Tuesday, February 10, 2015

Study group discussion: Grave's disease

I have a few review questions!

In which condition is pretibial myxedema seen?

Grave's. That and the ophthalmoplegia are specific to graves

Yes! Paradoxically Graves is hyperthyroidism not hypo!

Which drug is used for hyperthyroidism in pregnancy? Why?

PTU. Cause it crosses the placenta in the least amount?

Absolutely correct! Propylthiouracil does cross the placenta. It's just that you give a lower dose.

Which is the only symptom of Graves disease that doesn't get better with anti thyroid medication?

Ophthalmoplegia! You need steroids to treat it.

Study group discussion: Microcytic and Sideroblastic anemia

Do we have any specific topic for discussion today?

You can start one!
Yes!

Anemias?

Just on nights..we hold a review question session. Those are based on specific topics.

As in Asian nights. Time zone differences everywhere!

Haha..yes.

Alright! Anemia!

Name the hypochromic mycrocytic anemia.

Iron deficiency anemia!
Alpha thalssemia
Anemia of chronic disease
Sideroblastic anemia

Not beta thalessemia? Isn't it all thalassemias?
Beta thalassemia too
So yes! Thalassemias in general.

Lead poisoning

Chronic diseases such as...Renal failure, TB, etc.

There is the SITA mnemonic for the question we just answered
Sideroblastic
IDA
thalassemia
ACD

Remember hypochromic mycrocytic anemia as SITAL.

What's the L for?

Lead poisoning.

Oh.. We consider it in Sideroblastic anemia!

It's different.

Is it?

In Sideroblastic anemia there is defective formation of heme due to a genetic or even a drug induced cause. The RBC blast cells contain stippling. But in cases of lead poisoning..The cause is restricted to only lead.. Which causes a similar picture.

The same happens due to alcoholism and lead poisoning, right?
Yup.

The heme formation is defective because lead inhibits an enzyme required in heme synthesis.
Yup.

So why shouldn't lead poisoning be considered a type of Sideroblastic anemia?

Cause the cause is different and cause they like to confuse us -_-

Haha.

I got this table on classification of Sideroblastic anemia. It all comes under the same roof.

*can not post the table due to copyright issues on the blog, but it showed congenital and acquired Sideroblastic anemias*

Hmm.

Which anemia does an antitubercular drug cause?

Pyridoxine! Sideroblastic anemia, again.

Study group discussion: Mechanism of anemia in anemia of chronic disease

Why in chronic diseases you get anemia?

Due to poor absorptiomu of iron

Because of the inflammatory factor.. It locks up iron in the bone marrow.

I don't think it's due to inadequate absorption.

It's due to reduced absorption. But there is a reason to it. You guys heard of the protein hepcidin?
In anaemia of chronic disease, liver synthesizes hepcidin.
Hepcidin is a key that locks up iron in the bone marrow and prevents it’s release to transferrin.
That’s why, ferritin is increased. (Stores are there, but unavailable!)

Hepcidin block transporters in the intestine.

Good explanation!

Study link! http://medicowesome.blogspot.in/2013/08/difference-between-iron-deficiency.html

So reduced absorption is true?

Maybe the bone marrow too..The stores are adequate in chronic disease of anemia.

But main cause is the hepcidin locking the stores.

I'll look it up.

It's true..But there are other reasons too.

The ferroportin is present in both intestinal cells and macrophages.
Hepcidin performs its different functions via a single biochemical mechanism: hepcidin-ferroportin interaction. Intestinal epithelial cells and reticuloendothelial macrophages use the same transporter, ferroportin, to transport iron in the plasma. Moreover, macrophages and enterocytes exhibit strong upregulated ferroportin expression in the erythropoietic response in an iron-restricted state.
So I guess both the mechanisms are absolutely correct!

Nice.

What is the regulatory factor in the absorption of iron from duodenum?

Is it the transferrin levels? Their level of binding?

It's the Ferroportin.

Oh yes..The channel that transfers iron from epithelial cells into the blood, right?

Ferroportin is present in the entrocytes (cells lining the duodenum)

The level of ferritin that indicates adequate stores?
It's 15mg/dl
Below that level, it is diagnostic of falling iron stores.

I just read a research paper on it.. The hepcidin stuff can be used therapeutically, theoretically.
Interesting stuff.
Hepcidin agonists could be used to prevent or improve the accumulation of iron in both transfused and non-transfused β-thalassemic patients and even in anemia with iron storage. Hepcidin antagonists could be used in patients with diseases that cause hepcidin excess and occur with a framework of IDA or systemic IDA.

Monday, February 9, 2015

Osgood Schlatter disease mnemonic

Mini mnemonic for the day!

OsGood SchaTTer: Oh God. Traction shattered my Tibial Tuberosity.

-IkaN

Study group discussion: Why NSAIDs are avoided in MI, why aspirin is an exception

Why NSAIDs are not given in acute Myocardial Infarction?

I think it's because they're not strong enough and don't act fast enough. The pain relief lowers the stress on the heart.

NSAIDs hamper the process of scar formation after MI, there is chance of  wall rupture.

Steroids too.

Yes.

Isn't aspirin an NSAID? We give that in MI.

Yes, aspirin should be an NSAID. It's not a steroid, and it's anti-inflammatory.  So I don't see any reason why it wouldn't be one.
Edit, I just looked it up on the internet, and it's listed as one of the most common NSAIDs (along with ibuprofen and naproxen).

You give aspirin in antiagregation range. In order to help  dissolve the cloth and prevent new ones.

Well, I asked in reference to the comment on why NSAIDs should not be given in MI. But I read and found out that Aspirin is permitted as an exception.
None other NSAID should be given.
Aspirin is essential in the management of patients with suspected STEMI and is effective across the entire spectrum of acute coronary syndromes. Rapid inhibition of cyclooxygenase-1 in platelets followed by a reduction of thromboxane A2 levels is achieved by buccal absorption of a chewed 160–325-mg tablet in the Emergency Department. This measure should be followed by daily oral administration of aspirin in a dose of 75–162 mg.
Glucocorticoids and nonsteroidal anti-inflammatory agents, with the exception of aspirin, should be avoided in patients with STEMI. They can impair infarct healing and increase the risk of myocardial rupture, and their use may result in a larger infarct scar. In addition, they can increase coronary vascular resistance, thereby potentially reducing flow to ischemic myocardium.
Source: Harrison.

I think aspirin has a different mechanism to other NSAIDs. Aspirin, can worsen a bleed, for example, but is unlikely to be the direct cause of gi bleeding. I'm assuming it works differently with regards to myocardial repair too.

Non-selective NSAIDs enter the channels in both (cox1 and 2) enzymes and, except for aspirin, block them by binding with hydrogen bonds to an arginine halfway down. This reversibly inhibits the enzymes by preventing the access of arachidonic acid. Aspirin is unique in that it acetylates the enzymes (at serine 530) and is therefore irreversible.

I was taught that aspirin is the only NSAID you give in myocardial Infarction.
You have to give it as soon as possible because the latter you give, the benefit decreases.
That is why the first step in management of a patient with MI is aspirin (Not O2, not nitroglycerin, not beta blockers, not morphine) because aspirin has a time dependent mortality benefit.

Aspirin and clopidogrel!

Study group discussion: Management of enuresis

What's the guidance for action in case of enuresis of the child?

You test for urinary tract infections and look for stressors. First try non pharmacological methods like alarms, avoiding water intake at night etc. Then you use drugs.

If there's no infection and the non pharmacological methods don't work, what's the treatement?

Desmopressin then Imipramine.

Study link!
Uses of tricyclic antidepressants mnemonic  http://medicowesome.blogspot.com/2015/02/uses-of-tricyclic-antidepressants.html

Study group discussion: Why adrenaline is NOT given by the intravenous route?

Why is adrenaline / epinephrine not given intravenously in anaphylactic shock? Why intramuscular injection?

Study group discussion: Calorie test and true coma

How will you find out whether the prisoner is faking a coma or not?

Cold caloric oculovestibular reflex - A highly sensitive and specific test.

That's one of the test I had read used to pronounce the person brain dead. You push cold water in the person's ear, it stimulates a reflex. Rapid movement towards opposite side is normal.

Mnemonic is COWS.
Cold: Opposite side
Warm: Same side

Sunday, February 8, 2015

Study group discussion: Mechanism of action of Digoxin

Oubain and digoxin got a connection. Both are cardiac glycosides.

Well, last I studied Digoxin used to block the NaKAtpase and thus stopping the secondary active transport of Ca leading to increased cardiac contractility. Look what I found. According to a new research its not the actual mechanism. Digoxin here, goes into the cardiac myocyte and act on Rynodine receptors instead. http://www.ncbi.nlm.nih.gov/m/pubmed/21642827/

Can somebody comment on the reliability of such articles?

Well, I had read about its action on rynodine recepters in my text book...What I know is that it acts on rynodine recepters (there is a specific name RY something which I don't remember), it increases Ca inside the sarcoplasmic reticulum of myocytes with each contraction... Meaning it sends some Ca which comes in from outside into the SR... So that the subsequent contraction is more forceful as the Ca now available from the SR is more than the prev contraction...

It's RyR2!

RyR2, yes!

Study group discussion: Why does ingestion of salt cause high blood pressure?

Why does salt increase blood pressure? I Googled it but there is no biochemical info.

Salt in the blood takes water out from cells into veins and here we got blood pressure.

Excessive NaCl ingestion or NaCl retention by the kidneys and the consequent tendency toward plasma volume expansion lead to hypertension. Nevertheless, the precise mechanisms linking salt to high blood pressure are unresolved. The discovery of endogenous ouabain, an adrenocortical hormone, provided an important clue. Ouabain, a selective Na+ pump inhibitor, has cardiotonic and vasotonic effects. Plasma endogenous ouabain levels are significantly elevated in approximately 40% of patients with essential hypertension and in animals with several forms of salt-dependent hypertension.
Source: http://www.ncbi.nlm.nih.gov/pubmed/16467498

I was reading about it and people on the internet believe that salt causing hypertension is a myth :/

It was also given on wikipedia, I donno how you missed it..

When too much salt is ingested, it is dissolved in the blood as two separate ions - Na+ and Cl-. The water potential in blood will decrease due to the increase solutes, and blood osmotic pressure will increase. While the kidney reacts to excrete excess sodium and chloride in the body, water retention causes blood pressure to increase inside blood vessel walls.

Study group discussion: Cardiac shunts and snowman sign

Congenital heart diseases

-> Right to left shunts:
Truncus arteriosus
Transposition of the heart arteries
Tricuspid atresia
Tetralogy of falloy
Total anomalous pulmonary venous return TAPVR

-> Left to right shunts:
VSD
ASD
PDA
Eisenmenger

The right to left shunts all start with T. It's a good memory aid!

Snowman sign X ray feature of?

Snow man is a type of the cardiac silhoutte, right?

Another name figure of 8 sign.

Study group discussion: Eisenmenger's syndrome

I think Eisenmenger (shunt reversal) is actually R to  L shunt.
It is observed in case of L to R shunt, with time right ventricle get hypertrophied and can overcome left ventricle.

It's due to pulmonary hypertension. Reversal shunt that is. Right ventricular hypertrophy is just a consequence of PH.

And why does Pulmonary hypertension arise in that case?

Too much blood going to the lungs causes edema and hypertrophy of the pulmonary vasculature.

Increased flow of blood through pulmonary vasculature in cases of left to right shunt.
Normally, the pulmonary system is a low pressure system 25 / 8 mm of hg in compared to the normal 120/80 mm hg of systemic vessels
The pressure increases in hope to reduce blood flow through the lungs..through the shunt.
But instead of being a protective response.. It ends up making the whole situation much more severe.

Plethoric lungs, basically.

Or it Is it due to hypoxia which causes pulmonary vasocontriction which leads to pulmonary hypertension?

Yes, that's a contributory factor too

Why too much blood going to lungs.. Is it due to compensatory effort by Increasing HR?

The left ventricle is stronger than the right. So more blood goes to the right ventricle. Hence, more blood to the lungs.

It's the shunt..Left side of heart has a higher pressure compared to the right side of heart..Hence in cases of ASD and VSD.
Due to free communication.. Blood flows from high pressure to low pressure system.
In case of right to left shunts..There is obstruction which doesnt let blood enter the lungs (eg tetralogy of fellot where there is pulmonary trunk stenosis)
So a right to left shunt.

Thanks for explaining it to me, you guys!

Study group discussion: Short PR interval causes

Review question c: What are 3 causes of a short PR interval?

Wolff Parkinson White syndrome is one.

Yeah, but in general? What physiological alterations can cause that?

The re-entrant pathway.

As in... WPW causes it because it works as an accessory AV pathway.

1. Accelerated AV conduction
2. Tachycardia
3. Accessory AV pathway

Other cause is rheumatic fever.
It's one of the minor criteria for diagnosis in the Jones criteria.
Oops.. Rheumatic fever is a cause for increased PR interval.. My bad.

Study group discussion: Wolff-Parkinson-White (WPW) and increased QRS interval

Causes of increased QRS interval?
BBBs (Bundle branch block)
Electrolyte abnormalities
WPW syndrome
Medications like:
Procainamide
Tricyclic antidepressants

Study group experience #6

Here's what we discussed:

Our first group reached 100 awesomites today. So happy! 

Here are a few messages from the group:
A century of awesomeness.
WOOTS PARTY AND LOTS OF MESSAGES HAHHAA.
Proud to be a part.
Proud to be a silent contributer to the 100. Been reading all your messages like a creep this entire time. Congrats!
I think I don't have enough knowledge to answer most questions here, but I do like reading yours!
Yup me too a silent one! But I really love this group. Boosts me to learn more.
Cheers to all 100 <3 

To all the new coming awesomites, since the first group is full, I'll make your group in a week irrespective of the number.

Uses of tricyclic antidepressants mnemonic

Amitryptyline for neuropathic pain.

When you say “Aah” in pain, remember Amitryptyline!

Clomipramine for obsessive compulsive disorder.

Clomi when you feel Compulsion ;)

Imipramine for nocturnal enuresis.

Eemi Eee.. will not let you pee in bed ^__^

Lame but helps :D

Saturday, February 7, 2015

Hematology and chemical pathology mnemonics

An awesomite requested for Pathology hematology bottles mnemonics. I asked him (or her) to send notes and attempted to make lame mnemonics on the same.

Uploading the notes + mnemonics for reference:

THE PURPLE ONE (aka “Lavender”)
These bottles are generally used for haematology tests where whole blood is required for analysis.

ADDITIVE: EDTA (ethylenediaminetetraacetic acid)

COMMON TESTS:
Full blood count (FBC)
Erythrocyte sedimentation rate (ESR)
Blood film for abnormal cells or malaria parasites
Reticulocyte
Red cell folate
Monospot test for EBV
HbA1C for diabetic control
Parathyroid hormone (PTH)*
less commonly used for: ciclosporin/tacrolimus levels, some viral PCR tests, G6PD, ACTH level*, porphyria screen*, plasma metanephrines*, fasting gut hormone screen*

Mnemonic: PurplE
P: Parasite, PTH, PCR, Porphyria
E: EDTA

Friday, February 6, 2015

Study group discussion: Safflower, Butter and Cholesterol.

Out of butter and safflower oil.. Which of it contains cholesterol? And which doesn't, and why?

This has to be tricky.

It wouldn't be fun if it wasnt! :D

Well, defying logic, butter doesn't and safflower does?

Haha. Wrong!

Oh man. I hate vivas.

What's the reason?

Butter does because it comes from animals. Plant products never contain cholesterol, only animal products do.

Correct!

Study group discussion: Weight loss in malignancy

What's the cause of weight loss in malignancy?

Malignancy is cachexia.. Due to increased TNF and IL - 1.

Malignancy: Due to decreased appetite.

The TNF and IL - 1 decrease appetite as well as increase protein catabolism.

Study group discussion: Sweet syndrome

Has anyone out here heard of sweet syndrome?

And I checked it's not related to diabetes. -__-

Acute febrile neutrophilic dermatitis.

It is caused due to?

Acute febrile neutrophilic dermatosis (Sweet syndrome) is a reactive process (a hypersensitivity reaction) that occurs in response to systemic factors, such as hematologic disease, infection, inflammation, vaccination, or drug exposure.

Named after Rober Sweet.

Study group discussion: Necrobiosis lipoidica

What is necrobiosis lipoidica?

Which condition causes it?

Papule on Lowerlimb seen in DM.

What's DM?

Diabetes mellitus.

It's not simply a papule. It's necrosis of the skin.

Study group discussion: Cushing's syndrome

What is Cushing Reflex?

It's related to cushing syndrome or disease?

Nah. It consist of signs of Raised I.C.T: Hypertension, bradycardia, dilatation of pupil and pyramidal tract sign.

It is caused due to raised ICT?

There is more entity..Cushing's ulcer and curling ulcer. One of them is caused due to raised ICT I think. The other being a stress ulcer. Both in the stomach.

Curling ulcer is due to burns.

They both are confusing terms.

Cushing ulcer is caused when there's brain injury. With ICT as mention above

Agree.

Does anyone know the mechanism?

Cushing ulcer and Curling ulcer are peptic ulcers caused by CNS injury and burns respectively.
One possible explanation for the development of Cushing ulcers is the stimulation of vagal nuclei due to the increased intracranial pressure which leads to increased secretion of gastric acid.
Curling ulcers may be explained by a reduced plasma volume, which leads to sloughing of the gastric mucosa or secretion of burn toxins (necrotic and carbonaceous materials released from burned cells) by the stomach.

There is the cushing sign too

Must you know the difference between Cushing's disease and Cushing syndrome then?

Cushing disease is the disease caused due to a tumor of the pituitary..With increased secretion of ACTH.
The other is the syndrome caused due to excess cortisol in the blood.. Exogenous commonly. I am not sure whether adrenal tumors are also included in Cushing syndrome or not.

Cushing sign occurs as a result of Cushing reflex.

Here are study links on Cushing's!
Cushing's ulcer mnemonic: http://medicowesome.blogspot.ae/2014/03/ulcers-of-stomach-mnemonic.html

Cushing syndrome notes: http://medicowesome.blogspot.ae/2014/12/how-to-make-concise-medical-notes.html (View image)

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!


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

Thursday, February 5, 2015

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!

Study group discussion: Cardiac mortality in diabetes mellitus reduction due to aspirin

If a patient has diabetes..Which drug would you prescribe to reduce the chances of mortality due to heart diseases?

Thiazolidineones?
Metformin? Or pioglitazone?
Nope nope.

It's aspirin.

What? Aspirin is not an anti diabetic drug, is it? You prescribe aspirin in general to lower mortality. What's so special about diabetes?

I am yet to find out why.. I would love it if someone out here knows why.

About the use of aspirin in diabetes.... I read a paragraph online... Here's what it said:
It is found that there is excess release of thromboxane in type 2 diabetes patients... Hence the use of aspirin (TXA inhibitor)

Thanks!

http://m.care.diabetesjournals.org/content/27/suppl_1/s72.full

It never ceases to surprise you. Medicine.

Woah.

Study group discussion: Immortal cells

What do you know about immortal cells?

Cancer cells are immortal?

Yeah, like HeLa cells.

I had written a blog on it long back. Let me find it!

The blog I wrote isn't really on HeLa cells. But people who reblogged it on tumblr added this to it -
Tumblr reblogs:
I have read some thing like this before in the nonfiction book called the immortal life of Henrietta lacks. They took her cancer cells and studied them finding that the cancer cells were still living even after she past and outside of her body. I think, if I am remember correctly the cells are called HeLa. It's a great read.
Tumblr reblogs:
You’re right. HeLa cells are still used in scientific research. It is the oldest and most commonly used human cell line. The line was derived from cervical cancer cells taken on February 8, 1951, from Henrietta Lacks, a patient who eventually died of her cancer on October 4, 1951.

It doesn't matter if it's not about HeLa cells specifically :)
I just want to understand better how it works.

Oh.. Here's the blog link to immortal cells then http://immense-immunology-insight.blogspot.ae/2014/08/7-reasons-why-cancer-cells-are-immortal.html

The HeLa cell line has a lot of ethical issues.. Because the person from whom the cells were taken from (without consent) didn't get any medical attention or superior care and the companies benefited a lot from it.

Thanks a lot :) and I didn't know any of the history.. It's really interesting

Yes, it's actually pretty wonderful that the cells are still alive. There were a lot of sci fi notes added to the tumblr post, I'll share them here as well.

Tumblr reblogs:
So if somehow we were to find a way to harness the cancer cell’s power, we could possibly live forever. We’d just have to find a way turn turn all the cells in the body into cancer cells, and then take away their ability to divide via mitosis. It sounds like sci-fi, but highly plausible in theory.
Tumblr reblogs:
Well there’s more to it than that, but in theory yes… You also have to consider that tumor cells don’t actually function other than continuously dividing. And often times, tumor cells build up a lot of free radical waste that can damage surrounding tissue.
Tumblr reblogs:
You have a point, but that isn’t entirely true. While most cancer cells are nonfunctional, many actually do function similar to a normal cell (though sub par). The main reason why cancer kills people is because the rapid growth of tumors causes pinched tissues and ruptures/hemorrhages. If we could figure out how to prevent mitosis and make all cancer cells functional, we could possibly become immortal.
Tumblr reblogs:
May I just say, I love sci-fi theories. Immortality through cancer cells.. Now that’s some brilliant imagination, right there!
Yes, some cancer cells can function. But it’s too much for the body to handle. If we could control metastasis, we could send some liver cells and gut cells at every waste generating site and have our free radicals scavenged!
Tumblr reblogs:
It's semi funny however those facts are not entirely true because the cancer cells die, usually you get necrosis in the tumors mostly bc the growth of the tumor is quicker than its ability to grow vessels, or vessels that actually can hold it together. "Cancer cells dont need anything" is another misconception. they are like any other cells but also not every cancer is the same either. Saying like the thing about being mostly anaerobic which is true for some and sometimes they are, however not always, thats why we do such things embolization therapy in tumors. And it can work. The oncogenesis and basically the whole process is way more complicated than it seems.
Tumblr reblogs:
They meant growth factors when they said they don’t need anything. Hell yeah, normal cell requirements without regulatory factors. Necrosis affects only the central portion of the tumor, doesn’t account for the fact that the cells are dividing on the edge of the lesion, making the tumor as a whole, immortal. Embolization cuts off the entire blood supply, artificially. They were talking about how they are immortal without considering interventions like chemotherapy, radiotherapy, resection and many other therapies that we can do, clinically. Biologically, they are immortal. I agree that not all cancers are the same, but the facts given out here are true.

I had only heard about immortal cells as a possible cancer therapy by using telomerase inhibitors or something like that.

As a therapy to treat cancer? Woah.

Let me look for it.

Links online say it's too risky to come true.

This article says telomerase inhibitors would treat cancer.

Or this one... www.ncbi.nlm.nih.gov/pmc/articles/PMC2937180

The article title though <3

Haha I know :)

Immortal army! *_*

My favorite cells come to the rescue.. T cells!

Interesting read. Thanks for the article!

There's another thing I read a while back that made me realise why any form of immortality is or will be problematic..
Remember the adenosine deaminase deficiency treated with gene therapy?
Trials have shown that the kids cured with gene therapy had a predisposition to cancer because of the virus (sarcoma virus or retrovirus, don't remember which) put in to carry the gene that treats the condition.
So it's like you go in to treat this and you come out with another disease.
It's why the gene therapy isn't out of trials yet. They're re-considering the risks vs benefits.

Oh... Well that's unfortunate... It seems like a cool idea. Genetics is only being developed anyway. There's a lot we don't know.

Awesome rock solid last discussion last night guys! Loving this group.
And concept of immortality marvellous!

Wednesday, February 4, 2015

Study group discussion: ECG in MI, potassium abnormalities, infectious diseases, pericarditis

Which is the most definitive sign on ECG that a transmural infarct has occured? 
For transmural is it ST SEgment elevation?
Nope.
Q wave is the most definitive sign on ECG that a transmural infarct has occured 



One quick question.. Whenever you see diffuse ST segment elevation? Diagnosis?
Pericarditis has characteristic diffuse ST segment elevations in all the leads.



What is ecg sign for hypokalemia and hyperkalemia?

Regarding hyperkalemia and hypokalemia
For hyperkalemia remember peaked T waves
For hypokalemia remember U waves

For hyperkalemia it occurs in characteritic sequence
1) peaked T waves
2) loss of P waves
3) widening of Qrs complexes(sine wave)


Why T wave being a repolarisation wave is also a positive wave?

Its not about depolarisation or repolarisation .
Its the direction of the effective vector component corresponding to the field of the leads that determines whether it will be a positive or a negative wave

Oh yes! Right.

Wave of repolarisation not only being opposite to depolarisation and is also negative in character so this gives t wave positive deflection


Infectious disease causing ecg changes?

Malaria causes st elevation, right?


Lyme disease causes? 
3rd degree AV Block! 

Study group discussion: Hydrocephalus ex vacuo, normal pressure hydrocephalus and cortical atrophy

What's cerebral cortical atrophy?

Shrinking of the brain tissues, ie loss of neurones, can be focal (small part) or generalized (affects all of the brain). Number of causes such as Alzheimer's or stroke.

There is a disease called hydrocephalus ex vacuo, in which the baby has a smaller brain. But the CSF production is normal. But mostly the doctors end up diagnosing it as hydrocephalus.

Hydrocephalus ex-vacuo occurs when there is damage to the brain caused by stroke or injury, and there may be an actual shrinkage of brain substance. Although there is more CSF than usual, the CSF pressure itself is normal in hydrocephalus ex-vacuo.

We had a case of this in my college, the girl was a three year old..With the grasp reflex still present and no stable head control.

Is it the same as normal pressure hydrocephalus?
Nope. Cause medication and surgery for normal pressure hydrocephalus won't work on this.

Revision question: Tell me the triad of normal pressure hydrocephalus!

Dementia
Gait disturbance
Urinary incontinence

In case you guys don't know, triad for NPH mnemonic: Wibbly wobbly, wacky and wet. For gait disturbances, dementia and urinary incontinence respectively.

Hydrocephalus ex vacuo and cortical atrophy are different entities?

Can't exactly say. May have a cause effect relation.

One causes the other?

Yep.

Got it.

Study group discussion: Type 3 diabetes and type 1.5 diabetes

Guys, I heard of another cool thing!
Type 3 diabetes!

Which is?

Alzheimers disease, apparently.

How?

Something related to IGF.. AD represents a form of diabetes mellitus that selectively afflicts the brain.

Woah.

Wow.

There is also diabetes type 1.5

What is that?

Latent Autoimmune Diabetes in Adults (LADA)

Interesting.

Can LADA also have a polyneuropathy a symptom like DM? As the link says it a Diabetes cause of Autoimmune reaction?

I would imagine every type of diabetes has the potential to cause secondary effects such as neuropathy.

I'd never heard of Alzheimers as diabetes though.

As an aside other forms of diabetes I've heard of are gestational diabetes and diabetes secondary to pharmaceuticals.

What's MODY and how is it different from LADA? 

LADA is autoimmune whereas MODY seems to be related to chromosomal mutations.

Study group discussion: Difference between rouleaux formation and agglutination of RBC's

I was asked in pathology viva, what is the difference between agglutination and rouleaux formation.

I think rouleax is the RBC's sticking to form a tube or a roll and agglutination with an immunological reaction?
Have to check.

Agglutination clumping of RBC due to Antigen - Antibody reaction,
whereas in rouleaux clumping occurs due to decrease negative charge during rouleaux formation stage in ESR.

Study group discussion: Human Papilloma Virus

*An image of papilloma virus warts was posted on the group as guess the diagnosis, I am unable to post it on the website due to copyright issues but here is the discussion we had*

Is that Hyperkeratosis? Abnormal thickening of stratum corneum?

Nope.

VPH?

What's VPH?

Papilloma virus. Sorry, I wrote in Spanish.

Espanol! Virus del papiloma humano :D

Those are large warts?!

After a severe Human Pappiloma Virus (HPV) infection, a 35-year-old man, was dubbed the "tree man" because of the gnarled warts all over his body. He first noticed the warts on his body after cutting his knee as a teenager. Over time, he was sacked from his job, deserted by his wife and shunned by neighbours as the horn-like extensions covered much of his body and stopped him working. He has two children. After his case received widespread publicity, donations from the public and government help allowed him to get treatment, six kilos of warts were surgically removed from his body.

I remember having seen this episode on discovery channel long time ago! Didn't remember the disease though.

Yeah, it was broadcasted once.

Me too. They earn their living by showing their disease to the locals as a display of how they look like trees. Very sad.

There's no other treatment besides surgery, right?

Sadly, no.

They cause is immunodeficency. The body is unable to fight the HPV infection.

There was a similar case shown on the TV series, Greys anatomy too.

Study group discussion: Splenic vein thrombosis and hepatic vein thrombosis

One quick review question!
What is the most likely cause of varices in the fundus of the stomach?

Umm varices in the fundus? Something to do with the splenic artery?

Artery?
Sorry vein! Or high pressure in the spleen? I don't know.

Yeah, splenic vein thrombosis!

Oh yes, which is the most common cause of splenic vein thrombosis?

Umm.. Something to do with compression?
Pregnancy?
Nope.

Hint: Something to do with alcohol
Short of knowledge here.

For splenic vein thrombosis, most common cause is chronic pancreatitis.

Oh do you know the mechanism for splenic vein thrombosis?

I don't know the mechanism of splenic vein thrombosis, I'll find out and let you know.

I think cytokines are probably producing hypercoagulable state in splenic vein.

Splenic vein thrombosis in acute or chronic pancreatitis results from perivenous inflammation caused by the anatomic location of the splenic vein along the entire posterior aspect of the pancreatic tail, where it lies in direct contact with the peripancreatic inflammatory tissue. The exact mechanism of thrombosis is likely multifactorial, including both intrinsic endothelial damage from inflammatory or neoplastic processes and extrinsic damage secondary to venous compression from fibrosis, adjacent pseudocysts, or edema. Obstruction of the splenic vein may also be caused by enlarged retroperitoneal lymph nodes or by pancreatic or perisplenic nodes that are located near the splenic artery, superior to the splenic vein. These nodes lie adjacent to the pancreas and the splenic vein and compress the splenic vein when involved in an inflammatory or neoplastic process.

Awesome.

Thanks for the explanation!

And speaking of thrombosis, which is the most common cause of hepatic vein thrombosis?

For hepatic vein thrombosis, most common cause is PNH. It's also known as Budd Chiari syndrome.

PNH?

Paroxysmal nocturnal hemoglobinuria.

Study link! http://medicowesome.blogspot.ae/2015/01/paroxysmal-nocturnal-hemoglobinuria.html

I think both are different entity.

They are! Sorry didn't make myself clear.
Paroxysmal nocturnal hemoglobinuria causes hepatic vein thrombosis.
Hepatic vein thrombosis causing liver dysfunction is known as Budd Chiari syndrome.

Study group discussion: Amantadine

Talking of antivirals... Amantadine is an antiviral used for Parkinson's disease! Anyone knowing it's mechanism in both these conditions?

Influenza is through M2 channel. Donno about Parkinsons.. Anticholinergic?

Amantadine increses the secretion of dopamine. Don't know the channels.

Mechanism of action of Amantadine: Prevents viral uncoating by binding to protein M2 (It's a protein which is a proton channel) that allows acidification of the viral core to activate viral RNA transcriptase.

Mnemonic: A man, to dine, takes off his coat!

Also, mutated M2 protein makes the virus resistant to the drug.

Woah! Thanks!

Amantadine MOA as a anti parkinsonian drug:
Increases release of DA
Increases synthesis of DA
Decreases reuptake of DA
Direct action NMDA receptors
*DA: Dopamine

Study group discussion: Why food doesn't taste good on high altitude, high pressure aeroplanes

I read an interesting article today, not very study related though.

It's why food tastes yucky in airplanes.

Wow! So they found out finally why food tastes bad in air planes!

Why is it yucky??

Change in pressure and altitude numbs 1/3 of our taste buds.

Haha nice!

And I blamed airlines!

Damn!!

Lack of humidity, noise and mass food production are contributory too but that's the main reason.

Interestingly, only salty and sweet sensation is affected. Bitter and spicy remain unaffected.

I wasted so many pleasurable gustatory senses by eating chocolates on the plane! I'll eat spicy next time!

Hahaha science rocks! Unfolding the mysteries of the world.

Yeah spicy in better than bitter!

So much better!

Study group discussion: Drugs that cause urinary calculi

Which diuretic agent is asociated with development of kidney stones?

Loop diuretics.
Potassium sparing diuretics.

So... Almost all of them?
Nope. Osmotic diuretics don't!

And thiazides are used for treating kidney stones!

Loop diuretics, carbonic anhydrase inhibitors and triamterene (Not all potassium sparing diuretics) are the ones that cause calculi.
Mechanism: Loops and CAI cause metabolic abnormalities.

Why only Triamterene?
The exact mechanism by which Triamterene promotes urinary calculus formation is unclear, although it is hypothesized that precipitation of triamterene and its metabolites provides a scaffold for nucleation and subsequent calculus growth.

Which carbonic anhydrase inhibitor cause renal stones? And what's the mechanism?

Prolonged use of carbonic anhydrase inhibitors may lead to a hyperchloremic metabolic acidosis, in which urinary pH is increased and urinary citrate is decreased.
Acidification of urine prevents calcium and phosphate stones but causes uric acid and cysteine stones. Link: http://medicowesome.blogspot.in/2012/12/acidification-of-urine.html

Speaking of stones, which antiretroviral drug causes nephrolithiasis?

Acyclovir?

I didn't know this. Just Googled and found that they cause crystalluria and obstructive nephropathy as well.

Indinavir was the drug I was asked about in a test.

A summary of drugs that cause stones (Source: ncbi)

Urinary calculi can be induced by a number of medications used to treat a variety of conditions.
Loop diuretics, carbonic anhydrase inhibitors, and abused laxatives can cause metabolic abnormalities that facilitate the formation of stones. Correction of the metabolic abnormality can eliminate or greatly attenuate stone activity

Magnesium trisilicate; ciprofloxacin; sulfa medications; triamterene; ephedrine, alone or in combination with guaifenesin; and indinavir may induce calculi via urinary supersaturation. Eliminating such calculi usually involves discontinuation of the medication or initiation of alternate therapy.

Thanks!

Study group experience #4

Discussions so far -
How to do percussion (A clinically oriented topic) 
Respiratory physiology (Interesting read for first years) 

When I first thought of the group, negative thoughts poured in and everyone thought it was a bad idea: What if I get too many spam messages? All you'll receive is advertisements! You'll lose your Whatsapp privacy! It's too risky man! Why would you do something so stupid? Give your number to the internet?

But one person encouraged me: Eh? So what? Business men take risks all the time. Keep a verification so the spammers can't get it. Block people, duh! Why is that feature available on Whatsapp? You can always throw away your number or change it.
For everyone who benefits from the group discussions, you guys should totally thank that positive soul for this!

What I learnt by making the study group:
Don't be so negative, don't fear the bad stuff so much.
Be courageous. Take calculated risks.
Encourage people, no matter how crazy they sound.
It's takes just one person to make a life changing decision, make sure it's you.

*OMG I STILL CAN'T BELIEVE IT WORKED OUT SO WELL AND I'M TALKING TO YOU GUYS EVERYDAY*

-IkaN

Tuesday, February 3, 2015

Equilibrium potential value of an ion and how to apply it to action potential ?

The equilibrium potential value of an ion or the Em value.
I will try making some sense out of this confusing term.

1. Ions across a cell membrane have two forces acting on them, the concentration gradient and the electrical gradient. Since, Na,K and Cl are the most abundant of ions, it is only needed to know the Em of these three ions.

2. The Em is the value of the membrane potential at which both the concentration gradient force and the electrical gradient force are equal and opposite. This means that these two forces will cancel each other and there will be no net flow of ions across the membrane.

3. Also, remember whenever given the chance ( permeability ) the ion will try to reach a stability, that is it will try to achieve a membrane potential equal to its Equilibrium potential.

There is an equation called the Nernst equation to measure the Em value. When you solve this equation the values of Em are

Na- (+61Mv)
K   ( -94.1Mv)
Cl  (-70Mv)

Lets apply these terms, to the action potential

Study group discussion: ECG sign of left ventricular aneurysm

On ECG after an MI infarction..What is the sign for left ventricular aneurysm?

It's persistent ST segment elevation. After MI, the ST segment does rise, but it falls gradually too, reaching a normal. But if its elevated then its aneurysm.

In any specific leads?

The same leads where infarction shows up.

2, 3 and AVF leads.

So basically the ST segment doesnot fall back to normal right?

Yup.

Great didn't know that concept.

Study group discussion: Right ventricular infarction

Since it's MI..Review question.. Name a disease associated with right ventricular infarction?

Atherosclerosis?

I meant name a cause for right ventricular infarction, other than atherosclerosis.

It's pulmonary embolism.

The pulmonary embolus puts the right side of heart in strain and it dilates. This dilation obstructs the right coronary artery. This was my viva question on an ECG of right ventricular infarct.

So does not it lead to hypertrophy of the right ventricle?
In an acute setting, no.
If the pulmonary thromboembolism  is chronic it will cause pulmonary hypertension. Then it causes right ventricular failure.

So the acute pulmonary embolus should be the answer.

Ohh that makes some sense! Good one!