Transcript Endo - Clark College

GOOD
MORNING
Endocrine System
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Regulates body systems
Hormones secreted into the blood stream
Each hormone has 1 or more target organs
(receptor sites)
Rhythmic pattern of release
Problems arise from either production or
receptor sites
Most problems are chronic requiring selfmanagement
Hormones
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Responsible for regulating:
– Reproduction
– Growth & Development
– Energy production & use
– Maintenance of internal environment
Catecholamines
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Amino Acid derivatives
– Epinephrine
– Norepinephrine
– Thyroxin
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Easily replaced
Many can be oral
Proteins & Peptides
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Chains of Amino Acids
Difficult to isolate & engineer
None survive the GI system
Proteins:
– Larger molecules
– Insulin, Calcitonin, Growth Hormone, FSH
Peptides:
– Releasing Factors in Hypothalamus & Posterior
Pituitary (Neurohypophysis)
– Oxytocin, Vasopressin
Steroids
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Formed from cholesterol
Easily produced for replacement
Most can be oral
Include Adrenal and Sex Glands:
– Aldosterone
– Cortisol
– Estrogen
– Testosterone
Pharmacologic Uses
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Diagnostic
– ACTH to stimulate the Adrenals
– Thyroglobin to check thyroid response
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Replacement
– Insulin
– Estrogen
– Thyroid
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Pharmacologic Effects
– Steroids to decrease inflammation
Feedback
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Secreted when the body identifies a need
Changes in the blood level or other hormones
may cause an increase or decrease in secretion
Negative Feedback:
– Hormone produces an effect, when it is
strong enough, further hormone secretion is
inhibited, decreasing physiologic effect.
Feedback Loops
Hypothalamus
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Releasing Factor
Pituitary
Hormone A
Target Organ
Hormone B
Biologic Effect
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Negative
Feedback
Loop
Physiologic Changes with
Aging
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Reduction in hormone production
Changes in hormone clearance
Decreased cellular responsiveness
Changes in;
– Physical activity level
– Nutritional status
– Body composition
Causes of Disease
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Over or Under Production
Transport abnormalities
Inability of target tissues to respond
Problems with the feedback
mechanism
Primary
Secondary
Pituitary
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Anterior Pituitary
– Hypothalamic releasing factors stimulate
the release or inhibit the release of
hormones
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Posterior Pituitary
– Hormones produced in the hypothalamus
are stored in the posterior lobe until
stimulated by the hypothalamus via nerve
impulses
Hypothalamus
Neuro Secretory
Cells
Releasing
Factor
Producing Cells
Portal Vessel
Anterior
Posterior
Hormone
Producing Cells
Anterior Pituitary
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Growth Hormone (GH)
Gonadotropic
– Lutenizing Hormone (LH)
– Follicle Stimulating Hormone (FSH)
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Adrenocorticotropic Hormone (ACTH)
Thyroid Stimulating Hormone (TSH)
Prolactin (PRL)
Melanocyte-stimulating Hormone
(MSH)
Anterior Pituitary
Growth Hormone
(Somatotropin)
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Growth Hormone increases bone growth and
tissue cell size by changing metabolism,
antagonizing the action of insulin, and
increasing fat mobilization for energy use.
Deficiency - Dwarfism = delay in all body parts
with no mental impairment.
Excess - Gigantism in childhood, acromeglia in
adults.
Acromegaly
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Acromegaly is the Greek word for "extremities" and
"enlargement”
Signs and symptoms vary, dependent upon how long the
patient has had the disease, but may include…
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Swelling of the hands and feet
Facial features become coarse as bones grow
Body hair becomes coarse as the skin thickens and/or darkens
Increased perspiration accompanied with body odor
Protruding jaw
Voice deepening
Anterior Pituitary
Gonadotropic Hormone
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Gonadotropin-releasing hormone (GnRH)
– Produced and released from the
hypothalamus. Stimulates the secretion
of follicle stimulating hormone (FSH) and
lutenizing hormone (LH), from the
anterior pituitary.
Anterior Pituitary
Adrenocorticotropic Hormone
(ACTH)
Stimulates the
adrenal cortex to
synthesize and
release cortisols
in response to
stress.
Anterior Pituitary
Thyroid Stimulating Hormone
(TSH)
Hypothalamus releases TRH
Stimulates the anterior pituitary to produce
TSH
Regulates the amount of thyroid hormone
produced and released into the
bloodstream by the thyroid gland
Posterior Pituitary
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Oxytocin
– Uterine contraction
– Milk let down
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ADH (Vasopressin)
– Renal conservation of water
– Vasoconstriction
– Increase GI motility
– Released in response to plasma
osmolarity
SIADH - Syndrome of
Inappropriate ADH
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ADH release
Water Reabsorption into circulation Renal Tubules
Extravascular Fluid
Plasma Osmolality
Glomerular Filtration Rate
Serum Sodium Levels
CEREBRAL EDEMA
Diabetes Insipidus
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ADH Deficiency
Water excretion and blood
concentration
ADH is a peptide and can not be taken
orally
Treatment:
– Vasopressin (Pitressin) - short acting
injection
– Lypressin and Desmopressin - nasal spray
Adrenal Cortex
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Glucocorticoids (Cortisol)
– Release is under ACTH control
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Mineral-corticoids (Aldosterone)
– Renin-Angiotensin system and K+ levels
– Stimulated by NaCl depletion
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Androgens
– Growth of hair follicles
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Stress increases cortisol and aldosterone to
maintain CV tone.
Impairment of release leads to adrenal crisis
Cushing Syndrome
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Excess of corticosteroids secreted by
the adrenal cortex
Iatrogenic - prolonged use
Lab - 240 urine for cortisol
Tx - Surgery, Radiation, Suppress
synthesis using drug therapy
Prolonged steroid use - TAPER doses
Post-op care
Addison's
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Adrenocorticol insufficiency
Autoimmune
Sxs - weight loss, anorexia, weakness,
low BP, low sodium, high potassium,
nausea & vomiting, diarrhea
Tx - Glucocorticoids
– Mineralcorticoids
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Adrenal Crisis
Adrenal Medulla
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Pheochromocytoma
– Neoplasm increasing catecholamines
– Surgical removal
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Sxs - episodic HTN, increased
metabolism, hyperglycemia
Lab - urine metanephrines
Monitor wide BP fluctuations
The Thyroid Gland
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Normal thyroid levels are essential to
regulate cellular metabolism, and for
normal growth and development.
Production of thyroid hormone is
caused by release of TSH (stimulated
by TRH)
– Thyroxin - T4
– Triiodothyronine - T3
Thyroid
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Essential to regulate metabolism
Caused by release of TSH:
– Thyroxin - T4
– Triiodothyronine - T3
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Stimulated by increased Ca++ in blood
– Calcitonin - lowers blood levels by inhibiting
bone re-absorption
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Low calcium levels suppress the release of calcitonin
Elevated levels increase it’s secretion
Prevalence of Thyroid
Disorders
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In the United States, approximately
7.5 percent of the population (about 1
in every 13 individuals) have been
diagnosed with thyroid disorders, and
nearly another 1 percent are estimated
to have undiagnosed thyroid maladies.
Hyperthyroid
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Graves Disease
Multinodular Goiter
Symptoms:
– Increased metabolism
– Increase stimulation of sympathetic nervous system
– Exopthalmos
Thyroid Storm – Thyrotoxicosis----Severe
and life
threatening
Treatment - Propylthiouracil, Inderol, Iodine, Radiation,
Surgery
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Hypothyroid
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Infants - long gestation, failure to thrive
Childhood - Autoimmune
Adult - Atrophy or Decreased TSH
– Myxedema - interstitial edema, fatigue,
lethargy, impaired memory leading to coma
high mortality rate.
– Long term - Sxs related to increased protein
turnover
– Cardiovascular, GI, and reproductive
Replacement Therapy
Parathyroid
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Maintains extracellular Ca++ levels
Parathormone - Calcitonin antagonist
– Release stimulated by low blood levels of
Ca++ or high levels of phosphates
– Increases Ca++ blood levels
– Reabsorption of Ca++ and Phos. from
bones
– Increase GI absorption
– Increase reabsorption in kidneys
Hyperparathyroid
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Primary - Parathyroid tumor or hyperplasia
Secondary - Response to Low Ca++ levels
– ESRD - Response to phosphate excretion
problems
– Nursing - increase fluids, low calcium diet,
avoid immobility
Mithramycin - antihypercalcemic agent
Post-op removal - observe for tetany, fluid and
electrolyte problems
Hypoparathyroid
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Accidental removal or vascular damage
during surgery
Sxs - Tetany, Chvostek’s sign
Lab- low calcium, low PTH, and high
Phos.
Tx - Vitamin D, Calcium supplements,
and Phosphate binders
Pancreas
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Insulin
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Beta cells of Langerhans
Stored in Beta Cells as Proinsulin
Catalyst to cellular metabolism
Promotes storage of CHO in liver, muscle cells, and
fat deposits
Glucagon
– Opposes the action of Insulin
– Alpha cells produce
– Acts to mobilize liver glycogen and convert to
glucose
Diabetes Mellitus
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Chronic hyperglycemia---main feature in all
types of diabetes mellitus. Resulting from:
– Insulin secretion
– Insulin action
– Or both
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Disease classified
– Age of onset
– Problem causing the lack of insulin
– Severity of the deficiency
Cost of Diabetes in the United
States, 2002
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Total (direct and indirect): $132 billion
Direct medical costs: $92 billion
Indirect costs: $40 billion (disability,
work loss, premature mortality)
Blood Glucose Values
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Normal – Fasting blood glucose levels
of <110 mg/dL
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Significant abnormal results –
Levels>126mg/dL obtained on at least
two occasions are diagnostic of
diabetes, even in older adults.
Diabetes Causes
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Inability to use CHO
Insulin action ineffective at tissue site
or not enough Insulin available
Diabetes Causes
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Glycogen fails to store in liver
– Conversion of glycogen to glucose NOT
affected
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Increased metabolism of proteins and
fats
– Leads to Ketone production
Insulin
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Glucose transport across cell membrane
Storage of glucose as glycogen
Increased fat deposits
Decreased protein breakdown
Increased transport of amino acids into the
cell for protein synthesis
Absence = Increased osmotic pressure
3 Poly’s
Type I
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Beta cell destruction
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Rapid onset
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Must be given Insulin
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Ketoacidosis prone
Type II
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Enough Insulin to prevent DKA
May have increased or decreased Insulin production
Decreased tissue response to Insulin
Abnormal liver glucose regulation
Oral Agent:
– Increase Insulin production
– Improve cell receptor binding
– Regulate liver glucose production
Impaired Glucose
Tolerance
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“Borderline Diabetes”
Blood Glucose levels above normal,
but below levels to Dx Diabetes
May progress to Diabetes
Need close monitoring
Diet and Exercise
Gestational
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Intolerance of glucose during pregnancy
Insulin resistance to increase glucose
available to the baby
Paced with placental hormones
GTT returns to normal in 3-5 weeks after
delivery
Approximately 30% develop Diabetes within
the next 5-10 years
Glucose Tolerance Test
Baby Effects
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Increase amounts of amniotic fluid
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Large fetus
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Hypoglycemic reactions after birth
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Respiratory Distress Syndrome
Tests
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Blood Sugar
Glycosylated Hemoglobin (HbA1c)
– The higher the number the poorer the
control.
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GTT - Glucose Tolerance Test
Capillary Blood Glucose (CBG)
Treatment
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Diet
– ADA Exchange list
– Individually prescribed
Exercise
– Type I - IDDM
 Increases Insulin sensitivity of cells
 Reduce Insulin dose or snack before
exercise
– Type II - NIDDM
 Increases Insulin binding at receptors
 May initially elevate blood sugars
Insulin Treatment
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Goal: Match Normal Secretion Patterns
of the Body
Multiple types of Insulin
Administration techniques
Site Rotations
Pumps
New Technology
Somogyi Effect
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Wide difference in CBG’s
– Low in early AM
– High after breakfast
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Counter regulatory to hypoglycemia
during the night
Treatment - lower Insulin dose in the
evening or increase food intake before
bed
Dawn Phenomenon
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High CBG’s and possibly Ketones in the
morning
Dawn release of Growth Hormone or
Cortisol
Treatment - Change Insulin times
and/or increase Insulin dose
Look at client’s entire management
program
Sulfonylureas
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Must be producing some Insulin
Action:
– Stimulate Beta cell release of Insulin
– Increase Insulin receptor sensitivity
– May decrease liver glucose production
Do Not Take Extra if Overeats!
Hypoglycemia may be prolonged
Hypoglycemics
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Alpha-Glycosidase Inhibitors
– Delay digestion and absorption of CHO
Biguanides
– Decrease glucose absorption, decrease glucose production in
liver, and improves insulin sensitivity in tissues
Meglitinides
– Stimulates Beta cells and improves insulin response to
glucose
Thiazolidinediones
– Lowers insulin resistance by re-sensitizing the body to its
own insulin
Hypoglycemia
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Too much Insulin or not enough food
Symptoms due to rapid drop in Blood
Sugar
Adrenergic (Fight or Flight) Symptoms
Glyconeurogenic (Brain) Symptoms
Beta Blockers mask the symptoms
Elderly often present with Brain
symptoms FIRST
DKA - Diabetic
Ketoacidosis
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No Insulin leads to:
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Use of glucose
– Breakdown of fats to fatty acids to Ketones
– Acidosis causes K+ to leave cells and water loss
– Severe dehydration with high serum K+ levels
Jamie
HHNK Hyperglycemic Hyperosmolar NonKetosis
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Enough Insulin to Avoid DKA
High Blood Glucose Levels lead to Osmotic
Diuresis
Hypovolemia
Treatment = Insulin and Rapid IV Fluid
Replacement
Prevent by Pushing Fluids When Serum
Osmolarity Nears 320
2(Na+K) + BS + BUN
18
2.8
Chronic Complications
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80% of Medical Spending
Increasing as Population Ages
Microvascular
Macrovascular
PATIENT EDUCATION
Arthur
Pattern Management Rule
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Target Glucose Goals
Regular CBG’s
Record CBG’s & events
Study a 3 day pattern
Determine Insulin responsible for problems
s Insulin by 1 or 2 Units
One change at a time
Treat low CBG’s FIRST
3 days before another change
Client #1
A.M. NOON
P.M.
H.S.
2/1
84
191
114
97
2/2
78
222
104
135
2/3
90
201
117
103
2/4
86
186
129
132
Client #2
A.M.
NOON
P.M. H.S.
2/1
64
191
114
67
2/1
68
262
204
135
2/3
50
201
47
103
2/4
86
66
129
132
Client #3
A.M. NOON
P.M.
H.S.
2/1 254
271
314
397
2/2 278
282
304
335
2/3 264
261
387
403
2/4 286
286
329
332
Home Causes
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Oral Medication Errors
– Dose, Timing, Double Medication
– Bring ALL Meds from home
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Insulin Errors
– Technique Problems
– Observe technique ASAP
– Check dose and timing at home
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Diet Misinformation / Changes