NURS 5315 Endocrine
Addison's Disease - ANS-Disease of the adrenal cortex that results in decreased cortisol and
aldosterone secretion. Patho is d/t autoimmune reaction which targets the adrenal cortex
and causes adrenal atrophy and hypofunction. May be caused by TB, metastatic tumors,
infection, HIV, fungal infections, amyloidosis or cessation of steroid therapy.
\Addison's disease S&S - ANS-Before S&S appear 90% of gland has been destroyed. S&S:
hypoglycemia, weakness, fatigue, apathy, mental confusion, avorexia, nvd, abdominal pain
and addisonia triad-hyperkalemia(not enough aldosterone to rid of potassium),
hyponatremia(not enough aldosterone to retain sodium), and hypotension(not enough
cortisol to maintain vascular tone)
\Adrenal Glands hormones - ANS-Made up of the cortex which secretes steroids such as
cortisone and aldosterone and the medulla which secretes catecholamines such as epi and
norepi
\Aging in the adrenal gland - ANS-After age 50, the adrenal cortex develops fibrous tissue.
As we age we cannot clear glucocorticoids that our bodies produce very well. Less cortisol is
used as we age as well. With decreased clearance and use of cortisol the circulating levels
of cortisol are elevated
\Aging in the pancreas - ANS-Decline in beta cell function which leads to glucose intolerance
or diabetes. Pancreatic cell regeneration declines. Growth hormone secretion decreases
with age which causes a decrease in muscle size and function. Elevated levels of PTH are
associated with increased mortality. Decreased vit. D levels has been associated with
osteoporosis, cancer, autoimmune disorders, diabetes, cardiovascular disease and mental
health disorders.
\Aging in the thyroid - ANS-Undergoes some atrophy and fibrosis. Inflammation and
nodularity also occurs. Signs of thyroid disease are more occult in the elderly. TSH secretion
is thought to be increased.
\Anorexia of aging risk factors - ANS-functional impairments and deficiencies, medical and
psychiaric conditions, loneliness and grief, medications, social isolation, and abuse or
neglect
\Anorexia or aging - ANS-Decrease in appetite or food intake. Results from reduced energy
needs, waning hunger, diminished senses of smell and taste, decreased production of
saliva, altered GI satiety control mechanisms and presence of comorbidities.
\Anorexia or aging consequences - ANS-malnutrition, physical frailty, mitochondrial
dysfunction, reduced regenerative capacity, increased oxidative stress and imbalanced
hormonal levels. Death rates are higher when this is present
\Bone density classifications - ANS-normal bone mass>833. Osteopenia: 648-833.
Osteoporosis<648
\Coronary artery disease - ANS-Most common cause of morbidity and mortality in DM.
Prevalence increases with duration but not severity of DM. MI's lead to death in 75% of
diabetics bc they are often asymptomatic d/t peripheral and autonomic neuropathies
\Cushing disease - ANS-Characterized by a chronic over secretion of cortisol. Etiologies
include exogenous steroid use, over-secretion of ACTH 2nd to pituitary tumor, ectopically
produced ACTH from a non-pituitary carcinoma or adrenal adenoma
, \Cushing disease results - ANS->increased glycogenolysis which results in hyperglycemia
and type 2 DM >abnormal redistribution of fat and elevated blood lipid products. Body
changes include truncal obesity, moon face and formation of a buffalo hump. "cushingoid"
appearance>weakened collagen fibers leads to skin fragility, bruising and skin tears. They
will have purple striae over areas of increased fat deposits>Increased ACTH will cause
hirsutism(increased hair growth) and acne>people will bleed more easily and are more
susceptible to infection
\Dawn phenomenon - ANS-Early morning rise in blood glucose concentration caused by
nocturnal elevations of GH which decreases metabolism of glucose by muscle and fat.
Increasing the dose of evening insulin manages the problem.
\Diabetic Ketoacidosis (DKA) - ANS-Complication which results from insulin deficiency and
the release of counter regulatory hormones(catecholamines, glucagon, cortisol). Most
common predisposing factors are illness, infection, trauma, surgery, MI and lack of
medication compliance. The lack of insulin causes an increase in hepatic glucose
production, a decrease in peripheral glucose utilization, initiation of gluconeogenesis and
formation of ketone bodies and metabolic acidosis.
\Diabetic Nephropathy - ANS-Hyperglycemia leads to activation of the polyol pathway,
hexosamine pathway, protein kinase C and inflammation and the production of advanced
glycation end products which all cause kidney tissue injury yet exact process is not known.
The glomeruli are also injured.
\Diabetic Nephropathy S&S - ANS-Microalbuminuria is the first manifestation and develops
within 5-10 years. Later, hypoproteinemia, reduction in plasma oncotic pressure, fluid
overload, anasarca and hypertension may occur. As it continues, people with type 1 may
have problems with hypoglycemia. Glomerular filtration rate drops, and nausea, lethargy,
acidosis, anemia and uncontrolled hypertension may occur.
\Diabetic neuropathies - ANS-Most common complication of diabetes
Affects all types of nerves
> peripheral (sensorimotor) nerves
> autonomic (somatic) nerves
> spinal nerves
Prevalence increases with age of person & duration of DM
May be the first symptom of diabetes
May appear during periods of "good" glucose control
If blood glucose controlled, neuropathies decreased by 60%
Capillary basement membrane thickening & capillary closure may be present
Demyelinization of the nerves related to hyperglycemia
> delayed conduction
> nerve degeneration
> sensory deficits/symptoms more common than motor
Cognitive dysfunction can occur with chronic hyperglycemia
Some neuropathies are progressive & some may improve spontaneously
\Diabetic Retinopathy - ANS-Leading cause of blindness. Results from damage to retinal
blood vessels and RBCs, platelet aggregation, relative hypoxemia and hypertension. S&S:
blurring or loss of vision, reduced visual acuity, cataracts, and defects in the eye muscle
\Diabetic Retinopathy patho - ANS-Stage 1 nonproliferative: characterized by thickening of
the retinal capillary basement membrane and an increase in retinal capillary permeability,
vein dilation, microaneurysm formation and hemorrhages. Stage 2 preproliferative:
progression of retinal ischemia with areas of poor perfusion that culminate in infarcts. stage
Addison's Disease - ANS-Disease of the adrenal cortex that results in decreased cortisol and
aldosterone secretion. Patho is d/t autoimmune reaction which targets the adrenal cortex
and causes adrenal atrophy and hypofunction. May be caused by TB, metastatic tumors,
infection, HIV, fungal infections, amyloidosis or cessation of steroid therapy.
\Addison's disease S&S - ANS-Before S&S appear 90% of gland has been destroyed. S&S:
hypoglycemia, weakness, fatigue, apathy, mental confusion, avorexia, nvd, abdominal pain
and addisonia triad-hyperkalemia(not enough aldosterone to rid of potassium),
hyponatremia(not enough aldosterone to retain sodium), and hypotension(not enough
cortisol to maintain vascular tone)
\Adrenal Glands hormones - ANS-Made up of the cortex which secretes steroids such as
cortisone and aldosterone and the medulla which secretes catecholamines such as epi and
norepi
\Aging in the adrenal gland - ANS-After age 50, the adrenal cortex develops fibrous tissue.
As we age we cannot clear glucocorticoids that our bodies produce very well. Less cortisol is
used as we age as well. With decreased clearance and use of cortisol the circulating levels
of cortisol are elevated
\Aging in the pancreas - ANS-Decline in beta cell function which leads to glucose intolerance
or diabetes. Pancreatic cell regeneration declines. Growth hormone secretion decreases
with age which causes a decrease in muscle size and function. Elevated levels of PTH are
associated with increased mortality. Decreased vit. D levels has been associated with
osteoporosis, cancer, autoimmune disorders, diabetes, cardiovascular disease and mental
health disorders.
\Aging in the thyroid - ANS-Undergoes some atrophy and fibrosis. Inflammation and
nodularity also occurs. Signs of thyroid disease are more occult in the elderly. TSH secretion
is thought to be increased.
\Anorexia of aging risk factors - ANS-functional impairments and deficiencies, medical and
psychiaric conditions, loneliness and grief, medications, social isolation, and abuse or
neglect
\Anorexia or aging - ANS-Decrease in appetite or food intake. Results from reduced energy
needs, waning hunger, diminished senses of smell and taste, decreased production of
saliva, altered GI satiety control mechanisms and presence of comorbidities.
\Anorexia or aging consequences - ANS-malnutrition, physical frailty, mitochondrial
dysfunction, reduced regenerative capacity, increased oxidative stress and imbalanced
hormonal levels. Death rates are higher when this is present
\Bone density classifications - ANS-normal bone mass>833. Osteopenia: 648-833.
Osteoporosis<648
\Coronary artery disease - ANS-Most common cause of morbidity and mortality in DM.
Prevalence increases with duration but not severity of DM. MI's lead to death in 75% of
diabetics bc they are often asymptomatic d/t peripheral and autonomic neuropathies
\Cushing disease - ANS-Characterized by a chronic over secretion of cortisol. Etiologies
include exogenous steroid use, over-secretion of ACTH 2nd to pituitary tumor, ectopically
produced ACTH from a non-pituitary carcinoma or adrenal adenoma
, \Cushing disease results - ANS->increased glycogenolysis which results in hyperglycemia
and type 2 DM >abnormal redistribution of fat and elevated blood lipid products. Body
changes include truncal obesity, moon face and formation of a buffalo hump. "cushingoid"
appearance>weakened collagen fibers leads to skin fragility, bruising and skin tears. They
will have purple striae over areas of increased fat deposits>Increased ACTH will cause
hirsutism(increased hair growth) and acne>people will bleed more easily and are more
susceptible to infection
\Dawn phenomenon - ANS-Early morning rise in blood glucose concentration caused by
nocturnal elevations of GH which decreases metabolism of glucose by muscle and fat.
Increasing the dose of evening insulin manages the problem.
\Diabetic Ketoacidosis (DKA) - ANS-Complication which results from insulin deficiency and
the release of counter regulatory hormones(catecholamines, glucagon, cortisol). Most
common predisposing factors are illness, infection, trauma, surgery, MI and lack of
medication compliance. The lack of insulin causes an increase in hepatic glucose
production, a decrease in peripheral glucose utilization, initiation of gluconeogenesis and
formation of ketone bodies and metabolic acidosis.
\Diabetic Nephropathy - ANS-Hyperglycemia leads to activation of the polyol pathway,
hexosamine pathway, protein kinase C and inflammation and the production of advanced
glycation end products which all cause kidney tissue injury yet exact process is not known.
The glomeruli are also injured.
\Diabetic Nephropathy S&S - ANS-Microalbuminuria is the first manifestation and develops
within 5-10 years. Later, hypoproteinemia, reduction in plasma oncotic pressure, fluid
overload, anasarca and hypertension may occur. As it continues, people with type 1 may
have problems with hypoglycemia. Glomerular filtration rate drops, and nausea, lethargy,
acidosis, anemia and uncontrolled hypertension may occur.
\Diabetic neuropathies - ANS-Most common complication of diabetes
Affects all types of nerves
> peripheral (sensorimotor) nerves
> autonomic (somatic) nerves
> spinal nerves
Prevalence increases with age of person & duration of DM
May be the first symptom of diabetes
May appear during periods of "good" glucose control
If blood glucose controlled, neuropathies decreased by 60%
Capillary basement membrane thickening & capillary closure may be present
Demyelinization of the nerves related to hyperglycemia
> delayed conduction
> nerve degeneration
> sensory deficits/symptoms more common than motor
Cognitive dysfunction can occur with chronic hyperglycemia
Some neuropathies are progressive & some may improve spontaneously
\Diabetic Retinopathy - ANS-Leading cause of blindness. Results from damage to retinal
blood vessels and RBCs, platelet aggregation, relative hypoxemia and hypertension. S&S:
blurring or loss of vision, reduced visual acuity, cataracts, and defects in the eye muscle
\Diabetic Retinopathy patho - ANS-Stage 1 nonproliferative: characterized by thickening of
the retinal capillary basement membrane and an increase in retinal capillary permeability,
vein dilation, microaneurysm formation and hemorrhages. Stage 2 preproliferative:
progression of retinal ischemia with areas of poor perfusion that culminate in infarcts. stage
