About me

Hey Medicowesomites :D 

I have been posting here since some time and I would like to introduce myself

I am Murad Almasri from Palestine, I finished my med school in Egypt then did my USMLEs (step 3 left though) and will start my residency in Pediatrics in the US soon  :)

I am a positive person and I always like to know more and more ...it's just like eating information 
I believe in sth called "encyclopedial knowledge"..try to know everything about everything.

 I love making mnemonics and collecting them, I think I've been doing that since high school maybe even before that and this helped me tremendously in the USMLEs.

 I like reading books especially novels - I am a big Harry Potter fan ^_^ .
I also like video games ( I sometimes ask myself who doesn’t :D ?) and of course moviesssss 

 Learning new languages is a passion for me too, I already know a few.

 Good luck Medicowesomites and enjoy this amaaaaaazing website :)

 -Murad

Neural Crest Cells : Mnemonic

Hi everyone !
Here's a short mnemonic post !

Neural Crest Cells are very special cells that form at around 2-3 weeks of gestation.
They're right next to the Neural folds of the Neural tube to begin with and then eventually come to lie lateral to the tube, after which they migrate to various parts of the body giving rise to a bunch of things.

It's kind of SUPER IMPORTANT to memories what structures arise out of the Crest cells.
One of the reasons for it is that neural crest cell tumors will express certain neuroendocrine markers and that will make it easier to detect them on histopathology.
The other reason is that it's literally the most favorite embryology question - whether it's  NEET PG or Step1!

So here goes :

Mnemonic - LAMAS BABy

L - Lepto meninges (Pia + Arachnoid)
A - Adrenal Medulla
M - Melanocytes
A - ANS Ganglia
S - Schwann Cells

B - Branchial Arches
A - Aortopulmonary windows + Endocardial Cushions
B - Bronchogenic cells - Pneumocytes
Y - Yo

This will also help you understand why Melanomas , Bronchogenic Carcinoma , Schwannoma, Pheochromocytoma and even Neuroblastoma are all positive for similar markers and have similar appearances at times along with similar histopathological fetaures.

Hope this list covers them all!
Happy Studying!
Stay Awesome!

~ A.P. Burkholderia

Tennis in medicine

This post is compiled by Devi :)

● Tennis Racquet Appearance
o A descriptor for the tennis racquet-like thickening of the mesangium seen by light microscopy in glomeruli affected by Kimmelstiel-Wilson disease

● Tennis Racquet Appearance on Xray Teeth
o odontogenic keratocyst, ameloblastoma, central giant cell granuloma and odontogenic myxoma

● Tennis Racquet Spore
o classical shape of Clostridium tetani bacterium containing a terminal spore.

● Tennis Racquet Cell
o A tennis-racquet-shaped variant of rhabdomyoblast seen in sarcoma botryoides, a form of rhabdomyosarcoma affecting children

● Tennis Racquet Granule
o A subcellular particle seen by electron microscopy in Langerhans’ cell histiocytosis.

● Tennis Racquet Sign
o finding in a blighted ovum in which the ultrasonically empty gestational sac is compressed—the racquet’s ‘handle’—and adjacent to a surrounding deciduoid reaction—the ‘paddle’

● Tennis Elbow
o chronic inflammation at the origin of the extensor muscles of the forearm from the lateral epicondyle of the humerus, as a result of unusual or repetitive strain (not necessarily from playing tennis).

● Tennis Leg
o a rupture of the gastrocnemius muscle at the musculotendinous junction, resulting from forcible contractions of the calf muscles; often seen in tennis players as the result of frequent quick stopping and starting movements.

● Tennis Thumb
o tendinitis with calcification in the tendon of the long flexor of the thumb (flexor pollicis longus) caused by friction and strain as in tennis playing, but also occurring in other exercises in which the thumb is subject to repeated pressure or strain.

● Tennis Toe
o Subungual hematoma of the great toe which may follow any vigorous exercise—e.g., tennis-in shoes with hardened toe protectors

● Tennis Wrist
o Tenosynovitis of wrist which may occur in tennis players.

● Tennis Racquet cavity
o Seen in TB
o When tuberculous process is virtually confined to the bronchus, resulting in narrowing or occlusion with dilatation beyond, or in local wall destruction with weakening and dilatation, the ring shadow is in fact a dilated bronchus, and the wall of the ‘cavity’ has the histological feature of bronchial wall with or without tuberculosis foci in it. The rest of the bronchus, extending proximally towards the hilum, is often dilated as well, and its wall thickened by tuberculous involvement, so that a so called ‘tennis racket’ shadow. The draining bronchus of the most of the tuberculous cavities, whatever the type, is either concurrently or secondarily infected, leading to tennis racket appearance

Written by Devi Bavishi 

Age of Gestation and Estimated Date of Delivery (EDD)

Hello,

This is a nice video explanation by Jay!

Pyruvate Carboxylase Vs Pyruvate Dehydrogenase (a mnemonic)

Biochemistry has a lot of enzymes and equations which may make it hard to memorize!
Mnemonics come in handy and make our lives easier :D

I used to mix the function of these two enzymes: PC (Pyruvate Carboxylase) and PD ( Pyruvate Dehydrogenase)
so let’s first write the “simplified equations" with their main outcomes then talk about the mnemonic:

Pyruvate ---Pyruvate Carboxylase → OXloacetate

Pyruvate --Pyruvate Dehydrogenase→ Acetyl-CoA

A good way to remember that PC gives Oxaloacetate is just saying: PC and Xbox ( 2 platforms used for gaming) with the X in Xbox referring to the X in oXaloacetate.

To remember that PD gives Acetyl-CoA, put in mind that we become DEHYRATED in HOT weather so we use AIR CONDITIONERS  (ACs).
Dehydrogenase in Pyruvate dehydrogenase will remind you of dehydration and the need of ACs, consider AC the acronym of Acetyl-CoA ;)

A friend drew this to help simplifying it:

And that’s it :)

-Murad

Depression: A Summary

Hey guys! Here’s a review of Major Depressive Disorder using a whiteboard as help.

Depression is a type of mood disorder with primary disturbance in internal emotional state causing subjective distress and socio-occupational dysfunction.

Learned helplessness is when the individual learns that he/she is helpless in situations where there is a presence of aversive stimuli, has accepted that there’s no control over it, and thus gives up trying.

CLINICAL FEATURES:

The classic mnemonic goes as-

• Depressed mood: Can show diurnal variation. Patient reported. Essential for diagnosis.
• Sleep disturbance: Patients have decreased slow wave sleep duration and R.E.M. latency while having increased total R.E.M. duration with early R.E.M. onset in sleep cycle.
• Interest loss or anhedonia: Inability to attain pleasure from almost any activity. Patient reported. Essential for diagnosis.
• Guilty: Patients have feelings of worthlessness or sin for events they have little or no role in/ control of.
• Energy loss or fatigue
• Concentration difficulties: Usually accompanied with indecisiveness.
• Appetite and weight changes: Can increases or decrease. Usually, there’s a loss of body weight by 5% or more, associated with GI complaints of constipation, dyspepsia etc.
• Psychomotor changes: Retardation or agitation.
• Suicidal ideations: Recurrent thoughts of death, recurrent suicidal ideation without a specific plan, or a suicide attempt or specific plan for committing suicide.

MANAGEMENT:

1st line-

Psychotherapy: Cognitive Behavioural Therapy, Problem Solving Therapy, Emotions Focused Therapy and Behavioural Activation etc.

Selective Serotonin Reuptake Inhibitors: Fluoxetine, Paroxetine, Fluvoxamine, Escitalopram and Sertraline.

2nd line-

Serotonin/ Norepinephrine Reuptake Inhibitors: Duloxetine, Venlafaxine, Desvenlafaxine.

Tricyclic Antidepressants: Amitriptyline, Nortriptyline, Clomipramine, Desipramine and Imipramine.

Monoamine Oxidase Inhibitors: Tranylcypromine, Phenelzine, Isocarboxazid, Selegiline.

Atypical antidepressants: Bupropion, Trazodone, Mirtazapine.

Last line-

Electroconvulsive therapy is reserved for:

-Need for a rapid antidepressant reponse

-Failure of drug therapies

-History of good response to ECT

-High risk of suicide

-High risk of medical morbidity and mortality

Further reading:

Normal vs. abnormal grief reaction

Cyclothymia vs Dysthymia

Types of psychotherapy

Hope this helps. Happy studying!

--Ashish Singh

USMLE Mentorship

Hey there. How's it going? So I had this idea of compartmentalizing mentorship for different phases of USMLE.

Normally, what happens is a person asks questions which aren't very specific to a particular phase, and ends up annoying the opposite person.

So what if we divide usmle into 3 steps as they already are, also about paper work, electives, observerships, lodging boarding in different parts of USA, and make a list of people  specific to each step who want to help and provide mentorship. This way many people who are looking to give back to this process, have a chance of passing on the kindness.

So if you are done with any of the steps or want to provide mentorship for any of the things listed above, or have a thing that should be added to the list, send us your name and which part of the process you would like to help with. This way there can be more focused distribution of knowledge and mentorship.

People willing to help, send us your details. If we have enough people willing to volunteer, we can grow this thing into something really helpful. Depending on the number of  responses of volunteers, we will take this thing forward.

Leave your ideas and suggestions, if you have any. Thanks for reading.

If you are willing to help - email me at medicowesome@gmail.com with "USMLE Mentor" in the subject.

If you have IkaNs number on Whatsapp, contact her.

Varicose Veins : Overview

Varicose Vein

Hello Awesomites!
Through this post I'm trying to share the high yielding points on Varicose Veins.

VARICOSE VEINS
Primary:
Congenital absence or incompetence of valves
Inheritance with FOXC2 gene
Klippel-Trenuanay syndrome
Congenital AV fistula
Cutaneous hemangiomas
Hypertrophy of involved limb
Absence of deep venous system

Secondary:
Recurrent thrombophlebitis
Occupational – prolonged standing
Obstruction to venous return –abdominal tumors, retroperitoneal mass, Pregnancy.
Iliac vein thrombosis

Clinical features

Lipodermatosclerosis (brawny induration), pigmentation, thickening, chronic inflammation and induration of skin in calf muscle and around ankle.

Brodie-Trendelenburg test
To assess the competence of SFJ
Patient lies flat, elevate the leg and gently empty the veins, palpate the SFJ and ask the patient to stand whilst maintaining pressure. If the veins do not refill- SFJ is incompetent. If the veins do refill SFJ may or may not be incompetent, presence of distal incompetent perforators.

Cough impulse (Morrisey's test)
Locate the saphenofemoral junction(2-4 cm inferolateral to pubic tubercle) and ask the patient to cough. Impulse or fluid thrill felt indicates saphenofemoral incompetence.

Modified Perthes Test:Ask the patient to stand and tourniquet is applied at SF junction and ask to walk. Superficial veins become prominent – indicate deep vein thrombosis.

Three tourniquet test - To find the site of incompetent perforator
Tourniquets at SFJ, above knee level, below knee level.

Fegan's test:Detect the perforators

Investigations:
Duplex Ultrasound imaging – gold standard
Doppler examination – only when duplex is not available
Phlebography – not needed in primary venous insufficiency. Only performed as preoperative adjuncts when deep venous reconstruction is being planned
Ascending phlebography – differentiates primary from secondary insufficiency
Descending phlebography - identifies specific valvular incompetence suspected on B mode scanning.

Medical treatment:
Calcium dobesilate
Diosmin
Hesperidin
Toxerutin

Surgical management:
Trendelenburg's operation (juxta femoral flush ligation + stripping the varicose vein) for SFJ incompetency

Subfacial ligation of Cockett and Dodd :perforator incompetence with SF competency

VNUS closure(ablation catheter introduced into the SF junction and slowly withdrawn)

TRIVEX – veins identified by subcutaneous illumination; injection of fluid & superficial veins are sucked

Endo venous laser ablation (EVLA)

Sclerotherapy

That's all. Thank you.

-MD Mobarak Hussain (Maahii)

Hutchinson in Medicine

Here's a summary of the important Hutchinson's in medicine!

1. Hutchinson Teeth 
Seen in -  Congenital Syphilis
Feature -  Peg shaped Incisors , Widely spaced and smaller teeth.
Associations - Mulberry Molars : Multi-cusped Molars.

2. Hutchinson Sign of the Nail
Seen in -  Subungual Melanoma
Feature -  Melano-nychia ( Black colored nail) , feature of a melanoma below the nail plate.

3. Pseudo Hutchinson Sign of the Nail
Seen in -  Melanocytic be of nail bed
Feature -  Melano-nychia like appearance.

4. Hutchinson sign
Seen in -  Varicella Zoster infection
Feature -  Vesicle at the tip of the nose - indicative of Zoster infection. May precede Herpes Zoster Ophthalmicus.

5. Hutchinson Triad
Seen in -  Congenital Syphilis
Feature -  Hutchinson teeth + Interstitial keratitis + Sensorineural Hearing loss.

6. Hutchinson Patch
Seen in -  Syphilitic Keratitis
Feature -  Salmon patch on the cornea

7. Hutchinson Mask
Seen in -  Tabes Dorsalis, Neurosyphilis
Feature -  Mask like sensation over the face due to involvement of trigeminal.

8. Hutchinson  Pupil
Seen in -  Raised Intracranial tension especially due to a mass.
Feature -  Pupil dilated and unreactive to light due to 3rd cranial nerve compression.

Those are all the Hutchinson I can think of !
Let me know if you got any more.
Happy Studying!
Stay Awesome !

Growth Rates in Dermatology

Hi everyone. My skin Lecturer just taught me this so I thought let's post this =)

So growth rates !
We need to know 3 of them - Hair , Finger nails and Toe Nails.

Hair is the fastest growing.
So remember just one number for it - 0.37 mm/day.

Now , next fastest is finger nails.
For this divide by 3.
0.12 so 0.1 mm / day is finger nails.

Now divide this by 3 to get the value for Toe nails.
So 0.03 mm/ day is for Toe nails !

That's all for this post !
Stay awesome !
Happy Studying !
~ A.P.Burkholderia

MIL : Tinea (Dermatophytosis)

Hi everyone ! 
This is my 2nd MIL! Hope it's illustrative and informative ! 

(Click on the image to see it in Full View). 

Description : 

This is an Image of Tinea Corporis (Ringworm) infection of the skin. 

Notice - the lesion is annular in shape , has a ring like appearance. 

The lesion seems to be erythematous and  elevated (papular) towards its outside, and shows central area of clearing. 

This is classic of Tinea! 

Tinea is actually a fungal infection caused by Dermatophytes. 

____________________________

Clinical Features -

- Include such a lesion over different body parts which are severely itchy. 

- Occur particularly in summers.

Tinea Corporis = Tinea infection occuring over the body. 

Some common forms are - 

Tinea Cruris = Tinea Infection in the groin area (Jock itch).

Tinea Glutealis = Tinea along the natal cleft and towards the Gluteal regions. 

Tinea Pedis = Athelete's foot, occuring in the feet. 

Tinea Capitis = Scalp and hair. 

- Predisposed to get this in areas of constant sweat and moisture. 

Hence dryness is very important to maintain. 

____________________________ 

Ix : 

Usually a clinical diagnosis. 

Differentiate from Psoriasis : Lesions are not clear centrally ; there are plaques with Scales in Psoriasis and there maybe history of pin point bleeders.

Can confirm using Biopsy / Analysis of skin scraping and obtaining a species specific diagnosis. 

____________________________

Rx : 

A. Topical Anti fungals 

- Resistance is rampant. 

- Most promising ones are Luliconazole and Terbinafine creams.

- Can try Clotrimazole and Ketoconazole Shampoo for the site of lesion.

B. Oral Anti fungals 

- Itraconazole is a wonderful drug , dose being 5mg/kg / day. Roughly 100 mg twice a day is good enough. 

- Griseofulvin was an option but resistance seen now.

C. Anti histaminic for allergy. 

D. Duration of Rx is almost 2-3 months. It's a hard fungus to kill..

E. Steroids not to be used strictly. ( I've seen some horrendous results where the whole body was covered with Tinea when the patient stopped applying the steroids. Best to avoid them as per clinical as well as literature review). 

Hope this was helpful! 

Happy studying ! 

Stay Awesome ! 

~ A.P.Burkholderia 

Being street-smart during interviews: Buses!

Match season is a a really unique life-time experience. You will travel for interviews, meet new friends, visit states you have never visited before and of course, spend some money.

Although flights in general are the fastest most-convenient way to travel, you may try “bus inter-state travelling” which is much cheaper than taking a flight.

I will briefly write about some bus companies that are there and their pros and cons:

Greyhound:

Pros:
> It covers most of the states in the US.
> they have stations where you can sit and wait in (which is very important especially during Winter when it is freezing and snow is everywhere!).
> Starting from late 2017, you can use an E-ticket (emailed to you) instead of a printed ticket.
> They have nice discounts up to 50% sometimes, be sure to sign in and check their website for promo codes especially on Thanksgiving, Black Friday, New Year’s Eve.
(If you are planning to travel in January, don’t rush and buy the ticket early)

Cons:
> in general, their prices are more expensive than other bus companies.
> slow wifi (sometimes non-existent :D).
> Be careful around the stations especially at night, stay indoors!
> If you buy the ticket using a visa card with a different card-holder name than your’s, they will charge you an extra 18 dollars :( .
> Some passengers may be really weird.

If you miss your trip, you will be charged 20$ to issue a new ticket and catch the next one.

Megabus:

Pros:
> Cheaper and can be as cheap as 1 dollar! Check their website regularly.
> E-tickets are available too.
> Buses are newer and more comfortable.
> Passengers are “less weird”.

Cons:
> less state coverage than Greyhound.
> No stations, you have to wait in the street which can be very bard especially if it is raining heavily or snowing.

You can change your trip (if more than 3 hours left till departure) after paying a fee of 20 dollars. This is good to avoid losing your money if you had to cancel your scheduled trip for any reason.


Bustogo:
Less state coverage but they have a nice feature which is using the ticket within a year of purchasing it.

This is based on a personal experience, so you are welcome to try anything you want and put in mind that delays may occur here or there especially with bad weather.


Before you travel to any state, check this website: http://www.smartmedtravel.com/
It will show you names of buses and trains that are available in that state in addition to airports and car rental options.

Wishing y’all a successful Match/interview season and safe travels :D

-Murad

Mixed Connective Tissue Disease : An Overview

Hi everyone ! Just a short post reviewing MCTD! References are Harrison's and Medscape!

Mixed Connective Tissue Disease (MCTD)

1. What is it ?
- It's a somewhat ambiguously used term for disease characterised by a collection of few symptoms from different autoimmune connective tissue disorders.

- Namely , features of Systemic Sclerosis (SSc) , Lupus , Myositis and sometimes RA are present in some proportion in the same patient.
________________________________________
2. What are its chief presenting features ?

A. Features of SSc :
- Raynaud's is often the presenting feature. May also get edematous fingers.
- Dactylitis and digital gangrenes may be + due to Raynaud's
- Sclerodactyly
- Other Limited Cutaneous SSc features like CREST.

B. Features of Lupus :
- Arthritis
- Photosensitivity and Malar rash
- Evidence of Anti phospholipid Antibody Syndrome - associated with SLE. 

C. Features of Myositis :
- Proximal myopathy features
- Muscle tenderness
- May get Cutaneous features of Dermatomyositis.

Also may have Pulmonary Hypertension, Pulmonary Fibrosis.
________________________________________
3. What are the criteria for diagnosis ?

• Immunologically = Anti U1 RNP +

• Clinically = ( any 3 )

Mnemonic = A REM Sleep

Acrosclerosis
Raynaud's
Edematous Hands
Myositis (proven)
Synovitis-Arthritis

________________________________________
4. When to suspect MCTD?
- When a Patient comes with features of Limited Scleroderma (Raynaud's) , but not enough to fulfill its criteria ;

- SSc specific antibodies are not generally positive. (Anti Histone or Topoisomerase) ;

- Suspected SSc patients with  unusually prominent features of Arthritis, Muscle Pain or Rash

________________________________________
5.What tests would one order if suspecting MCTD ?

A. CBC with ESR -
May see Leucopenia with fairly elevated ESR

B. Serology -

• Confirm absence of SSc - Anti Centromere and Anti Topoisomerase.

• For MCTD -
U1 RNP Ab's are fairly specific

• For Myositis -
Anti Jo Ab's (Especially polymyositis)
Anti Mi Ab's (Especially Dermatomyositis)

• For Lupus -
ANA
Complement levels.

• For RA -
Anti CCP Ab's

C. Blood profile -
• Creatine Kinase - Elevated in Myositis
• Urine Routine + Microscopy for Lupus Nephritis type changes
• Electrolytes

D. For Complications -
• Chest X Ray for any ILD or fibrosis
• HRCT if needed.
• Pulmonary Function Tests
• MRI Brain for multi infarct lesions if APLA is + and if neurological changes are +
• ECG - For myocarditis
________________________________________
6. How is the treatment like ?

- NSAIDs - Symptomatic Relief.
- Steroids confer some Relief unlike in SSc. So it's important to differentiate the two!
- Hydroxy chloroquine and Methotrexate may be used to keep disease activity in check.
- Treatment of complications.

Hope this was helpful!
Happy Studying!
Stay Awesome!

~ A.P.Burkholderia