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phase 2a mine > GI top tier > Flashcards

GI top tier Flashcards

1
Q

IBD conditions=

- what are they both in general terms

A

crohn’s
ulcerative colitis

chronic, inflammatory conditions - inappropriate immune responses against gut flora

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2
Q

ulcerative colitis

  • age
  • gender
  • race
A

20-40
m>f
more prevalent in western populations than general world

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3
Q

risk factors for crohns and UC

A

Crohn’s
- Smoking damages

UC

  • Smoking protects so if smoking – decreases the severity of symptoms
  • Some link to HLAB27 (as with ankylosing spondylitis - but less strong of a link)
  • Primary sclerosing cholangitis
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4
Q

crohn’s vs UC: distrubtuion

A

crohns
= Can be anywhere along gut, from mouth to anus
- Most common in terminal ileum - where bile salts and B12 are absorbed

UC
= Starts at the rectum and progresses up.
- Up to colon- can’t go into the ileum past the ileocaecal valve.
- (backwash ileitis = reflux back into ileum but not intrinsically inflamed ileum)
- Classified by how much of colon is affected

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5
Q

crohns vs UC pattern of inflammation

how do inflamed areas appear?

A

crohns
=Patchy inflammation, not continuous (has skip lesions)

UC
=Continuous inflammation, not patchy. Distinct cut off between normal and inflamed regions:
- Inflamed = ulcerated and darker (hyperaemic = red in colonoscope but more brown in resections)

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6
Q

crohn’s vs UC bowel wall affected how

A

crohn’s =The full thickness of the bowel wall can be affected (can be transmural) - mucosa, submucosa, muscularis propria, fat

UC=Only the mucosal layer can be affected

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7
Q

crohns vs UC ulcers

what about fistula?

A

crohns= Deep fissuring ulcers

UC = ulcers also present

chrons = Yes (deep fistula go through to other bits of bowel)
UC = no
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8
Q

crohns’ vs UC granulomas

+ what is a granuloma

A

granuloma = collection of epithelial macrophages surrounded by lymphocytes

crohns = yes
UC= no
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9
Q

crohn’s vs UC effect on gut cells / features / looks like

A

crohns = cobblestone mucosa - as a result of fibrosis and strictures

UC =
goblet cell depletion
crypt abscesses and distortion

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10
Q

crohns vs UC- style of chronic disease

A

both = remission and relapse

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11
Q

signs/ symptoms of IBD (C+UC)

only crohns presentation

A

BOTH

  • Finger clubbing
  • Maybe mouth ulcers
  • Abdominal tenderness
  • Spondylarthropathies
  • Diarrhea, sometimes bloody – bowel urgency. Nocturnal diarrhea YES ( not in IBS)
  • Abdominal pain, cramps
  • Weight loss/failure to thrive/anorexia
  • Fatigue, fever, malaise, anorexia, tachycardia
  • and complications

CROHNS

  • Perianal abscess /fistulae/ skin tags (See complications)
  • Malnutrition effects
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12
Q

IBD investigations

A

Stool sample

  • Exclude pathogenic cause
  • Faecal calprotectin is present → highly sensitive, indicates GI inflammation

Colonoscopy / sigmoidoscopy / rectal biopsy
- Biopsy taken- Histology

Capsule endoscopy= capsule swallowed and takes pictures as it travels – useful for small bowel

AXR

  • No faecal shadows
  • Mucosal thickening in UC
  • Free air if perforated

Barium x ray

  • UC =Lead pipe colon on barium x ray
  • Crohns =String sign on barium x ray

Bloods -

  • may show elevated wbc
  • esr/crp raised with inflammation
  • LFTs- UC has strong link with primary sclerosing cholangitis)
  • Blood culture - rule out other things
  • pANCA in UC (and PSC)
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13
Q

crohns non-surgical treatment

A
  • Questran—Causes bile salts to be absorbed more in the terminal ileum so can be reused by the liver. It also means there are less in the large bowel so more water is reabsorbed into colon and less diarrhea.
  • Quit smoking
  • Diet- enteral = liquid
  • Prednisolone- then taper it off (induces but doesnt maintain remission - may relapse)
  • Thiopurine - maintain remission (Azathioprine )
  • If severe: IV fluid and IV steroids. Consider blood transfusion
  • Biologics
  • – Anti TNF (infliximab)
  • – Anti IL 12/ 23 (ustekinumab)
  • – Anti integrin (targets adhesion molecules)
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14
Q

UC non surgical treatment

A
  • Mesalazine - 5-aminosalicylic acid (for mild) - Not for crohns
  • Prednisolone (for moderate)
  • IV fluids, IV steroids (for severe)
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15
Q

surgery for IBD

- for each

A

Resection!

  • For UC:
  • – removal is curative!!!
  • – I think do if medication isn’t working
  • For crohns:
  • – When a stricture forms
  • – Perforation
  • – Fistulae
  • – Abscess
  • – Drugs arent working adequately
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16
Q

crohns complications

A

Bowel mainly
- Malabsorption
— If sections are resected /mucosal damage is extensive in the small bowel
- Obstruction
— Due to acute swelling, or chronic fibrosis → obstruction and dilatation
- Perforation -Of the deep fissuring ulcers → acute abdomen
- Fistula formation
When deep ulcers go through to other bits of bowel
- Anal skin tags
— Most skin tags checked for crohn’s at histopathology (but most are neg)
- Anal fissures and fistulas
— fissure= dead end, fistula = tunnel
- Neoplasia : Increase in risk of colorectal cancer. Worse if uncontrolled crohns. UC risk is worse

Non bowel = systemic
- Amyloidosis = deposition of beta pleated sheet proteins (rare)

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17
Q

amyloidosis =

A

deposition of beta pleated sheet proteins (systemic)

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18
Q

UC complications

A

Colon - due to inflammation
- Ulceration → blood loss
- Toxic dilatation (really swollen)- can rupture → peritonitis
- Colorectal cancer (rare), worse if uncontrolled UC
Larger increase in risk than crohns

Joints

  • Ankylosing spondylitis (spine joints fused, bamboo spine)
  • Arthritis

Eyes

  • Iritis
  • Uveitis
  • Episcleritis

Skin

  • Erythema nodosum = red nodules
  • Pyoderma gangrenosum (ulcer wounds)

Liver

  • Sclerosing cholangitis
  • Fibrosis of bile ducts → obstruct bile flow
  • Chronic pericholangitis
  • Fatty change
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19
Q

IBS

  • age
  • gender
  • commonnes
  • risk factors
A
  • Age onset less than 40
  • F >m
  • Very common in westerm world
  • anxiety,
  • previous severe/ long diarrhea
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20
Q

IBS causes -5

what exacerbates it -4

A

Unknown organic cause (this absence is key)

Causes

  • Depression
  • Anxiety
  • stress/ trauma (Sexual, physical/ verbal abuse)
  • GI infection
  • Eating disorders

Symptoms exacerbated by

  • Stress
  • Gastroenteritis
  • menstruation
  • food
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21
Q

IBS ! - differences from IBD

A

INVESTIGATION
- normal investigation results

PRESENTATION

  • no fever
  • no symptoms outside GI tract
  • no blood in stool inc meleana (dark/black poo - blood higher in tract)
  • no weight loss
  • bloating present
  • no mouth ulcers
  • more constipation
  • no nocturnal diarrhea
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22
Q

IBS! - similarities to IBD

A
  • persistant / fluctuating symptoms
  • food triggers
  • excarbated by stress
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23
Q

IBS

  • term describes what?
  • chornic/ acute
  • types
A

IBS = group of symptoms, Without any evidence of underlying cause
chronic

4 groups
IBS-D : diarrhea common
IBS-C : constipation common
IBS-M : both diarrhea and constipation common
IBS-U: neither diarrhea and constipation common

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24
Q

IBS symptoms

A

A- Abdominal pain
Relieved by defecation
(Pain 1 day/week for last 3 months (symptoms started 6 months ago - chronic))

B- bloating

C -Change in bowel habit

  • often Increased frequency/ loose stool
  • Also can be constipation
  • No blood
  • NO NOCTURNAL DIARRHEA
  • Painful period
  • Back pain
  • Fatigue
  • Urinary frequency/ urgency/ nocturia/ incomplete bladder emptying
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25
Q

IBS investigation

A 
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)
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26
Q

IBS management

A
  • 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
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27
Q

name the 5 broad causes of malabsorption

A 
1 defective intraluminal digestion
2 insufficient absorptive area
3 lack of digestive enzymes
4 defective epithelial transport 
5 lymphatic obstruction
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28
Q

defective intraluminal digestion - causes of malabsorption

A

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
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29
Q

insufficent absorptive area cause of malabsorption

A

= 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)
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30
Q

coeliac pathophysiology

A

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

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31
Q

lack of digestive enzyme causes of malabsorption

A

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
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32
Q

Disaccharide deficiency =

  • process
  • explanation of symptoms
  • commonness
A

= 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!!!)
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33
Q

defective epithelial transport causes of malapbsorption

how common are these?

A
  • 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
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34
Q

lymphatic obstruction cause of malabsorption including examples

A

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

Lymphoma
TB

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35
Q

what is the differential diagnosis of malabsorption

A

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

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36
Q

general presentation of patient with malabsorption

A
  • anaemic
  • Weight loss - despite normal calorie intake
  • Abnormal faeces
  • – High fat in stool as fat not absorbed
  • – Pale
  • – Floating
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37
Q

coeliac - which part of the bowel is predominantly affected

what malabsorption disorders may result

A

proximal bowel

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

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38
Q

coeliac disease

  • gender
  • age
  • commonness
A
  • Common - over 1% in Europe. Prevalence increasing worldwide
  • Normally diagnosed middle-aged, or as a child
  • m=f
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39
Q

coeliac risk factors

A

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
40
Q

coeliac symptoms

  • classic
  • non-classic
  • are many asymptomatic? how could we catch these
A

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
41
Q

coeliac investigation

A

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

42
Q

marsh score for coeliac

A 
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)
43
Q

coeliac disease management

A

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

44
Q

complications of coeliac disease

A
  • 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
45
Q

appendicitis complications (and how to treat them)

A

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
46
Q

appendicitis management

A
  • Appendectomy (lapropscopic) = removal of appendix
  • IV anitbiotics pre-op to reduce wound infections
  • Drain any abscesses
47
Q

appendicitis investigations inc exclusions

A

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

48
Q

symptoms and signs of appendiciits

A
  • 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
49
Q

appendicitis

  • age
  • commonness
  • gender
A

10-20y
common
m>f

50
Q

appendicitis causes

A
  • 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
51
Q

appendicitis differential diagnosis

name 3

A
  • Ileitus due to crohns
  • Salpingitis (fallopian tube inflammation)
  • Ectopic pregnancy
  • UTI
  • Diverticulitis
  • Perforated ulcer
  • Food poisoning
52
Q

appendicitis pathophysiology

A
  • 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
53
Q

complications of peptic ulcers

A

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
54
Q

peptic ulcer investigations

A

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
55
Q

peptic ulcer symptoms

A
  • Upper abdominal pain – Burning pain- indigestion/heartburn = what patient says feels like
  • Nausea
56
Q

what are peptic ulcers

peptic/gastric ulcer found where

A
  • 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
57
Q

what are peptic ulcers

4 causes of peptic ulcer (titles only)

A
  • 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
58
Q

what are the warning signs of GI cancer and how to confirm

A

ALARMS

  • Anaemia
  • Loss of weight
  • Anorexia
  • Recent onset/ progressive symptoms
  • Melaena = black stools from blood / haematemesis = vomiting blood
  • Swallowing difficulty = dysphagia

biopsy to confirm

59
Q

normal stomach tissues loooks like?

A
  • acidic stomach
  • neutral buffered mucin layer (complete)
  • glandular gastric cells
  • capillary underneath
60
Q

reduced blood flow cause of ulcer

  • pathophysiology
  • signs
  • treatment
A
  • 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
61
Q

increased acid in stomach cause of ulcer

  • pathophysiology
  • causes of increased acid
  • treatment
A
  • 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)

62
Q

how does aspirin / NSAIDs cause ulceration. and how do we counteract this

A
  • 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
63
Q

bile reflux cause of ulcer

  • where
  • causes
A
  • 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
64
Q

infection cause of ulcers

  • causative organism
  • pathophysiology
  • how to see
  • treatment
A

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

65
Q

long term response to helicobacter infection

A

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
66
Q

risk factors for GORD

A
  • 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
67
Q

pathophysiology of GORD

inc normal and resulting histology

A

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
68
Q

presentation GORD

A
  • 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
69
Q

GORD histological change

A

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

70
Q

GORD investigations

A

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

71
Q

GORD management non iatric / advice

A
  • Encourage weight loss
  • Smoking cessation
  • Small, regular meals
  • Avoid: hot drinks, alcohol, citrus fruits, spicy foods, eating 3h before bed
  • Raise bed head
72
Q

GORD management surgical

A

Nissen fundoplication = increases the resting lower oesophageal sphincter pressure

  • If not responding to therapy
  • May cause bloating and dysphagia
73
Q

GORD management pharmacological

drugs
and which to avoid

A

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
74
Q

GORD complications

A

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)

75
Q

cancer of upper/ lower GI

which cancer is v rare

A

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

76
Q

oesophageal cancer

  • commonness
  • age
  • gender
A
  • Increasing frequency
  • — Obesity increasing
  • — reclassification from upper gastric → oesophageal cancers
  • Not as common as colon cancer
  • M >f
  • Peaks in 60s/70s
77
Q

gastric cancer

  • commonness
  • age
  • gender
  • where in world
A
  • Incidence decreasing
  • — May be due to reclassification from upper gastric → oesophageal cancers
  • M >f
  • E europe
  • E asia
  • Peaks in 70s
78
Q

large bowel cancer

  • gender
  • age
  • where in world
  • commonness
A
  • 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
79
Q

risk factors for oesophageal cancer

A

= 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
80
Q

types of hiatus hernia

A

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
81
Q

gastric cancer risk factors

A
  • 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
82
Q

small bowel cancer

  • commonness
  • risk factors
  • types
  • symptoms
  • investigations
  • treatment
A

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

83
Q

colorectal cancer genetic risk factors

A

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)
84
Q

colorectal cancer non genetic risk factors

A
  • adenomas
  • Low fibre diet
  • – Better = veg, milk, garlic, - exercise
  • Sugar
  • Alcohol
  • Smoking
  • Obesity
  • Age
  • Conditions
  • – UC
  • – Primary sclerosing cholangitis (PSC)
85
Q

two types of oesophageal cancer

A

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
86
Q

gastric cancer

  • type of cancer
  • types, and their features
A
  • 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
87
Q

gastric cancer staging

A

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
88
Q

colon cancer

  • where
  • how does where affect prognosis
  • type of cancer
A
  • Anywhere in colon - most in distal end !
  • The proximal ones have a worse prognosis !
  • Adenocarcinoma (glandular)
89
Q

colon cancer staging

  • dukes
  • tnm
A

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)

90
Q

colorectal cancer presentation

A

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

91
Q

gastric cancer presentation

A

classic cancer signs

vom/ naus/ anorexia

dysphagia if tumour in fundus

92
Q

oesophageal cancer presentation

A

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)

93
Q

GI cancer investigations

A

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
94
Q

GI cancer management

A

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)
95
Q

coeliac first line investigation

A

IgA TTG

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

phase 2a mine (38 decks)

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