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Patho QOD Exam 3 Questions And Correct Answers
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Patho QOD Exam 3 Questions And Correct AnswersExogenous Steroids:
People who are being treated with exogenous steroids often experience diminished
levels of ACTH and endogenously produced cortisol. Explain why this might be,
referencing the hypothalamic-pituitary feedback mechanism in your answer.
Start a New Thread - ANSWER Exogenous steroids will reduce ACTH secretion by the
pituitary gland through a negative feedback loop. As cortisol rises (even if it is
exogenous), the rise is sensed by the hypothalamus, which stops production of
corticotropin releasing hormone (CRH), and the reduction in CRH will result in less
ACTH being produced (remember the function of CRH is the get the pituitary to release
ACTH). Without the release of ACTH, the adrenal glands are not stimulated to produce
endogenous cortisol, and so levels endogenous cortisol levels drop.
This can be an issue if a patient is on long-term steroid therapy and we discontinue
steroids abruptly. In such a case, there is insufficient endogenous steroid production,
which could lead to life threatening adrenal insufficiency (much like an Addisonian
crisis). Remember that cortisol is a vital hormone, and we cannot handle physiologic or
psychologic stress without it. This is why those with Addison's disease must have
lifelong cortisol (and aldosterone) replacement. Additionally, the amount of cortisol
administered in someone with Addison's disease will be increased in times of stress!
Adrenal Insufficiency:
Explain why someone with adrenal insufficiency might develop hyperkalemia. - ANSWER
Adrenal insufficiency is a deficit of all hormones produced by the adrenal gland,
including the hormone aldosterone. Recall from our fluid-electrolyte lecture that one of
the primary roles of aldosterone is to regulate blood potassium. Aldosterone facilitates
secretion of potassium into the urine, and so a lack of aldosterone will compromise the
body's ability to rid itself of excess potassium. This can lead to higher levels of
potassium within the blood (hyperkalemia). Thus, patients with conditions such as
Addison's disease are at risk for hyperkalemia.
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, Hypothyroidism and TSH:
A patient with Hashimoto's thyroiditis presents with increased levels of TSH.
A. What kind of hypersensitivity reaction is this?
B. Why is the TSH increased?
Start a New Thread - ANSWER A. This is a Type II hypersensitivity reaction, in which the
body is generating auto-antibodies that target self antigens. Remember, a type III would
be the accumulation of antigen-antibody complexes in the tissues. Type I would be IgE
mediated (allergy/anaphylaxis) and Type IV would be T cell mediated.
B. The TSH is increased due to the nature of the feedback loop controlling its release.
When the problem is in the thyroid itself, then the thyroid is not producing enough T3
and T4. In an effort to address the problem, the pituitary gland releases more TSH
(resulting in increased TSH levels) in an effort to stimulate the thyroid gland to produce
more thyroid hormone. Unfortunately, the thyroid gland is unable to do so.
Now, contrast this to secondary hypothyroidism. In secondary hypothyroidism, the
problem could be the pituitary itself. For example, there might be damage to the
pituitary and it no longer produces TSH. This would result in low TSH and low thyroid
hormone.
Diabetic Complication:
A 6-year old boy is admitted to the emergency department with nausea, vomiting, and
abdominal pain. He is very lethargic, his skin is warm, dry, and flushed. His pulse is
rapid and he has a sweet smell to his breath. His parents relate that he has been very
thirsty during the past several weeks, his appetite is increased, and he has been
urinating frequently. Current blood glucose is 420 mg/dL and urine test for ketones is
strongly positive.
What is the most likely cause of the boy's elevated glucose and ketonuria? How does
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