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.