The Day Before the Exam Is High Yield for the USMLE

Sounds weird but I think its true. The day before the exam you are at a set point to achieve for the day of the exam. The height of this set point is in direct relation to the amount and quality of effort you have put into the exam. The day before, you might be tempted to try to push that set point higher. I instead suggest to work on keeping the set point from dropping any lower, that is make it your duty to keep your set point stable. Don't harm your score by a little pre-test jiggers.

Make sure not to panic about any details you may not be able to remember. This exam won't be testing details as much as it will test your concepts. For example, the day(s) before the exam you might close your eyes and try to recall all you know. Some people report having a feeling of emptiness but do not panic; No one will be asking you to give a lecture on any of this stuff but only to circle the best answer. Please, DO NOT FREAK YOURSELF OUT THE DAY BEFORE THE EXAM as that is low low yield and this is a high yield blog.

This is not to say you should go into denial about tomorrow. Forcing yourself to not think about the exam on the day before is about as or more stressful as studying another day. I tried to keep my day before the exam as stress free as possible so that I could be relaxed and most importantly confident on test day. In order to keep yourself focused on the exam I have a simple solution and here it is. The day before I would do NBME questions that you have already answered and have figured out the correct answers. This will work to keep the concepts of the most important practice questions fresh but also it should further build up your self confidence as you'll probably score much more correct this time around.

Also note that I do not suggest that you do practice questions over and over again throughout your study period just to falsely build up your self confidence - to me (but many disagree and do fine their way) doing Q-bank more than once for whatever reason is a waste - how about you move on to USMLE World? All I'm saying is that a boost of self confidence the day before the exam is just what a 1st time boards test taker needs.

The Tuberculous Granuloma is High Yield for the USMLE

Ahh the Granuloma - a great example of topic that overlaps multiple subjects and any topic that brushes borders with the likes of pathology, immunology and microbiology make for great questions. Here are 5 steps to the granuloma in perfect 3^rd grader doodle form:

Step 1: Inhale the red, ACID FAST rod

M. tuberculosis is only acid fast why?

B/c of the MYCOLIC ACID in the cell wall resists decolorization with acid-alcohol and so it remains red which is the color of the initial stain, carbol fuchsin.

What else stains acid fast? Nocardia which is “partially acid fast”

Step 2: Phagocytosis by alveolar macrophages

Circulating monocytes roll on the vascular endothelium (d/t selectins) and adhere to it (d/t ICAMs) and then transmigrate into the affected area where they are called tissue macrophages.

Macrophages are the main players in the formation of a granuloma

Step 3: Antigen Presentation

Step 4: T Cell Activation

CD4 T Cells are involved

The TH1 subtype

No CD4 T Cells? No Granuloma. AIDS patients who loose their CD4 t-cells well before loosing their CD8 T Cells will make very weak if any granulomas.

Step 5: Macrophage Activation

Did I mention what the main player of a granuloma is? Oh yea, its the macrophage.

The Caseous Granuloma

Note that the caseous necrosis is cottage cheese like and is due to the destruction of the M. TB organism's cell wall's mycolic acids (mycolic acids are lipids).

Fundamentals of Biochemistry are High Yield for the USMLE

Sorry for the infrequent posting as of late but I've been traveling. Here's a great link if you are having trouble picturing the various molecular events not only in biochem and cell biology but also micro and immuno. It contains many animations that really helps you picture this stuff.

The page is called Max Animations

I especially suggest the lac operon, HIV virus lifecycle but there are tons of animations there so I just though I would point out this potentially useful link for you.

Viruses are High Yield for the USMLE Step 1

I suggest when trying to memorize viral structures make a priority list. Common viruses and ones that also overlap with pathology are the ones to focus on here since they can be asked about in many different ways.

Knowing DNA vs RNA is the most important distinguishing feature. Furthermore, f you know if its DS or SS you'll probably get the points.

Enveloped vs Naked: If you can memorize enveloped vs. naked for each virus then god bless, but I like this:
Envelopes are made of a lipid bilayer which are prone to destruction by the environment whereas naked viruses are more resistant to environmental stresses.

A 46 year old female who has genital warts (d/t HPV) takes a shower in her home during which time the virus sheds on the floor. Later her child presents with a wart on his toe.

This all happened since this virus had its tough nucleocapsid for protection and not a wimpy envelope. Take home message is if the virus is capable of fomite transmission it is probably naked.

Play odds, especially for rare viruses with less of a chance of being asked. I walked into the exam knowing that if I saw an RNA virus that looked deadly or pretty rare I would guess that it is SS (-) linear w/envelope.

Here is my list of High Yield Viruses and why I think they have a great chance of being asked

• Herpesviruses - DS linear DNA
  
• this family includes so many viruses that overlap with pathology I list it first since I think this is most important.
  
• All the viruses that cause hepatits - see First Aid for them since these are important!
  
• Note that Hep B carries the reverse transcriptase enzyme with it just like the retroviruses do.
  
• HIV - SS (+) linear RNA
  
• If you don't get at least 1 question on AIDs I will give you my blog. Seeing if you know virus structure is a possible secondary question.
• Papovavirus - DS (-) linear
• besides HPV causing cervical cancer don't forget about molluscum contagiosum which causes the umbilicated wart (center of wart is depressed like an "innie" belly button).
• Paramyxoviruses - SS (-) linear RNA with helical capsid symmetry
  
• this family is responsible for causing croup (parainflunza virus), bronchiolitis (d/t RSV), measles and mumps.
• Parvovirus - SS linear DNA
  
• It, along with Hepadnavirus, is exception to the rule that all DNA viruses are linear.
  
• It overlaps with pathology since it causes aplastic anemia in patients with sickle cell disease
  
• Pt might give you a history of having recent contact with a kid who had a slapped cheek appearance.
• Blood labs will give you a low RBC count with low reticulocytes (less than or equal to 3% of hematocrit - I wouldn't freak out about not knowing how to correct a reticulocyte count).
• Influenza virus (an orthomyxovirus) - SS (-) linear segmented RNA
• the NBME and practice questions I've seen love the fact that this genome is segmented since:
• Genetic shift - if our influenza virus recombines with a pig's or chickens genome we get pandemics - we're all screwed (small minor mutations lead to drifts causing an epidemic in a much smaller area w/ much less people). involved)
• If you digest the genome and view it with northern blotting you will see each of these (7 or 8) segments as separate bands.
  

Motivation is High Yield for the USMLE Step 1

Not that any med student goes into medicine for the money BUT if you happen to find yourself stuck inside studying for the boards all day, maybe feeling a little down, then this might cheer you up some.

Dr. X of ValueMD points out that a browse through Physician Salaries might just be the boost you need to go the extra mile.

Make sure to study the heart and anesthetics really well (you'll see what I mean)!

If you read this and immediately start day dreaming about the car you'll get or the kind of place you plan on living in then I want you to shut down your computer and open up a review book right this minute.

So stay motivated and keep your head in the game.

Vitamin K is High Yield for the USMLE Step 1

• Vit. K is needed for the γ-carboxylation of clotting factors 2, 7, 9 and 10
• This gives them a Ca binding site
• This explains why the vit. K dependent factors are the same factors that are dependent on calcium
• Deficiency:

o Primary problem is an inability to γ-carboxylate factors 2, 7, 9 and 10

• therefore, factors ARE made but can NOT be activated by Ca
• Involves several factors, including factor 7 which:
• has the shortest t½ of all the clotting factors
• therefore, factor 7 is the first factor unable to be activated
• Since factor 7 is specific to the extrinsic pathway the extrinsic pathway is affected first
• Since the prothrombin time (PT) is a measure of the extrinsic pathway, it is the value expected to be elevated first
• Leads to ↑↑PT (AND eventually ↑PTT) – therefore, PT is most sensitive since its ↑’d 1^st
• Bleeding time, a measure of platelet function, is normal since platelets are not affected
• Deficiency can be seen in the following patients:
• Newborns born at home
• Breast milk has low levels of vit K
• All babies in the US are given vit. K shots @ birth in the hospital to prevent hemorrhagic disease of the newborn
• Pts on broad spectrum antibiotics
• Bacteria in colon synthesize much of our vit. K
• Pts w/ steatorrhea
• Loss of fat in the stools also leads to a loss of the fat soluble vitamins, including vit. K
• Vitamin E toxicity
• Inhibits vitamin K dependent carboxylation of clotting factors
• Treatment
• Vitamin K Injection
• If bleeding is serious then give fresh frozen plasma

Testable Anemias That Do Not Always Make It To The Books

Here are some anemias that aren't always thought of in the same breath as many other anemias.

• Vitamin C deficiency - since vitamin C enhances non-heme iron absorption in the gut, a vitamin C deficiency can cause a iron deficiency (microcytic and hypochromic) anemia.
• Vitamin E (alpha-tocopherol) deficiency - Vit. E prevents the peroxidation of lipid cell membranes by free oxygen radicals since vit. E is an anti-oxidant. When deficient in vit. E, one sign is acanthocytes in the peripheral blood smear. When these spiny RBCs burst it causes a hemolytic anemia
  
• Similarly, in abetalipoprotinemia, an autosomal recessive disorder of lipid absorption may manifest with acanthocytosis in part because vitamin E (a fat soluble vitamin) is also not being absorbed.
• Orotic Aciduria - megaloblastic anemia unresponsive to folate or B12. A number of wordy enzymes may be deficient but the essential problem here is pyrimidine synthesis and so DNA synthesis is subsequently impaired.
  
• This is very similar to B12 and folate deficiencies since in both of these cases, DNA synthesis is also impaired.
  

Lymphatic Drainage is High Yield for the USMLE

Here's some basic information about lymphatic drainage:


Pretty simple, which is how I like it. Apo B48 is on chylomicrons which carry the dietary lipids. I remember this by its the apolipoprotein that is in the food before (B4) you ate (8). Okay, its not really before you ate it its after you ate it, but I think it gets the point across that ApoB48 is for the lipids that you eat and so is therefore found on chylomicrons. Since lipid soluble vitamins are absorbed with your dietary lipids, chylomicrons also contain fat soluble vitamins.

The right lymphatic duct also drains into venous blood but instead of the left internal jugular/subclavian vein, its into the right ones.

So it was just a quick doodle and explanation today about these straight forward points. I'm sure you can think of a lot of other integrated info about lymphatic system which I encourage you to share in the comments section.

Targeting Your Weakest Area(s) is HY for the USMLE

This one seems pretty obvious but its not always as easy as it seems. Instead of preaching how you should do it, I'll just tell you what I did.

With about 2 weeks before my exam I took a timed NBME exam (link in the sidebar to the right). The results are broken down by subject and your performance is shown as a shaded area in each subject and organ system. For example:

___________________P E R F O R M A N C E____________
SUBJECT ________Lower___ Borderline______Higher
Behavioral___________xxxxxxxxx
Pathology__________________________xxxxxxxxxxxx
etc...

This student obviously needs a lot of work in Behavioral science. That student was me. Much of my other subjects were further to the right and overlapped. If the bars overlap then they should be interpreted as similar.

Now, I think we can all agree that Pathology and pharmacology seem like much more important
subjects for the exam, and they are. But my theory was that if I'm doing pretty good in most and pretty bad in some then it would be much higher yield for me to focus on my weaknesses. It hurts too because nothing satisfies your soul more than reading the same stuff you already know over again 2 weeks before test day. It builds up your confidence (indeedimportant) but also it may induce you to overlook a gaping hole in your knowledge bank as it did for me.

Face your fears today: A good strategy would be to look at the table of contents or quickly flip the pages of first aid. Your body will let you know when you're at the right page. For me, I get a tight feeling in my stomach and hold my breath on inspiration (not long enough to cause a respiratory acidosis though) while my heart pounds through my chest (apex beat is found at the left 5th intercostal space). Bingo! Weakness area found.

As painful as it was to drop pathology and pharmacology, for me it was the right choice. I focused on behavioral and it paid off since behavioral science overlaps pathology and pharm on my actual performance profile from the USMLE.

Take home message is this:
A weak area brings your score down
Fixing your weak area can bring your score up much easier and higher than strengthening other already strong areas to compensate.

Burkitt's Lymphoma is High Yield for the USMLE Step 1

Burkitt Lymphoma
a form of non-Hodgkin's lymphoma

Associated with Epstein Barr Virus and is commonly located in the jaw of Africans (the classic patient)

(source)

Classic Translocation = t(8;14) which moves the c-myc gene on chromosome 8 right next to the Immunoglobulin (Ig) Heavy Chain.

Here is a joke for you. I hope you find it hilarious. Okay, a giggle will do. Tell it to someone else, embrace the awkwardness that ensues and that should tattoo it to your brain for a while.

How come Mick ate one for?

-----Here is what the joke really means----
come Mick = c-myc
ate = 8 - since c-myc is on chromosome 8
one = 1
for = 4

To get heavy!
heavy = Ig Heavy chain which is on chromosome 14


And here's a little doodle to drive it on home:


That big guy there is Mick (myc) who has just ate (8) one (1). For (4) what? To get heavy.
c-myc is on chromosome 8
Ig Heavy chain is on chromosome 14

Believe me, this joke is much funnier if you're telling it to yourself when you are looking at a question on it.

Here is what some practice questions I've seen ask and is mentioned in various review therefore I made sure I knew this for my exam although I had to look it up again for this post.

The function of c-myc: c-myc is a proto-oncogene which codes a protein that regulates nuclear transcription. When it is moved next to the gene for the Ig heavy chain it becomes constantly active since the body is constantly making Ig heavy chains. At this point it is now called an oncogene. c-myc now causes the B-cells to constantly reproduce themselves over and over again. This results in a high grade lymphoma

This is in contrast to B-cell follicular lymphomas in which BCL-2 (a gene which promotes apoptosis). When BCL-2, a tumor suppressor gene, is translocated it becomes functionally inactive and so B-cells can't undergo apoptosis the same anymore. This is an example of low grade tumor.

So I think this is how you should think about it: Burkitt's lymphoma is when B-cells actively divide whereas in B-cell follicular lymphomas, B-cells don't die.

Also, here's the classic"Starry Sky Appearance"

(source: pathguy.com)

I just want to point out here what that refers to. The dark purple areas are really just a bunch of neoplastic B-cells that are dividing much more rapidly now that c-myc is always active. ("Dark is Dividing") The stars are the lighter areas which are much fewer in number - these are the macrophages. I'm not sure what they are doing there, but I do know that they are NOT the problem. Perhaps they are trying to help out in getting rid of the tumor.

That's what I think is really important for this tumor that seems to be a pretty hot topic for the exam.

Thiamine is HY for the USMLE Step 1

THIAMINE aka Vitamin B1

Active form: Thiamine Pyrophosphate (TPP)

Main reactions in which thiamine is a cofactor:
These dehydrogenase reactions generate NADH in the mitochondria which enter the electron transport chain to generate ATP, therefore the patient has a problem making ATP.

Cofactors required by the above 2 enzymes are
Thiamine
Lipoic acid
CO2
Folate
NAD+
Which can be remembered by the phrase, "Tender Love and Care for Nancy"

(Thiamine is also a cofactor for transketolase which catalyzes 2 Carbon transfers in the HMP shunt (pentose phosphate pathway) - required to make Ribose 5 phosphate for nucleotide synthesis)

Classic patient is a Malnourished Alcoholic

Signs and symptoms of deficiency:

Wernicke's Encephalopathy

• Peripheral neuropathy
  
• due to Wallerian degeneration; not drawn (source: Boards and Wards, 3rd Edition)
• occurs since ATP is needed for myelin production and ATP isn't being made to the same quantity
  
• Neuropathy may manifest as foot drop or wrist drop much like lead poisoning does in adults
  
• Wernicke's encephalopathy is reversible (We-versible Wernicke's)

________

Say the above patient was given glucose without correcting his thiamine deficiency, it would precipitate...

Korsakoff's Amneisa

These are the Mammillary Bodies:

These are the mammillary bodies on drugs:

Any questions?
(source: The Medical Journal of Australia )

• anterograde and retrograde amnesia
  
• Bilateral hemorrhagic necrosis of mammillary bodies
  
• mammillary bodies are in the hypothalamus and are part of the limbic system
  
• irreversible
  

Treatment: IV Thiamine and THEN glucose

Developmental Milestones are HY for the USMLE Step 1

Questions I saw while preparing for the USMLE would often give the amount of blocks stacked as an important clue to figure out how old the child is

A formula that may help you to guess the age among the multiple choices
(AGE in years) x 3 = blocks stacked
I doubt that you will have to rely on the amount of blocks stacked alone, but rather as a piece of a larger picture in real life and therefore also on the exam.

Other Clues:
Something I dreaded trying to memorize were the ages of different milestones. Childhood and adolescent milestones are often easier to guess at but infants just seemed much harder for me.

Some sources list so many milestones in tables it was daunting to have to try to cram that in a brain filled with a lot of other stuff that seemed more important for a 2nd year medical student.

I figured I would make myself an easy way to actually REMEMBER it for answering questions. It wasn't all inclusive or exact, it was a little silly, but it worked pretty good to weed out wrong choices. Again, if the below works for you - awesome, use it.

I admit some are a stretch (for example, making a 12 look like a baby laying on its back is no easy task), but at least you can draw them yourself and maybe it will stick this time!

So without further adieu...

Mike's Milestone Chart

(click the image to make it larger)

Each age (in months) is written in a different color on the left. Then, on the right is the sketch that may help you to remember the milestones - the number in the sketch and the number written in the left column match so you can see where I stuck it. I used dark blue in each row to add the "fluff" that makes the numbers represent the different milestones.

In the "7-9 months" column I also included the pincer grasp, even though its normal for a child upto 12 months to not have one. 12 is also looks more similar to an 'R' than a 9 does, which is also nice.

Myocardial Infarctions Are HY for the USMLE

The formula for a Myocardial Infarction essentially is

Oxygen demand > (greater than) Oxygen supply

Myocardial tissue must therefore switch from aerobic to anerobic metabolism which generates only 2 ATP.

***AT REST THE HEART IS EXTRACTING ALMOST ALL OF THE O2 FROM ITS BLOOD SUPPLY***

therefore, for oxygen supply to increase, more blood must be pumped to the heart tissue (MOA of nitrates for ischemic chest pain). If supply cannot meet demand, the heart tissue may infarct.

Hacking Myocardial Infarctions on the EKG
The leads these changes are seen are listed in my drawing (see below)

• Peaked or Inverted T Waves - often earliest sign of ischemia
  
• ST segment
• Elevation
• Differential diagnosis: Prinzmetal's Angina
  
• a vasospasm of the smooth muscle of the artery
• Si/Sx: chest pain at rest
• cardiac enzymes = negative (differing it from an MI)
• Depressed in stable angina and subendocardial MI
  
• Deep Q waves
  
• These do not go away after the MI. Ever.
  
• therefore, deep Q waves indicats the patient may have suffered an MI

Effects of Aldosterone are High Yield for the USMLE

Scientists want to study the effect of that 1 mg of aldosterone will have on a healthy human volunteer. What changes can they predict in Na⁺ in grams, [Na⁺], pH, Urinary output, and K?

• Na⁺ in grams increases
• Aldosterone causes sodium (and water since water follows Na⁺) reabsorption in the principal cells of the distal convoluted tubule (DCT)
• Concentration of Na⁺ stays the same
• Since sodium is reabsorbed with water, the concentration will remain the same
• pH will increase
• Aldosterone causes H ion excretion in the intercalated cells of the DCT (via a Na/H-ATPase antiport pump)
• Urinary output decreases
• Since aldosterone causes the reabsorption of sodium and water from the DCT less remains in the urine that is forming
• Potassium in grams will decrease in concentration and grams
• Aldosterone is sodium sparring and potassium wasting (repeat this line to yourself 5 times)

Know Your Dermatomes For The USMLE

I won't attempt to cover them all, but I can give you a few pearls here.
It's something random that over the years have gotten me a bunch questions right without trying much.

• C6 includes your thumb and index finger (medial half)
• to remember this, make the number 6 with your left hand by touching your index finger to your thumb now look at your hand and say to yourself "C6"
• knowing this I can deduce C7 and C8 which I give C8 the lateral digit and half of the 4th while C7 just gets whats inbetween C6 and C8
  
• L5 vs S1 = very HY
  
• intervetebral discs commonly herniate at this level
• L5 affects the big toe
• I remember it by saying "L5 = Largest of the 5"
• L5 root is compressed by a herniated disc at the L4-L5 level
  
• S1 affects the smallest toe
• "S1 = the smallest one"
• S1 root is compressed at the L5-S1 level
• (If your toes don't follow this order you may need a different memory tool, sorry buddy.)
• L1 = Skin overlying the inguinal ligament
• L for ligament, 1 for 1nguinal
• S5 = Anus
• "S5 is the doodie hive"
  
• Other ones everyone probably knows but listed here just in case
• T10 = Umbilicus
• BellybuT-TEN
• L4 = Knee
• "L4 hits the floor" (when standing on your knees)

Remember that the above list isn't meant to be complete, and some dermatomes include more, but I hope this helps you to think of it in a way where you won't forget it! For exams knowing this usually gets me the point and when it comes to the USMLE, that is all I care about.

The NBME Exams Are High Yield

Off to the right hand side of my blog I've posted the link to the NBME page where you can sign up for 1 or all 4 self-assessment exams. It is in your very best interest to go through these exams in as much detail as you can before your actual exams. You will see very very similar, dare I say the same, questions on the USMLE step 1 exam.

Squamous Cell Lung Carcinoma's Paraneoplastic Syndrome is HY

A 56 year old male has a 65 pack year smoking hx. He is seeing you today about recently having coughed up blood. He knows that this might be lung cancer and asks you for your expert opinion. Labs show hypercalcemia. Bronchoscopy reveals cells with atypical mitosis with some nuclei containing 3 to 4 metaphases.
The question is, it squamous or small cell cancer?


You really have to remember that squamous cell carcinoma releases PTHrP causing hypercalcemia.

Squamous Cell = Hypercalcemia

And since small and squamous both start with the letter S, I often mistake the 2 so here is what I made up to remember calcium when I hear squamous cell.

Calcium’s abbreviation is Ca²⁺ which looks like Calcium squared (Calcium²).

Squamous ≈ squared. And there you have it.

Pharmacology Formulas are High Yield

For this I would point you to pg. 209 of First Aid 2007, there you would find all the formulas you will need.

If I was to ask you this,
"An extremely old medication used by African witch doctors for curing one's "voodoo" is being studied in NIH labs for a possible benificial effect in the treatment of beningin prostatic hyperplasia. The drug is initially studied on 2 rats with enlarged prostates (poor fellows), Rat A and Rat B.

I now, as the question writer proceed to write of bunch of BS and you'll want to read through this and tag it as such real fast on exam day

Rat A and B were born from the same mothers and both have lived in the same cage and blah blah blah and (end BS)

It is calculated that Rat A has a clearance time of 60 seconds where as rat B has a clearance time of one minute and 50 seconds.

Now I ask you this:

1) Given the same dose of the African drug, which of the following must be different.

2) If the 2 rats are found to have the same rate of elimination, which of the following explains the difference in clearance.

Answers to be posted after I receive at least one comment on this post.

Tabes Dorsalis

• This is a manifestation of tertiary (late) syphilis called neurosyphilis
• caused by infection with treponema pallidum, a spirochete
• tertiary syphilis also turns the vasa vasora (blood vessels that supply other blood vessels, eg aortic root) into a bunch of granulomas →:
• Aortic regurgitation – know how to recognize!
• Diastolic decrescendo murmur heard best along the left sternal border
• Aneurysm of the ascending aorta
• Note that tabes dorsalis only affects the dorsal horns.
• This patient had a positive (+ve) Rhomberg's sign
• Rhobmerg's sign
• Patient's balance is fine with his eyes open
• Visual input supplies spatial awareness/proprioception
• Upon closing his eyes the pt sways
• loss of proprioception from dorsal column

(If patient is swaying with eyes open and closed, this is likely a lesion in the cerebellum or vestibular system (eg. CN VIII) and would NOT qualify as a +ve Rhomberg's sign)

• Can you guess the level from which this spinal cord section was taken

A) C1
B) C4
C) T4
D) L4
E) S1

Answer posted on 4/2/07

Note the lateral horns (sometimes called intermediolateral cell column):
(I have circled the right one and have drawn an arrow to the left one)
This area of white matter contains preganglionic sympathetics which arise from the hypothalamus and will synapse onto a postganglionic sympathetic fiber in the paravertebral (aka chain) ganglion. Question for you... would the neurotransmitter used here be
a) norepinephrine (Norepi)
b) epinephrine (Epi)
c) acetylcholine (ACh)
d) glycine (Gly)
e) glutamate (Glu)
f) seratonin (5-HT)

Answer is c) Ach
Remember, all preganglionic autonomic fibers use ACh
Epinephrine is released from the adrenal medulla when preganglionic sympathetic fibers release ACh onto it.

Now, back to the level of the spinal cord:
Since we are talking about sympathetic (aka thoraco-lumbar) outflow, you should know right away that this slide must therefore have been sliced from somewhere between T1-L2.
Knowing this would have gotten you the right answer to my question.

If the question writer is out for your blood he may ask you to distinguish between 2 choices within the range of the lateral horn. Notice the shape of the above section. Now compare it to an upper lumbar section. See the difference? The lumbar section has only one dorsal column and it is just a lot more round. That "just a lot more round" part (I bet) is enough to differentiate for purposes of the exam. But feel free to knock yourself out, I know I did.

Molecular Mechanisms of Apoptosis

Apoptosis is HY for the USMLE Step 1. Here is my attempt to illustrate the molecular basis of apoptosis summarized from Robins.

Urea Cycle

• Urea contains 2 molecules of nitrogen derived from:
• NH3
• **Aspartate**
• Carbamoyl phosphate synthetase is the rate limiting enzyme
• located in the mitochondria
• activated by N-acetylglutamate

Epstein Barr Virus

• Attaches and activates B-lymphocytes CD21 (CR2) receptor
• These activated B cells promotes T cell proliferation
• The effected B-lymphocytes are NOT what are detected by the monospot test.
• Atypical lymphocytes (“Downy Cells”)
• Detected by the monospot test
• AKA (heterophile antibody test)
• Are CD8⁺ T lymphocytes
• Associated with:
• Heterophile positive infectious mononucleolus
• Burkitt's Lymphoma
• Nasopharyngeal Carcinoma
• Structure
• a "HAPPy" double-stranded linear DNA virus (see First Aid virus section)
  

Glucagon for Beta Blocker Overdose

Here's a great board question that I don't know if its ever been asked, but can you think why you would want to give glucagon for a beta blocker overdose? Hint: It’s all about cAMP

• Beta blockers at toxic doses would dangerously ↓ HR.
• The heart has β1 receptors which act through a G_s to raise intracellular cAMP
• Glucagon, via its own receptor can ↑ cAMP independently of the blocked β1 receptor
• Also note, that this is an example of physiologic antagonism
• Giving a β1 agonist to overcome the β-block would be an example of competitive antagonism

Can you say, "Gunner Level?"

2nd Messangers

bangledoc writes:

Thanks miky.It will hep greatly every one taking step 1.
could u write more about other 2nd messenger with application (as cGMP).As this are highly asked in exam.
Thanks again

I agree, 2nd messengers are very HY and therefore should be in any blog called HY for the USMLE


Lets start with this:

For the USMLE Step 1, it is more important to understand how each different 2nd messenger system works individually then to memorize if alpha 1 is a cAMP or cGMP or Gs or Gi. It happens to be cAMP and Gs.

I overlooked this point and placed greater emphasis on which receptor goes with which 2nd messenger system. The basic mnemonics in First Aid should suffice for the exam but there is a little more I would add, and since it is so late it will have to wait for tomorrow. (It involves the regulatory subunits of protein kinase A)

I also have a drawing to help you remember Gq, though I admit its corney!

Hypomagnesemia and PTH

One point which gets you an easy point but otherwise easy to miss is that hypomagnesemia can cause hypocalcemia since magnesium is necessary for the production of PTH.

	PTH	Calcium	Phosphate	Si/sx
Primary Hyperparathyroidism	↑	↑	↓	stones, bones, abdominal groans and psychic moans"
Chronic Renal Failure (→Vit D def.)	↑	↓	↑ - can’t be excreted
Hypercalcemia (malignancy)	↓	↑	↑
Hypomagnesemia	↓	↓	↓	Hypocalcemia that responds to Mg 2+ infusion

Cyanide Toxicity

• Causes
• Infusion with Nitroprusside
• Smoke Inhalation (MCC)
• Combustion of polyurathane (found in mattresses – just look at the tag)
• Effects
• Inhibits cytochrome oxidase (cytochrome a/a3) of the electron transport chain
• NOT cytochrome C (commonly mistaken)
• Blocks the use of oxygen → tissue hypoxia and rapid death
• Si/Sx
• Bitter almond-scented breath
• Agonal respiration
• Nausea and headache
• Treatment
• Amyl and Sodium Nitrite
• Produces methemoglobin (met-HB)
• note: nitrates used for anginal therapy do not cause formation of cy
• Met-HB sucks up CN from the mitochondria
• Iron in met-HB (Fe3+) has stronger affinity for CN than does cytochrome oxidase’s iron
• Results in formation of cyanomethemoglobin
• Sodium Thiosulfate
• Converts cyanomethemoglobin into:
• Thiocyanate
• less toxic & easier to excrete than cyanomethemoglobin
• Methemoglobin
• Methemoglobinemia is treated with methylene blue

cGMP is High Yield

• Know that the drugs acting via cGMP are
• Nitrates (Nitroglycerin, isosorbide dinitrate)
• Increases production of cGMP
• Activation (denitration) to NO occurs within the smooth muscle cells enwrapped around vascular endothelium.
• NO activates guanylyl cyclase → ↑cGMP → dephosphorylates myosin light chain kinase → smooth muscle relaxation
• Note, tolerance develops rapidly
• Addressed by telling pt to take a break from the particular drug or Rx w/ a different anginal drug
• Occupation exposure → Monday Disease
• Nitroprusside
• Rx: Hypertensive emergencies
• Same mechanism as nitrates
• AE: Cyanide toxicity (rx: sodium thiosulfate)
• Sildenafil
• Decreased breakdown of cGMP
• Inhibits 5’-phosphodiesterase
• The enzyme that breaksdown cGMP
• Do not give a pt on a nitrate sildenafil (will synergistically cause their diastolic BP to fall through the floor!)
• Instead give Alprostadil
• If you accidentally did combine the 2 above what drug would you want to give?
• α-1 agonist
• Hydralazine
• dilates arterioles more than veins= reduces afterload; AE: SLE like syndrome
• Know that ANP (Atrial Natriuretic Peptide) acts by activating guanylyl cyclase