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Homeostasis and The Stress Response. Homeostasis. Homeostasis. - PowerPoint PPT Presentation
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Homeostasis and The Stress Response
1
Homeostasis
2
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/Homeostasis
• 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. 3
Stressors
4
Stressors
5
Three Components to Physiologic Stress Response
6
Three Components to Physiologic Stress Response
1. Stressor
2. General adaptationsyndrome
3. Adaptationresponse &return to
homeostasis
7
Neuroendocrine Pathways and Physiologic Responses to Stress
Description
8
Neuroendrocrine Pathways and Physiologic Responses to Stress
Description• 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
9
Neuroendrocrine Pathways and Physiologic Responses to Stress
Diagram
10
Neuroendrocrine Pathways and Physiologic Responses to Stress
11
Adapted from Porth, 2011, Essentials of Pathophysiology,3rd ed., Lippincott, p. 213
(CorticotropinReleasing Factor)
(AdrenocorticotropicHormone)
Activation of the RAAS
Activation of the Sympathetic Nervous System (SNS)
12
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 13
Release of Norepinephrine
14
15
Norepinephrine
Vasoconstrictionof arteries and veins(↑Venous return to the heart/CO and ↑Blood Pressure)
Pupil Dilation
1 2 1
Heart rateContractilityRelease of reninAll of these increase blood pressure
1
Release of Norepinephrine
Epinephrine Released byAdrenal Medulla
16
17
Epinephrine
VasoconstrictionBlood pressureVenous return/CO
Pupil dilation
1
Heart rateContractility Release of renin
1
1 2
Dilation of skeletal muscle vascular beds and bronchi
2
Epinephrine Released byAdrenal Medulla
-Activates alpha 1 and alpha 2 as well as beta 2 receptors
Role of Epinephrine on B2 Receptors
18
19
Epinephrine
Degradation of cholesterol to bile Salts
Free fatty acids that canbe used for ATP synthesis
- maximizes energy production
Cholesterol to be available for the repair of cell membranes
Lipolysis of triglycerides2
2
20
Epinephrine
Liver
Skeletal Muscle
Gluconeogenesis Glycogen Breakdown
Blood Glucose
2
2
Protein breakdown/amino acid release
Norepinephrine stimulates beta-1 receptors to cause
21
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
22
25% 25%25%25%
Release of Renin and ADH (Antidiuretic Hormone)
23
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-aldosterone 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 24
ReninAngiotensin
Aldosterone System (RAAS)Diagram
25
ReninAngiotensin
Aldosterone System (RAAS)
Diagram
26
Must know this!!!
Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 420.
Hypothalamus-Anterior Pituitary FunctionDiagram
27
Hypothalamus-Anterior Pituitary Function
28Porth, 2007, Essential of Pathophysiology, 2nd ed., Lippincott, p. 666
Hypothalamus-Anterior Pituitary Function
Description
29
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
30
Feedback InhibitionDiagram
31
32
Feedback InhibitionDiagram
Porth, Essentials of Pathophysiology, 3rd ed., 2011, Lippincott, p.770.
Peripheral Glands Controlled by the PituitaryDiagram
33
Peripheral Glands Controlled by the Pituitary
34Porth, 2011, Essential of Pathophysiology, 3rd ed., Lippincott, p. 770
Regulation of Cortisol Synthesis and Secretion
Description
35
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
36
Regulation of Cortisol Synthesis and SecretionDiagram
37
Regulation of Cortisol Synthesis and Secretion
38
Lehne, 2009, Pharmacology for Nursing Care, 7th ed., Elsevier, p. 711
Diurnal Secretion of CortisolDiagram
39
Diurnal Secretion of Cortisol
40
When we administer corticosteroids pharmacologically, we try to mimic this diurnal rhythm.
Stewart, Paul, 2003, The adrenal cortex in Larson, et al, eds., Williams’ Textbook of Endocrinology, Saunders.
CortisolPhysiologic Effects
41
CortisolPhysiologic Effects
• Carbohydrate metabolism• Fat metabolism• Protein metabolism• Cardiovascular• Central nervous system• Stress
42
CortisolCarbohydrate Metabolism
43
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!
44
Glucocorts
45
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. 46
CortisolProtein Metabolism
47
CortisolProtein Metabolism
• Promote catabolism
• Amino acids provide substrate for hepatic gluconeogenesis
48
CortisolFat Metabolism
49
CortisolFat Metabolism
• Promote lipolysis– Increases the amount of energy that is available to
the cells
• Free fatty acids provide substrate for the Krebs cycle.
50
CortisolCardiovascular System
51
CortisolCardiovascular System
• Required for the integrity of the blood vessels, including their ability to constrict
52
CortisolCentral Nervous System
53
CortisolCentral Nervous System
• Increases excitation
• Euphoria
• Alertness
54
CortisolStress Response
55
CortisolStress Response
• Stress:– Stress increases CRH secretion by the
hypothalamus• CRH secretion stimulates ACTH (adrenocorticotropic
hormone) secretion, which increases cortisol secretion
56
Effect of Acute Stress
57
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 activated58
Chronic Stress
59
Chronic Stress
• Prolonged activation of the system
• Stage of exhaustion may be reached of the system
• Health problems may result
60
Chronic Activation of the Stress Response May Exacerbate
Diseases
61
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
62
Coping and AdaptationDescription
63
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
64
Coping and AdaptationDiagram
65
Coping and Adaptation
66
Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 216.
Coping
67
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
68
Nursing Care and Stress
69
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
• Today’s 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?
70
Types of EnvironmentsDiagrams
71
This Environment
72
Or this Environment…
73
Nurse’s Role in Dealing with Stress
74
Nurse’s Role in Dealing with Stress
• Nurses can help patients deal with the stress of injury, disease, or psychological stressors
–Augment the patient’s own methods of coping
–Provide the means for adapting to stressors
75
Supportive Care
76
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 77
Non-Pharmacologic Methods
78
Non-Pharmacologic Methods
• Music therapy
• Relaxation techniques
• Guided imagery
• Massage therapy
• Biofeedback
79
Disorders Affecting the Stress Response: Hypothalamic
Pituitary Adrenal Axis
80
Cushing’s SyndromeGlucocorticoid Excess
81
Cushing’s SyndromeCauses
82
Cushing’s SyndromeCauses
• Primary causes
• Secondary causes
83
Cushing’s SyndromePrimary Causes
84
Cushing’s SyndromePrimary Causes
• Hypersecretion of ACTH by pituitary adenomas (benign tumors) (Cushing’s disease)
• Hypersecretion of glucocorticoids by adrenal adenomas and carcinomas
• These are rare– Hardly ever see primary Cushing’s syndrome
85
Cushing’s SyndromeSecondary Causes
86
Cushing’s 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
87
Signs/symptoms of Cushing’s Syndrome
88
Signs/symptoms of Cushing’s 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
89
Cushing’s SyndromeDiagram
90
91
Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 695.
Signs & Symptoms ofCushing’s Syndrome
Treatment for Cushing’s Syndrome
92
Treatment for Cushing’s Syndrome
• Primary Cushing’s 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 Cushing’s syndrome– If glucocorticoid administration is the cause, decrease
the dose as much as possible.
93
Etiology of Adrenal Insufficiency
94
Etiology of Adrenal Insufficiency
• Primary hypoadrenalism
• Secondary hypocortisolism
95
Etiology of Adrenal InsufficiencyPrimary Hypoadrenalism
96
Etiology of Adrenal InsufficiencyPrimary Hypoadrenalism
• Primary hypoadrenalism – Addison’s disease
– Can be contracted via infection, hemorrhage, surgical removal of the adrenal glands
– Glucocorticoid deficiency, and possibly mineralocorticoid (aldosterone) insufficiency
97
Etiology of Adrenal InsufficiencySecondary Hypocorticolism
98
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)
99
Regulation of Cortisol Synthesis and Secretion
Description
100
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
101
Regulation of Cortisol Synthesis and Secretion
Diagram
102
Regulation of Cortisol Synthesis and Secretion
103Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 791.
Signs and Symptoms of Addison’s Disease
104
Signs and Symptoms of Addison’s 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
105
Addisonian Crisis
106
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
107
Treatment of Addisonian Crisis
108
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
109
Normal secretion of cortisol from the adrenal cortex is the
HIGHEST at
110
Normal secretion of cortisol from the adrenal cortex is the HIGHEST at:
1. 8:00 am2. 12 noon3. 4:00 pm4. 12 midnight
111
25% 25%25%25%
Agents for Replacement Therapy in Adrenal Insufficiency:
112
Agents for Replacement Therapy in Adrenal Insufficiency:
•These apply if the person has primary adrenal issues
•Glucocorticoids
•Mineralocorticoids
113
Fludrocortisone (Florinef)
114
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
115
Glucocorticoids
116
Glucocorticoids• Cortisol• Very commonly used
• Physiologic vs. pharmacologic effects– Physiologic = low levels for
replacement in primary Addison’s disease
– Pharmacologic = high levels for immunosuppression (organ transplant) or anti-inflammatory activity.• Pharmacological steroids are
more commonly given in large doses
117Lehne, 2009, Pharmacology for Nursing Care, 7th ed., Elsevier, p. 711
Oral Glucocorticoid Drugs Used to Treat Adrenal Insufficiency
118
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.
119
Hydrocortisone for Adrenal Insufficiency
120
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!
121
High Dose Glucocorticoid Therapy for Non-Endocrine
Disorders
122
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.
123
Anti-inflammatory/Immunosuppressive Effects of
Pharmacologic Doses of Glucocorticoids
124
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
125
Therapeutic Use of Glucocorticoids in Nonendocrine
Disorders
126
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 127
“Local” Administration of Glucocorticoids
128
“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
129
Oral Dosing Guidelines
130
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
toxicity131
Steroid Use for Acute Conditions
132
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
133
Diurnal Secretion of CortisolDiagram
134
Diurnal Secretion of Cortisol
135
When we administer corticosteroids pharmacologically, we try to mimic this diurnal rhythm.
Stewart, Paul, 2003, The adrenal cortex in Larson, et al, eds., Williams’ Textbook of Endocrinology, Saunders.
Adverse Reactions of Pharmacologic Glucocorticoid
Therapy
136
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.
137
Glucocorticoid TherapyEffects on Metabolism
138
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
139
Glucocorticoid TherapyEffects on Bones: Osteoporosis
140
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
141
Osteoporosis
142
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)
143
OsteoporosisPrevention
144
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.
145
Glucocorticoid Effects on Fluid and Electrolytes
146
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).
147
Glucocorticoid Effects on Immune System Infection
148
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
149
Glucocorticoid Treatment and Myopathy
150
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
151
Glucocorticoids and the Development of Cataracts and
Glaucoma
152
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 153
Glucocorticoids and Peptic Ulcer Disease
154
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)
155
Glucocorticoids and Growth Retardation in Children
156
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
157
Glucocorticoids and Psychiatric Side Effects
158
Glucocorticoids and Psychiatric Side Effects
• Most people experience increased alertness, energy, etc.
• Psychosis with hallucinations, mood changes, and other psychological disturbances is unusual.
159
Long Term Corticosteroid Therapy
160
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.
161
Regulation of Cortisol Synthesis and Secretion
Description
162
Regulation of Cortisol Synthesis and Secretion
Description• 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 can’t 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
163
Regulation of Cortisol Synthesis and Secretion
Diagram
164
Regulation of Cortisol Synthesis and Secretion
165
Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 791.
Glucocorticoid Withdrawal
166
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.
167
Strategies for Weaning People off of Glucocorticoids
168
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
169
Adrenal Suppression and Physiologic Stress
170
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
171
Pregnancy and Lactation
172
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.173
Preparations
174
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).
175
Integrative Body Functions II: Alterations in Temperature
Regulation
176
Body Temperature Regulation
177
Body Temperature Regulation
• Core body temp maintained • 36-37.5C (97-99.5 F)
• Individual differences, diurnal variations• Lowest in the morning and then
increases• Maximum body temperature is
around 6pm
178
Normal Diurnal Variations in Body Temperature
Diagram
179
180
Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 65.
Normal Diurnal Variations in Body Temperature
Thermoregulatory Center
181
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 182
Responses to Conserve Heat
183
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
184
Responses to Produce Heat
185
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.
186
Responses to Decrease Heat
187
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.
188
Mechanisms of FeverDescription
189
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
190
Mechanisms of FeverDiagram
191
Mechanisms of Fever
192
Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 68.
Fever Mechanisms
193
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
194
Core Temperatures
195
Core Temperatures
• Greater than 41C (105.8F) or less than 34C (93.2F) indicate the normal thermoregulation is impaired
196
Elevations of Temperature
197
Elevations of Temperature
• Fever (pyrexia)
• Hyperthermia
• Neurogenic fever
198
Elevations of TemperatureFever
199
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 100°F (37.8°C).
200
Elevations of TemperatureHyperthermia
201
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
202
Elevations of TemperatureNeurogenic Fever
203
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
204
Caution Related to Temperature Changes
205
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 elderly206
Purpose of Fever
207
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
208
Patterns of Fever
209
Patterns of Fever
• Intermittent
• Remittent
• Sustained
• Relapsing
210
Patterns of FeverIntermittent
211
Patterns of FeverIntermittent
• Temp returns to normal every 24 hours• Seen in children a lot
212
Patterns of FeverRemittent
213
Patterns of FeverRemittent
• Temp does not return to normal and varies a few degrees in either direction
214
Patterns of FeverSustained
215
Patterns of FeverSustained
• Temp remains above normal with minimal variation.
216
Patterns of FeverRelapsing
217
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
218
Physiologic Behaviors of Fever
219
Physiologic Behaviors of Fever
220
Chill Plateau DefervescenceSetpoint --->
Actual temp->
Time
Pre-dromal
Chill
Flush
Defervescence
RR, HR, Sweating metabolic rate, need for 02, use of body proteins for energy, metabolic acidosis•Headache•Changes in mentation
Treatment of Fever
221
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
222
Anti-pyretics
223
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.
224
Heat Exhaustion
225
Heat Exhaustion
• Heat exhaustion: related to loss of salt and water through the sweat.– Temp between 37.8 and 40°C but not terribly
elevated– May be exhausted, sweating profusely– Treat with cooling, rehydration
226
Heat Stroke
227
Heat Stroke
• Heat stroke: Severe life threatening failure of thermoregulatory mechanisms resulting in an excessive rise in body temp (> 40C, 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.
228
Hypothermia
229
Hypothermia• Core temps less than 35C (93F)– Accidental: Environment– Controlled: Surgery
• Lower the person’s metabolic rate in order to protect themselves
• Those at risk for accidental hypothermia:– Infants, elderly, malnourished,
alcohol/sedatives, hypothyroidism– Hikers, swimmers
230
Manifestations of Hypothermia
231
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). 232
Treatment of Hypothermia
233
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.
234
Which of the following alters the hypothalamic temperature set-
point?
235
Which of the following alters the hypothalamic temperature set-point?
1. Fever2. Hyperthermia3. Hypothermia4. Cortisol
236
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Integrative Functions IIIThyroid
237
Thyroid HormonesDescription
238
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
239
Thyroid HormonesDiagram
240
241Guyton & Hall, Textbook of Medical Physiology, 10th ed., 2000, Saunders, p. 860.
Thyroid HormonesDescription
242
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
243
Thyroid HormonesDiagram
244
245Porth, 2011, Essential of Pathophysiology, 3rd ed., Lippincott, p. 783
Thyroid Hormone ReceptorsDescription
246
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
247
Thyroid Hormone ReceptorsDiagram
248
249
Thyroid Hormone Effects
250
Thyroid Hormone Effects
• Regulates cell breakdown• Stimulates metabolic rate• Growth and development• Cardiovascular system• Gastrointestinal system• Central nervous system
251
Thyroid Hormone EffectsRegulation of Cell Breakdown
252
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.
253
Thyroid Hormone EffectsStimulation of Metabolic Rate
254
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.
255
Thyroid Hormone EffectsCardiovascular System
256
Thyroid Hormone EffectsCardiovascular System
• Thyroid hormone affects the cardiovascular system.
1. Increases blood flow and cardiac output.2. Increases heart rate.3. Increases the cardiac contractility.
257
Thyroid Hormone EffectsGrowth and Development
258
Thyroid Hormone EffectsGrowth and Development
• Thyroid hormone is important in growth and development.
1. Promotes CNS development in utero
2. Stimulates growth hormone secretion and skeletal maturation- Previously women who were hypothyroidic gave
birth to babies who were mentally retarded (cretins)
259
Thyroid Hormone EffectsGI Tract
260
Thyroid Hormone EffectsGI Tract
• Thyroid hormone affects the GI tract.
1. Increases GI motility.2. Increases secretion of digestive juices.
261
Thyroid Hormone EffectsCentral Nervous System
262
Thyroid Hormone EffectsCentral Nervous System
• Thyroid hormone affects the CNS
1. Increases the speed of impulse conduction (can be estimated from deep tendon reflexes).
2. Increases neuronal activity in the CNS.
263
Hypothalamic-Pituitary-Thyroid Feedback
264
Hypothalamic-Pituitary-Thyroid
Feedback
265Porth, 2011, Essential of Pathophysiology, 3rd ed., Lippincott, p. 784
Considerable Lag Time Built into the Thyroid System
266
267Guyton & Hall, Textbook of Medical Physiology, 10th ed., 2000, Saunders, p. 861.
Considerable Lag Time Built into the Thyroid System
Both Hypo- and Hyper- Thyroidism Come on Slowly and Have Vague, Systemic Symptoms
268
Both Hypo- and Hyper- Thyroidism Come on Slowly and Have Vague, Systemic
Symptoms
269
•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.
Screening for Thyroid Disease
270
Screening for Thyroid Disease
271
•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.
Primary Hypo or Hyper Thyroidism
272
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.
273
Secondary Hypo- or Hyper- Thyroidism
274
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
275
Pituitary Cause for Hypo- or Hyper- Thyroidism is Rare
276
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.
277See “Interesting Articles section of “Course Documents” in Blackboard.
Common Cause of Hypo- or Hyper-Thyroidism
278
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
279
A patient's TSH is low and his/her T3 and T4 are high. What
is wrong?
280
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
281 H
ypot
hyro
idis
m...
Hyp
erth
yroid
is...
Hyp
othy
roid
ism
...
Hyp
erth
yroid
is...
25% 25%25%25%
Thyroid Replacement Therapy
282
Thyroid Replacement Therapy
283
•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).
Thyroid Supplementation Drugs
284
Thyroid Supplementation Drugs
285
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.)
Thyroid Replacement TherapyPreferred Replacement Drugs
286
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.
287
Treatment of HyperthyroidismIntroduction
288
Treatment of HyperthyroidismIntroduction
• Radioiodine, medical management, or surgical ablation.
• Either may destroy too much or all of the gland and make the patient hypothyroid.• In this case, thyroid replacement would be given
289
Treatment of HyperthyroidismSurgery
290
Treatment of HyperthyroidismSurgery
• While the patient is waiting for thyroid ablation, they must be given drugs that relieve symptoms.• This is necessary because the person does not do well in
treatment if they are hyperthyroidic
• If surgical ablation is planned, a euthyroid state should be achieved prior to operation to prevent the development of intraoperative thyroid storm.
291
Treatment of HyperthyroidismMedications
292
Treatment of HyperthyroidismMedications
• Beta blockers can be used to block tremulousness, tachycardia, and anxiety.
• Calcium channel blockers can be used to control heart rate.
293
Drug Treatment of Hyperthyroidism
294
Drug Treatment of Hyperthyroidism
295
Drugs that affect the thyroid gland or thyroid hormone.
DrugBlock thyroid hormone synthesis?
Block peripheral conversion of T4
to T3?
Propylthiouracil (PTU)
yes yes
Methimazole yes no
Preferred Drug Treatment of Hyperthyroidism
296
Preferred Drug Treatment of Hyperthyroidism
• Methimazole is usually preferred because of its longer half-life and because PTU sometimes causes very severe liver toxicity.
• In some cases, especially thyroid storm, PTU would be preferred because of its ability to block the conversion of T4 to T3.
297
Which of the following medications blocks peripheral
conversion of T4 to T3?
298
Which of the following medications blocks peripheral conversion of T4 to T3?
1. Propylthiouracil 2. Methimazole 3. Liothyronine sodium 4. Levothyroxine sodium
299
Pro
pylth
ioura
cil
Met
himaz
ole
Lio
thyr
onin
e so
dium
Lev
othyr
oxine
sodi
um
25% 25%25%25%
Thyroid StormThyrotoxic Crisis
300
Thyroid StormThyrotoxic Crisis
• Sudden worsening of hyperthyroidism due to increased release of thyroid hormones.
• Symptoms such as tachycardia, cardiac failure, uncontrolled fever and delirium are of most concern.
• As for hyperthyroidism, treatment consists of agents to block release of thyroid hormone, β-blockers and/or calcium channel blockers to control heart rate, and supportive care.
301
Treatment for Thyroid Storm
302
Treatment for Thyroid Storm
1. Iodide may be given, which impairs release of thyroid hormone from the gland. Iodide is also given preoperatively in surgical ablation to prevent intraoperative thyroid storm.
2. Steroids are commonly given.– (Steroids also inhibit the conversion of T4 to T3)
303