Study group discussion: Smallest, largest and longest muscle

Which is the smallest muscle in the body?

Stapedeus. 

Nope, stapedius ain't the answer.

Then?

Erector pili muscle. The one responsible for goose bumps.

Oh yes! I forget it's a muscle cause it is so small and seems insignificant.

Haha me too!

Awesome.

Largest muscle?

Gluteus maximus!

The longest muscle?

Sartorius. Originates from ASIS to Pes anserinus.

Updated on 22nd February, 2015:

I read the previous  posts, errector pili -smallest smooth musle, smallest skeletal muscle -stapedius!

Smooth muscle not in our control , innervated by sympathetic system,triggering agents - cold, fear. 

Which is the strongest muscle in the body?

Ahh makes sense. 

Strongest would be the one in the thigh?

Gluteus maximus!

Nope. 

Masseter. 

True! Well done!

Shouldn't it be the quadriceps? I don't see the masseter kicking foot balls and running with the weight of the body :P

Yes, based on its weight, with all muscles working together it can close the teeth with a force of 25 kgs on the incisors. 

Ooh. 

Or 90 kgs on molars! 

I got a good link on that!

There are lots of ways to measure strength. One is brute force, in which case biggest is best. All skeletal muscles are bundles of many individual fibers that contain small force generating structures called sarcomeres. “Generally speaking, more muscle tissue means a larger total number of sarcomeres, which means greater maximum force generation,” Tasko says. That means the largest muscles—the quadriceps on the front of your thighs and the gluteus maximus on your rear—produce the most force.

I thought the strongest was the tongue! 

I was told that it was the muscle that can do the most amount of damage - the tongue (Obviously, not physical damage, you know what I mean, right?)

Oh oh most hard working muscle in the body? 

Heart <3 

Why not diaphragm?

Umm I donno.. Because you can have a paralyzed diaphragm and live but you can't have a paralyzed heart?

I personally think that heart is made popular for no reason :P

Study group discussion: Babinski sign

What is pyramidal tract sign?

Did you mean Babinski sign ?
There are a specific set of clinical signs for pyramidal tract disease..I haventy heard of just one particular one.. But yes, out of the many..Babinski is the most specific for pyramidal tract disease.

A few days after UMN syndrome, motor signs appear
These include spasticity,  hyperactive reflexes, extensor plantar responses.

That's because the CSF will press on the cortical neurons.. And cause a upper motor neuron type of lesion.

UMN lesion is due to lesion in corticospinal tract between cerebral cortex and SC.

Well, not all pyramidal signs are called Babinski. Babinski is the extensor response to plantar reflex when the lateral surface of the feet is striken/scratched.

Achcha what are the components of the positive babinski reflex? - review question.

Extension of great toe, fanning of other toes, contraction of tensor fascia lata.

Plus, dorsiflexion of ankle and knee joint.

Yeah, that.

Other ways to elicit a babinski ?
Plus the equivalent of babinski in the upper limbs?

It's plantar reflex. It can be elicited different ways, one's babinski, others are Oppenheim and Chaddock.

Schaeffer too.

Yep.

And do you elicit Babinski with sharp end or blunt end of the hammer? (Viva question)

In Babinski, you have to produce pain and pressure both at same time so I guess blunt end if the hammer is used.

To support my answer - I have also seen many doctors using their keys (blunt end) for eliciting Babinski.

The tip of a pen can also be used to elicit Babinski.

Yeah, they taught us that we could use keys if we didn't have a hammer handy.

Always red, it looks better on a patient's foot.

In paediatrics.. We used our own nails to elicit Babinski!

I was doubtful that it would work.. But it did.. Especially, children aged below 3-5 years.

Study group discussion: Monospot test for EBV infection

Anyone explain Monospot test please!

Heterophile antibodies in the blood?

I was just reading this. The test works with the agglutination of  horse's RBC when in contact with heterophile antibodies.

Yes.. Used in detection of these antibodies in infectious mononucleosis.

When you have infectious mononucleosis you produce antibodies anti-epstein barr virus and other unspecific antibodies which are called heterophile antibodies.

Aren't anti sheep antibodies produced in monospot test ?
I mean Heterophile anti sheep red cell antibodies?

That would be Paul Bunnel test.

But infected B cells secrete anti sheep red cell antibodies that are diagnosed for mononucleosis. .

I think the only difference between monospot and paul bunnel test is the origin of the RBC. In monospot they come from horses and on Paul Bunnell, from sheeps.

Study group discussion: Sarcoidosis and calcium regulation

I have a review question for sarcoidosis.

What is the characteristic appearance of sarcoidosis radiological imaging?

Lambda sign?
Panda sign?

No. Hint..That's also what tuberculosis shows positive.

BL hilar lymphadenopathy.

Tree in the bud sign.
You then differentiate it from TB ..Based on whether the lymph nodes are showing necrosis or not.

Can you elaborate on the tree in bud sign?

It's an appearance on chest CT. I read it is specific for TB and sarcoidosis.

Oh so if there is necrosis, it's Tb? If not, it's sarcoidosis?

Yup. That too can be differentiated on CT.. By looking at the lymph nodes.

I have a review question. Which cells will you see in sputum examination of a patient with sarcoidosis?

Elevated CD4/CD8 ratio.

Why is that?

I don't know exactly but CD 4 + inflammation is specific to sarcoidosis. Helps differentiate it from other non granulomatous interstitial lung diseases.

*A parallel discussion on calcium was going on, since they both are related to each other, I'm posting the calcium discussion here as well*

Percentage of dietary calcium absorbed is inversely related to intake. How is this possible?

If you take more calcium, it absorbs less? I don't know how that is possible.

The body has to maintain a homeostasis for calcium.. If reduced intake..There will be paradoxical increased receptors via Vitamin D. To maintain a constant absorption.
If increased intake..The body reduces the absorption. The mechanism..PTH is stimulated via low serum calcium.. And PTH is the one responsible to make the final active form of vitamin D.
So if calcium in the blood stabilizes, there will be reduced impulses by PTH..conversely less vitD and less absorption.

It means that if your body's need/absorption of calcium equals x.
If your intake equals x, you'd be absorbing 100% of it.
If your intake equals 2x , you'd be absorbing 50% of it.
If it equals 4x you'd be absorbing 25% of it, and so on.
At a normal steady state of absorption, the more the intake is, the less the absorption percentage of it.

Excellente.

Can anyone associate calcium and sarcoidosis?

Hypercalemia.

Why?

Because of increase in Vitamin D by granulomas.

PTH decreases then.

Which enzyme?
And which cell is involved?

It's the interstitial alveolar macrophages that secrete alpha hydroxylase that activates vitamin D.

Is sarcoidosis a cause for dystrophic calcification then?

No, metastatic.

Bravo!

Medicowesome study group on Whatsapp: The Official invitation

It started as a small experiment and turned out to be one word - AWESOME.

What's the study group for?
A bunch of medical students from all over the world, discussing study related concepts!
You may share your experiences, what you studied today, ask interesting questions to help other people learn or simply revise, ask doubts about things you don't understand, answer other people or just tell a fact you learnt that fascinates you.
We learn something new on a daily basis <3

How do I sign up for the group?
All you've got to do is message me your number. You can email me at medicowesome@gmail.com with "Whatsapp study group" in the subject.

Important: Make sure you include your proper country code when you email me your number. (Otherwise your number won't be displayed in my Whatsapp list and I might miss you out!)

After you have emailed me your number, you'll receive instructions from us. 

The group is for medical students only. We do not add pharmacy / nursing / pre med students.

"I want to join but.. I'm hesitant because I'll be sharing my number to a lot of people."
It's risky, I know, but we have solutions - Block users. So I don't think you should hold back on your awesomeness. I have added over 800 people so far and they are loving it.

We have had a few spammers, flirts and inappropriate members, but we removed them. We highly encourage awesomites to report such people to the admins (We have more than 5 admins) and necessary action will be taken.

Your number will be shared with at least 100 other medical students who are strangers - So if you aren't comfortable, don't join.

-IkaN

Related post: More information on study group

Study group experience #5

Here's what we discussed!

Drugs that cause urinary calculi

Amantadine

Cardiac mortality in diabetes mellitus reduction due to aspirin 

ECG in MI, potassium abnormalities, infectious diseases, pericarditis

Splenic vein thrombosis and hepatic vein thrombosis 

Difference between rouleaux formation and agglutination of RBC's

von Willebrand factor and disease 

O negative blood group 

Type 3 diabetes and type 1.5 diabetes

Hyperthyroidism and decreased appetite

Somatostatin 

Hydrocephalus ex vacuo, normal pressure hydrocephalus and cortical atrophy 

Wernicke Korsakoff syndrome 

Ziehl Neelsen staining uses

Human Papilloma Virus

Immortal cells 

Why food doesn't taste good in aeroplanes

I particularly like how when one person answers correctly in the group, even if it's to a simple question, someone says a positive word like, "Excellent!", "Well done" or "Bravo!"

If you answer incorrectly, we'll tell you, "We are here to make mistakes so that we can avoid them in real life."

Oh and the science discussions! They make me lose my sense of time.. I feel completely enraptured. We end up in deep thought, amazed by the wonders of nature when those insightful discussions happen. 

It's this kind of positive reinforcement that makes it not just a study group but a vast, open, refreshing and fascinating learning group to me. 

Thank you, good hearted awesomites, to make this such a beautiful experience.

To all the future awesomites, hope you continue the legacy. 

-IkaN

The illusion of ST segment elevation in transmural myocardial infarction

To, understand the WHY of it all, we need to understand what is the electrical vector?

      1.Before the incoming of any impulse, the heart muscle is polarized- meaning the outside of heart muscles is more positive in compared to the inside of the heart muscle. This means that the ECF all over the heart has a positive charge

2.       With the incoming of the impulse from the S.A node, the heart muscle depolarizes..means positive ions are going inside. Which means the overlying ECF is becoming negative in compare to the surrounding area

3.       This change  in electrical charge, generates a current in the ECF ..this current flows from negative to positive and thus generates what is called the electrical vector
4.       The electrical vector changes in size and direction as the wave of depolarization spread

5.       Also, our body is a volume conductor..which means when the electrical energy flows..there is an electrical field generated around it. And different points on the field have a potential, based on their location from the electrical vector
6.       When we connect two potential in this field, and measure the potential difference between them, we get the electrocardiogram (ECG)

Next important point to be understood is how the strength of the vector is measured, whether the wave will be negative, or positive..and what will be its strength?

The axis of the electrical field is determined from negative to positive

Suppose there is a vector AB,  what we do to measure the value of this vector is project the same vector on this electrical field.

Hence, the strength of the voltage is +4 mv, and since the value is positive we get a positive wave

On the other hand, this vector has a value of -3mv, and it will be a negative wave

Whenever, there is an infarction in the myocardial tissue..the cell looses its polarity, meaning it becomes depolarized.

So even when the whole heart is in the resting stage..there is some amount of current flow from the infarcted tissue ( this is called funny currents-If)

Also remember, the ST segment is an isoelectic line, meaning there is no flow of charge in the heart muscle during this time..that is either the heart is completely polarized ( resting stage- all over positivity outside) or the heart is completely depolarized (all over negativity outside)

So now when you take an ecg of this heart..example with an infarction in the anterior wall, on the V1 lead, the overall voltage of the heart is reduced, this is because the constant flow of funny currents from anterior to posterior. This modifies the electrical vector ( with change in its direction and size)

But now as the wave of depolarization is completed (the QRS complex), the funny currents are abolished..cause they too are in the depolarized state (negativity outside). Hence, no flow of funny currents.

This makes the st segment isoelectric (that is 0mv)

When we see this graph, it seems the st segment has elevated, but in reality it is just an illusion, cause the st segment is right where it was supposed to be, what has changed is the voltage of the rest of the ECG

Study group discussion: Wernicke Korsakoff syndrome

Review question:
What triad is present in Wernicke's encephalopathy?

Opthalmoplegia, ataxia and confusion.

Excellent!

What is the treatment?

Thiamine.

Route?

Intravenous or parenteral route is used.

Do we give glucose before the thiamine or after the thiamine?

Study group discussion: Somatostatin

What is the function of the hormone somatostatin? In relation to the regulation of blood sugar level?

Somatostatin is the hormone which keeps the blood glucose level smooth... Prevents fluctuation.

It inhibits both insulin as well as glucagon release, plus decreases the overall transit time of food in your GIT

Somatostatin is the reason why you need only three meals a day... It doesn't allow all the glucose to enter your body at once and maintains a continuous supply.

There is something a professor always says, "Somatostatin never met a hormone it didn't like to inhibit."

coOl.

True. I haven't come across one thing it stimulates ^_^"

Study group discussion: O negative blood group

Review question time!

Which is the universal donor?
And why?

O negative. No antigens.

But it still has anti-A and and anti-B antibody... Won't they react to the RBC present in the recipient?

Confused at the O negative thing. Will read it.

The things is when you give blood to the recipient.. The plasma in the O- blood is rapidly mixed with the 5 litres of the recipients plasma.

So the antibodies are diluted..they are not effective in causing agglutination of the recipients RBC

Why doesn't this happen with any other mis matched blood groups?

Cause in those cases the RBC's are having antigens... So they are rapidly agglutinated.

Mismatched blood transfusions are due to agglutination of donors RBC, never the recipients RBC.

Oohh yes... Cool.

Study group discussion: von Willebrand factor and disease

Drug of choice for Von Willebrand factor deficiency?

I know this! Vasopressin!

Route? :D

I think.. Nasal spray?

Yes! The drug can't be used chronically but cause it just causes release of preformed vWF factors.

vWF is for platelet adhesion.. Right? In normal haemostasis?

Yes, vWF sticks platelets to the blood vessel wall. Gp 1b helps in platelet adhesion.

It's present in Weibel Palade bodies.

What are these bodies?

Weibel–Palade bodies store and release von Willebrand factor and P-selectin. Mnemonic: http://medicowesome.blogspot.ae/2014/01/cell-mnemonic.html

And can any one name another disease related to Von Willebrand's factor? (Indirectly related)

Bernard
Sullivan syndrome.

Umm woah I didn't know so many diseases with vWF.
I was thinking of thrombotic thrombocytopenic purpura.
ADAM TS 13 is defective, which is involved in the degradation of vWF

I didn't find any Sullivan syndrome!
I think he meant Bernard - Soulier syndrome.
Bernard Soulier, you mean?
Yeah. Still spelt it wrongly.
Haha it's okay! I was spelling "Wobble palade" bodies myself. I Googled before typing it though.

Study link! http://medicowesome.blogspot.ae/2013/12/anti-platelet-drugs-receptor-and-their.html

Study group discussion: Ziehl Neelsen staining uses

Another one.. Name the substance that stain positive with Ziehl Neelsen staining.

Microbes.

Examples?

Tuberculosis, cryptosporidium.

M. Leprae.

Nocardia!

Others are rhodococcus, isospora, smegma bacillus.

Ooh did not know those!

And?

Sperms!

Study group discussion: Hyperthyroidism and decreased appetite

Why in hyperthyroid states there is loss of weight despite increased appetite?

High metabolism?

There is one more reason to it.

Do they have increased bowel movements? Maybe that reduces nutrient absorption?

Hyperthyroid is a protein catabolic state..Hence no matter the external energy provided..The preformed proteins are broken down.

Aah yes!