6364
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- Pituitary(Hypophysis)
-
* “Master Gland”
* Located in skull beneath the hypothalamus
* Regulates many body functions
* Two parts (anterior, posterior) - PITUITARY DISORDERS
-
* ANTERIOR PITUITARY GLAND (ADENOHYPOPHYSIS)
- GH; SOMATOTROPIN
- PROLACTIN
- TSH
- ACTH
- FSH
- LH
- MSH
* POSTERIOR PITUITARY GLAND (NEUROHYPOPHYSIS)
- ADH (VASOPRESSIN)
- OXYTOCIN - INCREASED TSH RESULTS IN
- HYPOTHYROIDISMÂ…
-
FEEDBACK LOOP LEADS TO A DECREASE IN T3 AND T4
WHICH RESULTS IN - HYPOTHYROIDISM
- WHAT ARE THE TWO THINGS THAT RESULT IN DIAGNOSIS OF THYROID DISORDERS?
-
1) CLINICAL MANIFESTATIONS
2) LABORATORY VALUES - WHAT IS A CONDITION THAT IS AN EXAMPLE OF HYPOTHYROIDISM?
- MYXEDEMA
- WHAT IS A CONDITION THAT IS AN EXAMPLE OF HYPERTHYROIDISM
- EXOPTHALMUS
- WHAT MIGHT BLURRED VISION INDICATE?
- PITUITARY TUMOR
- T3 AND T4 LEVELS ARE USED FOR DX OF WHAT?
- THYROID DISEASES
- WHAT IS AN IMPORTANT CONDSIDERATION WHEN DOING HORMONE REPLACEMENT THERAPY ON ELDERLY?
- LOWER AMOUNTS ARE TO BE USED
- HYPERPITUITRISM IS TYPICALLY CASUED BY?
- TUMOR
- WHAT IS THE SELLA TURCICA?
- THE SADDLE PART OF THE PITUITARY
- INCREASED PROLACTIN _____ THE SEXUAL HORMONES?
- INHIBITS
- WHAT MIGHT GALACTORRHEA SUGGEST?
- PITUITARY TUMOR
- IF INCREASED LEVELS OF GH BEFORE PUBERTY WHAT MIGHT RESULT?
- GIANTISM
- IF INCREASED LEVELS OF GH AFTER PUBERTY WHAT MIGHT RESULT?
- ACROMEGALYAN
- INSULIN ANTAGOINIST RESULTS IN ?
- HYPERGLYCEMIA
- WHAT IS PROGNATHISM?
- JAW PROJECTION
- WHAT DOES THE DRUG PARLODEL DO?
- STIMULATES DOPAMINE RECEPTORS AND INHIBITS RELEASE OF GH
- GIVE PARLODEL WITH?
- FOOD
- WHEN IS PARLODEL CONTRAINIDCATED?
- PREGANANCY
- WHAT IS AN EXPECTED S/S OF DIABETES INSPIDUS?
- LOTS OF URNINATION
- DIURETICS INCREASE?
- SECRETOIN
- ANTI-DIURETICS DO WHAT
- PULL FLUIDS BACK IN
- DIABETES INSPIDIS IS A DISRODER OF WHAT GLAND?
- PITUITARY
- DURING DIABETES INSIDISUS WHAT IS HAPPENING WITH THE KIDNEYS?
- THE KIDNEYS ARE NOT PULLING WATER BACK INOT THE DISTAL TUBEULS
- WHAT ARE IMPORTANT NURSING INTERVENTIONS FOR INDIVUDUALS WITH DIABETES INSIPUS?
-
* GOOD ORAL CARE
* SKIN CARE - WHAT TEST IS DONE FOR DEFINITIVE DX OF DIATBETES INSIPUDIS?
- 24 HOUR URINE
- WHAT IS NORMAL URINE SPECIFIC GRAVITY?
- 1.005 – 1.030
- WHAT IS PULSE PRESSURE ?
- SYSTOLIC MINUS DIASTOLIC
- DURING SIADHÂ…BASIC PRINCIPLE?
-
HYPERTONIC URINE
HYPOYONIC BLOLOD - SYMPTOMS OF ADDISONÂ’S?
-
- BRONXE COLOR
- SALT CRAVINGS - AUTOMIMMUNE DISEASE DO NOT RESULT IN ?
- SKIN PIGMENTATION CHANGES
- PHEOCHROMOCYTOMA REUSLTS FROM ?
- TOO MANY CATECHOLAMINES
- NITORGEN MANIFETSS ITSELF AS?
- MUSLE WASTING
- CUSHINGÂ’S DIEASES MAY RESULT FROM TOO MANY?
- STEROIDS
- AN INDIVUDIUAL WITH CUSHINGÂ’S SYNDROME MAY BE IMMUNSUPPRESED BECAUSE?
- LYMPHOCYTRES ARE SHRUNK AND SUPPRESSED
-
Pituitary
* Feedback loop/Target site
- Primary dysfunction
- Secondary dysfunction -
* HYPOPITUITARISM
- One or more hormones
- All hormones: Panhypopituitarism
* Decrease more common
* ACTH and TSH = most critical
- Gonadotropins (LH and FSH) = sexual changes -
hypopituitarism
* Etiology (primary) -
- Benign/malignant tumors
- Severe malnutrition
- Rapid loss of body fat (eg anorexia nervosa)
- Inadequate perfusion
- Surgery
- Radiation
- Infarction (postpartum hem Sheehan's)
- Trauma - * Secondary hypopituitarism
-
- Infection
- Trauma
- Brain tumor
- Congenital disorders
* Idiopathic = etiology unknown - * ASSESSMENT Secondary Hypopitutarism
-
- Physical appearance changes
- Target organ dysfunction
* Gonadotropin deficiencies (p 1400)
* Tumor etiology = visual changes
- Visual acuity
- Depth perception
- Peripheral changes
- Headaches
- Diplopia
* Laboratory Values
- Effects of hormones assessed
- Some actual pituitary hormone levels
* T3 and T4
* Testosterone/estradiol (from gonads)
* Measured easily
* Low levels may indicate disorder
* Abnormalities changes in sella turcica - * INTERVENTIONS Secondary Hypopituitarism
-
- Replacement of deficient hormone(s)
- Elderly lower amounts - Hyperpituitarism
-
* PRL (prolactin) most common fr adenoma
- Excess PRL inhibits gonadotropins
- Galactorrhea (men and women)
- Amenorrhea
- Infertility
* GH, results in gigantism, ACROMEGALY - * Acromegaly
-
- Gradual onset
- Slow progression
- Years before dx
- Early ID to reverse S/Sx
- Soft tissue affected, may be reversed
- Skeletal changes, permanent - * Giantism
-
- When before puberty
* Rapid proportional growth/length in bones - - After puberty
-
* Skeletal thickness
- Occur slowly
* Hypertrophy of the skin
* Bones have already reached limit
* Enlargement of visceral organs (liver/heart)
* After puberty
- Tufting of terminal phalanges (arrowhead)
- Bone cell overgrowth
- Degeneration of cartilage
- Hypertrophy of ligaments, vocal cords, eustacian tubes
- INSULIN ANTAGONIST (BLOCKS ACTION)
* RESULTS IN HYPERGLYCEMIA
* Hypersecretion leads to overstim of adrenal cor
- Produces excess glucocorticoids, mineralcorticoids, androgens, which lead to CUSHING's DISEASE - * ETIOLOGY (hyperpituitarism)
-
- Most from adenomas from pituitary
- May result from hypothalamus dysfunction causing overstimulation of pituitary
- Adenomas (may be genetically related)
* Incidence/prevalence
- Rare
- Most common tumors: prolactin, GH
- Least common: TSH - * Assessment Hyperpituitarism
-
- History: symptomatology imp to identify which hormone is produced in excess
- Accurate data about changes in apparel, ring sz
- Fatigue/lethargy?
* Hypersecretion of prolactin, decreased libido
- Women: menstrual changes, infertility, sexual functioning, painful intercourse (dyspareunia)
- Men: decreased libido, imnpotence
* Physical Changes:
- Facial appearance, coarse
* Increase in lip and nose size
* Increase in head, hand, and foot sizes
* Prominent supraorbital ridge
* Prognathism (jaw projection) - Assessment Hyperpituitarism - Acromegaly
-
* Assess for difficulty chewing
* Dentures no longer fit
* Arthritic changes, joint pain
* Arrowhead or tufted shape on x/rays of fingers, toes (thickened appearance)
* Onset: INCR. STRENGTH/ENERGY (metabolism) is replaced with lethargy
* Visual Changes (optic nerve compression)
* Organomegaly (cardiac, hepatic)
* HTN
* Dysphagia (enlarged tongue)
* deepening of voice (larynx)
* Hypersecretion of prolactin
- Galactorrhea (more in females, but both) - Generalized Assessment - Hyperpituitarism
-
* Psychosocial
- Seeks health care for physical changes
- Depression
- Infertility
* Laboratory Tests
- Most common: PRL, ACTH, GH
- Rare: TSH, FSH, LH
* Radiographic Assessment
- Sella turcica
- Xray CT MRI
* Misc
- Supression tests for hyperpituitarism
* Administration of agents to suppress pituitary
* Example high cortisol should suppress adrenal gland...with hyperpituitarism...not suppressed - Nsg Dx - Hyperpituitarism
-
- Disturbed body image
- Sexual dysfunction
- Acute/chronic pain - Intervention - Hyperpituitarism
-
* Goal: return to normal hormonal levels
* Correct secondary problems, eg visual - Nonsurgical Management Hyperpituitarism
-
- drug therapy (alone or with surgery)
* DOPAMINE AGONISTS (EG PARLODEL)
- STIMULATES DOPAMINE RECEPTORS IN BRAIN
* INHIBITS THE RELEASE OF MANY PITUITARY HORMONES
* INHIBITS RELEASE OF PRL AND GH
* TUMORS MAY SHRINK - SE OF PARLODEL
-
- ORTHOSTATIC HYPOTENSION
- CONSTIPATION
- GASTRIC IRRITATION
- NAUSEA
- ABDOMINAL CRAMPS
* GIVE WITH FOOD
* CONTRAINDICATED WITH PREGNANCY
* RADIATION THERAPY = NOT VERY EFFECTIVE - Surgery Hyperpituitarsim
-
* Removal of pituitary gland adenoma
* Preop care:
- Teaching: procedure decreases hormones
- Relieves HA
- May reverse sexual dysfunctions
- NASAL PACKING X2-3 DAYS
* MOUTH BREATHING
* DRESSING UNDER NOSE
* DO NOT BRUSH TEETH, COUGH, SNEEZE, BLOW NOSE OR BEND FORWARD (OPEN MUSCLE GRAFT, INCREASE ICP)
* NASAL AND ORAL C&S (EG SEPTICEMIA)
* Operative procedure p 1406
- Transsphenoidal
- craniotomy
* Postoperative procedure
- Routine post op vital signs
- Neuro checks
* Visual changes
* Loc
* Glascow coma scale
* COMPLICATIONS: DIABETES INSIPIDUS - Postop Hyperpituitarism Surgery
-
* Monitor IV
* Encouarge fluids
* Postnasal discharge noted/reported by pt
* CSF leakage (monitored by glucose)
- light yellow color at edge of drsg
- c/o HA
- Spinal tap may be indicated
* Semifowler's position
* Coughing avoided
- Increases pressure in incisional area
- May lead to CSF leakage
* Deep breathing exercises
* Incentive spirometry
* Mouth dryness from mouth breathing
* Frequent oral rinses, no brushing
* infection
* Alert for meningitis
* Entire gland removed: hormone replace.
* TEACHING
- Avoid activities that impair healing
- No bending except at knees
- No straining with BM
- No coughing
- No brushing x 2 wks (rinses, flossing)
- Decreased sense of smell (~4mos)
* Hormone replacement critical
- Laboratory values periodically
* Fluids
* Medications
* Report any symptoms of hyperpituitarism (previous s/sx) to MD - DIABETES INSIPIDUS
-
* DEFICIENCY OF ADH = DISORDER OF WATER METABOLISM
* INSUFFICIENT PRODUCTION
* INABILITY OF KIDNEYS TO RESPOND
* LARGE VOLUMES OF DILUTE URINE = DEHYDRATION
* S/S RELATED TO DEHYDRATION
* TYPES
* NEPHROGENIC
* PRIMARY
* DRUG-RELATED - Primary diabetes insipidus
-
- Hypothalamus/pituitary gland defect
- Lack of ADH production/release - Secondary diabetes insipidus
-
- Tumors hypothalamus, pituitary gland
- Head trauma
- Infectious processes
- Surgical procedures
- Tumors (breast or lung mets) - Drug related diabetes insipidus
-
- Lithium
- See pg 1409 - ASSESSMENT Diabetes Insipidus
-
- Most clinical signs are r/t dehydration
- Polyuria
- Polydipsia
- History: recent trauma, surgery, infection, or medication use (lithium)
* Increased fluid intake mediates s/sx
- Some may not have access to fluids
- Shock, caused by fluid loss
- Plasma hyperosmolality
- Poor skin turgor
- Dry, cracked mucous membranes
- Boggy, sunken eyeball sockets
* Blood/urine test changes
- 24 hour urine
- No restriction on oral intake
- >4 liters for definitive diagnosis (4->30)
- Urine is dilute, spec gravity is low
- Hyperosmolar urine
* Irritability
* Cognitive changes -
Assessment Diabetes Insipidus
CVS -
- Hypotension
- Decreased pulse pressure
- Tachycardia
- Weak peripheral pulses
- Hemoconcentration
* Increased hemoglobin
* Increased hematocrit
- Hypotension
- Decreased pulse pressure
- Tachycardia
- Weak peripheral pulses
- Hemoconcentration
* Increased hemoglobin
* Increased hematocrit
* Renal/urine
- Increased u/o
* Integumentary
- s/sx d/t dehydration
* Neurological
- Sensation of thirst
- Irritability
- Cognitive changes
- Lethargy, coma
- ataxia - Interventions - Diabetes Insipidus
-
* Medical management
- Drug therapy to control s/sx
- See page 1410
- Drugs increase ADH action (from hypothalamus)...undesirable SE
- When ADH severe, ADH replacement to maintain water balance
* DESMOPRESSIN ACETATE (DDAVP) DOCHOICE
- SPRAY, ULCERATION OF MB, ALLERGY, CHEST TIGHTNESS
* Nsg action: early detection of dehydration
* Maintain adequate hydration
* Accurate I&O
* Urine spec gravity
* Daily weight
* Monitor intake and output rigorously!
* Permanent IS: lifelong vasopressin tx
- Thorough teaching on medication, need for
* Teach patient polyuria, polydipsia
* Daily weights are a must!
- Same scale
- Same time of day
- With similar clothing, etc
- Any weight gain: Notify provider
* Medical alert braclet with Dx/meds - Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
-
* Regulation of ADH not functioning
* Dilutional hyponatremia
* Associated with pathologic conditions/specific drugs
* Clinical manifestations
* Water retention
* GI disturbances
* Weight gain
* Neurologic symptoms
* Tachycardia
* Hypothermia
* Vasopressin (ADH) is secreted
- Even when plasma osmolality is low/normal
* Decrease plasma osmolality ¡ý ADH production/secretion
* "Schwartx-Bartter" syndrome
- Feedback mechanism that regulate ADH do not function properly
SIADH
* ADH continues to be released even with plasma is hyperosmolar
* Water is RETAINED
* Results in: dilutional hyponatremia
* Decreased serum sodium
* Expansion of ECF
* Increased serum volume leads to increased GFR
- decreased renin release and decreased aldosterone release - SIADH
-
* DRUG THERAPY
- DIURETICS MAY BE USED
- NURSE MUST MONITOR ELECTROLYTES
* (REVIEW ELECTROLYTE LAB VALUES)
* SODIUM LOSS MAY BE EXACERBATED
* HYPERTONIC SALINE (3% SOLN) MAY BE USED
- CAUTION: HEART FAILURE
* LITHIUM (OPPOSITE EFFECT) MAY BE USED, BEING EXPLORED
* Safe environment
- Neurological status
- Muscle twitching and other s/sx
- LOC q 2 hr
- Avoid environmental overstimulation - Nursing Management SIADH
-
- History, p 1411
- Assessment
* Sx of SIADH r/t water retention - GI disturbances - SIADH
-
- Loss of appetite
- N/V
- Weight changes
- Free water retained, dependent edema usually not present
- Hyponatremia and fluid shifts affect CNS
* Serum Na < 115 mEq/L (CNS involvement)
* Lethargy, HA, hostility, disorientation - ADRENAL GLAND HYPOFUNCTION
-
Hypofunction-Adrenals
* Adrenocortical steroids DECREASED
* ACTH (adrenocorticotropic hormone)DECREASED
* May be sudden or slow developing
* Adrenal crisis = life-threatening s s/sx - Pathophysiology of Adrenal Gland Hypofunction
-
- Insufficiency LEADS TO problems fr loss of mineralcorticoid (aldosterone) and glucocorticoids (cortisol) action
* Impaired cortisol LEADS TO DECREASED gluconeogenesis (glucose from proteins)
- Depletion of liver/muscle glycogen leading to hypoglycemia -
Pathophysiology of Adrenal Gland Hypofunction
DECREASED aldosterone LEADS TO - K, Na, H2O imbalances
-
Pathophysiology of Adrenal Gland Hypofunction
DECREASED K excretion = - hyperkalemia
-
Pathophysiology of Adrenal Gland Hypofunction
INCREASED Na/water excretion = - hyponatremia and hypovolemia
-
Pathophysiology of Adrenal Gland Hypofunction
K+ retention LEADS TO reabs of - H+ WHICH LEAD TO acidosis
-
Pathophysiology of Adrenal Gland Hypofunction
DECREASED adrenal androgen levels - - Loss of secondary body hair
- Addisonian crisis =
-
acute adrenal insufficiency, life threatening
- Glucocorticoid
- Mineralcorticoid
- Both are lacking -
* Acute adrenal insufficiency
- Stress related
* Etiology (p 1413, table 63-4)
- Primary
- Secondary
* Abrupt cessation of long-term high-dose glucocorticoid therapy (negative feedback loop)
* Withdraw gluclocorticoid medica - -
- History re: adrenal hypofunction
-
- Neuromuscular
* Muscle weakness
* Fatigue
* Joint/muscle pain
- Integumentary
* Vitiligo
* hyperpigmentation - adrenal hypofunction - GI
-
- ANOREXIA, N/V
- ABDOMINAL PAIN
- BOWEL CHANGES (CONSTIPATION/DIARRHEA)
- WEIGHT LOSS
- SALT CRAVING
* CVS
- ANEMIA
- HYPOTENSION
- HYPONATREMIA, HYPERKALEMIA, HYPERCALCEMIA
* RADIATION TO ABDOMEN/HEAD
* MEDICATIONS? STEROIDS?
* PHYSICAL ASSESSMENT
- SEVERITY OF SX R/T SEVERITY OF DEFICIENCY
- PRIMARY HYPOFUNCTION
* PLASMA ACTH/MSH ARE ELEVATED BECAUSE LOSS OF ADRENAL-HYPOTHALAMIC-PITUITARY FEEDBACK LOOP
* INCREASED MSH LEADS TO INCREASED PIGMENTATION
* AUTOIMMUNE DISORDER LEADS TO DECREASED PIGMENTATION, BODY HAIR
- SECONDARY DISEASE, NO INCREASED SKIN PIGMENTATION - ASSESS S/SX HYPOGLYCEMIA
-
- SWEATING, HA, TACHYCARDIA, TREMORS
* ASSESS FOR VOLUME DEPLETION
- POSTURAL HYPOTENSION
- DEHYDRATION
* HYPERKALEMIA
- IRREGULAR HEART RATE
- DYSRHYTHMIAS - PSYCHOSOCIAL ASSESSMENT - ADRENOCORTICAL INSUFFICIENCY
-
- LETHARGIC
- APATHETIC
- DEPRESSED
- CONFUSED
- PSYCHOTIC
- VALIDATE WITH FAMILY AS APPROPRIATE - DIAGNOSTIC ASSESSMENT - ADRENOCORTICAL INSUFFICIENCY
-
* Laboratory (p. 1414)
- Low serum cortisol
- Decreased FBS
- Low sodium
- Elevated K+
- Elevated serum BUN
- Primary: INCREASED eosinophil and INCREASED ACTH - Interventions Adrenocortical Insufficiency
-
* Aim: promote fluid balance/monitor fluid deficits
* Daily weights
* I&O
* Vital signs q 1-4 hr
* Lab values
* Medication replacement of hormones
- Glucocorticoid/mineralcorticoids replaced - Adrenal Insufficiency
-
* Hyperkalemia ¨C promote balance
- Administer Kayexalate (electrolyte-binding)
- Monitor lab values for lytes/acid-base
- Administer meds to shift K+ into cell
- Avoid K+ sparing diuretics
- Maintain K+ restrictions
- Adminster diuretics prn
- Monitor fluid status
- Monitor cardiac status - hypoglycemia
-
* Provide simple CHO prn
* Administer glucagon
* Maintain IV access
* TEACH patient/family
* Instruct patient to wear appropriate emergency identification - Adrenal Hyperfunction
-
* Excessive secretion of adrenal hormones
- Hypercortisolism (Cushing's syndrome)
- Hyperaldosteronism (INCREASED mineralcorticoids)
- INCREASED androgen production
* May be caused by a tumor (pheochromocytoma) INCREASED catecholamines (80% epinephrine, 20% norepinephrine) - CUSHING'S SYNDROME
-
INCREASED androgens LEADS TO acne, hirsutism
interupt feedback mech to ovary, DECREASE the production of estrogen/progesterone
Etiology: excess cortisol (fr adrenal cortex) or administered exogenously - Assessment history - CUSHING'S SYNDROME
-
* PHYSICAL ASSESSMENT
- GENERAL APPEARANCE
- FAT DISTRIBUTION
- FAT PADS ON MECK, BACK, SHOULDERS
- ENLARGED TRUNK WITH THIN ARMS/LEGS
- MOON FACE
- MUSCLE WASTING/WEAKNESS
- SKIN CHANGES: FROM INCREASED BLOOD VESSEL FRAGILITY, EG, ECCHYMOSIS, WOUND HEALING
* Reddish purple striae, collagen breakdown
* Fine hair growth over face/body
* Hirsutism, clitoral hypertrophy
* Male pattern balding
* Psychosocial: depression, irritability, mood swings, confusion, etc - Diagnostic Assessment - CUSHING'S SYNDROME
-
* Plasma cortisol levels elevated
- Obtain same time q d
* Plasma ACTH vary
- Cushings: low to immeasurable
* INCREASED blood glucose
* INCREASAED WBC, lymphocytes
* INCREASED Na+ level
* DECREASED serum Ca++, K+ - Urine - CUSHING'S SYNDROME
-
- Measure free cortisol levels
- Measure adrenal metabolites
- 24 hour urine collection
* Interventions
- Aim: reduction of plasma cortisol level
- Removal of tumor, prevent complications
- Restore normal body appearance - Cushing's Syndrome -
-
* Nonsurgical (wts, I&O, fluid restriction)
* Medication
- Endogenous hypercortisolism = surgery
- Drugs that interfere with ACTH, palliative
* Radiation
- Tx for hypercortisolism from adenomas
* Surgical, depends on cause
- Pituitary or adrenal removal - Hyperthyroidism
-
* Glucose tolerance DECREASED = hyperglycemia
* Fat metabolism increased
* Etiology
- Numerous
- Most common: Grave's disease aka toxic diffuse goiter - Clinical manifestations - HYPERTHYROIDISM
-
- Excess appetitie (polyphagia)
- Energy demands excessive
cont
* Goiter
* Exophthalmos
* Pretibial myxedema
* Autoimmune disorder ¨C immunoglobulins are made and attach to the TSH receptor sites on the gland
* Antibodies bind to gland, ¡ü size ¡ü hormone
* Other etiologies: toxic multinodular goiter
cont
* Caused by overmedication with hormone (exogenous hyperthyroidism)
* Thyroid storm/crisis results when not treated appropriately, poorly controlled, or when client is ¡ü stressed
cont
* Assessment
- History
* Client may notice ∆s ¨C all systems affected
* Weight loss
* Increased appetite
* Diarrhea
* Heat intolerance
* Diaphoresis
* Palpitations/chest pain
* Visual changes ¨C blurred, diplopia, tiredness
cont
* Visual changes ¨C earliest notied
* Energy level change ¨C fatigue, weakness, insomnia
* Irritability
* Derpression
* Women: menstrual changes (amenorrhea, decreased flow)
* Increased libido, initially
cont
- Hx: radiation to neck, thyroid surgery
- Medications
* Physical S/Sx
- Ophthalmopathy ¨C Two changes
* Eyelid retraction (eyelid lag)
- Upper eyelid fails to descend when the client gazes slowly downward
- Globe lag: upper eyelid pulls back faster than eyeball when client gazes upward
* Infiltrative ophthalmopathy (esp c Grave¡¯s disease)
- Leads to exophalmus
cont
* Due to fatty tissue behind eyeball
* Pressure on optic nerve
* Incomplete closure = dryness, irritation
* Thyroid gland ¨C palpable with bruits
* Hair ¨C fine, soft, silky hair
* Skin ¨C moist, smooth
* Photophobia
* Gross motor activity, e.g., tremors, ¡ü DTR
cont
* Psychosocial Assessment
- Irritable, labile moods
- Fatigue d/t insomnia
* Laboratory Assessment (p 1427)
- T3, T4, TSH, TRH
* Other tests
- Thyroid scan
* Radioactive iodine
* Scan reveals position, size, function
cont
* Interventions
* Grave¡¯s disease ¨C most common form ¨C treatment next secion
* Heart: Increased systolic BP, widened pulse pressure, tachycardia, other dysrhythmias
* Nonsurgical management
- Comfort measures for q s/sx
cont
* Drug therapy:
- Propylthiouracil (PTU)
- Methimazole (Tapazole)
* Both block thyroid hormone production
* Response delayed d/t circulating hormones which are stored/released
- Iodine preparations decrease blood flow through the gland, reduces thyroid hormone production
cont
* ~2 weeks before improvement noted
* Take weeks before metabolism regulated
* May result: hypothyroidism
* Lithium ¨C inhibits hormone release and may be ordered (monitor SE: depression, nephrogenic diabetes insipidus, tremors, N/V, etc.)
cont
* Radioactive Iodine Therapy (RAI)
- Contraindicated in pregnancy
- RAI in form of oral I (Iodine)
- Destroys some of the cells in the gland
- May take 6-8 weeks for relief
- Outpatient tx
- A type of ¡°radiation¡± treatment
- Assure that radioactivity short-lived
- May result: hypothyroidism
cont
* Surgical management
- Drugs more common
- Surgery may be indicated
- Large goiter ¨C tracheal/esophageal compression
- Thyroidectomy ¨C lifelong hormone replacem
* Preop: antithyroid drugs given¡ú euthyroid state
* Iodine prep ¡ý size/vascularity of gland
- ¡ý hemorrhage and ¡°thyroid storm¡±
cont
* Cardiac (HTN, dysrhythmias, and ¡üHR) problems must be controlled
* High prot/high CHO diet for nutrition
* Cough/DB exercises
- Place both hands behind neck when moving
- Hoarseness may be common (endotracheal tube placement)
* Fear d/t neck area ¨C alleviate fear
cont
* Operative
* Postoperative
- Vital signs
- Comfort ¨C sandbags/pillows for support
* Pain medications
- Semi-Fowler¡¯s when awake
- ¡ý tension on sutures (No neck extension)
- Humidifcation of air (easier resps)
cont
* CDB exercises
* Monitor for complications:
- Hemorrhage ¨C 1st 24 h, check dressing
- Respiratory distress
* Swelling or tetany may cause
* Stridor (harsh, high pitched noise)
* Emergency tracheostomy at bedside
* Oxygen/suctioning equipment at bedside
- Parathyroid gland injury (hypocalcemia)
cont
* Parathyroid ¨C monitors calcium
- Note paresthesias ¨C numbness, tingling, twitching.
- Calcium gluconate or calcium chloride IV must be available for stat administration
* Laryngeal Nerve Damage ¨C hoarseness and weak voice; monitor voice q 2 h
* Thyroid Storm, i.e., ¡°thyroid crisis¡±
* Occurs with uncontrolled hyperthyroidism
* Usually taken care of with medications
* Usually caused by Grave¡¯s disease
* Triggered by stress/injury, i.e., surgery
* S/Sx: goiter palpatations, iodine exposure, radioactive iodine therapy
* Usually occurred when patient not treated with antithyroid drugs
cont
* Thyroid storm
- Fever
- Tachycardia
- Systolic HTN
- GI sx: abdominal pain, N/V
- Agitation, anxiety
- Tremors
- Restless, confused, psychotic, SZs, coma
- MORTALITY: 25%
CONT
* Infiltrative Ophthalmopathy
- Treatment is symptomatic
- Dry eyes: drops
- Incomplete closure: covering
- Photophobia: sunglasses
- Steroids may be prescribed for swelling and to stop the process
- Diuretics may be prescribed (edema)
cont
* Health Teaching
- s/sx hyperthyroidism/hypothyroidism
- Hormone replacement need
- Regular f/u
- Suture removed 3-4th day
- Incision area ¨C infection
- Emotional lability
Hypothyroidism
* Pathophysiology
- Gland may not produce hormone
- Cells may be damaged
- Cells may be intact but person does not receive adequate dietary precursors for hormone , e.g., iodine, tyrosine
- Inadequate hormones, blood levels low and decreased metabolism
- ¡ý met ¡ü TSH
cont
* TSH binds to gland results in goiter
* Most tissues/organs affected
* Low metabolic rate
* Cellular energy decreased
* Metabolites build up
* Metabolites: glycosaminoglycans build up in cells, increases mucous and water, forms cellular edema and ∆ organ structure
cont
* Cellular edema, mucinous edema called myxedema
* Changes appearance of the patient
* Nonpitting edema
* Edema around eyes, hands, feet, between shoulder blades
* Cause tongue to thicken
* Edema in larynx, voice more husky
cont
* Changes in other organs
* Myxedema coma rare, life-threatening
* Decrease metabolism of cardiac cells causes heart to become flabby, chamber size increases
* Decreased CO
* Decreased perfusion to the brain
cont
* Etiology:
- Thyroid surgery
- RAI treatment
- Endemic goiter ¨C soil/water ¡ý iodine
- Midwest US ¨C resulted in iodized salt
* Incidence/Prevalence
- Women 30-60 years (7-10X more)
- Link DM and hypothyroidism established
cont
* Assessment ¨C History
- Variety of s/sx produced
- Sleeping ¨C 14-16 hr/d
- Weakness
- Anorexia
- Muscle aches
- Paresthesias
- Constipation
- Cold intolerance
cont
* Decreased libido
* Infertility
* Menstrual changes (amenorrhea, excess)
* Medication use: lithium, etc (p 1432)
* Features: coarse, edema around eyes, face, blank expression, thick tongue
* Slow, muscle movement
cont
* Psychosocial
- Depression
- Lethargic
- Stuporous
* Laboratory Values
- T3 and T4 diminished
- TSH elevated
cont
* Etiology
- Thyroidectomy
- Thyroid destruction (radiation)
- Autoimmune disorder, Hashimoto¡¯s disease
- Cancer
- Iodine deficiency
- Excessive exposure to iodine
- Medications (lithium, etc)
- Infection, stress, trauma
cont
* Intervention for decreased CO
- Cardiac monitoring/assessment
- Monitor for shock,
- Decreased u/o
- Mental status changes
- Chest pain/discomfort
- Lifelong hormone replacement
* Most common, T4 Levothyroxine Synthroid
* Low dose and build up gradually
* Monitor lab values closely
cont
* Ineffective Breathing Pattern Interventions
- Observe/record respiratory pattern
- Monitor lungs
- Severe distress assoc with myxedema
* Thought Processes
- Sx decrease with hormone replacement, may take awhile
- Work with family, very difficult to accept s/sx
cont
* Myxedema Coma
- Coma
- Resp failure
- Hypotension
- Hyponatremia
- Hypothermia
- Hypoglycemia
- Shock
- Organ damage/death
cont
* Care for Myxedema Coma
- Maintain airway
- Replace fluids
- IV levothyroxine
- IV glucose
- Corticosteroids prn
- Monitor temp (blanket, keep warm)
- Monitor BP, HR
- Mental status changes
cont
* Health Teaching:
- Hormone replacement therapy for life
- s/sx of hyper and hypothyroidism
- OTC meds may interact
- Well-balanced diet (fiber/fluids)
- Medic alert bracelet
Thyroiditis
* Acute
- bacterial
* Subacute
- viral
* Chronic
- Hashimoto¡¯s disease, autoimmune
- Gland invaded with lymphocytes, destroys gland
Parathyroid Disorders
* Parathyroid Gland
- Maintains calcium and phosphate levels
- Serum calcium ¨C has a range
- Phosphate ¨C has more leeway
- PTH acts on kidneys
* Reabsorption of calcium
* Excretion of P
* Hyperparathyroidism
- Hypercalcemia; hypophoxphatemia
cont
* Assessment
- Ask about any fx, recent sugery/trauma to head and neck, weight loss, arthritis, or distress
- Skin may be waxy and there may be bone deformities (long-standing disease)
- Clinical s/sx r/t to either PTH effects or hypercalcemia effects
cont
* High PTH:
- Renal calculi
- Nephrocalcinosis (Ca in soft tissue of kidney)
- Bone lesions d/t increased bone destruction
- Pathological fractures
- Bone cysts
- Osteoporosis
cont
* GI
- Anorxia, nausea, vomitting, epigastric pain, constipation, and weight loss (hypercalcemia)
- Hypergastrinemia (¡ü serum gastrin levels) caused by hypercalcemia and ¡ú PUD
- Fatigue/lethargy
- Ca levels > 12 mg/dL, psychosis with mental confusion may result (see p 1437)
cont
- Laboratory Values: serum PTH, calcium, phosphate levels & cAMP
- Most common for hyperparathyroidism
- Xrays ¨C kidney stones, deposits, changes
* Interventions
- Nonsurgical
* Diuretics and fluid therapy
- Most common therapy for ¡ý CA++ (Lasix)
- IV with saline to ¡ú renal Ca++ excretion
cont
* Monitor cardiac function
* I&O q 2-4 hr
* Cardiac monitoring
* Serum Ca++ monitoring
- Report any ∆s immediately (hypocalcemia and paresthesias)
* Drug Therapy ¨C when IV insufficient
- Phosphates - ¡ý bone resoption
* Interfere with calcium absorption
* Used when Ca++ levels need to come down quickly
cont
* Calcitonin
- Decreases skeletal Ca++ release
- Increases kidney excretion of calcium
- Used with other meds (ineffective alone)
* Calcium Chelators
- Mithramycin, most effective
cont
* Surgical ¨C Parathyroidectomy
* Preop
- Client stabilized
- Calcium levels decreased to normal
- Teach about coughing, deep-breathing and pain postop (hands behind neck)
* Postoperative
- Resp distress
cont
* Emergency equipment
- Tracheostomy set
- Suctioning
- Intubation
- Oxygen
* Vital signs
* Identifies any change
* Monitor dressing
cont
* Sm amt (1-5 cc) normal
* Hypocalcemic crisis may occur ¨C critical
- Serum calcium levels monitored frequently
- s/sx: tingling, twitching
- Trousseau¡¯s sign (BP cuff)
- Chvostek¡¯s sign (face)
* Damage to laryngeal nerve, monitor for
* If all 4 glands removed, forearm implant
cont
- Lifelong treatment:
* Calcium
* Vitamin D
* HYPOPARATHYROIDISM
- Uncommon disorder
- Parathyroid gland function decreased
- Lack of PTH or tissue malfunction
* Net result: HYPOCALCEMIA
cont
* Iatrogenic hypoparathyroidism
- Most common form
- From removal of parathyroid tissue during thyroidectomy
- From removal of parathyroid tissue
* Idiopathic hypoparathyroidism
- Rare, may occur spontaneously
- Etiology unknown, may be autoimmune
cont
- Adrenal insufficiency
- Hypothyroidism
- DM
- Pernicious anemia
* Hypomagnesemia
- may cause disease
- Alcoholics
- Malabsorption syndrome
cont
- Chronic renal disease
- Malnutrition
* Assessment
- Ask about head/neck surgery, trauma, infection
- Radiation therapy
- Ask about s/sx of hypoparathyroidism
* Mild tingling
* Numbness
* tetany
cont
- Tingling/numbness around mouth, hands, or feet
- Severe muscle cramps ¨C more serious
- Carpopedal spasms
- Seizures
* Physical Assessment
- Excessive/inappropriate muscle contraction
- Chvostek¡¯s sign
- Trousseau¡¯s sign
cont
* Parkinsonian-like syndrome
* Cataracts (hypocalcemia)
* Teeth: bands, pits (encircle the crowns)
* Diagnostic tests
- EEG ¨C nonspecific; revert to normal with Ca
- Blood tests
- CT
cont
* Interventions
* Correction of hypocalcemia
- IV Ca++ (10% soln Ca Cl, Ca Gluconate)
* vit D def
- Calcitriol 0.5-2.0 mg/d
* Hypomagnesemia
- 50% Mg sulfate in 2 mL doses IM or IV
cont
* Long term therapy
- Vit D 50,000 ¨C 400,000 units qd
* Monitor levels
* Diet: high in calcium, low in phosphorus
- Milk, yogurt, processed cheese ¨C AVOID