Block 4 Quiz Flashcards
Phenobarbital, Pentobarbital, Thiopental, & Secobarbital
MOA:
Clinical use:
Adverse effects:
Barbiturates
MOA:
Facilitates GABA(A) by increasing the duration of Cl- channel opening to reduce neural firing
Clinical use:
1) Sedative
2) Anesthesia
Adverse effects:
1) Cardio-respiratory failure (fatal)
2) CNS depression
3) Dependence
AVOID in porphyria patients
Phenobarbital, Pentobarbital, Thiopental, & Secobarbital
Barbiturates
MOA:
Facilitates GABA(A) by increasing the duration of Cl- channel opening to reduce neural firing
Clinical use:
1) Sedative
2) Anesthesia
Adverse effects:
1) Cardio-respiratory failure (fatal)
2) CNS depression
3) Dependence
AVOID in porphyria patients
Barbiturates
Diazepam, Lorazepam, Triazolam, Temazepam, Oxazepam,
Clonazepam, Clorazepate, Midazolam, Chlordiazepoxide, & Alprazolam
Clonazepam, Clorazepate
MOA:
Clinical use:
Adverse effects:
Overdose treatment:
Which ones are used in liver diseased patients:
Benzodiazepines
MOA:
Facilitate GABA(A) by increasing the frequency of Cl- channel opening to reduce neuronal firing & REM sleep
Clinical use:
1) Anxiety, Panic disorder, Epilepsy, Spasticity (L, D, M)
2) Eclampsia & Alcohol detox (C & D)
3) Night terrors/Sleep walking
4) General anesthesia
Adverse effects:
1) CNS & Respiratory depression
2) Dependence
OD Rx:
Flumazenil
Liver diseased drank a LOT
Barbiturates Toxicity can be treated with which drug?
Sodium bicarbonate (to alkalinize urine and enhance renal excretion)
Diazepam, Lorazepam, Triazolam, Temazepam, Oxazepam,
Clonazepam, Clorazepate, Midazolam, Chlordiazepoxide, & Alprazolam
MOA:
Facilitate GABA(A) by increasing the frequency of Cl- channel opening to reduce neuronal firing & REM sleep
Clinical use:
1) Anxiety, Panic disorder, Epilepsy, Status epilepticus (acute seizures) (L, D, M)
2) Eclampsia & Alcohol/benzo withdrawal (delirium tremens) (C & D)
3) Night terrors/Sleep walking
4) General anesthesia
Adverse effects:
1) CNS & Respiratory depression
2) Dependence
OD Rx:
Flumazenil
Liver diseased drank a LOT
Benzodiazepines
Zolpidem, Zaleplon, & esZopiclone
MOA:
Clinical use:
Adverse effects:
Non-Benzodiazepine hypnotics
MOA:
Bind & potentiate potentiating BZ1 (increase frequency of chloride channel opening) to induce sleep
Clinical use:
Insomnia
Adverse effects:
1) Ataxia
2) Headaches/Confusion
3) Mild psychomotor depression
Clonazepam is useful in the therapy of __________
Absence seizures and myoclonic seizures in children
Diazepam currently is the drug of choice for the treatment of __________
status epilepticus
Zolpidem, Zaleplon, & esZopiclone
MOA:
Bind & potentiate potentiating BZ1 (increase frequency of chloride channel opening) to induce sleep
Clinical use:
Insomnia
Adverse effects:
1) Ataxia
2) Headaches/Confusion
3) Mild psychomotor depression
Non-Benzodiazepine hypnotics
Suvorexant
MOA:
Clinical use:
Adverse effects:
MOA:
Antagonizes orexin (hypocretin)
Clinical use:
Insomnia
Adverse effects:
1) CNS depression
2) Headache
MOA:
Antagonizes orexin (hypocretin)
Clinical use:
Insomnia
Adverse effects:
1) CNS depression
2) Headache
Suvorexant
Ramelteon
MOA:
Clinical use:
MOA:
Binds MT1/2 (Melatonin) in suprachiasmatic nucleus
Clinical use:
Insomnia
No dependence
MOA:
Binds MT1/2 (Melatonin) in suprachiasmatic nucleus
Clinical use:
Insomnia
No dependence
Ramelteon
Carbidopa & Levodopa
MOA:
Clinical use:
Adverse effects:
MOA:
Peripheral DOPA decarboxylase inhibitor (given with L-DOPA which crosses the BBB) to increase the availability of L-DOPA in the brain
Clinical use:
Parkinsons
Adverse effects:
1)“On-off” phenomenon with long-term
MOA:
Peripheral DOPA decarboxylase inhibitor (given with L-DOPA which crosses the BBB) to increase the availability of L-DOPA in the brain
Clinical use:
Parkinsons
Adverse effects:
1)“On-off” phenomenon with long-term
Carbidopa & Levodopa
Amantadine
MOA:
Clinical use:
Adverse effects:
NMDA receptor antagonist that
blocks muscarinic receptors to increase DA release & reduce its uptake in presynaptic neurons
Clinical use:
Parkinsons
Adverse effects:
1) Anticholinergic
2) Livedo reticularis **
3) ankle edema
4) Ataxia
NMDA receptor antagonist that
blocks muscarinic receptors to increase DA release & reduce its uptake in presynaptic neurons
Clinical use:
Parkinsons
Adverse effects:
1) Anticholinergic
2) Livedo reticularis **
3) ankle edema
4) Ataxia
Amantadine
Selegine & Rasagiline
MOA:
Clinical use:
Adverse effects:
MOA:
Inhibit MAO-B, increasing the availability of DA in the brain
Clinical use:
Parkinson & combats the “wearing off” effect of long-term L-DOPA use
Adverse effects:
1)May enhance adverse effects of L-DOPA
MOA:
Inhibit MAO-B, increasing the availability of DA in the brain
Clinical use:
Parkinson & combats the “wearing off” effect of long-term L-DOPA use
Adverse effects:
1)May enhance adverse effects of L-DOPA
Selegine & Rasagiline
Tolcapone & Entacapone
MOA:
Clinical use:
Adverse effects:
MOA:
COMT inhibitor that increases levodopa availability in brain
Tolcapone (peripheral + central)
Entacapone (peripheral only)
Clinical use:
Parkinsons (Only given with levodopa)
Adverse effects:
1) Hepatotoxicity (tolcapone only)
MOA:
COMT inhibitor that increases levodopa availability in brain
Clinical use:
Parkinsons (Only given with levodopa)
Adverse effects:
1) Hepatotoxicity
Tolcapone & Entacapone
Ketamine
MOA:
Clinical use:
Adverse effects:
NMDA receptor antagonist (PCP analog) that blocks excitation by glutamate to reduce neural conductivity
Clinical use:
1) Analgesia & Amnesia
2) Catatonia
3) Induction &
maintenance of anesthesia
Adverse effects:
1) Dissociative amnesia **
2) Increased intracranial pressure
3) Emergence reactions
Avoid in HTN & IHD
NMDA receptor antagonist (PCP analog) that blocks excitation by glutamate to reduce neural conductivity
Clinical use:
1) Analgesia & Amnesia
2) Catatonia
3) Induction &
maintenance of anesthesia
Adverse effects:
1) Dissociative amnesia **
2) Increased intracranial pressure
3) Emergence reactions
Avoid in HTN & IHD
Ketamine
Pramipexole & Ropinirole
MOA:
Clinical uses:
Adverse effects:
Non-ergot dopamine agonist that activates DA
Clinical uses:
1) Parkinson
2) Restless leg syndrome
Adverse effects:
1) Impulse control disorder
2) Hallucinations
3) Postural hypotension
4) Confusion
Non-ergot dopamine agonist that activates DA
Clinical uses:
1) Parkinson
2) Restless leg syndrome
Adverse effects:
1) Impulse control disorder
2) Hallucinations
3) Postural hypotension
4) Confusion
Pramipexole & Ropinirole
Bromocriptine
MOA:
Clinical uses:
Adverse effects:
Ergot dopamine agonist
acting selectively on D2 receptors
Clinical use:
1) Parkinsons
2) Hyperprolactinemia
Adverse effects:
1) Anticholinergic effects
2) Raynaud Phenomenon
Ergot dopamine agonist
acting selectively on D2 receptors
Clinical use:
1) Parkinsons
2) Hyperprolactinemia
Adverse effects:
1) Anticholinergic effects
2) Raynaud Phenomenon
Bromocriptine
Donepezil (1#), Rivastigmine, Galantamine
MOA:
Clinical uses:
Adverse effects:
MOA:
AChE inhibitors
Clinical use:
Alzheimer’s
Adverse effects:
1) Insomnia
Avoid in patients with cardiac conduction issues
MOA:
AChE inhibitors
Clinical use:
Alzheimer’s
Adverse effects:
1) Insomnia
Avoid in patients with cardiac conduction issues
Donepezil (1#), Rivastigmine, Galantamine
Memantine
MOA:
Clinical use:
Adverse effects:
MOA:
Regulates glutamate to prevent excitotoxicity.
Clinical uses:
1) Alzheimer’s (moderate to advanced dementia)
Adverse effects:
1) Confusion & Hallucination
MOA:
Regulates glutamate to prevent excitotoxicity.
Clinical uses:
1) Alzheimer’s (moderate to advanced dementia)
Adverse effects:
1) Confusion & Hallucination
Memantidine
Riluzole
MOA:
Clinical uses:
MOA:
Reduces glutamate excitotoxicity in neurons
via (Na+, GABA, glutamate, NMDA) to reduce motor neuron degeneration
Clinical use:
ALS (slows progression)
MOA:
Reduces glutamate excitotoxicity in neurons
via (Na+, GABA, glutamate, NMDA) to reduce motor neuron degeneration
Clinical use:
ALS (slows progression)
Riluzole
Tetrabenazine
MOA:
Clinical use:
MOA:
Inhibits VMAT to reduce DA release & degradation from monoamine oxidase
Clinical use:
Huntington’s
MOA:
Inhibits VMAT to reduce DA release & degradation from monoamine oxidase
Clinical use:
Huntington’s
Tetrabenazine
Desflurane, Halothane, Enflurane, Isoflurane, Sevoflurance, Methoxyflurane, & N2O
MOA:
Clinical use:
Adverse effects:
Inhaled anesthetics
(slow onset of action and slow recovery)
Clinical use:
1) Anesthesia maintenance
Adverse effects:
1) Hepatotoxicity (halothane)
2) Cardiorespiratory depression
3) Increased cerebral blood flow & ICP
4) Malignant hyperthermia
5) Nephrotoxicity (methoxyflurane)
Inhaled anesthetics
(slow onset of action and slow recovery)
Clinical use:
1) Anesthesia maintenance
Adverse effects:
1) Hepatotoxicity (halothane)
2) Cardiorespiratory depression
3) Increased cerebral blood flow & ICP
4) Malignant hyperthermia
5) Nephrotoxicity (methoxyflurane)
Inhaled anesthetics
Malignant hyperthermia
Pathology:
Triggers:
Treatment:
Path:
RYRI (ryanodine) mutation exposed to inhaled anesthetics causing Ca2+ release from the SR resulting severe muscle contractions & hyperthermia
Triggers:
Inhaled anesthetics
Treatment:
Dantrolene
Path:
RYRI (ryanodine) mutation exposed to inhaled anesthetics causing Ca2+ release from the SR resulting severe muscle contractions & hyperthermia
Triggers:
Inhaled anesthetics
Treatment:
Dantrolene
Malignant hyperthermia
Thiopental
MOA:
Clinical uses:
Adverse effects:
short-acting barbiturate that facilitates GABA channels in the brain, it has high lipid solubility & fast onset.
(increasing the duration that the chloride channels opening)
Clinical use:
IV anesthetic
Adverse effects:
1) CNS & Respiratory depression
short-acting barbiturate that facilitates GABA channels in the brain, it has high lipid solubility & fast onset.
(increasing the duration that the chloride channels opening)
Clinical use:
IV anesthetic
Adverse effects:
1) CNS & Respiratory depression
Thiopental
Midalozam
MOA:
Clinical use:
Adverse effects:
Benzodiazepine
that Facilitate GABA(A) (increasing the frequency of Cl- channel opening) to reduce neuronal firing (REM sleep)
Clinical Use:
1) Induce general anesthesia
Adverse effects:
1) Severe post-operative respiratory depression
2) Low BP
3) Anterograde amnesia
Benzodiazepine
that Facilitate GABA(A) (increasing the frequency of Cl- channel opening) to reduce neuronal firing (REM sleep)
Clinical Use:
1) Induce general anesthesia
Adverse effects:
1) Severe post-operative respiratory depression
2) Low BP
3) Anterograde amnesia
Midalozam
Propofol
MOA:
Clinical use:
Adverse effects:
GABA agonist
Clinical use:
IV anesthetic with strong sedative properties
Adverse effects:
1) profound hypotension (combo of reduced SVR and cardiac depression)_
GABA agonist
Clinical use:
IV anesthetic with strong sedative properties
Adverse effects:
1) profound hypotension (combo of reduced SVR and cardiac depression)_
Propofol
Haloperidol
MOA:
Clinical use:
Adverse effects:
Typical antipsychotic
that Inhibits D2 receptors
Clinical uses:
1) +ve Schizophrenia symptoms
2) Tourette’s syndrome
3) Acute psychosis
4) Bipolar delirium
5) Huntington
6) OCD
Adverse effects:
1) NMS
2) EPS
3) Hyperprolactinemia
4) Prolonged QT
5) Anticholinergic
Typical antipsychotic
that Inhibits D2 receptors
Clinical uses:
1) +ve Schizophrenia symptoms
2) Tourette’s syndrome
3) Acute psychosis
4) Bipolar delirium
5) Huntington
6) OCD
Adverse effects:
1) NMS
2) EPS
3) Hyperprolactinemia
4) Prolonged QT
5) Anticholinergic
Haloperidol
Neuroleptic malignant syndrome
Pathology:
Triggers:
Treatment:
Path:
Life-threatening reaction to antipsychotics
characterized by:
1) Fever
2) Muscle RIGIDITY (“lead pipe” rigidity)
3) Elevated creatinine kinase (CK)
4) Altered mental status
5) Autonomic dysfunction
6) Unstable vitals (BP, HR)
Triggers:
Haloperidol & Antipsychotics
Treatment:
1) Stop drug then give
2) Dantrolene
(Muscle relaxant → Reduces muscle rigidity and metabolic demand)
3) Bromocriptine or Amantadine
(Dopamine agonists → Counteract dopamine blockade)
Path:
Life-threatening reaction to antipsychotics
characterized by:
1) Fever
2) Muscle RIGIDITY (“lead pipe” rigidity)
3) Elevated creatinine kinase (CK)
4) Altered mental status
5) Autonomic dysfunction
6) Unstable vitals (BP, HR)
Triggers:
Haloperidol & Antipsychotics
Treatment:
1) Stop drug then give
2) Dantrolene
(Muscle relaxant → Reduces muscle rigidity and metabolic demand)
3) Bromocriptine or Amantadine
(Dopamine agonists → Counteract dopamine blockade)
Neuroleptic malignant syndrome
Extrapyramidal symptoms- Acute dystonia
Pathology:
Treatment:
Acute (hours),
MUSCLE
Treatment:
1)Anticholinergics
- Trihexyphenidyl
- Benztropine
2) Antihistamines
- diphenhydramine
Acute (hours),
MUSCLE
Treatment:
1)Anticholinergics
- Trihexyphenidyl
- Benztropine
2) Antihistamines
- diphenhydramine
Extrapyramidal symptoms- Acute dystonia
Extrapyramidal symptoms- Akathisia
Pathology:
Treatment:
Sub chronic (days)
RUSTLE
Treatment:
- Benztropine
- Benzodiazepines
Sub chronic (days)
RUSTLE
Treatment:
- Benztropine
- Benzodiazepines
Extrapyramidal symptoms- Akathisia
Extrapyramidal symptoms- Akinesia/Parkinsonism
Pathology:
Treatment:
Sub chronic (weeks)
1) Bradykinesia
2) Cogwheel rigidity
3) Tremor/Shuffling gait
Treatment:
Benztropine or Amantadine
Sub chronic (weeks)
1) Bradykinesia
2) Cogwheel rigidity
3) Tremor/Shuffling gait
Treatment:
Benztropine or Amantadine
Extrapyramidal symptoms- Akinesia/Parkinsonism
Extrapyramidal symptoms- Tardive dyskinesia
Pathology:
Trigger:
Treatment:
Path:
Chronic (months to years)
1) Involuntary repetitive movements, primarily of the face, tongue, and neck (lip smacking, sticking out tongue, grimacing)
IRRIVERSIBLE! unless caught early
Trigger:
- DA Antagonist
- VMAT 2 Inhibitor
Path:
Chronic (months to years)
1) Involuntary repetitive movements, primarily of the face, tongue, and neck (lip smacking, sticking out tongue, grimacing)
IRRIVERSIBLE! unless caught early
Trigger:
- DA Antagonist
- VMAT 2 Inhibitor
Extrapyramidal symptoms- Tardive dyskinesia
Procaine, Tetracaine, Benzocaine, & Chloroprocaine
MOA:
Clinical uses:
Adverse effects:
Local Anesthetics
Esters
Block sodium (Na+) channels (no depol) in sensory nerves resulting in loss of
(1) pain → (2) temperature → (3) touch → (4) pressure (last)
Clinical uses:
Analgesia/Anesthesia
(minor surgical procedures or administered as spinal/epidural anesthetic)
Adverse effects:
1) allergic reactions
2) Cardiovascular toxicity
3) Methemoglobinemia (benzocaine & prilocaine)
Procaine, Tetracaine, Benzocaine, & Chloroprocaine
MOA:
Block sodium (Na+) channels (no depol) in sensory nerves resulting in loss of
(1) pain → (2) temperature → (3) touch → (4) pressure (last)
Clinical uses:
Analgesia/Anesthesia
(minor surgical procedures or administered as spinal/epidural anesthetic)
Adverse effects:
1) allergic reactions
2) Cardiovascular toxicity
3) Methemoglobinemia (benzocaine & prilocaine)
Local Anesthetics
Esters
Lidocaine, Mepivacaine, Bupivacaine, Ropivacaine, & Prilocaine (all have 2 i’s)
MOA:
Clinical uses:
Adverse effects:
Local anesthetics
(Amides)
MOA:
Block sodium (Na+) channels (no depol) in sensory nerves resulting in loss of
(1) pain → (2) temperature → (3) touch → (4) pressure (last)
Clinical use:
Analgesia/Anesthesia in patients with ESTER ALLERGY
(minor surgical procedures or administered as spinal/epidural anesthetic)
Adverse effects:
1) Cardiovascular toxicity
Lidocaine, Mepivacaine, Bupivacaine, Ropivacaine, & Prilocaine (all have 2 i’s)
MOA:
Block sodium (Na+) channels (no depol) in sensory nerves resulting in loss of
(1) pain → (2) temperature → (3) touch → (4) pressure (last)
Clinical use:
Analgesia/Anesthesia in patients with ESTER ALLERGY
(minor surgical procedures or administered as spinal/epidural anesthetic)
Adverse effects:
1) Cardiovascular toxicity
Local anesthetics
(Amides)
Na+ channel blockers used in epilepsy?
“Crappy FLiP TV”
Carbamazepine
Fosphenytoin
Lamotrigine
Phenytoin
Topiramate
Valproate
Carbamazepine
Fosphenytoin
Lamotrigine
Phenytoin
Topiramate
Valproate
Are all examples of which class of drug?
Na+ blockers used in epilepsy treatment
Valproic Acid (Valproate)
MOA:
Clinical use:
Adverse effects:
MOA:
Increases Na+ channel inactivation to increase GABA concentration by inhibiting GABA transaminase & inhibiting NMDA channels (affecting potassium current)
Clinical uses:
1) Seizures (antiepileptic)
- 1st line for generalized/tonic-clonic & myoclonic seizures
- 2nd line for partial/focal seizures, absence seizures
2) Bipolar disorder
3) migraine prophylaxis and trigeminal neuralgia
Adverse effects:
1) Hepatotoxicity
2) Teratogen (NTD)
3) GI distress, pancreatitis, tremor, weight gain
4) P450 inhibitor (avoid warfarin & theophylline)
MOA:
Increases Na+ channel inactivation to increase GABA concentration by inhibiting GABA transaminase & inhibiting NMDA channels (affecting potassium current)
Clinical uses:
1) Seizures (antiepileptic)
- 1st line for generalized/tonic-clonic & myoclonic seizures
- 2nd line for partial/focal seizures, absence seizures
2) Bipolar disorder
3) migraine prophylaxis and trigeminal neuralgia
Adverse effects:
1) Hepatotoxicity
2) Teratogen (NTD)
3) GI distress, pancreatitis, tremor, weight gain
4) P450 inhibitor (avoid warfarin & theophylline)
Valproic Acid (Valproate)
Clinical Presentation: Characterized by sudden muscle rigidity (tonic phase) followed by synchronous muscle jerks (clonic phase), loss of consciousness.
Valproic Acid (Valproate)
Carbamazepine
MOA:
Clinical use:
Adverse effect:
MOA:
Inhibits Na+ channels stabilizing the inactivated state & reducing neuronal activity
Clinical uses:
1) Trigeminal neuralgia
(1st line)**
2) SJS
3) Focal seizures
4) Manic Bipolar episodes
Adverse effects:
1) Agranulocytosis/aplastic anemia (stop drug!!!)
2) Osteoporosis
3) SIADH
4) Teratogen (NTD)
5) Steven Johnson Syndrome (SJS)
6) Diplopia, ataxia, liver toxicity
Avoid with warfarin, theophylline,
MOA:
Inhibits Na+ channels stabilizing the inactivated state & reducing neuronal activity
Clinical uses:
1) Trigeminal neuralgia
(1st line)**
2) SJS
3) Focal seizures
4) Manic Bipolar episodes
Adverse effects:
1) Agranulocytosis/aplastic anemia (stop drug!!!)
2) Osteoporosis
3) SIADH
4) Teratogen (NTD)
5) Steven Johnson Syndrome (SJS)
6) Diplopia, ataxia, liver toxicity
Avoid with warfarin, theophylline,
Carbamazepine
Ethosuximide
MOA:
Clinical uses:
Adverse effects:
MOA:
Inhibits thalamic T-type Ca2+ channels to block action potential propagation in thalamic neurons
Clinical uses:
Absence seizures (1st line)
Adverse effects:
1) Steven-Johnson Syndrome (SJS)
2) Fatigue, GI distress, headache, itching (and urticaria)
MOA:
Inhibits thalamic T-type Ca2+ channels to block action potential propagation in thalamic neurons
Clinical uses:
Absence seizures (1st line)
Adverse effects:
1) Steven-Johnson Syndrome (SJS)
2) Fatigue, GI distress, headache, itching (and urticaria)
Ethosuximide
Gabapentin & Pregabalin
MOA:
Clinical uses:
Adverse effects:
MOA:
Primarily inhibits high-voltage-activated Ca+ channels via the α2δ subunit
Clinical uses:
1) Neuropathic pain (Post herpetic neuralgia)
2) Shingles/Varicella pain (with pregabalin)
3) Partial (focal) seizures
Adverse effects:
Somnolence, dizziness, ataxia and fatigue
MOA:
Primarily inhibits high-voltage-activated Ca+ channels via the α2δ subunit
Clinical uses:
1) Neuropathic pain (Post herpetic neuralgia)
2) Shingles/Varicella pain (with pregabalin)
3) Partial (focal) seizures
Adverse effects:
Somnolence, dizziness, ataxia and fatigue
Gabapentin & Pregabalin
Lamotrigine
MOA:
Clinical use:
MOA:
Inhibits voltage-gated Na+ channels & it
inhibits the release of glutamine
Clinical use:
1) Broad-spectrum antiepileptic
Treats partial (focal) seizures, tonic-clonic seizures, absence seizures
2) Depressed episode of Bipolar disorder
3) Lennox Gastaut Syndrome
Adverse effects:
1) Steven Johnson Syndrome (SJS) (slow dose titration!)
2) Hemophagocytic lymphohistiocytosis (severe anemia!!!)
3) Toxic epidermal necrolysis
4) Dizziness, ataxia, blurred/double vision
MOA:
Inhibits voltage-gated Na+ channels & it
inhibits the release of glutamine
Clinical use:
1) Broad-spectrum antiepileptic
Treats partial (focal) seizures, tonic-clonic seizures, absence seizures
2) Depressed episode of Bipolar disorder
3) Lennox Gastaut Syndrome
Adverse effects:
1) Steven Johnson Syndrome (SJS) (slow dose titration!)
2) Hemophagocytic lymphohistiocytosis (severe anemia!!!)
3) Toxic epidermal necrolysis
4) Dizziness, ataxia, blurred/double vision
Lamotrigine
Levetricetam & Brivaracetam
MOA:
Clinical uses:
Adverse effects:
MOA:
SV2A inhibitor that helps modulate GABA & Glutamate release to inhibited voltage-gated Ca+ channels to alter vesicle fusion
Clinical use:
1) Broad spectrum antiepileptic (1st line)
Treats partial (focal) seizures, generalized (tonic-clonic) seizures (safe in preggos)
Adverse effects:
1) Neuropsychiatric symptoms (e.g. personality changes)
2) Fatigue/Drowsiness, headache
3) Somnolence, asthenia, dizziness
MOA:
SV2A inhibitor that helps modulate GABA/Glutamate release, inhibited voltage-gated Ca+ channels to alter vesicle fusion
Clinical use:
1) Broad spectrum antiepileptic (1st line)
Treats partial (focal) seizures, generalized (tonic-clonic) seizures (safe in preggos)
Adverse effects:
1) Neuropsychiatric symptoms (e.g. personality changes)
2) Fatigue/Drowsiness, headache
3) Somnolence, asthenia, dizziness
Levetiracetam & Brivaracetam
Topiramate
MOA:
Clinical uses:
Adverse effects:
MOA:
Inhibits Na+ channels (no AP) & increases
the action of GABA
Clinical uses:
1) Broad-spectrum antiepileptic
- treats focal (partial) and generalized (tonic-clonic) seizures
2) Migraine prophylaxis
Adverse effects:
1) Kidney stones
2) Sedation/Slow cognition (word-finding diff)
3) Weight loss
4) Glaucoma (rare)
MOA:
Inhibits Na+ channels (no AP) & increases
the action of GABA
Clinical uses:
1) Broad-spectrum antiepileptic
- treats focal (partial) and generalized (tonic-clonic) seizures
2) Migraine prophylaxis
Adverse effects:
1) Kidney stones
2) Sedation/Slow cognition (word-finding diff)
3) Weight loss
4) Glaucoma (rare)
Topiramate
Vigabatrin
MOA:
Clinical uses:
Adverse effects:
MOA:
Increases GABA concentration (by
Inhibiting GABA transaminase) causing CNS depression and inhibition of neuronal impulses
Clinical uses:
1) Partial (focal) seizures
2) Infantile spasms ass with tuberous sclerosis
Adverse effects:
1) Permanent visual loss!!!! (retinal atrophy)
MOA:
Increases GABA concentration (by
Inhibiting GABA transaminase) causing CNS depression and inhibition of neuronal impulses
Clinical uses:
1) Partial (focal) seizures
2) Infantile spasms ass with tuberous sclerosis
Adverse effects:
1) Permanent visual loss!!!! (retinal atrophy)
Vigabatrin
Fill in the missing drug names!
Barbiturates (Phenobarbital, Thiopental, Primidone, Mephobarbital)
MOA:
Clinical uses:
Adverse effects:
MOA:
Increases GABA-A receptor activity by increasing duration of Cl- channel opening to
inhibit neuronal firing
Clinical uses:
Tonic-Clonic and Partial seizures
1) 1st line seizure in neonates
2) 3rd line for status epilepticus kids (phenobarbital)
3) Sedative for anxiety, insomnia, induction of anesthesia
Adverse effects:
1) Induces cytochrome P-450 (int with warfarin & theophylline)
2) Acute intermittent porphyria
3) Sedation (CNS depression)
4) Cardiorespiratory depression
5) Tolerance/dependence
MOA:
Increases GABA-A receptor activity by increasing duration of Cl- channel opening to
inhibit neuronal firing
Clinical uses:
Tonic-Clonic and Partial seizures
1) 1st line seizure in neonates
2) 3rd line for status epilepticus
3) Sedative for anxiety, insomnia, induction of anesthesia
Adverse effects:
1) Induces cytochrome P-450 (int with warfarin & theophylline)
2) Acute intermittent porphyria
3) Sedation (CNS depression)
4) Cardiorespiratory depression
5) Tolerance/dependence
Barbiturates (Phenobarbital, Thiopental, Primidone, Mephobarbital)
Barbiturate toxicity
Effects:
Toxicity:
1) Sedation
2) Agitation
3) Confusion (elderly)
4) Irritability/Hperactivity
Primidone (Barbiturate) treats:
Focal or generalized epilepsy but it has a lower incidence of sedation
Adverse effects:
Dose-dependent pronounced drowsiness & barbiturate side effects
Phenytoin & Fosphenytoin
MOA:
Clinical uses:
Adverse effects:
MOA:
Na+ channel blockers to reduce AP & decrease neuronal firing
(changes from 0 to 1st order kinetics)
Clinical use
1) Partial (focal) seizure
2) Status epilepticus
Adverse effects: “PHENYTOIN”
1) P450 induction (warfarin & Theophylline int)
2) Hirsutism
3) Enlarged gums
4) Nystagmus
5) Yellow-Brown skin
6) Teratogen
(Fetal hydantoin syndrome, cleft palate/lip, microcephaly)
7) Osteopenia
8) Inhibited folate synthesis
9) Neuropathy
MOA:
Na+ channel blockers to reduce AP & decrease neuronal firing
(changes from 0 to 1st order kinetics)
Clinical use
1) Partial (focal) seizure
2) Status epilepticus
Adverse effects: “PHENYTOIN”
1) P450 induction (warfarin & Theophylline int)
2) Hirsutism
3) Enlarged gums
4) Nystagmus
5) Yellow-Brown skin
6) Teratogen
(Fetal hydantoin syndrome, cleft palate/lip, microcephaly)
7) Osteopenia
8) Inhibited folate synthesis
9) Neuropathy
Phenytoin & Fosphenytoin
Diplopia, Ataxia, & Sedation represents which type of toxicity?
Phenytoin toxicity
Lithium
MOA:
Clinical use:
Adverse effects:
Acute toxicity:
MOA:
Reduces Gq pathway via inositol monophosphate dehydrogenase inhibitor
(reduces transmission)
Clinical Use:
1) Acute Mania/Mood episodes (bipolar disorder)
2) Major Depression
3) SIADH
Acts as ADH antagonist to induce diabetes insipidus and intentional fluid volume loss
Adverse effects: LiTHIUN
1) Low thyroid *
(hypothyroidism)
2) Tremor (involuntary movements)
3) Heart (Ebstein anomaly)*
3) Insipidus **
(nephrogenic DI)
4) Nephrotoxicity (chronic interstitial nephritis)
Acute toxicity:
- Nausea/vomiting, diarrhea, slurred speech, seizures, ataxia
Drug-drug interaction: Avoid thiazide diuretics
MOA:
Reduces Gq pathway via inositol monophosphate dehydrogenase inhibitor
(reduces transmission)
Clinical Use:
1) Acute Mania/Mood episodes (bipolar disorder)
2) Major Depression
3) SIADH
Acts as ADH antagonist to induce diabetes insipidus and intentional fluid volume loss
Adverse effects: LiTHIUN
1) Low thyroid *
(hypothyroidism)
2) Tremor (involuntary movements)
3) Heart (Ebstein anomaly)*
3) Insipidus **
(nephrogenic DI)
4) Nephrotoxicity (chronic interstitial nephritis)
Acute toxicity:
- Nausea/vomiting, diarrhea, slurred speech, seizures, ataxia
Drug-drug interaction: Avoid thiazide diuretics
Lithium
Treatment of acute lithium toxicity includes…
Thiazide diuretics, ACE inhibitors, & NSAIDS
Buspirone
MOA:
Clinical uses:
MOA:
A partial 5-HTA1 agonist
Clinical uses:
1) GAD **
(2nd line, slow onset ~2wks)
No dependence/abuse
MOA:
A partial 5-HTA1 agonist
Clinical uses:
1) GAD **
(2nd line, slow onset ~2wks)
No dependence/abuse
Buspirone
Methylphenidate (Ritalin)
MOA:
Clinical uses:
Adverse effects:
CNS stimulant
MOA:
Inhibits NE & DA reuptake to increase the concentration of catecholamines in the synaptic cleft
Clinical uses:
1) ADHD**
2) Narcolepsy
3) Binge Eating Disorder
Adverse effects:
1) Nervousness/Agitation/Anxiety/Anorexia
2) Restlessness/Insomnia
3) Tachycardia/HTN
4) Bruxism/Tics
CNS stimulant
MOA:
Inhibits NE & DA reuptake to increase the concentration of catecholamines in the synaptic cleft
Clinical uses:
1) ADHD**
2) Narcolepsy
3) Binge Eating Disorder
Adverse effects:
1) Nervousness/Agitation/Anxiety/Anorexia
2) Restlessness/Insomnia
3) Tachycardia/HTN
4) Bruxism/Tics
Methylphenidate (Ritalin)
Valproic acid, Phenytoin, Carbamazepine, & Lamotrigine all treat which type of seizures?
Partial (focal) & general (tonic-clonic) seizure
Lorazepam, Diazepam, Phenytoin, & Fosphenytoin all treat which type of condition?
Status epilepticus
Ethosuximide & Valproic acid both treat which type of seizures?
Absence seizures
Fluoxetine, Fluvoxamine, Paroxetine, Sertraline, Escitalopram, & Citalopram
MOA:
Clinical uses:
Adverse effects:
SSRI’s
MOA:
Inhibits serotonin (5-HT) reuptake transporters on presynaptic neurons
(takes 4-8 weeks)
Clinical uses:
1) 1st line for MDD
2) 1st line for anxiety conditions
- GAD
- PTSD
- Panic disorder
- OCD
- Social anxiety disorder
3) 2nd line for Bulimia nervosa & Binge-eating disorder
4) Adjustment disorder (depressed mood) & Premature ejaculation
Adverse effects:
1) Serotonin syndrome**
2) Sexual dysfunction
(Anorgasmia, low libido)
3) SIADH
4) GI distress & Sleep disturbances
5) Antidepressant discontinuation syndrome
Fluoxetine, Fluvoxamine, Paroxetine, Sertraline, Escitalopram, & Citalopram
MOA:
Inhibits serotonin (5-HT) reuptake transporters on presynaptic neurons
(takes 4-8 weeks)
Clinical uses:
1) 1st line for MDD
2) 1st line for anxiety conditions
- GAD
- PTSD
- Panic disorder
- OCD
- Social anxiety disorder
3) 2nd line for Bulimia nervosa & Binge-eating disorder
4) Adjustment disorder (depressed mood) & Premature ejaculation
Adverse effects:
1) Serotonin syndrome**
2) Sexual dysfunction
(Anorgasmia, low libido)
3) SIADH
4) GI distress & Sleep disturbances
5) Antidepressant discontinuation syndrome
SSRI’s
Venlafaxine, Desvenlafaxine, Duloxetine, Milnacipran, & Levomilnacipran
MOA:
Clinical uses:
Adverse effects:
SNRI
MOA:
Inhibit 5-HT & NE reuptake
Clinical use:
1) MDD
2) Anxiety disorders
- GAD
- Panic disorder
- Social anxiety
- PTSD
- OCD
3) Neuropathic pain
(Especially for diabetic peripheral neuropathy & fibromyalgia)
4) Migraine prophylaxis
Adverse effects:
1) Serotonin syndrome
2) Sexual dysfunction
(Anorgasmia, low libido)
3) Antidepressant discontinuation syndrome
4) HTN
Venlafaxine, Desvenlafaxine, Duloxetine, Milnacipran, & Levomilnacipran
SNRI
MOA:
Inhibit 5-HT & NE reuptake
Clinical use:
1) MDD
2) Anxiety disorders
- GAD
- Panic disorder
- Social anxiety
- PTSD
- OCD
3) Neuropathic pain
(Especially for diabetic peripheral neuropathy & fibromyalgia)
4) Migraine prophylaxis
Adverse effects:
1) Serotonin syndrome
2) Sexual dysfunction
(Anorgasmia, low libido)
3) Antidepressant discontinuation syndrome
4) HTN
SNRI
Serotonin syndrome
Pathology:
Treatment:
Path:
Happens when SNRI’s are taken with another 5-HT elevating drug
Characterized by:
1) Hyperactivity (CLONUS, hyperreflexia, hypertonia, seizures)
2) Autonomic instability (high temperature, sweating, tachycardia, diarrhea)
3) Altered mental status
AVOID THESE
TCAs, MAOIs, linezolid, St. John’s wort
Treat with: Cyproheptadine
A 5-HT2 receptor antagonist
Antidepressant discontinuation syndrome
Pathology:
Treatment:
Pathology:
Flu-like symptoms (nausea,fatigue, headaches) that happens when patients
Discontinue an SSRI/SNRI without a taper (sudden)
Characterized by:
- GI distress
- fatigue/flu-like
- depressed/irritable mood, fatigue
- feeling of electric shocks
Basically, if someone feels bad after stopping an SSRI/SNRI, think about this!
Treat by:
Restarting the antidepressant or raising the dose
Bupropion
MOA:
Clinical uses:
Adverse effects:
Atypical antidepressant
MOA:
Inhibits NE, DA, & 5-HT reuptake
Clinical use:
1) Promotes smoking cessation
2) Depression (2/3rd line)
Side effects:
1) Seizures **
(AVOID in bulimia/anorexia nervosa and seizure disorders)
Atypical antidepressant
MOA:
Inhibits NE, DA, & 5-HT reuptake
Clinical use:
1) Promotes smoking cessation
2) Depression (2/3rd line)
Side effects:
1) Seizures **
(AVOID in bulimia/anorexia nervosa and seizure disorders)
Bupropion
Stimulant effects (tachycardia & insomnia), Headache, Seizures in patients with eating disorders indicated which type of drug toxicity?
Bupropion
Amitriptyline, Nortriptyline, Imipramine, Desipramine, Clomipramine, Doxepin, & Amoxapine
MOA:
Clinical uses:
Adverse effects:
TCA’s
MOA:
Block reuptake of norepinephrine (NE) and serotonin → Increased concentration in the synaptic cleft. Additionally, block cholinergic, histamine, and alpha-1 adrenergic receptors.
Clinical uses:
1) 2nd line MDD
2) Neuropathic pain (fibromyalgia or MS)
3) Headache prophylaxis (Amitriptyline)
4) OCD (clomipramine)
5) Nocturnal enuresis (imipramine)
Adverse effects:
1) Anticholinergic effects
2) Cardiotoxicity
(prolonged QT, prolonged QRS, torsade’s de pointes)
3) Seizures (convulsions)
4) Serotonin syndrome
Amitriptyline, Nortriptyline, Imipramine, Desipramine, Clomipramine, Doxepin, & Amoxapine
TCA’s
MOA:
Block reuptake of norepinephrine (NE) and serotonin → Increased concentration in the synaptic cleft. Additionally, block cholinergic, histamine, and alpha-1 adrenergic receptors.
Clinical uses:
1) 2nd line MDD
2) Neuropathic pain (fibromyalgia or MS)
3) Headache prophylaxis (Amitriptyline)
4) OCD (clomipramine)
5) Nocturnal enuresis (imipramine)
Adverse effects:
1) Anticholinergic effects
2) Cardiotoxicity
(prolonged QT, prolonged QRS, torsade’s de pointes)
3) Seizures (convulsions)
4) Serotonin syndrome
TCA’s
Acute TCA overdose presents with severe anticholinergic symptoms, arrhythmias, seizures, and hypotension can be treated with what?
NaHCO3
Theorized that the Na+ helps to relieve Na+ channel blockade
Baclofen
MOA:
Clinical uses:
Adverse effects:
Antispasmodic
MOA:
GABA(B) receptor agonist in spinal cord
Clinical uses:
1) Muscle spasticity (ALS)
Adverse effects:
1) CNS depression
2) Respiratory depression
Mediated by GABA = inhibitory
Antispasmodic
MOA:
GABA(B) receptor agonist in spinal cord
Clinical uses:
1) Muscle spasticity (Dystonia & Multiple sclerosis)
Adverse effects:
1) CNS depression
2) Respiratory depression
Mediated by GABA = inhibitory
Baclofen
Triptans (Sumatriptan)
MOA:
Clinical uses:
Adverse effects:
MOA:
5-HT 1B & 1D agonists that inhibit the release of vasoactive peptides, promoting vasoconstriction & It inhibits trigeminal nerve activation to block pain paths in the brainstem
Clinical uses:
1) Abortion of acute migraine
2) 1st line acute cluster headaches
Adverse effects:
1) Coronary vasospasm
(AVOID in CAD or vasospastic angina)
2) Mild paresthesia
3) Serotonin syndrome
MOA:
5-HT 1B & 1D agonists that inhibit the release of vasoactive peptides, promoting vasoconstriction & It inhibits trigeminal nerve activation to block pain paths in the brainstem
Clinical uses:
1) Abortion of acute migraine
2) 1st line acute cluster headaches
Adverse effects:
1) Coronary vasospasm
(AVOID in CAD or vasospastic angina)
2) Mild paresthesia
3) Serotonin syndrome
Triptans (Sumatriptan)
Benztropine & Trihexyphenidyl
MOA:
Clinical uses:
Adverse effects:
MOA:
Act as Anticholinergic
Clinical Uses:
1) Parkinson’s disease (tremor & rigidity)
2) Drug-induced parkinsonism (1st line)
Adverse Effects:
Anticholinergic side effects
MOA:
Act as Anticholinergic
Clinical Uses:
1) Parkinson’s disease (tremor & rigidity)
2) Drug-induced parkinsonism (1st line)
Adverse Effects:
Anticholinergic side effects
Benztropine & Trihexyphenidyl
Tetrabenazine
MOA:
Clinical uses:
MOA:
Inhibits vesicular monoamine transporter (VMAT) to reduce dopamine release, dopamine vesicle packaging, & increase monoamine oxidase degradation of dopamine
Clinical Uses:
Treats Huntington Chorea & Tardive Dyskinesia
MOA:
Inhibits vesicular monoamine transporter (VMAT) to reduce dopamine release, dopamine vesicle packaging, & increase monoamine oxidase degradation of dopamine
Clinical Uses:
Treats Huntington Chorea & Tardive Dyskinesia
Tetrabenazine
Morphine, oxymorphone, hydromorphone
Heroin
Fentanyl
Codeine, oxycodone, hydrocodone
Methadone
Meperidine
MOA:
Clinical uses:
Adverse effects:
Full Opioid Agonists
MOA:
Mu opioid receptor agonist that reduces pain transmission by opening postsynaptic K+ channels & closing presynaptic Ca2+ channels. Mimicking the effects of endorphin, enkephalin & dynorphin.
Clinical uses:
Analgesia (pain relief)
Adverse effects:
1) Constipation
2) Miosis (pupil constriction, except meperidine, which causes mydriasis)
3) Respiratory Depression
4) Sphincter of Oddi spasm (biliary colic)
5) CNS Depression (sedation or coma)
6) Dependence
7) Withdrawal (when suddenly stopped)
Morphine, oxymorphone, hydromorphone
Heroin
Fentanyl
Codeine, oxycodone, hydrocodone
Methadone
Meperidine
MOA:
Mu opioid receptor agonist that reduces pain transmission by opening postsynaptic K+ channels & closing presynaptic Ca2+ channels. Mimicking the effects of endorphin, enkephalin & dynorphin.
Clinical uses:
Analgesia (pain relief)
Adverse effects:
1) Constipation
2) Miosis (pupil constriction, except meperidine, which causes mydriasis)
3) Respiratory Depression
4) Sphincter of Oddi spasm (biliary colic)
5) CNS Depression (sedation or coma)
6) Dependence
7) Withdrawal (when suddenly stopped)
Full Opioid Agonists
Buprenorphine
Nalbuphine
Pentazocine
Butorphanol
Individual MOA’s
Clinical uses:
Adverse effects:
Buprenorphine:
Partial mu opioid receptor agonist & Kappa and delta-opioid receptor antagonist
Nalbuphine:
Partial mu opioid receptor agonist
Kappa receptor partial agonist
Pentazocine:
Partial mu opioid receptor agonist
Kappa receptor agonist
Butorphanol:
Partial mu opioid receptor agonist
Kappa receptor agonist
Clinical uses:
1) Analgesia (with naloxone to prevent abuse)
2) Wean patients off full opioid agonists, (avoiding withdrawal from sudden termination)
Adverse effects:
1) Opioid withdrawal
2) Respiratory and CNS depression
Buprenorphine:
Partial mu opioid receptor agonist & Kappa and delta-opioid receptor antagonist
Nalbuphine:
Partial mu opioid receptor agonist
Kappa receptor partial agonist
Pentazocine:
Partial mu opioid receptor agonist
Kappa receptor agonist
Butorphanol:
Partial mu opioid receptor agonist
Kappa receptor agonist
Clinical uses:
1) Analgesia (with naloxone to prevent abuse)
2) Wean patients off full opioid agonists, (avoiding withdrawal from sudden termination)
Adverse effects:
1) Opioid withdrawal
2) Respiratory and CNS depression
Partial Opioid Agonists
Dextromethorphan
MOA:
Clinical uses:
MOA:
Opioid receptor agonist
Clinical Use:
1) Cough suppressant/antitussive
It’s the main ingredient in Robitussin
MOA:
Opioid receptor agonist
Clinical Use:
1) Cough suppressant/antitussive
It’s the main ingredient in Robitussin
Dextromethorphan
Tramadol
MOA:
Clinical uses:
Adverse effects:
MOA:
Weak opioid agonist that increases synaptic signaling by inhibiting reuptake NE & 5-HT
Clinical Uses
1) Analgesia
Adverse Effects:
1) Constipation
2) Miosis
3) Respiratory depression
4) Decreased seizure threshold
5) Serotonin syndrome
MOA:
Weak opioid agonist that increases synaptic signaling by inhibiting reuptake NE & 5-HT
Clinical Uses
1) Analgesia
Adverse Effects:
1) Constipation
2) Miosis
3) Respiratory depression
4) Decreased seizure threshold
5) Serotonin syndrome
Tramadol
Naloxone (Narcan)
MOA:
Clinical uses:
Adverse effects:
MOA:
Opioid receptor antagonist
Has high affinity for receptors (displaces opioids) but no activity (antagonist)
Clinical indications:
1) Acute opioid intoxication
Adverse Effects
1) Opioid withdrawal
(Sudden stopping of opioid signaling causes withdrawal symptoms and seizures)
MOA:
Opioid receptor antagonist
Has high affinity for receptors (displaces opioids) but no activity (antagonist)
Clinical indications:
1) Acute opioid intoxication
Adverse Effects
1) Opioid withdrawal
(Sudden stopping of opioid signaling causes withdrawal symptoms and seizures)
Naloxone (Narcan)
Naltrexone
MOA:
Clinical uses:
MOA:
Opioid receptor antagonist
Clinical uses:
1) Alcohol craving 1st-line
2) Opioid dependence maintenance
Effects are slow (cannot be used for acute intoxication)
MOA:
Opioid receptor antagonist
Clinical uses:
1) Alcohol craving 1st-line
2) Opioid dependence maintenance
Effects are slow (cannot be used for acute intoxication)
Naltrexone
Methylnaltrexone
MOA:
Clinical uses:
MOA:
Opioid receptor antagonist
Similar to naltrexone, except it acts peripherally ONLY
Clinical uses:
1) Opioid-induced constipation
Does not cause opioid withdrawal (due to lack of CNS penetration)
MOA:
Opioid receptor antagonist
Similar to naltrexone, except it acts peripherally ONLY
Clinical uses:
1) Opioid-induced constipation
Does not cause opioid withdrawal (due to lack of CNS penetration)
Methylnaltrexone
Phenelzine
Isocarboxazid
Iproniazid
Selegiline
Tranylcypromine (non-hydrazine)
MOA:
Clinical uses:
Adverse effects:
Non-Selective Monoamine Oxidase Inhibitors (MAOIs)
MOA:
1) Phenelzine, Tranylcypromine: Inhibit monoamine oxidase (MAO) enzyme non-selectively to reduce DA, 5-HT, NE breakdown & Increase neurotransmitters.
Selegiline: Selectively inhibits MAO-B at lower doses, affecting primarily dopamine breakdown.
Clinical uses:
1) Atypical Depression & treatment resistant depression
2) Anxiety disorders
3) Parkinsons (Selegine)
Adverse effects:
1) Hypertensive crisis (with tyramine-rich foods), less risk with Selegiline at low doses.
Treat with phentolamine
2) Causes Serotonin Syndrome
3) CNS stimulation, Orthostatic hypotension, Weight gain.
4) Insomnia (Selegine)
MAOI hypertensive crisis (tyramine from cheese/wine)
What is the treatment?
take phentolamine
history of taking general anesthetics with muscle relaxant (halothane + succinylcholine)
what is the condition? & the treatment?
Malignant hyperthermia treat with Dantrolene
Phenelzine
Tranylcypromine
Isocarboxazid
MOA:
Non-selective inhibition of monoamine oxidase (MAO) results in increased levels of
NE, 5-HT, & DA
Clinical uses:
Treat Atypical Depression
Adverse effects:
1) Causes Hypertensive crisis
(AVOID tyramine cheeses, cured meats, draft beer, etc.)
2) Causes Serotonin Syndrome
Non-Selective Monoamine Oxidase Inhibitors (MAOIs)
Mirtazapine
MOA:
Clinical uses:
MOA:
An antagonist at alpha-2 adrenergic receptors, 5-HT and H1 receptors
Clinical uses:
1) MDD
2) Anorexia Nervosa
Adverse effects:
1) Weight gain/Increased appetite
2) Sedation (insomnia)
MOA:
An antagonist at alpha-2 adrenergic receptors, 5-HT and H1 receptors
Clinical uses:
1) MDD
2) Anorexia Nervosa
3) Insomnia
Adverse effects:
1) Weight gain/Increased appetite
2) Sedation (insomnia)
Mirtazapine
Trazodone
MOA:
Clinical uses:
Adverse effects:
MOA:
An antagonist 5-HT, H1, and alpha-1 adrenergic receptors
Clinical uses:
1) MDD
2) Insomnia
Adverse effects:
1) Priapism
2) Sedation (insomnia)
3) Postural Hypotension
4) Serotonin Syndrome
5) Nausea
MOA:
An antagonist 5-HT, H1, and alpha-1 adrenergic receptors
Clinical uses:
1) MDD
2) Insomnia
Adverse effects:
1) Priapism
2) Sedation (insomnia)
3) Postural Hypotension
4) Serotonin Syndrome
5) Nausea
Trazodone
Vilazodone
MOA:
Clinicla uses:
Adverse effects:
MOA:
Acts as a partial agonist of 5-HT1A receptor to inhibit 5-HT reuptake
Clinical uses:
1) MDD
Adverse effects:
1) Serotonin Syndrome
2) Causes nonspecific symptoms (nausea, diarrhea, headache)
MOA:
Acts as a partial agonist of 5-HT1A receptor to inhibit 5-HT reuptake
Clinical uses:
1) MDD
Adverse effects:
1) Serotonin Syndrome
2) Causes nonspecific symptoms (nausea, diarrhea, headache)
Vilazodone
Vortioxetine
MOA:
Clinical uses:
Adverse effects:
MOA:
Increase 5-HT signaling, primarily by inhibiting the reuptake at neuronal synapses
Clinical uses:
MDD
Adverse effect:
1) serotonin syndrome
2) Nausea
3) Sleep disturbances
4) Anticholinergic effects.
MOA:
Increase 5-HT signaling, primarily by inhibiting the reuptake at neuronal synapses
Clinical uses:
MDD
Adverse effect:
1) serotonin syndrome
2) Nausea
3) Sleep disturbances
4) Anticholinergic effects.
Vortioxetine
Varenicline
MOA:
Clinical uses:
Adverse effects:
MOA:
Partial Agonist of Nicotinic Receptor
Clinical Use:
1) Smoking Cessation
(To reduce nicotine cravings - useful for nicotine withdrawal)
Adverse Effects:
Toxicity: Sleep disturbance, depressed mood
MOA:
Partial Agonist of Nicotinic Receptor
Clinical Use:
1) Smoking Cessation
(To reduce nicotine cravings - useful for nicotine withdrawal)
Adverse Effects:
Toxicity: Sleep disturbance, depressed mood
Varenicline
Curare-derivatives
-curarine (Tubocurarine, Rubocurarine)
-curium (Atracurium, Mivacurium)
-curonium (Pancuronium, Vecuronium, Rocuronium)
MOA:
Clinical uses:
Reversal agents:
Adverse effects:
Nondepolarizing Neuromuscular Blocking Drugs
MOA:
Competitive ANTAGONIST at nicotinic receptors in skeletal muscle (preventing depolarization)
Clinical Use:
1) Induction of anesthesia (muscle relaxation and diminish reflexes) give with atropine to avoid bradycardia
Reversal agents:
1) AChE inhibitor reversal (neostigmine, edrophonium)
Adverse Effects
1) Hypotension
2) Respiratory depression
Curare-derivatives
-curarine (Tubocurarine, Rubocurarine)
-curium (Atracurium, Mivacurium)
-curonium (Pancuronium, Vecuronium, Rocuronium)
MOA:
Competitive ANTAGONIST at Nm nicotinic receptors in skeletal muscle (preventing depolarization)
Clinical Use:
1) Induction of anesthesia (muscle relaxation and diminish reflexes) give with atropine to avoid bradycardia
Reversal agents:
1) AChE inhibitor reversal (neostigmine, edrophonium)
Adverse Effects
1) Hypotension
2) Respiratory depression
Nondepolarizing Neuromuscular Blocking Drugs
Succinylcholine (Depolarizing Paralytic)
MOA:
Clinical uses:
Reversible agents:
MOA:
Agonist at nicotinic receptors causing
continuous depolarization at neuromuscular junction & not allowing the muscle to repolarize resulting in flaccid paralysis (can manifest as transient fasciculations)
Clinical uses:
1) Paralysis for Anesthesia
Rapid sequence intubation (RSI), short surgical procedures, emergency airway management.
Reversible agents:
1) AChE inhibitors (e.g. neostigmine)
Adverse effect:
1) Malignant hyperthermia (give dantrolene)
2) Hyperkalemia
3) Hypercalcemia
4) Prolonged paralysis
5) Bradycardia
MOA:
Agonist at nicotinic receptors causing
continuous depolarization at neuromuscular junction & not allowing the muscle to repolarize resulting in flaccid paralysis (can manifest as transient fasciculations)
Clinical uses:
1) Paralysis for Anesthesia
Rapid sequence intubation (RSI), short surgical procedures, emergency airway management.
Reversible agents:
1) AChE inhibitors (e.g. neostigmine)
Adverse effect:
1) Malignant hyperthermia (give dantrolene)
2) Hyperkalemia
3) Hypercalcemia
4) Prolonged paralysis
5) Bradycardia
Succinylcholine (Depolarizing Paralytic)
Cyclobenzaprine
(Mephenesin, Chlorzoxazone, Methocarbamol, Carisoprodol, & Chlormezanone)
MOA:
Clinical uses:
MOA:
Act centrally on the brainstem and spinal cord to inhibit motor neurons
Clinical Use:
1) Treats muscle spasms (antispasmodic)
Adverse effects:
1) Anticholinergic
2) Heart block
(AVOID) MAOIs
MOA:
Act centrally on the brainstem and spinal cord to inhibit motor neurons
Clinical Use:
1) Treats muscle spasms (antispasmodic)
Adverse effects:
1) Anticholinergic
2) Heart block
(AVOID) MAOIs
Cyclobenzaprine
(Mephenesin, Chlorzoxazone, Methocarbamol, Carisoprodol, & Chlormezanone)
Dantrolene
MOA:
Clinical uses:
MOA:
Inhibits ryanodine receptors to prevent
Ca2+ release from the sarcoplasmic reticulum of skeletal muscle (reduce contraction)
Clinical uses:
1) Treats Malignant hyperthermia
2) Treats Neuroleptic malignant syndrome (NMS)
MOA:
Inhibits ryanodine receptors to prevent
Ca2+ release from the sarcoplasmic reticulum of skeletal muscle (reduce contraction)
Clinical uses:
1) Treats Malignant hyperthermia
2) Treats Neuroleptic malignant syndrome (NMS)
Dantrolene
Oxcarbazepine
MOA & Benefits over carbamazepine?
Adverse effect:
MOA/Benefits:
Prodrug of carbamazepine, induction capacity is low BUT it’s less likely to be involved in drug
Adverse effects:
Hyponatremia
MOA/Benefits:
Prodrug of carbamazepine, induction capacity is low BUT it’s less likely to be involved in drug
Adverse effects:
Hyponatremia
Oxcarbazepine
Tiagabine
MOA:
Clinical uses:
Adverse effects:
MOA:
Inhibits GABA Transporter GAT1 to
Reduces GABA uptake into neurons & glia
Clinical uses:
Add on therapy for Partial/Focal seizure with/without generalization
Adverse effects:
Dizziness, somnolence, tremor
MOA:
Inhibits GABA Transporter GAT1 to
Reduces GABA uptake into neurons & glia
Clinical uses:
Add on therapy for Partial/Focal seizure with/without generalization
Adverse effects:
Dizziness, somnolence, tremor
Tiagabine
Status epilepticus
Pathology:
Treatments:
3 lines of treatment
Alternatives for resistant cases
Path:
A seizure lasting longer than 5 minutes, or having more than 1 seizure within a 5 minute period, (without returning to a normal level of consciousness between episodes)
Treatments:
1# I.V. diazepam (10mg slowly)in adults, followed by slow infusion titrated to control convulsions.
Alternatives: clonazepam, lorazepam
2# I.V. phenytoin : (15-20 mg / kg )- Slowly Maintain BP, ventillation
Prevent physical injury, tongue injury & aspiration.
3# I.V. –Line with NS (phenytoin incompatible with glucose)
Resistant cases :
general anaesthetic with NMBs phenobarbitone
Antiseizure meds to avoid in preggos
& which drug is safe to use in preggos????
- valproate:
‘Spina bifida’ and ‘encephalocele’ - carbamazepine &
Phenytoin
‘fetal hydantoin syndrome – IUGR, microcephaly, mental retardation, hypoplastic nails, distal phalages’
Levetiracetam is SAFE IN PREGGOS
A 62-year-old female is brought to the emergancy with severe shortness of breath, tachypnea and pleuritic type chest pain. She had a similar episode two months ago and has been treated with warfarin since then. She says that she has been compliant with her medications. Her prothrombin time (PT and INR) is found to be sub-therapeutic. Which of the following concurrent medications is she most likely taking?
A.Aspirin
B.Phenylbutazone
C.Oxycodone
D.Acetaminophen
E. Metronidazole
F.Cimetidine
G.Phenytoin
H.Amiodarone
I. Diazepam
H. Amiodarone
A 20-year-old man is brought to the emergency department (ED) by his mother after having seizures. The patient’s mother says that he suddenly lost consciousness, had several jerky movements of his muscles, and had total loss of postural control. Over the next half hour while still in the ED, the patient has a series of rhythmic contractions of all four limbs, without a return to full consciousness. Which of the following is the most appropriate medication that should be administered first to this patient?
A. Carbamazepine
B. Ethosuximide
C. Lorazepam
D. Lamotrigine
E. Valproic acid
C. Lorazepam
A 40-year-old man with a history of epilepsy presents to the emergency department actively seizing. Paramedics have already administered two doses of IV lorazepam. Which of the following is the mechanism of action of the drug that should be given next?
A. Increased duration of GABAAchloride ion channel opening
B. Increased frequency of GABAAchloride ion channel opening
C. Inhibition of GABAAchloride ion channels
D. Inhibition of T-type calcium channels
E. Inhibition of voltage-dependent sodium channels
D. Inhibition of T-type calcium channels
A 25-year-old woman with a history of epilepsy presents to the clinic inquiring about her medication. She states that she is hoping to get pregnant within the next few months. Which of the following medications carries the highest risk of birth defects?
Carbamazepine
Gabapentin
Levetiracetam
Phenytoin
Vigabatrin
Phenytoin
(Levetiracetam is safe for Preggos)
Which of the following medications causes a decrease in the efficiency of the cytochrome p450 system?
Carbamazepine
Lamotrigine
Levetiracetam
Topiramate
Valproic acid
Lamotrigine
A 29-year-old man has epilepsy treated with phenytoin. He confuses his medications and accidentally takes four times his normal dose of phenytoin. Which of the following may occur in this man as the earliest sign of phenytoin toxicity?
(A) Megaloblastic anemia
(B) Unsteady gait
(C) Hirsutism
(D) Gingival hyperplasia
(E) Purple discoloration of the hand
(E) Purple discoloration of the hand
A 6-year-old girl presents after having “episodes” at school. During these episodes, she stares into space and does not
respond to verbal or tactile stimuli. The episodes last for a few seconds. She has no confusion after these events. A drug with
which of the following mechanisms of action is recommended for the treatment of her condition?
(A) Binds post-synaptic GABA receptors
(B) Blocks T-type calcium channels
(C) Increases activity of GABA
(D) Binds to a voltage-dependent Na channel
(E) Inactivates sodium channels
(B) Blocks T-type calcium channels
A patient with focal seizures has been treated for 6 months with carbamazepine but, recently, has been experiencing breakthrough seizures on a more frequent basis. You are considering adding a second drug to the antiseizure regimen. Which of the following drugs is least likely to have a pharmacokinetic interaction with carbamazepine?
A. Topiramate
B. Tiagabine
C. Levetiracetam
D. Lamotrigine
C. Levetiracetam
- A 22-year-old woman recently began medical treatment for a seizure disorder. She presents with dysuria,and a urine dipstick shows microhematuria but no leukocytes and no nitrites. A KUB X-ray shows calcifications in the renal pelvis, although she has neither personal nor family history of kidney stones. Which seizure medicine is she likely taking?
(A) Ethosuximide
(B) Phenobarbital
(C) Phenytoin
(D) Topiramate
(E) Valproic acid
(D) Topiramate
68-year-old woman comes to the physician because of persistent burning pain along the right side of her chest and back for the past 5 months. Her current symptoms were preceded by a painful red rash over the same area; the rash has since resolved. On physical examination, the patient moves due to pain when the area along her right back is lightly touched. The patient is started on medication that disrupts calcium channels to reduce her symptoms.
Which of the following medications was the patient most likely prescribed?
1) Carbamazepine
2) Gabapentin
3) Morphine
4) Glucocorticoid injections
5) Nortriptyline
1) Carbamazepine
A 5-year-old boy is brought to the pediatrician by his mother because the child frequently ceases his activities and “stares blankly into space” while smacking his lips. He resumes his normal activities shortly thereafter. These episodes happen both at school and at home. The pediatrician starts him on ethosuximide to treat his symptoms.
Which of the following is the most likely mechanism of action of the patient’s medication?
A. Activates chloride channel opening
B. Blocks N-type calcium channels
C. Blocks T-type calcium channels
D. Blocks glutamate receptors
E. Blocks voltage-gated sodium channels
C. Blocks T-type calcium channels
Absent seizures (child stares without blinking)
What is the best treatment?
Ethosuximide (T-type calcium channel blocker)
Tonic-clonic seizures best treatment?
Valproic acid
Neuroleptic malignant syndrome can be caused by which classes of drugs?
1) Dopamine blocker drug (metoclopramide)
2) Antipsychotics (Haloperidol, risperidone, chlorpromazine)
Rx Dantrolene
Serotonin syndrome is caused by any drug that increases 5-HT (SSRIs, SNRIs, MAOIs, TCAs, Triptans, St. John’s Wort, Illicit drugs (e.g., MDMA, LSD), and others when combined → Increase serotonin levels) & results in: Fever, rigidity, neuromuscular hyperreactivity
what do you treat it with?
cyproheptadine
Presentation
Confusion, agitation, headache, hallucinations.
Autonomic Symptoms: Hyperthermia, tachycardia, hypertension, diaphoresis, nausea, diarrhea, Tremor, clonus (spontaneous, inducible, ocular), hyperreflexia, muscle rigidity.
Diagnosis: High levels of urinary 5-HIAA
What is the condition & the treatment?
Serotonin syndrome treatment with Cyproheptadine: A serotonin antagonist → Reduces serotonin effects.
Cheese Reaction
Effect: Tyramine promotes norepinephrine (NE) release from presynaptic vesicles → Excessive NE → Vasoconstriction and increased heart rate → Hypertensive crisis.
What’s the treatment?
Treatment
Phentolamine: A non-selective alpha-adrenergic blocker, can be used to counteract the vasoconstriction.
Nitroprusside: A vasodilator, for severe cases to rapidly reduce blood pressure.
Cheese reaction caused by mixing TCA + MAOI can be treated with which drug?
Phenelzine
Which drug treats Alcohol dependence by Reducing cravings?
naltrexone (Mu receptor antagonist)
Amyotrophic lateral sclerosis can be treated with which drug types?
1) Riluzole which increases survival of patient
(slows disease progression)
2) Baclofen which used for muscle spasticity (acts on GABA B receptor)
Parkinson’s disease
What are the best treatment options:
- COMT inhibitor – tolcapone (hepatotoxic) and entacapone
- MAOI: selegiline and rasagiline
- Amantadine -
NMDA receptor antagonist causing livedo reticularis - Centrally acting anticholinergic - benztropine, trihexyphenidyl, bipyridine
(Also used to treat extrapyramidal side effect treatment)
- COMT inhibitor – tolcapone (hepatotoxic) and entacapone
- MAOI: selegiline and rasagiline
- Amantadine -
NMDA receptor antagonist causing livedo reticularis - Centrally acting anticholinergic - benztropine, trihexyphenidyl, bipyridine
(Also used to treat extrapyramidal side effect treatment)
Parkinson’s disease treatments
What’s the best treatment for Wilson diseases?
copper chelating agent – penicillamine
Opioid receptor Mu & kappa receptor agonists toxicity, what is the best treatment?
Patient presents with Sedation, analgesia, constipation, respiratory depression, dysphoria and constipation
Naloxone > Loperamide > Naltrexone
Note -Opioid withdrawal associated with diarrhea
Proton pump inhibitors (PPIs) -prazole
MOA:
MOA: Irreversibly inhibit H+/K+ -ATPase
Adverse effects:
C difficile infection, pneuminia, acute intersistal nephritis
H2 blocker -tidine
MOA:
MOA: blocks histamine receptors
Ondansetron
MOA:
Clinical uses:
MOA: 5-HT3 antagonist
Uses:
Chemotherapy induced nausea and vomiting
Metoclopramide
MOA:
Clinical uses:
Adverse effect:
MOA: D2 antagonist
Clinical uses:
Weight-loss
Adverse effects:
It causes NMS or extrapyramidal side effects
MOA: D2 antagonist
Clinical uses:
Weight-loss
Adverse effects:
It causes NMS or extrapyramidal side effects
Metoclopramide
Lubiprostone
MOA:
Clinical uses:
Adverse effects;
MOA:
A laxative that increases chloride ion secretion
Uses:
IBS associated with constipation
Adverse effects:
Diarrhea
MOA:
A laxative that increases chloride ion secretion
Uses:
IBS associated with constipation
Adverse effects:
Diarrhea
Lubiprostone
Loperamide
MOA:
Clinical uses:
Adverse effects:
MOA:
Mu receptor agonist
Uses:
For IBS associated with constipation
Adverse effect:
Constipation
MOA:
Mu receptor agonist
Uses:
For IBS associated with constipation
Adverse effect:
Constipation
Loperamide
What should you give a patient with IBD that has not be improved with traditional drugs?
give TNF-alpha antagonist –
infliximab
adalimumab
certolizumab
give TNF-alpha antagonist –
infliximab
adalimumab
certolizumab
In cases of what?
IBD that’s not be improved with traditional drugs
Sildenafil
MOA:
Clinical use:
Adverse effects:
MOA:
PDE5 inhibitor that increases cGMP to increase NO signalling & vasodilation
Uses:
Limp wiener
Adverse effects:
Severe hypotension if given with beta blockers
MOA:
PDE5 inhibitor that increases cGMP to increase NO signalling & vasodilation
Uses:
Limp wiener
Adverse effects:
Severe hypotension if given with beta blockers
Sildenafil
Anti-obesity drug that are available?
1) Orlistat a lipoprotein lipase inhibitor
2) Liraglutide a GLP1 agonist (FDA approved)
1) Orlistat a lipoprotein lipase inhibitor
2) Liraglutide a GLP1 agonist (FDA approved)
Are both used for which condition?
Obesity
Signs of miosis, respiratory depression constipation
Morphine
Signs of mydriasis, “crawling bugs”
Cocaine toxicity
varenicline
MOA:
Clinical uses:
MOA:
partial agonist activity on nicotine acetylcholine receptor (A4B2)
Uses:
Nicotine toxicity
fomepizole (#1) & ethanol
MOA:
Clinical use:
MOA:
inhibit alcohol dehydrogenase enzyme
Use:
Methanol toxicity
MOA:
inhibit alcohol dehydrogenase enzyme
Use:
Methanol toxicity
Fomepizole (#1) & ethanol
- Signs of ocular damage or respiratory failure
Methanol toxicity
Treat with fomepizole > ethanol
Signs of garlic breath, rice-water stool, and abdominal pain
Arsenic poisoning
Rx:
dimercaprol
Iron toxicity what is the treatment?
deferoxamine or deferasirox
Acetaminophen toxicity
N-acetylcysteine
Atropine poisoning
Rx:
physostigmine
Organophosphate poisoning
atropine (lifesaving; crosses BBB) or pralidoxime
Amphetamine poisoning (mydriasis)
ammonium chloride (acidification of urine)
Cyanide toxicity
hydroxocobalamin, sodium nitrate, and sodium thiosulfate
Ethylene glycol poisoning can cause what? & how is it treated?
- Nephrotoxicity (antifreeze)
ethanol and fomepizole
TCA poisoning
sodium bicarbonate
Disulfiram poisoning
aldehyde dehydrogenase
Reboxetine
Maprotiline
MOA:
MOA:
Selective NA reuptake inhibitors(NARIs)
St John’s wort (Hypericum perforatum)
MOA:
Clinical uses:
Effects:
MOA:
Monoamine reuptake inhibitors, MAOI, GABA stimulant
Enzyme inducer
Clinical use:
Natural antidepressant
Active ingredients – hypericin, hyperforin
Effects:
Enzyme inducer it reduces the concentration of:
Warfarin, OCP, antipsychotics, reverse transcriptase inhibitors (Zidovudine)
MOA:
Monoamine reuptake inhibitors, MAOI, GABA stimulant
Enzyme inducer
Clinical use:
Natural antidepressant
Active ingredients – hypericin, hyperforin
Effects:
Enzyme inducer it reduces the concentration of:
Warfarin, OCP, antipsychotics, reverse transcriptase inhibitors (Zidovudine)
St John’s wort (Hypericum perforatum)
MAO-A
VS
MAO-B
MAO-A:
Metabolizes NA, 5-HT and DA and is present in the intestine, peripheral nerve endings and liver.
MAO-B:
Metabolizes DA and is present in the brain, platelets and liver.
Moclebemide
MOA:
MOA:
Inhibits MAO-A selectively and reversibly. Its reversible and short acting, it does not exhibit cheese reaction with foods
Selective MAO -B inhibitors
_________ inhibits only MAO-B and is useful in Parkinsonism.
Selegiline
Major Depressive Disorder treatments options: SSRI & SNRIS
SSRIs –Escitralopram, Sertraline
SNRIs – Venlafaxine, Desvenlafaxine
Generalized anxiety disorder treatment SSRI’s
SSRI (paroxetine, fluoxetine)
OCD – SSRI treatments options
SSRI (Fluoxamine, Clomipramine)
ADHD – TCA treatment options
TCA (Imipramine, Desipramine, Atomoxetine)
Phobia, PTSD, impulse control SSRI treatment options
SSRI (Paroxetine), MAOI (moclobemide)
Nocturnal enuresis treatment options
–Amitriptyline, Imipramine, Desipramine
Bulimia nervosa treatment options
–Fluoxamine, Fluoxetine
Migraine (prophylaxis) treatment
– Amitriptyline
Smoking cessation and nicotine dependence & toxicity
Bupropion & Varenicline
Chronic pain (neuropathic pain)- treatment options
Amitriptyline,Imipramine,Dulaxetine
Fibromyalgia – treatments
Milnacipran
Alcohol dependence - treatments
Citalopram
TCAs
Adverse effects:
1) Anticholinergic S/E - Dry mouth, metallic taste, constipation, urinary retention, tachycardia, blurred vision.
2) Anti- adrenergic action: postural hypotension
3) Anti- histaminic effect: sedation, weakness, fatigue
4) CNS - Lowering of seizure threshold
5) Cardiac: depressant action(similar to Class I antiarrhythmics)
6) Weight gain, jaundice, rashes, leukopenia
1) Anticholinergic S/E - Dry mouth, metallic taste, constipation, urinary retention, tachycardia, blurred vision.
2) Anti- adrenergic action: postural hypotension
3) Anti- histaminic effect: sedation, weakness, fatigue
4) CNS - Lowering of seizure threshold
5) Cardiac: depressant action(similar to Class I antiarrhythmics)
6) Weight gain, jaundice, rashes, leukopenia
All side effects of which drugs?
TCA’s
SSRIs
Adverse effects:
1) Stimulation of 5HT2: Insomnia, increased anxiety, irritability, decreased libido
2) Stimulation of 5HT3: GIT Effects – nausea, vomiting
3) Withdrawal syndrome: headache, dizziness, nausea, insomnia
4)Teratogenic: Paroxetine – congenital cardiac malformations
5) Coadministration of SSRIs with MAO inhibitors can result in serotonin syndrome
1) Stimulation of 5HT2: Insomnia, increased anxiety, irritability, decreased libido
2) Stimulation of 5HT3: GIT Effects – nausea, vomiting
3) Withdrawal syndrome: headache, dizziness, nausea, insomnia
4)Teratogenic: Paroxetine – congenital cardiac malformations
5) Coadministration of SSRIs with MAO inhibitors can result in serotonin syndrome
Are all adverse effects of which drug class
SSRIs
SNRIs
Adverse effects:
1) Nausea, constipation, headache, insomnia, sexual dysfunction
2) Venlafaxine- Perinatal complications
1) Nausea, constipation, headache, insomnia, sexual dysfunction
2) Venlafaxine- Perinatal complications
Are all adverse effects of which drug class?
SNRIs
Atypical Antidepressants
Adverse effects
-Trazodone
- Nafazodone
- Mirtazapine
- Reboxetine
- Bupropion
Trazodone - priapism
Nafazodone: Nausea, antimuscarinic action, bradycardia, low BP, sedation, hepatotoxicity
Mirtazapine:↑appetite, weight gain, sedation
Reboxetine: Tachycardia, dry mouth, constipation, sexual dysfunction
Bupropion – seizures
Trazodone - priapism
Nafazodone: Nausea, antimuscarinic action, bradycardia, low BP, sedation, hepatotoxicity
Mirtazapine:↑appetite, weight gain, sedation
Reboxetine: Tachycardia, dry mouth, constipation, sexual dysfunction
Bupropion – seizures
Atypical Antidepressants
A 64-year-old nurse is presentation brought to the emergency room with confusion and fever. On physical exam, her skin is flushed, her oral mucosa is dry, and her pupils are dilated and poorly responsive to light. A bottle of atropine is found in her pocket. Which of the following drugs can cause a similar clinical?
A.Diazepam
B.Amitriptyline
C.Propranolol
D.Carbamazepine
E.Prazosin
B. Amitriptyline
Tricyclic antidepressants
A. have anticonvulsant activity
B. should not be used in patients with glaucoma
C. may increase oral absorption of levodopa
D. are sometimes used as antiarrhythmics
B. should not be used in patients with glaucoma
The ability of several drugs to inhibit the reuptake of CNS amine neurotransmitters is shown in the table below (number of arrows ↓ indicates the intensity of inhibitory actions). Which one of the drugs is most likely to have therapeutic effectiveness in the management of both obsessive-compulsive disorders (OCD) and major depressive disorders?
Drug C appears to be a selective inhibitor of the reuptake of serotonin,
A 60-year-old man is found by his daughter to be confused at home. Emergency medical services are called and he is brought to the emergency department by ambulance. The patient’s daughter, who accompanies him, says that she found an empty bottle of amitriptyline next to his bed. He has not been taking any other medications. In the emergency department, the patient is delirious and says that he sees small animals running around in the corner of the room. He appears flushed. The patient has a brief seizure and becomes unconscious. Temperature is 37.2 C (99 F), blood pressure is 90/62 mm Hg, and pulse is 120/min. Both pupils are dilated and equally reactive to light, and his skin and mucous membranes are dry. Initial ECG shows QRS widening and QTc prolongation. He is transferred to the intensive care unit but dies despite resuscitation attempts. Which of the following pharmacological effects
most likely contributed to the patient’s death?
A. Increased antihistamine effect
B. Sodium channel inhibition
C. Synaptic norepinephrine accumulation
D. Synaptic serotonin accumulation
E. Uncontrolled presynaptic dopamine release
B. Sodium channel inhibition
A 32-year-old woman comes to the office because she has felt sad and worthless for the past 3 months and often cries for no obvious reason. The patient has difficulty sleeping, her appetite is decreased, and she no longer enjoys spending time with friends. She has no significant medical history. A pregnancy test is negative, and TSH is within normal limits. The physician discusses the diagnosis with the patient and initiates first-line pharmacologic treatment. Two days later, the patient is brought to the emergency department after being found lying down next to an empty bottle of the prescribed medication. Temperature is 38.9 C (102 F), blood pressure is 146/92 mm Hg, and heart rate is 118/min and regular. The patient is disoriented, tremulous, and diaphoretic. She has abdominal cramps and diarrhea. Neurologic examination reveals pupillary dilation, bilateral hyperreflexia in the lower extremities, and bilateral, inducible ankle clonus. Which of the following amino acids is a precursor of the neurotransmitter most likely responsible for this patient’s current symptoms?
A. Glutamic acid
B. Histidine
C. Methionine
D. Tryptophan
E. Tyrosine
D. Tryptophan
≥2 of following during a 1m period & social dysfunction
- Delusions
- Hallucinations
- Disorganized speech
- Grossly disorganized/ catatonic behaviour
- Negative symptoms
For a minimum of least 6m
Schizophrenia
Clozapine
MOA:
Clinical uses:
Adverse effects:
MOA:
D2 and 5-HT2A receptor antagonism → Balanced dopamine and serotonin inhibition.
Uses:
Treatment-resistant schizophrenia, reduction in risk of suicidal behavior in schizophrenia or schizoaffective disorder.
Adverse effects:
Agranulocytosis!!!
seizures, myocarditis, weight gain.
MOA:
D2 and 5-HT2A receptor antagonism → Balanced dopamine and serotonin inhibition.
Uses:
Treatment-resistant schizophrenia, reduction in risk of suicidal behavior in schizophrenia or schizoaffective disorder.
Adverse effects:
Agranulocytosis!!!
seizures, myocarditis, weight gain.
Clozapine
Risperidone
MOA:
Clinical uses:
Adverse effects”
MOA:
MOA: 5-HT2A and D2 receptor antagonism → Decreased dopamine and serotonin neurotransmission.
Use:
Indications: Schizophrenia, bipolar I disorder, irritability in autism.
Adverse effect:
1) EPS at higher doses, weight gain, increased prolactin levels, QT prolongation.
1) agitation ,weight gain ,new onset DM ,Hyperprolactinemia (Avoid in old plp)
2) E.P.S.!!!
MOA:
MOA: 5-HT2A and D2 receptor antagonism → Decreased dopamine and serotonin neurotransmission.
Use:
Indications: Schizophrenia, bipolar I disorder, irritability in autism.
Adverse effect:
1) EPS at higher doses, weight gain, increased prolactin levels, QT prolongation.
1) agitation ,weight gain ,new onset DM ,Hyperprolactinemia (Avoid in old plp)
2) E.P.S.!!!
Risperidone
Olanzapine
MOA:
Clinical uses:
Adverse effects:
MOA:
: 5-HT2A and D2 receptor antagonism; histaminergic and anticholinergic actions.
Use:
Mania / Bipolar Disorder (I)
Schizophrenia
Adverse effects:
Significant weight gain, diabetes, dyslipidemia.
MOA:
: 5-HT2A and D2 receptor antagonism; histaminergic and anticholinergic actions.
Use:
Mania / Bipolar Disorder (I)
Schizophrenia
Adverse effects:
Significant weight gain, diabetes, dyslipidemia.
Olanzepine
Quetiapine
MOA:
Clinical uses:
Adverse effects:
Short acting
MOA: 5-HT2A and D2 receptor antagonism; additional action on histamine and adrenergic receptors.
Indications: Schizophrenia, bipolar disorder, major depressive disorder (as adjunct).
Adverse effects:
Sedation & postural hypotension , cataract formation, less Weight gain & hyperprolactinemia
Short acting
MOA: 5-HT2A and D2 receptor antagonism; additional action on histamine and adrenergic receptors.
Indications: Schizophrenia, bipolar disorder, major depressive disorder (as adjunct).
Adverse effects:
Sedation & postural hypotension , cataract formation, less Weight gain & hyperprolactinemia
Quetiapine
Ziprasidone
MOA:
Clinical uses:
Adverse effects:
MOA:
Atypical antipsychotic with combined D2+5-HT2a/2c+H1+a1 blocking activity
Uses:
Schizophrenia & mania
Adverse effects:
QT prolongation & arrhythmia
MOA:
Atypical antipsychotic with combined D2+5-HT2a/2c+H1+a1 blocking activity
Uses:
Schizophrenia & mania
Adverse effects:
QT prolongation & arrhythmia
Ziprasidone
Arpiprazole
MOA:
Clinical uses:
Adverse effects:
MOA:
MOA: Partial agonist at D2 and 5-HT1A receptors; antagonist at 5-HT2A → Modulation of dopamine and serotonin activity.
Indications: Schizophrenia, bipolar disorder, adjunct for major depressive disorder, irritability associated with autism.
Adverse Effects: Less weight gain compared to other atypicals, headache, anxiety, insomnia, nausea.
MOA:
MOA: Partial agonist at D2 and 5-HT1A receptors; antagonist at 5-HT2A → Modulation of dopamine and serotonin activity.
Indications: Schizophrenia, bipolar disorder, adjunct for major depressive disorder, irritability associated with autism.
Adverse Effects: Less weight gain compared to other atypicals, headache, anxiety, insomnia, nausea.
Arpiprazole
Perioral tremor (“Rabbit syndrome”)
Pathology:
Treatment:
Path:
Perioral tremors (lips only)
after months/years of D2 blocker therapies
Treatment
Antiparkinsonian agents often help. Ex .Amantadine
Chlorpromazine
MOA:
Clinical uses:
Adverse effects:
MOA:
D2 dopamine receptor antagonism; anticholinergic effects.
Indications: Schizophrenia, manic phase of bipolar disorder.
A/E
Cholestatic jaundice & Corneal deposits
Anticholinergic effects, sedation, EPS, QT prolongation.
Thioridazine side effect
Pigmentary retinopathy & Cardiotoxicity
Clozapine side effects:
↑ Seizure ,Paradoxical hypersalivation, Agranulocytosis
Olanzapine side effects:
Weight gain & Dysglycemia
Quitiapine side effect:
Cataract
sublingually antipsychotic
Uses:
1) Acute schizophrenia
- Negative symptoms & paranoid schizophrenia
2) Mania in bipolar disorder
A/E-anxiety ,weight gain & insomnia.
Asenapine
MOA : Blocking dopamine D2receptor.
Uses : Clozapine-resistant cases of schizophrenia, Unipolar depression (adjunct, at low dosages)
A/E:
EPS
Amisulpride
MOA:
Potent 5HT2A inverse agonist with no D2 affinity
USE:
Parkinsons
Pimavanserin
A 24-year-old man comes to the emergency department complaining of sudden onset of pain and stiffness on one side of his neck. He was diagnosed with a psychiatric disorder 5 days ago and started on a new medication. His vital signs are within normal limits. The patient’s head is tilted to one side and he cannot straighten it without considerable pain. The most likely cause of his symptoms is inhibition of which of the following receptors?
A. Adrenergic α1
B. Dopaminergic D2
C. GABAA
D. Histaminergic H1
E. Muscarinic M1
F. Serotoninergic 5-HT2A
B. Dopaminergic D2
The data shown in the table below concern the effects of drugs on transmitter in the CNS. Which one of the drugs is most likely to alleviate extrapyramidal dysfunction caused by typical antipsychotics? (The + signs denote intensity of drug action)
Letter A
Letter B
Letter C
Letter D
Letter E
Letter C
A 43-year-old male patient treated with antipsychotic drug for a history of schizophrenia is seen in the emergancy because of complaints of fever, stiffness, and tremor. Her temperature is 104°F, and her. What has occurred?
a. Akathesia
b. Allergy
c. Neuroleptic malignant syndrome (NMS)
d. Tardive Dyskinesia
e. Parkinsonism
c. Neuroleptic malignant syndrome (NMS)
A 38-year-old woman comes to the office due to breast tenderness and absence of menstrual periods over the last 3 months. The patient has a history of schizophrenia and familial hypercholesterolemia. Medications include risperidone, which has led to significant improvement in psychotic symptoms, and atorvastatin. BMI is 26 kg/m?, down from 30 kg/m? 6 months ago after following a strict dietary plan. Basic serum chemistry panel and thyroid function tests are normal, and urine pregnancy test is negative. Which of the following is the most likely explanation for this patient’s amenorrhea?
A. 21-hydroxylase deficiency
B. Asherman syndrome
C. Drug-induced amenorrhea
D. Polycystic ovary syndrome
E. Primary ovarian insufficiency
F. Weight loss
C. Drug-induced amenorrhea
A 23-year-old woman comes to the office describing restlessness in her legs and inability to lie or sit still. The patient was diagnosed with schizophrenia a month ago and medication therapy was initiated. Her dose was increased after 2 weeks. She says, “I haven’t heard any voices since a few days after the medication was increased.” Blood pressure is 140/90 mm Hg and pulse is 90/min. The patient is alert, oriented, fidgety, and anxious. Which of the following is the most likely diagnosis in this patient?
A. Acute dystonia
B. Akathisia
C. Drug-induced parkinsonism
D. Neuroleptic malignant syndrome
E. Psychotic agitation
F. Tardive dyskinesia
B. Akathisia
D1 VS D2 receptor pathways & effects:
D1 acts via Gs Path to increase adenylate cyclase to increase cAMP & activate protein kinase A = increase Ca2+ in heart
D2 acts via Gi Path to inhibit adenylate cyclase & reduce cAMP inhibiting protein kinase A = relaxation
a1/m1/m3 =
a2/m2/D2 =
B1/B2/D1 =
a1/m1/m3 = Gq (+ve phospholipase c to increase IP3, DAG & Ca2+)
a2/m2/D2 = Gi (inhibit AC (reduce cAMP)
B1/B2/D1 =GS (+ve AC (increase cAMP)
Levodopa
A/E of initiation of therapy
A/E of initiation of therapy:
Nausea and vomiting
Postural hypotension
Cardiac arrhythmias
Exacerbation of angina
Altered taste sensation
Levodopa Contraindications
Contraindications:
Psychotic patients
Angle-closure glaucoma
Active peptic ulcer
Melanoma
Levodopa interactions with pyridoxine
Reduces the efficacy of l-dopa
Levodopa interactions with amino acids
Reduces the absorption
Levodopa interactions with antipsychotics, metoclopramide, reserpine
Reduced efficacy
Levodopa interactions with decarboxylase inhibitors
Beneficial interaction (potentiation)
MOA:
selective D2/3 agonists
Parkinsons drugs
Adverse effects
Nausea
Dizziness
Hallucinations
Postural hypotension
Ropinirole
Pramipexole
Rotigotine
Ropinirole
Pramipexole
Rotigotine
MOA:
USE:
A/E
MOA:
selective D2/3 agonists
Parkinsons drugs
Adverse effects
Nausea
Dizziness
Hallucinations
Postural hypotension
Benhexol (trihexyphenidyl)
Benztropine
Procyclidine
Biperedine
moa:
Anti-cholinergics (atropine derivatives)
Use;
‘drug-induced parkinsonism’
A/E
Sedation (anti-hisamines)
Mental confusion
Constipation
Urinary retention
Blurred vision through cycloplegia (Avoid in narrow - angle glaucoma)
MOA:
Directly stimulates both D1 and D2 receptors
(More effective than bromocriptine)
Status: no longer available because its use has been associated with valvular heart disease
Pergolide
ALS treatment:
Edaravone, Baclofen, Tizanidine, Riluzole
: free radical scavenging properties that may reduce oxidative stress,
Used for ALS spasticity
Edaravone
:GABA B receptor agonist used for ALS
Baclofen
agonist of α2 adrenergic receptors in the CNS. It reduces muscle spasticity, probably by increasing presynaptic inhibition of motor neurons.
Used for ALS
Tizanidine :
Na+ channel & glutamate blocker used in ALS
Riluzole
MS treatment:
Natalizumab
Ocrelizumab
Alemtuzumab
Fingolimod
Modulator
IFN-β
Glatiramer acetate
Teriflunomide
Monoclonal antibody against integrin α4 USED IN MS
Prevents lymphocytes from binding to endothelial cells (blocking BBB entry)
Natalizumab
First line Rx in MS
Depletes B cells via mAB against CD20 (B cells)
Ocrelizumab
2nd line Rx for MS
mAB against CD52 (many side effects though)
Alemtuzumab
Sphingosine S1P-R agonist Used for MS
It traps lymphocytes in the spleen & LN by preventing their egress
A/E:
1st degree heart block & bradycardia
Fingolimod
Immunomodulator used in MS
It down regulates MHC expression on APC to reduce pro-inflammatory cytokines & Tcell production
A/E:
Flu-like & Injection site reaction
IFN-β
Immunomodulator used in MS SAFEST IN PREGGOS
It suppresses Tcells by binding MHC to reduce proinflammatory cytokines
A/E:
Flushing
Chest tightness/Dyspnea
Palpations/Anxiety
Lipoatrophy
Glatiramer acetate
Pyrimidine synthesis inhibitor used in MS
AVOID IN PREGGOS!!!!
Teriflunomide
Q
What Is the rationale for combining levodopa with carbidopa?
A. Carbidopa stimulates dopamine receptors
B. Carbidopa increases levodopa entry into the CNS by inhibiting peripheral dopa decarboxylase
C. Carbidopa enhances levodopa absorption
D. Carbidopa enhances the peripheral conversion of levodopa to dopamine
E. Carbidopa blocks peripheral COMT
B. Carbidopa increases levodopa entry into the CNS by inhibiting peripheral dopa decarboxylase
A study is performed to evaluate the effects of a high-potency typical antipsychotic drug on neurons in vitro in a bath that contains acetylcholine, dopamine, norepinephrine, and serotonin. The receptor being studied is believed to be responsible for the therapeutic efficacy and extrapyramidal side effects of this drug in schizophrenic patients. Which of the following effects would most likely occur intracellularly after the addition of this typical antipsychotic agent (D2 Blocking ) to the bath?
A. Increased Ca
B. Increased cAMP
C. Increased cGMP
D. Increased CI
E. Increased Na
B. Increased cAMP
A 72-year-old man is brought to the physician for a follow-up examination by his wife. For the past year, his wife has noticed that when the patient is reading the newspaper, he continually moves his fingers and hands. At first, the movements were only on the right side, but they have since spread to the left side too. His movements subside when he performs acts such as picking up a glass of water. Which of the following drugs acts by inhibiting the metabolism of the neurotransmitter that is deficient in this patient?
A. Benztropine
B. Bromocriptine
C. Levodopa
D. Ropinirole
E.Selegeline
E.Selegeline
A 58-year-old man with Parkinson’s disease presents to the clinic for follow-up. Recently, he has experienced an increase in his resting tremor and rigidity. He was wondering if there is a medication that could help these symptoms. What anticholinergic is the most appropriate treatment?
(A) Benztropine
(B) Bromocriptine
(C) Ipratropium
(D) Scopolamine
(E) Tropicamide
(A) Benztropine
A 48-year-old man with schizophrenia on thioridazine for 1 week develops restlessness and spasm of his arm and leg. Physical examination of the heart, lungs, and abdomen are unremarkable. Blockage of which neurotransmitter is responsible for extra pyramidal symptoms in this man?
(A) Acetylcholine
(B) Dopamine
(C) Epinephrine
(D) Norepinephrine
(E) Serotonin
(B) Dopamine
A 60-year-old man is brought to the physician by his wife because of progressive weakness of his hands and arms and difficulty walking. There is spasticity with flexion and extension at the elbows, and moderate spasticity with flexion and extension at the knees. Patient diagnose with ALS . Which of the following drugs will most likely prolong this patient’s life?
A. Bromocrptine
B. Clonazepam
C. Dantrolene
D. Riluzole
E. Tizanidine
D. Riluzole
A 27-year-old man with a history of paranoid schizophrenia is being treated with an antipsychotic drug. He comes to the physician because of a painful, involuntary twisting of his neck, a feeling of inner restlessness, tremor, and a difficulties initiating movement. His physician starts him on benztropine. Which of the following is the most likely side effect from this medication?
A. Bradycardia
B. Bronchoconstriction
C. Lacrimation
D. Miosis
E. Xerostomia
E. Xerostomia
MOA:
GABAB agonist
Uses
1. ALS
A/E:
Tolerance
Baclofen
Central α2 agonists
A/E
Clonidine & Tizanidine
A/E:
Tizanidine may cause asthenia, drowsiness, dry mouth, and hypotension
A 54-year-old quadriplegic man with suspected bacterial pneumonia is admitted to the hospital and started on intravenous antibiotics. Over the next 24 hours, he develops progressive respiratory failure requiring mechanical ventilation. Prior to intubation, a skeletal muscle relaxant is administered and the patient subsequently goes into cardiac arrest. His attached cardiac monitor shows ventricular fibrillation. While he is being resuscitated, his serum potassium level is drawn and later comes back as 10.0 mEq/L. Which of the following drug administration is most likely responsible for this patient’s condition?
A. Atracurium
B. Baclofen
C. Dantrolene
D. Succinylcholine
E. Vecuronium
D. Succinylcholine
A 66-year-old man is admitted to the hospital for a COPD exacerbation. While being cared for by the internal medicine service, he develops hypercapnic respiratory failure. He is transferred to the intensive care unit, where he undergoes rapid sequence intubation with muscle relaxant drug X and an appropriate sedative. He then is started on mechanical ventilation, however, he remains apneic longer than expected. Anesthesiology is consulted, and the patient’s neuromuscular blockade is assessed using train-of-four stimulation. The results are shown below.
When the anesthesiologist sees the responses obtained at 20 minutes, she administers neostigmine and the patient soon resumes spontaneous respirations. Drug X is most likely which of the following?
A.Dantrolene
B.Pancuronium
C.Succinylcholine
D.Midazolam
E.Tubocurarine
C.Succinylcholine
A 63-year-old man underwent abdominal surgery for prostate cancer. General anesthesia was supplemented with tubocurarine. Which of the following anatomical
structures most likely represents the main site of action of the drug for this clinical application?
A. Ganglionic neuron membranes
B. Adrenal medulla
C. Postjunctional folds of motor end plates
D. Autonomic cholinergic nerve terminals
E. Skeletal muscle cell membranes
C. Postjunctional folds of motor end plates
A 49-year-old man diagnosed with inguinal hernia was prepared for surgery. Shortly after the initiation of general anesthesia with halothane and succinylcholine, the patient developed muscle rigidity, tachycardia, labile blood pressure, profuse diaphoresis, and high fever (104.2°F, 40.1°C). The anesthesia was discontinued at once, and a drug was administered by rapid intravenous push. Which of the following was most likely the mechanism of action of the administered drug for management ?
A. Activation of GABAB receptors in the spinal cord
B. Blockade of excitatory neurotransmitter release in the
brain
C. Blockade of Ca2+ channels in the sarcoplasmic reticulum
D. Increased K+ conductance in the skeletal muscle membrane
C. Blockade of Ca2+ channels in the sarcoplasmic reticulum
A 74-year-old man underwent abdominal surgery to remove a colon carcinoma. The patient had severely impaired hepatic and renal function, and the anesthesiologist decided to supplement general anesthesia with a muscle relaxant that is inactivated primarily by a form of spontaneous breakdown (also known as Hoffmann elimination). Which of the following drugs was most likely given?
A. Succinylcholine B. Dantrolene
C. Tubocurarine D. Atracurium
E. Mivacurium
D. Atracurium
A 34-year-old woman suffering from hemifacial spasms started treatment with botulinum toxin injected directly into the abnormally contracting muscles. Which of the following molecular actions most likely mediated the therapeutic effect of the drug in the patient’s disorder?
A. Long-last ing activation of Nm acetylcholine receptors
B. Inhibition of acetylcholine storage into synaptic vesicles
C. Inhibition of cholineacetyltransferase
D. Inhibition of acetylcholine exocytosis from cholinergic terminals
E. Stimulation of acetylcholinesterase
F. Opening of Ca2+ channels in cholinergic terminals
D. Inhibition of acetylcholine exocytosis from cholinergic terminals
A 41-year-old man suffering from amyotrophic lateral sclerosis presented to his physician with muscle fasciculations, limb spasticity, hyperactive deep tendon reflexes, and extensor plantar re flexes. Baclofen was prescribed to reduce spasticity and cramps. Which of the following actions most likely mediated the therapeutic effect of the drug in the patient’s disease?
A. Activation of GABA B receptors in the spinal cord
B. Blockade of Nm receptors of motor end plates
C. Increased substance P release in the spinal cord
D. Blockade of Ca2+ channels in skeletal muscle membranes
E. Increased K+ conductance in skeletal muscle
A. Activation of GABA B receptors in the spinal cord
A 45-year-old man is brought to the emergency department 20 minutes after being involved in a motor vehicle collision. The patient has a pneumothorax, several rib fractures, and an orbital fracture. His temperature is 37.5°C (99.5°F), pulse is 106/min, respirations are 14/min (ventilated mechanically), and blood pressure is 105/75 mm Hg. He is administered vecuronium when intubated and admitted to the intensive care unit for several days. The effects of vecuronium are reversed to examine the patient’s neurologic status. Which of the following will be most effective in reversing the paralysis caused by vecuronium?
A. Atracurium
B. Dantrolene
C. Neostigmine
D. Succinylcholine
E. Tubocurarine
C. Neostigmine
A 30-year-old man with asthma has a severe attack and comes to the emergency department. Because of increasing pCO2and decreasing oxygenation, the resident opts to perform an endotracheal intubation. Which of the following neuromuscular blocking agents would be most appropriate to use before this procedure?
A) Atracurium
B) Cisatracurium
C) Mivacurium
D) Succinylcholine
E) Vecuronium
D) Succinylcholine
Which of the following neuromuscular blocking agents is most likely to increase serum potassium?
A) Atracurium
B) Cisatracurium
C) Mivacurium
D) Succinylcholine
E) Vecuronium
D) Succinylcholine
Which of the following neuromuscular blocking agents is safest for patients who have chronic kidney disease?
A) Cisatracurium
B) Mivacurium
C) Pancuronium
D) Rocuronium
E) Vecuronium
A) Cisatracurium
A 71-year-old man will undergo a prostate needle biopsy under anesthesia because of his low pain tolerance and high level of anxiety. The procedure is estimated to take approximately 10 min to complete. Which of the following is the most appropriate anesthetic agent for the patient to receive?
(A) Doxacurium
(B) Mivacurium
(C) Pancuronium
(D) Rocuronium
(E) Tubocurarine
(B) Mivacurium
Clinical Presentation: Symptoms depend on the brain region involved; may have motor, sensory, autonomic, or psychic symptoms without loss of consciousness (simple partial) or with impairment (complex partial).
“PartiaL/focaLseizure involve Consciousness”
Partial (Focal) Seizures
Carbamazepine
Phenytoin
Lamotrigine
Levetiracetam
Clinical Presentation: Sudden, brief, involuntary muscle jerks.
Myoclonic Seizures
Valproate
Levetiracetam
Topiramate
Clinical Presentation: A seizure lasting more than 5 minutes or two or more seizures within a 5-minute period without the person returning to normal between them.
Topiramate
Benzodiazepines (Lorazepam, Diazepam)
Phenytoin
Valproate
Levetiracetam
Esters
MOA:
Clinical uses:
A/E:
Examples: Procaine, Benzocaine (Note that these have one “i” in their generic name.)
MOA: Block sodium channels, inhibiting nerve impulse conduction.
Clinical Uses:
Procaine: Infiltration anesthesia, nerve block.
Benzocaine: Topical anesthesia for skin and mucous membrane.
A/E:
Allergy (more common with esters due to PABA metabolite).
Examples: Procaine, Benzocaine (Note that these have one “i” in their generic name.)
MOA: Block sodium channels, inhibiting nerve impulse conduction.
Clinical Uses:
Procaine: Infiltration anesthesia, nerve block.
Benzocaine: Topical anesthesia for skin and mucous membrane.
A/E:
Allergy (more common with esters due to PABA metabolite).
Esters
Examples: Procaine, Benzocaine (Note that these have one “i” in their generic name.)
Amides
MOA:
Clinical uses:
A/E:
Examples: Lidocaine, Bupivacaine, Ropivacaine (Note that these have two “i” in their generic name.)
MOA: Block sodium channels, inhibiting nerve impulse conduction. Unlike esters, they are metabolized primarily in the liver.
Clinical Uses:
Lidocaine: Topical, infiltration, nerve block, epidural, and IV for cardiac arrhythmias.
Bupivacaine: Epidural, spinal, and peripheral nerve blocks; longer duration than lidocaine.
Ropivacaine: Similar to bupivacaine but with less cardiotoxicity; used for surgical anesthesia and pain management.
S/E:
CNS toxicity (e.g., seizures), especially at high doses or with accidental intravascular injection.
Cardiovascular toxicity (more pronounced with bupivacaine), including arrhythmias and cardiac arrest.
Examples: Lidocaine, Bupivacaine, Ropivacaine (Note that these have two “i” in their generic name.)
MOA: Block sodium channels, inhibiting nerve impulse conduction. Unlike esters, they are metabolized primarily in the liver.
Clinical Uses:
Lidocaine: Topical, infiltration, nerve block, epidural, and IV for cardiac arrhythmias.
Bupivacaine: Epidural, spinal, and peripheral nerve blocks; longer duration than lidocaine.
Ropivacaine: Similar to bupivacaine but with less cardiotoxicity; used for surgical anesthesia and pain management.
S/E:
CNS toxicity (e.g., seizures), especially at high doses or with accidental intravascular injection.
Cardiovascular toxicity (more pronounced with bupivacaine), including arrhythmias and cardiac arrest.
Amides
MAC: ~105% (High MAC, Low Potency)
Advantages: Minimal cardiac effects, rapid onset and recovery.
Disadvantages: Low potency, must be used with other anesthetics.
Clinical Uses: Analgesia, minor surgical procedures.
HY S/E: Expansion of trapped gas in body cavities.
Nitrous Oxide (NO) (inhaled)
MAC: 0.75%
Advantages: Potent with smooth induction.
Disadvantages: Hepatotoxicity, sensitization to catecholamines.
Clinical Uses: Mostly pediatric anesthesia.
HY S/E: Malignant hyperthermia, hepatotoxicity
Halothane (inhaled)
MAC: 1.15%
Advantages: Potent, muscle relaxing, stable hemodynamics.
Disadvantages: Pungent, can cause respiratory irritation.
Clinical Uses: Maintaining anesthesia.
HY S/E: Mild respiratory irritation.
Isoflurane (inhaled)
MAC: 6.0%
Advantages: Very rapid onset and emergence.
Disadvantages: Airway irritation, requires special vaporizer due to high vapor pressure.
Clinical Uses: Rapid adjustment of anesthetic depth.
HY S/E: Coughing, laryngospasm, especially upon induction.
Desflurane (inhaled)
Clinical Uses: Induction of anesthesia, short surgical procedures.
Advantages: Rapid onset, short duration.
Disadvantages: Poor analgesic properties,
respiratory and cardiovascular depression.
HY S/E: Respiratory depression, hypotension.
Thiopentone Sodium (Thiopental)
IV Anesthetics
Clinical Uses: Induction and maintenance of anesthesia, sedation for procedures.
Advantages: Rapid onset and recovery, antiemetic properties.
Disadvantages: Pain on injection, respiratory and cardiovascular depression.
HY S/E: Propofol Infusion Syndrome (rare but serious).
Propofol
(IV)
Clinical Uses: Induction of anesthesia, especially in patients with risk of hypotension and asthma.
Advantages: Preserves airway reflexes, stimulates heart rate and blood pressure.
Disadvantages: Emergence reactions (hallucinations), increased intracranial pressure.
HY S/E: Emergence reactions, increased secretions.
Ketamine (IV)
Clinical Uses: Analgesia during and after surgery, component of general anesthesia.
Advantages: Potent analgesia, stable hemodynamics.
Disadvantages: Respiratory depression, nausea, pruritus.
HY S/E: Respiratory depression, risk of opioid addiction.
Opioids (e.g., Fentanyl)
(IV)
Clinical Uses: Pre-anesthetic sedation, induction of anesthesia, procedural sedation.
Advantages: Anxiolysis, anterograde amnesia, muscle relaxation.
Disadvantages: Respiratory depression, hypotension.
HY S/E: Sedation, amnesia.
Benzodiazepines (e.g., Midazolam)
(IV)
Clinical Uses: Rarely used for anesthesia due to better alternatives; used in controlling certain types of seizures.
Advantages: Seizure control.
Disadvantages: Respiratory depression, cardiovascular effects.
HY S/E: Respiratory depression, dependency.
Barbiturates (e.g., Phenobarbital)
(IV)
Drug inducers
“St.Johns Pheny pheny Mom Never Refuses Greasy Carbs & Chronic alcohol”
*Chronic alcohol
Smoking
*Rifampin
*Phenobarbital
*Carbamazepine
*Griseofulvin
*Phenytoin
St. John’s Wort
Drug inhibitors
Isoniazid
*Erythromycin
*Cimetidine
*Azoles
*Grapefruit juice
*Ritonavir (HIV)
Omeprazole
Acquired resistance to Penicillin’s
B-lactamase
Mutated PBP
Mutated porin proteins
Acquired resistance to Vancomycin
Mutated Peptidoglycan cell wall
Efflux pumps
Acquired resistance to Quinolones
Mutated DNA gyrase
Efflux pump
Acquired resistance to Aminoglycosides
Modifying enzymes
Mutated ribosomal & or prion protein
Acquired resistance to TCA’s
Efflux pump
Inactivates enzyme
Acquired resistance to Rifamycin’s
Mutated RNA polymerase
30 S inhibitors “buy AT 30”
Aminoglycosides
TCAs
50 S inhibitors “CCEL at 50”
Chloramphenicol
Clindamycin
Erythromycin (Macrolides)
Linezolid
Mydriasis
Drugs
Anticholinergics (Atropine, TCAs, Topicamide, Scopolamine, Antihistamines)
Drugs of abuse (Amphetamines, cocaine, LSD) Meperidine
Miosis
Drugs
alpha-2 agonists
Drugs of abuse (Heroin & opioids)
Pilocarpine & organophosphates
Methanol
OD & Treatment
OD:
Respiratory failure
Severe anion gap met acidosis
Ocular damage
Rx:
Fomepizole
