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Endocrine

Terms in this set (101)

what are hormones?
-Chemical messengers
-Function:
-Can work on distant cells
-Can work on nearby cells (paracrine)
-Can work on itself (autocrine)

-Affects all body systems/organs as they are controlled or influenced by some hormone
bound hormone
- transported through protein carriers
free hormone
- Needs to be free to send the message to the target tissue
- Excess is conjugated through liver
deficient hormone
due to autoimmunity, infection, inflammation, infarction, tumor
excess hormone
tumor, autoimmunity, genetic mutation
hormone resistance
causing dysfunctional receptor sites
Hypothalamus-pituitary-hormone axis
-Primary: at the site of the gland
-Secondary: Pituitary
-Not releasing the stimulating hormone
-Tertiary: Hypothalamus
primary
at the site of the gland
secondary
pituitary (not releasing the stimulating hormone)
tertiary
hypothalamus
tropic hormone
hormone that goes to the gland and tells it to release it's hormone
negative feedback
increased amount of hormone causes inhibition of release
positive feedback
increased amount of hormone causes more to be released
down regulation
-Prolonged, excessive stimulation of the endocrine system
-Leads to
-Decrease in number of receptor sites
-Receptor insensitivity
-System is depleted; hormone cannot cause desired effects
-Example: taking excessive steroids
hypothalamus
-Hypothalamic hormones regulate the synthesis and secretion of pituitary gland hormones
anterior pituitary gland
-Growth Hormone (GH ) (is not a tropic hormone)
-Thyroid Stimulating Hormone (TSH)
-Adrenocorticotropic Hormone (ACTH)
-Follicle Stimulating Hormone (FSH)
-Luteinizing Hormone (LH)
-Prolactin
-Melanocyte-Stimulating Hormone (MSH)
posterior pituitary gland
-Antidiuretic Hormone (ADH)
-Oxytocin
posterior pituitary does not
synthesize hormones (it only stores them)
hypopituitarism
-Decreased secretion of anterior pituitary gland
-The pituitary is dysfunctional, so the negative feedback system is rendered useless***
-Symptoms are secondary to which tropic hormone (or precursor hormone) is decreased
-Target gland hormone is decreased
causes of hypopituitarism
-Congenital
-Destruction of anterior pituitary
-Deficiency of hypothalamic hormones: due to stress, change in body weight, anorexia, bulimia, heart failure
clinical manifestations of hypopituitarism
-depends on hormones affected
-Growth defects in children and organ dysfunction in adults.
-Decreased growth in children
-Amenorrhea
-Decreased libido
-Erectile dysfunction
-Cold intolerance
-Dry skin
-Mental dullness
-Weakness
-Nausea
-Anorexia
-Fever
Postural Hypotension
hyperpituitarism
-Over secretion of anterior pituitary gland
-All hormones (except GH) control the biosynthesis and secretion of hormones from other target endocrine glands
causes of hyperpituitarism
-Pituitary Adenomas
-Hypothalamic lesions
clinical manifestations of hyperpituitarism
-depends on hormones affected
-Amenorrhea
-Galactorrhea
-Visual disturbances
-Headache
Acromegaly
ADH: Antidiuretic Hormone
-Synthesized by hypothalamus
-Stored and secreted by posterior pituitary
-Essential to maintain body's fluid balance through reabsorption of water by the kidneys
-Also known as Vasopressin
-in the nephron in your kidneys
-Anti-urinate****
diabetes insipidus
-Decreased ADH secretion or renal response to ADH resulting in excess water loss
-Fails to concentrate urine
clinical manifestations of diabetes insipidus
-Extreme thirst
-Dehydration
-Polyuria
-Enuresis (bed wetting)
-Hypernatremia
-pee a lot****
causes of diabetes insipidus
-Neurogenic (Central)
-Diseases that affect hypothalamic-neurohypophyseal system
-Head injury
-Brain surgery
-Gestational
-Nephrogenic
-Congenital
-Pyelonephritis
-Lithium toxicity
-Electrolyte disorders
-Chronic hypercalcemia
-Hypokalemia
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Failure for negative feedback system to regulate ADH resulting in excess water retention (too much ADH)
clinical manifestations of SIADH
-Water retention/intoxication
-Dilutional hyponatremia
-Muscle cramps/weakness
-N/V/D
-Lethargy, disorientation, HA
-Confusion, depression of DTR
-Seizures, coma
-Decreased urine output
-dont pee enough*****
causes of SIADH
-Surgery, trauma, tumors secreting ADH
-Pain/stress
-Temperature changes
-Tumors secreting ADH
-HIV
-Intrathoracic conditions (pneumonia, ventilation)
-Conditions that affect CNS
-Hydrocephalus
-Head injury
-Encephalitis
growth hormone
-Hormones essential for growth
-GH
-Insulin (insulin allows glucose to be stored in adipose tissue to be used as energy)
-Thyroid Hormone
-Androgens
-Somatotropin
-Peak levels secreted occurs after onset of sleep
increased secretion of growth hormone
-gigantism
-acromegaly
gigantism
-Excess of GH before puberty and fusion of long bones
-Normally die from cardiac disease
acromegaly
-GH excess after puberty and fusion of long bones
-Soft tissues continue to grow—not bones
decreased secretion of growth hormone in children causes
-Abuse/Neglect (Increased cortisol levels d/t fight or flight occurring often—negative feedback says to stop releasing hormones from ant pit)
-Pituitary Tumors
-Agenesis of Pituitary
decreased secretion of growth hormone in children clinical manifestations
-Normal intelligence usually but can have mental retardation or minor learning disabilities
-Short stature or dwarfism
-Obesity with immature facial features
-Growth hormone works against insulin
-Delay in skeletal maturation
-Delayed puberty
Microphallus in males
thyroid
-Butterfly-shaped structure located immediately below the larynx in the anterior middle portion of neck (not normally palpable)
-Efficient in use of iodine
thyroid hormones (T3 & T4)
-Released from anterior pituitary
-Growth and development of children
-Regulate metabolism and protein synthesis
-Affect cardiovascular and respiratory functions
-Affect GI motility
-Affect neural control of muscle function and tone
Thyroid Tests
-TSH (precursor hormone)
-Test to differentiate between primary or secondary thyroid disorders
-T3
-Triiodothyronine
-Active form of hormone
-Measures amount of T3 available
-T4 : body metabolism regulator
-Thyroxine
-Has to be converted to T3 to be used
Measures how much T4 is available
Hypothyroidism
-Decreased secretion of thyroid hormones
hypothyroidism causes
-Congenital
-Thyroidectomy
-Ablation of thyroid
-Medications
-Iodine Deficiency
-Hashimoto thyroiditis (autoimmune disorder)
clinical manifestations of hypothyroidism
-Slows metabolism
-Weight gain
-Myxedematous features
-Impaired growth in children
-Mental sluggishness
-Decreased cardiac output
-Constipation (from decreased gastric metabolism)
-Cold intolerance
-Decreased sweating
-Dry, coarse hair and skin
myxedema coma
-End stage hypothyroidism or severe hypothyroidism
pathiophysiology of myxedema coma
-Carbon dioxide retention and hypoxemia
-Fluid and electrolyte imbalance
clinical manifestations of myxedema coma
-Coma
-Hypothermia
-Cardiovascular collapse
-Hypoventilation
-Hyponatremia
-Hypoglycemia
-Lactic acidosis
hyperthyroidism
-Hypersecretion of thyroid hormones
causes of hyperthyroidism
-Grave's Disease (autoimmune disorder)
-Thyroid tumor
-Diffuse goiter (does not always cause dysfunction of thyroid)
clinical manifestations of hyperthyroidism
-Weight Loss
-Increased appetite
-Exophthalmos
-Heat intolerance
-Muscle shakes
-Thin, silky hair and skin
-Nervousness, anxiety
-Irritability
-Fatigue
-Tachycardia and palpitations, dysrhythmias
-Tachypnea, Dyspnea
-Excessive sweating
thyroid storm
-Extreme and life-threatening form of thyrotoxicosis
-Mortality rate is high!
thyroid storm precipitating factors
-Infection
-Stress
-Diabetic Ketoacidosis
-Trauma
Manipulation during thyroidectomy
clinical manifestations of thyroid storm
-Tachycardia, angina, dysrhythmias -> fatal
-Extreme hyperthermia
-Agitation, restlessness
-Delirium, coma
-Hepatomegaly with jaundice
-Weakness with muscle wasting
adrenal gland
-Bilateral glands that lie at apex of kidney (ACTH is the precursor secreted by ant. pit.)
adrenal cortex secretes
-Mineralocorticoids: Aldosterone
-Corticosteroids: Cortisol (ACTH)
-Adrenal androgens (DHEA)
-Adrenal cortex is vital for life (loss will result in death in 4-14 days)
adrenal medulla secretes
-Catecholamines: Epinephrine & Norepinephrine
Addison's disease
-Decreased secretion of adrenal cortical hormones
-Destruction of adrenal cortex
causes of Addison's disease
-*Autoimmune destruction
-Tuberculosis
-Cancer
-Childbirth/Major trauma
-AIDS
-Medications
clinical manifestations of Addison's disease
-Hyponatremia (d/t aldosterone loss)
-Hypochloremia
-Dehydration
-Hyperkalemia
-Increased appetite for salt
-Poor tolerance to stress
-Orthostatic hypotension
-Hypoglycemia
-Lethargy, weakness
-Fever
-N/V/D
-Anorexia and weight loss
-Hyperpigmentation
Cushing's syndrome
-Excess secretion of glucocorticoid hormones
-Also called Cushing's Disease
causes of Cushing's syndrome
-Pituitary adenoma
-Adrenal tumor
-Nonpituitary ACTH-secreting tumor
-Long-term corticosteroid therapy*
ex: prednisone
clinical manifestations of Cushing's syndrome
-Fat deposits that cause pendulous abdomen, buffalo hump and moon face: blocked insulin
-Muscle weakness and wasting
-Thin skin
-Osteoporosis (accelerates bone reabsorption)
-Hypokalemia, hyperglycemia, hypernatremia
-Hypertension
-Susceptibility to infection (inflammatory protection)
-Gastric ulceration/bleeding
-Hirsutism
-Acne
-Male balding pattern
-Emotional lability (mood swings)
-Acini
-Responsible for digestive secretions
-Amylase, Lipase (enzymes)
-Islets of Langerhans
-Beta Cells
-Secretes insulin and amylin
-Alpha Cells
-Secretes glucagon
-Delta Cells
-Secretes somatostatin
beta cells
-Secretes insulin and amylin
alpha cells
secretes glucagon
delta cells
secretes somatostatin
-Insulin (beta cells)
-Has direct effect on lowering glucose levels
-Promotes glucose uptake by cells from bloodstream
-Provides for glucose storage as glycogen in the liver
-Prevents glycogen breakdown (when there is too much glycogen and no more storage space, insulin converts the excess into fatty acids that become stored as adipose tissue)
-Inhibits glucose production from amino acids, lactate, and glycerol in liver and increase protein synthesis
-Glucagon (alpha cells)
-Maintains blood glucose between meals and during fasting
-Breaks down glycogen stores in the liver to raise blood sugar
-Breaks down fatty acids (in high concentrations in adipose tissue)
-Epinephrine
-During stress, stimulates glycogenolysis in the liver
-Floods blood stream with glucose
-Inhibits insulin release from beta cells
Growth Hormone
-Increases protein synthesis
-Mobilizes fatty acids from adipose
-Antagonizes the effects of insulin
-Decreases cellular uptake and use of glucose
-Fasting, exercising, stresses increase GH
-Glucocorticoid Hormones
-Cortisol (most activity)
-Stimulate gluconeogenesis by liver
-Decrease tissue use of glucose
-Hypoglycemia stimulates cortisol secretion
diabetes mellitus
-Disorder of macronutrient metabolism due to lack of insulin or a reduction in the effects of insulin (glucose stays in the bloodstream)
classifications of diabetes mellitus
-Type 1: no insulin
-Type 2: decreased sensitivity to insulin
-Gestational Diabetes: estrogen
-Other Specific Types of Diabetes
-Secondary diabetes associated with other diseases (ex: pancreatitis)
Type 1 Diabetes Mellitus
-Caused by autoimmune or idiopathic destruction of beta cells
-Unable to secrete insulin
-Lipolysis goes unchecked
-Releasing ketones
-Rapid onset in children
-Slower onset in adults
-All type 1 DM require exogenous insulin replacement
-Strong genetic influence
Type 2 Diabetes Mellitus aka: Glucose intolerance
-Pathophysiology
-Insulin resistance
-Increased glucose production by liver
-Impaired secretion of insulin by pancreatic beta cells (insulin deficiency)
-Risk Factors
-Obesity
-Age
-Family history
-Physical inactivity
Gestational Diabetes
-Glucose intolerance that develops during pregnancy
-Occurs in 3-7% of pregnancies
risk factors of gestational diabetes
-Glycosuria
-Family history
-Polycystic Ovarian Syndrome
-Prior history of GDM
-Delivery of previous large for gestational (LGA) infant
diabetes mellitus clinical manifestations
All types of diabetes:
-Polyuria
-Polydipsia
-Polyphagia
Type 1 specifically:
-Weight loss
-Fruity breath (acidosis)
-Weakness
-Fatigue
-Blurry vision
-Paresthesia
Skin infections
-Random blood glucose test
-Blood draw without any regard to time of last meal
->200 mg/dL with symptoms x2 on 2 separate occasions
-Fasting blood glucose test
-Glucose test after not eaten for 8 hours
->126 mg/dL x2 on 2 separate occasions
-Capillary blood glucose monitoring
-Most common test RN performs
-Allows patients to monitor at home
-90-110 mg/dL is normal
-Oral Glucose Tolerance Test (OGTT)
-Drink concentrated sugar drink and test plasma glucose after 2 hours
-Remain elevated if diabetic
-Glycosylated hemoglobin (A1C)
-Measures the hemoglobin that has undergone glycosylation
-Helps to identify unregulated hyperglycemia in last three months
->6.5%
Type 1 DM: Acute ComplicationsDiabetic Ketoacidosis (DKA)
Acute life threatening complication of uncontrolled diabetes in Type 1
Diabetic Ketoacidosis (DKA) characteristics
-Hyperglycemia of 250 or greater
-Ketosis
-Metabolic acidosis (decreased HCO3 < 18, pH <7.3, increased CO2)
clinical manifestations of diabetic ketoacidosis
-Lethargy, unresponsiveness
-Nausea, vomiting
-Abdominal pain
-Fruity breath (acidosis)
-Kussmaul's respirations (blow off excess CO2)
-DEHYDRATION
-Stupor, Coma
Type 2 DM: Acute Complications Hyperosmolar Hyperglycemic Syndrome (HHS)
-Also known as Hyperosmolar Hyperglycemic Non-Ketoacidosis (HHNK)
-Acute complication seen in DM Type 2
-Characteristics
-Hyperglycemia >600
-Hyperosmolarity (more concentrated blood)
-Dehydration
clinical manifestations of Hyperosmolar Hyperglycemic Syndrome (HHS)
-Weakness
-Dehydration
-Polyuria
-Polydipsia
-Visual hallucinations
-Seizures
-Coma
Aphasia
-Hypoglycemia
-Excess of insulin in blood stream with low glucose levels
-Medical Emergency!
clinical manifestations of hypoglycemia
-Disturbed or altered behavior
-Coma
-Seizures
-Anxiety
-Tachycardia
-Sweating
-Cool and clammy skin
-Mental confusion
-<60 mg/dL
-Diabetic Neuropathies
-50% people with diabetes
-Thickening of the walls of the nutrient vessels that supply the nerve and/or demyelination
clinical manifestations of diabetic neuropathies
-Paresthesia
-Impaired sensation
-Muscle weakness/wasting
-Impaired GI or GU system
-Diabetic Nephropathies
-Lesions that develop on kidneys due to damage to microvascular system
risk factors of Diabetic Nephropathies
-Family history
-Smoking
-Hypertension
-Poor glycemic control
-Hyperlipidemia
-Ethnicity
clinical manifestations of diabetic neuropathies
-Increased urinary albumin excretion
-Kidney failure
diabetic retinopathies
-Very common chronic complication of DM
-Characteristics
-Hemorrhage
-Scarring
-Diabetic macular edema
-Retinal detachment
risk factors of diabetic retinopathies
-Smoking
-Poor glycemic control
-Dyslipedmia
-Hypertension
diabetic foot ulcers
-Most common complication leading to hospitalization in DM
-Caused by impaired sensation and vascular insufficiency
infections
-Cellulitis, osteomyelitis, urinary tract infection, pyelonephritis, dental caries, yeast infections
-High glucose environment with high incidence of skin breakdown contribute to severe infection
-Infection often more serious in person with DM
-Somogyi Effect
-Cycle of insulin-induced posthypoglycemia episodes
-Hypoglycemia stimulates surge of counter-regulatory hormones leading to hyperglycemia
-Often occurring at night
-Dawn Phenomena
-Increased levels of fasting blood glucose (or insulin requirements) between 5 am and 9 am
-May be due to GH
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