ETOH and drugs of abuse Flashcards
Define alcohol use disorder as per the DSM-V criteria
1) Alcohol is taken in larger amounts or over a longer period than was intended
2) There is a persistent desire or unsuccessful efforts to cut down or control alcohol use
3) A great deal of time is spent in activities necessary to obtain alcohol , use alcohol or recover from its effects
4) craving or a strong urge to use alcohol
5) Recurrent alcohol use results in a failure to fulfil
major role obligations at work, school or home
6) Important occupational or recreational activities are given up or reduced due to ETOh use
7) Alcohol use continues despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effect
8) Alcohol use is continued despite knowledge of having a persistent physical or psychological problem that is likley to be cause or exacerbated
9) Recurrent alcohol use occurs in situation in which it is physically hazardous
10) Tolerance occurs defined as either
- - A need for markeldy increased amounts of alcochol to achieve intoxication or desired effect
- – markedly diminished effect with continued use of the same amount of ETOH
11) Withdrawal occurs as minifested by either of the following
- - The characteristic withdrawal syndrome for ETOH
- ETOH or closely realted substance is taken to avoid withdrawal symptoms
The presence of at least 2 of the above inticates alchole use disorder
Mild -2-3 symptoms
Moderate -4-5 symptoms
Severe - 6 or more symptoms
Discuss the alcohol use disorders identification test (AUDIT)
Identifies patietn at-risk of hazardous or harmful drinking with a sensitivity of 51-97%
Questions include (questions are scores 0-4 pointes )
1) How often do you have drink containing ETOH
2) How many drinks containing alcohol do you have on a typical day when you are drinking
3) How often do you have 6 or more drinks on one occasion
4) How often during the last year have you found that you were not able to stop drinking once you had started
5) How often during the last year have you failed to do what was normally expected from you because of drinking
6) How often during the last year have you needed a first drink in the morning to get yourself going after a heavy drinking session
7) How often during the last year have you had a feeling of guilt or remorse after drinking
8) How often during the last year have you been unable to remember what happened the night before because you had been drinking
9) Have you or someone else been injured as a result of your drinking
10) Has a relative or friend or doctor been concerned by your drinking
Discuss CAGE questions
Detect ETOH abuse and dependence with a sensitivity of 43-94% and specificity of 70-97%
Two or more positive responses identify patients with lifetime risk of ETOH problems
Cut Down - have you ever tried to cute your drinking
Annoyed - have you ever been annoyed by criticism of your drinking
Guilty : do you ever feel quilty about your drinking
Eye-opener: do you need an eye opener when you get up in the morning
Discuss FRAMES strategy to decrease ETOh consumption in a non-dependent patient
F: feedback - review problems caused by ETOH with the patient
R: respondibility - point out that changing behaviour is the patients responsibility
A: advise the patient to cut down or abstain from ETOH
M: Provide options to assist the patient to change behaviour
E: use an empathetic approach
S: self efficacy - encourge optimis that the patient can change behvaioru
Discuss ETOH withdrawal
Usually develops within 6-24 hours of cessation or reduction in ETOH consumption
Dependence affects multiple neurotransmitter systems. Down regulation of neuro-inhibitory GABA receptors leads to symptoms of GABA excess in withdrawal
It also inhibits the excitatory NMDA glutamate receptor and withdrawal abruptly removes this inhibition. Increased Dopaminergic and noradrenergic neurotransmission also occurs.
Discuss clinical features of ETOH withdrawal
Autonomic excitation Occurs within hours of cessation and peaks at 24-48 hours
- Tremor
- anxiety and agitation
- Sweating
- Tachycartdia
- HTN
- Nausea and Vomiting
- Hyperthermia
Neuro-excitation occurs within 12-48 hours
- Hyperreflexia
- Nightmares
- hallucinations
- generalised tonic clonic seizures - usually singular or breif flurry seizures - recurrent or status seizure need to prompt further investigation
DT - typically begins 48-96 hours post last drink
- Severe form with mortality approaching 8%
- Associated with medical co-morbidities and delayed presentation
- Hallucination, confusion, clouding of consciousness, autonomic hyperactivity, Respiratory and CVs collapse
Discuss co-morbidities associated with ETOH abuse
GIT
- Acute gastric erosions
- GIT bleeding from varicies, erosions, mallory weiss tear, PUD
- Pancreatitis
- Diarrhoea - watery due to ETOH itself or steatorrhea from chornic alcoholism
- Hepatamegaly - fatty liver or Chronic liver disease
- Chornic liver disease (alcoholic hepatitis, cirrhosis) and associated complications
- Cancer (oesophagus, cardia of stomach, liver and pancreaus)
CVS
- Cardiomyopathy
- arrythmias
- HTN
CNS
- Wernickes/korsakoffs
- peripheral neuopathy
- Pellagra ( 4ds, diarrhoea, dematitis, dementia and death)
- Withdrawal
- Alcoholic dementia
- alcoholic myopathy
- increase risk of subdural
Haem
- Anaemia (folate deficiency from diet, iron deficiency from blood loss, direct toxic effect of ETOH causing bone marrow suppression, rare b12 deficiency, or sideroblastic)
- Thrombocytopenia from bone marrow suppression or hypersplenism
Metabolic
-Hypoglycaemia
Discuss Signs of Wernickes
Acute confusion Reduced LOC Memory disturbance Ataxia Othalmoplegia Nystagmus Unexplained hypotension Hypothermia
Discuss management of ETOH withdrawal
Mild forms are treated with simple supportive care
Symptoms typically settle in 2-7 days but relapse is exceedingly common wihtout appropriate pychosocial supports put in place
Severe - RSI -Florid DT is a medical emergency and is managed in resus area -ABC -Seizure control wtih benzoes -Detection and treatment of hypoglycaemia AWS scorring - 5-20mg of oral diazapem thiamine supllementation Fluids and electrolyte balance
Labs
- EUC, FBC, LFT, coags, lipase
Discuss AWS score
Orientation -0-2
- fully oriented
- disoriented but co-operative
- disoriented and uncoperative
Agitation/anxiety
- Rest normally
- appears anxious
- very agitated all the time, panics or gets out of bed for no reason
Hallucination
- none
- anxious
- cant dissuage
Perspiration
- nil
- mil
- soaking
Tremor
- nil
- with intention
- at rest
Temperature
- 0-37.6
- 37.6-38.5
- > 38.5
Discuss opioid withdrawal syndrome
Physiologcical response that develops when there is abrupt cessation or rapid reduction in opiod dose in a dependent individual
Opioids exert their analgeisic effect by agonist activity at the CNS U receptroes - by decreasing cAMP via membrane bound G proteins. Prolonged opiod use leads to cellular adaptation and down-regulation through multiple mechanisms.
Discuss clinical features of opioid withdrawal
Although unpleasent is not a life threat unlike those seen from ETOH withdrawal or sedative hypnotics.
Onset of symptoms depends on the elimination kinetics of the specific opiate.
Symptoms may begin wtihin 6 hours of the last heroin dose and peak at 36-48hours and resolve within a week - compared to onset at 2-3days for methadone peak at several days and last up to 2 weeks/.
Clinical manifestation include
- intense craving
- dysphoria
- autonomic hyperactivity
- GIT distress
- myalgia and arthralgia
Discuss management of opiate withdrawal syndrome
Most patient can be managed in an outpatient setting Admission to hospital is requried if -severe withdrawl syndrome -signfiicant complications -significant intercurrent illness -psychiatric co-morbidity
Pharmalogical treatment of opioid withdrawal is categorized into 3 types
- opioid replacement therapy (e.g methadone, buprenorphine)
- antagonist detoxifications (naltrexone)
- symptomatic management
Discuss Opioid replacement therapy
Methadone is used in opioid withdrawal and for maintenance in abstinence progmas
Typically starts at 20-40mg/day and is tapered over many weeks
Buprenorphine is a high affinity partial Uopioid agnoist used as an alternative to methadone – as effective in maintenance treatment of heroin dependence but less effective in achieving treatment retnetion
Discuss detoxifications programs
Rapid detoxification using naltrexone, buprenorphine and clonidine in various combinations or rapid tapering of methadone has been successful in select patients
Discuss symptomatic treatment of opioid withdrawal
Dehrdation
-fluid resus
Nausea and vomiting
-antiemetics choose your poison
Abdominal cramping and diarrhoea
-Hyoscine 20mg PO QID
Myalgia and arthralgia
-paracetamol and ibuprofen
Anxiety, dysphoria and insomnia
- Diazepam 5-10mg PO Q6hourly for 2-3days
- Clonidine -centrally acting A2 agonist is useful in attenuating physical and psychological symptoms of opioid withdrawal.
Discuss sedative hypnotic abuse
There is a high degree of interindividual difference in the rate of onset , type and severity of withdrawal symptoms
Onset is generally within 2-10 days of abrupt cessation although withdrawal of vershortacting agents may produce symptoms within hours.
Severe and potentially lethal syndrome similar to DT- Similar symptomology as ETOH withdrawal
Discuss management of sedative hypnotic abuse
If withdrawal develops as a result of an interruption in regular benzodiazepine use due to intercurrent medeical illness it is best to reeverse the withdrawal with re-introduction of the offending agent.
If goal is cessation of abuse – long acting benzopdiazpems are used and weened slowly/
Most patients can be managed in an outpatient setting
Describe solvent
A solvent is defined as a liquid that has the ability to dissolve suspend or extract another material without chemical change to either the material or solvent
Organic solvents include hydrocarbons, nitrates and oxygenated compounds
Common solvents include isopropanol, toluene and xylene - other volatile hydrocarbons more commonly used as fuels such as petrol kerosene and butane
The most commonly abused inhlational agent is toluene found primarly in glues, spray paints and lacques
Discuss physiochemical properties of solvents
The organic solvents are all volatile liquids and well absorbed via the inhalation route – peak blood concentrations are chieved within 15-30 minutes – hihgly lipid soluble and a preferentially distributed to lipid rich organs notably the liver and CNS
After inhalation stops excretion is via the lungs – they are also metabolised by the liver with elimination half lives in the order of 15-72 hours
Discuss mechanisms of toxicity of organic solvents
Toxcitiy generally correlates with the volatility of an agent. They are lipophilic and potent CNS depressions
Higher volatility is associated with a greater risk of microaspiration and pneumonitis
Myelin toxicity is thought to be the cause of the neuropsychiatric consequences associated with long term inhlation abuse
Myocardial sensitisation to chatecholamines may also lead to arrythmias and sudden death
Discuss clinical features of aucte inhalational exposure
ACute inhalation predominantly affect the CNS causing altered cognition that resembles ETOH intoxication
There is general impairement of psychomotor function - reduced reaction time, manual dexterity and balnce
Patient are often euphoric , disinhibited, lethargic and ataxic
Ihalational exposure to solvent also causes intense irritation to the mcuous membranes of the eye, nose, thorat and lower airways. Inadvertent aspiration can induce chemical pneumonitis
Sudden death particuarly seen with butane or propane may be due to asphyxiation or cardiac dysrhythmias induced by sensitisation of the myocardium to chatecholamines
Discuss clinical features of chronic inhalational exposure
Strong evidence that long term toluene exposure leads to persistent neurotoxcicity characterised by strucutral and functional brain abnormalities as well as neuropsychoklogical impairement.
Chronic toluene abuse is also asscoiated with a NAGMA largely due to distal renal tubular acidosis - the acidaemia, hyperchloraemia and hypokalaemia may be prfound
Dicsuss management of solvent abuse
ABCD
Electrolyte and acid base management
management of seizure activity if present
Solvent use in pregnancy leads to syndrome similar to foetal ETOH syndrome and has withdrawal in the postpartum period as a symptoms
Discuss body packer and stuffers
Packers - internal concealment of illicit drugs – most often meticulously packed and swalloed – rare to use rectum or vagina as more likley to be found - use constipating agent to delay transit
Stuffers – hast conceralment of illicit drugs – more often to be multiple agents, less carefully packed and more like to spill
Discus presentations of body packers
3 seperate presnetions
1) acute drug intoxication or fear of pending rupture - can have take many times the lethal dose
2) Request by authorities for medical assessment following arrest
3) Development of surgical complications usually bowel obsturction but bowel perforation, oesophgeal obsturction and oesophageal rupture are also reportted
Discuss amphetamines and other sympathomimetics and there complications
Amphetamines and other sympathomimetics produce central and periperhal sympathomimetic effect
Lethal complciations include severe hyperthermai, ACS, cardiac dysrhythmias, arotic dissection and ICH. Repeated use leads to long term neuropsychiatirc sequalae
The prinicples of managements for almost all are supportive management and benzo at the same time
Discuss risk assessment of amphetamines
Small doses particularly in non toelrant pateints may result in significant intoxication
The presence of hyperthermia, headache, impaired level of consciousness, focal neurological signs or chest pain herald potentially life threatenign ocmplciation and warrant aggressive management and ix
Seizure occur in up to 4% of amphetamine emergency presentation
Children: on illicit amphetamine derivative pill may lead to life threatening sympathomimetic toxicity
Discuss toxic mechanism (TM) and toxicokinetics (TK)
TM: Structually related to ephedrine- amphetamines enahance catecholamine release and block reuptake. Inhibition of MAO also occurs. CNS and peripheral norad dpaminergic and serotnergic stimulation occurs. Long term CNS effects occur due to neurotransmitter and recepter adapation as well as permanent destruction of the dominergic neruopathways. MDMA at standard recreational doses somtimes induces SIADH leading ot profound hyponatraemia and coma.
TK: Well absorbed follwoing ingestion
lipid soluble weak bases and have a large VG. Most amphetamines undergo hepatic metabolism to form metaboities that are excreted in the urine. Elimiantion half-life varies from 8-30 hours.
Discuss clinical features of Amphetamine use
CNS:
- Euphoria
- anxiety, dysphoria, agitation and aggression
- paranoid psychosis with visual and tactil hallucinations
- hyperthermia, regidity and mycoclonic movements
- seizures
CVS
- Tachycardia and HTN
- Dysrhythmias
- ACS
- Acute cardiomyopathy
- APO
- Haemoptysis
Peripehral sympathomimetic
-mydrias sweating and tremor
Clinical features
- Rhabdo, dehydration and AKI
- Hyponatraemia and cerebral oedema following MDMA
- Aortic and carotid dissection
- Subarachnoid and intracerebral haemorrhage
- ischaemic colitis
Discuss IX for amphetamine use
ECG, BSL paracetamol
EUC - hyponatreami
ECG, TNI - ACS
CK - rhabdo
CXR - dissection and aspiration
Discuss management of amphetamine use
Resus
- potentially life threatening emergency and patient with serious intoxication should be managed in an area capable of CPR
- Features that require immediate intervention
1) HTN (Treat with titrated benzodiasapine. If refractory to benzo use phentolamine 1mg IV 5 minuted or GTN/SNIP) - do not use b blockade due to unapposed alpha effect
2) ACS (As per normal ACS apart from the avoidance of B blocade, also ischaemia is normally due to coronary vessel spasm or dissection rather than plaque rupture and thrombolysis is not indicated)
3) Seizures and agitated delirium - benzo
4) Hyperthermia
- >38.5 is indication for continuous core monitoring, benzo sedation and fluid resus
- >39.5 indication for rapid external cooling, paralysis, I&V likley needed
5) Hyponatraemia – treate as per SIADH
D: Charcoal not advised
E: nil
A: nil
D: Depends on severity
Discuss risk assessment of ccannabinoids
No reported deaths directly attributed to recreational use of marijuana
Adults may experience unpleasant symptoms ina dose dependant manne
- low dose :50mic/kg are associated with mild sedation, disinhibioitn, mild disorientation and euphoria
-high dose 250mic/kg are associated with tachycardai, postural hypotension, CNS depression, anxiety, perceptual disturbances and even psychotic symptoms
-Co ingestion of other CNS depressants has an additive effect
-chronic long term use leads to neuropsychiatirc sequelae
Children: ingestion can lead to life threatening coma in a child
Discuss TM and TK of cannabinoids
Tm: central sympathomimietic and antiemetic properties. it acts on cannabinoid receptors in the central and peripehral nervous system (CB1) and on immune cells (CB2). Augments dopamine release. Delta-9-tetrahydrocannabinoid (THC) is the most potent component
TK: radpidly and completed absorbed by inhaliation. Bioavalbility reduced if ingested
Highly protein bound lipid soluble and have a large VD
Hepatic metabolism to form active and inactive metabolites taht are excreted in urine.
Elimination half life is several days
Discuss clinicall features
CNS:
- Ataxia, incoordination, imparied judgement
- sedation
- CNS depression
- coma in children that can last up to 35 hours
CVS
- tachycardai
- orthostatic hypotension
- syncope
Psychiatric
- euphoria and relaxation
- agitation
- anxiety and panic attacks
- time distortion, hallucinations, delusions
- acute psychosis
Resp (rare)
- peumothorax
- pneumomediatinum
Cannaboid hyperemesis syndrome also sequalae
Discuss managemnt of cannaboid use
RESUS
ABCD
-agitation with 5mg of diazepam
Discuss cocaine risk assessment
Powerful sympathomimetic and LA properties. It is potentially lethal in overdose if severe hyperthermia, HTN, MI or prodysrhythmic effect occur
Ingestion >1g are potentially lethal
- the toxic dose is highly variable and small doses particularly in non tolerant patient may result in significant intoxication
- The presence of hyperthermia, headache cardiac conduction abnormalities, focal neurological signs or chest pain heralds potentially life threatening complications
Dose
-1-3mg/kg –> safe local anaethetic dose
20-30 mg usual dose in a line of cocaine to be snorted
1G potentially lethal
Pregnancy - cocaine is teratogneic and associated with an increased incidence of miscarraige and foetal demise
- lacatation cocaine is excreted in breast milk and can result in infant intoxication
- children ingestion is potentially lethal
Discuss TM and TK of cocaine
TM: - results from sympathomimetic, vasospastic and sodium channel blocking effect. Sympathomimetic effects due to blockade of presynaptic catecholamine reuptake and can result in vascular dissection, intracranial haemorrhage and acute caridomyopathy. Vasospasm and endothelial fissuring result in acute coronary syndrome. Blockade of myocardial fast sodium channels may result in ventricular dysrhythmias, as occur in TCA cardiotoxicity. CNS excitation may result in psychomotor acceleration seizures and hyperthermia.
TK: Well absorbed thorugh the mucous memrbneas of the nasopharynx, pulmonary alveolar tree and GIT>
Peak concentration achieved fastest with IV and inhalational administration.
Bioavailability depends on route
-IN 25-80%
-smoked 60-70%
Highly lipid soluble with a VD of 2l/kg
Cocaine is rapdialy metabolised by liver and plasma cholinesterase to water soluble metabolites
Metabolites may persist in the blood and urine for up to 36 hours. Clinical duration of effect is approxiamtly 60 mintues with biological half lives being reported between 0.5-1.5 hours
Discuss clinical features of cocaine
The onset of cocaine is rapid with major clincial manifestation occuring wihtin the first hour and usually lasting several hours
CNS
- Euphoria
- Anxiety, dysphoria, agitation and aggression
- paranoid psychosis with visual and tactile hallucinations
- hyperthermia rigidty and myclonic movements
- seizures
CVS:
- Tachy and hypertension may be severe
- dysrhythmias and cardiac conduction abnormaitlies
- acute coronary syndroms - vasospatic and thrmobotic
- qt prlongation
- APO
Peripheral sympathomimetic
- Hyperthermia
- muscle fasciculations
- mydriasis, sweating and tremor
CLinical features associated with the following medical complications
- hyperthermia induced rhabdomyolysis, renal failure and cerebral oedema
- aortic and carotid dissection
- subarachnoid and intracerebrla haemorrahges
- ischaemic colitis
- pneumothorax
- penumomediastinum
DIscuss IX of cocaine OD
12 lead
- detect MI
- Brugada-type pattern of ECG changes (RBBB with ST elevation in leads V1-3) can occur in cocaine
- Overal the sensitivty of ECG for detecting myocardial infarction is lower in cocaine users
- CXR +- CTA
- CT head
Discuss management of cocaine OD
RESUS
ABCD
CLinical features that require immediate intervetnion
-Cardiac dysrythmias (treated as per TCA overdose) ventricular dysryhtmias refractory to bicarb and defib are treated with lignocaine 1.5mg/kg IV followed by 2mg/min infusion
-ACS- treated by standard therapy apart from b blocakers which are contraindicated -Thrombolytics are contraindicated in the presence of severe HTn, seizures, ICH or aoritc dissection
-Sinus tachycardia and hypertension are treated with titrated parenteral benzo
-SVT treated with benzo if not workingnthen verapamil or adenosine with cardioversion if unstable
-HTN refractory to benzo consider
— phentolamine
—titrated vasodilator infusion (SNIp or GTN)
—B blocker contraindiacted
-Seizure treated as per toxic seizures
-Hyperthermia
—T 38.5 indication for continous core monitiring, benzo + fluid
—T >39.5 indication for rapid extenral cooling - paralysis intuabtion and ventialtion may be required
D: Not indicated unless a body packer
E: nil
A: nil
D:
Discuss risk assessment for gamma-hydroxytbutryrate (GHB)
When taken in excessive doses this illicit drug causes rapid onset of CNS and respiratory depression, myoclonic jerking and bradycardia.
Duration of toxic effects is short with complete recovery occuring within 4-8 hours
Dose estimates are virtually impossible beavuse concernrtaion varies widely and is almost never knonw OD usually occurs becuase the concentration supplied was higher than anticipated
Standard rec doses are 30mg/kg
ingestion of >50mg/kg can cause coma and respiratory depression.
Childrne - anu ingestion may be associated with rapid onset of coma and is regarded as potentionally fatal
Discuss TM and TK of GHB
TM: GHB is a short chain carboxylic acid that occurs naturally in the brain. It is both a precursor and metabolite of GABA and may be a neurotransmitted itsefl. MOA is unclear. Hypotheses include agonist activity at GABAb receptors activity at GHB receptors, dopaminergic modulation, increased ach or serotonin levels
TK: Rapidly absorbed following oral administration with peak plasma concentration occuring at 25-60 minutes. THe presence of food reduces bioavailability.
Gamma butryolcatone is rapidly transfomred in the liver to GHB. 1-4 butnediol is metabolised rapidly to GHB by alcohol dehydrogenase. THe presence of alcohol competitively inhibtis metbaolism and delays onset of effect.
Discuss clinical features of GHB
Occur wihtin 20 minutes and peak at 30-60 minutes
- Standard rec doses produce rapid onset of euphoria and drowsiness as well as enhanced sexual desire, performance and orgasm.
- in overdose the patient can be rousd with an external stimulus only to become deeply somnolent again when not distrubed
- Sudden recovery of consciousness occurs usually within 2-3 hours. Recovery is characterised by a short period of agitation or delirium and vomiting.
CNS
- CNS depression
- Agitation and delirium
- Miosis
- Myoclonic movemmetns may be noted in rare cases
Resp
- Airway obstruction
- resp depression
- Cheyne-Stokes type breathing
CVS:
- Bradycardia
- mild hypotension responsive to IV fluids
- non specific ecg changes
General:
-nmil hypothermia
-vomiting
0sweating
Tolerance to GHB devleops with regular use and a withdrawals sydnrome is recongnised -Hallucination paranoia insomnia -anixety -sweating -palpitations -agitation
Discuss management of GHB overdose
RESUS
- ABCD
- Potential early life threates that require immediate interveiton
- COMA
- resp depression
- loss of ariway protective relfex
Bradycardai is common but rarely needs intervention and only if cocurrent hypotension
D: Not indicated
E: nil
A: Nil
D: clinically well 2 hours following ingestion can be dsicharged home
What is a unit of alcohol and approx amounts of different drinks to get 1 unit what are the recommended safe intake levels
1 unit = 8-10 grams of alcohol
1 shot of spirits - 1 glass of wine - 200ml of beer are approximatly = 1 unit
No more than 10 units a week and no more than 4 in a single sitting
