Injury to Lungs Flashcards

1
Q

Most common form of high altitude sickness? Symptoms?

A

Acute mountain sickness. Headache, malaise, dyspnea, anorexia, lightheadedness, fatigue, insomnia

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2
Q

Most common fatal manifestation of sever high altitude illness?

A

High Altitude pulm. edema. Causes vasoconstriction in the lungs. Increased capillary permeability and pulm edema.

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3
Q

Clinical presentation of pulm edema?

A

Begin dry, non-productive cough and DOE, Progess to dyspnea at rest, pink, frothy sputum & blood in cough, tachycardia, tachypnea, low grade fever, inspiratory crackles

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4
Q

Treatment of HAPE?

A

Get down to lower altitude and supp. oxygen. Nifedipine (red. PA pressure and pulm vasc resistance) OR Tadalafil and sildenafil-vasodilators

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5
Q

AMS can change to this?

A

High altitude cerebral edema. Vasodilation in the brain

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6
Q

Manifestation of HACE?

A

Ataxic gait, lassitude, declining mental function and consciousness, can progress to coma and death.

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7
Q

This is the earliest sign of HACE and last finding to resolve?

A

Ataxia

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8
Q

Treatment of HACE?

A

Get down, oxygen, hyperbaric chamber, Dexamethasone, Acetazolamide

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9
Q

Medications used to help with acclimatization?

A

Acetazolamide (DOC)- 125mg q12h. Dexamathasone 2mg q6h or 4mg q12h. Above 4000m, 4mg q6h for active exertion

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10
Q

Type 1 decompression sickness (milder)

A

Joint pain (elbow/shoulder>hip/knee), numbness of extremities, skin pruritis, erythema, and cyanosis, lymphatic obstruction

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11
Q

Type 2 decompression sickness (more severe)

A

Cardiopulmonary (cough, substernal chest pain, tachypnea, wheezing) neurologic impairment, otic damage, air embolism

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12
Q

Other complications of scuba diving?

A

Nitrogen narcosis, otic narotrauma, pulm barotrauma, pneumothorax and pneumomediastinum

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13
Q

Mechanism of injury in smoke inhalation?

A

Thermal injury to airways, toxicity froom soot and gases, hypoxia and asphyxiation

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14
Q

Thermal injury generally occurs where?

A

Oropharyngeal airway

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15
Q

Obstruction of the airways from soot can lead to?

A

Bronchoconstriction

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16
Q

Clinical presentation of burns or smoke inhalation of the face and upper airways?

A

Burns, blisters or edema of mouth, hoarse voice, stridor, upper airway lesions of mucosa, black sputum

17
Q

Clinical presentation of burns or smoke inhalation of the lower airways?

A

Tachypnea, dyspnea, cough, wheezing, rales, decreased breath sounds, retractions

18
Q

These individuals should be intubated?

A

Stridor, use of accessory muscles, resp. distress, hypoventilation, deep burns of face or neck, edema or blistoring of oropharynx

19
Q

Because of the hypoxic events of burns and trauma, these levels can be measured?

A

Lactate levels

20
Q

Signs of carbon monoxide poisoning?

A

Headache (most common), nausea, dizziness, breathlessness, collapse, loss of consciousness

21
Q

Why should ABGs with oxyhemoglobin, methemoglobin, and carboxyhemoglobin be measured?

A

Because pulse ox cant differentiate b/w hemoglobin and carboxyhemoglobin

22
Q

Treatment of CO poisoning?

A

Remove pt from CO, ABGs, high-flow O2, hyperbaric oxygen treatment (CO>25%, LOC, metabolic acid ph

23
Q

These individuals will have the highest risk of radiation pneumonitis?

A

Lung cancer pt’s b/c they receive the largest volumes of radiation to the lungs

24
Q

Clinical manifestations of radiation pneumonitis?

A

Cough, pleuritic chest pain, fever, DOE, hypoxia, red. PFT

25
Initial phase of radiation pneumonitis begins ______ after therapy ends with what complications?
3-4 weeks, alveolitis, inflammation, capillary leak, pulm. edema. Pt usually asymptomatic
26
Early phase of radiation therapy beging ______ after therapy and has what complications?
3weeks-6months. acute pneumonitis, patient becomes symptomatic, alveoli desquamate and air spaces fill w/ fluid
27
What happens in the late phase of radiation pneumonitis?
Pulm. fibrosis developes
28
What is the mainstay treatment of radiation pneumonitis?
Oral corticosteroids. Prednisone 1mg/kg/day and tapered over weeks to months.
29
After transfusion, these antibodies attach to leukocytes and release cytokines and oxidative products which cause damage to pulmonary capillary endothelium?
Neutrophil specific antibody
30
TRALI presentation?
Minutes to 6 hours, hypoxia, bilateral infiltrates on CXR, pink frothy respiratory secretions, fever, hypotension, cyanosis