Sunday, May 28, 2017

Lesions of the Central Nervous System.


Hello everybody!

So today we'll review a series of lesions and their presentation starting from the cortex till the spinal cord.

Will try and include as many lesions as I can without making it redundant or boring.

To start with.

1)Disorders of the Meninges and Ventricular System.

Many conditions can affect the meninges, like infections, neoplasia, sarcoidosis.The most common being infections.

Some meningeal infections may be extremely indolent and lack the classical signs associated with infection.
Chronic meningitis can also present as dementia or AMS.
Abnormalities of the ventricular system can occur due to congenital anomalies, such as aqueductal stenosis leading to dilatation of the ventricular system and may cause increased head circumference in children.
In adults, acquired conditions, such as normal pressure hydrocephalus usually present with evidence of increased intracranial pressure or with dementia, AMS, gait problems,difficulty with bladder control. The classic triad of Normal pressure hydrocephalus is - WET WHACKY WOBBLY.

2)Cerebral Hemisphere Disorders. Characteristic of unilateral hemispheric pathology is a “hemi” deficit.
Hemisensory loss,
Hemiparesis,
Hemianopsia,
Hemiseizures.

Other manifestations are hyperreflexia and pathologic reflexes.

Disease affecting the cerebral cortex behave differently from disease of subcortical structures.

Cortical involvement:
Aphasia,
Apraxia,
Astereognosis,
Impaired two-point discrimination, Memory loss,
Cognitive defects,
Focal seizures, or other abnormalities that reflect integrative role of the cortex.

Dominant hemisphere involvement:
Language dysfunction in the form of aphasia, alexia, or agraphia. 

Non dominant hemisphere involvement:
Higher cortical function disturbances involving functions other than language, such as apraxia.

Subcortical structures :
The clinical picture includes the hemidistribution of dysfunction but lacks those elements that are typically cortical (e.g., language disturbance, apraxia, seizures, dementia).

Certain processes involve wide areas of the cerebrum, causing diffuse dysfunction.

3) Basal Ganglia Disorders:
Diseases of the basal ganglia cause movement disorders such as Parkinson’s disease (PD) or Huntington's Disease. Movement disorders may be hypokinetic or hyperkinetic, referring to whether movement is in general decreased or increased.
PD causes bradykinesia and rigidity. Huntington’s disease, in contrast, causes increased movements, which are involuntary and beyond the patient’s control (chorea).  Tremor is a frequent accompaniment of basal ganglia disease.

4)Brainstem Disease: (So I have a  separate blog on these do check them out,where I have enlisted individual syndromes.)

The classic distinguishing feature of brainstem pathology is that deficits are “crossed,” with cranial nerve dysfunction on one side and a motor or sensory deficit on the opposite side.

There are often symptoms reflecting  dysfunction of other posterior fossa structures, such as vertigo, ataxia, dysphagia, nausea - vomiting, and abnormal eye movements.

Unless the process has impaired the reticular activating system, patients are normal, mentally awake, alert, able to converse (though perhaps dysarthric), not confused, and not aphasic. 

DeepTendon Reflexes are usually hyperactive with accompanying pathologic reflexes in the involved extremities; pain is rare untill Thalamus is involved and sphincter dysfunction occurs only if there is bilateral involvement.

5) Cranial Neuropathy Disease :
Selectively involve one, or more than one, cranial nerve.
The long tract abnormalities, vertigo, ataxia, and similar symptoms and findings that are otherwise characteristic of intrinsic brainstem disease are lacking.

Common cranial neuropathies include Optic neuropathy due to MS,
Third nerve palsy due to aneurysm
Bell’s palsy.
Involvement of more than one nerve occurs in conditions such as Lyme disease, sarcoidosis, and lesions involving the cavernous sinus

6)Cerebellar Disease:
Leads to combinations of tremor, incoordination, difficulty walking, dysarthria, and nystagmus, depending on the parts of the cerebellum involved. 

There is no weakness, sensory loss, pain, hyperreflexia, pathologic reflexes, sphincter dyscontrol, or abnormalities of higher cortical function.

Cerebellar abnormalities resulting​ from dysfunction of the cerebellar connections in the brainstem, usually are accompanied by other brainstem signs.

7)Spinal cord disorders:
Produce characteristic patterns of clinical abnormalities, with motor and sensory deficits in a certain distribution.

In addition to weakness below the level of the lesion, patients with spinal cord lesions also have paresthesias, numbness, tingling, and sensory loss with a discrete sensory level, usually on the trunk.

The pattern of weakness is typically more localizing than sensory abnormalities in lesions of the cervical spinal cord, while demonstration of a sensory level on the trunk is more helpful in localizing lesions of the thoracic cord.

Some important findings depicting the syndromes are :

Dorsal cord syndrome : Loss of position and vibratory sensation in the feet with preserved ankle jerks.

Central cord Syndrome (syringomyelia) :
Bilateral segmental sensory loss (i.e., sensory loss in the hands and forearms), not in a peripheral nerve distribution, with normal sensation in the legs and trunk and in the upper arms and neck.

Thoracic Cord Syndrome : Bilateral loss of position and vibratory sensation in the feet with a definite level of pinprick loss on the abdomen or chest.

Brown-Séquard syndrome : Loss of pinprick sensation on one side of the body with loss of position and vibration sensation on the other.

Intramedullary lesion or anterior extramedullary compression :
Loss of pinprick sensation over the legs and trunk with normal sensation in the perianal area.

Conus medullaris or L5–S1 cauda  equina lesion:
Loss of pinprick sensation in the perianal area and in the upper part of both posterior thighs.

Anterior Cord Syndrome :
Loss of pinprick sensation on the legs and trunk with normal position and vibration sense in the toes and fingers.

Phew😅 that was alot.
I hope this was helpful.
If you have any doubts or you need a detailed explanation of some part, do let me know.

Let's learn Together!
-Medha.

Authors diary: Have fun while studying

If you are not having fun while studying, you are doing it wrong.

I crack really lame jokes. It keeps me sane :P

Saturday, May 27, 2017

Low Weight in Cerebral Palsy : Possibilities

Hi everyone ! Here's a short post on Causes of Weight loss or Poor gain of weight in Cerebral palsy (CP) patients.

1. Feeding problems due to motor deficit -
- Patients with CP have poor feeding due to problems with sucking and swallowing. - They may have  palato-pharyngeal incoordination due to the UMN lesions - especially if there's an accompanying Bulbar or Pseudobulbar palsy.
-So there's impaired oral motor control.
- Repeated aspirations may be present.

2. GERD -
- Gastro esophageal reflux is a common co-morbidity with CP.
- This can be very bothersome for the baby and reduces appetite and may even cause repeated vomiting.

3. Reliance on Care taker -
- The child cannot use his own hands to feed a lot of times.
- This causes excess reliance on the caretaker.
- The caretaker may underfeed the baby weary of the aspirations and Dysphagia of the baby.

4. Poor hygiene -
- Poor hygiene practices are more likely to cause infections (Feco-oral ).
- This is more likely to cause undernutrition due to the infective agents.

Hope this felt clinically relevant and helpful to you !
Stay awesome !

~A.P.Burkholderia

Syndromes associated with Ventricular Septal Defect : Mnemonic

Here's a short post.
So a fair bit of genetic mutations are associated with VSD's.

Remember :
ACED 2
(As in You ACED your exam ! )

A- Apert Syndrome
Features are mainly Cranio-digital. Causes Craniosynostosis, Syndactyly and mandibulo-facial deformities.

C- Cri du chat Syndrome
Notorious for the kitten like cry.
Other features are hyperagrresivenes, skin tags in front of eyes , microcephaly and wide eyes.

E - Edwards Syndrome
Trisomy 18. Other features - Omphalocele , esophageal atresia, low set ears, Microcephaly, Ptosis and Rocker bottom feet , Hypertelorism. Also associated with ASDs.

D - DiGeorge Syndrome
CATCH 22
C - CHD
A - Abnormal facies
T - thymic aplasia
C - Cleft palate
H - Hypocalcemia
22 - Chr 22 abnormality.

D - Down Syndrome
(You all know about that one !)

That's all!
Hope this helped.
Happy Studying and like always , Stay awesome !

~ A.P.Burkholderia

Medicowesome secret project : Lets talk about 'adjustments'

“Hello, I'm sure you would relate to me,
You will understand how I feel,
Because you might have felt it for a few moments like I feel most of the time.”

I was diagnosed with clinical depression a year back. Although the labeling never led to any improvement but it made me understand that I have a medical problem and I need help. Being from a smaller city, where everyone knew each other, where life moved at its own pace and where things were easier to understand, moving to Delhi away from my family proved stressful for me. The constant pressure to fit in, to dress, talk, sit in a particular manner and being ridiculed for being little different only made things worse. There would be days in row when I wouldn't feel like getting up, the day would stretch far too long and I wouldn't understand what exactly was I going through. I would stay awake till 4am crying with feeling of helplessness. From being the topper of my school I became one of the lowest scorers of my class.  Nothing would seem to motivate me to keep going because I had already given up. Fortunately, two failed suicide attempts made me feel like seeking for help. My treatment is ongoing. People close to me understand that it's something which I wasn't in control of. Depression is something which can break you into innumerable pieces, loosen your ability to look at positivity and get up to fight back with zeal. I hope you understand. - maybe this is what someone with depression goes through (I guess). So will you help them stay strong? :)

You, out of all these people have the capacity to love yourself the most, trust yourself the most and build yourself stronger with each passing day. Then why be worried if someone doesn't love you back or breaks your trust? It's you who is important. It's your life, you make your own decisions. Let no one ever tell you your worth or take away your happiness. You deserve all of the good things like everyone else.  You is important. Yes, you are :)

Thanks Purnima Bhatia for sharing this story ( a part of it is hers, rest is fiction ) with us and spread awareness on the matter. :)

Friday, May 26, 2017

Ewing's Sarcoma- A review.

Hello everybody!

Let's review a few important points on Ewing's sarcoma.

Ewing sarcoma is one of the small, round cell lesions of bone
Second most common malignant bone tumor in children (after osteosarcoma)
Common in males than females.
Occurs between the ages of 5-30 years.

 Location:
Arise in medullary cavity, usually of long bones in the lower extremities. Commonly involves metadiaphysis of long bones.
Most commonly occurs in long bones and pelvis but they can occur in virtually any bone.

Clinical Findings:
Most common symptoms are localized pain and swelling.
Additional symptoms:
Fever
Weight loss
Anemia
Leukocytosis
Elevated erythrocyte sedimentation rate 

Imaging Findings:
Most lesions are visible on conventional radiographs
However, their degree of spread is better evaluated with MRI

Common manifestations on conventional radiography include
1)Poorly marginated, lytic, destructive lesion
2)Permeative (small holes) or moth-eaten (mottled) appearance
3)Rarely, they can be sclerotic,Soft tissue mass or infiltration is common
4)Soft tissue mass may occur without destruction of cortex.Soft tissue mass may produce saucerization (scalloped depression in cortex)
5)Periosteal reaction is common
6)Lamellated - onion-skinning due to successive layers of periosteal development
7)Sunburst or spiculated - hair-on-end appearance when new bone is laid down perpendicular to cortex along Sharpey’s fibers.
8)Codman’s triangle - formed between elevated periosteum with central destruction of cortex
9)Osteosclerosis may be present secondary to reactive bone formation

Prognosis:60-75% five-year survival.

Treatment:Systemic chemotherapy is the mainstay of treatment with surgery and/or radiotherapy playing a role depending of the location and size of the tumour.

Hope this was useful.
Let's Learn Together!
-Medha.

Types of barium-contrast imaging.

Hello everybody!

Let's quickly revise the types of Barium investigations.

So to enlist the investigations are: Barium swallow, barium meal, barium follow-through, and barium enema.

The barium swallow, barium meal, and barium follow-through are together also called an upper gastrointestinal series (study), whereas the barium enema is called a lower gastrointestinal series (study).


Procedure:

In upper gastrointestinal series examinations, the barium sulfate is mixed with water and swallowed orally, whereas in the lower gastrointestinal series (barium enema), the barium contrast agent is administered as an enema through a small tube inserted into the rectum.


Let's review individual examinations breifly:

Barium swallow X-ray examinations are used to study the pharynx and esophagus.

Barium meal examinations are used to study the lower esophagus, stomach and duodenum.

Barium follow through examinations are used to study the small intestine.

Enteroclysis also called small bowel enema is a Barium X-ray examination used to display individual loops of the small intestine by intubating the jejunum with a small tube and administering Barium sulfate followed by methylcellulose or air.

Barium enema examinations are used to study the large intestine and rectum.

Hope this was useful!

Let's learn Together!

-Medha.

Thursday, May 25, 2017

Authors' diary: How to study during Ramzaan

This video has been requested since last year! Finally made it! :)

Autism and ADHD : The clinical intersection

Hello

Autism and Attention - Deficit Hyperactivity Disorder (ADHD) may co - occur in upto 80% of children and they share about 50 - 75% of their genetic factors and pathologic features, thus resulting in some clinical intersection.

Wednesday, May 24, 2017

NBME 7 question on muscle weakness

Disclaimer: This is an NBME form 7 question for step 2 CK. If you are planning to take USMLE step 2 CK in the future, I would recommend that you DO NOT read this post because it will bias your assessments.

CMS neurology form 2 question on fibromuscular dysplasia with paresis, occulomotor palsy

Disclaimer: This is an CMS neurology form 2 question for step 2 CK. If you are planning to take USMLE step 2 CK in the future, I would recommend that you DO NOT read this post because it will bias your assessments.

CMS neurology form 2 question on headache, seizures, urinary incontinence, broad based gait

Disclaimer: This is an CMS neurology form 2 question for step 2 CK. If you are planning to take USMLE step 2 CK in the future, I would recommend that you DO NOT read this post because it will bias your assessments.

NBME 7 question on intoxication

Disclaimer: This is an NBME form 7 question for step 2 CK. If you are planning to take USMLE step 2 CK in the future, I would recommend that you DO NOT read this post because it will bias your assessments.

Tuesday, May 23, 2017

Fact of the day : Pinenes for refreshing your Airways

Hello

Did you know? One of the reasons your lungs feel refreshed ( increased mental focus and energy ) when you walk through the shades of beautiful pine forest is because of an anti - inflammatory compound called alpha -Pinene, that is found in conifers. It is used as a bronchodilator in the treatment of asthma and is abundantly present in marijuana.

- Jaskunwar Singh

Pill induced esophagitis mnemonic

Pill induced esophagitis is caused by a pill! :D

Causes of pill induced esophagitis mnemonic: A PILL.

Aspirin
Alendronate
Antibiotics like tetracycline, clindamycin

Potassium chloride
Iron
Less water
Lying down immediately

Interesting anatomy correlation:
The most common sites of injury are the proximal esophagus near the compression from the aortic arch and the distal esophagus in patients with left atrial enlargement.

The typical endoscopic appearance of pill-induced esophageal injury is a discrete ulcer with relatively normal surrounding mucosa.

That's all!
-IkaN

Motor nuclei in the brainstem : An overview

Hi everyone. Just thought of doing an overview of the various motor nuclei of cranial nerves in the brain stem.

So we can classify the motor nuclei into 3 groups -
1. Somatic motor efferent - 4
2. Branchial motor efferent - 4
3. Visceral motor efferent - 4
Now how are these classified ?

1. Somatic Motor Efferent

- In the embryological stage , there are certain precursors to muscle and skin segment groups called 'Somites'. These are processes of the paraxial mesoderm.
- Sach somite gives rise to a particular set of muscles called its myotome. 
- There 4 such important somite groups -->

A. Pre otic somites = 3.
So this is simple.
There are 3 pre otic somites giving rise to distinct groups of extraocular muscles supplied by their own cranial nerve.

Somite 1  =
Muscles -
All Extra ocular muscles except Lateral Rectus and Superior oblique.
Nerve -
Oculomotor nerve (III)
Nucleus -
Oculomotor nucleus in the Upper Midbrain.

Somite 2  =
Muscles -
Superior oblique.
Nerve -
Trochlear nerve (IV)
Nucleus -
Trochlear motor nucleus in the Lower Midbrain.

Somite 3  =
Muscles -
Lateral Rectus.
Nerve -
Abducent nerve (VI)
Nucleus -
Abducent motor nucleus in the Pons.

(I'm sure you remember the popular mnemonic - LR6 SO4)

B. Occipital somites
Muscles -
All muscles of the tongue except Palatoglossus
Nerve -
Hypoglossal I'm nerve (XII)
Nucleus -
Hypoglossal nucleus in the Medulla.

Since these nuclei represent the motor innervation to the derivatives of Somites , they're called Somatic Motor or General Somatic Efferent (GSE) Fibres. 


2. Branchial Motor Efferent - 

- In the embryological stage , there are various branchial or Pharyngeal arches that give rise to muscles , bones and cartilage supplied by a particular nerve of that arch.

- Each nucleus that supplies the muscles from such a Branchial arch is called Branchiomotor Efferent or Special Visceral Efferent. (SVE) 
- There are 4 such important arches - 

A. 1st Pharyngeal arch (mandibular arch)
Muscles -
All muscles of mastication + TT (Tensor tympani + Tensor veli Palatini) + Digastric anterior belly. ( And Meckel cartilage)
Nerve -
Mandibular branch of Trigeminal
Nucleus - 
Trigeminal motor nucleus in Pons 


B. 2nd Pharyngeal arch (hyoid arch) 
Muscles -
All muscles of facial expressions + Stapedius + Digastric posterior belly.  ( And Reichter cartilage)
Nerve -
Facial nerve (VII)
Nucleus - 
Facial motor nucleus in Pons 


C. 3rd Pharyngeal arch
Muscles -
Stylopharyngeus
(And the hyoid bone funnily.)
Nerve -
Glossopharyngeal nerve (IX)
Nucleus - 
Nucleus Ambiguus in Medulla


D. 4th and 6th Pharyngeal arches
Muscles -
- All muscles of  Soft palate ( except Tensor veli which is up in the 1st arch) by the 4th. + cricothyroid muscle of Larynx. 
- All muscles of Larynx by the 6th except cricothyroid which is by the 4th. 
(All laryngeal cartilage as well)
Nerve -
4th arch - Superior laryngeal nerve of the Vagus.(X)
6th arch - Recurrent laryngeal nerve of the Vagus (X)
Nucleus - 
Nucleus Ambiguus of Medulla 

Now there's another Motor nucleus - The Accessory nerve. It supplies Trapezius and Sternomastoid muscles but it's doubtful if it's Branchial or Somatic. 


3. Visceral Motor Efferent - General

- These nuclei are parasympathetic and stimulate a particular gland to secrete or a ganglion to function. 
- These are called Secretomotor or General Visceral Efferent Fibres 

Again , there are 4 of these. 

A. Ciliary ganglion 
Function mediated by - 
Sphincter pupillae - Constricts pupil 
(Mnemonic = Remember C and C - Cholinergic Constricts )
Nerve -
Oculomotor nerve
Nucleus - 
Edinger Westphal in Midbrain 


B. Pterygopalatine ganglion 
Function mediated by - 
Lacrimal glands, nasal mucosal, sinuses mucosal glands and pharynx mucosal - Secretomotor. 
Nerve -
Facial nerve  (Greater Petrosal)
Nucleus - 
Superior salivatory nucleus - Pons. 

C. Submandibular ganglion 
Function mediated by - 
Submandibular glands , sublingual glands - Secretomotor.
Nerve -
Facial nerve  (Chorda tympani)
Nucleus - 
Superior salivatory nucleus - Pons. 

D. Otic ganglion 
Function mediated by - 
Parotid gland
Nerve -
Glosspharyngeal nerve  (Lesser Petrosal)
Nucleus - 
Inferior salivatory nucleus - Pons. 

The Vagus nerve has the largest parasympathetic discharge and supplies a lot of visceral with this input in the guy as well.

Hope this helps you to re-orient yourself to neuroanatomy and grasp the roles of various brainstem structures ! 
Happy studying ! 
~ A.P.Burkholderia

Monday, May 22, 2017

Lacunar strokes : An Overview


      Hi everyone ! Here's a short post on Lacunar infarcts. Credits to IkaN without whom IKant have done this post. Haha ;;) here goes.

- A Lacunar infarct is an infarction occurring    in the deep penetrating branches supplying the deep subcortical structures - Mainly the Internal capsule and parts of thalamus. 

- These are some of the most common infarctions seen. 

- Causes of lacunar infarction include Hypertensive bleeds and Microthrombi. 

- So these infarcts can present as one of the following​ Syndromes --> 

1. Pure Motor 
2. Pure Sensory 
3. Combined Sensorimotor 
4. Ataxic 
5. Dysarthria- Clumsy hand syndrome. 

- The illustrations I've drawn below clearly depict the syndromes , their anatomical localization and the arteries commonly involved. 

- The commonest of the lot is the Pure Motor type of stroke that affects mainly the Internal capsule containing the motor corticospinal fibres. Since a multitude of Fibres is concentrated very judciously in the Internal capsule , the hemiplegia resulting from this type is a 'Dense' or total hemiplegia affecting both upper and lower limbs in equal measure. 
(click on the image to see them in better resolution ) 




- The management is much like the other strokes - 
1. Airway Breathing Circulation to be established. 
2. Check Blood sugar and BP.
3. Send for an emergency Non contrast CT scan to rule out hemorrhage. 
4. If within 3-4.5 hours and absence of hemorrhage = Thrombolyse. 
5. If hemorrhage - BP control and ICT management.
6. If beyond 4.5 hours = Symptomatic and Palliative care and treat risk factors.


- I hope all of these Syndromes are clear to you now !
 Let me know if you'll have any doubts. 
Happy Studying ! 
Stay awesome.
~ A.P.Burkholderia

Fact of the day: Marchiafava-Bignami disease

Marchiafava-Bignami disease is a rare disorder of demyelination or necrosis of the corpus callosum and adjacent subcortical white matter that occurs predominantly in malnourished alcoholics. Dementia, spasticity, dysarthria, and inability to walk may present as an acute, subacute or chronic condition.

Lesions appear as hypodense areas in portions of the corpus callosum on CT and as discrete or confluent areas of decreased T1 signal and increased T2 signal on MRI. Alcohol abusers without liver disease, amnesia, or cognitive dysfunction show thinning of the corpus callosum at autopsy and on MRI, suggesting that alcohol or malnutrition damages the corpus callosum commonly in the absence of the necrotic lesions of Marchiafava-Bignami disease.

Interesting, isn't it?
-IkaN

High ankle and low ankle sprain mnemonic

Hello!

High ankle and low ankle sprain

Sunday, May 21, 2017

Atrial fibrillation begets Atrial fibrillation: Explanation

Hi ! Short post on pathophysiology of Atrial Fibrillation!

- Atrial Fibrillation is a fairly common disorder of rhythm, where the atria begin to beat at random , irregular and very high rates. Like 300-600 beats / min !
- Some of these MANY contractions get transmitted to the ventricles causing an Irregular , yet High , Ventricular rate - around 100-160 per minute or even higher.

Now how this occurs is a very interesting yet much-ignored mechanism.

- Due to some pre existing factors like Rheumatic heart disease , Myocardial ischemia or Thyroid abnormalities among many others, the atria get electrically irritated and begin to fire on their own.

- These ectopic foci are common along the opening of the pulmonary veins = called the pulmonary sleeve.
This area of hyperactivity and automaticity begins to fire from the left Atrium creating a wavefront of abnormal impulses.

- Say one of these myocytes becomes ectopic one day and produces an abnormal wavefront. This wavefront progresses across the atrium and in turn stimulates the other Atrial myocytes to inturn fire ectopically -- causing formation of multiple Daughter ectopic foci.

- These daughter ectopic foci produce daughter wavelets that then propagate through the atria , in turn producing more duaghter wavefronts.

- Eventually there are A LOT of Atrial foci causing multiple wavelets to produce multiple electrical wavefronts.

- Thus A-Fib causes multiple wavefronts which in turn cause more wavefronts eventually propogating A fib as a positive feedback mechanism​.

- In the long term, due to this constant irregular beating there is fibrosis and electrophysiological remodelling making the atrium more irritable and automatic.

Thus A-Fib begets A-Fib!

Hope you liked this !
Happy Studying !
Stay awesome.
~A.P.Burkholderia

Mitral Regurgitation Begets Mitral Regurgitation : Explanation


Hi everyone just a short explanation of the famous phrase 'MR begets MR'.
Here goes.

- Mitral Regurgitation is a disease where the mitral valve is incompetent or insufficient and leaks or pukes when it should be shut. (Rather like a blithering idiot who keeps talking at the wrong time. =}. )

- So it allows the blood to puke back into the Left Atrium from the Ventricle during systole.

- So assume - 100 ml of blood would flow into LV from the LA normally which the LV would pump into the Aorta.

- Now because fo the weird and incompetent valve , the LV can pump only like 70 ml into the Aorta and the rest of the 30 ml goes back into the LA.

- So now the LA volume is 30 ml + 100 ml
And it'll pour in 130 ml into the LV.

- So effectively, the LV has an overload of volume in it and over a period of time it would undergo Dilatational changes and increase in size.

- As the Ventricle increases in size , the mitral valve apparatus is stretched all the more.

-This is because the mitral valve is attached to the Ventricular myocardial tissue directly at the annulus as well as via the papillary muscles. Both of these are stretched. 

- The stretching causes further increase in MR. This causes further volume overload. Which causes further MR.

- Thus it is like a positive feedback response and a vicious cycle is formed.

This phenomenon is referred to as ' MR begets MR' which means MR basically causes Ventricular changes which stretch the heart and cause more MR which continues the cycle further.

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

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