NUR 239 Lecture Notes - Lecture 7: Adrenal Insufficiency, Adrenal Tumor, Anterior Pituitary
21 May 2018
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NUR 239/Pathophysiology and Pharmacotherapeutics in Nursing I
Unit 2/Drugs affecting the immune system
Complete the following study guide and submit on Reggie Net by the due date on the Course Calendar
1
Frandsen Chapter 17
Key Terms
Addison’s disease: primary adrenocortical insufficiency with inadequate production of cortisol and
aldosterone
Addisonian crisis: condition that mimics hypovolemic and septic shock; also known as adrenocortical
insufficiency
Aldosterone: mineralocorticoid hormone secreted by the adrenal cortex to increase sodium reabsorption
by the kidneys and indirectly regulate blood levels of potassium, sodium, and bicarbonate; also regulates
pH, blood volume, and blood pressure
Corticosteroid: steroid hormone produced by the adrenal cortex; examples include androgens,
glucocorticoids, and mineralocorticoids
Cortisol: the main glucocorticoid secreted as part of the body’s response to stress
Cushing’s disease: adrenocortical hyper function; may result from excessive corticotrophin or primary
adrenal tumor
Glucocorticoid: adrenal cortical hormone that protects the body against stress and affects protein and
carbohydrate metabolism
Immunosuppression: suppression of the immune system
Mineralocorticoid: steroid hormone released by the adrenal cortex to promote sodium and water
retention and potassium excretion
Negative feedback mechanism: when the output of a system affects the stimulus for the system (e.g.
hormone secretion produces an effect that shuts off the stimulus for further hormone secretion)
Steroid: lipid-soluble hormone produced by the gonadal organs or the adrenal cortex
Key Learning Objectives
▪ What is the difference between endogenous and exogenous corticosteroids?
o Exogenous: used as drugs in a variety of disorders; must be monitored due to
profound therapeutic and adverse effects
▪ Where is the endogenous secretion of corticosteroids controlled?
o Hypothalamus, the anterior pituitary, and adrenal cortex
▪ What events stimulate the secretion of corticosteroids?
o Low plasma, levels of corticosteroids, pain, anxiety, trauma, illness, being placed
under anesthesia cause the hypothalamus of the brain to secrete corticotrophin-
releasing hormone or factor, which stimulates the anterior pituitary gland to secret
corticotrophin, and corticotrophin then stimulates the adrenal cortex to secrete
corticosteroids
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NUR 239/Pathophysiology and Pharmacotherapeutics in Nursing I
Unit 2/Drugs affecting the immune system
Complete the following study guide and submit on Reggie Net by the due date on the Course Calendar
2
▪ Describe the negative feedback mechanism. How does stress affect this mechanism?
o Usually the rate of corticosteroid secretion is maintained within limits but changes
according to need. When plasma corticosteroid levels rise, secretion of the steroids
slows or stops. The mechanism by which the hypothalamus and anterior pituitary
“learn” that no more corticosteroids are needed is negative feedback.
o Negative feedback does not work during stress responses. The stress activates the
sympathetic nervous system to produce more epinephrine and norepinephrine and the
adrenal cortex to produce as much as 10x the normal amount of cortisol. The
interaction of the hormones increases the ability to respond to stress. The increased
SNS activity continues to stimulate cortisol production (main glucocorticoid secreted
as part of the body’s response to stress) and overrules the negative feedback.
▪ What percentage of cortisol is protein bound? How does this affect the half-life?
o Cortisol is 90% protein bound to plasma proteins, and this high degree of binding
slow cortisol movement out of the plasma, so that is has a relatively long plasma half-
life of 60 to 90 minutes.
▪ See Box 17.1 (p. 329) – summarize the effects glucocorticoids on the body processes and
systems.
o Carbohydrate Metabolism:
▪ increase formation of glucose by breaking down protein into amino acids →
transported to the liver where enzymes convert them to glucose → returned to
the circulation for use by body tissues or storage in the liver as glycogen
▪ Increase the production and decrease use of glucose promote higher levels of
glucose in the blood and can lead to DM; also increase the amount of GLU
stored as glycogen in liver, skeletal muscles, and other tissues
o Protein Metabolism:
▪ breakdown of protein into amino acids (catabolic effect), increase rate of AA
transport to the liver and convert to glucose
▪ Decrease rate of new protein forming from dietary and other AA (anti-
anabolic effect)
▪ Increase breakdown of cell protein and decrease protein making leads to
protein depletion in virtually all body cells except those of liver.
▪ Glycogen stores in the body are higher and protein stores are lower.
o Lipid Metabolism
▪ Increase breakdown of adipose into fatty acids, FA are transported in the
plasma and used as a source of energy body cells
▪ Increase oxidation of fatty acids within body cells
o Inflammatory and Immune Response
▪ Decrease inflammatory response. Inflaming is the normal bodily response to
tissue damage and involves three stages:
• Large amount of plasma-like fluid leads out of capillaries into
damaged area and becomes clotted
• Leukocytes migrate into the area
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Complete the following study guide and submit on reggie net by the due date on the course calendar. Addison"s disease: primary adrenocortical insufficiency with inadequate production of cortisol and aldosterone. Addisonian crisis: condition that mimics hypovolemic and septic shock; also known as adrenocortical insufficiency. Aldosterone: mineralocorticoid hormone secreted by the adrenal cortex to increase sodium reabsorption by the kidneys and indirectly regulate blood levels of potassium, sodium, and bicarbonate; also regulates ph, blood volume, and blood pressure. Corticosteroid: steroid hormone produced by the adrenal cortex; examples include androgens, glucocorticoids, and mineralocorticoids. Cortisol: the main glucocorticoid secreted as part of the body"s response to stress. Cushing"s disease: adrenocortical hyper function; may result from excessive corticotrophin or primary adrenal tumor. Glucocorticoid: adrenal cortical hormone that protects the body against stress and affects protein and carbohydrate metabolism. Mineralocorticoid: steroid hormone released by the adrenal cortex to promote sodium and water retention and potassium excretion.
