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PTH560 Pathology > Exam 2 - obstructive lung diseases > Flashcards

Exam 2 - obstructive lung diseases Flashcards

1
Q

What is COPD

A

“chronic obstructive pulmonary disease”

- progressive, largely irreversible obstruction to airflow OUT of the lungs

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2
Q

COPD - epidemiology

A
  • most common cause = cig smoking

- majority of patients have emphysema AND chronic bronchitis

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3
Q

Basic -

Emphysema vs chronic bronchitis

A

emphysema = air space destruction

chronic bronchitis = conducting airway inflammation

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4
Q

Emphysema

A

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

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5
Q

Causes and types of Emphysema

A

Smoking
AAT deficiency

types = centriacinar and panacinar

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6
Q

Emphysema pathogenesis

A

***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)

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7
Q

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

A

expriation: distal terminal bronchiole collapses

trapped air distends everything distal to that

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8
Q

Centriacinar emphysema

A

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
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9
Q

Panacinar emphysema

epidemiology, pathogen

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

pathogen:

  • lower lobes
  • loss of elastic tissue (entire respiratory unit, distention of unit)
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10
Q

Emphysema clinical findings

A
  • progressive dyspnea and hyperventilation
  • hypoxemia late
  • cor pulmonale UNCOMMON

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

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11
Q

emphysema PFT’s

A
  • inc TLC
  • dec FEV1
  • dec FVC => dec FEV1/FVC
  • late in disease = dec PaO2
  • normal to dec PCO2 (“pink puffer”)
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12
Q

Emphysema treatment

A
  • stop smoking
  • pulmonary rehab
  • oxygen to maintain SaO2 over 90%
  • bronchodilators
  • anticholinergics
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13
Q

Chronic bronchitis definition and causes

A

chronic cough for at least 3 months for 2 consecutive years

causes = cig smoking, cystic fibrosis

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14
Q

Chronic bronchitis: general? pathogenesis

A
  • hypersecretion of mucus
  • obstruction of airflow from mucus plugs (segmental bronchi, prox bronchioles)
  • irreversible fibrosis in chronically inflamed airways
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15
Q

Chronic bronchitis: BRONCHI pathogenesis

A
  • hypersecretion of submucosal mucus-secreting glands (sputum overproduction)
  • acute inflammation (neutrophil invasion, superimposed on chronic inflammation)
  • loss of ciliated epithelium (squamous metaplasia)
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16
Q

Chronic bronchitis: BRONCHIOLES pathogenesis

A
  • mucus plugs in lumens (CO2 trapped)
  • goblet cell metaplasia
  • chronic inflammation and fibrosis (lumen narrowing)
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17
Q

chronic bronchitis clinical findings

A
  • productive cough
  • dyspnea late
  • hypoxemia and respiratory acidosis early
  • cyanosis (“blue bloaters”)
  • obese
  • expiratory wheezing or rhonchi
  • cor pulmonale
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18
Q

Chronic bronchitis PFT’s

A
  • less inc in TLC and RV than emphysema
  • chronic respiratory acidosis
  • moderate to severe hypoxemia early
19
Q

Chronic bronchitis treatment

A
  • stop smoking
  • pulmonary rehab
  • oxygen to maintain SaO2 over 90%
  • bronchodilators
  • anticholinergics
20
Q

What is asthma?

A

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

21
Q

What are the 2 types of asthma?

A 
Extrinsic = type 1 hypersensitivity
Intrinsic = non-immune
22
Q

Asthma epidemiology

A
  • most common respiratory disease in kids

- >50% develop symptoms before age of 5

23
Q

Extrinsic asthma: Pathogenesis

A
  • 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
Q

Extrinsic asthma mediator functions

A
  • histamine (bronchoconstriction, mucus production, and leukocyte infiltration)
  • leukotrienes (prolonged bronchoconstriction)
  • acetylcholine (airway muscle contraction)
25
Q

Extrinsic asthma: changes in bronchi

A
  • thicken basement membrane
  • edema
  • mixed inflammatory infiltrate
  • hypertrophy of submucosal glands
  • hypertrophy/hyperplasia of smooth muscle
26
Q

Extrinsic asthma: changes in bronchioles

A
  • 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
Q

Extrinsic asthma: signs and symptoms

A
  • Expiratory wheezing (inspiratory wheezing when severe)
  • nocturnal cough
  • increase AP diameter of chest wall (air trapping)
28
Q

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

A

position = tripod during attacks

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

FEV1 = dec with severity

29
Q

Intrinsic asthma (causes)

A

-non immune

  • virus-induced infection
  • air pollutants
  • stress
  • exercise
  • cigarette smoke
  • ASA or NSAIDs (block COX, LOX takes over, produces leukotrienes, bronchoconstriction)
30
Q

What is bronchiectasis?

A
  • permanent dilation of the bronchi and bronchioles causing repeated episodes of airway infection and inflammation
  • destruction of cartilage and elastic tissue
31
Q

Causes of bronchiectasis

A
  • cystic fibrosis (most common cause in US!)
  • tuberculosis (most common WORLDWIDE)
  • infections
  • bronchial obstruction
  • primary ciliary dyskinesia
32
Q

Bronchiectasis: Pathology

A
  • lower lobes

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

33
Q

Bronchiectasis: clinical findings

A
  • productive cough
  • hemoptysis
  • digital clubbing
  • cor pulmonale

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

34
Q

What is cystic fibrosis?

A

-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
Q

Cystic fibrosis: pathogenesis

A

-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
Q

Cystic fibrosis: clinical findings

A
  • 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
Q

Cystic fibrosis diagnosis

A
  • infant screen: inc serum trypsin levels

- sweat chloride test (diagnosis)

38
Q

Cystic fibrosis: treatment

A
  • bronchodilators
  • antibiotics
  • pancreatic enzyme replacement
  • steroids
  • vitamins
  • recombinant human deoxyribonuclease aerosol
39
Q

OSA - obstructive sleep apnea

A

-excessive snoring with intervals of apnea

causes

  • obesity (most common)
  • tonsillar hypertrophy
  • nasal septum deviation
  • hypothyroidism
40
Q

OSA pathology

A
  • airways obstructed
  • CO2 retention (resp. acidosis)
  • hypoxemia
41
Q

OSA clinical findings

A
  • excessive snoring
  • apnea episodes
  • daytime somnolence
  • headaches
42
Q

OSA complications

A
  • pulmonary HTN (vasoconstriction of smooth muscle cell)
  • RVH (due to pulmonary HTN)
  • secondary polycythemia (hypoxemia inc erythropoietin)
43
Q

OSA: labs, diag, treatment

A

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

diag
(polysomnography-sleep study)

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

PTH560 Pathology (15 decks)

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