G1Pathologies
Upper Gl ·
9PIs inhibit
gastric secretions including Intrinsic Factor,
so
they can... cause malabsorption/B12 Deficiency.
Referred for
Foregut Epigastrium 991s be tapered off & notabruptly stopped,
·
is
pain must
·
1
otherwise symptoms return more
severely
·
Gastro-Desophageal Reflux Disease (GORD):due stimulation.
to accumilation of
1. has reduced tone, causing squamous
oesophageal sphincter mucosa
damage from acid reflux.
Squamous epithelium infilrated by Eosinophils/Basophils and
undergoes hyperplasia.
·
and causeoesophagitis and Barret's
metaplasia.
·
can
progress
Barrett's Metaplasia metaplasia from Squamous to Specialised Columnar
-
epithelium
symptoms: Dyspepsia, Heartburn, salivation, belching, chronic cough, hoarse voice.
·
oesophageal sphincter hypotonia, oesophageal dysmotility, delayed gastric emptying.
·
Causes:1.
Complications:haematemesis, oesophageal stricture, ulceration.
·
Risk factors:repeatvomiting,
obesity, pregnancy, Hiatus
Hernia, smoking, alcohol.
·
·
Treatment: lifestyle changes, Antacids, add 991 (end in -zole, e.g. Omeprazole), H2 blocker.
Eosinophilic Jesoghagitis:
·
Eosinophil build-up oesophagus, presenting with trachealised mucosal
in
rings.
mimic GORD
OESINOPHILIC
symptoms Dysphagia.
· +
OESOPHAGITIS
associated with hypersensitivity reaction/allergy.
·
·
Barrett's Metaplasia:
GORD/Oesophagitis leads to changing of
Chronic
Squamous to Specialised Columnar epithelium
-
akin to Gastric/ Intestinal columnar epithelium.
BARRET'S METAPLASIA
Pre-malignant, into dysplasia then adenocarcinoma.
·
can
progress
·
Gastritis:Stomach inflammation
can lead to stomach ulceration, dysplasia, adenocarcinoma.
·
·
Risk Factors:H. Pylori, NSAIDS I
Alcohol.
Atrophic Gastritis to replacement
Chronic gastritis autoimmunity leading of
-
or
mucosa with fibrous or intestinal tissue. Can be
asymptomatic.
, Lower Gl
·
Referred pain for Midgut is Umbilicus.
·
Referred pain for Hindgut is
Hypogastrium. IBD
·
Inflammatory Bowel Disease (IBD):encompasses UC and hy's.
CROHN'S
Both
genetic autoimmune
·
responses.
only mitigate symptoms.
·
No cure, can
·
Crohn's Disease:
mostly affects ileo -cecal junction,
·
but can affectanywhere in G1 in skip lesions, whole wall thickness.
·
Character:
thickening wall
of (smaller lumen), cobblestoning of mucosa, strictures possible,
deep ulceration, fatwrapping, granulomas present, smoking increases risk.
IBD
Complications:Obstruction, perforation, strictures,
·
Fistula, malabsorption/anaemia, Arthritis.
symptoms:Diarrhoea, fever, Haematochezia, clubbing,
·
weightloss, fatigue, abdo gain, oral ulcers.
Treatment:same UC, but without ASAs for maintenance.
·
as
·Ulcerative Collitis:
affects Rectum/Descending
superficially, only mucosa.
Colon
·
Character:
haemorrhagic mucosa, surviving mucosa presentas pseudo-polyps, strictures,
·
no
larger lumen, granulomas absent, smoking reduces risk.
·
Symptoms:episodic/chronic Diarrhoea, fever, Haematochezia, clubbing.
Complications:adenocarcinoma, Arthritis/Ankylosing Spondylitis, Toxic Megacolon, Diff, PSC.
·
C.
mild/severe
Treatment:treat differently, escalate if notresponding. Goal is to induce remission.
·
IBDincreases risk Thrombosis in Acute scenario,
of
always give thromboprophylaxis.
so
Maintenance Therapy: oral/enema ASAH-Azathioprine immunosupp. HInfliximab antibody.
·
no steroids
long-term
Aminosalicylates (ASAs): Differentials/Investigations:
e.g. mesalazine.
Acute Therapy: Differentiating IBD and IBS: Faecal Calprotectin and CRP
· ·
-
Oral Prednisalone steroid. are raised during Glinflammation, suggesting IBD over IBS.
Hydrocortisone steroid.
IV
-
-Oral Infliximab antibody. Infections Colitis symptoms of colitis due to
· -
Colon Resection it infection from contaminated food, commonly after travel.
-
responding.
not commonly caused by Shigella, Salmonella, E. Coli.
Do stool culture to rule in/out
infections colitis.
AVOID ANTI-DIARRHOEA DRUGS
