For the third time I heard " (name ) if you read my brochure, you will realize that I don't say it definitely." 
I have read the brochure about 4 times but because of that, am reading again.

what's the brochure's name? Dr.J's handwritten brochure about  Thyroid eye disease ~*

Proptosis, lid retraction, diplopia, optic nerve compression, strabismus, thy name is  Thyroid/Grave's disease.

Thyroid eye disease is interesting. These are so far, things I have observed and maybe noticed traits of patients with this pathology. (perhaps because I was told that the patient is often by my much experienced predecessors)

• talkative (have to cut them in middle of conversation while I'm screening, or else I will fall behind...)
• may not be pleasant.
• sometimes aggressive/paranoid

However, although I might have met paranoid person, luckily I have not had any extensive unpleasant experience... actually I can only recall seeing friendly thyroid patients who might have been more talkative than other patients.

*side note: what I do when I see thyroid patients. I write the code 0906A.

What's weird is that Thyroid eye disease (or thyroid orbitopathy, Grave's disease, Grave's orbitopathy etc) is an autoimmune disease that occurs in people 'with a history of thyroid problems...[but]...occur before or decades after the development of thyroid gland disease.' Another curious thing is that it can manifest even after the thyroidectomy. WHY?!?!? you don't have thyroid, so shouldn't you be free from these problems? 

Actually I just found out through U of M website, that ophthalmic manifestation is divided into 2 groups.  

Hypermetabolic and infiltrative 

(http://www.kellogg.umich.edu/theeyeshaveit/acquired/graves-disease.html)

Hypermetabolic: excess thyroid hormone --> sympathetic pathway activation --> retraction of lids 

= the "stare sign" -- when the patient is to look downward, the upper eyelids remain elevated or begin moving downward only after a delay -- a sign called "lid lag" 

Infiltrative: lymphocytic infiltration of the orbital soft tissue, NO RELATIONSHIP to the LEVELS of the THYROID hormone. 

so that's why Mr.K, even after thyroidectomy had this problem. back to it being an autoimmune disease...

As the inflamed conjunctiva becomes hyperemic (red) and boggy, the eyes tear and discharge mucus. The patient reports a feeling of tightness (yes), irritation (yes), and intermittent blurring of vision (yes), much as one might experience with infectious conjunctivitis ("pink eye"). The lower eyelids become boggy, and palpation elicits a sense of rubbery induration that is only mildly tender.

When the extraocular muscles and orbital fat become inflamed, the eyes are displaced forward in the orbit (proptosis, exophthalmos), and the movements of the eyes may be limited. At first, the impaired eye movements are due to swollen, inefficient extraocular muscles. If the inflammation persists beyond a year, the muscles scar in a contracted, noncompliant state. Typically, some extraocular muscles are affected more than others, driving the eyes out of alignment in some fields of gaze, and causing the patient to experience double vision.

As the muscles swell, they may compress the optic nerve in the posterior orbit, where they are packed in a tight space. If the compression is not relieved, axoplasmic flow within the nerve comes to a halt, and vision fails. This compressive optic neuropathy is the most dreaded ophthalmic consequence of Graves' disease.

Another outcome of marked swelling of extraocular muscles and orbital fat is massive proptosis which interferes with the protective function of the eyelids and results in drying of the cornea. This "exposure keratopathy" is the second most feared ophthalmic manifestation of Graves' disease.

The combination of hypermetabolic and infiltrative ophthalmic signs gives away the diagnosis of Graves' disease.

But when the hypermetabolic component is absent and infiltrative signs are mild, the condition is often misdiagnosed as infectious or allergic conjunctivitis.

When one side is relatively spared, the physician may incorrectly diagnose an orbital tumor.

And when inflammation relatively spares the most visible tissues—the conjunctiva and eyelids—the physician may fail to consider Graves' disease as the explanation for diplopia or visual loss.

But Mr.K had other problem. and that is what prompted me to write this post. He developed a Retinal Hemorrhage (bleeding behind retina) so he has to get injection in his eye with a needle ever 3 weeks in addition to chronic predinisolone drops.

"What were you injected with", I asked.

" Oh, I'm not sure..."

"Is it the steroid?"

"Oh, I use that drop everyday, but it's not that."

Dr.J must know. surely. 

So I asked Dr. J and he answered "anti-VEGF" 

Vascular endothelial growth factor.
as VEGF encourage the development of new blood vessel so in order to stop the evolution of bleeding. You use this. The most commonly marketed drug for this. LUCENTIS.
I asked if this anti-VEGF is must be used for cancer and he said yes..
Turned out the drug named AVASTIN is used to treat colorectal, lung, breast and brain cancer. The difference is that LUCENTIS is used specifically for the eyes and therefore smaller molecule.


It amazed me that this procedure was just implemented 3 years ago.
Before it was all corticosteroid.





side note:

Retinal Hemorrhages

Shape Mechanism Common Associated Conditions Dot Hemorrhage Rupture of deep capillaries Diabetes Flame Hemorrhage Rupture of superficial pre-capillary arterioles, small veins Systemic hypertension, leukemia, severe anemia, thrombocytopenia, retinal vein occlusion, trauma Boat Hemorrhage Rupture of large superficial retinal veins into the space between the retina and vitreous; sometimes these bleeds break into the vitreous cavity Sudden increase in intracranial pressure, anemia, thrombocytopenia, trauma Submacular Hemorrhage Rupture of choroidal vessels under the fovea Age-related macular degeneration Vitreous Hemorrhage Rupture of superficial retinal vessels or vessels on a fibrovascular stalk extending into the vitreous Proliferative diabetic retinopathy, hypertension, trauma

November 06 2012 - Lessons with Dr.J

If you ask me if I know someone who is an ideal husband, without a second thought I would say Dr.J.
The way he approaches the problem so logically with grace, you can almost say that I idolize him ("I never met anyone so perfect....") and then there is this love he has for his wife..that makes him the perfect husband.
(Women are often more attracted to hard-working men!)

Anyways, during the sloppy day it was yesterday, very important lessons were taught to me.


Do I want to be data gatherer, or a problem solver?


Why was the patient 20/400 in one eye and 20/20 in the other?
What was the reason? follow follow follow. Just like Sherlock Holmes would, look for clues that will tell the 'story'.
This was the very important lesson that was taught and I shall remember it.




Mental disease: Morgellon's disease
--why did I write Mental disease? it was described me to as a skin condition and I just typed up mental before I looked up the definition from Wikipedia.

Morgellons (also called Morgellons disease or Morgellons syndrome) is a name that was given in 2002 by Mary Leitao^[1] to a proposed condition characterized by a range of cutaneous (skin) symptoms including crawling, biting, and stinging sensations (formication); finding fibers on or under the skin; and persistent skin lesions (e.g., rashes or sores). Doctors,^[2] including dermatologists^[3] and psychiatrists,^[4] regard Morgellons as a form of delusional infestation (also called delusional parasitosis), i.e. the belief that there is a pathogenic infestation despite contrary medical evidence.^[5]

Despite the lack of evidence that Morgellons is a novel or distinct condition and the absence of any agreed set of diagnostic symptoms,^{[6][not in citation given]} the Morgellons Research Foundation and self-diagnosed Morgellons patients successfully lobbied members of Congress and the U.S. government's Centers for Disease Control and Prevention (CDC) to investigate the proposed condition.^[2][7] The CDC researchers issued the results of their multi-year study in January 2012, indicating that there were no disease organisms present in Morgellons patients, the fibers found were normal clothing fibers, and suggested that patients' sensations were manifestations of "delusional infestation".^[8][9]




Lambert-Eaton syndrome: (LEMS often associated with lung cancer... 50-70%)

Lambert–Eaton myasthenic syndrome (LEMS, sometimes Lambert–Eaton syndrome or Eaton–Lambert syndrome) is a rare autoimmunedisorder that is characterised by muscle weakness of the limbs. It is the result of an autoimmune reaction, where antibodies are formed against presynaptic voltage-gated calcium channels in the neuromuscular junction (the connection between nerves and the muscle that they supply).^[1]Around 60% of those with LEMS have an underlying malignancy, most commonly small cell lung cancer; it is therefore regarded as a paraneoplastic syndrome (a condition that arises as a result of cancer elsewhere in the body).^[2]

People who develop LEMS are usually over 40, although it may occur at any age. The diagnosis is usually confirmed with electromyography and blood tests; these also distinguish it from myasthenia gravis (MG), a related autoimmune neuromuscular disease.^[1]

If the disease is associated with cancer, direct treatment of the cancer often relieves the symptoms of LEMS. Other treatments often used aresteroids, azathioprine and intravenous immunoglobulin, which suppress the immune system, and pyridostigmine and 3,4-diaminopyridine, which enhance the neuromuscular transmission. Occasionally, plasma exchange is required to remove the antibodies.^[1]

Canaliculitis

One of the most misdiagnosed condition and this family physician wonderfully got it right.
The infection was caused by none other than Actinomyces Israelii and it is half yeast/bacterial like infection that is managed by minor surgery and antibiotic.

Actinomyces israelii is a species of rod-shaped bacteria within the Actinomyces. Known to live commensally on and within humans, A. israelii is an opportunistic pathogen and a cause of actinomycosis. Many physiologically diverse strains of the species are known to exist, though all are facultative anaerobes.^[1]

Actinomycosis is most frequently caused by Actinomyces israelii and is sometimes known as the "most misdiagnosed disease,"^[who?] as it is frequently confused with neoplasms. A. israelii is a normal colonizer of the vagina, colon, and mouth. Infection is established first by a breach of the mucosal barrier during various procedures (dental, GI), aspiration, or pathologies such as diverticulitis. The chronic phase of this disease is also known the "classic phase" because the acute, early phase is often missed by health care providers. This is characterized by slow contiguous growth that ignores tissue planes and forms a sinus tract that can spontaneously heal and recur, leading to a densely fibrotic lesion. This lesion is often characterized as "wooden." Sulfur granules form in a central purulence surrounded by neutrophils. This conglomeration of organisms is virtually diagnostic of Actinomyces israelii.^{[citation needed]}