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RANZCP exam preparation > EMQ Part 2 > Flashcards

EMQ Part 2 Flashcards

1
Q

Memantine
Mechanism of action
5HT1A partial agonist, MAO-B inhibitor, NMDA R antagonist, butylcholinesterase inhibitor, MAO-A inhibitor, GABA-B, 5HT 2A R stimulation, Alpha 2 agonist, 5HT1A partial agonist, GABA-A agonist

A

NMDA R antagonist

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2
Q

Side effect-Tolerance to hallucinogens
Mechanism:
M3 R blockade, D2 antagonism, M1 R blockade, 5HT1A autoreceptor, 5HT2 R activation, H2 R antagonism. 5HT2A R desensitisation, decreased brain GABA function, H1 R antagonism, Alpha 1 adrenergic R blockade

A

5HT2A R desensitisation eg LSD

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3
Q

Benzodiazepine withdrawal symptoms
Mechanism:
M3 R blockade, D2 antagonism, M1 R blockade, 5HT1A autoreceptor, 5HT2 R activation, H2 R antagonism. 5HT2A R desensitisation, decreased brain GABA function, H1 R antagonism, Alpha 1 adrenergic R blockade

A

Decreased brain GABA function. Benzo’s are GABA agonists. Bind to gamma sub-unit of GABA A R. Binding causes an allosteric modification of the R that results in an increase in GABA A receptor activity

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4
Q

Sedative action of trazodone
Mechanism:
M3 R blockade, D2 antagonism, M1 R blockade, 5HT1A autoreceptor, 5HT2 R activation, H2 R antagonism. 5HT2A R desensitisation, decreased brain GABA function, H1 R antagonism, a1 R antagonism

A

H1 R antagonism

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5
Q

Postural hypotension with antipsychotics
Mechanism:
M3 R blockade, D2 antagonism, M1 R blockade, 5HT1A autoreceptor, 5HT2 R activation, H2 R antagonism. 5HT2A R desensitisation, decreased brain GABA function, H1 R antagonism, a1 R antagonism

A

Alpha 1 R antagonism. Risperidone particularly ++

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6
Q

Constipation, dry mouth with TCA
Mechanism:
M3 R blockade, D2 antagonism, M1 R blockade, 5HT1A autoreceptor, 5HT2 R activation, H2 R antagonism. 5HT2A R desensitisation, decreased brain GABA function, H1 R antagonism, a1 R antagonism

A

M3 antagonism

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7
Q

Irregular menstural periods with antipsychotics
Mechanism:
M3 R blockade, D2 antagonism, M1 R blockade, 5HT1A autoreceptor, 5HT2 R activation, H2 R antagonism. 5HT2A R desensitisation, decreased brain GABA function, H1 R antagonism, a1 R antagonism

A

D2 antagonism

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8
Q

Haloperidol-induced NMS
Mechanism:
M3 R blockade, D2 antagonism, D2 R blockadeM1 R blockade, 5HT1A autoreceptor, 5HT2 R activation, H2 R antagonism. 5HT2A R desensitisation, decreased brain GABA function, H1 R antagonism, a1 R antagonism, 5HT2C,

A

D2 R blockade
Risks- young age, high potensy and high dose neuroleptic use, rapid increase in dose, depot medication, prior episodes of NMS, agitation, dehydration, exhaustion, organic illness, recent episode of catatonia

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9
Q

SSRI induced anorgasmia
Mechanism:
M3 R blockade, D2 antagonism, M1 R blockade, 5HT1A autoreceptor, 5HT2 R activation, H2 R antagonism. 5HT2A R desensitisation, decreased brain GABA function, H1 R antagonism, a1 R antagonism

A

5HT2C agonism. Mirtazapine is a 5HT2C antagonist and hence indicated to treat sexual dysfunction with SSRI.
Mirtazapine augmentation for SSRI-induced sexual dysfunction: a retrospective investigation

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10
Q

Trazodone-induced priapism
Mechanism:
M3 R blockade, D2 antagonism, M1 R blockade, 5HT1A autoreceptor, 5HT2 R activation, H2 R antagonism. 5HT2A R desensitisation, decreased brain GABA function, H1 R antagonism, a1 R antagonism, a2 R antagonism

A

A1 R antagonism

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11
Q

Mirtazapine-induced weight gain and sedation
Mechanism:
M3 R blockade, D2 antagonism, M1 R blockade, 5HT1A autoreceptor, 5HT2 R activation, H2 R antagonism. 5HT2A R desensitisation, decreased brain GABA function, H1 R antagonism, a1 R antagonism

A

H1 R antagonism

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12
Q

SSRI induced GIT
Mechanism:
M3 R blockade, D2 antagonism, M1 R blockade, 5HT1A autoreceptor, 5HT2 R activation, H2 R antagonism. 5HT2A R desensitisation, decreased brain GABA function, H1 R antagonism, a1 R antagonism

A

5HT3 R agonism

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13
Q

In a case-control study looking at the association between the use of antihypertensive medication and depression, subjects with depression may be more likely to remember what medication they had had, due to the potential importance of this issue to them
Bias? Recall bias, Neyman’s bias, Selection bias, confounding bias, informatioin bias, unmasking bias, publication bias, membership bias, Barkson’s bias, Attrition bias

A

Recall bias
when cases and controls recall exposures differently.
Rumination bias or search for meaning bias is where people with diseases will think harder about their prior exposures than disease free people.

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14
Q

In a cohort study looking at the long term association between cannabis use and schizophrenia, subjects in the cannabis group were more likely to drop out of follow up.
Bias? Recall bias, Neyman’s bias, Selection bias, confounding bias, informatioin bias, unmasking bias, publication bias, membership bias, Barkson’s bias, Attrition bias

A

Attrition bias

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15
Q

A case-control study investigating the association, between poor social support and depression recruits, depressed subjects from psychiatric hospital in-patients
Bias? Recall bias, Neyman’s bias, Selection bias, confounding bias, informatioin bias, unmasking bias, publication bias, membership bias, Barkson’s bias, Attrition bias

A

Berkson’s bias . Hospital controls- usually higher response rates than population controls, but more likely to have sampling bias (hospital controls likely to have different exposures than population controls.)

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16
Q

Case-control study looking at smoking and Alzheimer’s disease shows a protective effect.
Bias? Recall bias, Neyman’s bias, Selection bias, confounding bias, informatioin bias, unmasking bias, publication bias, membership bias, Barkson’s bias, Attrition bias

A

Neyman bias: incidence-prevalence bias, selective survival bias. When a series of survivors is selected, if the exposure is related to prognostic factors, or the exposure itself is a prognostic determinant, the sample of cases offers a distorted frequency of the exposure.
Can occur in cross sectional and case-control.
Bias occurs only if the risk factor influences mortality from the disease being studied

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17
Q

In a placebod-controlled trial for a new antidepressant, group allocation is based on hospital numbers, so the psychiatrist who enters patients for the study knows in advance which treatment group they will be in.
Bias? Recall bias, Neyman’s bias, Selection bias, confounding bias, informatioin bias, unmasking bias, publication bias, membership bias, Barkson’s bias, Attrition bias, membership bias

A

Selection bias. The selection bias in an RCT is called allocation bias. Allocation concealment is necessary to minimise allocation bias

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18
Q

Priapism
R mechanism? 5HT1D stimulation, 5HT1A stimulation, 5HT3 stimulation, 5HT2A/2C antagonism, D2 blockade, a1 blockade, a2 blockade

A

A1 blockade

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19
Q

Obsessive-compulsive symptoms with antipsychotics
R mechanism? 5HT1D stimulation, 5HT1A stimulation, 5HT3 stimulation, 5HT2A/2C antagonism, D2 blockade, a1 blockade, a2 blockade

A

5HT1D stimulation. Acting on the autoreceptors, to reduce serotonin fucntion. May explain delay in optimal beneficial effects of SSRIs

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20
Q

Weight gain
R mechanism? 5HT1D stimulation, 5HT1A stimulation, 5HT3 , 2C antagonism, stimulation, 5HT2A/2C antagonism, D2 blockade, a1 blockade, a2 blockade

A

5HT2C
Most associated with weight gain. H1, H3 autoreceptors also. M3 in pancreatic beta cell, mostly due to SGA, induces alterations in glucose metabolism, due to reduction in insulin secretion and increased insulin resistance. SGA also stimulate ghrelin release. Also stimulate orexin from lateral hypothalamus, which increases appetite,. Orexin stimulated due to blockade of histaine receptors.
Leptin levels which control insulin sensitivity, increade by SGA. Ziprasidone is a potent 5HT1A R agonist and modest 2C R antagonist, which along with reuptake inhibition of serotonin and NE, potentially increase metabolic rate and decreases appetite.

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21
Q

GI side effects with SSRIs
R mechanism? 5HT1D stimulation, 5HT1A stimulation, 5HT3 stimulation, 5HT2A/2C antagonism, D2 blockade, a1 blockade, a2 blockade

A

5HT3 stimulation

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22
Q

Temporal intermittent rhythmic dealta slowing
?HSE, CJD, Sub-acute sclerosing pan encephalitis, generalised anxiety, absence seizures, complex partial seizures, myoclonic epilepsy, metabolic encephalopathy

A

Herpes simplex encephalitis. Focal abnormalities or diffuse slowing may be observed. Periodic complexes and periodic lateralising epilpetiform discharges (PLEDs) in the proper clinical context, are strongly suggestive of HSE. PCR analysis of CSF for the detection of HSV DNA is now gold standard.

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23
Q

Bilateral synchronous high amplitude with wave slowing
?HSE, CJD, Sub-acute sclerosing pan encephalitis, generalised anxiety, absence seizures, complex partial seizures, myoclonic epilepsy, metabolic encephalopat

A

Subacute sclerosing pan encephalitis

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24
Q

3 Hz diffuse spike and wave activity?HSE, CJD, Sub-acute sclerosing pan encephalitis, generalised anxiety, absence seizures, complex partial seizures, myoclonic epilepsy, metabolic encephalopathy

A

Absence seizures

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25
Q

Agent that binds the receptor but produces the opposite pharmacological effect
?inverse agonist, presynaptic R, irreversible antagonist, partial agonist, full agonist, second messenger system, competitive antagonist, potency, non-competitive antagonist

A

Inverse agonist

Partial agonist have a weaker preference than an agonist fofr the same R. Inverse agonist has all the properties of a full agonist, shifts equilibrium in the opposite direction.

Anatgonist reduces the effect of an agonist by preventing it from binding to receptors. Antagonists do not have any effect in the absence of an agonist

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26
Q

Buspirone acts via this mechanism
?inverse agonist, presynaptic R, irreversible antagonist, partial agonis, full agonist, second messenger system, competitive antagoist, potency, non-competitive antagonist

A

5HT1A partial agonist
The degree of response of a partial agonist depends on availability of neurotransmitter in the vicinity. If large concentration, partial agonist can actually inhibit transmission.

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27
Q

Lithium’s postulated mechanism of action
?inverse agonist, presynaptic R, irreversible antagonist, partial agonis, full agonist, second messenger system, competitive antagoist, potency, non-competitive antagonist

A

Second messenger system

  1. Modulatioin of neurotransmitters likely readjusts balances between excitatory and inhibitory activities, and decreased glutamatergic activitiy may contribute to neuroprotection.
  2. Lithium modulates signals impacting on the cytoskeleton, a dynamic system contributing to neural plasticity, at multiple levels, including glycogen synthase kinase-3beta, cAMP K, PKC, which may be critical for the neural plasticity involved in mood recovery and stabilisation.
  3. Lithium adjusts signalling activities regulating second messengers, transcription factors and gene expression
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28
Q

These antagonists alter the receptor site so that effects cannot be reversed completely by increasing dose of agonist
?inverse agonist, presynaptic R, irreversible antagonist, partial agonis, full agonist, second messenger system, competitive antagoist, potency, non-competitive antagonist

A

Allosteric modulator
(Non-competitive antagonists)
Binds at a site distinct from active site. Conformational change, which alters the affinity of the receptor for the endogenous ligand.
Positive increase affinity whilst negative decrease the affinity

Reversible antagonist binds non-covalently, “washed out.” An irreversible binds covalently and cannot be displaced.

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29
Q

Tigabine
?Increased GABA B R density and neural responsiveness, u R, cGMP, inhibition of GAT-1, prolonged sodium and calcium channel activation, adenosine R, inhibitioin of kainate mediated conductance at AMPHA glutamae R

A

Inhibition of GAT-1 Tiagabine is a potent inhibitor of GABA uptake into neurons and glial cells by inhibiting the GABA transporter

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30
Q

Caffeine
?inverse agonist, presynaptic R, irreversible antagonist, partial agonist, full agonist, second messenger system, competitive antagonist, potency, non-competitive antagonist, cGMP

A

Adenosine receptors. Mechanism of action

  1. Mobilisation of IC calcium and inhibition of specific phosphodiesteraes only occur at high non-physiological concentrations of caffeine.
  2. Antagonism at the level of adenosine receptors
  3. Caffeine increases energy metabolism throughout the brain but decreases at the same time cerebral blood flow, inducing a relative brain hyperperfusion
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31
Q

Involved in sexual arousal
?inverse agonist, presynaptic R, irreversible antagonist, partial agonist, full agonist, second messenger system, competitive antagonist, potency, non-competitive antagonist, cGMP

A

cGMP

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32
Q

Carbamazepine
?inverse agonist, presynaptic R, irreversible antagonist, partial agonist, full agonist, second messenger system, competitive antagonist, potency, non-competitive antagonist

A

Prolonged sodium and calcium activation. Inhibits sustained repetitive firing by blocking use-dependent sodium channels. CYP3A4. CYP3A4 is the priary isoform respondible for the formation of carbamazepine -10,11 epoxide. This metabolite is active and shown to be equipotent to carbamazepine as an anticonvulsant.

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33
Q

Topiramate
?inverse agonist, presynaptic R, irreversible antagonist, partial agonist, full agonist, second messenger system, competitive antagonist, potency, non-competitive antagonist

A

Inhibition of kainate mediated conductance at AMPA glutamate R, considered to produce its antiepileptic effect through several mechanisms, including modification of Na and Ca dependent action potnetials, enhacement of GABA-mediated Clo-fluxes into neurons, and inhibition of kainate-mediated condictance at glutamate R of the AMPA/kainate type. Vigabatrin is a selective and irreversible GABA transaminase inhibitor that greatly increases whole-brain levels of GABA

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34
Q

Non-opioid present up to 48 hours
Time in urine
?Phenylcyclidine, benzodiazepine, cannabis, alcohol, cocaine, heroin, codeine, morphine, amphetamine, methadone

A

Amphetamine

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35
Q 
Time in urine:
Marijuana
Opiates
Benzo's
Alcohol
A 
Marijuana
-single: 3 days
-moderate: 5-7 days
-daily: 10-15 days
-long term heavy: >30 days
Opiates
-codeine 48 hrs
-heroin 2-4 days
-morphine 48-72 hrs
-oxycodone 2-4 days
Benzo's
-short-acting 3 days
-long-acting 30 days
Alcohol
-7-12 hrs
Amphetamine
-48 hours
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36
Q

Opioid present for 3 days or more

A

Methadone

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37
Q

Present in urine for up to 8 days

A

Phenylcyclidine

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38
Q

Rewarding and aversive qualities of sensations are represented in this area
?Substantia nigra, periaqueductal grey, anterior cingulate, locus coeruleus, subthalamic nucleus
orbitofrontal cortex, hippocampus, amygdala, VTA

A

VTA
midbrain, situated adjacent to SN
dopaminergic neurons

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39
Q

Area is activated in tasks involving cognition and motor tasks
?Substantia nigra, periaqueductal grey, anterior cingulate, locus coeruleus, subthalamic nucleus
orbitofrontal cortex, hippocampus, amygdala, VTA

A

Anterior cingulate
1. detection of errors or shortfalls from some standard
2. Anticipation and preparation before task performance
3. Regulation of emotions
connects t the PFC, parietal cortex and both motor and visual systems

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40
Q

Damage to this area leads to amnesic syndrome
?Substantia nigra, periaqueductal grey, anterior cingulate, locus coeruleus, subthalamic nucleus
orbitofrontal cortex, hippocampus, amygdala, VTA

A

Hippocampus

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41
Q

This area is involved in mediating the flight/fight response
?Substantia nigra, periaqueductal grey, anterior cingulate, locus coeruleus, subthalamic nucleus
orbitofrontal cortex, hippocampus, amygdala, VTA

A

Amygdala

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42
Q

A substance found in the neuron type A, which is secreted from it, acts on neuron B

A

Neurotransmitter

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43
Q

Peptide secretions from neurons that are secreted directly into the blood stream that also act on other neurons as neurotransmitters

A

Neurohormone

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44
Q

A substance that influences neuronal activity and originates from non-synaptic sites

A

Neuromodulator

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45
Q

Post-synaptic compounds that participate in the generation of post-synaptic responses

A

Neuromediator

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46
Q

Substances released by post-synaptic structures, which maintain pre-synaptic neuronal structure

A

Neurotrophin

Survival, development and function of neurons

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47
Q

Ligand gated ion channels which are inhibitory and concentrate at the inhibitory synapses of the brain
?NMDA, Kainate, Glycine receptors, GABA R, muscarinic R, AMPA, Glutamate

A

GABA R

Acetylcholine, Glutamate also of this type

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48
Q

Ligand gated ion channel which are excitatory and is the major binding site for phenylcyclidine
?NMDA, Kainate, Glycine receptors, GABA R, muscarinic R, AMPA, Glutamate

A

NMDA

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49
Q

G protein coupled receptors that exist in 5 subtypes situated on the CNS and peripheral tissues

A

Muscarinic R

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50
Q

This receptor is involved in a type of encaphlitis and is associated with ovarian tumours

A

NMDA
Prodromal phase- fever, headache, URTI, NVD.
over 2 weeks develop psychiatric sx- insomnia, delusions, hallucinations, paranoia, autonomic instability, apathy and depression.
Catatonic sx, seizures, abnormal movements, autonomic instability, memory deficits,
GluN1 subunit of NMDAR

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51
Q

Beta adrenoreceptor agonist that has tremors as side effect
?Black widow spider venom, partial nicotinic agonist, acetylcholinesterase, verenicicline, lofexidine, xanomeline, salbutamol,L-Dopa, disulfuram

A

Salbutamol

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52
Q

Drugs acting through this mechanism are currently in development for treatment negative symptoms in schizophrenia
?Black widow spider venom, partial nicotinic agonist, acetylcholinesterase, verenicicline, lofexidine, xanomeline, salbutamol,L-Dopa, disulfuram

A

Partial nicotinic agonists
The alpha 7 nicotinic acetylcholine receptor gene CHRNA7, is associated with genetic transmission of schizophrenia and related cognitive and neurophysioogical sensory gating deficits. Cognitive dysfunction is responsible for significant psychosocial disability in schizophrenia. Nicotine, a low potency agonist at the alpha 7 R has some positive effects on neurophysiological and neurocognitieve deficits associated with schizophrenia, which suggests that moree effective receptor activation might meaningfully enhance cognition in schizophrenia.

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53
Q

Nicotinic receptor agonist which can cause neuropsychiatric side effects
?Black widow spider venom, partial nicotinic agonist, acetylcholinesterase, verenicicline, lofexidine, xanomeline, salbutamol,L-Dopa, disulfuram

A

Verenicicline

high affinity and high selectivity for binding at the a4B2 receptor and is a partial agonist at the receptor.

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54
Q

This substance causes a rapid release of acetylcholine
?Black widow spider venom, partial nicotinic agonist, acetylcholinesterase, verenicicline, lofexidine, xanomeline, salbutamol,L-Dopa, disulfuram

A

Black widow spider venom

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55
Q

This neuropeptide increase appetite, leads to weight gain and promote slow wave sleep in humans
?Oxytocin, vasopressin, orexin, BDNF, neurotensin, ghrelin, CCK, CRF, leptin, NPY

A

Ghrelin

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56
Q

Released from the paraventricular nucleus of the hypothalamus, elevated levels of this substances are found in depression
?Oxytocin, vasopressin, orexin, BDNF, neurotensin, ghrelin, CCK, CRF, leptin, NPY

A

Corticotrophin released factor
++corticosteroid secretion endangers neurons in the hippocampus, amygdala, and PFC, by increasing their vulnerability to oxidative stress.

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57
Q

Part of the neuropeptide family, this chemical is labelled as the social neuropeptide because of its ability to regulate social recognition, affiliation, modulation of anxiety, mood and aggression
?Oxytocin, vasopressin, orexin, BDNF, neurotensin, ghrelin, CCK, CRF, leptin, NPY

A

Oxytocin

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58
Q

A deficiency of this substance is found in narcolepsy. The neurons secreting this substance cease discharge during sleep
?Oxytocin, vasopressin, orexin, BDNF, neurotensin, ghrelin, CCK, CRF, leptin, NPY

A

Orexin
Hypocretins
Produced in lateral hypothalamus. Orexin neurone project to VTA, locus coeruleus and dorsal raphe. Narcolepsy shows low CSF orexin or hypocretin

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59
Q

Acute and chronic stress decreases the expression of this neurotrophin and SSRI’s elevate levels
?Oxytocin, vasopressin, orexin, BDNF, neurotensin, ghrelin, CCK, CRF, leptin, NPY

A

BDNF
Hippocampal long term potentiation up regulates BDNF mRNA and BDNF by itself can induce a glutamate independent form of LTP. BDNF levels have bee correlated with expression of CAG releats from mutant huntingtin

60
Q

Subcortical Leucoencephalopathy is associated with late onset illness and treatment resistance
?Autism, PD, mood, substance, schizophrenia, anxiety, eating disorder, alzheimer’s dementia

A

Mood disorder
Subcortical Leucoencephalopathy is another term for White Matter Hyperintensities which is associated with late life depression. Also increased prevalence of WMH in bipolar disorder that extends to adolescent years

61
Q

Reduced concentration of phospholipids and NAA in frontal and temporal lobes
?Autism, PD, mood, substance, schizophrenia, anxiety, eating disorder, alzheimer’s dementia

A

Schizophrenia

62
Q

Increased activity in the insula and amygdala

?Autism, PD, mood, substance, schizophrenia, anxiety, eating disorder, alzheimer’s dementia

A

Anxiety disorder

63
Q

Medial PFC dysfunction

?Autism, PD, mood, substance, schizophrenia, anxiety, eating disorder, alzheimer’s dementia

A

Mood disorder

64
Q

Increased brain volume

?Autism, PD, mood, substance, schizophrenia, anxiety, eating disorder, alzheimer’s dementia

A

Autism
Increased volume, not cortical thickness, suggest early brain enlargement may be associated with increased cortical surface area.

65
Q

Increases in 5HT1A R binding and reductions in 5HT2A R binding

A

Eating disorder
Repeat length polymorphism in the promoter region of hman serotonin transporter gene 5HTT regulates gene expression in vitro. Individuals carrying one or two copies of the relatively low expressing Short allle of the serotonin transporter linked polymorphic region, exhibit elevated neuroticism. S-carriers exhibit elevated amygdala reactivity to threatening stimuli, as assessed by functional MRI.
S carriers exhibit elevated depressive sx, diagnosable depression, suicidality after experiencing stressful life events and childhood maltreatment.
Suicide victims tend to have low CSF 5HIAA and high CSF cortisol. Abused suciide victims had higher CSF cortisol compared to suicide victims with low exposure to interpersonal violence as a child.

66
Q

A 24 yo M with mood disorder has been started on anti mani agent. 1 week after initiation he reports confusion, irritability and seizures. He has an inherited disorder of carnitine metabolism
?Amitryptiline, lithium, agomelatine, ECT, statins, lamotrigine, valproate, carbamazepine, methylphenidate, olanzapine

A

Valproate
The metabolism of valproate by mitochondrial oxidation produces propionyl Co-A and valproyl Co-A, which inhibit N acetylglutamate synthetase and consequent deletion of N acetylglutamate. Leads to inhibition of carbamylphosphatase synthetase resulting in decreased clearance of ammonia.
Another mechanism if the reduction of hepatic carnitine levels by valproate.
Deficiency in carnitine results in decreased beta-oxidation of fatty acids, in turn results in reduced levels of acetyl co-A- which is substrate for N AG synthetase as above. Thus decrease in acetyl co-A ultimately disruppts urea cycle resulting in ammonia accumulation

67
Q

A 25 yo female with mood disorder is initiated on mood stabilised. On day 14, she reports swollen lymph nodes, fever and ulcers around her eye and mouth
?Autism, PD, mood, substance, schizophrenia, anxiety, eating disorder, alzheimer’s dementia

A

Lamotrigine

68
Q

A 35 yo man with treatment resistant depression complains that he is unable to remember important events in his childhood that he was able to previously remember
?Autism, PD, mood, substance, schizophrenia, anxiety, eating disorder, alzheimer’s dementia

A 
ECT
Adverse effects
1. memory
Autobiographical
Amnesia
Retrograde
Working memory
Memory disability
2. cognition
higher mental function, attention, concentration, flexibility, problem solving, analytical and abstract thinking, reasonaning, executive function, intelligence
69
Q

56 yo M with psychosis develops metabolic syndrome. Complains of severe muscle cramps after initiation of medication
?Autism, PD, mood, substance, schizophrenia, anxiety, eating disorder, alzheimer’s dementia

A

Statins

70
Q

Choice of opioid substitution when risk of diversion in high

?methadone, naltrexone, disulfuram, acamprosate, oxazepam, lofexidine, buprenorphine, suboxone

A

Suboxone
Combination bupr + naloxone.
Bup is long acting partial mu agonisst and full kappa antagonist administered SL in opioid replacement therapy. Buprenorphine is well suited medication for opioid replacement therapy due to its activity as a partial opioid agonist. Naloxone being an opioid antagonist can be used to avoid diversion.

71
Q

Choice of opioid substituation therapy in pregnancy

v?methadone, naltrexone, disulfuram, acamprosate, oxazepam, lofexidine, buprenorphine, suboxone

A

Methadone

72
Q

Alpha 2 receptor agonist used in opioid detoxification

?methadone, naltrexone, disulfuram, acamprosate, oxazepam, lofexidine, buprenorphine, suboxone

A

Lofexidine

73
Q

Opioid antagonist that reduces cravings for alcohol and is used in relapse prevention
?methadone, naltrexone, disulfuram, acamprosate, oxazepam, lofexidine, buprenorphine, suboxone

A

Naltrexone
Selective competitive antagonist at mu receptors, activity may explain anti-relapse action either because enogenous opioids are involved in the positively reinforcing effects of alcohol/or because these same transmitters are involved in conditioned anticipation of these effects.

74
Q

This drug used in alcohol relapse prevention acts on the GABA and glutamate receptor systems
?methadone, naltrexone, disulfuram, acamprosate, oxazepam, lofexidine, buprenorphine, suboxone

A

Acamprosate

75
Q

Drug of choice in alcohol detoxification in liver disease

?methadone, naltrexone, disulfuram, acamprosate, oxazepam, lofexidine, buprenorphine, suboxone

A

Oxazepam

76
Q

A partial opioid agonist with action at mu and kappa Receptors
?methadone, naltrexone, disulfuram, acamprosate, oxazepam, lofexidine, buprenorphine, suboxone

A

Buprenorphine
Reduces cravings for heroin and enhances treatment retention
Can be used for maintenence or withdrawal
diminishes psychological reinforcement of continued heroin use. May complicate attempts at analgesia with opioid agonists
Once daily to 3 times a weeks
Less sedating than full agonists
safer in overdose
treatment with naltrexone can be commenced within 5-7 days of bup
May complicate mx of opioid overdose requiring high naloxone doses
Doses >12mg may not increase opioid agonist effects, but will prolong the duration of action.

77
Q

Important aspects/points with buprenorphine

Mechanism, half life, administration with CYP3A4 inhibitors, affinity, timing of first administration

A

Partial opioid agonist at Mu R.
“Ceiling on maximal opioid activity”
Higher affinity for u R than full opioid agonist, therefore can block effects in dose-dependent fashion
Reducing craving + attenuating response
Half life 24-37 hours
Peak effect 4 hours after SL
Low dose- effects last 12 hours, high dose 16-32 mg lasts 48-72 hours.
When administered with CYP3A4 hibitors (protease inhibitors, CCBm macrolide antibiotics, azoles) can ++ plasma levels.
In some circumstances, may precipitate withdrawal one to four hours after first dose, as higher affinity and lower intrinsic activity than full agonists sch as methadone, morphine and heroin.
Displaces agonists and in short term, may not provide enough agonist activity.
Therefore during induction, first dose should be administered when the patient is experiencing features of opioid withdrawal 6-12 hours after last heroin use

78
Q

Is she the kind of person who likes to be the centre of attention at social gatherings
?Antisocial, schizotypal, anankastic, dependent, anxious-avoidant, histrionic, borderline personality, schizoid, paranoid

A

Histrionic

79
Q

Do you find it difficult to make decisions about trivial things such as what to wear, which restaurant to go to
?Antisocial, schizotypal, anankastic, dependent, anxious-avoidant, histrionic, borderline personality, schizoid, paranoid

A

Anankastic

80
Q

Has he made complaints against people and taken them to court
?Antisocial, schizotypal, anankastic, dependent, anxious-avoidant, histrionic, borderline personality, schizoid, paranoid

A

Paranoid

81
Q

Do you go to excessive lengths to please others, so you can get approval from them
?Antisocial, schizotypal, anankastic, dependent, anxious-avoidant, histrionic, borderline personality, schizoid, paranoid

A

Dependent

82
Q

70 yr old man from Fiji presents with bilateral foot drop, blurred vision and CSF showing elevated protein and increased cell count
?Hypocalcemia, meningitis, neurosyphillis, hypercalcemia, WE, Korsakoff’s encephalopathy, CJD, vit B12 def, hypomag, hypothyroid

A

Neurosyphillis
Tabes dorsalis- degeneration of ascending fibers of DRG. Pain, parasthesia and gait disturbance characteristic.
Lightnigh pain, general paresis, “Dementia paralytica”
Personality change
Change in affect, blunted, grandiosity

83
Q

22 yo F, living in army baracks, presents with headache, fever, photophobia and lethargy
?Hypocalcemia, meningitis, neurosyphillis, hypercalcemia, WE, Korsakoff’s encephalopathy, CJD, vit B12 def, hypomag, hypothyroid

A

Meningitis

84
Q

52 yo man with long standing history of alcohol intake presents with sore tongue, parasthesias in extremeties of hands and feet
?Hypocalcemia, meningitis, neurosyphillis, hypercalcemia, WE, Korsakoff’s encephalopathy, CJD, vit B12 def, hypomag, hypothyroid

A

Vitamin B12 deficiency

85
Q

50 yo Italian male who has recently had an eye operation presents with a change in personality namely irritability. Brain scan revealed abnormality in the thalamic region
?Hypocalcemia, meningitis, neurosyphillis, hypercalcemia, WE, Korsakoff’s encephalopathy, CJD, vit B12 def, hypomag, hypothyroid

A

CJD
Variant CJD: onset in young adults, 13-14 months duration. Prominent psychiatric sx, painful dysasthesias. Neurological signs delayed. Periodic sharp waves absent. Pulvinar sign on MRI which is symmetrical hyperintensity of pulvinars (posterior) thalamic nuclei. Sign present in 100% of cases diagnoses with FLAIR imaging.
Florid plaques on histopathology. Dense core with paler outer layer of amyloid fibrils surrounded by spongiform change.
Sporadic- most common. 5-6th decade. 44-5 month duration. Dementia early (ataxia, myoclonus). periodic shrp and slow wave complexes present.
Synchronous triphasic sharp wave complexes at 1-2 h.
Signal hyperintensity in caudate nucleus and putamen on diffuse weighted and FLAIR MRI.

86
Q

67 yo G started on Venlafaxine 2 weeks ago, presents with confusion, headache and muscle cramps and has a seizure in ED. sodium is 115
?Water intoxication, WE, serotonin syndrome, NMS, inappropriate SIADJ, hyperparathyroidism, addison’s , korsakoff’s psychosis, hypothyroidism, neuropsychiatric SLE

A

SIADH

Low serum osmolality and low serum sodium with increased urine osmolality

87
Q

23 yo woman who is intoxicated comes to the ED appears confused and cross eyed
?Water intoxication, WE, serotonin syndrome, NMS, inappropriate SIADJ, hyperparathyroidism, addison’s , korsakoff’s psychosis, hypothyroidism, neuropsychiatric SLE

A

Wernicke’s encephalopathy
Confusion, ataxia, opthalmoplegia
Mammillary bodies, mamillothalamic tract, anterior thalamus key structures involved.

88
Q

52 yo F with depression complains of feeling cold and easily fatigues on exertion
?Water intoxication, WE, serotonin syndrome, NMS, inappropriate SIADJ, hyperparathyroidism, addison’s , korsakoff’s psychosis, hypothyroidism, neuropsychiatric SLE

A

Hypothyroidism

89
Q

32 yo F with diagnosis of BPAD on mood stabilisers presents with loin pain, worsening of mood and lethargy
?Water intoxication, WE, serotonin syndrome, NMS, inappropriate SIADH, hyperparathyroidism, addison’s , korsakoff’s psychosis, hypothyroidism, neuropsychiatric SLE

A

Hyperparathyroidism
Lithium is associated with hypothyroidism, hyperthyroidism, hyperparathyroidism and hypoparathyroidism. Hyperpara- “bones, stones, abdominal groans and psychic moans”
Loin pain- renal stones

90
Q

23 yo M diagnosed with treatment resistant schizophrenia is started on Clozapine due to its unique mechanism
?Serotonin dopamine antagonist w/ strong affinity D2, glutamate R, SR antagonist, serotonin dopamine antag with rapid dissociation from D2, strong D2 block, SR agonis, kainate R, downreg of DA R supersensitivty of DA R, normal psychopath of Schziophrenia

A

Serotonin DA antag with rapid dissociation of D2

91
Q

22 yo M with untreated acute psychosis, neuroleptive naive presents with slow writhing movements of his neck
?Serotonin dopamine antagonist w/ strong affinity D2, glutamate R, SR antagonist, serotonin dopamine antag with rapid dissociation from D2, strong D2 block, SR agonis, kainate R, downreg of DA R supersensitivty of DA R, normal psychopath of Schziophrenia

A

Normal psychopathology of Schizophrenia
Abnormal dyskinesis in Schizophrenia documented for 140 years
Need to differentiate this from neuroleptic induced movement disorder

92
Q

42 yo F with long standing Schizophrenia, on typical depot preparation presents with chewing and writhing neck movements
?Serotonin dopamine antagonist w/ strong affinity D2, glutamate R, SR antagonist, serotonin dopamine antag with rapid dissociation from D2, strong D2 block, SR agonis, kainate R, downreg of DA R supersensitivty of DA R, normal psychopath of Schziophrenia

A

Supersensitivity of DA R
Upregulation of DA R responsiveness leads to supersensitivity
Neurodegeneration secondary to lipid peroxidation and excitotoxicity

93
Q

A new development targeting drug antagonists at the R
?Serotonin dopamine antagonist w/ strong affinity D2, glutamate R, SR antagonist, serotonin dopamine antag with rapid dissociation from D2, strong D2 block, SR agonis, kainate R, downreg of DA R supersensitivty of DA R, normal psychopath of Schziophrenia

A

Glutamate R

94
Q

32 yo G who was changed from Olanzapine to Ziprasidone for weight gain, showed a 6kg weight decrease
?Serotonin dopamine antagonist w/ strong affinity D2, glutamate R, SR antagonist, serotonin dopamine antag with rapid dissociation from D2, strong D2 block, SR agonis, kainate R, downreg of DA R supersensitivty of DA R, normal psychopath of Schziophrenia

A

Serotonin R agonism
R most associated with wt gain= 5HT2Cm H1m H3 autoreceptors
M3 antagonism induces alterations in glucose metabolism due to reduction in insulin secreion and increased insulin resistance
SGA also stimulate Ghrelin release which has an active role in the homeostasis of glucose and insulin secretion
They also stimulate release of orexin from Lateral hyothalamus, increasing appetite. Increased orexigenic activity occurs due to blockade of histamine R.
Leptin levels which control insulin sensitivity, are increased by Ziprasidone’s potent 5HT1A agonism and modest 5HT2C R antagonist, which along with synaptic reuptake inhibitor of serotonin and NE potentially increases metabolic rate and decreases appetite

95
Q

A female therapist comes back from a 3 week leave to see her client who is homosexual says he has changed and had a date with a lady he met at a cafe
?anger turned inwards, splitting, acting out, persecutory spiral, erotic countertransference, projective identification, transference, ambivalence, projection, displacement

A

Ambivalence

96
Q

A young lady complains about how difficult her mother is and how demanding she was on her recent visit. he therapist agrees with the patient. The patient then opposes the therapist and supports the mother
?anger turned inwards, splitting, acting out, persecutory spiral, erotic countertransference, projective identification, transference, ambivalence, projection, displacement

A

Persecutory spiral
escalating destructive interaction between both the patient and therapist feels persecuted.
Factors are “all knowing, authoritarian, and rigid attitudes and beliefs”

97
Q

Middle aged man who had marital discord for years. His wife died recently and new he says its all because of him. He is guilty and has suicidal thoughts
?anger turned inwards, splitting, acting out, persecutory spiral, erotic countertransference, projective identification, transference, ambivalence, projection, displacement

A

Anger turned inwards

98
Q

A therapist has a patient with borderline personality disorder who is seductive towards the therapist. After a few weeks the therapist develops feelings of attraction towards the patient
?anger turned inwards, splitting, acting out, persecutory spiral, erotic countertransference, projective identification, transference, ambivalence, projection, displacement

A

Erotic countertransference

99
Q

A woman who is attracted to her fellow workers accuses him of sexual advances
?anger turned inwards, splitting, acting out, persecutory spiral, erotic countertransference, projective identification, transference, ambivalence, projection, displacement

A

Projection

100
Q

Primitive defence mechanisms

A

Acting out- rather than remember and tolerate difficult past experiences, the patient will enact them.
Splitting- person will divide off parts of themselves that they find bad
Projection- split off parts attributed to other people
Projective identification- projected part taken on by other person who is then affected ad may react
Idealisation/denigration- ensures person does not have to tolerate ambivalence
Dissociation- patient will absent himself from reality s as to not be in contact with painful feelings/thoughts

101
Q

Immature neurotic defences

A

Undoing/Magical thinking- person will feel that ding a certain thing will magically negate an unacceptable thought or wish
Isolation of affect attempting to avoid a painful thought or feeling by objectifying and emotionally detaching oneself from the feeling
Identification with the aggressor- person takes on the abusive aspects of the abuser, so as to not feel victims of abuse themselves
Displacement- channelling a feeling or thought from its actual source to something or someone more acceptable.
Reaction formation- adopting beliefs, attitudes, and feelings contrary to what you really believe
Rationalisation- justifying thoughts, feelings and actions using logical, plausaible explanations

102
Q

Mature defence mechanisms

A

Sublimation- redirecting unacceptable instinctual drives into personally and socially acceptable channels
Altruism- selflessly acting for others and thereby avoiding the difficulty of attending to one’s own needs.
Humor

103
Q

70 yo female who has been on dothiepin for many years presents with slow movements oon face and extremities. She has never been exposed to a neuroleptic and has no family history of movement disorders
?NPH, huntington’s, blepharospasm, TD, CJDm senile chorea, PD, SNP, T dystonia, Hemiballismus

A

Senile chorea- gradual onset of symmetric chorea with slow progression and specifically excluding mental deterioration, emotional disturbances or family history. To rule out possible HD, genetic testing is recomended because FHx can be inaccurate and distinguishing age related mental changes and early features of HD in an elderly person may be difficult

104
Q

50 yo man has been on SSRI for many years, now has stiffness of his right hand and a low frequency tremor?NPH, huntington’s, blepharospasm, TD, CJDm senile chorea, PD, SNP, T dystonia, Hemiballismus

A

Parkinson’s disease

  1. Resting tremor
  2. Rigidity
  3. Bradykinesia - micrographia, hypomimia, hypophonia
  4. Postural instability

REM behaviour disorder- loss of normal atonia during REM sleep, “act out their dreams”
Prominent autonomic dysfunction esp urinary incontinence or profound orthostatic hypoT, may suggest MSA (Shy Drager Syndrome) rather than Parkinson’s.

Loss of DA neurons of SN pars compacta.
Lewy bodies and Lewy neuritis
Levodopa + carbidopa (PDI)
MAOi B treatment in early disease
Pramipexole provide mod symptomatic benefit and delay development of dyskinesia compared to levodopa
DBS- 3 key gray matter structures, the thalamus, globus pallidus, and STN (most targeted site)

105
Q

50 yo M on fluphenazine for years has now developed arching of trunk backwards
?NPH, huntington’s, blepharospasm, TD, CJDm senile chorea, PD, SNP, T dystonia, Hemiballismus

A

Tardive dystonia

106
Q

65 yo M on risperidone for years now has developed slow writhing movements of heald and neck to right side
?NPH, huntington’s, blepharospasm, TD, CJDm senile chorea, PD, SNP, T dystonia, Hemiballismus

A

Tardive dyskinesia

107
Q

32 yo M who complains of an excessive focus on not getting much sleep. He has difficulty falling asleep at his bedtime but has no difficulty falling asleep during other periods of inactivity
?Narcolepsy, psychophysiological insomnia, parasomnias, nightmares, somnambulism, sleep tremors, RLS, paradoxical insomnia, cataplexy, REM sleep disorder

A

Psychophysiological insomnia. Heightened arousal and learned sleep-preventing associations resulting in insomnia with associated decreased functioning during wakefullness.

108
Q

17 yo boy presents with recurrent episodes of abrupt awakening with intense fear, rapid breathing and sweating. On awakening he is confused, and disorientated and is not able to recall what woke him up
?Narcolepsy, psychophysiological insomnia, parasomnias, nightmares, somnambulism, sleep tremors, RLS, paradoxical insomnia, cataplexy, REM sleep disorder

A

sleep terrors
NREM sleep arousal disorder
Recurrent episodes of abrupt terror arousals from sleep, beginning with panicked scream, intense fear and signs of autonomic arousal
Relative unresponsiveness to effort to comfort the individual during the episode.
Little or no recall of dream imagery
Amnesia for episode
Sleep studies demonstrate that sleep terrors occur during stage 3 and 4 NREM sleep

109
Q

A 50 yo man with parkinsonism is brought in by his wife reporting that he is often found kicking and punching in his sleep and has hurt her as a result. He recalls his dreams vividly
?Narcolepsy, psychophysiological insomnia, parasomnias, nightmares, somnambulism, sleep tremors, RLS, paradoxical insomnia, cataplexy, REM sleep disorder

A

REM sleep disorder
DSM 5- recurrent episodes of arousal during sleep associated with vocalisation/or complex motor behavioyrs that arise during REM.
Either presence of REM sleep without atonia on polysomnograph or an established synucleinopathy diagnosis (PD, MSA) is a criterion.
Pontine nuclei may be involved anatomically. Studies have suggested that RBD may be associate d with alpha-synnuclein mediated degeneration of sleep regulating nuclei in the pontine tegmentum. Clonazepam is effective. AD such as mirtazapine and Venlafaxine can worse RBD. L-dopa is indicated in whom RBD is associated with PD

110
Q

A 55 yr old female complains of lack of sleep due to a constant urge to move her legs mainly at night due to unpleasant sensations in her legs.
?Narcolepsy, psychophysiological insomnia, parasomnias, nightmares, somnambulism, sleep tremors, RLS, paradoxical insomnia, cataplexy, REM sleep disorder

A

Restless legs syndrome
Symptoms increase in the evening, especially when a person is lying down and remaining still. Dysesthesias cause difficult falling asleep and are often accompanied by periodic limb movements. 85%. Iron deficiency anemia is important to rule out. Medications used in treatment include- Dopaminergic agents (pramiprexoles, bromocriptine, L dope/carbidopa, iron supplements, anticonvulsants, clonazepam, clonidine,
Paradoxical insomnia- complaint of severe insomnia, in the context of no objective evidence of sleep disturbance

111
Q

60 yo M presents with first episode psychosis, AH, and visual difficulties with light reflex absent on examination
?MRI- T1 weighted, serum VDRL, MRI- sella turcica, MRI-T2, SPECT, serum prolactin, CSF examination of lymphocytes and protein, brain biopsy, CSF for VDRL, RPR

A

CSF for VDRL

112
Q

30 yo M presents with dysphoria, ataxia and involuntary movements of the upper and lower limbs
?MRI- T1 weighted, serum VDRL, MRI- sella turcica, MRI-T2, SPECT, serum prolactin, CSF examination of lymphocytes and protein, brain biopsy, CSF for VDRL, RPR

A

SPECT- for huntington’s
can show caudate and putamen hypometabolism
functional nuclear imaging, evaluate regional cerebral perfusion.

113
Q

40 yo F who has been on risperidone depot for 10yrs complaining of galactorrhea, headache and homonymous hemianopia
?MRI- T1 weighted, serum VDRL, MRI- sella turcica, MRI-T2, SPECT, serum prolactin, CSF examination of lymphocytes and protein, brain biopsy, CSF for VDRL, RPR

A

MRI- sella turcica

Prolactinoma

114
Q

32 yo F presents with 2 wk history of depression and deteriorating vision in her left eye with dipolpia on lateral gaze
?MRI- T1 weighted, serum VDRL, MRI- sella turcica, MRI-T2, SPECT, serum prolactin, CSF examination of lymphocytes and protein, brain biopsy, CSF for VDRL, RPR

A

MRI T2 weighted
MS is key diagnosis
hyperintense lesions which are plaques

115
Q

Subarachnoid hemorrhage
?Dopamine transporter scan, PET scan, MRI visualisation of pulvinar nuclei, CT scan, SPECT, FLAIR, raclopride SPECT scan, pneumoencephalography, cerebral angiography, nerve conduction studies

A

CT scan

116
Q

MS
?Dopamine transporter scan, PET scan, MRI visualisation of pulvinar nuclei, CT scan, SPECT, FLAIR, raclopride SPECT scan, pneumoencephalography, cerebral angiography, nerve conduction studies

A

FLAIR - more sensitive than T2 in detectioin of periventricular plaques. Location can be infratentorial, deep white matter, periventricular, juxtacortical or mixed white grey matter lesions

CT- non-specific. Plaques can be homogenously hypoattenuating
MRI T1- black holes hypointense lesions, venus necklace (Callososeptal interface may have hypointense lesions),
T2 hyperintense lesions, ependymal dot dash sign, alternating small foci of hyperintensity alog callososeptal interface

117
Q

Variant CJD
?Dopamine transporter scan, PET scan, MRI visualisation of pulvinar nuclei, CT scan, SPECT, FLAIR, raclopride SPECT scan, pneumoencephalography, cerebral angiography, nerve conduction studies

A

MRI visualisation of pulvinar nuclei

High intensity signal bilaterally in the pulvinar nuclei of the Thalamus is considered a useful sign in CJD

118
Q

Differentiating Alzheimers from lewy body
?Dopamine transporter scan, PET scan, MRI visualisation of pulvinar nuclei, CT scan, SPECT, FLAIR, raclopride SPECT scan, pneumoencephalography, cerebral angiography, nerve conduction studies

A

Dopamine transporter scan

86/5% sensitivity

119
Q

Explore D2/D3 receptor binding
?Dopamine transporter scan, PET scan, MRI visualisation of pulvinar nuclei, CT scan, SPECT, FLAIR, raclopride SPECT scan, pneumoencephalography, cerebral angiography, nerve conduction studies

A

Raclopride SPECT scan

120
Q

55 yr old female presents with dysarthria and hypokinesia
?Huntington’s disease, CJD, Binswanger’sdisease, HIV dementia, Multiple sclerosis, benign intracranial hypertension, Kluver Bucy syndrome, Parkinson’s disease, neurosyphillis, progressive supranuclear palsy

A

Parkinson’s disease

121
Q

A 35 yo IV drug user presents with forgetfullness, poor concentration, apathy and withdrawal
?Huntington’s disease, CJD, Binswanger’sdisease, HIV dementia, Multiple sclerosis, benign intracranial hypertension, Kluver Bucy syndrome, Parkinson’s disease, neurosyphillis, progressive supranuclear palsy

A

HIV dementia
presentation predominantly those of subcortical dementia
deficits in cognitive, motor and behavioural domains

122
Q

35 yo with chronic hypertension presents with gradually deteriorating memory
MRI reveals white matter demyelination in the periventricular area
?Huntington’s disease, CJD, Binswanger’sdisease, HIV dementia, Multiple sclerosis, benign intracranial hypertension, Kluver Bucy syndrome, Parkinson’s disease, neurosyphillis, progressive supranuclear palsy

A

Binswanger

Subcortical leukoencephalopathy

123
Q

A 65 yo M with severe head nijury shows hyperororailty, inappropriate sexuality and hypermetamorphosis
?Huntington’s disease, CJD, Binswanger’sdisease, HIV dementia, Multiple sclerosis, benign intracranial hypertension, Kluver Bucy syndrome, Parkinson’s disease, neurosyphillis, progressive supranuclear palsy

A

Kluver Bucy
Bilateral lesions of anterior temporal lobe
visual agnosia, excessive oral tendency, hypermetamorphosis (excessive visual attentiveness), placidity with loss of normal fear and anger responses, altered sexual behaviour, indiscriminate hypersexuality, changing in eating behaviours
Occurs as a consequence of neurological disorders that cause destruction/dysfunction of bilateral mesial temporal lobe structures
(TL epilepsy, Picks, Alzheimers, cerebral trauma, CVA, herpetic encephalopathy, heat stroke)

124
Q

Comprehension is impaired and speech consists of paraphasias
?Global aphasia, conduction aphasia, wernicke’s, dysarthria, alexia, broca’s aphasia, transcortical mortor aphasia, progressive fluent aphasia, pure word deafness

A

Wernicke’s aphasia

Posterior superior temporal lobe

125
Q

This aphasia is most associated with depression, right hemiparasesis and hemisensory loss
?Global aphasia, conduction aphasia, wernicke’s, dysarthria, alexia, broca’s aphasia, transcortical mortor aphasia, progressive fluent aphasia, pure word deafness

A

Broca’s aphasia

126
Q

Conprehension is intact but speech is fluent with paraphasias and neologisms
Repetition is impaired
??Global aphasia, conduction aphasia, wernicke’s, dysarthria, alexia, broca’s aphasia, transcortical mortor aphasia, progressive fluent aphasia, pure word deafness

A

Conduction aphasia
Central dysphasia, syntactical dysphasia)
Repetition of speech is severely impaired. Wernicke’s and Broca’s areas are spared and the connection between them arcuate fasiculus is involved.
No ifs ands or buts on MMSE

127
Q

Repetition is intact, but speech is non-fluent
?Global aphasia, conduction aphasia, wernicke’s, dysarthria, alexia, broca’s aphasia, transcortical mortor aphasia, progressive fluent aphasia, pure word deafness

A

Transortical motor aphasia. The broca’s. wernickes and connection are intact but the whole system is cut off from other parts of the cortex. In transcortical sensory, presentation is similar to Wernicke’s, but repetition is intact. Echholalia is prominent. In transcotical motor, presentation is similar to Broca’s, but repetition is intact.

128
Q

Lack of awareness of neurological deficit
?Hemisomatagnosia, simultanagnosia, visual object agnosia, prosopagnosia, heuautoscopy, apprecetive visual agnosia, color agnosia, anosognosia, associated visual agnosia, autotopagnosia

A

Anosognosia- lack of awareness of disease. R) hemisphere damage is the hallmark, but bilateral damage is frequently reported. Deficit seems to be equally frequent in frontal, parietal and temporal cortical structures.

129
Q

Inability to recognise, move or point on command, various parts of the body
?Hemisomatagnosia, simultanagnosia, visual object agnosia, prosopagnosia, heuautoscopy, apprecetive visual agnosia, color agnosia, anosognosia, associated visual agnosia, autotopagnosia

A

Hemisomatognosia
(Hemidepersonalisation/Asomatognosia) Patient feels like the limbs on one side are missing. Involvement of the parietal lobe.

130
Q

Patient recognises the object, but is unaware of it use
?Hemisomatagnosia, simultanagnosia, visual object agnosia, prosopagnosia, heuautoscopy, apprecetive visual agnosia, color agnosia, anosognosia, associated visual agnosia, autotopagnosia

A

Associative visual agnosia- oerception is intact, but person does not recognise the object

In visual object agnosia- object cannot be named by sight, but is readily identified by other means, such as touch or hearing.

131
Q 
Prosopagnosia?
Colour agnosia?
Simultanagnosia?
Finger agnosia?
Autoscopy? Heuautoscopy
A

Inability to recognise familiar faces- defects in fusiform gyrus

Defective appreciation of the different skin colours, and fail to relate colours to objects correctly, even though primary colour vision is intact- dominant occipital lobe

Pt fails to recognie meaning of a complex picture, whilst detailsare correctly appreciated- post occipitoparietal lobe

Inability to recognise, name, identify, indicate or select individual fingers- dominant parietal lobe Gertsmann = f, agnosia, R/L disorientation, dyscalculia, dysgraphia. )

Doppleganger phenomenon- hallucinatory experience of one’s own body image projected into external visual space, heuautoscopy- both feels and sees awareness of presence of double

132
Q

Neurons rich in dopamine project from this area to the nigrostriatal pathway
?Angular gyrus, LC, nat geniculate nucleus, nucleus tractus solitaries, suprachiasmatic nucleus, medial geniculate nucleus, nucleus basalis, nucleus accumbens, ventral tegmental area

A

VTA

Motivation, reward and addiction

133
Q

Playing a role in reward, motivation and drug addiction
?Angular gyrus, LC, lat geniculate nucleus, nucleus tractus solitaries, suprachiasmatic nucleus, medial geniculate nucleus, nucleus basalis, nucleus accumbens,

A

Nucleus accumbens- in basal forebrain, important in reward pathway.
Mesolimbic pathway

134
Q

Major cholinergic site involved in the pathogenesis of Alzheimer’s dementia
?Angular gyrus, LC, nat geniculate nucleus, nucleus tractus solitaries, suprachiasmatic nucleus, medial geniculate nucleus, nucleus basalis, nucleus accumbens, ventral tegmental area, dorsal raphe nucleus,

A

Nucleus basalis of myenert- primary source of ACh in cerebral cortex

135
Q

Noradrenergic neurones
?Angular gyrus, LC, nat geniculate nucleus, nucleus tractus solitaries, suprachiasmatic nucleus, medial geniculate nucleus, nucleus basalis, nucleus accumbens, ventral tegmental area

A

Locus ceruleus- upper dorsolateral pontine tegmentum
immunorectiity for tyrosine hydroxylase- rate limiting enzyme for catecolamine synthsis
Arousal, attention, stress response

136
Q

Part of the brain involved in visual processing
??Angular gyrus, LC, lt geniculate nucleus, nucleus tractus solitaries, suprachiasmatic nucleus, medial geniculate nucleus, nucleus basalis, nucleus accumbens, ventral tegmental area

A

Lateral geniculate nucleus is part of the thalamus involved in visual processing and the medial geniculate nucleus is involved in auditory processing

137
Q

Involved in feeding, sexual behaviour and lactation
?Angular gyrus, LC, nat geniculate nucleus, nucleus tractus solitaries, suprachiasmatic nucleus, medial geniculate nucleus, nucleus basalis, nucleus accumbens, ventral tegmental area

A

Ventromedial

Lateral- hunger and thirst

138
Q

Associated with laughing seizures
?Orbitofrontal cortex, right subthalamis nucleus, hippocampus, inferior olivary nucleus, internal capsule, thalamus, hypothalamus, superior temporal cortex, cerebellum, amygdala

A

Hypothalamus
Gelastic seizures are epileptic events characterised by bouts of laughter.
Laughter-like vocalisation is usually combined with facial contraction in the form of a smile. GS have been related classically with hypothalamic hamartomas

139
Q

Patient pepsents with swinging movements of L arm and leg
?Orbitofrontal cortex, right subthalamis nucleus, hippocampus, inferior olivary nucleus, internal capsule, thalamus, hypothalamus, superior temporal cortex, cerebellum, amygdala

A

R subthalamic nucleus

Hemiballismus- swinging movements.
Emergence points to a sructural lesion or metabolic dysfunction in the region of the subthalamic nucleus, usually on the side contralateral to the movements.

140
Q

Patients with significant change in personality with childlike behaviour and disinhibition
?Orbitofrontal cortex, right subthalamis nucleus, hippocampus, inferior olivary nucleus, internal capsule, thalamus, hypothalamus, superior temporal cortex, cerebellum, amygdala

A

Orbitofrontal cortex

  1. inhibited, impulsive (Pseudopsychopathy), witzelsucht (jocular affect and euphoria)
  2. Medial frontal syndrome
141
Q

Patient with hypertension has a stroke. He develops and intense pain on the left side of the body
?orbitofrontal cortex, amygdala, inferior olivary nucleus, internal capsule, hypothalamus, R) subthalamic nucleus, hippocampus, cerebellum, superior temporal cortex, thalamus,

A

Thalamus
1. Translator of prethalamic inputs into readable form, 2. process and relay sensory infor selectively, 3. regulation of sleep and wakefullness, 4. Thalamo-cortico-thalamic circuits involved in consciousness/arousal, level of awareness and activity

Thalamic syndrome: contralateral hemianaethsia, often accompanied by mood swings

142
Q

The patient shows an ipaied finger nose test
?orbitofrontal cortex, amygdala, inferior olivary nucleus, internal capsule, hypothalamus, R) subthalamic nucleus, hippocampus, cerebellum, superior temporal cortex, thalamus,

A

Inferior olivary nucleus- of the cerebellum linked to finger nose

143
Q

The dose above which the risk of seizures with clozapine increases
?20-30mg/kg, 300mg, 50g, 350mg, 250mg, 100mg, 100mcg, 10mg/kg, 600mg

A

600mg

144
Q

Loading doses of valproate

?20-30mg/kg, 300mg, 50g, 350mg, 250mg, 100mg, 100mcg, 10mg/kg, 600mg

A

20-30mg/kg

145
Q

Usual maintenance dose of thyroxine

?20-30mg/kg, 300mg, 50g, 350mg, 250mg, 100mg, 100mcg, 10mg/kg, 600mg

A

100mcg

RANZCP exam preparation (119 decks)

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