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.

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: Eculizumab- It is an Antibody to C5 and prevents its clevage to C5a and C5b, so no MAC.

-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)

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