Nursing Care of Patient with Endocrine Disorders Flashcards
Cellular regulation of body functions - maintained by various hormones regulated by endocrine sys - lots glands and hormones
Neuroendocrine sys - neurotransmitters interact with endocrine sys
Primary goal: Maintain homeostasis - controls body funcs and regulated largely due to hormone release
Hormone release
Positive and Negative Feedback mechanisms
Endocrine sys: major concepts
Included: growth metabolism, sexual development and function
Primary goal: Maintain homeostasis - controls body funcs and regulated largely due to hormone release
occurs as a Response to altered cellular environment
Maintain level of another hormone or substance
Hormone release
Disorders caused by
Over (HYPER) or under(HYPO) secretion of any hormone produced or secreted by gland
Endocrine issue - treatment - replace missing hormone (natural hormone/synthetic analog)
Goals: control symptoms experience as a result of hyper/hypo
Positive and Negative Feedback mechanisms
More is more!
Less common
Childbirth
Clotting cascade
Trigger happens - body creates hormones/clotting cascade and keep adding until desired outcome reached
Positive feedback loops
Changing response to stimulus decreases synthesis and secretion of a hormone
More common
Once appropriate level reached, shut down because at homeostatic level - levels added or sensed because circulating blood levels
Thyroid sys: Ex: Decrease serum T3 T4; stimulates TRH; stimulates TSH: secretes T3 T4; level normalizes; turns off TSH & TRH because have appropriate levels
Negative feedback loops
RBC
WBC
Platelets
Hemoglobin
Hematocrit
CBC
4.2-6.1 x10^6/microL
RBC
5000-1000 mm^3
WBC
150,000-400,000 mm^3
Platelets
12-18 g/dL
Hemoglobin
37-52%
Hematocrit
Calcium
Carbon dioxide
Chloride
Creatinine
Glucose
Potassium
Sodium
Urea nitrogen, or BUN
BMP
9.0-10.5 mg/dL
Calcium
23-30
Carbon dioxide
98-106
Chloride
0.5-1.2
Creatinine
70-110
Glucose
3.5-5.0
Potassium
135-145
Sodium
10-20
Urea nitrogen, or BUN.
INR
PT
PTT
Clotting cascades
Ref range: 0.8-1.1
INR
Ref range: 11-12.5 sec
PT
Ref range: 60-70 sec
PTT
Does lots things - two separate glands
Anterior Lobe Hormones:
Posterior Lobe Hormones:
Pit gland: master gland review
Adrenocorticotropic hormone (ACTH)
Follicle-stimulating hormone (FSH)
Growth hormone (GH)
Luteinizing hormone (LH):
Prolactin:
Thyroid-stimulating hormone (TSH)
Anterior Lobe Hormones:
Antidiuretic hormone (ADH)
Oxytocin
Posterior Lobe Hormones:
Most common cause of pituitary disorders; 95% are benign; with ant and post pit
Two main Types
Posterior pit tumors
Anterior
Pit tumors
Pituitary (adenoma) tumors
Most common cause of pituitary disorders; 95% are benign; with ant and post pit
Secretory – secrete too much hormone
Non-secretory- cause pressure
Two main Types
Ex: tumor secretes TSH-hyperthyroidism - completely disrupt negative feedback - create more T3 and T4
Oversecretion - levels too high having negative effects
Secretory – secrete too much hormone
Not secreting but extra pressure can cause pit gland or other structures within the brain to become squished
Not like extra pressure (skull - tissues not expand far - lead to ICP - confusion, pit or hypo - not func appropriately, too high - brain herniation) - want to relieve it
Non-secretory- cause pressure
ADH deficiency or excess - too much or too little - causes body to hold onto fluid
Posterior pit tumors
Hypopituitarism
Hyperpituitarism
Anterior
Deficiency of one or more anterior pituitary hormones results in metabolic problems and sexual dysfunction.
Growth hormone stimulates liver
Hypopituitarism
Excess secretion
Hormone oversecretion
Neurologic symptoms may occur-compression of brain tissue (ICP) - tymor increasing size and mass - putting pressure on brain structures and increased ICP
Galactorrhea, amenorrhea, and infertility can result.
Hyperpituitarism
Opp of SIADH
Peeing too much - lots of urine
Insipid - cause not understood - void lot for cause unknown at time
Deficiency of ADH
Cause:
Clinical manifestations
Treatment:
Diabetes Insipidus - Disorders: post pit: diabetes insipidus and SIADH
Excessive urination; manifestations of dehydration (thirsty all time - drink lot because excrete lot fluid - as soon as drink thirsty because excreted immediately)
Deficiency of ADH
Genetics, trauma, tumors, renal problem
Lifelong issue
Trauma - brain surgeries - and tumors most common
Not always permanent - recent brain surgery: swelling in area caused ICP - swelling resolves see DI go away
Cause:
Excessive/ALWAYS thirst, urination
Large volumes of dilute urine - really light colored/clear
250mL/hr or more - 1 cup of urine/hr
Clinical manifestations
ID cause/Replace vasopressin (hormone of ADH - replace for pt - desmopressin - intranasally bid)
Lifelong - esp if genetic
Treatment:
Excess ADH
Daily weights imp with vast amt water retained
Vast amount Water retained, causes dilutional hyponatremia
Causes:
Clinical manifestations
Treat underlying cause once ID
Syndrome of Inappropriate ADH (SIADH) - Disorders: post pit: diabetes insipidus and SIADH
Sodium Is Always Down!
(135-145 mEq/L)
Sodium is dilute
Vast amount Water retained, causes dilutional hyponatremia
Cancer, certain respiratory infections, CNS disorders, certain drugs, drug abuse
Neuro surgery
Causes:
Neuro impairment - hallmark: confusion
Pt gets huge with all amount water retain
low Na: sx: confusion/altered mental status - fluid volume overloaded and confused
Clinical manifestations
Put on fluid restriction - not add to fluid retained
Diuretics - lasix/furosemide
Hypertonic saline - slowly bring Na up as bring fluid level down - not want Na too low for too long: KNOW: as make alterations to Na DO SLOWLY - not rapidly correct imbalances - can cause dangerous fluid shifts for your pt
Safe environment
Frequent neuro assessments every few hrs
Treat underlying cause once ID
Close monitoring of I & O
Daily weight
Blood chemistries, electrolytes - trend is imp as single lab level - show getting better/worse
Monitor changes in neurologic status
Nursing - Disorders: post pit: diabetes insipidus and SIADH
Growth hormone (GH) hypersecretion before puberty
too much GH
RARE
Height and girth affected
Grow to be very large
Treatment: most time pit tumor cause - remove tumor excessive growth slowed
Manifestations: headaches, visions problems, nausea, excessive sweating, weakness, insomnia, delayed puberty in boys and girls, irregular menstrual periods - putting weird pressure on pit affect other things
Gigantism - Disorders of ant. pit (AP)
Hyposecretion of GH
too little GH
Discovered early - supplemental GH can be admin
Gen: type (100s diff) - respond well to supplemental GH
When has same body proportions as unaffected person respond well to treatment
Dwarfism - Disorders of ant. pit (AP)
Can be confused for gigantism
GH hypersecretion after puberty - no issues during puberty
Pituitary adenoma
Onset of growth hormone hypersecretion after puberty.
Slow changes: - gradual - can be diff for pt and people close to pt unless look at pics from 10-20 yrs ago
Enlarged tongue, lips, nose, hands, feet, facial bone growth - squaring of jaw
Organ enlargement
Skeletal changes cannot be reversed - bone changes occur: permanent
Diagnosed: 10-20 yrs in - excess GH - bone structure not revert once hormone imbalance fixed
Acromegaly - Disorders of ant. pit (AP)
Good H&P
Visual acuity/visual field tests - tumor growing to point putting pressure on other structures of the brain - can cause other issues
CT and MRI - diagnostic imaging
Lab-Pituitary hormones
Measurement of target organ of the hormones
Remove/destroy tumor
Medications:
Diagnosis and medical management - Disorders of ant. pit (AP)
Surgery directly
Undergo Radiation Therapy prior to surgery to shrink tumor before removed - shrink tumor - affect part gland tissue itself
Replacement hormones required after destruction - injure organ - body needs hormones so replacement hormones required
Remove/destroy tumor
If cannot get rid of tumor or is inoperable
Inhibit production/release GH
Bromocriptine (Parlodel)
Octreotide (Sandostatin)
Medications:
Scope through nose - poke through back of nasal cavity into brain - transphenoidal approach
Comps:
Nursing: pre-op teaching
Nursing: postop care
Discharge instructions
Total hypophysectomy and complications - Disorders of ant. pit (AP)
Transient diabetes insipidus
Due to manipulation of posterior pituitary
Cerebral Spinal Fluid (CSF) Leakage
Observe for clear fluid from nose
Higher risk for meningitis
Visual disturbances, post op meningitis, pneumocephalus (air in intracranial cavity - air should not be in skull besides sinuses) and SIADH - SIADH and DI can happen as a result of surgical procedures in the skull
Comps:
Do as much teaching before prior to procedure - chance after be confused - ICP
Avoid actions that increase intracranial pressure cause pressure on surgical site leading to leak of CSF:
Teach patient
Nursing: pre-op teaching
Vigorous coughing/Blowing nose/sneezing
Sucking through straw
Bending over or straining during urination/defecation
Avoid actions that increase intracranial pressure cause pressure on surgical site leading to leak of CSF:
Deep breathing techniques
About dressing and packing in nose
Do not mess with the dressings
Further aftercare - in hospital for awhile and nurses may monitor dressings
Nurse will check visual acuity often - how many fingers seen; follow finger with eyes - watch for increased pressure on optic nerve
Need for accurate I&O - early signs of SIADH/DI
Head of bed at least 30 degrees (min 2 weeks - reduce ICP) - help with venous return and keep pressure down
Teach patient
Monitor
Head of bed raised 30 degrees
Mouth care every 2-4 hours
Cool vaporizer in room
Hormones and glucocorticoids as ordered
Nursing: postop care
Neurologic checks including visual acuity and visual fields - compare pre-op and post-op for changes
Accurate I&O
Incision / packing (keep dry and clean) - repack - nothing that ICP
Potential complications
DI
SIADH
s/s of meningitis - nasty infection to treat - esp if see CSF leaks - look for clear drainage from nose - halo sign (on pillowcase/bed sheets - disperses in that shape) - sample from nose and send to lab - see if clear mucus or CSF; make feel continuous postnasal drip - down back throat - swallow more frequently - more CSF down back of throat
Monitor for visual disturbances
Mustache dressing and packing - removed 3-4 days post-op: tell pts not mess with it
Monitor
Avoid blowing your nose, coughing, sneezing, drinking with a straw, or bending over/straining on the toilet for 4 weeks - hard, esp during allergy season - lots edu on why
Extended period not want ICP
Report to Surgeon
Use only nasal medications/rinsed as prescribed - not automatically resume stuff used prior to surgery to understand what meds they are to go back on and ones to hold on
Keep follow up appt.: 1 week after discharge
Risks
Discharge instructions
Increased Hunger, Increased thirst, Increased body swelling, Increased mood swings, increased urine output, weight loss (hormone deficiencies) - SIADH/DI looking for
Continual postnasal drip, nasal drainage, or excessive swallowing (cerebrospinal fluid leakage)
Pain with bending neck (hallmarks - meningitis - reported; treat ASAP)
Vision loss/changes (damage to optic chiasm)
Report to Surgeon
Damage to normal pit gland - rare - underlying healthy tissue - replacement hormone therapy
Sinus congestion as everything heals
Adhesions form
Nasal deformity
Nasal bleeding
Small chance of stroke - rare
Risks
Sit on top kidneys - 2
Aldosterone
Cortisol/ne
Adrenal glands: major hormone secretion
Regulates blood volume
Sodium reabsorption (water follows Na) and potassium excretion renal tubules (AldosteRoNe = Reabsorption Na+) - body gets rid K
Aldosterone
Stress hormone
Increases circ blood glucose by inhibiting insulin secretion and promoting gluconeogenesis - non-carb sources break down into glucose - proteins and AA broken down - liver major role
Increases breakdown of proteins and lipids - through gluconeogenesis
Suppresses the inflammatory and immune response
Increases sensitivity of vascular smooth muscle to norepinephrine and angiotensin II (both result in vasoconstriction) - stressed - keep BP and circulating volume delivering more O2 to tissues
Increases breakdown of bony matrix
Promotes bronchodilation - optimal airway exchange
Cortisol/ne
Less of hormones available
Addison’s Disease
Adrenal gland: hypofunction
Deficient of salt, sugar, steroid - hyponatremia, hypoglycemia because not having appropriate cortisol and aldosterone production
Decrease ACTH and adrenocortical steroids from adrenal cortex
Can have pit involvement with ACTH as well as adrenal gland involvement with decrease in aldosterone and cortisol
Cause:
Common clinical manifestations:
Addison’s Disease
Autoimmune; Meds: corticosteroids suppression (2-4wks) - abruptly stops taking them - used to artificial steroid coming in - not reused normal homeostatic steroid production - why must taper off slowly
Cause:
Hyper-pigmentation - particularly gum lines; tan and not out in sun
Fatigue/weakness/anorexia/unexplained wt loss (not hungry)
confusion/emotional lability (going between all diff emotions - quickly)
Decreased body hair
Hypoglycemia
Blood volume depletion
Hyperkalemia: cardiac arrhythmias - make sure on telemetry - tall peaked T waves which can go to v-tach which is lethal
Hyponatremia
Common clinical manifestations:
Life threatening
Sudden loss of cortisol and aldosterone
Sudden loss in func of adrenal glands
Typically after stressful event (surgery, trauma, severe infection) - physiologic stress - wreaks havoc on endocrine sys
Clinical Manifestations
Diagnosis
Medical
Nursing
Acute adrenal crisis
Vomiting - comes from shunting of blood away from GI tract - stomach and intestines not getting supply supposed to
Abdominal pain - comes from shunting of blood away from GI tract - stomach and intestines not getting supply supposed to
Low glucose/Low sodium/High potassium
Severe hypotension (loss of blood volume (lack of aldosterone) - Na not retained - fluid not retained - Hypovolemic Shock - not enough circulating volume to move blood and blood products effectively around the body
Clinical Manifestations
Early morning Plasma cortisol provocation tests
Injection of ACTH adm.; blood drawn 60 min later: measure cortisol - TIMING IMP; cortisol excreted in rxn to ACTH admin
Performed to differentiate primary from secondary adrenal insufficiency
Primary - affects gland directly; stress, surgery, trauma to KIDNEYS
Secondary - pit tumor - ACTH affected
Primary: greater increase in plasma ACTH and lower than normal cortisol concentration
Fasting blood glucose, electrolytes (Na, K), BUN
Diagnosis
Restore circulation blood volume and prevent shock - correct hypovolemia and do correctly - first line: crystalloid fluids: NS - depending on Hgb - may replace lost blood products
Replace hormones (hydrocortisone/dexamethasone - replace hormones lost)
Treat Hyponatremia (confusion - worry about safety - NS helps with this - bring level up slowly) and Hyperkalemia (dialysis may be required, lot fluid, insulin to cause intracellular shift of K following by d50 or kayexalate)
Treat Hypoglycemia - care with BG level; monitor - esp if using insulin to lower K
Administer LOTS fluids, monitor I&O
Monitor VS - high HR with low circulating volume and low BP; hopeful BP rise and HR down as fluid improves
Vasopressors for hypotension - levofed, neosinephrine - causes vasoconstriction
Determine cause
Medical
Monitor VS every 1 to 4 hours, assess for dysrhythmias or postural hypotension. - lack circulating volume
Daily weight - daily weights monitor fluid volume status
Promote fluid balance and monitor for fluid deficit.
Accurate I&O
Monitor Lab values - renal func (BUN and creat), electrolytes (Na - , and K - careful with loop diuretics because low circulating volume)
Give cortisol and aldosterone replacement therapy. - get overall situation fixed
Nursing
Cushing’s syndrome
Clinical manifestations (Cushing’s)
Diagnosis:
Medical management
N. interventions -
Adrenal gland: adrenocortical excess
Pheochromocytoma (common pit tumor 85% that can lead to this sydrome)
High sodium and high sugar
Cushing’s syndrome
Acne, muscle wasting, weakness, fragile skin, moon face - rounded face, buffalo hump - hump on the bag, enlarged trunk - tiny arms and legs with muscle wasting
Virilization: hirsutism, male pattern balding, clitoral hypertrophy, breast shrinkage, menses ceases, voice deepens (permanent because lengthening of vocal cords), loss of libido
Retention of sodium and water: hypertension and heart failure with excess fluid volume
Hyperglycemia
Clinical manifestations (Cushing’s)
Three tests: 2 must be abnormal for diagnosis
Serum cortisol - blood level of cortisol
Urinary cortisol (24 hr collection) - orange jug that tall milk jug - collect over 24 hr period time - imp because diff times of time for diff people the proteins excreted in the urine vary - get full 24 hours worth: make sure get adequate sample - collect all urine - not miss void - then start over because might have crucial substances - stay on top of pt - often send home with pt but teach that stay on top of it; must stay on ice and kept cold
Low dose dexamethasone suppression test
Diagnosis:
Surgery:
Drug therapy: adrenal enzyme inhibitors
Radiation possible if not surgical candidate - takes long time before see effects
Medical management
If cause pituitary tumor or primary adrenal hypertrophy/adrenal tumor
Adrenal insufficiency 12-48 hrs post op
Support with steroids - overproducing steroids - removed source steroid and no longer have source to produce steroid that is necessary for life so much supplement with hydrocortisone - remove cause - give at norm levels
Surgery:
Used to suppress ACTH if tumor cannot be removed
Mitotane (Lysodren) if surgery not possible
Drug therapy: adrenal enzyme inhibitors
priority depends on pt and scenario
Decrease risk for injury
Decrease risk of infection
Prepare patient for surgery
Encourage rest and activity
Promote skin integrity
Improve body image
Improve coping
Monitor for potential complications
Promote home and community care after d/c
N. interventions -
Affecting the source
Caused by functioning tumor-excessive production of aldosterone
Clinical Manifestations:
Medical management and Nursing
Adrenal tumor: primary aldosteronism
Profound decline in serum potassium levels (hypokalemia) and hydrogen ions (alkalosis) with increase in serum bicarb - metabolic alkalosis
Hypertension common universal sign
Muscle weakness, cramping, fatigue, excessive urine volume (polyuria) serum concentration - blood concentrated because losing lot fluid, polydipsia (thirsty)
Clinical Manifestations:
Surgical removal of adrenal tumor - best course of agent
Treat hypertension with spironolactone (helps hold onto K) - have low K - not want to give loop diuretic because decreases K;
Monitor serum potassium and creatinine for 4-6 weeks while of drug therapy
Nursing
Post Op care - monitor surg site for s&s of infection/bleeding
Assist with collaborative care - social services, rehab: meds need upon discharge
Medical management and Nursing
Primary Function: Controls cellular metabolic activity
Influences every major organ system with cellular metabolic rate control
Thyroid - Thyroid and parathyroid disorders
Regulate calcium and phosphorus metabolism - Ca and phosphorus inverse relationship
Tiny and at back
Most time have issues with this - because hyperparathyroid glands removed during thyroid surg procedure
Parathyroid glands - Thyroid and parathyroid disorders
Characterized by inflammation of thyroid tissue, resulting in fibrosis and lymphocytic infiltration (lymph tissue building up around thyroid)
Symptoms: neck pain, swelling, dysphagia
Three types of thyroiditis:
Nonsurgical management, drug therapy (levothyroxine to replace low thyroid levels)
Surgical management if drug therapy not successful
Thyroiditis
Acute -infection
Subacute (granulomatous)
Chronic (Hashimoto’s disease)—the most common type - hypothyroid sx with this
Three types of thyroiditis:
More on the hypervigilant, anxious side
Fast forward of metabolic processes
Excessive output of thyroid hormones
Women 8 x greater than men
Graves Disease most common type
Other types
Clinical Manifestations:
Lab and diagnostic tests
Thyroid storm and medical management
Nursing interventions
Medical management: ablation/removal
Radioactive iodine therapy
Precautions for hospitalized I-131 thyroid therapy patients
Nursing post-op of thyroid pt
Hyperthyroidism (thyrotoxicosis)
caused by abnormal stimulation by immunoglobulins - bond irregularly to thyroid tissue resulting in excess secretion of T3 and T4 - too much thyroid hormone (autoimmune)
Graves Disease most common type
Formation of nodules from iodine deficiency (toxic multinodular goiter)
Viral infection of the thyroid gland (thyroiditis)
Excessive pituitary secretion of TSH (secondary hyperthyroidism) - ultimately result too much T3 and T4
Other types
Nervous, apprehensive, cannot sit still (anxious all the time) perspire, poor heat tolerance (hot flashes), high HR (120-140 at rest), flushed, skin moist, tremors, increased appetite, weight loss, weakness, amenorrhea (no period)
Exophthalmos when had for long time (bulging eyes) - permanent; thyroid enlargement; bruit heard over thyroid arteries
Clinical Manifestations:
Thyroid labs
Radioactive Iodine Uptake
Fine-Needle aspirate biopsy- tissue sample to detect cancer
Thyroid Scan
Lab and diagnostic tests
TSH will be low and T3, T4 elevated - negative feedback loop
TSH low because T3 and T4 enough but thyroid gone rogue and produce more despite pit saying not need more
Thyroid labs
Measures rate of iodine uptake by thyroid - produce T3 and T4 needs iodine as a trace
Hyperthyroid exhibit high uptake - use more of it; hypothyroid low intake
Radioactive Iodine Uptake
Radionuclide injected and test determines “Hot” areas of increased activity and “cold” areas of decrease activity (cancer)
Thyroid cancer - may order Entire body may be scanned to determine metastatic thyroid disease
Thyroid Scan
Emergent situtions with alterations in thyroid hormones
Worsening of hyperthyroid signs and symptoms worse - HR increased even more
Rare complication of hyperthyroidism - not seen often; can be fatal if not quickly recognized
Develop heart failure (heart not working for extended period of time, full circulatory collapse, high fever (102+ - high risk for seizures)
Antithyroid medications - block T3 and T4) - methymizal
Plasmapheresis or dialysis to remove excessive T3 and T4 from circulation - not long-term but want get levels down quickly
Ablation (burn or cautarize part gland) or full removal of gland
Cardiac monitoring dysrhythmias - not used to working hard for extended period time
Oxygen to treat dyspnea (even if 90% to max O2 to tissues) and (possible) heart failure
Beta blockers to decrease sympathetic activity symptoms - slow HR
Acetaminophen to reduce temperature - high temp - seizure threshold lower
Thyroid storm and medical management
Monitor vital signs with special attention on temperature and heart rate elevations
Provide a calm and quiet environment to decrease anxiety and irritability - no extra stimulation - increases chance of seizures as well - may reduce visitors
Maintain a cool room (heat intolerant - and fever - not want add more - that warm - metabolic and O2 demands very high increasing risk for seziures) and environment
Provide eye care (exophthalmos - not comfy): Administer artificial tears (reduce dryness)
Elevate the head of bed at night. - may eyes more comfy
Corticosteroids to reduce inflammation. - taper when reduce off
Collaborate with a registered dietician
Teach patient and family diff needs
need for antithyroid medication.
Encourage follow up with HCP and any specialist
Provide information about online resources and support groups to learn how others handled them
Exophthalmos - sensitive to light - Treat photophobia with dark glasses available
Nursing interventions
Hypermetabolic state, caloric intake must be increased to 4000-5000 calories per day.
Encourage six meals per day
Collaborate with a registered dietician
Radioactive Iodine therapy (I 131)
Surgical removal of the thyroid if I 131 not option; relapse 19% at 18 mo
Total thyroidectomy/Ablation will need lifelong thyroid hormone replacement - removed source that produced thyroid hormone - necessary for life still
Medical management: ablation/removal
Most common treatment; successful for most; remission with high dose 80%
Radioactive Iodine therapy (I 131)
As destroy active thyroid - hormone go somewhere - has go somewhere - released all at once - observe for thyroid storm/thyrotoxic crisis - artificially induce by destroying part thyroid tissue
Ablative dose of I-131 administered
Causes acute release of thyroid hormone as it is destroyed
Observe for thyroid storm (thyrotoxic crisis)
Management
Radioactive iodine therapy
Fever 101.3 or greater, HR > 130 beats/min; effects on organs: abdominal pain, diarrhea, edema, chest pain, dyspnea, delirium, psychosis
Observe for thyroid storm (thyrotoxic crisis)
Cooling blanket; hydrocortisone (monitor for shock and adrenal insuf; methimazole (anti-T3 and T4; impede formation of thyroid hormone); iodine decrease T4 output)
Actively Support cardiac, respiratory, renal systems if pt goes into full thyroid storm
Management
Cooling blanket; hydrocortisone (monitor for shock and adrenal insuf; methimazole (anti-T3 and T4; impede formation of thyroid hormone); iodine decrease T4 output)
Actively Support cardiac, respiratory, renal systems if pt goes into full thyroid storm
Management
Wear gloves and shoe covers
Wear dosimetry badge - monitors radiation exposed to
Minimize time spent with patient - longer around them, more radiation exposed to; cluster care;
Remain at least 3 ft away when possible
Contaminated linens collected - bagged and laundered separately
Pt remain in room at all times - separate rooms; bathroom in room
Pt must use disposable utensils - disposable tray - reduce chance of exposing others to radiation
No minors or pregnant visitors are allowed
Radiation safety must release the room before cleared for another pt - room inspection before another pt can be admitted
Precautions for hospitalized I-131 thyroid therapy patients
Observe for Potential Complications: - in neck - pay attention to AIRWAY
Hemorrhage
Respiratory distress - signs of swelling around neck and airway
Hypocalcemia and tetany (parathyroid often comes with thyroid) -
Laryngeal nerve damage
Thyroid storm or thyroid crisis
Adm. hormone replacement as necessary (synthroid/levothyroxine)
Nursing post-op of thyroid pt
Everything running slow motion
95% primary due to low levels of thyroid hormones
Clinical manifestations:
Medical management: levothyroxine (synthroid)
Compensatory mechanisms: enlarged thyroid gland
N. management
Hypothyroidism
Women 5x more than men
Autoimmune (Hashimoto’s - more commonly seen), thyroid surgery - hyperthyroid or thyroid tumor, iodine deficiency - not enough iodine to make T3/T4, tumors, drugs
95% primary due to low levels of thyroid hormones
Early: Fatigue, c/o cold all time (subnormal temp), low HR, weight gain with poor appetite, constipation
TSH high T3 and T4 low - negative feedback loop - need more T3 and T4 to stimulate production but not respond with T3 and T4 that within norm ranges
Clinical manifestations:
Aka Goiter
Not seen in US as often
Abnormal enlargement of thyroid
Hypothyroid
Hyperthyroid
Rare in US - main causes lack iodine
Compensatory mechanisms: enlarged thyroid gland
Hypothalamus signals release of more TSH binds to thyroid cells and causes thyroid to enlarge in attempt to trigger release of T3 and T4 - adv hypothyroid - may see slight goiter
Hypothyroid
too much thyroid hormone released
may also see goiter where have too much released
Hyperthyroid
Modify activity
Monitor physical status
Promote physical comfort
Enhance coping mechanisms
Promote home and community based care
N. management
Risk of immobility problems - everything slowed down and low energy levels
Modify activity
VS and mental status; manifestations of medications and potential effects; feel like brain foggy
Monitor physical status
Keep room warm; no heating pads if possible - since cold intolerant - not overheat an area - warm the room; nutrition adequate; increase fluids, help with ADLs
Promote physical comfort
May have extremes of emotion (more depressive)-need support and counseling
Enhance coping mechanisms
Teach: meds; keep appts for checking lab levels and provider, self-care, support groups and how manage caring for their condition
Promote home and community based care
Emergent case of hypothyroidism
60% mortality rate
Tissue and organ failure due to decreased metabolism
Occurs with undiagnosed hypothyroidism and untreated or poorly treated hypothyroidism
Can lead to a coma
Clinical Manifestations
N. interventions
Myxedema crisis
Mucinous Edema-mucous and water: more solid edema - not the pitting edema - form cellular edema non-pitting edema forms everywhere (eyes, hands, feet, between shoulder blades, tongue …)
Hypothermia (low body temp), increasing lethargy, stupor, loss of consciousness, depressed respiratory drive, coma, can have cardiovascular collapse, can lead to shock and death
Super slow motion
Very sensitive to sedating drugs! - on ventilator which can happen if depressed resp drive and add sedative meds - little bit long way - start low and go slow
Clinical Manifestations
Ineffective Breathing Pattern
Decreased Cardiac Output
N. interventions
Observe and record rate and depth of respirations - rate: very imp - need accurate count
Auscultate the lungs
Assess for respiratory distress
Assess the client receiving sedation for respiratory adequacy - on ventilatory - resp status for meeting O2 demands
Ineffective Breathing Pattern
Monitor circulatory status - monitor BP, HR, peripheral pulses
Signs of inadequate tissue oxygenation. - cold fingers and toes, cold fingers and toes, change color and extremities
Changes in mental status. - hard if on ventilator
Fluid status and heart rate - edematous; HR on lower side
Administer oxygen or mechanical ventilation, as appropriate
Decreased Cardiac Output
Papillary, follicular, medullary, and anaplastic
Collaborative management with oncologist, HCP
Surgery treatment of choice: thyroidectomy - removing cancerous tissue
Suppressive doses of thyroid hormone for 3 months after surgery - want ensure got all cancerous tissue
Study performed after drugs are withdrawn
Genetic counseling - many times thyroid cancers are genetic
Thyroid cancer
Excessive secretion of PTH
Clinical Manifestations
Diagnosis: elevated calcium; xray, scans - look at area of decalcifications and bone density
Medical Management:
Nursing: pre-op
Nursing: post-op
Hyperparathyroidism
Causes increase calcium in blood, bone decalcification, and renal calculi - as PTH tells bones to decalcify - Ca goes into bloodstream and can start to build up leading to kidney stones
Excessive secretion of PTH
Fatigue, muscle weakness, constipation, skeletal pain, hypertension, dysrhythmias, peptic ulcers (build up Ca in GI tract inferring with mucosal lining), and pancreatitis
Clinical Manifestations
Diuretics, fluids, mobility, diet restriction (calcium rich food) - fluid adequate but not too much; Ca already too high - not add to it
Meds: Phosphates, calcitonin (hormone of replacement - Ca already high - increase phosphate because low
Surgery - option remove overactive parathyroid gland
Medical Management:
Parathyroidectomy preoperative care:
Client stabilized; calcium levels normalized
Studies: bleeding and clotting times - Ca factor in clotting cascade, CBC
Teaching: limit coughing, deep-breathing exercises (will be painful), neck support - since surgery to the neck; montior airway
Nursing: pre-op
Postoperative care includes:
Observe for respiratory distress - in neck and close to airway - make sure airway maintained
Keep emergency equipment at bedside/close to pt in case airway shuts off
Hypocalcemia crisis can occur
Watch for symptoms hypocalcemia: of tetany, seizures
Watch for Trousseu’s sign - occurs when put BP cuff on them - tighten BP cuff - wrist flops over - worried about low Ca levels
Recurrent laryngeal nerve damage can occur - know prior to surgery as well because can impact ability to communicate
Nursing: post-op
Decreased PTH secretion
Common cause: inadvertent removal of gland during removal of thyroid or other radical neck surgery
Medical
Hypoparathyroidism
Lack of hormone causes increase phosphate and decrease calcium (5-6 mg dl)
Decreased PTH secretion
Correcting hypocalcemia - supplemental Ca, adequate supplemental vitamin D deficiency
Keep patient in quiet environment free of bright lights, drafts, to decrease neurologic stimuli - for acute phase when have low Ca
Long-term: adequate Ca and D for pt
Medical
