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Clinical Conditions > 11. Gastrointestinal > Flashcards

11. Gastrointestinal Flashcards

1
Q

What is an appendicitis?

A

Inflammation of the appendix due to either lymphoid hyperplasia (infection) or obstruction by hardened stool (faecalith).

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2
Q

What is the presentation of appendicitis?

A

Midgut referred pain in periumbilical region. Localisation of pain to McBurney’s point (right iliac fossa, 1/3rd between ASIS and umbilicus) when overlying parietal peritoneum is irritated.

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3
Q

When does appendicitis cause peritonitis?

A

When it bursts and colonic flora gets into the peritoneum.

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4
Q

How is appendicitis managed?

A

By an appendectomy using grid iron incision to split muscle fibres of the external oblique, internal oblique, and transversus abdominis.

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5
Q

What is parotitis?

A

Inflammation of the parotid gland, often from bacteria travelling up Stensen’s duct.

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6
Q

Why is parotitis so painful and even lethal?

A

Because the tight fascia means the gland can’t expand so there is intense pain and swelling. The external carotid artery, facial nerve, and retromandibular vein can be compressed - lethal.

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7
Q

What is halitosis?

A

Failure of minute salivary glands to destroy pathogenic bacteria causing bad breath.

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8
Q

What is achlasia?

A

Failure of relaxation of either of the oesophageal sphincters due to nervous disorganisation.

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9
Q

What causes achlasia?

A

Lupus or idiopathic.

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10
Q

What is the presentation of achlasia?

A

Dysphagia, nausea/vomiting, epigastric pain. Aspiration pneumonia may result from aspiration of vomit in sleep.

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11
Q

What is referred cardiac pain?

A

Retrosternal - left arm, neck, jaw. Tightening or crushing.

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12
Q

What is referred stomach/oesophagus pain?

A

Burning, epigastric - visceral, foregut.

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13
Q

What is referred gall bladder pain?

A

Epigastrium - visceral foregut, left upper quadrant - somatic, right upper quadrant - site of bladder, inferior to right scapula on posterior body wall - body and neck are extraperitoneal, colic.

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14
Q

What is referred pancreatic pain?

A

Epigastric - visceral foregut, left upper quadrant - somatic, back - T10 retroperitoneal excluding tail.

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15
Q

What is referred small bowel pain?

A

Umbilicus - visceral midgut, colic.

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16
Q

What is referred large bowel pain?

A

Suprapubic - visceral hindgut, colic.

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17
Q

What is referred kidney pain?

A

In loin (posterior T11-L3, retroperitoneal), refers to testicles as mesonephric duct is converted into vas deferens in adult males. Excruciating colic pain - rolling on floor.

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18
Q

What is referred uterus pain?

A

Suprapubic with lower lumbosacral.

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19
Q

What is referred bladder pain?

A

Suprapubic.

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20
Q

What is referred diaphragmatic pain?

A

Left shoulder tip - C3-5 on left side (right side blocked by liver).

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21
Q

What is a hernia?

A

Protrusion of an organ through the wall or cavity in which it normally resides.

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22
Q

What is a direct inguinal hernia?

A

Pierces the posterior wall of the inguinal canal (transversalis fascia) at a weak point - Hesselbach’s triangle. Appears medial to inferior epigastric vessels.

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23
Q

What is an indirect inguinal hernia?

A

Enters through the deep inguinal ring within the posterior wall of the inguinal canal, herniates through superficial inguinal ring within anterior wall. Appears lateral to inferior epigastric vessels.

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24
Q

What is an epigastric hernia?

A

Occurs along linea alba between the xiphoid proces and umbilicus.

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25
Q

What are the risk factors for epigastric hernias?

A

Obesity and pregnancy.

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26
Q

How is an epigastric hernia differentiated from a divarication of recti?

A

It doesn’t disappear when laying flat or get worse when abdominal muscles are tensed as divarication of recti do.

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27
Q

What is an umbilical hernia?

A

Hernia through the umbilicus.

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28
Q

What is a femoral hernia?

A

Herniation into the femoral canal.

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29
Q

What hernia is more common in females and why?

A

Femoral hernia as females have a wider pelvis.

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30
Q

What affects the size of femoral hernias?

A

Small due to not a lot of space for hernia, until it reaches the great saphenous opening - can expand.

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31
Q

What complications are femoral hernias prone to and why?

A

Incarceration and strangulation due to pectineal, lacunar, and inguinal ligaments.

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32
Q

What is Richter’s hernia?

A

Partial hernia where only the anterior bowel wall protrudes through the abdominal wall. Posterior wall still within the abdominal cavity.

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33
Q

What are Richter’s hernia prone to?

A

Strangulation without obstruction.

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34
Q

What is a Spigelian hernia?

A

Hernia that appears along the linea semilunares at the point where the posterior rectus sheath ends - intersection with arcuate line.

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35
Q

What is a diaphragmatic hernia?

A

Usually from a developmental defect, abdominal viscera herniates into the thoracic cavity.

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36
Q

What are the two types of diaphragmatic hernia?

A

Sliding and rolling.

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37
Q

What is a sliding hiatus hernia?

A

Gastroesophageal junction moves through the oesophageal hiatus (T10) along with the cardia of the stomach.

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38
Q

What is a rolling hiatus hernia?

A

Gastroesophageal junction remains fixed above the oesophageal hiatus (T10) and a portion of the stomach follows it in.

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39
Q

What is an incisional hernia?

A

Herniation from abdominal wall weakness due to previous surgery.

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40
Q

What makes incisional hernias more likely?

A

Obesity and pregnancy.

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41
Q

What is divarication of recti?

A

Widening of the linea alba that causes the two opposing sides to oppose each other during muscular contraction and recede on relaxation.

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42
Q

What is incomplete rotation of the midgut?

A

Only 90 degree counter clockwise rotation, limbs don’t cross so the cranial limb ends up on the left hand side and the entire colon is left instead of framing the abdomen.

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43
Q

What is reversed rotation of the midgut?

A

90 degree clockwise rotation so normal disposition apart from the fact the duodenum is anterior to the transverse colon.

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44
Q

What can incorrect rotation of the midgut lead to?

A

Volvulus so interruption of blood supply, ischaemia and loss of gut.

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45
Q

What is a vitelline cyst?

A

Fluid filled sac that is anchored to the anterior abdominal wall and the small intestine.

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46
Q

What is the risk of a vitelline cyst?

A

Volvulus leading to loss of blood supply, ischaemia, adn loss of gut.

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47
Q

What is a vitelline fistula?

A

Incomplete obliteration causing communication between the small intestine and the umbilicus so faeces externally.

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48
Q

What is the risk of vitelline fistulas?

A

Infection.

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49
Q

What is Meckel’s diverticulum?

A

Blind ended outcropping from the small intestine.

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50
Q

What is the rule of 2s for Meckel’s diverticulum?

A

2% of the population have it, 2x as common in men than women, 2ft from ileo-caecal valve, 2 inches long, contains 2 ectopic tissue types - gastric or pancreatic.

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51
Q

What is failure of recanalisation?

A

In embryological development, the oesophagus, bile duct, and small intestine lose some or all of their patency so rely on recanalisation for function. If this fails, there is atresia or stenosis.

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52
Q

Where is failure of recanalisation most common?

A

In the duodenum.

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53
Q

What can cause failure of recanalisation?

A

Vascular accident during development - malrotation, volvulus etc.

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54
Q

Wha is pyloric stenosis?

A

Excessive hypertrophy of pyloric sphincter so there is a narrowed exit from stomach to duodenum.

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55
Q

What is the presentation of pyloric stenosis?

A

Projectile vomiting.

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56
Q

How is pyloric surgery managed?

A

Surgery to fix it.

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57
Q

What is gastrochisis?

A

Failure of fusion of the somatic mesoderm during lateral folding of the embryo so vertical anterior abdominal wall defect. Bowel isn’t covered in amnion but loops normally healthy.

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58
Q

What is exomphalos/omphalocele?

A

Incompletion of physiological herniation during midgut rotation so bowel protrudes through umbilicus. Still covered in amnion.

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59
Q

What is imperforate anus?

A

Failure of cloacal rupture.

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60
Q

How is imperforate anus managed?

A

Surgery to fix it.

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61
Q

What is anal/anorectal agenesis?

A

Failure of development of the rectum to the point it reaches the cloaca.

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62
Q

What is GORD (gastro-oesophageal reflux disease)?

A

Chronic presence of gastric acid within the lower third of the oesophagus.

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63
Q

What are the symptoms of GORD?

A

Dyspepsia, heartburn - epigastric burning, persistent cough, dysphagia, early satiety, nausea.

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64
Q

What are the causes of GORD?

A

Dysfunction of the lower oesophageal sphincter from change of angle or right crus weakness. Delayed gastric emptying so increased intragastric pressure and reflux. Hiatus hernia. Obesity causes increased intraabdominal pressure so increased gastric pressure.

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65
Q

What are the consequences of GORD?

A

Oesophagitis, chronic inflammation and scarring leading to oesophageal stricture, Barrett’s oesophageal - stratified squamous non keratinised to columnar epithelia with goblet cells.

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66
Q

What is acute gastritis?

A

Inflammation of the stomach mucosa.

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67
Q

What are the symptoms of acute gastritis?

A

Often asymptomatic but can present with dyspepsia or bleeding.

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68
Q

What are the causes of acute gastritis?

A

Heavy NSAID use - blocks prostaglandins so decreased mucosal blood flow and epithelial renewal so acid damages mucosa.
Alcohol dissolves mucus.
Chemotherapy attacks rapidly dividing cells like stomach epithelia.
Bile reflux from duodenum but uncommon.

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69
Q

What is chronic gastritis?

A

Chronic inflammation of the stomach mucosa.

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70
Q

What are the causes of chronic gastritis with their typical presentations?

A

Helicobacter pylori infestation - like acute gastritis and peptic ulcer.
Autoimmune antibodies raised to parietal cells. Pernicious/megaloblastic anaemia, glossitis, anorexia/cachexia.

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71
Q

What is a peptic ulcer?

A

Erosion of mucosa and subsequent ulceration of the submucosa.

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72
Q

What is a common cause of peptic ulcers?

A

Helicobacter pylori.

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73
Q

How does helicobacter pylori survive in the stomach?

A

Contains urease that creates NH3 to form a local alkaline cloud to protect against stomach acid. Reaches epithelial by positive chemotaxis to alkaline pH.

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74
Q

What is the pathogenesis of peptic ulcers from helicobacter pylori?

A

Bacteria burrows into epithelia and colonises at several many sites: antrum - increases gastrin and causes duodenal epithelial metaplasia, body - atrophic, 1st part of duodenum - tendency to bleed heavily.
Cytotoxic compounds cause direct epithelial insult, NH3 levels are toxic to epithelia, inflammatory response causes self injury.

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75
Q

What are the symptoms of peptic ulcers?

A

Mild - epigastric pain following meals.

Severe - bleeding, early satiety.

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76
Q

How are peptic ulcers diagnosed?

A

Endoscopy to looks for inflammation/ulcers/metaplasia of oesophagus.
Urease breath test - shows presence of H pylori.
Chest X ray - perforated ulcer is visible under diaphragm as pneumopreitoneum.
Haematoocrit - reduced due to bleeding.

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77
Q

How are peptic ulcers treated?

A

Conservative treatment - cease insult (alcohol, NSAIDs), dietary modification - smaller and more frequent healthy meals, no lying down after meals.
Pharmacological - H pylori eradication with clarithromycin and amoxicillin, H2 histamine blockers to block receptors on parietal cells and decrease acid production (ranitidine), PPIs block H+ extrusion across apical membrance so decrease acid production (omeprazole), antacids neutralise excess acid.
Surgical - cauterize bleeding ulcers via endoscopy.

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78
Q

What is Zollinger-Ellison syndrome?

A

Rare gastrin secretion from tumour of the pancreas leading to severe polyulceration.

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79
Q

What is stress ulceration?

A

Ulceration of the stomach following large physiological insult like burns, sepsis etc.

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80
Q

What is mesenteric adenitis?

A

Inflammation of lymph nodes within mesentery proper.

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81
Q

How does mesenteric adenitis present and what can it be confused with?

A

Right iliac fossa pain. Confused for appendicitis.

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82
Q

What is typhoid fever?

A

Infestation with and proliferation of salmonella typhi within the GI tract causing inflammation and subsequent rupture of Peyer’s patches so haemorrhage.

83
Q

What is gut ischaemia?

A

Interruption of blood supply to a section of gut causing necrosis and dangerous sequelae.

84
Q

What are the causes of gut ischaemia?

A

Systemic hypoperfusion (shock), arterial disease (superior mesenteric artery atherosclerosis), abdominal aortic aneurysm, thrombus/embolus etc.

85
Q

What is alcoholic liver disease?

A

Spectrum of progressively worsening liver damage due to high concentration of alcohol.

86
Q

What are the disease involved in alcoholic liver disease?

A

Steatosis and acute alcoholic hepatitis.

87
Q

What is steatosis?

A

Part of alcoholic liver disease, fatty change of liver from increased alcohol metabolism so acetic acid creates NADH which promotes fat storage.

88
Q

What is the presentation of steatosis?

A

Usually asymptomatic and reversible in two weeks.

89
Q

What is acute alcoholic hepatitis?

A

From chronic overexposure to or large binge drinking of alcohol. Toxins badly damage liver and cause inflammation so targeted hepatic necrosis occurs.

90
Q

What is the presentation of acute alcoholic hepatitis?

A

Fever, jaundice, tenderness. Reversible over a few weeks.

91
Q

What is liver failure/cirrhosis?

A

Loss of liver function as a result of cancer or infection or cirrhosis.

92
Q

What is cirrhosis?

A

Fibrous remodelling so loss of function of hepatocytes.

93
Q

What are the causes of liver failure/cirrhosis?

A

Chronic alcohol abuse, paracetamol overdose (NAPQI build up which is hepatotoxic), untreated chronic hepatitis B/C, primary biliary cirrhosis (autoimmune obliteration of bile duct so complete obstructive jaundice), hereditary haemochomatosis (iron deposition in tissues), Wilson’s disease (deposition of copper in tissues), a1-antitrypsin deficiency so overactivity of porteases and breakdown of liver parenchyma.

94
Q

What is the presentation of liver cirrhosis?

A

Hepatic jaundice, anaemic and easily bruised, bone/Ca2+ disorder, palmar erythema and Dupytren’s contracture (thickened palmar fascia so flexion deformity at MCP and IP joints), portal hypertension.

95
Q

How does cirrhosis cause portal hypertension?

A

Cirrhosis impairs blood flow and hydrostatic pressure backs up throughout the portal venous system.

96
Q

What are the characteristic signs of portal hypertension?

A

Ascites and splenomegaly, oesophgeal varices (azygous and left gastric vein), haemorrhoids (superior rectal and pudendal vein), caput medusae (dilation of superficial veins of abdominal wall).

97
Q

What are the investigations for liver cirrhosis?

A

AST/ALT - if under 1 then non-alcohol but if over 1 then alcoholic. Increased clotting time, hyponatraemia and hypoalbuminia, ALP increased, hyperbilirubinaemia (jaundice) unconjugated and conjugated.

98
Q

What is the treatment for liver cirrhosis?

A

Stop drinking and cease other insults. Treat symptoms, e.g. sprionolactone to minimise ascites. Manage all drugs to avoid more hepatotoxic drugs.

99
Q

What is fulminant hepatic failure?

A

Severe, acute decompensation of liver function accompanied by hepatic encephalopathy within 2 months of diagnosis of liver failure.

100
Q

What is fulminant hepatic failure accompanied by?

A

Hypokalaemia, hypocalcaemia, and hypoglycaemia.

101
Q

What is hepatic encephalopathy?

A

Reversible neurological deficit caused by increased NH3 levels.

102
Q

What causes hepatic encephalopathy?

A

Stress - physiological insult to liver, e.g. constipation, GI bleeding.
Hypokalaemia - so avoid non-K+ sparing diuretics with liver failure.

103
Q

What are the signs of hepatic encephalopathy?

A

Liver flap - extend wrists with arms pronated, not steady.

Constructional apraxia - can’t draw a 5 point star.

104
Q

What is cholelithiasis?

A

Gall stones, solid mass within the biliary tree.

105
Q

What are the risk factors for cholelithiasis?

A

Female, increasing age, obesity, increased bilirubin.

106
Q

What are the types of stones in cholelithiasis?

A

Cholesterol, pigment (Ca2+ and bilirubin), mixed (most common).

107
Q

What is the presentation of cholelithiasis?

A

Asymptomatic if just in gallbladder and not obstructing the neck.
Anywhere else in the biliary tree - biliary colic: ache in RUQ that becomes acute and peristaltic after eating, post-hepatic jaundice.

108
Q

What are the complications of cholelithiasis?

A

Cholecystitis - inflammation of the gallbladder due to colonisation by pathogen.
Ascending cholangitis - colonisation of the biliary tree by bacteria from the duodenum to liver leading to sepsis.
Biliary-enteric fistula - communication between the duodenum and biliary tree due to erosion as a result of irritation.

109
Q

What is the treatment of cholelithiasis?

A

Surgical removal - laparoscopic cholecystectomy.

Non-surgical - ERCP (endoscopic retrograde cholangio-pancreatography).

110
Q

What is pancreatitis?

A

Inflammation of the pancreas as a result of pancreatic enzymes being activated within the pancreas.

111
Q

What are the causes of pancreatitis?

A

GET SMASHED: gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion bites, hyperlipidaemia, ERCP/iatrogenic, diabetes.

112
Q

What is the presentation of pancreatitis?

A

Pain, nausea/vomiting, ecchymosis, SIRS, jaundice.

113
Q

What are the investigations for pancreatitis?

A

Increased pancreatic amylase, hypocalcaemia, hyperbilirubinaemia (conjugated) and increased ALP, hyperglycaemia.

114
Q

What is the presentation of chronic pancreatitis?

A

Duct stenosis leads to post-hepatic jaundice, pain, malabsorption from lack of bile salt delivery so steathorrea, hypoalbuminaemia leading to oedema, diabetes.

115
Q

What is diverticulitis?

A

Inflammation of the diverticuli (outcropping of weakened large intestinal wall as a result of age/pressure exerted by stools).

116
Q

What causes diverticulitis?

A

Colonic flora become trapped in the diverticuli and start to multiply causing swelling.

117
Q

What is a risk of diverticulitis?

A

Abscess can form and rupture, causing peritonitis.

118
Q

What is inflammatory bowel disease?

A

Umbrella term for two distinct diseases - Crohn’s disease, and ulcerative colitis.

119
Q

What is the presentation of Crohn’s disease?

A

15-30 or over 60 years, 6 weeks of non-bloody stools, fever, perianal disease, affects entire GI tract (mouth to anus), ileum involved usually so right lower quadrant pain.

120
Q

What is the presentation of ulcerative colitis?

A

18-25 years, 8 week history of bloody stools, no fever, no perianal disease, affect rectum, colon, and terminal ileum, colon involved so suprapubic pain/bloating.

121
Q

What is the gross pathology of Crohn’s disease?

A

Cobblestone ulceration, non-friable, potential fibrosis/narrowing, potential fistulae formation as transmural.

122
Q

What is the gross pathology of ulcerative colitis?

A

Continuous ulceration - blanket red and irritated appearance, friable, no fibrosis/narrowing, only affect submucosa.

123
Q

What is the microscopic pathology of Crohn’s disease?

A

Transmural inflammation forms granulomas, microscopic fibrosis, no crypt abscesses.

124
Q

What is the microscopic pathology of ulcerative colitis?

A

Non transmural inflammation, no granulomas, no microscopic fibrosis, no crypt abscesses.

125
Q

What are the investigations of Crohn’s disease?

A

Decreased haematocrit as bleeding ulcers leads to loss of B12 absorption and pernicious anaemia.
CT/MRI shows fibrosis/obstruction.
Colonoscopy shows skip lesions and cobblestone appearance.
Barium studies show string sign of Kantour.

126
Q

What are the investigations of ulcerative colitis?

A

Haematocrit decreased due to bleeding ulcers.
CT/MRI not very useful.
Colonoscopy gold standard, shows inflammation.
Barium studies used in mild cases only and shows lead pipe colon from inflammation so loss of haustra.

127
Q

What is the treatment for Crohn’s disease?

A

Stop smoking, avoid trigger foods, use antibiotics sparingly.
Aminosalicylates - trap free radicals so reduce damage, mesalazine.
Corticosteroids - dampen immune system in acute flare ups so reduce damage, prednisolone.
Immunomodulators - permanently dampen immune system for fistulae or remission, azathioprine.
Surgery isn’t curactive but used as last resort for fistulae repair/excise of really badly damaged bowel.

128
Q

What is the treatment for ulcerative colitis?

A

Avoid trigger foods, use antibiotics sparingly.
Aminosalicylates - trap free radicals so reduce damage, mesalazine.
Corticosteroids - dampen immune system in acute flare ups to reduce damage, prednisolone.
Immunomodulators - permanently dampen immune system for fistulae or remission, azathioprine.
Surgery is curative to have hemi/total colectomy.

129
Q

What is noma (aka cancrum oris/gangrenous stomatitis)?

A

Rapid polymicrobial infection of the mouth and surrounding tissues due to physiological dysfunction.

130
Q

What causes noma/cancrum oris/gangrenous stomatitis?

A

Malnutrition, dehydration.

131
Q

What is oral candidiasis?

A

Thrush from overgrowth of candida albicans, manifests as white furring in the oral cavity.

132
Q

What are the risk factors for oral candidiasis?

A

Newborns, diabetics, inhaled steroids, HIV, antibiotics.

133
Q

How is oral candidiasis treated?

A

With antifungals.

134
Q

What is dental caries/gingivitis?

A

Damage to teeth and gums due to colonisation by mouth bacteria as a result of poor oral hygeine.

135
Q

What is the causative organisms of gingivitis?

A

Streptococcus mutans (viridans strep).

136
Q

How can gingivitis lead to bacterial endocarditis?

A

Over vigorous brushing to remedy leads to damage and a route into the systemic circulation.

137
Q

What is Ludwig’s angina?

A

Laryngoedema as a result of overactivity in response to strep throat/tonsilitis.

138
Q

What is a sequelae of Ludwig’s angina?

A

Breathing problems and death from type II respiratory failure.

139
Q

What is tonsillitis?

A

Inflammation of the tonsils within the pharynx due to infection leading to dysphagia and odynophagia.

140
Q

What is quinsy?

A

Abscess with infected palatine tonsil leading to pharyngeal obstruction so breathing difficulty.

141
Q

What is the treatment for quinsy?

A

Needs excising and abscess needs lancing - careful of internal carotid artery that lies right next to it.

142
Q

What is oesophageal candidiasis?

A

Thrush of the oesophagus.

143
Q

What is oesophageal candidiasis indicative of?

A

AIDS.

144
Q

What is a perianal abscess?

A

Secretory anal gland blocked leading to stasis and infection by perianal flora.

145
Q

What are the complications of perianal abscesses?

A

Can progress to anal fistula and cause incontinence.

146
Q

What is vaginal candidiasis?

A

Thrush within and around the vagina, usually post-antibiotic usage.

147
Q

How does the vagina normally prevent candidiasis?

A

Lactobacillus converts glycogen to lactic acid which keeps the pH low and prevents yeast growth.

148
Q

How can antibiotics leads to vaginal candidiasis?

A

If the antibiotic acts against gram positive rods (i.e. is broad spectrum) there will be loss of lactobacillus so the pH will become less acidic and there is no inhibition of Candida growth.

149
Q

What is the presentation of oesophageal carcinoma?

A

Progressively worsening dysphagia/weight loss from difficulty swallowing.

150
Q

What are the investigations of oesophageal carcinomas?

A

Endoscopy and barium swallow.

151
Q

What are the types of oesophageal carcinoma?

A

Squamous cell carcinoma (at any level), adenocarcinoma (in lower 1/3 from Barrett’s oesophagus).

152
Q

What is the treatment for oesophageal carcinoma?

A

Curative intent - resection, combined chemotherapy and radiotherapy.
Palliative care - canalisation of tumour to facilitate swallowing.

153
Q

What is the five year survival for oesophageal carcinoma?

A

5%.

154
Q

What is the presentation of gastric cancer?

A

Epigastric pain, nausea/vomiting, weight loss, malaise, haematemesis, melena, raised Virchow’s node (left supraclavicular).

155
Q

How is gastric cancer investigated?

A

Endoscopy and biopsy.

156
Q

What are the macroscopic features of gastric cancer?

A

Fungates (breaks epithelia), ulcerates, and infiltrates).

157
Q

What are the microscopic features of gastric cancer?

A

Intestinal type - glandular formation.

Diffuse type - signet ring cells.

158
Q

What are the causes of gastric cancer?

A

Chronic H pylori infestation, high smoked/salty food diet.

159
Q

What is the treatment for gastric cancer?

A

Early stage - surgical resection, chemotherapy, targeted herceptin.
Late stage - chemotherapy, and targeted herceptin.

160
Q

What is gastric lymphoma?

A

The most common gastric cancer.

161
Q

What are the causes of gastric lymphoma?

A

HIV, chronic immunosuppression, or H pylori.

162
Q

What is the treatment of gastric lymphoma?

A

Eradicate H pylor to regress tumour, chemotherapy and radiotherapy.

163
Q

What are gastrointestinal stromal tumours?

A

Tumours of the pacemaker cells of peristalsis.

164
Q

What is the presentation of GISTs?

A

Asymptomatic early on the epigastric pain, nausea and vomiting, weight loss, etc.

165
Q

How is a GIST diagnosis confirmed?

A

Check for CD117 marker.

166
Q

What is the pathology of GISTs?

A

Wildly unpredictable - varied pleopmorphism, mitotic figures, and necrosis.

167
Q

What is the treatment for GISTs?

A

Imatinib - targets cancer cells due to CD117 markers, surgical resection.

168
Q

What is the five year survival for GISTs?

A

Over 80%.

169
Q

What is familial adenomatous polyposis?

A

Autosomal dominant failure of tumour suppressor genes leading to huge adenoma formation, particularly in the colon.

170
Q

What is the risk of familial adenomatous polyposis?

A

One of the adenomas becomes malignant (each have a chance of this) so colorectal cancer.

171
Q

How is development to colorectal cancer prevented with familial adenomatous polyposis?

A

Excise colonas prophylaxis.

172
Q

What is the presentation of colorectal carcinoma?

A

Elderly, fresh blood in stool, changes in bowel motions, suprapubic pain.

173
Q

How are colorectal carcinomas investigated?

A

Colonoscopy and PR exam.

174
Q

What is the pathology of colorectal carcinomas?

A

Variation in anatomical size, descending colon are stenotic so can cause obstruction but ascending colon are fungating so don’t. Microscopically, adenocarcinoma or mucinous/signet cell type.

175
Q

What are the causes of colorectal carcinomas?

A

Familial adenomatous polyposis, low fibre/high fat diet, genetic factors like loss of p53 gene, ulcerative colitis.

176
Q

What is the treatment for colorectal carcinomas?

A

Local radiotherapy (via rectum), palliative chemotherapy, colectomy.

177
Q

What is the presentation of pancreatic carcinomas?

A

Late symptoms: back/epigastric pain, post-hepatic jaundice, pain and vomiting, malabsorption, diabetes, Trousseau’s sign - systemic microthrombophlebitis.

178
Q

How are pancreatic carcinomas investigated?

A

ERCP and biopsy followed by staging CT.

179
Q

What is the macroscopic appearance of pancreatic carcinomas?

A

Firm, pale mass, necrotic, haemorrhagic, and cystic.

180
Q

What is the microscopic appearance of pancreatic carcinomas?

A

80% are ductal (glands with or without mucin).

181
Q

What are the causes of pancreatic carcinomas?

A

Chronic pancreatitis (alcohol), smoking etc.

182
Q

What are the treatments for pancreatic carcinomas?

A

Whipple’s procedure - removal of most of the pancreas, all of the duodenum, gall bladder, pylorus, lymph nodes, and sometimes small intestine. Only for early cancer.

183
Q

What is the presentation of hepatic cancer?

A

Hepatic jaundice, right upper quadrant pain, pruritus, nausea/vomiting, weight loss.

184
Q

How is hepatic cancer investigated?

A

Biopsy.

185
Q

What are the causes of hepatic cancer?

A

Chronic inflammation - alcoholism, hepatitis B/C, drugs.

186
Q

What is the treatment for hepatic cancer?

A

Resection of deposits, transplant, radiofrequency ablation.

187
Q

What is the 5 year survival for hepatic cancer?

A

10%.

188
Q

What is bowel obstruction?

A

Blockage of the bowel leading to constipation, vomiting and bloating depending on how proximal or distal obstruction is.

189
Q

What are the causes of small bowel obstruction?

A

Adhesions, strangulated or incarcerated hernias, tumours, infections.

190
Q

What are the symptoms of small bowel obstruction?

A

Early vomiting, late absolute constipation, and minimal distension. Colic every 2-3 minutes.

191
Q

What is the appearance of small bowel obstruction on abdominal X rays?

A

> 3cm wide, central position, thin valvulae conniventes visible.

192
Q

What are the causes of large bowel obstruction?

A

Cancer, diverticular disease, incarcerated or strangulated hernias, volvulus.

193
Q

What are the symptoms of large bowel obstruction?

A

Late, faeculant vomiting, early absolute constipation and significant distension. Colic every 10-15 minutes.

194
Q

What is the appearance of large bowel obstruction on abdominal X rays?

A

> 6cm wide, frames the small intestine, haustra visible.

195
Q

What is a sigmoid volvulus?

A

Twisting of the sigmoid colon around its mesentery leading to obstruction, ischaemia, and possible perforation.

196
Q

What is the sign of sigmoid volvulus?

A

Coffee bean sign of obstructive bowel from left lower quadrant to right upper quadrant.

197
Q

What is peritonitis?

A

Inflammation and infection of the peritoneum by bacteria that requires a perforation within the GI tract for colonic flora to leak out.

198
Q

What are the causes of peritonitis?

A

Appendicitis leading to ruptured appendix, toxic megacolon rupturing, diverticulitis rupture, severe Crohn’s with complete erosion of intestinal wall and fistula.

199
Q

What are the symptoms of peritonitis?

A

SIRS/sepsis, ache across entire abdomen with worsening pain, nausea/vomiting, oliguria/anuria.

200
Q

How is peritonitis treated?

A

Peritoneal washout and sepsis six - O2, fluids, broad spectrum antibiotics, catheterise, lactate, and blood culture/source control.

201
Q

What is gastroenteritis?

A

Acute inflammation of the stomach and intestine in response to a viral or bacterial infection.

202
Q

How can gastroenteritis cause dehydration?

A

Interference with water, salt, and sugar absorption.

203
Q

How is gastroenteritis treated?

A

Usually self limiting, increase fluid intake and wait it out.

204
Q

What are the common causative organisms of gastroenteritis?

A

Norovirus, campylobacter (direct epithelial damage so loss of function), salmonella, E coli.

Clinical Conditions (13 decks)

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