GI 5 Flashcards
(91 cards)
1
Q
What are the three cell types in the small intestine?
A
Goblet cells
Columnar absorptive cells (villi)
Endocrine cells
2
Q
What is the histology of the large bowel?
A
Flat – no villi Tubular crypts Surface columnar absorptive cells Crypts Goblet, endocrine + stem cells
3
Q
What are the histological changes in ulcerative colitis?
A
Inflammatory of mucosa Cryptitis + crypt abcesses Mucosal atrophy Ulceration into submucosa – pseudopolyps No granulomas Submucosal fibrosis
4
Q
What are the complications of ulcerative colitis?
A
Haemorrhage
Perforation
Toxic dilation
Cancer
5
Q
What is the pathology of crohn’s?
A
Granular serosa – dull gray
Wrapping mesenteric fat
Mesentery thickened oedematous and fibrotic
Narrowing of lumen due to thick wall
Sharp demarcation of disease segments from adjacent normal tissue – skip lesions
Ulceration in cobblestone fashion
6
Q
What are the histological changes in Crohn’s?
A
Cryptitis + crypt abcesses Deep ulcerations Atrophy – leads to crupt destruction Non-caseating granulomas Fibrosis Lymphangiectasia Hypertrophy of mural nerves Paneth cell metaplasia
7
Q
What is ischaemic enteritis?
A
An acute occlusion of one of the three major supply vessels - leads to infarction. (Coeliac, Inferior + Superior mesenteric ateries)
Gradual occlusion can have little effect - anastomotic circulation
Small end arteries - lesion small and focal
Mesenteric venous occlusion less common
Major occlusion - transmural injury
Acute/chronic hypofusion - mucosal +/- submucosal injury
8
Q
What are the predisposing conditions for arterial thrombosis (ischaemia)?
A
Severe atherosclerosis Systemic vasculitis Dissecting aneurysm Hypercoagulable states Oral contraceptives
9
Q
What are the predisposing conditions for ischaemia - arterial embolism?
A
Cardiac vegetations
Acute atheroembolism
Cholesterol embolism
10
Q
What are the predisposing conditions for non-occlusive ischaemia?
A
Cardiac failure
Shock/dehydration
11
Q
What is the pathology of acute ischaemia?
A
Oedema
Interstitial haemorrhages
Sloughing necrosis of mucosa-ghost outlines
Nuclei indistinct
Initial absense of inflammation
1-4 days - nacteria - gangrene and perforation
Vascular dilation
12
Q
What occurs with chronic ischaemia?
A
Mucosal inflammation Ulceration Submucosal inflammation Fibrosis Stricture
13
Q
What is radiation colitis?
A
Abdominal irradiation that impairs the normal proliferative activity of the small and large bowel epithelium
Usually rectum - pelvic radiotherapy
Damage depends on dose
Targets actively diving cells esp. blood vessels and crypt epithelium
Symptoms: anorexia; abdominal cramps; diarrhoea and malabsorption
Chronic- mimics IBD
14
Q
What are the histological changes in radiation colitis?
A
Bizarre cellular changes Inflammation -crypt abscesses and eosinophils Later-arterial stenosis Ulceration Necrosis Haemorrhage Perforation
15
Q
What is appendicitis?
A
Acute inflammation of appendix
Cause from obstruction
Feocolith or enterobius vermicularis
Increased intraluminal pressure - ischaemia
16
Q
What is the histologu of appendicitis?
A
Macro-fibrinopurulent exudate, perforation, abscess
Micro-
Acute suppurative inflammation in wall and pus in lumen
Acute gangrenous - full thickness necrosis +/- perforation
17
Q
What is the difference between high and low grade adenoma dysplasia?
A
Low grade - increased nuclear numbers, size, reduced mucin
High grade - carcinoma in situ, crowded, very irregular, not yet invasive
18
Q
What are the differences between left and right sided colorectal adenocarcinomas?
A
98% of colorectal carcinomas are adenocarcinomas
Obstruction in both
Right sided - exophytic/polypoid. Left - annular
Left sided - bleeding, altered bowel habit
Right sided - vague pain, weakness, anaemia
19
Q
What is IBD?
A
Chronic, replapsing, inflammatory conditions of the bowel I.E Crohn’s Ulcerative colitis Indererminate colitis Appendicitis Ischaemic + radiation colitis
20
Q
What is ulcerative colitis?
A
Presents with abdominal pain Bloody diarrhoea Weight loss Continuous inflammation with variable distribution (only colon)/severity Pseudopolyps + ulceration More common in females
21
Q
Who does crohn’s disease affect?
A
Early adulthood and over 60s, mainly.
M/F equal Children also affected
22
Q
What are the clinical features of crohn’s disease?
A
Depends on regions affected: Diarrhoea Abdominal pain Weight loss Malaise Lethargy Anorexia N&V Low grade fever Malabsorption – anaemia, vitamin deficiency
23
Q
What are the complications of crohn’s disease?
A
Inflammation
Stricture
And fistula (all of the small bowel)
24
Q
What are the inflammatory indications of IBD?
A
High ESR + CRP High platelet count High WCC Low Hb Low albumin
25
What is the difference histologically between Crohn's and UC?
```
Crohn's- granulomas
Fistulae and peri-anal disease in crohns
Crohn's is patchy "cobblestone" disease from mouth to anus.
>UC is only in colon
Goblet cells depleted in UC
Crypt abscesses (UC> crohns)
```
26
What conditions can arise outwith the GI system with IBD?
Eyes – uveitis, episcleritis, conjunctivitis
Joints – sacroiliitis, monoarcticular arthritis, ankylosing spondylitis
Renal calculi (only in crohns)
Liver and biliary tree – fatty change, pericholangitis, sclerosing cholangitis, gall stones
Skin – pyoderma gangrenosum, erythema nodsum, vasculitis
27
What are the risk factors of colonic cancer?
Pancolitis – (inflammation of whole colon) !!!
Left colitis !!
Proctitis – minimal
Time you’ve had colitis – risk increases with time
28
How do you manage UC?
In hospital – steroids, anticoagulation, rest, surgery?
| Out patient – steroids, 5ASA (anti-inflammatory drug), immunosuppression
29
What drugs are available for IBD?
```
Aminosaclicylates:
Mesalasine (5ASA)
Pro-drugs – balsalazide, olzalaine, sulfasalazine
Steroids
Thiopurines
Methotrexate
Ciclosporin (brdige for azathiprine)
Biologics
Metronidazole
```
30
How is Mesalasine used in IBD? (5ASA)
acrylic resin or ethylcellulose microgranules
Mild - 3g/day, sometimes rectal admission for distal/extensive, 1st line
Moderate – 1st line, reduces relapses, lifelong therapy 2g/day
31
What steroids are used in IBD?
prednisolone (40mg/day- reduce over 4 weeks), budenoside (less effective, but less side effects – for ileal and asc colon)
32
What are the unacceptable side effects of steroids?
Diabetes
Severe osteoporosis
Psychosis
33
What thiopurine is used in IBD, what are its side effects?
```
azathiopurine,
significant side effects –
>leucopenia,
>hepatoxicity,
>pancreatitis
```
34
What are the surgery options for Ulcerative colitis?
When chronic
Either pouch procedure – no ileostomy
Or protctocolectomy – an ileostomy
```
Acute illness (severe)
Iseostomy
```
35
What are the surgical indications for crohns?
```
Failure of medical management
Relief of obstructive symptoms – small bowel
Management of fistulae
Management of intra-abdominal abscess
Management of anal conditions
Failure to thrive
```
36
What is the epidemiology of colorectal cancer?
95-98% adenocarcinomas
2 thirds colonic, 1 third rectal
3rd commonenst cancer diagnosis
37
What are the risk factors for colorectal cancer?
Age
Male
Previous adenoma/CRC
Environmental influences (diet, obesity, lack of exercise, smoking, diabetes)
38
What are colorectal polyps?
Protuberant growths
Variety of histological types
Epitherlial or mesenchymal
Benign or malignant
39
What are adenoma colorectal polyps?
Benign, pre malignants
Epithelial in origin
3 main histological types - tubulars (75%), vilous 10%, indeterminate tubulovillous 15%
Morphologically - pedunculated or sessile
High risk legions - size, number, degree of dysplasia, villous architecture
40
What is the presentation of colorectal cancer?
rectal bleeding
Altered bowel opening - diarrhoea (each symptom by self - investigate >60, both investigate >40 yrs)
Iron deficiency anaemia - men of any age, non menstrating women - more likely to have right sided colonic malignancy
Palpable rectal or right lower mass
Acute colonic obstruction if stenosing tumour
Systemic symptoms of malginancy )weight loss, anorexia)
41
How do you investigate colorectal cancer?
Colonoscopy (preferred) - allows biopsies, therapeutic as well as diagnostic - polypectomy
>Sedation, bowel prep; risks - perforation, bleeding
Radiological - barium enema, CT colonography, CT abdo/pelvis
42
What is Duke's classification?
A - tumour confirmed to mucosa
B - tumoour extended form mucosa through muscle layer
C - onvolvement of lymph
D - Distant metastatic spread
43
How do you treat colorectal cancer?
```
Surgery is basis of therapy
Dukes A - endoscopic or local resection
Operative procedure depends on site, size, and stage of tumour
Laparotomy vs laparoscopic
Stoma formation - colostomy
Removal of lymph for analysis
Partial hepatectomy for metastases
Chemo - ajunctive, Dukes C, B
radio - rectal only, +/- chemo to control tumour if neoadjunctive
```
44
How do you scren for colorectal cancer?
```
Faecal occult blood test (every 2 yrs - if positive, then colonoscopy))
Faecal immunochomical test
Flexible sigmoidoscopy
Colonoscopy
CT colonography
```
45
What high risk groups are screened for colorectal cancer?
Heritable conditions - FAP, HNPCC
inflammatory bowel disease - 10 yrs post diagnosis
Familial risk - colonscopy every 5 yrs from 50 (high risk), once age 55 low risk
Previous adenomas/colorectal cancer
46
What is FAP (familial adenomatous polyposis)?
Autosminal dominant condition
Many adenomas throughtout colon - 50% by age 15
25% due to new mutations (APC gene chromosome 5)
Anual colonoscopy from age 10-12
Prophylatic proctocolectomy usually 16-25
Desmoids tumours make up 10-20%
47
How does FAP present outside the colon?
Benign gastric fundic cyuctic hyperplastic
| Duodenal adenomas in 90% w/ periampullary cancer
48
What is HNPCC (hereditary non-polyposis colorectal cancer)?
Autosomal dominant
Mutation in DNA mismatch repair
Early onset (40s) colorectal cancer rhs
assoc. w/ cancers at other sites - endometrial, genitourinary, stomach, pancreas
Diagnose with genetic testing
Screen from age 25, colonoscopy every 2 years
49
What is adaptive starvation?
Patients become adapted to starvation with reduced intake of carbohydrate, they reduce secretion of insulin
They reduce intracellular phosphate (extracellular may be normal)
Low micronutrient reserves
50
What can cause refeeding syndrome?
```
Refeeding after:
Adaptive starvation
Laxative abuse
Dehydration
Eccentric diets
```
51
What happens in refeeding syndrome?
```
There is a rapid:
>rise in insulin
>Generation of ATP
Phosphate moves into cells
Hypophosphateamia develops rapidly
```
52
what are the consequences of refeeding syndrome?
```
Rhabdomyloysis
Resp failure
Cardiac failuire
Leucocyte dysfunction
Hypotension
Arrhythmias
Seizures
Coma
Sudden death
```
53
What is the criteria for high risk for refeeding syndrome?
1+ of:
BMI less than 16
Unintention weight loss >15% in last 3-6 months
Little/no nutrition for last 10 days
Low levels of potassium, phosphate, or magnesium prior to feeding
OR 2+ of:
BMI <18.5
Unintetional weightloss >10% within last 3-6 months
Little/no intake last 5 days
History of alcohol abuse or drugs inc. insulin, chemo, antacids or diuretic
54
How do you treat refeeding syndrome?
```
Start slow
Correct fluid depletion – cautiously
Thiamine at least 30mins before feeding
Feed @5-10 kcal/kg over 24 hours
Gradual increase to req. over 1 week
Replace
If phosphate < 0.3 mmol/l – 40mmol in 500mls 5% dextrose over 6 hrs
K <2.5mmol/l
Mg <0.5
Thiamine
```
55
What behaviours can be seen in eating disorders?
```
Self starvation
Self induced vomiting
Compulisive activity and exercise
Use of laxatives
Diet pills
Herbal medicines
Deliberate exposure to cold
```
56
What is anorexia nervosa?
Core feature – deliberate weight loss + fear of weight gain + problem with body image
To meet diagnostic criteria – at least 15% of minimum weight must have been lost – adults BMI below 17.5
Menstration is absent
Often obsession with exercise
57
What is bulimia nervosa?
Recurrent episodes of binge eating followed by:
Eating in a discrete period of time an amount greater than what most people would eat. With a sense of lack of control during the episode
Recurrent compensatory behaviour to prevent weight gain
Self induced vomiting, laxatives, diuretics/other medications or enemas misuse
Episodes occur at least twice a week for three months
Self evaluation unduly influenced by body shapes/weight (not just during episodes of anorexia)
58
What are the risks of eating disorders?
Highest rate of mortality of any psychiatric illness
High risk of suicide
Many deaths from malnutrition
Cardiac muscle can be unstable
59
How do you treat eating disorders?
```
Firm+ consistent approach
Team approach
Dietician etc, decide as a team management options
Watch for refeeding
Listen to patient carefully
Treat seriously
Diagnosis from evidence, not exclusion
```
60
What are the features of an upper GI bleed?
Usually fresh blood/ coffee ground vomiting
Melaena
Dyspeptic symptoms
Epigastric pain
Elevated urea
Can be caused by NSAIDs, Aspirin, Clopidogrel, warfarin
61
What are the features of a lower GI bleed?
Usually, but not always fresh blood
More common with increasing age
Normal urea
62
What is haematemsis?
Vomiting of blood
| Bright red haematemesis -active haemorrhage from the oesophagus, stomach or duodenum.
63
What is coffee-ground vomit?
vomiting of brown-black material which is assumed to be blood
64
What is melaena?
Passage of black, tarry, loose stools per rectum – considered to be partially digested blood
Associated with upper GI bleed
However, consuming black liquorice, lead, iron pills, blueberries or bismuth medicines can have same effect
65
What is Hematochezia?
Passage of fresh or altered blood per rectum – may be from upper GI cause as “fast transit” or lower GI
66
What can cause a UGI bleed?
```
Peptic ulcer
Gastric erosions
Oesophagitis
Ersoive duodenitis
Varices
Portal Hypertensive gastropathy
Malignancy
Mallory Weiss tear
Vascular malformation
```
67
What can cause oesophagitis?
```
Reflux oesophagitis
Hiatus hernia
Alcohol
Bisphosphonates
Systemic illness
```
68
What is a mallory weiss tear?
Linear tear in the lower oesophagus
Follows recurrent retching and vomiting
Bleeding stops spontaneously in 80-90% of patients
Haemodynamic instability and shock may occur in up to 10% of patients
69
How do you manage an upper GI bleed?
Resuscitation/indemnification of shock
Consider blood tranfusion
Upper GI endoscopy once stable
Embolisation or surgery if unable to control endoscopically
PPIs
Terlipressin + broad spectrum antibiotics - variceal bleed
70
What are the risk factors for UGI bleed?
```
Age (>50years)
Co-morbities
Liver, cardiac, respiratory
Inpatients
Initial presentation with
Haematemesis
Melaena
Shock
Collapse
Continued bleeding after admission
Elevated blood urea
```
71
What are the treatments for a peptic ulcer?
```
Endoscopy
Endotherapy
Proton pump inhibitors
Check Helicobacter pylori status
Discontinue causative/contributory medications
```
72
What drugs should be withheld in a UGI?
Oral anticoagulants,
Aspirin
NSAIDs acutely
73
How do you manage variceal bleeding?
Band ligation
Or glue injection
IV terlipressin
IV antibiotics
74
What is terlipressin?
Vasoconstrictor of splanchnic blood supply
| Reduces blood flow to portal vein, reducing portal pressures
75
What are the major causes of lower GI bleeds?
```
Diverticular disease
Vascular malformations (angiodysplasia)
Haemorrhoids
Neoplasia (carcinoma or polyps)
Ischaemic colitis
Radiation enteropathy/proctitis
Inflammatory bowel disease (eg. ulcerative proctitis, Crohn’s disease)
```
76
What is diverticular disease?
Protrusion of the inner mucosal lining through the outer muscular layer forming a pouch.
>Diverticulosis - presence
>Diverticulitis - inflammation
Bleeding occurs in 10-20% during the lifetime
10% chance of recurrence at one year and 25% at four years.
Usually self-limiting- 75%
Risk of further bleeding
77
What is chronic angiodyslpasia?
Small Vascular malformation
>Degeneration
Friable and bleeds easily
May be association with valvular abnormalities
Bleeding often precipitated by anticoagulants/antiplatelets
Treatment with Argon Phototherapy
78
What is ischaemic colitis?
```
Disruption in blood supply to colon
>Presents with crampy abdominal pain
More common over 60 years
Usually self-limiting
Dusky blue, swollen mucosa
Restricted to a specific area
Complications include gangrene and perforation
```
79
What are the small bowel causes of a LGI bleed?
```
Small bowel angiodysplasia
Small bowel tumour/GIST
Meckel’s diverticulum
Small bowel ulceration
Aortoentero fistulation – following AAA repair
```
80
What is Meckel's diverticulum?
Gastric remnant mucosa
2% of population
Can be seen on nuclear scintigraphy
81
What are the signs of shock?
```
a high respiratory rate (tachypnoea)
a rapid pulse (tachycardia)
anxiety or confusion
cool clammy skin
low urine output (oliguria)
low blood pressure (hypotension)
```
82
What are the common presentations of anorectal disorders?
Pain
Haemorrhage
Dysfunction
83
How can they be classified?
Inflammation
Infection
Malignancy
Trauma
84
What are the congenital ano-rectal abnormalities
Imperforate anus
Uro-Genital Fistulae
Hirschprung’s Myenteric Plexus Deficiency
85
What are the aquired ano-rectal abnormalities
```
Haemorrhoids
Fissure
Abscess
Fistula-in-ano
Ulceration
Cancer
Control of Continence
```
86
What is the procedure for haemorrhoids?
```
Stapled anopexy
>Also for prolapse
Circular staple inserted
Staple haemorrhoids
Excise haemorrhoids
```
87
How do you treat an anal fissure?
```
Relax internal anal sphincter
Medical
Topical Nitric Oxide
Surgical
Internal Lateral Sphincterotomy
```
88
How do you treat a fistula in Ano?
```
Superficial
>Lay open by fistulotomy
Trans-sphincteric
>Seton Suture
>“Cook SIS” Fistula Plug
>Aim to close Primary Opening
>88% Success
```
89
How do you treat anorectal cancer?
Anal squamois cancer - radiotherapy
Rectal adenocarcinoma
>Neoadjuvant chemoRad
>Laparoscopic resection
90
What can cause anal ulceration
Crohn’s Disease
Malignancy
Syphilis “Chancre”
Nicorandil
91
Describe a sacral nerve root stiumlator implant
```
Before - objective anorectal manometry and endoanal ulstrasoind
Implants for S2-4
Somatic motor nerves to spiincters
Percutaneous access to Sacral Foramena
Implant Trial then Permanent Implant
```
