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Emily Phase 2a > Liver + > Flashcards

Liver + Flashcards

1
Q

What are the 2 types of liver injury?

A

Acute = usually recover, but then goes to liver failure
Chronic = cirrhosis, liver failure, varies, hepatoma

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2
Q

What does the liver do?

A
  • protein synthesis
  • defence against infection (reticuloendothelial system)
  • glucose and fat metabolism
  • detoxification and excretion
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3
Q

What are the causes of acute liver injuries?

A
  • viral (A,B, EBV)
  • drug
  • alcohol
  • vascular
  • obstruction
  • congestion
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4
Q

What are the causes of chronic liver injury?

A

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

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5
Q

What are the symptoms of acute liver failure?

A
  • Malaise
  • nausea
  • anorexia
  • jaundice

rarer
- confusion
- bleeding
- liver pain
- hypoglycaemia
(^suggestive that it has moved form liver injury to liver failure)

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6
Q

What are the presentations of chronic liver injury?

A

ascites,
oedema
haematemesis (vomiting of blood, varices)
malaise,
anorexia,
wasting
easy bruising,
itching
hepatomegaly,
abnormal LFTs

rarer:
- jaundice
- confusion

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7
Q

What is measured in serum liver function test?

A
  • serum bilirubin <20
  • albumin
  • prothrombin time = elevations shows liver disease

Serum liver enzymes
- alkaline phosphatase
- gamma GT
- transaminases

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8
Q

What is ALT and what is it a marker for?

A

ALT is found in high concentrations within hepatocytes and enters the blood following hepatocellular injury.

It is a useful marker of hepatocellular injury.

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9
Q

What is ALP and what is it a marker for in an LFT?

A

ALP is particularly concentrated in the liver, bile duct and bone tissues. ALP is often raised in liver pathology due to increased synthesis in response to cholestasis.

ALP is a useful indirect marker of cholestasis.

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10
Q

What is GGT and what is it a marker for in a LFT?

A

Gamma-glutamyl transferase
- a raised GGT suggests biliary epithelial damage + bile flow obstruction
- also raised in response to alcohol + drugs

Raised ALP + GGT indicates cholestasis

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11
Q

What does an isolated rise of ALP indicate?

A

ALP in the absence of a raised GGT signifies a NON-hepatobiliary pathology

  • ALP is also in bone
  • increased bone breakdown can elevate ALP
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12
Q

What does ALT > AST signify?

A

Chronic liver disease

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13
Q

What does AST >ALT signify?

A

cirrhosis + acute alcoholic hepatitis

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14
Q

What goes up in LFT in hepatocellular liver disease?

A

AST and ALT

(normally found in liver cells but when the liver is damaged, can be released into the blood, making serum ALT/AST levels to rise.
1st sign of a liver problem)

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15
Q

What is elevated in the LFT in cholestatic liver disease?

A

alkaline phosphatase
gamma-GT

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16
Q

What is jaundice?

A

Raised serum bilirubin

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17
Q

What conditions elevate unconjugated bilirubin?

A

‘pre-hepatic’
- gilberts (genetic condition where you have raised unconjugated bilirubin in your blood)
- haemolysis

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18
Q

What conditions elevate conjugated bilirubin?

A
  • Liver disease ‘hepatic’
  • bile duct obstruction ‘post hepatic’
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19
Q

What does it mean if a patient is jaundiced but ALT + ALP levels are normal?

A

An isolated rise in bilirubin is suggestive of a pre-hepatic cause of jaundice
- Gilbert’s syndrome
- Haemolysis

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20
Q

What causes hepatic (conjugated) jaundice?

A

Hepatitis: viral, drugs immune, alcohol
Ischaemia
Neoplasm
Congestion (CCF)

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21
Q

What causes post-hepatic (conjugated) jaundice?

A

Gallstone: bile duct, Mirizzi
Stricture: malignant, ischaemic, inflammatory

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22
Q

What are the visible signs of pre-hepatic jaundice?

A

Urine = normal
stools = normal
itching = no
liver tests = normal

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23
Q

What are the visible signs of cholestatic jaundice?

A

urine = dark
stools = may be pale
itching = maybe
liver tests = abnormal

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24
Q

What is cholestatic jaundice?

A

stopping or slowing of bile flow from the liver to the small intestine due to a block (obstruction) in the biliary duct system that connects the liver and small intestine, causing the bile to remain in the liver.

It is therefore a form of obstructive jaundice.

Either hepatic or post hepatic

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25
Q

What investigations should be done for jaundice?

A
  1. liver enzymes = very high AST/ALT suggests liver disease
  2. USS for biliary obstruction = 90% have dilated intrahepatic bile ducts on ultrasound
  3. further imaging: (see duct blockage/dilation)
    - CT
    - Magnetic resonance cholangiogram MRCP
    - Endoscopic retrograde cholangiogram ERCp
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26
Q

What does a fall in albumin indicate?

A
  • liver disease
  • inflammation triggering an acute phase response
  • excessive loss of albumin due to protein-losing enteropathies or nephrotic syndrome
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27
Q

What is the epidemiology and RF of gallstones?

A
  • very common: 1/3 women over 60
  • 70% due to cholesterol and 30% pigment
  • RF: female, fat, fertile
  • most ar asymptomatic
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28
Q

What are the different types of gallstones?

A
  1. Gallbladder stones = contain cholesterol
  2. Intrahepatic bile duct stones = contain mainly brown pigment + cholesterol stones
  3. extrahepatic bile duct stones = primary mainly brown pigment but secondary mainly cholesterol
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29
Q

What are the different presentations for stones in the gallbladder vs bile duct?

A

Gallbladder:
biliary pain = yes
cholecystitis (inflammation of bile duct system) = yes
obstructive jaundice = maybe
cholangitis = no
pancreatitis = no

Bile duct:
biliary pain = yes
cholecystitis = no
obstructive jaundice = yes
cholangitis = yes
pancreatitis = yes

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30
Q

What is the management for gallbladder stones?

A
  • Laparoscopic cholecystectomy
  • Bile acid dissolution therapy (<1/3 success)
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31
Q

What is the management for bile duct stones?

A
  1. ERCP with sphincterotomy and: removal (basket or balloon)
    crushing (mechanical, laser..)
    stent placement
  2. Surgery (large stones)
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32
Q

What are the types of drug induced liver injury?

A
  1. Hepatocellular = ALT >2 ULN, ALT/Alk Phos ≥ 5
  2. Cholestatic = Alk Phos >2 ULN or ratio ≤ 2
  3. Mixed = Ratio > 2 but < 5

(ULN = upper limit of normal)

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33
Q

What is ALT and why do we test for it?

A

Alanine aminotransferase (ALT) is an enzyme found inside liver cells that helps your liver break down proteins to make them easier for your body to absorb.

When your liver is damaged or inflamed, it can release ALT into your bloodstream.

High ALT –> indicate liver problem

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34
Q

What is ALP?

A
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35
Q

What is the time frame for developing drug induced liver injury?

A

5 days to 6 months after starting medication
(won’t be from taking a medication for years)

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36
Q

What is the most common cause of drug induced injury?

A

paracetamol

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37
Q

What are the main drugs that cause drug induced liver disease?

A

1) 32-45% Antibiotics (Augmentin, Flucloxacillin, Erythromycin, Septrin, TB drugs)
2) 15% CNS Drugs (Chlorpromazine, Carbamazepine Valproate, Paroxetine,
3) 5% Immunosupressants
4) 5-17% Analgesics/musculskeletal
(Diclofenac…)
5) 10% Gastrointestinal Drugs (PPIs…)
6) 10% Dietary Supplements
7) 20% Multiple drugs

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38
Q

What is the management of paracetamol induced fulminant hepatic failure?

A

N acetyl Cysteine (NAC)

Supportive treatment to correct:
- coagulation defects
- fluid electrolyte and acid base balance
- renal failure
- hypoglycaemia
- encephalopathy

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39
Q

What are the indicators of severe paracetamol induced liver failure?

A
  • late presentation (the longer left after taking the paracetamol the worse the effect)
  • acidosis (pH <7.3)
  • prothrombin time >70s (due to liver damage)
  • serum creatinine > 300 (due to renal damage)

consider emergency liver transplant otherwise 80% mortality

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40
Q

What are symptoms just specific to chronic liver disease?

A
  • muscle wasting
  • spider naevi (dilated blood vessels - discolouration of mole with redness around it)
  • ascites (obtruding umbilicus)
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41
Q

What conditions cause ascites?

A
  1. chronic liver disease
    - portal vein thrombosis
    - hepatoma
    - TB
  2. Neoplasia (ovary, uterus, pancreas…)
  3. pancreatitis, cardiac causes
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42
Q

What are varices?

A

abnormal, enlarged veins
MC at gastro oesophageal junction

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43
Q

What is the pathogenesis of ascites?

A
  1. increased intrahepatic resistance (from obstruction)
  2. portal hypertension
  3. Ascites (low serum calcium)
    OR
  4. systemic vasodilation
  5. secretion of:
    - renin-angiotensin
    - noradrenaline
    - vasopressin
  6. fluid retention
  7. fluid spills out into peritoneal cavity
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44
Q

What is the management of ascites?

A

Fluid and salt restriction
Diuretics = Spironolactone
+/- Furosemide
Large-volume paracentesis + albumin
Trans-jugular intrahepatic portosystemic shunt (TIPS)

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45
Q

What effect does alcohol have on the liver?

A

Alcohol changes the way that hepatocytes metabolise and produce fat
- causes fat accumulation within hepatocytes (steatosis)
- either large droplet (macro vesicular) or small droplet (micro vesicular)

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46
Q

What can fatty liver disease lead to?

A

either:
1. alcoholic hepatitis
Or
cirrhosis

and both lead to acute decompensation

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47
Q

What are the risk factors for alcoholic liver disease?

A
  • female
  • drinking pattern, binge + quantity
  • obesity
  • HCV
  • Genetics
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48
Q

What is the progression of alcoholic liver disease?

A
  1. normal
  2. steatosis (fatty liver)
  3. alcoholic steatohepatitis/fibrosis
  4. cirrhosis
  5. hepatocellular carcinoma
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49
Q

What is the management of ALD?

A

Stop drinking alcohol
Nutrition
corticosteroids (reduce inflammation)
liver transplant

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50
Q

What is the epidemiology of alcoholic liver disease?

A

most deaths are aged 55-59yrs
main cause of liver death in UK

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51
Q

What are the causes of portal hypertension?

A

cirrhosis
fibrosis
portal vein thrombosis

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52
Q

what is the pathology of portal hypertension?

A

Increased hepatic resistance
increased splanchnic blood flow
(blood flow to liver, stomach, spleen, pancreas, intestines)

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53
Q

What are the consequences of portal hypertension?

A

Varices (oseophageal, gastric…)
splenomegaly

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54
Q

What is the Lille score?

A

To assess the patient response to a liver transplant

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55
Q

What are some factors that cause chronic liver disease to become worse?

A
  • constipation
  • drugs (sedatives, analgesics, NSAIDs, diuretics, ACE blockers)
  • GI bleed
  • infection
  • HYPO: Na, K, Glycaemia
  • alcohol withdrawal
  • other (cardiac, intracranial…)
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56
Q

Why are liver patients vulnerable to infection?

A
  • impaired reticulo-endothelial function
  • reduced opsonic activity (bind to substances to induce phagocytosis)
  • reduced leucocyte function
  • permeable gut wall
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57
Q

What are common sites of infection in liver patients?

A
  • spontaneous bacterial peritonitis
  • septicaemia (blood poisoning)
  • pneumonia
  • skin
  • urinary tract
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58
Q

What are the causes for renal failure in liver disease?

A

Drugs:
- Diuretics
- NSAIDS
- ACE Inhibitors
- Aminoglycosides
Infection
GI bleeding
Myoglobinuria
Renal tract obstruction

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59
Q

What are the causes of coma in patients with chronic liver disease?

A

Hepatic encephalopathy (ammonia …)
- infection
- GI bleed
- constipation
- hypokalaemia
- drug (sedatives, analgesics)
Hyponatraemia / hypoglycaemia
Intracranial event

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60
Q

What are the bedside tests for encephalopathy?

A

Serial 7’s
WORLD backwards
Animal counting in 1 minute
Draw 5 point star
Number connection test

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61
Q

What are other 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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62
Q

What analgesia do you give in liver disease?

A

sensitive to opiates
- NSAIDs cause renal failure
- paracetamol safest

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63
Q

What drug can you use for sedation in liver disease?

A

use short-acting benzodiazepines

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64
Q

How do you treat the consequences of liver disease?

A

Malnutrition
- naso-gastric feeding
Variceal bleeding:
- endoscopic banding
- propranolol, terlipressin
Encephalopathy:
- lactulose
Ascites / oedema:
- salt / fluid restriction
- diuretics, paracentesis
Infections:
- antibiotics

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65
Q

What steps should you follow when liver patients get worse?

A

1 ABC: Airway, Breathing, Circulation
2 Look at chart
- vital signs, O2, BM(glucose), drug chart
3 Look at patient
- focus of infection? bleeding?
4 Tests
- FBC, U&E, blood cultures, ascitic fluid clotting, LFTs …

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66
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
- Wilson’s
- 1 antitrypsin deficiency…
Vascular
- Budd-Chiari

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67
Q

What are the investigations of chronic liver disease?

A

Viral serology
- hepatitis B surface antigen, hepatitis C antibody
Immunology
- autoantibodies
- AMA, ANA, ASMA,
- 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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68
Q

What are the normal levels in an LFT?

A

Bilirubin n<21
Albumin n>35
AST n<60
ALT n<41
Prothrombin time n<11.8

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69
Q

What is hepatitis?

A

Inflamed liver

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70
Q

What are the types of autoimmune liver disease?

A
  1. Primary biliary cholangitis
  2. sclerosing cholangitis
  3. autoimmune hepatitis
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71
Q

What is primary biliary cholangitis?

A

Is a chronic disease in which the intrahepatic bile ducts in your liver are slowly destroyed

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72
Q

What are the symptoms of primary biliary cholangitis?

A
  • severe itching
  • dry eyes
  • joint pains
  • variceal bleeding
  • liver failure: ascites, jaundice
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73
Q

What is the treatment for the 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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74
Q

What is the effect of Ursodeoxycholic acid in Primary Biliary Cholangitis?

A
  • improvement in liver enzymes, bilirubin
  • subtle reduction in inflammation (not fibrosis)
  • reduced portal pressure and rate of variceal development
  • reduces rate of death or liver transplantation
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75
Q

What is primary sclerosing cholangitis?

A

Progressive chronic inflammation of intrahepatic AND/OR extrahepatic bile ducts
- inflammation causes scars within the bile ducts

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76
Q

What autoimmune disease is PSC associated with?

A

Inflammatory bowel disease

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77
Q

What are the symptoms of PSC?

A
  • itching
  • pain +/- rigors
  • higher rate of developing cholangiocarcinoma
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78
Q

What is haemochromatosis?

A

An inherited condition where iron levels in the body slowly build up over years
- accumulates around the body damaging organs, including the liver
- autosomal recessive

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79
Q

What are the symptoms of haemochromatosis?

A
  • fatigue all the time
  • weight loss
  • weakness
  • joint pain
  • erectile dysfunction
  • irregular period or absent period
  • skin pigmentation (bronze)
  • hair loss
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80
Q

What is alpha 1 anti trypsin?

A
  • is a protein made by neutrophil cells in the liver to protect the lungs from damage
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81
Q

What is alpha 1 anti trypsin deficiency?

A

Alpha-1 antitrypsin (AAT) deficiency is a genetic disorder with an autosomal inheritance pattern and codominant expression of alleles.

Allele mutations cause ineffective activity of alpha-1 antitrypsin, the enzyme responsible for neutralising neutrophil elastase.

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82
Q

What are the risk factors fro non-alcoholic fatty liver?

A

Obesity
diabetes
hyperlipidaemia

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83
Q

What are the investigations for NAFL?

A
  • LFTs = mildly elavted
  • biopsy = to distinguish from NASH (non-alcoholic steatohepatitis)
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84
Q

What is the management for NAFL?

A

Still no effective drug treatments
- weight loss works

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85
Q

What are the presentations for hepatic vein occlusion?

A
  • abnormal LFTs
  • ascites
  • acute liver failure
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86
Q

What are the causes of hepatic vein occlusion?

A
  • thrombosis
  • membrane obstruction
  • veno-occlusive disease

congestion causes acute or chronic liver injury

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87
Q

What is the treatment for hepatic vein occlusion?

A
  • anticoagulation
  • transjugular intrahepatic portosystemic shunt

-liver transplantation

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88
Q

What bacteria are found in the GI tract?

A

Gastro intestinal flora with a predominance of anaerobes
e.g. Clostridium difficile

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89
Q

What are the defence mechanisms of the GI tract?

A

Intestinal Microflora:
- Prevent infection by interfering and competing with pathogens
- Produce its own antibacterial substances
- Gastric acid kills most organisms that are swallowed
- Bile has antibacterial properties

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90
Q

Define diarrhoea.

A

the passage of loose or watery stools, typically at least 3 times in 24hr period

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91
Q

What is the management of pseudomembranous colitis?

A
  • faecal transplant = aims to restore the ‘normal flora’
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92
Q

What are the types of diarrhoea?

A

Acute = 14 days or fewer, viral, infective

Persistent diarrhoea = more than 14 but fewer than 30 days

Chronic = more than 30 days

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93
Q

What are the causes of infective diarrhoea?

A

Infective :
- intraluminal infection
- systemic infections e.g. sepsis, tropical infections, covid

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94
Q

What are the causes of non-infective diarrhoea?

A
  • Cancer
  • chemical (poisoning, sweeteners, medications)
  • inflammatory bowel disease
  • IBS/malabsorption
  • endocrine (thyrotoxicosis)
  • radiation
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95
Q

What are the characteristics of watery diarrhoea?

A

Non-inflammatory
Location = proximal small bowel
bacteria = S. aureus, C.difficile. E.coli
Viral = rotavirus, norovirus
Parasitic = Giardia, cryptosporidium

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96
Q

What are the characteristics of blood diarrhoea?

A

Inflammatory (invasion)
Location: colon
Bacteria: shigella, campylobacter, salmonella
Parasitic: Entamoeba histolytica

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97
Q

What is travellers diarrhoea?

A

occurs within 10 days of arrival from foreign country

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98
Q

What are the characteristics of cholera?

A

Vibrio cholerae
- from contaminated food/water
- produce cholera toxin
- profuse watery ‘rice water’ diarrhoea

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99
Q

What investigations should be done for diarrhoea?

A

Stool tests:
Microscopy
Culture
Multi-pathogen molecular panels (GE PCR panel)
Ova, cysts and parasites x3
Toxin detection (C difficile)

Blood tests
Blood culture
Inflammatory markers
Electrolytes and creatinine

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100
Q

What are the characteristics + treatment of peptic ulcer disease?

A

Helicobacter pylori
- organisms produce ammonia that damages the gastric mucosa
- stool antigen test
- treatment = omeprazole, clarithromycin and amoxicillin

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101
Q

What is acute cholecystitis?

A
  • gallbladder inflammation, cystic duct obstruction by gall stones
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102
Q

What are the symptoms for acute cholecystitis?

A
  • RUQ or epigastric pain
  • fever
  • leucocytosis
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103
Q

How do you diagnose acute cholecystitis?

A

Ultrasound

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104
Q

What is the treatment for acute cholecystitis?

A

IV fluids
analgesia
antibiotics

Surgery = cholecystectomy

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105
Q

What is ascending cholangitis?

A

Obstruction of the cystic bile duct

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106
Q

What are the symptoms of ascending cholangitis?

A

Fever
abdominal pain
jaundice
(charcots triad)

107
Q

What is the management for ascending cholangitis?

A

Prompt admission and IV antibiotics
ERCP
Cholecystectomy

High mortality!

108
Q

What are the types of liver abscesses?

A

Pyogenic :
following biliary sepsis, or haematogenous spread
Usually polymicrobial: enteric gram-negative bacilli and anaerobes.

Amoebic:
Entamoeba histolyti

109
Q

What are the investigations for liver abscesses?

A

Diagnosis:
-Abdo CT or ultrasound
-Blood cultures + E. histolytica serology
-Aspiration and culture of the abscess material + E. histolytica molecular testing

110
Q

What is the treatment for liver abscesses?

A

Drainage (surgical or imaging guided) + antibiotics

111
Q

What is the cause and presentation of enteric fever?

A

Salmonella Typhi (Typhoid), Paratyphi (Paratyphoid)
High incidence in Central Asia, Southeast Asia, and southern Africa

Presentation:
Generalised abdominal pain, fever, and chills
Headache and myalgia
“Relative bradycardia”
Rose spots
Constipation/green diarrhoea

112
Q

What are the complications of enteric fever?

A

Complications: (week 2-3)
GI bleed
Perforation / peritonitis
Myocarditis
Abscesses

113
Q

What is the management of enteric fever?

A

antibiotics:
azithromycin, ciprofloxacin, cephalosporins, Meropenem

Mortality 20% –> < 1% with antibiotics!
2-3% become carriers….

114
Q

What is a unit of alcohol?

A

A UK unit is 8g or 10ml of pure alcohol

115
Q

How do you calculate the units of a drink?

A

Strength of the drink (%ABV) x amount if liquid (L)

116
Q

What are the safe drinking guidelines?

A

Low risk drinking (1% lifetime risk of death for those drinking at this level):
No more than 14 units per week (for men + women)
Spread drinking over 3 days or more

117
Q

What are the acute effects of alcohol consumption?

A

Accidents and injury
Coma and death from respiratory depression
Aspiration pneumonia
Oesophagitis/ gastritis
Mallory-Weiss syndrome (gastric tears)
Pancreatitis
Cardiac arrhythmias
Cerebrovascular accidents
Neurapraxia due to compression
Myopathy/rhabdomyolysis
Hypoglycaemia

118
Q

What are the chronic effects of alcohol consumption?

A

Pancreatitis
CNS toxicity (dementia)
Liver damage
Cancers

119
Q

What are the different types of reactions to alcohol withdrawal?

A
  1. Tremulousness - “the shakes”
  2. Activation syndrome - characterized by tremulousness, agitation, rapid heartbeat and high blood pressure
  3. Seizures - acute grand mal seizures can occur in alcohol withdrawal in patients who have no history of seizure or any structural brain disease
  4. Hallucinations - usually visual or tactile in alcohol dependence
  5. Delirium tremens - can be severe/fatal
    - Tremors, agitation, confusion, disorientation, hallucinations, sensitivity to light and sound, and seizures [medical emergency]
120
Q

What are the effects of foetal alcohol spectrum disorder?

A
  • Pre and post-natal growth retardation
  • CNS abnormalities including learning disabilities, irritability, incoordination, hyperactivity
  • Craniofacial abnormalities

Associated abnormalities including congenital defects of eyes, ears, mouth, cardiovascular system, genitourinary tract and skeleton, and an increase in the incidence of birthmarks and hernias

121
Q

What are the psychosocial effects of excessive alcohol consumption?

A
  1. Interpersonal relationships = violence, rape, depression
  2. Problems at work
  3. criminality
  4. social disintegration = poverty
  5. driving incidents/offences
122
Q

What are example of opiates and their effects?

A

Heroin
Codeine

Effects = euphoria, analgesia

123
Q

What are example of depressants and their effects?

A

alcohol
Benzodiazepines

effects = sedation, anxiolytic

124
Q

What are example of stimulants and their effects?

A

Amphetamines
Cocaine
Crack
ecstasy

effects = increase alertness and alter mood

125
Q

What are example of cannabinoids and their effects?

A

Cannabis

effects = relaxation, mild euphoria

126
Q

What are example of hallucinogens and their effects?

A

LSD
magic mushrooms

effects = altered sensory perceptions, thinking

127
Q

What are example of anaesthetic drugs and their effects?

A

Ketamine
Nitrous oxide

Effects = anaesthesia and sedative

128
Q

What are the effects of drug misuse?

A

Mortality
Morbidity (physical and psychological impact on quality of life)
Social (criminal justice involvement, crime, violence, acceptability)
Economic (productivity, tax)
Personal (identity, stigma, relationships

129
Q

Define addiction.

A

Involves compulsive use of a substance despite harmful consequences
- often involves structural and biochemical changes to parts of the brain linked to reward, self-control and stress

130
Q

What is ‘acute on chronic’ liver failure?

A

liver failure as a result of decompensation of chronic liver disease

131
Q

What is fulminant hepatic failure?

A

clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function. Sudden onset.

132
Q

What is the West-Haven grading system for an HE?

A
  • Grade I: change in behaviour with minimal change in level of consciousness. May have mild asterixis or tremor.
  • Grade II: gross disorientation, drowsiness, asterixis and inappropriate behaviour
  • Grade III: marked confusion, incoherent speech, sleeping most of the time but rousable to verbal stimuli. Asterixis less noticeable, elements of rigidity.
  • Grade IV: coma that is unresponsive to verbal or painful stimuli. Evidence of decorticate or decerebrate posturing.
133
Q

What is the structure of HBV?

A

It is a DNA virus that contains a nucleocapsid and outer envelope. Its small DNA genome is contained within the nucleocapsid.

134
Q

How many genotypes of HBV?

A

HBV is classified into eight separate genotypes termed A-H.
These genotypes are distributed differently throughout the world. The predominant genotype in the UK is A.

135
Q

What are the 4 major genes within the HBV genome?

A

There are four major genes within the HBV genome.

  • Surface (S) gene: encodes the small surface protein HBsAg
  • Core (C) gene: encodes the hepatitis B core antigen (HBcAg), which also helps form the e antigen (HBeAg)
  • Polymerase (P) gene: encodes DNA polymerase/reverse transcriptase
  • X gene: encodes the hepatitis B x (HBx) protein
136
Q

What are the 5 HBV protein products?

A
  • HBsAg: needed for construction of the outer HBV envelope
  • HBcAg: composed within the nucleocapsid that contains the viral DNA.
  • HBeAg: acts as an immune decoy to promote viral persistence. Presence is a marker of viral replication and infectivity.
  • DNA polymerase: involved in the synthesis of DNA molecules. Has reverse transcriptase activity, which means it can form DNA from RNA.
  • X protein: a transcriptional regulator that promotes cell cycle progression.
137
Q

What is anicteric hepatitis?

A

Present without jaundice

138
Q

What is fulminant liver failure?

A

defined as the rapid development of encephalopathy, coagulopathy, and jaundice in someone without known preexisting liver disease (deteriorates very quickly)

139
Q

What is hepatic encephalopathy?

A

is a decline in brain function that occurs as a result of severe liver disease.
- In this condition, your liver can’t adequately remove toxins from your blood.
- This causes a buildup of toxins in your bloodstream, which can lead to brain damage.

140
Q

What is melaena and haematemesis?

A

Melaena = black stool (blood in it)
Haematemesis = vomiting blood

141
Q

What is the Glasgow-Blatchford score?

A

assess the likelihood that a person with an acute upper gastrointestinal bleeding will need to have medical intervention such as a blood transfusion or endoscopic intervention.

142
Q

What is a vatical bleed?

A

Variceal (dilated vein in GI tract)
- suspect in patient with a history of liver disease or alcohol excess
- antibiotics + terlipressin (reduce pressure it portal veins) reduce mortality
- endoscopy

143
Q

What is a non-variceal bleed?

A

Suspect in patients with a history of peptic ulcers, using certain medications; NSAIDs, anticoagulation or antiplatelets.

Consider proton pump inhibitors.

Endoscopy within 24 hours.

144
Q

Why is a upper GI bleed important?

A

Acute upper GI bleeding is a very common medical emergency

145
Q

What are the different types of gut obstructions?

A
  • block lumen of gut
  • in the wall
  • something outside the gut squashing it closed
146
Q

What causes intraluminal obstruction?

A
  • tumour = carcinoma and lymphoma
  • diaphragm disease
  • meconium ileus
  • gallstone ileus (erodes through wall of gallbladder into ileum)
147
Q

Why is obstruction more likely to occur lower down the gut?

A

Facies become more solid so are more likely to get stuck

148
Q

What causes intramural obstruction?

A
  • inflammatory = Crohn’s disease + diverticulitis
  • tumours
  • neural = Hirschsprung’s disease
149
Q

What is diverticulitis?

A

Inflammation of the diverticular disease
- mucosa pushed through muscularis (dead-end outpouch)

150
Q

What is peritonitis?

A

when faeces are pushed through diverticulum into the perineum space of the gut

151
Q

What is Hirschsprung’s disease?

A

nerve cells in the colon don’t form completely causing in to contract and move food from the bowels
- without the contractions the stool stays in the large intestine
- severe constipation and intestinal obstruction (becomes dilated)

152
Q

What causes extraluminal obstruction?

A
  • adhesions
  • volvulus
  • tumour = peritoneal deposits
153
Q

How do fibrous adhesions occur in the gut?

A
  • from previous surgeries
  • cause tissues/ organs to be attached to each other
154
Q

What is volvulus?

A

Twisting of the bowel
- occurs most in sigmoid colon as less fixed and more floppy

155
Q

What is small bowel obstruction?

A

Mechanical blockage of the small intestine

156
Q

What is the difference between small bowel obstruction and illeus?

A

Ileus = is where the gut stops pushing food forward but there is no obstruction

157
Q

What is aetiology of SBO?

A
  • adhesions = scar tissue, too much fibrous tissue formed causing bowel to kink
  • hernia (bulges) = bowel gets stuck in inguinal canal hole etc.
  • cancer = primary tumour (obstruction) or secondary
158
Q

What is colic pain?

A

Sharp intense pain and then it will go away and come back in waves

159
Q

What investigations are done for SBO?

A

Full blood count
* Urea and electrolytes = renal function
* Lactate = marker of anaerobic respiration
* C-reactive Protein =
* CT scan = can identify cause and location of obstruction

160
Q

What would you assess in a patient with a SBO?

A
  • Hydration status
  • Weight loss
  • Pulse/BP
  • O2 Sats
  • Scars
  • Abdominal distension
  • Abdominal tenderness/peritonism
  • Hernia orifices
  • PR exam
161
Q

What is the treatment for SBO?

A
  1. manage pain = analgesia
    - assess fluid balance = nasogastric tube, urinary catheter
    - resuscitate = IV fluids
    - alleviate nausea = nasogastric tube, select antiemetics
    - nutrition = if >5 days without intake, may need parenteral feed
162
Q

How to treat SBO due to adhesions?

A
  1. signs of ischaemia/shock = resuscitate and operate
  2. non-operative management for up to 3 days
  3. Gastrografin challenge = take something and then do X-ray to see how far it has travelled
163
Q

What is involved in SBO operations?

A
  • Key hole or open
  • Divide scar tissue
  • Risk of future scar formation
  • Minimally invasive surgery can help
164
Q

Where do hernias most commonly occur?

A

in inguinal or femoral space in groin

165
Q

What is the different treatment for SBs due to hernias?

A

High risk patient = Taxis (push it back through)
High BMI = conservative Mx
Incisional hernia = treat as adhesive SBO

166
Q

What are the characteristics of SBO due to cancer?

A
  • Right sided colon cancer
  • Peritoneal disease from ovaries
  • May be advanced
  • Nutrition a problem
  • Active treatment vs palliation
167
Q

What is Barrett’s oesophagus?

A

Changes in the cells lining the oesophagus go from squamous cells to glandular columnar epithelium
(metaplasia)

168
Q

What is metaplasia?

A

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

169
Q

Why does Barrett’s oesophagus occur?

A

Acid from stomach refluxes up into oesophagus and kills off the squamous cells
- metaplasia into glandular epithelium with layer of protective mucin that is protective against stomach acid

170
Q

What are the complications of Barrett’s oesophagus?

A

risk of developing oesophageal adenocarcinoma
- glandular epithelium gets annoyed by stomach acid

171
Q

What are the different risk factors for squamous cell carcinomas and adenocarcinoma?

A

squamous cell
- alcohol
- smoking

adenocarcinoma
- obesity

172
Q

What is the difference between Adenocarcinoma and Squamous Cell Carcinoma?

A

*Adenocarcinoma may occur anywhere with glandular tissue while squamous cell carcinoma mostly occurs on the skin surface.

  • Adenocarcinoma arises from glands while squamous cell cancers arise from flat squamous cells.
  • Adenocarcinoma can metastasize frequently while squamous cell cancers rarely metastasize.
  • Local excision is mostly curative in squamous cell cancers while it may not be the case in adenocarcinoma.
173
Q

What causes the transition of normal gastric mucosa to a invasive carcinoma?

A

normal gastric mucosa
↓ (pickled food, H.pylori, pernicious anaemia)
intestinal metaplasia
↓ (genetic change)
dysplasia
↓ (genetic change)
intramucosal carcinoma
↓ (genetic change)
invasive carcinoma

174
Q

Who gets colorectal cancer?

A

people with adenomas
- dysplastic epithelium

175
Q

What is familial adenomatous polyposis?

A
  • rare hereditary condition
  • causes loads of small growths (polyps) in the large intestine
    (if develop could develop colorectal cancer)
176
Q

What are the reasons for identifying Hereditary Non-Polyposis Colorectal cancers HNPCC?

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
177
Q

What are HNPCC cancers?

A

hereditary non-polyposis colorectal cancer (Lynch Syndrome)
- no DNA repair protein produced

178
Q

What is Duke’s staging for bowel cancer?

A

A = cancer is in the inner lining of the bowel. Or it is slightly growing into the muscle layer.
B = cancer has grown through the muscle layer of the bowel
C = cancer has spread to at least 1 lymph node close to the bowel
D = cancer has spread to another part of the body, such as the liver, lungs or bones (stage 4 cancer)

179
Q

What are the main treatments for colon cancer?

A

surgery
chemotherapy

180
Q

What are the main treatments for rectal cancer?

A

surgery
radiotherapy
chemotherapy
chemotherapy and radiotherapy together (chemoradiotherapy)

181
Q

What treatment should be done at each stage of the progression to bowel cancer?

A

Normal epithelium = prevention
Adenoma = endoscopic resection
Colorectal adenocarcinoma = surgical resection
Metastatic colorectal carcinoma = chemotherapy palliative care

182
Q

What are the 2 types of benign liver tumours?

A

Hemangiomas
Adenomas

183
Q

What are the characteristics of hemangiomas?

A
  • Commonest benign tumour
  • Usually small and single but can be multiple and large
  • Often incidental finding on US or CT
  • Don’t require treatment
184
Q

What are the characteristics of adenomas?

A
  • Common
  • Caused by anabolic steroids, oral contraceptive pill, pregnancy
  • Can present with abdominal pain or intraperitoneal bleeding
  • Only treat if symptomatic or >5cm
185
Q

How is bilirubin metabolised?

A
  1. RBCs broken down –> releasing Hb
  2. Hb –> Haem + Globin
  3. Haem –> iron + unconjugated bilirubin
  4. UGT converts unconjugated bilirubin into conjugated bilirubin (now water soluble)
  5. Conjugated bilirubin secreted into the bile and stored in the gall bladder
  6. when released into ileum –> broken down into urobilinogen and stercobilin by bacteria
  7. Stercobilin excreted in faeces
  8. urobilinogen either recycled back to bile or excreted in urine
186
Q

What is the difference in pathology between primary biliary cholangitis and primary sclerosis cholangitits?

A

PBC
- progressive destruction of ONLY intrahepatic bile ducts

PSC
- progressive chronic inflammation of intrahepatic and/or extra hepatic bile ducts

187
Q

What is the difference in epidemiology between primary biliary cholangitis and primary sclerosis cholangitits?

A

PBC
- Middle Aged women
- associated with other autoimmune diseases

PSC
- middle aged men
- associated with inflammatory bowel disease

188
Q

What is the difference in management of primary biliary cholangitis and primary sclerosis cholangitits?

A

PBC
- Ursodeoxycholic acid
- colestyramine
- fat soluble vitamins supplements
- end stage: liver transplant

PSC
- observation and lifestyle optimisation
- colestyramine
- fat soluble vitamins supplements
- end stage: liver transplant

189
Q

What is Budd-Chiari syndrome?

A
  • very rare condition
  • The condition is caused by occlusion of the hepatic veins that drain the liver.
  • It presents with the classical triad of abdominal pain, ascites, and liver enlargement.
190
Q

What is schistosomiasis?

A

is an infection caused by a parasitic worm that lives in fresh water in subtropical and tropical regions.

191
Q

What is ascites?

A

Abnormal build up of excess fluid in the abdominal cavity

  • When patients suffer from cirrhosis, the liver and kidneys stop working properly and fluid stops being exchanged within the cells in the way it should.
192
Q

What is hepatic encephalopathy?

A

refers to changes in the brain that occur in patients with advanced, acute (sudden) or chronic (long-term) liver disease.
- It is one of the major complications of cirrhosis.
- liver unable to remove toxins in blood so build up in brain

193
Q

What is haematemesis?

A

Vomiting blood
- It is caused by bleeding from part of the upper portion of the gastrointestinal tract.
- It may be bright red or look like coffee grounds.

194
Q

What is the aetiology of haematemesis?

A

Common causes:

  • Peptic ulcers - ulceration can result in erosion into the blood vessels and can result in significant haemorrhage.
  • Mallory-Weiss tear - typified by episodes of severe or recurrent vomiting, then followed by minor haematemesis. Such forceful vomiting causes a tear in the epithelial lining of the oesophagus, resulting in a small bleed.
  • Oesophageal varices - caused by portal hypertension
  • Gastritis/ gastric erosions
  • Drugs - NSAIDs, aspirin, steroids, thrombolytics, anticoagulants
  • Oesophagitis - inflammation of the intraluminal epithelial layer of the oesophagus, most often due to either gastric acid reflux (GORD) or less commonly from infections (typically Candida Albicans), medication (such as bisphosphonates), radiotherapy, ingestions of toxic substances, or Crohn’s disease.
  • Duodenitis
  • Malignancy

Rare causes

  • Bleeding disorders
  • Portal hypertensive gastropathy - refers to changes in the mucosa of the stomach in patients with portal hypertension
  • Aorto-enteric fistula - pathologic communications between the aorta (or aortoiliac tree) and the gastrointestinal tract
  • Angiodysplasia - abnormality with the blood vessels in the gastrointestinal (GI) tract.
  • Haemobilia - bleeding into the biliary tree.
  • Dieulafoy lesion - large arteriole most commonly in the stomach wall (submucosal) that erodes and bleeds
  • Meckel’s diverticulum - outpouching or bulge in the lower part of the small intestine (congenital defect)
  • Peutz-Jegher’s syndrome - benign hamartomatous polyps in the gastrointestinal tract
  • Osler-Weber-Rendu syndrome - leads to abnormal blood vessel formation
195
Q

What are the investigations for haematemesis?

A
  • FBCs = acute bleeds may not show anaemia
  • LFTs = may show liver failure as cause
  • U&Es = high urea out of proportion to creatinine, indicative of massive blood meal.
  • Oesophagogastroduodenoscopy (OGD) = definitive investigation and should be performed within 12hrs in most cases of acute haematemesis
  • Erect chest X-ray = if a perforated peptic ulcer is suspected as the underlying cause.
  • CT abdomen = can be useful in assessing any active bleeding in an unstable patient
196
Q

What is the management for haematemesis?

A
  • Rapid = ABCDE assessment
  • High flow O2
  • FBC, LFT, U&E, clotting and crossmatch.
  • Startfluid resuscitationif needed
  • Insert urinary catheter to monitor and guide fluid replacement.
  • Transfuse if significant Hb drop
  • Correct clotting abnormalities - Vit K, fresh frozen plasma, platelets

Most cases will warrant anupper GI endoscopy.

Variceal bleed = terlipressin + antibiotics
Peptic ulcer = endoscopic haematemesis

197
Q

What are the non-infective causes of diarrhoea?

A
  • neoplasm
  • inflammatory
  • irritable bowel
  • anatomical
  • hormonal
  • radiation
  • chemical
198
Q

What are the infective causes of diarrhoea?

A
  • non- bloody
  • bloody (dysentery)
199
Q

What are all the steps in the steps in the chain of infection?

A
  1. Agent
  2. mode of transmission
  3. portal of entry
  4. Host
  5. Person to person spread
  6. reservoir
  7. portal of exit
    (back to start)
200
Q

What are the different types of transmission for a disease?

A
  1. Direct
    - STIs, faeco-oral
  2. Indirect
    - vector-borne, malaria, HepB
  3. Airborne
    - respiratory route, TB
201
Q

What are the characteristics of norovirus?

A
  • major cause of ‘winter vomiting’
  • mainly causes vomiting
  • lasts 1-3 days
  • immunity short lived
202
Q

How is clostridium difficile spread?

A
  • widely distributed in soil and digestive tract
  • spores resistant to heat, drying & chemicals
  • spread by faeco-oral route or spores in environment
203
Q

Which conditions are caused by C.difficile?

A
  • associated with antibiotic use (cause 20% of antibiotic associated diarrhoea)
  • antibiotic associated colitis
  • pseudomembranous colitis
204
Q

How to prevent the spread of C.difficile?

A
  • produces spores highly resistant to chemicals
  • alcohol hand rubs will not destroy the spores
  • hand washing using soap + water will remove the microorganisms from the hands
205
Q

What is the pneumonic to deal with C.difficile?

A

SIGHT
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

206
Q

What is the management for C.difficile?

A
  • control antibiotic use
  • standard infection control procedures
  • surveillance + case finding
  • any patents with diarrhoea = isolate, test stool, cleaning, treat with metronidazole or vancomycin
207
Q

Who are the groups at risk of diarrhoea diseases?

A

A – Persons of doubtful personal hygiene or with unsatisfactory hygiene facilities at home, work or school

B – Children who attend pre school or nursery

C – People whose work involves preparing or serving unwrapped/uncooked food

D – HCW/Social care staff working with vulnerable people

208
Q

What are the control measure to reduce diarrhoea diseases?

A

Hand-washing with soap
Ensure availability of safe drinking water
Safe disposal of human waste
Breastfeeding of infants & young children
Safe handling and processing of food
Control of flies/vectors
Case management including exclusion
Vaccination

209
Q

What are the causes of acute hepatitis?

A
  1. viral
    - Hep ABCDE
    - human herpes virus
    - influenza
  2. Non-viral
    - spirochetes
    - mycobacteria = TB
    - bacteria
    - parasites
  3. Non-infection
    - drugs
    - alcohol
    - other toxins/poisoning
    - NAFLD
    - pregnancy
    - autoimmune hepatitis
    - hereditary metabolic causes
210
Q

What are the causes of chronic hepatitis?

A
  1. Viral
    - Hep ABCDE
  2. Non-infection
    - drugs
    - alcohol
    - other toxins/poisoning
    - NAFLD
    - autoimmune hepatitis
    - hereditary metabolic causes
211
Q

What are the signs + symptoms of acute hepatitis?

A

Symptoms
- malaise, lethargy, myalgia
- abdominal pain
- jaundice

Signs
- tender hepatomegaly
- signs of fulminant hepatitis (acute liver failure)

Bloods
- raised transaminases (ALT/AST&raquo_space;GGT/ALP) + raised albumin

212
Q

What are the signs + symptoms for chronic hepatitis?

A
  • can be asymptomatic
  • signs of chronic liver disease (clubbing, spider naevi)
  • Transaminases (ALT/AST) can be normal

Compensated = liver function maintained
Decompensated = coagulopathy, jaundice, low albumin, ascites

213
Q

What are the characteristics of Hep A?

A
  • Faeco-oral transmission
  • contaminated food + water
  • usually symptomatic
  • short incubation time = 15-50 days
  • self-limiting = no chronic disease
  • 100% immunity after infection
214
Q

What are the different virus types for each hepatitis?

A

Hep A = PicoRNAvirus
B = hepaDNAvirus
C = Flavivirus
D = Linked to B

215
Q

What is the management for Hep A?

A

Supportive
- monitor liver function
- acute liver failure
- vaccine

216
Q

What are the characteristics of Hep E?

A
  • Faeco-oral transmission
  • blood + organ transplant recipients
  • Usually self-limiting
  • extra-hepatic manifestations e.g. neurological
  • risk of chronic infection in immunosuppressed
217
Q

What is the management for Hep E?

A

Acute infection
- supportive
- monitor for fulminant hepatitis/acute-on-chronic liver failure

Chronic infection
- reverse immunosuppression
- treat with Ribavirin >3months

218
Q

How to prevent getting Hep E?

A

Avoid eating undercooked meats (especially if immunocompromised)

Screening of blood donors

Vaccine available in China only (HEV 239 (Hecolin®) against HEV genotype 1

219
Q

How is Hep B spread?

A

blood borne virus = transmission via blood and bodily fluids
- mother to child
- household contact
- blood products
- iatrogenic
- occupational
- sexual
- injecting drug use

220
Q

What is the progression of Hep B in immunocompetent adults?

A
  1. Acute HBV infection
  2. 95% Spontaneous resolution
    OR
    5% Chronic infection
    –> cirrhosis, hepatocellular carcinoma
221
Q

What is the progression of Hep B in neonates and infants?

A
  1. Acute HBV infection
  2. 10% Spontaneous resolution
    OR
    90% Chronic infection (asymptomatic)
    –> cirrhosis, hepatocellular carcinoma
222
Q

What is the management of Hep B?

A

Supportive
- monitor liver function
- rarely fulminant hepatitis failure
- management of close contacts = vaccine

223
Q

What are the treatment options for Hep B?

A
  1. Pegylated interferon- alpha 2a
  2. Oral nucleotide analogues
    - inhibit viral replication
224
Q

What are the methods of prevention for Hep B?

A
  • Antenatal screening of pregnant mothers
  • universal chilhood immunisation
  • immunisation of healthcare workers
  • Screening +/- immunisation of sexual + household contacts
  • barrier contraception
  • universal screening of blood products
  • sterile equipment
225
Q

What are the characteristics of Hep D?

A
  • blood borne virus = transmission via blood and body fluids
  • defective RNA virus
  • Requires HBsAg presence to replicate (increases severity)
226
Q

What is the management for Hep D?

A
  • test Hepatitis D antibody, if positive test HDV RNA
227
Q

How do Hep D interact with Hep B?

A

Hep D requires HBsAg to replicate

Either:
- can be acquired simultaneously with HBV
(increased risk of fulminant hepatitis in acute infection)
OR
- acquired after HBV
(acute on chronic hepatitis, accelerated progression to liver fibrosis)

228
Q

How is Hep C spread?

A

Blood borne virus = transmission via blood and bodily fluids
Mother-to-child
Household contact
Blood products
Iatrogenic
Occupational
Sexual (MSM)
Injecting drug use***
Tattoos, piercings, etc

229
Q

What is the treatment for Hep C?

A

Directly-acting antiviral (DAA) therapy

230
Q

What is the method of prevention for Hep C?

A

No vaccine
Previous infection does NOT confer immunity: can be re-infected
Screening blood products (in UK since 1991)
Universal precautions handling bodily fluids
Sterile medical equipment + safe disposal
Opiate addiction treatment (OAT), e.g. methadone, buprenorphine
Provision of sterile injecting equipment
Treatment and cure of “transmitters”, e.g. active PWIDs
Safe sex, e.g. condoms

231
Q

What does it mean if a patient is jaundiced but ALT + ALP levels are normal?

A

An isolated rise in bilirubin is suggestive of a pre-hepatic cause of jaundice
- Gilbert’s syndrome (bilirubin not passed into bile at the normal rate)
- Haemolysis

232
Q

What does a fall in albumin indicate?

A
  • liver disease
  • inflammation triggering an acute phase response
  • excessive loss of albumin due to protein-losing enteropathies or nephrotic syndrome
233
Q

What does ALT > AST signify?

A

Chronic liver disease

234
Q

What does AST >ALT signify?

A

cirrhosis + acute alcoholic hepatitis

235
Q

What does amylase tell us?

A

high amylase = pancreatic damage

236
Q

What is the 1st line investigation for biliary disease?

A

Ultrasound
- can see if gallbladder wall is thickened or inflamed
- any gallstones
- to get more detail ask for an MRCP (MRI scan of bile system)

237
Q

What are the treatment options for gallstones?

A
  • conservative management = analgesia/antibiotics
  • radiological drain (cholecystostomy) = tube through skin in gallbladder, relieves infection
  • ERCP = endoscopy passes through stomach to biliary tree
  • cholecystectomy = keyhole surgery, definitive
238
Q

What does colic pain indicate?

A

Smooth muscle sneezing on something e.g. gallstones
- comes and goes in waves

239
Q

what does it mean when gallstones pain radiates to the shoulder blade?

A

diaphragmatic irritation
(share same nerve root endings)

240
Q

What happens as a conseqeucen of obstructive jaundice?

A
  • coagulopathy (2, 7, 9, 10)
  • no bile secretion = no absorption of ADEK vitamins
241
Q

If pain is relieved sitting forward what condition does that signify?

A

Pancreatitis
- reduces pressure on parietal peritoneum, esp during inspiration

242
Q

What is the difference between cholangitis and cholecystitis?

A

Cholangitis = gallstone in common bile duct (-ang = vessel)

Cholecystitis = gallstone in gallbladder (-cyst = sac)

243
Q

What are the symptoms, location, investigation and treatment of Asymptomatic Gallstones?

A

S = none
L = gallbladder
I = None
T = none

244
Q

What are the symptoms, location, investigation and treatment of Biliary colic?

A

S = colicky pain
L = gallbladder
I = USS
T = analgesia/surgery

245
Q

What are the symptoms, location, investigation and treatment of Acute Cholecystitis?

A

S = Pain, fever, tenderness
L = gallbladder
I = USS
T = antibiotics/drain/surgery

246
Q

What are the symptoms, location, investigation and treatment of Gallbladder Empyema?

A

(collection of pus in the gallbladder lumen)
S = pain, fever, rigors
L = gallbladder
I = USS/CT
T = antibiotics/drain/surgery

247
Q

What are the symptoms, location, investigation and treatment of Gallbladder Mucocoele?

A

(over-distended gallbladder filled with mucus or clear watery content)
S = pain/discomfort
L = gallbladder
I = USS/CT
T = surgery

248
Q

What are the symptoms, location, investigation and treatment of Choledocholithiasis?

A

(bile duct stones)
S = colicky pain, jaundice
L = common bile duct
I = USS/MRCP
T = antibiotics/ ERCP/surgery

249
Q

What are the symptoms, location, investigation and treatment of Cholangitis?

A

S = colicky pain, jaundice, rigors
L = common bile duct
T = USS/MRCP
T = antibiotics/ERCP/surgery

250
Q

What are the symptoms, location, investigation and treatment of pancreatitis?

A

s = epigastric pain, radiating to back
L = common bile duct
I = USS/MRCP/CT
T = analgesia/(ERCP)/surgery

251
Q

What are the symptoms, location, investigation and treatment of Gallstone Ileus?

A

S = bilious vomiting, abdominal pain
L = ileocaecal valve
I = CT
T = surgery but leave gallbladder

252
Q

Where are all the locations gallstones can occur (+names)?

A

Gallbladder = cholecystolithiasis
Common bile duct = choledocholithiasis
Pancreatic duct = pancreatolithiasis
Hepatic ducts = hepatolithiasis

253
Q

What are the long term side effects of being on steroids?

A

CUSHINGOID
C Cataracts
U Ulcers
S Striae or skin thinning
H Hypertension and hirsutism
I Immunosuppression and infections
N Necrosis of femoral head
G Glucose elevation
O Osteoporosis and obesity
I Impaired wound healing
D Depression and mood changes

254
Q

What’s the mechanism of action of N-acetyl cysteine in Paracetamol?

A

Replenishes the supply of glutathione that conjugates NAPQI to non-toxic compounds

255
Q

How does menopause affect ALP levels?

A

increases ALP
- bone lacks a protective factor against osteoporosis from reduced oestrogen
- main sourced of ALP are the liver, bones and placenta

256
Q

What are the symptoms of Charcot’s triad? And what do they indicate?

A

fever, jaundice and abdominal pain
- signify biliary obstruction

257
Q

What is the most likely iatrogenic cause of chronic pancreatitis?

A

past history of ERCP

258
Q

what does having both IBD and primary sclerosing cholangitis increase your risk of?

A

Colorectal and biliary system malignancy
- so require annual colonoscopy

259
Q

What type of hepatitis virus consists of DNA?

A

Hepatitis B
- the rest are RNA viruses

260
Q

What are the key symptoms of haemochromatosis?

A
  • fatigue
    weakness
    non-specific abdominal pain
    erectile dysfunction
    arrhythmias
    irritability
    skin bronzing
    hepatomegaly
261
Q

What does the presence Hepatitis B surface antigen indicate in Hep B serology test?

A

Indicates infection with Hep B virus
(positive in both acute and chronic)

262
Q

What does the presence Hepatitis B surface antibody indicate in Hep B serology test?

A

Indicates recovery and immunity from Hep B virus
- anti-HBs also develops in a person who has been successfully vaccinated

263
Q

What does the presence Hepatitis B DNA indicate in Hep B serology test?

A

indicates infectivity and active hepatitis B virus replication

264
Q

What does the presence Total Hepatitis B core antibody indicate in Hep B serology test?

A

Appears at the onset of symptoms in the acute hepatitis and persists for life
- presence of anti-HBc indicates previous or ongoing infection with Hep B virus in an undefined time frame

Emily Phase 2a (15 decks)

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