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!

Study group discussion: Management of enuresis

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

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

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

Desmopressin then Imipramine.

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

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

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

Study group discussion: Calorie test and true coma

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

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

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

Mnemonic is COWS.

Cold: Opposite side

Warm: Same side

Study group discussion: Mechanism of action of Digoxin

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

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

Can somebody comment on the reliability of such articles?

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

It's RyR2!

RyR2, yes!

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

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

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

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

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

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

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

Study group discussion: Cardiac shunts and snowman sign

Congenital heart diseases

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

-> Left to right shunts:
VSD
ASD
PDA
Eisenmenger

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

Snowman sign X ray feature of?

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

Another name figure of 8 sign.

Study group discussion: Eisenmenger's syndrome

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

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

And why does Pulmonary hypertension arise in that case?

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

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

Plethoric lungs, basically.

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

Yes, that's a contributory factor too

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

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

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

Thanks for explaining it to me, you guys!

Study group discussion: Short PR interval causes

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

Wolff Parkinson White syndrome is one.

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

The re-entrant pathway.

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

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

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

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

Causes of increased QRS interval?

BBBs (Bundle branch block)
Electrolyte abnormalities
WPW syndrome

Medications like:

Procainamide
Tricyclic antidepressants

Study group experience #6

Here's what we discussed:

Smallest, largest and longest muscle 

Sarcoidosis and calcium regulation

Weight loss in malignancy 

Metformin and weight 

Cushing's syndrome 

Necrobiosis lipoidica 

Babinski sign 

Sweet syndrome 

Monospot test for EBV infection 

Safflower, Butter and Cholesterol

Our first group reached 100 awesomites today. So happy! 

Here are a few messages from the group:

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

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

How to sign up for the group: Medicowesome study group on Whatsapp - The Official invitation

Uses of tricyclic antidepressants mnemonic

Amitryptyline for neuropathic pain.

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

Clomipramine for obsessive compulsive disorder.

Clomi when you feel Compulsion ;)

Imipramine for nocturnal enuresis.

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

Lame but helps :D

Hematology and chemical pathology mnemonics

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

Uploading the notes + mnemonics for reference:

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

ADDITIVE: EDTA (ethylenediaminetetraacetic acid)

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

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

Study group discussion: Safflower, Butter and Cholesterol.

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

This has to be tricky.

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

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

Haha. Wrong!

Oh man. I hate vivas.

What's the reason?

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

Correct!

Study group discussion: Weight loss in malignancy

What's the cause of weight loss in malignancy?

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

Malignancy: Due to decreased appetite.

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

Study group discussion: Sweet syndrome

Has anyone out here heard of sweet syndrome?

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

Acute febrile neutrophilic dermatitis.

It is caused due to?

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

Named after Rober Sweet.

Study group discussion: Necrobiosis lipoidica

What is necrobiosis lipoidica?

Which condition causes it?

Papule on Lowerlimb seen in DM.

What's DM?

Diabetes mellitus.

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

Study group discussion: Cushing's syndrome

What is Cushing Reflex?

It's related to cushing syndrome or disease?

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

It is caused due to raised ICT?

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

Curling ulcer is due to burns.

They both are confusing terms.

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

Agree.

Does anyone know the mechanism?

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

There is the cushing sign too

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

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

Cushing sign occurs as a result of Cushing reflex.

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

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

Study group discussion: Smallest, largest and longest muscle

Which is the smallest muscle in the body?

Stapedeus. 

Nope, stapedius ain't the answer.

Then?

Erector pili muscle. The one responsible for goose bumps.

Oh yes! I forget it's a muscle cause it is so small and seems insignificant.

Haha me too!

Awesome.

Largest muscle?

Gluteus maximus!

The longest muscle?

Sartorius. Originates from ASIS to Pes anserinus.

Updated on 22nd February, 2015:

I read the previous  posts, errector pili -smallest smooth musle, smallest skeletal muscle -stapedius!

Smooth muscle not in our control , innervated by sympathetic system,triggering agents - cold, fear. 

Which is the strongest muscle in the body?

Ahh makes sense. 

Strongest would be the one in the thigh?

Gluteus maximus!

Nope. 

Masseter. 

True! Well done!

Shouldn't it be the quadriceps? I don't see the masseter kicking foot balls and running with the weight of the body :P

Yes, based on its weight, with all muscles working together it can close the teeth with a force of 25 kgs on the incisors. 

Ooh. 

Or 90 kgs on molars! 

I got a good link on that!

There are lots of ways to measure strength. One is brute force, in which case biggest is best. All skeletal muscles are bundles of many individual fibers that contain small force generating structures called sarcomeres. “Generally speaking, more muscle tissue means a larger total number of sarcomeres, which means greater maximum force generation,” Tasko says. That means the largest muscles—the quadriceps on the front of your thighs and the gluteus maximus on your rear—produce the most force.

I thought the strongest was the tongue! 

I was told that it was the muscle that can do the most amount of damage - the tongue (Obviously, not physical damage, you know what I mean, right?)

Oh oh most hard working muscle in the body? 

Heart <3 

Why not diaphragm?

Umm I donno.. Because you can have a paralyzed diaphragm and live but you can't have a paralyzed heart?

I personally think that heart is made popular for no reason :P

Study group discussion: Babinski sign

What is pyramidal tract sign?

Did you mean Babinski sign ?
There are a specific set of clinical signs for pyramidal tract disease..I haventy heard of just one particular one.. But yes, out of the many..Babinski is the most specific for pyramidal tract disease.

A few days after UMN syndrome, motor signs appear
These include spasticity,  hyperactive reflexes, extensor plantar responses.

That's because the CSF will press on the cortical neurons.. And cause a upper motor neuron type of lesion.

UMN lesion is due to lesion in corticospinal tract between cerebral cortex and SC.

Well, not all pyramidal signs are called Babinski. Babinski is the extensor response to plantar reflex when the lateral surface of the feet is striken/scratched.

Achcha what are the components of the positive babinski reflex? - review question.

Extension of great toe, fanning of other toes, contraction of tensor fascia lata.

Plus, dorsiflexion of ankle and knee joint.

Yeah, that.

Other ways to elicit a babinski ?
Plus the equivalent of babinski in the upper limbs?

It's plantar reflex. It can be elicited different ways, one's babinski, others are Oppenheim and Chaddock.

Schaeffer too.

Yep.

And do you elicit Babinski with sharp end or blunt end of the hammer? (Viva question)

In Babinski, you have to produce pain and pressure both at same time so I guess blunt end if the hammer is used.

To support my answer - I have also seen many doctors using their keys (blunt end) for eliciting Babinski.

The tip of a pen can also be used to elicit Babinski.

Yeah, they taught us that we could use keys if we didn't have a hammer handy.

Always red, it looks better on a patient's foot.

In paediatrics.. We used our own nails to elicit Babinski!

I was doubtful that it would work.. But it did.. Especially, children aged below 3-5 years.

Study group discussion: Monospot test for EBV infection

Anyone explain Monospot test please!

Heterophile antibodies in the blood?

I was just reading this. The test works with the agglutination of  horse's RBC when in contact with heterophile antibodies.

Yes.. Used in detection of these antibodies in infectious mononucleosis.

When you have infectious mononucleosis you produce antibodies anti-epstein barr virus and other unspecific antibodies which are called heterophile antibodies.

Aren't anti sheep antibodies produced in monospot test ?
I mean Heterophile anti sheep red cell antibodies?

That would be Paul Bunnel test.

But infected B cells secrete anti sheep red cell antibodies that are diagnosed for mononucleosis. .

I think the only difference between monospot and paul bunnel test is the origin of the RBC. In monospot they come from horses and on Paul Bunnell, from sheeps.

Study group discussion: Sarcoidosis and calcium regulation

I have a review question for sarcoidosis.

What is the characteristic appearance of sarcoidosis radiological imaging?

Lambda sign?
Panda sign?

No. Hint..That's also what tuberculosis shows positive.

BL hilar lymphadenopathy.

Tree in the bud sign.
You then differentiate it from TB ..Based on whether the lymph nodes are showing necrosis or not.

Can you elaborate on the tree in bud sign?

It's an appearance on chest CT. I read it is specific for TB and sarcoidosis.

Oh so if there is necrosis, it's Tb? If not, it's sarcoidosis?

Yup. That too can be differentiated on CT.. By looking at the lymph nodes.

I have a review question. Which cells will you see in sputum examination of a patient with sarcoidosis?

Elevated CD4/CD8 ratio.

Why is that?

I don't know exactly but CD 4 + inflammation is specific to sarcoidosis. Helps differentiate it from other non granulomatous interstitial lung diseases.

*A parallel discussion on calcium was going on, since they both are related to each other, I'm posting the calcium discussion here as well*

Percentage of dietary calcium absorbed is inversely related to intake. How is this possible?

If you take more calcium, it absorbs less? I don't know how that is possible.

The body has to maintain a homeostasis for calcium.. If reduced intake..There will be paradoxical increased receptors via Vitamin D. To maintain a constant absorption.
If increased intake..The body reduces the absorption. The mechanism..PTH is stimulated via low serum calcium.. And PTH is the one responsible to make the final active form of vitamin D.
So if calcium in the blood stabilizes, there will be reduced impulses by PTH..conversely less vitD and less absorption.

It means that if your body's need/absorption of calcium equals x.
If your intake equals x, you'd be absorbing 100% of it.
If your intake equals 2x , you'd be absorbing 50% of it.
If it equals 4x you'd be absorbing 25% of it, and so on.
At a normal steady state of absorption, the more the intake is, the less the absorption percentage of it.

Excellente.

Can anyone associate calcium and sarcoidosis?

Hypercalemia.

Why?

Because of increase in Vitamin D by granulomas.

PTH decreases then.

Which enzyme?
And which cell is involved?

It's the interstitial alveolar macrophages that secrete alpha hydroxylase that activates vitamin D.

Is sarcoidosis a cause for dystrophic calcification then?

No, metastatic.

Bravo!

Medicowesome study group on Whatsapp: The Official invitation

It started as a small experiment and turned out to be one word - AWESOME.

What's the study group for?
A bunch of medical students from all over the world, discussing study related concepts!
You may share your experiences, what you studied today, ask interesting questions to help other people learn or simply revise, ask doubts about things you don't understand, answer other people or just tell a fact you learnt that fascinates you.
We learn something new on a daily basis <3

How do I sign up for the group?
All you've got to do is message me your number. You can email me at medicowesome@gmail.com with "Whatsapp study group" in the subject.

Important: Make sure you include your proper country code when you email me your number. (Otherwise your number won't be displayed in my Whatsapp list and I might miss you out!)

After you have emailed me your number, you'll receive instructions from us. 

The group is for medical students only. We do not add pharmacy / nursing / pre med students.

"I want to join but.. I'm hesitant because I'll be sharing my number to a lot of people."
It's risky, I know, but we have solutions - Block users. So I don't think you should hold back on your awesomeness. I have added over 800 people so far and they are loving it.

We have had a few spammers, flirts and inappropriate members, but we removed them. We highly encourage awesomites to report such people to the admins (We have more than 5 admins) and necessary action will be taken.

Your number will be shared with at least 100 other medical students who are strangers - So if you aren't comfortable, don't join.

-IkaN

Related post: More information on study group

Study group experience #5

Here's what we discussed!

Drugs that cause urinary calculi

Amantadine

Cardiac mortality in diabetes mellitus reduction due to aspirin 

ECG in MI, potassium abnormalities, infectious diseases, pericarditis

Splenic vein thrombosis and hepatic vein thrombosis 

Difference between rouleaux formation and agglutination of RBC's

von Willebrand factor and disease 

O negative blood group 

Type 3 diabetes and type 1.5 diabetes

Hyperthyroidism and decreased appetite

Somatostatin 

Hydrocephalus ex vacuo, normal pressure hydrocephalus and cortical atrophy 

Wernicke Korsakoff syndrome 

Ziehl Neelsen staining uses

Human Papilloma Virus

Immortal cells 

Why food doesn't taste good in aeroplanes

I particularly like how when one person answers correctly in the group, even if it's to a simple question, someone says a positive word like, "Excellent!", "Well done" or "Bravo!"

If you answer incorrectly, we'll tell you, "We are here to make mistakes so that we can avoid them in real life."

Oh and the science discussions! They make me lose my sense of time.. I feel completely enraptured. We end up in deep thought, amazed by the wonders of nature when those insightful discussions happen. 

It's this kind of positive reinforcement that makes it not just a study group but a vast, open, refreshing and fascinating learning group to me. 

Thank you, good hearted awesomites, to make this such a beautiful experience.

To all the future awesomites, hope you continue the legacy. 

-IkaN

The illusion of ST segment elevation in transmural myocardial infarction

To, understand the WHY of it all, we need to understand what is the electrical vector?

      1.Before the incoming of any impulse, the heart muscle is polarized- meaning the outside of heart muscles is more positive in compared to the inside of the heart muscle. This means that the ECF all over the heart has a positive charge

2.       With the incoming of the impulse from the S.A node, the heart muscle depolarizes..means positive ions are going inside. Which means the overlying ECF is becoming negative in compare to the surrounding area

3.       This change  in electrical charge, generates a current in the ECF ..this current flows from negative to positive and thus generates what is called the electrical vector
4.       The electrical vector changes in size and direction as the wave of depolarization spread

5.       Also, our body is a volume conductor..which means when the electrical energy flows..there is an electrical field generated around it. And different points on the field have a potential, based on their location from the electrical vector
6.       When we connect two potential in this field, and measure the potential difference between them, we get the electrocardiogram (ECG)

Next important point to be understood is how the strength of the vector is measured, whether the wave will be negative, or positive..and what will be its strength?

The axis of the electrical field is determined from negative to positive

Suppose there is a vector AB,  what we do to measure the value of this vector is project the same vector on this electrical field.

Hence, the strength of the voltage is +4 mv, and since the value is positive we get a positive wave

On the other hand, this vector has a value of -3mv, and it will be a negative wave

Whenever, there is an infarction in the myocardial tissue..the cell looses its polarity, meaning it becomes depolarized.

So even when the whole heart is in the resting stage..there is some amount of current flow from the infarcted tissue ( this is called funny currents-If)

Also remember, the ST segment is an isoelectic line, meaning there is no flow of charge in the heart muscle during this time..that is either the heart is completely polarized ( resting stage- all over positivity outside) or the heart is completely depolarized (all over negativity outside)

So now when you take an ecg of this heart..example with an infarction in the anterior wall, on the V1 lead, the overall voltage of the heart is reduced, this is because the constant flow of funny currents from anterior to posterior. This modifies the electrical vector ( with change in its direction and size)

But now as the wave of depolarization is completed (the QRS complex), the funny currents are abolished..cause they too are in the depolarized state (negativity outside). Hence, no flow of funny currents.

This makes the st segment isoelectric (that is 0mv)

When we see this graph, it seems the st segment has elevated, but in reality it is just an illusion, cause the st segment is right where it was supposed to be, what has changed is the voltage of the rest of the ECG

Study group discussion: Wernicke Korsakoff syndrome

Review question:
What triad is present in Wernicke's encephalopathy?

Opthalmoplegia, ataxia and confusion.

Excellent!

What is the treatment?

Thiamine.

Route?

Intravenous or parenteral route is used.

Do we give glucose before the thiamine or after the thiamine?