Step 2 CK: Differentials of proximal muscle weakness

Hello!

Here's a short post about proximal muscle weakness!

CHF treatment mnemonic

Hello
Here's a simple updated mnemonic on pharmacotherapy of congestive heart failure: UNLOAD FAST

U- Upright position/ Ultrafiltration
N- Nitrates
L- Lisinopril (ACE inhibitors)
O- Oxygen therapy
A- Aquapheresis/ ARBs/ Aldosterone inhibitors
D- Digoxin/ Diuretics

F- Furosemide/ Fluid restriction
A- Arterial dilators (to decrease Afterload)
S- Sodium restriction
T- Theophylline/ Thiamine/ Taurine

Latest updates suggest new classes of drugs for the treatment of CHF, approved by the USFDA -
- Angiotensin receptor-neprilysin inhibitors (a combination tablet of valsartan and sacubitril)
- Sino-atrial node modulator (ivabradine)


Thats all
- Jaskunwar Singh

Lesch-Nyhan syndrome mnemonic

Here's a mnemonic on Lesch-Nyhan disease!

Edward syndrome mnemonic

Trisomy 18 is the second most common autosomal trisomy after trisomy 21. Here's a mnemonic for it!

Why do infants of diabetic mothers develop polycythemia?

Why do infants of diabetic mothers develop polycythemia?

It's due to hyperinsulinemia!

Second Heart sounds: Quick review

Hello everyone,
Heart sounds are quite interesting and musical topic, something that makes more sense by practicing rather than just reading theoretically. This post is completely dedicated to second heart sound.

Second heart sound (S2)
It is produced during closure of pulmonary and aortic valve.
It is a high pitched sound.

A neonate with cyanotic heart disease (Case #1)

A 24-hour-old newborn, born to a diabetic mother, appears blue in all extremities. He is found to have a single, loud S2 murmur. He is given NICU support. CXR hows cardiomegaly with, an apparent narrowing of the superior mediastinum and increased pulmonary vasculature markings.

Diagnosis? Treatment till surgery is performed?

Anti-epileptic drugs, CYP450 induction and inhibition mnemonic

Cytochrome P450 aka CYP450 has the alphabets C and P:

C for Carbamazepine
P for Phenytoin

GABA A and GABA B receptor agonist antagonist mnemonic

Here's a super short post.

Flumazenil acts on the GABA-A receptor and baclofen acts on the GABA-B receptor.

How do you remember this?

Whatsapp study group (Public)

This is... Experimental.

We do realize the group capacity is just 256 members, so all of you guys won't necessarily fit in.

Because all members will be added without verification... This is more risky. Even though we have 10+ admins :)

The rules are obvious - No forwards, no non medical talks, no wishing / greeting on occasions & no bothering other people via personal message.

Updated on Jun 17, 2017

Since the first public group is full (and a huge success), we created a second one: https://chat.whatsapp.com/561vU4UDy7V99K1ZmG6miH

To join one of the private strictly monitored study groups, follow the email procedure.

Psoriatic arthritis mnemonic

A simple one: PSORIATIC

P- Pencil-in-cup deformity

Pencil-in-cup deformity

S- Sausage-like digits

O- Onycholysis and Onychodystrophy

R- Rheumatoid factor negative

I- Ivory phalanx (increased bone density)

A- Arthritis multilans

T- Telescopic fingers

I- Itchy skin

C- Cold weather (more severe)

Thats all

- Jaskunwar Singh

Noonan syndrome mnemonic

Hey Awesomites!

NOONan syndrome- the name tells it all :D

Liposomal Preparations : A Quick Review

Hello everyone !
This is a short post about Liposomal delivery systems. Hope this introduces you to the concept nicely.

∆ What are Liposomes ?
- They are vesicles made of Cell membrane phospholipids. In pharmacology, they can be used as Drug delivery systems.

∆ What advantage does a Liposomal preparation offer in comparison to a regular preparation?
- The Liposomal preparation consists of the desired drug loaded into the Liposomal vesicle. This vesicle is resistant to degradation in the gut and can be customized to open up in selective tissues.
- Thus , it increases Bioavailability of the drug and hence , the action of the drug is more predictable and sustained !

∆ Is this even used at all? Or is it just an extra thing we learn which is never used ?

(- I'm  so glad you asked. )
Here's a list of drugs that have commercially available Liposomal preparations :

Remember : ABCD GIV

Amphotericin B
Bupivacaine
Vitamin C
Doxorubicin And Daunorubicin

Glutathione
Irinotecan
Vincristine

- Liposomal preparations have totally revolutionised the usage of Amphotericin B! Which is the drug of choice for a host of fungal infections and even Leishmaniasis.

- With the anti cancer drugs like Doxorubicin​ , innovative methods such as targeting the drug to a specific organ have been formulated so that the cytotoxicity is limited to the organ in question only ! Thus optimizing the absorption as well as the action !

What a marvellous delivery system , isn't it ?

I hope this post helped you!
Stay awesome.

H. pylori infection : Facts and Fallacies

Here are some interesting facts about cytotoxin- associated gene A (CagA)- positive strains of H. pylori and its role in esophageal and gastric carcinoma.

- Chronic Helicobacter pylori infection results in lower gastric acid secretion by inducing atrophic gastritis, thus hinting to have an inverse association with EC.
- H. pylori infection reduces ghrelin synthesis due to loss of P/D1 cells in the fundus and body of stomach which decreases gastrointestinal motility and induces delay in gastric emptying, thus increasing the risk of GERD.
- Also the CagA positive strains induce fluctuations in the levels of somatostatin, gastrin, dopamine and other essential hormones, which might cause increased reflux symptoms and metaplastic changes in chronic cases.
- Upregulation of proinflammatory cytokines and impaired TNF-alpha levels might play a role in pathogenesis of esophageal and gastric carcinoma. Extragastric diseases such as Colorectal polyps, nonalcoholic fatty liver disease, dental caries, coronary heart disease, the parkinson's disease, and iron deficiency anemia are also associated with H pylori infection through multiple signaling pathways.

Inspite of much evidence, there have been arguments and debates on the underlying mechanisms in causing esophageal carcinoma. A meta- analytic study, on the other hand has recently concluded that CagA- positive strains of H. pylori have a protective role in EAC while there is no such clear association with ESCC.

Thats all
- Jaskunwar Singh

Steroids and the Eye : Utility Review

Hello everyone ! I'm back with another post on Opthalmology ! Hope you like it.

∆ Uses of Steroids in Ophthalmology -

1. Prophylactic - PC
- Post op Cataract - 6w
- Corneal grafting.

2. Therapeutic - Go from anterior to posterior. We use it in every layer of the eye !

- Lids - Intralesional for Chalazion

- Conjunctiva - Phlyctenular Conjunctivitis.

- Sclera and Episcleral tissue - Scleritis and Episcleritis.

- Cornea - Contra indicated - As it affects healing and may cause super infections.

- Uvea - Anterior and Posterior Uveitis. Purulent Uveitis - Endophthalmitis ; Panopthalmitis.

- Retina - Diabetic Retinopathy Intravitreal Triamcinolone.

- Nerve - Optic Neuritis ( Multiple Sclerosis ) - Methyl Prednisolone

3. Others :
- Secondary Glaucoma due to the Inflammatory etiology.

~~~~~~~~~

∆ Precautions :

- Avoid in any ulcer cases as it can delay healing of the ulcer or aggravate fungal or herpetic ones.

- Can cause Cataract - Posterior Subcapsular. (Generally when given systemically)

- Can cause Glaucoma ( Generally when used Topically. )

Hope you liked it !
Stay awesome !

Colles' fracture

Hey Awesomites! Today I am gonna talk about Colles' fracture (a short post).

"It is an extra-articular fracture of the distal metaphyseal region of the Radius (at its cortico-cancellous junction) with dorsal impaction and angulation, caused due to a fall on outstretched hand (FOOSH) resulting in displacement of the fractured part of bone distally as well as radially."

Fall on outstretched hand resulting in displacements seen in Colles' fracture

Note that there is dorsal angulation and impaction in Colles' fracture as opposed to volar angulation in Smith's fracture, when seen in X-ray (AP and lateral views).

Displacements seen in Colles' fracture mnemonic- SLID
- Supination
- Lateral shift and tilt
- Impaction of bone fragments
- Dorsal shift and tilt.

Clinical features: mnemonicise the features here.

Dinner Fork deformity- Normally the styloid process of radius is at a lower level than the ulnar styloid. In Colles' fracture, the dorsal displacement and impaction of Radius results in shortening of the bone and places the radial styloid at the same level or a little higher than the ulnar styloid. Hence the patient presents with such a deformity resembling a dinner fork.

Thats all
- Jaskunwar Singh

Churg Strauss Syndrome

Hello awesomites, I am kind of obsessed with fancy syndromes. So here is one of them.

Churg Strauss Syndrome (CSS) also known as Eosinophilic granulomatosis with polyangitis or allergic granulomatosis.
It is a rare  autoimmune condition, that causes inflammation of small and medium sized blood vessels.

Manifests in 3 stages-
Early stage (Prodromal stage) : Present as
Asthma or
Allergic Rhinitis
Sometimes with nasal polyps and sinusitis
(Remember 'A'  is the first letter, so it should always come first)

Second stage : Abnormally increased eosinophils= Hypereosinophilia
Which causes tissue damage mostly lung and digestive tract.
Manifestations are Night sweats, weight loss, cough, abdominal pain, GI bleeding, fever, purpura

Third stage: vasculitis- which leads to infarction which further leads to atrophy
Further progression leads to complications.
But not all patients develops all three stages, or progress in the same order.

Pathophysiology - Its a Autoimmune disorder where different cell types are responsible for immune response especially Eosinophils, T&B cells, endothelial and epithelial cells. Mainly it is Th2 mediated reaction.

Complications can be life threatening -
(Most Grievous)
M- Myocardial involvement is the most common complication and most common cause of death in CSS patients
G- GI bleeding, GI perforation, Glomerulonephritis, Glomerulosclerosis,
Granulomatous appendicitis

Treatment - Conventional treatment includes glucocorticoids like Prednisolone and immuno suppressive drugs like Azathioprine, cyclophosphamide.
Newer drugs direct against specific cytokines like mepolizumab have additional steroid sparing property angood tolerability. Use of  Rituximab is under investigation and limited to few cases.

That's all.  :)

Galeazzi fracture- dislocation

This is a counterpart of Monteggia fracture- dislocation.
It also has two components: Fracture of distal- third of Radius and dislocation of the distal radio- ulnar joint. Mnemonicise it from here.

The mechanism of injury is the same as in Monteggia fracture and dislocation (fall on an outstretched arm causes an axial load on a hyperpronated forearm; Hyperpronation injury). The more distal the fracture, greater are the problems encountered in wrist and hand movements and more are the deforming forces that cause muscular and soft- tissue injuries.

A must to mention here is about Anterior Interosseous nerve (AIN) palsy and Wrist drop.

A patient with Galeazzi fracture and dislocation may present with the AIN palsy (while PIN is common in case of Monteggia fracture and dislocation) that may cause paralysis of flexor policis longus and flexor digitorum profundus thus resulting in a loss of pinch mechanism between thumb and index finger.

Wrist drop may also be a presenting complaint that results from an injury to the radial nerve and also due to weakness of brachioradialis and extension of wrist and thumb. The patient cannot bear the weight of the hand.

Diagnosis:- X- rays of forearm (AP and lateral view)

Treatment:- Complete reduction and fixation is important to restore the functions of limb. Galeazzi fracture and dislocation is best treated with Open Reduction and Internal fixation (ORIF). In children, closed reduction is the procedure of choice due to skeletal immaturity.

Monteggia fracture- dislocation

Monteggia fracture- dislocation has two components- fracture of upper- third part of ulna (bone of medial side) and simultaneous dislocation of proximal part (the head) of Radius. Check out the mnemonic to memorise it here.

The injury is caused by a fall on an outstretched hand with the forearm forced into excessive prone position (hyperpronation injury).

Types of Monteggia fracture and dislocation (Bado's classification) :-
Type I- Extension type- Angulation of proximal part of ulna anteriorly and dislocation of the head of Radius anteriorly. This type is seen in 60% patients.

Bado type I lesion (most common)

(Note- Posterior Interosseous nerve may get paralysed in Monteggia fracture and dislocation that is a result of anterior radial head dislocation in type I of Bado, unless reduced by manual pressure).

Type II- Flexion type- Fracture of proximal part of ulna and posterior dislocation of radial head.
Type III- Lateral type- Fracture of ulnar metaphysis and dislocation of head of Radius laterally.
Type IV Combined type Fracture of ulnar as well as radial shafts with dislocation of radial head anteriorly.


Diagnosis of Monteggia fracture and dislocation:- Check for both components- the fracture as well as displacement coz there could be an isolated fracture of ulna as due to nightstick injury.
X- rays of the forearm (Antero-posterior and lateral view) are diagnostic.

Treatment- Conservative management in children with closed reduction (resetting of bones and casting) accompanies the high risk of displacement thus causing malunion.
Standard treatment procedure in Monteggia fracture and dislocation is Osteosynthesis of the ulnar shaft (Open Reduction and Internal fixation) in children as well as adults to improve stability of the radio-ulnar joint and mobilise so as to prevent stiffness.


Thats all
- Jaskunwar Singh

Aminoglycoside made easy, simplified and decoded!

Hey everyone!
In this post, I write about everything about Aminoglycosides antibiotic in Mnemonic form :)

Potter syndrome mnemonic

Hey wait its not the Harry potter syndrome or sequence ;p
The term was first coined by Edith Louis Potter but it's a misnomer and more of a Potter sequence or the Oligohydramnios sequence. So here's the mnemonic of some of the clinical features: POTTER

P- Pulmonary hypoplasia
O- Oligohydramnios
T- Twisted face (Potter facies)
T- Twisted skin (wrinkly skin)
E- Extremity (limb) defects
R- Renal agenesis (bilateral)


That's all
- Jaskunwar Singh

Occupation and Ophthalmology : Clinical Pearl

Hello everyone.
I'm back with another ophthalmology post. This one is more of a clinical post , something that would be important to you in any specialty! Hope you like it. :)

So our life is all about being a successful doctor at the moment. Cause we wanna be good at our jobs !
Everyone wants to succeed at the work place. But there are loads of occupational hazards or diseases that we end up acquiring or aggravating due to the kind of job we do.

In this post I'll be talking to you about what ocular diseases can occur in Association with certain occupations.

1. Pterygium
- Occur commonly in farmers, driving school teachers and construction workers.
- Due to  exposure to sunlight for a long duration of time.

2. Fungal corneal ulcer or other fungal infections of the eye
- can occur commonly in farmers again. Because they are at a higher risk of vegetative trauma

3. Computer vision syndrome :
- seen in people working with electronic devices on an extensive level.
- the complains include dry eye , headache , eye strain , neck and shoulder aches.
- Simple tip for prevention - called the 20 20 20 rule.
Every 20 minutes look away from the screen for at least 20 seconds at an object about 20 feet away.
- Frequent blinking.
- Use of Lubricant for the eye.
- Use of anti glare screen/ spectacles.

4. Miner's nystagmus :
- seen in coal workers.
- Photophobia and night blindness may accompany the Nystagmus.

5. Glass blower's cataract :
- Occurs in glass makers.
- infrared rays cause damage to the lens producing this kind of cataract.

6. Welder's flash :
- seen in welders.
- It's a form of Photokeratitis
- Occurs due to UV rays
- causes abrasion , conjunctivitis and eye strain.

That's all for today !
Hope this helped.
Stay awesome !

~A.P.Burkholderia

Glycogen Storage Diseases : Mnemonic

Hi everyone.
I'm back with a short post. This one is about Glycogen storage diseases which, again,  we all hate to remember  :'D Hope you like it.

So Remember :

Very Pompously CAMe Her Tears.

1. Very =  Von Gierke's
2. Pompously = Pompe's
3. C = Cori's / Forbe's 
4. A = Anderson
5. M = McArdle's
6. Her = Her's (we'll at least Remember this one :'D)
7. Tears = Tarui's

So that's that.
Now how do we remember which is Muscular and which is hepatic ?
Simple.

Remember :
The Muscular get kissed under the Mistle Toe.

So the ones involving the Muscles are :
Mistle = McArdle
Toe = Tarui's.

Also remember :
Pompeii the city was a wh*re. So it went everywhere and hence Pompe's is both Muscular and Hepatic.

That's all for now. It may seem like a lot of crap to simply memorize these Glycogenosis but you'll realise they form an excellent aid for memory :D and are super important whether you want to do USMLE or Indian PG.
So c'mon ! Burn those Glycogens in your liver and get some Glucose into your head ;)
Stay awesome.
Happy studying.

At risk babies criteria mnemonic

Hey Awesomites

How do we define and on what basis do we label a newborn as an "at risk baby"? Well, it is very important to make a right approach to the risks and factors which affect the health of a newborn. So I just mnemonified the factors in a very simple way. Just remember the words: RISK APPROACH 

R- Referral weight- check for the weight of the baby. It should not be less than 70% of the referral weight (taken to be approximately 2500g), i.e. a newborn less than 1800g body weight must be referred to a paediatric health care centre for further investigation.
I- Insufficient breastfeeding- check for maternal and infant factors affecting the supply of milk.
S- Spacing (between subsequent pregnancies) less than 2 years
K- Kilograms of weight loss during first 2 months after birth- 5-10% weight loss in the first 10 days of life in a breastfed baby is normal. Investigate into the matter if the baby loses excess weight.
A- Acute episodes of illness (congenital or environmental factors)
P- Plural birth (or twin birth) or Premature birth
P- Parental illness is a must to check to determine risk of inherited disorders and illness in the newborn.
R- Raised birth order (five or more)
O- One parent
A- Active mother- Ask about her occupation and if she is working and about her lifestyle.
C- Constant failure to gain weight during the first few months of life
H- History of previous pregnancy and death of any sibling, if any must be taken into consideration.


Thats all
- Jaskunwar Singh

The GLUT's : Mnemonic

Hello everyone !
I'm back with another short post on biochemistry.
It's about the Glucose transporters which we all hate :D So let's get down to it.

GLUT - Short for Glucose Transporters , are channels present in our body that bring about glucose uptake. They are forms of Facilitated transport mechanism and basically occur across a Concentration gradient.

Now it's important for us to understand their location , function and regulation if we want a good understanding of Glucose metabolism. But this can get a little tedious , hence this post.

There are a total of 4 major GLUTs. Out of which one is dependent on insulin and the others are not.
So first we're doing insulin independent ones.

Remember :

BBB
Kid's LiPs are
PiNK.

~~~~~

GLUT 1 -
Remember : BBB.

B - Blood ( The RBCs)
B - Baby  (So fetal tissue)
B - BBB ( The Blood brain barrier itself )

~~~~~

GLUT 2 -
Remember :  Kid's LiPs

Kid's - Kidneys
Li - Liver
Ps - Pancreatic Beta cells

~~~~~

GLUT 3 -
Remember : PiNK

Pi - Placenta
N - Neurons
K - Kidneys

_____________________________
Now we come to the Dependent one.
~~~~~
GLUT 4 -
Remember :
Father Mother Depend.

Father - Fat
Mother - Muscles ( Cardiac / Skeletal)

Now how do we remember this ?
In general the Mother and Father are who we depend on ! But in biochemistry the mother and father themselves depend on insulin. ! And the baby ( BBB etc) are independent.

Got it ?
Hope this helped.
It's something I've struggled with.
Anyway.
Happy studying. !
Stay awesome

~A.P.Burkholderia

Electronic Fetal Heart Rate monitoring interpretation (VEAL CHOP mnemonic)

Hello!

So do you guys know about the VEAL CHOP mnemonic?

Variable decelerations - Cord compression
Early decelerations - Head compression
Accelerations - Oxygenation
Late decelerations - Placental insufficiency

Well, it has one kind of periodic FHR change pattern missing. That's the sinusoidal pattern associated with fetal anemia!

For those who don't know, let's run through them quickly :)

Step 2 CK: Screening for Gestational Diabetes Mellitus (GDM)

Hello!

As you guys already know, GDM diagnosis can be accomplished with either of two strategies:
“One-step” 75-g OGTT or “Two-step” approach with a 50-g (nonfasting) screen followed by a 100-g OGTT for those who screen positive.

But what if, in the exam, you are asked to choose a screening test for GDM...
And the options contain both:
- One hour 50 gram glucose load test (1-h 50-g GLT)
- Two hour 75 gram oral glucose tolerance test (2-h 75-g GTT)
... Then which one do you choose?

Niemann-Pick disease notes and mnemonic

Hello!

Niemann-Pick disease (NPD; also called sphingomyelin-cholesterol lipidosis) is a group of autosomal recessive disorders associated with splenomegaly, variable neurologic deficits, and the storage of sphingomyelin.

The Burkholderian Culture : From the Authors' Diary

Hello everyone ! I'm A.P.Burkholderia , and I'm back with another post

Now a lot of people have been asking me why my name is that. Some have assumed it's my actual surname (Like our very own IkaN, but that's a whole 'nother story) while others have unraveled the mystery of the Burkholderian terminology (Like the ardent PSM-proponent Jay ). So before any more of you are boggled by this Burkholderian business I figured let's talk about why this organism is fancy enough to earn the charm of being my pen-surname. :P

So Burkholderia is a Gram negative rod. And it is one of a kind - Cause It's a Non Fermenter ! So if you were to make a TSI plate it would give you alkaline in the slant as well as the butt (LOL). Only few other organisms like Pseudomonas and Acinetobacter are non fermenters. So it's a total Aerobe and it can be checked with "High and Leifson Oxidation Fermentation media". Another cool name :D 

It's got 3 different types : 

B. cepacia 

B. mallei 

B. pseudomallei.

Now I love how it's called "Mallei". In Hindi 'Malai' means 'Milk Skin'. I find that hilarious. 

Also, 'Mai Lai' means 'I shall bring '. I find that really funny too. ( Burkholderia , Main Laiii !)

But other than that , it's a pretty serious bug. 

It causes Cepacia syndrome in Cystic Fibrosis,  which presents as a form of Bronchiectasis or Serious pneumonia. 

It can cause Meiloidosis which has a presentation similar to TB and another one called 'Glanders'. 

It shows a safety pin appearance when seen under the microscope on staining with Geimsa. 

Other than this , it's a very hard big to get rid of. 

It's almost resistant to all antibiotics and only the Carbapenems may work ! 

So this is why I love this bug. 

It's cool , it's classy and it's hard to get. :p 

Other than that , I love saying the name! *Burkholderia* 

I might do a video some day on this :p and how to say it right. 

Till then , Ciao! 

Stay awesome. 

*Burkholderia out*

Top 10 series: Digoxin

Klein waardenburg syndrome mnemonic

Here's a small post :)

Waardenburg syndrome is a rare genetic disorder most often characterized by varying degrees of deafness, minor defects in structures arising from the neural crest, and pigmentation changes.

Synonyms: Waardenburg Shah syndrome, Waardenburg-Klein syndrome.

Acute Post-hemorrhagic anemia

Hey Awesomites

Today I am gonna talk about the Anemias of blood loss, particularly the acute cases of posthemorrhagic anemia.

The Basics- Anaemia

Hey Awesomites

"Anaemia is defined as a decrease in the level of haemoglobin due to loss of a significant amount of red blood cells which decreases the oxygen- transporting capacity of blood."

Top 10 series: Everolimus

Post MI complications mnemonic

Hey Awesomites!

Complications due to an attack of myocardial infarction mnemonic: DARTH VADER (I loved his character in Star wars you know :p )

D- Dressler's syndrome
A- Arrhythmia
R- Rupture
T- Tamponade
H- Heart failure
V- Valvular defects
A- Aneurysm
D- Death!
E- Embolism
R- Recurrence


That's all
- Jaskunwar Singh

Cushing's Reflex in Meningitis : Mnemonic and Explanation

Hello everyone !
Another short post on a very important triad. Cushing's!

Cushing's reflex
It occurs in response to raised Intracranial Pressure (ICP/ICT)

Mnemonic : 

HIB

H - Hypertension
I   - Irregular Breathing
B - Bradycardia

Mechanism :
So just imagine :
Due to some reason you develop an increase in the ICT.
We know that blood flows from High Pressure to Low Pressure. Generally , the CSF pressure is lower than the BP.
However after a point , the ICT is bound to become equal to or even more than the systemic BP!
If that happens , the blood flow to the brain is decreased and the Brain can get ischemic (cause the Cranial pressure would be higher. So the body won't be able to pump the blood into it.)

Thus, in order to compensate for this , the sympathetic system is activated. The body's peripheral vessels undergo constriction to raise the BP. This would keep them at a higher pressure than the Cranium thus keeping the blood flow intact for a while at least. This causes the Systemic Hypertension.

In a way it's the last ditch effort to save the brain!
Due to sympathetic stimulation the respiratory centers get stimulated too and it's all weird so it causes Irregular Respiration.

Now you'd expect Tachycardia when there is so many Sympathetic juices flowing through your body.
But no. Things aren't as simple as that.

The aortic baroreceptors sense the increased BP and end up decreasing the Heart Rate. Resulting in Bradycardia. So in a way that's the 2nd phase of this Reflex!

The Reflex serves as a marker of raised ICT as that is the event that puts the whole cycle into place.
This generally occurs as the body's last resort to restore blood to the brain.
What a wonderful Homeostatic mechanism !!

Hope this helped !
Stay awesome !

Reynolds pentads

Hello readers ! Today's blog is sweet and simple.

Reynolds pentads are collection of signs and symptoms appearing when there is obstructive cholangitis -infection of bile duct usually caused by bacteria .Following are the diagnostic features of the reynolds pentads with simple  mnemonic.
   RJ -FHC.
R-Right upper quadrant pain .
J-Jaundice .
F-Fever .
H-Hypotension.
C-Confusion .

By the way the first three diagnostic features are also called as Charcot's triad so we can also say Reynolds traid is combination of charcot's triad with low blood pressure and mental confusion .

Stay awesome:)

~Ojas

Neonatal reflexes mnemonic

Hey Awesomites!

Here's a mnemonic for the reflexes seen in neonates and infants: GRASPMEN

G- Grasp reflex/ Glabellar tap
R- Rooting reflex (to assist breastfeeding)
A- Automatic walking reflex
S- Suckling reflex (during breastfeeding)
P- Plantar Reflex
M- Moro's reflex
E- Extrusion reflex
N- Neck (tonic reflex)

That's all
- Jaskunwar Singh

Tuberculosis : Ocular Manifestations

Hello everyone !
This is a short post about the manifestations of Tuberculosis in the eye.

TB is associated with a lot of findings in the eye.
We can classify them as :
1. Disease related.
2. Therapy related.

Let's look at the first one.

1. Disease related :

A. Extra Ocular structures -

    I. Appendages :
       Eyelid - Lupus Vulgaris. Lid granuloma.
       Lacrimal apparatus - TB Dacryoadenitis. Dacryocystitis.
      
    II. Orbit :
         Orbital Cellulitis.
         Orbital Pseudotumor.

B. Ocular manifestations -
    
     I. Conjunctiva -
         Phlyctenular Conjunctivitis - due to hypersensitivity to Tuberculin. Seen as intense itching , discharge , redness and nodules.

     II. Cornea -
          Interstitial Keratitis

     III. Uvea -
          Granulomatous uveitis ( Chronic anterior Uveitis ). Shows Mutton Fat appearance.

          Choroiditis - Choroid Tubercles - classic of TB Uveitis. Tuberculoma may be seen. Miliary choroid nodules may be seen.

      IV. Retina -
            Eale's disease - may be a result of Hypersensitivity to Tuberculin. Although causality is not established clearly.
           Sub retinal Tubercles.

2. Therapy Related :

       A. Ethambutol - may cause Optic Neuritis - generally retrobulbar type. With Color Blindness.

      B. INH - Isoniazid can cause retrobulbar optic neuritis, although this is much rarer.

     C. Immune Reconstitution Inflammatory Syndrome - When a person recuperates from TB /HIV his immune system may become hyperactive and show Immunologically mediated uveitis.

Hope this helps !
Happy studying.
Stay awesome. 

~A.P.Burkholderia

Nodule at the Limbus : Mnemonic

Hello everyone !
Here's a way to remember the D/D's of Nodules at the Limbus.

Mnemonic :
Please Please Please ! Eat Spicy MCDonald's Tortilla.

Please - Pterygium.
Please - Pinguecula.
Please - Phlycten.
Eat - Episcleritis.
Spicy - Scleritis.
M - Melanoma. 
C -  Choristoma
Donald - Dermoid.
Tortilla - Trachoma. Tranta spots.

1. Out of these Pterygium , Pinguecula and Phlyctens are Conjunctival lesions.
Pterygium is a fold of conjunctiva that encroaches towards the pupil.
It can be vascular and nodule like. Can cause Foreign body sensation and decreased vision if it covers the pupil.
It may also cause Diplopia and a Squint due to its traction over the eye.
A pinguecula is milky like nodular swelling of the conjunctiva.
A Phlycten is a lesion in Phlyctenular Conjunctivitis which is an allergic or Hypersensitivity response to Tuberculin or staph Antigens. There is intense itching , discharge and nodules in the eye - called Phlyctens.

2. The lesions of Episcleritis and Scleritis are similar. They're both associated with systemic disease like Rheumatoid Arthritis , SLE, Sarcoidosis etc.
Scleritis is a more severe one of the two. There's marked redness and congestion of the eye along with multiple vascular nodules. The eye is very inflamed. There is intense pain and watering. It needs urgent treatment. It may causes various types of staphylomas.
Episcleritis is a more benign form. There is intense itching , nodular vascularity and discharge with some amount of congestion.

3. Tumors like Choristoma , Dermoid tumor and Melanoma mainly arise from the uvea. They're not very common.

4. Trachoma : presence of lesions in trachoma at the nodule may be prominent. You may also get 'Horner Tranta spots' in Vernal Keratoconjunctivitis which is an allergic Conjunctivitis.

Hope this helped !
Stay awesome !
Happy Studying!

How to check for the Pupils : Clinical Pearl

Hello everyone !
This is a post about how to look for a normal pupil while doing an ophthalmological examination.
So here goes :

1. The Setting.
- Relax the Patient
- Take the patient to a semi dark room.
- Make the patient Fixate on a distant point to eliminate any error that Accomodation may produce.
- Place an obstruction between the two eyes.
- Always shine your torch laterally and bring it in only from the sides to avoid light shining directly on the other eye.

2. The Parameters.
Look for the following in the pupils :
- Size
- Shape  ( for eg. You may get a Festooned pupil on adding your Mydriasis if the patient has adhesions)
- Number ( for eg. You may get Poly Coria which causes Diplopia )
- Location  ( for eg. You may get Corectopia)

3. Reaction to light.
- Unless you've met the criteria above ( The setting) , you cannot say 'Direct and indirect reflex present' .
So unless you're in a semi dark room (and the other 3 criteria mentioned above) you would plainly shine the torch and look for constriction. This plainly shows the pupils are reactive to light.

4. Light Reflexes.   
- Check for your direct and consentual (indirect) reflexes in both your eyes after meeting the listed Criteria in the *Setting* !

Hope this helps !
Happy studying !
Stay aweosme.

~A.P.Burkholderia

Argyll Robertson Pupil : Mnemonic

Hello everyone ! I'm back with a short and sweet post on Argyll Robertson Pupil.

Mnemonic for Argyll Robertson  Pupil (ARP) :
ARP Accomodation reflex present
PRA Pupillary reflex absent.

It's seen in conditions like Neurosyphilis for which it is extremely specific. 
You could also see it in some form of strokes or Diabetic Neuropathy.

Another similar Pupillary reaction is Aedes pupil. The difference is Aedes is a  dilated pupil while Argyll's is constricted. How to remember this ?
Mnemonic : AeDes.
So Aedes is tonically Dilated.

Hope this helped !
Stay aweosme.
Thanks.

Treatment of Narcolepsy

Hey Awesomites!
This is the last post of the four-post series on Narcolepsy. So let's begin.

Diagnosis of Narcolepsy

Hello friends!!

This is the third one in the four-post series on Narcolepsy. Let's commence.

Diagnosing a not so common disorder, that too neurological is quite tricky. The greatest difficulty is separating it from the normal daytime and postprandial sleepiness of most people. Admit it, most of us feel like sleeping in the afternoon period after lunch, especially while reclining in the sofa, while watching television or in the theatres watching matinee shows. :p  

What distinguishes the typical narcoleptic attack from commonplace postprandial drowsiness and napping is the frequent occurrence of the former(2 to 6 times everyday), their irresistibility, and their occurrence in unusual situations, as while eating, standing, or carrying on a conversation.

Excessive daytime sleepiness can also be present with heart failure, hypothyroidism, use of antihistaminics, alcohol intake, head trauma, certain brain tumours like craniopharyngioma etc.

 

Overnight polysomnography followed by a standardized multiple sleep latency test can exclude other causes of excessive daytime sleepiness like obstructive sleep apnea. In the test, the patient is given 5 opportunities to nap at 2 hour intervals in a day

. 

If there are more than 2 Sleep-onset REM periods and a mean sleep latency of less than 8 minutes, it strongly suggests narcolepsy. 

Actually, in Narcolepsy, there is characteristic reversal in the order of the two states of sleep, with REM (rather than NREM) phase occurring  at the onset of sleep attacks. And the sleep latency is nothing but the interval between the point when an individual tries to sleep and the point of onset of sleep with the respective EEG patterns.

Measurement of hypocretin(orexin) levels in the CSF may help establish the diagnosis; a level lower than 110pg/ml is diagnostic of narcolepsy.

Cataplexy must also be distinguished from syncope, drop attacks and atonic seizures. In atonic seizures, there is temporary loss of consciousness, while in narcolepsy consciousness is perfectly preserved. 

That's all! Do go through the other posts in this series.

Role of Orexins in Narcolepsy
Clinical features of Narcolepsy
Treatment of Narcolepsy

-VM

Clinical Features of Narcolepsy

Hello friends!!

This is the second one in the four-post series on Narcolepsy. So let's begin.

Narcolepsy is not just a disorder in which the patient sleeps a lot, believe it or not the number of hours in a day spent in sleep by the narcoleptic is no greater than that of a normal individual!!

Narcolepsy is characterized by the classic tetrad of excessive daytime sleepiness, cataplexy, hypnagogic hallucinations and sleep paralysis. There is also a disorder of REM sleep. So let us try to understand these major clinical features.

The essential disorder is one of frequent attacks of irresistible sleepiness several times a day, usually after meals or while sitting in class or in other boring and sedentary situations. Now let us try to picturize the patient.

The eyes close, the muscles relax, breathing deepens slightly and it seems that the individual is dozing. A noise, a touch or even the cessation of lecturer’s voice is enough to awaken the patient. So the periods of sleep rarely last longer than 15min unless the patient is reclining, or if he is in an appropriately comfortable situation to sleep. At the conclusion of the nap, the patient feels somewhat refreshed.

Cataplexy refers to a sudden loss of muscle tone brought on by strong emotion- that is, circumstances in which hearty laughter or, more rarely, excitement, surprise, anger, intense athletic activity. So you can basically “tickle” a Narcoleptic into a Cataplectic state. 

The patient’s head will fall forward, jaw will drop, knees will buckle with sinking to the ground – all with perfect preservation of consciousness (scary, right?). Most attacks of cataplexy are partial, eg., only dropping of the jaw or weakening of the knees.

In about half the patients, there is hypnagogic hallucination and sleep paralysis. Please do not confuse sleep paralysis with cataplexy; sleep paralysis is brief loss of control(not tone) of voluntary muscles that occurs during the period of falling asleep or less often when awakening.

There are two terms which we should know, hypnagogic and hypnopompic. Hypnagogic or predormital refers to the period of falling asleep while hypnopompic or postdormital refers to the period of awakening. Sometimes there may be vivid and terrifying hallucinations with or before the onset of sleep paralysis, which may be visual, auditory, vestibular or somatic, called hypnagogic hallucinations.

That's all. Do go through the other posts in this series.

Role of Orexins in Narcolepsy
Diagnosis of Narcolepsy
Treatment of Narcolepsy

-VM 

Role of Hypocretins/Orexins in Narcolepsy

Hello friends!!

This is the first of the four-post series on Narcolepsy.

So let's start. The hypocretins were thought in the past to regulate feeding behaviour and energy metabolism, the word “orexin” is derived from the Greek word for appetite. But later through animal experimentation it was found that in mice, inactivation of two hypocretin receptors reproduces Narcolepsy.

First of all, let us learn that monoaminergic neuronal projections from Tuberomammilary nucleus(histaminergic), Locus Ceruleus(noradrenergic) and the Raphe nucleus(serotonergic) inhibit the Ventrolateral Preoptic Nucleus(VLPO) of hypothalamus.

To put it simply, the transition between sleep and waking is determined by the state of activity of the VLPO. Now imagine a see-saw, on one side we have all these nuclei wanting the person to wake up and on the other side we have VLPO forcing the person to sleep. Whoever gets heavier, metaphorically speaking, chooses the person’s state. 

So what’s the role of orexin/hypocretin ? We can say that it enables a smooth transition between wakefulness to sleep by reinforcing the monoaminergic firing from those three nuclei; hence it indirectly inhibits the VLPO. Hence if we remove orexin from the picture, the person will fall asleep immediately without being able to control; and roughly this is what occurs in Narcolepsy. 

That's all. Do go through the subsequent posts in this series.

Clinical features of Narcolepsy
Diagnosis of Narcolepsy
Treatment of Narcolepsy

-VM

Basics of Immunoglobulin G

Hey  readers!! ,So I have started with immunoglobulin section where I will be putting facts about a single immunoglobulin ,so today it is IgG!.

Immunoglobulin G or IgG occupies about 80% of serum antibodies.! .It's normal concentration is about 8-16mg/ml.They are created and release by plasma B cells .
There are two unique facts about IgG
1)It's catabolism.
2)Suppression of homologus antibody synthesis by a feedback process.

What's unique in catabolism?.
Well we can say body has complete control over the catabolism and to make it simpler let's say body and IgG both acts opposite to each other !.(Just a saying :p,Infact we know IgG works for body).For example In some diseases like chronic malaria ,kala azar or myeloma IgG level rises and as we know body has complete control and it acts against it So, IgG synthesis its gonna catabolised it rapidly !
Conversely,In hypogammaglobulinemia IgG given for treatment is metabolised slowly.

Suppression of homologus antibody synthesis
IgG has another unique property of suppressing the antibody synthesis which looks like it or performs similar kind of functions or simply homologus antibody.
Now let's say IgG is quite insecure about its true but dominating love -"Body". It doesn't want any competition so it kicks away all the antibodies which looks like it or perform similar function like him
(Such a insecure antibody it is  !)and this unique property is utilised in the Iso-immunisation of a women by administration of anti-Rh(D) IgG during delivery.

Well some more characteristics of our hero IgG is
It's the only maternal immunoglobulin that is transported across placenta and provides "Natural passive immunity"in new born (Not present in infants )

It has 4 subclasses due to presence of gamma 1,gamma 2 , gamma 3 and gamma 4 chains .

IgG1=65%
IgG2=23% (By the way 23 is also half life of IgG)
IgG3=8%
IgG4=4%

Here are functions of IgG molecule

Immunohemolytic anemias part-2

Hello readers, here is the continuation of the previous topic, Immunohemolytic anemias. Today we will discuss the next two types, its more like winter special.

B) Cold agglutinin type-  Cold agglutinin derives their name from the fact that they show maximal activity at temperature lower than normal body temperature.
It is present in low titres in healthy individuals.
Physiological cold agglutinin develops naturally after birth as a result of change in expression of Red cell antigens and reacts maximally at 4°C.
While pathological cold agglutinin maximally reacts at around 28-31° C and tend to occur at very low titres.

Mnemonic is "Cold MILL"
C     -  Complement mediated hemolysis. 
         
M    -  IgM is the causative antibodies

  I     -  Cold agglutinin antibodies appear  
           transiently following Infections 
            [Mycoplasma pneumoniae, EBV,
            HIV, influenza virus, CMV]
          - I antigen is the most common
              target
           
L     - Chronic cold agglutinin AIHA is
          associated with Lymphoid 
           neoplasm
          (esp B cell neoplasm), leukemias     
           like CLL

Mechanism- IgM binds to red cell where the temperature may fall below 30°C. It agglutinates red cells, and fixes complement rapidly. As blood recirculates and warms, IgM is released,but sufficient deposition of complements leads to phagocytosis of affected red cells in spleen, liver, bone marrow.

Clinical presentation- Exerts their pathological effects either via hemolysis and red cell destruction in RE system predominantly liver or by vaso occlusion due to agglutination.
-Mild anemia, purplish discoloration of fingers, toes, earlobes [ Acrocyanosis],  mild hepatospleenomegaly,
Raynaud phenomenon in peripheral cold exposed parts.

C) Cold hemolysin type -
Also known as paroxysmal cold hemoglobinuria.
It's a rare fatal disorder causing intravascular hemolysis and hemoglobinuria when auto antibodies binds to P blood group antigens in cool, peripheral regions of body.

Paroxysmal Cold HemoGlobinuria:
P- P blood group antigens
C- Complement mediated lysis occurs.

    IgGs auto antibodies binds to red cell in  
    cool peripheral regions, Complement
    mediated lysis occurs when affected
    red cell recirculates to warm regions,
    because complement cascade 
    functions
    more efficiently at 37°C

H- Hemoglobinuria
G - Auto antibodies belong to class IgG

Symptoms of the patients aggravates on exposure to cold.

Winter is coming, we know what's coming with it.
Stay warm :)

Immunohemolytic anemias part-1

Hello awesomites!
This is my very first post, so am starting with my favorite subject Hematology.
Today's post is about Immunohemolytic anemias, commonly ignored type of anemia

Also referred as Autoimmune hemolytic anemias(AIHA)
Where antibodies are responsible for premature destruction of red blood cell.
Types- warm antibody type
            - cold agglutinin type
            - cold hemolysin type

Warm antibody type  -  It is the most common type of AIHA.
you can remember it by mnemonic
" WARM GRILLED "
W - Warm because, antibodies are active  
       at 37°C
A -  Associated with other Autoimmune        
       disorders ( secondary causes like 
       SLE)
R - Red cell hemolysis is mainly
      extravascular
M- Moderate spleenomegaly due to
       hyperplasia of splenic phagocytes      

G- Ig G class - most common causative
      antibodies ( IgA sometimes too)

R- Rh blood group antigens are the main
      target 
I- 50% primary cases are  Idiopathic
       Secondary causes can be

L- Lymphoid neoplasm

ED-  Exposure to Drugs.
Examples - penicillin, cephalosporins, quinidine, methyl dopa etc

Mechanism - A) Antigenic drugs-
Drugs such as penicillin binds to red cell membrane and they are recognized by the antidrug antibody. The antibody either recognizes the drug and bind to it or both drug and membrane protein,ultimately results in hemolysis.

B) Tolerance breaking drugs- In drugs such as methyl dopa, antibodies are formed against red cell antigens particularly Rh antigens.

Stay awesome✌️

Nasal spray that prevents suicide.

0Hello readers! Being in medical field we are quite acquainted with the word "Stress out" .Todays article is just about a simple nasal spray that can prove to be a boon to entire human kind.(I think specially our field ! :p)

Everything in a brain is carried out by special substances called as "Hormones" .Even the simplest change in mood is concerned with hormonal changes.For example in first trimester of pregnency a rapid rise in estrogen and progesterone can cause mood swings in woman.Similary when there is depletion of hormones or its metabolites or less production of hormone this can leads to depression ,low -emotional state ,anxiety etc.Suicide can be triggered by serious illness ,can also be triggered by low self-esteem or emotional pain .
Scientists are developing a nasal spray that can prevent suicides! .This nasal spray consists of Thyrotropin releasing hormone(TRH) also known as thyroliberin . Thyrotropin is actually hormone released by hypothalamus ,it actually stimulate release of thyrotropin and prolactin from anterior pituitary.Recent findings have found out that TRH  also shows  anti-depressant and anti-suicidal effects.Thus preventing suicidal behaviour and depression.Researchers want to figure out ,a way to deliver it to a brain when it is given through nose  .Brain is protected by Blood brain barrier (BBB),which is acting has a hinderence to pass TSH to brain.
Clinically it is related  in spinocerebellar degeneration and disturbance of  consciousness in humans.Pharmacological form is known as protirelin.

I hope scientists find it soon how to cross  BBB  :p
Exams are near and I am already freaking out :p
Keep smiling :)
Have a day with high level of TSH in brain :)

~Ojas