Wednesday, March 4, 2015

Study group discussion: HOCM

A young, apparently healthy athlete, while playing collapses to the ground and dies.. Diagnosis?

Hypertrophic obstructive cardiomyopathy.

Right, as always!

Will probably also have family history!

Oh oh review question - what is the site of obstruction in HOCM?

Ventricular septal wall?

Interventricular septum.

Left ventricular outflow is obstructed.

Yup. Basically below the outflow tract of the aorta.

What will happen to the intensity of the murmur in HOCM during Valsalva maneuver?

It will increase. HOCM and MVP are the only two conditions in which a decrease in blood volume to the heart increases the intensity of the murmur.

What's Brugada syndrome??

In Brugada syndrome there's risk of sudden cardiac death.. And it's also genetic..

Oh.. Didn't know. What is the defect in brugada syndrome? In HOCM it is beta myosin I guess.

Some defect in sodium or calcium channels I guess.. Not sure.

Ohh okay. Thanks!

Study group discussion: Differentials of discharge in a pregnant woman

Differentials of 28 week primi presenting with white discharge?

You wanna see for pooling of fluid in the fornices and check for pH.
It could be premature rupture of membranes. It could be stress incontinence. It could also be a normal excessive discharge.

Could it be infection?

Yep, it could be.

Depends on the quantity of discharge.

Um okay..

I had a case on this in my final year university exam
The entire viva went on it!

Mine was normal physiological discharge with oligohydramnios.

Study group discussion: Aortic regurgitation

What are the characteristic physical findings in aortic regurgitation?

You mean the characteristics signs from head to toe?

No, some special findings are present.

Collapsing pulse.

Yes, the water hammer pulse!

It was my viva question. I was asked to demonstrate it!

What else?

Like signs? Like pulsations at nail bed!

Yeah what's that called?

Pulsations at nail bed?

Quinckes sign!

Yes, exactly Quincke.

Hills sign.

The hills sign is the most significant.

What is hill sign?

Low BP in the upper limbs.

Upper limb bp is higher than lower limb.. Or vice versa.

Yup..right.. Cuz there's a difference of >10mmhg in upper and lower limbs..

And obviously, wide pulse pressure.

Plus, there is this austin flint murmur characteristic of severe AR.

Mullers sign - Pulsations of the uvula

Corrigans sign - Carotid pulsation visible

Landlof's sign

Oh landolf's sign is alternate dilatation and constriction of pupil with each heart beat.

I know Mussetts - the head bobbing

Traubes, I think, is shotty femoral pulse!

Lighthouse sign!

Lighthouse sign is blanching and flushing of forehead with each heart beat..

Duroziez - murmur over femoral artery

Locomotor brachii.

What's that?

Oh yes.. Locomotor brachii is the Thickened, tortuous brachial artery on Inspection.. You can see the twitchings clearly especially on the medial side of arm.. It basically indicates hypertension but commonly associated with AR.. I've seen it in patient with AR..

Which is the most diagnostic sign? Which is the most important of all the signs of aortic regurgitation?

The diastolic murmur is diagnostic of all!

Even mitral stenosis has a diastolic murmur! It should be Hills!

In MS, we also have the opening snap.. You need practice to be quick in identifying the psa and opening snap. Where as hills can be diagnosed with a BP cuff!

And there is difference in the sounds too.

Theoretically, we read that.. Frankly, I find it a great achievement if I can only say with confidence whether it's diastolic or a systolic murmur.

True!

Haha that's the truth actually!!

Aortic regurgitation -Soft blowing early diastolic decrescendo murmur.
Heard best at the left 2nd ICS without radiation.
May also hear systolic flow murmur and diastolic rumble (Austin Flint)

Mitral stenosis -Low frequency rumbling mid-diastolic murmur, with presystolic component possible.
Heard best at apex.
Accentuated in left lateral decubitus position.

What's the amount of blood regurgitated in aortic regurgitation?

Its 25% of ejection fraction

In mild AR?

Ya

What about moderate and severe types?

Maybe increases, I have to check.

It does. But since you were specific to say 25% There has to be specific values of the other two classes as well.

In severe, its more than 50%  I think, correct me if I'm wrong.

Will check out my books.

I had an aortic regurgitation case in my finals too.
I thought I was reading the blood pressure wrong but... The diastolic was 20mm Hg.
It can go so low.. The diastolic can even go till zero is what my professor said!

Tuesday, March 3, 2015

Study group discussion: Diabetes

I've noticed one thing with my "swedish" medical book.... It always give glucose values in ( mmmol/l ) and not ( mg/dl )

fP-Glucose > 7,0 mmol/l
How much mg/dl is that ?

The conversion factor is   mg/dl= 18 x mmol/l
So 7mmol/l is 126mg/dl
I'm actually majoring in pharmacology :) we had a lot of those ^^

HbA1c < 52 mmol/l = 6 %
For diabetes type 1
Hemoglobin A1c level should be held at 6%
I'm reading about diabetes type 1 treatment
And it's written here HbA1c level should be held < 52 mmol/mol
equals to 6%

*a conversion table was posted on the group by someone which sorted this dilemma*

That might be possible but for the diagnosis it is >6.5

You don't use A1c for diagnosis. It is used only for evaluating control over the last few months!

But now if it's >6.5 he is diagnosed diabetic.

Umm but.. Why would you use such a test when there are better screening tests?

Ummm its part of one of the criteria for diagnosis!! Though getting fasting samples and all are easy but you have to make the patient fast right!! In this one benefit would be take the samples anytime!

Oh yep.. Makes sense!

A diabetic patient is undergoing contrast angiography for some reason. He was asked to stop his oral hypoglycemic, metformin before the procedure. Why?

Lactic acidosis.
Renal failure will worsen it.
Contrast leads to renal damage.

Correct! You are concerned about lactic acidosis. Even slight renal failure due to the dye will precipitate lactic acidosis!

A diabetic patient controlled on Insulin develops fainting episodes. On investigations, he was found to have an elevated creatinine. What is the mechanism for the hypoglycemia?

Insulin excreted renally?

Yes, the half life of insulin is increased in renal failure!

A nurse presents with hypoglycemia. Her insulin levels are up but C peptide levels are low. Diagnosis?

Taking exogenous insulin.

Alright. You confront the patient and goes into counselling.

Now the same patient comes with hypoglycemia but this time her insulin and C peptide levels, both are elevated!
What happened this time?

Using sulphonylureas
Oral diabetic drugs - Glipizide, glimipiride, glyburide

Correct! How will you prove it?

proInsulin levels? Just guessing don't know that!!

U/A

What's u/a?

U/A is shortening for urine analysis

Correct! Urine for Sulfonylureas

If the urine test came negative, what could it be?

Insulinoma

And he scores again!

Wonderful questions!!

That'll be all for today!

Thank you for the great questions IkaN.

Never thought questions would be this much fun!

*After which someone else asked us a few review questions based on what he had studied! *

Which antidiabetic drug can lead to SIADH?

Chlorpropamide

I would take that!! All sulphonylureas lead to SIADH.

Ok one more!! How would you access severity of diabetic ketoacidosis?

*since no one could guess, we were given hints!*

Let me put in this way.. Which electrolyte would you Check in serum to access severity of DKA?

If you had to check just 1.

Bicarbonate.

Yes!!!

Why bicarbonate?

Because it is acidosis

Yes, you are right!!

Low bicarbonate would lead to what? This one entity is very important in DKA management!  If this is corrected patient is well and good!! Some difference in the cations and anions!! What's that called?

Anion gap

Yes, it is!! Finally!!

This anion gap is very important.

What the normal value?

10 to 15

Does this gap increase or decrease?

Increases.

ABG would tell is about acid base imbalance.

How does neuropathy occur in diabetes? What's the mechanism?

Occlusion of small venules?

Damage to autonomic NS..?

Microvascular occlusion?

Yes, nerves themselves have a supply of blood vessels. Diabetes damages these small blood vessels, thus decreases supply to nerves!!

You all were correct!!

I've read somewhere that sorbitol deposits also damage nerves?

Lens! It causes cataract.

Alright guys!! That's it!! I can't remember any more!!

Any mnemonics?

Here are all the study links!

http://medicowesome.blogspot.ae/2015/01/oral-hypoglycemic-drugs-and-weight.html

http://medicowesome.blogspot.com/2015/02/study-group-discussion-pharmacological_15.html

http://medicowesome.blogspot.ae/2015/02/study-group-discussion-metformin-and.html

http://medicowesome.blogspot.ae/2015/02/study-group-discussion-cardiac.html

http://medicowesome.blogspot.ae/2015/02/study-group-discussion-type-3-diabetes.html

Study group discussion: Pre-eclampsia and HELLP syndrome

Anybody up for discussion on eclampsia? :D

What is cause of right upper quadrant Pain in HELLP syndrome?
Stretching of the liver capsule.

What's the earliest sign of pre-eclampsia?
It's excess weight gain.

Why?
Due to retention of water.

Study group discussion: Electrolyte abnormalities that cause constipation

Q) Which electrolyte abnormalities can lead to constipation?

My friend says calcium.

Yes, hypercalcemia.

He screamed in my ear because he got excited :L

Hahaha

Hypercalcemia
Hypermagnesemia
Hypokalemia
Hypophophatemia

How does hypercalcemia lead to constipation??

Hypercalcemia increases the action potential threshold and hence decreased contraction n peristalsis.

Sounds good!! Thanks!!

Study group discussion: Chionablepsia and Anisakiasis

Learnt some new words today!
Chionablepsia - its inflammation of eyes due to UV rays!

What a word. I can't even pronounce it!

And this word has no -itis😃

They should've come up with uv-eye-itis instead! :P

Hehe

One more!

Anisakiasis !

A parasitic infection by anisakid (nematodes)

What does this parasite infect?

Stomach walls!

Caused by ingestion of larvae...say, by consuming infected squid or fish

Since it affects the stomach walls, wouldn't bleeding or abdominal pain be most prominent symptoms?

Nothing special ....abdominal pain, nausea, vomiting, diarrhea.

Oh alright!

Deceptive appearances.

A few medical conditions have presentations that are more or less the same to a layman but in reality, are polar opposites of each other. There are though, a few subtle clues which help in differentiating these conditions. Some of them are as follows-

1. The Somogyi effect and the dawn     phenomenon.
These are the conditions which occur in diabetic patients which are undergoing treatment.

In the Somogyi effect, there is a rebound hyperglycemia (in the mornings) following hypoglycemia(during the night) due to the release of counter regulatory hormones.

On the other hand,the dawn phenomenon is characterized by morning hyperglycemia due to inadequate insulin dosage. It may be a possibility that the raised blood sugar is due to nocturnal GH release or increased insulin clearance in the mornings.

So, what does the patient think? That the treatment is not working, is inadequate, but the reality may be starkly different.

To pinpoint, the patient may be asked whether he feels excessive hunger during the night, experiences persistent nightmares or any other symptom during night pertaining to hypoglycemia.

3am and morning blood samples reveal hypo and hyperglycemia in the case of Somogyi effect, while hyperglycemia both the times with dawn phenomenon.

Hence, the modification in Somogyi effect is actually to decrease the insulin dose and increasing it if the patient has dawn phenomenon.

2. Anorexia and Bulimia nervosa.
Both these conditions are characterised by the patient having weight concerns and multiple episodes of self induced vomiting ,laxative abuse or extreme exercise and fasting.One might get confused as to what exactly is the underlying condition.

The primary difference between the two according to me is the patient's attitude and the quantity of food consumed.

Anorexics are primarily worried about their weight(they tend to be ballet dancers or actresses) and hence consume very less amount of food to begin with and vomit out or use laxatives to get rid of whatever is consumed. The patient tends to be almost emaciated, they have a distortion of the bodily image and beliefs that they are still overweight.

Bulimia patients too, engage in similar kinds of behaviours to lose calories but these are more driven out of guilt rather than extreme weight concerns,they usually have a normal weight.The patients have a sense of achievement that they can eat whatever they want and in any quantity until they are losing calories through vomiting, excessive exercise or laxative abuse. Contrary to anorexia, patients have episodes of binge eating then compensatory behaviours followed by hunger and then again binge eating.


Monday, March 2, 2015

Study group discussion: Difference between antibody and anti-toxin

What is the difference between an antibody and an antitoxin? Wikipedia says that antitoxin is also an antibody. But what's the difference between the two?

And if we take a vaccine, what is formed-an antibody or an antitoxin?

My understanding is a toxin cam be an antigen. An antigen is not necessarily a toxin. So an antitoxin can be an antibody, but not all antibodies are antitoxins.

Anti-toxin is something that neutralizes the toxins released by bacteria. Ex: Tetanospasmin released by Cl. tetani.
These conditions are life threatening acutely.. So you give pre-formed anti-toxin from horse serum or from multiple plasma donors.

Anti-toxin are antibodies. But you need to remember it is especially for neutralizing toxins released by bacteria.
Whereas, antibody is a very vast term. They can be formed against the cellwall of bacteria as well as one's own antigens (autoimmunity).

Multiple plasma donour means from many organisms?

When people donate blood, the antibodies from several of these people's blood is collected and given

Good explanation, Sakkan!

Study group discussion: Aspirin

Which is the classical triad of aspirin poisoning?

Idk the triad though... I just know some symptoms.

What are the symptoms?
Dehydration
Petechiae
Fever

The triad is hyperpyrexia, confusion and later death.

Death? :O

A very rare case.

Death is due to Respiratory collapse.

Fever? A drug used for pyrexia causes fever :D

Haha ironic, yes.

Pyrexia because of uncoupling of oxidative phosphorylation.

Yep. The energy in ATP gets disseminated in the form heat.

What is the treatment of aspirin overdose?

No specific antidote.
Symptomatic.. Cooling.
Vit k - For petechiae.

Increasing urine pH.

Right on! Aspirin is a weak acid.. Hence you increase its ionization to reduce absorption.. By giving sodium bicarbonate!

Yes!! Alkaline diuresis it's called!

Aspirin you just manage patient. Give iv fluid, increase urine pH, dialysis.

Dose of aspirin for prevention of MI?
Dose of aspirin in ongoing MI?

For prevention it is 81-160
For ongoing.. It is 160-325
Moving on

Why salicylates are contraindicated in children?

Reyes syndrome. They result in increase in liver transaminases plus encephalopathy.

Especially, when used for kids with viral fever.

Study group discussion: Cycloserine

I just came to know that One of the important side effects Cycloserine is suicidal tendencies!

And Cycloserine is used in MDR TB.

Exactly.

Does it have any other uses? Apart from TB?

Mental retardation... I searched online.

Hmm.

The person with MDR TB...Dies of suicide more often.

Now we know why!

No other infections?

Certain UTIs. It's antimicrobial action is due to inhibition of bacterial cell wall.

I see.

Study group discussion: Lymph nodes in various diseases

Characteristic lymph nodes in diseases:

Matted- Tuberculosis, LGV

Rubbery- Hodgkin's lymphoma.

Shotty- Syphilis.

Hard, fixed - Malignancy.

Do you know any more? Let us know in the comments section below!

Study group discussion: Biceps femoris reflex

Does anyone know what biceps femoris reflex is?

Biceps femoris reflex is a highly sensitive and reliable clinical tool for evaluation of the S1 spinal reflex pathway in radiculopathy.

It's the contraction of biceps femoris muscle when it is tapped on the lower part of its head just above its attachment on the head of fibula, with the limb slightly flexed at hip and knee.

Hope this helps :)

Thanks!