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Year 3 > Block 32 Week 7&8 > Flashcards

Block 32 Week 7&8 Flashcards

1
Q

history of acute liver failure?

A
  • alcohol use
  • jaundice and encephalopathy
  • meds & herbal meds
  • exposures
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2
Q

FHx to ask abt in ALF

A

WIlson disease

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3
Q

RF for viral hepatitis?

A
  • travel
  • transfusions
  • sexual contacts
  • occupation
  • body piercing
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4
Q

exposure to hepatic toxins?

A
  • mushrooms
  • organic solvents
  • phosphorous contained in fireworks
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5
Q

ALF?

A
  • characterised by coagulopathy of hepatic origin and altered levels of conciousness due to hepatic encephalopathy
  • drug induced liver injury is the most common cause of ALF
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6
Q

What is ALF usually accompanied by?

A
  • ALF is usually accompanied by transaminitis and hyperbilirubinaemia and usually initated following severe acute liver injury
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7
Q

ALF =

A

severe acute liver injury with development of coagulopathy and hepatic encephalopathy within 28 weeks of disease onset

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8
Q

Acute liver injury =

A

severe acute liver injury from primary liver aetiology -hepatic encephaolpathy is absent

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9
Q

what is the key difference between ALF and ALI?

A
  • development of HE is the key differentiating factor between ALF and ALI
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10
Q

Secondary liver injury?

A
  • secondary liver injury - similar to ALI but no evidence of a primary liver insult
  • e.g.s severe sepsis or ischeamic hepatitis
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11
Q

classifying ALF?

A
  • hyperacute
  • acute
  • subacute
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12
Q

hyperacute ALF?

A

HE within 7 days of noticing jaundice. Best prognosis as much better chance of survival and spontaneous recovery.

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13
Q

Acute ALF?

A

HE within 8-28 days of noticing jaundice

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14
Q

Subascute ALF?

A
  • HE within 5-12 weeks of noticing jaundice (ALF may be defined up to 28 weeks).
  • Worst prognosis as usually associated with shrunken liver and limited chance of recovery.
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15
Q

CLD?

A
  • HE occuring more than 28 weeks after onset of jaundice is categorised as CLD
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16
Q

Most common cause of acute liver failure in europe vs rest of the world?

A
  • In europe: DILI
  • worldwide: viral hepatitis
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17
Q

primary causes of ALF?

A
  • viruses (A, B, E)
  • paracetmol
  • toxin induced - death cap mushroom
  • pregnancy related e.g fatty liver of pregnancy
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18
Q

Conditions causing ALF?

A
  • Budd chiari syndrome
  • wilson’s disease
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19
Q

drugs linked to ALF?

A
  • statins, carbamazepine, ecstasy
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20
Q

secondary causes of ALF?

A
  • ischeamic hepatitis
  • severe infection e.g. malaria
  • heat stroke
  • liver resection e.g. post-hepatectomy liver failure
  • malignant infiltration
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21
Q

Pathophys of ALF?

A
  • Most cases of ALF are associated with a direct insult to the liver leading tomassive hepatocyte necrosisand/orapoptosis, which prevents the liver from carrying out its normal function.
  • as it progresses it can lead to hyperdynamic circ state with low systemic vascular resistance
  • this can lead to poor peripheral perfusion and multi organ failure
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22
Q

How is cerebral autoreg disrupted in ALF?

A
  • marked cerebral oedema occurs due to hyperammonaemia causing cytotoxic oedema and increased cerebral blood flow that disrupts cerebral autoregulation.
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23
Q

CFs of ALF?

A
  • characterised by jaundice, confusion and coagulopathy
  • key features are jaundice and HE
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24
Q

How does HE present?

A
  • HE may manifest as confusion, altered mental status, asterixis (i.e. flapping tremor) and/or coma.
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25
Q

features that suggest decompensated cirrhosis rather than ALF?

A
  • in patients w ALI or ALF look for features of CLF e.g. spider naevi, palmar erythema, leuconychia that might suggest first pres of decompensated cirrhosis rather than ALF
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26
Q

signs and symptoms of ALF?

A
  • altered mental status, confusion, asterixis, jaundice
  • RUQ pain
  • hepatomegaly
  • ascites
  • bruising
  • GI bleeding: hamaetemsis, meaena
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27
Q

Systemic signs of ALF?

A
  • hypotension and tachycardia from reduced systemic vascular resistance
  • raised ICP
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28
Q

Raised ICP?

A

papilloedema, bradycardia, hypertension, low GCS

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29
Q

Imaging for ALF?

A

CT abd pelvis

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30
Q

ALI vs ALF?

A
  • The key differentiation between ALI and ALF is the development of HE.
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31
Q

contra-indications to liver transplant ?

A
  • previous cirrhosis, which would indicate decompensated cirrhosis rather than ALF, heavy alcohol use, significant co-morbidities (e.g. major cardiac or respiratory disease) or terminal illness (e.g. cancer).
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32
Q

ALF management principals - CV, resp, GI, metabolic

A
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33
Q

ALF management principals - renal, coagulopathy, spesis, neurological, liver

A
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34
Q

complications from ALF?

A
  • sepsis due to marked immune dysfunction and progressive multi organ failure - AKI, metabolic disturbance, haemorrhage (GI bleeding) and cerebral dysfunction
  • cerebral dysfunction e.g. seizures, irreversible brain injury, cerebral dysfunction is commonly the result of raised intercranial pressure
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35
Q

Why are ppl at risk of high output cardiac failure with ALF?

A

due to slow vascular resistance

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36
Q

Reducing

Alcohol misuse?

A
  • alcohol licensing laws
  • taxation
  • alcohol control zones
  • driving legistation
  • gov funded education campagins e.g. ‘know your limits’
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37
Q

tobacco misuse?

A
  • tobacco licensing laws
  • taxation
  • smoking in public places bans
  • advertising bans
  • smoking cessation services
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38
Q

illicit substance law?

A
  • misuse of drugs act 2010
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39
Q

Risk minimisation w ilicit substances?

A
  • risk minimisation: needle exchange services, maintenance Tx to prevent wider public health problems associated w substance misuse (BBV spread, crime, impact on children)
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40
Q

service for illicit substances?

A
  • gov funded internet and phone advice services (FRANK)
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41
Q

proactive public health policies?

A
  • Proactive policies attempt to reduce substance misuse related harm prior to initiation, for example by classifying new substancesas they are developed and therefore attempting to limit supply to the market.
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42
Q

reactive policies?

A
  • Reactive policies aim to respondquickly to epidemics in substance misuse.
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43
Q

e.g. reactive policy

A
  • For example, as new substances or diseases emerge educational campaigns respond to provide early advice to limit potential harms andappropriate interventions have been initiated (e.g. needle exchange services).
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44
Q

acute cholangitis?

A
  • infection of the biliary tree which characteristically results in pain, jaundice and fevers
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45
Q

acute cholangitis almost always occurs due to

A

bacterial infection secondary to biliary obstruction.

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46
Q

acute cholangitis a.k.a

A

ascending cholangitis

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47
Q

biliary obstruction is often seen secondary to?

A

choledocholithiasis (gallstones in the biliary tree) or biliary strictures (both benign and malignant).

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48
Q

AC epidemiology?

A
  • median presenting age is 50-60 affecting men and women equally
  • can occur following ERCP
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49
Q

Most common cause of AC?

A
  • choledocholithiasis (stones in bile duct) most common cause
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50
Q

Cholelithiasis =

A

gallstomes

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51
Q

acute cholangitis occurs due to?

A

impaired drainage and bacterial overgrowth

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52
Q

AC: benign strictures leading to obstruction can occur due to:

A
  • chronic pancreatitis
  • iatrogenic injury
  • radio/chemo
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53
Q

AC and PSC?

A
  • primary sclerosing cholangitis is associated w UC and is characterised by inflammation and stricturing of bile ducts
  • Although the strictures are typically benign, patients are at increased risk of many cancers including cholangiocarcinoma, gallbladder cancer and hepatocellular carcinoma.
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54
Q

Malignant stricture?

A
  • can lead to acute cholangitis
  • such as cholangiocarcinoma, pancreatic cancer and GB cancer
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55
Q

other causes of AC?

A
  • post ERCP
  • blocked biliary stent
  • extrinsic compression
  • parasites - (Ascaris lumbricoides)
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56
Q

How does acute cholangitis typically present?

A

RUQ pain, fever, jaundice - Chracots triad

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57
Q

AC - reynolds triad (5)?

A
  • RUQ pain, fever, jaundice, shock, confusion
  • shock and confusion tends to be seen in the more serious cases w systemic sepsis
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58
Q

symptoms of AC?

A
  • RUQ / epigastric pain
  • Fevers
  • Malaise
  • Nausea/vomiting
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59
Q

Signs of AC?

A
  • RUQ/ epigastric tenderness
  • pyrexia
  • jaundice
  • hypotension and confusion in severe cases
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60
Q

Ix of acute cholangitis?

A
  • Acute cholangitis is most commonly investigated withUSS, CT abdomen/pelvis and MRCP.
  • Blood tests reveal elevated inflammatory markers and an obstructive picture (raised bilirubin and ALP, though transaminases may also be elevated) on liver function tests.
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61
Q

US?

A

allows assessment of the gallbladder for gallstones and assessment of the CBD

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62
Q

CT?

A

good visualisation of the biliary tree, including the distal portion, used where USS inconclusive, to evaluate for abnormal lesions/tumours or where other diagnoses are suspected.

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63
Q

MRCP?

A

Magnetic resonance cholangiopancreatography offers excellent visualisation of the biliary tree. Often used where CT/USS are inconclusive.

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64
Q

ERCP?

A

involves endoscopic intubation of the ampulla of Vater. Allows good view of biliary tree whilst allowing therapeutic intervention such as drainage

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65
Q

Management of AC?

A
  • ppts w infected obstructed biliary system require urgent drainage - ERCP is first line or PTC if it fails/ unavailable
  • antibiotics
  • fluids
  • analgesia
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66
Q

Bile =

A
  • exocrine secretion of the liver
  • produced continously by hepatocytes
  • contains cholesterol and waste products like bilirubin and bile salts which aid in digestion of fats
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67
Q

mechanical causes of biliary obstruction can be divided into

A

intrahepatic and extrahepatic

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68
Q

intrahepatic causes of obst?

A
  • intrahepatIc cholestasis generally occurs at the level of the hepatocyte or biliary canalicular membrane
  • causes include viral hepatitis, drug induced hepatitis, drug induced cholestasis, biliary cirrhosis, ALD
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69
Q

drugs that cause cholestasis?

A
  • drugs like anabolic steroids and chlorpromazine are known to directly cause cholestasis
  • thiazide diuretic use increases risk of gallstones
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70
Q

what is a common cause of acute cholestatic injury that can mimic biliary obstruction?

A
  • Amoxicillin/clavulanic acid is one of the most frequent causes of acute cholestatic injury that can mimic biliary obstruction.
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71
Q

extrahepatic obstruction?

A
  • Extrahepatic obstruction to the flow of bile can occur within the ducts or secondary to external compression
  • overall, gallstones are the most common cause of biliary obstruction
  • Other causes of blockage within the ducts include malignancy, infection, and biliary cirrhosis.
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72
Q

extrahepatic obstruction causes predominantly?

A

conjugated bilirubinaemia

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73
Q

obst jaundice - Mirrizi syndrome?

A
  • Mirizzi syndrome is the presence of a stone impacted in the cystic duct or the gallbladder neck, causing inflammation and external compression of the common hepatic duct and thus biliary obstruction.
  • A fistula may form between the gallbladderand the CBD and the gallstone may then come to lie in the CBD.
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74
Q

ALT/ AST are markers of?

A
  • found within liver cells at high concentrations
  • marker of hepatocellular injury: hepatitis, liver cirrhosis, drug induced e.g. paracetamol overdose, HCC
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75
Q

classical LFT of alcoholic liver disease?

A
  • TheAST:ALT ratiocan help determine the aetiology of hepatocellular injury, with a >2:1 ratio classical of alcoholic liver disease
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76
Q

ALP production?

A
  • ALP is derived from biliary epithelial cells and bones
  • Raised ALP levels can therefore be caused bycholestasisorbone disease.
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77
Q

cholestasis?

A

interruption in bile flow from hepatocytes to duodenum

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78
Q

ALP rise w normal GGT?

A
  • An ALP rise withnormal GGTsuggests bone disease (e.g. Paget’s disease, vitamin D deficiency, bony metastases)
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79
Q

ALP and GGT rise?

A
  • An ALP rise withassociated GGT riseis more suggestive of cholestasis
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80
Q

isolated GGT rise?

A

alcohol excess.

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81
Q

bilirubin ?

A
  • breakdown product of hb breakdown
  • predominantly metabolised and excreted by the liver
  • jaundice usually absent until bilirubin levels exceed 50micromol/L
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82
Q

pre-hepatic jaundice?

A
  • increased red blood cell breakdown -> too much bilirubin
  • overwhelms the metabolism pathways
  • most common cause is haemolysis and patients are often anaemic
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83
Q

type of bilirubin that accumulates in pre-hepatoc jaundice?

A
  • Bilirubin isunconjugatedin the blood, as the hepatocytes have not yet metabolised it. The remainder ofLFTs are generally normal, as the liver is otherwise working well.
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84
Q

Deficiency of

gilberts syndrome?

A
  • congenital disorder
  • deficiency of glucosyltransferase - enzyme resp for the conjugation of bilirubin
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85
Q

how does gilberts typically present?

A
  • Gilbert’s syndrome classically presents following viral infection withraised bilirubinbut normal LFTs/ full blood count.
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86
Q

hepatocellular jaundice?

A
  • hepatocyte damage -> inability to metabolise unconjugated bilirubin
  • high unconjugated bilirubin levels
  • high ALT/AST levels
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87
Q

cholestatic/ obstructive jaundice ?

A
  • cholestasis is an interruption in bile flow
  • build up of conjugated bilirubin
  • high ALP levels associated with high GGT
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88
Q

obst jaundice ->

A

pale stools and dark urine

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89
Q

why might stools also be pale in hepatocellular jaundice?

A
  • Stools may also be pale in hepatocellular jaundice, as there is decreased bilirubin metabolism/excretion, however as the bilirubin in the blood is unconjugated, it will not be able to pass into the urine.
  • Therefore, the urine should remain a normal colour.
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90
Q

causes of cholestasis - intrahep obstruction?

A
  • hepatitis
  • cirrhosis
  • maligancy
  • drugs (e.g. antibiotics, oral contraceptive pills, anabolic steroids)
  • pregnancy
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91
Q

causes of extrahepatic obstruction ?

A
  • gallstones
  • PSC
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92
Q

Causesof predominantly unconjugated hyperbilirubinaemia:

A
  • Pre-hepatic jaundice (e.g. haemolysis)
  • Gilbert syndrome
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93
Q

Causesof predominantly conjugatedhyperbilirubinaemia:

A
  • Cholestasis
  • Hepatocellular jaundice
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94
Q

what suggests a hepatocellular injury?

A
  • greater than 10 fold inc in ALT
  • less than 3 fold inc in ALP
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95
Q

What suggests cholestasis?

A
  • less than 10 fold inc in ALT
  • more than 3 fold inc in ALP
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96
Q

what suggests bone pathology?

A

isolateed ALP rise without GGT -

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97
Q

isolated bilirubin rise?

A

Anisolated bilirubin risewithout further LFT derangement suggests pre-hepatic jaundice or Gilbert’s disease.

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98
Q

summary table for LFTS

A
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99
Q

bilirubin metabolism pathway

A
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100
Q

Acute on chronic liver failure precipitating factors?

A
  • most common precipitating factors for developing ACLF are bacterial infections and alcohol
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101
Q

CLD cause?

A
  • Caused by repeated insults to the liver which can result in inflammation, fibrosis and cirrhosis
  • variety of aetiological factors including alcohol, toxins, viruses and many others.
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102
Q

CLD is defined as?

A
  • CLD is generally defined as progressive liver dysfunction for six months or longer.
  • The end result of chronic liver disease is cirrhosis
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103
Q

Causes of CLD?

A
  • alc
  • viral
  • primary biliary cholangitis
  • primary scleorsing cholangitis
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104
Q

Syndromes linked to CLD?

A
  • inherited e.g. Wilsons disease and alpha-1-antitrypsin deficiency
  • budd-chiari syndrome
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105
Q

CLD pathophys?

A
  • Chronic liver disease may result from repeated insults that causeinflammation(i.e. chronic hepatitis) orcholestasis(i.e. impairment of bile flow).
  • Excess deposition of fat in the liver (i.e. steatosis) can also promote an inflammatory response, which is seen in conditions like non-alcoholic fatty liver disease.
  • overtime, fibrosis -> cirrhosis - irreversible liver remodeling
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106
Q

compensated cirrhosis?

A
  • patients are typically asymptomatic as a small amount of residual function allows the liver to continue carrying out normal function despite extensive damage.
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107
Q

decompensated cirrhosis?

A
  • in this state the liver no longer has the capacity to carry out its normal functions, which results in multiple complications.
  • If the insult is removed, the liver may ‘recompensate’ over time to a state of compensated cirrhosis.
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108
Q

features of decomp cirrhosis?

A
  • coagulopathy - bruising and deranged coagulation tests
  • jaundice
  • encephalopathy - confusion
  • ascites - poor albumin synthesis
  • GI bleeding from varices
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109
Q

Scoring system for cirrhosis?

A
  • classification of decompensated cirrhosis
  • child pugh score
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110
Q

classical features of CLD?

A
  • spider naevi
  • palmar erythema
  • jaundice
  • hair loss
  • leuconychia
  • asterixis
  • ascites.
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111
Q

early features of CLD?

A
  • early clinical features are usually non specific: anorexia, lethargy, weight loss, hepatomegaly, nausea, distrubed sleep pattern
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112
Q

stigmata of CLD?

A
  • Caput medusa
  • palar erythema
  • splenomegaly
  • Dupuytrens contracture
  • Leuconychia
  • Gynaecomastia
  • Spider Naevi
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113
Q

Caput medusa?

A

distended and engorged superficial epigastric veins around the umbilicus.

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114
Q

Palmar erythema?

A

red discolouration on the palm of the hand, particularly over the hypothenar eminence.

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115
Q

Duputrens contracure?

A

thickening of the palmar fascia. Causes painless fixed flexion of fingers at the MCP joints (most commonly ring finger).

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116
Q

Leuconychia?

A

appearance of white lines or dots in the nails. Sign of hypoalbuminaemia.

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117
Q

gynaecomastia?

A

Reduced hepatic clearance of androgens leads to peripheral conversion to oestrogen.

118
Q

spider naevi?

A

due to excess oestrogen, usually found in distribution of SVC

119
Q

encephalopathy?

A

confusion, often present with a flapping tremor (asterixis)

120
Q

features of decompensation - CAGEJ?

A
  • Encephalopathy
  • ascites
  • jaundice
  • GI bleeding
  • coaglopathy
121
Q

Diagnosis of cirrhosis?

A
  • liver biopsy - gold standard diagnostic method for idenfi of cirrhosis
  • non invasive liver screen, LFTs, liver biopsy, imaging
  • transient elastography
122
Q

transient elastography?

A

A quick painless test that assesses liver stiffness. Itmeasures sound wave velocityusing an ultrasound probe to indicate the ‘degree’ of fibrosis and thus the likelihood of cirrhosis.

123
Q

imaging for cirrhosis?

A
  • US
  • CT - more detailed view of the abd viscera and good for secondary findings - e.g. features of portal hypertension
  • MRI
124
Q

management of cirrhosis?

A
  • treating underlying cause - alcohol cessation, stopping medications, use of anto-virals in chronic hepatitis
125
Q

encephalopathy - main driver ?

A
  • constipation
  • first line = laxatives
126
Q

second line for encephalopathy?

A

involves the long-term use of antibiotics (i.e. rifaximin) to reduce the proportion of ammonia-producing colonic bacteria.

127
Q

ascites?

A
  • combination of portal hypertension and loss of oncotic pressure
  • due to widespread vasodilation and underperfusion of kidneys, RAAS is active leading to excess water and sodium reabsorption that exacerbates ascites.
128
Q

Tx of ascites?

A
  • aldosterone antagonists like spironolactone which can be combined with loop diuretics like furosemide
129
Q

Tx of ascites - paracentesis?

A

ppts w grade 3 ascites, draianage of ascites w human albumin soltuion

130
Q

GI bleeding?

A
  • development of portal hypertension from cirrhosis
  • Cirrhosis leads to the development of portal hypertension because of extensive scarring and increased pressure through the portal system.
  • blood is shunted into the systemic circulation atportosystemic sites(i.e. where the portal venous system joins the systemic venous syste
131
Q

how are varices treated?

A

non selective BBs like propanolol

132
Q

what increases risk of HCC?

A
  • increased risk w cirrhosis or chronic hep B
  • 6 monthly survelluence US and AFP blood test
133
Q

A on L liver failure?

A
  • syndrome characterised by acute decompensation of CLD associated w organ failure
  • up to half of the cases have no identificable trigger
134
Q

most common causes of AonC liver failure?

A
  • in the remaining patients, sepsis, active alcoholism and relapse of chronic viral hepatitis are the most common reported precipitating factors
135
Q

how is diagnosis of ACLF made?

A
  • The diagnosis of ACLF is made in patients with acute decompensation of liver cirrhosis with organ failure
136
Q

causes of hepatomegaly

137
Q

reducing risk of liver damage?

A
  • stopping alc
  • healthy diet
  • stopping meds
138
Q

intervention for management of hepatic ascites?

A
  • Refractory ascites may require transjugular intrahepatic portosystemic shunt (TIPSS), which creates a connection between a hepatic vein and an intrahepatic portal vein.
  • A PTFE graft is then left between this connectin to allow blood to flow from the portal vein to the inferior vena cava under little resistance.
139
Q

CLD risks?

A
  • alcohol
  • blood borne viruses - hep B and C paticularly
  • obesity
  • diabetes
140
Q

prevention of CLD?

A
  • lifestyle - healthy weight and diet, exercising regularly, avoiding alcohol
  • liver disease screeninf
  • Tx for conditions that can lead to CLD e.g. diabetes, hep B and hep C, NASH
    `
141
Q

Liver function?

A
  • Bilirubin
  • ALT - hepatocellular inflammation
  • ALP - biliary or bone
  • Gamma GGT - biliary disease, alcohol, fatty liver
  • Alb - liver synthetic function
142
Q

raised igG?

A

Autoimmune hepatitis

143
Q

raised IgM?

A

Primary biliary cirrhosis

144
Q

raised IgA?

A

Alcoholic liver disease

145
Q

Investigation of patient w LFT abn

146
Q

RF for liver disease?

A
  • blood transfusion
  • IV drug use
  • surgery
  • contacts - sexual
  • chemical exposure
147
Q

Wilson disease?

A
  • abn copper deposition in liver, cornea and brain
  • Kayser-Fleischer rings in eyes
148
Q

causes of acute liver failure?

A
  • viral hepatitis
  • hepatitis due to other viruses: CMV, EBV. herpes viruses 1,2 and 6
149
Q

metabolic cause of acute liver failure?

A
  • Acute fatty liver of pregnancy
  • Reye’s syndrome
150
Q

vascular causes of ALF?

A
  • heat stroke
  • acute circulatory failure
  • veno-occlusive disease
151
Q

Miscellanous causes of ALF?

A
  • wilson disease
  • autoimmune hepatitis
  • massive tumour infiltration
  • liver transplant with primary graft dysfunction
152
Q

Enterically transmitted hepatitis?

153
Q

Blood borne hepatitis?

A

B, C, D, G

154
Q

typical biopsy findings in viral hepatitis?

155
Q

hereditary haemochromatosis ?

A
  • increased pigmentation
  • typical arthopathy with joint swelling in 2nd aand 3rd MCP joints
156
Q

kayser fleisher rings in wilson disease?

A
  • sunflower cateracts also seen w wilsons disease
157
Q

phase 1 metabolism?

A
  • consist of oxidative and reductive processes.
158
Q

phase 2 reactions?

A
  • products of oxidation, reduction, and hydrolysis are coupled with endogenous substrates such as glucuronic acid, sulfuric acid, and glutathione.
  • These processes render polar lipophilic compounds.
159
Q

how are phase 2 products excreted?

A

bile if the molecules are large or in urine ifsmall

160
Q

phase 3 reactions?

A
  • drugs are actively transported from the cell
161
Q

varices?

A
  • caused by portal hypertension
  • varices at the GO junction and pa;osade zone are located more superficially within the wall of the oesophagus so they have a thinner coat and are more likely to bleed
162
Q

what predicts risk of haemorrhage w varices?

A
  • red signs such as red wheal marks - red streaks on varices predict risk of haemorrhage
163
Q

causes of ascites

164
Q

SBP from ascites 2 mechanisms?

A
  • Direct spread: bacterial translocation across the bowel wall
  • Haematogenous spread: bacteria enter ascites via the bloodstream in the context of an immunosuppressed state
165
Q

how can SBP present?

A

SBP may present in a number of ways including peritonitis (i.e. abdominal pain), hepatic encephalopathy, upper gastrointestinal bleeding, acute kidney injury or overt sepsis.

166
Q

intrahepatic cause of biliary disease?

A
  • Primary Biliary Cirrhosis (PBC)
  • Primary Sclerosing Cholangitis (PSC)
167
Q

causes of cholestasis?

A
  • Drug induced i.e. Steroids
  • Pregnancy
  • Infections
  • i.e. Cholangitis
168
Q

hepatic causes of jaundice?

A
  • acute on chronic liver disease
  • drug induced/ alcohol/viral/autoimmune
169
Q

post hepatic causes of jaundice?

A
  • gallstones/ panc tumours
  • always do a clotting screen for jaundice
170
Q

what doe we check for primary biliary cholangitis?

A
  • AMA for primary biliary cholangiting
  • more associated w female patients in 40s-50s
171
Q

what do we check for autoimmune hep?

A
  • anti SM antibody - autoimmune hepatitis (usually raised IgG too)
172
Q

what is often raised in PBC?

173
Q

what is often up in alcoholic liver disease?

174
Q

primary sclerosing cholangitis?

A
  • PSC - scarring and inflammation of bile ducts, more common in younger male patients
  • associated w UC
175
Q

what can you gte w PSC?

A

raised p-ANCA

176
Q

Which types of hepatitis can cause chronic viral hepatitis?

177
Q

Wilsons disease presents in which patients?

A

younger males in their teens-twenties

178
Q

non liver causes of deranged LFTs?

A
  • can occassionally get raised ALT in celiac
  • thyrotoxicosis can cause deranged LFTs
179
Q

INR?

A
  • Short history of jaundice
  • young lady
  • signs of confusion
  • no stigmata of CLD
  • acute liver failure from paracetamol overdose
180
Q

alf?

A
  • rapidly progressive liver injury occuring in absence of chronic liver disease
  • most common in previously healthy adults in their 30s
181
Q

what causes most cases of ALF in the UK?

A

Paracetamol

182
Q

history taking for liver failure?

A
  • all meds taken in past 6 months: gym supplements (anabolic steroids - usually cholestatic liver injury) , antibiotics, herbal meds
  • travel history
  • sexual history
183
Q

causes of cirrhosis?

A
  • alcoholic liver disease
  • non alcoholic FLD (most don’t progress though)
  • chronic viral hep - usually hep B and C
  • cirrhosis increases risk of hepatocellular carcinoma
184
Q

complications of portal hypertension ?

A
  • GI bleeding - variceal
  • encephalopathy
  • ascites - spotaneous bacterial peritonitis
  • HCC
  • hepatorenal syndrome
  • hepatic hydrothorax
185
Q

what is often the first presentation of decompensation in cirrhosis?

A
  • most common complication of decompensation in cirrhosis - often the first presentation of decompensated liver disease
  • average survival is 9 months
  • develop malnutiriton and reduced appetite
186
Q

impacts of ascites on ppts?

A
  • impairs working and social life
  • freq leads to hospitalization
187
Q

management of ascites?

A
  • spironolactone +/- furosemude - tends to be better for peripheral oedema
  • no salt diet
  • fluid restriction
188
Q

what to avoid w ascites?

A
  • NSAIDs and ace inhibitiors
  • aminoglycosides - renovascular risks
  • iV dextrose
189
Q

dextrose and ascites?

A

leads to hyponatreamia - bc the diuretics cause hyponatreamia

190
Q

SBP - what is needed in the first 24 hrs?

A

ascites tap

191
Q

how does SBP present?

A
  • fever, abd pain, hypotension, encephalopathy
  • neutrophil count in ascitic fluid of >350/mm3
  • usually gram negative bac e.g. E coli
192
Q

Dysentery =

A

gastroenteritis characterised by diarrhoea with visible blood or mucus. Associated with fever and abdominal pain

193
Q

viruses causing GE?

A

Rotavirus
Norovirus
Adenovirus

194
Q

Bacterial vs viral GE?

A
  • Watery is more viral
  • bloody (inflammatory) - bacterial
195
Q

watery diarrhoea in GE?

A
  • due to predominant small bowel involvement.
  • Causes a large volume watery diarrhoea with features of abdominal cramping/bloating and weight loss.
196
Q

Bloody (inflammatory diarrhoea)?

A
  • due to predominant large bowel involvement.
  • Causes frequent, smaller-volume bloody or mucoid diarrhoea that is associated with fever and severe abdominal pain.
197
Q

Typical causes of watery diarrhoea:

A
  • Clostridioides (formally Clostridium) difficile
  • Clostridium perfringens
  • Enterotoxigenic Escherichia coli (ETEC)
198
Q

typical causes od bloody diarrhoea?

A
  • non typhoidal salmonellosis
  • campylobacter
  • shigella
  • EHEC
199
Q

Parasites?

A
  • Parasitic gastroenteritis is commonly associated with foreign travel.
  • Giardia spp. is the most commonly identified pathogen in prolonged travellers’ diarrhoea.
200
Q

rotavirus?

A
  • most common cause of GE in children
  • oral vaccine in the child immunisation programme
201
Q

rotavirus GE?

A
  • Commonly causes a watery diarrhoeal illness with vomiting.
  • Vomiting often settles within 1-3 days and diarrhoea within 7 days.
203
Q

Norovirus?

A
  • most common cause of GE
  • common in winter months
  • full recovery usually within 2 days
204
Q

campylobacter?

A
  • undercooked poultry and other contaminated food/water
  • C. jejuni is the most commonly implicated species and causes either a watery or bloody diarrhoeal illness 2-5 days after exposure.
205
Q

Campylobacter gastroenteritis has been linked to the development of…

A

several autoimmune conditions following an acute episode (e.g. reactive arthritis, Guillain-Barré syndrome).

206
Q

bacilus cereus - vomiting illness?

A
  • vomiting illness after reheating starchy foods - 1-5hrs of ingestion and resolution within 6-24 hrs
207
Q

bac cereus - diarrhoeal illness?

A

Ingestion of contaminated food with the diarrhoeal enterotoxin leads to a watery diarrhoeal illness 8-16 hours following ingestion with quick resolution (i.e. < 24 hours).

208
Q

bacilus vs staphlycoccus?

A
  • Staphylococcus aureus can also produce an enterotoxin that contaminates food and leads to a rapid-onset gastroenteritis illness.
  • the vomiting with S. aureus enterotoxin is usually accompanied with diarrhoea.
209
Q

salmonella transmission?

A
  • ingestion of contaminated food such as undercooked poultry (most commonly red and white meat, raw eggs and diary products).
210
Q

Salmonella GE?

A
  • typical watery diarrhoeal illness, but can be bloody, with associated abdominal pain, fever and vomiting.
  • The illness typically starts within 3 days of exposure and resolves within a week.
211
Q

Shigella?

A
  • classic cause of dysentery in young children
  • bloody/mucoid diarrhoea associated with fever and abdominal pain
212
Q

when is shigella most common?

A

most common in late summer and spread by direct human-to-human transmission because the bacteria only colonises humans and some nonhuman primates.

213
Q

shigella GE?

A

illness usually begins 1-3 days following exposure and resolves within 7 days.

214
Q

Enterohaemorrhagic E. coli ?

A
  • Classically causes a bloody diarrhoeal illness
  • the UK, E. coli O157 is the most common serotype of EHEC that commonly infects children < 5 years old.
215
Q

EHEC transmission?

A
  • most commonly transmitted by contaminated food (e.g. meat, salad, water) - also seen from direct human-to-human spread, which can be due to contact with infected animals (e.g. petting zoos).
216
Q

EHEC infection?

A

Infection may be asymptomatic or cause a diarrhoeal illness (classically dysentery-type illness), which begins within 3-4 days of exposure and resolves within 10 days

217
Q

EHEC 0157?

A

can cause haemolytic uraemic syndrome (HUS) in up to 20% of infected children and accounts for 90% of cases of HUS in children

218
Q

HUS symptoms?

A
  • microangiopathic haemolytic anaemia,
  • thrombocytopaenia and
  • acute kidney injury
219
Q

ETEC?

A

Commonly associated with a watery diarrhoeal illness in travellers or resource-limited countries.

220
Q

Entamoeba?

A
  • travellers
  • mainly asymptomatic
  • presentation ranges from mild diarrhoeal illness to severe dysentery.
221
Q

Giardia?

A
  • commonly implicated in Travellers’ diarrhoea.
  • watery diarrhoea
222
Q

GE history taking?

223
Q

symptoms of GE?

A
  • Diarrhoea: may be described as watery, bloody or mucoid
  • Nausea & vomiting
  • Fever
  • Abdominal pain
  • General malaise
  • Bloating/cramping
  • Weight loss
224
Q

Ix of GE?

A
  • stool cultures
  • virology
  • C diff
  • OCP - used to detect parasitic organisms. Usually only performed in Travellers’ diarrhoea or significant travel history
225
Q

Complications of GE?

A
  • Dehydration
  • AKI
  • HUS
  • sepsis
  • toxic megacolon
  • post infective IBS
226
Q

Inflammatory diseases after GE occur paticularly w?

A
  • reactive arthritis, Guillain-Barré syndrome. - Particularly with Campylobacter spp
227
Q

Ecoli TP?

A
  • Common amongst travellers
  • Watery stools
  • Abdominal cramps and nausea
228
Q

Giardiasis TP?

A
  • Prolonged,
  • non-bloody diarrhoea
229
Q

Cholera TP?

A
  • Profuse, watery diarrhoea
  • Severe dehydration resulting in weight loss
  • Not common amongst travellers
230
Q

shigella TP?

A
  • Bloody diarrhoea
  • Vomiting and abdominal pain
231
Q

Staph aureus TP?

A
  • Severe vomiting
  • Short incubation period
232
Q

Campylobacter GE?

A
  • A flu-like prodrome is usually followed by crampy abdominal pains, fever and diarrhoea which may be bloody
  • May mimic appendicitis
  • Complications include Guillain-Barre syndrome
233
Q

bac cereus TP?

A

2 types of illnesses:

  • vomiting within 6 hours, stereotypically due to rice
  • diarrhoeal illness occurring after 6 hours
234
Q

Amoebiasis TP?

A
  • Gradual onset bloody diarrhoea, abdominal pain and tenderness which may last for several weeks
235
Q

1 to 6 hr incubation period?

A

Staphylococcus aureus, Bacillus cereus - vomiting subtype, the diarrhoeal illness has an incubation period of 6-14 hours

236
Q

12 - 48 hrs incubation period?

A

Salmonella, Escherichia coli

237
Q

48-72 incubation period?

A

Shigella, Campylobacter

238
Q

> 7 days?

A

Giardiasis, Amoebiasis

239
Q

PBC?

A
  • The M rule
  • IgM
  • anti-Mitochondrial antibodies,M2 subtype
  • Middle aged females
240
Q

Antibodies

PSC?

A

p-anca ab, linked to UC

241
Q

PPIs can cause?

A

hyponatreamua

242
Q

electrolyte disturbances in refeeding syndrome?

A

Hypophosphataemia, hypokalaemia and hypomagnesaemia are the characteristic electrolyte disturbances seen in patients with refeeding syndrome

243
Q

what can cause torsades?

244
Q

coeliac disease is assoc w ?

A

iron, folate and vitamin B12 deficiency -> Koilonychia - nail spooning

245
Q

dysphagia is ? unless proven otherwise

A

oesophageal carcinoma

246
Q

Dysphagia, aspiration pneumonia, halitosis → ?

A

pharyngeal pouch

247
Q

prophylaxis vs treatment of variceal bleeds?

A

PROPhylaxis = PROPanolol
Treatment = Terlipressin

248
Q

beta blockers naming?

A

A-M = Cardio-Selective e.g. Bisoprolol,Metoprolol
N-Z = Non-Selective e.g. Propranolol

249
Q

C diff Infection Tx?

A

1st: oral vancomycin 10 days

2nd: oral fidaxomicin

3rd: oral vancomycin +/- IV metronidazole

250
Q

Area most likely to be affected by ischaemic colitis?

A

splenic flexure i

251
Q

presentation of ischaemic colitis?

A
  • RF for IHD like HTN
  • the pain gets worse after eating, when the bowel requires more blood flow for its increased energy demands for digestion
252
Q

splenic flexure?

A
  • The splenic flexure marks the point where the majority of blood supplied changes from the superior mesenteric artery (SMA) to the inferior mesenteric artery (IMA) - Watershed area
253
Q

acute mesenteric ischaemia?

A
  • Acute mesenteric ischaemia is typically caused by an embolism resulting in occlusion of an artery which supplies the small bowel, for example the superior mesenteric artery.
    -Classically patients have a history of atrial fibrillation.
254
Q

pain in acute mesenteric ischaemua?

A

The abdominal pain is typically severe, of sudden onset and out-of-keeping with physical exam findings.

255
Q

chronic mesenteric ischaemia?

A
  • Chronic mesenteric ischaemia is a relatively rare clinical diagnosis due to it’s non-specific features and may be thought of as ‘intestinal angina’.
  • Colickly, intermittent abdominal pain occurs.
256
Q

Common predisposing factors in bowel ischemia?

A
  • increasing age
  • atrial fibrillation - particularly for mesenteric ischaemia
  • other causes of emboli: endocarditis, malignancy
  • cardiovascular disease risk factors: smoking, hypertension, diabetes
257
Q

ischaemic colitis can be seen following ? in young ppts

A

cocaine use

258
Q

Common features of bowel ischemia?

A
  • abd pain - out of prop in AMI
  • rectal bleeding
  • diarrhoea
  • fever
  • bloods typically show an elevated white blood cell count associated with alactic acidosis
259
Q

most common cause of spont bac pertionitis?

260
Q

prophylaxis for SBP?

A

Patients who have had an episode of SBP require antibiotic prophylaxis - ciprofloxacin

261
Q

birds beak appearance?

A

bird’s beak’ appearance of the lower oesophagus that is seen in achalasia

262
Q

Causes of liver decompensation?

A

constipation, infection, electrolyte imbalances, dehydration, upper GI bleeds or increased alcohol intake.

263
Q

Mesenteric ischemia vs IC from 34.2 notes page 8

264
Q

Patients with ascites secondary to liver cirrhosis should be given

A

ald antagonist - spironolactone

265
Q

CD involves inc?

A

goblet cells

266
Q

which 2 things are seen more freq in UC?

A

crypt abcseses: UC, UC also causes pseudopolyps more than crohns

267
Q

PPI are a RF for

268
Q

New onset dysphagia?

A

New-onset dysphagia is a red flag symptom that requires urgent endoscopy, regardless of age or other symptoms

269
Q

most affected site in crohns?

A

Terminal ileum

270
Q

Histology of coeliac

A

Histology of coeliac disease: villous atrophy, raised intra-epithelial lymphocytes, and crypt hyperplasia

271
Q

duodenal vs gastric ulcers?

A

duodenal ulcers being relieved by food, and gastric ulcer worsening with food.

272
Q

right heart failure assoc w ?

A

Right heart failure is associated with a firm, smooth, tender and pulsatile liver edge

273
Q

ppts w T1D should be screened for?

A

Patients with type 1 diabetes or autoimmune thyroid disease should be screened for coeliac disease on diagnosis

274
Q

mild UC flare?

A
  • mild: < 4 stools/day, only a small amount of blood - topical aminosalicyclate , if no improv add oral aminosalicyclaye
275
Q

moderate UC flare?

A
  • moderate: 4-6 stools/day, varying amounts of blood, no systemic upset - topical aminosalicyclate , if no improv add oral aminosalicyclaye
276
Q

severe UC flare?

A
  • severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers) - IV steroids in hosp
277
Q

loss of hausta ->

A

leadpipe colon -> UC

278
Q

HNPCC is assoc w?

A

increased risk of pancreatic cancer

279
Q

DKA management - FIG PICK?

A

F - Fluids
I - Insulin (Fixed rate 0.1u/kg/hr)
G - Monitor glucose
P - Monitor / give potassium
I - Treat any underlying infections / triggers
C - Monitor for signs of cerebral oedema
K - Monitor ketones & pH

280
Q

first-line to maintain remission in patients with Crohn’s

A

azathioprine or mercaptopurine

281
Q

recommended test for H pylori post erad?

A

urea breath test

282
Q

uc + cholestasis?

A

(e.g. jaundice, raised ALP) → ? primary sclerosing cholangitis

283
Q

risk of ? w PSC?

A

Cholangiocarcinoma develops in around 10% of primary sclerosing cholangitis patients

284
Q

what suggests panc cancer?

A

The presence of painless obstructive jaundice and steatorrhoea is highly suggestive of pancreatic cancer. The presence of a right upper quadrant mass is suggestive of a palpable gallbladder

285
Q

inducing vs remaining remission in CD?

A
  • pred to induce remission
  • azathioprine/ mercaptopurine to maintain it
286
Q

C diff ->

A

C diff -> psuedomembranous colitis

287
Q

high SAAG ascites?

A
  • Ascites: a high SAAG gradient (> 11g/L) indicates portal hypertension
  • Causes of this include liver cirrhosis, hepatic failure, venous occlusion (e.g. Budd Chiari syndrome), alcoholic hepatitis, and kwashiorkor malnutrition.
288
Q

low SAAG ascites?

A
  • A low SAAG (<11g/L) suggests the ascitic fluid is an exudate.
  • Causes of this include malignancy, infection, pancreatitis and nephrotic syndrome.
289
Q

Budd chiari presentation?

A

triad of sudden onset abdominal pain, ascites, and tender hepatomegaly

290
Q

alcoholic hep ALT/AST ratio?

A

The AST/ALT ratio in alcoholic hepatitis is 2:1

Year 3 (45 decks)

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