Saturday, June 24, 2017

Mnemonico diagnostico: Opacities that may be confused with renal calculus

Hey Awesomites

Mnemonic for opacities on a plain abdominal radiograph that may be confused with renal calculus:
TOP GAME

Tubercular calcified lesions in the kidney
Ossified tip of 12th rib
Phleboliths (calcifications in the wall of pelvic veins)

Gall stones
Appendicular/ Adrenal gland concretions
Mesenteric lymph node calcifications
External (foreign) bodies in alimentary canal (ex., cyclopenthiazide)


Thats all
- Jaskunwar Singh

Answer is not always antibiotics!

Clinical vignette:
Young, non smoker, female comes with complaints of sore throath, dry cough, nasal congestion for 10 days. Now, she feels better however she coughs out yellowish expectoration.
There are scattered wheezes and crackles that clear with coughing.
You've ordered relevant labs and meanwhile the patient asks you if she would need antibiotics. What would your next step be?

Answer: Symptomatic management.
Reason: Since there is a history of preceding viral infection and her current situation indicated Acute Bronchitis, the expectant management would be fairly Symptomatic!
Infact, there are articles that state that giving antibiotics could worsen the patient condition! Also, judicious use of antibiotics can help prevent antibiotic resistance.

Let's fight antibiotic resistance!

Stay awesome!
-Rippie

FENO in asthma: routine clinical testing

Hey Awesomites

One of the additional tests for determining the present status of airways in asthmatics is the measurement of Fraction of Nitric Oxide in Expired air (FENO).

The levels of Nitric oxide are elevated in the presence of inflammation in the airways, that is eosinophilic in nature.

In children <12 years, normal FENO is usually less than 36 ppb. However, in case of allergic inflammation of airways, the levels rise to >50 ppb.

Note that FENO is not diagnostic, but a test for independent prediction of exacerbations in asthmatic patients and is now done routinely in clinical practice, as approved by US- FDA.

Thats all
- Jaskunwar Singh

Friday, June 23, 2017

My Elective experience

Hey guys,

I was off blogging for a while for obvious reasons and I apologise for that. But, hey! Let me share the reason behind it :D
I was off to the States for my Clinical Electives at Mayo Clinic and Cleveland Clinic, so I'm going to briefly write about Electives in this post.

Overview of US Clinical Experience:

A) HANDS-ON Clinical Experience:
- One to one patient contact, can elicit history, perform physical examinations, write notes, suggest plan of care, have full access to patient records
- Considered better as what can be better than hands-on!
- Can be done only before a Medical Student graduates. ( Therefore, you can't do electives if you're already a Doctor -_-)

1. Sub-Internship equivalent to a 4th year US Medical Student
2. Clinical electives are equivalent to a 3rd year US Medical Student
3. Clerkship (This typically is for US Medical students; not applicable to IMGs)
4. Externships

B) NOT HANDS-ON Clinical Experience:
- You only get to observe (hence, Limited role in patient care)
- Can be done while you're a Medical Student or even after you graduate
- Controversial if it can be considered as USCE?

C) RESEARCH ELECTIVE:
- Usually, longer the elective, the better it is! (Increases yield of getting a fruitful publication out of it.
- No outlined criteria, eligibility varies from place to place.

Now,
I typically like to classify Clinical Electives into: (Although, others may classify them based on different criteria, I believe, classifying this way is logical in terms of expenses majorly)
1. USMLE Step 1 required
2. USMLE Step 1 NOT required
[I shall soon write a separate blog on this, pre requisites for elective application and rough expenses soon, so stay tuned as always :D]

About my elective experience:

I had given my USMLE Step 1 while I was in Third year. So, when I got into Fourth year I applied to Universities that had USMLE Step 1 criteria.
As now a days, getting electives is becoming more and more competitive, along with my friends, I applied to IMG friendly elective places well in advance  (about 10 months prior for a few places). This also meant that we had to wait for a long time to get our acceptances as they don't send out acceptances until 3-1 month prior to your elective start date.

Fortunately, I got accepted at Mayo Clinic, Rochester for Infectious Diseases elective and at Cleveland Clinic, Ohio for Endocrinology elective! Yippie!! (Big thank you to Ikan for guiding me with the application process)

Both, Mayo Clinic and Cleveland Clinic are amazing places to work at! (And if you don't already know, Mayo Clinic has been ranked no.1 and Cleveland Clinic has been ranked no.2 on U.S. News and World Report's Honor Roll :D)

What to do while you're there?

- Be professional, dress professionally, follow code and conduct of your Hospital or Clinic.
- Take histories, perform physical examinations as required, write patient notes, suggest plan of action and so on...
- Volunteer for case presentations/ talks
- If you find an interesting case while you're rotating there, discuss with your residents/ fellows/ attendings if you can submit it to a journal or present it at any conference.
- If you're interested in research, talk to your attending and try to get involved in one.
- Most importantly, As an IMG, it is crucial for us to get A Strong Letter of Recommendation. If you've been working hard, I am sure, most attendings would agree to write you a Strong LoR! Hurray!

Also, once you are done with your elective, in the following week or so, it is good to write your attendings a courtesy/ Thank you email, so that they know you really learnt during your elective!

Stay awesome!
-Rippie


Lymphedema - High yeild Information.

Hello there!
So today in the surgery OPD I happened to see a case of Lymphedema feet ,and hence thought of reviewing some important points on same.

So, Congenital lymphedema may involve a single lower extremity, multiple limbs, the genitalia, or the face. 

The edema typically develops before 2 years of age and may be associated with specific hereditary syndromes -Turner syndrome,Milroy syndrome, Klippel-Trenaunay-Weber syndrome.

 Lymphedema praecox is the most common form of primary lymphedema, accounting for 94% of cases. 

Lymphedema praecox is far more common in women, with the gender ratio favoring women 10:1. 

The onset is during childhood or the teenage years, and the swelling involves the foot and calf. 

Lymphedema tarda is uncommon, accounting for <10% of cases of primary lymphedema. The onset of edema is after 35 years of age. 

Secondary lymphedema is far more common than primary lymphedema. Secondary lymphedema develops as a result of lymphatic obstruction or disruption.

 Other causes of secondary lymphedema include radiation therapy, trauma, infection, and malignancy. 

Globally, filariasis (caused by Wuchereria bancroftiBrugia malayi, and Brugia timori) is the most common cause of secondary lymphedema.

Hope It helps.
Let's Learn Together!
-Medha.

Pathophysiology and Radiologic patterns of Atelectasis


Hey guys!

This post will be on the classification of Atelectasis based on its pathophysiology and a brief overview of its radiology patterns. 

Let us deal with the radiology aspects first:

1. Opacification of airless lobe and displacement of fissures,

2. displacement of hilar and cardiomediastinal structures toward the side of collapse,

3. narrowing of the ipsilateral intercostal spaces,

4. elevation of the ipsilateral hemidiaphragm,

5. compensatory hyperinflation and hyperlucency of the remaining aerated lung and

6. obscuration or desilhouetting of the structures adjacent to the collapsed lung (eg, diaphragm and heart borders).

Google the Chest X ray scans for atelectasis to consolidate the above points.


Now the lengthy part, The Pathophysiology. Let us start with active or obstructive atelectasis. 

1. Active/Obstructive Atelectasis.

Obstructive atelectasis is a consequence of blockage of an airway. Air retained in the alveoli distal to the occlusion is absorbed into the pulmonary capillary blood since the pressure of gases in the blood plasma (PvO2) is lower than that in the alveoli. For this reason, it is also called absorptive atelectasis. This causes the affected regions to become totally gasless and then collapse. 
Obstruction of a segmental bronchus is less likely to result in segmental atelectasis than obstruction of a lobar bronchus is to produce lobar atelectasis. This difference is because of collateral ventilation between bronchopulmonary segments within a lobe. 
Collateral ventilation occurs via the age-old physiologic adaptive process of recruitment and distension of neighbouring bronchioles. But three are three other players here, or brothers as I like to call them. A small anecdote to remember these three brothers:
Once there was a priest named Kohn who decided to help out a fellow bronchopulmonary segment in aeration. Brother Kohn being eldest and hence weak could only manage to dig a pore. His work was carried on by Brother Boren who bored (as his name suggests) and made this pore into a fenestration. There was still some work left. And for that Brother Boren asked the help of the engineer Brother Lambert. Brother Lambert, after much hard work was eventually able to dig up a canal all the way upto the neighbouring segment so that they can share the aeration bestowed upon them by Lord Almighty!
So we have three distinct collateral connections: 1. Pores of Kohn, 2. Fenestrations of Boren and 3. Canals of Lambert.
So you need to defeat these three if you want to cause obstructive atelectasis.
Let's dig a bit deeper into Fenestrations of Boren. These collateral channels are extensively prominent in an emphysematous lung. Now take a case of a 60 year old male smoker with emphysema who has now developed small cell carcinoma. Suppose there is a tumor mass obstructing the right bronchus, this patient will take a lot of time to develop obstructive atelectasis in the right lung because of the presence of extensive network of fenestrations of Boren. Hence, this patient will become symptomatic late and thereby will be diagnosed late. Blessing or Curse!
One more thing, it has been observed that atelectasis occurs more rapidly in patients on oxygen therapy. Why? There is a simple reason behind this. Oxygen is more soluble than nitrogen in water, when you give inhalational O2 with a FiO2 take 50%, you are altering the partial pressures of gases in the alveoli, Nitrogen which was 79% will fall down to below 50% and O2 which was 20% will rise upto 50%. Hence overall solubility rises, this elevates the tendency and spontaneity of gases diffusing into the blood plasma.

Honestly speaking, rest of the causes are nowhere as important as the one mentioned above so let us try to ace them quickly. 
2. Nonobstructive Atelectasis

A. Relaxation (ie, passive) atelectasis ensues when contact between the parietal and visceral pleurae is eliminated. While this is usually due to a pleural effusion or pneumothorax, a large emphysematous bulla can have a similar effect. In this case, the residual physiologic elastic recoil of normal lung parenchyma allows the normal lung to collapse away from the chest wall with consequent loss of volume.
The middle and lower lobes may shrink more than the upper lobe in the presence of a pleural effusion, while the upper lobe may be affected more by a pneumothorax.

B. Adhesive atelectasis is a consequence of alveolar instability due, in part, to surfactant deficiency or dysfunction. As its name suggests, the alveoli walls will collapse into the alveolar space sticking with each other. In the normal lung, surfactant reduces the surface tension of alveoli and decreases the tendency of alveoli to collapse. Decreased production or inactivation of surfactant leads to alveolar instability and collapse. Adhesive atelectasis is a major problem in respiratory distress syndrome of premature infants(IRDS), acute respiratory distress syndrome (ARDS) in adults, acute radiation pneumonia, and posttraumatic lung contusion.

C. Cicatrization (ie, cicatricial atelectasis) results from diminution of lung volume due to severe parenchymal scarring. Common underlying etiologies include granulomatous disease (eg, sarcoidosis), necrotizing pneumonia, and radiation pneumonia.
D. Acceleration Atelectasis- This type of atelectasis has been described in pilots subjected to very high, vertical accelerative forces between 5G and 9G: at 5G, up to 50 percent of pulmonary airways are distorted and closed due to gravitational forces. The atelectasis is exacerbated by breathing a high fractional concentration of oxygen. Decreases in vital capacity are a reflection of this type of atelectasis in pilots. Acceleration atelectasis can cause symptoms like chest pain, coughing, and dyspnea.
E. Rounded atelectasis (also called folded lung, Blesovsky’s syndrome, or atelectatic pseudotumor) is a distinct form of atelectasis associated with pleural disease, particularly following asbestos exposure and in India following pleural tuberculosis. Asbestosis is associated with pleural plaques and diffuse pleural thickening while pleural TB will have pleural thickening alongwith pleural effusion which eventually resolves with or without organization and pleural septations(Harbingers of Fibrothorax). 
In this condition, there is a subpleural mass mainly in the middle or lower lobes from which bronchi and blood vessels arise and they form a structure like a comet tail which traverses through the underlying atelectatic lung parenchyma to join at the hilum. Some un-astronomical sources compare this to a Vacuum Cleaner, with the dirt box as the subpleural mass and the hose as the comet tail. 

P.S. Blesovsky's Syndrome is not the only syndrome connected to pneumoconiosis, there is also Caplan's syndrome(Rheumatoid pneumoconiosis); which has a well-known mnemonic CAPlaN;
C- Coal workers' pneumoconiosis
A- Rheumatoid Arthritis
PlaN- Pulmonary nodule

That's all! 
-VM

Thursday, June 22, 2017

Pills of knowledge in Ophthalm- Nodal cataract

The condition where 'day blindness' is present is a cataract at the nodal point. Nodal point of the eye is where the rays of light pass through the lens without any refraction, usually at the centre of the lens. Thus, during the day, especially when out in the sun, the pupil contracts and the light has to pass through the cataractous area, causing diminution of vision.


Immunotherapy for Prostate cancer

Hey Awesomites

Immunotherapy is now an emerging and much promising intervention in the treatment of prostate cancer, apart from the traditional cancer treatments - chemotherapy, radiation and surgery.

Research Update - The Multitasking Brain.

Hello there!
So you must be probably Studying (I assume and if not,you better be!)with your Cellphone besides you,
And you hear the Pinggg!!!
Aha.. GOTHAM needs you!! You shift your focus from the task of studying to the task of on your cellphone,and simultaneously thinking about how good you are at multitasking!
 Well don't pat your Backs yettt.
Although “multitasking” is a popular buzzword, research shows that only 2% of the population actually multitasks efficiently.
Most of us just shift back and forth between different tasks, a process that requires our brains to refocus time and time again — and reduces overall productivity by a whopping 40%.

 Told ya! No need to pat your backs,for decreasing your efficiency. So the next time your Read ,you only Read.

New Tel Aviv University research identifies a brain mechanism that enables more efficient multitasking. 

The key to this is “reactivating the learned memory,” a process that allows a person to more efficiently learn or engage in two tasks in close conjunction.

How does this work???

Starts with - Training the brain.

“When we learn a new task, we have great 
difficulty performing it and learning something else at the same time.

This is due to interference between the two tasks, which compete for the same brain resources.

The research demonstrates that - By pairing the brief reactivation of the original memory with the exposure to a new memory, long-term immunity to future interference was created.

For example- researchers first taught student volunteers to perform a sequence of motor finger movements with Right hand. 
After acquiring this learned motor memory, the memory was reactivated on a different day, during which the participants were required to briefly do some task with their Left hand — with an addition of brief exposure to the same learned motor task being performed by the Right hand.
By utilizing the memory reactivation paradigm, the subjects were able to perform the two tasks without interference.

So well we now have an overview of how the brains circuits are intimately connected and how they can still constantly evolve.

Hope this was helpful.

With this I finish the blog and my cup of tea!!
So much for Multitasking! 

Let's Learn Together.
-Medha 😊


Wednesday, June 21, 2017

Hematuria: A clinical pearl

Hey Awesomites

Hematuria (blood in urine) may be microscopic or macroscopic/ gross.

The American Urological Association (AUA) defines microscopic hematuria as 3 red blood cells/ high - power field on microscopic examination of the centrifuged urine specimen in two of the three freshly voided, clean- catch, midstream urine samples.

Gross/ visible hematuria can result from as little as 1mL of blood in 1L of urine, and therefore, the color of urine does not necessarily reflect the degree of blood loss.

Now lets have a brief review of the clinical presentation of hematuria on the basis of its source -

- A glomerular source of bleeding (nephronal/ glomerular hematuria) usually results in persistent microscopic hematuria that may be with/ without intermittent periods of gross hematuria.

- Total hematuria (present throughout the void) indicates bleeding of bladder/ upper tract origin.

- If renal sources of hematuria are present, the blood is equally dispersed throughout the urine stream  and does not clot.

In cases of clotting, its localisation is a must to evaluate the underlying cause:

- Hematuria/ clots at the beginning of the urine stream ( initial hematuria ) is a symptom of a urethral cause.

Terminal hematuria occurring at the end of stream may be caused due to either prostatic, bladder, or trigonal source of bleeding.


Thats all
- Jaskunwar Singh

Grossing the thyroid and differentials to be considered

Thyroidectomy is often received for lesions found suspicious on FNA or in cases where goitrous enlargement causes clinical symptoms of obstruction. Hemi includes the lobe and the isthmus, lobectomy only the lobe, while near total includes almost the entire thyroid except a small part of the thyroid left behind.
The following key factors should be described of the received specimen:

1. Type of the specimen
2. Dimensions of all the lobes
3. Size- If enlargement seen, is it diffuse or focal
4. Colour- Brown ( Normal); yellowish white/ beefy red/ mahogany brown
5. Consistency of the lesion - cystic ( single or multiple; bilateral or unilateral lobe involvement); solid; solid- cystic
6. Relation of the lesion to the adjacent thyroid
7. Surface of the thyroid - Smooth/ infiltrated - hemorrhagic irregular areas
8. Whether received intact or in pieces due to extensive extrathyroidal adhesions ( Reidel thyroiditis)

Serotonin receptor agonist and antagonist notes

1. 5-HT 1A receptor :- 
Partial agonists of this receptor are BusPIRONE,
IsaPIRONE, GePIRONE.
These are useful as anti-anxiety drugs.

2. 5-HT 1B/1D receptor :-
Agonists at this receptors are sumaTRIPTAN, NataTRIPTAN.
These are useful for the treatment of acute migraine attacks.

3. 5-HT 2A/2C receptor :-
Antagonists are clozapine and risperidone.
These are used as atypical antipsychotic agents.

4. 5-HT 3 receptor :-
Antagonists are ondanSETRON, graniSETRON, tropiSETRON.
These agents are used in chemotherapy induced vomiting.

5. 5-HT 4 receptor :-
Agonists on this receptors are cisaPRIDE, 
mosaPRIDE.
These are useful in the treatment of GERD.

-Upasana Y. :)





mPFC activation in depression: The Associations

Hey Awesomites

I had talked about how people with neuroticism also have an advantage of being creative in a previous post.
Lets now know the basis of this in brief -

Sinus of Morgagni- Contents

There occurs a gap in the pharyngeal wall between the base of the skull and superior constrictor muscle called as Sinus of Morgagni. This space is closed by the pharyngeobasilar fascia.

Contents- (mnemonic PLATE)

1. Palatine branch of ascending pharyngeal artery
2. Levator palati muscle
3. Ascending palatine artery
4. Tensor vetli palatini
5. Eustatian tube


In nasopharyngeal carcinoma, the tumor may extend laterally and involve this sinus involving the mandibular nerve. This produces a triad of symptoms known as Trotter's Triad. 
These symptoms are:
1) Conductive deafness 
2) Ipsilateral immobility of the soft palate
3) Trigeminal Neuralgia

Hope that helped!
Ashita Kohli

Zenker's Diverticulum

Zenker's Diverticulum is a posterior pulsion diverticulum which occurs through the Killian's Dehiscence.

Killian's Dehiscence is a potential gap between the oblique and transverse fibres of the inferior constrictor muscle. It is also known as the gateway of tears as it is a potential site of perforation during oesophagoscopy. 

Zenker's diverticulum occurs due to the outpouching of the pharyngeal mucosa at the site of Killian's dehiscence.
There is incoordination between the descending peristaltic wave and the cricopharyngeus muscle at the upper oesophageal spincter which leades to high intra luminal pressure and the mucosal herniation through the weak area of Killian's Dehiscence.

It is not a true diverticulum as it has just the herniation of the pharyngeal mucosa. ( A true diverticulum has all the layers of the oesophageal wall)

It is usually seen in elderly above the age of 60.

Symptoms-

1. The most common symptom is Dysphagia, which is intermittent initially and later becomes progressive.
2. Halitosis ( ie. bad breath, well ofcourse because food can get trapped in this pouch)
3. Regurgitation of food and cough.
4. There maybe regurgling sounds in the neck, gurgling sensation on palpation is known as Boyce sign.

Malignancies may develop in 0.5-1% cases.

Diagnosis- Barium Swallow and videofluoroscopy

Treatment-
1. Endoscopic stapling of the diverticulo esophageal sphincter.
2. In patients not fit for major surgeries, Dohlman's surgery may be done.

Hope that helped!
Ashita Kohli

Waldeyer's Ring

Waldeyer's Ring is an aggregation of lymphoid tissue seen in the subepithelial lining of pharynx guarding the nasopharynx and oropharynx in the form of a ring.

The ring is bounded by-

1. Palatine Tonsils ( also called as Faucial Tonsil)- Situated in between the anterior and posterior pillars on each side of oropharynx
2. Adenoids (aka Lushka's Tonsil)- Lies at the junction of roof and posterior wall of nasopharynx
3. Tubal Tonsils ( aka Gerlach's Tonsil)- Lies in the fossa of rosenmuller behind the eustatian tube opening
4. Lateral Pharyngeal Band and Nodules



Hope that helped!
Ashita Kohli

Rhinolalia Aperta

Rhinolalia Aperta is a speech disorder which involves hypernasality in voice.
The defect is seen in the failure of the nasopharynx to cut off from oropharynx.

Some fibres of palatopharyngeus muscle make the posterior pillar, go posteriorly in the posterior wall of nasopharynx and along with the lower fibres of the superior constrictor muscle forms a ridge known as the Passavant's Ridge

During swallowing and speaking the passavant's ridge closes the nasopharyngeal isthmus.
When this doesn't happen (eg- cleft lip, paralysis of palate) it leads to nasal regurgitation of food and nasal tone in speech known as Rhinolalia Aperta.

Treatment-

1. In children with cleft palate, special exercises can help in strengthening the muscles so as to reduce the nasality in voice.

2. Surgery- Posterior Pharyngeal Flap
                   Sphincter Pharyngeoplasty


Hope this helps!
Ashita Kohli 

Tuesday, June 20, 2017

Differentials of lower limb ulceration: Venous, arterial or neuropathic?

Hello!


Q. Today, in our OPD, a 45 year old diabetic Male, farmer by profession presented with an ulcer on left lateral malleolus.
He had a history of edema in lower limb associated with an itching 2 years ago. Since 6 months he got a non-healing ulcer on left lateral malleolus.

On examination:-
Pigmentation of skin, eczema lipodermatosclerosis, atrophied Blanche are present and dilated veins on the medial aspect of left lower limb.

My question is how to differentiate whether the ulcer is due to neuropathy, venous stasis or obliteration of artery.

Why do the above doubt arise?
Because venous ulcer are commonly found at the lower third of the leg usually on the medial side and even on the foot.

Ans.

(I) to rule out neuropathy,
1. Ask whether he feel the ground and pebble while walking barefoot
2. Test for the pain sensation, whether it is intact or not.

(II) Venous ulcer have characteristic findings. History is utmost important. They are shallow and flat. The edge is sloping and purple blue color.
The floor: - appears pink due to presence of granulation tissue. If it is a chronic ulcer there is more white fibrous tissue. Most important is A FAINT BLUE RIM of advancing epithelium may be seen at the margin.

(III) To check for arterial obliteration

1. Feel the dorsal pedis pulsation.
2. Ask for claudication also.

Conclusion: - It was venous ulcer.

Then why did it appear on the lateral side? Remember! On inspection dilated veins were found on the medial side.

Before answering the above question. Let us ask why is it most common on medial side?

There are more perforating veins on the medial side means more pressure in that area. But that doesn't mean lateral side is spared .There is some rise in pressure on lateral side also. The only thing that precipitated this was “Trauma”. Due to more itching on lateral side, he traumatised that area .It was initially small in size, non-healing ulcer which is gradually increasing in the size.

Found this great article on the lower limb ulcers.


Take care:)
-Upasana Y.



Authors diary: Tip for solving multiple choice questions

So this random tip comes from a fun conversation that I was having with my study partner today.

Baclofen for treatment of alcohol dependence

Hello!

Recent evidence suggest that the gamma-aminobutyric acid-B receptor agonist baclofen is a promising agent for the treatment of alcoholism.

Yep!

Baclofen produces an effortless decrease or suppression of alcohol craving. It decreases alcohol consumption including in those with poor motivation. The drug causes few side effects and does not add to the intoxication effect of alcohol.

It benefits patients with alcohol dependence (even those who are still in precontemplation stage of motivation!)

Research has shown that baclofen reduces withdrawal symptoms of alcohol and is safe in those with liver impairment.

Although further studies that compare long-term alcohol-related outcome of baclofen with established drugs such as naltrexone and disulfiram are needed.

Interesting, isn't it?

-IkaN

More than what you know about vitamins!

Hello! :)

These were the questions asked during my pharmacology vivas. And I found it fascinating after studying. I have never studied these points about vitamins before! 

Q. Which vitamin deficiency is related with lowering of seizure threshold?

Ans. Pyridoxine Vitamin B6. 

Why? As it is associated with synthesis of neurotransmitter GABA. Therefore, it is indicated during isoniazid induced convulsions. :)

Q. Why laropiprant (20mg) + Niacin (1g) is used in combination?

Ans. Nicotinic acid (a derivative) results in flushing of face.

Why? Vasodilation of cutaneous vessels.

Therefore, we combine it with specific anti-flushing drug called laropiprant.

Q. In hyperemesis gravidarum, what do you give for associated Wernicke's encephalopathy following hyperemesis? 

Ans. I thought of anti-emetics at first but the answer is vitamin B1. (Wernicke's encephalopathy doesn't always result from alcohol :P )

That's for today.
Take care. :)
-Upasana Y.
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