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Flashcards in Pathology 1 & 2 Deck (55):
1

Atelectasis:

incomplete expansion of lungs (neonatal) or collapse of previously inflated lung substance; usually reversible; hypoxia; predisposes to infection

2

types of atelectasis in adults:

1) resporption-
-follows complete airway obstruction
-excessive secretions
-mediastinal shift TOWARD atelectatic lung
2) compression-
-excessive air, fluid, blood or tumor in pleural space
-mediastinum shifts AWAY from affected lung
3) patchy
-loss of surfactant
-RDS
-postsurgical
4) contraction
-fibrosis around lung (cicatrization)

3

2 types of pulmonary edema:

-hemodynamic disturbances (hydrodynamic or cardiogenic pulmonary edema)
-edema caused by microvascular injury (dierct increases in capillary permeabiity 2ndary to microvascular injury)

4

hemodynamic pulmonary edema:

-most commonly due to inc hydrostatis pressure (ex: Left sides CHF)
-heavy WET lungs
-HEART FAILURE CELLS

5

edema caused by microvascular injury:

-mechanism: injury to capillaries of alevolar septa (vascular endothelium damage or damage to alveolar epithelial cells)
-fliud and proteins leaked
-LOCALIZED (Pneumonia & ALI) or diffuse (ARDS)

6

Obstructive pulmonary disease

-HARD TO GET AIR OUT
airway is obstructed=dyspnea

7

obstructive pulmonary diseases:

-emphysema
-Chronic bronchitis
-asthma (reversible)
-bronchiectasis
-COPD = emphysema+chronic bronchitis

8

emphysema =

SMALL AIRWAYS - ACINUS
-alveolar wall destruction
-overinflation-airspace enlargement
-DYSPNEA

smoking!

9

chronic bronchitis =

-LARGE AIRWAYS-BRONCHUS
-productive cough
-airway inflammation

-mucous gland hyperplasia, hypersection

-smoking!

10

bronchiectasis

-BRONCHUS
-airway dilation and scarring

-peristent severe infections

11

asthma

-Bronchus
-smooth muscle hyperplasia
-excess mucus
-inflammation

immune mediated or undefined cause

12

small airway disease-bronchiolitis

-Bronchiole
-inflammatory/scarring
-obliteration

-smoking!

13

COPD

RESERVE VOLUME INCREASED BC AIR IS TRAPPED IN LUNGS

14

Ratio FEV1/FVC in COPD

Ratio FEV1/FVC in restrictive disease?

DECREASES (BC FEV1 DECREASES more than FVC)

NORMAL OR INCREASED (TOTAL LUNG CAPACITY DECREASED)

15

Emphysema - obstructive:

-more common and severe in males
-associated with ****smoking**** and environmental pollutants
-SYMPTOMS NOT APPARENT UNTIL 1/3 OF PULMONARY PARENCHYMA INCAPACITATED

16

Emphysema defined:

-irreversible enlargement of airspaces DISTAL to terminal bronchiole accompanied by destruction of airway walls but WITHOUT obvious fibrosis

17

2 types of emphysema??

-alpha1 anti-trypsin
-smoking (pure chronic bronchitis)

18

factors associating smoking and emphysema

-smokers have inc neutrophils in lun = neutro and macro accumulate in lung
-smoking stimulates release of ELASTASE from neutro and macro
-Macro elastase NOT inhibited by alpha1-antitrypsin
-oxydants in cig soke and oxygen derived free radicals from neutrophils INHIBIT antiprotease = tissue damage via radicals

19

process to get emphysema: (protease antiprotease mechanism) (MOST POPULAR THEORY)

1) smoking=
a) dec alpha1-AT--antielastase
b) inc elastase secretion neutro and macro
==> ELASTIC DAMAGE
=====> emphysema

20

alpha1-antiprotease (antitrypsin)
genes:

-normal phenotype=PiMM (90%)
-deficiency phenotype = PiZZ most common
===> >80% of people with PiZZ develop symptomatic panacinar emphysema @ earlier age and inc severity if smoking

21

wHat does smoking do to alpha1 antiprotease?

-functionally inactivates it == altered balance between proteases and anti-proteases = destruction of elastin and collagen

22

types of emphysema
-how defined?

-defined by anatomic distribution within lung lobule - related to acinus

*1) Centriacinar (centrilobular)
*2) panacinar (panlobular)
3) Paraseptal (distal acinar)-adjacent to areas of fibrosis, scarring or atelectasis
4) irregular (airspace enlargement with fibrosis)- associated with scarring- very common

23

centriacinar emphysema

-most cases = heavy smokers
***-respiratory bronchioles affected and distal alveoli spared
-greatest severity in APICAL segments of upper lobes!**** --> MAJOR ROLE OF TOBACCO AND COAL

24

panacinar emphysema

-acini uniformly enlarged from respiratory bronchioles to terminal blind alveoli
-associated with alpha1-AT deficiency
-MOST COMMON IN BASILAR PORTIONS OF LUNG
-often occurs TOGETHER with centriacinar
-Histology/Gross- enlarged - tissue looks pulled apart- alveoli look huge

25

Distal Acinar (paraseptal emphysema)

-enlargement with destruction of distal portion of acinus - usually worse in upper lung zones
-usually ADJACENT to pleura or to areas of scarring, fibrosis, or atelectasis
-can form cyst like structures
-Associated with SPONTANEOUS PNEUMOTHORAX & bullous disease of lung in young adults
-NOT ASSOCIATED WITH SMOKING

26

irregular emphysema (airspace enlargement with fibrosis)

-acinus is IRREGULARLY involved
-associated with SCARRING usually from inflammatory process
-usually asymptomatic and insignificant

27

bullous emphysema-

can give rise to pneumothorax and possibly death= dangerous

28

death in emphysema

-respiratory acidosis and coma
-right sides heart failure (LATE)
-massive collapse of lungs secondary to pneumothorax

29

Emphysema tx:

-bronchodilators
-steroids
-bullectomy
-lung volume reduction surgery
-lung transplants
-substitution of a1-AT

30

chronic bronhcitis and R sided HF?

-EARLIER EVENT
(as opposed to emphysema where R sided HF is a late complication)

31

Pink puffers:

-severe emphysema
-over-ventilate and remain relatively well oxygenated
-dec diffusion capacity
-relatively normal blood gas values
-not significant bronchitis
-barrel cehst
-DOE
-PURSED LIP BREATHING
-WL

32

Blue bloaters

-major component of chronic bronchitis
-hypercapnia
-abundant purulent sputum
-severe hypoxemia (BLUE)
-cor pulmonale and cardiac failure are resulting complications

33

Chronic bronhcitis defined

CLINICAL DIAGNOSIS!
-persistent cough with production of sputum for at least 3 months of year for at least 2 consecutive year
-ma yhave dec airflow (dec FEV1)

34

Chronic bronchitis

-chronic irritation by inhaled substances (SMOKING!!!!!, air pollution, grain, cotton, silica dust...)

35

most common population affected by chronic bronchitis:

-middle-aged male smokers

36

histology changes in chronic bronchitis:

-chronic inflam (lymphs)
-hypertrophy of submucosal glands of rachea and bronchi (REID INDEX)
-**goblet cell metaplasia**
-mucus hypersecretion with pluggin
-bronchial epith may show squamous metaplasia and dysplasia
-marked narrowing of bronchioles = possible BRONCHIOLITIS OBLITERANS (obliteration of lumen 2ndary to fibrosis)

37

Reid index=

ratio of distance from BM to cartillage compared to distance of mucous gland
(mucus gland/normal bronchial wall)
- should be less and 0.4
-just pathology after death --> only have clinical diagnosis

38

Chronic bronchitis
clinical picture:

-persistent cough and sputum production
-lead to COPD with outflow obstruction, hypercapnia (high CO2), hypoxemia, possible cyanosis
-pulmonary HTN
-HF
-recurrent infections
-resp failure
-may cause squamous metaplasia and dysplasia of bronchial epithelium --> potential for cancer

39

Chronic bronchitis - usual bacterial and viral infection:

-bac=
H influenza
strep pneumo
-viral=
adenovirus
RSV

40

How does smoking predispose chronic bronchitis patient to infection?

-interfering with ciliary action
-direct damage to epith
-inh the ability of bronchial and alveolar leukocytes to clear bacteria

41

review slide 48

review slide 48

42

Chronic bronchiolitis

-small airway disease
-lumen filled with mucus
-tall epithelium with goblet cell metaplasia
-fibrous thickening of wall
-INCREASED PROMINENCE OF SMOOTH MUSCLE

43

What is asthma:

-chronic inflammatory disorder fo airways
-recurrent episodes of wheezing, breathlessness, chest tightness, coughing at night or early morning usually
-WIDESPREAD BUT VARIABLE BRONCHOCONSTRICTION = airflow limitation

-REVERSIBLE!

44

Process of asthma:

-inflammation
-hyperreactive airways
-episodes of reversible bronchoconstriction

45

Rare potentially fatal asthma=

status asthmaticus (CO2 goes)

46

Atopic (extrinsic) asthma

-initiated by a type 1 hypersensitivity reaction after exposure to an extrinsic allergen

47

Non-atopic asthma

-initiated by diverse nonimmune mechanisms such as ingestion of aspirin, pulmonary infections, inhalants, and exercise

48

Allergic asthma (atopic)

1) initial sensitization to inhaled antigens stimulaet induction of CD4 cells of TH2 type**
2) **TH2 cells release cytokines (IL4 & IL5)
-production of IgE by B-cells (IL4)
-growth of mast cells (IL4
-growth and activation of eosinoph (IL5)
3) subsequent IgE mediated reaction to inhaled antigens --> acute response and late phase reaction

49

Late phase allergic asthma how?

binding to left over IgE tiggers attack 4-8 hrs later

50

Asthma histology:

**-curschmann spirals - whorls of shed epithelium
**-charcot-leyden crysals-crystalloids made of eosinophillic proteins
-many eosinophils!!

51

bronchiectasis defined:

-permanent dilation of bronchi and bronchioles caused by destruction of muscle and elastic supporting tissue, resulting from or associated with chronic necrotizing infections

IRREVERSIBLE

52

***Two condition requsite for bronchiectasis?

-obstruction (tumors, foreign body, concretions, secretions)
-chronic persistent infection

53

Assocaited conditions with bronchiectasis:

-obstructive
-congenital or hereditary
-necrotizing (suppurative) pneumonia aka Staph, kleb...
-kartagener syndrome

54

Kartagener syndrome

-abnormal cilia - loss of radial spokes
-on histology have disordered radial spokes = cilia dont work

55

clinical featuers ofbronchiectasis

-chronic productive cough
-hemoptysis
-fould sputum
-blood sputum
-SYSTEMIC=fever WL weakness
-COMPLICATIONG=pulm HTN, brain abscess, rare cor pulmonale, LUNG ABSCESS!