1
Q
Q: Where are WBCs produced?
A
A: In the bone marrow.
2
Q
Q: What are the two main lymphocytes and their roles?
A
A: B cells (humoral response) and T cells (cell-mediated response).
3
Q
Q: What is the function of the spleen?
A
Acts as a filter:
Red pulp → removes old/injured RBCs
White pulp → stores lymphocytes.
4
Q
Q: What is the function of lymph nodes?
A
A: Filter lymph, remove foreign material before it enters the bloodstream.
5
Q
Q: What is natural immunity?
A
A: Nonspecific, first-line defense present at birth; immediate (minutes) or delayed (days).
6
Q
Q: What are the barriers of natural immunity?
A
A: Physical (skin, mucous membranes, cilia), chemical (mucus, gastric acid, tears, saliva enzymes, sweat).
7
Q
Q: What happens if natural immunity fails?
A
A: Host is considered immunocompromised.
8
Q
Q: What is acquired immunity?
A
A: Develops after exposure to an antigen (disease or vaccination); body “remembers” antigens for future defense.
9
Q
Q: What are the two types of acquired immunity?
A
Passive acquired (short-term, from immunization or maternal antibodies)
Active acquired (long-term, developed by person’s own immune system).
10
Q
Q: What are the three responses to invasion?
A
Phagocytic (ingests foreign particles, removes dead cells)
Humoral/antibody (B lymphocytes → antibodies)
Cellular (T lymphocytes → cytotoxic T cells).
11
Q
Q: What are the 4 stages of immune response?
A
A: Recognition → Proliferation → Response → Effector.
12
Q
Q: What do B lymphocytes do in humoral immunity?
A
A: Produce antibodies (may need help from T cells).
13
Q
Q: What conditions are associated with humoral responses?
A
A: Phagocytosis, anaphylaxis, allergies, immune complex diseases, bacterial/viral infections.
14
Q
Q: What do T lymphocytes recognize antigens with the help of?
A
Macrophages
15
Q
Q: What conditions are associated with cellular responses?
A
A: Transplant rejection, delayed hypersensitivity, graft vs host, tumor surveillance, intracellular infections (viral, fungal, parasitic).
16
Q
Q: What are Helper T cells (CD4) responsible for?
A
A: Secrete cytokines, activate B cells, cytotoxic T cells, NK cells, macrophages.
17
Q
Q: What are Cytotoxic T cells (CD8) responsible for?
A
A: Directly attack and destroy antigens.
18
Q
Q: What are Suppressor T cells responsible for?
A
A: Decrease B cell production to regulate immune response.
19
Q
Q: What is the function of Memory cells?
A
A: Recognize antigens from past exposure to mount faster immune responses.
20
Q
Q: What is the complement system?
A
A: A cascade of proteins in the inflammatory process that defend against bacteria, bridge natural/acquired immunity, and dispose of immune complexes.
21
Q
Q: What are autoimmune disorders caused by?
A
A: Defects in the complement cascade.
22
Q
Q: What are interferons?
A
A: Natural antiviral proteins that activate components of the immune system.
23
Q
Q: What are colony-stimulating factors?
A
A: Cytokines that regulate production and activation of hematopoietic cells.
24
Q
Q: What are monoclonal antibodies?
A
A: Lab-produced antibodies that target specific organisms, destroy pathogens while sparing normal cells.
25
Q: How does gender affect immunity?
A: Autoimmune disorders occur more often in females.
26
Q: How does aging affect immunity?
A: Increased illness and mortality risk.
27
Q: How does nutrition affect immune response?
A: Poor nutrition delays healing, worsens infections, and prolongs recovery.
28
Q: What infection/immunization history is assessed?
A: Childhood/adult vaccines, TB, STIs, hepatitis B/C/D, HIV, prior lesions/infections.
29
Q: What allergy information is important?
A: Types of allergens, symptoms, severity, seasonal variations, medication/food allergies.
30
Q: What disease history is assessed for immune function?
A: Autoimmune disorders, cancers, chronic illnesses (diabetes, renal disease, COPD), transplant or surgical removal of spleen, lymph nodes, thymus.
31
Q: Which meds can suppress immunity?
A: Antibiotics, corticosteroids, cytotoxic agents, salicylates, NSAIDs, anesthetics (large amounts).
32
Q: What other exposures must be documented?
A: Blood transfusions, OTC/herbal use.
33
Q: What lifestyle factors impair immunity?
A: Smoking, alcohol, illicit drugs, poor nutrition, extreme exercise, radiation/pollutant exposure.
34
Q: How does stress affect immunity?
A: Stress and psychological illness alter immune function through brain-immune system regulation.
35
Q: What diagnostic tests help evaluate immune status?
A: CBC with differential, immunoglobulin levels, allergy tests, imaging if indicated.
36
Q: What is the nurse’s role in managing immune disorders?
A: Provide education, support, and counseling; help reduce patient anxiety during diagnostic process.
37
Q: How is HIV transmitted?
A: Through body fluids, mother-to-child (delivery/breastfeeding), blood products, and sexual contact.
38
Q: What increases the risk of transmission?
A: Breaks in skin/mucosa, IV drug use, HIV-positive sexual partners, infants born to HIV+ mothers, organ transplant or blood products before 1985.
39
Q: What are gerontologic considerations for HIV?
A: Older adults are less likely to be tested, have weaker immune systems, engage in unprotected sex, and may have received transfusions before 1985.
40
Q: What are the key preventive strategies for HIV?
Safe sex (abstinence or condoms)
Partner viral load suppression before conception
Circumcision (reduced transmission risk)
Needle exchange programs
No breastfeeding if HIV+
Avoid hormonal contraceptives (higher HIV risk).
41
NI for HIV pt
Meticulous infection prevention: hand hygiene, enforce infection-control policies, continuous monitoring for early signs of infection
Education for immunodeficient patients: avoid skin breaks, no contact sports, avoid injury, maintain good dental care, practice coughing/deep breathing, avoid crowds, avoid sick people/children
Priority intervention: antibiotics must be given on time (NO late doses)
42
Q: What is PrEP and its purpose?
A: A daily pill with 2 HIV meds that prevents sexual HIV acquisition; requires HIV testing every 3 months.
43
Q: What is the prevention protocol for healthcare workers?
A: Post-exposure prophylaxis (PEP) within 72 hours.
44
Q: What are the 5 stages of HIV infection?
Stage 0: Initial infection, no antibodies yet.
Stage 1: CD4 high, highly contagious.
Stage 2: CD4 dropping, no AIDS-defining condition.
Stage 3: AIDS, very low CD4 + defining conditions.
Unknown: HIV confirmed but no CD4/AIDs info.
45
Q: What tests are used for HIV diagnosis?
Antibody tests (rapid/home, less reliable)
Antigen/antibody tests (blood test for both)
Nucleic acid (RNA) tests — most reliable.
46
Q: What is the purpose of viral load testing?
A: Measures amount of virus in blood; lower viral load = lower transmission risk, better survival, treatment effectiveness.
47
Q: What is the treatment goal for HIV?
A: Suppress the virus as much as possible.
48
Q: What are the main medications for HIV?
A: ART (antiretroviral therapy): NRTIs, NNRTIs, protease inhibitors, fusion inhibitors, integrase inhibitors, CCR5 antagonists.
49
Q: What are common side effects of HIV medications?
A: Bone marrow suppression, anemia, neutropenia, osteopenia, neuro/hepatotoxicity, skin rashes, diarrhea, body image changes.
50
Q: What is the patient education for ART?
A: Strict compliance; avoid alcohol and acetaminophen.
51
Q: What respiratory infections are common in HIV?
PCP (fungal pneumonia): chills, SOB, nonproductive cough; treat with sulfa drugs (bactrim).
TB: risk high in IV drug users, homeless; test HIV+ pts for TB.
52
Q: What GI complications occur in HIV?
Diarrhea (Sandostatin/Octreotide injection helps)
Wasting syndrome (weight loss, malabsorption, muscle wasting; treat with nutrition, supplements, THC meds- marinol, magace).
53
Q: What are common cancers in HIV patients?
Kaposi’s Sarcoma (purple/brown lesions, most common malignancy, treated with chemo/radiation).
AIDS-related lymphoma (aggressive, outside lymph nodes, poor prognosis).
54
Q: What neurologic complication is linked to HIV?
Cryptococcus neoformans meningitis — fever, headache, stiffness, seizures; treated with IV amphotericin B (nephrotoxic, hepatotoxic).
55
Q: What psychosocial issue is common in HIV patients?
A: Depression due to chronic illness, body image issues, and isolation.
56
Q: What skin complication is linked to HIV?
A: Candidiasis (white patches in mouth/esophagus, vaginal infections).
57
Q: What gynecologic conditions are HIV+ women at higher risk for?
A: PID and cervical cancer.
58
Q: What should be assessed in HIV patients?
A: Nutritional status, skin integrity, respiratory status, neuro status, fluid/electrolytes, knowledge level, and risk factors.
59
Q: What are common nursing diagnoses for HIV/AIDS?
A: Risk for infection, activity intolerance, impaired skin integrity, ineffective airway clearance, imbalanced nutrition, social isolation, grief.
60
Q: What are key nursing interventions for HIV/AIDS?
Promote skin integrity
Prevent infection (timely antibiotics, NO late doses)
Relieve pain/discomfort
Encourage rest/conserve energy
Improve nutrition
Reduce isolation
Support coping and grief.
61
Q: What are major complications of HIV/AIDS?
A: Opportunistic infections, respiratory failure, wasting syndrome, med side effects, body image changes.
62
Q: What immunoglobulin is responsible for allergic responses?
A: IgE – elevated in allergic reactions
63
Q: What is the function of antigens in allergic disorders?
A: Trigger immune responses when recognized as foreign (noted in hypersensitivity reactions).
64
Q: What are the 2 types of chemical mediators?
Primary mediators: Histamines from mast cells → redness, swelling, itching; treated with H1 antihistamines like Benadryl
Secondary mediators: Released later to sustain inflammation
65
Q: What is a Type I reaction?
A: Anaphylactic; most severe, rapid onset, can last up to 24 hrs
66
Q: What is a Type II reaction?
A: Cytotoxic; body mistakes a normal body part as foreign (seen in blood transfusions, hemolytic anemia)
67
Q: What is a Type III reaction?
A: Immune complex (e.g., lupus, rheumatoid arthritis), can damage organs especially kidneys
68
Q: What is a Type IV reaction?
A: Delayed-type (24–72 hrs); itching, redness, raised lesions, e.g., poison ivy
69
Q: What assessment is needed for allergies?
A: Ask about allergens, symptoms, severity, and seasonal variations
70
Q: What diagnostic tests are used for allergies?
A: CBC with differential (↑ eosinophils), serum IgE level, skin tests (stop allergy/steroid meds 48–96 hrs before), provocative testing, serum specific IgE test
71
Q: What is the pathophysiology of anaphylaxis?
A: Type I reaction; rapid IgE release triggered by allergens (e.g., insect stings, latex, contrast dye, antibiotics)
72
Q: What are the clinical manifestations of anaphylaxis?
Mild: tingling, throat itching, watery eyes
Moderate: anxiety, flushing, wheezing, edema
Severe: dyspnea, cyanosis, hypotension, cardiac arrest
73
Q: How can anaphylaxis be prevented?
A: Avoid allergens, allergy shots, carry EpiPen, education
74
Q: What is the medical/nursing management of anaphylaxis?
A: Administer epinephrine (EpiPen) go to ER after, vasopressors, steroids, antihistamines; immediate hospital care
75
Q: What type of hypersensitivity is atopic dermatitis?
A: Type I reaction
76
Q: How is atopic dermatitis managed?
A: Antihistamines, topical corticosteroids, cotton fabrics, hand hygiene, monitor for infection from scratching
77
Q: What type of hypersensitivity are drug reactions?
A: Type I
78
Q: What are the 3 most common drugs causing dermatitis medicamentosa?
A: Penicillin, sulfa drugs, cephalosporins
79
Q: What is the key management for dermatitis medicamentosa?
A: Rash resolves when med is stopped, but can progress to anaphylaxis
80
Q: What type of hypersensitivity is food allergy?
A: Type I
81
Q: What foods are most commonly responsible for food allergy?
A: Seafood, peanuts, tree nuts, wheat, berries, eggs, milk, chocolate
82
Q: How are food allergies managed?
A: Avoid allergens, use antihistamines, corticosteroids, and carry an EpiPen
83
Q: What patient education is important?
A: Recognize anaphylaxis, know how/when to use an EpiPen, avoid cross-contamination, always read food labels
84
Q: Who is at high risk for latex allergy?
A: Healthcare workers, factory workers, police, hairdressers, patients with spina bifida
85
Q: What foods may cross-react with latex allergy?
A: Bananas, pineapples, avocados
86
Q: What are clinical manifestations of latex allergy?
A: Contact dermatitis, redness, itching, possible anaphylaxis
87
Q: How is latex allergy diagnosed and managed?
A: Diagnosis: skin patch testing.
Management: strict avoidance, medical alert identification
88
Q: What are the 3 key mechanisms in rheumatic diseases?
A: Inflammation, autoimmunity, and degeneration
89
Q: What symptoms are assessed in rheumatic diseases?
A: Pain, joint swelling, limited movement, stiffness, weakness, and fatigue
90
Q: What lab tests are used?
A: CBC, ESR, CRP, BUN, urinalysis, calcium, alkaline phosphatase, LFT, ANA (positive = autoimmune)
91
Q: What other diagnostics are used?
A: X-ray, MRI, CT
92
Q: What is the patho of RA?
A: Immune system attacks joints → pain, swelling, stiffness
93
Q: Key manifestations of RA?
A: Symmetric joint pain, morning stiffness >1 hr, swelling, redness, warmth, nodules, loss of function
94
Q: Diagnostics for RA?
A: CRP, ANA, arthrocentesis (cloudy synovial fluid)
95
Q: Medications for RA?
DMARDs: Methotrexate (watch for infection, immunosuppression, toxicity; NO live vaccines)
NSAIDs: Ibuprofen, others for inflammation
Corticosteroids for symptom control
96
Non-pharmacologic management for RA
Encourage exercise and activity to maintain mobility, and help patients develop regular sleep patterns in a quiet environment
97
If DMARD dose increases for RA tx....?
closely monitor for immunosuppression or toxicity
98
Q: Who is most at risk for SLE?
Women
99
Q: Key manifestations of SLE?
A: Butterfly rash, fever, Raynaud’s, weight loss, alopecia, joint pain/swelling, HTN, kidney problems
100
Q: Diagnostics for SLE?
A: ANA+, BUN/creatinine, urinalysis
101
Q: Medications for SLE?
Methotrexate (monitor infection; immunosuppression risk)
Steroids to control inflammation
Nursing: Avoid sun (triggers exacerbations), monitor kidney function
102
NI for SLE
Monitor kidney function (BUN, creatinine, urine output) since nephron damage is common
Avoid sun exposure to prevent exacerbations
103
Q: What is scleroderma?
A: Build-up of fibrous tissue in skin → skin tightening, fingers curl
104
Q: Key manifestations of scleroderma?
A: Raynaud’s, hard/dry skin, no wrinkles, mask-like face
105
Q: Diagnostics & Management of scleroderma?
A: No specific test; X-rays for organ involvement. No modifying meds; treat symptoms, focus on exercise and skin care
exercise and skin care to maintain mobility and circulation
Raynaud’s: Teach to wear gloves in cold settings
106
Q: What causes gout?
A: Uric acid >6.8 mg/dL (protein breakdown); immune system reacts
107
Q: Risk factors for gout?
A: Age, high BMI, alcohol, HTN, diuretic use, males
108
Q: Key manifestations of gout?
A: Abrupt pain, redness, swelling (esp. big toe); attacks last 3–10 days, recurrent
109
Q: Diagnostics for gout?
A: Synovial fluid with uric acid crystals
110
Q: Medications for gout?
Colchicine for acute attack (↓ uric acid, ↓ pain)
Allopurinol for long-term maintenance
NSAIDs, steroids as needed
Lifestyle: ↓ alcohol, weight loss, diet modification
111
NI for gout
Nursing management: Reinforce lifestyle modifications (reduce alcohol, encourage weight loss)
Encourage dietary changes (avoid purine-rich foods such as meats)
112
Q: What is fibromyalgia?
A: Chronic pain syndrome, non-inflammatory, neurologic/psych-related, pain in multiple areas
113
Q: Management of fibromyalgia?
NSAIDs for pain
Antidepressants to help with symptoms
Exercise programs to reduce stiffness
114
Q: What are the major functions of the skin?
A: Protection, sensation, fluid balance (prevents excess water/electrolyte loss; ~600mL/day insensible loss), and vitamin D synthesis from sun exposure
115
Q: What are gerontologic skin considerations?
A: Dryness, wrinkles, diminished hair growth; higher damage risk with sun, systemic disease, poor nutrition, and thinning skin junctions
116
Q: What should be asked in skin history?
A: Medications, allergies, systemic disease history, sun exposure, nutrition, and family history.
117
Q: What skin, hair, and nail changes are significant?
Skin: rashes, lesions, vitiligo (white patches)
Vascularity/hydration: assess for dryness, fragile skin
Nails: spoon nails (iron deficiency), clubbing (COPD/hypoxia, smoking)
Hair: loss or diminished growth in older adults
118
Q: What skin findings are associated with diabetes?
Dermopathy: “shin spots” (brown, scaly, bilateral).
Stasis dermatitis: ↓ blood flow, fragile/dry skin, ulcers.
Skin infections: folliculitis → carbuncles if BG uncontrolled
119
Q: What skin conditions are linked with HIV?
A: Kaposi’s sarcoma, viral/bacterial infections.
Nursing note: Educate patients that acute flare-ups of chronic skin conditions may indicate new infection → notify PCP
120
Q: What is the purpose of a skin biopsy?
A: Rules out malignancy, used for diagnosis
121
Q: What does a skin scraping test for?
A: Infection/infestations
122
Q: What is Wood’s light examination used for?
A: Detects fungal or pigmentary changes
123
Q: What are other diagnostic tools?
A: Patch testing (allergies), Tzanck smear (zoster, varicella, simplex)
124
Q: What are nursing priorities for skin care?
Protect skin (mild lipid-free soaps, blot dry, avoid harsh detergents).
Prevent secondary infection (wear gloves for dressings, proper disposal).
Match treatment to skin state: dry/scaly = creams/ointments; hot/inflamed = cool soothing ointment
Teach self-care: apply meds/dressings correctly, assess wound (color, smell, drainage)
125
Q: What meds are used for skin management?
- Corticosteroids: reduce inflammation; taper pack; avoid use on face/eyes (risk for glaucoma, cataracts); may mask fungal infection
- Antihistamines: relieve pruritus/itching
Moisturizers: prevent dryness
- SSRIs: sometimes used for chronic pruritus
- Lidocaine (topical): pain/itch relief
Side Effects:
- Corticosteroids: risk of glaucoma, cataracts, fungal infection.
- Antihistamines: sedation, dry mouth.
- SSRIs: GI upset, sexual dysfunction, serotonin syndrome (rare).
- Topical lidocaine: possible local irritation, systemic toxicity if overused.
126
Q: What are nursing tips for managing pruritus (itching)?
A: Warm (not hot) baths, blot dry, avoid scratching, apply ointment/lotion, cold compresses, wear cotton clothes, avoid spicy foods/alcohol
127
Q: What’s the nurse’s main priority for skin care and how?
A: Protect skin with mild lipid-free soaps, rinse well, blot dry, avoid heavy deodorant soaps & detergents. Match product to skin state: dry/scaly → creams/ointments; hot/inflamed → cool soothing ointment.
128
Q: How do we prevent secondary skin infection in wound care?
Wear gloves for dressings and ensure proper disposal; teach self-care for medication and dressing application; if a dressing is removed, assess color, smell, consistency, amount of drainage.
129
Q: Which meds are used to calm inflammation in skin conditions and key cautions?
Corticosteroids—use as ordered, taper, avoid face/eyes (risk glaucoma/cataracts), can mask fungal infections
130
Q: What are some debridement types?
Natural: no intervention; takes weeks–months.
Mechanical: during dressing changes; wet-to-damp.
Chemical: topical enzymes.
Surgical: operative removal
131
Q: What are the types and categories of dressings?
Types: Passive (protect/moist—e.g., DuoDERM, Tegaderm), Interactive (absorb exudate—hydrocolloids, hydrogels), Active (improve healing—skin grafts, biologic dressings).
Categories: Occlusive (airtight film, often medicated, ~12 hr), Wet (rare; inflamed skin, cools), Moisture-retentive (interactive; saline/antibiotics, infrequent changes up to 2 weeks)
132
Q: Which meds are listed for wound/skin management and key cautions?
A: Corticosteroids (taper; avoid face/eyes; mask fungal infxn). Education: fragrance-free lotions/creams.
133
Q: What specific wound-care teaching points should nurses include?
A: Teach application of meds/dressings, washing wound, and after removing dressings assess color/smell/consistency/amount of drainage.
134
Q: Why is pruritus clinically important?
A: It may be the first sign of systemic disease (CKD, liver, thyroid).
135
Q: What meds relieve pruritus?
A: Antihistamines, skin moisturizers, SSRIs, topical lidocaine. (SE to know from set: antihistamines can sedate; topical lidocaine can irritate if overused.)
136
Q: What non-drug measures help itching?
A: Warm (not hot) baths, avoid heat, blot dry, no scratching, apply ointment/lotion, cold compresses, cotton clothing, mild soap, avoid spicy foods & alcohol.
137
Patho of Seborrheic Dermatoses
Excess sebum production; influenced by genetics, hormones, stress, infection, nutrition. Common on face, scalp, axillae, skin folds. Oily (greasy patches) & dry (dandruff) forms.
138
Mgmt of Seborrheic Dermatoses
Medicated shampoos, rotate 2–3 kinds, leave 5–10 min 3×/week; may use corticosteroids for relief.
Nursing: no cure; avoid irritants/heat, avoid rubbing/scratching; air-dry; chronic.
139
Herpes Zoster (Shingles) patho
Latent VZV reactivates; risk ↑ with age, low cellular immunity, immunosuppression
140
S/S herpes
Unilateral red rash with fluid-filled blisters, pain, pruritus; common on face & trunk;
major complication post-herpetic neuralgia.
141
medical mgmt of herpes
Start within 24 h of eruption/within 72 h of onset; acyclovir, valacyclovir, famciclovir
For pain gabapentin, topical lidocaine; corticosteroids to prevent complications
vaccinate ≥50.
142
Nursing Mgmt/Teaching of herpes
Not spread person-to-person by air; spread is via direct contact with fluid; once crusted → not infectious. Cover area, hand hygiene, avoid infants, pregnant women, immunocompromised until crusted.
143
Contact dermatitis
Type IV (delayed) hypersensitivity triggered by skin contact with an allergen/irritant such as soaps and detergents; usually not systemic.
144
Clinical manifestations of dermatitis
Itching, burning, skin lesions, edema.
145
Assessment/Diagnostics dermatitis
Patch test (can be difficult) to identify the culprit.
146
Medical & Nursing management of dermatitis
Protect the skin: use mild lipid-free soaps, rinse well & blot dry, avoid heavy deodorant soaps/laundry detergents.
Prevent secondary infection / match product to skin state: dry/scaly → creams/ointments; hot/inflamed → cool, soothing ointment
If anti-inflammatory meds are ordered: corticosteroids—taper, avoid face/eyes (risk glaucoma/cataracts), can mask fungal infection. (Use exactly as prescribed.)
147
Psoriasis patho and s/s
Patho/Triggers: Chronic, non-infectious inflammatory skin disease; stress/anxiety triggers.
Clinical Manifestations: Red, raised plaques with silvery scales, ± pruritus.
148
Med Mgmt of Psoriasis
Topicals: Corticosteroids (gently remove scales with moisture/soft brush; occlude ≤8 h; low-potency on face to avoid thinning), NSAIDs (slow skin growth), calcipotriene + betamethasone, salicylic acid, coal tar, intralesional injections.
Retinoid: Tazorac—contraindicated in pregnancy/child-bearing age.
Systemic: Methotrexate (1st-line moderate/severe; no alcohol, no pregnancy, hepatotoxicity), Cyclosporine (HTN, kidney issues, short-term only).
149
Nursing/Teaching of Psoriasis
Watch skin integrity; facial ointments can cause cataracts; address body-image/sexual disturbance; prevent flare-ups, check with MD before OTC.
150
S/s of BCC
Small, waxy nodule with a rolled, translucent “pearly” border; occurs on sun-exposed sites (face, neck, hands, scalp); rarely metastasizes
151
S/s of SCC
Rough, thickened, scaly tumors that may bleed; common on face, lower lip, ears, nose, forehead, upper extremities; metastasizes via blood/lymph.
152
Medical mgmt of BCC
Surgical excision, Mohs, electrosurgery, cryosurgery, radiation; follow-up every 4–6 months.
153
Medical mgmt of SCC
Mohs, cryosurgery, radiation; follow-up every 4–6 months
154
Nursing mgmt for skin cancer
- Sun protection & surveillance: Teach high-SPF sunscreen use and monthly self-skin checks; stress that early-childhood sunburns increase future risk; review high-risk groups (e.g., <30 and >50, many nevi, immunosuppressed, outdoor workers).
- After treatment: Reinforce the need for regular 4–6 month follow-ups per provider plan.
155
Melanoma
- Most lethal
- Atypical cells in epidermis + dermis; risks include sun exposure/tanning beds, genetic factors
- Common on hands/feet/scalp; torso lesions metastasize more.
- Lesions circular, multi-color, mole changes (size/color), bleed easily;
- Diagnosis: biopsy with 1 cm margin.
- ABCDEs
156
Topical antimicrobials commonly used on burn/wounds
silver sulfadiazine 1%, mafenide acetate 5–10% (very painful), silver nitrate 0.5%. (Topicals penetrate eschar, gram+/− coverage, not systemically toxic.)
157
Dressings over grafts
Apply topical agents → several layers of dry dressings; light dressings over joints; fingers/toes dressed individually; face wounds left open to air.
Occlusive gauze dressings (impregnated with antibacterial) may be used. Leave graft dressings on 3–5 days to allow microcirculation growth.
158
Care of the graft site
Immobilize and create humid environment; 1st dressing change at 3–5 days; begin exercise 5–7 days after grafting.
Donor site: moist dressing, thrombostatic agent, very painful, infection risk, heals 7–14 days.
159
Q: What gerontologic changes increase burn risk/severity?
A: Decreased sensation/coordination increase risk; thinning skin & ↓ elasticity increase morbidity/mortality in older adults.
159
Graft/biologic options
- Autograft (own skin)
- CEA
- homograft/allograft (cadaver; best infection control but expensive)
- Xenograft/heterograft (pig skin; used for deep burns; ↓ infection, ↓ fluid/protein loss, ↓ contractures; cosmetic/psych benefits)
160
Q: Who experiences burn injuries most often (incidence)?
Burns occur most often in males.
161
Q: What home prevention teaching should you give?
A: Change smoke-detector batteries annually; keep lighters/matches from kids; set water heater ≤120°F; don’t run cords under rugs; keep a fire extinguisher; never pour flammables on fires.
162
Q: Early outlook for survival: the top immediate killer and key risk factor?
A: Pulmonary injury is the most common cause of death at the scene; mortality risk relates to hypoxemia (and age).
163
Q: What determines burn severity?
A: Age, depth, extent (TBSA), inhalation injury, location, past medical history.
164
Q: Define superficial (1st-degree) burns.
A: Epidermis only; sunburn/low-intensity flash; painful, red, minimal edema; heals in days.
165
Q: Define partial-thickness (2nd-degree) burns (cause/S&S/healing).
A: Epidermis + part dermis; scalds/flash flame; painful, red, blisters, cold-air sensitive, edema; heals in 2–3 weeks.
166
Q: Define full-thickness (3rd–4th-degree) burns (cause/S&S/healing).
A: Epidermis + dermis ± subQ; flame/hot liquids/electric/chemicals; often painless, white/leathery, no blanching; months to heal. 4th-degree extends to muscle/bone/fat, often amputation.
167
Q: What is the Rule of Nines for TBSA?
A: Anterior trunk 18%, posterior 18%, each arm 9%, head 9%, each leg 18%, genitals 1%.
168
Q: When do you refer to a burn center?
A: ≥10% partial-thickness, any face/hands/feet/genitalia/major joints, third-degree, electrical/chemical, inhalation, trauma, children.
169
Q: Key cardiovascular alterations after burns?
A: Cardiac depression, edema, hypovolemia, circulatory issues; risk of compartment syndrome → remove eschar or fasciotomy.
170
Q: Typical fluid & electrolyte shifts?
A: Early hyperkalemia → later hypokalemia, hyponatremia, hemoconcentration.
171
Q: Hallmark pulmonary concerns and S/S of inhalation injury?
A: Pulmonary injury is the leading early killer; S/S: burned nasal/facial hair, SOB, red-tinged throat, stridor, swollen neck, with symptoms delayed 24–36 h; upper airway = heat/edema; lower = chemical irritation.
172
Q: Key renal risk after severe burns?
A: Rhabdomyolysis may occur.
173
Q: Major immunologic risk?
A: Wound infection → septic shock; GI tract is a major source of bacteria.
174
Q: Thermoregulatory concern during care?
A: Prevent hypothermia by maintaining water & room temperature during wound care.
175
Q: Key GI complications to watch for?
A: Paralytic ileus; Curling’s ulcer (watch for coffee-ground emesis/melena).
176
Q: Initial ED medical management?
A: 100% humidified O₂; encourage coughing/bronchial suction; large-bore IV (LR); ensure sheets not sticking; place catheter and NG for decompression.
177
Q: What are on-the-scene priorities (ABCDE)?
A: Airway, breathing, circulation, disability, examine; extinguish flames, loosen/remove restrictive items, cool the burn, cover wound, irrigate, keep NPO, position to prevent aspiration.
178
Q: What urine output targets guide resuscitation?
A: Thermal/chemical: 0.5–1 mL/kg/hr; electrical: 75–100 mL/hr.
179
Q: What clinical endpoints suggest adequate fluids in the first 24 h?
A: Use patient response: pulse <110, SBP >100, T >95°F, adequate UOP.
180
Q: Emergent-phase nursing priorities?
A: First aid, prevent shock & respiratory distress, treat other injuries, wound assessment & initial care.
181
Overall goals in Acute/Intermediate Phase (≈ 48–72 h post-burn)
A: Maintain respiratory & F/E, wound care/closure, prevent/treat complications.
182
Q: High-yield infection prevention steps?
A: Burns may progress to septic shock; bacteria under eschar; GI is major source. Use cap/gown/mask/gloves, clean hydrotherapy, take cultures (admission/each cleaning/PRN), no prophylactic antibiotics, control hyperglycemia (insulin).
183
Q: Key steps in wound cleaning?
A: Remove non-viable tissue/exudate/topicals; premedicate with narcotics; mild soap + water; clip/shave hair (not eyebrows); encourage activity; maintain water & room temp; hydrotherapy as ordered.
184
Q: Core dressing principles?
A: Apply topical, then several layers dry dressings; light over joints; separate fingers/toes; face left open to air; occlusive antibacterial gauze options; leave skin-graft dressings on 3–5 days.
185
Q: What debridement methods are listed?
A: Natural (weeks–months), mechanical (wet-to-damp, during dressing changes), chemical (topical enzymes), surgical.
186
pain management of burns
A: IV bolus morphine pre-procedure; IV PCA morphine, fentanyl, MS-Contin, oxycodone ER, benzodiazepines; Ativan/Versed for sedation; NSAIDs; non-pharm adjuncts.
187
Q: How do we modulate hypermetabolism/nutrition?
A: Need up to 5000 kcal/day; calories double/triple days 4–12; ~60% carbs, limit fats; tube feeds/TPN PRN; keep room temp; insulin therapy; oxandrolone (Oxandrin); beta-blockers.
188
Q: How do you restore normal fluid balance?
A: Daily weights; monitor urine output; diuresis usually begins 48–72 h post-burn.
189
Q: Best practices to prevent infection?
A: PPE (cap/gown/mask/gloves), clean hydrotherapy, frequent cultures, no prophylactic ABX, control hyperglycemia.
190
Q: How to promote skin integrity?
A: Follow wound cleaning, topicals, and dressing steps; protect grafts; separate digits to prevent adhesions.
191
Q: How to relieve pain & discomfort?
A: Use the analgesia/sedation regimen above and premedicate before procedures.
192
Q: How to promote physical mobility & prevent contractures?
A: Encourage activity during treatments; exercise starts 5–7 days post-graft; xenografts help prevent contractures.
193
Q: Safe unit placement & VAP prevention tips?
A: Place chest-burn/smoke-inhalation patients near the nurses’ station; prevent VAP with oral care, repositioning, sitting up.
193
Q: Name common complications to anticipate in this phase.
A: Airway obstruction (≤48 h), VAP, septic shock; respiratory mucosal slough 3–4 days (team may use aerosol heparin).
194
Q: When does rehab begin and what’s the aim?
A: Immediately, continues for years; after major wound closure, aim for optimal physical & psychosocial function.
195
Q: What abnormal wound healing should you teach about?
A: Hypertrophic scars (esp. joints: red/raised/hard), keloids, contractures (also linked to infection, shearing, pressure, poor nutrition).
196
Q: High-yield home-care teaching from your notes?
A: Correct topical/dressing application; monitor for infection (erythema, warmth, tenderness, malodorous exudate); maintain room/water temp during care.
197
Q: Which topical antimicrobials are used for burn wounds?
A: Silver sulfadiazine 1%, mafenide acetate 5–10% (Sulfamylon—extremely painful), silver nitrate 0.5%; all penetrate eschar, not systemically toxic, effective vs gram +/−, no single agent preferred.
198
Q: What are some analgesia/sedation meds?
A: Morphine IV bolus/PCA, fentanyl, MS-Contin, oxycodone ER, benzodiazepines, Ativan/Versed, NSAIDs.
199
Q: Which hypermetabolism supports/meds are listed?
A: Up to 5000 kcal/day; ~60% carbs, limit fats; tube feeds/TPN PRN; room temp; insulin, oxandrolone (Oxandrin), beta-blockers.
MS2
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