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.