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Bateman - Phase 2a COPY > Gastrointestinal and Liver > Flashcards

Gastrointestinal and Liver Flashcards

1
Q

What are common hepatitides for each of these hepatitis?

Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E

Yellow fever

A

Epstein-Barr V
Cytomegalovirus
Toxoplasma

Influenza
Adenoviruses
Coxsackie B

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2
Q

What is the route of transmission for each of the hepatitis’?

A 
A Faeco-oral.
B blood/ sexual.
C Blood/ sexual.
D Blood/ sexual
E Faeco-oral.
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3
Q

Is there chronic infection in each of the hepatitis’?

A 
A No
B Yes
C Yes
D Yes
E No
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4
Q

How can you prevent each of the hepatitis’?

A

A Pre and post-exposure immunisation.
B Pre and post-exposure immunisation, behaviour modification.
C Blood donor screening. Behaviour modificationtion.
D HBV immunisation. behaviour modification.
E Clean drinking water.

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5
Q

What are the symptoms of acute hepatitis?

A 
Malaise
Myalgia
Fever
Nausea/vomiting
Jaundice
RUQ pain.
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6
Q 
What are the different levels of these in acute hepatitis?
AST
ALT
Alk Phos
Albumin.
Bilirubin.
A 
AST raised
 ALT raised
 Alk Phos same or raised
 Albumin lower or same
 Bilirubin raised.
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7
Q

What is a typical case history for hep A?

A

Travelled to Malaysia for 4/52 - stayed in hostels, local food - ‘sea-food banquet’ on last night
Well throughout holiday
Travelled overseas before - “thought was up-to-date on vaccinations”

Unwell 3 weeks after return to UK - headache - lethargy - aching all over - poor appetite - hot and cold
10/7 later notices eyes/skin yellow
(but feels better

Jaundiced
Temp 37.8C
Dehydrated
Tender hepatomegaly

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8
Q

What is the name for hep A?

A

Picornavirus.

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9
Q

Where is hepatitis A found?

A

Contaminated food or water.
Shellfish
Travellers.
Infected food handlers.

Close personal contact.
Household.
Sexual.
Childcare groups.

Blood - IVDU.

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10
Q

What is ALT?

A

Alanine aminotransferase.

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11
Q

When does ALT rise in hep A?

A

Within 1 month.

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12
Q

When does IgM anti-HAV show an increase in hep A?

A

2-4 months.

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13
Q

What is the hep A vaccination?

A

Inactivated hepatitis A virus
Grown in human diploid cells
Dose - 0.5ml im - repeat at 6-12 months - booster every 10 years
HAV immunoglobulin - post exposure prophylaxis.

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14
Q

When do you notice a rise in IgM anti-HBc in hep B?

A

From 8-24 weeks.

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15
Q

What is a typical case for Hep B?

A

No PMH of note
Works as a solicitor
Not left UK >12 months
Divorced - new partner for last 8/12 - Egyptian

Feeling tired ‘long time’	-	thought due to work stress	-	worse in last week or so
Poor appetite 2/12	-	5 kg weight loss
Noticed eyes yellow 5 days ago
Skin very yellow last 24 hours
Urine ‘dark orange’

Afebrile
Deeply jaundiced
Tender hepatomegaly
Mild pitting oedema of ankles

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16
Q

What would be found out from the investigations for hep B?

A

USS abdo:

- enlarged liver, bright echogenic texture- no focal abnormality

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17
Q

When do anti-HBs starting b being produced?

A

After 32 weeks.

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18
Q

What would you find in a chronic hep B sufferer?

A

A high hep B surface antigen.

Total anti-HBc is also high.

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19
Q

What is Hep B called?

A

Hepadnavirus.

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20
Q

Where does hep B replicate?

A

Hepatocytes.

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21
Q

What is hep B infection?

A 
incubation 6/52 - 6/12
may be asymptomatic - esp <5 yrs
symptoms can last 6-12 weeks
>90%	adults will clear infection
<50%	children <5 yrs will clear infection
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22
Q

What are the facts of chronic hep B infection?

A

<50% adults develop chronic infection - HBsAg >6/12
Highly infectious - HBeAg +ve
2% carriers / year clear infection and develop natural immunity - female>male

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23
Q

What is the hep B vaccine types?

A

Inactivated HBsAg
Recombinant DNA (biosynthetic)
Dose: 1ml - 3 doses at 0, 1 and 6/12 - booster every 5 years - accelerated course 0, 1, 2/12
HBV immunoglobulin - post-exposure prophylaxis

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24
Q

What is the hep B treatment?

A 
Alpha Interferon
Nucleoside Analogues
   Tenofovir, Entecavir
Success rate:   20-40% HBeAg clearance 
     Long-term control of HBV DNA
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25
Q

What is the typical case for hep C?

A

Intravenous drug use for 12 yrs - heroin +/- crack cocaine - often shared ‘works’ - smokes cannabis ‘occasionally’
In rehab for 6/12 - not injected 5/12 - attended for health check

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26
Q

What would you find on examination of Hep C patient?

A 
Underweight
Multiple tattoos
Scars both arms and groins
Not jaundiced
Afebrile
Tender liver edge.
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27
Q

What is hep C called?

A

Flavivirus (RNA).

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28
Q

What happens in hep C patients, what percentage have acute and chronic?

A

Acute hepatitis ~20% patients - majority asymptomatic - incubation 2-26/52
Chronic hepatitis ~ 80%
cirrhosis 15%
hepatocellular carcinoma 5%

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29
Q

How is Hep C characterised in the liver?

A

Lymphocytic inflammation.

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30
Q

What is the serology for hep B acute?

A 
HBcAb negative.
HBsAb negative.
HBeAb negative
HBsAg positive.
HBeAg positive.
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31
Q

What is the serology for hep B previous?

A 
HBcAb positive.
HBsAb positive.
HBeAb positive.
HBsAg negative.
HBeAg negative.
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32
Q

What is the serology for hep B chronic HBV: low infectivity?

A 
HBcAb positive.
HBsAb negative.
HBeAb positive.
HBsAg positive.
HBeAg negative.
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33
Q

What is the serology for hep B: high infectivity?

A 
HBcAb positive.
HBsAb negative.
HBeAb negative
HBsAg positive.
HBeAg positive.
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34
Q

What is the serology like in a hep C patient?

A

HCV Ab - in all patients - appears up to 4/52 after infection
HCV RNA - detected by PCR - present in chronic infection
No vaccine available.

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35
Q

What is the hep C treatment?

A

Pegylated Interferon weekly injections
Plus: Ribavirin tablets
70-80% cure rate in non-1 genotype - 6/12 treatment
60% cure rate in genotype 1 - 1 year treatment
Newer drugs (eg Sofofbuvir) 90% cure
Interferon free regimes available soon.

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36
Q

How can you prevent hep C?

A

Screening blood products - since 1991
Lifestyle modification - needle exchanges etc
Universal precautions - for handling all bodily fluids

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37
Q

What is hep D?

A 
Co-infection with acute HBV	
-	increased severity of infection
Super-infection in patients with chronic HBV	
-	2o acute hepatitis	
-	increases risk of fulminant hepatitis	
-	increased progression of liver disease
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38
Q

What is hep E?

A

Small RNA virus
Similar to Hep A - faeco-oral transmission - acute hepatitis - no chronic disease
Less infectious
Increased mortality 1-2% - pregnant women 10-20%
now endemic in UK

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39
Q

What does the liver do?

A 
Glucose and fat metabolism.
Detoxification and excretion.
-bilirubin
-ammonia
-drugs / hormones / pollutants
Protein synthesis.
-albumin
-clotting factors
Defence against infection.
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40
Q

How is the liver arranged? How does the blood flow through it?

A

Regular way (acing or lobular models). Blood enters via the portal vein and hepatic artery, which lie together with a small bile duct within the portal tract. Blood flows into a system of sinusoids which bathe the liver cells arranged in plates, with blood, before exiting via the hepatic vein.

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41
Q

How many zones does the liver have?

A

Three, each receiving progressive less oxygenated blood.

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42
Q

What are the types of liver injury?

A

Acute and chronic.

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43
Q

What can acute liver injury lead to?

A

Liver failure or recovery.

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44
Q

What can chronic liver failure lead to?

A 
Recovery.
Cirrhosis.
Liver failure.
varices.
Hepatoma.
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45
Q

What does acute liver injury lead to?

A

Results in damage to and loss of cells.
Cell death may occur by necrosis (associated with neutrophils).
Or apoptosis.

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46
Q

What does chronic liver injury lead to?

A

Leads to fibrosis, termed cirrhosis in severest form.

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47
Q

What can cause acute liver injury?

A 
Viral (A,B, EBV).
Drug.
Alcohol.
Vascular.
Obstruction.
Congestion.
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48
Q

What can cause chronic liver injury?

A

Alcohol.
Viral (B,C).
Autoimmune.
Metabolic (iron, copper).

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49
Q

How does acute liver injury present?

A

malaise, nausea, anorexia, jaundice

rarer:
- confusion
- bleeding
- liver pain
- hypoglycaemia

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50
Q

How does chronic liver injury present?

A

ascites, oedemahaematemesis (varices)malaise, anorexia, wasting easy bruising, itchinghepatomegaly, abnormal LFTs

rarer:
- jaundice
- confusion

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51
Q

What are some serum ‘liver function tests’?

A

Serum bilirubin, albumin, prothrombin time: (give some index of liver function)

Serum liver enzymes:

  • cholestatic: alkaline phosphatase, gamma-GT
  • hepatocellular: transaminases (AST, ALT) (give no index of liver function)
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52
Q

What is jaundice pre-hepatic in relation to bilirubin? Give examples of diseases?

A

Unconjugated.

- Gilberts, Haemolysis.

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53
Q

What is jaundice hepatic in relation to bilirubin? Where is it seen?

A

Conjugated, liver disease.

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54
Q

What is jaundice post hepatic in relation to bilirubin? Where is it seen?

A

Conjugated, bile duct obstruction.

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55
Q 
Compare pre hepatic and hepatic or post hepatic for these.
Urine.
Stools.
Itching.
Liver tests.
A

Urine. Normal Dark.
Stools. Normal May be pale.
Itching. No Maybe.
Liver tests. Normal Abnormal.

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56
Q

What are some causes of liver disease?

A 
Hepatitis - Viral
                   - Drug
                   - Immune
                  - Alcohol
Ischaemia
Neoplasm
Congestion (CCF).
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57
Q

What are some causes of obstruction?

A 
Gallstone- Bile duct  
                   - Mirizzi   
Stricture - Malignant
                  - Ischaemic
                  - Inflammatory

Blocked stent

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58
Q

What liver tests would tell you which jaundice it is?

What further tests could be done?

A

Liver enzymes: Very high AST/ALT suggests liver disease, some exceptions
Biliary obstruction: 90% have dilated intrahepatic bile ducts on ultrasound
Need further imaging:
CT
Magnetic resonance cholangioram MRCP
Endoscopic retrograde cholangiogram ERCP

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59
Q

What are gallstones made up of?

A

70% cholesterol, 30% pigment +/- calcium.

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60
Q

What are some risk factors for gallstones?

A

Female, fat, fertile.

liver disease, ileal disease, TPN, clofibrate

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61
Q 
Compare gallstones for the gallbladder and bile duct locations.
Biliary pain.
Cholecystitis.
Obstructive jaundice.
Cholangitis.
Pancreatitis.
A

Gallbladder Bile Duct
Biliary pain. Yes Yes
Cholecystitis. Yes No
Obstructive jaundice. Maybe Yes
Cholangitis. No Yes
Pancreatitis. No Yes

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62
Q

How do you treat gallbladder gallstones?

A

Laporoscopic cholecystectomy

- Bile acid dissolution therapy (<1/3 success).

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63
Q

How do you treat Bile duct gallstones?

A

ERCP with sphincterotomy and: removal (basket or balloon)
crushing (mechanical, laser..)
stent placement
- Surgery (large stones)

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64
Q

What are the different types of drug induced liver injury?

A

Hepatocellular.
Cholestatic.
Mixed.

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65
Q

What drugs are known to have drug induced liver injury?

A 
Antibiotics.
CNS drugs.
Immunosuppresents.
Analgesics/musculoskeletal.
Gastrointestinal drugs.
Dietary supplements.
Multiple drugs.
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66
Q

What happens in paracetamol poisoning?

A

Paracetamol conveyed by Cy P450 into reactive intermediate and then into cellular macromolecules which causes cellular necrosis.

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67
Q

What is needed to help paracetamol poisoning? What does it do?

A

Start N-acetylcystine.

Increases Reactive intermediate to stable metabolite conversion. Increases glutathione transferase activity.

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68
Q

What does N-acetylcystine correct?

A

coagulation defects

  • fluid electrolyte and acid base balance
  • renal failure
  • hypoglycaemia
  • encephalopathy
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69
Q

What are some paracetamol induced liver failure poor prognosis indicators?

A 
Late presentation 
          (NAC less effective >24 hr)
Acidosis (pH <7.3)
Prothrommbin time > 70 sec
Serum creatinine ≥ 300 µmol/l

Consider emergency liver transplant - otherwise 80% mortality

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70
Q

What is Leukonchia?

A

White spots on fingernails.

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71
Q

What is spider naevus? Why is it important?

A

Swollen blood vessels below the skin. Extensive could indicate liver disease.

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72
Q

What is ascites?

A

Ascites is the accumulation of protein-containing (ascitic) fluid within the abdomen. Many disorders can cause ascites, but the most common is high blood pressure in the veins that bring blood to the liver (portal hypertension), which is usually due to cirrhosis.

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73
Q

What are the causes of ascites?

A 
Chronic liver disease (most)	
-	+/- Portal vein thrombosis	
-	Hepatoma	
-	TB
Neoplasia (ovary, uterus, pancreas...)
Pancreatitis, cardiac causes
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74
Q

What is the pathogenesis of ascites?

A

Increased intrahepatic resistance leads to portal hypertension which leads to ascites.

Systemic vasodilation leads to portal hypertension and also secretion of
-       Renin-angiotensin	
-	Noradrenaline	
-	Vasopressin
This then leads to fluid retention.

Low serum albumin also contributes to ascites.

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75
Q

What happens in acute alcohol-related injury?

A

Acute alcohol-related injury causes hepatocyte ballooning and is mediated by neutrophils (acute alcoholic hepatitis). Injured liver cells may accumulate a cytoskeletal protein which appears irregular and red on an H&E stain – Mallory’s hyalin. This is not specific to alcoholic liver disease, but when seen with neutrophils and fat is a clue as to the cause of liver disease.

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76
Q

What does alcohol do to the liver?

A

Alcohol changes the way that hepatocytes metabolise and produce fat. Fat accumulation within hepatocytes is termed steatosis. This may be large droplet (macrovesicular) or small droplet (microvesicular). It may be associated with acute liver injury, or as in the picture, chronic injury mediated by lymphocytes.

Alcohol and many other drugs and toxins have most affect on the cells with the lowest oxygen and blood supply (zone 3). Damage results in fibrosis, with pericellular fibrosis in zone 3 being more common in alcohol-related injury than fibrosis of portal tracts.

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77
Q

What does fatty liver cause?

A

Alcoholic hepatitis.
Cirrhosis.

Acute decompensation.

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78
Q

What does the progression of ALD look like?

A

Alcoholic hepatitis coming and going whilst fat and fibrosis rise.

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79
Q

What are the causes of portal hypertension?

A

cirrhosis, fibrosis, portal vein thrombosis.

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80
Q

What is the pathology of portal hypertension?

A

increased hepatic resistance

increased splanchnic blood flow

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81
Q

What are the consequences of portal hypertension?

A

varices (oesophageal, gastric…)

splenomegaly

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82
Q

Why can patients who have chronic liver disease ‘go off’?

A 
Constipation
Drugs 	- 	sedatives, analgesics
              	-	NSAIDs, diuretics, ACE blockers
Gastrointestinal bleed
Infection (ascites, blood, skin, chest …)
HYPO: natraemia, kalaemia, glycaemia ...
Alcohol withdrawal (not typically)
Other (cardiac, intracranial ...).
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83
Q

Why are liver patients vulnerable to infection?

A
  • impaired reticulo-endothelial function
  • reduced opsonic activity
  • leucocyte function
  • permeable gut wall
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84
Q

What are the sites of infection for liver patients vulnerable to infection?

A
  • spontaneous bacterial peritonitis
  • septicaemia
  • pneumonia
  • skin
  • urinary tract …
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85
Q

What are some causes of renal failure in liver disease?

A 
Drugs:  	
-	Diuretics	
-	NSAIDS	
-	ACE Inhibitors	
-	Aminoglycosides
Infection
GI bleeding
Myoglobinuria
Renal tract obstruction …
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86
Q

What can happen at end-stage liver disease?

A

End-stage liver disease, represented by cirrhosis. At the bottom of the picture are residual nodules of hepatocytes. If these nodules remain small the result is a micronodular cirrhosis. If they are able to regenerate, they may become large, giving a macronodular cirrhosis. The constant replication of hepatocytes in this condition make them liable to replication errors, which may result in neoplasia developing. Hepatocellular carcinoma is a risk in patients with long-standing cirrhosis.

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87
Q

What are some consequences of liver dysfunction?

A 
Malnutrition
Coagulopathy	
-	impaired coagulation factor synthesis	
-	vitamin K deficiency (cholestasis)
-	thrombocytopenia
Endocrine changes	
-	gynaecomastia
-	impotence                     	   	
-	amenorrhoea
Hypoglycaemia (+/-)
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88
Q

What are some causes of chronic liver disease?

A 
Alcohol
Non Alcoholic Steatohepatitis (NASH)
Viral hepatitis (B, C)
Immune  	
- 	autoimmune hepatitis	
-	primary biliary cirrhosis	
- 	sclerosing cholangitis
Metabolic	
- 	haemochromatosis	
- 	Wilson’s	
- 	1 antitrypsin deficiency…
Vascular 
-      Budd-Chiari
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89
Q

What can be seen in the liver which indicates autoimmune hepatitis?

A

Autoimmune hepatitis usually requires liver biopsy for diagnosis, although the appearances are not always specific. There are usually lymphocytes and plasma cells within portal tracts and within lobular parenchyma. The resultant damage causes apoptosis (pictured), or in severe cases, the death of swathes of hepatocytes - bridging necrosis or massive necrosis.

The inflammationate is often in the portal tracts, with damage to the adjacent, or interface, hepatocytes - interface hepatitis. Hepatocytes may become “stranded” in small groups or form rosettes at the interface. Numerous plasma cells are a clue to the diagnosis. Chronic disease leads to fibrosis around the portal tracts and eventually to cirrhosis.

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90
Q

What happens to the value of bilirubin, AST, albumin and PT when steroids are started?

A

AST, bilirubin and PT decreases.

Albumin increases.

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91
Q

What happens in primary biliary cirrhosis?

A

In Primary biliary cirrhosis, the immune damage is directed towards the small bile ducts s. The disease is patchy and so all stages may co-exist in the same liver. There is a small chance because of this, that disease may not be detected on an initial biopsy. Staging is by the Ludwig system: stage 1 (pictured) is the florid duct lesion - a dense mixed inflammatory infiltrate, rich in lymphocytes, is present within the portal tract, centred on the bile duct. Granulomas may be present in association with this inflammation.
Epithelium distrusted and damaged by infiltrating lymphocytes.
Eventually, this will result in the destruction of the bile duct branch.

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92
Q

How does primary biliary cirrhosis present?

A 
Asymptomatic lab abnormalities.
Itching and/or fatigue.
Dry eyes.
Joint pain.
Variceal bleeding.
Liver failure: ascites, jaundice.
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93
Q

How can you treat cholestatic itch?

A 
UDCA, antihistamines - little help
Cholestyramine helps in 50% of cases
Rifampicin effective; occasionally damages liver
Opiate antagonists
Also: ultraviolet light 
             plasmapheresis
             liver transplantation
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94
Q

What is primary sclerosis cholangitis?

A

Primary sclerosing cholangitis is another disease of bile ducts, the cause of which is not fully known yet. Histologically it is characterised in the early stages by peri-ductal oedema, giving a concentric “onion ring” appearance. Lymphocytes are also present, apparently mediating the damage. The lesions are present in an irregular fashion along the ducts. A secondary cholangitis (bile duct acute inflammation), with neutrophils within the bile ducts may also be present.

Eventually scarring and damage lead to loss of the bile duct branch. PSC is another cause of ductopaenia.

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95
Q

How does primary sclerosis cholagitis present?

A

Leads to strictures (areas of narrowing) ± gallstones
Over 50% have inflammatory bowel disease
Presents
- itching
- pain ± rigors
- jaundice
10% develop cholangiocarcinoma (bile duct cancer)
Ursodeoxycholic Acid: unclear benefits; may reduce colon cancer risk
Good results from Liver Transplantation

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96
Q

What is haemochromatosis?

A

Genetic disorder
90% have mutations in HFE gene: C282Y, H63D
Autosomal recessive; incomplete penetrance
Uncontrolled intestinal iron absorption with deposition in liver, heart and pancreas

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97
Q

How can you diagnose haemochromatosis?

A

Diagnosis suggested by raised ferritin and transferrin saturation, confirmed by HFE genotyping and liver biopsy
When cirrhosis present, increased risk of hepatocellular carcinoma
Iron removal may lead to regression of fibrosis

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98
Q

What is hepatocellular carcinoma?

A

Hepatocellular carcinoma is an adenocarcinoma formed of cells resembling normal hepatocytes. Instead of the normal orderly growth in plates, they form large groups, acini or glands. Several growth patterns exist (eg. glandular, clear cell, fibrolamellar) and these may mimic metastatic cancer from another primary. We can distinguish hepatocellular carcinoma using immunohistochemistry for cytokeratins 8/18, HePar1 and CD10. The latter stains the bile cannaliculi that run at the edges of the hepatocytes.

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99
Q

When is a hepatocellular carcinoma likely to occur?

A

Most occur in patients with cirrhosis
Risk: highest for hepatitis B,C, haemochromatosis
lower: cirrhosis from alcoholic, autoimmune disease
Males >Females

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100
Q

How will a hepatocellular carcinoma present?

A

May presents with decompensation of liver disease, wt loss ascites, or abdominal pain
50% produce a fetoprotein

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101
Q

What are the treatments for hepatocellualr carcinomas?

A

Treatments limited: Transplantation, resection or local ablative therapies
Sorafenib recently shown to prolong life

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102
Q

What is non-alcoholic fatty liver disease?

A

The hepatocytes are distended by fat, forming an empty white droplet in the biopsy (the fat dissolves out during processing). Most drugs and toxins lead to initial fat deposition in zone 3, but when severe, the whole acinus may be affected, as here. A scattering of chronic inflammatory cells may be present, as here. Bile ducts and blood vessels are normal. If there is no history of alcohol excess, a diagnosis of Non-Alcoholic Steato-Hepatitis may be made, although for histological diagnosis, features identical to that of an acute alcoholic hepatitis must be present.

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103
Q

What are the risk factors for non-alcoholic liver?

A

Risk factors: Obesity (70%) diabetes (35-75%), hyperlipidaemia (20-80%)…

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104
Q

What are the symptoms of non-alcoholic liver?

A

Usually no symptoms; liver ache in 10%
Commonest cause of mildly elevated LFTs
Usually ALT; Alk phos, GGT often normal
Fat, sometimes with inflammation, fibrosis (NASH)

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105
Q

What investigations can you do for non-alcoholic liver?

A

Need biopsy to distinguish NAFL from NASH

NASH: Important cause of “cryptogenic” cirrhosis

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106
Q

How can you treat non-alcoholic liver?

A

Still no effective drug treatments

Wt loss works- the more the better

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107
Q

What is anti-1-antitrypsin deficiency?

A

Alpha-1-antitrypsin deficiency. This causes chronic liver disease and emphysema. Eventually this will lead to cirrhosis. The liver biopsy appearances are of chronic inflammation with eosinophilic -1-antitrypsin protein globules on H&E.
Results in inability to export 1-antitrypsin from liver

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108
Q

What can anti-1-antitrypsin deficiency lead to?

A

liver disease (protein retention in liver) - emphysema (protein deficiency in blood)

Phenotypic expression variable - neonatal jaundice - chronic liver disease in adults

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109
Q

What is the treatment for anti-1-antitrypsin deficiency?

A

No medical treatment

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110
Q

What is hepatic vein occlusion?

A

Veno-occlusive disease - this rare disease has characteristic biopsy appearances. The terminal or central veins become occluded by fibrous tissue, which can be seen to be increased, in this plate. It is an irregular disease, so may be patchy or absent in a liver biopsy. The back pressure as a result leads to portal hypertension. The dilated sinusoids around this vein and the haemorrhage hint at a rise in pressure. There are many causes of veno-occlusive disease, including alkaloid ingestion, chemotherapy and following solid organ transplantation. The clinical picture may mimic Budd-Chiari syndrome.

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111
Q

What are the causes of hepatic vein occlusion?

A
  • thrombosis (Budd-Chiari syndrome) may be underline thrombotic disorder
  • membrane obstruction
  • veno-occlusive disease (irradiation, antineoplastic drugs)
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112
Q

What may hepatic vein occlusion present with?

A
  • abnormal liver tests
  • ascites
  • acute liver failure.
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113
Q

What is the treatment for hepatic vein occlusion?

A
  • anticoagulation
  • transjugular intrahepatic portosystemic shunt
    Liver transplantation
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114
Q

What are the causes of chronic liver disease?

A 
Alcohol
Non alcoholic steatohepatitis (NASH)
Viral hepatitis (B, C)
Immune  	
-	autoimmune hepatitis	
-	primary biliary cirrhosis	
-	sclerosing cholangitis
Metabolic 	
- 	haemochromatosis	
- 	Wilsons	
- 	1 antitrypsin deficiency…
Vascular 	
-       Budd-Chiari
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115
Q

What investigations can you do for chronic liver disease?

A

Viral serology - hepatitis B surface antigen, hepatitis C antibody

Immunology

  • autoantibodies
  • AMA, ANA, AMA,
  • coeliac antibodies
  • immunoglobulins

Biochemistry

  • iron studies
  • copper studies
  • caeruloplasmin
  • 24 hr urine copper
  • 1-antitrypsin level
  • lipids, glucose

Radiological investigations - USS / CT / MRI

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116
Q

What is heliocbacter pylori?

A

Gram negative, curved motile rod, microaerophilic.

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117
Q

What is heliocbacter pylori’s key biochemical feature?

A

Urease positivity-used in testing.

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118
Q

How is heliocbacter pylori spread?

A

Oro-fecal or oral-oral.

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119
Q

What is the pathogenesis of heliocbacter pylori?

A

Adapted to living in gastric mucus
Colonises over gastric but not intestinal epithelium.
Induces inflammation
Stimulates increased gastrin

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120
Q

Why is heliocbacter pylori adapted to live in gastric mucus?

A

Microaerophilic, motile, urease generates ammonium to buffer acidity.

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121
Q

How does heliocbacter pylori induce inflammation?

A

mononuclear and neutrophilic cellular infiltrate in lamnia propria
role for ammonia produced by urease, cagA and vacA
inflammatory response maladapted so pathogen is not cleared; Treg and TH17 responses.

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122
Q

How does heliocbacter pylori stimulate gastrin?

A

Increased parietal mass but also may modulate gastric acid production.

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123
Q

What are the usual symptoms of heliocbacter pylori?

A

Acquisition usually asymptomatic
but may cause nausea and epigastric pain.
Chronic diffuse superficial gastritis
Followed by a period of achlorrydria.

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124
Q

How does heliocbacter pylori alter the production of gastrin and what does this result in?

A
  1. In Antrum: H.pylori reduces somatostatin release by D cells. This leads to loss of inhibition of gastrin release.
  2. G cells now produce increased gastrin levels in the stomach
  3. Increased gastrin levels increases basal acid output
  4. In duodenum: Increased aciditiy leads to gastric metaplasia, H.pylori is then able to colonise duodenum and causes further mucosal damage.
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125
Q

What are some disease associations with heliocbacter pylori?

A

Ulcers. In the absence of NSAIDS or Zollinger-Ellison syndrome.
Gastric cancer.
Gastric lymphoma.
Oesophageal disease. Barrett’s oesophagus.
Others.

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126
Q

What is gastric cancer associated with? Why is this strange? HP?

A

Reduced gastric acid, strange because in some patients H.pylori reduces gastric acid in some patients.

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127
Q

What is the spectrum of gastric acid due to in HP?

A

Bacterial strain.
Genetics.
Diet.

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128
Q

What investigations can you do for HP?

A

Serology
rapid but gives no assessment of clinical state
rapid testing cards can have lower sensitivity
Stool antigen
also no assessment of clinical state but can assess response to therapy after 6-8wk
Urea breath test
requires equipment and more invasive but quantitative and rapidly responsive to treatment
Endoscopy with urease test, histology ± culture
Best if clinical symptoms and need to identify syndrome.
More invasive
Can allow culture and antibiotic sensitivity but not widely available
Urease test only 60% sens if 1h incubation but 905 if 24h
All can have sensitivity over 95%

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129
Q

What is the treatment for HP?

A

Omeprazole 20-40mg bd
Amoxicillin 1gm BD
Clarithromycin 500mg bd

OR

Omeprazole 20-40mg bd
Bismuth compound 2tablets BD
Metronidazole 400mg tds
Tetracycline 500mg qid or doxycycline 100mg bd

14d vs. 7-10d treatment circa 10% better eradication rate and quadruple also a bit better than triple

Acid suppression for 1mo heals 70-80% and for 2mo 90% ulcers but 50-90% relapse within 1-2 yrs.
Reduce relapse to 20-30% with continued suppression
<5% with HP eradication

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130
Q

What can infectious diarrhoea be from?

A 
Viral e.g. Rotavirus
Foodborne
Antibiotic associated diarrhoea
Travel related e.g E. coli, Giardiasis etc.
Diarrhoea in the immunocompromised host.
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131
Q

What are the mechanisms by which E. coli cause diarrhoea?

A

Toxin producing.
Invasive.
Adherent.

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132
Q

What is clostridium difficile infection?

A

Gram positive with terminal bulge due to spore
Toxin and B:
glucosyltransferases that target Rho family GTPases blocking their activation.
Induce actin depolymerisation and cytoskeletal rearrangement effecting epithelial tight junctions and permeability
Spores
Allow persistence in environment
Ingested by feco-oral route
Germinate in colon on exposure to bile salts

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133
Q

What are clostridium difficile’s clinical features

A 
Cause antibiotic associated diarrhoea
Clinical features:
Abdominal pain
Watery diarrhoea
May develop bloody diarrhoea
WBC 
Complicated by toxic megacolon and perforation
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134
Q

How can you diagnose clostridium difficile?

A

Glutamate dehydrogenase (GDH) or PCR screen to establish if C difficile present in stool
Then ELISA for toxin A and B (many strains only make toxin B)
Tissue culture cytotoxicity assay gold standard but not used routinely.

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135
Q

How can you prevent clostridium difficile?

A

Antimicrobial stewardship limit use of cephalosporins, fluoroquinolones and other agents associated with CDI
Effective cleaning of rooms with sporicidal agents.

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136
Q

What is the treatment for clostridium difficile?

A

metronidazole
oral vancomycin (for relapse, failure to respond or more severe infection)
fidaxomicin (expensive but reduces relapse rate).

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137
Q

What is biliary disease example?

A

Acute cholangitis

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138
Q

What are the symptoms of acute cholangitis?

A

Charcot’s triad jaundice, Abdo pain and fever with rigors

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139
Q

How can you diagnose acute cholangitis?

A

US, MRCP or ERCP.

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140
Q

How do you treat acute cholangitis?

A

IV Abx and fluids.
ERCP and sphincterotomy for stone removal (basket, mechanical crushing, lithotripsy)
If acutely ill may place stent first before definitive procedure
If gall bladder stones better outcome if laparoscopic cholecystectomy plus duct exploration than if ERCP and subsequent cholecystectomy
If not amenable to ERCP may need open surgical or percutaneous trnanshepatic cholangiography

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141
Q

What is acute cholecystitis?

A

RUQ pain plus abdominal tenderness, Fever, WBC, symptoms > 6 h and thickened GB on US suggest diagnosis and distinguish from biliary colic.

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142
Q

How can you treat acute cholecystitis?

A

Rx IV Abx Amoxicillin plus clavulinic acid, Piperacillin plus tazobactam, Ampicillin plus gentamicin and metronidazole, IV fluids
Early cholecystectomy.

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143
Q

What can liver abscess’ be?

A

1) Pyogenic (bacterial)
a) Biliary
b) Hematogenous;
bacteremia or from portal vein (mesenteric infections)
c) Direct extension e.g from empyema of Gall bladder
d) Trauma
e) Infection of tumour or cyst
2) Hydatid cysts
3) Amoebic liver abscesses

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144
Q

What is a pyogenic liver abscess caused by?

A 
Commonest sites from biliary tract, dental source , renal or intestinal.
Micro-organisms
E. coli
K. pneumoniae
Streptococcus milleri
Bacteroides spp. and other anaerobes
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145
Q

What are the symptoms for a pyogenic liver abscess?

A 
Fever
Weight loss
RUQ abdominal pain ± pleuritic or R shoulder pain
Tender hepatomegaly (50%)
± obstructive jaundice
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146
Q

What investigations can be done for a pyogenic liver abscess?

A 
Blood cultures  (+ve in 50-80%)
CT abdomen and US guided aspiration
Colonoscopy and other investigation if intestinal source.
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147
Q

What is the treatment for a pyogenic liver abscess?

A

Amoxicillin-clavulinic acid, piperacillin –tazobactam ampicillin +gentamicin+metrondiazole or meropenam
US guided catheter drainage if large
Definitive surgery of source; biliary, gut, dental etc..

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148
Q

What is a diverticular abscess?

A

Complication of diverticulosis
Fecolith obstructs lumen of diverticulum
Micro Colonic flora; E coli, other GNB and anaerobes

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149
Q

What are the symptoms of diverticulum abscess?

A

Fever, colicky abdominal pain, acute abdomen ±diarrhoea/constipation
WBC
CT paracolic abscess

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150
Q

How is diverticulum abscess treated?

A

Treated with amoxicillin-clavulinic acid and percutaneous drainage of large abscess.
Conservative management better than surgical resection unless indicated by a major complication

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151
Q

What is Hepatic abscesses (non-pyogenic)?

A

Hydatid cyst
Echinococcus granulosis dog tapeworm (and other spp.)
Multi-layered cysts, single or with with daughter cysts
May calcify.

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152
Q

What are the symptoms of a Hepatic abscess (non-pyogenic)?

A

Pain associated with infection or rupture

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153
Q

What can you diagnose a Hepatic abscess (non-pyogenic)?

A

serology ELISA

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154
Q

How can you treat a Hepatic abscesses (non-pyogenic)?

A

albendazole

PAIR (percutaneous aspiration, injection of scolicidal agent and re-aspiration)

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155
Q

What is amoebic liver abscess?

A

Entamoeba histolytica

Usually history of residing in endemic area.

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156
Q

What are the symptoms of amoebic liver abscess?

A

Fever and abdominal pain
Usually large single abscess
Aspiration of cyst shows ‘anchovy sauce’ chocolate-brown type material

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157
Q

How can you diagnose amoebic liver abscess?

A

Serology EIA

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158
Q

What is the treatment for amoebic liver abscess?

A

Treated with metronidazole plus luminal agent

Aspiration if large

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159
Q

What is peritonitis?

A

Inflammation of peritoneum.

160
Q

What are the symptoms of peritonitis?

A

Pain, tenderness and guarding
Fever
WBC

161
Q

What are the investigations of peritonitis?

A

XR/CT showing pneumato-peritoneum consistent with rupture
Ascitic tap
in spontaneous bacterial peritonitis >250 polymorphonuclear leukocytes (PMN)/ml and positive culture
in 2° bacterial peritonitis >250 polymorphonuclear leukocytes (PMN)/ml and polymicrobial infection on Gram stain or culture or two of LDH> upper limit of normal for serum, protein> 10g/L and glucose < 2.8mmol/L)
in chronic ambulatory peritoneal dialysis (CAPD) infections >100 WBC ≥ 50% PMN and cloudy fluid

162
Q

How can you treat peritonitis?

A

Treatment antimicrobials empiric to likely source

intraperitoneal preferred for CAPD infection)

163
Q

What are some infectious causes of peritonitis?

A
  • Surgical
    2° bacterial peritonitis due to to perforation or trauma; polymicrobial with gut flora
  • Spontaneous bacterial peritonitis (SBP)
    complication of ascites in cirrhosis, E coli and other GNB, S. pneumoniae,
  • Paediatric in absence of ascites
    S. pneumoniae and other streptococci
  • Infection 2° peritoneal dialysis
    with Staph. aureus , coagulase negative staphylococci or other skin flora, E. coli, , P. aeruginosa or other GNB
  • Pelvic inflammatory disease (PID)
    As complication of chlamydial or gonococcal sexually transmitted infection (STI) in young women
  • Tuberculous
  • Distinguish from non-infectious/sterile causes;
    Foreign body post surgical, endometriosis, pancreatitis, Familial Mediterranean fever, porphyria
164
Q

What are some physiological characteristics of the gut?

A 
Distensibilty
Motility
Segmented
Peristalsis
Physiological sphincters
Secretion
Faeces.
165
Q

What is the definition of the gut?

A

Mouth to Anus.

166
Q

What is the definition of intestinal obstruction?

A

Intestinal Obstruction= Blockage to the lumen of gut Intestinal Obstruction commonly refers
to blockage of intra- abdominal part of the intestine.

167
Q

What is a Volvos?

A

A twist / rotation of segment of bowel

168
Q

What is adhesions?

A

Sticking together
abdominal structures to one another,
bowel loops or omentum,
other solid organs, abdominal wall.

169
Q

What is intesusspition?

A

Telescoping

one hollow structure into its distal hollow structure

170
Q

What is atresia?

A

Absence of opening or failure of development of hollow structure.

171
Q

How is bowel obstruction classified?

A 
- According to site
Large bowel / Small bowel /Gastric
- Extent of luminal obstruction
Partial / complete
- According to mechanism
Mechanical / True ( intraluminal /
extraluminal)
Paralytic (Pseudo obstruction)
- According to pathology
Simple
Closed loop
Strangulation
Intussusception
172
Q

What happens if there is a small bowel obstruction?

A

Proximal dilatation
Increased secretions + swallowed air (small bowel) or bacterial fermentation (large bowel)
More dilatation- decreased absorption – mucosal
wall oedema
Increased pressure – intramural vessels compressed- Ischaemia- perforation.

173
Q

What does increased secretions and distention in the small bowel cause?

A

Anorexia, nausea, vomiting / distension with pain
Fluid and electrolyte imbalance- hypovolemia
Bacterial overgrowth faeculent vomiting

174
Q

What does small bowel obstruction lead to if untreated?

A

Ischaemia
Necrosis
Perforation.

175
Q

What happens in the large bowl lis obstructed?

A

Similar to SBO with difference
The colon proximal to obstruction dilates
Increased colonic pressure decreased mesenteric
blood flow
Mucosal oedema - transudation of fluid and electrolytes- lumen.
The arterial blood supply compromised - mucosal ulceration - full thickness necrosis - perforation.
Bacterial translocation – sepsis

176
Q

What happens in large bowel obstruction if the ileocaecal valve is competent?

A

If ileocaecal valve competent –
The caecum - usual site of perforation

If ileocaecal valve incompetent –
faeculent vomiting.

177
Q

What happens in a colonic Volvulus?

A

Axial rotation –at mesenteric attachments:
A 360° twist -a closed loop obstruction is produced.
Fluid and electrolyte shifts into the closed loop
Increase in pressure and tension - impaired colonic blood flow
Ischaemia, necrosis, and perforation of the loop of bowel

178
Q

What is the Small Bowel Obstruction (SBO)- Epidemiology?

A

Most obstructions due to a previous surgery, second is a inflammatory bowel disease.

179
Q

What are some caused of small bowel obstruction in adults?

A

Adhesions (developed world)- previous surgery
Hernia ( developing world)
Crohns
Malignancy.

180
Q

What are some causes of small bowel obstruction in children?

A 
Appendicitis
Intesussuption
Volvulus
Atresia
Hypertrophic pyloric stenosis.
181
Q

What are some uncommon causes of small bowel obstruction?

A 
Radiation
Gall stones
Diverticulitis, appendicitis
Sealed small perforation, intra abdominal collection / abscess
Foreign Bodies ( Bezoars).
182
Q

What is large bowel obstruction normally due to?

A

functional (due to abnormal intestinal physiology)
Mechanical obstruction
partial or complete.
Acute presentation-abdominal pain and obstipation,
Chronic - a progressive change in bowel habits.

183
Q

What are the causes of large bowel obstruction in adults?

A

Age and Race dependent
US/Europe – 90% colorectal malignancy
Age 70y ; Men and women equal
» Only 30% colorectal malignancy present as Obstruction
» 5% Volvulus
» 3% strictures Ischaemic, radiation, inflammatory, gynaecological
other malignancy
» 2% rare causes –FB, hernia, abscess
» Functional obstruction - faecal impaction
African countries – 50% Volvulus

184
Q

What are the causes of large bowel obstruction in children?

A

Paediatric
Anatomical development
» Imperforate anus
» Hirshsprung disease ( congenital absence of ganglion cells in bowel wall).

185
Q

What is the most common cause of small bowel obstruction? What are the common surgeries beforehand?

A

Adhesive obstruction.

Pelvic surgery
Gynaec surgery
Colorectal surgery

186
Q

What is the definition of a hernia?

A

Abnormal protrusion of viscus thro normal or abnormal defects of body cavity.

187
Q

What is the risk with hernias?

A

Untreated – strangulation

smaller hernias greater risk

188
Q

What does a hernia normally present as?

A

Lump

Pain.

189
Q

What does a volvulus always occur? What is it?

A

Always occurs at the part of bowel with mesentery

Type of closed loop bowel obstruction

190
Q

What is the cause of a volvulus?

A

Uncommon cause of SBO
– Caused by Caecal rotation, congenital or Adhesional

Caused narrow base and wide apex
Caused by rotation by 360 degree proximal limb around distal
Cuts of blood supply

191
Q

Where does a volvulus mostly occur in the large bowel?

A

Sigmoid (76%), Caecum (22%).

192
Q

What are the two types of intesusspition?

A

idiopathic
enteroenteral intussusception (jejunojejunal, jejunoileal, ileoileal),
Associated with special medical situations HSP, cystic fibrosis, hematologic dyscrasias

193
Q

What is the mechanism of intesusspition?

A

an imbalance in the longitudinal forces along the intestinal wall.
a mass acting as a lead point or
disorganized pattern of peristalsis
The invaginating portion - the intussusceptum)
the receiving portion - the
intussuscipiens.

194
Q

What happens if the mesentery of the intesusspition is lax?

A

The progression is rapid
The intussusceptum - prolapse out the
anus.
Invagination causes the classic pathophysiologic process of any bowel obstruction.

195
Q

What time do the different symptoms show in small and large bowel obstruction?

A 
-  Pain
Colicky – poorly localised
-  Vomiting
Early – proximal bowel obstruction  
Late – in large bowel obstruction
-   Constipation
Early in distal large bowel obstruction  
Late in small bowel obstruction
Absolute constipation=Obstipation
-  Abdominal distension
The more distal the obstruction the
greater the distension
196
Q

How do small bowel obstruction present?

A 
-   Vomiting
Projectile
Faeculent
-   Pain
Colicky to constant- diffuse
-   Constipation
Late ( one of more motion after onset of pain not
uncommon)
Obstipation – absence of faeces or flatus
-   Distension
-   Tenderness
197
Q

How does large bowel obstruction present?

A 
Common Symptoms – malignancy, strictures
-   Abdominal discomfort
-   Fullness / Bloating / Nausea
-   Altered bowel habit
Increasing difficulty to open bowels - tenesmus
Blood in stools
-   Constipation - obstipation
-    Abdominal pain
Colicky, tenderness, constant
-    Vomiting
late
-   Weight loss
-    Volvulus
Sudden
Pain
Localised tenderness and distension
198
Q

What are the different ways a bowel can be obstructed?

A

Inside the bowel.
In the wall of the bowel.
Just outside the bowel.

199
Q

What can obstruct inside the bowel?

A 
tumour
carcinoma
lymphoma
diaphragm disease
meconium ileus
gallstone ileus
200
Q

What is diaphragm disease?

A

Fibrous tissue with a little hole.

201
Q

What is diaphragm disease caused by?

A

NSAIDs Continuous ulceration.

202
Q

What is gallstone ileus?

A

Huge gallstone in gall bladder, inflamed, sticks onto small bowel and erodes through

203
Q

What can cause obstruction in the wall of the gut?

A 
intramural obstruction
inflammatory
Crohn’s disease
diverticulitis
tumours
neural
Hirschsprung’s disease.
204
Q

What does Crohn’s disease cause?

A

Inflammation and fibrosis.

205
Q

What is classic in Chohn’s disease?

A

Parts of the bowel fibrous, parts not, granulomas also common.

206
Q

Where is Crohn’s disease most common?

A

Terminal Ilieum.

207
Q

What is diverticular disease?

A

Sigmoid colon abnormality. Little pouches at the side.

208
Q

What is diverticular caused by?

A

Low fibre.

209
Q

What does the gut wall have in it?

A

Little holes where the vessels come in and out.

210
Q

What can diverticulitis become?

A

Peritonitis.

211
Q

What is a tumour of the pacemaker cells called?

A

Gastrointestinal stromal tumours.

212
Q

What happens in Hirschsprung’s disease.

A

No ganglion cell in it, no moving.

213
Q

What are some extraluminal obstruction problems?

A

adhesions
volvulus
tumour
– peritoneal deposits

214
Q

What is an example of a adhesion problem?

A

After appendix removal.

215
Q

What does volvulus affect the most?

A

Sigmoid colon.

216
Q

What does graphs of colorectal cancer show?

A

Environmental causes.

217
Q

What do older people have?

A

Polyps in colon.

218
Q

What causes a predisposition to cancer?

A

polyps.

219
Q

What can happen with cancer in the colon?

A

Go to a dysplastic epithelium but not to cancer.

220
Q

What is the normal progression of the colon into cancer?

A

Normal epithelium.
Adenoma.
Colerectal adenocarcinoma.

221
Q

What is a genetic condition that can predispose to colorectal cancer?

A

familial adenomatous polyposis

222
Q

How does familial adenomatous polyposis cause cancer?

A

APC bound GSK suppose to break down beta catenin, APC ascent in FAP, beta catenin builds up and causes epithelial proliferation.

223
Q

What is hereditary nonpolyposis colorectal cancer

HNPCC?

A

Two hits of DNA repair protein. No DNA repair.

224
Q

What are the reasons for identifying HNPCC cancers?

A 
risk of further cancers in index patient and  relatives
possible implications for therapy
tolerance of 5-FU etc.
do not recognise DNA damage
apoptosis not activated.
225
Q

Where is the most common site for cancer?

A

Rectum.

226
Q

What is colorectal cancer called?

A

Adenocarcinoma.

227
Q

What is important is cancers?

A

Can do staging, using whether it has spread to lymph nodes, how big tumour is.

228
Q

What is the resection margin?

A

Area around a tumour that has been cut out which is not cancerous.

229
Q

What are the different resection coding?

A

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

230
Q

Why should you stage a tumour?

A

To give prognosis and see life expectancy.

231
Q

How does staging of tumour work?

A

As it progresses it goes higher.

232
Q

What are the Duke stage prognosis?

A

A 95% 5 year survival
B 75% 5 year survival
C 35% 5 year survival
D 25% 5 year survival.

233
Q

What are Dukes classification?

A

Duke A in gut.
Duke B just outside gut.
Duke C lymph node.
Duke D high tie lymph node.

234
Q

How do you treat normal epithelium going to adenomas?

A

prevention.

Low dose aspirin.

235
Q

How do you treat an adenoma?

A

endoscopic resection

236
Q

How do you treat a colorectal adenocarcinoma?

A

surgical resection.

237
Q

How do you treat a metastatic colorectal adenocarcinoma?

A

chemotherapy and palliative care

238
Q

What does Duke’s classification not take into account?

A

Peritoneum.

239
Q

Why are specific diseases notifiable diseases?

A

Stuff that makes you very scared
Stuff that is quite nasty
Vaccine preventable diseases
Diseases that need specific control measures

240
Q

What is the role of survelliance in notifiable diseases?

A

Detection of any changes in a disease
Outbreak detection
Early warning
Forecasting

Track changes in disease
Extent and severity of disease
Risk factors

Allows development of interventions targeted at vulnerable groups

241
Q

How do the NHS protect people of notifiable diseases?

A

Investigate: contact tracing, partner notification, lookback exercises, etc…

Identify and protect vulnerable persons: e.g. chemoprophylaxis, immunisation, isolation

Exclude high risk persons or from high risk settings

Educate, inform, raise awareness, health promotion

Coordinate multi-agency responses

242
Q

What is the route of transmission for diseases?

A

Source
Pathway
Receptor.

243
Q

What are the two forms of immunity?

A

Active and Passive.

244
Q

What are the different types of active immunity?

A

Cell-mediated immunity

Antibody-mediated immunity

245
Q

What is passive immunity?

A

Protection provided from the transfer of antibodies from immune individuals
Most commonly cross-placental transfer of antibodies from mother to child
(e.g. measles, pertussis)
Or, via transfusion of blood or blood products including immunoglobulin
(e.g. Hep B)
Protection is temporary – usually only a few weeks
or months.

246
Q

What is human normal immunoglobulin?

A

Human normal immunoglobulin (HNIG) derived from the pooled plasma of donors and contains antibodies to infectious agents that are currently prevalent in the general population.

247
Q

What is pooled immunoglobulin used for?

A

Used to protect immunocompromised children exposed to measles and of
individuals after exposure to hepatitis A.
Specific immunoglobulins available for tetanus, hepatitis B, rabies and varicella zoster.

248
Q

What can vaccines be made of?

A

inactivated (killed) (e.g. pertussis, inactivated polio)
attenuated live organisms (e.g. yellow fever, MMR, polio, BCG)
secreted products (e.g. tetanus, diphtheria toxoids)
the constituents of cell walls/subunits (e.g. Hep B) or
recombinant components (experimental).

249
Q

What are the properties of polysaccharide vaccines?

A

Polysaccharide antigens not as immunogenic as protein antigens.
Protection is not long-lasting
Response in infants and young children often poor.
Conjugation helps improve immunogenicity (e.g. Hib, Men C)

250
Q

What are the properties of live attenuated vaccines?

A

Live attenuated organism must replicate in the vaccinated individual to produce an immune response.
Takes time (days or weeks).
Usually does not cause disease but some may cause a mild form
of the disease.

251
Q

What is herd immunity?

A

Enough of the population is immunised that it is unlikely that you will be infected.

252
Q

What is primary vaccine failure?

A

Person doesn’t develop immunity from vaccine.

253
Q

What is secondary vaccine failure?

A

Initially responds but protection wanes over time

254
Q

What can Meningococcal infection present as?

A

Meningitis or septicaemia.

255
Q

What causes Meningococcal infection?

A

Neisseria meningitidis

256
Q

How is Meningococcal infection spread?

A

Transmitted from person to person by inhaling respiratory secretions from the mouth and throat or by direct contact (kissing).

257
Q

What sequelae can Neisseria meningitidis cause?

A 
Brain abscess
Brain damage
Seizure disorders
Hearing impairment
Focal neurological disorders
Organ failure
Gangrene
Auto-amputation
Death
258
Q

What is the management of Neisseria meningitidis?

A

Clinical management
Antibiotic therapy: Cefotaxime or Ceftriaxone
Supportive treatment

Outcomes
Case fatality rate ~10%
More deaths caused by septicaemia than by meningiti

259
Q

What does meningococcaemia cause?

A

Meningococcaemia causes arterial occlusions leading to

gangrene of extremities & auto-amputations.

260
Q

What is contact tracing in meningitis?

A

Contact for meningitis is taken to be any person having close contact with a case in the past 7 days

Close contact includes kissing, sleeping with, spending the night together or spending in excess of eight hours in the same room

261
Q

What is the glass test for meningitis?

A

Petechial spots do not blanch on pressure.

262
Q

What is the antibiotic chemoprophylaxis for meningitis?

A

Ciprofloxacin (older children & adults) or Rifampicin (not pregnant women)
For nasal carriage
Reduces spread
Does not stop disease if already incubating it

Could offer vaccine if serotype is preventable.

263
Q

What vaccines are given at eight weeks?

A 
DTaP/IPV/Hib/HepB
Diphtheria, tetanus, pertussis (whooping cough), polio, Haemophilus in uenzae type b (Hib) and hepatitis B
Pneumococcal conjugate vaccine (PCV)
Pneumococcal (13 serotypes)
MenB
Meningococcal group B (MenB)
Rotavirus
Rotavirus gastroenteritis
264
Q

What vaccines are given at twelve weeks?

A

DTaP/IPV/Hib/HepB
Diphtheria, tetanus, pertussis, polio, Hib and hepatitis B
Rotavirus
Rotavirus

265
Q

What vaccines are given at sixteen weeks?

A 
DTaP/IPV/Hib/HepB
Diphtheria, tetanus, pertussis, polio, Hib and hepatitis B
PCV
Pneumococcal (13 serotypes)
MenB
MenB
266
Q

What vaccines are given at one years old?

A 
Hib/MenC
Hib and MenC.
PCV.
Pneumococcal.
MMR.
Measles, mumps and rubella.
MenB booster.
MenB.
267
Q

What vaccines are given at two years old?

A

Live attenuated in uenza vaccine LAIV

268
Q

What vaccines are given at three years old?

A

Diphtheria, tetanus, pertussis and polio

Measles, mumps and rubella

269
Q

What vaccines are given at twelve years old girls?

A

Cervical cancer caused by human papillomavirus (HPV) types 16 and 18 (and genital warts caused by types 6 and 11)

270
Q

What vaccines are given to fourteen years old?

A

Td/IPV (check MMR status)
Tetanus, diphtheria and polio
MenACWY
Meningococcal groups A, C, W and Y disease

271
Q

What are the notifiable diseases?

A 
Acute encephalitis
Acute infectious hepatitis
Acute meningitis
Acute poliomyelitis
Anthrax
Botulism
Brucellosis
Cholera
Diphtheria
Enteric fever (typhoid or paratyphoid fever)
Food poisoning
Haemolytic uraemic syndrome (HUS)
Infectious bloody diarrhoea
Invasive group A streptococcal disease
Legionnaires’ disease
Leprosy
Malaria
Measles
Meningococcal septicaemia
Mumps
Plague
Rabies
Rubella
Severe Acute Respiratory Syndrome (SARS)
Scarlet fever
Smallpox
Tetanus
Tuberculosis
Typhus
Viral haemorrhagic fever (VHF)
Whooping cough
Yellow fever
272
Q

What are the causes of Diarrhoeal diseases?

A

Infective causes and non-infective.

273
Q

What are some non-infective causes of diarrhoea?

A 
Neoplasm.
Hormonal.
Inflammatory.
Radiation.
Irritable bowel.
Chemical.
Anatomical.
274
Q

What are the infective causes of diarrhoea?

A

Non-bloody and bloody (dysentery)

275
Q

What are some different types of transmission?

A 
Direct
Direct route.
STIs
Faeco-Oral route.
Viral GE
Indirect
Vector-bourne
Malaria
Vehicle-bourne
Viral GE

Airborne
Respiratory route
TB

276
Q

27 year old student just returned from backpacking holiday around South Asia.
Presents with frequent bouts of diarrhoea, flatulence, nausea and abdominal discomfort.
What is this a case of?

A

Vibrio cholerae

277
Q

2 year old child presents with loose stools for 2 days. Miserable. Loss of appetite but drinking ok. No fever.
Attends nursery and playgroup.
Recently been to a petting zoo.
What is this a case of?

A

Escherichia coli

278
Q

87 year old resident of a care home presents with confusion, altered consciousness, dehydration and a history of diarrhoea.
What is this a case of?

A

Norovirus

279
Q

What is the norovirus?

A 
Major cause of “Winter Vomiting”
Mainly occurs in the winter
Mainly causes vomiting
May cause diarrhoea, nausea,  cramps	headache, fever, chills,  myalgia
Lasts 1-3 days
Immunity is short lived
280
Q

36 year old man presents with bouts of low volume bloody stools.
He works in a take-away.
What is the a case of?

A

Shigella.

281
Q

84 year old patient at the Northern General Hospital presents with diarrhoea.
She is recovering from a surgical operation a few days ago.
What is the a case of?

A

Clostridium difficile.

282
Q

What is clostridium difficile associated with?

A

Associated with antibiotic use
Especially broad spectrum antibiotics

In hospitalized patients cause
Antiobitic-associated diarrhoea
Antibiotic-associated colitis
Pseudomembranous colitis

Mortality high
Especially as patients tend to be elderly and ill

283
Q

What is the epidemiology of clostridium difficile?

A

Asymptomatic carriage occurs in
2-3% of healthy adults,
2/3 of babies
~36% of hospital patients
Spread by faeco-oral route directly or through spores in the environment.
Asymptomatic carriers without diarrhoea unlikely to spread it.
80% of symptomatic cases in persons > 65 years
Causes 20% of antibiotic-associated diarrhoea

284
Q

How can you prevent clostridium difficile?

A

Clostridium difficile produces spores highly resistant to chemicals (spores)

Alcohol hand rubs will not destroy the spores.

Hand washing using soap and water will remove the microorganisms (including spores) from the hands.

285
Q

What is SIGHT?

A 
S	uspect C diff as a cause of diarrhoea
I	solate the case
G	loves and aprons must be worn
H	and washing with soap and water
T	est stool for toxin.
286
Q

How do you manage a clostridium difficile patient?

A 
Control antibiotic usage
Esp. Ampicillin, amoxicillin &amp; cephalosporins
Standard infection control procedures
Surveillance &amp; case finding
Any patient with diarrhoea
Isolate
Enteric precautions
Test stool samples
Environmental cleaning
Treat cases with metronidazole or vancomycin
287
Q

What do you test for clostridium difficile?

A

Test stool samples for the toxin

Can also culture it (in order to identify which strain it is)

Tissue samples (histology) obtained at sigmoidoscopy

Don’t need to screen or treat asymptomatic carriers

288
Q

What does a normal gut look like?

A

Buffer on top on normal cells to neutralise the acid.

289
Q

What can upset the gut?

A

Lack of blood flow.

290
Q

What happens when the blood flow slows to the gut?

A

Cells break down as the buffer is not produced as much, the acid the attacks the cells and an ulcer forms.

291
Q

What can happen from a breach in the cells in the mucosa?

A

Acid attack adjacent cells.

292
Q

What is a lack of blood flow to the gut called?

A

Mucosal ischaemia.

293
Q

What would a patients stomach with a low blood pressure in ITU look like?

A

Bleeding points.

294
Q

How could you treat gastritis and ulceration?

A

Reduce the acid - H2 blocker or proton pump inhibitor.

295
Q

What else can cause ulceration?

A

Increased acid.

296
Q

What causes increased acid?

A

Stress.

Helicobacter pylori.

297
Q

What does aspirin do?

A

Inhibit COX-2.

298
Q

When COX-2 is inhibited what happens?

A

Cells break down and ulceration occurs.

299
Q

How can you avoid COX-2 inhibition by aspirin?

A

Produce aspirin with enteric coat on it, therefore won’t dissolve in stomach but lower down in gut.

300
Q

What can cause a stomach ulcer?

A

Decreased blood flow.
Increased acid.
Bile reflux.

301
Q

What does bile reflux do?

A

Cause ulcers.

302
Q

Where do helicobacter live?

A

In the mucus layer in the stomach.

303
Q

What does helicobacter do?

A

Secrete chemicals that attract neutrophils polymorphs into the cells.
Also increase acid production.

304
Q

What can happen to the epithelial lining in helicobacter pylori?

A

Change from stomach epithelium to intestinal epithelium.

Intestinal metaplasia.

305
Q

What can happen in ulceration to an artery?

A

Can eat into the artery and start haemorrhaging.
Stomach - will come straight up
Intestine - black stools.

306
Q

What can happen in ulceration to the muscle?

A

Ulceration through the muscle, which allows free flow of contents in the peritoneum causing peritonitis.

307
Q

What can ulceration lead to on the posterior side?

A

Erode through into the pancreas to give pancreatitis.

308
Q

What is the structure of the small intestine?

A

Villi and crypts.

Crypts provide new cells for the villi.

309
Q

What is located in the tips of the villi?

A

Lymphocytes.

310
Q

What are the different types of malabsorption?

A 
Insufficient intake.
Defective intraluminal digestion.
Insufficient absorptive area.
Lack of digestive enzyme.
Defective epithelial transport.
Lymphatic obstruction.
311
Q

What can defective intraluminal digestion be caused by?

A
  • Pancreatic insufficiency
    pancreatitis
    cystic fibrosis
  • Defective bile secretion (lack of fat solubilisation)
    biliary obstruction
    ileal resection – decreased bile salt uptake
  • Bacterial overgrowth
312
Q

What is a type of insufficient absorptive area?

A

Gluten sensitive enteropathy.

313
Q

What happens to the small intestine in celiacs disease?

A

Villi disappear and crypts are bigger to produce more cells for the villi.
Villi atrophy.
Crypt hyperplasia.

Increased amount of lymphocytes.

314
Q

What causes the changes to the small intestine in celiacs disease?

A

Gliadin protein gets absorbed into the gut.

Gliadin reacts with lymphocytes which produces T cells and produce chemicals which damage the cells.

315
Q

How do you diagnose celiacs disease?

A

Transglutaminase antibody

316
Q

What is Giardia lamblia?

A

Giardia lamblia, also known as Giardia intestinalis, is a flagellated parasite that colonizes and reproduces in the small intestine, causing giardiasis. The parasite attaches to the epithelium by a ventral adhesive disc, and reproduces via binary fission.

317
Q

What is involved with small intestine resection or bypass?

A

procedure for morbid obesity
Crohn’s disease
infarcted small bowel

318
Q

What is involved with lack of digestive enzymes?

A

disaccharidase deficiency (lactose intolerance)
bacterial overgrowth
– brush border damage.

319
Q

What is involved with defective epithelial transport?

A

abetalipoproteinaemia
primary bile acid malabsorption
– mutations in bile acid transporter protein

320
Q

What is involved with lymphatic obstruction?

A

lymphoma

tuberculosis

321
Q

What are the chronic idiopathic inflammatory bowel disease conditions?
What are the other inflammatory conditions?

A

Crohn’s disease.
Ulcerative colitis.

Diverticulits.
Ischameic colitis.
Infective colitis - bacterial and protozoal.

322
Q

What is Crohn’s disease?

A

Massive inflammation and associated ulcers.

Transmural granulomatous inflammation

323
Q

Where can ulceration/granulomatous inflammation be found in Crohn’s?

A

Throughout the mucosa, submucosa, muscular propriety and fat of the gut.

324
Q

What are some Crohn’s disease complications?

A 
Malabsorption
-disease extent
-surgical resections
Obstruction
-acute swelling
-chronic fibrosis
Perforation 
-acute abdomen
Fistula formation
Anal
-skin tags
-fissure
-fistula
Neoplasia 
-colorectal cancer
325
Q

What different surgical resections are there?

A

Ileocolonic anastomosis
Jejunocolonic anastomosis
End-jejunostomy

326
Q

What can ulcerative colitis involve?

A

Inflammatory disorder of the colonic mucosa.

May just affect rectum, or extend to involve part of the colon or all of the colon.

327
Q

How do you distinguish ulcerative colitis from Crohn’s disease?

A

Ulcerative colitis only involves mucosa whilst Crohn’s involves many layers of the gut.

328
Q

What is the pathology of ulcerative colitis?

A

Hyperaemic/haemorhagic granular colonic mucosa and maybe pseudo polyps formed by inflammation.

329
Q

What are the symptoms of ulcerative colitis?

A

Episodic or chronic diarrhoea; cramps abdominal discomfort; bowel frequency relates to severity; urgency/tenesmus.
Fever, malaise, anorexia, weight.

330
Q

What are some complications of ulcerative colitis in the skin?

A

Erythema nodosum

pyoderma gangrenosum

331
Q

What are some complications of ulcerative colitis in the colon?

A

blood loss
toxic dilatation
Colorectal cancer.

332
Q

What are some complications of ulcerative colitis in the liver?

A

fatty change
chronic pericholangitis
sclerosing cholangitis

333
Q

What are some complications of ulcerative colitis in the joints?

A

ankylosing spondylitis

arthritis

334
Q

What are some complications of ulcerative colitis in the eyes?

A

iritis
uveitis
episcleritis

335
Q

What investigations can be done for ulcerative colitis?

A

Bloods.
Stools.
Colonoscopy.

336
Q

What are the principles of management for ulcerative colitis?

A

Inducing remission - mesalazine, Steroids e.g. prednislone.

Suppositories.

Surgery.

Maintain remission.

337
Q

What is the oesophagus lined by?

A

Squamous epithelium.

338
Q

What is the stomach lined by?

A

Glandular epithelium.

339
Q

What happens in barrett’s oesophagus?

A

Change from squamous epithelium to glandular.

Columnar lined lower oesophagus.

340
Q

What is metaplasia?

A

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

341
Q

What does reflux of acid into the oesophagus cause?

A

Destruction of the squamous cells and ulceration.

342
Q

What can cause acid reflux?

A

Obesity - increased intra-abdominal pressure.

343
Q

What can develop from this acid reflux and changing of cells?

A

Adenocarcinoma.

344
Q

What is the progression of cell type in Barrett’s oesophagus?

A

Normal
Metaplasia
Dysplasia
Neoplasia.

As a result of on going acid reflux.

345
Q

What are the different types of oesophageal cancers for different parts of the world and why?

A

China have squamous cancer by smoking and drinking.

Europe has adenocarcinoma by acid reflux and obesity.

346
Q

What happens when a cancer grows in the oesophagus, at what point can you not remove it?

A

Could metastasise into the wall of the oesophagus, could move to far so that it comes into close contact with the superior vena cava and other major vessels.

347
Q

What is a risk factor for gastric cancer?

A

Eating certain foods such as pickled and smoked foods,.

Asia.

348
Q

What can helicobacter pylori put you at a predisposition to? Why is this?

A

Gastric cancer.

Due to intestinal metaplasia.

349
Q

What is limits plastica?

A

Cancer cells everywhere producing a plastic like feel.

350
Q

What is early gastric cancer?

A

Anything that doesn’t go into the muscular wall.

351
Q

What is late gastric cancer?

A

Into the muscular wall and lymph nodes.

352
Q

Why is the prevalence of coeliac’s disease increasing?

A

Change in endoscopic techniques

Antibody screening

Increased awareness of the spectrum of diversity in the presentation of coeliac disease

An actual increase in disease incidence!?

353
Q

How does coeliac’s disease present?

A 
Classical
Diarrhoea
Steatorrhoea
Weight loss
Failure to thrive
Non-classical
Irritable bowel type  symptoms
Iron Deficiency Anaemia
Osteoporosis
Chronic Fatigue
Dermatitis Herpitiformis
Ataxia
Peripheral neuropathy
Hyposplenism
Ammenorhoea
Infertility
354
Q

What is Dermatitis Herpetiformis?

A

Rash common with coeliac disease patients.

355
Q

What commonly happens with the presentation of coeliac’s disease?

A

More non-common presentations then common.

356
Q

How do you test for coeliac’s disease?

A 
Serology:
Tissue transglutaminase (tTG)  Anti-endomysial antibody (EMA)  Immunoglobulins.

Endoscopy + Duodenal biopsies.

Histology: Villous atrophy.

357
Q

Who would need a duodenal biopsy?

A

High risk antibody positive.

Low risk antibody positive.

358
Q

What do patients need to do when undergoing testing for coeliac’s?

A

testing is accurate only if they follow a gluten-containing diet
when following a gluten- containing diet they should eat some gluten in more than one meal every day for at least 6 weeks before testing
they should not start a gluten- free diet until diagnosis is confirmed by intestinal biopsy

359
Q 
What are the different stages of coeliac's disease? 
0.
1
2
3a
3b
3c
A
  1. Normal
  2. Raised Intra epithelial Lymphocytes (IEL)
    >30/100 enterocytes
  3. Raised IEL + Crypt Hyperplasia
    3a. Partial Villous Atrophy (PVA)
    3b. Subtotal villous atrophy (SVA)
    3c .Total villous atrophy TVA)
360
Q

Where will a duodenal biopsy be taken from for coeliac’s?

A

1 x Duodenal bulb (new)

4 x D2 (traditional)

361
Q

How many duodenal biopsy’s should be taken to make sure the most severe lesion is identified?

A

5.

362
Q

What are the macroscopic signs in coeliac’s disease?

A

Reduced Folds in Duodenum

Scalloping

363
Q

How do you manage coeliac’s disease?

A 
Gluten free diet – strict and lifelong
Dietician review
DEXA scan- osteoporotic risk
Coeliac UK info.
Prescription entitlement
Inform 10% risk in 1st degree relatives.
364
Q

What happens if coeliac’s disease is left untreated?

A

Persistent symptoms Osteoporosis Subfertility

Cancer risk Quality of life.

365
Q

What is the percentage of osteoporosis in coeliac’s disease?

A

40-60% of untreated adult CD

Fracture risk

Clinical, subclinical and silent affected

Adherence improves BMD

366
Q

What is the associated cancer risk with coeliac’s disease?

A

2 fold increase in cancer and mortality compared with controls
Small bowel lymphoma
Oesophageal and ENT malignancies
Lung and breast cancer LESS likely

367
Q

What is the definition of peritonitis?

A

Inflammation of the peritoneum.

368
Q

How is peritonitis classified?

A

Based on onset Acute Chronic
Source of origin Primary Secondary
Cause Bacterial Chemical
Localised Generalised

369
Q

What are the primary causes of peritonitis?

A 
Extremely rare -less than 1% adults &amp; 2% children
Cause haematogenous or lymph nodes
Risk groups
Liver disease (Spontaneous Bacterial Peritonitis – SBP)
Females
Immune compromised
Post Splenectomised
Peritoneal dialysis patient
Ascites
370
Q

What are the secondary causes of peritonitis?

A

Secondary
Perforation of hollow viscus
Contamination of cavity with secretions, organism
eg peptic ulcer, colonic diverticulum, appendix, bladder
Inflammation of abdominal organs
Appendix, pancreas, small bowel, colon , gall bladder,
Peritoneal dialysis patient
Tuberculosis
Ischaemia hollow viscus
Chemical
contamination – starch – surgical glove.

371
Q

How does peritonitis present?

A 
Acute ( most peritonitis )
Pain
Site, nature , progress
Tenderness
Localised – progression to generalised
Systemic symptoms
Nausea, chills and rigor
Dizziness, Weakness and inability to move due to pain.
372
Q

What clinical examinations could you do to diagnose peritonitis?

A 
Clinical
General examination
Pyrexia, tachycardia
Confusion ( encephalopathy)
Patients lie still
Localised peritonitis – avoid strain on part affected
Generalised peritonitis – lie very still
Hypotension, hypoxia are late signs of shock
Abdominal examination
Guarding, rebound, rigidity
Silent abdomen – ominous sign
373
Q

What investigations can you do to diagnose peritonitis?

A

Investigations
Needed for definitve in management
Blood tests
Full blood count, urea, electrolytes, amylase, liver function tests
Plain X ray
chest –erect perforation, Abdomen -supine
CT scan abdomen
In primary
Culture – blood , ascitic, dialsysate fluid
An ascites lactate level of more than 25 mg/dL was found to be 100% sensitive.

374
Q

What is SBP?

A

Spontaneous bacterial peritonitis

375
Q

How is spontaneous bacterial peritonitis defined?

A

Assessing Ascitic fluid
Defined by an absolute neutrophil count (ANC) >250 cells/mm^3.
Culture-negative neutrocytic ascites (CNNA)
Defined by an ANC >250 cells/mm^3, with no culture growth, this is considered a variant of SBP.
Bacterascites
positive ascitic fluid culture
● + ANC <250 cells/mm
● + no evidence of systemic or local infection.

Recent advances ( 100% Sensitivity)
Leucocyte esterase
Ascitic fluid lactate > 25mg/d

376
Q

How can you treat peritonitis?

A 
Resuscitate
ABC principle
Airways, breathing , circulation
Antibiotics
Treat the cause

MEDICAL – only for primary peritonitis
SBP , Pelvic inflammatory disease, PD related peritonitis

SURGICAL TREATMENT
Repair of perforated viscus – peptic ulcer
Excision of perforated organ
With or without drainage
With or without restoring continuity
377
Q

What is the clinical definition of ascites?

A

Detectable collection of Fluid in the peritoneal cavity
Chronic accumulation of Fluid within the peritoneal
cavity.

378
Q

How much fluid is there in the peritoneal cavity in a man and woman?

A

Healthy men – no fluid.

Women up to 20ml.

379
Q

What are the different stages of ascites?

A

Stage 1 detectable only after careful examination / Ultrasound scan (Mild)
Stage 2 easily detectable but of relatively small volume.
Stage 3 obvious, not tense ascites. (moderate)
Stage 4 tense ascites. (Large)

380
Q

What are the clinical features of refractory ascites?

A

not mobilised
or early recurrence (after therapeutic paracentesis) <4 weeks
Cannot be prevented by medical therapy

381
Q

What are the different refractory ascites?

A

Diuretic resistant
Na restriction and diuretics for atleast 1 wk

Diuretic intractable
Diuretic complications
Mean weight loss <0.8kg over 4d
Urinary Na excretion > Na intake

382
Q

What are the different causes of ascites?

A 
Cirrhosis
Malignancy  
Heart failure  
TB
Pancreatitis
Other Causes
383
Q

What is ascites - portal hypertension?

A

A state of sodium water imbalance
Interplay of various neurohormonal agents – renin, aldosterone, sympathetic nervous
system, nitric oxide

384
Q

What are the different theories for ascites - portal hypertension?

A

Three theories
Under filling-
Portal Hypertension – redistribution fluid – splanchnic volume high, effective circulating volume low – enzymes cascade –Na + H2O retention
Over filling-
Inappropriate Na + H2O retention – no volume depletion – hypervolemia
Peripheral arterial vasodilatation

385
Q

What is ascites - non portal hypertension?

A

Malignancy
Cardiac Failure
Nephrotic syndrome
Associated with Anasarca – generalised oedema including skin and subcutaneous tissue.

386
Q

What is chylous ascites?

A

abdominal surgery/ trauma, malignancy, radiation, congenital

387
Q

What does exudate mean?

A

High protein content.

388
Q

What does transudate mean?

A

Low protein content.

389
Q

What causes a exudate?

A

Occlusion / obstruction of lymphatic /venous drainage

390
Q

What causes a transudate?

A

passage of fluid through a membrane – osmotic pressure, hydrostatic pressure.

391
Q

What diseases cause exudates?

A 
Congestive cardiac failure
Constrictive pericarditis
Nephrotic syndrome
Myxoedma
Bud Chiari Syndrome –  Hepatic venous  thrombosis
Chylous ascites.
392
Q

What diseases cause transudate?

A 
Cirrhosis
Hypoproteinemic states
Protein losing enteropathy
Malnutrition
Tuberculosis ( minority)
Malignancy ( minority).
393
Q

What is the clinical presentation of ascites?

A 
Abdominal distension
Clothes getting tighter
? Gaining wait
	Nausea, Loss of appetite
	Constipation
Cachexia, weight loss
Associated symptoms of underlying cause
Jaundice &amp; Other Stigmata of
liver disease
Abdominal distension
	( up to 1.5 to 2 l)
	Puddle sign (150ml)
	Shifting dullness (500ml)
	Flanks fullness 1500+ ml
	Fluid thrill
394
Q

How do you analyse the ascitic fluid?

A 
Analysis of Ascitic fluid
Naked eye assessment
Chemistry
» Proteins
» Amylase
Microscopy
» Cytology
» Organisms
Culture
395
Q

How can you view the ascites?

A

Radiological
X-Ray ( 500ml)
Ultra sound scan ( at least 20ml)
CT abdomen (< v small amt )

396
Q

What biochemical analyses can you do? What would these help to show?

A

Serum Ascites Albumin Gradient [SAAG]
Value 1.1 g/dl important cutoff ( 97% accuracy)
>1.1 g/dl – Portal hypertension
<1.1 g/dl – non portal hypertensive causes

Total proteins
Accuracy 57% for causes
Exudate > 2.5 g/dl
Transudate < 2.5 g/dl

Amylase
Triglycerides

397
Q

How can you treat ascites?

A

Treatment of underlying cause
Adjuncts

95% portal hypertension
Diuretics
Spironolactone, Furosemide,
Amilioride, Metalazone, Mannitol
Salt and Fluid restriction
Albumen / colloid replacement
– Paracentesis
Shunts
Portosystemic shunts (liver
cirrhosis)
Peritoneovenous shunt

Bateman - Phase 2a COPY (15 decks)

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