Bye bye primary exams

28 09 2013

So I finally passed the primary exam last week.
After 2 years ….. looking back it was a bloody struggle. Few failed attempts…. juggling work and busier shifts.

Am so relieved and thankful that I vow to help those in need of passing the primary too.

Posts coming up :

a. tips + tricks
b. ways to motivate
c. tools I used

Probably the most important viva resource I found was from a website by the Auckland team :

ED Thursday Teaching

27 07 2013

as with our department – – with people calling in sick and lack of motivation (the tyranny of distance for some ; not being a trainee) or recreational leave : our attendance was minimal.

having said that : we had a great session!

1st session :


got grilled in the resus bay about the knobology and stuff.

The key messages taken away is to be aware of plateau pressures and hot to measure them.

Found some good links from the great LITFL crew courtesy of Chris Nickson :


Case presentations

few great cases : 1 about a rather rare cause for abdominal pain (epiploic appendigitis), 1 about Kawasaki’s and mine about perilunate dislocations.


Grand Rounds

had Dr Louise Cullen from RBWH presenting about chest pains (and the new diagnostic strategy to safely rule out the super duper low risk ones)



Exams in 20 days time ! EEEPS



friday at shift

13 07 2013

started out wither another fast AF Seconday to cessation of beta blocker. given some magnesium ; slowed down …yay


next case was interesting 10 y/o bilateral conjunctivitis for 1 week, followed by urinary symptoms; fevers and possibly a painful left knee ?? – possibly trauma from the day prior

? kawasakis vs reiters vs septic arthritis…

will have to see what happened

bloods and a knee joint aspirate were sent


next case INR of >10 and jaundiced….. hmmm

diverticulitis on CT ! as well as HOP incidentally.

needed prothrombinex.


3rd middle prox metacarpal # – oblique —> volar slab

another sporadic post

12 07 2013

thought i’d put a note to my shift yesterday.

Patient 1.

A flutter with syncope – admit telemetry

cause ? (probably too much flecainide and all the agents – alpha blocker/beta blocker/CCB/flecainide)

need to revise : Drugs for anti-arryhmics esp flecainide

Physiology : cardiac AP


2. Man seen yesterday w ? gastritis (used NSAIDs for weeks for arthritis) and today presents with worsening tummy pain and rash.


Rash – confluent maculopapular kind – distributed all over – not specific distribution. blanching. looks like drug rash.

Tummy – RLQ pain +++


diagnosis – perforated appendix w free fluid on CT. 

lessons : good disposition for ppl with abdo pain – rash is a bad sign

need to look up literature about rash + abdo pain. ( i thought that was from nurofen !)


3. # cuboid + tuberosity of 5th metatarsal

anatomy – good to revise bones of feet and muscles of ant part of leg.


4. Scans done :

a. 1 FAST

b. 1 LUS – B lines in LLL suggestive of infiltrative process.


5. I+D right upper lip abscess

used infraorabital nerve block.

anatomy : revise face / triangle of danger

Sporadic and tachycardic

23 05 2013

infrequent. sporadic. intermittent.

my posts are like these. am a big procrastinator.

the primaries are in 83 days again.

(flunked anatomy and physiology…ouch)


anyway would put relevant cases I see with my primaries.



Saw a Cat 2 2 days ago.

22 y/o F. Palpitations HR 170.

right…. straightaway comes to mind SVT ain’t it ?


brought to Resus. Adenosine drawn up, my senior doing cannula and bloods.

and then I saw the patient’s mum carrying 2 things in their hand :

a. Path results from 1 week ago showing T3 of 30 ; TSH < 0.01

b. Carbimazole





turns out this poor lass has been sick for the last 1 week with nausea/vomiting/headaches/URTI symptoms. NO rigors though and only could manage her carbimazole half the days. Had bloods with her GP and endocrinologist 1 week ago and only got the results on that day – her endo asked her to take 60mg carbimazole and see him in 1week’s time.

she had palpitations from the onset of 1400 pm and couldn’t sleep. (didn’t tell her mum until her mum saw her being pale and SOB)


HEr BP was 140/90 Sats 99% on R RR20 and Temp 36. NO focal signs of infection. CXR normal.

BLooods reassuring show normal K / renal function and her ECG showed a sinus tachy of 130.


Settled with some fluids to 125. but she felt palpitations still…..



SO…not SVT.

probably palpitations from sinus tachy precipitated by URTI +- UTI (Urine stil pending) ; complicated by hyperthyroidism.

We ended up given lots of anti emetics and made her chug some propranolol and another 20mg carbimazole and admitted under telemetry

Lessons learnt:


a. A little bit of thyroid physiology revised.

Spent 7 minutes watching this video :

b. Antithyroid medications.


Revised carbimazole/prophylthiouracil

Happy New Year…and a rant

9 01 2013

Happy new year guys. or myself.

So far, studying has been slow and work tiring —-been procrastinating my 1 drug a day….

Just a rant…

its a new year !

We had a little boy 6 years of age with 8 days of intermittent nausea/lower abdo cramps/vomiting/diarrea (non billous) whom mum says has lost 4 kg !

He had some right lower quadrant aches , otherwise soft tummy (and looked really well – afebrile, HR 80 and good blood pressure and BSL 5!) Boss assessed him too and agrees —- appendicitis vs gasto vs mesenteric adenitis

Urine dipstick normal

got the line in, bloods sent – – called our nearby Paediatric Surgical colleagues at the Paediatric hospital (we don’t have paediatrics in our hospital)

Paeds Surg Reg was slightly obstructive as adamant about bloods not being ready and not impressed w the story.

He wanted a paediatric USS.

Now at this point :

a. i was slightly thrown off track – – could we organise one ? (well…i think we shouldn’t as : our USS guys mainly do adults and ths kids not be assessed CLINICALLY)

b. my diagnostic thoughts and confidence in my disposition weren’t strong anymore.


I thought : hey this young boy has 8 days of nausea/lower abdo pain/vomiting w RLQ pain and needs to be assessed AT A PAEDIATRIC hospital and we thought hey lets let the surgeon know first up b4 we send the boy in.


At this point, (might be lack of caffeine or the presumed junior position that I thought i was) I wanted to defer the phone call and let my boss speak to the surg reg directly. I asked the surg reg to do you want to speak to my boss “yes, please” and politely asked my boss that the surg reg would like to speak to him.


My boss says ” NO I WON’T TALK TO HIM, that kid is going to that PAEDS ED, and that’s that!”


AM like WTF

At this point in time, I think the paeds surg reg could have hear this from the phone and probably felt sorry for me (his tone did soften, and said he’ll call me back after talking to HIS boss)

He called back saying “ok, send him over”


My rant is :

if you are a boss (i.e. Consultant) and don’t want to step in and STAND Up for your juniors. thats fine.

I’ll learn to harden the f*** up and sort my shit myself.

This is a bad example to set in front of the juniors.

As a consultant/registrar – – – if a specialty you are referring to is obstructive, you NEED to step in and STAND UP for your juniors. This is why as juniors we seek guidance and LEARN from you. If you agree with our assessment and disposition – please have the guts and take the effort to stand up for your juniors.


The genders may or may not be representative of the parties involved.





9 01 2013

Did my first Bier’s block yesterday. unwitnessed fall in a lady (high care nursing home patient) with significant comorbidities : COPD and newly diagnosed malignancy.

I’ve done them twice at least with senior registrars (me being the lever or the counter-traction guy) during the manipulation.

Yesterday was a first adjusting the cuff etc (but the boss still insisted on giving the drug himself)

biers_block —this is a page pdf file produced by the Gold Coast hospital which serves as a good intro and explanation including step by step about the Bier’s block. More goodies from : (you need to register – FREE)

Addit as of Dec 2012, the Gold Coast Hospital has limited the access to to only their staff.

So….drug of choice we gave was : PRILOCAINE

Let’s talk about local anaesthetics with Prilocaine as our star drug

WHAT is it ?

Local anaesthethic. Amide type


  • Absorption : systemic absorption affected by :
  1. dosage
  2. site of injection – high vascular area e.g. trachel mucosa means rapid absorption ; peak serum level highest esp intercostal block while sciatic and femoral lowest
  3. drug-tissue binding
  4. local tissue blod flow
  5. use of adrenaline (vasoconstrictor)
  • Distribution :
  1. Localised >>>
  2. Systemic …2 compartment model : initial alpha phase – rapid distribution and highly perfused organs. Slower beta phase – less perfused tissue ( muscle/gut) protective effect by uptake in lungs – serves to attenuate arterial concentration.
  • Metabolism
  1. amides converted to water soluble metabolites in liver


  • Mechanism of Action
  1. Membrane potential – blockade of voltage-gated sodium channels
  2. Sodium channel isoforms
  3. Channel blockade
  4. Other effects :
  • Structure activity characteristics of Local Anaesthetics
  1. smaller + more lipophilic LAs, faster rate of interaction w sodium channel R
    —-lignocaine/procaine/mepivacaine more water soluble than tetracaine/bupivacaine/ropivacaine (more potent and have longer duration, also bind more ext to proteins)


  • Neuronal factors affecting block
  1. differential block

Amides vs esters. Usual questions in MCQ for the primary ?which is a amide or ester ?

local anaesthetics that are Esters :have just one ” i ” in their names eg procaine ,cocaine but …
Amides : have more than one ” i ” in their names lidocaine, bupivacaine,prilocaine


1 12 2012

I came home late. (oh please time management)

would you really handover to your colleague to do 2 punch biopsies ?

we had this lady with a phototoxic drug eruption ( i mean hey we knew this 30 minutes after doing a history and physical) but the offending agent ?

had to wait for hours before derm got back to us (i blame it on a very small email system…where are you NBN!!)


anyway lets talk about indapamide as our drug today.


Indapamide belongs to the Thiazide group.




inhibit NaCk reabsorption from luminal side of epithelial cells in DCT by blocking the Na+/CL= transporter (NCC)

enhance Calcium reabsorption



only thiazide for parenteral : chlorothiazide
excretion : indapamide (biliary)
all thiazides secreter by organic acid secretory system in proximal tubule


1. Hypertension
2. Heart failure
3. Nephrolithiasis – from idiopathic hypercalciuria
4. nephrogenic Diabetic insipidus


1. Hypokalaemic metabolic alkalosis and Hyperuricemia
2. Impaire glucose tolerance
3. Hyperlipidaemia
4. Hyponatreamia
5. Allergic Reactions


30 11 2012

What is it ?

Lasix. oral + IV forms.
loop diuretic. selectively inhibit NaCl reabsorption in the Thick Ascending Loop (TAL)



Thick ascending loop of Loop of Henle


inhibit NKCC2, the luminal Na+/K+/2CL-transporter in the TAL of Henle’s loop.
hence :
a. REDUCING the reabsorption of NaCl
b. also diminish the lumen-positive potential that comes from K+ recycling >>>> increase in M+ and Ca2+ excretion

induce expression of cyclooxygenases (COX-2) >>>more synthesis of PG from AA

increases renal blood flow via PG actions on kidney vasculature


rapid absorption.
eliminated via glomerular filtration + tubular secretion.
duration of effect ~2-3 hours.



Acute pulmonary oedema

Acute hypercalcemia.


Acute Renal Failure

Anion OVerdose


Hypoklaemic Metabolic Alkalosis




Allergic reactions



MCQ questions :

3. which is NOT true of diuretics?

a. Loop diuretics can be used to treat hypercalcaemia
b. Frusemide is used in the prophylaxis of acute mountain sickness
c. Cirrhotic oedema responds to spironolactone
d. They may enhance the efficiency of ACE inhibitors
e. Hydrochlorothiazide is useful in diabetes insipidus

Viva questions :

1 Drug a day :Acetazolamide

28 11 2012

Apologies for the long hiatus —-had bouts of personal problems including a mishap involving a loved one.

I do have a few cases to dissect. My original aims for this blog was to try and do something like what this fella Chris Partyka  (an EM registrar in NSW i think) does i.e. his blog : 

However before that I have my primaries coming up and its daunting. Only 78 days to go !

I thought i’ll do something different….while am trying to compile cases and lessons I learnt I’ll also revise my drugs so….

…………….presenting ONE DRUG A DAY.


Today’s drug—–drumroll please


with every drug the format will be







  • What is it ?

diuretic. sold under trade name Diamox. Carbonic anhydrase inhibitor.



inhibits carbonic anhydrase (CA) blocking NaHCO3 reabsorption,
where >>> at the Proximal convoluted tubule PCT

What is CA used for ?
see diagram below (photo taken from Katzung)Image

CA does 2 things :

a. Carbonic acid (H2CO3) is rapidly dehydrated by CA to carbon dioxide and water within the lumen
b. the same carbon dioxide and water (within the PCT) is rehydrated by CA to become carbonic acid again

    well absorbed orally. Excretion by secretion in proximal tubule S2 segment.


  1. Glaucoma-via reduction in aqueous humor formation
  2. Urinary Alkalinization -increasing urine pH for hyperuricia/cystinueia
  3. Metabolic Alkalosis- esp in CHF patients
  4. Acute Mountain Sickness-decreasing CSF and decreasing pH of CSF/brain : increases ventilation
  5. Others – adjuvants in epilepsy/hypokalaemic periodic paralysis/CSF leak
  1. Hyperchloremic MEtabolic Acidosis
  2. Renal stones
  3. Renal Potassium Wasting
  4. Drowsiness + parasthesia

Worth watching this :

Youtube video on brief physiology :’s critical care manual book by Dr Paul Young :