GI top tier Flashcards

Question

IBS investigation

Answer 1

``` No diagnosis - no objective evidence - histology is useless - Rome IV criteria = Recurrent abdominal pain 1 day/week for last 3 months (symptoms started 6 months ago) + 2 of - Pain relieved with defecation - Stool frequency change - Stool appearance change ``` Instead just rule out things - Aneamia (FBC) - Inflammation (ESR/CRP) - Coeliac (tTG antibodies/ alpha gliadin / EMA antibodies) - Faecal calprotectin (IBD)

Answer 2

- Education - Reassurance Dietary modification - Low FODMAP = carbs which are poorly absorbed - Lots of fluids - Small, regular meals - Reduce caffeine, alcohol, fizzy drinks - Less insoluble fibre and fruit if bloating/ IBS-Dv(not dissolved, passes through gut unchanged, bulks up faeces and increases gut motility) - Fibre good for IBS-C (softens stool, slows down sugar release) - Low sugar - Pain treatment - Psychological - Laxatives vs antimotility agents (loperamide aka imodium) depending on IBS-C or IBS-D respectively

Answer 3

``` 1 defective intraluminal digestion 2 insufficient absorptive area 3 lack of digestive enzymes 4 defective epithelial transport 5 lymphatic obstruction ```

Answer 4

Pancreatic insufficiency - Pancreas produces the majority of digestive enzymes - amylases, proteases, lipases. Lack of these in the intestines → lack of digestion - Pancreatitis : causes damage to most of the glandular pancreas meaning less or no enzymes are released - Cystic fibrosis : results in the blockage of the pancreatic duct due to excess mucous meaning enzymes aren’t excreted Defective bile secretion - → Lack of fat solubilisation so cannot be absorbed - Biliary obstruction eg gallstone - Ileal resection - terminal ileum is where we absorb bile salts so reuptake decreased (eg Crohn’s) Bacterial overgrowth - Inhibits intraluminal digestion - Bugs eat the nutrients

Answer 5

= Microvilli damaged, so surface area decreased, so less absorption potential Coeliac (gluten sensitive enteropathy) - Villi short if even present (villous atrophy, crypt hyperplasia), due to allergic reaction to gliadin in gluten Crohns - Causes inflammatory damage and then scarring to the lining of the bowel, particularly in the terminal ileum, resulting in cobblestone mucosa → SA for absorption decreased Giardia lamblia (extensive surface parasitisation) - Extensive surface of villi and microvilli covered by parasite so food can’t be absorbed - Cleared with antibiotics Surgery - resection/ bypass of small intestine removes surface area - Procedure for - -- Morbid obesity (less so now - weight loss good but malabsorption aspect is bad) - -- Crohns - -- Infarcted small bowel (atherosclerosis)

Answer 6

Gliadin protein from gluten - absorbed into intestine. Processed by transglutaminase (TG) and then presented to an APC Th cell. This causes an allergic reaction to gliadin → toxic T cells → intestinal epithelium damage → villous atrophy villous atrophy and crypt hyperplasia are typical signs - villi short if present inflamed mucosa increased epithelial lymphocytes due to autoantibodies created and inflammatory response

Answer 7

Disaccharide deficiency = lactose intolerance - lactase enzyme deficient so Lactose in milk can not be broken down/ absorbed - Undigested lactose passes to colon where bacteria eat --> overgrowth - they damage brush border

Answer 8

= lactose intolerance - Lactose in milk can not be broken down so can not be absorbed as lactase enzyme is deficient - Undigested lactose passes to colon. - Bacteria in colon eat this, releasing CO2, causing wind and diarrhea - Bacteria overgrowth as a result too → damages brush border - Very common, and distribution varies - 80% china, 10% UK (ish!!!)

Answer 9

- Abetalipoproteinemia - lack of specific transporter protein to transport lipoprotein across so particular nutrient not absorbed - Primary bile acid malabsorption - due to mutation in bile acid transporter protein - Rare

Answer 10

This is the route that absorbed nutrients go: lymphatics → thoracic duct → inferior vena cava → blood Lymphoma TB

Answer 11

Insufficient intake -- Not malabsorption (would absorb correctly if they were taken in)

Answer 12

- anaemic - Weight loss - despite normal calorie intake - Abnormal faeces - -- High fat in stool as fat not absorbed - -- Pale - -- Floating

Answer 13

proximal bowel B12, iron, folate, vitamin D, calcium bile salts aren't absorbed so maybe prob with fat too

Answer 14

- Common - over 1% in Europe. Prevalence increasing worldwide - Normally diagnosed middle-aged, or as a child - m=f

Answer 15

genetics - Expressing HLA DQ2/8 (mainly the 2 one)- lots have this antigen but no coeliac but it is needed for disease - First degree relative of coeliac sufferer Other autoimmune disorders - igA deficiency environmental - Breast feeding - Rotavirus in infancy - gluten (gliadins) trigger

Answer 16

Classic (but not necessarily more common) - Diarrhea - Steatorrhea - Weight loss - Failure to thrive - Abdominal pain - Bloating Non-classic (but not uncommon) - IB symptoms - Iron deficiency anaemia - Osteoporosis - Dermatitis herpetiformis - -- Chronic autoimmune skin blistering - -- Itchy blisters, red, clusters - -- Cutaneous manifestation of coeliac - -- Diagnosis = skin biopsy to see IgA deposits - Chronic fatigue - Ataxia - Amenorrhea - Infertility - Peripheral neuropathy - Hyposplenism - Angular stomatitis = inflammation in one/both corners of mouth - *associated autoimmune disorders about ⅓ are silent - Look at 1st degree relatives of patients - -- Serological screening - Test if associated disease including autoimmune

Answer 17

Serology - IgA transglutaminase (tTG) antibody * - IgA anti-endomysial antibody (EMA)* - Coeliac antibodies but if someone is IgA deficient, test for IgG * - Alpha gliadin antibody levels * - Often (but not diagnostic) low ferritin, B12, Hb * Upper GI endoscopy AND * duodenal biopsy Histology - * villous atrophy - Crypt hyperplasia - Increase in intraepithelial lymphocytes need to keep gluten up (6w+) for investigations

Answer 18

``` 0 - normal mucosa 1 - increased number of intraepithelial lymphocytes 2- proliferation of crypts of lieberkuhn 3 - variable villous atrophy 3a - partial villous atrophy 3b - subtotal villous atrophy 3c - total villous atrophy 4 hypoplasia of the small bowel architecture (not all contain this stage) ```

Answer 19

Gluten free diet - Symptoms reverse. Some have persistent symptoms (Sometimes due to low adherence) . Symptoms despite 12month strict gluten free diet = “unresponsive” DEXA scan to monitor risk of osteoporosis Correction for vitamin deficiencies (eg folate, B12, iron, calcium, vitamin D) pneumococcal vaccine given due to risk of hyposplenia

Answer 20

- Lymphoma - Osteoporosis - Anaemia - Micronutrient deficiencies - Dermatitis herpetiformis - Hyposplenia - So pneumococcal vaccine given - Secondary lactose intolerance - Increased risk of malignancy due to increased cell turnover - Other autoimmune conditions - Infertility- see symptoms

Answer 21

Rupture - Releases infected tissue and faecal matter into peritoneum → peritonitis (serious) Appendix mass - If inflamed appendix becomes covered in omentum to form a mass - Antibiotics and then surgery to remove appendix Abscess - Pus and fluid around appendix - Antibiotics and drain appendix

Answer 22

- Appendectomy (lapropscopic) = removal of appendix - IV anitbiotics pre-op to reduce wound infections - Drain any abscesses

Answer 23

Blood tests - Raised CRP/ESR - Raised wbc - neutrophil esp Ultrasound - Inflammed appendix/ appendix mass/ diff diganoses CT = gold standard Pregnancy test- to exclude ectopic pregnancy Urinalysis- to exclude UTI

Answer 24

- pain - -- Umbilical region - -- Migrates to R iliac fossa - -- Mcburney's point - Anorexia - naus/vom - Constipation. Or sometimes diarrhea - Oedema - Fever - Tachycardia - Tenderness in R iliac fossa with guarding -- due to localised peritonitis!! - Tender mass in R iliac fossa

Answer 25

10-20y common m>f

Answer 26

- Faecolith = a stone made of faeces, can block appendix lumen - Lymphoid hyperplasia - block lumen -- Especially children/teenagers - Filarial worms (pinworms) block lumen == most common - Undigested seeds

Answer 27

- Ileitus due to crohns - Salpingitis (fallopian tube inflammation) - Ectopic pregnancy - UTI - Diverticulitis - Perforated ulcer - Food poisoning

Answer 28

- Occurs when lumen of appendix becomes obstructed, - Appendix continues to produce mucous secretions. These build up and increase appendix pressure - It gets physically bigger and presses on nerves - Inflammation - pus accumulates --Serum wbc increase - Oedema - Ischaemia - -- Swelling presses on blood vessels nearby and these cuts of the blood supply to appendix → cells die - -- Flora in gut now trapped in appendix, they are able to proliferate resulting in the invasion of gut organisms into the appendix wall - -- This means bacteria can invade the wall - Necrosis - Perforation --- Wall is dead so is very weak so pressure can burst the wall

Answer 29

If ulcer erodes through arterial vessel → big bleed/haemorrhage - Vomiting up blood If ulcer erodes past the muscle layer - → peritonitis - -- gas under diaphragm in erect CXR - -- Acute abdominal pain - → pancreatitis

Answer 30

Endoscopy - These are benign ulcers (not gastric cancer ulcers) - Punched out - No heaped up epithelium at edge - Sharply demarcated Breath test - C-urea - Tests for helicobacter pylori - Quick and reliable, sensitive + specific - Can monitor after eradication - No antibiotics/ PPIs before test Stool antigen test - Also detects helicobacter - No PPIs beforehand - Increase in inflammatory cells

Answer 31

- Upper abdominal pain -- Burning pain- indigestion/heartburn = what patient says feels like - Nausea

Answer 32

- Duodenal ulcers most commonly found in the duodenal cap (first part) - 2-3x more common than gastric ulcers. Gastric ulcers most commonly seen on lesser curve of stomach but can be anywhere

Answer 33

- Peptic ulcers: are ulcers (break in superficial epithelial cells penetrating down to muscularis mucosa) in either stomach, duodenum and lower oesophagus - Associated with an increase in inflammatory cell - Results in gastritis causes - reduced blood flow - increased acid in stomach - bile reflux - infection

Answer 34

ALARMS - Anaemia - Loss of weight - Anorexia - Recent onset/ progressive symptoms - Melaena = black stools from blood / haematemesis = vomiting blood - Swallowing difficulty = dysphagia biopsy to confirm

Answer 35

- acidic stomach - neutral buffered mucin layer (complete) - glandular gastric cells - capillary underneath

Answer 36

- Mucosa becomes ischaemic - Cells unable to produce mucin - layer depletes - Not protected from acidity of stomach - Those cells die (under no mucin) --> Microulcers (“curling’s ulcers” ) x lots as capillary exposed to acid - Bleeding - Cells either side are damaged - acute - tachy - low BP - maybe haemodynamic shock due to haemorrhage - restore blood volume (fluids ) --> more bloody supply to mucosa - reduce stomach acidity with PPI

Answer 37

- more acid so able to overcome mucosal mucin barrier - cells beneath mucin exposed and damaged by acid - ulceration as capillary and other gastric cells exposed to acid - Stress!! - Helicobacter pylori - Aspirin/aproxen - -- NSAIDs PPI - reduce acidity (and antibiotics if helicobacter)

Answer 38

- NSAIDs sit on mucosa and releases salicylic acid - This inhibits prostaglandin synthetase (=COX2 or COX1?) - So less prostaglandins. Prostaglandins needed for mucous secretion - Ulceration - SO.. aspirin can be coated in an enteric coat so that is doesn't dissolve in acid, sit on mucosa and cause ulceration

Answer 39

- Bile is okay in duodenum but not in the stomach. so if it refluxes, it is bad (irritation, inflammation) Causes - Spirits (rather than wine/beer). These ‘fix’ the stomach (i think this means like preserve it stiff?) - so food passes out less? - Partial gastrectomy - intestine blockage

Answer 40

helicobacter pylori - Can live in mucin layer in stomach, after being ingested 1. Helicobacter produce chemicals downwards to the cells → causing acute inflammatory cells to be attracted (neutrophils) 2. These move into the gastric epithelium → release things that damage the mucosal cells so they produce less mucus→ ulceration 3. G cells increase acid secretion from parietal cells --> stomach more acidic --> ulceration 4. also causes decrease in duodenal HCO3- secretion (more acidic in duodenum --> ulceration) - Can see them with alcian blue toll yellow stain - Blue little thin tic tacs in yellow stomach antibiotics + PPI

Answer 41

Long term response : mucosa changes into intestinal epithelium = intestinal metaplasia - More resistant to acid and bugs - Increased risk of gastric cancer (slight) . By chronic inflammation and becoming meta/dysplasia

Answer 42

- Obesity and overeating -- increased intraabdominal pressure! - Hiatus hernia - stomach bulges through diaphragm hiatus - --Rolling (paraesophageal) - 20% -- Fundus of stomach prolapses through but gastroesophageal junction remains intact. Reflux less common - -- Sliding - 80% -- Both gastro-oesophageal junction and part of stomach slide up into chest through the hiatus. Reflux more common as the sphincter is less competent - Smoking - Alcohol - Pregnancy - Systemic sclerosis

Answer 43

Should be a clear junction between oesophagus and stomach - Oesophagus = squamous epithelium (for abrasion eg crisps) - Stomach = glandular epithelium (acid secretion + mucin layer) - Lower oesophageal sphincter relaxes more transiently and frequently, not only following swallowing to allow bolus entry into the stomach - Lower oesophageal sphincter may have less tone - Acid reflux through the lower oesophageal sphincter causes the oesophageal cells to die quickly because the squamous cells have no mucin barrier - Ulceration - Pain - Continued acid reflux means that this squamous epithelium cannot regrow - Instead: metaplasia - This is a stem cell change rather than the individual squamous cells themselves - Now there is glandular epithelium in the oesophagus and it is covered with the associated secreted mucin layer - This protects it from acid reflux

Answer 44

- Weight loss maybe - Haematemesis = vomiting blood - Anaemia from iron deficiency - Pain - Heartburn = middle of chest - Burping - Painful swallowing = odynophagia - Cough , hoarse voice - Bad breath, unpleasant taste in mouth - Feel sick - May be triggered by particular foods

Answer 45

oesophagus : squamous epithelium to glandular epithelium covered with associated mucin layer (like in stomach)

Answer 46

Endoscopy - If palpable mass, vomitting, GI bleed, dysphagia, weight loss, haematemesis, persistant symptoms (4w), old (55) - Normal oesophagus (squamous over oesophageal mucus gland) reflects light - white/pale pink - Barrett’s oesophagus = columnar lined lower oesophagus (CELLO) = redder, less reflective. This is glandular mucosa overlying oesophagus mucus gland - Biopsy this Barium swallow - May show hiatus hernia

Answer 47

- Encourage weight loss - Smoking cessation - Small, regular meals - Avoid: hot drinks, alcohol, citrus fruits, spicy foods, eating 3h before bed - Raise bed head

Answer 48

Nissen fundoplication = increases the resting lower oesophageal sphincter pressure - If not responding to therapy - May cause bloating and dysphagia

Answer 49

Antacids - Eg magnesium/aliginate containing - Reduce reflux with ‘foam raft’ PPI - Eg lansoprazole - Reduces gastric acid production Avoid drugs that lower oesophageal motility - Nitrates - Anticholinergics - CCB H2 antagonist - ranitidine - not 1st line AVOID drugs that damage the mucosa - NSAIDs - Potassium salts - Bisphosphonates

Answer 50

Barrett's oesophagus - Hiatus hernia always present - Oesophageal cancer. The dysplastic epithelium can become neoplastic epithelium == adeniocarcinoma Peptic stricture - Inflammation of oesophagus (oesophagitis) resulting from gastic (peptic) acid - Gradually worsening intermittent dysphagia Iron deficiency Ulcers Mallory weiss tear (in mucosa at eosophagogastric junction)

Answer 51

upper - oesophageal , stomach (Small bowel rare) lower - colorectal

Answer 52

- Increasing frequency - --- Obesity increasing - --- reclassification from upper gastric → oesophageal cancers - Not as common as colon cancer - M >f - Peaks in 60s/70s

Answer 53

- Incidence decreasing - --- May be due to reclassification from upper gastric → oesophageal cancers - M >f - E europe - E asia - Peaks in 70s

Answer 54

- M > f - Old age- 60/70. Rare under 30 - HICs eg N europe , rather than asia/africa - Incidence rising with time - Colorectal is v common

Answer 55

= risk factors for reflux/ GORD : - Obesity -- Increased intraabdominal pressure!! - Hiatus hernia - stomach bulges through diaphragm hiatus - -- Rolling (paraesophageal) - 20%. Fundus of stomach prolapses through but gastroesophageal junction remains intact. Reflux less common - -- Sliding - 80%. Both gastro-oesophageal junction and part of stomach slide up into chest through the hiatus. Reflux more common as the sphincter is less competent - Smoking - Alcohol - Pregnancy - Systemic sclerosis

Answer 56

Hiatus hernia - stomach bulges through diaphragm hiatus Rolling (paraesophageal) - 20% - Fundus of stomach prolapses through but gastroesophageal junction remains intact - Reflux less common Sliding - 80% - Both gastro-oesophageal junction and part of stomach slide up into chest through the hiatus - Reflux more common as the sphincter is less competent

Answer 57

- Smoking - Smoked food - Pickled food - High salt/nitrates in diet - Genetic, family history - Helicopacter pylori - -- Causes chronic gastritis - -- Can lead to atrophic gastritis → metaplasia → dysplasia → cancer - Pernicious anaemia ``` decreased risk: Low salt Non-starchy veg Fruit Garlic ```

Answer 58

rare coeliac crohns (not UC- doesnt pass caeco-ileal valve) adenocarcinoma non-hodgkins lymphoma anaemia, weight loss, diarrhea, pain, mass, anorexia endoscopy and biopsy, CT/US radiotherapy resection

Answer 59

Genetic predisposition: - Familial adenomatous polyposis (FAP) = born with lots of polyps (100s-1000s) - -- Apc gene keeps beta catenin levels low - -- Apc mutation→ (misfolding)→ beta catenin levels rise → epithelial proliferation → adenoma - -- Dominant inheritance - -- May be given a prophylactic colectomy and ileorectal anstamosis - Lynch syndrome : Hereditary nonpolyposis colorectal cancer (HNPCC) - -- No DNA repair protein produced (hMSH2/hMSH1) - -- Increased risk of damage so increased risk of cancer development - DNA damage accumulates - -- Identifying this is important: relatives' cancer, and doesn’t respond well to chemo - so saves patients the side effects for little gain - -- Polyps develop into cancer more rapidly (normally 10y)

Answer 60

- adenomas - Low fibre diet - -- Better = veg, milk, garlic, - exercise - Sugar - Alcohol - Smoking - Obesity - Age - Conditions - -- UC - -- Primary sclerosing cholangitis (PSC)

Answer 61

Adenocarcinoma : Continued acid reflux - Affects lower ⅓ of oesophagus!! - This causes change in epithelium → meta → hyper plasia meaning there is glandular epithelium in the oesophagus (stem cell change) - This can develop to NEOPLASTIC glandular epithelium Tumour can - Protrude into lumen of oesophagus -- Dysphagia - If goes along oesophagus wall -- Difficult to resect - If goes outward into surrounding structures -- may compress/ enter lymph/ vascular channels / trachea/bronchi (Small vessels quite near and vena cava/ aorta further but not miles off) ``` squamous cell carcinoma - v common in china, SE asia, ethiopia risk factors - Smoking - Drinking - Obesity - Low fruit/veg low prognosis Upper ⅔ of oesophagus ```

Answer 62

- Adenocarcinoma as well (As oesophageal) - Stomach changes to intestinal metaplasia, then dysplasia - Then intramucosal carcinoma and then invasive carcinoma Intestinal - well formed, well differentiated heaped up, ulcerated lesions - Distal stomach - Environmental association Diffuse - Poorly cohesive undifferentiated cells - Infiltrate gastric wall - Any part of stomach, esp cardia - Worse prognosis

Answer 63

In situ = only in mucosa Early gastric cancer = into submucosa only - May or may not have spread to lymph nodes - This is good prognosis, but is rare as often caught having spread further - This is invasive. As soon as it leaves the mucosa, it is invasive - May appear as a shallow ulcer Late gastric cancer = into muscular wall - +/- lymph nodes - Linitus plastica = “leather bottle stomach” = Rigid , doesn’t move, Thickened wall, Cancer all the way through

Answer 64

- Anywhere in colon - most in distal end ! - The proximal ones have a worse prognosis ! - Adenocarcinoma (glandular)

Answer 65

Do in lab (histopathology) at margins ``` Dukes A - mucosa/submucosa B - bowel wall (muscular) C - lymph nodes --- High tide lymph node = lymph node on the mesentery that is furthest from the colon D - metastases ``` pT pN // TNM system Pt1- no deeper than submucosa (stage 1) Pt2 - in muscularis propria but no further (stage 1) Pt3 - has exitted muscularis ( to serosa/fat/lymph nodules) (stage 2) Pn1 - 1-3 lymph node metastases(stage 3) Pn2 - 4+ lymph node metastases (stage 4) M - distant metastases ( stage 4)

Answer 66

classic cancer signs blood/mucus in poo (the nearer the cancer to the anus, the more visible these will be) bowel habit change - diarrhea abdom pain

Answer 67

classic cancer signs vom/ naus/ anorexia dysphagia if tumour in fundus

Answer 68

classic cancer signs progressive!! dysphasia -- solids first, then liquids (if sudden liquids and solids difficulty from beginning- indicates benign disease eg leiomyomas. these are slow growing, narrowing the lumen)

Answer 69

Endoscopy + Biopsy - Rule out pathogens ``` Barium meals (uses contrast) - To see strictures ``` CT/MRI/PET - May show bowel wall thickening - May show lymph node involvement (lymphoma) - For tumour staging - PET esp for metastases ``` Colorectal - Faecal occult blood (FOB) - screening - Fbc - microcytic anaemia - Colonoscopy is best Biopsy , polyps removal - Barium enema - contrast CT - better for the elderly ```

Answer 70

All - Palliative care - Pain relief - Chemotherapy /radiotherapy if is spread - Surgical resection (endoscopic/surgical) Then look in the lab at resection margins -- is all cut out? RO= completely resected locally, R1 = microscopic involvement of margin by tumour R2 =macroscopic involvement of margin by tumour - Monitor to see if any development - oesophagus stenting allows swallowing - radiotherapy good for small bowel - rectal cancer hard to remove (chemo/surgery)

Answer 71

IgA TTG small bowel histology also NEEDED for diagnosis, but isnt first line