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!

Chediak Higashi syndrome.

Hello! This is Ultra short post regarding Chediak higashi syndrome! Hope you like it.

In normal person, when bacteria is engulfed by WBCs, they are carried to lysosome enzyme by LYST protein.
LYST protein stand for Lysosomal transfer protein.

Defect in LYST protein causes Chediak Higashi syndrome. It is autosomal recessive disorder.
No LYST protein so no phagocytosis of macrophages. Hence recurrent infections.

Clinical features:

1) Recurrent infections.

2) Absence of Melanin - Albinism.
LYST also helps in transfer of melanin to superficial layer of skin

3) Decrease in Myelin formation - Delayed conduction.

4) Hemorrhage.
LYST helps in maturation of megakaryocytes to platelets.

Confirmation: Incomplete digestion of bacteria leads to formation of  "Giant granules inside cell"

Mnemonic:
CHEDIAK

C- CNS involvement
HE- Hemorrhage
DI- Decrease immunity
A-Albinism

That's it!

-Demotional bloke.

Horner Syndrome

Horner syndrome is a classic neurologic syndrome whose signs include miosis, ptosis, and anhidrosis.

NEUROANATOMY - Horner syndrome can result from a lesion anywhere along a three-neuron sympathetic pathway that originates in the hypothalamus:
●The first-order neuron descends caudally from the hypothalamus to the first synapse, which is located in the cervical spinal cord (levels C8-T2, also called ciliospinal center of Budge).

●The second-order neuron travels from the sympathetic trunk over the lung apex. It then ascends to the superior cervical ganglion, located near the bifurcation of the common carotid artery.

●The third-order neuron from superior cervical ganglia then ascends within the adventitia of the internal carotid artery, through the cavernous sinus. In the orbit and the eye, the oculosympathetic fibers innervate the iris dilator muscle as well as Müller's muscle, a small smooth muscle in the eyelids responsible for a minor portion of the upper lid elevation and lower lid retraction.

First-order syndrome - Lesions of the sympathetic tracts in the brainstem or cervicothoracic spinal cord can produce a first-order Horner syndrome.
The most common causes are:
(a)occlusion of PICA, which produces Horner syndrome as part of the Wallenberg syndrome.
(b)Brown-Séquard syndrome above T1, patient may present with ipsilateral Horner syndrome due to damage of oculosympathetic pathway.

Second-order syndrome — Second-order or preganglionic Horner syndromes can occur with trauma or surgery involving the spinal cord, thoracic outlet, or lung apex.Other causes include pancoast tumor involving the lung apex.

Third-order syndrome — Third-order Horner syndromes often indicate lesions of the internal carotid artery such as an arterial dissection, thrombosis, or cavernous sinus aneurysm

CLINICAL FEATURES -The classic signs of a Horner syndrome are ptosis, miosis, and anhidrosis.
1)The ptosis occurs as a result of paralysis of the Müller's muscle.
2)The degree of anisocoria is more marked in the dark than in light.
3)Anhidrosis is present in central or preganglionic (first- or second-order) lesions because the sympathetic fibers responsible for facial sweating branch off at the superior cervical ganglion along the external carotid artery and its branches.
4)Horner syndrome is also a common feature of cluster headache.

SOURCE-UpToDate, Kaplan.

-Srikar Sama.

True or False #10

Hallux valgus is also known as bunion. T or F

T

●Hallux valgus (HV) deformity (ie, bunion) is a common, potentially debilitating deformity consisting of lateral deviation of the hallux on the first metatarsal . The etiology is unknown. The deformity is more common among women and shod populations.

●Although HV is easily recognized by clinical examination, radiographs may be necessary to determine the presence of articular damage . Neither radiographic nor clinical appearance provides the basis for surgical referral, which is determined by patient pain and disability.

●There is little evidence that conservative treatments are useful in the treatment of HV. Nevertheless, we suggest patients without debilitating symptoms avail themselves of conservative therapies before being referred for surgery.

Possible treatments include:

•Shoe modification: wide, low-heeled shoes, or specially altered shoes with increased medial pocket for first metatarsophalangeal (MTP) joint to minimize deforming forces

•Orthoses to improve support and alignment

•Night splinting to improve toe alignment

•Stretching and/ormobilization/manipulation to maintain joint mobility

•Medial bunion pads to prevent irritation

•Ice applied after activity to reduce inflammation
•Analgesics: acetaminophen or NSAIDs

●We suggest that patients with severe pain or dysfunction and those whose symptoms do not improve under a conservative treatment regimen be referred for surgical repair.

Approximately 150 surgical procedures for the correction of HV deformity have been described. Few prospective, randomized trials evaluating these procedures have been performed. Patients should be referred to a foot surgery specialist with experience repairing HV deformity.

●Managing patient expectations about surgery is important. Patients should understand that 10 to 25 degrees of valgus angulation is normal at the MTP joint, and that resolution of postoperative pain and swelling may require several months. Most patients will remain unable to fit into narrower shoes.

Do not forget to look up pictures of how a bunion looks.

Over and out.