Official Step 1 HY Renal Concepts & Discussion Thread

Mr. Mojo Risin · Jan 8, 2015

dfib slim · Jan 15, 2015

Common cause and pharmacological treatment for nephrogenic diabetes insipidus?

IndiaInk567 · Feb 12, 2015

AmphoB. Demeclocycline. Good q. Thx.

CodeRedDew · Feb 13, 2015

Why is HCTZ (diuretic) used to treat someone with nephrogenic DI (ie. why do you diurese these pts. even though they're volume depleted due to non-responding ADH receptors?)

faisal 2000 · Feb 13, 2015

dfib slim said:
Common cause for nephrogenic diabetes insipidus?

the problem here is kidney unable to use ADH may be due to inherited mutations or drugs like lithium and demeclocycline ,so patient develop
hypo-osomlar urine

dfib slim · Feb 13, 2015

CodeRedDew said:
Why is HCTZ (diuretic) used to treat someone with nephrogenic DI (ie. why do you diurese these pts. even though they're volume depleted due to non-responding ADH receptors?)

The sodium loss from inhibition in the DCT leads to increased reabsorption of sodium and water in the PCT.

faisal 2000 · Feb 13, 2015

where can i get more explanation about changes of cytidine concentration in the kidney ? or can anyone explain that

syoung · Feb 14, 2015

CodeRedDew said:
Why is HCTZ (diuretic) used to treat someone with nephrogenic DI (ie. why do you diurese these pts. even though they're volume depleted due to non-responding ADH receptors?)

you trick the kidneys into holding onto Na/H2O due to the HCTZ forcing more Na to be lost in the urine -> basically turning up the RAAS since the ADH is ineffective at the kidneys' receptors

CodeRedDew · Mar 12, 2015

42 y/o man arrives in ED and found to have been stabbed in the chest. HR is 135/min and BP is 65/40 mmHg - extremities are pale and cold to touch. BUN/creatinine values are significantly elevated.

Which of the circumstances listed best describes the kidney's response to pt's current condition?

Hormone Produced - Afferent arteriole response - Efferent arteriole response
A) Aldosterone - Constricts - Constricts
B) Aldosterone - Constricts - Dilates
C) ANP - Dilates - Constricts
D) Renin - Dilates - Constricts
E) Renin - Constricts - Constricts
F) Vasopressin - Dilates - Constricts

What's your answer and why?

syoung · Mar 13, 2015

F
vasopressin is a vasoconstrictor, can directly vasoconstrict systemic vascular vessels; i'd argue that it dilates afferent and constricts efferent because it's trying to preserve GFR in the kidneys
aldosterone acts mainly as a K waster and a Na reabsorber
ANP helps you natriurese
renin doesn't have direct effects on the arterioles, rather it acts on angiotensinogen and converts it to angiotensin I
Angiotensin II is the actual protein that acts on the arterioles, as well as upregulating ADH and aldosterone release; AII acts preferentially on efferent > afferent

So if not F then D, but that's a bit more indirect effects of renin on the arterioles' response

Slade009 · Mar 16, 2015

IndiaInk567 said:
AmphoB. Demeclocycline. Good q. Thx.

Democycline is an ADH antagonist so technically it can be a Secondary cause of Nephrogenic DI not a treatment. Democycline is the DOC for SIADH.

CodeRedDew · Mar 16, 2015

syoung said:
F
vasopressin is a vasoconstrictor, can directly vasoconstrict systemic vascular vessels; i'd argue that it dilates afferent and constricts efferent because it's trying to preserve GFR in the kidneys
aldosterone acts mainly as a K waster and a Na reabsorber
ANP helps you natriurese
renin doesn't have direct effects on the arterioles, rather it acts on angiotensinogen and converts it to angiotensin I
Angiotensin II is the actual protein that acts on the arterioles, as well as upregulating ADH and aldosterone release; AII acts preferentially on efferent > afferent

So if not F then D, but that's a bit more indirect effects of renin on the arterioles' response

Answer is D; however, I chose E since I thought that a severe hemorrhage as such where the BP <80mmHg, that the body would try and 'conserve' the blood for more vital organs (ie. heart/brain) instead of using it to make pee. So I figured both the efferent and afferent would constrict to DECREASE filtration. Aren't pts. with severe hemorrhage oliguric? If I'm thinking about this wrong, could someone please explain?

dfib slim · Mar 16, 2015

I would pick D because the question asks what is the "kidney's" response, it makes renin.

seminoma · Mar 17, 2015

CodeRedDew said:
42 y/o man arrives in ED and found to have been stabbed in the chest. HR is 135/min and BP is 65/40 mmHg - extremities are pale and cold to touch. BUN/creatinine values are significantly elevated.

Which of the circumstances listed best describes the kidney's response to pt's current condition?

Hormone Produced - Afferent arteriole response - Efferent arteriole response
A) Aldosterone - Constricts - Constricts
B) Aldosterone - Constricts - Dilates
C) ANP - Dilates - Constricts
D) Renin - Dilates - Constricts
E) Renin - Constricts - Constricts
F) Vasopressin - Dilates - Constricts

What's your answer and why?

D, but Renin isn't a hormone. Regardless, Renin is produced and angiotensin II constricts the efferent arteriole. Prostaglandins are also produced in hemorrhage, which produces dilation of the AA.

CodeRedDew said:
Answer is D; however, I chose E since I thought that a severe hemorrhage as such where the BP <80mmHg, that the body would try and 'conserve' the blood for more vital organs (ie. heart/brain) instead of using it to make pee. So I figured both the efferent and afferent would constrict to DECREASE filtration. Aren't pts. with severe hemorrhage oliguric? If I'm thinking about this wrong, could someone please explain?

They're oliguric because of aldo and ADH. Also, when you increase FF you increase peritubular capillary oncotic pressure, which increases reabsorption of sodium/water. The oliguria isn't because the kidney is being blocked off, it's because the kidney is reabsorbing everything it can.

seminoma · Mar 17, 2015

Slade009 said:
Democycline is an ADH antagonist so technically it can be a Secondary cause of Nephrogenic DI not a treatment. Democycline is the DOC for SIADH.

Cecil's says demeclocycline and lithium work, but aren't used often. Instead the treatment of choice is fluid restriction and, if that doesn't work, then it's one of the vaptans.

CodeRedDew · Mar 17, 2015

seminoma said:
D, but Renin isn't a hormone. Regardless, Renin is produced and angiotensin II constricts the efferent arteriole. Prostaglandins are also produced in hemorrhage, which produces dilation of the AA.

They're oliguric because of aldo and ADH. Also, when you increase FF you increase peritubular capillary oncotic pressure, which increases reabsorption of sodium/water. The oliguria isn't because the kidney is being blocked off, it's because the kidney is reabsorbing everything it can.

Gotcha. So in hemorrhage, the compensatory vasoconstriction that is seen in multiple vessels throughout the body DOES NOT occur in the afferent arteriole?

If so, is it safe to assume that hemorrhage will always be accompanied by an increase in FF (via vasodilation of afferent and vasoconstriction of efferent arterioles)?

seminoma · Mar 17, 2015

CodeRedDew said:
Gotcha. So in hemorrhage, the compensatory vasoconstriction that is seen in multiple vessels throughout the body DOES NOT occur in the afferent arteriole?

If so, is it safe to assume that hemorrhage will always be accompanied by an increase in FF (via vasodilation of afferent and vasoconstriction of efferent arterioles)?

Yes and no to the first question. High levels of ATII constricts both the AA and EA, but prostaglandins released locally in the kidney counteract the AA constriction. If it weren't for the prostaglandins, both would get constricted.

I think yes for the second question as long as there is normal physiology and no kidney damage or drugs involved.

CodeRedDew · Mar 17, 2015

seminoma said:
Yes and no to the first question. High levels of ATII constricts both the AA and EA, but prostaglandins released locally in the kidney counteract the AA constriction. If it weren't for the prostaglandins, both would get constricted.

I think yes for the second question as long as there is normal physiology and no kidney damage or drugs involved.

Guess that's where my confusion was because I thought the question was asking what was the response to the hormone (ie. AT-II coming from renin). But your response cleared it up, thanks for clarifying!

Slade009 · Mar 17, 2015

seminoma said:
Cecil's says demeclocycline and lithium work, but aren't used often. Instead the treatment of choice is fluid restriction and, if that doesn't work, then it's one of the vaptans.

From what I learned Demeclocyline and Lithium were used until their effects were later found out. What is Cecil's? Do you mean Goldman's Cecil?
Chronic Lithium use is the most common cause of drug-induced Nephrogenic DI and Demeclocycline causes reversible nephrogenic DI.

As far as what you've said regarding the treatment for SIADH, that's correct 👍. I forgot about Vaptans lol, before Vaptans Demeclocyline was the DOC.

Btw of all the books I been through I don't recall ever coming across Ampho B as a common cause of DI. Interesting.

theTruth_97 · May 4, 2015

How would hyperuricosuria increase risk for calcium nephrolithiasis? Uworld states that in one of their explanations and that us not making sense to me. Like wouldn't hyperuricosuria just increase risk of uric acid stones?

dfib slim · May 4, 2015

theTruth_97 said:
How would hyperuricosuria increase risk for calcium nephrolithiasis? Uworld states that in one of their explanations and that us not making sense to me. Like wouldn't hyperuricosuria just increase risk of uric acid stones?

http://www.mayomedicallaboratories....scripts/2010/2010-2a-kidney-stones/2a-22.html

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