describe the short term effects of alcohol misuse
1-2units - tachycardia, vasodilation giving you the warm sociable and talkative feeling
4-6units - brain and NS starts to be affected affecting the part associated with judgement and decision making. affects your reaction time and coordination
8-9units - reaction time much slower, speech starts to slur and vision loses focus
10-12units - coordination severely impaired, serious risk of accident. level of alcohol has a depressant effect on the on mind and body (drowsy). toxic levels, increase urine output, which cause you to be dehydrated
> 12units - considerable risk of developing alcohol poisoning . occurs when excessive volumes of alcohol art to interfere with body’s autonomic functions (breathing, heart rate, gag-reflex). coma and death in severe cases
other risks: violence and anti-social behaviour, accidents and injury, unsafe sex
describe the long term effects of alcohol misuse
Organs known to be damaged by long-term alcohol misuse include the brain and nervous system, heart, liver and pancreas
CVS + Resp:
- arrhythmia (AF/SVT)
- hypertension
- strep pneumonia, klebsiella TB
- Ca of lung
GI:
- gastritis
- fatty liver
- alcoholic hepatitis
- alcoholic liver cirrhosis
- acute or chronic pancreatitis
CNS:
- hepatic encephalopathy
- head injuries and subdural haemorrhages
- peripheral neuropathy
GU:
- impotence
- renal failure
- infertility
Alcohol withdrawal syndrome:
uncomplicated, with seizures or delirium tremens
what is involved in the clinical assessment of people who misuse alcohol?n
- > Alcohol consumption In units (how much) = Hx + biopsychosocial + risk assessment
- > when, where, with whom, why, what happens afterwards?
- > establish alcohol use disorder (WHO categories = hazardous, harmful, dependent, binge drinking)
- > treat complications
- > ask about driving
- > use screening tools
what screening tools can be used to assess alcohol misuse?
CAGE
AUDIT
FAST
blood tests (MCV, GGT, ALT)
Discuss the management of alcohol addiction
medical, psychological, and social interventions
medically assisted withdrawal from alcohol:
- benzodiazepines (chlordiazepoxide) - help reduce impact of AWS
- vitamins (IV high dose B vitamins)
- naltrexone - opioid antagonist, modulating euphoric effect
- baclofen - GABA agonist
relapse prevention:
- naltrexone (oppio antagonist. modulating euphoric effect)
- disulfiram (Antabuse)- irreversible inhibition of acetaldehyde dehydrogenase (ALDH) which converts alcohol to CO2 and H2O. acute sensitivity to alcohol causing flushing, headache, nausea, vomiting
- acamprosate (anti-craving drug) - enhancing GABA transmission in the brain; NMDA antagonist.
psychosocial:
- AA/Mutual Aid
- CBT
- MET (motivational enhancement therapy)
why is it important that someone doesn’t stop drinking alcohol suddenly?
can cause withdrawal symptoms (agitation, hallucinations, tremor, seizures, tachycardia, sweating, hypertension)
in severe cases can cause delirium tremens or Wernikes encephalopathy
define delerim tremins
severe and potentially fatal (5-15%) manifestation of alcohol withdrawal. dangerous mainly because of its effect on the ANS causing cardiac arrhythmias and respiratory depression
what is the triad that defines Wernikes encephalopathy
ophthalmoplegia, nystagmus (cerebral dysfunction) and confusion/acute confusional state (+ataxic gait)
acute neurological condition which can be precipitated by withdrawal that occurs due to vitamin B1/thiamine deficiency
list some risk factors of substance abuse
- genetic predisposition
- psychological factors (stress/ personality traits like impulsivity/ depression/ anxiety/ eating disorders/ personality and other psychiatric disorders)
- environmental influences (exposure to physical, sexual or emotional abuse)
list some risk factors of substance abuse
- genetic predisposition
- psychological factors (stress/ personality traits like impulsivity/ depression/ anxiety/ eating disorders/ personality and other psychiatric disorders)
- environmental influences (exposure to physical, sexual or emotional abuse)
what may make substance abuse more harmful?
- live alone
- not eating
- unemployed
what are the physical signs of chronic liver disease?
hands:
- clubbing
- leukonychia
- Dupuytren’s contracture
- palmar erythema
- flapping tremor
skin:
- purpura
- scratch marks (itch due to accumulation of bile salts in skin)
- bruising
- spider nevi - dilated blood vessels
- jaundice
- pallor
- hair loss
abdominal signs:
- splenomegaly
- hepatomegaly
- ascites
other:
- testicular atrophy
- oedema
- gynaecomastia
why is thiamine used in alcohol misuse management?
thiamine levels are low in alcohol abusers
vitamin supplement, advised to protect the brain as there is a risk of damage when someone has been drinking alcohol excessively, particularly when they are not eating a good diet
a) what are we particularly looking for in blood tests querying alcoholic liver disease.
b) what are markers of severe liver disease?
a) GGT enzymes often raised. can also be raised for other reasons like drugs, smoking, prostate/liver/breast cancer and pancreatitis.
b) low albumin and thrombocytopenia
(raised Hb and MCV are typical of alcohol excess.
low platelets are due to bone marrow suppression and increased portal hypertension and pooling of platelets in the spleen)
what other blood test might you consider if screening for chronic liver disease
coagulation screen, hepatitis B and C, anti-smooth muscle and antimitochondiral antibodies, immunoglobulins, Alpha-1 antitrypsin (particularly if Hx of lung disease; deficiency is a genetic disorder that may result in lung disease or liver disease), caeruloplasmin (Wilsons disease), ferritin (haemachromatosis)
what are the two most common medications to help pt’s remain abstinent from alcohol?
Disulfiram and Acamprosate (in combo with counselling)
Describe how addiction can be understood using psychological models
Temperance model:
- substance has the power of addiction and destruction
- that the individual is powerless against the addiction
- abstinence is the only salvation/Tx + understanding through abstinence you are able to remain well
Moral model:
- not used anymore as have neurological understanding
- frames addiction as a result of human weakness—a defect in character
- implication is that addiction is the result of poor choices made because of a lack of willpower or moral strength
Disease model:
- addiction is a disease with biological, neurological, genetic, and environmental sources of origin –> loss of control when drug is used
- person in control of managing their disease (don’t use)
medical model:
- physiological factors that put the person at risk
- control is related to risk management
psychodynamic model:
- related to psychodynamic factors such ACE’s or trauma
- addictive personality disorder/ self medication
- psychotherapy to address underlying factors
sociocultural models:
- factors within community that increase risk within a population (quality of living)
- these factors should be addressed
systems and family models:
- related to functioning of family and social systems
- for people to change need to consider relationships within system
- much more difficult to change system problem
learning model:
- is a learned behaviour therefore it can be unlearned and replaced by another learned behaviour
- person is responsible for learning and practising
describe the mechanisms of tolerance
Decrease of a behavioural response - with repeated admission more of a substance is required in order to achieve the same effects.
Exact mechanism unknown. possibility = accelerated metabolism from hepatic enzymes OR there is a decrease in binding affinity between a drug and receptor and a decrease in the number of receptors.
describe the mechanism of dependence
altered physiological state induced by long-term drug exposure that leads to a withdrawal syndrome on cessation of drug administration.
describe the neural mechanisms of addiction
long term administration of drug elicits changes in the neurones of the CNS that alter the functioning of neural circuits. depends on the drug and where they act (disrupt the reward circuit)
- at the receptor and transporter level. increased or decreased number of binding sites
e. g. cocaine blocks dopamine transporter so it is not taken back up –> pleasure and euphoria - at structural level. rearranging of synapses and connections. neuroplasticity and learning (where psychosocial interventions feature)
(2 mechanism neurobiological and psychosocial)
list some classes of substances that can be misu
- stimulants (cocaine)
- empathogens (MDMA)
- hallucinogens (ketamine, mushrooms)
- dissociative (ketamine)
- cannabinoids cause euphoria, enhancement of sensory perception, tachycardia, antinociception, difficulties in concentration and impairment of memory
- depressants inhibit the function of the CNS (diazepam, gabapentin)
- opioids, act on receptors to produce morphine like effects(heroin, methadone, codeine)
what are the main viruses associated with Hepatitis?
*NB inflammation is the wound-healing response of the liver to many causes of chronic injury
- hepatitis A, B, C, D, E, F and G
- cytomegalovirus
- EBV
- herpesvirus (immunocompressed)
- others like yellow fever virus, dengue virus
describe the natural history of liver damage
normal liver becomes damaged because of alcohol/ drugs/ viral infection/ autoimmune disorders etc –> inflammatory damage, parenchyma cell death, matrix deposition and angiogenesis –>early fibrosis –> disrupted architecture, loss of function and aberrant hepatocyte regeneration –> cirrhosis –> liver failure/ portal hypertension –> HCC (->) or liver transplant
can get regression from cirrhosis to early fibrosis or resolution from early fibrosis to normal liver with removal of underlying cause or anti-fibrotic drug or cell therapy
what are the clinical features of viral hepatitis
prodromal symptoms that are generally systemic and variable
constitutional symptoms (anorexia, flu-like, fatigue, malaise, weight loss, headache, low-grade fever) can precede symptoms of liver dysfunction
liver dysfunction symptoms - jaundice, dark burins, abdomen pain, hepatomegaly, tender RUQ
