Lower GI Flashcards
What is erythema multiforme?
A skin reaction usually mild as allergic reaction to virus or drug etc
What is leukoplakia?
Oral mucosal white patch that will not rub off and is not attributable to any other known disease
Fluconazole?
Anti-fungal medication. Eg. to treat candidiasis - orally or IV administration
Nystatin
Anti-fungal medication. Candidiasis is particularly sensitive
Amphotericin
Anti-fungal medication. Sometimes used IV for systemic fungal infections
Achalasia
Failure of oesophageal smooth muscle to relax. Aka sphincter can remain closed and fail to open when needed. Can happen throughout GIT
What can masses in the right iliac fossa be due to? (x11)
Appendix mass/abscess Caecal carcinoma Intussusception Crohn's Disease Pelvic mass TB mass Amoebic abscess Actinomycosis Transplanted kidney Kidney malfunction Tumour in undescended testes
5 F’s of abdominal distension
Flatus, Fat, Fluid, Faeces, Fetus
2 tests to confirm ascites
Shifting dullness, fluid thrill/fluid wave test (pushing down prevents vibration from being transmitted through the abdominal wall)
Causes of ascites (without portal hypertension) x6
Malignancy, Infection (eg. TB), low albumin (nephrosis/nephrotic syndrome) CCF, pancreatitis, myxoedema
Causes of ascites with portal hypertension x4
Cirrhosis, Budd-Chiari syndrome, IVC or portal vein thrombosis, Portal nodes
4 causes of pancreatic cysts (pseudocysts)
Congenital, cystadenomas, retention cysts of chronic pancreatitis, cystic fibrosis.
Pseudocysts = fluid in lesser sac from acute pancreatitis
What are GIT synchronous tumours?
Two different GIT tumours at the same time
What are metachronous tumours?
Second cancer, presents months to years after first cancer but in another part of GIT
What met is sometimes present at presentation of colorectal cancer? What %?
37% have liver mets at presentation
Where are colorectal cancers most commonly found?
Sigmoid or rectum (or unspecified descending colon)
Typically colorectal presentation?
Rectal bleeding, change in bowel habits, lower abdominal discomfort, 1/2 stone weight loss
Left sided colorectal cancer?
Bleeding and mucus PR, altered bowel habit or obstruction, tenesmus, mass PR (60%)
Right-sided colorectal cancer?
Weight loss, low Hb, abdominal pain and obstruction less likely
What is sister mary joseph nodule?
Peritoneal metastasis, tumour grows out umbilicus
Importance of FHx in CR cancer
10% have FHx
Risk factors for CR cancer x 10
age (8/10 >60), male, family history, alcohol, smoking, diet (red meat, processed meat, low fibre), abdominal fatness, previous cancer, previous polyp, pre-morbidities (IBD, PSC, acromegaly)
Prevention of CR cancer x3
Aspiring >75mg/day, physical activity, foods containing dietary fibre
Drug treatment for CR cancer
Chemotherapy - usually 5-fu with oxaliplatin
Drugs used in palliation of advanced CR cancer
Bevacizumab (anti-vegF antibody), Cetuximab and Panitumumab (in KRAS wild type CR cancer - anti-EGFR agents)
Surgery for CR cancer x6
Right hemicolectomy (for caecal, ascending or proximal transverse colon tumours) Left hemicolectomy (for distal transverse or descending colon tumours) Sigmoid colectomy (for sigmoid tumours) Anterior resection of rectum (for low sigmoid or high rectal tumours) - usually no colostomy Abdomino-perineal excision of rectum (for tumours low in rectum) - colostomy
Hartmann’s procedure - usually emergency bowel surgery - removal of sigmoid colon and/or rectum - hartmann’s because making a colostomy and leaving other end of bowel inside but closed off
Use of radiotherapy in CR cancer
Mostly palliation, occasionally pre-op to allow resection, post-op only in patients with rectal tumours at high risk of local recurrence
CR cancers - histologically
98% of colonic cancers are adenocarcinomas - from glandular epithelium
What do Duke stage C and D mean
C = Involvement of lymph nodes D = distant mets
Indications for surgery to treat liver mets
Non-radiographic involvement of important vessels or lymph nodes
Complete resection must be feasible
Need enough liver left for function post-resection
No unretractable extra-hepatic sites
Bowel Cancer Screening
60-74
Home stool testing
Every 2 years
Colonscopy if positive test
Causes of CR cancer?
75% - sporadic CR cancer - isolated polyp becomes malignant
15% familial gene increases risk of polyp becoming malignant
5% hereditary non polyposis - multiple cancers run in family and increased risk of solid organ malignancies
Development of CR cancer
Lose APC protective gene and normal epithelium becomes early adenoma
Activation of promotor gene
Protective gene TP53 inactivated
Definition of Crohn’s
Chronic inflammatory GI disease characterised by transmural granulomatous inflammation affecting any part of GIT. Skip lesions (unlike UC)
Especially affects terminal ileum and proximal colon
Genetic mutations which increase risk of Crohn’s
NOD2 / CARD15
Prevalence and incidence of Crohn’s vs UC
P of C = 0.5-1/1000, P of UC 1-2/1000
I of C = 5-10/100,000/year, I of UC = 10-20/100,000/year
Age of presentation for Crohn’s vs UC
Crohn’s two peaks 20-30 years and 60-70years - worser prognosis if younger presentation
UC = 15-30
Associations of Crohn’s vs UC
Smoking = 3-4x increase risk of Crohn’s and decreases risk of UC
NSAIDs may exacerbate Crohn’s disease
Symptoms of Crohn’s x9
Diarrhoea/urgency, abdominal pain, weight loss, failure to thrive, malaise, fever, anorexia, putrid smelling stool, fluctuating symptoms
Signs of Crohn’s x4 GIT and x4 systemic
Aphthous ulcerations, abdominal tenderness/mass, perianal abscess/fistulae/skin tags, anal strictures
Skin, joint and eye problems, clubbing
Complications of Crohn’s x 14
Small bowel obstruction Toxic dilatation (colon >6cm) - rarer than in UC Abscess formation Fistulae Perforation Rectal haemorrhage Colon Cancer Fatty Liver PSC Cholangiocarcinoma Renal stones Osteomalacia Malnutrition Amyloidosis
Stool tests - CDT and MC &S
CDT = c.diff toxin
MC & S = microbiology, culture and sensitivity
Ileal disease detection test
Small bowel enema
Signs indicative of worse Crohn’s severity x6
↑ Temperature ↑ Pulse ↑ ESR ↑ WCC ↑ CRP low albumin
Treating a mild Crohn’s attack
Prednisolone PO - decrease dose if symptoms resolve
Treating a severe Crohn’s attack
NMB and IVI
Hydrocortisone IV
Metronidazole IV helps
If improving after 5 days switch to PO prednisolone
If not improving then monoclonal ab’s may help
Rate of surgery in Crohn’s and indications
50-80% need an operation in their life
I = drug failure, GI obstruction from stricture, perforation, fistulae, abscess
Treatment for perianal disease in Crohn’s (prevalence and x4 treatment)
Occurs in 50%
Oral antibiotics, immunosuppressant therapy
Local surgery +/- seton insertion
Definition of UC
Relapsing, remitting inflammatory disorder of the colonic mucosa
3 different types of UC
Proctitis - 50% - just rectum
Left-sided colitis - 30% - extends from rectum to affect part of the colon
Pancolitis - 20% - affects entire colon
Symptoms of UC x 6 and x2 for rectal UC
Diarrhoea (blood and mucus), abdominal discomfort, fever, malaise, anorexia and weight loss
Rectal UC = urgency and tenesmus
Acute severe UC signs x3
Fever, tachycardia, distended tender abdomen
Extraintestinal signs of UC x 15
Clubbing Aphthous oral ulcers Erythema nodosum Pyoderma gangrenosum Conjuncitivitis Episcleritis Iritis Large joint arthritis Sacroiliitis Ankylosing spondylitis
Fatty liver PSC Cholangiocarcinoma Nutritional deficits Amyloidosis
AXR is UC - 3 signs
No faecal shadows, mucosal thickening and colonic dilatation
Complications of UC x5
Perforation, bleeding, toxic dilatation of colon, venous thrombosis, colonic cancer 15% increased risk with pancolitis
Mild UC maintenance treatment and remission induction
Anti-inflammatories - 5ASA
eg. Sulfasalazine, mesalazine or olsalazine
Steroids eg. prednisolone to induce remission
Moderate UC remission induction
Prednisolone with 5-ASA and steroid enemas
Severe UC remission induction
Admit - NBM and IVI
IV hydrocortisone, rectal steroids
Transfer to prednisolone with 5asa if improving
If no improvement - may need colectomy
Or immunosuppression can be used if no remission with steroids - azathioprine, methotrexate, monoclonal ab’s
Surgery in UC - rates, indications and type
20% need it at some stage
Indications = perforation, massive haemorrhage, toxic dilatation, failed medical therapy
Proctocolectomy + terminal ileostomy
Side effects of 5ASA x8
Nausea, headache, anorexia, temperature, rash, haemolysis, hepatitis and pancreatitis
Maintenance therapy in Crohn’s
Steroid sparing agents - because patients flare up every time you take them off steroids - mainstay is Azathioprine. Also steroid sparing in UC is 5asa not working.
6mp 6mecactopurine - used for steroid dependant UC or Crohn’s
What are GI diverticulum and where do they occur?
Outpouchings of gut wall and usually at entry sites of perforating arteries
What is diverticulosis vs diverticular disease?
Presence of diverticulum vs symptomatic diverticulum
Where are most important/common diverticulum?
Colonic - sigmoid colon - where most complications occur
Pathology of diverticulum?
Lack of dietary fibre causes high intraluminal pressure - forces mucosa to herniate through muscle wall
How common are diverticulum?
30% of westerners by age 65
Symptoms of diverticulum?
Many are asymptomatic - can have bleeding, altered bowel habit, colic, nausea and flatulence
Symptoms of diverticulitis?
Same as diverticulum (nausea, colic, altered bowel habit, flatulence, bleeding) but also pyrexia, raised WCC and CRP and tender colon/localised peritonitis
Treatment of diverticulitis?
Bowel rest (fluid only- may be only treatment if mild), antibiotics if needed, analgesia, surgery not for abscesses but yes for peritonitis
Indications for elective surgery in diverticulitis?
Stenosis, fistula or recurrent bleeding
Signs of perforation in diverticulitis?
Ileus, peritonitis, shock
Management of haemorrhage in diverticulitis?
Usually just bed rest and it will stop - if bad may need surgery - diathermy can prevent need for this
Signs of abscesses in diverticulitis?
Treatment?
Swinging fever, leucocytosis, localising signs (eg. Mass)
Treatment = antibiotics - CT/US guided drainage may be needed
What is angiodysplasia?
Submucosal arteriovenous malformations that typically presents as fresh PR bleeding in the elderly - cause unknown
Where does angiodysplasia occur?
Can affect anywhere in the GI tract but 70-90% of lesions occur in right colon
What is good for diagnosis of angiodysplasia?
Mesenteric angiography - shows early filling at site and then extravasation
Treatment of angiodysplasia
Embolisation, endoscopic laser electro coagulation, resection
What is a hernia?
Protrusion of a viscus through a defect of the walls of its containing cavity into an abnormal position
What is an incarcerated hernia?
Contents of hernial sac are stuck inside by adhesions
What is a strangulated hernia?
One where ischaemia occurs
Indirect vs direct inguinal hernia
Indirect - through internal inguinal ring. Direct - through abdominal wall through posterior wall of inguinal canal
What is defect in abdominal wall called and what are its boundaries?
Hesselbach triangle - laterally - inferior epigastric artery, medially - rectus abdominis, inferiorly - inguinal ligament
Risk factors for inguinal hernia x7
Male (8:1), chronic cough, constipation, urinary obstruction, heavy lifting, ascites, previous abdominal surgery
Differentiating direct from indirect
Gold standard is surgically - direct are lateral to inferior epigastric vessels and indirect arise medially
Direct vs indirect - which is more common?
Which strangulates more?
Which is more
Often reducible?
Indirect more common 80%
Direct reduce more easily
Indirect strangulate more easily
Repairs of hernia x2
Polypropylene mesh to reinforce posterior wall. Laparoscopic repair
Where do femoral hernias appear?
Mass in upper medial thigh or above inguinal ligament (points down the leg as opposed to inguinal pointing to the groin)
3 features of femoral hernias
More common in women, irreducible and strangulate easily due to rigidity of canal borders
Boundaries of femoral canal
Anteriorly - inguinal ligament, medially - lacunar ligament and pubic bone, laterally - femoral vein, posteriorly - pectineal ligament and pectineus
DDX of femoral hernia x6
Inguinal hernia, saphena varix, enlarged cloquets node, lipoma, femoral aneurysm, psoas abscess
Risk factors for paraumbilical hernia x2
Obesity and ascites
Where do epigastric hernias go?
Through linea alba above umbilicus
What is gastroschisis?
Congenital defect causing protrusion of abdominal contents through a defect in the anterior abdominal wall
Definition of IBS
Mixed group of abdominal symptoms for which no organic cause can be found
Prevalence of IBS, age at onset and F:M ratio
10-20% (probably higher)
Features required for IBS diagnosis
1) Abdominal pain/discomfort is relieved by defecation
OR
2) Altered stool or bowel frequency - constipation and diarrhoea alternate
Plus >2 of Urgency Incomplete evacuation Abdominal bloating/distention Mucus PR Worsening of symptoms after food
DIAGNOSIS OF EXCLUSION
Other symptoms present in IBS
Nausea Bladder symptoms Chronic >6months Backache Exacerbated by stress, menstruation or gastroenteritis
Treatment of IBS
Rarely successful Just make symptoms less intrusive Things which may worsen disease: - Fibre - Lactose - Fructose - Wheat - Starch - Caffeine - Sorbitol - Alcohol - Fizzy drinks
Management of IBS if constipation
High fibre can make worse
Avoid insoluble fibre
Bisacodyl and sodium picosulfate can make better
Ispaghula has non-fermentable water-soluble fibre
Management of IBS if diarrhoea
Avoid sorbitol sweeteners
Try bulking agent +/- loperamide after each loose stool
Management of IBS if colic/bloating
Oral antispasmodics
Active bacillus
Symptoms of gastrointestinal malabsorption
Diarrhoea Weight Loss Lethargy Steatorrhoea (hard to flush away) Bloating
Signs of deficiencies due to GI malabsorption
Anaemia (Iron, folate and B12) Bleeding disorders (vitamin K) Oedema (protein) Metabolic bone disease (vitamin D) Neurological features
Tests in GI malabsorption
Bloods - low b12, folate, iron, calcium
Stool - fat globules (Sudan stain), microscopy (infestation)
Barium-follow through (Diverticula, crohns)
Breath hydrogen (bacterial overgrowth)
ERCP - pancreatitis, biliary obstruction
Common causes of GI malabsorption in UK
Coeliac disease
Chronic pancreatitis
Crohn’s disease
Rarer causes of GI malabsorption
PBC
Ileal resection
Biliary obstruction
Pancreatic cancer
CF
Tropical disease
Surgery to have removed part of digestive system
What is Coeliac’s disease
T-cell mediated autoimmune disease of small bowel
Where prolamin intolerance (in wheat etc) causes villous atrophy and malabsorption
When do you suspect Coeliacs?
All with diarrhoea, weight loss and anaemia
Prevalence of Coeliacs
1 in 300-1500
More common in the Irish
Peaks in infancy and 50-60 years
Associations of Coeliacs
Familial component
HLA DQ2 in 95% (rest are DQ8)
Presentation of Coeliacs
Stinking stools/steartorrhea
Diarrhoea
Abdominal pain
Bloating
N and v
Weight loss
Fatigue and weakness
Aphthous ulcers
Angular somatitis
Osteomalacia
Easy bruising
Children fail to thrive (wasted buttocks)
Diagnosis of Coeliacs - blood test
Low Hb and ferritin
RCDW increase
Low B12
Antibodies in Coeliacs
IgG Anti-gliadin
IgA, IgG Anti-endomysial transglutaminase
Last diagnosis for Coeliacs
Biopsy at endoscopy
Shows subtotal villous atrophy
Raised intraepithelial WBCs
Features reverse on gluten-free diet
Treatment of Coeliacs
Life-long gluten free diet
Rice, maize, soya, potatoes, oats and sugar are okay
Complications of Coeliacs
Anaemia
Secondary lactose-intolerance
GI T-cell lymphoma
Increase risk of other malignancy (gastric, oesophageal, bladder, breast, brain)
Myopathies
Neuropathies
Hyposplenism
Osteoporosis
Digestion of carbohydrates
Starch breakdown - starts in mouth but most occurs under action of pancreatic amylase in upper intestine - sugars!!
Digestion of protein
Pancreatic proteolytic enzymes into amino acids and peptides - occurs in duodenum
Digestion of fat
Digestion by bile and pancreatic lipase in duodenum
Bile salts absorbed in terminal ileum
Water and electrolyte absorption
Upper jejunum - ileum - colon
Water soluble vitamins
Small intestine, vitamin B12 and bile salts - terminal ileum
Treatment of pruritus ani?
Careful hygiene
Moist wipe post-defecation
No spicy food
Anaesthetic cream
No steroid/antibiotic cream
What is an anal fissure?
Painful tear in squamous lining of lower anal canal
Where are anal fissures usually located?
90% are posterior
Causes of anal fissure
Most are due to hard faeces
Spasm may constrict inferior rectal artery - causing ischaemia - making healing difficult and perpetuating the problem
Other rare causes of anal fissure
Syphilis, herpes, trauma, crohn’s, anal cancer and psoriasis
Medical treatment of anal fissure
5% lidocaine ointment
GTN ointment
Topical diltiazem (calcium channel blocker) Botox injections
Conservative treatment of anal fissure
Increase dietary fibre
Fluids + stool softener
Hygiene advice
What is anal fistula? How arise pathologically?
Track communicates between skin and anal canal/rectum
Blockage of deep intramuscular glands thought to predispose to formation of abscesses - this discharge to the skin to form fistulas
Symptoms of anal fistula
Pain and irritation
Causes of anal fistula
Perianal sepsis
TB
Abscesses
Crohn’s disease
Diverticular disease
Rectal carcinoma
Tests in anal fistula
MRI
Endoanal US scan
Treatment of anal fistula
Fistulotomy and excision
What needs to happen in excision of a high fistula?
Continence of muscles of anus affected therefore ‘seton suture’ needed - tightened over time to maintain continence
What usually causes anorectal abscesses?
Normally gut organisms
Treatment of anorectal abscess
Incise and drain under GA
Associations of anorectal abscess
DM
Crohn’s
Malignancy
Fistulae
What is a perianal haematoma, what does it look like and how treated?
Thrombosed external pile. 2-4mm ‘dark blueberry’ under skin at anal margin
Can be evacuated under LA or left to resolve spontaneously
What is pilonidal cyst?
Ingrowing hair 6cm above anus - causes foreign body reaction - foul-smelling discharge
M:F = 10:1
More common in obese caucasians and people from Asia, Middle East and Mediterranean (more bodily hair)
Treatment of pilonidal cyst
Excision of sinus tract +/- primary closure
Ab’s pre op
What happens in rectal prolapse?
Mucosa - partial/type 1
Or all layers - complete/type 2 (more common)
protrude through the anus
Incontinence in 75%
Descent of >3cm when asked to strain
Causes of rectal prolapse
Lax sphincter, prolonged straining
Also related to chronic neurological disease
Treatment of rectal prolapse - 2 approachs
1) Abdominal approach
- Fix rectum to sacrum (rectopexy) +/- mesh insertion +/- rectosigmoidectomy (prolapsed bit removed and two ends joined up) = Altemeier’s procedure
2) Perineal approach = Delorme’s procedure - resect mucosa close to the dentate line - push muscle back up and suture mucosal boundaries - mucosa excess stitched back to cover repair
- Anal encirclement with a Thiersch wire
Treatment of anal warts?
imiquimod and podophyllotoxin
What is Proctalgia fugax?
Idiopathic, intense brief stabbing, crampy rectal pain
Often worse at night
Mainstay treatment is reassurance
How do you test muscular and sensory innervation?
Anocutaneous reflex - lightly stroking anal skin - sphincter should contract briefly
Risk factors for anal cancer?
Syphilis
Anal warts
Anoreceptive homosexuals
What sort of cancer is anal cancer normally?
Squamous cell - 85%
When are anal canal tumours associated with poor prognosis?
If spread above dentate line
Poorly differentiated
Non-keratinizing
Where does anal cancer spread to?
Above dentate line - to pelvic lymph nodes
Below dentate line - to inguinal lymph nodes
Presentation of anal cancer
Bleeding Pain Altered bowel habit Pruritus ani Masses/stricture
Treatment of anal cancer
Chemo-irradiation - usually preferable to anorectal excision & colostomy
Prognosis of anal cancer
75% retain normal anal function
What are piles/haemorrhoids?
Anus is lined by spongy vascular tissue = anal cushions - where 3 major arteries feed the vascular plexuses and enter the anal canal
These contribute to anal closure
Piles is when they get disrupted and dilated
What causes the cushions to form piles?
Effects of gravity
Increased anal tone
Straining at stool - constipation
All cause them to become bulky and loose and then they protrude
Why called haemorrhoids?
Because they bleed readily from the capillaries underlying
Bright red blood because from capillaries
Are haemorrhoids painful?
No because there are no sensory fibres
But can thrombose when protrude if they are gripped by the anal sphincter as this blocks venous return = painful
Classification of piles
1st degree - remain in rectum
2nd degree - prolapse through anus on defecation but spontaneously reduce
3rd degree - same as 2nd but require digital reduction
4th degree - persistently prolapsed
Difference between external and internal haemorrhoid
External - origin below dentate line (ex.rectal plexus)
Internal - origin above dentate line (int.rectal plexus)
Symptoms of piles
Bright red rectal bleeding
May be mucous discharge and pruritus ani
Severe anaemia can occur
Medical treatment of piles - when and what? x4
For 1st degree Increase fluid and fibre Topical analgesics Stool softener Topical steroids for a short period
Non-operative treatment of piles - when and what? x4
For 2nd and 3rd degree
1) Rubber band ligation - produces an ulcer therefore bleeding pain and infection are SE’s
- lowest recurrence rate
2) Sclerosants - 2ml of 5% phenol in almond oil injected into pile
- recurrence higher
- SE: impotence, prostatitis
3) Infra-red coagulation
- as successful as banding and might be less painful
4) Cryotherapy
- Not recommended as high complication rate
Surgical treatment of piles - when and what? x2
For 4th degree piles
1) Excisional haemorrhoidectomy
- Most effective
- Excision of piles and ligation of vascular pedicles
- Day-case surgery
2) Stapled haemorrhoidectomy
- Less pain maybe
- When there is a large internal component
- Higher recurrence rate
Treatment of prolapsed thrombosed piles
Analgesia, ice packs and stool softeners
Pain usually resolves in 2-3 weeks
Some say surgery
What is dermatitis herpetiformis
Intense, itchy blisters seen on elbows, knees or buttocks
Skin condition linked to coeliacs
Tumour markers in CR cancer
CEA (used to monitor disease progression and Ca 19-9
Type of surgery for CR cancer in caecum, ascending colon, proximal transverse colon
Right hemicolectomy
Type of surgery for CR cancer in distal transverse colon, descending colon
Left hemicolectomy
Type of surgery for CR cancer in sigmoid colon
Sigmoid colectomy
Type of surgery for CR cancer in high rectum
Anterior resection
Type of surgery for CR cancer in low rectum
Abdo-perineal resection and end colostomy formation
What is Duke Stage B
CR cancer staging
Breached serosa but negative lymph nodes
What is Duke Stage A
CR cancer confined to bowel wall
Investigation features of Crohns
Cobblestone mucosa
rose-thorn fissures
Barium showing fissures or strictures (string sign of kantor)
What is ischaemic colitis?
Ischaemia of the colon due to decreased colonic blood supply which can lead to muscosal inflammation, oedema, necrosis and ulceration
Where is most commonly affected by ischaemic colitis
Splenic flexure - watershed between superior and inferior mesenteric arteries
Cause of ischaemic colitis normally
Occlusion of large vessels by thrombosis/embolism
therefore increased risk with atherosclerosis and AF
Cause of ischaemic colitis in young patients
Small vessel vasculitis
Vasospasm (cocaine)
Hypercoagulable states
Symptoms of ischaemic colitis
Can be acute or chronic in onset
Crampy abdominal pain, may be post-prandial ‘gut claudication’ therefore ‘food fear’
Fever, nausea, bloody diarrhoea
Signs of ischaemic colitis
Abdominal distention and tenderness Local peritonism (worse on left) Fever and tachycardia depending on severity
Blood in ischaemic colitis
Raised LDH, lactate and CK
Imaging signs in ischaemic colitis
Thickening of wall, intramural air - thumbprinting (submucosal oedema)
Management of ischaemic colitis
Supportive, NBM and surgery if necrosis or perforated bowel
What is pseudomembranous colitis
Large bowel inflammation with mucosal destruction and inflammatory exudates forming pseudomembranes on bowel wall - due to toxin releasing C-Diff
Features of pseudomembranous colitis
Recent antibiotic therapy
Watery diarrhoea, may become bloody with crampy abdominal pain
Pyrexia and abdominal tenderness
Treat with metronidazole and vancomycin
Faecal test for UC
Faecal calprotectin (marker for disease severity)
Barium enema signs with UC
Loss of haustral pattern - leadpipe or hosepipe appearance
