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Gastrointestinal > Liver pathologies and ano-rectal disorders > Flashcards

Liver pathologies and ano-rectal disorders Flashcards

1
Q

What are the 3 pathways of lipid metabolism in the liver?

A

Reverse transport pathway (HDL)
Exogenous pathway (Chylomicrons)
Endogenous pathway (LDL)

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2
Q

Describe the metabolism of lipids in the liver?

A

Bile digests lipids in the gut, forming chylomicrons
Remnant receptors on liver take in chylomicrons
VLDL and HDL released by the liver
VLDL converted to LDL by lipoprotein lipase and taken up by the liver
HDL delivers cholesterol to tissue that needs it

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3
Q

Describe the metabolism of protein in the liver

A

Proteins are broken down into amino acids in the small intestine
Hepatocytes transport amino acids which are metabolised via the krebs cycle, forming hormones, neurotransmitters, plasma protein, nucleotides and ammonia

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4
Q

Describe the metabolism of ammonia in the liver

A

Ammonia is detoxified in the liver by conversion to urea by the krebs cycle, which is consumed in the conversion of glutamate to glutamine, a reaction that depends upon glutamine sythetase

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5
Q

Describe the metabolism of vitamin D by the liver

A

Vitamin D is metabolised to cholecalciferol and then to 25-hydroxy-cholecalciferol

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6
Q

What are the 3 phases of drug metabolism in the liver?

A

Phase I
Phase II
Phase III

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7
Q

What occurs in phase I of drug metabolism?

A

The drug can undergo oxidation, reduction and hydrolysis by cytochrome P450 in the endoplasmic reticulum
Some of these P450 proteins include CYP1, 2, 3 and 3A4

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8
Q

What occurs in phase II of drug metabolism?

A

The drug undergoes conjugation in the cytoplasm of hepatocytes
These conjugation processes include addition of glucuronic acid, sulphate, acetate, glycine or glutathione

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9
Q

What occurs in phase III of drug metabolism?

A

The drug is secreted into the bile, mediated by ATP

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10
Q

What is the function of albumin?

A

It is involves in the transport of insoluble molecules such as bilirubin, hormones and fatty acids in the blood

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11
Q

What are some proteins that are synthesised by the liver?

A

Ferritin
Caeruloplasmin
Transferrin
Ferritin
Alpha 1 anti-trypsin
CRP
AFP
Complement system components
Fibrinogen
Vitamin K dependant coagulation factors (X, IX, VII, II, V)

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12
Q

What role does the liver play in bile synthesis?

A

Primary bile is made up in the liver
Secondary bile acids are absorbed by the liver

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13
Q

What are some components of bile?

A

Phospholipids
Cholesterol
Bilirubin
Conjugated drugs
Electrolytes (e.g. Na+, Cl-, HCO3-, Cu)

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14
Q

Describe the pathway from formation to excretion of bilirubin

A

Haem -> In spleen
Biliverdin ->
Unconjugated bilirubin -> In blood
Conjugated bilirubin -> In liver
Urobilinogen -> In intestines and kidneys
Urobilin (kidneys) or Sterocobilin (Intestine)

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15
Q

Describe the role of the liver in immune response

A

The liver contains Kupffer cells which phagocytose gut pathogens
It also produces interleukins and tumour necrosis factors

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16
Q

What is liver cirrhosis?

A

The development of regenerative nodules, surrounded by fibrous bands in response to chronic liver injury

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17
Q

Describe the pathophysiology of liver cirrhosis

A

Injury causes inflammation, matrix deposition, parenchymal cell death and angiogenesis

Damage to cells releases cell contents and ROS which activates stellate cells

Stellate cells release CCL2 which activates macrophages

Phagocytosis of liver cells releases pro-inflammatory mediators which activates neutrophils, and releases TGFß which transdifferentiate stellate cells into myofibroblasts

Myofibroblasts release collagen and alpha-SMA causing scarring, which neutrophils cause damage

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18
Q

What occurs when chronic injury to the liver is stopped during fibrosis pathophysiology?

A

There is a decrease in MMP release from immune cells, which causes net matrix degradation

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19
Q

How can liver cirrhosis lead to portal hypertension?

A

An increase in type I and III collagen as well as angiogenesis and sinusoidal remodelling leads to increased sinusoidal resistance

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20
Q

What are some general symptoms of liver cirrhosis?

A

Jaundice
Fever
Loss of body hair

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21
Q

What are some presentations of compensated liver disease?

A

Xanthelasma
Parotid enlargement
Spider naevi
Gynaecomastia
Splenomegaly
Liver palms
Scratch marks
Testicular atrophy
Perpura pigmented ulcers

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22
Q

What is meant by liver palms?

A

Clubbing
Duputren’s contracture
Xanthoma

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23
Q

What are some presentations of decompensated liver disease?

A

Neurological conditions (e.g. disorientation, drowsiness, stroke)
Encephalopathy - Hepatic flap
Fetor hepaticus
Ascites
Caput medusae
Oedema

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24
Q

What are some investigations in liver cirrhosis?

A

Liver biopsy
Serum markers
Elastography

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25
Q

What are some of the serum markers that can be used in liver cirrhosis?

A

Albumin - Decreased in end stage
Prothrombin time - Decrease synthesis of clotting factors
Bilirubin - Increased in end stage cirrhosis due to decreased clearance
Platelets - Decreased thrombopoetin decreases megakaryocytic growth

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26
Q

What occurs in alcoholic liver disease?

A

Ethanol is absorbed into hepatocytes, altering their micrometabolism, especially their fat metabolism, which causes cell injury and death, manifested by formation of Mallory’s hyalin

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27
Q

Describe the progression of alcoholic liver disease

A

Fatty liver
Hepatitis
Fibrosis
Cirrhosis

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28
Q

How will 2-3 days of drinking alcohol affect the liver?

A

Cause reversible fatty liver

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29
Q

How will 4-6 weeks of chronic high alcohol intake affect the liver?

A

Cause reversible hepatitis

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30
Q

How will months of chronic high alcohol intake affect the liver?

A

Cause reducible liver fibrosis

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31
Q

How will years of chronic high alcohol intake affect the liver?

A

Cause irreversible cirrhosis

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32
Q

What occurs in fatty liver disease?

A

There in an increased number of fat vacuoles within the hepatocytes

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33
Q

What are some possible complications of alcoholic liver disease?

A

Cirrhosis
Portal hypertension
Malnutrition
Hepatocellular carcinoma
Social disintegration

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34
Q

How are units of alcohol calculated?

A

. Volume (mls) x ABV (%)
. ———————————
. 1000

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35
Q

What does CAGE stand for in alcohol misuse screening?

A

do you think you should (C)ut down
do you get (A)nnoyed by criticism of your intake
do you feel (G)uilty about your drinking
do you use alcohol as an (E)ye opener

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36
Q

What is the alcohol misuse screening test used in A&E?

A

PAT (Paddington Alcohol Test)

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37
Q

What is the cycle of change in alcohol misuse?

A

1 - Pre-contemplation
2- Contemplation
3 - Preparation
4 - Action
5 - Maintenance
6 - Established change or Relapse

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38
Q

What are the 2 stages of alcoholism treatment?

A

Detox
Maintenance of abstinence

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39
Q

What are some methods of abstinence maintenance in alcohol misuse?

A

White knuckling
Peer support (AA)
Disulfiram
Acomprasate

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40
Q

How does disulfiram work?

A

It creates an increase ethanol sensitivity and so causes adverse effects if alcohol in taken in

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41
Q

What is non-alcoholic fatty liver disease?

A

This is a spectrum of disease ranging from steatosis to steatohapatitis to fibrosis and cirrhosis, with an identical pathology to alcoholic liver disease

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42
Q

What causes non-alcoholic fatty liver disease?

A

Increased fat intake and insulin resistance

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43
Q

How is steatohepatitis pathologically characterised?

A

Inflammation
Hepatocyte degeneration
Ballooning
Mallory bodies
Eventual fibrosis

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44
Q

How is simple steatosis diagnosed in NAFLD?

A

Ultrasound

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45
Q

What is NASH?

A

Non-Alcoholic SteatoHepatitis

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46
Q

How is NASH diagnosed?

A

Liver biopsy

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47
Q

What is the management of simple steatosis in NAFLD?

A

Weight loss
Exercise

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48
Q

What is the management of NASH in NAFLD?

A

Weight loss
Exercise
Some experimental treatments

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49
Q

What are some viruses that can cause hepatitis?

A

Hepatitis A, B, C, D, E
Epstein-Barr Virus (EBV)
Yellow fever virus
Hepres Simplex Virus (HSV)
Cytomegalovirus (CMV)

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50
Q

How is hepatitis A spread?

A

Faecal-oral route

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51
Q

Who is most at risk of hepatitis A?

A

Children and young adults
Those in the tropics
Those with poor sanitation

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52
Q

How will hepatitis A show on LFTs?

A

High ALT and AST
Possible high bilirubin

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53
Q

How is a diagnosis of Hepatitis A made?

A

Blood clotting testing for HAV IgM

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54
Q

Does hepatitis A cause acute or chronic hepatitis?

A

Acute

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55
Q

Does hepatitis B cause acute or chronic hepatitis?

A

Both

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56
Q

How is hepatitis B transmitted?

A

Vertical transmission (Mother to child)
Blood
Sexually

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57
Q

Who is most at risk of hepatitis B?

A

People born in high prevalence areas
Children of infected women
PWID
People who have many partners in high prevalence areas
Men who have sex with men

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58
Q

What is the incubation period for hepatitis B?

A

30-180 days

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59
Q

When would a patients with Hepatitis B require treatment?

A

If there’s acute liver failure, coagulopathy or prolonged course of illness (>4 weeks)

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60
Q

What are the 7 diagnostic markers of hepatitis B?

A

HBsAg = Viral surface antigen
Anti-HBs = Antibody to surface antigen
HBeAg = Viral replication protein
Anti-HBe = Antibody to replication protein
HBcAg = Viral core antigen
Anti-HBc = Antibody to core antigen
HBV DNA = DNA of hepatitis B

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61
Q

How is a neonate treated for hepatitis B?

A

Immunoglobulin infusion and vaccination

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62
Q

What are the 2 nucleoside analogues for hepatitis B treatment in adults?

A

Tenofivir
Entecavir

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63
Q

Does hepatitis C cause acute or chronic infection?

A

Chronic

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64
Q

How many genotypes of hepatitis C are there and which are most common in the UK?

A

6 genotypes
I and III are most dominant in UK

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65
Q

How is hepatitis C transmitted?

A

Blood
Sexual (rare)

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66
Q

What are the main risk factors of hepatitis C?

A

PWID
Transfusions in the developing world
Tattoos in the developing world

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67
Q

Who is offered treatment in hepatitis C?

A

Everyone who will accept, as there is a low rate of spontaneous clearance

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68
Q

What are the 3 classes of drugs that can be used in hepatitis C treatment?

A

Protease inhibitors
Polymerase inhibitors
NS5A inhibitors

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69
Q

How is hepatitis C diagnosed?

A

HCV IgG = Indicated exposure
HCV RNA = Indicates active infection

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70
Q

How does hepatitis D cause infection?

A

It causes progressive or acute hepatitis in patients with pre-existing HBV infection as it required the HBsAg

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71
Q

What are the treatment options for hepatitis D?

A

Pegylated interferon - 48 weeks treatment
Bulveritide

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72
Q

Is hepatitis E acute or chronic?

A

Acute

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73
Q

What are some symptoms of hepatitis E?

A

Jaundice
Nausea
Vomiting

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74
Q

How is hepatitis E transmitted?

A

Faecal-oral route
Significant zoonotic spread (Pigs)

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75
Q

What is the incubation time for hepatitis E?

A

15-60 days

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76
Q

What are the 4 serotypes of hepatitis E and where are they found?

A

Type I and II are found most in Asia
Type III and IV are found most in Europe

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77
Q

How is hepatitis E diagnosed?

A

HEV IgM

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78
Q

Which forms of hepatitis virus cause acute infection?

A

A
B
E

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79
Q

Which forms of hepatitis virus cause chronic infection?

A

B
C

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80
Q

What are some symptoms of acute viral hepatitis?

A

Abdominal pain
Nausea
Vomiting
Jaundice
Diarrhoea (Occasionally)

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81
Q

Describe the LFTs of acute viral hepatitis?

A

Raised ALT and AST (>1000)
Possibly raised bilirubin
Normal ALP
Normal Gamma-GT

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82
Q

When will chronic hepatitis infection cause symptoms?

A

If it progresses to decompensated cirrhosis

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83
Q

What are some symptoms suggestive of chronic hepatitis infection?

A

Jaundice
Ascites
Encephalopathy

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84
Q

What is primary biliary cholangitis (Cirrhosis)?

A

This is a genetic condition leading to inflammation of the cholagiocytes lining the biliary tree

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85
Q

What causes primary biliary cholangitis (PBC)?

A

This is an autoimmune condition in which anti-mitochondrial antibodies target the pyruvate dehydrogenase enzyme of the inner leaflet of the mitochondrial membranes of cholangiocytes

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86
Q

Describe the pathology of primary biliary cholangitis?

A

Damage to cholangiocytes causes inflammation and granuloma formation, which can cause obstruction, leading to cholestasis, necrosis and fibrosis

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87
Q

Who is most at risk of PBC?

A

Females (10:1 ratio)

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88
Q

What are some symptoms of PBC?

A

Fatigue
Itch without rash (Due to bile build up in blood)
Xanthelasma
Xanthoma
RUQ pain or discomfort

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89
Q

How is PBC diagnosed?

A

Positive AMA test
Cholestatic LFTs
Liver biopsy

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90
Q

How is PBC treated?

A

Treatment is mostly to prevent symptoms such as itching, with urseodeoxycholic acid or obeticholic acid
Liver transpantation can be performed

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91
Q

How many types of autoimmune hepatitis are there?

A

2

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92
Q

What is the age distribution for Type I autoimmune hepatitis?

A

Bimodal age distribution
Ages 15-25
ges 45-70

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93
Q

What gender is most at risk of autoimmune hepatitis?

A

Females (3.6:1 ratio)

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94
Q

What are some conditions associated with Type I autoimmune hepatitis?

A

Autoimmune thyroiditis
Grave’s disease
Pernicious anaemia
Systemic sclerosis

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95
Q

What antibodies are the cause of type I autoimmune hepatitis?

A

ANA - Anti-Nuclear Antibodies
ASMA - Anti-Smooth Muscle Antibodies

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96
Q

What antibodies are the cause of type II autoimmune hepatitis?

A

LKM-1 - Liver Kidney Microsomal
AMA - Anti-Mitochonrial Antibodies

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97
Q

What age is most at risk of type II autoimmune hepatitis?

A

Children and young adults

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98
Q

What are some common mutations that can lead to autoimmune hepatitis?

A

HLA mutations
IgG mutations
T-cell receptor mutations

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99
Q

What are some drugs that can trigger autoimmune hepatitis?

A

Oxyphenistan
Methyldopa
Nitrofurantoin
Diclofenac
Minocycline
Statins

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100
Q

What are some symptoms of autoimmune hepatitis?

A

Malaise
Fatigue
Nausea
Abdominal pain
Anorexia
Jaundice

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101
Q

What are some clinical signs of autoimmune hepatitis?

A

Hepatomegaly
Jaundice
Splenomegaly

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102
Q

How will autoimmune hepatitis affect LFTs?

A

Elevated AST and ALT (100-800)
Elevated prothrombin time
Antibodies

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103
Q

What tests are used in diagnosis of autoimmune hepatitis?

A

LFTs
Liver biopsy

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104
Q

What is the treatment regime used in autoimmune hepatitis?

A

Prednisolone (30mg to 15mg at week 4 then 10mg daily)
Azathioprine (50-100mg)

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105
Q

What are some common drugs that can cause chronic drug induced hepatitis?

A

Antibiotics (Co-amoxiclav, flucloxicillin)
NSAIDs
Paracetamol
Methotrexate

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106
Q

How does paracetamol cause a hepatitis?

A

Paracetamol (Acetaminophen) is a common drug that can lead to liver injury and failure due to overdose

In the correct dose, paracetamol is conjugated by the liver via addition of glucuronide or sulfate

In large doses, excess paracetamol is converted into NAPQI (N-Acetyl-P-Benzo-Quinone Imine) which is hepatotoxic and binds to hepatocytes, causing damage

107
Q

What is the treatment for paracetamol induced hepatitis?

A

NAC (N-Acetyl cysteine) can be given, which adds glutathione, converting NAPQI into cysteine and mercapturic acid conjugates

108
Q

What is primary sclerosis cholangitis?

A

This is an autoimmune destructive disease of the large and medium sized bile ducts

109
Q

What gender is more at risk of primary sclerosing cholangitis?

A

Males (4:1 ratio)

110
Q

Describe the pathology of PSC?

A

Periductal fibrosis and duct destruction can cause stricture formation, leading to jaundice and recurrent cholangitis
There is also an increased risk of malignancy

111
Q

How is a diagnosis of PSC usually made?

A

Imaging of the biliary tree showing inflammation and stricture formation
This is by Ultrasound or MRCP (Magnetic Resonance Cholangiopancreatopgraphy)

112
Q

What are some signs and symptoms of PSC?

A

RUQ pain
Fever, weight loss, sweats and fatigue
Jaundice and pruritus
Hepatomegaly

113
Q

Describe the LFT derangement in PSC

A

Cholestatic - ALP > ALT/AST, ↑ GGT and bilirubin

positive p-ANCA (Anti neutrophilic cytoplasmic antibodies)

114
Q

How is PSC treated?

A

Maintenance of bile flow using ballon dilatation or stent implantation
Surveillance for carcinoma

115
Q

What is haemochromatosis?

A

This is a mono-genetic autosomal recessive disease, resulting in overload of iron in the blood and liver

116
Q

What are some causes of primary haemochromatosis?

A

Genetics leading to an increased absorption of iron, despite having a normal diet

117
Q

Describe the complications of haemochromatosis

A

Iron is deposited in the liver, which can stimulate fibrosis, if it reaches the portal connective tissue
This can lead to cirrhosis, carcinoma, diabetes, cardiomyopathy and impotence

118
Q

What are some causes of secondary haemochromatosis?

A

Iron overload from diet, blood transfusions or iron therapy

119
Q

What is the treatment option for haemochromatosis?

A

Venesection of the liver

120
Q

What is wilsons disease?

A

A mono-genetic autosomal recessive disorder of copper metabolism

121
Q

Describe the pathophysiology of Wilson’s disease

A

A mutation causes loss of function of caeruloplasmin
This is a copper binding protein, and a mutation of this causes massive copper deposition and accumulation in the liver and basal ganglia of the brain

122
Q

What are some some neurological symptoms of Wilson’s disease?

A

Choreo-astheitoid movements
Neurological deterioration

123
Q

What is meant by choreo-atheitoid movements (Choreoatheitosis)?

A

Involuntary muscle spasms and movements

124
Q

What are some hepatic symptoms of Wilson’s disease?

A

Cirrhosis
Sub-fulminant liver failure
Jaundice (In children)

125
Q

What are some systemic symptoms of Wilson’s disease?

A

Kayser-Fleischer rings (Golden rings) at the corneal limbus
Low serum caeruloplasmin levels

126
Q

What investigations can be performed in Wilson’s disease?

A

24hr urinary copper excretion high
Serum copper and ceruloplasmin levels low
Liver biopsy if other tests inconclusive

127
Q

What are the treatment options for Wilson’s disease?

A

Copper chelation drugs:
- Zinc
- Penicillamine
These block copper absorption in the GI tract

128
Q

What is an alpha-1 anti-trypsin deficiency?

A

An autosomal recessive disorder of production of an enzyme inhibitor, alpha-1 anti-trypsin

129
Q

Describe the role of alpha-1 anti-trypsin in the body

A

A1AT is produced by the liver and plays a role in inhibiting the action of elastases produced in the liver and lungs

130
Q

How can an A1AT deficiency cause liver cirrhosis and COPD?

A

If there is a deficiency of A1AT, elastases in the liver and lungs can cause destruction of the liver and lung parenchyma

131
Q

How will an A1AT deficiency present clinically?

A

Pulmonary - Cough, exertion dyspnoea, wheeze
Hepatic - Hepatitis, cirrhosis

132
Q

What are some investigations that can be performed in A1AT deficiency?

A
  • Plasma AAT level
  • PFTs
  • CXR
  • CT chest
133
Q

What are some treatment options in A1AT deficiency?

A

Smoking cessation
Bronchodilator therapy

134
Q

What is Budd-Chiari syndrome?

A

This is a condition resulting in thrombosis of the hepatic veins, either caused by congenital webs or thrombotic tendency due to protein C or S deficiency

135
Q

What is the main cause of primary Budd-Chiari syndrome?

A

Direct internal occlusion of the hepatic veins, usually caused by atheroma formation

136
Q

What is the main cause of secondary Budd-Chiari syndrome?

A

Usually caused by occlusion of the hepatic veins by an external stimulus, usually compression by a tumour or drugs such as the combined oral contraceptive pill

137
Q

How does acute Budd-Chiari syndrome usually present?

A

This usually presents with jaundice and tender hepatomegaly due to portal congestion

138
Q

How does chronic Budd-Chiari syndrome usually present?

A

It can present with ascites due to chronic portal congestion

139
Q

How is Budd-Chiari diagnosed?

A

Ultrasound or MRI to visualise the hepatic veins

140
Q

How is Budd-Chiari syndrome treated?

A

Recanalisation
TIPSS

141
Q

What supplement is required in treatment of decompensated liver disease due to alcohol?

A

Vitamin B - Thiamine, as excess alcohol intake can cause severe neurological disturbance if forgotten

142
Q

How does decompensated liver disease cause ascites?

A

Liver damage can cause release of vasodilators, causing renal hypotension, therefore causing sodium retention by the kidneys, leading to water retention

143
Q

How should new ascites be treated?

A

Spironolactone first, then loop diuretics such as furosemide

144
Q

What are some risks of ascites paracentesis?

A

Infection
Encephalopathy
Hypovolaemia

145
Q

What should be given to the patients in ascites paracentesis to prevent recurrence?

A

Albumin, therefore causing fluid retention in the blood, so fluid doesn’t move back into the perineal cavity

146
Q

What are the 4 grades of encephalopathy?

A

I - Can’t draw 5 point star or house
II - Hepatic flap
III - Unconscious but pain responsive
IV - Unconscious and unresponsive to pain

147
Q

What causes encephalopathy?

A

An increase in NH3 in the blood caused by a decrease in ammonia metabolism by the liver, causes the conversion of glutamate to glutamine in the astrocytes of the brain
Glutamine is highly osmotic, so causes astrocytes to swell as water moves in

148
Q

How is encephalopathy usually treated?

A

Lactulose to clear the gut
Rifazamin to treat the cause

149
Q

What scoring system is used to determine the probability of death in cirrhosis without transplant?

A

UKELD score

150
Q

How are ruptured oesophageal varicise treated and managed?

A

Resuscitation with fluids as bleeding can cause hypovolaemic shock
Terlipressin to prevent bleeding
Band ligation to cut off blood flow or balloon tamponade to compress the varicose

151
Q

What is meant by the lithotomy position?

A

The patient lies supine with their legs held in the air by stirrups

152
Q

What are the 2 ways in which wounds can heal?

A

Primary tension - wounds sutured together grow together
Secondary tension - Wound grows upwards, while being left open

153
Q

What are haemorrhoids?

A

Haemorrhoids are enlarged vascular cushions in the lower rectum and anal canal

154
Q

What are some common causes of haemorrhoids?

A

Excessive straining due to constipation
Increased intra-abdominal pressure (e.g. pregnancy, chronic cough, pregnancy)
Increasing age

155
Q

Where are the haemorrhoids found (Clockface)?

A

3, 7 and 11 on a clockface in the lithotomy position

156
Q

What are the 4 stages of internal haemorrhoids?

A

I - No protrusion, possible bleeding
II - Protrusion during defection
III - Protrusion but can be pushed in
IV - Cannot be mechanically pushed in

157
Q

What are the 2 types of haemorrhoid tissue?

A

Internal haemorrhoids
External haemorrhoids

158
Q

Where are the internal haemorrhoids usually found?

A

Above the dentate line

159
Q

Where are the external haemorrhoids usually found?

A

Below the dentate line, around the anus

160
Q

What are some symptoms of haemorrhoids?

A

Painless, bright red bleeding
Perianal itchiness
No changes in bowel habit or weight loss

161
Q

What are some investigations that can be performed in haemorrhoids?

A
  • PR exam
  • Proctoscopy
  • Flexible sigmoidoscopy in patients over 50 or where malignancy is a possibility
162
Q

What are some management options for haemorrhoids?

A

Do nothing if asymptomatic
Rubber band ligation
Open haemorrhoidectomy
HALO (Haemorrhoidal artery ligation)

163
Q

What are some symptom relief treatments in haemorrhoids?

A

Stool softeners
High fibre diet
Topical creams (Hydrocortisone)

164
Q

What are some possible complications of haemorrhoids?

A

Possible thrombosis
Strangulation
Necrosis

165
Q

What is meant by a rectal prolapse?

A

A condition in which the walls of the rectum protrude through the opening of the anus and become visible

166
Q

Who is most at risk of rectal prolapse?

A

The elderly, although it can occur in children

167
Q

What are some risk factors for rectal prolapse?

A

Increasing age
Female gender
Multiple deliveries
Straining
Previous traumatic vaginal delivery

168
Q

What are the 2 stages of rectal prolapse?

A

Partial - Anterior mucosal prolapse
Full - Full thickness prolapse

169
Q

How will rectal prolapse usually present?

A

A protruding mass from the anus, especially during defecation
Bleeding or passing of mucus per rectum
Poor anal tone on examination

170
Q

What are some investigations that can be performed in rectal prolapse?

A

Barium enema and/or colonoscopy
Stool microscopy and cultures
Sweat test

171
Q

What are some surgical procedures in rectal prolapse?

A

Delorme’s procedure
Altmaier procedure
Abdominal rectoplexy
Anterior resection

172
Q

What are some non-surgical treatment options in rectal prolapse?

A

Do nothing if asymptomatic
Laxatives may reduce prolapse
High fibre diet
Education of manual reduction

173
Q

What is an anal fissure?

A

A tear in the anal tissue, found below the dentate line

174
Q

What disease can cause multiple anal fissures?

A

Crohn’s disease

175
Q

What is meant by a sentinel pile?

A

A small skin tag caused by anal fissure formation

176
Q

What is the usual cause of anal fissure formation?

A

Constipation and straining

177
Q

What should the list of differentials be in a patient with fresh red bleeding PR?

A

Anal fissures
Haemorrhoids
Diverticulitis
IBD (Mainly UC)
Colorectal cancer

178
Q

What are some treatment options in anal fissures?

A

High fibre diet
Stool softeners
Pharmacological sphincterotomy
Botox injection

179
Q

What is a pharmacological sphincterotomy?

A

This is an ointment containing 0.3% GTN and 2% Diltiazem ointment, allowing for dilatation of blood vessels which allows healing

180
Q

Why is botox used in anal fissures?

A

This paralyses the sphincter to allow relaxation, meaning that the fissure can heal

181
Q

What are some consequences of chronic high alcohol intake?

A

Alcoholic Liver Disease
Hepatocellular carcinoma
Alcohol Dependence and Withdrawal
Wernicke-Korsakoff Syndrome (WKS)
Pancreatitis
Alcoholic Cardiomyopathy

182
Q

What is Wenicke-Korsakoff syndrome?

A

This is a syndrome caused by thiamine defieicny as a result of chronic high alcohol intake, leaidng to Wernicke encephalopathy and Korsakoff syndrome

183
Q

What are some symptoms of Wernicke’s encephalopathy?

A

Confusion
Oculomotor disturbances (disturbances of eye movements)
Ataxia (difficulties with coordinated movements)

184
Q

What are some symptoms of Korsakoff syndrome?

A

Memory impairment (retrograde and anterograde)
Behavioural changes

185
Q

What is meant by a fistula-in-ano?

A

This is an abnormal communication between the epithelium surface of the rectum and the perianal skin

186
Q

What are some possible causes of perianal fistulas?

A

Untreated anorectal abscess
Crohn’s disease
Tuberculosis
Anal cancer

187
Q

How do perianal fistulas form from an abscess or ulcer?

A

Pressure within the abdomen can cause burrowing through the ulcer or abscess, into the connective tissue and out onto the skin

188
Q

What disease will often cause multiple fistulas?

A

Crohn’s disease

189
Q

What are some possible presentations of perianal fistulas?

A

Painful tender swellings
Discharge of pus, faeces or blood onto the perianal surface

190
Q

What are some investigations that can be carried out in perianal fistulas?

A

PR examination
Proctoscopy
MRI in complex fistulas

191
Q

What are some surgical procedures that can be performed in cases of perianal fistulas?

A

Laying open
Insertion of seton (Drain)
LIFT or VAAFT (Video Assisted Anal Fistula Treatment)
Fistula plug

192
Q

What are some complications of surgery on anal fistulas?

A

Pain
Bleeding
Incontenence of stool or flatus

193
Q

What is the most common form of anal cancer?

A

Squamous cell carcinoma

194
Q

What are some risk factors of anal cancer?

A

Smoking
Immunosuppression
HPV
History of vulval, cervical or vaginal cancer

195
Q

What are some possible symptoms of anal cancer?

A

Pain
Bleeding
Lumps near anus

196
Q

What is the usual first line treatment in anal cancer?

A

Chemotherapy and radiotherapy with palliative surgery if this fails

197
Q

What are some benign lesions of the liver?

A

Haemangioma
Focal nodular hyperplasia
Adenoma
Liver cysts

198
Q

What are haemangiomas?

A

These are dense, hyper vascular tumours, usually small with a demarcated capsule

199
Q

Which gender is more at risk of haemangioma?

A

Female

200
Q

How is a diagnosis of haemangioma usually made?

A

US - Echogenic spot, demarcated
CT - Venous enhancement
MRI - High intensity area

201
Q

What is focal nodular hyperplasia?

A

This is a benign nodule formation of liver tissue and is commonly a congenital vascular anomaly, associated with Osler-Weber-Rendu and liver haemangioma

202
Q

Describe the pathology of focal nodular hyperplasia

A

There is usually a central scar containing a large artery, with radiating branches to the periphery (Hub and spoke)

203
Q

Who is more at risk of focal nodular hyperplasia?

A

Young and middle aged women

204
Q

How does focal nodular hyperplasia usually present?

A

It is usually asymptomatic

205
Q

How is a diagnosis of focal nodular hyperplasia usually made?

A

US - Nodule with varying echogenicity
CT - Hypervascular mass with central scar
MRI - iso or hypo intense
FNA - Normal hepatocytes and kupffer cells

206
Q

What is a hepatic adenoma?

A

This is a benign neoplasm, composed of normal hepatocytes, but with no branch of the portal triad

207
Q

What are some risk factors of hepatic adenoma?

A

Female (10:1)
Contraceptive hormones
Anabolic steroids

208
Q

at are some possible complications of hepatic adenoma?

A

Rupture
Haemorrhage
Malignant transformation

209
Q

Who is more at risk of melignant transformation of hepatic adenoma?

A

Males

210
Q

Where are most hepatic adenomas found?

A

Right lobe

211
Q

What are some side effects of larger hepatic adenomas?

A

RUQ pain
Bleeding

212
Q

What is the presence of multiple adenomas known as?

A

Adenomatosis - Associated with glycogen storage diseases

213
Q

How is diagnosis of hepatic adenomas made?

A

US - Filling defect
CT - Diffuse arterial enhancement
MRI - Hypo or hyper intense location

214
Q

How are hepatic adenomas treated in males?

A

Surgical excision due to risk of malignancy

215
Q

How are hepatic adenomas treated in females?

A

MRI scan after 6 months:
<5cm or reducing = Annual MRI
>5cm or increasing = Surgical excision

216
Q

What are cystic lesions of the liver?

A

These are fluid containing lesions

217
Q

What is meant by a simple liver cyst?

A

This is a liquid collection, lined by an epithelium, which is solitary and unallocated, with no biliary tree communication

218
Q

What are some possible complications of simple liver cysts?

A

Intracystic haemorrhage
Infection
Rupture
Compression

219
Q

What is a hydatid cyst?

A

This is a cyst caused by the tapeworm echinococcus granulosus

220
Q

Where are hydatid cysts most commonly found?

A

Eastern Europe
Central and South America
Middle East
North Africa

221
Q

How are hydatid cysts diagnosed?

A

History
Serological testing for anti-echinococcus anti-bodies

222
Q

What are some common management strategies in hydatid cysts?

A

Surgery
Albendazole
Percutaneous drainage

223
Q

What are embryonic ductal plate malformations?

A

These are embryonic malformations of the intrahepatic biliary tree, leading to the formation of numerous cysts throughout the liver parenchyma

224
Q

What are the 3 types of ductal plate malformations?

A

Von Meyenburg complexes (VMC)
Polycystic liver disease
Autosomal dominant polycystic kidney disease

225
Q

What are Von Meyenburg complexes?

A

These are microhamartomas, which are benign nodules that develop throughout the liver, caused by cystic bile duct malformations

226
Q

What is polycystic liver disease?

A

This is a genetic disease causing the formation of many cysts, however, liver function is normally preserved and renal failure is rare

227
Q

What are some symptoms of more severe polycystic liver disease?

A

Abdominal pain
Abdominal distension
Compression of adjacent tissue

228
Q

What is the usual treatment in polycystic liver disease?

A

Conservative treatment is recommended, with liver transplantation only required in cases of advanced disease or liver failure

229
Q

What is autosomal dominant polycystic kidney disease?

A

This is a genetic disease which leads to renal failure due to polycystic kidneys

Non-renal extra-hepatic features are common, leading to potential massive hepatic enlargement

230
Q

What are liver abscesses?

A

These are infections of the liver

231
Q

What are some symptoms of liver abscesses?

A

High fever
leukocytosis
Abdominal pain
Complex liver lesions

232
Q

Who is most at risk of liver abscesses?

A

Those with an abdominal or biliary infection
Those after a dental procedure

233
Q

What is the management strategy in liver abscesses?

A

Empirical borad spectrum antibiotics
Then needle aspiration
Then Echocardiogram
Then surgery if no clinical improvement

234
Q

What is the most common primary liver cancer?

A

Hepatocellular carcinoma

235
Q

What are some risk factors of hepatocellular carcinoma?

A

Males
Cirrhosis
Hepatitis B
Heoatitis C
Alcohol
Aflatoxin (Peanuts)

236
Q

How will hepatocellular carcinoma usually present?

A

Weight loss
RUQ pain
Worsening of pre-existing chronic liver disease
Acute liver failure

237
Q

What are some clinical signs of hepatocellular carcinoma?

A

Signs of cirrhosis
Hard enlarged RUQ mass
Liver bruit (Rare)

238
Q

What are some common sites of metastases from the liver?

A

Portal vein
Lymph nodes
Lung
Bone
Brain

239
Q

What is the first diagnostic test performed in hepatocellular carcinoma?

A

Alpha fetoprotein - HCC tumour marker, with values >100ng/ml being highly suggestive of HCC

240
Q

What are some other tests that can be performed in HCC?

A

Ultrasound
Triphasic CT
MRI

241
Q

What is the best available treatment in hepatocellular carcinoma?

A

Liver transplantation

242
Q

What are some more palliative treatment options in hepatocellular carcinoma?

A

Transarterial chemoembolisation (TACE), in which chemotherapy gents are directly injected into the hepatic artery

Immune checkpoint inhibitors can also be used

243
Q

What are some examples of immune checkpoint inhibitors used in hepatocellular carcinoma?

A

Atezolizumab (Anti-PDL1)
Sorafenib (Multikinase inhibitor)

244
Q

What is fibrolamellar carcinoma?

A

This is an aggressive form of liver malignancy that occurs in young, healthy patients, usually aged 5-35, with no cirrhosis

245
Q

What will be shown on Ct scanning in fibrolamellar carcinoma?

A

Typical stellate scar with radial septa, showing persistent enhancement

246
Q

What are some common cancers that metastasis to the liver?

A

Colon
Breast
Lung
Stomach
Pancreas
Skin (Melanoma)

247
Q

What are LFTs?

A

Liver Function Tests

248
Q

What are some tests that are performed in LFTs?

A

Albumin
Prothrombin time
Bilirubin
ALT and AST
ALP (Alkaline phosphate)
GGT

249
Q

What are some things that should be asked about when taking a liver history?

A

Alcohol
Tattoos
Blood transfusions
Medications
Illicit drug use
Travel history

250
Q

What are the main categories of tests within liver screening?

A

Virology
Immunology
Iron studies
Storage disorder studies
History specififc tests

251
Q

What are some viruses tested for in liver screening tests?

A

HCV - Hepatitis C virus
HBV - Hepatitis B virus
CMV - Cytomegalovirus
EBV - Eppstein-Barr virus

252
Q

What are some auto-antibodies (Immunology) tested for in liver screening?

A

ASMA (Anti-smooth muscle antibodies)
AMA (Anti-mitochondrial antibodies)
ANA (Anti-nuclear antibodies)
ALKM1 (Anti-liver kidney microsomal 1)

253
Q

What iron studies are performed in a liver screening test?

A

Transferrin saturation
Ferritin

254
Q

What are some storage disorder studies performed in a liver screen ?

A

Alpha 1 anti-trypsin
Caeruloplasmin

255
Q

What are some history specific tests that can be carried out in liver screening?

A

HEV (Hepatitis E Virus)
HAV (Hepatitis A Virus)
Paracetamol levels

256
Q

What are the 3 patterns of derrangement in liver function tests?

A

Hepatitic
Cholestatic
Mixed

257
Q

What will be seen in a hepatitic derangement of LFTs?

A

Predominant rise of ALT and AST (Transaminases) >55
This suggests injury to hepatocytes

258
Q

What are some conditions that will show hepatitic derangement of LFTs?

A

Autoimmune hepatitis (100<ALT<800)
HBV, HCV, Viral liver conditions
NAFLD (ALT < 250)

259
Q

What is cholestasis?

A

This is the slow movement or lack of movement of bile, usually caused by obstruction or a disease of the bile ducts

260
Q

What will be seen in a cholestatic derangement of LFTs?

A

Predominant rise in ALP and Bilirubin
Mild rise in ALT and GGT

261
Q

What is the upper limit of normal for bilirubin?

A

22

262
Q

What are some conitions that can cause a cholestatic pattern on LFTs?

A

Gallstones
Primary Biliary Cirrhosis
Obstructing tumours
Primary Sclerosing Cholangitis

263
Q

What are some conditions that can cause a mixed derangement of LFTs?

A

Alcoholic fatty liver disease
Drug induced liver injury
Obstructing or parenchymal tumours

Gastrointestinal (22 decks)

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