Week 4 Flashcards

Question

Treatment of gallstones?

Answer 1

1. Lap Chole | 2. Ursodeoxycholic acid to dissolve gallstones

Answer 2

Biliary colic: - V painful so may require morphine / pethidine (opioids) or diclofenac (NSAID) by suppository - Parenteral/rectal route chosen as overcomes difficulties in absorption caused by vomiting If pain continues for 24hrs+ or accompanied by fever = HOSPITAL ADMISSION

Answer 3

Main example: Colestyramine (an anion-exchange resin) Mechanism: Froms an insoluble complex with bile acids in the intestine Uses: - Relives pruritus associated with partial biliary obstruction and primary biliary cirrhosis -Diarrhoea episodes e.g. Crohn's disease cirrhosis -Hypercholesterolaemia

Answer 4

A bile acid sequestrant. It works by helping the body remove bile acids, which can lower cholesterol levels in the blood. The medicine is also used to relieve itching that's caused by a bile duct blockage.

Answer 5

Benign: - Mesenchymal e.g. Leiomyomas (Smooth muscle) - Squamous papillomas Malignant: - Squamous cell carcinoma - Adenocarcinoma

Answer 6

Benign: - Polyps: Non-neoplastic, adenomas - Mesenchymal Malignant: - Carcinoma (epithelial cells) - Lymphoma - Carcinoid - Mesenchymal

Answer 7

SSC Incidence: ->50 -More males Associated factors: - Diet: Vitamin deficiency, fungal contamination of foods, high content of nitrites/nitrosamines - Lifestyle: Hot food/drinks, alcohol, tobacco - Oesophageal disorders: Long standing oesophagitis and achalasia - Genetic predisposition Morphology: - Location: Mainly in middle 1/3 of oesophagus - Small, gray/white, plaque-like thickenings that become tumours masses - Three patterns: 1. Protruded polypoid exophytic 2. Flat, diffuse, infiltrative, 3. Exacavated, ulcerated Clinical features: - Dysphagia - Extreme weight loss - Haemorrhage and sepsis - Metastases to lymph nodes - Cancerous TEF Prognosis: 5% overall five-year survival

Answer 8

In lower 1/3 of oesophagus Incidence: Age 40 Associations: - Arise from Barrett Mucosa (intestinal metaplasia caused by gastric reflux) - Tobacco and obesity Morphology: - Flat/ raised patches or nodular masses - May be infiltrative or deeply ulcerative Histology: Mucin producing glandular tumours ``` Clinical features: • Dysphagia • Progressiveweightloss • Bleeding • Chestpain • Vomiting • Heartburn • Regurgitation ``` Prognosis: 20% overall five year survival

Answer 9

Tis carcinoma in situ T1 invasion of submucosa T2 invasion of muscularis propria T3 invasion of adventitia T4 invasion of adjacent structures N0 no node spread N1 regional node metastases M0 no distant spread M1 distant metastases

Answer 10

Module or mass that projects above the level of the surrounding mucosa, usually at the Antrum

Answer 11

Gastric carcinoma

Answer 12

Environmental: - Infection ny H pylori - Diet - Low socioeconomic status - Cigarette smoking Host: - Chronic gastritis - Gastric adenomas - Barrett oesophagus Genetic: - Increased risk with blood group A - Family history - Hereditary non-polyposis - Familial gastric carcinoma syndrome

Answer 13

Location: -Pylorus and Antrum ** Classification on the basis of: 1. Depth of invasion 2. Macroscopic growth pattern 3. Histological subtype Macroscopic growth patterns: - Exophytic - Flat or depressed --> Linitis plastica - Excavated Morphology: - All carcinomas eventually spread to regional and more distant lymph nodes. - ->Supraclavicular node - ->Local invasion to duodenum, pancreas and retroperitoneum - Metastases to the liver and lungs are common - Metastases to the liver and lungs - Metastases to the ovaries called Krukenberg tumour ``` Clinical features: • Asymptomatic until late • Weight loss • Abdominal pain • Anorexia • Vomiting • Altered bowel habits • Dysphagia • Anaemic symptoms • Haemorrhage ``` Prognosis: 90-95% for early gastric cancer. Less than 15% for advanced

Answer 14

Intestinal type: - Composed of neoplastic intestinal glands resembling those of colonic adenocarcinoma - Cells often contain apical mucin vacuoles Diffuse type: - Composed of gastric-type mucous cells which permeate the mucosa and wall as scattered individual cells or small clusters in a n "infiltrative" growth pattern - Mucin formation expands the malignant cells and pushes the nucleus to the periphery, creating a "signet ring" Mixed type

Answer 15

What are they? B cell lymphomas of mucosa-associated lymphoid tissue (MALT lymphomas) Associations: Chronic gastritis and H. pylori infection Prognosis: 50% five year survival Morphology: - Occurs in mucosa and superficial submucosa - Lymphocytic infiltrate of the lamina propria surrounds gastric glands massively infiltrated with atypical lymphocytes and undergoing destruction

Answer 16

METABOLIC: Breakdown down carbohydrates, hormones, lipids, drugs and proteins STORAGE: Glycogen, vitamins, iron PROTECTIVE: Detoxification and elimination of toxin compounds, kupffer cells ingest bacteria and other foreign material from blood BILE: Produced and excreted. Formed in biliary canaliculi, emulsifies fats and provides route for waste removal

Answer 17

Hepatic artery= Oxygenated blood | Portal vein - Nutrient rick blood

Answer 18

Liver lobule: - Hexagonal in shape - Hepatocytes arranged in plates - In contact with bloodstream one one side and bile canaliculi on the other - Between the plates are vascular spaces (sinusoids) containing Kupffer cells (phagocytic macrophages)

Answer 19

Infection- Viral, bacterial, parasitic Toxic/drug induced Autoimmune Biliary tract obstruction- Tumours, gallstones Vascular Metabolic : Haemochromatosis, Wilson's, hereditary hyperbilirubinaemias Neoplastic

Answer 20

Failure to produce or excrete bile - Intrahepatic = Problems in secretion of bile by hepatocytes due to damage - Extrahepatic = Problems with flow of bile out of the liver due to obstruction Result: - Accumulation of bilirubin in the blood leading to JAUNDICE. - Urine darkens - Stool becomes lighter

Answer 21

Excessive haemolysis, so bilirubin is uncongutated and does not appear in urine

Answer 22

Acute: Development of severe hepatic dysfunction within 24wks of onset of disease Chronic: Progressive decline in liver function with established disease

Answer 23

Poisoning e.g. from paracetamol Infection (Hepatitis A-C) Inadequate perfusion

Answer 24

Resolution Progression to acute hepatic failure Progression to chronic hepatic damage

Answer 25

Common: - Alcoholic fatty liver - Chronic active hepatitis - Primary biliary cirrhosis Unusual causes: - Alpha-1 AT deficiency - Wilson's disease - Haemochromatosis

Answer 26

1. Cirrhosis 2. Portal hypertension 3. Ascites 4. Renal failure 5. Easy bruising due to lack of production of clotting factors 6. Oedema as osmotic pressure is reduced

Answer 27

Irreversibile shrinkage of the liver and fibrosis

Answer 28

Increased blood pressure in the portal vein leading to: - Haemorrhage of oesophageal / gastric varices - Hepatic encephalopathy (detoxifying function bypassed) - Hypersplenism - Decreased resistance to infections

Answer 29

Accumulation of fluid in the peritoneal cavity

Answer 30

Inadequate synthesis of albumin Inadequate synthesis of clotting factors Inability to eliminate bilirubin Inability to eliminate nitrogenous waste

Answer 31

Poorly defined neuro-psychiatric disorder that occurs when products normally metabolised by the liver accumulate in the systemic circulation. Ammonia: Decreased liver capacity to synthesize urea and glutamine means the ammonia is no longer adequately metabolised and accumulates in the systemic circulation

Answer 32

1. Aminotransferases: ALT and AST for liver cell damage 2. Bilirubin- For cholestasis (suggesting bile flow blockage) 3. ALP and gamma-GT for biliary epithelial damage and obstruction 4. Albumin for synthetic function

Answer 33

Albumin is a main plasma protein Used as an assessment of liver synthetic function but low albumin also found in the following: - Post surgical/ITU patients due to redistribution - Significant malnutrition - Nephrotic syndrome

Answer 34

Breakdown product of haemoglobin

Answer 35

Taken up by the liver and then conjugated. This can then be excreted in bile. It is then attacked by bacteria in the colon and excreted in faeces. Small amounts are reabsorbed and excreted in urine as urobilinogen

Answer 36

AST and ALT Bilirubin ALP gamma-GT NOT EXCLUSIVELY FOUND IN LIVER TISSUE

Answer 37

These are non-specific markers of acute damage to hepatocytes

Answer 38

Increase in liver disease due to increased synthesis in response to cholestasis

Answer 39

Raised in colestasis, also affected by ingestion of alcohol and drugs such as phenytoin

Answer 40

1. Lack of complete organ specificity 2. Lack of disease specificity 3. May be over sensitive 4. "I have this abnormal result, what do I do with it?"

Answer 41

Haemolysis | Gilbert's syndrome

Answer 42

Physiological change e.g. pregnancy, adolescence

Answer 43

Skeletal muscle disorders | MI

Answer 44

Alcohol | Drugs

Answer 45

Pros: - Cheap - Widely available - interpretable - Direct subsequent investigation Cons: - Outdated by new diseases - Little prognostic value in liver transplantation - Little value for evaluating therapeutic success - Do not assess liver function

Answer 46

The spleen lies with ribs 9-11 to the left and posteriorly

Answer 47

``` 1,3,5,7,9,11 The spleen is: 1 inch thick; 3 inches wide; 5 inches long; weighs 7oz (200g); lies between the 9th and11th ribs ```

Answer 48

1. Mechanical filtration of red blood cells 2. Active immune response through humeral and cell mediated pathways 3. Haematopoesis until 5th month of gestation

Answer 49

Stomach in the gastric area Left kidney in the renal area Splenic flexure in the colic area

Answer 50

The spleen is surrounded by peritoneum that was derived from the dorsal mesentery of the stomach

Answer 51

It is connected to the stomach by the Gastrosplenic ligament Carries: Left gastro-epiploic and short gastric branches of the splenic artery (and equivalent veins) It is connected to the posterior abdominal wall, adjacent to the left kidney, by the Lienorenal (Splenorenal) ligament Carries: Splenic artery and vein alongside the tail of the pancreas

Answer 52

Rupture spleen causing intraperitoneal haemorrhage

Answer 53

When removing the spleen, great care must be taken to avoid injuring the tail of the pancreas when ligating the splenic vessels

Answer 54

The splenic artery is the largest branch of the coeliac artery [It has a tortuous course as it runs along the upper border of the pancreas] The artery then divides into about six branches, which enter the spleen at its hilum

Answer 55

The splenic vein leaves the hilum and runs behind the tail and the body of the pancreas Behind the neck of the pancreas, the splenic vein joins the superior mesenteric vein to form the portal vein (L1, Transpyloric Plane)

Answer 56

The lymph vessels emerge from the hilum and pass through a few lymph nodes along the course of the splenic artery and then drain into the coeliac nodes

Answer 57

The nerves accompany the splenic artery and are derived from the coeliac plexus (foregut T 5 to 9))

Answer 58

``` Uncinate process Head Neck Body Tail ```

Answer 59

lower 1/3 of oesophagus Spleen Pancreas Gall bladder

Answer 60

Branches and supplies the sinusoids, from which blood passes into the hepatic veins that join the inferior vena cava In the sinusoids, the portal venous blood mixes with oxygenated blood from the hepatic artery

Answer 61

Splenic vein | Superior Mesenteric Vein

Answer 62

Lower oesophagus | Left end of the lesser curve of the stomach

Answer 63

The inferior mesenteric vein drains the hindgut and joins the splenic vein in very variable positions behind the pancreas, often joining the portal vein itself

Answer 64

``` Splenic vein ( + IMV) SMV Left gastric vein Right gastric vein Cystic vein ```

Answer 65

Drains the right end of the lesser curve of the stomach directly to the portal vein

Answer 66

1. At the lower third of the oesophagus 2. Halfway down the anal canal 3. The para-umbilical veins 4. The veins of the retroperitoneal ascending colon, descending colon, duodenum, pancreas and liver

Answer 67

At the lower third of the oesophagus, the oesophageal branches of the left gastric vein (portal tributary) anastomose with the oesophageal veins draining the middle third of the oesophagus into the azygos veins (Varices)

Answer 68

Halfway down the anal canal, the superior rectal veins (portal tributary) draining the upper half of the anal canal anastomose with the middle and inferior rectal veins that are systemic tributaries of the internal iliac and internal pudendal veins, respectively (Piles or Haemorrhoids)

Answer 69

The para-umbilical veins connect the left branch of the portal vein with the superficial veins of the anterior abdominal wall (systemic tributaries). The para-umbilical veins travel in the falciform ligament and accompany the ligamentum teres (Caput Medusae)

Answer 70

The veins of the retroperitoneal ascending colon, descending colon, duodenum, pancreas, and liver (portal tributaries) anastomose with the renal, lumbar, and phrenic veins (systemic tributaries)

Answer 71

Supra-hepatic causes: Cardiac disease Hepatic vein thrombosis IVC thrombosis Hepatic causes: -Cirrhosis (due to alcohol, hepatitis) Infra-hepatic causes: - Portal vein thrombosis - Splenic vein thrombosis Consequences - Oesophageal varices - Haemorrhoids - Caput medusa

Answer 72

3 unpaired, anterior branches: - Coeliac trunk T12 - Superior mesenteric artery L1 - Inferior mesenteric artery L3 3 paired branches to viscera: - Middle suprarenal arteries - Renal arteries L1 - Testicular and ovarian arteries (L2)

Answer 73

1. Inferior phrenic arteries 2. Lumbar arteries 3. Median sacral artery

Answer 74

It is formed by the union of the common iliac veins behind the right common iliac artery at the level of L5 vertebra

Answer 75

1. Two or three anterior visceral tributaries: the hepatic veins 2. Three lateral visceral tributaries: the right suprarenal vein (the left vein drains into the left renal vein), both renal veins, and the right gonadal vein (the left vein drains into the left renal vein) 3. Five lateral abdominal wall tributaries: the inferior phrenic vein and four lumbar veins 4. Three veins of origin: two common iliac veins and the median sacral vein

Answer 76

Primary: X-ray, CT and USS Secondary: MRI, Fluoroscopy (e.g. Barium meals, barium enemas)

Answer 77

Types: Spine AXR, Crest CXR Excludes bowel obstruction perforation

Answer 78

The normal portal venous pressure is 5 - 10mm Hg If elevated above this the term ‘portal hypertension’ is used

Answer 79

Sensitivity of CT vs USS- 89% vs 70% CT results in 46%-60% change in management :)

Answer 80

Radiation exposure | Renal impairment

Answer 81

Pros: No radiation Good soft tissue delineation esp in pelvis Con's: Long examination time Not 24/7 in Fife Contraindications/ claustrophobia

Answer 82

Symptoms: Periumbilical pain, nausea & vomiting Localises at RIF USS first, then CT

Answer 83

80yrs + Misdiagnosis: Appendicitis, colorectal Ca Complications: Abscess, obstruction, perforation, fistulae Scans: Plain x-ray, CT

Answer 84

Almost always secondary gallstones Diagnosis based on: • One local sign of inflammation (RUQ pain etc) • One sign of inflammation (fever ,WCC, CRP) • Confirmatory imaging Scans: USS: Reveals gallstones, GB wall thickening, local fluid CT: Can be false -ve MRI: If biliary tree dilatation

Answer 85

MR cholangiopancreatography

Answer 86

Air in gallbladder wall. Common in diabetics Treatment: Medical, interventional radiology, surgery

Answer 87

* Common – adhesions, cancer, herniae and gallstone ileus * Symptoms: vomiting, pain and distension * Signs: Increased bowel sounds, tenderness, palpable loops * Imaging defines: site, cause, severity and detects complications (eg perforation, ischaemia) Scans: X-ray: For initial inspection. Can miss fluid filled loops. CT: Transition point revealed, key. Adhesions not seen.

Answer 88

Causes: • Colorectal cancer 60% • Volvulus 15% • Diverticulitis 10% Clinical presentation often variable Surgeon wants to know: Site, cause, distant disease ``` Scan used:CT • sens/. Spec >93% • Transition point • Underlying mass • State of caecum • Distant disease ```

Answer 89

Perforated ulcer Diverticular ** (Less common: 2ndary to cancer, ischaemia)

Answer 90

``` CT: • High sens and spec • Shows free fluid • Will often show clues to site of origin (86%) -Distribution gas -Defect in wall -Localised inflammatory change ```

Answer 91

If <10% CO to GI, then ischaemia develops Cause: • Arterial occlusion – 60-70% • Venous occlusion – 5-10% • Non-occlusive hypoperfusion – 20-30% S/S: • Severe abdominal pain • Vomiting, diarrhoea, distension inconsistent • Borderline amylase, raised WCC, acidotic Scan: Biphasic CT -Shows site of occlusion, length of affected bowel

Answer 92

Role of plain film: obstruction orperforation Role of USS – RUQ/ RIF pain Role CT – Primary imaging technique for acute abdominal pain except for acute cholecystitis/ appendicitis

Answer 93

Cystic duct | Common hepatic duct

Answer 94

Bile duct Hepatic artery Hepatic portal vein

Answer 95

Synthesises: Albumin, clotting factors, complement, alpha-1-antitrypsin, thrombopoietin Produces: Bile through conjugation of bilirubin Breaks down: Drugs, insulin, ammonia

Answer 96

Phagocytose old blood cells, bacteria and foreign materials from the bloodstream/gut

Answer 97

Jaundice is the yellowing of the skin and mucosal surfaces. When bilirubin levels are >40micromol/L Can cause intense itch Unconjugated is water insoluble. Conjugated is water soluble so can be excreted in the urine, leading to dark urine.

Answer 98

Prehepatic: Haemolysis --> Release for bilirubin from RBCs Intrahepatic: Liver disease --> Excess bilirubin in liver and bloodstream Post-hepatic (obstructive): Obstruction of bile outflow --> Dark urine and pale stools

Answer 99

Viral infections *Alcohol* Adverse drug reactions Biliary obstructions

Answer 100

Jaundice, malaise Raised serum bilirubin and transaminases Liver failure: decrease in albumin, ascites, bruising, encephalopathy

Answer 101

``` Zone 1 (on outskirts): Greatest blood supply so most susceptible but also most reliant Zone 3 (inner zone): If injury in this zone then that's when symptoms are experienced as cells cannot regenerate ```

Answer 102

Steatosis Cirrhosis Acute hepatitis with Mallory's hyaline

Answer 103

Fat deposition altered by metabolism | Mallory’s hyaline builds up due to hepatocyte damage

Answer 104

1. Acetaldehyde binds to hepatocytes causing damage → Inflammatory reaction 2. Inflammation → fibrosis 3. Fibrosis (collagen) + Regeneration → Cirrhosis

Answer 105

Micronodular: Nodules <3mm Macronodular: Nodules >3mm Mixed

Answer 106

* Liver Failure – hepatic encephalopathy (ammonia), build up of steroid hormones → hyperoestrogenism (palmar erythema and gynaecomastia), bleeding * Portal hypertension –↑ hepatic vascular resistance, AV shunting – oesophageal varices, haemorrhoids, caput medusae * Hepatocellular carcinoma

Answer 107

Paracetamol= Injury to liver cells (hepatocellular) overdose Methyl testosterone= Injury to bile production/secretion cells (cholestatic)

Answer 108

* This is usually due to gallstones * Causes colicky pain and jaundice * Can be complicated by infection of the blocked CBD - cholangitis

Answer 109

Viral Alcohol Drugs Autoimmune

Answer 110

6 months | With sustained elevation of transaminases which requires liver biopsy to classify cause

Answer 111

Females > Males Stages: 1. Autoimmune destruction of bile duct epithelium: Dense lymphocytic infiltration 2. Proliferation of small bile ducts 3. Architectural disturbance: Portal and bridging fibrosis 4. Cirrhosis Presentation: Jaundice, pruritus, xanthelasmata Raised ALP + IgM, AMA

Answer 112

Iron deposition in the liver causing alteration of architecture --> Fibrosis --> Cirrhosis

Answer 113

Lobule: Blood on outside going inwards Acinar: Blood supply in between

Answer 114

``` Alcohol Hep B and C Iron overload Gallstones Cirrhosis Autoimmune liver disease ```

Answer 115

Females > Males Usually presents in mid-late teens Features: - Interface hepatitis - Plasma cells and swollen hepatocytes present - Fibrosis - ANA, SMA, raised IgG and transaminases, Anti-LKM (liver-kidney microsomal) Treatment: Patients may benefit from steroids

Answer 116

HFE (autosomal recessive)

Answer 117

Regular venesection (test iron and ferritin levels)

Answer 118

Autosomal recessive disorder Leads to low levels of alpha-1 -antitrypsin Leads to protein build up in hepatocytes as hyaline as transport protein is deficient -->Cirrhosis (associated with emphysema)

Answer 119

Non-alcoholic steatohepatitis / Non- alcoholic fatty liver disease Associated with Metabolic Syndrome (DM II, hypertension, ↓HDL cholesterol, ↑ triglycerides Mechanism: Fat deposition in hepatocytes – can lead to cirrhosis

Answer 120

• Autosomal recessive disorder • Failure of the liver to excrete copper in bile → build up of copper in liver → cirrhosis • Copper also deposits in brain tissue → neurological dysfunction Clinical signs: Kayser-Fleischer rings

Answer 121

Malignant liver tumour Often multifocal Often arises in cirrhotic liver Aetiology: - Aflatoxin (fungal origin) - Hep B and C viruses - Cirrhosis

Answer 122

1. Gallstones (cholelithiasis) 2. Cholecystitis 3. Cholangiocarcinoma 4. Obstruction Congenital malformations 5. Atresia 6. Cholesocal cysts

Answer 123

* Arises from bile duct epithelium anywhere in the biliary system (intra- and extra-hepatic) * Associated with ulcerative colitis Causes: obstructive jaundice, itch, weight loss and lethargy Can lead to rupture of common bile duct or gallbladder – prognosis poor

Answer 124

Female, Fair, Fat, Forty, Fertile | Diabetes mellitus

Answer 125

Cholesterol (yellow), bile pigment (green) , *mixed*

Answer 126

Cholecystitis, obstructive jaundice, cholangitis, pancreatitis, cholangiocarcinoma

Answer 127

Acute – • Usually caused by gallstones • Initially sterile then becomes infected • May lead to abscess/rupture • Symptoms – RUQ pain (biliary colic), fever, nausea/vomiting Chronic – • Invariably related to gallstones • Chronic inflammation with wall thickening

Answer 128

At 2nd part of duodenum Causes obstruction Presentation: Polyhydramnios, low birth weight, poor feeding

Answer 129

``` Acutely leads to: • Causes catastrophic metabolic consequences – ↓ calcium, ↓ albumin, ↑ glucose • High serum amylase – diagnostic • Massive fluid losses → SHOCK • High mortality rates ``` Chronic leads to; • Multiple episodes of acute • Causes fibrosis of pancreas – may lead to diabetes mellitus • Reduced production of enzymes – require supplements (creon)

Answer 130

* Adenocarcinoma * Associated with smoking and diabetes mellitus * Presents with painless, progressive jaundice * Weight loss * Poor prognosis * May be operable if small and close to ampulla

Answer 131

``` Mucosa Muscularis mucosae Submucosa Submucosal plexus Circular later Myenteric plexus Longitudinal muscle Serosa ```

Answer 132

``` • Multifactorial • Genetic factors • Autoimmune / Immune dysfunction • Environmental factors -External -Internal ```

Answer 133

* Ulcerative Colitis * Crohn’s Disease * Indeterminate colitis (either Crohn's or ulcerative) * Pseudomembranous Colitis * Diverticulitis

Answer 134

Variable length of colon + rectum inflamed If entire colon = PANcolitis Inflammation: - Contiguous - Circumferential - Superficial inflammation Consequences: - Anaemia due to iron deficiency - Raised inflammatory markers - Dehydration

Answer 135

``` Inflammation characteristics: • Characterised by inflammatory change anywherein the GI tract • Discreet, focal ulceration • ‘Skip lesions’ • Terminal ileitis ``` S/S: - Anaemia (absorption/ blood loss) - Raised inflammatory markers - Dehydration Body trying to contain inflammation so fat wraps around the inflammation. Leading to the lumen being compressed

Answer 136

Fistula. | When ulcer permeate through bowel wall. Leading to faeces leakage and infections elsewhere in the body

Answer 137

* Inflammatory arthropathies * Erythema nodosum (Crohn’s) * Pyoderma gangrenosum * Primary sclerosing cholangitis (UC) * Iritis/Uveitis * Aphthous stomatitis

Answer 138

In diverticular disease, small bulges or pockets (diverticula) develop in the lining of the intestine. Diverticulitis is when these pockets become inflamed or infected.

Answer 139

SI- Benign: Adenoma, Mesenchymal tumours Malignant: Adenocarcinoma & Carcinoid, Lymphomaand Sarcomas Colon and rectum- Benign: Non-neoplasticpolyps, Neoplastic-Adenoma Malignant: Adenocarcinoma(98%), Carcinoid, Anal zone carcinoma, Lymphoma. Leiomyosarcomas

Answer 140

Ampulla of vater, becomes enlarged and exhibits a velvety surface

Answer 141

30- to 60-year-old patient with occult blood loss.

Answer 142

Usual presentation: – occur in the duodenum, usually in 40- to 70-year-old patients – napkin-ringencircling pattern – polypoidexophytic masses May cause: intestinal obstruction, obstructive jaundice Symptoms: cramping pain, nausea, vomiting, and weight loss

Answer 143

• Non-neoplastic polyps: – Hyperplastic (90%) – Hamartomatous • Neoplastic–Adenoma: – Tubular – Villous – Tubulovillous

Answer 144

Benign tumour of the colon and rectum that is non-neoplastic Structure: Nipple-like, hemispheric, smooth, moist protrusions of the mucosa 1/2 found in rectosigmoid colon No malignant potential Found in 60yrs+

Answer 145

Benign tumour of the colon and rectum that is non-neoplastic What are they? Malformations of the mucosal epithelium and lamina propria Age? Less that 5yrs 80% found in rectum No malignant potential

Answer 146

Benign tumour of colon and rectum, non-neoplastic Associated to Peutz-Jeghers autosomal dominant syndrome Involved the mucosal epithelium, lamina propria, and muscularis mucosa No malignant potential • Increased risk of the pancreas, breast, lung, ovary, and uterus carcinoma

Answer 147

Structure: - Small, pedunculate lesions - Large neoplasms that are usually sessile Gender: Equal Age: Most after 60yrs Classifications: Tubular adenomas, villous adenomas, tubulovillous adenomas Arise as a result of epithelial proliferative dysplasia

Answer 148

denomas are a precursor lesion for invasive colorectal adenocarcinomas Risk is correlated with: • Polypsize • Histological architecture • Severity of epithelial dysplasia IMPOSSIBLE from gross inspection of a polyp to determine its clinical significance

Answer 149

Location: Colon Shape: Small = Smooth-contoured and sessile. Large= Coarsely lobulated and have slender stalks raspberry-like Histology: - Stalk is composed of fibromuscular tissue and prominent blood vessels - Dysplastic low grade epithelium - Carcinomatousinvasioninto the submucosal stalk of the polyp constitutes invasive adenocarcinoma Clinical features: - May be asymptomatic - Evaluation of anaemia or occult bleeding Treatment: Endoscopic removal of a pedunculate adenoma. If invasive and sessile polyp further surgery may be required. BENIGN

Answer 150

Age: Older persons Location: Rectum and rectosigmoid Shape: Sessile, up to 10cm Histology: - Frond (1/2 leaf) like villiform extensions of the mucosa - Covered by dysplastic columnar epithelium - All degrees of dysplasia present - When invasive carcinoma occurs, there is no steak as a buffer zone and invasion is directly into the wall of the colon Clinical features: - May be asymptomatic - Evaluation of anaemia or occult bleeding - More symptomatic than colorectal tubular - Overt rectal bleeding Treatment: Endoscopic removal of a pedunculate adenoma. If invasive and sessile polyp further surgery may be required. BENIGN

Answer 151

Must be a pedunculate adenoma (1) the adenocarcinoma is superficial and does not approach the margin of excision across the base of the stalk (2) there is no vascular or lymphatic invasion (3) the carcinoma is not poorly differentiated

Answer 152

Gender: Rectum, more men. More proximal tumours, equal. Age: 60-79 Aetiology: Dietary factors: Excess calorific intake, lowe veg fibre intake, high content of refined carbs, intake of red meat, decreased intake of protective micronutrients Location? Mainly rectosigmoid colon Histology? - Range from tall, columnar cells to undifferentiated, anapaestic masses - May produce mucin Clinical features? - Asymptomatic for years - In caecum and right colonic = fatigue, weakness, iron deficiency - In left side = occult bleeding, changes in bowel habit, cramps in LLQ - Iron deficiency anaemia in an older male means gastrointestinal cancer until proven otherwise - Significiant manifestations such as weakness, malaise and weight loss signify more extensive disease - All colorectal cancers spread. Mainly to liver, lungs and bones. Classification of lesion by Duke's stage: A = Confined to the submucosa or muscle layer. 90% 5yr survival B= Spread through the muscle layer, but does not yet involve lymph nodes. 70% 5yr survival C= Involving lymph nodes. 35% 5yr suvival.

Answer 153

– Polypoid,exophytic masses – Obstructionis uncommon – Penetrate the bowel wall as subserosal and serosal white, firm masses

Answer 154

– Annular, encircling lesions - napkin-ring constrictions – Themarginsareclassically heaped up, beaded, and firm, and the mid-region is ulcerated – Thelumenismarkedly narrowed, and the proximal bowel may be distended – Penetratethebowelwallas subserosal and serosal white, firm masses

Answer 155

Derived from endocrine cells Make up 2% colorectal malignancies but almost 50% of small intestinal malignant tumours Age: 60yrs+ Histological features: No reliable difference between benign and malignant Appendix is the most common site Clinical features: -Rarely produces local symptoms -Caused by obstruction of SI -Can be associated with a distinctive carcinoid syndrome Appendiceal and rectal carincinoi do not metastasise. Whereas clean, gastric and colonic will spread to liver once lymph nodes are reached

Answer 156

Due to excess of serotonin - -> - Cutaneous flushes and apparent cyanosis - Diarrhoea, cramps, nausea, vomiting - Cough, wheezing and dyspnoea

Answer 157

Primary gastrointestinal lymphomas exhibit no evidence of liver, spleen, mediastinal lymph node, or bone marrow involvement at the time of diagnosis B cell: - MALT (mucosa- associated lymphoid tissue) mainly in stomach and SI - IPSID (Immunoproliferative small intestinal disease) - Burkitt lymphoma T cell: - Associated with long standing malabsorption syndrome - Poor prognosis

Answer 158

Lipomas (within submucosa or muscular is propria) Leiomyomas Leiomyosarcomas (intramural that ulcerate into lumen)

Answer 159

* the upper (covered with rectal mucosa) * the middle (partially covered with a transitional mucosa) * lower (covered by stratified squamous mucosa)

Answer 160

1. Basaloid pattern • immature proliferative cells derived from the basal layer of a stratified squamous epithelium 2. Squamous cell carcinoma • closely associated with chronic HPV infection 3. Adenocarcinoma • extension of rectal adenocarcinoma 4. Malignant Melanoma (very rare)

Answer 161

Fat Soluble: A, D, E, K | Water soluble: C, B1, B2, Niacin, B6, B5, Biotin, B12, Folic acid