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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
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)

PTH560 Pathology (15 decks)

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