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

Digoxin toxicity presentations

I came across a patient few days ago, 80 year old M with CCF on digoxin presented with an episode of sudden onset of dizziness lasting for around 3-4 minutes. The patient worried about digoxin toxicity. I used this opportunity to remind myself on the signs and symptoms of digoxin toxicity.

We can divide digoxin toxicity into acute or chronic:

Acute:
- GI: anorexin, vomiting, nausea, diarrhoea and abdominal pain
- Metabolic: hyperkalaemia (early sign of significant toxicity)
- CNS: enhanced automaticity with AV block, VF, VT, ventricular ectopic beats, bradyarrhythmias, hypotension and shock
- CNS: lethargy and confusion

Chronic digoxin toxicity:

Other features of chronic toxicity commonly described in textbooks are visual disturbances (e.g. reduce acuity, yellow halos (xanthopsia) and altered color perception (chromatopsia)}

Reference:

http://lifeinthefastlane.com/ccc/digoxin-toxicity/

Hepatitis B serology interpretation

I have struggled with Hepatitis B serology interpretation for a long time. I am trying to learn it properly for the exam, and also it is a common infection. In Australia, around 1 % of the population has Hepatitis B.

Key point:

- We are testing for 2 things here. One is antibody and one is antigen.

- Diagnostic test: To diagnose Hepatitis B. Only need to order 3 tests.

1. Hepatitis B surface Antigen: The presence of Hepatitis B surface antigen indicates infection.
2. Hepatitis B core antibody: The presence of antibodies to Hepatitis B core antibody indicates past infection or current infection. 
3. Hepatitis B surface antibody: present after vaccination and resolved infection.

- The following is a table which summarises the interpretation of the test results:

- How I remember this is that I remember HbsAg as a thief, anti-HBc as a security guard and anti-HBs as the policeman. HBsAg means the thief is in the shop and it means infection. When the thief is caught by the security guard (anti-HBc), the problem is still not solved completely until the policeman arrives (anti-HBs). If the policeman is there (anti HBs), no thief will come in and indicates immunity.

- Markers of hepatitis B virus infection : HBV antigens and host antibodies, HBV DNA and genotype, biochemical markers, and the degree of hepatic fibrosis and inflammation. 

- HBeAg: it promotes persistent infection 

- Antibody to e-antigen: not a protective antibody but its presence indicates better immunological control.

- HBV DNA

- ALT: indications for liver damage. Recent studies have shown that normal range of ALTs are <30 in men and < 19 in women 

- The following picture summarises the 4 phases to treatment decisions

- Immune tolerance: The immune tolerance phase is characterised by hepatitis B e antigen (HBeAg) positivity, high HBV DNA levels (>20,000 IU/mL, and commonly over 1 million IU/mL), normal ALT levels and minimal level liver injury. During this phase, which may persist for decades, liver inflammation or fibrosis is either absent or minimal. This phase is associated with a low risk of progression to advanced liver disease, and it is thought to occur most commonly in those who acquire the infection vertically from HBeAg-positive mothers. 

- Immune clearance phase: the immune clearance phase is also called the immune competent or active phase. The liver injury in HBV is determined by the immune response to the virus. The host's immune system recognises the HBV as foreign, and mounts a cytotoxic response to infected hepatocytes. This phase is characterised by fluctuating HBV DNA and ALT levels. Recurrent bouts of active inflammation and , eventually, fibrosis can occur int he liver following these repeated immune 

Mediated attacks. An important outcome of this phase is the seroconversion of HBeAg to anti-heb, which is associated with a lower level of viraemia. The observed rate of clearance of HBeAg in those with or without elevated ALT levels averages 8%-12% per year. However, a number of people will still develop active liver disease after HBeAg seroconversion, generally owing to immune escpape; that is, emergency of HBV mutant variants, particularly the core or preacher mutation that renders the virus unable to encode for HBeAg.

Reference:

Hepatitis B for GP

seborrhoeic dermatitis

I saw a lady with seborrhoeic dermatitis today. Her persentation is very similar to the following photo:

I thought it is almost time to review the treatment of seborrhoea dermatitis.

1. Cause: unknown. Malassezia is an aetiology factor, hence, the use of anti fungal.
2. Infantile seborrhoeic dermatitis and adult seborrhoea dermatitis are two different conditions.

3. Scalp seborrhoeic dermatitis: treat with anti fungal shampoo or steroid lotion (apply on wet hair and leave overnight and wash it off in the morning)

4. Facial, flexural and scrotal seborrhoeic dermatitis

• Cleansed the skin thoroughly using non soap cleanser daily 
• Apply ketoconazole cream once daily for 2 to 4 weeks 
• Hydrocortisone cream can be used, apply twice daily for 1 - 2 weeks 
• LPC and Tar can be used instead of steroid. 

5. Finally just to remind myself of different classes of topical steroid:

References:

1. Australian therapeutic guideline: dermatology

2. Dermnet

Give me the money!!!!

I love money. Who doesn't? I whinge all the time about how poor I am. Single income, mortgage, a baby on the way, university debt, cars to pay off etc. But the statistics I came across today just reminded about how lucky I am:

Key features:

1. Have $ 2200 (asset not cash) place you on the top 50% of the wealthiest people on earth.

2. If you earn more than $ 50,000 annually, you are in the top 1% of the world's income earners.

3. If you have more than $ 500,000 in assets, you are part of the richest 1% of the world.

For those who live in Australia, the full time weekly earnings for an adult is around $1484.50. So if you earn more than this per week, congratulations! You are earning above average.

  

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. 

Q fever - What is it?

Key points:

- Q fever is a zoonosis caused by Coxiella Burnetii. Usually found in farm animals: cow, sheep and goats but also present in other animals such as dogs, cats, camels and lama.
- People who work closely with animals are at risk. More common in rural area.
- Q fever is difficult to diagnosis because symptoms are non-specific and similar to a common cold.
- Diagnosis is made by serology.
- People at risk should be vaccinated.
- Q fever usually resolves in 2 weeks without any treatment. If diagnosis is made early, doxycycline 100mg x 2 weeks is the drug of choice. In pregnant women, use trimethoprim + sulfamethoxazole 12 hrly.
- Post infection, some people may develop fatigue symptoms for the next few months.
- Vaccination is one single subcutaneous dose. A serological and a skin test (comes with the vaccine) must be performed and tested negative before the vaccine is given.

Refereneces:
- Australian Q Fever Register
- eTG Complete

Hypercalcaemia

I saw a patient today with a recently diagnosed Paget's disease. He thinks that he has had symptoms for years but none of the GPs picked it up despite multiple abnormal ALPs. Eventually it was picked up by a GP registrar when he presented with palpitations and she ordered a Calcium, Magnesium and Phosphate. Looking back to my practice, I always forget to order calcium when people presented with palpitations. When I remembered to order them, I don't think I have ever had one came back elevated. The followings are just some key points on Calcium homeostasis and hypercalcaemia.

Key points:

- Common presentations can be summarised as "Bones, stones, groans and psychic moans."
- Causes of metastatic calcification can be summarised using a mnemonic, " Parathormone"

• Parathormone (PTH) increase and causes of Ca increase eg. Sarcoidosis 
• Amyloidosis 
• Renal failure (relates to increase PO4)
• Addison's disease (adrenal calcification)
• TB nodes; Toxoplasmosis (CNS)
• Histoplasmosis (e.g. in lung)
• Overdose in vitamin D
• Raynaud's - associated diseases , e.g. SLE; CREST; Dermatomyositis
• Muscle primaries/leiomyosarcomas
• Ossifying metastases (osteosracoma) or ovarian mets
• Nephrocalcinosis
• Endocrine tumours (e.g. gastrinoma)

- a basic flowchart from oxford handbook of clinical medicine, I think this is a good place to start.

Reference:
Oxford handbook of clinical medicine 8th edition

Acute Otitis Media

Acute Otitis Media 

I see so many ear pain everyday, however, I still feel that I don't have a good grasp on this topic. Parents are often anxious and pushing for antibiotics. I believe that GPs do have a standard to uphold and should only prescribe it only when it is clinically indicated. 

Key Points:

- The diagnosis of AOM is difficult to make especially in children under the age of 3. Studies have shown that the accuracy was: ENT surgeons 74%, paediatricians 51% and GPs 46%.

- Recurrent otitis media is 3 or more episodes in 6 months or 4 or more in 12 months. 

- Common organisms which cause AOM are: streptococcal pneumoniae, Haemophilus influenza-nontypeable and moraxella catarrhalis. 

- Treatment of AOM involves the following:

• Adequate analgesia: paracetamol, amethocaine, benzocaine or lidocaine.
• Antibiotic therapy recommendations:
• well, older than 2 years, no ABx for 48hrs
• Children under the age of 2 as they are more likely to develop complications
• children with severe illness with pain, or a tympanic membrane perforation 
• a child with known immunodeficiency 
• indigenous children, including aboriginal, Torres Strait islander and Maori and other Pacific Islander children
• Children with a cochlear implant
• antibiotic regime: amoxycillin 15mg/kg 3 times per day x 5days; allergic to penicillin, use cefuroxime 10mg/kg to 500 mg twice per day for 5 days or ceflacor 10mg/kg up to 250 mg 3 x per day for 5 days
• topical antibiotics (mainly ciprofloxacin) can be used with tympanic membrane perforation
• Vaccination with the polyvalent pneumococcal vaccine reduces the incidence of am BY 8 % 

- Prevention of recurrent otitis media

• avoid childcare
• avoid smoking 
• breastfeed x 6 months to 12 months
• avoid pacifiers/dummies
• polyvalent pneumococcal vaccines
• 2 weeks after an episode of AOM, 70% of children will have middle ear effusion but most perforation would have healed.
• Treating blocked nose may not help with acute otitis media. Saline to clear the nose and steroid spray to reduce the size of adenoid
• Adenoidectomy has not been shown to be effective in preventing recurrent AOM

References:

- Check program : ENT 

Fish Oil

Fish Oil

Key points:

- Fish oil has been reported to have anti-inflammatory and immunosuppressive effects, and it also result in decreased platelet activity. (beware of procedures)
- Long chain omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have anti-inflammatory properties when taken in doses greater than 2.7g daily.
- It is safe to use but compliance and cost is an issue as to have the inflammatory effect, patient needs to take quite many tablets per day. The following table is from therapeutic guideline:

References:
therapeutic guideline: rheumatology. Getting to know your drug.

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

Visible Haematuria

I have been seeing a 57 M in the last few weeks. He is a new patient to the clinic. He has significant history of ETOH abuse and heavy smoker. Around 2 weeks ago, he came to me with a jar which had his urine in it. There was visible haematuria. I sent him for a renal ultrasound and it was returned normal. I was re-assured by the result until I discussed this with one of the GPs today and did a bit of reading myself.

Some key points about visible haematuria:

1. 20 % of people with haematuria has urological malignancy.
2. Visible haematuria requires urgent urology referral.
3. CT urography is the preferred imaging investigation
4. Women have a poorer outcome in bladder cancer often because of delay in investigations.
5. The following flow chart shows the recommended approach:

6. Do not delay referral because you need to wait for the investgating results

7. Risk factors for bladder malignancies:

References:

Australian Doctor How to treat series Visible haematuria.