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
Q

Initial phase of radiation pneumonitis begins ______ after therapy ends with what complications?

A

3-4 weeks, alveolitis, inflammation, capillary leak, pulm. edema. Pt usually asymptomatic

26
Q

Early phase of radiation therapy beging ______ after therapy and has what complications?

A

3weeks-6months. acute pneumonitis, patient becomes symptomatic, alveoli desquamate and air spaces fill w/ fluid

27
Q

What happens in the late phase of radiation pneumonitis?

A

Pulm. fibrosis developes

28
Q

What is the mainstay treatment of radiation pneumonitis?

A

Oral corticosteroids. Prednisone 1mg/kg/day and tapered over weeks to months.

29
Q

After transfusion, these antibodies attach to leukocytes and release cytokines and oxidative products which cause damage to pulmonary capillary endothelium?

A

Neutrophil specific antibody

30
Q

TRALI presentation?

A

Minutes to 6 hours, hypoxia, bilateral infiltrates on CXR, pink frothy respiratory secretions, fever, hypotension, cyanosis