Download The Thyroid: Too Much, Too Little and Under the Weather

The Thyroid: Too Much, Too
Little and Under the Weather
Bonnie is a 52 year old woman with a 25 year
history of MS. She has been quadriplegic for the
past 20 years, living in a group home until 8
months ago when she became ventilator
dependent.
She has become drowsier in the past few days,
Temp 34, HR 58 and BP 138/65. Her WBC has
increased to 22. Cultures reveal pseudomonas in
her PICC blood.
Brenda Lynn Morgan RN BScN MSc CNCC(C)
Clinical Nurse Specialist, Critical Care Trauma Centre
Victoria Hospital, London Health Sciences Centre
Cases
What treatment is indicated?
TSH: 105
Euthyroid: 0.27-4.20 mIU/L
Suppressed: < 0.10 mIU/L
Elevated: > 15.00 mIU/L
 FT4: 3.2 (10-24 pmol/L)
 FT3: 1.5 (3.0-6.5 pmol/L)
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David was involved in an MVC and has
been declared neurologically dead.
What medications are indicated in
preparation for organ donation.
Mrs. Beems is admitted with
hypertension, hypoglycemia and
decreased LOC. She is in rapid atrial
fib with warm, moist skin. Thyroid
function reveals:
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Cases
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TSH: 0.01
Euthyroid: 0.27-4.20 mIU/L
Suppressed: < 0.10 mIU/L
Elevated: > 15.00 mIU/L
Cases
Mrs. Kilbert has been in the ICU for the past 3
months, with failure to wean following recovery
from urosepsis. Screening thyroid function
reveals the following.
Thyroid Hormone
TSH: .22
Euthyroid: 0.27-4.20 mIU/L
Suppressed: < 0.10 mIU/L
Elevated: > 15.00 mIU/L
 FT4:7.8 (10-24 pmol/L)
 FT3: 1.9 (3.0-6.5 pmol/L)
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Thyroid Hormone
Thyroid hormone requires iodine; iodine is
essential to diet
 Thyroid traps and stores iodine
 If dietary iodine is low, thyroid works
overtime to try to make more thyroid
hormone, producing goiter
 Seafood and seaweed highest food source
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growth and development
beta stimulation
metabolism
temperature regulation
energy production
Thyroid Hormone
Increased dietary iodine initially
decreases thyroid production
 Prolonged high intake can cause
hyperthyroid
 Low iodine levels or high thyroid
production can cause goiter
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Thyroid Releasing
Hormone (TRH)
Thyrotopin Releasing Hormone (TRH)
From hypothalamus
Stimulates anterior pituitary to release
thyrotropin (TSH)
 Increased TRH triggered by decreased
thyroid hormone output
 Decreased TRH triggered by increased
thyroid hormone output
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Thyrotropin (TSH)
From anterior pituitary
Transports iodide from serum into the
cells
 Stimulates oxidation of iodide and
iodination of tyrosine residues
 Stimulates synthesis of T4 and T3
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Thyroid Hormones (T4, T3)
Thyroxine (T4) and Triiodothyronine (T3)
Both composed of a phenyl ring attached
to tyrosine with two idodine atoms on the
inner tyrosine ring
 T4 has two additional iodine atoms on its
outer tyrosine; T3 has only one
 Thyroid gland has large storage of
thyroglobulin; the protein within which T4
and T3 are synthesized and stored
 Storage in thyroglobulin enables rapid
secretion
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Thyroid Hormones (T4, T3)
Thyroxine (T4) made soley in thyroid gland
T3 is made in thyroid gland AND in
peripheral tissues and liver by deiodination
of T4
 rT3 (reverse T3) is formed in liver if an
iodine atom is removed from inner ring of
T4; rT3 has no biological activity
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Drug Interaction
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T4, T3
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I
Colloid: rich
bath of
thyroglobulin
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Many drugs interact
Heparin can raise T4
Salicylates and furosemide can lower T4, T3
Calcium carbonate reduces absorption of
levothyroxine
Dose adjustment needed with many
anticonvulsants
Beta blockers inhibit T4 conversion to T3
Drug Interaction
IV contrast administration can cause
hyperthyroidism (within several weeks of
administration)
 Amiodarone (contains iodine): can cause
hyperthyroidism after ~21 months of
therapy; can be treated with prednisone
 Amiodarone and lithium can both cause
hyper or hypothyroidism; depends on
underlying thyroid function
 Dopamine and somatostatin inhibit TSH
secretion
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Thyroid Hormone Disorders
Thyroid Hormone Disorders
• Hyperthyroidism
• Hypothyroidism
• Non-thyroidal Hormone Disorders
Hyperthyroidism
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Graves Disease
• Most common cause of
hyperthyrodism
• Autoimmune disease
• Autoantibodies that stimulate TSH
recepter
• Stimulates T4, T3 production
• Unusual activity for antibody (most
block)
Graves Disease
Graves Disease
• Woman > men (3% vs 0.3% US)
• Family history of autoimmune disease
• Pregnancy
• Goiter; bruit
• Puffy eyes
Graves Ophthlmopathy
Graves Ophthlmopathy
• Swollen, red and/or bulging eyes
• Believed to be due to autoimmune
interactions on TSH receptor within
orbit
• May appear before, during or after
hormone secretion increases
Three Phases:
• Active period of inflammation
• Regression
• Inactive “burnt out” period
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Graves Ophthlmopathy
• Increased production of
gycosaminoglycans that attract large
amounts of water to orbit
• Increased pressure causes bulging
(proptosis)
• Can put pressure of blood supply and
threaten vision
• Extra-orbital lid retraction does not
threaten vision
Clinical Findings: Hyperthyroidism
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Anxiety, Emotional lability
Weakness
Tremor
Palpitations
Heat intolerance, sweating
Weight loss despite normal or
increased appetite (some may have
increased weight)
Clinical Findings: Hyperthyroidism
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Hyperdefecation (not diarrhea)
Urinary frequency
Oligomenorrhea/amenorrhea
Gynecomastia/erectile dysfunction
Heart failure, shortness of breath,
arrhythmias, hyperclacemia
• Beta stimulation (cardiac with
vasodilation)
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Clinical Findings: Hyperthyroidism
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“Stare” (lid retraction) and lid lag
Rapid speach, hyperactivity
Skin warm and moist
Hair thin and brittle
Tachycardia/atrial fibrillation
Exophthalmos only in graves
Enlarged thyroid
Single palpable nodule
Treatment; Hyperthyroidism
Treat peripheral effects of hormone
beta blockers
 blocks CVS effects
 mildly blocks conversion of T4 to T3
corticosteroids
 replace cortisol deficit triggered by thyroid hormone
 blocks conversion of T4 to T3
 augments PTU
Clinical Findings: Hyperthyroidism
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Low TSH
High T4
High T3
Overt hyperthyroidism due to
graves or nodular disease, T3
increase > T4 (increased production
and peripheral conversion of T3)
• Amiodarone toxicity inhibits T3
conversion; T4 > T3
Treatment; Hyperthyroidism
Block thyroid gland
 propylthioruracil (PTU)
 inhibits T3 conversion from T4
 inhibits new hormone synthesis
 methimazole (MMI)
 more potent
 inhibits new hormone synthesis
 potassium iodide (SSKI)
 May be used preop or for the most severe hyperthyroid
crisis
 Short term administration decreases thyroid hormone
release
 Temporarily blocks iodine uptake by thyroid gland (maximum
effect ~10 days)
 Lithium carbonate has similar effect
Treatment; Hyperthyroidism
Removal of circulating hormone
 plasmapheresis, charcoal perfusion
Supportive
Hypothyroidism
 fluid and electrolyte replacement
 correct hypoglycemia
 fever management
 cardiovascular support
Corrective
 Removal
 Radioactive iodine
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Primary (thyroid gland), Secondary
(pituitary) and Tertiary
(hypothalamus)
Hashimoto’s Disease
• Similar risk (female, history of
autoimmune) to Graves
• Autoimmune is most common cause
• Instead of stimulation, antibodies
cause thyroid destruction
• Congenital or childhood
hypothyroidism can lead to stunted
growth/impaired mental development
Hashimoto’s Disease (chronic
lymphocytic thyroiditis)
Hashimoto’s Disease
• Goiter (despite thyroid cell
destruction) due to lymphocyte
infiltration
• Increased TSH (due to low T4, T3)
stimulates hyperplasia
• Diffuse goiter, with rubbery feel
• Goiter rarely causes problems or
requires surgery
Diagnosis: Primary Hypothyroidism
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Goiter
High TSH
Low T4, T3
Thyroid antibodies (if Hashimoto)
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Iodine Deficiency
• Goiter
• Rare in Canada, more common in
mountanous regions
• Replace iodine deficiency
Central (secondary) Hypothyroid:
• Infrequent
• Inappropriately low TSH despite low T4
and T3
• Pituitary disease: adenoma most common
(may be associated with other endocrine
deficiencies)
• Similar presentation to primary
hypothyroidism
• Treatment of hypothryoidism same as
other causes
Central (tertiary) Hypothyroid:
• Inappropriately low TRH (testing not
readily available)
• Low TRH causes inappropriately low
TSH andT4 and T3
• Most common reason is acute
intracranial hypertension/lesion
• Treatment of hypothryoidism same
as other causes
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Clinical Findings: Hypothyroidism
Common:
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Fatigue
Cold intolerance
Depression, poor concentration
Anemia
Brittle hair/hair loss, dry skin
Bradycardia
Aches and pains
Carpal tunnel
Puffy eyes
Treatment
• Levothyroxine (T4)
• T4 to T3 conversion at periphery is
physiologically regulated
• Dose adjusted to TSH
Myxedema Coma
• Mortality 30-40%
• Acts like beta blockade: bradycardia, heart
failure, mild hypertension
• Hypothermia (aggressive peripheral warming
may cause hypotension)
• Hyponatremia
• Hypercapnea
• Anemia
Clinical Findings: Hypothyroidism
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Constipation
Hoarse voice
Menorrhagia
Edema
Cerebellar signs
Deafness
Psychiatric
Myxedema
• Severe form of hypothyroid with
coma
• Non-goitrous myxedma may be the
result of total destruction of thyroid
cells
• Often triggered by stressor such as
infection
Treatment of Myxedema Coma:
• IV levothyroxine (T3 not available in
Canada)
• Steroids (due to risk of
simultaneous adrenal insufficiency
known as Schmidt’s syndrome)
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Treatment; Myxedema
Supportive
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respiratory
cardiovascular
fluids
correct anemia
prevent further heat loss
Non-Thyroidal Thyroid Hormone
Dysfunction
 avoid aggressive rewarming
 treat cause
Critical Illness
Non-thyroidal Disorders
• Critical illness commonly associated
with thyroid hormone disorders that
are not due to thyroid gland disease
• Normal or low TSH, low or normal T4
and/or T3
• rT3 elevation (produced by breakdown
of T4 in liver; no biological activity)
• rT3 binds to T3 receptor sites
impacting activity
• May be bodies attempt to reduce
metabolism
• Failure to wean associated with
abnormal thyroid hormones
• Kidney contributes to clearance of
iodide (by glomerular filtration)
• Cortisione and renal failure decrease
T4 conversion to T3
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