Study group discussion: Sickle cell anemia

Name the three crisis of sickle cell anaemia.

Aplastic crisis
Vaso-occlusive crisis
Sequestration crisis

What causes aplastic crisis?
Parvovirus B19

*doubt discussion*
In sickle cell anemia what analgesic do we use? I've heard that morphine can cause vasoconstriction and that would make it worse, but I'm not sure that's true.

Yup, opiates are used.

One cause of death in sickle cell anemia is acute chest syndrome, if I give the patient morphine (that has a secondary coronary vasoconstrictor effect) that will kill the patient.

Correct.

Acute chest syndrome is due to occlusion of the pulmonary vessels.

The major issue hear is to given oxygen to the patient..Cause hypoxia aggravates the whole situation.

So I'm not supposed to worry about Myocardial Infarction?

Not that I've heard of.

Doesn't it cause CHF?

"The acute chest syndrome may mimic CHF however it is uncommon." Says the internet.

New drug for SCA. Read in Harrison. Azacytidine.

Mechanism of action of azacytidine?

Azacytidine increases HbF production and reduces anemia in sickle cell disease.

There's a drug which blocks gardos channel in RBC membrane. It's under trials too. It's the one I was talking about.

The mechanism is interesting because it prevents dehydration of the RBC.. That's the cause of sickling.

I like the sound of it - Gardos channel.

It's a potassium channel!

A greek god!

Me too.. It guards the RBC!

Gargoyle ..thats what my mind said.

Haha. They were guardians too!

Another interesting thing.. An anti fungal we use also blocks this channel in vitro!

Study group discussion: Electrolyte abnormalities that cause QT prolongation

Which electrolyte abnormalities lead to QT prolongation?

Study group discussion: Gate control theory of pain

Just had my first class of pain physiology. I loved it!

What was the most interesting thing that you learnt in class?

Melzack and Wall's theory. About the gate control of pain. I had to google the english term lol.

Aw that's so nice of you. It's an interesting concept. Why soldiers don't feel pain when they are injured in battle.. But feel it in the hospital.

What is it called in Brazilian? (I donno what language you'll speak)

Portuguese. In portuguese, it's 'teoria das comportas'

I feel better now for not recognising "Melzack and wall's theory" but I do remember learning teoria das comportas!  hahahaha I have to Google the translation all the time too.

Must be because of increase in Endorphins and adrenaline?

Not exactly. You should read more about it!

The brain determines which stimuli are profitable to ignore over time. Thus, the brain controls the perception of pain quite directly, and can be "trained" to turn off forms of pain that are not "useful". This understanding led Melzack to assert that pain is in the brain.

Awesome stuff!

Study group discussion: Type 2 polyglandular syndrome

Came across a new question today. Let me ask you guys -

So what is Type II polyglandular autoimmune syndrome?

Schmidt syndrome?

Yes, also known as Schmidt syndrome.

What are the components?

Adrenal insufficiency (Addisons)

Hypothyroidism (hashimoto)

Also gonadal insufficiency

And ?

Abs pancreatic insufficiency!

Yeah, Type 1 DM.

Good job!

Study group discussion: Vitamins (Antioxidants, Vitamin E and vitamins in egg)

Name the vitamins which are anti-oxidants?

Vitamin A, C, E.

Mnemonic: Ace the oxidants!

Which is the anti-oxidant important to prevent lipid peroxidation?

Vitamin E

Study group discussion: Tissues that are exclusively dependent on glucose for metabolism

Which things in our body are exclusively dependent in glucose for energy?

The lens.

Correct

Liver too?
Nope.
Brain?
No. It uses ketone bodies too!
Muscle?
No.

Cornea?

Cornea correct!

Heart.
Heart, no.
Interesting: Heart can use lactate.

Sperm
No. Sperm uses fructose!

It's RBC!
Oh ya. They are exclusively dependent on glucose! RBC can't metabolize anything else!

Study group discussion: Mechanism of hypercoagulability in obesity and smoking

How does smoking and obesity promote hypercoagulability?

Smoking increases reactive oxygen species. ROS reacts with LDLs causing increasing oxidized LDL, when deposited in intima becomes atherosclerotic plaques. Also ROS causes endothelial damage itself, increasing its permability to LDL.
Atherosclerotic plaques can rupture, exposing tissue factor. Or the plaque itself causes turbulent blood flow, increasing chance of thrombosis.

Nicotine causes vasculitis and thus causes turbulence of bood flow!

And obesity?

The various mechanisms by which obesity may cause thrombosis include: the actions of so-called adipocytokines from adipose tissue, e.g. leptin and adiponectin; increased activity of the coagulation cascade and decreased activity of the fibrinolytic cascade; increased inflammation; increased oxidative stress and endothelial dysfunction; and disturbances of lipids and glucose tolerance in association with the metabolic syndrome.
Source: Obesity and Thrombosis — ScienceDirect - http://www.sciencedirect.com/science/article/pii/S107858840600579X

Study group discussion: Virchow's triad

What is Virchow's triad for thrombosis? Explain please.

Virchow's triad... If there is stasis (Blood ain't flowing to wash out the collected coagulation factors), hypercoagulability (More coagulation factors) or endothelial injury (Stuff that activates coagulation factors) there'll be a predisposition to thrombosis.

In Virchow's triad 2 things are missing:
1. Role of platelets
2. Coagulation system

Study group discussion: Most common site of intraperitoneal abscess

Which is the most common site of intraperitoneal abscess?

It's pelvic.

The reason being gravity, common sites are subphrenic, paracolic, pelvic and right iliac fossa.

Pelvic is most common due to pelvic position of appendix and fallopian tubes, and due to leakages from colorectal surgeries.

I had a MCQ asking me to choose between paracolic, subphrenic and pelvic and stuff as options for the most common site.

So in that case, what would be the answer?

Pelvic would be the most common site, according to my teachers.

What is the best way to get to a pelvic abscess sample?

Through rectum? They usually burst into rectum and resolve.

In women, from the umm what do you call it..
Pouch of Douglas!

Nice Ikan :)

I tried so hard to recall the name. Almost blanked out for a moment there!

In women vaginal drainage is done.. Through posterior fornix vaginl drainage in women.

And if the abscess is pointing in rectum, rectal drainage is done.

In males, you would pass a needle through the rectum

Laparotomy is almost never necessary and rectal drainage is preferred over suprapubic which risks exposing the general peritoneal cavity to infection.

Study group discussion: Heparin induced thrombocytopenia and leech therapy

What's Heparin induced thrombocytopenia??

Antibodies are formed in the blood platelets due to heparin in certain individuals. This causes widespread petechia.

You discontinue heparin and give something else in HIT.

Lepirudin
Bivalrudin
Argatroban

And now the cool part :D
The drug Lepirudin is derived from the salivary glands of LEECH!

I know!!!

Haha ain't this cool?

Leech.. Didn't know that!

In school, they used to say if a leech bites you, you die. I never found out the truth though.

Maybe cause it releases these substances in your system..And you are not able to clot inside?

My 12th standard books also mentioned about leech having anticoagulant properties....Now I find out that it's used to prepare drugs!

HIRUDIN is the substance that is secreted by the salivary glands of leech!

I just Googled can a leech bite kill you :D
I don't think they can kill you, they don't take enough blood in a fast amount of time unless you put a few 100,000 on your body and left them there for a while.

100, 000...That's a lot of leech!

Lol I think it was a hyperbole!

I don't remember exactly....but I had heard of alopecia being treated with leech.

How? :O

The leech would suck blood... So keeping them for just the right amount of time they would increase the blood supply... I'm not sure though.

Leech therapy is known to increase blood circulation, therefore when therapy is applied to thinning or bald areas, the increase of blood circulation helps enhance the concentration and delivery of nutrients that assist in making hair follicles strong, thereby assisting in the promotion of hair growth. People suffering alopecia caused by fungal infections or dandruff can also benefit through the antibacterial component in the leeches saliva, which helps combat fungal infections.

It's also used in arthritis :O

The FDA approved the use of leeches in the USA in 2004. In October 2005 the first American hospital 'Beth Israel Medical Center New York' offered Leech Therapy to treat Osteoarthritis of the knee.

Arthritis?! Woah.

Study group discussion: Heparin, warfarin and the anti-fibrinolytics

Name the drugs which inhibit fibrinolysis.

TACA! Tranexaemic acid, amino caproic acid.

Describe the mechanism of action of heparin.

Binds to anti thrombin 3, blocks factor 10.

Which coagulation factors does warfarin affect?

Vitamin K dependent ones: 10, 9, 7, 2, protein C.

Why there is a lag of 2 - 3 days for warfarin to act?

Study group discussion: Management of Parkinson's disease

50 year old male, has no expressions, walks to your office, slowly. He complains of tremor while watching television. He says he can do tasks without the trembling his hands. His fingers keep moving as if he is rolling a pill as he is talking to you. Which drug will you prescribe to relieve his tremor?

It is Parkinson's disease. Anticholinergics will be prescribed.

Why not L-dopa? With carbidopa?

Study group experience #9

What is the kussmaul's sign? Is it seen in cardiac tamponade?

Mitral stenosis auscultatory findings

AV blocks simplified

Enzymes checked through RBCs 

G6PD deficiency and Myoglobinuria

How to study pharmacology (Most requested post ever)

Short course chemotherapy

Pharmacological management of diabetes

Mechanism of atropine induced hyperthermia 

Lepra type 1 and type 2 reaction 

Types of hypersensitivity reactions  (A simple Q&A at the end!)

Studying physiology 

Single Breath Count test in Guillain Barre syndrome

It was my birthday this week (13th February, to be precise). One of the awesomites got to know through Google plus and everyone wished me on my birthday which made it really special. Thanks everyone!

Happy belated Valentine's day everyone! May we all love what we do and do what we love.

I'm unable to access tumblr fan mails and ask messages at the moment. Sorry for the delay! I'll be back on tumblr in mid March but I'll try posting the study group experiences as and when possible!

-IkaN

Study group discussion: AV blocks simplified

Tell me little bit about what do you know about AV Block?

They occur when atrial depolarizations fail to reach the ventricles or when atrial depolarization is conducted with a delay. There are 3 degrees which we can recognize.

First degree consists of prolongation of the PR interval on the ECG (>200 msec in adults and >160 msec in young children).

In second degree, we can find atrial impulses that fail to conduct to the ventricles. And variations like mobitz I and II.

And finally, third degree, where we get multiple P waves that don't conduct at all.

Tell me differences in type 1 and 2 mobitz?

Well, in type I there is a prolongation of the PR interval until it drops and doesnt conduct

And in type 2, there is a constant PR interval and then it drops (:

Poem:
If your R is far from P, then you have a 1st degree.
Longer, longer, longer, drop...Then you have a Wenckebach.
If your PS don't go through, then you have a Mobitz 2.
If your PS don't agree, then you have a 3rd degree.

What's the treatment? For all of them?

First and second degree (mobitz I) only require treatment if they are symptomatic.

Mobitz II and 3rd degree usually require temporary and/or permanent cardiac pacing.

This was fun, thanks for the drawings!

*the drawings of medcomic were shared on the group, you should check them out*

Review question:
Which of the following is not a feature of complete heart block on the ECG:
a) Constant RR interval
b) Constant PP interval
c) Constant PR interval
d) PP interval shorter than RR interval

Answer: C

How to study pharmacology

First, you need to get the concepts right. Speed read and get a big picture, then understand the little details.

I dived into minute things I didn’t understand right away.. Now that I look back, I think I should’ve been patient.
Anyway, lil doubts made great blog posts!
Example: Why is lidocaine preferred in patients with arrhythmias following myocardial infarction?

It’ll take time to get a hang of the names of various drugs.. If mnemonics work for you, you should try making em! Try to put mechanism in the mnemonic to make it simpler (That’s what I do!)
Here are some recent examples of how I make my pharmacology mnemonics -
Antifungal drugs with mechanisms
Antiparkinsonism drugs with mechanisms

There are certain drugs which are unique and that is why remembering mechanism of action or their pharmacological property becomes very difficult :/
I talk about how to remember them in this post --> http://medicowesome.blogspot.ae/2014/06/pharmacology-study-tip.html

I requested my study group awesomites to contribute their tips so that I can share them. Here are the suggestions, tips, tricks, life hacks they told us! :D

One awesome way is to make a self constructed table. Side by side drugs.. Uses. Side effects and specific points. Helps a lot.
- Great tip by Sakkan.

I had small classification charts put up all over my cupboard and wall! I Would revise them at night....Since I found classifications a bit volatile.
- The repetitive memorization trick was submitted by Priyanka. (I made flash cards for the same!)

One useful tip is whenever you see a sachet of drug.. Just read the contents and dosages.
- Awesome tip by Sakkan. (Wish I did that earlier!)

And try explaining uncles and aunties taking them what's going on :D
- I like how Sakkan said, "Try" explaining. (She says she gets a lot off oooo, aaa and even a couple of blank faces too!)

I always discussed pharmacology with my friends, and mostly, taught juniors. You get good karma + revision.
- Manisha (Good karma always helps!)

It is very volatile but this subject manages appear everywhere.. All subjects. Everywhere there are therapeutic drugs mentioned. Makes it really difficult to grab the essence if you don't do pharmacology.
- Sakkan's way of telling us take pharmacology seriously.

I drew small cartoons...Of concepts I found difficult to remember.
- Priyanka (Send us your cartoons soon, girl!)

Book recommendations by awesomites:

A very good book for pharmacology is Colored Atlas pharmacology. For retaining most of it. By thieme. A page of drug and a page of illustration. Very helpful.

And there's at a glance series. Exists for all subjects. Comprises cool diagrams, flowcharts and accompanied with a page of description. Pretty standard text in her very easy format.

Motsbys pharmacology memory note cards. If you like cartoons this little book is great. (It's very adorable.) I have to admit there are drawings which I dont really get. Thats why doing your own drawings also comes in handy :)

I wonder if all international students refer Katzung or whether they have local authors too.
I think Lippincott is the standard, internationally.
Lippincott is simple to understand- standard and interesting book to read.
A book very commonly referred to in India is KD Tripathi.
We have Farrukh Jabbar, here, in Pakistan.

That's all!

I'll keep updating the post, adding new tips and tricks, till then, stay awesome!

-IkaN

Study group discussion: Types of hypersensitivity reactions

*We were discussing lepra reactions when we diverted to hypersensitivity reactions the other day*

I can't remember the types.

Here's a life saver for your soul -  http://medicowesome.blogspot.ae/2012/03/hypersensitivity-types-mnemonic.html

Apparently there is type 5 and type 6 hypersensitivity reactions too.

5? What's type 6? Oh my god.

I had received a long fan mail on it a few days back:
We had a test about 4 days ago on hypersensitivity reaction type 5 and a lot of people left it blank because they thought it was a typo. Well, I later found out that it is the same as type 2 non cytotoxic (In fact, there is a type 6. Can you believe it? ). In situations like this, I always imagine there is a bored researcher sitting in a corner of his office, maybe eating a donut and taking a sip of milk from a beaker or conical flask, who thinks the best pass time activity is to screw around with the heads of medical students. So he gets his iPad, types a whole new ( and sometimes unnecessary) classification, sends it to a journal thus forcing medical students to add one more thing to that cramped up space called the head.

Hahahahha. The fanmail is hilarious. Made my day! :D

Myasthenia gravis? Which type of hypersensitivity reaction?

Myasthenia is type 2. So is Grave's.

Nope. It's Type 5.

Why?

Type 5 is an extension of 2.

It is because of it's blocking antibody, right? Or because it doesn't incite any inflammation?
In that case what would Graves be that antibody is stimulating?

Graves and gravis are caused due to effect of cellular functions. Graves - Increase in cellular functions. Gravis decrease in cellular functions.

"Instead of binding to cell surface components, the antibodies recognise and bind to the cell surface receptors, which either prevents the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signaling.

Some clinical examples:

Graves' disease
Myasthenia gravis

The use of Type 5 is rare. These conditions are more frequently classified as Type 2, though sometimes they are specifically segregated into their own subcategory of Type 2."
- Source: Wikipedia

So type 5 includes autoimmunity, right?

Yes.

I didn't know they had classified it under autoimmunity now. Got it!

Type 6 is Antibody Dependent Cell Mediated Cytotoxicity.. The NK cell stuff.

They kill viruses laden cells and tumors.

Basically, any antibody that causes a effect besides inflammation due to binding to cell receptors is type 5.

Immunology comics on ADCC :D http://immense-immunology-insight.blogspot.ae/2013/10/functions-of-antibodies-simplified.html

Okay, review questions!
Name type of hypersensitivity!

Poison ivy reaction after 48 hours in a camping trip.

Type 4.

Correct!

A person who was given horse serum for something.

Type 3. Type 1 if he presents early!

Good job!

Person underwent a screening test for tuberculosis.
Type 4.

Excellent!

Person develops hemolysis after receiving penicillin.

Type 2.

Oh kid gets a bee sting.

Type 1.

Person with leprosy develops new lesions after starting drug therapy.

Type 3.

Awesome!

Hypersensitivity pneumonitis?

It is both type 3 as well as type 4.

Inhibitors of electron transport chain mnemonic

Inhibitors of electron transport chain mnemonic

Submissions: Vancomycin emotified

This was submitted to us by Priyanka Parekh. Thanks, girl!

Study group discussion: Mechanism of atropine induced hyperthermia

Even atropine high dose causes hyperthermia. But I don't know, the mechanism to it.

Atropine is because it inhibits sweating.

Children are especially susceptible.

Oh.

Study group discussion: Pharmacological management of diabetes

Review question time B)

Name the oral anti-diabetic drugs which increase release of insulin?

Sulphonyl urea.

One more!

Meglitinides such as repaglinide and nateglinide are prandial insulin releasers that stimulate rapid insulin secretion.

So which oral diabetic drugs will you give in a thin person and a overweight one? And why?

Overweight - Metformin
Thin - Sulphonylurea

Metformin decreases gluconeogenesis.

Sulfonylurea have weight gain as a side effect. Metformin have anorexia and weight loss as a side effect.

Which of the oral drugs class is cardiotoxic? Because of which many have been with drawn from the market.

Rosaglitazone.

Correct!

Name the sulfonylureas you know.

Chlorpropamide
Tolbutamide
Glipizide
Glimipiride
Gliclazide
Glyburide

Which of these is most likely to cause hypoglycemia?

All of them?

They all do. Right.. But one of them is most likely to do so.

Glibenclamide. It is the most potent.

Nice to meet glibenclamide :P

Which type of insulin do you give in ketoacidosis?

Intravenous.

Not which route, which type?

Regular.

Correct.

The lente rapid acting type is given.

Which is given in pregnancy?

Regular insulin? The same?

Correct.

Which of these oral drugs have nausea as the main side effect?

Nausea - Umm the alpha glycosidase inhibitor?

They cause hepatitis and flatulence.  So they are generally not preferred so much is what I read.

Nope. It's incretin mimetics. 40-50% patients taking incretin mimetics have nausea

Oh. I didn't know that.

An easy question - Which oral hypoglycemic drug causes lactic acidosis?

Metformin

Correct!

Which drug will you not use in renal failure? Why?

Metformin not used in renal. Same reason.

A patient has an attack of hypoglycemia while on a oral diabetic drug..He eats a spoonful of sugar. But even then he collapses and worsens. What went wrong?

Sugar needs to be metabolized @_@
^Random guesses!

Haha. No.

Must have taken complex carbohydrate. Need to use simpler ones like candy and all.

Yup. Sugar contains sucrose.

Hey I said the same thing.. Needs to be metabolized! T_T
I didn't use complex words :P

Haha! Not a convincing enough answer. But you on the right path.

Awww.
Examiner is strict!

It's okay. One point to R!

Hahaha.

Yay!

The sugar he ain't couldn't be broken down to simple sugars. Why?

He used an alpha glucosidase inhibitor! Acarbose!

Oooo that's interesting.

Correct.

Bang on!

Yaay!

He had to take glucose. Since he took sucrose (table sugar) it didn't help him.

Oh I lost the point now! :O
Nice question!

Haha we're equal now, R :P

Acarbose stops conversion to monosaccharides! So if he is on acarbose and takes a complex carbohydrate for increasing glucose levels, he won't be able to break it. Acarbose is a glucosidase that acts upon 1, 4 - alpha bonds which breaks down starch and disaccharides to glucose.
Sucrose is a disaccharide (table sugar) so yeah.

Easy question - what is the effect of insulin on potassium?

Hypokalemia.

Why is it clinically relevant in a patient with diabetic keto acidosis?

Need potassium supplementation along with insulin. Otherwise hypokalemia occurs. Causing cardiac and other emergency conditions.

Causes insulin causes the uptake of potassium by cells. Therefore, in hyperkalemia, the main line of management is giving insulin along with glucose.

Correct!

Why isn't bicarbonate preferred in patients with DKA?

Good question. I wonder about that answer too.

Tell us?

It causes cerebral edema.

Oh. If given in large doses?

Nope. Not dose related. Only in children though.

Can you explain?

Needed a research paper to back me up -

Adverse effects of bicarbonate therapy in DKA: In essence, possible mechanisms include initial cerebral vasoconstriction and reduced cerebral blood flow from acidosis and hypocapnia, cytotoxic edema, and cerebral injury, followed by cerebral hyperemia, reperfusion injury, and vasogenic edema, coupled with increased blood brain barrier permeability, during the rehydration phase of DKA. Several reports of sudden death following irreversible coma in children and young adults with DKA were published in the 1960s, including development of diabetes insipidus in some, with postmortem findings of CE and neuronal degeneration.

I'll send you the link.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3224469/
Read: Clinical impact of bicarbonate therapy in DKA
The paper is huge, read that specific part.

Thanks!

Multiple system atrophy (Shy Drager syndrome) mnemonic

Multiple system atrophy with orthostatic hypotension is the current classification for a neurological disorder that was once called Shy-Drager syndrome. I'll be sharing a mnemonic for this syndrome today!

Imagine a guy who has urinary incontinence (That's why he is shy!). He puts (or parks) his dagger knife (drager) into his brain (Cerebellum, to be precise).

So the mnemonic goes:
SHy Parked his Drager into his Cerebellum.

S: System atrophy (Multiple system atrophy)
H: Hypotension
Y: Why is he shy? Urinary involvement (urgency/incontinence).
Also remember autonomic symptoms like constipation, sexual impotence, vision disturbances, difficulty breathing and swallowing, sleep disturbances, and decreased sweating.

Parked: Symptoms of Parkinson's disease such as slow movement, stiff muscles, and tremor.

Cerebellum: Cerebellar problems like coordination and speech.

That's all!
-IkaN

Study group discussion: Single Breath Count test in Guillain Barre syndrome

I was reading about Guillain Barre syndrome and came across single breath count test.

Does any one know what is it / how to perform it?

GBS can cause respiratory paralysis. So you do the breath count test to know the level of respiratory compromise. The exact mechanism.. I am not sure..But you ask the patient to take a breath and count as many numbers he can starting from one.

Is it done to measure inspiration or expiration? They say that inspiration is affected in GBS but I think counting is expiration.. So I am confused.

I haven't read much into it..Can't answer that with confidence.

I tried Googling. No satisfactory answers. Maybe someone else in the group knows!

SBC is measured by asking patients to take a deep breath and count as far as possible in their normal speaking voice without taking another breath. It's measure your fvc (forced volume capacity).
Normal values are 40 to 44.

If the patient can count to 10 on one breath they likely have a forced vital capacity of about 1000 ml, if they can count to 25 then the vital capacity can be estimated at about 2000 ml.

Normal fvc values are 3000 ml to 4000 ml.

FVC is sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume.

Meaning SBC value is not just for your inspiration or expiration. But the whole capacity of lung to perform either of the function.

Thank you so much!

Study group discussion: Lepra type 1 and type 2 reaction

Can somebody explain lepra reaction in leprosy?

When the bacteria is killed, it's toxins are released & these toxins exaggerate the lesions.. More painful more red etc..

Lepra reaction 1 and 2?

I know that Lepra reaction 1 is type 4 HR and Lepra reaction 2 is type 3 HR.

Yes, 1 is 4, 2 is 3. The sum should be 5, that was my mnemonic

Oh okay ! Thanks for clearing this!!

This is a good way of remembering! 4+1=5 & 2+3=5!

Mnemonic you have to sum up so that total comes out to be 5
So in Lepra 1 + 4 HR = 5
And Lepra 2 + 3 HR =5

It's similar to the Jarisch Herxheimer reaction in syphilis right?!

Yes, the antigens cause the reaction.

Sometimes it happens when the patient begins treatment and loses faith in the doctor because of the reaction!

Woah! Loses faith in doctor!

Yes, so you have to explain the patient well. Maybe inform about the possibility before hand.

Is ENL the same? Or the severe form of lepra reaction?
Type 2 is ENL.
What's the difference between type 2 and 1?

The 2 is a type 3 hypersensitivity. Meaning deposition of antigen-antibody complexes.

Type 4 reaction is a delayed hypersensitivity due to t- lymphocytes. Which is seen lepra reaction type 1.

Type 1 is mediated by Th1 cells and type 2 is mediated by Th2 cells

In lepra reaction type 1 - there is widespread new lesions all over the body, cause those  Ag-ab reactions get deposited everywhere.

In type 2, the existing lesions become more pronounced, more red.

There are other differences based on extent of nerve damage and blah blah..Which I don't remember!

Treatment?

Aspirin!

Treatment is aspirin, steroids and even an anti leprosy drug, I guess.

Chloroquine.

Thalidomide used to be ...Not used now, right? Thalidomide is completely discarded due to  phocomelia.

Oh no.. It is still used. But strictly avoided in pregnancy.

In which case?

Used in behcet disease, Multiple myeloma.

Thalidomide is used only for type 2 reaction, not type 1.

And which anti leprosy drug was it? Clofamizine?

Yes.

*the discussion went on types of hypersensitivity reactions, which will be continued in the next post!*

Study group discussion: G6PD deficiency and Myoglobinuria

If a person has presents with hemolysis after ingestion of flava beans and dapsone, when will you ask to get G6PD levels?

Study group discussion: Short course chemotherapy

What's short course chemotherapy?

Earlier Tb treatment was given for 1.5 to 2 years, Tb drugs have lots of side effects and patient adherence to such long treatment is not good either. So after various research WHO introduced short course chemotherapy treatment for Tb under the name of Dots which gives treatment for 6-8 months. Good patient adherence and compliance.

Study group discussion: Studying physiology

Could you share with me tips to study pre med subject? Like physiology perhaps?

Physiology is my major, I draw diagrams basically. Understanding the stimulus and response first, then learn the steps in the middle.

Yup, flow charts for physiology!

Physiology is easier when you start at the big picture then elaborate on each pathway.

And make lots of notes. Here's a link on that http://medicowesome.blogspot.ae/2014/12/how-to-make-concise-medical-notes.html

I used to draw a lot of flow charts in physiology..and Youtube, try subscribing to armando hasudungan or medcram..They have nice videos!

Study group discussion: Enzymes checked through RBCs

Why is LDH non specific for MI?

LDH is elevated in many other diseases too!!

There is a much more specific reason for it.

The LDH -2 isoform is present in RBC, any sort of slight hemolysis will increase it as well.

Oh that's why! Didn't have the faintest idea.

Great!! So LDH -2 Isoform is also the one for MI?

Nope it's LDH-1.

But no one gets the specific enzyme type. Too expensive I guess.

I guess electrophorectically you can't differentiate both. Maybe.

Which poisoning is checked through RBC?
Lead!
Basophilic strippling.

Yes, one more!

Cobalt.

Which other poison then?

OPP. Organophosphorous poisoning.

How?

You check the acetylcholinesterase levels in mature RBC.

Which vitamin levels can be checked through RBCs?
Hint: A vitamin that affects enzymes.

Transketolase, Vitamin B1 deficiency.

How does it affect the RBC the transketolase?

Umm it's just a level that can be checked through RBCs. I don't think they do it in clinical practice.

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 (:

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.