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NBDE II boards > Pharm > Flashcards

Pharm Flashcards

1
Q

What is a cholinergic or cholinomimetic drugs?

A

stimulates the parasympathetic nervous system

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2
Q

Pilocarpine

A

Cholin agonist

Treats glaucoma + used to treat xerostomia after radiotherapy

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3
Q

Bethenacol

A

Cholin agonist

stims urination

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4
Q

Succinylcholine

A

Cholin antagonist

Muscle relaxant for surgery

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5
Q

Mecamylamine

A

Cholin antag

Treats hypertension

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6
Q

Carbachol

A

Treats closed angle glaucoma

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7
Q

Methacholine

A

test reactivity of airway

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8
Q

Cevimeline

A

cholin agonist

increase salivary flow

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9
Q

Nicotine

A

smoking cessation

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10
Q

what are 2 anti-muscarinics ? or anti-muscarinics?

A

atropine

scopolamine

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11
Q

what are the effect of anti- muscarinics?

A

dry mouth, blurry vision, urinary retention, constipation

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12
Q

what is pralidoxime?

A

a cholinesterase reactivator; use to treat organophosphate poisoning (found in pesticides); relives paralysis of the muscles of respiration.

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13
Q

What is glycopyrrolate (Robinul)

A

synthetic anticholinergic

Inhibit salivation pre-operatively; control upper airway secretions

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14
Q

What is benztropine mesylate (Cogentin)?

A

synthetic anticholinergic

Anti-Parkinsonism

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15
Q

What is Propantheline bromide (Pro-Banthine)?

A

synthetic anticholinergic

Traveler’s diarrhea

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16
Q

What is Trihyxphenidyl HCl (Artane)?

A

synthetic anticholinergic

Anti-Parkinsonism

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17
Q

List the alpha 1 agonists

A

Epi > NE

phenylephrine

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18
Q

List alpha 2 agonists

A

Epi > NE
clonidine
guanfacine

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19
Q

List beta 1 agonist

A

Epi = NE
isoprotenerol
dobutamine

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20
Q

list beta 2 agonist

A

Epi&raquo_space; NE
isoprotenerol
albuterol
terbutaline

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21
Q

What are the tissues that alpha 1 agonists affect?

A

radial muscle of the eye
vasculature
genitourinary/GI sphincters

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22
Q

What are the tissues that alpha 2 agonists affect?

A

vasculature
brainstem
NE terminals

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23
Q

What are the tissues that beta 1 agonists affect?

A

Heart

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24
Q

What are the tissues that beta 2 agonists affect?

A

lungs
vasculature to muscle
ciliary muscle of the eye
genitourinary/uterus

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25
Q

what is the antagonist for alpha 1?

A

prazosin; terazosin

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26
Q

what is the antagonist for alpha 2?

A

yohimbine

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27
Q

what is the antagonist for beta 1?

A

propranolol
atenolol
metoprolol

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28
Q

what is the antagonist for beta 2?

A

propranolol

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29
Q

What are the common medications for Parkinson’s Disease?

A 
L-dopa and carbidopa 
Benztropine 
Trihexyphenidyl 
Selegiline 
Entacapone
Azilect 
Pramipexole
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30
Q

What are common drugs that are used in combo with carbidopa-levodopa?

A

Azilect and Entacapone

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31
Q

What is azilect?

A

Used in conjunction with carbidopa and levodopa (Parkinsons disease) to prevent DA breakdown.

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32
Q

What is entacapone?

A

Used in conjunction with carbidopa and levodopa (Parkinsons disease) to improve carbidopa and levodopa effectiveness

It does this by being an inhibitor of COMT (catechol o methyltransferase); slows down break down of DA

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33
Q

What is levodopa?

A

used to treat parkinson’s disease but effectiveness diminishes as disease progresses;
controls the shake, tremors, shuffling

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34
Q

What do we combo levodopa with carbidopa?

A

The problem with levodopa on its own is that it gets metabolized before it gets into the brain by enzymes.

Large doses of L-DOPA = worked but affected other organs, and changed from LDOPA to NE

Resolution was to add Carbidopa to the mix because it is not permeable to the BBB and blocks LDOPA metab occuring outside the blood brain barrier. allowing conversion of LDOPA to DA in the blood brain barrier ie CNS.

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35
Q

What are side effects of levodopa and carbidopa?

A

dyskinesia - abnormal movements

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36
Q

If you have a patient that is taking LDOPA and Carbidopa, what should you be concerned with in the dental office?

A

Be concerned with administering local anesthetics with epinephrine due to the conversion of LDOPA to NE. Synergistic effects of NE and EPI. Avoid epinephrine when possible. But can limit to 3 cartidges of lidocaine 1:100,000 epi per 30 min period to avoid tachycardia and hypertension

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37
Q

What is benztropine (cogentin)?

A

an anticholinergic, to help with sialorrhea since these patients tend to excessively drool

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38
Q

what is trehexyphenidyl?

A

an anticholinergic; to help with sialorrhea since these patients tend to excessively drool

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39
Q

what is Pramipexole

A

D2 agonist

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40
Q

what is selegiline?

A

an MAO (monoamine oxidase inhibitor) used to increase dopaminergic activity

MAO plays an important role in the catabolism of catecholamines (dopamine, norepinephrine and epinephrine) and serotonin.

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41
Q

what is pramipexole?

A

A D2 agonist. Dopamine agonists may be used first to avoid some of the side effects seen with levodopa-carbidopa therapy. Due to breakdown of levodopa into NE during metabolism

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42
Q

what are the D1 agonists?

A

DA

fendolapam

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43
Q

what are the D2 agonists?

A

DA

selegiline

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44
Q

What tissues do D1 agonists affect?

A

kidney
vasculature
heart
CNS

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45
Q

What tissues do D1 agonists affect on the kidney?
Heart?
Vasculature?

A

Kidney- increase renal blood volume, GFR, and sodium excretion

Heart/vasculature- vasodilation in renal, cerebral, cardiac, and mesenteric vasculature

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46
Q

What tissues do D2 agonists affect?

A

Post ganglionic sympathetic nerve terminals
Chemoreceptor trigger zone
CNS

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47
Q

What tissues do D2 agonists affect on the:
Post ganglionic sympathetic nerve terminals
Chemoreceptor trigger zone
CNS

A

Post ganglionic sympathetic nerve terminals - decrease NT release
Chemoreceptor trigger zone - nausea/vomitting

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48
Q

what is halperidol?

A

A D2 antagonist

Treats schizophrenia

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49
Q

What should you do if your parkinson’s patient is taking selegiline?

A

do not administer agents with epinephrine because of adverse interactions, causing hypertension

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50
Q

What are side effects of L-dopa?

A

glossodynia (burning tongue), trismus, sialorrhea, dark saliva, dysphagia, bruxism, trismus

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51
Q

what are side effects of selegiline?

A

sublingual oral ulcerations, burning lips, mouth, facial grimacing and supraorbital pain

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52
Q

Explain Parkinson’s disease

A

involves degeneration of dopaminergic neurons in the nigral-striatal pathway in the basal ganglia, cause is unknown, but typically associate with hypoxia, toxic chemicals, cerebral infections, and head trauma

Histology: those with parkinson’s find lewy bodies

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53
Q

What is the strategy behind treating Parkinson’s?

A
  1. increase DA in basal ganglia
  2. Block muscarinic receptors in the basal ganglia ince cholinergic functions opposes the actions of dopamine in the basal ganglia
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54
Q

What system does Huntington’s disease affect?

A

GABA pathways

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55
Q

What are the clinical manifestations of huntington’s disease?

A

Abnormal moves (ie corea form) sudden large movements, lack of control with sudden jerky movements.

Cognitive systems begin to deteriorate; progressive intellectual dysfunction

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56
Q

What is the pathophysiology of huntington’s disease?

A

Affects GABA and cholinergic striatal cells

Excessive dopamine activity

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57
Q

Medications for huntingtons disease

A

Antipsychotics (DA antagonists)

Reserpine (DA depletion for choreiform movement)

SSRIs (target seratonin) for depression

Heloperidol (Haldol)- D2 antagonist and antipsychotc

Olanzepine (antipsychotic, binds to DA receptors not just D2)

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58
Q

What are the clinical manifestations of early Alzheimer’s disease?

A

short term memory loss; can fake really well, they still value and prioritize information – determines how well they remember that piece of info
Get lost frequently
Still functional

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59
Q

What are the clinical manifestations of moderate Alzheimer’s disease?

A

decrease functions, difficulty doing jobs, almost impossible to work ability to cope and be productive is gone at this stage –> stop working
This occurs even in the home

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60
Q

What are the clinical manifestations of late Alzheimer’s disease?

A

decrease motor function; no judgement; routine doesn’t work, need assistance from family
Eventually they become immobile and stop eating
Most wil ldie via cachexia

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61
Q

What is the pathophysiology of Alzheimer’s disease?

A 
Beta amyloid (senile palques) form and becomes sticky 
Neurofibrillary tangles – clusters of  tau protein- it’s a microtuble protein that transports

App (amyloid precursor protein)that has been abnormally formed from genetic factors which causes to form sticky Beta amyloid which decrease Ach

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62
Q

What type of drugs are used to treat alzheimer’s disease?

A

cholinesterase inhibitors- targets cognitive and functional decline

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63
Q

What are examples of cholinesterase inhibitors used for alzheimer’s?

A

donepezil
galantamine
rivastigmine

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64
Q

What is multiple sclerosis?

A

A demyelinating disease, An autoimmune disease that destroys myelin, decreasing action potentials thus becoming less functional.

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65
Q

What are the clinical manifestations of MS?

A

Not all the neurons in the brain are demyelinated but can have multiple sites affected.

Its progressive and relapsing – means a lot of on and off, remission varies in time; with each cycle it gets worse, worse and worse
Diverse effects- dependent on where the damage is located

Autonomics- alters cardio, breathing, GI (super serious)

Senses- hearing, taste, vision

Cognition- ant. Cortex affects how you think and make decisions

Mood- depression, fatigue

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66
Q

What medications treat MS?

A

Steroids to treat inflammation

ex. Prednisone

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67
Q

What is myasthenia gravis?

A

a chronic autoimmune neuromuscular disease that causes weakness in the skeletal muscles, which are responsible for breathing and moving parts of the body, including the arms and legs.

Myasthenia gravis is caused by an error in the transmission of nerve impulses to muscles. It occurs when normal communication between the nerve and muscle is interrupted at the neuromuscular junction—the place where nerve cells connect with the muscles they control.

In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction, which prevents the muscle from contracting.

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68
Q

What is the treatment for myasthenia gravis?

A

Acetylcholinesterase inhibitors such as prostigmine and neostigmine

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69
Q

What are anti-psychotic drugs?

A
  1. phenothiazines
  2. haloperidol
  3. thiothixane
  4. atypical antipsychotics
70
Q

What are the 3 derivatives of phenothiazines?

A
  1. aliphatic
  2. piperidine
  3. piperazine
71
Q

Name the aliphatic derivates of phenothizines

A

chlorpromaxine

72
Q

Name the piperidine derivates of phenothizines

A

thioridazine

mesoridazine

73
Q

Name the piperazine derivates of phenothizines

A

fluphenazine
perphenazine
prochlorperazine
trifluoperazine

74
Q

which med is resembles piperazine phenothiazines?

A

halperidol

75
Q

List atypical antipsychotics

A 
clozapine 
olanzapine
quetiapine 
risperidone
ziprasidone
aripiprazole
76
Q

What is the mech of action for treatment of psychosis?

A

Based upon DA hypothesis.
Drugs in the phenothiazine class block DA receptors in the mesolimbic and mesocortical pathways
The key antipsychotic receptor is D2

77
Q

What is mech of action of atypical antipsychotics?

A 
Preferentially inhibit selective DA receptors; 
Inhibit seratonin (5HT) receptors
78
Q

What are adverse effects of antipsychotic drugs?

A

acute dystonias - sustained muscle contractions

akathisia - a movement disorder characterized by a feeling of inner restlessness and inability to stay still.

parkinsonism - tremor, bradykinesia, rigidity, and postural instability.

perioral tremor

malignant syndrome- idiosyncratic reaction to neuroleptic medications that is characterized by fever, muscular rigidity, altered mental status, and autonomic dysfunction. NMS often occurs shortly after the initiation of neuroleptic treatment, or after dose increases

tardive dyskinesia - stiff, jerky movements of your face and body that you can’t control

extrapyramidal effects

antimuscaric effects - adverse motor

orthostatic hypotension

convulsions

photosensitivity

cardiac arrhythmias (long QT)

79
Q

How do antidepressants work?

A

based on increasing seratonin or NE or both at synapses in selective tracts in the brain; treatment takes several weeks to reach full clinical capacity

80
Q

List antidepressant drugs

A
  1. tricyclic antidepressants
  2. SSRIs
  3. MAOIs (monoamine oxidase inhibitiors)
  4. Misc antidepressants
81
Q

Dopaminergic cells groups and related effects of antipsychotics

  1. mesolimbic and mesocortical
  2. nigro-striatal
  3. tubero-infundibular
  4. chemoreceptor trigger zone
  5. medullary-periventricular
A
  1. mesolimbic and mesocortical - antipsychotic effects
  2. nigro-striatal - motor side effects
  3. tubero-infundibular - stim of prolactin release, galactorrhea
  4. chemoreceptor trigger zone - antiemetic (effective against vomiting and nausea)
  5. medullary-periventricular - increased appetite
82
Q

List of trycyclic antidepressants

A 
amytriptyline 
desipramine
doxepin
imipramine
protriptyline
83
Q

List of SSRIs

A 
fluoxetine - prozac
paroxetine - paxil
sertraline - zoloft
fluvoxamine
citalopram - celexa
84
Q

List of MAOIs

A

tranylcypromine

phenelzine

85
Q

Other antidepressants

A 
bupropion
maprotiline
mirtazapine
trazadone
st.johns wort
86
Q

What is the action of many antidepressants?

A
  1. Inhibition of reuptake of 5HT, NE, or both
  2. increase in synaptic concentrations of NT
  3. Desensitization of nerve terminal autoreceptors
  4. increase of neuronal release of NTs
  5. Selective changes in postsynaptic receptors
87
Q

What is the mechanism of action of tricyclic antidepressants?

A

inhibit reuptake of 5HT and NE; inhibition of reuptake leads to a sequence of events which eventually result in an antidepressive effect

88
Q

What is the mech of action of SSRIs?

A

inhibit 5HT

89
Q

what is the mech of action of MAOIs?

A

inhibit metabolism of NE and 5HT in nerve ending

90
Q

what is the mech of action of St.Johns Worts?

A

reduces membrane potential of nerves and thus may indirectly reduce uptake of NE and 5HT

91
Q

what is the mech of action of maprotiline

mirtazapine?

A

inhibit reuptake of NE and 5HT to varying degrees

92
Q

what is the mech of action of bupropion?

A

increasing DA in synapses

93
Q

What are the pharmacokinetics of antidepressants?

A

lipid soluble
long half life
able to be metabolized

94
Q

What are the side effects of tricylic antidepressants?

A

xerostomia (especially amytriptyline)
hypotension
sedation
antimuscarinic effects***

95
Q

What are the “what not to do’s” when administering MAOIs?

A

to not take it with meds that release 5HT and catecholamines and do not take with other antidepressants

96
Q

What are the side effects of SSRIs?

A

nausea
vomiting
diarrhea

97
Q

What are the side effects of MAOIs?

A

hypotension

98
Q

What are the side effects of trazadone?

A

sedation

hypotension

99
Q

What are the side effects of bupropion?

A

very low degree of effects: seizures, hypotension

100
Q

What is the function of dopamine pathways?

A
  • reward (motivation)
  • pleasure,euphoria
  • motor function
  • compulsion
  • decision making
101
Q

What is the function of serotonin pathway?

A
  • mood
  • memory processing
  • sleep
  • cognition
102
Q

Why do we use SSRIs to treat depression?

A

People with depression typically have low serotonin levels thus we want to increase the number or concentration of serotonin in the synapse of nerves.They do this by inhibiting 5ht receptors from re-uptaking 5HT thus accumulation of 5HT begins.

103
Q

What drugs are considered antimania drugs?

A

lithium
carbamazepine
valproic acid

104
Q

what is the mechanism of action of lithium?

A

works inside the cell to block conversion of inositol phosphate to inositol; It inhibits excitatory neurotransmitters such as dopamine and glutamate, and promotes GABA-mediated neurotransmission.

105
Q

what is the mechanism of action of carbamazepine?

A

blocks sodium channels; which prevents repetitive and sustained firing of an action potential

106
Q

what is the mechanism of action of valproic acid

A

blocks sodium and calcium channels;

attributed to the blockade of voltage-gated sodium channels and increased brain levels of gamma-aminobutyric acid (GABA).

107
Q

What happens chemically is manic (bipolar) patients?

A

Dopamine neurotransmission is increased. This elevated state would cause downregulation of dopamine receptors. A consequence of downregulation would be decreased dopaminergic neurotransmission associated with clinical depression.

Lithium inducing downregulation of NMDA receptors. As a reminder, the NMDA receptor is a subtype of glutamate receptor. Glutamate is an excitatory neurotransmitter that is elevated during mania.

Lithium increases GABA levels in cerebrospinal fluid. At the presynaptic level, lithium facilitates GABA release. At the postsynaptic level it upregulates GABA-B receptors. (people with manic disorder have low levels of GABA)

108
Q

what are signs of lithium toxicity?

A

nausea, diarrhea, convulsions, coma, cardiac arrythmias, hypotension,

thyroid enlargement – increase TSH secretion, may cause hypothyroidism

polydipsia, polyuria

109
Q

What are the clinical applications concerning lithium?

A
  1. patients must be warned against sodium restricted diets because sodium restriction leads to greater retention of lithium by the kidney.
  2. lithium inhibits the effect of antidiuretic hormone of the kidney
  3. patients must have regular blood checks due to margin of safety is so narrow
110
Q

What are the drug to drug interactions with lithium?

A

diuretics and newer non-steroidal anti-inflammatory drugs reduce lithium excretion and may cause lithium toxicity

111
Q

what channels are inhibitory?

A

chloride channels

112
Q

which channels are excitatory?

A

sodium channels

113
Q

What channels do sedative hypnotics enhance?

A

chloride channels

114
Q

List sedative hypnotics?

A
  1. benzodiazepines
  2. barbituates
  3. zolpidem
  4. chloral hydrate
  5. buspirone
  6. baclofen
  7. antihistamines
  8. ethyl alcohol
115
Q

Benzodiazepines mechanism of action

A

enhance the effect of GABA at GABAa receptors on chloride channels - increases chloride channel conductance in the brain

116
Q

Barbituates mechanism of action

A

enhance the effect of GABA on the chloride channel but also increase chloride channel conductance independently of GABA

117
Q

Zolpidem mechanism of action

A

enhances GABA by BZ1 receptor

118
Q

Choral hydrate mechanism of action

A

same as barbituates

119
Q

buspirone mechanism of action

A

partial agonist at a specific serotonin receptor

120
Q

baclofen mechanism of action

A

stims GABA b receptors – increase K+ conductance and decrease in Ca2+ conductance

121
Q

antihistamines mechanism of action

A

block H1 histamine receptors – leads CNS to sedation

122
Q

what are the pharm effects of benzos?

A 
antianxiety 
sedation
anticonvulsant
amnesia 
relax skeletal muscle
123
Q

List 3 benzos
Metabolism?
How fast do these drugs metabolize?

A

triazolam midazolam alprazolam
rapid route of metabolism via alpha hydroxylations
short sedative actions

124
Q

what are adverse effects of benzos?

A 
ataxia (lack of muscle coordination) 
confusion
excessive sedation 
amnesia 
altered sleep patterns
125
Q

Long lasting barbituates
List the name of drug?
used for?

A

phenobarbital

treats seizures

126
Q

Intermediate lasting barbituates

used for?

A

amobarbitol, pentobarbital, secobarbital

sleep

127
Q

short lasting barbituates

used for?

A

hexobarbital, methohexital, thiopental

rarely used as IV anesthetics

128
Q 
Benzos: 
Dose response profile
therapeutic index
inducer of liver enzyme
respiratory depression
shortens REM sleep 
potential for abuse
A 
Dose response profile- less steep, reaches a plateau at higher doses
therapeutic index- high 
inducer of liver enzyme- weak
respiratory depression- lower potential
shortens REM sleep- somewhat
potential for abuse- significant
129
Q 
Barbituates 
Dose response profile
therapeutic index
inducer of liver enzyme
respiratory depression
shortens REM sleep 
potential for abuse
A 
Dose response profile- steep no plateau
therapeutic index- low
inducer of liver enzyme- strong
respiratory depression- high potential 
shortens REM sleep- to a sig degree
potential for abuse- higher
130
Q

Zolpidem
metabolism?
used for?
receptors?

A

short half lives (about 2 hours)
used for insomnia
selective action at BZ1 receptor -reduces risk of tolerance and dependence

do not have anticonvulsant action
does not greatly affect sleep patterns

131
Q

Chloral hydrate
metabolism?
used for?
receptors?

A

short acting sleep inducer- metabolized to trichloroethanol
little change on REM sleep
used for conscious sedation in dentistry

132
Q

Buspirone
metabolism?
used for?
abuse potential?

A 
short half life (2-4 hours)
relieves anxiety 
doesnt act as a anticonvulsant
not a good muscle relaxant
minimum abuse potential
133
Q

baclofen

used for?

A

used in spasticity to relax skeletal muscle

occasionally used in trigeminal ganglia

134
Q

example of antihistamines used for sedation

A

diphenhydramine

135
Q

Sedatives used for muscle relaxation

A

carisoprodol
cyclobenzaprine
methocarbamol
baclofen

136
Q

What causes seizures?

A

Inappropriate and excessive activity of motor neurons in the CNS.

137
Q

What are the major receptor targets for antiepileptic drugs?

A
  1. sodium channels
  2. receptors assoc with chloride channels
  3. T-type calcium channels
  4. drugs that inhibit sodium channels, T-type calcium channels, or increase conductance at chloride channels
138
Q

What is the mechanism of phenytoin?

A

blocks sodium channels

139
Q

What is the mechanism of phenobarbitol?

A

binds to chloride channel and increases its conductance

140
Q

What is the mechanism of primidone?

A

binds to chloride channel and increases its conductance

141
Q

What is the mechanism of carbamazepine?

A

blocks sodium channels

142
Q

What is the mechanism of gabapentin?

A

increases synthesis and release of gaba

143
Q

What is the mechanism of tiagabine?

A

binds to chloride channel and increases its conductance

144
Q

What is the mechanism of topiramate?

A

blocks sodium channels

145
Q

What is the mechanism of lamotrigne?

A

blocks sodium channels

146
Q

What is the mechanism of vigabatrin?

A

inhibits GABA reuptake

147
Q

What is the mechanism of valproic acid?

A

blocks sodium channels and T-type calcium channels

148
Q

What is the mechanism of ethosuximide?

A

blocks T-type calcium channels

149
Q

What is the mechanism of clonazepam?

A

binds to chloride channel and increases its conductance

150
Q

What is the mechanism of diazepam?

A

binds to chloride channel and increases its conductance

151
Q

What is the mechanism of zonisamide?

A

blocks sodium channels and T-type calcium channels

152
Q

Pharmokinetics of phenytoin

A
  1. slow absorption with oral use
  2. antacids may decrease absorption
  3. highly bound to plasma protein
  4. often zero order elimination kinetics
  5. metabolized in liver
153
Q

what are other indications for phenytoin?

A

trigeminal neuralgia

154
Q

what are the adverse effects of phenytoin?

A
  1. gingival hyperplasia
  2. CNS: nystagmus, ataxia, vertigo, diplopia
  3. hyperglycemia
  4. lymphadenopathy
  5. osteomalacia
  6. hirsutism
  7. deficiency of folate and megaloblastic anemia
  8. congenital defects due to utero effects
155
Q

what are other indications for carbamazepine?

A
  1. trigeminal neuralgia

2. manic-depressive illness

156
Q

pharmokinetics of carbamazepine

A

metabolized in the liver; inducer of liver enzymes

157
Q

what are the adverse effects of carbamazepine?

A 
GI upset
dizziness, blurred vision
visual disturbances
peripheral neuritis
rashes
jaundice 
aplastic anemia and agranulocytosis (rare)
158
Q

What are the adverse effects of phenobarbital?

A
  1. sedation
  2. neurological and behavioral effects
  3. hepatic toxicitiy
  4. hypersensitivity leading to hematological effects
  5. osteomalacia
  6. respiratory depression
159
Q

What are the adverse effects of primidone?

A

acute systemic and CNS toxicity; sedation, vertigo, nausea, ataxia, diplopia, nystagmus, and hepatic and hematological toxicity

160
Q

what are other indications of gabapentin?

A

neuropathic pain

161
Q

what are the adverse effects of gabapentin?

A

sedation

ataxia

162
Q

what are other indication for valproic acid?

A

manic depressive illness

163
Q

What are the adverse effects?

A 
hair loss
GI upset
hyperglycemia
hyperuricemia
weight gain 
hepatic toxicity 
thrombocytopenia 
teratogenic- may cause spina bifida
164
Q

What are the adverse effects of ethosuximide?

A

GI irritation
CNS depression
Hematological side effects
Lupus

165
Q

what are the drugs of choice for partial seizures?

A

carbamazepine
phenytoin
topiramate

166
Q

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

A

valproate, topiramate

167
Q

what are the drugs of choice for absence seizures?

A

ethosuximide (uncomplicated)

valproate (complicated)

168
Q

What do general anesthetics do?

A

reduces pain and consciousness

169
Q

list inhaled anesthetics

A

halothane
enflurane
isoflurane
sevoflurane

170
Q

list injectable anesthetics

A 
propofol 
thiopental
droperidol
ketamine
etomidate

NBDE II boards (5 decks)

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