Life – up and down, pass and fail

It is so embarrassing to write such a post about my failure but it is worth if you get something after reading this little note. I just did my MRCP (UK) part 1 exam in May which was unsurprisingly end up with a negative result for me. How stupid I am? Those board exams are not so easy but not so difficult either. Once you know what they want you to know and you have the resources, you are on the right track. All you have to do is practice, practice, practice. The revision tests and mock tests can give you the nearest score that you can get in the real test with a minor deviation. In other words, you can guess how much score you will get before the exam.

The reasons why I failed in this exam is clearly the lack of proper practice. I did not even do a full timed mock test one time before the exam. I kept working and working leaving too little study hours. One big predisposing factor would be my weakness in basic sciences as I was just an average student in med school and never had a strong ambition to be a great physician. When I was young, I wanted to be a surgeon because I love operating theatre, obvious nature of surgical disease process, quick recovery rather than vague internal medicine, never changing human anatomy and artistry of surgical techniques because I know I am good at drawing, patient and I love art. However, I realized that surgical field is much more complicated and competitive than I have thought as soon as I started my practice. And I never have a chance to get continuous training close to surgery. Our government could not give the newly graduated doctors of our batch and so many of my friends move on to different faculties such as private practice, INGOs, pharmaceutical companies, business and go abroad. I am the one who chose to go abroad to continue my career as a clinician (after 2 years doing charitable works and wasting some precious time) and hence here in Jamaica.
To start, I had to do the registering exam that contains theory and clinical parts and as my first big failure I had to do the clinical part twice. And I started over my internship which I have done in my country before the graduation. I feel like I am lagged way behind my colleagues that give me depression sometimes until now.
As a matter of fact, I made up my mind to do MRCP which was a dream when I was a student. Again, 2nd time in life, I did not hit the score. Well, it was a lot of money and time I spent to buy such a bitter experience. What a shame! 5 years passed and I am just a mere M.B.B.S. And I still have no proper training either in internal medicine or any other specialties yet.

This cannot beat me down. If this is just my fate, I created somehow. So, why can’t I change or control that. I keep running while my target is there, not moving and waiting for me.

Paracetamol Poisoning

Toxic dose = 150mg/kg (75mg/kg if malnourished) or 12g in adults may be fatal (10-15g ~ 20-30 tablets)
Max. Therapeutic dose = 4g/day

Acute poisoning:
1 hr = larvage + activated Charcoal
4 hr = Paracetamol level
8 hr = N-acetylcysteine (within 8 hr, effectiveness is the same, afterwards it declines); alternative – Methionine
12 hrs = Review and repeat INR q12h
24 hr = review with results (see criteria for transfer)
48 h = review (if INR normal and pt stable, possible home)

N-acetylcysteine

  • to replenish hepatic glutathione

IVI regieme

1. 150mg/kg in 200mL of 5%DW x 15min
2. 50mg/kg in 500mL of 5%DW x 4 hr
3. 100mg/kg in 1L of 5%DW x 16 hr

 

Crieteria for transfer

  • Encephalopathy or increased ICP
  • INR >2.0 at <48 hr – or >3.5 at <72h (peak at 72-96h) N.B. LFTs are NOT good markers
  • Renal impairment ( Creat > 200), consider HD if >400) * monitor urine output and daily U&Es
  • Acidosis / Blood pH <7.3
    • Lactate > 3.5 mg/dL (0.39 mmol/L) 4 hrs after early fluid resuscitation
    • Lactate > 3 mg/dL (0.33 mmol/L) after full fluid resuscitation at 12 hours
  • Systolic BP < 80mmHg

 

King’s College Hospital Criteria for Liver transplantation

Paracetamol liver failure

  • Arterial pH <7.3 24 h after ingestion

Or all of the following:

  • PT > 100s
  • Creat > 300
  • Grade III or IV encephalopathy

Non-paracetamol liver failure

  • PT > 100s

Or 3 out of 5 of the following:

  1. Drug-induced liver failure
  2. Age <10 or >40y old
  3. >1wk from 1st Jaundice to encephalopathy
  4. PT > 50s
  5. Bilirubin > 300

Things I like about Jamaica

Once you heard somebody saying “Jamaica”, a beautiful island with white sandy beaches and the relaxing reggae music will come into your mind. Yes, it has many beautiful beaches and resorts and I love that. However, I can enjoy those in my homeland Myanmar (aka Burma) too.

So, what are the things really impressive to me? It would be nothing important for other people but directly affect my job or profession, which is the fact that there are –

NO Rabies

NO Malaria, and

NO Snake Bites.

When I was a house surgeon (internship after med school) back home, I came across with several cases of malaria and snake bites. These cases are really stressful and need prompt management including intensive care as they have dreadful complications and high mortality rate. And, I also had to concern with the vaccination of the rabies for every dog bite cases, even though I never saw a case of rabies.

Once I reached Jamaica, I put aside my knowledge about the management of cerebral malaria, differentiation and management of neurotoxic and hemorrhagic snake bites, management of thalassemia and so on. Instead, I focused on the sickle cell disease, obesity and other metabolic diseases. I see my very first case of sickle cell disease here, which is a JFK (just for knowledge) or GTK (good to know) topic in our med school. And I swear to god that I have never seen and manage a gunshot case until I reach Jamaica.

Before I forget to mention, I notice that there is also a relatively low prevalence of tuberculosis which really ease me a lot as you all know how difficult to control and deal with the TB patients. Patient compliance on long treatment regime and follow-up, social support, and the threat of MDR-TB, HIV vs TB are all the challenges. I remembered the days of my ward rounds with a face-mask on TB ward in my home-town hospital. I just made a shallow breathing during the ward round, and felt like I am choking until the round is finished. I am not exaggerating, the mask that I wore was not N-95 and even if it said N-95, you cannot trust and rely on all those equipments, right?

You can have a very unlucky day with your condom burst.

You can have a needle-prick from a HIV positive patient and PEP (post-exposure prophylaxis) failed.

This is our damn LIFE. We live in the world of uncertainty and are risking our lives everyday.

In the end, it’s not going to matter how many breaths you took, but how many moments took your breath away
-shing xiong

Fork in the mouth !

No, it is not about Fork to Mouth Disease (FTMD) (i.e. fat / overweight people living in denial and believing that their weight gain is from an over-active pituitary or thyroid gland – urban dictionary). It is literally a fork stuck in the mouth.

One evening, in fact, it is my very first week as a junior resident in casualty, my senior colleague came into the SMO’s office, where the SMO and I were having a conversation, reporting that he was just seeing a case with a fork in the mouth. Instantly, we all considered she is stabbed. We went there right away and saw a young lady about in her 30s, sitting in bed comfortably with the fork coming out from her mouth.

She mumbled that she was just eating and nobody stabbed her. We said “Ok, let’s have a look”. She could open her mouth normally, meaning her temporomandibular (TM) joint is normal, and we found out the fork just trapped between the floor of the tongue without any penetration. I regret that I didn’t take any picture of it. I really wish you guys to see. Anyway, don’t worry, I just drew a sketch by “FreshPaint” which I like most among windows 8 apps.

Image

Sorry for the eye pain with the bad drawing 😉

We tried to pull out with normal force but it didn’t work and she was in pain. I never know tongue muscle is that strong gripping the fork as if that is its own. Also, the lower teeth seemed to be a kind of barrier to come out easily. The SMO asked us to ascertain that the fork is not penetrating at all by putting finger between the tongue and the fork. And then, he asked the nurse to prepare a gauze soaked with adrenaline explaining us just in case it bled or hematoma formed. Then, he asked the lady to relax and just pulled out with a brisk force like we pull out the chest tube. Everything was perfect then.

So, how could that happen? The SMO admitted that he has never seen such a case in his life with the experience of over 35 years of medical practice. Is it something wrong with hypoglossal nerve? When I googled it, I just found a few possible differential diagnoses that can cause tongue spasm or involuntary contraction of the tongue muscle.

The first one is Meige’s syndrome. (Don’t confuse with Meigs syndrome which is a triad of ovarian tumor, ascites and pleural effusion) That one is also know as Brueghel’s syndrome and oral facial dystonia. It mainly affects TM joint and eye muscles (blepharospasm)Another possible differential should be Tourette syndrome.

Share your knowledge in the comment session below please.

Foothritis or arthritis?

I have been in Jamaica for almost three years and I don’t catch and understand their so called “Patois” (or sometimes “Pattwa”) language yet, especially when they speak fast. As expected, I learned greeting word like “Wa Gwan” or Whatta Gwan, something like “what is going on” or “What’s up” and of course, a bad word like “Bumbaclot“. Please don’t ask me what does it mean. Google it if you are curious enough.
Fortunately, 99% of them understand and talk standard English, so I don’t have any problem working here.
Yesterday, I just heard a new word which is neither Patois nor English. It is the word that I have not learnt in medical school and I have never been heard throughout my experience working with them.
This old gentleman just said “Doc, me havin’ foothritis” (or footathritis, I don’t know how he spells)”. I was explaining about arthritis – joint pain and he said ” no doc, me called it foothritis”. I said ok and use footathritis whenever I am using arthritis throughout our conversation.

Words or the language don’t matter, it is COMMUNICATION and the mutual understanding that matters, don’t?

Learn some Jamaican words here – http://members.tripod.com/~Livi_d/language/patois_dictionary.htm;

http://jamaicans.com/speakja/

First week in a type C hospital of a third world country

I couldn’t write any posts for a while because I was busy during these days just making a new move in my life. Since July 2013, when I finished my SHO period, I couldn’t make new contract at the government hospitals and was just doing sessions at a private clinic.

Finally, I was assigned as a junior resident in Linstead Hospital in St. Catherine parish of Jamaica, which is a downgraded type C hospital meaning nothing much more than a comprehensive health center except 24 hour emergency service with a capacity of 25 beds for inpatient management and a maternity unit. Basic lab and an X-ray department are just setting up and not ready yet.

There are no consultants here and so if we need some specialist opinion and consultation, we have to contact other tertiary hospitals and transfer the patient if necessary.

This is not what I really want to do. I would like to treat the patient rather than asking for help, writing referral letters and transferring patients. I would like to do procedures, academic ward rounds and case discussions. So, this place is just a crap? No, I believe I would learn something that I cannot get from tertiary hospitals here. As a matter of fact, I can learn emergency management along with case differentiation, spot diagnosis, prioritization, work up with limited resources, judgement and so on. As it is not as busy as the Type A hospital I used to work at before, I think I can get spare time to study for my MRCP and post graduate goals.

By far, I drive to my work from Kingston and it takes about an hour at least. The roads in Jamaica are hilly, narrow and rough in many areas, so I better relocate even though I don’t want to move from my current place, which is the house next to my girlfriend’s.  It is what we called life, isn’t it? Sometimes you have to do what you should do rather than what you really want to do.

Cheers !

Compilation of Drugs involved in specific conditions (2)

Enzyme Inducers  (NO GAS in CaR)
  • NNRTIs – Nevirapine *
  • Omeprazole – Induces P-450 1A2 **
  • Griseofulvin, Glucocorticoids
  • Alcohol (chronic)
  • Sulphonyureas/ St John’s Wort
  • Carbamazepine,  Pheytoin, barbiturates, Primidone
  • Rifampicin, Quinine
*    NNRTIs either induce or inhibit depending on the concomitantly administered drug
**  competitive inhibitor of the enzymes CYP2C19 and CYP2C9
Enzyme Inhibitors  (DOG RAISE)
  • Diltiazem, Verapamil
  • Omeprazole, Cimetidine,
  • Gemfibrozil, Grapefruit juice
  • Ritonavir (PI in HAART)
  • Amiodarone/ Allopurinol/ Acute alcohol intake, metahnol(acute), Disulfiram;
  • Isoniazid, Imidazoles (ketoconazole, fluconazole)
  • Sulphonamides, Sodium valproate, SSRIs (fluoxetine, sertraline)
  • Erthyromycin, Ciprofloxacin, quinupristin, metronidazole, quinidine
  • * Drugs that cause displacement of warfarin from protein
NSAID, OHA, metronidazole, salicylates, Co-trimoxazole
Drugs which are known to cause impaired glucose tolerance include:

  • Thiazides, furosemide (less common)
  • Steroids
  • Tacrolimus, Ciclosporin
  • Interferon-alpha
  • Nicotinic acid
  • Atypical Antipsychotics e.g. Olanzapine
  • Beta-blockers cause a slight impairment of glucose tolerance.
They should also be used with caution in diabetics as they can interfere with the metabolic and autonomic responses to hypoglycaemia
Drug-induced thrombocytopenia (probable immune mediated)

  • quinine
  • abciximab
  • NSAIDS
  • diuretics: furosemide
  • antibiotics: penicillins, sulphonamides, rifampicin
  • anticonvulsants: carbamazepine, valproate
  • heparin
Drug causes of gingival hyperplasia

  • phenytoin
  • ciclosporin
  • calcium channel blockers (especially nifedipine)

Other causes of gingival hyperplasia include

acute myeloid leukaemia (myelomonocytic and monocytic types)
Drug-induced liver disease is generally divided into hepatocellular, cholestatic or mixed.
There is however considerable overlap, with some drugs causing a range of changes to the liver
The following drugs tend to cause a hepatocellular picture:

  • Paracetamol (Acetaminophen)
  • Diclofenac
  • Sodium Valproate, Phenytoin
  • MAOIs
  • Halothane
  • Anti-Tuberculosis: isoniazid, rifampicin, pyrazinamide
  • Statins
  • Alcohol
  • Ecstasy/ amphetamine
  • Amiodarone
  • Methotrexate
  • Methyldopa
The following drugs tend to cause cholestasis (+/- hepatitis):
  • Oral Contraceptive pill
  • Antibiotics: ciprofloxacin, flucloxacillin, co-amoxiclav, erythromycin*, nitrofurantoin
  • anabolic Steroids, testosterones
  • Phenothiazines: chlorpromazine, prochlorperazine
  • Sulphonylureas
  • Fibrates
  • rare reported causes: nifedipine
*risk may be reduced with erythromycin stearate
Drugs affected by acetylator status

  • isoniazid
  • procainamide
  • hydralazine
  • dapsone
  • sulfasalazine