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Neuro Pharm Flashcards

1
Q

Lithium

Mechanism (not established)
Clinical use
Adverse effects

A

Mechanism: Not established; possibly related to inhibition of
phosphoinositol cascade.

Uses: Mood stabilizer for bipolar disorder;
blocks
relapse and acute manic events.

Adverse effects Tremor, hypothyroidism, polyuria (causes
nephrogenic diabetes insipidus), teratogenesis.
Causes Ebstein anomaly in newborn if taken by pregnant mother.
Narrow therapeutic
window requires close monitoring of serum
levels. Almost exclusively excreted by
kidneys; most is reabsorbed at PCT with Na+.
Thiazides (and other nephrotoxic agents) are implicated in lithium toxicity.

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2
Q

PCP

A

“hallucinogen”

  • dissociative anesthetic
  • long half life: 24 hours
  • taken orally, IV, smoking, snorted
  • PCP intoxication: psychosis resembling schizophrenia (paranoid, agitated, hallucinating)
  • marked neurological signs: vertical nystagmus, ataxia
  • profound autonomic effects (rapidly changing blood pressure, pulse)
  • NMDA receptor/glutamate (which people found was linked to schizophrenia so it helped understand it.
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3
Q

Riluzole

A

Drug that can slow down progression of ALS by several months. It does this by blocking glutamate which is implicated in neurodegenerative diseases like ALS, Alzheimers, Parkinsons

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4
Q

Name the major types of autonomic receptors and where they are located

A

M1: CNS neurons, sympathetic postganglionic neurons, some presynaptic sites

*M2: myocardium, smooth muscle, some presynaptic sites

M3: exocrine glands, smooth muscle, vessels

*M4: expressed in CNS, forebrain, striatum, cortex, hippocampus

M5: predominant muscarinic receptor in neurons in VTA and substantia nigra

  • opens K+ channels directly (beta subunit)
  • rest works through increased IP3 and DAG, with increased intracellular calcium (alpha subunit)
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5
Q

List therapeutic uses for cholinesterase inhibitors

A

Short acting:
edrophonium •  binds weakly and reversibly to anionic domain of AChE •  rapid renal clearance, brief duration of action
*•  used to diagnose myasthenia gravis (MG)

Intermediate acting inhibitors -

  • rivastigmine for treating Alzheimer’s disease
  • neostigmine, pyridostigmine, ambenonium, treat MG
  • demecarium, physostigmine (physo cross BBB but is used topically)- treats glaucoma

Long-acting inhibitors of acetylcholinesterase: Covalent, not readily reversible
•  organophosphate
insecticides
•  chemical warfare agents

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6
Q

Recognize the major signs and symptoms of cholinergic excess with treatment

A 
. Muscarinic: 
CNS stimulation 
•  miosis (pupil constriction)
•  reflex tachycardia 
•  bronchoconstriction (fight or flight you want to breath more)  
•  excessive GI and GU
smooth muscle activity 
•  increased secretory
activity (sweat, airway,
GI and lacrimal glands) 
•  vasodilation (sympathetic causes vasodilation of arteries carrying blood to muscles but at same time cause vasoconstriction of arteries carrying blood to unnecessary organs 
Nicotinic 
•  CNS stimulation
(convulsions) followed
by depression 
•  neuromuscular end
plate depolarization
(fasciculations, then
paralysis)

Treatment •  if insecticide exposure, decontaminate to
prevent further absorption •  maintain respiration, vital signs •  administer atropine (muscarinic antagonist) •  benzodiazepines for seizures

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7
Q

Cholinesterase inhibitor poisonning DUMBBELSS

A 
Diarrhea
Urination
Miosis
Bronchospasm
Bradycardia 
Excitation (of skeletal muscle and CNS)*
Lacrimation 
Sweating 
Salivation
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8
Q

Understand the mechanism of action of LA’s

Be able to describe the basic chemical structure of LA’s

Understand the effects of pH on the action of LA’s

A

Drug that reversibly blocks impulse
conduction along nerve axons and other
excitable membranes that utilize voltage gated sodium channels as the primary means of action potential generation.
Block Na+ channels in excitable
membranes without changing resting potential.
Reduce aggregate inward sodium
current
-Fibers that fire at a faster rate are more susceptible to the effects of local
anesthetics
Repeated depolarizations produce more effective anesthetic binding

This phenomenon is known as Frequency Dependent Block

Local anesthetics are weak bases
Therefore, the more acidic the pH, the
greater ionized, the more basic, the more neutral [B] form

The neutral form is required to get to site of action but charged form is required for activity.

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9
Q

Cocaine

A
  • stimulant, vasoconstrictor

- used in ENT surgeries because it is a LA and also blocks nasal leakage

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10
Q

Tetracaine

A

A long duration, potent ester primarily used for spinal anesthesia, toxic at relatively low doses
(***exception to short acting ester rule)
-experienced a shortage and basically never made it back to market

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11
Q

Chloroprocaine

A

Used to have a bad rep, now a commonly used quick onset, short duration LA
-primarily used now for pregnancies, used for the last part of labor

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12
Q

Lidocaine

A
  • the perfect local anesthetic
  • non-irritating
  • transient effect
  • low systemic toxicity
  • quick onset
  • action to span duration of surgery

does have TNS implication

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13
Q

Mepivacaine

A

Longer duration than lidocaine

  • *lowest pKa of injectable LA’s so it has one of the quickest onset
  • acts as a vasoconstrictor
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14
Q

Prilocaine

A

Prilocaine: **known associated with methemoglobinemia

-component of EMLA

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15
Q

Bupivacaine

A

Excellent long duration LA with devastating potential for cardiac toxicity.
Sensory block>Motor block - great for pregnancies

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16
Q

Ropivacaine

A

Single enantiomer long duration
LA with properties similar to bupivacaine but
with less cardiotoxicity; vasoconstrictor

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17
Q

Understand the concepts of lipophilicity, pKa, and protein binding as they relate to potency, onset of action, and duration of LA’s

A

The greater the lipophilicity, the greater the potency and duration. However there is also slower onset of action. Often there is a lipid depot surrounding the nerve so there is greater diffusion.

A greater pKa of drug means slower onset of action because it will be more ionized and have difficulty entering cells.

Increased protein binding means increased duration of action

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18
Q

Understand the adverse effects of LA’s

SLAM

A

Systemic toxicity
Local toxicity
Allergic Reactions
Methemoglobin formation

Systemic toxicity: Results from effects of LA on excitable
membranes and tissues other than
target nerves
-Manifest first as CNS toxicity then cardiotoxicity (rule
of thumb)

CNS Toxicity
>Tinnitus, perioral numbness, blurred vision, metallic taste, change in mental state, convulsions.

Cardiotoxicity
>Depression of excitability and
(ventricular prolonged QRS) as well as arteriolar dilation (Calcium channel effect)
> Bupivacaine is very cardiotoxic (R+)
> Ropivacaine less toxic (S-)
> Systemic acidosis or hypercarbia ­ increased sensitivity to LA toxicity (their pH is more acidic, trapping the LA in circulation)
>Pregnancy ­ sensitivity to toxic effects **Rescue is by IV Lipid Emulsion (drawing the lipophilic drugs out)

Local injury:
Neural Injury
High concentrations of local for extended periods can lead to nerve tissue destruction via membrane damage, cytoskeletal disruption, etc. but not due to blockade of the Na channel
-Motor and sensory loss are seen (e.g. cauda equina syndrome): If patients with cauda equina syndrome do not receive treatment quickly, adverse results can include paralysis, impaired bladder, and/or bowel control, difficulty walking
-Paralysis and paresis may result
*Transient Neurologic Symptoms (TNS)
Transient pain syndrome associated with spinally administered Lidocaine and certain surgical positions (e.g. lithotomy)
**NOT associated with motor or sensory loss, it just hurts! A self limited neuropathic pain syndrome

Esters
>PABA ® hapten formation ® true IgE mediated allergy

Amides
-do not form the same metabolites and *Methylparaben, preservative, can cause allergic reactions irrespective of LA type

Prilocaine metabolites (O-toluidine)
act as an oxidizing agent to convert
Hb++ to Hb+++
Benzocaine has also been implicated Chocolate colored blood
Pulse oximeter = 85% saturation w Treatment is with methylene blue

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19
Q

Understand the concept of methemoglobinemia as it relates to LA’s

A

Prilocaine metabolites (O-toluidine)
act as an oxidizing agent to convert
Hb++ to Hb+++

Benzocaine has also been implicated
Chocolate colored blood
Pulse oximeter = 85% saturation
Treatment is with methylene blue

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20
Q

What are the mechanisms of opioids (assuming mew opioid)

A

Presynaptic neuron
• Inhibits adenylyl cyclase-catalyzed formation of cAMP [cAMP]↓
•Closes Ca2+ channels [Ca2+]↓
→ ↓ synaptic transmission
→ ↓ release of neurotransmitters
that convey pain perception (e.g., ACh, substance P, glutamate)

Postsynaptic neuron 
• Opens K+ channels [K+]↑
→ hyperpolarization of cell
• ↓ firing of neuron 
• ↓ neuron excitability & pain
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
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21
Q

Morphine/Heroin

A

Hydrophilic drug, so CNS penetration and exit are slow, slow onset and long duration, T1/2 = 2-4 hr.
• Fairly rapid absorption, wide distribution, rapid hepatic clearance.
 Polar active metabolites cleared by kidney (caution in renal dysfunction).  Heroin (diamorphine), a more lipophilic prodrug of morphine, exhibits faster CNS penetration.

____________________________
analgesia for acute pain
• pain associated with severe injuries, post-surgery, bone/joint/muscle ailments
 major exception: contraindicated in head injuries** (they tend to increase intracranial pressure)
• myocardial infarction (MI) and angina (most important uses of morphine today)
• pulmonary edema (left ventricle hypertrophy - LVH ) - because of vasodilating effects
• cancer patients (fentanyl IM or IV is an alternative if patient becomes tolerant to morphine).

22
Q

Oxycodone/Hydrocodone

A

Oral analgesics for moderate, chronic pain.

23
Q

Fentanyl

A

regional anesthesia (e.g., spinal or epidural anesthesia)

80-100 times more powerful than morphine.
• Lipophilic drug, so very fast CNS penetration, fast onset and short duration, T1/2 < 1 hr.
• Multiple delivery routes: patch, intrathecal, intranasal spray, and buccal mucosa (fentanyl “lollipop”).

24
Q

Codeine or dextromethorphan

A

cough suppressant

cough suppressed by d-isomers of opioids (e.g. dextromethorphan) which have no analgesic activity

25
Q

Diphenoxylate or loperamide

A

.for relief from diarrhea (preferred due to lower BBB penetration).

26
Q

Methylnaltrexone

A

for relief of opioid-induced constipation.

27
Q

Vicodin, Percocet

A

Hydrocodone/acetaminophen (Vicodin)

Oxycodone/acetaminophen (Percocet) are two widely prescribed orally active opioid formulations for moderate to severe pain.

 Dosage is monitored by the need to limit acetaminophen (APAP) to <4 g/day in normal person (much
lower doses for alcoholics and for patients with impaired liver function).  Over past decade, the number of overdose deaths from prescription opioids has increased sharply
(Opioid Crisis).

28
Q

Describe respiratory depression

A

Opioids decrease the brain’s response to CO2 in the respiratory center.

This increase arterial CO2 which causes vasodilation in the brain.

This is why there is an increase in ICP.

  • Subnormal drive to breathe, despite normal respiratory rate.
  • Effects are dose-dependent: Very high doses may cause irregular breathing and apnea.

-Respiratory depression is the major toxicity of opioids and nearly always the cause of death from overdose.

Equi-analgesic doses of all opioids produce equivalent amounts of respiratory depression. (this is the consistency)

 Difficult to reverse respiratory depression w/o losing some analgesic effects.

However, do not give O2, give naloxone, an opioid antagonist.

29
Q

What are the acute clinical effects of opioids

  1. PBU His M N C My CS E R A
A

EFFECTS - all “u” opioid agonists
1. ANALGESIA

  1. RESPIRATORY DEPRESSION > increase in ICP
  2. EUPHORIA
    (decrease release of GABA in neuron, relieves inhibition resulting in release of dopamine in neighboring neuron)
  3. COUGH suppression
    (Depression of cough centers in the medulla.
    -Different molecular mechanism from analgesia or respiratory depression.
    - cough suppressed by d-isomers of opioids (e.g. dextromethorphan) which have no analgesic activity.
    - codeine or dextromethorphan is the preferred agent, rather than morphine.
  4. MIOSIS (pupil constriction): Miosis caused by stimulation of Edinger-Westphal (parasympathetic) nucleus of the oculomotor nerve.  Miosis (pinpoint pupils) is a visible signature of opioid overdose.
     Reversed by naloxone, atropine.
    *one exception is meperidine (demerol) which produces mydriasis
  5. CONSTIPATION:
    GI: Intestine and Stomach
    • ↓peristalsis in small and large bowels, constipation, cramping.
    • Chronic administration of opioids frequently requires laxatives.
    • Methylnaltrexone approved for treatment of opioid-induced constipation.
    Note: Opioids are useful for treatment of diarrhea. Diphenoxylate (Lomotil®) and loperamide (Imodium®) are preferred due to their lack of central effects (not CNS absorbed).
  6. Nausea and Vomiting
     Stimulation of the chemoreceptor trigger zone *(CTZ) in the area postrema - activates vomiting center.
     Emetic effects caused by stimulation of vestibular apparatus - ambulatory patients more likely to vomit than
    those lying quietly.
  7. Muscle Rigidity (skeletal tonus)
    • Large IV doses can cause generalized stiffness of skeletal muscle.
    • Most common with fentanyl and related opioids.
    • May play a role in some overdose fatalities.
  8. Histamine Release
    • Full agonists (e.g. morphine, fentanyl) can cause non-immunologic release of histamine,
    inducing vasodilation and hypotension. • May cause skin redness, urticaria (hives, rash), and pruritus (itchy skin) near injection site. • Not an allergic reaction - true allergic responses to opioids are rare.
    urticaria
  9. BILIARY + URINARY
    Can induce spasmotic effects on smooth muscle along the biliary tree
    and sphincter of Oddi.
    • Can precipitate biliary colic (gall bladder attack).
    c. Urinary Tract • Anti-diuretic effect can cause urinary retention.
  10. Effects on Pregnancy and the Neonate
    • Opioids are sometimes used sparingly to relieve labor pain (e.g., fentanyl, butorphanol, meperidine). • All opioids cross the placenta, thus may cause respiratory depression in baby. • Chronic use may cause physical dependence in utero and life-threatening neonatal withdrawal after delivery. • Treatment of choice for opioid addicted mother & newborn: methadone.
    Effects on Pregnancy and the Neonate
    • Opioids are sometimes used sparingly to relieve labor pain (e.g., fentanyl, butorphanol, meperidine). • All opioids cross the placenta, thus may cause respiratory depression in baby. • Chronic use may cause physical dependence in utero and life-threatening neonatal withdrawal after delivery. • Treatment of choice for opioid addicted mother & newborn: methadone.
30
Q

Describe the chronic effects of opioid

A
  1. Opioid Tolerance
    • Reduction in effect with repeated dosing (need higher dose to produce same effect).
    • Cross-tolerance to other opioids (additivity effect).
    • Tolerance develops rapidly (2-3 wks) to analgesia, *respiratory depression, euphoria.
    • No tolerance to miosis and constipation – they occur immediately with 1st dose.

Clinical Characteristics: • Heroin addicts or methadone maintenance patients may have little euphoria from high doses but continue
to experience constipation and miosis. • Terminal cancer patients requiring high doses for analgesia are also tolerant to respiratory depression, but
they frequently require laxatives for constipation.

  1. Physical Dependence
    • Giving opioid antagonist (e.g., naloxone) to physically dependent person causes abrupt withdrawal
    (abstinence) syndrome - usually not life-threatening to adult.
    • Symptoms stop when small dose of opioid is given.
    • Withdrawal symptoms: sweating, rhinorrhea (runny nose), vomiting, diarrhea, piloerection (goose bumps),
    mydriasis, shaking chills, drug seeking behavior.
    • Management of withdrawal: Supportive care, methadone.
    • Distinction between physical dependence (natural need for higher doses for analgesia) and psychological
    dependence (addiction, craving a “high”). Mild physical dependence is common in clinical setting.
14. Opioid overdose (intoxication)
Classic triad (MAR-means to spoil) 
Miosis 
Apnea, coma
Respiratory depression
31
Q

Buprenorphine

A

only partial agonist

Buprenorphine (alternative to methadone)
• Partial agonist at µ receptor - higher doses do not increase effects, ↑ margin of safety.
• Long-lasting: T½ >24 hrs, less likely to cause respiratory depression.
• Prescribed as buprenorphine/naloxone combo (Suboxone®), given orally as a sub-lingual tablet or film (don’t swallow).
• The naloxone is added to make the combo “abuse resistant”.

32
Q

Naltrexone

A

Antagonist of all opioid receptors (µ, κ, δ).
Blocks effects of heroin, morphine, methadone, etc. • Prescribed for patients after opioid detoxification to prevent relapse.
• To detoxify patient, Methadone or Buprenorphine/Naloxone dosage is slowly tapered to wean patient off drug.
• Once sufficiently detoxified (withdrawal free), patient is often prescribed Naltrexone PO for relapse prevention.

  • Long-acting opioid antagonist used for maintenance therapy and relapse prevention once detoxified.
  • Orally active
  • Not recommended for emergency overdose treatment.
33
Q

Naloxone

A

Intravenous Naloxone (Narcan) is widely used for emergency opioid overdose/intoxication.
• Pure, competitive antagonist at µ, κ, and δ receptors.
• Rapidly reverses opioid overdose when injected IV or IM, but it has short duration (T1/2 ~ 1 hr). Gives
immediate relief from acute respiratory depression, but can induce severe withdrawal symptoms – not life-
threatening to adult. Multiple or continual dosing may be required due to its short T1/2.
• Not orally active.
• Naloxone is added to many abuse-prone opioid drugs (e.g., oxycodone, buprenorphine) to render them
“abuse resistant”.

Mechanism: naloxone’s effects are minimal when taken orally with oxycodone or buprenorphine due to its poor absorption but will induce rapid withdrawal symptoms if oxycodone/naloxone or buprenorphine/naloxone is injected for a ‘high’.

34
Q

Nalorphine, pentazocine, nalbuphine, butorphanol

A

Act as κ agonists to produce analgesia, and as µ antagonists.

Developed in search for analgesics with less abuse potential and lower respiratory depression.

Clinical Characteristics of Mixed Agonist-Antagonists:
• Effective analgesics for moderate to severe pain.
• Limited toxicity (reduced respiratory depression or smooth muscle effects). • Decreased abuse potential, but also decreased patient acceptance due to side effects (dysphoria)- a state of unease or generalized dissatisfaction with life .

• Drawback: As µ antagonists, they can precipitate acute withdrawal in heroin or morphine addicts.

35
Q

What is the treatment of shingles

A

An antiviral (like acyclovir) and local anesthetic lidocaine.

36
Q

Tenzolomide

A

a commonly used anti-glioma chemotherapy agent.

MGMT (methylguanine-DNA-methyltransferase) removes the DNA adduct formed by DNA’s reaction

So the more methylated the MGMT gene, the more vulnerable a tumor will be to tenzolomide

37
Q

succinylcholine: clean up crew gets shock while cleaning up “SUCKS grafity”

A

succinylcholine: a nicotinic agonist
less readily hydrolyzed than ACh prolongs channel opening leads to muscle relaxation administered parenterally
charge limits penetration to CNS

Prolonged agonist occupancy prevents recovery of the membrane potential and the muscle relaxes

It is the only DEPOLARIZING NMJ blocking agent.

38
Q

M2 & M3

A

M2: smooth muscle, MYOCARDIUM - opens K+ channels, inhibition of adenylyl cyclase

M3: smooth muscle, EXOCRINE glands, vessels - IP3, DAG, intracellular calcium increases.

so think muscle, two, three, plant the tree

1,4,5 - makes you feel alive

39
Q

M1, M4, M5

A

All are expressed in the CNS!

M1: sympathetic postganglionic neurons - increases IP3, DAG and intracellular calcium

M4: forebrain especially, striatum, cortex, hippocampus - opens K+ channels, inhibits adenylyl cyclase

M5: VTA and substantia nigra - increases IP3, DAG and intracellular calcium

40
Q

Sweat glands are sympathetic nervous system (evidenced by Horner’s syndrome). Then why would muscarinic antagonists lead to “dry as a bone” presentation?

A

Sweat glands are special! Despite being sympathetic they feature M3 (muscarinic) receptors with an acetylcholine NT. So anti-muscarinic drugs will interfere with sweat.

41
Q

What is edrophonium

A

It is a short acting reversible inhibitor of acetylcholinesterase.

binds weakly and reversibly to anionic domain of AChE
•  rapid renal clearance, brief duration of action
•  used to diagnose myasthenia gravis (MG)
-on an exam, a patient could be currently treated for MG. She is either undertreated or overtreated leading to too much acetylcholine and causing refractory NMJ receptors. A small dose of edrophonium, if she improves that means she needs more acetylcholine.
Or exacerbates the crisis. Cholinergic excess.

-it removes muscle weakness symptoms for 5-15 min so its not useful for treatment.

42
Q

What are signs of cholinergic excess?

A

Muscarinic:

CNS stimulation - seizures
Miosis
Reflex tachycardia
Bronchoconstriction
Excess GI and GU smooth muscle activity

increased secretory activity (sweat, airway, GI and lacrimal glands, vasodilation)

Treatment •  if insecticide exposure, decontaminate to
prevent further absorption
•  maintain respiration, vital signs
•  administer atropine (muscarinic antagonist) + pralidoxime (organophosphate poisoning treatment)
•  benzodiazepines for seizures

43
Q

Phenylephrine: (neuro)

A

alpha agonist

-dilator muscle of eye has alpha receptors, this is to facilitate increase in pupil size similar to effects of tropicamide.

44
Q

Bevacizumab

A

In age related macular degeneration, there is neovascularization mediated by VEGF which is leaky and can cause blindness.

Bevacizumab is an antibody that soaks up all the free vegf.

45
Q

Bethanechol: “Beth the construction worker”

A

Muscarinic agonist:

-increases secretion of the gut (cement spilling out). “Do not obstruct”, used for non-obstructive GI issues, post op ileus. It can also be used for urinary retention since it activates the detrusor muscles.

46
Q

Pilocarpine (pile o carp),

A

dripping water,

Pilocarpine increases salivation (dry mouth caused by Sjogren’s syndrome).

Can also be used for glaucoma. (activating the ciliary body) “net”.

Also causes miosis- important for acute glaucoma.

47
Q

Carbachol varenicline

A

-glaucoma treating agent: constricted hood blocking carbon fumes

it is a muscarinic and nicotinic agonist.

48
Q

Pyridostigmine

Neostigmine

A

Pyridostigmine is the drug of choice for Myasthenia gravis - an autoimmune disease targetting nicotinic receptors.

They increase acetylcholine at NMJ’s so it can outcompete with the antibodies.

Neostigmine is not as widely used for this. It can also treat ileus and reversal of neuromuscular blockade.

49
Q

Physostigmine (phys ed)

A

acetylcholinesterase with central effects - works through competitive effects.

-treats atropine in wonderland: atropine overdose (mad as a hatter, hot as a hare, blind as a bat)

Belladonna flower -nightshade, which contains naturally occurring atropine.

Jimson week (gym) - also overdose of atropine (gardeners mydriasis)

50
Q

DUMBBELS - sweaty kid struggling with weights, too weak to lift them.

A

diarrhea, urination, miosis, bronchospasm, bradycardia, lacrimation, salivation

Cholinesterase inhibitor toxicity effects

Important is that cholinesterase inhibitors can also activate nicotinic receptors which with over activation causes flaccid paralysis

Commonly - organophosphate poisoning. Parathion, malathion,. Muscarinic and nicotinic symptoms. CNS involvement follows rapidly causes convulsions.

Person brought to ER, after gardening, he has bradycardia, tearing excessively, and can’t breath. Acute organophosphate have to recognized immediately. Aging organophosphate+acetylcholinesterase will become irreversible. Pralidoxime

51
Q

PraLIDoxime + Atropine

A

regenerates acetylcholinesterase to reverse cholinergic toxicity induced by organophosphate including flaccid paralysis. However it will NOT reverse the symptoms of CNS. because it can’t enter

Atropine an muscarinic antagonist “alice was here”. It can’t reverse the paralysis since it only acts muscarinic

52
Q

Donepezil, galantamine, rivastigmine

A

All three penetrate the CNS to treat alzheimers, “brain puzzle”

Alzheimers GALA , REVERSE the STIGMA, DONE with the puzzle.

With extra acetylcholine, these elderly patients can have serious side effects.

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