NUR 335 Final Exam QUESTIONS AND
ANSWERS WITH COMPLETRE
SOLUTIONS ALREADY PASSED!!!!
Question 1
When executing an initial emergency assessment on a burn patient, how does the
triage nurse apply the Rule of Palms to estimate total body surface area (TBSA)
burned, and which specific burn depths are included in this calculation?
✔✔ The Rule of Palms states that the surface area of the patient's own hand
(including the palm and fingers) represents approximately 1% of their Total
Body Surface Area (TBSA). This rapid assessment tool is used specifically to
measure irregular, scattered, or smaller partial-thickness (2nd-degree) and
full-thickness (3rd-degree) burns. Superficial (1st-degree) burns are excluded
from TBSA calculations.
Question 2
Inhalation injuries severely complicate burn trauma management. What are the key
environmental irritants involved, the primary toxic gases encountered, and how do
clinicians differentiate between upper and lower airway anatomical inhalation
trauma?
✔✔ Inhalation injuries involve complex pulmonary insults classified by
exposure type and anatomical location:
Etiology: Lung injury is driven by the inhalation of dense smoke, irritating
chemical toxins, and toxic products of incomplete combustion.
Toxic Gas Exposure: The most critical systemic threats are carbon
monoxide (CO) poisoning and hydrogen cyanide poisoning, both of
which disrupt cellular respiration.
Supraglottic Injury (Upper Airway): Primarily a thermal (heat) injury
occurring above the vocal cords. The upper airway effectively acts as a heat
sink, absorbing thermal energy, which can trigger rapid, life-threatening
airway swelling (epiglottic and laryngeal edema).
Subglottic Injury (Lower Airway): Primarily a chemical injury occurring
below the vocal cords. Because steam or chemical particulates travel deep
, into the lungs, they cause direct chemical burns to the bronchioles and
alveoli.
Question 3
When a patient sustains an inhalation injury, what are the underlying
pathophysiological mechanisms and the subsequent clinical outcomes that progress
from initial exposure to late-stage pulmonary complications?
✔✔ The mechanical breakdown and clinical progression of inhalation injuries
follow a predictable pathological cascade:
Pathophysiological
Clinical Outcome / Result
Mechanism
Displaces oxygen from hemoglobin and halts
Carbon Monoxide &
cellular ATP production, resulting in profound
Cyanide Inhalation
systemic hypoxia.
Inhalation of Chemical Triggers immediate smooth muscle
Stimulants constriction, causing severe bronchospasms.
Dead epithelial cells and soot form thick plugs
Mucosal Edema, Tissue
within the bronchioles, causing airway
Sloughing, & Cast
occlusion and intrapulmonary shunting
Formation
(blood flows past unventilated alveoli).
Destroys the fluid that keeps alveoli open,
Loss of Surfactant & leading to micro-atelectasis, diminished lung
Alveolar Collapse compliance, and severe ventilation-
perfusion (V/Q) mismatch.
Strips the lungs of their natural defense
Endothelial Ulceration,
mechanisms, leaving the patient highly
Necrosis, & Loss of Ciliary
vulnerable to superimposed bacterial
Clearance
pneumonia.
,Inhalation Injuries: S/S
Exposure in confined area
Facial burns/ singed nose hair
Soot around mouth/ nose
Carbonaceous sputum
Hypoxemia
Abnormal breath sounds
Respiratory distress
Elevated carboxyhemoglobin levels
Abnormal ABGs
Inactivation of surfactant
-alveolar collapse
-pneumonia
-pulmonary edema
Toxic Gases: Carbon Monoxide Poisoning
Binds to hemoglobin more rapidly than oxygen
Tissue hypoxia
Toxic Gases: Cyanide Poisoning
Binds to respiratory enzymes in the mitochondria
, Inhibits cell metabolism
Impaired oxygen utilization
Carbon Monoxide Poisoning
Carboxyhemoglobin levels (COHgb)
Pulse oximetry unable to differentiate b/t oxyhemoglobin/ carboxyhemoglobin
-less than 10-15%
--no sx
--HA or visual acuity
-15-40%
--CNS dysfunction
-40-60%
--LOC
--tachycardia/ tachypnea
--seizures
--cherry red/ or cyanotic color
->60%
--coma/death
Multi-Organ Effects of Burns
Integumentary
-skin loss, sensory loss, decreased temp
Cardiovascular
ANSWERS WITH COMPLETRE
SOLUTIONS ALREADY PASSED!!!!
Question 1
When executing an initial emergency assessment on a burn patient, how does the
triage nurse apply the Rule of Palms to estimate total body surface area (TBSA)
burned, and which specific burn depths are included in this calculation?
✔✔ The Rule of Palms states that the surface area of the patient's own hand
(including the palm and fingers) represents approximately 1% of their Total
Body Surface Area (TBSA). This rapid assessment tool is used specifically to
measure irregular, scattered, or smaller partial-thickness (2nd-degree) and
full-thickness (3rd-degree) burns. Superficial (1st-degree) burns are excluded
from TBSA calculations.
Question 2
Inhalation injuries severely complicate burn trauma management. What are the key
environmental irritants involved, the primary toxic gases encountered, and how do
clinicians differentiate between upper and lower airway anatomical inhalation
trauma?
✔✔ Inhalation injuries involve complex pulmonary insults classified by
exposure type and anatomical location:
Etiology: Lung injury is driven by the inhalation of dense smoke, irritating
chemical toxins, and toxic products of incomplete combustion.
Toxic Gas Exposure: The most critical systemic threats are carbon
monoxide (CO) poisoning and hydrogen cyanide poisoning, both of
which disrupt cellular respiration.
Supraglottic Injury (Upper Airway): Primarily a thermal (heat) injury
occurring above the vocal cords. The upper airway effectively acts as a heat
sink, absorbing thermal energy, which can trigger rapid, life-threatening
airway swelling (epiglottic and laryngeal edema).
Subglottic Injury (Lower Airway): Primarily a chemical injury occurring
below the vocal cords. Because steam or chemical particulates travel deep
, into the lungs, they cause direct chemical burns to the bronchioles and
alveoli.
Question 3
When a patient sustains an inhalation injury, what are the underlying
pathophysiological mechanisms and the subsequent clinical outcomes that progress
from initial exposure to late-stage pulmonary complications?
✔✔ The mechanical breakdown and clinical progression of inhalation injuries
follow a predictable pathological cascade:
Pathophysiological
Clinical Outcome / Result
Mechanism
Displaces oxygen from hemoglobin and halts
Carbon Monoxide &
cellular ATP production, resulting in profound
Cyanide Inhalation
systemic hypoxia.
Inhalation of Chemical Triggers immediate smooth muscle
Stimulants constriction, causing severe bronchospasms.
Dead epithelial cells and soot form thick plugs
Mucosal Edema, Tissue
within the bronchioles, causing airway
Sloughing, & Cast
occlusion and intrapulmonary shunting
Formation
(blood flows past unventilated alveoli).
Destroys the fluid that keeps alveoli open,
Loss of Surfactant & leading to micro-atelectasis, diminished lung
Alveolar Collapse compliance, and severe ventilation-
perfusion (V/Q) mismatch.
Strips the lungs of their natural defense
Endothelial Ulceration,
mechanisms, leaving the patient highly
Necrosis, & Loss of Ciliary
vulnerable to superimposed bacterial
Clearance
pneumonia.
,Inhalation Injuries: S/S
Exposure in confined area
Facial burns/ singed nose hair
Soot around mouth/ nose
Carbonaceous sputum
Hypoxemia
Abnormal breath sounds
Respiratory distress
Elevated carboxyhemoglobin levels
Abnormal ABGs
Inactivation of surfactant
-alveolar collapse
-pneumonia
-pulmonary edema
Toxic Gases: Carbon Monoxide Poisoning
Binds to hemoglobin more rapidly than oxygen
Tissue hypoxia
Toxic Gases: Cyanide Poisoning
Binds to respiratory enzymes in the mitochondria
, Inhibits cell metabolism
Impaired oxygen utilization
Carbon Monoxide Poisoning
Carboxyhemoglobin levels (COHgb)
Pulse oximetry unable to differentiate b/t oxyhemoglobin/ carboxyhemoglobin
-less than 10-15%
--no sx
--HA or visual acuity
-15-40%
--CNS dysfunction
-40-60%
--LOC
--tachycardia/ tachypnea
--seizures
--cherry red/ or cyanotic color
->60%
--coma/death
Multi-Organ Effects of Burns
Integumentary
-skin loss, sensory loss, decreased temp
Cardiovascular
