Exam 2 - obstructive lung diseases Flashcards Preview

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Flashcards in Exam 2 - obstructive lung diseases Deck (43):
1

What is COPD

"chronic obstructive pulmonary disease"
- progressive, largely irreversible obstruction to airflow OUT of the lungs

2

COPD - epidemiology

-most common cause = cig smoking

-majority of patients have emphysema AND chronic bronchitis

3

Basic -
Emphysema vs chronic bronchitis

emphysema = air space destruction

chronic bronchitis = conducting airway inflammation

4

Emphysema

-permanent enlargement of all or part of the respiratory unit (respiratory bronchioles, alveolar ducts, alveoli)

5

Causes and types of Emphysema

Smoking
AAT deficiency

types = centriacinar and panacinar

6

Emphysema pathogenesis

***increased compliance and decreased elasticity!

imbalance of elastase (and anti) as well as oxidants (and anti) which are released by neutrophils and macrophages.

*smoking is chemotactic to phagocytes

***net effect = destruction of elastic tissue. (at junction of terminal and respiratory bronchiole)

7

Emphysema patho: obstruction and air trapping *****

expriation: distal terminal bronchiole collapses

trapped air distends everything distal to that

8

Centriacinar emphysema

aka centrilobular
***most common type of emphysema in smokers

Pathogen:
-apical segments of upper lobes
-loss of elastic tissue (distal terminal and respiratory bronchioles)
-distended respiratory bronchioles

9

Panacinar emphysema
(epidemiology, pathogen)

epidemiology:
AAT deficiency (acquired from smoking or genetic - dominant)

pathogen:
-lower lobes
-loss of elastic tissue (entire respiratory unit, distention of unit)

10

Emphysema clinical findings

-progressive dyspnea and hyperventilation
- hypoxemia late
-cor pulmonale UNCOMMON

CXR - hyperlucent lung fields, increased AP diameter, vertical heart, hyperinflation

11

emphysema PFT's

-inc TLC
-dec FEV1
-dec FVC => dec FEV1/FVC

-late in disease = dec PaO2
-normal to dec PCO2 ("pink puffer")

12

Emphysema treatment

-stop smoking
-pulmonary rehab
-oxygen to maintain SaO2 over 90%
-bronchodilators
-anticholinergics

13

Chronic bronchitis definition and causes

chronic cough for at least 3 months for 2 consecutive years

causes = cig smoking, cystic fibrosis

14

Chronic bronchitis: general? pathogenesis

-hypersecretion of mucus
-obstruction of airflow from mucus plugs (segmental bronchi, prox bronchioles)
-irreversible fibrosis in chronically inflamed airways

15

Chronic bronchitis: BRONCHI pathogenesis

-hypersecretion of submucosal mucus-secreting glands (sputum overproduction)
-acute inflammation (neutrophil invasion, superimposed on chronic inflammation)
-loss of ciliated epithelium (squamous metaplasia)

16

Chronic bronchitis: BRONCHIOLES pathogenesis

-mucus plugs in lumens (CO2 trapped)
-goblet cell metaplasia
-chronic inflammation and fibrosis (lumen narrowing)

17

chronic bronchitis clinical findings

-productive cough
-dyspnea late
-hypoxemia and respiratory acidosis early
-cyanosis ("blue bloaters")
-obese
-expiratory wheezing or rhonchi
-cor pulmonale

18

Chronic bronchitis PFT's

-less inc in TLC and RV than emphysema
-chronic respiratory acidosis
-moderate to severe hypoxemia early

19

Chronic bronchitis treatment

-stop smoking
-pulmonary rehab
-oxygen to maintain SaO2 over 90%
-bronchodilators
-anticholinergics

20

What is asthma?

an episodic and reversible airway disease that targets bronchi and its subdivisions and non-respiratory bronchioles

21

What are the 2 types of asthma?

Extrinsic = type 1 hypersensitivity
Intrinsic = non-immune

22

Asthma epidemiology

-most common respiratory disease in kids
- >50% develop symptoms before age of 5

23

Extrinsic asthma: Pathogenesis

-Type 1 hypersensitivity
-exposed to allergens
-sensitized to allergens (Th cells activated)
-inhaled allergens crosslink IgE on MAST cells and release mediators (histamine, leudotrienes, ACh)

24

Extrinsic asthma mediator functions

-histamine (bronchoconstriction, mucus production, and leukocyte infiltration)

-leukotrienes (prolonged bronchoconstriction)

-acetylcholine (airway muscle contraction)

25

Extrinsic asthma: changes in bronchi

-thicken basement membrane
-edema
-mixed inflammatory infiltrate
-hypertrophy of submucosal glands
-hypertrophy/hyperplasia of smooth muscle

26

Extrinsic asthma: changes in bronchioles

-mucus plug formation (shed epithelial cells)
-crystalline granules in eosinophils coalesce
-patchy loss of epithelial cells
-goblet cell metaplasia
-thickening of basement membrane
-smooth muscle cell hypertrophy/hyperplasia

27

Extrinsic asthma: signs and symptoms

-Expiratory wheezing (inspiratory wheezing when severe)
-nocturnal cough
-increase AP diameter of chest wall (air trapping)

28

Extrinsic asthma: clinical findings (position, labs, FEV1)

position = tripod during attacks

labs = initial (resp. alkalosis) and later (resp. acidosis)

FEV1 = dec with severity

29

Intrinsic asthma (causes)

-non immune

-virus-induced infection
-air pollutants
-stress
-exercise
-cigarette smoke
-ASA or NSAIDs (block COX, LOX takes over, produces leukotrienes, bronchoconstriction)

30

What is bronchiectasis?

- permanent dilation of the bronchi and bronchioles causing repeated episodes of airway infection and inflammation

-destruction of cartilage and elastic tissue

31

Causes of bronchiectasis

-cystic fibrosis (most common cause in US!)
-tuberculosis (most common WORLDWIDE)
-infections
-bronchial obstruction
- primary ciliary dyskinesia

32

Bronchiectasis: Pathology

-lower lobes
-dilated bronchi/bronchioles (extend to lung periphery, pus-filled)

33

Bronchiectasis: clinical findings

-productive cough
-hemoptysis
-digital clubbing
-cor pulmonale

CXR:
-crowded, bronchial markings all the way to periphery

34

What is cystic fibrosis?

-autosomal recessive disorder
(carrier asymptomatic)

-body produces unusually thick, sticky mucous due to gene defect
-decrease of exocrine gland function (multiple organ systems - lungs, pancreas)

-most common fatal hereditary disorder in caucasians in US (median survival = 30 yrs)

35

Cystic fibrosis: pathogenesis

-3 nucleotide deletion on chromosome 7 that normally codes for phenylalanine
-defective protein folding CFTR
(regulates chloride ion permeability in sweat glands)
(dec Cl reabsorption in sweat glands)

-inc Na+ and water reabsorption
-dec Cl- secretion
(=dehydration of body secretions) (lack NaCl, secretions thickened everywhere)

36

Cystic fibrosis: clinical findings

-nasal polyps
-heat exhaustion (lose Na+ from fluid from skin)
-respiratory infection (P.aeruginosa)
-cor pulmonale
-pneumothorax
-malabsorption (pancreatic exocrine deficiency)
-type 1 diabetes
-infertility
-meconium ileus
-rectal prolapse
-gall stones
-biliary cirrhosis

37

Cystic fibrosis diagnosis

-infant screen: inc serum trypsin levels

-sweat chloride test (diagnosis)

38

Cystic fibrosis: treatment

-bronchodilators
-antibiotics
-pancreatic enzyme replacement
-steroids
-vitamins
-recombinant human deoxyribonuclease aerosol

39

OSA - obstructive sleep apnea

-excessive snoring with intervals of apnea

causes
-obesity (most common)
-tonsillar hypertrophy
-nasal septum deviation
-hypothyroidism

40

OSA pathology

-airways obstructed
-CO2 retention (resp. acidosis)
-hypoxemia

41

OSA clinical findings

-excessive snoring
-apnea episodes
-daytime somnolence
-headaches

42

OSA complications

-pulmonary HTN (vasoconstriction of smooth muscle cell)
-RVH (due to pulmonary HTN)
-secondary polycythemia (hypoxemia inc erythropoietin)

43

OSA: labs, diag, treatment

labs
(PaO2 dec, O2 sat dec, PaCO2 inc)

diag
(polysomnography-sleep study)

treatment
(CPAP -airway splint, surgery, weight loss)