Study group discussion: Cardiac biomarkers

Which all troponins are used as cardiac biomarkers?

I and T.

Troponin- T type 2.

Correct!

Which biomarker is used to differentiate breathlessness of cardiac origin from that of COPD?

BNP.

Correct!

BNP?
Brain natriuretic peptide.

Woah. I didn't know this.

Yeah. BNP is a marker for heart failure.

It's also used to monitor COPD patients.. That is the levels will increase if there is cor pulmonale

Also pro BNP.

BNP is present in ventricles. The ANP (Atrial natriuretic peptide) version in atria.

Amazing!

Study group discussion: Alcohol and liver enzymes

Which is the most sensitive enzyme for alcohol abuse?

Gamma glutamyl transaminase (GGT). 

What is the ALT:AST ratio specific for alcoholic hepatitis? 

1:2

2:1 is AST ALT. That was the catch if you got it wrong! Scotch and tonic is the mnemonic!

Which is more specific for liver disease.. ALT or AST?

ALT.

Why? 

ALT is more specific for liver disease than AST because AST is found in more types of cell (e.g. heart, intestine, muscle).

Kawasaki disease mnemonic and notes

Kawasaki, a Japanese name, reminds me of anime!

So I drew this anime character, having Kawasaki's disease. Can you label the 5 things she'll have besides the fever to make a clinical diagnosis of the disease?

Study group discussion: Vasculitis

This review question session was held by Sakkan!

Examples of large, medium and small arteries?

Large arteries: Aorta, pulmonary. Also, the major branches of aorta are large arteries - Brachiocephalic, common carotid and subclavian.

Mediucm sized arteries: Brachial and temporal, femoral are medium.

Small sized artery: Digitalis artery.

A patient comes with rhinitis and dyspnea, he also complains of hematuria. Which is the most probable vasculitis?

Study group discussion: Classification of enzymes

Which class of enzymes does carboxylase come under? (IUMB class for enzymes, 1 to 6.)

It belongs to transferases... Because you transfer a CO2 compound. 

Study group discussion: Competitive and non competitive inhibition

Define Km value of an enzyme.

In types of enzyme inhibition..Where does the value km and where does the value Vmax decrease?

It is the substrate concentration at which reaction rate is half the maximum rate.

Study links!
http://medicowesome.blogspot.ae/2013/12/competitive-and-non-competitive.html

http://medicowesome.blogspot.ae/2013/11/competitive-vs-non-competitive.html

In types of enzyme inhibition..Where does the value km and where does the value Vmax decrease?

Vmax decreases in non competitive inhibiton.

Kmax in competitive.

There is one more thing.. Uncompetitive inhibition.
Anybody knows about that?

Some placental enzyme inhibited by phenylalanine. Donno for sure.

Biochemistry.. It's fun when you have recently read it.

Study group discussion: Malaria

Review questions! Which are the types of parasites for malaria?

Plasmodium species!
Vivax, falciparum, ovale, malariae.

One more.
Plasmodium knowelsi.

How do you differentiate cause of malaria based on the fever

It's quartan in malarie.. After every third day.
It's tertian in the rest of them.. Every alternate day.

What's algid malaria?
Circulatory collapse

Fever and shock. That's algid malaria.

Which are the rapid diagnostic test for malaria?
Dip stick test
Pfhrp
Pfldh

Of HRP and LDH , which is specific for falciparum malaria?
HRP?

True.
LDH just shows infection with plasmodium. Not which sub type.

But what was the significance of LDH? I read somewhere it's super important.

It detects all other forms. Hrp is just to check whether it is falci or not.

Which forms have a latent phase in liver?
P. vivax & P. ovale

What is the clinical significance of liver forms?
They remain dormant in ovale & vivax, also known as hypnozoites & they cause relapse.
Yes.

Drug of choice for relapse?
Primaquine!

Why do we give primaquine in P. Falciparum malaria?

To destroy gametes!

Yes. Gametocides. It helps in control of spread. 45 mg is gametocidal.

Which test is more preferred if you are suspecting relapse?
Peripheral blood smear is preferred.

Correct!
Why don't you perform rapid diagnostic test when you are suspecting a relapse for malaria?

You don't do rapid diagnostic test cause.. These remain positive several weeks after an initial infection.
So it will show positive even if it's fever for some other cause.

I was asked this in viva, why we combine chloroquine and primaquine in combination?

In Vivax, primaquine is used for hypnozoites.

Which is the gold standard for detecting malaria?
Gold standard is that centrifuge thing.
QBC? Quantitative Buffy Coat? We add acridine orange?

Hmm. Peripheral blood smear is gold standard. Never heard of buffy test. Could be because in the buffy coat what you get is WBC's in maximal amount. Plasmodium are within RBC.

How will you diagnose cerebral malaria?

You can't diagnose malaria by CSF.
It's on clinical symptoms. Based on altered sensorium and coma you diagnose it.

Interesting.

But first you infuse glucose to rule out hypoglycaemia..If the patient fails to improve then its  cerebral malaria.

Yes, I remember that.

Which anti malarial drug can cause hypoglycaemia?

Quinine and chloroquine too.

Correct!

Introduction to the new author

Greetings mortals

I am sakkan. I am new here

New as in, I have just recently taken up blogging seriously. And as ikan told me..”welcome to everyday blooging “ =D

Its fun

Hobbies include. 

I am a passionate reader of fantasy novels.

 I like food, but I wont call myself passionate about it, cause I have to watch those calories.

I like sitting on a bench facing a park, with a cool breeze. That’s peace

I like knowing the why behind everything. Its very hard for me to remember things if I don’t understand whats going on.

 This blog has provided me a portal to be more demanding of those answers.

I have a couple of groups to my whatsapp. From junior college, medical college, classes. But truth be told none of them is as humongamous as the medicowesome study group. Diversity, sharing, thoughts, questions and most of all answers, and everybody just jumps in to answer your questions. It feels like a tiny virtual world of awesomites who just care to learn and nothing else.

p.s ‘ the word humongamous- cause even enormous seemed small to describe you guys’

hope we provide you with as much of knowledge through this blog, in equivalence to what you guys have provided us.

thank you

-sakkan

Study group discussion: Typhoid

When do complications of typhoid happen? Which week?

3rd week, intestinal perforation.

Correct. 3rd week is the week for complications.

Describe fever in typhoid?

Step ladder..the fever increases in the first week step by step. Later it becomes continuous.

When do rose spots appear?

End of first week.

Shape of ulcers?
Typhoid are longitudinal or parallel to the axis of the gut.

Most sensitive test?

WIDAL?
Widal is neither sensitive or specific.

Bone marrow for typhoid?

Yes, typhoid infects the RE cells..Hence, if the culture is inconclusive, there is higher chance of positivity from a bone marrow culture.

Urine and gall bladder cultures can also be performed.

Study group discussion: High output cardiac failure and beri beri

Name some hyperdynamic states

Fever, anemia
Beriberi
Infections
Paget disease
Hyperthyroidism

Infections are hyperdynamic cause they cause fever.
Hahaha true

What about any valvular heart disease?
Aortic regurgitation

Pregnancy
AV malformation

Correct!

Why beri beri is a high CO state which  leads to heart failure?
I don't know but is it due to Beri beri due to B1 deficiency?

For carbohydrate metabolism, B1 is required so for fulfilling body energy demands body has to burn other fuels fats and protein. They are limited and generate less energy so body need more cycles/min with more CO to wash out the products of metabolism to maintain metabolism. If condition not treated the heart gets hypertrophied and will eventually fail.

Yes. Beri beri leads to increased metabolic demand and increased need for blood flow causing high output cardiac failure.

Study group discussion: Systemic Lupus Erythematosus

*Review question session on SLE*

Which is the most sensitive antibody?
ANA

Most specific?
Ds DNA

Drug induced lupus?
Anti histone

I have mnemonics on these!

Please share!

http://immense-immunology-insight.blogspot.ae/2013/12/its-never-lupus-mnemonics.html

Most common type of lung involvement in SLE?
Pleurisy

Skin changes in SLE?
Malar rash
Discoid rash

Butterfly rash, discoid lesions

And?

Photosenstivity

Good.

How do you differentiate between discoid lupus and SLE?
Discoid lupus is a milder form of SLE.

I will approach the question in a different way.. Do we do skin biopsy in SLE?
Yes.

And what test we do?
Band test.
Correct!

Where?? Which level of the skin?

Between dermis and epidermis.

Dermo-epidermal junction. Correct!

So what do you think will be the difference in DLE and SLE?

Skin biopsy shows a green band under fluorescence.
In DLE..you will have a positive band test only in regional areas.
Whereas in SLE..the test is common all over the body, and not only the affected areas.

Ok so this differentiates DLE vs SLE.

Never heard about this thing. Thanks all!

This crazy skin test.

I didn't know this either. Amazing.

Also, nephritis is much more common in SLE.
Wire loop deposit.
Great!!

Which drugs cause drug induced SLE?

There is a very big list for sure.

The most common causes to remember are
1) Procainamide
2) Hydralazine
3) Isoniazid

Easy question would be..Which drugs don't cause SLE.

Yes. Because they are related to acetylators. The slow and fast acetylators.

Can you explain I mean how does it effect? The slow and fast acetylators?

I'm not sure.. But the slow acetylators are more prone to DILE. I'll cross check and let you know

Slow acetylators metabolize the drug slowly.. Hence a higher chance of toxicity.

Presumably, this is because acetylation of the aromatic amine or hydrazine functional group leads to a non-toxic product. Several other drugs which have been implicated in drug-induced lupus also contain an aromatic amine or hydrazine group. The clinical and laboratory characteristics of drug-induced and idiopathic lupus are similar but the degree to which the pathophysiological mechanisms are related, if at all, is unknown.
Source: http://www.ncbi.nlm.nih.gov/pubmed/7011656

Complex.

Ok so which symptoms you won't see in drug induced lupus?

Donno.. I know they'll disappear on discontinuation of the medication.

You won't see
CNS involvement and renal involvement in drug induced.

One last.

What happens to complement levels in lupus flare up?

Decreases.

Brilliant.

And what happens to dsDNA in flare up?

And what about levels of complement and anti ds Dna in drug induced lupus?

Anti dsDNA levels decrease in the lupus flare up.

Lol hope I am not bugging you guys!! Haha so I will answer the last one!!

Oh you're not. Medicine is addicting.
If we knew the answers we'd be jumping and answering :P

Haha yeah medicine is addicting once you get to know some of it.
You just can't back off! If when you have learnt there is much more that you don't know!

Complement levels and anti dsDNA levels are normal in drug induced lupus.

They do have positive ANA.

Ah. Makes sense.

Alright guys! It was wonderful! Keep learning medicine.
And keep rocking!

Study group discussion: Anti-phospholipid antibody syndrome

What is secondary anti-phospholipid syndrome?

Anti-phospholipid antibody syndrome?

In antiphospholipid syndrome, your body mistakenly produces antibodies against proteins that bind phospholipids.

Antibodies bind with phospholipid of every cell membrane?

It can be idiopathic or secondary when associated with another autoimmune dissorder as lupus. Oh, secondary can also be caused by infections (syphilis, HIV) or medication

It causes thrombosis, abortions, strokes...

Treatment?

Steroids.

Any specific steroid that is preferably used?

Don't know.

Mainly blood thinners and steroidal

Sapporo criteria used for APLA.

Interesting.

APLA is also a cause of recurrent abortions.

In fact I have seen a case female reproductiveage group having habitual abortions and anticardiolipin antibodies positive.

What is the significance of anticardolipin antibody?
(Microbiology related)

Syphillis test?

Yes, it gives false positive results.

APLA is differential diagnosis for false positive for syphilis.

Cool!

Study group discussion: Folate deficiency in hemolysis and alcohol

Here's an interesting thing I read.. Let me put it in a form of a hypothetical question.

A person suffers from chronic hemolysis due to sickle cell anemia. Has a high MCV. Which vitamin is he most likely to be deficient in?

Folic acid.

Correct!

Why not B12?

Cause it is stored in the body in high doses.

Yes :D

Folic acid on the other hand gets extinguished very fast.

Exactly!

And in every case of excessive RBC production..you always give folic acid supplements. Like even in thalassemia.. And other various chronic hemolytic conditions.

Ooh.

Why are alcoholics more prone to B9 deficiency?

Cause they eat less maybe. The commonest cause of deficiency is reduced intake in case of folic acid.

Correct!
Alcohol affects the body's ability to absorb folate and also increases folate in the urine. Many alcohol abusers have poor quality diets that do not provide the suggested intake of folate.

Study group experience #7

JVP during inspiration 
Holiday heart syndrome and Atrial fibrillation 
Wolff-Parkinson-White (WPW) and increased QRS interval 
Short PR interval causes 
Cardiac shunts and snowman sign
Eisenmenger's syndrome 
Why does ingestion of salt cause high blood pressure? 
Mechanism of anemia in anemia of chronic disease
Microcytic and Sideroblastic anemia
Folate deficiency in hemolysis and alcohol 
Grave's disease
Caloric test and true coma
Mechanism of action of Digoxin
Why NSAIDs are avoided in MI, why aspirin is an exception
Why adrenaline is preferably given by the intravenous route
Management of enuresis

 

We created the second group with a few members. It's as awesome as the first group!

I learnt  that we are all the same from the Whatsapp groups.. Even though we are medical students from different schools and countries, every one feels so similar in some unexplainable way. 

"Have you dissected cadavers? Looked inside the bodies of dead men? I have. And I can tell you we are all the same on the inside." - Amazing quote by a group member on equality with differences (:

Study group discussion: JVP during inspiration

Systolic BP decreases in inspiration.....then what about JVP? It also decreases...But I'm not getting how?

During inspiration, there is increased negative pressure in the thorax..therefore the venous blood is forced to enter the heart. Hence the JVP reduces because the suction effect is more. But the venous blood supply to the heart reduces..that is via the pulmonary veins. Resulting in a reduced cardiac output. And reduced systolic. The left side of the heart I mean.

During inspiration a negative pressure is created which sucks the blood into the heart. That's why blood from the veins goes into the heart, the pressure or the JVP decreases (less volume).

Conditions where you dont see fall in blood pressure or JVP during inspiration?

Cardiac tamponade
Constrictive pericarditis
Restrictive cardiomyopathy

Yes, when the heart can't fill up blood!

*someone had a confusion on rise or fall in JVP in tamponade, this was explained by Sakkan*

Most kussmaul sign is positive in cardiac tamponade. That is paradoxical rise in JVP in inspiration.

In cardiac tamponade.. Due to increased external pressure on the right side of heart..the blood can't enter during inspiration. This leads to rise in JVP.

This also leads to bulging of the interventricular septum Upon the left ventricle. This decreases the preasure more than the normal fall of 10 mm of Hg.

Related to this.. Cardiac tamponade has a classical triad..called becks traid. That is silent chest, increased JVP and reduced BP.

Muffled heartsound.
Yeah cause the pericardial fluid accumulation dampens the sounds.

Yeah JVP will be elevated in cardiac tamponade! Thanks for a nice explanation.

Study group discussion: Holiday heart syndrome and Atrial fibrillation

What's holiday heart syndrome?

Atrial fibrillation.. Due to alcohol.
Heart takes a holiday with you :P

Yup when people do binge drinking for the first time. Or after a long time!

Meaning of fibrillation?
I'm not clear about it.

It's paroxysmal..The patient can die. It's like when your atria dont contract in one motion.
There are several simultaneous impulses generated that stimulate the atria. Hence rather then contracting in a syncitium the atria simply fibrillate. Meaning many many sad attempts at contraction, none of them strong enough to push blood in the ventricles.

Thank you!

Flutter is like a less severe form of fibrillation.

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.

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!