Showing posts with label Physiology. Show all posts
Showing posts with label Physiology. Show all posts

Monday, October 16, 2017

Na-K ATPase and Donnan effect

Hello Awesomites :D

In Previous post, I gave an overview on Gibbs Donnan equilibrium.
This is to clear the doubt that Could animal cells attain Gibbs Donnan equilibrium?

Animal cells could never attain equilibrium. Plasma membrane can't sustain hydrostatic pressure gradient without evolution of some means of avoiding Gibbs-Donnan equilibrium.
Why do we need some new means? Because we couldn't afford to have "Protein free cell or no protein containing cell".
Na-K ATPase counteract Gibbs Donnan equilibration.
The bottom line effect of this is to make cell effectively impermeable to NaCl. Gibbs Donnan equilibrium do not reached and cell does not swell inspite of the presence of protein ion.
Hope you got it.
-Upasana Y. :)

Donnan Effect

Hello Awesomites :D

I was reviewing my 1st year physiology notes then I found this topic.
Let us begin. :D

We know that ions move across the membrane depending on 2 gradients :-
1. Concentration gradient (No. Of ions)
2. Electrical gradient (Charge of ions)

 The net movement of ion  is decided by the Electrochemical gradient.

I will do some calculations below. Caution point is when I will talk about electrical neutrality, I consider charge of ions.

Donnan Effect  ON DISTRIBUTION OF IONS has three effects:-
1. Because of charged proteins in cells, there are more osmotically active particles in cells than outside.
So what does it means? Animal cells do not have cell wall. Osmosis would make them swell and eventually rupture.

How to prevent this?
This implies need for evolution of pump (Na-K ATPase) to maintain osmotic equilibrium between cells and interstitial fluid across cell membrane.

2. At equilibrium the distribution of the permanent ions across the membrane is assymetric, an ELECTRICAL difference exists across the membrane.

What does it means?
K+ moves along its concentration gradient (as it is free to move)  lead to electrical disequilibrium.

This disequilibrium influence K+ to move continuously. Chloride also move it's side to equilibrate with charge.

Eventually ion concentration would stabilise (in diagram 64=64)  and individual solute concentration would not change over time (means 6 Na+ 4 Cl- 10 K+ 3 prot4- inside)
Gibbs Donnan force are responsible for development of a membrane charge due to passive process.

3.Because there are more proteins in plasma than in interstitial fluid,there is Donnan effect on ion movement across the capillary wall.

What do you mean by Donnan equilibrium?

Have a great day.
-Upasana Y. :)

Thursday, August 10, 2017

Factors increasing iron absorption in the intestine mnemonic

Hello! Long time, no see!

Did you know a number of dietary factors influence iron absorption?

Ascorbate (vitamin C) and citrate increase iron uptake in part by acting as weak chelators to help solubilize it in the duodenum.

Monday, July 3, 2017

REM, NREM and dream content recall mnemonic

My friend had difficulty remembering whether dreams can be recalled from REM sleep or NREM sleep.

I have a mnemonic!

REM REMembers nightmares.

Similarly, NREM does Not REMember night terrors.

That's all!
The North remembers.

Antiarrhythmic drugs: Classification, Mechanism of Action and ECG changes

Hello guys, this is a much important topic especially in Emergency Medicine. And before going through this post, if you may, brush up your concepts of cardiac action potential.

A quick recap: Imagine a non-pacemaker AP with a flat phase 4, phase 0 upstroke, then a phase 1 downward notch, then phase 2 plateau phase, phase 3 downstroke slow at first, rapid later. Now the channels.
Phase 0- Na+ channels in the open state, it is inactivated in all other phases.
Phase 1- Transient-outward K+ channels
Phase 2- L type Ca2+ channels and Slow K+ channels (IKs)
Phase 3- Delayed rectifier K+ channels; Slow K+ channels(IKs) to Rapid K+ channels(IKr) and finally ultrarapid K+ channels(IKur).
Phase 4- Inward rectifier K+ channels(IKi)

First, Classification:

We have the Vaughan-Williams classification, the Sicilian gambit which is the most accepted albeit with some significant limitations which will be discussed later.

Class I: 
These are the Na+ channel blockers and "membrane stabilizers". So, they reduce slope of phase 0 and hence the peak of action potential. And they all prolong effective refractory period(ERP).  Because of subtle differences in its members, they are further classified as three subclasses.
It has moderate efficacy, i.e., it moderately reduces the slope of phase 0. And now look at the letter A, it is pointing upwards. That is coz it increases APD (Action Potential Duration) and ERP(Effective refractory period) both since it blocks IKr channels which are a part of delayed rectifier K+ channels involved in repolarization phase 3, so they prolong both QRS(ventricular depolarization) and QT intervals(Due to increased APD).

Note: This class of drugs have a cumulative effect. They block Na+ channels in the open state during phase 0 and then dissociates from them slowly and incompletely during the diastolic period after QRS complex so that in next beat, some Na+ channels are already blocked from the previous beat. So the QRS prolongation will rise with each beat. And this effect will be exaggerated at higher rates since diastolic period will shorten and more no of Na+ channels will be stuck with drugs.

Hence, in a way, it attacks more strongly if the rate is uncontrollably higher.

Eg. Quinidine, Procainamide, Disopyramide

It has low efficacy, it weakly reduces the slope of phase 0. Unlike the above class, it decreases APD. On the ECG, it slightly shortens QT interval and have little effect on QRS complex although both are considered therapeutically irrelevant.
Now why does it shorten APD? In the quick AP recap above I lied a bit, in phase 2 plateau phase the depolarizing Ca2+ channels are helped by residual(still open) depolarizing Na+ channels which are blocked by these drugs, so the repolarizing K+ channels dominate earlier and shorten phase 2.

IA vs IB:

IA is like a friend who attaches to you quickly and then doesn't like to leave you. Wheareas, IB is like a friend who takes his good time to attach but then leaves you quickly.
So based on this, unlike IA, IB blocks both open and inactivated Na+ channels, but they do it so slowly that they miss most of the open Na+ channels in phase 0 (the reason behind them producing little changes in QRS complex) and their real effect starts after phase 0 when they block the inactivated Na+ channels and prolong ERP. They detach relatively quickly so they show less cumulative blocking effect, but at higher rates when the diastolic repolarization phase is so short that even these fast-detaching fellas fail to detach and remain stuck on producing cumulative blocking effect beat after beat.

Another question, why are IB drugs not effective in tackling down Atrial arrhythmias?

2 reasons:
1.Unlike ventricular myocyte AP, atrial myocyte AP has a very short plateau phase and APD and as stated above phase 2 is where IB drugs exert their major effect.
2. IB drugs have negligible effect on normal cardiac cells, they mainly show their effect on ischaemic cells. And atrial myocytes by virtue of their less thickness, less demand and adequate blood supply rarely become ischaemic.

Eg., Lidocaine, Phenytoin, Mexiletine

It is very strong, it significantly reduces the slope of phase 0. But coz its C, it doesn't Care about APD and ERP, so no effect. On the ECG, it prolongs QRS complex significantly and shows cumulative blocking effect in a very similar way to IA drugs.

Eg., Flecainide, Propafenone, Moricizine

Class II: These are Beta-blockers. They prolong phase 4 of AP, which reduces the automaticity and hence controls rate as well as conduction. On ECG, they prolong PR interval.

Class III: These are K+ channel blockers. They prolong phase 3 of AP, so it delays repolarization and prolongs APD and ERP.
Eg., Amiodarone, Dronedarone, Dofetilide, Sotalol, Ibutilide

Class IV: The Ca2+ channel blockers or more specifically the L-type Ca2+ channel blockers. In SA node and AV node, it prolongs both phase 0 and 4, so controls the rate. In myocardial cells, it prolongs phase 2 of AP, so it impedes conduction.  On ECG, they prolong PR interval.
Eg., Verapamil, Diltiazem

Class V: Variable Mechanism; including Magnesium Sulfate, Adenosine, Digoxin, Atropine.

The major drawback of this classification is that some drugs like Amiodarone have overlapping features of other classes.

Mnemonic by iKan :) -

Remember, VeraPamil has P in the name so PR interval is Prolonged.

(Cain) from Flecainide sounds like Quain, Q is for QRS interval prolongation.

That's all!
My next post will be on what, why and how of indications of anti-arrhythmics. Stay tuned! :)


Thursday, June 22, 2017

Pathophysiology and Radiologic patterns of Atelectasis

Hey guys!

This post will be on the classification of Atelectasis based on its pathophysiology and a brief overview of its radiology patterns. 

Let us deal with the radiology aspects first:

1. Opacification of airless lobe and displacement of fissures,

2. displacement of hilar and cardiomediastinal structures toward the side of collapse,

3. narrowing of the ipsilateral intercostal spaces,

4. elevation of the ipsilateral hemidiaphragm,

5. compensatory hyperinflation and hyperlucency of the remaining aerated lung and

6. obscuration or desilhouetting of the structures adjacent to the collapsed lung (eg, diaphragm and heart borders).

Google the Chest X ray scans for atelectasis to consolidate the above points.

Now the lengthy part, The Pathophysiology. Let us start with active or obstructive atelectasis. 

1. Active/Obstructive Atelectasis.

Obstructive atelectasis is a consequence of blockage of an airway. Air retained in the alveoli distal to the occlusion is absorbed into the pulmonary capillary blood since the pressure of gases in the blood plasma (PvO2) is lower than that in the alveoli. For this reason, it is also called absorptive atelectasis. This causes the affected regions to become totally gasless and then collapse. 
Obstruction of a segmental bronchus is less likely to result in segmental atelectasis than obstruction of a lobar bronchus is to produce lobar atelectasis. This difference is because of collateral ventilation between bronchopulmonary segments within a lobe. 
Collateral ventilation occurs via the age-old physiologic adaptive process of recruitment and distension of neighbouring bronchioles. But three are three other players here, or brothers as I like to call them. A small anecdote to remember these three brothers:
Once there was a priest named Kohn who decided to help out a fellow bronchopulmonary segment in aeration. Brother Kohn being eldest and hence weak could only manage to dig a pore. His work was carried on by Brother Boren who bored (as his name suggests) and made this pore into a fenestration. There was still some work left. And for that Brother Boren asked the help of the engineer Brother Lambert. Brother Lambert, after much hard work was eventually able to dig up a canal all the way upto the neighbouring segment so that they can share the aeration bestowed upon them by Lord Almighty!
So we have three distinct collateral connections: 1. Pores of Kohn, 2. Fenestrations of Boren and 3. Canals of Lambert.
So you need to defeat these three if you want to cause obstructive atelectasis.
Let's dig a bit deeper into Fenestrations of Boren. These collateral channels are extensively prominent in an emphysematous lung. Now take a case of a 60 year old male smoker with emphysema who has now developed small cell carcinoma. Suppose there is a tumor mass obstructing the right bronchus, this patient will take a lot of time to develop obstructive atelectasis in the right lung because of the presence of extensive network of fenestrations of Boren. Hence, this patient will become symptomatic late and thereby will be diagnosed late. Blessing or Curse!
One more thing, it has been observed that atelectasis occurs more rapidly in patients on oxygen therapy. Why? There is a simple reason behind this. Oxygen is more soluble than nitrogen in water, when you give inhalational O2 with a FiO2 take 50%, you are altering the partial pressures of gases in the alveoli, Nitrogen which was 79% will fall down to below 50% and O2 which was 20% will rise upto 50%. Hence overall solubility rises, this elevates the tendency and spontaneity of gases diffusing into the blood plasma.

Honestly speaking, rest of the causes are nowhere as important as the one mentioned above so let us try to ace them quickly. 
2. Nonobstructive Atelectasis

A. Relaxation (ie, passive) atelectasis ensues when contact between the parietal and visceral pleurae is eliminated. While this is usually due to a pleural effusion or pneumothorax, a large emphysematous bulla can have a similar effect. In this case, the residual physiologic elastic recoil of normal lung parenchyma allows the normal lung to collapse away from the chest wall with consequent loss of volume.
The middle and lower lobes may shrink more than the upper lobe in the presence of a pleural effusion, while the upper lobe may be affected more by a pneumothorax.

B. Adhesive atelectasis is a consequence of alveolar instability due, in part, to surfactant deficiency or dysfunction. As its name suggests, the alveoli walls will collapse into the alveolar space sticking with each other. In the normal lung, surfactant reduces the surface tension of alveoli and decreases the tendency of alveoli to collapse. Decreased production or inactivation of surfactant leads to alveolar instability and collapse. Adhesive atelectasis is a major problem in respiratory distress syndrome of premature infants(IRDS), acute respiratory distress syndrome (ARDS) in adults, acute radiation pneumonia, and posttraumatic lung contusion.

C. Cicatrization (ie, cicatricial atelectasis) results from diminution of lung volume due to severe parenchymal scarring. Common underlying etiologies include granulomatous disease (eg, sarcoidosis), necrotizing pneumonia, and radiation pneumonia.
D. Acceleration Atelectasis- This type of atelectasis has been described in pilots subjected to very high, vertical accelerative forces between 5G and 9G: at 5G, up to 50 percent of pulmonary airways are distorted and closed due to gravitational forces. The atelectasis is exacerbated by breathing a high fractional concentration of oxygen. Decreases in vital capacity are a reflection of this type of atelectasis in pilots. Acceleration atelectasis can cause symptoms like chest pain, coughing, and dyspnea.
E. Rounded atelectasis (also called folded lung, Blesovsky’s syndrome, or atelectatic pseudotumor) is a distinct form of atelectasis associated with pleural disease, particularly following asbestos exposure and in India following pleural tuberculosis. Asbestosis is associated with pleural plaques and diffuse pleural thickening while pleural TB will have pleural thickening alongwith pleural effusion which eventually resolves with or without organization and pleural septations(Harbingers of Fibrothorax). 
In this condition, there is a subpleural mass mainly in the middle or lower lobes from which bronchi and blood vessels arise and they form a structure like a comet tail which traverses through the underlying atelectatic lung parenchyma to join at the hilum. Some un-astronomical sources compare this to a Vacuum Cleaner, with the dirt box as the subpleural mass and the hose as the comet tail. 

P.S. Blesovsky's Syndrome is not the only syndrome connected to pneumoconiosis, there is also Caplan's syndrome(Rheumatoid pneumoconiosis); which has a well-known mnemonic CAPlaN;
C- Coal workers' pneumoconiosis
A- Rheumatoid Arthritis
PlaN- Pulmonary nodule

That's all! 

Sunday, June 18, 2017

Micturition and Neurological diseases

Here, presenting you a detailed description of Pathologies of Bladder in Neurology. I believe this is the best resource on this topic available online for free. :)

Saturday, June 17, 2017

Effects of Angiotensin-II on GFR

So this is a highly confusing topic. No matter how many times you read it, some amount of doubt is always there in your mind. So an advice to the readers, bookmark this post because you will be needing to read it more than once to get the drift.

First of all, let us review the effects of Angiotensin II on Glomerulus.

It constricts both the afferent and efferent arterioles but preferentially increases efferent resistance. Why? 3 reasons:

1. Efferent arterioles have a smaller diameter in their basal state.

2. Ang II stimulates the release of vasodilator NO from the afferent arteriole.

3. Ang II minimizes vasoconstriction at the afferent arteriole via the stimulation of Ang II type 2 (AT-2) receptors, which result in vasodilatation through a CYP450 dependent pathway.

The net effect of preferential rise in efferent arteriolar resistance is that the glomerular pressure is increased or stabilized(in hypoperfusion states), which helps to maintain or increase GFR. But in the long run, lots of fluid have been filtered out leaving behind the proteins which raise the colloid osmotic pressure, eventually enough to overrule the hydrostatic pressure and hence it leads to decrease in GFR.

Ang II also reduces GFR by causing constriction of the mesangial cells which reduces the effective surface area for filtration. 


Sunday, June 11, 2017

Study Group Discussion: Salisbury Phenomenon

Whats Salisbury effect?

It's a very interesting phenomenon.

It states that when coronary collaterals develop in the face of myocardial ischemia, they improve the blood supply. However they physically restrict left ventricular dilation and thereby raise LVEDP(LV end diastolic pressure) and reduce LV compliance.
This is because they act like tendrils/scaffold which prevent ventricular dilation.

Nice one!


Saturday, May 20, 2017

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)

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

Saturday, May 13, 2017

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

Monday, May 8, 2017

The basics: Lesions of Spinal Cord

Here is a basics video on Spinal cord with mnemonics for first year med students by Chaitanya Inge. Enjoy :)

Friday, May 5, 2017

Auditory Transduction simplified

Basics of auditory transduction simplified by Chaitanya Inge in his first awesome video! Check it out! :D

Thursday, May 4, 2017

Easy way to memorise Organ of Corti

Hello Everyone!

               Here is a easy way to memorise the Organ of Corti structure.

We've also upload a video explaining the same. Check it out =) 

Thank you,
Chaitanya Inge

Monday, May 1, 2017

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

Sunday, April 30, 2017


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?

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

Monday, April 24, 2017

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

Sunday, April 23, 2017

'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 :

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

Friday, April 14, 2017

Nerve fibres : A clinico-physiological approach.

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


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

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

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

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

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

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

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

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

Thus to summarize the small fibres -

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

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

Coming to the large fibres.

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

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

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

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

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

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

Hope this was helpful !
Happy studying !
Stay awesome.

~ A.P. Burkholderia

Thursday, April 13, 2017

Cerebellum and Motor learning!

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

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

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

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

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

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

I hope this was informative.

Let's learn together!