Zollinger Ellison syndrome mnemonic

Hello! Here's a short concept for the day!

Normally, secretin decreases gasrtin and gastric acid production,

In Zollinger Ellison syndrome, however, secretin increases gastrin production.

Non caseating granulomas mnemonic

Hello!

The mnemonic for non caseating granulomas is RBCS

Bernard Soulier syndrome mnemonic

This mnemonic would not help you to remember all the aspects of the syndrome but two quite important points would be on the tip of tongue for sure.

Remember the dog - St. Bernard's

Age of completion of ossification mnemonic

Hello!

For those who forget the age at which ossification centres close, this post is for you!

Bartters, Gitelmans and Liddles syndrome mnemonic

Hello!

Bartters, Gitelmans and Liddles syndrome present with chloride resistant (high urinary chloride) hypokalemic metabolic alkalosis.

What differentiates them:
Bartters: Hypercalciuric (Furosemide like! Loops lose calcium, remember?)
Gitelman: Hypocalciuric (Thiazides don't!) and Hypomagnesemia. Presents with cramping and spasms.
Liddles: Presents with hypertension, metabolic alkalosis and hypokalemia (Aldosterone excess like, but it is truly pseudohyperaldosteronism!)

It is characterized by: Hyporeninemic hypoaldosteronism, hypertension, hypokalemia and enhanced erythrocyte sodium influx

Here's a mnemonic for it!

"FaceBook GoT ALL pseudo HYPER about a Little syndrome"

FB - Bartter's is like Furosemide
GoT - Gitelman Thiazide
All pseudo hyper little - Liddles is like pseudo HyperALdosteronemia (Remember, it is pseudo - aldosterone levels are normal/low)

These syndromes are rare, so it’s important to rule out more common causes (Like diuretics)

That's all!

Here's an aphorism by Sir William Osler: “Care more for the individual patient than for the special features of his disease.” :)

-IkaN

Bile acid sequestrants mnemonic

Hello! The bile acid binding resins are:
Cholestyramine
Colestipol
Colesevelam

I'll talk about Cholestyramine in this post!

Iron deficiency anemia

   IRON DEFICIENCY ANEMIA

-The commonest nutritional anemia in India

-Causes:
Decreased Intake
Lack of absorption (eg. Celiac disease)
Increased loss ( in the form of blood loss through any system)

- More common in women d/t menstrual bleed, increased requirement in pregnancy and lactation.

 CLINICAL PRESENTATION
Increased fatiguability
Pica
May present as a triad with dysphagia and esophageal web in Plummer Vinson syndrome
Glossitis

INV:
Low Hb
Low Rbc count
Low MCV, MCH And MCHC
Low S. Ferritin
Raised TIBC
Reduced Transferrin saturation
Microcytic hypochromic picture on Peripheral blood smear; Pencil cells may be seen

Heyde's syndrome mnemonic

Greetings! Short post for the day about Heyde's syndrome!

The mnemonic is: Heydes' hidden bleeding heart.

Pathophysiology of achalasia mnemonic

Hello!

This post is about the pathophysiology of achalasia!

In achalasia, there is loss of NO and VIP releasing inhibitory neurons. Thus, the loss of the inhibitory innervation in achalasia results in the manometric consequence of failure of LES relaxation as well as loss of esophageal peristalsis.

Classification of enzymes mnemonic

Hello!

This mnemonic on classification of enzymes was submitted by Mohd. Ayub Ali.

The mnemonic is, "On The Himalayas, Lyf (life) Is Lightened."

Intermediates in Gluconeogenesis mnemonic

Hi guys!

So today I wanted to talk to you about Gluconeogenesis.

The first thing is that gluconeogenesis takes place in the mitochondria.

Now when anyone says, "mitochondria", I (and probably all of us) immediately jump to, "mitochondria is the powerhouse of the cell".

Why does Digoxin toxicity result in increased automaticity?

Hey everyone!

Digitalis and other cardiac glycosides are known to cause an AV nodal delay.

Then why does too much Digoxin result in some arrhythmias that are due to increased automaticity? Brady arrhythmias are explainable. But why tachy arrhythmias?

Atrial fibrillation in WPW syndrome

Random fact that I learnt today!

If a patient with WPW syndrome develops symptomatic atrial fibrillation, what is the drug of choice?

Answer is procainamide.

Stable patients suspected of having WPW with atrial fibrillation should not receive agents that predominantly block atrioventricular conduction, but they may be treated with procainamide or ibutilide.

Why?
Because if you block the AV node using beta blockers, calcium channel blockers or digoxin, you will favour conduction to the accessory pathway. This will worsen the arrhythmia.

That's why, in stable patients, chemical cardioversion is preferred.

If instability is present, electrical cardioversion is required.

That's all!
-IkaN

Related post: Supraventricular tachycardia mnemonic