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Homeostasis and The Stress Response

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Page 1: Homeostasis and The Stress Response

Homeostasis and The Stress Response

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Homeostasis

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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

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Stressors

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Stressors

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Three Components to Physiologic Stress Response

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Three Components to Physiologic Stress Response

1. Stressor

2. General adaptationsyndrome

3. Adaptationresponse &return to

homeostasis

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Neuroendocrine Pathways and Physiologic Responses to Stress

Description

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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

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Neuroendrocrine Pathways and Physiologic Responses to Stress

Diagram

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Neuroendrocrine Pathways and Physiologic Responses to Stress

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Adapted from Porth, 2011, Essentials of Pathophysiology,3rd ed., Lippincott, p. 213

(CorticotropinReleasing Factor)

(AdrenocorticotropicHormone)

Activation of the RAAS

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Activation of the Sympathetic Nervous System (SNS)

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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

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Release of Norepinephrine

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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

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Epinephrine Released byAdrenal Medulla

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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

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Role of Epinephrine on B2 Receptors

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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

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Epinephrine

Liver

Skeletal Muscle

Gluconeogenesis Glycogen Breakdown

Blood Glucose

2

2

Protein breakdown/amino acid release

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Norepinephrine stimulates beta-1 receptors to cause

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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

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25% 25%25%25%

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Release of Renin and ADH (Antidiuretic Hormone)

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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

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ReninAngiotensin

Aldosterone System (RAAS)Diagram

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ReninAngiotensin

Aldosterone System (RAAS)

Diagram

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Must know this!!!

Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 420.

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Hypothalamus-Anterior Pituitary FunctionDiagram

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Hypothalamus-Anterior Pituitary Function

28Porth, 2007, Essential of Pathophysiology, 2nd ed., Lippincott, p. 666

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Hypothalamus-Anterior Pituitary Function

Description

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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

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Feedback InhibitionDiagram

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Feedback InhibitionDiagram

Porth, Essentials of Pathophysiology, 3rd ed., 2011, Lippincott, p.770.

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Peripheral Glands Controlled by the PituitaryDiagram

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Peripheral Glands Controlled by the Pituitary

34Porth, 2011, Essential of Pathophysiology, 3rd ed., Lippincott, p. 770

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Regulation of Cortisol Synthesis and Secretion

Description

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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

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Regulation of Cortisol Synthesis and SecretionDiagram

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Regulation of Cortisol Synthesis and Secretion

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Lehne, 2009, Pharmacology for Nursing Care, 7th ed., Elsevier, p. 711

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Diurnal Secretion of CortisolDiagram

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Diurnal Secretion of Cortisol

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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.

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CortisolPhysiologic Effects

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CortisolPhysiologic Effects

• Carbohydrate metabolism• Fat metabolism• Protein metabolism• Cardiovascular• Central nervous system• Stress

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CortisolCarbohydrate Metabolism

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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!

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Glucocorts

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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

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CortisolProtein Metabolism

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CortisolProtein Metabolism

• Promote catabolism

• Amino acids provide substrate for hepatic gluconeogenesis

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CortisolFat Metabolism

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CortisolFat Metabolism

• Promote lipolysis– Increases the amount of energy that is available to

the cells

• Free fatty acids provide substrate for the Krebs cycle.

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CortisolCardiovascular System

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CortisolCardiovascular System

• Required for the integrity of the blood vessels, including their ability to constrict

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CortisolCentral Nervous System

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CortisolCentral Nervous System

• Increases excitation

• Euphoria

• Alertness

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CortisolStress Response

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CortisolStress Response

• Stress:– Stress increases CRH secretion by the

hypothalamus• CRH secretion stimulates ACTH (adrenocorticotropic

hormone) secretion, which increases cortisol secretion

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Effect of Acute Stress

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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

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Chronic Stress

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Chronic Stress

• Prolonged activation of the system

• Stage of exhaustion may be reached of the system

• Health problems may result

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Chronic Activation of the Stress Response May Exacerbate

Diseases

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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

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Coping and AdaptationDescription

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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

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Coping and AdaptationDiagram

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Coping and Adaptation

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Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 216.

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Coping

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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

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Nursing Care and Stress

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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?

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Types of EnvironmentsDiagrams

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This Environment

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Or this Environment…

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Nurse’s Role in Dealing with Stress

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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

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Supportive Care

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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

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Non-Pharmacologic Methods

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Non-Pharmacologic Methods

• Music therapy

• Relaxation techniques

• Guided imagery

• Massage therapy

• Biofeedback

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Disorders Affecting the Stress Response: Hypothalamic

Pituitary Adrenal Axis

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Cushing’s SyndromeGlucocorticoid Excess

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Cushing’s SyndromeCauses

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Cushing’s SyndromeCauses

• Primary causes

• Secondary causes

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Cushing’s SyndromePrimary Causes

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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

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Cushing’s SyndromeSecondary Causes

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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

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Signs/symptoms of Cushing’s Syndrome

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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

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Cushing’s SyndromeDiagram

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Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 695.

Signs & Symptoms ofCushing’s Syndrome

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Treatment for Cushing’s Syndrome

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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.

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Etiology of Adrenal Insufficiency

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Etiology of Adrenal Insufficiency

• Primary hypoadrenalism

• Secondary hypocortisolism

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Etiology of Adrenal InsufficiencyPrimary Hypoadrenalism

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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

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Etiology of Adrenal InsufficiencySecondary Hypocorticolism

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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)

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Regulation of Cortisol Synthesis and Secretion

Description

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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

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Regulation of Cortisol Synthesis and Secretion

Diagram

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Regulation of Cortisol Synthesis and Secretion

103Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 791.

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Signs and Symptoms of Addison’s Disease

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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

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Addisonian Crisis

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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

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Treatment of Addisonian Crisis

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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

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Normal secretion of cortisol from the adrenal cortex is the

HIGHEST at

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Normal secretion of cortisol from the adrenal cortex is the HIGHEST at:

1. 8:00 am2. 12 noon3. 4:00 pm4. 12 midnight

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Agents for Replacement Therapy in Adrenal Insufficiency:

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Agents for Replacement Therapy in Adrenal Insufficiency:

•These apply if the person has primary adrenal issues

•Glucocorticoids

•Mineralocorticoids

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Fludrocortisone (Florinef)

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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

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Glucocorticoids

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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

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Oral Glucocorticoid Drugs Used to Treat Adrenal Insufficiency

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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.

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Hydrocortisone for Adrenal Insufficiency

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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!

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High Dose Glucocorticoid Therapy for Non-Endocrine

Disorders

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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.

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Anti-inflammatory/Immunosuppressive Effects of

Pharmacologic Doses of Glucocorticoids

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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

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Therapeutic Use of Glucocorticoids in Nonendocrine

Disorders

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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

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“Local” Administration of Glucocorticoids

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“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

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Oral Dosing Guidelines

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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

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Steroid Use for Acute Conditions

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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

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Diurnal Secretion of CortisolDiagram

134

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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.

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Adverse Reactions of Pharmacologic Glucocorticoid

Therapy

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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.

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Glucocorticoid TherapyEffects on Metabolism

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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

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Glucocorticoid TherapyEffects on Bones: Osteoporosis

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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

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Osteoporosis

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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)

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OsteoporosisPrevention

144

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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

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Glucocorticoid Effects on Fluid and Electrolytes

146

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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

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Glucocorticoid Effects on Immune System Infection

148

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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

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Glucocorticoid Treatment and Myopathy

150

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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

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Glucocorticoids and the Development of Cataracts and

Glaucoma

152

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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

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Glucocorticoids and Peptic Ulcer Disease

154

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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

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Glucocorticoids and Growth Retardation in Children

156

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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

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Glucocorticoids and Psychiatric Side Effects

158

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Glucocorticoids and Psychiatric Side Effects

• Most people experience increased alertness, energy, etc.

• Psychosis with hallucinations, mood changes, and other psychological disturbances is unusual.

159

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Long Term Corticosteroid Therapy

160

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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

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Regulation of Cortisol Synthesis and Secretion

Description

162

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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

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Regulation of Cortisol Synthesis and Secretion

Diagram

164

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Regulation of Cortisol Synthesis and Secretion

165

Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 791.

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Glucocorticoid Withdrawal

166

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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

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Strategies for Weaning People off of Glucocorticoids

168

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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

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Adrenal Suppression and Physiologic Stress

170

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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

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Pregnancy and Lactation

172

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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

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Preparations

174

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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

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Integrative Body Functions II: Alterations in Temperature

Regulation

176

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Body Temperature Regulation

177

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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

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Normal Diurnal Variations in Body Temperature

Diagram

179

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180

Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 65.

Normal Diurnal Variations in Body Temperature

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Thermoregulatory Center

181

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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

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Responses to Conserve Heat

183

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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

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Responses to Produce Heat

185

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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

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Responses to Decrease Heat

187

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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

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Mechanisms of FeverDescription

189

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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

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Mechanisms of FeverDiagram

191

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Mechanisms of Fever

192

Porth, 2011, Essentials of Pathophysiology, 3rd ed., Lippincott, p. 68.

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Fever Mechanisms

193

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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

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Core Temperatures

195

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Core Temperatures

• Greater than 41C (105.8F) or less than 34C (93.2F) indicate the normal thermoregulation is impaired

196

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Elevations of Temperature

197

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Elevations of Temperature

• Fever (pyrexia)

• Hyperthermia

• Neurogenic fever

198

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Elevations of TemperatureFever

199

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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

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Elevations of TemperatureHyperthermia

201

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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

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Elevations of TemperatureNeurogenic Fever

203

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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

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Caution Related to Temperature Changes

205

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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

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Purpose of Fever

207

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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

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Patterns of Fever

209

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Patterns of Fever

• Intermittent

• Remittent

• Sustained

• Relapsing

210

Page 211: Homeostasis and The Stress Response

Patterns of FeverIntermittent

211

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Patterns of FeverIntermittent

• Temp returns to normal every 24 hours• Seen in children a lot

212

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Patterns of FeverRemittent

213

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Patterns of FeverRemittent

• Temp does not return to normal and varies a few degrees in either direction

214

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Patterns of FeverSustained

215

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Patterns of FeverSustained

• Temp remains above normal with minimal variation.

216

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Patterns of FeverRelapsing

217

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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

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Physiologic Behaviors of Fever

219

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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

Page 221: Homeostasis and The Stress Response

Treatment of Fever

221

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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

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Anti-pyretics

223

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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

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Heat Exhaustion

225

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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

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Heat Stroke

227

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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

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Hypothermia

229

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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

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Manifestations of Hypothermia

231

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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

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Treatment of Hypothermia

233

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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

Page 235: Homeostasis and The Stress Response

Which of the following alters the hypothalamic temperature set-

point?

235

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Which of the following alters the hypothalamic temperature set-point?

1. Fever2. Hyperthermia3. Hypothermia4. Cortisol

236

25% 25%25%25%

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Integrative Functions IIIThyroid

237

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Thyroid HormonesDescription

238

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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

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Thyroid HormonesDiagram

240

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241Guyton & Hall, Textbook of Medical Physiology, 10th ed., 2000, Saunders, p. 860.

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Thyroid HormonesDescription

242

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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

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Thyroid HormonesDiagram

244

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245Porth, 2011, Essential of Pathophysiology, 3rd ed., Lippincott, p. 783

Page 246: Homeostasis and The Stress Response

Thyroid Hormone ReceptorsDescription

246

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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

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Thyroid Hormone ReceptorsDiagram

248

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249

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Thyroid Hormone Effects

250

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Thyroid Hormone Effects

• Regulates cell breakdown• Stimulates metabolic rate• Growth and development• Cardiovascular system• Gastrointestinal system• Central nervous system

251

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Thyroid Hormone EffectsRegulation of Cell Breakdown

252

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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

Page 254: Homeostasis and The Stress Response

Thyroid Hormone EffectsStimulation of Metabolic Rate

254

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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

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Thyroid Hormone EffectsCardiovascular System

256

Page 257: Homeostasis and The Stress Response

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

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Thyroid Hormone EffectsGrowth and Development

258

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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

Page 260: Homeostasis and The Stress Response

Thyroid Hormone EffectsGI Tract

260

Page 261: Homeostasis and The Stress Response

Thyroid Hormone EffectsGI Tract

• Thyroid hormone affects the GI tract.

1. Increases GI motility.2. Increases secretion of digestive juices.

261

Page 262: Homeostasis and The Stress Response

Thyroid Hormone EffectsCentral Nervous System

262

Page 263: Homeostasis and The Stress Response

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

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Hypothalamic-Pituitary-Thyroid Feedback

264

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Hypothalamic-Pituitary-Thyroid

Feedback

265Porth, 2011, Essential of Pathophysiology, 3rd ed., Lippincott, p. 784

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Considerable Lag Time Built into the Thyroid System

266

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267Guyton & Hall, Textbook of Medical Physiology, 10th ed., 2000, Saunders, p. 861.

Considerable Lag Time Built into the Thyroid System

Page 268: Homeostasis and The Stress Response

Both Hypo- and Hyper- Thyroidism Come on Slowly and Have Vague, Systemic Symptoms

268

Page 269: Homeostasis and The Stress Response

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.

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Screening for Thyroid Disease

270

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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.

Page 272: Homeostasis and The Stress Response

Primary Hypo or Hyper Thyroidism

272

Page 273: Homeostasis and The Stress Response

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

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Secondary Hypo- or Hyper- Thyroidism

274

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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

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Pituitary Cause for Hypo- or Hyper- Thyroidism is Rare

276

Page 277: Homeostasis and The Stress Response

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.

Page 278: Homeostasis and The Stress Response

Common Cause of Hypo- or Hyper-Thyroidism

278

Page 279: Homeostasis and The Stress Response

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

Page 280: Homeostasis and The Stress Response

A patient's TSH is low and his/her T3 and T4 are high. What

is wrong?

280

Page 281: Homeostasis and The Stress Response

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

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yroid

is...

Hyp

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roid

ism

...

Hyp

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yroid

is...

25% 25%25%25%

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Thyroid Replacement Therapy

282

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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).

Page 284: Homeostasis and The Stress Response

Thyroid Supplementation Drugs

284

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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.)

Page 286: Homeostasis and The Stress Response

Thyroid Replacement TherapyPreferred Replacement Drugs

286

Page 287: Homeostasis and The Stress Response

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

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Treatment of HyperthyroidismIntroduction

288

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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

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Treatment of HyperthyroidismSurgery

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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.

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Treatment of HyperthyroidismMedications

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Treatment of HyperthyroidismMedications

• Beta blockers can be used to block tremulousness, tachycardia, and anxiety.

• Calcium channel blockers can be used to control heart rate.

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Drug Treatment of Hyperthyroidism

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Drug Treatment of Hyperthyroidism

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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

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Preferred Drug Treatment of Hyperthyroidism

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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.

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Which of the following medications blocks peripheral

conversion of T4 to T3?

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Which of the following medications blocks peripheral conversion of T4 to T3?

1. Propylthiouracil 2. Methimazole 3. Liothyronine sodium 4. Levothyroxine sodium

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Pro

pylth

ioura

cil

Met

himaz

ole

Lio

thyr

onin

e so

dium

Lev

othyr

oxine

sodi

um

25% 25%25%25%

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Thyroid StormThyrotoxic Crisis

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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.

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Treatment for Thyroid Storm

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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)

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