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Meg Surg 155-02 > Week 12 > Flashcards

Week 12 Flashcards

1
Q

Terms in Front of Chapter

A

-

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2
Q

Primary Immunodeficiency vs Secondary (acquired)

A

-Primary = results from genetic effects
Secondary = results from environmental factors like HIV/AIDS

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3
Q

X- Linked Agammaglobulinemia (XLA) (3 Q’s)

A
  • Most common primary immune deficiency, but still rare -> 1 : 250k male babies
  • X-Linked Recessive, women more often carriers, men more often with disease.
  • Females have 2 X chromosomes, so the bad one doesn’t matter? Males have 1 X and 1 Y, so the bad X is screwed?
  • B-Cells don’t develop normally-> resulting with tons of immature B-Cells
  • Immature B-Cells do not make immunoglobulins like they should (antibodies)
  • No B-Cells = no IG = frequent infections
  • Medical Treatment:
    *IV Immunoglobulins (IVIG) every 3-4 weeks
    *Prophylactic ABX
    *Immunizations that are not live vax
    *Protect from risk through teaching/ lifestyle changes

PRIORITY NURSING CONSIDERATIONS
- Risk for infection #1 (skin, nasal, none, eyes)
- Sepsis of infection of blood stream
- Bronchitis, meningitis, pneumonia

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4
Q

DiGeorge’s Syndrome (2 Q’s)

A
  • Defect in chromosome 22 that causes poor development of the body functions
  • Immune problems from Thymus involvement AND potentially parathyroid, heart issues, facial deformities, learning disabilities
  • Autosomal dominant genetic condition that makes the thymus malformed AND potentially other issues as well
  • A poorly-built thymus means T-cell deficiency
  • T-Cell deficiency means frequent infections
  • Treatment:
    *IV Immunoglobulins (IVIG) every 3-4 weeks
    *Prophylactic ABX
    *Immunizations that are not live vax
    *Protect from risk through teaching/ lifestyle changes
    *Treat hypoparathyroid/ hypocalcemia issues from parathyroid
    *Surgery for heart issues and face deformities

PRIORITY NURSING CONSIDERATIONS
- Calcium levels, and interventions
- Heart issues
* RISK OF INFECTION

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5
Q

NOT ON TEST

A

Other B-Cell and T-Cell Abnormalities
- Rare but similar to the other ones

Severe Combined Immune Deficiency (SCID)
- Problem with t and b cells
- Disease the (in)famous ‘bubble boy’ David Vetter had
* Lived until the age of 12 in an isolated, germ free environment
- Now with early bone marrow transplants, 5-year survival rates can be 80%, but untreated has a 2 year lifespan

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6
Q

Secondary Immune Dysfunction ( 3 Q’s)

A
  • AKA Therapy-induced immune dysfunction
  • Caused by outside source -> chemotherapy, radiation, immune condition, surgical removal of spleen/thymus, long term and/or high-dose corticosteroids
  • More common than primary immune issues
  • Most common cause: severe malnutrition

TREATMENT
- Fix underlying problem, may not want to or be able to
- Prevention of infection
- Early treatment of infection

RISK PREVENTION
- HAND WASHING**, do not clean the litter box, avoid risky food (undercooked meat, raw fruits/veggies), practice safe sex, use bottled or guaranteed safe water, avoid amphibians/reptiles, avoid crowds and exposure to sick people, self-monitor for infection, be careful when traveling

PRIORITY NURSING CONSIDERATIONS

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7
Q

Excessive Immune Response

A
  • Auto-immunity: Immune response activated against self
  • Failure to recognize self as ‘self’ and causes a reaction against the body’s own cells or tissues
  • Cause not entirely understood
  • Hypersensitivity Reaction: Immune system over-reacts to a foreign antigen (such as pollen, medications, incompatible blood products, bee stinger toxins, even viral/bacterial/fungal cells)
  • Can range from mildly annoying (hay fever) to fatal (anaphylaxis)
  • Overlap exists between the two – Autoimmune diseases have hypersensitivity reactions as part of their disease process
  • Example: Grave’s disease is started by a hypersensitivity reaction leading to autoimmune reaction
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8
Q

Hypersensitivity Reaction TYPE 1

*Hypersensitivity Reactions – 9
*2 specifically about anaphylaxis
*3 regarding risk reduction
*3 regarding type/Ig mediator

A
  • Immediate Allergic Rxn
  • Histamine & Mast cell activation, IgE mediated
  • CAUSES: pollen, dust, food allergies, medication allergies, etc
  • Localized symptoms: nasal discharge, sneezing, itching, sinus pressure, headache, itchy watery eyes
  • Systemic symptoms: dyspnea, SoB, skin reaction/rash, N/V/D, angioedema around mouth/eyes, stridor, wheezing -> hypotension, tachycardia, fever -> shock

TREATMENT
- Mild to moderate: antihistamine, nasal decongestants, steroids, bronchodilators
- Severe: anaphylaxis (Epinephrine IV, IM, SQ)

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9
Q

Hypersensitivity Reaction TYPE 2-5

A

II Cytotoxic Reactions: IgG, IgM - Transfusion reaction, Goodpasture’s syndrome,

III Immune Complex Reactions: IgG, IgM - Systemic lupus erythematosus, serum sickness

IV Delayed hypersensitivity reactions; T-cell mediated: NONE - contact dermatitis to poison ivy, positive TB test, Latex allergy

V Stimulated: BLANK - Grave’s disease, B-cell, gammopathies (increased levels of gamma globulin’s

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10
Q

Osteoarthritis

A
  • Overuse damage within the joints, typically weight-bearing joints (hips)
  • Age-related and overuse related. (More overuse than age)
    -RISK FACTORS: obesity causing stress on weight-bearing joints, increasing age, women, repetitive stress jobs, sports, previous injuries to the joint
    TREATMENT
  • heat, cold, and exercise
  • Tylenol, NSAIDS, steroid injections into affected joints, opioids
  • Total joint replacement surgery in severe cases
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11
Q

Side Effects of the Meds Table 20.1

A

Acetaminophen: hepatic toxicity especially with ETOH, potentiation of warfarin

NSAIDS: nephrotic toxicity, GI bleeding, anticoagulation

Nonacetylated salicylates: ototoxicity

Opioid analgesics: N/V, constipation, confusion, drowsiness, resp. depression, addiction

Intra-articular corticosteroids: local discomfort, increase in blood glucose level,

Intra-articular hyaluronans: local discomfort, increase in synovitis

Topical NSAIDS: local skin irritation

Topical capsaicin: local skin irritation

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12
Q

Rheumatoid Arthritis (RA) (4 Q’s)

A
  • Autoimmune condition causing symmetrical inflammation of the joints —– Immune system targets synovial membrane of joints -> causes inflammation that leads to permanent damage, pain, and impaired function/movement R/T joint deformities
  • Genetic predisposition with environment triggers:
    • Happens 3x more often to women
    • Strong genetic predisposition - 1st degree relatives 1.5x more likely than general public
    • Environmental triggers can be things like bacterial infection, viral infection, cigarette smoke

MEDICATIONS:
- NSAIDS/Analgesics- help with pain, doesn’t prevent damage
- DMARDS- suppress the immune system to slow the rate it damages the joints (Side Effects= hepatotoxicity, immunosuppression, teratogenic, must be carefully dosed in the renal compromised

PRIORITY NURSING CONSIDERATIONS

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13
Q

Scleroderma (1 Q)

A
  • Causes unknown, possible autoimmune in nature
  • S&S: abnormal collagen production and depositing
    *Localized= patches of hardened skin, lines of thickened skin going full thickness and effecting organs breathing (leads to loss of elasticity/ movement, plus pain and itching)
    *Systemic= Lung, heart, kidney, musculoskeletal involvement (can affect so many different body systems and each body system would need to be managed specifically R/T individual issues in that system - so focus on the localized variant for this class

-TREATMENT: no one-size-fits-all. Uses immunosuppressant medications (corticosteroids or methotrexate). Topical ointments and moisturizers to soften skin and relieve itching/pain

PRIORITY NURSING CONSIDERATIONS

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14
Q

Systemic Lupus Erythematosus (SLE) (Lupus) (1 Q)

A
  • Systemic chronic inflammatory condition with periods of remission and flare-ups
  • S&S very from patient to patient
    *Makes diagnosis complicated, may take a long time for diagnosis to occur - a diagnosis of exclusion
    *A few to note: butterfly rash across the bridge of nose and checks after sun exposure or during a flare- up, urticaria/rashes, fatigue, fever, muscle pain and weakness, joint pain and weakness

TREATMENT
- Prevent flares- avoid sun and use high SPF sunscreen, good diet, lots of rest and good sleep, stress reduction
- Medication- focused on treating symptoms of the disease *Hydroxychloroquine frequently used (though we don’t fully know why it helps), others as needed to treat pain and/or suppress immune system

COMPLICATIONS: eventually leads to long-term damage of many different body systems: heart, kidneys, lung + problems from side effects of treatment like immunosuppression or medication toxicity

PRIORITY NURSING CONSIDERATIONS

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15
Q

Gout (5 Q’s)

A
  • Painful uric acid crystals depositing in joints
  • RISK FACTORS: obesity, HTN, thiazide diuretics, lifestyle (large amounts of red meat, organ meat, seafood, ETOH, high sugar foods/drinks
    *“Disease of the kings” because only the rich had access to risk factors
  • Patho: Uric acid accumulate in body D/T factors listed above. Uric acid in high concentration/ supersaturation settles out of solution as urate crystals into the soft tissue of joints like the toe (like sugar crystals formed in rock candy) Masses of spiky crystals causes the pain and the inflammatory process exacerbates it an causes the other symptoms. Eventually leading to joint damage and destruction
  • S&S: horrible pain, swelling, warmth, redness
    TREATMENT
  • Lifestyle changes: lose weight, avoid ETOH, change diet to have less red meat and triggering food/drink
  • Medication: Indocin or Colchicine during attacks to reduce symptoms, Allopurinol between attacks to prevent them
    *Allopurinol CAN’T be used during an attack - PREVENTATIVE ONLY. Allopurinol during an attack makes the pain and swelling and potential damage worse

PRIORITY NURSING CONSIDERATIONS

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16
Q

Fibromyalgia (1 Q)

A
  • Poorly-understood chronic pain disorder of connective tissue
  • S&S: widespread, diffuse pain and possibly symptoms like fatigue, stiffness, executive dysfunction
  • Seems to affect more women than men
  • May have genetic factors
  • Onset usually in middle adulthood

TREATMENT
- Lifestyle: physical therapy and exercise, cognitive-behavioral therapy, relaxation techniques and stress minimization
- Medications: brain chemistry modification meds like antidepressants, nerve pain medications like Lyrica, OTC pain medications
*OPIOIDS DO NOT WORK WITH THIS PAIN

*PRIORITY NURSING CONSIDERATIONS

17
Q

Muscular Dystrophy (3 Q’s)

A
  • Characterized by progressive muscle weakness, muscle wasting, and muscle breakdown
  • Many different subtypes:
    * Vary in severity
    * Vary in muscle groups effected
    * Vary age onset
  • Duchenne & Becker MD are the most severe forms and the most common in children
18
Q

*Duchenne & Becker MD

A
  • Caused by a mutation in the gene that produces the protein Dystrophin
  • Dystrophin strengthens and stabilizes muscle fibers
  • Without dystrophin, enzymes can break down muscle fibers
  • This breakdown leads to the muscle weakness and muscle wasting that MD is known for
  • S&S: progressive muscle weakness, chronic pain
  • Diagnosis: Monitoring muscle enzymes like CK and liver enzymes like ALT, AST can give us a clue… but the gold standard for diagnosis is a muscle biopsy
  • On microscopy, if MD is present, visible and obvious changes of the muscle tissue will be visualized.
19
Q

Duchenne Muscular Dystrophy (DMD)

A
  • Onset = 2-4 years

S&S
- Limb muscle weakness (proximal more than distal)
- Positive Grower’s sign (muscle weakness of the proximal muscles, more commonly seen in lower limbs
- Calf enlargement
- Leg pain
- Progressive scoliosis
- Equinovarus (clubfoot) deformities of the feet
- Mental retardation
- Progressive cardiomyopathy
- Respiratory failure

20
Q

Becker Muscular Dystrophy (BMD)

A
  • Delayed onset, slower progression
  • 5- 25 years of age

S&S
- Similar to DMD
- Muscle waisting affecting hips, pelvic area, thighs, and shoulders
- Calves enlarged
- Cardiac involvement less common, but if present, more severe
- Mental retardation less common

21
Q

Emery- Dreifuss Muscular Dystrophy (EDMD)

A
  • Delayed onset, slower progression
  • Usually
22
Q

Treatment of Muscular Dystrophy

A
  • Prevent progression of disease, support patient, manage pain
  • Glucocorticoids can slow disease progression but have a whole host. of side effects
  • Supplements can help (Coenzyme Q10, amino acids, antioxidants)
  • Psychosocial support
  • Supportive care focuses on functional ability - support mobility, avoid falls, RoM exercises, OT/PT support
  • NO CURE
  • Goal: avoid disability and maintain functional ability for as long as possible

PRIORITY NURSING CONSIDERATIONS/ DIAGNOSES

23
Q

Osteoporosis (5 Q’s)

A
  • Chronic condition in which bone density decreases with bones becoming fragile and prone to fracture
  • 10 million Americans have osteoporosis, 43 million have osteopenia (low bone density, but not severe enough to qualify as osteoporosis)

RISK FACTORS
- Primary (non-modifiable + lifestyle factors): age, postmenopausal, gender, family history, low Ca+ intake, low Vitamin D intake, inadequate nutrition, smoking, excessive ETOH, sedentary lifestyle, lows body weight
- Secondary (related to having another issue/concern): medications like long term corticosteroids, anticonvulsants, and thyroid medications. Medical conditions like hyperthyroid, RA, Cushings, inflammatory bowel diseases

24
Q

Osteoporosis

A

Patho:
- OsteoCLASTS and osteoBLASTS keep bone in homeostasis
- Clasts break down bone, (B)lasts (b)uild new bone
- If osteoclasts activity over rules osteoblast activity, you result in loss of bone density
- Bone density peaks between 25-30 yrs. then slowly decreases with age
- Decrease in bone density, fractures increase

S&S: None until they fall and break something - spine, hip, legs, arms
* “Silent disease”

25
Q

Osteoporosis Diagnosis

A
  • Dual - energy x-ray absorptiometry (DEXA) scan
  • Gold standard
  • Literally scans important weight- bearing bones and provides a density as compared to a young, healthy adult
  • Goal is to be within standard deviation
  • > 2.5 SD from the goal is osteoporosis, between 1 and 2.5 SD is osteopenia
26
Q

Osteoporosis Treatment

A
  • Healthy Lifestyle: weight-bearing exercise, no smoking, no drinking, good nutrition
  • Meds: can be really useful in preventing bone loss
  • Bisphosphonates: suppress osteoclast activity, which is useful in long-term but…
    *Take on empty stomach to absorb
    *Ton of GI issues (inflammation and erosion of esophagus, upset stomach
    *Remain upright for 1 hour after taking meds can help
    *Can be associated with a weird complication called osteonecrosis of the jaw, where your jaw rots inside of you.
27
Q

Osteoporosis Complications

A
  • FACTURES
  • Nursing considerations: keep patients from falling, keep activity and nutrition levels where they ought to be, medication administration and medication teaching
28
Q

Paget’s Disease (1 Q)

A
  • Disease of excessive bone remodeling that leads to bone that is structurally abnormal
  • Osteoclasts and osteoblasts both working at an increased rate, but not working in an organized way
  • Some areas of the bone you get weakness from excessive breakdown of bone and on other areas you have excessive deposits of bone that impede functionally

S&S
- Asymptomatic until severe
- When severe, pain and deformity in the affected bone

  • Treatment: no affective treatments for Paget’s disease
  • The goal is to reduce pain, increase mobility
  • Complications: bone deformities, pain, loss of functional mobility, fractures, bone tumor formation
29
Q

Scoliosis (3 Q’s)

A
  • Abnormal sideways curvature of the spine

S&S
- most obvious, sideways curvature of the spine >10 degrees
- pain, uneven shoulder blades, uneven waist, uneven hem line
- Severe: cardiopulmonary compromise

TREATMENT
- mild: conservative treatment- physical therapy/ occupational therapy, exercise regimen, pain management
*Exercise can reverse pain and curvature
- severe: surgery with rods and pins
*Wound healing is critical after surgery, so teach patients to wear prescribed brace, get adequate nutrition, stop smoking, avoid ETOH

30
Q

Total Joint Replacement Surgery (2 Q’s)

A
  • Take out the old worn out and damaged joint, replace it with a metal
  • Most commonly in knees, hips, and shoulders. Can be done in ankle, wrist, elbow
  • Lasts about 10-15 years
  • Indications: loss of function in the joint related to pain, deformity, tissue damage, etc
  • Osteoarthritis, rheumatoid arthritis, hx of traumatic injury to joint, avascular necrosis (death of bone related to trauma), ankylosing spondylitis
31
Q

TJRS Post-Surgery

A
  • Need for physical and occupational therapy to regain movement and functional ability
  • Pain control
  • Anticoagulant therapy (such as Lovenox)
  • Precautions that need to be taught to avoid damage to new joint *ESPECIALLY IN TOTAL HIP REPLACEMENT
  • HIP PRECAUTIONS
    *2-3 mo. do not allow flexion of >90 degree when sitting (raised toilet seats and no recliners), avoid crossing affected leg past midline, avoid moving affected leg out to the side, use walker until follow-up appointment
32
Q

Bone CA

A
  • Rare, only 1% of all cancers in the U.S.
    -In kids, Ewings sarcoma which is very malignant and deadly

S&S
- Similar to other musculoskeletal disorders and traumas
- Pain with motion that is unrelieved by rest, pain severe enough to cause a limp, swelling, redness, fracture, decreased RoM
- Management: surgery, chemo, radiation

Meg Surg 155-02 (5 decks)

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