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
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
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
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)
5
Q
Septic Shock: Pathophysiology & Possible Causes
A
Pathophysiology: Widespread sepsis or infection leading to hypovolemia
Causes:
- Bacteremia
- Pneumonia
- Urosepsis
- Wounds, foleys, central lines
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)
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
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)
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)
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
11
Q
Irreversible Stage of Shock: Treatment
A
Does not respond to treatment; cannot survive
12
Q
Risks & Treatment for Each Stage of Shock (4): All Types
A
- Support respiratory system
- Fluid replacement
- Vasoactive meds
- Nutritional support
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
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
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
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
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
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
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)
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
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
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
23
Q
Superficial thickness burn
A
1st degree burn
- Painful
- Does not blister or scar
24
Q
Partial or intermediate-thickness burn
A
2nd degree burn
- Blisters & weeps
- ⬆ Depth ➡ ⬆ Risk of infection & scarring
- Deep partial thickness requires surgery
25
**Full** thickness burn
**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
26
**4th degree** burn
- Involves muscle or bone
- Leads to loss of the burned part
27
Identify levels of **sodium, potassium, hematocrit,** and **metabolic acidosis** in each phase of burn injury.
- ⬇ 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
Describe when to assess for an **inhalation injury** with a burn patient and the treatment options.
**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
**Emergent/Resuscitative** Phase of Burn Management
**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
**Acute/Intermediate** Phase of Burn Management
**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
**Rehabilitation** Phase of Burn Management
**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
How to "**cool the burn**"
- 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
What is needed to determine the depth of a burn?
- 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
**Local** Effects of Burn Injury
- Burns < 20% TBSA
- Pain, redness, numb
35
**Systemic** Effects of Burn Injury
- Burns > 20% TBSA
- Cytokines & mediators released into circulation (shift in fluids, electrolytes, proteins)
- Tissue hypoperfusion & organ dysfunction
36
Describe what to assess for with **circumferential burns**.
*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
Identify types of skin debridement:
1. **Natural**
2. **Mechanical**
3. **Chemical**
4. **Surgical**
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
Wound Care for Burns
- 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
Describe the nurse’s role for a patient after a skin graft.
- 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
Discuss pain management options for burn patients.
- 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
List discharge teaching for a patient going home with pressure garments.
- 23 hours per day
- Only remove for bathing or wound care
42
List strategies to reduce scarring and contractures for the burn patient.
- 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
Describe strategies for HIV prevention.
- 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
Discuss how HIV medications are ordered and monitored for effectiveness and adherence.
**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
Identify the difference between HIV infection and AIDs pertaining to the CD4+ T-lymphocyte count (4 different stages).
**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
HIV Opportunistic Infections & Treatment: **CMV retinitis**
- Foscaret
- Ganciclovir
- Vanganciclovir
- Cidofavir
46
HIV Opportunistic Infections & Treatment: **Respiratory**
**PCP (pneumocystis pneumonia)**
Treatment: Bactrim (trimethoprim-sulfamethoxazole); chemoprophylaxis, corticosteroids
**MAC (mycobacterium avium complex)**
Treatment: Azithromycin, clarithromycin, ethambutol (antimycobacterials)
46
HIV Opportunistic Infections & Treatment: **Cryptococcal Meningitis**
- Amphotericin B
- Fluconazole
47
HIV Opportunistic Infections & Treatment: **Herpes**
Acyclovir
48
Identify how to manage chronic diarrhea in the HIV patient.
**Octreotide acetate** (synthetic analogue of somatostatin)
49
List medications used to increase appetite.
- Megestrol acetate *(PO progesterone, promotes weight gain, increase fat stores)*
- Dronabinol *(modest weight gain)*
50
Medications to treat MAC
- Clarithromycin (first agent)
- Azithromycin (can be substituted d/t adverse drug reactions, intolerance)
- Ethambutol (second drug)
51
Identify the rationale for knowing how HIV integrates itself into a person’s immune system.
- 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
List the most common diagnoses that encompass cognitive decline & the most common respiratory infection in a patient with HIV.
**Cognitive decline**
- Subcortical neurodegenerative disease
- HIV encephalopathy
**Most common resp. infection**
- Pneumocystis pneumonia
53
Identify why older adults are often left out of the HIV risk group.
- Less likely than younger people to get tested
- Unknowingly become infected with HIV
- Medicare after 65
- Embarrassed to share activities to provider
54
Identify how a positive HIV mother can spread the virus to their infant.
May occur in
- Utero
- At time of delivery
- Breast-feeding
55
Identify signs, symptoms and diagnostic tests for meningitis.
**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
List the risk factors for an unfavorable outcome in meningitis treatment.
- First-year college students & military members not vaccinated
- Tobacco use
- Viral upper respiratory infection
- Otitis media, mastoiditis
57
Discuss discharge teaching strategies for a patient with trigeminal neuralgia.
- 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
Describe what triggers may precipitate pain in a patient with trigeminal neuralgia.
- Washing face
- Combing hair
- Brushing teeth
- Eating too hot or too cold foods
- Draft of air
59
Determine what other diseases to screen for in a patient with trigeminal neuralgia.
Multiple sclerosis
60
Discuss management for a patient taking carbamazepine.
- 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
Identify clinical signs of Bell’s Palsy and interventions to prevent complications (discharge teaching strategies).
**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
List diagnostics to test for Creutzfeldt-Jakob disease.
- Brain biopsy not recommended (only after death)
- Immunologic assessment of CSF *(protein kinase inhibitors indicate neuronal cell death)*
- EEG (brain patterns)
- MRI
63
Identify priorities of care for a patient with a brain abscess.
- Control ICP
- Drain abscess
- Administer abx; corticosteroids for cerebral edema
- Frequent neurologic assessment
