2.02 - Opioid Dependence, Hepatitic C

Front 1

What are the three types of opioid receptor?

Back 1

mu
kappa
delta

Front 2

To which type of opioid receptor does morphine have greatest affinity?

Back 2

Mu

Front 3

To which type of opioid receptor does codeine have greatest affinity?

Back 3

Equally weak affinity to all 3

Front 4

To which type of opioid receptor does naloxone have greatest affinity?

Back 4

Almost equally strong affinity to all 3

Front 5

To which type of opioid receptor does beta-endorphin have greatest affinity?

Back 5

Equally strong affinity to all 3

Front 6

T/F: beta endorphin is naturally occuring

Back 6

true

Front 7

Stimulation of kappa opioid receptors has what effect?

Back 7

1.Analgesia at spinal level
2. Dysphoria

Front 8

stimulation of mu and delta receptors has what effect?

Back 8

1. Analgesia (spinal and supraspinal)
2. Euphoria
3. Respiratory depression [decr. sensitivity to arterial CO2]
4. Decr. GI motility, incr. sphincter tone->constipation
5. Pupillary constriction [receptors in occulomotor nuc.]
6. Nausea and vomiting [area postrema feeds into chemoreceptor trigger zone]
7. Reduced cough reflex

Front 9

Are opiates effective for neuropathic pain?

Back 9

No

Front 10

Why does stimulation of mu receptor cause respiratory depression?

Back 10

Dampens brainstem sensitivity to incr. in PaCO2 --> won't get increased ventilatory response to rises in CO2

Front 11

What is the bioavailability (F) and half life of morphine?

Back 11

F = 20-30%
t1/2 = short [2-3hrs]

Front 12

Describe metabolism of morphine

Back 12

Phase II conjugation with GLUCURONIC ACID (added at 3rd and 6th position)

Get M-6-glucuronide and M-3-glucuronide

Front 13

T/F: M-3-glucuronide is twice as potent as morphine

Back 13

False. M-6-glucuronide is twice as potent

Front 14

What is the net analgesic effect of morphine and its metabolites?

Back 14

Combination of morphine actions AND M-6-glucuronide actions.

M-3-G is inactive.

Front 15

What is the structural difference between codeine and morphine?

Back 15

Codeine = 3-methyl-morphine (i.e. has methyl group at 3rd carbon, otherwise same)

Front 16

What is the bioavailability of codeine cf. morphine? and why?

Back 16

Codeine = 50%
Morphine = 20-30%
due to the methyl group at 3rd carbon

Front 17

Which enzyme converts codeine to morphine?

Back 17

CYP 2D6

to remember: coDEine (i.e. D)

Front 18

What is a "poor metaboliser of codeine"

Back 18

Someone who has a polymorphism in their gene for CYP 2D6 --> can't convert codeine to morphine and don't get as much analgesia

[7-10% Caucasians are poor metabolisers]

Front 19

Difference between oxycodone and codeine?

Back 19

Oxycodone NOT a pro-drug (c.f. codeine)
Oxycodone binds DIRECTLY to opiate receptors (i.e. full agonist)
Oxycodone bioavailability - 80% (c.f. 50% codeine)

Front 20

Difference between endone and oxycontin?

Back 20

Both oxycodone.
Endone - short acting (4-5hr duration)
Oxycontin - sustained release (12hr duration)

Front 21

Give features of fentanyl

Back 21

- mu agonist
- 60-80x more potent than morphine
- lipid soluble (crosses BBB)
- Short half life (3hrs)

Front 22

Give features of buprenorphine. What is it used for?

Back 22

- partial mu agonist
- full kappa antagonist

Used in treatment of opioid dependence

Front 23

What are some benefits of taking Tramadol?

Back 23

Less constipation
Less respiratory depression
Less addiction potential
.....cf morphine

Front 24

Give features of Tramadol

Back 24

Good oral bioavailability (70%)
Weak mu agonist
inhibits NA uptake
Enhances serotonin release

Front 25

Why should pethadine not be used?

Back 25

Very short half life (2hrs) --> more addiction potential
Metabolite accumulates with renal impairment --> convulsions
Lot of potential drug interactions

Front 26

Why is methadone used in oral maintenance programs for addicts?

Back 26

- similar molecular actions to morphine
- little euphoria --> less potential for abuse
- slow release from extracellular compartments (i.e. take once daily)

Front 27

What is heroin? Why can it cross the BBB so fast?

Back 27

Di-acetyl morphine
--> more lipophilic than morphine so crosses the BBB

Front 28

Endogenous opioids are derived from...?

Back 28

Larger polypeptide structures that have undergone post-translational modifications .
All contain enkephalin

Front 29

T/F: all opioid receptors are ionotropic

Back 29

False. they are all metabotropic

Front 30

What are the actions of opioids on their receptors?

Back 30

1. Close Ca2+ channels
-->inhibit NT release
2. Open K+ leakage channels
-->hyperpolarisation
3. Decrease AC activity
--> less cAMP

Front 31

Why do mu receptors cause euphoria and kappa receptors cause dysphoria?

Back 31

Depends on LOCATION OF RECEPTORS in mesolimbic dopaminergic pathway.
Cell bodies in VTA project to NAC and release DA.

Mu receptors are on inter-neurons at the VTA. Stimulation will inhibit the inhibitory interneuron --> firing --> DA release in NAC

Kappa receptors are found on nerve terminals in the NAC. Stimulation will decr. Ca2+ influx --> direct inhibition of DA release in NAC

Front 32

Difference between naltrexone and naloxone?

Back 32

Naloxone = reversal of opioid overdose (short half life, give subQ because low oral availability, reverses opioid effect in seconds)

Naltrexone = used in management of opioid dependence. Longer acting (half life 14 hrs), high oral bioavailability

Front 33

What is a problem with using naltrexone?

Back 33

Risk of OD if patient relapses, because their tolerance will have decreased if they haven't been using regularly

Front 34

What is the normal nociceptive ascending pathway?

Back 34

Peripheral pain receptors --> dorsal horn --> PAG in midbrain --> thalamus --> somatosensory cortex, anterior cingulate gyrus (emotional experience)

Front 35

What role does the PAG play in pain perception?

Back 35

The peri-aqueductal grey acts as a "gate" in the midbrain.
The PAG receives input from higher brain regions which activate a descending inhibitory system limiting the amount of nociception reaching brain.

Basically STIMULATE PAG --> shut the gate to the ascending pain pathway at level of dorsal horn

Front 36

The limbic system is proposed to be involved in which part of pain perception?

Back 36

Emotional

Front 37

How do opioids provide analgesia at the level of the PAG?

Back 37

Opioid receptors located on GABA interneurons in PAG.
Stimulate receptor --> inhibit GABA interneuron --> "take off the brakes" --> descending pathway activated --> ascending pain pathway inhibited (gate closes)

Front 38

T/F: Systemic NSAIDs potentiate opioid analgesia synergistically

Back 38

FALSE.
Systemic NSAIDs potentiate opioid analgesia ADDITIVELY.

Front 39

Which route of administration of NSAIDs potentiates opioids synergistically?

Back 39

SPINAL NSAIDs

Front 40

How does combining opioids and spinal NSAIDs increase analgesia?

Back 40

1. Opioid binds mu receptor on GABA interneuron in PAG.
2. G-protein activates PLA pathway
3. Arachidonic acid cleaved from cell membrane and converted to 12-lipoxygenase
4. Increased conduction of K+ channels
5. Inhibition of GABA interneuron
6. Excitation of descending pathway to inhibit ascending pain pathway.

BUT - arachidonic acid is also converted to cyclooxygenase. NSAIDs inhibit cyclooxygenase --> more arachidonic acid to be converted to 12-lipoxygenase --> more analgesia (synergism)

Front 41

What percentage of the world's human population is infected with Hep C?

Back 41

Approx. 3%

Front 42

What percentage of acute Hepatitic C infections display overt clinical disease?

Back 42

25%

Front 43

T/F: People who have had clinical disease with acute Hep C infection are more likely to clear the infection entirely and not progress to chronic infection

Back 43

True.

Front 44

T/F: Majority of people will die from Hepatitis C

Back 44

False.
Majority of infected individuals will die WITH disease, not FROM.

Front 45

What percentage of people will progress to chronic Hep C infection?

Back 45

Approx 80%

Front 46

What percentage of chronic Hep C infections will develop liver cirrhosis within 10 years?

Back 46

Approx 40%

Front 47

What percentage of chronic Hep C infections will develop hepatocellular carcinoma within 10 years?

Back 47

Approx 20%

Front 48

T/F: Hepatitis C virus ONLY infects hepatocytes

Back 48

True

Front 49

Why does the Hepatitis C virus mutate rapidly?

Back 49

RNA virus --> RNA Pol has no proof-reading ability.

Front 50

Hepatitis C Virus genotype 4 is predominent in which locations?

Back 50

Egypt and Africa

Front 51

Which Hepatitis C virus genotype is most difficult to treat?

Back 51

Genotype 1

Front 52

Which Hepatitis C virus genotype is most common?

Back 52

Genotype 1 - responsible for 60% infections

Front 53

What is the predominant mode of Hep C infection in Australia and North America?

Back 53

IV drug use

Front 54

What percentage of haemophiliacs are infected with Hep C and why?

Back 54

Approx 90%
High transfusion rate-->high risk

Front 55

T/F: Prophylactic treatment can be given after Hep C virus exposure?

Back 55

False - have to wait 12 weeks to see if become RNA +ve

Front 56

What are some exposures known to be associated with Hep C infection?

Back 56

- Injecting drug use
- transfusion, transplant from infected donor
- occupational exposure to blood
- unsafe injections
- birth to HCV-infected mother (vertical transmission rate <6%)
- Sex w/ infected partner

Front 57

Factors that are associated with faster HCV progression / worse response to treatment = ?

Back 57

- Age at infection - better prognosis if younger
- Gender --> males are worse – less response to treatment, higher prevalence of chronic infection
- Race – eg African-Americans have lower response rates to treatment and more severe cirrhosis
- Alcohol – heavy alcohol drinking concurrent with infection --> more severe liver disease
- HIV infection
- Obesity (more likely to have fatty liver disease)
- Haemachromatosis
- Schistomiasis
- Genetics

Front 58

How long does it take for anti-HCV antibodies to be detected in blood?

Back 58

8-12 weeks

Front 59

T/F: ALT levels predict liver damage

Back 59

False

Front 60

What serological features would you see with acute Hep C virus infection with RECOVERY?

Back 60

- Initial HCV RNA which becomes and remains negative
- Rise in ALT which then drops
- Still have anti-HCV Abs after cleared infection

Front 61

What serological features would you see with acute Hep C virus infection with PROGRESSION TO CHRONIC DISEASE?

Back 61

- HSV RNA positive (because don't clear infection)
- Anti-HCV Abs
- Initial peak in ALT which then fluctuate throughout chronic infection

Front 62

How do you test for HCV infection?

Back 62

1. ELISA
if positive:
2. PCR - very sensitive to RNA

Front 63

When is treatment of Hep C NOT recommended?

Back 63

- Persistently normal ALT
- Advanced or decompensated liver cirrhosis
- Excessive alcohol use
- Active drug use

Front 64

When is treatment of Hep C recommended?

Back 64

- Detectable HCV RNA
- Persistently elevated ALT
- Abnormal liver biopsy showing portal or bridging fibrosis, or at least moderate inflammation

Front 65

What are the predictors of a favourable response to HCV treatment?

Back 65

- Genotype 2 or 3
- Low viral load
- No or only portal fibrosis
- Female
- <40 yo

Front 66

The IL-28B gene on chromosome 19 encodes what?

Back 66

IFN - lambda 3

Front 67

Having the IL-28B gene on chromosome 19 is associated with what?

Back 67

Encodes for IFN - lambda 3. (This is favourable!!)

People with this gene are
-->MORE LIKELY to CLEAR THE VIRUS
-->MORE LIKELY to RESPOND TO THERAPY

Different polymorphisms in the promoter region of the gene have been linked to different success rates with treatment and also the rate of spontaneous clearance

Front 68

At 12 week follow-up after initiating HCV treatment, what drop in viral load is needed in order to continue treatment?

Back 68

Need a 2 log drop in viral load

--> if less than that, the treatment isn't working!

Front 69

How do you treat HCV infection? What are some contra-indications?

Back 69

IFNs and ribavirin

IFNs - side effects (constant flu like symptoms)

Ribavirin - teratogenic, must take in conjunction with contraception

Front 70

What are the three levels of protection against viruses?

Back 70

1. Physical barriers
2. Innate immune system
3. Adaptive immune system

Front 71

What are they 'key players' in the innate immune response against viruses?

Back 71

Type I IFN, NK cells, inflammatory mediators (eg cytokines)

Front 72

Outline the Herpesvirus life cycle

Back 72

1. Attachment
2. Penetration
3. Uncoating
4. Gene expression and DNA replication
5. Assembly
6. Release of progeny virus

Front 73

Viral infection stimulates production of which type of interferon?

Back 73

Type 1 IFN

Front 74

Type I interferons function to:
1. _____
2. _____
3. _____

Back 74

1. Inhibit viral infection and replication by inducing ANTI VIRAL STATE

2. Enhance cytotoxic T cell acvitiy

3. Enhance cytotoxic activity of NK cells

Front 75

What is an "anti viral state"

Back 75

Whereby enzymes are induced within a cell to block viral replication.
IFN also acts on bystander cells - priming them to an anti-viral state

Front 76

How does type 1 IFN enhance T cell cytotoxicity?

Back 76

IFN binds R on infected cell --> signalling cascade results in upregulation of class I MHC --> increased chance will be seen by CD8+ T cells

Front 77

How does type 1 IFN block viral replication

Back 77

Binding of IFN to receptor induces a signalling cascade that results in enzymes, such as those that degrade newly synthesised mRNA

Front 78

NK cells recognise what?

Back 78

Cells that fail to express MHC Class I

Front 79

T/F: NK cells contain T cell genes

Back 79

False

Front 80

What type of cell are NK cells?

Back 80

Large, granular lymphocytes

Front 81

Which cytokines are involved in the innate immune response to viral infection?

Back 81

TNF
IFN-gamma
IL-1
IL-2

Front 82

T/F: Antibodies are effective against viruses primarily during the intracellular phase of their life cycle

Back 82

False. Extracellular

Front 83

What type of antibodies are most effective in the extracellular phase?

Back 83

Neutralising Abs - prevents virus binding to cell surface receptor

Front 84

What process involving antibodies is most effective in the intracellular phase?

Back 84

ADCC

Front 85

What cytokine stimulates movement of DCs to the secondary lymphoid organs

Back 85

TNF-alpha

Front 86

Outline process of ADCC

Back 86

1. Viral infected cell expresses viral proteins on surface
2. IgG binds infected cell (Fab region)
3. Fc region binds FcR on NK cells
4. NK cells activated, degranulate
5. Apoptosis of infected cell

Front 87

What do perforin and granzymes do?

Back 87

Perforin = forms poly-perforin ring (i.e. hole) in infected cell membrane

Granzymes activate caspases - induce apoptosis

Front 88

How do viruses passively evade immune system?

Back 88

- infect immune priviledged sites that don't have MHC (eg neurons)
- establish latent infections

Front 89

How do viruses aggressively evade immune system?

Back 89

Infect and kill immune cells --> immunosuppression (e.g. HIV)

Front 90

How do viruses actively evade innate immune system?

Back 90

1. Interfere with type 1 IFN
-->some viruses encode IFN-R homolog that lacks transmembrane region
-->inhibit intracellular signalling cascade

2. Interfere with other cytokine signalling networks e.g. TNF-R homologs

3. Evade NK killing
--> HCMV expresses MHC-I homolog on surface that engages NK cells but not T cells

Front 91

How do viruses actively evade adaptive immune system?

Back 91

1. Modulate ADCC
--> HCMV encodes surface protein that binds FcR so that it can't bind to NK cells

2. Antigenic variation by RNA viruses

3. Inhibit Class I or II pathways

Front 92

How do viruses interfere with MHC Class I presentation

Back 92

- inhibition of generation of antigenic peptide

- Antigenic peptides transported via TAP complex

- inhibition of MHC I surface expression

Front 93

How do viruses interfere with MHC Class II presentation

Back 93

- inhibition of surface expression of MHC-II molecules (i.e. post-translational effects)

- inhibition of IFN-induced expression of MHC-II molecules (i.e. transcriptional effects)

Front 94

What are the 3 most common bloodborne viruses?

Back 94

Hep B
Hep C
HIV

Front 95

Outline features of Hep A

Back 95

- transmitted by faecal-oral route
- acute infection = jaundice, yellow eyes, flu symptoms
- body rapidly clears virus
- 0.05% people get serious liver damage
- virus in faeces when viraemic

Front 96

What proportion of community are anti-HCA Ab positive?

Back 96

20-80%

Front 97

Outline features of Hep B

Back 97

- DNA virus
- Abs directed against core and surface proteins (vaccine only gives against surface)
- infected for life (inserts into host genome)

Front 98

What does the E antigen in Hepatitis B indicate?

Back 98

E antigen = marker of virulence
If positive for E antigen, indicates virus in high replicative state, probable high viraemia

Front 99

What is the most reliable predictor of long term sequelae from infection with Hep B?

Back 99

DNA levels

Front 100

How do you treat Hep B?

Back 100

nucleotide analogs

Front 101

What are transaminases?

Back 101

released from dying hepatocytes in either acute or chronic infections

Front 102

what is gGT?

Back 102

inducible enzyme --> elevated after drinking a lot of alcohol

Front 103

What liver function test results would you expect with IMPAIRED SYNTHETIC FUNCTION?

Back 103

Raised bilirubin
Raised INR
Decr. albumin levels

Front 104

what is INR?

Back 104

coagulation factor - raised when have impaired synthetic function

Front 105

Bilirubin relates to what?

Back 105

Hepatocyte clearance and excretion into bilary tree

Front 106

Raised levels of bilirubin indicates what

Back 106

- Liver problems (conjugation of free bilirubin insufficient/obstruction of bilary ducts)

-RBC problem (incr. RBC turnover --> too much bilirubin for healthy liver to process)

Front 107

What is alpha-fetoprotein

Back 107

marker for liver cancer

Front 108

For example with a needlestick injury, what is the risk for bloodborne transmission of the following viruses:
1. Hep B
2. Hep C
3. HIV

Back 108

1. Hep B - very high (about 50% if not already immune)

2. Hep C - about 2%

3. HIV - 0.3%

Front 109

Raised ALT and AST suggest what?

Back 109

Hepatocellular injury

Front 110

What can 'collateral damage' in the liver cause?

Back 110

- Acute swelling obstructs bile ducts
- Chronic inflammatory response causes fibrosis

Front 111

What are the steps in drug dependence treatment?

Back 111

1.Establish a therapeutic relationship
2.Individualised assessment – look at them as an individual
3.Personalised feedback
4.Clarification of THEIR values and goals - not yours
5.Encouragement
6.Medication if necessary
7.Follow-up monitoring of their progress

Front 112

What is therapeutic Nihlism?

Back 112

Therapeutic Nihilism = the generally untrue but continuing belief that drug users do not care about their health, don’t want to stop using, don’t want treatment and won’t benefit from it

Front 113

T/F: addiction involves neurobiological dysfunction and is not just behavioural

Back 113

TRUE.
Initial drug use may be voluntary, but established dependence is neurobiological syndrome

Front 114

What are some treatments for drug dependence that have sound clinical evidence?

Back 114

Methadone
Buprenorphine
Naltrexone
Motivational interviewing

Front 115

T/F: Alcohol and opioid dependence have the worst compliance rates when compared with other chronic diseases

Back 115

FALSE.
Treatment compliance is the same compared with other chronic diseases.

Adherence is a concern for all chronic disorders!

Front 116

If treatment is intervention directed to an affected individual, which populations are the following aimed at:

1. Primary prevention
2. Secondary prevention
3. Tertiary prevention

Back 116

1. Primary prevention - NON-USERS
2. Secondary prevention - NON-DEPENDENT
3. Tertiary prevention - DEPENDENT

Front 117

What are the key differences between incidental and planned withdrawal states?

Back 117

Incidental - typically severe (not motivated to reduce drug use, no preparation)

Planned - less severe (motivated to reduce drug use)

Front 118

What are the principles of withdrawal management?

Back 118

- Establish relationship and goals
- stop substance use
- monitor for withdrawal symptoms/signs
- reduce dose steadily to zero/maintenance level

Front 119

What is the drug of choice in alcohol withdrawal management?

Back 119

Diazepam, up to 1/52

Front 120

T/F: Buprenorphine is more effective at 'detoxifying' than methadone

Back 120

True

Front 121

Difference between methadone and buprenorphine USE

Back 121

Methadone - long term maintenance

Buprenorphine - partial agonist, daily dose for about 1 week permitting transition to maintenance treatments

Front 122

Who is at risk of benzodiazepine withdrawal?

Back 122

Risk if >3 tablets/day for >3 months

Front 123

What are the 3 stages that amphetamine/cocaine users go through once stopped using?

Back 123

1. CRASH [9hrs-4days]
-->dysphoria, fatigue, depression

2. WITHDRAWAL [1-10wks]
-->Anhedonia, fatigue, outbursts, intense craving

3. EXTINCTION [indefinite]
--> Normal mood/interest in life
--> Episodic craving in response to conditioned cues

Front 124

What percentage of regular ecstacy (MDMA) users develop DSM-IV criteria for dependence?

Back 124

50%

Front 125

List properties of buprenorphine

Back 125

1. Long duration of action - not needed daily

2. Partial agonist - safer in OD

3. High receptor affinity- naloxone ineffective

4. High first pass metabolism - given sublingually

Front 126

What does combining naloxone and buprenorphine achieve?

Back 126

Abuse deterrent preparation!
--> if taken as directed sublingually, only the buprenorphine is active

--> if taken IV, buprenorphine is more active but naloxone also active and precipitates withdrawal symptoms

Front 127

What does disulfiram ("antabuse") do ?

Back 127

Inhibits conversion of acetaldehyde to acetate

Alcohol: accumulation of acetaldehyde --> flushing syndrome

Front 128

What are some introduced diseases to the Indigenous population

Back 128

Smallpox
TB
Influenza
Measles
Whooping cough
Venereal diseases

Front 129

When was smallpox officially eradicated?

Back 129

1980

Front 130

Who were the "missionaries" and when were they around?

Back 130

1820s-1830s
Southeastern Australia - wanted to save Indigenous people from destruction

Front 131

What happened in Jervis Bay 1890?

Back 131

Aboriginals petitioned for better conditions, boats, nets, schools, etc

Front 132

What/when was the Australian Aboriginal Progress Association?

Back 132

1925
First Aboriginal political organisation to create formal links b/w communities over wide area

Front 133

When was the Aboriginal Progressive Association established? by whom?

Back 133

1937
By Bill Fergusen and Pearl Gibbs

Front 134

When did the Council for Aboriginal Rights make a film in Warburton Ranges?
What did they film?

Back 134

1957
Short film documenting appaling living conditions

Front 135

When and what was the "Freedom Ride"

Back 135

Ted Noffs + Charles Perkins
1965 - 30 Sydney University students (including Aboriginal people) undertook a 2,300 km bus tour of northern NSW towns investigating and protesting discrimination against Aborigines

Front 136

What was the result of the 1967 referendum?

Back 136

92% voted YES to include Aboriginals in the Census

Front 137

When was the Land Rights Legislation passed?

Back 137

Mid-late 1970s

Front 138

when was the Royal Commission into Aboriginal Deaths in Custody established?

Back 138

1987

Front 139

When did Kev say sorry?

Back 139

February 2008

Front 140

T/F: Sclerosed veins (site of chronic injecting drug use) increase maternal morbidity in obstetric emergency

Back 140

true

Front 141

Microdeficiencies of which substances is often seen in injecting drug users

Back 141

Vitamin B6 (pyroxidine)
Folate
Vitamin B1 (thiamine)
Significant anaemia

Front 142

What is hyperemesis gravid arum

Back 142

Vomiting and nausea. Common in injecting drug users - futher diminishes macronutrient intake

Front 143

What are the fetal risks of maternal heroin use during pregnancy

Back 143

No specific congenital malformations attributible to heroin, BUT high rate of perinatal mortality reflects high incidence of antenatal problems
-->intra-uterine death
-->retarded intra-uterine growth
-->prematurity
-->risk of fetal acquisition of infection

Front 144

Which mechanisms are responsible for antenatal problems in heroin users?

Back 144

Repeated hypoxic episodes secondary to maternal withdrawal.
Chorioamnionitis (inflam. of fetal membranes)
Chronic nutritional inadequacy
Cigarette smoking

Front 145

What are the risks to baby after birth to a heroin using mother?

Back 145

- Newly delivered baby may be OBTUNDED and require ventilation
- Specific opioid abstinence syndrome
- Post-discharge failure to thrive, neglect, abuse

Front 146

T/F: Needle exchange programs contain the spread of HIV and Hep C equally

Back 146

False.
Contain spread of Hep C LESS effectively. This may be due to ancillary equipment s.a. touriquets

Front 147

What are the common clinical presentations of infections resulting from injection of BACTERIALLY contaminated drugs

Back 147

- local abcess at injection site
- acute bacteremia
- prostration (abrupt failure of function or complete physical exhaustion)
- acute septicaemia (commonly Staph aureus)
- acute Staphylococcal bacterial endocarditis (commonly tricuspid valve)

Front 148

Infections from injection of VIRUS contaiminated drugs include:

Back 148

- HIV infection with acute presentation (fever, rash, lymphadenopathy)

- Hepatitis B with acute or chronic presentation (jaundice, prodrome)

- Hepatitis C with acute or chronic presentation (similar to Hep B)

RARELY, other viral infections s.a. Hepatitis G, Hepatitis A, HTLV-1

Front 149

T/F: Methadone injection may lead to extensive venous thrombophlebitis

Back 149

True.

Note, thrombophlebitis = Inflammation of the wall of a vein with associated thrombosis

Front 150

What characterises opioid intoxication?

Back 150

Drowsiness
Stupor
Pin-point pupils

Higher doses-coma, respiratory depression

Front 151

How is opioid intoxication managed?

Back 151

Initial as for alcohol i.e. SEDATIVE
Establish airway, ensure adequate ventilation

Naloxone if depressed breathing. [titrate against response as not to induce withdrawal state]

Front 152

What are some symptoms of opioid withdrawal? When do they begin / peak / end?

Back 152

Begin 8-16hrs after last dose.
Peak @ 2-3 days
End after 4-7 days

Yawning, sweats, runny eyes and nose, hot and cold flushes, muscle and joint pain, restlessness, insomnia, nausea, vomiting, diarrhoea

Front 153

What is the Five Factor Model of personality?

Back 153

Describes major measures/descriptors of personality (OCEAN)

Openness
Conscientiousness
Extroversion
Agreeableness
Neuroticism/emotional stability

Front 154

How does the Big 5 model differ from the Five Factor model of personality?

Back 154

Big 5 replaces "openness" with INTELLECT

Front 155

What is a personality disorder?

Back 155

personality traits are inflexible and maladaptive and cause significant functional impairment or subjective distress

Front 156

Which pre-morbid personality characteristics can be identified in people who later become addicts?

Back 156

1. Disregard for rules of society/antisocial behaviour/diagnosis of antisocial personality disorder

2. Impulsive/sensation seeking traits

3. Low self-esteem/depression/anxiety

Front 157

What are the 4 types of Child Abuse

Back 157

Physical
Sexual
Emotional
Neglect

Front 158

What are the 5 broad categories of domestic violence?

Back 158

1. Physical abuse [criminal offence]
2. Psychological abuse
3. Economic abuse
4. Social abuse
5. Sexual abuse [criminal offence]

Front 159

What percentage of reported incidents of domestic violence involve victim = woman, perpetrator = man?

Back 159

85-97% cases

Front 160

What percentage of women have experienced an episode of domestic violence whilst in a married or de-facto relationship?

Back 160

Estimated 23%

Front 161

T/F: Women are more at risk of physical violence cf. sexual

Back 161

True

Front 162

Which populations are more at risk of domestic violence?

Back 162

- Female
- Younger
- Living in remote regions
- Indigenous

Front 163

What percentage of women reported that their children had witnessed their experience of violence?

Back 163

38%

Front 164

What is the most frequently used drug in Australia and what percentage of adults use it? What percentage use weekly?

Back 164

Alcohol.
82% adults drink it.
40% drink weekly.

Front 165

What proportion of the population drinks at levels which place them at risk of long-term harm

Back 165

1 in 10

Front 166

What proportion of the population smoke cigarettes regularly? What proportion of the population are "ex-smokers"?

Back 166

1 in 5 smoke
1 in 4 ex-smokers

Front 167

Which is the most frequently used illicit drug? What proportion of population has tried it?

Back 167

Cannabis.
1 in 3 have tried

Front 168

What proportion of the population has ever injected drugs?

Back 168

1 in 50

Front 169

What are the factors associated with higher risk of drug use?

Back 169

Male
20-29yo
English speaking b/ground
Lower SES group
Lower education level
Unemployment
Indigenous