Efenem quits USMLE

After giving very serious considerations about pros and cons, yes and no, asking and forumming around, many months of studying experience, I decide to quit USMLE Step 1.

People might ask me why do I have to quit? Here are the reasons:

1. Efenem is stupid and talentless.
2. Efenem is a quitter.
3. Efenem is a loser.
4. Efenem is freaking out.
5. Efenem sucks!

I made some calls, reread the information booklets; the total $835 I paid earlier will only be charged $100. The remainder will be refunded. That is a much better deal than to fail (which is very very likely for me) and lose the whole damn $835!!!

For those who are really willing to take this exam, please do so. You have what it takes to ace USMLE Steps, but I know I don’t. Do not be discouraged by my coward act.

I am currently not willing to explain any further. Please understand. After a year of mental preparation, half a year of studying, money spent on study materials, I feel deeply hurt to quit sitting USMLE Step 1. This is one of the worst pain in my whole life.

I am not ready to expose my face to the real world… For the time being, let me simply feel like the sore loser at the comfort of my own home.

Perhaps I should think about quitting medicine altogether.

Saturday June 14th 2008

1. The side effects of mannitol include headache, nausea, vomiting and the most severe is pulmonary edema. It is due to increase extracellular osmolality causing water extraction to extracellular space.
2. Constipation is due to inactivity, low-fiber diet, opiods and TCAs, hypercalcemia. Magnesium hydoxate, an osmotic laxative has similar effect to osmotic diarrhea in lactase deficiency.
3. Hypothyroid myopathy presentation:
1. Muscle fatigue, pain, cramping
2. Biopsy: pale muscle fibers, decreased striation and mucinous deposition.
3. atrophy of type II muscle fibers
4. increase in creatinine phosphokinase (CPK)
4. AV shunt bypasses capillary beds and is a major resistance in vascular system. On palpation; thrill pulsatile mass and bruits on auscultation. It increases preload (increase voluma and rate of blood flow back to the heart), thus increase diastolic volume, and prolong diastolic filling.
5. Hydroxyurea (for Sicke Cell Disease) increases HbF to protect sickle cells from polymerization.

Friday 13th June 2008

Half of UW:

1. Paget’s Disease increases in osteoclastic bone resorption. The end product is pattern of lamellar bone with irregular sections linked by cement lines.
2. Hydatiform mole have 2 types:
1. Complete (46 XX) = all chromosomes are from paternal origin, no fetal structure, large edemtaous and disordered chorionic villi. Looks like a bunch of grapes. The sperm replicates chromosome while eliminating maternal chromosome.
2. Partial (69 XXY), (69 XXX) = formation of fetal structure grossly. Fertilization of ovum by 2 or more sperm.
3. HCV is genetically unstable because it lacks proofreading 3′->5′ exonuclease activity in its RNA polymerase. It makes many errors during replication. Its envelope glycoprotein contains hypervariable region prone to mutation. An infected individual may present with several dozen subspecies.
4. In paroxysmal SVT, Valsalva manuever or carotid sinus massage is performed. Rectus abdominis muscle of AAW is most important muscle in achieving intraabdomina/intrathoracic pressure of Valsalva maneuver.
5. In calculating FF = GFR x RPF. GFR can be measured using creatinine or inulin clearance. RPF is estimated with PAH clearance.

Saturday June 7th 2008

I have neurology exam very soon, so I have to hold my studies for USMLE again but at the mean time I tried to listen to USMLE lectures of neuroscience which is not really helping with my forthcoming neurology exam but I am very impressed I can understand the very basics of neuroscience.

For example today I listened to the lectures about the 3 important tracts in spinal cord. I learned that the motor (corticospinal tract) only needs 2 neurons (UMN + LMN) while sensory (dorsal columns and spinothalamic tract) needs 3 neurons.

The lecture also taught me about the points of decussation and its clinical importance. For example the lesion in spinothalamic tract always manifest itself contralaterally because it decussates almost immediately upon entering the dorsal horn of grey matter. Meaning any pain and temperature loss in a patient always mean a contralateral lesion in spinothalamic tract!

This is very helpful to understand lesions on spinal cord; Brown-Sequard syndrome, Lou Gehrig’s disease, polio, tabes dorsalis etc.

But lesions on any part of brainstem will result in contralateral spastic paresis/ loss of touch sensation/ loss of pain sensation. How to know if this is really a lesion in brainstem? The cranial nerve involvement! For example; Weber’s syndrome = ipsilateral oculomotor nerve palsy (down n’ out) + contralateral hemiparesis/hemiplegia.

Wednesday June 4th 2008

A little late in updating because I was finishing urology case report. My neurology exams is in next 5 days so I will be focusing on neurology also from now on. Here are the half of UW discussion I did:

1. Pregnant women should be immunized by tetanus toxoid so that protective IgG can be transferred into neonate to avoid tetanus.
2. In urine, the pathogens that can be found are CMV, adenovirus, E. Coli, Staph. saprophyticus, Klebsiella.
3. This is probably the easies, but still I have to remember; lecithin/sphingomyelin ration > 2 indicates fetal lung maturity.
4. cryptpococcosis -> capsular polysaccharide have antiphagocytic properties; stained by India ink -> round yeast with peripheral clearing.
5. Listeria is the only gram +ve bacteria to produce lipopolysaccharide (LPS) endotoxin. Cell-mediated immunity is needed to eliminate listeria. It has very small zone of beta-hemolysis on sheep blood agar; catalase +ve and motile. Neonates up to 3 years, AIDS patients, pregnant and lymphoma are at high risk.
6. HPV causes cutaneus (straisn 1-4) & genital warts (strains 6 & 11), benign and malignant epithelial neoplasia. Koilocytosis is the hallmark of HPV infection.Koilocyte = pyknotic superficial or immature squamous cells with dense, irregularly staining neoplasm & perinuclear clearing.
7. Here are some things about antiHPTs in moderate to severe hypertension:
1. Hydralazine is safe and useful in pregnancy-induced hypertension.
2. Nitroprusside can cause cyanide toxicity and sodium & water retention.
3. Fenoldopam is  a new dopamine-1 receptor agonist. Dopamine-1 receptor stimulation activates adenylyl cyclase, increasing cAMP and vasodilation. Besides improving renal blood flow, it also increases excretion of sodium and water (natriuresis). It can be used in patients with renal insufficiency.
8. Homeobox codes for DNA-binding transcription factors play role in morphogenesis.
9. Power = 1 – beta; beta = probability of not seeing any difference while in reality it exists.
10. Risk factors for osteoporosis: smoking, menopause, corticosteroid therapy, physical inactivity, caucasian, low BMI, alcohol. Mechanism of corticosteroid therapy in inducing osteoporosis:
1. decreases GIT absorption of calcium.
2. inhibits collagen synthesis by osteoblasts.
3. decrease GnRH -> hypogonadism.
4. increases urinary calcium loss.
11. Skeletal muscles have two types – Slow Twitch (type I) and Fast Twitch (type II):
1. Type I – low level sustained force for maintenance (soleus, paraspinal). Aerobic metabolism, high in myoglobin (oxygen storage) and high mitochondria.
2. Type II – divides into IIa and IIb. It is responsible for rapid and forceful movements (muscles of the arm). IIb = anerobic glycogenolysis and glycolysis.
12. Depolarization (phase 0) in ventricle of the heart = sodium influx. In pacemaker cells (SA and AV nodes) = calcium influx.
13. Shine-Dalgarno sequence. 16s rRNA component of 30S ribosomal subunit can form complementary nucleotide sequence to the mRNA.
14. Common peroneal nerve lesion causes foot drop:
1. motor: superficial everts and deep dorsiflexes.
2. sensory: dorsum of the foot.
15. Metformin (biguanide). Side effects include Gi upset and lactic acidosis. Lactate is formed in anerobic glycolysis. Lactate then converts to glucose via GNG. GNG is inhibited by metformin. so the lactic acidosis. Contraindication of metformin:
1. renal failure (creatinine > 1.4 mg/dL)
2. liver dysfuction
3. patients taking heart failure meds
4. alcoholism
5. sepsis, hypersensitivity.

Tuesday June 3rd 2008

Ok here are some things from UW I did yesterday:

1. In lac operon (genetic regulation)
1. lactose induces gene expression by preventing binding of repressor protein which binds to the operator region.
2. glucose represses gene expression by reducing cAMP; causing poor binding of catabolite activator protein (CAP).
2. MHC class II needs lysosomal acidification to express itself.
3. Oral bioavailability = oral route/IV route (at the same dose)
4. Imperforate anus is associated with:
1. urogenital tract anomalies (urorectal, urovesical, urovaginal fistulas) – meconium may discharge from urethra/vagina
2. renal agenesis, hypospadias, epispadias, bladder extrophy
3. VACTERL = vertebral defects, anal atresia, cardiac defects, tracheoesophageal fistula, renal defects, limb defects.
5. Enteric bacteria that may cause sepsis: E.Coli, Salmonella typhi, pseudomonas, klebsiella and proteus.
6. Bacteria that cause proliferation of mesenteric lymph nodes are salmonella typhi and yersinia enterocolitica.
7. Shigellosis is bacterial infection that causes mucosal invasion, along with EIEC. Clinical manifestations include cramping abdominal pain, pus and bloody diarrhea in late manifestations. It enters M-cells in Peyer’s patches, disabling 60s ribosomal subunit -> failing protein synthesis in host and mucosal cell death.

I did UW again today 40 questions. And I am proud that my score has improved a significant 15-20% and I am quite happy. But that improvement has not reached the real target that I want, so I shouldn’t get really complacent. But for the time being, a little happy and grateful is fine.

Yep, that’s my motivation besides the very superb Goljan lectures!

Monday June 2nd 2008

I finished my ordeal with surgery and have a couple more exams to go, in which I have to confirm the dates of both.

I start with UW for USMLE studies of the day:

1. Actin filaments are anchored at the Z-lines of sarcomere. Z-line is at the center of I-band.
2. In sickle cell disease, HbS in hemoglobin electrophoresis can be distinguished because it moves slower than normal hemoglobin, due to loss of negatively charged amino acid, glutamate.
3. Ascending loop of Henle is impermeable to water. Reabsorption of water in collecting tubule is regulated by vasopressin (ADH). Osmolarity can reach 1200 mOsm/L.
4. Congenital hypothyroidism causes reduced T4 and T4 is very essential for brain development in early life of an infant thus mental retardation.
5. Bilateral agenesis in potter syndrome causing oligohydramnios.
6. Ataxia-telangiectasia is an autosomal recessive disorder due to defect of DNA repair (can cause cancer). The immune system is compromised and patient may suffer repeated sinopulmonary infection. Ataxia is caused by cerebellar atrophy while oculocutaneus telangiectasia is due to dilated the capillary vessels. Among other DNA repair disorders:
   1. Xeroderma Pigmentosum = DNA sensitive to UV causing premature skin aging and malignancy (melanoma and squamous cell cancer).
   2. Fanconi’s anemia = hypersensitivity of DNA to cross-linking agents.
   3. Bloom syndrome = chromosomal instability, susceptible to neoplasm.
   4. HNPCC = defect in DNA mismatch repair.
7. Pulmonary Hypertension pathogenesis:

   ETIOLOGY	PATHOGENESIS
   Left-sided heart failure	reactive pulmonary vasoconstriction due to dysregulation of pulmonary vascular smooth muscle tone and structural remodelling of pulmonary vasculature.
   Massive pulmonary embolism	mechanical obstruction of pulmonary tree.
   COPD	hypoxia-induced vasoconstriction
   Polycythemia	obliteration of vascular flow
   Pulmonary vasculitis (Wegener’s, Churg-Strauss)	inflammatory pulmonary vascular reaction
   Congenital heart diseases (ASD, VSD)	Flow volume and pressure

 

Listened to Goljan’s lecture on Liver diseases. Awesome reviews on viral hepatitis, parasitic infections, alcoholic hepatitis, drugs affecting the liver, metabolic liver diseases etc!

I did UW again, and I see little improvement. I am a bit happy but can’t be complacent since 40% of the wrong ones are because of my wrong intuition and carelessness! If I eliminate the 40% by getting most of the facts and ideas organized, I’m sure I will be fine! For the time being, I am targeting that if 60% of UW users answered the question right, I have to get it right too! No excuses!

Sunday June 1st 2008

I was browsing the surgery notes and I stumbled on Colorectal cancer. I am quite impressed. Although it’s not really complete, but the note is decent. What it didn’t mention was about genetic factors, which may not be tested in my med school but is highly tested in USMLE: APC mutation on chromosome 5q, DCC, p53 and K-ras oncogene.

The Duke’s staging is quite incomplete; the classes B and C have their own subdivisions, especially when it deals with invasion thru muscularis propria.

I was listening to Goljan’s lecture since yesterday on GIT pathology and the information I got was too much I can’t put it in the journal. Basically the one essential thing I learn is that the USMLE tests whether I can put things together. If I can, means I can answer fine. I have to organize the facts, ideas and stuffs – and put in on the MCQ.

I was bored with surgery for a while and I did several UW questions on GIT. I discovered that diphenoxylate is an opiate antidiarrheal binds to mu receptor which slows the motility of bowel. Among its side effects are bloating, sedation, euphoria in high doses.

S cells in duodenum increases pancreatic bicarbonate secretion under the stimulus of HCl. I also learn that prokaryotic mRNA (e.g. E.Coli) are polycistronic – meaning one mRNA can code into several proteins. Diarrhea causes by cholera and ETEC (traveler’s diarrhea) does not excrete blood or pus, only mucos and epithelial cells – because they are secretory type of diarrhea.

I listened to Dr. Goljan again and learn more about liver function tests and jaundice. It’s pretty amazing I can understand him. Jaundice isn’t one of my best areas, and somehow after listening to his lecture, I feel quite fine with the topic.

He also gave some tips on the topics for my surgery such as Crohn’s Disease and Ulcerative Colitis. Colon cancer; left side obstructs and right side bleeds. Appendicitis in adult has the same mechanism as diverticulitis, which is due to impacted fecalith pressing on the tissue -> ischemia. Appendicitis in children is different because the etiology is measles and adenovirus infection causing lymphoid tissue hyperplasia -> ischemia!

Saturday May 31st 2008

I opened the surgery notes. It’s incomplete. I criticize the notes not because I disrespect the people who wrote it, in fact I am very thankful for the notes. But I criticize the notes so that I can understand and memorize better, it’s for my own benefit.

The first thing in the morning I learnt was the Paget’s Disease of the breast. Clinical includes ulceration, nodules and oozing in the eczematous lesion at the nipple. But actually this is another form of malignancy in breast; in which the underlying ductal carcinoma cells migrate thru ducts to the epidermis -> causing the eczematous skin lesion.

Treatment includes mastectomy and trastuzumab (herceptin). Trastuzumab is a monoclonal antibody that kills the breast cancer cells which overexpress oncogene erb-B2. Prognosis depends on axillary lymph nodes (especially pectoral) involvement.

I was a little bored with surgery and I went to UW to do some questions which I got incorrect previously.

1. Reiter’s Disease is associated with HLA-B27, usually develops after GI or GU infection. Skin lesions on soles and feet may occur and sacroilitis in 20%. The classic triad is:
1. non-gonococcal urethritis
2. conjunctivitis
3. aysmmetric arthritis
2. Turner syndrome (45,XO):
1. Lymphedema of hand and feet (the most prominent sign)
2. Webbed neck
3. Coarctation of aorta
4. Horseshoe kidney
3. Acanthosis nigricans is a skin lesion most commonly found in axilla, posterior neck and groin. There are:
1. benign: increase in insulin (not hyperglycemia) stimulate epidermal and dermal proliferation (in DM, acromegaly, obesity etc)
2. malignant: underlying neoplasms of GIT (e.g. gastric adenocarcinoma) or GUT.
4. VZV infection is usually unilateral vesicular rash on a single dermatome. Postherpetic neuralgia is a complication, especially in the elderly – manifested by persistent local pain.
5. Injury of ulnar nerve (claw hand) can happen in:
1. medial epicondyle of humerus
2. canal of Guyon in hook of hamate and pisiform bone in wrist.
6. Mucormycosis is a fungal infection affecting paranasal sinuses (periorbital pain) in immunocompromised , leukemic and DKA patients. Morphologically non-septate hyphae (mucor, rhizopus and abisidia spp.)
7. Mutation at splicing sites (during posttranscriptional modification) causes formation of a larger non-functional protein but still retained its immunoreactivity.
8. Myoglobin dissociation curve is parabolic in shape because it has only one heme molecule to bind to oxygen. Hemoglobin dissociation curve is sigmoid in shape because after one heme binds to oxygen molecule, the other 3 heme molecules have increases affinity for oxygen (heme-heme interaction).

A short discussion with my favorite senior made me learn that pseudomonas aeruginosa (non-lactose fermenting, oxidase +ve, blue-green pigment producing) is the bacteria responsible for hot-tub folliculitis.

Friday May 30th 2008

Today in my Urology rotation, I saw operation on stage IV bladder cancer – in which the cancer has metastasized to AAW. It’s very long and tiring operation, especially the part when the surgeon was making artificial bladder from sigmoid colon. I asked the surgeon a lot of questions and the surgeon asked what vessel did the blood spurt out just now.

Since it’s AAW – I simply answered inferior epigastric artery. The surgeon said excellent or something. I guess, there’s nothing really to brag about here…

Yesterday was an operation on bladder cancer too – I suspect transitional cell carcinoma. I just remembered the wonderful mnemonic of causes of TCC. Pee SACS = Phenacetin, Smoking, Aniline dyes, Cyclophosphomide and Schistosomiasis.

But I have General Surgery exam this Monday, so I have to hold my studies for USMLE again. But it’s not a big problem since I believe the notes in General Surgery and USMLE complete each other. If anything, those two push me towards betterment in both med school and USMLE.

And now the sad part is I learnt that the only med school in Russia that incorporated USMLE instructions into its curriculum is in Saint Petersburg. To be honest, I don’t think NNSMA is preparing the med students for USMLE sigh…

I was browsing thru my surgery notes – now on the one with breast cancer. They are really incomplete, but I used my USMLE notes to add up.

For example the notes on fibrocystic breast is messy. The nipple discharge notes are incomplete for example certain antipsychotics which are dopamine antagonist can also stimulate prolactin causing galactorrhea.

One new accidental point I learnt is that Leydig cell tumor (of the testes)causes precocious puberty in boys and gynecomastia in men.

I also learnt that among chemotherapeutic agents used in breast cancer are methothrexate and 5-fluorouracil, which have similar mechanisms – inhibits thymidilate synthase thus decreasing dTMP. Their use in breast cancer are synergystic.

Tamoxifen can also be used, but it can cause endometrial cancer because it’s partial endometrial agonist, but raloxifene won’t because it’s endometrial antagonist.