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pathophysiology 3801 > obstructive pulmonary disease > Flashcards

obstructive pulmonary disease Flashcards

1
Q

increased secretions and increased spasms

A

asthma

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2
Q

increased secretions

A

bronchitis

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3
Q

loss of surrounding supporting tissue

A

emphysema

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4
Q

chronic inflammation of the airway and variable airflow obstruction; presence of intermittent symptoms

A

asthma

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5
Q

what is the cause of asthma?

A

immune-mediated airway inflammation caused by exposure to an allergen or an irritant

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6
Q

what are some symptoms of asthma

A

-sob
-wheezing
-coughing
-chest tightness
-feeling of breathlessness

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7
Q

what are some signs of a severe asthma episode

A

-wheezing
-orothpnea
-tachypnea
-tachycardia
-use of accessory muscles
=qgitation
-intercostal retractions

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8
Q

what are some common allergens

A

-dust mites
-smoke
-foods
-animal dander
-excersie
-pollution

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9
Q

true/false: type 2 inflammation involves innate and adaptive immune systems

A

true

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10
Q

type 2 inflammation: _____ induces B-cell isotope (antibody) switching to production of IgE

A

IL-4

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11
Q

type 2 inflammation: IgE, through its binding to _______ and ______ results in environmental sensitivity to allergens

A

basophils and mast cells

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12
Q

type 2 inflammation: what are the products from the cross linkage of IgE on the surface of basophils and mast cells

A

type II cytokines and direct activators of smooth muscle contraction and edema

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13
Q

type 2 inflammation: ____ has a critical role in regulating eosinophils. it controls formation, recruitment and survival of these cells

A

IL-5

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14
Q

type 2 inflammation: _____ induces airway hyperresponsivemess, mucus hyper secretion, and goblet cell metaplasia.

A

IL-13

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15
Q

type 2 inflammation: ____ can produce IL-5 and IL-13. they can be activated by epithelial cytokines known as alarming, which are produced in response to “nonallergic” epithelial exposures such as irritants, pollutants, oxidative agents, fungi or viruses.

A

type 2 innate lymphoid cells (ILC2)

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16
Q

non-type 2 inflammation: true/false: non-type 2 processes can exist either in combination which type 2 inflammation or without type 2 inflammation

A

true

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17
Q

non-type 2 inflammation: which type of inflammation is more commonly seen in severe asthma, that has not responded to the common anti-inflammatory therapies such as corticosteroids, that usually suppress type 2 inflammation

A

neutrophilic inflammation

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18
Q

these 3 cytokines are the major cytokines associated with type 2 inflammation, and have been targeted successfully in asthma therapies

A

Il-4,5, and 13

19
Q

true/false: thymic stromal lymphopoetin (TSLP), IL-25 and IL-33 also play a role in the signalling cascade and have been targeted successfully in asthma therapies

A

false - actively being studied as targets for tx of asthma

20
Q

these cytokines have been implicated in non-type 2 inflammation

A

IL-6, IL-17, TNF alpha, IL-1beta and IL-8

21
Q

what are pre-disposing (risk) factors of asthma

A
  • genetics *mutation on chromosome 17q21
  • family history of asthma
  • positive skin test to an allergen
  • tobacco (second hand and maternal smoke)
  • air pollution
  • diets (vitamin D deficiency)
  • obesity
  • medications
  • occupational exposures
22
Q

this type of inflammation is eosinophilic predominant and an IgE response is common.
clinical manifestations include: elevated IgE levels, eczema, allergic rhinitis, positive fam history of allergen and attacks associated with seasonal, environmental or occupational exposure

A

type 2 inflammation

23
Q

know the IgaE dependant pathway of the pathogenesis of asthma

A

an allergen is present -> mast cells and eosinophils are activated -> prostaglandins, leukotrines, interleukins and cytokines are released -> there is acute/chronic inflammation -> bronchoconstriciton, mucus and edema production, airway hyperresponsiveness

24
Q

know the IgE independent pathway of the pathogenesis of asthma

A

cold/exercise, osmotic stimuli, irritant exposure -> mast cells and eosinophils activated -> prostaglandins, leukotrienes, interleukins and cytokines released -> acute/chronic inflammation -> bronchoconstriction, mucus & edema production and airway hyperresponsiveness

25
Q

know the epithelial cell activation pathway of the pathogenesis of asthma

A

cyokines and chemokine are released -> mast cells and eosinophils growth, influx and proliferation of T lymphocytes, differentiation of B lymphocytes (IgE/A) and TH2 differentiations - IL production -> acute/chronic inflammation -> bronchoconstriciton, mucus and edema production and airway hyperresponsiveness

26
Q

what does the activation of local inflammatory cells produce?

A
  • acute bronchospasm
  • mucosal edema
  • mucus plug formation
  • airway wall remodelling
27
Q

what are some immunohistopathologic features of asthma

A
  • denudation of airway epithelium ‘
  • collagen deposition beneath basement membrane
  • edema
  • mast cell activation
  • infiltration by neutrophils, eosinophils and lymphocytes
28
Q

what medical conditions/findings may be associated with obstructive lung disease?

A
  • sensitive
  • GERD
  • allergic rhinitis
  • cough
  • wheezing
  • hyper inflated chest
29
Q

know the mechanism of bronchial smooth muscle relaxation

A
  • epinephrine binds to adrenergic receptors
  • adenyl cyclase is stimulated
  • increased cAMP production
  • increased Ca2+ pump activity = Ca2+ returned to sarcoplasmic reticulum in muscle
  • decreased activity of myosin light chain kinase
  • dephospho rylation of myosin-P and changes to shape and binding site
  • actin-myosin cross bridges are broken
  • decrease in contraction of bronchial smooth muscle = smooth muscle relaxation
30
Q

a term used to represent a process characterized by presence of chronic bronchitis or emphysema (usually both).

A

COPD

31
Q

type B COPD “blue bloater” - resting hypoxemia
- chronic or recurrent cough > 3 months > 2+ successive years
- persistent, but sometimes reversible airway obstruction
- commonly caused by: cigarette smoking, repeated airway infections, genetic predisposition and inhalation of chemical irritants

A

chronic bronchitis

32
Q

in chronic bronchitis, elevated _____ levels recruit neutrophil activation

A

IL-8

33
Q

in chronic bronchitis, ciliated epithelium are replaced by _____- type

A

squamous

34
Q

what are some clinical manifestations of chronic bronchitis

A
  • sob on exertion
  • cyanosis
  • excessive sputum
  • chronic cough
  • evidence of excess body fluids
35
Q

how do you know someone has bronchitis based on their pulmonary function tests (e.g. TLC, RV and FEV)

A
  • normal total lung capacity (TLC)
  • increased residual volume (RV)
  • decreased FEV (forced expiratory volume) and FEV/FVC (forced expiratory volume/forced vital capacity)
36
Q

how do you know someone has bronchitis based on their arterial blood gases (e.g. pCO2 and pO2)

A
  • elevated pCO2
    -decreased pO2
37
Q

type A COPD “pink puffer”
- develops overtime usually > 50 years of age
- usually caused by smoking and air pollution, as well with certain occupations e.g. mining, welding, working withs asbestos

A

emphysema

38
Q

what cells are effected in emphysema

A
  • macrophages
  • neutrophils
  • epithelial cells
  • lymphocytes
39
Q

know the pathogenesis of emphysema

A
  • reduction in pulmonary capillary bed: exchange of O2 and CO2 between capillary and alveoli is impaired
  • loss of elastic tissue: results in a decrease in size of smaller bronchioles and results in loss of radial traction (hold airway open)
40
Q

this type of emphysema is associated with chronic bronchitis and it destroys the respiratory bronchioles

A

centraicinar (centrilobular)

41
Q

this type of emphysema destroys the alveoli and is mostly seen in smokers

A

panacinar (panlobular)

42
Q

this type of emphysema affects the peripheral lobules

A

paraseptal

43
Q

what are some clinical manifestations of emphysema

A
  • pursed lip breathing
  • use of accessory muscles
  • thin
  • cough is minimal or absent
  • increased SOB for past 3-4 years
43
Q

what are some clinical manifestations of emphysema

A
  • pursed lip breathing
  • use of accessory muscles
  • thin
  • cough is minimal or absent
  • increased SOB for past 3-4 years
  • barrel chest
  • digital clubbing
  • decrease3d breath sounds

pathophysiology 3801 (8 decks)

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