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AMC MCQ > Neuropharmacology > Flashcards

Neuropharmacology Flashcards

1
Q

ANTYPSYCHOTICS
highest weight gain and cardiometabolic risk drugs

A
  • FGAs: Chlorpromazine
  • SGAs: “The PINEs”: Olanzapine, Clozapine, Quetiapine
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2
Q

ANTYPSYCHOTICS
parameters to monitor in prevention of cardiometabolic adverse effects

A

Monitor all patients

Monitoring parameters should consist of:
– weight, BMI, and waist circumference
– blood pressure
– fasting blood glucose concentrations
– full lipid profile (triglycerides, total cholesterol, HDL-C, LDL-C)

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3
Q

ANTIPSYCHOTICS
Cardiometabolic adverse effects Monitoring, when??

A
  • baseline
  • 3-monthly for the first year
  • 6-monthly for the duration of therapy
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4
Q

“Metabolic Syndrome”
Definition

A

INCREASED WAIST CIRCUMFERENCE

+

ANY TWO of the following factors:

  • reduced (HDL-C) levels
  • raised triglyceride levels
  • hypertension
  • hyperglycaemia
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5
Q

ANTIPSYCHOTICS
Which drugs can be affected by Tobacco, why, and how to manage

A

Olanzapine & Clozapine

  • SMOKING = reduces serum levels (inducer) => increase doses
  • smoking cessation = increases serum levels => dose reduction
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6
Q

ANTIPSYCHOTICS
Which drugs are MORE likely to cause Hyperprolactemia

A
  • FGAs = ALL
  • SGAs = amisulpride & risperidone
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7
Q

ANTIPSYCHOTICS
Which drugs are LESS likely to cause Hyperprolactemia

A
  • Aripiprazole
  • Clozapine
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8
Q

ANTIPSYCHOTICS
What is the plasma concentration of Prolactin that defines drug-induced Hyperprolactemia

A

Hyperprolactinemia (>2000 mIU/L)

values > 5000mIU/L are more likely due to a prolactinoma

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9
Q

ANTIPSYCHOTICS
Hyperprolactemia
Signs & Symptoms

A
  • galactorrhea
  • gynaecomastia
  • sexual dysfunction (decreased libido, impaired sexual arousal, impotence and anorgasmia)
  • infertility (novulation, impaired spermatogenesis)
  • amenorrhoea
  • reduction in bone mineral density (which is of concern in young people who have not yet reached their peak bone mass and in patients with osteoporosis)
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10
Q

ANTIPSYCHOTICS
less-sedating drugs

A
  • Haloperidol
  • Aripiprazole
  • Amisulpride
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11
Q

ANTIPSYCHOTICS
most sedating SGA drugs

A

“The PINEs”

  • olanzapine
  • Clozapine
  • Quetiapine
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12
Q

QTc normal ranges

A
  • Men: 350–450 ms
  • Women: 360–460 ms
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13
Q

ANTIPSYCHOTICS
QT prolongation

A
  • FGAs: All in general
  • SGAs: all, but Clozapine has is most commonly associated
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14
Q

ANTIPSYCHOTICS
Most common Anticholinergic effects

A

“Hot & Dry”
- Hyperthermia
- Decreased secretions
+
- Tachycardia
- sedation
- urinary retention

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15
Q

ANTIPSYCHOTICS
Which antipsychotic has the highest anticholinergic effects?

A

Clozapine

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16
Q

ANTIPSYCHOTICS
What is Clozapine unique adverse effect profile

A

Agranulocytosis (recurrent infections)

+

Cardiomyopathy

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17
Q

ANTIPSYCHOTICS
How to monitor for Agranulocytosis caused by Cloxapine

A
  • WEEKLY WBC and neutrophil counts for at least the first 18 weeks
  • MONTHLY after initial period, if no complication
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18
Q

ANTIPSYCHOTICS
WBC count and Neutropenia
MILD range values and Management

A

WBC >3.500

AND

NC >2.000

⬇︎

Clozapine therapy can continue

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19
Q

ANTIPSYCHOTICS
WBC count and Neutropenia
MODERATE range values and Management

A

WBC 3.000 - 3.500

     AND/OR

NC 1.500 - 2.000

			 ⬇︎

Requires increasing frequency of monitoring, to twice weekly

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20
Q

ANTIPSYCHOTICS
WBC count and Neutropenia
SEVERE range values and Management

A

WBC < 3.000

  AND/OR

NC < 1.500

     ⬇︎
  • CEASE clozapine immediately
  • Daily CBC
  • patient in protective isolation
  • Contact Consultant Psychiatrist and arrange urgent medical review
  • Clozapine may be restarted if Agranulocytosis resolved
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21
Q

ANTIPSYCHOTICS
How to monitor for Cardiomyopathy caused by Cloxapine

A
  • WEEKLY Troponins and C-reactive protein for the first 4 weeks
  • body temperature, pulse rate, BP and RR at baseline
  • (ECG) echocardiogram, are recommended at baseline and should be repeated on the basis of the other observations and results
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22
Q

ANTIPSYCHOTICS
which drugs are more commonly associated with Movement Disorders (EPS)?

A

FGAs

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23
Q

ANTIPSYCHOTICS
Which are the moviment disorders associated with Antipsychotics?

A

“AdAPT”
- Acute Dystonia
- Akathisia
- Parkinsonism
- Tardive Dyskinesia

https://australianprescriber.tg.org.au/articles/the-management-of-acute-dystonic-reactions.html

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24
Q

ANTIPSYCHOTICS
Acute Dystonia onset

A

Sudden (min-days)

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25
Q

ANTIPSYCHOTICS
Acute Dystonia Sx

A
  • Twisting movements
    – Oculogyric crisis
    – Buccolingual crisis
    – Blepharospasm
  • Abnormal postures
    – Torticollis
    – Opsthotonos
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26
Q

ANTIPSYCHOTICS
Acute Dystonia Mx

A

Benztropine (IV or IM)

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27
Q

ANTIPSYCHOTICS
Akathisia onset

A

Days - months

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28
Q

ANTIPSYCHOTICS
Akathisia Sx

A

abnormal, uncomfortable sensation of restlessness combined with an urge to move about

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29
Q

ANTIPSYCHOTICS
Akathisia Mx

A

FIRST LINE : propranolol VO
(avoided in asthma, severe peripheral vascular disease and CHF)

SECOND LINE: diazepam VO

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30
Q

ANTIPSYCHOTICS
Parkinsonism Onset

A

Gradual
(early weeks)

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31
Q

ANTIPSYCHOTICS
Parkinsonism Sx

A
  • Resting tremor
  • Muscle rigidity
  • Bradykinesia
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32
Q

ANTIPSYCHOTICS
Parkinsonism Mx

A
  • Benztropine VO
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33
Q

ANTIPSYCHOTICS
Tardive Dykinesia (TD) onset

A
  • gradual onset after prolong therapy (> 6 months)
  • can also be seen when withdrawing an atipsychotic
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34
Q

ANTIPSYCHOTICS
Tardive Disknesia Sx

A

uncontrolled involuntary movements
- grimacing
- lip smacking
- Rapid eye blinkning
- rapid eye movement
- tongue protruse
- lip puckering and pursing
- choreifomr movements of limbs and trrunks

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35
Q

ANTIPSYCHOTICS
Tardive Disknesia Mx

A

Switch to CLOZAPINE

36
Q

ANTIPSYCHOTICS
Drugs that can Cause of Neuroleptic Malignant Syndrome (NMS)

A
  • Most commonly associated with anti-psychotics (Dopamine antagonists)
  • anti-emetics (eg domperidone, metoclopramide)
  • cessation of a dopamine agonist
37
Q

ANTIPSYCHOTICS
Neuroleptic malignant syndrome (NMS) Cause

A

lethal adverse effect from treatment with a drug that affects dopaminergic transmission (↓DA)

  • Antipsychotics (LEADING CAUSE)
  • antidepressants
  • antiemetic drugs
  • lithium
  • after the cessation of dopamine agonist drugs (Parkinson’s)
38
Q

ANTIPSYCHOTICS
Neuroleptic malignant syndrome (NMS) Diagnostic criteria

A
  • GRADUAL ONSET
    -severe muscle rigidity (bradykinesia/hyporeflexia)
  • increased temperature (VERY HIGH FEVER)
  • autonomic instability (diaphoresis, elevated or labile blood pressure, tachycardia, tachypnoea, no occular clonus or mydriasis)
  • no GI tract symptoms
  • Alltered Mental Status (delirium)
  • raised creatine kinase (CK)
39
Q

ANTIPSYCHOTICS
Neuroleptic malignant syndrome (NMS) Mx

A
  • cessation of dopamine antagonists
  • Respiratory and circulatory support (muscle rigidity involving the chest wall)
  • Aggressive fluid replacement for hypotension
    should be given fluid replacement
  • Cooling for hyperthermia If temp. > 39 °C
    – the patient should be cooled with tepid sponging and ice packs. Antipyretic drugs are ineffective
  • Sedation - LORAZEPAM
  • Antidotal therapy = BROMOCRIPTINE (a dopamine agonist)
  • DANTROLENE - muscle rigidity

Bromocriptine should be titrated to clinical effect, looking for a lowering of the temperature and reduction of muscle rigidity.

40
Q

ANTIDEPRESSANTS
Long acting SSRI

A

Fluoxetine

41
Q

ANTIDEPRESSANTS
Best choice in post-MI patients with depression

A

Fluoxetine

42
Q

ANTIDEPRESSANTS
SSRIs/SNRIs drug interaction mechanism

A

SSRIs are substracts for metabolism by CYP450 system

Although SSRIs/SNRIs aren’t inducer or inhibitoirs of the CYP450 system, they can inhibit the metabolic clearance of other drugs (eg benzodiazepines, warfarin, clozapine) increasing their circulation concentration. this occurs because of the SRS drugs competition with other drugs for metabolism by the CYP450 system.

43
Q

ANTIDEPRESSANTS
Which SSRIs/SNRIs cause least drug interaction

A
  • Citalopram
  • Sertraline
  • Venlafaxine
44
Q

ANTIDEPRESSANTS
SSRIs -
risk of BLEEDING

A

SSRIs block the uptake of serotonin into platelets

The risk is increased by:
- concurrent use of NSAIDs
- concurrent use of anticoagulant drugs and antiplatelet drugs
- Patients with liver cirrhosis or liver failure
- patients susceptible to gastrointestinal bleeding
(eg patients with a history of peptic ulcer disease or
oesophageal varices, or who are undergoing surgery)

45
Q

ANTIDEPRESSANTS
SSRIs -
management if risk of BLEEDING

A
  • Consider an alternative class of antidepressant
  • consider addition of a gastroprotective drug (eg PPI)
  • If NSAID use must be continued, a less gastrotoxic NSAID is recommended (eg ibuprofen, diclofenac).
46
Q

ANTIDEPRESSANTS
SSRIs - what drugs have the highest risk of SEDATION/PSYCHOMOTOR IMPAIRMENT

A
  • Fluvoxamine
  • Paroxetine
47
Q

ANTIDEPRESSANTS
SSRIs - menagement of SEDATION/PSYCHOMOTOR IMPAIRMENT

A
  • tolerance develops over a period of days
  • Commencing treatment at a lower dose and increasing the dose slowly reduces the degree of sedation.
  • Avoid concomitant use of other CNS depressants (eg alcohol, benzodiazepines).
48
Q

ANTIDEPRESSANTS
Citalopram notable adverse effect

A

QT prolongation
(it is dose related)

49
Q

ANTIDEPRESSANTS
Drugs that can induce Hyponatraemia?

A
  • SSRIs
  • SNRIs
  • TCAs
  • MAOIs
50
Q

ANTIDEPRESSANTS
Risk factors for Hyponatraemia with concurrent use of Antidepressives?

A
  • older age
  • female gender
  • low body weight
  • drug interaction (eg diuretics, NSAIDs, carbamazepine, chemotherapy)
  • impaired renal function
  • comorbidity (eg hypothyroidism, diabetes, chronic obstructive pulmonary disease, hypertension, stroke, head injury)
  • hot weather.
51
Q

ANTIDEPRESSANTS
Prevention of Hyponatraemia & management

A

serum sodium may be considered in patients at high risk of hyponatraemia approximately 3 to 4 weeks after initiating treatment

If hyponatraemia occurs, discontinuation of the causative drug normalises serum sodium concentration within 2 weeks.

52
Q

ANTIDEPRESSANTS
Drugs that cause Sexual Dysfunction

A
  • SSRIs
  • SNRIs
  • TCAs
53
Q

ATIDEPRESSANTS
Which SSRIs are associated with the highest risk of sexual dysfunction?

A

Paroxetine and sertraline

54
Q

ANTIDEPRESSANTS
Drugs with minimal to negligeable Sexual Dysfunction

A
  • MAOIs
  • Bupropion
  • Mirtazpine
55
Q

ANTIDEPRESSANTS
antidepressant- induced sexual dysfunction Mx

A
  • Consider other causes
    ( alcohol use, diabetes, atherosclerosis, cardiac disease, central and peripheral nervous system conditions, medication)
  • Wait
    (remits spontaneously over time as patient develops tolerance = Consider this approach for patients with mild sexual dysfunction)
  • Reduce dose
    (considered if the condition being treated is well controlled)
  • Switching between the same class
    (Paroxetine and Setraline have the highest risk)
  • Switching to an antidepressant with less risk of sexual dysfunction
    – Mirtazapine
    – Bupropion ( not subsidesed through the PBS) = better option in females
  • Adjunctive treatment
    (with the addition of a non- antidepressant adjunctive treatment would be most reasonable for patients who have obtained substantial clinical benefit from the implicated antidepressant, and where sexual dysfunction is of moderate severity)
    – Sildenafil or Tadalafil
  • Non-pharmacological treatments
    – CBT and couples therapy
    – Exercise before sexual activity

chrome-extension://efaidnbmnnnibpcajpcglclefindmkaj/https://www.mja.com.au/system/files/issues/212_07/mja250522.pdf

56
Q

ANTIDEPRESSANTS
Mirtazapine notable side effects

A
  • waight gain
  • Sedation
  • Priapism
57
Q

ANTIDEPRESSANTS
TCA’s
Side effecrs

A
  • anticholinergic side effects (dry mouth, urinary retention, and dry skin)
  • QT prolongation (cardiotoxic)
  • Weigh gain
  • Sedation

Nortriptylinene has lower incidence of these side effects

58
Q

ANTIDEPRESSANTS
MAOIs interacts with which compound found in some drugs and foods?

A

Tyramine

59
Q

ANTIDEPRESSANTS
What can the interaction of MAOIs and Tryamine cause?

A

Hypertensive Crisis

60
Q

ANTIDEPRESSANTS
what drugs and foods contain Tyramine?

A
  • Drugs: TCAs
  • Foods:
    – matured, aged or out-of-date cheese
    – liver products (eg pâté);
    – fermented, matured or aged meat (eg salami,
    pepperoni, mortadella);
    – pickled herring;
    – improperly stored or spoilt meat, fish, poultry or eggs
    – fava or broad bean pods (not beans),
    – banana peel
    – all tap and home-brewed beers
61
Q

ANTIDEPRESSANTS
Bupropion contraindication

A

in patients suffering from seizures
it reduces seizure threshold

62
Q

ANTIDEPRESSANTS
Venlafaxine contraindication

A
  • Diastolic Hypertension
  • Breast feeding
63
Q

ANTIDEPRESSANTS
Drugs associated with Serotonin Syndrome

A
  • SSRIs
  • SNRIs
  • TCAs
  • MAOIs
  • Amphetamines
  • MDMA
  • Lithium
  • St John’s Wort with antidepressant
64
Q

ANTIDEPRESSANTS
Serotonin toxidrome
Clinical presentation

A
  • onset within hours of commencing the serotonergic agent or interacting drugs

TRIAD of clinical effects:

  • neuromuscular clonyc excitation
    —hyperreflexia, clonus (inducible or spontaneous), ocular clonus, myoclonus, shivering, tremor, hypertonia or rigidity
  • autonomic effects
    —hyperthermia (mild: < 38.5 °C; severe: > 38.5 °C or rapidly rising), diaphoresis, flushing, mydriasis, tachycardia
    —GI tract symptoms (nausea & vomiting, diarrhoea, increased bowel sounds)
  • central nervous system (CNS) effects
    —agitation, anxiety, confusion, seizure
65
Q

ANTIDEPRESSANTS
Serotonin toxicity Mx

A
  • cease inciting agent(s)
  • if mild to moderate serotonin toxicity
    – treatment is not usually required
  • If severe
    – sedation + intubation + paralysion
    – temperature control
  • If significant neuromuscular agitation = Cyproheptadine VO
    – In patients with severe serotonin toxicity who are unable to take oral medications, Chlorpromazine IV may be used
66
Q

ANTIDEPRESSANTS
Saint John’s Wort combined with COCP

A
  • SJW reduces the effectiveness of COCs and increases the risk of unintended pregnancy

SJW’s extracts induce the cytochrome P450 enzymes and increase intestinal P-glycoprotein expression. This stimulating the liver to break down the oestrogen and progestogen more rapidly, making COCs less effective and increasing chance of unintended pregnancy

67
Q

ANTIDEPRESSANTS
Saint John’s Wort combined with Warfarin

A

SJW reduces the effectiveness of warfarin and increases the risk of stroke, ischaemia, arterial blockage etc.

  • SJW’s extracts induce the cytochrome P450 enzymes, therefore metabolising warfarin at a faster rate therefore decreasing its effectiveness.
68
Q

MOOD STABILISER
common adverse effects seen in chronic use of Lithium

A

“LitHIUm”
- Low thiroid (Hypothyroidism)
- Heart (Ebstein anomaly)
- Insipidus (Nephrogenic Diabetes insipidus)
- Unwanted movements
+
- Alopecia/hair thining
- Acne

Lithium per si doesn’t cause kidney injury or affect clearance

69
Q

MOOD STABILISER
Most common setting of Lithium toxicity

A

Chronic usage

Acute lithium poisoning rarely leads to significant toxicity due to:
- the rapid elimination by the kidneys
- slow uptake into the CNS

Acute ingestions of < 25 g lithium are unlikely to cause major effects
unless patients have kidney failure.

In acute lithium poisoning, patients may have a concentration greater than 5 mmol/L and yet this may not indicate severe poisoning.

70
Q

MOOD STABILISER
Risk factors for chronic lithium poisoning

A
  • change in dose
  • decreased elimination (kidney function impairment)
  • dehydration
  • age > 50 years
  • drug interactions ((notably [NSAIDs], diuretics, ACEis/ARBs))
  • nephrogenic
  • diabetes insipidus
  • thyroid dysfunction.
71
Q

MOOD STABILISER
Clinical presentation

A
  • gastrointestinal effects
    —nausea, vomiting and diarrhoea
  • CNS effects
    —tremor, hyperreflexia, ataxia and dysarthria in mild to moderate toxicity;
    —confusion, coma and seizures in severe toxicity
  • cardiovascular effects
    — QT prolongation and hypotension in severe cases.
72
Q

MOOD STABILISER
Key investigations in lithium poisoning

A
  • ECG
    — QT prolongation occurs with severe poisoning, but rarely results in arrhythmias.
  • Lithium concentration
  • Creatinine and urea
    —check kidney function.
73
Q

MOOD STABILISER
Lithium toxic concentration

A

In chronic lithium poisoning, a concentration > 2 mmol/L is associated with severe poisoning.

Lithium concentrations can be difficult to interpret, and the lithium concentration in blood only reflects the
concentration in the CNS in chronic poisoning.

74
Q

MOOD STABILISER
Acute Lithium poisoning Mx

A

Most patients with acute poisoning require no specific treatment except:

  • All patients with chronic lithium toxicity require admission.
  • serial measurement of lithium concentrations to confirm elimination.
  • fluid replacement (essential in all patients with lithium poisoning)
75
Q

MOOD STABILISER
Chronic poisoning Mx

A

SIMILAR INITIAL MANAGEMENT

  • All patients with chronic lithium toxicity require admission.
  • serial measurement of lithium concentrations to confirm elimination.
  • fluid replacement (essential in all patients with lithium poisoning)

Intravenous fluid therapy with NaCl 0.9% is the first-line treatment and increases lithium elimination in patients with normal kidney function.

Many patients on long-term lithium therapy have diabetes insipidus, so it is essential that this is taken into
consideration when giving intravenous fluids (ie larger fluid requirements to replace increased urine output).

76
Q

MOOD STABILISER
Is activated charcoal used in the management of ACUTE Lithium poisoning?

A

NO

Activated charcoal does not bind lithium.

77
Q

MOOD STABILISER
What amount of lithium ingested would indicate decontamination

A

> 50 g

78
Q

MOOD STABILISER
What type of decontamination would be indicated in massive Lithium poisoning and what criteria shoulb met

A

whole bowel irrigation

  • if given within the first 6 hours
  • patient is awake and cooperative
79
Q

MOOD STABILISER
Indications for Haemodyalisis in Lithium poisoning

A
  • lithium concentration > 2.5 mmol/L (in chronic intake)
  • severe clinical effects —delirium, seizures, coma or hypotension
  • lithium concentration > 1.5 mmol/L associated with
    — persistent clinical effects
    — little response to intravenous fluids
    — persistent kidney impairment despite fluids.
80
Q

MOOD STABILISER
whento stop Dyalisis in lithum poisoning

A

Dialysis should be continued until lithium concentrations < 1 mmol/L

Lithium clearance is proportional to flow rate, so either haemodialysis or high-flux continuous veno-venous haemodialysis should be used to rapidly remove lithium.

81
Q

MOOD STABILISER
three features of clinical recovery from Lithium Poisoning

A
  • can take days to weeks
  • is significantly delayed compared with the decrease in serum lithium concentrations
  • Some neurological effects may be permanent.
82
Q

PSYCHOACTIVE SUBSTANCES
“Cannabinoids”

A
  • THC (Tetra-hydrocannabinol) = agonist
  • CBD (Cannabidiol) = antagonist
83
Q

PSYCHOACTIVE SUBSTANCES
“Cannabinoids” THC

A

↑ THC = greater high effect

84
Q

PSYCHOACTIVE SUBSTANCES
“Cannabinoids”

A

↑ CBD = greater analgesic, anti-inflamatory, anti-anxiety effects

85
Q
A

Contraindications to benzodiazepine
severe hepatic insufficiency
alcohol abuse
opioids
old age
COPD

AMC MCQ (57 decks)

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