Tommy’s
HY Concepts for the USMLE Step I
(# 1 - 1863)
Copyright © 2003-2005 ValueMD, Inc. All rights reserved.
Tommyk posts ( 1-147)
Q. Patient, young, with obesity, hypotonia, mental
retardation, short stature, hypogonadotropic hypogonadism, strabismus, and small
hands and feet. What disease and what is tx?
A. Prader Willi Syndrome. Treat with GH
Q. Pt w/ symptoms include tall stature, ectopia lentis,
mitral valve prolapse, aortic root dilatation, and aortic dissection? What gene
is missing and what is treatment of choice? Don't peek below w/o guessing.
A. Marfan's Syndrome (This WILL be on your test). Defect
in fibrillin gene. Treat the aortic dissection with B-Blockers. Warn them about
pneumothorax and strenous exercise. Tell patients that they are AD inheritance.
Warn them about weird things like an elevator that travel up too fast or an
airplane without decompression.
You have to know that many test takers said it really
"helped" to do the NBME Step 2 questions and the NBME Step 3 questions that they
have on the website. Please do not neglect them. Just ignore the "next step"
questions, and do the diagnosis problems
Q. IF you are given a diagram with an LDL receptor
molecule, and ...
Then if you are asked what ion binds to it, what would
you guess?
Choices: Na, Ca, Fe?
A. The answer is Ca. You should look at the concept of
diagrams of receptors. Remember, many of the writers of the questions are
MD-PhDs and they specialize in their own receptor research.
Q. Uric acid stones (which are transLUCENT on x ray
unlike Ca stones), are common in what three diseases? Bonus: what do uric acid
stones cause symptom wise
A. the three diseases are:
HGPRT deficiency
PRPP synthetase overactivity
Glucose-6-phosphatase deficiency
The stones will present most commonly with hematuria,
then fever/nausea/vomiting, then UTI!!
Q. You HAVE to know this...
Sorry to be patronizing, but you will get this concept
most likely...
What is the primary treatment for the uric acid stones?
2nd treatment if refractory?
A. 1st thing is to alkalinize the urine and hydrate!
Wait for the stone to pass.
If that doesn't work, give allopurinol!
BUT, if the stone is more than .5cm, then use
lithotripsy because the stone will not pass by itself!
Stones are SO common and SO common stuff are all over
the USMLE
Q. A patient who had her gall bladder removed for stones
STILL feels colicky pain, what could be the reason? This is a very HY
concept....
A. loss of inhibitory enteric innervation (motor)
Q. YOU WILL definitely be asked to understand the
concept that a person with an injury to the SURGICAL neck of the humerus/or the
dislocation of anterior shoulder will have which nerve injury?
A. AXILLARY nerve, not the radial nerve.
Q. You HAVE to know this crucial concept tested on most
exams and in clinic!
A woman who diets and cuts out all fats but still eats
carbohydrates. Will she lower her LDL? HDL
A. Everyone will be tested on the concept that
chylomicrons are blood lipoproteins produced from dietary fat.
It is the VLDLs that are produced mainly from dietary
carbohydrate. IDL and LDL are produced from VLDL.
Thus, HER LDL level will still BE HIGH. Crucial
concept!!!
Q. Methinks that every single human taking USMLE had to
know that a man with:
Diffuse demineralization of the bone associated with
hypercalcemia, anemia, hypergammaglobulinemia, proteinuria, and normal serum
alkaline phosphatase is most suggestive of?
A. Multiple Myeloma. I CAN BET MY BOTTOM DOLLAR THAT YOU
WILL SEE MULTIPLE MYELOMA ON YOUR TEST. I definitely did.
Q. A woman with sarcoidosis or with hypercalcemia (there
are a thousand ways to ask this concept) enters your clinic, which is the
diuretic of choice?
A. Furosemide, NOT thiazides or mannitol, or
acetazolamide
Q. A Super high yielder is Hardy Weinberg. If the number
of homozygotes is 1/4900, can you tell me the number of heterozygotes
A. use q2 and then use equation 2pq
Q. Everyone is reporting that they MUST master the
concept of transgenic mice. Here is one concept you must understand:
Transgenic mouse with defect in B2 microglobulin gene.
What is the immuno defect?
A. The B2 microglobin is part of the MHC Class I
molecule. So, a defect here will cause a problem with CD8 + cells so cell
mediated immunity is crushed!
The MHC includes a polymorphic set of genes encoding
cell surface glycoproteins, designated class I and class II molecules, whose
function is to present antigenic peptides to CD8+ and CD4+ T cells,
respectively. Peptides generated in the cytosol from denaturated proteins
fragmented by proteasomes, some components of which are MHC-encoded are
transported into the endoplasmic reticulum (ER) by peptide pumps or transporters
associated with antigen processing (TAP) whose encoding genes are again located
in the MHC. Peptide binding to the class I heavy chain facilitates association
with b2-microglobulin (b2-M) and stabilizes the complex allowing it to migrate
to the cell surface.
B2 microglobin, a component of MHC I molecules,
functions to transport MHC I to cell surface,ditto.
Lack B2 microglobin, no MHC on cell surface. CD8+
cytotoxic T cell needs to bind to MHC I molecules.
result: defect on CD8+ cytotoxic T cells mediated
immunity
Q. A wise man said that you cannot avoid understanding
Biochem thoroughly. So, if I gave you a pic of cbiochem ycles and asked where is
it inhibited by acetyl CoA and enhanced by citrate, would you succeed
A. During fatty acid synthesis in the CYTOSOL, Citrate
will activate aceytl CoA into malonyl CoA, Acyl CoA will block this. (SORRY, in
the question above I meant to say Acyl CoA, not Acetyl CoA)
Nevertheless, this is a crucial biochemical step
underappreciated...by all
Q. Aside from drug abuse and high exercise, which is a
given, what is the next most common cause of lactic acidosis? There are a
thousand poss. ways to ask this concept
A. shock, like septic shock or hypoperfusion.
Q. ubiquitous question in USMLE, clinic, life, and love
is:
A child comes in with meconium ileus, other than
Hirshsprung's, what is the other MAIN common disease you see?
Like on Family Feud, the game show, the best answer is
A..Cystic Fibrosis.
It is too easy to merely ask about salty sweat and fatty
stools, although some will invariably get the easy questions about this disease.
Q. Speaking of my previous question about Meconium ileus,
there is a disease EVERYONE will get on their test, and in clinic...Meconium
ileus is a block of the terminal ileum and is the most common cause of
obstruction and congenital GI anomaly. What is the other name of this that
starts with the letter M?
A. Meckel's diverticulum, persistecne of the vitelline
duct. This is SO HY
You will see this concept everywhere you turn:
Q. A pt. comes in with overdose of scopolamine because
she went on a roller coaster in Disneyland. The doctor in line slips her
physostigmine instead of neostigmine, etc. why?
and now>
A. it is because of the cholinomimetics, physostigmine
crosses the blood brain barrier to CNS.
Neostigmine is better for urinary retention after
plastic surgery (or any surgery).
You will see this concept in your life....soon...
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Q. A med student grabs gentamicin for you to treat
Bacteroides. You will hit him over the head because he is wrong. Why? (What is
MOA of Aminoglycosides)
A. Bacteroides is an anaerobe. Aminoglycosides do not
work on anaerobes b/c they need O2 for uptake, thus blocking formation of 30S
initiation complex!
Q. Young girl has early acne, you give tetracycline,
then years later family comes back at her homecoming and kicks you. Why? (What
is SE of TETRAcycline)
A Tetracycline has the famous concept of discoloring
teeth and blocking bone growth in children, along with photosensitivity.
Q .Anatomical common injuries are super duper HY.
A football player comes in with an injury in the shaft
of his humerus. What nerve is crushed (choices: radial, median, ulnar, axillary)
and what prob. does he have?
Radial nerve is damaged. He is lose his triceps,
brachioradialis, and have wrist drop.
This is a must know...
The aforementioned athlete breaks his supracondyle of
humerus. What nerve is crushed?
(Radial, median, ulnar, or axillary)
(All of you will get a variation of the upper arm
injuries)
A. MEDIAN nerve is blown. He loses his finger flexing
ability and some thumb movements and some loss of sensation over lateral palm
and thumb and radial 2.5 digits
Q. Everyone I hear is asked about brachial plexis
injuries. But they are not easy direct questions. E.g.
A supermodel in a car crash looks at you with a "claw
hand". What two cord segments contribute to the nerve which is damaged?
A. Cord segments are C8 and T1! See, not so easy, right?
Q. Adenosine deaminase def can cause what problem
immunologically?
A. Adenosine deaminase def can cause SCID.
Q. Most I spoke to got this on their test. Distinguish
the Rinne and Weber TEST!?
A. absolutely HY. Weber test- tuning fork in midline of
skull- localizes hearing loss to one side or the other- if it is a conductive
loss, patient hears better on side of defect. If it is sensorineural hearing
loss, hearing is better on opposite side of defect. Rinne test- place tuning
fork on mastoid process until patient can no longer hear vibrations, then place
tuning fork next to external auditory meatus- if patient cannot perceive
vibrations- BC ( bone conduction) is better than AC(air) and patient has a
conductive hearing loss on that side.
If AC is better than BC, then that is the normal ear
Q. Everyone seems to need to understand that:
A Bicornuate uterus, which prevents a woman from
fertility, is caused by what?
A. it is due to the incomplete fusion of the
PARAMESONEPHRIC ducts. Amen
Q. YOU WILL be asked this question:
There will be a person with a history of travel who goes
to Mexico or thereabouts. Then he or she will return with bloody bloating crampy
diarrhea. They will ask you either what is the bug and the disease, and the
treatment. So what are the answers? Look below
A. Ambiasis, dx is dysentery, and you treat with
Metronidiazole and the bug is Entamoeba histolytica.
Q. Since taking the test, I spoke to "a Lot" of people
and the US licensing board wants everyone to know a certain fixed "universe" of
diseases and txs, if you master those, you will at least PASS. That is what I am
trying to help to do for all of us family VALUE MDs!
I "got" this question, my "roommate" got this question,
in 2030 probably, my sons/daughters will get this concept:
What is the MOA of Acyclovir
A. Acyclovir blocks viral DNA polymerase when
phosphorylated by viral thymidine kinase.
Some people will be asked to understand that Acyclovir
is used for the HSV, Varicella, Epstein Barr Virus
The boards LOVE Acyclovir
Q. So common, definitely on everyone's test:
A baby come to your clinic with loud cough that
resembles the barking of a seal, difficulty breathing, and a grunting noise or
wheezing during breathing. What is the dx? And the secondary question they WILL
ask is is it enveloped and what is the structure?
A. Dx is Croup!
Paramyxovirus,
It Has an envelope, has single strand, nonsegmented.
Q. Case: Cilia lack ability to move, so your patient is
sterile, no sperm, and he has ongoing sinus inflammation. What is syndrome and
the protein that is lacking?
A. Kartagener's Syndrome, due to dynein arm defect!
Q. EVERYONE, seriously, EVERYONE I talked to needed to
master this concept for the test:
Case: Child with multiple fractures and BLUE sclera. The
two secondaries are
What is specific defect?
What is the inheritance pattern?
A. Osteogenesis Imperfecta, with abnormal collagen type
I, and inheritance pattern is autosomal dominant! Good Luck!
Q. Hard one, but def. a must!
Here it is..
A child has defect in eustachian tube and middle ear,
which pharyngeal pouch is defective?
A. The first pouch... some of my friends last year got a
whole slew of arches and pouches, a favorite of the NBME, KNOW IT
Q. YOUR SOUL MUST UNDERSTAND that if you have a patient
with probs with his circadian rhythms and autonomic regulation and a DETAILED
diagram with arrows of brain pops up, which nucleus is affected?!
A. The suprachiasmatic nucleus of the hypothalamus!
Peace to Everyone on Earth!
Yoda says rather asks you:
Q. Which one of the following is responsible for
peripheral myelin production?
(Choices: Ependymal cells, Oligodenroglia, Astrocytes,
Microglia, Schwann cells)
A. Schwann cells! Remember that Oligodendroglia are
CENTRAL myelin production
Q.Even my grandmother I think had to understand this for
USMLE:
Case: A patient with a defect in apo C-II and
Lipoprotein Lipase. How will her labs look like? I.E. What is her disease
You WILL get questions PLURAL on the big three:
Diabetes, Hypertension, Hyperlipidemia. so, ...
A.The answer to my question was HYPERLIPIDEMIA
hyperlipidemia type I is associated with :
uncontrolled diabetes mellitus, obesity, and sedentary
habits, all of which are more prevalent in industrialized societies than in
developing nations. In both epidemiologic and interventional studies, hTG is a
risk factor for coronary disease.
Two rare genetic causes of hTG (lipoprotein lipase [LPL]
deficiency and apolipoprotein [apo] C-II deficiency) lead to triglyceride (TG)
elevations
Q. Consequence: cardio disease! They love porphyrias.
Maybe they watched the movie "The Madness of King George" over and over, I dunno,
but in order to pass the test, you have to understand that if you get a patient
with bizarre symptoms like stomach pains with very mild photosensitivity,
delirum, and his urine darkens in the light, you are looking at ACUTE
INTERMITTENT PORPHRIA! So you have to know four things:
What is the deficient enzyme? AND, What substances
accumulate in the urine? AND what two amino acid begin this synthesis of
porphrin molecule? AND what metallic ion cofactor is required. YOU HAVE TO KNOW
THIS TO PASS.
A. Deficient enzyme: uroporphyrinogen 1 synthetase
Porphobilinogen and aminolevulinic acid accumulate in
urine
Glycine and Succinyl CoA are precursors of porphrin
Metallic ion is Fe!
Q. Pt. who drinks his whole life, say the question
describes to you he has Wernicke-Korsakoff syndrome (you know how to spot this
right?), and say the question asks what vitamin is missing AND what DOES THIS
VIT DO. Can you tell me? (It is not enough to know just the vitamin)
A. Vitamine B1 (thiamine), it functions as a cofactor
for OXIDATIVE DECARBOXYLATION OF PYRUVATE and is involved in the crucial HMP
shunt!
REMEMBER...thiamine and the word DECARBOXYLATION RXN
Q. Ahh... the all important Folic Acid def. Everyone
will see this, guaranteed since it is the most common vit deficiency.
YOU HAVE to understand that if you see a slide with
macrocytic megaloblatic anemia, what is missing vitamin (I gave it away, Folic
Acid, but it could also be Vit B12 but without Neuro sym)....anyways, I
digress...What IS the EXACT function of it, and type of reaction?
A. Methylation reactions ...
and it is an enzyme for the all important one carbon
transfers.
Folic acid=METHYLATION reactions
Q. with meowing catlike cry and later is mentally
retarded. But always it is the SECONDARY QUESTION, so what is the disease, the
genetic defect, and the organ that is primarily affected and how? I sound like a
broken record, but EVERY DOCTOR-TO-BE SHOULD KNOW THE CONCEPTS THAT ARE ON THESE
POSTS!
A. Cri-du chat syndrome...BUT did you know that...
chromosome 5's short arm is deleted AND pt has cardiac
defects primarily VSD and ASD!!!!!!!!
Q. Guaranteed you have to know:
Case: A college student comes into your clinic with
fever, hepatosplenomegaly, lymphadenopathy and + heterophil Ab test. What is the
"bug" and most crucial, is it:
SS or DS? (single stand or double strand)
Envelope or no envelope?
linear or circular?
What is the family?
{Believe me, you will see this question}
A. Pt has Mono, and it is Epstein Barr Virus. Most
importantly, the NBME will not stop there!!!! You will have to answer it is a
Herpesvirus family, DS, linear, and it has an envelope. Failure to master this
concept will result in a veil of tears
Q. Older patient comes to you with bone pain, Visual
inspection may reveal bony deformities, such as an enlarged skull, spinal
kyphosis, and bowing of the long bones of the extremities. Localized pain and
tenderness may be elicited with manual palpation. Labs: elevated alk phos.
What is this common disease and drug Rx? You have to
catch this diagnosis b/c it can lead to cancer!!!!!
A. Paget's Disease, treat with bisphosphonates, physical
therapy, could have viral etiology.
Q. Suppose you are a pathologist to be and are shown a
pic of lymph node. Could you point to EXACTLY where the T-cells are housed on a
histo slide? You have to know this
A. Hey, look up on Webpath and pick out the PARACORTEX,
where the T-cells are housed. You have to know this on a pic, not just on
words...
Q. case: skin manifestations include peripheral nerve
involvement with fibromas and plexiform neurofibromas; the iris, with Lisch
nodules; optic nerve gliomas; pheochromocytomas in some patients; skeletal
abnormalities, including craniofacial dysplasia. What is this disease that you
are SURE to have on your USMLE? What is inheritance pattern?
A. Neurofibromatosis, AD (Don't confuse with McCune
Albright which is assoc with girls and precocious puberty) Cheers!!!
Q. Pt appears healthy at birth. Diagnosis is usually
made in infants aged 6-24 months. Inguinal and umbilical hernias are commonly
seen at birth. On physical examination, these patients are observed to have
corneal clouding, hepatosplenomegaly, skeletal deformities (dysostosis
multiplex), coarse facial features, large tongue. You will see this presentation
likely on your test because it is so serious.
They will ask, "What is the missing enzyme?"
A. Hurler's Syndrome and you are having a deficiency of
alpha L iduronidase. Love for everyone!!!
Q EVERYONE I CONSULTED SAID THEY HAD THE UREA CYCLE ON
THEIR TEST AND IT IS SO IMPORTANT IN OUR CLINICS AND LIVES. Know the cycle COLD
until you can draw it out from memory.
For example, we know that an ammonium ion comes in in
the mitochondria with carbamoyl phosphate, BUT urea has TWO nitrogens, which
compound provides the second nitrogen? KNOW THIS. IT is essential for life.
A Answer is aspartate feeds it in!
NOBODY, but NONE of US will give up. We will ALL succeed
and become doctors. Let's let none of us give up and be left behind with their
dreams.
Q. Don't be surprised if you are asked to know this
classic common concept:
Pt with right sided ataxia, loss of pain temp of right
face and left upper and lower extremities, hoarseness, dysphagia, loss of taste
of right tongue, with vertigo and nystagmus. This IS SO CLASSIC FOR WHAT LESION
YOU WILL see in your clinic and a famous test?
A. PICA, posterior inferior cerebellar artery stroke! Be
SURE you can identify it on a brainstem slide.
Q. Invariably, you will be asked:
Pt, older gentleman with visual field defects from a
Circle of Willis (they'll give a pic) hemorrhage. Point to the artery in Webpath.
for now, though, what is the name of this most famous artery?
A This is a case of anterior communicating artery
stroke, the most common circle of Willis aneurysm! Got it? Got Milk?
Q.LIVE to know that:
Niacin, Melatonin and serotonin are derived from what
amino acid? Think hard first before looking!
A. answer is tryptophan! Don't forget....
Q. Sorry to continue to bug you all, but the galaxy
members informed me that all need to know that if:
Given a midsagittal section of the brain, there is an
arrow pointing to the different structures, but the question is:
Case: a child come to your clinic with symptoms of
hypopituitarism. Where is the lesion? POINT TO IT! What is the dx?
A. Pick the answer choice where the arrow is point to
the pituitary (it is next to the hypothalamus, find it on your atlas). This is a
classic question of a craniopharyngioma which is the most common cause of
hypopituitarism in children and it compresses the optic chiasm and hypothalamus.
Q. This is a question that a 99%er told me he knew but
for the rest of us we can be OK if we are clueless:
A man comes in with bilateral and multicentric retinal
angiomas, central nervous system (CNS) hemangioblastomas; renal cell carcinomas;
pheochromocytomas; islet cell tumors of the pancreas; endolymphatic sac tumors;
and renal, pancreatic, and epididymal cysts. CNS hemangioblastoma is the most
commonly recognized manifestation of and occurs in 40% of patients. What is the
dx? No secondary here. Just the diagnosis is Hard enough! BUT common enough for
USMLE CONSIDERATION!
A. Von Hippel Lindau Disease. There will be a MRI of a
brain with a cyst in the cerebellum from a hemangioblastoma. Excellent work my
brothers and sisters
Q. A patient presents with recurrent viral infections
from T-cell deficiency and symptoms pointing to hypocalcemia. Can you tell me
disease (dx) and what failed to develop? A USMLE glorious favorite!!! Kinda hard
though, but popular. You HAVE to know this.
A. Faulty development of 3rd and 4th POUCH caused
DiGeorge's syndrome and thymic hypoplasia and hypocalcemia.
Warning, I heard a lot of students messed this with the
arches, and put 3rd and 4th ARCH (so close and yet so far!)
Q.What is the precursor for heme, which aa? Know this
concept like your mom's birthday
A. glycine. don't forget!
Q. You WILL see a pic and case presentation of a woman
with a picture of an atypical mole (big hint is dysplastic nevus). What is the
associated neoplasm, is it benign or not?
A. It predisposes to malignant melanoma. The NBME wants
you to know the stuff that you CANNOT AFFORD to miss that are COMMON.
Q. Speaking of skin stuff, Suppose you are dreaming and
you see a color photo of a hyperpigmented skin lesion in the axillary area on an
obese person that you have nailed as acanthosis nigricans (as an aside KNOW THAT
THIS LESION IS MORE COMMON WITH DARKER SKINNED INDIVIDUALS). Say they ask you
the most notable associated malignancy, what will you say?
A.Commonly associated with cases with dark skinned obese
individuals, you must be wary that they may get GASTRIC adenocarcinoma! You
cannot miss this and the NBME won't let you off if you don't know this.
Q. Here we go:
There is a young person who comes in with mild tachypnia
because of acidosis, he has enlarged liver, is slightly to moderately icteric;
accompanying hypoglycemia (watch for seizures). What is the MISSING ENZYME?
A.This is a classic presentation of Aldolase B
deficiency. They may want you to know it is autosomal recessive inheritance and
you must terminate BOTH fructose and sucrose in the diet
Q.will faint with disbelief if you don't get this on
your test and also in clinic and in life:
Case: Visual field defect of homonymous hemianopsia,
there will be a series of diagrams of the eye nerves (you guys know with pic I
am talking about right?) with arrows everywhere. Where exactly is the lesion?
A There are at least two dozen questions that can be
asked from this crucial concept with those visual field defects. Master them
all.
an arrow point to the nerves behind the optic chiasm
contralateral.
Q.You WILL see this on your test because in clinic you
will prob see it everywhere:
Case: There is a older man with signs of LOWER (not
upper) GI bleeding. What is the most common disease (hint, neoplasm is not the
answer), secondaries are What area of the bowel is affected and what drug can be
given if surgery is not indicted?
A.This is classic diverticulosis/itis of the lower
descending colon and sigmoid (all proximal to the ligament of Treitz). You can
give vasopressin as a drug.
Watch for distractor answer choices like Meckel's
Diverticulum and Intususception and IBD, these are found in children and
adolescents more often. Always always first consider your age and gender and
ethnicity and travel and meds of your patients!
Q. This USMLE FAVORITE is kinda easy but just in case:
Patient is older gentleman and had a history of lytic
lesions and M protein spike and now present w/ lesion in the kidney, lesion was
stained w/Congo Red? What is the dx and the name of the tissue stained
(condition)?
A. Multiple Myeloma and the stain is amyloidosis. These
two diseases are EVERYWHERE, like Britney Spears pictures on magazines
Q. The NBME declares that you must know your basic
oncogenes, guaranteed. So...
Case: You are given a clinical case where the gene that
is active is c-myc (this is a oncogene, not TSG), what is the related tumor and
specific gene translocation?
A. This is Burkitt's lymphoma, some of you will be asked
that it is a t8;14 gene translocation
Q. Speaking of oncogenes, many will be forced to address
this point (not in Error! Hyperlink reference not valid. but def. in NBME's
brain:
Case: A clinical presentation of MENI and or MENII
(review this quick), then you have to pick the oncogene that is activated. What
will you chose?
we are talking about the ret oncogene. repeat that in
your mind ten times NOW
Again, you are given a blood smear photo (medium
quality) that you know to be follicular lymphomas (review on Webpath). But of
course, the answer is a secondary. So tell me, give a series of answer choices,
what is the oncogene responsible
A. It is bcl-2 which block apoptosis. YES! YOU GOT IT!
Q. So Classic, so repeated, so in vogue, so know it...
A clinical presentation is given where a pupil
constricts with accommodation and is not reactive to light. What is the
treatment? The bug? The name of the syndrome? AND give me the method to
visualize the bug!
A. Penicillin G = Tx
Bug = Syphillis, T. Pallidum
Syndrome = Argyll-Robertson pupil
Visualized by = dark field microscopy
THIS IS A NBME FAVORITE! And you should know it for life
for your patients!
Q. Here is a hard one, but certain to appear:
Case: One of your patients is in childhood with
hepatosplenomegaly, pancytopenia, and crippling skeletal disease. He is Jewish
and a liver biopsy shows glycolipid laden cells. What is the disease name and
the enzyme deficiency given 5 choices that are agonizingly difficult?
A. This is Gaucher's Disease and the enzyme def. is B-glucocerebrosidase!
KNOW that Gaucher's like most other enzyme deficiencies
are AUTOSOMAL RECESSIVE! YES! Go and kick TUSH on this test!
Q. This is an interesting and crucial case seen around
the world in testing centers:
A baby patient of yours has loss of sensation around the
jaw, and suppose the answer choices ask which brachial arch is defective? What
will you answer? (NBME loves those arches)
A. Answer is Brachial arch 1,
cranial nerve V3 is affected along with all the "m"
muscles (e.g. Muscles of mastication, masseter, medial pterygoid), Malleus, and
a couple of others
Q. On test day, you see a question which asks you for
the mechanism of RESISTENCE of bacteria to norfloxacin or ciprofloxacin and then
asks you also the side effects? Will you know?
A. Resistence comes from a mutational change of the
bacterial DNA gyrase. This drug is eliminated renally so don't give to renal
compromised patients. A scary side effect of this is inflammation of tendons and
cartilage damage.
NOTE: These Quinolones have NO EFFECT on anaerobes!
Q. Quickly, you see that oh-so-familiar diagram of th
Cardiac Cycle/EKG. And you are asked what valve corresponds with the END of the
first heart sound (Arrow is pointing there) and is it closing or opening? What
do you say?
A. The Aortic Valve OPENS at the end of the first heart
sound (KNOW THIS)
Q.While we are on the subject, everyone in the world
will face the Cardiac cycle/EKG graphs. So, There is an arrow points to the
place where the S2 STARTS. What valve is opening or closing?
A. The Aortic Valve closes at the beginning of the 2nd
heart sound (KNOW THIS)
Q. Simply, what is the MOA of Cyclosporine
A. inhibits IL-2
Q. Case: You are given a classic presentation of an
older man with Benign Prostatic Hypertrophy (this disease is everywhere). What
is the drug of choice and what is the mech of action
A. You should choose finasteride, a 5 alpha reductase
inhibitor.
Q. You will not get away from Step 1 without seeing a
case of...
An obese woman with infertility, acne, alopecia,
hirsuite. Now, I must ask you what is the hormonal abnormality and the drug of
choice? You could also be asked what cancer is she most at risk of?
(THIS CONCEPT IS A MUST KNOW
A. This is a case of PCOS. There is elevated LH/FSH
ratio, and the LH stimulates testosterone. The lack of progesterone predisposes
the woman to endometrial cancer.
Treat with Oral Contraceptive Pills or an anti androgen
like Spironolactone
Q. EVERY MAN EVERY SINGLE MAN who lives long enough will
get this disease:
Case: Older gentleman with urinary control problems and
complaints include back and hip pain as well as other symptoms such as fatigue,
malaise, and weight loss. There may also be a history of bone fractures. What is
the disease, and the drug of choice (2 NBME favorite choices)?
A. This is sadly prostate cancer with mets to spinal
cord. You need to aim to stop testosterone production. Although castration is
best (seriously), the choice most men opt for is Lupron or generic name
Leuprolide (A LHRH agonist) or Flutamide.
Q. You will get a case of a patient with ptosis and
inability to turn the eye up, down, or inward. At rest, the eye is deviated down
and temporally, and the iris sphincter may be involved or spared. He has a
history of an aneurysm, and his eye does not constrict. Two secondaries: What
nerve is lesioned, AND if you are given a picture of the circle of Willis and a
bunch of arrows, which artery will you pick?!
A. This is an aneurysm of the posterior communicating
artery which is causing CN III to be affected!
Q. Friends, this concept comes up I hear on every exam
and hospital pimp session:
If you get a man with a history of atherosclerosis, and
he dies very suddenly, and he had no thrombus to cause an MI, he died of a
VENTRICULAR ARRYTHMIA
Q. I present you with a patient who has angina at rest
with atherosclerosis, is this:
Prinzmetal angina
Stable angina
or Unstable angina
or MI
UNstable angina,
A. KNOW if you get a version asking Prinzmetal's, you
see ST elevation on stress ECG and ST depression with exertional/stable angina
Q. Here is one that rings through eternity on USMLE
(rhymes!):
Case: A 15 year old soccer player named Goober comes
into your clinic because of acute, serious throbbing pain in the right knee and
is limping. He was "clipped" on his lateral right side of the knee. What three
structures are affected
A. This super HYer is the triad of anterior cruciate
ligament, medical meniscus, and medial collateral ligament. (Think in
abbreviations, ACL, MM, MCL)
Q. If I give you a case with a lumbar puncture (w/ a pic),
and ask with arrows where do I get CSF from, can you tell me?
(Choices: Dural, Subdural, Subarachnoid, Arachnoid)
Also asked is between what two spaces is CSF taken?
A. IT is Subarachnoid, the most common wrong answer is
arachnoid or pia mater.) between L4 and L5
Q. Some patient comes with a history of arrhythmias and
is on a med and she presents with antinuclear antibodies, arthralgias, rash.
What med is she on
Procainamide, KNOW that this and HYDRALAZINE gives SLE
like symptoms (drug induced
You will be given a diagram with the Arachidonic acid
products pathways with arrows everywhere. You have to know which arrow is
pointing to where Zafirlukast acts. (Don't confuse with Zileuton)
Zafirlukast acts on the arrrow pointing at the end step
where Leukotrienes are inhibited. Zileuton acts before and the level of
Lipoxygenase BEFORE HPETE. Don't forget! Review that classic diagram, it is in
BRS and
FA
A pt complains to you about his skin thinning and mild
osteoporosis and saying his esophagus burns. What med is he on that causes this?
(Very popular point)
He is on a Glucocortoicoid, notice that I did not say
"buffalo hump", or central obesity. The boards avoids "clicker" words.
Case: If I present a sideways angiogram of the head,
choose the arrow pointing exactly to the sigmoid sinus AND, can you point to the
cavernous sinus?
The cavernous sinus is right behind the eyes and the
sigmoid floats along the back. LOOK at WEBPATH
Case: What is the proposed mech of action of Lithium,
and does your patient have hyper or hypothyroidism? What about poly- or
oligouria? A MUST KNOW
You bipolar patient has hypothyroidism and polyuria, Li
blocks PIP cascade.
YOU WILL KNOW THIS CONCEPT!:
Case: A 27 yo AID patient has pulmonary complications.
Exam of tissue shows yeast-like with capsules. What does he have? Secondary seen
is how do you treat? Very tricky.
He has Cryptococcus Neoformans, NOT Pnemocystis carinii
due to ID of the capsule. Treat Cryptococcus with Amphotericin B. KNOW
Cryptococcus usually causes meningitis, BUT, it also easily hits the lungs.
While on the SUPER HY topic of AIDS: I remembered I have
to tell you...
Case: 32 yo male has demonstrated AIDS and you see cysts
containing sporozoites can be seen with silver-stained preparations in the
lungs, and he is rather asymptomatic. X-ray shows interstitial infiltrates. What
now are you thinking and what drug will you grab!
He has PCP, the most common disease of the AIDS, treat
with TMP-SMX!!!!!
USMLE LOVES...
Case that you nailed as Influenza...secondaries seen are
where does it replicate? Pick among answer choices does it have envelope? Linear
or NOT?
It along with HIV are the only RNA viruses to replicate
in the NUCLEUS, and.... it has an envelope and is linear single strranded!!!!!!!!!!!!!!!!!
BIGGIE CANDY KWESCHON
A thousand times you will see...
A pt or question defining the subject of DOPAMINE (A
million dollar concept). Which dopamine receptors are excitatory, which are
inhibitory, and is the second messenger cAMP or Ca? This concept alone will let
you answer a thousand questions, seriously...
The oh so important Dopamine has:
D1 and D5 which are excitatory which rev up kidney
perfusion in shock, AND
D2, 3, 4 are inhibitory. Most schizophrenic drugs work
on the D2 receptor which is inhibitory!!!! Wow, I feel great!
Finally, dopamine works on G-protein coupled cAMP second
messengers...
Easily one of the most missed because people THOUGHT
they knew:
PIC: HISTO of muscle fiber. Can you do these if arrows
are everywhere?
1) Point to myosin fibers
2) Point exactly where ATP works/acts in EM.
3) To what does Ca bind to (answer is diff for smooth
and skeletal muscle)
ANSWER ME, PLEEEAASE! (Well, silently, I cannot actually
hear you)
1) Myosin are the middle lines/area (Look up Histo
atlas)
2) ATP is bound to myosin on the Head
3) Ca binds to troponin in skeletal muscle and
CALMODULIN (which activates MLCK)
See, isn't it easy to forget? So DON"T!
HARD ONE:
Patient complain of gradually worsening shortness of
breath, progressive exercise intolerance, and fatigue, and swollen feet. He is
an older man with amyloid deposits everywhere? From 4-6 answer choices of
-myopathies, what does he have? (Hint: Loud diastolic S3 heard)
he has the rather rare but often quizzed Restrictive
Cardiomyopathy (myocardium is stiff)
Case: (VERY COMMON)
Young child with clinical triad of mental retardation,
epilepsy, and facial angiofibromas. What associated cancer is common
CNS hamartomas and cardiac rhabdomyomas You will see
skin lesions so don't pick neurofibromatosis as the answer choice for the pre
cancerous condition or I will cry.
You are given a case and asked to quickly calculate the
ejection fraction. What's the equation?
Stroke vol/ EDV
You will be asked questions about Down Syn. Tell me:
What is the organ most commonly affected (although
Down's hits all systems)?
What cancer is associated?
What hormone do you often treat them with?
Is alpha feto protein low or high at 14 week gest?
Cardiac (e.g. VSD)
Cancer is ALL
Hormone is thyroid hormone
Alpha fetoprotein is low in testing
Copyright © 2003-2005 ValueMD, Inc. All rights reserved.
You will know Jedi Knight,
A pic with B1 receptor, which neurotransmitter acts here
(Epi, norepi, Ach, Dopamine)?
Now you see a pic of Lung with B2 receptors. Does same
neurotransmitter act there?
BIG CONCEPT:
Norepinephrine acts on B1 receptors but NOT B2 receptors
(epi does though)
Picture like on Webpath of LOBAR Pneumonia. Histo shows
encapsulated orgs. Then you see myriads of bact/fungi/viruses as possibilities.
What is your first choice
Strep Pneumoniae!
Slide with megaloblastic anemia, pt looks like a B12
def. Intrinsic factor administered. Patient improves. What disease did he have?
(Pick between terminal ileum deficiency and atrophic gastritis) Also, could
there be a bug involved? Which one?
He has atrophic gastritis fr. H. Pylori.
Quick! Can you tell me what is the term for the most
appearing number amongst a given series of number values
it is called the MODE. Came up before
Fast! Tell me the ABCs or name three anaerobes and what
is name of enzyme lacking which makes them vulnerable to oxidative damage?
Actinomyces
Bacteroides
Clostridium
They are missing catalase. Treat with Clinda above the
diaphragm and Metronidazole below the diaphragm!!!
You are given a case with a druggie and he has Hepatitis
C. Choose and tell me if it is RNA/DNA/SS/DS/Helical/Square
RNA, SS, LINEAR (remember that all RNA viruses are
single stranded except Reovirus, AND the letter PCR denote the NON-ENVELOPED
VIRUSES or P-Picorna, C-Calic, R-Reo)
You will see this:
A man comes into your office acting very strange,
sticking out his swollen tongue, and complaining of numbness and prickling. He
is a vegetarian. What two crucial reactions cannot occur because of the missing
diet cofactor
This is classic triad for Vit B12 deficiency.
Homocysteine METHYlation and Methyl malonyl CoA step into TCA cycle is blocked!
Ain't that awesome, I mean the knowledge, I feel sorry for the patient though
valuemd.com
Here is a biggie:
Your patient goes for plastic surgery to look like
Michael Jackson and he is given succinylcholine (muscle relaxant). He suffered
prolonged respiratory paralysis and muscle paralysis afterwards! What enzyme or
mineral is defective? (Hypomagnesium, Hypokalemia, Pseudocholinesterase def)
It is pseudocholinesterase deficiency. Many causes, but
pregnancy, neonates, elderly, burn victims, pesticide poisoning, can be
presented by the Boards
Banana-split question! A patient presents with
epigastric symptoms and melena.. You should pick PUD or peptic ulcer disease
(this disease is everywhere, like air), BUT there is a secondary! Labs rule out
H.Pylori (most common). What is the next HUGE cause?
Chronic NSAID use. Man, I had to do so many anal exams
for this (checking for bleeding with those little Heme cards). They call it the
M-3 student consult.
Wow this a biggie fry with a biggie drink question:
You have a patient with a description of allergic
rhinitis (some 50 million Americans suffer this, you will see this tested), and
he is taking steroids, antihistamines, and pseudoephedrine. He is depressed and
wants anti depressants. You pick one from 5 choices and your attending knocks
you silly. Which one did you pick that is a no-no?
MAO inhibitors cause hypertensive crisis. You deserved
the punch.
Every single person sitting for USMLE gets one of the
Immune def questions, no exception I hear. So, you have a young patient with a
gene defective in making myeloperoxidase, thus the cause of his recurrent
infections. What cells are weakened, what is the MECHANISM LOST, what is the
metal ion in MPO?
(You will see this case, or DiGeorge's, SCID, etc.)
The ability of the immune cells to engage in respiratory
burst is cut off. Myeloperoxidase, MPO, catalyzes the conversion of hydrogen
peroxide and chloride ions (Cl) into hypochlorous acid. Hypochlorous acid is 50
times more potent in microbial killing than hydrogen peroxide.
Neutrophils are weakened which contain Fe
Hey, compare and contrast this oft seen lingering
factoid!
Case: You get another child just like the previous case
with bacterial infections. BUT, this time you discover there is a defect in
microtubules and phagocytics. You see severe gingivitis and oral mucosal
ulceration PLUS albinism on the skin. Secondaries: What is the disease, what two
bugs eat at you, and what is the first drug you reach for?
Here is Chediak-Higashi disease (not too common). But
you get strep and staph infections and you treat with Acyclovir. The KEY to this
diagnosis is the mouth stuff and hypopigmentation! You start with Acyclovir THEN
give the missing globulins through IV because Chediak Higashi is an IMMUNE
DISEASE and Acyclovir boosts the recovery while fighting the viruses. The
globins you transfuse will address the Staph and Strep. OK?
IMPOSSIBLE ODDS, but, look...
Still in your peds rotation, your next patient comes in
with recurrent bronchpulmonary, bacterial, neurologic disease, thymus aplasia,
telangiectasias, growth retardation, and impaired organ mutation, and is walking
funny and waddling. What are you looking at NOW?
HERE,
you are looking at Ataxia telangiectasia, where both the
T and B cells are busted. The alpha fetoprotein levels are always elevated, and
they key finding is ATAXIA!
OOHHMIGOSH!
ANOTHER, would you believe, child, younger this time, 2
years old walks in, again with recurrent bacterial, fungal, infections. His mom
say he suffers often from candida. And you note he has IL-2 def, poss. reticular
or ZAP-70 gene def. Your attending walks in and says he will suffer from PCP and
Herpes. She (attending) asks you to write a prescription for .... ???? What
disease? What med?
This unfortunate child has Severe combined
immunodeficiency or SCID. They usually die by age 2 from PCP. You must
prophylaxis with TMP-Sulfmethoxazole. Consider IV globin transfusion if counts
stay low.
YOU are starting to hear TWILIGHT ZONE MUSIC BECAUSE....
YET ANOTHER CHILD comes into your peds clinic with an
immune def. But this time, the child is hyperreflexic on exam, has abnormal
facies, congenital heart disease, hypocalcemia on labs, and increased
susceptibility to infections. A radiograph shows he has no thymus! What do you
tell your chief? What do you prescribe?
This child has DiGeorge's Disease or thymic aplasia. His
3rd and 4th arch failed to develop. This concept is a favorite of NBME.
Including considering marrow transfusion, you must prescribe Calcium salts and
Vit D!!!!
106. Fiddlesticks, just when you thought you were free,
ANOTHER child walks in with his mom with another immune
deficiency. (I keep on with rhymes, he-he-he). Here he is 4 years old, with
recurrent otitis media, eczema, and thrombocytopenia from Strep pneumoniae. AND,
he bleeds a lot. His IgM is low. Your attending and chief are wondering if you
are able to distinguish all these immune def. diseases. Will you get an honors
grade(Name disease)? What will you treat with? What is mech that is broken?
He has X-LINKED Wiskott-Aldrich syndrome. This is often
confused with the others and Bruton's on exams..hint, hint. But remember the
tendency to get attacks from capule bugs like Strep, with otitis, eczema , and
BLEEDING. The key is LOW IgM, High IgA,and the bleeding. IgM response curtailed.
He is not nearly as bad as SCID case, and you must give him amoxicillin (there
are a lot of options here, like you can give ceftriaxone too) plus globins.
FOR ALL OF THESE IMMUNO CASES STAY AWAY FROM LIVE
VACCINES. The NBME will ask you this, if not now, then later, if not later, then
someone will ask you.......
107. Oh no mate! Another ONE! BUT YOU HAVE TO KEEP
GOING! EVERY TEST WILL HAVE ONE OR MORE OF THESE DISEASES BECAUSE YOU CANNOT
AFFORD TO MISS THEM. IT AIN"T JUST ANOTHER COLD BABY.
This boy has low IgG and presents like WAS syndrome with
continued bacterial infections, diarrhea. And you find out this is X-linked too!
In the absence of functional Btk, mature B cells expressing surface
immunoglobulin and the marker CD19 are few to absent. What disease?
Here is the first immune def. described by Dr. Bruton.
So similar to WAS syndrome, but WAS boys will BLEED. OK? Get them straight in
your head!!! IT IS HARD!
108. This is just a day that won't end! Another child,
this time let's make it a GIRL, comes in with OF COURSE, an immune deficiency
with bacterial and fungal infections. HOWEVER, the NBME has to give up some info
(er...I mean the girl's features do I mean..). {This knowledge is good to know
for life of course, not just a test}.
Soo...you note that all the immune def. choices are
mixing but you see her presenting with lymphadenopathy, hepatosplenomegaly,
growth failure, and stigmata of chronic skin infections. Your fellow med student
(star student) whispers something about def. w/ phagocytes. TWO distinct hints.
AND culture comes back and she has Aspergillus. TELL YOUR ATTENDING WITH CONFID
ENCE......!?????
This is Chronic Granulomatous Disease. This is marked by
the granulomas (skin stuff) and key words phagocyte def. and Aspergillus
infection. Are you getting it all down. YOU HAVE TO IN ORDER TO PASS. All the
immune def. will be among answer choices, they differ so slightly. Master them!
The clock is approaching 5:30, AND the nurse squeezes in
another patient and whaddaknow, he has immune def. with recurrent bacterial
sinopulmonary infections. The NBME, er, I mean attending starts pimping you with
choices...but you note that the patient is OLDER, LESS SYMPTOMATIC (i.e. less
severe disease), and complains of GI symptoms too like diarrhea. What words are
coming out of your mouth?
This is the OH SO COMMON IgAD or Immunoglobulin A def.
Many stay asymptomatic, IgG and Neutrophil levels could be normal. Give
antibiotics....Confused yet? I hope not, I hope I gave you cues to distinguish
the diseases
As an aside, I spoke to 100 people and they all scream
back, KNOW ENDOCRINE!}
Soo...........
Now it is 5:00 pm. You are beat, but happily this time
your patient is not an immune def. case. BUT, you rub your eyes because standing
in front of you are 3 answer choices..errr, i mean fraternal triplets (listen I
am tired, I have not slept yet)...
LISTEN CLOSE, THEY ALL HAVE systemic symptoms such as
weakness, fatigue, malaise, and fever low-grade, two have neck pain, one does
not. Physical exam shows hypothyroidism. But here is the concept that comes
again again again again:
Child A has hypothyroidism, neck pain, and fever chills
and dysphagia
Child B has hypothyroidism, neck pain, and sort of looks
a little like he was hyperthyroid last week from history
Child C is shorter and his neck is NOT tender and gets
constipation a lot
SUPER CONCEPT: Who has what??????????????????? A must
know!!
Child A has ACUTE THYROIDITIS (bacterial) so you must
manage aggressively with antibiotics (penicillin G is DOC)
Child B has SUBACUTE THYROIDITIS (viral) so you just
give aspirin and return visit. (KEY!!, HYPER, then HYPOthyroid features)
Child C has AUTOIMMUNE THYROIDITIS. This is bad because
it is a life-long condition. Treat with levothyroxine.
THIS QUESTION WAS WORDED VERY ODDLY, BUT YOU WILL REGRET
IT IF YOU DON'T TAKE HOME THE CONCEPT!!!!
as to the HY Concept 110, consider that...
someone I knew said they had to distinguish the
hypothyroiders (I did not say it, but you KNOW TSH is high right), and then, he
was given a series
of graphs pointing to thyroid levels. Recall Subacute
thyroiditis can start with HYPER then HYPO thyroidism. The NBME likes to ask
things in a scary way that makes you forget everything, even your own name
during the exam. HOLD YOUR WITS. YOU KNOW MORE THAN YOU THINK
What MAJOR MAJOR drug other than trimethoprim blocks the
loved enzyme dihydrofolate reductase?
Methotrexate:
KNOW you often use it for rheumatoid arthritis,
hydatiform mole, leukemias and it works its magic in the synthesis phase,
stopping thymidine (thymidineless death) and blocks protein synthesis. As I
mentioned, I AM NOT REPEATING "EXAM CONTENT" but know that the NBME will give
you a picture and ask you to POINT to where methotrexate works its magic. They
like doing that. Last year, I wish someone told me just how the NBME likes us to
understand stuff. No one told me. Now I want to lift others up.
AGAIN BEING VAGUE AFTER AZSKEPTIC's warning...
I think that is ridiculous to say that I am
disseminating material with all due respect to AZSKEPTIC. Like I said, there is
a purpose to this very very hard test. There are trillions are pieces of info,
and you HAVE to pick and choose. But the NBME needs to know that you are not
going to come to the US and kill people, soooo..... I relay the concepts like
"Don't give ACE inhibitors to a pregnant woman". This is SURE to be on the USMLE
Step 1,2,3, but am I breaking a RULE to tell people this VITAL piece of info? I
am giving out "exam content" in the sense that I am relaying that IL-5 revs UP
IgA and IL-6 (like IL-1) revs up the acute phase response...BUT THESE ARE the
BASICS that NBME wants US doctors to master. That is why if I recall from my
test a case of a drug overdose and how to treat it, I FEEL COMPELLED to say it
on this board in such a way that does not violate copyright laws or "giving out
answers". Because....every doctor in the world SHOULD know what drug a person
probably took based on his or her symptoms and how to treat them. I encourage
everyone to share the concepts after their exams. The NBME should not mind
unless I tell everyone that "if you get test version KX-115 then the answer to
#1 is B, #2 is A, #3 is E, etc." But to share knowledge that the difference
between ALS and multiple sclerosis is that ALS has no sensory deficits, well
that is just making everyone wiser and better doctors. What do you guys believe?
Anyhow, let truth reign! Let's say a patient comes into
your office at 6:00 pm, my my, and he has vertigo and remarks that he has
difficulty with taste and swallowing. Before you give a prescription for
antivert, is this a dysfunction of the vestibular apparatus of the inner ear? Or
is it a brain stem issue? If it is a brain stem issue, what two nuclei and
nerves are involved
Tricky case. Because vertigo has many causes, note the
DIFFICULTY with taste and swallowing. This pushes up the suspicion of a lesion
to the nucleus solitarius and ambiguus with nerves 7,9, and 10 also lesioned.
AND for the cherry, we see that all the time with a POSTERIOR INFERIOR
CEREBELLAR ARTERY stroke which supplies that area! See?
SO, don't just send them home with antivert and a
reminder slip for a return 3 month visit!! (This IS USMLE MATERIAL, but a MUST
KNOW FOR LIFE!) IF we avoid all discussion and thought of USMLE material, what
is the USE
DRAT! AGAIN...to BE VAGUE....
KEY KEY KEY point. if a patient has no pupillary
reaction to light shined on the right side but there is a reaction to light in
both eyes, when light is shined on the left. The lesion is what? NOW I change
the patient so there is pupil rxn to light on only the right side, when light is
shined in either eye. NOW, where is the lesion?
ABSOLUTELY USMLE BEGS FOR YOU TO UNDERSTAND THIS. IT
WILL BE ON YOUR TEST, IN YOUR LIFE, IN YOUR PRACTICE, IN HUMANITY FOREVER....
For the first patient, the lesion is the right CN2. For
the second, the lesion is left CN3. KNOW IT!
NEURO IS PRIZED LIKE A CHILD FOR THE NBME... so,
Say your pt comes in and you touch both her corneas one
at a time with a q-tip, and you note that ONLY the LEFT eye blinks, then which
cranial nerve is activated?
KEY TO THE CITY point!
Right CN7 (NOT THE LEFT ONE, common mistake)
will try to be vague so I don't anger azskeptic or NBME,
without peeking, what drug blocks out enzyme dihydrofolate reductase!!??? (This
is NBME's 10 ten list of favorite enzymes)
Trimethoprim blocks it. NOW FOR THE NEXT QUESTION...
valuemd.com
Here is a King Kong Koncept!
Two patients walk into your office. Listen close.
Patient A has a stroke in motor cortex that lesions UMN
tract to central facial n.
Patient B went on a camping trip and has a lesion to the
LMN CN VII.
Tell me how each patient will present on physical
exams...
Patient A will have CONTRALATERAL, and LOWER QUADRANT
paralysis.
Patient B will have same side Bell's Palsy features
(can't smile and may drool on affected side)
PROMISE ME that you will know this for LIFE for your
PATIENTS' HEALTH! because tx are distinct! Review neuro pictures, it will be
clear.
Presenting the GODZILLA of concepts:
Now it is 6:30 in your peds clinic (and you are
wondering if you are actually in a surgery rotation), and the nurse brings in a
15 year old boy with "fatty" thick calf muscles. The child trips on a toy and
strangely uses his proximal muscles to assist in standing....
Ahh...you are thinking Duchenne's (gave it away), BUT
WAIT, your attending says NO! What is the disease and what is the defective
protein? And what are the labs? Crucial...crucial... What is the only drug with
known effectiveness for his condition?????
The disease is Becker's, a milder form of progressive
muscular dystrophy.
The defective protein is DYSTROPHIN!
The labs show elevated CPK!
The ONLY drug with current known effectiveness is
prednisolone.
BAD, BAD, disease. Treat well....and be sincere.
To avoid angering AZSKEPTIC, I will make my concepts
less and less sharp and more vague and fuzzy so that I can still feel I am
helping and yet not feel worried that powers greater than me will get
upset...even though I cannot imagine why...but then then again, the world is
MAD...sometimes...
OOOHHH!! What is bigger and stronger than King Kong or
Godzilla. Maybe that new Transformers Robot. This concept is at least that big!
Anemias, SO COMMON, SO TESTED, SO SEEN, SO DIFFICULT ON
EXAMS...SO DON'T NEGLECT...
You see a female with a blood smear with RBCs small
n'round, physical is anemia, hyperbilirubinemia, and abnormal results on the
osmotic fragility test. OK OK she has hereditary spherocytosis (so common in
clinics). But of course, you need to know:
1) What protein is defective?
2) What is the inheritance pattern?
3) What are the main two complications?
4) Surgical treatment?
5) What do you, an intern prescribe to them?
KNOW IT AS YOUR LIFE DEPENDED ON IT!
1) spectrin
2) AD inheritance
3) cholecystitis and aplastic anemia
4) Splenectomy
5) They need folic acid!
What's next, yes, the MECA-Godzilla or maybe Mothra of
Concepts:
Another patient comes in weak with signs pointing to
anemia. You take a blood smear and whoa! cytopenia...blast cells, reticulocytes,
sparse RBCs. And you know this is not autoimmune because it is recent. Hold
it...she mentions she had a gonorrheal infection and is on a med. OH YES! OK, so
what is the disease, name of the med she is on AND what will be the name of the
med you give her as you transfuse bone marrow!?!?!
Copyright © 2003-2005 ValueMD, Inc. All rights reserved.
Chloramphenicol is the drug she is on that caused
aplastic anemia. AND you can give cyclosporine or a steroid along with her
transfusion. REMEMBER, aplastic anemia has many causes so be careful. Benzene,
pregnancy, CMV, HIV, EBV, and autoimmune causes are all to be considered
Can we do it over Godzilla? Yes, here is the Pillsbury
Dough Boy of Concepts:
An African American male comes into your office with
signs of very very mild anemia, almost no symptoms, a little jaundice. His main
complaint--a UTI. Your senior hints this is the most common enzyme pathology. A
smear shows Heinz bodies (review please). Now your senior starts a pimping away.
1) What is his disease?
2) Why is it so prevalent?
3) What does the enzyme catalyze? What is the end
product?
4) You grab some sulfamide and nitrofurantoin to treat
his Urinary Tract Infection and your attending smacks you on the other side of
the face that she missed before. Why was she so upset with you?
1) G6PD Deficiency
2) It confers protection against malaria
3) The G6PD enzyme catalyzes the oxidation of
glucose-6-phosphate to 6-phosphogluconate while concomitantly reducing the
oxidized form of nicotinamide adenine dinucleotide phosphate (NADP+) to
nicotinamide adenine dinucleotide phosphate (NADPH). NADPH, a required cofactor
in many biosynthetic reactions, maintains glutathione in its reduced form. RBCs
need NADPH to protect itself against oxidative stresses. (Long winded
explanation, but you have to know it., sorry).
4) You cannot give an oxidizing agent like primaquine,
choroquine, or a sulfa drug, or nitrofurantoin to a patient with G6PD def. Their
RBC will hemolyse and you will lose your license and your attending will lose
her's and your hospital will close and turn into an apartment complex.
Case: an elderly psych patient of yours complains of
arrhymias, what drug is she on? (amitriptyline or thioridazine or lithium or
olanzapine?)
she's on amitrypyline, a tri cyclic antidepressant.
(OTHER tricyclics are imipramine and nortriptyline.
Bad side effect: arrhythmias. Review MOA.
Another elderly psych patient comes to your office with
complaints of colds and a peripheral smear shows low WBCs, what drug caused
this? MOST LIKELY one..Secondaries: which two receptors does it block
Clozapine, blocks 5HT-2 and dopamine. Causes leukopenia.
Yet another elderly psych patient comes into your office
this time with constipation and rigid muscles and (hint other antimuscarinic
sym). He was given a med FOR an ACUTE psych episode where he shouted and hit
others. What is the drug? 2nd: Receptor/MOA? And Name at least two other drugs
in this family
Answer: He is on Haloperidol (used for Positive symp, in
ACUTE cases), the drug blocks D2 receptors, and fluphenazine and thioridazine
are within this family named NEUROLEPTICS,
assoc of course too tardive dyskinesia!
(these are different from the atypicals, make sure you
know the atypicals are risperidone, but also clozapine and olanzapine--neg
symptoms controlled more, diff receptors involved)
An M&M candy question:
Woman walks in with chronically sore right knee. She is
neg. on labs for rheumatoid factor. Under microscope, you see crystals appearing
shorter and often rhomboidal. Under a polarizing filter, crystals do not change
color depending upon their alignment relative to the direction of the red
compensator.
What on earth does she have and what is the name of the
crystals deposited!
Answer IS NOT rheumatoid arthritis or gout, BUT, the
answer is pseudogout, and you see calcium pyrophosphate crystals as ooposede to
birefringent needle crystals in gout! P=Pseudo=Positively birefringent
an M&M peanut candy question:
Next a child enters your clinic with chronic diarrhea
and fatty stools. A younger med student asks you if he has Cystic Fibrosis,
Giardia, or Ulcerative Colitis, or Chron's. But, YOU go further and order labs.
They come back with weird D-xylose test, anti-IgA antibodies, B-cells in the
lamina propia
You go Hoorah because you know:
1) Disease
2) Etiology (viral/immune/etc)
3) is there a specific substance or drug he should take
or avoid?
1) He has Celiac sprue
2) Autoimmune/hereditary/Europe
3) Avoid gliadin wheat in diet
An OVERSIZED CANDY question (BIG FAVORITE)
Next, you have a older African American male who comes
in with chronic CHF and began a new medication. But he suddenly one morning
found his left foot joints swollen and so tender even the weight of the
bedsheets are so painful! (BIG HINT COMING). Labs come back and you see crystals
with needle shapes (shown a pic), (-) birefring...
But NOT SO FAST, THIS IS USMLE!
1) Tell me the likely med he was on and at least two
other meds which could cause this condition.
2) What is the short term and LONG term treatment?
3) MOA (Mech of Action) of disease?
4) What compound builds up?
5) What foods should he avoid?
6) Bonus Biggie: He had a great grandfather who had
similar symptoms but was mildly retarded and scratched himself like crazy! Dx?
) Thiazide diuretics, Cyclosporine, Nicotinic Acid and a
LONG LONG list can do this.
2) Colchicine short term/and Indomethacin and
Allopurinol long term
3) Uric acid precipitates from supersaturated
extracellular (ie, synovial) fluid. The resulting crystals stimulate
phagocytosis by neutrophils and initiation of the inflammatory cascade. OUCH.
4) PRPP
5) (Purine rich foods (especially of anchovies,
sardines, sweetbread, kidney, liver, meat extracts)
6) Lesch-Nyhan syndrome, (a NBME favorite)
NOT IN THE FORM OF A QUESTION BUT THIS IS A LIFE POINT:
People keep missing Goodpasture's and Wegner's, you
know, the diseases with BOTH kidney damage and Lung damage. Can't discern.
POINT IS THAT WITH WEGNER'S GRANULOMATOSIS LOOK FOR
UPPER RESIRATORY SIGNS LIKE SINUSITIS TO DIFFERENTIATE ON THE BOARDS, ER, I MEAN
CLINICS!!!!!
So hard, but the reason so many friends of mine failed
is because they could not differentiate the subtle differences of:
Case; Pt comes in and says she has: Inability to eat dry
food, such as crackers, which sticks on the roof the mouth Tongue sticking to
the roof of the mouth She always has to be putting a glass of water on their bed
stand to drink at night. She has difficulty speaking for long periods of time,
and her eyes are dry and her right wrist is starting to hurt.
HERE'S THE MONEY:
1) Disease?
2) Which HLA is involved?
3) Drug of Choice (DOC)?
4) What dx, is she at increased risk for?
Answers:
1) Sjogren's syndrome (they'll give choices like
Reiter's, PSS, etc.)
2) HLA 3
3) Pilocarpine to stim. secretions! And eye drops!
4) a lymphoproliferative disorder
This one's is KEY:
Next, a male patient comes in with myalgias and low back
pain. He also has reddish (infection like) tinge on his left eye. Your
subordinate med student yells out! "Ankylosing spondylitis!, Rheum. Arthritis!.
But not so fast! You note that labs came back positive for HLA B27, BUT so did
chlamydia culture!!!!!
You scold your med student.
1 Why? Because he had picked the wrong disease, the
right one is?
1.. Reiter's syndrome!
The KEY finding is the Chlamydia or could be Salmonella
and urethral connections. The closing of the triad is the conjunctivitis. Don't
be tricked my brothers and sisters!
YOU COULD BE ASKED BY YOUR ATTENDING/BOARDS WHICH BUG IS
HE MOST SUSCEPTIBLE TO...(they have millions of ways to twist the questions but
the concept remains the same!) MINOR ADDENDUM on hy concept 129, Reiter's= male
Sjogren's=female
This one's is a MAGIC KEY:
Next, another male patient comes in with myalgias and
low back pain! He also has reddish (infection like) tinge on his left eye.
HLA-B27+ Unreal! You are about to say that you have another case of Reiter's,
but you note his labs reveal cardiac anomalies....Your subordinate med student
yells out....What?
(This time your med student is RIGHT!)
This one is ankylosing spondylitis, compare carefully
with Reiter's. One triad has the heart, the other has the urethra!!!! Got It?
Got Milk? Got Love? Got God?
Oh boy..
Another patient comes with lower back pain and the usual
suspects. But she says her arthritis often comes with a fever and is WORSE IN
THE MORNING! You know this dx of course, you know it is NOT osteoarthritis,
which has osteophytes, but what if I presented a pic of the hands with arrows to
all joints. WHICH ONE(S) OF THE THREE JOINTS ARE AFFECTED (DIP, MCP, PIP)? (See,
you HAVE to know pictorially the secondaries.)
Besides NSAIDS, what other three drugs are often tried?
She has rheumatoid arthritis, + rheumatoid factor. This
autoimmune dx has systemic symptoms like her fever and malaise. The answer is:
MCP and PIP joints
OSTEOarthritis has DIP joint inflammation
Q. So depressing...a young girl comes into your office
with a fever and history of weakness, infections, cardiac flow murmur and
petechaie. You order a CBC and find that her smear shows what looks like
immature leukocytes...but you cannot seem to distinguish between ALL and AML
(THIS IS A MAJOR TEACHING POINT, BECAUSE THE SMEARS CAN LOOK VERY VERY SIMILAR
AND THERE WILL BE BOTH ON THE ANSWER CHOICES, SO LOOK IT UP IN A HISTO ATLAS!).
You sud
TOMMYPOSTS 2 ( 149-200)
Q. I present you with a LM image of the thyroid with
arrows everywhere. Tell me the cell and the exact location on the image where
calcitonin is secreted
A. The parafollicular or C-cells secrete calcitonin.
Make sure of it!!!!
Q. The parafollicular or C-cells secrete calcitonin.
Make sure of it!!!!
A. It binds TUBULIN AND BLOCKS POLYMERIZATION OF
MICROTUBULES, THUS BLOCKING MITOSIS.
PARASITE S
Q. NBME wants you to understand all the HELMITHS, one of
my students said he got a whole block of them! (he was prob. exaggerating
though)
So, one by one...
A pt of yours comes in with abd pain after eating raw
fish. He looks lk he has cholecytitis. What drug do you give? What is the bug?
(PIC GIVEN)
A. This is a fluke (looked weird like a worm), Bug is
CLONORCHIS SINENSIS, treat with PRAZIQUANTEL.
Q. A young boy comes to your clinic with diarrhea after
eating "mud pies", what is the bug and the tx?
A. But is the infamous Strongloides stercoralis, tx.
with Thiabendazole
Q. Oh, please note that ALL OF THE CASES YOU WILL SEE ON
THE USMLE WILL LIKELY HAVE A HISTORY OF TRAVEL!
That said, you have a male pt, 30, with epilepsy coming
in after eating "raw pork". What is the helminth and the treatment?
A. the bug is a tapeworm--Taenia solium and you give
Praziquantel and Niclosamide and a steroid to relieve CNS pressure because this
bug swims everywhere, even in the CNS! (Pic given. slide)
THE CASE WILL give travel to Southeast Asia or maybe
Africa.
Q. A traveler comes from Africa (could also be a West
Alaskan Indian), and had told you he ate coyote and dog poop as a college dare!
He is ASYMPTOMATIC but you see cysts in his lungs on X-ray. What's the bug and
TX?
A. Give him Albenza which is trade name for Albendazole
which works by depleting ATP, and the bug if asked is Echinococcus. For this and
the other tapeworm, Taenia, the guy could be scratching his rear end a lot so
wash your hands!
Q. A pt of yours came back from Brazil and has dysuria
and nausea. Plus he told you he ate a bunch of snails at a local exotic
restaurant. What's the bug and tx?
A. He has the famous Schistosoma Haematobium. In US it
is rare because they don't usually eat a lot of snails! But know this fluke has
many subtypes and can clinically present LIKE ANTHING! The NBME will have to be
very specific. One key is it results in granulomas! Treat with Biltricide which
has generic name Praziquantel.
Q. A pt returns to your clinic fr. Latin America with
signs of Asthma. But a stool sample shows a round curved worm (slide is given).
YOUR ATTENDING TELLS YOU THIS IS THE MOST COMMON HELMINTH INFECTION IN THE
WORLD! You are looking at what and will treat with what? AND also seen is what
is MOA of the drugs? BONUS, you must know.
A. YOU are looking at ASCARIASIS. So common. Treat with
Mebendazole (WHICH WORKS BY BLOCKING GLUCOSE UPTAKE). AND pick Pyrantel pamoate
(WHICH IS A NEUROMUSCULAR BLOCKING AGENT WHICH PARALYSIZES THE ROUNDWORM). I
THINK Kaplan AND Error! Hyperlink reference not valid. mentions these bugs but
not ALL THE NECESSARY and tested material is given.
This is FECAL ORAL SPREAD
Q. Don't you dare confuse this with Ascariasis. This
nematode is quite prevalent in the US. That will be the give away and so will
the fact that your peds patient is scratching his behind. Give me bug and drug
A. Watch out, this one I am told is confused with
Ascariasis, but it is Enterobius vermicularis and the case seen is a kid with an
itchy "butt".
Treat with Pyrantel pamoate.
Q. This is a BIGGIE in the US, so you don't need a
history of travel: HERE goes:
A woman patient comes to you after sampling raw spiced
pork sausage links (classic case). She has myalgias and PERIORBITAL EDEMA.
What's the bug and drug and MOA of drug?
A. This helminth is the ubiquitous Trichinella. Very
common the US.
FOR ALL OF THE HELMINTHS QUESTIONS, THE NBME USUALLY
GIVES A EM OR HISTO SLIDE BECAUSE MANY OF THEM PRESENT WITH SIMILAR VAGUE
SYMPTOMS LIKE DIARRHEA, MYALGIA, ETC. SO WATCH CAREFULLY FOR THEIR CLUES WHICH
THEY HAVE TO PROVIDE.
Treat Trichinella with Thiabendazole!
Again, Trichella is assoc. with pigs if all else fails.
Q. This helminth is rather distinct so you likely won't
have trouble!
Hey, you get a patient who came from a trip
photographing wild animals in AFRICA (let's say Ethiopia). He comes to your
clinic and you see hypopigmented (leopard spot like) lesions on his legs. He
photographed from a riverbank (HINT). Give me bug and drug and MOA of drug?
A. HERE we are:
This is "river blindness" or Onchocerca volvulus. BUT
THE MOST COMMON PRESENTATION IS NOT BLINDNESS WHICH IT MAY EVENTUALLY CAUSE, BUT
SKIN LESIONS!
Transmission is by black flies, along riverbeds, mostly
all in Africa. Treat with IVERMECTIN, which works and binds selectively with
glutamate-gated chloride-ion channels in invertebrate nerve and muscle cells.
Q. Here is a MUST KNOW:
A post college grad comes to you who came back from the
PEACE CORPS. She volunteered her time so well, but this is a crisis. She is thin
and athletic, and pretty but sadly one of her legs looks swollen like an
ELEPHANT'S. What's the bug and drug you give?
A. This is too bad, she was trying to do good...This is
a classic NBME example and very common case of Bancroftian Filariasis or
Wuchereria bancrofti where a person is bit by a mosquito and has lymph node
swelling everywhere. Common is a foot and/or leg elephantiasis. Treat FAST with
Ivermectin or Diethylcarbamazine or she will lose her precious leg
Q. While we are on the subject of these parasites, here
Nematodes, we spoke of a drug often used called Mebendazole. What is the MOA?
A. Mebendazole is often used for treatment of
eosinophilic enteritis; inhibits microtubule polymerization by binding to
cytoplasmic b-tubulin; by affecting parasite's intestinal cells, prevents use of
nutrients and essentially starves parasite to death! Sorry parasites...esp. if
you are Buddhist, I guess even a parasite would be sacred!
Q. We are slowly winding down the NBME's list of
parasites...
BUT HERE IS A BIGGIE THAN AFFECTS UP TO ONE BILLION
PEOPLE!
You see one of your dear patient who came back from
Puerto Rico (could be other places too). Now, he complained that a month ago he
started itching, THEN coughing, THEN having diarrhea! Terrible! He is begging
you to diagnose him because he is starting to look anemic!!
What is the bug and drug???????? Oh, also what does his
blood smear show?
A. You are staring at Anclostoma or HOOKworm disease
which is SOOOOO prevalence around the world. You should look for travel history.
Another related hookworm is Necator Americans.
When the bug hatches in the intestine, you get IRON DEF.
ANEMIA, so blood smear will show microcytic RBCs.
You treat with Albendazole or Mebendazole.
Q. This is a mediumee, but you have to know this too:
In your peds clinic, a kids comes in with vision
problems and his mom said he had gotten a couple of new puppies. He also has
wheezing urticaria and he lives in Southeast US. What is the bug and drug?
This is kinda hard because the differential is HUGE, but
the association of:
puppies=southeast US=eye stuff gives it away easy. OK,
so go ahead!
A This is classic for Toxocariasis. You treat with a
drug called Diethylcarbamazine but Thiabendazole can be used too. Puppy poop has
this. You cannot miss this and accidentally treat with antibiotics thinking you
have Pasturella (bacteria).
So how will you KNOW? Well, the NBME will give you a
picture and labs. Remember eosinophilia? It can be as high as 80% with high
IgM!!!!! Oh, I should make that my next CONCEPT!
We have been going over the parasite bugs the NBME WILL
test you on. And they frequently have things that will distinguish them from
bacteria.
1) You may see a clinical history with stages (first
intestines, then lungs, etc. because these guys lay down larvae)
2) You MUST look for the clue for labs and sometimes my
students say they completely skip the lab section because they are in a hurry.
ONE TWO MILLIMETER SPACE has the info HIGH EOSINOPHILIA! If you miss this, you
may treat your patient with antibiotics on your test and get the question wrong.
3) Also, a lot of these bugs are not endemic to the US.
So look for a history of travel.
4) There are only a few drugs here, so please don't
forget them
valuemd.com
Q. Here is one that has been reported POPing up, so you
better know it because it was in a newspaper and...
A Japanese family just came to the US 3 months ago and
then went straight to your clinic. One of the kids has serious pulmonary signs
and was treated for Tuberculosis. HE IS NOT BETTER. Worried parents gave you a
history that he was treated by his older grandma in Japan with raw crayfish for
health. You are glad they came to you because you know you are not looking at TB
but rather....? And you will treat with ???
A finally the drug was what MOA????
A. This is popular with NBME because doctors mistake
this deadly PARASITE with other things like TB or coccidomycosis and then a BIG
lawsuit occurs.
So here you have a big clue about the Japanese ethnicity
and the ingestion of crayfish and the lung findings.
This is pathognomic for....Paragonimiasis.
Please treat with Praziquantel. You must know...
Praziquantel again that it inhibits microtubule
polymerization by binding to cytoplasmic b-tubulin; by affecting parasite's
intestinal cells, prevents use of nutrients and essentially starves parasite to
death. I think I mentioned this before, but I am repeating it because it is very
important.
thought as I finish up the parasites that you really try
to LUMP them somehow. I think of these because they work for me, but you should
use some pneumonic because they are kinda hard to distinguish.
Taenia> Sounds like Tan-in-sol (sun) while Praying
(praziquantel)
[These are weird pneumonics but I think you need some
and personalize them like since I like to pray a lot, I can think of Tanning and
Praying so I associate Taenia with Praziquantel for the drug treatment]
Strongyloides> "strong thighs" (Thighs sounds like)
Thiabendazole
Onchocerca > "On cocaine via IV" (IV for Ivermectin)
Corny, but the parasites need this because their names
are weirder.
Again, try not to confuse the parasites and bacteria.
Look for Travel, look at labs, and look for symptoms that wax and wane over a
month as the parasite goes through larvae stages
Copyright © 2003-2005 ValueMD, Inc. All rights reserved.
Let's move on,
I'm quizzing you from before...
Remember my original case of the 2 year old with Chronic
Granulomatous Disease which we discovered is REALLY BAD, what is the name of the
enzyme that was lacking? Do you remember? Were you paying attention? If not,
that is OK, I am not upset at all, but you should keep reviewing my HY posts!
A. Answer is NADPH OXIDASE
Our phagocyte oxidase system is an NADPH oxidase enzyme
complex consisting of 4 component proteins. Membrane-bound gp91 and p22 make up
the b and a subunits of the heterodimer cytochrome b558 portion of phox gene.
But for us, we need to only remember NADPH OXIDASE, not distractors like NADH
OXIDASE or NAD+OXIDASE or NADPH REDUCTASE!
IMMUNO
Q. The NBME wants you to know a simple point about VDJ
recombination. It is a very basic concept which explains antibody diversity. But
if I say it exactly I would be repeating NBME material b/c it is so specific so
instead I'll ask you to read on it for just two seconds. Of course, if I can
think of a way to present it indirectly which I am always doing then I will. But
HERE, let me ask you guys, at the very least, which chain, the H (Heavy) or L
(Light) carries the 3 gene segments? And in CLASS SWITCHING, which antibody,
IgM, IgG, IgA, IgD, or IgE is most "primitive"?
BIG CONCEPT, and some tests had a disproportionate
amount of IMMUNO.
A. While you read up on VDJ, know that the Heavy chain
has the VDJ and there is DNA rearrangement. Know the L and H chains are made
SEPARATELY in the CYTOPLASM by means of DISULFIDE BONDS!!! The LAST step is the
addition of the CARBOHYDRATE moiety. (Look and remember my capital letters...).
Second, at first, all B lymphocytes carry IgM specific
then after undergo class switching to the others (If you were lost here, YOU
REALLY NEED TO KNOW IMMUNO AND REVIEW)
Q. OK, here we go, a patient presents with dyspnea,
endless differential, but here are the secondaries for ARDS:
1) Pretend you already diagnosed ARDS, a deadly illness,
what cell is responsible for the distress?
2) OK, they NBME wants you to understand they will ask
you cases (so what are the main causes?)
3) We know there are a lot of causes of Pulmonary Edema,
but how can you differentiate ARDS edema and Cardiogenic edema?
ARDS carries a 50% death rate. Know it or Die!
A. 1) Neutrophils
2) Ischemic shock/Endotoxic shock/DIC; breathing really
hot air; acute pancreatitis (weird, eh?), drug use
3) It is called Pulmonary Capillary Wedge Pressure test
(LV) LOW in ARDS, HIGH in CARDIOGENIC!
Q. THIS IS A GREAT CONCEPT:
OK, let's dabble in immune just for a change of pace,
for just a second, we will revisit later. We need to know the following..
Whew! I am getting tired again, I need a break so I will
lump a couple of KEY factoids:
1) Could you pick out the right ratio of T to B cells?
2) YOU know the T cells pass through thymus for thymic
education (review if what I just said is foreign), do the B cells pass thru
thymus? If not, where (amongst a series of choices of course)?
3) Which IL type boosts up T helper cells?
A 1) 3:1
2) B cells don't pass thru thymus but the precursors
mature in GALT and Peyer's patches.
3) IL-2
ALL OF THOSE ARE MUST MUST KNOWS, THE CONCEPT ARE IN THE
BRAIN OF THE NBME, BUT I PICKED MY OWN WAYS TO MAKE SURE YOU UNDERSTAND!!! KNOW
THAT NBME WILL ASK THE ABOVE CONCEPTS IN WEIRD WAYS, SO AFTER THE FIRST READING
OF THE QUESTION, YOU WILL BE LIKE "HUH?" THEN FOR EXAMPLE THE ABOVE THREE
CONCEPTS WILL COME TO YOU AND THEN YOU WILL SAY "OH, I KNOW THIS!"
Q. OK, after this I need a few minutes break....
OK, remember that to really learn you need to compare
and contrast so that is why I think I will "LUMP" my HY by subjects if I can at
times. To know what is BLACK, you need to see WHITE, etc.
SOO>>>...
We know IL-1 and TNF-alpha makes your temperature go up,
so
which IL revs up IgA?
A. IL-5
Q. All, the NBME likes to ask things in weird ways:
We just covered helminths. Which IL is most involved?
A. BIGGIE POINT: SAME ANSWER AS BEFORE IL-5. That is how
NBME tricks you. You may "memorize" what I just asked, IgA is stimulated by
IL-5, but then when I bring up the concept that IL-5 revs up both IgA
(intestinal mucosa) and Eosinophils, your brain may hiccup! See, are you
starting to understand????
Q. IMMUNO:
Which mediator is responsible for endotoxin septic shock
and makes you have cachexia (like in cancer)? And then, what is the MECH?
HARD HARD, BUT MAJOR POINTS.
A.
TNF alpha,
1) secreted by MACROPHAGES
2) It causes cachexia by inhibiting lipoprotein lipase
in adipose tissue.
ALSO, FOR ICING ON THE CAKE, KNOW TNF-A also revs up
IL-2 and B-cells.
Q. Here's one more at least:
A patient of yours is predisposed to TYPE I
hypersensitivity. Which IL is mostly responsible. This is a great great
question.... look below after guessing...
A. Surprise, I bet you guessed IL-1 or TNF-a BUT
NNOOOOO!
The answer is IL-4 IL-4 revs up IgE, WHICH THEN is
responsible for anaphylactic shock.
THIS IS AN ULTIMATE CONCEPT. MANY STUDENTS JUST LINK
IL-4 TO IgE, which is fine because some versions of the test will be that
straightforward. BUT SOME OF THE TEST TAKERS WILL BE ASKED JUST LIKE I JUST DID,
INDIRECTLY AND WITH A SECONDARY. It is not a HARD question, but you can GET
EASILY DISTRACTED!
DO YOU GUYS AGREEE????? YOU HAVE TO PONDER AND REALLY
THINK!
Q. Some of you will be asked:
Which IL revs up stem cells?
A. WOW, the answer is IL-3
But some of my students got it wrong because they read
Error! Hyperlink reference not valid. and it said
IL-3 = Bone marrow.
So they Blanked! They KNEW the answer, but they blanked
because they did not stop to recall that stem cells are in the bone marrow.
See, see how easy it is to get tricked? Please let me
know if you agree.
© 2003, 2004 ValueMD Incorporated. All rights reserved.
Q. We MUST BE LUMPERS, (lump info together), it is more
efficient, believe me it is educational theory...
So, which IL is part of the acute phase other than IL-1?
Also, which IL does the same as GM-CSF?
A. IL-6
then IL-3 is like GM-CSF!!!!
Q. You KNOW MHC I = T=cells
AND MHC II =B-cells (these are loose associations), but
tell me,
Mature MONOCYTES secrete which two cytokines?[/b]
A. Mature monocytes are macrophages and they are the
ones that secrete IL-1 and TNF-alpha
Q. Great question:
Give a place where macrophages are fixed in tissues and
name a mediator that activates them to move!!!!!
SUPER DUPER POINT(s)!
A. Kupffer cells of the LIVER and C5a!!!!
YOU MAY THINK I AM BEING TRIVIAL, BUT HINT HINT, I AM
NOT!!! KNOW THESE!!!!!!!! DON"T FORGET!
Q. Differentiate NK T-cells with cytotoxic T-cells!!! It
is things like this which keep students from passing!
A. NK, or natural killer cells specialize in killing
virus infected cells and cancer cells but unlike cytotoxic T cells, THEY ARE
ACTIVE WITHOUT PRIOR EXPOSURE TO THE VIRUS, ARE NOT REVVVEEED UP BY CONTACT, AND
ARE NOT SPECIFIC!
AND, THEY DO NOT HAVE TO PASS THRU THE THYMUS TO MATURE.
(You DO know the cytotoxic T-cells have a receptor, NK's
don't!)
(NK's don't need MHC to act)
Since NKs activated by IL-2 are being used in cancer
research, is there any wonder that what I JUST WROTE WILL BE ON YOUR TEST?!
Q. IT is the WONDER WOMAN of concepts:
Which ILs rev up growth and maturity of B-lymphocytes?
A. The answer is IL-2,4,5!!!
Say it again, 2,4,5
Again, 2,4,5
You "may" be shown a pic.
I KNOW THIS STUFF IS HARD AND BORING AND SO ROTE MEMORY,
BUT IT IS HY, YOU MAY NOT THINK IT IS, BUT IF I CAN HELP EVEN ONE OF YOU GET
THEM ALL STRAIGHT, WE WILL DANCE TOGETHER IN HEAVEN.
Q. This is the KENTUCKY FRIED CHICKEN 20 PACK concept:
You all know CD-8 binds to MHC-1, but if I give you 5
mult choices, which IL revs it UP!!!!!
A. IT is IL-2 !!!!!!!!!!!!!!!!!!!!!!!!!!!! Which also
stimulates itself (Kinky, eh)
NBME LOVES THESE, DRAW A PICTURE UNTIL YOU KNOW IT COLD,
IT IS VERY CONFUSING.
Q. LOOk, you all know all T cells have CD3 (That factoid
alone can help eliminate wrong choices like the leukemia stuff), but, what does
CD3 do?
Is it using the cAMP pathway?
A. This,,,,my friends, is the BATMAN of facts:
CD3 molecules transmit into that the antigen receptor is
OCCUPIED!
This works NOT by cAMP but by the IP3 Ca pathway.
(Music PLaying..) Instead of hearing "This is CNN", you
are hearing "This is the NBME"
WE ARE IN THE NBME MATRIX, where's Keanu?
RE: HY Concept 182,
KNOW COLD that B Cells do not have CD3!!!! AND
B-cells have IgM on the surface BUT T-cells DO NOT!!!
Repeat this over over over over over over over again!
Q. This is the Green Lantern of concepts:
Which 3 cytokines bring neutrophils to the scene
(pretend I show you a histo slide pointing to a neutrophil and THEN ask the same
question)
Secondaries, secondaries...
A. They are
IL-1, IL-6 and TNF-alpha = acute phase response
Are We Getting Anywhere Yet?
Q. FRIENDS, I told you IL-3 revs up bone marrow, now
tell me:
What is different about the T-cells that make IL-3 (vs.
others)?
Now tell me which mediator is used in cancer
chemotherapy to rev up some neutrophils to stave off infection?
A. IL-3, unlike the others are ACTIVATED first
AND WHAT A CONNNECTION:
IL-3 IS SIMILAR TO GM-CSF (colony stim. factor)
KEY: IT IS GM-CSF THAT IS USED IN CHEMOTHERAPY
Q. Oh boy, now we get to complement!!!
This can get really really confusing! If I merely post
my HYers, you will be lost unless you quickly review an IMMUNO book and look at
the COMPLEMENT CASCADE. You WILL be asked which complement factor does what,
NBME is very specific! There are literally 100 questions possible and more just
on the diagram of the complement cascade!
So, I will ask only one or two questions here:
HOPEfully you know for example that C3b opsonizes
bacteria, but which factor (s) neutralize viruses?
A. C1, 2, 3, and 4 neutralizes viruses in the CLASSIC
pathway, and complement:
1) kills GRAM-NEGATIVE BACTERIA
2) IgM and IgG activate complement in the classic
pathway,
3) But, Endotoxin and nonspecifics work in the
alternative pathway!!!
(THE NBME can ask SO many questions on just the words
above, that is why this test is concept based. They could give a list of bugs
and ask which one does C3a work on and you are scratching your head, but then
you notice that all the bugs are gram positive except ONE! And then you will
pick the Gram NEGATIVE bug!) (You may be distracted for 10 minutes trying to
recall what C3a does (anaphylaxis), but YOU WASTED YOUR TIME!
Also, of course, I could ask you what OTHER complement
works like C3a? Then you have to know it is C5a....
And so on , and so on and so on. Do you see how
EVERYTHING IS INTERCONNECTED AND WHY SIMPLE RECALLS DON'T WORK? If you take the
time, you can see into the NBME's mind and KNOW it all.
Q. So after reviewing, which complements are part of the
membrane attack complex (MAC)?
And, which complement do both pathways meet at?
(two questions of candy bars
A. C5b thru C9 = MAC
And both classic and alternative pathways meet at C5.
Tattoo the above facts into your brain!
Q. CANNOT BELIEVE IT, I ALMOST FAINTED BECAUSE I ALMOST
FORGOT TO TELL YOU THAT THE COMPLEMENT SYSTEM MUST BE REGULATED OR..
The system can overreact and destroy our good cells.
So..I told you C1 is an esterase right (no, I didn't, and there is a another
possible question!). OK, what factor blocks C1 and what happens if you lack C1?
Next, give me another case: Human cells have DAF or
(decay accelerating factor) to protect themselves. What factor does DAF work on?
What diseases arise if the above controls are LOST?
A. Your body has C1 inhibitor (rather unoriginal name)
to block C1.
Your DAF blocks C3b thus protecting your cells.
If C1 inhibitor and/or DAF is gone, your capillaries
will weak, you will get PNH (hemoglobin in your urine at night) OUCH!
Q. SPEAKING OF IMMUNO, YOU WILLL SEEEEE..
Interferons, becuase they are DRUG and part your body's
defense..
They are GLYCOPROTEINS (Everything I sort of BOLD is an
unforgettable word/point), and they protect healthy cells and virus
replicaition. KNOW there are alpha, beta, and gamma interferons:
alpha (fr. WBCs) interferons and beta (fr. fibroblasts)
are triggered by viruses and target viral mRNA.
1)NOW, GAMMA interferon are the third interferon, they
are produced by?
2) They active what process?
3) Gammas rev up what cells?
A. 1) Gammas are made by activated CD4 and CD8 T-cells.
2) THEY rev up PHAGOCYTOSIS.
3) This by those NK, macrophages, neutrophils and revs
up MHC I and II antigen presentation, which is like a plate of food that
attracts the phyagocytes. Finally, Gammas revs up B-cell antibody production.
valuemd.com
Q. ok, BIG POINT:
You have to understand the basics of activation. IF say
an antigen presenting cell (Dendrocyte, B-cell, Macrophage) [T-CELL ARE NOT
ANTIGEN PRESENTING!!!!], binds an antigen (virus), then CROSSLINKING occurs and
the cell gobbles up antigen and then PRESENTS IT ON THE SURFACE. A lot of you
know that, but THEN you must follow the storyline. And lovely young helper T
cell comes along and attaches or holds hands with the antigen presenting cell.
THEN, the T-helper cell "blushes red" and is so happy she throws out IL-2, IL-4,
and IL-5 that stimulate both B-cells and T-cells (IL-2 here). Some of the
activated B-cells from what kind of cells in the secondary response and what is
the most common surface Ig?
A. A few activated B-cells turn INTO MEMORY CELLS
(BEFORE, THEY WERE PLASMA CELLS), and they usually have IgG on top of them for
rapid response to reexposure.
IMMUNO IS REALLY TOUGH SO I HOPE YOU GUYS DON'T GET TOO
MANY QUESTIONS, BUT THE GOOD THING IS THAT THE NBME IMMUNO QUESTIONS OFTEN RANGE
FROM SUPER BASIC TO SUPER DUPER HARD.
GET THE EASY ONES RIGHT!
Q. cannot break the copyright rules, but there was a
question where the concept I can describe so you won't miss it.
IT is very very basic. They, many of you will get
variations of the same concept where you are given a pic. of that infamous Y
shaped Antibody and there are like a thousand questions about same concept.
Like, let me make up something original but applicable:
1) Is the Constant Light Chain region part of Fab
fragment or Fc fragment?
2) Is the CARBOXY terminal part of the constant or
variable region?
(There are ways with arrows to address this, so know
this)
3) What kind of bonds KEY PT, holds the chains together?
A. 1) Fab fragment
2) Heavy chain
3) Disulfide bonds, know which drugs can cleave
these....
GET the concepts
Q. 1) Give that famous Y antibody with arrows, where
does complement bind (Fc or Fab portion?)?
2) POINT to where CMV virus attaches.
3) Where can I find sugar side chains?
A. 1) Fc portion
2) Both L and H hypervariable regions
3) Fc fragment
Q. KNOW that LIGHT chains only lie in the AMINO TERMINAL
and are part of only the Fab fragment!!!!
Q. SUPER DUPERS:
MOst know that babies have IgG from Mom until 6 months
of age (a key pt like ..uh on a graph), can the baby defend itself against
syphilis at one month?
A.
YES, the feus can make IgM.
Q. 1)Whoa! you see an EM of an Ig that is a dimer. Where
in the body is it found and MOA? Does this fix complement?
2) Whoa! you see an EM of an Ig pentamer! What's so
special here?
3) The only Ig to cross the placenta, this dude is most
dominant in 2nd response about is what percent of total Ig?
4) You see an Ig in a baby's cord blood that the
IMMUNOLOGIST tells you is rather unknown what it does? what is it?
5) You see an EM of an Ig that binds a basophil on a
smear! Does this one fix complement? What else is special here?
A. 1) IgA (also can be monomer). See in saliva, tears,
gut, vagina, etc.
2) IgM is the PRIMARY response, most efficient in
aggultination
3) IgG of course - 75% of all
4) IgD
5) IgE, anaphylactic allergies DOES NOT FIX COMPLEMENT.
[for example you may be asked a patient has a hookworm
infection, which Ig is reved up? = IgE, right, remember?]
Q. OHHHH! Superkey!
T/F, Delayed hypersenitivity is a function of antibodes,
right, huh?
A. NOOOOO.
Type IV Delayed is CD4 T-cells! Common mistake!
Q. Great question:
A patient of yours tries a new cosmetic cream and then
presents in a couple of days with eczema. Which HYPERSENSITIVITY (I, II, III,
IV) is this?
KEY POINT, I won't bug you with all the possibilities,
but you must MASTER ALL THE FOUR HYPERSENSITIVIES AND THE POSSIBLE OFFENDING
AGENTS, THEY WILL BE ASKED!
A. This is not not not Type I (common mistake), but Type
IV. Often is you see stuff like a case of neomycin or soaps, and then a reaction
a day after after reapplication, you are looking at TYPE IV. Review al of
them...
like Glomerulonephritis is TYPE III (NOT TYPE II)
like Goodpasture's is TYPE II (NOT TYPE III)
(see look above, some student just think kidney
stuff-Type III, and they get stuff wrong!)
like the complement system is activated in TYPE III
like Coombs Test is associated with TYPE II
Q. I heard of 500 questions/ways to address the concept
that:
You know T-cells have CD3,4,and 8 on their surface.
Which CD is a suppressor function?
A. YEAH, CD8 has both cytotoxi and suppressor functions
they suppress B cells and cellular immunity.
Q. Quiz to know if you are reviewing wisely:
1) What cells are involved in AUTOIMMUNITY?
2) Graft rejection?
A. 1) B cells
2) T cells
Copyright © 2003-2005 ValueMD, Inc. All rights reserved.
[I CONFESS I CANNOT COVER ALL OF IMMUNO, IT IS SO
CONFUSING AND ENDLESS, BUT I JUST PRESENTED SOME OF THE HIGHEST YIELDING STUFF
Q. There exists out there a diagram of the difference
between:
TH1 and TH2 cells. YOU HAVE TO KNOW THE DIFFERENCES!
1) Which ILs are made by what?
2) IL-12 induces TH1 or TH2
(you have to read these stuff also on your own)
A. Th1 revs up CD8 (T-cells) and macrophages (APCs)
Th2 revs up B-cells via IL-4 and IL-5
Gosh these are ultra high yield but so much I think I
need to SCREEEAAMMM!