Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm SJSM > Block 4 Quiz > Flashcards

Block 4 Quiz Flashcards

1
Q

Phenobarbital, Pentobarbital, Thiopental, & Secobarbital

MOA:

Clinical use:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Barbiturates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Barbiturates Toxicity can be treated with which drug?

A

Sodium bicarbonate (to alkalinize urine and enhance renal excretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

Benzodiazepines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Zolpidem, Zaleplon, & esZopiclone

MOA:

Clinical use:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clonazepam is useful in the therapy of __________

A

Absence seizures and myoclonic seizures in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Diazepam currently is the drug of choice for the treatment of __________

A

status epilepticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

Non-Benzodiazepine hypnotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Suvorexant

MOA:

Clinical use:

Adverse effects:

A

MOA:
Antagonizes orexin (hypocretin)

Clinical use:
Insomnia

Adverse effects:
1) CNS depression
2) Headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MOA:
Antagonizes orexin (hypocretin)

Clinical use:
Insomnia

Adverse effects:
1) CNS depression
2) Headache

A

Suvorexant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ramelteon

MOA:

Clinical use:

A

MOA:
Binds MT1/2 (Melatonin) in suprachiasmatic nucleus

Clinical use:
Insomnia

No dependence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

MOA:
Binds MT1/2 (Melatonin) in suprachiasmatic nucleus

Clinical use:
Insomnia

No dependence

A

Ramelteon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Carbidopa & Levodopa

MOA:

Clinical use:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

Carbidopa & Levodopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Amantadine

MOA:

Clinical use:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Amantadine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Selegine & Rasagiline

MOA:

Clinical use:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

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

A

Selegine & Rasagiline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tolcapone & Entacapone

MOA:

Clinical use:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

MOA:
COMT inhibitor that increases levodopa availability in brain

Clinical use:
Parkinsons (Only given with levodopa)

Adverse effects:
1) Hepatotoxicity

A

Tolcapone & Entacapone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Ketamine

MOA:

Clinical use:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

Ketamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pramipexole & Ropinirole

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A

Pramipexole & Ropinirole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Bromocriptine

MOA:

Clinical uses:

Adverse effects:

A

Ergot dopamine agonist
acting selectively on D2 receptors

Clinical use:
1) Parkinsons
2) Hyperprolactinemia

Adverse effects:
1) Anticholinergic effects
2) Raynaud Phenomenon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Ergot dopamine agonist
acting selectively on D2 receptors

Clinical use:
1) Parkinsons
2) Hyperprolactinemia

Adverse effects:
1) Anticholinergic effects
2) Raynaud Phenomenon

A

Bromocriptine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Donepezil (1#), Rivastigmine, Galantamine

MOA:

Clinical uses:

Adverse effects:

A

MOA:
AChE inhibitors

Clinical use:
Alzheimer’s

Adverse effects:
1) Insomnia

Avoid in patients with cardiac conduction issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MOA:
AChE inhibitors

Clinical use:
Alzheimer’s

Adverse effects:
1) Insomnia

Avoid in patients with cardiac conduction issues

A

Donepezil (1#), Rivastigmine, Galantamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Memantine

MOA:

Clinical use:

Adverse effects:

A

MOA:
Regulates glutamate to prevent excitotoxicity.

Clinical uses:
1) Alzheimer’s (moderate to advanced dementia)

Adverse effects:
1) Confusion & Hallucination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

MOA:
Regulates glutamate to prevent excitotoxicity.

Clinical uses:
1) Alzheimer’s (moderate to advanced dementia)

Adverse effects:
1) Confusion & Hallucination

A

Memantidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Riluzole

MOA:

Clinical uses:

A

MOA:
Reduces glutamate excitotoxicity in neurons
via (Na+, GABA, glutamate, NMDA) to reduce motor neuron degeneration

Clinical use:
ALS (slows progression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

MOA:
Reduces glutamate excitotoxicity in neurons
via (Na+, GABA, glutamate, NMDA) to reduce motor neuron degeneration

Clinical use:
ALS (slows progression)

A

Riluzole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Tetrabenazine

MOA:

Clinical use:

A

MOA:
Inhibits VMAT to reduce DA release & degradation from monoamine oxidase

Clinical use:
Huntington’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

MOA:
Inhibits VMAT to reduce DA release & degradation from monoamine oxidase

Clinical use:
Huntington’s

A

Tetrabenazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Desflurane, Halothane, Enflurane, Isoflurane, Sevoflurance, Methoxyflurane, & N2O

MOA:

Clinical use:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

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)

A

Inhaled anesthetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Malignant hyperthermia

Pathology:

Triggers:

Treatment:

A

Path:
RYRI (ryanodine) mutation exposed to inhaled anesthetics causing Ca2+ release from the SR resulting severe muscle contractions & hyperthermia

Triggers:
Inhaled anesthetics

Treatment:
Dantrolene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Path:
RYRI (ryanodine) mutation exposed to inhaled anesthetics causing Ca2+ release from the SR resulting severe muscle contractions & hyperthermia

Triggers:
Inhaled anesthetics

Treatment:
Dantrolene

A

Malignant hyperthermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Thiopental

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

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

A

Thiopental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Midalozam

MOA:

Clinical use:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

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

A

Midalozam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Propofol

MOA:

Clinical use:

Adverse effects:

A

GABA agonist

Clinical use:
IV anesthetic with strong sedative properties

Adverse effects:
1) profound hypotension (combo of reduced SVR and cardiac depression)_

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

GABA agonist

Clinical use:
IV anesthetic with strong sedative properties

Adverse effects:
1) profound hypotension (combo of reduced SVR and cardiac depression)_

A

Propofol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Haloperidol

MOA:

Clinical use:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

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

A

Haloperidol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Neuroleptic malignant syndrome

Pathology:

Triggers:

Treatment:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

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)

A

Neuroleptic malignant syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Extrapyramidal symptoms- Acute dystonia

Pathology:

Treatment:

A

Acute (hours),
MUSCLE

Treatment:
1)Anticholinergics
- Trihexyphenidyl
- Benztropine
2) Antihistamines
- diphenhydramine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Acute (hours),
MUSCLE

Treatment:
1)Anticholinergics
- Trihexyphenidyl
- Benztropine
2) Antihistamines
- diphenhydramine

A

Extrapyramidal symptoms- Acute dystonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Extrapyramidal symptoms- Akathisia

Pathology:

Treatment:

A

Sub chronic (days)
RUSTLE

Treatment:
- Benztropine
- Benzodiazepines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Sub chronic (days)
RUSTLE

Treatment:
- Benztropine
- Benzodiazepines

A

Extrapyramidal symptoms- Akathisia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Extrapyramidal symptoms- Akinesia/Parkinsonism

Pathology:

Treatment:

A

Sub chronic (weeks)
1) Bradykinesia
2) Cogwheel rigidity
3) Tremor/Shuffling gait

Treatment:
Benztropine or Amantadine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Sub chronic (weeks)
1) Bradykinesia
2) Cogwheel rigidity
3) Tremor/Shuffling gait

Treatment:
Benztropine or Amantadine

A

Extrapyramidal symptoms- Akinesia/Parkinsonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Extrapyramidal symptoms- Tardive dyskinesia

Pathology:

Trigger:

Treatment:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

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

A

Extrapyramidal symptoms- Tardive dyskinesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Procaine, Tetracaine, Benzocaine, & Chloroprocaine

MOA:

Clinical uses:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

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)

A

Local Anesthetics
Esters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Lidocaine, Mepivacaine, Bupivacaine, Ropivacaine, & Prilocaine (all have 2 i’s)

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

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

A

Local anesthetics
(Amides)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Na+ channel blockers used in epilepsy?

“Crappy FLiP TV”

A

Carbamazepine
Fosphenytoin
Lamotrigine
Phenytoin
Topiramate
Valproate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Carbamazepine
Fosphenytoin
Lamotrigine
Phenytoin
Topiramate
Valproate

Are all examples of which class of drug?

A

Na+ blockers used in epilepsy treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Valproic Acid (Valproate)

MOA:

Clinical use:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

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)

A

Valproic Acid (Valproate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Clinical Presentation: Characterized by sudden muscle rigidity (tonic phase) followed by synchronous muscle jerks (clonic phase), loss of consciousness.

A

Valproic Acid (Valproate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Carbamazepine

MOA:

Clinical use:

Adverse effect:

A

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,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

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,

A

Carbamazepine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Ethosuximide

MOA:

Clinical uses:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

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)

A

Ethosuximide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Gabapentin & Pregabalin

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

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

A

Gabapentin & Pregabalin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Lamotrigine

MOA:

Clinical use:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

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

A

Lamotrigine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Levetricetam & Brivaracetam

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

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

A

Levetiracetam & Brivaracetam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Topiramate

MOA:

Clinical uses:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

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)

A

Topiramate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Vigabatrin

MOA:

Clinical uses:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

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)

A

Vigabatrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Fill in the missing drug names!

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Barbiturates (Phenobarbital, Thiopental, Primidone, Mephobarbital)

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

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

A

Barbiturates (Phenobarbital, Thiopental, Primidone, Mephobarbital)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Barbiturate toxicity

Effects:

A

Toxicity:
1) Sedation
2) Agitation
3) Confusion (elderly)
4) Irritability/Hperactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Primidone (Barbiturate) treats:

A

Focal or generalized epilepsy but it has a lower incidence of sedation

Adverse effects:
Dose-dependent pronounced drowsiness & barbiturate side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Phenytoin & Fosphenytoin

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

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

A

Phenytoin & Fosphenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Diplopia, Ataxia, & Sedation represents which type of toxicity?

A

Phenytoin toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Lithium

MOA:

Clinical use:

Adverse effects:

Acute toxicity:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

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

A

Lithium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Treatment of acute lithium toxicity includes…

A

Thiazide diuretics, ACE inhibitors, & NSAIDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Buspirone

MOA:

Clinical uses:

A

MOA:
A partial 5-HTA1 agonist

Clinical uses:
1) GAD **
(2nd line, slow onset ~2wks)

No dependence/abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

MOA:
A partial 5-HTA1 agonist

Clinical uses:
1) GAD **
(2nd line, slow onset ~2wks)

No dependence/abuse

A

Buspirone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Methylphenidate (Ritalin)

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

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

A

Methylphenidate (Ritalin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Valproic acid, Phenytoin, Carbamazepine, & Lamotrigine all treat which type of seizures?

A

Partial (focal) & general (tonic-clonic) seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Lorazepam, Diazepam, Phenytoin, & Fosphenytoin all treat which type of condition?

A

Status epilepticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Ethosuximide & Valproic acid both treat which type of seizures?

A

Absence seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Fluoxetine, Fluvoxamine, Paroxetine, Sertraline, Escitalopram, & Citalopram

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

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

A

SSRI’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Venlafaxine, Desvenlafaxine, Duloxetine, Milnacipran, & Levomilnacipran

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

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

A

SNRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Serotonin syndrome

Pathology:

Treatment:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Antidepressant discontinuation syndrome

Pathology:

Treatment:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Bupropion

MOA:

Clinical uses:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

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)

A

Bupropion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Stimulant effects (tachycardia & insomnia), Headache, Seizures in patients with eating disorders indicated which type of drug toxicity?

A

Bupropion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Amitriptyline, Nortriptyline, Imipramine, Desipramine, Clomipramine, Doxepin, & Amoxapine

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

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

A

TCA’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Acute TCA overdose presents with severe anticholinergic symptoms, arrhythmias, seizures, and hypotension can be treated with what?

A

NaHCO3

Theorized that the Na+ helps to relieve Na+ channel blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Baclofen

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

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

A

Baclofen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Triptans (Sumatriptan)

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

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

A

Triptans (Sumatriptan)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Benztropine & Trihexyphenidyl

MOA:

Clinical uses:

Adverse effects:

A

MOA:
Act as Anticholinergic

Clinical Uses:
1) Parkinson’s disease (tremor & rigidity)
2) Drug-induced parkinsonism (1st line)

Adverse Effects:
Anticholinergic side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

MOA:
Act as Anticholinergic

Clinical Uses:
1) Parkinson’s disease (tremor & rigidity)
2) Drug-induced parkinsonism (1st line)

Adverse Effects:
Anticholinergic side effects

A

Benztropine & Trihexyphenidyl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Tetrabenazine

MOA:

Clinical uses:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

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

A

Tetrabenazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Morphine, oxymorphone, hydromorphone
Heroin
Fentanyl
Codeine, oxycodone, hydrocodone
Methadone
Meperidine

MOA:

Clinical uses:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

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)

A

Full Opioid Agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Buprenorphine
Nalbuphine
Pentazocine
Butorphanol

Individual MOA’s

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

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

A

Partial Opioid Agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Dextromethorphan

MOA:

Clinical uses:

A

MOA:
Opioid receptor agonist

Clinical Use:
1) Cough suppressant/antitussive
It’s the main ingredient in Robitussin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

MOA:
Opioid receptor agonist

Clinical Use:
1) Cough suppressant/antitussive
It’s the main ingredient in Robitussin

A

Dextromethorphan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Tramadol

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

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

A

Tramadol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Naloxone (Narcan)

MOA:

Clinical uses:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

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)

A

Naloxone (Narcan)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Naltrexone

MOA:

Clinical uses:

A

MOA:
Opioid receptor antagonist

Clinical uses:
1) Alcohol craving 1st-line
2) Opioid dependence maintenance
Effects are slow (cannot be used for acute intoxication)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

MOA:
Opioid receptor antagonist

Clinical uses:
1) Alcohol craving 1st-line
2) Opioid dependence maintenance
Effects are slow (cannot be used for acute intoxication)

A

Naltrexone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Methylnaltrexone

MOA:

Clinical uses:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

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)

A

Methylnaltrexone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Phenelzine
Isocarboxazid
Iproniazid
Selegiline
Tranylcypromine (non-hydrazine)

MOA:

Clinical uses:

Adverse effects:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

MAOI hypertensive crisis (tyramine from cheese/wine)

What is the treatment?

A

take phentolamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

history of taking general anesthetics with muscle relaxant (halothane + succinylcholine)

what is the condition? & the treatment?

A

Malignant hyperthermia treat with Dantrolene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

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

A

Non-Selective Monoamine Oxidase Inhibitors (MAOIs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Mirtazapine

MOA:

Clinical uses:

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

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)

A

Mirtazapine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Trazodone

MOA:

Clinical uses:

Adverse effects:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

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

A

Trazodone

141
Q

Vilazodone

MOA:

Clinicla uses:

Adverse effects:

A

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)

142
Q

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)

A

Vilazodone

143
Q

Vortioxetine

MOA:

Clinical uses:

Adverse effects:

A

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.

144
Q

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.

A

Vortioxetine

145
Q

Varenicline

MOA:

Clinical uses:

Adverse effects:

A

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

146
Q

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

A

Varenicline

147
Q

Curare-derivatives
-curarine (Tubocurarine, Rubocurarine)
-curium (Atracurium, Mivacurium)
-curonium (Pancuronium, Vecuronium, Rocuronium)

MOA:

Clinical uses:

Reversal agents:

Adverse effects:

A

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

148
Q

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

A

Nondepolarizing Neuromuscular Blocking Drugs

149
Q

Succinylcholine (Depolarizing Paralytic)

MOA:

Clinical uses:

Reversible agents:

A

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

150
Q

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

A

Succinylcholine (Depolarizing Paralytic)

151
Q

Cyclobenzaprine

(Mephenesin, Chlorzoxazone, Methocarbamol, Carisoprodol, & Chlormezanone)

MOA:

Clinical uses:

A

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

152
Q

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

A

Cyclobenzaprine

(Mephenesin, Chlorzoxazone, Methocarbamol, Carisoprodol, & Chlormezanone)

153
Q

Dantrolene

MOA:

Clinical uses:

A

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)

154
Q

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)

A

Dantrolene

155
Q

Oxcarbazepine

MOA & Benefits over carbamazepine?

Adverse effect:

A

MOA/Benefits:
Prodrug of carbamazepine, induction capacity is low BUT it’s less likely to be involved in drug

Adverse effects:
Hyponatremia

156
Q

MOA/Benefits:
Prodrug of carbamazepine, induction capacity is low BUT it’s less likely to be involved in drug

Adverse effects:
Hyponatremia

A

Oxcarbazepine

157
Q

Tiagabine

MOA:

Clinical uses:

Adverse effects:

A

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

158
Q

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

A

Tiagabine

159
Q

Status epilepticus

Pathology:

Treatments:
3 lines of treatment

Alternatives for resistant cases

A

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

160
Q

Antiseizure meds to avoid in preggos

& which drug is safe to use in preggos????

A
  1. valproate:
    ‘Spina bifida’ and ‘encephalocele’
  2. carbamazepine &
    Phenytoin
    ‘fetal hydantoin syndrome – IUGR, microcephaly, mental retardation, hypoplastic nails, distal phalages’

Levetiracetam is SAFE IN PREGGOS

161
Q

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

A

H. Amiodarone

162
Q

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

A

C. Lorazepam

163
Q

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

A

D. Inhibition of T-type calcium channels

164
Q

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

A

Phenytoin

(Levetiracetam is safe for Preggos)

165
Q

Which of the following medications causes a decrease in the efficiency of the cytochrome p450 system?
Carbamazepine
Lamotrigine
Levetiracetam
Topiramate
Valproic acid

A

Lamotrigine

166
Q

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

A

(E) Purple discoloration of the hand

167
Q

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

A

(B) Blocks T-type calcium channels

168
Q

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

A

C. Levetiracetam

169
Q
  1. 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

A

(D) Topiramate

170
Q

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

A

1) Carbamazepine

171
Q

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

A

C. Blocks T-type calcium channels

172
Q

Absent seizures (child stares without blinking)

What is the best treatment?

A

Ethosuximide (T-type calcium channel blocker)

173
Q

Tonic-clonic seizures best treatment?

A

Valproic acid

174
Q

Neuroleptic malignant syndrome can be caused by which classes of drugs?

A

1) Dopamine blocker drug (metoclopramide)
2) Antipsychotics (Haloperidol, risperidone, chlorpromazine)

Rx Dantrolene

175
Q

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?

A

cyproheptadine

176
Q

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?

A

Serotonin syndrome treatment with Cyproheptadine: A serotonin antagonist → Reduces serotonin effects.

177
Q

Cheese Reaction

Effect: Tyramine promotes norepinephrine (NE) release from presynaptic vesicles → Excessive NE → Vasoconstriction and increased heart rate → Hypertensive crisis.

What’s the treatment?

A

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.

178
Q

Cheese reaction  caused by mixing TCA + MAOI can be treated with which drug?

A

Phenelzine

179
Q

Which drug treats Alcohol dependence by Reducing cravings?

A

naltrexone (Mu receptor antagonist)

180
Q

Amyotrophic lateral sclerosis can be treated with which drug types?

A

1) Riluzole which increases survival of patient
(slows disease progression)

2) Baclofen which used for muscle spasticity (acts on GABA B receptor)

181
Q

Parkinson’s disease

What are the best treatment options:

A
  1. COMT inhibitor – tolcapone (hepatotoxic) and entacapone
  2. MAOI: selegiline and rasagiline
  3. Amantadine -
    NMDA receptor antagonist causing livedo reticularis
  4. Centrally acting anticholinergic - benztropine, trihexyphenidyl, bipyridine

(Also used to treat extrapyramidal side effect treatment)

182
Q
  1. COMT inhibitor – tolcapone (hepatotoxic) and entacapone
  2. MAOI: selegiline and rasagiline
  3. Amantadine -
    NMDA receptor antagonist causing livedo reticularis
  4. Centrally acting anticholinergic - benztropine, trihexyphenidyl, bipyridine

(Also used to treat extrapyramidal side effect treatment)

A

Parkinson’s disease treatments

183
Q

What’s the best treatment for Wilson diseases?

A

copper chelating agent – penicillamine

184
Q

Opioid receptor Mu & kappa receptor agonists toxicity, what is the best treatment?

Patient presents with Sedation, analgesia, constipation, respiratory depression, dysphoria and constipation

A

Naloxone > Loperamide > Naltrexone

Note -Opioid withdrawal associated with diarrhea

185
Q

Proton pump inhibitors (PPIs) -prazole

MOA:

A

MOA: Irreversibly inhibit H+/K+ -ATPase

Adverse effects:
C difficile infection, pneuminia, acute intersistal nephritis

186
Q

H2 blocker -tidine

MOA:

A

MOA: blocks histamine receptors

187
Q

Ondansetron

MOA:

Clinical uses:

A

MOA: 5-HT3 antagonist

Uses:
Chemotherapy induced nausea and vomiting

188
Q

Metoclopramide

MOA:

Clinical uses:

Adverse effect:

A

MOA: D2 antagonist

Clinical uses:
Weight-loss

Adverse effects:
It causes NMS or extrapyramidal side effects

189
Q

MOA: D2 antagonist

Clinical uses:
Weight-loss

Adverse effects:
It causes NMS or extrapyramidal side effects

A

Metoclopramide

190
Q

Lubiprostone

MOA:

Clinical uses:

Adverse effects;

A

MOA:
A laxative that increases chloride ion secretion

Uses:
IBS associated with constipation

Adverse effects:
Diarrhea

191
Q

MOA:
A laxative that increases chloride ion secretion

Uses:
IBS associated with constipation

Adverse effects:
Diarrhea

A

Lubiprostone

192
Q

Loperamide

MOA:

Clinical uses:

Adverse effects:

A

MOA:
Mu receptor agonist

Uses:
For IBS associated with constipation

Adverse effect:
Constipation

193
Q

MOA:
Mu receptor agonist

Uses:
For IBS associated with constipation

Adverse effect:
Constipation

A

Loperamide

194
Q

What should you give a patient with IBD that has not be improved with traditional drugs?

A

give TNF-alpha antagonist –
infliximab
adalimumab
certolizumab

195
Q

give TNF-alpha antagonist –
infliximab
adalimumab
certolizumab

In cases of what?

A

IBD that’s not be improved with traditional drugs

196
Q

Sildenafil

MOA:

Clinical use:

Adverse effects:

A

MOA:
PDE5 inhibitor that increases cGMP to increase NO signalling & vasodilation

Uses:
Limp wiener

Adverse effects:
Severe hypotension if given with beta blockers

197
Q

MOA:
PDE5 inhibitor that increases cGMP to increase NO signalling & vasodilation

Uses:
Limp wiener

Adverse effects:
Severe hypotension if given with beta blockers

A

Sildenafil

198
Q

Anti-obesity drug that are available?

A

1) Orlistat a lipoprotein lipase inhibitor

2) Liraglutide a GLP1 agonist (FDA approved)

199
Q

1) Orlistat a lipoprotein lipase inhibitor

2) Liraglutide a GLP1 agonist (FDA approved)

Are both used for which condition?

A

Obesity

200
Q

Signs of miosis, respiratory depression constipation

A

Morphine

201
Q

Signs of mydriasis, “crawling bugs”

A

Cocaine toxicity

202
Q

varenicline

MOA:

Clinical uses:

A

MOA:
partial agonist activity on nicotine acetylcholine receptor (A4B2)

Uses:
Nicotine toxicity

203
Q

fomepizole (#1) & ethanol

MOA:

Clinical use:

A

MOA:
inhibit alcohol dehydrogenase enzyme

Use:
Methanol toxicity

204
Q

MOA:
inhibit alcohol dehydrogenase enzyme

Use:
Methanol toxicity

A

Fomepizole (#1) & ethanol

205
Q
  • Signs of ocular damage or respiratory failure
A

Methanol toxicity

Treat with fomepizole > ethanol

206
Q

Signs of garlic breath, rice-water stool, and abdominal pain

A

Arsenic poisoning

Rx:
dimercaprol

207
Q

Iron toxicity what is the treatment?

A

deferoxamine or deferasirox

208
Q

Acetaminophen toxicity

A

N-acetylcysteine

209
Q

Atropine poisoning

A

Rx:
physostigmine

210
Q

Organophosphate poisoning

A

atropine (lifesaving; crosses BBB) or pralidoxime

211
Q

Amphetamine poisoning (mydriasis)

A

ammonium chloride (acidification of urine)

212
Q

Cyanide toxicity

A

hydroxocobalamin, sodium nitrate, and sodium thiosulfate

213
Q

Ethylene glycol poisoning can cause what? & how is it treated?

A
  • Nephrotoxicity (antifreeze)

ethanol and fomepizole

214
Q

TCA poisoning

A

sodium bicarbonate

215
Q

Disulfiram poisoning

A

aldehyde dehydrogenase

216
Q

Reboxetine
Maprotiline

MOA:

A

MOA:
Selective NA reuptake inhibitors(NARIs)

217
Q

St John’s wort (Hypericum perforatum)

MOA:

Clinical uses:

Effects:

A

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)

218
Q

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)

A

St John’s wort (Hypericum perforatum)

219
Q

MAO-A

VS

MAO-B

A

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.

220
Q

Moclebemide

MOA:

A

MOA:
Inhibits MAO-A selectively and reversibly. Its reversible and short acting, it does not exhibit cheese reaction with foods

221
Q

Selective MAO -B inhibitors
_________ inhibits only MAO-B and is useful in Parkinsonism.

A

Selegiline

222
Q

Major Depressive Disorder treatments options: SSRI & SNRIS

A

SSRIs –Escitralopram, Sertraline
SNRIs – Venlafaxine, Desvenlafaxine

223
Q

Generalized anxiety disorder treatment SSRI’s

A

SSRI (paroxetine, fluoxetine)

224
Q

OCD – SSRI treatments options

A

SSRI (Fluoxamine, Clomipramine)

225
Q

ADHD – TCA treatment options

A

TCA (Imipramine, Desipramine, Atomoxetine)

226
Q

Phobia, PTSD, impulse control SSRI treatment options

A

SSRI (Paroxetine), MAOI (moclobemide)

227
Q

Nocturnal enuresis treatment options

A

–Amitriptyline, Imipramine, Desipramine

228
Q

Bulimia nervosa treatment options

A

–Fluoxamine, Fluoxetine

229
Q

Migraine (prophylaxis) treatment

A

– Amitriptyline

230
Q

Smoking cessation and nicotine dependence & toxicity

A

Bupropion & Varenicline

231
Q

Chronic pain (neuropathic pain)- treatment options

A

Amitriptyline,Imipramine,Dulaxetine

232
Q

Fibromyalgia – treatments

A

Milnacipran

233
Q

Alcohol dependence - treatments

A

Citalopram

234
Q

TCAs

Adverse effects:

A

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

235
Q

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?

A

TCA’s

236
Q

SSRIs

Adverse effects:

A

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

237
Q

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

A

SSRIs

238
Q

SNRIs

Adverse effects:

A

1) Nausea, constipation, headache, insomnia, sexual dysfunction

2) Venlafaxine- Perinatal complications

239
Q

1) Nausea, constipation, headache, insomnia, sexual dysfunction

2) Venlafaxine- Perinatal complications

Are all adverse effects of which drug class?

A

SNRIs

240
Q

Atypical Antidepressants

Adverse effects
-Trazodone
- Nafazodone
- Mirtazapine
- Reboxetine
- Bupropion

A

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

241
Q

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

A

Atypical Antidepressants

242
Q

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

A

B. Amitriptyline

243
Q

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

A

B. should not be used in patients with glaucoma

244
Q

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?

A

Drug C appears to be a selective inhibitor of the reuptake of serotonin,

245
Q

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

A

B. Sodium channel inhibition

246
Q

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

A

D. Tryptophan

247
Q

≥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

A

Schizophrenia

248
Q

Clozapine

MOA:

Clinical uses:

Adverse effects:

A

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.

249
Q

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.

A

Clozapine

250
Q

Risperidone

MOA:

Clinical uses:

Adverse effects”

A

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.!!!

251
Q

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.!!!

A

Risperidone

252
Q

Olanzapine

MOA:

Clinical uses:

Adverse effects:

A

MOA:
: 5-HT2A and D2 receptor antagonism; histaminergic and anticholinergic actions.

Use:
Mania / Bipolar Disorder (I)
Schizophrenia

Adverse effects:
Significant weight gain, diabetes, dyslipidemia.

253
Q

MOA:
: 5-HT2A and D2 receptor antagonism; histaminergic and anticholinergic actions.

Use:
Mania / Bipolar Disorder (I)
Schizophrenia

Adverse effects:
Significant weight gain, diabetes, dyslipidemia.

A

Olanzepine

254
Q

Quetiapine

MOA:

Clinical uses:

Adverse effects:

A

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

255
Q

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

A

Quetiapine

256
Q

Ziprasidone

MOA:

Clinical uses:

Adverse effects:

A

MOA:
Atypical antipsychotic with combined D2+5-HT2a/2c+H1+a1 blocking activity

Uses:
Schizophrenia & mania

Adverse effects:
QT prolongation & arrhythmia

257
Q

MOA:
Atypical antipsychotic with combined D2+5-HT2a/2c+H1+a1 blocking activity

Uses:
Schizophrenia & mania

Adverse effects:
QT prolongation & arrhythmia

A

Ziprasidone

258
Q

Arpiprazole

MOA:

Clinical uses:

Adverse effects:

A

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.

259
Q

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.

A

Arpiprazole

260
Q

Perioral tremor (“Rabbit syndrome”)

Pathology:

Treatment:

A

Path:
Perioral tremors (lips only)
after months/years of D2 blocker therapies

Treatment
Antiparkinsonian agents often help. Ex .Amantadine

261
Q

Chlorpromazine

MOA:

Clinical uses:

Adverse effects:

A

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.

262
Q

Thioridazine side effect

A

Pigmentary retinopathy & Cardiotoxicity

263
Q

Clozapine side effects:

A

↑ Seizure ,Paradoxical hypersalivation, Agranulocytosis

264
Q

Olanzapine side effects:

A

Weight gain & Dysglycemia

265
Q

Quitiapine side effect:

A

Cataract

266
Q

sublingually antipsychotic

Uses:
1) Acute schizophrenia
- Negative symptoms & paranoid schizophrenia

2) Mania in bipolar disorder

A/E-anxiety ,weight gain & insomnia.

A

Asenapine

267
Q

MOA : Blocking dopamine D2receptor.

Uses : Clozapine-resistant cases of schizophrenia, Unipolar depression (adjunct, at low dosages)

A/E:
EPS

A

Amisulpride

268
Q

MOA:
Potent 5HT2A inverse agonist with no D2 affinity

USE:
Parkinsons

A

Pimavanserin

269
Q

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

A

B. Dopaminergic D2

270
Q

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

A

Letter C

271
Q

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

A

c. Neuroleptic malignant syndrome (NMS)

272
Q

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

A

C. Drug-induced amenorrhea

273
Q

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

A

B. Akathisia

274
Q

D1 VS D2 receptor pathways & effects:

A

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

275
Q

a1/m1/m3 =

a2/m2/D2 =

B1/B2/D1 =

A

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)

276
Q

Levodopa

A/E of initiation of therapy

A

A/E of initiation of therapy:
Nausea and vomiting
Postural hypotension
Cardiac arrhythmias
Exacerbation of angina
Altered taste sensation

277
Q

Levodopa Contraindications

A

Contraindications:
Psychotic patients
Angle-closure glaucoma
Active peptic ulcer
Melanoma

278
Q

Levodopa interactions with pyridoxine

A

Reduces the efficacy of l-dopa

279
Q

Levodopa interactions with amino acids

A

Reduces the absorption

280
Q

Levodopa interactions with antipsychotics, metoclopramide, reserpine

A

Reduced efficacy

281
Q

Levodopa interactions with decarboxylase inhibitors

A

Beneficial interaction (potentiation)

282
Q

MOA:
selective D2/3 agonists

Parkinsons drugs

Adverse effects
Nausea
Dizziness
Hallucinations
Postural hypotension

A

Ropinirole
Pramipexole
Rotigotine

283
Q

Ropinirole
Pramipexole
Rotigotine

MOA:

USE:

A/E

A

MOA:
selective D2/3 agonists

Parkinsons drugs

Adverse effects
Nausea
Dizziness
Hallucinations
Postural hypotension

284
Q

Benhexol (trihexyphenidyl)
Benztropine
Procyclidine
Biperedine

A

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)

285
Q

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

A

Pergolide

286
Q

ALS treatment:

A

Edaravone, Baclofen, Tizanidine, Riluzole

287
Q

: free radical scavenging properties that may reduce oxidative stress,

Used for ALS spasticity

A

Edaravone

288
Q

:GABA B receptor agonist used for ALS

A

Baclofen

289
Q

agonist of α2 adrenergic receptors in the CNS. It reduces muscle spasticity, probably by increasing presynaptic inhibition of motor neurons.

Used for ALS

A

Tizanidine :

290
Q

Na+ channel & glutamate blocker used in ALS

A

Riluzole

291
Q

MS treatment:

A

Natalizumab
Ocrelizumab
Alemtuzumab
Fingolimod
Modulator
IFN-β
Glatiramer acetate
Teriflunomide

292
Q

Monoclonal antibody against integrin α4 USED IN MS

Prevents lymphocytes from binding to endothelial cells (blocking BBB entry)

A

Natalizumab

293
Q

First line Rx in MS

Depletes B cells via mAB against CD20 (B cells)

A

Ocrelizumab

294
Q

2nd line Rx for MS

mAB against CD52 (many side effects though)

A

Alemtuzumab

295
Q

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

A

Fingolimod

296
Q

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

A

IFN-β

297
Q

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

A

Glatiramer acetate

298
Q

Pyrimidine synthesis inhibitor used in MS

AVOID IN PREGGOS!!!!

A

Teriflunomide

299
Q

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

A

B. Carbidopa increases levodopa entry into the CNS by inhibiting peripheral dopa decarboxylase

300
Q

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

A

B. Increased cAMP

301
Q

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

A

E.Selegeline

302
Q

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

(A) Benztropine

303
Q

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

A

(B) Dopamine

304
Q

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

A

D. Riluzole

305
Q

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

A

E. Xerostomia

306
Q

MOA:
GABAB agonist

Uses
1. ALS

A/E:
Tolerance

A

Baclofen

307
Q

Central α2 agonists

A/E

A

Clonidine & Tizanidine

A/E:
Tizanidine may cause asthenia, drowsiness, dry mouth, and hypotension

308
Q

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

A

D. Succinylcholine

309
Q

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

A

C.Succinylcholine

310
Q

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

A

C. Postjunctional folds of motor end plates

311
Q

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

A

C. Blockade of Ca2+ channels in the sarcoplasmic reticulum

312
Q

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

A

D. Atracurium

313
Q

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

A

D. Inhibition of acetylcholine exocytosis from cholinergic terminals

314
Q

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

A. Activation of GABA B receptors in the spinal cord

315
Q

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

A

C. Neostigmine

316
Q

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

A

D) Succinylcholine

317
Q

Which of the following neuromuscular blocking agents is most likely to increase serum potassium?
A) Atracurium
B) Cisatracurium
C) Mivacurium
D) Succinylcholine
E) Vecuronium

A

D) Succinylcholine

318
Q

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

A) Cisatracurium

319
Q

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

A

(B) Mivacurium

320
Q

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”

A

Partial (Focal) Seizures

Carbamazepine
Phenytoin
Lamotrigine
Levetiracetam

321
Q

Clinical Presentation: Sudden, brief, involuntary muscle jerks.

A

Myoclonic Seizures

Valproate
Levetiracetam
Topiramate

322
Q

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.

A

Topiramate

Benzodiazepines (Lorazepam, Diazepam)
Phenytoin
Valproate
Levetiracetam

323
Q

Esters

MOA:

Clinical uses:

A/E:

A

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).

324
Q

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).

A

Esters

Examples: Procaine, Benzocaine (Note that these have one “i” in their generic name.)

325
Q

Amides

MOA:

Clinical uses:

A/E:

A

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.

326
Q

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.

A

Amides

327
Q

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.

A

Nitrous Oxide (NO) (inhaled)

328
Q

MAC: 0.75%

Advantages: Potent with smooth induction.

Disadvantages: Hepatotoxicity, sensitization to catecholamines.

Clinical Uses: Mostly pediatric anesthesia.

HY S/E: Malignant hyperthermia, hepatotoxicity

A

Halothane (inhaled)

329
Q

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.

A

Isoflurane (inhaled)

330
Q

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.

A

Desflurane (inhaled)

331
Q

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.

A

Thiopentone Sodium (Thiopental)

IV Anesthetics

332
Q

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).

A

Propofol
(IV)

333
Q

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.

A

Ketamine (IV)

334
Q

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.

A

Opioids (e.g., Fentanyl)
(IV)

335
Q

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.

A

Benzodiazepines (e.g., Midazolam)
(IV)

336
Q

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.

A

Barbiturates (e.g., Phenobarbital)
(IV)

337
Q

Drug inducers

“St.Johns Pheny pheny Mom Never Refuses Greasy Carbs & Chronic alcohol”

A

*Chronic alcohol
Smoking
*Rifampin
*Phenobarbital
*Carbamazepine
*Griseofulvin
*Phenytoin
St. John’s Wort

338
Q

Drug inhibitors

A

Isoniazid
*Erythromycin
*Cimetidine
*Azoles
*Grapefruit juice
*Ritonavir (HIV)
Omeprazole

339
Q

Acquired resistance to Penicillin’s

A

B-lactamase
Mutated PBP
Mutated porin proteins

340
Q

Acquired resistance to Vancomycin

A

Mutated Peptidoglycan cell wall
Efflux pumps

341
Q

Acquired resistance to Quinolones

A

Mutated DNA gyrase
Efflux pump

342
Q

Acquired resistance to Aminoglycosides

A

Modifying enzymes
Mutated ribosomal & or prion protein

343
Q

Acquired resistance to TCA’s

A

Efflux pump
Inactivates enzyme

344
Q

Acquired resistance to Rifamycin’s

A

Mutated RNA polymerase

345
Q

30 S inhibitors “buy AT 30”

A

Aminoglycosides
TCAs

346
Q

50 S inhibitors “CCEL at 50”

A

Chloramphenicol
Clindamycin
Erythromycin (Macrolides)
Linezolid

347
Q

Mydriasis

Drugs

A

Anticholinergics (Atropine, TCAs, Topicamide, Scopolamine, Antihistamines)

Drugs of abuse (Amphetamines, cocaine, LSD) Meperidine

348
Q

Miosis

Drugs

A

alpha-2 agonists

Drugs of abuse (Heroin & opioids)

Pilocarpine & organophosphates

349
Q

Methanol

OD & Treatment

A

OD:
Respiratory failure
Severe anion gap met acidosis
Ocular damage

Rx:
Fomepizole

Pharm SJSM (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions