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Year 2 > GI Diseases 2 > Flashcards

GI Diseases 2 Flashcards

1
Q

What are the types of Liver function tests?

A

ALT- Markers of hepatocellular damage, localised to liver

AST- Markers of hepatocellular damage, synthesised by liver, heart, skeletal muscle and brain

Billirubin- Assessing degree of jaundice

gGT- Cholestasis

ALP- Cholestasis – sources are bone and liver

Albumin- Synthetic function

Prothrombin time - Synthetic function

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2
Q

Liver function tests- imaging

A
  • USS- Ultrasound is usually first line. Identifies any obstructive pathology present or gross liver pathology
  • Fibroscan
  • MRI
  • MRCP- Used to visualise the biliary tree. Usually performed if obstructive jaundice is suspected or US is inconclusive
  • X rays – hepatic angiogram
  • CT
  • Biopsy- Performed when the diagnosis has not been made despite the above investigations
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3
Q

What is Jaundice?

A

yellow appearance of the skin, sclerae and mucous membranes resulting from an increased bilirubin concentrations in body fluids

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4
Q

What are the types of jaundice?

A
  • Pre-hepatic
  • Hepatic/ intrahepatic/ hepatocellular
  • Post-hepatic
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5
Q

Pre-hepatic jaundice and also be called?

A

haemolytic jaundice

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6
Q

What is pre hepatic jaundice?

A

Excessive red cell breakdown which overwhelms the liver’s ability to conjugate bilirubin 🡪 unconjugated hyperbilirubinemia

Any bilirubin that manages to become conjugated is excreted normally

Unconjugated bilirubin in the blood causes jaundice

ALT, AST, ALP will be normal

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7
Q

Examples of conditons that can see pre hepatic jaundice?

A
  • Examples
  • Haemolytic anaemia
  • Malaria
  • Sickle cell thalassemia
  • SLE
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8
Q

What is hepatic jaundice?

A
  • Due to dysfunction of the hepatic cells
  • Liver loses the ability to conjugate bilirubin
  • Liver may become cirrhotic 🡪 compromises the intra-hepatic portions of the biliary tree to cause some obstruction
  • Both unconjugated and conjugated bilirubin are found in blood
  • High ALT, AST and ALP (higher ALT&AST)
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9
Q

Examples of conditions where you can hepatic jaundice?

A
  • Alcoholic liver disease
  • Viral hepatitis
  • Primary biliary cirrhosis
  • Hepatocellular carcinoma
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10
Q

What is Post-hepatic jaundice

A
  • AKA obstructive jaundice
  • Due to obstruction of biliary drainage
  • Bilirubin that has been conjugated by the liver is not excreted
  • Excess conjugated bilirubin = conjugated hyperbilirubinemia
  • High ALP, AST and ALT (higher ALP)
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11
Q

What is Acute liver failure?

A

Onset of hepatic decompensation within 6 months, results in loss of function in 80-90%

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12
Q

Causes of Acute Liver failure?

A
  • Drugs

50% of cases in the UK due to paracetamol overdose

others inc NSAIDs and ecstasy

  • Infection

Viral hepatitis, CMV, HSV, EBV

  • Acute fatty liver in pregnancy

Unmetabolized fetal fatty acids enter maternal circulation and accumulate in mothers liver

  • Wilsons disease

AR, copper accumulates in the liver

  • Budd-Chiari

Occlusion of hepatic vein

Abdo pain + ascites + liver enlargement

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13
Q

Clinical features of Acute liver failure?

A
  • Jaundice
  • Bruising (coagulation disturbance)
  • Ascites
  • Tachycardia and hypotension
  • Due to reduced systemic vascular resistance
  • Signs of encephalopathy
  • Sweet smell on breath
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14
Q

Complications of acute liver failure

A
  • Hepatic encephalopathy = altered level of consciousness
  • Impaired protein synthesis = measured by serum albumin + prothrombin time in blood
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15
Q

What is Chronic liver failure

A

Progressive destruction/regeneration of liver parenchyma leading to fibrosis and cirrhosis (> 6 months

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16
Q

Causes of chronic liver failure

A
  • Metabolic

Hereditary haemochromatosis -Accumulation of iron, reacts with H2O2 to form free radicals

NAFLD

Wilsons disease

  • Toxic and drugs

Alcohol

Drug induced is rare 🡪 methotrexate, amiodarone

  • Infections – hep b & c
  • Autoimmune

Primary biliary cholangitis, primary sclerosing cholangitis, autoimmune hepatitis

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17
Q

Clinical features of Chronic liver failure?

A
  • Nail clubbing
  • Palmar erythema
  • Spider nevi
  • Gynaecomastia
  • Feminising hair distribution
  • Small irregular shrunken liver
  • Anaemia
  • Caput medusae
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18
Q

Complications of chronic liver failure?

A
  • Portal hypertension
  • Synthetic dysfunction
  • Hepatopulmonary syndrome
  • Hepatorenal syndrome
  • Encephalopathy
  • Hepatocellular carcinoma
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19
Q

What is portal hypertension?

A
  • Increased blood pressure in the hepatic portal system (portal venous system) usually due to hepatic cirrhosis
  • Obstruction may prevent the blood flow from the portal vein into the IVC
  • Causes the blood to accumulate in the hepatic portal system 🡪 increasing the pressure 🡪 PORTAL HYPERTENSION
  • Portosystemic Shunts- anastomoses between portal and systemic systems, due to portal HTN the blood backs up and varices form- these can rupture
  • Features (ABCDE)- ascites, bleeding, caput medusae, diminished liver function and enlarged spleen
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20
Q

What is hepatic encephalopathy?

A

Reduced blood to liver 🡪 reduced liver function

Increased ammonia crosses BBB

Can be gradual or sudden

In advanced stages 🡪 coma

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21
Q

Clinical features of heaptic encephalopathy

A

Asterixis, lethargy, movement problems, changes in mood or changes in personality, altered consciousness, seizures

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22
Q

What is treatment for hepatic encephalopathy?

A

Treatment = Oral lactulose

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23
Q

What is Hepatopulmonary syndrome

A

Syndrome of shortness of breath and hypoxemia caused by vasodilation in lungs of patients with liver disease

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24
Q

Causes of hepatopulmonary syndrome?

A

Due to formation of microscopic intrapulmonary arteriovenous dilations

Thought to be due to increased liver production or decreased liver clearance of vasodilators, e.g. NO

Dilation of blood vessels 🡪 over-perfusion relative to ventilation 🡪 V/Q mismatch

Increased gradient between the partial pressure of O2 in alveoli and adjacent arteries

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25
Q

What is Hepatorenal syndrome?

A

Life-threatening medical condition that consists of rapid deterioration of kidney function in individuals with cirrhosis or fulminant liver failure

Occurs due to portal hypertension

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26
Q

What is HEpatocellular carcinoma

A

Malignant tumour of the liver which occurs primarily in patients with pre-existing liver cirrhosis or chronic hepatitis

Most common type of primary liver cancer

Malignant tumour of the liver which occurs primarily in patients with pre-existing liver cirrhosis or chronic hepatitis

Most common type of primary liver cancer

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27
Q

What is the adenoma- carcinoma sequence?

A

A stepwise pattern; of mutational activation of oncogenes ( ie Kras) and inactivation of tumour suppressor genes (eg p53) that results in cancer

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28
Q

Environmental factors that leads to GI cancer development

A
  • Smoking
  • Alcohol
  • Diet; processed meat ( especially red meat), increased obesity risk, green vegetables and diet high in fibre protective against colorectal cancer
  • Chronic inflammation ie patients with ulcerative colitis have increased risk of developing colorectal cancer
  • Upper GI cancer; H pylori infection?
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29
Q

Hallmarks of cancer

A
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30
Q

APC KRA and P53

which of these are tumour supressor genes?

A

APC and P53

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31
Q

APC KRas and P53

Which of these are oncgenes?

A

KRas

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32
Q

what is Colorectal cancer development in relation to TSG and Oncogenes

A
  1. Inactiviation of APC
  2. Activation of Kras
  3. Inactivation of p53
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33
Q

what is Colorectal carcinogenisis in IBD development in relation to TSG and Oncogenes?

A

Same genes different order

  1. P53
  2. Kras
  3. APC
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34
Q

Typical upper GI cancer would be

A

Oesophageal cancers

Gastric cancers

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35
Q

Typical lower GI cancer would be

A

colorectal cancers

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36
Q

Colorectal cancer is the __ most commone cancer in the UK

Most occur in the ___

___ most common cause of cancer death in the UK

A

4th

rectum

2nd

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37
Q

Risk factors of colorectal cancer?

A

family history, those that have FAP or HNPCC, diet with lack of fibre, inflammatory bowel disease (ie ulcerative colitis)

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38
Q

What are familial adenomatous polyposis?

A

Classic familial adenomatous polyposis, called FAP or classic FAP, is a genetic condition. It is diagnosed when a person develops more than 100 adenomatous colon polyps. An adenomatous polyp is an area where normal cells that line the inside of a person’s colon form a mass on the inside of the intestinal trac

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39
Q

How are Familial adenomatous polyposis inherited?

A

Autosomal dominant inheritance

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40
Q

How is HNPCC (hereditary non polyposis colon cancer) inhertied?

A

Autosomal dominant inheritance

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41
Q

HNPCC (hereditary non polyposis colon cancer)

Mutations occur where

A

Mutations in the DNA mismatch repair genes (MSH2 (60%)) and MLH1 (30%)), causing microsatellite instability. These genes normally maintain stability of DNA during replication

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42
Q

Difference between HNPCC and FAP

A
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43
Q

RED FLAG symptoms for colorectal cancer?

A
  • Unintentional / unexplained weight loss
  • Rectal bleeding
  • Change in bowel habit
  • Abdominal masses
  • Iron deficiency anaemia
  • In history; ask about family history- family members with ovarian and bowel cancer can be significan
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44
Q

Pathology of Colorectal Cancer

A

Most common : adenocarcinoma ( a malignant tumour formed from glandular structures of the epithelial tissue)

Less common; mucinous adenocarcinoma, signet ring cell carcinoma, small cell carcinoma

Glandular dysplasia is the premalignant lesion, when it forms a poly it is commonly referred to as an adenoma

Adenomas classified as tubular, tubulovillous and villous (the is the worst one)

Adenomas are also graded in terms of dysplasia (low or high)

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45
Q

Staging using TNM for Corectal Cancers

Tumour staging

A
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46
Q

Staging using TNM for Corectal Cancers

Lymph nodes staging

A
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47
Q

Staging using TNM for Corectal Cancers

Metastasis staging

A
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48
Q

If a tumour that invades the muscularis propria, metastasizes to 1-3 lymph nodes but does has no distant metastasis how would you use TNM?

A

T2N1M0

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49
Q

Pathology of gastric cancers?

A
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50
Q

Gastric cancer clinical features

A

Epigastric pain; may be relieved by food and antacids

Dysphagia especially if tumour involves stomach fundus

Anaemia

Nausea, vomiting and weight loss

Can have Liver, bone , brain and lung involvement

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51
Q

What is Zollinger- Ellison syndrome?

A

Zollinger–Ellison syndrome is a disease in which tumours cause the stomach to produce too much acid, resulting in peptic ulcers. A gastrin secreting tumour (gastrinoma) - Excess gastric acid secretion leads to (unusual/severe peptic ulceration, oesophagitis, diarrhoea and

52
Q

WHat are gastrinomas?

A
  • Neuroendocrine tumours
  • Gastrin secreting
  • Cause severe peptic ulcer disease and diarrhoea (referred to as the Zollinger Ellison Syndrome)
  • Can either be sporadic (75-80% of cases) or associated with Multiple endocrine neoplasia type 1 (20-30% of cases)
53
Q

What is acute pancreatitis?

A

Sudden inflammation, haemorrhage of pancreas due to autodigestion from inappropriate activation of zymogen (trypsinogen → trypsin)

Reversible

54
Q

What are the causes of acute pancreatitis?

A

Gallstones - Obstruct sphincter of Oddi causing reflux . Bile salts irritates pancreatic duct

Ethanol - Increases acinar cell secretion, decreases ductal cell secretion → thickened pancreatic juice . ROS damages the cells

Trauma - Usually ruptured duct in the body of the pancreas from direct trauma (vertebral column)

Drugs - sodium valporate, furosemide, thiazides, Azathioprine

55
Q

Investiagtions for acute pancreatitis?

A

Elevated serum amylase >1000 IU/L

Elevated serum lipase (2-5x normal value)

LFTs: gallstones aetiology (jaundice)

Imaging

CT: swollen gland with inflammation, necrosis, pseudocyst

USS: gallstones

56
Q

What is chronic pancreatitis?

A
  • Chronic inflammation causing irreversible structural damage

Atrophy of acinar cells

Fibrosis

Calcification

Dilation of ducts/ narrowing

  • Formation of chronic pseudocysts, intrapancreatic cysts
57
Q

What is pathogenesis of Chronic pancreatitis?

A

Obstruction in the pancreatic ducts

Ductal dilatation and damage to tissue (atrophy of acinar cells)

Stellate cells lay down fibrotic tissue

Further resulting in atrophy of acinar cells, intraluminal calcification, narrowing of ducts

58
Q

Causes of chronic pancreatitis?

A
  • Recurrent episodes of acute pancreatitis (alcohol)
  • Duct obstruction: tumour, gallstones, structural abnormalities (annular pancreas, pancreas divisum), traumatic strictures
  • Cystic fibrosis
59
Q

Investiagtions for chronic pancreatitis?

A

Serum lipase and amylase may or may not be elevated

Glucose tolerance test (endocrine function)

Imaging

CT : calcification, intrapancreatic cysts or chronic pseudocysts

ERCP: dilated and strictured ducts (chain of lakes pattern)

To differentiate from carcinoma

Pancreatic imaging + EUS + targeted needle biopsy

60
Q

Complications of chronic pancreatitis?

A

Increased risk of pancreatic carcinoma

Pancreatic pseudocysts, fistula, ascites

Biliary obstruction

Malnutrition

Diabetes mellitus

61
Q

Risk factors for Pancreatic carcinoma

A

Western lifestyle

Cigarette smoking

High-fat diet

Liver cirrhosis

Chronic pancreatitis

Obesity

Family history/genetic factors (BRCA1/BRCA2/FAP/HNPCC)

62
Q

Name some congenital anomalies

A

Hirschprung’s Disease

Meckel’s Diverticulum

Omphalocele

Gastroschisis

63
Q

What is Hirschprung’s Disease

A

Agangliosis of myenteric and submucosal plexus in the distal colon and rectum which causes lack of peristalsis

Functional obstruction from spasms in denervated colon

Severe constipation within first 2 months

Investigations

X ray: colon distension

Biopsy to identify transition zone

Management: surgical removal of affected segment

64
Q

What is Meckel’s Diverticulum?

A

Persistence of vitellointestinal duct

Rule of 2s

2% of population

Present in first 2 years

2 inches in length

Approximately 2 ft from ileocaecal valve

65
Q

What is Omphalocele?

A

Herniation of intestines (sometimes liver and other organs) out of umbilicus at birth due to abdominal wall defects

Failure to return to abdomen after natural protrusion during development

Covered by peritoneal membrane and amnion

Investigations: USS antenatal scan shows herniated loop contained within peritoneum

Associated with severe malformations, 25% mortality

66
Q

What is Gastroschisis?

A

Herniation of bowel loops (sometimes stomach and liver) through para-umbilical wall defect (lateral to the umbilicus)

Not covered by surrounding membrane

Investigations: Antenatal USS show herniation to lateral of umbilicus, free-floating

67
Q

What is alcoholic liver disease?

A

Alcoholic liver disease results from the effects of the long term excessive consumption of alcohol on the liver. The onset and progression of alcoholic liver disease varies between people, suggesting that there may be a genetic predisposition to having harmful effects of alcohol on the liver.

68
Q

What are the 3 stepwise pricess of progression of alcoholic liver disease?

A

1. Alcohol related fatty liver

Drinking leads to a build-up of fat in the liver. If drinking stops this process reverses in around 2 weeks.

2. Alcoholic hepatitis

Drinking alcohol over a long period causes inflammation in the liver sites. Binge drinking is associated with the same effect. Mild alcoholic hepatitis is usually reversible with permanent abstinence.

3. Cirrhosis

This is where the liver is made up of scar tissue rather than healthy liver tissue. This is irreversible. Stopping drinking can prevent further damage. Continued drinking has a very poor prognosis.

69
Q

What is the recommended alcohol consumption

A

That latest recommendations (Department of Health, 2016) are to not regularly drink more than 14 units per week for both men and women.

If drinking 14 units in a week, this should be spread evenly over 3 or more days and not more than 5 units in a day.

The government guidelines also state that any level of alcohol consumption increases the risk of cancers, particularly breast, mouth and throat.

Pregnant women should avoid alcohol completely.

70
Q

What is AUDIT Questionnaire

A

The Alcohol Use Disorders Identification Test (AUDIT) was developed by the World Health Organisation to screen people for harmful alcohol use. It involves 10 questions with multiple choice answers and gives a score. A score of 8 or more gives an indication of harmful use.

71
Q

Complications of Alcohol

A
  • Alcoholic Liver Disease
  • Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
  • Alcohol Dependence and Withdrawal
  • Wernicke-Korsakoff Syndrome (WKS)
  • Pancreatitis
  • Alcoholic Cardiomyopathy
72
Q

Signs of Liver Disease

A
  • Jaundice
  • Hepatomegaly
  • Spider Naevi
  • Palmar Erythema
  • Gynaecomastia
  • Bruising – due to abnormal clotting
  • Ascites
  • Caput Medusae – engorged superficial epigastric veins
  • Asterixis – “flapping tremor” in decompensated liver disease
73
Q

Ix for Alcohol Liver Disease

A

Bloods

FBC – raised MCV

LFTs – elevated ALT and AST (transaminases) and particularly raised gamma-GT. ALP will be elevated later in the disease. Low albumin due to reduced “synthetic function” of the liver. Elevated bilirubin in cirrhosis.

Clotting – elevated prothrombin time due to reduced “synthetic function” of the liver

U+Es may be deranged in hepatorenal syndrome.

Ultrasound

An ultrasound of the liver may show fatty changes early on described as “increased echogenicity”. It can also demonstrate changes related to cirrhosis if present.

“FibroScan” can be used to check the elasticity of the liver by sending high frequency sound waves into the liver. It helps assess the degree of cirrhosis.

Endoscopy

Endoscopy can be used to assess for and treat oesophageal varices when portal hypertension is suspected.

CT and MRI scans

CT and MRI can be used to look for fatty infiltration of the liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites.

Liver Biopsy

Liver biopsy can be used to confirm the diagnosis of alcohol-related hepatitis or cirrhosis. NICE recommend considering a liver biopsy in patients where steroid treatment is being considered.

74
Q

What is general management for alcohol liver disease

A
  • Stop drinking alcohol permanently
  • Consider a detoxication regime
  • Nutritional support with vitamins (particularly thiamine) and a high protein diet
  • Steroids improve short term outcomes (over 1 month) in severe alcoholic hepatitis but infection and GI bleeding need to be treated first and do not improve outcomes over the long term
  • Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy)
  • Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral
75
Q

Withdrawal symptoms

Symptoms occur at different times after alcohol consumption ceases:

  • 6-12 hours:
  • 12-24 hours:
  • 24-48 hours:
  • 24-72 hours:
A
  • 6-12 hours: tremor, sweating, headache, craving and anxiety
  • 12-24 hours: hallucinations
  • 24-48 hours: seizures
  • 24-72 hours: “delirium tremens”
76
Q

What is Delirium Tremens

A

Delirium tremens is a medical emergency associated with alcohol withdrawal with a mortality of 35% if left untreated. Alcohol stimulates GABA receptors in the brain. GABA receptors have a “relaxing” effect on the rest of the brain. Alcohol also inhibits glutamate receptors (also known as NMDA receptors) having a further inhibitory effect on the electrical activity of the brain.

77
Q

When alcohol is removed from the system, GABA under-functions and glutamate over-functions causing an extreme excitability of the brain with excess adrenergic activity. This presents as:

A
  • Acute confusion
  • Severe agitation
  • Delusions and hallucinations
  • Tremor
  • Tachycardia
  • Hypertension
  • Hyperthermia
  • Ataxia (difficulties with coordinated movements)
  • Arrhythmias
78
Q

What is CIWA-Ar

A

(Clinical Institute Withdrawal Assessment – Alcohol revised) tool can be used to score the patient on their withdrawal symptoms and guide treatment.

79
Q

Which benzodiazepine is used to combat the effects of alcohol withdrawal.

What is alternative?

A

Chlordiazepoxide (“Librium”)

Diazepam

80
Q

Wernicke-Korsakoff Syndrome (WKS)

What is it?

A

Alcohol excess leads to thiamine (vitamin B1) deficiency. Thiamine is poorly absorbed in the presence of alcohol and alcoholics tend to have poor diets and rely on the alcohol for their calories. Wernicke’s encephalopathy comes before Korsakoffs syndrome. These result from thiamine deficiency.

81
Q

What are the Features of Wernicke’s encephalopathy

A
  • Confusion
  • Oculomotor disturbances (disturbances of eye movements)
  • Ataxia (difficulties with coordinated movements)
82
Q

What are the Features of Korsakoffs syndrome

A
  • Memory impairment (retrograde and anterograde)
  • Behavioural changes
    *
83
Q

Korsakoffs syndrome reversible or irreversible

A
84
Q

What is NAFLD?

What is the extreme form of this called ?

A

Non alcholic fatty liver disease (NAFLD) forms part of the “metabolic syndrome” group of chronic health conditions relating to processing and storing energy that increase risk of heart disease, stroke and diabetes. It is estimated that up to 30% of adults have NAFLD. It is characterised by fat deposited in liver cells. These fat deposits can interfered with the functioning of the liver cells. NAFLD does not cause problems initially, however it can progress to hepatitis and cirrhosis.

Non-alcoholic steatohepatitis (NASH) is most extremeform and→cirrhosis in 10%

85
Q

NAFLD stages?

A
  1. Non-alcoholic Fatty Liver Disease
  2. Non-Alcoholic Steatohepatitis (NASH)
  3. Fibrosis
  4. Cirrhosis
86
Q

NAFLD Risk factors

A
  • Obesity
  • Poor diet and low activity levels
  • Type 2 diabetes
  • High cholesterol
  • Middle age onwards
  • Smoking
  • High blood pressure
87
Q

Investigation in Non-Alcoholic Fatty Liver Disease

A

Liver Ultrasound can confirm the diagnosis of hepatic steatosis (fatty liver). It does not indicate the severity, the function of the liver or whether there is liver fibrosis.

Enhanced Liver Fibrosis (ELF) blood test. This is the first line recommended investigation for assessing fibrosis but it is not currently available in many areas. It measures three markers (HA, PIIINP and TIMP-1) and uses an algorithm to provide a result that indicates the fibrosis of the liver:

  • < 7.7 indicates none to mild fibrosis
  • ≥ 7.7 to 9.8 indicates moderate fibrosis
  • ≥ 9.8 indicates severe fibrosis

NAFLD fibrosis score is the second line recommended assessment for liver fibrosis where the ELF test is not available. It is based on an algorithm of age, BMI, liver enzymes, platelets, albumin and diabetes and is helpful in ruling out fibrosis but not assessing the severity when present.

Fibroscan is the third line investigation. It involves a particular ultrasound that measures the stiffness of the liver and gives an indication of fibrosis. This is performed if the ELF blood test or NAFLD fibrosis score indicates fibrosis.

  • BMI
  • Glucose, fasting lipids
  • ↑transaminases: AST:ALT <
  • Liver biopsy
88
Q

Management NAFLD

A
  • Weight loss
  • Exercise
  • Stop smoking
  • Control of diabetes, blood pressure and cholesterol
  • Avoid alcohol

Refer patients with liver fibrosis to a liver specialist where they may treat with vitamin E or pioglitazone.

89
Q

What is liver cirrhosis?

A

Liver cirrhosis is the result of chronic inflammation and damage to liver cells. When the liver cells are damaged they are replaced with scar tissue (fibrosis) and nodules of scar tissue form within the liver.

90
Q

This fibrosis affects the structure and blood flow through the liver, which causes increased resistance in the vessels leading in to the liver. This is called ________ __________

A

portal hypertension

91
Q

4 most common causes of Liver cirrhosis

A
  • Alcoholic liver disease
  • Non Alcoholic Fatty Liver Disease
  • Hepatitis B
  • Hepatitis C
92
Q

Rarer Causes of cirrhosis?

A
  • Genetic:Wilson’s,α1ATD, HH, CF
  • AI:AH, PBC, PSC
  • Drugs:Methotrexate, amiodarone, methyldopa,INH
  • Neoplasm:HCC, mets
  • Vasc:Budd-Chiari, RHF,constrict. pericarditis
93
Q

Signs of Cirrhosis

What do they suggest?

A

Hands

  • Clubbing (± periostitis)
  • Leuconychia (↓albumin)
  • Terry’s nails (white proximally, red distally)
  • Palmer erythema- caused by hyperdynamic cirulation
  • Dupuytron’s contracture
  • Asterixis – “flapping tremor” in decompensated liver diseas

Face

  • Pallor: ACD
  • Xanthelasma: PBC
  • Parotid enlargement (esp. c̄EtOH)
  • Jaundice – caused by raised bilirubin

Trunk

  • Spider naevi (>5, fill from centre)- these are telangiectasia with a central arteriole and small vessels radiating away
  • Gynaecomastia- in males due to endocrine dysfunction
  • Loss of sexual hair
  • Brusing- due to abnormal clotting

Abdo

  • Striae
  • Hepatomegaly (may be small in late disease)
  • Splenomegaly- due to portal hypertension
  • Caput Medusae – distended paraumbilical veins due to portal hypertension
  • Testicular atrophy- in males due to endocrine dysfunction
94
Q

Ix for liver cirrhosis?

A

Bloods

  • FBC:↓WCC and↓plats indicate hypersplenism
  • ↑LFTs
  • ↑INR
  • ↓Albumin

Find Cause

  • EtOH:↑MCV,↑GGTNASH:hyperlipidaemia,↑glucose
  • Infection:Hep, CMV, EBV serology
  • Genetic:Ferritin,α1AT, caeruloplasmin (↓in Wilson’s)
  • Autoimmune:Abs (there is lots of cross-over)
  • AIH:SMA, SLA, LKM, ANA
  • PBC:AMA
  • PSC:ANCA, ANA
  • Ig:↑IgG – AIH,↑IgM – PBC
  • Ca:α-fetoprotein

Abdo US + PV Duplex

  • Small / large liver
  • Focal lesions
  • Reversed portal vein flow
  • Ascites

Ascitic Tap + MCS

PMN >250mm3indicates SBP

Liver biopsy

95
Q

Majority of pancreatic cancers are?

A

adenocarcinomas

96
Q

Pancreatic Cancer

Pre hepatic/hepatic/Post hepatic

A

Post Hepatic

Obstructive jaundice

97
Q

Where does pancreatic cancers spread to usually?

A

liver, then to the peritoneum, lungs and bones.

98
Q

Presentation of pancreatic cancer?

A
  • Painless Obstructive jaundice
  • Yellow skin and sclera
  • Pale stools
  • Dark urine
  • Generalised itching
  • Non-specific upper abdominal or back pain
  • Unintentional weight loss
  • Palpable mass in the epigastric region
  • Change in bowel habit
  • Nausea or vomiting
  • New‑onset diabetes or worsening of type 2 diabetes
99
Q

It is worth noting that a new onset of diabetes, or a rapid worsening of glycaemic control type 2 diabetes, can be a sign of __________ ______

A

Pancreatic cancer

100
Q

What are the NICE guidelines for when to refer for suspected pancreatic cancer:

A
  • Over 40 with jaundice – referred on a 2 week wait referral
  • Over 60 with weight loss plus an additional symptom (see below) – referred for a direct access CT abdomen
101
Q

When does GP directly refer to accesss CT abdomen to assess pancreatic cancer?

A

if a patient has weight loss plus any of:

  • Diarrhoea
  • Back pain
  • Abdominal pain
  • Nausea
  • Vomiting
  • Constipation
  • New‑onset diabetes
102
Q

What is the sign called for palpable gallbladder along with jaundice

A

Courvoisier’s law

suggests cholangiocarcinoma or pancreatic cancer

103
Q

What is Trousseau’s sign of malignancy

A

refers to migratory thrombophlebitis as a sign of malignancy, particularly pancreatic adenocarcinoma. Thrombophlebitis is where blood vessels become inflamed with an associated blood clot (thrombus) in that area. Migratory refers to the thrombophlebitis reoccurring in different locations over time.

104
Q

Ix for pancreatic cancer?

A

Diagnosis is based on imaging (usually CT scan) plus histology from a biopsy.

Staging CT scan involves a full CT thorax, abdomen and pelvis (CT TAP). This is used to look for metastasis and other cancers.

CA 19-9 (carbohydrate antigen) is a tumour marker that may be raised in pancreatic cancer.

Magnetic resonance cholangio-pancreatography (MRCP) may be used to assess the biliary system in detail to assess the obstruction.

Endoscopic retrograde cholangio-pancreatography (ERCP) can be used to put a stent in and relieve the obstruction, and also obtain a biopsy from the tumour.

Biopsy may be taken through the skin (percutaneous) under ultrasound or CT guidance, or during an endoscopy under ultrasound guidance.

105
Q

Management for pancreatic cancer

A

Surgery

  • Total pancreatectomy
  • Distal pancreatectomy
  • Pylorus-preserving pancreaticoduodenectomy (PPPD) (modified Whipple procedure)
  • Radical pancreaticoduodenectomy (Whipple procedure)

In most cases, curative surgery is not possible. Palliative treatment may involve:

  • Stents inserted to relieve the biliary obstruction
  • Surgery to improve symptoms (e.g., bypassing the biliary obstruction)
  • Palliative chemotherapy (to improve symptoms and extend life)
  • Palliative radiotherapy (to improve symptoms and extend life)
  • End of life care with symptom control
106
Q

What is Whipple Procedure?

A

A Whipple procedure (pancreaticoduodenectomy) is a surgical operation to remove a tumour of the head of the pancreas that has not spread. A Whipple procedure is a massive operation so patients need to be in good baseline health.

107
Q

Whipple Procedure involves the removal of ?

A
  • Head of the pancreas
  • Pylorus of the stomach
  • Duodenum
  • Gallbladder
  • Bile duct
  • Relevant lymph nodes
108
Q

A modified Whipple procedure is called

A

pylorus-preserving pancreaticoduodenectomy (PPPD).

leave pylorus in place

109
Q

Symptoms of Meckels’ Divertculum

A

Symptoms

  • GI bleeding (May contain gastric mucosa → gastric ulcerations)
  • Abdominal pain and cramping
  • Tenderness near the belly button
  • Obstruction of bowels
110
Q

Causes of pre-hepatic jaundice

A

Excess (billirubin) BR production

  • Haemolytic anaemia
  • Ineffective erythropoiesise.g. thalassaemia
111
Q

Causes of unconjugated hepatic jaundice

A

↓BR Uptake

  • Drugs: contrast, RMP
  • CCF

↓BR Conjugation

  • Hypothyroidism
  • Gilbert’s (AD)
  • Crigler-Najjar (AR)

Neonatal jaundice is both ↑production +↓conju

112
Q

Causes of conjugated hepatic jaundice

A

Hepatocellular Dysfunction

  • Congen:HH, Wilson’s,α1ATD
  • Infection:Hep A/B/C, CMV, EBV
  • Toxin:EtOH, drugs
  • AI:AIH
  • Neoplasia:HCC, mets
  • Vasc:Budd-Chiari

↓Hepatic BR Excretion

  • Dubin-Johnson
  • Rotor’
113
Q

Causes of post hepatic jaundice

A

Obstruction

  • Stones
  • Ca pancreas
  • Drugs
  • PBC
  • PSC
  • Biliary atresia
  • Choledochal cyst
  • Cholangio Ca
114
Q

What convertes uBR to cBR

A

BR-UDP-glucuronyl transferase in live

115
Q

what are normal billirubin levels

at what levels can jaundice obvious

A
  • Normal BR = 3-17uM
  • Jaundice visible @ 50uM (3 x ULN
116
Q

Name some drug induced Jaundice

A
117
Q

What is Gilbert’s syndrome

How is it inherited?

What percentage of population is affected?

Dx:

A

In Gilbert’s syndrome, slightly higher than normal levels of a substance called bilirubin build up in the blood.

  • Auto dom partial UDP-GT deficiency
  • 2% of the population
  • Jaundice occurs during intercurrent illness
  • Dx:↑uBR on fasting, normal LFTs
118
Q

What is Crigler-Najjar

What is treatment

A
  • Rare auto rec total UDP-GT deficiency
  • Severe neonatal jaundice and kernicterus
  • Rx:liver Transplant
119
Q

What grading is used for Liver Cirrhosis

Explain it

A

Child-Pugh Grading of Cirrhosis

  • Predicts risk of bleeding, mortality and need for Tx
  • Graded A-C using severity of 5 factors
  • Albumin
  • Bilirubin
  • Clotting
  • Distension: Ascites
  • Encephalopathy
  • Score >8 = significant risk of variceal bleeding
120
Q

Viral Hepatitis

There are types A-E

explain how they are spread and their cause

A
121
Q

Patho of autoimmune hepatitis

A
  • Inflammatory disease of unknown cause characterisedby Abs directed vs. hepatocyte surface antigens
  • Predominantly young and middle-aged women
122
Q

Classification of autoimmune hepatitis

A

Classified according to Abs

  • T1:Adult, SMA+ (80%), ANA+ (10%),↑IgG
  • T2:Young, LKM+
  • T3:Adult, SLA+
123
Q

What are some associated diseases with autoimmune hepatitis

A

Autoimmune thyroiditis

DM

Pernicious anaemia

PSC

UC

GN

AIHA (Coombs +ve)

124
Q

Ix for autoimmune hepatitis

A
  • ↑LFTs
  • ↑IgG
  • Auto Abs: SMA, LKM, SLA, ANA
  • ↓WCC and↓plats = hypersplenism
  • Liver biopsy
125
Q

Mx for autoimmune hepatitis

A

Immunosuppression

  • Prednisolone
  • Azathioprine as steroid-sparer

Liver transplant (disease may recur)

126
Q
A

Year 2 (33 decks)

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