Why do we feel sleepy when we are sick?

Hellooo Everybody,
Let's delve into some sleep physiology and learn about some sleep producing substances breifly!

The chemical agents which might be responsible​ for induction of sleep have been obtained from experiments on sleep-deprived animals.
The first experiments of this type were performed by Henri Pieron in 1913 on dogs. He demonstrated that dogs receiving CSF from sleep-deprived donor dogs slept for hours, while the recipients of CSF from normal donors remained awake. Recent work has confirmed these observations and identified several candidate sleep producing substances (SPS)

Sleep-deprivation presumably leads to a rise in the production of these substances in the brain tissue, cerebrospinal fluid,and even urine, through a negative feedback effect.

The best known SPS :
1) Muramyl dipeptide (MDP)
2) Delta sleep-inducing peptide (DSIP)
3) Arginine vasotocin (AVT)
4) Interleukin-1 (IL-1).

Besides these, there are about 20 more putative sleep-inducing factors.

Most of the known sleep producing substances induce Slow Wave Sleep.

After learning the physiology let's answer our question:
Muramyl dipeptide (MDP) is a component of bacterial cell( which acts via IL-1.) walls ,whereas IL-1 is released in infections.
IL-1 potentiates GABA-induced increase in permeability to chloride at synapses causing inhibitory effect on the Brain.

Nitric oxide may be part of a second messenger system which mediates the effect of IL-1 on sleep.

Lastly, IL-1 induces release of growth hormone releasing hormone (GHRH) which in turn releases growth hormone. Growth hormone itself enhances REM sleep and inhibits Slow wave sleep.

This explains why we feel sleepy when sick!

IL-1 also induces fever, and is therefore also called endogenous pyrogen.  Antipyretics, such as aspirin, suppress the fever induced by IL-1 but do not affect the sleep-inducing effect of IL-1.
Like fever, sleep is a smart response  which perhaps helps recovery by compelling the patient to take rest.

Isn't it truly remarkable, how our bodies work!

Let's Learn Together!
-Medha.

Brain Function Imaging.

Hello everybody!
Today we shall breifly learn as to how we can study the brain function using imaging techniques.

Positron Emission Tomography (PET)made debut in 1980s; two more imaging techniques came in the 1990s: functional magnetic resonance imaging (fMRI) and magnetoencepalography (MEG).

1) Positron Emission Tomography:

This technique makes it possible to see in an image which part of the brain is active during a particular task.
As we also know that although brain as a whole does not consume significantally more energy when it is active than when it is idle, metabolic activity does increase in circumscribed regions of the brain when these regions are functionally active.
This increased metabolic activity in the brain is the basis of PET.

In this technique a positron-emitting isotope is tagged to a molecule of biological interest such as glucose or a neurotransmitter.

For example, the positron-emitting isotope of fluorine (18F) is tagged to deoxyglucose and it is injected intravenously.
Deoxyglucose is taken up by neurons in the same way as glucose, but it can neither be fully metabolised nor can it come out of the neurons.
Since functionally active neurons take up more glucose, active regions of the brain accumulate more deoxyglucose.
So , following visual stimulation, 18F-deoxyglucose accumulation can be seen in the visual cortex. This signifies increased glucose metabolism in the visual cortex. Thus we have evidence for involvement of specific regions of the brain in specific functions

Positron emission is detected by appropriate detectors which construct a series of computerised images of the brain similar to those seen in computerised tomography (CT).

2) Functional MRI :
It is based on the principle that increased neuronal activity leads to a local increase in blood flow through the active part of the brain.

The increase in blood flow is somewhat greater than is warranted by the increase in oxygen consumption.
Therefore, blood flowing through the active, hyperemic region of the brain has more oxygenated haemoglobin than the blood flowing through less active regions of the brain.
The magnetic properties of oxygenated and deoxygenated haemoglobin are different, the magnetic resonance signals from the active region of the brain increase.

Functional MRI systems currently in common use give a spatial resolution of about 1 mm, but a resolution of 0.5 mm has been achieved in experimental settings. This is an important breakthrough because cortical columns also have a width of about 0.5 mm.

3)Magnetoencephalography (MEG):

It can complement the information obtained from the conventional electroencephalography (EEG). MEG is based on the principle that neuronal activity in the cerebral cortex generates not only fluctuations in electrical potential (detected by EEG) but also magnetic fields. Unlike EEG signals, MEG signals are not distorted by the intervening tissues. These technical advances have given hope for rapid progress in localization of functions in the human brain.

So I hope ,this helps you guys to have a better picture on Brain Imaging.

Let's Learn Together!
-Medha.

Absolute contraindications for trial of labor

Here are a few conditions in which trial of labor is absolutely contraindicated:

1. Classical cesarean section. (Vertical incision)

2. Abdominal myomectomy with uterine cavity entry.

Previous cephalopelvic disproportion is not an absolute contraindication for trial of labor (Because if the fetus is small in this pregnancy, a trial of labor can be done.)

Previous low transverse cesarean section (Horizontal incision) is not a contradiction for trial of labor.

These are the ones I found out about. Lemme know if there are more, we'll add them to the list!
That's all!
-IkaN

Toxic Ventral Horn Cell disease

Hey guys!

The only ventral horn cell disease famous in India is Polio which was successfully eradicated. During it's era, other diseases with similar clinical picture, such as Kugelberg-Welander syndrome, Cerebral palsy, Friedreich's Ataxia, Spina Bifida etc were rampantly misdiagnosed​ as Polio.
Hence after it's eradication the incidence of these rare disorders has increased!

The disease is also known as "Infantile paralysis" and this moniker can't be more inaccurate. The commonest manifestation of this disease is Aseptic meningitis presenting with headache, photophobia, etc. And only 1% cases develop into paralytic poliomyelitis. And another point is that adults are 15 times more likely to become paralysed and are more likely to die.

Sorry for going off topic above; couldn't help it. Fortunately there are no drugs that are known to cause ventral horn cell disease. But there is one chemical called- TriocP, full form is tri-ortho-cresyl phosphate. It is illicitly used as a component of country liquor especially in USA; and in Mediterranean countries it was used as an adulterant in cooking oil.

Another toxic cause is Tick paralysis. The ixodes tick secretes a toxin that can cause Ataxia, flaccid asending paralysis, bulbar palsy etc closely mimicking Guillian barre's syndrome.

That's all!

-VM

Lasegue's Test

Hey guys here's another clinical sign!

Lasegue’s sign is another name for the modified straight leg maneuver used in the diagnosis of lumbosacral radiculopathy.

To perform the straight leg test, the clinician lifts the extended leg of a patient in a supine position. A positive response occurs when the pain pattern of the lumbar radiculopathy is reproduced. The test should be stopped when the pain is reproduced or maximum flexion is achieved.

But this sign is difficult to evaluate clinically especially for students. The reason being as simple as that it has been performed many a times before and patient already knows that he is going to suffer pain. So it was modified a bit by Lasague, he proposed that the leg should be raised while the knee is flexed by flexing the thigh at the hip joint. And then the knee is slowly extended until the patient complains of pain. In severe cases patient will complain of pain even during the flexion of hip.

More useful than the straight leg maneuver is the crossed straight leg test. This test has a lower sensitivity but a higher specificity​. The crossed straight leg maneuver is performed by raising the unaffected leg in a similar manner to the straight leg test. The examiner looks for the reproduction of radicular pain with elevation of the opposite leg.

A supplement to this straight leg raising test is Braggard's test. First we have to start raising the leg of the patient while his knee is extended until he complains of pain and then dorsiflex his foot, if the pain worsens, it's a positive Braggard's test.

But as given in most books, these signs are not only positive in case of lower lumbar vertebral disc lesions but also in a no of other conditions. The differential diagnosis of a positive straight leg test includes:
1. disc protrusion with impingement of nerve roots below L4;
2. meningismus;
3. any intraspinal lesion such as tumor below L4;
4. malignant disease or
5. osteomyelitis of the ilium or upper femur;
6. ankylosing spondylitis;
7. fractured sacrum and more.

That's all!

-VM

Tinel's Test

Heyy guys!!

Tinel's sign is the sign that a nerve is irritated. Tinel's sign is positive when lightly banging or percussing over the nerve elicits a sensation of tingling, or 'pins and needles,' in the distribution of the nerve.

For example, in carpal tunnel syndrome, where the median nerve is compressed at the wrist, the test for Tinel's sign is often positive, eliciting tingling in the thumb, index, and middle fingers.

Procedure: First you have to hyperextend the wrist to get the median nerve in the carpal tunnel more juxtaposed to the flexor retinaculum. Then tap the skin over the flexor retinaculum midway between pisciform bone and hook of hamate and then observe the patient's response.

This test can also be useful in the diagnosis of Tarsal tunnel syndrome where the tibial nerve is entrapped.

Another test in Carpal tunnel syndrome is Phallen's test.

-VM

Pathophysiology of atrophic vaginitis

Hello!
Here's a short post on the pathophysiology of atrophic vaginitis!

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Alien Hand Syndrome!

Hello everybody!

So today I will be writing a post on the movie Dr.Strangelove, suggested to me by a dear friend!
In the movie..the character called as 
Peter Sellers constantly has to restrain his alien hand from giving the Nazi party salute.

The condition the character was suffering is called as Alien Hand Syndrome.

Let's understand what exactly is alien hand syndrome.

In this Syndrome there is complex, goal directed but involuntary activity in one hand; the hand moves as if it had a mind of its own.
It is usually due to interruption of the cortical connections that control smooth bimanual operations.
The hands no longer work as a team.The affected hand begins to function autonomously and loses the ability to cooperate with its fellow. 
If the patient tries to eat with the good hand, the alien hand may grasp the good hand and force it away from the mouth.

There are two forms of it:

Callosal form:
In this form there is a lesion in the anterior corpus callosum.
Intermanual conflict is typical and it nearly always affects the left hand.

Frontal form:
In the frontal form, there is a lesion of the medial frontal lobe.  The alien hand is uncooperative but not contentious. It may display reflex grasping and other autonomous behavior, but there is little or no intermanual conflict.

Patients may complain of the hand’s behavior, and may criticize it ,
on the other hand (No pun intended here) patients regard the hand’s behavior as amusing.

A sensory alien hand syndrome has also been described following right posterior cerebral distribution stroke. There are typically parietal sensory deficits and hemineglect involving the left side of the body, which resemble anosognosia. 
The right arm may then involuntarily attack the left side of the body. 

I hope this was informative!
I love watching Movies which integrate medical conditions, do let me know your suggestions too!

Let's Learn Together!
-Medha!

Drugs causing Hyperkalemia mnemonic

Hello

Lets remember drugs which cause rise in serum potassium levels:

Fisher's Rules.

Hello Everybody!

So today I will be telling you guys about the “Fisher’s rules” that I came across while striving to develop good clinical skills while doing my internship!

So these rules are basically clinical maxims collected from observing C. Miller Fisher, a clinician of legendary diagnostic acumen. Some of these axioms are particularly helpful to bear in mind and are relevant for Clinical Reasoning and useful as diagnostic Principles.

So here we go, while seeing the patient for the first time we better keep the following 6 rules in our mind.

1) In arriving at a clinical diagnosis, think of the five most common findings (historical, physical findings, or laboratory) found in a given disorder.

If at least three of these five are not present in a given patient, the diagnosis is likely to be wrong.

2) Resist the temptation to prematurely place a case or disorder into a diagnostic cubbyhole that fits poorly.

Allowing it to remain unknown stimulates continuing activity and thought.

3) The details of a case are important; their analysis distinguishes the expert from the journeyman.

4) Pay particular attention to the specifics of the patient with a known diagnosis; it will be helpful later when similar phenomena occur in an unknown case.

5) Fully accept what you have heard or read only when you have verified it yourself.

6) Maintain a lively interest in patients as people.

I found these extremely useful while seeing patients in real and so thought of sharing these.

Medicine in practice is more than just Studying the Standard textbooks, It's an Art that we should all strive to Master,so we can help our patients better.

Its a long journey ahead... Let's Learn Together!

-Medha!

Can watching Pokémon cause seizures?

Hello everybody,

So this is an interesting post about Stimulus Sensitive seizures also known as Reflex Seizures.

The major stimuli precipitating these seizures are Sensory in nature but as there is no known "Reflex" to cause such seizures they are better termed as Stimulus Sensitive Seizures!

So in order to study these seizures Japanese children were exposed to   Pokémon  cartoon that induced seizures, surprisingly​ out of all the children who had an episode of seizure only 24% had a  history of spontaneous seizures. These children had the Photosensitive type of Stimulus Sensitive seizures.

Photosensitive or pattern-induced  seizures as experimented in the Japanese kids are, well-recognized and stimulated by bright or flashing lights  (TV,  video  games,  discotheques,  concert  light  shows)  or  by patterns  (lines on the road  while traveling).  These may occur 1 in 4,000 people in age group of 5-25yr but are outgrown in their 30s.

For patients with isolated  photosensitive  or pattern-induced seizures, avoidance  or  modification of stimuli is the initial  approach in the form of wearing blue or  polarized  sunglasses, avoiding  highcontrast flashing-light video games, 
avoiding discotheques, watching TV in a  well-lit room at a distance of  >8  feet,  and covering 1 eye when in a provocative  situation.

Well generally it is observed that many patients with epilepsy can identify precipitating or provoking events that  predispose them to having a seizure. 

Common events include :
stress
lack of sleep
fever
fatigue.

In another group, patients have seizures in response to a very specific, identifiable sensory stimulus or activity.
These stimuli may be :
External :(light, patterns,  music,  brushing  teeth)
Internal :(math, reading, thinking, self-induced). 

The manifestation of these seizures can be either:
Generalized
Partial
Nonconvulsive
Absence
Myoclonic. 

One common pattern is photomyoclonic seizures characterized by forehead  muscle twitching or repetitive eye opening or closing.

So till the next time you play Pokèmon Go or you see Pikachu in action do remember about Stimulus Sensitive Seizures!  ;)

Hope this was informative!

-Medha!

Sudden Unexpected Death in Epilepsy - SUDEP.

Hello everybody,

Let's today learn about Sudden  Unexpected  Death  in  Epilepsy.

It is the most common epilepsy related  mortality in patients with chronic  epilepsy.

Incidence: ranges  from  1-5 per 1000 patients.

Etiology:  unknown, but some of the risk factors include :

1)Polypharmacology, 
2) Poorly controlled generalized  tonic clonic seizures
3) Male gender, 
4) Age  younger than 16 yr, 
5) Long duration of epilepsy, and  frequent seizures. 

Potential mechanisms include :
1) Respiratory  arrest  or  dysfunction, 
2) Drug-induced  cardiac  toxicity, 
3) CNS dysfunction  (hypoventilation,  arrhythmia,  suppression  of  brain  electrical  activity)
4) Pulmonary  edema.

Patients are usually found dead in their  bed in prone  position  with  evidence  suggestive of a recent seizure.   

Some of the Preventive measures include:

1)Reduction of tonic–clonic seizures:  optimum  treatment,  good drug  compliance,  lifestyle  advice  (e.g. avoiding sleep deprivation)

2)Treatment changes: change drugs in a  gradual staged manner; when switching, introduce the new drug before  withdrawing the old one.

3)Supervision at night for patients at high risk.

4) Choice of drugs:  caution  with  antiepileptic drugs with potential cardiorespiratory adverse  effects.
 
5) Action on ictal warning signs: 
tonic–clonic  seizures  that  are prolonged, associated  with  marked  cyanosis, severe bradycardia or apnea,    complex  partial seizures with marked  atonia  (drop  attacks); 

Lastly counseling on the risks, lifestyle modifications. The treatment  decisions are the patient’s  prerogative, the physician’s role is to provide a risk-vs-benefit analysis.

Hope it was informative.

Let's learn together!
-Medha!

Micro-organism series -Salmonella

Introduction: Salmonella belongs to the type of parasites which infects the intestine of vertebrates and causes infection.It causes following infections  (Mnemonic - "GAS".)
G - Gastro-enteritis
A - Abdominal fever or enteric fever
S - Septicemia

The species Salmonella-typhi was first observed by Eberth in mesenteric lymph nodes and  spleen and was first isolated by Gaffky and hence is also known as Eberth -Gaffky or Eberthella -typhi .
S.cholerae - suis the first organism to be isolated from animals and human beings.

Salmonella is divided into two groups :-
1)Typhoidal Salmonella :Causes typhoid fever eg S.typhi and  S.paratyphi A,B,C
Man is the only reservoir
2)Non-typhoidal : They have many animal reservoir .To remember species name, here is a mnemonic
"Hodor held typhimurium  to enter into port "

Hodor -S.hadar

Held- S.heidelbrurg

typhimurium-S.typhimurium (to)

Enter-S.enteridies

Port-S.new port

Morphology:
Aerobes and facultative anaerobes
Gram negative bacilli
It is motile with peri-trichate flagella except S.Gallinarum and S.Pullorum .
Non-capsulated and non-sporing .

Cultural characteristics:
Can grow on simple media over pH-6-8
Temperature:15-41℃
Colonies are circular ,low-convex and smooth .
1)Mac-Conkey's agar(Differential media) :Non-lactose fermenting colonies

2)Deoxycholate citrate and XLD(Selective media): Black head due to hydrogen sulphide production
(Deoxycholate citrate agar and Mac-Conkey's agar are selective as well as differential media)

3)Wilson & Blair bismuth sulphite medium(Indicator medium):Black colony with metallic sheen due to production of hydrogen sulphide.Only S.typhi produces black colony .Paratyphi A produces green colony as it does not form hydrogen sulphide.

4)Selenite F broth and tetrathionate broth  is the enrichment media used for both shigella and salmonella

Biochemical tests:-
1)It ferments Glucose ,mannitol and maltose producing acid and gas
2)IMViC : - + - +
3)Most salmonella produces hydrogen sulphide in Triple sugar iron(TSI) test except S.parathyphi A and S.Cholerae suis .
4)S.Gallinarum and Pullorum cannot be differentiated but can be identified by biochemical reactions .S Gallinarum ferments dulcitol unlike Pullorum .

Resistance:
Killed in 1 hour at 55℃ or in 15 mins at 60℃
Boiling ,chlorination and pasteurisation destroys bacteria .
Killed in 5 minutes by using mercuric cholride / 5% Phenol .
Survives for weeks in polluted air & water
Survives for months in ice
Survives for years  if prevented from drying .

Antigenic structure:
There are 3 antigens present in salmonella
1)Flagellar antigen H:
- Heat labile
- Present on flagella
- Highly immunogenic and hence form high titre of antibodies
- Destroyed by alcohol or boiling
- When mixed with antisera  , agglutination is rapid producing large ,loose and fluffy clumps.
- H persists longer than O agglutinins

2)Somatic antigen "O"
- Integral part of cell wall
- Identical to endotoxin
- Less immunogenic

3)Vi antigen :
- Heat labile polysaccharide and it prevents the agglutination of O antigen
- Act as virulence factor by preventing phagocytosis.
- Persistance of Vi antigen indicates carrier state

Pathogenesis:
Transmission:Normally food contaminated by the faeces of the animal or humans who carries salmonella

Mode of transmission:Ingestion

Incubation period :7-14 days for enteric fever

Pathogenicity :
Salmonella infection usually causes
Gastroenteritis
Enteric fever
Septicemia

Clinical symptoms:
Clinical course  may vary from mild to undifferentiated pyrexia (Also called as ambulant typhoid)
- Onset :Gradual with headache ,malaise ,anorexia ,a coated tongue and constipation or diarrhea.
- Step ladder pyrexia.
- Palpable spleen
- Rose spot appearence on chest during 3rd or 4th week .
- Complications occurs in 3rd and 4th week causing intestinal perforation and GI hemorrhage (most common )
- Pea soup stools in 3rd week of typhoid fever
- Some degree of bronchitis or bronchopulmonary spasm is always seen
- Osteomyelitis is rarely seen mainly in patients affected with  sickle cell anemia  .

Laboratory diagnosis :
Specimen :
Blood is collected for culture ,as in urine or stool .
Serum for Widal test .
(A very famous mnemonic for collection of sample depending upon time duration is
"BASU")
B - Blood culture in 1st week of infection
A - Antibody (Widal in 2nd week of infection)
S - Stool culture in 3rd week of infection
U - Urine  culture for 4th week of infection.
Best diagnosis is  made by blood culture at any stage .
Detection of Vi antigen indicates carrier state.
If antibiotics is started we must use faeces or bone marrow for laboratory diagnosis .Since antibiotics kills bacteria from the circulation  and if not started then we can use blood culture .

Treatment:
Ceftriaxone is the DOC
Ciprofloxacin is the DOC for susceptible organism .
Other drugs used are azithromycin ,amoxicillin,chloramphenicol
Carrier :Ampicillin or amoxicillin given for six weeks

Salmonellosis:
Non Thyphoidal salmonellosis(NTS) is -commonest type of salmonellosis

Factor causing NTS
Immunosuppressive agents like increase in age ,Disease such as HIV etc.

Clinical manifestation:
Gastroenteritis most common .Diagnosis is done by gastroenteritis .
Localized infection like abscess ,meningitis , Osteomyelitis.

Treatment:
DOC either ceftriaxone or Ciprofloxacin .

That's it :P
Stay awesome and cool:)

~Khushboo and Ojas

Testosterone and Dihydrotestosterone

Hello awesomites today I am going to share my notes on functions of Testosterone and Dihydrotestosterone .

Testosterone is regarded as the circulating prohormone.In most of the target cells , testosterone is reduced to Dihydrotestosterone (DHT) which is more potent than the testosterone.

Testosterone function:

Remember: LISE
-LH inhibition .
-Internal genitals development .
-Spermatogenesis
-Erythropoiesis.

Dihydrotestosterone function

Remember :"PG says hair growth,behaviour changes and development of external genitals is due to DHT "

(Half of the things you all  must have got through it!)
PG-Prostrate growth .
Behaviour changes ,Sexual growth .
Hair growth .
External genital development.

Function which is done by both hormones?

-Increase in muscle  mass and strength of bones

Stay cool and awesome:)
~Ojas

Watermelon stomach- GAVE!

Helloooo everybody....

So today's post is summer special ... A condition called as Watermelon stomach...

I am sharing here the most important points related to it... 

Do lemme know your thoughts on the same....And any important points that I may have missed...

Let's learn together!!

-Medha!

Ion-exchange resins and Laxatives

In my last post on Hyperkalemia, I asked this question that why do we give laxatives with ion-exchange resins, eg. Sodium polystyrene sulfonate.

The reason is that if there is constipation due to Hyperkalemia or any other condition we are treating, besides these ion-exchange resins can themselves cause constipation; these resins will be stuck in the colon and the ion to which it is bound to will be reabsorbed into the circulation hence foiling the whole agenda.

-VM

Difference between polysaccharide vaccines and conjugated vaccines

Polysaccharides are strings of sugars. Some bacteria, such as Streptococcus pneumoniae and Neisseria meningitidis, have large amounts of polysaccharide on their surface, which encapsulate the bacteria. The polysaccharide capsules protect the bacteria from the host’s immune system and can make the bacteria more virulent. 

Polysaccharide vaccines are poorly immunogenic. They produce low affinity antibodies (which do not bind well to the antigen) and, because they do not elicit T-cell responses, immune memory does not develop. 

The new generation conjugate vaccines contain carrier proteins that are chemically attached to the polysaccharide antigens. Attaching relatively non-immunogenic polysaccharides to the highly immunogenic carrier proteins means that by activating a T-cell response, conjugate vaccines induce both high-affinity antibodies against the polysaccharide, and immune memory.

So in conclusion:

Polysaccharide vaccine - T cell independent B cell response

Conjugate vaccine -  Carrier proteins - T cell dependent B cell response

Mnemonic:
CT (Like a CT scan?)
ConjugaTe has a T cell response

That's all! 

-IkaN 

Trastuzumab notes + mnemonic

Trastuzumab (Herceptin) is a humanized monoclonal antibody directed against the extracellular domain of the tyrosine kinase receptor HER2.

ARDS pathophysiology Q&A

In Acute Respiratory Distress Syndrome (ARDS), what happens to the following parameters? (Increase / decrease / normal) 

Compliance
Pulmonary artery pressure
Pulmonary capillary wedge pressure
A-a gradient (Alveolar-arterial gradient)
PaO2 / FiO2

Answers given below!

Medicowesome secret project: Cyclothymia

What is the secret project? How can I participate?

Fact of the day : Neuroticism and creative thinking

Hey Awesomites

While the medial prefrontal cortex is a part of the brain that shows high levels of activity in the neurotics, innovation of new ideas is also something the frontal areas of our ( mainly right ) brain function for.

There is often a preponderance to generation of self - generated thoughts and a perception of threat appraisal when there is no such actual external stimulus. The neurotics tend to 'create' situations of threat in their mind and respond accordingly, but they also come up with creative ideas to find solutions to such 'internal' problems by overthinking and overactivating their thought - provoking areas of brain. They also have oversensitive amygdalae, that is concerned with panic attacks, excess fear and anxiety.


Thats all
- Jaskunwar Singh

Did you know? Sir Isaac Newton suffered from bouts of depression and once had a mental breakdown. Inspite of that he made use of his creative mind and formulated laws of gravity, and fathomed several mathematical theories.

Pregnancy risks related to hypertension

Important for multiple choice questions (=

Pre-eclampsia
Post partum hemorrhage
Placental abruption
Gestational diabetes

Preterm delivery
Oligohydramnios
Growth restriction (Asymmetric IUGR, Head spared, Head abdominal ratio increased)
Still birth

-IkaN

Calcium Gluconate in Hyperkalemia

Hey guys!!

In this post I will try to explain why Calcium gluconate is the first line drug in managing hyperkalemia.

First of all, please form a mental image of normal cardiac action potential with the-
1- Very steep phase 0 caused by Na+ influx,
[Note: Vmax is the rate of build-up of membrane potential in phase 0]

2- A short, sharp phase 1 caused by K+ efflux via Transient outward K+ channel
( and some books say Cl- influx)

3- Phase 2 plateau phase caused by Ca2+ influx and K+ efflux via slow delayed rectifier channels.

4- And finally, the downsloping, not so steep repolarization phase caused by K+ efflux via Ikr (Rapid delayed rectifier channels) and also a few other channels which you can afford to forget.

Now what changes Hyperkalemia bring in this sequence of normal action potential?

1. Initially it increases myocardial excitability by raising the RMP from -90mv to approx -75mv; hence bringing it closer to the threshold potential. This is coz of the K+ concentration gradient alteration.

2. But as Hyperkalemia progresses, it causes myocardial depression by decreasing Vmax, essentially slowing down phase 0, hence causing increase in QRS complex duration. This is because the no of Na+ channels activated decreases if RMP becomes less negative.

3. Conversely, it increases the rate of Repolarization, hence causing shortening of QT interval. This is because of a strange reason. The Ikr which I have mentioned above becomes more active if the extracellular K+ levels are high.

Now that we know what happens in Hyperkalemia, let us learn how calcium gluconate amends these changes.

1. It makes the threshold potential become less negative, thereby restoring the normal difference between it and RMP. Myocardial excitability amended!

2. It increases Vmax. Myocardial depression amended!

3. It acts on the SA node and AV node and increases their automaticity further rectifying myocardial depression.

A word of caution! In patients having Hyperkalemia due to digitalis toxicity, hypercalcemia can potentially kill the patient. So in such conditions we use calcium gluconate cautiously only if-
1. There is loss of P waves
2. Widened QRS complex.

Other treatment modalities:

1. Insulin with Dextrose
2. Beta-2 Agonists​ like Albuterol

Both 1 and 2 work by increasing the activity of Na+-K+ ATPase.

3. Bicarbonate. It will cause increased pH which will increase the activity of H+-K+ exchangers.

4. Haemodialysis if it's readily available

5. Ion exchange resins like Sodium Polystyrene Sulfonate along with a laxative like Sorbitol.

A question for you guys, Why is it recommended to give a laxative with an ion exchange resin? ;)

-VM

Education - a vaccine for violence

Hello

We are often so engulfed with racks of books to study and revise for exams that some might even go unrevised or untouched !! Many a times we notice poor children roaming on the streets and asking for coins and notes that are not of much value in their life. These children need education and proper guidance to re - track their life routes and help them fulfil their dreams. Poverty and lack of education in life makes such people feel helpless and force them to use illegal ways to fill their pockets.

" Brian was a poor boy. Born to a poor family, he worked all day to help his parents earn some money. Wearing a half - torn  white - turned - black tee and a faded brownish - black shorts, the eight -year old roamed here and there on the roads while holding some beautiful soft toys for being sold to the so-called 'high class' passers - by. Little did he know why was he doing all that. He was just told that he has to give the toys to some people and in return, he would get something called 'money'.

Then one day, he saw other boys of his age, carrying bags full of books and going to school. Fully energized, cheerful and in high spirits, they went on to their place. And Brian just saw them going. At that moment, he decided to change his life for the better. :)

Brian squandered his bag of toys on the roadside and started searching for a book store. A few hours passed but he couldn't find one. He knew nothing about shops, places, or any people around. He felt lone. It was a new place for him. He felt suffocated in the rising shades of darkness. The sun was getting closer to the horizon. The street lights scattered blue on the dusty road. He felt helpless and tired. Unable to get back to his home, he just slept on the footpath. Not even one eye focused on him inspite of busy streets and the flux of vehicles on the roads.

It was 8 in the morning. Seeing him still there and crying, an old man came up to him. Brian couldn't respond to any of his questions. The old man gave him some food to eat, and then took him to his house. There the little boy saw a library of books - just what he was finding since so long. He got overjoyed and went on to reach the shelves. The old man felt his curiosity to study. He asked the boy if he goes to school.

Brian told him his story after which the old man decided to help the little boy. He got him admitted to a reputed school. He gave him all he could. Books, clothes, food, shelter and work so that the little boy could help his family. And so now the boy was not poor any more. He got the treasure of his life - the books. :) "

In view of the Dhule incident a few days back, it is unethical and unacceptable for parents and relatives to demonstrate any act of physical and mental abuse towards a doctor if a patient with head injury cannot be saved due to the unfortunate circumstances such as the patient being brought late to the hospital and shortage of staff and equipment. These factors attract the need to shift the patient to a higher centre for provision of better treatment facilities and medical care.

The poor prefer to visit government hospitals and clinics because it suits their pockets. Referring the patient to a higher centre means more expensive and more delay in treatment. But that absolutely does not mean you argue with and abuse the doctor to force the treatment which cannot be done !!

Education is a key component to ensure that the person who has met with an accident and severely injured is immediately brought under medical care and treated successfully with suitable measures to save the life.

We, as responsible and educated citizens of the country must take steps to help the poor children and give them their weapons to fulfil dreams which seemed impossible to them. :)


That's all
- Jaskunwar Singh

Fact of the day: Histoplasmosis can present like sarcoidosis

Patients with histoplasmosis who have hilar lymphadenopathy, arthralgias, and erythema nodosum can be mistakenly given the diagnosis of sarcoidosis (“pseudosarcoidosis.”)

Steroids mistakenly given for sarcoidosis can cause acute exacerbation of histoplasmosis.

Fact of the day: Ferritin is an inflammatory disease marker

Ferritin is an acute phase reactant.

Serum ferritin arises from damaged cells, and is thus a marker of cellular damage.

Medicowesome secret project: Hemispheres of the brain

What is the secret project? How can I participate?

An overview of the NEET PG entrance exam

AN OVERVIEW OF THE NEET PG ENTRANCE EXAM
by Dr. Prateek Charuchandra Joshi (DNB AIR 291, MH state rank 51)

Brainstem Syndromes-Pons!

Hellooo people!

After travelling from the Midbrain  I we have reached  the Pons.. which literally means a Bridge... So .... Let's study the important eponymous Pontine syndromes today...

1) Millard-Gubler Syndrome:
Lesion location:Pons
Structures affected: CN VII ,Corticospinal tracts!!
Clinical features: Ipsilateral peripheral facial palsy; contralateral hemiparesis ,CN VI not involved

Foville's Syndrome(Raymond-Foville) :
Lesion location:Pons
Structures affected:CN VII; lateral gaze center; Corticospinal tracts.
Clinical features • Ipsilateral facial palsy and horizontal gaze palsy; contralateral hemiparesis

Raymond's (Yelloly, Landry) Syndrome: Lesion Location: Pons
Structures affected: CN VI; Corticospinal tracts
Clinical Features: Ipsilateral abducens palsy; contralateral hemiparesis ,it is  often lumped with Foville's syndrome.

There are other Pontine syndromes ...And an Anatomical classification of them makes them easy to understand !

I shall in the next post put up the respective syndromes along with associated diagrams..

Till then... Study Well Guys!
Also I would like to say... Medicine is not just science and theory but also an art to be understood.... So we all need to have the artists eyes and spot out the subtle presentations of the  diseases in our patients and treat them with all our hearts!

-Medha!

Fact of the day: High maternal cortisol good for foetal brain

Hey Awesomites

Neurodevelopment attained in the foetal period is greater than in any other period of an individual's life. Foetal exposure to "optimal levels" of maternal cortisol in third trimester has been linked to better cognitive and functional performance in the child.

Maternal cortisol acts on its receptors present in amygdala, hippocampus and the pre - frontal cortex ( PFC ) in high amounts. This hormone influences various stages of neurodevelopment including neurogenesis, axonal development, and myelination of nerve fibres and thus it leads to increased cortical thickness in frontal part of the brain and increased brain maturity.
( Source )

Thats all
- Jaskunwar Singh

Brutons disease (X linked agammaglobulinemia) mnemonic

Hello! 

Guess who made a new video?

Differentials of Unilateral Central Scotoma

Hey, guys this post will be on the differential diagnosis of "Blurred Vision in one eye" due to a central scotoma.

So a central scotoma can be usually due to retrobulbar neuritis(inflammation of the optic nerve) or optic nerve compression.

Now when you have detected a central scotomata in one eye it is essential to do the confrontation test in the other eye also. If in the other eye you detect a defect in upper temporal field, a superior temporal quandrantonopia; it is higly likely that this is a case of optic nerve compression.

How so? Well refer the attached pic with the illustrated diagram and I am sure you will understand. :)

-VM

Studying made simple: Ocular signs of thyrotoxicosis

Hey Awesomites

I read about ocular signs seen in patients with thyrotoxicosis. On googling and partly my work, studying these signs has become so simple to remember. -

Lhermitte's sign Variants!

Helloooo....

Well we all know about the Lhermitte’s sign... The famous Barber's Chair sign!

For the people who are reading for the first time... Lhermitte's sign  is a sensation of tingling or electric shocks running down the back and legs on flexion of the neck.

Some other actions giving rise to similar sensations are:  Neck rotation, arm abduction, coughing ,Yawning 

It is common in multiple sclerosis, and other demyelinating diseases  but can occur with other conditions involving the cervical spinal cord.

But...Some variants to Lhermitte’s sign have also been described.

1) Delayed typical Lhermitte phenomenon can follow contusion of the spinal cord from neck trauma.

2) Reverse Lhermitte phenomenon
Paresthesias induced by neck extension have been described in extrinsic compression of the cervical spinal cord.

3) Inverse Lhermitte's sign:
Upward moving paresthesias with neck   flexion have been described in myelopathy from nitrous oxide inhalation.

I hope this was informative!

-Medha!😊

Brainstem syndromes-Midbrain!

Here we shall review three syndromes in the Midbrain occuring majorly due to a vascular event.

Weber's Syndrome:
Lesion Location: Midbrain base

Structures involved :CN III fibers; cerebral peduncle

Features: Ipsilateral CN III palsy; contralateral hemiparesis

(The image showing the involved 3 nerve and the crus! The lesion is anterior—in the cerebral peduncle—in  Weber’s syndrome, causing hemiparesis.)

Claude's Syndrome:
Lesion location :Midbrain tegmentum

Structures involved: CN III fibers; red nucleus; SCP

Clinical features: Ipsilateral CN III palsy; contralateral ataxia and tremor (“rubral tremor”)

(The sky blue line depicts the sup. Cerebellar peduncle! Lesion is more posterior—in the tegmentum—in Claude’s syndrome, causing hemiataxia.)

Benedikt's Syndrome:
Lesion location: Midbrain tegmentum

Structures involved: CN III fibers; red nucleus; CST (corticospinal tract)SCP(superior cerebellar peduncle)

Clinical features:
•Ipsilateral CN III palsy; contralateral hemiparesis with ataxia, hyperkinesia and tremor “rubral tremor

(The blue fibers being the sup. Cerebellar peduncle. In Benedikt’s syndrome, the lesion is more extensive, involving both the tegmentum and the peduncle, causing hemiparesis with tremor and ataxia of the involved limbs)

These three midbrain syndromes are variations on a theme.

Benedikt’s is essentially  Weber’s + Claude’s.

Because the fascicles of cranial nerve (CN) III are scattered in their course through the midbrain, the third nerve palsy in any of these syndromes may be partial.

Last on the list....
 Nothnagel's Syndrome mainly due to neoplasms ...affecting the Midbrain tectum involving Ipsilateral or bilateral CN 3 causes Oculomotor palsies; ataxia.

We finish Alll the midbrain syndromes !!!!!😎

Hope it helps!

-Medha😊

Facts and Fallacies: Vitamin D link to cancer

Hey Awesomites

Vitamin D has been shown beneficial for a variety of disorders and diseases. Recent studies now suggest that those deficient in vitamin D are at a  higher risk of developing cancer compared to those with adequate levels.

Brainstem Syndromes!

So let's get done with all the important brainstem syndromes once and for all !

I would be writing on all of them one by one...

Also ...I will try and incorporate many of my diagrams to help you guys make it seem less daunting...

Starting from the Midbrain the first syndrome is..

(The image shows the level of the lesion)

1):Parinaud's Syndrome

Lesion location:Midbrain dorsum ,superior  collicculi.

Structures involved: Quadrigeminal plate region; pretectum; periaqueductal gray matter

Etiology: •Due to mass lesion in the region of the posterior third ventricle, most often pinealoma, or due to midbrain infarction.

Clinical features:
•Impaired upgaze as centre for upward gaze is affected
convergence retraction nystagmus;
Argyll Robertson pupil :dilated pupils with light near dissociation.

A closer look at the structures involved .

I hope it helped !Also do share your Neuroanatomy diagrams and and more information on Parinaud Syndrome.

Have a nice day!

-Medha!

How I remember the duration of symptoms for Generalized anxiety disorder (GAD) required for diagnosis

The symptoms of generalized anxiety disorder should be present for at least 6 months. For me, it's hard to remember the duration of the symptoms in psychiatry. So I mnemonic-ify them :D

I remember G6PD, and say G6AD instead!

For those who don't know what GAD is here is the DSM V criteria for diagnosis of Generalized Anxiety Disorder...

Transposition of Great Arteries!

Hello!

So I have divided the post into two parts - A short summary for those who don't have the time to read everything (#TLDR) and a nice long explanation for those who want to read everything :)

Let's start with TLDR.

Buzz words for congenital syphilis!

Following are some important signs and buzzwords that are testable ...And high yeild for entrances.

Olympian Brow: Bony prominence of the forehead caused by persistent or recurrent periostitis

Clavicular or Higoumenakia sign:Unilateral or bilateral thickening of the sternoclavicular third of the clavicle

Saber shins :Anterior bowing of the midportion of the tibia

Scaphoid scapula :Convexity along the medial border of the scapula

Hutchinson teeth:Peg-shaped upper central incisors; they erupt during 6th yr of life with abnormal enamel, resulting in a notch along the biting surface

Mulberry molars :Abnormal 1st lower (6 yr) molars characterized by small biting surface and excessive number of cusps

Saddle nose :Depression of the nasal root, a result of syphilitic rhinitis destroying adjacent bone and cartilage

Rhagades:Linear scars that extend in a spoke-like pattern from previous mucocutaneous fissures of the mouth, anus, and genitalia

Juvenile paresis :Latent meningovascular infection; it is rare and typically occurs during adolescence with behavioral changes, focal seizures, or loss of intellectual function

Juvenile tabes : Rare spinal cord involvement and cardiovascular involvement with aortitis

Hutchinson triad :Hutchinson teeth, interstitial keratitis, and 8th nerve deafness

Clutton joint :Unilateral or bilateral painless joint swelling (usually involving knees) from synovitis with sterile synovial fluid; spontaneous remission usually occurs after several weeks

Interstitial keratitis: Manifests with intense photophobia and lacrimation, followed within weeks or months by corneal opacification and complete blindness

8th nerve deafness: May be unilateral or bilateral, appears at any age, manifests initially as vertigo and high-tone hearing loss, and progresses to permanent deafness.

Well all these are late manifestations of congenital syphilis occuring after 2 years of life.
It is important to recognise these signs clinically and also on the exams...

-Medha.