Non-Alcoholic fatty liver disease (NAFLD)

• What is Non-Alcoholic fatty liver disease?

• It is a clinical histopathological entity with evidence of hepatic steatosis, either by imaging or by histology and, by definition, occurs in patient with little or no history of alcohol consumption. The disease ranges from fat accumulation in liver cells to a necro-inflammatory component, known as non-alcoholic steatoheaptitis (NASH).

• Why do we worry about NAFLD?
• It can become Non alcoholic steatohepatitis (NASH)
• NASH is histologically indistinguishable from alcoholic steatoheaptitis, and may progress to cirrhosis in up to 20 % of patients
• NAFLD does not increase short morbidity or mortality but if it progresses to NASH, it increases chance of cirrhosis and may require liver transplant

• Who gets NAFLD?
• Anyone can get it but criteria require the person to be diagnosed to have no history of ETOH abuse 
• Other risk factors 
• central obesity 
• type 2 diabetes mellitus 
• dyslipidaemia 
• metabolic syndrome 

• What causes it?
• Unknown 

• How do you diagnose it?
• Demonstration of hepatic steatosis by imaging or biopsy 
• Exclusion of significant alcohol consumption 
• Exclusion of other causes of hepatic steatosis 
• No coexisting causes for chronic liver disease
• Other investigations to exclude other causes
• anti hepatitis C virus antibody 
• hepatitis A IgG
• Hepatitis B surface antigen 
• Plasma iron, ferritin, and total iron binding capacity 
• Serum gamma-globulin level, antinuclear antibody, anti-smooth muscle antibody, and anti-liver/kidney microsomal antibody - 1

• What is the treatment?
• Weight lose 
• lifestyle changes

Gastroenterology index page

• Giardiasis
• Gastroenterology examination video 
• Non alcohol fatty liver disease (NAFLD)
• 
  

Approach to Diarrhoea

A diagnostic approach

Probability diagnosis

• Acute:
• Gastroenteritis/infective enteritis
• Dietary indiscretion 
• Antibiotic reaction 
• Chronic
• Irritable bowel syndrome
• Drug reaction 
• Chronic infections 

Serious disorders not to be missed

• Neoplasia
• Colorectal cancer
• Ovarian cancer
• Peritoneal cancer
• HIV infection (AIDS)
• Infections
• Cholera
• Typhoid.paratyphoid
• Amoebiasis
• Malaria
• Enterohaemorrhagic E.coli enteritis
• Inflammatory bowel disease
• Crohn/ulcerative colitis
• Pseudomembranous colitis
• Intussusception 
• Pelvic appendicitis/pelvic abscess
• Acute ischaemic colitis

Pitfalls

• Coeliac disease
• Faecal impaction with spurious diarrhoea 
• Lactase deficiency 
• Giardia lamblia infection 
• Cryptosporidium infection 
• Malabsorption states
• Vitamin C and other oral drugs
• Nematode infections
• Strongyloides
• whipworm
• Radiotherapy
• Diverticulitis
• Post GIT surgery
• Ischaemic colitis 
• Rarities
• Addison disease
• Carcinoid tumours
• short bowel syndrome
• amyloidosis
• toxic shock
• Zollinger Ellison syndrome

Red flag pointers for diarrhoea 

• unexpected weight loss
• persistent/unresolved
• Fever
• Overseas travel
• Severe abdominal pain 
• Family history: bowel cancer, crohn disease

Acute gastroenteritis

Condition

• Acute Gastroenteritis

Potential causes

• Rotavirus and adenovirus
• Bacterial: C. jejuni and Salmonella sp, E. Coli and Shigella
• Protozoal: G. Lamblia, E. histolytica, Cryptosporidium 
• Food poisoning: staphylococcal toxin 

Investigation

• No investigation is usually required if < 7 days
• if > 7 days, send Stool MCS

Management

• Invariably a self-limiting problem
• No antibiotic is required
• If antibiotic is required, wait for culture

Coeliac disease

Condition

• Coeliac disease: an autoimmune condition characterised by chronic inflammation at the small intestinal mucosa caused by gluten 

History

• can present in many different ways e.g. tiredness, change of bowel habits etc
• low threshold of ordering coeliac serology for non specific symptoms e.g. fatigue, depression 
• The following is from NICE guideline, the following presentation warrants coeliac blood test

• 
  

Examination

• often normal 

Investigation

• Coeliac serology: IgA tTg, IgA EMA, IgA DGP , IgG tTg
• HLA DQ2 / HLA DQ 8: negative test essentially excludes coeliac disease
• micronutrient levels 

Management

References:

• http://www.racgp.org.au/afp/2014/october/coeliac-disease-where-are-we-in-2014/

Pseudomembranous colitis

Condition

• Pseudomembranous colitis

Clinical features

• Profuse, watery diarrhoea
• Abdominal cramping and tenesmus +/- fever
• Within 2 days of taking antibiotic (can start p to 4 to 6 weeks after usage)
• Persists 2 weeks (up to 6) after ceasing antibiotic
• Augmentin duo forte is the common culprit 

Treatment

• Metronidazole 400 mg tds for 10 days

I have seen multiple C. Diff colitis as a registrar last year. Most of the time secondary to inappropriate antibiotic prescription. For some reasons, some GPs like to prescribe augmentin duo forte as the first line antibiotic. If we follow the antibiotic guideline, there are not many conditions which requires augmenting duo forte. Ironically, the cases I saw they didn't even require antibiotic at the first place. 

** Reminder to myself: prescribe antibiotic according to the antibiotic guideline **

Irritable bowel syndrome

Condition

• Irritable bowel syndrome

History

• chronic abdominal pain 
• altered bowel motions in the absence of an organic cause
• more common in women
• can present with wide array of symptoms including gastrointestinal and extra-intestinal complaints such as tiredness, sleeping difficulties and poor concentration

Examination

• apart from mild abdominal tenderness over the sigmoid colon, which is common, abdominal examination should be normal 

Diagnostic criteria

• ROME III Criteria for the diagnosis of IBS
• 
  

Investigations

• mainly to exclude other diseases
• FBE, Iron studies, UEC, CRP, TFTs, coeliac disease 
• the presence of the following symptoms usually suggest other disease 

• 
  

Management:

• Non pharmacological treatment
• Fibre restriction 
• dietary restrictions of lactose and/or fructose or FODMAPs 
• Probiotics: bifidobacteria and combination strains containing this bacteria, have shown some benefit in reducing IBS symptoms 
• Pharmacological treatment
• Antispasmodics - peppermint oil, hyoscine and mebeverine
• Antidiarrhoeals - loperamide 
• Antibiotics - rifaximin
• Antidepressants - TCAs and SSRIs
• Psychological therapies
• CBT and psychotherapy

Approach to dysphagia

Approach to dysphagia 

Murtagh's diagnostic models 

** Excluding oropharyngeal infections and strokes**
** Although dysphagia is a common psychogenic symptom, it must always be taken seriously and investigated.**

Probability diagnosis 

• Functional 
• Tablet-induced irritation 
• Pharynotonsillitis
• Reflux oesophagitis

Serious disorders not to be missed 

• Neoplasia
• Cancer of the pharynx, oesophagus, stomach
• extrinsic tumour
• AIDS (opportunistic oesophageal infection)
• Stricture, usually benign peptic stricture
• Scleroderma
• Neurological causes:
• pseudobulbar palsy
• multiple sclerosis 
• motor neurone disease (amyotrophic sclerosis) 
• Parkinson disease

Pitfalls (often missed)

• Foreign body 
• Drugs
• Subacute thyroiditis
• Extrinsic lesion (lymph nodes, goitre)
• Upper oesophageal web (e.g. Plummer-Vinson syndrome)
• Eosinophlic oesophagitis
• Radiotherapy
• Achalasia
• Upper oesophageal spasm 
• Globus sensation 
• Rarities 
• sjogren syndrome
• aortic aneurysm
• aberrant right subclavian artery
• lead poisoning 
• cervical osteoarthritis (large osteophytes)
• other neurological causes
• other mechanical causes

Red Flag Pointers 

• Age > 50 
• Recent or sudden onset
• unexplained weight loss
• Painful swalloing 
• Progressive dysphagia 
• Dysphagia for solids 
• Hiccoughs
• Hoarseness
• Neurological symptom/signs 

Achalasia

Condition

• Achalasia 

Definition 

• failure for smooth muscle to relax, which can cause a sphincter to remain closed and fail to open when needed.

Main features

• Gradual onset of dysphagia for both liquids and solids 
• Fluctuating symptoms 

Investigations

• Diagnosis confirmed by barium swallow or manometry 

Treatment 

• Attacks are often triggered by GORD, so treatment for GORD is sometimes helpful
• Ingestion of warm water at the commencement of an attack can be helpful
• GTN spray may shorten an attack 
• If attacks are frequent and disabling, try:
• Diltiazem controlled release 180 mg orally, once daily, increasing 240 to 360 mg orally, once daily depending on response and adverse effects
• isosorbide dinitrate 10 to 20 mg orally, 3-4 times daily 
• Nifedipine controlled release 20 to 30 mg orally, once daily, increasing to 60 mg orally, once daily depending on response and adverse effects
• Refractory symptoms may require : injecting botulinum toxin type A into the lower oesophageal sphincter or myotomy of the lower oesophagus

References:

• John Murtagh's general practice 5th edition 
• eTG 

Oesophageal cancer

Condition 

• Oesophageal cancer

Definition

• Metaplasia of the squamous carcinoma to columnar epithelium 

Main features

• Dysphagia at beginning of meal 
• Dysphagia for solid food steadily progressive over weeks
• Can remain silent and tends to be invasive when diagnosed
• Hiccoughs may be an early sign
• Hoarseness and cough (upper third) 
• Discomfort or pain-throat, retrostenral, inter scapular
• Weight loss can be striking 
• Associations: GORD, tobaccco, Barrett oesophagus --> weak evidence that PPIs help to prevent development of malignancy

Investigations

• Endoscopy
• SCC (most common) and adenocarcinoma
• Adenocarcinoma associated with Barrett oesophagus (0.5% per cent per year, life time risk of less than 5%)

Treatment

• Depends on staging, most likely palliative surgery. 

References

• John Murtagh's General Practice 5th edition 

Functional dyspepsia

Condition

• Functional dyspepia 

Definitions

• Dyspepsia with normal investigations 

Main features

• heart burn 
• postprandial fullness
• early satiety 
• epigastric pain or burning 

Investigations

• Serology: FBE, UEC, LFT, Lipase and H. Pylori serology.
• Endoscopy if indicated 

Management plan

• lifestyle management 
• PPI 

References

• John murtagh's general practice 5th edition 
• eTG 

Stomach cancer

Condition

• Stomach cancer

Definitions

• Cancer develops from the lining of the stomach 

Main features

• Male to female ratio of 3:1 
• Usually asymptomatic early 
• Recent onset dyspepsia in middle age
• Dyspepsia unresponsive to treatment 
• Vague fullness or epigastric distension 
• Dysphagia
• Onset of anaemia 
• Risk factors
• Increasing age
• blood group A
• smokers
• Atrophic gastritis
• Examination findings
• conjunctival pallor 
• enlarged supraclavicular lymph node 
• epigastric mass
• Hepatomegaly - hard and irregular edge

Diagnostic triad

• Malaise + anorexia + dyspepsia + weight loss = stomach cancer
• Triple loss of appetite + weight + colour = stomach cancer

Treatment

• surgical excision 

Peptic ulcer

Condition

• Peptic ulcer 

Definitions

• a break in the lining of the stomach typically in the stomach or duodenum 

Main features

• Epigastric pain or discomfort 
• nausea
• vomiting 
• heartburn 
• nocturnal waking with epigastric pain 
• An ulcer diagnosis is more likely if there is a family history of ulcer disease or if the patient its making aspirin or another NSAID, and even more so if there is a documented past history of an ulcer

Investigations

• Office base: none 
• Pathology test: FBE, UEC, LFT, Lipase to look for anaemia and exclude other pathologies such as pancreatitis or hepatitis 
• Imaging: probably not useful but one of the surgeons I know always order one before endoscopy 
• Endoscopy provides the definite diagnosis. Biopsy can help to determine whether H. Pylori is present or not. Antibiotics within the last 4 weeks, or proton pump inhibitor therapy within the past 2 weeks, reduce the accuracy of these biopsies. 

Management 

• In uncomplicated duodenal ulcer, If H.Pylori is present, eradication. First line therapy is triple therapy. 
• Omeprazole 20 mg orally twice daily for 7 days 
• Amoxycillin 1g orally twice daily for 7 days
• Clarithromycin 500 mg twice daily for 7 days 
• If patient is hypersensitive to penicillin, metronidazole may be substitued for amoxycillin
• Omeprazole 20 mg orally twice daily for 7 days
• Metronidazole 400 mg orally twice daily for 7 days
• Clarithromycin 500 mg orally twice daily for 7 days 
• Post treatment test
• C13 or C14 urea breath test is preferred
• No antibiotics or bismuth 1 month before the test
• PPI should be suspended for at least 1 week 
• Follow up endoscopy is usually not required, exceptions are for gastric ulcer and complicated duodenal ulcers)
• For more complicated ulcers, large gastric ulcers, ulcers occurring in high risk patients or ulcers associated with NSAID use, ongoing antisecretory therapy with a PPI for about 8 weeks is appropriate.

References:

• John Murtagh 5th edition genenral practice 
• eTG

Gastro-oesophageal reflux disease

Condition: GORD

Definition:

• Extremely common 

Main features:

• Nausea
• Bloating and belching 
• Heartburn 
• Acid regurgitation, especially lying down at night 
• Water brash
• Nocturnal cough with possible asthma like symptoms 
• Diagnosis usually made on history 
• investigation usually not needed unless red flag features present

Red flag features

• Anaemia 
• Dysphagia 
• Odynophagia (painful swallowing)
• Haematemesis or melaena 
• Unexplained weight loss > 10%
• Vomiting 
• Older age > 50 years 
• Chronic NSAID use
• Severe symptoms
• Family history of upper GIT or colorectal cancer
• short history of symptoms 

Investigations

• Gastroscopy (around 2/3 patients have normal gastroscopy)

Murtagh's diagnostic triad

Management plan:

• If mild intermittent symptom (no more than once per week), trial of lifestyle management first:
• weight reduction 
• eating smaller meals 
• drinking most fluid between meals rather than with them
• avoiding lying down after eating 
• avoid eating or drinking 2 to 3 hours before bedtime or vigorous exercise
• elevating the bedhead
• losing weight 
• Stopping smoking 
• Decreasing alcohol consumption 
• Pharmacological intervention 
• MgOH + Aluminium hydroxider preparations 10 to 20 ml orally 
• antacid plus alginate prepartions 10 to 20 ml orally 
• A histamine h2 receptor antagonist e.g. ranitidine 150 mg once or twice daily 
• PPI 
• Fail to respond to PPI after 8 weeks warrants further investigation
• If moderate to severe symptoms (twice or more per week) --> start on PPI
• Maintenance therapy
• try stopping PPI (30% of people have prolonged remission of symptoms)
• step down to the lowest dose possible 
• NPS has an educational module on how to stop PPIs. 
• PPIs are fairly safe to use but the safety profile in long term use is uncertain. Some potential side effects associated with long term use include: fracture, increase enterc infection, vitamin b12 deficieny, iron and magnesium deficiency and pneumonia. (Please see reference 3) 

References:

• John Murtagh's general practice 5th edition 
• eTG 
• http://www.nps.org.au/publications/health-professional/medicinewise-news/2015/proton-pump-inhibitors

Approach to dyspepsia

Dyspepsia

** Consider heartburn as ischaemic heart disease until proved otherwise **

Murtagh's diagnostic model

Probability diagnosis

• Irritable upper GIT (functional dyspepsia)
• Gastro-oesophageal reflux
• Oeosphageal motility disorder (dysmotility)

Serious disorders not to be missed

• Neoplasia: stomach, pancreas, oesophagus
• Cardiovascular: ischaemic heart disease and congestive cardiac failure
• Pancreatitis
• Peptic ulcer 

Pitfalls 

• Myocardial ischaemia
• Food allergy (e.g. lactose intolerance)
• Pregnancy (early)
• Biliary motility disorder
• Other gall bladder disease
• Post vagotomy
• Duodenitis
• Rarities
• Hyperparathyroidism
• Mesenteric ischaemia
• Zollinger - Ellison syndrome
• Kidney failure
• Scleroderma

Stomach cancer

Condition	Stomach cancer
Demographics	M: F 3:1 Risk factors: increase age, blood group A, smoking, atrophic gastritis
Murtagh Triad	Malaise + anorexia + dyspepsia + weight loss = stomach cancer Triple loss of appetite + weight + colour = stomach cancer
History features	Weight loss New symptoms > 40 years old  dyspepsia unresponsive to treatment  anorexia, nausea+/- vomiting  Dysphagia - late sign  Onset of anaemia
Examination	Epigastric mass Hepatomegaly - hard and irregular  Anaemia  Enlarged supraclavicular lymph node
Investigations	Gastroscopy
Management	Surgical excision  Chemotherapy  Usually poor prognosis

GORD in infants

I have seen multiple infants presented with "reflux". In fact, their symptoms are inconsolable crying. (Irritable, wake up from their sleeps.) They often presented with young worrying parents. Maternal child health nurses often come up with different diagnoses to explain crying babies e.g. UTI, reflux, cow's milk protein allergy. Their favourite ones seem to be reflux. It is very easy just to prescribe the parents a PPI and send them home. I have done it before when I cannot be bothered arguing with the parents but it is not the right thing to do and I will not do it again.

Key points on how to approach the situation:

1. Explained GOR is normal. Everyone gets reflux, including adults, we all get reflux on average 3 times per day.

2. Reflux rarely causes crying.

3. GORD is the complication of GOR which includes oesophagitis, failure to thrive and aspiration. Make sure check their weight and height.

4. The symptoms of GORD are vomiting with:

• pronounced irritability and arching
• refusal to feed
• weight loss or crossing centimes
• haematemesis 
• chronic cough, wheeze 
• apnoeas

5. Don't suggest changing of formula 

6. It is normal for babies to cry. Make sure mum is ok. Encourage symptom diary. (RCH symptom diary)

7. Try 5s to console a crying baby:

- swaddling- firm clothing, not too loose

- lie baby on side or stomach (only on awake baby with parents present)

- Shush

- Swing - sway them from side to side

- Suckling

8. If you think it is reflux, refer them to paediatrician and start them on PPI. 

References:

- Royal children's hospital guideline
- John Murtagh 8th edition

Hepatitis C

Hepatitis C

key features:

1. Hepatitis C virus is responsible for most cases of viral hepatitis in Australia. 
2. 25% of people will clear Hepatitis C virus spontaneously
3. there are at least 6 major genotypes of HCV and treatment decisions are based n the genotype
4. Diagnosis and progress:
1. HCV Ab (Anti HCV) +ve = exposure (current or past)
2. HCV RNA + ve = chronic viraemia, -ve spontaneous clearance
3. HCV/CD4= Viral load
4. ALTs on LFTs indicate disease activity (tested 3 times over 6 months)
5. ALTs persistently normal = good prognosis
6. ALT increases = referral for treatment
7. If PCR +ve + significant viral load + ALT increases perform HCV genotype - determines treatment
5. current treatment is ribavirin orally daily and pegylated alpha-interferon. At present the determination of the genotype and the viral load will identify those groups most likely to respond to therapy. e.g. genotype 1 will have a good response, genotype 2 and 3 have excellent response
6. Patients with hepatitis c should be tested for hepatitis A and B 
7. They should avoid ETOH
8. Factors associated with faster disease progression include significant ETOH ingestion, co-infection with hepatitis B or HIV, age over 40 years at acquisition, marijuana use and obesity
9. Those at increased risk of having hepatitis c
1. Blood transfusion recipients (prior to HBV and HCV)
2. Intravenous drug users 
3. Male homosexuals who have practised unsafe sex
4. kidney dialysis patients
5. sex industry workers
6. those with abnormal LFTs with no obvious cause
7. Tattooed people/body piercing
10. Advice to those who are positive for HCV
1. Do not donate blood or any body organs or tissues
2. Do not share needles
3. Advise health care workers, including your dentist
4. Do not share intimate equipment such as tooth brushes, razors, nail files and nail scissors
5. Wipe up blood spills in the home with household bleach
6. Cover up cuts or wounds with an adequate dressing
7. Dispose of blood stained tissue, sanitary napkins and other dressings safely
8. Use safe sex practices such as condoms 
9. Avoid tattooing
10. 
11. 
12. 
13. 
14. 

Coeliac disease

I think I may have made my first diagnosis of coeliac disease in a child of 14 year old. Her presentation was atypical. She saw me for something unrelated and when I was about to conclude the consultation. Mum told me that school wants her daughter to have a mental health assessment. Upon further questioning, Mary has not been going to school. She feels tired all the time and she cannot wake up in the morning. She has a normal examination. Her weight and height are appropriate for her age. Blood tests revealed iron deficiency and positive IgA tTG and IgG to deaminated glaidin.


Key points:

- It is common, affects 1% of the population.
- It is very easy to miss as it can present atypically.
- IgA transglutaminas and IgG deaminated glaiden are the current recommendation for coeliac disease investigations
- HLA DQ2 and HLA DQ8 are present in 99% of people with coeliac disease but they are also present in 50% of the populations. Patients who don't have the above genes, can't have coeliac disease.
- The golden diagnosis is small bowel biopsy
- It is associated with other autoimmune conditions
- Management is lifelong gluten free diet. It can cause complications such as malnutrition. Need to refer to dietitian. Don't forget some medications have gluten in it too !
-

References:
- Common sense pathology: https://www.rcpa.edu.au/getattachment/5f4e8920-65cb-4ec1-8a66-29c7887f336f/Celiac-Diseases.aspx

H. Pylori

H. Pylori 

Key features: 

1. H. pylori is a gram negative bacillus that has naturally colonised the human stomach for at least 50,000 years. Usually acquired in childhood, it colonises the gastric mucosa of about 50% of the world’s population at some time in their life. 
2. Infection with H. pylori induces a persistent immune response. Because the organism has numerous adaptions to prevent immune detection, clearance by the body is never complete. The resulting sustained inflammatory processes in the stomach cause a reduction in the population of somatostatin-producing D cells. This causes a subsequent rise in gastrin secretion followed by an increase in gastric acid release which may lead to peptic ulceration in some patients. 
3. Most patients colonised with H. Pylori do not develop peptic ulcers. 
4. It would not be appropriate to investigate for H. pylori initially in the presence of alarm symptoms such as weight loss, bleeding, dysphagia or symptoms in a patient above the age of 55 years. In this context, investigations should first be directed at excluding malignancy, for example with a gastroscopy.
5. Current Therapeutic Guidelines in Australia, revised in July 2013, recommend PPI-based triple therapy as the first line measure for eradication of H.pylori. (Esomeprazole 20 mg twice daily, amoxicillin 1 g twice daily and clarithromycin 500 mg twice daily)
6. The conclusion to be drawn from the Swedish study is that in all traditionally prescribed regimens, eradication is only partially successful. 

Reference:

http://www.racgp.org.au/afp/2014/may/helicobacter-pylori-eradication/