Thursday, March 16, 2017

How I remember the duration of symptoms for Generalized anxiety disorder (GAD) required for diagnosis

The symptoms of generalized anxiety disorder should be present for at least 6 months. For me, it's hard to remember the duration of the symptoms in psychiatry. So I mnemonic-ify them :D

I remember G6PD, and say G6AD instead!

For those who don't know what GAD is here is the DSM V criteria for diagnosis of Generalized Anxiety Disorder...

Transposition of Great Arteries!

Hello!

So I have divided the post into two parts - A short summary for those who don't have the time to read everything (#TLDR) and a nice long explanation for those who want to read everything :)
Let's start with TLDR.

Buzz words for congenital syphilis!

Following are some important signs and buzzwords that are testable ...And high yeild for entrances.

Olympian Brow: Bony prominence of the forehead caused by persistent or recurrent periostitis

Clavicular or Higoumenakia sign:Unilateral or bilateral thickening of the sternoclavicular third of the clavicle

Saber shins :Anterior bowing of the midportion of the tibia

Scaphoid scapula :Convexity along the medial border of the scapula

Hutchinson teeth:Peg-shaped upper central incisors; they erupt during 6th yr of life with abnormal enamel, resulting in a notch along the biting surface

Mulberry molars :Abnormal 1st lower (6 yr) molars characterized by small biting surface and excessive number of cusps

Saddle nose :Depression of the nasal root, a result of syphilitic rhinitis destroying adjacent bone and cartilage

Rhagades:Linear scars that extend in a spoke-like pattern from previous mucocutaneous fissures of the mouth, anus, and genitalia

Juvenile paresis :Latent meningovascular infection; it is rare and typically occurs during adolescence with behavioral changes, focal seizures, or loss of intellectual function

Juvenile tabes : Rare spinal cord involvement and cardiovascular involvement with aortitis

Hutchinson triad :Hutchinson teeth, interstitial keratitis, and 8th nerve deafness

Clutton joint :Unilateral or bilateral painless joint swelling (usually involving knees) from synovitis with sterile synovial fluid; spontaneous remission usually occurs after several weeks

Interstitial keratitis: Manifests with intense photophobia and lacrimation, followed within weeks or months by corneal opacification and complete blindness

8th nerve deafness: May be unilateral or bilateral, appears at any age, manifests initially as vertigo and high-tone hearing loss, and progresses to permanent deafness.

Well all these are late manifestations of congenital syphilis occuring after 2 years of life.
It is important to recognise these signs clinically and also on the exams...

-Medha.

Pathophysiology of myopathy caused during hypothyroidism and hyperthyroidism

Hello awesomites! Today's topic of discussion is - Myopathy in thyroid disease.
Interestingly, it is caused by both, hypothyroidism as well as hyperthyroidism.

What is myopathy?
It is a disease of muscle tissue where, ultimately, muscles get weak and are unable to perform work due to deficiency of ATP.

Why is there myopathy in hyperthyroidism?
The thyroid hormone is a catabolic hormone. Hyperthyroidism increases energy expenditure, glucose turnover, lipolysis, and protein breakdown (proteolysis). But here is the catch - Hyperthyroidism increases whole-body protein turnover and breakdown before any measurable changes in energy expenditure or glucose and fat metabolism, suggesting that amino acid and protein metabolism is an early and primary target for thyroid hormone action in humans. It was therefore concluded that the thyroid-hormone concentration may be an important factor in regulating muscle proteolysis. The altered protein metabolism causes myopathy.

Then, one may ask, why myopathy in hypothyroidism? Less thyroid hormone should lead to less protein breakdown, shouldn't it?

Well, this is a good question! Slightly complex and tricky to answer though. 

In hypothyroidism, there is abnormal glycogenolysis, defective mitochondrial oxidative metabolism and triglyceride storage.

Abnormal glycogenolysis and triglyceride storage: Less glucose is released and utilised because of this. The body starts using more proteins usually derived from muscles leading to myopathy.

Mitochondrial oxidative metabolism defect: Thyroid hormone is responsible for activation of bc1 complex also known as complex 3 & succinate dehydrogenase. Less activation of bc1 leads to less formation of ATP from glucose.... So again, the body switches to proteins from muscles as a source of energy!

That's all!
Stay cool :)
~Ojas

Medicowesome secret project: Exam time

Medicowesome secret project: Embryo – Male or female?

Medicowesome secret project: Ghrelin

Medicowesome secret project: Biostatistics

Wednesday, March 15, 2017

Fact of the day: Regulate brain activity with your type of music

Hey Awesomites

Which genre or type of music do you like the most? Well, it surely has to do a lot with the functioning of our brain. Some of you may like slow music while others like to rock n roll on the floor while listening to their favourite beats. I am more of the latter type too, depending on the mood. ;p

Saturday, March 11, 2017

Fact of the day: Paradoxical undressing in fatal hypothermia

Hypothermia causes paradoxical undressing.

This typically occurs during moderate to severe hypothermia, as the person becomes disoriented, confused, and combative. They may begin discarding their clothing, which, in turn, increases the rate of heat loss. It is estimated that twenty to fifty percent of hypothermia related deaths are due to paradoxical undressing.

Why does this happen?

Friday, March 10, 2017

Fact of the day: Psychosomatic symptoms love to travel

Hey Awesomites

Yes, you read it right. The symptoms of psychosomatic disorders flit from one body part to another, and just too easily and quickly ( they love to travel a lot ;p ) . Just as one symptom is discovered, it disappears and another one emerges in some other part of the body.

The psychosomatic symptoms have been linked to a chameleon. Every time a medicine tries to pin them down,  they become something different.

That's all
- Jaskunwar Singh

The colours of a chameleon are not more numerous and inconstant than the varieties of the hypochondriac and hysteric disease.
 - Robert Whytt

NYHA Classification Mnemonic

Hey guys, this post will help you to remember the definitions of the four NYHA classes.

So first just remember two phrases-
"Patient with a heart disease" and "in ordinary or accustomed activities". For convenience I will use letters A and B to refer to these phrases respectively. Now I will just fill in the gap between them.

1. NYHA Class I:
A--- will not get dyspnea ---B.

2. NYHA Class II:
A--- will get dyspnea ---B.

3. NYHA Class III:
A--- will get dyspnea in less than ---B.

4. NYHA Class IV:
A--- will get dyspnea at rest.

This system of classification has its flaws since the definition of "ordinary and accustomed activities" is entirely subjective. Like for example if a rich businessman gets breathless after walking 1 km, you may label him as NYHA Class II, but the same case in a hard working labourer will have to be labelled as NYHA Class III.

And another thing that NYHA has recently clarified NYHA Class III a bit further, it has included self-care activities in it's spectrum. As a supposition, if a 56 year old male person gets breathless while shaving or bathing then it is NYHA Class III.

-VM

Authors' diary: Medicowesome secret project


We initially introduced the secret project very mysteriously and kept the details highly confidential just for fun! Let me tell you more about it...

Thursday, March 9, 2017

Grave's ophthalmopathy features mnemonic

Hey Awesomites

Grave's disease, a common cause of primary hyperthyroidism causes some epic features of ophthalmopathy apart from lid retraction and lid lag. Mnemonic: EPIC

E- Exophthalmos
P- Periorbital Edema
I- Involvement of ocular muscles (diplopia)
C- Conjunctival irritation and chemosis

- Jaskunwar Singh

Amiodarone- induced thyroid dysfunctions

Hello

Amiodarone, a potent class III anti- arrhythmic drug is contraindicated in thyroid patients or those with subclinical disease. The reason lies in the pharmacokinetic profile of this drug.

The drug has a structural resemblance to triiodothyronine (T3) and thyroxine (T4). In the body, it is metabolized by dealkylation to Desethylamiodarone (DEA), the intrathyroidal concentration of which is higher than the parent drug.

Normal daily recommended intake of iodine for adults is approx. 0.15mg (150mcg).  Each 200mg tablet of amiodarone contains about 74.4mg of iodine with 7.4mg (10%) being released as free form. This is roughly 50- fold higher than the normal. Therefore, total body stores may remain increased for upto 9 months after stopping the drug.

High iodine content of this drug inhibits  local type-1 5'- deiodinase activity (blocking conversion of T4 to T3) and type- II 5'- deiodinase activity in the pituitary. As a result, TSH is increased initially (mild elevation) and then return to normal or may even decrease in euthyroid patients after weeks, while T4 is normal or raised, and T3 levels decrease.

The increased delivery and uptake of iodine by the thyroid gland may cause increase in hormone production and release, a condition called type-1 Amiodarone- induced thyrotoxicosis (AIT) . In other cases, excessive thyroid tissue destruction due to destructive thyroiditis may lead to type-2 Amiodarone- induced thyrotoxicosis. These are hyperthyroid states!!
Discontinuation of the drug is recommended, if not, then high doses of thioamides and corticosteroids may work in AITs.

Amiodarone may also cause hypothyroidism (AIH) in  patients depending upon the iodine status of individuals and prior thyroid disease. Wolff- chaikoff effect is shown by thyroid cells due to failure of thyroid hormonogenesis. Levothyroxine is the drug of choice.


Thats all
- Jaskunwar Singh