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103 Cards in this Set

  • Front
  • Back
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
HYPOTHYROIDISM…
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 SIADH…BASIC PRINCIPLE?
HYPERTONIC URINE
HYPOYONIC BLOLOD
SYMPTOMS OF ADDISON’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
CUSHING’S DIEASES MAY RESULT FROM TOO MANY?
STEROIDS
AN INDIVUDIUAL WITH CUSHING’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
* Oversecretion of hormones
* Pituitary tumors/hyperplasia
- Adenomas, most common (benign)
- CLASSIFIED BY SIZE/HORMONE SECRETED
- INVASIVE INVOLVES SELLA TURCICA
- "ENCLOSED" DOES NOT INVOLVE SELLA TURCICA
- ADENOMA ENLARGES, COMPRESSES TISSUE
* VISUAL CHANGES, HAS, INCREASED ICP
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
Diabetes Insipidus
* Posterior pituitary gland
* Inadequate ADH (vasopressin)
- Insufficient ADH synthesis
- Inability of kidneys to respond
* ADH deficiency results in:
- Excretion of large volumes of dilute urine
- DISTAL TUBULES/CDS OF KIDNEY IMPERMEABLE TO WATER
- THUS, WATER IS EXCRETED AS URINE RATHER THAN BEING REABSORBED
Diabetes Insipidus
* Polyuria, excess excretion of urine that is predominately water
* Dehydration
* Increased plasma osmolality
- Simulates osmoreceptors to relay thirst
* Classified as:
- Nephrogenic (genetic) renal tubules do not respond to the actions of ADH
- Results in inadequate water reabsorption
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
* Causes INCREASED Na loss in urine
- Further causes hyponatremia
* SIADH assoc with several complications
* Many medications utilized
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
SIADH
* SZ, COMA
* DTR SLUGGISH/ABSENT
* VS CHANGES
- TACHYCARDIA (INCREASED FLUID ON BOARD)
- HYPOTHERMIA
* DIAGNOSTIC ASSESSMENT
- PLASMA OSMOLAR CHANGES
- URINE OSMOLAR CHANGES
SIADH
* PLASMA VOLUME INCREASES, OSMOLALITY DECREASES
* URINE VOLUME DECREASES, OSMOLALITY INCREASES
* ELEVATED URINE SODIUM
* ELEVATED SPEC GR
* INTERVENTIONS
- FOCUS ON FLUID RESTRICTION
- PROMOTE URINE/WATER EXCRETION
- REPLACE SODIUM LEVELS
- PREVENT INJURY
SIADH
* FLUID RESTRICTION
- ESSENTIAL (FLUID DILUTES FURTHER)
- 500-600 ML/24 HOUR RESTRICTIONS
- TUBE FEEDINGS DILUTED NOT WITH WATER
- I& O, WEIGHTS DETERMINE FLUID PERMITTED
- 2 POUNDS/DAY CONCERN
- 1 KG WEIGHT INCREASE = 1000 ML FLUID
- PATIENT UNCOMFORTABLE DURING RESTRICTION
* MUCOUS MEMBRANE CARE
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
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 medications gradually-- pituitary production of ACTH & cortisol (adrenals)
-
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
ADRENAL INSUFFICIENCY
* HYPOGLYCEMIA MANAGEMENT
- MONITOR FOR S/SX HYPOGLYCEMIA
* SHAKINESS, TREMOR, SWEATING, NERVOUSNESS, ANXIETY, IRRITABILITY, IMPATIENCE, TACHYCARDIA, PALPITATIONS, CHILLS, CLAMMINESS, LIGHTHEADEDNESS, PALLOR, HUNGER, NAUSEA, HA, TIREDNESS, DROWSINESS, WEAKNESS, WARMTH, DIZZINESS, FAINTNESS, BLURRED VISION, NIGHTMARES, CRYING OUT IN SLEEP, PARESTHESIAS, DIFFICULTY CONCENTRATING, DIFFICULTY SPEAKING, INCOORDINATION, BEHAVIOR CHANGE, CONFUSION, COMA, SEIZURE, ETC
- MONITOR BLOOD GLUCOSE LEVELS
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
* EXAGGERATES ACTION OF GLUCOCORTICOIDS
* INCREASED ACTH PRODUCTION
* ABNORMAL N, CHO, MINERAL METABOLISM
* INCREASE IN TOTAL BODY FAT
* REDISTRIBUTION OF FAT
- "BUFFALO HUMP"
- "MOON FACIES"
* INCREASE PROTEIN CATABOLISM
CUSHING'S SYNDROME
* Increase in urine nitrogen excretion
* Decreased muscle mass = atrophy
- Thin skin, bone density loss
* High corticosteroids kill lymphocytes
- Shrink organs that contain lymphocytes (liver, spleen, lymph nodes)
- Immunosuppression
- Inflammatory response impaired
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
- Excessive thyroid hormone production
- Clinical manifestations: thyrotoxicosis
- Thyroid hormone: cellular metabolism
- Pathophysiology: normal feedback control impaired with excess thyroid hormone
* Hormone directly stimulates the heart
* Increased HR and SV ¡ú increased CO
* Affects protein, CHO, & lipid metabolism
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