Initiation factors in eukaryotic translation mnemonic

Hello Everyone,

Lets discuss Initiation factors today. Here's the the mnemonic:

1. elF-1: 1 looks like i . So it causes Dissociation of 80 S

2. eLF-2: Two- Formation of Ternary complex. Also GTP needed

3. eLF-3: 3 looks like B. hence it causes Breakdown(dissociation of 80 S)

4. elF-4:   

cap binding protein complex elF-4F=  elF-4E + elF-4G+ elF-4A . Binds to 5’End of mRNA through elF-4E  

elF-4A and elF-4B: A has helicAse activity.Makes use of ATP 

                                B makes things Better. :)

                                Both help  reduce complex secondary structure of 5’end of m-RNA.                                                                                                           (A+B=reduce Complexity)

5. eLF-5: 5 looks like S. So it causes: 

      1. releaSe of initiation factors

      2. aSSociation of 40S and 80S Subunits

Here are some diagrams that will help you:

That’s all,

Thank you,
Chaitanya Inge

Rubeola vs Rubella mnemonic

Hello!

RubeOla - Ordinary measles ( kOplik spots on buccal mucosa are pathognomic )

RuBella ( German measles ) - Well, I remember Bella B. Felsenheimer, a German musician and drummer ( Foschheimer spots on the soft palate are characteristic ).


Thats all
- Jaskunwar Singh

Torres bodies mnemonic

Okay, to be honest this one is not quite a very good mnemonic but I like to remember Torres bodies in yellow fever by the footballer Fernando Torres wearing his club jersey in yellow color, even if he doesn't. Well, yeah, that's about it! :-p

-Sushrut Dongargaonkar

Diagnostic Enzymes in Myocardial Infarction

   

Hello Everyone,

Here’s a quick mnemonic on Sequence of elevated enzymes in myocardial infarction. I got it from https://imgusmlestep1.blogspot.in. Originally it was  like this Time to CALL 911. I have modified it. It goes like this

                             Time to CALL 12 24 30 48.

The numbers represent time of peak elevation of the enzymes.

Sequence of elevated enzymes are:

        Troponin: Cardiac Troponin I and Cardiac Troponin C (12 hours)

        Creatine Phosphokinase (MB) (24 hrs)

        Aspartate Transaminase (30 hrs)

        Lactate Dehydrogenase 1 (48 hrs) 

Important Facts:

Cardiac troponin I (cTnI) is highly sensitive and specific for damage to cardiac tissue. cTnI appears in plasma within 4–6 hours after an MI, peaks in 8–28 hours, and remains elevated for 3–10 days.Elevated cTns, in combination with the clinical presentation and characteristic changes in the electrocardiogram, are currently considered the “gold standard” in the diagnosis of a MI.

Creatine Phosphokinase (MB):Appearance of this hybrid isoenzyme in plasma is virtually specific for infarction of the myocardium .Following an acute MI, CK2 appears approximately 4–8 hours following onset of chest pain, reaches a peak of activity at approximately 24 hours, and returns to baseline after 48–72 hours.

A quick comparison between Cardiac troponin and Creatine Phosphokinase:

Troponin is more sensitive than CK-MB because more troponin is found in the heart per gram of myocardium and that a greater percentage depleted from the heart by cardiac injury arrives in the blood 

With regard to specificity, troponin elevations are almost always specific for cardiac injury, except for the infrequent analytical false positives caused by fibrin interference and/or cross-reacting antibodies. CK-MB is not specific for cardiac injury, as a small amount is found in skeletal muscle.

I am very thankful to IkaN for helping me with Troponin and CK-MB.  :)

Thats all,

Thank you

Chaitanya Inge  

Drugs that prolong QT interval mnemonic

Hello!

Here are drugs that can prolong QT interval and cause Torsades de Pointes! The mnemonic is TOOOOORSADES!

Cerebral ring enhancing lesions Mnemonic

Cerebral Ring enhancing lesions are a common finding in MRI based questions asked in the boards. ;)

The mnemonic to help you remember it is: Suppose there is a Dr Grams who is missing his wedding ring and is searching for it fervently. So if you're doing an MRI and you see a ring what should you do?

CAL DR GRAMS

C- Contusion
A- Abscess
L- Lymphoma

D- Demyelinating disease
R- Radiation necrosis

G- Glioblastoma
R- Resolving Haematoma
A- Abscess
M- Metastatic lesion
S- Subacute infarct

Here's a mnemonic submitted by Jaskunwar Singh. It includes Tuberculosis and toxoplasmosis!

CAL DR SMART

C - Contusions
A - Abscess
L - Lymphoma

D - Demyelinating diseases
R - Radiation necrosis

S - Subacute infarct
M - Malignancy / Metastatic lesions
A - AIDS
R - Resolving haematoma
T - Toxoplasmosis / TB

I assume that everybody knows about toxoplasmosis and tuberculosis so I didn't include them in my mnemonic. Use the mnemonic that suits you =)

That's all :)

-VM

Study group discussion: A mnemonic for yawning? (pandiculation)

Hello!

Pandiculation definition: A stretching and stiffening of the trunk and extremities, as when fatigued and drowsy or on waking, often accompanied by yawning. 

Here's a study group discussion xD

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Vitamin B3 and pellagra mnemonics

Hello!

This post is all about niacin aka vitamin B3 and it's deficiency with loads of mnemonics. Who is excited?

1. How to remember Niacin is vitamin B3:

- You can remember the three vowels in nIAcIn, so it's vitamin B three.
- N has 3 strokes, so Niacin is B3
- NIA - B3

2. Vitamin B3 deficiency, Pellagra, is clinically manifested by photosensitive dermatitis, diarrhea, dementia.

Pellagra mnemonic:
"B3 causes D3"
Diarrhea, Dermatitis, Dementia.

3. Pellagra tends to occur in areas where people eat maize (or corn, the only grain low in digestible niacin) as a staple food.

Mnemonic: Corny people can't be nice. (Corn can't have niacin)

People - Pellagra. PP!

Corny people can't be nice and amazing! Get it? A-maize-ing! Hahahahha! I'm so pun-ny and funny!

4. The amino acid tryptophan is needed to make niacin, serotonin and melatonin.
Mnemonic: Have a nice trip to serotonin land (Serotonin rhymes with Melatonin).

Why is this fact clinically significant?
Carcinoid syndrome leads to excess production of serotonin, which depletes  tryptophan. There's not enough tryptophan to produce niacin, resulting in pellagra.

5. Isoniazid (INH) use can cause vitamin B3.

Mnemonic: INH has 3 letters. B3 deficiency!
Also, isoNIAzid. For NIAcin deficiency.

6. Lastly, you should know about Hartnups disease which is due to defective neutral amino acid transporter on renal and intestinal epithelial cells 

Here's a mnemonic by usmle1mikmonics:
HARTNUP Disease
Hartnup
Aminoaciduria
Renal (also intestinal) / Recessive
Transporter defect / Tryptophan deficiency
Neutral amino acids / Niacin deficiency / Nicotinamide supplements (Treatment)
Urine (Tryptophan lost in urine)
Pellagra / high Protein diet (Treatment)
D’s - Dermatitis, Dementia, Diarrhea

That's all!
-IkaN

Anterior Abdominal Wall : Mnemonics

Hi everyone. So I've just started Surgery and it makes me go back to Anatomy. A lot.
Here are some helpful Mnemonics on the Anterior abdominal wall

The External Oblique muscle is the SIR of  all muscles.
It's the SIR of all muscles.
Hence , This SIR forms the Superficial Inguinal Ring.
Because it's the SIR , it forms the Sir of all ligaments too - the Inguinal Ligament.

The Fascia Transversalis is a scary thing. Whenever I see it , I get DAR. ( Dar is the Hindi word for Fear)
So I get DIR when I look at it. :P
And hence the Deep Inguinal Ring is in the Fascia Transversalis.
Since this is such a scary muscle , the important artery Inferior Epigastric Pierces this muscle. Making it more DIR-avna.

Finally,
How should one remember the direction of the External and Internal oblique muscles ?
Hands in your pocket is External Oblique.
So medially and downwards.

Hands on the Tits is Internal Oblique.
So medially and upwards.

Hope these help you !
Happy Studying !
Stay aweosme.

~ A.P.Burkholderia

How is Visual Contrast achieved?

Hello everyone,
Let us discuss Visual contrast today. This question has haunted me for a long time.

Let's start with the basics, the cells in various layers of retina and their function.

Here's a quick review of things you have already read:

1. What is photoreceptor?
It is a rod or cone. It detects light.

2. What is horizontal cell?
It is present between rods and cones. It is inhibitory in function. (It is involved in lateral inhibition which we will discuss later!)

3. What is bipolar cell?
It transmits information from photoreceptor to ganglion cells.



Now, lets come to the details.

4. What are metabotropic receptors?

First of all what you must understand is Metabotropic receptors and Inotropic receptors are receptors present on bipolar cells.

They recieve stimulas from photoreceptors (mostly decreased glutamate is the stimulas).

Metabotropic receptors cause depolarisation that is excitation of centre of receptive field of bipolar cells

5.What are inotropic receptors?
They cause inhibition of centre of receptive field i.e. hyperpolarization. (remember, I for Inhibition)

6. Receptive field - What is it?
It is a region of retina where if the light falls it is going to alter the firing of neurons. (By firing I don’t mean guns :P) It means the action potentials generated and transmitted by the photoreceptors. So each cell has a characteristic receptive field. It can be as small as a dot or as large as this page itself. But don't limit this concept to a photoreceptor only. Almost all sensory cells example in somatosensory system or in auditory system possess a receptive field.

Receptive field of a bipolar cell is arranged into a central disk,
the “center” and a concentric ring, the “surround”, each region responding oppositely to light.

Coming to the crux of the topic i.e. Visual Contrast.

How do the things we have discussed so far help us achieve that?

Visual Contrast is achieved by two mechanisms:
1. Lateral Inhibition
2. Excitation of Some Bipolar Cells and Inhibition of Others — The Depolarizing and Hyperpolarizing Bipolar Cells.

1. How does lateral inhibition help?
First: It does not allow the signal to spread through the dendritic and axonic trees. Hence point to point transmission occurs.
Second: The direct and indirect pathways accentuate each other. This can be easily understood. Photoreceptor sends excitatory signals to bipolar cell. But the adjacent photoreceptor sends a inhibitory signal through the horizontal cell. Mostly these two neutralize each other so no net stimulus is transmitted to bipolar cell.
      But If the adjacent cell is  unstimulated by light, It will not inhibit the excitatory signals transmitted by the photoreceptor which is stimulated by light. Hence it will allow excitation of bipolar cell.
This allows extra excitation of bipolar cell. We get a better contrast. The area which is dark remains dark. But the area which is bright becomes even brighter. This is what visual contrast is all about.
The fun part of all this is, a lot of visual illusion make use of this principle. Do google "Simultaneous Contrast"  :) .

2. How do different Bipolar cells help?
Because depolarizing and hyperpolarizing bipolar cells lie immediately against each other, this provides a mechanism for separating contrast borders in the visual image, even when the border lies exactly between two adjacent photoreceptors.
We will take a simple example. Suppose light is striking at periphery of two receptive fields. Remember it is shaped like a disk, with a centre and periphery both opposite in nature.Suppose One is On centre bipolar cell and other is Off centre bipolar cell(On centre: Activated when light hits centre but periphery is inactivated and vice versa for Off centre). So only the Off centre bipolar cell will detect it. Hence mixing up of signals is avoided. Again what I get is a sharper border. That is what contrast is all about.

That is how it is all done.

Interesting fact: The cells in the retina don't follow the "all or none" law. Transmission is by Electrotonic conduction. From ganglionic cell onwards cells  follow all or none law.

Thats all,
Thank you,
Chaitanya Inge

Lewy body dementia mnemonic

Hey there.

Dementia with Lewy Bodies (DLB) is characterized clinically by deficits in attention and visuospatial function; fluctuating cognition; recurrent visual hallucinations; and spontaneous motor features of parkinsonism. Other associated symptoms include repeated falls, syncope, autonomic dysfunction, neuroleptic sensitivity, delusions, hallucinations in other modalities, sleep disorders, and depression.

Here are mnemonics and how I remember these points!

Lewy has halLEWYcinations.
Visual hallucinations are common.

Lewy is slowy.
Slow movements for Parkinson's disease .

Lewy is sleepy.
REM sleep abnormalities like drowsiness.

Lewy is slippy.
DLB is associated with frequent falls.

Lewy is slow-y, sleepy, slippy and sees things (halLEWYcinations)

lEwy also has an E for eosinophilic intracytoplasmic alpha synuclein aggregates.

That's all!
-IkaN

Authors' diary: Jas a year

Hello!

Our admin and author, Jaskunwar Singh, completed 1 year of writing with Medicowesome today :D

Causes of coma : mnemonic

Hello

Coma ( unresponsive and unarousable state ) causes mnemonic

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Collier's Sign

Hey guys!

Collier’s sign (“posterior fossa stare,” “tucked lid” sign) is elevation and retraction of the upper eyelids, baring the sclera above the cornea, with the eyes in the primary position or looking upward.

This may be seen with upper dorsal midbrain supranuclear lesions (e.g., Parinaud’s syndrome). There may be accompanying paralysis of vertical gaze (especially upgaze) and light-near pupil-
lary dissociation.

The sign is thought to reflect damage to the posterior commissure levator palpebrae superioris inhibitory fibers; causing overactivity of this muscle.

-VM

Hydatid cyst mnemonic

Here's a mini mnemonic on hydatid cyst. Caused by E. Granulosus.

H - Hepatic cysts common
Y -
D - Dogs are definitive host
A - Albendazole treatment (Remember, anaphylaxis risk if aspirated)
T -
I -
D -

C - Calcification (eggshell calcification)
Y -
S -
T -

That's all!
-IkaN

Phencyclidine intoxication mnemonic

A combative, agitated, psychotic patient with multi directional nystagmus, tachycardia and hypertension. 

Yup. You guessed it right. It's PCP intoxication. 

Here's a mnemonic 

Melanoma marker mnemonic

The immunohistological marker for melanoma is HMB 45.

You can remember it by remembering the gorilla named 'Harambe' (HaraMBe) of Cincinnati zoo who was in the news as he unfortunately had to be put down because a child entered his enclosure.

You can correlate melanoma's black pigment with that of Harambe's black fur.

That's​ all!

- Sushrut Dongargaonkar

Chronic granulomatous disease mnemonic

Chronic granulomatous disease mnemonic

CGD - GRANULES!
G - chronic Granulomatous disease
R - Rhodamine (Dihydrorhodamine abnormal flow cytometry)
R - ROS, Respiratory burst decreased
A - Abscess / Granulomas
N - Nitroblue tetrazolium dye test
N - NADPH oxidase defective

Catalase positive organisms mnemonic: CATALASE!
Candida
Aspergillus
Tuberculosis
Listeria
Staphylococcus aureus
Serratia
pSeudomonas
E coli

That's all!

-IkaN

Deglutition

Hello Everyone!

 Today lets discuss deglutition. Human's love this process :) .

1.What is Deglutition?

Process by which food  moves from mouth into stomach.

2.What are the different stages?

Oral

Pharyngeal

Oesophageal

3.Is it voluntary?

No, Only the Oral stage is voluntary.

4.What is the oral stage?

Bolus is pushed by the tongue into the Oropharynx.

What is the pharyngeal stage?

It is a involuntary stage. Here bolus moves from pharynx to oesophagus. Bolus has got 4 paths in pharynx

Back in mouth: This is prevented by position of tongue against soft palate.
Upward into nasopharynx: Prevented by elevation of soft palate.
Forward into larynx: Prevented as follows(Only if you don’t talk while swallowing food :P

• Approximation of vocal cords
• Forward and upward movement of vocal cords
• Backward movements of epiglottis to seal opening of larynx
• This causes Deglutition Apnea

Enters the Oesophagus:

• Pharyngoesophageal sphincter relaxes.
• Also upward movement of larynx stretches opening of oesophagus.

What is Oesophageal Stage?

Food from oesophagus enters the stomach.Peristaltic waves aid in this process.Two types of Waves are seen:
Primary peristaltic contractions
Secondary peristaltic contractions

What is the role of lower oesophageal sphincter(LES)?

It undergoes Receptive Relaxation. i.e. it relaxes only upon entry of bolus. Otherwise it is constricted.We have 2 clinical conditions associated with it:

1.Achlasia cardia : Failure of sphincter to relax during swallowing. Causes accumulation of food in oesophagus.

2.Gastroesophageal Reflex disease(GERD): Due to incompetence of LES. Acidic content from stomach regurgitates back into pharynx.

That's all,
Thank you,
Chaitanya Inge

Condyloma acuminata vs condyloma lata mnemonic

Hello!

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Mnemonic for Sulci And Gyri of the cerebrum

Hello everyone,
  Memorising sulci and gyri of the cerebrum consists of two parts:

1. Memorising the names of the sulci and gyri
2. Memorising the locations

Today I will help you with the first part. Please bear with me, it will be a lengthy one.
Lets start with Superolateral surface
We have 4 regions on superolateral surface. They are

1. Frontal 
2. Parietal
3. Temporal
4. Occipital

Trick for superolateral surface revolves around 3 letters, they are: PSI

Frontal

Sulci- PSI      Gyri- PSIM
Sulci:

1. Precentral 
2. Superior frontal
3. Inferior frontal

Gyri

1. Precentral
2. Superior Frontal
3. Inferior frontal
4. Middle frontal 

Temporal
Sulci:SI  Gyri: SMI
  Names of Sulci are:

1. Superior Temporal
2. Inferior Temoral

Gyri

1. Superior Temporal
2. Middle Temporal
3. Inferior Temporal

Parietal
Sulci: PI Gyri: PSI

Sulci

1. Postcentral
2. Intraparietal

Gyri

1. Post central 
2. Superior Parietal
3. Inferior Parietal

For occipital. Remember a simple mnemonic : Sulci- SaLLTy C    Gyri- Gisa.

Sulci
SaLLTy C

1. Superior and Inferior Polar
2. Lunate
3. Lateral Occipital
4. Transverse Occipital
5. Calcarine

And the gyri

GISA

1. Gyrus descendens
2. Inferior Occipital
3. Superior Occipital
4. Arcus parieto-occipitalis.

So that completes the superolateral surface.

Now moving on to Medial Surface

  Here's the mnemonic CAPS. Men wear CAPs.  

Now  it goes like this Sulci- CCCAPPS. Gyri- Men wear CCaPPPPs

Sulci 

1. Calcarine
2. Callosal 
3. Cingulate
4. Anterior parolfactory
5. Posterior Parolfactory
6. Parieto-Occipital
7. Suprasplenial or subparietal

Gyri

1. Median frontal
2. Cuneus
3. Cingulate
4. Paraterminal
5. Paraolfactory
6. Paracentral
7. Precuneus

Finally moving to the Inferior Surface

 Here's the mnemonic

     when Cars HOORns  PeoPle LAugh LoudLy on boys playing GaMMes on streets!

Sulci (red coloured in mnemonic)

1. Collateral
2. H shaped orbital sulci
3. Olfactory
4. Occipitotemporal
5. Rhinal

Gyri(purpled coloured in mnemonic

1. Parahippocampal
2. Posterior Orbital
3. Lateral orbital
4. Anterior Orbital
5. Lingual
6. Lateral Occipitotemporal
7. Gyrus rectus
8. Median Occipitotemporal
9. Medial Orbital

Lets hope it will make memorising these things a bit easier.

That's all,
Thankyou,
Chaitanya Inge

Blood Supply And Nerve Supply of the Scalp

 Hello Everyone!
                Today we will discuss blood supply and nerve supply of the scalp. Just too many nerves and arteries out there. But there is a way out.

     First let us talk about nerves.

Nerve Supply:

1.  Sensory
2. Motor

Sensory:

Here's the trick

 In front of the auricle we have 4 nerves, and all are branches of trigeminal nerve.They are:

1. Supratrochlear (Opthalmic division)
2. Supraorbital  (Opthalmic division)
3. Zygomaticotemporal (Maxillary division)
4. Auriculotemporal (Mandibular division)

The remaining 4 are located behind the auricle. They are very simple to remember:

GaLeO Go To

1. Great Auricular(C2,C3)
2. Lesser Occipital(C2)
3. Greater Occipital(C2)
4. Third Occipital(C3)

Motor Supply:

In front of auricle: Temporal branch of facial nerve

Behind the auricle: Posterior auricular branch of facial nerve

Nerve supply of the Scalp 

Coming to the  Blood Supply:

1. Arterial supply:
1. Supratrochlear
2. Supraorbital
3. Superficial Temporal
4. Posterior Auricular
5. Occipital

1. Venous Drainage: Common, thats simple. Names corresponds to arteries.
• But there's a twist. The superficial temporal along with maxillary vein wants to drain in external as well as internal jugular. So they form retro mandibular vein whose course is pretty clear in diagram.

Blood Supply of the Scalp

That's all,

-Chaitanya Inge 

How to draw midbrain sections and lesions (Fun mnemonic diagrams)

Hello everyone!

Brain sections are super hard to remember, I imagine them as monsters and this is how I draw them:

Paraneoplastic Dermatoses - Bazex Syndrome.

Hello everybody,

So to continue our series on cutaneous manifestations of internal malignancies
Let's quickly learn about Bazex Syndrome.

Bazex syndrome — acrokeratosis
paraneoplastica is a paraneoplastic phenomenon associated with squamous cell carcinoma of the upper digestive tract.

Presents more commonly in Males and over the age of 40.

Presentation: Erythematous to violaceous psoriasiform plaques predominantly located in acral areas (especially the fingers, toes, nose, and helices).

Nail dystrophy, palmoplantar keratoderma, and alopecia are common.

In most patients, manifestations of Bazex syndrome precede the diagnosis of malignancy or the malignancy is diagnosed concurrently.

The lesions of Bazex syndrome are usually resistant to targeted therapies, but treatment of the neoplasm usually leads to resolution of the cutaneous findings, although not always.

Let's learn together!
-Medha!

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Exam Prep Hacks -Tips for a lazy person

Hola everyone!

This post is for those people who really struggle during exam time, not because they can't understand studies or are stressed, but for someone who is really lazy and no amount of stress can change that (believe me I'm one of those :P)

So if you're someone who puts on their best game forward during exams and becomes a ninja  - this post is not for you! :P

Okay, so you know your exams are just around the corner and you have shit loads of syllabus to complete and you know there will be last minute panic yet you do not make a strategy and  "go with the flow", completely regret it later and are desperate to change this.

Understand that this post won't make you active all of a sudden, this post is all about embracing your laziness and turning into an asset and to rock your exams always without being under constant stress ;)

Let's get down to the basics then.

1. Always set rewards for yourself.

Sitting continuously for 5-6 hours IS JUST NOT POSSIBLE. Your concentration span is of a fly and you get distracted very easily, so instead of setting a target of studying for 5-6 hours continuously and then being disappointed later, make short targets. Like finishing one or two topics in one sitting and then maybe watching an episode of friends or going out for a walk. This way you feel like you've "earned" the break and will keep you motivated.

2. JUST SWITCH OFF YOUR PHONE.

Let's face it. Our phone's are the greatest source of distraction. Be it a whatsapp text, facebook notification or instagram post, we are constantly checking our phones. Either turn the internet off or put it on do not disturb mode, check the phones during your breaks.

3. Exercise!!!

Okay yes I get it, how is exercise gonna help me study? Remember endorphins- feel good hormones? Yeah well, they are secreted whenever we exercise. Exercise also help increase the blood flow and makes us more active. So, go for a walk for 20 min, skip in your room or dance, Whatever keeps you going, believe me, it's really gonna help. Will increase your concentration too!

4. Coffee.

I do not need to explain this. This is like a godsent drink!!  Everyone swears by it, but honestly, whatever will help you stay up.

5. Make realistic targets.

DO NOT set your goals according to others. Forget how your roommate is studying, how the lights of the topper of your class is always turned on. You know yourself the best. Do what suits you. Set targets for yourself. Setting targets according to others will just leave you disappointed and demotivated. It's a vicious cycle. Don't do it.

6. Select a time best suited for you.

Decide if you're a morning or a night person. And stick to that. Again, do not follow others. If you're a morning person, sleep well in time and wake up as early you can. If you're a night owl, prolong your study for as late as you can. Push yourself a little. Lol, just a little though :P

7. Sleep is your best friend.

Haha. Sleep to your rescue. It has been documented that sleep is very important to convert your short term memory to long term memory, so don't shy away taking those naps! :P Lack of sleep will cause dark circles too :P

But obviously not too long, 4-5 hours is adequate during exam time :P

8. Good diet.

Last but the most important part. Keep yourself hydrated and try to have a healthy diet, something which isn't too heavy. Heavy or oily food will just make you sleepy, tired and of course gain weight. Keep drinking water and fluids. Your brain needs food to function!

Hope all these things help you guys in acing your exams!

So the next time someone calls you lazy, Be Proud ;)

Ashita Kohli

The Basics : Deviated Nasal Septum

Hello

Deviated Nasal Septum - "Abnormal and asymmetrical alignment of the nasal septum that results in acute nasal obstruction and other symptoms of upper respiratory tract."

AETIOLOGY -

1. Trauma : Abnormal pressure ( lateral or frontal ) applied to nasal septum results in its deviation to one side or another.
- The lateral blow may cause displacement of septal cartilage from the vomerine groove and maxillary crest.

Groove on which septal cartilage sits ( encircled ) - lateral view
Diagram by IkaN.

- Frontal blow causes crushing injuries to the nose, usually occurs in sportspersons especially the boxers.

2. Developmental anomalies : Palate forms the base of nasal septum. Highly arched palate, cleft palate or lip, and dental abnormalities can all lead to deviation of the septum.

3. Racial factors : Caucasians have more incidence of DNS.

4. Hereditary : Familial predisposition.


TYPES of DNS -

1. Anterior dislocation : dislocation of nasal septum into one of the chambers. ( unilateral nasal obstruction )
2. C - shaped dislocation : simple curve to one side with compensatory hypertrophy of turbinates in other side. It causes unilateral nasal obstruction.
3. S - shaped deformity : causes bilateral nasal obstruction
4. Spurs : shelf - like projections may lead to headache and epistaxis. ( unilateral obstruction )
5. Thickening : due to septal hematoma

CLINICAL FEATURES of DNS mnemonic

TREATMENT - Only required if the symptoms are severe. The procedures are to be done once the patient is more than 17 years old.

- Septoplasty : The most deviated parts of nasal septum are removed and rest of the parts are surgically corrected and repositioned.

- Submucous resection ( SMR ) : Mucoperiosteal and mucoperichondral flaps that overlie one side of the septum are lifted. Most of the septum is removed and flaps repositioned.

Thats all
Hope this helped :)

- Jaskunwar Singh

External Carotid Artery branches mnemonic

Hello

External Carotid Artery branches mnemonic - Seven Angry Ladies Fighting Over PMS

Cranial nerve III damage (Oculomotor nerve damage mnemonic)

Hello!

The CN III has both motor (central) and parasympathetic (peripheral) components.

Which fibers get affected in diabetes?
Which would lead to loss of pupillary light reflex?
Which fibers are compressed first?
Which would cause the down and out pupil?

Don't know? Check the video out!

Mnemonic : Deviated Nasal Septum clinical features

Hey Awesomites

The clinical features ( s/s ) that are presented by a patient with DNS are : NOSE MASH

NO - Nasal Obstruction
S - Septal cartilage and bone deformity
E - Epistaxis

M - Middle Ear infection
A - Anosmia
S - Sinusitis
H - Headache


- Jaskunwar Singh

C Peptide levels : An Overview

Hello everyone!So I ended up uttering 'C peptide' recently in my Medicine Viva and my professor screwed me over it.
(Clearly I didn't C it through :'D )
So I thought of doing a brief summary on it.
Here goes.

1. What is C peptide ?
- When pro- insulin is cleaved , it gives insulin and C peptide.
- C peptide in general has a longer half life than insulin and is easier to detect.
- The pathway is something like this :

Pre proinsulin produced in Rough Endoplasmic Reticulum of Pancreas --> Transported to the Golgi apparatus and cleaved to form Proinsulin -->  Packed into secretory granules --> In these granules proinsulin is converted to : Insulin and C peptide. 

- Traditionally it is said to have no intrinsic activity but recent studies say it might have anti oxidant and anti inflammatory properties.   

2. What does it indicate ?
- So , its presence indicates presence of Insulin in the body in a proportionate amount.
- Hence in a case of Hypoglycemia if C peptide levels are high, it's likely to be due to increased endogenous Insulin levels.

3. C peptide levels increased in -
- Insulinoma
- Sulfonylurea induced Hypoglycemia ( As they are Insulin Secretagogues)
- Type 2 Diabetes Mellitus ( Hyperinsulinism due to resistance)
- Insulin Resistance states like Obesity , PCOS , Cushing's.

4. C peptide levels reduced in -
- Type 1 Diabetes as Insulin secretion is reduced
- Latent Autoimmune Diabetes of Adult (LADA )
- Factitious hypoglycemia - Due to excess exogenous Insulin administration.
- Hypoglycemia due IGF secreting tumors.

So if you get a patient with Hypoglycemia with elevated insulin levels , C peptide levels help you decide if due to exogenous Insulin , or Endogenous Insulin  ( Sulfonylurea induced or Insulinoma).

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

The Basics : Middle Ear

Hey Awesomites

In this post, I will be talking about the middle ear structures and its relations with its neighbors ( just a summary ).

The Middle Ear is an air filled and bilaterally compressed/ concaved cavity lined by mucous membrane located in between the external and internal parts of ear. It is divided into:
- Epitympanum or the Attic ( 6mm ) - lies  above pars tensa and medial to pars flaccida
- Mesotympanum ( 2mm ) - lies opposite to pars tensa
- Hypotympanum ( 4mm ) - lies below the level of pars tensa

BOUNDARIES of the middle ear ( homologous to structure of a cube ) :-

Roof : Tegmen tympani - a thin bony plate that is a part of petrous part of temporal bone, separates the middle ear cleft from middle cranial fossa.
- Infection in the middle ear may spread superiorly and lead to formation of abscess in the meninges ( especially Extradural abscess ), meningitis or if severe, it may even lead to abscess formation in the temporal lobe.

Floor : Jugular bulb - The middle ear cavity is separated from jugular bulb by a thin piece of bone that if deficient may lead to formation of a layer of fibrotic tissue and mucous membrane in between. The contents of jugular bulb are:
- Internal Jugular vein
- Glossopharyngeal nerve ( IX )
- Vagus ( X )
- Accessory nerve ( XI )

The tympanic branch of glossopharyngeal nerve enters the middle ear at the junction of the floor and medial wall to play an important role in formation of tympanic plexus.

Anterior wall : The upper part of the narrow anterior wall has two openings or tunnels for - ( mnemonic : TEA )
- Canal for Tensor tympani muscle
- Pharyngotympanic ( or Eustachian ) tube

The lower part of anterior wall is separated from the Internal Carotid Artery by a thin plate of bone. The ICA is surrounded by a plexus of sympathetic nerves that enter middle ear through openings in this bony plate to form tympanic plexus.

Posterior wall : Posteriorly, it is related to middle ear cleft ( Aditus, Antrum and mastoid air cells )
- Infection in this region may spread posteriorly into the sigmoid sinus ( in posterior cranial fossa ) and cause thrombophlebitis !!

Medial wall : Medially the middle ear cavity is related to the promontory, oval and round window

Lateral wall : Tympanic membrane separates the middle ear from the external ear.

A brief about the functions of middle ear:
On the incoming of sound waves, the tympanic membrane oscillates and these oscillations are sensed by the strongly attached and faithful middle ear ossicle, the Malleus. The sound energy is transmitted as such by the ossicles ( Malleus - Incus - Stapes ) to the internal ear for further processing.

The major function of these ossicles is amplification of sound waves - Tympanic membrane is 17 times larger than the oval window - So that means the sound energy is picked up by the larger area ( TM ) and impinged over a much smaller area ( oval window ) thus amplifying it 17 times.

In addition, the lever action of the ossicular chain is approx. 1.3 units. Thus the intensity ( force ) of sound waves/ vibrations changes ( increased by ~20 times ) and not the frequency !! If the sound waves are not amplified ( in case OC is removed ), the Air Conduction would be lost. So BC > AC and thus hearing would then be poor.


Thats all
Hope this helped :)
Stay Awesome!

- Jaskunwar Singh

Craniopharyngioma mnemonic

The C's of Craniopharyngioma

Children

Calcification
Cholesterol crystals
Cyst formation

Central diabetes insipidus

Compresses chiasm, can't C (see, because butemporal hemianopia)

CR: CRAniopharyngioma RAthkes pouch remnant

Yup. That's all!

-IkaN

Medicowesome secret project: Organ series

What is the secret project? How can I participate?

Medicowesome secret project: Heart art

What is the secret project? How can I participate?

Medicowesome secret project: Let's talk about depression in medical professionals

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

Medicowesome secret project: Let's talk about finding love

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

Medicowesome secret project: Earth Day

'A' wave in JVP : Mnemonic and explanation

Hi everyone. So JVP is one of the most theoretical clinical signs I've ever studied. And though parts of it are logical , I find it tedious to memorize all causes for a particular finding.
So I've prepared a Mnemonic for prominent a waves.
Here goes.

The A wave is a positive wave of the JVP.
It represents the Right Atrial pressure during systole.

Causes of a prominent a wave
Remember :
CRePT's

C - Cor Pulmonale
R - Right heart Failure
P - Pulmonary stenosis
T - Tricuspid stenosis
S - The S tells you it's Stenosis for P and T.

The a wave essentially represents the pressure in the Right atrium during systole.
So any condition that causes this pressure to increase would cause a prominent A wave.

Cor Pulmonale and RVF are basically congestion in RV causing elevation of pressure in the RV.
This means the atrium needs to pump with greater force into the Ventricle for the venous return to enter the Ventricle. This increases the RA pressure causing prominent a wave.

Pulmonary Stenosis leads to accumulation of blood in the RV and this follows a similar fate as the above mentioned causes.

Tricuspid stenosis causes obstruction to the flow of blood from RA to RV. Thus accentuating the pressure in the RA.

That's the Prominent a wave for you !

~~~~~~~~~~~
Now there's something called the Cannon a wave.
These represents contraction of the RA against a closed Tricuspid valve.
The causes of this include -
A- V dissociation.
Heart blocks.
Ventricular arrhythmias - V tach , Ventricular premature complexes and Ventricular pacing.
~~~~~~~~~~~
The a wave would be absent in Atrial fibrillation as the atrium is functionally not pumping at all , and just vibrating.

These are the a wave findings for you !
Hope this helped
Stay awesome.
~ A.P. Burkholderia

Number needed to treat and number needed to harm mnemonic

Hello!

Number needed to treat = 1 / Absolute risk reduction

Mnemonic: TARR - Treat Absolute Risk Reduction

Number needed to harm = 1 / Attributable risk

Mnemonic: HARM - Harm Attributable Risk M

That's all
-IkaN

The Basics : Lateral wall of Nasal cavity

Hey Awesomites

In this post, I will be talking about the anatomical structures in the lateral wall of the nasal cavity. 

Clubbing : Why it occurs.

Hi everyone !
This is a short post on why clubbing happens.
So it's simple !
It's cause people like to go out and get drunk. 
Just kidding. Here goes.

1. What is clubbing ?
- It's the bulbous enlargement of the terminal digits​ and the nail bed.

2. What are its causes ?
- Symmetrical clubbing can occur due to a host of causes.
- To summarize :
  A. Respiratory
   : Lung  cancer
   : Suppurative lung conditions like   

     Bronchiectasis , lung abscess and Chronic TB.
    : Pulmonary  Fibrosis

   B. Cardiac
   -  Cyanotic heart disease
   - Eisenmenger Syndrome
   - Infective endocarditis

    C. GIT
     -  Inflammatory bowel disease
     -  Cirrhosis - esp Biliary

     D. Endocrine
     -  Thyroid Acropachy
     -   Acromegaly

3. Why does it occur 

So I've spent a lot of time researching theories on how clubbing occurs. And let me tell you in the start itself, they're not clear on why it occurs.
But what makes sense to me , I want to share with you'll! And it was an absolute pain to find something convincing enough. So just stick with me here ;;) 

So the crux of clubbing lies in vasodilation of the digital vessels causing proliferation of the tissue there in.
The most widely accepted theory right now is the megakaryocyte theory.

So in the figure above , the left side in white shows the normal course of a megakaryocyte through the blood. 

In altered  cardiorespiratory conditions , these large platelets either bypass the Pulmonary circulation owing to the shunting produced due to Heart defects or the lung parenchyma itself proves to be less to purify the blood of the platelets.

 This causes these giant platelets to go lodge into the digital circulation causing release of cytokines like Platelet derived growth factor (PDGF) and TGF beta amongst others. These GF's cause vasodilation and in return , nail bed proliferation and collagen deposition.

How do we explain the Clubbing in GI causes ?
IBD - especially Crohn disease seen to have thrombocytosis eventually which may aggravate the PDGF.
In cirrhosis of liver , especially biliary , pulmonary arteriovenous shunting is observed. This could result in the megakaryocyte entrapment as explained.

Another theory suggests inflammation triggers a vagal response causing Vasodilator effects. ( Neurogenic).

Other theories -
Hypoxia induced
Reduced ferritin related
Neurogenic
Humoral - various PG's and other humoral molecules.

The most widely accepted theory is the Megakaryocyte theory.

Hope this satisfied you ! 
Thank you.
Stay awesome. 

~A.P.Burkholderia

Preparing for NEET - Part 2

Hello everyone.

So now for my part 2 post on NEET PG prep, I will provide you with a seventh month schedule, but before that let’s  talk about the pros and cons of joining classes and how to deal with studies if you don’t join one.

Now in my earlier post I did mention that classes will help YOU with only 20% of the entire prep that also with sustained proper attention in the 12 hour class with proper notes and revision.

     1. The biggest thing you achieve by attending class is that the professors don’t beat around the bush, they give you point to point details and explain the things which they know by experience that the students are bound to screw up the most.

This is not something you can’t achieve by your own.  If you can get your hand on any class notes, then that’s enough, just thoroughly read that book, be regular in solving mcq’s and discuss your issues in group chats or with your study buddies. This does take care of it plus you gain a lot more, because here you are actively seeking answers and not being spoon fed like in classes

If you don’t have any class notes and our reading standard books, I suggest only read the bold lines, don’t read anything else. If you clearly don’t know anything about a particular topic then only read it in depth.

2. Weekly test series and grand test with ranking. This is beneficial only if you stick to the schedule, sadly I feel only 3 out of 10 students are regular at these exams. Also even if you don’t join the regular course, you can just join the test series, which I feel is a great option .

The bad point is that sometimes students feel torn between their own study speed, the subjects they want to study first and the test series schedule. Sometimes the test series just overwhelms you a lot cause every week you need to prepare for a different subject.  This has happened to me, and I feel that if I hadn’t join the test series to begin with, maybe I  wouldn’t have been so confused as to whether what to study and what to revise.

So it’s very important that you all know your own study patterns and your comfort. Don’t do things just because everyone else is doing it.  Chart down your schedule, and once you start with it, stick to it. Don’t listen to people and try doing things their way, you are your own person and you are awesome.

NOW for the study schedule.  This way of prep is bold and ridiculous. Its exhausting and It will demand that you trust the process, but it will work. It was taught to me by one of my friend. Its esp for the ones who haven’t joined any classes.

·         This first phase is for you to grab onto all the possible books on mcq’s you can for the last ten year mcq’s. And then you go crazy, just solve the mcq. Don’t read the explanations. Just solve and solve, just  reading the answers. Thats it. This whole process should take you a month at the max of rigorous solving.

·         Take a break..chill out for a couple of days

·         Phase two. repeat the phase one, now I  have tried this. And by experience I will tell you this is when it gets tough, monotonous and downright stupid but keep going at it. This will take you two months max.

·         Breaktime

·         Phase three is when you repeat it all over again, but now you will see the difference. You will love solving cause now the answers will flow out of you. Cause you have just learned 30.000 important one liners of all the 20 subjects. This process will take you 20 days.

·         Phase four is when you read and solve your doubts, read any damn book you want. Search for pictures, make your own picture library.

Remember 75% mcq are repeats, so this plan is made in a way that you learn all of those 75% first

You need to solve atleast all the mcq a minimum of five times to score a decent rank

Your speed of solving should reach 300 questions in one hour with atleast 65- 70% right.

These above are your goals after you are done with phase four

Irrespective you choose to follow this plan or any of the tips in my part 1 post, or if you choose to modify it according to you. Remember the most important thing is that you have to be consistent and do smart studies and not study like a dog. Have your wits about yourself and don’t  waste your time on reading unnecessary details.

Thank you

Sakkan

Authors' diary: Homemade cheap DIY alternatives for a smartphone camera stand

This video is from the authors diary!
In this video, I show how I keep my camera stable while shooting videos of my notes / whiteboard.
I use paper cups and books as my camera stand.