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Haroon Phase 2A > GI > Flashcards

GI Flashcards

1
Q

What does inflammatory bowel disease comprise of? (IBD)

A

Ulcerative colitis Chron’s disease

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2
Q

Pathophysiology of IBD?

A

Inflamed intestines Associated with HCAB27 (Seronegative spondyloarthropathy) Has a Bimodal age distribution (15-20, 55+)

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3
Q

Cause of Chron’s disease?

A

Environmental and genetic - CARD15/NOD2 mutation => strong genetic component - bacteria trigger an immune mediated response (t-cells)

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4
Q

What part of the gut does Chron’s disease affect?

A

Whole gut Especially terminal ileum and proximal colon (usually rectum is spared)

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5
Q

Risk factors for Chron’s

A

Family history Jewish HLA-B27 gene Smoking (2x as likely) Caucasian

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6
Q

Pathophysiology of Chron’s

A

-Characterised by skip lesions (lesions with gaps in between) arising anywhere between the mouth and the anus -End result is transmural inflammation (in all layers) with granuloma formation => resulting in fistulas, strictures and adhesions

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7
Q

Signs and symptoms of Chron’s disease?

A

Diarrhoea- most significant symptom in adults -Abdominal pain- most significant symptom in kids -Gallstones and kidney stones -Weight loss and lethargy -B12/folate/ Fe deficiency due to malabsorption in small intestine -Apthous mouth ulcers

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8
Q

Extraintestinal manifestations of both Chron’s and Ulcerative Colitis

A

Eyes:Episcleritis = chrons> Uveitis = UC> Cutaneous: Erythema nodosum Pyoderma gangrenosum Musculoskeletal: Arthritis (most common manifestation in both) Spondylarthritis “spine ache” Osteoporosis Clubbing Also 90% of UC patients have PSC but also sometimes present in patients with Chron’s

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9
Q

Investigations to diagnose Chron’s

A

-Feacal calprotectein = raised (inflammation in GI tract + differentiates IBD from IBS) -FBC -CRP/ESR -U&Es -Colonoscopy = skip lesions, cobblestone mucosa, deep ulcers -Biopsy = transmural inflammation, granulomas and goblet cells

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10
Q

How to differentiate UC from Chron’s particularly in the peadiatric population?

A

Serum antibody markers: - pANCA more associated with UC - ASCA more associated with Chron’s

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11
Q

How to differentiate IBD from IBS?

A

Faecal calprotectin Raised in IBD and not IBS

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12
Q

General management tips for Chron’s

A

Smoking cessation advice = crucial -Some evidence that NSAIDs and/or combined oral contraceptive pill can increase risk of relapse

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13
Q

Treatment given to induce remission in mild and moderate Chron’s

A

Elemental diet (alone or with meds, particularly in young people) Mild Chron’s: FIRST LINE : glucocorticoids (PO predinsolone or IV hydrocortisone) SECOND LINE: aminosalicylate (eg mesalazine) Moderate Chron’s: Add in: FIRST LINE: azathioprine or mercaptopurine SECOND LINE: Methotrexate

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14
Q

Treatment for severe Chron’s to induce remission that is unresponsive to conventional therapy

A

Infliximab or adalimumab as monotherapy or combined with other immunosuppressant

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15
Q

Treatment for Chron’s if it is refractory to medical therapy or disease limited to the distal ileum to induce remission

A

Surgery

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16
Q

How to classify severity of Chron’s

A

Mild: - first prevention or - 1 exarcerbation in 12 months Moderate: - >= exarcerbations in 12 months or - glucocorticoid cannot be tapered for management of mild disease Severe: - unresponsive to conventional therapy AND - >= symptoms eg weight loss, fever, severe abdominal pains - usually >3 loose stools per day

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17
Q

How to maintain remission in Chron’s

A

1st line: azathioprine or metcaptopurine 2nd line: Methotrexate Post surgery: consider azathioprine with or without methotrexate

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18
Q

Frequency of surgery in Chrons patients?

A

Approx 80% of patients with Chron’s will require surgery but this is not curative as entire bowel can be affected. By removing ‘x’, ‘y’ can flare up.

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19
Q

Complications of Chron’s

A

Peri-anal abscess Anal fissure Anal fistula Strictures and obstruction

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20
Q

Location of ulcerative colitis

A

COLON ONLY start at rectum—> sigmoid colon—> proximal colon Never proximally beyond illeocaecal valve Doesn’t affect the anus

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21
Q

Aetiology of ulcerative colitis

A

Not well understood Autoimmune colitis associated with HCA B27 gene Involves polygenic predisposition and env factors

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22
Q

Risk factors for ulcerative colitis

A

Family history HLA b27 Caucasian Non-smokers Bimodal age distribution 15-25 and 55-70yrs

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23
Q

Physiopathology of ulcerative colitis

A

Histopathology will show mucosal and submucosal ulceration as well as crypt abscesses with neutrophil infiltration

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24
Q

Symptoms of ulcerative colitis

A

Abdominal pain in left lower quadrant -Urgency and tenesmus (pain on defecation) -Bloody mucosy watery Diarrhoea

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25
Q

Investigations to diagnose ulcerative colitis

A

-Increase in feacal calprotectin -pANCA +ve -FBCs -CSR\ESR - colonoscopy = continuous, “leadpipe sign” - biopsy = raw/red mucosal with widespread shallow ulceration with crypt abscesses and goblet cell depletion

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26
Q

How is disease activity measured in ulcerative colitis patients?

A

Truelove and Witt’s severity index

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27
Q

Treatment for ulcerative colitis to induce remission

A

Generally: First line: topical ASAs Second line: Add high-dose oral ASA Third line: Add topical or oral corticosteroid For acute severe colitis admit into hospital and start iV corticosteroids Add ciclosprin if no improvement in 72hr Still no improvement consider surgery

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28
Q

Treatment for maintenance of remission of ulcerative colitis

A

Low maintainance dose of ASA

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29
Q

Surgery with ulcerative colitis?

A

Total/partial colectomy is often curative

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30
Q

Complications of ulcerative colitis

A

Toxic megacolon is the most common complication cause ulcerative colitis deaths

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31
Q

What is Coeliac’s?

A

Systemic autoimmune T4 hypersensitivity to gluten that effects the small intestine

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32
Q

Pathophysiology of Coeliac’s

A

Pathogenic component of gluten = gliadin -Once absorbed, it is deamidated by tissue transglutaminase (tTG) -in coeliacs, deamidated peptides are presented by antigen-presenting cells via HLA DQ2 or DQ8 to T helper cells to trigger immune response. -immune activation —> villous atrophy, lymphocyte accumulation and intestinal crypt hyperplasia —> malabsorption

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33
Q

Risk factors for Coeliacs

A

Family history HLA-DQ2 and HLA-DQ8 Autoimmunity (thyroid disorders + addisons) IgA deficiency Down’s syndrome Turner’s syndrome

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34
Q

Signs and symptoms of coeliacs

A

Indigestion Diarrhoea or steatorrhoea Bloating and/or constipation Weight loss and fatigue Unexplained iron, vit b12 or folate deficiency IBS in adults Dermatitis herpetiformis- vesicular itchy rash that occurs due to IgA deposition along the dermal papillae

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35
Q

Investigations to diagnose coeliacs

A

If possible patients should be on a gluten containing diet for 6 weeks prior to investigations Screening: 1st line: serological test for IgA antibodies against tTG (anti-tTG) - total IgA must also be measured as may get false -ve in IgA deficient patients 2nd line: endomysial antibodies (IgA) if anti-tTG is weakly positive Diagnostic: gold standard Duodenal biopsy for all patients with positive serology Findings: crypt hyperplasia, villous atrophy, intraepithelial lymphocyte infiltration

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36
Q

Treatment for coeliacs

A

Gluten-free diet Avoid : wheat, rye, barley sometimes oats -Rice, potatoes and corn are gluten free -Replace vitamins and mineral’s deficiency if needed -Offer pneumococcal vaccination with boosters every 5 years

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37
Q

Complications of coeliacs

A

Dermatitis herpetiformis Malignancy Increased risk of osteoporosis Calcium and vit D deficiency

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38
Q

Differental diagnosis with coeliacs

A

Sprue or tropical sprue (associated with tropical travel) = malabsorption syndrome -Similar biopsy to coeliacs- crypt hyperplasia and villous atrophy -Treatment = often antibiotics eg tetracycline

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39
Q

What is IBS?

A

Chronic, relapsing and often lifelong disorder that affects lower GI tract - no discernible structure or biochemical cause => considered ‘functional’

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40
Q

Cause of IBS

A

Multi factorial Genetics + environmental + psychological (stress, anxiety) + dietary Exact mechanism unknown

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41
Q

Categorisation of IBS

A

IBS-C —> mostly constipation IBS-D —> mostly diarrhoea IBS-M —> mostly mixed; alternating C/D

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42
Q

Risk factors of IBS

A

Young adults Females Family history Dietary factors Psychosocial cavities Drugs

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43
Q

Symptoms of IBS

A

Abdominal pain and bloating relieved from defecation -Altered stool form/frequency

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44
Q

Diagnosis to exclude before diagnosing IBS

A

Coeliacs (serology) IBD (check fecal calprotectin) Infections (ESR/CRP/Blood cultures)

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45
Q

Investigations to diagnose IBS

A

IBS is a diagnosis of exclusion so no specific investigation to confirm diagnosis May use following to exclude other conditions: - FBC - ESR/CRP - coeliac serology

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46
Q

Treatment for IBS

A

1st line: conservative patient education, dietary advice and patient reassurance, address any cormorbid stress or anxiety For IBS-C consider more fibre and for IBS-D consider probiotics 2nd line: IBS-C —> laxatives (senna/Fybogel) IBS-D —> antimotility drug (loperamide) 3rd line: For severe abdominal pain consider low-dose trycyclic antidepressant (TCA eg amitriptyline) - consider CBT for psychological support - refer to gastroenterologist

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47
Q

Complications of IBS

A

Mood disorders: more severe and frequent depression and anxiety Poor quality of life: miss three times as many days off work

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48
Q

What is GORD

A

Gastric-oesophageal reflux disease = reflux of gastric contents into oesophagus due to decreased pressure across lower oesophageal sphincter

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49
Q

Causes of GORD

A
  • raised intragastric pressure= obesity + pregnancy - hiatal hernia (mostly with LOS sliding up through diaphragm) - Drugs anti-muscarinics, CCBs - Scleroderma (LOS = scarred)
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50
Q

Symptoms of GORD

A

“Heartburn” -Retrosternal burning chest pain that is exacerbated by lying flat -Sour/bitter taste of acid in the back of the mouth -dysphagia -nausea -chronic cough

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51
Q

Investigations to diagnose GORD

A

If no red flags go a traight to treatment (PPI) Red flags (dysphagia, haematemeis, weight loss) - endoscopy —> oesphagitis or Barrett’s - oesophagal manometry —> measure functionality of LOS and gastric acid pH

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52
Q

Treatment for GORD

A

-Conservative lifestyle changes (smaller meals, 3+hrs before bed, avoidance of trigger foods) -medication review: consider reducing or stoppping medications that are causing symptoms eg CCB -PPI offer full dose for 1-2 months If symptoms persists use PPI at lowest dose possible as maintenance If symptoms still persist or CI then use H2RA

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53
Q

Last resort for GORD treatment?

A

Surgical treatment- laparoscopic fundoplication = mobilisation of funded of stomach which is then wrapped around the lower oesophageal sphincter to tighten it

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54
Q

Complications of GORD

A

Barrett’s oesophagus-oesophageal stricture - fibrous scarring and therefore narrowing of oesophageal lumen -dental problems

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55
Q

Barrett’s oesophagus

A

-10-15% develop Barrett’s -Always involves hiatal hernia -Metaplasia (SSNKE —>simple columnar) -Increased risk of adenocarcinoma -Diagnose with a Biopsy Pathway for oesphagus changes: Normal—> metaplasia (Barrett’s) —> dysplasia (adenocarcinoma)

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56
Q

What is Mallory Weiss Tear?

A

Linear lower oesophageal mucosal tear due to sudden increase in intra-abdominal pressure at the border of the gastro-oesophageal junction Limited to mucosa and submucosa

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57
Q

Typical presentation of Mallory-Weiss Tear?

A

Presents typically as a young male with acute history of retching and vomiting after a night out eventually causing haematemesis Causes a laceration resulting in an upper GI bleed that is usually self-limiting.

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58
Q

Differential diagnosis for MWT?

A

Boerhaave’s syndrome -spontaneous perforation of the oesophagus -usually due to vomiting -ruptures all the layers of the oesophageal wall (transmural) -unlike MWT it’s a surgical emergency

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59
Q

Risk factors of a Mallory Weiss Tear?

A

-Any condition that predisposes to retching or vomiting: gastroenteritis, bulimia, hyperemesis - Alcoholism - chronic cough - hiatus hernia - GORD - Male - age 40-60

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60
Q

What if a patient has haematemesis and pulmonary hypertension?

A

oesophageal varices rupture

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61
Q

Symptoms of MWT

A

Background of alcohol excess presenting with episodes of violent retching or vomiting - Haematemesis (Usually small to moderate volume of bright red blood which is self limiting) - hypotensive in severe cases but unlikely

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62
Q

Investigations to diagnose MWT

A

Upper GI endoscopy (gold standard) required for all patients depending on the Glasgow Blatchford score - usuallay shows a single longitudinal tear (can be multiple) in the mucosa at the gastro-oesophageal junction

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63
Q

Scoring system for upper GI bleeds

A

Glasgow Blatchford Score Score >0 means patient require admission for inpatient endoscopy Score 0 means patient can be discharged Most accurate in identifying risk patients in need of transfusion

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64
Q

What is the Rockall score?

A

Calculated after endoscopy to identify patients at risk of adverse outcomes after treatment for an upper GI bleed

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65
Q

Treatment for MWT

A

Most spontaneously heal within 24h!

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66
Q

What type of peptic ulcer is more common?

A

Gastric>Duodenal Gastric is 2/3x more common

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67
Q

What are peptic ulcer diseases?

A

Punched out round holes in either stomach or stomach or duodenum

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68
Q

Where do gastric ulcers occur

A

Mostly at a lesser curve

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69
Q

Causes of gastric ulcers

A

-H.pylori (causes of 75% of gastric ulcers) -NSAIDs -Zolinger Ellison syndrome: - pancreatic tumour - gastric acid hypersecretion - widespread peptic ulcers

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70
Q

Symptoms of gastric ulcers

A

Epigastric pain - worse on eating - better between meals + with antacids * typically weight loss

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71
Q

Investigations to diagnose gastric ulcers

A

If no red flags (55+, haematemesis/melaena, anaemia, dysphasia) - non invasive tests: c-urea breath test Stool antigen test If red flags - urgent endoscopy + biopsy

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72
Q

Complications of peptic ulcer disease

A

-Bleeding -Perforation: life threatening as ulcer penetrates the duodenum or stomach into the peritoneal cavity; requires surgical intervention -Gastric outlet obstruction: caused by obstruction at pylorus due to an ulcer and subsequently scarring. Presents with vomiting and nausea after food

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73
Q

Location of Duodenal ulcers?

A

mostly at D1 and sometimes D2 -the gastroduodenal artery is located at the posteromedial aspect of D2 so deeply penetrating ulcers in this region can result in a torrential upper GI bleed

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74
Q

Causes of duodenal ulcers

A

H. Pylori (causes 95% of duodenal ulcers) NSAIDS ZE Syndrome

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75
Q

Symptoms of duodenal ulcers

A

Epigastric pain - worse between meals - better with food * typically weight gain

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76
Q

Investigations to diagnose duodenal ulcers

A

If no red flags: - non-invasive testing 1. Urea breath test 2. Stool antigen test If red flags: Urgent endoscopy + biopsy (Will see Brunner’s gland hypertrophy- more mucous production)

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77
Q

What do you have to make sure of before testing for H.pylori?

A

If testing for h.pylori, patient must be off PPI for 2 weeks+ (all ulcers) - otherwise you can get a false -ve

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78
Q

Treatment for both gastric and peptic ulcers?

A

Stop NSAIDs 1) H.pylori +ve -> triple therapy CAP Clarythromycin Amoxicillin PPI (omeprazole) (If they have a penicillin allergy replace amoxicillin with metronidazole) 2) H.Pylori -ve give PPI at initial high dose for a month until ulcer healed Ensure all patients who have a proven ulcer have a repeat endoscopy 6-8 weeks later to confirm healing as well as h.pylori retesting

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79
Q

What is gastritis?

A

Mucosal inflammation and injury

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80
Q

Causes of gastritis

A

Autoimmune (related to pernicious anaemia + anti intrinsic factor antibodies) H. Pylori NSAIDs (causes gastropathy- injury without inflammation) Mucosal ischaemia Campylobacter (GBS) + viral (CMV)

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81
Q

Symptoms of gastritis?

A

Epigastric pain with diarrhoea Nausea and vomiting Indigestion

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82
Q

What is PUD a complication of?

A

Gastritis

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83
Q

Investigations to diagnose gastritis?

A

If H.pylori suspected: - stool antigen test/ urea breath test Gold standard= endoscopy + biopsy

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84
Q

Treatment for gastritis?

A

H. Pylori = triple therapy CAP Clarythromycin Amoxicillin PPI

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85
Q

Pathophysiology of H.Pylori?

A

Commences in stomach- not usually diarrhoea causing - Decreased virulence and is typically opportunistic 1) decreases stomatostatin 2) decreases luminal HCO3 3) secretes urease 4) inscreases gastrin release Urea —urease—> CO2 + NH3 NH3 + N+ —reversible—> NH4+ (toxic)

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86
Q

What is autoimmune gastritis?

A

Affects funds portion of the stomach Especially causes atrophy of parietal cells

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87
Q

What is appendicitis?

A

Acute inflamed appendix, usually due to luminal obstruction SURGICAL EMERGENCY

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88
Q

Epidemiology and risk factors of appendicitis?

A

10-20yrs old Male Frequent antibiotic use Smoking

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89
Q

Causes of appendicitis?

A

Blockages: - Faecolith (hard mass of stool) - foreign body - lymphoid hyperplasia of Peyer’s patches (teens) - fibrous strictures Blockage is typically infected with e.coli and as pressure inside appendix increases, so does rupture risk

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90
Q

Mechanisms of pain in appendicitis?

A

Peri umbilical pain: inflammation of appendix and visceral peritoneum irritates autonomic nerves of the embrylogical midgut —> referred pain to the umbilical region Right iliac fossa: due to localised inflammation of the parietal peritoneum

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91
Q

Classic triad presentation of appendicitis?

A

1) central abdominal pain that migrates to right iliac fossa 2) low-grade pyrexia 3) anorexia 50% of patients present with this characteristic history

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92
Q

Symptoms of appendicitis?

A

1) periumbilical pain that migrated to the right iliac fossa (McBurney’s point) (rebound or percussion tenderness) 2) low grade fever >38°C 3) reduced appetite and anorexia 4) nausea and vomiting 1) McBurney’s point 2) umbilicus 3) right ASIS

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93
Q

Signs of appendicitis?

A

1) Rosving’s sign (pressing on left Illiac fossa causes right illiac fossa pain to get worse) 2) Psoas sign (pain worsened by lying on left side and extending the right leg) 3) Obturator sign (pain worsened by flexing and internally rotating the hip)

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94
Q

Complications of appendicitis?

A

Perforation (15-20%) - appendiceal rupture Appendiceal mass Periappendical abscess

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95
Q

Investigations to diagnose appendicitis?

A

CT abdominal + pelvis = gold standard Pregnancy test to rule out ectopic pregnancy ( presents with right iliac fossa pain)

96
Q

Treatment for appendicitis?

A

Antibiotics and then appendectomy (laproscopic) -Must drain abcesses - resistant to Antibiotics

97
Q

Why must abscess be drained in appendicitis?

A

Abscess = walled off bacterial collection -Resistant to systemic antibiotics so not useful -Needs to be directly dealt with - drainage + intra abscess antibiotic

98
Q

What is diverticular disease?

A

Outpouching of colonic mucosa -most frequently affects the sigmoid due to its small diameter -due to increased intra-colonic pressure at naturally weaker parts of the colon, where penetrating arteries enter walk of the colon

99
Q

Define diverticulum

A

An outpouching at perforating artery sites

100
Q

Define diverticulosis

A

An asymptomatic outpouching

101
Q

Define diverticular disease?

A

A symptomatic outpouching

102
Q

Define diverticulitis

A

Inflammation of outpouching - infection

103
Q

What percentage of diverticula are asymptomatic?

A

95% and only 5% are symptomatic (diverticular disease)

104
Q

What is Meckel’s diverticulum?

A

Paediatric disorder -Failure if obliteration of vitelline duct -Rule of 2s: 2 years old 2 inches long 2ft from illeocaecal valve (umbilical) Diagnostic= technetium scam

105
Q

Risk factors for diverticular disease?

A

Connnective tissue disorders (ED + M) Ageing Increased colon pressure COPD + chronic cough Age

106
Q

Complications of diverticulitis?

A

SBP Obstruction Fistulae

107
Q

Symptoms of diverticulitis?

A

1) Left lower quadrant pain 2) constipation 3) fresh rectal bleeding

108
Q

Investigations to diagnose diverticulitis?

A

CT abdominal/ pelvis with contrast = gold standard

109
Q

Treatment for diverticulosis?

A

Nothing, watch and wait

110
Q

Treatment for diverticular disease

A

Bulk forming laxatives “isphagula husk” Surgery is gold standard

111
Q

Treatment for diverticulitis

A

Antibotics (Co amoxiclav) Paracetamol IV Fluid + liquid food Rarely surgery

112
Q

Two types of intestinal obstruction?

A

Small Bowel Large Bowel

113
Q

Percentage of intestinal obstruction that is small bowel?

A

60-75% of all cases

114
Q

Causes of small bowel obstruction?

A

Adhesions (most common) 50% Hernias 15% Cancer 10% Chron’s

115
Q

Symptoms of intestinal obstruction?

A

Vomiting then constipations Mild abdominal distension + pain Tinkeling bowel sounds (*hyperresonant bowels on percussion in both types of intestinal obstruction)

116
Q

Percentage of intestinal obstruction cases that involve large bowel?

A

25-40% of all cases

117
Q

Causes of large bowel obstruction?

A

Malignancy (90%) Volvulus- mostly sigmoid colon, children Intussusception (bowel telescopes in on itself -> most common in children)

118
Q

Symptoms of large bowel obstruction?

A

First constipation Then vomiting Gross distension + pain Hyperactive, then normal, then absent bowel sounds

119
Q

Investigations to diagnose both types of intestinal obstruction?

A

1st line- X-Ray = shouldn’t be used however might be your exam answer according to lecturer but he is trying to get exam boards to change it💀💀 Gold standard = CT abdomen and pelvis with contrast, and is now often used as initial imaging modality where possible - can idenitify dilated bowel loops, evidence of ischaemia and perforation as well as underlying cause

120
Q

What is a pseudo obstruction?

A

No mechanical obstruction, often a result of post operative state -still have symptoms of intestinal obstruction

121
Q

Treatment for intestinal obstruction?

A

Most patients are two days without food before admission

122
Q

Types of diarrhoea?

A

watery - secretory - osmotic - functional (IBS) - steatorrhoea - inflammatory

123
Q

What is diarrhoea?

A

A presenting symptom with many differential diagnoses Classed as 3+ watery stools daily which are level 5-7 on Bristol stool cahrt

124
Q

What is bloody diarrhoea?

A

Dysentery Eg. Amoebic dysentery E.coli + salmonella + shigella

125
Q

Levels of diarrhoea?

A

Acute < 14 days Subacute 14-28 days Chronic > 28 days

126
Q

Causes of diarrhoea?

A

IBD (Chron’s, UC) Coeliac disease Hyperthyroidism Inflammation or malignancy Infective causes

127
Q

Infective causes of diarrhoea?

A

Viral = most common - rotavirus (kids <3y) - norovirus (adult) Bacterial: - campylobacter (most common bacterial cause) - c. Diff - salmonella - shigella - cholera - E.coli Worms Parasites- Giardiasis (most common parasite cause)

128
Q

Antibiotics as a cause of diarrhoea?

A

They increase the risk of C. Diff infection 4C’s - Clarythromycin, co-amoxiclav, ciprofloxacin, cephalosporins

129
Q

Treatment of diarrhoea?

A

Depends on underlying cause Viral (mc) = self limiting Fluids and diroalyte to rehydrate patient

130
Q

Complications of diarrhoea?

A

Dehydration Electrolyte loss

131
Q

Two types of osphageal cancer?

A

Adenocarcinoma Squamous cell carcinoma

132
Q

Adenocarcinoma location and association?

A

Lower 2/3 of oesophagus Associated with Barrett’s oesophagus

133
Q

Squamous cell carcinoma location and association?

A

Upper 2/3 oesphagus Smoking and alcohol

134
Q

Symptoms of oesophageal cancers?

A

Presents when advanced ALARMS Anemia Loss of weight Anorexic Rescent sudden symptom worsening Melenea/Haematemesis Swallowing progressive difficulty

135
Q

Key symptom of osphageal cancer and differential diagnosis?

A

Progressive swallowing difficulty - first hard to swallow potatoes, now it’s hard to swallow soup If it’s non progressive it could be aschalasia

136
Q

Investigations to diagnose osphageal cancer

A

OGD (oesophago-gastro-duodenoscopy) + biopsy with barium swallow CT/PET for staging

137
Q

Treatment for oesphageal cancer?

A

Medically fit = chemo/radio + surgery Unfit = palliative

138
Q

What are gastric carcinomas?

A

Mostly adenocatcinomas

139
Q

Grading of gastric carcinomas?

A

T1 = well differentiated = better prognosis (mc) T2 = undifferentiated “signet ring carcinomas” typically at proximal stomach = worse prognosis

140
Q

Causes of gastric carcinomas

A

H.pylori Smoking CDH-1 mutation cashed in gene= 80% risk Family history Pernicious anemia (autoimmune chronic gastritis)

141
Q

Symptoms of gastric carcinomas?

A

Severe epigastric pain (Same as gastritis, but worse) Anemia (Fe deffieciency, occult loss) - weight loss - Tired all the time - progressive dysphagia Metastatic signs: -jaundice due to liver metastases -krukenbergtumour due to ovarian metastases from gastric cancer

142
Q

Investigations to diagnose gastric carcinomas?

A

Gastroscopy+ biopsy CT\mri for staging, PET to iD metastases Staging= TNM

143
Q

Treatment for gastric carcinomas?

A

Surgery + “ECF” chemo regimen, if resectable

144
Q

Chance of small intestine carcinomas?

A

Small intestine is pretty tumour resistant so decreased chance of tumour here 1% of all GI tumours Most are adenocarcinomas

145
Q

Risk factors of small intestine carcinomas

A

Chronic SI disease: -Chron’s -Coeliac’s

146
Q

Diagnosis and treatment of small intestine carcinoma?

A

Same as gastric carcinomas

147
Q

What are colorectal polyps vs adenomas?

A

Polyps = small growths on the inner lining of the colon => very common Adenomas = type of polyp that may become cancerous => precursor - mostly spontaneous and benign - common with age

148
Q

Risk factors for colorectal polyps and cancer?

A

Familial inherited genetic predisposition -Adenomas/ polyps -Alcohol, Smoking, ulcerative colitis

149
Q

2 inherited conditions that massively increase the risk of polyps

A

1) familial adenomatous polyposis (FAP) - Auto dom APC gene mutation - causes 1000s of duodenal polyps - inevitably will get colorectal cancer (93% risk by 50) 2) hereditary non polyposis colon cancer (HNP C-Lynch syndrome) - auto dom MSH-1 mutation (or MSH-2) - a DNA mismatch repair gene -Rapidly increases progression adenomas-> carcinoma

150
Q

Common metastases of colon polyps/adenomas?

A

Liver and Lung

151
Q

Symptoms of colorectal polyps/adenomas?

A

Mostly in distal colon (from sigmoid onwards) => LLQ pain, bloody mucosy stools (fresh blood because in the distal colon closer to the anus) Tenesmus (if rectal involvement)

152
Q

Investigations to diagnose colorectal polyps/adenomas?

A

FIT test (fecal occult) - screening for microscopic blood in poop - done in all 60+ with Fe deficient anaemia and change in bowel habits Gold standard= colonoscopy and biopsy Patients with a +ve FIT and suspected colorectal cancer get referred for colonoscopy/biopsy within 2weeks

153
Q

How are colorectal polyps/adenomas classified?

A

TNM system

154
Q

Treatment for colorectal adenomas/polyps cancer?

A

Surgery and chemo is the only curative option if there are no metastases

155
Q

What is dyspepsia?

A

Not a disease A presenting symptom of “indigestion”

156
Q

Signs of dyspepsia?

A

early satiation -epigastric pain + reflux (GORD like pain) -extreme fullness

157
Q

Cause of dyspepsia?

A

Often unknown (“Functional disorder”) Maybe related to ulcers (especially gastric)

158
Q

Diagnosis and treatment of dyspepsia?

A

Need endoscopy to find underlying cause

159
Q

What is H.pylori?

A

Gram -ve bacteria Has a decreased virulence in the GIT

160
Q

Pathology of H.pylori?

A

1) causes decreased stomatostatin 2) increased luminal gastric acid (as more gastrin) 3) urease results in ammonia generation 4) therefore decreased HCO3- secretion

161
Q

Causes of h.pylori?

A

PUD -gastritis -gastric carcinomas

162
Q

Investigations to diagnose H.Pylori?

A

Biopsy (Stool antigen + C-urea breath test often 1st line)

163
Q

Treatment for H.pylori?

A

Triple therapy: Clarythromycin + amoxicillin + PPI

164
Q

What is E.Coli?

A

Major player in UTIs also Gram -ve bacteria Often commensal flora of GIT Some strains/ “serotypes” are very virulent

165
Q

Strains of E.coli that lead to watery diarrhoea?

A

ETEC EAEC EPEC

166
Q

Strains of E.coli that lead to bloody diarrhoea?

A

EHEC

167
Q

Cause of haemolytic uremic syndrome?

A

Serotype 0157:H7 of E.coli Leads to haemorrhagic diarrhoea Nephrotic syndrome

168
Q

Treatment of E.coli?

A

Often amoxicillin, trimethoprim, nitrofurantoin

169
Q

What is C.difficile?

A

Gram +ve spore forming bacteria

170
Q

What is C.difficile mainly induced by?

A

Ciprofloxacin Co-amoziclav Cephaolosporins Clindamycin 4 Cs

171
Q

What’s Meleana?

A

Blood in the stool that appears black

172
Q

Likely causes of GI bleeding?

A

Peptic ulcer= most common (50%) Osephageal varices Mallory-Weiss syndrome Gastric carcinoma (uncommon)

173
Q

How to manage patients with GI bleeds?

A

img

174
Q

How to differentiate between variceal and non-variceal bleed?

A

img

175
Q

What is most important when it comes to GI bleeding?

A

Initial assessment and management rather than endoscopy in most cases

176
Q

In the UK how often do you see upper GI bleeding?

A

Nearly one presentation every 6 minutes = very common medical emergency

177
Q

Causes of intraluminal obstruction?

A

tumour - carcinoma - lymphoma - diaphragm disease (becoming more common due to NSAIDs) - meconium Ileus - gallstone disease

178
Q

Causes of intramural obstruction?

A

inflammatory - Chron’s disease - diverticulitis - tumours - neural - Hirschsprung’s disease

179
Q

Causes of extraluminal obstruction?

A

adhesions - volvulus - tumour - peritoneal deposits

180
Q

What is small bowel obstruction?

A

A form of intestinal failure causing malabsorption requiring iV supplementation or replacement

181
Q

Presenting history of small bowel obstruction?

A

pain in umbilical region that comes in waves = colic -Bilious vomiting (dark green) - bloating/ distension - when did they last eat and drink?

182
Q

What to assess in a patient with potential small bowel obstruction?

A

hydration status - Weight loss - pulse/bp - O2 stats - scars - Abdominal distension - Abdominal tenderness - hernia orifices - PR exam

183
Q

Investigations to diagnose small bowel obstruction?

A

Full blood count Urea and electrolytes Lactate C-reactive protein CT SCAN = 🔑 NOT X RAY

184
Q

Why use a CT scan for suspected small bowel obstruction?

A

3D representation of problem Localises site of obstruction Indicates cause Tells you if bowel is ischaemic: - poor enhancement - free fluid - twisted mesentery

185
Q

How to treat patients with Small bowel obstruction due to adhesions?

A

Gastrograffin Challenge = administer soluble contrast and do x-ray to assess if operation needed

186
Q

Types of operation given for small bowel obstruction?

A

Key hole or open -divide scar tissue -risk of future scar formation -minimally invasive surgery can help

187
Q

How to treat small bowel obstruction due to hernia?

A

Groin or umbilical - operate (almost always groin- ie. femoral) High risk patient- Taxis (local anaesthesia and push back in) High BMI- conservative measures Incisional hernia- treat as adhesive SBO

188
Q

Most common complication of small bowel obstruction?

A

Renal failure

189
Q

When would you advise surgery in adhesive SBO?

A

Signs of ischemia on a CT scan

190
Q

What does C. difficile cause and how?

A

Pseudomembranous colitis - normal GIT flora killed by antibiotics and C.diff replaces these - results in dangerous severe diarrhoea ( very watery so increased dehydration) and is highly infectious

191
Q

Treatment for C.difficile?

A

Stop using these 4 antibiotics ( ciprofloxacin, Co-amoxiclav, cephalosporins, clindamycin) => give Vancomycin (now first line according to nice)

192
Q

What is Achalasia?

A

Osephageal dysmotility (impaired peristalsis) - LOS fails to relax - rate and idiopathic

193
Q

Symptoms of achalasia?

A

Non progressive dysphagia (struggle swallowing anything) -Chesty Substernal pain -Food regurgitation -Aspiration pneumonia

194
Q

Investigations to diagnose Achalasia?

A

Barium swallow with “bird beak” - manometry (measure pressure across LOS) = diagnostic

195
Q

Complication of Achalasia?

A

May increase risk of oesphageal squamous cell lung cancer

196
Q

Treatment for Achalasia?

A

Only surgery is curative (balloon stenting) * drugs may help pre-surgery - nitrates, nifedipine

197
Q

What is ischemic colitis?

A

Ischemia if colonic arterial supply - colon gets inflamed due to hypoperfusion

198
Q

Causes of ischemic colitis?

A

Affecting inferior mesenteric artery; - thrombosis (+/- atherosclerosis) = most common - emboli - decreased CO + arrhythmias (eg history of AF) or due to shock - combined oral contraceptive pill

199
Q

Most common sites effects with ischemic colitis?

A

Watershed areas - splenic flexure (most common) - sigmoid colon + cecum

200
Q

Symptoms of ischeamic colitis?

A

LLQ pain + bright bloody stool +/- signs of hypovolemic shock

201
Q

Investigations to diagnose ischemic colitis?

A

Colonoscopy + biopsy = gold standard (Only after patient is fully recovered, prevents stricture formation + normal healing) (first rule out other causes- eg. Stool sample for h pylori)

202
Q

Complications of ischemic colitis?

A

Perforation - tissue death - strictures (therefore obstruction)

203
Q

Treatment do ischeamic colitis?

A

If just symptomatic- IV fluids + antibiotics (prophylactic) If gangrenous (infected colon)- only SURGERY

204
Q

What is mesenteric ischemia?

A

Ischemia of small intestine

205
Q

Two types of mesenteric ischemia?

A

AMI- acute attack “abdominal MI” CMI- chronic and over a longer period of months “abdominal angina”

206
Q

Causes of mesenteric ischemia?

A

Affecting superior mesenteric artery - Thrombosis (most common) - Emboli (due to AF often)

207
Q

Symptoms of mesenteric ischemia?

A

Triad: 1) central/ RIF acute severe abdo pain 2) no abdo signs on exam (eg. Guarding, rebound tenderness) 3) rapid hypovolemic shock

208
Q

Investigations to diagnose mesenteric ischemia?

A

CT angiogram FBC+ABG = persistant metabolic acidosis

209
Q

Complication of mesenteric ischemia?

A

SBP (spontaneous bacterial peritonitis)

210
Q

Treatment of mesenteric ischemia?

A

Fluid resuscitation Antibiotics IV heparin ( decrease thromboemboli) —> infarcted bowel is treated by surgery

211
Q

What are haemorrhoids?

A

Swollen veins around anus disrupt anal cushions - parts of the anal cushions prolapse through tight anal passage (Google pics at ur own discretion 🤮)

212
Q

Most common cause of haemorrhoids?

A

Constipation with increase straining - also anal sex

213
Q

2 types of haemorrhoids?

A

1) internal - originate above internal rectal plexus (dentate line) - less painful as has decreased sensory supply - may feel “incomplete emptying” 2) external haemrrhoids - originate below dentate line - so painful patients can’t sit down!

214
Q

Symptom of haemorrhoids?

A

-Bright red flesh PR bleeding and mucosy bloody stool -bulging pain +/- pruritas ani (itchy bum)

215
Q

Investigations to diagnose haemorrhoids?

A

External haemorrhoids = PR exam (digital) - may be visible though Internal haemorrhoids = proctoscopy

216
Q

Treatment for haemorrhoids?

A

Stool softener Definitive= rubber band ligation

217
Q

What is a perianal abscess?

A

Walled off collections of stool + bacteria around anus

218
Q

Most common cause of perianal abscess?

A

Anal sex causing anal gland infection

219
Q

Symptoms of perianal abscess?

A

Pus in stool + constant pain (tender)

220
Q

Treatment for perianal abscess?

A

Surgical removal + drainage if walled off and resistant to oral antibiotic therapy

221
Q

What is an anal fistula?

A

Abnormal “tracks” form between inside of anus —> elsewhere Eg subcutaneous skin (mostly)

222
Q

What does an anal fistual typically progress from?

A

Perianal abscesses - abscess discharges (toxic substances) which aid fistula formation as abscess grows (also Chron’s and rectal cancer)

223
Q

Symptoms of anal fistulas?

A

Bloody/ mucosy discharge Often very viable and painful

224
Q

Treatment for anal fistula?

A

Surgical removal + drainage (with antibiotics if infected)

225
Q

What is an anal fissure?

A

Tear in abal skin lining below dentate line => very painful due to strong sensory supply

226
Q

Most common causes of anal fissure?

A

Hard feaces

227
Q

Other less common causes of anal fissures?

A

Trauma (eg childbirth) Chron’s UC

228
Q

Symptoms of anal fissures?

A

extreme defecation pain -very itchy bum (pruritus ani) -anal Bleeding

229
Q

Treatment for anal fissures?

A

Stool softening (increase fibre intake + more fluids) Topical creams (lidocaine ointment) Definitive treatment=surgery (not usually done)

230
Q

What are pilondial sinus/abscesses caused by?

A

Hair follicles that get stuck in natal cleft (bum crack) Which : 1) forms small tracts (sinus) 2) get infected (abscesses)

231
Q

In which people are pilondial sinus and abscess commonly seen in?

A

In very hairy people (eg Asians)

232
Q

Symptoms of pilondial sinus and abscesses?

A

Swollen pus filled smelly abscess on bum crack (Visible on exam)

233
Q

Treatment for pilondial sinus / abscess?

A

Surgery + hygiene advice

234
Q

What is Zenker’s diverticulum?

A

A pharyngeal pouch when some food goes down the pouch instead of totally down oesphagus

235
Q

Symptoms of Zenker’s diverticulum?

A

Smelly breath (food is accumulating in oesphagus) Regurgitation and aspiration of food

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