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RHS > L3- Pulmonary Pathology II > Flashcards

L3- Pulmonary Pathology II Flashcards

1
Q

ALI = (1- include alternate name) is characterized by (slow/rapid) onset of (3) and (4) in the absence of (5).

A 
1- acute lung injury // noncardiogenic pulmonary edema
2- abrupt / rapid onset
3- significant hypoxemia
4- bilateral pulmonary infiltrates
5- cardiac failure
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2
Q

(1) is the histological manifestation of ALI/(2)/(3). (1) is the root cause of (4).

A

1- DAD, diffuse alveolar damage
2/3- (acute lung injury), noncardiogenic pulmonary edema, shock lung syndrome
4- ARDS (acute respiratory distress syndrome)

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3
Q

DAD is the main cause of (1) during one of the following settings: (2). (1) is characterized by (3).

A

(diffuse alveolar damage)
1- ARDS, acute respiratory distress syndrome
2- sepsis, severe trauma, diffuse pulmonary infection (etc)
3- progressive respiratory insufficiency

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4
Q

list the ‘direct’ causes of pulmonary insult in ARDS (hint- 6)

A
  • pneumonia
  • aspiration
  • emboli
  • inhalation injury
  • drowning
  • oxygen toxicity
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5
Q

list the ‘indirect’ causes of pulmonary insult in ARDS (hint- 7)

A
  • sepsis
  • trauma with shock
  • acute pancreatitis
  • severe burns
  • blood transfusion (or its products)
  • uremia
  • drugs
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6
Q

list the risk factors for ARDS

A

Non-heritable: smoking and alcohol

Heritable: several genes, includes variants that map genes linked to inflammation and coagulation

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7
Q

list the steps of ARDS/ALI pathogenesis

A

1) endothelial activation
2) adhesion and extravasation of neutrophils
3) accumulation of intra-alveolar fluid and formation of hyaline membranes

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8
Q

In ARDS/ALI, endothelial activation occurs in response to….

A

(1st of 3 steps of pathogenesis)

  • directly by circulation inflammatory factors
  • secondary to pneumocyte injury
  • *mediated by alveolar macrophages
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9
Q

In ARDS/ALI, after endothelial activation, (1) is increased on the endothelium in order to (2) and migrate them into (3). Once (2) enters into (3), (4) will occur.

A 
(2nd of 3 steps of pathogenesis)
1- adhesion molecules
2- bind neutrophils
3- interstium and alveoli
4- degranulate and release inflammatory mediators
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10
Q

In ARDS/ALI, inflammatory molecules from neutrophils leads to (1) within the alveoli. (1) will lead to the loss of (2) and the deficiency of (3). As a result (4) and (5) accumulate within the alveoli in order to form (6).

A 
(3rd of 3 step of pathogenesis)
1- leaky capillaries
2- diffusion across alveolar membrane
3- surfactant (type II pneumocyte damage)
4- protein rich fluid
5- cellular debris
6- hyaline membrane
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11
Q

list the chemical mediators involved in the pathogenesis of ARDS/ALI

A 
CKs
oxidants
GFs
TNF
IL-1, IL-6, IL-10
TGF-β
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12
Q

In the resolution of ARDS/ALI, (1) enter the intra-alveolar space in order to remove debris and (2) leading to (3). (4) will proliferated to replace pneumocytes. Endothelium will restore as a result of (5).

A 
1- macrophages
2- release fibrogenic factors
3- fibrosis of alveolar wall
4- bronchiolar stem cells
5- proliferation of uninjured capillary endothelium
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13
Q

list the phases exhibited histologically for ARDS

A

(DDD- diffuse alveolar damage)

1) acute / exudative phase, 0-4 days
2) organizing / proliferative phase, 4 days - 3 wks

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14
Q

Acute phase, aka (1), occurs for (2) duration after onset of ARDS. It is characterized by a (3) gross appearance of the lungs, (4) of the interstitium and intra-alveolar spaces, and (5) of the alveolar epithelium in order to create (6), the main characteristic feature.

A 
1- exudative phase
2- (days 0-4)
3- heavy, firm lungs
4- edema / hemorrhage
5- necrosis and sloughing of cells
6- Hyaline Membranes
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15
Q

Organizing phase, aka (1), occurs for (2) duration after onset of ARDS. It starts with the proliferation of (3) and the organizing of (4) in order to establish (5) as the end result.

A 
1- proliferative phase
2- (day 4 - week 3)
3- type II pneumocytes
4- fibrin exudates into Fibrosis
5- alveolar septal thickening

(Note- there is resorption of the Hyaline Membranes created in the acute phase)

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16
Q

list the sign and symptom progression of ARDS/DAD

A
  • rapid onset, w/in wks
  • severe dyspnea –> tachypnea –> hypoxemia (refractory to O2 therapy)
  • cyanosis
  • respiratory failure
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17
Q

how is ARDS/DAD investigated

A

1) diffuse bilateral infiltrates on radiograph (i.e. CXR)

2) V/Q mismatch (ventilation perfusion mismatch)

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18
Q

ARDS/DAD has a (1) mortality rate, where (2) are factors that indicate a poor prognosis. If there is recovery, normal function may take up to (3- time) to return. It is treat with (4).

A

1- 40% (although decreasing)
2- advanced age, bacteremia/sepsis, progression to multi-system organ failure
3- 6-12 mos
4- supportive therapy

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19
Q

Obstructive lung diseases are considered (1) disorders and affect the (2) parts of the lung. (3) is increased and is exhibited by (4) on spirometry.

A

1- airway disorders
2- trachea to terminal bronchioles
3- airflow resistance (limits expiratory rates on forced expiration)
4- reduced FEV1/FVC ratio

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20
Q

Restrictive lung diseases are considered (1) disorders and affect the (2) parts of the lung. (3) are decreased and is exhibited by (4) on spirometry.

A

1- parenchymal disorder
2- respiratory bronchioles to alveoli / alveolar ducts
3- TLC, O2 diffusing capacity, other lung volumes, lung compliance
4- inc FEV1/FVC ratio (or normal)

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21
Q

Obstructive lung disease spirometry, indicate inc, dec, or no change to the following:
TLC, FEV1, FVC, FEV1/FVC, FRC, RV

A 
TLC- inc
FEV1- large dec
FVC- dec
FEV1/FVC- dec, <0.7 
FRC- inc
RV- inc
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22
Q

Restrictive lung disease spirometry, indicate inc, dec, or no change to the following:
TLC, FEV1, FVC, FEV1/FVC, FRC, RV

A 
TLC- dec
FEV1- dec
FVC- large dec
FEV1/FVC- inc/normal. >0.8
FRC- dec
RV- dec
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23
Q

list the common obstructive lung diseases (hint- 4)

A

emphysema
chronic bronchitis
asthma
bronchiectasis

24
Q

list the common restrictive lung diseases (hint- 4)

A
  • Acute Restrictive Disease: ARDS
  • Chronic Restrictive Disease: interstitial fibrosis, pneumoconiosis, granulomatous
  • chest wall deformities
  • neuromuscular
25
Q

COPD affects (men/women) more

A

affects men and women equally

26
Q

compare COPD to Asthma in terms of types of airflow obstruction

A

COPD (+ emphysema, bronchiectasis): loss of elastic recoil –> expiratory obstruction secondary to airway collapse // Irreversible

Asthema: anatomic airway narrowing // Reversible

27
Q

list the 3 reasons why chronic bronchitis and emphysema are grouped together in COPD

A

1) smoking is common trigger
2) overlapping features: many Pts present with features of both conditions
3) management of disease is similar

28
Q

Emphysema is characterized by (1) occurring in the (2) part of the lung. It is accompanied by (3), but (4) is importantly absent.

A

1- abnormal permanent airspace enlargement
2- distal to terminal bronchioles
3- destruction of airspace walls
4- fibrosis

29
Q

list the 4 types of Emphysema

A
  • Centrilobular / Centriacinar
  • Panlobular / Pananinar
  • Para-septal / Distal Acinar
  • Irregular / Paracicatricial
30
Q

In centrilobular, aka (1), emphysema, the (2) parts of the respiratory tract is affected and the (3) part of the lung is most affected. (4) is the common cause. (5) is a unique feature seen in individual lobules.

A

1- centriacinar
2- respiratory bronchiole (spares distal alveoli)
3- upper lungs
4- smoking
5- diseased and normal airspaces in same lobule

31
Q

the most common emphysema is (1); (2) is the other common emphysema seen in practice

A

1- centrilobular / centriacinar

2- panlobular / panacinar

32
Q

In panlobular, aka (1), emphysema, the (2) parts of the respiratory tract is affected and the (3) part of the lung is most affected. (4) is the common cause.

A

1- panacinar
2- respiratory bronchiole to distal alveoli affected
3- lower lung
4- AAT-1 deficiency

33
Q

describe the 2 rare or less common emphysemas

A

Para-septal / Distal acinar:

  • next to atelectasis, along septa, margins of lobes, subpleural
  • more common in upper lobes
  • bullae may form
  • may lead to pneumothorax

Irregular / Paracicatrical: surrounding scar, asymptomatic

34
Q

Emphysema pathogenesis is based on (1). The (2) component of one is released from (3) after its infiltration, and functions to (4). The (5) factor plays a protective role in the lung. Therefore an increase in (2) or decrease in (5) can lead to (6).

A

1- imbalance of protease-antiprotease mechanism
2- protease
3- neutrophils (+ other leukocytes)
4- destroy lung tissue
5- antiprotease (ex. AAT, inhibits neutrophilic proteasses)
6- destruction of alveolar parenchyma

35
Q

what are the 3 genetic factors that play a role in emphysema

A

A1AT deficiency: antiprotease deficiency, accompanied by abnormal protein accumulating in liver => chronic liver disease

TGF-β gene polymorphism: dec signaling => inadequate elastin repair

MMP gene polymorphisms: inc in emphysema

36
Q

A1AT is a (1) type protein. Its abnormal form from (2) genotype found on chromosome (3), can have abnormal folding, leading to accumulation in (4) causing (5).

A 
1- antiprotease (in lung)
2- Pi-ZZ (Pi-MM is normal)
3- chr.14
4- liver
5- chronic liver disease
37
Q

list the 3 major histological features of emphysema

A
  • large alveolar spaces
  • alveolar septa destruction w/o fibrosis (septa is free flowing in air spaces)
  • elastin destruction in small airways => lung collapse during expiration, a functional obstruction
38
Q

describe the symptoms or patient presentation for emphysema

A
  • dyspnea, insidious/progressive onset
  • productive cough, variable
  • weight loss, hyperventilation and excessive puffing/panting => pink puffers
39
Q

describe the signs seen on patient exam for emphysema

A
  • barrel chest
  • prolonged expiration + pursed lips
  • sitting forward, hunched trying to squeeze air out of lungs
40
Q

describe the spirometry results for emphysema

A
  • inc lung volumes: TLC, RV
  • dec FVC, FEV1 (more so) => FEV1:FVC dec
  • dec DLCO (diffusing capacity for the lungs) due to loss of SA in lung for diffusion
41
Q

describe the results of CXR and blood gases seen in emphysema

A

CXR: inc air trapping, flat domes of diaphragm

Blood Gases: normal until later presentation (pink puffers), showing hypoxia, hypercapnia, respiratory acidosis

42
Q

The main end progression of emphysema is (1), and (2) is the main complication seen.

A

1- irreversible lung damage

2- Cor Pulmonale

43
Q

describe how to diagnose chronic bronchitis

A 
(clinical Dx)
persistent productive cough:
->3 consecutive mos in a yr
->2 consecutive yrs
-no other identifiable cause
44
Q

Chronic bronchitis is mostly caused by……

A

inhaled irritants: smoking or urban dweller inhalation of SO2, NO2

45
Q

describe the steps of pathogenesis for chronic bronchitis in response to inhaled irritants

A

1) submucosal gland hypertrophy => mucus hypersecretion
2) goblet cell metaplasia in bronchioles
3) smooth muscle hyperplasia + peribronchiolar fibrosis => small airway obstruction distally
4) inflammation: Tc cells, macrophages, neutrophils

46
Q

describe the gross appearance of the lung in chronic bronchitis

A
  • hyperemia and edema of mucous membranes

- excessive mucinous or mucopurulent secretions

47
Q

describe the histological appearance of the lung in chronic bronchitis

A
  • inc Reid index = thick mucus gland layer
  • goblet cell metaplasia
  • smooth cell hyperplasia
  • peribronchiolar fibrosis
  • irritant => squamous metaplasia
48
Q

describe Reid index and its relationship to chronic bronchitis

A

Reid Index- ratio of thickness of mucous gland layer to thickness of wall between epithelium and cartilage

-chronic bronchitis, >40%

49
Q

describe the symptoms or patient presentation for chronic bronchitis

A
  • persistent cough (see criteria in other slide)
  • progression to dypsnea upon exertion
  • cyanosis (blue bloaters)
50
Q

describe the signs seen on patient exam for chronic bronchitis

A
  • hypoxia, hypercapnea, cyanosis
  • persistent hypercapnea –> desensitizes PCO2 sensitive centers –> switch to respiration drive based on PO2 –> caution needed with O2 therapy
51
Q

what are the 2 main complications that stem from chronic bronchitis

A
  • secondary infections

- pulmonary HTN –> Cor Pulmonale

52
Q

compare i) age of onset and ii) CXR results between emphysema and chronic bronchitis

A

i) age of onset
Emphy: 50-75 y/o
CB: 40-45 y/o

ii) CXR
Emphy: hyperinflation, small heart
CB: prominent vessels, large heart

53
Q

compare i) airway resistance and ii) elastic recoil between emphysema and chronic bronchitis

A

i) airway resistance:
- Emphy: normal or slight inc
- CB: inc

ii) elastic recoil:
i) Emphy: low
ii) CB: normal

54
Q

compare presentation of i) dyspnea, ii) cough, and iii) general appearance between emphysema and chronic bronchitis

A

Emphysema:

i) severe and early dyspnea
ii) late, scanty sputum in cough
iii) pink puffer

CB:

i) mild and late dyspnea
ii) early, copious sputum in cough
iii) blue bloater

55
Q

compare presentation of i) infections, ii) respiratory failure, and iii) cor pulmonale between emphysema and chronic bronchitis

A

Emphysema:

i) occasional
ii) terminal
iii) rare, terminal

CB:

i) common
ii) repeated (cyclic)
iii) common

RHS (35 decks)

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