Learning Objectives (Non-CLIC) Flashcards

1
Q

What are the synthetic Functions of Healthy Liver?

A
▪ Conjugation + elimination of bilirubin
	▪ Synthesis of albumin 
	▪ Synthesis of clotting factors
	▪ Gluconeogenesis 
	▪ Glycogen storage
	▪ Production of bile - needed to digest fat, and absorb vitamin A, D, E and K.
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2
Q

What are LFT’s used for?

A
  • Confirm clinical suspicion

* Differentiate between hepatocellular and cholestasis/post-hepatic/obstructive

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3
Q

Which of the LFT’s are used to differentiate between Hepatocellular and cholestasis?

A
  • ALT (High concentrations in Hepatocytes)
    • AST
    • ALP (High concentrations in liver, bile duct, and bone tissues - produced as a response to cholestasis - indirect marker)
    • GGT
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4
Q

Which of the LFT’s are used to assess liver synthetic function?

A

• Albumin
• Bilirubin
• Prothrombin Time
(Also check serum glucose as one function of gluconeogenesis - the production of glucose from non-carbohydrates)

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5
Q

What proportion of ALT to ALP indicates likelihood of hepatocellular injury?

A

• Greater than 10 fold increase in ALT with Lower than 3 fold increase in ALP

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6
Q

What proportion of ALT to ALP indicates likelihood of cholestasis?

A

• Lower than 10 fold increase in ALT with Higher than 3 fold increase in ALP

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7
Q

List reasons to why GGT might be raised in a patient.

A

▪ Biliary obstruction/epithelial damage
▪ Alcohol
▪ Drugs (phenytoin)

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8
Q

Raised ALP with raised GGT is highly suggestive of obstruction. What can raised ALP alone be indicative of?

A

▪ Bony metastases / primary bone tumours
▪ Vitamin D deficiency
▪ Recent bone fracture
▪ Renal Osteodystrophy

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9
Q

What would an ALT>AST ratio indicate in relation to liver disease?

A

▪ Chronic Liver Disease

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10
Q

What ratio of ALT to AST would cirrhosis or acute alcoholic hepatitis show?

A

▪ AST>ALT

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11
Q

List three reasons why there might be a drop in Albumin levels?

A

▪ Decreased production due to liver disease
▪ Inflammation triggering acute phase response
▪ Loss (e.g nephrotic syndrome)

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12
Q

What other screening would you do for liver?

A

▪ Ferritin (haemochromatosis)
▪ Anti0mitochondrial Antibody (AMA) - primary biliary cirrhosis (cholangitis)
▪ Viruses in the blood (hepatitis etc…)

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13
Q

What is the definition of an addiction?

A

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

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14
Q

What is the most prevalent addiction in the world?

A

Alcohol

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15
Q

A) Name a psychological model that is used to understand addiction

B) Describe this model

A

A) The PRIME model

B)
- there is an internal and external influences/elements. Dysfunction in any of these elements can contribute to the addiction.

▪ The Internal Environment has 5 element (PRIME):
	○ Plans (Malfunction = the person cannot create effective plan to quit the addiction, or they cannot retrieve the plan from their memory etc.. So less likely to quit)
	○ Evaluations (Malfunction = the person views the information or memory of doing the drug in a biased manner - so they will have this unrealistic belief that when they drank their problems got solved)
	○ Motives (Malfunction = powerful urges to take part due to previous experiences - motivations are affected by the good times when they were on it, and the bad feelings when they didn’t have it)  
	○ Impulses (Malfunction = there is a strong association between certain cues and taking part in the addictive behaviour - for example they are used to smoking after they have their dinner, so every time they have their dinner there is a strong urge to smoke which may make them relapse)
	○ Response
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16
Q

PRIME is now the chosen theory and model through which addiction is considered. Name other models that are used understand addiction.

A

▪ Temperance - drug is dangerous and causes the problem. Moderation is not the answer, the answer is total prohibition. Once you start using you cannot stop.
▪ Moral - this model states that it is the person who decides whether to use or not. Biology doesn’t matter. If they use it’s a reflection of their weak character. And its their social and religious norms that dictate all this. This model is now rejected.
▪ Disease - this one states that certain people have physiological process where if they use it leads to loss of control. So here its completely based on the biological factor, it’s a disease!
▪ Medical - this is similar to disease model. There is a number of physiological factors which put a certain individual at risk of addiction. Again very biology based.
▪ Psychodynamic - misuse is primarily related to psychodynamic facotrs such as early childhood experiences of trauma. They need psychotherapy
▪ Socio-cultural - Its not biology, or individual experiences, but there is sociocultural factors which increase likelihood of addiction. If you address these you can solve the problem.
▪ Systems and families - the use of alcohol and other drugs should be considered in the light of the relationships that the individual has with their family, and other social circle elements. So in order to change the behaviour, those relationships have to be healthy… so its not about the person, but about the relationships that person has with everyone around them.
▪ Learning theory - using and drinking are learnt behaviours… if you can learn something you can unlearn it.

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17
Q

List the DSM-5 criteria scores for the following Substance Use Disorders Categories:

1) Mild
2) Moderate
3) Severe

A

1) 2-3
2) 4-5
3) >6

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18
Q

Define 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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19
Q

Define Tolerance.

A

A state of reduced responsiveness to the effects of a drug caused by previous administration of the drug. The repeated administration means that more is required for the same effects.

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20
Q

Define Withdrawal.

A

▪ Physical withdrawals - can be fatal particularly in alcohol, seizures, death
▪ Psychological withdrawal state of anhedonia, characterised by dysphoria, irritability, emotional distress

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21
Q

List the viruses that are associated with hepatitis.

A

▪ Hepatitis viruses (Hepatitis A, B, C, D, E, G)
▪ Cytomegalovirus
▪ Epstein-Barr Virus
▪ Herpesviruses (mostly in immunosuppressed)
▪ Other: yellow fever virus, dengue virus

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22
Q

• Discuss the global disease burden of Viral Hepatitis

A

▪ 1.34 million deaths globally in 2015
▪ Hep B and C prevalent all over the world but mainly in Africa and Asia
▪ Hep C most prevalent in Europe
▪ Hep E rare in Europe and more prevalent in Africa and Asia

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23
Q

Explain the epidemiology of Hepatitis A?

A

▪ High risk in developing countries where there is poor sanitation, hence faeces, contaminated foods, and water are sources of infection

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24
Q

A) Name 5 of the constitutional symptoms that may precede symptoms and signs of liver dysfunction in a patient with hepatitis.

B) Name symptoms of liver dysfunction in hepatitis.

A
A)
▪ Anorexia
▪ Flu-like symptoms
▪ Fatigue
▪ Malaise
▪ Headache
B)
▪ Jaundice
▪ Dark Urine
▪ Abdominal Pain
▪ Enlarged/tender Liver
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25
Q

What can LFT’s show in regards of hepatitis.

A

▪ Whether it is chronic or acute

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26
Q

State the incubation periods for Hep A, B, C, E.

A

▪ Hep A: 28 days (15-50d)
▪ Hep B: 3 months (can be up to 6 months in some patients - becomes chronic in 5%)
▪ Hep C: 45 days (up to 6 months possible - 70% chronic)
▪ Hep E: 40 days

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27
Q

A) What are some of the most common routes of transmission of Hepatitis B.

B) Risk Factors.

A

A)
▪ Heterosexual transmission
▪ Nosocomial (infection originating in a hospital)
▪ Mother-to-child transmission

B)
▪ IV Drug Use/shared needles
▪ Unprotected sex (especially multiple sexual partners, sex with someone from a high risk area, men who have sex with men)
▪ Infant born to an infected mother

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28
Q

What is the most common hepatitis in Europe?

A

Hep C

29
Q

Describe what the following serological results indicate in regards to the course of Hep B infection:

A) HBV Surface Antigen  (HBsAg)
B) HBV core antibody (IgG anti-HBc)
C) HBV IgM core antibody (IgM anti-HBc) 
D) HBV anti-surface Antibody (Anti-HBsAg) 
E) HBV DNA PCR
A
A) Active/current infection
B) Chronic HBV or past infection
C) Diagnostic for acute infection
D) Vaccine/Natural Immunisation
E) Not a screening test
30
Q

Describe Acute Hepatitis B Management.

A
  • Acute Hep B usually spontaneously clear
  • Does not usually need specific treatment
  • Offer supportive treatment to relief symptoms
  • Repeat blood in 3-4 weeks to ensure development of antibodies and recovery
  • Advice to use protection
  • Advice to vaccinate household contact and partner
31
Q

Which other Hepatitis Virus only invades a host when they have a Hep B infection?

A

HDV - causes a superinfection with HBV

32
Q

A) Describe the serological features of a chronic HBV infection.

B)
What is the requirement in terms of investigations for patients with chronic hepatitis?

C) Current treatment options for chronic HBV?

A

A)

    • HBsAg positive for more than 6 months
    • IgG anti-HBc - positive
    • Anti-HBsAg - Negative

B)
▪ Regular (minimum 6 months) LFTs, HBV markers, and fibroscan due to increased risk of HCC

C)
▪ Pegylated interferon (PegIFNa): Subcutaneous for 48 weeks
▪ Nucleos(t)ide analogue (NA) therapy: oral treatment, long term until HBsAg Loss
• E.g Lamivudine (LAM), adefovir dipivoxil (ADV), entecavir (ETV)

33
Q

Describe the serological features of a acute HBV infection.

A
  • HBsAg positive
  • IgM Anti-HBc positive
  • Anti-HBsAg - negative
34
Q

What are the main routes of transmission of Hepatitis C.

A

▪ Injecting drug use

▪ Men who have sex with men (especially acute)

35
Q

Describe the serology of Hepatitis C Virus.

A

Anti-HCV = past of chronic infection

HCV Antigen = active

HCV RNA PCR = not a screening test

36
Q

Describe the management of chronic HCV.

A

▪ Aim is to avoid complications (liver and extra-hepatic): hepatic necroinflammation, fibrosis, HCC
▪ Improve quality of life
Prevent onward transmission

37
Q

What are treatment options for HCV.

A

▪ Oral direct acting antivirals achieving sustained virological clearance

38
Q

List common routes of hepatitis A transmission (transmission = faecal-oral).

A

▪ Person-to-person

▪ Contaminated food (certain shellfish like mussels, oysters, and clams + also seen in vegetables) or drink

39
Q

What are some of the risk factors based on recent outbreaks in the UK.

A

▪ MSM
▪ IVDU
▪ Consumption of contaminated frozen berries

40
Q

Describe management of acute HAV. (Infectious period = two weeks before onset of first symptoms and until 1 weeks after)

A

▪ Advice on good hygiene practice
▪ Exclude work until 7 days post onset of jaundice or in absence of jaundice, from onset of compatible symptoms
▪ Identify possible source of infection
▪ Undertake risk assessment

41
Q

Describe Hep E global distribution.

A

▪ Highly endemic area = developing countries

▪ Europe however is also endemic

42
Q

List common routes of hep E transmission (transmission = faecal-oral).

A

▪ Contaminated water
▪ Undercooked pork or deer meat
▪ Person-to-person
▪ Contaminated Blood

NOTE: this can be asymptomatic infection, or acute self-limiting hepatitis

43
Q

What group of people are at most risk of HEV chronic infection.

A

▪ Immunosuppressed

▪ Patients with pre-existing liver disease

44
Q

How do you differentiate hepatitis from cholangitis/cholecystitis?

A
  • those infections have fever while hepatitis doesn’t
45
Q

List three consquences/implications (economic and social) of substance misuse.

A
  • Increased mortality
  • Increased morbidity and hospital admissions
  • Social implications like family break down
46
Q

Describe the short term effects of alcohol misuse.

A

1-2 units = vasodilation, tachycardia (warm talkative feeling)
4-6 units = Effects on CNS. Part of the brain that control judgment and decision making.
8-9 units = slower reaction time, slurred speech, loss of focus
10-12 = impaired coordination, depressant effects of alcohol lead to drowsiness, can also cause nausea, vomiting, diarrhoea, indigestion
Over 12 = increased risk of alcohol poisoning and as result coma

47
Q

Over how many units does alcohol poisoning become a risk?

A

over 12 units

48
Q

What are the physical implications of alcohol on the CVS?

A
  • Arrhythmias
  • Hypertension
  • Cardiomyopathy
49
Q

What are the potential complications of alcohol on the respiratory system?

A
  • Strep pneumoniae
  • TB
  • Klebseilla infection
50
Q

What are the alcohol misuse complications on the GI and Hepatic system?

A
  • Gastritis
  • Fatty Liver
  • Alcoholic hepatitis
  • Alcoholic liver cirrhosis
  • Acute pancreatitis
51
Q

What are the CNS complications of alcohol misuse?

A
  • Head injuries and subdural haemorrhages
  • Hepatic encephalopathy
  • Cerebral degeneration
52
Q

What are GU complications of Alcohol misuse?

A
  • Impotence
  • Renal Failure
  • STI
53
Q

List the different conditions associated with Alcohol Withdrawal syndrome.

A
  • Uncomplicated Alcohol Withdrawal Syndrome
  • AWS with seizures
  • Delirium Tremens
  • Wrenicke-Korsakoff Syndrome
54
Q

Describe uncomplicated Alcohol Withdrawal Syndrome.

A
  • 4-12 hours after last drink
  • Peaks at 48 hours
  • Lasting 2-5 days

Sx = Tremor, Sweating, Insomnia, Nausea, Vomiting, Increased craving

55
Q

Describe Alcohol Syndrome with seizures.

A

5-15% AWS are complicated with seizures

RF:

  • Previous AWS episode with seizures
  • Head injury
  • Idiopathic epilepsy
  • Hypokalaemia or hypomagnesnaemia
56
Q

Describe Delirium Tremens.

A

▪ Definition:
○ Potentially fatal manifestation of alcohol withdrawal
○ 5-15% mortality
○ Occurs after heavy drinking periods and especially if the person isn’t eating enough
▪ Symptoms:
○ Delirium (sudden confusion)
○ Body tremors
○ Changes in mental function
○ Agitation
○ Hallucinations
○ Seizures (most common 12-48 hours after last drink)
▪ Risks:
○ Previous alcohol withdrawal problems
○ Heavy drinking for several months; and
○ Having other co-morbidities such as: head injuries, intercurrent infection, hepatitis, pancreatitis
▪ Complications:
Cardiac Arrhythmias (du

57
Q

Describe Wrenicke-Korsakoff Syndrome.

(Wernicke’s encephalopathy ( WKS is caused by a deficiency in the B(1) vitamin thiamine. Thiamine plays a role in metabolizing glucose to produce energy for the brain.)

and

Korsakoff psychosis)

A

Def:

  • Haemorrhages and secondary gliosis in periventricular and periaqueductal grey matter
  • Involves Mamillary, hypothalamus
  • acute and chronic phases of a single disease process (Wrenicke = acute, Korsakoff = chronic)
  • Neuronal Degeneration secondary to thiamine deficiency

Sx:

  • Tetrad for WD = confusional state, opthalmoplegia (paralysis of the muslces within or surrounding the eye - double vision, ptosis, , nystagmus, ataxic gait)
  • For WKS = you also get hallucinations, exaggerated story telling, amnesia of stuff happened after onset of disorder, difficulty understanding words

Tx:

  • High potency parenteral vitamins (Pabernix B Vitamins)
  • Prophylaxis in detox
58
Q

List the categories of alcohol misuse disorder in terms of severity of drinking.

A

Hazardous - above limit but no experience of harm
Harmful - above the recommended limit and experiencing physical or psychological harm
Dependent - above limit and experience physical/psychological harm + central characteristic is strong/overpowering desire to drink
Binge Drinking - originally episodic heavy drinking, now heavy drinking in a single session (ie twice the daily limit in one session)

59
Q

Describe the assessment of people who misuse alcohol.

A

1- History
a. Consumption in units? (how much/many?) (Units = ABV (Alcohol By Volume - so percentage of alcohol) x Volume of Cup)
b. When, where, with whom, why, what happens afterward?
c. Establish alcohol use disorder (categories above)
d. Ask about driving
2- Screening tools
a. CAGE
b. AUDIT (highly sensitive and specific test) – Use Audit-consumption questions (Audit-C) which takes 1 minute. If the results is positive (ie 5+) then administer the full AUDIT
c. Blood tests (MCV, GGT, ALT)
3- Treat Complications

60
Q

Describe the management of alcohol misuse.

A
  • You are not required to prescribe medications in all those who misuse alcohol
  • You should determine which stage they are at at take non-pharmachological advice/planning- based action:

Stages of change:
1- Pre-contemplation (intervention unlikely to succeed, give info about risks)
2- Contemplation (offer advice and motivational work to move them along)
3- Preparation (set date and make plan)
4- Action (encourage, support, offer follow-up)
5- Maintenance (you just reinforce success)

61
Q

Describe pharmacological management options for alcohol dependency disorder.

A

1- Medically assisted withdrawal from alcohol (Benzos and vitamins)
2- Relapse Prevention:

    • Naltrexone (opioid receptor antagonist - had modest effects in getting people to reduced amount drinking as it takes away the positive effects of consumption of alcohol or opiates)
    • Baclofen
    • Acamprosate
    • Disulfiram
62
Q

Describe non-pharmacological management options for alcohol withdrawal.

A

Psychosocial:

  • AA/Mutual Aid
  • CBT (e.g. diaries where you reflect on how you felt doing something and amount of money being spent)
  • MET
63
Q

Describe the MOA and contraindications of Disulfiram.

A

▪ MOA: Irreversible inhibition of acetaldehyde dehydrogenase (ALDH) which converts CO2 and H2O
▪ Build of Acetaldehyde –> flushing, headache, nausea
▪ This is contraindicated in cardiovascular problems!

64
Q

Describe the MOA, Dose, and SE’s of Acamprosate.

A

▪ MOA: Enhance GABA and NMDA Antagonist reducing cravings and withdrawal
▪ Dose: usually 666mg
▪ SE: GI Upsets, Pruritis, rash, altered libido
▪ No role in controlled drinking, no aversion action, no addictive potential

65
Q

List health strategies for tackling substance misuse.

A

▪ Systemic learning from drug-related deaths (there is no systemic learning from drug-related deaths at the moment)
▪ Housing support as a key element of commissioned services for tackling substance misuse (homelessness is well established in its relationship with substance misuse)
▪ A human right-based approach to ensure that physical health of all are met

66
Q

What are the screening tools for substance misuse disorders?

A

DSM-5 and ICD-11

67
Q

Describe opioid substitution pharmacological treatment.

A

1- Methadone (synthetic form of heroin but not with the same buzz of high, used to get people to come off, dose gradually reduced over time)
2- Buprenorphine (this is a partial agonist for opioids)
3- Naltrexone (they take this, it has an effect, if they inject heroin on top of it, it acts as a complete blocker of the receptors)
4- Naloxone (Administered in the event of an overdose - a public health measure)

68
Q

Part of Substance misuse assessment is history, collateral history, use of DSM-5 and ICD-11 as criteria, the use of a formulation, investigation tests, and risk assessment and management.

What is meant by formulation?

A
  • A Formulation model allows you to identify the factors that influence the addictive behaviour and helps develop a care plan
  • The 5 P’s:
    1- Predisposing
    2- Precipitating
    3- Perpetuating
    4- Presenting
    5- Protective