Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology Semester 2 > Anti Depressants > Flashcards

Anti Depressants Flashcards

1
Q

Antidepressants

A

capable of improving mood in patients with depression acts on lack of interest and energy, loss of appetite, sleep disturbances, concentration problems, feeling guilty or worthless, suicidal ideas, newer ones are used in anxiety, panic attack, phobia, pain. Goal is remission (symptom free 4-9 months) or recovery of patient (symptom free for more than 12 months)

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

Depression appears because of

A

serotonin (responsible of satisfaction, decreased anxiety), norepinephrine (energy, concentration) or dopamine deficiency. Inhibition of monoamine transport proteins.

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

Antidepressant effects

A

acute, sedative, and vegetative effects (healthy and depressive) and the antidepressant effect (weeks after treatment in patients with depression).

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

During the entire treatment association with

A

CNS depressants (alcohol, old histaminic, barbiturates, benzodiazepines, hypnotics, opioids, antipsychotics) should be avoided.

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

Tricyclic antidepressants - tertiary amine tricyclic antidepressants

A

Amitryptiline, imipramine, clomipramine, trimipramine, doxepin

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

TCA - secondary amine tricyclic antidepressants

A

nortriptyline, desipramine

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

Tetracyclic antidepressants

A

mapotiline, mianserin

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

SSRIs

A

citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline

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

serotonine norepinephrine reuptake inhibitors

A

venflaxine, desvenlafaxine, duloxetine, milnacipran

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

Atypical - NE and Dopa reuptake inhibitors

A

bupropion

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

Atypical -selective NE antagonist/reuptake inhibitors

A

Nefazodone, trazodone

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

Atypical - alpha 2

A

mirtazapine

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

MAO inhibitors

A

moclobemid, tranycypromine

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

TCAS

A

oldest class, contains 3 rings of atoms, most effective, but not first line due to side effects.

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

SSRIS

A

decreased serotonin level may play a role in depression. Serotonin is responsible for increased satisfaction and happiness, decreased anxiety, impulsivity, libido, and appetite and can cause nausea, diarrhea, decreased clotting function (decrease platelet and VC), fewer side effects, reduced danger of drug-drug interactions, less likely to excACERBATE other illness and less toxic in overdosage, agents of choice in treating depression.

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

Fluoxetine

A

widely prescribed, standard antidepressant, selective inhibitor of serotonin uptake in CNS, little effect on central norepinephrine or dopamine function, less adverse effects bc of minimal bleeding to cholinergic, histaminic, adrenergic receptors,

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

Venflaxine, desvenlafaxine, duloxetine, milnicarpan

A

inhibit reuptake of serotonin and norepinephrine,Indications
major depressive disorder;
social phobia (Venlafaxine);
generalized anxiety disorder (Venlafaxine, Duloxetine);
fibromyalgia (Duloxetine, Milnacipran);
attention deficit hyperactivity disorder (Venlafaxine);
premenstrual symptoms (Duloxetine);
stress urinary incontinence (Duloxetine).
Adverse effects
nausea, constipation or diarrhea;
xerostomia;
hypertension;
sleeping disturbances (Duloxetine).

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

Atypical antidepressants are

A

not structurally related to tricyclic antidepressants and do not have the same mechanism of action, no anticholinergic effects.

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

Bupropion

A

mild inhibitor of dopamine reuptake, inhibitor of norepinephrine reuptake; I: major depressive, smoking cessation, SAD, adjunct to SSRIs, substance abuse, ADHD, weight loss; AE : seizures in bulimic

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

Atomoxetine

A

blocks norepinephrine transporters, I: depression, ADHD

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

Mirtazapine

A

blocks presynaptic a2 adrenergic on noradrenergic and serotonergic neurons, blocks 5HT etc; I: major depressive (first line), panic attacks, nausea after chemotherapy/surgery, AE:Sedation, headache, dizziness, increased appetite, weight gain

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

Nefazodone, trazodone

A

block… I:major depressive, anxiety (trazodone), PTSD (nefazodone), depression with comorbid substance abuse (nefazodone), AE: liver toxicity, priapism (trazodone), increased QT (trazodone)

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

MAOI

A

effective antidepressants, third line drugs due to adverse effects

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

Opioid analgesics and antagonists - Strong agonists

A

morphine, fentanyl, meperidine, heroin, methadone

25
Q

Opiod and antagonists - moderate agonists

A

codeine, prorpoxyphene

26
Q

Mixed agonists and antagonists

A

buprenorphine, pentazocine

27
Q

Opioid (antagonists)

A

naloxone, naltrexone; natural/synthetic, opiates reserved for drugs like morphine and codeine obbtained from juice of opium poppy

28
Q

Opiod mechanism of action

A

bind specific opiod receptors found in areas of CNS for pain signal transmission, binding to receptors mediate pharmacological effects; see receptor table

29
Q

Morphine

A

major analgesic. drug contained in opium and is prototype agonist, high affinity for mu receptors and varying for delta and kappa receptors.

30
Q

Meperidine

A

entirely synthetic analgesic; I:severe, acute pain (1/8 potent Morphine), AE: respiratory depression, addiction liability (withdrawal effects less severe than morphine), duration of 2-4 hours (shorter than morphine

31
Q

Methadone

A

controlled withdrawal of addicts from heroin and morphonine, oral, substitute for injected opioid, then slowly weaned; AE: similar to morphine, milder withdrawal syndrome, develops more slowly than morphine

32
Q

fentanyl

A

80x analgesic potency and respiratory depressant properties of morphine, rapid onset and short duration of action (15-30 min)

33
Q

codeine

A

obtained from opium or methylation of morphine, much less potent than morphine, higher oral efficacy, 30mg codeine = 6oomg aspirin, cough suppressant; AE: less sedation or respiratory depression, fewer GI effects, addiction liability lower than with morphine and withdrawal less sever

34
Q

Pentazocine

A 
Pentazocine acts as an agonist on kappa receptors and is a weak antagonist at mu and delta receptors;
despite its antagonist action, Pentazocine does not antagonize the respiratory depression of Morphine, but it can precipitate a withdrawal syndrome in Morphine abusers; Pentazocine should not be used with agonists such as Morphine, since the antagonist action of Pentazocine may block the analgesic effects of Morphine;
Indications
moderate pain.
Adverse effects
less euphoria compared to Morphine;
respiratory depression;
increased blood pressure;
hallucinations, nightmares;
tachycardia;
dizziness;
tolerance and dependence.
35
Q

Buprenorphine

A

partial agonist on mu receptors, long duration of action due to tight binding on receptor, administered parenterally/sublingual; AE: respiratory depression, nausea, dizziness, decrease in blood pressure

36
Q

Naloxone

A

Mechanism of action
Naloxone, like other competitive receptor antagonists, blocks the opioid receptors; administration of antagonists produces no profound effects in normal individuals; however, in patients addicted to opioids, antagonists rapidly reverse the effect of antagonists, such as Heroin, and precipitate the symptoms of opiate withdrawal; the sedative effects, respiratory depression and adverse cardiovascular effects of opioid agonists are reversed within 1–2 minutes after parenteral administration of Naloxone.
Therapeutic notes
if Naloxone is administered to opioid-addicted patients, a withdrawal syndrome is easily precipitated;
mothers who have received opioids during labor receive Naloxone prior to delivery, to minimize neonatal respiratory depression.

37
Q

Naltrexone

A

action similar to naloxone, opiate dependance maintenance programs, single dose blocks effect of heroin for up to 48 hours

38
Q

TCA mechanism

A

block reuptake of noradrenaline and serotonin, block major route of neurotransmitter removal, increased concentrations of monamines in synaptic cleft, result in antidepressant effects, block H1 and muscarinic, work as sodium and calcium inhibitors

39
Q

TCA pharmokinetics

A

well absorbed from the GI tract;
because of their lipophilic nature, this agents become widely distributed and readily penetrate into the CNS;
lipid solubility also causes TCAs to have a long t1/2 (e.g. 4-17 hours for Imipramine);
as a result of their variable first pass metabolism in the liver, TCAs have low and inconsistent bioavailability; therefore the patient’s response is used to adjust dosage; the initial treatment period is typically 4-8 weeks;
metabolized in the liver and excreted as inactive metabolites via the kidney.

40
Q

TCA phrarmodynamic effects

A

CNS effects: TCAs elevate mood, improve mental alertness, increase physical activity and reduce morbid preoccupation; the onset of this effects is slow, requiring 2-3 weeks or more; they do not produce CNS stimulation or mood elevation in normal individuals;
cardiovascular effects: orthostatic hypotension, arrhythmias, tachycardia;
autonomic nervous system effects: anticholinergic effects;
increase effectivenes of analgetics, without having an analgetic effect themselves.
the TCAs have a narrow therapeutic index (TI = 7); for example 5-6 times the maximal daily dose of Imipramine can be lethal; remember that this drugs are being given to patients with high risk of suicide, the overdosage can be life-threatening and that is why depressed patients who are suiciidal should be given limited quantities and monitored closely.

41
Q

TCA indication

A 
severe major depression (second line, after SSRI);
nocturnal enuresis (Imipramine).
42
Q

TCA adverse effects

A 
orthostatic hypotension, tachycardia;
drowsiness, sedation, confusion;
dry mouth, constipation, urinary retention, blurred vision;
weight gain;
sexual dysfunction.
43
Q

TCA contraindication

A

acute intoxication with CNS inhibitors (opioids, sedativ-hypnotics, alcohol);
acute mania;
glaucoma, prostate adenoma, ileus;
severe cardiovascular diseases (grade III AV block);
combination with MAOI (2 weeks pause).

44
Q

SSRI indication

A

major depressive disorder (Fluoxetine, Venlafaxine are first line drugs);
obsessive-compulsive disorder (except Citalopram, Escitalopram);
social phobia (Sertraline, Fluvoxamine, Paroxetine);
posttraumatic stress disorder (Sertraline, Paroxetine);
generalized anxiety disorder (Fluoxetine, Fluvoxamine, Paroxetine, Escitalopram are first line drugs);
premenstrual disphoric disorder (Fluoxetine, Paroxetine, Sertraline).

45
Q

SSRI adverse effect

A

loss of apetite, nausea, vomiting, diarrhea;
decreased libido, delayed ejaculation;
headache, insomnia or somnolence, nightmares;
increase of QT interval (Citalopram, Escitalopram);
in case of abrupt stopping: agitation, flu-like symptoms, increased suicidal risk.

46
Q

SSRI contraindication

A

acute mania;
combination with MAOI;
caution in patients with diabetes (glycemia oscillations), on anticoagulant therapy (increased bleeding risk) or epilepsy (increased seizure senzitivity).

47
Q

Fluoxetine Pharmokinetics

A

well absorbed after oral ingestion;
it undergoes extensive hepatic biotransformation to the active metabolite norfluoxetine; the elimination t1/2 is 1–3 days for Fluoxetine and 7-15 days for Norfluoxetine; the inactive metabolites are excreted in the urine;
the onset of action is within 1-3 weeks after beginning treatment.

48
Q

FLuoxetine indications

A 
depression;
bulimia nervosa;
obsessive-compulsive disorders;
anorexia nervosa;
panic disorders;
pain associated with diabetic neuropathy;
premenstrual syndrome.
49
Q

Fluoxetine adverse effects

A 
nausea;
headache;
insomnia, fatigue;
sexual dysfunction;
hypoglycemia in patients with diabetes.
50
Q

MAOI mechanism of action

A

MAO is a mitochondrial enzyme found in neural and other tissues; in the neuron MAO functions as a “safety valve” to degrade and inactivate any excess of neurotransmitter molecules (norepinephrine, serotonin and dopamine) that may leak out of synaptic vesicles when the neuron is at rest; the MAOIs may irreversibly (for 7-10 days; Tranylcypromine, nonselective) or reversibly (for 24 hours; Moclobemid, selectiv on MAO-A) inactivate the enzyme, permitting neurotransmitter molecules to escape degradation and therefore to both accumulate within the presynaptic neuron and to leak into the synaptic space; this causes activation of norepinephrine and serotonine receptors, and may be responsible for the antidepressant action of these drugs.

51
Q

MAOI pharmacokinetics

A

rapidly absorbed from the GI tract, but, inexplicably, the observed therapeutic response does not occur for 2–3 weeks;
enzyme regeneration terminates the drug effect, but this frequently takes several weeks after use of the drug is stopped; thus, when switching antidepressant therapy, a minimum of 2 weeks delay is required after termination of MAOI therapy.

52
Q

MAOI indications

A

atypical depression: hypersomnolence, hyperphagia and hyperanxiety;
depression in patients who are unresponsive or allergic to other antidepressant drugs or who experience strong anxiety.

53
Q

MAOI adverse effects

A

drug-food interactions;
orthostatic hypotension;
weight gain.

54
Q

MAOI interactions

A

MAO (from the gut) normally inactivates tyramine, contained in certain foods (cheese, chicken liver, beer and red wines); individuals receiving a MAOI are unable to degrade tyramine obtained from the diet; tyramine causes the release of large amounts of stored cathecolamines from nerve terminals, resulting in headache, tachycardia, nausea, HBP, cardiac arrhythmias and stroke; patients must therefore be educated to avoid tyramine-containing foods;
concurrent use of MAOIs with SSRIs can cause a “serotonin syndrome” which includes hyperpyrexia, agitation, neuromuscular irritability, hypotension, coma, and death; if the treatment has to be changed: allow 2 weeks washout period between administrations if we switch from MAOI to SSRI and 5 weeks between administrations if we switch from Fluoxetine (long t1/2) to MAOI.

55
Q

Morphine pharmacodynamic effect

A

analgesia, primarily by interacting with mu receptors;
respiratory depression (dose-dependent), due to decreased sensitivity of the respiratory center chemoreceptors to CO2 and direct effects to decrease respiratory rhythmicity; respiratory depression is variable from patient to patient and the most common cause of death in acute opioid overdose;
sedation;
mood changes;
miosis (as a result of increased activity in the parasympathetic nerve innervating the pupil);
nausea and vomiting (as a result of direct stimulation of the chemoreceptor trigger zone for emesis);
cough suppression;
truncal rigidity (as a result of increased tone in large trunk muscles probably due to increased impulse activity from supraspinal sites);
orthostatic hypotension;
cutaneous flushing, hypothermia;
bronchoconstriction;
constipation;
constriction of biliary smooth muscle and the sphincter of Oddi;
increased tone in the ureter, detrusor muscle of the urinary bladder and vesicle sphincter can produce urinary retention.

56
Q

Morphine pharmacokinetic

A

it is well absorbed from the GI tract;
Morphine rapidly enters all body tissues, including the fetuses of pregnant women, and should not be used for analgesia during labor;
significant first pass metabolism of Morphine occurs in the liver; therefore IM, SC or IV injection produce the most reliable responses; Morphine is metabolised in the liver to glucuronides; Morphine-6-glucuronide is a very potent analgesic;
the duration of action of Morphine is 4–6 hours.

57
Q

Morphine indications

A

severe pain;
diarrhea;
cough;
dyspnea due to pulmonary edema.

58
Q

Morphine adverse effects

A

respiratory depression (dose-dependent);
nausea;
increased biliary tract pressure;
tolerance (after 1-3 weeks) to all effects except miotic and constipating effects;
physical dependence;
the elevation of intracranial pressure, particularly in head injury;
acute urinary retention (important in prostatic hypertrophy);
toxicity (depressed respiration, pinpoint pupils, coma).

Pharmacology Semester 2 (7 decks)

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