gastro meds Flashcards
Medications used in GI disease
1 antacids (ELIMINATING acids)
REDUCING acid secretion
2. H2 receptor blockers
3. Proton pump inhibitors
examples of Antacids
- gaviscon
- rennie
- alkalis that neutralises acid
function of H2 receptor blockers
- preventing histamine activation of acid production
- limited effectiveness because gastrin and Ach pathways still operative
function of Proton pump inhibitors
- blocks acid secretion irrespective of whether the simulation continues at the bottom
- much more effective clinically than H2
what is ome/lanso/pantoprazole
PPI
what is cimetidine
- cimetidine
- ranitidine
both are H2 receptor blockers
Upper GI disease
- Oral diseases
- Oesophageal
o Dysphagia
o GORD - Gastric
o Hiatus hernia
Dysphagia
- difficulty swallowing
- dysmotility = fibrous replacement of elastic and muscle tissue
- external compression
- feel of food sticking
causes of dysphagia
- external compression
- GORD
- scleroderma
- neuromuscular dysfunction
o Parkinsons
o Diabetes
o Achalasia
refer to the notes for more info
GORD Causes
- defective lower oesophageal sphincter
- impaired lower clearing
- impaired gastric emptying
effects of GORD
- ulceration
- inflammation – erythema due to burning by acid
- Barrett’s oesophagus metaplasia – change in oesophagus epithelium from stratified squamous to columnar epithelium
- Precancerous adenocarcinoma – chronic inflammation can lead to potentially malignant lesion
- Dysphagia
Signs and symptoms of gord
- epigastric burning
- abdominal pressure
increasing - dysphagia
- stricture
- oesophagitis
- dysmotility
- GI bleeding FOB test
- severe pain
- heartburn after excessive food or drink mimicking MI
- oesophageal muscle spasm
Management of Gord
- stop smoking improves sphincter
- lose weight as abdominal fat can pressure ad force food back up
- stop excess coffee
- antacids
- H2 blockers
- PPI
- drugs to increase gut motility and gastric emptying to reduce backfilling into the oesophagus
2 types of hernia
- part of stomach in thorax
o 1 => sliding hernia where the hernia moves with the oesophagus
o 2=> rolling hernia where the oesophagus and hernia behave independently
symptoms of hernia
- similar symptoms to GORD
- the diaphragmatic muscles cannot help to compress the lower sphincter making it easier for gastric contents to pass up from stomach back into oesophagus and cause GORD
Peptic ulcer disease affects which part of the git
- oesophagus
- stomach
- duodenum often affected by PUD
causes of peptic ulcer disease
- High acid secretion in ddn and oesophagus
- Normal acid secretion but lost ability to neutralise acids (Helicobacter pylori) (stomach)
- Drugs like nsaids and steroids
Types of peptic ulcer disease
- bleeding ulcer – gone through lining and submucosa, eroded to an artery causing significant bleeding
- perforated ulcer – burn can extend through artery or viscous wall into peritoneum
where does Helicobacter pylori usually affect
- infects lower part of stomach (antrum)
what does h pylori do to the stomach
- bacteria gets through the mucus layer, removes it, allows attack on stomach lining, leading to inflammation
- loss of mucus layer protection
- chronic gastric wall inflammation
- activates lymphoid tissues in gastric wall
can lymphoma caused by H.pylori disappear?
yes, with triple therapy. (2 antibiotics and 2 PPI)
- when stimulus is removed ie H. pylori, the lymphoma will disappear
what is MALT
lymphoma on the stomach (peptic ulcer disease) is a MALT (mucosa associated lymphoid tumour)
Signs and symptoms of PUD
- asymptomatic
- epigastric burning pain
- significant bleeding and perforation ulcers may cause there to be change in amount of blood in circulation, could be a drop in blood pressure
Investigations for peptic ulcer diseases
- endoscopy, biopsy
- radiology
- anaemia
o FBC and FOB
o chronic bleeding in the stomach may cause a decrease in Hb content (fbc)
o bleeding in git shown by positive test of Hb in stools for FOB - H. pylori
o antibodies in blood
o mucosa biopsy
o metabolic products of bacteria in breath sample
Complications of peptic ulcer disease
Local more serious
o perforation
o haemorrhage
o stricture
o malignancy
Systemic
o anaemia
refer to notes for more info
tx of peptic ulcer disease
o stop smoking
o small regular meals
o eradication therapy, removing H.pylori using triple therapy
o ulcer healing drugs like PPIs
o reduce acid secretion using H2 receptor blockers and PPI
o improve mucosal barrier by eliminating H.pylori with triple therapy and stopping NSAIDs and steroids
Surgical
o gastrectomy used when there is stricture, ACUTE bleeding, perforation, malignancy
what is gastrectomy
surgical excision of the ulcer, part of the stomach
Bilroth 1 vs 2
Bilroth 1 – duodenum connected to upper part of stomach
Bilroth 2 – duodenum sewn up, stomach connected to small bowel
what is vagotomy
vagotomy – divide the main vagus trunk into small branches to the stomach to reduce acid secretion
what is coeliac disease
sensitivity to alpha-gliaden component of gluten!
Gluten found in wheat, barley, rye etc
Where does coeliac disease affect?
- Small bowel
- mainly JEJUNUM
what disease has to do with malabsorption
disease of the small intestines like
a. Pernicious anaemia
b. Coeliac disease
c. Crohn’s
d. Small bowel disease
where are haematinics absorped in git?
b12 terminal iluem
iron and folate in jejunum
** iron and folate deficiency may be due to coeliac disease
b12 deficiency due to diseases affecting terminal ileum like crohns
coeliac disease may cause what deficiency
iron and folate
crohns may cause what deficiency
b12
Causes of coeliac disease
- genetic susceptibility
- environmental triggers
- gluten ALPHA GLIADEN COMPONENT
what does alpha glaiden do to the small intestine?
o alpha gliaden in gluten passes through the bowel wall causing an immune reaction that produces antibodies
o T cells and antibodies destroy the villous tissue resulting in villous atrophy
- loss of projections
- decrease in SA
- reduction in absorption
signs and symptoms of coeliac
- failure to grow due to malabsorption
- abdominal pain
- oral aphthae (ulcers)
- tongue papilla loss
- steatorrhea (oily stools)
- dysphagia
- iron, folate deficiency
- fat deficiency
Investigations for coeliac
- autoantibody test
o serum transglutaminase (TTG)
o anti gliaden antibodies - jejunal biopsy
- loss of projections seen on endoscopy
- faecal fat increased if malabsorption
- haematinics
can Gluten free diet reverse coeliac disease?
yes , FULLY reverses jejunal villous atrophy
- complete and full absorption restored
what is dermatitis herpetiformis
Coeliac disease associated diseases
o little blisters on skin filled with fluid
o autoantibodies against the skin
o granular IgA deposited in skin and mucosa
o itch and blisters
o antibodies binding to the JE between the connective tissue and the epithelial surface, loss of adhesion causing the epithelium to lift up
which disease has granular IgA deposited in skin and mucosa
- dermatitis herpetiformis which is a coeliac disease associated disease
if you see oral aphthous ulcer and blisters, what could you link it to?
Coeliac disease associated diseases
deficiency of haematinics
what is Pernicious anemia
disease caused by vitamin b12 deficiency either because
a. B12 intake not enough
b. B12 not absorbed in terminal ileum
what might cause lack of b12 absorption in terminal itleum?
a. parietal cells disease, usually autoimmune, Intrinsic factor not produced
b. inflammatory bowel disease of the terminal ileum like Crohn’s
c. bowel cancer at ileocaecal junction
Treatment of Pernicious anaemia
- increase b12 intake
- supplements
- IM injections of b12
Importance of B12
- nerve function without it may have permanent neuromuscular damage
- bone marrow production of RBC
where is bowel cancer occuring
- usually means colonic cancer
- large bowel
who gets bowel cancer more commonly
UK screening from age 50
man > woman
Symptoms of bowel cancer
- usually none
- low level anaemia
- rectal blood loss (high risk symptom)
- abdominal pain/tenderness
how to screen for bowel cancer?
o Faecal immunochemical test (FiT)
o endoscopy if positive ie see blood in stool
causes of bowel cancer?
- carcinomas arise from POLYPS
- patient controlled factors
- medical and familial factors
how to stage bowel cancer?
Staged by degree of invasion into bowel wall
- A => SM
- B => Muscularis
- C => Lymph nodes
- D => Liver
best Treatment of bowel cancer
best tx is to detect early and remove polyps
- surgery
- hepatic metastases drugs to control spread in liver
- radiotherapy
- chemotherapy
what are intestinal polyps
genetically inherits a tendency to form lots of polyps in the bowel, each polyp has a risk of developing a cancer therefore increase polyp number = increase risk of cancer
is small intestine polyps high risk or low risk
low risk
large intestine -> high risk
how long for polyps to progress to malignancy?
about 5 years
frequent screening is good, remove early polyps can prevent bowel cancer
what gene may increase risk of bowel cancer
o genetics p53 gene in 75% of bowel cancer patients
what gastro diseases may increase risk of bowel cancer?
o Ulcerative colitis
what diet might cause increased risk of bowel cancer?
o diet low in fibre, high in fat, low vegetables
o alcohol
where does crohns and ulcerative colitis appear?
crohns - anywhere in git but popular site is ileocaecal junction
UC - colon and rectum, always in rectum
cause of crohns
- Crohn’s could be caused by transmission of mycobacteria through milk from cattle with Johne’s disease
- Food intolerance
- persisting viral infection
- smoking
- genetics
is drinking pasteruised milk safer to prevent crohns?
no
- Ultra heat transmission kills mycobacteria, pasteurisation does not kill mycobacteria
Microscopic features of crohns
oedema
granuloma
transmural
narrowing of lumen
why is there odema in crohns?
o giant cells occupying the drainage channels and preventing fluid from draining
o fluid build up causing oedema
what disease has a cobblestone appearance?
crohns
o areas of oedema between fibrous bands causing a cobblestone appearance
can crohns appear in the mouth?
yes
- extend onto skin or perianal tissues
symptoms of crohns
if crohns in small bowel,
o pain
o malabsorption
o obstruction
if crohns in the mouth
OFG
orofacial granulomatosis vs oral crohns disease
OFG if only mouth affected
oral crohns if extension of crohns disease from other parts of git
presentation of ofg
o lip and oral swelling
o no identifiable trigger
o oedema of mouth and face
o cobblestone/ fissures
o full thickness inflammation to surface of skin from mouth
why do we need Growth monitoring for kids with OFG
, May go on to develop Crohn’s later in life, if there is failure to grow according to normal rate, failing to absorb nutrients, necessary for other investigations maybe calprotectin levels or endoscopy
which disease has continuous level of inflammation throughout the bowel?
UC
- start as the distal part and moves forward through the large intestine
- continuous level of inflammation throughout the bowel
Microscopic features of UC
VASCULAR
mucosal only, doesnt extend through the wall, superficial layers only
clinical appearance of UC
- erythema
- inflammatory change
Symptoms of UC
- diarrhoea
- abdominal pain
- rectal bleeding
Investigations for Inflammatory bowel disease
- blood tests
o anaemia
o c reactive protein
o erythrocyte sedimentation rate - faecal calprotectin
- endoscopy
- leukocyte scan
- barium studies
- bullet endoscopy
what calprotectin?
inflammatory protein secreted by epithelial cells in large or small bowel into lumen
link between UC and bowel cancer or carcinomas in general
- ulcerative colitis can develop into carcinoma
- inflammatory change present for many years
TX of Inflammatory bowel disease
- Medical (immunosuppressive drugs) both steroidal and non steroidal
- Surgical colectomy; drain abscess/ close fistulae; remove obstructed bowel segments
what steroidal drugs are used for crohns and what are used for UC
crohns -
systemic steroidal + antiinflammatory 5ASA drugs
UC -
systemic and local (topical rectal) steroidal + antiinflammatory 5ASA drugs
Non steroidal drugs for inflammatory bowel disease
NS immunosuppressant
* keeps inflammatory response under control
anti TNFa therapy
* suppress part of inflammatory process
* biological drugs
* monoclonal antibodies
* moderate to severe disease
* change quality of life
be aware of the oral lesions seen in Crohns
OFG
The detection of specific oral manifestations often preceded by painless gingival enlargement (diffuse lip and buccal mucosal swelling, oral cobblestoning, buccal sulcus ulceration and mucosal tags)
and/or unspecific or ancillary ones (cheilitis, scaly perioral erythematous rashes and frank intraoral abscess formation, labial and tongue fissuring, glossitis and aphthous stomatitis) is mandatory for the early diagnosis of intestinal Crohn’s disease.
crohns vs UC need to know
comparing location, site, serosa, clinical appearance, continuity, rectum involvement, anal fissures, vascularity, carcinoma potential etc
** transmural vs mucosa only
** discontinuous vs continuous
** rectum always involved in UC
** crohns non vascular
** UC has carcinoma potential
can a colectomy fully cure uc?
yes
