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Discussion Starter · #1 ·
A 40-year-old man comes to the emergency department with a temperature of 39° C (102° F) and a heart rate of 95 beats/minute. He has Gram-negative bacteria in his blood. Which type of transport mechanism is most likely responsible for his elevated pulse rate?

A. Active transport
B. Antiporter
C. Passive diffusion
D. Symporter
E. Uniporter
 

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E. Uniporter

Since nobody wants to take a stab at it I shall try, even though I'm not sure...

---->gram negative org in blood could be due to septicemia, or initial stages of septic shock.

---->since pulse rate is high = tachycardia (+ive chronotropic effect? I dunno if that has any relevance to this), moderate in this case (95beats/min) upper human threshold is 100beats/min.


if the cardiac contractility increases in frequency and mechanism of muscle contractility involves the Ca2+ channels for Facilitated diffusion through carrier proteins, thus it means it can't be Passive diffusion or Active since this is a question for myocardial contractility.

so the only answer choice left is Uniporter, which is a form of carrier protein diffusion. ANY other GUESSES? :eek:

PM me to lemme know, I'm anxious to see if i got this right!!!! :sorry: hope I'm getting stronger in concepts!!! :D or maybe i'm still thinking waaaaaay toooooo much into it! :confused:


I have made a bad habit of doing this, any suggestions how not to OVER COMPLICATE the question than it already is? :eek:
 

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Discussion Starter · #3 ·
well u really overcomplicated it.....:eek:
btw u r wrong....try another concept...:D
its really out of our mind so dont worry....:)
 

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My guess

Okay so we need two more people guess wrong and come up with a crazy explanation and we'll have the right answer ;)

So my crazy guess is C - passive diffusion

Heart rate increase = increased SA node stimulation due to steeper phase 4 due to If sodium funny current.

Sympathetic stimulation increases chances the If funny current channels are open according to First Aid

So if the channels are open then Na can just go through moving the voltage inside up towards threshold and depolarization.

Although, according to wiki the funny current channels are actually a sodium / potassium channel, but i'm thinking the primary system is still passive - i haven't read anywhere that ATP is involved so that is my reasoning for kicking out anything involving energy.

Someone else take a shot?
 

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hmmm i would also go with

C. Passive diffusion

But the rationale would be gram -ve bactaremia ---> septic shock----> hypovolemia ----> tachycardia.


@khusboo............. Another atypical question. Thanks for shariing !!!!!
 

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hmmm i would also go with

C. Passive diffusion

But the rationale would be gram -ve bactaremia ---> septic shock----> hypovolemia ----> tachycardia.
Yeah sorry - I should have thrown that part in there.. Once you have hypovolemia you decrease the stimulation of the carotid sinus receptors and then this in turn causes increased sympathetic stimulation and tachycardia through the funny current mechanism...

Does that sound about right?
 

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Yeah sorry - I should have thrown that part in there.. Once you have hypovolemia you decrease the stimulation of the carotid sinus receptors and then this in turn causes increased sympathetic stimulation and tachycardia through the funny current mechanism...

Does that sound about right?
Yes u rite it doesn't make any sense... i totally misunderstood the question.......:eek:

I am changing my option to E. Uniporter

Shock would dec. pulse pressure due to dec stroke volume and inc. peripheral resistance.

The cause of increased pulse pressure is "Fever" alone.

Fever is mediated through prostaglandin's acting on the hypothalmic nuclei, so i guess... option E. Uniporter fits.

I hope i am right...........:scared:
 

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Discussion Starter · #11 ·
well tried guys.....

@ step1an.....never change ur first choice..... :D

Option C (Passive diffusion) is correct. The patient is experiencing endotoxic shock, which triggers a release of the vasodilator nitric oxide. This vasodilator readily moves across membranes by passive diffusion.

Option A (Active transport) is incorrect. The patient is experiencing endotoxic shock, which is mediated by passive transport of nitric oxide.

Option B (Antiporter) is incorrect. The patient is experiencing endotoxic shock, which is mediated by passive transport of nitric oxide.

Option D (Symporter) is incorrect. The patient is experiencing endotoxic shock, which is mediated by passive transport of nitric oxide.

Option E (Uniporter) is incorrect. The patient is experiencing endotoxic shock, which is mediated by passive transport of nitric oxide.

Most cases of septic shock (approximately 70%) are caused by endotoxin-producing gram-negative bacilli (Chapter 9), hence the term endotoxic shock. Endotoxins are bacterial wall lipopolysaccharides (LPSs) released when the cell walls are degraded (e.g., in an inflammatory response); LPS consists of a toxic fatty acid core common to all gram-negative bacteria (lipid A), and a complex polysaccharide coat that is unique for each species (O antigens). Analogous molecules in the walls of gram-positive bacteria and fungi can also elicit septic shock.

With moderately severe infections, and therefore with higher levels of LPS (and a consequent augmentation of the cytokine cascade), cytokine-induced secondary effectors (e.g., nitric oxide and platelet-activating factor; Chapter 2) become significant. In addition, systemic effects of TNF and IL-1 may begin to be seen, including fever, increased synthesis of acute-phase reactants, and increased production of circulating neutrophils
 

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Where did you get this question from? could I have the source please, cuz this is a pretty good question. The only problem I foresee is why didn't it list the reasons of why the rest of them couldn't be the answer instead of the repeat of the "Right answer" :)

I am still kind of shaky about the explanation, haha its probably because I over complicated it too much in my mind.....so NO creates hypotension in septic shock, thus SNS takes over and tachycardia results as a compensation mechanism? Is that it? cuz I just flew all the way to Fiji with the way I thought about this question! lol :eek:

Thanks for the question, you rock!
 

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Discussion Starter · #13 ·
Where did you get this question from? could I have the source please, cuz this is a pretty good question. The only problem I foresee is why didn't it list the reasons of why the rest of them couldn't be the answer instead of the repeat of the "Right answer" :)

I am still kind of shaky about the explanation, haha its probably because I over complicated it too much in my mind.....so NO creates hypotension in septic shock, thus SNS takes over and tachycardia results as a compensation mechanism? Is that it? cuz I just flew all the way to Fiji with the way I thought about this question! lol :eek:

Thanks for the question, you rock!
well its from usmle consult...
 

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@ step1an.....never change ur first choice..... :D
yes u r rite i will keep that in mind..... Its easier to advise than follow urself :eek:

I guess i was sleepy at that time.....it was just a straight forward question.
 

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Yeah, I really overthought that one too... I love how explanations are so clean and neat after you've answered... :)

Thanks again for the question and the lively discussion, keep it up guys!
 
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