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week 36: substance abuse > general > Flashcards

general Flashcards

1
Q

describe the short term effects of alcohol misuse

A

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

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2
Q

describe the long term effects of alcohol misuse

A

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

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3
Q

what is involved in the clinical assessment of people who misuse alcohol?n

A
  • > 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
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4
Q

what screening tools can be used to assess alcohol misuse?

A

CAGE

AUDIT

FAST

blood tests (MCV, GGT, ALT)

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5
Q

Discuss the management of alcohol addiction

A

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)
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6
Q

why is it important that someone doesn’t stop drinking alcohol suddenly?

A

can cause withdrawal symptoms (agitation, hallucinations, tremor, seizures, tachycardia, sweating, hypertension)

in severe cases can cause delirium tremens or Wernikes encephalopathy

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7
Q

define delerim tremins

A

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

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8
Q

what is the triad that defines Wernikes encephalopathy

A

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

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9
Q

list some risk factors of substance abuse

A
  • 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)
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10
Q

list some risk factors of substance abuse

A
  • 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)
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11
Q

what may make substance abuse more harmful?

A
  • live alone
  • not eating
  • unemployed
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12
Q

what are the physical signs of chronic liver disease?

A

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
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13
Q

why is thiamine used in alcohol misuse management?

A

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

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14
Q

a) what are we particularly looking for in blood tests querying alcoholic liver disease.
b) what are markers of severe liver disease?

A

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)

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15
Q

what other blood test might you consider if screening for chronic liver disease

A

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)

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16
Q

what are the two most common medications to help pt’s remain abstinent from alcohol?

A

Disulfiram and Acamprosate (in combo with counselling)

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17
Q

Describe how addiction can be understood using psychological models

A

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
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18
Q

describe the mechanisms of tolerance

A

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.

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19
Q

describe the mechanism of dependence

A

altered physiological state induced by long-term drug exposure that leads to a withdrawal syndrome on cessation of drug administration.

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20
Q

describe the neural mechanisms of addiction

A

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)

  1. 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
  2. at structural level. rearranging of synapses and connections. neuroplasticity and learning (where psychosocial interventions feature)

(2 mechanism neurobiological and psychosocial)

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21
Q

list some classes of substances that can be misu

A
  • 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)
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22
Q

what are the main viruses associated with Hepatitis?

*NB inflammation is the wound-healing response of the liver to many causes of chronic injury

A
  • hepatitis A, B, C, D, E, F and G
  • cytomegalovirus
  • EBV
  • herpesvirus (immunocompressed)
  • others like yellow fever virus, dengue virus
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23
Q

describe the natural history of liver damage

A

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

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24
Q

what are the clinical features of viral hepatitis

A

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

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25
Q

how is a diagnosis of viral hepatitis made?

A

usually done by detailed Hx taking: Understand clinical details and incubation period. Ask questions about risk factors e.g. IVDU/ travel/ vaccination Hx/ tattoos/ blood transfusion/ unprotected sex/ medication/ food/ drink/ hospitalisation. Examination and LFT pattern (Pt’s mostly present in similar way but LFT’s can tell you if it is acute or chronic case)

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26
Q

what single blood result would make you worried about/ suggest liver failure in a pt with suggestive liver dysfunction?

A

high lactate

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27
Q

a) what antibody blood result would be suggestive of acute viral hepatitis B infection?
b) what marker is an indication of past or chronic infection HBV?
c) what other blood result is suggestive of current/ active HBV infection
d) what serum marker is suggestive of past vaccine for HBV?

A

a) IgM antibody to core antigen –>found in serum shortly before onset of symptoms and peaks during LFT elevation. undetected within 6months if pt doesn’t progress to cirrhosis state
b) IgG core antibody
c) surface antigen marker. undetectable within 6mnth if pt doesn’t progress to chronic. also
d) anti-surface antibody

28
Q

what is the incubation period for hepatitis viral infection?

A

Hep A: 28days/1month
Hep B: 3months
Hep C: 45days
Hep D: 40days - generally present early

29
Q

name some functions of the healthy liver

A
  • conjugation and elimination of bilirubin
  • synthesis of albumin, clotting factors
  • gluconeogenesis
  • glycogen storage
  • production of bile - needed to digest fat, and absorb vitamins A, D, E and K
30
Q

describe the role of LFTs

A
  • confirm clinical suspicion

- differentiate between hepatocellular and cholestasis/post-hepatic/ obstruction

31
Q

describe the role of liver ‘function’ tests

A

synthetic function:

  • PTT
  • albumin
  • bilirubin

measure of excretion:

  • bile acids
  • dye clearance tests

measure of metabolic function:
- breath tests

biochemical/ enzymes:

  • ALT (hepatocytes)
  • AST(hepatocytes, cardiac muscle, skeletal muscle, kidney, brain etc)
  • -> released in response to liver damage or disease
  • -> ALT+AST >1000: ischaemic hepatitis, viral hepatitis, paracetamol
  • -> AST>ALT: acute alcoholic hepatitis, drugs, cirrhosis
  • -> ALT>AST: chronic liver disease, viral hepatitis unless cirrhosis is present
  • ALP (biliary epithelium, bone, placenta)
  • GGT (liver and other viscera; main role is to help interpret ALP)
  • ->ALP»GGT: bone disease, pregnancy
  • -> GGT»ALP: alcohol, medications

*an increase in AST, ALT reflects hepatocellular damage. increase in ALP, GTT reflects cholestasis (biliary obstruction/epithelial damage)

32
Q

why would there be low platelets in portal hypertension?

A

(acute; chronic would be ascites/ varices) more blood shunted to spleen which then traps platelets

33
Q

a. what proportion of ALT to ALP indicates likelihood of hepatocellar injury?

A

greater than 10 fold increase in ALT

lower than a 3 fold increase in ALP

34
Q

what proportion of ALT to ALP indicated likelihood of cholestasis?

A

lower than 10 fold increase in ALT

higher than 3 fold increase in ALP

35
Q

list 3 reasons why there might be a drop in albumin levels?

A
  1. decreased production due to liver disease
  2. inflammation triggering acute phase response
  3. loss (e.g. nephrotic syndrome)
36
Q

list the common liver imaging techniques

A

USS:

  • check for structural changes (hepatomegaly, masses), obstructions in the biliary tree, help distinguish between intrahepatic and extrahepatic causes
  • common Ix of cholelithiasis and cholecystitis

doppler USS:
- assess direction of blood flow and patency of blood vessels (especially portal vein)

CT:
-good for detecting masses and fatty liver

ERCP:

  • detailed imaging and Tx
  • can remove stones, insert stents and used for sphincter dysfunction
37
Q

define addiction

A

addictions are chronic conditions ‘resulting in a powerful motivation to engage in a given behaviour with a significant potential to harm’

NB: addiction and dependence are usually used interchanheably
: physical dependence refers to physiological adaptions (tremors and other withdrawal effects)
: psychological dependence refers to powerful motivation to use a drug to to engage in a particular behaviour repeatedly

38
Q

what are the global prevalence levels of addiction?

A

alcohol = most prevalent 43.5%

tobacco = 22.5%

cannabis = 3.5%

39
Q

analyse the psychological model of addiction: PRIME

A
  • there is an ‘external’ and ‘internal’ environment inside the person who is suffering the addiction
  • the external environment influences the internal
  • the internal environment has 5 elements (PRIME), any dysfunction in any elements can contribute to addiction:
  • > plans: malfunction = person cannot create effective plan to quit addiction
  • > evaluation: malfunction = unrealistic/bias processing leading to think that the addiction is helping them e.g. coping mechanism
  • > Motives: malfunction = powerful urges to take part due to previous experiences with (good) and without it (bad)
  • > impulses: malfunction = there is a strongg association between certain cues and taking part in the behaviour
  • —-> resposes
40
Q

what chemical is released when the reward system is activated?

A

dopamine (and serotonin??)

41
Q

liver fibrosis is not normally an problem. when does it become clinically relevant?

A

dysreggulation and excessive scarring occurs in response to persistent injury –> tissue disfunction

42
Q

what is the route of transmission of viral hepatitis?

A 
A - F/O. food (shellfish) 🦞 🦐 . MSM.
B - sex. IVDU. childbirth.
C -sex. IVDU.
D - only if infected with HBV.
E - F/O. food 🐖  (undercooked pork).
43
Q

what is the management of acute and chronic HBV?

A

acute:

  • symptom relief
  • likely spontaneous clear
  • repeat blood to make sure they develop antibodies
  • advice to use protection
  • vaccinate close contacts

chronic:

  • if surface antigen is positive for >6mnths or IgG is positive, anti-surface antigen is negative
  • referral
  • regulate LFTs, HBV markers, fibroscan (increased risk of HCC)
  • some require Tx: pegylated interferon SC for 48weeks. nucleoside analogue therapy oral long term until surface antigen is lost
44
Q

what virology tests are there for HCV?

A
  • anti-HCV antibody -> past or chronic infection

- HCV antigen -> active/current infection

45
Q

what is the management of chronic HCV?

A

oral direct acting antivirals achieving sustained virological response/clearance

goal = prevent the complications of HCV-related liver and extra-hepatic diseases, including hepatic necroinflamfmation, fibrosis, cirrhosis, decompensation of cirrhosis, HCC, severe extra-hepatic manifestations and death

46
Q

T or F. hep A only causes acute infection?

A

True

47
Q

what hepatitis viral infection can cause extra hepatic manifestations, neurological, renal and haematological disorders?

A

Hep E

48
Q

what virology tests are available for HAV and HEV?

A

HAV:
anti-HAV IgM -> recent infection
anti-HAV IgG -> past infection/vaccination

HEV:
Anti-HEV - IgM -> recent infection

49
Q

what is the management of acute hep A infection?

A
  • advice on good hygiene practice
  • exclude from work until 7days post onset jaundice or in absence, from onset of compatible symptoms
  • identify possible source
  • undertake risk assessment/ inform public health

*infectious period is taken from 2 weeks before onset of first symptoms and until one week after the onset of jaundice

50
Q

what diagnosis gives the following serology results?…

a) anti-HAV IgM - positive, anti-HAV IgG - positive, HBsAg - negative, Anti-HC V Ab - negative, Anti-HEV IgM - negative, HIV Ag/Ab - negative

b) HBsAg - positive,
IgM anti-HBC - positive, IgG anti-HBcAb - negative, HCV Ag - negative, Anti-HCV Ab - negative, HIV Ag/Ab - negative

c) HBsAG - negative, anti-HBc IgG - positive, anti-HBs -positive
d) HBsAg - negative, anti-HBc IgG - positive, anti-HBs - negative
e) HBsAg - negative, anti-HBc IgG negative, anti-HBs positive

A

a) acute Hep A infection
b) acute Hep B infection
c) past HBV infection with immunity (NB if anti-HBs is positive, means that the pt developed immunity through previous infection)
d) past HBV infection without immunity (NB if anti-HBs is negative. means that the pt did not develop immunity through previous infection and these pt’s are still at risk of acquiring HBV again)
e) immunity via vaccination (if pt is only positive for anti-HBs)

51
Q

if a pt has had past HBV infection without immunity what is the concern?

A

can acquire again.

if they become immunosuppressed, they could have reactivation of HBV

could give HBV vaccination to promote antibody development to ensure the pt;s become immune

52
Q

what is functional cure of HBV?

A

clearance of HBsAg

53
Q

describe the epidemiology of drug use in Scotland, and some of the causes

A

epidemiology:

  • 57,300 estimated drug users in 2015/16
  • drug-death rate 3.4 times that of UK as whole in 2018 and continues to increase
  • increased rates amongst the deprived and homeless

trends/causes:

  • male and females higher in 35-64y/o
  • deprivation/ poverty
  • homelessness
  • mental health dual diagnosis
  • trauma
  • violence
  • neglect
  • stigma
  • lack of access to effective, high-quality treatment and support
54
Q

list the potential implications of the recent trends in substance use in Scotland

A
  • risk of mortality increases in drug users ( + from other causes, exacerbated by drug use)
  • increasing rates of morbidity, especially hospital admissions
  • burden of disease increasing
  • costs (8,546 general acute hospital stays with Dx of drug misuse in 2016/17). economic impact (total economic and social costs of illicit drug use is around 3.4bn/yr in 2009)
  • pose risk to children, family breakdown, unemployment and homelessness
  • injecting is associated with risk of transmission of BBV like HIV, Hep C
  • increasing geographical and deprivation-related disparity
55
Q

discuss some of the problems and priorities in relation to tackling drug use-related disorders at a population level

A
  • current approaches have been ineffective in reducing drug-related harm
  • do not exclude people with severe mental illness because of their substance misuse
  • complex issue requires a whole systems approach
  • work together across agencies and localities to develop action plans
  • quick access to quality services is key
56
Q

how do you calculate QALY?

A

length of life (years) X quality (0-1)

  • 0 = dead
    1 = perfect
57
Q

list 4 signs and symptoms of alcohol dependence

A
  • recurrent intoxication, nausea, sweating, tachycardia, hypertension
  • mood swings, depression, anxiety, suicide
  • poor nutrition, poor immunity and personal neglect
  • dyspepsia, diarrhoea, bloating, hematemesis, jaundice
58
Q

what are the CVS and Rest complications of alcohol misuse?

A
  • arrhythmia: AF and SVT
  • hypertension
  • cardiomyopathy
  • cerebrovascular accident/ stroke
  • weaker immune system so, strep pneumonia, TB, klebsiella infection
  • Ca lung
59
Q

what are the GI and hepatic complications of alcohol misuse?

A
  • gastritis
  • fatty liver
  • alcohol hepatitis
  • alcoholic liver cirrhosis
  • acute or chronic pancreatitis
  • malert weiss syndrome
60
Q

what are the CNS complications of alcohol misuse?

A
  • head injuries and subdural haemorrhages
  • hepatic encephalopathy
  • peripheral neuropathy
  • cerebral degeneration
61
Q

define the different types of AWS

A

uncomplicated AWS:

  • 4-12hrs after last alcoholic drink, peak at 48hrs, lasting 2-5days
  • coarse tremor, sweating, insomnia, nausea, vomiting
  • increased craving

AWS with seizure:

  • complicated by grand Mal seizure in 5-15% of cases of withdrawal
  • predisposed by previous withdrawal seizures, idiopathic epilepsy, head injury, hypokalaemia

delirium tremens:

  • acute confusional state, medical emergency
  • onset 1-7days after last drink
  • risks = severe dependence, co-morbid infection, pre-existing liver damage
  • marked psychomotor agitation, hallucinations, persecutory delusions, febrile

Wenicke-Korsakoff syndrome:

  • haemorrhages and secondary gliosis in periventricular and periaqueductal grey matter involving the maxillary bodies, hypothalamus, mesodorsal thalamic nucleus, colliculi and tegmenjtum of the midbrain
  • neuronal degeneration secondary to thiamine deficiency
62
Q

what are the 4 groups od the DSM-V criteria for substance use disorders?

A
  1. impaired control - substance often taken in larger amounts or over a longer period than was intended
  2. risky use of substance - recurrent use in situation in which it is physically hazardous
  3. social impairment - recurrent substance use resulting in a failure to fulfil major role obligations at work, school, or home
  4. pharmacological criteria - tolerance or withdrawal
63
Q

list criteria for substance misuse disorders

A
  • cravings
  • wanting to cut down or stop and not being able to
  • taking substance in larger amounts for longer than meant to
  • neglecting other parts of your life because of the substance
  • continuing to use even though it causes problems with relationships
  • using substance even when it puts you in danger
64
Q

what is involved in assessment and management of someone misusing drugs?

A

assessment. …
1. biopsychosocial
- stages of change and how you intervene
2. formulation:
- predisposing
- precipitating
- perpetuating
- presenting
- protective
3. risk:
- self (neglect, harm, suicide), others, exploitation (financial, perpetrator)

management. …
1. short and long term recovery
- opiod dependency disorder -> substitution Tx - methadone, buprenorphine, HAT
- alcohol - medically assisted withdrawal with benzodiazepines and vitamins. relapse prevention with naltrexone (dont get pleasure from substance when take it), disulfiram, Acamprosate
2. body maps/ diaries

65
Q

what are the stages of change

A
  1. pre-contemplations (unaware/unready) - intervention unlikely to success, give information about risks
  2. contemplation (aware) - offer advice and/or motivational work to move patient along
  3. preparation (planning) - set date, make plans, be specific, anticipate difficulties
  4. Action (ready) - encourage, support, offer follow-up
  5. maintenance (keeping it up) - reinforce success, advise on managing slips/relapse prevention

week 36: substance abuse (1 decks)

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