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103 Cards in this Set
- Front
- Back
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Pituitary(Hypophysis)
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* Master Gland
* Located in skull beneath the hypothalamus * Regulates many body functions * Two parts (anterior, posterior) |
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PITUITARY DISORDERS
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* ANTERIOR PITUITARY GLAND (ADENOHYPOPHYSIS)
- GH; SOMATOTROPIN - PROLACTIN - TSH - ACTH - FSH - LH - MSH * POSTERIOR PITUITARY GLAND (NEUROHYPOPHYSIS) - ADH (VASOPRESSIN) - OXYTOCIN |
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INCREASED TSH RESULTS IN
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HYPOTHYROIDISM
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FEEDBACK LOOP LEADS TO A DECREASE IN T3 AND T4
WHICH RESULTS IN |
HYPOTHYROIDISM
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WHAT ARE THE TWO THINGS THAT RESULT IN DIAGNOSIS OF THYROID DISORDERS?
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1) CLINICAL MANIFESTATIONS
2) LABORATORY VALUES |
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WHAT IS A CONDITION THAT IS AN EXAMPLE OF HYPOTHYROIDISM?
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MYXEDEMA
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WHAT IS A CONDITION THAT IS AN EXAMPLE OF HYPERTHYROIDISM
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EXOPTHALMUS
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WHAT MIGHT BLURRED VISION INDICATE?
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PITUITARY TUMOR
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T3 AND T4 LEVELS ARE USED FOR DX OF WHAT?
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THYROID DISEASES
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WHAT IS AN IMPORTANT CONDSIDERATION WHEN DOING HORMONE REPLACEMENT THERAPY ON ELDERLY?
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LOWER AMOUNTS ARE TO BE USED
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HYPERPITUITRISM IS TYPICALLY CASUED BY?
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TUMOR
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WHAT IS THE SELLA TURCICA?
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THE SADDLE PART OF THE PITUITARY
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INCREASED PROLACTIN _____ THE SEXUAL HORMONES?
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INHIBITS
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WHAT MIGHT GALACTORRHEA SUGGEST?
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PITUITARY TUMOR
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IF INCREASED LEVELS OF GH BEFORE PUBERTY WHAT MIGHT RESULT?
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GIANTISM
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IF INCREASED LEVELS OF GH AFTER PUBERTY WHAT MIGHT RESULT?
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ACROMEGALYAN
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INSULIN ANTAGOINIST RESULTS IN ?
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HYPERGLYCEMIA
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WHAT IS PROGNATHISM?
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JAW PROJECTION
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WHAT DOES THE DRUG PARLODEL DO?
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STIMULATES DOPAMINE RECEPTORS AND INHIBITS RELEASE OF GH
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GIVE PARLODEL WITH?
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FOOD
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WHEN IS PARLODEL CONTRAINIDCATED?
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PREGANANCY
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WHAT IS AN EXPECTED S/S OF DIABETES INSPIDUS?
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LOTS OF URNINATION
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DIURETICS INCREASE?
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SECRETOIN
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ANTI-DIURETICS DO WHAT
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PULL FLUIDS BACK IN
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DIABETES INSPIDIS IS A DISRODER OF WHAT GLAND?
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PITUITARY
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DURING DIABETES INSIDISUS WHAT IS HAPPENING WITH THE KIDNEYS?
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THE KIDNEYS ARE NOT PULLING WATER BACK INOT THE DISTAL TUBEULS
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WHAT ARE IMPORTANT NURSING INTERVENTIONS FOR INDIVUDUALS WITH DIABETES INSIPUS?
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* GOOD ORAL CARE
* SKIN CARE |
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WHAT TEST IS DONE FOR DEFINITIVE DX OF DIATBETES INSIPUDIS?
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24 HOUR URINE
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WHAT IS NORMAL URINE SPECIFIC GRAVITY?
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1.005 1.030
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WHAT IS PULSE PRESSURE ?
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SYSTOLIC MINUS DIASTOLIC
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DURING SIADH
BASIC PRINCIPLE?
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HYPERTONIC URINE
HYPOYONIC BLOLOD |
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SYMPTOMS OF ADDISONS?
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- BRONXE COLOR
- SALT CRAVINGS |
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AUTOMIMMUNE DISEASE DO NOT RESULT IN ?
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SKIN PIGMENTATION CHANGES
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PHEOCHROMOCYTOMA REUSLTS FROM ?
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TOO MANY CATECHOLAMINES
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NITORGEN MANIFETSS ITSELF AS?
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MUSLE WASTING
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CUSHINGS DIEASES MAY RESULT FROM TOO MANY?
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STEROIDS
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AN INDIVUDIUAL WITH CUSHINGS SYNDROME MAY BE IMMUNSUPPRESED BECAUSE?
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LYMPHOCYTRES ARE SHRUNK AND SUPPRESSED
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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 |
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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 |
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* Secondary hypopituitarism
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- Infection
- Trauma - Brain tumor - Congenital disorders * Idiopathic = etiology unknown |
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* ASSESSMENT Secondary Hypopitutarism
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- 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 |
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* INTERVENTIONS Secondary Hypopituitarism
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- Replacement of deficient hormone(s)
- Elderly lower amounts |
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Hyperpituitarism
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* 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 |
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Hyperpituitarism
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* PRL (prolactin) most common fr adenoma
- Excess PRL inhibits gonadotropins - Galactorrhea (men and women) - Amenorrhea - Infertility * GH, results in gigantism, ACROMEGALY |
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* Acromegaly
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- Gradual onset
- Slow progression - Years before dx - Early ID to reverse S/Sx - Soft tissue affected, may be reversed - Skeletal changes, permanent |
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* Giantism
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- When before puberty
* Rapid proportional growth/length in bones |
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- After puberty
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* 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 |
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* ETIOLOGY (hyperpituitarism)
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- 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 |
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* Assessment Hyperpituitarism
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- 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) |
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Assessment Hyperpituitarism - Acromegaly
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* 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) |
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Generalized Assessment - Hyperpituitarism
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* 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 |
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Nsg Dx - Hyperpituitarism
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- Disturbed body image
- Sexual dysfunction - Acute/chronic pain |
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Intervention - Hyperpituitarism
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* Goal: return to normal hormonal levels
* Correct secondary problems, eg visual |
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Nonsurgical Management Hyperpituitarism
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- 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 |
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SE OF PARLODEL
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- ORTHOSTATIC HYPOTENSION
- CONSTIPATION - GASTRIC IRRITATION - NAUSEA - ABDOMINAL CRAMPS * GIVE WITH FOOD * CONTRAINDICATED WITH PREGNANCY * RADIATION THERAPY = NOT VERY EFFECTIVE |
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Surgery Hyperpituitarsim
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* 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 |
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Postop Hyperpituitarism Surgery
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* 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 |
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DIABETES INSIPIDUS
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* 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 |
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Diabetes Insipidus
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* 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 |
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Diabetes Insipidus
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* 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 |
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Primary diabetes insipidus
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- Hypothalamus/pituitary gland defect
- Lack of ADH production/release |
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Secondary diabetes insipidus
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- Tumors hypothalamus, pituitary gland
- Head trauma - Infectious processes - Surgical procedures - Tumors (breast or lung mets) |
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Drug related diabetes insipidus
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- Lithium
- See pg 1409 |
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ASSESSMENT Diabetes Insipidus
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- 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 |
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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 |
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Interventions - Diabetes Insipidus
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* 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 |
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Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
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* 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 |
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SIADH
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* Causes INCREASED Na loss in urine
- Further causes hyponatremia * SIADH assoc with several complications * Many medications utilized |
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Nursing Management SIADH
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- History, p 1411
- Assessment * Sx of SIADH r/t water retention |
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GI disturbances - SIADH
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- 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 |
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SIADH
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* SZ, COMA
* DTR SLUGGISH/ABSENT * VS CHANGES - TACHYCARDIA (INCREASED FLUID ON BOARD) - HYPOTHERMIA * DIAGNOSTIC ASSESSMENT - PLASMA OSMOLAR CHANGES - URINE OSMOLAR CHANGES |
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SIADH
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* 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 |
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SIADH
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* 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 |
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SIADH
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* 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 |
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ADRENAL GLAND HYPOFUNCTION
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Hypofunction-Adrenals
* Adrenocortical steroids DECREASED * ACTH (adrenocorticotropic hormone)DECREASED * May be sudden or slow developing * Adrenal crisis = life-threatening s s/sx |
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Pathophysiology of Adrenal Gland Hypofunction
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- 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 |
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Pathophysiology of Adrenal Gland Hypofunction
DECREASED aldosterone LEADS TO |
K, Na, H2O imbalances
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Pathophysiology of Adrenal Gland Hypofunction
DECREASED K excretion = |
hyperkalemia
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Pathophysiology of Adrenal Gland Hypofunction
INCREASED Na/water excretion = |
hyponatremia and hypovolemia
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Pathophysiology of Adrenal Gland Hypofunction
K+ retention LEADS TO reabs of |
H+ WHICH LEAD TO acidosis
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Pathophysiology of Adrenal Gland Hypofunction
DECREASED adrenal androgen levels |
- Loss of secondary body hair
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Addisonian crisis =
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acute adrenal insufficiency, life threatening
- Glucocorticoid - Mineralcorticoid - Both are lacking |
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* 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) |
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History re: adrenal hypofunction
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- Neuromuscular
* Muscle weakness * Fatigue * Joint/muscle pain - Integumentary * Vitiligo * hyperpigmentation |
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adrenal hypofunction - GI
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- 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 |
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ASSESS S/SX HYPOGLYCEMIA
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- SWEATING, HA, TACHYCARDIA, TREMORS
* ASSESS FOR VOLUME DEPLETION - POSTURAL HYPOTENSION - DEHYDRATION * HYPERKALEMIA - IRREGULAR HEART RATE - DYSRHYTHMIAS |
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PSYCHOSOCIAL ASSESSMENT - ADRENOCORTICAL INSUFFICIENCY
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- LETHARGIC
- APATHETIC - DEPRESSED - CONFUSED - PSYCHOTIC - VALIDATE WITH FAMILY AS APPROPRIATE |
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DIAGNOSTIC ASSESSMENT - ADRENOCORTICAL INSUFFICIENCY
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* Laboratory (p. 1414)
- Low serum cortisol - Decreased FBS - Low sodium - Elevated K+ - Elevated serum BUN - Primary: INCREASED eosinophil and INCREASED ACTH |
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Interventions Adrenocortical Insufficiency
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* 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 |
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Adrenal Insufficiency
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* 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 |
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ADRENAL INSUFFICIENCY
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* 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 |
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hypoglycemia
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* Provide simple CHO prn
* Administer glucagon * Maintain IV access * TEACH patient/family * Instruct patient to wear appropriate emergency identification |
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Adrenal Hyperfunction
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* 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) |
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CUSHING'S SYNDROME
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* 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 |
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CUSHING'S SYNDROME
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* 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 |
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CUSHING'S SYNDROME
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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 |
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Assessment history - CUSHING'S SYNDROME
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* 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 |
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Diagnostic Assessment - CUSHING'S SYNDROME
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* 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+ |
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Urine - CUSHING'S SYNDROME
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- 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 |
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Cushing's Syndrome -
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* 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 |
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Hyperthyroidism
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- 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 |
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Hyperthyroidism
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* Glucose tolerance DECREASED = hyperglycemia
* Fat metabolism increased * Etiology - Numerous - Most common: Grave's disease aka toxic diffuse goiter |
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Clinical manifestations - HYPERTHYROIDISM
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- 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 |
