Submission: Direction of growing end of bone, opposite to direction of nutrient artery

submitted by: Mayank Kesharwani

Upper limb joints types mnemonic

Hey Awesomites

From proximal to distal, the joints and its types are:

Shoulder joint - Ball and socket type
Elbow joint - Hinge joint
Radio carpal ( wrist ) joint - Ellipsoidal and biaxial type
Carpo metacarpal joint - Saddle joint
Metacarpo phalyngeal joint - Ellipsoidal ( condylar ) joint
Interphalyngeal joint - Hinge joint

Mnemonic to remember the types, from proximal to distal : BaSu ( Ball and Socket ) writes Hindi ( hinge ) in elliptics ( Ellipsoidal ) but is sadly (Saddle ) condemned ( Condylar ) without hinges .


Thats all
- Jaskunwar Singh

Submission ( notes and mnemonic ) by Mayank Kesharwani - ( PS: This is a Hindi Urdu mnemonic )
Bhaiya Hum ESE Hain

Bhaiya - Ball and Socket joint
Hum - Hinge joint
E - Ellipsoidal
S - Saddle
E - Ellipsoidal
Hain - Hinge

Thanks Mayank for sharing :)

Submissions : Tonsillar Bed mnemonic

Hello

Tonsillar bed mnemonic ( from within outwards ) :

P(b) S S B(p)

Pharyngo Basilar fascia
Superior constrictor
Styloglossus
Bucco pharngeal fascia

- Submitted by Mayank Kesharwani

Submissions : Important vertebral levels

Hello

Important vertebral levels for bifurcations:
- Common carotid artery bifurcation - C4 vertebra
- Tracheal bifurcation - T4 ( may ascend or descend upto two vertebrae higher or lower with breathing )
- Abdominal Aorta bifurcation - L4

Important vertebral levels for formations:
- Cricoid cartilage-  C5- C6
- Thoracic duct crosses right to left - T5 ( and enters left IJV )
- Inferior Vena Cava formation - L5 ( from two common iliac veins )

Submitted by Mayank Kesharwani

Submissions: Rolando fracture mnemonic

Hello

TATA truck ROLLS on wheels

The shape of this fracrure is T- shaped or Y ( bent- T ) shaped, which resembles the sign of the Tata motors truck, and Roll is for "Rolando fracture"

Mnemonic submitted by Mayank Kesharwani

Diagram by Jaskunwar Singh 

Medicowesome secret project: Let's talk about unpleasant changes

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Let's talk about providing psychological support

What is the "Let's talk" project? How can I talk about mental illnesses?

Bartonella henselae and Pasteurella multocida infection mnemonic

Hello!

Sometimes I confuse the clinical manifestations of these two cat related diseases - Cat scratch disease caused by Bartonella henselae and Pasteurella multocida infection caused by cat bites. 

I probably wouldn't have confused these two in my step 1 days, but the older you get, the more confusing rare diseases become,

Sooo... Mnemonic!

Preparing for NEET: Part 1

Hello folks,

This is a common post requested as to how to prepare for NEET PG exams.
And as to whether joining classes is really required to get a decent rank.

So today I will share with you a study schedule told to me by my professor. Which takes around 7 month hardcore prep.

Now for a general approach to it
1. Classes are not essential. Classes add only 20% to the entire PG prep of yours.. That's with like max optimum attention and taking down notes vigorously.

2. Don't read standard books. The competition is so high, that the publishers end up increasing the number of pages. Just to make the book more appealing. Reading those books is a waste of your time cause they repeat the explanations over and over again with unnecessary details which will make you take a month atleast to finish a subject like obstetrics.
The only decent book I found was modit khanna for medicine, like the initial pages of high yield notes and the questions and not the explanations. Don't read the explanations unless the answer is not known to you through the high yeild section.

3. Try getting your hands on class notes. Be it DAMS, Bhatia or IAMS. They are all amazing and to the point. And that's what is needed.

4. Get the NEET PG question booklet, by Arvind Arora. A minimum of last five years questions of NEET is a must to solve.

5. Never sit with a pen and a paper or a marker during your first read for any subject. You will end up marking the whole book and write unnecessary notes  and wasting a lot of precious time. Save it for your second and third read or when you are confident enough that you know the flow of the subject and now just need to focus on details.

6. While reading if you have any doubts make a point to jot it down and find answers before sleeping or at the end of the week. But do solve them. Cause at the end just before exams these are the doubts that trouble you the most.

7. You need to score only a 75% aggregate to score a decent rank. Like to be in the top 3000. That is very much possible with a 7 month smart prep. For the the fight in between the top 3000 see the next para

8. Imagine yourself after a 24hr emergency duty, back to back and just next day you have to write theory paper of your uni exam.That's a near about situation of how mind stressed you are before neet.
Like it's 20 subjects..and you need to shift your focus from ophthalmology to psm in a matter of seconds. If you can't do that and if you waste your time even like an extra 5 mins on one question then you will be compromising the tail questions and that's when the stress gets to you. You keep looking at the timer and boom you black out.

A solution to this is you need to train your brain to deal with this situation. I have an aggregate of tips from medicowesome authors to deal with this.

- Solve the grand test. Just don't stick to one subject solving be as varied as possible. Like your best shot is solving 100 random questions every day doesn't matter if you know only 5subjects out of the 20, you only need to train your brain to deal with it.

- Solve the questions after an on call or after a very stressful day, give yourself the taste of it. So that your brain will be able to switch attentions during exams.

I feel the battle between the top 3000 rankers all comes down to who switched their attention between questions the fastest. The knowledge is the same it all matters that whether you were able to use it to your best or not.

9. Follow medicowesome :D
A bit cheeky but seriously it helps. Every now and then try reading the various posts. It will help you to condition your brain to all the subjects piece by piece.

10. A lot of questions are photo based. Try making your own picture library like jot down the things of pics you want to search for and look for it at the end of the day or the week end.

11. We don't promote apps and stuff but I would seriously advice downloading the pg prep app from Google play. It has stats to show your progress, daily exams, a 55 thousand question bank, photo questions, subject wise and grand test questions. It is amazing. Go ahead download it if you haven't and stick to it.

12. Have a way to destress yourself during the prep. Like be it running , movie, at a cafe or a novel.
Pg prep is a monotonous dumb thing to do , let's not lie to our selves -_-
You need to keep your engine at a steady pace so that you are able to fast track during the last month before your exam.
Like I personally read manga :D
Weekly updates were my solace and paradise. That's the way I treated myself after I had completed my schedule for the week.

I will upload a seven month prep schedule in part 2.

- Sakkan

Myopic Shift : Explanation

Hi everyone ! So this is a short post on the Second Sight or the Myopic Shift seen in Cataract.

So in people who  have a hypermetropic / presbyopic power , tend to experience a reduction in their refractive errors when Cataract starts to develop. This is called Myopic Shift or Second sight.
This​ occurs most commonly in nuclear cataracts. Now why this occurs is , the lens in early stages of Cataract undergoes sclerosis. That increases the Power of the lens ( this increases the refractive index).
Thus it makes the lens slightly more Powerful , or Convex. Due to this it acts as a correction for Hyperopia/ Presbyopia (Where the error was due to a weaker lens. )
This transient Myopic nature of the eye is called the Myopic Shift.
It does go away when the Cataract progresses as the sclerosis begins to reduce refractive surface in the lens.

Hope this helped! Stay awesome  !
Happy Studying :)

~ A.P.Burkholderia

Infants of Diabetic Mothers (IDM) : A clinical overview

Hello

With the prevalence of insulin - dependent diabetes mellitus and maternal hyperglycemia, serious consequences to the ingrowing foetus may occur during its organogenesis. Lets have a quick review of the clinical problems in the infants of diabetic mothers ( IDM ) with some lame mnemonics :p -

GENERAL BUILT :
- Macrosomia ( birth weight >4,000 gm ) resulting in difficult labor and complications such as traumatic asphyxia, shoulder dystocia, BP injury, etc.
- Large for gestational age

CONGENITAL ANOMALIES :-

1. CARDIOVASCULAR - mnemonic : CASTeD
- Cyanotic heart disease
- Asymmetric septal hypertrophy ( resulating in small LV )
- Septal defects ( VSD, ASD )
- Transposition of blood vessels
- Decreased cardiac output ( due to perinatal asphyxia and metabolic acidosis )

2. SKELETAL AND CNS -
- Caudal regression syndrome
- Mental retardation

3. NEURAL TUBE DEFECTS - mnemonic : HAM

- Holoprosencephaly

- Anencephaly

- Meningomyelocoele

4. RENAL and GENITOURINARY - mnemonic : HURT

- Hydronephrosis

- Urethral dysplasia

- Renal agenesis

- Thrombosis of renal vein

( patient presents with flank mass, intermittent hematuria, and thrombocytopenia )

5. GASTROINTESTINAL - mnemonic : GAS

- Gastrointestinal obstruction ( due to duodenal atresia )

- Anorectal malformations

- Small left colon syndrome

6. RESPIRATORY -
- Hyaline membrane disease ( Infantile RDS )
- Persistent Pulmonary Hypertension

7. METABOLIC changes -

- Hyperbilirubinemia ( due to polycythemia )

- Hypoglycemia occurs 30 - 90 mins post delivery which may take several days to resolve. Rebound hypoglycemia may occur in response to rapid, large boluses of glucose ( 10-15 mg/kg/min ).

- Hypocalcemia ( levels <7 mg/dL ) occurs within hours to days after birth due to a delay in PTH synthesis after birth, often accompanied with Hypomagnesemia.


Thats all
Hope this helps :)

- Jaskunwar Singh

Mnemonico diagnostico : Risk approach to Antenatal cases

Hello

'High - risk' antenatal cases contribute to 70 - 80% of perinatal morbidity and mortality rates. The screening and diagnostic tests to evaluate and identify such cases is a must so as to provide special care to the mother - child duo. Risk approach for antenatal cases according to WHO includes : ( mnemonic - RISK APPROACH )

Prader-Willi syndrome and Angelman syndrome mnemonic

Hello! Let me start with the mnemonic and then I'll explain these syndromes in detail.

Hypersensitivity types mnemonics

Hypersensitivity types are:

Type 1 RTA pathophysiology, notes and mnemonic

Hello! This post is on type 1 renal tubular acidosis.

What causes Type 1 RTA?
Defective H+ ion secretion in the distal tubule.
Impairment in H+ ions secretion result in an inability to acidify the pH beyond 5.5 (Used in the diagnosis of type 1 RTA)


The plasma bicarbonate is significantly reduced and may fall below 10 meq/L.
These patients tend to have urinary K+ wasting and hypokalemia (thought to be due to increased potassium secretion by distal tubular cells in the setting of diminished H+ ion secretion.)

What type of RTA is associated with an enhanced chance if nephrolithiasis?
Distal or type 1 RTA can cause nephrocalcinosis / calcium oxalate kidney stones.
Mnemonic: ONE predisposes to stONEs

Pathophysiology: Hypercalciuria, hyperphosphatemia, nephrolithiasis (calcium phosphate stones) and nephrocalcinosis are frequently associated with untreated type 1 RTA. The hypercalciuria is thought to be due to:
1) increased calcium phosphate release from bone as a result of bone buffering of excess acid and
2) reduction in tubular calcium reabsorption secondary to chronic acidosis.
The hypercalciuria, alkaline urine, and reduced excretion of citrate in the urine (which normally prevents calcium crystallization) promote the precipitation of calcium phosphate and stone formation.

Which conditions are associated with type 1 RTA?
diStal RTA is associated with the 3 S's:
Sjogren's
SLE

Sickle cell anemia

Treatment: Bicarbonate administration

That's all!
-IkaN

Mnemonico diagnostico : Vitamin D deficient Rickets

Hey Awesomites

The clinical features specific for Rickets due to vitamin D deficiency are : Vit D BHP RICKETS

V - Visceroptosis ( due to ligament laxity )
D - DEXA scan / low bone Density
B - Bossing of skull
H - Harrison's groove
P - Ping pong ball sensation
R - Rachitic rosary
I - Iron deficiency and other anemias
C - Coxa vara
K - Kyphosis
E - Eruption of teeth ( delayed )
T - Thoracolumbar ( Lordosis )
S - Sternum and ribs protrusion ( Pigeon chest )


Thats all
- Jaskunwar Singh

Difference between Duodenal and Gastric Ulcer

Hello everyone, let’s talk about the ever confusing difference between Duodenal and Gastric Ulcer. Both the ulcers are a type of Peptic Ulcer which occurs due the action of acid resulting in the damage of alimentary mucosa. The main cause for both of them could be infection with H. pylori or intake of NSAIDs.

Mnemonico diagnostico : Klinefelter's syndrome

Hey Awesomites

Criteria for diagnosis of Klinefelter's syndrome in males mnemonic : KLINEFELTER

K - (K) Cryptorchidism
L - Leydig cells hypertrophy
I - Increased gonadotrophins
N - Negative/ Positive chromatism (aberrations)
E - Elongated legs
F - Failure of secondary sexual characters
E - Eunuchoidism
L - Late pubic hair
T - Testicular failure
E - Erectile dysfunction / Elbow deformities
R - Retardation (mental)


Thats all
- Jaskunwar Singh

Non Contraceptive uses of the Condom

Hi everyone. So we know what we use a condom for generally :p
But there are a few non Contraceptive uses for this magical device that prevents babies :').

So here goes -

1. Prevention of STD's.
2. Can be used in Balloon Tamponade to control PPH.
3. Used to cover the USG probe inserted into the female tract.
4. Can be used as a mould for the vagina during Vulvoplasty.
5. Women with Anti Sperm antibodies during the initial phase. (Controversial).

So that's about it.
We know no 5 more reasons to use condoms !
Go get em ; )
Happy studying.
Stay awesome.

~ A.P.Burkholderia

How to remember Hepatitis B is associated with membranous glomerulonephritis

Writing this post because I confused it with focal segmental glomerulonephritis yesterday.

Hepatitis B is associated with membranous glomerulonephritis.

Mnemonic: Happy memory - Heppy membory - Hepatitis B Membranous nephropathy :D

That's all!
-IkaN

Bromocriptine : Utility Review

Hi everyone ! Here's a brief review on the drug Bromocriptine which happens to be one of my favorite drugs. So here goes.

- Bromocriptine is a Dopaminergic agonist , specifically acting on the D2 Receptors.

- It is a very widely used drug , with various and multi systemic uses.

Uses :

1. Parkinson's disease.
- Bromocriptine and other D2 agonists like Rotigotine , Ropinirole and Pramipexole can be used to treat Parkinsonism.
- They act by providing a sort of  replacement for the depleted dopamine in the circuits of the basal ganglia.
- They are quite effective , especially in case of L Dopa resistance , or deterioration of symptoms when on L dopa.

2. Neuroleptic Malignant Syndrome.
- NMS is perhaps caused by D2 blockade due to drugs like Haloperidol and Fluphenazine.
- Thus it makes sense if you give this D2 agonist to treat this disorder.

3. Hyperprolactinemia.
- Dopamine acts as a Prolactin Inhibitory Factor (PIF) at the Hypthalamo-Pituitary level.
- In cases of Hyperprolactinemia where there is gynecomastia and galactorrhea,  giving D2 agonists counteracts the elevated prolactin levels.
- Thus it's useful in Anti psychotic/ Metoclopramide induced Hyperprolactinemia.
- Can be used in Ovulation induction due to elevated prolactin by a Pituitary adenoma.

4. Diabetes Mellitus.
- Bromocriptine modulates the Dopaminergic discharge at the Hypothalamus level.
- This modulates the circadian rhythm and resets the abnormal metabolic drive of the Hypothalamus and reduces the insulin resistance.
- The specific Quick Release formulation is used for this indication.
- It may be used in conjunction with Insulin and does not cause hypoglycemia.
- It cannot however be used for DKA

5. Acromegaly.
- Inhibits the excess Growth Hormone secretion by acting at the Hypothalamus level.

Hope this helped !
Happy studying and stay awesome!
~ A.P.Burkholderia

Neuroleptic Malignant Syndrome : A Crisp Overview

Hi everyone ! So I recently saw a patient who possibly had Neuroleptic malignant syndrome. So I though I would do a post on it !

1. The Syndrome -

NMS is an idiosyncratic reaction to Anti psychotic drugs. It causes a host of symptoms like Rigidity , Hyperpyrexia and altered consciousness.

2. The Etiology -

- All Antipsychotic drugs can cause NMS. But most commonly implicated are Haloperidol, Fluphenazine and Chlorpromazine.
- Especially at risk are those taking Depot preparations.
- Even lithium in high doses can precipitate this.
- Atypical Antipsychotic drugs have a lower propensity to cause this.

3. The Pathophysiology -
- Although largely speculative , the cause is said to be the dopaminergic blockade by the anti psychotic drugs.
- Blockade of D2 in Hypothalamus is responsible for the Behavioral and Temperature changes.
- Blockade of D2 in the basal ganglia ( nigro striatal pathway) causes the Rigidity.
- increased muscular activity can cause muscle break down.

4. The Clinical Features - 

- generally within 4-10 days after starting the Antipsychotic drug. But can even occur years later.
- Hyperthermia ( Hypothalamus is conked off )
- Lead pipe Rigidity ( Basal ganglia are screwed)
- Altered mental state - delirious.
- Sweating/ Diaphoresis  ( compensation for high temp)
- Tachycardia
- Dyspnea
- Urinary incontinence
- Dysphagia
- Pallor.

Symptoms develop over a period of 24-72 hours.

5. Tests -
- Creatine Phosphokinase (CPK MM) is raised
- Leukocytosis
- Low Iron
- Deranged LFT and LDH

( Can be used to differentiate from serotonin syndrome)

- Diagnosis requires Hyperthermia + Rigidity +   2  other features ( including riased leukocytes and CK MM)

6. Management -
- ABCD
- Ventilatory support if needed
- stop Antipsychotic drugs.
- Anti pyrectics . Ice packs. Cooling blankets.
- BDZ
- Specific -->
Dantrolene - Muscle relaxant and Hyperthermia management. 400 mg/D.

- Bromocriptine - D2 agonist.

- ECT may be needed.

Hope this was helpful ! Happy studying and Stay awesome.

~ A.P.Burkholderia

Reversible Causes of Dementia : Mnemonic

Hi everyone ! This is a short post on causes of dementia that can be corrected. This is very important as most causes other than these have no available treatment ! (One Reversible cause of dementia is the Demeantor's kiss ;;) Treat using  Expectro Patronum)

So the medically treatable causes include the following.

Remember : ABCD2E

- Alcoholism
- Vitamin B deficiency - Thiamine / Niacin /B12
- CNS infections - HIV , Chronic Meningoencephalitis , Whipple Disease, Neurosyphilis.
- Depression
- Drug induced
- Endocrine - Thyroid disturbances

Let's look at how these can be corrected medically.
- A = Alcohol abuse. May be a result of Alcoholic delirium/ Wernicke-Korsakoff syndrome. So the management would include giving Thiamine to the patient , and alcohol withdrawal using Disulfiram ans other anti craving drugs like Ondansetron, Acamprosate, Topiramate and Naltrexone.

- Vitamin B Deficiency = Thiamine deficiency we've seen above.
Niacin Deficiency causes 3 D's - Diarrhea , Dermatitis and Dementia. So treat that using Niacin.
B12 Deficiency and possibly folic acid can also cause Dementia.

- CNS Infections = They cause transient cognitive changes that are reversible on treating the disease.

- Depression = may cause depressive pseudodementia or even true dementia. (pseudo dementia = no confabulation or impaired recent memory)

- Drug induced = Chronic use of drugs like BDZ , Opiates and TCA's.

- Endocrine = Hypothyroidism is notorious to cause Dementia.

~~~~~~~~~~~~~~~~~~~~~~~

The surgically correctable causes are below.
Remember = T2 H2

- Tumors  (esp frontal lobe tumors )
- Trauma (Subdural Hematoma)
- Normal Pressure Hydrocephalus (NPH)
- Hydrocephalus

- Tumors are resected surgically.
-  For the hydrocephalus group , ventriculo peritoneal shunting is performed.
- NPH = Triad of symptoms showing Gait disturbances , Urinary incontinence and Dementia. (GUD)

Hope this post helped you and didn't leave you too demented. !  If it did, have some chocolate like Lupin would offer ;;)
Happy studying.
Stay awesome.

~ A.P.Burkholderia

Fact of the day: Nightmares are a warning for serious mental problems

Hello

Not one or two, but frequent nightmares are major caveats for underlying serious mental problems. Rapid Eye Movement sleep disorder is a rare disorder that causes the person to act violently during dreamy state. This may be a warning sign for major neurologic disorders like Parkinson's and neurodegenerative diseases like Alzheimer's !!

Night owls are more likely to have frequent sleep and mood disturbances than the early sleepers. Evidences suggest people suffering from nightmares and related sleep disorders are more likely to have suicidal tendencies than those not, in addition to other contributing factors.


- Jaskunwar Singh

Drugs causing hyperkalemia mnemonic

Hello!

I modified the K BANK mnemonic and added more to it to cover a few more drugs.

The mnemonic for drugs causing hyperkalemia is: K BANK Digs, cycles, sucks, self help (Sulf hep!)

K - Potassium sparing diuretics (Obviously!)

B - Non selective beta blockers

A - ACEI, ARBs

N - NSAIDs

K - Potassium supplements

Digs - Digoxin

Cycles - Cyclosporine

Sucks - Succinylcholine

Sulf - Sulfonamides, Trimethoprim

Hep - Heparin

That's all!

-IkaN

Direct acting cholinomimetic agonist mnemonic

Hi everyone, 

Here's the mnemonic for direct acting cholinomimetic drugs: ABC VPN

Nerve fibres : A clinico-physiological approach.

Hello everyone. So I've not been active at all lately , cause Final Year ! Pretty depressing 🙄. Anyway. Here's a post about the nerves and what we need to know for clinical application!

Nerves

So Erlanger and Gasser classified the nerves into A, B and C based on Myelination and size.

So you have :
A
(Which has Alpha , Beta , Gamma , Delta fibres )
B
C

Out of these , the first 3 : 
A - Alpha , Beta , Gamma = Large fibres which are largely Myelinated.

And next 3 :
A - Delta , B , C = Small fibres which are not Myelinated as much.

How I remember these fibres is as per evolutionary significance.
The least Myelinated fibres , which are the smallest are the ones all living creatures need. As we progress from C to B to A , we continue to gather more and more well developed and specialised fibres.

C -
The smallest fibres.
Least Myelinated.
Most basic fibres and most primitive from an evolutionary stand point !
Control sensations of Dull Pain and Temperature (Heat)

B -
Small fibres.
Low Myelination.
Next most Basic Instinct - Urination.
Controls your Autonomic nervous system.
Remember- B = Bladder

A Delta -
Moderately Small fibres.
Lower Myelination than other A fibres.
Responsible for sensation of Sharp pain and Temperature ( Cold )

Thus to summarize the small fibres -

We have C , B and A Delta.
Out of these
C and A Delta control Pain and Temperature
( where C controls Dull pain and Heat ; A Delta controls Sharp pain and Cold )
And B controls Bladder /ANS.

(How to remember A Delta vs C.
C is more primitive. Hence controls Dull pain. Sharp pain is a little more specialized and hence is controlled by the relatively more modern fibre - the A Delta)

Coming to the large fibres.

We progress from A gamma to A beta to A alpha.

A Gamma :
Large but smaller then Alpha and beta.
Myelinated but not as much as alpha and beta.
Responsible for muscle tone.
Remember : A Gamma = Gamma motor neuron which is responsible for tone.

A Beta :
Very large.
Well Myelinated.
Responsible for modern sensations like Fine touch, Pressure and Vibration.

A Alpha :
Largest.
Most Myelinated.
Responsible for Muscle Contraction and Most modern sense - Proprioception.
It's the Bomb of the fibres hence responsible for muscle contraction.

Thus , demyelinating diseases like Guillian Barre syndrome and CIDP would affect the fibres that are used to being Myelinated.
So your presentation in these diseases would generally involve loss of:
A Alpha - Motor + Proprioception
A Beta -  Modern sensations of fine touch and vibration.
A Gamma - Tone

And Axonal Polyneuropathic Diseases like Metabolic or Post infectious ones would involve loss and abnormalities of -
A Delta - Sharp Pain and Cold
B - ANS
C - Dull pain and Heat.

Hope this was helpful !
Happy studying !
Stay awesome.

~ A.P. Burkholderia

Case control study vs Cohort study mnemonic

Super short post :)

Case control study - Start with an outcome and go back in time to study the risk factor.
Simplified: Case (Diseased) vs Control (No disease)

Cohort study - Start with risk factor and see who developed the disease and who did not.
Mnemonic: cOhOrt has two O's.
One O has an R (cohORt), which means one group has the risk factor.
Other O does not have an R (cOhort), which means the other group does not have the risk factor.
Compare the two to see who gets the disease.

How to remember that case control studies measure odds ratio and cohort studies measure relative risk:

You take surgical "cases" to the "OR" (Operating room)
Case control study - Odds Ratio

cohoRRRRRRt measures Relative Risk.

kthxbye!

-IkaN

Abdominal Pain in Pregnancy

Hey guys

In this post I will mention the most common and must-know causes of abdominal pain in pregnancy which is a very common complaint during gestation. I will also mention certain salient points which will be helpful in the differential diagnosis.

1. Implantation Bleeding. There is a mild abdominal pain 6-12 days after conception along with a small amount of vaginal bleeding called spotting. Be careful so as not to confuse this bleeding with the menstrual bleeding.

2. Ectopic Pregnancy. This is the leading cause of first trimester mortality of the foetus. If there is a serum HCG level more than 2400 mIU/ml (The discriminatory zone is 1500-2400mIU/ml) and on USG there is no gestational sac in the uterus, then you should strongly suspect this. The most common sites are Tubal, Ovarian, Interstitial, Cervical.

3. Spontaneous Abortion. It is common in the early pregnanacy( upto 20 weeks) and is divided into 4 stages: Threatened, Inevitable, Incomplete, Complete. If there is vaginal bleeding without cervical dilatation or any change in cervical consistency, then it is Threatened abortion, if the cervix is dilated, it is Inevitable; if some products of conception are discharged per vaginally, it is incomplete abortion.

4. Abruptio Placentae. It is due to premature separation of placenta from its implantation site causing vaginal bleeding and pain due to uterine cramps caused by myometrial irritation. In some cases there is no vaginal bleeding, and we call those Concealed abruption. If the abruption is large enough to cause uteroplacental insufficiency the fetus is at risk. And the mother is at risk of haemorrhagic shock.

5. Ovarian Cyst

6. Ovarian Torsion 

7. Appendicitis

8. Uterine leiomyomas (Fibroids)

9. HELLP Syndrome. Haemolysis, Elevated liver enzymes, Low platelets syndrome is a complication of Preeclampsia characterized by nausea, vomiting and right upper quadrant pain and tenderness. If this condition has progressed, there is risk of seizures and in the worst case hepatic rupture causing hypovolemic shock and severe pain. Peripheral blood smear will show schistocytes and low platelets.

10. Cholelithiasis. This condition will have characteristic biliary colic, i.e., intermittent right upper quadrant pain associated with nausea and vomiting.

11. Cholecystitis.

12. UTI. There will be suprapubic pain with dysuria, frequency and urgency.

13. Urolithiasis.

14. Round Ligament Pain.  Enlargement of uterus during pregnancy leads to traction in the round ligament which pulls on the nearby nerve fibres causing sharp pain; such a pain can also be caused by round ligament spasm or cramps. This pain is usually present on the right side because of the dextro-deviation of the uterus and managed by acetaminophen and exercise.

That's all!

-VM

Ischial Spines - Important Obstetric Landmark.

Hello There!

So let's enlist few important points in relation to the ischial spines.

Ischial spines can be generally be palpated at about a finger-length into the vagina, at 4 & 8o'clock.
They are felt as bony prominences and their palpation may cause a little discomfort to the patient.

These spines serve as a landmark for:

1) Engagement of Fetal Head.(Most commonly used for determining the Fetal Station during labor.
Ischial spines are considered as Station0)
2) Internal Rotation of the fetal head.
3) Pudendal Nerve Block.
4) External os.
5) Obstetric Curve (J shaped) takes forward curve at this level.
6) Insertion of levator Ani.
7) Plane of least pelvic dimension.
8) Ring pessary is kept at the level of ischial spines.

These are the few things I know about at the level of the Ischial spines.
Do let me know some additional points you know of, to add to the list.

Let's learn Together!
-Medha.

Umbilical Cord Knots.

Hello everybody!

Recently during my Ob-Gyn internship while delivering the placenta, the Umbilical cord that I held, was very lumpy bumpy. Little knowing about the reason at that moment, I came home found out the reason.
Let's see how the Umbilical cord can get knotty sometimes.

So there are two types of knots seen in the cord.
1)True Umbilical Knots
2)False Umbilical Knots.

True Knots :
These are noted after delivery. 

The umbilical vessels, are protected by the thick myxomatous Wharton jelly, and can rarely be occluded completely. The jelly protects the vessels and the fetal blood supply, as there is only flattening or dissipation of Wharton jelly when a Knot is formed.
Due to the knot some amount of venous congestion distal to it and some  partially or completely occlusive vascular thrombi may also be observed.

A true knot is formed when a loop of cord slips over the infant’s head or shoulders during delivery.
If the knot is pulled tightly it can cause fetal demise due to restriction of the circulation in the cord. 

The True Knots can occur due to:
1)A long cord, 
2)Large amounts of amniotic fluid
3)A small infant,
4)An overactive fetus
5)As a result of external version. 

(All the above causes lead to increased fetal movements in utero)

However the fetal mortality rate associated with true knots is low.

False Knots:
In the cord the blood vessels are longer than the cord and are often folded on themselves producing nodulations on  the surface of the cord. These nodulations are lumps and bumps I saw!
These have been termed as false knots.

So guys the next time you see a lumpy bumpy cord, unlike me, you now know the reason.
That's​ all, on the Umbilical cord and it's knots.

Let's learn Together!
-Medha.

Laryngomalacia vs tracheomalacia mnemonic

Laryngomalacia casuses inspiratory stridor.

Tracheomalacia causes expiratory stridor.

Terson Syndrome.

Hello everybody!

In this post let's quickly learn about Terson Syndrome.

So what is it?
This Syndrome is a combination of intraocular and subarachnoid haemorrhage secondary to aneurysmal rupture, most commonly arising from the anterior communicating artery.

Terson Syndrome along with other bleeding disorders is included amongst the Systemic causes of vitreous hemorrhage!

Intraocular haemorrhage is also seen to occur with:
1)Subdural haematoma
2)Acute elevation of intracranial pressure

The mechanism of intraocular bleeding:

There is increase in cavernous sinus pressure due to the subarachnoid/subdural hemorrhage leading to stasis in the retinal veins. This stasis in the retinal veins leads to increased intraluminal pressure in the veins making them susceptible to bleed.

The haemorrhage is often Bilateral.
Typically intraretinal and/or preretinal. With this hemorrhage there is a possibility of it leaking in the vitreous.

The vitreous haemorrhage usually resolves in a few months and the long-term, the visual prognosis is good.

I hope you guys found it useful. Do let me know about some neuro-opthalmology syndromes you know about.

Let's learn Together!
-Medha.

Innate Cellular Anti-retroviral Mechanisms

This post will focus on the mechanism by which a cell fights against HIV, mainly by interfering with its life cycle. There are only 3 such mechanisms discovered and elucidated till date.

As it says on the post, these are innate mechanisms most of which are upregulated by Interferons (alpha and gamma).The adaptive immune system is mostly ineffective against retroviruses. How? Earlier the most accepted hypothesis was that this is because of error-prone Reverse trancriptase which makes a lot of errors while forming the proviral ds DNA, hence causing hypermutations(mainly G to A) resuting in change in the viral antigenic domains. This is true for both HIV and HBV. 

1. APOBEC3G: The full form is Apolipoprotein B mRNA editing enzyme and catalytic polypeptide like 3g which you will easily forget and you should. It is basically a cytidine deaminase which acts on the negative cDNA strand and converts dC into dU; hence converting G into A in the positive strand. These hypermutations ultimately lead to failure of viral replication by unknown processes. So the latest most accepted hypothesis explaining the G to A hypermutations in virion DNA is this. This is more effective against HBV than HIV, guess why? Its because HIV-1 has Vif (Viral Infectivity Factor) that inactivates APOBEC3G.

2. TRIM5: This is the reason why Rhesus monkeys are innately resistant to HIV. Its an awesome protein in my opinion. What it does is as soon as the viral nucleocapsid enters the cell, it forms a cage around it and cause it to "uncoat" prematurely hence inactivating the reverse transcriptase and other enzymes present within the capsid. Then it performs a Kamikaze!

It ubiquitinates itself (auto-ubiquitination); hence causing its own proteasomal degradation and destroying the viral proteins in the process as collateral damage.

3. Tetherin: Now this is a case of Stockholm Syndrome! Tetherin are proteins that tethers or chains the virion to the cell membrane, hence preventing its release from the cell. The cell is not letting the virus leave her. So that when the cell dies either by apoptosis or inflammatory processes, the virions die with it. <3

Unfortunately however cool these may appear, these are mostly ineffective and hence the standard microbiology textbooks choose to ignore these proteins. Hopefully in future, drugs will be designed to make them more effective. :)

That's all!

-VM

Cerebellum and Motor learning!

Hello everybody!
Let's today learn about cerebellum and how amazing it is.

So all of us know that walking, swimming or typing needs conscious effort while being learnt for the first time, but after learning, one can continue these activities mechanically without having to think about them.

After learning, the responsibility for these activities seems to shift more and more to the cerebellum leaving the cerebral cortex free for other tasks.

That is why a child who is learning to walk has to put all his mind into it. Any distraction may make him fall. But as adults we can multitask along with walking.

Let's see how this happens.
There is evidence that cerebellar circuits can undergo functional changes as a result of experience.
The climbing fibres play an important role in this process. (bring information only from the inferior olivary nuclei, and establish excitatory synapses with Purkinje cells)
In a new situation, the climbing fibre activity is high, and it tends to reduce mossy fibre activity.
(Mossy fiber excitation not only stimulates Specific Purkinge cells but also inhibits the neighbouring Purkinge Cells.)
On repeated exposure to stimulus while learning, the mossy fibre response gets stabilized at the low level without an increase in the climbing fibre activity and the Cerebellar efferents perform the function semiautonomously on stabilized afferent input.

Thus Cerebellar learning may spare the cerebral cortex in the learnt movements.

I hope this was informative.

Let's learn together!
-Medha.

Drug: Evolocumab

This post will be on Evolocumab, a monoclonal antibody drug recently approved by FDA for use in refractory cases of Primary Hyperlipidemia and Homozygous(Not used in heterozygous) Familial Hypercholesterolemia alongwith Statins and appropriate diet and lifestyle modifications. 

Mechanism of Action:

As you know, LDL-Cholesterol is the bad cholesterol which is cleared by hepatocytes via surface LDL-receptors. These receptors are catabolized in hepatocytes by the enzyme proprotein convertase subtilisin/kexin subtype 9, fondly called PCSK9.

This enzyme is inhibited by Evolocumab, hence decreasing the intracellular clearance of LDL-R, thereby increasing the clearance of LDL-C from the body.

And Statins also help in raising the expression of LDL-R in hepatocytes by inhibiting HMG-CoA Reductase, hence decreasing cholesterol synthesis forcing the hepatocyte to extract more cholesterol from the blood.

The most common adverse effect is Nasopharyngitis which is easily manageable. And the black box warning is Hypersensitivity Reaction.

Look out for new drugs and ever-changing treatment and management guidelines and try to stay updated! :)

-VM

Medicowesome secret project: Let's talk about unhappiness

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Let's talk about depression

What is the "Let's talk" project? How can I talk about mental illnesses?

Thalamus.

Helloooo everybody!
 let's quickly learn a few basics and beyond in today's post on Thalamus.

So thalamus is nothing but a collection of neurons which are organized well-defined nuclear masses.

The nuclei have confusing names and are difficult to remember too.

But from a functional point of view they are divisible into four groups to keep our lives simple.

1) Specific Sensory Nuclei
2) Association Nuclei
3) Nonspecific Nuclei
4) Motor Nuclei.

Specific Sensory Nuclei :These receive all sensory afferents. The arrangement of fibres is topographic and so is their projection to the somatosensory cortex. 

Corresponding to the thalamocortical projection fibres, there are also corticothalamic fibres which provide feedback information to the relay nuclei.

Let us now see how the sensory relay nuclei work.

A specific sensory stimulus activates neurons in the sensory relay nucleus.
                           
The thalamic nuclei activate some thalamic interneurons as well as an area in the sensory cortex. Activated sensory cortex also sends impulses back to the thalamic relay nucleus, thereby modulating the thalamic output.

In short, the sensory relay nuclei really do not act as simple relays.  They process the sensory signal by local intrathalamic circuits and descending corticothalamic  fibres before sending it to the sensory cortex.

Association Nuclei :
These help achieve integration of different types of sensory information.

Nonspecific​ Nuclei:
These also receive sensory information but project to the cortex in a diffuse manner.  Therefore they seem to be involved in the arousal induced by sensory stimuli.
They also project to the limbic system, thereby suggesting their involvement in the emotional impact of sensory stimuli.

Motor Nuclei :
They relay and process messages from the basal ganglia and cerebellum to the motor and premotor cortex.

All nuclear groups have to and fro connections with the cerebral cortex. Thus the thalamus and cortex function as one functional entity, the thalamocortical​ system.

Possibly the thalamus prepares a crude blue pint of the  final product achieved by the cortex.

The global involvement of the thalamus in central nervous function is revealed when its function is impaired, as in the thalamic syndrome.

Let's now quickly learn about Thalamic Syndrome.

Level of lesion : Posteroventral thalamus.

Etiology: Thrombosis of  Posterolateral branch of the posterior cerebral artery.

Manifestations :

1) Impairment of discrimination in sensory perception,
2) Hypotonia, muscular weakness and incoordination,
3) Volatile emotions, pleasant or unpleasant. 

After a few weeks to months, partial recovery may occur.

The sensations, regardless of the nature of the stimulus, may be very painful. 

The symptoms are thought to arise partly because the medial nuclei of the thalamus are spared by the lesion. 

 The medial nuclei are the nonspecific nuclei which receive major projections from pain  fibres.Hence the dominance of pain among the sensations. 

Well that's all on Thalamus,Hope it was helpful!

Let's learn Together!
-Medha.

Medicowesome secret project: Let's talk about seeking help

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Let's talk about low self esteem

What is the "Let's talk" project? How can I talk about depression?

Treatment of migraine headaches mnemonic

Hello! Here's a short post on treatment of migraines!

Treatment of acute migraine attacks mnemonic: NSAiDs

N: NSAIDS like Naproxen, S, Aspirin, Ibuprofen, Diclofenac

S: Sumatriptan (And other Triptans such as rizatriptan, eletriptan, almotriptan, zolmitriptan, naratriptan, and frovatriptan)

AiDs: Antiemetic/dopamine receptor antagonists: Chlorpromazine, prochlorperazine, and metoclopramide

Ds: Dihydroergotamine and ergot derivatives

Prophylaxis of migraine mnemonic: ABC

Antidepressants: Amitriptyline and venlafaxine

Beta blockers: Metoprolol, propranolol, and timolol

AntiConvulsants: Valproate and topiramate

Calcium channel blockers (less effective): Verapamil, Flunarizine

That's all!
-IkaN

Why do we feel sleepy when we are sick?

Hellooo Everybody,
Let's delve into some sleep physiology and learn about some sleep producing substances breifly!

The chemical agents which might be responsible​ for induction of sleep have been obtained from experiments on sleep-deprived animals.
The first experiments of this type were performed by Henri Pieron in 1913 on dogs. He demonstrated that dogs receiving CSF from sleep-deprived donor dogs slept for hours, while the recipients of CSF from normal donors remained awake. Recent work has confirmed these observations and identified several candidate sleep producing substances (SPS)

Sleep-deprivation presumably leads to a rise in the production of these substances in the brain tissue, cerebrospinal fluid,and even urine, through a negative feedback effect.

The best known SPS :
1) Muramyl dipeptide (MDP)
2) Delta sleep-inducing peptide (DSIP)
3) Arginine vasotocin (AVT)
4) Interleukin-1 (IL-1).

Besides these, there are about 20 more putative sleep-inducing factors.

Most of the known sleep producing substances induce Slow Wave Sleep.

After learning the physiology let's answer our question:
Muramyl dipeptide (MDP) is a component of bacterial cell( which acts via IL-1.) walls ,whereas IL-1 is released in infections.
IL-1 potentiates GABA-induced increase in permeability to chloride at synapses causing inhibitory effect on the Brain.

Nitric oxide may be part of a second messenger system which mediates the effect of IL-1 on sleep.

Lastly, IL-1 induces release of growth hormone releasing hormone (GHRH) which in turn releases growth hormone. Growth hormone itself enhances REM sleep and inhibits Slow wave sleep.

This explains why we feel sleepy when sick!

IL-1 also induces fever, and is therefore also called endogenous pyrogen.  Antipyretics, such as aspirin, suppress the fever induced by IL-1 but do not affect the sleep-inducing effect of IL-1.
Like fever, sleep is a smart response  which perhaps helps recovery by compelling the patient to take rest.

Isn't it truly remarkable, how our bodies work!

Let's Learn Together!
-Medha.

Brain Function Imaging.

Hello everybody!
Today we shall breifly learn as to how we can study the brain function using imaging techniques.

Positron Emission Tomography (PET)made debut in 1980s; two more imaging techniques came in the 1990s: functional magnetic resonance imaging (fMRI) and magnetoencepalography (MEG).

1) Positron Emission Tomography:

This technique makes it possible to see in an image which part of the brain is active during a particular task.
As we also know that although brain as a whole does not consume significantally more energy when it is active than when it is idle, metabolic activity does increase in circumscribed regions of the brain when these regions are functionally active.
This increased metabolic activity in the brain is the basis of PET.

In this technique a positron-emitting isotope is tagged to a molecule of biological interest such as glucose or a neurotransmitter.

For example, the positron-emitting isotope of fluorine (18F) is tagged to deoxyglucose and it is injected intravenously.
Deoxyglucose is taken up by neurons in the same way as glucose, but it can neither be fully metabolised nor can it come out of the neurons.
Since functionally active neurons take up more glucose, active regions of the brain accumulate more deoxyglucose.
So , following visual stimulation, 18F-deoxyglucose accumulation can be seen in the visual cortex. This signifies increased glucose metabolism in the visual cortex. Thus we have evidence for involvement of specific regions of the brain in specific functions

Positron emission is detected by appropriate detectors which construct a series of computerised images of the brain similar to those seen in computerised tomography (CT).

2) Functional MRI :
It is based on the principle that increased neuronal activity leads to a local increase in blood flow through the active part of the brain.

The increase in blood flow is somewhat greater than is warranted by the increase in oxygen consumption.
Therefore, blood flowing through the active, hyperemic region of the brain has more oxygenated haemoglobin than the blood flowing through less active regions of the brain.
The magnetic properties of oxygenated and deoxygenated haemoglobin are different, the magnetic resonance signals from the active region of the brain increase.

Functional MRI systems currently in common use give a spatial resolution of about 1 mm, but a resolution of 0.5 mm has been achieved in experimental settings. This is an important breakthrough because cortical columns also have a width of about 0.5 mm.

3)Magnetoencephalography (MEG):

It can complement the information obtained from the conventional electroencephalography (EEG). MEG is based on the principle that neuronal activity in the cerebral cortex generates not only fluctuations in electrical potential (detected by EEG) but also magnetic fields. Unlike EEG signals, MEG signals are not distorted by the intervening tissues. These technical advances have given hope for rapid progress in localization of functions in the human brain.

So I hope ,this helps you guys to have a better picture on Brain Imaging.

Let's Learn Together!
-Medha.

Absolute contraindications for trial of labor

Here are a few conditions in which trial of labor is absolutely contraindicated:

1. Classical cesarean section. (Vertical incision)

2. Abdominal myomectomy with uterine cavity entry.

Previous cephalopelvic disproportion is not an absolute contraindication for trial of labor (Because if the fetus is small in this pregnancy, a trial of labor can be done.)

Previous low transverse cesarean section (Horizontal incision) is not a contradiction for trial of labor.

These are the ones I found out about. Lemme know if there are more, we'll add them to the list!
That's all!
-IkaN

Toxic Ventral Horn Cell disease

Hey guys!

The only ventral horn cell disease famous in India is Polio which was successfully eradicated. During it's era, other diseases with similar clinical picture, such as Kugelberg-Welander syndrome, Cerebral palsy, Friedreich's Ataxia, Spina Bifida etc were rampantly misdiagnosed​ as Polio.
Hence after it's eradication the incidence of these rare disorders has increased!

The disease is also known as "Infantile paralysis" and this moniker can't be more inaccurate. The commonest manifestation of this disease is Aseptic meningitis presenting with headache, photophobia, etc. And only 1% cases develop into paralytic poliomyelitis. And another point is that adults are 15 times more likely to become paralysed and are more likely to die.

Sorry for going off topic above; couldn't help it. Fortunately there are no drugs that are known to cause ventral horn cell disease. But there is one chemical called- TriocP, full form is tri-ortho-cresyl phosphate. It is illicitly used as a component of country liquor especially in USA; and in Mediterranean countries it was used as an adulterant in cooking oil.

Another toxic cause is Tick paralysis. The ixodes tick secretes a toxin that can cause Ataxia, flaccid asending paralysis, bulbar palsy etc closely mimicking Guillian barre's syndrome.

That's all!

-VM

Lasegue's Test

Hey guys here's another clinical sign!

Lasegue’s sign is another name for the modified straight leg maneuver used in the diagnosis of lumbosacral radiculopathy.

To perform the straight leg test, the clinician lifts the extended leg of a patient in a supine position. A positive response occurs when the pain pattern of the lumbar radiculopathy is reproduced. The test should be stopped when the pain is reproduced or maximum flexion is achieved.

But this sign is difficult to evaluate clinically especially for students. The reason being as simple as that it has been performed many a times before and patient already knows that he is going to suffer pain. So it was modified a bit by Lasague, he proposed that the leg should be raised while the knee is flexed by flexing the thigh at the hip joint. And then the knee is slowly extended until the patient complains of pain. In severe cases patient will complain of pain even during the flexion of hip.

More useful than the straight leg maneuver is the crossed straight leg test. This test has a lower sensitivity but a higher specificity​. The crossed straight leg maneuver is performed by raising the unaffected leg in a similar manner to the straight leg test. The examiner looks for the reproduction of radicular pain with elevation of the opposite leg.

A supplement to this straight leg raising test is Braggard's test. First we have to start raising the leg of the patient while his knee is extended until he complains of pain and then dorsiflex his foot, if the pain worsens, it's a positive Braggard's test.

But as given in most books, these signs are not only positive in case of lower lumbar vertebral disc lesions but also in a no of other conditions. The differential diagnosis of a positive straight leg test includes:
1. disc protrusion with impingement of nerve roots below L4;
2. meningismus;
3. any intraspinal lesion such as tumor below L4;
4. malignant disease or
5. osteomyelitis of the ilium or upper femur;
6. ankylosing spondylitis;
7. fractured sacrum and more.

That's all!

-VM

Tinel's Test

Heyy guys!!

Tinel's sign is the sign that a nerve is irritated. Tinel's sign is positive when lightly banging or percussing over the nerve elicits a sensation of tingling, or 'pins and needles,' in the distribution of the nerve.

For example, in carpal tunnel syndrome, where the median nerve is compressed at the wrist, the test for Tinel's sign is often positive, eliciting tingling in the thumb, index, and middle fingers.

Procedure: First you have to hyperextend the wrist to get the median nerve in the carpal tunnel more juxtaposed to the flexor retinaculum. Then tap the skin over the flexor retinaculum midway between pisciform bone and hook of hamate and then observe the patient's response.

This test can also be useful in the diagnosis of Tarsal tunnel syndrome where the tibial nerve is entrapped.

Another test in Carpal tunnel syndrome is Phallen's test.

-VM

Pathophysiology of atrophic vaginitis

Hello!
Here's a short post on the pathophysiology of atrophic vaginitis!

Medicowesome secret project: Let's talk about not quitting

What is the "Let's talk" project? How can I talk about mental illnesses?