Study group discussion: Grave's disease

I have a few review questions!

In which condition is pretibial myxedema seen?

Grave's. That and the ophthalmoplegia are specific to graves

Yes! Paradoxically Graves is hyperthyroidism not hypo!

Which drug is used for hyperthyroidism in pregnancy? Why?

PTU. Cause it crosses the placenta in the least amount?

Absolutely correct! Propylthiouracil does cross the placenta. It's just that you give a lower dose.

Which is the only symptom of Graves disease that doesn't get better with anti thyroid medication?

Ophthalmoplegia! You need steroids to treat it.

Study group discussion: Microcytic and Sideroblastic anemia

Do we have any specific topic for discussion today?

You can start one!
Yes!

Anemias?

Just on nights..we hold a review question session. Those are based on specific topics.

As in Asian nights. Time zone differences everywhere!

Haha..yes.

Alright! Anemia!

Name the hypochromic mycrocytic anemia.

Iron deficiency anemia!
Alpha thalssemia
Anemia of chronic disease
Sideroblastic anemia

Not beta thalessemia? Isn't it all thalassemias?
Beta thalassemia too
So yes! Thalassemias in general.

Lead poisoning

Chronic diseases such as...Renal failure, TB, etc.

There is the SITA mnemonic for the question we just answered
Sideroblastic
IDA
thalassemia
ACD

Remember hypochromic mycrocytic anemia as SITAL.

What's the L for?

Lead poisoning.

Oh.. We consider it in Sideroblastic anemia!

It's different.

Is it?

In Sideroblastic anemia there is defective formation of heme due to a genetic or even a drug induced cause. The RBC blast cells contain stippling. But in cases of lead poisoning..The cause is restricted to only lead.. Which causes a similar picture.

The same happens due to alcoholism and lead poisoning, right?
Yup.

The heme formation is defective because lead inhibits an enzyme required in heme synthesis.
Yup.

So why shouldn't lead poisoning be considered a type of Sideroblastic anemia?

Cause the cause is different and cause they like to confuse us -_-

Haha.

I got this table on classification of Sideroblastic anemia. It all comes under the same roof.

*can not post the table due to copyright issues on the blog, but it showed congenital and acquired Sideroblastic anemias*

Hmm.

Which anemia does an antitubercular drug cause?

Pyridoxine! Sideroblastic anemia, again.

Study group discussion: Mechanism of anemia in anemia of chronic disease

Why in chronic diseases you get anemia?

Due to poor absorptiomu of iron

Because of the inflammatory factor.. It locks up iron in the bone marrow.

I don't think it's due to inadequate absorption.

It's due to reduced absorption. But there is a reason to it. You guys heard of the protein hepcidin?
In anaemia of chronic disease, liver synthesizes hepcidin.
Hepcidin is a key that locks up iron in the bone marrow and prevents it’s release to transferrin.
That’s why, ferritin is increased. (Stores are there, but unavailable!)

Hepcidin block transporters in the intestine.

Good explanation!

Study link! http://medicowesome.blogspot.in/2013/08/difference-between-iron-deficiency.html

So reduced absorption is true?

Maybe the bone marrow too..The stores are adequate in chronic disease of anemia.

But main cause is the hepcidin locking the stores.

I'll look it up.

It's true..But there are other reasons too.

The ferroportin is present in both intestinal cells and macrophages.
Hepcidin performs its different functions via a single biochemical mechanism: hepcidin-ferroportin interaction. Intestinal epithelial cells and reticuloendothelial macrophages use the same transporter, ferroportin, to transport iron in the plasma. Moreover, macrophages and enterocytes exhibit strong upregulated ferroportin expression in the erythropoietic response in an iron-restricted state.
So I guess both the mechanisms are absolutely correct!

Nice.

What is the regulatory factor in the absorption of iron from duodenum?

Is it the transferrin levels? Their level of binding?

It's the Ferroportin.

Oh yes..The channel that transfers iron from epithelial cells into the blood, right?

Ferroportin is present in the entrocytes (cells lining the duodenum)

The level of ferritin that indicates adequate stores?
It's 15mg/dl
Below that level, it is diagnostic of falling iron stores.

I just read a research paper on it.. The hepcidin stuff can be used therapeutically, theoretically.
Interesting stuff.
Hepcidin agonists could be used to prevent or improve the accumulation of iron in both transfused and non-transfused β-thalassemic patients and even in anemia with iron storage. Hepcidin antagonists could be used in patients with diseases that cause hepcidin excess and occur with a framework of IDA or systemic IDA.

Osgood Schlatter disease mnemonic

Mini mnemonic for the day!

OsGood SchaTTer: Oh God. Traction shattered my Tibial Tuberosity.

-IkaN

Study group discussion: Why NSAIDs are avoided in MI, why aspirin is an exception

Why NSAIDs are not given in acute Myocardial Infarction?

I think it's because they're not strong enough and don't act fast enough. The pain relief lowers the stress on the heart.

NSAIDs hamper the process of scar formation after MI, there is chance of  wall rupture.

Steroids too.

Yes.

Isn't aspirin an NSAID? We give that in MI.

Yes, aspirin should be an NSAID. It's not a steroid, and it's anti-inflammatory.  So I don't see any reason why it wouldn't be one.
Edit, I just looked it up on the internet, and it's listed as one of the most common NSAIDs (along with ibuprofen and naproxen).

You give aspirin in antiagregation range. In order to help  dissolve the cloth and prevent new ones.

Well, I asked in reference to the comment on why NSAIDs should not be given in MI. But I read and found out that Aspirin is permitted as an exception.
None other NSAID should be given.
Aspirin is essential in the management of patients with suspected STEMI and is effective across the entire spectrum of acute coronary syndromes. Rapid inhibition of cyclooxygenase-1 in platelets followed by a reduction of thromboxane A2 levels is achieved by buccal absorption of a chewed 160–325-mg tablet in the Emergency Department. This measure should be followed by daily oral administration of aspirin in a dose of 75–162 mg.
Glucocorticoids and nonsteroidal anti-inflammatory agents, with the exception of aspirin, should be avoided in patients with STEMI. They can impair infarct healing and increase the risk of myocardial rupture, and their use may result in a larger infarct scar. In addition, they can increase coronary vascular resistance, thereby potentially reducing flow to ischemic myocardium.
Source: Harrison.

I think aspirin has a different mechanism to other NSAIDs. Aspirin, can worsen a bleed, for example, but is unlikely to be the direct cause of gi bleeding. I'm assuming it works differently with regards to myocardial repair too.

Non-selective NSAIDs enter the channels in both (cox1 and 2) enzymes and, except for aspirin, block them by binding with hydrogen bonds to an arginine halfway down. This reversibly inhibits the enzymes by preventing the access of arachidonic acid. Aspirin is unique in that it acetylates the enzymes (at serine 530) and is therefore irreversible.

I was taught that aspirin is the only NSAID you give in myocardial Infarction.
You have to give it as soon as possible because the latter you give, the benefit decreases.
That is why the first step in management of a patient with MI is aspirin (Not O2, not nitroglycerin, not beta blockers, not morphine) because aspirin has a time dependent mortality benefit.

Aspirin and clopidogrel!

Study group discussion: Management of enuresis

What's the guidance for action in case of enuresis of the child?

You test for urinary tract infections and look for stressors. First try non pharmacological methods like alarms, avoiding water intake at night etc. Then you use drugs.

If there's no infection and the non pharmacological methods don't work, what's the treatement?

Desmopressin then Imipramine.

Study link!
Uses of tricyclic antidepressants mnemonic  http://medicowesome.blogspot.com/2015/02/uses-of-tricyclic-antidepressants.html

Study group discussion: Why adrenaline is NOT given by the intravenous route?

Why is adrenaline / epinephrine not given intravenously in anaphylactic shock? Why intramuscular injection?

Study group discussion: Calorie test and true coma

How will you find out whether the prisoner is faking a coma or not?

Cold caloric oculovestibular reflex - A highly sensitive and specific test.

That's one of the test I had read used to pronounce the person brain dead. You push cold water in the person's ear, it stimulates a reflex. Rapid movement towards opposite side is normal.

Mnemonic is COWS.

Cold: Opposite side

Warm: Same side

Study group discussion: Mechanism of action of Digoxin

Oubain and digoxin got a connection. Both are cardiac glycosides.

Well, last I studied Digoxin used to block the NaKAtpase and thus stopping the secondary active transport of Ca leading to increased cardiac contractility. Look what I found. According to a new research its not the actual mechanism. Digoxin here, goes into the cardiac myocyte and act on Rynodine receptors instead. http://www.ncbi.nlm.nih.gov/m/pubmed/21642827/

Can somebody comment on the reliability of such articles?

Well, I had read about its action on rynodine recepters in my text book...What I know is that it acts on rynodine recepters (there is a specific name RY something which I don't remember), it increases Ca inside the sarcoplasmic reticulum of myocytes with each contraction... Meaning it sends some Ca which comes in from outside into the SR... So that the subsequent contraction is more forceful as the Ca now available from the SR is more than the prev contraction...

It's RyR2!

RyR2, yes!

Study group discussion: Why does ingestion of salt cause high blood pressure?

Why does salt increase blood pressure? I Googled it but there is no biochemical info.

Salt in the blood takes water out from cells into veins and here we got blood pressure.

Excessive NaCl ingestion or NaCl retention by the kidneys and the consequent tendency toward plasma volume expansion lead to hypertension. Nevertheless, the precise mechanisms linking salt to high blood pressure are unresolved. The discovery of endogenous ouabain, an adrenocortical hormone, provided an important clue. Ouabain, a selective Na+ pump inhibitor, has cardiotonic and vasotonic effects. Plasma endogenous ouabain levels are significantly elevated in approximately 40% of patients with essential hypertension and in animals with several forms of salt-dependent hypertension.
Source: http://www.ncbi.nlm.nih.gov/pubmed/16467498

I was reading about it and people on the internet believe that salt causing hypertension is a myth :/

It was also given on wikipedia, I donno how you missed it..

When too much salt is ingested, it is dissolved in the blood as two separate ions - Na+ and Cl-. The water potential in blood will decrease due to the increase solutes, and blood osmotic pressure will increase. While the kidney reacts to excrete excess sodium and chloride in the body, water retention causes blood pressure to increase inside blood vessel walls.

Study group discussion: Cardiac shunts and snowman sign

Congenital heart diseases

-> Right to left shunts:
Truncus arteriosus
Transposition of the heart arteries
Tricuspid atresia
Tetralogy of falloy
Total anomalous pulmonary venous return TAPVR

-> Left to right shunts:
VSD
ASD
PDA
Eisenmenger

The right to left shunts all start with T. It's a good memory aid!

Snowman sign X ray feature of?

Snow man is a type of the cardiac silhoutte, right?

Another name figure of 8 sign.

Study group discussion: Eisenmenger's syndrome

I think Eisenmenger (shunt reversal) is actually R to  L shunt.
It is observed in case of L to R shunt, with time right ventricle get hypertrophied and can overcome left ventricle.

It's due to pulmonary hypertension. Reversal shunt that is. Right ventricular hypertrophy is just a consequence of PH.

And why does Pulmonary hypertension arise in that case?

Too much blood going to the lungs causes edema and hypertrophy of the pulmonary vasculature.

Increased flow of blood through pulmonary vasculature in cases of left to right shunt.
Normally, the pulmonary system is a low pressure system 25 / 8 mm of hg in compared to the normal 120/80 mm hg of systemic vessels
The pressure increases in hope to reduce blood flow through the lungs..through the shunt.
But instead of being a protective response.. It ends up making the whole situation much more severe.

Plethoric lungs, basically.

Or it Is it due to hypoxia which causes pulmonary vasocontriction which leads to pulmonary hypertension?

Yes, that's a contributory factor too

Why too much blood going to lungs.. Is it due to compensatory effort by Increasing HR?

The left ventricle is stronger than the right. So more blood goes to the right ventricle. Hence, more blood to the lungs.

It's the shunt..Left side of heart has a higher pressure compared to the right side of heart..Hence in cases of ASD and VSD.
Due to free communication.. Blood flows from high pressure to low pressure system.
In case of right to left shunts..There is obstruction which doesnt let blood enter the lungs (eg tetralogy of fellot where there is pulmonary trunk stenosis)
So a right to left shunt.

Thanks for explaining it to me, you guys!

Study group discussion: Short PR interval causes

Review question c: What are 3 causes of a short PR interval?

Wolff Parkinson White syndrome is one.

Yeah, but in general? What physiological alterations can cause that?

The re-entrant pathway.

As in... WPW causes it because it works as an accessory AV pathway.

1. Accelerated AV conduction
2. Tachycardia
3. Accessory AV pathway

Other cause is rheumatic fever.
It's one of the minor criteria for diagnosis in the Jones criteria.
Oops.. Rheumatic fever is a cause for increased PR interval.. My bad.