-
The anterior pituitary produces what hormones
- Growth hormone (GH)
- Thyrotrotropic hormone (TSH)
- Adrenocorticotropic Hormone (ACTH)
- Melanocyte stimulating hormone (MSH)
- Somatotropin
- Prolactin
- Luteotropic hormone
- Follicle stimulating hormone
- interstitial cell stimulating hormone
-
The posterior pituitary produces what hormones
Antidiuretic Hormone (ADH)
Oxytocin
-
The tyroid produces
- Triiodithyronine (T3)
- Thyroxine (T4)
- Calcitonin
-
The parathrroid produces
Parathormone (PTH)
-
The Pancreas produces
- Endocrine function insulin
- Glucagon
- Digestive enzymes
-
The Adrenal Cortex produces
- Glucocorticoids (cortisone, cortisol)
- mineral corticoids (aldosterone)
- sex hormones (androgens)
-
The Adrenal medulla produces
Catechaloamines (Epinephrine, norephinephrine)
-
Growth Hormone (GH)
- Comes from the Anterior Pituitary
- Acts directly on bones and other tissues to stimulate growth
-
Thyrotrotropic hormone (TSH)
- comes from the Anterior Pituitary
- stimulates the thyroid gland
-
Adrenocorticotropic Hormone (ACTH)
- comes from the Anterior Pituitary
- stimulates the adrenal cortex
-
Melanocyte stimulating hormone (MSH)
- comes from the Anterior Pituitary
- stimulates darking of the skin
-
Antidiuretic Hormone (ADH)
facilitates reabsorption of H2O in the kidneys
-
Triiodithyronine (T3)
Control body metabolism and influence physical and mental
-
Thyroxide (T4)
growth, nervous system activity, protein, fat, carbohydrate metabolism, reproduction
-
Calcitonin
lowers serum calcium levels, inhibits bone reabsorption
-
Parathormone (PTH)
regulates calcium and phosphorus metabolism
-
Insulin
enables glucose to freely enter cells, helps muscles and tissue oxidation of glucose, promotes stoarge of glycogen
-
Glucagon
increases gluconeogenesis in the liver
-
Glucocorticoids (cortisone and cortisol)
decreases protein synthesis, regulate serrum glucose by increasing rate of gluconeogenesis, suppress the inflammatory and immune responce, increase fat mobiliaztion, support adaptation during stressful situations
-
Mineralocorticoids (Aldosterone)
Facilitate reabsorption of NA+ and elimination of K+
-
Androgens
responsible for development of secondary sex characteristics
-
Epinephrine
initiates stress response
-
Norepinephrine
causes vasoconstriction
-
Estrogen
Responsible for secondary sex characteristics, mammary duct system growth of graafian follicle in women
-
Why do hormonal alterations occur?
- Decrease in the # of receptors
- imparied receptor function
- andtibodies against receptors (autoimmune)
- abnormal receptor number
-
Hypofunction of endocrine
- absence or impaired development of gland
- gland destroyed
- decline in function
-
Hyperfunction of endocrine
- excessive stimulation
- hyperplasia
- hormone producing hormone
-
Primary hormone alteration
defect in target gland responsible for producing the hormone
-
secondary hormone alteration
- target gland normal
- deficient RH and SH from pituitary system
-
Tertiary hormone alteration
results from hypothalamic dysfunction
-
Alterations of the Hypothalamic-Pituitary System
interruption of the physical connections between the hypothalamus and the pituitary gland can cause disease
-
Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
A syndrome characterized by high levels of ADH in the absence of normal physiologic stimuli for its release
-
The most common causes of SIADH
Ectopic secretion of ADH by tumor cell
-
Who is at risk for SIADH
pituitary surgery, post-op clients, positive pressure ventilation, medications, disease and injury to the CNS
-
Pathophysiology of SIADH
water intoxication due to water retention that leads to hyponatremia, hypoosmolarity, urine inappropriately concentrated w/ respect to serum osmolarity
-
osmolarity
- concentration of the blood
- Normal 270-295
-
Normal sodium levels
135-145
-
-
-
Clinical manifestations of SIADH
- decreased serum osmolality
- decreased sodium level
- increased urine osmolality
- decreased hematocrit
- decreased BUN
-
Diabetes Insipidus "Tasteless diabetes"
- insufficiency of ADH, leading to polyuria and polydipsia
- hx of head injury, pituitary tmor, craniotomy
-
Types of Diabetes Insipidus
- Neurogenic (central)
- Nephrogenic
-
Neurogenic Diabetes Insipidus
- insufficient ADH
- may follow head injury or surgery near the lesion area
-
Nephrogenic Diabetes Insipidus
- End organ failure
- insensitivity of the renal tubule to ADH
- drugs and disorders damage the renal tubule
-
Pathophysiology of Diabetes Insipidus
- Partial or total inabilty to concentrate urine. Insufficient ADH secretion causes secretion of large volumes of dilute urine, leading to an increase in plasma osmolatity
- urine out put 3 to >12 L/day
- Specific Gravity 1.00-1.005
- Dehydration can develop rapidly
-
Specific Gravity
- measure of concentration of urine
- Normal 1.010 - 1.020
-
Nursing Care for Diabetes Insipidus
- Monitor fluids
- Replace Fluids
- Check neuro states
- Check vital signs
- check muccous membranes
-
Clinical Manifestations of Diabetes Insipidus
- Polyuria, nocturia, thirst, polydipsia
- increase plasma osmolality
- decrease urine spenific gravity
- decreased urine osmolality
- hypovolemia, tachycardia, decreased b/p
-
Microadenoma
pituitary tumors < 10 mm
-
Macroadenoma
pituitary tumors >10 mm
-
Acromegaly
occurs in adults who are exposed to continuously excessive levels of GH
- slow progression, increased amounts of GH can't stimulate further lone bone growth, the result is connective tissue and bony proliferation
- Diabetes mellitus may occur when the pancreas is unable to secrete enough insulin to offset the effects of GH
-
The most common cause of Acromegaly
GH secreting pituitary adenoma
-
Clinical manifestations of Acromegaly
enlaged tongue, interstitial edema, large sebaceous and sweat glands, coarse hair, enlarged bones of face, hands, feet, soft tissue overgrowth, HTN, heart failure
-
Gigantism
occurs in childern and adolescents, excessive secretion of GH by adenomas. Epiphyses not fused, excessive skeletal growth occures
-
Dwarfism
low GH in children can lead to
-
Hyperthyroidism (Thyrotoxicosis)
condition that results from increased levels of thyroid hormone. could be due to graves disease, adenomas, carcinomas, pituitary issue
-
Most common cause of hyperthyroidism
Graves disease
-
Clinical Manifestations of Hyperthyroidism (Thyrotoxicosis)
- result of increased circulating thyroid hormones
- increased T3, T4, decreased TSH
- clubing fingers, Tremors, increaed diarrhea, Menstrual changes (amenorrhea), intolerance to heat, fine straight hair, bulging eyes, facial flushing, enlarged thyroid, tachycardia, increase systolic BP, breast enlargement, weight loss, muscle wasting, nervousness, increased appetite
-
Graves Disease
- more common in women, Familial tendency, autoimmune disease
- Thyroid autoantibodies are found in more than 95% of clients
-
The hyperfunction of the thyroid gland leads to
suppression of TSH and TRH, increased iodine uptake, increaed thyroid gland metabolism, lead to enlargment of the gland
-
Goiter
- enlarged thyroid gland
- can be seen ini both hypo and hyperthyroidism
-
Myxedema
subcutaneous swelling legs and hands
-
Ocular Manifestations of Grave's Disease
Exophthalmos (Bulging eyes), Edema of the orbital contents, protrusion of the globe can occur which can lead to visual disturbances, irritation, pain
-
Thyroid Storm
- excerbation of hyperthyoidism
- worsened thyrotoxic state that can be fatal if not treated
- death can occur w/i 48hrs
- most frequently occurs in undiagnosed, partially treated and stressed individuals
-
Whos at risk for Thyroid Storm?
infections, cardiopulmonary disorders, emotional distress, poor preparation for thyroid surgery
-
Systoms of Thyroid storm
Hyperthermia, tachycardia, high-output heart failure, agitation, NVD
-
Hypothyroidism
most common throid disorder due to deficient productoin of thyroid hormone by the throid gland
-
Primary Hypothyrodism
- loss of functional throid tissue
- leads to decreased production of TH
- that leads to increased production od TSH
- that may lead to goiter
-
Secondary Hypothyrodism
- due to problem w/ pituitary gland and insufficient TSH
- pituitary tumors
- Decreased TSH, decreased TH
-
Subacute thyroiditis
nonbacterial inflammation preceded by a virus
-
Autoimmune Thyroiditis
- destruction of thyroid tissue
- ex-Hashimoto disease
-
Clinical Manifestations of Hypothyroidism
hair loss, apathy, lethargy, dry skin (coarse & Scaly), muscle aches and weakness, constipation, intolerance to cold, receding hairline, facial & eyelid edema, Dull-blank expression, extreme fatigue, thick tongue, slow speech, anorexia, brittle nails and hair, menstrual disturbances
late: subnormal temp, bradycardia, weight gain, decresed LOC, thickened skin, cardiac complications
-
Myxedema in Hypothroidism result from
- alteration in the composition of the dermis and other tissues
- protein-mucopolysaccharide complex binds w/ water
-
Myxedema Coma
- excerbation of Hypothroidism
- decreased LOC, hypothermia, hypoventilation, hypoglycemia,
- LIFE THREATENING
-
Congenital Hypothyroidism
occurs in infants as a result of absent thyroid tissue and hereditary defects in thyroid hormone synthesis
-
Cretinism
due to untreated congenital hypothyroidism
-
Thyroid Carcinoma
- most common cause is exposure to ionizing radiation during childhood. Small thyroid nodule or metastatic tumor in lungs, brain, bone
- s/s due to pressure on surrounding tissue
-
Cushing Syndrome
- manifestation of hypercortisolism from any cause
- Cushing disease
- Benign or Malignant adrenal tumor
- Ectopic Cushing
- Iatrogenic Cushing
-
Cushing diseases is due to
excessive anterior pituitary secretion of ACTH. Most individuals have a pituitary microadenoma which secretes ACTH
-
Ectopic Cushing's
non-pituitary ACTH secreting tumor small cell carcinoma of the lung
-
Iatrogenic Cushing's
longterm use of pharmacologic glucocorticoids
-
Clinical Manifestations of Cushing's Syndrome
personality changes, moon face, increase susceptibility to infection, gynecomastia, fat deposits on back, osteoporosis, hyperglycemia, CNS irritability, NA and Fluid retension, Thin extremities, GI distress (Increase acid), amenorrhea, hirsutism, thin skin, purple striae, bruises and petechiae
-
Hirsutism
excess facial hair
-
In Cushing's Syndrome weight gain due to
- adipose accumulation in trunk, face, cervical areas, sodium and water retention,
- "Moon face, truncal obesity, buffalo hump"
-
In Cushing's Syndrome glucose intolerance due to
insulin resistance and increased gluconeogenesis
-
In Cushing's Syndrome protein wasting due to
catabolism effects of cortisone on peripheral tissues, collagen loss leads to thin skin, easy bruising, capillaries more visible
-
In Cushing's Syndrome hyperpigmentation due to
high levels of ACTH, stimulates increased MSH
-
In Cushing's Syndrome elevated blood pressure due to
NA+ retention
-
In Cushing's Syndrome susceptible to infection due to
suppression of immune system
-
In Cushing's Syndrome irritability and depression due to
cortisol effect
-
In Cushing's Syndrome hair growth, acne, oligomenorrhea in females due to
increased androgen levels
-
In Cushing's Syndrome high risk for gastric ulcers due to
increased gastric acid secretions
-
In Cushing's Syndrome high risk for osteoporosis due to
destruction of bone proteins and aalteration in Ca+ metabolism
-
An example of Primary Adrenal Cortical Insufficiency
Addison disease
-
Addison Disease
- autoimmune destruction of the adrenal glands is the most common cause
- 90% of tissue destroyed before symptoms
- characterized by elevated serum ACTH levels with inadequate corticosteroid synthesis and output
- add hormones
-
Clincal Manifestations of Addison Disease
bronze skin pigmentation of skin, change in distrubution of body hair, GI disturbances, weakness, hypoglycemia, postural hypotension, weight loss
-
Clinical Manifestations of Adrenal Crisis
- profound fatigue
- dehydration
- vascular collapse
- renal shut down
- decreased serum NA
- increased K
-
Clincal Manifestations of Mineralcorticoid effect in Addison Disease
- urinary loss of NA(Hyponatremia, loss of ECF), Cl, H2O
- decreased excretion of K+ (hyperkalemaia)
-
Clincal Manifestations of Glucocorticoid effects in Addison Disease
- Hypoglycemia
- Lethargy
- Weakness
- GI Symptoms
- Weight loss
-
Secondary Adrenal Cortical Insufficiency
low ACTH levels cause inadequate adrenal stimulation, adrenal atrophy, and corticosteroidogenesis
due to Exogenous steroids use (cannt be abruptly stoped due to "shutting off" of adrenal gland
-
Acute Adrenal Crisis
- LIFE THREATENING
- precipitated by illness, stress, abrupt discontinuing of steroids
can cause N/V, muscular weakness, hypotension, dehydration, vascular collapse
care focused on dehydration
-
5 S's of Acute Adrenal Crisis
- S=salt (replace)
- S=sugar (replace)
- S=Steroids (replace)
- S= support
- S= search for cause
-
Hypersecretions of Adrenal Androgens and Estrogens are due to
adrenal tumors, cushing syndroms, defects in steroid synthesis
-
Feminization
- hypersection of estrogen (excess)
- development of female charcteristics
-
Virilization
- hypersecretion of androgens (excess)
- development of male charcteristics
-
Pheochromocytoma
- A catecholamine producing tumor derived from the chromaffin cells of the adrenal medulla that contain sympathetic nevre cells
- most common 40-60 yrs, men and women affected equaly
-
CLinical Manifestations of Pheochromocytoma
hypertension, headaches, diaphoresis, tachycardia, palpitations, hypermetabolism, glucose intolerance, warmth, heat intolerance
-
Pheochromocytoma cause an excess productin of...
cathecholamines
-
Hyperparathyroidism
increased PTH levels results in increase serum Ca levels
-
Primary Hyperparathyroidism
greater than normal secreations of PTH by one or more of the parathyroid glands, cause unknown, maybe due to adenoma, carcinoma, inheritance
-
Secondary Hyperparathyroidism
caused by increased PTH secondary to a chronic disease state. the most common cause is renal failure. Vitamin D metabolism is impaired in renal failure results hypocalcemia. The chronic renal failure induced hypocalcemia serves as a stimulus for increased PTH secretions
-
Hypoparathyroidism
- abnormally lof PTH levels
- most common cause by damage to parathyroid glands during surgery ,
- a lack of PTH causes a depressed serum calcium level and an increased serum phosphate level due to increased renal reabsoprtion of phosphate
-
Clinical Manifestations of hypocalcemia
- muscle spasm (Chvostek's)
- hyperflexion (Trousseau's)
- Dry Skin
- Hair loss
- done deformities
-
To Diagnosis Diabetes Mallitus
- 1. more than one fasting plasma glucose level >or = 126 mg/dl
- 2. plasma glucose value in the 2 hr sample of OGTT > 200 mg/dl
- 3. Casual plasma glucose level > or = 200mg/dl with symptoms
- 4. HgbA1C= normal <7%
-
HgbA1C
shows overal status of a person BS for the past few months
-
Classifications of Diabetes Mellitus
- Type 1
- Type 1.5
- type 2
- Gestational
-
1A Immune Mediated Diabetes Mellitus
- environmental-genetic factors result in Bcell destruction
- autoantibbodies detected of pancreas and B cells
- 95%
- peakage 11-13 years
-
1B Idiopathic Diabetes Mellitus
- cause unknown
- no evidence of autoimmunity
-
Clincal Manistations of Type 1
Polyuria, polydipsia, polyphagia, weight loss, fatigue, increase frequency of infection, rapid onset, insulin dependent, familial tendency, peak incidence from 10-15 years
-
In Type 1 Diabetes Mellitus hyperglycemia due to
lack of insulin
-
In Type 1 Diabetes Mellitus polydipsia is due
to elevated glucose levels pull water from cells which results in intracellular dehydration
-
In Type 1 Diabetes Mellitus polyuria is due to
the effects of hyperglycemia as an osmotic diuretic renal threshold for glucose excreded
-
In Type 1 Diabetes Mellitus Polyphagia is due to
depletion of cellular stores of CHO, fats, proteins, resulting in cellular starvation
-
In Type 1 Diabetes Mellitus weight loss is due to
fluid loss w/ osmotic diuresis, loss of body tissue
-
In Type 1 Diabetes Mellitus fatigue is due to
metabolic changes
-
Pathophysiology of Type 2 Diabetes
- 1. Peripheral insulin resistance
- 2. Deranged secrections of insulin by pancreatic cells
- 3. increased glucose production by the liver
-
The biggest risk factor for type 2 diabetes
obesity, diabesity, visceral fat
-
Syndrome X (Metabolic Syndrome, Insulin Resistance syndrome)
- 1. hyperglycemia
- 2. hypertension
- 3. hyperlipidemia
- High triglycerides (>150
- 4. Abdominal obsesity
-
-
-
-
-
Clinical Manifestations of Type 2 Diabetes
genital pruritus, visual changes, parethesias, fatigue
-
Impaired fasting Glucose (Borderline/Previsional Diabetics)
Fasting glucose >100 and <126 mg/dl
-
Impaired Glucose Tolerance (IGT)
2 hour postload glucose level greater than or equal to 140 but less that 200 mg/dl
-
Gestational Diabetes mellitus (GND)
glucose intolerance first recognized during pregnacy, most likely in the third trimester. Following pregnancy glucose may normalize remaini impaired or progress to Diabetes Mellitus.
-
Hypoglycemia
- lowered plasma glucose 45-60 mg/dl
- occcurs more frequently in individuals treated w/ insulin
-
Symptoms of hypoglycemia
tachycardia, diaphoresis, pallor, tremors, dizziness, headahcem visual changes
- Adrengic-pallor, sweating, tachycardia, sweating, palpitations, hunger, restlesness, anxiety, tremors, clammy skin
- Neurogenic- Fatigue, irritabilty, headache, visual changes, dizziness, convulsions
-
Diabetic Ketoacidosis
- most commonly occurs in Type 1 diabetics
- develops when ther is an absolute or relative deficiency of insulini and an increase in insulin counterregulatory hormones. Hepatic glucose production increases. peripheral glucose usage decreases, fat mobiliaztion increase and ketogenesis is simulated
-
Counterregulatory Hormones
catecholamines, cortisol, glucagon, growth hormone
are realses during a stress responce
-
Precipitating Factors of DKA
type 1, illness, infection, trama, surgery, mi, stress evernt
-
Metabolic Components of DKA
- Hyperglycemia (BG 300-750)
- Ketosis (Ketones come from fat metabolism)
- Metabolc Acidosis (ketones acid) ,low bicarb <15, low pH <7.3
-
Clinical Manifestations of DKA
polyuria, polydipsia, N/V, Fatigue, hypotension, tachycardia, stupor leads to coma, abdominal pain, fruity breath, kussmauls respirations
-
Kussmauls Respirations
- Hyperventilation
- rapid , deep
-
why is a person woth DKA at risk for dehydration?
fluid loss from osmotic diuresis due to hyperglycemia
-
What metabolic changes are seen in DKA
K+ normal or elevated (Met Acid= high K+), shift of H20 and K+ from EC due to hyperosmolarity of ECF due to hyperglycemia, NA normal or decreased
-
Hyperglycemia Hyperosmolar Nonacidotic diabetes (HHNKS)
- more commonly seen w/ type 2 diabetes, levels of free fatty acid are in HHNKS are consistently lower than in DKA and is charcterized by a lack of ketosis
- insulin levels are sufficient to prevent excessive lipolysis but not to use glucose properly
-
factors contributing to development of HHNKS
- Glucose levels>600-2000 mg/dl
- Hyperosmolarity >350 mOsm/l
-
HHNKS presentation
- 1.Major stress event
- 2. increased cortisol, glucagon, catecholamines
- 3. hyperglycemia
- 4. inadequate insulin secretion
- 5. Hyperglycemia
- 6. Osmotic Diuresis, Electrolye imblance
- 7.Extreme dehydration and intracellular dehydration
- 8. Nonketotic COMA, Death
-
Clinical Manifestations of HHNKS
- dehyration
- neurological signs-changes in LOC, seizures, visual loss, may mimic strock
- excessive thirst
- electrolye loss
- Potassium phosohorus sodium relacement needed, also rapid fluid replacement
-
Peripheral Neuropathies
- thickened vessel walls
- caused by ischemia, segmental demyelinization
-
Somatic Neuropathies
- affects nerves that control sensations and muscle in the body
- loss feeling, touch, sensation
- burning pain
-
Autonomic Neuropathies
affects involuntary nerves controlling many body systems i.e bladder, GI sytem
-
Diabetic Retionpathy
retinal ischemia resulting from blood vessel changes and red blood cell aggregation
-
Diabetic Nephropathy
the glomeruli are injured by protein denaturation by high glucose levels and adverse effects of intraglomerular hypertension. Glomerular enlargement and glomerular basement membrane thickening result in diffuse intercapittary glomerulonecrosis. Proeinuria is a consistent sign of renal damage
-
Macrovasular Disease
- arise from development of atherosclerosis
- damage to endothelial later of arteries
coronary artery disease, Cerebrovascular diease, Peripheral vascular disease(see discolorarion, necrosis)
-
Diabetic Foot Ulcer
- common problem
- due to sensory impairment and motor weakess
-
Why is diabetic at high risk for infection
- impaired vision
- impaired touch
- pathogens multiply
- decreased blood supply
- WBC function impairment
|
|