Jackson Lectures 4 Flashcards
(50 cards)
Actions of cortisol are essential under non-stress conditions, but they can become damaging when
cortisol is elevated for long periods of time and combined with chronic activation of the SNS
• cortisol is highly catabolic on substrates used to produce needed
glucose;
tissue can be rebuilt when stress is over, but catabolism continues as long as stressor is present
• cortisol has anti-inflammatory and anti-immune effects to inhibit
cytokines and phagocytosis, and block proliferation of white blood cells
- this conserves energy in the short term, but damaging with chronic stress
• mobilization of metabolic fuels increases
lipids in the blood which, when combined with increased blood pressure (sympathetic response), can lead to development of atherosclerosis and hypertension
So problems arise when a continued physical or psychological stressor turns a short-term response into
chronic activation of CRH (cortisolreleaseing hormone) neurons.
Evidence for an interaction between immune function and activation of the stress response.
- HSV + psychiatric illness → increased recurrences and duration of outbreak
- influenza + family dysfunction → increased frequency and severity of illness
- hepatitis B + exams → delayed antibody response to vaccine
Adrenal insufficiency or
Addison’s Disease
Causes of primary adrenal insufficiency: disease
disease – tuberculosis destroys adrenal cortex
Causes of primary adrenal insufficiency: congenital disorder
– improper development or mutation in enzyme
Causes of primary adrenal insufficiency: autoimmune disorder
– affects all cortex cells,
Causes of secondary adrenal insufficiency: pituitary problem
– aldosterone not typically affected, as aldosterone is stimulated by something else.
Causes of secondary adrenal insufficiency: glucocorticoid therapy
– use of exogenous corticosteroids for a number of conditions has feedback effects on CRH and ACTH and can impair a normal stress response.
Adrenal insufficiency: This is an important consideration for dental patients because
there may be complications with maintaining blood pressure during anesthesia, and diminished immune and inflammatory responses.
Symptoms of adrenal insufficiency
- low cortisol and high ACTH
- weakness, lethargy, decreased appetite
- low blood pressure
- low glucose when fasting
- hyperpigmentation due to lack of negative feedback control of POMC production
Adrenal insufficiency: Treat with
exogenous glucocorticoids and/or dietary control
Hypercortisolinemia or
Cushing’s disease
Hypercortisolinemia is typically due to a
pituitary tumor (or administering too much exogenous glucocorticoid), and can be treated by removing the tumor.
Hypercortisolinemia Symptoms are related to =
elevated basal concentrations of cortisol
• excessive tissue catabolism, especially bone, skin, and muscle
- diabetes – like symptoms – increased appetite and circulating glucose, redistribution of fat stores
- impaired immune function
- threat of hypertension
Hypercortisolinemia: In dental patients, the primary concern is
impairment of immune function after a procedure, but hypertension, osteoporosis, and increased bleeding are also problematic.
The three major classes of sex steroids differ with respect to the
number of carbons they contain: or pregnanes (21 C), androgens or androstanes (19 C), and estrogens or estranes (18 C).
start with progesterone, converted to
androgens, converted to estrogens.
The primary male hormone is
testosterone (T) which is an androgen
. T is more potent than
DHEA and androstenedione.
T is converted to the most potent androgen, DHT, by the
enzyme 5α-reductase. All for 1 recepter = higher affinity.
