TOMMYK POST 149-200

[mommd]

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




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


[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!

[Anonymous]

i am overwhelmed
thank you again

[Anonymous]

thank u sooooo much...i have been wanting to do it but havent gotten around to it....i really appreciate it.

[mommd]

HERE R THESES POSTS

[mommd]

here are early posts

[kris2c]

149-200 from mommy