Small + large intestine conditions Flashcards
Name 2 malabsorption disorders of the SI
Coeliac disease
Crohn’s (doesn’t just affect SI)
Define maldigestion v malabsorption
Maldigestion = Impaired breakdown of food in the intestinal lumen, e.g. lack of pancreatic enzymes, following gastric resection, bile acid deficiency
Malabsorption = Impaired absorption of digested food caused by alterations of the intestinal mucosa
Are Crohn’s disease and coeliac disease malabsorptive or maldigestive disorders
Malabsorptive
General symptoms (3) /signs (5) of malabsorption
Increased appetite
Bloating
Fatigue
Weight loss Diarrhoea Steatorrhoea (fat malabsorption --> fatty stool) Clubbing Apthous ulcers (crohn's)
Signs of iron deficiency (4)
Anaemia:
- Fatigue
- Pale skin
- Dyspnoea on exertion
- Koilonychia
Sign of vitamin A deficiency
Night vision impaired
Sign of vitamin K deficiency
Raised prothrombin time
Signs of vitamin
-B1
-B3
deficiency
Vitamin B1 (thiamine) deficiency –> memory loss
Vitamin B3 (niacin) deficiency –> dermatitis
Sign of vitamin C deficiency
Scurvy
Investigations of small intestine disorders (6)
Endoscopy + biopsy Barium follow through Enteroscopy - longer version of endoscopy CT MRI enterography Capsule enterography - pillcam
Investigations of bacterial overgrowth in SI (2)
H2 BREATH TEST (diagnostic of SI bacterial overgrowth and carbohydrate malabsorption)
Endoscopy + aspiration of duodenal/jejunal fluid –> then culture
What is coeliac disease
Autoimmune disease triggered by gluten (specifically gliadin component of gluten)
Sensitivity to gluten
Pathophysiology of coeliac disease
Immune activation –> inflammatory response to gliadin –> body produces anti-tissue transglutaminase) antibodies attacking the enzyme, tissue transglutaminase (tTG)), –> villous atrophy, hypertrophy of crypts and increased lymphocytes
Risk factors of coeliac disease (3)
Family history of coeliac
PMH or FH of autoimmune diseases - type 1 DM, thyroid disease
IgA deficiency
Symptoms (4) /signs (5) of coeliac disease
abdo pain
DIARRHOEA - most common
bloating,
fatigue
Steatorrhoea Weight loss Dermatitis herpetiformis (IgA deposit on skin) IgA deficiency Anaemia
Investigations of coeliac disease (4)
- serology (3)
- gold standard
Serology (test for antibodies): -Total IgA - for IgA deficiency -IgA-tTG antibody -anti-endomysial IgA (Some coeliacs are IgA deficient so ALWAYS measure total IgA)
Distal duodenal biopsy – GOLD STANDARD
Treatment of coeliac disease (2)
Gluten free diet
Nutritional support - calcium, vitamin D supplements
What is the characteristic histological finding of coeliac disease
+ other histological findings (3)
Villous atrophy
intraepithelial lymphocytes,
mucosal atrophy
crypt hyperplasia
What is the diagnostic investigation of coeliac disease
Distal duodenal biopsy
Other causes of small intestine malabsorption (4)
Infection, e.g. tropical sprue, HIV, giardiasis
Whipple’s disease
Iatrogenic - e.g. following gastric resection
Pancreas insufficiency
Treatment of small intestine bacterial overgrowth (3)
2 weeks each of:
Metronidazole
Tetracycline
Amoxycillin
What is IBD
A collective name for chronic inflammatory conditions of the bowel
Results from inappropriate and persistent activation of the mucosal immune system
Name the 3 types of IBDs
Crohn’s disease
Indeterminate colitis
Ulcerative colitis
Pathophysiology of IBD
Unknown activation of the immune system –> immune response against normal flora of the colon
Cause of IBD
Idiopathic
Thought to be due to combo of:
- Environmental triggers
- Immune dysfunction - possibly autoimmune
- Genetic predisposition
What is ulcerative colitis + is it superficial/deep + where does the inflammation begin (3)
CONTINUOUS inflammation of the colon
Inflammation is SUPERFICIAL – limited to mucosa
Inflammation always starts from the rectum and moves proximally
Risk factors of UC (3)
Family history of UC
HLA-B27 gene
Infection
Symptoms (2) /signs (4) of UC
Abdo pain (LLQ) Diarrhoea
Abdo tenderness
Rectal bleeding
Blood in stool
Malnutrition –> vit deficiencies, inable to maintain ideal weight
Symptoms/signs of a flare up/relapse of UC (worsened or additional symptoms to usual) (4)
Arthritis
Mouth ulcers
Irritated red eyes
Painful red swollen skin
Signs (4) of a severe UC attack
Stool frequency >6 a day with blood
Fever
Tachycardia
Dyspnoea
Investigations of UC (6)
- biochem
- imaging (2)
Stool test - elevated calprotectin
FBC - high WBC, high platelets
ESR - elevated
CRP - elevated
Flexible sigmoidoscopy
Colonoscopy + biopsy - DEFINITIVE
Treatment of UC (4 medical, 2 surgical)
Medication:
- 5ASA (aminosalicylates) - e.g. mesalazine, sulfasalazine
- immunosuppressants
- —–> steroids (prednisolone)
- —–> azathioprine*
- biologics (anti-TNFa antibodies - infliximab)**
Surgery
- proctocolectomy (rectum + colon removal) + permanent ileostomy (stoma) - most standard
- total colectomy + ileorectal anastomosis
*only used in refractory disease = if not responsive to normal treatment, i.e. 5ASA and steroids
**only used in refractory or severe disease
Pathological findings (i.e. if you were to look at it specimen physically) of UC (3)
Continuous pattern of inflammation
Inflamed RED granular mucosa
Pseudopolyps - projecting masses of scar tissue that have healed from ulceration (so old ulcer remnants)
Histological findings of UC (6)
Inflammatory infiltrates - high neutrophils
Mainly mucosal inflammation/ulcers + mucosal atrophy
CRYPT ABSCESSES/CRYPTITIS
NO GRANULOMAS
May get atypia (abnormal structure) of cells –> adenomatous change –> invasive cancer
Pathological findings (i.e. if you were to look at it physically) of Crohn’s disease (4)
GRANULAR serosa/dull grey
Mesentery - thickened and fibrotic
THICK COLON WALL –> NARROW lumen
‘Skip/cobblestone lesions’ - bits of normal colon then abnormal colon
Histological findings of Crohn’s (6)
NON-CASEATING GRANULOMAS
Cryptitis/ distortion of crypt cells
DEEP ulceration - TRANSMURAL inflammation
Fistula/stricture formation –> narrowing intestine
Fissuring ulcers
Lymphoid aggregates and neutrophil infiltrates
Is ulceration superficial/deep in UC vs crohn’s
UC - superficial
Crohn’s - deep
What is crohn’s disease
Disorder of unknown aetiology characterised by transmural inflammation (=all layers of bowel wall) of ANYWHERE in the GI) tract - from mouth to peri-anal area
Symptoms (3) /signs (4) of Crohn’s disease
Abdo pain/cramp - RLQ
CHRONIC diarrhoea - not usually bloody
Fatigue
Peri-anal lesions - skin tags/fistula/abscess
Blood in stool - more so microscopic, NOT GROSS BLEED
Oral lesions/ulcers
Weight loss
Risk factors of Crohn’s disease (3)
White
Age 15-40 or 60-80
Family history of crohn’s
Extra-intestinal manifestations of IBD (4)
Eyes - irritated, red eyes, e.g. uveitis
Joints - arthritis
Skin - painful red patches, often on legs
Liver - primary sclerosis cholangitis (risk of cholangiocarcinoma)
Investigations of Crohn’s disease (7) + which of these is the definitive diagnosis
- biochem (4)
- imaging (3)
FBC - low Hb, high WBCs
CRP
ESR
Stool test - elevated faecal calprotectin only significant in UC
AXR
Abdo CT
Colonoscopy + biopsy - definitive diagnosis
Treatment of Crohn’s disease
- medical (6)
- surgery indicated if
5ASA (aminosalicylates) - e.g. mesalazine, sulfasalazine
Immunosuppressants
- Steroids (prednisolone/budesonide) - MORE USED
- azathioprine, methotrexate
Manage extra-intestinal manifestations - uveitis, arthritis,
Biologics (anti-TNFa antibodies - infliximab) -
Antibiotics - only if septic complications suspected
Surgery - if no improvement with medical therapies
Are antibiotics used for UC or crohn’s
Crohn’s
Complications of Crohn’s disease (4)
Intestinal obstruction
Abscess formation
Fistulas
Extra-intestinal manifestations - uveitis, arthritis
Complications of UC (5)
Pseudopolyps Toxic megacolon Perforation Stricture --> fistulas Colonic adenocarcinoma
Are immunosuppressants such as azathioprine and biologics (anti-TNFa antibodies) such as infliximab used more in crohn’s or UC
Crohn’s
Only used in UC if refractory disease = if not responsive to normal treatment, or severe disease
Pathophysiology of acute appendicitis (4)
Obstruction of the lumen of the appendix usually by a calcified stone of faeces (faecolith) –> lumen distal to obstruction fills with mucus and swells –> increasing intraluminal pressure
Bacteria multiply rapidly and eventually leak out through the dying walls –> pus forms within and around appendix
Histological features of appendicitis (3)
Fibrinopurulent exudate - pus + fibrin rich substance
Abscess
Full thickness necrosis of wall
Risk factors of appendicitis (4)
Young adult
Smoking
Pre-existing infection spread to appendix
IBD
Symptoms (3) /signs (3) in acute appendicitis
Abdominal pain (starts in umbilical region then moves to right lower quadrant)
Nausea
Anorexia
FEVER
RLQ tenderness (McBurney’s point)
Tachycardia
Investigations of appendicitis (2)
- bloods
- imaging
FBC - elevated leukocytes (WBCs)
CT abdo/pelvis
Treatment of appendicitis (3)
IV fluids
IV antibiotics
Appendectomy ASAP
+/- abscess drainage
Complications of appendicitis (3)
Perforation
Peritonitis
Appendicular abscess
What is dysplasia
Structural change of cells/ abnormal development of cells
How is dysplasia related to colon cancer
Dysplasia can lead to formation of adenomas
2 Types of dysplasia
Low grade or high grade
Colorectal carcinoma is usually what type of tumour
Adenocarcinoma
Risk factors of colorectal cancer (7)
Increasing age
APC mutation
Lynch syndrome (aka hereditary non-polyposis colorectal cancer (HNPCC))
IBD
Obesity
Family history of CRC
Previous history of colorectal adenoma or CRC
Colorectal cancers are more often in the colon or rectum
Colon
Symptoms (2) /signs (3) of colorectal cancer
Rectal bleeding - esp left sided CRC
Altered bowel habit - esp left sided CRC
Anaemia - esp right sided CRC
Rectal mass
Constitutional symptoms/signs - weight loss, anorexia - if advanced disease
Common clinical features of a left sided CRC (3)
Altered bowel habit - more frequent, loss stools
Rectal bleeding - fresh blood
Annular shaped colon - apple core lesion
Clinical features of a right sided CRC (3)
Tumour grows outwards like a polyp
ANAEMIA
Vague visceral pain
Investigations of colorectal cancer (3 - imaging)
+ staging investigations (4)
Colonoscopy + biopsy
Barium enema
CT colonography (virtual colonoscopy)
CT chest/abdo/pelvis
Pelvic MRI
Rectal endoscopic ultrasound - better than CT for T staging
PET scan
Are most CRCs sporadic or genetic
Sporadic
Where does colorectal cancer spread to commonly (3)
Liver
Lungs
Lymph nodes
Pathophysiology of CRC development (3)
High grade dysplasia of colonic/rectal epithelial cells –> adenomatous polyps –> carcinoma
Colorectal polyps are…
Pre-malignant adenomas
3 histological types of colorectal polyps
Tubular (majority)
Villous
Tubulovillous
What do sessile polyps look like
Flat, blend in with lining
What do pedunculate polyps look like
Raised growths
Treatment of colorectal cancer
- colon cancer (surgical (2) /non surgical candidate (1))
- rectal cancer (surgical (2) /non surgical candidate (1))
- may need removal of what organ with metastases
Colon cancer
- if surgical candidate: surgical resection + chemotherapy
- if non-surgical candidate: chemotherapy
Rectal cancer
- if surgical candidate: surgical resection +/- neoadjuvant RADIOTHERAPY*/CHEMORADIOTHERAPY
- if non-surgical candidate: chemotherapy
Partial hepatectomy if liver metastases
*radiotherapy for rectal cancer only
Is neoadjuvant radiotherapy used in rectal or colon cancer
Rectal
Staging systems used in colorectal cancer (2)
TNM
Dukes
Name 2 inherited syndromes that can predispose you to colorectal cancer
FAP (Familial adenomatous polyposis)
HNPCC (hereditary non-polyposis colorectal cancer) aka Lynch syndrome
Explain the Dukes staging system (4)
Dukes A - limited to mucosa and submucosa
Dukes B - invades through muscularis externa
Dukes C - regional lymph nodes involved
Dukes D - distant metastases
Explain the TNM staging system
- T (3)
- N (3)
- M (2)
T1 - involves mucosa/submucosa
T2 - involves muscularis externa
T3 - involves serosa
N0 - no lymph node metastases
N1 - 1-3 local lymph nodes
N2 - 4+ local lymph nodes involved
M0 - no distant metastases
M1 - distant metastases
Name 2 screenings tests for CRC
Faecal occult blood test (FOBT)
Faecal immunochemical test (FIT)
How does Faecal occult blood test (FOBT) work - to screen for CRC
+ how frequently is it done in Scottish bowel screening programme
Faecal sample placed on guaiac paper and hydrogen peroxide applied which, in the presence of blood, gives a blue reaction product
Every 2 years in Scottish bowel screening programme
How does Faecal occult blood test (FOBT) work - to screen for CRC
Finds hidden blood in faeces
Uses specific antibodies that recognise human haemoglobin
Faecal occult blood test has high … but low …
Specificity
Sensitivity
Screening programme for CRC in people with FAP
annual colonoscopy from age 10-12
Screening programme for CRC in people with HNPCC
from age 25, bi-annual colonoscopy
What mutation occurs in FAP
APC gene mutation
What mutation occurs in HNPCC
Mutation in DNA mismatch repair (MMR) genes
Screening programme for people with family history of CRC
5 yearly colonoscopy from age 50 if high moderate risk
Screening programme for CRC in people with IBD
colonoscopy 10 years post IBD diagnosis
Screening programme for people with previous history of CRC
5 yearly colonoscopy
Causes of small bowel/intestinal obstruction (7)
Adhesions/scar tissue post surgery Inguinal hernia Foreign bodies Intussusception (when part of the intestine slides into an adjacent part of the intestine Tumour Appendicitis Crohn's disease
Symptoms (3) /signs (2) of bowel obstruction
Failure to pass wind/stool Abdo pain Nausea Vomiting Abdo distension
Treatment of small bowel obstruction (5)
IV FLUIDS
NASOGASTRIC DECOMPRESSION - NG tube put in to decompress air/fluid
Analgesia
Anti-emetics
Correction of underlying cause, e.g. appendicitis, hernia, tumour
Causes of large bowel obstruction (3)
Colorectal tumour - 90%
Colonic volvulus - loop of intestine twists around itself
Stricture
Definitive treatment of large bowel obstruction (1)
+ acute treatment (6)
Surgery to correct the cause
Acute
- Supplemental oxygen
- IV fluids
- electrolyte imbalances should be corrected
- Blood transfusion/blood products may be required to correct anaemia or coagulopathy
- Nasogastric decompression - to decompress the air/fluid in the intestinal tract
- Pre-op antibiotics
Low risk features of rectal bleeding (3)
Temp symptoms <6wks
Anal symptoms
<40yrs age = watch and wait for 6 wks, if symptoms persist/deteriorate –> refer for LI imaging
High risk features of rectal bleeding (4)
Persistent change in bowel habit >6wks
Persistent bleeding WITHOUT anal symptoms
Rectal/abdominal mass
Unexplained iron deficiency anaemia
Other causes of small intestine malabsorption apart from coeliac disease + crohn’s
Infection
- tropical sprue
- HIV
- giardia lamblia
Define a severe flare up of UC
> 6 bowel movements a day with lots of rectal bleeding
