Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IPAP JUNIOR SEM. > Occupational Lung Dz And Toxic Lung Injury > Flashcards

Occupational Lung Dz And Toxic Lung Injury Flashcards

1
Q

What are the three effects of smoke inhalation

A

1) Impaired tissue oxygenation
2) Thermal injury to upper airway
3) Chemical injury to the lower airways and lung parenchyma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe Impaired tissue oxygenation 2/2 smoke inhalation injury

A

Carbon monoxide avidly binds with hemoglobin!
—Greater affinity than oxygen

S/S: severe headache or acutely altered mental status, seizures, coma, cherry red skin (rarely seen)

Tx: high flow O2 followed if needed by hyperbaric oxygen and supportive care
—100% NRB Mask:
—Despite the Pulse Ox reading 100%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the resting level of Carbon o oxide in smokers and non smokers

A

Nonsmokers may have up to 3 percent carboxyhemoglobin at baseline

smokers may have levels of 10 to 15 percent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What effect does cyanide have in smoke inhalation injuries

A

Causes impaired Tissue Oxygentaion

Cyanide disrupts cell function and prevents tissue from taking up oxygen leading to lactic acidosis

S/s: Dyspnea, confusion, hypotension, headache, dizziness, syncope
Seizures, coma, cardiovascular collapse, death

Tx: cyanide antidote kit (Cyanokit®) and supportive care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the cyanide kit

A

Contains hydroxocobalamin
precursor to vitamin B-12

Binds to cyanide and neutralizes it
Eliminated harmlessly from the body through urination

ADE of RX: temporary discoloration of the skin and urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe thermal injury with smoke inhalation

A

inhalation of hot gases injures mucosal surfaces

—Complications become evident w/in 18-24 hours

S/S: Mucosal edema, Upper airway obstruction ,increased secretions,
inspiratory stridor
—Respiratory failure possible

Tx: Humidifed O2, with suction PRN,
Elevated HOB 30*
Racemic Epi to reduce edema,

Order ABGS and monitor pulse ox

Intubation as necessary
Or Trach if unable to intubate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe chemical injury in smoke inhalation injury

A

from toxic gases & products of combustion

Early S/S: Bronchorrhea, bronchospasm with dyspnea, tachypnea & tachycardia

Late S/s: Labored breathing & cyanosis

+diffuse wheezing/rhonchi
Bronchial edema & sloughing leading to obstruction, atelectasis, and increasing hypoxemia

—ARDS possible in 1-2 days
—Pneumonia common 5-7 days after exposure

Tx: humidified O2, Bronchdilators, with suction of secretions,
Intubation as necessary with PEEP
Chest physical therapy
IVF and Fluid MGMT

Daily Sputum Gram Stains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Are Routine corticosteroids & antibiotics recommended for the tx of smoke inhalation chemical injury

A

Routine corticosteroids & antibiotics are ineffective & not recommended

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define bronchiolitis obliterans

A

A ground glass hazy opacities on CXR 2/2 to damage to the bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In a pt post fire with a markedly elevated lactate think

A

Cyanide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

DO pts with burns typically have long term pulm problems ?

A

Patients who survive burns and recover generally do not have long-term pulm problems

May get impaired PFTs
—Reactive airway dysfunction syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the Tx for Vaping Lung Injury

A

E-VALI
—E-cigarette or vaping associated lung disease

S/s:
Cough, fever, bilateral infiltrates

Vitamin E acetate – now removed
Reduced incidence of E-VALI

Treatment: supportive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

These are a group of chronic fibrotic dz caused by inhalation of INORGANIC dusts
Usually asymptomatic with diffuse nodular opacites on CXR

Think

A

Coal works lung
Silicosis
Asbestosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pneumoconioses from inhalation of coal dust that leads to coal macules from alveolar macrophage ingestion

Leads to severer lung impairment and premature death

Think? CXR? tx?

A

Coal workers lung

CXR: diffuse 2-5mm opacities on CXR, prominent in upper lung fields

Tx: Supportive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pneumoconioses from prolonged inhalation of free silica particle that leads to small rounded nodules in the lungs

2/2 Quartz, granite, sandstone
Quarries, mines, etc

Think? CXR? Tx?

A

Silicosis

CXR: Small rounded opacities throughout the lung
—Calcification of hilar lymph nodes (“eggshell” calcification)
-strongly suggests silicosis

Simple silicosis usually asymptomatic & normal PFTs

Complicated silicosis – conglomerates of irregular masses >1cm leading to large upper lung densities, dyspnea, obstructive & restrictive PFTs

Tx: supportive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pts with silicosis are at an increased risk of what infection

A

TB!

Silica is cytotoxic to alveolar macrophages; pts with silicosis are at greatest risk of acquiring lung infections that involve macrophages as a primary defense
(TB, Atypical mycobacteria and fungi)

All silicosis pts should have tuberculin skin test & current CXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

This pneumoconioses presents with nodular interstitium fibrosis

Common to Shipyard & construction workers, pipe fitters, insulators
—10-20 years of exposure

S/s : progressive dyspnea, inspiratory crackles; sometimes clubbing, cyanosis

THink? CXR? Tx?

A

Asbestosis

CXR: Linear streaking at lower lung fields
Opacities of various shapes/sizes
—Honeycomb changes – advanced disease
—Pleural calcifications may be best diagnostic clue

DX: High rest CT
—Parenchymal fibrosis & coexisting pleural plaques

Tx: supportive
O2 for SOB
Resp. physiotherapy to remove secretions

18
Q

What pattern of pct will pts with asbestosis Present with

A

Restrictive dysfunction
Reduced FVC & FEV1

Normal or elevated FEV1/FVC ratio

Reduced DLCO
(Diffusing capacity for carbon monoxide)

19
Q

This is an inflammatory D/o of the lung involving the alveolar walls and terminal airways

Induced by exposure to ORGANIC agents that leads to an acute illness

(Avian droppings, microorganisms, avian proteins, fungi, mold)

S/s acute: Sudden malaise, chills, fever, cough, dyspnea, nausea, onset after leaving work/ at night .

Subacute: Insidious onset (weeks to months) of chronic cough, slowly progressive dyspnea, anorexia, wt loss

Chronic: progressive respiratory insufficiency & fibrosis

THink? CXR? Tx?

A

Hypersensitivity Pneumonitis

CXR acute: small nodular densities, sparing apices & bases

Chronic: pulmonary fibrosis and honeycombing

Dx: increased WBCs with neutrophilia, elevated ESR, CRP
PFTs: restrictive dysfunction & reduced DLCO

Lung Bx may be necessary for chronic

Tx: Identification of offending agent & avoidance of further exposure

Severe/protracted cases: oral corticosteroids in long (4-6 week) followed by long taper (3 months)

20
Q

This D/o presents like asthma but recovers when away from work

Think? Dx? Tx?

A

Occupational Asthma

Can develop weeks to years after exposure

Dx: Spirometry before & after exposure
Peak flow measurements in the workplace

Tx: bronchodilator’s and Pulm consult

21
Q

Chronic bronchitis is commonly seen in what professions

A

Coal miners

Exposures to Cotton, flax & hemp dust

22
Q

Which is worse occupational or non occcupations COPD

A

Occupational

23
Q

This is an asthma like d/o in textile workers from inhalation of cotton dust

S/s Chest tightness, cough, dyspnea characteristically worse on Monday (or the first day back to work)

Think?

A

Byssinosis

24
Q

This is an acute toxic pulmonary edema caused by inhalation of nitrogen dioxide from recently filled silos

Think? Tx? And progression?

A

Silo filers Disease

Tx: early cortiosteroids

Progresssion to bronchilitis obliterans and death

25
Q

This is from chronic inhalation of diacetyl that leads to bronchilitis obliterans

A

popcorn lung

26
Q

Describe what happens if you acutely aspirate gastic contents

A

Pure gastric acid (pH<2.5) leads to extensive desquamation of bronchial epithelium, bronchiolitis, hemorrhage, pulmonary edema

This is one of the most common causes of ARDS

S/s Cough, wheeze, fever even in the absence of infection, tachypnea, crackles at the bases

With early hypoxemia and leukocytosis

CXR: patchy alveolar opacities in dependent lung fields

27
Q

What is the Tx for Acute aspiration of gastric contents

A

O2
Airway MGMT
Possible intubation and mech vent

MGMT with IVF

No need to prophylaxis with ABX

28
Q

What are the complications of chronic aspiration of gastric contents

A

Achalasia

Esophageal stricture

Systemic sclerosis (scleroderma)

Esophageal carcinoma

Esophagitis

Gastroesophageal reflux Dz (GERD)

Relaxation of LES (lower esophageal sphincter) – esp at night

29
Q

What effect does Cigarette smoking, etoh, caffeine, theophylline have on the lower esophageal sphincter?

A

Relaxes it leading to chronic aspiration of gastric content

30
Q

What is the tx for Hydrocarbon pneumonitis–caused by aspiration of ingested petroleum distillates

A

Tx: supportive, protect lungs from repeated aspiration

Cuffed endotracheal tube if necessary

31
Q

What is the onset, S/s, PFT, CXR and Tx for Radiation pneumonitis

A

Onset is 2-3 months after rads exposure

PFT: reduced lung volume/lung compliance, diffusing capacity

S/S: Insidious onset of dyspnea, intractable dry cough, chest fullness/pain, weakness, fever

CXR: alveolar or nodular opacities limited to irradiated area

Tx: prednisone

32
Q

This fibrosis is common in pts after a full treatment for lung or breast cancer

Presents with slow progressive dyspnea

Think?
CXR?
Tx?

A

Pulm Radiation Fibrosis

CXR: tented diaphragms, obliteration of normal lung markings, reduced lung volumes, reticular and dense opacities

TX; corticosteroids x2-3wk with taper

33
Q

What is the onset of O2 Toxicity

A

It appears to occur with exposure to Fio2of 50 to 60% after exposures as short as 6 hours in duration

34
Q

A pt is receiving blood products and within minutes goes into respiratory distress with a PaO2 less than 60 and a PaCO greater than 45 with tachypnea and tachycardia

What happened? What should we do ? What would you see on CXR ?

A

TRALI

This is indistinguishable from ARDS

Ts: STOP THE TRANSFUSION
Supportive care and O2 with IVF and pressure support ventilations

(Recovery in 2-5 days)

35
Q

A climber gets a headache and malaise at 7,000 feet

What is this called

A

Acute mountain sickness

36
Q

A native of the mountains gets headache, fatigue, dyspnea, and indigestion at 10,000 feet

What is this called

A

Chronic mountain sickness

37
Q

At 950o feet a climber gets dyspnea, cough and tachycardia

What is this called

A

High altitude pulm edema

38
Q

A climber at 15000 feet gets vision changes

What is this callled

A

High alt retinal hemorrhage

39
Q

At 15,000 feet a pt gets confusion ataxia, hallucinations, and a coma

This is called

A

HACE

40
Q

What is the prevention and treatment for High Altidue injuries

A

Prevention: gradual ascent, acclimatization, meds (acetazolamide)

TX: immediate descent, O2/hyperbaric chamber,
—If mild: sildenafil, acetazolamide, theophylline SR, NSAIDS, Tylenol, aspirin

IPAP JUNIOR SEM. (43 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions