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 -

Histrionic personality disorder, Munchausen syndrome and MSBP  

Dissociative identity disorder, Post-Traumatic Stress Disorder and Shutter Island  

Migraine, aura and floaters  

Schizophrenia and Schizotypal disorder 

Malignant hypertension discussion 

Renal tubular acidosis types mnemonic 

How to do percussion (A clinically oriented topic) 

Cause of decreased glucose levels in CSF in bacterial meningitis  

Respiratory physiology (Interesting read for first years) 

Physiology books  

Transpulmonary pressure 

Case control and cohort study mnemonic  

Legionella confusion   

Compliance of the lungs  

Urinalysis  

Lateral spinothalamic tract mnemonic  

Trial of scar  

Management of ARDS 

Diagnostic tests for pulmonary embolism  

Amyloid  

Bone tumors 

Myocardial infarction markers  

Right ventricular infarction 

ECG sign of left ventricular aneurysm 

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

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!

Study group discussion: Myocardial infarction markers

Which is the reinfarction cardiac marker?

It's CK MB. The levels fall in 3-4 days. So if you get a reinfarction and see your troponin you can't be sure if it's from last time.

CK MB falls in 36-48 hrs.

Why isn't it myoglobin? Myoglobin rises and falls the fastest.

Because myoglobin is not a specific cardiac marker.

No but in these cases, it is the most preferred. Cause it returns to normal within 24 hours.

Dunno.

I think the time after which re-infarction occurs also matters.

Do let us know.

These things are confusing. Good thing is we are trying to sort them out.

Yes, it is.

We had a confusion between myoglobin and CK MB in the diagnosis of re-infarction.

The answer is CK MB simply because it is cardiac specific and falls within 2 days.

The only use for myoglobin is ruling out a Myocardial Infarction, early. (Cause it's the first to rise and is very sensitive!)

If the levels are not up, it's not a MI.
If myoglobin levels are up - it could be a skeletal muscle injury or a MI, you don't know until you look at the other markers.

Even though myoglobin levels fall early, it is not used for the diagnosis of reinfarction because it's not specific and if the levels are up after an infarction, it could mean something else as well.

Harrison says both CK MB and myoglobin can be used for reinfarction. I would hate the question maker for asking us to choose between the two & go with CK MB because it's specific.

Woah... Awesome discussion... Thank you everyone for the cocepts... I so love this group.

Study group discussion: Amyloid

Does anyone have awesome things for amylodosis pathology?

Another concept you must understand is that the protein deposits in tissues depending upon where it was derived from.

For example, amyloid from immunoglobulins deposit in tissues of mesodermal origin like kidneys, heart, muscle, tongue.

When it's due to chronic inflammatory disease, it involves parenchymal organs like liver adrenals and pancreas.

Good concept.

Review question! Which amyloid protein is associated with Alzheimers disease?

Beta amyloid

Yes!

And why are patients with downs syndrome more susceptible to early Alzheimers?

Extra chromosome 21 which means extra copy of the presilline gene, I think.

Absolutely right!

Great.

Never knew that!

Oh oh one more!

Which condition is associated with amyloid deposition in the thyroid gland?

Are we talking about the medullary thyroid carcinoma?

Yep. The amyloid deposits are derived from calcitonin in that condition!

Which is the one in patients on dialysis?

Beta micro globulin?
B2 - microglobulin is seen in dialysis associated amyloid.
Derived from the MHC class 1 protein.

Yes. It's because the beta micro globulin is not filtered from the dialysis membrane.

Excellent stuff.