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CNS > [PHARMA] ANTIPSYCHOTICS > Flashcards

[PHARMA] ANTIPSYCHOTICS Flashcards

1
Q

all antipsychotics act on

A

D2 receptor in mesolimbic system

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2
Q

atypical pyschotics also act on

A

5HT2 in mesocortical pathway

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3
Q

advantages of typical antipsychotics

A

cheaper
fast acting IMI & inhalation
long-acting injectable formula for patients struggling to adhere to therapy

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4
Q

central D2 receptors targeted by typical antipsychotics are present in

A

1-mesolimbic system
2-CTZ
3-Hypothalamus & Pituitary gland
4-Basal ganglia (nigrostriatal area)

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5
Q

blockade of mesolimbic D2 receptor leads to

A

antipsychotic effect:
-violent patient calms down
-1ry psychosis
-2ry psychosis

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6
Q

blockade of CTZ D2 receptor leads to

A

antiemetic effect

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7
Q

blockade of basal ganglia D2 receptor leads to

A

Extrapyramidal side effects (EPS)

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8
Q

blockade of hypothalamus & Pituitary gland D2 receptor leads to

A

↑prolactin
↑ body weight
gynecomastia ♂
infertility ♂
galactorrhea ♀
amenorrhea ♀

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9
Q

autonomic receptors include

A

H1
M
α

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10
Q

blockade of H1 receptor leads to

A

sedation
↑ body weight

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11
Q

blockade of M receptor leads to

A

atropine-like effects:
dry mouth
confusion
constipation
urine retention

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12
Q

blockade of α receptor leads to

A

postural hypotension
reflex tachycardia

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13
Q

miscellaneous side effeccts of D2 blockade

A

cardiotoxic ↑QT
convulsions
corneal-lens deposits
cholestatic jaundice

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14
Q

EPS disorders

A

akathisia
dystonia
parkinsonism
tardive dyskinesia

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15
Q

neuroleptic malignant syndrome symptoms

A

muscle rigidity
hyperpyrexia
altered mental status
stupor
unstable BP
myoglobinemia

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16
Q

neuroleptic malignant syndrome occurs due to

A

rapid excessive central DA blockade in patients sensitive to EPS

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17
Q

management of neuroleptic malignant syndrome

A

discontinue
muscle relaxants
antiparkinsonian drugs
bromocriptine

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18
Q

akathisia is characterized by

A

motor restlessness

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19
Q

dystonia is characterized by

A

muscle spasms
neck torticollis

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20
Q

parkinsonism is characterized by

A

rigidity
hypokinesia
tremors

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21
Q

parkinsonism is characterized by

A

rigidity
hypokinesia
tremors

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22
Q

tardive dyskinesia is characterized by

A

abnormal involuntary movements:
chewing
sucking
fly catching movement of tongue

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23
Q

akathisia occurs due to

A

blockade of D2 receptors in basal ganglia

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24
Q

dystonia occurs due to

A

blockade of D2 receptors in basal ganglia

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25
Q

parkinsonism occurs due to

A

relative increase in cholinergic Ach activity following D2 blockade in basal ganglia

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26
Q

tardive dyskinesia occurs due to

A

upregulation of DA receptors supersensitivity to DA following chronic blockade of D2 receptors in basal ganglia

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27
Q

akathisia management

A

propanolol (DOC)

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28
Q

dystonia management

A

propanolol (DOC)

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29
Q

parkinsonism management

A

anticholinergics (benztropine)

30
Q

tardive dyskinesia management

A

least possible dose
minimal duration
replace w/ atypical antipsychotics or clozapine
antidyskinesia drugs
AVOID ANTICHOLINERGICS

31
Q

tardive dyskinesia is exacerbated by

A

anticholinergics

32
Q

parkinsonism in EPS is relieved by

A

anticholinergics

33
Q

low potency typical antipsychotics include

A

chlorpromazine
thioridazine

34
Q

high potency typical antipsychotics include

A

haloperidol
fluphenazine

35
Q

low potency typical antipsychotics side effect

A

less central side effects
more autonomic

36
Q

high potency typical antipsychotics side effect

A

more central side effects
less autonomic

37
Q

high potency typical antipsychotics are preferred in

A

elderly
cardiac patients

38
Q

atypical antipsychotics advantages

A

-less central side effects
-less EPS
-less amenorrhea, galactorrhea, -gynecomastia (except w risperidone)
-more efficacy

39
Q

more selective on mesolimbic system

A

atypical antipsychotics

40
Q

improve negative symptoms

A

atypical antipsychotics

41
Q

improve positive symptoms

A

typical antipsychotics

42
Q

DOC in resistance cases

A

clozapine

43
Q

risperidone characteristics

A

less autonomic
less EPS
less weight gain
↑QT
↑Prolactin

44
Q

least likely to cause EPS

A

clozapine

45
Q

clozapine characteristics

A

↑autonomic side effects
↑ seizures risk
nocturnal salivation
↑body weight
↑hyperlipidemia (DM risk)
insulin resistance
↑agranulocystosis risk

46
Q

most likely to ↑ body weight

A

Olanzapine

47
Q

olanzapine differs from clozapine in that

A

it has no risk of agranulocytosis

48
Q

DOC in psychosis in Parkinson disease

A

Quetiapine

49
Q

has extrapyramidal effects & causes akathisia

A

Aripiprazole

50
Q

DOC in children

A

Aripiprazole

51
Q

DOC in obese & DM patients

A

Aripiprazole

52
Q

therapeutic uses of antipsychotics (9)

A

1-Schizophrenia
2-Mania
3-Bipolar disorder
4-Tranquilizer= Haloperidol
5-Intractable hiccups= Chlorpromazine
6-Antiemetic= Chlorpromazine
7-Autism= Aripiprazole
8-Adjuncts in refractory depression= Quetiapine, Aripiprazole
9-off label hypnotics in insomnia= Quetiapine, Clozapine, Chlorpromazine

53
Q

monovalent cation

A

Li+

54
Q

gold standard in bipolar manic depression

A

Li+

55
Q

Li+ uses

A

mood stabilizers
antimanic
recurrent endogenous depression
refractory unipolar depression

56
Q

first line TTT for bipolar depression

A

Li+ or lamotrigine

57
Q

Li+ onset

A

5-20 days

58
Q

Li+ T½

A

24h

59
Q

adverse effects of Li+

A

-CNS= fine tremors, ↓cognition
-GIT= NVD
-Renal= antagonizes ADH->polyuria->thirst
Renal tubular damage
Nephrogenic diabetes insipidus

-Thyroid= benign enlargement with/without hypothyroidism

60
Q

Li+ toxicity is due to

A

Narrow TI
Long T½
cumulative

61
Q

precautions to be taken w/ Li+ therapy

A

monitor kidney function
monitor thyroid function
monitor serum Li+
adjust dosage in ↓ Li+ excretion

62
Q

↓Li+ excretion can be due to

A

Na+ depletion
renal dysfunction
elderly (↓renal function)

63
Q

Lithium toxicity range

A

toxic: Li+ >1.5 mEq/l
lethal: Li+ > 2 mEq/l

64
Q

Lithium toxicity range

A

toxic: Li+ >1.5 mEq/l
lethal: Li+ > 2 mEq/l

65
Q

Li+ toxicity manifestations (11)

A

1-Vomiting
2-Diarrhea
3-Coarse tremors
4-Convulsions
5-Confusion
6-Coma
7-CV collapse
8-arrhythmia
9-ataxia
10-drowsiness
11-slurred speech

66
Q

Li+ antidote

A

NONE

67
Q

Li+ toxicity management

A

Stop intake
gastric lavage
Activated charcoal in acute ingestion
Diuresis (NEVER thiazide/loop D)
Hemodialysis

68
Q

hemodialysis is continued for

A

6-8hr till nontoxic Li+ range

69
Q

Hemodialysis is most effective in

A

1-Fluid intake is CI (CHF
Cirrhosis)
2-severe symptoms
3- Li > 3 mEq/l
4-RF

70
Q

DOC in hepatic impairement

A

Li+

71
Q

how does the body deal with Li+

A

excretes it completely
no metabolism

72
Q

Li toxicity occurs in Na depletion due to

A

Li is carried by Na/H exchanger & Na channels
in Na depletion, Li is reabsorbed in place of Na= ↑serum Li= TOXICITY

CNS (29 decks)

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