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SRNAPharmacology I > EXAM 4-Antidepressant Agents > Flashcards

EXAM 4-Antidepressant Agents Flashcards

1
Q

Antidepressant target

A

Targeting neurons in the NS< and specific neurotransmitter altered (NE or 5-HT pathways)

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2
Q

Antidepressants lacks

A

dopamine 2 receptor antagonists

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3
Q

High incidence of adverse effects

A

CV, CNS and anticholinergic toxicities

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4
Q

Clinical uses of TCAs

A

Depression
Migraine
Anxiety
Enuresis

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5
Q

Classification of TCAs

A

Tertiary amine

Secondary amine

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6
Q

• TCAs block the reuptake of both NE and 5-HT into the presynaptic nerve
terminal via inhibiting NET and SERT and thus enhance noradrenergic and
serotonergic transmission

A
  • TCA’s ALSO block/antagonize other types of receptors to varying degrees which contributes to the different adverse effect profile of the individiual agent
  • α1-adrenergic antagonism
  • H1 antagonism – antihistamine effects
  • Muscarinic antagonism – anticholinergic effects
  • Block Na+ channels – leads to cardiac conduction abnormalities
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7
Q

Pharmcokinetics of TCA

A

Highly protein bound >90% extensive liver metabolism

high Vd

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8
Q

Quinidin like effect

A

because block fast na channel

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9
Q

TCA and cardiac effects

A

Cardiac conduction abnormalities occur primarily in overdose situations

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10
Q

TCA and seizures

A

Decrease seizure threshold.

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11
Q

What can cause Withdrawal symptoms

A

Abrupt cessation of treatment may produce withdrawal symptoms

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12
Q

• Tertiary amines are metabolized into

A

active secondary amines

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13
Q

Short half life predict withdrawal

A

Pharmacokinetics : half life

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14
Q

TCA drug to drug, never give which drug?

A

MAOIs – NEVER GIVE AT THE SAME TIME!!!

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15
Q

*****TCA can do what to sympathomimetic agents?

A

Potentiate/decreases

Interaction is COMPLEX AND PREDICTABLE

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16
Q

Recently started on TCA,

A

an exaggerated pressor response should be anticipated from direct or indirect acting sympathomimetics.. MORE PRONOUNCED such as EPHEDRINE (primarily indirect)

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17
Q

Induction of anesthesia may be associated with an increase risk
of cardiac arrhythmias in patient’s treated with TCAs
• The dose of exogenous epinephrine necessary to produce
cardiac dysrhythmias during anesthesia with a volatile
anesthetic is decreased by TCAs

A

Normal dose of epinephrine, may be associated with higher risk

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18
Q

A potential for an increase in cardiac arrhythmias may be observed in patients treated with ______ _____ and _____

A

Halothane, pancuronium and TCAs

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19
Q

• Because the anticholinergic (antimuscarinic) effects of drugs are additive, the use of centrally acting anticholinergic (antimuscarinic) agents for preoperative medication of patients treated with TCAs. Exception is this medication ______

A

may be associated with increased risk of postoperative delirium and confusion; Glycopyrrolate

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20
Q

Glycopyrrolate

A

is less likely to have this drug interaction in patients being treated with

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21
Q

Centrally acting , name 2 medications

A

Scopalamine

Glycopyrrolate

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22
Q

TCA can cause_____and using _________can increase the risk

A

HYPOTENSION

Alpha 1 antagonists.

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23
Q

TCA overdose can be

A

life threatening
CNS and cardiotoxicity
Severe hypotension and cardiac depressant “quinidine -effect)
CNS depression, respiratory depression, coma, seizures

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24
Q

GI decomtamination

A

Large volume gastric lavage

EMESIS is contraindicated

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25
Q

TCA overdose management

A
  • ECG and monitoring
  • Airway, IV
  • GI decomtaminiation
  • Hyperventilation or serum alkalinization with IV sodium
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26
Q

TCA, those antiarrhythmics contraindicated

A

1A and 1 C

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27
Q

SSRI clinical use

A

do not need to know

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28
Q

SSRI MOA

A

Selectively inhibit the re-uptake into the pre-synaptic nerve terminal by inhibiting SERT

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29
Q

SSRI do not block those 2 receptors

A

do not block histamine or alpha adrenergic receptors.

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30
Q

SSRI most common to remember

A

NAUSEA

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31
Q

Less common of SSRI

A

Increase risk of bleeding post op (because of serotonin on platelet)

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32
Q

Withdrawal: Least common with Fluoxetine due to

A

long-half life of both fluoxetine and its active metabolite, norfluoxetine.

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33
Q

Drugs to drug interaction with SSRIs

A

CYP 450 enzymes

SSRIs are inhibitors of many CYP450 Enzyme systems

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34
Q

What is the most potent CYP450 inhibitor of all SSRIs?

A

Fluoxetine

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35
Q

MOAI

A

do not use any SSRI within 14 days of stopping an MAOIs

MUST WAIT AT LEAST 5 weeks after stopping fluoxetine before starting any MAOI

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36
Q

Zyvox (Linezolid)

A

non-selevitve MAOI propertises

Combined use of risk SEROTONIN SYNDROME

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37
Q

Serotonin Syndrome

A

rare but severe, potentially life threatening condition that can occur with the use of SSRI.

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38
Q

Symptoms of serotonin syndrome

A

AMS: Agitation, hallucinations, coma
Tachycardia, hyperthermia, hypertension

in more severe: resemble NMS which include hyperthermia, muscle rigidity, myoclonus and coma.

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39
Q

MEMORIZE Differential diagnosis of serotonin sydrndome KNOW chart table43-5

A

SS : serotonin agonists

NMS

40
Q

Longest half life of all SSRI

A

Fluoxetine

41
Q

Pharmacokinetics of fluoxetine

A

prolonged half life

highly protein bound

42
Q

SSNIs

A

Serotonin NE uptake inhibitors.

43
Q

SSNIs MOA

A

primarily block reuptake and NE and dopamine in pre-synaptic terminal

44
Q

Adverse effects of SSNI

A

Nausea, nausea, nausea,
HTN
Increased bleeding post op

45
Q

MOAIs

A

monoamine oxidase inhibitors

46
Q

MOAis MOA

A

Nonselective IRREVERSIBLE of MOA-A and MOA-B both peripheral and Central actions

47
Q

MOA inhibit what ?

A

inhibit enzyme responsible for the breakdown of NE, 5-HT, Dopamine, Epi, and EXOGENOUS MONOAMINES( Tyramine)

48
Q

Since MAOis are IRREVERSIBLE

A

it takes up to 2 weeks for MAO activity to recover

49
Q

MAOis major adverse effects

A

ORTHOSTATIC HYPOTENSION

50
Q

Must maintain a _______ on MAOIs

A

Strict diet

51
Q

Foods that contain tyramine and beta-phenylethanolamine

A

should avoided in patient with MAOis due to increased risk of developing hyptertensive crisis (hypertension and Hyperpyrexia)

52
Q

MAO-A in the intestinal wall and MAO-A and MOA-B in the liver normally degrade dietary tyramine?

A

Mao inhibition leads to the accumulation of tyramine in adrenergic nerve terminals and neurotransmitter vesicles and induces NE release and this increase release of NE stimulates post-synaptic receptors in the periphery increasing blood pressure to dangerous levels.

53
Q

Esmolol and MAOIs consideration?

A

Use in caution because ESMOLOL is cardio-selective for beta 1 and may leave alpha 1 unblock, and MAOIs release NE which will bind to alpha 1 receptor.
Give labetalol, or other drugs.

54
Q

Prohibited food in MAO-A

A 
Pork
Liver, fava beans
Avocados, cheese
alcohol 
wines
55
Q

Sympathomimetic such as ephedrine and phenylephinre

A

reduce the dose to 1/3

56
Q

Do not give any with MAOs

A

in-direct symptomimetics (ephedrine)

57
Q

Do not give with MAOs ( 2 )

A

induce skeletal muscle rigidity

SERTONIN SYNDROME

58
Q

Post op shivering harder to manage because what is contraindicated with MAOIs?

A

CANNOT give meperidine or meperidine derivatives

59
Q

Do not use these class of meds within 14 days of

A

TCAs
SSRIs
SNRIs

60
Q

Use caution with _____ and_____why>

A

cocaine and local anesthetics; potentiation effects.

61
Q

Anesthetics requirements for volatile anesthetics with MAOis

A

increased

62
Q

General anesthesia and spinal anesthesia with the MAOIs

A

HYPOTENSION may be exaggerated.

63
Q

Are responses to Nondepolarizing NMB altered by MAOIs

A

NO

64
Q

For MAOIs recovery of normal enzyme function is dependent of what?

A
  • Synthesis and transport of new MAO enzyme to monoaminergic nerve terminals.
65
Q

MAOIs are the

A

3rd line or last line agents

Limited use for patient resistant to other forms of therapy because on toxicities risk of drugs and food interactions.

66
Q

Trazodone act as a _____

what receptors does it block?

A

Acts as a potent antagonist at 5-HT2 receptors and to a lesser
degree also selectively inhibits neuronal reuptake of 5-HT
• It also significantly blocks alpha1 adrenergic (postural
hypotension) and histamine (H1) receptors

67
Q

Cases of life-threatening hepatic failure have been reported in patients treated with

A

Nefazodone!!!

68
Q

Weight loss managmenet
smoking cessation
ANti-depressant

A

Bupropion

69
Q

Buproprion

A

causing seizures.

70
Q

Combining anesthetics that causes seizure with Buproprion

A

would increase seizure threshold

71
Q

Serotonin Reuptake inhibitor.

A

Vilazodone

72
Q

Vortioxetine (BRintellix)

A

Complex medication
SSRI and also antagonist at multiple receptors
DOES MANY THINGS
Antagonist, partial agonist, agonist

73
Q

Sent apart Brintellix

A

TERMINAL HALF LIFE 66 Hours

74
Q

Buspirinone
Used for ______
does it interact with GABA?
lack?

A

Anti -anxiety ( not related to any other class)
Mimi the anti anxiety proper of benzo BUT DOES NOT interact with GABA receptors and lack prominent sedative, anticonvulsant and skeletal muscle relaxants

75
Q

Lithium

A

Acute and maintenance therapy for Bipolar disorder

Lithium is the gold standard in bipolar treatment.

76
Q

Lithium indications

A

Bipolar disorder

Depression (manic)

77
Q

Exact mechanism of lithium

A

NO ONE KNOWS

78
Q

Lithium is route _____, bioavailability is _____

A

PO ; 100

79
Q

Lithium half life is a _____and excreted via______

A

24 hours; Kidney

80
Q

Lithium competes with

A

Na for reabsorption in the proximal renal tubule, therefore , lithium retention can be increased by Na+ loss

81
Q

NA depletion

A

dehydration will increase lithium reabsorption by the proximal tubule.

82
Q

General range for most indications

A

0.6- 1.2 mmol/L

83
Q

Drugs to Drug Lithium (increase reabsorption)

A

Thiazide —> Increase
LoOP—>Increase
NSAIDS–>Increase (this is KETOROLAC, Ibuprofen)
ACEi and ARBs

84
Q

Drugs to Drug Lithium (increase reabsorption)

A

Neuromuscular
Carbamazepine
Antipsychotics

85
Q

Neuromusclular blockade

A

Lithium prolonged effects of non-depolarizing and depolarizing NMB
CCB –> Increase CNS toxicity

86
Q

Lithium may potentiate ________or increase the risk for

A

EPS, NMS

87
Q

Haldol with lithium

A

encephalopathic syndrome with

irreversible brain syndrome

88
Q

Renal adverse effects

A

polyuria polydipsia VERY COMMON

2L /day

89
Q

Lithium induced nephrogenic DI

A

Amiloride can be given to treat

90
Q

Lithium with any sedatives

A

InCREASE RISK OF SEDATION

91
Q

Lithium

A

EKG changes - T wave flattening and inversion (U waves

QRS complex prolongation, sinus Brasdy, AV blocs when level are >2.5 mol/L

92
Q

Lithium toxicity

A

> 2 toxic

93
Q

Lithium less than 1.5 mol/L

A

Fine hand tremor, nausea, vomiting, diarrhea, skeletal muscle weakness, mild polyuria and polydipsia

94
Q

Lithium 1.5 -2.5

A

Muscle twitching, nygstamus

95
Q

Lithium Over 2.5

A

BRAIN (seizure, coma) and CARDIAC symptoms

96
Q

Name anesthesia implications & Lithium

A

NMB MAY BE prolonged

Lithium associated sedation suggests anesthetic requirements for injected and inhaled anesthetics could be DECREASED

97
Q

CNS and lithiums

A

HIGH PLASMA concentration may delay recovery from the CNS depressant effects of barbiturates.

SRNAPharmacology I (29 decks)

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