Study group discussion: Venous ulcer

*a picture of an ulcer was posted on which this discussion took place in the group*

Which side is the lesion on? Medial or lateral?

If it is medial, it can be venous ulceration too! Mass obstructing the venous outflow.

Yup could be as it is superficial.. And also it could be venous ulcer because it looks like the ulcer is in gaiters area..above the medial malleolus..

What is gaiters area?

Gaiters area is where venous ulcers are usually seen. Above medial malleolus!

Where there is highest preasure in vein due to gravitational pull! And incompetent valve also in varicose vein

What's the name of the perforator in that area?

They are cockett boyd dodd and hunter from below upwards.

I have a mnemonic for the perforators

Do share!

http://medicowesome.blogspot.ae/2014/09/types-of-perforators-of-lower-limb.html

Study group discussion: Kartageners syndrome

What is Kartagener syndrome?

Immotile cilia syndrome

May result in Situs inversus
Bronchiectasis
Sinusitis

Glue ear too!

Infertiliy? Sperm motility is also affected i guess

Sperm motility is affected.
The protein involved is 'dynein'.

I've seen a case of Kartageners in my hospital. The auscultation and looking at radiographs was fascinating!

Study group discussion: Gallstone ileus

*a picture of gall stone ileus was posted in the group as guess the diagnosis after which this discussion took place*

Commonest position of obstruction by gallstone in ileum

Ileocaecal junction?

Not ileocaecal valve. The position in books have been mentioned terminal ileum. A little proximal to the ileocaecal valve.

Most commonly, obstruction occurs at the distal ileum.

I didn't know gallstone ileus could be this big. I imagined them to be tiny!

Me too!

I've heard there has to be a fistula for the stone to be that big to obstruct the ileum. Something that connects the gall bladder to the intestine.. Because a stone this big wouldn't pass the common bile duct

I agree with IkaN

Yup I'm sure the patient suffered from a fistula too..

It enters the intestine through cholecystoduodenal fistula commonly..

I've heard my resident mention fistula once

Yep.. And the predisposed patients are those with Crohn's disease! Thanks, just wanted to confirm it :D

Large stones, >2.5 cm in diameter, are thought to predispose to fistula formation by gradual erosion through the gallbladder fundus...

Ohh that makes sense! The huge stone itself causes fistula formation which is why they are common!

"A fistula develops between a gangrenous gallbladder and the duodenum or other parts of the gastrointestinal tract, allowing passage of the stone. Occasionally the stone may enter the intestine through a fistulous communication between the bile duct and the gastrointestinal tract."

Study group discussion: Colorful amino acids and pH

Colorful aminoacids?

Donno. Maybe tyrosine because they add pigment?

Trytophan phenylalanine tyrosine. Tryptophan is major!

They add color to us! Makes sense. At first, I have to admit, I was imagining colors of the rainbow xD

Yeah and remaining are colorless!

At physiological pH what is the charge of amino group and Carboxyl group?

Positive amino negative carboxyl
PANCard

That's a good mnemonic! Will never forget this!

I just remember histidine is the one who is neutral at physiological pH.

Name the positively charged amino acids!

Basic are positively charged I guess. Histidine lysine arginine.

Mnemonic! http://medicowesome.blogspot.ae/2013/11/amino-acids-with-electrically-charged.html

IkaN mnemonic wow <3
Lady gaga is always negative hahaha!

Study group discussion: Cytochrome c

What is moonlight effect of cytochrome c?

Sounds interesting!

Cytochrome c in cytosol cause cell death by apoptosis. Cytochrome c in mitochondria helps in electron transport. This dual function!

Ooo.. Yes, the life maintainer and the killer! Why moonlight though?

Moon light means a job on the side, one that you wouldn't wanna disclose.
I have a question, what is the differences between cytochrome c1 and cytochrome c?

I think cyt c is mobile and the other is not.

Yep.

Study group discussion: Agranular cytoplasmic reticulum

What are the functions of agranular cytoplasmic reticulum?

Synthesise lipids, transportation of proteins,enzymes for detoxification of drugs,enzymes of glycolysis.

Study group discussion: Atrial septal defects - Why do they present late?

Why do ASD present later in life?

You mean atrial septal defects?

Yup.

The left atria is stronger than the right, so it's a left to right shunt, initially (Oxygenated blood getting more oxygenated kind of shunt.)
This is why, ASD is acyanotic at birth. It won't present till there is pulmonary hypertension (The lungs get fed up of the excess blood!)
This will cause a reversal of shunt - turning it into right to left. (Now, the deoxygenated blood is getting thrown into circulation!)
This reversal is also known as Eisenmenger's syndrome.
This is why, ASDs present late in life.

Okay.. So I think the compensatory mechanisms make up for the disturbances in circulation in early years but fail later hence the features appear later..

Also the atria contribute very little as compared to the ventricles.

Atrial defects are usually very small thus, less complications in infancy. And also murmurs heard in ASD are not very loud, so its difficult for a physician to detect it.
I think, it becomes complicated due to development of Eisenmenger syndrome in later years.

Yes.. And the patient hardly survive 5-6 yrs after development of Eisenmenger syndrome..

Sometimes, ASDs never get severe enough to present as a heart disease. A paradoxical embolus is the initial presentation of an ASD in some cases!

Study group discussion: Cardiac embryology and fetal heart sounds

Cardiac Embryology review question! Which blood vessel does the 6th arch artery give rise to?

Pulmonary arteries!

Common carotid artery derived from..??

3rd arch

Right!

Here's a mnemonic on the derivatives of arch arteries http://medicowesome.blogspot.ae/2013/11/aortic-arch-derivatives-mnemonic-images.html

The coronary arteries develop from which structure?

From aortic sinuses of valsalva..??

Endothelial tissue grows out of the aortic wall and connects with the subepicardial vessel plexus while the heart is developing to form coronary arteries.. Is that right??

Ya.. At first the cells are derived from venous sinus  then they transform to become arteries.

When does heart start pumping ?

I am guessing its 4wks?

First heart beat by 4 weeks!

When does the fetal heart beat for the first time in utero? And when is the heartbeat detected by ultrasound? I know 4 weeks is when the heart starts pumping but is it the same time we detect through USG?

I think there are 2 different terms!!
Fetal heart motion around 5-6 weeks
Fetal heart sounds can be heard around 8-10 weeks

Ohh.

Fetoplacental unit establishes around 21-22 days following fertilization.
Fetal heart motion: 9 weeks by doppler USG.
Fetal heart sounds 18-20 weeks by stethoscope.

When does the  fetal movements start?

18-20 weeks?

That's probably right. I know mothers start noticing moviments from 20th week on. a bit later if it is their first child and they don't how to recognise the sensation.

Yep. Multigravidas appreciate fetal movements earlier than primis

In 16 to 18 wks - That's for multigravida.

But fetal movements start at 8-9 weeks. They are perceived late I guess!

In what case foetal heart fails to mature enough such that we can't detect sounds even at 8w?

One case would be hydatidiform mole. No heart sounds heard.

I don't know what is a hydatidiform mole.

Hydatidiform mole isn't a fetus. It's a edematous condition of the Placental villi. You'll learn this is second year, Pathology!
There is no fetus or fetal parts. Not compatible with life... You'll have to read it up from books.

Here are some study links!
Embryology and gestational trophoblastic disease 

Difference between complete and partial mole mnemonic

Hydatidiform mole (Complete vesicular mole) mnemonic

Why is such a gap between starting of heart beats and its detection by US ??

I mean heart starts beating at around 4w and heart beats are detected at around 8w .. why so ?

That's a very interesting question.. But I have no idea regarding that!

Theories:
Maybe because motion is there but structurally heart is immature so no sound is there (av valve)

I think we don't have equipment to detect faint sounds. We could detect heart sounds along with the motion if we had the technology!
Maybe you guys will invent a fetoscope that detects it earlier in the future! :D

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!

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.

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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!

Study group discussion: ACE in lung diseases

Can anyone please explain why Serum ACE is elevated in Sarcoidosis?

ACE activity is increased in sarcoidosis, a systemic granulomatous disease that commonly affects the lungs. In sarcoidosis, ACE is thought to be produced by epithelioid cells and macrophages of the granuloma.

Serum ACE also appears to reflect the activity of the disease so we can estimate the severity or response to treatment..

You mean : Higher the ACE level , more the disease severity?

Yes.. Higher the level more the severity.

Got it . Thank yoh!

Both TB and sarcoidosis has increased levels of Adenosine Deaminase but Sarcoidosis can be distinguished from tuberculosis by serum ACE levels (In tuberculosis, decreased levels of serum ACE.)

Woah.

Study group discussion: Drug for neurological manifestations of Wilson's disease

Review question-
Which drug is used for neurological manifestations of Wilson's disease?

Penicillamine (cuprimine and depen) and trientine (syprine and trientine dihydrochloride).
Both of these drugs act by chelation of binding of copper, causing it's increased urinary excretion.

Yes, but any specific drug for neurological involvement?

It's Ammonium tetrathiomolybdate.

Glycogen storage diseases mnemonic

Hey everyone! Long time no see!

I was requested mnemonics for glycogen storage diseases recently so I thought I'd write about it -

Glycogen storage diseases from 1-6 are:
von Gierke's disease
Pompe's disease.
Cori's disease
Anderson’s disease
McArdles disease
Hers disease

The memory aid for remembering this one is actually a dirty mnemonic, I found it on tumblr (Can't remember where I read it!)

Anyway the mnemonic is -

Viagra
Pills
Cause
A
Massive
Hardon

Also, heart pumps (Pomps) blood. So that's how you can remember that the heart is affected in Pompe's disease!

And for the enzymes -

Glycogen storage disease type 1 mnemonic:
Geirke - Glucose 6 phosphatase. Both have a G!

Glycogen storage disease type 2 mnemonic:
The Pompe's disease mnemonic is a drag but for whoever this helps.. Do you guys know about the volcanic eruption in Pompeii?
The fires of Pompeii makes me think of acid (burns-fire-acid?) and how it killed children.
So acid alpha-glucosidase and affects children!

Glycogen storage disease type 3 and 4 mnemonic:
Mnemonic for Anderson’s and Cori’s is, "ABCD"
A-B(ranching)
Anderson’s - Branching enzyme.
C-D(ebranching)
Cori’s - Debranching enzyme.

Glycogen storage disease type 5 mnemonic:
Muscle phosphorylase for McArdles. Both have a M in the name!

Glycogen storage disease type 6 mnemonic:
LivHER. So Liver phosphorylase is affected in Hers disease.

That's all!

Hope you're having a wonderful time  and see you in the next post xo

-IkaN

Study group discussion: Thyroid surgery practicals viva questions

Anyway, speaking of triangles of the neck.. Do you guys know they are super important for surgery vivas?

I have surgery viva coming up !!

Omg. If you have a thyroid case, they are bound to ask you this!

I have thyroid - surgery review questions :D

Who is father of thyroid surgery?

Answer: Kocher

Which artery is ligated in thyroid surgery?

Answer: Superior  thyroid artery

Why don't you ligate two?

Answer: Superior thyroid artery is only ligated. The inferior one is left. If you ligate the inferior thyroid artery, the two inferior parathyroids will necrose. Hence the current dictum is not to ligate the ITA.

What about which artery to be ligated near the gland and which one far?

Answer: You ligate STA as near to the gland as possible to avoid injury to the nerve which runs along with it.

Differential diagnosis of midline neck swelling?

Thyroglossal cyst and thyroid are the common ones.

Thyroglossal cyst is embryological remanant of?

Thyroglossal duct.

Most early cause of respiratory difficulty postoperatively?

It's tracheomalacia. Immediately as soon as you withdraw the ET tube.. The trachea collpases. 

Reason?

Tracheomalacia is an inherent condition of weakness of the tracheal cartilage. The thyroid keeps it patent. After thyroidectomy, it might collapse. 

Interesting.. Didn't know this!

Which thyroid cancer can form renal stones?

Medullary. Due to calcitonin. 

At abnormally high levels, it increases urinary excretion of calcium causing renal stones. Medullary carcinoma can also present with hypocalcemia. 

In thyroid surgery, why are we ligating middle thyroid vein first?

To prevent metastasis or to prevent formation of seedling in case of cancer.

Can anyone please elaborate why hyperthyroidism causes oligomenorrhea and hypothyroidism causes menorrhagia?

Hypothyroidism increases TRH.
TRH increases prolactin.
Prolactin decreases GnRH.
GnRH decreases LH and FSH.

What are the complications of multinodular goitre?

Complications of MNG - Due to obstruction - Dyspnea, dysphagia.
Malignant change, calcification are also complications.

Thanks :) 

Study group discussion: Pressure and volume reservoir in the human body

Why arteries are labelled as pressure resevoir?

All artery..especially, arterioles are the main site of pressure regulation.
Veins on the other hand are called capacitance. They store at a time 60% of the total blood volume.
Therefore arterioles regulate the pressure.  On the other, hand..Veins monitor the volume of blood reaching the heart

I think that is true.
And vein also called main blood resevoir.

I found out a good explanation on - Why arteries are known as pressure reservoirs?

Arteries also contain an elastic layer in their walls. Elastin is a protein fiber that has elastic qualities. During systole, large arteries distend with blood as their elastic walls stretch. During diastole, the walls rebound, thus pushing blood along. In this way the arteries act as a pressure reservoir that maintains a constant flow of blood through the capillaries despite pressure fluctuation during the cardiac cycle.

Veins on the other hand, are known as blood reservoirs.

Veins are larger and more compliant (stretchable) than arteries, thus they can hold more blood. In fact, the veins act somewhat like a blood reservoir, containing 60% of the total blood volume at rest.

Study group discussion: Morphine and atropine

* Our discussion started with this: Acute LVF management
LMNOP:
Lasex (frusemide)
Morphine (diamorphine)
Nitrates
Oxygen (sit patient up)
Pulmonary ventilation (if doing badly)*

Morphine used even in the absence of infarction?

To treat severe pain.. Morphine is powerful analgesic.

Yes, but in which cases other than MI, pain is a significant symptom?

Post surgical pain, Cancer pain.

Morphine is indicated in only acute stabbing visceral pain. Except in abdominal emergency's.
Abdominal emergencies if due to biliary spasm. Give nitrous oxide. Or else pethidine.

Even for abdominal pain, if it's severe once after the examination of abdomen.

No, we don't use morphine in abdominal emergencies.

I think we do apart from biliary conditions.

Posting this again, since it's relevant. Opioids, morphine mnemonic http://medicowesome.blogspot.ae/2014/04/opioids-and-other-analgesics-mnemonic.html

Biliary spasm is due to contraction of sphincter of Oddi. Right?

Yep.

Is morphine used alone in biliary spasm??

No, no. It's specifically contraindicated in acute abdominal pain. Because it cause biliary spasm.

Yes, but if used along side of some particular drug it releives spasm.. What drug is it??

I think it's atropine.. Is that right?

Yes!

Atropine is used with morphine for treatment of renal and biliary colic.. Morphine alone may aggravate pain by causing spasm of sphincter of oddi.. Atropine relaxes the smooth muscle of gallbladder and increases the intrabiliary capacity and counteracts the spasmogenic effect of morphine..

I was asked this in a viva, why is atropine given before procedures like drainage of pleural effusion aka pleural tap?

Ummm don't know!!

Okay, I'll give you a hint.. What will happen when you push the needle into the patient

Bleeding?!

And?

Bleeding is minor, think of other things!

Atelectesis?!!

Think Neurologic.

Shock?

Yep. Vasovagal shock. That's why atropine is administered half an hour before the procedure.

Oooh.

Wow! Didn't know that!!

This should apply to all procedures then!

Yes, all procedures. But I was asked this specially because my case in finals was pleural effusion.

Thanks IkaN!

Study group discussion: Central trachea in pleural effusion

In which pleural effusions the trachea is central??

Bilateral ??

Okay.. But in which unilateral conditions?

Due to bronchogenic ca?
When there is pull + push of trachea, nullifying it?

Umm.. It's because of mesothelioma

Why?? I mean why specifically I'm mesothelioma?

If pleural effusion is because of mesothelioma then the negative pressure created by it doesn't effect that much... Sorry.. Don't know exactly.. I'll let you know..

In absorption collapse such as in bronchiogenic ca or foreign body impaction,
Bronchus is obstructed, intrapleural pressure remains negative and trachea is shifted to the same side.

In cases of compression collapse due to pleural effusion, pneumothorax or hydropneumothorax,
Bronchus is patent, intrapleural pressure is positive n so trachea is pushed to the opposite side.

So, if there is bronchogenic ca with pleural effusion, both mechanisms take place,
If pulling effect by bronchogenic ca plays more, trachea remains on the same side of effusion.
If both plays equally, trachea remains in central

Ah.. Push and pull which I mentioned earlier. Thanks a ton!

Study group discussion: Scissoring posture

1 and a half year old child when suspended by the axillae, his legs maintain scissoring posture. What can you think of?

Cerebral palsy!
Or UMN lesion!

Which type?

Spastic diplegia

What is the reason for such kinda posture?

Scissoring is a sign of hypertonia.

Patient tone is increased!!

Yes

Everything related to UMN lesion

Spasticity, hyper reflexia, upgoing plantar.. You will see in this patient!

What can be the possible treatment?

Baclofen + physiotherapy.
A pillow or ball between the legs while sleeping!

Yeah, baclofen will relieve the spasticity.

Study group discussion: Cutaneous signs of insulin resistance and lipoproteinemia

These are skin tags. What do you think of when these are present?

Aren't these harmless with no associated risk?

Nope. They represent something! Ok! These are signs of insulin resistance!

What are other cutaneous signs of insulin resistance?

Acanthosis nigricans

Yes!!

One more.. Although that one is associated with hyperlipidemia too.

Xanthelasma?

Yes!!! Xanthelesma.

Since we are on hyperlipidemia http://medicowesome.blogspot.ae/2013/08/how-to-remember-lipoprotein-disorders.html

So cutaneous signs of insulin resistance include:
Skin tags
Acanthosis Nigricans and
Xanthelesma

Mnemonic: SAX!

In which condition do you see orange tonsils?

Rifampicin intake?

Haha nope. It's related to the topic.. A high cholesterol condition!

Lol no idea then!

Tangier disease.. It's due to lack of cholesterol transporter gene. The disease is characterized by atherosclerosis, hepatosplenomegaly, polyneuropathy and orange tonsils.

Ohh!!!

Another review question.. Why is type 1 lipoproteinemia associated with pancreatitis?

Short of knowledge on this topic maybe someone else would answer it?

It's because chylomicrons obstruct the pancreatic duct.

Study group experience #13

Ligamentum venosum and ligamentum arteriosum

Shift to left 

Uncouplers of oxidative phosphorylation 

What does emulsification mean in fat digestion 

Chagas disease 

Parasites that cause carcinoma of the gall bladder 

Lemierre's syndrome

Acute lymphangitis

Chain messages 

Alcohol and sex

How and when do children understand the concept of death

Abnormal breath sounds: Crackles, Wheeze, Rhonchi and Stridor 

Mechanism of tet spells 

CHARGE syndrome and related case 

Pfeiffer disease and Pfeiffer syndrome

Heyde's syndrome 

Fontanelles and thyroid hormone

Fixed specific gravity 

Neurological emergencies and isoniazid overdose 

Medial medullary syndrome and crossed paralysis

Locked in syndrome and total locked in syndrome

Cool fact about optic nerve

Marcus gunn jaw winking syndrome and Ptosis

Relative afferent pupillary defect (Marcus Gunn pupil) vs Optic nerve lesion

Water intoxication syndrome

Hernia

Varicocele

Leriche syndrome

45 centimetres in length and tubes

To vaccinate or not to vaccinate

Non contraceptive uses of condom

Hyperuricemia

Drug causing hypertrophic pyloric stenosis

Beta blockers

Drug therapy for asthma

Low molecular weight heparin vs unfractionated heparin

Thiazides

Fluoroquinolones

Cool fact about GLP 1 agonists

Phew! That was a lot, was it not? So much more to come! I could create a separate blog for these xD

We also reached 100 awesomites in group 2! Yaay!

Which also means new comers will have to wait till there are enough awesomites to form group 3. Sorry for the delay!

How sign up for the study group

Study group discussion: Relative afferent pupillary defect (Marcus Gunn pupil) vs Optic nerve lesion

*A picture was posted on the group on which this discussion took place.

Description of the picture for the readers convenience:
In the first picture, we see normal pupils.
In the second picture, light is shone in the left eye. Right and left pupil constrict.
In the third picture, light is shone in the right eye. Right and left pupils do not constrict.
In the fourth picture, light is again shone on the left eye and again, both pupils constrict*

RAPD?
Also know as Marcus Gunn eye!
Aka prostitute's pupil :P

Nope. Optic nerve is affected on the left side. As there are absolutely no afferents from left eye, indirect is absent.

Yes.. The 3rd nerve efferent is intact and optic nerve is affected.

There is crossing of the afferent fibres of each eye. That's why when you stimulate one eye the other eye also dilates via the efferent fibres. That's how the other eye also constricts (indirect). In this picture, there is complete afferent defect. The optic nerve is completely transected.

Why not RAPD?

In RAPD, when light is shone to the diseased eye, direct absent.. Therefore, doesn't constrict.
Mnemonic: Direct Diminishes in a Diseased eye, indirect present.

RAPD is diagnosed by swinging light test. When you alternate the flashlight.. The affected pupil ( less number of afferent fibres ) has a release phenomenon and dilates instead of constricts. The affected pupil initially constricts..But when you swing the flashlight repeatedly it dilates. The pic hasn't shown frequent swinging. And the pupil remains dilated in the first go when the light is shown. So there is no relative afferent defect.

I haven't heard of the release phenomenon, I've thought it's because relative to the normal eye, the disease eye appears to dilate. It always constricts but because you compare it with the normal eye, it seems to dilate.

But why do we call it relative? The direct being present and the indirect being absent?

I dont think we call it relative cause efferent is intact. We call it relative cause, relative to the normal eye..The affected eye has reduced optic nerve fibres. This is done to detect early loss of fibres in optic neuritis.

I'm such type of patient. I mean my left optic nerve is affected.

Really? How were you diagnosed and when?

I met with an accident. It was a severe injury on left  eye. 3rd nerve got damaged at first. Doctors said it's severe. It will heal with time. But doctors were not sure it will heal completely or not.

Oh I'm so sorry!
Can you see?

After 1 yr, I again went for checkup.. Doc said 3rd nerve is alright now but optic nerve is affected due to increased stress. Now, I have only partial vision left eye. It's 6/24 (Normal is 6/6)
And it'll not heal completely for whole life.

Optic field shows that the person can't see through different angles with the defective eye. That's why, it's called Partial Vision.
Because of damage to optic nerve.. Healing depends upon the degree of damage. Meconerv Forte is the medicine for that.. But chances of complete healing are rare..

Difficulties make us more strong! Just keep going no matter what.

Yeah, of course. Thanks!

Study group discussion: Marcus gunn jaw winking syndrome and Ptosis

Interesting one - congenital ptosis associated with winking motion of the affected eyelid on the movement of the jaw. Known as Marcus gunn jaw winking syndrome.

On opening, side ward movements of jaw, increase of palpebral aperture!

Usually jaw movement to opposite side! Jaw winking.

What are the causes of Ptosis?

Neurologic causes of Ptosis include Horner's syndrome, in which the pupil is constricted, and third nerve palsy, in which there are abnormalities of eye movements and the pupil may be dilated. Local causes include congenital and acquired disorders of the levator muscle complex and tumors and infections of the eyelid. Myasthenia should always be considered.

Study group discussion: Medial medullary syndrome and crossed paralysis

Which of the following are clinical features of medial medullary syndrome?

A. Ipsilateral numbness of arm and trunk
B. Horners syndrome
C. Ipsilateral 12th cranial nerve palsy
D. Contralateral pyramidal tract sign

Study group discussion: Water intoxication syndrome

Water intoxication syndrome! I remember this from first year physiology!

How does water intoxication syndrome work? How much water does the person have to take?

The water that causes intoxication is mostly through intravenous fluids. I doubt a human being would have the capacity to drink enough water to cause an intoxication orally. I have heard of psychiatric disorders associated with a high water consumption though.

But if you're looking for a number - it's 16 ml/min

If you consume that much in any amount of time, you'll have exceeded intake more than the maximal urine flow.

Ummm, got it! it makes more sense than what I was thinking hahaha

Surely, drinking too much water would cause vomiting or something before the body would allow itself to become intoxicated?
Or massive impermeability of the kidney nephrons?

Does drinking too much water cause vomiting?   How permeable is the upper alimentary canal to water?  Could a large amount of water be absorbed before it reaches the stomach?

Too much water does cause vomiting! The most common symptoms suffered by this group were changes in mental status, emesis, nausea, and seizures. Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770067/

I think there have been documented cases of people drinking enough water to die.  I imagine it's very difficult, though, and therefore rare.

Mostly psychiatric patients.

Water intoxication also occurs in SIADH and surgical trauma.

Risk factors include low body mass (infants), endurance sports, competitive drinking or latrogenic.
Treatment normally follows strict fluid restriction. In more serious cases, diuretics or vasopressin receptor antagonists are given.

Similar to SIADH treatment!

You know the artist Andy Warhol? He died of water intoxication!

Oh.

Study group discussion: Drug therapy for asthma

Which is the physiological antagonist of histamine?

Acetylcholine?

No.

It's ephedrine or adrenaline.

Which are the classes of drugs used for acute control of asthma?

B 2 agonists.

Epinephrine.

Yes, epinephrine.. But that too comes under b2 agonist.

Steroids?

No, steroids is for long term control

Two more classes of drugs!

Methylxanthine? Theophylline!
Montelukast?
Ipratropium!

Yup. Second class is theophylline or aminophyline. The third class is anti-cholinergics.

But not montelukast..That's also for chronic use.

What is the function of montelukast?

Leukotriene receptor antagonist!

Leukotrienes when binding to their receptors it cause bronchoconstriction. Monteluekast used in maintenance therapy of asthma. But not useful in acute exacerbation.

Mast cell stabilizers, that is, ketotifen and sodium chromoglycate?

Mast cell stabilizers are also chronic for use.

And IgE antibody? Omalizumab?

That too for chronic use.

Even MgSO4 is used in acute management of asthma.

Yup.

Next one.

Why does use of aspirin cause asthma?

Arachidonic acid forms two type of substances via the cyclo-oxygenase and lipo-oxygenase pathways. Aspirin inhibits the cyclooxygenase pathway.
Hence, all of the arachidonic acid gets diverted to lipo-oxygenases.
And if you remember L4, B4 are the major mediators of acute attack of asthma.

Oh yeah.. That's why leukotriene antagonists are used, they inhibit LT C4 , D4

Exactly.

There are the major cause of bronchoconstriction!

As cyclo cycle is inhibited..arachidonic acid is used more in lipo cycle!

LT antagonists act on cysLT1!

Study group discussion: Low molecular weight heparin vs unfractionated heparin

Something regarding heparins! So which one is better to use? LMWH or UFH? Why?

LMWH (Low molecular weight heparin)

Why?

Less incidence of thrombocytopenia with LMWH!
Better bioavailability, t1/2 , APTT not affected.

Right. Why APTT not affected?

Because LMWH has more predictable pharmacokinetics and anticoagulant effect, LMWH is recommended over unfractionated heparin for patients with massive pulmonary embolism.

Because LMWH acts only on AT3... Does not have the scaffolding effect of UFH.

On which part it doesn't act?
LMWH doesn't affect on thrombin..

Yes! That's the answer!

LMWH acts on AT3 only and doesn't affect thrombin.

UFH acts by 2 mechanisms
1. On AT3
2. By providing a scaffolding on which AT3 can interact with Thrombin

In LMWH, the second effect is absent, hence less interference...

Yes!! Correct!!

Which situation you would prefer UFH?

For cardiac surgeries, UFH is preferred as it can be titrated dose - by - dose with protamine sulphate.

Cardiopulmonary bypass.

Why?

Cardiopulmonary bypass....Because it's effects can easily be reversed fully by protamine. And its more effective.

Exactly! Any conditions with high risk of bleeding we prefer UFH.

Yep. Cause we will be able to reverse if we give more heparin by giving protamine sulphahte same is not possible with LMWHs.

Why?

Because action of LMWH cannot be reversed completely..

Yes, correct. It's because of the molecular weight.

So which test would you like to do before deciding whether to give UFH or LMWHs?

Any other conditions?

Ok so in cases of advanced renal failure UFH are preferred over LMWHs

Now tell me why?

No idea.. Please explain!

So we would check creatinine before starting heparin

This was the test I was taking about! LMWHs are excreted renally.

Right...UFH is metabolised by liver

On the other hand UFHs are cleared by reticuloendothelial system.

Good work guys! Hope it helped!

Yes, thanks a lot!

What about pregnancy?

Are UFH still preferred or do you give LMWH?

The major limiting factor is the cost or HIT. Heparin is still ruling the world and saving millions of lives.

Also i heard..senior doctors still prefer UFH, inspite of LMW

Ummm!! I would say LMWHs are much better!! Many trials have proved that! It's only in certain scenarios that UFHs are preffered. Nobody wants to keep monitoring APTT so just making the life easy LMWHs are good!!

Yeah. But they are more experienced in using UFH.
This was told by our residents. If a senior external asks you whether UFH or LMWH is better.. Be diplomatic in your answer.

Ohh! Yeah that can be the thing!

Updated later:
And also an addition to a previous discussion on oral anti-coagulants. Why heparin is given for the initial 5 to 7 days, when warfarin has already been started?
One reason is the preformed coagulant factors need to get depleted before warfarin starts taking effect. The other reason is that in the initial days warfarin acts as a prothombotic. Cause it depletes protein c and protein s!

Study group discussion: Fixed specific gravity

What is fixed specific gravity? Like what is the cause?

Because of renal failure, the remaining functional nephrons undergo compensatory structural and hypertrophic changes,these compensatory changes result in urine that is almost isotonic with plasma.  Therefore, a patient experiencing renal failure will present with specimens measuring the same, or fixed, specific gravity regardless of water intake

Thanks! Is there any value associated with it? Numerals?

Low specific gravity in renal failure, which results in a fixed specific gravity is between 1.007 and 1.010.

Study group discussion: Fluoroquinolones

Fluoroquinolones with
maximum phototoxicity -  sparfloxacin
100% bioavailibity - pefloxacin
Highest efficacy against tuberculosis - moxifloxacin

I don't know what is the meaning of 100 % bioavailability.

100% bioavailability means no first pass metabolism. Usually achieved on IV administering.