This was submitted to us by Priyanka Parekh. Thanks, girl!
Sunday, February 15, 2015
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?
Saturday, February 14, 2015
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.
Friday, February 13, 2015
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
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
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
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
-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
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!
Thursday, February 12, 2015
Study group experience #8
Here's what we learnt!
Vasculitis (Question and answer discussion. Must read!)
Kawasaki disease quiz!
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!
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