GI Flashcards
presentation of coeliac disease
indigestion, diarrhoea, abdominal bloating, constipation
fatigue
faltering growth in children
iron, vitamin B12 or folate deficiency
uncommon:
osteopenia/osteoporosis
dermatitis herpetiformis
cerebellar ataxia
pathophysiology of coeliac disease
associated with HLA-DQ2 or HLA-DQ8 (although most people with these don’t have coeliac)
these present gluten peptides (after de-amidation by tTG) that activate an immune response
Th1 –> villous atrophy and crypt hyperplasia
Th2 –> plasma cell maturation and anti-gliadin and anti-tTG antibody production from these plasma cells
investigations for coeliac disease
Confirm that the person has eaten gluten-containing foods (with wheat, barley, or rye as an ingredient) at least twice every day over the previous 6 weeks
Send off serology - use IgA tTG and total IgA as first line
(IgA EMA can be used if IgA tTG is unavailable)
FBC - IDA
small bowel histology (GOLD STANDARD) - will show intra-epithelial lymphocytes, villous atrophy and crypt hyperplasia - do the duodenum because this is where most of the damage occurs (probs cos this is the first bit exposed to the gliadin)
skin biopsy in patients with skin lesions suggestive of dermatitis herpetiformis
management of coeliac disease
gluten free assess and manage osteoporosis risk consider annual blood test: - coeliac serology - FBC and ferritin - TFT, LFTs, electrolytes (addison's) - vitamin D, B12, red cell folate, serum calcium
most common infections leading to acute diarrhoea
noravirus, sapovirus, rotavirus
salmonella species, campylobacter jejuni, shigella species, E coli, C difficile (can cause pseudomembranous colitis)
parasitic are the most common causing persistent diarrhoea - cryptosporidium, giardia, entamoeba histolytica and cyclospora
causes of acute diarrhoea other than infection
drugs - antibiotics, chemo, metformin, NSAIDs, PPIs, SRTIs, ARBs, allopurinol
diverticulitis, ischaemic colitis, IBD, anxiety, food allergy, acute appendicitis, pelvic radiation, intestinal ischaemia
or overflow diarrhoea due to constipation
anti-mobility agents for diarrhoea
loperamide
o Uses: gastroenteritis, non-specific diarrhoea, mild traveller’s diarrhoea, IBS, IBD
o SHOULD NOT BE USED for cases of bloody diarrhoea, acute exacerbation of UC or bacterial enterocolitis
anti-secretory agent for diarrhoea
racecadotril
BNF - has better tolerability than loperamide - causes less constipation + flatulence
antispasmodics for diarrhoea
hyoscine butylbromide
mebeverine - used specifically in IBS to relieve symptoms like pain, cramping, flatulence and diarrhoea
C difficile treatment
metronidazole 400mg TDS or vancomycin (check current guidelines)
diverticulosis vs diverticular disease vs diverticulitits
diverticulosis = diverticula are present but without symptoms
diverticular disease = diverticula cause symptoms
diverticulitis = diverticula becomes inflamed and infected - causing severe symptoms
aetiology of diverticular disease
multi-factorial - both genetic and environmental factors have been linked
- low fibre, >50, genetics, smoking, obestiy, NSAIDs, opiods, steroids
low fibre diet increases intestinal transit time and decreases stool volume –> results in increased intraluminal pressure and colonic segmentation
symptoms of diverticular disease
left lower quadrant pain - may be triggered by eating and relieved by the passage of stools or flatus
constipation, diarrhoea or occasionally rectal bleeds
symptoms of diverticulitis
severe abdominal pain starting in the hypogastrium then localising in the LLQ
fever
change in bowel habit and possible significant rectal bleeding
nausea and vomiting
complications of diverticulitis
abscess formation perforation and peritonitis - abdominal rigidity, guarding, rebound tenderness sepsis stricture and fistula formation intestinal obstruction
investigations for diverticulitis
colonic diverticulosis should only be diagnosed after diverticula have been noted on imaging (barium enema or CT) or after direct visualistation (via sigmoidoscopy or colonoscopy)
FBC, CRP - diverticulitits
blood culture - if patient has signs or symptoms of sepsis
CXR - if obstruction and suspecting perforation
angiogram - can be used in acute bleeding - considered if bleeding is too profuse to enable identification using colonoscopy
AXR - if thinking obstructio n
peak age of ulcerative colitis
most are 20-40 years but there is another peak at 60 years
treatment for diverticulosis
- Recommend eating a healthy, balanced diet and having regular meals
- The person’s meals should contain whole grains, fruits and vegetables
- Fibre intake should be increased gradually (to minimize flatulence and bloating) - adults should aim to consume 30g/day
treatment for diverticular disease
patient education
recommend 30g fibre/day
public health England’s ‘the eatwell guide’
drink adequate fluid
consider bulk-forming laxatives if symptoms of constipation and diarrhoea persist despite diet changes
paracetamol for abdo pain
Advise the person to avoid NSAIDs and opioid analgesia (such as codeine) if possible, due to the potential increased risk of diverticular perforation
Arrange to review the person, for example after one month, depending on clinical judgement to check how they are managing (if there are persistent or refractory symptoms, consider alternative causes for the symptoms)
treatment of diverticulitis
arrange urgent hospital admission if suspected complications and cannot be managed at primary care of risk of dehydration or significant co-morbidities
hospital: IV ABx, fluids, analgesia, surgery for complications (e.g. abscess drainage)
oral abx in primary care - at least one week of co-amoxiclav
analgesia as needed
if managed in primary care, arrange a review within 48 hours or sooner if worsen
causes of peptic ulcers
H pylroi (gram -ve rod that produced urease --> ammonia, damages gastric mucosa) NSAID use
rarer causes: gastric ichaemia (stress ulcers), Zollinger Ellison syndrome (gastrin secreting neuro-endocrine tumour), medications (SSRIs, cocaine), infections (CMV), CD
peptic ulcer presentation
dyspepsia/indigestion causing abdominal fullness, heartburn, nausea, belching or upper abdominal pain
with duodenal ulcers - may radiate into the back - Nausea or vomiting
Bleeding causing haematemesis, ‘coffee ground’ vomiting and melaena
pointing sign - can show pain with one finger
early satiety - may indicate pyloric stenosis
symptoms of anaemia - fatigue, pica, nail changes
investigations for peptic ulcer disease
assess for alarm symptoms that might suggest a complication
FBC - anaemia
H pylori urea breath test or stool antigen test
upper GI endoscopy -Get a biopsy – can do urease testing on this and histology for neoplasm (cancers can look similar to ulcers). Biopsy will also show if there is evidence of an NSAID being the cause
repeat the endoscopy 6-8 weeks later to confirm healing
conservative treatment of peptic ulcer disease
patient education
conservative - lose weight, avoid trigger foods (coffee, chocolate, tomatoes, fatty or spicy food). eat smaller meals and eat evening meal 3-4 hrs before bed. stop smoking, reduce alcohol
assess for stress/anxiety which may worsen symptoms
review medication - e.g. stop NSAIDs/aspirin, bisphosphonates, SSRIs
ask about any previous courses of ABx that may affect the choice of H pylori eradicaiton regimen used
medical treatment of peptic ulcer disease
h pylori confirmed - 7 day triple regimen of
- PPI 2x daily
- amoxicillin 1g 2x daily
- either clarithromycin 500mg 2x daily or metronidazole 400mg 2x daily
h pylori confirmed and associated with NSAIDS - prescribe full-dose PPI therapy for 2 months THEN first line eradication therapy afterwards
h pylori negative - prescribe a full dose PPI for 4-8 weeks
PPI options = lansoprazole, omeprazole….
surgical options for peptic ulcer disease
include antrectomy (antrum removal) with a gastro-duodenal anastomosis or gastro-jejunal anastomosis, a vagotomy and pyloroplasty, or a highly selective vagotomy
management of an actively bleeding peptic ulcer
perform A–>E
check their Hb - transfuse if <70g/L
Erythromycin (as a prokinetic agent) and proton pump inhibitor may be considered prior to endosopy
Injection therapy (e.g. adrenaline), thermal probes (e.g. bipolar electrocoagulation, heater probe), or clips should be used
differentials of dyspepsia
functional dyspepsia H pylori infection GORD oesophagitis peptic ulcer disease gastroparesis - DM and previous abdominal surgery may result in vagal nerve injury gastritis lactose intolerance coeliac disease upper GI malignancy
