Case control study vs Cohort study mnemonic

Super short post :)

Case control study - Start with an outcome and go back in time to study the risk factor.
Simplified: Case (Diseased) vs Control (No disease)

Cohort study - Start with risk factor and see who developed the disease and who did not.
Mnemonic: cOhOrt has two O's.
One O has an R (cohORt), which means one group has the risk factor.
Other O does not have an R (cOhort), which means the other group does not have the risk factor.
Compare the two to see who gets the disease.

How to remember that case control studies measure odds ratio and cohort studies measure relative risk:

You take surgical "cases" to the "OR" (Operating room)
Case control study - Odds Ratio

cohoRRRRRRt measures Relative Risk.

kthxbye!

-IkaN

Abdominal Pain in Pregnancy

Hey guys

In this post I will mention the most common and must-know causes of abdominal pain in pregnancy which is a very common complaint during gestation. I will also mention certain salient points which will be helpful in the differential diagnosis.

1. Implantation Bleeding. There is a mild abdominal pain 6-12 days after conception along with a small amount of vaginal bleeding called spotting. Be careful so as not to confuse this bleeding with the menstrual bleeding.

2. Ectopic Pregnancy. This is the leading cause of first trimester mortality of the foetus. If there is a serum HCG level more than 2400 mIU/ml (The discriminatory zone is 1500-2400mIU/ml) and on USG there is no gestational sac in the uterus, then you should strongly suspect this. The most common sites are Tubal, Ovarian, Interstitial, Cervical.

3. Spontaneous Abortion. It is common in the early pregnanacy( upto 20 weeks) and is divided into 4 stages: Threatened, Inevitable, Incomplete, Complete. If there is vaginal bleeding without cervical dilatation or any change in cervical consistency, then it is Threatened abortion, if the cervix is dilated, it is Inevitable; if some products of conception are discharged per vaginally, it is incomplete abortion.

4. Abruptio Placentae. It is due to premature separation of placenta from its implantation site causing vaginal bleeding and pain due to uterine cramps caused by myometrial irritation. In some cases there is no vaginal bleeding, and we call those Concealed abruption. If the abruption is large enough to cause uteroplacental insufficiency the fetus is at risk. And the mother is at risk of haemorrhagic shock.

5. Ovarian Cyst

6. Ovarian Torsion 

7. Appendicitis

8. Uterine leiomyomas (Fibroids)

9. HELLP Syndrome. Haemolysis, Elevated liver enzymes, Low platelets syndrome is a complication of Preeclampsia characterized by nausea, vomiting and right upper quadrant pain and tenderness. If this condition has progressed, there is risk of seizures and in the worst case hepatic rupture causing hypovolemic shock and severe pain. Peripheral blood smear will show schistocytes and low platelets.

10. Cholelithiasis. This condition will have characteristic biliary colic, i.e., intermittent right upper quadrant pain associated with nausea and vomiting.

11. Cholecystitis.

12. UTI. There will be suprapubic pain with dysuria, frequency and urgency.

13. Urolithiasis.

14. Round Ligament Pain.  Enlargement of uterus during pregnancy leads to traction in the round ligament which pulls on the nearby nerve fibres causing sharp pain; such a pain can also be caused by round ligament spasm or cramps. This pain is usually present on the right side because of the dextro-deviation of the uterus and managed by acetaminophen and exercise.

That's all!

-VM

Ischial Spines - Important Obstetric Landmark.

Hello There!

So let's enlist few important points in relation to the ischial spines.

Ischial spines can be generally be palpated at about a finger-length into the vagina, at 4 & 8o'clock.
They are felt as bony prominences and their palpation may cause a little discomfort to the patient.

These spines serve as a landmark for:

1) Engagement of Fetal Head.(Most commonly used for determining the Fetal Station during labor.
Ischial spines are considered as Station0)
2) Internal Rotation of the fetal head.
3) Pudendal Nerve Block.
4) External os.
5) Obstetric Curve (J shaped) takes forward curve at this level.
6) Insertion of levator Ani.
7) Plane of least pelvic dimension.
8) Ring pessary is kept at the level of ischial spines.

These are the few things I know about at the level of the Ischial spines.
Do let me know some additional points you know of, to add to the list.

Let's learn Together!
-Medha.

Umbilical Cord Knots.

Hello everybody!

Recently during my Ob-Gyn internship while delivering the placenta, the Umbilical cord that I held, was very lumpy bumpy. Little knowing about the reason at that moment, I came home found out the reason.
Let's see how the Umbilical cord can get knotty sometimes.

So there are two types of knots seen in the cord.
1)True Umbilical Knots
2)False Umbilical Knots.

True Knots :
These are noted after delivery. 

The umbilical vessels, are protected by the thick myxomatous Wharton jelly, and can rarely be occluded completely. The jelly protects the vessels and the fetal blood supply, as there is only flattening or dissipation of Wharton jelly when a Knot is formed.
Due to the knot some amount of venous congestion distal to it and some  partially or completely occlusive vascular thrombi may also be observed.

A true knot is formed when a loop of cord slips over the infant’s head or shoulders during delivery.
If the knot is pulled tightly it can cause fetal demise due to restriction of the circulation in the cord. 

The True Knots can occur due to:
1)A long cord, 
2)Large amounts of amniotic fluid
3)A small infant,
4)An overactive fetus
5)As a result of external version. 

(All the above causes lead to increased fetal movements in utero)

However the fetal mortality rate associated with true knots is low.

False Knots:
In the cord the blood vessels are longer than the cord and are often folded on themselves producing nodulations on  the surface of the cord. These nodulations are lumps and bumps I saw!
These have been termed as false knots.

So guys the next time you see a lumpy bumpy cord, unlike me, you now know the reason.
That's​ all, on the Umbilical cord and it's knots.

Let's learn Together!
-Medha.

Laryngomalacia vs tracheomalacia mnemonic

Laryngomalacia casuses inspiratory stridor.

Tracheomalacia causes expiratory stridor.

Terson Syndrome.

Hello everybody!

In this post let's quickly learn about Terson Syndrome.

So what is it?
This Syndrome is a combination of intraocular and subarachnoid haemorrhage secondary to aneurysmal rupture, most commonly arising from the anterior communicating artery.

Terson Syndrome along with other bleeding disorders is included amongst the Systemic causes of vitreous hemorrhage!

Intraocular haemorrhage is also seen to occur with:
1)Subdural haematoma
2)Acute elevation of intracranial pressure

The mechanism of intraocular bleeding:

There is increase in cavernous sinus pressure due to the subarachnoid/subdural hemorrhage leading to stasis in the retinal veins. This stasis in the retinal veins leads to increased intraluminal pressure in the veins making them susceptible to bleed.

The haemorrhage is often Bilateral.
Typically intraretinal and/or preretinal. With this hemorrhage there is a possibility of it leaking in the vitreous.

The vitreous haemorrhage usually resolves in a few months and the long-term, the visual prognosis is good.

I hope you guys found it useful. Do let me know about some neuro-opthalmology syndromes you know about.

Let's learn Together!
-Medha.

Innate Cellular Anti-retroviral Mechanisms

This post will focus on the mechanism by which a cell fights against HIV, mainly by interfering with its life cycle. There are only 3 such mechanisms discovered and elucidated till date.

As it says on the post, these are innate mechanisms most of which are upregulated by Interferons (alpha and gamma).The adaptive immune system is mostly ineffective against retroviruses. How? Earlier the most accepted hypothesis was that this is because of error-prone Reverse trancriptase which makes a lot of errors while forming the proviral ds DNA, hence causing hypermutations(mainly G to A) resuting in change in the viral antigenic domains. This is true for both HIV and HBV. 

1. APOBEC3G: The full form is Apolipoprotein B mRNA editing enzyme and catalytic polypeptide like 3g which you will easily forget and you should. It is basically a cytidine deaminase which acts on the negative cDNA strand and converts dC into dU; hence converting G into A in the positive strand. These hypermutations ultimately lead to failure of viral replication by unknown processes. So the latest most accepted hypothesis explaining the G to A hypermutations in virion DNA is this. This is more effective against HBV than HIV, guess why? Its because HIV-1 has Vif (Viral Infectivity Factor) that inactivates APOBEC3G.

2. TRIM5: This is the reason why Rhesus monkeys are innately resistant to HIV. Its an awesome protein in my opinion. What it does is as soon as the viral nucleocapsid enters the cell, it forms a cage around it and cause it to "uncoat" prematurely hence inactivating the reverse transcriptase and other enzymes present within the capsid. Then it performs a Kamikaze!

It ubiquitinates itself (auto-ubiquitination); hence causing its own proteasomal degradation and destroying the viral proteins in the process as collateral damage.

3. Tetherin: Now this is a case of Stockholm Syndrome! Tetherin are proteins that tethers or chains the virion to the cell membrane, hence preventing its release from the cell. The cell is not letting the virus leave her. So that when the cell dies either by apoptosis or inflammatory processes, the virions die with it. <3

Unfortunately however cool these may appear, these are mostly ineffective and hence the standard microbiology textbooks choose to ignore these proteins. Hopefully in future, drugs will be designed to make them more effective. :)

That's all!

-VM

Cerebellum and Motor learning!

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

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

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

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

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

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

I hope this was informative.

Let's learn together!
-Medha.

Drug: Evolocumab

This post will be on Evolocumab, a monoclonal antibody drug recently approved by FDA for use in refractory cases of Primary Hyperlipidemia and Homozygous(Not used in heterozygous) Familial Hypercholesterolemia alongwith Statins and appropriate diet and lifestyle modifications. 

Mechanism of Action:

As you know, LDL-Cholesterol is the bad cholesterol which is cleared by hepatocytes via surface LDL-receptors. These receptors are catabolized in hepatocytes by the enzyme proprotein convertase subtilisin/kexin subtype 9, fondly called PCSK9.

This enzyme is inhibited by Evolocumab, hence decreasing the intracellular clearance of LDL-R, thereby increasing the clearance of LDL-C from the body.

And Statins also help in raising the expression of LDL-R in hepatocytes by inhibiting HMG-CoA Reductase, hence decreasing cholesterol synthesis forcing the hepatocyte to extract more cholesterol from the blood.

The most common adverse effect is Nasopharyngitis which is easily manageable. And the black box warning is Hypersensitivity Reaction.

Look out for new drugs and ever-changing treatment and management guidelines and try to stay updated! :)

-VM

Medicowesome secret project: Let's talk about unhappiness

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Let's talk about depression

What is the "Let's talk" project? How can I talk about mental illnesses?

Thalamus.

Helloooo everybody!
 let's quickly learn a few basics and beyond in today's post on Thalamus.

So thalamus is nothing but a collection of neurons which are organized well-defined nuclear masses.

The nuclei have confusing names and are difficult to remember too.

But from a functional point of view they are divisible into four groups to keep our lives simple.

1) Specific Sensory Nuclei
2) Association Nuclei
3) Nonspecific Nuclei
4) Motor Nuclei.

Specific Sensory Nuclei :These receive all sensory afferents. The arrangement of fibres is topographic and so is their projection to the somatosensory cortex. 

Corresponding to the thalamocortical projection fibres, there are also corticothalamic fibres which provide feedback information to the relay nuclei.

Let us now see how the sensory relay nuclei work.

A specific sensory stimulus activates neurons in the sensory relay nucleus.
                           
The thalamic nuclei activate some thalamic interneurons as well as an area in the sensory cortex. Activated sensory cortex also sends impulses back to the thalamic relay nucleus, thereby modulating the thalamic output.

In short, the sensory relay nuclei really do not act as simple relays.  They process the sensory signal by local intrathalamic circuits and descending corticothalamic  fibres before sending it to the sensory cortex.

Association Nuclei :
These help achieve integration of different types of sensory information.

Nonspecific​ Nuclei:
These also receive sensory information but project to the cortex in a diffuse manner.  Therefore they seem to be involved in the arousal induced by sensory stimuli.
They also project to the limbic system, thereby suggesting their involvement in the emotional impact of sensory stimuli.

Motor Nuclei :
They relay and process messages from the basal ganglia and cerebellum to the motor and premotor cortex.

All nuclear groups have to and fro connections with the cerebral cortex. Thus the thalamus and cortex function as one functional entity, the thalamocortical​ system.

Possibly the thalamus prepares a crude blue pint of the  final product achieved by the cortex.

The global involvement of the thalamus in central nervous function is revealed when its function is impaired, as in the thalamic syndrome.

Let's now quickly learn about Thalamic Syndrome.

Level of lesion : Posteroventral thalamus.

Etiology: Thrombosis of  Posterolateral branch of the posterior cerebral artery.

Manifestations :

1) Impairment of discrimination in sensory perception,
2) Hypotonia, muscular weakness and incoordination,
3) Volatile emotions, pleasant or unpleasant. 

After a few weeks to months, partial recovery may occur.

The sensations, regardless of the nature of the stimulus, may be very painful. 

The symptoms are thought to arise partly because the medial nuclei of the thalamus are spared by the lesion. 

 The medial nuclei are the nonspecific nuclei which receive major projections from pain  fibres.Hence the dominance of pain among the sensations. 

Well that's all on Thalamus,Hope it was helpful!

Let's learn Together!
-Medha.

Medicowesome secret project: Let's talk about seeking help

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Let's talk about low self esteem

What is the "Let's talk" project? How can I talk about depression?

Treatment of migraine headaches mnemonic

Hello! Here's a short post on treatment of migraines!

Treatment of acute migraine attacks mnemonic: NSAiDs

N: NSAIDS like Naproxen, S, Aspirin, Ibuprofen, Diclofenac

S: Sumatriptan (And other Triptans such as rizatriptan, eletriptan, almotriptan, zolmitriptan, naratriptan, and frovatriptan)

AiDs: Antiemetic/dopamine receptor antagonists: Chlorpromazine, prochlorperazine, and metoclopramide

Ds: Dihydroergotamine and ergot derivatives

Prophylaxis of migraine mnemonic: ABC

Antidepressants: Amitriptyline and venlafaxine

Beta blockers: Metoprolol, propranolol, and timolol

AntiConvulsants: Valproate and topiramate

Calcium channel blockers (less effective): Verapamil, Flunarizine

That's all!
-IkaN

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!

Medicowesome secret project: Let's talk about not quitting

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Let's talk about going to a doctor

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Let's talk about the stigma

What is the "Let's talk" project? How can I talk about depression?

Medicowesome secret project: Let's talk anthem

What is the "Let's talk" project? How can I talk about mental illnesses?

Vascular smooth muscle: Effect of sympathetic stimulation mnemonic

Pancreatic beta cell: Effect of sympathetic stimulation mnemonic

Calcium channel blockers and muscles they act on mnemonic

Medicowesome secret project: Let's talk about asking for help

What is the "Let's talk" project? How can I talk about mental illnesses?

Medicowesome secret project: Substance dependency

What is the secret project? How can I participate?

Medicowesome secret project: Depression - Let's talk

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.