Score 99 USMLE blog

Testicular torsion - Key points for the USMLE

2011-12-19T01:22:00.000-05:00

Torsion is the most common cause of acute scrotal swelling and pain
-Underlying cause is a high attachment of tunica vaginalis that occurs in 12% of males
-Symptoms may include nausea and vomiting and even fever (in addition to testicular symptoms)
-Examination may demonstrate a horizontal and elevated testis
-The cremasteric reflex is usually absent, but its presence does not rule out testicular torsion.
-Elevation of the scrotum does not relieve the pain
-Doppler can confirm diagnosis although it is often not needed
-If surgery is done after 6 hours of onset the chances of testicular atrophy are extremely high
-During surgery the opposite (normal) testis is also fixed because the high attachment anomaly is often bilateral

Differential diagnosis:
1) Acute epididymitis and/or orchitis
-Onset is more gradual with fever and dysuria.
-Elevation of the scrotum may reduce discomfort
-Cremasteric reflex may or may not be present
-Teatment is with rest, analgesia, and antibiotics if there is concern about a bacterial infection

2) Torsion of the appendix testis
-Localized tenderness over the upper portion of the testis
-Blue dot sign
-Cremasteric reflex is present
-Treatment is analgesia

Asperger syndrome vs Autism key points

2011-12-18T00:21:00.000-05:00

Asperger disorder
-Impairment in social interaction (few interests)
-They are aware that they do not fit in socially.
-Unlike autistic children, they do not express basic language impairment (only minor problems)
-Treatment is behavior modification and cognitive-behavioral therapy are used to improve level of function.
-Some consider this condition as high functioning autism

Autism
-Usually manifests itself before age 3 years (Asperger may be later)
-Triad of
---Impairment in social interaction (no friends, no empathy)
---Language delay
---Ritualistic behaviors and a strong need for sameness and consistency
-Treatment includes intense family support, behavior modification, speech and language training, auditory integration training, and medication.

Epstein's pearls and Bohn's nodules

2011-12-15T17:20:00.001-05:00

Epstein's pearls are tiny cystic lesions of the palate found in approximately 2/3rds of newborns. They are visible over the region of fusion of the posterior palatal segments and are a result of the inclusion of epithelial cells during palatal fusion. Bohn's nodules are also benign and much less frequent than Epstein's pearls. They occur along the junction of the hard and soft palate or adjacent to the midpalatal raphe and are derived from epithelial remnants of developing palatal salivary glands. Distinction between Epstein's pearls and Bohn's nodule is difficult and clinically irrelevant because both of these lesions regress and require no treatment.

Do not confuse these with the following conditions:

Congenital epulis is a very rare tumor seen in the newborn period (especially in females). It is usually firm and pedunculated and visible on the anterior alveolar ridge of the maxilla. It is benign in nature but may lead to difficulty with feeding and/or respiration requiring excision.

Mucoceles are clear fluid-filled, well-circumscribed, small lesions usually visible on the labial mucosa of the lower lip. These occur as a result of trauma to a submucosal salivary duct, usually from blunt trauma or lip biting. They usually also require no treatment. Large lesions may be de-roofed.

Rett syndrome key points

2011-12-15T03:26:00.000-05:00

Rett syndrome
-X-linked dominant (Affects girls).
-Onset is in the second year of life.
-Typically there is regression in motor and language development
-Autistic behaviors are common
-There is acquired microcephaly
-Characteristic hand-wringing behavior

Poor prognosis. No specific treatment.

Vitiligo

2011-12-09T02:15:00.001-05:00

Vitiligo is characterized by hypopigmentation of the skin. It is an autoimmune condition that results from melanocyte dysfunction.

Image from Wikimedia Commons.
Available here:http://en.wikipedia.org/wiki/File:Vitiligo2.JPG

Signs and symptoms

-Hypo or depigmented patches that often enlarge and change shape.
-Most prominent on the face, hands and wrists.

Treatment

-UVB phototherapy with or without Psoralen, a material that increases the effect of the UV light. It can be done at home or a few times a week in the clinic.
-Studies have shown that immunomodulators such as topical tacrolimus (Protopic) and pimecrolimus (Elidel) may also cause improvement in some cases, when used with UVB narrowband treatments
-Psoralen and Ultraviolet A light (PUVA) therapy is generally performed in clinic setting.
-Skin camouflage/make up
-Depigmenting with topical drugs like monobenzone, mequinol or hydroquinone may be considered to make the not vitiligous skin appear fairer and uniform. It increases risk of melanoma and consistent sun protection should be advised.

Differential diagnosis

-Pityriasis alba
-Tuberceloid Leprosy
-Post inflammatory hypopigmentation
-Tinea versicolor
-Albinism
-Piebaldism

USMLE pearl: Vitiligo is often associated with other autoimmune diseases including Hashimoto thyroiditis, type I Diabetes Mellitus, Addison's disease, pernicious anemia etc.

Strategies, Tips and Tricks to succeed in the USMLE Step 1 and 2 CK

2011-12-09T00:22:00.000-05:00

Five keys to success

1-Know the content
2-Learn how to apply the knowledge at solving multiple choice questions
3-Keep your calm. There will always be questions you will not know the answers to. In fact there will be many!
4-Practice questions and develop expertise at solving multiple choice questions.
5-Know the exam software really well. Practice again and again. You should know where every button is and what they do. You should know exactly how many questions are going to be there in how many blocks. Things keep changing so refer to the latest material from the official website www.usmle.org)

How to approach a question:

1. Read the question stem well

This sounds obvious but believe me (and I am sure others have told you) when I say this is the most important thing. In the stress of the real exam it is easy to overlook key facts. Spend time reading every word. When reading try to pick key facts and if it is a clinical scenario try to think of the diagnosis even if that is not what the question might ultimately ask. It is better to read well in the first go but re-reading is a good idea (although takes more time) if you think you didn't do a good job at the first time around.

2. Guess the answer before reading the options

Once you had read the question stem try to think of the right answer BEFORE reading the options. It is understandably difficult to do this under stress of a real exam but it is well worth trying. This is because most USMLE questions have traps or distractors. Traps are options that sound right but are not. If you read options before giving a good thought to what the answer might be, it might be difficult to think without a bias.

3. Is your answer present in the options provided?

If the answer you thought as above is actually present as one of the options, it is probably right answer but you have to read the other options to make sure that it fits the best. Remember, if two answers seem to be almost the same, then neither one is probably right.

4. If not start excluding the wrong options

If you do not know the right answer try to exclude the wrong ones and narrow down to 2 or 3 options. Depending on how much time you have at hand you might consider re-reading the question stem at this point to find a hint in favor or against any of the options.

5. Guess!

In the end, even after exclusions if you can't reach to a final answer, Guess. There is no negative marking in the USMLE. No answer is as good or bad as wrong answer so simply guess an answer and do not leave any question unanswered.

And on your big day

1) Be confident but at the same time prepared to feel stupid. You might feel like you did not know more than half the questions. I have multiple friends who cried after the exam thinking they will fail but ended up getting scores >240 (99)

2) Arrive on time. In fact, I recommend you arrive 30-45 minutes before time. Take the scheduling permit and a government issued photo ID. In countries outside the US they sometimes insist on a passport and may not recognize other IDs (for e.g. like driving license). Don't let any of these be additional anxiety proving issues. The exam itself is enough!

3) Drink strong coffee. Take some along. Also take some snacks with lots of sugar. Remember, glucose is the only fuel our brain can use. It can not use amino-acids, fatty acids etc. unlike other body organs. (You can store everything in the locker which they will provide).

4) Taking breaks: I recommend that at the end of each block when it gives you option to take a break or go to next block, hit 'Take a break'. Then ask yourself: 'Do I need to pee', 'Do I need to eat', 'Do I need to drink'. If the answer to those questions is 'No'. Take a few seconds (or minutes) while sitting on your seat to refresh your brain and tell your self, 'I am ready for more' and then start another block. If the answer is 'Yes', you can leave your seat and do the needful! I recommend taking a slightly longer break of about 10-15 minutes after 3-4 blocks to refresh your brain.

5) Start with question 1 and go till the end. Time yourself so that you do not miss any questions because of lack of time. Every 10 questions or so check to ensure you have enough time for the remaining questions and if not try to speed up.

6) Do not leave a question unanswered to come back to it. You can mark it with a check mark to come back if you have time left at the end of your block and change the answer but do not leave a question without choosing an answer because you may never get back to it.

7) Try not to mark too many questions to come back. If you think that you might get the correct answer if you give it a thought mark it. I would say mark no more than 5-6 questions in a block. One good example is questions on biostatistics that require some math. I always marked a random answer and came back to do the math at the end unless it was very simple. Because it is easy to do the math wrong in a hurry.

8) Some people say when you change an answer, you are more likely to choose a wrong answer. I disagree. In my opinion, if you think a different answer is right, go ahead an change it. In all the practice tests that I had done in preparation for the boards, I found that I changed from a wrong answer to right more often than I did from right to wrong.

Good luck for the test!

Key points to remember about sideroblastic anemia for the USMLE

2011-11-13T04:04:00.000-05:00

-Sideroblastic anemia results from hereditary (X-linked) or acquired disorder of heme synthesis.

-It is a microcytic hypochromic anemia with a high RDW (red cell distribution width) Same as iron deficiency anemia.

-Iron studies will distinguish the two. In sideroblastic anemia serum iron, serum ferritin and transferrin saturation are increased.

-The impaired synthesis of heme leads to retention of iron in the mitochondria. The nucleated RBC's show aggregation of iron in the mitochondria and has a perinuclear distribution. These cells are called ringed sideroblasts, which are characteristically seen in sideroblastic anemia.

-Severity can be mild or severe enough to need frequent transfusions.

-Treatment: Pyridoxine helps in some rare inherited cases but manu need periodic transfusions. Stem cell transplantation has been used to treat children who are dependent on blood transfusion.

Treatment of Gout (Acute and Chronic)

2011-10-30T06:12:00.001-04:00

Gout is an important topic for all 3 USMLE steps. Below is a summary of key potential facts that may be questioned in these exams with regards to the treatment of Gout.

Treatment of Acute Attacks of Gout

-First the diagnosis should be confirmed. Septic arthritis has the potential to look exactly like gout, hence the initial step is always arthrocentesis unless the patient has a known diagnosis.

-Next step is pain management. Nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and ACTH are the mainstays of treatment. Co-existent health conditions determine which drugs are used. For example renal failure may contraindicate use of certain NSAIDS.

-When comorbidities limit the use of NSAIDs or colchicine, intra-articular steroid injection may be indicated.

-One must remember that control of the underlying hyperuricemia is contraindicated until the acute attack is controlled as it may intensify and prolong the attack. However if the patient is already on allopurinol or probenecid, they should be continued.

Medications for acute gout:

Nonsteroidal anti-inflammatory drugs
NSAIDs are the first drugs of choice in most patients (typically indomethacin is used except in elderly because of CNS adverse effects). Contraindications to NSAIDS use include peptic ulcer disease or GI bleeding, renal failure, abnormal liver function and patients on warfarin (selective COX-2 inhibitors like celecoxib can be used). Additional caution in needed for those patients who are on ACE inhibitors as both ACE inhibitors and NSAIDS can decrease the GFR. NSAIDS are given at full dose for about 4-5 days and then dose is gradually decreased.

Colchicine
Colchicine is a mitotic inhibitor and has now become a second line treatment because of risk of adverse effects. To be effective colchicine therapy must be initiated within 24 hours of onset of the acute attack. Common adverse effects include diarrhea and vomiting, in 80% of patients. A number of dosing regimens are proposed with recent recommendations favoring lower doses with a maximum of 2.5 mg/24 hours and 6 mg over 4 days. Contraindication to colchicine include severe renal insufficiency (GFR less than 10 mL/min), hepatic dysfunction and biliary obstruction.

Colchicine is one agent that can be used in acute gout as well as for Gout prophylaxis (0.6mg BID). Myopathy is an important side effect of chronic colchicine therapy.

Corticosteroids
Corticosteroids can be given to patients with gout who cannot use NSAIDs or colchicine, but ACTH is generally preferred over steroids.

Treatment of Chronic Gout

-Firstly attempt should be made at avoiding the use of medications that elevate uric acid. For example thiazides should be avoided and losartan should be considered in stead. (Losartan is uricosuric at 50 mg/day doses). If the patient has tophaceous disease, probenecid should not be used.

-Probenecid (uricosuric agent) and allopurinol (decrease production of uric acid) are the two main drugs used. Probenecid is preferred by some.

-Patients with very high uric acid excretion will benefit from Allopurinol. It is also the drug of choice in patients with existing renal disease.

Medications for chronic gout:

Probenecid
Probenecid inhibits tubular reabsorption of uric acid. Some physicians recommend alkalizing the urine when starting probenecid to reduce the risk for renal stone formation. All patients should be advised to drink plenty of liquids (>2L a day).

Allopurinol
Allopurinol is xanthine oxidase inhibitor and thus reduces the generation of uric acid. Therefore, it should be used in patients who overproduce uric acid (also used in patients at risk of tumor lysis syndrome). Common side effects include dyspepsia, headache, diarrhea, and rash. Allopurinol hypersensitivity is a wellknown but rare complication with high mortality. Allopurinol is also associated with the drug rash with eosinophilia and systemic symptoms (DRESS) syndrome. For these reasons Allopurinol should be discontinued in patients who develop a rash.

Febuxostat
Febuxostat is a newer nonpurine selective inhibitor of xanthine oxidase, and is a potential alternative to allopurinol.

Other treatments:

Rasburicase
Rasburicase is an extremely potent (and expensive) drug that can metabolize uric acid into soluble substances. It is used in treatment of tumor lysis syndrome. It is very prone to causing allergic reaction and its role in treatment of gout is not clear.

Diet and Activity
Foods very high in purines include hearts, sweetbreads (eg, pancreas, thymus), smelt, sardines, mussels, anchovies, trout, haddock, scallops, mutton, veal, liver, bacon, salmon, kidneys, and turkey. These should be avoided as much as possible. Patients with gout should limit alcohol as it can precipitate gout. This is especially true for beer and hard alcohol but mild-moderate wine drinking is well tolerated by most.

Increasing dairy intake, folic acid intake, and coffee consumption may reduce gout flares. Weight reduction in patients who are obese can improve hyperuricemia.

Angelman Syndrome vs. Prader Willi Syndrome: Genetics and Clinical Features

2011-10-08T23:39:00.009-04:00

Prader-Willi and Angelman syndromes are the two most common genetic disorders of imprinting. The concept of imprinting lies in the fact that the function of certain genes is dependent on their parents: maternal or paternal. Basically there is something wrong with the 15q11 region of the paternally derived chromosome in Prader Willi syndrome and that of the maternally derived chromosome in Angelman syndrome.

Prader-Willi phenotype can occur as a result of one of the following

1. Deletion of 15q11-q13 including the Prader-Willi critical region of the paternally derived chromosome 15 (most common)

2. Abnormality of the structure of Prader-Willi critical region of 15q11-q13 (for example translocation)

3. If the child has two maternally derived chromosome 15s. (Hence absence of paternal chromosome 15)

4. Mutations of imprinting control center genes (rare)

The critical region of chromosome 15 for Angelman syndrome is located very close to the Prader-Willi critical region. But, when deletion of the Angelman critical region results, it is the maternally derived chromosome that is affected.

Mechanisms leading to Angelman syndrome include the following:

1. Deletion of the 15q11-q13 including the Angelman critical region of the maternally derived chromosome 15 (most common)

2. Abnormality of the structure of the Angelman critical region of 15q11-q13 (e.g. translocation)

3. If the child has two paternally derived chromosome 15s. (Hence absence of maternal chromosome 15)

4. Mutations of imprinting control center genes (rare).

5. Mutations of the ubiquitin-protein ligase gene (UBE3A)

6. No identifiable etiologic mechanisms but a positive family history of other affected individuals and a classic phenotype

Clinical features of Prader Willi syndrome:

Newborns: hypotonia, poor sucking and swallowing, weak cry
Infancy: Delayed motor and speech development
Toddler: Hypotonia goes away! Extreme appetite leading to morbid obesity.

In addition hands and feet are noticeably small from birth, height is short and the penis and testes are hypoplastic. Patients have emotional lability and extreme temper tantrums.

Clinical features of Angelman syndrome:

Severe cognitive deficits; speech is heavily impared. Inappropriate paroxysms of laughter (happy puppets). Physical features include microcephaly, maxillary hypoplasia, large mouth, and short stature.Seizures are common. Except for case reports, all patients are infertile.

Miliaria rubra or prickly heat

2011-10-08T06:58:00.000-04:00

Miliaria rubra, or prickly heat is caused by obstruction of sweat ducts in epidermal or dermal layers. This rash is common in infants and children, especially in the summer. It appears over the face, upper trunk, and intertriginous area of the neck, as a result of tight-fitting clothing. Wearing lightweight, loose-fitting clothing, eliminating greasy topical agents, and using corn starch or even talcum powder help get rid of the rash.

Hashimoto Thyroiditis/ Chronic Lymphocytic Thyroiditis

2011-09-25T23:00:00.000-04:00

Hashimoto's thyroiditis a.k.a. chronic lymphocytic thyroiditis is an autoimmune condition affecting young females. It is sometimes known as Prasad syndrome. It is the most common cause of primary hypothyroidism in North America.

Pathophysiology: Antibodies against thyroid peroxidase and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland. There is infiltration of thyroid tissue by leukocytes, mainly T-lymphocytes. It is associated with non-Hodgkin lymphoma.

Clinical features: Features of hyperthyroidism can be seen initially (and sometimes intermittently), however the predominant feature is hypothyroidism. The thyroid gland is firm and mildly enlarged and sometimes lobulated.

Diagnosis: Hashimoto's thyroiditis is diagnosed by detecting the presence of anti-thyroglobulin antibodies (anti-Tg), anti-thyroid peroxidase antibodies (anti-TPO) and anti-microsomal antibodies.

Differential diagnosis: Depression, cyclothymia, PMS, chronic fatigue syndrome, fibromyalgia and, anxiety disorder.

Treatment: Hypothyroidism is treated with thyroid hormone replacement agents such as levothyroxine. Aim of treatment is to keep TSH levels be kept under 3.

Embryology of the heart and fetal circulation

2011-08-28T16:29:00.000-04:00

This is an old but awesome video on embryology of the heart and fetal circulation.

Complications of myocardial infarction

2011-08-23T01:29:00.000-04:00

Myocardial infarction (MI) due to coronary artery disease is a leading cause of death in the United States.

Complications of MI include:
-Arrhythmic
-Mechanical
-Inflammatory

-Thrombo-embolic
-Circulatory/Shock

Arrhythmic Complications of MI:

About 90% of patients with MI develop some form of cardiac arrhythmia. These arrhythmias can be broadly classified into the following categories:

Supraventricular tachyarrhythmias
Accelerated junctional rhythms
Bradyarrhythmias
Atrioventricular (AV) blocks
Intraventricular block
Ventricular arrhythmias
Reperfusion arrhythmias

Mechanical Complications:

-Ventricular free wall rupture and pericardial tamponade
-Ventricular septal rupture
-Papillary muscle rupture with severe mitral regurgitation
-Left Ventricular Aneurysm

Inflammatory complications:

-Pericarditis: Occurs in 10% patients within the first 4 days of MI)
-Post-MI syndrome (Dressler syndrome): Occurs in 1-5% after MI and can present 2-3 weeks after MI.

Thrombo-embolic complications:

Occur secondary to regional myocardial hypokinesia and stasis as well as secondary to arrhythmias such as atrial fibrillation.

Circulatory/Shock:

Can be seen in right ventricular infarction (treatment is IVF) and in massive left ventricular infarction (treatment is supportive with careful administration of IVF.

Caput succedaneum vs. Cephalhematoma

2011-08-05T15:25:00.001-04:00

Caput succedaneum is a common and benign condition in which head compression against the cervix impedes venous return. It has the following characteristics
- Apparent usually at birth
- Crosses suture lines
- Reabsorbs within 1-3 days

Cephalhematoma (also spelled as cephalohematoma cephalhaematoma and cephalohaematoma) on the other hand is collection of blood below the periosteum. It has the following characteristics.
- Typically becomes apparent 1-2 days after birth
- It does not cross the suture lines (because it is under the periosteum).
- Takes 3-4 weeks or longer for it to be reabsorbed
- Can lead to jaundice from degradation of the extravasated blood
- Often associtated with birth trauma and a fracture in the newborn's skull bones (most commonly parietal bone)

Mechanism of action of common antibiotics

2011-07-27T12:19:00.000-04:00

Betalactams (e.g. penicillins and cephalosporins): Inhibit cell wall synthesis.

Fluoroquinolones (e.g. ciprofloxacin and nalidixic acid): Bind to bacterial DNA gyrase and topoisomerase IV, interfering with bacterial DNA synthesis.

Tetracyclines: Bind to the bacterial 30S ribosome, inhibiting bacterial protein synthesis.
Aminoglycosides (e.g. gentamicin): Bind to 30S ribosome unit as well.

Macrolides (e.g. azithromycin): Reversibly bind to the 50S ribosomal subunit.

Sulfonamides (e.g. sulfamethoxazole): Inhibit steps in bacterial folic acid synthesis.

This stuff is high yield for Step 1.

Take a quick break!

2011-07-26T15:06:00.000-04:00

Two molecules are walking down the street; one bumps into the other and says:
"Oh, my fault. Are you okay?”
The second molecule says: "No, I'm not okay. I've lost an electron!"
The first molecule says: "Are you sure"
The second molecule answers: "I'm positive!"

Now get back to work! Click on any topic above to start reading useful pearls for the USMLE.

Lead screening, levels and treatment in children

2011-07-20T14:34:00.000-04:00

Current guidelines state that health-care professionals should use blood lead tests to screen children at ages 1 and 2 years. Older children should be screened in certain high risk situations.

The American Academy of Pediatrics policy statement recommends the use of venous samples for initial screening whenever possible. If capillary testing is performed and the lead concentration is greater than 10 mcg/dL, the lead concentration must be confirmed by a venous sample because capillary sampling is more likely to yield false-positive results due to contamination from skin.

Chelation therapy should be considered if lead concentrations are higher than 44 mcg/dL. The role of chelation is not clearly defined for children whose blood lead concentrations range from 20 to 45 mcg/dL. Levels below 20 mcg/dL can be monitored periodically.

Succimer is the drug of choice for children whose blood lead concentrations are > 45 mcg/dL. For levels >70 mcg/dL calcium-disodium EDTA can be added. The first dose always is succimer, followed 4 hours later by EDTA, because EDTA when given alone can worsen lead encephalopathy.

Hemolytic-uremic syndrome

2011-07-20T04:14:00.000-04:00

Hemolytic-uremic syndrome (HUS), is essentially a vasculopathy characterized by hemolytic anemia, acute renal failure and thrombocytopenia. It is caused by a variety of agents but most commonly by E. coli O157:H7, which is a gram negative bacteria acquired via contaminated food or drinks.

Pathophysiology:
-Shiga toxin-producing E. coli (STEC) or enterohemorrhagic E. coli (EHEC) produce a toxin called verotoxin or shiga-like toxin.
-Toxin enters the bloodstream and causes damage to the body's vascular endothelium.
-Endothelial damage leads to platelet activation that causes thrombocytopenia. The renal glomerular endothelial cells express a receptor for the toxin.

Clinical features:
-HUS is characterized by the triad of hemolytic anemia, thrombocytopenia, and acute renal failure.
-Preceding bloody diarrhea may or may not be present.
(HUS must be distinguished from Thrombotic thrombocytopenic purpura (TTP) which in addition to the triad above has fever and neurological signs. TTP is caused by an acquired defect in the protein ADAMTS13.)

Treatment:
-Supportive treatment for low platelets (transfusion if bleeding)
-Supportive treatment of renal failure (electrolyte balance, dialysis as needed)
-Plasmapheresis is often used in early cases to get rid of the circulating toxin
-With supportive care majority of the patients have good renal outcomes

Take a break. Read a joke!

2011-07-19T14:27:00.001-04:00

On their honeymoon, the new husband told his bride, "I have a confession to make that I should have made before, but I was concerned that it might affect our relationship.

"What is it?" his new bride asked lovingly.

"I'm a golf fanatic," he said. "I think about golf constantly. I'll be out on the golf course every weekend, every holiday, and every chance I get. If it comes to a choice between your wishes and golf, golf will always win."

His new bride pondered this for a moment and said, "I thank you for your honesty. Now in the same spirit of honesty, I should tell you that I've concealed something about my own past that you should know about. The truth is, "I'm a hooker."

"No problem," said her husband, "just widen your stance a little, and overlap your grip, and that should clear it right up."

Caisson Disease or Decompression Sickness

2011-07-19T01:44:00.000-04:00

Caisson disease is also known as decompression sickness or diver's disease. When the body is subjected to high surrounding pressure (e.g. scuba diving), more than usual amount of Nitrogen gets dissolved in the blood. If the pressure is relieved suddenly, the dissolved Nitrogen can become gaseous quicker than the body can get rid of. These bubbles can lead to ischemia by blocking blood vessels. Clinical situations when such sudden depressurization can occur include scuba diving, caisson working, mining, flying in unpressurised aircraft, and extra-vehicular activity from spacecraft.

Depending upon the location of ischemia a variety of symptoms can results. Classically the symptoms are described as the bends, the chokes and the staggers!

The bends: refers to pain in the joints from ischemia of joint capsules
The chokes: refers to dyspnea
The staggers: refers to neurological symptoms.

Prevention:

-Divers should limit their ascent rate to about 10 metres per minute.
-Oxygen pre-breathing

Treatment:

-Administer 100% oxygen by face mask until re-compression with 100% oxygen until hyperbaric oxygen therapy is available.
-Treat dehydration

Systemic Lupus Erythematosus (SLE) Nephritis Classes and Prognosis

2011-07-15T07:59:00.001-04:00

Class I has no histologic changes and has the best prognosis.

Class II has proliferation in the mesangium and has good prognosis.

Class III has focal proliferation. It has variable prognosis.

Class IV has diffuse proliferation and bad prognosis.

Class V has membranous changes and relatively better progrnosis.

Class VI has scarred glomeruli and end stage disease.

This letter M has five red circles. (Membranous)

Extrapyramidal side effects of antipsychotics

2011-07-13T15:05:00.000-04:00

Akathisia refers to an urge to keep moving. Typicallythe patients will pace about in the house and sit down and get upagain. First line treatment of akathisia is propranolol althoughbenzodiazepines have also been used. Akathisia can occur any time after starting the medication.

Tardive duskinesia (TD) refers toinvoluntary movements which can be perioral (such as lip smaking,chewing and darting tongue movements) or choreoathetoid movements ofextremities or other body parts. TD usually does not occur within thefirst 3 months of starting the medications. TD can be difficult totreat and may require changing to medications that do no cause thisside effect such as clozapine.

Dystonia occur withinhours or days of starting the therapy. Characteristic featuresinclude muscle spasms (e.g. torticollis). Treatment of dystonia isacomplished by antihistaminic medications like diphenhydramine(Benadryl) or anticholinergics like benztropine or trihexphenidyl.

Neurolept maligant syndrome is a knownside of antipsychotics that presents with hyperthermia, muscle rigidityand mental status changes. It usually occurs after 1-2 weeks ofstarting the therapy. Treatment includes stopping the medication anduse of dantrolene, bromocriptine and amantidine.

Commonest antipsychotics leading to these side effects inlcude: chlorpromazine (Thorazine, Largactil), Fluphenazine (Prolixin) - Available in decanoate (long-acting) form, Perphenazine (Trilafon), Prochlorperazine (Compazine), Thioridazine (Mellaril, Melleril), Trifluoperazine (Stelazine), Mesoridazine, Periciazine, Promazine, Triflupromazine (Vesprin), Levomepromazine (Nozinan), Promethazine (Phenergan), Pimozide (Orap), Chlorprothixene (Cloxan, Taractan, Truxal), Clopenthixol (Sordinol), Flupenthixol (Depixol, Fluanxol), Thiothixene (Navane), Zuclopenthixol (Cisordinol, Clopixol, Acuphase)

DLCO - Diffusion Capacity of Lungs for Carbon Monoxide

2011-06-30T13:41:00.000-04:00

DLCO measures the ease with which CarbonMonoxide can diffuse across the alveolar lining. Normal would be 100 +/- 20. There areconditions in which it can increase as well as decrease as listed below.

DecreasedDLCO:

With restrictive pattern on PFTs (poulmonary function tests)then diagnosis could be restrictive lung diseases such as fibrosis,pneumonitis, elveolitis, idiopathic pulmonary fibrosis, firbrosis secondary tobleomycin therapy.

With obstructive pattern on PFTs then diagnosis is usuallyemphysema.

If there is noPFTs and clinical scenariosare suggestive the following two could be possible:
1) Pulmonary embolism (longplane journey, after pregnancy, on oral contraceptives etc.)
2) Pulmonary hypertension (idiopathic, h/o heartdisease etc.)

IncreasedDLCO:

With increased circulating lungblood volume e.g. exercise, heart failure

Asthma

Polycythemia

Normal DLCO

Can be seen in extrinsic conditions affecting the ventilation for example scoliosis. PFTs will show restrictive pattern but DLCO will be normal.

USMLE Ethics Question 8

2011-06-30T05:47:00.000-04:00

Q: Jacob is a 37 year old man who is brought to the emergency room by police after being arrested for suspected driving under influence of alcohol. Police requests you to give him sample of his gastric aspirates to prove alcohol consumption and test for other substances. The patient refuses to consent for insertion of a gastric tube. What should you do?

A: Follow the patient's requests. A physician cannot take orders from police. Patient has full right to refuse any medical treatment. A blood alcohol level can be performed. Rules vary from state to state with regards to refusal of breath or blood testing. Some states mandate either of the two while in some states the patient can refuse but will lose their driving license for a variable period of time. For the sake of USMLE I would advice that doing breath alcohol testing or blood alcohol levels should be chosen as the answer.

USMLE Ethics Question 7

2011-06-26T16:07:00.000-04:00

Q: 72 year Ms. Smith has chronic renal failure from diabetes and decides to stop getting dialysis. She understands that not getting dialysis will kill her. As her physician if you do not intervene she is certainly going to die. His 45 year old son urges you to save her life. What do you do?

A: Patients have the absolute right to refuse medical intervention. They can refuse cardiopulmonary resuscitation, mechanical ventilation, artificial nutrition or IV fluids, dialysis etc. even if it results in his or her death. Such a decision to withdraw or withhold life-sustaining treatment is not considered suicide and physician participation is not considered physician-assisted suicide. Physicians do not have any legal liability.

Osteogenesis Imperfecta

2011-06-26T08:38:00.001-04:00

The term Osteogenesis imperfecta was coined by Lobstein. The term is some what self explanatory! It is one of the relatively common bone dysplasias (1 in 20000 live births). OI involves all parts of the body that contain type 1 collagen to some extent giving rise to a variety of clinical presentations. Underlying mechanism in simple words is functional or actual decrease in collagen type 1 secondary to mutations in genes (most are inherited in autosomal dominant manner) coding for the same.

Clinical features include blue sclera, triangular facies, macrocephaly, hearing loss, dentition problems, chest deformity, scoliosis, limb deformities, fractures, joint laxity, constipation, sweating and growth retardation. There are several types, some being more severe than others (classified according to Sillence Classification). Type II has the most severe clinical presentation with most babies dying in newborn period. Type I is the mildest and commonest sub-type.

Diagnosis of OI is usually made clinically and confirmed by genetic testing for mutations. Radiological tests are useful and confirmatory in many cases. Findings include: fractures, excessive callus formation and popcorn bones (multiple radiolucent areas with radiodense rims), wormian bones in the skull, enlargement of frontal and mastoid sinuses, deformities of ribs, narrow pelvis. In mild cases dual x-ray absorptiometry (DEXA) scan can be useful and will show decreased bone mineralization.

Treatment is essentially supportive. Bisphosphonates, especially pamidronic acid, are drugs that inhibit osteoclast-induced bone resorption. These are given in a cyclic manner (every few weeks) and have been shown to decrease the fracture rate (especially in type III and IV OI). Side effects of pamidronic acid include hypocalcemia (usually not severe), leukopenia, increase in bone pain (which is typically transient), and scleritis.

Other drugs with unclear roles in the treatment of OI include: Human growth hormone, teriparatide (which is human parathyroid hormone, brand name is Forteo). Bone marrow transplantation and gene therapy are being investigated. Aggressive physical therapy, occupational therapy and education of parents about injury prevention is essential.

Above article also serves as explanation to Quiz 28: 'Femur X-Ray of a 3 year old boy' on the website www.pedsquiz.com

USMLE Ethics Question 6

2011-06-25T12:02:00.000-04:00

Q: Dr. Austin is a 42 year old obstetrician who is recently diagnosed with HIV infection. Is she required to tell her patients or fellow doctors about her HIV status?

A: No. She is not obliged to tell anyone. She should take appropriate universal precautions (which all doctors should, irrespective of their HIV status). She does need to authorize the hospital authority but this information cannot be used to terminate her job.

USMLE Ethics Question 5

2011-06-25T00:17:00.006-04:00

Q: John is a 2nd year pediatric resident and is asked to order a particular medicine for his patient by his attending physician. He thinks that the treatment is not appropriate and could be potentially harmful. What should he do?

A: He should ask the attending to explain the rationale. In most cases the attending will be able to convince the resident why the medicine is important. If he still doesn't agree with the attending he should not order the medicine and seek advice/consultation from senior resident, senior attending or division chief.

USMLE Ethics Question 4

2011-06-24T23:33:00.000-04:00

Q: Mr. Jameson is a 56-year old patient of yours who you have recently diagnosed with pancreatic carcinoma. You have referred him to an oncologist who plans to treat him aggressively with chemotherapy, radiation and surgery. The patient urges you not to tell his wife who is also a patient of yours about his diagnosis. His wife asks you about his diagnosis. What should you do?

A: Do not discuss Mr. Jameson's medical condition without his permission. However, you should encourage him to reveal his diagnosis to his wife.

Requirements of various state medical and osteopathic boards

2011-06-24T23:28:00.006-04:00

State	Minimum Postgraduate Training Required	Number of attempts at Licensing Examination	Time Limit for Completing Licensing Examination Sequence
Alabama	1 year; 3 years IMG	3+ attempts at USMLE Step 3; 10 attempts at all USMLE Steps; No limit on COMLEX	7 years to successfully complete all USMLE Steps; No limit on COMLEX
Alaska	2 years; 3 years IMG	2 attempts per USMLE Step; 2 attempts per COMLEX Level	7 years to complete USMLE; 10 years for MD/PhD candidates; 7 years to complete COMLEX
Arizona Medical	1 year; 3 years IMG	No limit on USMLE	7 years to complete USMLE if initial licensure / No limit if already licensed
Arizona Osteopathic	1 year	No limit on COMLEX	No limit on COMLEX
Arkansas	1 year; 3 years IMG unless currently enrolled in training program through Univ of Arkansas for Medical Sciences	3 attempts per USMLE Step; No limit on COMLEX	7 years to complete USMLE; 10 years for MD/PhD candidates; No limit on COMLEX
California Medical	1 year; 2 years IMG	4 attempts at USMLE Step 3	Passing scores on a written/computerized exam shall be valid for a period of ten (10) years from the month of the examination
California Osteopathic	1 year	No limit on COMLEX	No limit on COMLEX
Colorado	1 year; 3 years IMG	No limit on USMLE; No information available on COMLEX	7 years from first sitting to complete USMLE or COMLEX; 10 years for MD/PhD or DO/PhD candidates
Connecticut	2 years	No limit on USMLE; No limit on COMLEX	7 years to complete USMLE; No limit on COMLEX
Delaware	1 year; 3 years IMG	No information at this time	No information at this time
Washington, DC	1 year; 3 years IMG	3 attempts at USMLE Step 3; after which one additional year of postgraduate training is required. No limit on COMLEX	7 years to complete USMLE; No limit on COMLEX
Florida Medical	1 year; 2 years IMG	No limit on USMLE	No limit on USMLE
Florida Osteopathic	1 year in an AOA-approved program	No limit on COMLEX	No limit on COMLEX
Georgia	1 year; 3 years IMG	3 attempts per USMLE Step; No limit on COMLEX	7 years to complete USMLE; 9 years to complete USMLE if in MD/PhD program; No limit on COMLEX
Guam	1 year; Applicants must complete 36 months progressive approved training in US program	No information at this time	No information at this time
Hawaii	1 year; 2 years IMG	No limit on USMLE or COMLEX	7 years to complete USMLE; No limit on COMLEX
Idaho	1 year; 3 years IMG	2 attempts per USMLE Step; No limit on COMLEX	7 years to complete USMLE (10 years for MD/PhD candidates); No limit on COMLEX
Illinois	2 years	5 attempts at all USMLE Steps combined; 5 attempts at COMLEX Levels combined	7 years to complete USMLE; No limit on COMLEX
Indiana	1 year; 2 years IMG	3 attempts per USMLE Step; 5 attempts per COMLEX Level	10 years to complete USMLE; 7 years to complete COMLEX
Iowa	1 year; 2 years IMG	6 attempts at both USMLE Step 1 and 2; 3 attempts at USMLE Step 3; 6 attempts at both COMLEX Levels 1 and 2; 3 attempts at COMLEX Level 3. Three years of approved postgraduate training required if outside the attempt limit	10 years to complete USMLE or COMLEX; 10 years for MD/PhD or DO/PhD candidates. Note: Board certification by ABMS or AOA is required if the applicant has not met the specified time period
Kansas	1 year; 3 years IMG (minimum 2 years must have been in US program)	3+ attempts at USMLE Step 3 or COMLEX Level 3	10 years to complete USMLE or COMLEX
Kentucky	2 years	4 attempts per USMLE Step; 4 attempts per COMLEX Level	No limit on USMLE or COMLEX
Louisiana	1 year; 3 years IMG	No limit at USMLE Step 1 or COMLEX Level 1; 4 attempts each at USMLE Steps 2 and 3 or COMLEX Levels 2 and 3	10 years to complete USMLE or COMLEX
Maine Medical	US/Canadian medical school graduates who graduated after 7/1/04 must complete 3 years of postgraduate training. (Those who graduated before 7/1/04 are only required to complete 2 years of PGT); IMGs 3 years	3+ attempts at USMLE Step 3. More than 3 attempts require a request for a waiver	7 years to complete USMLE. More than 7 years requires a request for a waiver
Maine Osteopathic	1 year in AOA approved program	No limit on COMLEX	No limit on COMLEX
Maryland	1 year; 2 years IMG	4 attempts at each USMLE Step or COMLEX Level	10 years to complete USMLE or COMLEX
Massachusetts	1 year; 2 years IMG	6 attempts at USMLE Step 3; No limit on COMLEX	7 years to complete USMLE with exceptions for MD/PhD or DO/PhD candidates; No limit on COMLEX
Michigan Medical	2 years	No limit on USMLE	5 years to pass USMLE Step 3
Michigan Osteopathic	1 year in AOA approved program	No limit on COMLEX	No limit on COMLEX
Minnesota	1 year; 2 years IMG	3 attempts at each USMLE Step; No limit on COMLEX. Effective 04/11/08, 4 attempts allowed if current license in another state and current certification by specialty board of ABMS, AOABPE, RCPSC, CFPC	Beginning 8/1/07 USMLE Step 3 must be passed within five years of Step 2 or before the end of residency training
Mississippi	1 year; 1-3 years IMG	3 attempts at USMLE Step 3; No limit on COMLEX	7 years to complete USMLE; No limit on COMLEX
Missouri	1 year; 3 years IMG	3 attempts at USMLE Step 3; 3 attempts on COMLEX	7 years to complete USMLE (waived for MD/PhD candidates); No limit on COMLEX
Montana	2 years; 3 years IMG	3 attempts at USMLE Step 3; No limit on COMLEX	7 years to complete USMLE (exceptions possible for MD/PhD candidates); No limit on COMLEX
Nebraska	1 year; 3 years IMG	4 attempts+ at each USMLE Step; 4 attempts+ at each COMLEX Level	10 years to complete USMLE or COMLEX beginning with date 1st Step/Level is passed
Nevada	3 years	Must pass all 3 Steps of USMLE in not more than a total of 9 attempts and must pass Step 3 in not more than a total of 3 attempts	MD must pass all Steps of the exam within 7 years after the date on which the applicant first passes any Step of the exam; PhD must pass all Steps of the exam within 10 years after the date on which the applicant first passes any Step of the exam
Nevada Osteopathic	3 years for full license OR 2 years if resident signs commitment to practice in NV	No limit on COMLEX	DO graduated before 1995 does not require 3 years residency. No limit on COMLEX
New Hampshire	2 years	3 attempts at each USMLE Step or COMLEX Level	No limit on USMLE or COMLEX
New Jersey	US and IMG graduates who graduated after 7/1/03 must complete 2 years of postgraduate training and have signed a contract for a 3rd year in an accredited program. At least 2 of the years must be in the same field. Graduates prior to 7/1/03: 1 year; 3 years IMG	5 attempts at USMLE Step 3; or COMLEX	7 years to complete USMLE; or COMLEX
New Mexico Medical	2 years	6 attempts per USMLE Step	7 years to complete USMLE; 10 years for MD/PhD candidates
New Mexico Osteopathic	1 year	No limit on COMLEX	No limit on COMLEX
New York	1 year; 3 years IMG	No limit on USMLE or COMLEX	No limit on USMLE or COMLEX
North Carolina	1 year; 3 years IMG	3 attempts per USMLE Step; 3 attempts per COMLEX Level	USMLE Step 3 shall be passed within seven years of the date of passing Step 1 OR within 10 years if the reason for the delay is based on applicant obtaining an MD/PhD degree
North Dakota	1 year; 3 years IMG	3 attempts at each USMLE Step or COMLEX Level	7 years to complete USMLE or COMLEX
Northern Mariana Islands	No information available at this time	No information available at this time	No information available at this time
Ohio	1 year; 2 years IMG	Four attempt limit on each Step or Level on USMLE or COMLEX	Ten years to complete USMLE or COMLEX (possible waiver good cause if over ten years)
Oklahoma Medical	1 year; 2 years IMG	3 attempts at each USMLE Step (Step 2 = CK & CS)	10 years to complete USMLE
Oklahoma Osteopathic	1 year	No limit on COMLEX	No limit on COMLEX
Oregon	1 year; 3 years IMG	3 attempts + 1 year postgraduate training at USMLE Step 3; 3 attempts + 1 year postgraduate training at COMLEX Level 3 (waiver of 1 year postgraduate training + 4th attempt if ABMS/AOA certified)	7 years to complete USMLE or COMLEX (possible waiver for dual degree candidates; individuals with personal illness; current certification by ABMS or AOA; or completion of postgraduate training equivalent to number of years to a dual degree program)
Pennsylvania Medical	2 years; 3 years IMG	No limit	No limit
Pennsylvania Osteopathic	1 year	No limit on COMLEX	No limit on COMLEX
Puerto Rico	1 year	No limit on USMLE	USMLE Step 3 shall be passed within 7 years of the date of passing Step 1
Rhode Island	2 years; 3 years IMG	3 attempts at each USMLE Step; 3 attempts at each COMLEX Level	7 years to complete USMLE; No information available on COMLEX
American Samoa	No information available at this time	No information available at this time	No information available at this time
South Carolina	1 year; 3 years IMG	4 attempts per USMLE Step and COMLEX Level	10 years to complete USMLE or COMLEX
South Dakota	Successful completion of residency program	3 attempts per USMLE Step and COMLEX Level	7 years to complete USMLE or COMLEX. 10 years for dual degree MD-PhD applicant
Tennessee Medical	1 year; 3 years IMG	No limit on USMLE	7 years to complete USMLE unless licensed and in good standing in three other jurisdictions
Tennessee Osteopathic	1 year	No limit on COMLEX	No limit on COMLEX
Texas	1 year; 3 years IMG	3 attempts at each USMLE Step or COMLEX Level. (Exceptions may apply - see TMB website for more information www.tmb.state.tx.us)	7 years+ to complete the USMLE or COMLEX. (Exceptions may apply - see TMB website for more information www.tmb.state.tx.us)
Utah Medical	2 years	3 attempts at USMLE Step 3	7 years to complete USMLE; 10 years for MD/PhD candidates
Utah Osteopathic	2 years	3 attempts at each COMLEX Level	7 years to complete COMLEX; 10 years for DO/PhD candidates
Vermont Medical	1 year; 3 years IMG	3 attempts at USMLE Step 3	7 years to complete USMLE
Vermont Osteopathic	Has satisfactorily completed one year's post-graduated training in a rotating internship program approved by the AOA or has satisfactorily completed three years of postgraduate training in an AOA or ACGME-approved residency program (Rule 2.1.2 (3))	No information available at this time	All three COMLEX examinations Level 1, 2 & 3) must be completed in sequential order within seven years of the successful completion of Level 1/Part 1. (rule 2.1.3)
Virgin Islands	6 months required after 2 attempts for SPEX exam	Must take SPEX (only given in May and November) and an oral exam. 2 attempts	3 years to pass the 2 attempts allowed re-examinations. 1 year limitation to take the oral exam after passing written
Virginia	1 year; 2 years IMG	No limit on USMLE	10 years to complete USMLE; Greater than 10 years if candidate is ABMS certified
Washington Medical	2 years	3 attempts at USMLE Step 3	7 years+ to complete USMLE
Washington Osteopathic	1 year	No limit on COMLEX	No limit on COMLEX
West Virginia Medical	1 year; 3 years IMG	3 attempts per USMLE Step	10 years to complete USMLE
West Virginia Osteopathic	1 year	No limit on COMLEX	No limit on COMLEX
Wisconsin	1 year	3+ attempts per USMLE Step; N/A on COMLEX	USMLE Step 3 shall be passed within 10 years of the date of passing Step 1; N/A on COMLEX
Wyoming	1 year	Seven total attempts on USMLE or COMLEX	Seven years (eight years if in combined DO or MD/PhD program)

USMLE Ethics Question 3

2011-06-23T12:08:00.002-04:00

Q: John is a 55 year old man who works as a bus driver for the city of Washington DC. He had a stroke 6 months ago from which recovered well except that he has had 2 seizures in last 4 months and has focal damage on an MRI from the stroke. As his physician you believe that he is at risk of having more seizures and you have started him on antiepileptics. He requests his doctor not to mention his seizures to his employer as this may result in loss of his job and he is the sole earner in his family. What should you do?

A: Try to convince him to tell his employer. If he refuses you have to inform the appropriate the authorities because you have a duty towards him as well as the society.

USMLE Ethics Question 2

2011-06-22T22:35:00.000-04:00

Q: Sam Smith is a 4th year medical student currently doing his AI (acting intern) rotation in a big teaching, university hospital. He carries his own patients on the general medicine team. How should he introduce himself? Can a patient refuse treatment from him?

A: He should introduce himself as a student. He cannot say 'I am Dr. Smith'. A patient can refuse a medical student from performing any procedure. However, students are allowed to perform a procedure under appropriate supervision if the patient agrees to that.

Click on Ethics label in the label cloud to see more posts on ethics in USMLE

USMLE Ethics Question 1

2011-06-22T22:23:00.002-04:00

Q: A 17 year old male was diagnosed with metastatic osteogenic sarcoma of the left leg. After thorough investigation and discussion with the family the oncology team decided that the only way to cure him was to perform above knee amputation. The patient refuses amputation after understanding all the risks including that the cancer will certainly kill him if his leg is not amputated. What should the medical team do?

A: Correct answer is almost always respecting the individual's wishes. If this was not an adolescent patient (say a 5 year old) then the parents wishes should be respected but if the boy would die without it then doctors can bring in a court ruling against parent's wishes to perform amputation. There is no sharp demarcation as to above what age a patient can make true informed decisions but for the purpose of USMLE I would say 16 years or older patient who is mentally sound should be his or her own decision maker.

Click Ethics on the label clould on the side to view more posts on ethics in the USMLE.

Histograms vs. Bar graphs: what is the difference.

2011-06-18T01:50:00.002-04:00

They both look very similar and can be confusing. Essentially histograms are a type of bar graphs. Both these charts have frequency on the Y (vertical) axis and categories on the X (horizontal) axis.

In a bar graph the variables on X axis are arbitrary. For example if you ask one hundred 8 year old students to pick their favorite ice cream flavor the result can be plotted as a bar graph as follows. Note that the bars do not touch each other.

Bar graph

On the other hand in a histogram the variables on X axis are part of a population and the data on Y axis is numerical. For example say we measured the heights of the same 100 children. We could plot the graph as a histogram as follows. The X axis has range for height in inches. Note that the bars touch each other. In the USMLE you might be given some data and asked what kind of a chart will be most appropriate to present that data. With increased emphasis on bio-statistics and evidence based medicine, interpretation and presentation of such data may be tested more frequently in the USMLE.

Histogram

Click biostatistics label on the label cloud to view more posts on statistics in the USMLE

Types of Vitamin K

2011-06-09T00:53:00.001-04:00

Three forms of vitamin K are known to humans as follows:

K1: Phylloquinone: It is the 'plant' form and is found in green leafy vegetables, vegetable oils, and dairy products. This is the form given to newborns as water soluble IM injection at birth.

K2: Menaquinone: It is the form manufactured by bacteria in the intestines.

K3: Menadione: This is artificially designed vitamin K that is not used any more because of its adverse effects (hemolysis).

Vitamin K is required for gamma carboxylation of GLU residues on coagulation factors (Factors II, VII, IX, and X are called vitamin K dependent factors). In absence of vitamin K abnormal/defunct proteins called PIVKAs (proteins induced by vitamin K absence) are formed. These cannot participate in the coagulation cascade leading to failure of clotting and bleeding.

Hemorrhagic Disease of the Newborn

2011-06-08T00:55:00.000-04:00

Three forms of hemorrhagic disease of the newborn are recognized. The phrase is a misnomer because these can be seen during infancy after the neonatal period.

1) Early-onset: Typically presents during first 24 hours after birth and is seen in infants born to mothers who are deficient in vitamin K (those who are on seizure or tuberculosis medications). Site of bleeding is variable and can be serious (intracranial).

2) Classic: Presents between day 1 to 7 of life and is secondary to failure of administration of vitamin K at birth. Site of bleeding can be umbilicus, GI, skin, circumcision. Intracranial bleeding is less common.

3) Late: Presents from 2 weeks up to 6 months (rarely later) and is seen in exclusively or predominantly breastfed infants who did not get vitamin K at birth. Most common presentation is intracranial hemorrhage.

Treatment: Symptomatic (transfusion, supportive care, site specific treatment), FFP for active bleeding, vitamin K administration.

Clinical Presentation, Diagnosis and Treatment of Celiac Disease

2011-04-25T00:01:00.005-04:00

Celiac disease immune mediated disease in which the body makes antibodies against tissue transglutaminase (tTG) enzyme. Gluten is the most important environmental trigger and the disease has specific association with class II haplotypes of HLA DQ2 (haplotypes DR17 or DR5 or 7) and, DQ8 (haplotype DR4).

Clinical presentation: Typically it presents with abdominal symptoms between 6 months to 2 years of age (Age at which gluten is introduced in the diet). Symptoms include diarrhea, poor appetite, abdominal pain, emesis and failure to thrive. Celiac crisis can be a rare presentation in which the patient has severe watery diarrhea, bloating, dehydration, electrolyte imbalance(low K) and shock. Older children can present with nausea, vomiting, recurrent stomachache, constipation, diarrhea, anemia and stunting of growth.

Diagnosis: Antigliadin (AGA) tests were commonly used but now have fallen out of favor due to low sensitivity and specificity. The IgA endomysium (EMA-IgA) and tissue transglutaminase (TTG-IgA) tests are currently the tests of choice due to their high specificity. Diagnosis has to be confirmed by duodenal biopsy A minimum of 4 biopsy samples are recommended as patchy involvement is common.

Treatment: Complete avoidance of gluten is the key. This means avoiding Wheat, rye, barley. Oats are considered safe.

GBS (Group B Strep) infections

2011-04-19T20:33:00.000-04:00

Group B Streptococcus (GBS, Streptococcus agalactiae) is a common gram positive coccus that colonizes the vaginal and gastrointestinal tracts in 20-40% of healthy women. About half of GBS positive mothers will pass on the bacteria to their newborns but only 1% of these newborns will have a clinical infection. Transmission and clincal GBS disease is more common in premature infants and in women who have prolonged rupture of the membranes.

Neonatal group B streptococcal disease classically presents either as early or late sepsis. Early sepsis typically presents within 24 hours of birth but by definition can be evident up to seventh day of life. With early sepsis bacteremia and pneumonia are classic findings. Late sepsis on the other had can present up to 3 months postpartum and classically has bacteremia and meningitis.

Prevention: Term women with GBS positive cultures are treated with ampicillin intrapartum. Penicillin allergic patients can be treated with clindamycin or erythromycin.

GBS infection is otherwise rare in healthy individuals but the following conditions may predispose to an infection: Diabetes mellitus, malignancy, old age with bedridden state, cirrhosis, steroids, AIDS, renal failure, peripheral vascular disease. Common manifestations in these scenarios are urinary tract infection, pneumonia, and soft-tissue infection.

Pseudomembranous colitis (PMC)/Clostridium Difficile Infection

2011-03-30T09:10:00.003-04:00

PMC is caused by Clostridium difficile which is a spore producing gram positive rod/bacillus. It's incidence is about 0.5% in hospitalized adults. PMC typically occurs in setting of altered gut flora due to antibiotics.

Common antibiotics impicated include: Clindamycin, Ciprofloxacin (and other fluoroquinolones), Cephalosporins and macrolides. Both Vancomycin and Metronidazole which are used in treatment of PMC can also cause PMC. Omeprazole(and other proton pump inhibitors) and chemotherapeutic drugs have also been shown to increase risk for PMC.

Treatment is typically done with oral metronidazole (Flagyl) or oral vancomycin. Of the two metronidazole is usually preferred because it is relatively inexpensive and to reduce the risk of developing vancomycin resistant enterococci (VRE) organisms.

International MD Program

2011-03-28T08:00:00.002-04:00

The MD program at the Vita-Salute San Raffaele University enjoys recognition from the World Health Organization (WHO Avicenna Database), the British General Medical Council (GMC), the US Educational Commission for Foreign Medical Graduates (ECFMG^®) as listed in the International Medical Education Directory (IMED) of the Foundation for Advancement of International Medical Education and Research (FAIMER^®).

The curriculum at San Raffaele has been designed to allow those students interested in US postgraduate training to spend their final year abroad and take part in the pre-residency programs required for their future enrollment to US residencies.

Only 60 spots are available each year and admissions will be based on an entrance test based on analytical and logical skills. Thirty positions are reserved for non European Union students. Visit this link for more information on the program.

The Admission Test is entirely in English and is the only means of selection. The last date to enroll is April 3rd. The test will be held in Milan, New York and Kuala Lumpur. Click here to apply online.

Melanomas

2011-03-24T18:31:00.003-04:00

When to suspect malignant change in a mole? Look for the following 5 changes (ABCDE):

Asymmetric shape

Border is irregular or blurred

Color is not uniform

Diameter greater than 6 mm

Evolving changes from past appearance

Various types of melanoma are described as follows:

Superficial spreading:

It is most common on the trunk and on the legs and commonly seen in 30-50 year olds. It typically is a flat or barely elevated brownish lesion with inhomogeneous color. Histology reveals buckshot scatter of malignant melanocytes.

Nodular:

Also seen commonly on legs and trunk. Starts as a dark papule which may become a nodule and ulcerate. It can lack the pigment sometimes and appear skin colored (amelanotic nodular melanoma). It is often well rounded and homogeneously pigmented leading to delay in diagnosis. This is the only relatively common melanoma that does not show a radial growth phase.

Lentigo maligna:

Commonly seen on head, face, neck, shoulders and arms in elderly light skinned individuals. It has extremely slow growth and it can exist in the in-situ form for years before growing.

Acral lentiginouS:

This is relatively less common in whites but accounts for upto 2/3rds of melanoma cases in dark skinned populations. The diagnosis is often delayed and hence prognosis is relatively poor. As the name suggests it occurs on hands and soles. It can also occur in the nail bed.

Amelanotic:

These are uncommon and appear as flesh-colored lesions often confused with carcinomas. As mentioned above it most commonly occurs in nodular form.

Treatment for melanoma is primarily surgical although trials of Interferon alpha have been successful to some extent. The most important predictor of prognosis is the thickness at the time of diagnosis (Breslow Index).

Hidradenitis Suppurativa

2010-09-28T14:43:00.000-04:00

Hidradenitis suppurativa is a chronic inflammatory condition characterized by painful lesions in various parts of the body with sweat glands. Typical sites are either groin or axillara (arm pit). The primary gland involved are the apocrine variety of sweat glands (those that produce the characteristic odor). It usually results from blockage of the duct of the gland which leads to distension and inflammation of the surrounding tissues.

Surgical drainage may be needed to relieve pain or if there is bacterial super-infection (evident by redness, exquisite tenderness, pus drainage or fevers). Antibiotics are usually indicated in that case to treat the surrounding cellulitis.

Salmonella infection in humans

2010-09-06T13:19:00.001-04:00

Salmonella infections occur mainly via ingestion of contaminated food. Ingested bacteria are usually killed by the acid in the stomach but when they do survive they can cause enteritis. Certain conditions that reduce the acidity in the stomach predispose to infection (e.g.infants, H2 pr Proton pump inhibitor use and pernicious anemia). It has been predicted that about one million organisms need to be ingested to cause infection.

Infection manifests with fever, loose stools, vomiting, dehydration and cramping pain.

Treatment

Salmonella enteritis is usually self-limiting and does not need antibiotic therapy. Fluid management and symptoms control are the mainstay of the treatment.

However, antibiotics may be indicated in the following high risk groups:

Infants especially in the first 3 months of life
Elderly
Immunocompromised hosts
Individuals with prosthetic heart valves or joints

Salmonella is sensitive to a variety of antibiotics including fluoroquinolones(ciprofloxacin, ofloxacin, levofloxacin), azithromycin, trimethoprim/sulfamethoxazole(Bactrim/Septran) or amoxicillin.

Carrier state

Carrier state is defined as having positive stool cultures for >12 months. It can occur in 1 in about every 200 patients with salmonella enteritis. The bacteria resides in the biliary tree. Chronic antibiotic therapy (Ampicillin) or surgery is needed.

Treatment of Acute Otitis Media (AOM) in Children

2010-08-21T22:28:00.000-04:00

Acute otitis media is the commonest diagnosis in sick children visiting the pediatrician's office in the United States.

Middle ear effusion is common after the resolution of acute symptoms. It may persist for three months in 10%. If persistent it can cause conductive hearing loss and may affect speech, language, and cognitive ability.

Treatment of involves pain relief and antibiotics.

Motrin (ibuprofen), Tylenol(crocin/parecetamol/acetaminophen) are effective for pain.

Less than 24 month olds should always get antibiotics. Older kids with bilateral infection should also always get antibiotics. Otherwise healthy, older children with unilateral infection may be observed without antibiotics.

Amoxicillin is the usual first-line therapy and duration is usually 7 days. If they persist to have symptoms despite 48-72 hours of treatment may be changed to Augmentin(amoxicillin-clavulinic acid).

Less than 2 year olds and older kids with language deficits should have a follow up visit 2-3 months from the acute infection to ensure resolution of effusion.

Female sexual disorders

2010-08-21T22:20:00.000-04:00

The American Psychiatric Association requires that the problem be recurrent or persistent and cause personal distress or interpersonal difficulty to establish the diagnosis of sexual disorder. Following are different types of female sexual disorders.

Hypoactive sexual desire disorder: lac of sexual fantasies and desire for sexual activity

Female sexual arousal disorder: inability to attain, or maintain adequate lubrication and other physiologic responses of sexual excitement

Female orgasmic disorder: absence of, orgasm following an apparent normal sexual excitement

Dyspareunia: pain associated with sexual intercourse

Vaginismus: involuntary contraction of the perineal muscles vaginal penetration attempted

Pyogenic Liver(hepatic) Abscess

2010-08-11T13:43:00.000-04:00

Pyogenic liver abscesses are usually secondary to peritonitis due to that subsequently spread to liver via the portal circulation or bile ducts. Other common form is as a result of hematogenous seeding in the setting of sepsis.

Clinical manifestations: fever, abdominal pain, nausea, vomiting, anorexia, weight loss and malaise.

Diagnosis of pyogenic liver abscess is confirmed by imaging (ultrasound r CT) followed by aspiration and culture of the abscess material. Most pyogenic liver abscesses are polymicrobial. Serology is useful in distinguishing pyogenic abscess from an amebic abscess.

Indications for drainage(less than 5cm usually aspiration is sufficient, greater than 5cm usually need in dwelling catheter):

- Loculated abscesses

- Abscesses with viscous contents obstructing drainage catheter

- Underlying disease requiring primary surgical management

- Inadequate response to percutaneous drainage within seven days
- Multiple abscesses (depends on number, position, and size)

Antibiotics:
A total of 4-6 weeks of therapy is needed.

Options for empiric gram-negative and anaerobic coverage include:

1) Penicillin derivatives: Ampicillin-sulbactam, Piperacillin/tazobactam or Ticarcillin-clavulanate
2) Cephalosporins: Ceftriaxone with metronidazole
3) Fluoroquinolone: Ciprofloxacin or Levofloxacin with metronidazole
4) Carbapenems: Imipenem, Meropenem or Ertapenem

Herpes labialis

2010-08-11T06:53:00.000-04:00

Image from CDC public health image library

Herpes labialis or 'cold sore' is caused by Herpes simplex virus (HSV) type 1 which is a double-stranded, enveloped, DNA virus. Diagnosis is clinical. Treatment is symptomatic. Topical acyclovir may be helpful in recurrent cases.

Sensitivity, Specificity, Positive Predictive Value, Likelihood Ratio explained with an example

2010-08-10T17:18:00.004-04:00

Sensitivity-SnOut: Sensitive test to rule-out a disease. Meaning it will try to not miss any case. Formula for Sensitivity is

Specificity-SpIn: Specific test to rule-in a disease. Meaning it will try not to misdiagnose a normal case as diseased. Formula for specificity is

Positive Predictive Value (PPV): Positive predictive value is also known as precision rate is the proportion of subjects with positive test results who are correctly diagnosed. It is a measure of the performance of a diagnostic method, as it reflects the probability that a positive test reflects the underlying condition being tested for. Its value does however depend on the prevalence of the outcome of interest. Hence the formula for PPV is as follows:

PPV can be calculated if the specificity, sensitivity and prevalence of the disease under question is known by the following formula.

Negative predictive value is the opposite of PPV hence the formula for NPV will be

Based on specificity, sensitivity and prevalence the formula is

Likelihood Ratio: The likelihood that a given test result would be expected in a patient with a disease compared to the likelihood that the same result would be expected in a patient without that disease.

Likelihood Ratio Positive (LR+): The odds that a positive test result would be found in a patient with, versus without, a disease. Formula for LR+ is as follows:
Likelihood Ratio Positive (LR+) = Sensitivity / (1 - Specificity).

Likelihood Ratio Negative (LR-): The odds that a negative test result would be found in a patient without, versus with, a disease.
Likelihood Ratio Negative (LR-) = (1- Sensitivity) / Specificity.

Now let us solve a question using all the above formulae

Imagine that a group of 203 patients had a Chest Xray to look for cancer. Of these 203 patients 20 patients had abnormal chest xray (positive test). 183 had a negative Chest XRay(negative test). 2 of the 20 with positive chest Xray actually had cancer while one of the normal chest xray patient had cancer.

True positives are those patients who had abnormal xray and had cancer so TP=2

False positives are those patients who had abnormal xray but did not have cancer so FP=18 (20 abnormal Xrays but only 2 cancers)

True negatives are those patients who had normal xray and did not have cancer so TN=182 (183 normal Xrays but 1 had cancer)

False negatives are those patients who had normal xray but had cancer so FN=1

Hence based on these numbers the sensitivity is:
TP/(TP+FN)
that is 2(2+1)=0.667 or 66.7%

Specificity is:
TN/(TN+FP)
that is 182/(182+18)=0.91 or 91%

PPV is:
TP/(TP+FP)
that is 2/(2+18)=0.1 or 10%

NPV is:
TN / (FN + TN)
that is 182/(1+182)= 0.995 or 99.5%

Propionic acidemia

2010-08-09T02:57:00.000-04:00

Propionic acidemia is an autosomal recessive disorder in which the body is unable to process certain parts of proteins and lipids. It is classified as an organic acid disorder (organic acids build up).

Diagnosis:

Symptoms appear within a few days of birth and include vomiting, poor feeding, hypotonia and lethargy. Leukocyte propionyl CoA carboxylase activity is the study required for definitive biochemical diagnosis and appropriate genetic counseling. Blood ammonia levels (elevated secondarily), Lactate levels, electrolytes, Urine ketones are other tests recommended in this condition. Anion gap will be increased due to increased unmeasured acids. ECG is recommended in all patients because of increased risk of prolonged QTc interval.

Pathophysiology:

The enzyme propionyl-CoA carboxylase is dysfunctional in propionic acidemia. Mutations in the PCCA and PCCB genes are responsible. As a result propionyl CoA accumulates in the body.

Treatment:

In acute illness - extra calories. No proteins. Once clinical condition improves can resume proteins at a very low concentration using special formulas that lack in isoleucine, valine, threonine, methionine

What to wear to the Step 2 CS (for the ladies)

2010-08-08T15:10:00.000-04:00

Your attire should make you look like a real doctor. Wear clothes similar to those you have seen doctors wear in a clinic in the US. Below are rough guidelines.

Bottoms:
Formal black/dark trousers or skirt.

Top:
Formal light colored shirt or top. May put on a sweater if it is winter time.

Hair:
Keep it all tied/gelled to the back. DO NOT play with/touch your hair during an encounter.

Jewelry:
KISS-Keep it simple stupid. I have heard conflicting things about wearing and not wearing rings. I don't think it matters!

Make up:
A light foundation and lipstick should do it. Careful when picking the color of your lipstick.

Shoes:
Black or dark brown formal shoes. No sandles, no open front shoes please.

Nails:
Cut short and clean. It's okay to paint them.

Perfume:
Take a shower and put on a mild deodorant.

Spinal Canal Stenosis

2010-08-08T12:06:00.000-04:00

Usually results from degenerative changes in the lumbar vertebrae. Predisposing factors include older age, history of back injury or surgery, and manual labor.

Clinical features: Leg pain (neurogenic claudication) and paresthesia that comes on while walking or running and gets better on rest.

Diagnosis: Imaging will show degenerative changes and spondylolisthesis (Sliding of one vertebra over another). MRI is diagnostic.

Treatment: Symptomatic with NSAIDs and physical therapy. Steroid injections(epidural) are rarely used if other methods fail. If features of cord compression are present surgery may be needed.

Hematuria(Blood in urine) causes and differential diagnosis

2010-08-05T19:47:00.000-04:00

Causes of visible blood urine/gross hematuria/macroscopic hematuria:

1) Trauma

Kidney injury is usually secondary to a blunt injury to the flank or abdomen. Penetrating injuries from gunshots and stab wounds are less common causes. Rarely deceleration injuries in motor vehicle accidents, and laceration by fractured lower ribs present with gross hematuria.

Ureteral trauma is rare and most commonly iatrogenic(during a surgery/endoscopic procedures).

Bladder trauma can be commonly seen in motor vehicle accidents with pelvic fractures.

Urethral injury is seen almost exclusively in males, and presents as blood at the tip of the urethra (It is important not to catheterize patients with suspected urethral injury before they have been evaluated by urology.)

2) Nephrolithiasis

Usually causes microscopic hematuria but gross hematuria can been seen. Family history of kidney stones is present in many but not all patients.

3) Hematologic

Sickle cell anemia, Bleeding disorders and patients on warfarin/heparin can present with gross hematuria. Renal vein thrombosis, which can happen in a setting of hyper-coagulable state such as renal cell carcinoma or nephrotic syndrome, generally presents with pain and gross hematuria.

4) Structural causes

Benign prostatic hyperplasia (BPH) increases chances of urethral bleed and gross hematuria. Kidney lesions such as polycystic kidney, medullary sponge kidney, and medullary cystic disease may be associated with gross hematuria. Vascular malformations and arterial-venous fistulas are rare causes of hematuria.

5) Infectious

Lower urinary tract infections and pyelonephritis are common causes of macroscopic hematuria.Urinary TB may present with hematuria.

6) Medical renal disease

Hints to a medical renal disease include: Proteinuria, Hypertension, Renal failure, Dysmorphic RBCs and casts in urine.(e.g. SLE, Glomerulonephritis etc)

Benign familial hematuria is a genetic disease resulting in thinning of the basement membranes. Alport syndrome is an inherited disorder which has hematuria in addition to proteinuria, deafness, and high BP leading to renal failure.

7) Oncologic

Renal cell carcinoma, transitional cell carcinoma and kidney metastasis can present with hematuria. Prostate cancer can present with intermittent gross hematuria. Therapy for certain other cancers for e.g. Cyclophosphamide for leukemia can cause hemorrhagic cystitis and hematuria. Radiotherapy can cause damage to bladder mucosa and hematuria.

8) Miscellaneous

Menstrual bleeding, pseudohematuria (due to certain medications or food - rifampicin, pyridium, beets, rhubarb etc) should be distinguished from real hematuria.

Febrile seizures

2010-08-04T18:34:00.000-04:00

A febrile seizure is defined by the following:
-3 months and 5 years of age
-associated with fever but without evidence of intracranial infection.
-Seizures with fever in children with history of nonfebrile seizures are excluded.

Typical febrile seizures:
-Lasts <15 minutes
-Occurs no more than once in 24 hours
-Is generalized tonic clonic

Lumbar puncture is Indicated only to rule out meningitis or encephalitis if signs or symptoms suggestive of these illnesses are present.

Treatment of simple/typical febrile seizures:

Treat the cause of fever (most are viral infections and do not require antibiotics). Antipyretics are used in adequate amounts until the risk of fever abates. Antipyretics are of no direct value in preventing febrile seizures or their recurrence nor do they slow temperature elevation during fever.

Diabetic Ketoacidosis

2010-08-03T19:41:00.000-04:00

Diabetic ketoacidosis (DKA) is characterized by hyperglycemia, ketonemia and acidemia, with rapid symptom onset.

Most common precipitating cause for DKA is non compliance with insulin regimen. Other precipitating factors include infections, dehydration and other stressful conditions.

Clinical features include weakness, abdominal pain, vomiting, tachycardia, tachypnea (Kussmaul breathing), acidotic breath, dry mucous membranes, poor skin turgor and hypotension. If cerebral edema has set in there may be altered mental status, seizures and abnormal neurological findings such as brisk knee jerks.

Treatment includes correction of volume depletion and insulin therapy. Special attention should be paid to electrolyte imbalances especially sodium and potassium. Potassium will fall with insulin therapy and will need to be replaced. Sodium will be falsely low in setting of hyperglycemia. Corrected sodium can be calculated as Measured sodium + 0/016x(Current glucose-150). In other words increase sodium by 1.6 for every 100mg/dl of glucose above 100.

End points for treatment:

Plasma glucose less than 200 mg/dL
Serum bicarbonate more than 18 mEq/L
Venous pH more than 7.3
Anion gap more than 10.

No vomiting/pain and able to eat PO

Urine ketones may persist at this point and some physicians will continue patients on IVF while urine has ketones.

Erectile Dysfunction and its treatment with PDE5 inhibitors(sildenafil, tadalafil, vardenafil)

2010-08-03T04:02:00.003-04:00

ED affects close to 20 million men in the US. It is often associated with cardiovascular risk factors like diabetes, hypertension and smoking.

International index of erectile dysfunction can assist in diagnosis.

Treatment includes ruling out treatable organic causes and sildenafil citrate. Sildenafil (Viagra) is an oral phosphodiesterase-5 inhibitor and works by increasing blood flow to the spongiform tissue of the penis.

PDE5 inhibitors(sildenafil, tadalafil, vardenafil) are relatively safe drugs. Contraindications to their use include cardiovascular disease(severe), heart attack within 3 months, stroke within 6 months, heart failure within 6 months(moderate or severe), unstable angina or coital angina, poorly controlled arrhythmias, poorly controlled blood pressure, and hereditary degenerative retinal disorders. Vardenafil can also cause QT-interval prolongation. Caution is recommended when using other vasodilator drugs because the resulting hypotension may be severe.

Pneumonia - causes and organisms

2010-07-13T15:05:00.001-04:00

1) Gram-Positive Bacteria

    -Streptococcus pneumoniae is the most common cause of pneumonia(20 - 60% of all community-acquired pneumonia-CAP in adults).
    -Staphylococcus aureus causes only about 2% of CAP but 10 - 15% of hospital-acquired pneumonias. It is the organism most often associated with viral influenza.
    -Streptococcus pyogenes or Group A streptococcus.

2) Gram-Negative Bacteria

    These cause infections in patients with chronic lung conditions like cystic fibrosis and chronic lung disease.

    -Haemophilus influenzae
    -Klebsiella pneumoniae may be responsible for pneumonia in alcoholics and other people who are physically debilitated.

    -Pseudomonas aeruginosa is an important cause of nosocomial pneumonia. It is a common cause of pneumonia.
    -Moraxella catarrhalis, Neisseria meningitidis and E. Coli are other rare gram negative bacteria causing pneumonia.

3) Atypical Pneumonia

    -Mycoplasma pneumoniae is the most common atypical bug causing pneumonia. Mycoplasma is a tiny bacterium that lacks a cell wall. The pneumonia caused by it is commonly called "walking pneumonia."
    -Chlamydia pneumoniae disease is usually mild but can be severe in babies and elderly.
    -Legionella pneumophila causes Legionnaires' disease. It is contracted by breathing in drops of contaminated water (especially from air coolers and air conditioners). Outbreaks are often reported in hotels, cruise ships, and office buildings.
    -Workers exposed to pigeons, parrots, parakeets, and turkeys are at risk for psittacosis, a lung disease caused by the bacteria Chlamydia psittaci.

4) Viral Pneumonia

    -Influenza. Pneumonia is a major complication of the flu and can be very serious(usually staphylococcal)
    -Respiratory syncytial virus usually infects infants and causes bronchiolitis. It can also cause pneumonitis.
    -Parainfluenza virus, Adenoviruses, Herpes viruses, Avian influenza(Type A influenza subtype H5N1 in birds/Swine flu) are other relatively uncommon causes of pneumonia.

5) Anaerobic Bacteria

This usually results from aspiration. This may happen in children and adults with chronic neuromuscular disorders, after a head injury or general anesthesia, or under the effects of drugs or alcohol.

6) Opportunistic infections

    -Pneumocystis carinii, renamed Pneumocystis jiroveci in 2002, is a parasite. It was originally thought to be protozoa but is now classified as a fungus.
    -Mycobacterium tuberculosis, avium etc.
    -Cytomegalovirus

7) Chemical pneumonia:

    Exposure to chemicals can also cause inflammation and pneumonia.

When to chelate for lead toxicity?

2010-07-03T22:26:00.000-04:00

Indication:

Chelation therapy should be considered for lead toxicity if lead concentrations are higher than 44.0 mcg/dL. For levels between 10 and 44 frequent monitoring is recommended.

Drugs:

Succimer is the drug of choice for children whose blood lead concentrations are 45.0 to 100.0 mcg/dL . At values higher than 69.0 mcg/dL, a second drug, Calcium Disodium EDTA (Not to be confused with Sodium EDTA), is added. The first dose always is succimer, followed 4 hours later by EDTA, because children who present with lead encephalopathy may deteriorate when treated with EDTA alone.

Blood lead levels fall rapidly after chelation, but rebound within weeks, even if there is no further exposure to lead, due to release of lead from bone stores. These levels usually are not high enough to indicate chelation but if they do a second round of chelation may be needed.

Kawasaki Disease

2010-07-02T23:25:00.001-04:00

Diagnostic Criteria for Kawasaki Disease

Presence of fever for at least 5 days and at least four of five criteria:

- Bilateral conjunctival injection without exudate
- Polymorphous rash
- Changes in lips and mouth (Reddened, dry, or cracked lips, Strawberry tongue, Diffuse redness of oral cavity or pharynx)
- Changes in extremities (Reddening of palms or soles, Indurative edema of hands or feet, Desquamation of skin of hands, feet, and groin (in convalescence)
- Cervical lymphadenopathy (More than 15 mm in diameter, usually unilateral, single, non-purulent, and painful)

Exclusion of other conditions with similar clinical picture like:

Staphylococcal scalded skin syndrome, toxic shock syndrome
Scarlet fever
Stevens-Johnson syndrome
Drug reaction
Juvenile rheumatoid arthritis

Sjogren's Syndrome

2010-07-02T18:25:00.001-04:00

Revised International Classification Criteria for Sjögren's Syndrome

I. Ocular symptoms: Yes to one or more of the following:

Have you had daily, persistent, troublesome dry eyes for more than 3 months?
Do you have a recurrent sensation of sand or gravel in the eyes?
Do you use tear substitutes more than 3 times a day?

II. Oral symptoms: Yes to one or more of the following:

Have you had a daily feeling of dry mouth for more than 3 months?
Have you had recurrently or persistently swollen salivary glands as an adult?
Do you frequently drink liquids to aid in swallowing dry food?

III. Ocular signs- objective evidence of ocular involvement defined as a positive result for at least one of the following two tests:

Schirmer's I test, performed without anaesthesia (
Rose bengal score or other ocular dye score (>/=4 according to van Bijsterveld's scoring system)

IV. Histopathology: Focal lymphocytic sialoadenitis in minor salivary glands. Requires a focus score >/=1, defined as a number of lymphocytic foci (which are adjacent to normal-appearing mucous acini and contain more than 50 lymphocytes) per 4 mm² of glandular tissue

V. Salivary gland involvement: objective evidence of salivary gland involvement defined by a positive result for at least one of the following diagnostic tests:

Unstimulated whole salivary flow (
Parotid sialography showing the presence of diffuse sialectasias (punctate, cavitary or destructive pattern), without evidence of obstruction in the major ducts
Salivary scintigraphy showing delayed uptake, reduced concentration and/or delayed excretion of tracer

VI. Autoantibodies: presence in the serum of the following autoantibodies:

Antibodies to Ro(SSA) or La(SSB) antigens, or both

Classification

Primary Sjogren's Syndrome

In patients without any potentially associated disease, primary SS may be defined as follows

1. The presence of any 4 of the 6 items is indicative of primary SS, as long as either item IV (Histopathology) or VI (Serology) is positive

2. The presence of any 3 of the 4 objective criteria items (that is, items III, IV, V, VI)

3. The classification tree procedure represents a valid alternative method for classification, although it should be more properly used in clinical-epidemiological survey

Secondary Sjogren's Syndrome

In patients with a potentially associated disease (for instance, another well defined connective tissue disease), the presence of item I or item II plus any 2 from among items III, IV, and V may be considered as indicative of secondary SS

Must exclude:

Past head and neck radiation treatment
Hepatitis C
Acquired immunodeficiency disease
Pre-existing lymphoma
Sarcoidosis
Graft versus host disease
Use of anticholinergic drugs

Polymyalgia Rheumatica

2010-07-01T18:21:00.000-04:00

Diagnostic Criteria for Polymyalgia Rheumatica

Bird's or Wood's criteria

Presence of three or more of the following, or at least one of the following plus positive results on temporal artery biopsy:

Bilateral shoulder pain and/or stiffness
Less than two weeks from onset of symptoms to maximal symptoms
ESR greater than 40 mm per hour
Morning stiffness lasting longer than one hour
Patient older than 65 years
Depression and/or weight loss
Bilateral upper arm tenderness

Jones and Hazleman's criteria

Presence of all of the following:

Shoulder and pelvic girdle muscle pain without weakness
Morning stiffness
Symptom duration of more than two months unless treated
ESR greater than 30 mm per hour or C-reactive protein level greater than 6 mg per L
No rheumatoid arthritis, inflammatory arthritis or malignant neoplasm
No objective signs of muscle disease
Prompt and dramatic response to systemic corticosteroid therapy

SLE Criteria/American College of Rheumatology 1982 revised criteria for lupus

2010-06-03T15:34:00.000-04:00

Any 4 or more of the 11 criteria are required to classify a patient as having SLE. These criteria do not have to be present all at once.

Malar rash: Fixed erythema, flat, or raised, over the malar eminences, characteristic sparing of the nasolabial folds.

Discoid rash: Erythematous raised patches with adherent keratotic scaling with or without plugging of the follicles; scarring may occur in older lesions.

Photosensitivity

Oral ulcers: Usually painless, Have to be observed by physician. History of ulcers is not sufficient.

Arthritis: Usually nonerosive arthritis

Serositis(inflammation of visceral membranes): Pleuritis or Pericarditis.

Renal involement: Persistent proteinuria >0.5 g/day or >3+ if quantification not performed OR Cellular casts.

Brain involvement: Seizures OR Psychosis.

Hematologic disorder: Hemolytic anemia OR Leukopenia: <4000/mm^3 on ≥2 occasions OR Lymphopenia: <1500/mm^3 on ≥2 occasions OR Thrombocytopenia: <100,000/mm^3.

Immunologic disorder:
Anti-DNA antibody
Anti-Smith antibody
Antiphospholipid antibodies based on:
- increased level of IgG or IgM anticardiolipin antibodies
-positive lupus anticoagulant
-A false-positive serologic test for syphilis

Antinuclear antibody:
An abnormal titer of antinuclear antibody by immunofluorescence or an equivalent assay at any point in time and in the absence of drugs known to be associated with drug-induced lupus syndrome.

Chronic Fatigue Syndrome

2010-06-02T15:09:00.000-04:00

Onset may be acute or subacute.
It is essentially a diagnosis of exclusion.

The 1994 CDC diagnostic criteria require the concurrent presence of at least 4 of the following symptoms over a 6-month period:

Impaired short-term memory or concentration
Sore throat
Tender lymph nodes/glands
Muscular pain
Joint stiffness in multiple areas
New-onset headaches
Unrefreshing sleep
Postexertional fatigue/malaise lasting more than 24 hours.

Treatments:

-Exercise
-Cognitive behavioral therapy

The syndrome is associated with depression, obstructive sleep apnea and other psychiatric illnesses.

Fibromyalgia

2010-06-01T15:05:00.000-04:00

The following points help make diagnosis:

-Women
-Chronic, widespread body pain
-Fatigue, stiffness, and unrefreshing sleep.
->11 of 18 defined tender points are tender on palpation.

Treatment of choice is patient education, graded exercise, and behavioral therapy.
Tricyclic antidepressants may be helpful.

Therapy for acne

2010-05-31T15:04:00.001-04:00

Mild acne

Comedonal acne is especially responsive to topical retinoids. Salicylic acid is not as effective a comedolytic as retinoids.

For inflammatory acne, combination therapy is the mainstay of treatment. Topical retinoids (tretinoin Evidence , adapalene Evidence and tazarotene) are prescribed in combination with benzoyl peroxide Evidence and/or topical antibiotics (clindamycin Evidence or erythromycin Evidence).

Moderate acne

Moderate comedonal acne with minimal inflammation may respond to topical retinoids alone. Inflammatory acne is best treated by a combination of systemic antibiotic with topical retinoid. If this does not make acne better in 8-10 weeks, benzoyl peroxide should be considered. This is mainly to reduce production of antibiotic resistant strains but also increase the efficacy of the treatment.

Severe nodulocystic acne

For severe or nonresponsive acne, oral isotretinoin for 6 months should be considered. Systemic steroids can be used as an adjunct.

U.S. Preventive Services Task Force (USPSTF) recommendationson mammography

2010-01-18T22:52:00.002-05:00

In November 2009, the U.S. Preventive Services Task Force (USPSTF) came out with new recommendations for routine mammography screening for woman aged 40 to 49 years. These are as follows:

-No routine screening mammography in women aged 40 to 49 years. The decision to start regular screening mammography before the age of 50 years should be an individualized one.

-The USPSTF recommends biennial (once every 2 years) screening mammography for women between the ages of 50 and 74 years

-The evidence is insufficient to assess the additional benefits and harms of screening mammography in women 75 years or older.

-The evidence is insufficient to assess the additional benefits and harms of clinical breast examination beyond screening mammography in women 40 years or older.

-The USPSTF recommends against clinicians teaching women how to perform breast self-examination.

-The USPSTF concludes that the current evidence is insufficient to assess additional benefits and harms of either digital mammography or magnetic resonance imaging instead of film mammography as screening modalities for breast cancer.

Pemphigus

2009-12-19T22:57:00.002-05:00

Pemphigus is an autoimmune disorder of the skin and mucous membranes characterized by blisters associated with the binding of IgG autoantibodies to epithelial cell surface. The common form is called Pemphigus vulgaris. Antigens in pemphigus are believed to be desmoglein 1 and desmoglein 3. Antibodies belong to IgG1 and IgG4 type.

Mean age of onset is approximately 50-60 years. Histologic changes consist of intercellular edema with loss of intercellular attachments in the basal layer. Suprabasal epidermal cells separate from the basal cells to form clefts and blisters. These findings can help differentiate phemphigus vulgaris from pemphigus foliaceous, which demonstrates a more superficial epidermal cleavage.

Primary Amyloidosis- Types, proteins and clinical associations

2009-12-18T20:31:00.002-05:00

Type	Deposited Protein	Clinical Associations
Systemic	Immunoglobulin lambda chains	Multiple myeloma
	Transthyretin	Familial amyloidosis, senile cardiac amyloidosis
	Amyloidosis – A protein	Inflammation-associated amyloidosis
	Beta₂ -microglobulin	Dialysis-related amyloidosis
	Immunoglobulin heavy chains	Systemic amyloidosis
Hereditary	Fibrinogen alpha chain, Apo A1 and Apo A2	Familial systemic amyloidosis
Hereditary	Lysozyme	Familial systemic amyloidosis
Central nervous system	Beta protein precursor	Alzheimer's
	Prion protein	Creutzfeldt-Jakob disease, Gerstmann-Strãussler-Scheinker disease, fatal familial insomnia
	Cystatin C	hereditary cerebral hemorrhage with amyloidosis (Icelandic)
Ocular	Gelsolin	Familial amyloidosis (Finnish)
	Lactoferrin	Familial corneal amyloidosis
	Keratoepithelin	Familial corneal dystrophies
Localized	Calcitonin	Thyroid Carcinoma (Medullary)
	Amylin	Insulinoma, type 2 diabetes
	Atrial natriuretic factor amyloid	Isolated atrial amyloidosis
	Prolactin	Pituitary amyloid
	Keratin	Cutaneous amyloidosis
	Medin	Aortic amyloidosis in elderly people

NYHA Classification for Congestive Cardiac Failure

2009-12-17T20:05:00.002-05:00

The New York Heart Association (NYHA) Functional Classification is used to grade the severity of congestive cardiac failure. Symptoms it refers to include dyspnea and chest pain.

NYHA Class	Symptoms
I	No symptoms and no limitation in ordinary physical activity, e.g. shortness of breath when walking, climbing stairs etc.
II	Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity.
III	Marked limitation in activity due to symptoms, even during less-than-ordinary activity, e.g. walking short distances (3-15 feet). Comfortable only at rest.
IV	Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients.

Complications of obesity

2009-11-27T06:01:00.002-05:00

CVS - Hypertension, coronary artery disease, cor pulmonale, pulmonary hypertension of obesity, obesity related cardiomyopathy, atherosclerosis

CNS - Stroke, Benign intracranial hypertension

Neoplastic - Increased endometrial, prostate, gall bladder, breast and colon cancer

Endocrine - Non Insulin Dependent Diabetes Mellitus(NIDDM), abnormal lipid profile

GIT - cholecystitis, cholelithiasis, nonalcoholic steatohepatitis (NASH), fatty liver, gastro esophageal reflux disease(GERD)

Pulmonary - Obstructive sleep apnea, Pickwickian syndrome(hypoventilation)

Psychosocial -Depression, stigma,

Orthopedic - Osteoarthritis, slipped capital femoral epiphyses, Blount and Legg-Calvé-Perthes disease, backache

Gynecologic - Anovulation and infertility, hyperandrogenism and polycystic ovarian disease

Obstetric - Pregnancy induced hypertension, large baby

Surgical - Deep venous thrombosis, pulmonary embolism

Aspirin for MI/angina

2009-11-25T18:21:00.003-05:00

162-325 mg of chewable aspirin should be promptly administered to patients who do not have bleeding tendency. Administration should not be delayed as the peak effect of aspirin can be seen as early as half hour after administration and it is important to prevent thrombus formation and propagation.

If the patient undergoes stenting 162-325 mg aspirin should be continued for 1 month after bare metal stent implantation, 3 months after sirolimus-eluting stent implantation, or 6 months after paclitaxel-eluting stent implantation.

Most subjects will get low dose (75-162 mg) all their life.

Koilonychia - Spoon shaped nails

2009-11-24T19:09:00.002-05:00

Koilonychia is relatively more frequent in children and usually resolves with aging.

When in doubt the diagnosis can be confirmed by keeping a drop of water on the nail. If the drop falls off koilonychia is unlikely.

Common causes include:

Iron deficiency anemia
Diabetes mellitus
Protein malnutrition
SLE
Raynaud's disease and phenomena

Anterior cruciate ligament anatomy

2009-09-20T03:58:00.000-04:00

ACL is attached to a depression on the posteromedial surface of the lateral condyle of femur. On the tibia it inserts into a fossa that is anterior and lateral to the anterior tibial spine. The tibial attachment is known to be stronger than the femoral attachment.

The ACL is intracapsular but is extrasynovial. Its course is anterior, medial, and distal from the femur to the tibia. Close your eyes and imagine this course. It will help you understand the mechanism of injury.

The Anterior Cruciate Ligament has 2 bands - the anteromedial band and the posterolateral band. During flexion when the back of the leg comes closer to the back of the thigh, the anterior band is taught. When the leg is straightened posterolateral band is tight.

Breast cancer, HER2 receptors and Monoclonal antibodies

2009-09-18T20:25:00.001-04:00

One thirds of all breast malignancies have amplification of the HER2 gene. HER2 stands for human epidermal receptor type 2. HER2 receptor is a transmembrane tyrosine kinase receptor whose stimulation leads to a number of molecular pathways associated with tumor growth and progression.

Cancers that express HER2 have poorer prognosis.

Trastuzumab also known as Herceptin is a recombinant monoclonal antibody specifically directed against the HER2 receptor and it has been shown to be improve the response rate in breast cancer patients. This antibody is used in combination with chemotherapy including doxorubicin, cyclophosphamide and paclitaxel.

Another antibody named Lapatinib (a.k.a. Tykerb) which is a 4-anililoquinazoline kinase that inhibits the tyrosine kinase domains of HER2 receptor is also being studied.

National Comprehensive Cancer Network recommends use of these agents in addition to chemotherapy for patients with HER2-positive breast cancers that are larger than 1 cm and have spread to lymphnodes.

***This topic is hot for the USMLE***

Anterior interosseous syndrome

2009-09-11T23:31:00.003-04:00

Anatomy: Few inches distal to the cubital fossa, the median nerve gives a branch named anterior interosseous nerve, which travels on the interosseous membrane and supplies the flexor pollicis longus (flexor of the thumb), the flexor digitorum profundus to the radial 2 digits, and the pronator quadratus at its termination. The nerve innervates the pronator teres, flexor capri radialis, the flexor digitorum sublimis, and the 2 radial flexor digitorum profundus tendons.

Symptoms: include pain in the proximal forearm and weakness of the thumb and index finger. Affected persons cannot form a circle by pinching their thumb and index finger (ie, hyperextension of index distal interphalangeal joint and thumb interphalangeal joint).

Treatment: Medical treatment includes rest, NSAIDs (Non Steroidal Anti Inflammatory Drugs), and splints. Surgical treatment includes exploration and release.

Vibrio cholera

2009-09-10T22:25:00.000-04:00

This organism can not survive in acidic pH. Hence any condition that causes decrease stomach acidity will cause it to proliferate.

Botulism

2009-09-10T20:28:00.002-04:00

Botulism is caused by a gram positive rod Clostridium botulinum. The toxin released by this bacteria binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions. This binding inhibits acetylcholine release, causing weakness and flaccid paralysis. The paralysis persists until the nerve endings regenerate.

The 3 types of botulism are as follows:

Infant botulism is caused by ingested spores of the bacteria which germinate in the gut releasing toxin inside the body.

Wound botulism results from contamination of a wound with toxin-producing clostridia.

Foodborne botulism occurs after consumption of contaminated food for e.g. canned vegetables.

Key points for USMLE:
-The binding of toxin is irreversible
-Infant botulism is associated with consumption of honey

Differential diagnosis of botulism:

* Guillain-Barré syndrome
* Myasthenia gravis
* Lambert-Eaton myastheic syndrome
* Polio
* Tick paralysis
* Stroke
* Diphtheric paralysis
* Congenital neuropathy or myopathy
* Snake bite (Cobra)

Legionnaire’s Disease

2009-09-09T22:20:00.001-04:00

Legionnaire’s Disease – caused by Legionella Pneumonia causes disease in smokers, with diarrhea, headache and confusion.

Alkaptonuria

2009-09-04T09:26:00.000-04:00

Alkaptonuria is caused by inherited deficiency of the liver enzyme homogentisic aicd dioxygenase. This leads to accumulation of homogentisic acid, which is rapidly cleared in the kidney and excreted.

When homogentisic acid comes on contact with air, it is oxidized to form a black colored compound. Hence the urine of these patient turns black on standing. Kidneys are efficient at clearing homogentisic acid initially but eventually it gets deposited in various tissues.

The earliest symptom may be the mother noticing a black diapers. Ochronosis, which is visible deposition of the pigment in tissues usually does not occur before the fourth decade. The tissues most commonly involved include cartilage, sclera. This leads to joint problems. It is speculated that heart disease including myocardial infarction may be more common but there is not enough statistical evidence.

Smith-Lemli-Opitz syndrome/RSH syndrome

2009-09-03T10:45:00.001-04:00

Initially described in 1964 this is an inborn error of metabolism of in the steroid synthesis pathway. This syndrome was initially called RSH after the first initial of the last names of the first 3 patients evaluated!

This syndrome is caused by a deficiency of the microsomal enzyme DHCR7(Dehydrocholesterol reductase 7), which is responsible for conversion of 7DHC to cholesterol as the last step in cholesterol synthesis. Affected children hence have low plasma cholesterol levels and elevated levels of cholesterol precursors (e.g. 7DHC).

Clinical features are variable and include llethargy, rrespiratory failure, deafness, feeding difficulties, failure to thrive, photosensitivity, mental retardation, autism, antisocial, self-destructive, and violent acts , intrauterine growth retardation (IUGR), microcephaly, broad nasal tip with anteverted nostrils, micrognathia, ptosis, squint, congenital cataracts, low-set ears, syndactyly and/or polydactyly, hypospadias or cryptorchidism in males and ambiguous genitalia in females, cleft palate and congenital cardiac defects.

Clinical manifestations of Aspergillus infection of the lungs(Pulmonary aspergillosis)

2009-09-03T09:20:00.001-04:00

There are four common manifestations of pulmonary aspergillosis namely - Allergic Broncho Pulmonary Aspergillosis (ABPA), Chronic Necrotizing Pulmonary Aspergillosis(CNPA), aspergilloma ('Fungal ball') and invasive aspergillosis.

1) ABPA - is almost exclusively seen in asthmatics or cystic fibrosis patients. It is basically an allergic reaction to aspergillus that is colonized in the airways. Patients have fever and respiratory symptoms (cough, hemoptysis, wheezing).

2) Aspergilloma - is seen in immunocompromised patients. or in lungs with pre-existing cavities. Aspergillomas are often silent or cause fever and respiratory symptoms similar to ABPA.

3) CNPA - Occurs in individuals with underlying disease, such as severe chronic obstructive pulmonary disease (COPD) and prolonged antibiotic therapy. They present with symptoms such as fever, cough, night sweats, and weight loss.

4) Invasive aspergillosis - occurs in patients with immunosuppression or ANC (Absoulute neutorphil count) and in patients post transplantation. These patients are usually sick and need urgent parenteral treatment.

Novel Risk Factors for Atherosclerosis (CRP, Lipoprotein-a, Fibrinogen and Homocysteine)

2009-09-02T19:43:00.001-04:00

CRP- C-reactive protein: High CRP reflects inflammation, and has been shown to correlate with the occurrence of myocardial infarction and peripheral arterial disease.

Homocysteine levels: It is a well known fact that homozygous hyperhomocystinemia is associated with early atherosclerosis and stroke. However, approximately 5-7% of the general population have mild elevations of plasma homocysteine, and recent research have focussed on refuting or establishing if this population is at a higher risk for cardiovascular events. A number of treatments have been postulated for those with high homocysteine levels including folic acid and pantothenic acid.

Fibrinogen: In recent studies high levels of fibrinogen have been found to be strongly related to cardiovascular events in apparently healthy individuals.

Lipoprotein-A: Lipoprotein A is an LDL like substance in the blood that remains bound to apolipoprotein A. It may promote atherosclerosis by its ability to be oxidized. Some studies have shown that Vitamin B3 (Niacin) can decrease its levels but the clinical significance is still unclear.

Syncope (Causes and Pathophysiology)

2009-09-01T10:53:00.001-04:00

Syncope is defined as loss of consciousness due to decreased cerebral perfusion. Causes of syncope can be classified as Neuroregulatory, Arrhythmias and Hemodynamic.

A. Neuroregulatory causes of syncope.

A.k.a.vasovagal syncope this is caused by a sudden decrease in blood pressure. Prolonged standing is a common cause especially is the subject is dehydrated.

The low BP is sensed by carotid baroreceptors, that increase cardiac rate and contractility. On the other hand pressure receptors in the walls of the underfilled left ventricle may sense high-pressure and cause paradoxical bradycardia and lower contractility.

B. Arrhythmia as a cause of syncope.

Common arrhythmias causing syncope include supraventricular tachycardia (SVT), ventricular tachycardia (VT), ventricular fibrillation, and severe bradycardia (eg, heart block).

C. Hemodynamic syncope

The following Structure defects in the heart can cause syncope.

•Hypertrophic obstructive cardiomyopathy (HOCM) or aortic stenosis leading to left sided outflow obstruction

•Pulmonary hypertension may cause syncope when the right ventricle fails to pump against the high pulmonary pressure.
•Ischemic heart disease due to anomalous coronary artery origin, hypercholesterolemia, or acute inflammatory diseases such as Kawasaki disease and myocarditis.

•Pericardial tamponade can cause hypotension and syncope secondary to decreased pre-load (ventricles can not fill well).

Vitamin K and Coagulation - High yield facts

2009-08-31T13:08:00.001-04:00

Vitamin K is a fat soluble vitamin needed for the gamma-carboxylation of clotting factors 2, 7, 9 and 10. Remember II VII IX and X

Initially PT is prolonged. PTT can be prolonged later on.

Clinical situations where vitamin deficiency can be seen:
-Newborns who did not receive Vit K at birth. (Breast milk has low levels of vit K).
-Patient on broad spectrum antibiotics (Because gut flora is disturbed. Normally the intestinal bacteria make a significant portion of our Vit K)
-Fat malabsorption syndromes. Vit K is a fat soluble vitamin hence it will go down the drain with the fat.

Management of Vit K deficiency:
-For acute bleeding give FFP (fresh frozen plasma)
-Vitamin K is available as injection and orally

Juvenile rheumatoid arthritis (JRA) - Classification and epidemiology

2009-08-30T10:56:00.003-04:00

JRA (Now also called Juvenile idiopathic arthritis or JIA) is one of the most common chronic joint disorders in kids. It is classified as follows.

1) Pauciarticular disease: (About 50% of all JRA cases) Less than 5 joints are involved. Usually large joints, such as the shoulder, elbow, hip, and knee are affected. Pauciarticular JRA is most common in kids younger than 8 years. There is 20-30% chance of developing iridocyclitis.

2) Polyarticular disease: (30% of all JRA cases) As the name suggests this type affects more than 5 joints. Unlike the pauciarticular type small joints such as those in the hands and feet are often involved.

3) Systemic onset JRA (a.k.a Stills disease, 20% of all JRA). Children present with high fevers, skin rashes, and joint pain. Acute leukemia must be excluded as it can present identically.

Churg-Strauss Syndrome (CSS)

2009-08-30T10:50:00.002-04:00

CSS was first described in 1951 by Jacob Churg and Lotte Strauss as a symptom complex with asthma, eosinophilia and vasculitis. CSS resembles polyarteritis nodosa (PAN) in many aspects. CSS however has characteristic granulomas while PAN does not.(Hence also called allergic granulomatosis).

CSS occurs in middle aged individuals. They present with new or worse asthma. Asthma can start many years before the other symptoms.

Marked by eosinophilia then follows. After that there is the phase vasculitis. Vasculitis can involve the lungs, skin, nerves, kidneys and sometimes other body organs.

EEG findings in Absense seizures/ Petit mal epilepsy

2009-08-22T15:16:00.004-04:00

Electroencephalographic findings in typical absence seizures (petit mal epilepsy) are as follows:

1) Background activity is normal.
2) Frontally dominant bursts of 3-Hz spike-and-wave complexes are seen during the seizures.
3) In syndromes with less frequent absence seizures (juvenile absence epilepsy or juvenile myoclonic epilepsy), an awake recording may be normal; a sleep or sleep-deprived recording may show evidence of generalized 3-Hz spike-and-wave complexes.
4) There is abrupt onset and ending. No postictal EEG slowing is noted.
5) Video EEG may demonstrate that clinical seizures at times occur after the the start of ictal EEG activity by a few seconds.

X linked Recessive diseases

2009-08-17T18:31:00.002-04:00

Adrenoleukodystrophy which leads to progressive brain damage, failure of the adrenal glands and eventually death.

Alport syndrome which includes glomerulonephritis-renal failure and deafness.

Androgen insensitivity syndrome with receptor resistance to the effect of androgens. The patient is typically a young woman (phenotypically) with XY chromosomes.

Charcot-Marie-Tooth disease which is a hereditary neuropathy.

Duchenne and Becker muscular dystrophy characterized by rapid progression of muscle degeneration, eventually leading to loss in ambulation and death.

Fabry disease- a lysosomal storage disease due to deficiency of the enzyme ceraminidase.

Fragile X syndrome resulting from expansion of a single trinucleotide gene sequence (CGG) on the X chromosome. Clinical features include long face, testicular enlargement, Mental retardation.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency.

Hemophilia A and B (Deficiency of factor 8 and 9 respectively). Hemophilia B is also known as Christmas disease.

Hunter's Syndrome which is one of the Mucopolysachharidosis.

Kabuki syndrome with multiple congenital anomalies and mental retardation.

Lesch-Nyhan syndrome is a disorder of purine metabolism with neurologic dysfunction, cognitive and behavioral disturbances including self-mutilation.

Lowe Syndrome- Oculo-cerebro-renal syndrome.

Menkes disease with sparse and coarse hair, growth failure, and neurological symptoms.

Ornithine transcarbamylase deficiency is relatively common disorder of protein metabolism.

Red-Green color blindness, also known as daltonism.

Rett syndrome with acquired microcephaly and small hands and feet. Stereotypic, repetitive hand movements.

Wiskott-Aldrich syndrome is the classic triad of eczema, thrombocytopenia and immune deficiency.

X-linked agammaglobulinemia (XLA) also known as Bruton's disease.

X-linked ichthyosis (fish skin) is a hereditary deficiency of the steroid sulfatase (STS) enzyme.

X-linked Severe Combined Immunodeficiency (SCID); is a severe form of immunodeficiency usually causing death in the first years of life.

prGCD - plant cell expressed recombinant Glucocerebrosidase enzyme (GCD) for use in Gaucher's disease

2009-08-17T17:02:00.002-04:00

This is a newly approved (partially approved for use by the Food and Drug Administration-FDA) drug for the treatment of patients with Gaucher's Disease.

Gaucher's disease is the most common lysosomal storage diseases in humans. It is caused by a hereditary deficiency of the enzyme glucocerebrosidase (also known as acid β-glucosidase). The enzyme acts on glucocerebroside which accumulates in its absence. Fatty material collects in the liver, kidneys, lungs, spleen, brain and bone marrow. The disease is inherited in autosomal recessive manner. The locus is on chromosome 1.

Traditionally Gaucher's disease has been classified in the following 3 types.

Type I (or non-neuropathic type) is the most common form of the disease. It occurs in 1 in 50,000 births. It is much more frequent in children of Ashkenazi Jewish heritage. Symptoms include enlarged liver and spleen. Bone marrow replacement can cause anemia, thrombocytopenia and leukopenia. The brain is usually not affected. Rarely there is lung or kidney impairment. These patients may live well into adulthood.

Type II (or acute infantile neuropathic form) typically begins in infancy and occurs in approximately 1 in 100,000 births. The diagnostic symptom of this type is extensive and progressive brain damage. Affected children do not usually live longer than 2 years of age.

Type III (the chronic neuropathic type) has a variable onset. Incidence is 1 in 100,000 births. It is characterized by slowly progressive but milder neurologic symptoms. Other major symptoms include an spleen and/or liver enlargement, seizures, bone marrow disorders and respiratory problems.

Challenging Questions

2009-08-14T22:15:00.004-04:00

There are 4 steps to answering a challenging question. Most people do the 2nd step but forget the rest.

1st- Express your understanding for the SP's concern
2nd-Answer the question
3rd-Counsel/Reassure
4th-Ask if they have more questions.

The basic idea to is to tell the SP that more diagnostic tests would be needed before one can be sure. Nevertheless read through the examples below .

Q "Can you give me some antibiotics to get better?"
A "I understand your concern Mr Smith. Antibiotics work only when there is a bacterial infection. While your symptoms could be due to it, there are many other conditions which

can cause similar symptoms. I would surely prescribe you antibiotics if they are indicated. However for me to know if you need them, we need to run some tests first. If we find any evidence of bacterial infection, we will go ahead and take antibitics. Does that answer your question Mr Smith?"

Q "Do you think I will be able to use my leg again like before?
A "I understand your concern Mr. Smith. I am hoping that you will be able to use your leg like before, but to be sure, we need to confirm whether it's broken or dislocated and if there is any nerve or muscle damage. We will know once we run a few tests. Iwould then treat accordingly and try my best to preserve the function of your leg and make you comfortable."

Q "Do I have cancer, doctor?"
A "I understand your concern, Mr. Smith. We cannot exclude the possibility of cancer at this point. We need to perform additional tests. Once we have the results in, we will know for sure. Regardless of the results Mr. Smith, I want to assure you that we as a team would do the best we can to make you comfortable and address your concerns. Does that answer your question Mr Smith."

Q "Will I get better if I stop smoking?"
A "Mr Smith I totally understand your concern. I am glad that you are thinking about quitting smoking. Although we still have to find out exactly what's making you sick, stopping smoking should help your chronic cough. Overall it will also decrease the risk of cancer and heart disease. We have excellent smoking cessation counsellors that I can refer you to if you so wish." Does that answer your question?

Q "Doctor, am I going to die?
A "I understand your concern Mr Smith. Your condition may be serious, but until I get the test results back, we cannot be sure of the diagnosis. There are many disease that cause symptoms similar as yours. We will know the exact diagnosis only when we have the results. So please do not worry at this time. Now that you are here, we will do everything we can to help you".

Dos and Don'ts during the CS exam

2009-08-13T11:00:00.004-04:00

DO

Explain what you are doing when you are examining the patient (Mr. Smith I am now going to feel for your thyroid gland...and that feels normal...)
Acknowledge everything that the SP tells you by OK or thank you or similar words or at least gestures. Use appropriate words/phrases. (For e.g. don't say OK when SP says "My sister died of lung cancer"!)
Ask permission before exam, before untying the gown
Congratulate, encourage whenever you get an opportunity
Speak slowly and clearly. Use can not in stead or can't and do not in stead of don't
Try to keep your eyes at the same level as the patient
Use open ended questions not leading questions
If you don't understand something ask the SP to repeat
Act confident and imagine as if you were seeing a real patient

DON'T

Do not interrupt when the SP is talking
Do not fill in words for the SP
Do not make the patient change too many positions
Do not forget to say "Did that answer your question ? Do you have another question
Do not put the pen in your mouth
Do not raise eye brows or frown
Do not repeat same questions again and again
Do not keep looking at the computer in the room!
Do not mumble. Be loud and clear

Ankylosing Spondylitis (AS)

2009-08-12T16:24:00.001-04:00

Characteristic symptoms of AS include back pain that is worst in the morning and improves with exercise. AS is more common in men, and patients usually present at a younger age (18-35 years) relative to patients with mechanical causes of back pain or arthritis.

AS is a clinical diagnosis, HLA B27 testing is positive in a large proportion of patients with AS but one should keep in mind that in the general population, about 8% Caucasian, 4% African, 2-9% Chinese, and 0.1-0.5% Japanese have the HLA-B27 antigen.

Commonest cause of death related to AS is renal failure secondary to amyloidosis in AS.

Myocarditis classification

2009-08-05T11:26:00.002-04:00

Myocarditis is inflammation of myocardium. It is usually viral and Cocksackie B is the commonest virus isolated. Myocarditis can be classified into the following 3 types based on pathologic findings per the Dallas Criteria (1987):

Active myocarditis - Characterized by abundant inflammatory cells and myocardial necrosis (subclassified into ongoing, resolving, or resolved myocarditis.)

Borderline myocarditis - Characterized by an inflammatory response that is too sparse for this type to be labeled as active myocarditis; degeneration of myocytes not demonstrated with light microscopy (subclassified into ongoing, resolving, or resolved myocarditis.)

Nonmyocarditis

Treatment of von Willebrand's Disease

2009-08-03T08:20:00.007-04:00

Desmopressin (1-deamine-8-D-arginine vasopressin [DDAVP]) is the mainstay of therapy for most patients with mild von Willebrand disease. DDAVP causes a 2-4-fold increase in plasma von Willebrand factor and FVIII concentrations in healthy responsive individuals.

DDAVP can be used to treat bleeding complications or to prepare patients with von Willebrand disease for surgery.

In type IIB von Willebrand disease, DDAVP may cause a paradoxical drop in the platelet count and should not be used without prior testing.

William Morrow in Bundle Branch Block

2009-07-22T15:50:00.001-04:00

You can distinguish between LBBB (Left Bundle Branch Block) and RBBB (Right Bundle Branch Block) simply by looking at the QRS morphology in V1 and V6.

If the QRS looks like W in V1 and M in V6 it is LBBB. (WiLLiaM)

If the QRS looks like M in V1 and W in V6 it is RBBB. (MoRRoW)

Lay man phrases for medical terms

2009-06-13T08:08:00.004-04:00

Food regurgitation: Bringing up food.
Amaurosis fugax: Sudden loss of vision that is usually transient.
Palpate: Feel for.
Percuss: Tap.
ECG: Records the electric activity of your heart.
CT scan: Imaging the inside of your brain. It is like taking many X-rays and pooling them together.
MRI: Stands for magnetic resonance imaging. Basically takes pictures of the inside of your brain
Ultrasound: Looking at the inside of your belly (or the part in question) using a device on the surface of your body. The waves produced by the device are similar to sound waves and are totally harmless.
Appendicitis: Swelling and inflammation of the appendix.
Inflammation: Swelling due to irritation of the tissue due to a variety of reason.
Ovarian torsion: Twisting of the ovary on its stem.
Pneumonia: Infection of the lung.
Gastroenteritis: Infection of the stomach and the intestines.

Cholecystitis: Swelling and inflammation of the gall bladder.

Hepatitis: Swelling and inflammation of the liver.

USMLE Step 2 CS pass/fail rates

2009-06-10T21:38:00.005-04:00

Above data indicate that almost 1 in every 4 international graduates will fail the USMLE Step2 CS. Commonest reason for failing used to be ICE (Integrated Clinical Encounter) but more and more IMGs are now failing the CIS (Communication and Interpersonal Skills). Unlike the popular belief, English proficiency is an uncommon cause of failure (see the table below)

Patient Note

2009-06-09T07:56:00.003-04:00

Importance of PNs in the USMLE Step 2CS is often underestimated. Many test takers score low on the data gathering because of a poor patient note. Here is a template that I suggest you use for every patient note. Make sure to include every heading. Even if you think it is not important in this particular case. I preferred writing down the Differential Diagnosis and Diagnostic Work Up part before writing the history and physical exam part but you can do either way that you feel comfortable.

History template

[Basic info] 30 yo female c/o [CC] pain in abdomen x 2 days.
[ODP and CC description] Pain is in the lower half of her abdomen, colicky, 7/10 without any radiation. Pain started at rest and gradually worsened to present state. Has taken 2 tabs of Tums today morning with partial relief. There is no specific aggrevating factor.
[Associated symptoms from the affected system] She has associated Nausea and Vomiting. She vomited 2 times today morning. Non bilious/non bloody. No diarrhea.
[Review of other systems] No cough. No pain elsewhere in the body, No trauma, No urinary complaints.

[P]Past medical history is significant for asthma for which she takes [M] budesonide and albuterol. No previous surgeries. [A]Allergic to penicillin and sea food. [S]Is sexually active with her husband and uses condom for contraception. [O] Has one living child that was born vaginally at term 3 years ago. No pregnancy or delivery related complications. [H] That was her only hospitalization. [U] No urinary complaints. [G] LMP was 4 weeks back. Is normally regular every month and lasts 2-3 days. [S] Does not smoke or drink alcohol. Works as a teacher in primary school. [F]Family history significant for grandmother with ovarian cancer. No DM or HTN in family.

Physical exam template

[General] Appears to be in pain but in no acute distress.

[Vitals] Vitals HR: 80/min, RR 20/min, BP 120/80mmHg, Temp 37 C

[GPE] No pallor or icterus. Neck supple. HEENT normal with moist mucous membranes.

[Sytemic Exam]Abdomen: Non distended, Normal bowel sounds in all 4 quadrants. Tenderness on palpation of thr right illiac fossa. No rebound tenderness. No masses or organomegaly.

Chest: Symmetric movements, Normal vesicular breath sounds bilaterally.

Heart: S1S2 normal. No murmur.

Differential diagnosis

1) Acute appendicitis

2) Ectopic pregnancy

3) Ovarian torsion

4) Pelvic inflamatory disease

[Remember to write the Differential in order or possibility]

Diagnostic Work Up

1) Pelvic exam

2) US abdomen and pelvis

3) CBC

4) Urine pregnancy test

[Remember to write Pelvic and other such exams in your Diagnostic Work Up. Examples of commonly forgotten things include

Pelvic exam

Digital rectal exam

Orthostatic vitals

Minimental state exam

Pure tone audiometry]

What to take to the Step 2CS test center

2009-06-04T18:14:00.003-04:00

The four things you need to take to the test center are as follows:

1) Stethoscope (If you forget they will provide one but it is generally recommended that you take your own)

2) White laboratory coat (If you forget they will provide one but it is generally recommended that you take your own. And of course make sure the pockets are empty!)

3) Scheduling permit

4) Photo ID [Acceptable forms of ID include the following forms of unexpired identification: passport, driver's license with photograph, national identity card, other form of unexpired government-issued identification, ECFMG-issued identification card. Your identification must contain both your signature and recent (no more than 10 years earlier) photograph. If it contains your photograph but not your signature, you can use another form of unexpired identification that contains your signature, such as a student/employee identification card or a credit card, to supplement your photo-bearing, governmentissued identification.]

Hardy–Weinberg equilibrium with example

2009-06-03T22:36:00.003-04:00

The Hardy–Weinberg principle states that both allele and genotype frequencies in a population remain in an equilibrium (are constant) as long as no specific disturbing influences are introduced.

Those disturbing influences could be mutations, non-random mating, selection, limited population size, gene flow and random genetic drift. Because these influences are universal in real life Hardy-Weinberg principle is never absolutely accurate. Although it sounds more theoretical it can help predict things with reasonable error.

Take for example a single gene that could occur as either dominant allele (A) or recessive(a) and their frequencies are denoted by p and q respectively. Assuming population equilibrium, frequency of occurrence of AA(A homozygosity) is p^2 and frequency of aa (a homozygocity)is q^2. Similarly the frequency of Aa (heterozygous) should be 2pq.

To better understand this consider an autosomal recessive mutation that causes sickle cell anemia in homozygous recessive children. The parents of a boy with this mutation wants to know the probability of their grandchildren inheriting the disease. In order to determine the chance that the child will reproduce with a carrier of the recessive mutation we can use the above equation. In order to know this we should know the incidence of heterozygous girls with this mutation and this can be derived if the incidence of homozygous (disease) state is known.

Let us assume that the homozygous state occurs at the rate of 64 per 10,000 people. Hence the occurrence of aa (disease) is 0.0064 hence q^2 0.0064 Hence q = 0.08

p+q=1 hence p=1-q=1-.08=.92. According to this, AA is p^2, which is .8464. Heterzygotic frequency is 2pq, which is 0.1472

Hence the chance that the young boy will mate with a heterozygous girl are about 14% and half of all their kids will be homozygous hence the chance that their kids will have the disease is about 30%

Common paraneoplastic syndromes

2009-06-02T14:49:00.001-04:00

Paraneoplastic Limbic Encephalitis :

PLE is characterized by irritability, seizures, short-term memory loss and depression. MRI reveals bilateral mesial temporal lobe hyperintensities on T2 weighted images. Small cell lung carcinoma is the most common associated cancer.

Paraneoplastic Cerebellar Degeneration :

PCD patients present with cerebellar signs. MRI may be normal in initial stages. Common malignancies associated with this syndrome include -Small cell lung cancer, ovarian cancer, breast cancer and Hodgkin's lymphoma.

Paraneoplastic Encephalomyelitis :

In this condition there is patchy inflammation involving multiple areas of the nervous system. The tumor most frequently involved is again Small Cell Lung Carcinoma.

Paraneoplastic Sensory Neuropathy :

It is usually sensory neuropathy.

Opsoclonus-myoclonus :

This syndrome usually affects young children. While 50% of children with this syndrome have neuroblastoma only about 2% of children with this tumor develop opsoclonus.

Lambert-Eaton Myasthenic Syndrome (LEMS):

This is a Neuromuscular junction disorder characterized by Acetylcholine release problems from the presynaptic terminal.Symptoms are similar to myasthenia gravis. Diagnosis is often made using EMG. LEMS results from immunologic attack against the presynaptic terminal that cause interference with the release of Acetylcholine.