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Years 1+2 > S4C5 > Flashcards

S4C5 Flashcards

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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
What is the prognosis of Hep B?
Fulminant hepatitis | Chronic disease
26
What viral family is Hep C from?
Flavivirus Enveloped virus Partially double-stranded circular DNA
27
What transmission route and incubation period for Hep C?
Parenteral | 14-180
28
What are the signs and symptoms for Hep C?
Often asymptomatic Acute hepatitis Stigmata of cirrhosis in chronic cases
29
What test do you do to serological diagnose Hep C?
Anti-HCV IgM | HCV RNA
30
What treatment is required for Hep C?
Acute: interferon-α or peginterferon-α Chronic: interferon-α plus ribavirin or DAAs Liver transplantation
31
How can you prevent Hep C?
Use of sterile instruments and needles Safe sex There is no vaccination available
32
What is the prognosis of Hep C?
Chronic disease
33
What viral family is Hep D from?
Deltavirus Enveloped virus Negative sense, single-stranded, circular RNA
34
What transmission route and incubation period for Hep D?
``` Co-infection with HBV Requires HBsAg for entry into hepatocytes Parenteral Coinfection: 45-160 Superinfection: 14-56 ```
35
What are the signs and symptoms for Hep D?
Acute hepatitis
36
What test do you do to serological diagnose Hep D?
HDV-RNA | Anti-HDV IgM
37
What treatment is required for Hep D?
peginterferon-α
38
How can you prevent Hep D?
Prevention of HBV infection
39
What is the prognosis of Hep D?
Fulminant hepatisis | High risk of severe chronic lover disease
40
What viral family is Hep E from?
Hepevirus Non-enveloped virus Positive sense, single-stranded linear RNA
41
What transmission route and incubation period for Hep E?
Fecal-Oral | 15-64
42
What are the signs and symptoms for Hep E?
Similar to Hep A, milder
43
What test do you do to serological diagnose Hep E?
Anti-HEV IgM
44
What treatment is required for Hep E?
Supportive
45
How can you prevent Hep E?
Food and water hygiene
46
What is the prognosis of Hep E?
Fulminant hepatitis | High mortality rate in pregnant women
47
What are the causes of prehepatic jaundice?
Haemolysis | Ineffective erythropoiesis
48
What type hyperbilirubinemia is prehepatic jaundice?
Unconjugated
49
What are the colours of the stool and urine prehepatic jaundice? What about urinary urobilinogen?
Stool - Dark Urine - Normal Urinary urobilinogen - very increased
50
What are the causes of intrahepatic jaundice?
Nonobstructive biliary disease | Mechanical biliary obstruction (within liver)
51
What type hyperbilirubinemia is intrahepatic jaundice?
Conjugated
52
What are the colours of the stool and urine intrahepatic jaundice? What about urinary urobilinogen?
Stool - Pale, clay coloured Urine - Dark Urinary urobilinogen - normal/ slightly increased
53
What are the causes of posthepatic jaundice?
Mechanical biliary obstruction (outside liver)
54
What type hyperbilirubinemia is posthepatic jaundice?
Conjugated
55
What are the colours of the stool and urine intrahepatic jaundice? What about urinary urobilinogen?
Stool - Pale, clay coloured Urine - Very dark Urinary urobilinogen - low
56
What are the causes of unconjugated hyperbilirubinemia?
Increased haemoglobin breakdown Defective hepatic uptake Defective conjugation of unconjugated bilirubin
57
What are the causes of conjugated hyperbilirubinemia?
Reduced drainage via biliary tract | Decreased reuptake
58
Explain Bilirubin metabolism
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
Describe urobilinogen break down
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
What gives stool is characteristic colour?
Stercobilin
61
What is Vd? (pharmokinetics)
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
What characteristic makes drugs highly distributed?
High lipid solubility
63
What is drug metabolism?
the enzyme-mediated conversion of a lipid-soluble compound into a more water-soluble one
64
Where does drug metabolism mainly occur?
Liver | In the SER and cytosol and mitochondria
65
What happens in phase 1 reactions?
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
What happens in phase 2 reactions?
Conjugation reactions
67
What are the conjugation reactions?
``` Glucuronidation * – most widespread Sulphation * Methylation Acetylation Amino acid (Damage to hepatocytes can restrict this) Glutathione Fatty acid ```
68
What are the products of phase 2 reactions?
Water-soluble and easily excreted Increased MW Inactive (Decrease receptor affinity and Enhance excretion)
69
What are the outcomes of drug metabolism?
``` Pharmacological activation (pro-drugs) Pharmacological inactivation Change in type of pharmacological response No change in pharmacological response Change in drug distribution ```
70
What internal factors affect metabolism?
``` Age Gender Pregnancy Disease Genetic ```
71
How does age affect metabolism?
Reduced as liver mass and blood flow decrease Drug inactivation is slower - mostly in phase 1 oxidation Decrease first-pass metabolism
72
How does pregnancy affect metabolism?
Increased hepatic metabolism | Increased blood flow to liver and kidney
73
What external factors affect metabolism?
``` Drug induced Lifestyle Environment Diet Inducers Inhibitors ```
74
What drugs can affect metabolism?
``` Licensed e.g. Co-amoxiclav, isoniazid, methyldopa, halothane, rifampicin, paracetamol Unlicensed herbal remedies: Comfrey Black cohosh Kava ```
75
What drugs does smoking increase the metabolism of?
``` Theophylline Caffeine Tacrine Imipramine Haloperidol Pentazocine Propranolol Flecainide Estradiol ```
76
What in the environment can affect metabolism?
Arsenic Toluene Fluorine
77
What foods can affect metabolism?
BBQ meat brussel sprouts increase metabolism grapefruit juice decrease metabolism
78
What are some inducers of metabolism?
Carbamazepine Alcohol St Johns wort
79
What are some inhibitors of metabolism?
Fluoxetine Erythromycin Ketoconazole Grapefruit juice
80
How does grapefruit juice affect metabolism?
Inhibits CYPA4 Metabolises ~30% of all drugs Increase in plasma levels - prolonged effect
81
What genetic type makes up a poor metaboliser?
Homozygous for defective CYP gene | Increased [drug}, decreased [metabolites]
82
What genetic type makes up a intermediate metaboliser?
Heterozygous for defective CYP gene | Increased [drug}, decreased [metabolites]
83
What genetic type makes up a extensive metaboliser?
Homozygous for functional CYP gene | decreased [drug}, increased [metabolites]
84
What genetic type makes up a ultra-rapid metaboliser?
Extra copies of functional CYP gene | decreased [drug}, increased [metabolites]
85
How does paracetamol normally metabolise?
Paracetamol gets glucuronide and sulphate conjugates of -OH group This produces an inactive metabolite which undergoes urinary excretion
86
How does an small increased dose of paracetamol metabolise?
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
What happens if too much paracetamol is consumed?
Undergoes N-hydroxylation (CYP450) This causes rearrangement N-acetyl-p-benzoquinone-imine This leads hepatotoxicity and cell death
88
What are type A ADRs?
augmented reactions, exaggerated response to drugs normal actions, dose dependent Causes 80% of hospital admissions
89
What are type B ADRs?
bizarre reaction, novel response to drug that was not expected based upon known pharmacological actions of the drug
90
What are type C ADRs?
Dose and time chronic reaction
91
What are type D ADRs?
delayed chronic reaction
92
What are type E ADRs?
Withdrawal reaction
93
What are type F ADRs?
Unexpected failure of therapy
94
How many hospital admissions are due to ADR (p.a.)? What are the death rates and cost of them?
1 in 16 admissions >2% die >£1 billion
95
What are the signs of hepatocellular injury?
Hepatocyte necrosis and inflammations V increased ALT and AST Increased γ-glutamyl transpeptidase
96
What are the signs of cholestatic injury?
Resembles bile duct obstruction V increased ALP and γ-glutamyl transpeptidase Increased AST and ALT
97
What are the signs of mixed hepatocellular-cholestatic injury?
Most characteristic pattern | Increased ALP and ALT

Years 1+2 (21 decks)

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