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Year 2 > GI Tumours and torsions > Flashcards

GI Tumours and torsions Flashcards

1
Q

What is a volvulus

A

Complete twisting of a loop of intestines around its mesenteric attachment

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2
Q

When can a volvulus occur

A 
Stomach
Small Intestines
Caecum
Transverse Colon
Sigmoid Colon
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3
Q

What is the most common part of the body in which a volvulus forms

A

Sigmoid

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4
Q

What age group do sigmoid volvulus effect

A

Elderly

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5
Q

When do volvulus tend to present

A

Children + babies

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6
Q

Clinical presentation of a volvulus

A
  1. Bilious vomiting
  2. Failure to thrive
  3. Anorexia
  4. Constipation
  5. Bloody stools
  6. Abdo pain
  7. malnutrition
  8. Immunodeficiency
  9. Regurgitation of saliva
  10. Dysphagia and noisy gastric peristalsis may occur in chronic volvulus
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7
Q

How common is volvulus of the stomach

A
  1. Quite rare
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8
Q

What is the classical triad of GI obstruction features

A
  1. Vomiting
  2. Pain
  3. Failed attempts to pass an nasogastric tube
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9
Q

What is differential diagnosis of volvulus

A
  1. Acute obstruction
  2. Appendicitis, cholecystitis, constipatoin
  3. Gastroenteritis
  4. GORD
  5. Hepatitis
  6. Peptic Ulcers
  7. Pancreatitis
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10
Q

What would an abdominal x-ray show for volvulus diagnosis

A
  1. Sigmoid shows inverted U shape loop of bowel that looks a bit like a coffee bean
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11
Q

Other than AXR, what is used to diagnose for volvulus

A
  1. ULTRASOUND
  2. MRI
  3. CT
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12
Q

How is volvulus treated

A

Surgical correction

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13
Q

Name the surgical correction for Volvulus

A

Ladd’s procedure

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14
Q

What is Ladd’s procedure

A

Anti-clockwise rotation to correct error

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15
Q

What is non-surgical treatment of volvulus

A

GI compression with naso-gastric tube

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16
Q

Complications of volvulus treatment

A
  1. Intestinal ischaemia, mucosal necrosis + sepsis
  2. Perforation, peritonitis + death
  3. Malabsorption
  4. Growth retardation
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17
Q

In what part of the oesophagus is squamous cell carcinoma common

A

Middle third and upper third

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18
Q

Where do adenocarcinomas of the oesophagus take place

A

Lower third and cardia

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19
Q

What age of people does oesophageal carcinoma tend to effect

A

60-70yrs old

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20
Q

How is the incidence of SCC changing

A

Decreasing

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21
Q

What gender do SCCs effect

A

Males

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22
Q

Causes of SCC

A
  1. High levels of consumption
  2. Achalasia
  3. Tobacco use
  4. Obesity
  5. Smoking
  6. Low fruit + veg consumption
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23
Q

Why does obesity contribute to SCC

A

Increased reflux

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24
Q

What is Achalasia

A

Disorder where oesophagus has reduced ability to do peristalsis and transport food down

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25
Q

What decreases the risk of SCC

A 
Diets rich in:
fibre
carotenoids
folate
Vit C
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26
Q

What epithelium do adenocarcinomas of the oesophagus occur in

A

Columnar-lined epithelium

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27
Q

Causes of adenocarcinomas

A
  1. Smoking
  2. Tobacco
  3. GORD
  4. Obesity (increased reflect)
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28
Q

Risk factors for adenocarcinomas

A

Same as SCC

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29
Q

Why are SCCs dangerous

A

People with SCCs are asymptomatic so when it is found it is EXTREMELY ADVANCED

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30
Q

Describe progressive dysphagia (SCC)

A
  1. Initially there is difficulty swallowing solids but dysphagia for liquids follows within weeks
  2. Dysphagia to solids AND liquids from the start this indicates banging disease
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31
Q

Clinical presentation of SCC/Adenocarcinoma

A
  1. Weight Loss
  2. Lymphadenopathy 3. Anorexia
  3. Pain due to impaction of food or infiltration of cancer into adjacent structures
  4. Oesophageal obstruction eventually causes difficulty in swallowing saliva, coughing and aspiration into lungs
  5. Signs from upper thirds of oesophagus (hoarseness and coughs)
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32
Q

How is oesophageal cancer diagnosed

A
  1. Oeosphagoscopy with biopsy
  2. Barium swallow
  3. CT scan/MRI/PET for tumour staging
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33
Q

Why is barium swallow for oesophagus cancer needed

A

Allows us to see strictures

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34
Q

How is oesophageal cancer surgically improved

A
  1. Combined with chemotherapy BEFORE SURGERY (improves outcome) + radiotherapy
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35
Q

When is there a best chance of oesophageal cancer cure

A

If tumour has NOT infiltrated outside the oesophageal wall (stage I)

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36
Q

If locally incurable or metastatic, how is oesophageal cancer treated

A

Systemic chemotherapy (stage II and III)

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37
Q

How is dysphagia treated

A
  1. Endoscopic insertion of expansing metal stent across tumour to ensure oesophageal potency
  2. Laser and alcoholic injections to cause TUMOUR NECROSIS and increase lumen size
  3. Palliative care
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38
Q

Survival rates of dysphagia

A

Low

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39
Q

What benign oesophageal tumour is most common

A

Leiomyomas

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40
Q

What other benign tumours can appear in the oesophagus

A
  1. Papillomas
  2. Fibrovascular types
  3. Haemangiomas
  4. Lipomas
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41
Q

What is a hemangioma

A

benign tumour of the blood vessels

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42
Q

What are leiomyomas

A

Smooth muscle tumours arising from the oesophageal wall

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43
Q

Characteristics of leiomyomas in the oesophagus

A
  1. Intact
  2. Well-encapsulated
  3. Within the overlying mucosa
  4. Slow-growing
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44
Q

Clinical features of leiomyomas

A
  1. Asymptomatic
  2. Dysphagia
  3. Retrosternal pain
  4. Food regurgitation
  5. Recurrent chest infections
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45
Q

How are benign oesophageal tumours diagnosed

A
  1. Endoscopy
  2. Barium Swallow
  3. Biopsy to rule of malignancy
46
Q

How are benign oesophageal tumours treated

A
  1. Endoscopic removal

2. Surgical removal

47
Q

In what gender do gastric tumours effect

48
Q

How does age effect incidence of gastric tumours

A

Increases with age

49
Q

How is the incidence of adenocarcinomas in the body and distal stomach changing

50
Q

Main causes of gastric tumours

A
  1. Smoking
  2. Helicobacter pylori
  3. Dietary factors
  4. Loss of p53 and APC genes
  5. First degree relative with gastric cancer
  6. Pernicious anaemia
51
Q

How do helicobacter pylori cause gastric cancer

A

Infection causes chronic gastritis which leads to atrophic gastritis and pre-malignant intestinal metaplasia -> dysplasia

52
Q

What things in the diet can cause gastric tumours

A
  1. High salt and nitrate increases risk

2. Non-starchy veg, fruit, garlic + low salt DECREASES risk

53
Q

What are all gastric cancers

A

ADENOCARCINOMAS

54
Q

Appearance of intestinal gastric cancers

A
  1. Well-formed + differentiated glandular structures
55
Q

Appearance of tumours in intestinal gastric cancers

A

Polypoid or ulcerating lesions with heaped-up, rolled edges

56
Q

What is seen in the mucosa of people with intestinal gastric cancers

A

Intestinal metaplasia with H. pylori

57
Q

In what part of the stomach does intestinal gastric cancer take place

A

Distal stomach in patients with atrophic gastritis

58
Q

Appearance of cells in diffuse intestinal gastric cancer

A
  1. Poorly cohesive undifferentiated cells that tend to infiltrate gastric wall
59
Q

What part of the stomach do diffuse gastric cancer effect

60
Q

What has the worse prognosis, intestinal or diffuse

61
Q

Clinical presentation of gastric cancer

A
  1. Epigastric pain indistinguishable from peptic ulcer disease (CONSTANT + SEVERE)
  2. Nausea, anorexia
  3. Weight loss
  4. Vomiting is frequent
  5. Anaemia
  6. Liver metastasis resulting in jaundice
62
Q

How is epigastric piani relived

A

Food and antacids

63
Q

When is vomiting most severe

A

If tumour encroaches on pylorus

64
Q

What symptom is seen if gastric cancer is in the fundus

65
Q

Where can gastric cancer metastasise

A

Liver, bone, brain and lung

66
Q

What lumps node is palpable in gastric cancers

A

In supraclavicular fossa on left side

67
Q

How i s gastric cancer diagnosed

A

gastroscopy and biopsy to confirm adenocarcinoma

68
Q

How many biopsies of the stomach are taken

69
Q

Why is an endoscopic ultrasound used to diagnose gastric cancers

A

Evaluate depth of invasion

70
Q

Why are CT/MRI used for gastric cancer diagnosis

71
Q

Why are PET scans used for gastric diagnosis

A

Identifies metastases

72
Q

How are gastric cancers treated

A

1, NUTRITIONAL SUPPORT

2. Surgery and combination chemotherapy followd by radiotherapy

73
Q

What combination chemotherapy is used for gastric cancers

A
  1. EPIRUBICIN
  2. CISPLATIN
  3. 5-FLUOROURACIL

ECF chemo

74
Q

When is chemo given

A

Around same time as surgery

75
Q

How common are small intestine tumours

76
Q

What kind of tumour is most prevalent in the small intestines

A

ADENOCARCINOMAS

77
Q

Where in the small intestines can non-hodgkin’s lymphoma be found

A

ILEUM (not as common as adenocarcinomas)

78
Q

Risk factors for small intestinal cancers

A
  1. Coeliac

2. Crohn’s

79
Q

Clinical presentation of small intestinal cancers

A 
Pain 
Diarrhoea
Anorexia
Weight loss
Anaemia
Palpable mass
80
Q

How are small intestinal cancers diagnosed

A
  1. ULTRASOUND
  2. ENDOSCOPIC BIOPSY
  3. CT SCAM
81
Q

What would a CT scan show

A

Small bowel wall and lymph node involvement

82
Q

What are clonal polyps

A

Abnormal growth of tissue projecting from colonimucosa

83
Q

What are adenomas

A

Benign, dysplastic tumour of columnar cells or glandular tissues
Precursor lesions to colon cancer

84
Q

Are adenomas common before age of 30

85
Q

When are polyps removed

A

At colonoscopy

86
Q

Clinical presentation of polyps in rectum and sigmoid colon

87
Q

How do FAPs form

A

Mutation in APC gene

88
Q

At what age do FAPs form

A

16 and cancer at 39

89
Q

How are FAPs characterised

A

Autosomal dominant

Colorectal and duodenal adenomas

90
Q

How are FAPs treated

A

Prophylactic colectomy and ileorectal anastomosis

91
Q

What is HNPCC (Lynch syndrome)

A
  1. Mutation in one of the DNA mismatch repairs genes (hMSH2 or hMSH1)
92
Q

Role of hMSH1 and 2

A

Maintain stability of DNA during replication causing highly repeated short DNA sequences known as micro satellites that are shorter or longer than normal (increases risk of DNA damage)

93
Q

What kind of cancer are colorectal carcinomas

A

ADENOCARCINOMAS

94
Q

Where do CRCs occur

A

Distal colon

95
Q

Risk factors for CRCs

A
  1. Increasing age
  2. Low fibre diet
  3. Saturated animal fat + red meat consumption
  4. Sugar consumption
  5. Colorectal polyps
  6. Alcohol + smoking
  7. Obesity
  8. Adenomas
  9. Ulcerative colitis
  10. Family History
96
Q

How to reduce risk of CRCs

A
  1. Veg
  2. Garlic
  3. Milk
  4. Excersise
  5. Low-dose aspirin
97
Q

What is the appearance of CRCs

A

Polyploid mass with ulceration

98
Q

How do CRCs metastasise

A

Direct infiltration through bowel wall and spread down lymphatics and blood vessels to liver and lungs

99
Q

When do right-sided adenocarcinomas stop being asymptomatic

A

Until they present with iron deficiency anaemia due to bleeding

100
Q

Clinical presentation of right-sided adenocarcinomas (CRCs)

A

Mass
Weight loss
Low Haemoglobin
Abdo pain

101
Q

Clinical presentation of left-sided adenocarcinomas (CRCs)

A
  1. Changes in bowel habit with blood and mucus in stools
  2. Diarrhoea
  3. Alteration constipation and diarrhoea
  4. Thin/altered stools
  5. Blood in stools
102
Q

What do patients with rectal carcinomas present with

A

Rect bleeding and mucus

When cancer grows will have thinner stool and tenesmus

103
Q

What is tenesmus

A

Cramping rectal pain

104
Q

In emergencies what are 4 signs of gastro obstruction

A
  1. ABSOLUTE constipation
  2. Colicky abdo pain
  3. Abdo distension
  4. VOMITING
105
Q

What can CRCs be mistaken for

A
  1. Haemorrhoids
  2. Fissures
  3. Anal Prolapse
  4. Diverticular disease
  5. IBD
  6. Ischaemic colitis
  7. Massive upper GI bleed
  8. Meckel’s diverticulum
106
Q

How are CRCs diagnosed

A
  1. Faecal occult blood
  2. Tumour markers (not specific)
  3. COLONOSCOPY
  4. Double contrast barium enema
  5. CT colonoscopy
107
Q

How is the uncomfortableness of a colonoscopy treated

108
Q

Risk of colonoscopy

A

Perforation (needs a stoma)

DEATH

109
Q

What is a double-contrast barium enema a replacement for

A

Colonoscopy

Doesn’t require sedation and avoids perforation

110
Q

Con of double-contrast barium enemas

A

Limited in detecting small lesions

111
Q

Why are CT colonoscopies used in the elderly

A

No sedation and avoids perforation risk (limited in detecting small lesions)

112
Q

Why is an MRI used in CRC diagnosis

A

Determines spread

Year 2 (155 decks)

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