Treatment of Narcolepsy

Hey Awesomites!
This is the last post of the four-post series on Narcolepsy. So let's begin.

Diagnosis of Narcolepsy

Hello friends!!

This is the third one in the four-post series on Narcolepsy. Let's commence.

Diagnosing a not so common disorder, that too neurological is quite tricky. The greatest difficulty is separating it from the normal daytime and postprandial sleepiness of most people. Admit it, most of us feel like sleeping in the afternoon period after lunch, especially while reclining in the sofa, while watching television or in the theatres watching matinee shows. :p  

What distinguishes the typical narcoleptic attack from commonplace postprandial drowsiness and napping is the frequent occurrence of the former(2 to 6 times everyday), their irresistibility, and their occurrence in unusual situations, as while eating, standing, or carrying on a conversation.

Excessive daytime sleepiness can also be present with heart failure, hypothyroidism, use of antihistaminics, alcohol intake, head trauma, certain brain tumours like craniopharyngioma etc.

 

Overnight polysomnography followed by a standardized multiple sleep latency test can exclude other causes of excessive daytime sleepiness like obstructive sleep apnea. In the test, the patient is given 5 opportunities to nap at 2 hour intervals in a day

. 

If there are more than 2 Sleep-onset REM periods and a mean sleep latency of less than 8 minutes, it strongly suggests narcolepsy. 

Actually, in Narcolepsy, there is characteristic reversal in the order of the two states of sleep, with REM (rather than NREM) phase occurring  at the onset of sleep attacks. And the sleep latency is nothing but the interval between the point when an individual tries to sleep and the point of onset of sleep with the respective EEG patterns.

Measurement of hypocretin(orexin) levels in the CSF may help establish the diagnosis; a level lower than 110pg/ml is diagnostic of narcolepsy.

Cataplexy must also be distinguished from syncope, drop attacks and atonic seizures. In atonic seizures, there is temporary loss of consciousness, while in narcolepsy consciousness is perfectly preserved. 

That's all! Do go through the other posts in this series.

Role of Orexins in Narcolepsy
Clinical features of Narcolepsy
Treatment of Narcolepsy

-VM

Clinical Features of Narcolepsy

Hello friends!!

This is the second one in the four-post series on Narcolepsy. So let's begin.

Narcolepsy is not just a disorder in which the patient sleeps a lot, believe it or not the number of hours in a day spent in sleep by the narcoleptic is no greater than that of a normal individual!!

Narcolepsy is characterized by the classic tetrad of excessive daytime sleepiness, cataplexy, hypnagogic hallucinations and sleep paralysis. There is also a disorder of REM sleep. So let us try to understand these major clinical features.

The essential disorder is one of frequent attacks of irresistible sleepiness several times a day, usually after meals or while sitting in class or in other boring and sedentary situations. Now let us try to picturize the patient.

The eyes close, the muscles relax, breathing deepens slightly and it seems that the individual is dozing. A noise, a touch or even the cessation of lecturer’s voice is enough to awaken the patient. So the periods of sleep rarely last longer than 15min unless the patient is reclining, or if he is in an appropriately comfortable situation to sleep. At the conclusion of the nap, the patient feels somewhat refreshed.

Cataplexy refers to a sudden loss of muscle tone brought on by strong emotion- that is, circumstances in which hearty laughter or, more rarely, excitement, surprise, anger, intense athletic activity. So you can basically “tickle” a Narcoleptic into a Cataplectic state. 

The patient’s head will fall forward, jaw will drop, knees will buckle with sinking to the ground – all with perfect preservation of consciousness (scary, right?). Most attacks of cataplexy are partial, eg., only dropping of the jaw or weakening of the knees.

In about half the patients, there is hypnagogic hallucination and sleep paralysis. Please do not confuse sleep paralysis with cataplexy; sleep paralysis is brief loss of control(not tone) of voluntary muscles that occurs during the period of falling asleep or less often when awakening.

There are two terms which we should know, hypnagogic and hypnopompic. Hypnagogic or predormital refers to the period of falling asleep while hypnopompic or postdormital refers to the period of awakening. Sometimes there may be vivid and terrifying hallucinations with or before the onset of sleep paralysis, which may be visual, auditory, vestibular or somatic, called hypnagogic hallucinations.

That's all. Do go through the other posts in this series.

Role of Orexins in Narcolepsy
Diagnosis of Narcolepsy
Treatment of Narcolepsy

-VM 

Role of Hypocretins/Orexins in Narcolepsy

Hello friends!!

This is the first of the four-post series on Narcolepsy.

So let's start. The hypocretins were thought in the past to regulate feeding behaviour and energy metabolism, the word “orexin” is derived from the Greek word for appetite. But later through animal experimentation it was found that in mice, inactivation of two hypocretin receptors reproduces Narcolepsy.

First of all, let us learn that monoaminergic neuronal projections from Tuberomammilary nucleus(histaminergic), Locus Ceruleus(noradrenergic) and the Raphe nucleus(serotonergic) inhibit the Ventrolateral Preoptic Nucleus(VLPO) of hypothalamus.

To put it simply, the transition between sleep and waking is determined by the state of activity of the VLPO. Now imagine a see-saw, on one side we have all these nuclei wanting the person to wake up and on the other side we have VLPO forcing the person to sleep. Whoever gets heavier, metaphorically speaking, chooses the person’s state. 

So what’s the role of orexin/hypocretin ? We can say that it enables a smooth transition between wakefulness to sleep by reinforcing the monoaminergic firing from those three nuclei; hence it indirectly inhibits the VLPO. Hence if we remove orexin from the picture, the person will fall asleep immediately without being able to control; and roughly this is what occurs in Narcolepsy. 

That's all. Do go through the subsequent posts in this series.

Clinical features of Narcolepsy
Diagnosis of Narcolepsy
Treatment of Narcolepsy

-VM

Basics of Immunoglobulin G

Hey  readers!! ,So I have started with immunoglobulin section where I will be putting facts about a single immunoglobulin ,so today it is IgG!.

Immunoglobulin G or IgG occupies about 80% of serum antibodies.! .It's normal concentration is about 8-16mg/ml.They are created and release by plasma B cells .
There are two unique facts about IgG
1)It's catabolism.
2)Suppression of homologus antibody synthesis by a feedback process.

What's unique in catabolism?.
Well we can say body has complete control over the catabolism and to make it simpler let's say body and IgG both acts opposite to each other !.(Just a saying :p,Infact we know IgG works for body).For example In some diseases like chronic malaria ,kala azar or myeloma IgG level rises and as we know body has complete control and it acts against it So, IgG synthesis its gonna catabolised it rapidly !
Conversely,In hypogammaglobulinemia IgG given for treatment is metabolised slowly.

Suppression of homologus antibody synthesis
IgG has another unique property of suppressing the antibody synthesis which looks like it or performs similar kind of functions or simply homologus antibody.
Now let's say IgG is quite insecure about its true but dominating love -"Body". It doesn't want any competition so it kicks away all the antibodies which looks like it or perform similar function like him
(Such a insecure antibody it is  !)and this unique property is utilised in the Iso-immunisation of a women by administration of anti-Rh(D) IgG during delivery.

Well some more characteristics of our hero IgG is
It's the only maternal immunoglobulin that is transported across placenta and provides "Natural passive immunity"in new born (Not present in infants )

It has 4 subclasses due to presence of gamma 1,gamma 2 , gamma 3 and gamma 4 chains .

IgG1=65%
IgG2=23% (By the way 23 is also half life of IgG)
IgG3=8%
IgG4=4%

Here are functions of IgG molecule

Immunohemolytic anemias part-2

Hello readers, here is the continuation of the previous topic, Immunohemolytic anemias. Today we will discuss the next two types, its more like winter special.

B) Cold agglutinin type-  Cold agglutinin derives their name from the fact that they show maximal activity at temperature lower than normal body temperature.
It is present in low titres in healthy individuals.
Physiological cold agglutinin develops naturally after birth as a result of change in expression of Red cell antigens and reacts maximally at 4°C.
While pathological cold agglutinin maximally reacts at around 28-31° C and tend to occur at very low titres.

Mnemonic is "Cold MILL"
C     -  Complement mediated hemolysis. 
         
M    -  IgM is the causative antibodies

  I     -  Cold agglutinin antibodies appear  
           transiently following Infections 
            [Mycoplasma pneumoniae, EBV,
            HIV, influenza virus, CMV]
          - I antigen is the most common
              target
           
L     - Chronic cold agglutinin AIHA is
          associated with Lymphoid 
           neoplasm
          (esp B cell neoplasm), leukemias     
           like CLL

Mechanism- IgM binds to red cell where the temperature may fall below 30°C. It agglutinates red cells, and fixes complement rapidly. As blood recirculates and warms, IgM is released,but sufficient deposition of complements leads to phagocytosis of affected red cells in spleen, liver, bone marrow.

Clinical presentation- Exerts their pathological effects either via hemolysis and red cell destruction in RE system predominantly liver or by vaso occlusion due to agglutination.
-Mild anemia, purplish discoloration of fingers, toes, earlobes [ Acrocyanosis],  mild hepatospleenomegaly,
Raynaud phenomenon in peripheral cold exposed parts.

C) Cold hemolysin type -
Also known as paroxysmal cold hemoglobinuria.
It's a rare fatal disorder causing intravascular hemolysis and hemoglobinuria when auto antibodies binds to P blood group antigens in cool, peripheral regions of body.

Paroxysmal Cold HemoGlobinuria:
P- P blood group antigens
C- Complement mediated lysis occurs.

    IgGs auto antibodies binds to red cell in  
    cool peripheral regions, Complement
    mediated lysis occurs when affected
    red cell recirculates to warm regions,
    because complement cascade 
    functions
    more efficiently at 37°C

H- Hemoglobinuria
G - Auto antibodies belong to class IgG

Symptoms of the patients aggravates on exposure to cold.

Winter is coming, we know what's coming with it.
Stay warm :)

Immunohemolytic anemias part-1

Hello awesomites!
This is my very first post, so am starting with my favorite subject Hematology.
Today's post is about Immunohemolytic anemias, commonly ignored type of anemia

Also referred as Autoimmune hemolytic anemias(AIHA)
Where antibodies are responsible for premature destruction of red blood cell.
Types- warm antibody type
            - cold agglutinin type
            - cold hemolysin type

Warm antibody type  -  It is the most common type of AIHA.
you can remember it by mnemonic
" WARM GRILLED "
W - Warm because, antibodies are active  
       at 37°C
A -  Associated with other Autoimmune        
       disorders ( secondary causes like 
       SLE)
R - Red cell hemolysis is mainly
      extravascular
M- Moderate spleenomegaly due to
       hyperplasia of splenic phagocytes      

G- Ig G class - most common causative
      antibodies ( IgA sometimes too)

R- Rh blood group antigens are the main
      target 
I- 50% primary cases are  Idiopathic
       Secondary causes can be

L- Lymphoid neoplasm

ED-  Exposure to Drugs.
Examples - penicillin, cephalosporins, quinidine, methyl dopa etc

Mechanism - A) Antigenic drugs-
Drugs such as penicillin binds to red cell membrane and they are recognized by the antidrug antibody. The antibody either recognizes the drug and bind to it or both drug and membrane protein,ultimately results in hemolysis.

B) Tolerance breaking drugs- In drugs such as methyl dopa, antibodies are formed against red cell antigens particularly Rh antigens.

Stay awesome✌️

Nasal spray that prevents suicide.

0Hello readers! Being in medical field we are quite acquainted with the word "Stress out" .Todays article is just about a simple nasal spray that can prove to be a boon to entire human kind.(I think specially our field ! :p)

Everything in a brain is carried out by special substances called as "Hormones" .Even the simplest change in mood is concerned with hormonal changes.For example in first trimester of pregnency a rapid rise in estrogen and progesterone can cause mood swings in woman.Similary when there is depletion of hormones or its metabolites or less production of hormone this can leads to depression ,low -emotional state ,anxiety etc.Suicide can be triggered by serious illness ,can also be triggered by low self-esteem or emotional pain .
Scientists are developing a nasal spray that can prevent suicides! .This nasal spray consists of Thyrotropin releasing hormone(TRH) also known as thyroliberin . Thyrotropin is actually hormone released by hypothalamus ,it actually stimulate release of thyrotropin and prolactin from anterior pituitary.Recent findings have found out that TRH  also shows  anti-depressant and anti-suicidal effects.Thus preventing suicidal behaviour and depression.Researchers want to figure out ,a way to deliver it to a brain when it is given through nose  .Brain is protected by Blood brain barrier (BBB),which is acting has a hinderence to pass TSH to brain.
Clinically it is related  in spinocerebellar degeneration and disturbance of  consciousness in humans.Pharmacological form is known as protirelin.

I hope scientists find it soon how to cross  BBB  :p
Exams are near and I am already freaking out :p
Keep smiling :)
Have a day with high level of TSH in brain :)

~Ojas

Can virus kill cancer cells ?

Hello awesomites !Today's topic is short ,simple and easy to understand.

Cancer is basically a disease where there is abnormal growth of cells in body and sometimes it is also malignant that is ,it can spread from one organ/site to another.These newly formed cells can disturb normal cycle of other cells .When a  cell suffers DNA damage from cancer,a virus or radiation a group of protein complex MRN is sent to repair DNA.MRN is protein complex ,it consists of Mre11,
Rad50 and Nbs1 .In eukaryotes initial processing of double strand DNA breaks prior to repair by homologus recombination or by non-homologus joining.
When a DNA virus is present in the cell,MRN instead focuses on removing it.
If both DNA damage & a DNA virus are present in a single cell .The MRN complex is unable to manage both threats at once and ends up ignoring the virus .
These new findings imply that scientist might be able to form a virus that targets and  kills only cancer cells.

Keep smiling:)
Good day:)

Artificial skin

Hello awesomites !!! Today's topic is something that really has created revolution in the entire human race - "Artificial skin"

Skin is the largest organ of our body. It consists of three parts Epidermis, dermis and fatty layer. Epidermis serves as the protective layer of the skin, it prevents the entry of the pathogen into body with the help of sebaceous and sweat glands along with long chain fatty acids, and dermis consists of all the nerves, artery and veins that supply skin. Fatty layer maintain the body temperature.
A damage to the skin through burns causes loss of large number of plasma and it provides free entry to pathogens into body. Artificial skin was discovered by Loannis yannas & his colleague surgeon Dr John burke.

Artificial skin was discovered to replace bandages, which cannot seal large damage areas. Patients with extensive burns often die as bandages cannot heal their wounds completely. Even if patient survives some scars are left behind on skin. Artificial skin consists of collagen polymers. Collagen is protein found in skin. Artificial skin helps patient to grow skin without forming any scars. It has been commercially prepared under name as IntegraTM.

It is also used in plastic surgery and also in chronic skin wounds.
 
Ahh!    That's it :)
            Keep smiling :)
            Have a nice day!
      
~Ojas

Replacement to open heart surgery

Hello awesomites today I am gonna tell you something that is really -really interesting and fascinating !.
We all know how crucial is open heart surgery in some conditions, here is one of the alternative methods of open heart surgery.(For some conditions)

Alternative method :-

For the 1st time a new catheter technology was used in place of open heart surgery.
Cardioband is a low impact method to fix leaky mitral or tricuspid valve in heart. The catheter technology offers a minimal invasive alternative to heal a leaky valve. It enables the tightening of a leaky annulus in the heart. During this procedure, the band is placed around the open valves using catheter. It is served with anchors & tightened using a wire until the valve is fully closed. Until now , only treatment of leaky tricuspid was open heart surgery.

Now patient  previously thought to be inoperable will have chance to be treated.
University Zurich hospital successfully performed first tricuspid surgery using cardioband .

Have a happy day
Keep smiling:)

~Ojas

Monteggia vs Galeazzi fracture mnemonic

Hey Awesomites

While studying the Monteggia and Galeazzi fracture and dislocation today, I googled and came up with a mnemonic. GRUesome MURder helps us remember which bone is fractured and which one is dislocated.

GRUesome-
G: Galeazzi
R: Radial fracture (lower- third)
U: Ulnar dislocation

MURder-
M: Monteggia
U: Ulnar fracture (upper- third)
R: Radial dislocation

Also in Monteggia fracture, bone of medial side is involved.


Thats all
- Jaskunwar Singh

Top 10 series: Empagliflozin

Here is the video!

Migraine- Research updates

Hey Awesomites

Now that we are clear on the basics, here's another post on recent updates and studies on the concepts of causation and treatment strategies of migraine.

The basics: Migraine

Hey Awesomites!

Lets understand the basics of migraine here-

Top 10 series: Colchicine

The video is up!

Pain killer in Human saliva.

Hello readers ,Here is something new information about human saliva !.

Human saliva and pain killer :-
Human saliva contains a painkiller that is naturally produced by human body .It is called as -"Opiorphin" in very low concentration.

Opiorphin's role:-
Opiorphin prevents the breakdown of chemicals called as enkephalins . Apart from this opiorphin inhibits 3 protease.-
a)Ecto-endo peptidase.
b)Ecto-amino peptidase .
c)Dipeptidyl peptidase.
This extends the duration of enkephalins.
The enkephalins activates opiate receptors .Activated opiate receptors blocks pain signals from reaching brain!!. opiorphin is 6 times more potent than morphine .Unlike morphine opiorphin is not addictive and prolonged use may not lead to tolerance .

Current status in research:
Painkiller was successfully tested on rats.Further research is still needed before it's use on humans .Research include modifying molecular structure to avoid rapid degeneration in intestine and it's poor BBB(Blood brain barrier !).Modification includes transformation of N-terminal glutamine into pyroglutamate .

~Ojas

New drug:Tideglusib

Hello awesomites ! Today's blog is about new drug -Tideglusib.

Tideglusib is actually Alzheimer's drug and is also used in paralysis of supranuclear palsy!
However this drug is currently in news because of its ability to stimulate repair of teeth .

Use of this drug can cause end of dental fillings .
Mechanism of action of drug
The mechanism is roughly known .It acts in 2 ways
1)It stimulates stem cells in the pulp of the teeth to generate new dentine and heal small cavities.(Dentine is hard dense bony tissue that forms your teeth)
2)Inhibits an enzyme called as GSK-3 which prevents formation of dentine !,

Progress in research:
Drug is successful tested on mice .They soaked biodegradable sponges in the drug and then placed them in cavity .The sponges melts away over time,leaving only the repaired tooth but for use in humans ,the drug is still under research.

Keep smiling :)
Happy day:)

~Ojas

Interesting and rare disease:Ectopic cordis

Hello awesomites ,really tired of all the bookish knowledge so for time being I switched my self to internet,and came across some of the rarest and the most interesting diseases of all the time !
Here is the first one -Ectopic cordis.

What is -Ectopic cordis?
It is the disease where the heart is located at abnormal position that is places other than thorax or sometimes partially at thorax.It is a congenital disorder

Cause :-
It is caused due to improper maturation of the mesoderm and ventral body wall durig embryonic development.Lateral wall is responsible for fusion at midline to form ventral wall any change in this process may lead to -Ectopic cordis.

Types:-
Depending upon situation of the heart in patient ,ectopic cordis is classified into 4 parts :-
1)Thoracic.
2)Cervical.
3)Thoracoabdominal.
4)Abdominal.

Defects seen:-
1) Ventricular septal defect .
2)Atrial septal defect.
3)Absence of tricuspid valve.(Tri-cuspid atresia)
4)Fallots tetralogy. (http://www.medicowesome.com/2017/01/teratology-of-fallot.html)

Treatment:
Unfortunately the only treatment is surgery !
Not all the surgeries are successful .
Patients of ectopic cordis hardly can live for long years as there are more chances of infections to heart .

That's it for today.
Internet is interesting:)
~Ojas

MBBS practical viva tips on examination

Smile, stay confident.
Keep calm.
And rock those vivas!

This video is on how to not make silly mistakes during pracs!

The SAAG solution (Serum-Ascites Albumin Gradient simplified)

Yo people!

A good friend of mine asked me to review the concept of SAAG. So let's dive into a "Puddle" of ascitic fluid. :P

As you guys all know, SAAG stands for Serum-Ascites Albumin Gradient and it helps to differentiate the causes of ascites. What it means is pretty self explanatory, it is the difference (gradient) between the levels of albumin (a plasma protein) in two compartments i.e. Serum and Peritoneal fluid.

Tetralogy of fallot

Hello  readers today's blog is small one -Fallot's tetralogy .

What is Fallot's tetralogy?
   It is a congenital disorder of heart .It is caused to foetus may be because of  alcoholic mother or who has  diabetes or may be due to rubella infection caused during pregnancy.It is caused due to deletion of chromosome 22

Signs and symptoms:-
As the name suggest ,there are four signs
All four of them are related to heart .
Mnemonic is PVR -f cinema.
-Pulmonary stenosis
-Ventricular septal defect .
-Right ventricular hypertrophy
-Over-riding of aorta ,due to which blood from both the ventricles may enter aorta.

Due to defect in heart ,there is low oxygen supply to tissue this may lead to cyanosis when there is high amount of pulmonary stenosis but when there is moderate amount of pulmonary stenosis this may lead to pink tit that is pinkish colouration of skin.There is also clubbing  .

Treatment:
Open heart surgery is only treatment for fallots tetralogy  .
The appropriate time for surgery depends on the pulmonary stenosis .
However patient should be on life long medication for healthy life

That's all :)
Have a happy day.

~Ojas

Top 10 series: Amphotericin B

Here is the video! :)

Microbiology of legionella mnemonic

Legionella: Facultative intracellular, gram negative rod

Pili: They are all involved in adherence and intracellular replication of L. pneumophila

Flagella: Within the host cell vacuole, legionella are nonmotile, whereas in the later stages of infection and cell lysis, legionella are flagellated and highly motile. Motility enables Legionella to escape from a spent host and facilitates its attempt to find a new host by dispersion into the environment.

Extra Ocular Muscles Insertion : Mnemonic

Hello everyone ! I hope you'll have been enjoying the Top 10 Series that we've started. This is a short post on the insertion of Extra ocular muscles in the eye.

So there are 4 Extra Ocular muscles whose insertion on the sclera we need to be aware of ( in terms of distance from the Limbus). The Recti.

Remember :
I'M Low Standard

I = Inferior Rectus. 5.5
M = Medial Rectus 6.6 (or 6.5 but just remember 6.6 for easiness)
L = Lateral Rectus  6.9 (Loser)
S = Superior Rectus 7.7

So basically it starts with 5.5 , 6.6, 6.9 and finally 7.7.
3 of these are the same number repeated (5.5 , 6.6 and 7.7) but LR is a loser. Hence it does not follow the rule and is a badass hence does a 69. :p

Hope this helped !
Thank you.
Happy studying!

~A.P.Burkholderia

Temporomandibular joint: Super old notes

Hey, these are my super ugly notes from 2010.

Temporomandibular joint: Notes for MBBS exam

In today's blog, we will be showing you how to write answers of joint in your theory exams.

Example question: TMJ

I would like you guys to know that since there is a lot of time limitation in theory exams, you should:

1. Draw diagrams ("Anatomy paper without diagram is as good as flower without fragrance!")

2. Name everything  you know

3. Elaborate

Before the exam, choose the diagrams you would draw for sure and optional diagrams ("If I get time...")

ADRs of Sulphonamides mnemonic

Hey Awesomites!

Adverse drug reactions of Sulphonamides mnemonic-
SULPHONAMIDES

S- Stevens- Johnson syndrome
U- Urinary crystals formation and bleeding
L- Lyell's syndrome (TEN)
P- Photosensitivity
H- Hepatic/ Hematologic
O- Ocular side effects
N- Neonatal jaundice/ Nausea and vomiting
A- Antimetabolites (inhibit folic acid synthesis)
M- Miscarriage (pregnancy and fetal abnormalities)
I- Intolerance
D- Dermatitis
E- Eosinophilia
S- Serum sickness


Thats all
- Jaskunwar Singh

Neurodevelopmental maturity and adulthood

Hey Awesomites!

When do you really attain adulthood?
18. That's when you are legally declared an adult. Right? Oh so you already got the answer. Hey no wait.. we are medical professionals and students of science. So talking in a legal way doesn't always seem right, because from a scientific perspective, adulthood is still an unsolved mystery. Let me tell you about it here..

Increased Intracranial pressure clinical features mnemonic

Increased intracranial pressure clinical features mnemonic- 5Ps

P- Persistent projectile vomiting (due to stimulation of CTZ)

P- Persistent headache (the patient presents it as the "worst" headache of his life)

P- Palsy (sixth nerve palsy and diplopia)

P- Papilledema (bilateral)

P- Personality disturbances (behavioral changes)

Thats all

- Jaskunwar Singh

The basics :Parkinson's disease

Hey,Hello! awesomites ,this blog is just a small review of some old and new things I learned about Parkinson's disease.
The very first thing I learned is:- parkinson's disease and parkinsonism are two different terms !!!.
-Parkinsonism is a complex term it includes many symptoms while parkinson's disease is a progressive neurodegenerative disorder .
-Parkinosons disease is actually cause of parkinsonism .
       Let's start with Parkinson's disease
-Main cause is decrease dopamine secretion in body mainly due to injury to substantia nigra which sends dopamine secreting nerve fibers to caudate nucleus and putamen.
Signs and symptoms:
- Characteristics features is tremors .Tremors occurs during all walking hours and therefore it is a type of involuntary tremor in case of cerebellar disease there is an intension tremor because tremors are seen when patient perform any work.
-Also  festinant gait is found
-Akinesia is also seen
-Lead-pipe rigidity is seen earlier in hands and legs followed by neck and trunk.

Causes:
-Any  serious injury that affects dopamine secretion !
-Also some medication which decreases dopamine secretion or blocks dopamine receptors.
-Apart from that certain drugs also induces Parkinson's disease  like drugs used to treat schizophrenia and other neuroleptic drugs like
Clozapine.
Risperdal.
Quetiapine.
Apart  neuroleptic drugs,others drugs  like prochlorperazine,metoclopramide.
Also calcuim channel blockers causes Parkinson's

Drug induced Parkinson's remains same ,it doesn't progress

Categories of drugs used for treatment of parkinsonism:-
-Dopamine agonist.
-Anticholinergic.
-COMI inhibitors.

~Ojas

Step 2 CK: Pancreatic pseudocyst notes

Pancreatic pseudocyst

How does it develop?

The basics : Constipation

Today I am gonna give some brief review about how to treat constipation .So let's start with basics

Why constipation occurs ?
-Water serves as a transporter of stools ,decrease in concentration of water in intestine can lead to constipation ,it may be either due to increase absorption from the extracellular space or decrease water content in body.
-Decrease bowel moment

How to treat constipation?
-As now we know cause of the constipation ,we can treat constipation either by :-increasing water content or decrease loss of water from intestinal lumen
And also by increasing bowel moments so less water or salts are absorbed (Yet some drugs uses another mechanism.)

Drugs used :-
1)We can use Dietary fibers which will just form a bulk in intestine and will increase water content of faeces ,also due to bacterial degradation some osmotic active substances are produces which further increases water content Hey but there is one drawback ,it may causes gas :D.
2)Stool softeners:
-They permit water and lipid to penetrate stool .
-They are either given orally or rectally!
(Yes a drug acting on intestine can also given rectally)
-Again there is one drawback ,prolong use can cause impair  absorption of fat soluble vitamins ( A,D,E,K)

3)Osmotic laxatives (Laxative is term used for drugs for treatment of constipation)
-Colon can neither concentrate /dilute fecal fluid  so fecal fluid is isotonic throughout the colon
-Generally we use non-absorable sugars /salts eg:-Magnesium citrate & sodium phosphate.
-Osmotic laxatives are commonly used but should not be used in patient with renal insufficiency.
-But patient using sodium phosphate must take adequate water to compensate fluid loss due to it
,It may causes hyperphosphatemia,hyper natremia , hypocalcemia,hypokalemia.
-So should not be used in cardiac patients

4)Stimulant laxatives
    a) Anthraquinones:It after hydrolysis produces bowel moment in 6-12hrs if given orally or within 2 hrs if given rectally.!
   -It may causes melanosis coli.
   b)Diphenylmethane derivatives : It increases  bowel moments in 6-10hrs when given orally and in 30-60mins when given rectally.
-It has minimum systemic absorption

5) Opioid receptor antagonism
-Now this is  an interesting type of drug mechanism rather than increasing motility it "decreases" motility .

Confused ?!!

Still it is used in prevention of constipation ?!

Yes ,by decreasing motility it prolonges the transient time required for absorption of water and salts from surrounding
Eg:-Methylnaltrexone & alvimopan.

~Ojas

Viva questions on bulb of Foley's catheter

Since it's exam season! :D

Top 10 series: Spironolactone

The video is up!

Top 10 series: Gabapentin

Here is the video!

The basics: Peptic ulcer

Peptic ulcer is excoriated area of stomach  or intestinal mucosa caused by  excessive gastric acid secretion or upper intestinal tract secretion .A type of peptic ulcer called as marginal peptic ulcer is caused during surgical process whenever there is opening made in between stomach and jejunum of small intestine like gastrojejunostomy.

Common site of peptic ulcer ?
Mostly on lesser curvature of antral end  of stomach and rarely on lower end of stomach.

Causes of peptic ulcer ?
1)Increase in acid secretion and peptic content in stomach .
2) Irritation to mucosa.
3)Poor blood supply .
4)Poor secretion of mucus.
5)Infection by H.pylori.

Treatment of peptic ulcer.
We give anti-ulcer therapy for peptic ulcer treatment
Following are goals of anti-ulcer therapy
a) Relief of pain.
b)Ulcer healing.
c)Prevention of complications.(like bleeding ,perforation)
d)Prevention of relapse.

Approach of  treatment of peptic ulcer :
(I have made some lame tricks for memorising drugs name:D ,if you have some mnemonics please comment !)
1) Decrease acid secretion :It includes total 4 categories ,they are described below .

a) H2 Anti-histamine (They all end with -tidine)
-Cimetidine .     
-Famotidine.
-Ranitidine.
-Roxatidine.

b)Proton -pump inhibitor.(ends with -prazole)
-Omeprazole.
-Esomeprazole.(Read it as Es-omeprazole)
-Lansoprazole.
-Pantoprazole.
-Rabeprazole.
-Dexrabeprazole
(Read it as Dex-rabeprazole!)

c)Anti-cholinergic drugs:
-Pirenzepine .
-Propantheline.
(Read it as Propan-the-line).
-Oxyphenonium .

d) Prostaglandin analogue:Misoprostol !

2)Neutralization of gastric acid secretion
    (Antacids) .It includes 2 categories
a) Systemic:
-Sodium bicarbonate .
-Sodium citrate.

b)Non-systemic:
-Magnesium hydroxide .
-Magnesium trisilicate.
-Aluminium hydroxide.
-Calcuim carbonates.

c)Ulcer protective:
-Sucralfate.
-CBS (Colloidal bismuth subcitrate!).

d)Anti-H pylori drugs:
-Amoxicillin.
-Tetracyclin.
-Clarithromycin.
-Tinidazole.
-Metronidazole.

~Ojas
 

Mental distractions

Hey Awesomites!

Let me ask you a question.. how much focused you are during your study time? Well, as a medical student you try your best to focus on what is written in the book and in making your own notes. You are not aware of your surroundings anymore. Someone comes nearby and calls you or sits just beside you but still your eyes are on those words and difficult medical terms of the diseases and syndromes and the drugs used to treat them. This is called Change blindness, a perceptual phenomenon that occurs when you don't notice a major change in the environment because you are too focused on one particular thing.

Let me give you another example. A young guy is standing in a long queue at a place while some people arrive from the opposite side. He starts staring on a cute little child who was looking at him too. They share smiles, and eye contact for several minutes while the mother carrying the child moves on. The guy just stands still there and is not aware of the surroundings when other people behind shout at him because he is not moving forward or letting them go. All of a sudden he realizes where he is and so walks ahead. This transient moment is the change blindness. :D
Note: Even maintaining an eye- contact with someone, even a child in this case may prove strenuous for the brain especially during reasoning and verbal processing and so is itself a distraction (distracting the young guy from the queue and instead focusing on that child). That is why we periodically avert our eyes during conversations.

During this particular moment this guy activated his visual association area (visual cortex) while looking at that child which meant he was just paying attention to the perceptual details (the depth of eyes of that child, cuteness, innocence, love).

On the other hand, the older adults may notice changes and patterns happening around while doing a particular task as well. Reduced focus (mental distractions) in the aging brain is responsible for the abstract thinking in them that is needed for problem solving and creative work.

In other words, the healthy aging people show thinking patterns that allow them to make connections among pieces of information that are right in front of them as well as information they have have encountered in the past. For example, an older adult involved in a conversation might pick up information on current road conditions from a television nearby, whereas a younger adult might be paying a closer attention to the conversation itself. Later on, the older adult might make use of the information from the TV broadcast while planning a route home. 

The study suggests that older adults tend to have more focused attention in the morning and more of the abstract thinking later in the day. College students on the other hand tend to have their peak attention in the afternoon or evening and are less focused in mornings.

Inability to remember details of major events or just the location of objects begins in early midlife (the 40s) which does not mean the brain function is deteriorating, instead it may be the result of the changing focus of brain on the particular information during the process of memory formation and its retrieval. The experiments on this study have concluded that the middle- aged and older adults don't really show the same level of visual cortex activation as the young do when they recall the information. Instead, their medial prefrontal cortex is activated, a part of the brain that is involved in learning associations between events and the corresponding adaptive responses. The mPFC likely relies on the hippocampus to support rapid learning and memory consolidation.


Thats all
- Jaskunwar Singh

Classification of closed globe injuries

Closed globe injury classification:-

- Based on the mechanism of injury (type) :
A. Contusion (blunt trauma)
B. Lamellar laceration (due to a sharp object or blunt trauma)
C. Superficial foreign body (organic matter or metals)
D. Mixed (combined injuries)

- Based on the visual acuity (grade) :
A. >20/40 (0.5)
B. 20/50 - 20/100 (0.4 - 0.2)
C. 19/100 - 5/200 (0.2 - 0.025)
D. 4/200 - Light Perception (0.02 - L+ P+ )
E. No Light perception

- Based on the pupillary defect :
A. Relative afferent pupillary defect (RAPD) positive
B. Relative afferent pupillary defect (RAPD) negative

- Based on the Zones of violations :
Zone I- External (superficial injuries of bulbar conjunctiva, cornea and sclera)
Zone II- violation of the Anterior segment (structures in anterior chamber and the pars plicata)
Zone III- violation of the Posterior segment (structures posterior to the posterior lens capsule- retina, vitreous and optic nerve)


Thats all
- Jaskunwar Singh

Blood Indices

Hello readers,today I am gonna tell you about some blood indices -there meaning, normal values, and units ! . Hopefully they will be useful . I always use to mess up them during my very first year :(

1)Mean corpuscular volume (MCV):It denotes the  volume in a single RBC .It correspond to size of RBCs ,so when MCV is in normal range it denotes normocyte .When MCV increases , RBCs are known as macrocytic  eg : megaloblastic anemia  and when it decreases ,cell are microcytic eg: iron deficiency anemia.
MCV can be calculated by automated hematology analyzer or by using hematocrit value
MCV:-Hematocrit (%) ×10/RBC count
                                        (million /cubic mm).

Unit of MCV is femtolitre(fL)
Normal value is 80-95 fL

2)Mean corpuscular hemoglobin(MCH):-
It's the quantity or amount of hemoglobin present in one RBC. It's normally expressed in picogram or microgram .
Normal range is 27-31 pg
Formula -
MCH :-Hb (gm per 100mL)/Total RBCs in blood(million per cubic mm) .                                  I think no need to tell MCH decreases in anemia :D

3)Mean corpuscular hemoglobin concentration: It is concentration of hemoglobin in one RBC.It is actually the amount of hemoglobin expressed in relation to volume of RBC.(It's actually
Combination of above two terms )
So we express it in gram /dL
Normal value is 33-36 gm/dL
Formula :
MCHC:
Hb(g/100mL)×100/Hematocrit(%).

When RBC size decrease , RBC is known as hypochromic
In pernicious anemia RBCs are macrocytic and normochromic While in iron deficiency RBCs are microcytic and hypochromic.

We don't have hyperchromic RBC because content of RBC is limited !

~Ojas

   

Mnemonic for personality disorders

Hello!

Soo here's a nice memory aid I came across...
A: Mad
B: Bad
C: Sad

If you write two A's (AA) It does look like an M!
B for cluster B, B for Bad!
C and Sea sounds similar for Sad xD

Mnemonic for personality disorders

"SPAS BAN His ACD"

Rickettsia mnemonic

We transferred this post here because we lost the diagram: https://www.medicowesome.com/2020/03/rickettsia-mnemonic.html

Here are a few things you should know about rickettsia!

Rickettsia, are small, gram-negative, nonmotile, rod-shaped bacterium.

Nervous regulation of blood pressure

Hello awesomites ! Some days back I revised my concepts on regulation of blood pressure  so would like to share with you ,so lets start it .This is short -term regulation of blood pressure.

Changes in blood pressure is normally detected by 9th cranial nerve from carotid sinus and by 10th cranial nerve from aortic arch both of them carries signal to NTS (nucleus of tractus solitarius) present in medulla oblongata which in turn co-ordinate 3 centres  present in medulla oblongata.
- Cardio inhibitory centre .
- Cardio stimulatory centre.
- Vasomotor centre.

Now suppose there is increase in blood pressure ,let's see microscopically what changes we are gonna seen in nerve endings of 9th and 10th nerve.
An increase in blood pressure will stretch carotid sinus and aortic arch ,which in turn will cause stretching or spreading of nerve endings ,which will increase influx of the sodium ions . Ultimately increase in depolarisation wave will cause stimulation of NTS (Even decrease in depolarisation wave  will stimulate NTS ,which happens during decrease in blood pressure).Now as we know there is increase in blood pressure , NTS-our main character in this process  will control these 3 centres to control blood pressure. Let's see what it do to these  three  centres  present in medulla oblongata.
1)Cardio-inhibitory centre : This centre will be   stimulated  which in turn send fibers to SA node and AV node via right and left vagus nerve respectively.Leading to decrease in heart rate ,obviously cardiac output will decrease so will be blood pressure!.
2)Cardio-stimulatory centre: This centre will be inhibited which causes decrease in heart rate and cardiac output via it's fibers (post-ganglionic) which passes to lateral horn of spinal cord and then post-ganglionic fibers goes to sympathetic ganglion from where post-ganglionic sympathetic fibers  acts on heart causing decrease in heart rate and cardiac output.
3)Vasomotor centre:This centre do's more work compared to above two mentioned centres .It acts on three areas ,
Arteries
Veins
Adrenal medulla
Let's see how it reacts when there is increase in blood pressure.
a) On arteries :It causes vasodilation leading to decrease in Total peripheral resistance which is directly proportional to diastolic pressure hence causes decrease in diastolic blood pressure.
b )On veins :It causes vasodilation leading to decrease in venous return which is directly proportional to EDV and which in turn causes decrease in Cardiac output and hence decrease in systolic blood pressure.
c )On adrenal medulla: Decreases release of epinephrine and nor-epinephrine which is responsible for decrease in HR,so decrease in blood pressure.

Woahh! Was such a long blog!
I think it's not necessary to mention occlusion of carotid artery causes false phenomenon of decrease in blood pressure so opposite effects will be seen:)

~Ojas.

Levels Of Prevention & Mode Of Intervention

Hi everyone,
this is notes on community medicine topic. levels of prevention and mode of intervention.
Hope it helps.
That's all
Shubham Patidar jmc 013

Metoclopramide

Hello awesomites ! Today I am gonna talk about a drug named as "Metoclopramide".
Basically it's a anti-emetic drug.First let us know what is emesis !.In simple words emesis means vomiting.Chemoreceptor trigger zone (CTZ) is  located in area postrema and the nucleus tractus solitarius (NTS) of medulla oblongata.They both act as a important relay areas for afferent impulses arising in g.i.t.,throat and other viscera.
Metoclopramide is a Pro kinetic drug
It acts on GIT causing increase in peristaltic movement with relaxation of  pylorus .

Mechanism of action includes :

a)D2 antagonism:It Decreases dopamine concentration  and obviously acetylcholine concentration increases  !.Which causes activation of ACh receptors leading to increase in LES tone and gastric pressure .

b)5-HT4 agonism:Activates 5-HT4 receptors on primary afferent neurons (PAN) of the ENS,via excitatory interneurons.

Gastric hurrying and LES tonic effects are mainly due to this action which is synergised by bethanechol and attenuated by atropine .

c)5-HT3 antagonism: At high concentrations  it can block 5-HT3 receptors present on inhibitory myenteric interneurons and in NTS/CTZ .Increase in ACh concentration is also seen in minor condition

Long term use can cause parkinsonism-since decrease in dopamine , galactorrhea and gynecomastia .

It hastens use of many drugs like aspirin and diazepam by its action

~Jaskunwar Singh & Ojas 

Triad of Charcot

Hello

Charcot's triad in acute cholangitis: FOR
- Fever
- Obstructive jaundice
- Right upper quadrant pain

Chracot's triad in multiple sclerosis: SIN
- Scanning speech
- Intention tremors
- Nystagmus


Thats all
- Jaskunwar Singh

Multiple sclerosis mnemonic

Hey awesomites!

Presenting to you the first post of 2017 :)

Multiple sclerosis clinical features mnemonic:

DONALD TRUMP

D- Demyelinating disease

O- Optic neuritis

N- Neuromyelitis optica

A- Autoimmune aetiology

L- Leg pain

D- Depression

T- Triad of Charcot

R- Relapsing and remitting type (most common)

U- Uhthoff's phenomenon

M- McDonald's criteria (diagnostic)

P- P100 latency of nerves (delayed)

Thats all

- Jaskunwar Singh

2016: the flashback

Hey all!

In this post, I just want to share a flashback to the year 2016 and what I have learnt through the journey of these 365 days.

2016, you will be missed

Remember I promised 2016 was going to be awesome?

It was, it was. It was a beautiful year, personally.

Here's my year in review:

Create the change

Hello everyone

So it's the last day of 2016. And everyone is now talking about new year resolutions and stuff. But what do we want to resolve as medical students?

Remember the first day you joined the medical college? That day you promised yourself something. To be a good doctor one day and serve humanity. To study and work hard all day and night seven days a week and gain knowledge in every subject you study. You had taken your life- changing resolution on that first day itself.

I believe in change. I have always tried to explore myself and learn new things each day of my life. That's what we all should do. And not just in the initial days or weeks of the new year. Because you are known by your actions and not what you think.

So stop making resolutions and start taking your real life decisions. Change is the law of nature. Create the change in yourself each passing day for the better. That will make you feel good. And because your ultimate goal in life is not just to be a doctor but also be a good human being. Then one day you will be what you ever wanted to be.


That's all
- Jaskunwar Singh