Study group discussion: Mitral stenosis auscultatory findings

What is the characteristic feature of mitral stenosis? In terms of murmur? And echo findings?

Opening snap.
Enlarged  left atria.
Mid diastolic murmur.
Left heart failure.. Left atrial enlargement.
Sam of mitral leaflet.

Also one more auscultatory finding.

Loud S1

Correct!

One more!

Pre systolic accentuation.

Yes!

Advanced stage S 1 goes soft.

What happens to this murmur in cases of atrial fibrillation?

Disappear.

What disappears?

Psa.

Correct. Now tell me why?

Because presystolic accentuation is due to contraction of the atria.

May be bcoz atria are in tremora!

Correct. The final phase of atrial contraction is absent in afib.

Which auscultatory finding indicates the severity of the disease?

Length of murmur. The longer, the more severe the disease.

Opening snap moves closer to s2 as the severity increases.

When I said OS S2 interval, the examiner wasn't convinced.
I checked..and then I read somewhere about the length of murmur. You see..As the level of stenosis increases..Blood takes a longer time to enter from atria to ventricles. Hence, the length of murmur.

Maybe it's not anymore. I read a research publication on it.. It's not OS A2 anymore. But let's not confuse exam going students :P

Haha. Could be the length of the murmur!
It could be our PG question :O

Here's the paper for those who are interested http://www.ncbi.nlm.nih.gov/pmc/articles/PMC487332/

Interesting.

Study group discussion: What is the kussmaul's sign? Is it seen in cardiac tamponade?

Kassmaul sign is never found in cardiac tamponade

i.e inspiratory rise in jvp is not present in cardiac tamponade

Kussmaul sign is present in cardiac tamponade. That's what was explained.

Bt kussmaul sign absent in cardiac tamponade.I will recheck my sources for the kussmaul sign
Okay i saw..increased jvp is present and it is common in cardiac tamponade

overall JVP rises bt inspiratory rise is nt dere
I had read somewhere

kussmaul's which is an inspiratory increase is also present..but it is more pathognomic sign of constrictive pericarditis. 
Hence, its not a sure sign of cardiac tamponade

We need harrison for this. Could you check?

On it B)

The table in Harrison says Kussmaul's sign is absent in tamponade. 

A positive Kussmaul sign (seebelow) is rare in cardiac tamponade. 
-Harrison

(***the table in harrison says it is absent, but the text says it is rare***)

So I guess we ain't wrong after all (:

Yaay!

during inspiration there is  RV enlargement to accommodate more blood and in cardiac tamponade it can’t dilate more due to the blood enveloping around it so it pushes the septum and dilates....dilatation causes decrease pressure of right atrium and hence decrease in JVP

I have read about the septum being pushed to the left

Ya septum is pushed to left

The abrupt x descent in jvp shows that  pressure is increased

Ya pushed to left

There are a couple of mcq's asked on the same topic many a times

In tamponade diastole filling affected so it is transmitted in jugular vein , and presence or absence of JVP is indicative of degree of tamponade severity
Pressure

Rapid 'Y' Decent Seen In Constrictive Pericarditis Is Called As Friedreich's sign

So the conclusion we can draw is, it might be present in cardiac tamponade but in rare cases. Kussmauls sign is more pathognomic of constrictive pericarditis and very non specific sign for cardiac tamponade.

Yes!

Study group experience #8

Here's what we learnt!

Thyroid, weight and ophthalmoplegia 

Competitive and non competitive inhibition 

Classification of enzymes

Alcohol and liver enzymes 

High output cardiac failure and beri beri

Cardiac biomarkers 

Vasculitis (Question and answer discussion. Must read!)

Kawasaki disease quiz!

Anti-phospholipid antibody syndrome 
Systemic Lupus Erythematosus

Acute myelogenous leukemia 

Pharmacological treatment of UTI in pregnancy

Colored side effects 

Typhoid 

Malaria 

As you all can guess, we discuss A LOT and I can't seem to keep up with it. So I'm planning to post one or two posts per day. The number of blogs per day will reduce but I'll post all the topics eventually, I promise! Maybe we'll post a weekly study group experience of 15 topics or something. Let's see!

How to join the study group

Study group discussion: Colored side effects

Which drug causes Red Man syndrome? Why?

Vancomycin!

The antibiotic causes histamine release - which causes flushing.

Which drug causes Grey baby syndrome? Why?

Chloramphenicol.

Due to a lack of glucuronidation reactions occurring in the baby, thus leading to an accumulation of toxic chloramphenicol metabolites. The UDP-glucuronyl transferase enzyme system of infants, especially premature infants, is immature and incapable of metabolizing the excessive drug load.

Which drug causes Blue man syndrome? Why?

Amiodarone.

Amiodarone is anti-arrhythmic drug which contains iodine, it's because of that the iodine accumulated in the skin gives the blue color.

Which drug causes blue halo effect?

Sildenafil. 

Which substance makes us look yellow? (It is something which you eat. It is a differential diagnosis for jaundice.)

Excess carotene... Especially, from carrots. But the sclera is spared.. So thats how you know its not jaundice.

Orange urine and tears? Side effect of?

Rifampicin!

Which drug cause blue urine?

Methylene blue.

Study group discussion: Acute myelogenous leukemia

A 67-year-old man presents to his physician with a 10-day history of fatigue, bleeding gums, cellulitis, and a recent weight loss of 9 kg (20 lb). On physical examination, the patient is pale but has no evidence of lymphadenopathy or hepatosplenomegaly. Results of a complete blood count are as follows: WBC count: 18,300/mm3 (75% blastocytes, 20% lymphocytes) Hemoglobin: 9.1 g/dL Hematocrit: 29% Platelet count: 98,000/mm3 diagnosis?

He has acute myelogenous leukemia. It's acute because of the blasts.

Yes, acute myelogenous leukemia.

What could be find in marrow biopsy?

Lots of cells! Sometimes there could be fibrosis though which would lead to a dry tap.

Can anyone tell why the platelet count is affected? (Conceptual review question)

Isn't it in normal limits? 100k-150k?

Then why did he have bleeding gums?

Megakaryocyte lineage affected.

Yup the excessive growth of myeloid series doesn't not allow growth of megakaryocyte.

It is AML M5.

Isn't the bleeding gums due to thrombocytopenia?

I have seen a patient with type 5 AML in my hospital. They don't have bleeding gums. Rather a swelling of gums due to infiltration of leukemic cells. Gingival infiltration it's called I think.

Chloroma.

What's chloroma?

Infiltration of leukaemic cells in soft tissues.

That happens in ALL too, right? The infiltration of leukaemic cells into tissues?

Yes, I think.

I had seen a picture with a child having a chloroma of the orbit.

I thought the WBC count goes in lakhs in AML.

The count doesn't really help because sometimes the counts are comparable to a normal infection.

Oh.

What do we use for differentiating leukemia from infection?

The LAP.

What are the other causes of leukemoid reaction?

The major causes of leukemoid reactions are severe infections, intoxications, malignancies, severe hemorrhage, or acute hemolysis.
Source: http://www.ncbi.nlm.nih.gov/pubmed/16962944

Study group discussion: Pharmacological treatment of UTI in pregnancy

Sharing some of the knowledge I learnt!

So what is the treatment of Urinary tract infection?

Antibiotic according to urine  culture report.

Yeah what's the most common cause?

E.coli

So what the treatment prescribed?

Norfloxacin. It's excreted unchanged in the urine.

The most commonly is trimethoprim sulfamethoxazole. But that's in case of chronic uti, right?

So the question I wanted to ask is what would you prescribe in a pregnant lady? Which drug.. Sulphamethoxazole and trimethoprim?

No. Its a PABA agonist.. Will inhibit folate synthesis. Risk factor for NTD.

NTD means?

Ntd-neural tube defects.

Amoxicillin and ampicillin. Those are the ones preferred for any infection.

Nitrofurantoin too.

That's prophylactically. Atleast that's what we were taught.

Even nalidixic acid.

Yeah! Not to give TMP-SMX that's what was the main point I wanted to convey.

Study group discussion: Thyroid, weight and ophthalmoplegia

We were told by our Pediatrics teacher that thyroid status and weight changes are not related. Weight gain in hypothyroidism, in fact due to myxoedema and not due to slow metabolism.
But almost every other book I read say weight changes are a part of symptomatology of thyroid disorders.
Would someone enlighten me about this?

In myxedema there is reduced breakdown of glycosoamimoglycans. Plus there is free fluid retention. A lot of factors come into play. I'll look it up and send a good resource on it.

And haan..also iy read in a book..that in thyrotoxicosis..30% of patients will have weight gain. So therefore, maybe the weight status are not characteristic to changes in thyroid profile.

Maybe.

The cause of the weight gain in hypothyroid individuals is also complex, and not always related to excess fat accumulation. Most of the extra weight gained in hypothyroid individuals is due to excess accumulation of salt and water.
Source: http://www.thyroid.org/weight-loss-and-thyroid

So, 'obesity' should not ideally be mentioned in symptoms of hypothyroidism?

Weight gain should be mentioned
Along with the various other signs and symptoms. The complete clinical picture is specific to thyroid diseases.

The mechanism maybe varied but weight gain is a symptom and should always be a differential for hypothyroidism.

Yup.

Also, in Grave's ophthalmopathy, GSGs are deposited in the retro orbital space. Shouldn't this be seen instead in hypothyroidism where there is reduced breakdown of GSGs?

It's because of autoimmunity
The antibodies stimulate deposition of GAGs. Has nothing to do with the effect of thyroid hormones. That's why, ophthalmoplegia can not be treated by anti thyroid medications.

Oh!

What is the treatment of ophthalmoplegia in Grave's?

It is symptomatic. Lubricants, steroids is all what we can prescribe.

Yes, steroids. To suppress the immune system.

Steroids are especially given in retinal pathologies.

What about a permanent cure?

I don't know about any permanent cure.

It's radioactive iodine 131 or thyroidectomy.

Permanent cure for opthalmopathy?

Hemithyroidectomy. Or if the graves is not too bad, we can give thyroid peroxidase inhibitors? And sometimes it will resolve by itself?
I was told the retro-orbital lipofibroblasts requires surgical removal of the mass behind the eye, but the lid lag will resolve once the thyrotoxicosis resolves?

Yes.

There are different surgeries for the opthalmoplegia..Don't remember the names.

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 (: