Drugs causing hyperkalemia mnemonic

Hello!

I modified the K BANK mnemonic and added more to it to cover a few more drugs.

The mnemonic for drugs causing hyperkalemia is: K BANK Digs, cycles, sucks, self help (Sulf hep!)

K - Potassium sparing diuretics (Obviously!)

B - Non selective beta blockers

A - ACEI, ARBs

N - NSAIDs

K - Potassium supplements

Digs - Digoxin

Cycles - Cyclosporine

Sucks - Succinylcholine

Sulf - Sulfonamides, Trimethoprim

Hep - Heparin

That's all!

-IkaN

Direct acting cholinomimetic agonist mnemonic

Hi everyone, 

Here's the mnemonic for direct acting cholinomimetic drugs: ABC VPN

Nerve fibres : A clinico-physiological approach.

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

Nerves

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

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

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

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

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

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

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

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

Thus to summarize the small fibres -

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

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

Coming to the large fibres.

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

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

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

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

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

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

Hope this was helpful !
Happy studying !
Stay awesome.

~ A.P. Burkholderia

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