Step 1 Complicated Concepts Thread

[TheSeanieB]

ASK AND ANSWER TOUGH QUESTIONS RELATED TO STEP 1.

Starting with me:
physiologic chloride shift - When CO2 diffuses into a RBC, it quickly converts with H2O to H+ and HCO3- so that CO2 will continue to passively diffuse into the RBC. The HCO3- is then excreted into the plasma by a Cl-/HCO3- exchanger. When the RBC enters the pulmonary capillaries, the process reverses. HCO3- is taken up by exchange for a Cl-. It combines with H+ to creates CO2 +H2O. The CO2 then diffuses out of the RBC and ultimately into the alveoli. This process allows for maximal CO2 excretion by a RBC.

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[loveoforganic2]

Correct me if I'm wrong but my general rule with the 2 porphyrias is that they are more or less alphabetical. AIP corresponds to HMB synthase (or whatever you call it) slash porphosomething deaminase slash uroporphowhatever 1.

In PCT, the deficient enzyme is only called uroporphosomething 3. P (as in PCT) comes after A (as in AIP), 3 comes after 1, and all the other AIP enzyme name synonyms start with letters that come before "U" as well.

It's also nice because the interruption for AIP occurs before the interruption for PCT. Once again, alphabetical order.

The substrate that builds up for AIP starts with the letter P, while the substrate that builds up for PCT starts with the letter U. Alphabetical as well.

If you somehow managed to follow that, I promise it's super helpful.

It took me like 5 minutes of rereading it 4 times and googling... but yes it was! thanks!

 

[tiedyeddog]

Correct me if I'm wrong but my general rule with the 2 porphyrias is that they are more or less alphabetical. AIP corresponds to HMB synthase (or whatever you call it) slash porphosomething deaminase slash uroporphowhatever 1.

In PCT, the deficient enzyme is only called uroporphosomething 3. P (as in PCT) comes after A (as in AIP), 3 comes after 1, and all the other AIP enzyme name synonyms start with letters that come before "U" as well.

It's also nice because the interruption for AIP occurs before the interruption for PCT. Once again, alphabetical order.

The substrate that builds up for AIP starts with the letter P, while the substrate that builds up for PCT starts with the letter U. Alphabetical as well.

If you somehow managed to follow that, I promise it's super helpful.

damn, thanks for this!! I am annoting this into my FA now so I don't forget it...

 

[dbeast]

I think this is exactly what happens. Think of it like this:

bloodsteam must fill before interstituim does.
Interstituim(ECF) must fill before ICF does.
When the drug hits the ICF, the effect starts.

The more soluble(lipophillic) the compound is, the more of it dissolves into the bloodsteam. I believe this has to do with the high amount of fat carriers, such as albumin, that bind to the compounds. The more more lipophillic they are, the more binding to albumin there is, the more you need to dissolve to fill that compartment.

This is a super dumb analogy, but think of it like this:

Top cup(highest one) is the bloodsteam. Compound won't flow into the cup below it until the top cup overflows. Same goes for the ECF to ICF.

I love this picture/analogy... So you could also say that something with low blood solubility would be similar to a smaller top cup so that it overflows quickly into the next compartment (aka fast induction)???

We're going places with this, guys. Also I plan on having a 4 cup drink in your honor after the test if I get one of these questions.

 

[sharklasers]

I love this picture/analogy... So you could also say that something with low blood solubility would be similar to a smaller top cup so that it overflows quickly into the next compartment (aka fast induction)???

We're going places with this, guys. Also I plan on having a 4 cup drink in your honor after the test if I get one of these questions.

hmm yeah id say thats exactly right!!

less beer would fit in the smaller upper cup so it would go into the next cup faster
less anesthestic fits into the blood so it goes into the brain faster

 

[tiedyeddog]

I love this picture/analogy... So you could also say that something with low blood solubility would be similar to a smaller top cup so that it overflows quickly into the next compartment (aka fast induction)???

We're going places with this, guys. Also I plan on having a 4 cup drink in your honor after the test if I get one of these questions.

lol, remember tiedyeddog when you nail that ****, rofl

 

[Pinkleton]

How does hyperkalemia decrease comtractility?

 

[sharklasers]

How does hyperkalemia decrease comtractility?

Just a guess here

Increase potassium causes increased activity of the Na/K pump making more Na go outside. This increases the Na gradient so it increases the activity of the Na/Ca exchange. This leads to more Ca being pumped out of the cell, decreasing contractility.

If this is correct, just think that it's the exact opposite of how digoxin increases contractility!

 

[sharklasers]

Is there some drug that is not effective if given with a particular vitamin? b6 maybe?

i know that isn't much info, but i vaguely remember reading something like that and am annoyed I can't remember exactly what it is

 

[tiedyeddog]

Is there some drug that is not effective if given with a particular vitamin? b6 maybe?

i know that isn't much info, but i vaguely remember reading something like that and am annoyed I can't remember exactly what it is

Tetracycline and cations? I dunno...

 

[dbeast]

Is there some drug that is not effective if given with a particular vitamin? b6 maybe?

i know that isn't much info, but i vaguely remember reading something like that and am annoyed I can't remember exactly what it is

L-DOPA yo. It gets converted to dopamine in peripheral tissues by B6 before it crosses the blood brain barrier. There's a question about an old guy with worsening parkinson's and they ask why it's getting worse... answer was "Daily multivitamin"

 

[sharklasers]

L-DOPA yo. It gets converted to dopamine in peripheral tissues by B6 before it crosses the blood brain barrier. There's a question about an old guy with worsening parkinson's and they ask why it's getting worse... answer was "Daily multivitamin"

YES this is exactly what i was thinking about lol thanks!

i definitely got that question wrong haha

 

[dbeast]

YES this is exactly what i was thinking about lol thanks!

i definitely got that question wrong haha

I did too... Don't worry it was definitely one of those 20% of people got it questions. I usually just write those off as a lost cuase.

 

[JP2740]

What is the difference between serum sickness and arthrus reaction?

 

[Pinkleton]

Just a guess here

Increase potassium causes increased activity of the Na/K pump making more Na go outside. This increases the Na gradient so it increases the activity of the Na/Ca exchange. This leads to more Ca being pumped out of the cell, decreasing contractility.

If this is correct, just think that it's the exact opposite of how digoxin increases contractility!

Hmmmm...Can concentration gradients change the rate of activity of ATP dependent pumps?

 

[Jamiu22]

What is the difference between serum sickness and arthrus reaction?

I've always looked at it as both being type 3 hypersentivities... but with

Arthus Rxn: you see local subcutaneous reaction./swelling... while with
Serum sickness.. the pathology seems more systemic - with fibrinoid necosis and neutorphilic infiltrates of small vessels (where complex is also deposited)

EDIT: I just checked with FA.... and yup..that's whats in there (FA2012; pg 233)

 

[blaqmamba]

Anyone know around how long it takes for bicarb to compensate a respiratory alkalosis, and if it's the same for a respiratory acidosis

Ie, when can we assume someone at high altitude has compensated by dumping their HCo3

 

[pvtbacon]

Anyone know around how long it takes for bicarb to compensate a respiratory alkalosis, and if it's the same for a respiratory acidosis

Ie, when can we assume someone at high altitude has compensated by dumping their HCo3

According to the UConn acid base tutorial, if resp alkalosis persists for 2-6 hours, renal elimination of HCO3- starts to kick in slowly and is complete by 2-3 days.

But since 2-6 hours is too much of a blur, I doubt they'd use that on the exam. Safe bet is 2-3 days.

 

[sharklasers]

So PE and blood gases...

I got a question and I figured with a PE, you have less gas exchange, so you have a decrease in O2, increase in CO2, and have a decrease in pH.

But they were going for a decrease in O2, decrease in CO2 and increase in pH due to hyperventilation.

so can you just assume that anytime you have a situation with low O2, you are going to hyperventilate and decrease CO2?

 

[Pinkleton]

So PE and blood gases...

I got a question and I figured with a PE, you have less gas exchange, so you have a decrease in O2, increase in CO2, and have a decrease in pH.

But they were going for a decrease in O2, decrease in CO2 and increase in pH due to hyperventilation.

so can you just assume that anytime you have a situation with low O2, you are going to hyperventilate and decrease CO2?

I know that the primary disturbance with PE is hypoxemia. I would think it's because you have a drop in perfusion, not ventilation. That will drop the PO2 below 60 and cause hyperventilation, which reduces PCO2 as well. I think you can get rid of the CO2 because it equilibrates faster than O2

Edit: got perfusion and ventilation reversed, now corrected

 

[tiedyeddog]

So PE and blood gases...

I got a question and I figured with a PE, you have less gas exchange, so you have a decrease in O2, increase in CO2, and have a decrease in pH.

But they were going for a decrease in O2, decrease in CO2 and increase in pH due to hyperventilation.

so can you just assume that anytime you have a situation with low O2, you are going to hyperventilate and decrease CO2?

You can't alway make that assumption, no. For instance, COPD leads to chronically high pCO2.

 

[pvtbacon]

So PE and blood gases...

I got a question and I figured with a PE, you have less gas exchange, so you have a decrease in O2, increase in CO2, and have a decrease in pH.

But they were going for a decrease in O2, decrease in CO2 and increase in pH due to hyperventilation.

so can you just assume that anytime you have a situation with low O2, you are going to hyperventilate and decrease CO2?

I banged my head against the wall trying to reason through this question. Every time I think of PE, my mind goes back to the drawing from BRS Physiology with the embolus blocking blood flow and so I automatically assume that no gas exchange is occurring. I mean, there's this plugged up vessel so how is blood going to get oxygenated?? And so I reasoned just like you that of course CO2 is gonna pile up and the guy's gonna go into metabolic acidosis

But then it hit me; our lungs don't have just one vessel. And if it were a massive saddle embolus that really plugged everything out, then maybe my case would still stand, but in that case he'd be dead. So I guess whenever there's a PE, there's gonna be hypoxic vasoconstriction that shunts blood flow elsewhere. Hence, the decrease in paO2 is more likely to result in hyperventilation because the pCO2 will have reached peripheral chemoreceptors.

 

[Akr]

So PE and blood gases...

I got a question and I figured with a PE, you have less gas exchange, so you have a decrease in O2, increase in CO2, and have a decrease in pH.

But they were going for a decrease in O2, decrease in CO2 and increase in pH due to hyperventilation.

so can you just assume that anytime you have a situation with low O2, you are going to hyperventilate and decrease CO2?

Sounds about right! If the problem is not in ventilation itself (I can think of way more scenarios in which it is, though: intoxication with any respiratory depressant... neuromuscular disorder... restrictive lung disease...)..So someone with PE, someone at high altitude, maybe someone with acute asthma would have a drop in O2, and hyperventilate to try to increase it. The way it's been explained to me before is that CO2 diffuses better than O2, so we'd see the hyperventilation decrease CO2 more than it increases O2.

 

[sharklasers]

You can't alway make that assumption, no. For instance, COPD leads to chronically high pCO2.

oh true yeah duh, because hyperventilation wouldn't help bc there is an intrinsic problem with the lungs.

can someone distinguish between blue bloater and pink puffer?

i know that in COPD, the person takes deep slow breaths to minimize work of breathing.

in restrictive lung diseases, the person takes fast shallow breaths to minimize work of breathing.


first aid says that chronic bronchitis blue bloater while emphysema = pink puffer. i'm not really sure why this is.

 

[tiedyeddog]

I know that the primary disturbance with PE is hypoxemia. I would think it's because you have a drop in ventilation, not perfusion. That will drop the PO2 below 60 and cause hyperventilation, which reduces PCO2 as well. I think you can get rid of the CO2 because it equilibrates faster than O2

Right.

When addressing these you have to think about perfusion defect vs diffusion defect. You can't fix a perfusion defect via intrapulmonary shunting, so you'll still be hypoxic. Hypoxic response is to so breath faster -> alkalosis.

I think of perfusion defects as the same thing as breathing at a high altitude.

 

[TheSeanieB]

Anyone have any recommendations (diagrams, websites, animations, etc) for embryology that have helped them?

 

[pvtbacon]

Right.

When addressing these you have to think about perfusion defect vs diffusion defect. You can't fix a perfusion defect via intrapulmonary shunting, so you'll still be hypoxic. Hypoxic response is to so breath faster -> alkalosis.

I think of perfusion defects as the same thing as breathing at a high altitude.

Arterial blood gas — Arterial blood gas (ABG) measurements and pulse oximetry have a limited role in diagnosing PE [2]. ABGs usually reveal hypoxemia, hypocapnia, and respiratory alkalosis. Patients with room air pulse oximetry readings <95 percent at the time of diagnosis are at increased risk of in-hospital complications, including respiratory failure, cardiogenic shock, and death [3].

The typical arterial blood gas findings are not always seen. As an example, massive PE with hypotension and respiratory collapse can cause hypercapnia and a combined respiratory and metabolic acidosis (the latter due to lactic acidosis). In addition, hypoxemia can be minimal or absent. A PaO2 between 85 and 105 mmHg exists in approximately 18 percent of patients with PE [4]. Up to 6 percent may have a normal alveolar-arterial gradient for oxygen.

Straight out of UpToDate. Looks like the textbook findings don't always play out clinically but we'll have to assume those findings for the purpose of this exam.

 

[pvtbacon]

Anyone have any recommendations (diagrams, websites, animations, etc) for embryology that have helped them?

GI: http://www.youtube.com/watch?v=AscKR_cQExY
http://www.youtube.com/watch?v=uPBEgBIvRcI

Cardio:http://www.youtube.com/watch?v=g5UTzj9LOhQ

Cardiac embryology seemed most complicated. The rest is primarily just memorizing germ layer derivatives.

 

[tiedyeddog]

Straight out of UpToDate. Looks like the textbook findings don't always play out clinically but we'll have to assume those findings for the purpose of this exam.

I was wondering about this, thanks for the info!

 

[TheSeanieB]

GI: http://www.youtube.com/watch?v=AscKR_cQExY
http://www.youtube.com/watch?v=uPBEgBIvRcI

Cardio:http://www.youtube.com/watch?v=g5UTzj9LOhQ

Cardiac embryology seemed most complicated. The rest is primarily just memorizing germ layer derivatives.

Awesome! Thanks.

 

[blaqmamba]

Can someone explain the situation behind vaccines? I feel like it's something I never fully learned and FA/UW isn't cutting it. Or maybe point me to where I can understand them?

Specifically:
Bacterial vaccines: I understand the whole "lets conjugate diptheria's protein to a polysach capsule to make it more antigenic," but why in some cases do you only generate IgM, vs forming memory cells, etc..?

Viral vaccines: why does a live vaccine induce a humoral and cell-mediated response, while killed vaccines only induce a humoral response? And does this mean that a humor response only = no memory?

any other info would be appreciated too

 

[pvtbacon]

Can someone explain the situation behind vaccines? I feel like it's something I never fully learned and FA/UW isn't cutting it. Or maybe point me to where I can understand them?

Specifically:
Bacterial vaccines: I understand the whole "lets conjugate diptheria's protein to a polysach capsule to make it more antigenic," but why in some cases do you only generate IgM, vs forming memory cells, etc..?

Viral vaccines: why does a live vaccine induce a humoral and cell-mediated response, while killed vaccines only induce a humoral response? And does this mean that a humor response only = no memory?

any other info would be appreciated too

I'll take a stab at it. There's a distinction between T-cell independent and T-cell dependent antigens.

T-cell independent:
polysaccharide
LPS

No isotype switching via CD40/CD40L. Stimulation of B cells alone enough to produce massive amounts of lower affinity IgM. Because they never associate with the T cells, there's no memory either. No somatic hypermutation.

T-cell dependent
peptide

Need to go through isotype switching to be effective. B cell presents antigen to TH2 cell TCR via MCHII, crosslinks TCR, TH2 cell starts making IL-4 to enhance switch to IgG. I don't understand how memory works but I suppose one of the lineages of the T helper cells will change into a memory cell.

Live vaccines: follows a similar course to natural infection and has the ability to MULTIPLY at site of injection and rapidly disseminate to tissues via blood supply
Killed vaccines: more localized response due to dendritic cells and it produces more of a TH1 response rather than TH2.

http://www.who.int/immunization/documents/Elsevier_Vaccine_immunology.pdf

 

[coolforschool]

Can someone explain the situation behind vaccines? I feel like it's something I never fully learned and FA/UW isn't cutting it. Or maybe point me to where I can understand them?

Specifically:
Bacterial vaccines: I understand the whole "lets conjugate diptheria's protein to a polysach capsule to make it more antigenic," but why in some cases do you only generate IgM, vs forming memory cells, etc..?

Viral vaccines: why does a live vaccine induce a humoral and cell-mediated response, while killed vaccines only induce a humoral response? And does this mean that a humor response only = no memory?

any other info would be appreciated too

I agree with you, man. The way I think about it is that conjugating a protein to the capsule will cause a T-cell response because T-cells need APCs to present stuff to them on MHC Class II receptors, and MHC II receptors require a protein in that slot. Therefore, you need that protein conjugate in order to present the whole thing to the T-cells. This will allow the T-cells to become activated and activate cells like memory B cells to produce antibodies against that protein conjugate.

It's the same thing with live and killed vaccines. Live vaccines can cause mild infection, so they're simulating a real infection but they aren't pathogenic per se. You mimic an infection, so you get all of the normal reactions to an infection and end up with a good cell-mediated response. For killed vaccines, you only have bits and pieces of the virus, so they can't establish an infection at all. You only get a response to their products, so it's not the same and thus you get a weaker, more general response.

Not really sure on the specifics, but that's how I think of it. Now I want somebody to come in and lay down the damn details to all of this crap.

 

[sharklasers]

oh true yeah duh, because hyperventilation wouldn't help bc there is an intrinsic problem with the lungs.

can someone distinguish between blue bloater and pink puffer?

i know that in COPD, the person takes deep slow breaths to minimize work of breathing.

in restrictive lung diseases, the person takes fast shallow breaths to minimize work of breathing.


first aid says that chronic bronchitis blue bloater while emphysema = pink puffer. i'm not really sure why this is.

just thought i would bring this back into attention

thanks for the invaluable help guys!

 

[pvtbacon]

just thought i would bring this back into attention

thanks for the invaluable help guys!

Blue Bloater has to do with early cyanosis seen with chronic bronchitis. Mucus plugs up your airways so bad that you can't get enough oxygen. Early hypoxia -> pulm vasoconstriction -> eventual right heart failure -> backup of blood to venous circulation -> edema

Pink Puffer. Cyanosis is often late so they don't turn blue. Hence, we call them pink instead to indicate that they are normal? Puffer because they need to breathe out through pursed lips to maintain positive airway pressure because the alveolar wall destruction produces functional obstruction.

 

[tiedyeddog]

I agree with you, man. The way I think about it is that conjugating a protein to the capsule will cause a T-cell response because T-cells need APCs to present stuff to them on MHC Class II receptors, and MHC II receptors require a protein in that slot. Therefore, you need that protein conjugate in order to present the whole thing to the T-cells. This will allow the T-cells to become activated and activate cells like memory B cells to produce antibodies against that protein conjugate.

It's the same thing with live and killed vaccines. Live vaccines can cause mild infection, so they're simulating a real infection but they aren't pathogenic per se. You mimic an infection, so you get all of the normal reactions to an infection and end up with a good cell-mediated response. For killed vaccines, you only have bits and pieces of the virus, so they can't establish an infection at all. You only get a response to their products, so it's not the same and thus you get a weaker, more general response.

Not really sure on the specifics, but that's how I think of it. Now I want somebody to come in and lay down the damn details to all of this crap.

Ok, I am going to give you a brief overview here. Look at these diagrams to get the gist of it:

In general, the polysacchride coats of encapsulated bacteria are made of sugars (except Bacillus Anthracis, which you should know has a protein coat and is one of the only clinically relevant bacteria to have one). Sugars are extremely poor antigens and APC's don't like to use them, instead they mainly use proteins.

So, eukaryotes have evolved T-cell independent methods of fighting these bacteria. Basically, they use toll-like receptors and stuff like that to start to fight these bacteria via the complement cascade and typically do NOT cause T cell activation. This is a problem because you need T cell activation for Ig class switching.

Scientists first tried making a vaccine of just polysaccaride. It didn't work. The immunity was poor and didn't last long. So, to combat this, they made conjugate vaccines. Conjugate vaccines are a protein carrier conjoined to the polysaccharide capsule bits. So, now what occurs is your B cells see the protein part of the vaccines. It likes protein, so it takes these up, chews them up, and now presents them on MHCII. When chewing them up, some bits of polysaccharide are left over. These are presented to T cell TCR receptors, which do two things:

1. make memory T cells or the next infection
2. create plasma cells that make high quality IgG for the future.

And there you go! one key thing to know is that often the protein carrier is something your body already recognizes, which is good because it makes it more likely a good immune response well occur. If I am not mistaken the HiB vaccine uses teninospam toxoid (tetanus toxin that is inactive, however you spell it) as the protein carrier.

 

[coolforschool]

Beautiful pictures, man. Thanks a lot.

 

[blaqmamba]

wow T-dogg! You the man

 

[JP2740]

Isoprotenerol pg.236 first aid. Why is there a decrease in systolic pressure there, when isoprotenerol is a beta1 agonist? Why isn't it mimicking what norepinephrine is doing? Because the increased HR disallows filling of the LV?

 

[pvtbacon]

Isoprotenerol pg.236 first aid. Why is there a decrease in systolic pressure there, when isoprotenerol is a beta1 agonist? Why isn't it mimicking what norepinephrine is doing? Because the increased HR disallows filling of the LV?

Isoproterenol is a b1 b2 agonist. b2 relaxes skeletal muscle vasculature so you decrease afterload

norepinephrine does b1, a1, a2 but no b2 so it will have higher sbp

 

[JP2740]

Isoproterenol is a b1 b2 agonist. b2 relaxes skeletal muscle vasculature so you decrease afterload

norepinephrine does b1, a1, a2 but no b2 so it will have higher sbp

I guess what I'm confused about is that the first aid chart has b1 on that line as if it's b1 activity is responsible for the systolic BP

 

[pvtbacon]

I guess what I'm confused about is that the first aid chart has b1 on that line as if it's b1 activity is responsible for the systolic BP

b1 is partly responsible for the increase in systolic BP. b1 by activation of Gs subunit increases cAMP and increases contractility. likewise activation of b2 is responsible for the decrease in diastolic pressure

The diagram on the left again shows b1 increasing sbp and a1 increases the dbp.

 

[dbeast]

I'm guessing that this is hardly a "complicated concept" for this thread, and maybe I'm overthinking things, but why does cholestasis cause hyperlipidemia? Is it just you can't excrete the cholesterol as bile due to obstruction/PBC/whatever? Same goes for diabetes. Does insulin just promote VLDL secretion? Thanks peeps.

 

[TheSeanieB]

What parasitic inflections can cause a patient to become and chonic carrier in their gallbladder?

 

[dbeast]

What parasitic inflections can cause a patient to become and chonic carrier in their gallbladder?

I'm thinking it's Clonorchis because it increases risk of cholangiocarcinoma although First Aid doesn't specifically say you're a chronic carrier, but also don't forget that Salmonella can chronically live in the gallbladder too.

 

[coolforschool]

I'm guessing that this is hardly a "complicated concept" for this thread, and maybe I'm overthinking things, but why does cholestasis cause hyperlipidemia? Is it just you can't excrete the cholesterol as bile due to obstruction/PBC/whatever? Same goes for diabetes. Does insulin just promote VLDL secretion? Thanks peeps.

Wish I could help but all of that sh** confuses me. It's probably my weakest subject along with some of repro path and behavioral. My exam's less than a week away.

 

[223556]

I'm guessing that this is hardly a "complicated concept" for this thread, and maybe I'm overthinking things, but why does cholestasis cause hyperlipidemia? Is it just you can't excrete the cholesterol as bile due to obstruction/PBC/whatever? Same goes for diabetes. Does insulin just promote VLDL secretion? Thanks peeps.

I had a similar question regarding bile stasis/blockage pages back and (2)coolforschool gave a great answer here: http://forums.studentdoctor.net/showpost.php?p=14070095&postcount=471

 

[TheSeanieB]

I'm thinking it's Clonorchis because it increases risk of cholangiocarcinoma although First Aid doesn't specifically say you're a chronic carrier, but also don't forget that Salmonella can chronically live in the gallbladder too.

For some reason, I have it in my head that there was a parasite that would chronically inhabit the gallbladder if the patient was given the wrong antbiotics. Does this sound familiary to anyone?

 

[dbeast]

I had a similar question regarding bile stasis/blockage pages back and (2)coolforschool gave a great answer here: http://forums.studentdoctor.net/showpost.php?p=14070095&postcount=471

Cool, that sounds about right to me. Thanks!

 

[MLT2MT2DO]

For some reason, I have it in my head that there was a parasite that would chronically inhabit the gallbladder if the patient was given the wrong antbiotics. Does this sound familiary to anyone?

Two things pop into mind.

1. Salmonella Typhi
2. Vivax/Ovale if you don't give primaquine

 

[sharklasers]

For some reason, I have it in my head that there was a parasite that would chronically inhabit the gallbladder if the patient was given the wrong antbiotics. Does this sound familiary to anyone?

maybe entameoeba? needs iodaquinol (or something like that) for cysts, but -bendazoles work for everything else

don't know about gallbladder in particular though