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Conditions + definitions > GI 5 > Flashcards

GI 5 Flashcards

1
Q

What are the three cell types in the small intestine?

A

Goblet cells
Columnar absorptive cells (villi)
Endocrine cells

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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
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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
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4
Q

What are the complications of ulcerative colitis?

A

Haemorrhage
Perforation
Toxic dilation
Cancer

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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

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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
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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

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8
Q

What are the predisposing conditions for arterial thrombosis (ischaemia)?

A 
Severe atherosclerosis
Systemic vasculitis
Dissecting aneurysm
Hypercoagulable states
Oral contraceptives
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9
Q

What are the predisposing conditions for ischaemia - arterial embolism?

A

Cardiac vegetations
Acute atheroembolism
Cholesterol embolism

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10
Q

What are the predisposing conditions for non-occlusive ischaemia?

A

Cardiac failure

Shock/dehydration

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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

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12
Q

What occurs with chronic ischaemia?

A 
Mucosal inflammation
Ulceration
Submucosal inflammation
Fibrosis
Stricture
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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

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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
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15
Q

What is appendicitis?

A

Acute inflammation of appendix
Cause from obstruction
Feocolith or enterobius vermicularis
Increased intraluminal pressure - ischaemia

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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

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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

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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

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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
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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
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21
Q

Who does crohn’s disease affect?

A

Early adulthood and over 60s, mainly.

M/F equal Children also affected

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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
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23
Q

What are the complications of crohn’s disease?

A

Inflammation
Stricture
And fistula (all of the small bowel)

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24
Q

What are the inflammatory indications of IBD?

A 
High ESR + CRP
High platelet count
High WCC
Low Hb
Low albumin
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25
Q

What is the difference histologically between Crohn’s and UC?

A 
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)
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26
Q

What conditions can arise outwith the GI system with IBD?

A

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

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27
Q

What are the risk factors of colonic cancer?

A

Pancolitis – (inflammation of whole colon) !!!
Left colitis !!
Proctitis – minimal
Time you’ve had colitis – risk increases with time

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28
Q

How do you manage UC?

A

In hospital – steroids, anticoagulation, rest, surgery?

Out patient – steroids, 5ASA (anti-inflammatory drug), immunosuppression

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29
Q

What drugs are available for IBD?

A 
Aminosaclicylates:
Mesalasine (5ASA) 
Pro-drugs – balsalazide, olzalaine, sulfasalazine
Steroids 
Thiopurines  
Methotrexate 
Ciclosporin (brdige for azathiprine)
Biologics 
Metronidazole
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30
Q

How is Mesalasine used in IBD? (5ASA)

A

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

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31
Q

What steroids are used in IBD?

A

prednisolone (40mg/day- reduce over 4 weeks), budenoside (less effective, but less side effects – for ileal and asc colon)

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32
Q

What are the unacceptable side effects of steroids?

A

Diabetes
Severe osteoporosis
Psychosis

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33
Q

What thiopurine is used in IBD, what are its side effects?

A 
azathiopurine, 
significant side effects – 
>leucopenia, 
>hepatoxicity, 
>pancreatitis
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34
Q

What are the surgery options for Ulcerative colitis?

A

When chronic
Either pouch procedure – no ileostomy
Or protctocolectomy – an ileostomy

Acute illness (severe)
Iseostomy
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35
Q

What are the surgical indications for crohns?

A 
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
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36
Q

What is the epidemiology of colorectal cancer?

A

95-98% adenocarcinomas
2 thirds colonic, 1 third rectal
3rd commonenst cancer diagnosis

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37
Q

What are the risk factors for colorectal cancer?

A

Age
Male
Previous adenoma/CRC
Environmental influences (diet, obesity, lack of exercise, smoking, diabetes)

38
Q

What are colorectal polyps?

A

Protuberant growths
Variety of histological types
Epitherlial or mesenchymal
Benign or malignant

39
Q

What are adenoma colorectal polyps?

A

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
Q

What is the presentation of colorectal cancer?

A

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
Q

How do you investigate colorectal cancer?

A

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
Q

What is Duke’s classification?

A

A - tumour confirmed to mucosa
B - tumoour extended form mucosa through muscle layer
C - onvolvement of lymph
D - Distant metastatic spread

43
Q

How do you treat colorectal cancer?

A 
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
Q

How do you scren for colorectal cancer?

A 
Faecal occult blood test (every 2 yrs - if positive, then colonoscopy))
Faecal immunochomical test
Flexible sigmoidoscopy
Colonoscopy
CT colonography
45
Q

What high risk groups are screened for colorectal cancer?

A

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
Q

What is FAP (familial adenomatous polyposis)?

A

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
Q

How does FAP present outside the colon?

A

Benign gastric fundic cyuctic hyperplastic

Duodenal adenomas in 90% w/ periampullary cancer

48
Q

What is HNPCC (hereditary non-polyposis colorectal cancer)?

A

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
Q

What is adaptive starvation?

A

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
Q

What can cause refeeding syndrome?

A 
Refeeding after:
Adaptive starvation
Laxative abuse
Dehydration
Eccentric diets
51
Q

What happens in refeeding syndrome?

A 
There is a rapid:
>rise in insulin
>Generation of ATP
Phosphate moves into cells
Hypophosphateamia develops rapidly
52
Q

what are the consequences of refeeding syndrome?

A 
Rhabdomyloysis
Resp failure
Cardiac failuire
Leucocyte dysfunction
Hypotension
Arrhythmias
Seizures
Coma
Sudden death
53
Q

What is the criteria for high risk for refeeding syndrome?

A

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
Q

How do you treat refeeding syndrome?

A 
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
Q

What behaviours can be seen in eating disorders?

A 
Self starvation
Self induced vomiting
Compulisive activity and exercise
Use of laxatives
Diet pills
Herbal medicines
Deliberate exposure to cold
56
Q

What is anorexia nervosa?

A

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
Q

What is bulimia nervosa?

A

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
Q

What are the risks of eating disorders?

A

Highest rate of mortality of any psychiatric illness
High risk of suicide
Many deaths from malnutrition
Cardiac muscle can be unstable

59
Q

How do you treat eating disorders?

A 
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
Q

What are the features of an upper GI bleed?

A

Usually fresh blood/ coffee ground vomiting
Melaena
Dyspeptic symptoms
Epigastric pain
Elevated urea
Can be caused by NSAIDs, Aspirin, Clopidogrel, warfarin

61
Q

What are the features of a lower GI bleed?

A

Usually, but not always fresh blood
More common with increasing age
Normal urea

62
Q

What is haematemsis?

A

Vomiting of blood

Bright red haematemesis -active haemorrhage from the oesophagus, stomach or duodenum.

63
Q

What is coffee-ground vomit?

A

vomiting of brown-black material which is assumed to be blood

64
Q

What is melaena?

A

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
Q

What is Hematochezia?

A

Passage of fresh or altered blood per rectum – may be from upper GI cause as “fast transit” or lower GI

66
Q

What can cause a UGI bleed?

A 
Peptic ulcer
Gastric erosions
Oesophagitis
Ersoive duodenitis
Varices
Portal Hypertensive gastropathy
Malignancy
Mallory Weiss tear
Vascular malformation
67
Q

What can cause oesophagitis?

A 
Reflux oesophagitis
Hiatus hernia
Alcohol
Bisphosphonates
Systemic illness
68
Q

What is a mallory weiss tear?

A

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
Q

How do you manage an upper GI bleed?

A

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
Q

What are the risk factors for UGI bleed?

A 
Age (>50years)
Co-morbities
Liver, cardiac, respiratory
Inpatients
Initial presentation with 
Haematemesis
Melaena
Shock
Collapse
Continued bleeding after admission
Elevated blood urea
71
Q

What are the treatments for a peptic ulcer?

A 
Endoscopy
	Endotherapy
	Proton pump inhibitors
	Check Helicobacter pylori status
	Discontinue causative/contributory medications
72
Q

What drugs should be withheld in a UGI?

A

Oral anticoagulants,
Aspirin
NSAIDs acutely

73
Q

How do you manage variceal bleeding?

A

Band ligation
Or glue injection

IV terlipressin
IV antibiotics

74
Q

What is terlipressin?

A

Vasoconstrictor of splanchnic blood supply

Reduces blood flow to portal vein, reducing portal pressures

75
Q

What are the major causes of lower GI bleeds?

A 
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
Q

What is diverticular disease?

A

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
Q

What is chronic angiodyslpasia?

A

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
Q

What is ischaemic colitis?

A 
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
Q

What are the small bowel causes of a LGI bleed?

A 
Small bowel angiodysplasia
	Small bowel tumour/GIST
	Meckel’s diverticulum
	Small bowel ulceration
Aortoentero fistulation – following AAA repair
80
Q

What is Meckel’s diverticulum?

A

Gastric remnant mucosa
2% of population
Can be seen on nuclear scintigraphy

81
Q

What are the signs of shock?

A 
a high respiratory rate (tachypnoea) 
a rapid pulse (tachycardia) 
anxiety or confusion
cool clammy skin
low urine output (oliguria)
low blood pressure (hypotension)
82
Q

What are the common presentations of anorectal disorders?

A

Pain
Haemorrhage
Dysfunction

83
Q

How can they be classified?

A

Inflammation
Infection
Malignancy
Trauma

84
Q

What are the congenital ano-rectal abnormalities

A

Imperforate anus
Uro-Genital Fistulae
Hirschprung’s Myenteric Plexus Deficiency

85
Q

What are the aquired ano-rectal abnormalities

A 
Haemorrhoids
Fissure
Abscess
Fistula-in-ano
Ulceration
Cancer
Control of Continence
86
Q

What is the procedure for haemorrhoids?

A 
Stapled anopexy
>Also for prolapse
Circular staple inserted
Staple haemorrhoids
Excise haemorrhoids
87
Q

How do you treat an anal fissure?

A 
Relax internal anal sphincter
Medical   
	Topical Nitric Oxide
Surgical 
Internal Lateral Sphincterotomy
88
Q

How do you treat a fistula in Ano?

A 
Superficial 
>Lay open by fistulotomy
Trans-sphincteric
>Seton Suture
>“Cook SIS” Fistula Plug
>Aim to close Primary Opening
>88% Success
89
Q

How do you treat anorectal cancer?

A

Anal squamois cancer - radiotherapy
Rectal adenocarcinoma
>Neoadjuvant chemoRad
>Laparoscopic resection

90
Q

What can cause anal ulceration

A

Crohn’s Disease
Malignancy
Syphilis “Chancre”
Nicorandil

91
Q

Describe a sacral nerve root stiumlator implant

A 
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

Conditions + definitions (68 decks)

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