The end is the beginning is the end...

I'd finally survived a spontaneous vertex delivery from medical school on Feb 28, 2008! No meconium aspiration in the process, it was a clear pass. No resuscitation required. Am receiving my birth cert called MBBS in May, with my surname "Doctor" imprinted on it! Aahhh... the air is so refreshing...

With my mates

Kumpulan Kongsi Gelap Anti-Sosial

With my group study members, "Kumpulan Gagak Hitam"

He said Dua, I say Diu!

The godfather of medicine Health Minister, Latok Chua announced yesterday that newly graduated medical doctors will have to undergo TWO years of hell-holeship housemanship compared to the previous one year! What pissed my willy off is that the salary will still be the same for the entire 2 years.

Today's paper said that those bargers will seek to promote doctors to the U43 Grade only AFTER housemanship. You and I know what "will seek" means in Malaysian context! In other words, for the first 2 years of fresh graduates' life, we need to eat shit to survive. They claimed the consolation for prolonging the housemanship for another year is that we can enjoy a RM500 pay raise (upon approval of "will seek") and be allowed to pursue further studies right after housemanship. Be realistic lah, we often hear stories in the past that people got into a postgrad program as early as during HO (the rule was 3 yrs after completing houseman). Why still need to "will seek this" and "will seek that" when you have confirmed the duration of housemanship? Just blardy confirm the salary lah! We are ready to give and take if the deal is right, don't make it so arbitrary ok latok?!

Footnote: Sigh... there goes my 4-year plan of replacing Latok Chua! Niamah...

Curbside.MD

This is a new search engine for EBM. In contrast to the other search engines which require the old school way of using keywords, Curbside.MD provides evidence-based answers to real medical questions! Forget the keywords, ask a question like you would ask a medical expert. Enter patient’s info, diseases, drugs, even paragraphs of information. The more the better. This is because Curbside.MD uses a technology called semantic fingerprinting, which essentially works quite similarly to geocoding.

Click here to read more on how it works, or go to the main page to start searching!

Mantoux Test

Mantoux test is a test for tuberculosis. The test involves injecting a small amount of tuberculin (an extract of the causative bacteria) into the forearm skin, and the skin reaction measured 72 hours later.

This is the staff nurse who administered my tuberculin injection.

The nurse said the injection itself is quite painful, and claimed that she was quite nervous administrating Mantoux test for a "doctor".

It's an intradermal injection, meaning the stuff is injected right under the skin.

The injection site is left untouched for 3 days; no soap around the injection site during shower. The site is inspected and interpreted by an experienced medical personnel after 72 hours.

The skin reaction on my forearm, 72 hours after injected with the tuberculin.

Simply put, the induration (the reddish hardening) on the skin is measured to arrive to the diagnosis of tuberculosis. An induration of 10mm or more in people with no BCG scar indicates a positive reading for tuberculosis. In most people who are vaccinated against TB and hence, a BCG scar is present, a reading of 15mm or more is needed to indicate a TB infection.

8mm!

My skin induration measured 8mm (and yes, I do have a BCG scar)! That means I don't have TB! Fuhhh... On why I did this test, that's a story for another day!

Subungual Haematoma

Haven't start training for Seremban Half Marathon yet, mainly due to my subungual haematoma (bruise under the nail, also known as runner's nail in this case) sustained from Penang Bridge Marathon. Not sure if I'm gonna train at all, with impending exam stress and the painless purplish toe I'm having!

Unlike tridoc who's going to Lumphini Park this Friday for a highly specialised training with the hope of gunning it under 2hrs for Seremban Half (LOL!), I'm lying low nursing my bruised toe!

Consulted my orthopaedic surgeon, Prof. H this morning, as I was contemplating of draining the clotted blood by poking a heated needle through my toe nail (the standard treatment for subungual haematoma). He advised me against it, as my bruise is not huge and it is painless. Most importantly I wouldn't want any bacterial infestation by creating a hole on my toenail. And the complications of onycholysis and what nots. Will try jog a little tomorrow. See how it goes. The blistering hot weather doesn't help at all!

My Middle Finger

This is actually a picture of my left middle finger. Notice the pinkish lesion? I've been having it for about 4 months now. It's mildly itchy at times, otherwise I don't feel a thing. I was hoping it would go away with time but it didn't! Let's have a closer look...

Can you guess what's that nasty-looking thingy that I'm having on my left middle finger? And no, I don't have a fetish for fingering stuffs.

Fellatio reduces incidence of Pre-eclampsia?

Fellatio, or "blow-job", is oral sex performed on the penis (as if you did not already know!). I was browsing the net and came across this journal that claimed fellatio with subsequent ingestion of semen reduces the incidence of pre-eclampsia.

But before you strip your partner's southern region naked, you must be wondering what the heck pre-eclampsia is. Pre-eclampsia is a condition of hypertension (high blood pressure of 140/90 mmHg and above) during second half of pregnancy, typically accompanied by proteinuria (passage of relatively high amount protein in the urine) with/without oedema (bodily swelling).The cause of pre-eclampsia remains unclear, although aberrant trophoblastic tissue and immune mechanisms have been implicated. Untreated pre-eclampsia can cause foetal death, maternal multi-system organ failure, vaginal bleeding, and seizure. Conventional treatment of pre-eclampsia is to admit the mother into a hospital, and medication given to control her blood pressure. Ultimately, the doctors would have to deliver the baby as delivery is the only way to bring the mother's blood pressure back to normal.But what if there's a way to prevent this from happening in the first place? No needles, no tablets, no surgeries, no pain, and most important of all, comes packed with erotic fun and pleasure with your partner!

The study by Koelman et. al. titled "Correlation between Oral Sex and a Low Incidence of Pre-eclampsia: A Role for Soluble HLA in Seminal Fluid" found that oral sex and swallowing of sperm is correlated with lower incidences of pre-eclampsia! Neat discovery aye?!Before you rush to get hold of that therapeutic fluid, the last line of the study abstract also stated that "An extension of the present study is necessary to verify this hypothesis". Ooops did the warning came too late?Bet you didn't know blow-job has health benefits (provided safe technique is observed). There's always a risk of sexually-transmitted infection, mind ya! You wouldn't want your oral cavity to look like our mate in the photo above, so say no promiscuity aight?! Should anyone wanna find out more on fellatio, you know, how to improve your fellatio prowess, there's a book written on it too:Imagine, if further studies verify that fellatio and sperm-drinking actually reduces incidences of pre-eclampsia, O&G specialists will go around telling patient "Give your hubby a blow-job and make sure you swallow his cum, twice daily for a fortnight before attempting conception". Or, "Drink a tablespoon of your husband's sperm everynight before going to bed". Eww, *shudders* I feel disgusted already.

Just in case the links to the study mentioned above didn't work, here's the study abstract by Koelman et. al.:

The involvement of immune mechanisms in the aetiology of preeclampsia is often suggested. Normal pregnancy is thought to be associated with a state of tolerance to the foreign antigens of the fetus, whereas in preeclamptic women this immunological tolerance might be hampered. The present study shows that oral sex and swallowing sperm is correlated with a diminished occurrence of preeclampsia which fits in the existing idea that a paternal factor is involved in the occurrence of preeclampsia. Because pregnancy has many similarities with transplantation, we hypothesize that induction of allogeneic tolerance to the paternal HLA molecules of the fetus may be crucial. Recent data suggest that exposure, and especially oral exposure to soluble HLA (sHLA) or HLA derived peptides can lead to transplantation tolerance. Similarly, sHLA antigens, that are present in the seminal plasma, might cause tolerance in the mother to paternal antigens. In order to test whether this indeed may be the case, we investigated whether sHLA antigens are present in seminal plasma. Using a specific ELISA we detected sHLA class I molecules in seminal plasma. The level varied between individuals and was related to the level in plasma. Further studies showed that these sHLA class I molecules included classical HLA class I alleles, such as sHLA-A2, -B7, -B51, -B35 and sHLA-A9. Preliminary data show lower levels of sHLA in seminal plasma in the preeclampsia group, although not significantly different from the control group. An extension of the present study is necessary to verify this hypothesis.

Intensive Care Unit

A panoramic view of Hospital Tuanku Jaafar's ICU. This week sees my first time stepping into an ICU. Full of mechanical gadgetry and sick people. Am posted there again tomorrow. Yawn!

Post Gynae Long Case Exam

My patient is a 54 year-old widow of parity 1, who presented with cyclical menorrhagia of 2 years duration with mild symptoms of anaemia. I wouldn't say it's a postmenopausal bleeding despite her age (mean age of menopause for Malaysian women is 50.7 years), as her menses were regular cycles of 40 days with duration of 7 days for the past 2 years. She's recently diagnosed to be hypertensive and on medication.

Dr. S: Are you ready?
Me: (Give it to me baybehh...) Err, yes...
Dr. S: Say you are the one who saw this patient for the first time, how would you investigate her?
Me: FBC to assess anaemia, PT/APTT to see if there's any coagulation defects, blood grouping and crossmatch in case she needs transfusion. Thyroid function test for hypothyroidism as she appeared sluggish. Then, a transabdominal or transvaginal ultrasound to look for uterine and pelvic mass. Followed by cervical smear, Pipelle sampling, and hysteroscopy for direct visualisation and directed biopsy.
Dr. S: What can be done during ultrasound examination to improve ultrasonographic view?
Me: ... ... ...
Dr. S: Distend the uterus with normal saline la. Do you think a renal profile is justified in her case?
Me: No?... err Yes, actually... given her age she may have diabetes...
Dr. S: Yes! And don't forget she has hypertension too! Now, they are going to insert a Mirena into her. What's Mirena?
Me: It's a levonorgestrel intrauterine system used to treat menorrhagia and dysmenorrhoea, and is also used as contraception. It releases the hormone levonorgestrel locally in the uterus in small doses for up to 5 years, making menstruation lighter, shorter, and less painful (lucky I curi the Mirena booklet from the clinic!).
Dr. S: Other than Mirena, how would you manage the patient, medically?
Me: I would prescribe her haematinics for her anaemia. Then, mefenamic acid and tranexamic acid to reduce her menstruation. Also, hormonal preparations such as Danazol, Gestrinone, GnRH analogues, and combined oral contraceptive pills (COCs). (Was basically regurgitating facts from textbook)
Dr. S: Do you think she needs COCs at her age?
Me: Oops, sorry, no COC for her.
Dr. S: And due to her age, we don't normally prescribe Danazol, Gestrinone, and GnRH analogues. What other management options would you give her?
Me: Surgical options, and these are divided into fertility sparing and non-fertility sparing procedures...
Dr. S: Why do you want to preserve fertility in this patient?
Me: Oh yeah, 54 year-old, suppose to be menopause edy... (sh!t... again!). Then the surgical option would be more radical, such as vaginal hysterectomy, transabdominal hysterectomy, and laparoscopic-assisted vaginal hysterectomy.
Dr. S: Riiiiggght... ok tell me the physical findings.
Me: On general inspection, she's overweight with BMI of 25. She has pallor of the conjunctivae but no jaundice, clubbing, oedema, or cyanosis. Blood pressure 160/90, pulse 60, respiratory rate 16 breaths per min, afebrile. Her lungs are clear. On heart exam, apex beat is not deviated, dual rythmn heard and no murmur detected. On abdomen exam, it's soft, non-tender, no organomegaly, no uterine enlargement and no mass palpable. If given enough time, I would proceed to pelvic examination.
Dr. S: What would you look for in pelvic exam?
Me: Starting with inspection of external genitalia, I'd look for any bleeding or discharge. On speculum exam, I'd look for any ulceration or exophytic growth on the cervix, and if there's any active bleeding. I'd do a bimanual palpation to assess mobility of pelvic organs, feel if the uterus is retroverted, if there's any adnexal pathology and palpate for pelvic masses.
Dr. S: Do you expect to find anything in this patient?
Me: Not likely.
Dr. S: What's your provisional diagnosis?
Me: Given her history, I would like to entertain the diagnosis of benign growth of the endometrium, such as endometrial polyps.
Dr. S: You're not wrong, but do you think she would be given Mirena if it's a polyp?
Me: No,... no Mirena if it's polyp.
Dr. S: What's your differential diagnosis?
Me: Malignancy, such as endometrial carcinoma.
Dr. S: Yes, don't forget about malignancy. Why do you think her cycles are getting prolonged?
Me: ... err... hormonal imbalance... the ovaries are failing...
Dr. S: What do you call that?... failing ovaries and cycles getting longer?
Me: ... anovulatory cycles?
Dr. S: Yea lah, why you so scared to say that? So what's your diagnosis for this lady now?
Me: (heh heh, actually I tembak oni...) Dysfunctional uterine bleeding!
Dr. S: (polyphonic ring tone blasting loudly) Ok la, thanks.
Me: (yeahh... balik tidorrr... Oh no... Dato' S. is still in the ward...)

Post SAQ Exam (Int. Med)

Just finished my 1-hour SAQ paper for the Internal Medicine posting. There are 6 questions all together, and here's my contribution to the infamous "IMU Past Year Questions" archive.

Question 1
A man came in with right-sided pan-systolic murmur, fever, breathless. Multiple venous puncture scar on arm hinting on IVDU. Chest X-ray showed multiple cavitating lesions. Diagnosis is right-sided infective endocarditis, involving the tricuspid valve with septic embolisation resulting in pneumonia. I find the question "Describe the chest X-ray findings" a bit confusing. Is it asking for the cause of the pneumonia, or is it asking for other possible causes besides pneumonia?

Question 2
Middle aged Indian man came in with jaundice, epigastric discomfort, ascites, oedema. Causes of hepatitis? Viral, drug-induced, alcohol, biliary diseases. A LFT is provided, increased ALT. Two probable diagnosis? And give eight physical signs of liver disease.

Question 3
Patient came in confused, dizzy, vomited. Bilateral leg oedema. A BUSE result was given, showing hyponatraemia. What is the cause of confusion and vomitting? Answer: Hyponatraemia. Pathophysiology? Cerebral oedema. How would you manage the electrolyte imbalance (3 steps)? Answer: fluid restriction, diuretics, treat underlying cause, etc.

Question 4
A male executive came in to check his BP. It was raised la. Smokes ciggies for 15 yrs 10 sticks per day. Height 1.75cm, weight 90kg. His dad had DM and died of CVA at age 60. Give 4 investigations for his general well-being (again non-specific, tibai anything also correct I guess). What are the risk factors for development of CVA/CVD in this patient (give 3)? What are the side effects of hydrochlorothiazide he was given (give 3 also)?

Question 5
Old lady, collapsed at home. Another BUSE result given (normal range not given!). History of DM for 10yrs on Metformin. Random blood glucose on admission = Read: 60mmol/L! Diagnosis clinched - Hyperosmolar Non-ketotic coma (HONK)! Pathophysiology? Four other investigations you would perform on her? Management.

Question 6
Esha's question. Female came in with right-sided hemiparesis, history of two abortions, joints swollen and painful, with characteristic facial rash. Diagnosis - Systemic Lupus Erythematosus. Give four complications associated with the underlying disease (again, what is this question asking for?? I wrote the other manifestations of SLE). A syndrome commonly associated with SLE? Anti-phospholipid syndrome. How would you investigate her.

That's it guys. Overall, quite an easy paper la, since I never study that much also can answer >60%. If study more than average sure score kao kao one. Chiao, gonna makan. Can't go back KL coz Sunday got marathon!

Post Long Case Exam (Int. Med)

My patient for the long case was an elderly Malay man in his 80's, having a massive right-sided pleural effusion (that's water in the lung) due to lung cancer. I had more than ample time to clerk him and perform a complete physical examination before Dr. J came in.

Dr. J seated me at the nurses counter and I started to present my history and clinical findings. I did ok I guess, although it was interrupted by phone calls for Dr. J. Clinical specialist mah! And here comes the first blunder of the day...

Dr. J: So what's your diagnosis?
Me: (damn confident) Lung cancer!
Dr. J: *frown* You can diagnose lung cancer clinically meh?
Me: ... ... ... (confidence decreasing at a rapid rate)
Dr. J: Ok, nemind, come let's examine the patient.

And then Dr. J greeted the patient and asked whether I had examine him justnow. And I proceeded to examine him. And here comes the second blunder/stupid mistake... I auscultated his chest before doing a percussion. I was silently hoping he didn't see that as he was busy flipping the case notes. Well... he did...

When I was done with my physical exam...
Dr. J: Shouldn't auscultation come after percussion?...
Me: (damn, he saw it...)
Dr. J: Ok, nemind, come...
We went back to the nurses' counter to look at some chest radiographs.


Dr. J: So tell me, what do you see on the chest x-rays?
Me: There's an air-fluid level on the right lung signifying a pleural effusion, and the left lung is hyperinflated.
Dr. J: Meniscus sign! Air-fluid level suggests lung abscess. What else do you see?
Me: Err... err... upper lobe diversions here and there, a patch of heterogenous opacification here, err... no cardiomegaly (dunno what else to say edy)...
Dr. J: Ya ok, why do you think the left lung is hyperinflated?
Me: It may be due to lung collapse due to pleural effusion (simply shoot).
Dr. J: You mean it's a compensatory hyperinflation (trying to help me with the answer he wants).
Me: Yes yes, compensatory...
Dr. J: If it's not compensatory, what else could it be due to, the hyperinflated left lung?
Me: COPD (chronic obstructive pulmonary disease) due to him being a chronic smoker?
Dr. J: Yeeeeessss... that's right... he smokes like nobody's business. Now tell me, what do you think has caused the pleural effusion?
Me: Lung cancer... lung carcinoma... (gulp!)
Dr. J: Can you be more specific on the lung cancer?
Me: Bronchogenic carcinoma (gulped again!).
Dr. J: Which type of lung cancer do you think he has?
Me: Small cell carcinoma, coz he presented acutely 2 months ago and has progressively worsen ever since.
Dr. J: But I thought his cough started last year?
Me: (Ugghh!) Ermm, in that case, I would say it's a non-small cell ca.
Dr. J: Yesssss... it's a non-small cell ca. What type of histology would you expect in the biopsy?
Me: Adenocarcinoma.
Dr. J: Why?
Me: Coz it's commoner in smokers.
Dr. J: Other than that?
Me: ... ...
Dr. J: Adenocarcinoma affects glands, and where are glands foung in the lung? In the alveoli. Right... and thus adenocarcinoma affects lung periphery. As opposed to squamous cell carcinoma. It affects bronchus more, thus more centrally located or known as bronchogenic carcinoma...
Me: (wah, he sibeh good! If I examiner I sure pass him.)
Dr. J: Ok, this patient has multiple admissions for the last 2 months for pleural effusion. What is your first line management?
Me: To drain his pleural fluid by doing a thoracocentesis.
Dr. J: Ok, if the patient kept coming back for the same problem, what's your long term management?
Me: Put an indwelling drainage tube...
Dr. J: You mean to put a chest tube lah...
Me: Yeh yeh, chest tube... chest tube...
Dr. J: Other than chest tube?
Me: .............................................
Dr. J: Have you heard of chemical pleurodesis?
Me: (Shake head...)
Dr. J: It is done to fuse the parietal and visceral pleura so that no fluid can accumulate inside the pleural space.
Dr. J: Ok, you did OK, although there's some blunders here and there.

This is how Dr. J looked like after taking me for my long case exam:

Sigh... "A" is out of question (Dr. J: muahaha! "A"? HAHAHA!). Hope the result won't turn out too bad... gotta buck up! Gambateh!!!

p/s: Read Dr. J's take on IMU exam bloopers here. Do read it! Got comment by Dr. LKY on ethical issues! Haha! On more IMU bloopers by Dr. J, click here and here.

Labioplasty

This short video is from one of the episodes of Girls Out Loud, a talk show broadcasted by Channel5 and hosted by Wendy Cheng a.k.a. XiaXue. Watch how silly and immature she was while the plastic surgeon explained why some females needed their genitals reconstructed, a procedure known as labioplasty.

Med Colleges Under Probe

Health Minister Datuk Seri Dr. Chua Soi Lek said, "After a six-month-probe, the ministry found the lecturer-student ratio of two local private medical colleges to be 1:20 when ideally it should be 1:6 to 1:8". These two medical colleges are under investigation by the Health Ministry of Malaysia for violating regulations pertaining to training of students in the clinical phase of their studies.

The colleges are believed to be taking in too many students and not providing adequate training for them, which is vital before they can be full-fledged doctors. “While Universiti Malaya alone is churning out about 200 students each year, these private colleges, which have been operating less than 10 years, have produced 300 students per year,” he said. Dr Chua said such acts by the private colleges would tarnish the name of the country as a centre of excellence for education.

Health director-general Tan Sri Ismail Merican, who was also at the event, said initial investigations also found that there was no full-time lecturer at the colleges. He said the ministry and the Malaysian Medical Council would send warning letters to the two colleges and their certification would not be renewed if they failed to heed the advice.

Why is IMU unlikely one of the two colleges? First of all, IMU had been operating more than 10 years (15 years to date). Secondly, although at some point of our clinical phase we do have a ratio of about 1:14 to 1:18 lecturer-student ratio, IMU did not produce as many as 300 students per year, at most 160. Thirdly, IMU does have many full time lecturers! Then who are the culprits? I personally think AIMST or UCSI could very likely be one (or both) of them! I'm sure in time, we would know which two colleges those are! (must be Manipal!!!) <--- damn another speculation!

Allergic Rhinitis

The term is allergic rhinitis, a condition I suspected I had been having since I was little. Being plagued with moderately severe childhood asthma in my early years, I'm clearly an allergic person! Although the asthma attacks had stop since I was 10, this nose problem I had been having persisted.

The symptoms are alternating nasal blocks; sometimes my left nostril is blocked, sometimes right, at times both. This disturbs sleep and made me a mouth-breather.

Being posted in Otorhinolaryngology (E.N.T.) for the past 2 weeks cleared up my doubts. My E.N.T. teacher examined me and said I had a grossly hypertrophied (enlarged) inferior turbinate, in which the mucosa is pale (signifies long-term, chronic allergic reaction).


My nasal septum (the flesh that divides your nostril into two orifice), is deviated to the left. These predisposes me to a great risk of having sinusitis, as an enlarged inferior turbinate and a deviated nasal septum could block the drainage of maxillary sinus, thus causing mucus overflow, infection, and subsequently mucopurulent explosion! I could die!

He also examined my throat, and discovered my posterior oropharyngeal wall is nodular (small lymphatic swellings), a sign of chronic postnasal drip.


I did not know I was so pathological! (whimpers)...

TFCC Injuries

It's been almost 4 weeks now since I injured my wrist, and after popping my 16th Celebrex (celecoxib) capsule today, there's still some dull pain even though I have regained my wrist's full range of motion. This triangular fibro-cartilage complex (TFCC) injury is disabling, and sure takes hell of a long time to heal completely!


The TFCC is a small piece of cartilage and ligaments on the little-finger side of the wrist, located just past the end of the forearm bone (ulna). Cartilage is a tough rubbery tissue that acts as a cushion for the joint. The ligaments are strong bands of tissue that attach the cartilage to bones in the wrist. The ligaments or cartilage can be torn during a wrist injury.


So how did I injure this little small piece of pain in the arse?
Answer: A violent twist to the wrist while handling that Yamaha Virago 500.

Of course, that's not the only way to have your TFCC torn. You could also achieve the same damage by falling on an outstretched hand (if you're lucky, you could break some bones in the process too!), a direct blow to the little finger side of the wrist or hand, or even when you're playing racquet games.

Once you've torn your TFCC, the symptoms are easy to spot. First, you will experience pain on the little-finger side (ulnar side) of the wrist. Secondly, there's a characteristic clicking sound or feeling of a catching sensation when moving the wrist. These 2 symptoms, coupled with a history of trauma, is enough to warrant you a course of non-steroidal anti-inflammatory drugs (ie. NSAIDs, eg. celecoxib, ibuprofen) for 3 weeks. But if you think that your surgeon is incompetent or has nothing much to do, you could ask for an X-ray, an arthrogram, or even an MRI just to be sure!

Here's how a TFCC injury looks like on a radiograph (that is, if you're good at interpreting one):


But it's just a small tear, why the long healing time? That's because only the peripheral 15-20% of the TFCC has a blood supply (Wheeless' Textbook of Orthopaedics - TFCC Anatomy). You may wanna read more on this at Wheeless' Textbook of Orthopaedics Online on TFCC, and TFCC examination.

To the guys who kept asking me "What the fuck happened to your wrist?" or "What the fuck happened to your biceps strength?" in the gym, that's what happened. And it's not in the biceps, fuck-heads!

Related post: The Diagnosis

The Diagnosis

I wished it was a simple case of a sprained wrist which would heal in a week or two. Turned out there were more to it than the naked eyes could see. While the pain on my right wrist had started to subside, I noticed some crackling noise on the ulnar side of my wrist in the past two days.

Concerned, I went to see two orthopaedic surgeons this morning and both concluded that I had a Triangular Fibrocartilage Complex (TFCC) injury.

This TFCC, also known as the 'wrist meniscus', functions very similarly to the knee meniscus. It provides a continuous gliding surface for the wrist's flexion, extension, and rotational movements, as well as cushioning the forces transmitted through the ulnocarpal axis, to name a few. Injuries to TFCC present with ulnar-sided wrist pain, often accompanied by clicking. Diagnosis clinched!

In my case, the cause of the injury was a distraction force applied to my right wrist when I attempted to stabilise the 500cc Yamaha Virago, with both my legs straight and astride the tractor-like bike. Moral of the story is, whenever you're gonna ride a low-seated cruiser bike, always place your arse on the seat before trying to lift it off the side stand. Simply because these bikes have lower seats and thus lower centre of gravity, making any pulling of stabilising them more difficult and injury-prone.

That said, I had to wallop these NSAID pills for 3 weeks. No weight-lifting for the next 1 month, I guess. Damn...

Sex Change

= VIEWER DISCRETION IS ADVISED =

Have you ever asked yourself:

(1) Why wasn't I born a male with a penis?
(2) Why can't I not have period pains?
(3) Why can't I not give birth but have children?
(4) Why can't I play a more active role in sexual intercourse?
(5) Why can't I be a man?
(6) Why am I branded the weaker sex?
(7) Why can't I have a penis to wank with?
(8) Why can't I be the US president?
(9) Why must I be the mother and not the father?
(10) Why am I such a lousy driver?

... and all the "why nots" you could think of. Look no more, if you have had asked yourself the why nots listed above, the solution is here. Read on. Again, viewer discretion is advised and if you're under the age of 18, please read the rest of the article without getting caught.

The following is a step-by-step guidethrough of a sex change op, female to male.

First, the surgeon would rip the labia majora apart and make a deep incision to expose the root of your clitoris. A catheter (tube) would be inserted into your urethra (your urine pipe) to drain any retained urine or blood.

Further incisions would be made to further expose the whole length of your clitoris and the urethra.

Next, tissue would be grafted along the length of your clitoris and its glands to create the your new penis. At this point it is essential to tell your surgeon before hand if you would like it to have a prepuce or come fully circumcised. At this juncture, the opening of your vagina would be sutured together, thus closing it.

The wounds are allowed to heal. Further reconstructions and refashioning of your newly acquired penis may be needed to achieve maximal satisfaction, cosmetic wise. The last operation would be insertion of an inert material, such as silicone, to create the testicles. You may call it a pair of silicone-balls or silicone-nuts.

And voila! You have your new penis to play with. It may appear small initially (baby-dick), but later on when revascularisation (growing of blood vessels) takes place, your new organ may grow in size, depending on the situation and mood.

Are you balding?

"Why do people bald, and why more men are affected compared to women?"

It is estimated that 50% of men develop "male pattern hair loss" (known medically as androgenetic alopecia) at some point in their lives. The main cause of balding involves the miniaturization of scalp hair follicles in site-specific areas.

So why some men have lush abundant locks while some start shedding in their 20's? Blame it on your gene. Male pattern hair loss is due to a genetic predisposition being translated by a hormonal mechanism. Current evidence indicates that dihydrotestosterone (DHT) (a hormone which is higher in males, the so-called "male hormone") is the culprit.

How do you grade the severity of your balding? Fret not. ҜαίخόρЋЯзпїα™ presents you the Hamilton-Norwood grading for androgenetic alopecia (AGA):

[Interpretation]
Mild: pattern I and II
Moderate: pattern IIa to IV
Severe: pattern IVa to VII

One example of the many popular personalities being plaqued by androgenetic alopecia is the famous blogger ShaolinTiger. He's Grade IV Grade IIIa!

Despite the many circulating myths, men suffering from AGA can be attractive too!

The onset of AGA may be any time after puberty and may be apparent by age 17 in normal Caucasian males and 25-30 years in normal Caucasian females.
In our Asian context, the prevalence of AGA in Chinese is less common than in Caucasians (phew!), milder and of later onset .
Japanese males for instance develop AGA 10 years later than Caucasoids and have 1.4 times less AGA in each decade of life.

Currently, the only pharmacological agents that are scientifically proven effective are oral Finasteride and Minoxidil sprays.

Examples of Minoxidil sprays available in the local market.

The setbacks of Minoxidil:
(1) It is expensive. A bottle costs RM 120-180, and lasts approxmately 1 ½ to 2 months.
(2) Need to apply twice per day: morning and night. Need discipline.
(3) Treatment duration is indefinite (lifelong). On stopping, all new hairs shed within 3-6 months.

The setbacks of oral Finasteride:
(1) Treatment duration is indefinite (lifelong). On stopping finasteride, the regrown hair persists, but the balding process resumes.
(2) Possible side effects, which are rare, include: ejaculation disorder; breast
tenderness and enlargement; hypersensitivity reactions including rash, pruritus, urticaria, and swelling of the lips and face; and testicular pain.

Who to see if you have AGA?
Be sure to consult your doc before starting any medications. Any competent family doctors are able to make the diagnosis. You may want to see a dermatologist if you're loaded. The treatments for now are essentially the same.

Females are affected too!

How long surgeries work?

Lengthy surgeries - how do they work?

Clinical scenario:

A pair of conjoined 4-year-olds who were separated last Tuesday have been off ventilators for 24 hours, and they've opened their eyes. It took a team of surgeons in Hospital Tuanku Jaafar (previously Hospital Seremban) more than a day (28 hrs to be exact) to divide the twins, who shared a body up to the mid-torso. How can surgeons work for so many hours in a row?

The How:

They work in teams. A conjoined-twin operation can be broken down into many stages, like the initial incision, the work around the bones, separation of the blood vessels, and reconstructive plastic surgery. A different team of surgeons scrubs into the operating room for each stage, most of which take only a few hours to complete. That way, most of the surgeons don't end up working for more than four or five hours in a row.

He's not that fierce looking in person, that Dr. K.K.Lim

The lead surgeons try to stay involved for the duration. They'll stay in the operating room for as long as they can, with a couple of breaks for snacks and rest. A surgeon who specializes in long-haul surgeries told the ҜαίخόρЋЯзпїα™ that he stops for food and drink every seven hours or so. He normally drinks Nes-Lo ice or teh-o-ais limau, and chomp down on a few pieces of roti prata. But that's besides the point.
"It really is like a marathon," he said. "You've got to keep hydrated."

There's no sunken eyeballs - signs of dehydration.

When surgeons at the Hospital Tuanku Jaafar Children's Centre separated a pair of twins who were conjoined at the head, they had a live feed of the procedure on a video display in a room upstairs. That way doctors who weren't involved in a particular stage could scrub out for a while and watch the operation on TV.

For the Tuanku Jaafar conjoined-twin procedure, four surgeons operated at any one time, with one pair assigned to each twin. Nurses shifted into the procedure every few hours, with two assigned to each pair of surgeons. Having so many people at the table could get a little confusing, so nurses and surgeons who worked together wore the same color stripe on their surgical caps.

MedikTV

Does anybody watch MedikTV? It's aired every Saturday evening on TV3 by this medical company known as KPJ Healthcare Bhd. Rach called me up and asked me to watch yesterday's episode featuring breast cancer biopsy.


I personally find it very educational, as it gives the public a glimpse of common diseases and their management and treatment procedures. I was actually impressed that they covered the psychological and social aspects of the patient too! This programme also features a very attractive host. The only downside is that it is in Malay language. They should air it in English to cater for non-Malay speaking viewers too!

A very comprehensive and "holistic" medical show. Highly recommended if you don't mind the Malay dialogues (with English subtitles).