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phase 2 > GI > Flashcards

GI Flashcards

1
Q

Which two diseases have a toxin with less than 6hour incubation time and cause diarrhoea, nausea and vomitting

A

S. aureus and bacillus cereus

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2
Q

Diarrhoea, nausea and vomitting from food handler. From dairy products, salads, ham, poultry

A

Staphylococcus aureus

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3
Q

Diarrhoea, nausea and vomitting from reheated rice

A

Bacillus cereus

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4
Q

Which two diseases have a toxin with 8-16h incubation time and causes abdominal cramps and watery diarrhoea

A

Clostridium perfingens and bacillus cereus

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5
Q

Abdominal cramps and watery diarrhoea from beef and chicken and gravies

A

Clostridium perfringens

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6
Q

Abdominal cramps and watery diarrhoea from reheated rice

A

Bacillus cereus

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7
Q

Which toxins have a 16-72hour incubation and caue abdominal cramps and watery diarrhoea

A

Vibrio parahaemolyticus

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8
Q

Abdominal cramps and watery diarrhoea from spring summer shellfish

A

Vibrio parahaemolyticus

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9
Q

Tissue invasion of which microorganisms causes fever, abdominal cramps an diarrhoea which can be bloody, 16-72hr incubation

A

Salmonella spp, campylobacter jejuni, shigella spp

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10
Q

Fever, abdominal cramps and diarrhoea which can be bloody, from poultry eggs beef dairy

A

Salmonella spp

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11
Q

Fever, abdominal cramps and diarrhoea which can be bloody from poultry other meat, milk, water

A

Campylobacter jejuni

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12
Q

What is the most common cause of gastroenteritis

A

Campylobacter jejuni

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13
Q

Fever, abdominal cramps and diarrhoea which can be bloody from egg, salad and lettuce

A

Shigella spp

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14
Q

What is the person to person spread of shigella spp

A

Low

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15
Q

Toxin production in the gut with 72-120hr incubation time causing bloody diarrhoea without fever

A

E. coli 0157

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16
Q

Bloody diarrhoea without fever from ground beef, apples, milk

A

E. coli 0157

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17
Q

Which microorganism causes shiga toxin and renal failure

A

E coli 0157

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18
Q

Which microorganism causes toxin production and tissue invasion 16-48hr incubation time. Fever and abdominal cramps without diarrhoea

A

Yersinia enterocolitica

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19
Q

Fever and abdominal cramps without diarrhoea from pork and milk

A

Yersinia enterocolitica

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20
Q

Fever and abdominal cramps without diarrhoea with an acute abdomen

A

Yersinia enterocolitica

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21
Q

Causes of diarrhoea

A

Bacterial, viral, parasitic, nosocomial, Hepatobilliary infections, travellers, whipples disease and H pylori infection. Malaria and sepsis can also cause.

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22
Q

What does nosocomial mean

A

A disease originating in hospital

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23
Q

What are the three categories of causes of intestinal obstruction

A

Intraluminal obstruction, intramural disease and extraluminal obstruction

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24
Q

Name four causes of intraluminal obstruction

A

Tumour, diaphragm disease, meconium ileus and gallstone ileus

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25
Q

Name three causes of intramural disease

A

Inflammatory, tumours and neural

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26
Q

Name two inflammatory causes of intramural disease

A

Crohns disease and diverticulitis

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27
Q

Name a neural cause of intramural disease

A

Hirschpung’s disease

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28
Q

What does intramural mean

A

Within the walls of the intestine

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29
Q

Name three causes of extraluminal obstruction

A

Adhesions, volvulus and tumour

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30
Q

Name a tumour cause of extraluminal obstruction

A

Peritoneal deposits

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31
Q

What bowel sounds can you hear when there is intestinal obstruction

A

High tinkling

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32
Q

What is a lymphoma

A

Malignant tumour of lymphoid cells

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33
Q

How do NSAIDs cause intestinal obstructoin

A

Recurrant ulceration causes fibrosis and fibrous diaphargm formation, with a narrow lumen

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34
Q

What is gallstone ileus

A

A large gall stone inflames the gall bladder then erodes through into the small bowel

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35
Q

What is meconium

A

A baby’s first poo

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36
Q

What is meconium ileus

A

Seen in CF, meconium adheres to intestinal wall and causes obstruction

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37
Q

Where does inflammatory bowel obstruction most commonly occur

A

Terminal ileum, inflammation causes fibrosis and bowel constricts down

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38
Q

What is diverticular disease and where does it occur

A

Outpouchings of mucosa in the sigmoid colon

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39
Q

What diet is associated with diverticular disease

A

Low fibre

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40
Q

How do diverticular form

A

Low fibre, so increased pressure in the lumen as contraction is reduced. Mucosa is pushed between holes in the muscularis. If they rupture, faecal material enters peritoneum.

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41
Q

Which bowel tumour is the most common and what does it do

A

Gastrointestinal stroma stumours are tumours of the bowel pacemaker cells

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42
Q

What is Hirschprung’s disease

A

Developmental, section of bowel without ganglion so doesnt move and it obstructs. Causes dilation and obstruction of all proximal bowel loops.

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43
Q

Which factor predisposes to bowel adhesions

A

Abdominal surgery

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44
Q

What is a volvulus

A

Where the sigmoid colon twists on it’s long mesentery causing obstruction and cutting off blood supply

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45
Q

Which cancer can easily spread to the peritoneal cavity

A

Ovarian

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46
Q

Is the peritoneum good for cancer and why?

A

Yes very good, moist, smooth mucosa and good blood supply

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47
Q

What percentage of faeces is water and what percentage solid

A

75%, 25%

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48
Q

Where does the gut start and end

A

Mouth to anus

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49
Q

Define intestinal obstruction

A

Blockage to the lumen of the gut

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50
Q

What is intesussuption

A

Telescoping, one hollow structure into its distal hollow structure

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51
Q

What is atresia

A

Absence of opening or failure of development of hollow structure

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52
Q

What is a volvus

A

A twist/rotation of a segment of bowel

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53
Q

What is a paralytic obstruction

A

A pseudo obstruction

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54
Q

What are the four pathologies of obstruction

A

Simple, closed loop, strangulation or intussusception

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55
Q

What can an incompetent ileocaecal valve cause

A

Faeculant vomiting

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56
Q

What can cause proximal dilation of the small bowel

A

Increased secretions or swallowed air

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57
Q

What can cause proximal dilation of the large bowel

A

Bacterial fermentation

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58
Q

What is the consequence of untreated obstruction

A

Ischaemia, necrosis and perforation

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59
Q

What is a simple obstruction

A

Where the bowel is blocked somewhere

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60
Q

What is closed loop obstruction

A

Where a twist has blocked the bowel at one point

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61
Q

What is a strangulation obstruction

A

Where the blood supply is at risk

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62
Q

Will the colon dilate proximal or distal to the obstruction

A

Proximal

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63
Q

Will the small intestine dilate proximal or distal to the obstruction

A

Distal

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64
Q

If the ileocaecal valve is competent where does large bowel obstruction normally occur

A

The caecum

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65
Q

What is a common cause of small bowel obstruction in the developing world

A

Hernia

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66
Q

What are common causes of small bowel obstruction in children

A

Appendicitis and intesussuption

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67
Q

Are bowel obstructions mainly large bowel or small bowel

A

Small bowel (75%)

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68
Q

What is the most common cause of large bowel obstruction in US/.Europe

A

90% colorectal malignancy

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69
Q

What is the most common cause of large bowel obstruction in African countries

A

50% volvulus

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70
Q

What is the most common developmental cause of large bowel obstruction

A

Imperforate anus or Hirschpungs disease

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71
Q

Define hernia

A

Abnormal protrusion of viscus through normal or abnormal defects of body cavity

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72
Q

Do smaller or larger hernias carry a bigger risk

A

Small, more likely to cause strangulation

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73
Q

Where can colonic volvuli occur

A

Sigmoid (76%) and Caecum (22%)

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74
Q

What causes intussusception

A

Imbalance in the longitudinal forces along the intestinal wall due to a mass acting as a lead point or disorganised pattern of peristalsis.

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75
Q

What is obstipation

A

Absolute constipation

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76
Q

How would you describe the pain in intestinal obstruction

A

Colicky and poorly localised

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77
Q

What is the vomiting and constipation like in small bowel obstruction

A

Early vomiting and late constipation

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78
Q

What is the vomiting and constipation like in large bowel obstruction

A

Late vomiting and early constipation

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79
Q

Obstruction of which part of the bowel causes more distension

A

The more distal the obstruction the greater the distension

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80
Q

What is tenesmus

A

Increasing difficulty to open bowels

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81
Q

Stretching of which layer of the bowel causes severe pain

A

Muscularis propria

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82
Q

How is pain relief given in intestinal obstruction

A

IV as wont absorb orally, avoid opiates because slow bowel

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83
Q

Why is NGT used

A

To relieve proximal pressure to the obstruction by decompressing

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84
Q

How big do bowels have to be on XRay to be classified as obstructed

A

369 rule. Small 3cm, Large 6cm, sigmoid/caecal 9cm.

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85
Q

How do you differentiate between small and large bowel on XRay

A

Large bowel’s haustral fols do not go all the way across the lumen and tend to be peripheral

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86
Q

How does intussusception appear on CT scan

A

Target shape

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87
Q

How does sigmoid volvolus appear on CT scan

A

Coffee bean sign

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88
Q

Whats the name of the mucosal folds in the small intestine

A

Valvulae conniventes

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89
Q

Which sections of the large intestine arent fixed and are on a mesentery

A

Transverse and sigmoid

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90
Q

Which types of obstruction require surgery

A

Strangulation and large bowel obstruction

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91
Q

What is the immediate treatment for intestinal obstruction

A

Drip and Suck: IV fluids and NGT

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92
Q

Which scan is used most commonly in GI

A

CT

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93
Q

Define malabsorption

A

Reduced or defective absorption of various nutrients in the small bowel

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94
Q

What provides the immune function of the small intestine

A

Lymphocytes in the tips of the villi

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95
Q

How does CF cause malabsorption

A

Pancreas fills with mucid secretions causing defective bile secretion and defective intraluminal digestion

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96
Q

Where are bile salts reabsorbed

A

Terminal ileum

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97
Q

Coeliac disease (gluten sensitive enteropathy) histologically

A

Short villi, much larger crypts as working much harder. Villous atrophy, crypt hypertrophy. Many more intravillous lymphocytes

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98
Q

What is the mechanism of gluten sensitive enteropathy

A

Lymphocytes with abnormal HLA, react to gliadin and cause and abnormal immune response. T cells subsequently target villi

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99
Q

Name four causes of malabsorption by insufficient absorptive area

A

Gluten sensitive enteropathy, Crohns, Parasites (giardia lamblia) and small intestine resection

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100
Q

What are the 6 categories of malabsorption causes

A

Insufficient intake, defective intraluminal digestion, insufficient absorptive area, lack of digestive enzymes, defective epithelial transport and lymphatic obstruction

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101
Q

What is a cause of malabsorption through lack of digestive enzymes

A

Disaccharide deficiency leads to lactose build up

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102
Q

What is a cause of malabsorption through defective epithelial transport

A

AB protein lipoeamia means lipoproteins cant be moved

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103
Q

What is a cause of malabsorption through lymphatic obstruction

A

Lymphatic oedema

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104
Q

Who mainly gets colorectal cancer and what does this show?

A

The elderly therefore mainly environmental cause

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105
Q

What is an adenoma

A

Group of cells showing dysplasia, a polyp

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106
Q

What is a genetic cause of colorectal adenocarcinoma

A

Familial adenomatous polyposis and hereditary nonpolyposis colorectal cancer (FAP and HNPCC)

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107
Q

What is familial adenomatous polyposis

A

Thousands of polyps (therefore high risk of cancer forming). Removing of colon is treatment.

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108
Q

What causes familial adenomatous polyposis

A

APC protein binds and removes beta cartenin, in familial adenomatous there is a mutant gene and therefore beta cartenin builds up and causes proliferation

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109
Q

What happens in BRCA

A

The DNA repair protein is absent so you get accumulation of cross linking and genetic damage

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110
Q

Why should you identify the genetic link in colorectal cancer

A

To identify further cancers in index patient and relatives and also possible implications for therapy

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111
Q

Malignant neoplasm of the colon must be a

A

Adenocarcinoma

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112
Q

What is the resection coding system

A

R0-tumour completely excised R1-microscopic involvement at margin R2-macroscopic involvement at margin

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113
Q

What does CRM mean in GI tumours

A

Circumferential resection margin, if +ve risk of local recurrence is 85%. If negative means total resection and recurrence rate 10%

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114
Q

Name two staging systems for lower GI tumours

A

Dukes and TIN

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115
Q

What is a Dukes A tumour

A

Not through the wall

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116
Q

What is Dukes B tumour

A

Through the wall but not into lymph nodes

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117
Q

What is Dukes C tumour

A

Through the wall and in nearby lymph nodes

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118
Q

What is Dukes D tumour

A

Through the wall and to higher lymph nodes

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119
Q

What is the treatment for adenoma

A

endoscopic resection

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120
Q

What is the treatment for adenocarcinoma

A

Surgical resection

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121
Q

What is the treatment for metastatic colorectal adenocarcinoma

A

Chemotherapy and palliative care (unless a small bit of liver resection cures)

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122
Q

What can be used to prevent adenoma formation

A

NSAIDs - low dose aspirin

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123
Q

Which cancers are classified as upper GI tract cancers

A

Oesophageal and stomach cancer

124
Q

What marks the junction between the stomach and oesophageal

A

Diaphragm

125
Q

What is the epithelium of the oesophageus

A

Squamous epithelium, resists food

126
Q

What is the epithelium of the stomach

A

Glandular

127
Q

Which epithelium change occurs in Barretts oesophagus

A

Squamous to glandular epithelium

128
Q

What is metaplasia

A

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

129
Q

Why are oesophageal cells susceptible to death and ulceration

A

As they dont have much mucin

130
Q

Which epithelium change occurs in vagina during puberty

A

Cervix invades into the vagina and due to vaginal pH becomes squamous

131
Q

Which population has a high prevalence of squamous cell carcinoma and why

A

The chinese due to heavy smoking and drinking

132
Q

Which population has a high prevalence of adenocarcinoma and why

A

Europe due to obesity causing acid reflux

133
Q

Why do eastern europe and eastern asia have higher rates of gastric cancer

A

Pickled and smoked foods

134
Q

Which microorganism predisposes to gastric cancer

A

Helicobacter pylori as causes metaplasia

135
Q

Which three factors can cause metaplasia of the gastric mucosa

A

Smoked/pickled diet, H. pylori, pernicious anaemia

136
Q

What is responsible for the progression of metaplastic oesophagus to neoplastic

A

GO reflux and other factors

137
Q

What is responsible for the progression of metaplastic gastric mucosa to neoplastic

A

Genetic change

138
Q

What are all gastric cancers classified as

A

Adenocarcinoma

139
Q

What is shallow gastric carcinoma

A

Early gastric cancer

140
Q

What is linitis plastic

A

Leather bottle stomach. Where cancer cells cause a fibrotic reaction causing widespread stiffness

141
Q

What is used for screening of upper GI cancer

A

Barium and endoscopy

142
Q

How is oesophagitis and hiatal hernia assessed

A

Endocopy

143
Q

How is oesophagitis treated

A

Endoscopic dilatation and long term proton pump inhibitor therapy

144
Q

What protects the gastric cells from damage

A

Mucin provides buffering

145
Q

Name factors which can cause disruption of mucin buffering

A

Mucosal ischaemia, ITU, shock, septicaemia, burns

146
Q

What is the treatment for gastric ulcers

A

Increase blood pressure and volume and reduce the amount of acid

147
Q

How can you increase blood pressure and volume

A

Fluids and ionotropes

148
Q

How can you reduce the amount of stomach acid

A

H2 blocker or PPI

149
Q

Which microorganism can PPIs increase the risk of further down the gut

A

C difficile

150
Q

Name causes of ulceration

A

Stress, helicobacter, aspirin, bile reflux and high concentrations of alcohol

151
Q

How does aspirin cause ulceration

A

Causes mucosal ischaemia as it moves into mucosa and inhibits prostaglandin production through COX2. Enteric coated tablets avoid this

152
Q

How does helicobacter pylori cause ulceration

A

Exists in an ecological niche within the mucin layer, secretes chemicals which cause acute inflammation via neutrophil polymorphs

153
Q

Will an ulcerated artery present earlier in the stomach or duodenum

A

Stomach, it will be vomitted out whereas if in the duodenum it would take days before excreted as black stools

154
Q

What will happen if an ulcer goes through connecctive tissue

A

Peritonitis

155
Q

What will happen if a gastric ulcer erodes through the posterior wall

A

It will cause pancreatitis

156
Q

Name chronic idiopathic inflammatory bowel diseases

A

Crohns disease and ulcerative colitis

157
Q

Name inflammatory bowel diseases other than Crohns and UC

A

Diverticulitis, ischaemic colitis, infective colitis (bacterial or protozoal)

158
Q

What is a complication of Crohns which isnt to do with the bowel

A

Amyloidosis

159
Q

What are potential bowel complications of crohns disease

A

Malabsorption, obstruction, perforation, fistula formation, anal, neoplasia

160
Q

What are the unique features of crohns

A

Only affects the colon and mainly the sigmoid and rectum, only mucosal layer, distinct cut off a wide ranging consequences

161
Q

What are some systems affected by UC

A

Colon, joints, eyes, liver, skin

162
Q

What is ascites

A

Abnormal accumulation of fluid within the peritoneal cavity

163
Q

What are capus medusi and whats it a sign of

A

Prominent veins running away from the umbilicus. Can be seen in ascites

164
Q

What are the three causes of ascites

A

Impaired blood outflow, leaky membrane and decreased oncotic pressure

165
Q

What is exudate

A

High protein fluid

166
Q

What is transudate

A

Low protein fluid

167
Q

What is the mechanism of transudate ascites

A

Outflow problem eg portal HTN, decreased oncotic pressure and high serum to ascites albumin gradient

168
Q

What are the causes of transudate ascites

A

Cirrhosis, cardiac failure and Budd-Chiari syndrome

169
Q

What is Budd Chiari syndrome

A

Post hepatic venous thrombosis

170
Q

What is the treatment of transudate ascites

A

Underlying cause, fluids, low salt diet, drainage

171
Q

What is the mechanism of exudate ascites

A

Membrane more porous, altered oncotic pressure. low serum to ascites albumin gradient

172
Q

What are the causes of exudate ascites

A

Cancer, sepsis, TB, nephrotic syndrome

173
Q

Which ascites is more serious

A

Exudate- extremely bad

174
Q

What does abdominal pain relieved by defecation suggest

A

IBS

175
Q

In which part of the colon is cancer more common

A

Distal

176
Q

In which part of the colon does cancer have a worse prognosis

A

Proximal

177
Q

What is Dukes A classification of bowel cancer

A

Invading through the bowel wall but not inot the muscularis propria

178
Q

What is the Dukes B classification of bowel cancer

A

Through the wall of the bowel but hasnt yet invade lymph

179
Q

What is the Dukes C classification of bowel cancer

A

It has invaded through the bowel wall and into the lymph vessels

180
Q

What is the Dukes D classification of bowel cancer

A

It has invaded through the bowel, into the lymph system and has also metastasised

181
Q

Define peritonitis

A

Inflammation of the peritoneum

182
Q

What are possible causes of peritonitis

A

Blood, GI content (faeces and bile), air and bacterial infection

183
Q

How can you identify a blocked bowel on XRay

A

You will see a fluid level

184
Q

What are the clinical signs of intestinal obstruction

A

Colicky central abdominal pain and bilious vomiting

185
Q

Why might you see air under diaphragm on XRay

A

Due to perforation, air in peritoneum

186
Q

Where will the pain be felt for gastric ulcer

A

Epigastric pain

187
Q

Which structure allows the movement of intraabdominal collections and spread of infections

A

Paracolic gutters

188
Q

Which nerves are responsible for dull pain

A

Visceral

189
Q

Which nerves are responsible for sharp pain

A

Somatic

190
Q

Where is the problem when epigastric pain

A

Stomach to duodenum

191
Q

Where is the problem when umbilical pain

A

Duodenum till left colon

192
Q

Where is the problem when pubic pain

A

Left colon onwards

193
Q

Sudden onset low abdominal pain, peritonism, tachycardia, hypotension. 23 yo woman

A

Ectopic pregnancy

194
Q

What is shock

A

Inadequate delivery of oxygen to tissues or organs

195
Q

Which screen is used to estimate survival in peritonitis

A

P-POSSUM

196
Q

Why is there increased physiological frailty with increasing age

A

There is increased use of the physiological reserve

197
Q

What is haematemesis

A

Vomitting of blood

198
Q

What are varices

A

Veins which are distended, lengthened and tortuous

199
Q

What is tachycardia

A

Increased pulse rate, above 100bpm

200
Q

What would die of first if you didn’t have a liver

A

Hypoglycaemia, the liver is the only producer of glucose

201
Q

What are the consequences of cirrhosis

A

Both scarring and disorganisation

202
Q

What are the functions of the liver

A

Glucose and fat metabolism, detoxification and excretion, protein synthesis and defended against infection

203
Q

What type of epithelium lines the portal tract

A

Cuboidal

204
Q

What are the three possible outcomes of acute livery injury

A

Recovery and liver failure

205
Q

What are the three possible consequences of chronic liver injury

A

Recovery, cirrhosis and liver failure

206
Q

Which cells are associated with necrosis

A

Neutrophils

207
Q

What is the histological appearance of necrotic liver cells

A

Dense eisonophilic cytoplasm and pyknotic nucleus

208
Q

What is pyknosis

A

Condensation of chromatin

209
Q

Causes of acute liver injury

A

Viral (A,B,EBV), drug, alcohol, vascular, obstruction, congestion

210
Q

Causes of chronic liver injury

A

Alcohol, viral (B,C), autoimmune, metabolic (iron, copper)

211
Q

Which hepatitis types cause acute liver injury

A

A and B

212
Q

Which hepatitis types cause chronic liver injury

A

B and C

213
Q

What are two manifestations of liver failure

A

Varices and hepatoma

214
Q

What are hepatoma

A

Hepatocellular carcinoma, the most common malignancy of the liver. Hep B and C greatly increase the risk

215
Q

What are varices

A

Varicose veins are veins that are distended, lengthened and tortuous

216
Q

Why does cirrhotic liver have an increased risk of turning into cancer

A

There is an increased rate of regeneration

217
Q

If someone presenets with liver pain what does this suggest

A

Obstruction or malignancy

218
Q

What are the common presentations of acute liver injury

A

Malaise, nausea, anorexia and jaundice

219
Q

What are the common presentations of chronic liver injury

A

Ascites, oedema, haematemesis, malaise, anorexia, wasting, easy bruising, itching, hepatomegaly, abnormal LFTs

220
Q

Why is the liver twice as likely to get ischaemic disease

A

As it has a dual blood supply

221
Q

Metabolic causes of chronic liver injury

A

Iron overload, haemochromatosis, copper overload

222
Q

When do you get liver pain

A

When the liver expands into the capsule. The liver doesnt have nerves but the capsule does

223
Q

What is the most common presentation of liver injury

A

Abnormal liver tests

224
Q

When will there be disease but normal LFTs

A

Compensatory cirrhosis

225
Q

Which serum liver enzymes are cholestatic

A

Alkaline phophatase and gamma-GT

226
Q

Which serum liver enzymes are hepatocellular

A

Transaminases (AST and ALT)

227
Q

What are two causes of yellow skin

A

Jaundice and carotenosis

228
Q

How would you differentiate between carotenosis and jaundice

A

Carotenosis does not affect the eyes

229
Q

What does raised serum unconjugated bilirubin suggest

A

Prehepatic problem (Gilbert’s or haemolysis)

230
Q

What does raised serum conjugated bilirubin suggest

A

Cholestatic problem

231
Q

What is a hepatic cause of raised serum conjugated bilirubin

A

Liver disease

232
Q

What is a post hepatic cause of raised serum conjugated bilirubin

A

Bile duct obstruction

233
Q

Dark stools, pale urine, itching and abnormal liver tests are suggestive of which type of jaundice

A

Cholestatic (hepatic and post hepatic)

234
Q

Which enzyme converts non conjugated bilirubin to conjugated

A

Glucorinotransferase

235
Q

What are the four causes of hepatitis

A

Viral, drug, immune and alcohol

236
Q

Name four causes of liver disease

A

hepatitis, ischaemia, neoplasm and congestion (CCF)

237
Q

What is mirizzis syndrome

A

Compression of the bile duct from the outside

238
Q

Name two ways gall stones cause obstruction

A

Bile duct and mirizzi

239
Q

Name three types of obstructive stricture

A

Malignant, ischaemic and inflammatory

240
Q

Name three causes of hepatic obstruction

A

Gallstone, stricture and blocked stent

241
Q

What do MRCP and ERCP liver scans stand for

A

Magnetic resonance cholangiogram and endoscopic reterograde cholangiogram

242
Q

How is paracetamol induced liver failure treated

A

NAC

243
Q

What is leukonychia

A

White nails

244
Q

What are three main risk factors for gall stones

A

Fat, female, fertile

245
Q

What are some additional risk factors for gall stones

A

Liver disease, ileal disease, TFN, clofibrate

246
Q

Gall bladder gallstone presentation

A

Biliary pain, cholecysitis, maybe obstructive jaundice

247
Q

Bile duct gallstone presentation

A

Biliary pain, obstructive jaundice, pancreatitis, cholangitis

248
Q

What is cholangitis

A

Inflammation of the bile duct system

249
Q

Management of gall bladder gallstones

A

laproscopic cholecystecomy or bile acid dissolution therapy

250
Q

Management of bile duct gallstones

A

ERCP sphincterectomy and removal, crushing and stent placement. Surgery for large stones

251
Q

What can be used for the removal aspect of bile duct gallstones

A

Basket or balloon

252
Q

What can be used for the crushing aspect of bile duct gallstones

A

Mechanical or laser

253
Q

What do raised ALT and AST suggest

A

hepatitis or liver injury, not obstruction

254
Q

Do atenolol and beta blockers cause liver injury

A

NO

255
Q

What enzyme levels will be present in hepatocellular DILI

A

Raised ALT and ALT/Alk ratio

256
Q

What enzyme levels will be present in cholestatic DILI

A

Raised Alk and low ALT/Alk ratio

257
Q

What enzyme levels will be present in mixed DILI

A

Ratio between 2 and 5

258
Q

What is used to treat paracetamol induced fulminant hepatic failure

A

N acetyl cysteine (NAC) and supportive therapy

259
Q

What is spider naevus

A

Swollen blood vessels beneath the skin. They have a central vessel and if you depress the lump the rash spreads

260
Q

What is the most common cause of ascites

A

Chronic liver disease

261
Q

Name causes of ascites

A

Chronic liver disease, neoplasia, pancreatitis and cardiac causes

262
Q

What are two causes of portal hypertension

A

Systemic vasodilation (flow) and increased intrahepatic resistance

263
Q

What is a TIPS

A

Transjugular intrahepatic portosystemic shunt, bypass from high pressure hepatic vein to low pressure portal vein

264
Q

What is steatosis

A

Fat accumulating in hepatocytes from alcohol changing the metabolism

265
Q

What is oliguria

A

Low urine output (<400-500mls a day)

266
Q

What is haematemesis

A

Vomitting blood

267
Q

Causes of portal hypertension

A

Cirrhosis, fibrosis and portal vein thrombosis

268
Q

Pathology of portal hypertension

A

Increased hepatic resistance and increased splanchnic blood flow

269
Q

Consequences of portal hypertension

A

Varices and splenomegaly

270
Q

Which drugs shouldnt be given to those with liver failure as they cause renal failure

A

NSAIDs, diuretics, ACE inhibitors and aminoglycosides

271
Q

Treatment for alcohol withdrawal

A

Lorazepam

272
Q

Do people with liver disease tend to have a high or low blood pressure

A

Low

273
Q

What is the most common cause of infection in liver patients

A

Spontaneous bacterial peritonitis

274
Q

What is spontaneous bacterial peritonitis on gram stain

A

Gram negative bacilli

275
Q

Why do liver patients have reduced opsonic activity

A

Reduced function of Kupffer cells

276
Q

What is primary biliary cholangitis

A

Cirrhosis - name changed to reduce stigma

277
Q

What is hepatic encephalopathy

A

Build up of nitrogenous waste in the brain due to liver failure

278
Q

amenorrhoea meaning

A

absense of periods

279
Q

Which analgesic is safest in those with liver failure

A

Paracetamol

280
Q

How is malnutrition treated

A

Nasogastric feeding

281
Q

How is variceal bleeding treated

A

Endoscopic banding, propanolol and telepressin

282
Q

How is encephalopathy treated

A

Lactulose

283
Q

How is ascites/oedema treated

A

salt/fluid restriction. Diuretics and paracentesis

284
Q

How are infections treated

A

Antibiotics

285
Q

Why do ferritin levels change

A

It is an acute phase protein so goes up when there is any inflammation

286
Q

How is autoimmune hepatitis treated

A

Prednisolone +- azathioprine

287
Q

Which system is used to stage primary biliary cirrhosis

A

Ludwig

288
Q

What is ductopenia

A

Destruction of the bile duct

289
Q

What are varices

A

Dilated blood vessels in the oesophagus or stomach

290
Q

Which prognostic score is used in primary biliary cirrhosis

A

Mayo clinic

291
Q

All autoimmune diseases are associated with which condition

A

Sjogrens, thyroiditis, scleroderma and RA

292
Q

What is sjogrens

A

Women: dry secretions eg tears

293
Q

Which mutation causes haemochromatosis

A

HFE gene C282Y on chromosome 6. It is autosomal recessive and shows variable penetrance

294
Q

What is the mechanism of haemochromatosis

A

Uncontrolled intestinal iron absoprtion with deposition in the liver, heart and pancreas

295
Q

How is haemochromatosis diagnosed

A

Suggested by raised ferritin and transferrin saturation, then confirmed by HFE genotyping and liver biopsy

296
Q

Who is at highest risk of hepatocellular carcinoma

A

Those with fibrosis from a viral cause or haemochromatosis

297
Q

Which groups get non alcoholic fatty liver disease

A

The obese and the diabetic

298
Q

Which disease is the most common cause of mildly raised LFTs

A

Non alcoholic fatty liver disease

299
Q

What does cryptogenic mean

A

Unknown cause

300
Q

What happens to the fat levels as cirrhosis increases in NAFL

A

They drop

301
Q

What is the best treatment of NAFL

A

Weight loss

302
Q

What defect accounts for alpha 1 antitrypsin deficiency

A

Z allelle of the alpha 1 antitrypsin gene

303
Q

How does alpha1 antitrypsin deficiency cause liver failure

A

Protein retention in the liver

304
Q

How does alpha1 antitryspin deficiency cause emphysema

A

Low protein in the blood

305
Q

Hepatic vein occlusion causes

A

Thrombosis, membrane obstruction and venocclusive disease

306
Q

What is the presentation of hepatic vein occlusion

A

Abnormal liver tests, ascites, acute liver failure

307
Q

What is the treatment for hepatic vein occlusion

A

Anticoagulation and TIPS

phase 2 (17 decks)

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