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.

Study group discussion: Wolff-Parkinson-White (WPW) and increased QRS interval

Causes of increased QRS interval?

BBBs (Bundle branch block)
Electrolyte abnormalities
WPW syndrome

Medications like:

Procainamide
Tricyclic antidepressants

Study group experience #6

Here's what we discussed:

Smallest, largest and longest muscle 

Sarcoidosis and calcium regulation

Weight loss in malignancy 

Metformin and weight 

Cushing's syndrome 

Necrobiosis lipoidica 

Babinski sign 

Sweet syndrome 

Monospot test for EBV infection 

Safflower, Butter and Cholesterol

Our first group reached 100 awesomites today. So happy! 

Here are a few messages from the group:

A century of awesomeness.
WOOTS PARTY AND LOTS OF MESSAGES HAHHAA.
Proud to be a part.
Proud to be a silent contributer to the 100. Been reading all your messages like a creep this entire time. Congrats!
I think I don't have enough knowledge to answer most questions here, but I do like reading yours!
Yup me too a silent one! But I really love this group. Boosts me to learn more.
Cheers to all 100 <3 

To all the new coming awesomites, since the first group is full, I'll make your group in a week irrespective of the number.

How to sign up for the group: Medicowesome study group on Whatsapp - The Official invitation

Uses of tricyclic antidepressants mnemonic

Amitryptyline for neuropathic pain.

When you say “Aah” in pain, remember Amitryptyline!

Clomipramine for obsessive compulsive disorder.

Clomi when you feel Compulsion ;)

Imipramine for nocturnal enuresis.

Eemi Eee.. will not let you pee in bed ^__^

Lame but helps :D

Hematology and chemical pathology mnemonics

An awesomite requested for Pathology hematology bottles mnemonics. I asked him (or her) to send notes and attempted to make lame mnemonics on the same.

Uploading the notes + mnemonics for reference:

THE PURPLE ONE (aka “Lavender”)
These bottles are generally used for haematology tests where whole blood is required for analysis.

ADDITIVE: EDTA (ethylenediaminetetraacetic acid)

COMMON TESTS:
Full blood count (FBC)
Erythrocyte sedimentation rate (ESR)
Blood film for abnormal cells or malaria parasites
Reticulocyte
Red cell folate
Monospot test for EBV
HbA1C for diabetic control
Parathyroid hormone (PTH)*
less commonly used for: ciclosporin/tacrolimus levels, some viral PCR tests, G6PD, ACTH level*, porphyria screen*, plasma metanephrines*, fasting gut hormone screen*

Mnemonic: PurplE
P: Parasite, PTH, PCR, Porphyria
E: EDTA

Study group discussion: Safflower, Butter and Cholesterol.

Out of butter and safflower oil.. Which of it contains cholesterol? And which doesn't, and why?

This has to be tricky.

It wouldn't be fun if it wasnt! :D

Well, defying logic, butter doesn't and safflower does?

Haha. Wrong!

Oh man. I hate vivas.

What's the reason?

Butter does because it comes from animals. Plant products never contain cholesterol, only animal products do.

Correct!

Study group discussion: Weight loss in malignancy

What's the cause of weight loss in malignancy?

Malignancy is cachexia.. Due to increased TNF and IL - 1.

Malignancy: Due to decreased appetite.

The TNF and IL - 1 decrease appetite as well as increase protein catabolism.

Study group discussion: Sweet syndrome

Has anyone out here heard of sweet syndrome?

And I checked it's not related to diabetes. -__-

Acute febrile neutrophilic dermatitis.

It is caused due to?

Acute febrile neutrophilic dermatosis (Sweet syndrome) is a reactive process (a hypersensitivity reaction) that occurs in response to systemic factors, such as hematologic disease, infection, inflammation, vaccination, or drug exposure.

Named after Rober Sweet.

Study group discussion: Necrobiosis lipoidica

What is necrobiosis lipoidica?

Which condition causes it?

Papule on Lowerlimb seen in DM.

What's DM?

Diabetes mellitus.

It's not simply a papule. It's necrosis of the skin.

Study group discussion: Cushing's syndrome

What is Cushing Reflex?

It's related to cushing syndrome or disease?

Nah. It consist of signs of Raised I.C.T: Hypertension, bradycardia, dilatation of pupil and pyramidal tract sign.

It is caused due to raised ICT?

There is more entity..Cushing's ulcer and curling ulcer. One of them is caused due to raised ICT I think. The other being a stress ulcer. Both in the stomach.

Curling ulcer is due to burns.

They both are confusing terms.

Cushing ulcer is caused when there's brain injury. With ICT as mention above

Agree.

Does anyone know the mechanism?

Cushing ulcer and Curling ulcer are peptic ulcers caused by CNS injury and burns respectively.
One possible explanation for the development of Cushing ulcers is the stimulation of vagal nuclei due to the increased intracranial pressure which leads to increased secretion of gastric acid.
Curling ulcers may be explained by a reduced plasma volume, which leads to sloughing of the gastric mucosa or secretion of burn toxins (necrotic and carbonaceous materials released from burned cells) by the stomach.

There is the cushing sign too

Must you know the difference between Cushing's disease and Cushing syndrome then?

Cushing disease is the disease caused due to a tumor of the pituitary..With increased secretion of ACTH.
The other is the syndrome caused due to excess cortisol in the blood.. Exogenous commonly. I am not sure whether adrenal tumors are also included in Cushing syndrome or not.

Cushing sign occurs as a result of Cushing reflex.

Here are study links on Cushing's!
Cushing's ulcer mnemonic: http://medicowesome.blogspot.ae/2014/03/ulcers-of-stomach-mnemonic.html

Cushing syndrome notes: http://medicowesome.blogspot.ae/2014/12/how-to-make-concise-medical-notes.html (View image)

Study group discussion: Smallest, largest and longest muscle

Which is the smallest muscle in the body?

Stapedeus. 

Nope, stapedius ain't the answer.

Then?

Erector pili muscle. The one responsible for goose bumps.

Oh yes! I forget it's a muscle cause it is so small and seems insignificant.

Haha me too!

Awesome.

Largest muscle?

Gluteus maximus!

The longest muscle?

Sartorius. Originates from ASIS to Pes anserinus.

Updated on 22nd February, 2015:

I read the previous  posts, errector pili -smallest smooth musle, smallest skeletal muscle -stapedius!

Smooth muscle not in our control , innervated by sympathetic system,triggering agents - cold, fear. 

Which is the strongest muscle in the body?

Ahh makes sense. 

Strongest would be the one in the thigh?

Gluteus maximus!

Nope. 

Masseter. 

True! Well done!

Shouldn't it be the quadriceps? I don't see the masseter kicking foot balls and running with the weight of the body :P

Yes, based on its weight, with all muscles working together it can close the teeth with a force of 25 kgs on the incisors. 

Ooh. 

Or 90 kgs on molars! 

I got a good link on that!

There are lots of ways to measure strength. One is brute force, in which case biggest is best. All skeletal muscles are bundles of many individual fibers that contain small force generating structures called sarcomeres. “Generally speaking, more muscle tissue means a larger total number of sarcomeres, which means greater maximum force generation,” Tasko says. That means the largest muscles—the quadriceps on the front of your thighs and the gluteus maximus on your rear—produce the most force.

I thought the strongest was the tongue! 

I was told that it was the muscle that can do the most amount of damage - the tongue (Obviously, not physical damage, you know what I mean, right?)

Oh oh most hard working muscle in the body? 

Heart <3 

Why not diaphragm?

Umm I donno.. Because you can have a paralyzed diaphragm and live but you can't have a paralyzed heart?

I personally think that heart is made popular for no reason :P