Sunday, April 28, 2013

What are the factors affecting diastolic blood pressure?

Hi everyone!

What is diastolic blood pressure?
It is the pressure that is exerted on the walls of the various arteries around the body in between heart beats when the heart is relaxed.
It is the minimum pressure in the entire cardiac cycle.
So it basically represents amount of blood in arterial system during diastole.

Monday, April 22, 2013

Lateral medullary syndrome and lateral pontine syndrome mnemonic

*Super super excited to share this mnemonic with you* ^__^
 But let's get to the basics first!

What is lateral medullary syndrome?
Neurological symptoms due to injury to lateral part of the medulla.
Also called Wallenberg's syndrome.

When does it happen?
When the posterior inferior cerebellar artery is occluded.

What is lateral pontine syndrome?
Neurological symptoms due to injury to lateral part of the pons.

When does it happen?
When the anterior inferior cerebellar artery is occluded.

Wednesday, April 17, 2013

Free water clearance

Hi everyone!
This is my attempt of explaining everything I know about free water clearance.. Hope you understand :)

What is free water clearance?
Free water clearance (CH2O) is the volume of blood plasma that is cleared of solute-free water per unit time.

What does it mean? @_@
Water follows salt everywhere it goes.
[Think of salt and water as a lovey dovey couple, in a very codependent relationship of course, water being the lead role xP ]

Tuesday, April 16, 2013

Virus mnemonic

Do you know viruses have various shapes?
The simple viruses are either icosahedral or helical.

Cool and important fact:
Icosahedral viruses can either be simply a naked caspid virus or it can be an enveloped caspid virus.
But if a virus is helical, it HAS to be enveloped and surrounded by a nice lipid bilayer (mostly derived from the host cell membrane)

How I remember that helical viruses are always enveloped is:
Think of our DNA!
We have a helical structure.. So the helical viruses can not survive without our cell membranes.
Helical virus forms can not be naked.

I know it's stupid but it makes life easy for me < 3

If you want to stuff your hippocampus with some other facts:

Sunday, April 14, 2013

Nervous system origins mnemonic

Hello everyone :)
Let's get to CNS and PNS origins =D

Neural crest derivatives:
Neural creSt cells have S
Schwann cells have S
Sensory neurons have S
How I remember that neural crest cells give rise to post ganglionic autonomic neurons is that I remember adrenal medulla is derived from neural crest cells which is as good as a post ganglionic neuron!

Note: The cells that give rise to the adrenal medulla are called chromaffin cells.

Mesoderm gives rise to Microglia which are Macrophages of the CNS

Saturday, April 13, 2013

Inactivated sodium channels and Lidocaine (Lignocaine)

Why is lidocaine preferred in patients with arrhythmias following myocardial infarction?

Hypoxic tissue is depolarized.
Na+ - K+ ATPase doesn't work.
Na+ has accumulated in the cell and no one pumps it out.
All the sodium channels are in the inactivated state.

These inactivated channels slow the conduction of electrical activity in ischemic tissue.
This is how arrhythmia arises.
It causes disparity in the way action potentials are propagated in the heart  muscle cells.
The normal fibres wanting to go fast and the hypoxic tissues slowly firing in between :|

That's why you use class Ib antiarrhythmic, lidocaine, in patients with arrhythmias following myocardial infarction.
They block inactivated sodium channels.

Blocking inactivated sodium channels doesn't change any flux of sodium into the cells.
But if you are keeping it inactive, you are preventing it's return back to the resting state.
So you are keeping those cells in hypoxic tissue refractory, keeping them from going back to resting and preventing them in firing new action potentials on their own.

Lidocaine also decreases action potential duration by blocking slow sodium window channels.
In any other healthy cell, this would be proarrhythmic.
But in hypoxic tissue over here, which is already slow in conduction, you'd help it recover faster and help it go back with the healthy tissue for electrical speed.
Or simply by decreasing APD, you'll have more time in disatole for filling.
Either way, you are improving the cardiac output of the ischemic heart :)

Since digoxin is also going to depolarize the heart by blocking sodium channels, lidocaine is also used in digitalis toxicity.

Cool fact:
Lidocaine is also a local anesthetic.
However, preparations for cardiac use contain no preservatives.
Local anaesthetic preparartions should not be used for cardiac purposes.
It is used i.v. due to high first pass metabolism.

Another cool fact:
Mexiletine and Tocainide are lidocaine like drugs and are available in oral formulations.

That's all for today!
 Have a happy healthy Saturday <3
-IkaN

Cardiac fast fibers and slow fibers - Why does a less negative membrane potential convert a normally fast fiber into a slow fiber?

Greetings everyone! :)

What are fast fibers?
Fast fibers have functioning fast channels.
Fast fibers include ventricular fibers, atrial fibers and Purkinje fibers.

What are fast channels?
They are sodium channels that quickly open and close on depolarization.
  
What are slow fibers?
SA node and AV node.
They lack functioning fast channels.
That's why depolarization is so slow in them.

So what will happen if fast fibers lose their fast sodium channels?
They'll convert into slow fibers!

When does this happen? @_@
When the resting membrane potential is less negative.

Why does this happen?
Less negative potential inactivates sodium channels.
Repolarization is necessary for returning the sodium channels to the ready state.

So.. what will depolarize a slow fiber?
L type Calcium channels! =D
Also known as slow channels.
They allow sodium to pass as well.
It's known as the sodium window current.
So you can appropriately call em slow calcium sodium channels.

Other ways of saying the same thing but worth noting:
Capacity of a cell to depolarize depends on the number of sodium channels in ready state.
The more negative resting potential, the faster the response.
(-90mV in atrial and ventricular cells, compared to -60mV in pacemaker cells)
Slow response fibers have no appreciable Na+ current during phase 0 in these cells because the Na channels are either absent or in an inactivate form because of the existing voltage (-60mV, remember?)

That's all!
^______^
-IkaN

Thursday, April 11, 2013

Behind the scenes: Subendocardial fibres lack phase 1

Hello everyone!

I know my "Why are there differences in cardiac action potential in different parts of the heart?" post is not like the regular posts where I tell the usual facts and mnemonics and it seems out of place.

So I thought of doing a behind the scenes version of it. Who said only videos have behind the scenes? Each writing, each painting, each piece of art has a behind the scenes!

Let's get to it =D

Behind the scenes of:

Why are there differences in cardiac action potential in different parts of the heart?


My quest started off with the statement, "Subendocardial fibres lack phase 1"
And when you Google "Subendocardial fibres" it tells you about "Purkinje fibers" which is not the same.


The lord is testing me
"Why do subendocardial fibres lack phase 1?" seemed impossible to answer at first!
"Quit, don't quit? Noodles, don't noodles? You are too concerned about what was and what will be." —Oogway (Kung Fu Panda)
I decided to keep going. After poking around here and there I discovered that purkinje fibers have a prominent phase 1. That means subendocardial fibers can NOT be purkinje fibres.

The heart cells in the subendocardial region lack phase 1 and the conducting cells (Purkinje fibres) in the same region have a prominent phase 1.
I believed there was beauty in how it was created. How our bodies are designed. But I didn't know why.
"What a piece of work is a man! How noble in reason, how infinite in faculty! In form and moving how express and admirable! In action how like an angel, in apprehension how like a god! The beauty of the world. The paragon of animals. And yet, to me, what is this quintessence of dust?"
—Shakespeare
I had to push further to find out why..

I learnt there was a difference: Cells in different regions of the heart do not have the same action potential. We have a tendency to generalize things and principles to everything. The statement was a mind opener for me!
"We are all equal in the fact that we are all different. We are all the same in the fact that we will never be the same. We are united by the reality that all colors and all cultures are distinct & individual. We are harmonious in the reality that we are all held to this earth by the same gravity. We don't share blood, but we share the air that keeps us alive."
 ― C. JoyBell C.
I learnt why was there a difference: The repolarization phenomenon being different in every cells. Repolarization in a cell occurs because the action pulse has only a certain duration; thus the cell repolarizes at a certain instant of time after its depolarization, not because of the repolarization of an adjoining cell.

Because it's the differences make life interesting!
"Sunshine is delicious, rain is refreshing, wind braces us up, snow is exhilarating; there is really no such thing as bad weather, only different kinds of good weather."
― John Ruskin
Then I learnt what causes the difference: The potassium channels conductance. The action potential notch is due to the presence of a transient outward current (Ito), which diminishes in amplitude from the epicardial to endocardial surfaces.
"There is little difference in people, but that little difference makes a big difference. The little difference is attitude. The big difference is whether it is positive or negative." 
― W. Clement Stone
I learnt why is that necessary: Help the heart contract in an organized fashion and prevent haywire spread of cardiac excitation.
"You can become blind by seeing each day as a similar one. Each day is a different one, each day brings a miracle of its own. It's just a matter of paying attention to this miracle."
 ― Paulo Coelho
In the process I also learnt that without something pushing you to find the answers it's just impossible to keep looking. Thank you for being my reason.
"Passion rebuilds the world for the youth. It makes all things alive and significant."
 ―Ralph Waldo Emerson
 And that's how I ended up finding my answers to the all my questions. It took me three days of asking and three hours of Google search to get to my answer. And I'd like to end by quoting the last quote on hard work :D
"So if you wanna do something, if you've thought about something you wanna do, take it head on. Decide that you're gonna face it; that whatever shortcomings you have, that you're gonna stiffen yourself there; whatever training that is required, that you're gonna get that training; that you're gonna get started right now; do what you can, where you are, with what you have and never be satisfied."
 ― Les Brown
That's all!
Hope you had fun learning with me and see you in the next post xoxo
-IkaN

Wednesday, April 10, 2013

Why are there differences in cardiac action potential in different parts of the heart?

Cells in different regions of the heart do not have the same action potential.

The difference is major between conducting system and the myocytes.
And there is a minor variation in the action potential in distinct parts of the ventricle (endocardial and epicardial)

What is epicardium and endocardium?
Epicardium is the outer side of the cardiac muscles and endocardium is the inner side (towards the cavity of the ventricle)

What causes the difference in action potential?
This is due to the nature of repolarization.
Unlike depolarization, the repolarization is not a propagating phenomenon.

When a cell depolarizes, another cell close to it then depolarizes and produces an electric field which triggers the depolarization phenomenon.
In this way, the depolarization proceeds as a propagating wave within cardiac tissue.

Repolarization in a cell occurs because the action pulse has only a certain duration; thus the cell repolarizes at a certain instant of time after its depolarization, not because of the repolarization of an adjoining cell.

If the action pulses of all cells are of equal duration, the repolarization would of course accurately follow the same sequence as depolarization.
In reality, however, this is not the case in ventricular muscle. The action pulses of the epicardial cells (on the outer surface) are of shorter duration than those of the endocardial cells (on the inner surface).

Coming back to our original statement.. What is the minor variation in the action potential of endocardial and epicardial fibres?

The epicardial action potential exhibits a prominent notch between phase 1 and phase 2 that results in a spike and dome configuration. The notch is smaller in midmyocardial cells and absent in endocardial cells.
Subendocardial fibres lack phase 1.
The action potential notch is due to the presence of a transient outward current (Ito), which diminishes in amplitude from the epicardial to endocardial surfaces.

This current is due to potassium efflux (potassium going out of the cell)
You see, if the sodium channels simply closed at phase 0 the action potential would stay up there. It is the closure of potassium channels which cause the repolarization and the phase 1.

It simply means epicardium has more outward current than endocardium.
Outward potassium current is little in endocardial cells.
So very little potassium is going out.. And that too is balanced by calcium coming in. That's why no phase 1. Hope that made sense ^_^"

In real heart muscle, since the action potential duration at the epicardium is actually shorter than at the endocardium, the recovery phase appears to move from epicardium to endocardium, that is, just the opposite to activation.

Why is there a difference in action potential?
According to me, the differences in action potentials cause a difference in conducting velocities and difference in refractory period (changing their respective response to stimulation rate)
It is these differences that help the heart contract in an organized fashion and prevent haywire spread of cardiac excitation.
I mean, we don't want the impulse transmitted to the epicardium from the endocardium go back into the endocardium now, do we?
So we let the epicardium repolarize first (shorter action potential) and make sure that the endocaridum is refractory till then.
Otherwise we'd have an impulse going back and forth from the epicardium to the endocardium!

That is why, during depolarization, the impulse is carried from endocardium to epicardium, and during repolarization, the impulse moves from epicardium to endocardium.

What helps one of my best friend's remember this is "What depolarizes last, repolarizes first"
So to sum it all up, it's the variation in potassium (potassium conductance) which plays a major role in impulses going here and there in the heart. That's why potassium injections are lethal if not in range.
Thank you so much for being there in my life (:

Cool fact: 
Purkinje fibres have a prominent phase 1.
The heart cells in the subendocardial region lack phase 1 and the conducting cells (Purkinje fibres) in the same region have a prominent phase 1.
It is breathtakingly beautiful how our body is designed :)

Another cool fact: The changes in action potential also change the response of various drugs on different parts of the heart. This I came to know during my extensive Google search :P
So all of these minor changes might have relevance in your future practice as a doctor =D

That's all!

If you search hard enough for something, you will find it.. Yes, even the answers to your silly questions! ^_^

Read behind the scenes, which questions lead me to which answers & making of this post by clicking here.

-IkaN

References: 
http://www.bem.fi/book/06/06.htm
http://cpt.sagepub.com/content/2/1/61.short
http://en.wikipedia.org/wiki/Endocardium
http://physrev.physiology.org/content/85/4/1205.full

Monday, April 8, 2013

Why does heart stop in diastole when plasma potassium level rises?

Normally, potassium has a tendency to move outside the cells due to the concentration gradient.

As plasma potassium rises, this concentration gradient is reversed. 
So potassium will move into the cells. 

The cell's resting membrane potential is very sensitive to changes in extracellular potassium ion concentration.
Elevated potassium, or hyperkalemia, causes the resting electrical potential of the heart muscle cells to be lower than normal (less negative). 

Without this negative resting potential, cardiac cells cannot repolarize. 

That means all your cells are depolarized.
This inactivates sodium channels. 

Inactivated sodium channels means the cells can not fire. 
The heart can not contract. 
That's why, heart stops in diastole. 

Hope you understand :)

This is the mechanism of execution by lethal injection, sudden depolarization of the cell without the ability to repolarize.

Increased extracellular potassium is also seen in rhabdomyoloysis, tumor cell lysis, hemolysis etc.

Cool fact:
In ischemic tissue, potassium in the surrounding interstitium rises. 
Wanna know why?
Ischemic tissue does not receive oxygen.
So there is lack of ATP.
Na+ - K+ ATPase doesn't work
K+ leaves the cell and no one can pump it back in.
(Special thanks to a friend for explaining this fact to me ^_^ )

Another cool fact:
Increased extracellular calcium tend to stop the heart in systole (contracted).
This is known as calcium rigor.

That's all!

-IkaN


Sunday, April 7, 2013

Cerebellum mnemonics

Hello everyone!
This post is for those having trouble remembering the cerebellum

I modified a mnemonic I got online :)
So if you have a little bit of anatomic imagination cerebellum should be a piece of cake for you!


Region: Hemisphere (lateral)
Principle input: Cerebrocerebellar
Function: Peripheral coordination and planning
How to remember: It’s location is around the periphery of cerebellum

Region: Flocculonodular lobe
Principle input: Vestibulocerebellar
Function: Ear, eye, balance, body co-ordination.
How to remember: Pops out to the edges, looks like bunny ears to me =P

Region: Vermis
Principle input: Spinocerebellar
Function: Axial equilibrium
How to remember: It is located in the axis of cerebellum
And looks like the spinal column

Also, the intermediate hemisphere influences the lower motor neurons via the rubrospinal and reticulospinal tracts

I think of climber plants and the fruit olive
And that's how the "climbing fibres" and "olivocerebellar tracts" come together xD

Superior Sends out
Superior cerebellar peduncle in the major outflow from the cerebellum

That's all the mnemonics I got
Feel free to add more in the comments ^__^

-IkaN


Thursday, April 4, 2013

Spinal cord organization mnemonic

Hello, all my Pokemon and cat fans =P

Spinal cord organization mnemonic
“SAD MEW”

S - Sensory
A - Afferent
D - Dorsal

M - Motor
E - Efferent
V V - Ventral


"Sad mew" Spinal cord organization mnemonic

-IkaN

Tuesday, April 2, 2013

Cochlear nerve, pathway and mnemonic

It's time to finish off the cochlear part of the vestibulocochlear nerve! :)

It starts off from the organ of corti, central processes of the spiral ganglion forms the cocchlear nerve and they terminate into the cochlear nuclei

From the cochlear nucleus, most of the axons cross to the opposite side in the trapezoid body and terminate in the superior olivary nucleus

The axons arising from the superior olivary nucleus form the lateral leminiscus
and reach the inferior colliculus

The fourth neurons pass through the inferior brachium to reach the medial geniculate body

The axons of the fifth neurons form the auditory radiation which passes through the sublentiform part of the internal capsule to reach the auditory area in the temporal lobe

How am I ever gonna remember all this? @_@
Mnemonic! =D
SLIM
S = Superior olivary nucleus
L = Lateral leminiscus
I = Inferior colliculus
M = Medial geniculate body

I sorted out the whole pathway for you :P

Now, all you need to remember is that lesion in the cochlear part of the 8th nerve of the cochlear nucleus will cause a unilateral sensorineural hearing loss
Because fibres haven't crossed yet

If it is a bilateral senorineural hearing loss, the lesion is at higher levels such as the brainstem, thalamus or cortex
These patients will also have a decreased ability to localize a sound source


I'll add the mnemonic for the auditory tests here too

W, for Webers test, is a symmetrical alphabet ie made up of two V's
So it tests both ears simultaneously
Also, tuning fork is placed on the Vertex

R, for Rinnes test, is asymetrical
Tests only one ear
It's kinda stupid but works for me :)


That's all!
-IkaN

Vestibular nerve, pathway and mnemonic for the receptors

Hello everyone! We'll finish off the vestibulocochlear nerve today :)
It isn't as hard as it seems, trust me <3

Vestibular receptors are:

The macuLae of the utricLe and saccuLe
And what do they sense? Linear acceLeration

The Cristae of the semiCircular canal
And what does it sense? Circular movements (rotatory)

It's a no brainer really =D

Sunday, March 31, 2013

Lipoproteins and apoproteins

Hey guys!
We have always had difficulty remembering lipoproteins and apoproteins and stuff.. And what makes it simpler? Mnemonics!

After you eat, dietary trigylcerides is transported via chylomicrons from the intestine to the adipose tissue.
VLDL carries endogenous triglycerides from the liver to the peripheral tissues.

Both triglyceride transporters contain apoB

Chylomicrons have micro
Micro means small
So they have a small number, that is, apoB 48

VLDL have the larger number, apoB 100

apoC II is a Cofactor for lipoprotein lipase
Which hydrolyzes the triglycerides into fatty acids and glycerol
LIpoprotein LIpase is activated by InsuLIn

apoE helps in rEmnant uptake by lEvEr (Liver =P )

Chylomicron (B48, C-II, E) > Chylomicron remnant (B48, E)
 

VLDL (B100, C-II, E) > IDL (B100, E) > LDL (B100)
VLDL loses apoC-II to become IDL
IDL loses apoE to become LDL
LDL will transport cholesterol to peripheral tissues

apoA-I Activates lcAt (LCAT)
Also, I looks like l
It's on HDL
Converts cholesterol to cholesterol esters
(LCAT transfers a polyunsaturated fatty acid from 2nd carbon of glycerol to cholesterol forming lysolecithin and cholesterol ester)

*phew* That was work!
Let's have a look at the deficiencies now =)

So what happens if you have apoB deficiency?
No triglycerides is incorporated into VLDL and chylomicrons
Serum triglycerides, cholesterol and phospholipids are low
Beta lipoprotein (LDL) is absent
Lipids and lipid-soluble vitamins (especially A and E) are poorly absorbed (steatorrhea)
Hemolytic anemia—lipid imbalance causes RBC membranes to pucker (acanthosis)

What happens in lipoprotein lipase deficiency?
Increased triglycerides in chylomicrons and VLDL!
(You can't breakdown triglycerides to fatty acid and glycerol for uptake)

What happens if you have a LDL receptor deficiency?
There will be and increased levels of LDL and cholesterol
(Because peripheral tissues can't take them without the LDL receptor)

What happens if you have LCAT deficiency?
You have increased unesterified cholesterol
(You can esterify the cholesterol you have)
You also have increased phoshatidyl choline which is a component of lecithin

That's all!
 Have an awesome week <3

-IkaN

Post is continued here

Southern, Northern, and Western blot mnemonic

Hello everyone!

The mnemonic to remember blotting techniques is "SNoW DRoP"

S -    Southern - DNA     - D
N -   Northern - RNA     - R
O -   Oooooo - Ooooo    - O
W -  Western - Protein   - P


Blotting techniques illustration and mnemonic :)
There's another simpler one for all those who can speak the language Hindi.. Southern in Hindi is Dakshin for DNA & Western in Hindi is Paschim for Protein!

Cool facts on blotting techniques that the mnemonic doesn't cover -
If you want to visualize DNA at replication level, you will use Southern blot. This will require a DNA probe attached to phosphate.
RNA at transcription level can be visualized with Northern blot. This will require a DNA probe attached to phosphate too.
Remember: If you want to visualize protein at transcription level, you will go with Northern blot!
Proteins at translation level are just antigens (Whether they are cell membrane, cytoplasmic or secretory proteins!) Therefore, antibodies (not probes) are used to visualize proteins byWestern blot.
DNA binding proteins also known as transcription factors go to the nucleus and bind to DNA. They are proteins but they work at the DNA level. They are different than just regular antigens and therefore, we use DNA probe (not antibodies!) to visualize them. This is known as the South Western blot :)

That's all!

Hope you won't go, "Which direction was that again?" in the exam =P

-IkaN

Updated on 4th December, 2013: Hindi mnemonic & illustration.
Updated on 5th December, 2013: Cool facts that you may have not known.

Sunday, March 24, 2013

Leukocyte adhesion deficiency mnemonic

Leukocyte adhesion deficiency mnemonic

Chemokines (chemoattractants) mnemonic

Here is something for chemoattractants..

Phagocytic cells are in blood vessels which is like street of city
Now they want to go in tissues which is like a dark forest

Somebody suggested phagocytic cells that if you want to go,
"Before (B4) going, make sure you can See five (C5a) clearly In Light (IL8) and form peptides (N-formyl peptides)"

So it is B4, C5a, IL8, N-formyl peptides.

-IkaN

HLA, MHC & CD T cell mnemonic

Hello everyone!
Time for another immmunology mnemonic =D

MHC class I:
CD8+ T-cells recognize MHC I.
It takes only 1 stroke of the pen to write “8

The genes have only one alphabet. (HLA-A, HLA-B, HLA-C)

CD8 x MHC1 = 8
CD8+ are Cytotoxic T cells because "EighT" has T for "Toxic"

All cells have one nucleus, so all nucleated cells have class I MHC.

MHC I has one chain (alpha chain) & one microglobulin (Beta 2 microglobulin).