Thursday, 29 December 2016

Dermatofibrosarcoma protuberans (DFSP)

What is dermatofibrosarcoma protuberans?

  • Rare tumour 
  • most likely to be of fibroblastic lineage
How does it present?
  • it has smooth appearance resembling a keloidal scar
  • its site on the trunk in young to middle-aged patients
What is the management
  • excision with wide surgical margins 
Reference:
  • Primary certificate of dermatology RACGP 

Benign lymphocytic infiltrates

What is benign lymphocytic infiltrates?

  • The are benign infiltrates of lymphocytes occurring in the dermis
  • They are categorised into B cell and T cell proliferations. 
  • Lymphocytoma cutis is the name used for B cell infiltrates
  • Jessner's lymphocytic infiltrate is an example of a T-cell pseudo lymphoma 
How does it present?
  • Rare
  • The presentation is often in the third or fourth decade of life, but may occur at any age 
  • They present as smooth red apple,es, plaques or nodules, which may be multiple and coalesce
  • The face is most commonly involved, including the ear lobes

What the skin biopsy shows?
  • moderately dense infiltrate lymphocytes within the dermis 
  • distinction from lymphoma is sometimes difficult

What is the management?
  • typical treatment includes
    • potent topical steroids 
    • intralesional steroids 
    • phototherapy 
    • hydroxychloroquine 
  • spontaneous resolution sometimes occur 
  • recurrence is common 
  • small number may progress to lymphoma 
Reference:
  • Primary certificate of dermatology RACGP 

Cutaneous B-cell lymphoma (CBCL)


What is cutaneous B-cell lymphoma (CBCL)?


  • It can be either primary disease of the skin or secondary from nodal (non-Hodgkin's) lymphoma
  • It is rare and less common than mycosis fungicides
  • Men are more commonly affected, most cases present in the sixth or seventh decade of life


How does it present?
  • solitary or multiple nodules localised to one area of the body
  • Usually pink or violaceous in colour, smooth, firm, non tender 
  • favour neck and head region
  • lymph nodes in other area may be involved 

What does it look like on skin biopsy?

  • dense infiltrate of lymphocytes throughout the mid and lower dermis 
  • B lymphocytes do not localise to the epidermis, hence, no scale
What is the treatment ? 
  • Referral to a dermatologist or oncologist is recommended for staging and treatment 
  • Treatment options 
    • radiotherapy 
    • surgery for localised lesion s
    • chemotherapy 
    • rituximab 
What is the prognosis?
  • In general good prognosis > 90 % 5 year survival rate for the follicle centre and marginal zone b cell lymphoma 
  • less so for the variant occurring on the legs 
  • Secondary CBCL is associated with a poor prognosis 
Reference:
1. primary certificate of dermatology RACGP 

Wednesday, 28 December 2016

Tennis Elbow


Tennis elbow is quite a common presentation at general practice. The diagnosis is usually quite straight forward, occasionally, it is complicated by referred neck pain. Most of the time, the patient will be able to tell you the diagnosis is Tennis Elbow.


What is the management?


  • There are many treatments available. Why ? Because none is effective. 
  • Treatments include:
    • physiotherapy: ultrasound, manual therapy
    • NSAIDs: oral, topical. Some mild benefit with topical NSAID gel. 
    • ESWT: no benefit. Cochrane recommended against it. 
    • Surgery: no evidence. Final Resort. 
    • Platelets rich plasma : no definite conclusion can be drawn. No benefit has been shown so far. 
    • orthotic device : no definite conclusion can be drawn. 
    • GTN patch: not mentioned in cochrane. Usually used in combination with an exercise program. 

I looked at cochrane review, there is no evidence for any particular treatment.

The following is a succinct summary from reference 1. 

Essentially, in acute stage, watch and wait. 
Subacute stage, refer to physiotherapy or structured exercise program. 
Chronic stage, can try cortisone injection. Refer for specialist opinion. 

Patient handout: https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/elbow-pain
(I read quite a few handouts online and I found the one from the victoria state government to be the most accurate and up to date)

References:
1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781883/
2. http://www.cochrane.org/CD001821/MUSKEL_orthotic-devices-for-the-treatment-of-tennis-elbow

Thursday, 22 December 2016

Acute sinusitis

I came across this article on Australian prescriber. It looks like all common management strategies that we use have little or no evidence.

Including: systemic steroid, sinus wash. There is small benefit using intranasal steroid in mild disease.

References:
https://www.nps.org.au/australian-prescriber/articles/acute-sinusitis

Thursday, 15 December 2016

Actinic keratosis

Key points:

  • estimated around 10% of them becomes Squamous cell carcinoma 
  • thought to be an intraepidermal lesion 
  • multiple treatment modalities, the most common one is cryotherapy
  • biopsy lesion if it does not respond to treatment

What is actinic keratosis?
  • They are keratotic lesions with malignant potential 
  • They are considered intraepidermal, pre-cursor or early lesions of squamous cell carcinoma 
  • lesions are most commonly found in the sun-exposed areas of elderly patients with fair skin types who have had significant sun exposure in their lifetime
What are the histological changes?

  • epidermal cell dysplasia 
  • dilated upper dermal blood vessels 
  • degeneration of collagen and elastin in the dermis (solar elastosis)
Who's at risk?
  • Celtic descents 
  • Skin types 1 and 2 
  • immunosuppressant therapy
  • elderly
What are the differential diagnoses?
  • BCCs
  • lupus erythematous
  • actinic porokeratosis
  • SCCs
How does it present?
  • usually in caucasians > 40 in sun exposed area
  • actinic keratoses initially present as a poorly defined area of redness or telangiectasia
  • over time, the lesion becomes more defined and develops a thin, adherent, yellowish or transparent scale
  • with time, the adherent scale becomes progressively thicker and yellow in colour 
How is it diagnosed?
  • most of the time by clinical examination 
  • advance lesions may require biopsies to differentiate from squamous cell carcinoma
  • the histologic hallmark is a disordered epidermis with intraepidermal keratinocyte atypia 
What is the prognosis?
  • small number of actinic keratoses will progress to SCC, and the trouble is we don't know which one is going to progress and which one is not 
  • We think the thicker ones are more worrisome 
  • SCC that develop on the ear, the scalp, or at the vermilion border are more likely to metastasise, so actinic keratoses in the above areas need to be treated aggressively
What treatment is available ?
  • cryotherapy
  • imiquimod
  • Efudix 
  • photodynamic therapy
  • emollients containing keratolytics e.g. 2-4% salicylic acid in sorbolene cream
  • Tretinoin 
  • Laser
Why are there so many treatments available?
  • None work 100 % 
Why do lesions recur after treatment?
  1. The lesion may have been treated inadequately
  2. Wrong diagnosis: could be BCCs, SCCs, Bowen's lupus erythematous or psoriasis. Therefore, failed treatment usually means biopsy


Reference:
  • Habif: skin disease diagnosis and treatment third edition

Saturday, 3 December 2016

Autistic spectrum disorder

I have absolutely no interest in dealing with behavioural problems in kids, unfortunately, it is part of the job as a GP. There is a strong push from parents and schools to label these children with a diagnosis. Once they have a diagnosis, they can receive extra fundings and extra help at school. Having said that, it is also important to diagnose children with ASD early so that there is a better chance for them to function independently in the future.

What is Autism?


  • Lifelong neurodevelopment disability that affects how an individual communicates and interacts with people and their environment. There are difficulties in 2 primary areas. 
    • social interaction 
    • repetitie behaviours and interests
How common is autism ?

  • Australia 1/160 - 1/100
  • USA & Europe 6-7/1000

What cause autistic spectrum disorder?

  • exact cause is unknown 
  • multifactorial is the keyword in exam 
  • some genetic factors in play
    • monozygotic twins 60%
    • dizygotic 3 %
  • More common in males than females 4:1
  • More common in certain chromosomal disorders e.g. Fragile X syndrome 
  • Increased in neurogenetic disorders e.g. tuberous sclerosis 

  • NOT CAUSED BY VACCINATION

How do children with Autistic spectrum disorder present?

  • Parents usually aware before 18 months 
  • Most common parental concerns include delayed speech and behaviour problems
What is the Role of GP?
  • Identify problem early and refer 
  • Need to conduct a full history and physical exam
  • Appropriate referrals e.g. hearing/vision, intervention services+/-therapy, paediatrician
  • ongoing multidisciplinary management and review
What are some absolute indications for immediate refer?
  • No Babbling, pointing or other gestures by 12 months
  • No sharing of interests in objects with another person
  • No single words by 16 months
  • No 2 word spontaneous phrases by 24 months
  • Any loss of language or social skills at any age

Any screening tools available ?
  • M-Chat (16-30 months) Free to download online. Just type M-Chat on google.
What are some key elements in intervention?
  • The earlier the better, the more the better
  • early intervention between 15-25 hours a week
  • Multidisciplinary supportive individualized
  • In collaboration with family 
  • Strategies to be able to generalise skills
  • Develop functional, spontaneous communication 
  • Reduction of maladaptive behaviours
  • Teach functional adaptive skills
  • Opportunity for neurotypical peer interaction 
  • Clear Goal setting, predictability and routine 
  • Continual review 
Does medication help?
  • In general, medication does not help. 
  • It is mainly used to treat other co-morbidities e.g. ADHD, insomnia, anxiety etc
What is the prognosis?
  • 10 % adults with ASD live independently 

References: 
  • Austism spectrum disorder by Dr. Gillian Brooks from diploma of child health webcast 2016






Wednesday, 5 October 2016

Attention Deficit Hyperactivity Disorder (ADHD)



What is ADHD?

  • It is a development problem which results in poor concentration and control of impulses. 
  • It can affect children's learning and social skills, and also family functioning
  • About 3-5 of every 100 children in Australia have ADHD

What are the symptoms and diagnosis ?
  • Inattention 
    • Difficult concentrating, forgetting instructions, moving from one task to another without completing anything 
  • Impulsivity
    • Talking over the top of others, losing control of emotions easily, being accident prone
  • Overactivity 
    • Constant fidgeting and restlessness
What are the treatments?
  • Stimulatns 
  • Behaviour strategies 
References:
  • RCH: ADHD 

Saturday, 17 September 2016

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



  • What is giardia? 
    • Giardia duodenalis is a parasite
    • It is the most common gastrointestinal protozoan that causes chronic diarrhoea 

  • How dose it spread?
    • It is transmitted by the ingestion of food or water contaminated by faeces, by exposure to faecally contaminated surfaces and through person-to-person contact. 

  • What are the signs and symptoms?
    • stomach cramps
    • excessive gas or bloating 
    • diarrhoea, which may be water, usually last 1 to several weeks
    • frequent loose or pale, greasy faeces which may float in the toilet bowl 
    • fatigue
    • weight loss
    • lactose intolerance may occur in 20 to 40% cases and last several weeks
    • fever and bloody diarrhoea are uncommon 
    • symptoms usually appear 1-2 weeks following infection and resolver within 2-4 weeks
** many infected have no symptoms**

  • How do you diagnose it ?
    • Diagnosis is made by stool MCS or multiplex

  • How do you treat it ?
    • Tinidazole 2 g orally 
    • metronidazole 2g orally daily for 3 days or 400 mg orally 8 hourly for 5-7 days 

Reference
  • http://www.sahealth.sa.gov.au/wps/wcm/connect/Public+Content/SA+Health+Internet/Health+topics/Health+conditions+prevention+and+treatment/Infectious+diseases/Giardia+infection/


Sunday, 11 September 2016

Iron deficiency

What is iron deficiency?

  • Royal College of pathologists of Australasia definition of iron deficiency is serum ferritin level of < 30 for an adult 
Who gets iron deficiency?
  • Basically everyone 
  • Pre-menopausal and pregnant women are at higher risk
  • Vegetarian with a balanced diet should not have iron deficiency
What causes iron deficiency?
  • 2 major categories
    • Not taking in enough iron such as coeliac disease, poor diet etc
    • Loosing iron such as blood loss
What are the clinical features of iron deficiency?
  • No clinical features in many cases and found out from routine blood test
  • Clinical features include: fatigue
How is it diagnosed?
  • It is diagnosed via iron studies, not as straight forward as it sounds 
    • Ferritin is the most reliable indicator of iron level but it elevates with acute inflammation so a CRP is recommended to order with ferritin together 
    • Transferrin saturation levels reflecting transport iron, if it is less than 20% indicate an iron supply that is insufficient to support normal erythropoiesis
    • Total iron binding capacity increases in iron deficiency in an attempt to increase iron uptake 
What is the treatment for iron deficency?
  • Dietary modification is inadequate to treat iron deficiency, only enough to prevent 
  • treatment is around 100 - 200 mg elemental iron daily in divided doses 
  • Over the counter product only contains very small amount of iron content
  • If iron replenish is required urgently (prior to operation or pre-obstetric delivery), IV iron can be used. (Usually ferronjet 1000 mg can be given over 15 minutes)
  • There are quite many iron oral formulas available: Here
What is the outcome?
  • Variable depends on the cause
  • takes 3 to 4 weeks to have a clinical significant impact
  • Hb level should increase by approximately 20 g/L every 3 weeks
References:
  • RACGP check program 2016 Blood disorder 
  • South Australia health. Blood safe iron deficiency anaemia resources

Thursday, 1 September 2016

Respiratory history

System review questions:

  • chest pain
  • shortness of breath
  • wheeze
  • cough
  • sputum
  • haemoptysis 
  • exercise tolerance
  • smoking history 

Tuesday, 30 August 2016

Breast lump

Key points:

  • History needs to include her mentrual and reproductive history, and any known risk factors for breast cancer 
  • Approach is clinical examination, U/S and FNA. If all came back negative, then you can re-assure patient. If equivocal, refer to breast surgeon
  • Risk factors for breast cancer
    • Family history of breast and ovarian cancer
    • increasing age
    • late childbearing (after the age of 30 years)
    • Nulliparity (no children)
    • Early menarche (<12 age="" li="" of="" years="">
    • Late menopause
    • Use of hormone replacement therapy
    • Ashkenazi jewish ethnicity
    • Obesity (post-menopausal women)
    • Lifestyle factors (e.g. high alcohol consumption, high-fat diet)
  • Tamoxifen
    • it is prescribed to treat early stage oestrogen receptor - positive breast cancer in premenopausal and postmenopausal women
    • Tamoxifen is usually taken for up to five years 
    • As tamoxifen is an anti oestrogen drug, the common side effects are hot flushes, night sweats and vaginal dryness. Less commonly, tamoxifen increases the risk of blood clots, stroke, cataracts, endometrial cancer, mood swings, depression and loss of libido
  • Only about 5% of women have breast cancer due to a genetic predisposition or inherited gene mutation, such as BRCA1 and BRCA2.

Friday, 19 August 2016

Anal pruritus

Key points:

1. Anal pruritus is estimated to affect up to 5% of the population, with a male to female ratio of 4:1

2. In up to 25% of cases the anal pruritus is idiopathic

3. Even mild degrees of faecal soiling, which the patient may not be aware of, may be enough to cause an itch-scratch cycle

4. Dietary associations with pruritus anti include caffeine, alcohol, chocolate, tomatoes, spices and citrus fruit

5. Important to educate the patient about the recurring, benign nature of this irritating condition and to ensure adherence to the following simple, yet essential, measures to eliminate irritants and resolve symptoms

6. Management strategies

  • Normalisation of bowel motions
  • Cleaning after defaecation: rubbing or scrubbing the area should be actively discouraged
  • Clothing
  • Soaps and cleansers: do not use soaps
  • Do not scratch: easy to say than done. May need help with topical steroid. Suggested regimen: start with methylprednisolone fatty ointment --> reducing to a moderate potency preparation such as betamethasone validate and then 1% hydrocortisone cream. Not curative. May need to return to high potency steroid from time to time 
  • topical capsaicin in a 0.006% preparation (only available in a compound pharmacy. needs to be mixed with white paraffin )
References:
http://www.racgp.org.au/download/documents/AFP/2010/June/201006maclean.pdf

Thursday, 18 August 2016

Male baldness

Key points:

1. 5AR converts testosteron to dihydrotestosterone, inhibition of 5AR improves hair growth and slows hair loss.

2. Finasteride (a type 2 5AR inhibitor) and dutasteride (type 1 and 2 isoenymes) are used to treat Androgenic alopecia

3. Main side effects of 5AIRs are effects on sexual function, breast enlargement and a possible increase in the risk of prostate cancer

4. Early onset of AGA is a strong predictor of early onset of severer coronary heart disease and metabolic syndrome

5. Hair thinning usually on ly becomes noticeable after losing 50 % or more of scalp hair

6. The typical history for a man with AGA is gradual onset of thinning after puberty. There is a gradual thinking of hair on the crown and vertex of the scalp, and frontal recession

7. When discussing treatment, emphasis

  • no treatment will completely reverse the process
  • the response to treatment is quite variable 
  • some people will not respond to particular treatments
8. Treatment options 
  • no treatment 
  • hair piece
  • medical treatment 
    • topical minoxidil 2-5%
    • oral finasterid 1 mg daily 
    • oral dutasteride 0.5 mg daily (not approved for hair loss use yet in Australia)
    • surgery 
Reference
http://gplearning.racgp.org.au/content/AFP/16Apr/Clarke.pdf

Saturday, 13 August 2016

Paresthesia and peripheral neuropathy

1. The author suggested that clarifying clearly the patients' symptoms is the first step.

2. To my surprise, the  medications commonly caused include amiodarone, STATINS (didn't know that), antiretrovirals, tacrolimus or levodopa.

3. Nutritional/Dietary history is important as well such B6, B12 and Thiamine.

4. Carpal tunnel and ulnar neuropathy can be usually managed at gp practice without referral to neurologist

5. The median nerve supplies only four muscles in then hand, represented by the mneumoni LOAF:

  • lateral two lumbricals
  • opponens pollicis
  • abductor pollicis brevis 
  • flexor pollicis brevis 
6. The ulnar nerve supplies the following muscles 
  • abductor digiti minimi
  • medial humeral epicondyle 
7. Treatment is very general and as it is a short article so the author essential can't list out all the possible treatments.  But for carpal tunnel, use night splints. Ulnar nerve compression use medial elbow padding. 

Reference:

Dermatology

Topics related to Dermatology:


Ingrown toenail

Pruritus ani

Male baldness

actinic keratosis

punch biopsy

shave biopsy

BCC

Cutaneous B cell lymphoma 

Benign lymphocytic infiltrates

Dermatofibrosarcoma protuberans


Wednesday, 10 August 2016

Approach to problem behaviour in children

Key points:

- Use the following table to take a focused history on things which can affect a child's behaviour

 


  • Use the mnemonic ABC to clarify events surrounding the behaviour
    • Antecedent - what were the events preceding the behaviour?
    • Behaviour - what is the behaviour exactly?
    • Consequence - what did the parents do to resolve the situation?
  • Examination 
    • physical examination 
    • brief developmental assessment 
  • General management (Box 1 lists out principles of behaviour management)
    • Encourage positive behaviour 
    • Ensure a consistent approach 
    • Set clear boundaries and expectations
    • Set clear consequences for actions and makes parents can follow through
  • Tantrums and oppositional behaviour in toddlers (1-3 years old)
    • Remain calm and do not raise your voice
    • ask the child to stop and re-direct them to another activity
    • if they do stop, praise them
    • it they do not stop, go to quiet time (same room)
    • if they keep coming out of quiet time, or are aggressive again, go to time out (in another room)
      • keep conversation minimal at this time as the child might be too agitate to understand explanations 
      • the child stays in time out until they are quiet and calm 
  • Anger and aggression in preschoolers (3-5 years)
    • Management involves prioritising behaviours in terms of severity level
      • low priority behaviours can be dealt with by 
        • ignoring the behaviour
        • distracting the child
        • logical consequences for the child's action 
      • High priority behaviour, such as behaviour with associated safety concerns should be dealt with through time out as described 
    • Hyperactivity or inattention in school aged children (5-11 years)
      • At school, teachers will be doing the work 
      • At school, removing/withdrawal of privileges 
  • When to refer 
    • all else fails 
    • not coping at school 
References
- http://www.racgp.org.au/download/documents/AFP/2011/September/201109luangrath.pdf
- http://www.racgp.org.au/afp/2015/december/finetuning-behaviour-management-in-young-children/



Monday, 8 August 2016

Approach to dysmenorrhoea


History

  • Pain
    • It is important to determine if the pain is actually related to the menstrual cycle or has another underlying cause
      • where is the site of the pain ?
      • How would you describe the pain ? e.g. continuous or colicky
      • How long has it been present 
      • Is the pain associated with gastrointestinal function; do you have nausea, vomiting or diarrhoea/loose bowels
      • does opening your bowels ease or make the pain worse?
      • Do you have pain on urination?
    • Menstrual history
      • How old were you when you first had your period?
      • How often do you have periods and how long does each one last?
      • is the period heavy ? if so, on which day of the period?
      • What size tampon or pad do you use? do you ever use both?
      • how often do you change them?
      • do you ever flood through tampon/pad or at night in bed?
      • Have your periods caused you to miss school/work/social actives before this period?
      • What associated symptoms, including pain and discomfort, do you have?
      • What pain relief have taken and does it help?
    • Medical and family history 
      • do you have any family members with 
        • diagnosed endometriosis?
        • pelvic pain or pain during menstruation?
        • problems getting pregnant or involuntary childlessness?
    • Sexual history 
      • when the first intercourse occurred
      • male or female partners
      • route of intercourse
      • use of contraception 
      • discussion of STIs
      • vaccination history including hPV 
      • pain or bleeding during sex 
  • Examination 
    • abdominal examination 
    • vaginal examination is often not required esp. in adolescent girls who have never had sexual intercourse before
  • Investigation 
    • Blood test + STD screen 
    • Vaginal or transabdominal ultrasound 
  • DDx
    • can be broadly classified in primary or secondary dysmenorrhoea 
    • for further details about primary dysmenorrhoea, please go to the following link 
    •  
  • Management
    • Analgesia: NSAID
    • Suppression of ovarian function: COCP, GnRH agonist, IUD, etonorgestrel implant and oral dienogest
    • surgical ablation 
    • management of infertility 30-35% of women with endometriosis have infertility
  • Prognosis
    • Chronic condition 
    • recurrence rate of 10-50% one year after surgery

Rosacea

Rosacea


  • Epidemiology
    • 2-3% of general population 
    • Rosacea tends to occur in adults over the age of 30 years.
    • In groups aged younger than 35 years or older than 50 years, men and women are affected equally, however, there is a predominance in women in the 36-50 year age group.
    • Most common in fair skinned, anglo-celts
  • Cause
    • multifactorial and exact mechanisms are not well understood
      • Genetics may play a role
      • Neurovascular dysregulation and augmented immune detection and response
      • infection:  the face mite demuxed folliculorum, an obligatory parasite of human pilosebaceous follicles, has been identified in elevated numbers in patients with rosacea
  • Clinical features
    • commonly affects the central convex areas of the face(cheers, nose, chin and forehead)
    • Diagnosis can be made using the following features
      • flushing 
      • erythema
      • inflammatory lesions 
      • telangiectasia 
  • Differential diagnoses of rosacea
    • Acne vulgaris
    • Seborrhoeic dermatitis
    • Perioral dermatitis
    • steroid induced acneiform eruption 
    • lupus erythematousus-discoid, systemic or subacute cutaneous 
    • Cutaneous sarcoidosis of the nose 
    • Tinea faciei
    • Essential telangiectasia
    • Carcinoid syndrome 
    • Drug reaction 
    • polymorphous light eruption 
    • atypical infections 
    • contact dermatitis 
    • Lupus vulgaris (cutaneous tuberculosis)
    • Acne agminata
    • Dermatomyositis
    • Polycythaemia rubra vera
    • Superior vena cava obstruction 
  • Treatment: 
    • Education 
    • Avoid precipitants
    • sun screen and hats

    • Oral agents
      • tetracycline 500 mg bd 
      • doxycycline 50 mg - 100 mg / day (intermittent use is preferable)
      • erythromycin 500 mg bd 
      • erythromycin ethyl succinate 800 mg bd
    • Topical agents
      • metronidazole 
      • erythromycin 
      • brimonidine 0.33% gel 
      • azelaic acid (available as a 20% lotion or 15% gel) 
      • other agents
        • diclofenac
        • isotretinoin for refractory cases
        • clonidine, spironolactone, beta blockers,  naloxone and ondansetron
        • ivermectin 
    • Recurrence is routine 
  • Complications 
    • depression 
    • ocular rosacea (symptoms include tearing, conjunctival hyperaemia, foreign body sensation, burning, stinging, dryness, itching, light sensitivity and blurred vision)
    • lymphoedema
    • salivary gland involvement --> reduce in salivary secretions and dry mouth 
References:
http://medicinetoday.com.au/system/files/pdf/medicine_today/article/MT2015-01-034-CHEE.pdf

Saturday, 6 August 2016

What vitamins should I take for my macula ?


  • General dietary and lifestyle advice to reduce the risk of a person developing macular degeneration and to minimise loss of vision if AMD is present is outlined below. 
  • Lutein and zeaxanthin are particularly important nutrients for good macular health, and are derived through the diet, mainly from green vegetables. 
  • Other nutrients important for macula health and general eye health are zinc, vitamin C, vitamin E and the omega 3 fatty acids
  • Supplements based on the Age-related Eye disease study (AREDS) formula may considered by people who have been diagnosed with AMD
  • In 2001, the Age related eye disease study (AREDS), large (n4757), multi centre prospective trial over 6 years, used 80 mg of elemental zinc. Lower since was used in subsequent study to improve safety and efficacy but the conclusion remained that 80 mg zinc is safe and more effective in preventive AMD. 
  • In patients who are not consuming enough lutein and zeaxanthin ( 3 quarters of a cup of cooked spinach), supplement helps to reduce 45% reduction in the progression of AMD. 
  • AREDS used tablet formula only as copper containing formulae is considered unsafe in capsule form. The combination of linoleic acid-rich oil and copper may produce toxic products. 
  • supplements that include copper and fish oil and/or LZ in the one tablet or capsule are not recommended because of potential for toxicity.
  • The author of the article takes Macuvision, Lutein-vision advanced tablet, coenzyme Q10 and B12 supplement as his B12 supplement is low, so he takes B12 as well. 
Reference:
http://medicinetoday.com.au/system/files/pdf/medicine_today/article/MT2014-05-048-BEAUMONT.pdf

Monday, 1 August 2016

Early pregnancy bleeding


  • 20 - 40 % of pregnant women will experience bleeding during the first trimester of pregnancy
  • Major causes are miscarriage (10-20%) and ectopic pregnancy (1-2%)
  • Establishing the site of the pregnancy is vital, as failure to correctly diagnose an ectopic can have potentially life threatening consequences
  • Initial assessment is haemodynamic stability. Unstable patients need to be transferred to the emergency department
  • History
    • gestational age of the pregnancy
    • the amount of blood loss
    • any associated pain symptoms 
    • the presence of syncope, chest pain and shortness of breath may point to anaemia from significant blood loss, and shoulder tip pain may be associated with intra-abdominal bleeding 
  • Examination 
    • Assess for haemodynamic instability 
    • abdominal examination 
    • speculum examination to assess the amount and origin of ongoing bleeding
    • bimanual examination allows assessment of uterine size, dilatation of the cervical os, pelvic tenderness and cervical motion tenderness
  • Investigation 
    • Beta HCG (Serum HCG levels rise exponentially up to six to seven weeks of gestation, increasing by at least 66 % every 48 hours)
    • Ultrasound assessment
    • Testing for maternal blood group and antibody status will determine the need for RhD immunoglobulin administration 
    • On TVS, a gestational sac will usually be visible from 4 weeks and 3 days after the last menstrual period
  • Management 
    • Rh D immunoglobulin is indicated for the prevention of Rh D sensitisation in Rh D negative women. This should be given within 72 hours of the sensitising event.
References:

http://www.racgp.org.au/afp/2016/may/early-pregnancy-bleeding/

Wednesday, 27 July 2016

Inflammatory arthritis


  • Rheumatoid arthritis is an autoimmune condition mainly affecting the joints of the body.

  • Typical features are morning stiffness, joint pain relieved by movements and aggravated by rest.

  • Basic investigations for patients with suspected rheumatoid arthritis/inflammatory arthritis
    • FBE
    • UEC
    • LFT
    • ESE
    • CRP
    • Anti CCP
    • RA
    • ANA
    • ENA 

  • DMARDs have made significant improvement in patients with RA. We don't see patients with RA with severe deformities anymore. The best outcome is when patients are started on DMARDs early, so refer early. 

  • Methotrexate is the first line DMARD for RA at the moment. Cheap, relatively easy and safe to take. Common side effects: nausea and mouth ulcers. Monitor LFT and FBE monthly. 



Tuesday, 26 July 2016

Anxiety disorder


  • Anxiety disorder is common. GPs encounter patients with anxiety disorders everyday, so it is important to have some basic understanding of the disorder and also management plans

  • Anxiety disorders include: general anxiety disorder, phobias, OCD, PTSDs, panic attack, substance induced anxiety and anxiety secondary to general medical condition

  • My personal approach is that I do not prescribe benzodiazepam to anyone who comes in with anxiety disorder. As it is often lifelong and most patients ended up becoming dependent on benzodiazepam. I will usually bring this straight up during the first consultation, which prevents them from coming in for benzodiazepam prescription in the future

  • Use DASS 21 or K10 to assess level of distress 

  • Substance abuse or comorbid psychiatric disorders are common in this population, make sure you screen for them 
  • Management plan
    • Avoid benzodiazepam. You are not doing the patient any good by prescribing them. 
    • Psychoeducation 
      • It is the key to many psychological condition 
      • use the flight/fight model to explain the purpose of anxiety
    • Cognitive behavioural therapy
      • Essential to mention this in the exam 
      • Do a mental health plan and refer to psychologist 
      • National e-therapy centre for anxiety
    • Medications
      • Some SSRIs have anti anxiety effect but only escitalopram is currently listed to use in GAD 
      • Avoid Paroxetine in young women who have not completed their family

   

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Monday, 25 July 2016

Approach to Dysnoea

Probability diagnosis

  • bronchial asthma
  • bronchioligitis (children)
  • COPD
  • Ageing; lack of fitness
  • Left heart failure
  • Obesity 
Serious disorders not to be missed
  • Cardiovascular
    • Acute heart failure
    • arrhythmia 
    • pulmonary embolism
    • fat embolism
    • pulmonary hypertension 
    • dissecting aneurysm 
    • cardiomyopathy
    • pericardial tamponade
    • anaphylaxis
  • Neoplasia
    • bronchial carncma, other malignancy
  • Severe infections
    • SARS
    • avian influenza
    • pneumonia
    • acute epiglottitis
  • Respiratory disorders
    • inhaled foreign body
    • upper airways obstruction 
    • pneumothorax
    • atelectasis
    • pleural effusion 
    • tuberculosis
    • acute respiratory distress syndrome
  • Neuromuscular disease
    • infective polyneuritis
    • poliomyelitis
Pitfalls
  • interstitial lung disease 
    • idiopathic pulmonary fibrosis 
    • extrinsic allergic alveolitis
    • sarcoidosis
  • chemical pneumonitis
  • metabolic acidosis 
  • radiotherapy 
  • kidney failure (uraemia)
  • multiple small pulmonary emboli
Severn masquerades checklist
  • Depression 
  • Diabetes
  • Drugs 
  • Anaemia 
  • Thyroid disorder 
  • Spinal dysfunction 
Is the patient trying to tell me something?
  • Consider functional hyperventilation 

Sunday, 24 July 2016

Approach to the disturbed patient

Approach to the disturbed patient

Probability diagnosis

  • The 4Ds
    • Dementia
    • Delirium 
    • Depression 
    • Drugs: toxicity, withdrawal
  • Serious disorders not to be missed
    • Cardiovascular 
      • CVAs
      • Cardiac failure
      • Arrhythmia 
      • ACS
    • Neoplasia
      • cerebral
      • Cancer
    • Severe infections 
      • septicaema
      • HIV infection 
      • infective endocarditis
    • Hypoglycaemia
    • Bipolar disorder/mania
    • Schizophrenia states
    • Anxiety/panic
    • Subdural haematoma 
  • Pitfalls 
    • illicit drug withdrawal
    • Fluid and electrolyte disturbances
    • Faecal impaction 
    • Urinary retention 
    • Hypoxia 
    • Pain syndromes
    • Rarities
      • Hypocalcaemia
      • Kidney failure
      • Hepatic failure
      • Prion diseases
  • Seven masquerades checklist 
    • Depression 
    • Diabetes
    • Drugs
    • Anaemia 
    • Thyroid disorder 
    • Spinal dysfunction 
    • UTI 
  • Is the patient trying to tell me something?

Approach to Diarrhoea

A diagnostic approach

Probability diagnosis

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
  • 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 **


Saturday, 23 July 2016

Myocardial ischaemia

Condition

  • Myocardial ischaemia
History
  • Any pain waist line and above is cardiac until proven otherwise
  • Quality of the pain is usually described as pressure, heaviness or tightness
  • May have associated symptoms: dysnoea, dizziness, nausea and vomiting and sweating
  • Ask family and risk factors
Examination
  • could be normal
  • variable ? arrhythmias
  • Gallop rhythm 
  • Murmur of MI
  • Basal crackles
Ix
  • ECG is a must
  • Troponin probably does not have a role at general practice unless you have a cath lab
  • CXR helps to exclude causes e.g. pneumothorax
  • Myocardial perfusion study
    • High negative predictive score
    • Risk stratify into 3 categories: reversible ischaemia, normal/equivocal and non diagnostic
    • Normal/Equivocal --> CTCA
    • Limitations: patients' compliance to the exercise requirements of the study, low sensitivity and radiation dose 
  • Stress echocardiagraphy
    • can use to risk stratify like myocardial perfusion study
    • needs expert operator
  • CTCA
    • Needs the HR < 60 bp
    • Be able to breath hold
    • very high negative value approaching 100 %
    • Limitations: sometimes can be difficult to get the heart rate down (anyone ever works at ED will tell you that) and high calcium in the arteries can also obscure the view
    • Scan protocol (Triple rule out) using CTCA to rule out PE, Aortic dissection and MI have been employed by some centres in the state. Watch out for this space in Australia
Management
  • For GPs, the main thing is recognising it and send the patient to ED. This could be life saving. 
  • I used to feel terrible for sending someone in who end up did not have a MI. Feeling that I have wasted their time and ED's time and ED's discharge letter will definitely make you feel that way. 
  • Don't forget that we will never be 100 % correct. We got some and we missed some. For those who did not have MI, you have just excluded a life threatening condition! Well done!

References
1. John Murtagh
2. http://www.racgp.org.au/afp/2014/may/imaging-for-cardiac-disease/

Friday, 22 July 2016

Idiopathic thrombocytopenia purport

Condition

  • Immune destruction of platelets
Clinical features
  • easy bruising
  • epistaxis and menorrhagia common 
  • no systemic illness
  • splenomegaly rare
  • isolated thrombocytopenia
  • other blood cells normal
  • normal physical examination 
  • normal bone marrow with normal or increased megakaryocytic
Murtagh's triad
  • bruising + oral bleeding + epistaxis = ITP

Management
  • no treatment 
  • avoid contact sports
  • watch and wait
  • likely to resolve spontaneously 
  • wide range of practice within Australia. At Westmead children's hospital, they are more pro-watch and wait and avoid treatment

Henoch-Schonlein purpura

Condition

  • Commonest vasculitis of children 
Classic triad 
  • non thrombocytopenic purpura 
  • large joint arthritis
  • abdominal pain 
History 
  • upper respiratory tract infection including a group A streptococcal tonsillopharyngitis
  • mainly in children
  • rash, mainly on buttocks and legs
  • arthritis: mainly ankles and knees
  • abdominal pain - colicky 
  • haematuria
  • associations
    • kidney involvement - deposition of IgA immune complex
    • Malaena
    • intussusception 
    • Scrotal involvement
Investigaions
  • FBE
  • UEC
  • Urine: protein and blood: spun specimen, micro for casts

Management
  • Analgesics 
  • Check UEC 
  • Beware of renal failure 

Tuesday, 19 July 2016

Approach to arthritis

**Red flags**

  • Fever
  • Weight loss
  • Profuse rash
  • Lymphadenopathy
  • Cardiac murmur
  • Severe pain and disability
  • Malaise and fatigue
  • Vasculitic signs 
  • 2 or more systems involved


Arhritis in children: causes to consider

Infections

  • rheumatic fever
  • septic arthritis
  • meningococcaemia
  • osteomyelitis
  • reactive arthritis
  • tuberculosis
  • viral infections
Inflammation - chronic arthritis
  • juvenile idiopathic/chronic arthritis
  • oligo articular
  • seropositive polyarticular
  • seronegative polyarticular
  • systemic onset arthritis 
  • enthesitis related arthritis
  • Psoriatic juvenile arthritis
Haematological disorders
  • thalassaemia
  • sickle-cell anaemia
  • haemophilia
Neoplasms
  • Leukaemia
  • Lymphoma
  • Neuroblastoma
Orthopaedic conditions
  • perthes
  • slipped upper femoral epiphyses
  • chondromalacia
Others
  • Henoch-schonlein purpura
  • kawasaki syndrome
  • scurvy
  • traumatic arthrits
  • osteochondritis
  • psychogenic rheumatism
  • malignant tumour
    • bone
    • cartilage
    • synovium

Monday, 18 July 2016

Approach to abdominal pain

**Red flags**

  • History
    • collapse at toilet 
    • lightheadedness
    • ischaemic heart disease 
    • progressive-vomiting pain, distension 
    • menstrual abnomalities
    • malignancy
  • Signs
    • Pallor and sweating 
    • Hypotension 
    • Atrial fibrillation or tachycardia
    • Fever
    • Prostration 
    • Rebound tenderness and guarding 
    • Decreased urine output
  • Key history
    • Dysphagia/odynophagia
    • Nausea/vomiting
    • Loss of appetite 
    • Reflux
    • Abdominal pain 
    • Abdominal distension 
    • Altered bowel habit
    • systemic symptoms: malaise/fatigue/jaundice/fever
Murtagh Triad
  • Pale child + severe colic + vomiting = acute intussusception
  • intense pain + pale and 'shocked' +/- back pain = ruptured AAA
  • Anxiety and prostration + intense central pain + profuse vomiting +/- bloody diarrhoea = mesenteric arterial occlusion 
  • Localised RIF pain + a/n/v + guarding = acute appendicitis 
  • Colicky central pain + vomiting + distension = SBO
  • Colicky pain + distension +/- vomiting = LBO
  • Sudden severe pain + anxious, still, 'grey', sweaty + deceptive improvement = perforated peptic ulcer
  • Intense pain (loin) --> groin + microscopic haematuria = ureteric colic
  • acute pain + left sided radiation + fever = acute diverticulitis

Indigenous health

Approach to indigenous health

**common exam topic**

**In your management plan, must mention aboriginal health worker**

Common clinical problems in children

Perinatal

  • Low birthweight
  • Asphyxia
  • Infections 

Preschool

  • Failure to thrive
  • Malnutrition 
  • Anaemia -- check for hookworm 
  • Respiratory infection 
  • Diarrhoea disease
  • hepatitis B
  • Skin infection/infestation 
  • Urinary tract infection 
  • Meningitis 
  • Joint and bone infection 
  • Chronic suppurative otitis media 
  • Trachoma

Later childhood and adolescence

  • Bacterial and viral infections 
  • Parasitic infestation 
  • Streptococcal infection:
    • Rheumatic fever
    • Glomerulonephritis
  • Trauma 
  • Substance abuse
  • Chronic suppurative otitis media 
Adults


  • Diabetes
  • Cardiovascular disease
  • Injury (and youth suicide)
  • Kidney disease
  • STIs
  • Mental health
  • Poor nutrition 
  • Ear infections 
  • Women's problems
Socioeconomic

  • Education of aboriginal children
  • Housing 
  • Water supply
  • Alcohol and substance misuse
  • Domestic violence and sexual abuse
  • Child abuse 
  • Gambling 
  • Unemployment
Immunisation schdule

Central retinal artery occlusion

Condition

  • Central retinal artery occlusion: infarction of retina 
What is it ?
  • Infarction 
  • Can either be caused by thrombosis or embolic occlusion
  • Thrombosis
    • systemic hypertension 
    • dyslipidemia 
    • hyper coagulable states
  • Embolus
    • cervical carotid bifurcation 
    • abnormalities of cardiac valves, wall or rhythm e.g. atrial fibrillation
How does it appear ?
  • Sudden painless loss of vision usually confined to one eye
  • Afferent pupil defect in affected eye
  • Milky appearance of retina because ischemic swelling causes loss of its transparency
  • Cherry-red spot in fovea (spared because it is nourished by choroidal rather than retinal arteries)
Management
  • Refer to hospital immediately for further evaluation 
  • Needs stroke workup
  • Massage globe digitally 
References
- the eye have it 

Thursday, 14 July 2016

Faecal incontinence


Key points:

  • most likely caused by constipation 
  • RCH website has good summary on laxatives
  • don't forget psychological cause 
  • refer early if not winning, as this can be problematic for the child and the family 


What causes faecal incontinence?
  • Functional 
    • constipation associated faecal incontinence, involuntary
    • non retentive faecal incontinence (encopresis)
      • may have a psychosocial basis 
  • Organic 
    • anorectal malformation, spinal disorders, hirschsprung's disease, CP, mental retardation etc
Assessment ?
  • General history
  • Bowel habit details
    • frequency of defecation 
    • consistency of stool 
    • intestinal hurry - soiling 
    • toilet posture, school practices re: toilet 
  • Fluid intake 
  • Diet/fibre intake/cow's milk history
  • Bristol stool chart. Normal is type 3 and 4.

Examination?
  • Developmental 
  • nutritional 
  • abdominal 
  • neurological 
    • spine/reflexes
  • anorectal exam ? PR (not necessary)
    • anal tone/sensation 
What are the investigations?
  • bowel chart/diary
  • abdominal x-rays (esp if no faecal retention found on rectal exam)
  • abdominal ultrasound (rectal diameter for rectal distention > 2.9 cm). Not every centre knows how to do it, check with radiology first, otherwise, it will just be wasting of time
  • anorectal manometry 
  • blood tests limited value (TFTs, Ca)
What is the management ?

  • Good flow chart from DCH lecture 
  • Education 
  • Laxatives 
    • disimpact if significant retention 
    • maintenance therapy, 6 months at least 
  • Toileting program: bowel opening post meals 
  • Treat anal fissures
  • Toilet diary (behaviour modification) 
Toileting program 
  • Ensure adequate fluid intake (50ml/kg/day)
  • Ensure adequate fibre intake
  • Toilet posture
    • support feet with a stool, it helps relaxing pelvic floor muscle
    • toilet sit after meals (gastrocolic reflex)

References
  • Diploma of child health: encopresis and enuresis lecture 

Approach to constipation


  • Constipation is common, occurring in 30 % of children

  • Red flags
    • constipation presents early in life < 6 weeks
    • functional constipation is the most common cause of constipation in childhood 

  • Some other less common causes 
    • Medical: cow milk allergy, coeliac disease, hypercalcaemia, hypothyroidism 
    • Surgical: hirschsprung disease, meconium ileus, anatomic malformations of anus and spinal cord abnormalities

  • History
    • Timing of meconium passage
    • Painful/frightening precipitant
    • Straining 
    • Toilet refusal, hiding while defecting, crossing legs or other withholding behaviour 
    • Faecal or urinary incontinence, day or night 
    • Weight loss, vomiting or PR blood loss - suggests possible organic disease
    • Stool description 

  • Examination 
    • Height and weight -- failure to thrive
    • Abdomen - palpable faeces
    • Spine - deep sacral cleft or tuft of hair 
    • Neurology - assessment of lower limbs 
    • Anal area - visually examine for fissures, internal examination not required

  • Management 

    • Behaviour modifications
      • Toilet sits - 5 minutes 3 times a day, preferably after meals 
      • use chart or diary 
    • Diet 
    • Medication
      • Titrate medicaion aiming for one soft, easy to pass bowel action per day 
      • children: stool softener or iso-osmotic laxative 
      • infants 6-12 months: colocyl drops or lactulose 
      • infants < 6 months: coloxyl drops 

References: 
  • RCH 
  • John Murtagh

Approach to enuresis


  • Enuresis can be defined as daytime wetting (diurnal enuresis) after age 4 years or night-time wetting (nocturnal enuresis) after 6 years. Usually no treatment is required before that. 

  • Red flags
    • Referral > 6 years old or any age with continual dripping to paediatric nephrologist
    • Any child with a febrile urinary tract infection with abnormal renal US
    • Any child with a congenital anatomic genitourinary concern  (posterior urethral valves, vesicoureteral reflux, hydronephrosis, ureteropelvic junction obstruction, bladder or urethral abnormalities or genital malformation)

  • It is very common. About 50% of children aged 3 years wet the bed, as do 20% of children aged 4 years and 15% of children aged 5. 

  • Usually there is no underlying cause found but we tend to blame:
    • parents: there is a genetic tendency
    • small bladder
    • deep sleeper
    • kidneys like to produce urine at night 
    • Constipation (make sure the child is not constipated)

  • Some disorders that we like to exclude:
    • urinary tract infection 
    • diabetes mellitus
    • diabetes insipidus
    • neurogenic bladder
    • urinary tract abnormality

  • Investigations
    • Urine MCS
    • Renal ultrasound 

  • Management for nocturnal diuresis
    • it is mainly behavioural
    • the most effective way is using a bed alarm 
    • it takes 6-8 weeks for it to work 
    • takes some effort and parents will need to be happy to get involved
    • first step: get a bed alarm. it sounds obvious but some parents do not want to because financial reasons
    • second step: practice using it with the child. Pour salting water on to it and listen to the alarm
    • Practice routine when the alarm goes off. The child needs to get up, turn the alarm off, go to the toilet and empty bladder completely, come back and change the sheet/material on top of the alarm and turn the alarm back, go back to sleep
    • The child is better only to wear underpants to go to sleep rather with trousers 
    • for parents handout: go to http://www.rch.org.au/kidsinfo/fact_sheets/bedwetting/

  • Medication if alarm fails:
    • DDAVP 200-400 mcg tablets 
    • if that fails, use that with an alarm 
References:
  • General practice 5th edition by John Murtagh
  • RCH 

Approach to common paediatric problems


Crying and fussing in infants

Blocked nasolacrimal duct

Failure to thrive (FTT)

Short stature

Enuresis

Encopresis

Constipation

Approach to delayed puberty

Definition

  • Absence of pubertal development in 
    • girls > 14 years 
    • boys > 15 years
Causes
  • Constitutional delay (commonest, usually familial)
  • Chronic illness (coeliac etc)
  • Poor nutrition and exercise
  • anorexia nervosa 
  • Turner syndrome and gonadal failure
Investigations
  • FBE and ESR
  • Kidney function 
  • Thyroid function tests
  • chromosomal analysis (usually in girls to exclude turner's syndrome 
  • serum FSH, LH, Prolactin, testosterone (exclude kallman syndrome) 
  • x-ray of the wrist to determine bone age 
  • pelvic ultrasound in girls 
Management 
  • Refer to endocrinologist 
References:
2. John Murtagh

Approach to short stature

The three major growth factors are genetic, nutritional and hormonal. The hormones that are essential for a normal growth process are growth hormone and insulin-like growth factor I (the key), thyroxine, cortisol and sex steroids.

Ten essential questions from murtagh

1. Is the child actually short ?
2. Is the child short compared with other children?
3. Is the child unexpectedly short from a genetic viewpoint?
4. Is the child's growth slowing ?
5. If the growth is slow, what is the reason?
6. How dose the child feel about the short stature?
7. How does the height percentile match against a growth velocity chart?
8. Has puberty commenced?
9. Is there any specific investigation warranted?
10. Is there any specific therapy warranted?

The causes of short stature can be grouped into the following categories:
1. Organic causes
2. Constitutional delay
3. Familial short stature

Examination
1. General inspections includes dysmorphic features and nutritional status. Measure all anthropometry (height, weight, GV, upper/lower segment ratio) and compare with percentile charts
2. Measure skeletal proportions
3. Assess pubertal status

Investigations
If GV is < 25th percentile for bone age, consider

  • TSH
  • FBE and ESR
  • Coeliac disease
  • Chromosomes in all girls. Karyotype to exclude Turnes 45 XO 
  • Growth hormone studies: IGF - 1 
  • Kidney function 
  • Bone age x-ray (left wrist) 

Management:
- May require growth hormone 

References:;
John Murtagh 
http://www.rch.org.au/uploadedFiles/Main/Content/MedEd/fracp/short%20stature%20NEJM.pdf

Wednesday, 13 July 2016

Failure to thrive / poor growth


Don't forget that there are two patients during the consultation. (Mum and baby)

Most common cause > 90 %. Normal variant and nutritional deprivation

History and examination is the key. No use ordering a lot investigations

Measure weight, height and head circumference and plot them on growth chart

** Feeding history is the key **

General observation is the key to this examination. Mother baby interaction, signs  of abuse and neglect, loss of muscle bulk and subcutaneous fat sores.

Red flags:

  • Signs of abuse or neglect
  • Poor carer understanding 
  • Signs of family vulnerability e.g. drug and etoh abuse, domestic violence, social isolation, no family support 
  • signs of poor attachment 
  • parental mental health issues
  • already/previously case managed by child protection services
  • did not attend or cancelled previous appointments
  • signs of dehydration 
  • signs of malnutrition or significant illness


Investigation (if required):

  • FBE, ESR
  • UEC, LFT
  • Iron studies
  • Calcium, phosphate
  • Thyroid function 
  • Blood glucose
  • Urine MCS
  • Coeliac screen
  • Stool MCS
  • Stool for fat globules and fatty acid crystals 
Management depends on the cause. Most of the time can be managed in the community. Admission may be required if the child is dehydrated and unstable social situation. 


References:
RCH
John murtagh


unsettled or crying babies


Background

- It is normal for babies to cry
- The mneumonic is PURPLE crying

  • P for peak of crying. Peaking at about 2 months
  • U for unexpected crying. 
  • R for resists soothing. 
  • P for pain like face
  • L for long lasting. Crying can last for several hours a day
  • E for evening. Cry more in the late afternoon and evening
- Common non pathological causes of crying 
  • Excessive tiredness
  • Hunger 
- Differential diagnoses to consider include:
  • Cow milk/soy protein allergy 
  • GORD
  • Lactose overload/malabsorption 

Red flags:

- Sudden onset of irritability and crying should not be diagnosed as colic, a specific cause is usually present
- The maternal and family psychosocial state must be taken into account. Maternal post-natal depression may be a factor in presentation. Note that excessive crying is the most proximal risk factor for shaken baby syndrome

- Suspect cow milk/soy protein allergy if

  • vomiting/blood or mucus in diarrhoea/poor weight gain/family history in first degree relative/signs of atopy (eczema/wheezing)/significant feeding problems (especially worsening with time) 
  • gastro-esophageal reflux is diagnosed
  • lactose malabsorption is diagnosed in formula fed babies


Investigation
  • really depends on the history 
  • for acute cry
    • Urine MCS (if acute crying and vomiting)
    • Fluoroscein staining of eyes (if history suggestive)
Management
  • Exclude medical cause (including mum--> ? depression) 
  • Explanation and reassurance
1. Engage in a partnership with the parents
2. Explain normal crying and sleep patterns
3. Assist parents to help their baby deal with discomfort and distress
  • Give mother permission to rest once per day 
4. Assess maternal and emotional state and mother baby relationship
5. Sometimes when you are really frustrated, it is ok to put your baby down few minutes and calm yourself down


Conclusion
  • Most of the time it is normal and no medical cause is found 
  • The most important thing is to gain the parents trust
  • Give them clear explanation 
  • Minimal intervention from us is the best intervention

References:
John Murtagh 
RCH website

Saturday, 9 July 2016

Hyphaema

Hyphaema : blood in the anterior chamber. When clot fills the anterior chamber it is called an 8-ball hyphema.

History:

  • symptoms: pain, blurred vision, loss of vision 
  • injury: blunt trauma? what happened ? when ? how ?
  • Bleeding diathesis: disorders, medications, history of sickle cell disease 
  • Use of eye protection 
Examination:
  • Visual acuity - variable 
  • External examination: check for concomitant head and facial injury 
  • pupillary reflex
  • Tonometry 
  • Slit lamp examination if there is one available 
  • Fundoscopy and red reflex 
Investigation and management
  • Oral analgesia and topical cycloplegics for comfort, Consider antiemetics.
  • Remain upright 
  • Apply an eye shield (how to pad an eye)
  • Avoid blood thinners
  • Treat secondary glaucoma
  • Surgical evacuation 
  • review by an opthalomologist within 24 hours 
Hospital admission criteria
  • non compliant patients
  • children 
  • increased IOPs
  • sickle cell disease
  • bleeding diathesis or blood dyscrasia 
Follow up and discharge advice
  • examine by an ophthalmologist on a daily basis (or on day 3 on a microhyphema)
  • refrain from strenous physical activities for 1 week after the initial injury or a rebleed
Complications
  • rebleeding 
  • glaucoma
  • corneal staining
  • traumatic iritis 
References: 
- life in the fast lane 

Burns

I am scared of burns. I don't know what to do but after seeing burns for a few times, I start to get some understandings of it. I tend to follow the following principles (hopefully most of the burns we see at GP clinic is just minor burns):

1.  Assess the whole person, follow the principle of ABC 

2.  Know when to refer, the burns unit is available 24/7 for you to get advice (please go to RCH website), refer 
  • All full thickness burn
  • Circumferential burns
  • All burns to face, eyes, ears, hands, feet, genitalia, perineum or a major joint, even if less than 10 %
  • Chemical burns
  • Electrical burns
  • Burns associated with significant fracture or other major injury 
  • All inhalation or airway burns
  • Burns in children under the age of 12 months
  • It is out of your/your hospital's comfort zone 
3. Assess the TBSA of burns. In children, their palm size is around 1 % of their body surface area. In adults, you can use your palm to gauge

4. Categorize burns into the following 3 categories and treat accordingly:
  • superficial: only epidermis is involved
  • superfical partial thickeness: dermis is involved, forms blister, fixomull 
  • superficial deep thickness: hist white slough, red mottled, sluggish capillary return
  • Full thickness: dry, charred whitish, absent capillary return 
5. 
superficial burn --> can leave it open, in infants  use non adherent dressing
partial thickness burn --> mepilex Ag Tm with crepe bandage or acticoat 3/7
Full thickness burn --> refer 

Reference:
1. RCH burns guideline 

Friday, 8 July 2016

About me

This site serves a few purposes:

1. Fulfil the RACGP training requirement

2. Capture some of my study notes and summarise notes for common presentations to general practice

3. Verbal diarrhoea

I am a GP registrar who finds out actually does not want to be a GP at all. Unfortunately, too deep into the training program and with no other specialty to turn to, is getting stuck being a GP for eternity.

After accepting this as a reality, trying hard to be a good GP and resist in prescribing antibioticss and benzos. Got into at least one argument per day with patients as I refuse to prescribe them the medications they want.

Also has a special interest in dermatology and trying to learn as much as I can on this topic. Hoping to get into dermatology training in my next life or the next next life.

My life is propelled forward by two external forces. One is my wife and one is my daughter. The reason I am going to work is mainly because of them. Children are expensive and I don't have the courage to rob a bank or smart enough to sell drugs on the street. The only option that left is continued being a gp.


Thursday, 7 July 2016

Approach to tiredness/fatigue

Tiredness/chronic fatigue: diagnostic strategy model

Probability diagnosis

  • Stress and anxiety
  • Depression
  • Viral/postviral infection 
  • Sleep-related disorder (e.g. sleep apnoea)
Serious disorders not to be missed
  • malignant disease
  • cardiac arrhythmia (e.g. sick sinus syndrome)
  • cardiomyopathy
  • anaemia 
  • hidden abscess
  • haemochromatosis
  • HIV infections 
  • Hepatitis C
Pitfalls
  • 'Masked' depression
  • Food intolerance
  • Coeliac disease
  • Chronic infection (e.g. lyme disease)
  • Incipient CCF
  • Fibromyalgia
  • Lack of fitness
  • Drugs: alcohol, prescribed, withdrawal
  • Menopause syndrome
  • Pregnancy
  • Neurological disorders
    • post-head injury
    • CVA
    • Parkinson disease
  • Kidney failure
  • Metabolic (e.g. hypokalaemia, hypomagnesaemia)
  • Chemical exposure (e.g. occupational)
  • Rarities
    • Hyperparathyroidism
    • Addison disease
    • Cushing syndrome
    • Narcolepsy
    • Multiple sclerosis
    • Autoimmune disorders
Minimal investigations from John Murtagh General practice 5th edition:
  • FBE
  • ESR/CRP
  • TFTs
  • Coeliac serology
  • LFT
  • CMP
  • BSLs
  • Iron studies
  • Urine MCS

Approach to sore throat

Sore throat: diagnostic strategy model

Probability diagnosis

  • Viral pharyngitis
  • Streptococcal tonsillitis
  • Chronic sinusitis with postnasal drip
  • Oropharyngeal candidiasis
Serious disorders not to be missed
  • Cardiovascular 
    • angina
    • myocardial infarction 
  • Neoplasia
    • cancer of oropharynx, tongue
  • Blood dycrasias (e.g. agranulocytosis, acute leukaemia)
  • Severe infections:
    • acute epiglottitis 
    • peritonsillar abscess
    • pharyngeal abscess
    • diphtheria 
    • HIV/AIDS
Pitfalls (often missed)
  • Foreign body 
  • Epstein-Barr mononucleosis
  • Candida
    • common in infants
    • steroid inhalers
  • STIs:
    • gonococcal pharyngitis
    • herpes simples (type II)
    • syphilis
  • Irritants (e.g. cigarette smoke, chemicals)
  • Reflux oesophagitis --> pharyngolaryngitis
  • Tonsilloliths
  • Cricopharyngeal spasm
  • Kawasaki disease
  • Chronic mouth breathing 
  • aphthous ulceration 
  • Thyroiditis
  • Rarities
    • scleroderma
    • behcet disease
    • sarcoidosis 
    • malignant granuloma 
    • tuberculosis

Wednesday, 6 July 2016

Breaking bad news

Unfortunately, it is part of the job. Everyone will develop their own styles. The following is the guideline I try to follow adopted from John Murtagh's general practice:

1. Plan the consultation, check facts, set aside ample time
2. Meet in an appropriate room with privacy and no interruption
3. Ask the patient if they would like company
4. Make good eye contact and be alert for non-verbal responses
5. Use simple, understandable language
6. Be honest and diplomatically to the point (don't cover up the issue)
7. Allow time, silence, tears or anger
8. Don't give precise predictions about life expectancy


References:
1. John Murtagh General Practice 5th edition

Paediatric sleep disorder

Paediatric sleep disorder is very common. Most of the time it is behavioural and does not require  medication. Recently, there is a huge surge in melatonin prescription and most of the scripts come from paediatricians. I also have parents coming in asking for melatonin to help their kids going to sleep. The following is a structured approach I use in a consultation:

History taking. I use this mneumonic called BEARS.

B: Bedtime problems.

E: Excessive daytime sleepiness

A: Awakenings during the night

R: Regularity and duration of sleep

S: Sleep disorder breathing

After history, you can usually able to categorise the child into one of the sleep disorder categories.
1. Not enough sleep (difficulty initiating or maintaining sleep)--> behavioural intervention
2. Increased need for sleep (excessive sleepiness or hyper somnolence) --> refer
3. Fragmented sleep  (episodic disturbances e.g. sleep related breathing disorders or movement disorder)--> refer

At GP setting, the most common sleeping disorder we encounter is not enough sleep. This often happens with infants or young children. Parents come in complaining that they are not getting enough sleep and demand something to be done straight away. They cannot handle this anymore. There is always a sense of urgency and as a GP, you always feel pressure to do something to relieve their distress.

There are some resources out there which I use as a guideline when I am under the pump from the parents or when I need some guidance:

Behavioural sleep problems in school aged children

Sleep health foundation has plenty of information about sleeping and children


The reality is that most parents want quick fix and when you tell them that there is no quick fix or you don't prescribe what they want. They get upset pretty quickly so parental rapport is very important at the beginning of the consultation.