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YR2 BCS Study Points SEM 1 > Block 6 - Psychiatry > Flashcards

Block 6 - Psychiatry Flashcards

1
Q

What is Consciousness? What is it dependent on? 4 components?

A

Consciousness: The state of being aware of and responsive to one’s surroundings. Dependent on ascending RAS system of brainstem (arousal) and cerebral cortex (content of consciousness).

The part of the brain that is responsible for consciousness is the extended reticular activating system.

  • Self-awareness
  • Access to memories
  • Ability to manipulate abstract ideas
  • Focus of attention
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2
Q

What are 4 Altered States of Unconciousness?

A

Altered States of Unconsciousness:

Sleep: A state of reduced interaction with the environment (reversible)

Delirium: Acute condition with altered mental state due to organic cause (syndrome not diagnosis)

Coma: Unarousable unresponsiveness usually with preserved brainstem function (no response to pain)

Brain Death: Loss of all brain function with no response to pain or brainstem reflexes (irreversible)

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3
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5
Q

What are the Basic Mechanisms of Unconsciousness?

A

Mechanisms and Causes of Unconsciousness:

  • Altered consciousness is due to loss of function of ARAS in the brainstem or thalamus, and/or widespread impairment of cortical function.
  • A single focal hemisphere (or cerebellar) lesion does not produce coma unless it compresses the brainstem.
  • Cerebral oedema frequently surrounds masses, increasing their pressure effects.
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6
Q

Causes of Altered Consciousness?

A
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7
Q

Explain the role of sodium in fluid balance, and the causes and consequences of sodium dysregulation.

  • Is it a cation or anion?
  • In which body fluid compartment is it mostly?
  • What is the sodium plasma level?
    • ECF?
    • ICF?
    • Bone?
  • Which 4 things regulate sodium reabsorption?
  • Where in the nephron is most sodium reabsorbed?
  • Effect of Na on water?
A

Role of Sodium in Fluid Balance:

  • Positively charged cation in the ECF
  • Major solute in ECF and so determines the osmolality and subsequent volume of ECF
  • Sodium plasma level around 140mmol/L
    • ECF: 50% (140mmol/L)
    • ICF: 5% (15mmol/L)
    • Bone: 45% (125mmol/L)
  • Sodium is regulated by RAAS, ADH, ANP, thirst and kidney reabsorption
    • 70% proximal tubule
    • 20% ascending loop
    • 5% distal tubule
    • 3% collecting duct

Acute changes in sodium will cause osmolality changes with free water shifting into and out of the vascular space until osmolality is equilibrated

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8
Q

What are the major fluid compartments of the body?

A
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9
Q

What is sodium dysregulation caused by overall?

  • What is Extrarenal hyponatraemia defined as?
  • What are 5 Extrarenal causes of hyponatraemia with decreased ECV (hypovolemia)?
  • What is Renal hyponatraemia defined as?
  • What are 6 Kidney causes of hyponatraemia with decreased ECV (hypovolemia)?
A

Sodium Dysregulation: Disturbances of sodium concentration are caused by disturbances of water balance.

Causes of hyponatraemia with decreased ECV (hypovolemia)

Extrarenal (urinary sodium <20 mmol/L)

  1. Vomiting
  2. Diarrhoea
  3. Haemorrhage
  4. Burns
  5. Pancreatitis

Kidney (urinary sodium >20 mmol/L)

  1. Osmotic diuresis (eg. hyperglycaemia, severe uraemia)
  2. Diuretics
  3. Adrenocortical insufficiency
  4. Tubulo-interstitial renal disease
  5. Unilateral renal artery stenosis
  6. Recovery phase of acute tubular necrosis
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10
Q

What are the causes of hyponatraemia with normal Extracellular volume (euvolemia)?

A
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11
Q

What are the 4 causes of hyponatraemia with increased Extracellular volume (hypervolemia)?

A

Causes of hyponatraemia with increased Extracellular volume (hypervolemia)

  1. Heart Failure
  2. Liver Failure
  3. Oliguric kidney injury
  4. Hypoalbuminaemia
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12
Q

What are the causes of hypernatraemia?

A
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13
Q
A
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14
Q

What is the mechanism behind Hyponatraemia (<135 mmol/L) with Hypovolaemia?

What happens to ADH?

A

Hyponatraemia (<135 mmol/L)

Hypovolaemia: Salt loss in excess of water loss. ADH secretion is initially suppressed (via the hypothalamic osmoreceptors) but as fluid volume is lost, volume receptors override the osmoreceptors and stimulate both thirst and the release of ADH.

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15
Q

What is the mechanism behind Hyponatraemia (<135 mmol/L) with Euvolaemia?

What is SIAHD? Causes?

A

• Euvolaemia: An intake of water in excess of the kidney’s ability to excrete it (dilutional hyponatraemia) with no change in body sodium content (plasma osmolality remains low). See SIAHD.

  • SIAHD: Syndrome of inappropriate ADH secretion is hyponatraemia due to an increase in concentration of ADH inappropriate to the current osmotic or volume status.

Due to major surgery, ADH production from tumour, drugs, CNS disorders, hormone deficiency, other and pulmonary disorders (MAD CHOP)

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16
Q

What is the mechanism behind Hyponatraemia (<135 mmol/L) with Hypervolaemia?

A

• Hypervolaemia: Water excess. Sodium retention with relatively greater water retention.

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17
Q

What are the consequences of Hyponatraemia (<135 mmol/L)? (12)

A

What are the consequences of Hyponatraemia?

Acute ↓Na will shift fluid into the interstitial space and cause cerebral oedema. Also results in nerve and muscle dysfunction.

  1. Nausea and vomiting
  2. Neuropsychiatric symptoms
  3. Muscular weakness
  4. Headache
  5. Lethargy
  6. Psychosis
  7. Raised ICP
  8. Confusion
  9. Delirium
  10. Seizures
  11. Coma
  12. Death
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18
Q

What are the causes and consequences of hypernatraemia (>148mmol/L)?

A

Hypernatraemia (>148 mmol/L) *RARE*

  • CAUSES
    • Dehydration: Due to unreplaced water that is lost from the gastrointestinal tract (vomiting or osmotic diarrhea), skin (sweat) or the urine
    • Excess Salt: Due to administration of salt in excess of water
    • ADH system failure (body unable to rectify hyperosmolarity)
    • Impaired thirst mechanism or responsiveness (infants and elderly) or limited access to water
  • CONSEQUENCES → Acute ↑NA will cause water to enter the vascular space
    • Symptoms are nonspecific
    • Nausea, vomiting, fever and confusion may occur
    • Convulsions occur in severe states
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19
Q

What is Osmolality?

What is Osmolarity?

A
  • *Osmolality**: Amount of dissolved solute per kilogram of solvent (Osm/kg)
  • *Osmolarity**: Amount of dissolved solute per litre of solution (Osm/L)
  • *NB:** Extreme variation in osmolarity causes cells to shrink or swell, damaging or destroying cellular structure and disrupting normal cellular function
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20
Q

Describe the mechanisms of action of commonly used illicit drugs.

  • What are 3 CNS Stimulants (Sympathomimetics)?
  • What are 3 CNS Depressants?
  • What are 2 CNS Hallucinogens (Psychotomimetics0?
A
  • CNS Stimulants (Sympathomimetics)
    1. Amphetamine
    2. Cocaine
    3. MDMA
  • CNS Depressant
    1. Opiates
    2. Benzodiazepines
    3. Ethanol
  • CNS Hallucinogens (Psychotomimetics)
    1. Cannabis
    2. LSD/Mushrooms
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21
Q

What are the Mechanism, Effects (9) and Side Effects (12) of:

CNS Stimulants (Sympathomimetics) - Amphetamine?

A

CNS Stimulants (Sympathomimetics) - Amphetamine

  • Mechanism
    • Enhances the release of catecholamines (noradrenaline, adrenaline and dopamine).
    • To a lesser degree also inhibits the reuptake of catecholamines and inhibits monoamine oxidase.
  • Effects
    1. α1: Vascular smooth muscle and iris
    2. β1: Myocardium
    3. β2: Skeletal muscles and
    4. vascular smooth muscle
    5. Impulsivity
    6. Euphoria
    7. Alertness/energy
    8. Concentration
    9. Confidence
  • Side Effects
    1. Aggression/agitation, hypertension, tachycardia
    2. Dilated pupils
    3. Hyperthermia
    4. Thirst
    5. Dysrhythmia
    6. Increased muscle activity
    7. Restless/teeth grinding
    8. Anorexia
    9. Psychosis
    10. Depression
    11. Seizures
    12. Coma
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22
Q

What are the Mechanism, Effects (9) and Side Effects (4) of:

CNS Stimulants (Sympathomimetics) - Cocaine?

A

CNS Stimulants (Sympathomimetics) - Cocaine

  • Mechanism
    • Inhibits catecholamines reuptake by blocking noradrenaline, dopamine and serotonin transporters (as opposed to amphetamines which mainly stimulates release)
    • Blocks sodium channels (local anaesthetic effect and dysrhythmia)
    • Vasoconstrictive effect (myocardial infarction)
  • Effects
    1. Anaesthetic
    2. α1: Vascular smooth muscle and iris
    3. β1: Myocardium
    4. β2: Skeletal muscles andvascular smooth muscle
    5. Impulsivity
    6. Euphoria
    7. Alertness/energy
    8. Concentration
    9. Confidence
  • Side Effects
    1. Cardiac arrhythmia (wide QRS)
    2. Muscle and nerve dysfunction (blocks Na)
    3. Myocardial infarction or stroke
    4. Nasal septum damage
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23
Q

What are the Mechanism, Effects (9) and Side Effects (16) of:

CNS Stimulants (Sympathomimetics) - MDMA?

A

CNS Stimulants (Sympathomimetics) - MDMA

  • Mechanism
    • An indirect serotonergic agonist which increases extracellualar serotonin by occupying and reversing serotonin reuptake transporters
    • Blocks adrenaline, noradrenaline and dopamine reuptake
  • Effects
    1. Hallucinations (5-HT)
    2. α1: Vascular smooth muscle and iris
    3. β1: Myocardium
    4. β2: Skeletal muscles and vascular smooth muscle
    5. Impulsivity
    6. Euphoria
    7. Alertness/energy
    8. Concentration
    9. Confidence
  • Side Effects
    1. Pupil dilation
    2. Hyperthermia
    3. Thirst
    4. SIADH
    5. Cerebral oedema
    6. Seizures and coma
    7. Hypertension
    8. Tachycardia
    9. Ischaemia
    10. Cerebral hemorrhage
    11. Rhabdomyolysis
    12. Metabolic acidosis
    13. Serotonin syndrome
    14. Rapid speech
    15. Psychosis and paranoia
    16. Aggression

NB: Treat with BZD for sedation

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24
Q

What are the some Examples, the Mechanism, Effects (8) and Side Effects (10) of:

CNS Depressants - Opiates?

Antidote?

A

CNS Depressants - Opiates

  • Examples → Opioids are a class of drugs that include the illegal drug heroin, synthetic opioids such as fentanyl, and pain relievers available legally by prescription, such as oxycodone (OxyContin®), hydrocodone (Vicodin®), codeine, morphine, and many others.
  • Mechanism
    • Agonist to the mu (mostly), kappa and delta opioid receptors
    • Pre-synaptically blocks voltage sensitive Ca2+ channels and inhibits vesicle docking and neurotransmitter release
    • Post-synaptically enhances K+ conductance, hyperpolarisation and decreases action potential propagation.
  • Effects
    1. μ1: Supraspinal analgesia, bradycardia and sedation
    2. μ2: Respiratory depression, euphoria and physical dependence
    3. δ: Spinal analgesia and respiratory depression
    4. κ: Spinal analgesia, respiratory depression and sedation
    5. Euphoria
    6. Analgesic
    7. Adjunct to anaesthesia
    8. Cough suppressant
  • Side Effects
    1. Pinpoint pupils, respiratory depression and sedation
    2. Slurred speech
    3. Itching
    4. Nausea and vomiting
    5. Urinary retention
    6. Constipation
    7. Hypotension
    8. CNS depression (low GCS)
    9. Confusion/ delirium
    10. Coma

NB: Antidote is naloxone. Has shorter half-life so may return to respiratory depression when wears off

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25
Q

What are the Mechanism, Effects (4) and Side Effects (11) of:

CNS Depressants - Benzodiazepines?

Antidote?

A

CNS Depressants - Benzodiazepines → YR Pharm lecture flashcards Benzodiazepines

  • Mechanism
    • Binds allosterically to GABAA and potentiates GABA inhibitory neurotransmitters in CNS.
  • Effects
    1. Sedation
    2. Anxiolytic
    3. Anticonvulsant
    4. Muscle relaxant
  • Sife effects
    1. Drowsiness and confusion
    2. Dizziness and hallucinations
    3. Respiratory depression
    4. Hypotension
    5. Slurred speech
    6. Amnesia
    7. Nystagmus
    8. Ataxia
    9. Coma paradoxical
    10. Agitation
    11. Aspiration pneumonia

NB: Antidote is Flumazenil but it is not widely used (seizures)

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26
Q

What are the Mechanism, Effects (4) and Side Effects (5) of:

CNS Depressants - Ethanol?

SEE SEM 1 Pharmacology notes Prof Carroll - 6. Alcohol Metabolism & 7. Benzodiazepines

A

CNS Depressants - Ethanol

  • Mechanism
    • Increases GABA receptor activity
    • Alcohol increases both the frequency and the duration of the opening of the GABAA receptor chloride ion channel
  • Effects
    1. Sedation
    2. Anxiolytic
    3. Anticonvulsant
    4. Muscle relaxant
  • Side Effects
    1. Disinhibition
    2. Euphoria
    3. Impulsivity
    4. Aggression
    5. As benzos
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27
Q

What are the Mechanism, Effects (5) and Side Effects (6) of:

CNS Hallucinogens (Psychotomimetics) - Cannabis?

A

CNS Hallucinogens (Psychotomimetics) - Cannabis

  • Mechanism
    • Binds and activates pre- synaptic CB1 and CB2 receptors
    • Decreases neurotransmitter release
  • Effects
    1. Analgesic
    2. Antiemetic
    3. Relaxation
    4. Sharpened sensory awareness
    5. Increased appetite
  • Side Effects
    1. Sedation
    2. Incoordination
    3. Ataxia
    4. Impairment of short-term memory
    5. Impairment of motor coordination
    6. Hypothermia
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28
Q

What are the Mechanism, Effects (5) and Side Effects (5) of:

CNS Hallucinogens (Psychotomimetics) - LSD/Mushrooms?

A

CNS Hallucinogens (Psychotomimetics) - LSD/Mushrooms

  • Mechanism
    • 5-HT receptor agonists (mostly 5-HT2A receptors)
  • Effects
    1. Hallucinations
    2. Energy
    3. Creative thinking
    4. Awareness of senses
    5. Distortion of perceptions
  • Side Effects
    1. Pupil dilation
    2. Dizziness
    3. Over-sensitisation to noises
    4. Paranoia
    5. Fear and panic
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29
Q

Explain the importance of the history and mental status examination of the patient who has taken a deliberate drug overdose.

  • What are 6 components of the history taking of mental status/drug overdose?
  • What is the SAD PERSONS assessment?
A

Importance of History and Mental State Examination:

  1. Risk Assessment: To determine agent, dose, time of ingestion, clinical features and patient factors to help treat patient
  2. Suicidality: To determine risk of suicide (SAD PERSONS)
  3. Medical Health: To assess medical health and presence of drug complications
  4. Psychiatric Health: To determine any mental disorders
  5. Dependence and Tolerance: To assess level of drug use (recreational, dependence, tolerance or withdrawal) and assess readiness to change
  6. Psychosocial Situation: To better understand situation of patient
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30
Q

Relate the potential sequelae of overdose with commonly prescribed medications.

  • What are 4 Potential Consequences of Drug Use?
A

Potential Consequences of Drug Use:

  1. Drug Dependence: A chronic relapsing condition characterised by…
    1. A compulsion to seek and take a drug
    2. Tolerance and loss of control in limiting intake
    3. Craving during periods of abstinence
    4. Withdrawal emergence of a negative emotional state when access to the drug is prevented
    5. Rapid reinstatement of dependence upon resumption of drug use
  2. Drug Tolerance: The need for increased amounts of the drug to achieve a given response OR a markedly diminished effect with continued use of the same amount of the drug
  3. Withdrawal: Onset of a set of syndromes when chronic drug use is ceased, circulating drug levels are significantly reduced OR an antagonist is administered
  4. Common Complications: Arrhythmias, seizures, hypoxic brain damage, aspiration pneumonia, and hepatoxicity
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31
Q

What are the Mechanism, Effects (2) and Side Effects (5) of:

Paracetamol?

See Prof Carrol Paracetamol lecture - SEM1 NSAIDs & Paracetamol

A

Paracetamol

  • Mechanism
    • Not fully understood
    • Analgesic effect may include inhibition of central prostaglandin synthesis and modulation of inhibitory descending serotonergic pathways
    • The antipyretic effect is probably due to reduced production of prostaglandins in the hypothalamus
  • Effects
    1. Analgesia
    2. Antipyretic
  • Side Effects
    1. Nausea and vomiting
    2. Hepatotoxicity (can cause acute hepatic failure in OD)
    3. Hypersensitivity reactions
    4. Thrombocytopaenia
    5. Neutropaenia

NB: Check 4/24 paracetamol levels and plot on nomogram, if over the level treat with N- acetyl-cysteine

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32
Q

Describe the metabolism of paracetamol.

  • Which phase?
  • Conjugates with what?
  • What happens in overdose? Which metabolite builds up?
A

Paracetamol Metabolism:

Paracetamol usually metabolised by phase II metabolism by conjugation with sulfate and glucuronide. Small portion is metabolised by CYP450 into toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI) which is usually conjugated by glutathione into less toxic cysteine and mercapturic acid. In OD the phase II metabolism is overwhelmed and more is diverted into the CP450 pathway. When the glutathione is depleted the toxic NAPQI metabolite builds up.
NAC replenishes glutathione hence deactivates and safely excretes NAPQI

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33
Q

What are the clinical features of paracetamol toxicity by timeframe?

A
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34
Q

What are the Mechanism, Effects (3) and Side Effects (13) of:

SSRIs (E.g. Fluvoxamine)?

A

SSRIs (E.g. Fluvoxamine)

  • Mechanism
    • Selectively inhibit the presynaptic reuptake of serotonin
    • Also weak affinity for noradrenaline and dopamine transporters
  • Effects
    1. Antidepressant
    2. Anxiolytic
    3. Chronic pain relief
  • Side Effects
    1. Serotonin syndrome
    2. Nausea
    3. Dry mouth
    4. Diarrhoea/constipation
    5. Decreased appetite
    6. Decreased libido, ED and anorgasmia
    7. Increased risk of bone fracture
    8. Sedation/insomnia
    9. Tremor
    10. Dizziness
    11. Sweating
    12. Photosensitivity
    13. Suicidal ideation (early)
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35
Q

What are the Mechanism, Effects (3) and Side Effects (14) of:

Tricyclic Antidepressants (E.g. Amitriptyline)?

A

Tricyclic Antidepressants (E.g. Amitriptyline)

  • Mechanism
    • Inhibit reuptake of noradrenaline and serotonin into presynaptic terminals
    • Also block cholinergic, histaminergic, alpha1- adrenergic and serotonergic receptors
    • Also blocks fast Na+ channels in myocardium
  • Effects
    1. Antidepressant
    2. OCD management
    3. Chronic pain relief
    4. Insomnia management
    5. Migraine prophylaxis
  • Side Effects
    1. Cardiotoxicity, palpitations, arrythmia and chest pain
    2. Hypotension
    3. Widened QRS, tall R in aVR, sinus tachycardia and long QT/ PR
    4. Seizures and coma
    5. Respiratory depression
    6. Metabolic acidosis
    7. Drowsiness
    8. Confusion
    9. Dry mouth
    10. Fever
    11. Urinary retention
    12. Pupil dilation and blurred vision
    13. Constipation
    14. Rigidity
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36
Q

What is the Serotonin Syndrome?

  • Which medicines can cause it?
  • Clinical Features?
  • Treatment?
A

Serotonin Syndrome

  • May be caused by drugs which increase the concentration of serotonin (5-hydroxytryptamine, 5HT) in the brain
  • Possibly caused by an overstimulation of 5HT1A and 5HT2A receptors in the central grey nuclei and medulla
  • Involves a triad of mental, autonomic and neurological effects
  • Condition may deteriorate rapidly and may cause death

Medicines Which May Cause the Serotonin Syndrome → Especially combinations of two or more serotonergic drugs e.g. SSRI, SNRI, TCA, tramadol, MAOI and amphetamines

  1. Antidepressants e.g. SSRIs, MAOIs, tricyclics, SNRIs
  2. Some opioid analgesics e.g. tramadol, pethidine, fentanyl
  3. Some cough suppressants e.g. dextromethorphan
  4. Sumatriptan, cocaine, ecstasy, St John’s wort

Clinical Features: Hyperthermia, hypertension, tachycardia, agitation, hyperreflexia, rigidity/ hypertonia, clonus, diaphoresis, tremor and salivation

Treat: Benzodiazepines, cooling, cyproheptadine (serotonin antagonist and call tox!

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37
Q

What are the Mechanism, Indications (3) and Side Effects (14) of:

Antipsychotics (E.g. Quetiapine)?

A

Antipsychotics (E.g. Quetiapine)

  • Mechanism
    • D2 antagonist
  • Indications
    • Schizophrenia, bipolar and psychosis management
  • Side Effects
    • Tachycardia, Hypotension, Sedation, Abnormal LFTs, Hypothyroidism, Anxiety, Dry Mouth, Hyperprolactinemia, Urinary retention, Sexual dysfunction, Parkinsonism, Extrapyramidal symptoms, Weight gain, Raised BSL, Hyperlipidaemia
    • OD: Arrythmia, hypotension, seizures, coma and delirium
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38
Q
A
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39
Q

What are 9 Substance Abuse Treatment Options?

A

Substance Abuse Treatment Options:

  1. Counselling and Motivational Interviewing
  2. Psychotherapy and Cognitive Behaviour Therapy
  3. Pharmacotherapy
  4. Self-Help AA/NA
  5. Residential/Therapeutic Communities
  6. Withdrawal Treatment
  7. Substitution Treatment
  8. Controlled Use
  9. Reduce Risks of Drug Use
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40
Q

What are the 10 general principles of treatment for substance abuse?

A

General Principles of Treatment for Substance Abuse:

  1. Addiction is a complex but treatable disease
  2. Match treatment to patient and their readiness to change (i.e. controlled use, withdrawal treatment or substitution treatment)
  3. Treatment should be patient’s choice following doctor’s recommendations
  4. No single treatment is right for everyone
  5. Effective treatment addresses all of the patient’s needs, not just their drug use
  6. Counselling and other behavioural therapies are the most commonly used forms of treatment
  7. Medications are often an important part of treatment, especially when combined with behavioural therapies
  8. Treatment plans must be reviewed often and modified to fit the patient’s changing needs
  9. Treatment should address other possible mental disorders
  10. Consider harm minimisation and reduction strategies if continual usage (i.e. needle exchange programs)
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41
Q

What are the pharmacological treatments available for ALCOHOL abuse?

  • Withdrawal = 2?
  • Relapse Prevention = 4?
  • Substitution/Maintenance?
A

Pharmacological Treatment of Substance Abuse - Alcohol

1) Withdrawal:

  1. Diazepam: Normalises the down regulation of GABA
  2. Thiamine: Replenish deficiency and prevent WKS

2) Relapse Prevention:

  1. Naltrexone (ReVia): Reversible antagonist at the μ opioid receptor. Blocks the effect of endogenous opioids and associated reward pathway. Reduces craving and pleasurable effects.
  2. Acamprosate (Campral): Chemical structure is similar to GABA. Restores activity levels of GABA and reduces glutamate in the brain. Blocks glutamate function.
  3. Combinations Naltrexone/Acamprosate
  4. Disulfiram (Antabuse): Not commonly prescribed. Deters alcohol use. Prevents usual alcohol metabolism. Irreversibly inhibits aldehyde dehydrogenase, blocking acetaldehyde breakdown. This causes unpleasant, potentially serious effects if alcohol is consumed e.g. flushing, sweating, nausea, vomiting, palpitations, headache, dyspnoea, chest pain, hypotension, cardiovascular collapse, seizures, arrhythmias.

3) Substitution/Maintenance: Nil

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42
Q

What are the pharmacological treatments available for OPIATES abuse?

  • Withdrawal = 3?
  • Relapse Prevention = 1?
  • Substitution/Maintenance = 2?
A

Pharmacological Treatment of Substance Abuse - Opiates

1) Withdrawal:

  1. Naloxone: Competitive opioid receptor antagonist. Reverses the effects of opioids/heroin.
  2. Clonidine: α2 adrenergic agonist to reduce autonomic symptoms of diarrhoea, nausea and sweating
  3. Buprenorphine: Partial opioid receptor agonist. Reduces withdrawal symptoms and craving in opioid dependence. Blocks effects of agonist (heroin) and displaces antagonists (naltrexone).

2) Relapse Prevention:

  1. Naltrexone: As described above.

3) Substitution/Maintenance:

  1. Methadone: Synthetic opioid agonist at the μ opioid receptor. Substitutes for heroin and is long-lasting. Gradual withdrawal.
  2. Buprenorphine: As described above.
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43
Q

What are the pharmacological treatments available for AMPHETAMINE abuse?

  • Withdrawal = 2?
  • Relapse Prevention = 1?
  • Substitution/Maintenance = 2?
A

Pharmacological Treatment of Substance Abuse - Amphetamine

1) Withdrawal:

  1. Benzodiazepines: Potentiate the inhibitory effects of GABA throughout the CNS, resulting in anxiolytic, sedative, hypnotic, muscle relaxant and antiepileptic effects.
  2. Tetracyclic Antidepressant (Mirtazapine): Postsynaptic blockade of serotonin 5HT2 and 5HT3 receptors and presynaptic blockade of central α2 adrenergic inhibitory autoreceptors (SNRI). Also a potent H1 antagonist which accounts for its sedative effects.

2) Relapse Prevention:

  1. Antidepressants: Inhibit the uptake of noradrenaline and serotonin
  2. Antipsychotics: Block D2 receptors and dopamine transmission in brain

3) Substitution/Maintenance: Nil

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44
Q

What are the pharmacological treatments available for TOBACCO addiction?

  • Withdrawal?
  • Relapse Prevention = 2?
  • Substitution/Maintenance = 1?
A

Pharmacological Treatment of Substance Abuse - Tobacco

1) Withdrawal: Nil

2) Relapse Prevention:

  1. Varenicline (Champix): Partial agonist at nicotinic acetylcholine receptors. It blocks nicotine binding to these receptors, preventing the pleasurable effects of smoking, while its partial agonist activity reduces symptoms of nicotine withdrawal.
  2. Bupropion (Zyban): Noradrenaline/dopamine reuptake inhibitor which reduces withdrawal symptoms and craving.

Substitution/Management:

  1. Nicotine Gum/Patches: Nicotine replacement reduces the severity of tobacco withdrawal symptoms and increases the likelihood of smoking cessation
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45
Q

Demonstrate the ability to communicate with families of seriously ill patients.

What is the SPIKES acronym for breaking bad news?

A

Delivering Bad News (SPIKES):

Setting: Mental and physical preparation for the discussion. Arrange for some privacy, involve significant others, sit down (don’t rush), make connection with patient and manage time constraints and interruptions. Also review the plan for telling the patient and how one will respond to patients’ emotional reactions or difficult questions.

Patient Perception: Elicit the patient’s perspective. Use open-ended questions to create a reasonably accurate picture of how the patient perceives the medical situation (what it is and whether it is serious or not).

Invitation: Ask patient what they would like to know. Invite patient to disclose level of information they would like to receive about diagnosis, prognosis, and details of illness. If patients do not want to know details, offer to answer any questions they may have in the future or to talk to a relative or friend.

Knowledge: Warn the patient that bad news is coming. Give information in small chunks and check patient’s understanding periodically. Start at patient’s level of comprehension, use simple language and avoiding excessive bluntness.

Explore Emotions and Empathise: Offer support and solidarity to the patient by making an empathic response. Observe patient for emotions, identify emotion, identify reason for emotion and let the patient know that you have connected the emotion after you have given the patient a brief period of time to express his or her feelings.

Summary and Strategy: Summarise what was discussed and set out a medical plan of action. Discuss prognosis and treatment options to patient if they are ready for the discussion.

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46
Q

What are some examples of Substance Abuse Assessments?

  • 2 for early recognition and screening?
  • 1 withdrawal scale?
A

Substance Abuse Assessment:

  1. Early Recognition and Screening:
    1. CAGE questionnaire
    2. AUDIT 10 Items Alcohol Use Disorder’s Identification Test
  2. Withdrawal Scales:
    1. CIWA-Ar → Clinical Institute Withdrawal Assessment - Alcohol revised
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47
Q

Describe the history and assessment of patients in relation to substance abuse.

  • What are 7 starting questions when taking a substance abuse history?
A

Substance Abuse History: Starting Questions

  1. “When did you start using?”
  2. “Have you stopped before and if so, for how long?”
  3. “What led you back to using”
  4. “Have you had any treatment and what was the outcome?”
  5. “What do you like about using drugs?”
  6. “In what way does drug use help you to cope?”
  7. “What concerns you about your drug use?”
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48
Q

Describe the history and assessment of patients in relation to substance abuse.

  • What information should be obtained when determining drug use history and dependence severity? (8)
  • What should you enquire about medical history, psychiatric hx, psychosocial hx and readiness to change?
A

Drug Use History and Dependence Severity: Drugs, dose, route, timing and type (accidental or recreational)

  1. Drug(s) used recently and ever
  2. Age of first use
  3. Age when first became dependent
  4. Pattern of use over time
  5. Recent use (method, quantity and frequency)
  6. Method(s) of use
  7. What happens when use is stopped? Withdrawal?
  8. Complications and problems from use
  • Medical History: Particularly, major co-morbidities, BBV, sepsis, trauma, overdose and pregnancy
  • Psychiatric History: Particularly, depression, anxiety, psychosis and personality disorder
  • Psychosocial History:
    • Relationships, family, social supports and activities
    • Education and employment
    • Legal issues
    • Living circumstances (stability and affordability)
    • Finances (legal sources of income and debts)
    • Involvement with other agencies (DCP)
    • Family history of substance use disorders
    • Social factors that may contribute to substance use or facilitate treatment
  • Readiness to Change: Ask about patient’s perception of their use and readiness to change
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49
Q

Describe the history and assessment of patients in relation to substance abuse.

  • What is involved in the Examination of someone with a Substance Abuse problem? (5)
A

Substance Abuse Examination:

  1. General Overview: Vital signs including heart rate, blood pressure, temperature, respiratory rate and oxygen saturation.
  2. Observation: Colour, injection sites, track marks, smell, bruising, skin changes, pressure sores, nutritional status, weight, teeth, stigmata of liver disease (i.e. jaundice, hepatomegaly), presence of intoxication or withdrawal.
  3. Neurological: Glasgow Coma Scale, pupils, tone, limb movements, reflexes, clonus and fasciculations
  4. Mental State: Appearance, behaviour, mood cognition and affect
  5. Other: Signs of aspiration, secretions and signs of injury or trauma
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50
Q

Which investigations should always be performed (3)/considered (7) for those with a substance abuse problem?

A

Substance Abuse Investigations: ECG, BSL and Paracetamol Screen ALWAYS!!

  1. Blood Glucose Levels
  2. Electrocardiogram
  3. Blood Gases
  4. ß-HCG (in women of childbearing age)
  5. Bloods: Paracetamol (in deliberate self-poisoning), drug screen, LFTs and hepatitis and HIV serology
  6. Urine and Saliva: Drug testing
  7. Breath Alcohol Screen
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51
Q

Describe the clinical approach to assessment of the unconscious patient including the use of Guedel airway.

What is the Glasgow Coma Scale?

A
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52
Q

Describe the clinical approach to assessment of the unconscious patient including the use of Guedel airway.

What is the AVPU scale?

A
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53
Q

Describe the steps in the Assessment of the Unconscious Patient (DRSABCDES)

  • DANGER?
  • RESPONSE?
  • SEND HELP?
  • AIRWAYS? (3)
    • Basic airway management? (5)
A

Assessment of the Unconscious Patient

  • DANGER → In any emergency situation, the safety of you and the other staff members comes first before the safety of the patient.
  • RESPONSE → Glasgow Coma Scale & AVPU Scale
  • SEND FOR HELP → Call for extra staff or a medical emergency team (MET)
  • AIRWAYS
    1. Is C‐spine immobilisation required? Apply collar and log roll patient if necessary.
    2. Is the airway patent? Inspect mouth, suction and apply airway manoeuvres if necessary.
    3. Basic Airway Management:“GCS 8 Intubate”
      1. Cervical spine control
      2. Clearance: Mouth examination and clearance of airways (only if not breathing due to risk of bite injury). Consider Yankauer suction catheter.
      3. Airway Manoeuvres: Chin lift +/- head tilt (not in spinal injury!) and jaw thrust
      4. Adjunctive Airway Devices: Nasopharyngeal airway (used in spontaneous breathing patients to help with upper airway obstruction) or Guedel airway (only for unconscious patients). Advanced options include laryngeal mask airway (LMA), endotracheal intubation or surgical airway (cricothyroidotomy).
      5. Oxygen Therapy Devices: Nasal prongs, simple Hudson mask, venturi mask, non- rebreather face mask or bag-valve mask (the lifesaver!)
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54
Q

Describe the steps in the Assessment of the Unconscious Patient (DRSABCDES)

  • CIRCULATION? (7)
  • DEFIBRILLATION?
  • DON’T EVER FORGET GLUCOSE/ DISABILITY? (5)
A

Assessment of the Unconscious Patient

  • CIRCULATION
    1. Check heart rate and rhythm, blood pressure and capillary refill (< 2 seconds)
    2. Auscultate precordium
    3. Perform an ECG as soon as possible
    4. Place IV access in order to take blood and give fluids/medications
    5. Take bloods including a venous/arterial blood gas
      1. VBG: pH, O2, CO2, Na+, K+, Hb and glucose
      2. Paracetamol screen
      3. U&Es including Ca2+, FBC, LFT, B-HCG, blood alcohol and toxicity/drug screen
    6. Give fluids and medications if required
    7. Look for a medicalert bracelet whilst assessing radial pulse
  • DEFIBRILLATION → Has the patient got a shockable rhythm? Defibrillate if needed.
  • DON’T EVER FORGET GLUCOSE/ DISABILITY
    1. Check glucose and treat if low
    2. Assess pupils for symmetry and size and gaze abnormalities
    3. Neurological Exam: Look for obvious asymmetrical neurological weakness, tone, abnormal posturing and reflexes (lateralising signs). It is important to assess these prior to intubation or sedation which will alter neurological findings.
    4. Assess for neck stiffness (only in patients where there is no concern of C ‐spine trauma)
    5. Battle Signs: Assess tympanic membranes for blood, perforation and otorrhoea (discharge), nose and ears for discharge (CSF fluid), behind the ears for bleeding, eyes for racoon eyes (hemorrhage), scalp for lacerations and skull for fractures.
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55
Q

Describe the steps in the Assessment of the Unconscious Patient (DRSABCDES)

  • EXPOSURE? (3)
  • EXTRAS? (6)
  • SECONDARY SURVEY? (5)
A

Assessment of the Unconscious Patient

  • EXPOSURE
    1. Re‐examine the patient from top to toe. This includes rectal examination for anal tone and perianal sensation (spinal trauma).
    2. ALWAYS remember to look at the back of the patient, this may mean log rolling the patient (if the cervical spine needs to remain immobilised).
    3. In trauma patients it is important to palpate each bone in the vertebral column to elicit localised tenderness that may suggest spinal injury.
  • EXTRAS
    1. Temperature
    2. Tetanus status (particularly if open dirty wounds)
    3. Confirm allergies if possible before administering medications
    4. Check pregnancy status before any irradiating imaging is performed
    5. Consider catheterisation (urine can be used for B-HCG and toxicity screen) if unconscious or low GCS
    6. Consider CXR to assess lungs and CT head and CT c-spine to assess head/neck trauma
  • SECONDARY SURVEY → Cardiovascular, respiratory, abdominal and renal exams
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56
Q

What is the AIRWAY MANAGEMENT PROTOCOL?

A
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57
Q

Discuss reasons why patients or families may demonstrate aggressive or disruptive behaviour in medical settings

5 Reasons for Aggressive/Disruptive Behaviour?

A

Reasons for Aggressive/Disruptive Behaviour:

  1. Person perceives that he or she is being treated unfairly or without respect
  2. Aggression may give people a feeling of power in order to compensate for feelings of inadequacy and anxiety
  3. Some neurological disorders (psychosis, mental disorders and substance-abuse disorders) have been associated with changes in personality that may also result in violence
  4. May be a result of the effect of some therapeutic medications for example corticosteroids
  5. Aggression or violence can occur when people have inappropriate skills for dealing with feelings of frustration, fear and anxiety, or as an expression of these feelings by people who are unwell (may be present in persons experiencing acute or chronic pain, drug or alcohol withdrawal, stroke, head injury or Alzheimer’s disease)

NB: Always remember confidentiality of the patient. May not be appropriate to disclose information to family members.

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58
Q

What is the pathogenesis and clinical findings of acetaminophen (paracetamol) overdose?

A
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59
Q

BENZODIAZEPINES

  • Mechanism of Action?
  • 3 Effects?
  • Side effects?
  • OD Rx?
A

BENZODIAZEPINES

  • MOA: potentiate GABA (inhibitory neurotransmitter in CNS). GABA binds to GABA A receptor which then opens its chloride channel, allowing chloride influx into neuron → cell hyperpolarises → inhibits cellular excitation.
    • Benzos are positive allosteric modulators: increase effect of GABA by increasing frequency of Cl channel opening → potentiates GABA effects. Binds to benzodiazepine site on GABA A receptor complex
  • Effects:
    1. Sedation/ anxiolytic
    2. Anticonvulsant
    3. Muscle relaxant
  • SE: drowsiness, confusion, dizziness, hallucinations, respiratory depression, hypotension, slurred speech, amnesia, nystagmus, ataxia, coma, paradoxical agitation, aspiration pneumonia, more dangerous in combination
  • Rx OD:- largely supportive, ABC, possible airway support
    Antidote:-there is an antidote Flumazenil but it is not widely used, has risk of precipitating seizures especially in chronic user
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60
Q

OPIATES

  • Opioid toxidrome symptoms?
  • MOA?
  • Opioid receptors: μ1, μ2, δ, κ
  • Heroin?
  • Naloxone?
  • SE?
  • Rx OD?
  • Antidote?
A

OPIATES: Common overdose either intentional or unintentional/ iatrogenic

  • Recognisable opioid toxidrome: pinpoint pupils, respiratory depression and sedation
  • MOA: bind to opioid receptors on neuronal cell walls that also bind endogenous enkephalins and endorphins.
  • Opioid receptors:
    • μ1 → supraspinal analgesia, bradycardia, sedation
    • μ2 → respiratory depression, euphoria, physical dependence
    • δ → spinal analgesia, respiratory depression,
    • κ → spinal analgesia, respiratory depression, sedation
  • Heroin = converted to morphine, acts on μ receptors in CNS also dopamine receptors → nausea/ vomiting, histamine release → pruritis
  • Naloxone = pure opioid μ, κ, δ receptor antagonist
    Effects/use: analgesic, adjunct to anaesthesia, cough suppressant
  • SE: pinpoint pupils, respiratory depression, CNS depression, constipation, hypotension, confusion/ delirium
  • Rx OD: supportive care ABC/ respiratory support/ ventilation, reverse with antidote
  • Antidote: naloxone → note naloxone has shorter half-life than the opioid so may return to respiratory depression when wears off (dangerous in heroin OD if pt discharges self). May need small aliquots titrated to response or infusion.
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61
Q

SSRIs

  • MOA?
  • Effects/Uses? (3)
  • SE?
  • OD Rx?
A

SSRIs: Common overdose, less toxic than many (relatively safe in OD, not usually cardiotoxic)

  • MOA: limit presynaptic reuptake serotonin, which increases its availability to bind to postsynaptic cleft. Also weak affinity for noradrenaline and dopamine transporters
  • Effects/ use:
    1. Antidepressant
    2. Anxiety
    3. Chronic pain
  • SEs: nausea, dry mouth, diarrhoea/ constipation, decreased appetite, decreased libido, retrograde ejaculation, anorgasmia, ED, increased risk bone #, akasthisia, tremor, sedation/ insomnia, dizziness, sweating, photosensitivity, suicidal ideation in early stages Rx, serotonin syndrome esp in combination with other drugs, discontinuation syndrome
  • Rx OD: largely supportive
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62
Q

PARACETAMOL

  • MOA?
  • Effects/Uses? (2)
  • SE?
  • OD Rx?
  • Metabolism?
  • Antidote?
A

PARACETAMOL: Common overdose (often in parasuicide context) potentially fatal

  • MOA: not fully understood, analgesic effect may include inhibition of central prostaglandin synthesis and modulation of inhibitory descending serotonergic pathways. The antipyretic effect is probably due to reduced production of prostaglandins in the hypothalamus.
  • Effects/ use:
    1. Analgesia
    2. Antipyretic
  • SE: hepatotoxic (can cause acute hepatic failure in OD), hypersensitivity reactions, thrombocytopaenia, neutropaenia
  • Rx OD: check 4/24 paracetamol levels and plot on nomogram, if over the level treat with N-acetyl-cysteine.
    • If given <8/24 after ingestion->almost zero mortality from OD.
    • If present >8/24 start NAC immediately while awaiting levels.
  • Paracetamol usually metabolised by phase II metabolism by conjugation with sulfate and glucuronide. Small portion is metabolised by CP450 into toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI) which is usually conjugated by glutathione into less toxic cysteine and mercapturic acid.
  • In OD the phase II metabolism is overwhelmed and more is diverted into the CP450 pathway, when the glutathione is depleted the toxic NAPQI metabolite builds up.

NAC replenishes glutathione hence deactivates and safely excretes NAPQI.

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63
Q

ANTIPSYCHOTICS

  • Example?
  • MOA?
  • Effects/Uses? (2)
  • SE?
  • Metabolic effects?
  • In OD?
  • Rx OD?
A

ANTIPSYCHOTICS - e.g. Quetiapine

  • MOA: D2 antagonist
  • Effects/ use:
    1. Schizophrenia
    2. Bipolar
    3. Psychosis
  • SE: tachycardia, hypotension, sedation, abn LFTs, hypothyroidism, anxiety, dry mouth, hyperprolactinaemia, urinary retention, sexual dysfunction, NMS Extrapyramidal SEs: acute dystonic reaction, tardive dyskinesia, akasthesia, Parkinsonism
  • Metabolic effects: hyperlipidaemia, wt gain, raised BGL
  • In OD: arrhythmias, hypotension, seizures, coma, delirium
  • Rx OD: supportive Rx, especially respiratory support: if large dose >3g or 10mg/kg likely to need intubation. Call tox
    Note Rx of acute dystonic reaction is anticholinergic (benztropine).
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64
Q

AMPHETAMINES

  • Recognisable amphetamine toxidrome symptoms?
  • 3 examples?
A

AMPHETAMINES: Common recreational overdose/ intoxication

  • Recognisable amphetamine toxidrome: aggression/agitation, hypertension, tachycardia, dilated pupils
  • 1) Methamphetamine (meth, base, crystal meth, ice) → stimulates release & stops reuptake of monoamines (dopamines & NA), serotonin.
    • First synthesised 1919-used in WWII
    • crystal meth/ ice=more potent distilled form, rock/crystal-like (smoke/ inject) -speed-white powder form often snorted
    • base-oily thick brown-yellow substance
  • 2) Amphetamine sulphate/ HCL-(speed) also prescription (e.g. dexamphetamine): initially used to Rx asthma, now used to Rx narcolepsy or ADHD
  • 3) MDMA (ecstasy)-competitively binds to monoamine uptake receptors- → stimulates release, increases dopamine, 5HT, NA. Greater effect on serotonin than meth (primary effect=indirect serotonin agonist. Has hallucinogenic as well as stimulant effects
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65
Q

AMPHETAMINES

  • MOA?
    • α1?
    • β1?
    • β2?
A

MOA: Sympathetic effects on:

  • α1 → vascular smooth muscle, iris
  • β1 → myocardium
  • β2 → skeletal muscles, vascular smooth muscle
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66
Q

AMPHETAMINES

  • Side effects?
    • CVS?
    • Neuro?
    • Psych?
    • Resp?
    • GIT?
    • GU?
  • OD Rx?
A

AMPHETAMINES - Side Effects:

  1. Hyperthermia
  2. Thirst, often volume deplete but may have water intoxication,
  3. SIADH (esp MDMA)
  4. Rhabdomyolysis
  5. Metabolic acidosis, AKI, DIC, microinfarcts, serotonin syndrome, skin infections
  6. CVS → hypertension, tachycardia, CCF, AMI,
  7. Neuro → cerebral haemorrhage/ SAH, cerebral oedema, seizures, intellectual impairment
  8. Psych → rapid speech pacing, trismus, hallucinations/ delusions, psychosis, paranoia, aggression, pupil dilation, jaw clenching, teeth grinding, sleep disturbance, memory impairment, depression/ anxiety long term
  9. Resp → ARDS (fm hyperthermia)
  10. GIT → hepatocellular necrosis (2 to hyperthermia)->hepatic failure, mesenteric ischaemia, wt loss, dental decay
  11. GU → fetal anomalies, miscarriages

OD Rx: benzodiazepine/ sedation (more extreme possibly propofol infusion/ intubation), dopamine antagonists e.g. droperidol, ketamine

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67
Q

CANNABINOIDS

  • Examples?
  • MOA?
  • Uses? (4)
  • SE?
    • CVS?
A

CANNABINOIDS - THC (tetrahydrocannabinol) & CBD (cannabidiol)

  • MOA: stimulating cannabinoid receptor type 1 (CB1) & type 2 (CB2) within the endocannabinoid system
  • Uses:
    1. Chronic pain
    2. Cancer
    3. MS
    4. Epilepsy
  • SE: dry mouth, conjunctivitis, tachycardia, hypotension, bradypnoea, impairment of short-term memory, judgment and sensation, altered reaction time & movement, increased appetite, panic, paranoia, cannabinoid hyperemesis syndrome, psychosis, addiction, altered brain development, cognitive impairment in adolescents, loss of volition, myoclonus
    • CVS: Increased risk MI, stroke, thromboembolic events, postural hypotension Resp: chronic bronchitis, ARDS, lung cancer, bronchospasm
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68
Q

SEROTONIN SYNDROME

  • Features? (10)
  • Which Drugs?
  • Rx?
A

SEROTONIN SYNDROME (another toxidrome)

  • Features:
    1. Hyperthermia
    2. Hypertension
    3. Tachycardia
    4. Agitation
    5. Hyperreflexia
    6. Rigidity/ hypertonia
    7. Clonus
    8. Diaphoresis
    9. Tremor
    10. Salivation
  • Drugs: especially combinations of two or more serotonergic drugs e.g. SSRI, SNRI, TCA, tramadol, MAOi, amphetamines.
  • Rx: benzodiazepines, cooling, cyproheptadine (serotonin antagonist)-call tox!
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69
Q
A
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70
Q

MOA of Cocaine?

A

COCAINE

  • MOA: blocks catecholamine/ serotonin reuptake, Na channel blockade, sympathomimetic, local anaesthetic, vasospasm, cardiotoxicity
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71
Q
  • What is SYNTHETIC CATHINONES?
  • What is LSD?
  • What is N-BOMe?
  • What is GBH?
  • What is Flakka?
A
  • SYNTHETIC CATHINONES (bath salts)
    • “New psychoactive substances”, stimulants, similar to amphetamines, found in plants called khat e.g. mephedrone, methylene
  • LSD
    • Lysergic acid diethylamide (LSD, acid)
    • Possibly stimulates glutamate release in the cortex->excitation, mainly serotonergic effects (stimulates 5HT1A & 2A receptors), dopaminergic (D2)
    • Hallucinogenic effects
  • N-BOMe
    • “N-Bomb” or “Smiles”
    • Synthetic hallucinogen similar to LSD
  • GBH (Gamma-hydroxybutyrate)
    • “Grievous Bodily Harm”
    • Sedative and anaesthetic properties
    • Can → agitation, hallucinations, seizures, coma
  • FLAKKA (alpha-pyrrolidinopentiophenone or alpha-PVP)
    • Newer generation bath salts
    • Euphoria, bizarre behaviour, paranoia, agitation, delusions
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72
Q

MEDICAL MANAGEMENT of HEROIN ADDICTION? (3)

Symptoms of Opioid Withdrawal?

A

MEDICAL MANAGEMENT of HEROIN ADDICTION

  1. Methadone → oral opiate, harm minimisation, long term maintenance or can gradually reduce dose, issues: ‘authorised prescriber’, daily collect from chemist, present to ED’s ‘medication stolen’ out of hours, can still use heroin
  2. Buprenorphine (subutuex) or Buprenorphine with naloxone (suboxone) → partial mu-opioid agonist (high affinity, low activity) & weak kappa antagonist
  3. Naltrexone – abstinence maintenance, opioid antagonist
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73
Q

MEDICAL MANAGEMENT of ALCOHOL ADDICTION? (5)

Clinical findings and complications of alcohol withdrawal?

A

MEDICAL MANAGEMENT of ALCOHOL ADDICTION

  1. Detox: management of withdrawal - e.g.benzos
  2. Naltrexone → opioid antagonist
  3. Acamprosate → structure alanalogue of GABA
  4. Disulfiram → less commonly used now, not first line. Inhibits aldehyde dehydrogenase, prevents the metabolism of alcohol’s primary metabolite, acetaldehyde → deterrent effect (feel sick when drink ETOH)
  5. Don’t forget thiamine
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74
Q

Paeds toxicology - What are 8 examples of ‘One Pill Kills’ drugs?

A
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75
Q

What is the primary brain structure responsible for maintaining consciousness?

3 Functions?

A

Primary brain structure responsible for maintaining consciousness: Reticular activating system

Functions:

  1. Maintain cerebral cortical alertness:
  2. Filters out repetitive stimuli (awareness) – Thalamus w RAS projections are responsible for awareness to the environment
  3. Regulates skeletal & visceral muscle activity
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76
Q

What is the Physiology of alertness?

Which neurotransmitters increase alertness? (3)

Which NT decreases alertness? (1)

A

Physiology of alertness: Maintains arousal of the whole brain by having ascending sensory pathways synapse with the RAS neurons, keeping them active and enhancing their arousing effect on the cerebrum

  • Increases alertness
    1. Serotonin
    2. Histamine
    3. Noradrenaline
  • Reduces alertness
    1. Acetylcholine
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77
Q

What is the RAS inhibited by?

What is the RAS depressed by?

A

RAS is inhibited by: sleep centres in the hypothalamus

RAS is depressed by: alcohol, tranquilisers, etc.

  • Depressed RAS system (semi-comatose) → inability to respond to sensory information as well (visual, auditory, proprioception, painful stimuli)
  • Depressed RAS system → unable to regulate skeletal & visceral muscle activity
  • Severely depressed RAS (comatose) → unable to respond to stimuli such as pain & irritation which could normally stimulate reflexes → inability to protect their airway consciousness?
78
Q
  • What is conciousness?
  • What is the difference between sleep and altered level of consciousness?
    • Sleep?
    • Altered LOC?
    • Coma?
    • Brain dead?
A

Consciousness: Ability to maintain awareness of self, access to memories, ability to manipulate abstract ideas and focus your attention

Difference between sleep and altered level of consciousness:

  • Sleep: reduced state of interaction with the environment. Still able to respond to auditory, light, painful stimuli Altered
  • LOC: Alteration between a normal alertness and comatose state (GCS 8-14)
  • Coma
    • Unrousable, unresponsive (no response to pain)
    • Brainstem reflexes intact (some CN intact, vasomotor centre intact)
  • Brain death
    • Irreversible loss of brain function
    • No response to pain
    • No brainstem reflexes intact (Very specific diagnostic criteria to pronounce someone braindead) o Must exclude: hypothermia, long acting drugs, endocrine dysfunction, etc.
79
Q

LO: Discuss the consequences (physical, psychological and social) of illicit drug use for: (a) the individual; (b) his/her family; (c) the community.

A
  • Individual level:
    • Physical health: Nausea, aches and pains, sleep disturbance, weight gain/loss, infection, accidents, illness or chronic disease
    • Mental health: Depression, anxiety, paranoia, psychosis
    • Personal relationships: Family problems, arguments, relationship breakdowns, loss of friends, social isolation, loneliness
    • Work or financial impact: Job loss, trouble at work or study, truancy and/or absenteeism, debt, unemployment
      • Financial strain to support habit and potentially stealing from family and friends
    • Social impact: Loss of interest or time to do other things for pleasure, reduced participation in social activities, anti-social behaviour (e.g. domestic violence), criminal conduct
  • Family level:
    • Stress for family and friends
    • Violence (physical and psychological) towards medical staff and the public (social costs)
  • Community level:
    • Lost productivity
    • Cost to healthcare system (if hospitalisation/ambulance service required)
    • Cost of policing, child/spouse protection
80
Q

What is the definition of Normal Human Behaviour?

What is the definition of Abnormal Human Behaviour? 3 Causes?

A

Normal Behaviour: Behaviour that is aligned to what is normal and expected within a given culture (depends on social group, generation and culture).

Abnormal Human Behaviour: Behaviour that deviates from what is normal (occurs frequently) and expected within a given culture (abnormality is a continuum rather than a category). It is culturally bound and developmentally influenced.

  1. Psychological Dysfunction: A set of symptoms that leads to an interruption in occupational and social roles
  2. Personal Distress: A set of symptoms that causes the person (or those close to them) to feel distressed
  3. Atypical Response: Behaviours and psychological characteristics that are not common in a given cultural context
81
Q

What are 6 issues with Abnormal Thoughts and Beliefs?

A

Abnormal Beliefs and Thoughts:

  1. Are difficult for others to understand
  2. Become distressing for the individual
  3. Give rise to avoidance, attack or other responses that are not expected or appropriate
  4. May be fixed and obsessional
  5. Impede on ability to meet cultural expectations (work in a job, manage hygiene, pay rent on time etc.)
  6. Often lead to alienation
82
Q

What is the Cultural Disorder ‘Amok’? Which country?

A

Cultural Context & Abnormal Human Behaviour

  • Name of Disorder - Amok
  • Culture - Malaysia
  • Description - Sudden and violent outbursts often leading to homicidal behaviour. Triggered in usually withdrawn men.
83
Q

What is ‘Zar’? Which culture?

A

Cultural Context & Abnormal Human Behaviour

  • Name of Disorder - Zar
  • Culture - North Africa
  • Description - A person believes he/she is possessed and may engage in random emotional expressions. May withdraw socially and so apathy to others.
84
Q

What is Kitsunetsuki? Culture?

A

Cultural Context & Abnormal Human Behaviour

  • Name of Disorder - Kitsunetsuki
  • Culture - Japan
  • Description - A disorder in which the victim believes he/she is a fox and changes their facial expressions accordingly.
85
Q

How can Adaptive Behaviours develop to Disordered behavior?

A
86
Q

What is Psychosis Syndrome?

A

Psychosis Syndrome:

  • A syndrome, not an illness, that warrants a diagnosis
  • A problem with brain function characterised by…
    • A loss of reality testing and impairment of mental functioning
    • Where patients incorrectly evaluate the accuracy of their perceptions and thoughts, and make incorrect inferences about external reality
87
Q

What are the clinical features of Psychosis?

Positive Symptoms? Negative Symptoms?

A

Clinical Features of Psychosis: Delusions, Hallucination, Disorganised behaviour, speech and thought and altered mood and affect (not core features)

  • Positive Symptoms:
    1. Delusions
    2. Hallucinations
    3. Passivity
  • Negative Symptoms:
    1. Affective flattening
    2. Alogia
    3. Avolition
    4. Anhedonia
    5. DEFICIT SYNDROME
88
Q

What is a Delusion? What is is a Disorder of? 7 Examples?

A

Delusions (Disorder of Thought Content): Fixed, false belief based on incorrect inference about external reality, firmly held despite evidence to the contrary, out of keeping with patient’s cultural background

Examples:

  1. Bizarre vs systematised delusions
  2. Mood congruent vs mood incongruent delusions
  3. Nihilistic, delusion of poverty
  4. Somatic
  5. Persecution, grandeur, reference
  6. Control (thought broadcasting, insertion, withdrawal)
  7. Jealousy, infidelity and erotomania (another person is in love with them)
89
Q

What are Hallucinations? Examples?

A
  • *Hallucinations (Perceptual Disturbances):** Sensory perception not associated with real external stimuli, there may or may not be delusional interpretation of the experience
  • *Examples:**
  1. Auditory, visual, olfactory, somatic, tactile or gustatory perceptions
  2. Lilliputian (very small person/being)
  3. Synesthesia (i.e. hearing colours), trailing
  4. Hypnagogic and hypnopompic (sleep/waking up hallucinations) → not a pathology
90
Q

What are Thought Disorders? What are they a Disorder of? Examples?

A
  • *Thought Disorders (Disorder of Thought Form):** When the flow of ideas, symbols and associations initiated by a problem/task are not goal-directed
  • *Examples:**
  1. Neologisms, word salad
  2. Circumstantiality, tangentially
  3. Derailment, loosening of associations
  4. Perseveration, verbigeration, clang association
  5. Flight of ideas
  6. Blocking
91
Q

What are the mood and affect of Psychosis?

A

Mood and Affect: Inappropriate affect

Examples: Blunting, flat, isolation/dissociation and incongruent affect

92
Q

Clinical Features of Psychosis - Appearance and Behaviour?

A
  • *Inappropriate appearance and behaviour**
  • *Examples:** Bizarre dress, catatonia, poor impulse control, anger, agitation and stereotypes
93
Q

Describe the MSE of Psychosis?

A
94
Q

Discuss the Differential Diagnosis of Psychosis - Medical?

  • 2 Common causes?
  • Brain insult causes?
  • Other?
  • What are 4 signs/symptoms that favour a medical cause of pyschosis?
A

Differential Diagnoses of Psychosis - Medical

  • Common: Dementia or Delirium
  • Brain Insult: Neoplasms, CVD (esp. late- onset psychosis), Trauma (esp. frontal or limbic), MS (esp. many periventricular lesions), Huntington’s Disease or Epilepsy (esp. TLE)
  • Other: Cushing’s Disease, Thyroid Disease, B12, porphyria, CO, CJD, HSE, Neurosyphilis, HIV, NPH, SLE or Wilsons Disease
  • Favours Medical Cause:
    1. Sudden
    2. Old age
    3. First episode
    4. Current illness or injury or neurological symptoms
  • NB1: Always consider non-psychiatric medical conditions especially in patients with previous diagnosis of schizophrenia (may overlook something more sinister such as a SAH)
  • NB2: Comorbidity is the rule rather than the exception
95
Q

Discuss the Differential Diagnosis of Psychosis - Medications and Substances?

  • 5 Drug Highs?
  • 3 Drug Withdrawal states?
  • 4 clinical signs/symptoms that favours drug-induced psychosis?
  • What favours SCZ?
A

Differential Diagnoses of Psychosis - Medications and Substances

  • Drugs:
    1. Amphetamines
    2. Cocaine
    3. Hallucinogens
    4. PSP
    5. Alcohol
  • Withdrawal States:
    1. BZD
    2. Barbiturates
    3. Alcohol
  • Favours Drug-Induced Psychosis:
    1. Visual hallucinations
    2. Hyperactivity
    3. Hypersexuality
    4. Confusion and incoherence
  • Favours SCZ: Presence of formal thought disorder and blunted or flattened affect
96
Q

Discuss the Differential Diagnosis of Psychosis - Mood Disorders?

  • 2 Mood Disorders?
  • What favours mood disorders?
  • What favours SCZ?
A

Differential Diagnoses of Psychosis - Mood Disorders

Bipolar: Bipolar affective disorder (mania with psychosis)

Depression: Major depressive disorder episode with psychosis

Favours Mood Disorder: Mood-congruent delusions

Favours SCZ: The affective and mood symptoms should be brief relative to the duration of active and residual periods

97
Q

Discuss the Differential Diagnosis of Psychosis - Anxiety?

  • Which anxiety disorder?
  • What clinical features favour anxiety disorder?
A

Differential Diagnoses of Psychosis - Anxiety

Anxiety: PTSD with traumatic hallucinosis or dissociative disorders

Favours Anxiety Disorder: Traumatic stressors and other anxiety symptoms to suggest anxiety disorder, derealisation and depersonalisation

98
Q

Discuss the Differential Diagnosis of Psychosis - Personality?

  • 5 Personality Disorders that can be a differential for psychosis?
  • What clinical features favour personality disorder?
A

Differential Diagnoses of Psychosis - Personality

Personality Disorder (PDs):

  1. Schizoid
  2. Schizotypal
  3. Paranoid
  4. Borderline personality disorder
  5. Obsessive compulsive personality disorder

Favours Personality Disorder: Longstanding pervasive and maladaptive personality traits

NB: PDs may often mask an underlying SCZ process and may often be comorbid with SCZ!

99
Q

Discuss the Differential Diagnosis of Psychosis - Malingering and Factitious Culture-Bound Syndromes?

A

Differential Diagnoses of Psychosis - Malingering and Factitious Culture-Bound Syndromes

  1. Koro in South East Asia
  2. Religious experiences
  3. Meditative states or belief in UFO’s etc.
100
Q

Discuss the Work up of a psychotic patient?

A

Work up of a Psychotic Patient

  • Good clinical history: include a complete Fam Hx, an in-depth Hx of medical, neurological and psychiatric disoders
  • Physical exam (Neuro etc)
  • Tests & Investigations
    1. FBC, UEC, LFT, TFT, B12, folate, ESR, CRP
    2. Consider: CMP, Vit D, Iron studies, syphiils, hepatitis, HIV (if indicated)
    3. Urinalysis, UDS
    4. If indicated: CT or MRI, EEG, LP
101
Q

What is the diagnosis in order of frequency of psychosis in the elderly?

A
102
Q

What are the 6 Primary Psychotic Disorders?

A

Primary Psychotic Disorders

  1. Brief Psychotic Episode
  2. Schizophreniform
  3. Schizophrenia
  4. Schizoaffective
  5. Delusional Disorder
  6. Folie A Deux
103
Q

What is a Brief Psychotic Episode? (4 points)

A

Primary Psychotic Disorders - Brief Psychotic Episode

  1. Presence of psychotic symptoms (delusions, hallucinations, disorganised speech and disorganised or catatonic behaviour), not better explained by other disorder
  2. Duration of disturbance 1 day to 1 month
  3. Not better explained by other illness
  4. Eventual full return to premorbid functioning
104
Q

What is Schizophreniform? 3 Features? Features of Good Prognosis?

A

Primary Psychotic Disorders - Schizophreniform

  1. Presence of psychotic symptoms for at least 1 month
  2. Episode (including prodrome, active and residual) lasts at least 1 month but less than 6 months
  3. Not better explained by other illness

Good prognosis features include absence of blunted/flat affect, good premorbid features, confusion on perplexity at the height of episode and onset of psychotic symptoms within 4 weeks

105
Q

What is Schizophrenia?

  • 4 Clinical features?
A

Primary Psychotic Disorders:** **Schizophrenia

  1. Presence of psychotic symptoms for at least 1 month
  2. Functional impairment
  3. Continuous disturbance for 6 months (may include prodrome and residual symptoms)
  4. Not better explained by other illness

Pure types are uncommon, mixtures of symptoms are more common.
Other subtypes include catatonic (rare), disorganised, paranoid or undifferentiated and residual type.

106
Q

What is Schizoaffective Disorder? 4 Clinical Features? 2 Subtypes?

A

Primary Psychotic Disorders:** **Schizoaffective

  1. An uninterrupted period of illness with a major depression episode, manic episode or mixed episode concurrent with symptoms of schizophrenia
  2. Presence of delusions or hallucinations for two weeks in the absence of prominent mood symptoms, during the same period
  3. Symptoms for a mood episode are present for a substantial proportion of the total duration, during the active and residual phase of the illness
  4. Not better explained by other illness

Subtypes include: bipolar type or depressive type.

107
Q

What is Delusional Disorder? 5 Clinical Features? 6 Subtypes?

A

Primary Psychotic Disorders: Delusional Disorder

  1. Presence of non-bizarre delusions (involving situations that occur in real life i.e. being followed, loved and poisoned) for at least one month duration
  2. Hallucinations may be present if they are related to the delusional theme
  3. Functioning or behavior not markedly impaired
  4. If mood episodes have occurred, they are brief
  5. Not better explained by other illness

Subtypes include: erotomanic, grandiose, jealous, persecutory, somatic and mixed types

108
Q

What is Folie A Deux? 3 Clinical features?

A

Primary Psychotic Disorders:** **Folie A Deux

  1. Delusion develops in an individual in the context of a close relationship with another person who already has an established delusion
  2. Delusion is similar in context
  3. Not better explained by other illness
109
Q

What 8 psychiatric comorbidities are most common in psychotic disorders?

A

Comorbidties are common among schizophrenia patients

  • PSYCHIATRIC include (Buckley, 2009):
  1. Substance abuse (47%)
  2. Anxiety (panic 15%, 29% PTSD, 23% OCD) disorders
  3. Depressive disorders (50%)
  4. •MEDICAL include (Lambert, 2003):
  5. Diabetes, Hyperlipidaemia, HT, arrhythmias, obesity
  6. Neoplasms
  7. HIV, hep C
  8. OP, hyperprolactinaemia
110
Q

Prevalence and Risk Factors of Schizophrenia?

  • What is the point prevalence of SCZ?
  • Lifetime prevalence?
  • Incidence?
  • Onset?
  • Cost?
  • Risk Factors?
  • Epidemiology?
A

Prevalence and Risk Factors of Schizophrenia:

No population is free of schizophrenia!

  • Point Prevalence: 5 per 1000 Australian have schizophrenia
  • Lifetime Prevalence: 0.5% to 1.5% world-wide (WHO) have schizophrenia
  • Incidence: 15.2 per 100 000
  • Onset: Males is mid 20s and females mid-late 20s (peak also in 40s). Males are more predisposed than females (3:2 ratio).
  • Cost: An estimated $1.45 billion per annum (Australian Government), while societal costs are at least $1.44 billion for schizophrenia alone
  • Risk Factors: Family history, CNS damage, bereavement and co-morbidities
111
Q

What are the most frequent symptoms of Schizophrenia?

A

Clinical Features of Schizophrenia:

Positive Symptoms: Delusions, hallucinations and thought disorders

Negative Symptoms: Affective flattening, alogia (poverty of speech), avolition (decreased motivation to complete purposeful tasks), anhedonia (loss of pleasure). Deficit Syndrome!

Cognitive Behavioural Disorganisation: Thought and speech disorder, disorganised behaviour, catatonic behaviour and cognitive impairment (attention, verbal memory, working memory and executive dysfunction)

112
Q

What is the Clinical Course of Schizophrenia? (4 Stages)

A

Course of Schizophrenia:

  1. Premorbid (Fetal-Childhood): Mild motor cognitive and social impairments
  2. Prodromal (Puberty-Adolescence): Unusual psychotic-like behaviours and negative symptoms
  3. Onset/Deterioration (Early Adulthood): Positive, negative, cognitive and mood symptoms
    1. Adult Onset: Most likely to exhibit positive and affective symptoms. Genetic predisposition drives manifestation of symptoms anywhere from BPAD, SCZA and SCZ.
    2. Late Onset (>45): Females more predisposed than males. Good premorbid functioning. Predominance of paranoid symptoms.
  4. Chronic/Residual (Adulthood-Senescence): Positive, negative and cognitive symptoms
113
Q

What is the Prognosis of Schizophrenia?

  • Prognostic features - 8 poor & 8 good outcome?
A

Prognosis of Schizophrenia:

  • 30% of individuals have complete or partial remission between episodes
  • 25% of individuals have negative symptoms between episodes
  • 45% of individuals experience functional decline with frequent or continuous psychotic symptoms
  • Positive psychotic symptoms tend to go away after first episode of psychosis (87%) with median time to remission 9 weeks (does not equate to functional recovery)
  • Perpetuating Factors: Suboptimal treatment, poor adherence, side effects of medications, substance abuse and family members with high expressed emotion (hostility, criticism and emotional over-involvement)
114
Q

Principles of Psychosis Pharmacotherapy: Do They Work?

A

Principles of Psychosis Pharmacotherapy: Do They Work?

  • 80% remission of positive symptoms during first episode psychosis (SCZ) within 9 weeks
  • 10-20% of first episode psychosis fail to fully remit after a trial of two antipsychotics. With time this increases to 30-50% in enriched populations (treatment resistance).
  • First line is atypical antipsychotics given better tolerability and less chance of tardive dyskinesia
  • Antipsychotics have variable or low efficacy in psychosis secondary to medical, substance use or delusional disorder
115
Q

Principles of Psychosis Pharmacotherapy: Why Take the Medication? (3)

A

Why Take the Medication:

  1. To prevent distress, disability and suicide
  2. First episode psychosis more responsive to treatment than subsequent episodes
  3. Prolonged duration of untreated psychosis has poor response and outcome
116
Q

Principles of Psychosis Pharmacotherapy: How Long For?

A

Principles of Psychosis Pharmacotherapy: How Long For?

  • After first episode psychosis continue for at least 12 months and then attempt to withdraw over several weeks with further specialist follow up for 12 months
  • For relapse, monotherapy with atypical antipsychotics is first choice (unless intolerable side effects or remission on typical antipsychotics)
  • People who respond early tend to stay on their medication
117
Q

Principles of Psychosis Pharmacotherapy: What Happens When They Stop?

A

Principles of Psychosis Pharmacotherapy: What Happens When They Stop?

  • Patient may not notice a difference initially
  • Possible relapse after 4-6 weeks
  • Stopping medication is the most powerful predictor of relapse
118
Q

Principles of Psychosis Pharmacotherapy: Which is The Right Medication?

  • Illness profile considerations?
  • Patient profile considerations?
  • Medication profile considerations?
A

Principles of Psychosis Pharmacotherapy: Which is The Right Medication?

  • Illness Profile: History of illness onset an course, present signs and symptoms and past treatment response
  • Patient Profile: Vulnerability to side effects, tolerance to side effects, insight to illness and comorbidities
  • Medication Profile: Tolerability (short term and long term), delivery formulations, availability, cost and pharmacokinetics
119
Q

Principles of Psychosis Pharmacotherapy: What Happens If It Doesn’t Work?

  • What is DR POSCAN?
  • Treatment Resistance management?
A

Principles of Psychosis Pharmacotherapy: What Happens If It Doesn’t Work?

  • Antipsychotics may take 4-6 weeks for effect. If no response at 4-6 weeks, then change. If partial response then wait 6-10 weeks
  • No Response: DR POSCAN
  • Treatment Resistance: Ensure at least 2 adequate trials of antipsychotics (>6 weeks and at least 1 atypical). Clozapine is treatment of choice, consider depot antipsychotic if there is poor adherence and if fails, resort to antipsychotic that gave best response.
120
Q

What are 2 examples of Typical Antipsychotics?

  • When are they each indicated?
  • What is the Mechanism of Action of Typical Antipsychotics?
  • 5 advantages?
  • 3 Disadvantages?
A

Typical APs (Older)

  • Examples
    1. Haloperidol (PO/IMI): Aroused or agitated patient (IMI for highly aroused/agitated)
    2. Chlorpromazine (PO): Aroused or agitated patient
    3. NB: Often combined with BZD but can worsen delirium
  • Mechanism of Action
    • Blocks D2 receptors which decreases hyperactivity of mesolimbic dopamine pathway (decreases positive symptoms)
    • Blocks the hypoactive mesocortical pathway (increases negative symptoms?)
    • Blocks nigrostriatal and tuberoinfundibular pathways (extrapyramidal symptoms and hyperprolactinemia)
  • Advantages
    1. Cheap (off patent)
    2. Have depot (IMI) preparations
    3. Many decades of experience
    4. Established side effect profiles
    5. Haloperidol lacks anticholinergic activity (hence is safer in the elderly)
  • Disadvantages
    1. Lowers the seizure threshold
    2. Low propensity to cause weight gain
    3. Higher likelihood of tardive dyskinesia
121
Q

What are 4 examples of ATypical Antipsychotics?

  • When are they each indicated?
  • What is their Mechanism of Action?
  • 2 Advantages?
  • 3 Disadvantages?
A

Atypical APs (Newer Except Clozapine)

  • Examples
    1. Olanzapine (PO): Aroused or agitated patient
    2. Quetiapine (PO): Aroused or agitated patient
    3. Risperidone (PO): Often used in short term Mx of A/A of delirium
    4. Clozapine
  • Mechanism of Action
    • DA and 5HT blockade (risperidone)
    • D2/D3 activity (amisulpride)
    • DA partial agonist (aripiprazole)
    • Complex (CLOZ)
    • Decreases positive symptoms and improves negative and neurocognitive symptoms
  • Advantages
    1. Generally have fewer side effects as decreases extrapyramidal symptoms and hyperprolactinemia (except risperidone)
    2. Virtually NO TARDIVE DYSKINESIA
  • Disadvantages
    1. More expensive (patents) but cost effective
    2. Less well established side effects profiles
    3. Limited depot options
122
Q

What are some additional side effects of clozapine? Why use it?

A
123
Q

Discuss which APs are metabolised by which CYP450 enzyme?

A
124
Q

What are 4 examples of clinically relevant drug interactions with APs?

A

EXAMPLES OF CLINICALLY RELEVANT DRUG INTERACTIONS

  1. 1A2 inhibited by fluvoxamine (SSRI): clozapine level ↑
  2. 1A2 Induced by smoking: clozapine ↓
  3. 2D6 inhibited by fluoxetine and paroxetine (SSRIs): ↑AP levels
  4. 3A4 inhibited by fluvoxamine and fluoxetine (SSRIs): ↑ AP levels
125
Q

What are the 11 Side effects of APs?

A

Side effects of APs

  1. Acute Dystonia
  2. Parkinsonism
  3. Akathisia (Psychomotor Restlessness):
  4. Tardive Dyskinesia:
  5. Hyperprolactinemia:
  6. 6. Prolongation of QTc Interval
  7. Anticholinergic
  8. Anti-Adrenergic (A1)
  9. Antihistaminergic
  10. Metabolic Syndrome
  11. Neuroleptic Malignant Syndrome
126
Q

Side Effects of Antipsychotics

  • What is Acute Dystonia?
  • When does it occur?
  • Complications?
  • How do we screen for it?
  • Treatment?
A

Acute Dystonia: Affects face, neck and trunk especially likely after IMI administration. Occurs within hours to days (24-72 hours after they leave ED), especially in young males.

Complications: Laryngeal spasm (potentially fatal), oculogyric crisis (involuntary contractions of eye muscles resulting in conjugate gaze usually in upward direction) and opisthotonus (tetanic spasm in muscle of back)

Screen: Abnormal involuntary movements scale (AIMS)

Treatment: Benztropine 1-2mg IMI, every 10-15 min if necessary (max 6mg/24hr)

127
Q

Side Effects of Antipsychotics

  • What is Parkinsonism?
  • Treatment?
A

Parkinsonism: Bradykinesia, resting tremor (high frequency, pill rolling) and muscular rigidity (increased tone, lead pipe rigidity, cogwheeling).

• Treatment: Benztropine 0.5mg

128
Q

Side Effects of Antipsychotics

  • What is Akathisia?
  • Complications?
  • Screening?
  • Treatment?
A

Akathisia (Psychomotor Restlessness): Severe sense of agitation and restlessness of the limbs, may present as a feeling of inner restlessness and develops within hours to days. Common with aripiprazole.

Complications: May lead to suicide

Screen: Barnes akathisia rating scale

Treatment: Propranolol 20-40mg orally TDS-QID or diazepam 2-5mg orally, TDS. Recent trial mirtazapine 15mg.

129
Q

Side Effects of Antipsychotics

  • What is Tardive Dyskinesia?
  • Diagnosis criteria?
  • Risk factors?
  • Screening?
  • Treatment?
A

Tardive Dyskinesia: Permanent oro-facial dyskinesia. Complex syndrome of involuntary hyperkinetic oral, lingual, buccal, facial, limb, trunk and finger movements.

  • For diagnosis, must be > 3 months of treatment and > 4 weeks of symptoms.
  • Risk factors: old age, potent typical antipsychotics (haloperidol 5% PA, 50-60% lifetime), long term use, head injury, drug and alcohol use, female and extra pyramidal side effects.
  • Screen: Abnormal involuntary movements scale (AIMS)
  • Treatment: No effect treatment! Slowly withdraw causative agent and consider alternative antipsychotic. Acting early can avoid onset. Prevent by using atypical antipsychotics (decrease incidence ten-fold).
130
Q

Side Effects of Antipsychotics

  • What is Hyperprolactinaemia? Mechanism?
  • Screening?
A

Hyperprolactinemia: inhibition of dopamine at tuberoinfundibular pathway leads to increased prolactin causing weight gain, galactorrhoea (lactation), gynecomastia, sexual dysfunction, amenorrhoea/menstrual irregularity and infertility. Often with typical antipsychotics, amisulpride and risperidone

  • Screen: Measure prolactin levels and consider other differentials of increased levels (consider MRI of pituitary fossa)
131
Q

Side Effects of Antipsychotics

  • How do APs cause prolongation of QTc interval?
  • Risk of Torsades?
  • Screening?
A

Prolongation of QTc Interval: Due to effects on K channels and delayed repolarisation. Resting QTc typically <420ms for male or <430ms for females. Risk of sudden death with Torsades de pointes and VF at QTc >500ms. High risk with thioridazine, droperidol, pimozide and ziprasidone. Low risk with atypicals.

• Screen: Dizziness, syncope, presyncope and palpitations

132
Q

Side Effects of Antipsychotics

  • 5 anticholinergic side effects?
A

Anticholinergic: Strong anticholinergic activity correlates with decreased extra pyramidal side effects (limits the procholinergic effect of dopamine blockade). Muscarinic blockade causes:

  1. Dry mouth
  2. Blurred vision (loss of accommodation)
  3. Constipation
  4. Urinary hesitancy/ retention
  5. Cognitive blunting such as with Olanzapine.
133
Q

Side Effects of Antipsychotics

  • 3 Anti-adrenergic effects?
A

Anti-Adrenergic (A1):

  1. Postural hypotension
  2. Hypothermia
  3. Impotence and failure to ejaculate such as with Risperidone.
134
Q

Side Effects of Antipsychotics

  • 1 Anti-histaminergic effect? Which AP?
A

Antihistaminergic: Drowsiness such as with Quetiapine

135
Q

Side Effects of Antipsychotics

  • What is Metabolic Syndrome?
  • Which APs are most offensive?
A

Metabolic Syndrome: Weight gain, obesity, impaired glucose tolerance, hyperlipidemia and hypertension.

  • Mechanisms are complex and multifactorial.
  • Most offensive is clozapine (+4kg at 10 weeks) and olanzapine (+4.1kg), risperidone (+2.1kg) and other atypicals.
136
Q

Side Effects of Antipsychotics

  • What is Neuroleptic Malignant Syndrome?
  • When does it occur?
  • Differentials?
  • Complications?
  • Investigations?
  • Management?
A

Neuroleptic Malignant Syndrome: Occur in 2% of patients on antipsychotics, at any time but usually in the first 30 days (mortality is 5-20%).

  • Symptoms evolve over 1-2 days and recover over 2-3 weeks.
  • Symptoms include change in mental state, autonomic dysfunction, neuromuscular hyperactivity (CAN).
  • Differentials: Serotonin syndrome, drug or alcohol intoxication/withdrawal or lithium toxicity
  • Complications: Metabolic acidosis, myoglobulinaemia, renal failure, pulmonary embolism, chronic cerebellar syndrome, disseminated intravascular coagulation (DIC) and death
  • Investigations: Observations, check med chart, IV access and measure CK, UEC, coagulation profile, lithium level, other drug levels and UDS
  • Management: Cease antipsychotics, resuscitate (cooling, BP, rehydrate), fluids, BZD, medical review and transfer to monitored ward (ICU for dopamine agonist, muscle relaxant, heparin and ECT).
137
Q

Compare Neuroleptic Malignant Syndrome and Serotonin Syndrome:

  • History?
  • Clinical Manifestations?
  • Lab results?
  • Distinguishing features?
A
138
Q

Mechanisms and Side Effects of First Generation Side Effects?

A
139
Q

Mechanisms and Side Effects of Second Generation Side Effects?

A
140
Q

Mechanisms and Side Effects of Third Generation Side Effects?

A
141
Q

What are the 4 Dominergic Nuclei and Pathways and their function?

A

Dopaminergic Nuclei and Pathways (Context):

  1. Mesolimbic Pathway: VTA to limbic structures (motivation, reward and executive functions)
  2. Mesocortical Pathway: VTA to prefrontal lobe (motivation, reward and executive functions)
  3. Nigrostriatal Pathway: Substantia nigra to the striatum (part of extrapyramidal system and motor control)
  4. Tuberoinfundibular Pathway: Arcuate nucleus of the hypothalamus to the anterior pituitary (inhibits prolactin release)
142
Q

Describe the dopaminergic hypothesis of schizophrenia.

  • Which pathway is hyperactive? Which symptoms does this produce?
  • Which pathway is hypoactive? Which symptoms does this produce?
A

Dopamine Hypothesis in Schizophrenia:

  • Theory: Dysregulated dopamine results in aberrant salience (tendency for irrelevant stimuli to be attributed motivational salience and thus to attract attention and influence behaviour inappropriately). Psychotic symptoms are driven by inappropriate processing of stimuli that would normally be considered irrelevant.
  • Mesolimbic Pathway: Hyperactivity (positive symptoms)
  • Mesocortical Pathway: Hypoactivity (negative symptoms/cognitive impairment)
143
Q

Understand the evidence for and against this hypothesis.

(3 for each)

A
144
Q

What is the Neurotransmitter Hypothesis of Schizophrenia?

  • Glutamate?
  • GABA?
  • Serotonin?
  • Dopamine?
A

Neurotransmitter Hypothesis of** **Schizophrenia

  • Glutamate: Low activity of the NMDA receptors of GABAergic inhibitory neurons in in prefrontal cortex. Antagonists of NMDA glutamate receptor such as phencyclidine (PCP) and ketamine transiently induce psychosis and symptoms of acute schizophrenia.
  • GABA: Loss of GABAergic neurons in hippocampus linked to psychosis.
  • Serotonin: 5HT receptor agonists such as LSD cause psychosis.
  • Dopamine: As described above.
145
Q

What is the Diathesis-Stress Hypothesis of Schizophrenia?

A

Diathesis-Stress Hypothesis: Underlying vulnerability (genetic and/or acquired) is acted upon by a stress, resulting in onset of disease. Vulnerability likely to be inherited (60-90% heritability).

146
Q

What is the Neurodevelopmental Hypothesis of Schizophrenia?

  • Histological changes?
A

Neurodevelopmental Hypothesis: Structural brain abnormality from early neurodevelopmental insult.

  • Decrease in elaboration of inhibitory pathways and excessive pruning of excitatory pathways leads to altered excitatory-inhibitory balance in the prefrontal cortex.
  • Could explain neurotransmitter imbalance and reduced function of prefrontal cortex.
  • Imaging (MRI and CT) shows regional volume reductions in medial temporal and limbic (hippocampus, amygdala, parahippocampal gyrus) structures and increased volume of ventricles.
  • Post-mortem investigations confirm imaging and show histological evidence of disrupted migration (no gliosis) in medial and frontal lobes.
    • Histological changes: ↓ neuropil (dendritic arborisation), smaller cell bodies, ectopic neurons, impaired cortical inter-neurons
147
Q

What is the Neurodegenerative Hypothesis of Schizophrenia?

A

Neurodegenerative Hypothesis: Brain changes progress over the course of the illness. Series of brain insults results in structural changes during early development which alters disease course, in patients with chronic, relapsing illness (but no gliosis in recent post-mortum studies).

148
Q

What are 6 Mechanisms of Development of Psychotic Symptoms and Disorders?

A

Mechanism of Development of Psychotic Symptoms and Disorders:

  1. Neurotransmitter Systems and Pathways: See neurotransmitter hypothesis above.
  2. Genetic Factors: See diathesis-stress hypothesis above.
  3. Exogenous Substances: Substance use can be linked to neurotransmitter changes, stress (diathesis model) and brain insult (neurodegeneration), see above.
  4. Structural Brain Abnormality: See neurodevelopmental and neurodegenerative hypothesis above.
  5. Information Processing: See changes to prefrontal cortex as described above.
  6. Stressful Events or Situations: See diathesis-stress hypothesis above.
149
Q

Demonstrate the ability to generate and present a ‘clinical formulation’ for a mental health problem.

  • What is a Clinical Formulation in Psych?
  • How is one generated/presented? (3)
A

Clinical Formulation (Clinical Intuition and Judgement):

  • A core clinical skill that links assessment information and treatment planning
  • It is a hypothesis about the mechanisms that cause and maintain the problem
  • Answers the Question: Why is this PARTICULAR patient here, with this PARTICULAR problem, at this PARTICULAR time in their life?
  • Performed after history and mental state examination but before diagnosis and treatment

Generate and Present a Clinical Formulation:

  1. Cross Sectional: Demographics, referral status, presenting complaint, history of presenting complain, mental state examination (observations and examinations) and current suicidality
  2. Longitudinal: Past medical history, medication history, family history and psychiatry history
  3. Integrative and Dynamic: Predisposing, precipitating, perpetuating and protective factors as well as prognosis and defense mechanisms, risk, strengths and gaps
150
Q

Outline An Approach to Patient with Psychiatric Presentation.

A

An Approach to Patient with Psychiatric Presentation:

  1. Psychiatric History
  2. Mental State Examination
  3. Physical Examination
  4. Gather Collateral (Family and Friends)
  5. Investigations (As Indicated)
  6. Formulate, Diagnose and Communicate
151
Q

Discuss the biological determinants of mood and mood disorders.

  • What is the difference between an emotion and a mood?
A

Emotion: Short-lived feelings that come from a known cause e.g. happy, ecstatic, sad and prideful.

Mood: Feelings that are longer lasting than emotions and have no clear starting point of formation e.g. positive or negative

152
Q

What is the difference between emotions and feelings?

A

Neural Basis of Emotions (Context):

Emotional Expression (Emotions): Set of physiological responses when the brain detects a positively or negatively charged stimulus. In the brain it involves changes in arousal levels and cognitive functions (attention, memory and decision strategy). In the body it involves endocrine, autonomic and musculoskeletal responses.

Emotional Experience (Feelings): The conscious experience of somatic and cognitive changes.

153
Q

Discuss the biological determinants of mood and mood disorders.

  • Which structures in the limbic system and connections to the limbic system are involved in emotions?
A

Neural Basis of Emotions

  • Limbic System: Cingulate gyrus and parahippocampal gyrus (cortical areas) and hippocampus, amygdala and septal areas (subcortical areas)
  • Connections to Limbic System: Ventral basal ganglia (nucleus accumbens), anterior and dorsomedial nuclei of the thalamus, prefrontal cortex, reticular formation and hypothalamus
154
Q

What role does the Hypothalamus-Pituitary Adrenal Axis (HPA) play in emotions and mood?

A

Neural Basis of Emotions - Hypothalamus-Pituitary Adrenal Axis (HPA):

  • Stress response which includes the release of cortisol from the adrenal glands and activation of the sympathetic nervous system (stress → Corticotrophin-releasing hormone → Adrenocorticotrophin hormone → cortisol).
  • Works with amygdala to stimulate avoidance behaviour and increased vigilance and arousal.
  • Hippocampal activation suppresses CRH release.
    • Glucocorticoid receptors on hippocampal cells bind cortisol and feedback to the HPA axis to inhibit CRH release.
155
Q

What role does the Amygdala play in emotions and mood?

  • Medial group?
  • Basal lateral?
  • Central & anterior group?
A

Neural Basis of Emotions - Amygdala:

Amygdala: Critical centre for coordinating behavioural, autonomic and endocrine responses to environmental stimuli, especially those with emotional content. Projections provide a key link between the experience of emotions and their expression (ink between sensory centres and hypothalamus outputs) and involved in emotional learning and memory through connections with hypothalamus (visceral and motor responses) and cortex dorsomedial nucleus of thalamus and orbitofrontal cortex.

  • Medial Group: Olfactory bulb and olfactory cortex
  • Basal Lateral: Orbital and medial prefrontal cortex and association cortex of anterior temporal lobe (especially large in humans)
  • Central and Anterior Group: Hypothalamus and brainstem
156
Q

Describe the Neuroanatomy and Physiology of Emotion?

A
157
Q

What is the Monoamine Theory (Basic Theory) of Depression?

A

Monoamine Theory (Basic Theory):
- Deficiency of one or more monoamines (DA, NA, A or 5HT) results in depression
- Deficiency states linked to depression
- Medication that decrease monoamines cause depression (B-Blockers)
- Medication that increase monoamines treat depression (SSRIs, NRIs or MAOI). Cause downregulation of receptors (balance neurotransmitters and receptors).
- Antidepressants increase monoamine neurotransmitters, and change gene expression in those neurons affected ( ↑ BDNF), which involves desensitisation of receptors.
- Ability to measure monoamine metabolites (i.e. 5HIAA) in blood or CSF and link to abnormality

158
Q

What is the Neurochemical Imbalance (Modern Theory) of Depression?

A
159
Q

What is the role of the Endocrine System, Cortisol and HPA Dysfunction in Depression?

A
160
Q

What is the role of Genetics in Depression?

A
161
Q

What is the role of Sleep and the Circadian Rhythm in Depression?

A
162
Q

What is a Schema?

A

Schema: A set of pre-programmed interpretations about the world that are activated by specific situations i.e. the world is unsafe and harsh (negative cognitive style) or the world is full of exciting opportunities (positive cognitive style). Maladaptive schema can distort reality and lead to negative thinking and altered mood.

163
Q

What is the Diathesis-Stress Model?
- What is a Diathesis?
- What are Stressors?

A

**Diathesis-Stress Model: **A psychological theory that attempts to explain a disorder as the result of an interaction between a pre-dispositional vulnerability and a stress caused by life experiences. Serves to explore how biological or genetic traits (diatheses) interact with environmental influences (stressors) to produce disorders such as depression, anxiety, or schizophrenia.

164
Q

List some Psychosocial Determinants of Mood and Mood disorders.

A
  1. Stressful life events
  2. Changes in life situation
  3. Childhood trauma
  4. Abuse and/or neglect
  5. Personality factors (hopelessness and worthlessness, low self-esteem, self-criticism and pessimism)
  6. Learned helplessness
  7. Poor social support and isolation
  8. Relationship breakdown, strain or problems
  9. Gender and cultural roles and expectations
165
Q

Which Mood Disorder Drugs are best? List in order.

A

ECT > MAOIs > SNRIs > SSRIs > TCADs

166
Q
A
167
Q
A
168
Q

What are the 5HT Receptor Effects?
- 5HT1A?
- 5HT2?
- 5HT3?

A
169
Q
A
170
Q
A
171
Q
A
172
Q
A
173
Q
A
174
Q

Treatment for Depression:
- Goal?
- Level 0?
- Level 1?
- Level 2?
- Level 3?

A
175
Q

Serotonin Syndrome
- Pathogenesis & Clinical Findings?

A
176
Q

Serotonin Syndrome
- Triad of symptoms?
- Hunter criteria?

A
177
Q

What is Discontinuation Syndrome?
- SSRI?
- TCA?
- MOAIs?

A
178
Q

Pharmacokinetics of Psychotropic Medications (Review)
- What is Absorption?
- 10 Factors which influence absorption?

A
179
Q

Pharmacokinetics of Psychotropic Medications (Review)
- What is Distribution?
- 4 Factors which Increase Distribution?

A
180
Q

Pharmacokinetics of Psychotropic Medications (Review)
- What is Metabolism?
- Location?
- Function?
- 5 important enzymes?

A
181
Q

3 examples of dangerous drug interactions with Psychotropic Medications?
- CYP450 Inhibition example?
- CYP450 Induction example?

A

Induction Example
Smoking induces CYP1A2 and metabolism of clozapine (antipsychotic), reducing plasma levels of the drug (if the patient ceases smoking, may need dose reduction of
clozapine).
Inhibition Example
SSRIs (especially fluvoxamine) inhibit CYP1A2 and metabolism of caffeine,
potentially leading to toxic plasma levels of the drug (fluvoxamine and theophylline potentially lethal together).

182
Q

Pharmacokinetics of Psychotropic Medications (Review)
- Most Common Route of excretion for Psychotropics?
- Examples of Drug Interactions Affecting Excretion?

A
183
Q

Describe how suicide risk can be assessed?

A

Suicide Assessment Tool:
SAD PERSONS Risk Assessment Scale

184
Q

Describe how suicide risk can be assessed?

A

Suicide Assessment Tool:
SAD PERSONS Risk Assessment Scale

185
Q

Suicide Assessment Protocol:
- 5 components?

A
186
Q

What are 6 Types of Mood Disorders?

A
  1. Major Depressive Disorder - An episodic mood disorder primarily characterised by depressed mood and anhedonia that lasts for at least 2 weeks
  2. Adjustment Disorder - Minor depressive symptoms following a stressor or bereavement
  3. Recurrent Major Depression - Repeated episodes of major depression
  4. Dysthymia - A chronic disorder of low mood for at least 2 years
  5. Personality Disorder - A persistent, pervasive and maladaptive pattern of coping since late adolescence or early adulthood that can be characterised by affect dysregulation (including periods of low mood)
  6. Bipolar Disorder - A history of episodic elevated mood (mania or hypomania) and at least one major depressive episode.
187
Q

8 Signs & Symptoms of Depression?

A
188
Q

Major Depressive Disorder (DSM V) Diagnostic Criteria? (10)

A
189
Q

Depression vs Mania Presentation?

A
190
Q

What is the DASS-21?

A

DASS-21: A clinical assessment that measures the three related states of depression, anxiety and stress. It has 21 questions and takes about 3 minutes to complete.

191
Q

What is involved in the physical examination of a patient presenting with mood disorders?

A
192
Q

What investigations might you consider for patients presenting with mood disorders? (9)

A

YR2 BCS Study Points SEM 1 (7 decks)

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