Saturday, May 20, 2017

Tay-Sachs disease notes and mnemonic

Hello!

Tay-Sachs disease is an autosomal recessive, neurodegenerative disease.

Plasma Proteins Mnemonic

Hello Everyone,
 Lets discuss plasma proteins.

1.How do we classify them?
  • They are classified into Albumin, Globulin and Fibrinogen.
  • Globulins are further classified into Alpha , Beta Globulins and Gamma Globulin.
  • Alpha Globulin is further divided into Alpha 1 and Alpha 2 Globulins.
Memorising the examples of them is simple. 






Examples of Beta Globulins can be remembered as follows:
         B PTH
B-Beta Lipoproteins(LDL)
P-Plasminogen
T-Transferrin
H-Hemopexin

Interesting Fact:

Acute-phase proteins are a class of proteins whose plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation. This response is called the acute-phase reaction.
  • Positive acute-phase proteins increase in inflammation e.g., C-reactive proteinmannose-binding protein, complement factorsferritinceruloplasminserum amyloid A and haptoglobin.
  • Negative acute-phase proteins decrease in inflammation. Examples include albumin, transferrin, transthyretin, retinol-binding proteinantithrombintranscortin


Thats all,
Thank you,
Chaitanya Inge


Friday, May 19, 2017

No cyanosis in cyanide poisoning. Why?

I was reading about cyanide poisoning today and saw "Cherry red skin" in the clinical manifestations. I know that carbon monoxide poisoning causes a cherry red color to blood. But why cyanide?

The curiosity lead to this post.

In normal cellular metabolism, most adenosine triphosphate (ATP) is generated from oxidative phosphorylation. .

Cyanide avidly binds to the ferric ion (Fe3+) of cytochrome oxidase a3, inhibiting this final enzyme in the mitochondrial cytochrome complex. When this enzyme's activity is blocked, oxidative phosphorylation ceases. The cell must then switch to anaerobic metabolism of glucose to generate ATP.

Anaerobic metabolism leads to the formation of lactic acid and the development of metabolic acidosis. Hydrogen ions produced by ATP hydrolysis are no longer consumed in aerobic ATP production, exacerbating this acidosis. Serum bicarbonate decreases as it buffers excess acid, leading to an increased anion gap.

Despite an ample oxygen supply, cells cannot utilize oxygen because of their poisoned electron transport chain. This functional (or "histotoxic”) hypoxia is particularly deleterious to the cardiovascular and central nervous systems (especially the basal ganglia).

Because of the decreased utilization of oxygen by tissues, the venous oxyhemoglobin concentration will be high, making venous blood appear bright red.

Therefore, despite hypotension, apnea, and/or bradycardia, the patient does not usually appear cyanotic in the setting of cyanide poisoning.

Clinical features:
Central nervous system toxicity is the most prominent in cyanide toxicity – Headache, anxiety, confusion, vertigo, coma, seizures.

Which should you suspect cyanide poisoning?
Victims of fires
Reported ingestions
Treatment with sodium nitroprusside

Antidote:
Hydroxocobalamin
Sodium thiosulfate
Nitrites (to induce methemoglobinemia)

That's all!
-IkaN

Thursday, May 18, 2017

CT scans and role of Contrast enhancement


Contrast enhancement and it's role in CT scan
The concept of Contrast enhancement in radiology is not new and it has been in practice even before the Advent of CT scans.
CT scan as a modality of imaging was invented by a British engineer Godfrey Hounsfield in the year 1972.

Purpose of Contrast enhancement

Contrast enhancement is a method of exaggerating  the visible difference between adjacent structures on scan by administrating contrast agents.The term Contrast enhancement in CT scan includes usage of radio opaque substances for better visualization of the anatomic structures as well as better localization and characterization of the pathologies, better differentiation of the pathology from the normal surrounding structures.

Principle of Contrast enhancement

The diffusion of contrast agents from the blood stream to the body tissue is physiologically limited. In pathologies such as cancer, blood vessels grow (angioneogenesis) with increased leaking of contrast agents resulting in lesions much more visible on Contrast enhanced scans.
In CNS, contrast diffusion is limited by Blood brain barrier. Disruption of BBB lead to enhancement after administration of contrast agents.

Indications of Non Contrast CT (NCCT )
For detection of
1.Stones in kidney,ureter, cbd
2.Calcification
3. Fat in various tumors
4. Head injury
5. Acute hemorrhage
6. Stroke
7. SAH


CECT

The pathologic lesions show enhancement or attenuation depending upon the phase of contrast enhancement. So if you are looking for a particular pathology,it is important to know in which phase of CECT to look for.
For that purpose,I've enumerated the phase in which CT scan is done and can be recorded.

1. Non enhanced phase (NECT)
Uses are same as those of Ncct. Many a times this scan is done before administration of the dye to compare pre and post contrast enhancement study.
Calcification, fat in tumors, inflammation and infarction can be seen in this phase well.

2. Early arterial phase (15-20 secs post injection)
When contrast is still in the arteries, it has not enhanced the organs.
This phase is useful to look for vascular abnormalities such as aneurysms, vascular stenosis, etc

3. Late arterial phase (35-40 secs post injection)
Sometimes known as arterial phase.
All the structures that get their blood supply from arteries will show optimal enhancement in this phase.

4. Hepatic or late portal phase (70-80 secs post injection)
Liver parenchyma enhance trough blood supply by portal vein and some enhancement of hepatic veins.

5. Nephrogenic phase (100 secs post injection)
This is when all of the renal parenchyma including medulla enhances. Particularly helpful for small renal cell carcinoma which are otherwise missed.

6. Delayed phase (6-10 mins post injection) called as wash out phase or equilibrium phase
Washout of contrast in all abdominal structures except for fibrotic tissues which become relatively more dense in this phase.

Factors affecting CECT
The timings depend on
1. Organs to be scanned and focussed
2. Type of CT machine available, number of slice
3. Amount of contrast given depending upon the body weight of the patient
4. Injection rate of the contrast
5. Route by which contrast given. (Mainly IV but can be oral,rectal too)

Lesions / pathologies visualized on CECT
1. Liver tumors
Due to it's dual blood supply, 80% by portal vein and 20% by hepatic artery normal parenchymal enhancement maximally in hepatic phase . On the contrary, all all liver tumors are supplied 100% by hepatic artery. So hyper vascular tumors are best seen in late arterial phase. Hypovascular tumors on the other hand are better seen in hepatic phase.
2. Fibrotic lesions
Fibrotic lesions like cholangiocarcinoma and fibrotic mets hold contrast much longer than normal parenchyma hence best seen in delayed phase.
3. Pancreatic tumors most of them being hypovascular are seen best in late arterial phase. In cases of acute pancreatitis, late arterial phase best detects necrosis. Remember chronic pancreatitis can be very well appreciated on NCCT due to calcification.
4. Anastomosis leakage 
CECT done in post op patients to check anastomosis leakage. Oral contrast play a role here for check scans done in post op bowel anastomosis.

5. Pulmonary embolism - 
Good quality scans are required to delineate the emboli in the pulmonary vasculature.
6.CT angiography 
For vascular studies.

Dr. Shil Pill

Coccidioidomycosis mnemonic

Coccidioidomycosis is caused by Coccidioides immitis!

Diabetes insipidus and water deprivation test

In this video I talk about pyschogenic polydipsia, central diabetes insipidus, nephrogenic diabetes inspidius, water deprivation test :)

Theophylline toxicity mnemonic

Theophylline's effects arise from antagonism of adenosine receptors and indirect adrenergic activity.
It is used as a bronchodilator for patients with asthma or chronic obstructive pulmonary disease.

Chest x-ray - Left Lung.

Hello everybody!
Let's see the image correlations of the left lung today.
The left lung has an apical lobe ,lingula and a basal lobe.
Apical lobe has 2 segments: Anterior and posterior.
Lingula : The tongue like extension and the alleged counterpart of the middle lobe has 2 parts to it : Superior and Inferior.
Basal lobe has 4 segments namely : Superior, Posterior, Medial, Lateral.
Carefully observe how the identification of these segments differs while seeing an X-ray.
Apical lobe:



Basal Lobe:



So that's it with the interpretation of lung fields on X-rays!
Hope this is helpful!
-Medha.

Wednesday, May 17, 2017

“PILL” Esophagitis.

Hello!

Let's review a very common preventable condition of pill/drug induced esophagitis. 

It is occurs due to prolonged contact of the esophageal mucosa with a medication, which acts like the damaging agent.

Medications implicated in
“pill”esophagitis are :
Tetracycline
Potassium chloride
Ferrous sulfate
Nonsteroidal antiinflammatory drugs
Alendronate

Most often the offending tablet is ingested at bedtime with inadequate  water, this leads to prolonged contact  u of the drug with the esophageal mucosa leading to focal damage and esophagitis.

This causes acute discomfort followed  by progressive retrosternal pain,  odynophagia, and dysphagia.

Endoscopy reveals a focal lesion localized to one of the anatomic narrowed regions of the esophagus or an unsuspected pathologic narrowing. 

Treatment is supportive.
Antacids, topical anesthetics, bland or  liquid diets are often used.

Let's Learn Together!
-Medha.

Flow volume loop notes and mnemonics

Here are my notes on the flow volume loops!

Flow volume loop explanation video and mnemonic

Hello!

I explain the flow volume loops seen in obstructive lung diseases, restrictive lung diseases, intrathoracic and extrathoracic - fixed variable obstruction in this video with mnemonics! :)

Chest X-ray - Right Lung!


Hello everybody!
So today let's go through the Right lung segments as seen on a Chest x-ray with the help of images.

This will help us identify the exact location of the pathology and the possible etiology for the same.

So the Right lung has 3 lobes.
Upper
Middle
Lower.

Let's start with the right UPPER LOBE.
It has 3 segments.


Now moving to the MIDDLE LOBE .
It has 2 segments Medial and Lateral.



Moving to the LOWER LOBES.
It has 5 segments.
Superior Basal
Lateral Basal
Antero Basal
Medial Basal
Posterior Basal.






(3D CT Images courtesy - CU medicine Hong Kong)

So well I hope this helps to correlate the various Bronchopulmonary segments while interpreting a Chest x-ray!

Let's Learn Together!
-Medha.








Tuesday, May 16, 2017

Difference between cauda equina syndrome and conus medullaris (with mnemonics)

Let's differentiate Cauda equina syndrome (CES) from conus medullaris today!
With mnemonics because they make life easier! (And because it is the IkaN style of doing things)

Ischioanal fossa (Fun Mnemonic Diagrams)

Hello Everyone,
Lets discuss Ischioanal fossa. I remember it as a Rocket!!
How to draw it?


Draw a rocket

Add 2 wings !!

Draw 2 snakes underneath the wings
                                             
Color it up.

And Label it.



That's all,
Thank you,
Chaitanya Inge


Methamphetamine intoxication mnemonic

Hello!
This post is about crystal meth.

Aortic stenosis murmur explained

In this video I talk about:

The systolic crescendo decrescendo murmur of AS
Early vs late systolic murmur - Which is more severe?
Why there is a soft S2 and paradoxical splitting of the second heart sound in AS?

And mnemonics! Yaay! :D

Cortisol and eosinophils

Today, I forgot the relationship between cortisol and esosinophils. Completely screwed up a practice question because I couldn't remember it.

Now I made a mnemonic to remember this :D

Mnemonic: In hypERcortisolism, Eosinophils Reduce.

Why do corticosteroids cause eosionopenia? Why does hypocortisolism cause an increase in eosinophil count?

Bankart's and Hill Sach's lesion mnemonic

These two lesions occuring in relation with shoulder dislocation can stump someone if asked in an MCQ as to which lesion is specifically related to which structure.

Remember the sentence-

" Sacks of money are deposited in a bank"

In a similar way, the head of humerus is 'deposited' (articulates within) the glenoid cavity.

Thus,
Hill Sach's lesion occurs on the humeral head.
Bankart's lesion occurs on the anterior glenoid labrum.

Now, how to remember whether is it the anterior or the posterior labrum?
Remember that anterior dislocation of the humeral head is the commonest occurence. That will leave no confusion.

That's all!

-Sushrut Dongargaonkar


How to interpret a Chest X-ray.


Hello everybody, so today's post will be a little long so kindly bear with me.

I hope that this post helps you and makes interpretation of an x-ray less daunting and more fun.

So let's get started.
Step 1:
Always place the x-ray in a such a way so that it seems you are facing the patient.

So naturally this is only possible with AP(Anteroposterior) and PA (Posteroanterior) views.

The technicians mark the X-ray indicating the side but chest x-rays are sort of independent of side markers due to the position of the left ventricle and the aortic knuckle.

Step 2:
To interpret a chest x-ray you need to think in layers as in from outside-in or from inside-out, with one type of structure at a time.
Do a targeted search rather than just staring at the radiograph, an abnormality is unlikely to strike unless you look for it in a planned manner.
Your eyes should scan each part of the film and one should always look twice in the regions where mistakes are more likely, like the Apices in a PA view and the region over the spine in a lateral view.

Step 3:
Scan the whole radiograph in a sequence:

Identify AP or PA view.
Check for side markers.
Radiographic exposure.
Check for integrity of bony cage.
Begin with lung Apices.
Upper middle and lower zones.
Check the Cardiophrenic angles.
Mediastinal structures.
Soft tissues.

Step 4:

Then Detect the lesion : Where is the lesion and what structures are affected by it. Starting with

Trachea and Bronchi:
Position,shift and deviation.

Mediastinal Lines:
Paratracheal stripes: visible or lost.
Aortopulmonary Window: Fullness or normal.
Paraspinal Lines: bulging or normal.

Hilum and Cardiac prominences, and see cardiogenic or mediastinal cause for the prominence.

Lungs :
Check for the Lung Volumes, Right or left lung densities,Diffuse lung abnormalities.
Whether the lesion is Pulmonary or Extrapulmonary. If pulmonary whether it is focal or diffuse.

Pleura and Fissures : Check for pleural effusion and pleural based masses.

Bones :
Focal injuries
Rib fractures, Notching.
Shoulder girdle and clavicles .

Step 5:
Directed search in an apparently normal chest x-ray.

Lungs :
See the Hidden lung areas like retrocardiac and retroclavicular areas.
Also check for Pulmonary Embolism.

Mediastinum :  Check for the Posterior mediastinal masses and hilar masses.

Step 6:
Describe the Lesion :
Location and Extent of the lesion.
Characteristics in the form of :
Shape
Homogeneity
Calcification
Necrosis
Associated features of trachea, lungs fissures etc.

Step 7:
In the end.
Put up a provisional diagnosis.
Differentiate from the closer/similar diagnoses.
Put up a final diagnosis.
A breif description on the Management.

Viola! We are through our way describing a chest x-ray!

Reading any radiograph has its learning curve and the more we see the more we learn.

Try and describe all the radiographs you see hence forth in the manner mentioned above or anyway you like it but follow a definite protocol and don't miss any important points.

I hope this post was helpful.

Let's Learn Together!
-Medha.

Monday, May 15, 2017

A neonate with cyanotic heart disease (Case #2)

A 3 day old new born is found to have cyanosis. On examination, a II/IV holosystolic murmur is heard. CXR shows decreased pulmonary vascular markings and cardiomegaly. ECG shows tall P waves and left axis deviation. Diagnosis?

Similar to the case we discussed last time (A neonate with cyanotic heart disease #1), let's narrow our differential.

Step 2 CK: Immunization schedule in the US mnemonic

Hey!

I did not create the mnemonic, I just created the table to put it all together for quick revision :)

Sunday, May 14, 2017

Why some people hate cheese!

Hello everybody!

So today let's learn a bit about how our brain circuits work.

Some people hate cheese. Like seriously?
How can you miss the warm fussy feeling you get while eating warm molten cheese in a Fondue!

Well some people might not feel any bit of it and rather feel disgusted when presented with cheese.( I feel bad for them )

Anyway let's see how these things work.

Why aversive to cheese per say? 

Cheese is the food that most frequently triggers aversion. 

 Among those with an aversion to cheese, 20% say they are intolerant to lactose. In 50% of cases, at least one of their family members does not like cheese either. These stats suggested that there is a genetic origin to this aversion, which might be related to lactose intolerance.

To find out what happens in the brain,  people who like cheese and who do not were selected and participated in a functional magnetic resonance imaging (fMRI) study. 

They observed that the ventral pallidum which is activated in people who are hungry was totally inactive in people who had an aversion to cheese but was active for all other food types. Also the Globus Pallidus and Substantia Nigra part ( the reward circuit) was more active in people who had aversion to cheese than in those who do. 

So in conclusion, the areas of reward centres of our brain the Globus Pallidus and Substantia Nigra have two types of neurons with complementary activity , one relating to the rewarding aspect of food and other to it's aversive nature.

So now we have a breif idea as to how the brains are wired differently and how we all our special in our own ways!

Let's learn Together!

-Medha.

Femoral Nerve Mnemonic

Hello Everyone,
Lets discuss Femoral nerve today. Doesn't femoral nerve sound feminine? Also I am writing this post on Mothers Day, what a coincidence!

Root value: L2-L4
   (Ladies work 24 hours.)

Motor innervation:
It innervates following muscles:

  • Anterior division branches innervates
    •   Sartorius 
    •   Illiacus
    •   Pectineus 
  • Posterior division branches (innervates Quadriceps femoris)
    •   Rectus femoris 
    •   Vastus medialis 
    •   Vastus lateralis 
    •   Vastus intermedius 

How to remember it? @_@
Queens hardly get time to SIP coffee  ^_^


Sensory innervation:

Anterior division branches provides sensation to anteromedial asepct of the thigh, consists of 2 branches:

  • Medial cutaneous nerve of thigh 
  • Intermediate cutaneous nerve

Posterior division:

  • Saphenous nerve : provides sensation to anteromedial aspect of lower leg.
  • Infrapatellar branches to knee :pierces the sartorius and fasica lata medial to the knee, and provides cutaneous innervation to the skin anteriorly over the patella.
How to remember it? @_@
MISs is Insensitive to pain. ^_^


Wish you Happy Mothers Day : )

That's all
Thank you,
Chaitanya Inge


Monteggia and Galeazzi fracture mnemonic

One can get confused on hours end as to what fracture is related to what bone. Hope this mnemonic comes in handy!

1. MUFC( Manchester united fan club)

- Monteggia upper ulnar fracture
With radial head dislocation

2. GFR low(Glomerular filtration rate)

- Galeazzi fracture radial, lower
With distal radio ulnar subluxation

That's all!

-Sushrut Dongargaonkar


Laughter Disorders - It might not be funny!

Hello everybody!
So today I am going to share some information on how laughter has a dark side too.
There are a lot of laughter related disorders and this gets the scientists more Intrigued to understand the neurocircuitry involved in laughter.The actual neural basis of laughter is still not very well known and what we do know about it largely comes from pathological clinical cases.
 So laughter can be classified,
 ranging from genuine and spontaneous to simulated (fake), stimulated (tickling), induced (by drugs) or even pathological.
Some of the laughter related disorders are:
1) Pseudobulbar affect : identified by Charles Darwin, It is characterised by frequent, involuntary and uncontrollable outbursts of laughing and crying. It arises due to disconnection of the descending pathways between the frontal lobes and brainstem.
Some disorders associated with the condition are : Traumatic brain injury, Alzheimer's, Parkinson's Disease, Multiple sclerosis and Most importantly Stroke.
2) Gelatophobia : Fear of being mocked at. It may lead to social ineptness to severe​ depression. It is thought to arise from negative early life experiences if being teased, ridiculed.
Imagining shows us that people who suffer from this condition have poor brain wiring and poor connections between frontal and medial temporal brain areas.
On the continum Gelatophilia is the joy of being laughed at and another related condition Katagelasticism is joy of laughing at others.
3) A twisted sense of humor and laughing at inappropriate times is thought to be an early sign of demetia.
4) Gelastic seizures : rare type of seizure that involves a sudden burst of energy, usually in the form of laughing. Mainly associated with Hypothalamic Hamartoma.
5) Angelman Syndrome : It's a chromosomal disorder affecting the Central Nervous  System.They laugh frequently due to heightened stimulation of parts of Brain involved in laughter.
So these were some pathologies and conditions of abnormal laughter.Do share if you know of any such conditions I may have missed.
So long as there are no underlying illnesses laughter is still the best medicine!
Let's Learn Together!
-Medha.

Saturday, May 13, 2017

Fact of the day : Loss of Olfaction is a prodrome of neurodegeneration

Hey Awesomites

Loss of the sense of smell is one of the first warning signs of neurodegenerative diseases such as Alzheimer's, Parkinson's and other diseases associated with dementia.

One of the common link evidenced in some studies is the damage to neurotransmitter and neuromodulator receptors ( particularly acetylcholine ) in the frontal part of brain.

Also, one of the pathogenic hallmarks of AD, the Neurofibrillary Tangles ( NFTs ) have been found in olfactory bulb, olfactory tract, the transentorhinal and entorhinal cortex, anterior olfactory nuclei and amygdale. The number of NFTs within these areas have been positively correlated with the disease progression.

Thus, olfactory testing at the 'right time' is essential to detect the presence of disease process in its 'preclinical phase' itself. It could help in the differential diagnosis of several neurodegenerative diseases. Early diagnostic interventions such as smell testing, brain imaging procedures like functional MRI and PET scan, olfactory epithelium biopsy, using radioactive neurochemicals help in evaluation.

The anosmic symptoms are much more common in old patients of more than 65 years of age.


Thats all
- Jaskunwar Singh

Research update : Genetic locus of Anorexia nervosa revealed

Hey Awesomites

A Research landmark study led by UN school of medicine has found the first genetic locus for the perplexing illness, anorexia nervosa. Previously it was known that this eating disorder runs in families with genetic and environmental factors both playing their role and there is ten - fold risk in first -degree relatives, but no particular association with a genetic locus was provided.

Thought to be associated with psychiatric disorders like neuroticism and schizophrenia, it has also been positively correlated with underlying metabolic abnormalities including body - mass index (BMI) and insulin - glucose metabolism. Genome - wide association studies ( GWAS ) have revealed a significant locus for anorexia nervosa on chromosome 12, in a region previously shown to be associated with type -1 diabetes mellitus and autoimmune disorders. This means that this eating disorder shares common roots with metabolic and psychiatric traits !!

These results may help in reconceptualizing the underlying aetiology and pathogenesis of such a lethal disorder and also coming up with new treatment interventions to cure the disease.


Thats all
- Jaskunwar Singh

Treatment of erythema migrans in early Lymes disease

Hi.

Like the title suggests, this post is on treatment of erythema migrans in early Lymes disease.

For non pregnant adults and children ≥8 years of age with early Lyme disease: Doxycycline, amoxicillin, or cefuroxime axetil.

Why is doxycycline preferred for most patients with early localized Lyme disease?

Because it is effective against both Lyme disease and human granulocytic anaplasmosis.

Children <8 years of age or pregnant women with early localized Lyme disease: Amoxicillin or cefuroxime axetil.

Doxycycline is not recommended for children under the age of eight years or for pregnant or lactating women. 

Why?

Because of severe adverse effects, including teratogenicity, permanent yellowish-brown teeth discoloration after in utero exposure and in children under 8 years of age and more rarely fatal hepatotoxicity reported in pregnant women.

That's all!
-IkaN

Dwarfism vs Cretinism

Hello Everyone,
   How do we differentiate between dwarfism and cretinism?
Just remember GIRL

G- Growth- Reduced in both
I- IQ- Normal in pituitary dwarfism and decreased in cretenism
R-Reproduction-Absent or delayed puberty in both
L-Limbs- Proportionate in Dwarfs and Disproportionate in cretins.
                (C follows D)(cretins have disproportionate limbs)

What are features seen in a cretin?
Remember 5P's
  1. Pot-bellied
  2. Pale
  3. Puffy-faced child
  4. Protruding umbilicus
  5. Protuberant tongue



That's all,
Thank you,
Chaitanya Inge




Authors' diary: Cerebellar tumor location and associated symptoms

Hello!

In 2013, I wrote this anatomy mnemonic on parts of the cerebellum and their functions.

I was tested this fact in a question today and I got it right. Yaay! :D

The question asked about a tumor, expected to know the most common location of the tumor and then expected you to know the symptoms caused due to it's location. Ooooh!

Anyway, lemme summarize what you should know:

Medulloblastomas usually occur in the vermis and spare the cerebellar hemispheres - They are more likely to cause truncal ataxia.

Pilocytic astrocytomas occur in the cerebellar hemispheres - They are more likely to cause intention tremors.

Added by VM:
An ependymoma can also cause truncal ataxia just like medulloblastoma. Ependymoma can be differentiated by it's location, again. Being more common on the floor of fourth ventricle, it will irritate area postrema and cause vomiting. It can also cause CN 7, CN 10 and CN 12 palsies. 

It's funny how in your preclinical years, all you ask is, "WHY DO I HAVE TO LEARN THIS?" 
And in your clinical years, you are always like - I wish I took my first and second year seriously! :P

-IkaN