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GOOD MORNING

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Problems arise from either production or receptor sites ... Acromegaly. Acromegaly is the Greek word for 'extremities' and 'enlargement' ... – PowerPoint PPT presentation

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Title: GOOD MORNING


1
  • GOOD MORNING

2
Endocrine System
  • 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
    self-management

3
Hormones
  • Responsible for regulating
  • Reproduction
  • Growth Development
  • Energy production use
  • Maintenance of internal environment

4
Catecholamines
  • Amino Acid derivatives
  • Epinephrine
  • Norepinephrine
  • Thyroxin
  • Easily replaced
  • Many can be oral

5
Proteins Peptides
  • 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

6
Steroids
  • Formed from cholesterol
  • Easily produced for replacement
  • Most can be oral
  • Include Adrenal and Sex Glands
  • Aldosterone
  • Cortisol
  • Estrogen
  • Testosterone

7
Pharmacologic Uses
  • Diagnostic
  • ACTH to stimulate the Adrenals
  • Thyroglobin to check thyroid response
  • Replacement
  • Insulin
  • Estrogen
  • Thyroid
  • Pharmacologic Effects
  • Steroids to decrease inflammation

8
Feedback
  • 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.

9
Feedback Loops
__
Hypothalamus
Negative Feedback Loop
Releasing Factor
__
Pituitary
Hormone A
Target Organ
Hormone B
Biologic Effect
10
Physiologic Changes with Aging
  • Reduction in hormone production
  • Changes in hormone clearance
  • Decreased cellular responsiveness
  • Changes in
  • Physical activity level
  • Nutritional status
  • Body composition

11
Causes of Disease
  • Over or Under Production
  • Transport abnormalities
  • Inability of target tissues to respond
  • Problems with the feedback mechanism
  • Primary
  • Secondary

12
Pituitary
  • Anterior Pituitary
  • Hypothalamic releasing factors stimulate the
    release or inhibit the release of hormones
  • Posterior Pituitary
  • Hormones produced in the hypothalamus are stored
    in the posterior lobe until stimulated by the
    hypothalamus via nerve impulses

13
Hypothalamus
Neuro - Secretory Cells
Releasing Factor Producing Cells
Portal Vessel
Anterior
Posterior
Hormone Producing Cells
14
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15
Anterior Pituitary
  • Growth Hormone (GH)
  • Gonadotropic
  • Lutenizing Hormone (LH)
  • Follicle Stimulating Hormone (FSH)
  • Adrenocorticotropic Hormone (ACTH)
  • Thyroid Stimulating Hormone (TSH)
  • Prolactin (PRL)
  • Melanocyte-stimulating Hormone (MSH)

16
Anterior PituitaryGrowth Hormone (Somatotropin)
  • 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.

17
Acromegaly
  • 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
  • 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

18
Anterior PituitaryGonadotropic Hormone
  • Gonadotropin-releasing hormone (Gn-RH)
  • Produced and released from the hypothalamus.
    Stimulates the secretion of follicle stimulating
    hormone (FSH) and lutenizing hormone (LH), from
    the anterior pituitary.

19
Anterior PituitaryAdrenocorticotropic Hormone
(ACTH)
  • Stimulates the adrenal cortex to synthesize and
    release cortisols in response to stress.

20
Anterior PituitaryThyroid 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

21
Posterior Pituitary
  • Oxytocin
  • Uterine contraction
  • Milk let down
  • ADH (Vasopressin)
  • Renal conservation of water
  • Vasoconstriction
  • Increase GI motility
  • Released in response to plasma osmolarity

22
SIADH - Syndrome of Inappropriate ADH
  • ADH release
  • Water Reabsorption into circulation -Renal
    Tubules
  • Extravascular Fluid
  • Plasma Osmolality
  • Glomerular Filtration Rate
  • Serum Sodium Levels
    CEREBRAL EDEMA

23
Diabetes Insipidus
  • 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

24
Adrenal Cortex
  • Glucocorticoids (Cortisol)
  • Release is under ACTH control
  • Mineral-corticoids (Aldosterone)
  • Renin-Angiotensin system and K levels
  • Stimulated by NaCl depletion
  • Androgens
  • Growth of hair follicles
  • Stress increases cortisol and aldosterone to
    maintain CV tone.
  • Impairment of release leads to adrenal crisis

25
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26
Cushing Syndrome
  • 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

27
Addison's
  • Adrenocorticol insufficiency
  • Autoimmune
  • Sxs - weight loss, anorexia, weakness, low BP,
    low sodium, high potassium, nausea vomiting,
    diarrhea
  • Tx - Glucocorticoids
  • Mineralcorticoids
  • Adrenal Crisis

28
Adrenal Medulla
  • Pheochromocytoma
  • Neoplasm increasing catecholamines
  • Surgical removal
  • Sxs - episodic HTN, increased metabolism,
    hyperglycemia
  • Lab - urine metanephrines
  • Monitor wide BP fluctuations

29
The Thyroid Gland
  • 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

30
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31
Thyroid
  • Essential to regulate metabolism
  • Caused by release of TSH
  • Thyroxin - T4
  • Triiodothyronine - T3
  • Stimulated by increased Ca in blood
  • Calcitonin - lowers blood levels by inhibiting
    bone re-absorption
  • Low calcium levels suppress the release of
    calcitonin
  • Elevated levels increase its secretion

32
Prevalence of Thyroid Disorders
  • 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.

33
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34
Hyperthyroid
  • 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

35
Hypothyroid
  • 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

36
Parathyroid
  • 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

37
Hyperparathyroid
  • 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

38
Hypoparathyroid
  • Accidental removal or vascular damage during
    surgery
  • Sxs - Tetany, Chvosteks sign
  • Lab- low calcium, low PTH, and high Phos.
  • Tx - Vitamin D, Calcium supplements, and
    Phosphate binders

39
Pancreas
  • Insulin
  • 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

40
Diabetes Mellitus
  • Chronic hyperglycemia---main feature in all types
    of diabetes mellitus. Resulting from
  • Insulin secretion
  • Insulin action
  • Or both
  • Disease classified
  • Age of onset
  • Problem causing the lack of insulin
  • Severity of the deficiency

41
Cost of Diabetes in the United States, 2002
  • Total (direct and indirect) 132 billion
  • Direct medical costs 92 billion
  • Indirect costs 40 billion (disability, work
    loss, premature mortality)

42
Blood Glucose Values
  • Normal Fasting blood glucose levels of lt110
    mg/dL
  • Significant abnormal results Levelsgt126mg/dL
    obtained on at least two occasions are diagnostic
    of diabetes, even in older adults.

43
Diabetes Causes
  • Inability to use CHO
  • Insulin action ineffective at tissue site or not
    enough Insulin available

44
Diabetes Causes
  • Glycogen fails to store in liver
  • Conversion of glycogen to glucose NOT affected
  • Increased metabolism of proteins and fats
  • Leads to Ketone production

45
Insulin
  • 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 Polys

46
Type I
  • Beta cell destruction
  • Rapid onset
  • Must be given Insulin
  • Ketoacidosis prone

47
Type II
  • 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

48
Impaired Glucose Tolerance
  • Borderline Diabetes
  • Blood Glucose levels above normal, but below
    levels to Dx Diabetes
  • May progress to Diabetes
  • Need close monitoring
  • Diet and Exercise

49
Gestational
  • 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

50
Baby Effects
  • Increase amounts of amniotic fluid
  • Large fetus
  • Hypoglycemic reactions after birth
  • Respiratory Distress Syndrome

51
Tests
  • Blood Sugar
  • Glycosylated Hemoglobin (HbA1c)
  • The higher the number the poorer the control.
  • GTT - Glucose Tolerance Test
  • Capillary Blood Glucose (CBG)

52
Treatment
  • 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

53
Insulin Treatment
  • Goal Match Normal Secretion Patterns of the Body
  • Multiple types of Insulin
  • Administration techniques
  • Site Rotations
  • Pumps
  • New Technology

54
Somogyi Effect
  • Wide difference in CBGs
  • Low in early AM
  • High after breakfast
  • Counter regulatory to hypoglycemia during the
    night
  • Treatment - lower Insulin dose in the evening or
    increase food intake before bed

55
Dawn Phenomenon
  • High CBGs and possibly Ketones in the morning
  • Dawn release of Growth Hormone or Cortisol
  • Treatment - Change Insulin times and/or increase
    Insulin dose
  • Look at clients entire management program

56
Sulfonylureas
  • 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

57
Hypoglycemics
  • 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

58
Hypoglycemia
  • 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

59
DKA - Diabetic Ketoacidosis
  • No Insulin leads to
  • 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

60
Jamie
61
HHNK - Hyperglycemic Hyperosmolar NonKetosis
  • 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(NaK) BS BUN
  • 18 2.8

62
Chronic Complications
  • 80 of Medical Spending
  • Increasing as Population Ages
  • Microvascular
  • Macrovascular
  • PATIENT EDUCATION

63
Arthur
64
Pattern Management Rule
  • Target Glucose Goals
  • Regular CBGs
  • Record CBGs 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 CBGs FIRST
  • 3 days before another change

65
Client 1
66
Client 2
67
Client 3
68
Home Causes
  • Oral Medication Errors
  • Dose, Timing, Double Medication
  • Bring ALL Meds from home
  • Insulin Errors
  • Technique Problems
  • Observe technique ASAP
  • Check dose and timing at home
  • Diet Misinformation / Changes
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