Chapter 7 (Stress/Adaptation)
Stress Response
Physiological and Psychological Responses to Stress
Effects of Hormones and Receptors
Non-Pharmacological Stress Relief Methods
- Debriefing
- Counseling
- Relaxation
- Massage
- Music Therapy
- Biofeedback
- Imagery
- Personal Preferences
Chapter 14 (Thermoregulation)
Need to Know:
- Core Body Temperature is
oReflection of the balance between heat gain and heat loss by the body
- The hypothalamus is the thermal control center
oHypothalamus is the “master regulator”
Regulates everything
oReceives information from peripheral and central thermoreceptors and compares
it with its temperature point
o
Methods of Heat Loss
- Radiation
oTransfer of heat through air or vacuum
oExternal temp has to be less than that of body to occur
- Conduction
oDirect transfer (Touch)
- Convection
oCirculation of air currents
oContinual removal of layer of warm air surrounding body
- Evaporation
oSweat glands
oUse of body heat to convert water on skin (sweat) to water vapor
oWater which diffuses independent of sweating is called
oInsensible perspiration
Methods of Heat Retention
- Vasoconstriction and Shivering
- Positions (Huddling)
Fever Patterns
- Intermittent
oTemp returns to normal at least once every 24 hours
oCome and go fever
- Remittent
oTemp never returns to normal
oVaries in either direction
oLong-term
- Sustained/Continuous
oTemp remains above normal with minimal variation (Despite medications)
- Recurrent/Relapsing
oOne or more episodes of fever as long as several days with one or more days of
normal temp between fever episodes
oFever, No fever for a day, Fever
Physiologic Behaviors of Fever
- Prodrome
oMild headache, fatigue, malaise, fleeting pain (feeling eh when coming down
from fever)
- Chill
oUncomfortable sensation of being chilled, shaking
Feeling colder than they should be
- Flush
oCutaneous vasodilation, skin warm and flush
Sweating
- Defervescence
oInitiation of sweating
Chapter 40/41 (Hormones)
Function of Anti-Diuretic Hormone (ADH/Vasopressin)
-Conserve Fluid Volume of the Body
oRetains water and sodium to be used elsewhere when the body is in shortage
-Path of ADH
oSynthesized in Hypothalamus
oStored in PPG
oReleased into blood stream and eventually reaches kidneys
oIncreases water and sodium retention
This increases BP (Holding all fluid in, distends kidney and blood vessels)
-Regulation of ADH (Peeing)
oDrops BP
Release of Pressure
oPlasma Osmolality
Brings electrolyte-water balance back
oVomiting
Release of Pressure
Physical effects of hypersecretion of adrenal medulla
-Adrenal Medulla secretes Nor-Epi and Epi
oWill cause a prolonged SNS response to stress
How do mineralcorticoids on maintaining BP
-The mineralcorticoid aldosterone, will activate the Na+/K+ pump
oThe pump will bring in Na+ and excrete K+
oNa+ will always bring in water with it
-The pump will cause Na+ and water retention in the blood streams that supply the kidney
-It will increase blood volume, which will raise the BP
Hormones which raise blood glucose
-Epinephrine
-Cortisol
-Growth Hormone
-Glucagon
Hypo and Hyper Thyroidism on Systems in the Body
-Hypothyroidism
oCardiac
Decreased Cardiac Output
Low BP
Bradycardia
Cardiac Collapse (Myxedematous Coma)
Hypothermia
Blood PH is thrown due to CO2
Cardiomegaly (Myxedematous Coma)
oDigestive
Low Metabolism
Decreased Appetite
Weight Gain
Constipation
Gastric Atrophy
oRespiratory
Low RR
Hypoventilation
Hypoxia
oPsych
Mental Sluggishness and Fatigue
Somnolence
Impaired Memory
oRenal
Fluid and Electrolyte Imbalance (Myxedematous Coma
oIntegumetary
Coarse Dry Skin and Hair
Peripheral Edema
Puffy Face
Periorbital edema
Cold intolerance
oReproductive
Menorrhea (Anovulatory Cycles)
-Hyperthyroidism
oCardio
Increased Cardiac Output
Tachycardia & Palpations
Heart Failure (Thyroid Storm)
Very High Fever (Thyroid Storm)
oPsych
Restlessness, Irritability, Anxiety, Wakefulness
Delirium
oDigestive
Weight Loss
Diarrhea
Increased Appetite
Increased Metabolism
oRespiratory
Dyspnea
oIntegumentary
Thin and silky hair and skin
Heat intolerance
Increased Sweating
Exophthalmos
oReproductive
Oligomenorrhea
Hypersecretion of APG (Disorders)
-Cushing’s (Excess ACTH leading to excess glucocorticoid from adrenal cortex)
oALL INFO UNDER CUSHING’S SYNDROME
-Hyperthyroidism (Excess TSH leading to excess thyroid function/hormone)
oCauses
Grave’s Disease
Multinodular Goiter
Adenoma of Thyroid
Ingestion of Excessive Hormone
oSigns/Symptoms
Increased Metabolic Rate, Hunger, Diarrhea
Weight Loss
Tachycardia and Excess cardiac output
Intolerance to Heat
Increased Sweating
Thin and silky hair and skin
Restlessness, Anxiety, Irritability
Exophthalmos (Eyes pop out)
oConditions caused by hyperthyroidism
Thyroidtoxicosis
Thyroid Storm
oTreatment
Reduce thyroid level
Eradication of thyroid gland
Antithyroid drugs
Beta adrenergic blocking drugs
Reduce effects of SNS (Slow HR and Lower BP)
-Excessive GH
oExcessive GH in Children
Rare Condition
Signs/Symptoms
Gigantism (Increased Linear Bone Growth)
Excess Skeletal Growth (Epiphyses not Fused Yet)
Treatment
Often related to adenoma of pituitary, treated prior to a disorder
developing
Medications octreotide and pegvisomant
oExcessive GH in Adults
Adenoma of pituitary of hypothalamic
Signs/Symptoms
Overgrowth of cartilaginous parts of the skeleton
Enlargement of heart and other parts of body
Metabolic disturbances (Altered fat metabolism and impaired
glucose tolerance)
Excess soft tissue
Enlarged Respiratory tract
Insulin resistance
Acromegaly (40-45 y/o)
Treatment
Remover Tumor, correct metabolic disorder
Medications to inhibit GH secretion
oAcromegaly
Caused by somatotroph tumor adenoma 95%
Other causes (<5%):
Excess secretion of GHRH by hypothalamic tumors
Ectopic GHRH secretion by non-endocrine tumors such as
carcinoid tumors or small cell lung cancers
Ectopic secretion of GH by non-endocrine tumors
Signs and Symptoms
Thickened calvana (Head/Skull)
Somatotrophic adenoma on pituitary
Goiter
Hyperostosis of thoracic vertebrae
Cardiomegaly (Hypertension)
Barrell Chest
Abdominal glucose intolerance and insulin intolerance
Increased hands and feet size
Degenerative Arthritis
Peripheral Neuropathy
Thickened Skin (Hypertrophy of sebaceous and sweat glands)
Large tongue
Swelling of esophagus
Treatment Goals
Normalize GH response to oral glucose load
Normalize IGF-1 Levels to age and sex-matched control levels
Removal/Reduction of tumor/mass
Relieving central pressure effects
Improvement of adverse clinical features
Normalize mortality rate
Big 3 Treatment
Remove tumor
Treat symptoms
Get GH level down
-Hyperprolactinemia
oIn women
Amenorrhea
Galactorrhea: Excessive milk production
oIn Men
Decreased Sex Drive
Decreased Sperm Count
Often Breast Enlargement (Gynecomastia)
Rare to produce milk
Hyposecretion of APG (Disorders)
-Second Adrenal Insufficiency (Lack of ACTH)
oSame signs and symptoms as Primary Adrenal Insufficiency
oMonitor and Replace Glucocorticoids to treat
-Secondary Hypothyroidism (Lack of TSH)
oSame signs and symptoms of Primary Hypothyroidism
oSame treatment of normal hypothyroidism
-GH Deficiency
oGH Deficiency in Children
Caused by lack of GH
Caused by lack of GHRH, Pituitary tumor, Larontype dwarfism
Signs/Symptoms
Normal intelligence
Short Stature (Interferes with linear bone growth)
Obesity due to delay of skeletal maturation (May caused bowed
legs)
Delayed Puberty
Treated By
GH Replacement
If Larontype Dwarfism (IGF-1 Replacement)
oGH Deficiency in Adults
Caused by Lack of GH as a Child, or Lack of GH as an Adult
(Hypopituitarism)
Sings/Symptoms
Increase Body Fat
Insulin Resistance
Dyslipidemia
Treated by GH Replacement
-FSH and LH Deficiency
oDeficiency in Release of Sex Hormones in the Gonads
-Prolactin Deficiency
oMoms Can’t make milk
Hormones Secreted by PPG and APG
-Hormones which trigger APG Release/Inhibition
oCorticotropin Releasing Hormone or Factor (CRH/CRF)
Stimulates release of ACTH
oThyrotropin Releasing Hormone (TRH)
Stimulates Release of TSH
oGrowth Hormone Releasing Hormone (GHRH)
Stimulates release of GH
oSomatostatin
Inhibits release of GH
oGonadotropin Releasing Hormone (GnRH)
Stimulates release of FSH
Stimulates release of LH
Stimulates release of Prolactin
-Hormones APG Releases
oAdrenocorticotropic Hormone (ACTH)
Acts on Adrenal Cortex
Release of Glucocorticoid (Cortisol)
Release of Mineralcorticoid (Aldosterone)
Release of Adrenal Sex organs (Androgens)
oThyroid Stimulating Hormone (TSH)
Acts on Thyroid
Stimulates secretion of thyroid hormones
oGrowth Hormone (GH)
Acts on Liver and Adipose tissue
Promotes growth indirectly
Control of protein, lipid, carbs metabolism
oFollicle Stimulating Hormone (FSH)
Acts on Ovary and Testis
Controls reproductive function
oLuteinizing Hormone (LH)
Acts on Ovary and Testis
Controls reproductive function
oProlactin
Acts on Mammary Gland
Milk production
-Hormones which trigger PPG Release
oOxytocin
oAntidiuretic Hormone (ADH)
-Hormones PPG Releases
oOxytocin
Stimulates milk ejection and uterine contractions
oADH
Conserves body water
Myxedema
-Presence of Non-pitting Edema (Swelling that does not indent with applied pressure)
Caused by:
-Primary
oDestruction of the thyroid gland
oThyroidectomy
oDeficiency in Iodine : Can Lead to goiter
oMedications or Large amounts of Iodine can cause original hypothyroidism which
can lead to myxedema
-Secondary
oImpaired pituitary function
-Tertiary
oImpaired hypothalamic function
Myxedema Coma
-Caused by progressed hypothyroidism
oLife-Threatening End Stage Coma
Signs and Symptoms
-Cardiovascular Collapse (Slow BP)
-Hypoventilation (Low RR 12-20 BPM)
-Metabolic Disorders
oHyponatremia, Hypoglycemia, Lactic Acidosis
3 Big Factors
-Carbon Dioxide Retention (Hypoxia)
oDue to Hypoventilation
oLow Blood Platelet
-Fluid and Electrolyte Imbalances
-Hypothermia (Common in elderly women)
Treatment
-Monitor High Risk Populations
oWomen with high risk of Hashimoto’s Disease
-Cardiovascular and Respiratory Support
-Fix the Hypothermia
-Fix hyponatremia and hypoglycemia
-Monitor physical condition, VS
-Fix thyroid imbalance
Thyroid Storm
-Hyperthyroid/Thyrotoxic Crisis
oLife-Threatening form of Thyrotoxicosis
oVERY HIGH MORTALITY RATE
-Undiagnosed/Untreated Hyperthyroidism
Signs/Symptoms
-Very High Fever (108 and above)
-Tachycardia
-Heart failure
-Restlessness and delirium
-Excessive sweating
oWill dehydrate from sweating and die
Treatments
-Cooling blanket to decrease body temp
-Replace fluids, glucose, and electrolytes
-B-adrenergic blocking drugs
-Glucocorticoids to replace loss due to increased metabolic rate
-DO NOT USE ASPRIN
oSame protein which carries aspirin also carries thyroid T-4
oOnly makes it worse
Diagnostic Tests and Treatments for Endocrine Disorders
-Blood Tests
oBlood Glucose or Insulin Levels
oHormone Levels in Plasma
-Urine Tests
oUrinary Hormone
oHormone metabolic excretion
o24-Hour urine Sample
oUrinary Cortisol Levels
-Hormone Stimulation and Suppression Tests
-Genetic Testing
oSpecific Genetic Pathophysiologic Markers
-Diagnostic Imaging
oNon-Isotopic
MRI
CT
DEXA
Ultrasonography
oIsotopic (Administering a Radioisotope
PET
PET/CT
Post-Op Concerns of Thyroidectomy
-Primary deficiency of thyroid hormones
-Acquired hypothyroidism
-Hypometabolic Rate
-Myxedema (non-pitting edema (No indent with applied pressure))
-Low amounts of Iodine: Can lead to formation of a goiter (Major Following Surgical)
-Thyroid Storm (Very unlikely)
-No TH
Physical Signs, Decrease in
-Metabolic Rate
-Bradycardia, Low BP
-Breathing/Respiratory Rate
Physical Signs, Observable
-Mental Sluggishness
-Weight Gain
-Cold intolerance
-Coarse/Dry Skin
-Coarse/Brittle Hair
-Constipation (Hypoactive GI Tract)
Role of ACTH
-Stimulate and regulate the secretion of hormones from the adrenal gland
oAdrenal Cortex
Corticoids and Androgens
Salt, Sugar, Sex
oAdrenal Medulla
Nor-Epi + Epi
Stress response and regulation
Parathyroid Hormone
-What does it do?
oRegulates Blood Calcium
Controls Bone Formation
-Signs and Symptoms of Hypoparathyroidism
oCalcium levels in serum drop
Tetany (Spasms) and Seizures
-Signs and Symptoms of Hyperparathyroidism
oCalcium levels in serum rise
Cardiac arrythmias
Muscle and bone weakness
All calcium is in the kidneys (Next bullet)
Renal Calculi (Kidney Stones)
Hypersecretion of Adrenal Cortex
-Hypersecretion of Mineralcorticoids (Aldosterone)
oHypernatremia which will lead to hypokalemia
-Hypersecretion of Glucocorticoids (Cortisol)
oCushing’s Syndrome
-Hypersecretion of Androgens (DHEA)
oIncreases Testosterone and DHT
What can occur in the body post adrenalectomy?
-Low BP
-Fatigue
-Elevation of Serum Potassium Levels
-Hormone Imbalance
-Infections
-Increased Stress Levels
-Excessive Cortisol Levels
SIADH
-What is it?
oFailure of negative feedback system that regulates the release and inhibition of
ADH (AKA Hypersecretion of ADH)
Very Diminished Urine Output
oCaused By:
Neoplasms (Abnormal growths of tissue somewhere, for SIADH often
cancer of pancreas, prostate)
Positive Pressure Ventilation (activation of baroreceptors which change in
response to intrathoracic pressure)
Disease/Injury to CNS (Meningitis, Encephalitis)
Excessive stress, surgery
Pain (produces and releases ADH independently of control mechanisms
High temp change
oTransient during stressful conditions, chronic with lung or brain tumors
-Effects on Serum and Urine Osmolality
oVery high urine osmolality (Low volume/High Concentration)
oVery low serum osmolality (High Volume/Low Concentration)
oSupposed to be even levels of volume and concentration
oOpposite Levels of Diabetes Insipidus Osmolality’s
-Signs/Symptoms (Diagnosis is only considered with all 5 Cardinal Features)
oHypotonic Hyponatremia (low sodium in the blood)
oNatriuresis (Urine is exceptionally saturated with sodium/very, very salty)
oUrine osmolality higher than serum osmolality
oAbsence of swelling AND Volume Depletion of Urine
oNormal Renal, Adrenal, Thyroid function
-Priority Nursing
oSTOP DRINKING (Could Drown Themselves)
#1 treatment
oDiuretics
Mannitol pulls liquid out of tissues
Lasix promotes free water clearance
oIn severe water intoxication
Hypertonic solution used with 3% NaCl to fly sodium levels
Cushing’s Syndrome and Addison’s Disease
Cushing’s Syndrome
-Refers to Hypercortisolism from any cause
oExcess glucocorticoid hormone (Cortisol is a glucocorticoid)
-3 Forms/Causes of Cushing’s Syndrome
oPituitary Form (Original Cushing’s Syndrome, Pituitary form is called Cushing’s
Disease)
Excess ACTH by a tumor on Pituitary Gland
ACTH Activates Adrenal Cortex (Which secretes cortisol)
oAdrenal Form
Adrenal Tumor (Benign or Malignant) causes excess of cortisol to secrete
oEctopic
Non-Pituitary ACTH Secreting Tumor
-Signs/Symptoms
oMoon Face & Buffalo Hump
Due to exaggerated effects of cortisol
oAltered fat metabolism (Cortisol causes lipolysis)
oAltered glucose metabolism
oIncreased facial hair
oThinning scalp hair
-Appearance
oEmotional disturbance
oEnlarged Sella Turcica
oMoon facies
oOsteoporosis
oHypertension (Cardiac)
oObesity
oHyperplasia of Adrenal Cortex
oThin, wrinkled skin
oAbdominal Striae
oAmenorrhea
oMuscle weakness
oPurpura
oPoor wound healing (Skin ulcers)
-How to Diagnose
o24-hour excretion of cortisol in the urine (Measure)
oBlood test to take ACTH Levels
oMRI/CT of head to look for tumor causing excess ACTH
-Treatment/Nursing Considerations
oRadiation or Removal of Tumor
oMedication to block steroid synthesis
oFor immune suppression, give pneumocystis prophylaxis
Hypercortisolism causes excess of glucose which causes suppression of
immune system
oMonitor Vital Signs as well as fluid & electrolyte levels/values, physical findings
Fluid & Electrolyte levels out of whack could bring other diseases that
would kill them before Cushing’s
Addison’s Disease
-Common destructive autoimmune disorder (Chronic)
-Caused by a decrease in available cortical hormones
oCauses elevation in ACTH due to lack of feedback from cortical hormones to
inhibit it
-Signs/Symptoms
oAnorexia, weight loss, fatigue, nausea, diarrhea, arthralgia, abdominal pain,
hyperkalemia, hyponatremia
Hyperkalemia and Hyponatremia causes extreme muscular deficit/atrophy
No sodium potassium concentration gradient
oDeficiency of Mineralcorticoids caused by elevated ACTH
Increased urinary loss of sodium, chloride, and water
Appetite for SALT
Hypoglycemia
Cortisol low=Glucose low
oLose No-Ep, Epi, Mineralcorticoids (Lose the 3 S’s)
Affects Stress Response (Can’t Deal with It)
Missing cortisol (Can’t fight nor produce cells)
Lack fluid=Drop in BP
-Treatment/Nursing Considerations
oH&P
oOral hormone replacement therapy
Higher doses given periods of stress
Should have both glucocorticoid and mineralcorticoid activities
Replace Glucose and Sodium and Monitor Electrolytes
oRegular Schedule of Meals and Exercise
oMonitor Stressors and Infections
oMedic Alert Bracelet
-Prolonged Addison’s Disease
oCaused by illness, stress, adrenal hemorrhage
oLose the ability to deal w stress
oAcute Adrenal Crisis (Life-Threatening Insufficiency of Cortisol)
oSigns/Symptoms
Weakness, Hypotension (Lack of Mineralcorticoid), Dehydration (More
evidence of tenting)
Vascular collapse due to significant dehydration
oTreatment
5 S’s:
Replacement of Salt, Sugar, Steroid
Support of Physiologic Function
Search for and treat any underlying conditions
Monitor Vital Signs, Electrolyte Values, and Physical Condition
Stimulation of Anti-Diuretic Hormone (ADH)
-Decrease in blood volume which decreases blood pressure which increases blood
osmolarity
oCaused by a deficiency in water and sodium
Relationship between hyposecretion of the adrenal cortex on serum sodium
-Primary Adrenal Insufficiency (Addison’s Disease)
-Hyposecretion of adrenal cortex (Adrenal deficiency) causes deficiency in sodium
oDeficiency in sodium is Hyponatremia
Causes extreme muscular deficit
Effect of Glucocorticoids on Blood Glucose
-Stimulates glucose production by
oLiver
-Promotes protein breakdown
oAmino acids mobilized and transported to liver and used in glucose production
-Mobilizes Fatty Acids
oCoverts cell metabolism to use fatty acids instead of glucose for energy
-Basically raises glucose level because usage is going down and production is going up
oAlso causes a moderate insulin resistance
Normal Blood Glucose Range
-70 to 110 mg/dL
