Nitroglycerin

Here are some facts about nitrates!

The prototype drug is nitroglycerin. Other nitrates are isosorbide mononitrate and isosorbide dinitrate.

Nitroglycerin taken sublingually bypasses the first pass metabolism of liver and acts quickly. That is why, it is preferred in termination of an acute attack of angina where a rapid action is needed.

Nitroglycerin in low doses, causes venodilation, decreasing preload. In higher doses, it causes arterial and venous dilation, causing a decrease in preload and afterload.

Repeated and frequent exposure causes tissue tolerance to nitrates. That is why, nitrate free interval is recommended daily, especially with the use of transdermal patches or ointment.

Side effects of nitroglycerin are headache, postural hypotension and reflex tachycardia.

Supraventricular tachycardia mnemonic

To remember about SVT, all you need to remember is the cause and you know the symptoms and treatment!

Internship diaries: Gamjee roll

Attending, burns ward: Bring the *list of things* and a Gamjee along and come for dressing x patient.

Me: What?! Gamjeee?

*inner me*: Samwise Gamgee :D

Study group discussion: Differentials of wasting of small muscles of the hand

What are causes of wasting of small hand muscles?

The approach is to start with the spinal cord and move towards the muscles.

Spinal cord

Syringomyelia
Cervical spondylitis with compression of c8 root segment
Tumour
Trauma

Anterior horn

Motor neuron disease
Polio
Spinal muscular atrophy

Root lesion

C8 compression

Lower trunk brachial plexus

Thoracic outlet syndrome
Trauma, radiation, infiltration, inflammation

Peripheral nerve

Median and ulnar nerve lesion
Peripheral motor neuropathy

Myopathy

Distal myopathy
Dystrophia myotonica

Trophic disorder

Arthripathies
Ischaemia including vasculitis
Shoulder hand syndrome

That's a long list!

You're right. The most important thing is to remember the categories and some of the more common things listed.

Yup I love the way you listed it out.

Entropy, Enthalpy and Gibbs free energy – The monsters of bioenergetics.

The first law of thermodynamics is very famous. It says, "Energy can neither be created nor be destroyed but is converted from one form to another."

So simple.

But can you explain the second law of thermodynamics? A bit puzzled, aren't you?

It's the very reason I call it the monsters of bioenergetics. Let's convert these monsters into cute little pixies :)

The second law of thermodynamics says, "The entropy of the universe goes on increasing over time."

What is entropy?
Entropy is the degree of randomness.

A solid has closely placed molecules. Hence, the randomness in molecules is less. On the on the other hand, in liquids, the distance between the molecules is more. Hence, they have more randomness and more entropy value.

Melting of ice is a good example which illustrates the second law of thermodynamics. When the ice melts, solid gets converted into it's liquid form. The distance between the molecules increases from solid to liquid and thus, the entropy increases!

Here's an interesting fact: The human body consumes carbohydrates, breaks it down and stores its energy as ATP, which is a high energy molecule. One would argue that storage of such high energy molecule is against the second law, as entropy of the body is not increasing in this reaction. The entropy increases, but in this case, the entropy of the universe increases because we release carbon dioxide into the surrounding!

Since we are on this topic, let's address two more terms - Gibbs free energy and enthalpy!

Gibbs free energy

It is the Gibbs free energy which determines whether the reaction will proceed spontaneously to equilibrium without any input from surrounding.

In a reaction, if reactants are unstable (Having more energy) and the products are stable (Having less energy), then the reaction tends to move forward spontaneously without any input from surrounding.

On the other hand, if reactant is more stable than products then for this reaction to happen there has to some input of energy from surrounding.

Hence, if products have less Gibbs free energy than the reactants (i.e. change in Gibbs free energy is negative) then the reaction is spontaneous/exergonic irrespective of whether it is exothermic or endothermic.

Exergonic reaction - Thermodynamics

If products have more Gibbs free energy than the reactants (i.e. change in Gibbs free energy is positive) then the reaction is non-spontaneous/endergonic.

Endergonic reaction - Thermodynamics

Enthalpy

Enthalpy (H) is a sum of useful energy and non-useful energy. The non-useful part is the Entropy (S) and the useful part is the Gibbs free energy (G).

ΔH = ΔG + TΔS

To summarize all the three terms: 
Entropy: Degree of randomness (Non-useful energy)
Gibbs free energy: Energy available to do work (Useful energy)
Enthalpy: Sum of Entropy and Gibbs free energy!

Written by Komal M. Kadam
Illustrated by Immense Immunology Insight
Related post: How to remember the sign and direction of Gibbs free energy change

How to remember the direction of torsion of testis

Torsion of the right testis occurs in the clockwise direction and left testis occurs in the anticlockwise direction.

Heterophile antibody test, CMV and EBV mnemonic

Hi everyone!

Now - a - days, monospot test is used to diagnose infectious mononucleosis rapidly. 

But heterophile antibody test was used in the past and remembering it is high yield for exams.

Infectious mononucleosis is caused by EBV, which gives a heterophile positive antibody test.

In a minority of cases, infectious mononucleosis is caused by CMV, which gives a heterophile negative antibody test.

How do I remember this?

Mnemonic!

Study group discussion: Tonsils and pharynx review questions

Most common organism causing tonsillitis?
Group B hemolytic streptococcus.

Most common artery which bleeds in tonsillectomy?
Facial artery. 

Paratonsillar vein also known as?
Denise brown vein.

What is facial artery also known as?
Artery of tonsillar hemorrhage.

Why is cleft palate a contraindication to tonsillectomy?

The tonsil is situated at the anterior end of oropharynx. So if the person already has cleft palate and you remove the tonsil.. You are removing an extra support to the palate. This can lead to velopharyngeal insufficiency, that is, nasal voice (rhinolaila aperta) and nasal regurgitation.

15 year old boy presents with recurrent epistaxis which can't be controlled by adrenaline douches. Diagnosis?

Nasopharyngeal fibroma.

Why adrenaline ain't working?
Vessels here are just endothelium lined with no muscle coat.

What are the parts of pharynx?

Oroparynx, nasopharynx and laryngopharynx.

70 year old guy comes with right upper lateral lymph node enlargement. On further questioning, he complains of recent onset reduced hearing on right side. Diagnosis?

Nasopharyngeal carcinoma.

Virus causing NPC?

EBV

What's the pathogenesis of hearing loss in nasopharyngeal carcinoma?

NPC arises from the fossa of rosenmuller.. It's the most common site of origin.  

This, if you remember, is just behind the nasal opening of eustachian tube. So due to blockage of ET.. You get serous otitis media. Which is the cause for deafness. 

While examining a newborn, you notice that there is a mass in the nasopharynx. What is the rationale for checking neural tube defects in such a patient?

Nasopharyngeal bursa represents the embryonic attachment of notochord. So if you see a mass in a newborn in the nasopharynx, the baby maybe suffering from a occult NTD.

A patient comes to you.. He has trismus, fever, and a swelling which is pushing the tonsil medially. Diagnosis? Past history: Molar extraction a few days back.

It's parapharyngeal abscess.

Study group discussion: Refsums disease

Ataxia + Ichthyosis + Retinitis pigmentosa  + Don't drink milk.

Associated with which inherited autosomal recessive condition?

Refsums disease.

It's a rare AR disease.. The signs and symptoms of Refsum disease result from the abnormal buildup of a type of fatty acid called phytanic acid. This substance is obtained from the diet, particularly from beef and dairy products. It is normally broken down through a process called alpha-oxidation, which occurs in cell structures called peroxisomes.

Milk, cabbage etc. contain phytanic acid. That's why, they should be avoided.

Study group discussion: Pathophysiology of liquefactive and coagulative necrosis in hypoxia

Why does hypoxia in the brain cause liquefactive necrosis? And why does hypoxia cause coagulative necrosis in all other tissues?

Let's take it step by step!

What's the basis of coagulative necrosis in hypoxia? How does it appear?

The framework and architecture of the cells is maintained.

The reason is - In hypoxia, there is early reduction of ATP. Hence, there is a switch to anaerobic pathways. Increased lactic acid production causes a decrease in pH which results in the inactivation of even the proteolytic enzymes.

The organelles dissolve to some extent, but as the pH increases, enzymes are inactivated, leaving behind the framework.

So.. Why is there no coagulative necrosis in the brain?

There is no anaerobic metabolism in the brain. Hence, no lactic acid to stop the proteolytic enzymes.

Also, in brain there is no supporting matrix. It is all neurons and supporting cells.
In other words,there are no acellular substances. Whereas in other tissues, there is an acellular supporting matrix.

When hypoxia strikes, everything dies in brain.
Hence, liquefactive. In other tissues, the ECM maintains the structure a little bit.

Cool concept. Made me go woah.

Interesting fact: It has been established that casseous necrosis is not necrosis per say, but it is mass apoptosis of macrophages. Robbins mentions it as necroapoptosis.

Study group experience #16

Temporal arteritis
Polymyalgia rheumatica and polymyositis
Headache in brain tumor 

Dua's membrane

Artery of Percheron
Pseudoganglion 

Differentials of epistaxis 

MAC deficiency in Waterhouse Friedreichson syndrome 

Fluoride bulb and glycolysis 

Vitamin K overdose and deficiency 
Vitamins and renal stones 

Diabetes and ACE inhibitors

Anti-epileptic drugs
Pathological basis of drugs used in the treatment of Alzheimers disease 
Side effects of cyclophosphamide

Facies in medicine 
Hutchinson's in medicine 
Physics in Medicine 
Alcoholic liver disease, hepatic encephalopathy and stigmata

How to determine which hemisphere is dominant 
REM Sleep Behavior Disorder and Parkinson's disease 

Signs in acute appendicitis 
Infantile hernia 

Serial interval and communicable period 

Pleural tap

Oxytocin

Clinical tips for pediatric rotations

Dirty mnemonics

We have 100 members in all 3 groups so we made group 4 :D

I can no longer keep up with the discussions (Internship is draining me T_T)

For this reason, all Whatsapp chats will not be published on the blog, only some :)

Thanks for the tumblr fanmail (:

-IkaN

Study group discussion: Diabetes and ACE inhibitors

Question: Which of the following drug is best for reducing proteinuria in a diabetic patient?
A. Metoprolol
B. Perindopril
C. Chlorthiazide
D. Clonidine

Study group discussion: Dirty mnemonics

*During a random discussion on Krebs*

There's a mnemonic for the entire sequence in Krebs! It's kinda inappropriate.

Study group discussion: Clinical tips for pediatric rotations

So I'm just going to start with my paediatrics posting and I really really wanna be a paediatrician. Could anyone share any tips on how to be a good paediatrician?

Spend time in clinic/wards..
take histories. Try to make differential diagnosis yourself and discuss it with your teachers..

Yaah..and examine as many kids as you can.

Take a lot of toys / chocolates with you to keep the child busy when you examine.
I used to gift my patients toys and they'd smile so huge! One kid, even though seemed uneducated, told me a thank you! :D

The parents seem really tense, it's a sick child after all. You wanna be very gentle with them and talk cuddly. If you treat the kid more as a patient and less like a child, they are more likely to get pissed.

Good tips, IkaN!

Oh and when you present the case to the attending and the patient's parents are around, don't start with, "Patient, Jane Doe, 2m old female.."
Say, "Child, Jane Doe.."
No one would like their child to be addressed as a patient.

IkaN *thumbs up*
My peds HOD won't let us examine children, if we don't bring candies for them :)

My peads attending said to my friend after a viva, "What did you bring for the kid?"
My friend had not got anything so the ma'am said jokingly, "Nothing for the kid? Okay then, no marks for you!" :P

Awesome tips for peds, IkaN!
They'll be super helpful even during volunteering.

Omg. So you can give them chocolates?

I guess you can give chocolates.. Unless they are lactose intolerant / allergic.
Toys are better, I guess. They keep kids busy for hours!
Give them under parental supervision just to be safe xD

How do you get kids to let you auscultate them? They cry and then you can't hear anything

That's a two people job then, one of you has to distract the baby while the other one auscultates!

And try warming the diaphragm of your stetho a little, the kid probably also cries because it's cold.

Worst case, ask the mother to feed/play with the child.

Distract it, that normally does the trick. Carry a small torch and distract it with the light, it's a trick that usually works.

Study group discussion: Headache in brain tumor

Why do people with brain tumor get headache in the morning?

Intracranial pressure increases in the brain after laying flat all night.

Why does it increase?

How to remember the side effect of quietapine is cataract

How to remember the atypical antipsychotic that causes cataract
If your lens shine,
you may have been taking quietapine.

Lens shining = Cataract

Related post: Side effects of atypical antipsychotics mnemonic

Study group discussion: Pathological basis of drugs used in the treatment of Alzheimers disease

Discussion on drugs for Alzheimer's.

What is the basic pathology in Alzheimers disease?

Amyloid deposition in the Ach neurons. Hence, decrease acetylcholine in the brain.

Amyloid precusor proteins in the circulation are acted upon by two enzymes -
Alpha secretase: Which forms soluble proteins. These are good.
Beta gamma secretase: Which forms insoluble proteins. These are bad.

These insoluble proteins polymerise to form the plaque. So these insoluble plaque get preferentially deposited in Ach neurons and cause a foreign body reaction.. Leading to inflammation and death of neurons. Hence Alzheimers.

How alpha secretase is good?

Cause it cause soluble products.. These can be washed out by blood. The insoluble ones will precipitate.

There are 5 classes of drugs.. Guess their mechanism based on the pathology discussion!

First class: AchE inhibitors. How do they help?

They will inhibit break down of Ach.. Indirectly, increasing their levels.
Donepezil, Rivastigmine and Galantamine are examples.
They are lipid soluble and cross the blood brain barrier easily. They are also called centrally acting anticholinesterase.

Interesting fact: Nicotine acts both presynaptic and post synaptically to release Ach hence smoking is thought to be protective against AD. However, one of the hypothesis for AD is free radical damage, which can be caused by smoking.

Second class: A drug which will increase activity of alpha secretase.

The name for this drug is deprenyl.

Third class: A drug that inhibits beta secretase.

Beta- gamma secretase has got an inhibitor called tarenflurbil.

Fourth class: These are primary drugs. Inhibit polymerization.

Drug named Tramiprostate

Fifth class: This one removes the pre formed polymers.

Bapineuzumab is the drug.

I love the way you explain things. Starting right from basics!

Extras -

Glutamate antagonists - Memantine. How would antagonism of glutamate help?

Block glutamate excitotoxicity.

Related post: Drugs used in the treatment of Alzheimers disease  http://medicowesome.blogspot.com/2015/03/study-group-discussion-drugs-used-in.html

Study group discussion: Infantile hernia

Can anyone mention something about infantile hernia?

The pathology or the physiological hernia that is normal?

Both!

Alright, there are a couple of hernias related to infants that I know about.

One of them is the physiological hernia, which is a thing that happens to all babies during fetal period. So it's normal.
The intestines herniate out of the body of the fetus and rotate 90 degrees at week 6 of development. Then at week 10 they rotate a further 180 degrees and come back into the body. This is the phenomenon that forms the spiral-like location of intestines.

Now there are two pathologies.

One is the Ompholocele, where the intestines fail to come back at week 10.

The other is Gastroschisis where the physiological hernia happens normally but the abdominal wall fails to close so the gastrointestinal system protrudes directly into the amniotic cavity.

Thanks for explaining! Here's a study link!
http://medicowesome.blogspot.ae/2014/09/gastroschisis-vs-omphalocele-mnemonic.html

Study group discussion: Side effects of cyclophosphamide

Side effect of cyclophosphamide?

Bladder carcinoma is the commonest one!!

It can also lead to Haemorrhagic cystitis!

Maximum cyclophosphamide can be given for 18 months.. After that it has to be replaced with Methotrexate or azathioprine..

May cause infertility in male patients who received high doses as children.

Okay.. Didn't know that.. Thanks

Risk of potentially fatal and irreversible interstitial pulmonary fibrosis if given over prolonged periods.

Study group discussion: Pseudoganglion

Which nerves have a pseudoganglion?

Nerve to teres minor!

Correct.

Others are lateral terminal branch of deep peroneal nerve and posterior interosseous.

But why name pseudoganglion..??

Pseudo ganglion is only a nerve thickening resembling the presence of a ganglion.

Ohh.

Study group discussion: Differentials of epistaxis

What could be the possible cause of a sudden episode of nose bleeding in a patient who has a history of open heart surgery?

It could be because of anticoagulation. Hypertension is also a cause.

Since we are on this topic, any one would like to go over the differentials of epistaxis?

Excessive scratching of nasal area
Anticoagulation meds or any coagulation disorder
Traumatic
Leukemia
ITP
Problems in liver
Rhinosporidiosis
Polyps
Foreign bodies