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IHD Part 2 306 > Hepatobilary system > Flashcards

Hepatobilary system Flashcards

1
Q

Hepatitis: What are the causes of hepatitis? (infectious and non infectious)

A

infectious:

  • viral - most common
  • bacterial
  • fungal
  • parasitic

non infectious

  • alcohol
  • drugs
  • autoimmune
  • metabolic diseases
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2
Q

Hepatitis: What are the signs and symptoms of hepatitis?

A

Malaise
Jaundice - elevation of bile in the blood causes
Dark urine
Pale fatty stools
Serum & urine biochemistry, specific serological tests for HepA, B, C, D & E antibodies for viral hepatitis

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3
Q

Hepatitis: What is the structure of a virus?

A

Consist of a strand of nucleic acid, either DNA or RNA, surrounded by a protective protein coat (the capsid).

Sometimes they have a further membrane of lipid, referred to as an envelope, surrounding the protein.

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4
Q

Hepatitis: What is a complete virus called?

A

vision

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5
Q

Hepatitis: What are the major hepatitis viruses?

A
  • do we have to know this, ask
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6
Q

Hepatitis: What is hepatitis A?

A
  • RNA, belongs to group
    Picornavirus
  • Genotypes I - VII.
    • Four associated with human disease I-III & VII; most being I (80%) & III

Jejunum-blood-liver, bile faeces

2- week incubation followed
by 4-10 day prodrome. Resolves in few weeks

Vaccine – formalin-killed virus

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7
Q

Hepatitis: What is the epidemiology of hepatitis A?

A

1.5 million cases worldwide; 6-7000 cases reported p.a. in UK
Children (3-5 years) often asymptomatic
Important in spread
- severity increases with age

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8
Q

Hepatitis: Which antibody is produced the first time a host is exposed to an antigen?

A

IgM

IgM will eventually decline, and then the host produces IgG, which lasts much longer

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9
Q

Hepatitis: Which antibody do you get in a secondary infection?

A

igG

Detection of IgM indicates acute or primary infection, IgG indicates past infection or immunity.

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10
Q

Hepatitis: In which phase is hepatitis A infective?

A

Asymptomatic phase

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11
Q

Hepatitis:What is chronic persistent hepatitis B?

A

Healthy carriers - can spread but no symptoms

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12
Q

Hepatitis: What is a Dane particle?

A

The whole outer vision (capsule) which is infective of the hep b virus

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13
Q

Hepatitis: What is HBE antigen used for?

A

Detect hep B infection

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14
Q

Hepatitis: What does the surface antigen split off to form in hep B?

A

The tubular and spherical forms

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15
Q

Hepatitis: What 4 genes are encoded by the hep B genome?

A

C, X, P, S

core protein - gene C
Dna polymerase - gene P
surface antigen - gene S
Gene x - regulatory?

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16
Q

Hepatitis: how can enzymes be used to determine whether liver cells are abnormal?

A

Liver cells happen to have lots of AST, ALT, and GGTP inside them. When cells die or are sick the enzymes leak out causing the blood level of these enzymes to rise, which is a way of determining if the cells in question are sick.

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17
Q

Hepatitis: What is laboratory diagnosis of hep B focused on?

A

detection of the hepatitis B surface antigen HBsAg

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18
Q

Hepatitis: What antigen is also seen in the initial phase of hep b infection?

A

hbeag

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19
Q

Hepatitis: What is high levels of hbeag an indication of?

A

HBeAg is usually a marker of high levels of replication of the virus.

The presence of HBeAg indicates that the blood and body fluids of the infected individual are highly contagious.

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20
Q

Hepatitis: What is chronic infection of hep b characterised by?

A

persistence of HBsAg for at least 6 months (with or without concurrent HBeAg). Persistence of HBsAg is the principal marker of risk for developing chronic liver disease and liver cancer (hepatocellular carcinoma) later in life.

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21
Q

Hepatitis: What is the epidemiology of hep b?

A

UK carriage approx. 0.1%
Carriage in Africa and Asia approx. 5%
Transmission; vertical, parenteral, sexual
>108 HBV/ml; 0.000001-0.00001ml blood;
Infection early in life > increased chance of chronicity
10% of chronic infection progress to chronic liver disease
Vaccine – genetically engineered HBsAg

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22
Q

Hepatitis:What is hep D caused by?

A

a ‘defective’ RNA virus which coexists with HBV

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23
Q

Hepatitis: What are the features of hep D?

A

Very small virus
Outer coat derived from HBsAg – cannot survive without HBV.
~5% HBV carriers are HDV positive.

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24
Q

Hepatitis: What is the delta antigen of hep D used for?

A

Used for diagnosis

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25
Q

Hepatitis: What hepatitis virus can only occur with HBV?

A

Hep D

Infection co-incident with HBV

  • HDV influenced by replication of HBV
  • rarely progressive or chronic

Superinfection on HBV disease

  • ideal for rapid HDV replication
  • commonly chronic

15 million HDV cases worldwide
- mainly iv drug users in UK

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26
Q

Hepatitis:What are the viral features of hep C?

A

Small enveloped SSRNA virus

Core of genetic material (RNA), surrounded by an icosahedral capsid

Two viral envelope glycoproteins, E1 and E2, are embedded in the lipid envelope - help it to attach to host cells of liver

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27
Q

Hepatitis: How is hep c released?

A

by budding

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28
Q

Hepatitis: What is hep c a member of? ( a family)

A

flaviviruses

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29
Q

Hepatitis: What is the epidemiology of HCV?

A

180 million carriers worldwide

  • 5 million in Western Europe
  • UK carriage ~0.08% (~40,000)

Transmission

  • IV drug abuse needle sticks, tattoos, ear piercing
    • -80% iv drug users infected
  • Previously
    • -blood products, haemodialysis, transplantation

minor routes - saliva; sexual; vertical

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30
Q

Hepatitis: Why is diagnosis of HCV unreliable?

A

antibody takes 6wk-6mnth to show up in blood) – 97% by 6mnth

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31
Q

Hepatitis: what is the treatment for HCV?

A

interferon a (interferes with replication) + Ribavirin (stimulates T cells to attack the virus)

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32
Q

Hepatitis: Why is there no vaccine for HCV?

A

Cure rate is dependent on the genotype, treatment history and presence of liver damage

re-infection can occur with the same type - lack of neutralising antibody

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33
Q

Hepatitis: Which types of HCV are the most common in the UK?

A

Types 1a and 1b

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34
Q

Hepatitis: What type of virus is hep E?

A

Rna hepevirus - 4 genotypes

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35
Q

Hepatitis: How is hep E spread?

A

Faecal-oral spread

36
Q

Hepatitis: What is the average incubation period for hep E?

A

6 weeks

37
Q

liver disease pathology: What is the most common cause of a lack of liver available to process things?

A

cirrhosis - end stage liver disease

38
Q

liver disease pathology: What is the general mechanism of cirrhosis?

A

Damage to liver cells

inflammation to liver cells

mostly the cells regenerate

other pathway - healing by fibrosis

leading to cirrhosis

39
Q

liver disease pathology: What are the causes of cirrhosis?

A

Anything that damages the liver and it is unable to recover

Hepatitis viruses - B, C, D, E

40
Q

liver disease pathology: What are the consequences of cirrhosis?

A

jaundice
portal hypertension
ascites - abnormal buildup of fluid in the abdomen and increases BP due to low albumin production (water potential)
Heptocellular cancer - due to increased cell turnover during repair of the liver

41
Q

liver disease pathology: What can block the outflow of bile from the liver?

A

Gall stones

42
Q

GI pathology 1: What cellular changes occur in Barett’s oesophagus?

A

turns from squamous into glandular mucosa (columnar lined lower oesophagus = Barett’s) = metaplasia

43
Q

GI pathology 1: What is metaplasia?

A

change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type

44
Q

GI pathology 1: What is the stomach lined by?

A

Glandular epithelium with layer of mucin for acid buffering

45
Q

GI pathology 1: What happens in Barrett’s oesophagus?

A

Reflux of acid into oesophagus, squamous cells cannot adapt so die - left with acellular gap that causes pain

so squamous changes into glandular with mucin on top - protects against acid reflux

eventually producing dysplastic (pre cancerous) glandular epithelium

then neoplastic glandular epithelium

46
Q

GI pathology 1: What are the differences in risk factors for squamous cell carcinoma and adenocarcinoma (oesophageal)

A

Squamous - alcohol and smoking

Adeno - obesity

47
Q

GI pathology 1: Why are survival rates of oesophageal cancer not good?

A

Presents late

48
Q

GI pathology 1: How does helicobacter gastritis occur?

A

helicobacter lives in the stomach mucin

attracting neutrophils from the capillaries which damage the lining cells

get ulcerations from the acid contacting

burning sensations in the stomach/ heartburn

49
Q

GI pathology 1: What are the causes of gastric cancer?

A

Smoked foods

pickled foods?

50
Q

GI pathology 1: What cellular changes occur from HP, pernicious anaemia, smoked/pickled food diet?

A

Normal mucosa

intestinal metaplasia

genetic change causes dysplasia

genetic change causes intramucosal carcinoma

genetic change causes invasive carcinoma

51
Q

GI pathology 1: What is gluten sensitive enteropathy coeliac disease?

A

Lack of villi/ atrophied villi reducing SA

crypt hyperplasia

hundreds of lymphocytes

allergic reaction to gluten in the blood

52
Q

GI pathology 1: What is the mechanism of coeliac disease?

A

Immune reaction to gliadin protein in gluten

gliadin absorbed by gliadin peptide

another enzyme (TG) causes it to attach to HLA (antigen presenting cell) - causing toxic T cells to be produced and cause injury

53
Q

GI pathology II: What is Crohn’s disease?

A

produces aphthous ulcers
patchy inflammation/ulcers all the way through the gut
can get scarring in the bower’s after long term - cobble stoned mucosa

drugs control inflammation well

most complications in the bowel
e.g. malabsorption, obstruction, perforation, fistula formation

54
Q

GI pathology II: What is ulcerative colitis?

A

Only affects colon not mouth

not patchy inflammation - continuous inflammation

idiopathic

55
Q

GI pathology II: What are the complications of ulcerative colitis?

A

Colon - blood loss, toxic dilation, some risk of cancer

joints - ankylosing spondylitis, arthiritis

eyes - iritis, uveitis, episcleritis

skin - erythema nodosum, pyoderma gangrenosum

liver - fatty change, chronic pericholangitis, sclerosing cholangitis

56
Q

GI pathology II: What is diverticular disease?

A

outpouchings in the sigmoid colon into the fat layer - punched out

taking out colon often cures

too much pressure when squeezing from inside of the bowel probably due to a low fibre diet pushes mucosa out - can get infection

faeces out into the peritoneal cavity - can die from it - peritonitis

treated by high fibre diet

57
Q

GI pathology II: What is happening to the incidence and mortality rates of colorectal cancer?

A

incidence increasing but mortality decreasing as treating earlier

58
Q

GI pathology II: What is familial adenomatous polyposis?

A

normal colon but get thousands of adenomas in teens and early adult hood - polyps

get cancer in 20’s - 30’s

APC gene is the problem gene

59
Q

GI pathology II: What are the cellular changes of colorectal cancer?

A

normal epithelium
adenoma
colorectoral adenocarcinoma

60
Q

GI pathology II: What is the cellular mechanism of familial adenomatous polyposis?

A

APC gene bound to GSK

when beta catenin rise - binds to it and take sit away to be broken down - prevents getting high

mutation - no APC or faulty APC
beta catenin rises, can’t remove this

moves through membrane and binds to the DNA - causes epithelial proliferation and causes adenoma

61
Q

GI pathology II: What is hereditary nonpolyposis colorectal cancer? HNPCC

A

born with a mutation in one of the repair genes

then another mutation occurs during life time

2 hit system

get tumours elsewhere more often and don’t respond as well to treatment

62
Q

GI pathology II: What is resection coding?

A

R0 - tumour completely excised locally
• R1 - microscopic involvement of margin by tumour
• R2 - macroscopic involvement of margin by tumour

63
Q

GI pathology II: What are the Dukes’ stages and prognosis?

A 
Dukes’ stage and prognosis
A - 95% 5 year survival 
B - 75% 5 year survival 
C - 35% 5 year survival 
D - 25% 5 year survival
64
Q

GI pathology II: What are the cellular stages of colorectal cancer?

A

prevention - low dose aspirin?
normal epithelium

endoscopic resection
adenoma

surgical resection
colorectal adenocarcinoma

chemotherapy palliative care
metastatic colorectal adenocarcinoma

65
Q

Liver and Gall bladder disease: What does bile do?

A

helps emulsify fat

changes pH into alkaline

66
Q

Liver and Gall bladder disease: What are the functions of the liver?

A

Detoxification: Filters & cleans blood of waste products (drugs, hormones)
Immune functions: Fights infections and diseases (RE system)
Involved in Synthesis of clotting factors, proteins, enzymes, glycogen and fats (advanced cirrhosis patients go from having glycogen to being starved very quickly)
Production of bile & breakdown of bilirubin
Energy storage (glycogen and fats)
Regulation of fat metabolism
Ability to regenerate

67
Q

Liver and Gall bladder disease: What is the metabolic role of the liver?

A

The liver maintains a continuous supply of energy for the body by controlling the metabolism of CHO and fats.
Its role varies during:
Fasting, absorption, digestion & metabolism
Multiple pathways
The liver is regulated by:
Endocrine glands eg pancreas, adrenal, thyroid
Nerves

68
Q

Liver and Gall bladder disease: What are the types of liver disease?

A

acute vs chronic

acute - recovery
causes - viral, drugs, vascular e.g. clot

chronic - cirrhosis to liver failured
causes - alcohol, viral B/C, autoimmune, vascular metabolic

69
Q

Liver and Gall bladder disease: How may acute liver injury present?

A

Asymptomatic
abnormal LFTs &coagulopathy
Malaise, nausea, anorexia
Jaundice

Confusion – think ALF !

Bleeding
Liver pain

70
Q

Liver and Gall bladder disease: How may chronic liver injury present?

A

abnormal LFTs
hepatomegaly,
malaise, abdo discomfort
itching

Ascites, oedema
Haematemesis (varices)
Easy bruising (coagulopathy)
Jaundice
Confusion
Anorexia, wasting
71
Q

Liver and Gall bladder disease: What are the serum liver function tests?

A 
Albumin - tells you if liver is working 
ALP – Alkaline phosphatase
GGT – gamma GT
ALT – Alanine Aminotransferase
AST – Aspartate Aminotransferase
Bilirubin - tells you if liver is working 
Globulin
72
Q

Liver and Gall bladder disease: What is jaundice due to?

A

High bilirubin (breakdown product of hmg)

73
Q

Liver and Gall bladder disease: What are the causes of jaundice?

A

Pre-hepatic
- Haemolysis (increased substrate)

Hepatic (intrinsic liver disease)
- Cirrhosis
- Infiltration of the liver by tumours
- Acute hepatitis 
   (viral, alcoholic, autoimmune, drug-induced)

Post-hepatic (obstruction of biliary outflow)

  • Gallstones
  • External compression: pancreatitis, lymphadeno-pathy, pancreatic tumour, ampullary tumour
74
Q

Liver and Gall bladder disease: What are the causes of chronic liver disease?

A

Most common

NAFLD & NASH
Alcohol
Viral hepatitis (B, C)

Less common

Auto-immune

  • autoimmune hepatitis
  • primary biliary cirrhosis
  • Primary sclerosing cholangitis

Metabolic

  • Haemochromatosis
  • Wilson’s - overload of copper
  • alpha1 antitrypsin deficiency…

Vascular

  • Budd-Chiari
  • Portal vein thrombosis

Drugs

  • Amiodarone
  • Chemotherpay
75
Q

Liver and Gall bladde disease: What are the risk factors for non alcoholic fatty liver disease?

A

diabetes, obesity, hypertension, dyslipidaemia = metabolic syndrome

76
Q

Liver and Gall bladder disease: What are the stages of fatty liver disease?

A

Fatty liver - deposits of fat cause enlargement
Liver fibrosis - scar tissue forms
Cirrhosis - growth of connective tissue destroys liver cells

77
Q

Liver and Gall bladder disease: Compare and contrast hep B and hep C

A 
Hepatitis B
DNA Virus
Reads in hepatocyte genome
Persists in liver even if no in longer in blood
Can reactivate
Mainly transmitted via intercourse/vertically
Early infection: chronicity
Vaccination available
Longterm treatment
Hepatitis C
RNA virus
Mainly transmitted through IVDA; needles blood products
Once cleared  = cleared
Reinfection possible – no immunity
Time limited treatment
 	well tolerated, 90 % cure
No vaccination
78
Q

Liver and Gall bladder disease: What are the stages of chronic liver disease?

A 
NCPH = non-cirrhotic portal hypertension
Often due to vascular problems in the liver
Tolerating bleeding well and clotting generally intact; 
Relatively rare (patients generally aware)

Pre-cirrhotic
No effect on dental work
May be asymptomatic

Liver cirrhosis
Compensated & decompensated

79
Q

Liver and Gall bladder disease: what is the difference between compensated and decompensated liver cirrhosis?

A

Compensated
Invisible
Blood can be normal
Risk low

Decompensated
Visible
Abnormal blood tests
Risks high

80
Q

Liver and Gall bladder disease: What is the prognosis of cirrhsis worsened by?

A

Malnutrition
Variceal bleeding
Infection (SBP)
Renal failure

81
Q

Liver and Gall bladder disease: What are the complications in chronic liver disease?

A

Acute:

- GI bleeding        Portal    - Ascites              hypertension
- Jaundice
- Hepatic Encephalopathy
- Renal impairment
- Coagulopathy
- Infection

Chronic:

- Malnutrition
- Bone disease
82
Q

Liver and Gall bladder disease: What are the signs and symptoms of chronic liver disease?

A 
Palmer erythema 
Spider naevi 
Gynaecomastia 
Leuconychia 
Clubbing
Jaundice 
Ascites
hepatic encephalopathy
83
Q

Liver and Gall bladder disease: How do you recognise HE?

A

Confusion
Altered behaviour
Coma
Collateral history

How test for HE
Serial 7s:	100 - 93 – 86 – 79 – 72 – 65
“baby hippopotamus”
5-star drawing
Number connection test
Ammonia level (>50) – poor correlation
84
Q

Liver and Gall bladder disease: How do you treat liver disease?

A

Symptomatic - Diuretics
Nutrition support
Supplements
Propranolol

Specific 
Antiviral
Immunosuppression
Relieving obstruction
Venesection
85
Q

Liver and Gall bladder disease: What are the dental considerations in liver diseasE?

A

Comprehensive medical and dental histories

Appropriate laboratory investigations
Full blood count (FBC)
Prothrombin Time (PT)
LFTs (and U&Es)

Consultation with and/or to referral to physician(s) prior to dental treatment

Minimization of soft tissue trauma during dental procedures

Consideration of hospital setting for advanced surgical procedures or severely coagulopathic patients

Potential for increased bleeding in patients with liver disease
Coagulopathy
Thrombocytopenia

Be aware of infection risks and consider extra precautions if higher risk of injury (double gloves)

Hep B vaccination

Caution should be used in prescribing medications that are metabolized in the liver and/or impair haemostasis

  • Anaesthetics - Local (amides) and General (halothane) - anaethetist
  • Antiplatelet (aspirin) stop 7 days before dental surgery/extraction
  • Increased DILI with Flucloxacillin and Co-Amoxyclav
  • Sedatives (long-acting benzodiazepines, barbiturates)

Potential for increased drug toxicity in patients with advanced liver disease

  • Caution should be used in prescribing medications metabolized in the liver
  • AVOID NSAIDs
  • Paracetamol – safest pain killer in liver disease
  • Opiates – slow and low

IHD Part 2 306 (23 decks)

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