REM, NREM and dream content recall mnemonic

My friend had difficulty remembering whether dreams can be recalled from REM sleep or NREM sleep.

I have a mnemonic!

REM REMembers nightmares.

Similarly, NREM does Not REMember night terrors.

That's all!
The North remembers.
-IkaN

Ultrasonography in Acute Appendicitis

Hey Awesomites

Ultrasonography ( graded compression technique ) is the investigation of choice in cases of acute appendicitis.

Antiarrhythmic drugs: Classification, Mechanism of Action and ECG changes

Hello guys, this is a much important topic especially in Emergency Medicine. And before going through this post, if you may, brush up your concepts of cardiac action potential.

A quick recap: Imagine a non-pacemaker AP with a flat phase 4, phase 0 upstroke, then a phase 1 downward notch, then phase 2 plateau phase, phase 3 downstroke slow at first, rapid later. Now the channels.
Phase 0- Na+ channels in the open state, it is inactivated in all other phases.
Phase 1- Transient-outward K+ channels
Phase 2- L type Ca2+ channels and Slow K+ channels (IKs)
Phase 3- Delayed rectifier K+ channels; Slow K+ channels(IKs) to Rapid K+ channels(IKr) and finally ultrarapid K+ channels(IKur).
Phase 4- Inward rectifier K+ channels(IKi)


First, Classification:

We have the Vaughan-Williams classification, the Sicilian gambit which is the most accepted albeit with some significant limitations which will be discussed later.

Class I: 
These are the Na+ channel blockers and "membrane stabilizers". So, they reduce slope of phase 0 and hence the peak of action potential. And they all prolong effective refractory period(ERP).  Because of subtle differences in its members, they are further classified as three subclasses.
             
IA:
It has moderate efficacy, i.e., it moderately reduces the slope of phase 0. And now look at the letter A, it is pointing upwards. That is coz it increases APD (Action Potential Duration) and ERP(Effective refractory period) both since it blocks IKr channels which are a part of delayed rectifier K+ channels involved in repolarization phase 3, so they prolong both QRS(ventricular depolarization) and QT intervals(Due to increased APD).

Note: This class of drugs have a cumulative effect. They block Na+ channels in the open state during phase 0 and then dissociates from them slowly and incompletely during the diastolic period after QRS complex so that in next beat, some Na+ channels are already blocked from the previous beat. So the QRS prolongation will rise with each beat. And this effect will be exaggerated at higher rates since diastolic period will shorten and more no of Na+ channels will be stuck with drugs.

Hence, in a way, it attacks more strongly if the rate is uncontrollably higher.

Eg. Quinidine, Procainamide, Disopyramide


IB:
It has low efficacy, it weakly reduces the slope of phase 0. Unlike the above class, it decreases APD. On the ECG, it slightly shortens QT interval and have little effect on QRS complex although both are considered therapeutically irrelevant.
Now why does it shorten APD? In the quick AP recap above I lied a bit, in phase 2 plateau phase the depolarizing Ca2+ channels are helped by residual(still open) depolarizing Na+ channels which are blocked by these drugs, so the repolarizing K+ channels dominate earlier and shorten phase 2.

IA vs IB:

IA is like a friend who attaches to you quickly and then doesn't like to leave you. Wheareas, IB is like a friend who takes his good time to attach but then leaves you quickly.
So based on this, unlike IA, IB blocks both open and inactivated Na+ channels, but they do it so slowly that they miss most of the open Na+ channels in phase 0 (the reason behind them producing little changes in QRS complex) and their real effect starts after phase 0 when they block the inactivated Na+ channels and prolong ERP. They detach relatively quickly so they show less cumulative blocking effect, but at higher rates when the diastolic repolarization phase is so short that even these fast-detaching fellas fail to detach and remain stuck on producing cumulative blocking effect beat after beat.

Another question, why are IB drugs not effective in tackling down Atrial arrhythmias?

2 reasons:
1.Unlike ventricular myocyte AP, atrial myocyte AP has a very short plateau phase and APD and as stated above phase 2 is where IB drugs exert their major effect.
2. IB drugs have negligible effect on normal cardiac cells, they mainly show their effect on ischaemic cells. And atrial myocytes by virtue of their less thickness, less demand and adequate blood supply rarely become ischaemic.

Eg., Lidocaine, Phenytoin, Mexiletine


IC: 
It is very strong, it significantly reduces the slope of phase 0. But coz its C, it doesn't Care about APD and ERP, so no effect. On the ECG, it prolongs QRS complex significantly and shows cumulative blocking effect in a very similar way to IA drugs.

Eg., Flecainide, Propafenone, Moricizine


Class II: These are Beta-blockers. They prolong phase 4 of AP, which reduces the automaticity and hence controls rate as well as conduction. On ECG, they prolong PR interval.

Class III: These are K+ channel blockers. They prolong phase 3 of AP, so it delays repolarization and prolongs APD and ERP.
Eg., Amiodarone, Dronedarone, Dofetilide, Sotalol, Ibutilide

Class IV: The Ca2+ channel blockers or more specifically the L-type Ca2+ channel blockers. In SA node and AV node, it prolongs both phase 0 and 4, so controls the rate. In myocardial cells, it prolongs phase 2 of AP, so it impedes conduction.  On ECG, they prolong PR interval.
Eg., Verapamil, Diltiazem

Class V: Variable Mechanism; including Magnesium Sulfate, Adenosine, Digoxin, Atropine.

The major drawback of this classification is that some drugs like Amiodarone have overlapping features of other classes.

Mnemonic by iKan :) -

Remember, VeraPamil has P in the name so PR interval is Prolonged.

(Cain) from Flecainide sounds like Quain, Q is for QRS interval prolongation.

That's all!
My next post will be on what, why and how of indications of anti-arrhythmics. Stay tuned! :)

-VM

Fact of the day: Sleep Apnea linked with Acute Gout attacks

Hey Awesomites

Those who suffer from sleep apnea are usually overweight, and so may be those with acute gout exacerbations.

In addition to lower body temperature and nighttime dehydration, hypoxic patients of sleep apnea are at upto 50% higher risk of having acute attacks of gout at night. This is due to excess tissue damage and cell breakdown, both of which increase uric acid levels that may accumulate in joints to cause exacerbations !!

- Jaskunwar Singh

Eagle Syndrome

Eagles Syndrome also known as Styalgia is due to elongated process or calcification of the styohyoid ligament.

Symptoms-
1. Pain in tonsillar fossa and upper neck which radiates to upper neck which gets aggrevated during swallowing.
2. Dysphagia

Diagnosis-
1. Transoral palpitation of the styloid process in tonsillar fossa.
2. X Ray of lateral view of skull or AP view with open mouth.

Treatment-
Many people may remain asymptomatic and do not need treatment.

Symptomatic patients may need excisition of styloid process by transoral or cervical approach.

Hope this helps!
Ashita Kohli

Fact of the Day : Pantaloon Hernia

So this is just a very interesting fun fact.

When a person has a Direct Inguinal Hernia along with an Indirect Inguinal hernia , the person is said to have a Dual / Pantaloon/ Romberg / Saddle bag hernia.

Tried a lot to find out why the name is 'Pantaloon'. Pantaloon = Saggy pants or a Foolish old man. So take your pick !

That's all!
Happy studying!
Stay Awesome.
~ A.P.Burkholderia

Placenta Previa : Why it occurs.

Here's a short discussion post on Placenta Previa Etiology.

So Placenta Previa is a dangerous condition that presents with bleeding after 28 weeks up to the 1st stage of labour. (So it could so happen that the baby needs to tear it open and come out - as it may cover the Os. Hence Previa , where Previa means 'In front of'. Of course the reality being that the placenta gets compressed and results in fetal Hypoxia along with bleeding ).

The main pathology is that the Placental gets abberantly deposited / implanted in the lower uterine segment in stead of the upper.

This could be due to :
1. Decidual area being defective in the upper segment (Due to maternal age , Multiparity, Curretage or Cesearan section in the past).
2. Large placenta - due to which some part may encroach over the lower segment. (Multiple pregnancy, Smoking etc).

Here's a way to remember the risk / etiological factors for this condition.

Risk Factors for Placenta Previa -

Mnemonic : M4 C3

M - Maternal Age - Decidua becomes weaker with age so the placenta ends up encroaching over the lower segment.
M - Multiparity (Similar reason. Especially in a grand multi para)
M - Multifetal pregnancy (Twins etc. There's less space in the fundal area hence gets lodged in the lower segment)
M - Maternal Serum AFP (Indicates high/persistent Chorionic activity - essentially invades into more and more of the Endometrium.)

C - Curretage - in the past if done , damages the uterine layer making the upper segment defective.
C - Caeserean sections in the past / other operations on the Endometrium/myometrium - Makes the uterus defective.
C - Cigarette smoking - causes Hypoxia to the baby leading to Placental Hypertrophy - larger placenta occupies larger area and may encroach downwards.

Hope this helped !
Stay Awesome and
Happy Studying !
~ A.P.Burkholderia

Step 2 CK: Algorithm for management of Atrial Fibrillation and Atrial Flutter

A patient presents with palpitations and irregular pulse-- What would you do next? The clock is ticking away.. and you might need to answer your multiple choice question!

This is a classic presentation of Atrial fibrillation - Palpitations and irregular pulse.
Next step in diagnosis: Do an EKG first--> if it does not show A.fib --> the next step depends on the patient's location --> If inpatient-> order Telemetry monitoring
If outpatient--> order Holter monitoring.

Now, once the diagnosis has been made, what they want you to know is the next best step in management.
The answer to this will depend on the HEMODYNAMIC status of the patient.
Patient can be either STABLE or UNSTABLE.
Now, what defines being UNSTABLE is any of the following:
* systolic blood pressure <90
* C.H.F.
* confusion
* chest pain

Once you know the status, follow the chart below.

Happy Doctors' Day!

-- Rajavee Panchal & Vikramjeet Kakade

Fact of the day: The link between Alzheimer's and Cancer

Hey Awesomites

People with a history of cancer are less likely  to suffer from Alzheimer's in the advanced age, while those with Alzheimer's disease are less likely to get cancer.
( Source )

- Jaskunwar Singh

Hemineglect mnemonic + clock drawing

Hemineglect - where is the lesion ? Which side is neglected?

Mnemonic: Hemineg-left. Left side is neglected. 

Lesion located in the right parietal lobe (non dominant lobe).

Interesting fact: Right-brain-damaged (RBD) individuals with spatial neglect often depict an object with left-sided features absent on drawing.

Usually, the patient is asked to draw a clock.

The drawing of patients with hemineglect contain empty space on the left, as if the clock were covered by an opaque semicircle.

However, this metaphoric occlusion frequently leaves the rim of the clock unaffected. The circular outline is rarely compromised in neglect patients’ clock drawings and is almost always the first feature produced in the task.

Interesting, isn't it?

-IkaN

Torn meniscus and inability to extend the knee

Doubt: Why does torn meniscus present with inability to extend the knee? I don't understand the anatomy correlation.

If there is complete tear, the meniscus (a piece of it) gets dislodged. It gets stuck in the knee joint.

This causes:
Inability to extend the knee.
Pain on extension of the knee.

Why is it called "bucket handle"?

A bucket handle meniscus tear represents a complete tear of the mensicus support or the ligament that holds the meniscus in place. This allows the meniscus to flop over like the handle on a bucket.  When the meniscus flips over it becomes stuck in the middle of the knee joint, you lose the ability to fully straighten the knee then you have a “locked knee”.

Explained by Dr. Mustufa Poonawala

The meaning of valgus (with doubt + mnemonic)

Meaning of valgus: A deformity involving oblique displacement of part of a limb away from the midline.

Doubt: Why is genu valgum knock knees? The knees (genu) are displaced towards the midline!

Answer: It's not the knees we consider during the deformity... It's the relationship of distal part with the proximal part at a joint.

Mnemonic: L in vaLgum is for Lateral displacement.

(Conversely, varuM is medial displacement.)

That's all!
Hate the inaccurate naming.
-IkaN

Study group discussion: Queckenstedt Sign

Suppose there is an obstruction to cerebral venous drainage in the left side, and u r doing an LP with manometry. If u occlude the left internal jugular vein, there will be no change in pressure but if u do it on the right side, there will be increase in csf pressure.