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Years 1+2 > S4C5 > Flashcards

S4C5 Flashcards

1
Q

What are the 8 principles of Confidentiality?

A

Use the minimum necessary personal information.
Manage and protect information.
Be aware of your responsibilities.
Comply with the law.
Share relevant information for direct care in line with the principles in this guidance unless the patient has objected.
Ask for explicit consent to disclose identifiable information about patients for purposes other than their care or local clinical audit, unless the disclosure is required by law or can be justified in the public interest.
Tell patients about disclosures of personal information you make that they would not reasonably expect, or check they have received information about such disclosures, unless that is not practicable or would undermine the purpose of the disclosure.
Support patients to access their information.

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2
Q

What does Hep B screening involve?

A

HBV has three antigens (surface, core, and e), some of which can be detected in the blood.

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3
Q

What does Hep B surface antigens suggest?

A

Determines whether a person currently has the infection
Detectable 4-10 weeks after exposure
After 6 months, if still present, infection considered chronic

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4
Q

What does Hep B core antibodies suggest?

A

Determines whether a person has ever been infected
Appears within a few weeks
Has or is infected

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5
Q

What does Hep B surface antibodies suggest?

A

Determines whether a person has cleared the virus after infection, or has been vaccinated and is now immune to future infections
Detects presence of the antibodies
A positive hepatitis B surface antibody screening test means the person has lifetime immunity from hepatitis B.

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6
Q

What does a positive HCV antibody test mean?

A

The person is a chronic carrier of HCV - 75-85%
Has been infected but has resolved infection 15-25%
Recently (acutely) infected
Takes 6-8 weeks

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7
Q

What does a qualitative HCV RNA test measure?

A

RNA is the genetic material of the virus, and the qualitative test determines whether the virus is present.
A quantitative RNA test—or quantitative viral load test—measures how much of the virus is present
If HCV RNA is present for at least 6 months, the HCV infection is considered chronic.

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8
Q

What is the pathology of the liver in viral hepatitis?

A

Hepatitis viruses: Non-cytopathic
Hepatocyte damage is immune-mediated
Antigen recognition by Cytotoxic T cells: Apoptosis
Chemokine driven recruitment of Ag-nonspecific cells
Depending on strength of immune response
Mild inflammation to massive necrosis of liver

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9
Q

What is hepatic encephalopathy?

A

A syndrome observed in patients with cirrhosis. Hepatic encephalopathy is defined as a spectrum of neuropsychiatric abnormalities in patients with liver dysfunction, after exclusion of brain disease

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10
Q

What are the mild symptoms of hepatic encephalopathy?

A 
confusion
forgetfulness
personality or mood changes
stale or sweet odour on the breath
poor judgement
poor concentration
change in sleep patterns
worsening of handwriting or small hand movements.
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11
Q

What are the severe symptoms of hepatic encephalopathy?

A 
unusual movements or shaking of hands or arms
extreme anxiety
seizures
severe confusion
sleepiness or fatigue
severe personality changes
jumbled and slurred speech
slow movement
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12
Q

What viral family is Hep A from?

A

Picornavirus
Non-enveloped
+ sense single-stranded linear RNA

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13
Q

What transmission route and incubation period for Hep A?

A

Fecal-Oral

15-50

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14
Q

What are the signs and symptoms for Hep A?

A 
Acute hepatitis
Fever
Malaise
Loss of appetite
Nausea
Abdominal pain
Jaundice
Increased AST/ALT
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15
Q

What test do you do to serological diagnose Hep A?

A

Anti-HAV IgM

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16
Q

What treatment is required for Hep A?

A

Supportive

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17
Q

How can you prevent Hep A?

A

Food and water hygiene

Immunisation

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18
Q

What is the prognosis of Hep A?

A

Full recovery with ~3 months

Does not become chronic

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19
Q

What viral family is Hep B from?

A

Hepadnavirus
Enveloped virus
Partially double-stranded circular DNA

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20
Q

What transmission route and incubation period for Hep B?

A

Parenteral
Sexual
Perinatal
30-180

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21
Q

What are the signs and symptoms for Hep B?

A

Often asymptomatic
Serum sickness-like reaction in prodome phase
Acute hepatitis
Stigmata of cirrhosis in chronic case

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22
Q

What test do you do to serological diagnose Hep B?

A

HBsAg
Anti-HBc
HbeAg

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23
Q

What treatment is required for Hep B?

A

Acute - supportive

Chronic - interferon-α or tenofovir

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24
Q

How can you prevent Hep B?

A

Safe sex; screening of blood products

HBV vaccination post-exposure prophylaxis

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25
Q

What is the prognosis of Hep B?

A

Fulminant hepatitis

Chronic disease

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26
Q

What viral family is Hep C from?

A

Flavivirus
Enveloped virus
Partially double-stranded circular DNA

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27
Q

What transmission route and incubation period for Hep C?

A

Parenteral

14-180

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28
Q

What are the signs and symptoms for Hep C?

A

Often asymptomatic
Acute hepatitis
Stigmata of cirrhosis in chronic cases

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29
Q

What test do you do to serological diagnose Hep C?

A

Anti-HCV IgM

HCV RNA

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30
Q

What treatment is required for Hep C?

A

Acute: interferon-α or peginterferon-α
Chronic: interferon-α plus ribavirin or DAAs
Liver transplantation

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31
Q

How can you prevent Hep C?

A

Use of sterile instruments and needles
Safe sex
There is no vaccination available

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32
Q

What is the prognosis of Hep C?

A

Chronic disease

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33
Q

What viral family is Hep D from?

A

Deltavirus
Enveloped virus
Negative sense, single-stranded, circular RNA

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34
Q

What transmission route and incubation period for Hep D?

A 
Co-infection with HBV
Requires HBsAg for entry into hepatocytes
Parenteral
Coinfection: 45-160
Superinfection: 14-56
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35
Q

What are the signs and symptoms for Hep D?

A

Acute hepatitis

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36
Q

What test do you do to serological diagnose Hep D?

A

HDV-RNA

Anti-HDV IgM

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37
Q

What treatment is required for Hep D?

A

peginterferon-α

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38
Q

How can you prevent Hep D?

A

Prevention of HBV infection

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39
Q

What is the prognosis of Hep D?

A

Fulminant hepatisis

High risk of severe chronic lover disease

40
Q

What viral family is Hep E from?

A

Hepevirus
Non-enveloped virus
Positive sense, single-stranded linear RNA

41
Q

What transmission route and incubation period for Hep E?

A

Fecal-Oral

15-64

42
Q

What are the signs and symptoms for Hep E?

A

Similar to Hep A, milder

43
Q

What test do you do to serological diagnose Hep E?

A

Anti-HEV IgM

44
Q

What treatment is required for Hep E?

A

Supportive

45
Q

How can you prevent Hep E?

A

Food and water hygiene

46
Q

What is the prognosis of Hep E?

A

Fulminant hepatitis

High mortality rate in pregnant women

47
Q

What are the causes of prehepatic jaundice?

A

Haemolysis

Ineffective erythropoiesis

48
Q

What type hyperbilirubinemia is prehepatic jaundice?

A

Unconjugated

49
Q

What are the colours of the stool and urine prehepatic jaundice? What about urinary urobilinogen?

A

Stool - Dark
Urine - Normal
Urinary urobilinogen - very increased

50
Q

What are the causes of intrahepatic jaundice?

A

Nonobstructive biliary disease

Mechanical biliary obstruction (within liver)

51
Q

What type hyperbilirubinemia is intrahepatic jaundice?

A

Conjugated

52
Q

What are the colours of the stool and urine intrahepatic jaundice? What about urinary urobilinogen?

A

Stool - Pale, clay coloured
Urine - Dark
Urinary urobilinogen - normal/ slightly increased

53
Q

What are the causes of posthepatic jaundice?

A

Mechanical biliary obstruction (outside liver)

54
Q

What type hyperbilirubinemia is posthepatic jaundice?

A

Conjugated

55
Q

What are the colours of the stool and urine intrahepatic jaundice? What about urinary urobilinogen?

A

Stool - Pale, clay coloured
Urine - Very dark
Urinary urobilinogen - low

56
Q

What are the causes of unconjugated hyperbilirubinemia?

A

Increased haemoglobin breakdown
Defective hepatic uptake
Defective conjugation of unconjugated bilirubin

57
Q

What are the causes of conjugated hyperbilirubinemia?

A

Reduced drainage via biliary tract

Decreased reuptake

58
Q

Explain Bilirubin metabolism

A

Haemoglobin is broken down into Haem and globin in the spleen (80%) and bone marrow (20%)
Macrophages break down haem to unconjugated bilirubin.
Unconjugated bilirubin binds to albumin and reaches the liver
Bilirubin is conjugated in the liver and secreted in bile
In order to be secreted, conjugated bilirubin enters the blood to reach the hepatocytes with direct connection to the bile canaliculi
Bilirubin reaches the intestine via the bile
Intestinal bacteria coverts bilirubin into urobilinogen

59
Q

Describe urobilinogen break down

A

Most urobilinogen is converted into stercobilinogen and then stercobilin
The rest of the urobilinogen is reabsorbed and follows 2 pathways; most of it undergoes hepatobiliary recirculation, while the rest is filtered in the kidney
In urine, urobilinogen oxidates to urobilin, which is responsible for its characteristic yellow colour

60
Q

What gives stool is characteristic colour?

A

Stercobilin

61
Q

What is Vd? (pharmokinetics)

A

the fluid volume that would be required to contain the total amount of absorbed drug in the body at a uniform concentration equivalent to that in the plasma at steady state
Dose/ conc in blood

62
Q

What characteristic makes drugs highly distributed?

A

High lipid solubility

63
Q

What is drug metabolism?

A

the enzyme-mediated conversion of a lipid-soluble compound into a more water-soluble one

64
Q

Where does drug metabolism mainly occur?

A

Liver

In the SER and cytosol and mitochondria

65
Q

What happens in phase 1 reactions?

A

Produce/uncover chemically reactive functional groups → ‘FUNCTIONALISATION’
Help with excretion
Oxidation, e.g. alcohol dehydrogenase, MAO, CYP450 (most important)
products slightly more polar → water-soluble
preparation for phase 2
pro-drugs > ‘pharmacological activation’

66
Q

What happens in phase 2 reactions?

A

Conjugation reactions

67
Q

What are the conjugation reactions?

A 
Glucuronidation * – most widespread
Sulphation *
Methylation
Acetylation
Amino acid (Damage to hepatocytes can restrict this)
Glutathione
Fatty acid
68
Q

What are the products of phase 2 reactions?

A

Water-soluble and easily excreted
Increased MW
Inactive (Decrease receptor affinity and
Enhance excretion)

69
Q

What are the outcomes of drug metabolism?

A 
Pharmacological activation (pro-drugs)
Pharmacological inactivation
Change in type of pharmacological response
No change in pharmacological response
Change in drug distribution
70
Q

What internal factors affect metabolism?

A 
Age
Gender
Pregnancy
Disease
Genetic
71
Q

How does age affect metabolism?

A

Reduced as liver mass and blood flow decrease
Drug inactivation is slower - mostly in phase 1 oxidation
Decrease first-pass metabolism

72
Q

How does pregnancy affect metabolism?

A

Increased hepatic metabolism

Increased blood flow to liver and kidney

73
Q

What external factors affect metabolism?

A 
Drug induced
Lifestyle
Environment
Diet
Inducers
Inhibitors
74
Q

What drugs can affect metabolism?

A 
Licensed e.g. Co-amoxiclav, isoniazid, methyldopa, halothane, rifampicin, paracetamol
			Unlicensed herbal remedies:
Comfrey
Black cohosh
Kava
75
Q

What drugs does smoking increase the metabolism of?

A 
Theophylline
Caffeine
Tacrine
Imipramine
Haloperidol
Pentazocine
Propranolol
Flecainide
Estradiol
76
Q

What in the environment can affect metabolism?

A

Arsenic
Toluene
Fluorine

77
Q

What foods can affect metabolism?

A

BBQ meat
brussel sprouts increase metabolism
grapefruit juice decrease metabolism

78
Q

What are some inducers of metabolism?

A

Carbamazepine
Alcohol
St Johns wort

79
Q

What are some inhibitors of metabolism?

A

Fluoxetine
Erythromycin
Ketoconazole
Grapefruit juice

80
Q

How does grapefruit juice affect metabolism?

A

Inhibits CYPA4
Metabolises ~30% of all drugs
Increase in plasma levels - prolonged effect

81
Q

What genetic type makes up a poor metaboliser?

A

Homozygous for defective CYP gene

Increased [drug}, decreased [metabolites]

82
Q

What genetic type makes up a intermediate metaboliser?

A

Heterozygous for defective CYP gene

Increased [drug}, decreased [metabolites]

83
Q

What genetic type makes up a extensive metaboliser?

A

Homozygous for functional CYP gene

decreased [drug}, increased [metabolites]

84
Q

What genetic type makes up a ultra-rapid metaboliser?

A

Extra copies of functional CYP gene

decreased [drug}, increased [metabolites]

85
Q

How does paracetamol normally metabolise?

A

Paracetamol gets glucuronide and sulphate conjugates of -OH group
This produces an inactive metabolite which undergoes urinary excretion

86
Q

How does an small increased dose of paracetamol metabolise?

A

Undergoes N-hydroxylation (CYP450)
This causes rearrangement N-acetyl-p-benzoquinone-imine
This undergoes Glutathione conjugation
This produces an inactive metabolite which undergoes urinary excretion

87
Q

What happens if too much paracetamol is consumed?

A

Undergoes N-hydroxylation (CYP450)
This causes rearrangement N-acetyl-p-benzoquinone-imine
This leads hepatotoxicity and cell death

88
Q

What are type A ADRs?

A

augmented reactions, exaggerated response to drugs normal actions, dose dependent
Causes 80% of hospital admissions

89
Q

What are type B ADRs?

A

bizarre reaction, novel response to drug that was not expected based upon known pharmacological actions of the drug

90
Q

What are type C ADRs?

A

Dose and time chronic reaction

91
Q

What are type D ADRs?

A

delayed chronic reaction

92
Q

What are type E ADRs?

A

Withdrawal reaction

93
Q

What are type F ADRs?

A

Unexpected failure of therapy

94
Q

How many hospital admissions are due to ADR (p.a.)? What are the death rates and cost of them?

A

1 in 16 admissions
>2% die
>£1 billion

95
Q

What are the signs of hepatocellular injury?

A

Hepatocyte necrosis and inflammations
V increased ALT and AST
Increased γ-glutamyl transpeptidase

96
Q

What are the signs of cholestatic injury?

A

Resembles bile duct obstruction
V increased ALP and γ-glutamyl transpeptidase
Increased AST and ALT

97
Q

What are the signs of mixed hepatocellular-cholestatic injury?

A

Most characteristic pattern

Increased ALP and ALT

Years 1+2 (21 decks)

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