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Author34 Posts
  #1

A 66-year-old male with chronic rheumatoid arthritis comes to the emergency department with fever and cough productive of yellow sputum for the past ten hours. He has had rheumatoid arthritis for the past twelve years. He has been taking methotrexate (5 mg/wk), prednisone (7.5 mg/d), and NSAIDs (as needed) for the last several years. Physical examination reveals a sick-appearing male with cushingoid features. His blood pressure is 90/70 mm Hg, heart rate is 110/min, temperature is 102 F(38.9C) and respirations are 24/min. His oxygen saturation by pulse oximetry is 92% on 2 liters of intranasal oxygen. His mucous membranes are moist. There is no pallor or icterus. Lung examination reveals crackles on the left base. The other systems are normal. Laboratory investigations reveal an increase in the total WBC count with a left shift. His basic serum chemistry profile is normal, except for a serum sodium level of 131 mEq/L and BUN level of 27 mg/dL. Chest x-ray reveals a left lower lobe infiltrate. EKG reveals sinus tachycardia with nonspecific ST-T wave changes.


What is the most likely cause of hypotension in this patient?


A. Sepsis
B. Aldosterone deficiency
C. Cortisol deficiency
D. ACTH deficiency
E. Cardiogenic shock


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  #2

First shot: patient in corticosteroid treatment-------->immunosupression------->risk of infections--------> Lung infiltrate-------->sepsis

A


Edited by Ivonne on 12/26/07 - 02:33 PM

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  #3

@ Ivonne

How do you explain hyponatremia?

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  #4

D

Exogenous corticosteroid leads to ACTH suppression, leading to less aldosterone production, leading to hypotension and hyponatremia.


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Que sera sera, whatever will be will be.

  #5

Interesting!

There are many points here:

i thought that the cessation of long-term glucocorticoid treatment will cause 2ry adrenal insufficiency (Patient is still in treatment)

i thought that in terciary adrenal insufficiency(due to chronic use of supraphysiological doses of corticoids) will decrease ACTH and cortisol but the aldosterone secretion is relatively preserved.

I though that any problem inside the brain or the lung could cause SIADH------->hyponatremia.

But i might be wrong since Arlete is always rightwink


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  #6

arlete wrote:
D

Exogenous corticosteroid leads to ACTH suppression, leading to less aldosterone production, leading to hypotension and hyponatremia.


i.e. B?

  #7

anastamosis wrote:
@ Ivonne

How do you explain hyponatremia?



you can't for sure tell what caused hyponatremia - you have not serum osm or/and ECF volume.
But the q is abt hypotension, and i agree with a - pt is septic and on immunosupressive drugs, so more likely A


  #8

i think it is cortisol deficiency..chronic exogenous steroid>adrenal atropy..now this patient needs more steroid to tide over the acute stress..the dose he is recieving is not enough and the adrenals cant produce it because they are atropied..ACTH would infact be raised as the pituatary tries to push the adrenals to produce more and the pituatary is normal..ACTH would be suppresed only as long as the body has sufficient steroid..as soon as the demand increases, the pituatary would go into overdrive..hypotension is explained by the fact that catecholamines cant produce the vasoconstriction in absence of the permissive action of cortisol..
sepsis is unlikely because septic shock is warm with increased cardiac output and wide pulse pressure not evident here..
also, ACTH deficiency doesnt affect alsosterone, since primary controller of alsosterone is angiotensin and ACTH has a negligible role..

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  #9

Gingko is in harmony with the UW Answer.

Arlete, ACTH does not control the secretion of mineralocorticoids from the zona glomerulosa of the adrenal glands. I agree that ACTH will be low under -ve feedback from exogenous steroids. But decreased ACTH will not casue Hypotension in this patient.

Hero, the question says,"His basic serum chemistry profile is normal, except for a serum sodium level of 131 mEq/L and BUN level of 27 mg/dL"

But there are a few queries.
1) Since the infection is the stress source here which precipiatated the hypotension, why is A. not the answer?

2) Will cortisol deficieny casue hyponatremia?

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  #10

septic shock would cause a wide pulse pressure due to vasodilatation..this patient has a low pulse pressure
as for hyponatremia, most likely cause may be aldosterone deficiency, but i am not sure with all the mineralocorticoid escapes etc..

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Old McDonald had an ERAS inbox..with a reject here and a reject there..here a reject, there a reject,everywhere a reject, reject.

  #11

narrow, i mean

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Old McDonald had an ERAS inbox..with a reject here and a reject there..here a reject, there a reject,everywhere a reject, reject.

  #12

Even i thought B should be the answer

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  #13

what abt BUN?
If BUN 27, serum creatinin is normal, BUN/creat ratio is 20 or more, what is prerenal RF.

bcs of what? low cortisol??

  #14

Pre Renal RF due to hypotension

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  #15

nice question!


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"I must, I can and I will"

  #16

It seems to be secondary adrenal insuf.---->lack of cortisol.
BUT
I dont understand why hyponatremiarolling eyes

  #17

Nice question! Thank you, anastomosis.

See, Ivonne: I am not always right! wink Actually, endocrinology was one of my weakest subjects in step 2 CK...

Doesn't cortisol have a weak mineralocorticoid action? Its deficiency wouldn't lead to hyponatremia (it's a relative deficiency, since under stress the normal body reaction is to increase its production)?


___________________
Que sera sera, whatever will be will be.

  #18

Arlete, it does not matter how you performed in S2CK. I got a STAR in endocrinology in step 2 ck, but now i am preparing for S3, its all boggled up. We all have the knowledge but the format of questions and the way we should look at them is drastically different for S3. I wonder why people say S3 is similar to S2CK?

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  #19

Next Step

Intravenous fluids and antibiotics were administered after drawing blood cultures. What is the most appropriate next step in management?


A. Place arterial line and start dopamine.
B. Administer intravenous methylprednisone.
C. Administer dexamethasone and perform cosyntropin stimulation test.
D. Start fludrocortisone.
E. Perform dexamethasone suppression test.


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THE HIGHER YOU AIM, THE HIGHER YOU REACH !! My contacts are as follows ==> yahoo id --> anastamosis_e2e;gmail id --> anastamosis;Skype id --> anastamosis

  #20

anastomosis, you're scaring me! sad

B (not even close to be sure on that, just a guess).


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Que sera sera, whatever will be will be.

  #21

Good Morning Arlete.

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  #22

We need to replace only glucocorticoid in this acute stage. So Dexamenthasone and its derivatives should be used. This also rules out prednisone. We are not using Hydrocortisone due to its interference with the COSYNTROPIN test. So we should use dexamethasone.

Correct me if i am wrong some where

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  #23

1)------------->C. Cortisol deficiency
2)------------->C. Administer dexamethasone and perform cosyntropin stimulation test.

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  #24

Aashi , can we have your reasoning behind those answers?

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  #25

nodnodnod
Aashi wrote:
1)------------->C. Cortisol deficiency
2)------------->C. Administer dexamethasone and perform cosyntropin stimulation test.









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