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NR 368 Exam 4 -Endocrine Disorders

NR 368 Exam 4 -Endocrine Disorders

NR 368 Exam 4 -Endocrine Disorders

Chapter 52 Assessment and Management of Patients With Endocrine Disorders

The endocrine system is closely linked with the nervous system and the immune system

  • Hormones

–             Steroid: act inside the cell

–             Peptide (protein): act on cell surface

–             Amine

  • Fatty acid derivative

HORMONES:

Hyopthalamus

CRH, TRH, GHRH, GnRH

Pituitary Gland (Hypophysis)

Anterior Hormones

                                        ACTH- Over production – Cushings or Acromegaly

GH (growth hormone)- Under production – dwarfism

TSH

Posterior Hormones

                                        Vasopression (ADH)

 

Hyposphysectomy– removal of pituitary gland- menses ceases, infertiliy (for pituitary tumors)

Diabetes Insipidus

  • Abnormally large amounts of urine excreted; >250ml per hour
  • Surgical brain tumors, failure of renal to secrete ADH

Medications:

Desmopression (SSAVP)- spray 2x a day

Chloropropamide (Diabinese)

Thiazide Diuretics

Syndrome of Inappropriate Antidiuretic Hormone Secretion

Dilutional hyponatremia

 

Thyroid Gland

–                            Thyroid hormones: T3 and T4

–                            Iodine is contained in the thyroid hormone

–                            TSH from the anterior pituitary controls the release of the thyroid hormone

–                            TRH from the hypothalamus controls the release of TSH

–                            Calcitonin is secreted in response to high plasma calcium level

–                            Hypothalamic-Pituitary-Thyroid Axisà increased T3/T4 = decreased TSH

Diagnostic Tests

  • TSH – screen all adults over 35 every 5 years if elevated then:
  • Normals:
  • T3- 80-200
  • T4- 5.4-11.5
  • TSH- 0.3-5.0
  • CALCITONIN- <10

 

Thyroid Disorders

Cretinism

  • Condition of severely stunted physical and mental growth; can be mild to severe

Hypothyroidism (low thyroid)

Causes: Hashimoto’s disease (most common cause)

Affects women 5X more frequently than men

  • Early symptoms may be nonspecific; fatigue; hair, skin and nail changes;
  • Myxedema (swelling of skin) may progress to stupor, coma, and death
  • Medical Management
  • Synthetic levothyroxine – replacement therapy (synthetic thyroid)
    • Effects of hypnotic and sedative agent; reduce dosage
    • Support of cardiac function and respiratory function- thyroid has direct effect

Hyperthyroidism

  • The second most prevalent endocrine disorder
  • Increase in thyroid hormone- Graves disease (most common cause)
  • Affects women 8X more frequently than men
  • Manifestations: palpitations; poor heat toleration; tremors; exophthalmos (bulging of eyes)
  • Medical Management of Hyperthyroidism?Surgery
  • Radioactive 131I therapyà inevitably causes hypothyroid
  • Medications:

–             Tapazole

–             Sodium and potassium iodine solutions

–             Dexamethasone- Decadrol

–             Beta blockers- Inderal

  • Thyroid Storm AKA thyrotoxic crisis or thyrotoxicosis
    • – Severe hyperthyroidism, usually abrupt onset
    • – If untreated, can be fatal

 

Thyroid Tumors– benign or malignant; diagnosed by scan; look for hot or cold

Thyroid Cancer– single, hard, fixed lesion

Thyroidectomy – Treatment of choice for thyroid cancer

  • Postoperative Care

–             Monitor dressing for potential bleeding/hematoma formation; check posterior dressing

–             Monitor respirations and protect airway

–             Potential hypocalcemia related to removal of parathyroid glands

 

Parathyroid Gland

  • Parathormone regulates calcium and phosphorus balance

–             Parathormone lowers phosphorus level

Hyperparathyroidism

  • Primary hyperparathyroidism is 2X to 4X more frequent in women
  • Treatment- Parathyroidectomy and reduce calcium excretion

–             Diet: encourage fluid and avoid excess or restricted calcium

  • Hypercalcemic crisis- Ca levels over 13 mg/dl; normal – 8.5-10.2

–             Medications: calcitonin, biphosphate, cytoxic agents (mithramycin)

Hypoparathryoidism

  • Deficiency of parathormone usually due to surgery such as thyroidectomy, parathyroidectomy, or radical neck dissection
  • Results in hypocalcemia and hyperphosphatemia
  • Management- Increase serum calcium level to 9 to 10 mg/dL

–             Calcium gluconate IV- in ICU need to be monitored

–             Parathormone may be administered; potential exists for allergic reactions

–             Consume diet high in calcium and low in phosphorus; Vitamin D supplementation

 

Adrenal Glands

  • Adrenal medulla
  • – Functions as part of the autonomic nervous system
  • – Catecholamines: epinephrine and norepinephrine
  • Adrenal cortex
  • – Glucocorticoids
  • – Mineralocorticoids
  • – Androgens
  • Pheochromocytoma- tumor which is usually benign in the adrenal medulla
  • – “5 Hs” (headache, hyperhidrosis, hypermetabolism, hyperglycemia, HTN
  • – Clonidine suppression test- measure level of catecholamine in blood; if level not suppressed then positive test
  • Adrenalectomy- removal of one or both adrenal glands; open or laparoscopic

Nifedipine (Procardia)

Sodium nitropursside (Nipride)à for hypertensive crisis

Corticoteroids

 

Adrenocortical Insufficiency/Addison’s Disease

  • May be the result of adrenal suppression by exogenous steroid use
  • Unable to produce ACTH
  • Manifestations include muscle weakness

Addisonian crisis

  • Hypotension, confusion
  • Diagnostic tests: adrenocortical hormone levels, ACTH levels, and ACTH stimulation test
  • Treatment: lifetime corticosteroid
  • – VS and postural blood pressures

Cushing’s Syndrome

  • Increased ACTH
  • Due to excessive adrenocortical activity or corticosteroid medications
  • Manifestations include hyperglycemia, central type obesity with “buffalo hump,” heavy trunk and thin extremities, “moon-face,” virilization in women
  • Dexamethasone suppression test- level less than 5 is a normal test
  • DISTURBED BODY IMAGE in women

 

Corticosteroid Therapy

  • Suppress inflammation and autoimmune response, control allergic reactions and reduce transplant rejection
  • Medications: Cortone, Solu-Medrol (prednisone), Azmacort
  • Prone to infection!

 

Chapter 51: Assessment and Management of Patients With Diabetes Mellitus

Functions of Insulin (pancreas secretes)

  • Transports and metabolizes glucose for energy
  • Stimulates storage of glucose in the liver and muscle as glycogen
  • Signals the liver to stop the release of glucose
  • Enhances the storage of dietary fat in adipose tissue
  • Accelerates transport of amino acids into cells
  • Inhibits the breakdown of stored glucose, protein, and fat

NR 368 Exam 4 -Endocrine Disorders

Classifications of Diabetes

  • Prediabetes – Impaired glucose tolerance (IGT) or impaired fasting glucose; need to monitor
  • Gestational
  • DM associated with other conditions/syndromes (AKA secondary DM)

Type 1 Diabetes

  • Insulin-producing beta cells destroyed by an autoimmune process, genetic susceptibility
  • Little or no insulin is produced – therefore, need insulin
  • Onset is acute and usually occurs before age 30
  • 5% to 10% of persons with diabetes

Type 2 Diabetes

  • Decreased sensitivity to insulin (insulin resistance) and impaired beta cell function results in insulin production
  • 90% to 95% of person with diabetes
  • More common in persons over age 30 and in the obese
  • Treated initially with diet and exercise
  • Oral hypoglycemic agents and insulin may be used
  • Insulin resistance may lead to metabolic syndrome:

–             1) HTN

–             2) increased cholesterol

–             3) abdominal obesity

Clinical Manifestations

  • “3 Ps”- Polyuria, polydipsia, polyphagia
  • Fatigue, weakness, vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, and recurrent infections
  • Type 1 may have sudden weight loss, nausea, vomiting, and abdominal pain if DKA has developed

Diagnostic Findings

  • Fasting (8H) blood glucose of 126 mg/dL or more
  • Random/casual glucose exceeding 200 mg/dL
  • Two hour glucose greater than 200mg/dl
  • Glycated (glycosylated) Hgb A1C: 4-6%. Goal <7% NOT on chart

Treatment Goalsà Normalize Blood Glucose Levels

Dietary Management (Medical Nutrition Therapy)

  • If change in prescription or diet; sick or hypo/hyperglycemic à check blood glucose

Meal Planning

  • Carbohydrates: 50% to 60% carbohydrates, emphasize whole grains
  • Fat: 20% to 30%, with >10% from saturated fat and >300 mg cholesterol
  • 10% to 20% Proteins
  • Alcohol- in moderation; alert for hypoglycemia
  • Nutritive and non-nutritive sweeteners

Exercise: Lowers blood sugar, aids in weight loss, Lowers cardiovascular risk

–             NO exercise:  blood sugar levels are elevated (above 250 mg/dL) and ketones in urine

–             Insulin normally decreases with exercise; patients on exogenous insulin should eat:

  • 15-g carbohydrate snack before moderate exercise to prevent hypoglycemia
  • Need to monitor blood glucose levels
  ONSET WHEN TO GIVE CHARACTERISTICS
Rapid-Acting- (Lispro (Humalog)

Aspart (Novolog)

 10-30 min 5-15 min before meal + Basal insulin for control of glucose (most given in combo)
Short Acting- Humalog R, Regular 30-60 min 30-60 min before meal Only insulin that can be given IV

-clear in color “R” on bottle
Intermediate Acting- Humulin N, lente, NPH, 70/30)

NPH/Lente- Basal

 1-3 hours   White, cloudy; only given subQ

Can be mixed with short acting
Long Acting- Ultralente 1-3 hours   Basal insulin; cant be mixed
Very long acting- Glargante, Lantus 1-2 hours   Cant be mixed; no peak

 

Insulin Regimens

Conventional- short/intermediate mixing; ex/terminally ill, older, bed-bound

Intensive- allows for more flexibility; ex/ very active people; eat a lot

Complications

  • Allergic
  • Lipodystrophy- when they keep injecting into same site
  • Resistance

Morning Hyperglycemia

  • Insulin Waning- progressive increase in blood sugar levels from nighttime to morning
    • Tx: increases evening dose
  • Dawn Phenomenon- good blood sugar until increase around 3 AM
    • Tx: give treatment later
  • Somogyi Effect- nocturnal hypoglycemia, followed by rebound hyperglycemia
    • Tx: hold injection before dinner (don’t need that much) OR give them snacks

Oral Antidiabetic Agents

–             Used for type 2 diabetes that cannot be treated with diet and exercise alone

–             Combinations of oral drugs may be used

  • Major side effects: hypoglycemia
  • Medications in textbook on page 1434-35

In the Hospital– NPO/Clear Liquids/Enteral Feeds

 

Hypoglycemia (Insulin Reactions)

  • Less than 70 mg/dL
  • Causes include too much insulin or oral hypoglycemic agents, too little food, and excessive physical activity

–      Adrenergic symptoms: sweating, tremors, tachycardia, palpitations, nervousness, and hunger

–      Central nervous system symptoms: inability to concentrate, headache, confusion, memory lapses, slurred speech, numbness of lips and tongue, irrational or combative behavior, double vision, and drowsiness

–      Severe hypoglycemia may cause disorientation, seizures, and loss of consciousness

  • Onset is abrupt and may be unexpected
  • Treatment must be immediate
  • Give 15 g of fast-acting, concentrated carbohydrate

–      3 or 4 glucose tablets

–      4 to 6 ounces of juice or regular soda (not diet soda)

–      6 to 10 hard candies

–      2 to 3 teaspoons of honey

  • Retest blood glucose in 15 minutes, retreat if < 70 mg/dL or if symptoms persist more than 10 to 15 minutes and testing is not possible

Emergency Measures

  • If the patient cannot swallow or is unconscious:

–      Subcutaneous or intramuscular glucagon 1 mg

–      25 to 50 mL 50% dextrose solution IV (CVL vs PVL)

 

“Sick Day Rules”

  • Shouldn’t skip treatment
  • Continue with fluids; consume small amounts of carbs
  • Testing BGM/urine ketones more frequently

 

Diabetic Ketoacidosis (DKA)

  • Caused by an absence of or inadequate amount of insulin resulting in abnormal metabolism of carbohydrate, protein, and fat
  • NA IMBALANCE
  • Clinical features

–      Hyperglycemia

–      Dehydration

–      Acidosis

Manifestations– blurred vision, acetone breath, Kussmaul respirations (deep labored breathing)

  • Blood glucose levels vary between 300 to 800 mg/ dL
  • Electrolytes vary according to water loss and level of hydration

Treatment of DKA

  • Rehydration with IV fluid
  • IV continuous infusion of regular insulin
  • Reverse acidosis and restoration of electrolyte balance

 

Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)

Hyperosmolality and hyperglycemia occur due to lack of effective insulin; ketosis is minimal or absent

  • Hyperglycemia causes osmotic diuresis with loss of water and electrolytes; hypernatremia and increased osmolality occur
  • K IMBALANCE
  • Med emergency for Type 2
  • Manifestations include hypotension, profound dehydration, tachycardia, and variable neurologic signs due to cerebral dehydration
  • High mortality
  • Treatment of HHNS

–             Rehydration

–             Insulin administration

–             Monitor fluid volume and electrolyte status

 

Long-Term Complications of Diabetes

  • Macrovascular- Coronary artery disease, cerebrovascular disease, and peripheral vascular disease
  • Microvascular- retinopathy (leading cause of blindness in diabetes) and nephropathy
  • Neuropathic/ Neuropathic Ulcers

 

Chapter 60:  Assessment of Integumentary Function 

Normal Aging Changes

 

  • Thinning of skin
  • Uneven pigmentation
  • Wrinkling, skin folds, and decreased elasticity
  • Dry skin
  • Diminished hair
  • Increased fragility and increased potential for injury
  • Reduced healing ability

 

Skin Appearance

 

  • Erythema
  • Rash
  • Cyanosis
  • Jaundice
  • Pruritus: itching

 

NR 368 Exam 4 -Endocrine Disorders

Diagnostic Procedures

  • Skin biopsy – “punch” biopsy
  • Immunofluorescence – microscopic to see antibodies on skin through dye
  • Patch testing – skin allergy testing
  • Skin scrapings – DX or rule out DX; used to detect fungal infection
  • Tzanck smear – test is to confirm viral infections; ex/Herpes, Varicella
  • Wood’s light examination – UV light done for fungal/bacterial infection OR detect pigment disorders; ex/Vitiligo
  • Potassium Hydroxide KOH test- used to confirm fungal infections

NR 368 Exam 4 -Endocrine Disorders 

Chapter 61:  Management of Patients with Dermatologic Problems

Wound care

Chronic wounds covered: 48-72 hours never leave without dressing

Acute wounds covered: 1 day unless really infected/heavy discharge

  • Types of wound dressings

Passive – have only a protective function and maintain a moist environment for natural healing

Interactive – capable of absorbing wound exudate white maintaining a moist environment and allowing surrounding skin to remain dry

  • Hydrocolloids, alginates, hydrogels

Active – improve the healing process and decrease healing time

  • skin grafts and skin substitutes

Rules of wound care

  1. Categorization
  2. Selection- proper dressing
  3. Change- change dressing if doesn’t work well
  4. Evolution- individualized care
  5. Practice- to learn/educate about dressing changes

Debridement

  • Autolytic– body’s own enzyme to break down necrotic tissue
  • Chemical– collagenase/santyl- covered with occlusive dressing and breaks up slough
  • Mechanical/Surgical– getting rid of dead tissue

 

Categories of dressings

  • Occlusive dressings – Transparent/clear; Plastic wrap (no more than 12 hours each day)
  • Moisture-retentive dressings – (Ex: DuoDERM, Convatec)

*CHECK manufacturer’s recommendations for time

  • Hydrogels, Hydrocolloids (can stay for 7 days), Foam dressings
  • Calcium Alginates- put into areas of tissue maceration into wound bed/cavity
  • Pharmacologic Therapy
  • Lotions – pruritic conditions
  • Topical Corticosteroids– these are absorbed better when skin is moist and then covered by occlusive dressing

Intralesional therapy– injection of corticosteroid under skin- Ex/ psoriasis/keloid conditions

  • Complications: lipodystrophy
  • Balneotherapy- bath to remove crusts/scales; ex/psoriasis and dermatitis

Pruritus– Tx: antihistamine, cortisone cream, topical lidocaine

Secretory disorders

  • Hidradenitis Suppurativa- abscess/lesions under armpits/perineal area; due to abnormalities of sweat glands
  • Seborrheic Dermatoses- “dandruff”
  • Acne Vulgaris- severe acne

Infectious Diseases of the Skin

Bacterial infections

  • Impetigo- contagious; use of antibiotics (topical)
  • Folliculitis, furuncles, and carbuncles

Viral infections

  • Herpes zoster (“shingles”)
  • Herpes simplex: orolabial, genital- Valtrax, acyclovir, valacyclovir administered within 24 hours of the initial reaction

NR 368 Exam 4 -Endocrine Disorders

Fungal infections (Review: Table 61-5 on page 1781)

Tinea Capitis Tinea Corporis Tinea Cruris Tinea pedis Tinea unguium

(onychomycosis)
head Body Groin/perineal Foot nailbeds

 

Parasitic Skin Infestations

  • Pediculosis (lice)
  • pediculosis capitis (head)- not a sign of uncleanliness; use of certain shampoos
  • pediculosis corporis (body)- poor hygiene; scabicide or OTC permethrin
  • Phthirus pubis (perianal)- spread by sexual contact
  • Scabies
    • 5% permethrin to entire body, except face/scalp; leave on for 12-24 hours
    • most common in nursing homes

Noninfectious inflammatory dermatoses

Contact Dermatitis

  • Eczema- reaction to irritant

Psoriasis

  • A chronic, noninfectious inflammatory disease of the skin in which epidermal cells are produced at an abnormally rapid rate
  • Improves and recurs; a lifelong condition
  • Appearance: Red, raised, silvery scales, dark red base
  • Treatment:
  • Baths – to remove scales
  • Medications:
    • Topical: Corticosteroids- evaluate and change every 8 hours
  • Phototherapy- UVA OR UVB
    • More effective with UVAà PUVA (Psolaren + UVA)
  • Systemic therapy (cytotoxic)- methotrexate
  • Biologic – new procedure/treatment

Blistering diseases

Appearance of the skin

  • Pemphigus vulgaris- oral lesions
  • Bullous pemphigoid- bubbly looking blisters
  • Dermatitis herpetiformis- highly pruritic; all over body

Toxic Epidermal Necrolysis and Steven Johnson Syndrome

  • Reactions to medications; FATAL
  • “Scalded skin syndrome”
  • Immunocompromised at risk
  • Initial treatment with systemic corticosteroid- Solu-medrol
  • IVIG
  • Cyclosporine (Neoral)
  • Biologic dressings/plastic semipermeable dressings

Skin Cancer

  • Frequently related to sun exposure—prevention: use of sunscreen and avoid sun exposure
  • Prevention of all types of skin cancer involves protection from excessive sun exposure
  • Basal cell carcinoma
  • Most common type and most successfully treated because tumors remain localized
  • Squamous cell carcinoma
  • Prognosis depends upon presence of metastasis
  • Treatment involves eradication of the tumor
  • Melanoma– VERY INVASIVE
    • Mortality rates increasing; quickly metastasizes
    • Irregular border; dark/color variation
  • Peak incidence occurs 20 to 45 years of age

Kaposi’s Sarcoma

  • A malignancy of endothelial cells that line the blood vessels: dark reddish-purple lesions of the skin, oral cavity, GI tract, and lungs
  • Usually benign
  • Categories
  • Classic KS
  • Endemic (African) KS
  • Immunosuppression-associated KS- worst one to have

Plastic Reconstructive and Cosmetic Procedures

Skin grafts- skin from one spot to another

  • Autografts – from patients own body
  • Allografts- from someone elses body
  • Xenografts- artificial skin/animal skin
  • Split thickness or full thickness

Conditions to be met:

  1. Adequate blood supply
  2. Graft must be in close contact with its bed to avoid accumulation of blood/fluid between graft and recipient site
  3. Area must be free of infection
  4. Graft must be immobilized so it remains in place

 

Chapter 62 Management of Patients With Burn Injury

Most burns occur in the home.

Priority: Young children and the elderly, over 25%, burns to face!

Burns are caused by transfer of energy from a heat source to the body. (thermal, chemical and radiation)

 

Factors to Consider in Determining Burn Depth Classification of Burns

  • First Degree: Superficial partial-thickness

Sunburn, low-intensity flash

Nikolsky’s signà (-)=skin doesn’t detach when you rub; (+) isn’t good

  • Second Degree: partial-thickness (2-3 weeks of healing)

Scalds, flash flame, contact

  • Third Degree: Full-thickness

Flame, prolonged exposure to hot liquids, electric current, chemical, contact

  • Fourth Degree: Full + fat, fascia, muscle, and/or bone

 

Methods to Estimate Extent of Total Body Surface Area (TBSA) Burned

Rule of Nines – body diagram of percentages

– Arm- 9%, leg- 18%, anterior/posterior- 18%, face- 9%

 

Physiologic Changes

Burns less than 25% TBSA produce a primarily local response.

MAJOR burns: (more than 25%) 30% – 1/3 – of TBSA –likely to produce a local and systemic response

Systemic response includes release of cytokines and other mediators into the systemic circulation.

Fluid shifts and shock result in tissue hypoperfusion and organ hypofunction.

 

Effects of Major Burn Injury (although may see smaller percentages of TBSA)

Cardiovascular effects

Fluid and electrolyte shifts – edema and hypovolemia- take weights/I&O’s

  • Might end up with contraction in lower extremities due to fluid obstruction; it will obstruct blood flow

Escharotomy- one way to relieve compartment syndrome

Fasciotomy-  another option for compartment syndrome

Pulmonary injury– especially inhalation injuries (carbon monoxide poisoning)

  • Cautious with face/neck injuries; always oxygen at bedside

Kidney alterations– may end up on dialysis because of decreased blood flow

GI alterations

Paralytic ileus- decreased or absent peristalsis;

Tx: gastric decompression

Curling’s Ulcer- ulcers that bleedà coffee grind; necrosis of stomach lining

– Usually >25% burns; will have low suction NG tube

  • Abdominal Compartment Syndrome (ACS)- b/c of increased pressure in abdominal cavity

NR 368 Exam 4 -Endocrine Disorders

Phases of Burn Injury

Emergent or resuscitative phase – Onset of injury to completion of fluid resuscitation

  • Prevent injury to rescuer.
  • Stop injury: extinguish flames, cool the burn, irrigate chemical burns.
  • ABC’s: Establish airway, breathing, and circulation.
  • Start oxygen and large-bore IVs.
  • Remove restrictive objects and cover the wound.
  • Assessment: surveying all body systems and obtaining history of incident and pertinent history.
  • Patient is transported to emergency department.
  • Patients with electrical burns should have an ECG.

Diagnosis:

  • Fluid volume deficit
    • Fluid resuscitation is begun. Maintain BP above 100 mm Hg systolic and urine output of 30-50 mL/hr. Maintain serum sodium at near-normal levels.
      • Fluid and Electrotype Shifts: Emergent Phase
        • Generalized dehydration
        • Reduced blood volume and hemoconcentration
        • Decreased urine output
        • Trauma causes release of potassium into extracellular fluid: hyperkalemia.
        • Sodium traps in edema fluid and shifts into cells as potassium is released: hyponatremia.
        • Metabolic acidosis
      • Acute pain- only IV medication should be administered.
        • Patients with burns exceeding 20-25% should have an NG tube inserted and placed to suction.

 

Acute or intermediate phase:  From beginning of diuresis to near completion of wound closure

  • 48-72 hours after injury
  • Continue assessment and maintain respiratory/circulatory support. At risk for infection!
  • Wound care
    • Debridement- removal of dead tissue; want pink, healthy tissue
    • Wound cleaning- Hydrotherapy
    • Topical Agents
      • General Antimicrobial ointment
      • Silver sulfadiazine
      • Mafaenide acetate
      • Silver nitrate
      • Grafting- know 4 needs
    • Fluid and Electrolyte Shifts: Acute Phase
      • Fluid re-enters the vascular space from the interstitial space.
        • Potential complication
      • Hemodilution
      • Increased urinary output
      • Sodium is lost with diuresis and due to dilution as fluid enters vascular space: hyponatremia.
      • Potassium shifts from extracellular fluid into cells: potential hypokalemia.

 

Rehabilitation phase: From wound closure to optimal physical and psychosocial adjustment

  • The patient may need reconstructive surgery to improve function and appearance.

 

Important:

  • Nutrition- gag reflex; afraid of aspiration
    • Enteral route (goes directly into organ- GI System) is preferred for feeding; jejunal feedings are used to maintain nutritional status with lower risk of aspiration

 

Chapter 11

  • Leading cause of death à heart diseases, malignant neoplasms, cerebrovascular disease
  • Presbycusis– decreased ability to hear high-pitched tones as result of irreversible inner ear changes
  • Presbyopia– decrease in visual accommodation that occurs with age
  • Mental Health Problems:
    • Depression– most common affective disorder from changes in reuptake of serotonin
    • Delirium– acute, confusional state that begins with confusion and progresses to disorienation
    • Dementia– characterized by general decline in higher brain functioning with pattern of eventual decline in ability to perform ADL’s
      • Ex/ alzheimers, vascular dementia (underlying disease like a TIA-mini stroke- where not enough oxygen is going to brain)
    • Use of MMSE, MINI COG AND CAM for confusion test methods

NR 368 Exam 4 -Endocrine Disorders

Chapter 35 Assessment of Immune Function

Immunity: the body’s specific protective response to invading foreign agent or organism

Components:

  • Phagocytic immune response à WBC’s
  • Bone marrow: T cells (cellular immune response) and B cells (humoral/antibody response)
    • B lymphocytes mature in bone marrow; antibodies=immunoglobulins(5)
      • IGM- 1st response to antigen
      • IGG- most common form; crosses placenta
      • IGE- histamine reactions and allergies
      • Antigen-antibody binding- if it fits well it will work well
    • T lymphocytes mature in thymus
      • Helper T cells(CD4)- activate the rest of immune system (HIV patients)
      • Cytotoxic T cells (killer)(CD8)- attack antigen directly and destroy cell membrane and cause cell lysis
    • Lymphoid Tissue: spleen and lymph nodes

–Autoimmunity- normal protective immune response

–Hypersensitivity reactions- allergic reactions

–Immunocompromised host- more susceptible to an infection

–Immune deficiencies

  • Primary- someone is born with it or develop it right after birth
  • Secondary- comes much later in life

 

Immune Function- fighting invading antigens

  • Natural immunity: nonspecific response to any foreign invader; acquired at birth

–Inflammatory/immediate response

–Physical barriers- skin, chemical barriers, acidic gastric secretions (enzymes in tears and saliva)

Acquired immunity: specific against a foreign antigen; develops after birth

–                            Result of prior exposure to an antigen; Active or passive

 

Non-T and Non-B Lymphocytes

  • Null cells–Destroy antigen coated with antibody
  • Natural killer cells–Defend against microorganisms and some malignant cells

Complement System– circulating plasma proteins made in the liver and are activated when antibody connects to antigen; important in defense

Immunomodulators– help with the immune response

NR 368 Exam 4 -Endocrine Disorders  

Chapter 36 Management of Patients With Immunodeficiency Disorders

Primary Immunodeficiencies- Genetic

–      May affect phagocytic function, B cells and/or T cells, or the complement system

  • Manifestations: vary according to type; severe or recurrent infections; failure to thrive or poor growth; and positive family history

Secondary Immunodeficiences- Acquired

  • Related to underlying disorders, diseases, toxic substances, medications
  • More common than primary
  • HIV, AIDS

Phagocytic Dysfunction

  • Defects of phagocytes affecting natural immunity
  • Increased WBC then Severe neutropenia (<1000 or <500)

Managing an IV Immunoglobulin Infusion

  • Side effects: hypotension, creatinine elevated
  • Important treatment for immune disorders; given very slowly
  • Patient needs to also get Tylenol or Benadryl 30 min prior to infusion; if patient has reaction, stop immediately

Chapter 52 Management of Patients With HIV Infection and AIDS

HIV/AIDS- CD4 Lymphocytes*

Prevention- **Standard precautions

 

Stages of HIV Disease – Category A-C

  1. Primary Infection- category A
    1. HIV infection or acute HIV syndrome
    2. No symptoms but viral load is high (very contagious); lack of HIV antibodies (may be negative on testing)
  2. HIV asymptomatic- Category A
    1. >500 CD4 & T lymphocytes
    2. Slow inset of symptoms
  3. HIV symptomatic- Category B
    1. 200-499 CD4 & lymphocytes; CD4 cells will gradually fall
    2. Patient develops symptoms
  4. AIDS- Category C
    1. CD4 COUNT LESS THAN 200(considered AIDS)- impairment of immune system

NR 368 Exam 4 -Endocrine Disorders

HIV Antibody Tests

?     HIV-1 antibody assay (EIA=ELIZA)  >> Western Blot (confirms ELIZA)

?     Rapid HIV-1 Antibody Test (ex/ Oraquick ADVANCE)

?     Viral loads (RT-PCR)- amount of virus circulating through blood stream

Treatment and protocols are continually evolving

  • Antiretroviral (ART) agents: see Table 37-3 (COMBOs) p. 1007
  • Goal: sustained viral suppression
  • Nucleoside Reverse Transcriptase Inhibitors (NRTI’s)- **Peripheral neuropathy
    • Didanosin (DDL)
    • TDF
    • Zidovudin

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Manifestations:

Respiratory

  • Pneumosystis pneumonia (PCP) – (OLD: Pneumocystis carinii pneumonia )

–      Initial symptoms may be nonspecific and may include nonproductive cough, fever chills, dyspnea, and chest pain

–      If untreated, progresses to pulmonary impairment and respiratory failure

–      Treatment: TMP-SMZ or pentamidine; prophylactic TMP-SMZ

GI

  • Oral candidiasis

–      May progress to esophagus and stomach

–      Treatment with Mycelex troches or nystatin and ketoconazole

  • Wasting syndrome

–      10% weight loss and chronic diarrhea or chronic weakness and fever – no other cause

–      Protein energy malnutrition

Neurologic

  • Peripheral Neuropathy
  • HIV encephalopathy- very common

–      Progressive cognitive, behavioral, and motor decline

–      Probably directly related to the HIV infection

 

Chapter 38: Assessment and Management of Patients with Allergic Disorders

Allergy- an inappropriate, often harmful response of the immune system to normally harmless substances

Allergens- substance that causes the allergic response

Mast cells- what the antibody attaches toà releases chemicals

 

Hypersensitivity- sensitivity to specific antigen

Anaphylactic (Type I)- (ex/asthma, allergic rhinitis)

Cytotoxic (Type II)- (ex/ thrombocytopenia, pernicious anemia)

Immune Complex (Type III)- (ex/fever, joint pain)

Systemic Lupus         and Rheumatoid arthritis

Delayed-Type (Type IV)- (ex/ contact dermatitis)

24-72 hours after exposure to allergen

Montoux reaction

Assessment

Allergy Assessment Form (p. 1034-35), CBC, Eosinophil Count, Total Serum IgE, Skin Tests, Provocative Testing, Radioallergosorbent Test (RAST)

Medications

  • Inhaled Corticosteroids
    • Prevent thrush by rinsing mouth out and using spacers
    • Cant stop corticosteroids abruptly
    • Major side effect: weight gain
  • Atarax- used for generalized itch disorders

Prevention of Anaphylaxis- Screen and prevent with use of Epipen

Allergic Rhinitis (runny nose)

  • Treat with antihistamines (cant be used in 3rd of pregnancy)
    • Non-sedating: Cetirizine (Zyrtec)
    • Sedating: benadryl (don’t use on elderly b/c of falls)
  • Also can use nasal sprays; may have rebound effect
    • Rebound reaction can occur in 4 hours