addiction

193
Q

When should you NOT use a narcotic analgesic

A 
d.	Contraindications:
•	History of substance abuse
•	Severe constipation or upset stomach
•	Respiratory problems (emphysema or asthma)
•	Use of CNS depressants
194
Q

Your pharm comp disoverd new analgesic caled Nopaine that claims to be a cox 1 inhibitor. FDA sees 4 studies and says your not pure cox 1 and tells you that its misclassified. Which of the following was most likely basis for rejection

a. improved gastric mucosal protection against acid reflux
b. nopaine had no effect on heart or blood vessels
c. nopain strengtheed bleeding time after tissue trauma
d. relieved pain assoc with prostaglandin mediated inflammation

A

Cox 1 typically has Gi issues, bleeding, kidney issues

a. is wrong because thats exactly the opposite of what cox 1 does

the others fall in line with cox 1 stuff

HD&T (7 decks)

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