tag:blogger.com,1999:blog-48654617657395829142024-03-12T18:04:05.988-04:00Score 99 USMLE blogA blog to help you prepare for USMLE Step1, Step 2CK, Step 2CS and Step 3Sunhttp://www.blogger.com/profile/15829446311285351529noreply@blogger.comBlogger247125tag:blogger.com,1999:blog-4865461765739582914.post-19015194948008558402012-07-16T23:49:00.003-04:002012-07-16T23:53:31.285-04:00Heriditary spherocytosis<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;">The following article covers most of the important points about Hereditary spherocytosis (HS) that are tested in the USMLE exam. Pay close attention to <strong>bold phrases</strong> as they are key points that appear in the exam as questions/hints.</span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;"><br /></span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;">HS is a common inherited
hemolytic anemia resulting from abnormalities in the proteins of the red
blood cell (RBC) membrane (<b>mainly spectrin but also ankyrin, protein 4.2, and band 3</b>).
</span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;"><br /></span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;">It is usually inherited in an <b>autosomal dominant</b> pattern, is most
common in whites of Northern European descent, and is <b>infrequent in
African Americans</b>. (Hereditary elliptocytosis (HE) is another disorder of
the red cell membrane that is a common cause of inherited hemolytic
anemia in African Americans.)</span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;"><br /></span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;">The membrane abnormalities of HS
cause fragility of the red cell membrane with loss of surface area and a
resultant spheroid shape instead of the normal biconcave appearance.
The <b>MCV is usually within the normal range</b> for age, but may be slightly
elevated if there is a brisk reticulocytosis. </span><span style="font-family: "arial", "helvetica", sans-serif; font-size: small;"><b>MCHC is high due to the
relative cellular dehydration.</b> </span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;"><br /></span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;">The abnormal RBCs become trapped in the
spleen where they are eventually hemolyzed (so-called<b> extravascular
hemolysis</b>). </span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;"><br /></span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;">This leads to an increase in <b>LDH,</b> unconjugated bilirubin.</span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;"><br /></span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;"><b>Haptoglobin</b> is a scavenger hor free
hemoglobin and is <b>normal or decreased in HS (as the hemolysis is extravascular)</b>.</span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;"><br /></span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;"><b>Osmotic fragility is <u>increased</u> in HS.</b></span><br />
<span style="font-family: "arial", "helvetica", sans-serif; font-size: small;"><b><br /></b><b>Splenectomy</b> is a common treatment but should be delayed until after school going age, if possible, due to the risk of pneumococcal sepsis.
<b>Penicillin prophylaxis</b> is recommended for at least the first 5 years
after splenectomy with some doctors recommending treatment for life.</span><div class="blogger-post-footer"><script type="text/javascript"><!--
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<br />
Pseudostrabismus can easily distinguished form strabismus by looking at the patient's corneal light reflex. The patient in the picture below has <b>true strabismus </b>as evident by presence of corneal light reflex in different parts of the cornea. <br />
<br />
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="http://3.bp.blogspot.com/-aZzeoqZ5ReI/UAIuaPDTfpI/AAAAAAAACQs/fsucSH7CJ9k/s1600/Strabismus.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" src="http://3.bp.blogspot.com/-aZzeoqZ5ReI/UAIuaPDTfpI/AAAAAAAACQs/fsucSH7CJ9k/s1600/Strabismus.jpg" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">(image modified from Wikipedia: http://en.wikipedia.org/wiki/File:Strabismus.jpg)
</td></tr>
</tbody></table>
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<br />
Diagnosis: In addition to delivery history the following features may point towards the diagnosis:<br />
-Decrease/assymetric movement of the limbs. (This may be evident by presence of an assymetric Moro's reflex)<br />
-Palpable crepitus or bony irregularity early on<br />
-A large callus forms quickly and is generally palpable by age 1 week. <br />
<br />
Prognosis is excellent. Treatment, if any, is limited to immobilization of the arm and shoulder on the affected side (simply pinning the sleeve to the side of the infant's shirt does the trick). Figure of 8 bandages are no longer used.<br />
<br />
Differential diagnosis: Congenital pseudoarthrosis of the clavicle<br />
<br />
This condition presents as a palpable lump in the center of the clavicle that does not change or heal with any amount of time. Its cause is unknown. The condition is more common on the right side and generally does not lead to any functional impairment. Surgery is rarely indicated.<div class="blogger-post-footer"><script type="text/javascript"><!--
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-Underlying cause is a high attachment of tunica vaginalis that occurs in 12% of males<br />
-Symptoms may include nausea and vomiting and even fever (in addition to testicular symptoms)<br />
-Examination may demonstrate a horizontal and elevated testis<br />
-The<u> cremasteric reflex is usually absent</u>, but its presence does not rule out testicular torsion. <br />
-<u>Elevation of the scrotum does not relieve the pain </u><br />
-Doppler can confirm diagnosis although it is often not needed<br />
-If surgery is done after 6 hours of onset the chances of testicular atrophy are extremely high<br />
<u>-During surgery the opposite (normal) testis is also fixed because the high attachment anomaly is often bilateral</u><br />
<br />
<strong>Differential diagnosis:</strong><br />1) Acute epididymitis and/or orchitis<br />
-Onset is more gradual with fever and dysuria. <br />
-Elevation of the scrotum may reduce discomfort<br />
-Cremasteric reflex may or may not be present<br />
-Teatment is with rest, analgesia, and antibiotics if there is concern about a bacterial infection<br />
<br />
2) Torsion of the appendix testis<br />
-Localized tenderness over the upper portion of the testis<br />
-Blue dot sign<br />
-Cremasteric reflex is present
<br />
-Treatment is analgesia<br />
<br /><div class="blogger-post-footer"><script type="text/javascript"><!--
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-Impairment in social interaction (few interests)<br />
-They are aware that they do not fit in socially. <br />
-<u>Unlike autistic children, they do not express basic language impairment (only minor problems)</u><br />
-Treatment is behavior modification and cognitive-behavioral therapy are used to improve level of function.<br />
-Some consider this condition as high functioning autism<br />
<br />
<strong>Autism</strong><br />
-Usually manifests itself before age 3 years (Asperger may be later)<br />
-Triad of <br />
---Impairment in <u>social</u> interaction (no friends, no empathy)<br />
---<u>Language</u> delay<br />
---<u>Ritualistic</u> behaviors and a strong need for sameness and consistency<br />
-Treatment includes intense family support, behavior modification, speech and language training, auditory integration training, and medication.<div class="blogger-post-footer"><script type="text/javascript"><!--
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<br />
Do not confuse these with the following conditions:<br />
<br />
<u>Congenital epulis</u> 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.<br />
<br />
<u>Mucoceles</u> 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.<div class="blogger-post-footer"><script type="text/javascript"><!--
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-X-linked dominant (Affects girls).<br />
-Onset is in the second year of life.<br />
-Typically there is regression in <strong>motor</strong> and <strong>language</strong> development<br />
-Autistic behaviors are common<br />
-There is <u>acquired microcephaly</u><br />
-Characteristic hand-wringing behavior<br />
<br />
Poor prognosis. No specific treatment.<div class="blogger-post-footer"><script type="text/javascript"><!--
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<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="http://upload.wikimedia.org/wikipedia/commons/7/75/Vitiligo2.JPG" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="240" src="http://upload.wikimedia.org/wikipedia/commons/7/75/Vitiligo2.JPG" width="320" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Image from Wikimedia Commons. <br />
Available here:http://en.wikipedia.org/wiki/File:Vitiligo2.JPG</td></tr>
</tbody></table>
<b>Signs and symptoms</b><br />
<br />
-Hypo or depigmented patches that often enlarge and change shape.<br />
-Most prominent on the face, hands and wrists.<br />
<br />
<b>Treatment</b><br />
<br />
-<b>UVB</b> 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.<br />
-Studies have shown that <b>immunomodulators</b> such as topical tacrolimus (Protopic) and pimecrolimus (Elidel) may also cause improvement in some cases, when used with UVB narrowband treatments<br />
-Psoralen and Ultraviolet A light (<b>PUVA</b>) therapy is generally performed in clinic setting.<br />
-Skin <b>camouflage</b>/make up<br />
-<b>Depigmenting</b> 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.<br />
<br />
<b>Differential diagnosis</b><br />
<br />
-Pityriasis alba<br />
-Tuberceloid Leprosy<br />
-Post inflammatory hypopigmentation<br />
-Tinea versicolor<br />
-Albinism<br />
-Piebaldism<br />
<br />
<b>USMLE pearl: </b>Vitiligo is often associated with other autoimmune diseases including Hashimoto thyroiditis, type I Diabetes Mellitus, Addison's disease, pernicious anemia etc.<div class="blogger-post-footer"><script type="text/javascript"><!--
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<br />
1-Know the <b>content</b><br />
2-Learn how to <b>apply </b>the knowledge at solving multiple choice questions<br />
3-Keep your <b>calm</b>. There will always be questions you will not know the answers to. In fact there will be many!<br />
4-<b>Practice </b>questions and develop expertise at solving multiple choice questions.<br />
5-Know the exam <b>software </b>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)<br />
<br />
How to approach a question:<br />
<br />
<b>1. Read the question stem well</b><br />
<br />
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.<br />
<br />
<b>2. Guess the answer before reading the options</b><br />
<br />
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.<br />
<br />
<b>3. Is your answer present in the options provided?</b><br />
<br />
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.<br />
<br />
<b>4. If not start excluding the wrong options</b><br />
<br />
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.<br />
<br />
<b>5. Guess!</b><br />
<br />
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.<br />
<br />
And on your big day<br />
<br />
1) Be confident but at the same time <b>prepared to feel stupid</b>. 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)<br />
<br />
2) <b>Arrive on time</b>. 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!<br />
<br />
3) Drink strong <b>coffee</b>. Take some along. Also take some snacks with lots of <b>sugar</b>. 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).<br />
<br />
4) Taking breaks: I recommend that at the end of <b>each block</b> when it gives you option to take a break or go to next block, hit '<b>Take a break</b>'. 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.<br />
<br />
5) Start with question 1 and go till the end.<b> Time yourself </b>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.<br />
<br />
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 <b>do not leave a question without choosing an answer because you may never get back to it.</b><br />
<br />
7) Try<b> not to mark too many questions</b> 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.<br />
<br />
8) Some people say when you<b> change an answer,</b> 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.<br />
<br />
Good luck for the test!<div class="blogger-post-footer"><script type="text/javascript"><!--
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-Sideroblastic anemia results from hereditary (X-linked) or acquired disorder of heme synthesis.<br />
<br />
-It is a microcytic hypochromic anemia with a<b> high RDW</b> (red cell distribution width)<u> Same as iron deficiency </u>anemia.<br />
<br />
-Iron studies will distinguish the two. In sideroblastic anemia serum iron, serum ferritin and transferrin saturation are <b>increased</b>.<br />
<div>
<br /></div>
-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.<br />
<br />
-Severity can be mild or severe enough to need frequent transfusions.<br />
<br />
-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.<br /><div class="blogger-post-footer"><script type="text/javascript"><!--
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<br />
<span class="Apple-style-span" style="font-size: large;">Treatment of Acute Attacks of Gout</span><br />
<br />
-First the <u>diagnosis should be confirmed</u>. Septic arthritis has the potential to look exactly like gout, hence the initial step is always arthrocentesis unless the patient has a known diagnosis.<br />
<br />
-Next step is <u>pain management</u>. 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.<br />
<br />
-When <u>comorbidities </u>limit the use of NSAIDs or colchicine, intra-articular steroid injection may be indicated.<br />
<br />
-One must remember that<u> control of the underlying hyperuricemia is contraindicated until the acute attack is controlled </u>as it may intensify and prolong the attack. However if the patient is already on allopurinol or probenecid, they should be continued.<br />
<br />
<b><u>Medications for acute gout:</u></b><br />
<br />
<b>Nonsteroidal anti-inflammatory drugs</b><br />
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.<br />
<b><br /></b><br />
<b>Colchicine</b><br />
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.<br />
<br />
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.<br />
<br />
<b>Corticosteroids</b><br />
Corticosteroids can be given to patients with gout who cannot use NSAIDs or colchicine, but ACTH is generally preferred over steroids.<br />
<br />
<span class="Apple-style-span" style="font-size: large;">Treatment of Chronic Gout</span><br />
<br />
-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.<br />
<br />
-Probenecid (uricosuric agent) and allopurinol (decrease production of uric acid) are the two main drugs used. Probenecid is preferred by some.<br />
<br />
-Patients with very high uric acid excretion will benefit from Allopurinol. It is also the drug of choice in patients with existing renal disease.<br />
<br />
<b><u>Medications for chronic gout:</u></b><br />
<b><br /></b><br />
<b>Probenecid </b><br />
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).<br />
<b><br /></b><br />
<b>Allopurinol</b><br />
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.<br />
<b><br /></b><br />
<b>Febuxostat</b><br />
Febuxostat is a newer nonpurine selective inhibitor of xanthine oxidase, and is a potential alternative to allopurinol.<br />
<b><br /></b><br />
<b><u>Other treatments:</u></b><br />
<b><br /></b><br />
<b>Rasburicase</b><br />
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.<br />
<b><br /></b><br />
<b>Diet and Activity</b><br />
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.<br />
<br />
Increasing dairy intake, folic acid intake, and coffee consumption may reduce gout flares. Weight reduction in patients who are obese can improve hyperuricemia.<div class="blogger-post-footer"><script type="text/javascript"><!--
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<br />
<u>Prader-Willi phenotype can occur as a result of one of the following</u><br />
<br />
1. <b>Deletion</b> of 15q11-q13 including the Prader-Willi critical region of the paternally derived chromosome 15 (most common)<br />
<br />
2. Abnormality of the <b>structure </b>of Prader-Willi critical region of 15q11-q13 (for example translocation)<br />
<br />
3. If the child has <b>two maternally derived chromosome</b> 15s. (Hence absence of paternal chromosome 15)<br />
<br />
4. Mutations of imprinting <b>control center</b> genes (rare)<br />
<br />
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.<br />
<br />
<u>Mechanisms leading to Angelman syndrome include the following: </u><br />
<br />
1. <b>Deletion </b>of the 15q11-q13 including the Angelman critical region of the maternally derived chromosome 15 (most common)<br />
<br />
2. Abnormality of the <b>structure </b>of the Angelman critical region of 15q11-q13 (e.g. translocation)<br />
<br />
3. If the child has <b>two paternally derived chromosome</b> 15s. (Hence absence of maternal chromosome 15)<br />
<div>
<br /></div>
4. Mutations of imprinting <b>control center genes </b>(rare).<br />
<br />
5. Mutations of the <b>ubiquitin-protein ligase gene</b> (UBE3A)<br />
<br />
6. <b>No identifiable etiologic mechanisms</b> but a positive family history of other affected individuals and a classic phenotype<br />
<br />
<u><b>Clinical features of Prader Willi syndrome:</b></u><br />
<b><u><br /></u></b><br />
Newborns: hypotonia, poor sucking and swallowing, weak cry<br />
Infancy: Delayed motor and speech development<br />
Toddler: Hypotonia goes away! Extreme appetite leading to morbid obesity.<br />
<br />
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.<br />
<br />
<b><u>Clinical features of Angelman syndrome:</u></b><br />
<br />
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.<div class="blogger-post-footer"><script type="text/javascript"><!--
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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.<br /><div class="blogger-post-footer"><script type="text/javascript"><!--
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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.<br />
<br />
<u>Pathophysiology:</u> 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.<br />
<br />
<u>Clinical features:</u> Features of <b>hyperthyroidism </b>can be seen initially (and sometimes intermittently), however the predominant feature is <b>hypothyroidism</b>. The thyroid gland is firm and mildly enlarged and sometimes lobulated.<br />
<br />
<u>Diagnosis: </u>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.<br />
<br />
<u>Differential diagnosis:</u> Depression, cyclothymia, PMS, chronic fatigue syndrome, fibromyalgia and, anxiety disorder.<br />
<br />
<u>Treatment:</u> Hypothyroidism is treated with thyroid hormone replacement agents such as levothyroxine. Aim of treatment is to keep TSH levels be kept under 3.<br /><div class="blogger-post-footer"><script type="text/javascript"><!--
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<br />
<embed id=VideoPlayback src=http://video.google.com/googleplayer.swf?docid=-129131776699704562&hl=en&fs=true style=width:400px;height:326px allowFullScreen=true allowScriptAccess=always type=application/x-shockwave-flash> </embed><div class="blogger-post-footer"><script type="text/javascript"><!--
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Myocardial infarction (MI) due to coronary artery disease is a leading cause of death in the United States.<br />
<br />
Complications of MI include:<br />
-Arrhythmic<br />
-Mechanical<br />
-Inflammatory<br />
<br />
-Thrombo-embolic<br />
-Circulatory/Shock<br />
<br />
<br />
<br />
<b><u>Arrhythmic Complications of MI:</u></b><br />
<b><br /></b><br />
About 90% of patients with MI develop some form of cardiac arrhythmia. These arrhythmias can be broadly classified into the following categories:<br />
<br />
Supraventricular tachyarrhythmias<br />
Accelerated junctional rhythms<br />
Bradyarrhythmias<br />
Atrioventricular (AV) blocks<br />
Intraventricular block<br />
Ventricular arrhythmias<br />
Reperfusion arrhythmias<br />
<br />
<b><u>Mechanical Complications:</u></b><br />
<br />
-Ventricular free wall rupture and pericardial tamponade<br />
-Ventricular septal rupture<br />
-Papillary muscle rupture with severe mitral regurgitation<br />
-Left Ventricular Aneurysm<br />
<br />
<b><u>Inflammatory complications:</u></b><br />
<br />
-Pericarditis: Occurs in 10% patients within the first 4 days of MI)<br />
-Post-MI syndrome (Dressler syndrome): Occurs in 1-5% after MI and can present 2-3 weeks after MI.<br />
<br />
<br />
<b><u>Thrombo-embolic complications:</u></b><br />
<br />
Occur secondary to regional myocardial hypokinesia and stasis as well as secondary to arrhythmias such as atrial fibrillation.<br />
<br />
<b><u>Circulatory/Shock:</u></b><br />
<b><br /></b><br />
Can be seen in right ventricular infarction (treatment is IVF) and in massive left ventricular infarction (treatment is supportive with careful administration of IVF.<br />
<br />
<br />
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- Apparent usually at birth<br />
- Crosses suture lines<br />
- Reabsorbs within 1-3 days<br />
<br />
Cephalhematoma (also spelled as cephalohematoma cephalhaematoma and cephalohaematoma) on the other hand is collection of blood below the periosteum. It has the following characteristics.<br />
- Typically becomes apparent 1-2 days after birth<br />
- It does not cross the suture lines (because it is under the periosteum).<br />
- Takes 3-4 weeks or longer for it to be reabsorbed<br />
- Can lead to jaundice from degradation of the extravasated blood<br />
- Often associtated with birth trauma and a fracture in the newborn's skull bones (most commonly parietal bone)<div class="blogger-post-footer"><script type="text/javascript"><!--
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<b>Betalactams </b>(e.g. penicillins and cephalosporins): Inhibit cell wall synthesis.<br />
<br />
<b>Fluoroquinolones</b> (e.g. ciprofloxacin and nalidixic acid): Bind to bacterial DNA gyrase and topoisomerase IV, interfering with bacterial DNA synthesis.<br />
<br />
<b><span class="Apple-style-span" style="color: #990000;"><u>Tetracyclines</u></span>:</b> Bind to the bacterial <u><b><span class="Apple-style-span" style="color: #990000;">30S</span></b> </u>ribosome, inhibiting bacterial protein synthesis.<br />
<b><span class="Apple-style-span" style="color: #990000;"><u>Aminoglycosides </u></span></b>(e.g. gentamicin): Bind to <u><b><span class="Apple-style-span" style="color: #990000;">30S</span></b> </u>ribosome unit as well.<br />
<br />
<b>Macrolides </b>(e.g. azithromycin): Reversibly bind to the 50S ribosomal subunit.<br />
<br />
<b>Sulfonamides </b>(e.g. sulfamethoxazole): Inhibit steps in bacterial folic acid synthesis.<br />
<div>
<br /></div>
<div>
This stuff is high yield for Step 1.</div><div class="blogger-post-footer"><script type="text/javascript"><!--
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<h6 class="uiStreamMessage" data-ft="{"type":1}">
<span class="messageBody" data-ft="{"type":3}" style="font-weight: normal;"><span class="Apple-style-span" style="font-family: inherit; font-size: small;">Two molecules are walking down the street; one bumps into the other and says:<br />"Oh, my fault. Are you okay?”<br />The second molecule says: "No, I'm not okay. I've lost an electron!"<br />The first molecule says: "Are you sure" <br />The second molecule answers: "I'm positive!"</span></span></h6>
<h6 class="uiStreamMessage" data-ft="{"type":1}">
<span class="Apple-style-span" style="font-size: small;"><span class="Apple-style-span" style="font-weight: normal;">Now get back to work! Click on any topic above to start reading useful pearls for the USMLE.</span></span></h6><div class="blogger-post-footer"><script type="text/javascript"><!--
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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.<br />
<br />
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.<br />
<br />
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.<br />
<br />
<b>Succimer is the drug of choice</b> 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.<br /><div class="blogger-post-footer"><script type="text/javascript"><!--
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<br />
<b>Pathophysiology:</b><br />
-Shiga toxin-producing E. coli (STEC) or enterohemorrhagic E. coli (EHEC) produce a toxin called verotoxin or shiga-like toxin.<br />
-Toxin enters the bloodstream and causes damage to the body's vascular endothelium.<br />
-Endothelial damage leads to platelet activation that causes thrombocytopenia. The renal glomerular endothelial cells express a receptor for the toxin.<br />
<br />
<b>Clinical features:</b><br />
-HUS is characterized by the triad of hemolytic anemia, thrombocytopenia, and acute renal failure.<br />
-Preceding bloody diarrhea may or may not be present.<br />
(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.)<br />
<br />
<b>Treatment:</b><br />
-Supportive treatment for low platelets (transfusion if bleeding)<br />
-Supportive treatment of renal failure (electrolyte balance, dialysis as needed)<br />
-Plasmapheresis is often used in early cases to get rid of the circulating toxin<br />
-With supportive care majority of the patients have good renal outcomes<div class="blogger-post-footer"><script type="text/javascript"><!--
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to make that I should have made before, but I was concerned that it
might affect our relationship. <br />
<br />
"What is it?" his new bride asked lovingly. <br />
<br />
"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." <br />
<br />
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." <br />
<br />
"No problem," said her husband, "just widen your stance a little, and overlap your grip, and that should clear it right up."<div class="blogger-post-footer"><script type="text/javascript"><!--
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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.<br />
<br />
Depending upon the location of ischemia a variety of <u>symptoms </u>can results. Classically the symptoms are described as the bends, the chokes and the staggers!<br />
<br />
<b>The bends:</b> refers to pain in the joints from ischemia of joint capsules<br />
<b>The chokes: </b>refers to dyspnea<br />
<b>The staggers:</b> refers to neurological symptoms.<br />
<br />
<u>Prevention:</u><br />
<u><br /></u><br />
-Divers should limit their ascent rate to about 10 metres per minute.<br />
-Oxygen pre-breathing<br />
<br />
<u>Treatment:</u><br />
<br />
-Administer 100% oxygen by face mask until re-compression with 100% oxygen until hyperbaric oxygen therapy is available.<br />
-Treat dehydration<br /><div class="blogger-post-footer"><script type="text/javascript"><!--
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<div style="margin-bottom: 0in;">
<b>Class I</b> has<b> no histologic changes</b> and
has the best prognosis.</div>
<div style="margin-bottom: 0in;">
<b>Class II</b> has <b>proliferation in the
mesangium</b> and has good prognosis.</div>
<div style="margin-bottom: 0in;">
<b>Class III </b>has <b>focal </b>proliferation. It
has variable prognosis.</div>
<div style="margin-bottom: 0in;">
<b>Class IV </b>has <b>diffuse </b>proliferation and
<u><span class="Apple-style-span" style="color: #cc0000;">bad prognosis.</span></u></div>
<div style="margin-bottom: 0in;">
<b>Class V</b> has <b>membranous </b>changes and
relatively better progrnosis.
</div>
<div style="margin-bottom: 0in;">
<b>Class VI </b>has <b>scarred </b>glomeruli and end
stage disease.</div>
<div style="margin-bottom: 0in;">
<br /></div>
<div style="margin-bottom: 0in;">
<br /></div>
<div style="margin-bottom: 0in;">
<a href="http://2.bp.blogspot.com/-HqbTRCgInmU/TiArjjRiZdI/AAAAAAAACA4/eX-ZeFz8dK4/s1600/m.png" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="http://2.bp.blogspot.com/-HqbTRCgInmU/TiArjjRiZdI/AAAAAAAACA4/eX-ZeFz8dK4/s1600/m.png" /></a></div>
<div style="margin-bottom: 0in;">
This letter M has five red circles. (Membranous)</div>
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<div style="margin-bottom: 0in;">
<b>Akathisia </b>refers to an urge to keep moving. Typically
the patients will pace about in the house and sit down and get up
again. First line treatment of akathisia is propranolol although
benzodiazepines have also been used. Akathisia can occur<u> any time</u> after starting the medication.</div>
<div style="margin-bottom: 0in;">
<br />
</div>
<div style="margin-bottom: 0in;">
<b>Tardive duskinesia (TD)</b> refers to
involuntary movements which can be perioral (such as lip smaking,
chewing and darting tongue movements) or choreoathetoid movements of
extremities or other body parts. TD usually <u>does not occur within the
first 3 months</u> of starting the medications. TD can be difficult to
treat and may require changing to medications that do no cause this
side effect such as clozapine.</div>
<div style="margin-bottom: 0in;">
<br />
</div>
<div style="margin-bottom: 0in;">
<b>Dystonia </b>occur <u>within
hours or days </u>of starting the therapy. Characteristic features
include muscle spasms (e.g. torticollis). Treatment of dystonia is
acomplished by antihistaminic medications like diphenhydramine
(Benadryl) or anticholinergics like benztropine or trihexphenidyl.</div>
<div style="margin-bottom: 0in;">
<br />
</div>
<div style="margin-bottom: 0in;">
<b>Neurolept maligant syndrome</b> is a known
side of antipsychotics that presents with hyperthermia, muscle rigidity
and mental status changes. It usually occurs after 1-2 weeks of
starting the therapy. Treatment includes stopping the medication and
use of dantrolene, bromocriptine and amantidine.</div>
<div style="margin-bottom: 0in;">
<br /></div>
<div style="margin-bottom: 0in;">
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)</div><div class="blogger-post-footer"><script type="text/javascript"><!--
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