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RHS > L2- Pulmonary Pathology I > Flashcards

L2- Pulmonary Pathology I Flashcards

1
Q

Define the following:

  • TV
  • IRV
  • ERV
  • RV
A

Tidal Vol.: volume of air inhaled and exhaled with normal respiration

Inspiratory Reserve Vol.: volume of air that can be inhaled beyond normal inspiration

Expiratory Reserve Vol.: volume of air that can be exhaled beyond normal expiration

Residual Vol.: left over air volume after maximal exhalation

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2
Q

Define the following:

  • TLC
  • VC
  • IC
  • FRC
A

Total Lung Capacity: maximal lung volume after maximal inhalation

Vital Capacity: maximal lung volume that can be inhaled/exhaled (TLC - RV = IRV + ERV + TV)

Inspiratory Capacity: maximal air volume that can be inhaled following normal expiration (TV + IRV)

Functional Residual Capacity: lung volume after normal expiration (ERV + RV)

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3
Q

Define the following:

  • FVC
  • FVC1
  • FEF
A

Forced Vital Capacity: volume of air exhaled with force following maximal inhalation

FVC-1: volume of air exhaled with force in first second following maximal inhalation

Forced Expiratory Flow (25%-75%): measure of airflow midway through expiration (middle half)

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4
Q

Describe how the following change in Restrictive Lung Disease:

  • FEV1/FVC
  • FEV1
  • FVC
  • TLC
A
  • FEV1/FVC: normal or inc (>80%)
  • FEV1: normal or slightly dec
  • FVC: dec
  • TLC: dec
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5
Q

Describe how the following change in Obstructive Lung Disease:

  • FEV1/FVC
  • FEV1
  • FVC
  • TLC
A
  • FEV1/FVC: dec (<70%)
  • FEV1: dec (significant)
  • FVC: dec or normal
  • TLC: inc or normal
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6
Q

list the 4 types of laboratory tests conducted in the respiratory system

A
  • Sputum analysis: cells, microbiology
  • Arterial blood gases (pCO2, pO2)
  • Pleural fluid
  • Blood Culture
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7
Q

describe the goal or types of tests conducted in sputum analysis

A

Cell analysis: WBCs, RBCs, malignant cells

Microbiological Studies:

  • bacteria (staining, culture, AB resistant)
  • fungal (KOH, culture)
  • viral (PCR, DNA, culture)
  • NAAT (nucleic acid amplification testing)
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8
Q

what are the blood gas changes seen in lung diseases and why are they monitored

A
  • pCO2: looking for INCreases
  • pO2: looking for DECreases

-the quantity of changes determines the severity of the disease progression

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9
Q

describe how pleural fluid is studied for lung diseases

A

-used as a therapeutic or diagnostic technique

i) Cell Count: HF (dec to normal) vs Infection (inc)
ii) Malignancy: primary vs secondary

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10
Q

list the techniques or procedures used to acquire lung sample for cytology (hint- 9)

A
  • bronchial washings (inject slime and aspirate it out)
  • bronchial brushing (scraping lesion)
  • TBNA, transbronchial needle aspiration
  • TTNA, transthoracic needle aspiration
  • EBUS-FNA, endobronchial ultrasound-guided fine needle aspiration

-navigational bronchoscopy

  • bronchoscopic biopsy: transbronchial, endobronchial
  • pleuroscopic biopsy

-Surgical biopsy / resection: VATS (video assisted transthoracic) biopsy or Open biopsy

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11
Q

foreign objects that are accidentally inhaled will generally go into the (R/L) lung because of (2)

A

R lung- the R main bronchus is shorter and more vertical than the L

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12
Q

Respiratory Zone function, (1)

Conducting Zone function, (2)

A

1- gas exchange

2- carry, warm, filter, humidify air

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13
Q

list the components of the Bronchial Walls (histology)

A 
[conducting zone only- no gas exchange]
(inside to outside)
1) Epithelium: ciliated columnar cells, goblet cells, basal cells, neuroendocrine cells
2) Basement Membrane
3) Smooth Muscle
4) Seromucinous Glands
5) Cartilage
6) Vasculature and Lymphatics
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14
Q

list the components of the Bronchiolar Walls (histology)

A

[conducting zone until terminal bronchioles –> respiratory zone and respiratory bronchioles]
(inside to outside)
1) Epithelium: ciliated columnar cells, Clara cells
2) Basement Membrane
3) Smooth Muscle
4) Vasculature and Lymphatics

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15
Q

compare the epithelium of Bronchi and Bronchioles

A

Bronchi: ciliated columnar cells, goblet cells, basal cells, neuroendocrine cells

Bronchioles: ciliated columnar cells, Clara cells

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16
Q

describe the histology of alveoli

A

(inside to outside)

1) epithelium: type I/II pneumocytes
2) alveolar macrophages
3) interstitium
4) capillaries (endothelial cells)

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17
Q

The alveolar epithelium is mostly type (I/II) pneumocytes.

  • type I function, (2)
  • type II function, (3)
A

1- type I, 95%
2- gas exchange
3- surfactant production, alveolar epithelium repair (generates type I and II pneumocytes)

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18
Q

______ cells are responsible for gas exchange in alveoli

A

type I pneumocytes

19
Q

______ cells are responsible for surfactant production

A

type II pneumocytes

20
Q

______ cells are responsible for repairing alveolar epithelium

A

type II pneumocytes (generates type I and II pneumocytes)

21
Q

Atelectasis refers to either (1) or (2). The loss of (3) is secondary to (1)/(2) and has the following progression, (4).

A

(atelectasis = collapsed lung)
1- incomplete expansion of lungs (neonatal atelectasis)
2- collapse of previously inflated lung
3- lung volume
4- dec oxygenation –> ventilation perfusion imbalance

22
Q

list the three types of atelectasis

A

(based on cause and mechanism)

  • resorption atelectasis (obstruction)
  • compression atelectasis
  • contraction atelectasis
23
Q

(1) atelectasis results do to some obstruction as a result of one of the following, (2)

A

Resorption Atelectasis

  • mucus/mucopurulent plug post-surgery
  • aspiration of foreign material
  • bronchial asthma, chronic bronchitis, bronchiectasis
  • bronchial neoplasms (if total obstruction)
24
Q

Resorption atelectasis results from (1) of the (2) part of respiratory tract. As a result, (3) is prevented and the (4) progression will occur to cause final (5) change to the lung.

A

1- complete obstruction
2- bronchi, subsegemental bronchi, bronchioles
3- airflow to alveoli
4- trapped air in distal spaces is resorbed thru Pores of Kohn (alveoli to alveoli) –> lack of air to distal airspaces –> (5)
5- lung collapse

25
Q

In resorption atelectasis, (1) is evident or presents 24-36 hrs post-lung collapse.

  • (2) and (3) are evident on imaging (X-Ray)
  • (4) is evident upon palpation and auscultation
A

1- fever, dyspnea

2- ipsilateral deviation of trachea / mediastinum
3- ipsilateral diaphragmatic elevation

4- absent breath sounds (no expansion upon inspiration –> dec air movement) + absent vocal vibratory sensation / tactile fremitus

26
Q

Compression atelectasis or lung collapse can occur due to accumulation of…… (include examples)

A
  • air
  • fluid
  • tumor

i.e. tension pneumothorax, pleural effusion

27
Q

_________ is the main clinical feature of compression atelectasis

A

(contralateral) trachea and mediastinum shift away from affected lung

28
Q

Contraction atelectasis, aka (1), occurs due to (2) affecting (3) or (4) which will prevent (5)

A 
1- cicatrization atelectasis
2- fibrosis (local or diffuse)
3- lung
4- pleura
5- lung expansion
29
Q

(T/F) atelectasis is a reversible process

A

T- Resorption and Compression atelectasis

F- Contraction atelectasis

30
Q

atelectasis is treated promptly in order to prevent….

A
  • hypoxemia

- superimposed infection of collapsed lung

31
Q

Surfactant is made out of….

A

(lipoprotein)
Lipids: phosphatidylcholine (lecithin), phosphatidylglycerol

Surfactant Proteins: SP- A, B, C, D

32
Q

surfactant production begins during (1) and is stored in (2)

A

1- week 28 of gestation

2- lamellar bodies of type II pneumocytes

33
Q
  • surfactant production is increased in response to (1) hormone(s)
  • surfactant production is decreased in response to (2) hormone(s)
A

1- (inc) cortisol, thyroxine

2- (dec) insulin

34
Q

describe the function of SP- A, B, C, D

A

(surfactant protein)
B, C: reduces surface tension at air-liquid barrier in alveoli –> prevents collapse on expiration

A, D: innate immunity

35
Q

SP-__ functions in the innate immune system

A

Surfactant Protein- A, D

36
Q

SP-__ functions to reduce air-liquid barrier surface tension to prevent lung collapse upon expiration

A

Surfactant Proteins- B, C

37
Q

Neonatal atelectasis causes (1) in newborns and occurs as a result from (2).
Risk factors: (3), (4), (5)

A

1- RDS (respiratory distress syndrome)
2- dec surfactant production

3- premature birth: before 28 wks
4- maternal diabetes: fetal hyperglycemia => insulin release => dec production
5- C-section: b/c dec cortisol => dec production // labor/vaginal delivery inc stress => inc production

38
Q

how does maternal diabetes affect surfactant production

A
  • fetal hyperglycemia => insulin release

- insulin dec surfactant production

39
Q

compare mechanism for increased surfactant production in vaginal delivery vs C-section

A
  • vaginal birth => inc stress => inc cortisol => inc surfactant production
  • C-section has less cortisol in neonate, less surfactant production
40
Q

Neonatal atelectasis results in hypoxemia and CO2 retention in the body, which is mainly exhibited by (1) in the blood. As a result of (1), (2) occurs which causes (3) and (4), where (2), (3), (4) all compound the hypoxemia and CO2 retention. The biggest consequence of (3) and (4) is (5).

A

1- respiratory acidosis
2- pulmonary vasoconstriction / hypoperfusion
3- endothelial damage
4- epithelial damage
5- plasma leaks into alveoli –> hyaline membrane of fibrin and necrotic cells

41
Q

_____ is the main histological feature of neonatal atelectasis

A

hyaline membrane (fibrin and necrotic cells) as a result of plasma leak into alveoli

42
Q

Neonatal atelectasis is evident by (1) at birth, with (2) evident in blood work and (3) evident on imaging

A

1- RDS (respiratory distress syndrome) w/in few hrs of birth
2- hypoxemia, respiratory acidosis
3- ‘ground glass appearance’ (CXR)

43
Q

list the common complications of neonatal atelectasis

  • (1) in the brain
  • (2) in the GIT
  • (3) blood labs
  • (4) blood vessel structure
  • (5) as a result of Tx / therapy
A

1- intraventricular hemorrhage
2- necrotizing enterocolitis b/c intestinal ischemia
3- hypoglycemia b/c excessive insulin release
4- PDA b/c persistent hypoxemia
5- [via O2 therapy] lung damage (bronchopulmonary dysplasia) and cataracts/blindness

RHS (35 decks)

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