Sunday, December 30, 2018

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. :)

Thursday, December 27, 2018

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

Monday, December 17, 2018

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.

Friday, December 14, 2018

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.

Wednesday, December 12, 2018

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.

Monday, December 10, 2018

Atropine poisoning

Atropine poisoning is also called as Anti-muscarinic poisoning.

It is caused due to ingestion of :-
1) Datura plant
2) ‎Atropa belladona
3) Hyoscyamus
4) ‎Anti-histamine drugs
5) Anti-psychotic drugs
6) ‎Anti-depressants like TCA
7) ‎Anti-Parkinsonism

Clinical features:

Let's go from head to toe!

1) Brain:
Atropine causes following symptoms
-Hallucinations
-‎Confusion
-‎Delirium

Also called as Mad as hatters!

Remember: Atropine drives you crazy!

2) Eyes:
AcH causes constriction of pupils. No or less AcH causes Mydriasis

Fun fact 1: In ancient times, women used to apply Atropa belladona in eye for attracting men by dilating pupil.

Fun fact 2: Most of the dinner dates are candle night dinner, why? To dilate pupils and look attractive.
Also described as "Blind as a bat"

Remember: Atropine makes you look seductive!

3) Eyes and Mouth:-
AcH is responsible for secretion of saliva and tears.
Lack of AcH action causes - Dry mouth and Dry eyes.

Also described as "Dry as a bone"
Most common feature in Adults.

Remember: Atropine Dries you!

4) Face:
AcH causes constriction of blood vessels. Atropine blocks this action and hence causes dilation of the blood vessel. Hence this causes flushing of face.

Also described as - Red as a beet.

Remember: Atropine makes you blush!

5) Body temperature:
AcH is responsible for secretion of the glands. Lack of secretion causes decrease or no cooling effect. Hence it causes-Hyperthermia.

Also described as - Hot as a hare
Most common feature in children.

Remember: Atropine makes you hot!

Most common cause of death is Respiratory paralysis.
Next common is Shock.

I remember all this feature with the help of story:

I went on a candle night dinner with hot girl. Ofcourse, she was blushing because I'm crazy to have dry resins after dinner! (Okay that's lame and I know!)

Key points:-

Candle night dinner - Mydriasis
Hot-Hyperthermia
Blushing-Flushing of face
Crazy-Deliruim, Hallucination and confusion
Dry resins-Dry secretion

Treatment:
1) Supportive treatment:

Gastric lavage using Tannic acid : To remove unabsorbed poison. Avoid potassium permagnate.

Forced acidic diuresis: Because Atropine is an alkaline drug

Seizures are treated by Diazepam

Patient is kept in dark quiet room-To avoid hallucination.

Ice bags given to treat maintain temperature.

2) Antidote: Physostigmine since it crosses BBB.

That's it
-Demotional bloke.

Friday, December 7, 2018

Wiskott-Aldrich syndrome

1)Wiskott-Aldrich syndrome is an X-linked recessive disorder caused by mutations in the gene that encodes the Wiskott-Aldrich syndrome protein (WASp).

2)All hematopoietic cells produce WASp protein, and there is WIPF1 that encodes WASp-interacting protein (WIP), a protein that stabilizes WASp. Both of these proteins are required to reorganize cell's cytoskeleton.

3)Its absence impairs the:
 (a)Formation of the immunologic synapse, the site of interaction between T cells and antigen-presenting cells leading to immunodeficiency.
 (b)NK cell function is impaired as a result of defective immune synapse formation on the cell surface which leads to increase risk of malignancy.
 (c)Regulatory T cells are incapable of controlling autoimmunity, so there is increased risk of Autoimmune disease.
 (d)Myeloid lineage cells exhibit impaired phagocytosis and chemotaxis - susceptible to recurrent pyogenic infections.
 (e)Impaired cytoskeleton in megakaryocytes → Decrease in size and number of platelets →microthrombocytopenia.

4)Clinical manifestations :
(a)Bleeding-microthrombocytopenia.
(b)Recurrent pyogenic infections.
(c)Eczema
(d)Increase in risk of autoimmune diseases and malignancy.

5)Laboratory findings :
(a)low to normal IgG and IgM and high IgA and IgE.
(b)Peripheral smear-Thrombocytopenia with small platelets.


Mnemonic: Remember the movie Antman and thewasp :p. So WASP helps you remember,
(1)WASp mutation  (2)wasp is a small bee like insect🐝→small platelets and if wasp bites, you get eczema(↑IgE).


SOURCE-UpToDate.

-Srikar Sama.

Sunday, December 2, 2018

Peculiar pattern of pulmonary edema

Usually left sided cardiac pathology causes bilateral pulmonary edema but still unilateral pattern is seen in fair number of cases, usually involving right lung parenchyma.

Likely mechanisms include:

1) Lymphatic drainage on right side is via low calibre right bronchomediastinal trunk as opposed to more robust thoracic duct on left side.

2) Numerous conditions ranging from hypertension to valvular pathology can cause enlargement of left side of heart.
This will preferentially impinge on left pulmonary artery causing reduced capillary perfusion and ultimately congestion of left lung parenchyma.

3) In cases of mitral regurgitation jet of regurgitate can preferentially impact either of the right or left pulmonary veins, hence explaining more profound edema on either side.

So, if according to patient's history and clinical examination suspicion of cardiac failure remains high, then immediate intervention with diuretics and nitrates is warranted in spite of unilateral pattern of pulmonary edema.

Kirtan Patolia

Obesity in Prader-Willi syndrome and WAGR syndrome

Delicate balance between food consumption and energy expenditure involves modulation of orexigenic and anorexigenic signals at hypothalamus.

OREXIGENIC PATHWAY- It involves peripheral mediators like ghrelin and neuropeptide-Y. 
They act on NPY-AgRP(neuropeptide-Y and agouti related peptide) neurons which subsequently mediates orexigenic signals via second order neurons that release peptides like orexin at hypothalamus.


ANOREXIGENIC PATHWAY- It involves peripheral mediators like leptin, amylin and PYY(Peptide YY).
They act on POMC/CART(Pro-opio melanocortin/Cocaine and amphetamine regulated transcript) neurons.
These neurons release alpha melanocyte stimulating hormone which in turn stimulates second order neurons that release TRH ,CRH and hence mediates catabolism.
They also simultaneously inhibit anabolic pathway.

Now back to pathogenesis of obesity in these syndromes.

In Prader-Willi syndrome levels of PYY are low due loss of imprinted genes on chromosome 15q11-q13.
This results in reduced catabolism and enhanced unihibited anabolism.
It is not uncommon for such patients to have BMI above 40.

In WAGR syndrome there is haplo-insufficiency of BDNF(Brain derived neurotrophic factor).
Alpha melanocyte stimulating hormone in catabolic pathway acts through melanocortin receptors(MC4R) on second order neurons.
Downstream signalling pathways of MC4R involves BDNF hence explaining obesity in these patients.

In fact efforts are already underway to reduce PPY levels and modulate BDNF to control obesity in these disorders.

Kirtan Patolia

Paroxysmal nocturnal hemoglobinuria

1)PNH originates from an acquired mutation ( frame-shift that creates a premature stop codon) in a myeloid stem cell, the acquired mutation in PNH occurs in the PIGA gene which is responsible for the first step in the synthesis of the GPI anchor that attaches CD55 and CD59 to the cell surface.

2)Complement detects self vs nonself cells by these complement inhibitors. Function of these complement inhibitors is to:
3)In the absence of these inhibitors, complement proteins bind cell membranes of our own cells and through the alternative complement pathway can lyse self-cells.

4)CD55/DAF decrease → More C3 convertase→Increase C3b→Increase opsonization→Extra Vascular Hemolysis.

   CD59/MIRL decrease→More MAC→Intra Vascular Hemolysis.


5)Why nocturnal hemoglobinuria- hemolysis occurs throughout day but its more at night because:   (a)Increased hemolysis in night due to respiratory acidosis(Shallow breathing).
 (b)Overnight concentration of urine is more and hemoglobinuria is clearly evident.

6)Diagnosis:(a)Flow cytometry- decrease CD55 and CD59 levels.
                     (b)HAM test-confirmatory.
                     (c)Direct coombs test-Negative (Helps to differentiate PNH and AIHA- its positive in AIHA)                                                                           

7)Treatment
(a)Ravulizumab- long acting C5 complement inhibitor
(b)Eculizumab- It is an Antibody to C5 and prevents its clevage to C5a and C5b, so no MAC. Ravulizumab has a half life that is three to four times longer than eculizumab.

-Srikar Sama

SOURCE: UpToDate, Uworld.

Friday, November 30, 2018

Psammoma Body

Psammoma body :

1)Psammoma bodies are round microscopic calcific collections.

2)A single necrotic cell act as a nidus and calcium deposits around it in laminated and concentric fashion.Psammoma body is an example for dystrophic calcification (Ca2+ deposition in abnormal tissues secondary to injury/necrosis in context of Normal calcium levels).

3)It is used in histopathology for diagnosis of certain tumours like:

Mnemonic : Remember it as SPAMmoma

          S- Serous cystadenocarcinoma of ovary

              Somatostatinoma


        PA-Papillary thyroid carcinoma

              Papillary renal cell carcinoma


       M- Mesothelioma

             Meningioma.


-Srikar Sama

Atrial myxomas

Myxomas are the most common primary cardiac neoplasm. 90% occur in the atria (mostly left atrium). The cells originate from a multipotent mesenchyme that is capable of neural and endothelial differentiation. Myxomas produce vascular endothelial growth factor (VEGF), which probably contributes to the induction of angiogenesis and the early stages of tumor growth.


GROSS FEATURES :Typical myxomas are pedunculated, the surface may be smooth, villous or friable.

HISTOLOGY : Gelatinous material, myxoma cells immersed in glycosaminoglycan. 

CLINICAL MANIFESTATIONS : 

1)Obstruction : Myxomas are usually described as "ball valve" obstruction of AV valves which may cause syncopal episodes, Dyspnea.

2)Influenced by position : Upright position may exacerbate the condition whereas lying down may decrease it.

3)Embolization : If the myxomas are friable or villous, fragments of mass can detach and present with systemic emboli.

4)Constitutional symptoms (eg: fever, weight loss) : Some myxomas release cytokines like IL6 which may produce constitutional symptoms.

5)Auscultation may reveal early diastolic "tumor plop".

TREATMENT : Prompt resection is required because of the risk of embolization or cardiovascular complications, including sudden death.
-Srikar Sama

Dietary Risk Factors For Calcium Stones

1)Fluids :
A lower fluid intake will lead to a lower urine output, thereby promoting stone formation by increasing the concentration of calcium and oxalate .
Type Of Fluid :
1)Coffee and tea have, in the past, been considered to have a high oxalate content but recent studies show they have negligible impact.

2)Alcoholic beverages had been purported to increase the risk of stones. However, prospective studies found that beer and wine were associated with a lower risk of stone formation

3)Orange juice(which contains both potassium and citrate) was associated with a lower calculated risk of crystal formation (possibly due in part to increased urinary citrate excretion)



2)Low Dietary Calcium :
This was a surprise to me because i always thought High Calcium in diet leads to formation of stones.Now to explain this- Normally  dietary Calcium binds to dietary Oxalate in gut to form non-dissociable complex which can't be absorbed into blood.If Calcium in diet is less, Oxalate will be in free form which is then absorbed into blood and excreted into urine and thus increases risk of stone formation.



3)High Dietary Oxalate :
High Oxalate is normally found in chocolate,nuts,spinach.If dietary oxalate is higher than Calcium,all the free oxalate is then absorbed into blood and thus increasing risk of stone formation.

NOTE:In Crohn's disease where there is fat malabsorption, Calcium in the gut binds to this fat and forms a complex thus decreasing the Calcium available for oxalate.So all the free oxalate is absorbed and risk of development of Oxalate stones is increased.



4)High Dietary Sodium :
If dietary sodium is high, we absorb less sodium from PCT and thus decreasing Calcium absorption.So there is increased calcium excretion which increase incidence of stone formation.



5)High Animal Protein :
Long term, a high-protein diet may lead to higher urine calcium excretion by increasing renal calcitriol production that may be mediated by an increase in renal mass.


SOURCE:UpToDate,UWorld.

-Srikar Sama

Warfarin Induced Skin Necrosis

Warfarin-induced skin necrosis is a complication of warfarin therapy in which the patient develops demarcated areas of purpura and necrosis of skin including the extremities, breasts, trunk, or penis.

Mechanism:
1)Mechanism of action of Warfarin is it inhibits VitK epoxide reductase,so there is decrease in synthesis of VitK dependent factors - (factors II, VII, IX, and X) and natural anticoagulants (protein S and protein C).


2)Now no new clotting factors are produced but the old circulating clotting factors are still present (warfarin has no effect on already circulating clotting factors).


3)Among the factors II, VII, IX, X, ProteinC that are already present,ProteinC has the shortest half life,So ProteinC is depleted more rapidly than the others.


4)Now there is no anticoagulant in the body to oppose the action of already present clotting factors,so there will be initial coagulation till factors II, VII, IX, X gets depleted i.e till their half lives are completed.


5)This initial coagulation occurs in dermal vasculature which causes Skin Necrosis.

Prevention:
Overlapping of warfarin with heparin during the first several days of warfarin administration(if Heparin is given along with warfarin, this prevents functioning of circulating factors since heparin inhibits the activity of circulating thrombin and factorXa) and then warfarin is continued for long term therapy.


Source: UpToDate, First Aid.

-Srikar Sama

New application process for ECFMG registration

Hello,

This post is regarding new application process for ecfmg registration.


STEP1 : The process for obtaining USMLE ID is still the same which has been described very clearly here http://www.medicowesome.com/2016/12/how-to-apply-for-usmle-exams.html#more


STEP2 - ECFMG CERTIFICATION USING IWA:

1)when you go to IWA and login to your account you will only have one option : apply for certification (no application for examination any more ) so you will just click on that.

2)simply follow the steps and confirm you information and you will end up getting a payment page of 125$.


STEP3 - FORM 186 :

1)After payment they will send you form 186 (unlike before you dont need to go to your medical school and have it signed by your deen)

2)You will simply go to the website :- https://www.notarycam.com/ecfmg/


STEP4 - INTERVIEW WITH ONLINE NOTARY :

1)Fill an application and upload form (186) and high quality image of your passport or photo ID preferably but not necessarily in english.

2)You will receive an email from one of the online notaries and schedule an appointment of an online meeting with him/her.

3)If you are ready at the moment you can schedule an appointment immediately(which is what i did) or you can schedule for an appointment later.

4)During your meeting with the notary please prepare your passport as you will be asked to show it, to confirm your identity.

5)Afterwards the notary will ask you to position your self to the mid of screen and ask your permission for taking a screenshot.(If your webcam is of low quality they will ask you to mail them a passport picture of yours,so be ready with that too)

6)Then you will have to electronically sign your form-no need to actually sign it,they will display your name in few fonts and you have select one.

7)Now you have done your part.The notary will seal the document and send it to the ecfmg.

8)You will get an 2 emails after this process-one from notary that they have sent your form186 to ECFMG and second email is from ECFMG which you will be getting after few days that they have accepted your form 186.

-Srikar Sama

Monday, November 26, 2018

A rare type of fistula-Arterioenteric fistula

As the name suggests, this type of fistula is characterized by anomalous connection between bowel and arterial lumen.

CAUSES- Diverticulitis, Inflammatory bowel disease, bowel wall perforation, penetrating ulcers, aneurysms, prosthetic vascular grafts, radiation, trauma or foreign body ingestion.

CLINICAL PRESENTATION- Depending on the cause it could include abdominal pain, hematochezia, hematuria (say if diverticulitis perforates bladder wall), sepsis, syncope (due to volume depletion from major bleed), gangreneous involvement of limbs due to vascular insufficiency etc...

MANAGEMENT- Prompt diagnosis with laparoscopic intervention to eliminate fistula and any revascularization procedures if needed is the key to reduce mortality in such patients.

Kirtan Patolia

A few USPSTF guidelines

Hello,

USPSTF guidelines are important to remember for step 2 CK, step 3 and residency!

Here are a few high yield ones!

Sunday, November 25, 2018

Ingenious Immune System

Hello friends, today let's take a moment to appreciate how amazing is our immune system.

In our immune system, just like any regular car there are brakes in place to regulate it's working. Removing brakes can certainly enhance it's function which underlies the concept of immune check-point blockade.

Two such molecules on surface of T-cells are CTLA-4(Cytotoxic T-lymphocyte associated protein 4) and PD-1(Programmed cell death protein 1).

When CTLA-4 binds to it's ligand B7-1 and B7-2 which are often expressed in increased numbers on tumor cells it results in inhibition of T-cells and hence allowing tumor cells to evade apoptosis and survive.

Similarly when PD-1 binds to PD-L1on tumor cells inhibitory signals are relayed to T-cells.

In macrophages signal regulatory protein alpha mediates inhibitory signals on interacting with CD47 on tumor cells.

In NK-cells KIR2DL1(killer cell immunoglobulin like receptor 2DL1) mediates inhibitory signals.

So blocking these inhibitory signals by monoclonal antibodies can remove "brakes" on immune system ultimately enhancing their ability to kill tumor cells.

Approved antibodies include:
Anti CTLA-4-Ipilimumab
Anti PD-1-Nivolumab,Pembrolizumab
Anti PD-L1-Avelumab,Durvalumab

Kirtan Patolia

Authors' diary: 53 facts about me

Another vlog before my long weekend ends =)

Pemphigus vulgaris vs Paraneoplastic Pemphigus vulgaris (PNP)

Hello friends , today let's talk about subtle differences between pemphigus vulgaris and Paraneoplastic Pemphigus vulgaris

1. SITE OF INVOLVEMENT
Pemphigus vulgaris usually involves buccal and labial mucosa.
PNP causes severe stomatitis as well as targetoid lesions on palms and soles much like erythema multiforme.

2. ANTIBODIES INVOLVED
In Pemphigus vulgaris antibodies are directed against intercellular adhesion molecules desmoglein-1 and desmoglein-3.
However, in PNP apart from desmoglein-1 and desmoglein-3 antibodies are also directed against envoplakin, plectin, desmoplakin,periplakin and BPAG-1. 

3. IMMUNOFLUORESCENT PATTERN
In Pemphigus vulgaris typical chicken-wire pattern is seen due to intercellular deposition of IgG and C3
In PNP, that is not the case as although there is IgG deposition in all layers but not intercellularly and furthermore C3 is deposited along basement membrane as in Bullous pemphigoid.

4. VISCERAL INVOLVEMENT
In Pemphigus vulgaris it is rare while in PNP often mucosa of esophagus, stomach, duodenum, intestines and pulmonary epithelium is seen.

Prognosis is quite poor in PNP with bronchiolitis obliterans and sepsis being chief complications.
Mostly seen in Non- Hodgkin's lymphoma and CLL.

Kirtan Patolia

Friday, November 23, 2018

Talazoparib: Zenith of novelty

Recently, talazoparib was approved by FDA for BRCA mutated breast cancer. Several other drugs related to it such as niraparib, olaparib are already approved for ovarian and breast cancer.

So how they work:

In eukaryotic cells, there is highly intricated network of sensors, transducers and mediators for DNA damage recognition and subsequent successful repair.

One of the such molecule is PARP (polyADP ribose polymerase) which serves to identify single strand breaks (SSBs) and seal them.

If PARP is inhibited (say, by talazoparib) then SSBs would progress to double strand breaks (DSBs). DSBs can also be effectively repaired by BRCA 1 and BRCA 2 complex by homologous recombination method.

However, in cancer cells with mutated BRCA, DSBs would not be repaired, ultimately causing apoptosis via molecules such as PUMA (p53 upregulated modulator of apoptosis), NOXA and p21.

Furthermore, talazoparib is known to induce formation of cytotoxic PARP-DNA complex, further contributing to it's mechanism.

That is definitely zenith of novel mechanism.

Stones in Crohn's disease

Hello everyone, 

In this post, I'll be talking about the different types of stones seen in Crohns disease. Let's learn why they form! 

CHOLESTEROL GALLSTONES: Either due to ileal involvement or ilectomy, in Crohn's, enterohepatic circulation of bile acids is perturbed resulting in supersaturation of bile with cholesterol altering delicate composition of bile acids , phospholipids and cholesterol of 10:3:1 in bile fluid.

CALCIUM BILIRUBINATE GALLSTONES: Due to alteration in colonic flora conjugated bilirubin is converted to unconjugated bilirubin, which along with seepage of excessive unabsorbed bile acids from ileum, results in enhanced absorption of bilirubin from colon causing increased concentration in bile.

CALCIUM OXALATE RENAL STONES:
Usually, calcium in the GI tract forms a complex with oxalate ions resulting in it's excretion in stool but in Crohn's due to steatorrhea excessive unabsorbed negatively charged fatty acids bind with calcium, leaving unbound oxalate to be absorbed and subsequently excreted by urine causing nephrolithiasis.

URIC ACID RENAL STONES: Diarrhea in Crohn's cause metabolic acidosis due to decreased bicarbonate absorption or increased excretion from colon which increases acidity of tubular fluid. The increased acidity, simultaneous dehydration, hypocitraturia and hypomagnesemia in such patients precipitate uric acid stones.

-Kirtan Patolia

Authors' diary: Residency and life so far (after moving to the US)

Hey!

I am video blogging now :)

Thursday, November 22, 2018

True or False #9

1.Atopic dermatitis presents on flexor surfaces in infants. T or F

ANSWER

F

Extensor surfaces

Flexor in older children and adults

How to remember this?

Infants slEEEEEEEp a lot right.

Hence EEEEEEEExtensor surface involved in infants in atopic dermatitis

That will help you remember the opposite ( flexor surfaces) involved in older children and adults

That's all.

Wednesday, November 21, 2018

Calcium monitoring in ethylene glycol poisoning

Seizures often occurs in ethylene glycol poisoning.  It has multifaceted pathophysiology but one of the major cause is hypocalcemia.

Hypocalcemia occurs in ethylene glycol poisoning because ethylene glycol is metabolized to oxalate, which forms calcium oxalate depleting calcium from ECF.

Also, correcting associated metabolic acidosis by bicarbonate supplementation can further cause hypocalcemia due to increased binding of calcium to albumin.

This is why, calcium levels should always be monitored meticulously in such patients.

- Kirtan Patolia ( BJ medical college)

Cryptic conundrum in ET: Thrombosis or bleeding?

In essential thrombocytosis, contrary to what might be surmised, bleeding is more of threat than thrombosis.

This is because high platelet count especially above 1 million/mm3 cause acquired von willebrand disease, much like type 2b von willebrand disease, where excessive affinity of vWF for platelet Gpib result in excessive removal of platelet-vWF complex by spleen results in  thrombocytopenia and loss of high molecular weight vWF multimers.

However, incidence of erythromelalgia , transient ischemic attack and other microvascular events are also high in patients with essential thrombocytosis.

Pretty complex and contradictory, right?

- Kirtan Patolia ( BJ medical college).

Sunday, November 18, 2018

Diabetic amyotrophy

Hello everyone!

Today, I will be talking about diabetic amyotrophy.

Diabetic amyotrophy has a lot of names!

It is also known as Bruns-Garland syndrome, diabetic myelopathy, proximal diabetic neuropathy, diabetic polyradiculopathy, diabetic motor neuropathy, diabetic radiculoplexopathy, diabetic lumbosacral plexopathy, and diabetic LRPN.

Diabetic amyotrophy typically occurs in patients with type 2 diabetes mellitus. The traditional features include the acute, asymmetric, focal onset of pain followed by weakness involving the proximal leg, with associated autonomic failure and weight loss. Progression occurs over months and is followed by partial recovery in most patients.

The diagnosis of diabetic amyotrophy is mainly based upon the presence of suggestive clinical features in a patient with known or newly diagnosed diabetes mellitus. Appropriate laboratory investigations, particularly electrodiagnostic studies, and neuroimaging in select patients, are useful to exclude other peripheral and central nervous system etiologies as a cause of the neurologic symptoms and signs.

No treatments are proven to be effective for diabetic amyotrophy or for idiopathic LRPN.

PS: Distal symmetric sensorimotor polyneuropathy is the most common type of diabetic neuropathy - it is characterized by a progressive loss of distal sensation correlating with loss of sensory axons, followed, in severe cases, by motor weakness and motor axonal loss. Classic "stocking-glove" sensory loss is typical in this disorder.

Source: UpToDate

That's all!

-IkaN

Zebra series: Lemierre's syndrome

Hello everyone!

Let's talk about Lemierre's syndrome today.

Lemierre's syndrome is characterized by disseminated abscesses and thrombophlebitis of the internal jugular vein after infection of the oropharynx. The predominant pathogen is a gram-negative anaerobic bacillus, Fusobacterium necrophorum.

That's the Zebra for the day!

IkaN

Saturday, November 17, 2018

True or False #8 Lower GI Bleed

1. Angiodysplasia is a high volume arterial bleed. T or F

2. Diverticulosis is a low volume arterial bleed. T or F

ANSWERS

1. FALSE

Angiodysplasia  more often than not involves low volume venous bleeding.

Angiodysplasias are composed of ectatic, dilated, thin-walled vessels that are lined by endothelium alone or endothelium along with small amounts of smooth muscle. Studies in which casts of angiodysplasias were made by injecting a silicone material demonstrated that the most prominent feature in angiodysplasias is the presence of dilated, tortuous submucosal veins.
Small arteriovenous communications are also present and are due to incompetence of the precapillary sphincter. Enlarged arteries may be seen in larger angiodysplasias and may be associated with arteriovenous fistulas, which explains why bleeding can be brisk in some patients.
Histologic confirmation is often difficult. When obtained, it shows dilated vessels in the mucosa and submucosa, sometimes covered by only a single layer of surface epithelium.

2. FALSE

Diverticular bleeding involves high volume arterial bleed

Diverticular bleeding — As a diverticulum herniates, the penetrating vessel responsible for the wall weakness at that point becomes draped over the dome of the diverticulum, separated from the bowel lumen only by mucosa. Over time, the vasa recta is exposed to injury along its luminal aspect, leading to eccentric intimal thickening and thinning of the media. These changes may result in segmental weakness of the artery, predisposing to rupture into the lumen. Diverticular bleeding typically occurs in the absence of diverticulitis


Monday, November 12, 2018

True or False #7

1.Depression increases the risk of morbidity and mortality in Cardiovascular disease. T or F

2. Patients with Cardiovascular disease are more likely to develop Depression. T or F

True or False #6

1. Nightmare is a REM sleep behavior disorder. T or F

2. Night Terror is a REM sleep behavior disorder. T or F

ANSWERS

1. True

Things you should REMember for Nightmare disorder are :

REM

Second half of the night

Responsive to comfort

REMembers the dream

2. False

Night terrors:  Abrupt arousals from sleep (panicked scream, terror, autonomic arousal, unresponsive to comfort)

- Little or no dream recall

- Amnesia for episodes


Sleep is a gift, always be grateful for it.

True or False #5

1. Narcolepsy exhibits a reduced REM latency. T or F



ANSWER

1. True

Narcolepsy: depletion of hypocretin secreting neurons in lateral hypothalamus that are involved in maintaining wakefulness

Diagnostic: recurrent lapses into sleep or napping several times in the same day, >3 times a week for >3mo. and at least 1 of the following
-Cataplexy: Conscious of bilateral loss of muscle tone precipitated by emotions or abnormal facial movement (without emotional triggers)

-Hypocretin - 1 (orexin A) deficiency in CSF

- REM sleep latency <15 minutes

Tetrad:
-Sleep attacks

-Cataplexy

-Hypnagogic or hypnopompic hallucinations

-Sleep paralysis

Dx: Shortened REM sleep latency on polysomnografy
Low levels of hypocretin 1 in CSF

You may feel weak, you may fall down, say no to Cataplexy, say yes to CATA GETUP!!

True or False #4

1. Imaging is contraindicated in pregnancy for diagnosing latent TB. T or F

2. Check for latent TB before prescribing Infliximab. T or F

ANSWERS

1. False

Diagnostic evaluation after positive test — Patients with a positive TST or IGRA must undergo clinical evaluation to rule out active tuberculosis. This includes evaluation for symptoms (eg, fever, cough, weight loss) and radiographic examination of the chest (with appropriate shielding), regardless of gestational age.

Patients with a positive TST or IGRA with no evidence of active TB may be presumed to have latent TB.

2. True

Toxicity of Infliximab includes :

Respiratory infection (possible reactivation of latent TB)

Fever

Hypotension



Last man standing wins. Keep grinding.

True or False #3

1. A high potassium diet, decreases risk of kidney stone. T or F

2. Increase Sodium intake  for reducing kidney stones. T or F

ANSWERS

1. True

A high potassium diet decreases urinary calcium excretion.

Foods rich in potassium enhance urinary Citrate excretion, likely from urinary alkalization, forming soluble calcium Citrate and thereby preventing stone formation

2. False

Decrease the sodium intake

So that when sodium is reabsorbed by the nephron, calcium is also passively reabsorbed and hence decreased calcium in urine.

You are your own Kingdom, pick up the Crown.

Bhopalwala. H

True or False #2

1. Herpangina involves the anterior oropharynx with grey vesicles and ulcers. T or F

2. Pleurodynia is also known as Bornholm disease. T or F

ANSWERS

1. False

Herpangina is caused by Coxsackievirus and involves the posterior oropharynx

Herpetic gingivostomatitis caused by HSV involves the anterior oropharynx and grey vesicles and ulcers

2. True

Pleurodynia — Pleurodynia is an acute enteroviral illness characterized by fever and paroxysmal spasms of the chest and abdominal muscles . Most cases occur during localized summer outbreaks among adolescents and adults. Regional and nationwide outbreaks involving a large number of older children and young adults have been reported at infrequent intervals, often separated by decades. The role of the group B coxsackieviruses, the most important cause of epidemic pleurodynia, was established in 1949 . Other agents rarely implicated in pleurodynia include echovirus serotypes 1, 6, 9, 16, and 19 and group A coxsackievirus serotypes 4, 6, 9, and 10 .

Pleurodynia can mimic more serious diseases, including bacterial pneumonia, pulmonary embolus, myocardial infarction, acute surgical abdomen, and herpes zoster infection. Most patients are ill for four to six days. Children have milder disease than adults, who are often confined to bed.

True or False #1

1. Vareniciline increases the risk of suicide and depression. T or F
2. Vareniciline increases the risk of CVS events. T or F

Saturday, November 10, 2018

Facebook: ANM registration

#Medicowesome
#PSM

In a subcenter population, Crude birth rate is 20. What is minimum expected number of pregnencies registered with ANM?

1) 110
2) 120
3)  55
4) 100

Answer within 24 hours.

Answer is Option 3)

Let's get to this tricky question.

Total subcentre population is 5000.
Total CBR =20 per 1000 mid year  population.
Hence, 20/1000* 5000
=100 births.

Now here comes the tricky part.

Abortion and still birth accounts for 10% wasted pregnencies.
So 100+10 (10% of total births)
=110.
As per rule, ANM should have 50% registration, therefore 110/2=55
Approximately C) 60

That's all.

-Demotional bloke.

Thursday, November 8, 2018

Management of Diabetic Ketoacidosis

Hi guys! Let’s look at how we manage one of the the most dreaded medical emergencies; a complication of Diabetes Mellitus type 2.

[Please click on the image to enhance it]

- Patients with DKA have a triad of hyperglycaemia, ketosis and metabolic acidosis and they are severely dehydrated due to osmotic diuresis.
- Those with altered sensorium or pH < 7.0 require intensive care. A comprehensive flow sheet of changes in vital signs, fluid intake/output and lab values must be maintained.
- Despite a bicarbonate deficit, most DKA patients often do not require bicarbonate replacement but may be given if arterial pH < 7.0
- Serum phosphate, magnesium and calcium may rarely need supplementation.
- Patient education is of utmost importance to prevent future recurrences.

Happy studying!
- Ashish Singh.

Assessment and plan: New onset atrial fibrillation with rapid ventricular response

Hello!

Here is case one for the A&P series!

Assessment and plan: 99 yo M with PMH of ... admitted for ... is being evaluated for new onset atrial fibrillation with rapid ventricular response.

Authors' diary: Assessment and plan

Hey everyone!

As a medical student rotating in the US, I would have a tough time "typing" the assessment and plan. I would have it straight in my head but putting it all into words was difficult. I guess because I came from a different medical system where we don't write assessment and plan in our notes.

Tuesday, November 6, 2018

Ventricular arrhythmia notes

Hello! 

Anti-Ro/SSA antibodies and neonatal lupus

Hello everyone!

Did you know? Anti-Ro/SSA antibodies are associated with neonatal lupus (congenital heart block (CHB), neonatal transient skin rash, hematological and hepatic abnormalities).

How do I remember this? 

Thursday, November 1, 2018

Algorithmic Management of Organophosphate Poisoning

Hey guys, this whiteboard provides a general overview of how to manage patients with OrganoPhosphorous Compounds (OPC) poisoning.

      [Please click on the image to enhance it]

*Use of benzodiazepines has been associated with decreased mortality and morbidity, even in the absence of convulsions.

Signs of atropinization refer to the target end-points for atropine therapy and includes:
- Clear chest on auscultation, no wheeze
- Heart rate >80 beats/min
- Systolic Blood Pressure >90 mmHg
- Dry axillae
- Pupils no longer pin-point (miotic)

Early treatment with oximes is necessary before phosphorylated cholinesterase enzymes undergo “aging” and become resistant to reactivation (due to loss of their alkyl group).

That would be all.
Happy studying!

- Ashish Singh.

Monday, October 29, 2018

Role of BNP in acute exacerbation of COPD

Hello Awesomites!

Heart failure and COPD are common and they commonly co-exist in the same patient. Diagnosis may be difficult during acute exacerbation.

BNP/nT-pro-BNP is good Negative predictive value to rule out the presence of heart failure.

Spirometry is useful when the patient’s volume status is optimized. During acute HF exacerbation, diagnostic accuracy may be limited.

ECHO may be helpful to rule out systolic or diastolic dysfunction.

Why is it important to know?

Some therapies in COPD may be associated with worsening cardiac events in HF patients.

1) Oral steroids: - increased sodium and fluid retention.

2) Beta2 agonist: - increased HR and increased oxygen demand.

3) Aminophylline: - increased risk of arrhythmia.

You can further read about this in Link between COPD and HF
HAPPY STUDYING !
-Upasana Y. :)

Sunday, October 28, 2018

IRIS (Immune reconstitution inflammatory syndrome)

Hello Awesomites!

In terms of understanding immunity, HIV and leprosy never fails to fascinate me.There is whole spectrum of change in response of immune system.

So let us begin with the immune system which begins to recover. (Fall down 7 times get up 8!)

Immune reconstitution inflammatory response abbreviated as IRIS is a condition seen in some cases of AIDS or immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse.

There are 2 presentations:-

1. Paradoxical IRIS: worsening of symptoms of a known disease during ART

2. Unmasking IRIS: present of an occult opportunistic infection, in which disease that was not clinically apparent prior to ART, manifests during ART

Proper history:

-Time course of symptoms

 -History of Opportunistic infection,

-Recently diagnosed Opportunistic infections

-Treatment of Opportunistic infection: date of initiation, adherence, duration and clinical response

 -ART initiation date,

- Specific antiretroviral regimen,

-medication adherence,

-Previous history of ART

 -CD4 cell count and HIV viral load before ART initiation

 -Current CD4 cell count and HIV viral load,

The risks of corticosteroid therapy should be weighed against the severity of the IRIS manifestations and the potential benefits.Risks of corticosteroid therapy include the following:

-Hyperglycemia.
-Hypertension.
-Mental status changes.
-Avascular necrosis.
-Worsening of an existing infection.
-Predisposition to a new infection.

It teaches me something about "Balance".
-Upasana Y. :)

Facebook:ENT X-rays part - 1

#Medicowesome
#Ent

Which is the last sinus to appear radiologically on X-ray?
1) Maxillary sinus
2) Ethmoid sinus
3) Sphenoid sinus
4) Frontal sinus

Answer with detail explanation through blog in 12 hours.

So, this post is regarding our Facebook page question on ENT X-rays.
Correct answer is Option 4- Frontal sinus.

Let's get into some details and all of them are potential one liner questions.

Order of development of Paranasal sinus is
Maxillary > Ethmoid > Sphenoid > Frontal

I remember this order with mnemonic - "MESs Food"

Maxillary sinus and (Anterior) Ethmoid sinus are present at birth.
Maxillary sinus appears at 4-5 months of age radiologically.
(Anterior) Ethmoid appears at 1 year of age radiologically.

Sphenoid sinus: Development start at 2nd or 3rd year after birth and continues till adulthood. Making it last sinus to complete development.
It appears radiologically after 4 year of birth.

Frontal sinus: Development starts after 4 year of birth and completed at 13-14 years of age.
It appears radiologically after 6 years of birth.

Happy learning :)

-That's all

-Demotional bloke.

CHA2DS2-VASc Risk Score

Hello Awesomites !

You all must be familiar with the complications of atrial fibrillation (AF). The management of atrial fibrillation is centered on these complications.
Thromboembolism is caused by AF. CHA2DS2VASc score is to estimate stroke risk in AF patients and to start OACs (oral anticoagulants).
Previously, we have CHADS2 Score.

HEART FAILURE OR LVEF LESS THAN OR EQUAL TO 40%
1
HYPERTENSION
1
AGE MORE THAN OR EQUAL TO 75
2
DIABETES MELLITUS
1
STROKE,TIA or THROMBOEMBOLISM
2
VASCULAR DISEASE (PREVIOUS MI,PERIPHERAL ARTERY DISEASE, OR AORTIC PLAQUE)
1
AGE 65-74 YEARS
1
FEMALE SEX (BUT NOT A RISK FACTOR IF FEMALE SEX IS THE ONLY FACTOR)
1
MAXIMUM SCORE
9

SCORE 0
RECOMMEND NO THROMBOTIC THERAPY
SCORE 1
CONSIDER RISK/BENEFIT AND HAS-BLED SCORE TO AID DECISION OF ANTI-THROMBOTIC OR ANTI PLATELET THERAPY 
SCORE 2
RECOMMEND OACs

HAS-BLED is a scoring system developed to assess 1-year risk of major bleeding in patients taking anticoagulants with atrial fibrillation.

-Upasana Y. :)

Studying for Step One

Studying for the USMLE can be a daunting task, especially when you're an International Medical Student/Graduate. Coming from a different background - culturally and educationally - the questions asked in these examinations reflect the health system and health needs of the US's population. Apart from the questions, the financial aspects of attaining residency in the United States may also be a setback for some. Overall, this journey is a test of patience and dedication to the profession and one's career goals.

Euvolemic hyponatremia algorithm

Just happened to create this image so I thought of sharing with you guys :)

-IkaN

Saturday, October 20, 2018

Wednesday, October 17, 2018

Why is the level of Vitamin B12 increased in CML?

Why is the level of Vitamin B12 increased in Chronic Myeloid Leukemia (CML)?

Pathophysiology: The transport of vitamin B12 in the blood as well as hepatic uptake require the presence of transcobalamins (TCBs).

TCB types I (TCB I) and III (TCB III) ensure the binding of ∼80% of circulating vitamin B12.

Monday, October 8, 2018

ACHOO SYNDROME.

HELLO PEOPLEEEE!

Well this is not a medical joke or something that I made up. This syndrome is legit and very irritatting for the people who suffer from it. As said by Pryse Phillips the acronym is slightly forced but remains the best of the decade.

The acronym ACHOO is for Autosomal Dominant Compelling Helio-Opthalmic Outburst reflex which is basically sneezing in response to looking at a bright light, there can be a burst of 2-10 sneezes at a time.

Photic sneeze reflexes don't seem to make any sense at first. The purpose of sneezing is to clear unwanted irritants or germs from the nose. Bright light produces neither.
The phenomenon was first described in the 1950s, after a French doctor discovered several patients sneezing in response to the light of his ophthalmoscope, (the device doctors use to examine the retina). Further investigation revealed that it wasn't just any light that brought on the sneezing, but sudden flashes. These patients would reliably sneeze when quickly exposed sunlight, flash photography, and, in a few cases, even ultraviolet light.
There is no clear understanding on how photic sneez reflex works and hence a variety of theories have been proposed. 
For us its important to understand the basics of a normal sneez reflex arc.
The opthalmic division of the trigeminal nerve innervates the the nasal mucosa over the nasal septum and the anterior nasal passages. The afferent limb of the reflex arc is carried over the opthalmic nerve and the efferent limb is by the cranial nerves 5 and 7,9,10 and the motor nerves of the cervical and thoracic spinal cord.
The reflex centre is situated in the brainstem and upper spinal cord.
Any stimulation of the afferent limb of this reflex arc by dust or any foreign material sets the reflex arc in action which ultimately makes us sneez!
The primary clinical use of this sneez (sternutatory) reflex is a cross check on the corneal reflex.
Are there any other weird stimuli that cause people to involuntarily sneeze?
  • Sneezing induced by feeling full. (One case study of a relatively normal 32-year-old man found that "fullness of the stomach immediately after meals invariably results in three or four uncontrollable sneezes."
  • And the weirdest: For some, eating chocolate can induce some unwanted sneezes how barbaric.
Well I hope this information was helpful. So the next time you hear some sneezing (ACHOO!) do remember this phenomenon.

Let's Learn Together.
-Medha Vyas.
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