Dermatophytes mnemonic

Let's learn a lil mycology today!

Lesions of small pox and chicken pox mnemonic

Same stage vs different stages of development!

Structure and properties of poxviruses mnemonic

Hello!

So we will be learning about the structure and multiplication of poxviridae today from the mnemonic: “Pox is in a big box”

Excited?

Memory aid for urease positive organisms

Hailo!

Here's a little memory aid for urease positive organisms.

Alcohol and Drug Interactions: 4th Part

Hii friends...

This is the last post in the series: Alcohol and Drug Interactions. The previous posts in this series were Disulfiram-like Reaction, 2nd Part, and 3rd Part.

With Warfarin

1. Binge drinking- Leads to inhibition of warfarin metabolism by CYP450 enzyme system. So it can precipitate warfarin toxicity with increased bleeding tendency in the body.

2. Chronic Alcohol consumption- Leads to induction of CYP450 enzyme system, so increases metabolism of Warfarin in the liver. So higher than usual dose of warfarin is needed to exert appropriate anticoagulant action in the patient.

With Opioids

Alcohol increases the sedative effects and also increases the risk of respiratory depression. It also attenuates cough reflex and gag reflex, so the patients have a higher risk of getting food stuck in their respiratory tract, remember Cafe Coronary.

With NSAIDs

1. NSAIDs have been implicated in an increased risk of ulcers and gastrointestinal bleeding in elderly
people. Alcohol may exacerbate that risk by enhancing the ability of these medications to damage the
stomach mucosa.

2. Alcohol also potentiates the antiplatelet actions of Aspirin, hence increase the risk of bleeding in the patients.

3. Intake of alcohol with acetaminophen can increase the risk of acetaminophen-related toxic effects
on the liver. Acetaminophen breakdown by CYP2E1 (and possibly CYP3A) results in the formation of a toxic product(NABQI) that can cause potentially life-threatening liver damage. As mentioned earlier, heavy alcohol use enhances CYP2E1 activity. In turn, enhanced CYP2E1 activity increases
the formation of the toxic acetaminophen product. In people who drink heavily or who are fasting
(which also increases CYP2E1 activity), liver injury may occur at doses as low as 2 to 4 grams per day.

That concludes this series. I hope it will help you to guide your patients towards drinking alcohol more judiciously. :p

-VM

Alcohol and drug interactions: 3rd part

Hey, guys.....

This is the third post in the series, Alcohol and drug interactions. The other posts are Disulfiram-like Reaction, 2nd Part and 4th Part.

With Antihistaminics

Alcohol increases the risk of sedation, drowsiness and falls, especially in the elderly population and with the 1st gen antihistaminics.

With Barbiturates and Benzodiazepines

Alcohol acts synergistically with them to increase their sedative effects and memory-impairing effects( This memory-impairing effect is misused in Date Rape drug, Flunitrazepam(Rohypnol)). Besides it also inhibits their metabolism in the liver, hence, increasing the drug's levels in the blood.

With H2-Receptor Antagonists

These agents(eg., Cimetidine, Ranitidine) inhibit the action of Alcohol dehydrogenase(ADH) present in gastric mucosa.  Cimetidine may also increase the rate of gastric emptying hence increasing the absorption of alcohol. So both of these effects contribute to increasing the Blood Alcohol levels.

With Muscle Relaxants

Several muscle relaxants (e.g., carisoprodol, cyclobenzaprine, and baclofen), when taken with alcohol, may produce a certain narcotic-like reaction that includes extreme weakness,
dizziness, agitation, euphoria, and confusion. For example, carisoprodol is a commonly abused and readily available prescription medication that is sold as a street drug. Its metabolism in the liver generates an anxiety-reducing agent that was previously marketed as a controlled substance (meprobamate). The mixture of carisoprodol with beer is popular among street abusers for creating a quick state of euphoria.

That's all!

-VM

Alcohol and Drug Interactions: 2nd part

Hey guys,

This is a continuation of the previous post on Disulfiram-like Reaction.

Let us start with a basic info. Pharmacokinetic drug interactions with alcohol are only seen in heavy drinkers whereas Pharmacodynamic drug interactions can be seen in moderate drinkers and even after a single episode of drinking. 

With Antibiotics

As already mentioned, the Disulfiram-like reaction can occur with Isoniazid, Cefotetan, Cefamandole, Cefoperazone, Chloramphenicol, Sulfamethoxazole, Sulfisoxazole.

Besides patients on Isoniazid should abstain from drinking alcohol since isoniazid is hepatotoxic and the liver damage can be exacerbated by concurrent alcohol consumption

With Antidepressants

1. With TCAs: Alcohol increases the sedative action of TCAs, especially Amitriptyline, Doxepin etc.
Alcohol also impairs the first-pass metabolism of Amitriptyline in the liver causing increased bioavailability of the drug. Excessive increase in levels of TCAs in the blood can precipitate convulsions and cardiac arrhythmias.

2. Among SSRIs, all are relatively safer with alcohol; the safest being Fluoxetine.

3. With MAOIs(eg., Phenelzine, Tranylcypromine): There can be severe high BP(cheese reaction) if taken together with red wine which contains Tyramine.

That's all! :)
Do go through the subsequent posts in this series, 3rd Part and 4th Part.

-VM

Alcohol and Drug Interactions: Disulfiram-like Reaction

Hey, guys...

So day before yesterday, there was my Forensic Medicine viva and the examiner asked me the causes of impotency. And I immediately started blabbing about Stress, Phimosis, Hypospadias, Peyronie's disease, I even mentioned Parkinson's disease. The examiner interjected me and asked the most common cause. I guessed heart disease and the related medications and he denied. Then he said it is excess consumption of alcohol and asked me not to underestimate alcohol and it's various interactions and correlations ever.
So here I am, trying to summarize the interactions of alcohol with the major classes of drugs.

Disulfiram-like Reaction

I am not going to go into the details of the mechanism. Just, in brief, Disulfiram-like reactions entails flushing(due to dilatation of blood vessels), nausea, vomiting, sweating, hypotension, so reflex tachycardia which can be deleterious to a patient of coronary artery disease(CAD).

Now let us try to use CAD as a mnemonic here while learning certain other things as well.

1. It starts with C, a lot of drugs starting with C have this reaction, like Cefamandole, Cefoperazone, Cefotetan, Chloramphenicol.

2. Patients with CAD have Pain, so let us now manage that some analgesics starting with P(for Pain), Phenylbutazone, Phenacetin.

3. Patients with CAD can have attacks of Angina, for which we give Nitrates, so let us take that. Drugs with Nitro group: Nitroglycerin, Isosorbide dinitrate, Nitrofurantoin, Metronidazole. Why leave Sulpha group behind?
Drugs with Sulpha group: Sulphamethoxazole, Sulfisoxazole.

4. CAD often co-exists with Diabetes Mellitus(DM). So let us manage that with some Sulfonylureas; Tolbutamide, Tolazamide, Chlorpropamide and even the 2nd gen drug Glyburide.

5. Patients with DM are immunosuppressed. Hence, they are predisposed to Mycoses and TB. Manage them with Griseofulvin and Isoniazid respectively.

That's all! :)
Do go through the other posts in this series, 2nd Part, 3rd Part, and 4th Part

-VM

Vibrio species: Halophilic and non halophilic vibrio mnemonic

Anyone up for a lil microbiology?

Non tubercular uses of: Streptomycin

Another super short video :)

Non tubercular uses of: Rifampicin

Super short video :D

Anticonvulsants: Inhibitors and inducers of CYP450 mnemonic

Although we have a text post on this... Let's upload a video too! :D

Pharmacology: Drugs causing hemolysis in G6PD deficiency

Here's Shilikas first video :)

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 :)