Deck 6 Flashcards
Q. What occurs to the epithelial cells of the oesophagus in Barrett’s oesophagus? What is the main cause of this?
A. Squamous cells become glandular/columnar due to acid reflux
B. CELLO = columnar lined lower oesophagus
C. Incidence increased with age, main cause due to obesity
Q. What is the most common cancer of the oesophagus; what are the two main types and who do they affect most?
A. Carcinoma: two main types squamous carcinoma and adenocarcinoma
B. Usually commences as an ulcer and spread to become annular, then constricts and pt develops dysphagia
C. Squamous: higher incidence in men, smoking, alcohol, thermal injury, HPV infection (squamous epithelium develops into squamous cancer)
D. Adenocarcinoma: higher incidence in men, recent increase in incidence in western countries (obesity)
E. GORD and Barrett’s oesophagus predispose
Q. What can metaplastic oesophageal glandular epithelium develop into?
A. Dysplastic oesophageal glandular epithelium
B. Then to neoplastic oesophageal glandular epithelium
C. Can develop into adenocarcinoma
D. (normal, metaplastic, dysplastic, neoplastic)
Q. What causes squamous cell carcinoma? How does it normally present?
A. Alcohol and smoking
B. Presents: late, often with dysphagia
Q. Describe the management of squamous cell carcinoma
A. Small tumours: resected with endoscope
B. Tumour in submucosa: oesophagostomy (incision in chest and abdo)
C. Large tumour: palliative, stents to allow feeding etc (invasion of muscle)
Q. Which common infection increases the chances of gastric cancer
A. Helicobacter
Q. Which parts of the GI tract are major sites of peptic ulcers and therefore cancer
A. First part of duodenum (due to acid from stomach)
B. Junction of antral and body mucosa in the stomach
C. Distal oesophagus (nearest to stomach)
D. Gastro-enterostomy site due to prev surgery (surgical creation of connection between stomach and jejunum)
Q. Name four risk factors of peptic ulcers, name 2 associated complications
A. Hyperacidity, helicobacter, duodenal-gastric reflux, NSAIDS, smoking, genetic factor
B. Complications: haemorrhage, penetration of adjacent organs, perforation, anaemia, obstruction due to fibrous strictures and malignancy
Q. What is a polyp?
A. Protuberant (bulging) masss of tissue (mass be neoplastic or due to excessive reparative or regenerative process)
Q. Where are gastric cancers likely to spread to?
A. Pancreas, transverse colon, liver, spleen
Q. Where is the most common site for intestinal cancer?
A. Small intestine: uncommon
B. Large intestine: common, often Lt side (sigmoid, then rectum, then left descending colon), then rt, then transverse
Q. Describe two (3) types of adenoma seen in the intestine
A. Tubular (75%): generally small, appearance like raspberry, stalk and broad base, numerous elongated crypts lined by mucus-secreting epithelium
B. Villous (10%): usually sessile, larger, extend over a wide area, elongated vili in papillary growth pattern
C. Tubulovillous (15%): intermediate
Q. What is the adenoma-carcinoma sequence?
A. Mechanism of polyp to adenocarcinoma
B. Normal epithelium, small polypoid adenoma, large polypoid adenoma, invasive adenocarcinoma
Q. Name a hereditary condition with a high risk of colorectal adenoma
A. Familial adenomatous polyposis (FAP)
B. Mutations in APC gene, autosomal dominant
C. Activation of MAPK pathway including cell proliferation, preventing apoptosis, and promoting invasion, metastasis and neovascularisation
D. Loss or mutation of tumour suppressor genes
1.
- Q. Name 3 different causes of peritionitis
A. Bacterial: gram +, gram –ve, perforated viscus, spontaneous bacterial peritonitis
B. Chemical: gall bladder burst or leakage: bile leak (post op?)
C. Haematological: ruptured ectopic pregnancy, trauma?
Q. Name 3 different causes of peritionitis
A. Bacterial: gram +, gram –ve, perforated viscus, spontaneous bacterial peritonitis
B. Chemical: gall bladder burst or leakage: bile leak (post op?)
C. Haematological: ruptured ectopic pregnancy, trauma?
Q. Name 3 differences between visceral and parietal viscera
A. Visceral: on organs, autonomic innervation, poor localised sensation
B. Parietal: found on abdominal wall, somatic innervation, well localised sensation
Q. Describe 4 key features in a classic presentation of peritonitis
A. Sudden onset of pain (due to perforation)
B. Severe pain on movement, lying still relieves
C. Poorly localised, then moves to one point on abdomen
D. Walking is painful
E. Systemically shocking (temp, high HR, low BP)
F. Point tenderness vs rigid abdo (muscle protective)
G. Localised v generalised
Q. Name two investigations for peritonitis
A. FBC – infection? CRP, amylase? B. CXR, abdo XR C. CT abdo: obstruction? D. (B-HCG = ectopic preg? E. ECG – MI – clot?
Q. Name 2 multisystem complications that may be present due to peritonitis
A. Hypovolaemia B. Kidney failure C. Systemic sepsis D. Paralytic ileus E. Pulmonary atelectasis/pneumonia F. Portal pyaemia
Q. What major factor may affect where an abscess forms?
A. The position of the patient!
B. Standing = pelvis
C. Supine = L/R paracolic gutter
D. Supine: suprahepatic/sub-phrenic
Q. Name 2 patients who are at a higher risk of primary peritonitits
A. Pts with liver damage, ascites, immunocompromised
Q. Where is pain due to appendicitis likely to be?
A. Generalised then moves to right iliac fossa
Q. What are ascites?
A. Accumulation of free fluid within the peritoneal cavity
Q. What is heard on percussion of abdomen in a pt with ascites?
A. Dull: due to gas/fluid – ‘shifting dullness’ – ask pt to roll over
Q. How should ascites be diagnosed?
A. Ultrasound of liver, ascetic tap, treat underlying cause
B. General management: restrict sodium, diuretics, drainage, ahint/TIPSS – poor prognosis
