Pharm Board Review Book

[Pox in a box]

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What book is everyone using besides First Aid for their board review? Katzung's text and review book are out of the picture. They are too lengthy for a high-yield, short board review. I'd also like to think that the Kaplan pharmacology (Trevor is a bit much) is out of the picture too for the same reasons as Katzung.

Any suggestions/experiences? Hoping to hear from bigfrank, Idiopathic, Long Dong, Zedpol, Jalby (yeah right 🙂 ), HYJunkie, Hiddentruth, and any others. TIA.

 

[omarsaleh66]

i did the pharm appleton lange 125q section from the Appleton Lange USMLE Queston book by Michael King the day before the shelf to prepare for the pharm NBME. it had pretty good q in my opinion. they were written by katzung. helped me get a 620/91 on the shelf. I dont know how much it helped but it did help me understand some of the difficult pharm concepts that u might not get from other sources.


EDIT: also, knowing mechanism of antimicrobials, antiparasitics is HY and so is the methods of resistance to these drugs. Also, knowing all those anticonvulsants, CNS and antidepressants is good too.

later

 

[HiddenTruth]

EDIT: also, knowing mechanism of antimicrobials, antiparasitics is HY and so is the methods of resistance to these drugs. Also, knowing all those anticonvulsants, CNS and antidepressants is good too.

later

Yo man, i think you missed cardiac, anticancer, resp, gi, inflammatory, immunologic drugs in that "HY" section of yours. 🙂

Pox: I don't know what others are doing out there, but I did Kaplan, and annotated my FA (it took FOREVER!). But, I thought it was a good text--but our pharm was taught really well too, (perhaps, the only class) so i may be biased.

But, from others have said, FA is all you really need. I don't know the validity of that, as I haven't taken the real deal yet. Maybe Automaton can shine some light, as he took the test already. Good luck!

 

[Jalby]

Any suggestions/experiences? Hoping to hear from bigfrank, Idiopathic, Long Dong, Zedpol, Jalby (yeah right 🙂 ), HYJunkie, Hiddentruth, and any others. TIA.

Hey, how come I got a yeah right??

 

[Pox in a box]

Hey, how come I got a yeah right??

Cause you're "No longer in service." I knew you'd come when your name was called.

 

[Pox in a box]

But, from others have said, FA is all you really need. I don't know the validity of that, as I haven't taken the real deal yet. Maybe Automaton can shine some light, as he took the test already. Good luck!

I have heard that too from bigfrank and some others but I don't know how confident I can be with FA alone. It seems pretty weak to me. 👎

 

[automaton]

i used katzung but only as a reference to look up things i didn't understand from first aid. things like mechanism, reason for certain side effects, etc. katzung is intimidating but it's actually pretty succinct. just don't try to read it cover to cover, since most of the drugs in first aid are pretty obvious in what they do and how. i also used pretest pharmacology and found it very helpful, but ran out of time and did only two chapters. i don't think i saw any drugs that weren't in first aid. i'm sure some random drugs might show up from time to time but it's probably low yield worrying about that when there are other subjects to master too.

 

[Pox in a box]

Anybody ever used Pharmacology Secrets ?

 

[Jalby]

Cause you're "No longer in service." I knew you'd come when your name was called.

Alright, you caught me. I search for my own name on here, and that's about it nowadays.

 

[Mike59]

If you're gonna go one step more detailed than first aid, I highly recommend "Pharmacology Recall". It's a great book and has tons of memory tricks to remember side effect profiles and other important info. Plus there's a "power review" section at the end that summarizes the essential drugs, mechanisms and side effects for all of medicine into about 40 pages (it's a small book).

Also, I have the feeling that FA is good, but it is bare bones. There are several drugs in each class that Pharm Recall has that aren't in FA (especially in the alpha/beta receptor chapters and chemotherapy agents) and I've seen them come up in qbank/ other practice question resources.

Good luck! 🙂

 

[Pox in a box]

What, J-a-l-b-y?

 

[HiddenTruth]

just to let u know--i took the CBSE today, and it had some pharm in there, which was much harder than what is prescribed in FA. There were several resistance questions, and questions in chart/diagram format.

Infact, here is one that i spent over 5-7 minutes, trying to figure out.
It was a line graph based question, but to sum it up, this is how it went.

On the y axis, it had PERCENT CHANGE IN VASOPRESSOR RESPONSE and X axis had time (min). And then they had two lines, one representing AT1 and the other ATII. Both AT1 and ATII were parallel, right next to each other, going across horizantally with time, corresponding with a -5-15% change in vasopressor response on the y axis.

So, here is the qusetion
So, at time 20 minutes (xaxis), you give drug X. Soon after, AT1 line dropped down to like in the negative percenatages of vasopressor response, while the ATII remain unchanged and kept treading along at the same vasopressor response change as it was before giving drug x). AT1, after 40 minutes or so, started climbing back up, but never quite made it back to where it was before drug x (or next to ATII, as it was before drug X). They wanted to know what drug X was. I could not figure this out for the life of mine.

Here were the asnwer choices.
a. Ketoconazole
b. Losartan
c. Captopril
d. Sildenafil
e. something bizarre

i was so, trying to convince myself that it was an ARB, but it just didn't play out. At first, I figured that's what it was, because i saw that ATII did not change, but the y axis did not have LEVELS of ATII, but rather VASOPRESSOR RESPONSE CHANGE, and that did not change after giving the drug. I couldn't figure out how you would get a decrease in AT 1 response, without a decrease in ATII response, based on the choices they gave above. Any thoughts?

 

[omarsaleh66]

yeah man I got a lot of resistance q on my pharm NBME haha.

Was choice E Angiotensin Converting Enzyme (ACE) or peptidyl dipeptase by any chance? This would inactivate ATI and decrease it by cleaving it and make more ATII?

It could not be losartan but i would think that ATII would increase cuz the receptors are blocked.

My guess is that its ketoconazole. Estrogen, Thyroid Hormone and corticosteroids increase angiotensin, and Im guessing that ketoconaozole inhibits steroids synthesis (i dont know if it also does that to corticosteroids) so maybe ketoconazole reduces AT1?? Big guess here, but i think captroril and losartan are traps.

 

[p53]

just to let u know--i took the CBSE today, and it had some pharm in there, which was much harder than what is prescribed in FA. There were several resistance questions, and questions in chart/diagram format.

Infact, here is one that i spent over 5-7 minutes, trying to figure out.
It was a line graph based question, but to sum it up, this is how it went.

On the y axis, it had PERCENT CHANGE IN VASOPRESSOR RESPONSE and X axis had time (min). And then they had two lines, one representing AT1 and the other ATII. Both AT1 and ATII were parallel, right next to each other, going across horizantally with time, corresponding with a -5-15% change in vasopressor response on the y axis.

So, here is the qusetion
So, at time 20 minutes (xaxis), you give drug X. Soon after, AT1 line dropped down to like in the negative percenatages of vasopressor response, while the ATII remain unchanged and kept treading along at the same vasopressor response change as it was before giving drug x). AT1, after 40 minutes or so, started climbing back up, but never quite made it back to where it was before drug x (or next to ATII, as it was before drug X). They wanted to know what drug X was. I could not figure this out for the life of mine.

Here were the asnwer choices.
a. Ketoconazole
b. Losartan
c. Captopril
d. Sildenafil
e. something bizarre

i was so, trying to convince myself that it was an ARB, but it just didn't play out. At first, I figured that's what it was, because i saw that ATII did not change, but the y axis did not have LEVELS of ATII, but rather VASOPRESSOR RESPONSE CHANGE, and that did not change after giving the drug. I couldn't figure out how you would get a decrease in AT 1 response, without a decrease in ATII response, based on the choices they gave above. Any thoughts?

p53 sez captopril. 100% guaranteed. Talk about EZ.

 

[HiddenTruth]

yeah man I got a lot of resistance q on my pharm NBME haha.

Was choice E Angiotensin Converting Enzyme (ACE) or peptidyl dipeptase by any chance? This would inactivate ATI and decrease it by cleaving it and make more ATII?

It could not be losartan but i would think that ATII would increase cuz the receptors are blocked.

My guess is that its ketoconazole. Estrogen, Thyroid Hormone and corticosteroids increase angiotensin, and Im guessing that ketoconaozole inhibits steroids synthesis (i dont know if it also does that to corticosteroids) so maybe ketoconazole reduces AT1?? Big guess here, but i think captroril and losartan are traps.

you have a good point there, and i thought abt that too. Azoles do decrease cortisol and androgens, and i guess in turn that can reduce angiotensinogen, but then again, ATII response did not change, so that doesn't quite fit the picture. And, on a side note, azoles actually cause mineralcorticoid excess, but that doesn't really have much to do with this.

Neither ACE, or dipeptidyl transpeptidiase were choices--choice E. was acutlaly some name that i have never seen, so technically, that may be an answer. Unfortunately, i don't remember it. Does ACE come as a drug?

 

[HiddenTruth]

i did the pharm appleton lange 125q section from the Appleton Lange USMLE Queston book by Michael King the day before the shelf to prepare for the pharm NBME.

later

hey, this is not pharm specific, is it? This is the same A&L q book with all the subjects that everyone talks abt, eh?

 

[omarsaleh66]

hey, this is not pharm specific, is it? This is the same A&L q book with all the subjects that everyone talks abt, eh?

yeah, this is the book by michael king that has been given much love by all the high scorers here. It's pretty good, Im tryign to finish it all right now, I got 4 weeks till the big exam, so I'll let u know how much it helps.

later

 

[caribsun]

actually im not sure about ketoconazole. losartan works at hte receptor site and you would see an decreased response of AII so its out. i would guess captopril because it causes a difference in AI and AII and that's seems to be what the graph shows

just to let u know--i took the CBSE today, and it had some pharm in there, which was much harder than what is prescribed in FA. There were several resistance questions, and questions in chart/diagram format.

Infact, here is one that i spent over 5-7 minutes, trying to figure out.
It was a line graph based question, but to sum it up, this is how it went.

On the y axis, it had PERCENT CHANGE IN VASOPRESSOR RESPONSE and X axis had time (min). And then they had two lines, one representing AT1 and the other ATII. Both AT1 and ATII were parallel, right next to each other, going across horizantally with time, corresponding with a -5-15% change in vasopressor response on the y axis.

So, here is the qusetion
So, at time 20 minutes (xaxis), you give drug X. Soon after, AT1 line dropped down to like in the negative percenatages of vasopressor response, while the ATII remain unchanged and kept treading along at the same vasopressor response change as it was before giving drug x). AT1, after 40 minutes or so, started climbing back up, but never quite made it back to where it was before drug x (or next to ATII, as it was before drug X). They wanted to know what drug X was. I could not figure this out for the life of mine.

Here were the asnwer choices.
a. Ketoconazole
b. Losartan
c. Captopril
d. Sildenafil
e. something bizarre

i was so, trying to convince myself that it was an ARB, but it just didn't play out. At first, I figured that's what it was, because i saw that ATII did not change, but the y axis did not have LEVELS of ATII, but rather VASOPRESSOR RESPONSE CHANGE, and that did not change after giving the drug. I couldn't figure out how you would get a decrease in AT 1 response, without a decrease in ATII response, based on the choices they gave above. Any thoughts?

 

[HiddenTruth]

actually im not sure about ketoconazole. losartan works at hte receptor site and you would see an decreased response of AII so its out. i would guess captopril because it causes a difference in AI and AII and that's seems to be what the graph shows

true, but you would see a difference in the ATII response change after giving captopril, which the graph did not reveal; the response of ATII remained the same after giving drug X.

 

[p53]

true, but you would see a difference in the ATII response change after giving captopril, which the graph did not reveal; the response of ATII remained the same after giving drug X.

Wrong again. The graph overlayed two different experiements onto one graph. One experiment simulated a competitive inhibition of ACE by adding captopril to AI, and the second experiment showed that captopril was added with AII (no action) and this showed that captopril acts BEFORE AII action. For those keeping score at home, the same question can be used again in scenario #2, if the graph shows changed response of AI and AII than the answer would be losartan.

Once again the answer is captopril.

If you want more correct answers from your exam, post them and I will give you the right answer for your Step 1 prep.

 

[Pox in a box]

Wrong again. The graph overlayed two different experiements onto one graph. One experiment simulated a competitive inhibition of ACE by adding captopril to AI, and the second experiment showed that captopril was added with AII (no action) and this showed that captopril acts BEFORE AII action. For those keeping score at home, the same question can be used again in scenario #2, if the graph shows changed response of AI and AII than the answer would be losartan.

Once again the answer is captopril.

If you want more correct answers from your exam, post them and I will give you the right answer for your Step 1 prep.

Post highjack?

 

[HiddenTruth]

Wrong again. The graph overlayed two different experiements onto one graph. One experiment simulated a competitive inhibition of ACE by adding captopril to AI, and the second experiment showed that captopril was added with AII (no action) and this showed that captopril acts BEFORE AII action.

The question did not mention of two experiements, infact it said "an experiement". I think you are making some assumptions in your theory.

Sorry, pox, for semi-hijacking the thread. Back to Pox's search for a pharm review book. 🙂

 

[Pox in a box]

The question did not mention of two experiements, infact it said "an experiement". I think you are making some assumptions in your theory.

Sorry, pox, for semi-hijacking the thread. Back to Pox's search for a pharm review book. 🙂

p53 is notorious for not doing his job, which I thought was just to guard the membrane. Apparently p53 didn't read the owner's manual (I mean listen). If you want to discuss whatever you were talking about, can you just repost in a new one? Thanks.

 

[p53]

p53 is notorious for not doing his job, which I thought was just to guard the membrane.

What does p53 have to do with "membrane", I can't find this info anywhere in BRS Pathology. 👎

 

[caribsun]

sorry for adding fuel to the hijack fire...speaking of review books, i have read 5 sections of the pharm recall book some ppl were talkin about and it pretty much sucks so far..

the format is questions on the left side of the page and answers on the right but because of this structure i think the information is all over the place when u read it. also, a lot of extraneous material is presented. but well see how i feel when i get through to antimicrobials.

 

[p53]

The question did not mention of two experiements, infact it said "an experiement". I think you are making some assumptions in your theory.

Sorry, pox, for semi-hijacking the thread. Back to Pox's search for a pharm review book. 🙂

This is common sense, Hidden. The graph showed two experiments overlayed into one graph to compare the results. Any other interpretation would not make any sense whatsover with the answer choices. The ketoconazole argument is pure crap because even if there was a decrease in metabolism of estrogen or corticosteroids. Estrogen increases ANGIOTENSINOGEN concentration. Angiotensinogen is before AI and AII so the effect would be the same for AI and AII.

 

[Pox in a box]

What does p53 have to do with "membrane", I can't find this info anywhere in BRS Pathology. 👎

What does the term BM mean to you?

By the way, you don't know dork.

 

[HiddenTruth]

This is common sense, Hidden. The graph showed two experiments overlayed into one graph to compare the results. Any other interpretation would not make any sense whatsover with the answer choices. The ketoconazole argument is pure crap because even if there was a decrease in metabolism of estrogen or corticosteroids. Estrogen increases ANGIOTENSINOGEN concentration. Angiotensinogen is before AI and AII so the effect would be the same for AI and AII.

Last time i checked, medical knowledge is not common sense, and secondly, i think I took the test and saw the question, and by no means, does your interpretation make any sense. Lets end this discussion here, so i don't get on pox's "dirty" list of hijacking a thread.

 

[p53]

What does the term BM mean to you?

By the way, you don't know dork.

What does p53 have to do with Basement Membrane? I'm sure Kumar, Robbins, and Coltran would like to know.

 

[p53]

Last time i checked, medical knowledge is not common sense, and secondly, i think I took the test and saw the question, and by no means, does your interpretation make any sense. Lets end this discussion here, so i don't get on pox's "dirty" list of hijacking a thread.

Just admit that you missed the question. The answer is captopril. If you did a poll of your question, captopril would win by a landslide. Don't miss this concept on Step 1. You are welcome, I will continue to help you for Step 1 prep.

 

[HiddenTruth]

Just admit that you missed the question. The answer is captopril. If you did a poll of your question, captopril would win by a landslide. Don't miss this concept on Step 1. You are welcome, I will continue to help you for Step 1 prep.

Thanks, Mr./Ms. spokesman from the NBME. I am glad you got to review my test and saw what answer I put, and now are returning back with the key. You should consider applying for a job at the NBME, if you haven't already. Your comments may hold more credibility. 😀

 

[Pox in a box]

What does p53 have to do with Basement Membrane? I'm sure Kumar, Robbins, and Coltran would like to know.

First, you're being a dolt. Here's one example of how you tried to explain your way through something and ended up leaving with your tail between your legs.

Step 1 Pimp Each Other Thread

Second, it's not even classified as a pathology topic. This is cell and molecular biology 101, something you've actually commented upon as being a heavier emphasis on the exam. You better go read Alberts now. Good luck!

Tumors may be resistant to programmed cell death, as a consequence of inactivation of p53 or other changes. p53 has a vital role in limiting invasion by its role in regulating apoptosis. Without the defined function of p53 or other checkpoint components, tumor cells detach from each other because of reduced adhesiveness, and cells then attach to the basement membrane via the laminin receptors and secrete proteolytic enzymes, including type IV collagenase. Degradation of the basement membrane and tumor cell migration follow. A carcinoma must first breach the underlying basement membrane, then traverse the interstitial connective tissue, and ultimately gain access to the circulation by penetrating the vascular basement membrane.

Third, it's Cotran, not Coltran. You better apologize. Fourth, Cotran isn't even affiliated with Robbins now. I forgot, you don't even have a Robbins.

 

[p53]

First, you're being a dolt. Here's one example of how you tried to explain your way through something and ended up leaving with your tail between your legs.

Step 1 Pimp Each Other Thread

Second, it's not even classified as a pathology topic. This is cell and molecular biology 101, something you've actually commented upon as being a heavier emphasis on the exam. You better go read Alberts now. Good luck!

Tumors may be resistant to programmed cell death, as a consequence of inactivation of p53 or other changes. p53 has a vital role in limiting invasion by its role in regulating apoptosis. Without the defined function of p53 or other checkpoint components, tumor cells detach from each other because of reduced adhesiveness, and cells then attach to the basement membrane via the laminin receptors and secrete proteolytic enzymes, including type IV collagenase. Degradation of the basement membrane and tumor cell migration follow. A carcinoma must first breach the underlying basement membrane, then traverse the interstitial connective tissue, and ultimately gain access to the circulation by penetrating the vascular basement membrane.

Third, it's Cotran, not Coltran. You better apologize. Fourth, Cotran isn't even affiliated with Robbins now. I forgot, you don't even have a Robbins.

You better read chapter 7 of Robbins. I wonder if p53 will be mentioned there. Once again, p53 has nothing to do with the extracellular basement membrane. p53 is an intracellular protein. It plays a role in guarding the cellular genome and inducing apoptosis. Every time you say p53 guards the basement membrane you sound like a complete idiot.

Good luck on Step 1. I will pray for you. Since I don't know dork, I'll spot you 75 points on our step 1 scores. Be a man and take the bet.

Hidden, if you want some of the action, I'll spot you 40.

 

[Prophecies]

Genes & Development (1996):
p53 plays multiple roles in cells. Expression of high levels of wild-type (but not mutant) p53 has two outcomes: cell cycle arrest or apoptosis. The observation that DNA-damaging agents induce levels of p53 in cells led to the definition of p53 as a checkpoint factor, akin, perhaps, to the product of the fad9 gene in yeast. While dispensable for viability, in response to genotoxic stress, p53 acts as an "emergency brake" inducing either arrest or apoptosis, protecting the genome from accumulating excess mutations. Consistent with this notion, cells lacking p53 were shown to be genetically unstable and thus more prone to tumors.

Science (2003):
Exposure to cellular stress can trigger the p53 tumor suppressor, a sequence-specific transcription factor, to induce cell growth arrest or apoptosis. The choice between these cellular responses is influenced by many factors, including the type of cell and stress, and the action of p53 co-activators. p53 stimulates a wide network of signals that act through two major apoptotic pathways. The extrinsic, death receptor pathway triggers the activation of a caspase cascade, and the intrinsic, mitochondrial pathway shifts the balance in the Bcl-2 family towards the pro-apoptotic members, promoting the formation of the apoptosome, and consequently caspase-mediated apoptosis. The impact of these two apoptotic pathways may be enhanced when they converge through Bid, which is a p53 target. The majority of these apoptotic effects are mediated through the induction of specific apoptotic target genes. However, p53 can also promote apoptosis by a transcription-independent mechanism under certain conditions. Thus, a multitude of mechanisms are employed by p53 to ensure efficient induction of apoptosis in a stage-, tissue- and stress-signal-specific manner. Manipulation of the apoptotic functions of p53 constitutes an attractive target for cancer therapy.

...obviously p53 has a role in cancer by not causing apoptosis or sending a cell into arrest, therefore causing the cancerous cells to divide and grow. I've done a small amount of work on this in undergrad (mostly the genetic coding, not the protein)...research suggests that activating p53 in tumor cells can specifically target and destroy tumors, without harming normal somatic cells.

Now can we get back to Pox's question? Pharm review books... ... ...

 

[p53]

From Genes & Development (1996):

...obviously p53 has a role in cancer by not causing apoptosis or sending a cell into arrest, therefore causing the cancerous cells to divide and grow. I've done a small amount of work on this in undergrad (mostly the genetic coding, not the protein)...research suggests that activating p53 in tumor cells can specifically target and destroy tumors, without harming normal somatic cells.

Now can we get back to the OP's question? Pharm review books... ... ...

I agree that p53 has a tumor suppressive action in the cell cycle. I am not questioning this fact. The point is that p53 does not guard the basement membrane, it acts as an tumor suppressor inside the cell.

Your argument is a separate one. Keep in mind there are metastatic cancers that have functional p53s and there are hamartomas that have null p53s.

 

[Prophecies]

Right now, no one else except the two of you really have an interest in what p53 does or does not do to the basement membrane...I'm not trying to argue with either of you, I just want this thread to get back on topic. The bickering between the two of you isn't helping anyone. 😡

 

[p53]

Right now, no one else except the two of you really have an interest in what p53 does or does not do to the basement membrane...I'm not trying to argue with either of you, I just want this thread to get back on topic. The bickering between the two of you isn't helping anyone. 😡

You are right. For some reason, pox likes a good old fashioned debate. However, the greater good is that we had a chance to review a high yield topic for Step 1.

 

[Pox in a box]

You better read chapter 7 of Robbins. I wonder if p53 will be mentioned there. Once again, p53 has nothing to do with the extracellular basement membrane. p53 is an intracellular protein. It plays a role in guarding the cellular genome and inducing apoptosis. Every time you say p53 guards the basement membrane you sound like a complete idiot.

Good luck on Step 1. I will pray for you. Since I don't know dork, I'll spot you 75 points on our step 1 scores. Be a man and take the bet.

Hidden, if you want some of the action, I'll spot you 40.

You win. Your prize will be sent to your mailbox as soon as our research and development team creates it. Just remember that p53 plays an indirect role in guarding the membrane. Without p53 and others, cancers would invade like wild. Yes, it has many other roles. We all know the concepts now. Back to the original question... 😴

 

[Samoa]

What does p53 have to do with Basement Membrane? I'm sure Kumar, Robbins, and Coltran would like to know.

p53, you're right about p53. Pox is associating it with basement membrane because the text talks about them in the same paragraph. However, it is the lack of p53-induced apoptosis that allows a completely separate process (development of metastatic potential) to proceed.

The text, though, is called Robbins and Cotran Pathologic Basis of Disease, and the authors are Kumar, Abbas and Fausto.

But back to the topic. I just got out of the pharm shelf, and seriously, all you need is FA, and an unshakeable confidence in your answers. If you're at all indecisive about an answer, and try to rely on test-taking strategies to guess, the test will trip you up. It's not nice.

 

[Pox in a box]

Pox is associating it with basement membrane because the text talks about them in the same paragraph.

Actually, no but we've already killed this thread's main objective.