March 20: Lesson with Dr. J

CN3, Oculomotor Nerve, Muscles in Eyes (rectus muscles, oblique muscles), Medication used in Grave's, tapazole, b-blocker, SNS, muller's muscle, Recession surgery, Difference between Horner's and Myasthenia Gravis



In my scrap sheet consisting of things that I-must-record-before-I-forget were above words.

What Dr.J went through with me during the surgery day on March 20th.






I remember from with my shameful response that I couldn't answer all the muscles in eyes innervated by which muscles (oculomotor muscle the obvious choice, but there are 2 other nerves that actually affect the eye movement, rather innervates muscles to the eyes moving it up, down, to sides and etc.)

Dr.J said in a teacher's tone, "Use the process of elimination. Everything is innervated by oculomotor nerve (CN 3) except lateral rectus muscle which abducts and thus innervated by abducens nerve (CN 6) and superior by trochelear (CN 4)." Actually I was able to say oculomotor after muttering to myself: ""Oh, oh, oh, to touch and feel very good velvet...ah, heaven."


That was very embarrassing and  I didn't have a chance to redeem myself by compensating with the cool knowledge that I had - last time I mentioned SJS (I looked it up!) after blundering the basic concept to compensate my stupidity (to save thy face!).


 The talk of extraocular muscle came after asking Dr.J about the recession surgery done on thyroid patients who has proptosis or exopthalmos. Typically with age, you have dermatochalasis and the two approach can be used to solve this problem. Blepharoplasty or ALR (anterior levator resection) surgery



See ALR surgery video here:

While the bleph surgery removes the fat and skin, ALR is the surgery for the muscle directly.
That is why patient have to practice "sit-ups" during the surgery to get the palpebral aperture right (so both eyes are symmetrical).


However, there's the exact opposite surgery which is called the recession surgery which reats the eyelid retraction - where the eyelids are abnormally wide (THYROID!).
Eyelid retraction recession weakens the muscle in the upper eye lid bring the eye lids down.
Anyway, for thyroid patients typically those with Grave's, their thyroid levels is up.

Thyroid level up -->
adrenergic up (that's why their heart beats very fast) -->
SNS activation (travel via carotid artery) -- Postganglionic sympathetic fibers originate in the superior cervical ganglion, and travel via the internal carotid plexus -->
muller's muscle activation (or superior tarsal muscle which is a smooth muscle adjoining the levator palpebrae superioris muscle that helps to raise the eye lid)-->
Proptosis!!



Tapazole and beta blockers are used to treat the grave's

and I have wrote alpha blockers too... interesting that Flomax which is a drug used to improve urination in men with benign prostatic hyperplasia....  is an alpha-blocker thus also treats high blood pressure.

I have to review medication yet again...used by patients and used during the surgery... 





Moving on from Thyroid now, I would like to talk about Horner's and myasthenia gravis.

I don't know why but it is very difficult for me to differentiate between the two and I have also confessed this difficulty to Dr.J.
Both are manifested by ptosis.

With Horner's there's miosis (pupil smaller) and anhydrosis (no sweating) 
With MG, acetycholine test and ice test.


I should know Horner's syndrome as my dad was suspected of having this due to possible tumors
Anyway, from Wikipedia:


Horner syndrome is due to a deficiency of sympathetic activity. The site of lesion to the sympathetic outflow is on the ipsilateral side of the symptoms. The following are examples of conditions that cause the clinical appearance of Horner's syndrome:

Myasthenia gravis (from Greek μύς "muscle", ἀσθένεια "weakness", and Latin: gravis "serious"; abbreviated MG) is an autoimmune neuromuscular disease leading to fluctuating muscle weakness and fatigability. It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction

March 14: Lesson with Dr. J

A patient comes in for consultation and possible (surgery) for ectropion repair.

Something like this.

Right side forehead smooth, eye pulled down - full of tears.
Keratinized and angry looking conjunctiva, man complained of 'hard of hearing' and loss of light perception and sensation from his right eye.

The man smelled certain way and I noticed the old stained overall holding his pants.

After he was seen, instead of ectropion repair, Medial Canthal Tendon repair was to be go ahead with it.

I've never seen the procedure and normally this would be done under Major OR (anesthetic)- but since this man had lost all sensation in his right face - including in his cornea - it was ok.







During the surgery - Dr.Johnson says,
"the one thing that I learned after medical school was that corneal cell regenerates as there are stem cells in limbus - so this man- not being able to feel anything indicates that this is not a normal bell's palsy - It's not just the CN 7 that's affected."

and then he asks me:

"which CN is the one for corneal sensation?"

of course I go, "um..."

"CN 5, trigeminal nerve" this was new to me. I think back from my book if I had ever read something about this. Nope, I didn't see it (later that night I went back to my text book and of course it doesn't say anything... through google I just confirmed this - as I almost wrote CN3 - oculomotor nerve)

And then the man says, "my hearing is bad in one ear (indicating his right where the bell's palsy was)"

Dr.J exchange looks with me and says, "and also the CN 8 - there's something going on."



I noticed that near his jaw and neck, there's a overly protruding bone (?) and I point at that as I wonder.
Dr.J nods then says "five."





No light perception..I wonder if his right pupil constricted? because this would indicate that his CN3 was also affected.









Back to limbal epithelial cells of the cornea.

During undergrad, I had the most difficulty wrapping around the concept of stem cells and to this day, I'm quite confident to say I don't understand whole lot what's going on with the cell development.
I know that there are different levels of stem cells such as totipotent (total: can make an individual!!)  and pluripotent (sublevel: not fixed as to developmental potentialities; especially : capable of differentiating into one of many cell types) cells and then it gets complicated....


To read the "Limbal epithelial stem cells of the cornea" click here!




Summary for myself (short copy and paste from the above link):

Ok, so what is cornea?
The cornea is responsible for protecting the eye against insults such as injury and infection. It also provides the majority (two thirds) of the total refractive power of the eye and is therefore the major refracting lens (Meek et al., 2003). So the LASIK, LASEK surgery is basically carving the corneal to correct the refractive power.

The corneal epithelium is a dynamic physical barrier preventing the entry of deleterious agents into the intraocular space. It consists of superficial squamous cells, central suprabasal cells and a single layer of inner columnar basal cells (Seckera& Daniels 2009).

Corneal integrity and therefore function is dependent upon the self-renewing properties of the corneal epithelium. The prevailing hypothesis is that this renewal relies on a small population of putative stem cells located in the basal region of the limbus (Seckera& Daniels 2009).  

that's what Dr.J said!!!

Throughout life, our self-renewing tissues rely upon populations of stem cells / progenitors to replenish themselves throughout life following normal wear and tear and injury. The corneal epithelium on the front surface of the eye is no exception as dead squamous cells are constantly sloughed from the corneal epithelium during blinking. At the corneo-scleral junction in an area known as the limbus, there is a population of limbal epithelial stem cells (LESCs). LESCs share common features with other adult somatic stem cells including small size (Romano et al., 2003) and high nuclear to cytoplasmic ratio (Barrandon and Green, 1987). They also lack expression of differentiation markers such as cytokeratins 3 and 12 (Kurpakus et al., 1990; Schermer et al., 1986).

Reading News March 20: Man of Integrity

Team player: Edmonton scientist turns down $100,000 ‘baby Nobel’ because it shut out colleagues

Republish Reprint

Sarah Boesveld | 13/03/20 | Last Updated: 13/03/20 3:32 PM ET
More from Sarah Boesveld | @sarahboesveld

The Canadian Press / Handout / University of Alberta-Michael Holly"What means the most to me is what our work means to patients. Some people think this may hurt my chances for the Nobel, but I felt that this is the time to stick my feet in," Michael Houghton told the Post

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It’s a respected medical research award, dubbed the “baby Nobels” as many of its winners have gone on to earn the coveted science prize. But Edmonton’s Dr. Michael Houghton has declined the Canada Gairdner International Award, worth $100,000, for his contribution to the discovery of the hepatitis C virus. He said he couldn’t accept the honour, also awarded to Dr. Harvey Alter of the National Institutes of Health, Dr. Daniel Bradley of the U.S. Centers for Disease Control and Prevention, if two other important researchers on his team were shut out. The Canada Excellence Research Chair in Virology said awards committees are stuck in the past, unwilling to acknowledge that research teams have grown since the time of Alfred Nobel. He spoke with the Post’s Sarah Boesveld from his office at the University of Alberta.

Q: Explain a bit further why you’re not taking the award.

A: I believe there were five key contributors: The three that received the Gairdner Award [which includes Dr. Houghton,] and Dr. George Quo and Dr. Qui-Lim Choo [who are employed by Chiron Corp.) Those two people worked with me for seven years to discover the virus in my laboratory.

Q: Do you think they were shut out because they work for a private company?

A: Oh, I don’t know. First of all let me say I’m pleased for Dr. Alter and pleased for Dr. Bradley  — those two individuals made important contributions. I just feel that this is yet another example — and this is not the first time — of where a major discovery is done by a number of people, but when it comes to recognizing that discovery, they’re exclusive rather than inclusive. The facts are, these big discoveries these days need big teams.

I haven’t told my wife that yet.

Q: Why are the awards so exclusive? The pot of money?

A: No, I don’t think it’s that. It’s all based on the Nobel prize. In his will, Dr. Nobel says there can be no more than three. All of the other major awards tend to copy that and limit it to three. It’s antiquated. In the days of Nobel, research was done by one or two people in small labs. Now it’s done by big teams in multiple labs. I’m very grateful to the Gairdner, I highly respect them, they do a fantastic job. On this one, unfortunately, I couldn’t accept.

Q: Why take such a stand when you could have accepted and acknowledged their major contributions?

A: I think I’ve evolved my philosophy after many, many years. When you make a big discovery, nobody trains you on how to handle it. In the 1990s, I got a call from the Robert Koch Foundation offering an award to myself and Dr. Bradley. I requested Dr. Choo and Dr. Quo be included and they said no. I took the award anyway. In the 2000s, I got a call from the Lasker Committee who said I got the award with Dr. Alter. I said ‘It’s really important that Dr. Quo and Dr. Choo be included.’ They said no. I agonized over the Lasker for many weeks and eventually I decided to accept it.

What means the most to me is what our work means to patients. Some people think this may hurt my chances for the Nobel, but I felt that this is the time to stick my feet in

Q: How do Drs. Quo and Choo feel about it all?

A: They feel they deserve direct recognition and I agree with them. I think it was after the Lasker that I decided ‘well, I really shouldn’t do this anymore.’ I never envisaged a situation when I was offered an award, I couldn’t persuade the committees to include my colleagues. That’s been a complete shock to me. It’s a huge disappointment. It takes a lot of the pleasure out of the whole process. It makes it awkward. It makes it unpleasant.

Q: Do you think this will hurt your chances at getting a Nobel prize?

A: I’m very respectful of the Nobel and the Gairdner and the Lasker and Robert Koch. What means the most to me is what our work means to patients. Some people think this may hurt my chances for the Nobel, but I felt that this is the time to stick my feet in. This was the opportunity to do it.

Q: I guess you don’t get the $100,000.

A: I haven’t told my wife that yet.

Read original article here!

My thoughts: it is so rare to see works credited to post docs and fellows who actually does bulk of the work in research. And when I say the bulk of the work, I mean: proposals, actual research - procuring specimen, experiment, statistic analysis, writing. Of course supervisors are some-what involved...actually the level of involvement between P.I (Primary Investigator) differs quite a lot that you can not generalize.

Knowing this, reading the article struck me with a thought.

'A True Man of Integrity'

March 11: Lesson with Dr. J - surgical debridement

First, Common drug names of the day: 

Atacand: angiotan: Diovan (Valsartan) = ACE 2 (receptor antagonist) inhibitor for HTN
Nexium (Esomeprazole) = H+ pump inhibitor for GERD

Second, Common medical condition of the day:

*Hiatus hernia (protrusion of upper part of stomach through opening of the thorax due to weakening of the diaphragm --> exacerbate GERD (Gastroesophageal reflux disease)

Third, quick office surgery of the day:

Debridement: Unbridle (to free from restriction)

Second last patient of the day flinched a little bit when alcaine drop was applied.
Just below his right upper lid, there was a big brown scab with a groove.
In a minute he was given xylocaine - after pressure application the area (brown scabby) was excised out, cauterized and was sutured.

Debridement - Dr.J said, I muttered to myself.
I asked if the groove was too big for the skin to heal properly and he said yes, that's why he had to debride the area so that it will heal after the closure - otherwise you get the scar like those who have chicken pox.
Groove, brown and forever lasting.
Debridement he said again.
I really appreciate it when he repeats.

Fourth, word from letters today that caught my attention: 

Stevens-Johnson Syndrome: Cell death separates epidemis from dermis. Main cause is certain medications, infections and rarely cancers. It is a milder form of toxic epidermal necrolysis (TEN) - SJS and TEN can be mistaken for erythema multiforme (type 3 hypersensitivity and more benign). Dermatologic emergency.