Causes of dilated cardiomyopathy mnemonic

Hi awesomites!

Here's a short note on causes Dilated cardiomyopathy.

It's mostly idiopathic.

Other causes are:

1. G enetic Mutation
2. Myocarditis

3.  Alcohol  abuse
4.  Drugs
5.  Pregnancy
6.  Hemochromatosis

Mnemonic.  GMM ADPH

That's all :)
 
H@Mid

Why do newborns have a higher heart rate?

Hey guys!

Have y'll ever wondered why do babies have heart rates as high as 160s?

Answer:
Babies have a high proportion of Body Surface Area to heart than that in adults. Therefore, in order to maintain adequate blood flow, baby's "li'l heart" has to pump more often to cover the "large Body Surface Area"!

I hope y'll find this interesting!

Till then, stay awesome!

-Rippie

Nasal Encephalocele vs Nasal Glioma

Both nasal encephalocele and nasal gliomas are congenital conditions in which there is herniation of glial tissues and meninges into the nasal cavity through the foramen cecum.

Both the masses are seen in the nasal cavity as bluish masses with nasal obstruction.

Nasal gliomas have no communication to the brain as the communication gets detached after the fusion of cranial bones in late IUL. Gliomas are firm and non compressible mass.

Encephalocele also presents as nasal mass with obstruction. The swelling increases in size in response to coughing. Most common site is occipital and then frontal.

Bilateral compression of the internal jugular vein also leads to the increase in the size of mass called as Frustenberg Test.
Frustenberg test is positive in encephalocele and negative in gliomas.

Investigation of choice for both is MRI.

Hope this helps!
Ashita Kohli

External Cephalic Version : An overview

Here's a short review on basics of External Cephalic Version.

So this Procedure is basically manipulating the baby externally to come in a favorable cephalic presentation.

Its indications need are limited and mainly include -
Breech Presentation and Transverse Lie.

The most important thing to remember is when not to do an ECV.

You can remember these contraindications as :

ABCDEF

A - Ante partum hemorrhage ( Previa and Abruptio.) It can result in detachment and more Accidental Hemorrhage (Abruption).

B - Bad Obstetric History

C -
Contracted Pelvis - ECV can cause fetal Hypoxia if the pelvis is small already

Congenital uterine Abnormalities - like bicornuate etc as can cause uterine rupture.

D - Dual Pregnancy (Twins/ Multifetal pregnancy).

E - Eclampsia PIH.

F - Fluid - Oligohydramnios

2 other C/I are important to remember -

Previous Cesarean section ( Uterine rupture chances are high).

Rh Incompatibility.

The best time for doing an ECV is around 36-38 weeks. It's easiest to perform the maneuver before 36 weeks but the fetus undergoes a lot of spontaneous movements before 36 weeks and may come back to being Breech.

Beyond 40 weeks best to avoid it as liquor reduces in amount and can cause cord compression amongst other things.

Another pre requisite is having the uterus relaxed. So it may be done in OT set up where anesthesia like Halothane can be used as a uterine relaxant. (Not so sure about the last part as some PG resident in college told us this. :P)

Hope this helps.
Happy Studying !
And as always ,
Stay Awesome !

~ A.P.Burkholderia.

Pancreatic cysts

The take home message for differentiating pancreatic cysts are-

1. When you see no epithelial lining to the cyst on microscopy, think of a pseudocyst
2. When you see a multilocular cyst with a central scar, think of a serous cystadenoma; if it is absent, think of a mucinious cystadenoma. Both are " NOT" connected to the main pancreatic ductal system
3. When you see a sizable (more than 1cm) growth within the pancreatic duct, think of IPMN!

That's it!

Mnemonic- Causes of saddle nose

Saddle nose is a nasal deformity due depressed nasal dorsum which may be bony, cartilaginous or may involve both.

Causes- HOT SALT

H- Hematoma
O- Operative (during SMR)
T- Trauma
S- Syphilis
A- Abscess
L- Leprosy
T- Tuberculosis

Hope this helps!
Ashita Kohli

Mikulciz Disease- Rhinoscleroma

Mikulciz disease aka Rhinoscleroma is a chronic granulomatous disease commencing in the nose and extending into the nasopharynx, oropharynx, larynx, trachea and bronchi

This disease may occur in either or the sexes at any age.

Causative organism- Klebsiella rhinoscleromatis (gram negative Frisch bacillius)

Three stages-

1. Atrophic Stage-
This stage typically resembles atrophic rhinitis and presents with nasal discharge which is purulent and foul smelling with nasal crusting.

2. Granulomatous Stage-
This is a proliferative stage. Characterised by granulomatous reaction and presence of mikulciz cells.
Presents as painless nodules in the nasal mucosa.
The subdermal infiltration into the lower part of external nose and upper lip gives a Woody feel to the nose.
There may occur broadening of the nose with thickened skin- Hebra nose

3. Cicatricial Stage-
There occurs fibrotic adhesions and fibrosis of nose, nasopharynx and oropharynx.
The fibrotic deformity of nose is known as- Taper nose.

Most common symptoms-
Nasal discharge and crusting> nasal deformity> epistaxis

Diagnosis-
Diagnosis can be done histopathologically which shows mikulciz cells and Russell bodies in the submucosa which is characteristic of rhinoscleroma.
Mikulciz cells are foam cells with central nucleus and vacuolated cytoplasm containing bacteria.
Russell bodies are eosinophilic inclusion bodies seen in the cytoplasm.

Treatment-
Streptomycin (2g/day) + teracycline (2g/day) for 4-6 weeks

Hope this helps!
Ashita Kohli

Polycythemia in newborn notes

Polycythemia in newborns

Definition: Venous hematocrit of 65%

Clinical manifestations:
Ruddy, plethoric skin.

CNS - Lethargy, hypotonia, tremulousness, irritability.

Seizures.

Hypoglycemia, hypocalcemia, hyperbilirubinemia.

GI - Vomiting, distension, NEC.

Kidney - Renal vein thrombosis, acute renal failure.

Cardiopulmonary - Respiratory distress syndrome, congestive heart failure.

Treatment: Partial exchange transfusion.

That's all!
Remember the association with infants of diabetic mothers.
-IkaN

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