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ESUN MS2Unit3 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What system that packages and store dopamine and make it ready to release?

A

VMAT2 (vesicular monoamine transporter 2)

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2
Q

How do you get rid of dopamine in the synapses?

A

Dopamine transport (DAT) to reuptake/COMT and MAO-B to degrade

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3
Q

Which dopamine pathway systems control movement? hyper function cause? hypo?

A

Nigrastriatal systems (between striatum and substantia nigra)/dyskinetic movement/Parkinsonism

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4
Q

Which dopamine pathway systems control reward and perception?hyper function cause? hypo?

A

Mesolimbic system (between nucleus accumbens and tagmentum)/addiction/amotivation and apathy

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5
Q

Which dopamine pathway systems make you alert, awake and focused? hyper function cause? hypo?

A

Mesocortical system (tagmentum and the front of your brain)/hypervigilance/inattention

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6
Q

Which dopamine pathway systems control prolactin function? hyper function cause? hypo?

A

Tuberoinfundibular system (hypothalamus and pituitary)/hypoprolactinemia/hyperprolactinemia

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7
Q

Loss of dopamine activity in what part of the brain causes ADHD?

A

Anterior cingulate

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8
Q

Block dopamine can alleviate?

A

Nausea

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9
Q

How does L-methylfolate increase the production of dopamine?

A

Folic acid—>MTHFR—>L-methylfolate—>cross BBB—>1 carbon cycle—>increase tyrosine—>increase dopamine

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10
Q

What chemical also stimulate the 1 carbon cycle?

A

s-adenosyl methionine

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11
Q

Which drug block DA and NE reuptake?

A

Bupropion

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12
Q

2 mechanism of amphetamine?

A

Block DAT and might reverse it/promote VMAT2—>release more DA

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13
Q

How does methylphenidate compare with amphetamine?

A

methylphenidate just blocks DAT

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14
Q

Example of class I and II addictive drugs?

A

Cocaine (illegal)/amphetamine (allowed to prescribe)

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15
Q

What does modafinil and armodafinil do? how does it work?

A

For ppl who are fatigue (class IV)/increase histamine activity in TMN/increase orexin (arousal)/might block DAT/might up NE receptor

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16
Q

Should you prescribe class IV drugs to ppl who has addiction problems?

A

No

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17
Q

Can modafinil and armodafinil make you loss weight?

A

Yes

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18
Q

High dose of selegiline block?

A

MAO A and B

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19
Q

What gives you HTN crisis (stroke/MI) when you are on MAOi?

A

NE and food with tyramine in it

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20
Q

What is serotonin syndrome and what causes it?

A

high level of 5HT—>tremor/muscle spasm/hyerthermia/delirium/coma/death
takes 5HT when you are on MAOi

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21
Q

What does entacapone and tolcapone treat?

A

Parkinson’s

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22
Q

What is the side effect of entacapone?

A

Fatigue and nausea (unusual in stimulant drugs)

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23
Q

Why don’t we want to use levodopa right away?

A

It stops working 10-20 years and give you dyskinesias

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24
Q

Side effect of D2 agonists?

A

Mania (one of them)/too happy

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25
Q

What is D2 receptor?

A

Phasic DA—>release DA in short puff

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26
Q

What is D3 receptor?

A

Tonic DA—>goes up and down slowly in a day to keep you awake

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27
Q

What else can aripiprazole treat besides schizophrenia?

A

Depression

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28
Q

you want to __ DA in treating schizophrenia?

A

Lower

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29
Q

What are reserpine and tetrabenazine?

A

DA depleters—>reserpine: Psychosis (DA blocker—>shooting blank)

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30
Q

What is high potency first gen antipsychotic drugs (typical) and its side effect?

A

High affinity for D2/cause DA to be too low—>extrapyramidal syndromes

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31
Q

What is extrapyramidal syndromes?

A

Caused by FGA—>akathisia/dystonia (torticollis—>stiff neck)/Parkinsonism/neuroleptic malignant syndrome (all muscles contract—>hyperthermia/muscle rigidity/rhabdomyolysis

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32
Q

Why use anticholingeric drugs for Parkinson’s?

A

Block cholingeric system—>release DA

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33
Q

What is diphenhydramine (Benadryl) used for?

A

Anticholinergic—>treat EPS caused by FGA/SGA

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34
Q

What happen if D2 receptor (high potency FGA) is blocked for years?

A

Highly sensitive D2 receptor emerge—>tardive dyskinesia (fast quirky movement usually on face)

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35
Q

What else does low potency FGA block besides D2 receptor?

A

They are also anticholinergic/anti H1/anti alpha 1—>more side effects

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36
Q

What are the 3 high potency FGAs?

A

Haloperidol/fluphenazine/thiothixine

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37
Q

What are the 2 low potency FGAs?

A

chlorpromazine/thioridazine

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38
Q

Difference of high and low potency FGAs regarding side effects?

A

High potency is more prone for EPS/low potency has more side effects

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39
Q

What is the difference between SGA (atypical) and FGA?

A

SGA is more specific—>it blocks D2 and 5HT2a—>blocking DA in mesolimbic system and allowing better transmission in other DA pathways

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40
Q

Do you get more or less EPS with SGA?

A

Way less/but SGA has more metabolic side effects—>also make younger people suicidal

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41
Q

What else does SGA treat?

A

depression

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42
Q

What are the side effects for pines (SGA)?

A

More antihistamine—>more sedative

Make ppl eat more and gain more weight—>diabetes

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43
Q

What are the side effects for dones (SGA)?

A

More EPS

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44
Q

What is so special about clozapine?

A

Most effective SGA/risk of agranulocytosis/most metabolic risk/little to zero EPS

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45
Q

What is the most common type of headache?

A

episodic tension type

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46
Q

What gender is more prone to migraine?

A

Female (3 times more frequent than men)

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47
Q

What is the migraine phases?

A

Prodrome—>aura—>headache—>resolution

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48
Q

What is positive and negative visual phenomenon?

A

Positive—>see something

Negative—>missing vision

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49
Q

What is aura regarding migraine?

A

Cortical spreading depression—>reduction of cerebral blood flow—>focal neurological problem (last about 20mins—>visual is most common (distortion) )

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50
Q

Would migraine headache relive by rest?

A

Yes

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51
Q

How long does migraine last?

A

4-72 hours

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52
Q

Symptoms of migraine headache?

A

osmo/photo/phonophobia (seek dark room)

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53
Q

Is migraine w/ aura more common than w/o?

A

No w/o is more common

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54
Q

What is familial hemiplegic migraine?

A

Mutation of Ca channel on chromosome 19—>cause one side of the body paralyzed

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55
Q

What is special about migraine pt’s brain?

A

It is much more sensitive—>high response to stimuli

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56
Q

What is the pathophys of headache?

A

Activation of trigeminovascular system—>nerve fibers release vasodilating/permeability promoting peptides—>sterile inflammation—>increase mechanosensitivity and hyperalgesia to previous normal stimuli (blocked by triptans)—>pain perceived by the surface of the brain

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57
Q

Behavioral treatment for migraine involves?

A

healthy habits/stress/trigger avoidance

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58
Q

Mild to moderate migraine can be treated with?

A

Nonspecific med—>NSAIDs/analgesics and so on (overuse can cause headache)

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59
Q

What is the precaustion for barbiturates and opioids for acute treatment use?

A

Risk of overuse—>medication overuse headache

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60
Q

When to use corticosteroids for migraine?

A

Prolonged migraine

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61
Q

Why is dihydroergotamine (DHE) preferred over ergotamine?

A

Less side effects

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62
Q

How does triptans work?

A

Cross BBB—>agonize 5HT1b/d—>shut down trigeminovascular system (must take early take about 20mins to work)

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63
Q

What are some adjunctive treatments for acute migraines?

A

Antiemetics/neuroleptics (antipsychotic)

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64
Q

What to use for preventive treatment for migraine?

A

Antidepressants (TCA and SSRI)/antihypertensive (beta blocker and Ca channel blockers)/antiepiletpic

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65
Q

What are the 3 TCA that are used to prevent migraine?

A

Amitriptyline/protriptyline/nortiptyline

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66
Q

What is Ca channel blockers used for migraine prevention?

A

When pt has prolonged or disabling aura

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67
Q

What is the major side effect for topiramate (antiepileptic)?

A

Change in cognition

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68
Q

What is botox used for migraines?

A

Chronic migraine

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69
Q

What is tension type headache like?

A

Non-pulsating/dull/achy pain/not worsen by movement/not that severe

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70
Q

What defines chronic tension type headache?

A

More than 15 times per month

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71
Q

What do you treat acute TTH with? and prevent it from happening?

A

Analgesics/TCA like amitriptyline

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72
Q

What is cluster headache?

A

Happen at night and at the same time every year/mostly men—>heave facial features

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73
Q

How is the pain in cluster headache?

A

Unilateral/temporal/peaks quickly/really severe pain

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74
Q

What to use to treat acute cluster headache?

A

O2/triptan/DHE

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75
Q

What to use for short term preventive treatment for cluster headache?

A

Steroids

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76
Q

What to use for long term preventive treatment for cluster headache?

A

Verapamil (Ca channel blockers)/topiramate/valproic acid/lithium (avoid indomethacin and Ca depleting diuretics)

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77
Q

How is aqueous (eye) produced and traveled?

A

Made in ciliary body—>pass through between lens and iris—>anterior chamber—>drain out via trabecular meshwork

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78
Q

What is the angle in angle closure and open angle glaucoma? and how to tell if it is angle closure (prevent drainage of aqueous)?

A

The angle between iris and cornea/shine light from temporal side of the eye—>if both temporal and nasal iris are illuminated—>deep anterior chamber

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79
Q

At the age of 45, you start to loss the ability to ___?

A

Accommodate (thickening of the lens)

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80
Q

What does epi and dipivalyl do for glaucoma?

A

They lowered the intraocular pressure

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81
Q

Topical cocaine for the eye is testing for?

A

If pupil do not dilate—->symp dysfunction (Horner’s)

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82
Q

If eyes do not respond to paredrine, what order of neuron is damaged?

A

3rd order neuron (postganglionic)

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83
Q

Parasymp paresis?

A

Loss of parasymp function—>pupillary dilation

Parasymp runs with 3rd cranial nerve—>loss of eye movement and ptosis

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84
Q

Adie’s symdrome?

A

Damage to ciliary ganglion—>parasymp synapse at ciliary ganglion—>parasymp damage—>large pupil—>don’t respond to light but respond to accommodation

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85
Q

What happens with internal carotid aneurysm for the eyes?

A

Trauma to 3rd nerve—>pupillary dilation/loss of eye movement/ptosis
Aneurysm also comes with headache (medical emergency)

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86
Q

Distinguish Adis’s from intracranial aneurysm?

A

Denervation hypersensitivity happens in Adi’s—>small amount of ACh stimulates nerve (low dose of methacholine and pilocarpine will work)

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87
Q

1% pilocarpine constricts everybody’s pupil but?

A

Not for pharmacologic blockade

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88
Q

Pilocarpine causes?

A

Bifrontal headache

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89
Q

What are the 3 light-near dissociation disorder?

A

Adie’s/Parinaud’s syndrome (mid brain tumor)/Argyll Robertson syndrome (tertiary syphilis)

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90
Q

Antidepressant is used for ?

A

Depression/anxiety (and its subtypes like OCD and PTSD/enuresis/neuropathic pain/bulimia

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91
Q

What are the major mechanisms for antidepression drugs?

A

Block amine reuptake/block MAO/block presynaptic amine autorecetpors

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92
Q

How long will you see the clinical improvement for antidepression drugs?

A

Not till weeks or months

93
Q

___ antidepressants are very effective especially for children and teens?

A

Placebo

94
Q

What is the difference between all the amine reuptake inhibitors?

A

Their selectivity against NE or 5HT reuptake transporter

95
Q

What are the side effects of tricyclics?

A

Also block muscarinic/alpha/histamine/DA reuptake pump

96
Q

Overdose of tricyclics causes?

A

Cardiac arrhythmias—>lethal

97
Q

Why is SSRI used more than TCAs?

A

SSRI has less side effects (might not as good)—->more compliance

98
Q

What is one of the major side effect of paroxetine and fluoxetine?

A

P450 inhibitor

99
Q

What is ketamine?

A

Party drug that has a faster clinical effect than other antidepression drugs

100
Q

Is resistant to depression meds common? and how do we deal with it?

A

It is common/switch, combine or augment different drugs

101
Q

What are the 2 atypical antidepressant?

A

Mirtazapine and bupropion

102
Q

What is the definition of local anesthetics?

A

Reversibly prevents nerve impulse transmission w/o affecting consciousness

103
Q

The cell membrane of neuron is permeable to __ and not to ___?

A

Permeable to K but not Na

104
Q

What is preemptive analgesia?

A

Nerve block before incision

105
Q

Local anesthetic works on Na channels that are ___?

A

being activated (less in resting or inactivated states)

106
Q

What are the 3 structural characteristics of local anesthetics?

A

Aromatic ring (lipophilic)/intermediate linkage either Ester or Amide/terminal amine

107
Q

Intermediate linkage of local anesthetics determine the way of biodegradation, how does Ester and Amide degraded?

A

Ester—>hydrolyzed in the plasma by pseudocholinesterase (CSF does not have this enzyme)/Amide—>transformed by P450 in the liver

108
Q

The terminal amine in local anesthetics can accept ___ and become ___?

A

Accept a proton and become a weak base—->thus hydrophilic and active

109
Q

Only the ___ form of local anesthetics can cross the lipid membrane and only the ___ form can act on the Na channel

A

unionized/ionized

110
Q

In physiologic pH, local anesthetics are ___?

A

Ionized

111
Q

What do we do when we have to inject local anesthetics into an infected tissues (acidic environment)?

A

Add bicarb first and then LA

112
Q

What kind of nerve would be blocked first by LA?

A

Smaller and myelinated nerves

113
Q

What are the 4 types of nerve fibers and their diameter and conduction speed?

A

Diameter and conduction speed in descending order: A-alpha—>A-beta—>A-delta—>B—>C

114
Q

Which 4 nerve fibers are myelinated and which 2 fibers conduct pain?

A

All the A fibers and B are myelinated and A-delta and C fiber conduct pain

115
Q

Which nerve fiber gets blocked first and which ones recovers first?

A

B/C get blocked first and then A fibers/A fibers recover first and then B and C fibers

116
Q

Pain and temp sensation can be blocked but ___ can not be blocked?

A

Pressure sensation

117
Q

What is Cauda Equina Syndrome and what caused it?

A

High dose of intraspinal lidocaine—>complete motor weakness and sensory lost/lost of bladder and bowel function

118
Q

Lidocaine and other LA can also cause ___?

A

Transient neurologic symptoms (transient pain)

119
Q

How to treat LA toxicity?

A

Intralipid infusion with ventilation to maintain normal blood pH

120
Q

Which LA causes allergy, esters or amide?

A

Esters (PABA metabolites)

121
Q

What is the difference between toxicity and adverse effect?

A

Toxicity is predicted reaction, adverse effects are not

122
Q

What kind of seizures do phenytoin treat?

A

Tonic-clonic and acute seizures

123
Q

Lamotrigine competes with __ for excretion?

A

Valproate

124
Q

What are the 2 drugs that bind to GABA A and for antiepileptic?

A

Phenobarbitol and benzodiazapines

125
Q

What is status epilepticus and what drug is for that?

A

Seizures that start right after one another (medical emergency)/benzodiazepine

126
Q

Which antiepileptic drug has cognitive toxicity (word finding)?

A

Topiramate

127
Q

Li can be used for ___ headache?

A

cluster

128
Q

What is MAC (minimal alveolar concentration)?

A

The concentration of anesthetic vapor in the lungs that 50% of pt would not response to noxious stimuli/additive

129
Q

GABA and Glutamate bind to and open ___ channels?

A

ligand-gated ion channels

130
Q

NMDA receptor conduct what ions?

A

Na/K/Ca

131
Q

GABA receptor conduct what ion and result in?

A

Cl/hyperpolarization

132
Q

Glycine is inhibitory or excitatory NT in CNS or spinal cord?

A

Inhibitory in spinal cord

133
Q

Anesthetics bind to ___ pockets of ___ protein?

A

Hydrophobic pockets of water soluble protein

134
Q

Volatile anesthetic (liquid) needs to be ___ before giving to pts?

A

Vaporized (specific drug goes with specific vaporizer)

135
Q

What is partial pressure regarding inhaled anesthetics?

A

concentration of gas dissolved in liquid is proportionate to the partial pressure of the gas above the liquid—>equilibrium exists between 2 phases (e.g. alveoli and blood)

136
Q

What is partition coefficient?

A

Ratio of solubilities of gas between 2 compartments/it describes how inhaled anesthetics distribute themselves

137
Q

What propel the anesthetic gas to go from the machine to the brain?

A

Partial pressure of the alveoli PA

138
Q

Partial pressure of alveoli PA/pulmonary papillary blood Pa/brain partial pressure Pbr are?

A

equal

139
Q

How to maintain a good partial pressure of anesthetic gas in the alveoli by increase delivery to alveoli?

A

Increase amount of gas/increase alveoli ventilation/ and decrease functional residual capacity

140
Q

How to maintain a good partial pressure of anesthetic gas in the alveoli by decreasing uptake of blood?

A

Decrease blood solubility/decrease CO/increase con. of gas in the blood—>so gas stay in the alveoli

141
Q

You can start with ___ con. of gas since the gas will be mixed with other gas in the lungs and get diluted

A

Higher

142
Q

What is concentration effect?

A

When the gas is rapidly absorbed into the blood stream in the lung, the remaining con. of gas in the alveoli increase because the volume shrinks

143
Q

What is the 2nd gas effect?

A

Potent gas and N2O are in the alveoli—>N2O got absorbed a lot faster than the potent one—>potent gas con. goes up

144
Q

Speed of anesthetic induction (speed of pt fall asleep) is determined by?

A

The rate of rise of alveolar concentration of anesthetic agent

145
Q

What kind of anesthetic agents achieve high PA and thus faster induction?

A

Poorly soluble ones (tend to stay in alveoli)

146
Q

MAC measures the response of ___?

A

spinal cord

147
Q

MAC is increased in?

A

hyperthermia/red hair ppl/increase catecholamine and NTs/hypernatremia/cyclosporin

148
Q

MAC is decreased in?

A

Increase age/pregnancy

149
Q

Why is N2O used with other volatile anesthetics?

A

So we don’t have to use too much of potent volatile anesthetics—>minimize side effects

150
Q

What are the Guedel’s 4 stages of CNS depression from anesthesia?

A

Analgesia—>excitement and delirium—>surgical anesthesia—>medullary depression (need ventilator)

151
Q

Volatile agents increase?

A

Cerebral blood flow (counted by hyperventilation)/increase ICP/blood flow to brain muscle and skin

152
Q

Volatile agents decrease?

A

systemic vascular resistance (vasodilate)/BP/ventilatory response to hypoxia

153
Q

Volatile agents’ effects on neuromuscular function?

A

Relax skeletal muscle/trigger malignant hyperthermia (genetic variant)

154
Q

Barbiturates and propofol causes __ and results in ___?

A

Vasodilation and HoTN

155
Q

For a elderly pt who can not tolerate drop in BP, use which general anesthesia?

A

Etomidate

156
Q

What is ketamine’s (general anesthesia) effect on cardiovascular system and respiratory system?

A

Stimulate sympathetic system/broncodilator

157
Q

What generalized anesthesia do we use for children with developmental delay?

A

Ketamine

158
Q

What is the difference between dexmedetomidine and other generalized anesthesia?

A

Pt on dexmedetomidine resembles natural sleep

159
Q

All neuromuscular blockers have ___ structure?

A

Quarternary ammonium

160
Q

Neuromuscular blockers can be countered with?

A

Anti cholinesterase

161
Q

What is the difference of Train of Four for depolarizing and non depolarizing neuromuscular blockade?

A

every succeeding twitch is smaller for non-depolarizing/decrease the same degrees for all 4 twitches for polarizing

162
Q

If a pt has renal failure and need non depolarizing NMB, which one you shouldn’t give?

A

Pancuronium

163
Q

Difference between sedative and hypnotic drugs?

A

Sedative—>calming/anti anxiety

Hypnotic—>induce sleep

164
Q

Does GABAa agonist bind directly to the binding site of GABA?

A

No, they bind onto the structure allosterically and then enhance the receptor (can’t open them themselves)

165
Q

GABA receptor has many subunits, resulting?

A

Different composition has different effect

166
Q

What is BDZ1 receptor?

A

The receptor that zolpidem binds to (they made that receptor up just for zolpidem, aren’t you special)

167
Q

Benzo binds to BDZ1 or 2?

A

Both

168
Q

Why is benzo safer than barb?

A

Benzo has ceiling effect—->they only enhance the receptor can’t open them
Barb (and alcohol) in high dose act as agonist themselves—>can lead to much severe effect like coma and death

169
Q

What determines the short and long acting benzo?

A

If they have active metabolites then they are long acting

170
Q

Triazolam and zolpidem are used as a ___ pills

A

Sleeping (short half life)

171
Q

___ is used for fear of flying (calm you down)

A

Alprazolam (Xanax)

172
Q

GABA antagonist cause?

A

Seizure

173
Q

Why Thiopental is rapid acting?

A

Lipid soluble—>access to brain fast—>redistribution out of the brain fast as well

174
Q

What kind of drugs treat long term and short term anxiety?

A

Antidepressant/benzo

175
Q

Alcohol is ___ in size therefore ___ absorbed

A

Small/rapidly

176
Q

What determines the rate of absorption of alcohol?

A

Concentration of alcohol/stomach fullness

177
Q

What happens to alcohol when there’s food in the stomach?

A

Dilute alcohol/delay stomach emptying/increase effective metabolism of alcohol

178
Q

Alcohol is distributed throughout the __ content of the body, and resulting women to have ___ alcohol

A

Water content/male has higher water fraction than females

179
Q

Where is alcohol metabolism takes place?

A

Liver and stomach

180
Q

What is the alcohol metabolism process in the liver?

A

Alcohol —(alcohol dehydrogenase ADH)—>acetaldehyde—(acetaldehyde dehydrogenase—>ALDH1/2)—>acetate

181
Q

Asians lack which enzyme that metabolize alcohol?

A

ALDH2—>higher ALD level—>higher alcohol sensitivity

182
Q

When will the P450 metabolism of alcohol kick in?

A

When you drink too much or you are a seasoned drunk

183
Q

What is the limiting factor for rate of alcohol oxidation, and how are other reactions involving this factor affected?

A

NAD+/all other NAD+ reaction are diverted to alcohol metabolism

184
Q

When our system is fully saturated with alcohol (ya drunk), what is the order of kinetics regarding alcohol elimination?

A

Zero order (NAD+ is the limiting factor)—>turn to 1st order when the concentration is really low

185
Q

Progression of alcohol intoxication?

A

Loss of inhibition—>impaired motor—>vision—>cerebellum—>medulla (respiration and temp)

186
Q

Chronic alcohol usage causes ___? which can lead to ___?

A

Fatty liver—>cirrhosis

187
Q

Moderate alcohol consumption can increase ___ and decrease ___?

A

HDL/coronary heart disease

188
Q

Acute drug interaction of alcohol?

A

Metabolism of other drugs might be inhibited

189
Q

Chronic drug interaction of alcohol?

A

Induce P-450—>enhance metabolism of other drugs

190
Q

Alcohol has an ___ effect with other CNS depressant

A

Additive

191
Q

What are methyl alcohol and ethylene glycol? and what is used for OD of these?

A

Their metabolites are toxic/use ethanol to compete with ADH (preferred substrate)—>pee out the toxic ones

192
Q

Cocaine can be hydrolyzed via ___ or ___?

A

plasma cholinesterase or spontaneously

193
Q

What is schedule I and II drugs?

A

Schedule I—>high potential for abuse and no medical use (hallucinogens/heroin/weeds and what not)
Schedule II—>high potential for abuse and some medical use (morphine/cocaine)

194
Q

What are some examples of indole alkyl amines?

A

Serotonin like—>psilocybin and LSD

195
Q

What is an example of phenylethylamines?

A

Mescaline

196
Q

LSD’s affects?

A

Distortion of perception and heightened sensory awareness

197
Q

Why it is hypothesized that LSD share the same site of action with mescaline and psilocybin?

A

Because there’s cross tolerance between LSD and mescaline and psilocybin

198
Q

What is the mechanism of LSD?

A

agonists at inhibitory 5HT2a at raphe nucleus (raphe nucleus usually inhibit downstream 5HT)—->inhibit the inhibitor—->uncontrolled 5HT release

199
Q

How is THC metabolized?

A

Highly lipid soluble/metabolized by P450

200
Q

What are the 2 cannabinoid receptors and what do they do?

A

CB1—>euphoria

CB2—>immune system

201
Q

What is endogenous opioid?

A

Endorphin

202
Q

Where does opioid receptor agonist act on?

A

decrease release of substance P/Ascending spinothalamic tract/descending pain modulatory system

203
Q

What kind of receptor is opioid receptor?

A

G protein coupled

204
Q

Opioid side effects include?

A

Miosis/lower seizure threshold/depressed respiration

205
Q

What is bolus effect for opioid and what do we do to prevent it?

A

Analgesic effect from bolus of opioid injected but then pain comes back with rapid excretion/give extended release or IV

206
Q

What should we worry about opioid with acetaminophen?

A

Pt might take too much acetaminophen

207
Q

What to do when a pt who’s on extended release opioid that is still in pain?

A

Use immediate release as a breakthrough, don’t escalate the extended release (OD)

208
Q

How do we administer opioid for pt who has renal or liver problems?

A

Decrease dose or interval/use as needed only for pt with no urine/opioid is conjugated in the liver and excreted in the urine

209
Q

What is peudoaddiction of opioid?

A

Under treatment of pain

210
Q

What is tolerance of opioid?

A

Decrease effectiveness w/ repeated dose/decrease side effects EXCEPT for constipation

211
Q

What is physical dependence of opioid and how to avoid it?

A

Pt goes through withdraw/decrease the dose slowly

212
Q

What is equianalgesic dosing?

A

Switch an opioid to another or from one route to another (has to change dose too)

213
Q

How do we adjust for cross-tolerance when equianalgesic dosing?

A

(might be more sensitive to new drug) Decrease dosing for new drugs—>give more if pain

214
Q

What to give pt for nausea vomiting caused by opioid side effect?

A

DA blocker

215
Q

Is there a limited dose of opioid (ceiling) that you can give?

A

No, limited by side effect

216
Q

Which opioid you shouldn’t use for malnourished pt?

A

Fentanyl (patch form)

217
Q

What are the 5 MS subtypes?

A

Clinically isolated syndrome (one location)
Relapsing-remitting (most common)
Primary progressive (slowly gets worse/no relapse)
Progressive relapse (has relapse, worse every time)
Secondary progressive (start like relapsing-remitting and then stop relapsing and just gets worse)

218
Q

What does MS cause to the appearance of the brain?

A

White matter atrophy—>enlarged ventricles

219
Q

Neutralizing antibodies interfere with ___ treatment?

A

IFN-beta for MS (antibodies neutralize IFN-beta)

220
Q

Which IFN-beta drug has the highest neutralizing antibodies?

A

Betaseron (trade name)

221
Q

Which MS drug slow disease progression?

A

IFN-beta-1a

222
Q

The key for MS treatment is to treat?

A

Early

223
Q

Which IFN-beta drug is preferably used over others?

A

Rebif (or glatiramer acetate)

224
Q

How many years before the risk of getting PML from Natalizumab is increased and you should switch to other drugs?

A

About 2 years (JC antibody + pt has a higher chance of getting PML)

225
Q

What are atypical antidepressants?

A

Mirtazapine and bupropion

226
Q

What to give for alcohol withdraw

A

Benzo

227
Q

What is Hoffman degradation

A

Spontaneous degradation

228
Q

What causes Adie’s syndrome and what is its eye presentation?

A

Bacterial or viral infection damage the ciliary ganglion of the postganglionic of parasymp/bilateral mydriasis—>react slowly to light but react normally to accommodation

ESUN MS2Unit3 (11 decks)

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