Thursday, February 5, 2015

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!

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.

Study group discussion: Bone tumors

Osteoclastoma is a giant cell tumor, right?

And these giant cells can be differentiated from other giant cells on the basis of the number of nucleoli present?

 Yo

These giant cells will have about a 100 nucleoli

Osteogenic sarcoma is osteosarcoma. it is a malignant tumor

 names are confusing
 Osteosarcoma, osteoblastoma, osteoclastoma
 The other two are benign?

GCT(osteoclastoma) is a special variant bone tumor
Does not come under either benign or malignant
 Based on number of giant celss an osteoclastoma is loosely classified from typical to aggressive to malignant
 More giant cells and less stroma its benign, less giant cells more stroma its aggressive.

Osteoblastoma is a rare primary neoplasm of bone, categorized as a benign bone tumor that is closely related to osteoid osteoma. It differs from osteoid osteoma in its ability to grow larger than 2.0 cm in diameter and its aggressive behavior in bone.

Monday, February 2, 2015

Turner's syndrome mnemonic

Turner's syndrome mnemonic

Cystic hygroma, webbed neck: You can't turn your neck because of it.

Aortic coarction: Aorta takes a sharp turn.

Some toxicology mnemonics

Acetaminophen toxicity is treated with N acetyl cyteine.
Mnemonic: ACETaminophen ACETyl cysteine!

Ethylene glycol is metabolized to oxalic acid. Ethylene glycol is found in anti freeze.
Mnemonic: Freeze your EGO.
Anti freeze
Ethylene Glycol
Oxalic acid

Methanol is metabolized to formic acid by alcohol dehydrogenase which causes visual disturbances. It is treated with fomepizole.
Mnemonic: There's more to me (FoMEpizol) than what meets (Methanol) the eye (Blindness).

Study group discussion: Diagnostic tests for pulmonary embolism

What is the commonest sign on ecg for PE?

Nonspecific ST changes?
Nope.

SQ3 T3 something like that?
Nope.

Most common sign is sinus tachycardia. Most specific is S1q3t3 pattern..Positive only in 20-30% cases.

Ohhh!! Nice question.

Ooh.. We tend to forget common ones when looking out for rare signs!

What is the screening test for PE?

Screening test is d-dimer. If d-dimer is negative you virtually exclude the diagnosis of PE.

Which is the most specific diagnostic test for pulmonary embolism?

Pulmonary angiography.

Depends if the person is low risk or high risk! CT angiography is done though.

Which is the most preferred test for PE?

Spiral CT is preferred next to know location, size and blah blah.

What about VQ scan?

That's done if the patient is allergic to contrast.
Or has kidney failure.
Or CT isn't available.
Or the patient is pregnant.

In our hospital setting angiography would key since most patients can't afford CT.

Oh. But its invasive..and can be very harmful. It's only preferred when you are planning for thrombectomy..Or as a last resort to diagnose PE if all the other test are negative but d-dimer is positive.

Well money for a CT can feed a peasants family for a year.

True.

Venous doppler is preferred when CT or V/Q are inconclusive.

Whats d-dimer?
The clot thingy. It interlocks fibrin strands.

It is released from the thrombus.

Fibrin is non specific for clots
Because it is elevated in some other conditions as well. So d dimer to the rescue!
*Fibrin degradation products are.

Study group discussion: Management of ARDS

Anyone over here who knows the management of ARDS?

PEEP

Positive end expiratory pressure and 100% oxygen.

It's like during expiration your alveoli collapse, especially in ARDS since their surfactant is gone, so to prevent that collapse you give a bout of positive pressure at the end of expiration.
I don't know how they generate it but this is the mechanism!

Aah.

PEEP is continuous flow generated at certain fixed pressure that stops the alveoli from collapsing during the expiration. Pressure usually kept around 5

So the pressure is kept continuous during the whole time?

Yeah it's continuous during the both inspiration and expiration!

Umm then why is it called "End expiratory"?

That's a very good question actually. Don't know exactly why it's named that way!

Ever heard of low tidal volume ventilation? Aka lung protective ventilation? Aka baby lung concept?
It's used in managing ARDS. Since many alveoli are fluid filled and the patient effectively will have lesser tidal volume than normal. If we give the normal tidal volume the patent alveoli will burst due to barotrauma!
Inspite of normal tidal volume - 8-12ml/kg, we give 4-6ml/kg body weight for ARDS.

Also, you treat the underlying cause of ARDS.

You even have to restrict fluid overload. That's the other most important point!

Yeah read that too, diuretics are beneficial to some extent. Steroids are of no use.

Yup.

Also NO (Nitrogen oxide) is of no use.

Yeah for ARDS. During the various trails for the treatment of ARDS they observed that increasing the tidal volume lead to worsening most probably due to inflammation due to repeated opening and closing of alveoli with each inspiration and expiration ultimately affecting the structure of alveoli and their ability to perform their job. Low tidal volume along with PEEP significantly reduced the mortality in the patients with ARDS. So that the standard treatment at present.

I read there is other device called high RR..it provides respiratory rate of 15 to 20 cycles per SECOND.

It has a very low tidal volume but..Almost 1-2 ml / kg

Study group discussion: Trial of scar

Can anyone tell me about the "Trial of scar" after C section procedures?
I have heard of trial of labour, not sure if its the same thing!

My searches lead me to trial of labour as well ..I guess they are.

It's especially indicated in cases of borderline cephalopelvic disproportion.

The obstetrician let's the lady go in to labour in a controlled environment. If the labour becomes to stressful and is prolonged unduly, the doctor immediately performs a C section

It's more like given the patient an opportunity to experience normal vaginal delivery.

Same thing i suppose can be applied to scar from previous C section.

You see the chances of rupture of the lower segment scar is highest during labour, so the patient is monitored especially for signs of impending scar rupture

Most common is pain and tenderness over the scar area.

A off topic thing due to c/s delivery a tv series named "the knick", a medicine based serie in the beginning of the 20th century in usa, i recommend it, the changes in surgery, hospitalization, treatments are baby steps, surgeons invent the tools they use, amazing!

Study group discussion: Lateral spinothalamic tract mnemonic

PAin and TEmperature sensation carried by LAteral spinothalamic tract. Mnemonic is "PaTeLa" (which is present knee).

Study group discussion: Urinalysis

Significance of difference findings in urine analysis-
1) WBC in urine - Pyelonephritis
2) RBC - Glomerulonephritis
3) Hyaline cast - No significance
4) Broad waxy cast - CRF
5) Dirty brown/granular cast - Acute tubular necrosis

RBC's may also be present in case of calculi or tumors!

Correct!

"Approach to hematuria"
1) Dipstick - blood positive
Microscopy- RBC negative
It is myoglobinuria.

2) Dipstick - blood positive
Microscopy- RBC positive
It may be kidney pathology or bladder.

In that case if RBC is isomorphic (not distorted) - urinary bladder pathology like stones, cystitis.

If RBC is Dysmorphic - Kidney pathology (When RBC is passing thru tubules shape get distorted)

The dysmorphic RBC are a characteristic of glomerular pathology not tubular.

Study group discussion: Compliance of the lungs

Can anyone simply compliance for me?

Compliance = Change in volume/change in pressure.

So it follows as lungs starting at zero before inspiration. At the end there will be 500mL of air. So 0.5L
The pressure of he lungs starting at -5cm H20 increases to -10cm after expiration.

It would be (Specific compliance)
0.5 L/ (-5cm H20 - (-10cm H20))
= 0.5L/5cm H20 = 0.1 per cm H20

Theres a few types of compliance. Static compliance and dynamic.
Static calculates the periods where here isnt any gas flow. So during the time where there isn't fas flow.
Dynamic calculates the periods of active(!) Inspiration.

But I know nothing about those two calculations.

What is dead space of lungs?

There are two types of dead space-

1.       Anatomical
2.       Physiological

Anatomical dead space is the area included in the first 16 generation of the bronchial tree. Its by virtue of the normal anatomical structure that this area is unable to take part of in the exchange of gases

The physiological dead space is when there is decreased blood supply to a particular part of the lung, but the air entering the same part is normal. Hence there is no exchange of gases. In other words there is an increase in V/Q ratio.

Extra-

Why secondary tuberculosis affects the upper lobe?

There is an entity called ventilation perfusion ratio (V/Q)
meaning the degree of air entering the alveoli of lung and the corresponding pulmonary blood supply to the same. The normal value of the V/Q ratio is 0.8

Pulmonary blood capillaries are a low pressure system, with an average pressure of 25/8 mm of Hg. Out here comes the effect of gravity, pulmonary blood is unable to perfuse the upper lobes that well .

On the other hand, Air when it enters the lungs it enters the upper lobes better than the middle and lower lobes

This fact can be applied to

Study group discussion: Legionella confusion

A few days back, we had a discussion on legionella.

Legionella affects three systems - Lungs, GIT (diarrhoea) and CNS (Altered sensorium, confusion, etc).

Why does it cause CNS symptoms?

Study group discussion: Case control and cohort study mnemonic

Any mnemonic for case control study vs cohort study and how to identify which study to conduct or not?

Sunday, February 1, 2015

Study group discussion: Transpulmonary pressure

What is transpulmonary pressure and its significance?

I remember it's something like... General lung pressure without alveolar pressure. I don't know.

It's the difference between the intrapleural pressure and the alveolar pressure. The athmosphere pressure is constant, but air still needs to flow in and out of our lungs, so we adjust the pressure inside our body.

The basic principle is that air flows from higher pressures to lower, so we constantly change the pressure in our lungs to higher or lower than the atmosphere.

Transpulmonary pressure (when everything is fine) is always positive.

I'm getting what he is saying, go on!

Transpulmonary pressure is always positive, intrapleural is always negative and alveolar fluctuates.

That's how I remember from my physiology classes, anyway.

Yeah, alveolar fluctuates so that air can flow in and out easily.

Transpulmonary pressure is basically the elasticity of the lungs. The recoil.

Since atmospheric pressure is relatively constant, pressure in the lungs must be higher or lower than atmospheric pressure for air to flow between the atmosphere and the alveoli. It is nothing but the elastic recoiling of the lungs. If 'transpulmonary pressure' = 0 (alveolar pressure = intrapleural pressure), such as when the lungs are removed from the chest cavity or air enters the intrapleural space (a pneumothorax), the lungs collapse as a result of their inherent elastic recoil. Under physiological conditions the transpulmonary pressure is always positive; intrapleural pressure is always negative and relatively large, while alveolar pressure moves from slightly positive to slightly negative as a person breathes. For a given lung volume the transpulmonary pressure is equal and opposite to the elastic recoil pressure of the lung.

Study group discussion: Physiology books

Which is the best physiology book? I find Guyton to be really dull and Rhoades lacks details.

Ganong is okay, I guess.

Ganong has always been my first love.

I usually go for Ganong, but Costanza and Berne-Levy are also pretty good.

Costanza is not as detailed though, it's good for refreshing your memory the week before exams.

Yep. BRS is good for last minute revision!

Which are the simpler books for physiology? I know of Ganong.

Which was the other one?

Guyton?

Guyton is too extensive.
I read Guyton only in 1st year.
Good for clearing basics.

Yes, I find Guyton better than other physiology books.

Try BRS physiology.. It's little and has everything you need to know. Like it's smaller than Ganong.

Smaller the better!

I think it's 100 -  200 pages.

Study group discussion: Respiratory physiology

Does anyone have a mnemonic for respiratory centers?

DIVE!
The Dorsal nucleus is for Inspiration (tidal).
The Ventral nucleus for Expiration.

The ventral nucleus is especially important for forced respiration because expiration in general is passive. In tidal respiration, during the inspiration phase, the diaphragm and external intercostal muscles work. But the tidal expiration is completely passive because of elastic recoil.

Review question: Which all values of lung volumes you cant measure by spirometry? And why?

Reserve volume.
Functional residual capacity.
Vital capacity.

It's because spirometry measures through expiration. And the stuff that stays inside the lungs can't be measured!

What is the importance of residual volume? Why is it crucial for your body to retain air even after forceful expiration?

So that the lungs don't collapse on themselves. That's the most important one. There are two other uses!

Gas exchange is a continuous process, just because you expire, doesn't mean the gas exchange stops.

Third, the residual volume doesn't allow sudden changes in the outside concentration of air to affect your internal homeostasis. It takes 16 to 20 breaths for the outside air to affect your residual volume. This gives ample of time for your chemoreceptors to detect the slight changes in pH and respond.

Oh wow.. I didn't know this. Cool stuff. The breaths part though. Our body is waaay ahead of us than we think.

Totally!

Another review question! Mechanism of chemoreceptors? What passes through the BBB?

CO2 is not polar and is small, the BBB allows hydrophobic substances to pass through, so CO2 would pass the BBB.
The chemoreceptors monitor the H+ concentration of cerebrospinal fluid (CSF), including the brain interstitial fluid.
CO2 readily penetrates membranes, including the bloodbrain barrier, whereas H+ and HCO3– penetrate slowly. The CO2 that enters the brain and CSF is promptly hydrated. The H2CO3 dissociates, so that the local H+ concentration rises. The H+ concentration in brain interstitial fluid parallels the arterial PCO2.

Mechanism of peripheral receptors?

Oxygen potassium sensitizer channel. Lack of oxygen closes this channel, leading to increase in potassium in the ICF, depolarising it.

Do you know about the conditions in which you do not give 100% oxygen to the patient?

In cases where the CO2 levels are increased. Example, emphysema.. Cause the problem here is the respiratory drive is completely dependent on the blood CO2 level. So if you give 100% O2 the patient will go in apnea.

Yep. There's one more besides the CO2 indication. The neonate. Why?

Causes retinopathy of prematurity due to oxidative stress!

Study group discussion: Cause of decreased glucose levels in CSF in bacterial meningitis

I have a question, my professor told us that the cause of decreased glucose in CSF relates to permeability changes caused by the exudates. Which I find a good reason for the protein levels but glucose is not the same. In books and other references, I found the reason being bacterial and brain tissue consumption of glucose and non replenishment of it being the cause.

Can someone tell me for sure the cause for glucose depletion in csf in meningitis?

I think it's the glucose consumption. Permeability changes play a minor role.

Yes I'd also go with consumption.

Because permeability changes occur in viral meningitis as well.

That's what I also thought because permeability changes occur in all of the forms even the non infective ones.