Hey guys!
As you all know, I'm preparing for USMLE and I wish to do an Internal Medicine residency in the USA. A part of the process for international medical students requires electives, which is, clinical experience in the US.
I am in Cleveland, Ohio in the months of January - April 2016 for my electives.
I will also be coming to Houston, Texas for my USMLE Step 2 CS exam.
If you're around at that time, I would love to meet you. Please come say hi.
For those of you who have been to the US for electives, please let me know do's and dont's. Anything you wish someone had told you prior to the experience.
I will also be blogging about every tiny detail - From preparation to what I experienced - So that it helps someone like me in the future :)
That's all!
Wish me luck and pray for me.
-IkaN
PS: I will not be disclosing the name of the hospital and specialty on the blog. Reason being patient confidentiality and privacy purposes.
Why do patients with multiple sclerosis experience worsening of neurological symptoms after heat exposure, that is, after taking a hot bath or after exercise?
It's known as Uhthoff's phenomenon.
Uhthoff's phenomena is due to ion channel modifications, in conjunction with thermoregulatory derangements that occur in MS, transiently altering the conduction properties of demyelinated axons.
This is from uptodate:
Heat sensitivity — Heat sensitivity (Uhthoff phenomenon) is a well-known occurrence in MS; small increases in the body temperature can temporarily worsen current or preexisting signs and symptoms.
This phenomenon is presumably the result of conduction block developing in central pathways as the body temperature increases. Normally, the nerve conduction safety factor decreases with increasing temperature until a point is reached at which conduction block occurs; this point of conduction block is reached at a much lower temperature in demyelinated nerves.
(This was discussed on our study group.)
Study group discussion: Why does ciprofloxacin cause tendinitis or tendon rupture?
The exact pathophysiology of FQ-induced tendinopathy remains elusive; however, some concepts have been suggested:
FQ: Fluoroquinolones
1. FQs are synthetic antibiotics that act by inhibiting bacterial DNA gyrase (topoisomerase II). DNA gyrase is directly involved in DNA replication and cell should not exert a negative effect on human cell lines because the affected bacterial enzymes have little homology with mammalian DNA gyrase. However, it is possible that FQs have a direct cytotoxic effect on enzymes found in mammalian musculoskeletal tissue.
2. FQs have chelating properties against several metal ions (e.g., calcium, magnesium, aluminum), and have been known to cause direct toxicity to type 1 collagen synthesis and promote collagen degradation.
3. Animal studies have shown that FQs cause cartilage damage by inducing necrosis of chondrocytes (36 hours after treatment), disruption of the extracellular matrix, and formation of vesicles and fissures at the articular surface.
(This was discussed in our study group)
Some review questions on drug induced pancreatitis!
Which diuretics can lead to pancreatitis?
Thiazides and furosemide
Which Antiretroviral drugs can lead to pancreatitis?
Didanosine and stavudine
Which antibiotics can lead to pancreatitis?
Metronidazole and tetracyclines
Seizure med leading to pancreatitis?
Valproate
Immunosuppressive drugs leading to pancreatitis?
Azathioprine
L asparaginase
Ok the last one.. Drugs for treatment of IBD leading to pancreatitis?
Sulfasalazine
5-ASA
(Mnemonic, if you need one)
FAV DAM - ATiTiS
Furosemide, Azathioprine, Valproate
Didanosine, Asparginase, Metronidazole
ASA, Tetracycline, Thiazides, Stavudine, Sulfasalazine.
Hello everyone!
I see a lot of patients in the casualty with fever, chills & thrombocytopenia but to my surprise, they've been diagnosed with malaria (Instead of dengue). I was wondering what the mechanism is.
The speculated mechanisms leading to thrombocytopenia are: coagulation disturbances, splenomegaly, bone marrow alterations, antibody-mediated platelet destruction, oxidative stress and the role of platelets as cofactors in triggering severe malaria.
In uncomplicated cases of malaria, thrombocytopenia is the result of splenic pooling of platelets aggravated by a moderate decrease in platelet life span.
That's all!
-IkaN
Mini bacteriology post! Yaay!
In which Lancefield group does Streptococcus pyogenes and Streptococcus agalactiae belong? How do you remember them?
Streptococcus Pyogenes belongs to Lancefield Group A mnemonic:
I remember GAP jeans (Because of the gap company manufactures amazing clothes) - Group A Pyogenes.
Streptococcus Agalactiae belongs to Lancefield Group B mnemonic:
Remember B for Baby. Streptococcus Agalactiae causes meningitis in babies and belongs to Lancefield Group B. Babies also love Galaxy chocolates and stars.
That's all!
-IkaN
I was reading Atrial fibrillation today and thought I'd write a small quick review blog on it.
A patient with atrial fibrillation will usually present with palpitations or fatigue.
On physical examination, irregularly irregular pulse is characteristic.
ECG is diagnostic.
Extra tip: Your patient may have his rhythm well controlled when you see him in the wards and you might not have the characteristic physical finding of an irregular pulse or have an ECG in hand. In that case and especially during vivas, do mention that you would like to rule out other causes of fatigue by ordering CBC, SE & LFT.
CBC: Complete blood count
SE: Serum electrolytes
LFT: Liver function tests
In an acute setting, you must provide symptom relief through rate control. Beta blockers, calcium channel blockers are preferred. Digoxin is considered if blood pressure is low.
Fun fact: Why isn't Digoxin an awesome drug for rate control in exercise and anxiety?
Because the increased rate in exercise and anxiety is primarily due to adrenergic stimulation and Digoxin works through Vagal stimulation.
You need to rule out reversible causes of atrial fibrillation like electrolyte imbalance, thyrotoxicosis, fever, alcohol and drugs. Always order TSH levels.
Extra tip: Also ask for a history of snoring since sleep apnea is a treatable cause of atrial fibrillation.
Rate control is usually done first since it mitigates symptoms. Rhythm control is preceded by measures to reduce stroke, which includes either 3 weeks of anticoagulation by dabigatran / warfarin or clot exclusion by TEE.
CHADS2 score is used to decide whether anticoagulation is required. It is based on risk stratification.
Dabigatran is preferred over warfarin because INR monitoring isn't required. However, it is expensive, contraindicated in renal failure and there is no reversal in major bleeding.
Electric cardioversion or chemical cardioversion may be done depending on patient symptoms.
Drugs used for chemical cardioversion are: Flecainide, Ibutelide, Procainamide, Amiodarone.
Curative catheter ablation may be tried in patients who have recurrent atrial fibrillation and in whom antiarrhythmic drug trial has failed.
Cool fact: Propafenone is "pill in pocket" drug used by patients when they feel onset of palpitations. It is used in conjunction with beta blockers to prevent fast dysrhythmias.
Here are a few mnemonics I got online:
Precipitants / causes of Atrial fibrillation: PIRATES
PE, Ischemia, Respiratory diseases like COPD, Atrial enlargement or myxoma, Thyroid, Ethanol, Sepsis or Sleep Apnea
Mnemonic for determining major risk of bleeding: HAS BLED
HTN, abnormal LFT / RFT, Stroke, Bleeding history, Liable INR, Elderly, Drugs that predispose to bleeding.
If score >3, higher risk of major bleeding.
That's all!
-IkaN
Related post: Antiarrhythmic drug classes mnemonic
Greetings everyone!
Here's a mini fact: Christmas tree rash is seen in Pityriasis rosea.
That's all!
Merry Christmas everyone!
-IkaN
Related post: Christmas disease mnemonic
What is the reason for pruritus and itching in obstructive jaundice?
Patients have differing sensitivities to elevated bile salt concentrations,
which act on peripheral pain afferent nerves to produce the sensation of itching. This stimulation involves
opiate-mediated pathways, and opiate antagonists can block cholestasis-associated itching.
Itching does not appear to be associated with histamine release, and antihistamine therapy is generally ineffective.
Ultraviolet B phototherapy has been successfully used to treat pruritus.
Thanks for explaining the mechanism to us, Benedict!
Hello.
Battles sign is ecchymosis over the mastoid process and is mostly indicative of a fracture of the skull.
Mnemonic:
Battle Sign
Bruises Seen
Basilar Skull fracture
I love this mnemonic posted online too: BattlE - Behind Ear.
That's all!
You're a warrior.
-IkaN
"Hello IkaN!
I hope you're okay and happy :)
Can you teach me how to be organized? How can I save my notes?
I don't know why I'm so untidy. I want to be just like you, helping others & having good grades! <3
Please help me out here!"
- Email by an awesomite
Hello! I'm okay and at peace (:
Your organization depends on where you study from.
I study from books and ebooks so my study life seems very complicated to others.
I can read while I'm in the bus or in the train on my phone, so I always have ebooks or audio lectures with me. I can't write while traveling so everything I learn is saved on my phone. When I study with my books at home, I like having the traditional pen & paper to write, doddle and draw. Or a white board.
Here's how I save the information I have studied:
1. Make subject wise notebooks and write notes in it:
This is effective when you're studying from multiple text books and you need to merge all information into one for fast review during exams. I recommend making notes after you've read from all the textbooks if you're using this technique. You don't need to be tidy!
PS: This is time consuming.
2. If you're using ebooks, highlight and bookmark:
I read Harrison (Which is a HUGE internal medicine book) this way. The bookmarks would show me the topics I've read and while revising, I'd go through the highlighted lines only.
(App I use: Adobe Reader)
3. Type your notes and make sure they're synchronised:
If I have too much information on the digital platform and too little time to write on paper, copy paste on a notes app. Make sure you sync and back em up.
(Apps I use: Google Keep, ColorNote)
4. Blog:
The internet a wonderful place to save everything! (Many a times, I look for my own notes on Google =P)
If you don't have time for a fancy blog, just a simple tumblr with your study material is a good way to keep things in one place.
(Apps I use: Blogger, Tumblr)
Extra tips:
- Make a separate book for points you write during lectures. They're not always important but you will want you refer that book for the one thing your teacher said that you can't recollect while studying.
- If you think it's important, always write / save it somewhere. In my experience, you regret the things you didn't save =P
- Don't always focus on making the notes. Understand the information first, then organize it so that you revise and remember it.
The fact that you find me someone you wish to be like makes me happy. I hope I live up to the image you have of me =)
Until next time!
Why isn't mannitol used in pulmonary edema? And why is it used in cerebral edema?
Mannitol would expand the intravascular volume, increasing cardiac output and causing pulmonary edema (more fluid going to the lungs than it can drain.)
(Assuming the pulmonary edema is due to CHF:) The increased hydrostatic pressure proximal to the left atrium causes transudation in the lungs. Although mannitol can act as a diuretic, it initially increases plasma volume due to its effects on elevating plasma oncotic pressure.
Increased plasma volume --> increased left atrial preload in the face of decompensation that already occurred even at a lower preload --> increased LAP (PCWP) with further decompensation --> exacerbation of pulmonary venular transudation.
So basically, it causes edema by volume overload.
It's blood brain barrier (BBB) that allow us to use mannitol for brain edema. Since no such barrier is there in lungs, mannitol can cross capillaries into alveoli and worsen it. Even in cerebral edema, we give mannitol only when the BBB is intact. Otherwise, mannitol can create havoc there too.
Infusion of hypertonic solutions of any effective small molecular weight solute (eg hypertonic saline, mannitol or urea) will dehydrate the brain. In the peripheral capillaries, these solutes are not effective at exerting an osmotic force because they can easily cross these capillary membranes.
Hey everyone!
Today, I felt like sharing random things that I learnt today. It's about neuropathic joint disease - Destructive joint disease due to loss of pain and proprioception.
Neuropathic joint resembles osteoarthritis (Osteophytes, loose bodies, loss of articular cartilage, etc.)
I couldn't think of neuropathic joint disease as a differential today because I was so caught up in osteoarthritis!
The distribution of joint involvement depends on the underlying neurologic disorder.
Tabes dorsalis: Hip, knee, ankle.
Syringomyelia: Glenohumeral joint, elbow, wrist.
Diabetes: Tarsal and tarsometatarsal joint.
This is a major clue. The joint distribution.
Diabetes mellitus is the most common cause of Charcot's joint.
Other causes of Charcot's joint include yaws, leprosy, Charcot Mary Tooth disease and meningomyelocele.
That's all!
I cannot feel, what is real..
- IkaN
Hey!
HOCM is hypertrophic obstructive cardiomyopathy.
HOCM is the most common cause of sudden cardiac death in ADolescents.
HOCM is Autosomal Dominant.
Fun fact: Most common cause of sudden cardiac death in children in Aortic Stenosis.
-IkaN
This is a discussion I had with a lot of people. My questions are put in inverted commas.
"I don't understand the next best step in the management in acute coronary syndromes. If there's ST elevation MI, you do angioplasty. But when there was a ST depression, they preferred heparin after aspirin even when angioplasty was in the options. Why is that? Why does the management change depending on elevation or depression?"
ST elevation means transmural ischemia so maybe angioplasty is the only way to restore flow. ST depression means subendocardial ischemia so occlusion isn't complete. Heparin and blood thinners might work.
"But then if you can do angioplasty (Catherization lab available), why give heparin?"
They do send for angioplasty later. Heparin can be given immediately to prevent the situation from getting worse.
"But then again, why wouldn't you do that with ST elevation too?"
ST elevation means the occlusion is complete. Heparin wouldnt be effective. In NSTEMI and unstable angina, there's still some lumen viable.
"Patients with MI with ST-segment depression should not be treated with fibrinolysis. Why isn't fibrinolysis done in ST depression angina?
We say that the occlusion isn't complete because there is subendocardial ischemia in ST depression and we give heparin to prevent further occlusion. But why not give streptokinase? Why not eradicate what is already formed instead of trying to prevent progression of clot?"
Because fibrinolysis treatment has it's own side effects and it's not effective in all the cases. It's contraindicated because studies have shown it does more harm than good in only ST depression.
Like, for example, there is reperfusion injury which would might make the only subendocardial infarct into a transmural one. 3 in ten patients end up with cerebral haemorrhage. There are so many other clauses.
Hence it's only indication is a transmural infarction.. The damage is already great. Irrespective of using t-PA the patient condition is critical.
That's all!
Thank you everyone who helped me out on this one.
-IkaN
By which mechanism, does medullary thyroid cancer cause secretory diarrhea?
Medullary thyroid carcinoma is usually associated with men syndrome in which we get VIPoma, which is associated with diarrhoea.
Upto date: "Systemic symptoms may occur due to hormonal secretion by the tumor. Tumor secretion of calcitonin, calcitonin-gene related peptide, or other substances can cause diarrhea or facial flushing in patients with advanced disease. In addition, occasional tumors secrete corticotropin (ACTH), causing ectopic Cushing's syndrome."
Colonic function was markedly impaired in three ways: (a) water absorption was decreased by half; (b) as the main excreted solutes were organic acids, a large electrolyte gap was recorded in faecal water, and (c) colonic transit time of the meal marker was very short, and was in agreement with the rapid transit of ingested radioopaque markers. These data strongly suggest that decreased absorption in the colon secondary to a motor disturbance is the main mechanism of diarrhoea in this case of medullary thyroid carcinoma, while calcitonin induced small intestinal fluid secretion suggested earlier is either non-existent, or only of minor importance.
Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1433550/
My dd for tumors and secretory diarrhea (someone wants to add):
- carcinoid tumor
- VIPoma
- Gastinoma
- Medullary thyroid cancer
Mnemonic for Macrocytosis (Non B12 causes):
ALPHA NERD
Alcohol
Liver disease
Pregnancy
Hemolysis (especially chronic)
Agglutination
Neoplasia (Including myelodysplasia)
Endocrine (Hypothyroidism)
Reticulocytosis
Drugs (Especially myelosuppressives like chemotherapy, anti-HIV meds)
This awesome mnemonic was written by Adnan Arif.
-IkaN
While Auscultating the Chest of patient and analysing Type of breathing, whether it's Bronchial or Vesicular.
Remember GRIP
1. Bronchial breathing:
Gap is present between Inspiration & expiration.
Respiration shows Inspiration & expiration equal length
Intensity is loud.
Pitch is high.
2. Vesicular Breathing:
Gap is absent.
Respiration shows Expiration is short.
Intensity is low.
Pitch is low.
This post was written by Adnan Arif. Thanks Adnan! (:
-IkaN
Related post: Abnormal breath sounds mnemonic
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| Ankylosing Spondylitis (Radiological signs notes) |
1. Durgs that inhibit hormone synthesis (Antithyroid drugs):
Propylthiouracil, methimazole, carbimazole.
Mnemonic: Professor Met Carby
2. Drugs that inhibit thyroid trapping (Ionic inhibitors):
Nitrates (NO3), thiocyanates (SCN), perchlorate (ClO4) .
Mnemonic: NTP
3. Inhibit hormone release:
Iodine, iodides of Na & K, organic iodides.
Mnemonic: I prevents release (Iodine, it's salts and organic form.)
4. Destroy thyroid tissue: Radioactive Iodine (I 131, I 123, I 125)
Mnemonic: Iodine normal is 128 (+3 &-3 are radioactive so is I 123)
That's all!
The mnemonics were submitted by Sareer. Thank you, Sareer, you're awesome.
-IkaN
When you are listening to a murmur, look for "SECRET Pi"
Site
Effect of posture
Character (Tapping, heaving, thrill)
Radiation ( Axilla, neck, shoulder)
Effect of Respiration
Timing
Pitch
This mnemonic was submitted by Adnan Arif =)
Thanks Adnan!
-IkaN
Hey everyone!
Someone requested me to make a mnemonic on reliability and validity. Let me tell you in short what these terms mean!
What is validity and reliability?
Let's take the example of measuring blood glucose levels.
Suppose, we have developed a test to measure glucose levels and we measure it in healthy man. Normal standard we have set is, let's say, 80.
Reliability means test will give the same value each time. Let's say, we measured three times it gave reading of 120, 120, 120 that is reliable. Reliability is consistency. Also called precision.
But validity means the test will give a value which is close to our standard value, that is, 80 in this case. The three readings we get this time are 82, 85, 79. So this test is reliable, but not valid. Validity is also called accuracy. Validity is not affected by sample size.
This interplay of words messes up with one of my readers brain, so I'm sharing the mnemonic I made on it. I thought it was silly at first, to use a mnemonic to remember words, but I'm glad you all are as weird as me.
VACuum = Validity + ACcuracy
PReCiSe = Precision + Reliability + Consistency + Sample size dependent
That's all!
Life is so good. I've never been so happy and calm. I'll tell you why soon, but for now, I just wanted you guys to know (:
-IkaN
Related post: Biostatistics mnemonic
Can someone explain how ethacrynic acid causes deafness?
Na+K+Cl+ transporter is also present in the ear. This transporter is the main site of action for ethacrynic acid. So when it acts the transporter Is inhibited leading to ionic imbalance. This results in hearing loss.
It is the diuretic which is most dangerous when it comes to causing sensorineural deafness.
Even then it's use indicated in one special condition. Guess which condition?
If a patient has reaction to sulpha drugs.. The DOC becomes ethacrynic acid.
Recent studies revealed that the ototoxic effect of EA is actually involved in selectively blocking the lateral spiral artery in the cochlea and suppressing the blood flow supply to the cochlear lateral wall. The epithelial ischemia and anoxia in stria vascularis resulted in a significant depression of endolymphatic potential which was equivalent to cutting off the power supply of the cochlea . During the ischemic damage to the epithelium and capillaries on the cochlear lateral wall, the vascular permeability and membranous permeability in stria vascularis were also affected so that the ototoxic drug can penetrate through the broken blood-cochlea barrier to enter the cochlea.the ototoxic drug can reach the cochlear hair cells either through the cuticular plate facing the endolymph or through the under parts of the hair cells in the cortilymph.
In short bro, hair cell damage directly by EA.
Oooh. So it first causes ischemia and then enters the hair cells. But at the end the outer hair cells are getting damaged. Nice!
In otosclerosis, why carharts notch at 2000 Hz in PTA?
Carhart attributed this phenomenon to "mechanical factors associated with stapedial fixation."
But why the greatest dip at 2 kHz?
The ossicular chain has two basic modes of vibration. The first mode, with a peak around 1200 Hz, is the primary mode for AC stimulation. This mode is associated with a "hinging" motion of the ossicles caused by AC stimulation of the tympanic membrane at the umbo. The second mode, with a peak around 1700 Hz, is described as a "pivoting" motion of the malleus/incus, with an axis of rotation somewhat orthogonal to the axis of rotation associated with the "hinging" motion. The second mode is less robust than the primary mode for AC stimulation, but it is the dominant mode when excited by BC stimulation. A decreased mobility of the ossicular chain at 1700 Hz due to otosclerosis also affects the surrounding frequencies, but is seen most prominently as a BC loss at 2000 Hz in audiometric testing.
