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Homeostasis and The Stress Response

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Title: Homeostasis and The Stress Response


1
Homeostasis and The Stress Response
2
Homeostasis
3
Homeostasis
  • Definition The tendency of an organism or a
    cell to regulate its internal conditions, usually
    by a system of feedback controls, so as to
    stabilize health and functioning, regardless of
    the outside changing conditions.
    http//www.biology-online.org/dictionary/Homeostas
    is
  • Influences that tend to deregulate internal
    conditions are termed stressors
  • This is a different definition than we are used
    to hearing
  • Stressors can be physical, emotional,
    environmental, etc.
  • Compensatory mechanisms to counteract the
    effect(s) of stressors involve
  • Autonomic nervous system
  • Adrenal cortex
  • Renin-angiotensin-aldosterone system (RAAS)
  • Many others.

4
Stressors
5
Stressors
Anxiety
Procedures
Disease
Old age
Obesity
Malnutrition
Pain
Fear
Trauma
Heat
Prolonged Exertion
Anger
Low 02 supply
Cold
Noise
Treatments
Lack of sleep
Drugs
Surgery
Radiation
Infection
6
Three Components to Physiologic Stress Response
7
Three Components to Physiologic Stress Response
8
Neuroendocrine Pathways and Physiologic Responses
to StressDescription
9
Neuroendrocrine Pathways and Physiologic
Responses to StressDescription
  • Shows the different responses to stressors
  • May perceive stressor in the cerebral cortex or
    the stressor may be unconscious
  • Activating the RAS (the part of the brain that
    keeps up awake) leads to increased muscle
    tension and alertness
  • Limbic system produces the emotional response
  • The locus ceruleus activates the ANS (sympathetic
    nervous system), which activates the adrenal
    medulla and the activation of the RAAS

10
Neuroendrocrine Pathways and Physiologic
Responses to StressDiagram
11
Neuroendrocrine Pathways and Physiologic
Responses to Stress
(Corticotropin Releasing Factor)
(Adrenocorticotropic Hormone)
Activation of the RAAS
Adapted from Porth, 2011, Essentials of
Pathophysiology,3rd ed., Lippincott, p. 213
12
Activation of the Sympathetic Nervous System (SNS)
13
Activation of the Sympathetic Nervous System
(SNS)
  • ? Heart rate
  • ? Blood pressure
  • Cool skin
  • All of the blood is being shunted away form the
    skin to the skeletal muscle
  • Diaphoresis to keep body cool
  • Pupil dilation
  • ? Blood glucose to have fuel for muscle
  • ? Peristalsis
  • ? Urine output
  • Do not want to devote metabolic energy to urine
    formation

14
Release of Norepinephrine
15
Release of Norepinephrine
Norepinephrine
?1
?1 ?2
?1
Pupil Dilation
Vasoconstriction of arteries and veins (?Venous
return to the heart/CO and ?Blood Pressure)
  • ?Heart rate
  • ?Contractility
  • Release of renin
  • All of these increase blood
  • pressure

16
Epinephrine Released byAdrenal Medulla
17
  • Epinephrine Released by
  • Adrenal Medulla
  • Activates alpha 1 and
  • alpha 2 as well as beta
  • 2 receptors

Epinephrine
?1 ?2
?1
?1
  • Vasoconstriction
  • Blood pressure
  • Venous return/CO

Pupil dilation
?2
Dilation of skeletal muscle vascular beds and
bronchi
?Heart rate ?Contractility ? Release of renin
18
Role of Epinephrine on B2 Receptors
19
Epinephrine
?2
?2
Lipolysis of triglycerides
?Degradation of cholesterol to bile Salts
  • Free fatty acids that can
  • be used for ATP synthesis
  • - maximizes energy
  • production

?Cholesterol to be available for the repair of
cell membranes
20
Epinephrine
?2
Skeletal Muscle
?2
? Protein breakdown/amino acid release
Liver
Gluconeogenesis
Glycogen Breakdown
? Blood Glucose
21
Norepinephrine stimulates beta-1 receptors to
cause
22
Norepinephrine stimulates beta-1 receptors to
cause
  1. Lipolysis of triglyerides beta 2
  2. Vasoconstriction of blood vessels - alpha
  3. Decreased heart rate muscarinic receptors
  4. Renin release

23
Release of Renin and ADH (Antidiuretic Hormone)
24
Release of Renin and ADH (Antidiuretic Hormone)
  • Renin is released in response to SNS stimulation
    of beta-1 receptors in the kidney
  • Release of renin initiates renin-angiotensin-aldos
    terone system (RAAS)
  • Angiotensin II causes vasoconstriction leading to
    ? Blood pressure
  • Aldosterone causes increased reabsorption of
    water in the kidneys causing ? venous return ? ?
    cardiac output
  • Aldosterone has a steroid structure, like
    cortisol, and is referred to as a
    mineralocorticoid.
  • -------------------------------------------------
    ----------------------
  • ADH (antidiuretic hormone) is released from the
    posterior pituitary in response to SNS
    stimulation
  • ADH causes increased reabsorption of water in the
    kidneys causing ? venous return ? ? cardiac output

25
ReninAngiotensinAldosterone System
(RAAS)Diagram
26
ReninAngiotensinAldosterone System
(RAAS)Diagram
Must know this!!!
Porth, 2011, Essentials of Pathophysiology, 3rd
ed., Lippincott, p. 420.
27
Hypothalamus-Anterior Pituitary FunctionDiagram
28
Hypothalamus-Anterior Pituitary Function
Porth, 2007, Essential of Pathophysiology, 2nd
ed., Lippincott, p. 666
29
Hypothalamus-Anterior Pituitary
FunctionDescription
30
Hypothalamus-Anterior Pituitary
FunctionDescription
  • The hypothalamus and the anterior pituitary are
    important in the stress response
  • Cells release releasing factors that travel
    through the vessels and cause cells in the
    anterior pituitary to release tropic hormones
  • Go to target glands to release peripheral
    hormones
  • The hormone has a negative feedback on the
    anterior pituitary and the hypothalamus to
    decrease the hormone

31
Feedback InhibitionDiagram
32
Feedback Inhibition Diagram
Porth, Essentials of Pathophysiology, 3rd ed.,
2011, Lippincott, p.770.
33
Peripheral Glands Controlled by the
PituitaryDiagram
34
Peripheral Glands Controlled by the Pituitary
Porth, 2011, Essential of Pathophysiology, 3rd
ed., Lippincott, p. 770
35
Regulation of Cortisol Synthesis and
SecretionDescription
36
Regulation of Cortisol Synthesis and
SecretionDescription
  • Adrenals do not store glucocorticoids
  • Amount released amount made
  • Regulated by negative feedback loop
  • Circadian rhythm
  • ? bedtime, ? sleep, peak on awakening, ? during
    day
  • Stress increases CRH synthesis and release.
  • Some of the inputs into the hypothalamus include
    stress and circadian rhythms
  • Also regulated by negative feedback from cortisol
    in the periphery
  • Also acts on cells in the anterior pituitary
  • ACTH circulates all over the body, such as the
    adrenal cortex
  • Biological effects of cortisol are on nearly
    every body cell
  • Cortisol secretion is low at night, at its
    highest in the morning

37
Regulation of Cortisol Synthesis and
SecretionDiagram
38
Regulation of Cortisol Synthesis and Secretion
Lehne, 2009, Pharmacology for Nursing Care, 7th
ed., Elsevier, p. 711
39
Diurnal Secretion of CortisolDiagram
40
Diurnal Secretion of Cortisol
Stewart, Paul, 2003, The adrenal cortex in
Larson, et al, eds., Williams Textbook of
Endocrinology, Saunders.
When we administer corticosteroids
pharmacologically, we try to mimic this diurnal
rhythm.
41
CortisolPhysiologic Effects
42
CortisolPhysiologic Effects
  • Carbohydrate metabolism
  • Fat metabolism
  • Protein metabolism
  • Cardiovascular
  • Central nervous system
  • Stress

43
CortisolCarbohydrate Metabolism
44
CortisolCarbohydrate Metabolism
  • Carbohydrate Metabolism
  • ?Gluconeogenesis the synthesis of new glucose
    molecules in the liver
  • ?Peripheral glucose utilization in the periphery
  • Increased gluconeogenesis and decreased
    peripheral glucose utilization will increase
    glucose levels in the body
  • ? glucose uptake muscle/adipose tissue
  • Promote glucose storage (glycogen)
  • All these make glucose more available to the
    brain!

45
Glucocorts
46
Glucocorts
  • Supplying the brain with glucose is essential for
    survival.
  • Glucocorts help meet this need with CHO
    metabolism thru the following 4 ways.
  • All 4 actions increase glucose availablility
    during fasting and thereby ensure the brain will
    not be deprived of its primary source of energy.
  • When present in chronically high levels for a
    prolonged period of time, glucocorts produce
    symptoms much like those of diabetics.
  • Pro metab promote pro breakdown.
  • If present at high levels for prolonged pd of
    time, glucorts will cause a thinning of skin,
    muscle wasting, and negative nitrogen balance
  • Fat metab glucocorts promote lipolysis (fat
    breakdown).
  • When present at high levels for an extended time,
    glucocorts cause fat redistribution, given the pt
    a potbelly, moon face, and buffalo hump on the
    back.

47
CortisolProtein Metabolism
48
CortisolProtein Metabolism
  • Promote catabolism
  • Amino acids provide substrate for hepatic
    gluconeogenesis

49
CortisolFat Metabolism
50
CortisolFat Metabolism
  • Promote lipolysis
  • Increases the amount of energy that is available
    to the cells
  • Free fatty acids provide substrate for the Krebs
    cycle.

51
CortisolCardiovascular System
52
CortisolCardiovascular System
  • Required for the integrity of the blood vessels,
    including their ability to constrict

53
CortisolCentral Nervous System
54
CortisolCentral Nervous System
  • Increases excitation
  • Euphoria
  • Alertness

55
CortisolStress Response
56
CortisolStress Response
  • Stress
  • Stress increases CRH secretion by the
    hypothalamus
  • CRH secretion stimulates ACTH (adrenocorticotropic
    hormone) secretion, which increases cortisol
    secretion

57
Effect of Acute Stress
58
Effect of Acute Stress
  • Goals survival, vigilance, alertness, arousal,
    aggression
  • Designed to be self-limiting and short term
  • Similar to the Fight or flight SNS
    activation shortest term
  • Activation of the HPA (hypothalamus pituitary
    adrenal) axis promotes energy utilization and
    availability of substrate for tissue repair.
    longer term.
  • Even though this is longer term, it is not
    designed to be continually activated

59
Chronic Stress
60
Chronic Stress
  • Prolonged activation of the system
  • Stage of exhaustion may be reached of the system
  • Health problems may result

61
Chronic Activation of the Stress Response May
Exacerbate Diseases
62
Chronic Activation of the Stress Response May
Exacerbate Diseases
Cardiovascular Heart disease, stroke
Immune Autoimmune diseases
GI Ulcers, irritable bowel syndrome, colitis, vomiting, diarrhea
Endocrine Diabetes mellitus, metabolic syndrome
CNS Fatigue, eating disorders, depression, insomnia, post-traumatic stress disorder
63
Coping and AdaptationDescription
64
Coping and AdaptationDescription
  • Humans have the capacity to adapt and cope with
    stressors based on a lot of different things
  • Very young and very old people do not respond to
    stress as well as middle-aged people
  • Hardiness the ability to go on despite problems
  • It is harder to adapt to a sudden stressor

65
Coping and AdaptationDiagram
66
Coping and Adaptation
Porth, 2011, Essentials of Pathophysiology, 3rd
ed., Lippincott, p. 216.
67
Coping
68
Coping
  • The coping response can exaggerate or moderate
    the consequences of the stress response
  • Outcome is determined by coping strategies
  • Effective coping moderates stress
  • Ineffective coping exacerbates stress

69
Nursing Care and Stress
70
Nursing Care and Stress
  • Nurses should put the patient in the best
    possible condition for nature to restore or
    preserve health, to prevent, or cure disease
    (Florence Nightingale)
  • This is still performed today
  • Todays hospital environment (stressful!)
  • Turbulence, frenzied pace, telephones, intercoms,
    electronic alarms, pagers, telemetry
  • The hospital environment is not very conducive to
    rest
  • Is the hospital a place of healing?

71
Types of EnvironmentsDiagrams
72
This Environment
73
Or this Environment
74
Nurses Role in Dealing with Stress
75
Nurses Role in Dealing with Stress
  • Nurses can help patients deal with the stress of
    injury, disease, or psychological stressors
  • Augment the patients own methods of coping
  • Provide the means for adapting to stressors

76
Supportive Care
77
Supportive Care
  • Should be given to every patient
  • Maintain/restore homeostasis by monitoring fluid,
    electrolytes, blood pressure, heart rate, etc.,
    and making necessary corrections.
  • Provide adequate nutrition to provide substrate
    for energy generation and repair/maintenance of
    tissues.
  • Provide appropriate sleep-wake cycles.
  • Postpone blood draws and other care
  • Darken the room as far as possible
  • Provide protection from stressful life events.
  • Appropriate visitors
  • Restful environment
  • Clear explanations and patience

78
Non-Pharmacologic Methods
79
Non-Pharmacologic Methods
  • Music therapy
  • Relaxation techniques
  • Guided imagery
  • Massage therapy
  • Biofeedback

80
Disorders Affecting the Stress Response
Hypothalamic Pituitary Adrenal Axis
81
Cushings SyndromeGlucocorticoid Excess
82
Cushings SyndromeCauses
83
Cushings SyndromeCauses
  • Primary causes
  • Secondary causes

84
Cushings SyndromePrimary Causes
85
Cushings SyndromePrimary Causes
  • Hypersecretion of ACTH by pituitary adenomas
    (benign tumors) (Cushings disease)
  • Hypersecretion of glucocorticoids by adrenal
    adenomas and carcinomas
  • These are rare
  • Hardly ever see primary Cushings syndrome

86
Cushings SyndromeSecondary Causes
87
Cushings SyndromeSecondary Causes
  • Caused by chronic administration of pharmacologic
    glucocorticoids (autoimmune diseases such as
    rheumatoid arthritis, organ transplant)
  • This is the most common cause of cushingoid
    changes

88
Signs/symptoms of Cushings Syndrome
89
Signs/symptoms of Cushings Syndrome
  • Obesity
  • Redistribution of fat to abdomen
  • Hyperglycemia/glycosuria
  • Hypertension
  • Fluid, electrolyte disturbances
  • Osteoporosis
  • Muscle weakness
  • Cataracts
  • Hirsutism
  • Menstrual irregularities
  • Decreased resistance to infection because
    steroids are immunosuppressant
  • Moon facies
  • Buffalo hump
  • Psychiatric changes

90
Cushings SyndromeDiagram
91
Signs Symptoms of Cushings Syndrome
Porth, 2007, Essentials of Pathophysiology, 2nd
ed., Lippincott, p. 695.
92
Treatment for Cushings Syndrome
93
Treatment for Cushings Syndrome
  • Primary Cushings syndrome - surgical removal of
    diseased adrenal gland or diseased pituitary
  • If bilateral adrenalectomy is required, patient
    will need replacement with both glucocorticoids
    and mineralocorticoids (aldosterone)
  • Secondary Cushings syndrome
  • If glucocorticoid administration is the cause,
    decrease the dose as much as possible.

94
Etiology of Adrenal Insufficiency
95
Etiology of Adrenal Insufficiency
  • Primary hypoadrenalism
  • Secondary hypocortisolism

96
Etiology of Adrenal InsufficiencyPrimary
Hypoadrenalism
97
Etiology of Adrenal InsufficiencyPrimary
Hypoadrenalism
  • Primary hypoadrenalism Addisons disease
  • Can be contracted via infection, hemorrhage,
    surgical removal of the adrenal glands
  • Glucocorticoid deficiency, and possibly
    mineralocorticoid (aldosterone) insufficiency

98
Etiology of Adrenal InsufficiencySecondary
Hypocorticolism
99
Etiology of Adrenal InsufficiencySecondary
Hypocortisolism
  • Secondary hypocortisolism
  • Abrupt discontinuation of chronic pharmacologic
    glucocorticoids
  • This is the most common cause of adrenal
    insufficiency!
  • Hypopituitarism creates a deficiency in cortisol
    due to insufficient ACTH secretion
  • Glucocorticoid deficiency, but not
    mineralocorticoid
  • (Aldosterone is controlled by Angiotensin II not
    ACTH from the pituitary gland)

100
Regulation of Cortisol Synthesis and
SecretionDescription
101
Regulation of Cortisol Synthesis and
SecretionDescription
  • Pharmacologic steroids produce a negative
    feedback effect on the hypothalamus and
    pituitary.
  • CRH and ACTH are decreased to zero
  • Over time, the adrenal gland becomes less able to
    produce cortisol.
  • If pharmacologic steroids are discontinued
    abruptly, CRH and ACTH will increase but the
    adrenal cannot respond.
  • The person will be out of corticosteroids
  • Can be very dangerous
  • There may also be a problem with physiologic
    stress such as surgery, infection, etc. extra
    steroids should be given.
  • Normally cortisol will increase
  • If a person is on pharmacologic steroids, the
    adrenal gland does not know about the stressor
    and cannot respond
  • Will have to increase steroids because the
    adrenal gland cannot increase its production of
    cortisol to meet the stressor

102
Regulation of Cortisol Synthesis and
SecretionDiagram
103
Regulation of Cortisol Synthesis and Secretion
Porth, 2011, Essentials of Pathophysiology, 3rd
ed., Lippincott, p. 791.
104
Signs and Symptoms of Addisons Disease
105
Signs and Symptoms of Addisons Disease
  • Glucocorticoid deficiency
  • Hypoglycemia, anorexia, nausea, vomiting,
    diarrhea, anxiety, depression, hyperpigmentation
  • Mineralocorticoid deficiency
  • If deficiency is due to malfunctioning or absent
    adrenal gland
  • Fluid volume deficit, hyperkalemia, hyponatremia,
    orthostatic hypotension due to dehydration

106
Addisonian Crisis
107
Addisonian Crisis
  • Major complication, life threatening
  • May occur with abrupt discontinuation of
    pharmacologic steroids or failure to administer
    extra steroids to a steroid-dependent patient who
    has additional stress (surgery, trauma).
  • Severe hypotension
  • Hyponatremia
  • Dehydration
  • Hyperkalemia

108
Treatment of Addisonian Crisis
109
Treatment of Addisonian Crisis
  • Immediate replacement of cortisol with
    hydrocortisone
  • Hydrocortisone is fast acting and has both
    glucocorticoid and mineralocorticoid activity
  • May also need mineralocorticoid replacement as
    well as the steroids

110
Normal secretion of cortisol from the adrenal
cortex is the HIGHEST at
111
Normal secretion of cortisol from the adrenal
cortex is the HIGHEST at
  1. 800 am
  2. 12 noon
  3. 400 pm
  4. 12 midnight

112
Agents for Replacement Therapy in Adrenal
Insufficiency
113
Agents for Replacement Therapy in Adrenal
Insufficiency
  • These apply if the person has primary adrenal
    issues
  • Glucocorticoids
  • Mineralocorticoids

114
Fludrocortisone (Florinef)
115
Fludrocortisone (Florinef)
  • The only drug for aldosterone replacement
  • Is an aldosteorne agonist
  • Aldosterone replacement, but also has some
    glucocorticoid activity.
  • Most of the time, is given with a glucocorticoid.
  • Renal effects
  • Like aldosterone, acts on the collecting ducts to
    promote Na reabsorption (?H20 ) in exchange for
    K, H
  • Cardiovascular effects (harmful effects with?
    levels)
  • Promotes myocardial remodeling and fibrosis
  • Vascular fibrosis

116
Glucocorticoids
117
Glucocorticoids
  • Cortisol
  • Very commonly used
  • Physiologic vs. pharmacologic effects
  • Physiologic low levels for replacement in
    primary Addisons disease
  • Pharmacologic high levels for immunosuppression
    (organ transplant) or anti-inflammatory activity.
  • Pharmacological steroids are more commonly given
    in large doses

Lehne, 2009, Pharmacology for Nursing Care, 7th
ed., Elsevier, p. 711
118
Oral Glucocorticoid Drugs Used to Treat Adrenal
Insufficiency
119
Oral Glucocorticoid Drugs Used to Treat Adrenal
Insufficiency
  • Hydrocortisone has some mineralocorticoid
    activity.
  • Dexamethasone
  • Prednisone
  • These drugs will be discussed in detail in the
    section on steroids for non-endocrine disorders.
  • When used for adrenal insufficiency (steroid
    replacement), doses are low to produce
    physiologic levels and effects.

120
Hydrocortisone for Adrenal Insufficiency
121
Hydrocortisone for Adrenal Insufficiency
  • Replacement therapy
  • Oral hydrocortisone is ideal for chronic
    replacement therapy
  • Parenteral administration used for acute adrenal
    insufficiency and to supplement oral doses at
    times of stress
  • May suffice as sole therapy since it has
    mineralocorticoid activity
  • Dirt cheap!

122
High Dose Glucocorticoid Therapy for
Non-Endocrine Disorders
123
High Dose Glucocorticoid Therapy for
Non-Endocrine Disorders
  • Glucocorticoids have powerful anti-inflammatory
    and immunosuppressive actions.
  • These do not occur at physiologic doses but at
    higher, pharmacologic doses.
  • When used at high doses for their
    anti-inflammatory or immunosuppressive effects,
    the physiologic effects are magnified and cause
    important side effects.
  • Non-endocrine use of glucocorticoids is much more
    common than use as replacement for adrenal
    insufficiency.

124
Anti-inflammatory/Immunosuppressive Effects of
Pharmacologic Doses of Glucocorticoids
125
Anti-inflammatory/Immunosuppressive Effects of
Pharmacologic Doses of Glucocorticoids
  • Inhibit synthesis of inflammatory mediators
  • Prostaglandins, leukotrienes, histamine
  • Reduce swelling, warmth, redness, pain
  • Suppress infiltration of phagocytes
  • Damage from lysosomal enzymes is averted
  • Suppress proliferation of lymphocytes in response
    to the immune system
  • Reduce immune component of inflammation
  • This could be both good and bad

126
Therapeutic Use of Glucocorticoids in
Nonendocrine Disorders
127
Therapeutic Use of Glucocorticoids in
Nonendocrine Disorders
  • Rheumatoid arthritis intra-articular or
    systemic
  • Systemic lupus erythematosus - oral
  • Inflammatory bowel disease - oral
  • Allergic conditions topical or systemic
  • Asthma inhaled or systemic
  • Cancer
  • Suppression of allograft rejection
  • Prevention of respiratory distress syndrome in
    preterm infants (administered to the mother in
    threatened preterm birth)
  • Promotes fetal lung maturation

128
Local Administration of Glucocorticoids
129
Local Administration of Glucocorticoids
  • Inhalation or intra-articular
  • On the skin
  • Since steroids are very lipid soluble, some of
    the locally-administered dose will get into the
    bloodstream but concentrations will be lower than
    if it were administered systemically
  • Because blood levels are lower with these routes
    of administration, side effects are lessened.
  • Local administration is the best for avoiding
    side effects

130
Oral Dosing Guidelines
131
Oral Dosing Guidelines
  • For chronic conditions, usually start with low
    dose and increase until symptoms improve
  • Daily dosing
  • Give entire dose before 9AM every morning (limits
    adrenal suppression since it coincides with the
    normal peak level of cortisol).
  • Some patients may require a 2nd dose in the
    afternoon.
  • Alternate day dosing
  • May be possible in some patients as the 1st step
    in tapering
  • Reduces adrenal suppression, risk of growth
    retardation, overall toxicity

132
Steroid Use for Acute Conditions
133
Steroid Use for Acute Conditions
  • Steroid pulse is given at a high dose initially
    with tapering over a week or 2-week period.
  • Example Oral prednisone, 60 mg. for 4 days, 50
    mg for 2 days, 40 mg for 2 days, 30 mg. for 2
    days and so on.
  • This type of regimen will not cause adrenal
    suppression.
  • Ex. poison ivy

134
Diurnal Secretion of CortisolDiagram
135
Diurnal Secretion of Cortisol
Stewart, Paul, 2003, The adrenal cortex in
Larson, et al, eds., Williams Textbook of
Endocrinology, Saunders.
When we administer corticosteroids
pharmacologically, we try to mimic this diurnal
rhythm.
136
Adverse Reactions of Pharmacologic Glucocorticoid
Therapy
137
Adverse Reactions of Pharmacologic Glucocorticoid
Therapy
  • When taken chronically in large doses
    (non-endocrine disorders), there are a
    multiplicity of adverse effects that must be
    monitored and dealt with.
  • Metabolism
  • Bone
  • Fluids and electrolytes
  • Immune system
  • Eye problems
  • Cataracts
  • Glaucoma
  • Peptic ulcers
  • Growth retardation in children
  • Psychiatric side effects
  • Often the patient has to take a 2nd or 3rd drug
    to counteract the bad effects of the steroids.

138
Glucocorticoid TherapyEffects on Metabolism
139
Effects on Metabolism
  • Intensified effects of physiologic doses
  • Hyperglycemia/diabetes
  • This is a significant adverse effect that
    frequently results in the patient being treated
    for diabetes and experiencing the long-term
    complications of diabetes.
  • Suppression of protein synthesis
  • Fat deposits mobilized and redistributed
    (cushingoid habitus)
  • Osteoporosis

140
Glucocorticoid TherapyEffects on Bones
Osteoporosis
141
Glucocorticoid TherapyEffects on Bones
Osteoporosis
  • Glucocorticoids cause bone loss by
  • Suppression of bone formation by osteoblasts
  • Acceleration of bone resorption by osteoclasts
  • Reduction of intestinal absorption of calcium

142
Osteoporosis
143
Osteoporosis
  • Osteoporosis with resultant fractures is a
    frequent, serious complication of therapy
  • Ribs and vertebrae most affected
  • More likely to occur with systemic therapy (as
    opposed to inhaled or intra-articular uses)

144
OsteoporosisPrevention
145
OsteoporosisPrevention
  • Bone mineral density test prior to treatment
  • Use routes of administration that do not result
    in high blood levels (topical, inhalation, or
    intra-articular).
  • Patients should receive calcium and vitamin D
    supplements
  • Bisphosphate therapy (alendronate, etidronate)
    preserves bone by inhibiting osteoclastic bone
    resorption.
  • Although these drugs are approved for
    glucocorticoid-induced osteoporosis, they are not
    approved for osteoporosis prophylaxis.
  • Calcitonin inhibits osteoclasts this drug is
    also not approved for osteoporosis prophylaxis.

146
Glucocorticoid Effects on Fluid and Electrolytes
147
Glucocorticoid Effects on Fluid and Electrolytes
  • Retention of water and sodium may result in
    hypertension and edema
  • Hypokalemia can lead to dysrhythmias
  • Precautions
  • Consider restricting sodium intake
  • Consider adding potassium rich foods to diet, or
    administration of supplements
  • Monitor BP
  • Instruct patient to notify practitioner of fluid
    retention and palpitations (a sensation of rapid
    heart beat).

148
Glucocorticoid Effects on Immune System Infection
149
Glucocorticoid Effects on Immune System
Infection
  • Immunosuppressant
  • Suppression of immune system increases
    susceptibility to infection
  • -New infection or reactivation of latent
    infection (TB)
  • Steroids prevent the inflammatory manifestations
    of infection such that fulminant infection may
    develop without detection.
  • The person may not develop a fever, redness,
    swelling, pain, etc.
  • Prevention and close monitoring are key
  • Pneumocystis carinii pneumonia common, therefore
    sulfamethoxazol/trimethoprim prophylaxis is
    recommended

150
Glucocorticoid Treatment and Myopathy
151
Glucocorticoid Treatment and Myopathy
  • Manifests as muscle weakness
  • Muscles of arms and legs affected most
  • Damage may prevent ambulation
  • If myopathy develops, dosage should be reduced

152
Glucocorticoids and the Development of Cataracts
and Glaucoma
153
Glucocorticoids and the Development of Cataracts
and Glaucoma
  • Extremely common complication
  • Cataracts are a common complication of long term
    therapy
  • Eye examination every six months
  • Advise patient to contact provider with changes
    in vision
  • Oral glucocorticoids can cause glaucoma
  • Usually develops rapidly, reverses within 2 weeks
    of cessation
  • However, the person should taper the dose

154
Glucocorticoids and Peptic Ulcer Disease
155
Glucocorticoids and Peptic Ulcer Disease
  • Glucocorticoids inhibit prostaglandin synthesis,
    augment secretion of gastric acid and pepsin,
    inhibit production of protective mucus, reduce
    gastric mucosal blood flow ? GI ulceration
  • Risk increases with other ulcerogenic drugs, such
    as NSAIDS
  • Early detection crucial through examination for
    occult blood in the stool
  • Instruct patient to notify practitioner if stools
    become black (melana)

156
Glucocorticoids and Growth Retardation in Children
157
Glucocorticoids and Growth Retardation in Children
  • Probably as result of reduced DNA synthesis,
    decreased cell division
  • Assess height and weight regularly
  • Growth suppression may be minimized with
    alternate day therapy

158
Glucocorticoids and Psychiatric Side Effects
159
Glucocorticoids and Psychiatric Side Effects
  • Most people experience increased alertness,
    energy, etc.
  • Psychosis with hallucinations, mood changes, and
    other psychological disturbances is unusual.

160
Long Term Corticosteroid Therapy
161
Long Term Corticosteroid Therapy
  • Bypasses negative feedback loop and results in
    gradual loss of adrenal and pituitary hormone
    reserves atrophy of ACTH secreting cell occurs.
  • Sudden withdrawal results in acute adrenal
    insufficiency the most common cause of adrenal
    insufficiency.
  • Could be fatal
  • Patients on glucocorticoids greater than 2 weeks
    have some degree of HPA suppression.
  • Secondary adrenal insufficiency is prevented by
    gradual weaning the patient from these drugs
    over weeks to months.

162
Regulation of Cortisol Synthesis and
SecretionDescription
163
Regulation of Cortisol Synthesis and
SecretionDescription
  • Pharmacologic steroids produce a negative
    feedback effect on the hypothalamus and
    pituitary.
  • CRH and ACTH are decreased.
  • Over time, the adrenal gland becomes less able to
    produce cortisol.
  • If pharmacologic steroids are discontinued
    abruptly, CRH and ACTH will increase but the
    adrenal cant respond.
  • There may also be a problem with physiologic
    stress such as surgery, infection, etc. extra
    steroids should be given.
  • Have adrenal insufficiency because of negative
    feedback mechanism on pituitary and hypothalamus
    and adrenal gland cannot respond to CRH and ACTH

164
Regulation of Cortisol Synthesis and
SecretionDiagram
165
Regulation of Cortisol Synthesis and Secretion
Porth, 2011, Essentials of Pathophysiology, 3rd
ed., Lippincott, p. 791.
166
Glucocorticoid Withdrawal
167
Glucocorticoid Withdrawal
  • Should be done slowly (taper)
  • Schedule is determined by degree of adrenal
    suppression
  • Strategies for weaning
  • Depending on the time the person has been on
    steroids and the dose used, the tapering period
    may be years or they may never be able to be
    completely weaned.

168
Strategies for Weaning People off of
Glucocorticoids
169
Strategies for Weaning People off of
Glucocorticoids
  • Multiple daily doses to single daily dose
  • Institute alternate day dosing
  • Taper gradually over months
  • Continue to monitor, adjust dose
  • Increase dose for major stressors, such as
    surgery
  • Even if steroids are discontinued, the patient
    may need supplementation in the event of a major
    stressor because the adrenal gland may be
    inadquate

170
Adrenal Suppression and Physiologic Stress
171
Adrenal Suppression and Physiologic Stress
  • Patient taking glucocorticoids long term require
    increased doses at times of stress
  • Patients should carry an identification to inform
    emergency personnel
  • Patients should always have emergency supply of
    glucocorticoids on hand

172
Pregnancy and Lactation
173
Pregnancy and Lactation
  • Use of steroids in pregnancy should be carefully
    weighed.
  • Animal studies show increased birth defects no
    studies in humans.
  • Discontinuation of steroids could be serious for
    the mother in terms of re-exacerbation of a
    disease, rejection of an organ, adrenal
    insufficiency, etc.
  • Adrenal hypoplasia with adrenal insufficiency is
    a possibility in the infant due to the action of
    the steroids
  • Large doses over long term in a lactating woman
    could cause growth retardation or other adverse
    events in the baby
  • If these are necessary, perhaps the mother should
    not breast feed.

174
Preparations
175
Preparations
  • The half-life, mineralocorticoid potency
    (aldosterone activation), and glucocorticoid
    potency are important variables (Table 71.1 in
    Lehne).
  • Long-acting steroids (betamethasone and
    dexamethasone) are more potent than
    hydrocortisone.
  • Depot preparations are available for
    intra-articular and intramuscular injection
    (Table 71.2 in Lehne).

176
Integrative Body Functions II Alterations in
Temperature Regulation
177
Body Temperature Regulation
178
Body Temperature Regulation
  • Core body temp maintained
  • 36-37.5?C (97-99.5 ?F)
  • Individual differences, diurnal variations
  • Lowest in the morning and then increases
  • Maximum body temperature is around 6pm

179
Normal Diurnal Variations in Body
TemperatureDiagram
180
Normal Diurnal Variations in Body Temperature
Porth, 2011, Essentials of Pathophysiology, 3rd
ed., Lippincott, p. 65.
181
Thermoregulatory Center
182
Thermoregulatory Center
  • Core body temp is regulated by the
    thermoregulatory center in hypothalamus.
  • The center receives input from cold and warm
    thermal receptors located throughout body and
    generates output responses that conserve body
    heat or increase dissipation.
  • Thermostatic set point is set so body core
    temperature is maintained within normal limits
  • With increased temperature, heat-dissipating
    behaviors are stimulated
  • With decreased temperature, heat-producing
    behaviors are stimulated

183
Responses to Conserve Heat
184
Responses to Conserve Heat
  • Vasoconstriction of superficial blood vessels
    reduces heat loss from the skin into the
    environment.
  • Contraction of piloerector muscles that surround
    hairs on skin if we had fur, it would be
    fluffed up to conserve heat.
  • Assumption of huddle position to conserve heat

185
Responses to Produce Heat
186
Responses to Produce Heat
  • Shivering muscle movement produces heat
  • Increased production of epinephrine which
    increases the availability of glucose and free
    fatty acids for fuel.
  • As we burn fuel, we generate heat
  • Increased production of thyroid hormone, which
    increases metabolism.

187
Responses to Decrease Heat
188
Responses to Decrease Heat
  • Dilation of the superficial blood vessels
  • Flushing of skin and dissipation of heat
  • Transfer of heat to the body surface where it is
    lost through convection or radiation
  • Sweating produces loss of heat through
    evaporation
  • Controlled by the SNS
  • Evaporative heat losses are dependent on ambient
    temperature and humidity
  • In temperatures greater than body temperature,
    evaporative heat loss is essential for control of
    body temperature.

189
Mechanisms of FeverDescription
190
Mechanisms of FeverDescription
  • The pyrogens cause the resetting of the
    thermostatic set point
  • Released by the inflammatory response
  • The set point is set to a higher level and the
    temperature-raising responses are initiated

191
Mechanisms of FeverDiagram
192
Mechanisms of Fever
Porth, 2011, Essentials of Pathophysiology, 3rd
ed., Lippincott, p. 68.
193
Fever Mechanisms
194
Fever Mechanisms
  • Elevation in body temperature that is caused by a
    cytokine-induced upward displacement of the set
    point of the hypothalamic thermoregulatory
    center.
  • Caused by a number of microorganisms and
    substances, exogenous pyrogens
  • Exogenous pyrogens induce host cells to produce
    fever-producing mediators, endogenous pyrogens
  • Interleukins, Prostaglandin E

195
Core Temperatures
196
Core Temperatures
  • Greater than 41?C (105.8?F) or less than 34?C
    (93.2?F) indicate the normal thermoregulation is
    impaired

197
Elevations of Temperature
198
Elevations of Temperature
  • Fever (pyrexia)
  • Hyperthermia
  • Neurogenic fever

199
Elevations of TemperatureFever
200
Elevations of TemperatureFever
  • Upward displacement of hypothalamic set point
  • Usually caused by inflammatory mediators like
    IL-1 or by bacterial products
  • In children over 6 mos or so and immunocompetent
    adults, we would expect to see a temperature of
    over about 100F (37.8C).

201
Elevations of TemperatureHyperthermia
202
Elevations of TemperatureHyperthermia
  • Set point is unchanged (unlike in fever when the
    set point is changed)
  • The mechanisms that control body temperature are
    ineffective in maintaining temperature within
    normal range when heat production may be
    excessive or when there is exposure to high
    ambient temperatures
  • Ex. status epilepticus, ambient temperatures are
    extremely high

203
Elevations of TemperatureNeurogenic Fever
204
Elevations of TemperatureNeurogenic Fever
  • Neurogenic Fever Origin in CNS, caused by damage
    to hypothalamus resistant to anti-pyretics
  • Seen in stroke or brain-injury patients

205
Caution Related to Temperature Changes
206
Caution Related to Temperature Changes
  • Certain individuals may not be able to mount a
    full-blown fever response! Therefore, we have to
    be careful in our evaluations of temperature
    elevations in these people.
  • Infants, especially newborns.
  • Immunosuppressed individuals
  • Chemotherapy
  • Organ transplant
  • HIV infection
  • Frail elderly

207
Purpose of Fever
208
Purpose of Fever
  • May not be harmful and may be helpful
  • Cook the poisons?
  • May enhance immune function
  • Inhibit microbial growth
  • If it is a low fever and the person is
    functioning fairly well, it is okay not to lower
    it immediately

209
Patterns of Fever
210
Patterns of Fever
  • Intermittent
  • Remittent
  • Sustained
  • Relapsing

211
Patterns of FeverIntermittent
212
Patterns of FeverIntermittent
  • Temp returns to normal every 24 hours
  • Seen in children a lot

213
Patterns of FeverRemittent
214
Patterns of FeverRemittent
  • Temp does not return to normal and varies a few
    degrees in either direction

215
Patterns of FeverSustained
216
Patterns of FeverSustained
  • Temp remains above normal with minimal variation.

217
Patterns of FeverRelapsing
218
Patterns of FeverRelapsing
  • One or more episodes of fever, each as long as
    several days, with one or more days of normal
    temps between.
  • Ex. malaria

219
Physiologic Behaviors of Fever
220
Physiologic Behaviors of Fever
Defervescence
  • ? RR, ? HR, Sweating
  • ? metabolic rate, ? need for 02, use of body
    proteins for energy, metabolic acidosis
  • Headache
  • Changes in mentation

221
Treatment of Fever
222
Treatment of Fever
  • Fever is a manifestation of disease state,
    important to determine cause
  • Treat infection, condition causing fever
  • Modify environment
  • Support hypermetabolic state
  • Protect vulnerable organs

223
Anti-pyretics
224
Anti-pyretics
  • Aspirin, acetaminophen
  • Aspirin should not be used to treat fever in
    children!
  • Acetaminophen or ibuprofen would be the drugs of
    choice
  • Anti-pyretics alleviate discomforts and protect
    vulnerable organs
  • Anti-pyretics reset the hypothalamic temperature
    control center to a lower level by blocking
    activity of COX-2, thereby inhibiting
    pyrogen-induced synthesis of prostaglandins.

225
Heat Exhaustion
226
Heat Exhaustion
  • Heat exhaustion related to loss of salt and
    water through the sweat.
  • Temp between 37.8 and 40C but not terribly
    elevated
  • May be exhausted, sweating profusely
  • Treat with cooling, rehydration

227
Heat Stroke
228
Heat Stroke
  • Heat stroke Severe life threatening failure of
    thermoregulatory mechanisms resulting in an
    excessive rise in body temp (gt 40?C, 104 ?F),
    absence of sweating, and loss of consciousness.
  • Common in elderly in non-air conditioned
    settings.
  • Also seen in military/police settings during
    excessive physical training on hot days.

229
Hypothermia
230
Hypothermia
  • Core temps less than 35?C (93?F)
  • Accidental Environment
  • Controlled Surgery
  • Lower the persons metabolic rate in order to
    protect themselves
  • Those at risk for accidental hypothermia
  • Infants, elderly, malnourished,
    alcohol/sedatives, hypothyroidism
  • Hikers, swimmers

231
Manifestations of Hypothermia
232
Manifestations of Hypothermia
  • Changes in mentation, poor coordination, slurred
    speech.
  • Intense shivering with mild hypothermia, but
    shivering decreases as hypothermia becomes more
    severe.
  • Vasoconstriction of surface vessels pale, even
    blue.
  • Cold diuresis
  • Dehydration and elevated hematocrit (Hct)
    (increases viscosity)
  • In moderate to severe hypothermia, metabolic rate
    decreases significantly (this is why hypothermia
    is used in surgery).

233
Treatment of Hypothermia
234
Treatment of Hypothermia
  • Re-warming
  • Passive Remove the person from the cold
    environment, cover with blankets, warm fluids to
    drink, etc.
  • Active Immerse in warm water, use a heating pad
    (careful!). When hiking/camping, get in a
    sleeping bag naked with another (warm) naked
    person.
  • Active core re-warming heated fluids into the GI
    tract or peritoneal cavity, extracorporeal
    re-warming of blood.

235
Which of the following alters the hypothalamic
temperature set-point?
236
Which of the following alters the hypothalamic
temperature set-point?
  • Fever
  • Hyperthermia
  • Hypothermia
  • Cortisol

237
Integrative Functions IIIThyroid
238
Thyroid HormonesDescription
239
Thyroid HormonesDescription
  • Thyroid hormone comes in two types
  • Triiodothyronine
  • Thyroxine
  • Get there using the amino acid tyrosine
  • Add iodine to create monoiodotryrosine and then
    add another iodine to create di and then hitch
    together a mono and a di to create T3 or two di
    to create T4

240
Thyroid HormonesDiagram
241
Guyton Hall, Textbook of Medical Physiology,
10th ed., 2000, Saunders, p. 860.
242
Thyroid HormonesDescription
243
Thyroid HormonesDescription
  • Hormones are synthesized in cells in the ducts
  • The duct is not empty, but rather is filled with
    colloid (or thyroid globulin)
  • When the T3 and T4 have been synthesized they
    secrete them into the duct, where are hitched to
    the

244
Thyroid HormonesDiagram
245
Porth, 2011, Essential of Pathophysiology, 3rd
ed., Lippincott, p. 783
246
Thyroid Hormone ReceptorsDescription
247
Thyroid Hormone ReceptorsDescription
  • Most body cells have thyroid receptors
  • The thyroid hormone receptor is a nuclear
    receptor that influences gene transcription.
  • Only T3 binds to the thyroid receptor T4 must
    be converted to T3 inside the target cells before
    it will activate the receptor.
  • T3 and T4 are synthesized by the thyroid and are
    synthesized
  • Thyroid receptor that is activated by T3
    influences the transcription of multiple genes,
    so it has multiple effects in many different cell
    types.
  • Thyroid receptor is a nuclear receptor, leading
    to synthesis to the proteins with a plethora of
    effects

248
Thyroid Hormone ReceptorsDiagram
249
(No Transcript)
250
Thyroid Hormone Effects
251
Thyroid Hormone Effects
  • Regulates cell breakdown
  • Stimulates metabolic rate
  • Growth and development
  • Cardiovascular system
  • Gastrointestinal system
  • Central nervous system

252
Thyroid Hormone EffectsRegulation of Cell
Breakdown
253
Thyroid Hormone EffectsRegulation of Cell
Breakdown
  • Thyroid hormone regulates protein, fat, and
    carbohydrate breakdown in all cells.
  • 1. Stimulates fat breakdown and release of
    free fatty acids.
  • 2. Decreases cholesterol and triglycerides.
  • 3. Stimulates carbohydrate metabolism.
  • 4. Stimulates protein breakdown.

254
Thyroid Hormone EffectsStimulation of Metabolic
Rate
255
Thyroid Hormone EffectsStimulation of Metabolic
Rate
  • Thyroid hormone stimulates the metabolic rate.
  • 1. Increases respiratory rate and oxygen
    utilization.
  • 2. Stimulates body heat production.
  • 3. Decreases body weight.

256
Thyroid Hormone EffectsCardiovascular System
257
Thyroid Hormone EffectsCardiovascular System
  • Thyroid hormone affects the cardiovascular
    system.
  • Increases blood flow and cardiac output.
  • Increases heart rate.
  • Increases the cardiac contractility.

258
Thyroid Hormone EffectsGrowth and Development
259
Thyroid Hormone EffectsGrowth and Development
  • Thyroid hormone is important in growth and
    development.
  • Promotes CNS development in utero
  • Stimulates growth hormone secretion and skeletal
    maturation
  • Previously women who were hypothyroidic gave
    birth to babies who were mentally retarded
    (cretins)

260
Thyroid Hormone EffectsGI Tract
261
Thyroid Hormone EffectsGI Tract
  • Thyroid hormone affects the GI tract.
  • Increases GI motility.
  • Increases secretion of digestive juices.

262
Thyroid Hormone EffectsCentral Nervous System
263
Thyroid Hormone EffectsCentral Nervous System
  • Thyroid hormone affects the CNS
  • Increases the speed of impulse conduction (can be
    estimated from deep tendon reflexes).
  • Increases neuronal activity in the CNS.

264
Hypothalamic-Pituitary-Thyroid Feedback
265
Hypothalamic-Pituitary-Thyroid Feedback
Porth, 2011, Essential of Pathophysiology, 3rd
ed., Lippincott, p. 784
266
Considerable Lag Time Built into the Thyroid
System
267
Considerable Lag Time Built into the Thyroid
System
Guyton Hall, Textbook of Medical Physiology,
10th ed., 2000, Saunders, p. 861.
268
Both Hypo- and Hyper- Thyroidism Come on Slowly
and Have Vague, Systemic Symptoms
269
Both Hypo- and Hyper- Thyroidism Come on Slowly
and Have Vague, Systemic Symptoms
  • Patients may not notice how severe the symptoms
    have become because they come on slowly
  • Caregivers may diagnose depression or a viral
    illness rather than thyroid disease.
  • Because it has systemic effects and is insidious
  • The thyroid may or may not be enlarged.

270
Screening for Thyroid Disease
271
Screening for Thyroid Disease
  • The TSH level is the accepted screening test.
  • If TSH is high or low, tests for T3 and T4 are
    obtained.
  • The diagnosis of hypo- or hyper- thyroidism is
    based on the combination of the TSH, T3 and T4
    levels.
  • The practitioner must differentiate between a
    problem in the thyroid and a problem in the
    pituitary.

272
Primary Hypo or Hyper Thyroidism
273
Primary Hypo or Hyper Thyroidism
  • The thyroid is not following the directions of
    the pituitary but rather is acting autonomously
  • Hypothyroidism --- TSH is high (saying that T3
    and T4 are low so need to make more so TSH is
    high) but T3 and T4 are low.
  • Hyperthyroidism --- TSH is low (pituitary says
    that there is too much T3 and T4 but the thyroid
    makes more anyway) but T3 and T4 are high.
  • In either case, the problem is in the thyroid.
    The pituitary is normal.

274
Secondary Hypo- or Hyper- Thyroidism
275
Secondary Hypo- or Hyper- Thyroidism
  • The thyroid is doing what it is told by the
    pituitary but the pituitary is giving it the
    wrong directions
  • Hypothyroid --- TSH is low and T3 and T4 are also
    low.
  • Hyperthyroid --- TSH is high and T3 and T4 are
    also high.
  • In either case, the problem is in the pituitary.
    The thyroid is normal.
  • The pituitary is telling the thyroid the wrong
    thing

276
Pituitary Cause for Hypo- or Hyper- Thyroidism is
Rare
277
Pituitary Cause for Hypo- or Hyper- Thyroidism is
Rare
  • Secondary hypothyroidism or hyperthyroidism is
    rare
  • Increased secretion of TSH by the pituitary is
    most commonly caused by a tumor that secretes
    TSH.
  • Decreased secretion of TSH by the pituitary could
    be caused by a tumor that does not secrete TSH
    and crowds out the TSH-producing cells.
  • Head trauma can cause ischemia or necrosis of the
    pituitary --- this might cause panhypopituitarism,
    a loss of all pituitary hormones.

See Interesting Articles section of Course
Documents in Blackboard.
278
Common Cause of Hypo- or Hyper-Thyroidism
279
Common Cause of Hypo- or Hyper-Thyroidism
  • Hypo- or Hyper- Thyroidism is most often caused
    by problems in the thyroid (primary hypo- or
    hyper- thyroidism)
  • Hypothyroidism is treated by thyroid hormone
    replacement therapy.
  • Hyperthyroidism is treated by ablation (getting
    rid of the thyroid) --- either surgical or with
    radioiodine

280
A patient's TSH is low and his/her T3 and T4 are
high. What is wrong?
281
A patient's TSH is low and his/her T3 and T4 are
high. What is wrong?
  1. Hypothyroidism, pituitary cause
  2. Hyperthyroidism, pituitary cause
  3. Hypothyroidism, thyroid cause
  4. Hyperthyroidism, thyroid cause

282
Thyroid Replacement Therapy
283
Thyroid Replacement Therapy
  • TSH levels are tested about 6 weeks after therapy
    has begun.
  • This must be done because of the lag time
    following the administration of the hormone
  • TSH levels should have fallen to normal. If not,
    the dose is increased and a TSH level obtained 6
    weeks later.
  • Normal TSH levels are under debate. One clinic
    uses 1.3 µU/ml as the target level (Lehne gives
    0.3-6 µU/ml as the normal range).

284
Thyroid Supplementation Drugs
285
Thyroid Supplementation Drugs
Thyroid supplementation drugs Thyroid supplementation drugs
T3 (liothyronine sodium) Cytomel, Triostat
T4 (levothyroxine sodium) Synthroid, Levoxyl, Levothroid, generic
T3 and T4 (liotrix) Thyrolar
T3 and T4 (thyroid extract) Various (rarely prescribed for newly diagnosed pts.)
286
Thyroid Replacement TherapyPreferred Replacement
Drugs
287
Thyroid Replacement TherapyPreferred Replacement
Drugs
  • Pharmacodynamically speaking, all thyroid
    replacement preparations will result in elevation
    of T3 levels and amelioration of the hypothyroid
    state, but there are pharmacokinetic reasons to
    pick one replacement over another.
  • T4 is preferred because of its longer half-life.
  • Blood levels of thyroid hormone are more constant
    with T4 therapy, even if a dose is missed.
  • T4 is converted to T3 in the target cell.

288
Treatment of HyperthyroidismIntroduction
289
Treatment of HyperthyroidismIntroduction
  • Radioiodine, medic
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