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

Medication Cessation

Key points:

1. patients who are on 5 drugs or more are at an increased risk, up to 30 %, of experiencing an adverse drug-related event (ADE) over the next 6 months, which may lead to hospitalisation.

2. When reviewing medications for patients who are on multiple medications, the following issues need to be established:

• the current indications for each drug
• Patient and carer's perception of the efficacy and side effects Phyllis has experienced with each drug
• whether there are any drugs she is not taking and reasons for non compliance
• scientific evidence for the benefits and harms of each drug
• a shared understanding with patient of the likely future course of illness and what she values as the goals of care

3. The CEASE protocol includes a systematic method for appraising the utility of individual medications and deciding which ones may be worthy of discontinuation and in which order. The following 6 questions are there to help with the process:

• Is there a valid indication for each medication?
• right diagnosis? active disease?
• evidence to use those medications?
• Is the drug part of a prescribing cascade seeking to counteract side effect of other medicines?
• Is the drug, on balance, more likely to do harm than confer benefit over the medium to longer term?
• Is the drug being prescribed for disease or symptom control despite either being ineffective of where symptoms have completely resolved or are amenable to non-drug interventions?
• Is the drug a primarily preventive medicine, which is unlikely to confer any patient-important benefit over the patient's remaining lifespan?
• Is the drug imposing unacceptable treatment burden?

4. The drugs that should take priority in being discontinued are those with the lowest utility and least likelihood of being associated with withdrawal syndromes or disease rebound. (Figure 1 Algorithm for deciding the order and mode in which could be discontinued)

5. Cease one drug at a time so that harms and benefits can be attributed to specific drugs and rectified.

6. Wean, not abruptly cease, drugs that are more likely to cause adverse withdrawal effects. Instruct the patient on what to look for and report in the event of such effects occurring, and what actions they can self-initiate if these were to occur

7. Fully document the reasons for, and outcomes of, de-prescribing

Melanoma

Condition

• Melanoma

Definition

History

• Risk factors for melanoma
• Older age
• Men > Women
• History of sun burn (Melanoma is more associated with episodic intense sunburns than more continuous sun exposure).
• past history of melanoma increases risks by 10 fold
• non melanoma skin cancer may increase the risk fourfold 
• Family history: first-degree relative doubles the risk of a person developing melanoma

Examination

• examine the whole skin surface under good lighting 
• if melanoma is suspected, the patient should be examined for enlarged lymph nodes in the appropriate draining area (e.g. axial or groins)

Investigation 

• excisional biopsy if possible: 
• stage 0 < 0.1mm
• stage 1 < 2 mm without ulceration or up to 1mm with ulceration 
• stage 2 > 2mm 
• Stage 3: spread to lymph nodes
• stage 4: distant spread

Management

• excisional biopsy 
• often requires referral

Key points:

• In Australia, it has been shown that up to 75% of patients detect their own recurrences.
• No evidence that earlier detection by routine scans or examinations improves the outcome.
• Instruct patient to gain awareness of lesions on their skin and report any persisting symptoms promptly.
• Sun protection when the ultraviolet (UV) index is 3 or above to prevent further skin damage and subsequent skin cancers

References:

Check program 2015 September Cancer

Dermatoscopy

Key points:

- Skin cancer is common in Australia and GPs need to be competent in assessing skin lesions.

- The use of a dermatosope in clinical practice has been shown to increase diagnostic accuracy and is considered the standard of care in assessing patients with pigmented skin lesions.

- All visible lesions that cannot be confidently diagnosed should be examined with a dermatoscope.

- Dermatoscope is more than a magnifying lens and light source. By eliminating reflection from the skin surface, the dermatoscope allows better visualisation of the patterns formed by pigment and blood vessels - critical features in the diagnosis of skin lesions. (Try to get one if you don't have one already)

- There are many different methods in analysing a pigmented lesions. (CASH, the ABCD method of dermatoscopy, the 7-point checklist, the Menzies method, the 3 point checklist, the revised pattern analysis and a short modification of revised pattern analysis called 'chaos and clues'.

- The method I learned is called Chaos and Clues.

- First, we need to learn how to describe pigmented structures, which are objectively defined using the following geometric terms:

• Line: a two dimensional continuous object with length greatly exceeding with 
• Pseudopod: a line with a bulbous end
• Circle: a curved line equidistant from a central point
• Clod: any well circumscribed, solid object larger than a dot; clods may take any shape
• Dot: an object too small to have a discernible shape 
• Lines are further classified into 5 types: reticular, branched, parallel, radial and curved, as these have diagnostic significance

- Blood vessels can be described the same way:

- Colour has great diagnostic significance in dermatoscopy. The main pigments are melanin and haemoglobin, and the colours produced are shown :

- The chaos and clues algorithm:

• The first step is to dermatoscopically assess the pigmented lesion for 'chaos', defined as asymmetry of structure or colour'. Chaos is assessed by pattern not shape. As perfect symmetry is biologically rare, some deviation from geometrical symmetry must be expected. It is helpful to imagine a piece of carpet that can be cut in any shape but which maintains uniform pattern.  It would be regarded as having no chaos regardless of how irregular the shape was and regardless of the presence of a little dust on one part. 
• If chaos are identified, look for clues. 
• As for all the algorithms, there are always exceptions: beware of dermatoscopic grey on head or neck, pigmented nodular lesions, parallel ridge pattern (palms or soles)

- As with many things in life, they don't come easily. It takes a lot of time to practice, practice and practice. If in doubt, do a biopsy. (Spoke to a surgeon in the past, he told me that he has never regretted taken out a normal appendix but he always regret on the ones which he didn't. Biopsy rarely results in major harms but melanoma kills.)

Reference:

1. Dermatoscopy in routine practice 'Chaos and Clues'. Australian Family Physician. 2012. 

Gout

Key points:

1. Gout is the most common inflammatory arthritis with a prevalence of about 2% in Australasia.
2. Key steps in the development of gout are 1)chronic hyperuricemia 2) monosodium rate monohydrate 3)interaction between the crystals and the inflammatory system, which is primarily responsible for the clinical features. 
3. Definition of hyperuricemia: serum rate level > 0.42
4. Hyperuricemia is caused by medications and genetic predisposition
5. Only 20% of patients with hyperuricemia develop gout 
6. Definite diagnosis can only be achieved via synovial fluid analysis. This needs to be done before recommending hypouricemic drug therapy.
7. Management of acute gout:
   
   8. There is an increase risk of gout when the patient is started on rate lowering therapy. Patients can be started on low dose colchicine 0.5 mg daily or daily NSAID or 5mg prednisolone. Usually prophylaxis is required for around 3-6 months.
   
   
   9. Serum rate target is less than 0.36 mmol/L, however for patients with a large rate crystal load (as reflected by the presence of tophi) erosions or chronic joint deformity due to gout, the target is a serum rate of less than 0.3 mol/L
   
   
   10. Diet and lifestyle modification alone usually is inadequate to lower serum urate level.
   
   
   11. Allopurinal hypersensitivity syndrome occurs with greater frequency in the setting of renal insufficiency, advanced age, HLA B58:01 positivity and higher initial doses but can occur in their absence. The syndrome usually occurs in the first 12 weeks of exposure, and thus the development of rash during this period should prompt immediate cessation of allopurinol, assessment of liver and renal function, and for the possibility of hypersensitivity. 
   
   
   12.Probenecid is another agent which can be used as rate lowering agent. But the patient needs to have renal function > 30-40ml/min. Because of the marked increase in urinary uric acid in the early phase of treatment, good hydration and urinary alkalisation are appropriate. 
   
   
   
   
   
   
   

Osteoporosis

Key points:

- Osteoporosis is under-recognised and under-treated, even in people who present with a minimal trauma fracture.

- A minimal trauma fracture is sufficient for a presumptive diagnosis of osteoporosis medicines can start prior to obtaining BMD results with dual energy x-ray absorptiometry (DXA).

- Guidelines recommend risk factor assessment and that modifiable risk factors be addressed in all postmenopausal women aged >45 years and men aged > 50 years.

- A full diagnostic investigation is indicated for:

• women> 50 YEARS and men> 60 years with other clinical risk factors 
• Patients > 45 years with a minimal trauma fracture or suspected vertebral fracture 
• patients who have causes of secondary osteoporosis (medical conditions or medicines such as long-term, high-dose corticosteroids)
• adults aged over 70 years 

- Clinical risk factors (CRFs), use the mneumonic of shattered 

Previous minimal trauma fracture, family history 

• S: steroid use (oral corticosteroid use > 5mg/day)
• H: hyperthyroidism, hyper parathyroidism and hypercalciuria 
• A: Alcohol and tobacco use 
• T: Thin (BMI < 22)
• T: Testosteron decrease (e.g. anti androgen ca, prostate Rx)
• E: Early menopause 
• R: renal or liver failure 
• E: Erosive/inflammatory bone disease (e.g. myeloma or rheumatoid arthritis)
• D: Dietary Calcium decrease/malabsorption , DM1 

- The strongest risk factor is age > 70. Peak bone mass is achieved by age 30. Bone loss occurs steadily from the age of about 40, with accelerated loss in perimenopausal period (4-6%) before slowing again after the age of 70 (1-2% per year).

- Basic investigations: DEXA, Ca, PO, ALP, FBE, UEC, LFT, myeloma screen if indicated

• Hip bone mineral density best predictor for hip fracture
• Lumbar spine bone mineral density best for monitoring treatment effect
• 
  

- Management:

• lifestyle measures
• quit smoking and reduce ETOH consumption 
• Weight bearing exercise may increase bone mineral density 
• Balance exercises such as tai chi reduce risk of falls 
• Calcium and vitamin D supplements 
• recommended dietary intake of calcium is between 1000 and 1300 mg per day, depending on age and sex
• Most Australians do not reach the recommended dietary intake so daily supplements of 500-600 mg of calcium are sometimes needed
• Safety of calcium is still a controversial topic as there is evidence that it may increase risks of MI
• Home based fall prevention program, with visual assessment and a home visit
• Medications 
• Bisphosphonates and Denosumab
• Criteria: minimal trauma fracture or age > 70 with T score <=-2.5
• Bisphosphonates: well tolerated, some significant side effects: oesophageal cancer? (not proven), osteonecrosis of the jaw (see dentist prior to commence treatment) and do not use with the other antiresorptive or anabolic agents
•  Denosumab: use with caution in patients with severely impaired kidney function as denosumab may exacerbate hypocalcaemia 
• Raloxifene 
• postmenopausal woman with a minimal trauma fracture and risk of vertebral fractures predominatly
• reduces vertebral fracture but not non vertebral fractures in postmenopausal women
• Reduces risk of breast cancer so suitable for women at high breast cancer risk
• Associated with increased risk of DVT or pulmonary embolism in meta-analyses
• Strontium ranelate
• Criteria: unable to tolerate other medications or contraindicated to other medications
• assess patient risk of developing CVD before treatment due to safety concerns in patients with history of CVD, embolism or stroke 
• Teriparatide 
• Reduces vertebral and non - vertebral fractures in postmenopausal women 
• limited evidence in men
• must be initiated by a consultant physician
• Vitamin D deficiency
• 600 IU per day for people under 70
• 800 IU per day of people over 70 
• 1000-2000 IU per day may be required for sun avoiders or those at high risk of deficiency
• Monitor treatment response and review therapy to encourage adherence
• BMD measurements 2 years after the commencement of therapy or 1-2 years after therapy changes significantly

Approach to ceasing medications in elderly patients

Key questions to ask:

1. Is there a valid reason for each medication ?

2. Is the drug part of a prescribing cascade to counteract side effects of other medication?

3. Is the drug more likely to do harm than good in medium to long term ?

4. Is the drug prescribed unnecessary or ineffective or amenable to non drug intervention?

5. Is the drug primarily preventive medicine, which is unlikely to confer any patient important benefit over the patient's remaining lifespan?

6. Is the drug imposing unacceptable treatment burden?

References:
RACGP check program

Polycystic ovarian syndrome

Key points :

- It is the most common endocrinological disorder (12-18 % women in reproductive age)

- Presentations: Menstrual irregularity (>35 or < 21 day cycles), overweight, hirsutism, fertility issues, pre diabetes, gestational diabetes or early onset type 2 diabetes, not high risk ethnic groups (Asian, indigenous, Nth African)

- Rotterdam Diagnostic criteria:

• Requires 2 of 
• Oligo- or anovulation 
• Clinical and/or biochemical hyperandrogegism
• Polycystic ovaries; and exclusion of other aetiologies

- Differential diagnosis investigations: TSH, Prolactin and FSH (if premature menopause suspected), free testosterone, DHEAS, SHBG, 17 hydroxy progesterone, FSH, LH

- Total testosterone is often normal in PCOS. cFT is often elevated. 

- PCOS management areas include:

• Emotional health: depresion and anxiety is more common. Assess mental health is the key. 
• Lifestyle : aim for 5-10 % weight loss 
• Cardiometaboic health: Smoking cessation, check BP annually, lipid profile and OGTT every 2 years
• Weight management:5-10% weight loss 
• Fertility: weight loss if BMI > 25 is the first line treatment, metformin (500 mg daily, increase by 500 mg per fortnight up to 1500 mg - 2000 mg average dose) and clomiphene 
• Menstrual cycle regulation: lifestyle and metformin, OCP 
• Clinical hyperandrogenism (eg hirsutism): OCP, if OCP alone doesn't work after 6 months, then try anti androgen (spironolactone) 
• Sleep apnoea 

References:
https://jeanhailes.org.au/contents/documents/Resources/Tools/PCOS_GP_tool.pdf

Achilles tendonosis

Key features:

- Often gradual and insidious onset.

- Diagnosis is mainly made via history and examination. Imaging is not indicated in most cases, however, if there are atypical features such as sudden onset and significant swelling. U/S may be appropriate

- U/S features of tendonosis: neb-vascularity and fusiform thickening

- X-ray is indicated when: insertional tenderness or posterior impingement

- Pathophysiology of tendonosis is not fully understood. May be related to overtraining.

- Management:

• Rest (may need to be off sports for 4 - 6 weeks)
• Gradual return to activities
• Eccentric exercise program (12 weeks, 3 sets, 15 reps of slow heel drop)
• NSAIDs
• Autologous blood injection and platelet rich plasma injection 
• GTN patch + eccentric exercise 

Ankylosing spondylitis

Key features:

- Ankylosing spondylitis encompasses a group of rheumatic disorders that share clinical, genetic and radiographic features and includes psoriatic arthritis, reactive arthritis or inflammatory bowel disease.

- Affects 1 in 200 individuals and is usually diagnosed many years after onset of symptoms . Chronic back pain is common and recognition of early disease requires clinical experience and a high index of suspicion. Further, inflammatory markers are not invariably elevated and radiographic changes are often late findings.

  - The presence of inflammatory back pain (IBP), the archetypal feature of AS, increases the likelihood of SpA to approximately 14%.

- Two very specific features of IBP are alternating buttock pain and awakening only in the second half of the night with spinal pain or stiffness. Table listed the difference between inflammatory and mechanical back pain

- Examination findings:

• Reduced spinal mobility: modified schober's test, lumbar side flexion and occiput to wall distance.
• Extra axial features: 50% asymmetric oligoarthrits (< 4joints), often targeting the lower limb joins, enthesitis and dactylitis.
• Extra-articular features: uniocular anterior uveitis in 40% of patients (presents with acute painful red eye, blurred vision and photophobia)

- Investigation findings: 

• Lab test: CRP, ESR (Only 50-70% of AS patients), HLA-B27
• Imaging: x-rays

References:

- http://www.racgp.org.au/download/Documents/AFP/2013/November/201311golder.pdf

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

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

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

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.

NSAIDs - How to prevent GI bleed?

NSAIDs - How to prevent GI bleed?


I saw a young man today with likely ankylosing spondylitis. I started him on NSAIDs. He told me that he suffers from reflux, this brings up a question, how can I reduce the GI side effect?

How does it work ? (This is to remind myself, I seriously can't remember)

Key points:

1. No one NSAID is safer another. 

2. Use low dose NSAIDs for the shortest time possible. 

3. COX-2 NSAIDs seem to have less GI side-effects

4. Co-infection of H. Pylori and the use of NSAIDs increase the risk of GI ulcer by 60 folds and bleeding by 6 folds. 

5. Other drugs which can increase bleeding risks include: anti platelets, anti coagulants, anti depressants, corticosteroids, cigarette, smoking and excessive ETOH consumption.

6. Some other risk factors of GI bleed: 

7. Consider the use of PPI in high risk groups: 

Reference:

Australian therapeutic guideline