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Psychiatry SC1 > Psychopharmacology > Flashcards

Psychopharmacology Flashcards

1
Q

MAOI
What are these drugs mainly used for?
What does it stand for?
Describe the mechanism of action.
Give a name of 3 where 2 of them are also used in Parkinson’s
Rarely used because of its side-effect profile and interactions with many drugs. What are the major side effects?

A

Antidepressants. Some are also used for Parkinson’s
Monoamine oxidase inhibitor
Inhibits enzyme responsible for metabolizing neurotransmitters AFTER reuptake. This would increase the concentration of neurotransmitters until drug wears off.
Phenelzine, Selegiline and Rasagiline. Giline = Used in Parkinson’s
Postural hypotension and Hypertensive reaction/crisis (with tyrosine-rich foods such as cheese and wine)

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2
Q

TCAs
What does it stand for?
Describe its mechanism of action.
Give 2 examples. One with each ending.
These drugs are known for having a wide range of effects and hence a wide range of side effects causing it to fall out of favor except with those who are young or those that are easily monitored. What are the major side effects?

A

Tricyclic Antidepressants
Inhibits reuptake of serotonin, noradrenaline, or both. Most also have some blocking of the Na and Ca channels hence causing Anticholinergic effects
Amitripyline (or Nortriptyline), Clomipramine
Side Effects:
Anticholinergic effects: Dry mouth, blurred vision, confusion, urinary retention
Postural hypotension, dizziness, sedation
Cardiac Toxicity: Risk of QT prolongation/arrhythmias

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3
Q

SSRI
What does it stand for?
Why does it have less side effects than TCA?
What should one consider when prescribing SSRIs? (Not an SE)
What are the main side effects of SSRIs? (Although rare)
Name 3

A

Selective Serotonin Reuptake inhibitor (Same MOA as TCA - inhibiting reuptake - but only of serotonin
Less widespread receptor affinity => less systemic side effects/toxicity. Also does not affect Ca and Na => no anti-cholinergic effects
Lag effect of SSRI (1-2weeks) 2-4 weeks is a myth. Maximal effect is in weeks 1-2 and minimal in weeks 4-6
GI disturbance (constipation) > Sexual Dysfunction, sedation > Serotonin syndrome, GI bleeding, Hyponatremia
Fluoxetine, Citalopram, Sertraline, Paroxetine

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4
Q

SNRIs
What does it stand for?
Give an example

A

Serotonin/Noradrenaline Reuptake Inhibitors
Venlafaxine

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5
Q

What type of Drug is Venlafaxine
What is the effect of increasing dose with this drug

A

SNRI
At low doses it primarily affects serotonin but as you increase the dose, there is an effect on noradrenaline.
Differences:
Dose-dependent effect on blood pressure => monitor at higher doses
Noradrenergic side effects at higher doses => anti-cholinergique effects (Dry mouth, urinary retention, constipation, blurred vision).

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6
Q

What are Anxiolytic medications used for?
Other than Pregabalin, what is the group of medications used for this?
What are the main side effects?
These drugs are prone to causing addiction. What are the symptoms of withdrawal?
What is the antidote for overdose?
Give 2 examples

A

They are used to treat ACUTE and severe symptoms of anxiety. They are prone to addition which is why. Only to be used in short periods of time.
Benzodiazepines.
Side effects: Sedation, Paradoxical Reaction (aggressive), dizziness/falls (do not give to elderly), Depersonalization/déréalisation
Withdrawal: sleep disturbance, anxiety/panic attacks, difficulty concentrating.
Flumazenil
Flurazepam, Temazepam, Lorazepam

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7
Q

Pregabalin
What is the MOA?
What type of drug is it?
What are the indications?
Is it long-acting or short-acting?

A

Inhibits release of neurotransmitters (esp glutamate) by inhibiting Ca influx
Anxiolytic medication
Generalized anxiety disorder, neuropathic pain, partial seizures
Short-acting (anxiolytics treat acute and severe anxiety symptoms

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8
Q

What drugs are used as sleeping tablets?

A

Melatonin
Z-drugs - Zopiclone, Zolpidem Zzzzz
Benzodiazepines - Flurazepam, Temazepam

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9
Q

Schizophrenia is treated via…
If a patient presents with positive symptoms are they early or late
Give examples of positive and negative symptoms of schizo

A

Antipsychotics
Late
Positive - Delusions, hallucinations, catatonia (strange movements, jerks, abnormal/uncomfortable sitting)
Negative - Anhedonia (loss of ability to feel pleasure), Avolition (lack of motivation), Alogia (poverty of speech), Affective Blunting (limited emotional reactivity)

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10
Q

What family of receptors are important in psychosis and what receptors belong to that family

A

D2 composed of D2,3,4

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11
Q

Dopamine Pathways
Where does the Mesolithic pathway run
what does it control
What occurs when it is overactive?
What condition is associated with overactivity of this pathway?

A

Mesolithic pathway: Projects from the ventral regimental area to the nucleus accumbens
It controls behavior and produces delusions and hallucinations when overactive

Schizophrenia

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12
Q

Dopamine Pathways
Where does the Mesocortical pathway run?
What does it control?

A

Mesocortical Pathway: Projects from the VTA (Ventral regimental area) to cortex.
It mediates positive and negative psychotic symptoms and cognitive side-effects of neuroleptics

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13
Q

Dopamine Pathways:
Where does the Nigrostriatal pathway run?
What does it control?
What disease affects this pathway? How?

A

Nigrostriatal pathway:
Projects from substantia nigra to the basal ganglia
Controls movement
Parkinsons- When post-synaptic dopamine receptors in the basal ganglia are blocked, movement disorders can appear => Drug induced Parkinsonism

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14
Q

Dopamine Pathways:
Where does the Tuberoinfundibular pathway run?
What does it control?

A

Projects from hypothalamus to the anterior pituitary = > controls prolactin secretion => Dopamine controls prolactin release by inhibiting it.
Note: This is the only pathway that runs downwards. All the others travel from the midbrain upwards

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15
Q

Dopamine Hypothesis:
Increased dopamine causes what symptoms in schizo patients? What are these symptoms called?
What dopamine pathway is mostly involved here?
What drugs mostly cause these symptoms?

A

Positive symptoms in schizo patients are due to increased dopamine. These symptoms include hallucinations, Catatonia (Movements + withdrawal), and delusions
Mesolimbic Pathway - controls behaviour and produces delusions and hallucinations when overactive
Cocaine, amphetamines, and L-dopa

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16
Q

Describe some changes to the brain in Schizo patients
What do you expect to see on FMRI?

A

Enlargement of lateral and 3rd ventricles => cortical volume (actual brain size) is lighter andsmaller. This change is more of decreased neuronal size rather than neuronal loss
Wider sulci gaps
Lower grey matter volume especially in medial temporal structures
Functional imagine shows dysconnectivity between frontal and temporal lobes

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17
Q

Give 1 similarity between all 3 types of antipsychotics and differentiate between them in terms of MOA and side effects

A

They all have dopamine antagonism
1st gen —> Typical => D2 blockade is the primary MOA
2nd gen —> Atypical => Newer and blockades many receptors
3rd Gen —> D2 partial agonism

Side effects of these drugs BOTH include extrapyramidal symptoms (EPSEs due to D-block) AND metabolic.
1st gen drugs mostly block D2 => extrapyramidal symptoms mostly
2nd gen drugs mostly have metabolic symptoms

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18
Q

Blocking the D2 receptor causes what family of symptoms?
How is it caused?
What are the symptoms?

A

Extrapyramidal symptoms (EPSEs)
Nigrostriatal neurons terminate on cholinergique neurons => dopamine inhibits neurons => antipsychotics cause acetylcholine release => antipsychotics with weak Anticholinergic properties display more EPSEs than potent ones since blocking more = more release
Parkinsonism (Bradykinesia, resting tremor, rigidity)
Acute Dystonia
Akathisia (inability to stay still —> always walking)
Tardive dyskinesia —> sudden, irregular, involuntary movements

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19
Q

What generation are typical drugs? Are they widely used?
Give 2 examples
When are they used

A

1st generation, not widely used anymore
Haloperidol
Chlorpromazine
Used in acute psychotic episodes

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20
Q

What is Acute Dystonia?
What is it caused by?
Acute Dystonia of the muscles of the eye is called?

A

Involuntary contraction of a muscle group leading to abnormal movements and postures
Body reaction to antipsychotics
Oculogyric crisis

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21
Q

What is Akathesia?
What behavior would you associate with Akathesia

A

Inner restlessness and compulsion to move
Usually constantly walking

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22
Q

Since Antipsychotics act by blocking dopamine receptors, acetylcholine release is not inhibited => causing EPSEs. If your patient is given an Antipsychotic and presents with acute Dystonia, what medication would you give them?

If your patient is experiencing Tardive Dyskinesia, what would you expect to see? What does this indicate?
How is it treated?

Dopamine also inhibits another pathway. What is that pathway and what are the SEs?

In unfortunate circumstances, a medical emergency may occur when administering these drugs. What is this medical emergency? What does it present similar to?
How could you confirm that this is occurring?
How would you treat?

A

Biperiden, Procyclidine

Involuntary muscle movements => usually chewing. This is a late onset (=> tardive)
Doesn’t usually go away = > considered irreversible. All you can do is reduce the dose or switch to another antipsychotic

Dopamine naturally inhibits prolactin which is controlled via the tuberoinfundibular pathway => raising prolactin levels. This causes gynacomastia, galactorrheoea and amenorrhea

Neuroleptic malignant syndrome is a reaction to antipsychotic drugs that is characterized by fever, altered mental status (confusion), agitation and muscle rigidity followed by hyperthermia, diaphoresis (sweating), autonomic instability (respiratory difficulties). This is similar to Malignant hyperthermia exhibited by anesthetics during surgery.
Labs: Patients would have raised CPK (Creatine Phosphokinase)
Treatment: Dantrolene (muscle relaxant), supportive to (rehydration)

23
Q

List the symptoms of first generation antipsychotics in the order that they occur!

Do these occur in 2nd generation antipsychotics?

A

Acute Dystonia
Akathisia (inability to stay still —> always walking)
Parkinsonism (Bradykinesia, resting tremor, rigidity)
Tardive dyskinesia —> sudden, irregular, involuntary movements (tardive=late onset)
Non-EPSE —> Sedation, Photosensitivity, and Cardiac Conduction defects

Yes but since they target a wide range of receptors, the side effects are mostly metabolic in 2nd gen meds.

24
Q

Name the 2 typical antipsychotic drugs

A

Haloperidol and Chlorpromazine

25
Q

Atypical antipsychotics:
What generation are these medications?
Name 3
What are the major side effects?

A

2nd Generation
Olanzepine and Clozapine. Others include Quetiapine and Risperidone
Weight gain, Dyslipidemia/hypercholesterolemia, and glucose intolerance (induced DM)

26
Q

Clozapine:
What type of antipsychotic is it?
When does it treat?
When is it indicated

Since it is considered the best antipsychotic out there, why dont we just give it to everyone?

What are the 4S side effects?

A

Atypical/2nd gen antipsychotic
Treatment of schizophrenia, negative symptoms, suicidal behavior, aggressive behavior, L-dopa psychosis
Only indicated after 2 other antipsychotics have been used for 6 weeks each AND one of them has to be atypical/2nd generation

1% risk of agranulocytosis which has very high mortality => must be closely monitored with WBC count every 3-4 weeks. If the patient fails a blood test they have to stop clozapine.

Sedation, hyperSalivation, Seizures, and Somatic (weight gain)

27
Q

What is Aripriprazole and how does it work?
Patients with these drugs do not often complain of sedation as much as they complain of…?

A

3rd generation D2 partial agonist
Agitation rather than sedation can be an issue.

28
Q

Antipsychotics are great for psychotic conditions (psychosis) such as in schizo. What else are they prescribed for?

A

Mania, to augment antidepressants, and to handle severe anxiety

29
Q

Define Euthymic
Define Hypomania
Define Subsyndromal Depression

A

Euthymic is a normal/balanced mood.
Hypomania is a mild/moderate mania.
Subsyndromal depression is depression of the same quality as major depression yet without anhedonia (no pleasure) and depressed mood

30
Q

How would you treat an episode of mania and depression in bipolar disorder and compare that to what you would use to treat the disorder.

A

The goal of treatment in an episode is to treat depression or mania NOW
Anti-manic medications are Antipsychotics that act quickly (tranquilisation) as well as lithium and anticonvulsants (Valproate, carbamazepine)
Anti-depressive medications are SSRIs, SNRIs etc… or augmentation of that with lithium

In terms of treating the disorder, our goal is to prevent future highs and lows => we use mood stabilizers
Mood Stabilizers: Lithium, Anticonvulsants (Valproate etc..) or an atypical antipsychotic (Olanzepine, Clopzapine)

31
Q

What are the main effective uses of Lithium

A

Anti-mania
Mood Stabilization
Antidepressants augmentation
Anti-suicidal
Anti-aggression

32
Q

Lithium is a salt and it is not protein-bound => does not act as a plasma buffer. Before administering lithium what investigations must be conducted?

After giving Lithium, what is a concern that one may have?

What is the therapeutic range for lithium?

A

Lithium Checklist:
Lithium levels in blood within FBC
Electrolytes: Nephrotoxicity from lithium can cause dehydration
As a salt, lithium is heavily influenced by Renal function => renal function test => Creatinine and BUN (blood urea nitrogen)
Lithium may cause widening of QRS complex => ECG
Lithium may cause hypothyroidism => thyroid function test (TSH)
Pregnancy test => Ebstein’s anomaly

As levels of lithium vary from person to person based on renal function, blood tests must be conducted after administration to ensure correct levels are present for the intended purpose.

1-1.2

33
Q

Give examples of what may affect levels of lithium in the body

A

As Lithium is a salt, it is affected by Renal elimination => levels are affected by renal failure, kidney damage, and dehydration
Most importantly concurrent use of diuretics will significantly affect levels
+NSAIDs

34
Q

List the common Side effects of lithium

At what levels does lithium toxicity occur and what are some signs of it?

How would you treat lithium toxicity?

What would happen if lithium is administered in pregnant women?

A

Polydipsia, polyurea, water retention
Hypothyroidism
Nephrotoxicity => Dehydration and diabetes insipidus
Mild fine tremor

Lithium toxicity begins at >1.5 mmol/L. Symptoms similar to being drunk
Neuromuscular: Ataxia (coordination) and tremor
CNS: Slurred speech, blurred vision, dizziness
CVS: Hypotension, widened QRS complex, lethargy

Remember that it is affected by kidney function and hence rehydrate + dialysis. Other than that the obvious reducing dosage

Lithium should never be administered in pregnant women as it can cause Ebstein’s anomaly which is the displaced tricuspid valve allowing for tricuspid regurgitation

35
Q

Valproic Acid/Sodium Valproate:
Mechanism of action:
Side effects:

A

Anticonvulsant
MOA: inhibits voltage-gated sodium channels (anticonvulsant property) and increases GABA (bonzo effect of sedation)
Side Effects: causes folate deficiency in the adult as well as the child in pregnancy => spina bifida (neural tube defect). Rarely, it can cause hepatic necrosis

36
Q

How do anxiolytic medications work? What effects does it induce?

Benzodiazepines are divided into 3 groups based on their half-life, each with clinical indications of their own. State them

A

They act by primarily act by increasing the release of GABA which has the effects of euphoria, relaxing muscles and reduced breathing (shallow breathing). This eliminates anxiety and seizures (muscle).

Short term (1-12hrs): Panic attacks (and status epilepticus)
Medium term (12-40hrs): anxiety, insomnia, panic disorder
Long term (40-250hrs): chronic panic disorder, alcohol withdrawal

37
Q

A patient with signs of serotonin syndrome presents to the ED. An intern asks for the “antidote”. What is it and give an example

A

Serotonin Receptor Antagonist e.g. Cyproheptadine

38
Q

NMS or neuroleptic malignant syndrome may occur in what class of drugs? Why does it occur?

A

1st generation anti-psychotics (such as haloperidol) due to dopamine antagonism

39
Q

List 3 metabolic side effects of 2nd generation antipsychotics.

A

Weight gain —> check weight
Dyslipidaemia —> check cholesterol levels
Glucose intolerance => NIDDM (non-insulin dependent diabetes mellitus -type 2) => HbA1c

40
Q

How long does it take mood stabilisers to take effect on average?

A

1 week

41
Q

What’re some indications of Lithium

A

Bipolar prophylaxis, recurrent depression prophylaxis, steroid-induced psychosis, suicidal behaviour, aggressive behaviour
Treatment of clozapine-induced neutropenia

42
Q

A patient presents to OPD with results of her clozapine blood test. it shows that the patient is severely neutropenic. What is your next step?

A

Prescribe Lithium (treats clozapine-induced neutropenia)

43
Q

1) Prior to prescribing lithium, state the investigations that must be performed and why they are being performed.
2) You will need to explain to the patient the commitments that come with lithium. After starting the dose, what should be done? (same for after changing the dose)
3) What should routinely be done during the tx process and how often should each be checked?

A

1)Before prescribing lithium, Bloods including RFTs, TFTs, and calcium levels. RFTs due to nephrotoxicity, TFTs for increased risk of hypothyroidism, Calcium is taken as lithium has increased resorption in the nephron => increase in PTH => hyperparathyroidism
ECG is conducted due to dysrhythmias (T wave/ST segment)
Exclude pregnancy (Ebstein’s tricuspid valve regurgitation)
Weight (weight gain)

2) After starting the medication, serum lithium should be taken 5-7 days later and it must be 12 after the patient last took lithium. Lithium dosage must be adjusted to reach 0.5-0.8

3) Serum Lithium must be checked every 3 months, other blood tests every 6 months (RFT, TFT, Calcium). Inform the patient that if they experience any symptoms of hypothyroidism (increased weight/feeling cold), that they should seek medical attention

44
Q

A patient on lithium is asking if she can breastfeed the baby. What do you tell her?

A

Lithium is excreted in breast milk and hence patient is advised to not breastfeed while on treatment. If they insist they may still be on lithium but it is under their discretion

45
Q

What are the immediate side effects of lithium?
What are the long term side effects?
What are the signs of toxicity?

A

Immediate: GI (Nausea, diarrhoea, vomiting), polyuria (increased urination) and polydipsia (increased thirst), drowsiness. FINE TREMOR (course tremor = toxicity)

Long term: (go through investigations) Nephropathy, nephrogenic diabetes insidious, hypothyroidism. hyperparathyroidism, cardiac dysrhythmias

Toxicity: COARSE TREMOR, Exacerbation of same side effects, slurred speech, convulsions. Occurs at >1.3mmol

46
Q

How would you treat lithium toxicity

A

Anticonvulsant, fluids, osmotic diuresis, hemodialysis (severe)

47
Q

Prior to prescribing valproate, what should be tested and why?
During (incl. frequency)?

A

Prior: Bloods (FBC, LFTs for drug-induced acute liver failure), weight, exclude pregnancy
During: Serum valproate checked every 3 months and FBC/LFTs every 6 months

48
Q

A 30 year old woman complains no improvement on lithium. She researched online that sodium valproate can be tried. What would you tell her?

She insists on trying this medication and promises to not get pregnant and has no intentions to do so. What is the protocol?

A

Valproate should never be prescribed in a woman of child bearing age due to congenital abnormalities such as Spina Bifida, facial anomalies, and congenital heart disease.

Pregnancy prevention protocol involves assessing the patient’s potential of becoming pregnant as well as educating patient on the risks. Pregnancy tests must be conducted annually during treatment and patient must be adhere to a contraceptive throughout. This provision must be confirmed and form signed.

49
Q

What are the immediate and long term side effects of Prescribing valproate

A

Immediate: GI disturbances and drowsiness
Long term (Investigations): Thrombocytopenia/agranulocytosis/Anaemia (FBC), Hyperammonemia (metabolic increase of ammonia), and Hepatic/pancreatic toxicity (LFTs)

50
Q

A patient prescribed clozapine is not noticing much improvement in their condition. You decide to give them a mood stabiliser. Which mood stabilisers would you give and which would you not. Give a reason as to why you would not give these meds.

A

Give: Lithium or Lamotrigine
Don’t give: Valproate or Carbamazepine due to also having the side effect of agranulocytosis

51
Q

Other than Depression, mania, or BPAD, where carbamazepine is not recommended as first line, what would it be used for?

A

Trigeminal neuralgia
Just a note: Investigation prior and during for this medication is exactly the same as that of lithium except for TFTs

52
Q

What are the major side effects of carbamazepine

A

Has the same immediate side effects as others (GI, drowsiness etc..). Major ones are agranulocytosis, thrombocytopenia, and aplastic anaemia. These are comparable to valproate. FBC checks every 6 months are essential. Lamotrigine and Carbamazepine may have SJ rash within first 8 weeks of starting.

53
Q

Lamotrigine is only licensed for use in BPAD. What should be monitored prior and during treatment?
What are the main side effects?
Can lamotrigine be used in pregnancy?

A

FBC and LFTs should be monitored every 6 months
Side effects: GI disturbances, Diplopia, Headaches, dizziness and SJ rash within first 8 weeks of starting dose
It is not recommended but may be used. Serum lamotrigine levels should be monitored in this case.

54
Q

SJ rash is a side effect that may occur when prescribing some mood stabilisers. What are the mood stabiliser that may cause it and when would this rash be expected to occur?

A

Lamotrigine and carbamazepine
First 8 week after starting.

Psychiatry SC1 (7 decks)

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