Brainscape's Knowledge GenomeTM

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


See full index

Neurology > Pharmacology > Flashcards

Pharmacology Flashcards

0
Q

Catecholamine

A

precursor to EP

DA, NE

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

Monoamine

A

NTs that contain one amino group that is connected to an aromatic ring
Ex) thyroid hormones, Histamine, catecholamines (EP, DA, NE), tryptamines (5-HT)

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

Where is ACh made?

A

Nucleus basalis of Meynert

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

Where is DA made?

A

substantia nigra and ventral tegmental area

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

Where is Histamine made?

A

Ventral Posterior hypothalamus (Tuberomammillary nucleus)

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

Where is NE made?

A

locus ceruleus in upper pons

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

Where is 5-HT made?

A

raphe nucleus in brain stem

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

NMJ-blocking Agents: What do they cause?

A

Used for skeletal muscle relaxation–> ONLY paralysis, NO analgesia or unconsciousness

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

Depolarizing Agents (mech, ex, use, side effects)

A

Mech: binds aggressively to AChR–> depolarizes–> resistant to AChE–> stays bound–> Na+ channels remain closed–> cannot depolarize. Cannot be reversed.
Ex) Succinylcholine
short-acting (onset 30sec, last 10min) due to Pseudocholinesterase
temporary muscle paralysis (surgery, intubation)

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

Non-depolarizing agents

A

Mech: competitive inhibition
Ex) MivaCURIUM, -curium
elimination depends on renal/hepatic activity
Side effects: resp. failure

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

How do you reverse Nondepolarizing Agents?

A

AChE inhibitors

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

Why can’t you give AChE inhibitor to person w/ Depolarizing Muscle agent?

A

AChE inhibitors will also block Pseudocholinesterase, which is the main way to eliminate depolarizing agents–> prolong Phase I (aggressive binding)

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

Cholinesterase Inhibitors

A

Mech: inactivate AChE
used to reverse nondepolarizing NMJ agents
Ex) neostigmine, physostigmine
Side effects: bradycardia, broncospasm, pupil constriction, increased bladder tone, etc.

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

Anticholinergic Drugs

A

Mech: competitive inhibition
used in anesthesiology
Ex) Atropine
Side effects: decreased secretions, urinary retention, CNS stimulation, cutaneous blood vessel dilation

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

Atropine

A

first-line tx for organophosphate poisoning, w/ pralidoxime (2-PAM)
Effects: reverses bradycardia, bronchial smooth muscle relaxation, decrease resp. secretions, reverse psychotic effects

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

What are the 2 biggest concerns with benzodiazepines and barbiturates?

A

tolerance and withdrawal

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

Barbituates

A

Mech: increase DURATION of Cl- channel opening
Uses: anesthesia, anticonvulsants, anxiolytics, insomnia
*withdrawal is dangerous and pts must be hospitalized

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

What are 3 side effects of barbituates?

A

induce CYP-450
suppress REM sleep (even though given for insomnia)
Contraindicated in pts w/ Acute Intermittent Poryphyria b/c barbs activate ALA synthase–> heme synthesis

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

Benzodiazepines

A

Mech: Increase FREQUENCY of Cl- channel opening
Uses: anxiolytics, muscle relaxants, amnesic agents, anticonvulsants

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

Benzodiazepines and pregnancy

A

can cross placental barrier

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

How to reverse effects of benzodiazepines? How does withdrawal compared to that of barbiturates?

A

Flumazenil (competitive antagonist)

Withdrawal similar, but NOT as severe as barb withdrawal

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

How do benzodiazepines and barbituates affect sleep?

A

Benzo: decrease latency, increase Stage 2 of NREM sleep, decrease REM and slow-wave sleep
Barb: suppress REM sleep

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

Opiods

A

Mech: agonist at M-opioid receptors, with varying strengths
Uses: local analgesia, systemic pain relief, chronic pain management, antitussive
Side effects: tolerance, dependence, overdose

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

Buspirone

A

Mech: partial agonist of 5-HT-1A receptors
* NO EFFECT on GABA rec, does NOT interact w/ EtOH, NO sedating effects or euphoria (like with benzo, barb). Less potential for abuse!
Use: Generalized Anxiety Disorder (NO muscle relaxant or anticonvulsant properties)

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

What are endogenous endorphins made from?

A

POMC (proopiomelanocortin)

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

Which NTs do Antidepressants target? What can extended treatment lead to?

A

5-HT, NE, and sometimes DA

Extended treatment can lead to downregulation of postsynaptic NT receptors

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

Selective Serotonin Reuptake Inhibitors

A

first-line tx for depressive and anxiety disorders
Increases 5-HT levels
Ex) Citalopram, fluoxetine, paroxetine, sertraline, fluvoxamine
see effects after 3-6wks
Uses: depressive disorders, panic disorder, generalized anxiety disorder, OCD, etc.
Side effects: diarrhea, sexual dysfcn, Discontinuation Syndrome

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

For whom are SSRI’s better to use? Who should NOT use them? For whom are they ineffective?

A

Good: Pregnant women, elderly
Bad: patients with Mania
Ineffective: mood is not elevated in non-depressed patients

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

What is the most common congenital defect with SSRI use?

A

ventral septum defect

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

SSRI Discontinuation Syndrome

A

dizziness, vertigo, nausea, fatigue, HAs, agitation, suicidal ideation, etc.

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

Monoamine Oxidase Inhibitors (contraindications)

A

IRREVERSIBLY inhibits MAO–> Increases NE levels
Ex) Phenelzine, tranylcypromine, isocarboxazid
Uses: depressive disorders, anxiety
Contraindications: tyramine-containing foods, SSRIs

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

What else is MAO responsible for?

A

breakdown of 5-HT and tyramine

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

What are some side effects if take MAOIs w/ tyramine-foods? What kinds of food have tyramine?

A

Side Effects: HTN crisis, diaphoresis, HA, vomiting

Foods: cheese, pepperoni, beer/wine, smoked/pickled meat, liver

33
Q

What can happen if take MAOIs w/ SSRIs?

A

“Serotonin Syndrome”: confusion, hyperthermia, myoclonus, hyperreflexia, diaphoresis

34
Q

Tricyclic Antidepressants

A

Inhibit reuptake–> Increase levels of NE and 5-HT
ex) amytriptyline, imipramine, amoxaprine
Uses: chronic pain, major depression, anxiety
Side effects: Constipation, cardiac arrhythmia, coma

35
Q

Noncyclic Heterocyclic Antidepressants (Bupropion)

A

inhibits reuptake of DA and NE–> Increase levels of DA and NE
Ex) Bupropion
Uses: 2nd and 3rd-line meds for major depression and smoking cessation. God for pts who do not tolerate TCAs.
Side effects: stimulant effects, tachycardia, insomnia

36
Q

Noncyclic Heterocyclic Antidepressants (Venalfaxine, Duloxetine)

A

Inhibit reuptake of 5-HT > NE–> increase levels

Uses: major depression, melancholia, anxiety, chronic pain, diabetic peripheral neuropathic pain

37
Q

Noncyclic Heterocyclic Antidepressants (Nefazodone, trazodone, mirtazapine)

A

5-HT modultors–> Block 5-HT2 receptors and inhibit 5-HT and NE reuptake
Uses: major depression, anxiety

38
Q

Noncyclic Heterocyclic Antidepressants (Maprotiline)

A

inhibits reuptake of NE. ONLY one that does not affect 5-HT levels!
Uses: Major depression
Side effects: orthostatic hypotension, sedation

39
Q

Neuroleptics

A

Anti-psychotics
Block Type 2 DA Receptors
Uses: positive symptoms of schizophrenia (hallucinations, delusions)

40
Q

First-Generation Antipsychotics

A

Ex) Thioridazine (Low-potency) Haloperidol (High-potency)
Uses: acute psychosis, schizophrenia, bipolar disorder
Side effects: extrapyramidal signs, tardive dyskinesia, dystonia, hyperprolactinemia, prolongation of QT interval, neuroleptic malignant syndrome.

41
Q

High-potency vs. Low-potency 1st generation antipsychotics

A

High-potency: greater affinity for D2 receptors

Low-potency: also have affinity for mAChRs, alpha-Adrenergic Rs, Histaminergic Rs

42
Q

Side effects of Low-potency 1st generation antipsychotics due to blockade of Histamine and mAChRs?

A

Histamine Rec: weight gain, sedation, orthostatic hypotension, tremor, sexual dysfunction
mAChRs: facial flushing, dry mouth, urine retention, constipation

43
Q

Neuroleptic Malignant Syndrome

A

Muscle rigidity, fever, autonomic instability, and cognitive changes such as delirium
Associated with elevated plasma creatine phosphokinase

44
Q

Second Generation (Atypical) Antipsychotics (advantages)

A

Ex) clozapine, Risperidone, olanzepine
Advantages: more effective against negative/chronic symptoms (flattened affect, alogia). Less risk for tardive dyskinesia, neuroleptic malignant syndrome, extrapyramidal signs
Side effects: cardiotoxicity, neuroleptic malignant syndrome, hyperprolactinemia, prolongation of QT interval

45
Q

Anticonvulsants (mechanisms?)

A

suppress uncontrolled neuronal discharge
epileptic seizures
Mech: 1) increase GABA-ergic activity 2) block VG-Na+ channels 3) block VG-Ca2+ channels

46
Q

Valporic Acidd

A

Mech: 1) binds to VG-Na channels–> keep in inactivated state. 2) block VG-Ca2+ channels (Type T channels in Thalamus)
Uses: partial and generalized tonic-clonic seizures, bipolar disorder
Side Effects: GI upset, sedation, increased appetite, weight gain

47
Q

Ethosuximide

A

Mech: Block VG-Ca2+ channels (Type T channels in Thalamus)–> stop rhythmic discharge
Uses: First-line for ABSENT seizures
Side Effects: GI upset, lethargy, HA, Stevens-Johnson Syndrome

48
Q

Phenobarbital

A

Mech: Barbiturate (increases DURATION of GABA receptor)
Uses: Status epilepticus
Side Effects: sedation, tolerance, dependence, Induce P450 (Barbiturate side effects)

49
Q

Carbamazepine

A

Mech: reduces rate of recovery of Na+ channels–> block rapid firing
Use: First-line for partial seizures, tonic-clonic seizures, TRIGEMINAL NEURALGIA, bipolar disorder
Side Effects: hyponatremia, Induces P450

50
Q

Phenytoin

A

Mech: reduces rate of recovery of VG-Na+ channels
Uses: First-line PROPHYLAXIS for Status Epilepticus, all types of partial/generalized seizures (EXCEPT Absent seizures)
Side Effects: nystagmus, diplopia, Fetal Hydantoin Syndrome, Induce P450

51
Q

Lamotrigine

A

Mech: reduces rate of VG-Na+ channels AND reduces glutamate release
Uses: partial seizures, generalized seizures, focal epilepsy, Lennox-Gastaut syndrome, bipolar disorder
Side Effects: Dizziness, Nausea, HA, Stevens-Johnson Syndrome

52
Q

Pregabalin

A

Mech: binds to alpha2-delta subunit of high-VG-Ca2+ channels, increases density of GABA transporter/increases rate of GABA transport, AND decreases glutamate, NE, and substance P release
Uses: Anitnociceptive AND antiseizure. Neuropathic pain (diabetic neuropathy and postherpetic neuralgia, fibromyalgia, partial seizures
Side Effects: dizziness, somnolence, weight gain

53
Q

Gabapentin

A

Mech: GABA-analog, BUT does NOT work at GABA receptor. Binds to alpha2-delta high-VG-Ca2+ AND decreases glutamate release
Uses: partial seizures, pain, peripheral neuropathy, bipolar disorder, anxiety
Side Effects: sedation, weight gain

54
Q

Lithium

A

Uses: Mood stabilizer. Bipolar disorder, augment antidepressants
Mech: UNKNOWN, may interfere w/ monoamine synthesis, release, reuptake.
Low Therapeutic Index
Side Effects: Can be toxic to thyroid and kidney–> MUST monitor. Hypothyroidism, nephrogenic diabetes insepidus

55
Q

What happens to NT levels in Alzheimer’s?

A

Decrease in ACh

Increase in glutamate–> influx of Ca2+ can lead to neuronal cell damage

56
Q

Memantine

A

Mech: Non-competitivelyblocks NMDA receptors in CNS
Uses: moderate to severe Alzheimer AND vascular dementia
Side effects: agitation, urinary incontinence, insomnia, diarrhea

57
Q

Tacrine, Donepezil, Rivastigmine, Galantamine

A

Mech: Selective AChE in the CNS! Crosses BBB (less peripheral side effects)
Use: Alzheimer
Side effects: nausea, vomiting, diarrhea, insomnia

58
Q

What are the 3 ways to increase CNS levels of DA?

A

1) prevent degradation of DA
2) add exogenous precursor
3) give D2 receptor agonists

59
Q

Bromocriptine (extra effects?), Pergolide, Ropinirole, Pramipexole

A

Mech: DA receptor agonists. Different effects on different types of receptors. Bromocriptine ALSO antagonizes D1 receptors in hypothalamus.
Uses: Parkinson. Bromocriptine can ALSO be used to reduce growth rate of pituitary adenoma (prolactinoma)
Side Effects: HA, nausea/vomiting, epigastric pain, Hypotension—> HTN

60
Q

Levodopa (L-dopa) (Contraindications?)

A

Mech: precursor of DA. Enters brain through L-amino transporter (DA canNOT cross the BBB). In CNS, metabolized to HVA and DOPAC.
Uses: First-line for Parkinson’s tx w/ Carbidopa.
Side effects: nausea/vomiting, tachycardia, dyskinesia, agitation, confusion, depression
Contraindications: psychosis and closed-angle glaucoma

61
Q

Carbidopa

A

reduces peripheral conversion of L-Dopa to DA–> increases availability of L-Dopa for CNS

62
Q

MAO Inhibitors (different Types)

A

MAO-A: metabolizes NE and 5-HT

MAO-B: metabolizes DA (striatum)

63
Q

Selegiline and Rasagiline

A

Mech: IRREVERSIBLE selective inhibitors of MAO-B (striatum).
Uses: Parkinson. Selegiline given in LOW-dose–> no interaction w/ tyramine-containing foods
Side effects: Serotonin syndrome if taken w/ SSRIs, TCAs, merperidine

64
Q

Tolcapone and Entacapone

A

Mech: COMT inhibitors–> prolong action of L-Dopa. Tolcapone (peripheral and central). Entacapone (peripheral ONLY)
Uses: Increase L-Dopa levels. Entacapone PREFERRED b/c less hepatotoxic.
Side effects: dyskinesia, nausea, confusion

65
Q

General Anesthetics

A

Cause analgesia, amnesia, unconsciousness, muscle relaxation, suppression of reflexes

66
Q

4 Stages of Anesthesia

A

1) Analgesia: “Conscious and Conversational”
2) Disinhibition: Autonomic variations (changes in BP, HR, RR)
3) Surgical anesthesia: Unconscious w/ relaxed muscles
4) Medullary depression: Respiratory and vasomotor center depression

67
Q

Inhaled Anesthetics

A

Uses: MAINTENANCE of anesthesia b/c depth of anesthesia can be rapidly altered.
Mech: poorly understood.
Ex) Halothane, isoflurane, sevoflurane, desflurane
Side effects: resp. depression, nausea, emesis, hypotension

68
Q

Toxicity of Inhaled Anesthetics

A

Hepatotoxicity, nephrotoxicity, convulsions, malignant hyperthermia (EXCEPT Nitrous Oxide)

69
Q

What determines speed of anesthesia induction?

A

1) alveolar gas and venous blood partial pressures
2) solubility in blood
3) alveolar blood flow

70
Q

MAC (Minimum Alveolar Concentration)

A

Similar to ED50–> Alveolar conc. of inhaled anesthetic that stops movt in 50% patients in response to incision

71
Q

What is the difference between anesthetics with LOW and HIGH solubility in blood?

A

LOW solubility: Rapid induction and recovery. Not as potent.
HIGH solubility (in oil/lipid): Slower induction/recovery. Increased potency.
Higher lipid solubility–> higher solubility in blood.
Tradeoff between potency and speed of induction.

72
Q

How do you treat Malignant Hyperthermia?

A

Dantrolene: interferes w/ Ca2+ release from SR in muscles by binding to ryanodine receptors

73
Q

Intravenous Anesthetics (Types)

A

Rapidly INDUCE anesthesia

1) barbiturates
2) benzodiazepines
3) ketamine
4) opiates
5) propofol (can ALSO maintain anesthesia)
6) Etomidate

74
Q

Benzodiazepines

A

Ex) Midazolam
Use: endoscopy
Side effects: severe postoperative respiratory depression and amnesia

75
Q

Barbiturates

A

Ex) Thiopental
Highly lipid-soluble–> enters brain rapidly
NOT analgesic–> need supplementary
Side effects: severe Hypotension in hypovolemic/shock patients

76
Q

Ketamine

A

Ex) Arylcyclohexylamine)
Dissciative anesthetic (Act via NMDA receptors)
Causes: sedation, amnesia, immobility, disorientation, hallucinations

77
Q

Opioids

A

Ex) Morphine, fentanyl, sufentanil
*Used w/ other CNS depressants during anesthesia
Toxicity: hypotension, respiratory depression, muscle ridigity

78
Q

Propofol

A

Rapid induction AND maintenance
*Excitatory phase: muscle twitching, hiccups
Uses: resection of spinal tumors. Can be used when assessing spinal cord function b/c less effect on CNS-evoked potentials

79
Q

How can you reverse opioids?

A

Naloxone and naltrexone (Mu-opioid receptor antagonists)

Neurology (11 decks)

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