Curriculum for Specialty Certificate Examination in Gastroenterology

Countdown to the Examination

Saturday 26 November 2016

Complications of polypectomy: Bleeding 1

Most frequent complication. 
Primary: Usually immediately visible.
Secondary: delayed.

Immediate haemorrhage:
Usually a slow ooze , can be arterial spurt.
Treat immediately.
Re-snare / endo-loop the remaining stalk.
If bleeding recurs try clip/ electrocoagulation. 
Selective arterial catheterization and embolization.

Secondary haemorrhage:
Up to 14 days after polypectomy.
Usually After the removal of large-stalked polyps. 
Hot biopsy, over-large polyps. 
Transfusion may occasionally be required

Sunday 24 August 2014

Schatzki ring

Schatzki ring, My Gastro room
The pathogenesis of Schatzki rings is not clear, and at least 4 hypotheses have been proposed. These hypotheses may not be mutually exclusive. Proposed hypotheses are as follows:
  1. The ring is a pleat of redundant mucosa that forms when the esophagus shortens transiently or permanently for unknown reasons.
  2. The ring is congenital in origin.
  3. The ring    actually a short peptic stricture occurring as a consequence of gastroesophageal reflux disease.
  4. The ring is a consequence of pill-induced esophagitis.
Schatzki ring is quite common and may be found in as many as 15% of all patients undergoing barium swallow studies; however, few of these patients exhibit any symptoms of dysphagia.
Most patients present with intermittent, episodic, nonprogressive dysphagia to solids. Dysphagia to liquids is usually not present.
Using a large French mercury bougie, polyvinyl bougie, or a balloon, esophageal dilatation is used with the intention of fracturing the ring—not merely stretching it.

Tuesday 22 April 2014

Hepatitis C viral infection: Questions and comments

1-a 34 year old man with hepatitis C attended for review after treatment for 12 weeks with peginterferon and ribavirin co-therapy. He complained of lethargy and SOB on exertion. I vestigation prior to treatment confirmed genotype 1 and a viral load of 1.3 x 10 to 6 with no evidence of cirrhosis.

Investigations:
Hb 10
Plt 65
neutrophils 0.8
LFT normal
U&E normal

what is most approperiate next step in management?
1-continue same treatment

2-Blood transfusion

3-reduce peginterferon

4-reduce ribavirin

5-stop treatment

During the treatment of HCV infection, assess for side effects at week 1,2,4 and then 4-8 weekly.
Ribavirin can cause anaemia.
Action: reduce dose, consider transfusion if Hb less than 10

Peg-interferon alfa can cause:
flu-like symptoms,usually subside in few weeks
neutropenia nad thrombocytopenia
consider dose reduction if neutrophills less than 0.75, Plts less than 50

other side effects includes: depression, irritability, sleeping disorders

stop treatment if hepatitis flare up ALT > 10 time ULN or severe bacterial infection.


Question, what is the diagnosis?

A 31 year old male had one episode of unprotected sex whilst in holiday 3 month ago. two month later he developed lethargy, fletting artheralgia and night sweats. He also complained of severe pain in the right hypochondrail area which radiate into the right testicle.his GP had recently started him on antidepressants. there is no history of diarrhoea or dysurea.six years previously he was treated for genital herpes simplex infection.
On examination he was febrile. there was no lymphadenopathy.he joints appeared normal. abdominal examination revealed a palpable liver edge and spleen. there was evidence of right epdidimorchitis.

Hb             13
WCC             5
Plt             230
AST             60
ALT             80
ALP             60
Bili             70

Urethral swap: no evidence of chlamydia or gonococcus

What is the diagnosis?

1)    HIV seroconversion
2)    Whipple’s disease
3)    Reiter’s disease
4)    Brucellosis

5)    Lymphoma

Bacterial causes of food poisoning


Organism
Source/vehicles
Incubation period
Symptoms
Diagnosis
Recovery
Staphylococcus aureus
Man - contaminated food and water
2-4 h
Diarrhoea, vomiting and dehydration
Culture organism in vomitus or remaining food
< 24 h
E. coli
Salads, water, ice
24 h
Watery diarrhoea
Stool culture
1-4 days
E. coli O157:H7
Cattle - meat, milk
12-48 h
Watery diarrhoea ± haemorrhagic colitis, HUS
Stool culture
10-12 days
Yersinia enterocolitica
Milk, pork
2-14 h
Abdominal pain, vomiting, diarrhoea
Stool culture
2-30 days
Bacillus cereus
Environment - rice, ice-cream, chicken
1-6 h
6-14 h
Vomiting

Culture organism in faeces and food
Rapid
Clostridium perfringens
Environment - contaminated food
8-22 h
Watery diarrhoea and cramping pain
Culture organism in faeces and food
2-3 days
Listeria monocytogenes
Environment - milk, raw vegetables dairy products, unpasteurized cheese
?
Colic, diarrhoea and vomiting
Stool culture
?
Vibrio parahaemolyticus
Seafood
2-48 h
Diarrhoea, vomiting
Stool, food
2-10 days
Clostridium botulinum
Environment - bottled or canned food
18-24 h
Brief diarrhoea and paralysis due to neuromuscular blockade
Demonstrate toxin in food or faeces
10-14 days
Salmonella spp.
Cattle and poultry - eggs, meat
12-48 h
Abrupt diarrhoea, fever and vomiting
Stool culture
Usually 3-6 days, but may be up to 2 weeks
Campylobacter jejuni
Cattle and poultry - meat, milk
48-96 h
Diarrhoea ± blood, fever, malaise and abdominal pain
Stool culture
3-5 days
Shigella spp.
Man - contaminated food and water
24-48 h
Acute watery, bloody diarrhoea
Stool culture
7-10 days

infectious diarrhea

Bloody diarrhoea:

1)    shigella
Basillary dysentery
IP 2-3 days
Oro-feacal
C/F:
Bloody diarrhoea
Sudden fever
Abd pain

Stool microscopy: no trophoziote
Association: spondyloartheritis
Treatment; cipro

2)    Amaebiasis
Amaebic dysentery
IP 1-4 weeks
Oro-feacal
C/F:
abd pain
diarrhoea ,start slowly ,then become perfuse and bloody

stool microscopy;trophozoite
treatment: metronidazole
diloxamide for chronic disease
   
3)    salmonella
IP 12-48 hrs
Gm –ve bacilli
Egg, meat and poultry
C/F:
Bloody diarrhoea
Abd pain
Vomiting
Local infection

Treatment: cipro

4)    compylobactor
IP 2-5 days
Gm –ve rods
C/F:
Severe abd pain (may mimic acute abdomen)
Bloody diarrhoea

Non bloody diarrhoea:

Giardiasis:
IP 1-4 weeks
Flagellate protozoa
Colonize duodenum and jejunum
C/F
Explosive diarrhoea
Offensive
Bloating



Monday 21 April 2014

what is your diagnosis?

A 62 years oled male presented with severe chest pain and hypotension after vomiting.


Ct shows bilateral pleural effusion and pneumomediastinum to the aorta and to the right of the oesophagus. Subsequent CT with oral contrast shows dense contrast in the oesophagus (arrow) and leakage into the irregular complex right mediastinal collection.

The diagnosis is Boerhaave syndrome.

Spontaneous rupture of the oesophagus during vomiting.
May follow alcohol ingestion or lage meal.
Rupture typically located at the left subdiaphragmatic portion of the oesophagus.
Classical presentation: Mackler traid:
-Vomiting
-Severe chest pain
-Subcutaneous emphysema

Ménétrier's disease

A rare disease that has a bimodal age distribution.  
The childhood form, more common in boys, is linked to CMV infection and o en resolves spontaneously, unlike the adult form.
The adult form, also more common in males, is thought to involve improper regulation of the epidermal growth factor receptor signaling pathway. 
Marked gastric mucosal hypertrophy secondary to hyperplasia of superficial mucosal epithelial cells leads to the characteristic large lobulated gastric folds. 
Giant rugal folds are most prominent along the greater curvature and tend to spare the antrum and cardia. 
Albumin loss across the gastric mucosa occurs at a high rate and is not only responsible for the clinical manifestation of peripheral edema, but also for intravascular hypovolemia which may account for the increased incidence of thrombotic events in the disease. 

Sunday 20 April 2014

Wernicke encephalopathy

Result from Thiamine (vitamin B-1) deficiency 
Characteristically associated with chronic alcoholism, because it affects thiamine uptake and utilization. However, may develop in nonalcoholic conditions, such as prolonged starvation, hyperemesis gravidarum, bariatric surgery, and HIV.

Triad of Wernicke encephalopathy are: 
1-Encephalopathy: profound disorientation, indifference, and inattentiveness
2-Ataxic gait:combination of polyneuropathy, cerebellar involvement, and vestibular dysfunction
3-Oculomotor dysfunction:Nystagmus is the most common finding and is typically evoked by horizontal gaze to both sides

All 3 features of the triad are recognized in only about one third of cases.

Other features: long-term alcohol abuse and/or malnutrition and any of the following: 
-acute confusion, 
-ataxia, 
-ophthalmoplegia, 
-memory disturbance, 
-hypothermia with hypotension.
-delirium tremens.

A high proportion of patients with acute Wernicke encephalopathy who survive develop Korsakoff psychosis, characterized by:
-potentially irreversible retrograde amnesia 
-anterograde amnesia (inability to assimilate new information)
-confabulation
-Hallucination ( visual/auditory)
-varying degrees of other cognitive deficits

Diagnosis:
Clinical, however tests to exclude other causes.

FBC
Blood glucose
Toxocology screen
Erythrocyte transketolase activity assay
Blood pyruvate and lactate measurements

MRI: not usually required. mamilary body haemorrhage and atropy.

Treatment:
Thiamine until the patient resumes a normal diet.
Empirical parenteral magnesium sulfate

Wernicke's encephalopathy may be precipitated by administration of intravenous glucose solutions to individuals with thiamine deficiency. In susceptible individuals glucose administration should be preceded or accompanied by thiamine 100 mg IV.
Thiamine supplementation, along with other multivitamin supplementation, is recommended for patients at risk for thiamine deficiency. 

Budd–Chiari Syndrome BCS

Hepatic vein obstruction/thrombosis
Caused by:
heamtological disorders
Anti-phospholipid sydrome
Malignancy/ HCC/leukemia
OCP

C/F:
Abd pain
Tender hepatomegaly/ caudate lope enlargement
Acites

Diagnosis:
Hepatic vengram/ doppler USS
Asitic tap: exudate SAAG less than 11 g/L (protein more than 25 g/L)
Liver Bx diagnostic

Treatment:
Underlying cause
Anticoagulant
Surgical: TIPS/Tx

 

Consider BCS if:
Picture of cirrhosis but no obvious cause + reason for hypercoagulable state
Acute hepatitis with ascites
Abnormal LFT with liver Bx showing centrilobular congestion with or with fibrosis
Acute presentation in female on OCP