What is the cause of mineralocorticoid deficiency in Addison's disease?
Explanation
This question assesses the fundamental pathology of Addison's disease, specifically the lack of aldosterone and its consequences.
Other questions
What percentage of cortisol in the plasma is bound to plasma proteins such as cortisol-binding globulin and albumin?
What is the approximate half-life of cortisol, and how does its high degree of plasma protein binding affect this?
What percentage of circulating aldosterone is in the free form, and what is its resulting half-life?
Which enzyme is responsible for the conversion of cholesterol to pregnenolone in the synthesis of steroid hormones?
What is the primary site of degradation for adrenal steroids, and what are the main conjugation products?
According to Table 78-1, how does the mineralocorticoid activity of aldosterone compare to that of cortisol?
What is the average secretory rate of cortisol, and how does this compare to the secretory rate of aldosterone?
What is the primary role of the enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) in renal epithelial cells?
A genetic deficiency of the enzyme 11beta-HSD2 can lead to a condition called apparent mineralocorticoid excess syndrome (AME). What is the expected plasma aldosterone level in a patient with AME?
Ingestion of large amounts of licorice can cause a syndrome similar to apparent mineralocorticoid excess (AME) because it contains glycyrrhetinic acid. How does this substance cause the effect?
What is the phenomenon known as 'aldosterone escape'?
What are the dual effects of aldosterone on renal tubular handling of sodium and potassium?
In a person with excess aldosterone secretion (e.g., from an adrenal tumor), what is the effect on plasma potassium concentration and why can this lead to muscle weakness?
How does a complete lack of aldosterone secretion affect the extracellular fluid potassium ion concentration and cardiac function?
What is the cellular mechanism of aldosterone action in tubular epithelial cells, starting from its entry into the cell?
How long does it typically take after aldosterone administration for the rates of sodium and potassium transport to begin increasing, according to the genomic mechanism?
Which two factors are described as the most potent in regulating aldosterone secretion?
What is the described role of ACTH in the regulation of aldosterone secretion under most physiological conditions?
What is the best-known metabolic effect of cortisol, and by how much can it increase the rate of this process?
How does cortisol cause mobilization of amino acids from extrahepatic tissues?
While cortisol reduces protein stores in most body cells, it has an opposite effect in the liver. What is this effect?
What is the condition called 'adrenal diabetes,' and why is insulin administration only moderately effective in treating it?
What is the primary mechanism by which cortisol promotes fatty acid mobilization from adipose tissue?
Excess cortisol secretion can lead to a peculiar type of obesity. How is this obesity characterized?
Which of the following is a primary anti-inflammatory effect of cortisol?
How does cortisol administration affect the numbers of eosinophils and lymphocytes in the blood?
What is the principal effect of ACTH on adrenocortical cells that leads to steroid production?
What is the 'rate-limiting' step for the synthesis of all adrenocortical hormones that is activated by ACTH?
Cortisol secretion exhibits a circadian rhythm. When are the secretory rates of CRF, ACTH, and cortisol typically highest?
What is the effect of administering an ACE inhibitor on plasma aldosterone and cortisol concentrations in sodium-depleted dogs, as shown in Figure 78-5?
Why do most people with Addison's disease develop melanin pigmentation of the skin and mucous membranes?
What is the most common cause of Cushing's syndrome?
How is the dexamethasone suppression test used to help distinguish between ACTH-dependent and ACTH-independent Cushing's syndrome?
Primary aldosteronism (Conn's syndrome) is characterized by the effects of excess aldosterone. What is a key diagnostic criterion for this condition related to plasma renin?
What is the effect of total loss of adrenocortical secretion on survival if left untreated?
In a state of aldosterone deficiency, why does hyponatremia (low plasma sodium) occur?
What is the primary function of dehydroepiandrosterone (DHEA) secreted by the adrenal cortex?
What is the role of aldosterone on sweat glands, salivary glands, and intestinal epithelial cells?
At least what percentage of the glucocorticoid activity of adrenocortical secretions results from the secretion of cortisol?
What is the primary effect of cortisol on the immune system that makes it useful in preventing rejection of transplanted organs?
What is the chemical name for the active form of cortisol and the inactive form to which it is converted by 11beta-HSD2?
How does cortisol provide negative feedback to regulate its own secretion?
What is the primary stimulus for the secretion of corticotropin-releasing factor (CRF) from the hypothalamus?
According to Figure 78-4, which drug can be used to block the epithelial sodium channel (ENaC) and antagonize the sodium-retaining effects of aldosterone?
In the adrenogenital syndrome, what is the effect of excessive androgen secretion from an adrenocortical tumor in a prepubertal male?
What is the primary reason that glucocorticoid deficiency in Addison's disease makes a person highly susceptible to stress?
Which of these synthetic steroids listed in Table 78-1 has the highest glucocorticoid activity relative to cortisol?
What is the primary purpose of the 'reservoir' function of plasma protein binding for adrenal steroids like cortisol?
In the pathways for synthesis of steroid hormones shown in Figure 78-2, which enzyme is required to produce mineralocorticoids like corticosterone but is NOT required for the main pathway to glucocorticoids like cortisol?