In the UK more than 130,000 adults had treatment for substance misuse in 2020.
Cannabis is the most widely used drug globally, followed by amphetamines. However, we will be discussing the use disorders of therapeutic as well as illicit drugs both. Many people who use drugs are polydrug users.
We will discuss a variety of substance use disorders, such as:
- Opioid use disorder and overdose
- Cocaine use disorder and toxicity
- Amphetamine use disorder and overdose
- Cannabis use disorder
- Inhalant use disorder
- Hallucinogen use disorder
- Benzodiazepine overdose
- TCA overdose
- Anabolic steroid use disorder
- Paracetamol overdose
- Chronic alcohol use
- Smoking cessation
Opioid use disorder includes heroin (diamorphine) and prescription opioid misuse. Opioids are synthetic/natural agents that stimulate the opioid receptor. Opiates are naturally derived from the opium poppy. These can be used to treat pain but also provide euphoric effects and as a result they are abused often.
Some common opioids that may be misused are:
- Diamorphine
- Fentanyl
- Methadone
- Oxycodone
- Hydrocodone
Pathophysiology
Dopamine is produced in the ventral tegmental area and projects to the nucleus accumbens. Opioid activation increases dopaminergic signalling to the nucleus accumbens → euphoria.
Opioid tolerance occurs due to a decrease in response by opioid receptors due to a previous dose of an opioid, therefore requiring a higher dose to achieve the same dopamine release.
Noradrenaline is produced in an area called locus coeruleus. When opioids are used, noradrenaline production decreases. However, with chronic use we get increased NA production and when we get a period of opioid deprivation, this NA is released in excessive amounts → muscle cramps, diarrhoea, anxiety, tremors.
😷 Presentation
- Rhinorrhoea (runny nose)
- Needle marks
- Pinpoint pupils
- Drowsiness
- Watering eyes
- Yawning
- Chronic constipation
- Weight loss
🚨 Complications
→ Opioid withdrawal
- Nausea and vomiting
- Dilated pupils
- Distress
- Insomnia
- Autonomic hyperactivity
- Tachypnoea
- Tachycardia
- Sweating
- Hypertension
- Hyperthermia
- Diarrhoea
→ Opioid overdose
- CNS depression - altered mental status
- Respiratory depression and apnoea - <10 breaths per minute is indicative of opioid intoxication.
- Pulse <40bpm or cardiac arrest
- Miosis
- Death
We can diagnose it clinically and by using a therapeutic trial of naloxone.
Ventilation, naloxone and CPR (if in cardiac arrest) is the treatment for i-opioid overdose.
→ Bacterial infection - infective endocarditis, septic arthritis, septicaemia, necrotising fasciitis.
→ Viral infection - HIV, Hep B, Hep C.
🔍 Investigations
🏆 Abuse and overdose are typically clinical diagnosis, however, we may consider a few tests.
🥇 Urine or saliva drug screen - >300nanograms/mL
🥈 Gas chromatography-mass spectroscopy - to determine which opioid is used
Bloods - U&Es, FBC, LFTs (may be elevated due to hepatitis).
Hepatitis and HIV serology
🧰 Management
- 🥇 Buprenorphine ± naloxone - it too is an opioid, however, it is only a partial agonist of the opioid receptor leading to a reduced effect of the abused opioid. It may be combined with naloxone which is an opioid antagonist.
- 🥇 Methadone - an alternative 1st line agent, it too is a partial agonist of the opioid receptor.
Supportive therapies are also required such as symptomatic relief for muscle cramps, sleep disturbances, nausea and vomiting, diarrhoea, anxiety. Food and hydration should also be adequate.
- 🥈 Clonidine/lofexidine ± naltrexone - clonidine and lofexidine are a2-adrenoreceptor agonists → decreased sympathetic nervous system response to counter autonomic hyperactivity that occurs with withdrawal.
We can monitor compliance with urinalysis once again. Detoxification should be for 4 weeks in an inpatient setting and up to 12 weeks in the community setting.
The majority of cocaine users do not have cocaine use disorder. This occurs when it significantly impairs or distresses the patient. It’s risk increases with smoking, injection or heavier use.
First, let’s take a look at the pathophysiology:
Cocaine performs multiple functions, but in this case the main mechanism is prevention of catecholamine re-uptake. This increases the effect of dopamine → euphoria and addiction. Noradrenaline is also not taken up → alertness, SNS hyperactivity.
Cocaine activates DNA which increase the amount of calmodulin-kinase II which can cause myocardial hypertrophy and increased calcium within cardiomyocytes. These two factors increase the risk of arrhythmias.
Most cocaine is mixed with levamisole (an antihelthmic that is a nAChR agonist). Adverse effects of levamisole is aplastic anaemia, and more commonly retiform vasculopathy that is accompanied by neutropenia, agranulocytosis, purpura of the face and ears. However, most concerningly levamisole is converted to a secondary substrate (aminorex) which causes idiopathic pulmonary hypertension.
😷 Presentation
⭐️ Cocaine causes a hyperadrenergic state, which means:
- Nausea
- Jitteriness
- Lack of concentration
- Anxiety
- Paranoia
- Euphoria
Other signs of cocaine abuse are:
- Crack lip/thumb - due to heat-related injury.
- Injection scars
- Nasal septum perforation
- Hypertension and tachycardia
- Diaphoresis
🚨 Complications
→ Cocaine withdrawal
Can induce a state resembling mania and can be associated with depression with suicidal ideation that can sometimes persist in patients.
→ Cocaine toxicity
Risk increases with high doses of the drug, high ambient temperature and concomitant sympathomimetic agent usage.
- Tachycardia
- Hypertension
- Hyperthermia
- Diaphoresis
- Mydriasis
- Agitation
It can cause sudden death as it can lead to dysrhythmias, seizures and hyperthermia, respiratory failure.
🔍 Investigations
🥇 Urine toxicology
🏆 GC-MS - interestingly, we look for levamisole as almost all cocaine nowadays is adulterated with it.
ECG can also be done, showing non-specific T-wave changes or Brugada pattern.
🧰 Management
Mental health counselling is the treatment for moderate cocaine use disorder. For severe cocaine use disorder, psychiatric referral is indicated.
→ Cocaine toxicity - there is no specific antidote so we have to treat symptoms and provide supportive measures within A&E.
Some symptoms to treat are:
- Agitation - diazepam/midazolam/lorazepam or propofol.
- Hypertension - diazepam/midazolam/lorazepam or anti-hypertensives.
- Seizures -diazepam/midazolam/lorazepam.
- Volume depletion - IV saline.
- Hyperthermia - external cooling.
Pathophysiology
Amphetamines include MDMA (ecstasy) and can be misused by oral, IV, nasal routes and also smoking. They have complex and diverse actions:
- They have similar structure to catecholamines (DA and NA) and as such it is transported into the presynpatic terminal by the DAT and NET → increased activity and acting as an indirect sympathomimetic. It causes euphoria, pleasure and reduced fatigue. However, with increased doses to can cause agitation.
- Tolerance is an issue as we get down-regulation of receptors after each dose. This can lead to depression, fatigue and tiredness.
😷 Presentation
- Hyper-vigilance
- Hyper-arousal and euphoria
- Anxiety
- Hallucinations
- Paranoia
- Gum disease and dental decay (meth mouth)
Signs we may see include:
- Hypertension
- Tachycardia
- Tachypnoea
- Dilated pupils
- Hyponatremia
🔍 Investigations
Urine toxicology
GC-MS
ECG
🧰 Management
For chronic misuse we give psychosocial + behavioural treatment and pharmacological treatment in the form of:
- Modafinil - 200mg OD. Reduces cravings supposedly
- Antidepressants
- Fluoxetine - an SSRI. Also decreases cravings.
🚨Complications
→ Methamphetamine toxicity
😷 Due to excessive intake. It causes exaggerated effects of the drug which cause excessive periods without food and sleep, followed by exhaustion and fatigue. It can also cause agitation and psychosis.
💊 We can treat it with:
- 🥇 Activated charcoal - it absorbs the toxins within the GI tract, preventing systemic absorption of the toxins.
- 🥇 Antipsychotic/sedative
- Olanzapine - an atypical antipsychotic.
- Lorazepam - a BDZ.
BDZ are the most prescribed medication for anxiety, sleep, sedation, and epilepsy. Overdose can be intentional, recreational error or accidental with medication.
Let’s quickly revise how BDZs work:
Benzodiazepines positively modulate the GABAa receptor by increasing the “open” state of the receptor → increasing Cl- influx → hyperpolarisation and preventing neurotransmitter release → CNS depression.
😷 Presentation
BDZs cause CNS depression and overdose presents similar to alcohol intoxication.
- Excessive sedation and drowsiness
- Impaired mental status
- Slurred speech
- Ataxia
🚨 Complications
Can occur with excessively large doses combined with other CNS depressants and alcohol too. A
- Coma
- Respiratory depression
- Rhabdomyolysis
🔍 Investigations
- Pulse oximetry
- ABG/VBG - hypoxia and/or hypercapnia.
- FBC - normal.
- U&Es - patients may develop AKI.
- LFTs - often normal.
- ECG
- Creatine kinase - if elevated it can indicate rhabdomyolysis.
- Plasma paracetamol concentration - if you suspect an intentional overdose mixed with paracetamol.
🧰 Management
- A - ensure patent airway as endotracheal intubation may be needed. If the patient can talk then there is no need to look for airway compromise.
- B - assisted ventilation may be required if the patient has respiratory arrest. Look for signs of breathing and check SpO2, check for cyanosis. ABG might quantify the degree of hypoxia.
- C - fluid resuscitation if the patient is hypotensive and also ensure cardiac rhythm is good with an ECG.
- D
- Consciousness - AVPU.
- Pupils - will be dilated in overdose. Opioid overdose may be suggested by pinpoint pupils.
- Drug chart review
- Assess for hypoglycaemia
- E
- Keep the patient warm
- Inspect any injection sites, injuries or infections.
- Catheterisation to monitor urine output.
- Flumazenil - antagonises the BDZ binding site on the GABAa receptor. It is not licensed in the UK and supposedly the risks outweigh the benefits as it is associated with convulsions. It is only to be used with patients who have pure BD.
- Activated charcoal - 50g dose in adults.
TCAs such as amitriptyline and dosulepin are used in the treatment depression. Their use has fell out of favour due to the availability of SSRIs but they still account for antidepressant overdoses annually.
TCAs are rapidly absorbed and bind to proteins rapidly and have high lipid solubility so they distribute into tissues rapidly (brain and myocardium concentrations are higher than blood concentrations).
They have multiple effects, such as:
- Anticholinergic effects
- a1-receptor antagonism
- Fast Na-channel blockade
- Increase post-synaptic NA, 5HT and DA
- H1 and H2 antagonism
As we can see, it affects multiple systems with a variety of mechanisms and as a result can cause a multitude of side effects. It affects our myocardium, the CNS, peripheral vascular resistance.
😷 Presentation
- Tachycardia - wide complex tachycardia is present with overdose.
- Hypotension - due to a1 antagonism → decreased PVR.
- Blurred vision, dilated pupils, dry mouth - due to anticholinergic effects.
- Mental status changes - drowsiness, delirium, coma. Due to anticholinergic effects once again.
- Absent bowel sounds - due to anticholinergic effects.
- Urinary retention - due to anticholinergic effects.
Presents with some typical clinical features:
- Hyperpyrexia
- Agitation/impaired consciousness
- Hypertonia and clonus
Drugs that may cause serotonin syndrome include:
- MAOIs - moclobemide, phenelzine, rasagiline, selagiline for example.
- SSRIs
- Ecstasy
- Amphetamines
🔍 Investigations
🥇 ECG - should be done immediately to assess for QRS prolongation >100 milliseconds. This increases risk of seizures. If it is >160 milliseconds it can indicate ventricular arrhythmias.
🥇 Sodium bicarbonate therapeutic trial - 2mmol/kg rapid IV bolus of sodium bicarbonate should be given as soon as QRS prolongation is confirmed. If that’s QRS doesn’t narrow then the QRS prolongation is probably not due to toxicological causes.
🧰 Management
- 🥇 IV bicarbonate - first-line for hypotension or arrhythmias.
Other antiarrhythmics such as magnesium may be used too. However, class 1a antiarrhythmics, such as Quinidine, class 1c antiarrhythmics, such as Flecainide, and class III antiarrhythmics such as amiodarone are too be avoided as they prolong depolarisation and the QT interval.
- IV lipid emulsion - such as intralipid can be used to reduce free drug concentrations and toxicity.
Pathophysiology
The maximum dose of paracetamol per day depends on age, but in adults, it is 4g per 24 hours.
Paracetamol has to undergo sulfation and glucuronidation to produce a non-toxic metabolite that can be really excreted.
It is metabolised by CYP2E1 to a toxic intermediate metabolite known as N-acetyl-p-benzoquinone imine (NAPQI).
NAPQI then binds with glutathione to produce the non-toxic metabolite.
However, in overdose, NAPQI production exceeds the capacity to detoxify it as glutathione availability depletes. NAPQI then binds to hepatocyte components → mitochondrial injury and hepatocyte death.
😷 Presentation
Patients are often asymptomatic or only have mild GI symptoms initially. However it can lead to hepatotoxicity within 2-4 days of ingestion and may lead to acute liver failure.
- ⭐️ Nausea and vomiting are common and occur within a few hours of overdose. However, it may indicate hepatic necrosis 2-3 days after an overdose.
- RUQ pain - indicative of acute liver injury.
- Jaundice
- Hepatomegaly
- Altered consciousness - a sign of hepatic encephalopathy.
- Asterixis - also a sign of acute liver injury. We test it by asking the patient to extend their hand, dorsiflexing the wrist, and spreading the fingers to observe a flap at the wrist.
⚠️ Risk factors
- Malnourished patients
- Chronic alcohol excess
- Rifampicin
- Phenytoin
- Carbamazepine
- St. John’s Wort
🔍 Investigations
- Serum paracetamol concentration - we can use this to stratify risk of liver injury and also to assess if acetylcysteine therapy is needed. Samples should be taken at 4 hours after ingestion. If the result is below the threshold of treatment, we should repeat it at 6 hours.
- LFTs - ALT >35IU/L. Indicates acute liver injury.
- PT and INR
- PT may be prolonged (>13.5s).
- Blood glucose - if hypoglycaemic (<3.3mmol/L) it may indicate ALI.
- Creatinine - may be acutely elevated.
- ABG/VBG - may show lactic acidosis.
INR may be increased (>1.1).
🧰 Management
Management depends on the time since the overdose:
<8 hours
Activated charcoal - is considered. 50g single dose if the patient presents within 1 hour of ingestion and has ingested more than 150mg/kg.
Acetylcysteine - is considered. If the patient has ingested more than 150mg/kg, administer acetylcysteine immediately without waiting for blood tests.
>8 hours
Acetylcysteine - may be considered, along the same protocol.
The same protocol applies, except acetylcysteine is 1st line if it is a staggered overdose (not a single dose or taken all within 1 hour) or if it is a therapeutic excess.
Alcohol-use disorder is a psychiatric disorder that is chronic and associated with a variety of medical and psychiatric disorders.
With excessive alcohol intake, we get tolerance, withdrawal and an inability to control drinking behaviour despite the apparent consequences it leaves on an individuals life.
Withdrawal is a serious condition and can be monitored using the Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar).
Pathophysiology
The pleasurable effect of alcohol comes from activation of the dopaminergic pathway from the VTA → nucleus accumbens. Continuous alcoholism sensitises the pathway and leads to dependence. Long-term exposure causes down regulation of GABA receptors, and up regulation of glutamate receptors and also NA activity (an excitatory state).
When an individual stops taking alcohol, this excitatory state is unopposed and we get hyperactivity of the nervous system and dysfunction. These are the issues that occur with withdrawal. Patients that have withdrawal symptoms experience cravings to drink alcohol.
Chronic alcohol use releases stress-producing neurotransmitters and hormones such that one needs alcohol to relieve chronic stress and dysphoria.
Episodes of withdrawal intensify the more episodes of withdrawal you have. This is known as kindling.
🔢 Classification
Alcohol-use disorder can be characterised as chronic alcohol use over a 12-month period that results in significant impairment/distress such as psychosocial problems (role impairment, legal issues, interpersonal difficulties risk-taking behaviours), cravings, compulsive alcohol use.
We can diagnose it in individuals who compulsively drink alcohol despite the adverse effects that it has on their life. The severity ranges from:
- Mild - 2-3 criteria met.
- Moderate - 4-5 criteria met.
- Severe - 6+ criteria met.
- Alcohol use in large quantities/ alcohol use over a longer period of time than intended.
- Persistent desire/unsuccessful attempts to decrease or control alcohol intake.
- Significant time spent in activities needed to obtain/use alcohol or to recover from its effects.
- Cravings
- Failure to fulfil major role obligations at home, work, or school due to alcohol.
- Forgoing important social, occupational or recreational activities due to alcohol.
- Recurrent use of alcohol in hazardous situations (e.g. while driving).
- Continued use despite knowing that alcohol is causing physical/psychological problems.
- Tolerance
- Withdrawal.
Remission criteria is time-dependant. It is determined by how long no criteria have been met (except for cravings). 3 months → early remission, while 12 months → sustained remission.
😷 Presentation
- Nicotine dependence comorbidity
- Social, economic, legal or psychological problems
- Nausea and vomiting/haematemesis - may be an indicator of alcohol-related gastritis and/or pancreatitis.
- Muscle cramps, pain, tenderness
- Peripheral neuropathy - relates to their poor nutrition and thiamine deficiency.
- Hypertension and tachycardia
- Cutaneous manifestations - flushing, psoriasis, pruritis, rosacea, urticaria.
- Dental/periodontal disease
Sometimes we can see people with a broad-based gait due to cerebellar degeneration.
Upon examination we may find pathologies of the abdomen such as:
- Increased/decreased liver size
- Jaundice
- Ascites
🚨 Complications
Alcoholic liver disease - a spectrum of conditions including:
→ Liver cirrhosis - the effects of cirrhosis will be discussed in its relevant CCC.
→ Chronic hepatitis
→ Fatty liver disease
We will discuss ALD more in the cirrhosis CCC.
WIthdrawal - presents with a multitude of issues. Symptoms start at 6-12 hours, these include:
- Sweating, tachycardia, anxiety.
At 36 hours seizures have peak incidence.
At 48-72 hours, delirium tremens is at its peak incidence.
Delirium tremens is an acute onset of delirium due to alcohol withdrawal. Features include:
- Coarse tremor
- Confusion
- Delusions
- Auditory and visual hallucinations
- Fever
- Tachycardia
To treat withdrawal we use:
🥇 Diazepam or oxazepam or chlordiazepoxide these are all BDZs that combat withdrawal effects.
🥈 Lorazepam
This is to diminish the delirium tremens and seizures.
🥇 IV pabrinex/Thiamine is also given to prevent Wernicke’s encephalopathy. Pabrinex is a combination of B vitamins. Thiamine can be given orally following pabrinex administration.
All of this is coupled with supportive care such as hydration and reassurance.
An acute neurological condition occurring due to thiamine deficiency. It presents with a clinical triad of:
- Ophthalmoparesis with nystagmus
- Ataxia
- Confusion
If this is not treated with urgent thiamine replacement, one could develop Korsakoff syndrome which can then be termed Wernicke-Korsakoff syndrome.
With WKS we add the amnesia (both anterograde and retrograde amnesia) to the aforementioned symptoms.
🔍 Investigations
- Diagnostic interview - using the DSM-5 criteria to make a diagnosis of alcohol-use disorder,
- CIWA-Ar - to assess the severity of alcohol withdrawal symptoms.
- Carbohydrate-deficient transferrin (CDT) - highly sensitive for heavy drinking. It is raised with excessive alcohol intake.
- LFTs - GGT in particular is closely correlated with alcohol consumption. AST>ALT more than 2:1 is typical with alcoholic liver disease. 3:1 is strongly suggestive of acute alcoholic hepatitis.
CAGE questions can be used as a brief screening tool for alcohol abuse:
- C - Cut down? Ever thought you should cut down?
- A - Annoyed? Do you get annoyed at others commenting on your drinking?
- G - Guilty? Do you feel guilty about your drinking ever?
- E - Eye opener? Do you ever drink in the morning to help with your nerves/hangover?
🚨 Management
🥇 For mild alcohol dependence, GP advice and brief interventions within the primary care setting or during inpatient hospitalisations. Ideally the patient and physician develop a plan for decreasing alcohol consumption.
🥇 For moderate-severe alcohol dependence, psychosocial interventions such as CBT/counselling is indicated. Pharmacotherapy is also indicated first-line.
The first-line medications used are (not all 3 at once, just 1 of the 3):
- Naltrexone - 50-100mg OD for 3-4 months. It can also be given once monthly for 6 months as a 380mg IM injection. Can precipitate opioid withdrawal if the patient has been using opioids recreationally.
- Acomprosate - 666mg orally 3x daily for 3-4 months.
- Disulfiram - 500mg OD for 1 week then 250mg OD.
Cigarette smoking is the most common cause of preventable death. As physicians are generally credible and trusted, they have the opportunity to convey the message to smokers and connect them to cessation counselling and treatments.
Smoking is strongly associated to heart disease, cancer, COPD and multiple comorbidities are put at a disproportionate risk as a result of smoking.
🏘 Epidemiology
Approximately 15% of the UK population smokes with men currently still being higher (17%), however, the trend of women smoking is an upward one (13.3%).
Pathophysiology
Nicotine within cigarettes is the active agent. It binds to nAChRs to stimulate the CNS mesolimbic dopamine system → reinforcing the reward pathway and causing addiction. Nicotine is extremely addictive as a result and abstinence can cause withdrawal as a result (symptoms are listed below). As mentioned above, the behavioural and learned aspects of smoking are also integral to the addiction mechanism.
😷 Presentation
- Tar staining on nails and fingers. They appear yellowish due to repeated exposure to smoke and tar. Moustaches with white hair show a pattern of yellowing in the centre with chronic smoke exposure.
- Lips and dentition - lips may have a bluish-black discolouration to them, while teeth may look yellowish.
- Burns
- Skin changes - premature wrinkling and dry skin.
- Smoke smell
- Dysphoria/depression
- Irritability
- Anger
- Anxiety
- Increased appetite and weight gain
These symptoms contribute to smoking persistence and relapse of smoking after cessation. There can be learned associations with smoking such as associations with other pleasurable activities like breaks, meals, socialising or relief from stress. So relapses often occur in social situations or during period of high stress.
⚠️ Risk factors
Smoking behaviour is due to biological, genetic, psychosocial factors.
- Low SES
- Mental health illness - for example depression, anxiety, bipolar, schizophrenia (almost 90% of schizophrenics smoke).
- Substance abuse
- It is far more likely in households with current smokers.
🚨 Complications
Complications of smoking cessation:
→ Withdrawal
→ Depression
→ Glycaemic control issues - smoking and NRT increases insulin resistance.
→ Weight gain - usually 4-6kgs due to increased appetite, hand-to-mouth substitution, decreased metabolism. It is important to tell the patient that the health risks of weight gain are small in comparison to the risks of continued smoking. It is not recommended to advise limiting calorie intake with cessation as hunger may trigger cravings.
Complications of smoking in general:
- Cancer
- CHD
- MI/stroke
- PVD and CVD
- COPD
- Pneumonia and other RTIs
- Impotence and reduced fertility
And countless other risks….
🧰 Management
Smoking cessation is notoriously difficult but there are a couple things we can do to aid smoking cessation, however, the management plan differs depending on where the individual stands currently with wanting to quit smoking:
- 🥇 Reinforcement and counselling
- 🥇 NRT - we will discuss the options for NRT below.
- 🥇 Bupropion - 150mg OD for 3 days then 150mg BD for 8 weeks.
- It works as nAChR antagonist as well as a NAT/DAT inhibitor.
- Risk of seizures (contraindicated in epilepsy, and pregnancy/breastfeeding).
- 🥇 Varenicline - 500mcg OD for 3 days. Then 500mcg BD for 4 days. Then 1mg BD for 11 weeks.
- Works as a partial nAChR antagonist.
- Used in caution with patients if depression or self-harm. Also contraindicated in pregnancy/breastfeeding
OR
- Adivse to stop - with clear, strong and personalised messages, focusing on their future health and current comorbidities if any. Also mention risk of second-hand smoke to family.
- Motivational messages - open-ended questions that allow the patient to think about stopping. Ask about the risks, rewards, roadblocks. Repetition is key also.
- Offer NRT or varenicline-assisted reduction
- First thing to do is take a smoking history:
- How long?
- How much do they smoke?
- What type?
- When do they smoke (any triggers)?
- How much would they save?
- Have they tried quitting?
- Withdrawal symptoms?
- PMH:
- Lung disease
- CVD
- DH:
- Previous NRT, bupropion or varenicline.
- SH:
- Alcohol
- Recreational drug use
- Stressors at home and work
- Employment
5 A’s approach:
Ask - about smoking status and record it.
Advise - on the risks of smoking and long-term effects. Reassure them that they will be supported throughout.
Assess - assess their understanding of the consequences. Assess their views on cessation and if they are motivated and where they stand according to the Stages of Change Model.
Assist - use the STAR approach to do so:
- S - Set a date, usually within 2-4 weeks.
- T - Tell family and friends to be more accountable.
- A - Anticipate any potential roadblocks and how they will overcome them.
- R - Remove all tobacco products. Recommend counselling and pharmacotherapy also. Counselling may be individual, group or telephone even.
Arrange - a follow-up appointment in 1-2 weeks to assess patient’s progress.
Another approach could be used is by asking:
- On a scale of 1-10 how important is it to you to give up smoking?
- Then ask “why did you choose that number and not the number lower”? (Assuming they do not pick 1).
https://www.uptodate.com/contents/image?imageKey=EM%2F71268&topicKey=EM%2F301&source=see_link
Dear future Sarmad,
Please open this link and write up on these common toxidromes when you revisit this condition.
Kind regards,
Present Sarmad Akram (21/12/2022)