Evaluating axis from ECG (Mnemonic)

Hi everyone! We are going to learn how to determine the axis from an electrocardiogram =D

First of all, do you know which two leads should be looked at to determine whether axis is in the normal quadrant or if it is Left Axis Deviation (LAD) or Right Axis Deviation (RAD)?

Look at lead I and lead II. Sounds simple! ^__^

An upright (positive) QRS in leads I and II is normal (–30 degrees to +105 degrees).
In left-axis deviation, there is an upright QRS in lead I and a downward (negative) QRS in lead II ( +105 degrees).

How do I remember this? @_@

Thumbs up method: Lead I = Left thumb, Lead II = Right thumb.

Wait, why lead I is left thumb and lead II is the right thumb?
Because left is a smaller word and it gets the smaller number, that is, one!
Right has more alphabets and it gets the bigger number, that is, two.

Left thumb up (I) + Right thumb up (II) = Normal.
Left thumb up (I) + Right thumb down (II) = LAD.
Left thumb down (I) + Right thumb up (II) = RAD.

Mnemonic method:
Left leaves, right returns.

That’s all!
Have a splendid week everyone

HLA associations mnemonic

Hi everyone!
Here’s a complete guide on how to remember the HLA associations. Let’s catch em all!

Doctors (DR) will turn into MD’s someday.. The thought makes you go, “Aah”
Starting with 2 and ending with 5, your mnemonic for DR associations is “MD.. AAH!”
HLA DR2 - Multiple sclerosis
HLA DR3  - Diabetes mellitus type 1
HLA DR4  - Arthritis (Rheumatoid, also the one associated with Lyme’s disease)
HLA DR5  - Anemia (Pernicious, causing B12 deficiency)
HLA DR5  - Hashimoto’s thyroiditis

If it’s not too much, you can remember “Hey! This Doctor is going to be good MS someday” to remember Hay fever, Goodpasture’s syndrome and Multiple Sclerosis for HLA DR 2.

External image

Hi5 is another way you can remember about Hashimoto’s relation to DR5.
HiPA5 will help you remember Pernicious Anemia with it too (If the A’s of Arthritis and Anemia confuse you!)

I use rhymes for all the other associations, make sure you sing em with a funny tone!

“Two, three S-L-EE.
Three, four, not so sour.”

HLA DR2 and HLA DR3 is associated with SLE
HLA DR3 and HLA DR4 is associated with Diabetes mellitus type 1
(not sour - sweet - sugar - diabetes lol)

You can also remember with the pokemon, “Two, three, butterfree” for the butterfly rash in SLE.. Whatever suits you.

External image

A threeFrEaking three.
HLA A3 is associated with Hemochromatosis.
(fe3+ - iron - hemochromatosis)

Be there at eight, don’t be late.
HLA B8 is associated with Grave’s disease.
(late - dead - grave)

Seven, heavenly pee.
 HLA DR7 is associated with steroid-responsive nephrotic syndrome.
(pee - kidney - nephrotic syndrome)
Seven rhymes with heaven, lee rhymes with pee, I don’t know what I was even thinking when I made this!

For HLA B27, the PAIR mnemonic is famous.
Psoriasis, Ankylosing spondylitis, Inflammatory bowel disease, Reiter’s syndrome.

The above mnemonics will suffice for the exam.

The below facts are not very high yield, but for the sake of completion here you go -
SCAM 3 - Sjogrens syndrome, Chronic active hepatitis, diabetes mellitus type 1 for HLA DR3.

If you extend the line in 4, it looks like an A.
A for Arthritis. Flip the A and it looks like V.
V for vulgaris, pemphigus vulgaris.
So HLA DR 4 is associated with Arthritis as well as Pemphigus vulgaris,

That’s all!
Hope it helps you all < 3

Credits here.

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

SVT occurs due to accessory conduction pathway through the AV node.



Beta blockers

Calcium channel blockers


V - Vagal maneuvers


Ice immersion

Carotid massage

SVT: Start Vagal Treatment - - > If fails, use pharmacotherapy (ABCD drugs)

The P in Pvst reminds us that it presents with Palpitations in a hemodynamically stable patient (HR: 160-180/min)

*PVST: Paroxysmal supraventricular tachycardia

Interesting fact: In an asthmatic patient with SVT, you can’t give adenosine or beta blockers. The drug of choice in an asthmatic patient is therefore, diltiazem (A calcium channel blocker)

That’s all!


Autonomic system drugs mnemonic

Please give some tips on remembering cholinergic and adrenergic drugs.

Drugs ending in

- ine are beta agonists
(Terbutaline, ritrodine)

-sin are alpha blockers
(Prazosin, terazosin)

- olol are beta blockers
(Propanolol, metoprolol)

- alol are alpha + beta blockers (Labetalol)

- stigmine are cholinergic drugs
(Neostigmine, physiostigmine)


Aortic arch derivatives mnemonic images  -HD images here

I made these diagrams guessing these will be helpful ^__^

The greater part of the first and second artery disappear. In adult life first arch artery is represented by the maxillary artery and the second arch persists for some part of fetal life as the stapedial artery.
The mnemonic people use for that is, “First is max” & “Second is Stapedial” =)

Mnemonic for third arch artery:
C for Carotid, C the third letter of the alphabet.”

The third arch artery gives off a bud that grows cranially to form the external carotid artery.

The internal carotid artery is derived from the distal part of the third arch artery and cranial most part of the dorsal aorta.

The brachiocephalic trunk is formed by the right horn of the aortic sac.

Mnemonic for fourth arch artery:
“fOUR rhymes with AOR for Aorta.
fouRS for Right Subclavian.”

The ascending aorta is formed from the truncus arteriosus.

The arch of aorta is derived from the vental part of the aortic sac, it’s left horn and the left fourth arch artery.

Mnemonic for sixth arch artery:
Well, this is lame but the letter 6 looks like lungs to me =D

Pulmonary trunk is derived from truncus arteriosus.

Mnemonic for subclavian artery:
“7 is S.”
Seventh InterSegmental Subclavian!

The right subclavian artery is derived from the right fourth arch artery and right seventh cervical intersegmental artery.

On the left side, the subclavian is derived entirely from the seventh cervical intersegmental artery.

That’s all!

Hope you had fun learning ^__^



Hey everyone! Here are some review questions about hyperkalemia:

What is the physical examination finding you are likely to see in a patient with hyperkalemia before you order an ECG?


What is the earliest EKG change seen in patients with hyperkalemia?
Peak T waves

What is the drug given if you see ECG changes in a patient with hyperkalemia? Why?
Calcium gluconate. It is cardioprotective.

Name three rapidly acting therapies:
Albuterol (I hear it is the fastest but the magnitude of action is small)
Insulin with glucose (Beware of hypoglycemia, it’s dangerous)
Bicarbonate (Causes hydrogen ions to come out and potassium to go into the cells)

Name any two therapies used to hasten potassium removal from the body:
Loop diuretics

What is the side effect of sodium polystyrene sulfonate (Kayexalate)? In which patients you do not administer it?
Intestinal necrosis. Do not give it in patients with ileus or bowel obstruction as it may cause perforation.

That’s all!

If you could answer all these questions, give yourself a pat on the back!
If not, give a pat anyway, you learnt something new :)


Related posts:
Why does heart stop in diastole when plasma potassium level rises?
Drugs and conditions that enhance Digoxin toxicity and the mechanism behind it

Heart murmurs mnemonic

Hello people with a pumping heart in their chests, obviously! <3
In this post, I’ll be taking about the few mnemonics I use in relationship to murmurs.

PASS” is a good mnemonic for remembering that pulmonic and aortic stenosis give a systolic murmur.

The opposite of PASS, ie, other two valves and the other defect gives a systolic murmur too. (Mitral and tricuspid regurgitation gives a systolic murmur!)

VSD has a S so that’s systolic.

Now, the other ones - pulmonic and aortic regurgitation, mitral and tricuspid stenosis will cause diastolic murmurs :)

Here’s another mnemonic submitted by one of the readers:
For the systolic murmurs: MR. P.V. TRAPSS (Mister Per Vaginum traps? :P)
MR. P. - Mitral Regurgitation or Prolapse
V. - VSD
TR - tricuspid regurg
APS - Aortic or Pulmonary Stenosis
S - Systolic

For the diastolic murmurs: MS. PAID
MS - Mitral Stenosis
PAI - Pulmonary or Aortic Insufficiency
D - Diastolic

Here are a few more lame mnemonics I made when I was in final year! =)
I remember GDP or Gross Domestic PRoduct.
Graham Steel murmur is a Diastolic murmur associated with Pulmonary Regurgitation.
Alternatively you can remember, Graham SED PR (Graham said per rectum? xD)
For Graham Steel, Early Diastolic, Pulmonary Regurgitation.

Carrey Coombs murmur is seen in rheumatic carditis.
RCCC (Renal cell carcinoma) is diagnosed by MD and MS”, is my mnemonic.
Rheumatic carditis, Carrey Coombs, Mid diastolic, Mitral Stenosis.

Austin flint murmur is seen in aortic regurgitation.
AFAR MD” helps me remember Austin Flint, aortic regurgitation and Mid Diastolic.

I am actually not a fan of using mnemonics for concepts like murmurs. But once, I was asked to name systolic murmurs in a viva. And you know how vivas are, if you don’t answer quickly, another question is thrown at you. Luckily, I remembered this mnemonic that day and could answer quickly. That’s when I realized, it’s okay (It’s awesome, actually!) to understand all the murmur mechanisms properly when you have time to imagine at home and it’s definitely okay to use mnemonics cheaply when you don’t have time to think, that is, in time bound exams.

That’s all!

Lub dub goes my heart…



How to remember lipoprotein disorders

Hello everyone!

Click here to read about Lipoproteins and apoproteins if you need a quick revision before we get started :)

In this blog post, I’ll be talking about lipoprotein disorders, how to remember them and some facts that you need to know about the disorders. Type I hyperlipoproteinemia
Chylomicrons increased in childhood.
VLDL increased later in life.

Lab findings: Increase in serum triglycerides.

CPL (Capillary lipprotein lipase) hydrolyzes triglycerides in lipoproteins.
It requires apo-CII as a co-factor.

Clinical findings: Acute pancreatitis (Pancreatic vessels filled with chylomicrons rupture), eruptive xanthomas.Type II hyperlipoproteinemia
Serum LDL is increased.

Lab findings:
In IIa, only cholesterol is increased.

Liver cholesterol synthesis is deprived of negative feedback.

In IIb, cholesterol and triglycerides are increased.

Liver overproduces VLDL in IIb

Acquired causes: Primary hypothyroidism, nephrotic syndrome, extrahepatic cholestasis.

Clinical findings: Tendon xanthomas, Xanthelasma, premature coronary artery disease and stroke. Type III hyperlipoproteinemia
This dysbetalipoproteinemia is also known as “remnant disease”.

Lab findings: Elevation in cholesterol and triglyceride levels.

Apo E is required to remove chylomicron remnants and IDL (remnant of VLDL).

Clinical findings: Palmar xanthomas, increased risk for coronary artery and peripheral vascular disease. Type IV hyperlipoproteinemia
Increase in VLDL.

Lab findings: TG accumulates
in preference to cholesterol, like IIb.

Acquired causes: Excess alcohol, OCPs, Diabetes mellitus, chronic renal failure, thiazides, beta blockers.

Clinical findings: Eruptive xanthomas, increased risk for coronary artery and peripheral vascular disease.
Type V hyperlipoproteinemia Increase in chVlomicrons and VLDL. It is a mixture of types I and IV familial dyslipidemias. Lab findings: TG levels are high, whereas cholesterol concentration increases only moderately. Clinical findings: Like type I, but unlike type IV, there is no major risk of atherosclerosis, so that pancreatitis and eruptive xanthomas remain the main complications. For the sake of completion, I’d like to add another disease -
Tangier disease is due to lack of ABC1 cholesterol transporter gene.
Cholesterol accumulates inside cells. Blood HDL and cholesterol are low.
The disease is characterized by atherosclerosis, hepatosplenomegaly, polyneuropathy and orange tonsils.

*phew* That’s all!

Like I always say, if you stare at a word long enough, you find the mnemonic in the word itself :P
I made these myself, hope you find them helpful ^__^

Happy Indian Independence Day :)


Hey! Everybody has their moments of low self esteem. We have different reasons for why we doubt our abilities.

I’ll tell you about mine, for example. After I cleared my exam and got into med school, I thought, “What if I really got through the entrance based on pure luck? What if I just marked the right answers, got a good score and I don’t really deserve to be here?" After being transferred to an academically better med school, "These kids are really smart. I just got here because of the transfer. I don’t belong here.”

Honestly, no one knows for sure whether they deserve it, whether anyone deserves anything. So that’s not even a valid question to ask ourselves, but we are so programmed to be negative that we still do. We drown ourselves with doubt and fear. We need to tell that negative inner voice to shut up!

You are not average. You have infinite potential within you. Your premed score doesn’t determine who you can or can not be. At this present moment of time, I think it doesn’t matter who you are or where you came from or how you got here - Here you are. So let’s do this!

Your dreams will drive you to work when you have low self, hold on to it. Write it down, why you really wanted to be here. Write about how your passion will separate you from others. Anything positive about you, write it down and read it thrice a day. It’ll really help you get out of the negativity you’ve created for yourself.

Once you get rid of your low self esteem and self doubt, you’ll start to work towards your dream. And it’s an uphill from there. The work reinforces you to learn more. You discipline yourself to achieve what you desire. Your work starts to speak for you. It glows out of your personality from within. Who you were separates out from what you do.

Also, in the movie Kung Fu Panda, Po thinks he fell out of the sky and didn’t deserve to be the Dragon warrior. But look what happens once he starts to believe in himself! So don’t doubt yourself. Believe and just start working. And watch the movie if you haven’t :)

Oh and here’s something by Les Brown that you should read:

“Be careful of your self-talk. Without monitoring your mind and your mouth, the majority of what you say to yourself can poison your attitude, weaken your spirit, drain your energy. Be aware that, left unchecked, the negative storyteller in your brain can shut down your faith, amplify your fears and activate a spirit of hopelessness and self-sabotage. Turn off and banish the automatic negative thoughts that will ruin your life if you let them.

Learn to keep your heart open and love yourself unconditionally. The universe is on your side waiting for your next move. Celebrate what’s working in your life. Focus on the positive and on what you can do right now. Give thanks for what you have and that you’re still here. That alone says that your life still matters. You have something special. You have GREATNESS within you!”

Why does oxygen cause hypercapnia in COPD?

In medical school, we learnt that oxygen administration in patients with chronic obstructive pulmonary disease (COPD) induces hypercapnia through the ‘hypoxic drive’ mechanism. I had talked about this in my previous blog here.

Today, I found out that it is a myth. Well, sort of. It has a minor role. At least, in COPD. Studies found out that the minute ventilation had a limited effect on PaCO2 :/

So… What caused the CO2 increase then?

The MAJOR mechanism on why you get hypercapnia due to oxygen administration is ventilation perfusion mismatch.

Normally, alveolar ventilation and perfusion are well matched.

Two extremes of ventilation-perfusion (V/Q) mismatch may occur:
1. No ventilation of an alveolus but adequate perfusion, resulting in shunting
2. Adequate ventilation but no perfusion, resulting in dead space ventilation

The body has protective mechanisms to optimize the V/Q ratio.When alveolar oxygen tension decreases (for example, in bronchoconstriction), local mediators induce vasoconstriction of pulmonary capillaries supporting this particular alveolus, counteracting possible shunting, a mechanism called hypoxic pulmonary vasoconstriction.
(So areas that don’t work, don’t get blood. The lungs are pretty smart and don’t pour blood in places where gas exchange can’t occur.)

The strongest mediator for hypoxic pulmonary vasoconstriction is alveolar pO2 (partial pressure of oxygen). Therefore, a high fraction of inspired O2 (FiO2) will increase O2 tension in alveoli with a low level of ventilation, inhibiting hypoxic pulmonary vasoconstriction. As a result, alveoli with relatively impaired ventilation are well perfused, leading to an increase in V/Q mismatch.
(Now the areas that don’t work are unnecessarily getting the blood causing a waste of everybody’s time and increasing CO2 in blood.)

Another mechanism is Haldane effect:
Hemoglobin combines with CO2 to form carbamino compounds.The ability of deoxygenated hemoglobin to bind CO2 is much higher than that of oxygenated hemoglobin.
Thus, oxygen induces a rightward shift of the CO2 dissociation curve and this is known as the Haldane effect. (I talk about it in this blog post.)
A rightward shift in the CO2 dissociation curve will increase PaCO2, which normally is excreted through elevated minute ventilation, normalizing PaCO2.
However, in patients with severe COPD, who are unable to increase minute ventilation, the Haldane effect will increase PaCO2.

Interesting, isn’t it?


It started as a small experiment and turned out to be one word - AWESOME.

What’s the study group for?

A bunch of medical students from all over the world, discussing study related concepts!

You may share your experiences, what you studied today, ask interesting questions to help other people learn or simply revise, ask doubts about things you don’t understand, answer other people or just tell a fact you learnt that fascinates you.

We learn something new on a daily basis <3

How do I sign up for the group?

All you’ve got to do is message me your number. You can email me at with “Whatsapp study group” in the subject.
Important: Make sure you include your proper country code when you email me your number. (Otherwise your number won’t be displayed in my Whatsapp list and I might miss you out!)

After you have emailed me your number, you’ll receive a verification email from us. It’s just some basic questions that helps us decide which group should you be added in (And whether you are a regular human being or a internet creep! :P ).

Replying to this mail is essential otherwise you might not be added to the group.

I’m a pre-med/nursing/pharmacy/EMS/other medical fraternity student. Can I join too?

I want to join but.. I’m hesitant because I’ll be sharing my number to a lot of people.

It’s risky, I know, but we have solutions - Block users. So I don’t think you should hold back on your awesomeness. I have added over 90 people so far and they are loving it.. No complaints so far. Take a chance and hop in! <3

You can read our previous experiences and discussions here:

Medicowesome study group on Whatsapp

Study group experience #1

Study group experience #2

Study group experience #3

Study group experience #4 

Study group experience #5

So.. See you in the group, awesomite!


Conn’s syndrome mnemonic

Hi. I keep forgetting that Conn’s syndrome is hyperaldosteronism. Can you help me out with this?

Sure! :D

The N’s are for sodium - Hypernatremia!

The C makes a K for potassium, which is less than the number of N’s, therefore, hypokalemia!

Also, Na+ is sodium. A could remind you of Aldosterone.
AL could remind you of ALkalosis.

That’s all!


Signs seen in Aortic regurgitation mnemonic

Hello! In this post, I talk about the signs seen in Aortic regurgitation and share a few mnemonics with you. I also inserted some gifs to make it fun.

I recommend using mnemonics for the signs you can’t remember after learning them thoroughly than trying to memorize the mnemonics first :)

Let’s get started :D

de Musset’s sign: Rhythmic nodding or bobbing of the head in synchrony with the beating of the heart.

Mnemonic: Imagine a musketeer, raising his hat and then bowing his head stylishly.

Originally posted by emmahb20

Muller sign: Systolic pulsations of uvula.
Mnemonic: M for Muller, M for mouth. Muller’s sign is seen in the mouth.
You could also think of MU in MUller - Muller, Uvula.

Originally posted by teded

Quincke’s sign: Regurgitant blood flow into a dilated left ventricle during diastole leads to a decrease in diastolic pressure and a consequent increase in stroke volume, resulting in blanching and flushing, respectively, of the nail bed.

PS: They are pulsations which are SEEN, they are NOT FELT.

Quincke’s pulse is the capillary pulsations and any thing that demonstrates these pulsations may be known as Quincke’s sign. (I don’t know for sure though.)

Other ways to see Quincke’s pulse:

- While drawing the thumb nail sharply across the forehead, one can cause a red mark, which can be seen paling and flushing with each beat of the heart.

- When pressing a glass slide on the inner part of the lower lip, the same capillary pulsation will be seen.

So these two can also be called Quincke’s signs! :)

Mnemonic: I honestly don’t have a mnemonic for this one. Uhh.. How about.. “Quickly keep Quiet with Quincke’s finger on your lips?” The Q’s to remind you of Quincke. Finger for nail bed. Lips for the glass slide thingy.

Originally posted by tennydr10confidential

Watson’s water hammer pulse: A pulse that is bounding and forceful, rapidly increasing and subsequently collapsing, it resembles the strike of waterhammer, a Victorian toy.

Mnemonic: This image. Look at the bounding of poor Donald’s head :P

Originally posted by gameraboy

Traube’s sign: A ‘pistol shot’ systolic sound heard over the femoral artery.

Mnemonic: You keep pistol (gun) in your trousers in the belt (which is near the femoral area). So pistol shot is traubes (trousers) sign which is the sound over the femoral vein.

Originally posted by blckdiamondss

Light house sign: Alternate flushing and blanching of forehead.
Mnemonic: Imagine a light house flashing lights on and off. Your forehead becomes a light house, going pale and flushed, as if lights are going on and off in your head.

Gerhardt’s sign: Also known as “Sailer’s sign”, in severe aortic valve regurgitation, Gerhardt’s  sign is present when pulsations of the spleen are detected in the presence of splenomegaly. This is from the large forward stroke volume that is present in this state.

Mnemonic: GPS - Gerhardt Pulsatile Spleen (Sailer too)

Here’s a sailor navigating with no GPS :P

Originally posted by littlehorrorshop

Landolfi’s sign: It is alternating dilation and constriction of the pupils in time with the patient’s heartbeat. The sign is a result of the increase in pulse pressure that occurs with aortic insufficiency.

Mnemonic: You dream of the lands you wish to visit with your wide eyes :P

Originally posted by magical-boy-rohariel

Becker’s sign: Presence of visible (through an opthalmoscope) pulsation of retinal arteries.

Mnemonic: BeckeR. Becker sign - Retinal artery pulsations.

Duroziez’s sign: Audible diastolic murmur which can be heard over the femoral artery when it is compressed with the bell of a stethoscope.

Mnemonic: D for Diastolic murmur, D for Duroziez, D for Deaf (It’s audible xD).

Originally posted by shootmesenpai

Got no mnemonic for these but posting them for the sake of completion :)

Mayne’s sign: Drop of at least 15 mmHg in the diastolic blood pressure on raising the arm.

Originally posted by d-epth

Okay.. Enough of stupid images :P

Rosenbach sign: The pulsation of the liver during systole caused by the high stroke volume.

Hill’s sign: Popliteal cuff systolic pressure exceeding brachial cuff systolic pressure by more than 10 - 20 mm Hg.

Lincoln sign: Pulsatile popliteal.

Sherman sign: Dorsalis pedis pulse is quickly located and unexpectedly prominent in age >75 yr.

Ashrafian sign: Pulsatile pseudo-proptosis.

Corrigan’s pulse: A jerky carotid pulse characterized by full expansion followed by quick collapse. Also known as Dancing carotid. *tempted to put a dancing gif*

Pulsus biferiens: Click here.

Locomotor brachii: Prominent pulsation of brachial artery seen in aortic regurgitation.

Did you know? Dilatation of the heart with hypertrophy is called “ox-heart” in AR.

That’s all!
I’m in America, having a wonderful time with other international medical students. Things aren’t going quite as expected so far but I am learning a lot. I need you guys to pray for me :)I hope I get a strong letter of recommendation from my professors and get acquainted with people who will make getting Internal Medicine residency in a University Hospital easier for me.
Pray for me, guys.

I was super super excited to share this mnemonic with you ^__^

What is lateral medullary syndrome?
Neurological symptoms due to injury to lateral part of the medulla
(also called Wallenberg 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

What do both the lesions have in common?

Ipsilateral horner’s syndrome
Why? Descending hypothalamic tracts affected

Contralateral loss of pain and temperature
Why? Lateral spinothalamic tract affected

Ipsilateral cerebellar ataxia
Why? Cerebellar peduncles affected
(Inferior - medulla, middle - pons)

Nausea, nystagmus, vertigo, vomiting
Why? Vestibular nuclei involvement

Ipsilateral loss of pain and temperature sensation from the face (facial hemianesthesia)
Why? Spinal trigeminal nucleus and tract involved

Ipsilateral hearing loss
Why? Cochlear nuclei and intraxial nerve fibers involved

So how do I tell the difference between the two? @__@

Lateral medullary syndrome:
Dysphagia, dysarthria, dysphonia
Why? Nucleus ambiguus involved

Lateral pontine syndrome:
Ipsilateral paralysis of the upper and lower face (lower motor neuron lesion)
Ipsilateral loss of lacrimation and reduced salivation
Ipsilateral loss of taste from the anterior two-thirds of the tongue

 Why? Facial nucleus & facial nerve involved

Cool fact:

There is a loss of pain and temperature sensation on the contralateral (opposite) side of the body and ipsilateral (same) side of the face This finding is diagnostic

That’s all!

I created the mnemonic all by myself =D
Hope that was fun and helpful :)


Hey everyone!

We recently got 500 followers on tumblr & I couldn’t think of a more fun way to celebrate it!! =D

I missed the 500th follower though ^__^“

I’d love to thank all of my followers for reblogging & liking my posts :)

Especially, My Notes for USMLEDr. Cranquis’ Mumbled Gripes

Thank you so much everyone for your love and support <3

As for the emoticon game, I won’t be posting the answers online but you can email me on for the answers and I’ll get back to you as soon as I can!

That’s all!