Shame, stain or mockery, because we are ignorant in mental illnesses it is difficult to accept, when we know it is a brain disease there is no more stigma

What is the percentage of people w/mental disordes?

1/4 of people will have mental disorder in their life, and the most serious obstacle for treatment will be stigma.

What are some fallacies and myths regarding mental illness?

Mental illness pt are violent and dangerous, unpredictable, irrational, retarded, lack willpower, incurable, cannot get into a relationship, toxic mediactions and talking therapies are useless. If we think about it most of diseases are chronic, and their treatments are chronic ones, just like mental illness drugs. Psychiatry is stigmatized since it is thought that they are unable to treat patients, saves people from dangerous people

What are the consequences of stigma?

Delay for diagnosis, poor access to mental and physical healthcare, reduced life expectancy, exclusion from higher education and employment, increased risk of contact with criminal justice systems, victimization, poverty Worst Outcome in psychiatry is Suicide, criminals are not psych pts, they are held accountable.

What is the genetic basis of suicide and mental illness?

We have in our genes the instinct of survival, but w/some diseases we get to suicide Ernest Hemingway (nobel prize, suicide, 5 suicides in family) Charolette Salomon (6 suicides in 4 gens) Van Gogh (was bipolar and shot himself) Elevated expression of Glutamate receptors in NE neurons from locus coeruleus in MDD is seen (higher NMDA receptor subunits, GRIN2B and GRIN2C and metabotropic receptor genes GRM4 and GRM5 all in locus coeruleus. Antagonists of Glut receptors reduce depressive symptoms faster than antidepressants, as glut is a prominent excitatory input to the NA LC so LC becomes overactive in MDD.

What is mood? What is affect?

Mood (sustained emotional state and how you subjectively feel) Affect (expression of mood observable) these two are used interchangbly but shouldn't be confused Mood episodes include depressive episodes , hypomanic episodes and manic episodes (w/ or w/o mixed features) Note that manic and hypomanic episodes are only seen in bipolar disorder

What are the depressive disorders?

Most important is major depressive disorder. others are disruptive mood dysregulation disorder, persistent depressive disorder (dysthymia), presmenstrual dysphoric disorder, substance-induced depressive disorder, other specific depressive disorder. They come in a spectrum, may get many small episodes or one big one

What are the MDD diagnostic criteria?

5+ of the following present most of the day nearly everyday for at least 2 weeks 1-depressed mood 2-Loss of interest or pleasure in all activities 3-Significant weight changes 4-Insomnia/Hypersomnia 5-Psychomotor Agitation/Retardation 6-Fatigue 7-Feeling worthlessness guilt 8-Diminished ability to think/concentrate 9-Recurrent thought of death/suicide These symptoms will cause a significant impairment of social, occupational or other important areas of functioning.

What is the definition of MDD?

Malady of stress adaptation in brain or disorder of stress response and adaptation (neuroplasticity)

What is the DD of MDD?

Hypothyroidism, hyperthyroid, hyperpara, addison, cushing, toxoplasmosis, mono, AIDS, RA, MS, Parkinsons, Abdominal cancer Hypothyroidism increased risk of MDD 3.56 pts, and anxiety disorders 2.32 pts Meds (steroids, reserpine, methyldopa, BB, cimetidine, indomethacin, cycloserine, vincristine, vinblastine).

What are diagnostic instruments used in MDD?

Structured interviews to dx MDD (MINI, SCID-5, CIDI, highly specific and sensitive, but used for research not therapy) Scales (BDI, HAMD, not diagnostic, gives severity)

How is epidemiology of depression?

20% of primary care pt have depressive symptoms, 2 time more in females, 2/3 have multiple episodes, each episode increases the risk of recurrence. Prevalence is unrelated to race, education , income or civil status, lifetime rates vary across countries (1.5-20%) Lifetime prevalence (16.2%) and 12 months (6-6%) Nationally, 1/6 met criteria for at least one year DSM V CIDI disorder, 27% serious and 36% moderate, MDD 5% 11% 1 year disorders got tx, 2/3 of tx are given by GP not psychiatrist Lifetime prevalence in Lebanon 26% (anxiety 16% mood 13% and substance use 2%) delay very much between onset and tx (6-28 years), war increased risk of first onset anxiety and mood disorder

How is the increasing importance of depression?

4th rank among major causes of disability worldwide in 2000, and became 2nd in 2020

What are biological etiologies of MDD?

We have molecular susceptibility genes, protective genes and transcription factors (BDNF, CREB,PCK) that predispose cell growth, and environment will affect growth, neurotransmission and neural networks then early life adverse effects will cause behavioral cognitive and sensory motor disruptions. Study of influence of life stress on depression revieled that genotype alone is not sufficient to predict depression, 5-HT transporter gene needs envirnomental life stress to cause depression, life events alone can cause it and if combined with genetics (5-HT transporter) doubled the risk short allele (s allele) of 5-HT transporter is strongly associated with stress sensitivity increase (childhood maltreatment and specific medical conditions) We get glial hypoactivity and death

How is the physiology of stress?

Normal physio, stress causes CRF release from PVN of hypothalamus, then ACTH release from ant pituitary then increased cortisol then mobilize energy as response to threat High cortisol will cause increased cell death in hippocampus (apoptosis), brief exposure will increase hippocampal activity helps remember acute stressor. Hippocampus - feedback on cortisol after we learn about the stressor. if more cortisol, less - feedback, keeps cortisol high so chronic stress causing hippocampal cell death, MI, ventricular arrhythmias, increased catecholamines thus atherosclerosis and HTN, cortisol antagonizes insulin and causes dyslipidemia

What are serotonin and NE pathways in brain?

Raphe nucleus, to sleep centers, frontal cortex, hypothalamus, limbic system and basal ganglia (serotonin) and LC to cerebellum, frontal cortex, limbic system and hypothalamus (NE) Role of monoamines (serotonin, NE and dopamine balance excitatory mechanisms in brain and prefrontal cortex (logic) and limbic system (emotions), any dysregulation causes depressive symptoms (cortex: depressive mood, hypothalamus weight change and pleasyre loss, limbic guilt and suicidal thoughts...

What is role of NE and serotonin in BDNF synthesis?

Serotonin and NE aid in BDNF synthesis, which is important for cell development and if inactivated leads to cell death So neurogenesis is upregulated by BDNF enriched environment, exercise, learning and antidepressants, and is downregulated by stress, adrenal steroids, age and drugs of abuse. Antidepressants may normalize BDNF levels promoting serotonin and NE conduction

What are stressful triggers for depression?

Stressful events undergo kindling phenomenon, when increased depressive episodes, we get increased risk of depression with decreased association with stressful life events.

What are brain areas regulating the mood?

Frontal cortex (cognitive function and attention), hippocampus, nucleus accumbens (reward), amygdala (emotions), hypothalamus (sleep, apetite, sex), ventral tegmental area (dopamine projections), dorsal raphe nuclei (serotonin projections), locus coeruleus (NE projections)

How is depression and inflammation?

Increased level of proinflammatory cytokines (IL6, IL1 and TNF-a), there is a direct correlation between severity of depression and cytokine elevation, celecoxib (COX-2 inhibitor), TNF-a antagonists showed antidepressant properties. There is an interplay between depression and inflammation, leading to obesity and diabetes in addition to other depression mediators

Who are the psychology talkers in etiology of MDD?

Freud and Beck

What is the relation between nurture and MDD?

Both adopted and non-adopted children w/mother w/MDD are likely to get MDD Childhood adversity increases risk of adulthood disease. effects of childhood trauma (mostly emotional and physical abuse + neglect, sex, separation, divorce and hospitalization.

How is course and comorbidities of MDD?

5 Rs of mental illness: after an episode, the patient gets response (better), then remission (stops episode) then relapse (another episode), then Recovery (complete resolution) then recurrence (after total recovery) Usually recurrence risk increases with episode numbers (1st episode: 50%, 2nd 70%, 3rd >90%) Comorbidities (CAD1 18% w/episode, MI 16% 6 months post MI, Cancer during illness 20-25%, HIV 1 year 36%, migraine lifetime 22-32%, alzheimer in episode 17-31%, MS lifetime up to 50% Depression in patients in 2 times more than normal individuals, up to 30% in acute hospitalized pt.

How is depression and CVD?

Depression doubles CV mortality/events, possible causes include sympathetic actiavtion, platelet reactivity and immune system reactions. Depression is associated w/2.7 times increased mortality risk of IHD independently of IHD risk factors.

How is depression and cancer?

MR >25% in pt w/depression symptoms and >39% in pt dx w/major/minor depression, without effect of diminishing those effects. Study of lebanon breast cancer w/depression, mixed cancer: psych comorbidity 46%, MDD 16% and minor depression 17.6%. Psychiatric morbidity increase MR by 4.13 times, and depression in breast cancer is 14%, cancer is diagnosed 70% in late stage due to health definition in middle east MDD can be influenced by social support of cancer patients, not related to treatment stage and related to stage of disease

How is religiousity with MDD?

No correlation between it and depression by study in syria pre and post war, even no difference for gender, demographics.

What is the Hamilton depression rating scale?

Treatment effect score,17 items, score from 0-52, MDD if above 15, 7-15 we are getting a response >50% reduction, <7 remission 67% of pt respond to antidepressants, 33% remit w/any type of AD, after 1 year of treatment w/4 ADs 67% will remit, relapse is less for pt who achieve remission

What are antidepressants indication?

Mood disorders (MDD, dysthymia, subthreshold depression, bipolar [combine with mood stabilizer], schizoaffective depressed type) Anxiety disorders (OCD, panic, GAD, PTSD, SAD) Impulse control disorders (Kleptomania, complusive shopping, trichotilo, binge eating, paraphilias) Affective-spectrum disorders (IBS, migraines, fibromyalgia, chronic pain, enuresis)

What are SSRIs?

Fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, escitalopram. Mode of action (at begining serotonin increases in somatodendritic area in midbrain raphe causing side effects, over time auto receptors downregulate and become desensitized, serotonin release isn't turned off increasing their release and neural impulse flow so therapy w/tolerance to side effects Side effects (CNS [nervousness, insomnia, fatigue, headache, tremor], GI [nausea, vomit 14%, diarrhea constipation, increased apetite and weight gain], sex [delayed orgasm, decreased libido], endocrine [DM], pregnancy [Fluoxetine OK others no data])

What are SNRIs?

Serotonin NE reuptake inhibitors, Venlafaxine XR, Desvenlafaxine XR, Duloxetine, Milnacipran Side effects (Same ass SSRI + alter blood pressure at high doses, alter heart rate, anticholinergic dry mouth, constipation and urinary retention)

What are NDRIs?

Bupropion (MDD, nicotine withdrawal, lowers seizure threshold, no sexual side effects and no weight increase)

What are SNDIs?

A2 antagonists (miratazapine (serotonin 1a agonist, others antagonist, main side effect weight gain and sedation)) SNDI action (LC [cut in brakes blocks presynaptic neurons NE increase release of NE, block presynaptic serotonin increase its release (by decreasing action)] Raphe [step on accelerator [increase NE release stimulating a1 Rs in post synaptic dendritic neurons of serotonin provoking serotonin release])

What are classic antidepressants?

Tricyclic AD's (Clomipramine, Imipramine, Amitriptyline, Nortriptyline, Desipramine, Doxepine) Actions (block reuptake pumps for NE, serotonin, serotonin 2A and 2C receptors and disinhibit DA and NE release. Overdose lethal, second-line for resistant depression) Side effects (Blockade of muscarinic cholinergic Rs M1 dry mouth, constipation and blurred vision, and M3 insulin action disruption. Histamine 1 Rs cause sedation and weight gain, a1 Adrenergic Rs cause orthostatic HTA, dizziness, and voltage-sensitive Na channels cause seizure, arrhythmia and arrest) Efficacy (acc to literature)

What are other biological/electrical treatments of MDD?

ECT (electroconvulsive therapy, severe depression w/suicide risk, psychotic features or resistant depression. Side effects include temporary memory loss, anesthesia effects) TMS, VNS, DBS Psychological therapies (psychodynamic, CBT, interpersonal therapy) Social-skills training Fitness seems to increase hippocampal volume for any age/sex/education level

What was Mozart's condition?

Incredible mental capacity but naive sometimes, he had cyclothymic disorder (mood swings), deeply religious, needs a lot of affection, loved Constanze faithful, unable to manage fincancially. Hideous laugh

How is misdiagnosis of bipolar?

69% of cases are misdiagnosed, 60% depression, 26% anxiety, 18% schizophrenia, 17% cluster B personality disorders and 14% alcohol abuse This is due to the flares and the presentation of the disorder

How is the manic episode of bipolar?

Abnormally perisitently elevated expansive or irritable mood abnormally and persistently increased goal directed energy lasting at least 1 week or any duration if it lead to hospitalization, 3 or more of [grandiosity, decreased need for sleep, more talkative, racing thoughts, distractability, increased activity, increased risky behavior], impairs social/occupational status may need hospitalization, no substance or medical condition leading to it. Note that a full manic episode during AD treatment persisting beyond physiologic effect of the AD is evidence for manic episode and bipolar I diagnosis

How is hypomanic episode of bipolar?

Abnormally elevated activity, irritability, energy for at least 4 days with 3 or more of same as manic episode effects. Episode is associated with an equivocal change in function, mood disturbance is evident, not severe enough to cause hospitalization, so if psychotic ->manic, not attributable to physiological effects of substance

What are mixed specifiers of bipolar?

1- Manic or hypomanic episode, w/ mixed features: Full criteria are met for a manic episode or hypomanic episode, and at least 3 of depressive symptoms present. 2- Depressive episode, w/ mixed features: Full criteria are met for a major depressive episode, & at least 3 of manic/hypomanic symptoms present.

What is the clinical spectrum of bipolar?

Bipolar I Disorder: characterized by the presence of at least one manic episode Bipolar II Disorder: one or more major depressive episode & at least one hypomanic episode Cyclothymic Disorder Substance/Medication-Induced Bipolar and Related Disorder Bipolar and Related Disorder Due to Another Medical Condition Other Specified Bipolar and Related Disorder Unspecified Bipolar and Related Disorder

What is bipolar disorder spectrum>

Bipolar ½ Schizobipolar disorder Bipolar I Manic-depressive illness Bipolar 1 ½ Depression w/ protracted hypomania Bipolar II Depression w/ spontaneous discrete hypomanic episodes Bipolar III Repeated depression plus hypomania occurring solely w/ antidepressant or other somatic tx Bipolar III ½ Depression, mood swings & hypomania occurring w/ substance & / or alcohol abuse Bipolar IV Depression superimposed on a hyperthymic temperament Bipolar V Recurrent depressions (≥ 5)

What is so peciuliar about bipolar?

Is it a continuum (mood episodes grading, severity, frequency, mixture of symptoms in same episode, many MDD shift bipolar in long term [first episode is depressive], residual manic episodes predict depressive recurrence, bipolar signs may be common in MDD makes difficult dx) So we have phenotype and its opposite and middle, diverse cluster of symptoms, self-lethality, multiple comorbidities, AD may be saviours or killers.

What are the 4 cluster of symptoms of bipolar?

Manic/hypomanic (euphoria, pressured speech, impulsive, irritable, violence, excess libido, reckless, social intrusiveness, diminished need for sleep) Depressive (sad, anhedonia, withdrawal, anxiety, suicide) Cognitive (racing thoughts, distractable, disorgnaized, inattetiveness) Psychotic (hallucination/delusion)

What are red flags in bipolar?

Age of onset (teens, 20s, 30s) Psychotic episodes (more common) Family hx high, temperament cyclothymic, numerous episodes, abrupt onset of episodes, postpartum increase, resistant to AD / poop out of AD treatment is common Clues for bipolar in depressive episodes that are found more in bipolar than depression are total sleep time, hypersomnia, psychomotor retardation, post-partum episodes, while weight loss is more in depressive than bipolar Other clues of bipolar in depressive disorders are seasonal depression, depression with sexual arousal, suicidal crisis

How is the transition from MDD to Bipolar?

Nearly quarter of adults w/MDD after 12-14 years followup developed BD w/greatest risk of transition in first 5 years, seen in pt w/family hx of BD, earlier age of onset of MDD and presence of psychotic symptoms

How is epidemiology of BD?

Estimates for lifetime prevalence worldwide: 0.5% to over 5%. Diagnostic assessment methods and criteria varied broadly from study to study, males=females, age onset 18-20 yrrs, no variation in ethnicity if other factors controlled, marital status is debatable whether its the cause or consequence

How is clinical assessment of BD?

Third-party information, Adequate exam time Diagnostic scales: Mood disorder questionnaire, Bipolar spectrum diagnostic scale…Longitudinal assessment, Family history. Van Gogh was thought to have it due to his difference in paintings.

What are comorbidities associated with BD?

Medical (migraine, pain disorders, DM, CVD, Obesity) Psychiatric (Personality disorders, ADHD, Impulse control, anxiety disorders, eating disorders, substance abuse) 30% obese, 43% hyperglycemia, 20% hypercholesterolemia, male, depressed/mixed and duration of illness more obesity. Older age, later disease onset and lower education more hyperglycemia Other (more hospitalization, poorer tx response, pharmaco conflicts, worse outcomes, higher suicide risk, violence) Suicide attempts most seen in Bipolar II, then Bipolar I and then unipolar

What are the objectives of BD treatments?

Control depression Control mixed specifiers Control Mania/Hypomania Relapse prevention… Control suicidality Control side effects

What are treatments of manic episodes?

FDA approved (Lithium, valproate, olanzapine, chlorpromazine, risperidone, queiapine) trials (carbamazepine, antipsychotics, ziprasidone, aripiprazole, ECT) Mood stabilizers (Mania minded [treat from above, reduce mania or stabilize it to prevent recurrence of mania], depression minded [treat from below, reduce bipolar depression symptoms or stabilize it to prevent relapse and recurrence]) 3 categories: Lithium, Anticonvulsants, and neuroleptics/antipsychotics.

How is Lithium tx?

50 years and still The Reference/first choice drug. 1- inhibition of second messenger enzymes inositol monophosphatase 2- modulation of G proteins 3- inhibition of glycogen synthetase kinase 3 (GSK3) and protein kinase C. Promotes neuroprotection long-term plasticity. Evidence as best for suicide prevention. Side effects: nausea, vomiting, and diarrhea, weight gain, hair loss, acne, tremor ... Long-term adverse effects on the thyroid and kidney -Prelithium workup: TSH, FT3, FT4, CBC, Electrolytes, BUN, Creatinine, Ca and EKG if more than 40 yrs. -Therapeutic level :0.6 - 0.9 and clinical assessment.

What are anticonvulsants tx?

Valproic acid, Carbamazepine, Lamotrigine Lamotrigine (May be effective in treatment of bipolar depression non FDA approved. FDA approved prevent the recurrence of both mania & depression ie maintenance. Well tolerated, except :rash, rarely Stevens—Johnson syndrome (toxic .epidermal necrolysis) minimized by very slow uptitration. Best as add on Mechanism of action: reduces the release of the excitatory glutamate, block calcium channel, block potassium channel

What are neuroleptics used in BD tx?

Old gen (Haloperidol, Chlorpromazine, Perphenazine, Pimozide, Zuclopenthixol) Atypical/second Gen (Risperidone, Olanzapine, Quetiapine, Lurasidone, Aripiprazole, Clozapine (for resistant schizophrenia)

What is the biggest tx challenge?

Maintenance Lifetime +++ for relapse prevention. Monotherapy (ex. Lithium…) rare. Combination is the rule +++ Regular follow-up for compliance and side-effect monitoring

Talk about stories regarding BD?

Churchill (his depression is his black dog, recorded to have manic episodes) Wolff felon committed suicide to overcome guilt Prephecy on marche sur la lune Antigone (Sopholces 441 BC Oedipus/antigone, Ismene/antigone and haemon/antigon problems, suicide (religion, family cardinal signs), Haemon suicide more emotional

What are types of addiction?

Substances (drugs, tobacco, alcohol, medications) Behavioral (gambling, sport, work, shopping, internet, sex, eating...)

How is screening for addiction?

Questions carefully designed to determine whether there is a need for more evaluation. Differs from assessment in terms of that it is just a tool of evaluation whether a problem is present (yes/no), while assessment is defining it, dx, tx recommendations... May be a single question (how many times have you used illegal drugs?) or scales/questionnaires

How is assessment of addiction?

Substance use: - type, frequency and amount - route of administration - overdose history - history of prior SUD, treatment Mental Health General Medical Family History Social History DSM5 Criteria Substance Use Disorder Substance-induced Disorders: - Intoxication - Withdrawal

What are the DSM-V criteria of SUD?

Impaired control (taken in larger amounts/longer periods than intended, persistent unsuccessful effort to cut down/control substance use, alot of time spent to get the substance use it or recover, craving/strong urge to use) Social impairment (failure in work and education by substance use, continuous usage regardless of all social issues caused by it, important social activities given up due to substance use) Risky use (recurrent use in physically dangerous situations, continuous usage despite knowledge of damage) Physical dependence (Tolerance [need for increased amount to achieve desire, or diminished effects of substance], and withdrawal [withdrawal symptoms or same substance taken to relieve the symptoms])

How do we assess SUD severity?

Mild: Presence of 2-3 symptoms Moderate: Presence of 4-5 symptoms Severe: Presence of 6 or more symptoms

What are diagnostic criteria for acute intoxication?

G1. There must be clear evidence of recent use of a psychoactive substance (or substances) at sufficiently high dose levels to be consistent with intoxication. G2. There must be symptoms or signs of intoxication compatible with the known actions of the particular substance (or substances), and of sufficient severity to produce disturbances in the level of consciousness, cognition, perception, affect, or behavior that are of clinical importance. G3. The symptoms or signs present cannot be accounted for by a medical disorder unrelated to substance use, and are not better accounted for by another mental or behavioral disorder.

What is intoxication?

Intoxication is the result of being under the influence of, and responding to, the acute effects of alcohol or another drug. The recognition of intoxication states is important in the appropriate treatment of substance-using patients Intoxication states can range from euphoria or sedation to life-threatening emergencies when overdose occurs The initial challenge to the clinician, however, is diagnosis, because intoxication can mimic many psychiatric and medical conditions. It is important to determine not only the severity of the substance ingestion but also the patient’s level of consciousness, the substances involved, and any complicating medical disorders. Often, more than one substance is involved, and it is critical to know what substances have been ingested, as well as how much of each substance.

What are diagnostic criteria of withdrawal?

G1. There must be clear evidence of recent cessation or reduction of substance use after repeated, and usually prolonged and/or high-dose, use of that substance. G2. Symptoms and signs are compatible with the known features of a withdrawal state from the particular substance or substances . G3. Symptoms and signs are not accounted for by a medical disorder unrelated to substance use, and not better accounted for by another mental or behavioral disorder.

How is addiction a developmental disease?

It starts early (1.5% <12, 67% teens, 26% 18-25 yrs, 5.5% >25 yrs) All adolescents brains are still developing, when reading emotions, adults rely more on frontal cortex while teens more on amygdala.

What is the SUD biopsychosocial model?

Biological factors (genetics [fam hx], brain chemistry [altered reward system, neurotransmitters, dependency], mental health disorders [co-occurring mental health disorders, depression, anxiety]) Psychological (self-medication hypothesis [high level of stress, coping mechanism], trauma [early trauma], personality traits [impulsive, excitement]) Social factors (peer pressure [adolescence], family environment [lack of supervision, hx of use], socioeconomic status [poverty, lack of access to education, unemployment])

What are environmental factors leading to SUD?

Availability: Easy access to substances can lead to higher rates of use and, subsequently, SUD. Cultural Norms: Societal attitudes towards substance use can influence individual behavior. Policy and Regulation: The legal status and regulation of substances affect their use and the potential for disorder.

What are genes and environment interplay in addiction?

What is the brain biology of drugs?

How is reward pathophysio?

Dopamine is central to reward in all pathways

What does prolonged use lead to?

Changes the brain in fundamental and long-lasting ways

What is driving addiction?

Positive Reinforcement - rewards that strengthen a conditioned response after it has occurred, such as the feeling of euphoria after taking a hit Negative Reinforcement – stimuli (e.g., stress, withdrawal) that are removed when the desired response (e.g., drug use) has been obtained

What are main substances in SUD?

Alcohol Cannabinoids Opiates Stimulants Psychedelics Dissociatives Ecstasy GHB Inhalants Sedatives

What are the main methods of use of substances in SUD?

Oral Intranasal (snorting, sniffing) Intravenous Subcutaneous Inhaling Smoking

What are different types of drinking?

Social (occasional, not causing problems) Harmful (causes damage, adverse social consequences) Dependence (compulsion to drink daily, gradual increase of amount to fell well)

What is the max alchohol consumption for low-risk drinking?

What is alcohol intoxication?

Recent ingestion of alcohol, one or more of the signs during/shortly after ingestion (slurred speech, incoordination, unsteady gait, nystagmus, impaired memory/attention, stupor/coma)

What are the different presentations of different blood alcohol levels?

What are CNS effects of alcohol?

Blackout (memory impairment [anterograde amnesia], remain awake) Sleep impairment (depress REM and inhibit stage 4 sleep, frequent alternations between sleep stages and more dreams late night as blood alcohol level falls)

What are general health problems caused by alcohol?

Brain damage, loss of memory, hallucination, fits, dementia. Risk of chest infection hepatitis and cirrhosis Tingling nerves, numbness and trembling hands Risk of STD and HIV and AIDS. Poor diabetes control Loss of muscle Carditis, HTA, irregular pulse Gastric ulcers, gastritis, vomit blood Pancreatitis Impotence (Men) infertility (women)

What are mental health issues caused by alcohol?

Psychological dependence, typical symptoms of common mental disorder (sleep problem, irritable, sad), hallucination (hears and sees things), unreasonable jealousy. Chronic cases memory loss, orientation and becomes helpless person. Epileptic fits, increased suicide risk

How is alcohol withdrawal?

Cessation of (or reduction in) alcohol use that has been heavy and prolonged. Two (or more) of the following, developing within several hours to a few days after Criterion A: (1) Autonomic hyperactivity (e.g., sweating or pulse rate greater than 100) (2) Increased hand tremor (3) Insomnia (4) Nausea or vomiting (5) Transient visual, tactile, or auditory hallucinations or illusions (6) Psychomotor agitation (7) Anxiety (8) Grand mal seizures

What are alcohol withdrawal symptoms?

What is Cannabis?

Marijuana, Hash... Prepared from dried flowering tops and leaves of plants, consists of dried cannabis resin, may be light brown to almost black

What is composition of Cannabis?

How is THC variations in Hash?

Great variation in concentration, Hash Oil very high THC concentration. Balance between of THC and CBD in street cannabis appears to have changed over the last decade

How is method of use of Hash?

Smoked (joints), Water-pipe (bong), Oral (cooked), no injection (THC does not dissolve in water)

How is pharmaceutical use of Hash?

Two human cannabinoid receptors (CB), THC and metabolites are highly fat soluble, slow rate of clearance. May be detected in blood for several days and traces may persist for several weeks. THC may be stored in body fat for more than 28 days

What are clinical effects of Hash?

Lower Doses (relaxation, euphoria, altered time and sensory perception, increased apetite) Higher Doses (hypervigilance, paranoia, anxiety or panic, derealization or depersonalization, hallucinations) Increased HR by 20-50% up to 3 hours, BP increased while person is sitting and decreases on standing. Healthy young users CV effects rarely significant, risk to pt with heart disease. Driving performance impairment, no fatal poioning in human medical lit.

How is cannabis withdrawal?

Cessation of use after heavy and prolonged usage. 3 or more of following 1 week prior cessation irritable, nervousness/anxiety, sleep difficulty, decreased appetite/weight loss, restlessness, depressed mood, one of physical symptoms causing discomfort [abdo pain, shakiness, sweating, fever, chills, headache].

What are effects of long-term cannabis use?

Medical, Gateway effects Neurotoxic effects (deficits in cognitive function memory and attention, education and occupational. Mechanism: THC induce cell death, decreased cerebral blood flow) Mental health (gateway drug, amotivational syndrome, psychosis/schizophrenia [psychosis among vulnerable, exacerbates symptoms and prolongs illness, helps self medicate psychiatric symptoms or medication side effects] Depression and anxiety increases + suicide attempts)

What is synthetic cannabinoids?

AKA spice/K2, Pot pourri herbal addictives with synthetic cannabinoid chemical compounds, less common may be sold as resin/powder, oils, e-liquid, card, vape... Smoked by cannabis pipe. Incentive (cannot be detected w/std urine drug test, affordable, promises a high stronger than cannabis.

Compare SC vs THC?

SC have four times more affinity for the CB1 receptor and ten times more affinity for the CB2 receptor SC are a full agonist In contrast to THC which is a CB1 partial agonist SC may exert activity on other receptor families as well, like NMDA and 5-HT2A Spice do not include cannabidiol SC are 2 to 100 times more potent than THC

What are acute/subacute effects of Cannabis?

Agitation, auditory/visual hallucinations, anxiety, intense feelings of paranoia, mood swings, suicidal ideation, suicide attempts…. Seizures, vomiting, hypertension, hypokalemia, respiratory depression… Both supraventricular and ventricular arrhythmias

What is Spiceophrenia?

Higher risk than cannabis: - no CBD - full agonist - dose variation Longer-lasting induced effects (many weeks) Psychotic relapse after smoking SC for a day

What are opiates?

Opium derivatives: Heroin, Morphine, Codeine Synthetic opioids: Fentanyl Opioid receptors: mu, kappa, delta Opioid drugs: µ agonists Heroin (diacetylmorphine): - more potent and more lipid soluble than morphine - crossing the blood–brain barrier more rapidly - more rapid onset of subjective effects

How are methods of use of opiates?

What are clinical effects of opiates?

Changes in mood (euphoria in some persons) Indifference to anticipated distress Reduced anxiety Increased self-esteem Better ability to cope with everyday problems Decreased sense of boredom. Physical effects: analgesia, respiratory depression