Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

(OMS2) CPR II Exam 2 > (14.1) Pulmonary Pathology (Singh) > Flashcards

(14.1) Pulmonary Pathology (Singh) Flashcards

1
Q

Describe the progression of normal fetal lung development

A

Embryonic (lung bud) –> Pseudoglandular –> Canalicular –> Saccular –> Alveolar

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

What are the clinical uses for knowing the stage of fetal lung development?

A

Knowing the stage can help the clinician determine the age of the fetus

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

What are the requirements for normal fetal lung development?

A
  • Space in the thoracic cavity
  • Ability to inhale (chest call must be able to move, and there must be enough material (amniotic fluid) present to inhale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the main structures you will see histologically of the trachea and main bronchi?

A

Cartilage

Glandular tissue

Respiratory epithelium

Smooth muscle layer

Lamina propria

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

Describe what you would encounter with a low-power image of lung parenchyma

A

Alveoli

Blood vessels

Bronchioles

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

Describe what you would encounter with a high-power image of lung parenchyma

A

Erythrocytes

Macrophages

Type 1/2 pneumocytes

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

What is CRUCIAL to the sucessful oxygen exchange occuring in the lungs?

A

A very THIN layer between the circulating erythrocytes and alveolar lumen so that there is easy exchange

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

Describe the function of Type I pneumocytes

A

Facilitate gas exchange

*Support and line the alveoli

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

Describe the function of Type II pneumocytes

A

Product surfactant

Replace type 1 pneumocytes (they are pluripotent)

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

What is the function of alveolar pores (of Kohn)?

A

“holes” that allow aeration but also bacteria/cells/exudate to travel between alveoli

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

What is this pathology?

A

Pulmonary hypoplasia

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

What causes pulmonary hypoplasia?

A

Reduced space in the thoracic cavity (eg. diaphragmatic hernia taking up the space by the lungs)

Impaired ability to inhale (eg. oligohydraminos from renal agenesis, airway malformation, chest wall motion disorders)

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

What is the mortality rate of pulmonary hypoplasia?

A

HIGH! (up to 95%)

If lung weight is <40%, immediate death occurs in neonatal period

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

What are foregut cysts?

A

Detached outpouchings of foregut

Seen along hilum and mediastinum

Can be respiratory, esophageal or gastroenteric

Often asymptomatic and seen incidentally; complications include rupture, infection, or airway compression

Tx: Excision is curative

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

What is congenital pulmonary adenomatoid malformation (CPAM)?

What are the complications?

A

“Arrested development” (stuck at a stage) of pulmonary tissue branching from the tracheobronchial tree with formation of intrapulmonary cystic masses that repeats itself; can be detected via US

can lead to hydrops fetalis, pulmonary hypoplasia (since the CPAM is taking up the space for the lung to grow) or get infected later in life

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

What are pulmonary sequestrations?

A

Nonfunctioning lung tissue that forms as an aberrant accessory“lung bud”, not connected to the tracheobronchial tree unlike CPAM

*Typically found in the region of the left lower lobe

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

How are pulmonary sequestrations characterized?

A

Lack of connection to the tracheobronchial tree

Independent (systemic) arterial supply, but they are non functional so they do not tend to get blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is this image an example of?

A

Intralobar pulmonary sequestration (ILS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are intralobar pulmonary sequestration (ILS)s susceptible to?

A

Lack of airway perfusion makes ILS’s susceptible to infection and absess formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is this an example of?

A

Extralobar pulmonary sequestrations (ELS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How are extralobar pulmonary sequestrations (ELS) different from ILS?

A

ELS have their own PLEURA, appears as a mass in the chest or abdomen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What comes to attention sooner…

ILS or ELS?

A

ELS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the differences between these congenital anomalies:

CPAM/CCAM

vs

Pulmonary sequestraion

A

CPAM/CCAM = INTRApulmonary cystic malformation w/ CONNECTION to tracheobronchial airways and pulmonary vasculature

Pulmonary sequestration = INTRA or EXTRA pulmonary lung tissue with NO CONNECTION to pulmonary vasculature or tracheobronchial tree

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is atelectasis?

A

Partial or complete collapse of the lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the three major types of **atelectasis?**
- Resorption - Compression - Contraction
26
What causes **resorption atelectasis?**
**Airway obstruction** - parenchyma does not get air = gradual _resorption_ of air reduces lung expansion
27
What causes **compression atelectasis?**
**Accumulated material** in pleural cavity **compresses** the lung parenchyma and prevents it from expanding
28
What causes **contraction atelectasis?**
**Fibrotic** or other **innate restrictive process** in the pleura or peripheral lung restricts lung expansion
29
What is the LEAST common form of **atelectasis?**
Contraction atelectasis
30
What pathologic process is occuring here?
Pulmonary edema
31
What are the major causes of **pulmonary edema?**
"Pushing out" --\> as in left sided heart failure (backing to pulm circ. = too much blood in pulm .circuit = leak out = pulm edema) "Leaking out" --\> pulmonary vessels cannot keep blood in and it leaks out in the lungs (e.g. low albumin/oncotic pressure) Injury to alveolar wall Unsure mechanisms (neurologic, high altitude pulmonary edema)
32
What are the clinical criteria for **acute lung injury (ALI)?**
Acute onset Hypoxemia (PaO2/FiO2 \<300) Bilateral infiltrates No evidence of cardiac failure
33
What is the clinical criteria for **acute respiratory distress syndrome (ARDS)?**
Abrupt onset of symptoms Hypoxemia (PaO2/FiO2 \<200) Bilateral infiltration Non cardiac in nature
34
What is **diffuse alveolar damage (DAD)?**
Histologic manifestation of ARDS
35
What is the pathology?
Acute respiratory distress syndrome (ARDS)
36
What is the pathophysiology of ARDS?
Fluid leaks into the endothelium from the capillary into the alveoli \> damage to the Type 1 and 2 pneumocytes \> debris forms hyaline deposits on the alveoli
37
What is the pathology?
Diffuse alveolar damage (DAD) Edema + Fibrin + Cell debris = HYALINE MEMBRANES
38
What are the three stages of ARDS?
1. Exudate 2. Proliferative 3. Fibrotic
39
What occurs during the **exudative stage** of ARDS?
Edema Hyaline membranes Neutrophils
40
What occurs during the **proliferative stage** of ARDS?
Fibroblast proliferation Organizing pneumonia Can lead to resolution or Early fibrosis
41
What occurs during the **fibrotic stage** of ARDS?
Extensive fibrosis Loss of normal alveolar architecture
42
ARDS : resolution After the fibroproliferative phase, 2 pathways may ensue... what are they?
Resolution OR Fibrosis (irreversible)
43
Describe the histologic differences b/w a normal lung and a lung w/ hyaline membranes
Lung w/ hyaline membranes has THICKENED walls that make oxygen exchange nearly impossible This is what accounts for the decreased PaO2/FiO2 values observed
44
What is **acute interstitial pneumonia (AIP)?**
Same clinical presentation as **ARDS** Same histology as **ARDS/DAD** **_\*\*\*​CANNOT BE ATTRIBUTED TO A SPECIFIC ETIOLOGY_**
45
What is restrictive lung disease?
aka interstitial lung dz, characterized by volume restriction (stiff lungs) = cannot fill the lung FEV1/FVC ratio is normal or increased (both are reduced BUT the ratio is not necessarily reduced) (FEV=force expiratory volume, FVC=forced vital capacity)
46
What is **obstructive lung disease?**
Decreased flow **LOW FEV1/FVC ratio** \*\*\*(FEV=force expiratory volume, FVC=forced vital capacity)
47
What are examples of **obstructive pulmonary diseases?**
Emphysema Chronic bronchitis Asthma
48
What is the most common cause of **COPD/Chronic bronchitis?**
Smoking
49
Describe what is occuring during a **chronic bronchitis** state
Smoke chemicals cause inflammation and mucus production - Mucus hypersecretion (mucinous layer with goblet cell hyperplasia/hypertrophy) \> cillia is "drowning" and cannot get rid of the debris/chemicals - predisposes to more inflammation and infection
50
What is the criteria for diagnosing chronic bronchitis?
Persistent cough **w/ sputum production** for _3 months out of 2 consecutive years_
51
What is the predominant pathophysiologic mechanism of chronic bronchitis?
Mucous gland **hyperplasia**
52
What are the complications of chronic bronchitis?
Squamous cell metaplasia of the bronchi \> dysplasia \> carcinoma Bronchiectasis Death for respiratory infection
53
What is the pathology?
Emphysema \*Notice the extremly dilated spaces within the lung parynchema
54
Why is **emphysema** considered an _obstructive process?_
There is a **compressed duct** proximal to the alveolar sac \> causes the destruction of the alveolar sacs that define emphysema Smoking induced emphysema: centriacinar emphysema (upper lobes)
55
What is the clinical presentation of **emphysema?**
Clear but enlarged lungs on CXR "Barrel chest" FEV1/FVC ratio is reduced
56
What does "blue bloaters" refer to?
Chronic bronchitis (actually the initial stage of emphysema) cyanotic and edematous (rhonchi - mucus) compensation still going on so Hgb is elevated
57
What does "pink puffers" refer to?
Emphysema Older and thin, severe dyspnea, pursed lips trying to prolong expiratory wheezing
58
What is alpha1-antitrypsin?
Alpha1-antitrypsin coats the lungs **protecting** them from **neutrophil elastase** Neutrophil elastase is produced by white blood cells to break down harmful bacteria
59
What is an **alpha1-antitrypsin deficiency?**
Lungs LACK alpha1-antitrypsin coating coded by Pi gene on Cr.14 (Homozygous mutatnt is PIZZ) This leaves lungs **vulnerable** to damage by **neutrophil elastase \> panacinar emphysema (lower lobes since it contacts more elastase from the capillaries in the setting of decreased a1-antitrypsin)** **presents as dyspnea + cirrhosis in genetically susceptible individuals**
60
Describe the type of emphysema associated with each image
61
Alpha1 antitrypsin deficiency demonstrates a ___________ emphysema pattern
BASILAR panacinar
62
What are the complications of emphysema?
Respiratory failure Pneumothorax with lung collapse CAD Right heart failure (cor pulmonale)
63
What are the basic mechanisms of **asthma?**
Inflammation \> airway hyperresponsiveness + airway obstruction (reversible)
64
What are the classifications of **asthma?**
Atopic (extrinsic) Non-atopic (intrinsic)
65
Describe **atopic** asthma
2/3 of all patients May be any age, usually children FH of asthma triggered by allergies, Elevated **IgE levels** (type I hypersensitivity) Triggers may include a variety of **allergens**
66
Describe the pathogenesis of atopic asthma
TH2 \> interleukins \> recruit inflammatory cells TH2 \> leukotrienes C4, D4, E4 \> bronchoconstriction, increased vascular perm, mucus secretion Mast cell cross linked to IgE \> histamine
67
Describe **non-atopic** asthma
1/3 of all patients Often older pts NORMAL IgE levels Triggers include **cold, exercise, infection**
68
Why is it SO important to make sure your asthmatic patients' have "controlled" asthma?
High potential for irreversible **airway remodeling with each subsequent asthma attack**
69
What are some of the results of **airway remodeling?**
Fibrosis Smooth muscle hyperplasia Increased goblet cells and submucosal glands \*now irreversible
70
Pharmacologically, what is a huge problem in patients that have undergone airway remodeling?
DECREASED response to therapeutic agents: Bronchodilators Corticosteroids
71
What is **status asthmaticus?**
Unremitting, potentially fatal asthma attack Characterized by **bronchial occlusion by thick mucus** \*Hallmark = **_curschmann spirals_** (coiled mucus plugs) and Charcot Leyden crystals (eosinophlic crystals) found in mucus
72
What is **aspirin-sensitive asthma?**
Unique sensitivity to aspirin that induces asthma Highly associated with: nasal polyps and recurring rhinitis (Samter's triad)
73
What is the pathogenesis of aspirin sensitive asthma?
Aspirin inhibits COX-1 \> AA accumulates \> becomes Leukotriene C4, D4, E4
74
What is **bronchiectasis?** ## Footnote **What conditions predispose to bronchiectasis?**
**Necrotizing inflammatory response** that is an end stage process of multiple processes that can include infection or obstruction ABPA, Cystic Fibrosis, Chronic Infection (TB), Primary ciliary dyskinesia
75
Describe the path of **cystic fibrosis**
CFTR gene is affected Chloride transport is impaired \> cells absorb extra Na+,Cl and H20 instead of lubricating the mucus --\> Leads to dehydrated mucus that forms plugs \> predispose to infection \> bronchiectasis
76
What is **kartagener's syndrome?**
Aka Primary ciliary dyskinesia --\> Dysfunction of **_dynein arm_** of microtubules --\> impaired ciliary function Triad of : Sinusitis, bronchiectasis, situs inversus dextrocardia (cillia helps rotate the organs in utero) \*\*\*Often male infertility (sperm cannot swim)
77
What is this pathology?
Allergic Bronchopulmonary Aspergillosis (ABPA)
78
What is **allergic bronchopulmonary aspergillosis (ABPA)?**
Exaggerated hypersensitivity response to **Aspergillus** infection overlying chronic lung disease --\> Background of **asthma** or **CF** -Increased **IgE** on serum testing, positive **skin test** \*\*\*Thick mucus in bronchi

(OMS2) CPR II Exam 2 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions