RACE protocol in Atrial fibrillation.

Hello! This is a short post regarding RACE protocol. Before starting it, here are some high yielding points regarding Atrial fibrillation.

Most common cause of embolic stroke: Non rheumatic Atrial fibrillation.
Examination shows
1) Pulse: Fast
2) Rhythm: Irregular
3) Pulse deficit more than 10/ min is diagnostic of Atrial fibrillation.

Ecg finding:

1) No P wave
2) R-R interval keep varying

R. A. C. E. protocol is followed in treatment of the Atrial fibrillation.

1) Rate control :

Short acting beta blockers are given to decrease heart rate. Decreasing heart rate leads to increase filling time of the heart. This in turn leads to increase diastolic time. It Increases end diastolic volume, stroke volume, cardiac output and increase BP.

2)Anticoagulation:

Atrial fibrillation causes increase clot formation in heart. Clots can be detected by Transesophageal Echo.

3) Rhythm control:

Antiarrythmic drugs are given to control rhythm.
Chemicals cardioversion is drugs used to terminate ectopic foci.

4) Electrical cardioversion:

If chemical cardioversion fails, go for electrical cardioversion. In this technique patient is sedated and DC shock of 200J biphasic is given.

That's it!

-Demotional bloke

Amiodarone and thyroid dysfunction

Amiodarone, a class III antiarrhythmic drug is associated with a number of side effects, including thyroid dysfunction (both hypo- and hyperthyroidism)

AMIODARONE INDUCED HYPERTHYROIDISM:
There are two types of amiodarone-induced thyrotoxicosis (AIT):

Type I: This type is typically seen in patients with preexisting multinodular goiter or latent Graves disease, the excess iodine from amIODarone results in enhanced thyroid hormone production.

Type II: In type II AIT there is destructive thyroiditis caused by the drug itself that results in excess release of T4 and T3(There is no hormone production). It typically occurs in patients without underlying thyroid disease.

AMIODARONE INDUCED HYPOTHYROIDISM:
1)Normally after exposure to an iodine load (eg, radiocontrast), iodine transport and thyroid hormone synthesis are transiently inhibited to prevent normal individuals from becoming hyperthyroid(the Wolff-Chaikoff effect). Normally patients escape this Wolff-Chaikoff effect and come back to normal within a few weeks, but patients with pre-existing subclinical thyroid disease fail to escape and develop hypothyroidism.

2)Amiodarone also inhibits 5'-deiodinase which is responsible for the peripheral conversion of T4 to T3. So there is a decrease in T3 production.

-Srikar Sama

Wolff-Parkinson's White syndrome

Hello! This post is regarding WPW syndrome. It is an Autosomal recessive disorder.
In Normal heart, conduction is from SA node to cardiac myocytes via AV node and Purkinje fibers. In WPW syndrome, SA node transfers electric activity directly to cardiac myocytes. This transfer is done by 'Bundle of Kent'.  Since AV node is responsible for delay of the conduction in normal heart, skipping of the AV node causes excitation prior to the expected time. Hence low Cardiac output is sign in WPW syndrome.

Investigation: ECG done

Findings in ECG.

1) Since AV node is skipped in conduction, short P-R interval is seen.

2) q wave is responsible for conduction in septal region, here also it is skipped in ECG (Remember conduction directly from SA node to cardiac myocyte!). At the same time we see Delta waves.

What are Delta waves?
-Change in the upswinging of the 'R' wave.

3) PJ interval is normal

What is PJ interval?
-J point is the point where S wave ends.
Starting point of P wave to J point is called as PJ interval.

(Remember: Segments does not include waves, interval loves waves! Example: ST segment is from end of S to start of T wave)

Now, as we can figure it out PJ interval is PR + qRS
PR becomes shorter and qRS becomes  broader in WPW syndrome. qRS is broader because conduction of cardiac myocytes is slower than Purkinje fibers. (Hope you remember clue sentence here - conduction from SA node directly to cardiac myocytes!) Hence PJ interval is normal.

Treatment:

Flecainide given orally is DOC.
Treatment of choice is Radio-frequency ablation.

Submission: Tips for Step 2 CK

Hello All,

I am currently preparing for my step 2 CS exam. I gave my step 2 CK in June 2018 and scored >250.

Here are the resources I used-

1) Onlinemeded lectures+MTB

2) U world Q bank

3) NBME /UWSA

Here is what I. Used to do-

Listen to Online meded lectures and take notes on MTB but I did not read them again. I just listened to OME lectures  2nd time while exercising.

I printed the pdf file circulating with UWorld tables and Followed listening lectures of online meded  with doing questions of Usmle World and taking notes on Tables file.

Then I used to revise whole system I did in the week on weekends

Initially I started with one system a week and in the end I did 2 systems in a week.

Some important points to note-

1) U world and Online meded are the basic resources. 

2) Listen to all the online meded lectures  before solving U world Qs. It helps alot and makes the process of going through Usmle world Qs a lot easier.

3) Memorise Usmle World tables on your tips. 

4) Every option of Usmle world Qs is important. Go through not only the right one but also the wrong options properly.

5) I used to give a NBME every 3-4 weeks to track my progress and gave UWSA in the end. I started with 200’s and went upto 250’s.

-Parneet kaur

Mechanistic insights regarding Lesch-Nyhan syndrome

Hello friends! Let's refresh our biochemistry knowledge today.

Lesch-Nyhan syndrome is characterized by choreoathetosis, dystonia, hyperuricemia, gout, self mutilatory behavior especially self-biting of fingers, and intellectual disability due to HGPRTase mutations.

So how do HGPRTase mutations actually cause dystonia and other extrapyramidal signs and symptoms?

1.)  For the synthesis of dopamine tetrahydrobiopterin as a cofactor for tyrosine hydroxylase is required.
Tetrahydrobiopterin itself is derived by a series of reactions in which GTP cyclohydrolase is a rate-limiting enzyme.
Now HGPRTase deficiency causes depletion of GTP thereby ultimately depleting tetrahydrobiopterin.

In fact, GTP cyclohydrolase mutations are known to cause dopa-responsive dystonia and phenotype similar to Lesch-Nyhan syndrome.

2.)  Secondly, dopamine receptors are linked to G-protein coupled receptors which alternate between GTP-GDP bound states, yet another link between GTP depletion and perturbation of dopamine signaling.

3.) Adenosine deficiency due to the reduction in salvage may adversely affect the role of adenosine as a neuroprotective agent.

Lastly, in Lesch Nyhan syndrome no characteristic imaging abnormalities are seen but reduced dendritic arborizations in the caudate nucleus, putamen, and nucleus accumbens are thought to underlie clinical manifestations.

So to summarise, Lesch Nyhan syndrome can be considered as one of the basal ganglia disorders with Wilson's disease and Huntington's disease being the other notable ones.

Have a great day!

-Kirtan Patolia

Submission :Dexmedetomidine and Bradycardia

-By Parneeet Kaur

Submission: Thyroid Acropachy

Let's go through quick review regarding Thyroid Acropachy! 

1)It is an uncommon finding of Graves disease.

2)It is a triad of clubbing+swelling of soft tissue of digits + periosteal reaction of extremity bones. 

3)It is usually associated with Thyroid Ophthalmopathy and Dermopathy.

X ray findings-Hands and feet involvement,soft tissue swelling, fluffy, asymmetric periosteal reaction

Skin biopsy- Fibroblast activation and GAG deposition.

Differentials: 

1)Pulmonary Osteoarthropathy-.

2)Symmetric periosteal reaction  -can involve long bones of forearms and legs

Treatment-
No Specific treatment available, Treatment directed at associated Ophthalmopathy and Dermopathy using Local corticosteroids and systemic immunosuppressive therapy.

By Parneet kaur

Cyanide poisoning

Cyanide is a mitochondrial toxin that causes death within minutes to hours of exposure.

PATHOPHYSIOLOGY:

1)Cyanide avidly binds to the ferric ion (Fe3+) of complex IV thus inhibiting the Electron transport chain.

2)The cell must then switch to anaerobic metabolism of glucose to generate ATP.Anaerobic metabolism leads to the formation of lactic acid and the development of metabolic acidosis.

TREATMENT:

1)Sodium nitrite and Amyl nitrite induce formation of methemoglobin. Cyanide has high affinity to metHb. This provides an attractive alternative binding site for cyanide which makes the ETC free.

2)Sodium thiosulfate can be given which converts cyanomethemoglobin to thiocyanate and metHb. Thiocyanate is then renally excreted and metHb can be converted back to normal Hb by using methylene blue.

3) Hydroxocobalamin, a precursor of vitamin B12, avidly binds to intracellular cyanide (with greater affinity than cytochrome oxidase) forming cyanocobalamin. This molecule is stable and readily excreted in the urine.

-Srikar Sama

Early morning workout and weight loss.

To reduce weight, early morning exercise is recommended but question is why?
Let's get back to basics before answering this question.

Body has three sources of blood glucose to maintain level uniformly.
1) Food.
2) Liver Glycogen.
3) ‎Gluconeogenesis.

Now, Liver Glycogen can provide energy for around 12-18 hours. Gluconeogenesis uses lots of energy to maintain blood glucose level. Between dinner and breakfast we have gap of around 12 hours. This mean before taking breakfast  liver glycogen stock is null! And body is using now gluconeogenesis to maintain blood glucose level and as you know it's going to take hell lots of ATPs to maintain it. Also, exercise uses lots of energy. Hence both in turn helps in reducing body weight.

What is wrong with evening workout?

Suppose a person has taken lunch around 2 pm and he's working out around 5-6 pm. Which stores will be used by body to maintain glucose level - food obviously! Hardly any Liver glycogen is used up. Also extra food will be stored.

That's all!

-Demotional bloke

Authors diary: Goodbyes

It's heart breaking when you leave work in the evening and show up 10 hours later only to find that the patient you were taking care of passed away during the night.

You don't get to say goodbyes. But my wish for you is that you get to give your condolences 💔 

-IkaN 

USMLE Step 3 CCS sheet guide

Hey guys,

So I recently took my USMLE Step 3 and I gathered some of this from various resources. I think this may be of some help to the beginners.

Let's get started!

In relevant emergency cases (order the ones that are relevant):
ABC:
Airway
Breathing
Circulation

P.O. ICESS:
Pulse oximetry
Oxygen
Intravenous line and fluids (Please remember to type NSS/Normal Saline or Dextrose, etc. CCS software won't take orders that are less than 3 characters!)
Cardiac monitor
ECG
Sugar (fingerstick)
Suction

For chest pain add MONA:
Morphine
Oxygen
Nitrates
Aspirin
~~~
Then order relevant Physical Exam (In Office cases, you'd want to order most physical exams and in the Emergency Department cases, you'd want to order more symptom-based system specific exam)
~~~
Laboratory orders: CBC LFT ICU PAX
Complete Blood Count (CBC), ESR
Basic Metabolic Profile (BMP)
Cardiac enzymes (if not ordered earlier)

Liver Function Tests (LFT) or Lipid profile
FOBT
TFT

Imaging (CT/MRI/USG/etc) Iron profile Immunologic tests (HIV/HepB/HepC/Rubella/etc)
Cultures (Blood/urine/fluid/etc)
Urine (routine, microscopy, culture & sensitivity)

Pregnancy test (urine) & Pap test (if female) PT/INR PTT d-Dimer PFT
Amylase ABG
Xray
~~~
You can now forward the time to get some results or decide whether the location needs to be changed
~~~
CCC
Comfort: if the patient is in pain- give NSAIDs/Morphine based on the situation; vomiting- antiemetic; etc
Cure: if you suspect a particular infection-give antibiotic; if it's an MI- angiography v/s other management options; etc
Consult: you may want to order a Psych or Surgery or OBGYN or any other relevant consult based on the case
~~~
If the patient needs to get admitted on floors or ICU:  ADIC

Activity: Bed rest/ ambulation
Diet
Input/output charting
Compression stockings

~~~

If the patient is scheduled to undergo a procedure: ABC PIN

Antibiotics

Blood grouping and crossmatching

Consent

PT/ PTT

INR

NPO

~~~

When you get your 2-minute screen: Counsel and order follow-up labs!

You may want to counsel them on their diagnosis, lifestyle habits, medication adherence/ compliance/ side effects and so on.

Hope this helps!

Stay awesome :)

-Rippie

Lifestyle modifications for managing hypertension

Hey guys,

Happy New Year!

Let's get started on lifestyle modifications for treating or managing hypertension.

We Decide to Eat less Salt & drink less Alcohol!

Weight loss: Reduce BMI to <25 
DASH: Diet high in fruits and vegetables and low in saturated fat and total fat
Exercise: 30minutes/day for 5-6 days/week
Dietary Sodium: <3 g/day
Alcohol: 2 drinks/day in men and 1 drink/day in women

The effect of these interventions is in descending order, with weight loss having an impact of about 5-20 mmHg lowering per 10 kg weight loss and reducing alcohol intake can lower BP by 2-4 mmHg!

Remember: If a patient's BMI is already lower than 25, you don't have to ask them to reduce weight any further for this therapeutic effect. Instead, you ask them to switch over to DASH diet!

Hope this is helpful!

Stay awesome!
-Rippie

In short: Vasopressin in the ICU

Hello!

Here are some quick points + mnemonics on Vasopressin!

1. Effects are preserved during hypoxia and severe acidosis and catecholamine-resistant states.

Mnemonic: Vasopressin presses when other pressors can't press the vasculature anymore.

2. Vasopressin decreases norepinephrine requirement.

3. Onset: fast, offset: fast.
Mnemonic: VasopressIN is IN and OUT fast.

4. It is often weaned off last in patients on multiple pressors for the same reason.

5. Used in:
- Refractory hypotension (potentiates the actions of over vasoconstrictors)
- Esophageal variceal bleed
- Cardiac arrest
Non ICU indications: vWD, DI, hemophilia

That's all!

-IkaN

In short: Dexmedetomidine and bradycardia

If a patient who is intubated and sedated develops bradycardia, go through the sedatives list - it might give you a hint on what is causing the bradycardia.

Dexmedetomidine (Precedex) is notorious for causing bradycardia. Another sedative associated with bradycardia is propofol.

That's all!

Will update this post at a later date. What you can do if you are free: Read up on it, write a small post on it and email it to us so we can post it and learn from you :)

-IkaN

Authors diary: In short

Hello!

I am planning to write short one line posts on things that I learn in the everyday.

Pediatrics residency series: 1. Intro

Hey Medicowesomites :) Happy new year everyone (writing this post on 1-1-19)

Residency is time-consuming as you know. It’s been a long time since I last posted but I came back to tell you that I will be starting a new series on “Pediatrics Residency”. Useful apps, cases and other things will be discussed.

Stay tuned :)

-Murad

Hair tansplant or follicular transplant

Hello Awesomites!

This is going to be fun. :D

Q. A male diagnosed with AGA (Androgenetic alopecia) came to me with grade 3 alopecia. Asking me that he is frustrated from taking medication and heard of hair transplant surgery. What advice would you give him?

A.I have seen lot of misconception regarding this concept. Hair transplant doesn't mean actual hair. We take follicle from occiput. Why? Because it is not responsive to androgen as there is no Androgen receptor.

Hair transplant is for already bald area. Androgen receptor blockade is given for remaining vellus hair. So that means hair transplantation surgery is not substitute for minoxidil/finasteride. For grade 3 AGA alopecia patient can undergo hair transplantation for bald area but have to take medication for remaining vellus hairs.
This is for AGA alopecia. Scarring alopecia won't show good response with hair transplantation surgery as much as AGA alopecia,

Q. AGA is genetic alopecia. So why don't it appear at birth itself?
A. At birth, androgen receptor is present but insensitive. When genetic component become active, the receptor become sensitive and balding occur.

Have a great day ahead.
Upasana Y. :)

Warfarin: a procoagulant or anticoagulant?

Hello Awesomites!

No doubt ! Warfarin is an oral anticoagulant.
Confused? Don't be. :D

Warfarin inhibits reduction of Vitamin K to its active form and leads to depletion of the vitamin K-dependent clotting factors II,VII,IX and X, and protein C,S and Z.

Because of the rapid depletion of the anti-coagulant Protein C and a slower depletion of factor II, patients might develop increased hypercoagulability during the first few days of warfarin therapy. So warfarin is combined with a parenteral initially. Treatment of DVT/PE with warfarin requires overlap therapy/bridging therapy with a parenteral anticoagulant (UFH,LMWH, or pentasaccharide) for atleast 4-5 days and until the INR reaches atleast 2.0.

The starting dose of warfarin depends on many factors. During warfarin therapy INR monitoring should occur frequently during the first month of warfarin therapy (e.g.twice weekly for 1-2 weeks, then weekly for 2 weeks, then less frequently).

Have a great day ahead.
Upasana Y. :)

ARNI

Hello Awesomites !

I have something with weird titles. :D

ARNI stands for Angiotensin receptor-neprilysin inhibitor.

This is combination of ARB Valsartan and neprilysin inhibitor Sacubitril recently approved for use in patients with HFrEF and NYHA Class II-IV symptoms.

NEPRILYSIN:- It is a neutral endopeptidase involved in the degradation of vasoactive peptides including natriuretic peptides, bradykinin, adrenomedullin. Inhibition of neprilysin increased the availability of these peptides, which exert favorable effects in HF.

Effects of Natriuretic peptides are-
1.Vasodilation
2.Lower blood pressure
3.Reduced sympathetic tone
4.Reduced aldosterone levels
5.Natriuresis/Diuresis

In a large trial, this agent was shown to be superior to enalapril in reducing death and rehospitalization among NYHA class II-IV patients with HFrEF.

Have a great day ahead.
Upasana Y. :)

Vestibulo ocular reflex

The vestibulo-ocular reflex is a reflex, where activation of the vestibular system causes eye movement. This reflex functions to stabilize images on the retinas during head movement by producing eye movements in the direction opposite to head movement, thus preserving the image on the center of the visual field. For example, when the head moves to the right, the eyes move to the left, and vice versa. Since slight head movement is present all the time, VOR is necessary for stabilizing vision.

Circuit:

1)It starts in the vestibular system, where semicircular canals get activated by head rotation and send their impulses via the vestibular nerve and end in the vestibular nuclei in the brainstem.In addition the hair cells of opposite ear are inhibited because endolymph in that ear flows away from hair cells.

2)From these nuclei, fibers cross to the contralateral cranial nerve VI nucleus.

3a)There they synapse with 2 additional pathways. One pathway projects directly to the lateral rectus of the eye via the abducens nerve.
  b) Another nerve tract projects from the abducens nucleus by the medial longitudinal fasciculus to the contralateral oculomotor nucleus, which contains motorneurons specifically activating the medial rectus muscle of the eye through the oculomotor nerve. 

4)For instance, if the head is turned clockwise, then excitatory impulses are sent from the semicircular canal on the right side via the vestibular nerve to the right vestibular nuclei in the brainstem. From this nuclei excitatory fibres cross to the left abducens nucleus.There they project and stimulate the lateral rectus of the left eye via the abducens nerve. In addition, by the right medial longitudinal fasciculus, fibers cross and go to right oculomotor nuclei, they activate the medial rectus muscles on the right eye. As a result, both eyes will turn counter-clockwise.

-Srikar Sama

Basics of Fat necrosis.

Hello, let's dissect fat necrosis in this post.

Fat necrosis is seen where fat concentration is more or lipase concentration is more.
Example- Injury to Breast or Omentum tissue or in Acute pancreatitis with gall stones or alcohol intake.

Alcohol intake leads to activation of lipase enzyme. This lipase enzyme converts lipids to fatty acids. Always remember fatty acids loves calcium! This love affair leads to formation of "Fatty acids - Calcium complex formation". This is called as "Saponification".
This gives yellow - white chalk like color. This helps surgeon to identify fat necrosis.

For prognosis we use serum calcium level. Why?

Suppose there is severe pancreatitis. This leads to more activation of the lipase enzyme. This leads to formation of the fatty acids. More fatty acids, more saponification. Hence less calcium level in serum!

Low calcium level suggest bad prognosis!