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Phase 2a - Jemima > Liver > Flashcards

Liver Flashcards

1
Q

what are the functions of the liver

A

where oestrogen level regulation
albumin production
clotting factors
sorage
metabolism of carbs
immunity (Kupfer)
detoxification
bilirubin metabolism

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2
Q

what are markers of liver function

A

bilirubin - conjugated vs unconjugated
albumin
prothrombin time (PT/INR)

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3
Q

what happens to levels of bilirubin in liver damage

A

increase

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4
Q

what happens to levels of albumin in liver damage

A

decrease

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5
Q

what happens to prothrombin time in liver disease

A

it increases

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6
Q

Where are ALT and AST found

A

found in the liver, heart, kidney and muscles

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7
Q

why do you test for ALT and AST

A

they will show an increase in liver damage (likely) as they spill out into the blood

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8
Q

what is the ratio of AST:ALT seen in alcoholic liver disease (typically)

A

> 2:1 (especially with an increased GGT)

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9
Q

what is the GGT test used for

A

it is the gamma-glutamyl transferase test - which measures the amount GGT in the blood, which increases when the liver is damaged

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10
Q

when might you see an increase in ALP levels

A

in biliary tree specific damage

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11
Q

what is acute liver damage

A

when there is liver injury which ic accompanied with HE, Jaundice and coagulopathy (>1.5INR) in a patient with a previously normal liver

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12
Q

what is the main cause of acute liver failure (fulminant liver failure) in the UK

A

Paracetamol overdose

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13
Q

what is fulminant liver failure

A

it is a rare syndrome of massive hepatocyte necrosis

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14
Q

what is seen histologically in acute liver failure

A

multiacinar necrosis

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15
Q

what is hyper acute fulminant liver failure

A

Hepatic encephalopathy within 7 days of jaundice

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16
Q

what is acute fulminant liver failure

A

it is hepatic encephalopathy within 8-28 days of jaundice

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17
Q

what is chronic liver failure

A

a patient which has a progressive history of liver disease

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18
Q

what are causes of acute liver injury

A

viral - HepA, B, E, CMV, EBV
autoimmune hepatitis
drugs - paracetamol, alcohol, ecstasy
HCC
metabolic - wilsons, haemochromotosis, A1ATD
Budd chiari

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19
Q

how does liver failure progress from hepatitis

A

hepatitis - fibrosis - compensated cirrhosis - decompensated cirrhosis

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20
Q

what are symptoms of acute liver failure

A

jaundice, coagulopathy, hepatic encephalopathy
- spider naevi
- fetor hepaticus
- caput-medusae
- Dupuytren’s contracture

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21
Q

what are the West haven criteria grades 1-4 for hepatic encephalopathy

A
  1. altered mood and sleep issues
  2. lethargy, mild confusion, asterixis
  3. marked confusion, somnolent
  4. comatose
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22
Q

How do you diagnose acute liver injury

A

Bloods (LFTs)
imaging: ECG to grade the HE, USS to check budd chiari
microbiology to rule out infection

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23
Q

what microbiological test will be performed in acute liver injury to rule out infection

A

blood culture
urine culture
ascitic tap

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24
Q

what would be seen on bloods in an acute liver injury

A

increased bilirubin, decreased albumin, increased prothrombin time and INR. There will be an increased serum AST and ALT, increased NH3 and a decreased glucose

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25
Q

how do you acutely treat acute liver failure

A

ITU - ABCDE
fluids
analgesia

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26
Q

how do you treat acute liver failure

A

treat the underlying cause and complications
- increase ICP give IV mannitol
- HE give lactulose
- ascites give diuretics
- haemorrhage - give vitamin K

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27
Q

what are the two outcomes for acute liver injury

A

can lead to liver failure or recovery

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28
Q

what is the presentation of acute liver injury

A

malaise, nausea, anorexia, jaundice
rare
- confusion
- bleeding
- liver pain
- hypoglucaemia

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29
Q

what is the presentation of chronic liver injury

A

ascites
oedema
haematemesis (varices)
malaise
anorexia
wasting
easy bruising
hepatomegaly
abnormal LFTs

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30
Q

what are the two types of liver enzymes tested for

A

cholestatic: alkaline phosphate and gamma GT
hepatocellular: transaminases (AST, ALT)

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31
Q

what are the reasons someone may develop pre-hepatic jaundice

A

Gilbert syndrome
Haemolysis

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32
Q

What are causes for conjugated bilirubin jaundice

A

liver disease - hepatic
bile duct obstruction - post hepatic

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33
Q

what is chronic liver failure

A

it is progressive liver disease over 6 months due to repeated liver insults

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34
Q

what are risk factors of developing chronic liver failure

A

alcohol, obesity, T2DM, drugs, inherited metabolic disease, autoimmunity

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35
Q

what are causes of chronic liver failure

A
  1. Alcohol related liver disease
  2. Non-alcoholic fatty liver disease
  3. Viral
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36
Q

what is the pathophysiology behind chronic liver failure development

A

Hepatitis/cholestasis - fibrosis (reversible) - cirrhosis (irreversible) - compensated or decompensated liver failure

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37
Q

what are the symptoms of decompensated liver failure

A

jaundice, hepatic encephalopathy, ascites, coagulopathy, low serum albumin

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38
Q

what is the Childpugh score

A

it assesses the prognosis and extent of the treatment required for chronic liver failure
- especially for decompensated cirrhosis

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39
Q

what are the classes scores of the Childpugh score

A

A = 100% 1y survival
B = 80% 1y survival
C = 45% 1y survival

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40
Q

what is a clear risk factor for developing hepatocellular carcinoma

A

end-stage liver failure with decompensated cirrhosis

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41
Q

what is the MELD score

A

it is the model for end-stage liver disease liver disease, which stratifies the severity of ESLD for transplant planning

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42
Q

what are symptoms of chronic liver injury

A

jaundice, ascites, hepatic encephalopathy, oesophageal varices, palmar erythema, gynecomastia, clubbing, setor hepaticus, Dupuytren’s contracture

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43
Q

how do you diagnose chronic liver failure

A

Liver biopsy - see the extent of CLD
Lifer function tests
Imaging: USS
Ascetic tap culture

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44
Q

what is the treatment for chronic liver failure

A

prevent progression - lifestyle modifying
consider liver transplant (if decompensated)
manage the complications

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45
Q

what lifestyle changes can be made to prevent chronic liver failure progression

A

drink less alcohol
decreased BMI

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46
Q

what do you give to manage hepatic encephalopathy

A

lactulose

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47
Q

how do you manage ascites

A

diuretics

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48
Q

what is ascites

A

build up of fluid in the belly

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49
Q

what are risk factors for alcohol liver disease

A

chronic alcohol consumption
obesity
smoking

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50
Q

how does alcoholic liver disease progress

A

steatosis - fatty liver undamaged
alcoholic hepatitis - mallory bodies
alcoholic cirrhosis - micronodular

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51
Q

what are the symptoms of alcoholic liver disease

A

early stages may show very little symptoms
in the more severe stages patients will develop chronic liver failure symptoms and alcohol dependency

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52
Q

what symptoms are seen in late stage alcoholic liver disease

A

jaundice
hepatomegaly
Dupuytren contracture
ascites
hepatic encephalopathy
spider naeiri
easy bruising

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53
Q

what is the maximum units of alcohol recommended per week

A

14 units a week

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54
Q

how do you work out the units using alcohol ABV

A

Strength (ABV) X Vol/ml ÷ 1000

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55
Q

how much is one unit of alcohol in g and mL

A
  1. 8g
  2. 10mL
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56
Q

what are the two types of gall stone

A
  1. Cholesterol stones (70%)
  2. Pigment stones (30%)
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57
Q

how do you manage gall stones

A
  • laparoscopic cholecystectomy
  • bile acid dissolution therapy
    if they are in the bile duct
  • ERCP with sphincterotomy and removal
  • surgery with large stones
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58
Q

what type of liver disease is itching associated with

A

cholestatic liver disease

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59
Q

what are the different types of drug-induced liver injury

A

hepatocellular
cholestatic
mixed

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60
Q

what are the common drugs which cause drug-induced liver disease

A

antibiotics - augmentin, flucloxacillin
CNS drugs
immunosuppressants
analgesics/MSK - diclofenac
Gastrointestinal drugs - PPIs
Dietary supplements
multiple drugs

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61
Q

what is the alcohol dependency questionnaire CAGE

A
  1. should you Cut down
  2. are people Annoyed by your drinking
  3. do you feel Guilty about drinking
  4. do you drink in the morning (Eye opening)
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62
Q

other than CAGE what other alcohol dependency questionnaires can be used

A

AUDIT - 10 questions: alcohol use disorder ID test

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63
Q

how do you diagnose alcohol liver disease

A

bloods - LFTs, FCB (macrocytic non megaloblastic anaemia)
Biopsy - to confirm extent of cirrhosis

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64
Q

what is the treatment for alcoholic liver disease

A

STOP ALCOHOL
give diazepam for tremors (withdrawal)
healthy diet and reduce BMI
steroids (short term)
B1 and folate supplements
liver transplant

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65
Q

what must someone with alcohol liver disease do if they need a liver transplant

A

must abstain for 3 plus months from alcohol before they are considered

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66
Q

what are complications of alcohol liver disease

A

pancreatitis
hepatic encephalopathy
ascites
hepatocellular carconoma
Mallory Weiss tear
Wernicke korsakoff syndrome

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67
Q

what is a mallory weiss tear

A

it is a tear of the tissue in the lower oesophagus which can be brought about by violent coughing or vomiting

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68
Q

what are the symptoms of a mallory weiss tear

A

blood in vomit
black or tar like stools
weakness
dizziness
faintness
shortness of breath
diarrhoea
pale
abdominal or chest pain

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69
Q

what are the infectious causes of liver failure

A

Viral hepatitis (B, C, CMV)
yellow fever
leptospirosis
EBV

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70
Q

what is Wernicke Korsakoff syndrome

A

it is B1 deficiency due to excess alcohol intake.
it is the combines presence of Wenicke encephalopathy and Korsakoff syndrome

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71
Q

What are the vascular causes of liver failure

A

Budd-Chiari syndrome
Veno-occlusive disease

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72
Q

what is Budd - Chiari syndrome

A

it is a condition where the hepatic veins are blocked or narrowed by a clot

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73
Q

what toxins cause liver failure

A

amanita phalloides mushroom
carbon tetrachloride
paracetamol overdose
halothane
isoniazid
alcohol

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74
Q

what are obstructive causes of liver failure

A

fatty liver of pregnancy
eclampsia

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75
Q

what are some other causes for liver failure

A

autoimmune disease
Wilsons disease
Cirrhosis

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76
Q

when will prothrombin time be high

A

in acute renal failure

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77
Q

what is asterixis

A

a tremor when the wrist is extended

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78
Q

what is fetor hepaticus

A

breath has a strong musty smell

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79
Q

what is constructional apraxia

A

you cant perform tasks which involve construction i.e drawing a star

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80
Q

how is liver failure monitored

A

fluids = Urinary and central venous cannulas
bloods = daily
glucose = 1-4 hr plus a dextrose IV

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81
Q

what are the complications of liver failure

A

hepatorenal syndrome
bleeding
sepsis
ascites
hypoglycaemia
seizures
cerebral oedema

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82
Q

what are the symptoms of Wernicke Korsakoff syndrome

A

ataxia
nystagmus = a rhythmical, repetitive and involuntary movement of the eyes
encephalopathy

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83
Q

what is non alcoholic fatty liver disease

A

chronic liver disease not due to alcoholism

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84
Q

what are risk factors of non alcoholic fatty liver disease

A

obesity, hypertension, hyperlipidemia, type 2 diabetes, endocrine disorders, drugs (NSAIDs, amiodarone)

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85
Q

what is the disease progression of non alcoholic fatty liver disease

A

hepatosteatosis (non alcoholic fatty liver) - non alcoholic steatohepatitis - fibrosis - cirrhosis

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86
Q

what are the patient symptoms of non alcoholic fatty liver disease

A

it is typically asymptomatic: any findings are incidental initially
- if it is very severe then they will present with liver failure signs

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87
Q

how do you diagnose non alcoholic fatty liver disease

A

bloods = rearranged LFTs (increased PT/INR, low albumin, high bilirubin). FBC (thrombocytopenia and hyperglycaemia)
imaging = 1st line for suspected NAFLD - USS abdomen

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88
Q

how do you assess the risk of fibrosis in NAFLD

A

the non invasive scoring system

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89
Q

what is the treatment for NAFLD

A
  • lose weight (reduce BMI)
  • control risk factors: statins, metformin, ACE-i
  • VITAMIN E
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90
Q

what are complications for NAFLD

A

hepatic encephalopathy
ascites
hepatocellular carcinoma
portal hypertension
oesophageal varices

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91
Q

what is viral hepatitis

A

inflammation of liver as a result of viral replication within hepatocytes

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92
Q

what are the features of Hep A induced hepatitis

A

Acute
Mild
Faecal - oral spread
Shellfish
ssRNA virus

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93
Q

what are risk factors of catching HepA

A

overcrowding
poor saturation
shellfish
travel

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94
Q

how long is the incubation period for Hep A

A

incubation is 2 weeks - replicated in the liver and excreted in the bile

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95
Q

what are the symptoms of HepA

A

prodromal phase - 1-2 weeks
- malaise, nausea, vomiting, fever
Then jaundice, dark urine, pale stools, hepatosplenomegaly

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96
Q

how do you diagnose HepA

A

bloods - increased ESR and leukopenia
LFTs - bilirubin increase
HAV serology - HAV IgM indicated acute infection

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97
Q

what is the treatment for hepatitis A

A

supportive treatment
- travelers vaccine is available

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98
Q

what is a rare complication of hepatitis A

A

fulminant (rapid) liver failure

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99
Q

what are features of Hep C infection

A

acute and chronic infection
ssRNA virus
blood bone
large association with IVDU, limited vertical and sexual transmission

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100
Q

what are the symptoms of Hep C infection

A

often asymptomatic
few patients with influenza like symptoms
resent later with chronic liver failure signs and hepatosplenomegaly

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101
Q

how do you diagnose Hep C

A

serology
- HCV RNA = current infection
- HCV Ab = presents within 4-6 weeks of infection

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102
Q

what is the treatment for Hep C

A

direct acting antivirals
- oral rivavarin plus NSSA-I, NSSB-I

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103
Q

what percentage of Hep C cases progress onto chronic liver failure

A

30%

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104
Q

what are the features of HepE

A

acute infection
ssDNA infection
associated with undercooked pork
faecal - oral spread
common in india and china

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105
Q

how do you diagnose Hep E infection

A

Bloods
- HEV IgM = acute infection
- HEV RNA

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106
Q

what is the treatment for Hep E

A

supportive
self limiting disease so will get better (usually)

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107
Q

what are features of Hep D

A

acute and chronic infection
ssRNA
blood born
dependent on HBV

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108
Q

why does Hep D require HBV for infection

A

it is incomplete - required HBV genome for viral assembly

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109
Q

what are the features of Hep B

A

it is an acute and chronic virus
dsDNA
blood born

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110
Q

how is Hep B transmitted

A

needles
Sexual
vertical
horizontal (between children)

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111
Q

What body fluids is HBV found in

A

saliva and semen

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112
Q

what are the risk factors for HBV

A

IV drug user
MSM
dialysis patients
healthcare workers

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113
Q

what are the symptoms of Hep B

A

similar to hepatitis A
1-2 week prodrome with a then deepening jaundice, dark urine and pale stool. Hepatosplenomegaly, urticaria, arthralgia

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114
Q

what is the incubation period for HBV

A

1-6 months

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115
Q

how do you diagnose Hep B

A

serology
- HBVsAg = present for 1-6 months of infection
- HBsAg = present after 6 months of infection (denotes immunity)
- HBcAg = exposed to HBV at some point
- HBcIgM = acute infection
- HBcIgG = chronic infection
- HBeAg = marker of patient infectiousness
- HBeAb = implies reduced infectivity, present in all chronic infections

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116
Q

what is the treatment for HepB

A

peglyated interferon
alpha 2A

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117
Q

what percentage of HBV cases progress to chronic liver failure

A

5-10% of cases, but in 90% of cases in children they will become chronic decompensated and associated with a very poor prognosis - will require a liver transplant

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118
Q

what do all types of hepatitis show

A

interface necrosis on histology

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119
Q

what is autoimmune hepatitis

A

very rare - an adaptive immunity that mounts a response against hepatocytes

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120
Q

what are risk factors of autoimmune hepatitis

A

female
other autoimmune diseases (such as SLE)
viral hepatitis
HLA DR3/4

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121
Q

what are the two types of autoimmune hepatitis

A

T1 = adult females (80%)
T2 = young females

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122
Q

what are the two types of antibody found in type 1 autoimmune hepatitis

A

antinuclear antibody
anti smooth muscle antibody

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123
Q

what are the two types of antibody found in T2 autoimmune hepatitis

A

anti liver cytosol
anti liver - kidney microsome

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124
Q

what are the symptoms of autoimmune hepatitis

A

25% of cases asymptomatic
many present with jaundice, fever and hepatosplenomegaly

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125
Q

how do you diagnose autoimmune hepatitis

A

serology
- ANA, ASMA plus or minus ALC-1 or ALKM1

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126
Q

how do you treat autoimmune hepatitis

A

corticosteroids (prednisolone) and azathioprine
- also have Hep A and Hep B vaccination
transplantation considered as last resort

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127
Q

what is jaundice

A

the yellowing of the skin/eyes due to the accumulation of conjugated or unconjugated bilirubin

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128
Q

what is the normal method of bilirubin metabolism

A

1 Haemoglobin is broken down into haem and globin
2 haem is converted into biliverdin (+ Fe++)
3 biliverdin reductase converts biliverdin to unconjugated biliruben
4 unconjugated bilirubin travels to the liver where its bound to glucuronic acid making conjugated bilirubin
5 this goes into the duodenum and becomes urobilinogen
6 urobilinogen converted into stercobilin (90%)
6 5% of urobilinogen becomes urobilin and excreted in the wee

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129
Q

what is the cause for pre-hepatic jaundice

A

it is when there is high unconjugated bilirubin due to an increased red blood cell breakdown
- haemolytic anaemia
- sickle cell
- C6PDH deficiency
- autoimmune haemolytic anaemia
- thalassemia
- malaria

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130
Q

what are causes for intrahepatic jaundice

A

parenchymal disease
- HCC
- ALD/NAFLD
- hepatitis (viral, autoimmune)
- hepatotoxic drugs (rifampicin)
- Gilberts syndrome
- crigler Nijar syndrome

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131
Q

what is gilbers syndrome

A

a mutation of UGT1A1 gene; causes underreactive UGT enzyme and therefore there is reduced conjugated bilirubin

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132
Q

What is Crigler Najjar syndrome

A

absence of UGT

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133
Q

what are causes of post hepatic jaundice

A

conjugated hyperbilirubinemia due to obstruction
- biliary tree pathology
- choledocholithiasis
- pancreatic cancer
- cholangiocarcinoma
- Mirizzi syndrome
- drug induced cholestasis (ampicillin)
- Autoimmune

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134
Q

what is Mirizzi syndrome

A

rarely gallstones get stuck and can externally compress the common bile duct and cause obstruction

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135
Q

why is there pale stool and dark urine in obstructive jaundice

A

as conjugated bilirubin affects stool and urine, when there is a blockage there is more in the blood and less in the intestine.

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136
Q

is gilberts syndrome more common in men or women

A

young men

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137
Q

What is Courvoisier sign

A

painless jaundice with a palpable gall bladder
- most likely pancreatic cancer

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138
Q

where is the most common site of pancreatic cancer

A

60-70% occurs at the head of the pancreas

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139
Q

what is charcots triad

A

fever
jaundice
Right upper quadrant pain

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140
Q

what are symptoms of cholecystitis

A

fever and right upper quadrant pain

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141
Q

what are features of biliary cholic pain

A

right upper quadrant pain

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142
Q

what are features of ascending cholangitis

A

fever
right upper quadrant pain
jaundice

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143
Q

what is reynolds pentad

A

ascending cholangitis (obstructive)
- fever, right upper quadrant pain, jaundice, confusion, hypotension

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144
Q

what is murphys sign

A

right upper quadrant tenderness; ask patient to take a breath in while pressing the right upper quadrant + cholecystitis

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145
Q

how do you diagnose jaundice

A

bloods and LFTs - bilirubin, albumin, PT/INR, AST, ALT, GGT, ALP, Urine, Bilirubin and urobilinogen
- imaging: first line is ultrasound scan

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146
Q

what are 99% of pancreatic cancer cases

A

adenocarcinoma of the exocrine pancreas, of ductal origin typically affecting the head

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147
Q

where does pancreatic cancer typically affect

A

the head of the pancreas

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148
Q

what are risk factors for developing pancreatic cancer

A

smoking
alcohol
Diabetes mellitus
family history
chronic pancreatitis
genetic predisposition - PRSS-1 mutation

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149
Q

what are the presentations of a pancreatic cancer of the head of the pancreas

A

Courvoisier sign - painless jaundice and palpable gall bladder with pale stoll and dark urine.

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150
Q

what are the presentations of pancreatic cancer of the body or tail of the pancreas

A

epigastric pain radiating to the back which is relieved by sitting forward

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151
Q

how do you diagnose pancreatic cancer

A

pancreatic CT protocol and then a bile duct drainage
- will have ca19-9 tumour marker (not diagnostic but used to monitor the patients)

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152
Q

what is the treatment for pancreatic cancer

A

prognosis is very poor
- surgery and post-operative chemo if there are no Mets
- palliative care otherwise

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153
Q

what is the five year survival for pancreatic cancer

A

3% 5 yr survival

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154
Q

what are primary types of liver cancer

A

hepatocellular carcinoma
cholarigiocarcinoma

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155
Q

what are secondary causes of liver cancer

A

metastasis - GIT, Breast, bronchial

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156
Q

what does hepatocellular carcinoma arise from

A

liver parenchyma

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157
Q

what are risk factors of hepatocellular carcinoma

A

chronic hepatitis virus - C and B
cirrhosis from ALD/NAFLD/haemochromotosis

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158
Q

where does HCC often metastasise to

A

lymph nodes
bones
lungs

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159
Q

what are patient symptoms of HCC

A

signs of decompensated liver failure
- jaundice
- ascites
- hepatic encephalopathy
- irregular hepatomegaly
Signs of cancer
- weight loss
- tired all the time

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160
Q

what are the steps in diagnosing HCC

A

may show an increase in serum AFP
imaging - ultrasound, GS CT for confirmation

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161
Q

why is biopsy often avoided with HCC

A

to prevent seeding of the tumour everywhere

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162
Q

how do you treat HCC

A

surgical resection of the tumour
when decompensated cirrhosis - liver transplant
prevention - HBV vaccination

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163
Q

what does a cholangiocarcinoma arise from

A

it arises from the biliary tree - typically adenocarcinoma

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164
Q

what are risk factors of developing cholangiocarcinoma

A

parasitic flukeworms
biliary cysts
IBD
Primary sclerosing cholangitis

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165
Q

what are symptoms of cholangiocarcinoma

A

abdominal pain
jaundice
weight loss
fevers
puritis
Courvoisier sign

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166
Q

when do symptoms present in cholangiocarcinoma

A

present late as it is a slow growing tumour

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167
Q

how do you diagnose cholangiocarcinoma

A

may show increased CEA and CA19-9
LFT shows increased bilirubin and ALP
ERCP is used to image the biliary tree
biopsy

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168
Q

how do you treat cholangiocarcinoma

A

Operation
majority of cases are inoperable as the patients present very late

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169
Q

what are examples of benign primary liver tumours

A

Haemangioma
hepatic adenoma

170
Q

what is seen on infants with haemangioma

A

seen as a strawberry mark on the skin within the first few weeks of life

171
Q

how o you diagnose secondary liver tumours

A

increased serum ALP
Ultrasound
CT/MRI of the chest and abdomen for staging and identifying the primary tumour

172
Q

how do you treat secondary cancer of the liver

A

surgical resection if possible (and of primary cancer)
chemotherapy

173
Q

what are the different types of biliary tract disease

A

gall stones
cholecystitis
ascending cholangitis

174
Q

what are risk factors for biliary tract disease

A

Overweight/high BMI
female
over 40
Fertile

175
Q

what are the symptoms of Gallstones

A

right upper quadrant pain “biliary cholic”
constant severe episodes of pain
pain is worse after a fatty meal

176
Q

wha are symptoms of cholecystitis

A

right upper quadrant pain
fever
tender gall bladder
may have referred pain to right shoulder
murphy sign positive

177
Q

at are the symptoms of ascending cholangitis

A

right upper quadrant pain
fever
jaundice
dark urine
pale stool
Charcots triad

178
Q

what is reynolds triad

A

charcots triad plus an altered mental state and hypotension

179
Q

how do you diagnose gallstones

A

abdominal ultrasound

180
Q

how do you treat gall stones

A

elective laparoscopic cholecystectomy if symptomatic
until then
- mild pain = NSAIDS
- severe pain = IM diclofenac
change lifestyle - reduce fatty diet

181
Q

how do you diagnose cholecystitis

A

FBC - leukocytosis and neutrophilia
LFT (normal)
Abdominal ultrasound - thickened gall bladder wall

182
Q

how do you diagnose ascending cholangitis

A

FBC - leukocytosis and neutrophilia
LFT - increased conjugated hyperbilirubinaemia
Abdominal ultrasound - CBD dilation and gallstones
MRCP - diagnostic and best pre-intervention management

183
Q

how do you treat cholangitis

A

surgery done within 1 WEEK (MUST by NICE) - laproscopic cholecystectomy
till then put on IV fluid, analgesia and antibiotics if necessary

184
Q

how do you treat ascending cholangitis

A

ERCP (bile duct clearance) and then a laparoscopic cholecystectomy one stable to prevent recurrence
- consider the risk of stenosis

185
Q

what is a MRCP

A

magnetic resonance cholangic pancreatography - magnetic resonance imaging (MRI) exam that produces detailed images of the hepatobiliary system

186
Q

what is ERCP

A

endoscopic retrograde cholangic- pancreatography

187
Q

What is primary biliary cirrhosis

A

intrahepatic autoimmune jaundice, affecting the intralobular bile ducts

188
Q

what are the risk factors of primary biliary cirrhosis

A

female
40-50 year olds
other autoimmune diseases
smoking

189
Q

what is the pathophysiology of primary biliary cirrhosis

A

autoantibodies cause intralobular bile duct damage: chronic autoimmune granulomatous inflammation
this results in cholestasis leading to fibrosis, cirrhosis, portal hypertension and infection

190
Q

what are the symptoms of primary biliary cirrhosis

A

it is initially often asymptomatic
the earliest symptoms are pruritis and fatigue
jaundice
hepatomegaly
xanthelasma - yellow growths on or near eyelids

191
Q

what are the complications of primary biliary cirrhosis

A

cirrhosis
malabsorption of fats and vitamins A, D, E and K
osteomalacia
coagulopathy

192
Q

how do you diagnose primary biliary cirrhosis

A

LFT - increase ALP, conjugated bilirubin and decreased albumin
rule out acute hepatitis in bloods
serology - 95% have AMA antibodies
ultrasound
liver biopsy - portal tract infiltrate and fibrosis

193
Q

what is the treatment of primary biliary cirrhosis

A

1st line = Ursdeoxycholic acid - bile acid analogue (life long)
for pruritis = cholestyramine
vitamin ADE and K supplements
may need liver transplant

194
Q

what is primary sclerossing cholangitis

A

chronic liver disease in which the bile ducts inside and outside the liver become inflamed and scarred, and eventually narrowed or blocked. When this happens, bile builds up in the liver and causes further liver damage.

195
Q

what are the risk factors for primary sclerosing cholangitis

A

male
40-50
strong link to IBD especially UC

196
Q

what are the symptoms of primary sclerosing cholangitis

A

initially asymptomatic
then pruritis and fatigue
charcot triad
hepatosplenomegaly
IBD

197
Q

how do you diagnose primary sclerosing cholangitis

A

LFT
Serology - HBVsAg/HCVAb negative, ANA negative, pANCA positive in some cases
GS imaging - MRCP

198
Q

how do you treat primary sclerosing cholangitis

A

conservative symptom management
- cholestyramine for puritis
- fat soluble A, D, E, K vitamin supplements
- consider liver transplant

199
Q

what other autoimmune conditions is PBC associated with

A

sjorgens
SLE

200
Q

what is acute pancreatitis

A

acute inflammation of the pancreatic gland

201
Q

what are reasons for acute pancreatitis

A

Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom or spider bite
hypercalcaemia or hyperlipidaemia
ERCP
drugs - azathioprine, NSAIDs, ACE -i

202
Q

what is the most common reason for acute pancreatitis

A

gall stones

203
Q

what is the most common reason for chronic pancreatitis

A

ethanol

204
Q

what causes autoimmune pancreatitis

A

an increase in serum IgG4 - autoimmune destruction of pancreas

205
Q

how do you treat autoimmune pancreatitis

A

oral prednisolone for 4-6 weeks

206
Q

what is the pathology of acute pancreatitis

A

gallstones obstruct pancreatic secretions and therefore there are accumulated digestive enzymes in the pancreas. This causes host defences to be overwhelmed and leads to autodigestion (inflammation and enzymes leak into the blood)

207
Q

what are the symptoms of acute pancreatitis

A

sudden severe epigastric pain radiating to the back
jaundice
pyrexia
steatorrhoea
grey turner sign - flank bleeding
cullen sign - periumbilical bleeding

208
Q

how do you diagnose acute pancreatitis

A

bloods - increased serum amylase and lipase
exclude gastroduodenal perforation
ultrasound to diagnose gall gallstones
CT and MRI = extent of damage

209
Q

for a diagnosis to be made of acute pancreatitis what must be present

A
  1. characteristic symptoms and signs
  2. increased amylase and lipase
  3. radiological evidence
210
Q

what are the two pancreatic scoring systems

A
  1. APACHE 2 - assesses severity within 24hours
  2. Glasgow and Rouson score - prediction of severe attack after 48 Hrs
211
Q

how do you treat acute emergency pancreatitis

A

IV fluid
NU by mouth
Analgesia (morphine)
Catheterize
antibiotic prophylaxis

212
Q

what are complications of acute emergency pancreatitis

A

systemic inflammatory response syndrome
- tachycardia
- tachypnoea
- pyrexia
- increased white cell count

213
Q

what is chronic pancreatitis

A

three month history or pancreatic deterioration: irreversible pancreatic inflammation and fibrosis

214
Q

what are the main causes of chronic pancreatitis

A

alcohol, chronic kidney disease, cystic fibrosis, trauma, recurrent acute pancreatitis

215
Q

what are symptoms of chronic pancreatitis

A

epigastric pain radiating to the back which is exacerbated by alcohol

216
Q

How do you diagnose chronic pancreatitis

A

bloods - lipase and amylase unlikely to be raised in severe cases
fecal elastase - typically increased
Abdominal ultrasound and CCT - detects calcification and dilated pancreatic duct

217
Q

how do you treat chronic pancreatitis

A

mainly alcohol cessation
NSAIDs for abdominal pain
Pancreatic supplements - enzymes and insulin

218
Q

what is portal hypertension

A

complications of cirrhosis
pathology increases pressure in the portal vein

219
Q

what are the three types of portal hypertension

A
  1. prehepatic
  2. intrahepatic
  3. post hepatic
220
Q

what are reasons of pre hepatic portal hpertension

A

portal vein thrombosis

221
Q

what causes intrahepatic portal hypertension

A

cirrhosis
Schistosomiasis - worms

222
Q

what are causes of post hepatic portal hypertension

A

Budd chiari (hepatic vein obstruction)
RHS heart failure
constrictive pericarditis

223
Q

what is the pathophysiology of portal hypertension

A

the normal pressure is between 5-8mmHg in the portal vein. Cirrhosis causes an increased resistance to flow and therefore splanchnic dilation and compensatory increase in cardiac output. this results in fluid overload in the portal vein
- leads to collateral blood shunting to gastroesophageal veins

224
Q

what are the symptoms of portal hypertension

A

mostly asymptomatic
present when there is rupture of oesophageal varices

225
Q

what are oesophageal varices

A

Oesophageal varices are extremely dilated sub-mucosal veins in the lower third of the esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis.

226
Q

how do you diagnose oesophageal varices

A

an oesophagogastroduodenoscopy

227
Q

How do you treat oesophageal varices

A

Acutely - resus until haemodynamically stable and consider blood transfusion
Stop the bleed - IV terlupressin, variceal banding and TiPPS
Prevent bleeding - non selective beta blocker and nitrates
Last resort is a liver transplant

228
Q

What is TiPPS

A

A transjugular intrahepatic partosystemic shunt - it decreases portal pressure by diverting blood to other larger veins

229
Q

what are ascites

A

accumulated free fluid in the abdominal cavity

230
Q

what is ascites a complication of

A

cirrhosis

231
Q

what are causes of ascites

A

local inflammation - peritonitis, TB, abdominal cancer
low protein - nephrotic syndrome, hypoalbuminemia
flow stasis - cirrhosis, Budd chiari, congestive heart failure, constrictive pericarditis

232
Q

what are symptoms of ascites

A

abdominal distension
shifting or dullness in flanks
may have jaundice and puritis
can have painful distension

233
Q

how would you examine a patient with suspected ascites

A
  1. tap on their central abdomen when supine (resonant)
    Tap on their flanks and this will sound dull due to the fluid
  2. ask the patient to lay on their side and tap the flank: resonant as the fluid will have moved to the other side
234
Q

how do you diagnose ascites

A

shifting dullness on exam
Ascitic tap
1. cytology, look at white blood cell counts
2. protein measurement

235
Q

what proteins are you measuring in ascites diagnosis

A

Transudate proteins - fluid found here due to increased hydrostatic pressure
Exudate proteins - fluid due to inflammation mediated exudation

236
Q

what causes transudate fluid to accumulate

A

portal hypertension, Budd Chiari, Constrictive pericarditis, chronic heart failure, nephrotic syndrome

237
Q

what causes exudate fluid to accumulate

A

malignancy, peritonitis, pancreatitis

238
Q

how do you treat ascites

A

treat the underlying cause
diuretic to increase fluid excretion = spironolactone
Paracentesis
Liver transplant

239
Q

what is peritonitis

A

an inflamed peritoneal cavity

240
Q

Where does nerves T5-9 give sensation to in the gut

A

Epigastric - the greater splanchnic nerve
supplies foregut up to the second part of the duodenum

241
Q

where does nerves T10-11 give sensation to in the gut

A

umbilical - lesser splanchnic nerve
supplies the midgut up to 2/3 of the transverse colon

242
Q

what does nerve T12 give sensation to in the gut

A

hypogastric region - lesser splanchnic nerve
supplies the hindgut up to the rectum

243
Q

what are primary causes for peritonitis

A

ascites
SBP (infection)

244
Q

what are secondary reasons for peritonitis

A

underlying cause i.e bile or malignancy

245
Q

what are bacterial causes for peritonitis

A

Gram negative = E.coli and klebsiella
Gram positive = Staphylococcus aureus

246
Q

what are symptoms of pericarditis

A

sudden onset of severe abdominal pain
collapse and septic shock, fever
pain is poorly localised at first and then it becomes well localised as it becomes more inflamed

247
Q

how can you help the pain in pericarditis

A

rigidity helps with the pain
- guarding, resting hands on the abdomen to stop it moving

248
Q

how do you diagnose ascites

A

Ascitic tap shows neutrophillia and cultures will show causative organism
increased EST and CRP
exclude pregnancy as a cause
exclude bowel obstruction as a cause
erect CXR will show air under diaphragm

249
Q

how do you treat ascites

A

ABCDE
treat the underlying cause: IV fluid and antibiotics
Surgery - peritoneal lavage - clearing out of peritoneum

250
Q

what are complications of ascites

A

septicemia if not treated early
subphrenic or pelvic abscesses
paralytic ileus

251
Q

what is haemochromotosis

A

it is a mutation of the HFE gene which results in excess body iron

252
Q

what are risk factors for haemochromotosis

A

males
women after menopause
over 50

253
Q

what is the pathophysiology of haemochromotosis

A

excess iron is taken up by transferrin-1 and there is reduced hepcidin synthesis (protein that regulated iron homeostasis) which causes iron accumulation. This normally accumulates in liver, pancreas, kidney, heart, skin and anterior pituitary and damages the organ

254
Q

what are the symptoms of haemocromotisis

A

fatigue
joint pain
hypogonadism (due to anterior pituitary damage)
slate grey skin
liver cirrhosis
osteroperosis
heart failure

255
Q

what is the gross Fe overload triad

A

bronze statue skin
hepatomegaly
type 2 diabetes

256
Q

how do you diagnose haemochromotosis

A

Fe studies - increased serum iron and ferritin, increased transferrin saturation and decreased TIBC
Genetic tests - HFE
Liver biopsy - assess extent of liver damage

257
Q

what is the treatment for haemochromotosis

A

Venesection - regularly removing blood
if contraindicated use desfernoxamine
change lifestyle and have a low iron diet

258
Q

what is wilsons disease

A

an a recessive mutation of ATP78 gene which causes an excess of copper

259
Q

what is the pathophysiology of Wilsons disease

A

impaired copper biliary secretion and normal transport bound to calculoplasmin which means there is an increased calcium accumulation in the liver and the CNS

260
Q

what are the symptoms of Wilsons disease

A

Hepatic - liver disease
Neurological - parkinsonism, memory issues
opthalmological - Kayser fleischer rings (green brown ringed appearance in cornea)

261
Q

how do you diagnose Wilsons disease

A

calcium tests = reduced serum calcium as more is deposited
liver biopsy = increased calcium and liver damage
MRI brain = cerebellar and basal ganglia degeneration

262
Q

what is the treatment for Wilsons disease

A

1st line = D-Penicillinamine (lifelong)
change in the diet to avoid high copper foods such as shellfish
a severe and last resort is liver transplant

263
Q

what is AIAT deficiency

A

an auto recessive mutation of the protease inhibitor gene (Serpina-1 gene) causing a deficiency of alpha 1 antitrypsin enzyme.

264
Q

what is the pathophysiology of AIAT deficiency

A

AIAT normally inhibits neutrophil elastase (which degrades elastic tissue). With a deficiency in AIAT it means there is an increase in neutrophil elastase. This is devastating for the lungs and liver

265
Q

what is neutrophil elastase

A

Neutrophil elastase is secreted by neutrophils during inflammation, and destroys bacteria and host tissue

266
Q

what does AIAT deficiency do to the lungs

A

an increase in neutrophil elastase degrades elastic tissue causing alveolar duct collapse and air trapping - panacinar emphysema

267
Q

what does AIAT deficiency do to the liver

A

the liver becomes fibrotic due to neutrophil elastase, leading to cirrhosis and hepatocellular carcinoma risk.

268
Q

where is AIAT normally made

A

in the liver

269
Q

what are the symptoms of AIAT deficiency

A

COPD like symptoms
dyspnoea
chronic cough
sputum production
barrel chest
jaundice

270
Q

how do you diagnose AIAT deficiency

A

serum AIAT is severely decreased (<20mmol/L)
barrel chest on exam
CXR will show hyperinflated lungs
panacinar emphysema on CT
LTF shows signs of obstruction
Genetic tests

271
Q

what is the treatment for AIAT deficiency

A

there is no curative treatment
stop smoking
manage emphysema - inhalers
consider hepatic decompensation patients for liver transplant

272
Q

how much paracetamol needs to be taken for it to be overdose

A

over 75mg per KG

273
Q

what are symptoms of liver failure

A

acute
severe right upper quadrant pain
severe nausea and vomiting

274
Q

What happens in normal paracetamol metabolism

A

90% of paracetamol undergoes phase 2 conjugation (glucuronidation) and is excreted
10% of paracetamol undergoes phase 1 conjugation and forms NAPQ1 and then undergoes phase 2 conjugation and is excreted

275
Q

what happens in paracetamol overdose to cause liver damage

A

the phase 2 pathway is saturated and therefore there is shunting down the phase 1 pathway. this means that there is accumulation of the toxic NAPQ1 in the liver

276
Q

what is the treatment for a paracetamol overdose

A

give activated charcoal within 1 hours of the paracetamol ingestion
N-acetyl-cysteine - increases availability of the phase 2 pathway

277
Q

What is Gliberts syndrome

A

An autosomal recessive mutation which causes hereditary jaundice

278
Q

what is the pathophysiology of Gilberts syndrome

A

You have an abnormal or deficient UGT therefore you have an increase in unconjugated bilirubin leading to unconjugated hyperbilirubinemia

279
Q

what are the symptoms of Gilberts syndrome

A

30% of cases are asymptomatic may present with a painless jaundice

280
Q

What is Gilberts + cirgler najjar

A

More severe
Jaundice with nausea and vomiting, lethargy

281
Q

How do you treat gilberts syndrome

A

Gilberts - most people are fine without treatment
Crigler Najjar - phototherapy as wit breaks down bilirubin

282
Q

What can people with Grigler Najjar die of

A

Can die of Kernicterus in childhood
- this is where you get an accumulation of bilirubin in the basal ganglia causing neurological defects

283
Q

what is hernia

A

it is the protrusion of an organ through a defect in its containing cavity

284
Q

What is the most common type of hernia

A

bowel

285
Q

what are the two types of hernias

A

Reducible
Irreducible

286
Q

What is a reducible hernia

A

One that can be pushed back into place

287
Q

What is a irreducible hernia

A

one that is
- obstructed
- strangled (ischema)
- incarcerated (contents are fixed)

288
Q

What is a hiatal hernia

A

it is where the stomach herniates through the diaphragm aperture

289
Q

What are the two types of hiatal hernia

A

Rolling and sliding

290
Q

what is a rolling hiatal hernia

A

the LES stays in the abdomen and part of the fundus rolls into the abdomen

291
Q

what is a sliding hiatal hernia

A

the LES slides into the abdomen

292
Q

what are the symptoms of a Hiatal hernia

A

GORD
dysphagia

293
Q

How do you diagnose a hiatal hernia

A

chest X ray
Barium swallow
OGD

294
Q

what is a femoral hernia

A

it is when the bowel moves through the femoral canal

295
Q

what is a femoral hernia likely to do

A

strangulate the bowel due to the rigid femoral canal boarders

296
Q

What are the symptoms of a femoral hernia

A

swelling in the upper thigh pointing down

297
Q

how do you diagnose a femoral hernia

A

you can ultrasound the abdominal/pelvis

298
Q

what is an inguinal hernia

A

it is when the bowel herniates through the inguinal canal

299
Q

What are the two types of inguinal hernia

A

Direct
Indirect

300
Q

What is a direct inguinal hernia

A

is in Hesselbachs triangle
- Medial to inferior epigastrics

301
Q

What is an indirect inguinal hernia

A

it is lateral to the inferior epigastrics

302
Q

what are the risk factors of an inguinal hernia

A

male
history of heavy lifting or abdominal pressure

303
Q

What are symptoms of a inguinal hernia

A

painful swelling in the groin, which points along the groin margin

304
Q

how do you diagnose an inguinal hernia

A

if you are clinically unsure you can perform an abdominal ultrasound or CT

305
Q

How do you treat hernia

A

SURGERY

306
Q

What is an acute on chronic liver failure

A

when there is an abrupt decline in a patient with chronic liver symptoms

307
Q

What are the blood investigations for liver failure

A

FBC - Infection, bleed, MCV
U&Es - low urea,high creatinine
LFTs - AST:ALT ratio, albumin, PT
Clotting
Glucose
ABG - acidosis
Ferritin
paracetamol levels

308
Q

What AST:ALT ratio is seen in alcoholic liver disease

A

AST:ALT >2

309
Q

What AST:ALT ratio is seen in viral liver disease

A

AST:ALT <1

310
Q

What microbiology investigations for liver failure

A

Hepatitis, CMV, EBV and serology
Ascites MCS and SAAG

311
Q

What are radiological investigations for liver failure

A

Chest X ray
Abdominal ultrasound
Portal vein duplex

312
Q

What are complications of liver failure

A

Bleeding
Hepatorenal syndrome
Sepsis
Ascites
Hypoglycaemia
Encephalopathy
Seizures
Cerebral oedema

313
Q

what is biliary colic

A

It is where you have sudden pain due to gallstone blockage - cystic obstruction or passing into the common bile duct

314
Q

what is the pathophysiology of biliary colic

A

There is gallbladder spasm against a stone in the neck of the gallbladder

315
Q

What are the risk factors of biliary colic

A

Family history
Female
Over forty
Overweight
Fertile

316
Q

What are the symptoms of biliary colic

A

Right upper quadrant pain radiating to back
Sweating, pallor, nausea and vomiting
May be precipitated with fatty food
right tender hypochondrium
possible jaundice

317
Q

What are the differential diagnoses of biliary colic

A

Cholecystitis or other gall stone disease
pancreatitis
bowel perforation

318
Q

What is the management of biliary colic

A

Rehydrate by mouth
Opioid analgesia - morphine 5-10mg
Laparoscopic cholecystectomy

319
Q

what are complications of biliary colic

A

Mirizzi syndrome
Gallbladder empyema
Chronic cholecystitis
Bouveret’s syndrome
Gallstone ileus

320
Q

What urine tests should be done with suspected biliary colic

A

Bilirubin
Urobilirubin
Haemoglobin

321
Q

What blood tests should be done with suspected biliary colic

A

FBC
U&Es
Amylase
LFTs
Clotting
CRP

322
Q

What imaging tests should be done with suspected biliary colic

A

AXR - 10% of gallstones are radio-opaque
Erect CXR
Ultrasound - stones, ducts and inflammation

323
Q

What test should be ordered when diagnosis of biliary colic is uncertain after an ultrasound

A

HIDA cholescintigraphy - shows failure of gallbladder filling

324
Q

If dilated ducts are seen on ultrasound of suspected biliary colic + can’t see gallstones, what test should be ordered?

A

Magnetic resonance cholangiopancreatography (MRCP)

325
Q

what is acute cholecystitis

A

Inflammation of the gall bladder which occurs over hours

326
Q

what is the pathogenesis of acute cholecystitis

A

Sludge or stone in Hartmanns pouch leads to chemical or bacterial inflammation of the gall bladder

327
Q

What can cause acute cholecystitis

A

Gallstones
tumour
Bile duct blockage
Infection
Blood vessel problems

328
Q

What is muphys sign

A

2 fingers over the gall bladder, ask patient to breathe in
Pain and breath catch - inflammation
Must be negative on left hand side

329
Q

What is Boa’s sign

A

Hyperaesthesia below right scapula

330
Q

what urine tests are done for acute cholecystitis

A

Bilirubin
Urobilinogen

331
Q

what blood tests are done for acute cholecystitis

A

FBC
High white cell count
U&Es
Dehydration from vomiting
Amylase
LFTs
Group and save
Clotting
CRP

332
Q

what are the imaging test for acute cholecystitis

A

AXR
Erect CXR
US

333
Q

What test is ordered if diagnosis of acute cholecystitis is uncertain after ultrasound?

A

HIDA cholescintigraphy

334
Q

What test is ordered if dilated bile ducts are found on ultrasound in suspected acute cholecystitis?

A

MRCP (magnetic resonance cholangiopancreatography)

335
Q

What are the differential diagnoses for acute cholecystitis?

A

Peptic ulcer disease
Liver disease
Pancreatitis
Cardiac disease

336
Q

What analgesia is given for acute cholecystitis?

A

Paracetamol
Diclofenac
Codeine

337
Q

What are the complications of acute cholecystitis?

A

Gangrene
Rarely perforation
Chronic cholecystitis
Empyema

338
Q

what are the symptoms of chronic cholecystitis

A

‘flatulent dyspepsia’
Vague upper abdominal discomfort
Nausea
Distension, bloating
Flatulence/burping

339
Q

what exacerbates the symptoms of chronic cholecystitis

A

fatty foods

340
Q

what investigations are done for chronic cholecystitis

A

AXR
US
Magnetic resonance cholangiopancreatography

341
Q

What are the differential diagnoses of chronic cholecystitis?

A

Peptic ulcer disease
IBS
Hiatus hernia
Chronic pancreatitis

342
Q

What is the management of chronic cholecystitis?

A

Bile salts - not great Elective cholecystectomy
ERCP (Endoscopic retrograde cholangiopancreatography) if ultrasound shows distended ducts and stones

343
Q

what is the general composition of gallstones

A

phospholipids
bile pigments
cholesterol

344
Q

what are characteristics of pigment stones

A

Small, black, gritty, fragile
Calcium bilirubinate
Associated with haemolysis

345
Q

what are characteristics of cholesterol stones

A

Often solitary
Large

346
Q

What is Admirand’s triangle

A

low bile salts
low lecithin
high cholesterol

347
Q

what are causes of gallstones

A

Lithogenic bile
biliary sepsis
gall bladder hypomotility
pregnancy/oestrogen contraceptive pill
total parenteral nutrition or fasting

348
Q

what can be done to confirm gallstones

A

Murphy’s sign
ultrasound scan

349
Q

Why might you order a cholangiography and CT for gallstones

A
  1. To assess the condition of the gallbladder
  2. Look for complications of gallstones
350
Q

what is the differential diagnosis for gallstones

A

Mirizzi syndrome
Gallbladder empyema
Chronic cholecystitis
Bouveret’s Syndrome
Gallstone Ileus

351
Q

what are the complications of gallstones in the gallbladder

A

Biliary colic
Acute cholecystitis +- empyema
Chronic cholecystitis
Mucocele
Carcinoma
Mirizzi’s syndrome

352
Q

what are the complications of gallstones in the common bile duct

A

Obstructive jaundice
Pancreatitis
Cholangitis

353
Q

What are the complications of gallstones in the gut?

A

Gallstone ileus

354
Q

what is the pathophysiology of ascending cholangitis

A

There is common bile duct obstruction which causes bacterial seeding of the biliary tree
- sludge formation creates a growth medium for bacteria

355
Q

what causes ascending cholangitis

A

Gallstones
Iatrogenic - ERCP
Cholangiocarcinoma
Ascending infection from duodenum junction

356
Q

what are risk factors for ascending cholangitis

A

Gallstones
Sclerosing cholangitis
HIV
Narrowing of common bile duct

357
Q

What are the differential diagnosis for ascending cholangitis

A

Acute cholecystitis
Peptic ulcer disease
Acute pancreatitis
Hepatic absess
Acute pyelonephritis
Acute appendicitis
Right lower lobe pneumonia
HELLP syndrome of pre-eclampsia

358
Q

what are the complications of ascending cholangitis

A

Acute pancreatitis
Hepatic abscess

359
Q

What blood tests are performed in suspected acute pancreatitis?

A

FBC - High WCC
Amylase and lipase - high
U&Es - dehydration and renal failure
LFTs - cholestatic picture (high AST and LDH)
Low calcium
High glucose
CRP raised in severe
ABG - low O2 suggests ARDS

360
Q

what urine tests are performed in suspected acute pancreatitis

A

glucose
high conjugated bilirubin
low urobilinogen

361
Q

what are the signs associated with acute pancreatitis

A

High heart and respiratory rate
Fever
Hypovolaemia - shock
Epigastric tenderness
Jaundice
Ileus (absent bowel sounds)
Ecchymoses (discolouration of skin due to bleeding underneath it)
Grey Turners: flank
Cullens: periumbilical

362
Q

what is the differential diagnosis for acute pancreatitis

A

Perforated duodenal ulcer
Mesenteric infarction
Myocardial infarction

363
Q

what is the Glasgow criteria in assessing acute pancreatitis severity

A

PaO2
Age
Neutrophils
Ca2+
renal function
enzymes
Albumin
Sugar

364
Q

what are the complications of acute pancreatitis

A

ARDS - O2
Hyperglycaemia - insulin
Alcohol withdrawal - chlordiazepoxide

365
Q

What are the indications for surgical management of acute pancreatitis?

A

Infected pancreatic necrosis
Pseudocyst/abscess
Unsure diagnosis

366
Q

what are the possible early complications of acute pancreatitis

A

Systemic:
-Resp
-ARDS
-Pleural effusion
Shock
-Hypovolaemic
-Septic
Renal failure
Disseminated intravascular coagulation
Metabolic
-Hypocalcaemia
-Hyperglycaemia
Metabolic acidosis

367
Q

What are the possible late complications of acute pancreatitis?

A

Pancreatic necrosis
Pancreatic infection
Pancreatic abscess
Bleeding
Thrombosis
Fistula formation
Pancreatic pseudocyst

368
Q

what is the pathophysiology of chronic pancreatitis

A

Progressive loss of lobular morphology and structure of pancreas due to necrosis/apoptosis, inflammation and/or duct obstruction

Deformation of the large ducts and severe changes in arrangement and composition of islets

Irreversible morphological and structure changes - impair exocrine and endocrine functions

369
Q

What are the characteristics of pain in chronic pancreatitis?

A

Bores through the back

Relieved by sitting forward or hot water bottle (erythema ab igne - hot water bottle rash)

Exacerbated by fatty foods/alcohol

370
Q

what are signs of chronic pancreatitis

A

Hyperglycaemia
Low faecal elastase (low exocrine function)
Pseudocyst in US
Speckled pancreatic calcification (AXR)
Pancreatic calcifications (CT)

371
Q

what are the differential diagnosis for chronic pancreatitis

A

Peptic ulcer disease
Reflux disease
Abdominal aortic aneurysm
Biliary colic
Chronic mesenteric ischaemia

372
Q

what is the indication for surgery in chronic pancreatitis

A

Unremitting pain
Weight loss
Duct blockage

373
Q

what is the surgical management of chronic pancreatitis

A

Distal pancreatectomy (Whipple’s)
Pancreaticojejunostomy (drainage)
Endoscopic stenting

374
Q

what are the complications of chronic pancreatitis

A

Pseudocyst
Diabetes mellitus
Pancreatic calcification
Pancreatic swelling (?cause duct obstruction)
Splenic vein thrombosis - splenomegaly

375
Q

what is fatty liver

A

build-up of fat within liver cells

376
Q

what is the pathophysiology of cirrhosis

A

Stellate cells are activated - major source of extracellular matrix

Accumulation of collagen in hepatic parenchyma and space of Disse

Space of Disse collagen accumulation called capillarisation of sinusoids - fenestration lost affection exchange

Activated stellate cells more contractile, increased portal resistance

Progressive process

377
Q

what are common causes of cirrhosis

A

Chronic alcohol
Chronic hepatitis C (and hepatitis B)
Non-alcoholic fatty liver disease/non alcoholic steatohepatitis

378
Q

what are symptoms of cirrhosis

A

Fatigue
Nausea
Anorexia
Weight loss
Jaundice
Haematemesis
Puritis
Dark pee and tarry-looking poo
Bleeding or bruising easily
Oedema
Low libido

379
Q

where can venous collaterals occur in portal hypertension

A

gastro-oesopageal junction
anterior abdominal wall
anorectal junction
veins from retroperitoneal viscera

380
Q

What is the sequelae of portal hypertension?

A

SAVE:
Splenomegaly
Ascites
Varices
Encephalopathy

381
Q

what are risk factors of portal hypertension

A

cirrhosis
congestive heart failure
arteriovenous malformations
hypercoagulable states

382
Q

What are the signs and symptoms of portal hypertension?

A

Ascites
Hepatic encephalopathy
Variceal bleeding
Splenomegaly
Associated with cirrhosis means liver failure symptoms may also be observed

383
Q

What investigations are ordered for patients with suspected portal hypertension?

A

Scans
Abdo US - dilated portal vein
Doppler US - slow velocity + dilated portal vein
Endoscopy - presence of oesophageal varices

384
Q

What is the management of portal hypertension?

A

Treat underlying cause
Salt reduction and diuretics
Beta-blockers and nitrate to reduce blood pressure

385
Q

what is the clinical presentation of oesophageal varices

A

Signs of chronic liver damage
Splenomegaly
Ascites
Hyponatraemia

386
Q

What is the clinical presentation of oesophageal varices if ruptured?

A

Haematemesis
Abdo pain
Shock
Fresh rectal bleeding
Hypotension and tachycardia
Pallor

387
Q

what are the differential diagnosis of oesophageal varices

A

Hiatal hernia
Gastric varices
Mallory-Weiss tear
PUD (peptic ulcer disease)
Gastric antral vascular ectasia

388
Q

What is transjugular intrahepatic portoclaval shunt (TIPS)?

A

Shunt between systemic and portal systems
Reduces sinusoial and portal vein pressures
Only used when variceal bleeding cannot be controlled acutely, or rebleeds

389
Q

what is the pathophysiology of alcoholic hepatitis

A

Liver main site of alcohol metabolism - main site of injury due to excessive drinking

Widespread hepatic lesions (steatosis, hepatitis, cirrhosis)

Malnutrition - protein-energy malnutrition (calories obtained from alcohol not food)

Alcohol induces hypermetabolic state in hepatocytes, leading to hypoxic damage

Direct damage from metabolites (free radicals and oxidative injury)

390
Q

what are risk factors for alcoholic hepatitis

A

female
obesity
genetics
ethnicity
binge drinking

391
Q

what is the management for alcoholic hepatitis

A

stop alcohol and treat withdrawal
high dose B vitamins
optimize nutrition
manage complications

392
Q

what is the monitoring of alcoholic hepatitis

A

Daily
- weight
- LFTs
- U&Es
- INR

393
Q

what hepatic signs are associated with the icteric phase of viral hepatitis

A

abdominal pain
hepatomegaly
cholestasis - dark urine/pale stools

394
Q

what are extrahepatic features of the icteric phase of viral hepatitis

A

Urticaria or vasculitic rash
cryoglobulinemia
polyarteritis nodosa
glomerulonephritis
arthritis

395
Q

what is type 3 autoimmune hepatitis

A

there is soluble liver antigen antibodies present, (antismooth muscle and antinuclear antibody negative)

396
Q

what are associated conditions of autoimmune hepatitis

A

Pernicious anaemia
Ulcerative colitis
Glomerulonephritis
Autoimmune thryoiditis
Autoimmune haemolysis
Diabetes mellitus
Primary biliary cirrhosis

397
Q

What investigations are ordered in suspected autoimmune hepatitis?

A

LFTs (raised)
IgG (raised)
Auto antibodies: SMA, LKM1, SLA, ANA
Low WCC and plateles (hypersplenisnm)
Liver biopsy

398
Q

What is the pathophysiology of pseudomembranous colitis?

A

C. diff replaces normal gut flora, aided by the use of antibiotics

Release of C. diff toxins causes necrosis and formation of pseudomembranes

399
Q

What are the viral causes of infective diarrhoea?

A

Rotovirus (children)
Norovirus (adults)
Adenovirus
Astrovirus

400
Q

what are the bacterial causes of infective diarrhoea

A

Campylobacter jejuni (poultry)
E. coli (children)
Salmonella (children)
Shigella spp (children)

401
Q

what are parasitic causes of infectious diarrhoea

A

Giardia lamblia
Entamoeba histolytia
Cryptosporidium

402
Q

what are antibiotic associated causes of infectious diarrhoea

A

(start with C) - antibiotic induced C. diff
Clindamycin
Ciprofloxacin (quinolones)
Co-amoxiclav (penicillins)
Cephalosporins

403
Q

what are risk factors for infective diarrhoea

A

Foreign travel
PPI or H2 antagonist use
Crowded area
Poor hygiene

404
Q

What are the risk factors for pseudomembranous colitis?

A

Elderly
Antibiotics
Long hospital admission
Immunocompromised (i.e. HIV)
Acid suppression (PPIs H2 antags etc)

405
Q

what are the clinical presentations of infective diarrhoea

A

diarrhoea - if bloody likely bacterial
vomiting
abdominal cramping
fever, fatigue, headache, myalgia

406
Q

what are the investigations ordered in infective diarrhoea

A

Bloods - look at MCV, iron and WCC
Stool culture
Sigmoidoscopy with biopsy

407
Q

What are the differential diagnosis for infective diarrhoea

A

Appendicitis
Volvulus
IBD
UTI
Diabetes mellitus
Pancreatic insufficiency
Short bowel syndrome
Coeliac disease
Laxative abuse

408
Q

how is pseudomembranous colitis treated

A

Antibiotics
Stool transplant
Stop C antibiotic

409
Q

what is the treatment for infective diarrhoea

A

Treat underlying causs
Oral rehydration and avoid sugary drinks
Anti-emetics (metoclopramide)
Antibiotics
Anti-motility agents (loperamide hydrochloride)

410
Q

what are the side effects of penicillamine

A

Skin rashes
fall in white blood cell, Hb and platelets
Haematuria
renal damage

411
Q

what are complications of a-1 antitrypsin deficiency

A

Emphysema
liver cirrhosis
hepatocellular carcinoma

412
Q

what is the pathophysiology of ascites

A

local inflammation - fluid accumulation
low protein
low flow - fluid cant move and raises the pressure in vessels

413
Q

what are the risk factors for ascites

A

high sodium diet
hepatocellular carcinoma
splanchnic vein thrombosis resulting in portal hypertension

414
Q

what are chemical causes of peritonitis

A

bile
old clotted blood
ruptured ectopic pregnancy
intestinal perforation

415
Q

what is an obstructed hernia

A

intestine obstructed due to pressure from edges of the hernia, but the blood flow is maintained

416
Q

what is an incarcerated hernia

A

contents of the hernial sac are stuck inside by adhesions

417
Q

what is a strangulated hernia

A

this is where the blood supply is cut off
Ischemia and gangrene/perforation of the hernial contents

418
Q

what are risk factors of inguinal hernias

A

Male
Chronic cough
Constipation
Urinary obstruction
Heavy lifting
Ascites
Past abdominal surgery

419
Q

what are risk factors for incisional hernias

A

Emergency surgery
Wound infection post op
Persistent coughing/heavy lifting
Poor nutrition

420
Q

what makes repair of incisional hernias more difficult to repair

A

obesity

Phase 2a - Jemima (11 decks)

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