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ADN 9 Transition to Practice > FINAL: Sepsis, Burns, HIV & Neuro > Flashcards

FINAL: Sepsis, Burns, HIV & Neuro Flashcards

1
Q

Anaphylactic Shock: Pathophysiology & Possible Causes

A

Pathophysiology:
- Severe allergic reaction in patient who already produced antibodies to antigen
- IgE response
- Causes widespread vasodilation

Causes:
- Foods (especially peanuts)
- Medications
- Insect stings & bites

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2
Q

Cardiogenic Shock: Pathophysiology & Possible Causes

A

Pathophysiology:
- Inability of the heart to pump blood
- Supply of oxygen is inadequate for the heart & tissues
- CO, SV, HR decrease

Causes:
Coronary: Acute MI
Noncoronary:
- Hypoxemia
- Hypoglycemia
- Hypocalcemia
- Acidosis
- Tension PTX
- Cardiomyopathy
- Dysrhythmias
- Cardiac tamponade
- Valvular damage

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3
Q

Hypovolemic Shock: Pathophysiology & Possible Causes

A

Pathophysiology:
Decreased intravascular volume from excessive fluid loss

Causes:
- Excessive fluid loss
- Blood loss
- Diuresis
- Vomiting/diarrhea
- Burns
- DKA

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4
Q

Neurogenic Shock: Pathophysiology & Possible Causes

A

Pathophysiology: Loss of sympathetic tone (increased parasympathetic) causing vasodilation, leading to hypovolemia

Causes:
- Nervous system damage
- SCI
- Epidural anesthesia
- Depressants
- Lack of glucose (i.e. insulin reaction)

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5
Q

Septic Shock: Pathophysiology & Possible Causes

A

Pathophysiology: Widespread sepsis or infection leading to hypovolemia

Causes:
- Bacteremia
- Pneumonia
- Urosepsis
- Wounds, foleys, central lines

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6
Q

Compensatory Stage of Shock: Manifestations

A
  • BP normal (cap refill normal)
  • Vasoconstriction: ⬆ HR > 100 bpm, ⬆ heart contractility
  • Body shunts blood from skin, kidneys, GI to vital organs (brain, heart, lungs):
    - Cold, clammy skin
    - ⬇ UOP
    - Hypoactive bowel sounds
  • Acidosis from anaerobic metabolism
  • ⬆ RR > 22 ➡ compensatory resp. alkalosis
  • Confusion possible
  • Hyperglycemia (⬆ catecholamines & cortisol)
  • Hypernatremia (RAAS activation: reabsorb sodium & water)
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7
Q

Compensatory Stage of Shock: Treatment

A
  • Oxygen
  • IV fluids
  • Blood cultures for suspected infection, antibiotic treatment
  • Assess LOC, V/S, UOP, skin, RR, & labs
  • Monitor hemodynamic status, report low BP
  • Continuous central venous oximetry
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8
Q

Progressive Stage of Shock: Manifestations

A
  • Systolic BP < 100; MAP < 65
  • ⬆ HR > 150 bpm
  • Rapid, shallow respirations; Crackles
  • Pulmonary edema; Hypoxemia
  • Mottling, petechiae, ecchymosis; DIC
  • Capillary refill > 3.5 s
  • Lethargy
  • Metabolic acidosis (anaerobic metabolism continues)
  • AKI (⬇ MAP ⬇ GFR)
  • Stress ulcers (risk for GI bleeding; GI ischemia)
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9
Q

Progressive Stage of Shock: Treatment

A
  • Monitor hemodynamics, ECG, ABGs, electrolytes, physical & mental status changes
  • Enteral nutritional support
  • Target hyperglycemic control with IV insulin
  • Reduce risk of GI bleeds (antacids, H-2 blockers, antipeptic meds)
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10
Q

Irreversible Stage of Shock: Manifestations

A
  • BP requires support
  • Erratic HR
  • Respirations require intubation, ventilation, oxygenation
  • Jaundiced (liver fxn fails)
  • Anuric; requires dialysis (renal fxn fails)
  • Unconscious
  • Profound acidosis (anaerobic metabolism worsens acidosis)
  • MODS ➡ MOFS
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11
Q

Irreversible Stage of Shock: Treatment

A

Does not respond to treatment; cannot survive

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12
Q

Risks & Treatment for Each Stage of Shock (4): All Types

A
  1. Support respiratory system
  2. Fluid replacement
  3. Vasoactive meds
  4. Nutritional support
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13
Q

Risks & Treatment for Each Stage of Shock: Fluid Replacement

A
  • Crystalloids: 0.9% NS, LR
  • Colloids: Albumin, dextran
  • Blood components
    Rapid crystalloids 30 ml/kg for hypotension or lactate >4
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14
Q

Risks & Treatment for Each Stage of Shock: Medications

A
  • Inotropic agents (dobutamine, dopamine, epinephrine)
  • Vasodilators (nitroglycerin, nitroprusside)
  • Vasopressors (phenylephrine, dopamine, nor/epinephrine, vasopressin)
  • Analgesics (morphine)
  • PPIs (pantoprazole)
  • Anticoagulants (LMWH)
  • Antihistamines (Benadryl)
  • Corticosteroids
  • Antibiotics
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15
Q

Risks & Treatment for Each Stage of Shock: Nutritional Therapy

A
  • Nutritional support needed to ⬆ metabolic & energy requirements
  • Parenteral or enteral nutrition
  • Administration of PPIs or H-2 blockers to prevent stress ulcers
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16
Q

Identify the rationale for nutritional needs in the patient with shock.

A

⬆ metabolic rates during shock ➡ ⬆ energy & caloric requirements

  • Release of catecholamines causes rapid depletion of glycogen stores
  • Energy met by breaking down lean body mass (skeletal muscle), instead of body fat
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17
Q

Identify MODS and the treatment options (4).

A

MODS:
- Altered function of two or more organs in an acutely ill patient
- Interventions necessary to support organ function

Treatment:
- Control initiating event
- Promote adequate organ perfusion
- Provide nutritional support
- Maximize patient comfort

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18
Q

Describe the risks & prevention for sepsis.

A

Risks:
- Older adults
- Malnutrition, immunosuppressive
- Undergoing surgery or invasive procedure
- Chronic illness (i.e. diabetes, hepatitis, CKD, immunodeficiency)
//
- Bacteremia, pneumonia, urosepsis
- Intra-abdominal infections, wound infections, catheters

Prevention:
- Fluid replacement
- Broad-spectrum antibiotics ➡ more specific ones
- Nutrition therapy

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19
Q

Sepsis Treatment: 1 hour bundle

A
  • Measure lactate
  • Blood cultures before broad-spectrum antibiotic therapy
  • Rapid crystalloids 30 ml/kg for hypotension or lactate > 4
  • Vasopressors if hypotensive during or after fluid resuscitation to maintain MAP > 65

Assessment Tools:
- Sepsis-Related Organ Failure Assessment (SOFA)
- Modified Early Warning System (MEWS)

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20
Q

Sepsis Treatment: 3 hour bundle

A
  • Remeasure lactate
  • Obtain blood culture before administering antibiotics (Blood cultures x 2)
  • Broad spectrum abx
  • IV fluids if hypotensive or lactate > 4
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21
Q

Sepsis Treatment: 6 hour bundle

A
  • Vasopressor if hypotensive (MAP < 65) AFTER IV fluid bolus
  • Repeat lactate if initial > 2
  • MD reassess volume status & tissue perfusion
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22
Q

List prevention strategies for burns in the community setting.

A
  • Matches, lighters, hot irons kept out of reach from children
  • Never leave children unattended around fire hazards
  • Smoke & CO detectors in home, change batteries annually
  • Home exit fire drill with all household members
  • Have a fire extinguisher
  • Avoid overhead electrical wires & underground wires when working outside
  • Store flammable liquids away from fire source
  • Be aware of loose clothing when cooking over a stovetop
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23
Q

Superficial thickness burn

A

1st degree burn

  • Painful
  • Does not blister or scar
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24
Q

Partial or intermediate-thickness burn

A

2nd degree burn

  • Blisters & weeps
  • ⬆ Depth ➡ ⬆ Risk of infection & scarring
  • Deep partial thickness requires surgery
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25
Q

Full thickness burn

A

3rd degree burn

  • Dry
  • Insensate to light touch & pin prick
  • Small areas will heal with substantial scar
  • Large areas require skin grafting
  • ⬆ Risk of infection
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26
Q

4th degree burn

A
  • Involves muscle or bone
  • Leads to loss of the burned part
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27
Q

Identify levels of sodium, potassium, hematocrit, and metabolic acidosis in each phase of burn injury.

A
  • ⬇ Na (hyponatremia): sodium traps in edema fluid & shifts into cells as K is released
  • ⬆ K (hyperkalemia): trauma/massive cell destruction results in release of K into ECF
    OR
  • ⬇ K (hypokalemia): later fluid shifts & inadequate K replacement
  • ⬆ Hct: due to plasma loss
  • Metabolic acidosis: hypoxia, poor renal & liver function
28
Q

Describe when to assess for an inhalation injury with a burn patient and the treatment options.

A

Assessment:
- Airway obstruction up to 48 hours
- Stridor, dyspnea
- Singed facial hair
- Carbonaceous sputum (black; soot)

Treatment:
- Early ET/vent
- Elevate HOB
- Perform X-rays, ABGs, carboxyhemoglobin tests, bronchoscopy

29
Q

Emergent/Resuscitative Phase of Burn Management

A

Onset of injury ➡ Complete fluid resuscitation

Treatment:
- Primary survey: ABCDE (disability, exposure); supply oxygen
- Fluid resuscitation (Large-bore IV)
- Foley catheter inserted
- Burns exceeding 20-25% ➡ NG insertion, placed to suction
- Cool & cover the burn
- Clean wounds (prevent infection)
- Prevent shock & respiratory distress

Types of burns:
- ECG for electrical burns
- Irrigate chemical burns

30
Q

Acute/Intermediate Phase of Burn Management

A

Beginning of diuresis ➡ near completion of wound closure

Treatment:
- Burn wound care & closure (topical antimicrobials, debridement, grafting)
- Pain management
- Continuous assessment of resp & circulatory, F&E, GI, kidneys
- Infection prevention & control
- Nutritional support
- Early positioning/mobility

31
Q

Rehabilitation Phase of Burn Management

A

Major wound closure ➡ return to individual’s optimal physical & psychosocial level

Treatment:
- Prevent & treat scars, contractures
- Physical, occupational & vocational rehabilitation
- Functional & cosmetic reconstruction
- Psychosocial counseling

32
Q

How to “cool the burn”

A
  • Soaked with cool water to cool the wound, halt burning process
  • Never apply ice directly to the burn, wrap person in ice, use cold soaks or dressings
    > 20 mins (worsen tissue damage, lead to hypothermia in larger burns)
33
Q

What is needed to determine the depth of a burn?

A
  • How the injury occurred
  • Causative agent (i.e. flame, scalding liquid)
  • Temperature
  • Duration of contact (with causative agent)
  • Thickness of skin at injury site
34
Q

Local Effects of Burn Injury

A
  • Burns < 20% TBSA
  • Pain, redness, numb
35
Q

Systemic Effects of Burn Injury

A
  • Burns > 20% TBSA
  • Cytokines & mediators released into circulation (shift in fluids, electrolytes, proteins)
  • Tissue hypoperfusion & organ dysfunction
36
Q

Describe what to assess for with circumferential burns.

A

Full thickness burns that affect the entire circumference of a torso, extremity, neck, chest, limb, digit

  • Bronchoconstriction (reduced respiratory movement, limited resp function)
  • Chest constriction
  • Poor circulation to extremities
37
Q

Identify types of skin debridement:
1. Natural
2. Mechanical
3. Chemical
4. Surgical

A
  1. Natural: affected tissue separates from underlying viable tissue spontaneously
  2. Mechanical: use of surgical tools to separate & remove eschar
  3. Chemical: topical agents to promote debridement
  4. Surgical: remove affected tissue along with early burn wound closure
38
Q

Wound Care for Burns

A
  • Wound debridement (natural, mechanical, chemical, surgical)
  • Wound excision & grafting (eschar removed, graft placed, wound covered with graft, appropriate coverage)
    Autografts, allografts, heterografts,
    synthetic dressings, skin substitutes
    (CEA, Integra, AlloDerm)
  • Topical antibacterial
  • Gentle cleaning with mild soap, water & washcloth
  • Wound dressing
39
Q

Describe the nurse’s role for a patient after a skin graft.

A
  • Restore fluid balance
  • Prevent infection
  • Modulate hypermetabolism (nutritional support)
  • Promote skin integrity
  • Relieve pain & discomfort
  • Promote mobility
  • Strengthen coping strategies
  • Support patient & family
  • Monitor & manage complications
40
Q

Discuss pain management options for burn patients.

A
  • Opioids, NSAIDs, anxiolytics, anesthetic agents
  • Long-acting analgesic; PCA for background pain (continuous level of discomfort)
  • Short-acting pain agents for breakthrough pain
  • Benzodiazepines with opioids for anxiety
  • Nonpharm: relaxation techniques, distraction, guided imagery, hypnosis, therapeutic touch, humor, music therapy, VR techniques
41
Q

List discharge teaching for a patient going home with pressure garments.

A
  • 23 hours per day
  • Only remove for bathing or wound care
42
Q

List strategies to reduce scarring and contractures for the burn patient.

A
  • Compression for early burns
  • Elastic bandage wraps to improve circulation
  • Custom pressure garments
  • Topical silicone enhances compression
  • Scar massage for contractures
  • Steroid injections to reduce scars
  • Avoid scratching (pruritus)
43
Q

Describe strategies for HIV prevention.

A
  • Abstain from sex or use protection
  • One sexual partner
  • Use latex condoms, do not reuse
  • Avoid using cervical caps or diaphragms without a condom
  • Avoid sharing needles, razors, toothbrushes, sex toys, or blood-contaminated items
  • Inform previous & present partners of HIV+ status
44
Q

Discuss how HIV medications are ordered and monitored for effectiveness and adherence.

A

Pre-exposure prophylaxis (PrEP)
- Taking one pill containing two HIV medications daily
- HIV status checked every 3 months to ensure person is not infected

ART (Antiretroviral Therapy)
- Take as prescribed (maintains viral suppression)
- No risk of transmitting HIV through sex

45
Q

Identify the difference between HIV infection and AIDs pertaining to the CD4+ T-lymphocyte count (4 different stages).

A

Stage 0: Primary Infection
Period of infection to development of HIV-specific antibody
Stage I: HIV asymptomatic
> 500 CD4+ T-lymphocytes
Stage II: HIV symptomatic
200-499 CD4+ T-lymphocytes
Stage III: AIDS
< 200 CD4 T-lymphocytes

46
Q

HIV Opportunistic Infections & Treatment: CMV retinitis

A
  • Foscaret
  • Ganciclovir
  • Vanganciclovir
  • Cidofavir
46
Q

HIV Opportunistic Infections & Treatment: Respiratory

A

PCP (pneumocystis pneumonia)
Treatment: Bactrim (trimethoprim-sulfamethoxazole); chemoprophylaxis, corticosteroids

MAC (mycobacterium avium complex)
Treatment: Azithromycin, clarithromycin, ethambutol (antimycobacterials)

46
Q

HIV Opportunistic Infections & Treatment: Cryptococcal Meningitis

A
  • Amphotericin B
  • Fluconazole
47
Q

HIV Opportunistic Infections & Treatment: Herpes

A

Acyclovir

48
Q

Identify how to manage chronic diarrhea in the HIV patient.

A

Octreotide acetate (synthetic analogue of somatostatin)

49
Q

List medications used to increase appetite.

A
  • Megestrol acetate (PO progesterone, promotes weight gain, increase fat stores)
  • Dronabinol (modest weight gain)
50
Q

Medications to treat MAC

A
  • Clarithromycin (first agent)
  • Azithromycin (can be substituted d/t adverse drug reactions, intolerance)
  • Ethambutol (second drug)
51
Q

Identify the rationale for knowing how HIV integrates itself into a person’s immune system.

A
  • Transmission by body fluids containing HIV or infected CD4 lymphocytes (blood, semen, vaginal secretions, amniotic fluid, breast milk)
  • Casual contact does not cause transmission
  • Breaks in skin or mucosa increase risk
52
Q

List the most common diagnoses that encompass cognitive decline & the most common respiratory infection in a patient with HIV.

A

Cognitive decline
- Subcortical neurodegenerative disease
- HIV encephalopathy

Most common resp. infection
- Pneumocystis pneumonia

53
Q

Identify why older adults are often left out of the HIV risk group.

A
  • Less likely than younger people to get tested
  • Unknowingly become infected with HIV
  • Medicare after 65
  • Embarrassed to share activities to provider
54
Q

Identify how a positive HIV mother can spread the virus to their infant.

A

May occur in
- Utero
- At time of delivery
- Breast-feeding

55
Q

Identify signs, symptoms and diagnostic tests for meningitis.

A

S/Sx:
- HA, fever
- Changes in LOC
- Behavioral changes
- Nuchal rigidity (stiff neck)
- (+) Kernig’s sign (knee extension painful)
- (+) Brudzinski’s sign (neck flexion → knee flexion)
- Photophobia

Diagnostics:
- CT prior to lumbar puncture
- Bacterial culture
- Gram staining of CSF & blood

56
Q

List the risk factors for an unfavorable outcome in meningitis treatment.

A
  • First-year college students & military members not vaccinated
  • Tobacco use
  • Viral upper respiratory infection
  • Otitis media, mastoiditis
57
Q

Discuss discharge teaching strategies for a patient with trigeminal neuralgia.

A
  • Cotton pads & room temperature water to wash face
  • Rinse with mouthwash after eating if toothbrush causes pain
  • Nutrition (soft food, chew on unaffected side, avoid hot & cold food)
  • Intervene for signs of anxiety, depression, & insomnia
58
Q

Describe what triggers may precipitate pain in a patient with trigeminal neuralgia.

A
  • Washing face
  • Combing hair
  • Brushing teeth
  • Eating too hot or too cold foods
  • Draft of air
59
Q

Determine what other diseases to screen for in a patient with trigeminal neuralgia.

A

Multiple sclerosis

60
Q

Discuss management for a patient taking carbamazepine.

A
  • Taken with meals
  • Serum levels must be monitored to avoid toxicity who require high doses to control pain
  • Monitored for bone marrow depression during long-term therapy
61
Q

Identify clinical signs of Bell’s Palsy and interventions to prevent complications (discharge teaching strategies).

A

S/Sx:
- Unilateral facial muscle weakness or paralysis with facial distortion
- Increased lacrimation
- Painful sensations in face
- Difficulty with speaking or eating

Treatment:
- Corticosteroid therapy (reduce inflammation & severity)
- Reassure stroke has not occurred
- Protect eye from injury (eye ointment, sunglasses, close eyelid, cover eye with shield at night)
- Facial exercises & massage to maintain muscle tone

62
Q

List diagnostics to test for Creutzfeldt-Jakob disease.

A
  • Brain biopsy not recommended (only after death)
  • Immunologic assessment of CSF (protein kinase inhibitors indicate neuronal cell death)
  • EEG (brain patterns)
  • MRI
63
Q

Identify priorities of care for a patient with a brain abscess.

A
  • Control ICP
  • Drain abscess
  • Administer abx; corticosteroids for cerebral edema
  • Frequent neurologic assessment

ADN 9 Transition to Practice (2 decks)

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