Gastro Flashcards
Discuss oropharyngeal dysphagia
Neuromuscular disease causes approximatly 80% of cases of oropharyngeal dysphagia with the other being caused by localized structural lesions
Describe UC
UC causes inflammation and ulceration throughout the colon rectum but spares the small intestine.
Inflammation is more superficial than Chrons.
Typically the inflammation exists as one continous lesions originating in the rectum and extending a variable distance into the colon.
Inflammatory arthropathies and primary sclerosing cholangitis are the most common extra-intestinal manifestations of UC.
Describe Chron’s disease
May affect any part of the GIT usually the distal small intestine and proximal colon and less commonly the oesophagus duodenum or stomach.
Due to the transmural inflammation the development of intestinal strictures abscesses or fistulae to adjacent organs are protentional complications
Extraintestinal manifestation occur more frequently than UC and include
- uveitis
- arthritis
- apthous stomatitis
- erythema nodosum
- ank spondylarthropathy .
Discuss clinical features of IBP
Typical presenting complaints in patients with IBD include abdominal pain and tenesmus with bloody diarrhoea
Patient with CD may have a history of nocturnal diarrhoea which helps differentiate CD from patients who have IBS
Patient with CD may have fissures, ulcerated haemorrhoids, stricutres or cutaneous abscessess around the anus. Onset of symptoms usually occurs before the age of 30.
Common compliactiosn of IBD include the formation of fistulae strictures and abcesss,
Less common but life threatening includ fulminant colitis, toxic megacolon and intestinal perforation.
Discuss or list extraintestinal manifestations of IBD
SKin
- erythema nodosum
- pyoderma gangrenosum
Eyes
- uveitis
- episcleritis
- scleritis
Joints
- arthritis
- sacroiliitis
Bone
-Osteoporosisii
SPine
-ank spondyliti
Liver
-primary sclerosing cholangitis
Thromboembolic events are overlooked and under-diagnosed - there is a 60% increase in thromboembolic disease compared to general population.
Central venous thrombosis is also more common
Discuss IX ibd
Endoscopic evaluation with biopsy is required to confrim the diagnosis.
CRP and or ESR
New patient should have infective gastro excluded and have micro for
- ecoli 0157:H7
- c-diff
- amoeba
CT for complications or MRI
Discuss management of IBD
Medical treatment is the mainstay
- aminosalicylates 5-ASA
- steroids for flairs
Surgery for complications
Supportive cares
Discuss toxic megacolon
Is total or segmental nonobstructive colonic dilations that occurs in the contest of systemic toxicity
Most commonly considered a complciation of IBD especially UC most inflammatory or infectious conditions of the colon can lead to the dilation
Discuss causes of toxic megacolon
Inflammatory
- UC
- CD
Infections Bacterial -clostridioides diccicile -salmonella -shigella -campylobacter Viral -CMZ
Discuss risk factors for the development of toxic megacolon
Metabolic/electrolyte
-hypokalaemia
Drugs
- antimotility agents
- opiates
- anticholinergics
- antidepressants
- abrupt cessation of steroids
- barium enemas
- bowel prep
Discuss imaging for toxic megacolon
> 6cm dilation in the large bowel
Discuss radiation proctocolitis
Common side effect to radiation
Radiation dose is the major determinant of the severity of acute and late toxicity.
The disease has two distinct presentations acute and chronic.
Acute
- during or shortly after a course of radiation therapy typically within 6 weeks is usually easily diagnosed and is slef limiting
Chronic
-begins any time after the end of radiation which can make the diagnosis challenging.
Describe acute radiation proctocolitis
The intestinal epithelium normally is sloguhed and replaced at a rapide rate.
After the start of radiation growth of replacement epitherlium is slowed but sloughing continues at the pre-exposure rate.
This mismatch lead to gaps in the epithelium which over time coalese into ulcerations. In addition oedema and inflammatory changes of the submucosa cause excessive mucous secretion and bleeding.
After radiation ceases the cycle of damage stops and healing occurs over the next few weeks
Discuss chronic radiation prctocolitis
Due to progressive endarteritis with abnormal tissue collagen deposition. The affected intestine ahs a decreased microvascular density with subsequent decreased perfusions. Over time the affected bowel gradually becomes more ishcaemic leading to ulceration scarring and narrowing of the bowel lumen.
Discuss clinical features of radiation proctocolitis
Abdominal and rectal pain
Diarrhoea
Bleeding
Tenesmus
Chronic RP has a more insidious onset with a variety of presentations including ulcerative disease stricture, obstruction, fistulae and bowel perf. Bleeding is common but is not usually HD signifiacnt
Discuss management of radiation proctocolitis
Measures to improve nutritional status should be considered.
Steroid enemas to reduce infllamtion
Describe oropharyngeal dysphagia
Neuromuscular disease causes approximately 80% of cases of oropharyngeal dysphagia, with most remaining causes being localized structural lesions.
Liquid especially at extremes of temperature are more common the cause than solids.
CVA causing pharyngeal weakness and failure of the cricopharyngeus muscle to relax are the most common cause of neuromuscular dysphagia.
The second most common cause of neuromuscular dysphagia is inflammtoray myopathy such as polymyositis or dermatomyositis.
Myasthenia gravis is an important cuase of oropharyngeal dysphagia. At least 40% of myasthenia patients have some dysphagia and it is the presenting complaint in 15% of cases.
Describe oesophageal dysphagia
Cause by mechanical lesions or motility disorders. Mechanical lesions may be extrinsic or intrinsic. Instrinsic causes include -strictures -webs -rings -tumours -oesophagitis -postsurgical changes -oesophageal foreign bodies Extrinsic lesions include -osteophytes -mediastinal masses -aortic aneurysms
Motor causes include
- achalasia - marked increase LES tone and absence of peristalsis in the middle portion of the oeosphagus
- diffuse oeosphageal spasm
- hypertensive lower oesophageal sphincter
Systemic connective tissue disease may cause secondary motor dysfucntion
- CREST
- Scleroderma
- paraneoplastic disorder
Briefly describe clinical features of oropharyngeal dysphagia
Characterized by
- inability or excessive dealy in initiation of swallowing
- aspiration
- nasopharyngeal regurgitation
- residual ingestate within the pharyngeal cavity following a swalloing event
Toungue weakness can result in oral regurg
Inability to seal the nasopharynx becuase of obstruction or muscular weaknesscan cause nasal regurgitation.
List the four most common places for FB to be lodged
1) cricopharyngeus muscle (upper oesophageal sphincter)
2) aortic arch
3) left mainstem bronchus
4) LES
Discuss IX of FB
Plane AP and lateral x-rays of the neck, chest and abdomen.
Flat objects in the oesophagus such as coins or button batteries typically orient in the coronal plane and appear as a circular object on an AP
Double density can indicate a button battery
List reasons for urgent endoscopy
- Large or sharp objects
- button batteries
- coins lodged in the proximal oeosphagus
- impactions that impairs the handling of secretions
- Food bolus causing high grade obstruction
List complications of prolonged FB
- Perforation
- aortoenteric fistula
- tracheooesophageal fistula
- Abscess
Discuss management of lower oeosphageal FB
Historically administration of glucagon IV 1-2mg has been thought to cause enough relaxation of the LES to allow passage of a food boluls. This has not been the case in studies and it can increase vomiting which places the patient at increased risk of perforation
List object that have passed into the stomach that still require removal via endoscopy
- Larger than 5cm or wider than 2.5cm in diameter rarely pass through the duodenum.
- All sharp and pointed FB (toothpicks/razers) should be removed prior to passing to reduce risk of perforation
Describe Eosinphilic oeophagitis
Results from eosinophilic infiltration within the oeophageal mucosa or deeper tissues. The cause is unknown although there is an associated with food allergens especially in the younger age group. More than 50% of patients have associaed atopy.
The criteria for diagnosis is
1) clinical symptoms of eosophageal dysfucntion
2) more than 15 eosinophils in one high powered field
3) lack of responsiveness to high dose PPI
Most common symptoms is solid food dysphagia in addition, nasuea and vomiting, food impaction and GORD can be present.
If untreated 40% develop strictures – referral to gastro - ?topical steroids
Describe infectious oesophagitis
Primarily seen in immunocompromised hosts. Candida is the most common oesophageal pathogen. HIV is a risk factors but rate have decreased since the advent of HARRT
As empierical antifungal prophylaxis in immunosuppressed states has become more common viral oeophgatitis has become more prominents. HSV and CMV are the most common viral pathogens.
Usually causes severe odynophagia. Dysphagai of solids and liquids is present. Pain may be so severe that the patients refuses to eat or drink.
Treatment of true candidial oeophagitis should be with fluconazole 400mg loading and than 100-400 Dailey for 2-4 weeks
List risk factors for GORD
Decreased LES pressure
- anticholinergic drugs
- benzo
- caffiene
- Ca blockers
- chocolate
- oestrogen
- ethanol
- Fatty foods
Decreased Oeophgeal motility
- Achalasia
- DM
- scleroderma
Increased Gastric emptying time
- Anticholinergic drugs
- dibaetic gastroparesis
- gastric outlet obstruction
Discuss PUD
The most common cause of gastritis is infection with H.Pylori.
H.Pylori is believed to cause mucosal inflammation that disrupts the normal defence mechanisms and leads to ulceration. It also increase the risk of gastric cancer
Suppurative gastritis also known as acute phlemonous gastritis is a rare and often fatal disease that results from acute bacterial infection. Strep are involved in nearly 75% of all cases
Use of aspirin and other NSAIDS is the second most common cause of PUD. The cause of NSAID related ulcers is the suppression of gastric prostaglandin synthesis.
Only 1% of cases of PUD are caused by acid hyper-secretion. Zollinger-Ellison syndrome is an acide hypersecretion syndrome caused by increased levels o circulating gastrin from gastrin secreting tumors.
Symptoms that awaken a patient between midnight and 3am are classic for PUD as most people gastric output is highest at about 2 am
Discuss complications of PUD
1) Haemorrhage
- ulceration into an artery can lead to life threatening haemorrhage.
2) perforation
- 2-10% of PUD patients experience a perforation
- duodenal ulcers account for 60% of cases , followed by antral (20%) and than gastric body (20%)
3) penetration
- Ulcer erodes into another organ (liver or pancreas)
4) gastric outlet obsturction
- result of oedema and scarring near the gastroduodenal junction
Discuss management of PUD
1) Antacids
- consider for symptomatic relief
2) Histamine blockers
- H2 receptor antagonist reduce the volume of gastric juice
3) PPI
4) Eradications of H.yplori
- 20mg of esompeprazole BD for 7 days
- Amoxicillin 1g BD for 7 days
- Clarithromycin 500mg orally BD for 7 days
Describe gastric volvulus
Rare cause of severe abdominal pain that occurs when the stomach rotates on itself more than 180 degrees creating a closed loop obstruction.
The stomach is fixed at only 2 points the oesophagocardiac junction and the pylorus.
Primary volvulus occurs when the stabilizing ligaments are too lax or are congenitally abnormal in such a way that the stomach is able to twist on itself
Secondary occur oin patients with diaphragmatic defects such as
- eleavated diaphragm
- paraoeophageal hiatus hernia,
- gastric ulcer or carcinoma
- abdominal adhesions.
Discuss clinical features and complications of gastric volvulus
Sudden onset severe abdominal pain. Borchardt's triad 1)Severe epigastrci pain 2) vomiting followed by violent non productive retching 3) inability to pass a NGT
Complications
- Gastric ischaemia
- perforation
- death
