Hypertension
Cushing's syndrome can be exogenous, resulting from the administration of glucocorticoids or adrenocorticotrophic hormone (ACTH), or endogenous, secondary to increased secretion of cortisol or ACTH. Hypertension is one of the most distinguishing features of endogenous Cushing's syndrome, as it is present in about 80% of adult patients and in almost half of children and adolescents patients. Hypertension results from the interplay of several pathophysiological mechanisms regulating plasma volume, peripheral vascular resistance and cardiac output, all of which may be increased. The therapeutic goal is to find and remove the cause of excess glucocorticoids, which, in most cases of endogenous Cushing's syndrome, is achieved surgically. Treatment of Cushing's syndrome usually results in resolution or amelioration of hypertension. However, some patients may not achieve normotension or may require a prolonged period of time for the correction of hypercortisolism. Therefore, therapeutic strategies for Cushing's-specific hypertension (to normalise blood pressure and decrease the duration of hypertension) are necessary to decrease the morbidity and mortality associated with this disorder. The various pathogenetic mechanisms that have been proposed for the development of glucocorticoid-induced hypertension in Cushing's syndrome and its management are discussed.
Muscle wasting
By contrast, glucocorticoids (cortisol) exert a clear catabolic effect, and their levels are frequently increased in diseased states. Cortisol activates a catabolic enzyme called ubiquitin-proteasome, which breaks down muscle tissue. Acute glucocorticoid treatment increases the expression of ubiquitin-proteases in muscle, resulting in catabolism.
Increased blood glucose
Other signs include polyuria (and accompanying polydipsia), persistent hypertension (due to cortisol's enhancement of epinephrine's vasoconstrictive effect) and insulin resistance (especially common in ectopic ACTH production), leading to hyperglycemia (high blood sugar) which can lead to diabetes mellitus.
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Showing posts with label Cushing's Syndrome. Show all posts
Showing posts with label Cushing's Syndrome. Show all posts
Wednesday, August 25, 2010
Cushing's Syndrome: Symptoms - Focus on moonface, central obesity, thin skin and fatigue.
Cushing’s Syndrome
It is basically high levels of cortisol or adrenocorticotropic hormone (which leads to high cortisol).
The reasons for the manifestations of the many symptoms relate directly to the actions of these hormones.
Overall symptoms
Most people with Cushing syndrome will have:
• Upper body obesity (above the waist) and thin arms and legs
• Round, red, full face (moon face)
• Slow growth rate in children
Skin changes that are often seen:
• Acne or skin infections
• Purple marks (1/2 inch or more wide) called striae on the skin of the abdomen, thighs, and breasts
• Thin skin with easy bruising
Muscle and bone changes include:
• Backache, which occurs with routine activities
• Bone pain or tenderness
• Collection of fat between the shoulders (buffalo hump)
• Thinning of the bones, which leads to rib and spine fractures
• Weak muscles
Women with Cushing syndrome often have:
• Excess hair growth on the face, neck, chest, abdomen, and thighs
• Menstrual cycle becomes irregular or stops
Men may have:
• Decreased fertility
• Decreased or no desire for sex
• Impotence
Other symptoms that may occur with this disease:
• Mental changes, such as depression, anxiety, or changes in behavior
• Fatigue
• Headache
• High blood pressure
• Increased thirst and urination
So how does excess cortisol cause the symptoms “moonface”, central obesity, thin skin and severe fatigue?
Cortisol counteracts insulin, contributing to hyperglycemia via stimulation of hepatic gluconeogenesis and inhibition of the peripheral utilization of glucose by decreasing the translocation of glucose transporters to the cell membrane, especially GLUT4. However cortisol increases glycogen synthesis (glycogenesis) in the liver. Cortisol also acts as an anti-diuretic hormone
Moonface
The reason why fat tends to accumulate where it does is not known, but perhaps it is because there are more stress hormone receptors in the face and body, which are more sensitive to insulin, where skeletal muscle is less sensitive to insulin. Another reason is due to increased mobilization of fat in extremities and deposition in the trunk.
Central obesity
It is generally suggested that stress-induced cortisol weight is usually gained around the waistline, because fat cells in that area are more sensitive to cortisol. The fat cells in your abdomen are richer in stress hormone receptors, are particularly sensitive to high insulin, and are very effective at storing energy – more so than fat cells you would find in other areas of the body.
Thin skin
In laboratory rats, cortisol-induced collagen loss in the skin is ten times greater than any other tissue. It is probable that increasing copper availability for immune purposes is the reason many copper enzymes are stimulated to an extent which is often 50% of their total potential by cortisol. This includes lysyl oxidase, an enzyme which is used to cross link collagen and elastin.
Severe fatigue
This is due to increased catabolism of protein for gluconeogenesis and decreased synthesis of protein (except for in the liver). This leads to muscle weakness and thus fatigue. As the effects of insulin are also reduced, glucose is not being effectively taken into cells, especially skeletal muscle which can also contribute to feeling fatigued.
It is basically high levels of cortisol or adrenocorticotropic hormone (which leads to high cortisol).
The reasons for the manifestations of the many symptoms relate directly to the actions of these hormones.
Overall symptoms
Most people with Cushing syndrome will have:
• Upper body obesity (above the waist) and thin arms and legs
• Round, red, full face (moon face)
• Slow growth rate in children
Skin changes that are often seen:
• Acne or skin infections
• Purple marks (1/2 inch or more wide) called striae on the skin of the abdomen, thighs, and breasts
• Thin skin with easy bruising
Muscle and bone changes include:
• Backache, which occurs with routine activities
• Bone pain or tenderness
• Collection of fat between the shoulders (buffalo hump)
• Thinning of the bones, which leads to rib and spine fractures
• Weak muscles
Women with Cushing syndrome often have:
• Excess hair growth on the face, neck, chest, abdomen, and thighs
• Menstrual cycle becomes irregular or stops
Men may have:
• Decreased fertility
• Decreased or no desire for sex
• Impotence
Other symptoms that may occur with this disease:
• Mental changes, such as depression, anxiety, or changes in behavior
• Fatigue
• Headache
• High blood pressure
• Increased thirst and urination
So how does excess cortisol cause the symptoms “moonface”, central obesity, thin skin and severe fatigue?
Cortisol counteracts insulin, contributing to hyperglycemia via stimulation of hepatic gluconeogenesis and inhibition of the peripheral utilization of glucose by decreasing the translocation of glucose transporters to the cell membrane, especially GLUT4. However cortisol increases glycogen synthesis (glycogenesis) in the liver. Cortisol also acts as an anti-diuretic hormone
Moonface
The reason why fat tends to accumulate where it does is not known, but perhaps it is because there are more stress hormone receptors in the face and body, which are more sensitive to insulin, where skeletal muscle is less sensitive to insulin. Another reason is due to increased mobilization of fat in extremities and deposition in the trunk.
Central obesity
It is generally suggested that stress-induced cortisol weight is usually gained around the waistline, because fat cells in that area are more sensitive to cortisol. The fat cells in your abdomen are richer in stress hormone receptors, are particularly sensitive to high insulin, and are very effective at storing energy – more so than fat cells you would find in other areas of the body.
Thin skin
In laboratory rats, cortisol-induced collagen loss in the skin is ten times greater than any other tissue. It is probable that increasing copper availability for immune purposes is the reason many copper enzymes are stimulated to an extent which is often 50% of their total potential by cortisol. This includes lysyl oxidase, an enzyme which is used to cross link collagen and elastin.
Severe fatigue
This is due to increased catabolism of protein for gluconeogenesis and decreased synthesis of protein (except for in the liver). This leads to muscle weakness and thus fatigue. As the effects of insulin are also reduced, glucose is not being effectively taken into cells, especially skeletal muscle which can also contribute to feeling fatigued.
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