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.