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GIT Pathology Flashcards

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1
Q

In what percentage of patients with familial adenomatous polyposis coli do desmoid tumours occur?

A

Up to 15%

This association highlights the importance of monitoring for desmoid tumours in these patients.

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2
Q

Desmoid tumours usually show bi allelic mutations of _______.

A

APC

The APC gene is crucial in the development of familial adenomatous polyposis and is implicated in desmoid tumour formation.

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3
Q

What is the preferred treatment for desmoid tumours?

A

Radical surgical resection

In some cases, radiotherapy and chemotherapy may be considered, but surgical options are usually prioritized.

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4
Q

In selected cases of abdominal desmoids, what may be preferred instead of immediate treatment?

A

A period of observation

Some abdominal desmoid tumours may spontaneously regress, making observation a valid strategy.

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5
Q

What cell type is most associated with Desmoid tumors?

A

Myofibroblasts

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6
Q

Post splenectomy blood film cells?

A

Howell- Jolly bodies
Pappenheimer bodies
Target cells
Irregular contracted erythrocytes

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7
Q

What are the primary causes of iliopsoas abscess?

A

Haematogenous spread of bacteria, primarily Staphylococcus aureus.

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8
Q

What is the recurrance rate for iliopsoas abscesses?

A

Up to 15-20%

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9
Q

What are the clinical features of iliopsoas abscess?

A

Fever, back/flank pain, limp, and weight loss.

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10
Q

How should a patient be positioned for clinical examination of iliopsoas abscess?

A

Supine position with the knee flexed and the hip mildly externally rotated.

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11
Q

What is another specific test for iliopsoas inflammation?

A

Lie the patient on the normal side and hyperextend the affected hip; this should elicit pain as the psoas muscle is stretched.

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12
Q

What is the gold standard investigation for iliopsoas abscess?

A

CT scan.

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13
Q

Stipple cells found in?

A

Lead poisoning

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14
Q

What happens to red blood cells after splenectomy?

A

The loss of splenic tissue results in the inability to readily remove immature or abnormal red blood cells from circulation.

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15
Q

What types of cells appear in circulation in the first few days after splenectomy?

A

Target cells, siderocytes, and reticulocytes will appear in circulation.

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16
Q

What is observed immediately following splenectomy?

A

A granulocytosis (mainly composed of neutrophils) is seen.

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17
Q

What changes occur in blood cell composition over the following weeks after splenectomy?

A

Granulocytosis is replaced by lymphocytosis and monocytosis.

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18
Q

What happens to the platelet count after splenectomy?

A

The platelet count is usually increased and may be persistent.
Will need antiplatelet

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19
Q

Which tumor supressor gene portects against neoplasm

A

p53

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20
Q

Coeliac disease is associated with what type of spleen?

A

hyposplenism

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21
Q

What is Li-Fraumeni Syndrome?

A

An autosomal dominant condition consisting of germline mutations to the p53 tumour suppressor gene, leading to a high incidence of malignancies, particularly sarcomas and leukaemias.

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22
Q

How is Li-Fraumeni Syndrome diagnosed?

A

Diagnosis occurs when an individual develops sarcoma under 45 years or when a first degree relative is diagnosed with any cancer below age 45 years and another family member develops malignancy under 45 years or sarcoma at any age.

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23
Q

What are BRCA 1 and BRCA 2?

A

Genes carried on chromosome 17 (BRCA 1) and chromosome 13 (BRCA 2) linked to a 60% risk of developing breast cancer and associated risks of developing ovarian cancer (55% with BRCA 1 and 25% with BRCA 2).

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24
Q

What is Lynch Syndrome?

A

An autosomal dominant condition where individuals develop colonic and endometrial cancer at a young age, with 80% of affected individuals likely to develop these cancers.
Stomach ca as well

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25
What are the Amsterdam criteria?
Criteria used to identify high risk individuals for Lynch Syndrome, requiring three or more family members with confirmed colorectal cancer, one being a first degree relative, two successive affected generations, and one or more colon cancers diagnosed under age 50 years.
26
What is Gardner's syndrome?
An autosomal dominant familial colorectal polyposis characterized by multiple colonic polyps and extra colonic diseases including skull osteoma, thyroid cancer, and epidermoid cysts.
27
What mutation is associated with Gardner's syndrome?
A mutation of the APC gene located on chromosome 5, leading to colonic polyps and often necessitating colectomy to reduce the risk of colorectal cancer.
28
How is Gardner's syndrome classified in relation to familial adenomatous polyposis?
It is now considered a variant of familial adenomatous polyposis coli.
29
What are the features of Morgagni hernia?
Anteriorly located, minimal compromise on lung development, minimal signs on antenatal ultrasound, usually present later, and usually good prognosis.
30
What are the features of Bochdalek hernia?
Posteriorly located, larger defect, often diagnosed antenatally, associated with pulmonary hypoplasia, and poor prognosis.
31
What are posterior hernias of Bochdalek?
The most common type of hernia that typically presents soon after birth with respiratory distress.
32
What is a classical finding in infants with Bochdalek hernias?
A scaphoid abdomen on clinical examination due to herniation of abdominal contents into the chest.
33
What chromosomal abnormalities are associated with Bochdalek hernias?
Trisomy 21 and 18.
34
What causes considerable respiratory distress in infants with Bochdalek hernias?
Hypoplasia of the developing lung.
35
What is the historical view regarding pulmonary hypoplasia in Bochdalek hernias?
It was considered to be due to direct compression of the lung by herniated viscera.
36
What complications are associated with pulmonary hypoplasia?
Pulmonary hypertension and abnormalities of pulmonary vasculature.
37
What risk does pulmonary hypertension pose to infants with Bochdalek hernias?
Risk of right to left shunting, resulting in progressive and worsening hypoxia.
38
What diagnostic workup is performed for infants with Bochdalek hernias?
Chest x-rays, abdominal ultrasound scans, and cardiac echo.
39
What is the mainstay of treatment for Bochdalek hernias?
Surgery utilizing both thoracic and abdominal approaches.
40
How are smaller and larger defects treated in Bochdalek hernias?
Smaller defects may be primarily closed, while larger defects may require a patch.
41
What is the mortality rate associated with Bochdalek hernias?
50-75%, related to the degree of lung compromise and age at presentation.
42
How does age at presentation affect mortality in Bochdalek hernias?
Mortality is considerably better in infants older than 24 hours.
43
What are the first blood components affected following splenectomy?
The granulocyte and platelet count are the first to be affected.
44
What happens to reticulocyte levels after splenectomy?
Reticulocytes increase following splenectomy.
45
How long does it take for lymphocytosis and monocytosis to develop after splenectomy?
Lymphocytosis and monocytosis take several weeks to develop.
46
Is the eosinophil component usually raised after splenectomy?
The eosinophil component is seldom raised following splenectomy.
47
What vaccines should individuals with hyposplenism receive?
Individuals with hyposplenism or those who may become so should receive pneumococcal, haemophilus type b, and meningococcal type C vaccines. These should be administered 2 weeks prior to splenectomy or two weeks following splenectomy.
48
What vaccination is recommended annually?
Annual influenza vaccination is recommended in all cases.
49
Who should receive antibiotic prophylaxis post-splenectomy?
Antibiotic prophylaxis is offered to all, especially those at greatest risk, including individuals under 16 years or over 50 years, and those with a poor response to pneumococcal vaccination.
50
What precautions should asplenic individuals take when traveling?
Asplenic individuals traveling to malaria endemic areas are at high risk and should have both pharmacological and mechanical protection.
51
What is the dosing for antibiotic prophylaxis post splenectomy?
Penicillin V 500mg BD or amoxicillin 250mg BD.
52
What occurs during vascular changes in acute inflammation?
Vasodilation occurs and persists, inflammatory cells exit circulation, and capillary permeability increases, leading to protein-rich exudate formation.
53
What is the role of fibrinogen in acute inflammation?
The high fibrinogen content of the fluid may form a fibrin clot, which has important immunomodulator functions.
54
What are the possible sequelae of acute inflammation?
The sequelae include resolution, organisation, suppuration, and progression to chronic inflammation.
55
What characterizes the resolution of acute inflammation?
Resolution typically occurs with minimal initial injury, where the stimulus is removed and normal tissue architecture is restored.
56
What is a histological diagnostic feature of acute inflammation?
The presence of neutrophil polymorphs is a histological diagnostic feature of acute inflammation.
57
What is Peutz-Jeghers syndrome?
Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous benign hamartomatous polyps in the gastrointestinal tract and pigmented freckles on the lips, face, palms, and soles.
58
What is the inheritance pattern of Peutz-Jeghers syndrome?
It is an autosomal dominant condition.
59
What gene is responsible for Peutz-Jeghers syndrome?
The responsible gene encodes serine threonine kinase LKB1 or STK11.
60
What are the main features of Peutz-Jeghers syndrome?
Features include hamartomatous polyps in the GI tract (mainly small bowel), pigmented lesions on lips, oral mucosa, face, palms, and soles, intestinal obstruction (e.g., intussusception), and gastrointestinal bleeding.
61
What is the prognosis for patients with Peutz-Jeghers syndrome?
Around 50% of patients will have died from a gastrointestinal tract cancer by the age of 60 years.
62
How is Peutz-Jeghers syndrome managed?
Management is conservative unless complications develop.
63
What may large villous adenomas of the rectum result in?
The development of hypokalaemia.
64
Why do large villous adenomas of the rectum cause hypokalaemia?
Because rectal secretions are rich in potassium.
65
What is Pseudomyxoma Peritonei?
A rare mucinous tumour that most commonly arises from the appendix, although other abdominal viscera can also be primary sites.
66
What characterizes Pseudomyxoma Peritonei?
The disease is characterized by the accumulation of large amounts of mucinous material in the abdominal cavity.
67
What is the usual treatment for Pseudomyxoma Peritonei?
The usual treatment is surgical, consisting of cytoreductive surgery (often peritonectomy) combined with intra peritoneal chemotherapy using mitomycin C.
68
What is Meckel's diverticulum?
A congenital abnormality resulting in incomplete obliteration of the vitello-intestinal duct.
69
What are some associated conditions with Meckel's diverticulum?
Enterocystomas, umbilical sinuses, and omphaloileal fistulas.
70
What is the arterial supply to Meckel's diverticulum?
Omphalomesenteric artery.
71
What is the prevalence and typical size of Meckel's diverticulum?
2% of the population, 2 inches long, and located 2 feet from the ileocaecal valve.
72
What type of mucosa typically lines Meckel's diverticulum?
Typically lined by ileal mucosa, but ectopic gastric mucosa can occur, with the risk of peptic ulceration.
73
What other types of mucosa can occur in Meckel's diverticulum?
Pancreatic and jejunal mucosa can also occur.
74
What is the clinical presentation of Meckel's diverticulum?
Normally asymptomatic and an incidental finding.
75
What complications can arise from Meckel's diverticulum?
Complications are the result of obstruction, ectopic tissue, or inflammation.
76
When is removal of Meckel's diverticulum indicated?
If narrow neck or symptomatic. Options are between wedge excision or formal small bowel resection and anastomosis.
77
What do carcinoid tumors secrete?
Carcinoid tumors secrete serotonin.
78
Where do carcinoid tumors primarily originate?
They originate in neuroendocrine cells mainly in the intestine (midgut-distal ileum/appendix).
79
In which other locations can carcinoid tumors occur?
They can occur in the rectum and bronchi.
80
When do hormonal symptoms mainly occur in carcinoid syndrome?
Hormonal symptoms mainly occur when the disease spreads outside the bowel.
81
What is the onset of carcinoid syndrome?
The onset is insidious over many years.
82
What are common clinical features of carcinoid syndrome?
Common clinical features include flushing face, palpitations, pulmonary valve stenosis, tricuspid regurgitation causing dyspnoea, asthma, and severe diarrhoea.
83
What type of diarrhea is associated with carcinoid syndrome?
The diarrhea is secretory and persists despite fasting.
84
What is a key investigation for carcinoid syndrome?
5-HIAA in a 24-hour urine collection.
85
What imaging technique is used in the investigation of carcinoid syndrome?
Somatostatin receptor scintigraphy and CT scan.
86
What blood test is performed in the investigation of carcinoid syndrome?
Blood testing for chromogranin A.
87
What is a common treatment for carcinoid syndrome?
Octreotide.
88
What is another treatment option for carcinoid syndrome?
Surgical removal.
89
Does rectal involvement occur with diverticular disease?
Rectal involvement with diverticular disease almost never occurs.
90
Why does diverticular disease almost never occur in the rectum?
Because the rectum has a longitudinal muscle coat, diverticular disease almost never occurs here.
91
What are the most common primary liver tumours?
The most common primary liver tumours are cholangiocarcinoma and hepatocellular carcinoma.
92
What percentage of liver malignancies are due to metastatic disease?
Overall metastatic disease accounts for 95% of all liver malignancies.
93
List the types of primary liver tumours.
Primary liver tumours include: • Cholangiocarcinoma • Hepatocellular carcinoma • Hepatoblastoma • Sarcomas (Rare) • Lymphomas • Carcinoids (most often secondary although primary may occur)
94
What percentage of primary liver tumours are hepatocellular carcinoma?
Hepatocellular carcinoma accounts for 75% of primary liver tumours.
95
What is the common background for hepatocellular carcinoma?
Its worldwide incidence reflects its propensity to occur on a background of chronic inflammatory activity.
96
In which conditions do most cases of hepatocellular carcinoma arise?
Most cases arise in cirrhotic livers or those with chronic hepatitis B infection.
97
What percentage of patients with hepatocellular carcinoma present with existing liver cirrhosis?
The majority of patients (80%) present with existing liver cirrhosis.
98
What imaging modalities are preferred for diagnosing hepatocellular carcinoma?
CT/MRI (usually both) are the imaging modalities of choice.
99
What biomarker is elevated in almost all cases of hepatocellular carcinoma?
Alpha-fetoprotein (aFP) is elevated in almost all cases.
100
Why should biopsy be avoided in hepatocellular carcinoma diagnosis?
Biopsy should be avoided as it seeds tumour cells through a resection plane.
101
What is the preferred strategy in cases of diagnostic doubt for hepatocellular carcinoma?
In cases of diagnostic doubt, serial CT and aFP measurements are the preferred strategy.
102
What staging procedures should be performed for hepatocellular carcinoma patients?
Patients should be staged with liver MRI and chest, abdomen and pelvic CT scan.
103
What additional examination should be done in males with hepatocellular carcinoma?
The testis should be examined in males (testicular tumours may cause raised AFP).
104
What is the mainstay of treatment for operable hepatocellular carcinoma cases?
Surgical resection is the mainstay of treatment in operable cases.
105
What consideration may be given for small primary tumours in cirrhotic livers?
Consideration may be given to primary whole liver resection and transplantation.
106
What are the operative risks associated with liver resections in hepatocellular carcinoma?
Operative risks and post-operative hepatic dysfunction are greater than seen following metastectomy.
107
How sensitive are hepatocellular carcinoma tumours to chemotherapy and radiotherapy?
These tumours are not particularly chemo or radiosensitive; however, both may be used in a palliative setting.
108
What is a more popular strategy for treating hepatocellular carcinoma?
Tumour ablation is a more popular strategy.
109
What is the overall survival rate for hepatocellular carcinoma at 5 years?
Overall survival is poor, at 15% at 5 years.
110
How is an enterocutaneous fistula treated?
This is treated with resection.
111
What are vitello intestinal duct anomalies?
Vitello intestinal duct anomalies are common and these are always distal.
112
Is LBO a feature of UC?
No. You will get megacolon
113
Does UC affect the anal canal?
No
114
How common is an anterior anal fissure?
10%

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