I've been doing a lot of thinking about the website and where I want it to go, and I've decided that I'd like to take a break for a while. The current plan is to eventually continue writing about medicine and my take on having a family during training (that was the main purpose when I started this) but I'm going to wait until I have a little bit more time. Besides, I have somehow unofficially become the webmaster of our new resident portal at work, so I imagine that'll keep me plenty busy. For family and friends, I'll periodically email new photos when I can.

I've also been more concerned about posting photos of the boys online, especially now that they are getting older. Privacy and safety issues are a big concern, so until I figure out how to best handle this, I'm going to take the archives offline.

I've left up some of my writings about medical school and kids, since those are the things I get emailed about the most. I've also left up my shopping resources.

Sorry for the abrupt message, and thanks for all your support.
-medstudentmom

It's been a long time since I've posted one of these (that probably means I am not reading enough).

No matter how hard I try to remember these, I always need a refresher. Here's the information straight from the CDC (click link to access a downloadable .pdf file).

This is a serious life-threatening obstetric complication that is believe to be related to pre-eclampsia. It is important to note that this syndrome can sometimes not present until after delivery. The pathophysiology is not well understood but a serious complication is consumption of coagulation factors, which can lead to disseminated intravascular coagulation (DIC). As in pre-eclampsia, the only effective treatment is delivery of the baby.

Hemolytic anemia, Elevated Liver enzymes, Low Platelets

Felty syndrome is characterized by the triad of chronic rheumatoid arthritis, splenomegaly, and granulocytopenia. Patients frequently have high titers of rheumatoid factor, and may also have subcutaneous nodules.

Although many patients are asymptomatic, some develop serious and life-threatening infections secondary to granulocytopenia.

Temporary blindness in one visual field. Often described as similar to "pulling down of a shade." Seen in TIAs (transient ischemic attacks).

I know it's been a while since I've posted one of these (sorry about that!).

This is classically defined as a fall in systolic blood pressure >10mm Hg on inspiration, which is an exaggeration of the normal response. Classically seen in pericarditis.

Here's a related mnemonic from First Aid:
PERICarditis
Pulsus paradoxus
ECG changes (PR-segment depression in precordial leads, low voltage, diffuse ST segment elevation)
Rub (friction)
Increased JVP
Chest pain

Classic triad of bilateral claudication in the hips, thighs and buttocks, symmetric atrophy of the lower extremities, and impotence in men. Suggestive of aortoiliac occlusion (leading to ischemia). Patients will have decreased peripheral pulses as well, and most will need an aortoiliac bypass graft.

Also known as obesity hypoventilation syndrome (OHS), this is defined to be alveolar hypoventilation while awake (resulting in hypoxemia and metabolic imbalance) in extremely obese patients. Other symptoms include hypersomnolence, dyspnea and pulmonary edema (from pulmonary hypertension). Patients often have obstructive sleep apnea (OSA) as well, which contributes to the symptoms.

"Pickwickian" refers to a Charles Dickens character (from the book The Posthumous Papers of the Pickwick Club). The symptoms resembled those of a character, Joe, in the book (commonly known as the Pickwick Papers).

Treatment includes noninvasive positive pressure therapy (for both OHS and OSA).

This is a rare, multisystem disorder that generally occurs in males younger than 20 years of age. There is a classic triad of mouth ulcers, genital ulcers, and uveitis. Focal neurological deficits may also be present.

Lab results usually show elevated ESR, and nonspecific changes on biopsy.

Treatment choices include corticosteroids, dapsone, colchicine, azathioprine, cyclosporine, and chlorambucil.

A simple, inexpensive method to assess the degree of vascular insufficiency in peripheral vascular disease. It is calculated by measuring the resting (and post-exercise if necessary) systolic blood pressures in the ankle and arm.

The highest of four measurements in the ankles and feet (posterior tibial and dorsalis pedis arteries) is divided by the higher of two brachial artery measurements.

Normal ABI ratio is 1 - 1.3 (pressure is higher in the ankle than the arm). Values > 1.3 suggest a noncompressible, calcified vessel.

ABI < 0.9 is associated with at least 50% stenosis in one or more major vessels.

Specifically,
0.4 - 0.9: arterial obstruction, claudication
< 0.4: advanced ischemia

This is an X-linked immunodeficiency disorder which presents with eczema, thrombocytopenia (bleeding), and recurrent otitis media. There is an increased risk of lymphoproliferative disease.

Patients have increased levels of IgE and IgA, and decreased levels of IgM. They get recurrent infections from S. pneumonia, S. aureus, H. influenza Type B, CMV, PCP, and HSV.

Treatment is supportive (IVIG and antibiotics), and patients frequently die of hemorrhage from the thrombocytopenia (rarely survive into adulthood).

Used to evaluate immediate health status of a neonate (not a predictor of health). Five parameters are measured and scored at one and five minutes after birth for a maximum score of 10 points. It is repeated at regular intervals if the scores are low (<3). Scores above 7 are generally considered reassuring.

Each parameter is given a score of 0-2 points (see below). There are several mnemonics to help you remember the parameters, but this is the one that I favor:

Score: 0, 1, 2
Appearance (color): blue, extremities blue, pink
Pulse (heart rate): absent, <100, >100
Grimace (reflex irritability): no response, grimace when stimulated, pull away when stimulated
Activity (tone): none, some flexion, active movement
Respiration: absent, weak or irregular, strong

McCune-Albright syndrome (MAS), is a genetic disease also known as familial gonadotropin-independent precocity. It affects the bones (fibrous dysplasia) and skin (cafe au lait spots), and causes precocious puberty, particularly early menarche in females.

MAS is believed to be caused by mutations in the GNAS1 gene. While there is no specific cure, it should be treated with drugs that inhibit gonadal steroidogenesis or gonadal steroid action to preserve fertility.

In girls, tamoxifen and bisphosphonate pamidronate have been shown to be helpful. Boys have been treated with ketoconazole (inhibits androgen synthesis), or a combination of spironolactone, (inhibits androgen action) and testolactone (blocks the conversion of androgen to estrogen), with good results.

Complications included broken bones, cosmetic bone deformities, blindness/deafness (pinched nerves as a result of bone deformities).

Classic triad for cardiac tamponade.

1. decreased arterial pressure (hypotension)
2. distended jugular veins
3. distant heart sounds

MEN1 is a rare, heritable (autosomal dominant) disorder, with a prevalence of approximately 2/100,000 people.

It is classically associated with a classic triad of tumors (parathyroid glands, anterior pituitary gland, and pancreatic islet cells) but has been expanded to include tumors of other organs as well (duodenum, thymus, lung (bronchial carcinoid), stomach, adrenal glands). Around 40% of patients also have Zollinger-Ellison syndrome or asymptomatic elevation in serum gastrin concentrations.

The initial presentation is most commonly primary hyperthyroidism (1-2% of all cases are due to MEN1). Treatment is variable and dependent on pathophysiology (similar to isolated tumor therapy). It also depends on the symptoms and severity (can be surgical or medical).

This refers to spinal cord damage involving the dorsal column, corticospinal tract, and spinothalamic tract unilaterally (hemisection). This causes weakness, Babinski sign, and loss of vibration and proprioception ipsilateral to the lesion, and loss of pain and temperature sensation on the contralateral side (2-3 segments below the lesion).

The most common causes of this syndrome are trauma (knife or bullet wound) and demyelination. Less common are tumors, herniation, and infection.

Mastocytosis, as the name implies, is a group of disorders caused by excessive mast cell production, and urticaria pigmentosa is a systemic condition. On skin exam, lesions composed of mast cells urticate/flush when rubbed (Darier's sign). Loss of weight and splenomegaly suggest systemic involvement. The bone marrow is the most commonly involved organ (besides the skin).

The infantile type is usually confined to the skin, whereas the adult type affects visceral organs as well. Bone marrow biopsy should be considered in adults with urticaria pigmentosa, elevated serum tryptase (>20ng/ml), or signs and symptoms of systemic involvement. If skin biopsy is performed, metachomatic staining with toluidine blue is used for visualization of mast cells in tissue sections. Other findings include elevated urinary histamine or a history of itching triggered by aspirin or alcohol ingestion.

The TST is a widely used test for detecting latent tuberculosis infection, and requires 2-12 weeks after primary infection for conversion to occur.

The Mantoux method (intradermal) is used in the United States, where 0.1mL (5 IU) of purified protein derivative (PPD) is injected into to volar surface of the forearm. The test should be interpreted 48 to 72 hours after administration of antigen by measuring the induration (not erythema) surrounding the injection site, in millimeters.

Interpretation
Induration greater than or equal to 5 mm: positive in highest risk population (HIV; recent contacts of TB-infected patients; patient with radiographic changes consistent with prior TB; immunosuppressed or taking >15mg/day prednisone for one month or more)
Induration greater than or equal to 10 mm: positive for individuals with an increased risk (recent immigrant (5 years) from Eastern Europe, Latin America, Asia, Africa; injection drug users; high-risk employees at hospitals, prisons, homeless shelters, nursing homes, laboratories; children exposed to adults at high risk, or any children under 4; patients with silicosis, chronic renal failure, hematologic disorders or other malignancies, weight loss of 10% of ideal body weight, gastrectomy, jejeunoileal bypass).
Induration greater than or equal to 15 mm: positive in low risk populations.

Outside the U.S., the two methods commonly used include intradermal injection of 2 IU of PPD (RT-23), or using a multiple puncture device (Heaf or tine test) on the volar or dorsal surface of the forearm. Individuals who have a history of BCG vaccination or previous tuberculous infection often test positive. Even so, tuberculin skin tests are not contraindicated in BCG-vaccinated persons and skin test reactivity should be interpreted and treated as for unvaccinated persons.

A new whole blood interferon assay (IFN-gamma, QuantiFERON-TB Gold) has been approved by the FDA and can be used instead of the TST. It is much less subjective, and only requires one patient visit.

Light's criteria is a traditional method used to determine whether pleural fluid is an exudate by measuring serum and pleural fluid protein and LDH. At least one of the following three criteria must be true for the fluid to be an exudate.
* Pleural fluid protein/serum protein ratio greater than 0.5
* Pleural fluid LDH/serum LDH ratio greater than 0.6
* Pleural fluid LDH greater than two thirds the upper limits of the laboratory's normal serum LDH

Light's criteria are often criticized for being redundant, and other diagnostic criteria are often used (with similar diagnostic accuracy), because they do not require concurrent measurement of serum protein or LDH.

Two-test rule
Pleural fluid cholesterol greater than 45 mg/dL
Pleural fluid LDH greater than two-thirds the upper limit of the laboratory's normal serum LDH

Three-test rule
Pleural fluid protein greater than 2.9 mg/dL
Pleural fluid cholesterol greater than 45 mg/dL
Pleural fluid LDH greater than two-thirds the upper limit of the laboratory's normal serum LDH

TORCHeS, a well-known mnemonic for the most common congenital newborn infections:

T: toxoplasmosis
O: other (HIV, parvovirus)
R: rubella
C: cytomegalovirus (most common)
H: herpes
S: syphilis

Reynold's pentad consists of the symptoms from Charcot's triad, plus shock and altered mental status. Presence of all of these symptoms suggests severe cholangitis.

You can find all my random medical facts here.

Charcot's triad consists of right upper quadrant pain, jaundice, and fever. The symptoms are present in 50 to 75% of patients with acute cholangitis.

Formerly known as Reiter syndrome, the classic triad of spondyloarthritis-related symptoms includes arthritis, nongonococcal urethritis, and conjunctivitis. Associated with HLA-B27, it can often follow an infection (Chlamydia trachomatis or pneumonia, Yersinia, Salmonella, Shigella, Campylobacter, or Clostridium difficile). Superficial oral and penile ulcers are not uncommon.

Diagnosis starts with laboratory testing to confirm a preceding or ongoing enteric or genitourinary infection, and to exclude other causes of mono- or oligoarticular arthritis. There is no single definitive test. The prognosis is usually good with most patients recovering spontaneously. In addition to treating any infection, NSAIDs (naproxen 500 mg three times daily or indomethacin 50 mg three times daily) may help as well. For those who don't respond to NSAIDs, intraarticular injections of glucocorticoids may be used. Completely refractory patients may be started on a trial of sulfasalazine (beginning with 500 mg twice daily and increasing, as tolerated to 1000 mg twice daily) or a trial of etanercept (50 mg subcutaneously weekly).

This classic multiple sclerosis (MS) sign is named for a French neurologist, Jean Lhermitte (1877-1959). It describes sudden transient electric-like shocks which extend from the neck down the spine when the head is flexed forward. It can be due to a disorder such as compression of the cervical spine (the portion of the spinal cord within the neck), and suggests a lesion of the dorsal columns of the cervical cord or of the caudal medulla.

Other possible causes include Behçet's disease, trauma, radiation myelopathy, vitamin B12 deficiency (subacute combined degeneration), and compression of the spinal cord in the neck (spondylosis, disc herniation, tumor, Arnold-Chiari malformation).

It's been a long time since I've posted one of these random medical facts (just goes to show how little I get to study these days). I am now cramming for the neurology shelf, which is probably going to be quite challenging, since my knowledge base for neuroanatomy is pretty weak right now (it's been several years). I still have a few days, so we'll have to see how it goes.

LEMS is a autoimmune disease, with the the main symptoms being slowly progressive proximal muscle weakness with hyporeflexia. Autonomic dysfunction is often present as well, with dry mouth being the most common complaint. It can also be a paraneoplastic syndrome associated with small cell lung cancer. It is due to autoimmune attack against voltage-gated calcium channels (VGCC) on the presynaptic motor nerve terminal, causing impaired released of acetylcholine (ACh). Because the presynaptic stores of ACh and postsynaptic response remain intact, repetitive nerve stimulation actually improves symptoms (unlike in myasthenia gravis, where repetitive nerve stimulation causes muscle fatigue).

It is a clinical diagnosis, but can be confirmed with both VGCC antibodies and nerve conduction studies. The differential diagnosis is broad, covering any diseases which present with proximal muscle weakness, but the most common consideration is myasthenia gravis.

Therapy includes both symptomatic (guanidine, 3,4-DAP, pyridostigmine) and immunologic (plasma exchange, IVIG, oral immunosuppressive agents) options.

This is a general rule for estimating %BSA (body surface area) affected in burn victims.

head: 9%
arm: 9%
back: 18%
chest: 18%
leg: 18%
perineum: 1%

I always forget the details about the different types of hemoglobin, which are important to understand when it comes to diseases like thalassemia.

The Parkland formula is used to estimate fluid repletion in a burn patient during the first 24 hours.

4 x patient's weight (kg) x %body surface area involved. Give 50% of the fluids over the first 8 hours, and then the rest over the next 16 hours.

To determine intravenous fluid rate in ml/hr:

Use 4 ml/kg/hr for the first 10 kg, 2mg/kg/hr for the second 10 kg, and 1 ml/kg/hr for any weight over 20 kg.

So, for a 25 kg child: 4 x 10 + 2 x 10 + 1 x 5 = 65 ml/hr

This is a popular method to calculate daily intravenous fluid (IVF) maintenance requirements in pediatrics.

For the first 10 kg of weight, give 100 mL/kg fluid.
For 11-20 kg, give 1000 mL + 50 mL/kg for each kg over 10 kg.
For children over 20 kg, give 1500 mL + 20 ml/kg for each kg over 20 kg.

Example: For a 25 kg child, you'd give 1500 + 20 x 5 = 1600 ml/day, or 66.6 ml/hr (if divided over 24 hours).

Dressler Syndrome, also called postcardiac injury syndrome (PCIS), postpericardiotomy syndrome, or postmyocardial syndrome, is an autoimmune pericarditis that usually occurs as a late (weeks to months) complication of an acute myocardial infarction (MI). It can happen in other settings, like after cardiac surgery or pulmonary embolism (PE).

Signs and symptoms include malaise, pleuritic chest pain, pericardial friction rub, fever, leukocytosis, pleural effusion, and pulmonary infiltrates. The pathogenesis is believed to be related to immunologic factors, where myocardial injury stimulates an antigen-antibody reaction, forming complexes that are deposited into tissues and elicit an inflammatory response.

It is mainly a clinical diagnosis based on the manifestations mentioned above. Erythrocyte sedimentation rate is often high as well.

Treatment is with NSAIDs (corticosteroids in refractory cases) and recurrence may occur.

Isovaleric acidemia is a rare disorder involving deficiency of isovaleryl-CoA dehydrogenase, which is needed in the leucine oxidative pathway. It is an autosomal recessive condition that can be diagnosed in utero. Symptoms include poor feeding, protein intolerance, metabolic acidosis, seizures, and an odor of sweaty feet during the first few days of life. Coma and death can result if not treated. Some patients have a more chronic course, with symptoms of vomiting, lethargy, hair loss, and pancreatitis. If suspected in a newborn, a urine organic acid chromatography test can consistently detect isovalerylglycine for diagnosis.

Treatment involves a low-protein, low-leucine diet. Conjugation with glycine or carnitine can help maintain metabolic stability.

Performed during the second trimester (~16-18 weeks) of pregnancy, the triple marker screen includes maternal serum alpha fetoprotein (msAFP), unconjugated estriol (uE3), and human chorionic gonadotropin (hCG). The markers are relative predictors of risk for abnormalities like neural tube defects and Down syndrome. Combined with maternal age and ultrasound dating of gestational age, the detection rate can be as high as 75%, with a 5% false positive rate.

As a medical student, it's important to remember some general trends. For example, hCG is usually elevated in Down syndrome, while msAFP and uE3 are decreased or normal. All three are decreased in Trisomy 18 (Edwards syndrome). For neural tube defects, msAFP is usually elevated. And the markers are not useful for detecting Trisomy 13 (Patau syndrome).

A quadruple marker test is also available, which adds inhibin A to the triple marker screen, and results in a higher detection rate (81%) for Down syndrome (inhibin A is increased).

Caput succedaneum is diffuse swelling due to accumulation of interstitial fluid in the soft tissues of the scalp in a neonate caused by pressure from the uterus or vaginal wall during vertex delivery. In other words, the baby's scalp gets swollen from being squished in the birth canal. It is caused by mechanical trauma and may occur on any part of the scalp. It can cross the midline (unlike a cephalhematoma) and is a common phenomenon that resolves in a few days without treatment.

Often called IIH, or idiopathic intracranial hypertension, pseudotumor cerebri is a disorder of unknown etiology which predominantly affects obese women of childbearing age. It is basically increased cranial pressure without a secondary cause (malignancy, for example) and most often presents with symptoms of headache and visual changes (particularly, papilledema). As such, the visual exam (visual field, fundoscopy, motility) is critical for diagnosis, and untreated disease may lead to progressive optic atrophy and blindness. The rest of the neurologic exam, as well as MRI and CT, can often be normal. Increased pressure on cerebrospinal fluid analysis is confirmatory. Treatment varies, but include using a carbonic anhydrase inhibitor (acetazolamide) to lower the ICP, corticosteroids, and surgery (CSF shunt or optic nerve sheath fenestration).

The question I was asked had to do with associated etiologic factors, particularly oral progestational drugs. Other associated conditions are mastoiditis and lateral sinus thrombosis, head trauma, marantic sinus thrombosis, cryofibrinogenemia, Addison disease, hypoparathyroidism, tetracycline therapy, and hypervitaminosis A.

What cardiac anomaly occurs with the highest frequency in fetuses exposed to lithium in utero (especially during the first trimester?)

I'll stick a random photo here, in case you didn't want the answer right away. It was taken a long time ago, during a pre-medical school vacation to my old college alma mater, but looking at it now, it could pretty much be anywhere.



And now, back to work.
The answer is Ebstein anomaly, which is a malformation of the tricuspid valve. Specifically, it is a congenital malformation that is characterized by downward (apical) displacement of the septal and posterior tricuspid valve leaflets, as well as malformation and abnormal attachment of the anterior leaflet to the right ventricular free wall. In other words, the tricuspid valve between the right atrium and right ventricle did not develop appropriately and does not work properly, so blood can leak backwards and cause atrial enlargement and potential heart failure.

Because of the increased pressure of backflow blood into the right atrium, many people with Ebstein anomaly also have an atrial septal defect, which allows blood to go directly from the right atrium to left atrium, bypassing the right ventricle and lungs, thus sending deoxygenated blood into the circulation.

Depending on severity, Ebstein anomaly can be asymptomatic, or present with cyanosis, heart failure, dyspnea, tricuspid regurgitation, fatigue, arrhythmias, or many other signs and symptoms. Definitive diagnosis is by echocardiogram study, and the treatment varies from none to surgery (repair/replacement).

A rare type of hypergonadotropic hypogonadism characterized by failure of the ovaries to respond to FSH and LH because of receptor defects. Apparently, this is rarely seen and a somewhat obsolete term. It is also known as ovarian resistance syndrome.

Okay, so it is a little weird (and gross?) to be posting about chancre, chancroid, gonorrhea and chlamydia between posts about my family and pictures of my babies. My Random Medical Facts section was started as a way for me to reinforce stuff that I have trouble remembering, but it often ends up being awkwardly placed among other, more pleasant, themes in my life. In some ways, that is how med school fits in with my family life, forcing its way into and in between a much different world. And I do enjoy them both, but they are really quite different, and equally demanding. But, no time to worry about that now. One day, when M and A are reading about what life was like when they were really little and mommy was a medical student, they might also be fascinated by the occasional random medical fact. Maybe not so much with this one though.

One common treatment of gonococcal cervicitis is ceftriaxone 125-250mg intramuscularly. We are always taught to look for and treat both gonorrhea and chlamydia together (they often coexist). Chlamydia treatment is azithromycin 1g orally or doxycycline 100mg twice daily for 7 to 10 days. Remember to treat partners too.

I can never remember the difference between chancre and chancroid. They are both sexually transmitted infections (STIs) but I always get them confused. Maybe typing this up will help me remember.

A chancre is the initial lesion of syphilis (primary), which is caused by the spirochete Treponema pallidum. The typical ulcer is painless, red, round, firm, with indurated borders. It arises three weeks after inoculation and disappears after two to six weeks without therapy. T. pallidum can be identified by serum antibody tests (MHA-TP, FTA-ABS), and material expressed from a chancre reveals motile spirochetes under dark-field microscopy. Treat with intramuscular benzathine penicillin G (alternative treatments are tetracycline and doxycycline).

Chancroid is also sexually transmitted, manifesting as a tender ulcer. It is more common in males, is usually painful, has ragged edges and a necrotic base. Tender inguinal lymphadenopathy is also common. It is caused by Haemophilus ducreyi, a small gram-negative rod and usually diagnosed clinically but can be confirmed with biopsy and/or culture (difficult). Treat with oral azithromycin or intramuscular ceftriaxone.

So, how will I try to remember the difference? A friend of mine suggested that "chancroid" could remind me of the word "android" (more common in males). A "lad" is male (common abbreviation for lymphadenopathy, which is painful). I could name the android "Duke," which might help remind me about H. ducreyi. Silly, I know, but sometimes this stuff really works!

Since I am on ob/gyn next, I'm reading a bit about it now. You would think that having gone through it (twice) would mean I knew most of this stuff already, but it's really different experiencing it from the other side. I really wasn't thinking like a medical student when I was going to my appointments, and whatever upper hand I might have had as a medical student in terms of exposure has clearly now been outweighed by my "mommy brain." And that doesn't even include the sheer lack of time and energy to read anything at the end of the day. You'd be amazed at what people have said to me regarding how much easier rotations must be because I experienced childbirth and have kids. Seriously? Perhaps in terms of patient empathy, but being a medical student mom doesn't make it any easier to remember things like the BPP (I don't remember ever having this assessed, and if it was, I certainly didn't get a hands-on lecture about it).

The Biophysical Profile (BPP) integrates 5 parameters as a tool for antenatal testing of fetal well-being, using real-time ultrasound:
1) nonstress test (NST) two or more episodes of fetal heart rate acceleration greater than 15bpm above baseline for at least 15 seconds, over a 20 minute period
2) breathing one or more episodes greater than 20 seconds long, within 30 minutes
3) movement two or more discrete body/limb movements or episodes within 30 minutes
4) tone one or more episodes of active extension with return to flexion of fetal limb(s) or trunk
5) amniotic fluid volume one or more pockets of fluid greater than 2cm in vertical axis, not to be confused with amniotic fluid index (AFI)*
Source: Manning FA: Fetal biophysical profile. Obstet Gynecol Clin North Am 1999 Dec; 26(4): 557-77

A score is assigned (0=abnormal, 2= normal) to each parameter, with a total score of 8-10 being reassuring for fetal well-being. First Aid includes a little mnemonic to help remember the parameters:
Test the Baby, MAN (tone, breathing, movement, amniotic fluid, nonstress test)

I have seen slight variations of the BPP in terms of scoring criteria, but are all pretty much the same in terms of assessing fetal well-being.

*An AFI measurement is the sum of highest vertical pocket of amniotic fluid (in cm) in each of four quadrants; <5cm = oligohydramnios, >25 = polyhydramnios. Along with the NST, it comprises the modified BPP.

This is one of the few obscure named diseases that I actually already knew about when I came across it in my studies. It is a nodular fibroblastic proliferation of palmar fascia, which leads to contracture of (most commonly) the fourth and fifth digits. It typically affects older men of Northern European heritage, can be hereditary, and has also been associated with chronic liver failure. Not too much more is known about the pathophysiology at this time, but there may be an association with certain genes (MafB), and myofibroblasts play a role in this disease. Treatment is surgical (fairly simple), but recurrence is common.

Basically, the patient will come to you because their ring and pinky fingers are curled and can't be fully extended. You can feel nodules in the palm and can often feel cords in the fingers. It is more common than I thought (saw quite a few cases on my hand surgery rotation). I also saw it a lot when I rotated through the Veterans Health Administration, which makes a lot of sense.

I could go on and on about named diseases, but here's one that I had never heard of before. It can be the presenting symptoms of sarcoidosis in some populations, especially Scandinavian women. The classic triad is polyarthritis, erythema nodosum, and bilateral hilar adenopathy. So the appropriate next step if you suspect this (according to my practice question) is to do a chest x-ray. Who knew?

I missed a practice question today about this syndrome, which I had never heard of before. It's also called "herpes zoster oticus," which is essentially varicella zoster virus (VZV) reactivation in the geniculate ganglion of cranial nerve VII. The classic triad of symptoms includes peripheral unilateral facial paralysis, ear pain, and vesicles in the auditory canal. Ouch. In any case, I didn't realize that VZV reactivation in the ear had a special name, other than shingles. Treatment is with antivirals (acyclovir) and analgesics. Some people like to use prednisone. Pretty picky question if you ask me. I don't think VZV reactivation in the other cranial nerves has a special name, or at least I hope not. The possibilities would be endless.

I have a little break before my next rotation (hand surgery), so I am trying to accomplish a few different things. I have a couple of research projects in the works, and I'm also studying for the USMLE Step 2 exam, which I'm going to schedule in the winter. I'm trying to get everything done early so that by this time next year, I will be coasting, and spending as much time with the kids as possible before I start residency. I'm also thinking about taking Step 3 early (is that even possible?) just to have one less thing to worry about when I am an intern.

I thought I'd occasionally write about some random facts I've learned during my studies. Today I read a bit about dermatitis herpetiformis, something that sounds familiar but I have no idea how to diagnose. It's an autoimmune vesicobullous disorder that presents as intensely pruritic papules, vesicles, or wheals (medical speak for itchy spots). The skin has IgA deposits along the dermoepidermal junction, and usually occurs on extensor surfaces of the elbows and knees, as well as the face and neck. The one factoid I didn't know was that there is an association with gluten-sensitive enteropathy (celiac disease). So you should suspect it and remember to ask about diarrhea and weight loss. Treatment is with dapsone or sulfapyridine, as well as a gluten-free diet.

I don't know how much stuff I overlooked in my preclinical years, or how much I have forgotten, but all of that sounded pretty new to me when I read it. In any case, for my med school friends, maybe it'll stick in your head now too!