Systemic Pathology 400 (respiratory pathologies 3-4) Flashcards

1
Q

allergic rhinitis

A

..

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2
Q

allegic rhinitis mostly where?

A

mostly nose and eyes

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3
Q

allergic rhinitis occurs in respones to

A

occur in response to breathing in allergens

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4
Q

allergens (example)

A

dust, dander, mold, cockroaches, pollen, grass, trees

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5
Q

allergic rhinitis is …

A

A collection of signs and symptoms

(mostly in the nose and eyes)

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6
Q

what are those collections of SSx?

A

Itching nose, mouth

Conjunctivitis (EYES)

Sneezing

Sinus and nasal obstruction

Coughing, wheezing

Coryza

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7
Q

SSx are in

A

eyes,

nose

throat, respiratory tract

sinuses

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8
Q

allergic rhinitis AKA

A

AKA HAY FEVER or SEASONAL ALLERGIES

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9
Q

how common is allergic rhinitis

A

VERY COMMON

not as common 50 years ago (?)

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10
Q

allergic rhinitis commonly co-occurs with …

A

Asthma

Atopic dermatitis
—> Atopy

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11
Q

atopy define

A

“Atopy is the tendency to produce an exaggerated immunoglobulin E immune response to otherwise harmless substances in the environment.”

“Atopy refers to the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (eczema).”

“derived from the Greek words a and topos, meaning “without” and “place,” respectively.”

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12
Q

allergic rhinitis — PATHOGENESIS

A

ACUTE VASOMOTOR response mediated by HISTAMINE and related vasoactive substances released locally in the nose from mast cells coated with IgE

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13
Q

what is the acute vasomotor response mediated by?

A

1) HISTAMINE

2) vasoactive substances
—> released locally in the nose
(from mast cells coated with IgE)

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14
Q

allergic rhinitis — Dx

A

History

Symptoms

Skin test

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15
Q

skin test – allergic rhinitis

A

“A skin prick test, also called a puncture or scratch test, checks for immediate allergic reactions to as many as 50 different substances at once. This test is usually done to identify allergies to pollen, mold, pet dander, dust mites and foods. In adults, the test is usually done on the forearm.”

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16
Q

allergic rhinitis – Tx

A

(Avoid triggers)

Antihistamines
Decongestants
Injections

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17
Q

how does decongestant work?

A

vasoconstrict

“They work by reducing the swelling of the blood vessels in your nose, which helps to open the airways. Examples include pseudoephedrine (sometimes called by the brand name Sudafed.”

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18
Q

ASTHMA

A

..

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19
Q

what is asthma?

A

Increased responsiveness of bronchial tree to certain stimuli

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20
Q

how is asthma multi-factorial?

A

Complex disorder involving…

biochemical,
autonomic,
immunologic,
infectious,
endocrine,
psychological factors

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21
Q

asthma – how is it chronic vs acute?

A

Chronic inflammatory condition

with acute exacerbations

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22
Q

asthma can be classified as …

A

Can be classified as reversible COPD

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23
Q

back to allergies —> “hygiene” theory related to allergies, hypersensitivities, autoimmune diseases, etc.

A

exposure to pathogens and a variety of substances from early age, reduces likelihood of allergies/hypersensitivities developing.

whereas, children who are sheltered, and don’t spend time outside, and around various substances/animals/people, are more likely to develop hypersensitivities/allergies, etc.

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24
Q

Asthma – Incidence

A

..

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25
Q

HOW COMMON IS ASTHMA?

A

The MOST COMMON chronic disease in adults and children

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26
Q

asthma, male to female ratio

A

Male > female 2:1

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27
Q

asthma, male to female ratio IN SEVERE CASES

A

Severe cases: Male = female

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28
Q

asthma – incidence vs country development level

and incidence vs socioeconomic class

A

More common in DEVELOPED countries, specifically those who are of LOW SOCIOECONOMIC STATUS

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29
Q

for asthma in developing countries, which group are more likely to have asthma?

A

In the developing world it is more common in those who are of high socioeconomic standing.

Why?
access to healthcare (?)
rich people living in cities more often in developing countries (?)
related to occupation (?)

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30
Q

Asthma risk factors

A

Environment
Small families
Lack of pets
Antibiotics
Age
Gender
Smoking while pregnant
Viral infections

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31
Q

other risk factors for asthma

A

Obesity
Urban settings
Low SE status
Overcrowding
BMI
Family history

Atopy (tendency for allergies)

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32
Q

allergies as risk factor for asthma?

A

“The chemicals released by your immune system lead to allergy signs and symptoms, such as nasal congestion, runny nose, itchy eyes or skin reactions. For some people, this same reaction also affects the lungs and airways, leading to asthma symptoms.”

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33
Q

asthma – etiology

A

Genetics
Viruses

Risk factors (outlined in previous slide)

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34
Q

EXTRINSIC ASTHMA
(atopic or allergic asthma)

results from?
occurs mostly in?
considered a _____ disorder

A

Results from an allergy to specific triggers

Occurs mostly in children and young adults

considered part of “Hypersensitivity disorders”

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35
Q

is family history a risk factor for asthma

A

yes

3-6 times more likely

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36
Q

Intrinsic asthma
((nonallergic asthma)

triggers?
onset age?
possibly d/t … ?

A

No known triggers

Adult onset

Possibly viral exposure
—> Post-viral asthma
(POST-VIRAL BRONCHOCONSTRICTION)

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37
Q

Occupation Asthma

A

NARROWING OF AIRWAYS

caused by workplace exposure

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38
Q

exercise-induced Asthma

A

Bronchoconstriction can occur in those without other forms of asthma
—> Up to 20% of the healthy population

(More common in cold temperatures)

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39
Q

asthma – pathogenesis

A

An inflammatory response in the airway causes:
Cellular infiltration
Epithelial disruption
Mucosal edema
Mucous plugging

The inflammatory mediators produce:
Smooth muscle spasm
Vascular congestion
Increased vascular permeability
Edema formation
PRODUCTION OF THICK, TENACIOUS MUCOUS
Impaired mucociliary function

Mediators also cause:
Thickening of airway walls
Increased contractile response of bronchial smooth muscle

This leads to airway hyper-responsiveness and, along with swollen airways and mucous plugs, causes trapping of distal air leading to:
HYPOXEMIA/hypoxia
Obstructed airflow
Increased work of breathing

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40
Q

in long run, what can asthma cause

A

barrel chest – but not as common

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41
Q

asthma – SSx, clinical manife

A

Cough
SOB
Wheezing

Degree – mild, moderate, severe
Frequency

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42
Q

asthma attacks are usually …

A

Most attacks are short-lived with asymptomatic periods between attacks.

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43
Q

long term asthma and repeated acute episodes can lead to…

A

Repeated episodes may leads to …
barrel chest,
elevated shoulders,

hypertonicity of accessory muscles of respiration, etc.

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44
Q

acute severe asthma — aka

A

formerly known as STATUS ASTHMATICUS:

“a severe condition in which asthma attacks follow one another without pause.”

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45
Q

acute severe asthma is …

A

Acute severe asthma (formerly status asthmaticus) –

an acute attack that cannot be altered with standard bronchodilators

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46
Q

acute severe asthma requires ____

can be ____

A

requires emergency medical care

can be fatal

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47
Q

asthma — Dx

A

History

Clinical manifestation

Pulmonary function tests (FEV-1) — FORCED EXPIRATORY VOLUME

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48
Q

fev-1 diagnostic tool

A

forced expiratory volume test

“FEV1 helps measure the progression of lung conditions such as chronic obstructive pulmonary disease (COPD) or asthma. FEV stands for forced expiratory volume, which is the air you exhale in 1 second. A low FEV1 suggests a breathing obstruction.”

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49
Q

asthma – Tx

A

Identify and avoid specific triggers

Medications
—> Corticosteroids
—> Bronchodilators

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50
Q

asthma – Px for children

A

Asthma resolves in many children, but for as many as one in four, wheezing persists into adulthood or relapse occurs in later years

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51
Q

asthma – mortality rate ?

A

About 4000 deaths/yr in the US are attributable to asthma, most of which are preventable with treatment. Thus, the prognosis is good with adequate access and adherence to treatment

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52
Q

long term asthma —-> structural effects on lungs

What can prevent these structural changes?

A

Over time, the airways in some patients with asthma undergo permanent structural changes (remodeling) that prevent return to normal lung functioning.

Early aggressive use of anti-inflammatory drugs may help prevent this remodeling

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53
Q

PNEUMOCONIOSES

A

Restrictive lung diseases

caused by inhalation of MINERAL DUSTS and various INORGANIC particulate

—> leads to permanent deposition of substantial amounts of particles in the lungs

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54
Q

which substances are commonly involved in PNEUMOCONIOSIS?

A

Particularly inorganic DUST such as IRON ore or COAL

—> inhaled and deposited in lung tissue

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55
Q

pneumoconiosis etymology

A

pneumo – of or related to lungs

konis – dust

osis – condition/disease

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56
Q

pneumoconiosis – commonly as a result of

A

Most classified as occupational and a consequence of long term exposure in the workplace

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57
Q

“coal worker’s pneumoconiosis”

(aka anthracosis)

A

etymology:

anthrax/anthrak – coal
osis – condition/disease

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58
Q

3 types of pneumoconiosis

A

1) coal worker’s pneumoconiosis (anthracosis)

2) silicosis

3) asbestosis

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59
Q

whether or not there is damage to lungs during pneumoconioses, depends on a THREE FACTORS

A

A) Duration of exposure

B) Concentration of particles

C) Size, shape and solubility of particles

D) Biochemical composition of the inhaled dust

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60
Q

how does size of particles determine whether a risk factor for pneumoconioses?

A

E.g.
Large dust particles retained in the nasal mucus and do not reach the lower respiratory tract

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61
Q

How does biochemical composition of the inhaled dust determine risk for developing pneumoconioses?

A

E.g. Inert particles, like coal particles, are less reactive

E.g. silica particles are more reactive and produce more prominent tissue injury

E.g. asbestos particles are insoluble and remain lodged in lungs permanently

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62
Q

pneumoconiosis – incidence and etiology

A

Occurs most commonly in miners, sandblasters, stonecutters, asbestos works, insulators

Increasing incidence with age because cumulative effects of exposure

Overall incidence decreasing (BETTER OCCUPATIONAL SAFETY STANDARDS)

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63
Q

1) Coal worker’s pneumoconiosis

A

Amorphous carbon particles retained in nasal mucosa

Ingestion of inhaled coal dust by alveolar macrophages; expectorated

—> Black lung

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64
Q

2) SILICOSIS

A

Cells membranes of macrophages destroyed; macrophages die and release silica which is ingested by macrophages

Dead macrophages release
biochemically active substances
that stimulate formation of
COLLAGENOUS NODULES

Confluent nodules destroy lung
parenchyma and cause
massive pulmonary fibrosis

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65
Q

____ is a common complication of SILICOSIS

A

TB common complication

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66
Q

if silicosis is caused by volcanoes it is called ____

A

Pneumonoultramicroscopicsilicovolcanoconiosis

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67
Q

silicosis define

A

“Silicosis is a type of pulmonary fibrosis, a lung disease caused by breathing in tiny bits of silica, a common mineral found in sand, quartz and many other types of rock.”

“Silicosis mainly affects workers exposed to silica dust in jobs such as construction and mining. Over time, exposure to silica particles causes scarring in the lungs, which can harm your ability to breathe.”

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68
Q

3) Asbestosis

A

Asbestos particles engulfed by macrophages

Macrophages activated to release inflammatory mediators

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69
Q

asbestos associated with increased risk of ____

whereas silicosis is associated with increased risk of _____

A

Associated with increased risk of LUNG CANCER

silicosis is associated with increased risk of TUBERCULOSIS

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70
Q

pneumoconiosis — Clinical manifestations

A

Progressive dyspnea
Chest pain
Chronic cough
Expectoration of mucus

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71
Q

pneumoconiosis — Dx

A

workplace exposure,
CXR,
clinical manifestation,
pulmonary function tests (FEV1?)

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72
Q

pneumoconiosis – safety measures

A

Prevention and safety measures

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73
Q

pneumoconiosis – is there Tx when it happens?

A

No standard treatment

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74
Q

pneumoconiosis – what about Px ?

A

Poor prognosis generally

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75
Q

HYPERSENSITIVITY PNEUMONITIS

A

Hypersensitivity reaction in the alveoli as a response to inhaled ORGANIC particulate

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76
Q

BOTH of these are considered to be OCCUPATIONAL PATHOLOGIES

A

Hypersensitivity Pneumonitis

Pneumoconiosis

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77
Q

BOTH of these are considered to be RESTRICTIVE LUNG DISEASES

A

Hypersensitivity pneumonitis

Pneumoconiosis

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78
Q

Hypersensitivity pneumonitis causes

A

“Hypersensitivity pneumonitis can happen when you repeatedly breathe in bacteria , mold, or chemicals in your environment that cause inflammation in your lungs. These harmful substances may be found in: Air conditioners, humidifiers, and ventilation systems. Bird droppings, feathers, and animal furs.”

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79
Q

one difference between pneumoconiosis and hypersensitivity pneumonitis

A

PNEUMOCONIOSIS usually involves inhalation of INORGANIC particles

HYPERSENSITIVITY PNEUMONITIS usually involves inhalation of ORGANIC particles

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80
Q

hypersensitivity pneumonitis – relation to allergies and allergens

A

“Hypersensitivity pneumonitis causes a different immune reaction in your body than pollen or pet allergies. Unlike common allergies that cause hay fever and asthma, repeated exposure to allergens that cause HP can lead to inflammation that can permanently damage your lungs.”

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81
Q

hypersensitivity pneumonitis — SSx

A

Fever
Cough
Dyspnea
Headache
Pleuritis

Clubbing (hypoxia?)
Honeycomb lungs
Bronchiolitis
Crackles (aka RALES)

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82
Q

hypersensitivity pneumonitis – Dx

A

History
Blood tests
X-ray
Biopsy
PFT (e.g. FEV1)

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83
Q

hypersensitivity pneumonitis — Tx

A

Avoid triggers

Anti-inflammatories

84
Q

pneumothorax

A

accumulation of air/gas in the PLEURAL CAVITY

caused by defect in VISCERAL pleura
or defect in PARIETAL pleura (chest wall)

85
Q

what is result of pneumothorax

A

COLLAPSE of lung (ATELECTASIS)

86
Q

atelectasis etymology

A

ateles (imperfect)

ektasis (extension)

87
Q

PRIMARY pneumothorax

A

no underlying pathology

idiopathic

88
Q

SECONDARY pneumothorax

A

typically result of COPD (esp emphysema), CF

or other lung pathologies/infections

89
Q

how does pneumothorax lead to atelectasis (lung collapse) ?

A

air leaking into pleural cavity causes compressive force on lung –> leading to lung collapse

90
Q

incidence (pneumothorax) – gender, age

A

MEN 5x more likely

Can develop at ANY AGE

esp TALL and SKINNY individuals

91
Q

pneumothorax – risk factors

A

100x

SMOKING increases risk by up to 100x

(Tobacco or cannabis)

92
Q

pneumothorax as a result of TRAUMA

A

IATROGENIC trauma
—> Surgery

or other ACUTE TRAUMA

93
Q

pneumothorax — pathogenesis

A

air enters pleural cavity

There is a separation between the visceral and parietal pleura
→ destroys the NEGATIVE pressure of pleural space
→ lung collapses towards the hilum

94
Q

pleural cavity pressure – typically negative or positive?

A

typically NEGATIVE

positive pressure means that it will exert pressure/force on the lungs —> leading to lung collapse

95
Q

what is the effect on mediastinum d/t pneumothorax

A

air pressure pushes mediastinum in OPPOSITE direction —> towards UNAFFECTED lung

“Result is a mediastinal
shift towards the unaffected side which
will compress the opposite lung”

96
Q

types of pnuemothorax

A

1) spontaneous (different from idiopathic)

2) traumatic

3) Iatrogenic (type of traumatic)

97
Q

spontaneous pneumothorax

generally d/t

A

blebs and bullae (usually)

TB, lung abscess and other lung disease (also possible)

98
Q

traumatic pneumothorax

A

occurs following penetrating or non-penetrating chest trauma (rib fracture, stab, bullet)

99
Q

iatrogenic pneumothorax (type of traumatic pneumothorax)

A

occurs during medical procedure
(biopsy, CPR, etc.) –

is considered to be traumatic

100
Q

other types of pneumothorax

A

1) Open & closed

2) tension pneumothorax

101
Q

open pneumothorax

A

air is drawn into lungs via hole
forced out of hole during expiration

____

a type of traumatic pneumothorax that occurs when air is drawn into the lungs upon inspiration and is forced out upon expiration.

This is the opposite of a closed pneumothorax.

102
Q

open pneumothorax is AKA

A

“sucking chest wound”

103
Q

closed pneumothorax

A

hole does not open to exterior

104
Q

2) TENSION PNEUMOTHORAX

A

any pneumothorax that leads to significant respiratory impairment or issues with blood circulation.

This is a medical emergency.

—> LEADS TO PRESSURE ON MEDIASTINUM

105
Q

open, closed, tension pneumothorax

VS.

pleural & atmospheric pressure

A

in CLOSED pneumothorax:
—> pleural cavity pressure is LESS THAN atmospheric pressure

in OPEN pneumothorax:
—> pleural cavity pressure is EQUAL TO
atmospheric pressure

in TENSION pneumothorax:
—> pleural cavity pressure is GREATER THAN atmospheric pressure
—> LEADS TO PRESSURE ON MEDIASTINUM

106
Q

pneumothorax – CLINICAL MANIFESTATIONS

A

Dyspnea
Sharp, pleuritic chest pain
Tachypnea

TRACHEAL DEVIATION
(when pleural cavity pressure is high enough to push against mediastinum)

Fall in blood pressure (?)
Weak (?) and rapid pulse

107
Q

why does PNEUMOTHORAX (esp TENSION pneumothorax) cause LOW BP & weak pulse?

A

“As the intrapleural pressure increases, the mediastinum shifts and the venous return to the superior vena cava is impaired. Tension pneumothorax causes hypotension, increases the central venous pressure, decreases cardiac output, and ultimately produces cardiovascular collapse.”

108
Q

which type (stage) of pneumothorax is more likely to cause CV Sx (low BP, weak pules) ?

A

TENSION PNEUMOTHORAX

—> increased pressure in pleural cavity exerts pressure on mediastinum (including structures such as vena cava)

109
Q

pneumothorax Dx

A

Patient history

Chest films
—> CT, CXR, US

110
Q

pneumothorax – Px

A

Good

However, recurrence is likely

111
Q

pneumothorax – treatment

A

Administration of oxygen

Repair and closure of defect

Chest tube insertion may be necessary

Surgery to control bleeding, remove large clots, and treat trauma

Not a good idea to travel on plane or do lung function tests at least 2 weeks after treatment

Watch and wait

112
Q

pneumothorax – Asherman chest seal (TREATMENT)

A

“This chest seal includes a one-way valve, intended to let air and blood escape as needed, while keeping both out of the pleural cavity. Features. Circular design with 1-way valve. Pressure-sensitive adhesive that offers effective seal (even on hairy areas)”

113
Q

pleurodesis (treatment for pneumothorax)

A

“Pleurodesis is a medical procedure in which part of the pleural space is artificially obliterated. It involves the adhesion of the visceral and the costal pleura. The mediastinal pleura is spared.”

“Pleurodesis is a procedure that sticks your lung to your chest wall. This procedure removes the space between your lung and your chest wall (pleural space)”

114
Q

pleurodesis etmyology

A

The term ‘pleurodesis’ comes from the Greek words pleurá (pleura) and desmos (bond)

refers to a procedure undertaken to create the symphysis between the parietal and visceral pleura in order to eliminate the pleural space.

115
Q

pleurodesis – flaws, risks, complications

A

“Sometimes patients experience chest pain from pleurodesis. Painkillers are given as needed to help relieve this.”

“Some patients experience fever for the first day or two after the procedure. This is usually controlled with paracetamol and is short-lived.”

“Sometimes pleurodesis can cause breathlessness due to too much inflammation in the lung. This usually settles down over a few days with oxygen treatment, although very rarely (about 1 in 1000) it can be serious.”

116
Q

PLEURISY

A

AKA pleuritis

117
Q

pleurisy is

A

An inflammation of the pleura

caused by infection (USUALLY VIRAL), injury, tumor, other lung pathologies

118
Q

pleurisy can be a complication of

A

pneumonia, TB, influenza, pneumothorax

SLE, RA, cancer

etc.

119
Q

pleurisy can also be

A

idiopathic

(PRIMARY?)

120
Q

pleurisy — clinical manifestations

A

Sharp, sticking pain when breathing
—> Can also be dull, constant pain

Cough
Fever
SOB
Tachypnea

121
Q

pleurisy symptoms develop quickly or slowly?

A

Symptoms develop suddenly

122
Q

pleurisy Sx worse when …

A

Worse on …

inspiration,
coughing, sneezing,
movement

123
Q

pleurisy pathogenesis

A

If serous fluid between the visceral and parietal layers
is unchanged, it is said to be “DRY”

Two layers get congested and swollen and rub against each other → PAIN

124
Q

DRY pleurisy

A

If serous fluid between the visceral and parietal layers is unchanged, it is said to be “DRY”

Two layers get congested and swollen and rub against each other → PAIN

125
Q

WET PLEURISY (pleurisy with effusion)

A

If serous fluid between visceral and parietal layers is increased, it said to be “wet” or “pleurisy with effusion”

Less likely to cause pain because there is no chafing

May interfere with breathing by compressing the lung

Can become infected - “purulent pleurisy” or “empyema”

126
Q

DIAPHRAGMATIC PLEURISY

A

Inflammation of part of the pleura reaches the diaphragm, called diaphragmatic pleurisy

→ secondary to pneumonia

→ sharp pain referred to the neck, upper traps or shoulder

127
Q

pleurisy types

A

dry pleurisy

wet pleurisy

diaphragmatic pleurisy

128
Q

pleurisy Treatment

A

Aspirin

NSAIDS

Antibiotics

Thoracentesis if effusion is present

129
Q

PLEURAL EFFUSION

A

..

130
Q

pleural effusion vs hydrothorax (?)

A

“When unspecified, the term ‘pleural effusion’ normally refers to hydrothorax.”

NOTE that if pleural effusion is blood it is hemothorax; if pus, empyema.

—> pleural effusion is more general term, doesn’t specify what is in excess in pleural cavity

131
Q

pleural effusion is

A

Increased fluid between visceral and parietal pleura

I.e.
In PLEURAL CAVITY

132
Q

(pleural effusion) fluid can be

A

blood, pus, serous fluid, urine

133
Q

how urine (pleural effusion)

A

kidney disease (?)

134
Q

pleural effusion — secondary vs primary

A

Can be secondary to any pathologies that cause pleural edema

135
Q

is pleural effusion an issue with DRAINAGE?

or is it an issue with SECRETION?

A

can be d/t DECREASED DRAINAGE

INCREASED SECRETION

or BOTH

136
Q

secondary pleural effusion – pathologies

A

E.g. congestive heart failure, liver disease, kidney disease, trauma, malignancy, PE, infection, etc.

137
Q

pleural effusion – clinical manifestations DEPEND ON

A

amount of fluid,
the degree of lung compression,
underlying health condition,

etc.

138
Q

pleural effusion – Sx may include …

A

progressive dyspnea on exertion,

pain,

etc.

139
Q

pleural effusion — Dx

A

history,

imaging,

biopsy

140
Q

pleural biopsy define

A

“Pleural biopsy is a procedure to remove a sample of the pleura. This is the thin tissue that lines the chest cavity and surrounds the lungs. The biopsy is done to check the pleura for disease or infection.”

“Pleural biopsy is often done to find the cause of a collection of fluid around the lung (pleural effusion) or other abnormality of the pleural membrane. Pleural biopsy can diagnose tuberculosis, cancer, and other diseases.”

141
Q

ventilatory failure

A

various mechanisms

E.g.
muscle issues
—> E.g. diaphragm not contracting

neural issues

142
Q

acute alcohol poisoning – medullary rhythmicity centre (DRG)

A

interferes with DRG

—> inhibits neural activity to lungs/diaphragm

143
Q

ventilatory failure is secondary to

A

Secondary to alveolar hypoventilation

—-> Gas isn’t being exchanged properly in the lungs for some reason, which leads to ventilatory/respiratory failure

144
Q

ventilatory failure occurs in several conditions that can affect …

A

1) Mechanical respiration
—> (neural control, muscular issues)

2) Lung circulation

3) Airways

4) Gas exchange

145
Q

neural control of respiration

A

Respiratory centers in the brainstem have chemoreceptors to measure the content of carbon dioxide

Brainstem lesions can depress spontaneous breathing

146
Q

respiratory muscles

A

Consist of the diaphragm, SCMs, intercostals, pec. minor, scalenes

→ are striated muscles controlled by cranial and spinal nerves

147
Q

how can respiratory muscles become dysfunctional?

A

Can become dysfunctional under several conditions

→ affect the nerves, the NMJ or muscles themselves

148
Q

various conditions and respiratory failure

A

Poliomyelitis

Spinal cord injury

Tetanus toxin

Myasthenia gravis

Muscular dystrophy

149
Q

Poliomyelitis vs respiratory failure

A

affects the SPINAL CORD can cause RESPIRATORY PARALYSIS

150
Q

Spinal cord injury and ventilatory failure

A

damage to nerves

151
Q

Tetanus toxin

A

muscle spasm

—>
“Respiratory failure because of muscle spasms is a major sequela of tetanus. Spasms can be controlled with sedation and adjunctive treatment, albeit at the expense of respiratory drive and weakness. Invasive ventilation under deep sedation with intensive care unit admission is the best practice.”

152
Q

what percentage of polio patients experience paralysis?

A

In less than 1% of cases, polio causes permanent paralysis of the arms, legs or breathing muscles.

153
Q

Myasthenia gravis and ventilatory failure

A

affects the NMJ to cause depression in breathing

(among other muscles of course)

154
Q

Muscular dystrophy & respiratory failure

A

esp. in Duchennes → causes muscle wasting → respiratory muscle failure

155
Q

Chest wall lesions & ventilatory failure

A

Restrict the expansion of the chest during inspiration

Happens in deformities of chest cage:
—>
(kyphoscoliosis),
pleural fibrosis,
pleural tumours,
extreme obesity

156
Q

airway pathologies and ventilatory failure

A

E.g. CF (with bronchial mucus plugs), COPD, asthma, etc.

157
Q

ARDS (acute respiratory distress syndrome)

A

Acute respiratory distress syndrome

Changes that occur in the lungs that cause acute respiratory failure

158
Q

ARDS vs NRDS

A

“Despite having a similar name, NRDS is not related to acute respiratory distress syndrome (ARDS).”

159
Q

ARDS causes

A

Shock – trauma, burns, acute cardiac failure

Pneumonia

Toxic lung injury – fumes, drugs, bacterial endotoxins

Aspiration of fluids – e.g. drowning

160
Q

ARDS etiology / pathogenesis

A

Can be due to a variety of conditions

161
Q

is ARDS to do with alveoli or capillaries?

A

EITHER / BOTH (?)

Can be either an injury to endothelial cells in pulmonary capillaries or injury to the alveolar lining cells

as a result
—>
Alveolar walls are affected and gas exchange is severely impaired

162
Q

what happens if impaired gas exchange?

A

Impaired oxygenation of blood results in hypoxia

163
Q

what can long term impaired gas exchange lead to?

A

fatal systemic conditions including
—>
shock,
sepsis,
SIRS
and/or respiratory acidosis

164
Q

SIRS

A

Systemic inflammatory response syndrome
—>
“In immunology, systemic inflammatory response syndrome is an inflammatory state affecting the whole body. It is the body’s response to an infectious or noninfectious insult.”

165
Q

cancer – primary vs secondary

A

not idiopathic

primary means it arose from lungs itself (E.g. lung cancer)

secondary means it was d/t metastasis

166
Q

lung cancer – AKA

A

AKA bronchogenic carcinoma

167
Q

lung cancer is malignancy of ____

A

epithelium
of the respiratory tract

168
Q

are most lung cancers primary or secondary?

A

Most PRIMARY

169
Q

lung cancer epidemiology

A

Leading cause of cancer death worldwide (men and women)

One of the world’s leading causes of preventable death

Up to 90% due to smoking cigarettes

170
Q

lung cancer deaths more than ___ + ___ + ___ (THREE CANCERS) combined

A

More deaths than from
—->
colon, breast, and prostate cancer combined

171
Q

when is lung cancer diagnosis most common?

A

Diagnosis typically occurs after 50 years old

172
Q

5 year survival (lung cancer, esp later stages)

A

5 year survival rate from diagnosis is 10-15%
—>
Largely because at diagnosis, 50% of lung cancer is already stage IV

173
Q

lung cancer etiology / risk factors

A

Cigarette smoking
—> More than 20 per day

Occupation
Environmental exposures
Industrial living

Asbestos
Radon gas

Age
Family history

174
Q

Radon gas

A

“Radon is a radioactive gas that has no smell, colour or taste. Radon is produced from the natural radioactive decay of uranium, which is found in all rocks and soils. Radon can also be found in water. Radon escapes from the ground into the air, where it decays and produces further radioactive particles.”

175
Q

types of lung cancers ?

A

1) Small cell lung cancer (SCLC)
—> AKA Oat cell lung cancer

2) Non-small cell lung cancer (NSCLC)

176
Q

1) small cell lung cancer (SCLC)

aka oat cell lung cancer

A

20% of all lung cancers

SCLC is highly aggressive and almost solely occurs in smokers.

177
Q

sclc & metastasis @ time of diagnosis (?)

A

It is rapidly growing, and roughly 60% of patients have widespread metastatic disease at the time of diagnosis.

178
Q

note that small cell cancer is not unique to lungs, and can occur elsewhere?

A

Can have small cell cancer in other tissues not related to the lungs (cervix, prostate, etc)

179
Q

2) Non-small cell lung cancer (NSCLC)

A

80% of all lung cancers

180
Q

NSCLC includes …

A

a) squamous cell carcinoma,

b) adenocarcinoma (most common),

c) large cell carcinoma

181
Q

lung cancer where does it commonly metastasize?

A

brain

182
Q

breast cancer – where commonly metastasize?

A

ovaries

183
Q

which type of lung cancer do non-smokers usually get?

A

Lung cancer that occurs in non-smokers is almost always NON-small cell lung cancer (NSCLC)

—> However, most cases of NSCLC are still smokers

184
Q

what percentage of NSCLC patients have metastasis @ time of diagnosis?

A

Clinical behavior more variable and depends on histologic type;

about 40% of patients will have metastatic disease at the time of diagnosis.

185
Q

metastasis @ diagnosis – SCLC vs NSCLC

A

60% vs 40%

186
Q

lung cancer pathogenesis

A

Various chemicals in tobacco smoke act as primary carcinogens

A)
DNA mutating agents
—>
ACTIVATE ONCOGENES

B)
and/or
—>
DEACTIVATE TUMOR SUPRESSOR GENES

C)
as well as
—>
mutate genes that detoxify (oxidative stress) and assist in DNA repair

187
Q

lung cancer, invasiveness & metastasis

A

Lung cancer is highly invasive and metastasizes early

→ extends into the mediastinum and spreads into pleural cavity and lymph nodes

188
Q

lung cancer Dx can be challenging …

A

A)
not many SSx until late stage

____

B)
can mimic symptoms of other disease
—> E.g. hyperproduction of cortisol
(PARANEOPLASTIC SYNDROME)
I.e.
—> Doesn’t necessarily indicate an issue with lungs

—> Also why websites like WEBMD always list CANCER as potential for MANY, MANY symptom types

189
Q

where does lung cancer metastasize?

A

liver and brain (most often),

bones, kidneys and adrenals

190
Q

where is lung cancer metastasis common?

A

brain (m/c)

191
Q

lung cancer and mass effect

A

Local extension of tumor into the mediastinum or pleural cavity (mass effect)

192
Q

lung cancer, mass effect, and ATELECTASIS

A

Cause obstruction → atelectasis → lung infection

193
Q

lung cancer, mass effect, and PLEURAL EFFUSION

A

yes

194
Q

mass effect & dyspnea (?)

A

Progressive dyspnea from lung compression

195
Q

lung cancer and pain/paralysis of diaphragm & vocal cords

(d/t MASS EFFECT?)

A

Pain and paralysis of muscles of diaphragm and vocal cords

___

“Diaphragmatic paralysis may be caused by tumor compression upon or invasion into the phrenic nerve or the C3–5 nerve roots.”

196
Q

lung cancer – SSx (esp late?)

A

Hemoptysis
Cachexia
SOB
Cough
Anorexia
Paraneoplastic syndromes
Digital clubbing

197
Q

Paraneoplastic syndromes

A

“A paraneoplastic syndrome is a syndrome that is the consequence of a tumor in the body. It is specifically due to the production of chemical signaling molecules by tumor cells or by an immune response against the tumor. Unlike a mass effect, it is not due to the local presence of cancer cells.”

“Paraneoplastic syndromes are rare conditions that can occur with cancerous tumors.”

198
Q

clinical manifestations of liver metastasis (lung cancer)

A

Liver → hepatomegaly

199
Q

clinical manifestations of bone metastasis (lung cancer)

A

Bone → fractures, pain

200
Q

clinical manifestations of adrenal gland metastasis (lung cancer)

A

“Cancer that has spread to the adrenal glands doesn’t usually cause any symptoms.”

“The adrenal glands produce hormones and if cancer has spread to both adrenal glands you might have low levels of adrenal hormones. This might cause: loss of appetite.”

201
Q

clinical manifestations of brain metastasis (lung cancer)

A

neurologic symptoms and high mortality

202
Q

lung cancer – Dx

A

Diagnosis includes chest x-ray and biopsy (best)
—> CT positives are 95% false positive

___
“One potential risk of low-dose CT is that it results in many false-positive findings, such as a lung nodule, that, upon further testing, turns out not to be cancer.”

203
Q

lung cancer – Tx

A

surgery (resection), chemotherapy, radiation

204
Q

lung cancer prognosis

A

Prognosis is very poor

(esp later dx, which is the most common dx d/t few clinical manifestations in early stage)

205
Q

most important thing for lung cancer is ____

A

prevention

not smoking

206
Q
A