New3 Flashcards

1
Q

Lithium Toxicity Signs Acute

A
  • GI - Nause, vomiting, diarrhea
  • Cardaic - can cause EEG changes but it is rare
  • Neurological - slugishness, ataxia, confusionm agitation, neuromuscular excitiability (tremor, fasciculations, myoclonic jerks)
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2
Q

SILENT

A
  • Syndrome of irriversible lithium neurotoxicity - prolonged neurological and neuropsychiatric symptoms.
  • Symptoms persist despite successful removal of the drug.
  • Cerebellar dysfunction, extrapyramidal symptoms, brainstem dysfunction, and dementia can develop as part of SILENT
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3
Q

Chronic toxicity

A
  • Neurologic - Ataxia, confusion or agitation, and neuromuscular excitability. Severe can result in seizure, nonconvulsive status epilepticus, and encephalopathy.
  • Cardiac - Can have EEG changes but its rare
  • Renal - diabetes inspidus. Volume depletion can occur, may develop hypernatremia
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4
Q

DSM-5 Depression Specifiers

A
  • Melancholic - nonreactive mood, anhedonia, weight loss, guilt, psychomotor retardation or agitation, moring worsening of mood, early morning awakening.
  • Atypical - reactive mood, oversleeping, overeating, leaden paralysis, interpersonal rejection sensitivity.
  • Psychotic - hallucination or delusions
  • Catatonic - waxy flexibility, catatonic excitement, negativism or mutism, mannerisms or stereotypes, echolalia or echopraxia
  • Anxious - tense, restless, worried, something awful may happen, afraid or losing control
  • Mixed- elevated mood, inflated self-esteem or grandosity, increase talking, racing thoughts, increase energy and activity, decrease sleep, risking impulsive activities
  • Seasonal affective - regular onset and remission of depressive episodes during particular season
  • Peripartum - onset duirng pregnancy or within 4 weeks
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5
Q

Serious (but uncommon) adverse effects of antidepressants

A
  • QT prolongation (surrogate marker for Torsafe de Pointes) is a warning for citalpram, escitalopram, and quetiapine. However, Torsade is an idiosyncratic events, and its association with antidepressant meds in unclear.
  • Long term use of SSRI - increase risk of falls and fractures
  • Hyponatremia in SSRI use in older patients
  • SSRIs can inhibit platelet aggregation by altering platelet serotonin receptors and increase risk of GI bleeds
  • Agomelatine - requires livers function testing as it has potentual to elevate liver enzymes
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6
Q

Clinically relevant drug-drug interactions

A
  • Antidepressants and antipsychotics are primarly metabolized through CYP450 enzymes
  • Agomelatine and duloxetine are metabolized via CYP1A2 pathways, and should not be coadministered with drugs that block this pathway.
  • Vilazodone is metabolized through CYP3A2 pathway and should be used cautiously when prescribed with CYP3A4 inhibitors
  • Clinically relevants interactions are usually caused by agents that are potent CYP inhibitors - fluoxetine, paroxetine, and fluvoxamine
  • Interactions with moderate CYP inhibitors (bupropion, duloxetine, and sertraline) are rarely clinically relevant except at higher doses.
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7
Q

Discontinuations Syndrome

A
  • Occurs when you stop using an antidepressant withut tapering
  • F - flu-like symptoms
  • I - insomnia
  • N - nausea
  • I - imbalance
  • S - sensory disturbances
  • H - hyperarousal
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8
Q

Adjunctive Strategies depression

A
  • Atypicals
    • Aripiprazole 2-15mg
    • Quetiapine 150-300mg
    • Risperidone 1-3mg
  • Antidepressants - mirtazapine
  • Other - lithoum, stimulatns
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9
Q

What defines a psychiatric disorder in children?

A
  • Developmentally inappropriate
  • Severity, frequency, duration are atypical
  • It impairs school performace, peer and family relationships, community activities
  • Not simply an unaccommodating environment
  • The behaviour is abnormal always
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10
Q

Evaluation of children and adolescents

A
  • Want information from multiple informants, multiple visits, and multiple forms of gathering the information
  • Review school reports, psychoeducation testing, and previous assessments
    *
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11
Q

Externalizing disorders children

A
  • ADHD
  • ODD
  • CD
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12
Q

ADHD

A
  • A neurodevelopmental disorder (disorder of brain structure and function)
  • 3 subtypes: inattentive, hyperactive/impulsive, combined
    • inattentive, distractbile, forgetful, “thoughtless”
    • Overactive, hyper, excessivelt talkative
    • Impulsive, intrusibe, insenstive, risk takers
  • M>F, however, female may be overlooked because they tend to be inattentive subtype which is less noticable.
  • In order diagnosis needs to be in multiple domains, persistent, and impairing
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13
Q

ADHD Treament

A
  • Pills and Skills
  • Stimulants - use long acting as first line treatment
    • Methylphenidate and related compounds
    • Amphetamine and related compounds
    • Must do cardiac screening if there is a family history of cardiac problems or personal history of cardiac symptoms
    • Side effects - weight loss, irritability, increase HR, and increase BP, tics if vulnerable
  • Non-stimulant - atomoxetime, bupropion, TCAs, Clonidione, Guanfacine
  • Skills - behaviour modification (parents behaviour training, school modifications), social skills training
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14
Q

ODD

A
  • Consistent pattern of negativistic, hostile, vindictive, and defiant behaviours. Generally in multiple environments, but can still have diagnosis if only in one environment
  • Behavioural management training is the treatment - parent-child interaction therapy, problem solving skills training, parent management training
  • There are no specific medications for ODD, but you can treat co-morbid conditions
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15
Q

ODD Prognosis

A
  • 2/3 will no longer meet critieria in 3 years
    • Younger age onset - more likely to continue to be symptomatic
  • Irritability sx predicts later anxiety and depression
  • Headstong sx predicts later CD
  • Hurtful (vindictive) sx predicts aggressive CD (most serious form of CD)
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16
Q

Conduct Disorder

A
  • Pattern of behaviours that is repetitve and persistnet in whcih the basic rights of others or social norms are violated
    • aggression, destruction, deceitfuless, rule violations
  • Symptoms tend to become more serious over time, may progress from overt or covert
  • Overall, 40% will progress to ASPD
17
Q

Internalizing disorders children

A
  • Anxiety disorders
  • Mood disorders
18
Q

Separation Anxiety

A
  • Developmentally inappropriate distress associated with separation
  • Separation anxiety is normal in early life and declines after age 30 months
  • Afe of onset 7-9years
  • High comorbid with other ADs
19
Q

Selective mutism

A
  • Children who are able to talk but refused to do so due to extreme anxiety. It is not social anxiety disorder, but it is very comorbid. Also comorid with notural enuresis, speech, and language delays
20
Q

Anxiety disorder treatments in children

A
  • SSRIs and CBT
  • SSRIs even in young children - you dont want to undermedicate if it can be helpful, however, you need to be cautious and thoughtful.
21
Q

Typical Antipsychotics

A
  • D2 receptor antagonism is responsible for the efficacy and side effects of the typicals. Thought that therapeutic actions is mainly due to D2 blockade in mesolimbic dopamine pathway (reduced positive symptoms). Unfortunately, in order to block an adequate number of D2 receptors in the mesolimbic D2 pathway to alleviate positive symptoms, you must stimultaneously block the same number of receptors throughout the brain, causing numberous side effects.
  • For most typicals, degree of D2 receptor binding in mesolimbic pathway needs to be 80%, while D3 receptor occupancy greater than 80% in dorsal striatum is associated with EPS and hyperprolactinemia.
  • Furthermore, since in schizophrenia mesocortibal DA pathways to DLPFC and VMPFC are thoughts to be hypoactive, administration of D2 antagonism may actually worsen these symptoms (cognitive, negative, and affective.
22
Q
  1. EPS
  2. Tardive dyskinesia
  3. Prolactinemia
A
  1. D2 blockade in nigrostriatal pathway
  2. Long-tern D2 blockade in nigrostriatal pathway can cause upregulation of these receptors, resutling in hyperkinetic movements, characterized by facial and tongue movements, and quick, jerky limb movements
  3. D2 antagonism in tuberoinfundibular pathway causes prolactin levels to rise. Can result in galactorrhea and amenorrhea
23
Q

Neuroleptic malignant syndrome

A
  • Extreme muscle rigiditym, high fever, coma, and even death. May be related to D2 receptor blockade in nigrostriatal pathway.
24
Q

Pharmacologic proterpties other than D2 blocking in typicals

A
  • Blocking of muscarinic M1-cholingeric receptors - can result in side effects such as dry mouth, blurried vision, constipation, and cognitive blunting.
    • May explain different rates of EPS among typicals. Specifically, increase EPS= weak anticholingeric properties; derease EPS= stronger anticholingeric properties (increase muscarinic blackage may reduce RPS due to the fact that dopamine and acetylcholine have a reciprocal relationship with each other in the nigrostriatal pthway.
  • Blockade of histamine H1 - causes weight gain and drowsiness
  • Blockade of alpha1- adrenergic - cause cardiovascular sie effects such as orthostatic hypotension and drowsiness
25
Q

Atypical Antipsychotics

A
  • Works effectively on positive symptoms, but low EPS, and less hyperprolactinemia when compared to they typicals.
  • Are considered serotonin-dopamie antagonists, with stimultaneous serotine 5HT2A receptor antagonism + D2 antagonis
    • Though that 5HT2A are “brakes” on DA release in the striatum and thus by antagonizing these receptors it actually stimulates downstream DA release in the striatum (reduced EPS)
  • 5HT2A also prevents hyperprolactinemia because serotonin usually promotes prolactin release (where DE blocks its). Thus, even though DA is blocked, promoting prolactin release, the antagonism of serotonin makes it so serotonin can no longer stimulated prolactin release.
  • “Pines” and “Done” bind more potently to 5HT2A receptor than D2
26
Q

Atypcials non Dopamine or serotonin binding

A
  • Potent antihistamine actions - clozapine, quetiapine, olanzapine, and ibperidone are all more potent H1 antagonists than D2 antagonists. All other antipsychotics have moderate potency, except lurasidone, which has no H1 bindings.
  • Potent anticholinergic actions - only clozapine, quetiapine, and olanzapine have high potency for muscarinic receptors
  • Potent alpha1 adrenergic antagonism - all atypicals have at least moderate bindings. Most potent are clozapne, quetipine, risperdione, and iloperidone
27
Q

Cardiometabolic actions atypicals

A
  • All atypicals carry risk for metabolic syndrome
  • High risk - clozapine, olanzapine
  • Moderate risk - risperidone, paliperidone, quetiapine, iloperidone (weight only)
  • Low risk - ziprasidone, aripiprazole, lurasidone, iloperidone, asenapne, brexpiprazole, cariprazine
  • Pharmacologic mechanisms for what propels people along the “metabolic highway” is not fully understood. Starts with appetite and weight gain, and progresses to insulin ressitance and increase TG levels. Hyperinsulinemia advances to B-cells failure, prediabetes, and then diabetes. Thought to be, at least partially, due to blocking of the H1 and 5HT2c receptors which leads to increase appetite. However, this does not fully explain the progression of metabolci syndrome. Furthermore, pateitns can experience the insulin resistance and dyslipidemia eben before gaining any weight.
28
Q

Benzodiazepines

A
  • Benzodiazepines work by bindings at the GABA-A ligand-gate chloride chanel compex. They enhance the inhibitory effects of GABA.
  • These drugs are rarely fatal in overdose, but can be deadly if combined with opioids or alcohol, generally, these overdoses are accidental
    • These drugs all supress breathing but in different ways - benzos and alcohol through GABA-A inhibiton and opioids through the medulla.
29
Q

Benzodiazepines in the elderly

A
  • Two major risk factors - falls and cognitive impairment
    • Falls - can lead to fractures, which can be fatal
    • Cognitive side effects of benzos tends to worsen over-time. Cognition gradually improves after drug is discontinued, but some impairment is still detectable up to one year
30
Q

Benzodiazepines fasting-acting to longest acting

A
  • Alprazolam > Lorazepam > Clonazpam > Alprazolam XR
  • Diazepam - acts quickly and lasts a long time
31
Q

Doses Benzos

A
  • Alprazolam
    • Anxiety - 0.25-0.5mg TID
    • Panic disorder - 0.5 TID
  • Lorazepam
    • Insomnia - 0.5-1mg HS
  • Clonazepam
    • Anxiety and panic - 0.25-0.5 BID
    • Seizure - 20mg/day
  • Diazepam
    • Anxiety/seizure - 2-10mg BID-QiD