Sunday, April 16, 2017

Difference between Duodenal and Gastric Ulcer

Hello everyone, let’s talk about the ever confusing difference between Duodenal and Gastric Ulcer. Both the ulcers are a type of Peptic Ulcer which occurs due the action of acid resulting in the damage of alimentary mucosa. The main cause for both of them could be infection with H. pylori or intake of NSAIDs.

Mnemonico diagnostico : Klinefelter's syndrome

Hey Awesomites

Criteria for diagnosis of Klinefelter's syndrome in males mnemonic : KLINEFELTER

K - (K) Cryptorchidism
L - Leydig cells hypertrophy
I - Increased gonadotrophins
N - Negative/ Positive chromatism (aberrations)
E - Elongated legs
F - Failure of secondary sexual characters
E - Eunuchoidism
L - Late pubic hair
T - Testicular failure
E - Erectile dysfunction / Elbow deformities
R - Retardation (mental)


Thats all
- Jaskunwar Singh

Non Contraceptive uses of the Condom

Hi everyone. So we know what we use a condom for generally :p
But there are a few non Contraceptive uses for this magical device that prevents babies :').

So here goes -

1. Prevention of STD's.
2. Can be used in Balloon Tamponade to control PPH.
3. Used to cover the USG probe inserted into the female tract.
4. Can be used as a mould for the vagina during Vulvoplasty.
5. Women with Anti Sperm antibodies during the initial phase. (Controversial).

So that's about it.
We know no 5 more reasons to use condoms !
Go get em ; )
Happy studying.
Stay awesome.

~ A.P.Burkholderia

How to remember Hepatitis B is associated with membranous glomerulonephritis

Writing this post because I confused it with focal segmental glomerulonephritis yesterday.

Hepatitis B is associated with membranous glomerulonephritis.

Mnemonic: Happy memory - Heppy membory - Hepatitis B Membranous nephropathy :D

That's all!
-IkaN

Bromocriptine : Utility Review

Hi everyone ! Here's a brief review on the drug Bromocriptine which happens to be one of my favorite drugs. So here goes.

- Bromocriptine is a Dopaminergic agonist , specifically acting on the D2 Receptors.

- It is a very widely used drug , with various and multi systemic uses.

Uses :

1. Parkinson's disease.
- Bromocriptine and other D2 agonists like Rotigotine , Ropinirole and Pramipexole can be used to treat Parkinsonism.
- They act by providing a sort of  replacement for the depleted dopamine in the circuits of the basal ganglia.
- They are quite effective , especially in case of L Dopa resistance , or deterioration of symptoms when on L dopa.

2. Neuroleptic Malignant Syndrome.
- NMS is perhaps caused by D2 blockade due to drugs like Haloperidol and Fluphenazine.
- Thus it makes sense if you give this D2 agonist to treat this disorder.

3. Hyperprolactinemia.
- Dopamine acts as a Prolactin Inhibitory Factor (PIF) at the Hypthalamo-Pituitary level.
- In cases of Hyperprolactinemia where there is gynecomastia and galactorrhea,  giving D2 agonists counteracts the elevated prolactin levels.
- Thus it's useful in Anti psychotic/ Metoclopramide induced Hyperprolactinemia.
- Can be used in Ovulation induction due to elevated prolactin by a Pituitary adenoma.

4. Diabetes Mellitus.
- Bromocriptine modulates the Dopaminergic discharge at the Hypothalamus level.
- This modulates the circadian rhythm and resets the abnormal metabolic drive of the Hypothalamus and reduces the insulin resistance.
- The specific Quick Release formulation is used for this indication.
- It may be used in conjunction with Insulin and does not cause hypoglycemia.
- It cannot however be used for DKA

5. Acromegaly.
- Inhibits the excess Growth Hormone secretion by acting at the Hypothalamus level.

Hope this helped !
Happy studying and stay awesome!
~ A.P.Burkholderia

Neuroleptic Malignant Syndrome : A Crisp Overview

Hi everyone ! So I recently saw a patient who possibly had Neuroleptic malignant syndrome. So I though I would do a post on it !

1. The Syndrome -

NMS is an idiosyncratic reaction to Anti psychotic drugs. It causes a host of symptoms like Rigidity , Hyperpyrexia and altered consciousness.

2. The Etiology -

- All Antipsychotic drugs can cause NMS. But most commonly implicated are Haloperidol, Fluphenazine and Chlorpromazine.
- Especially at risk are those taking Depot preparations.
- Even lithium in high doses can precipitate this.
- Atypical Antipsychotic drugs have a lower propensity to cause this.

3. The Pathophysiology -
- Although largely speculative , the cause is said to be the dopaminergic blockade by the anti psychotic drugs.
- Blockade of D2 in Hypothalamus is responsible for the Behavioral and Temperature changes.
- Blockade of D2 in the basal ganglia ( nigro striatal pathway) causes the Rigidity.
- increased muscular activity can cause muscle break down.

4. The Clinical Features

- generally within 4-10 days after starting the Antipsychotic drug. But can even occur years later.
- Hyperthermia ( Hypothalamus is conked off )
- Lead pipe Rigidity ( Basal ganglia are screwed)
- Altered mental state - delirious.
- Sweating/ Diaphoresis  ( compensation for high temp)
- Tachycardia
- Dyspnea
- Urinary incontinence
- Dysphagia
- Pallor.

Symptoms develop over a period of 24-72 hours.

5. Tests -
- Creatine Phosphokinase (CPK MM) is raised
- Leukocytosis
- Low Iron
- Deranged LFT and LDH

( Can be used to differentiate from serotonin syndrome)

- Diagnosis requires Hyperthermia + Rigidity +   2  other features ( including riased leukocytes and CK MM)

6. Management -
- ABCD
- Ventilatory support if needed
- stop Antipsychotic drugs.
- Anti pyrectics . Ice packs. Cooling blankets.
- BDZ
- Specific -->
Dantrolene - Muscle relaxant and Hyperthermia management. 400 mg/D.

- Bromocriptine - D2 agonist.

- ECT may be needed.

Hope this was helpful ! Happy studying and Stay awesome.

~ A.P.Burkholderia

Reversible Causes of Dementia : Mnemonic

Hi everyone ! This is a short post on causes of dementia that can be corrected. This is very important as most causes other than these have no available treatment ! (One Reversible cause of dementia is the Demeantor's kiss ;;) Treat using  Expectro Patronum)

So the medically treatable causes include the following.

Remember : ABCD2E

- Alcoholism
- Vitamin B deficiency - Thiamine / Niacin /B12
- CNS infections - HIV , Chronic Meningoencephalitis , Whipple Disease, Neurosyphilis.
- Depression
- Drug induced
- Endocrine - Thyroid disturbances

Let's look at how these can be corrected medically.
- A = Alcohol abuse. May be a result of Alcoholic delirium/ Wernicke-Korsakoff syndrome. So the management would include giving Thiamine to the patient , and alcohol withdrawal using Disulfiram ans other anti craving drugs like Ondansetron, Acamprosate, Topiramate and Naltrexone.

- Vitamin B Deficiency = Thiamine deficiency we've seen above.
Niacin Deficiency causes 3 D's - Diarrhea , Dermatitis and Dementia. So treat that using Niacin.
B12 Deficiency and possibly folic acid can also cause Dementia.

- CNS Infections = They cause transient cognitive changes that are reversible on treating the disease.

- Depression = may cause depressive pseudodementia or even true dementia. (pseudo dementia = no confabulation or impaired recent memory)

- Drug induced = Chronic use of drugs like BDZ , Opiates and TCA's.

- Endocrine = Hypothyroidism is notorious to cause Dementia.

~~~~~~~~~~~~~~~~~~~~~~~

The surgically correctable causes are below.
Remember = T2 H2

- Tumors  (esp frontal lobe tumors )
- Trauma (Subdural Hematoma)
- Normal Pressure Hydrocephalus (NPH)
- Hydrocephalus

- Tumors are resected surgically.
-  For the hydrocephalus group , ventriculo peritoneal shunting is performed.
- NPH = Triad of symptoms showing Gait disturbances , Urinary incontinence and Dementia. (GUD)

Hope this post helped you and didn't leave you too demented. !  If it did, have some chocolate like Lupin would offer ;;)
Happy studying.
Stay awesome.

~ A.P.Burkholderia

Saturday, April 15, 2017

Fact of the day: Nightmares are a warning for serious mental problems

Hello

Not one or two, but frequent nightmares are major caveats for underlying serious mental problems. Rapid Eye Movement sleep disorder is a rare disorder that causes the person to act violently during dreamy state. This may be a warning sign for major neurologic disorders like Parkinson's and neurodegenerative diseases like Alzheimer's !!

Night owls are more likely to have frequent sleep and mood disturbances than the early sleepers. Evidences suggest people suffering from nightmares and related sleep disorders are more likely to have suicidal tendencies than those not, in addition to other contributing factors.


- Jaskunwar Singh

Friday, April 14, 2017

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.

Thursday, April 13, 2017

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