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Applied Pathophysiology > Asthma & COPD > Flashcards

Asthma & COPD Flashcards

1
Q

Respiration Functions of Lungs:

A
  1. Make O2 available for metabolism (“internal respiration”)
    - ventilation (6000L/day at rest)
    - gas exchange (lung)
    - transport to tissues
  2. Remove CO2 - metabolic byproduct
    - transport from tissues to lung
    - gas exchange
    - expiration
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2
Q

Non-respiratory functions of lungs:

A

defence against infection, particulate matter & noxious chemicals
- lung ventilation ~6000L per day without exertion
- pulmonary capillary bed is only 1 in body through which entire blood supply flows! (therefore lung is a high risk area (non-sterile)

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3
Q

Why is the lungs deemed a high risk area?

A

pulmonary capillary bed is only 1 in body through which entire blood supply flows! (therefore lung is a high risk area (non-sterile)

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4
Q

What are non-specific defenses?

A

clearance - cough, mucociliary escalator (mucous, bugs, debri, etc. gets pushed up & coughed out)

secretions - mucous, surfactant

cellular - epithelium, phagocytes

biochemical - proteinase inhibitors (a1-antitrypsin), antioxidants

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5
Q

What is a1-antitypsin?

A

its genotype determines whether someone who smokes will get COPD for ex

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6
Q

What are specific immune defenses?

A

antibody mediated immunity
- b cells

antigen presentation
- dendritic, epithelial cells & macrophages

cell mediated immunity
- regulate local inflammation
- t-lymphocytes, mast cells, eosinophils

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7
Q

What is the path of airflow?

A

mouth/nose –> larynx –> trachea –> airways –> alveolae

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8
Q

What are features of the bronchi?

A
  • cartilage in wall
  • airway smooth muscle encircle
  • Ciliated psuedostratified epithelium
  • Mucous glands
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9
Q

What are features of Bronchioles?

A

No cartilage with reducing smooth muscle, cilia & mucous glands

Respiratory bronchioles:
• No smooth muscle or cilia
• First alveolar buds

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10
Q

What are features of Alveolar Sacs?

A

• Type I and II epithelium
• Surfactant (surface tension reducing agent)
• Gas exchange!

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11
Q

What do the vagus (parasympathetic) fibers do?

A

(cholinergic)

ACh regulation:
- Muscarinic 2 receptors (M2R)
- Muscarinic 3 receptors (M3R)

  1. stimulate mucous secretion from glands
  2. stimulates contraction of airways smooth muscle
  3. stimulates vasodilation
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12
Q

What do the sympathetic fibres do?

A

(adrenergic)

norepinephrine regulation:
- B2 adrenergic receptors
- A1 adrenergic receptors

  1. causes inhibition of mucous glands
  2. causes dilation of airways smooth muscle
  3. causes vasoconstriction
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13
Q

What pathway do anticholinertics inhibit for Asthma/COPD?

A

the parasymp. ganglion releasing ACh which binds to M3-receptors to trigger rxn - it prevents constriction

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14
Q

Where is the greatest resistance in the lungs & how does it relate to total cross-sectional area?

A

• Greatest resistance: 2nd-5th generation airways (conducting)

• Airflow resistance inversely ~ to total cross-sectional area
- meaning: if a few small airways collapse; won’t have as huge of an effect as a couple of large ones

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15
Q

Features of Asthma:

A
  • Thickened airway smooth muscle & mucus plugging
  • Airway hyperresponsiveness (bronchoconstriction)
  • Airway wall swelling –> edema
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16
Q

Features of Chronic Obstructive Pulmonary Disease (COPD):

Chronic bronchitis:

A
  • Smoking related chronic inflammation of lower airways
  • Airway edema & mucus plugging
  • Airway hyperresponsiveness (bronchoconstriction)

(similar to asthma but trigger is diff.)

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17
Q

Features of Chronic Obstructive Pulmonary Disease (COPD):

Emphysema:

A
  • Loss and collapse of terminal bronchioles (tiny airways)
  • Alveolar wall destruction(trypsin mediated)
    – b/c of overwhelmed antitrypsin mech’s
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18
Q

What are airway resistance determinants?

A

radius and patency (ability to stay open rather than collapse) of conducting airways – Contraction of airway smooth muscle
– Mucous plugging
– Airway wall remodeling (physical change over time)

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19
Q

Smaller radius, ___ R

A

higher

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20
Q

Higher R, ___ air flow

A

less

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21
Q

Bronchoconstriction

Pathologic, physical, physiologic, & pharmacologic dynamic control

A

Pathologic
- Allergen, histamine

Physical
- Mucous, edema
- Airway collapse

Physiologic
- Parasympathetic stimulation
- Local decrease CO2

Pharmacologic
- Methacholine (binds to M3 receptors); triggers constriction

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22
Q

Bronchodilation

Pathologic, physical, physiologic, & pharmacologic dynamic control

A

Pathologic
- None

Physical
- None

Physiologic
- Sympathetic
neural stim
- Hormone (adrenaline)
- Local increase CO2 (cause opening)

Pharmacologic
- β2 adrenergic receptor ligands (salbutamol, salmeterol) (relax smooth muscle cells)

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23
Q

What is lost with emphysema (COPD)?

A

radial traction - b/c lung is being broken down

Larger lung has lower R; air flows greater

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24
Q

Compliance:

A

a measure of the dispensability of a structure - the degree that volume changes in response to a change in pressure = ∆V/∆P

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25
Q

Compliance is a determinant of airway-lung interpendence:

A

• Deep breath stretches open airways
• Lung stiffness keep airways open when
exhaling

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26
Q

Lung elastic recoil determined by:

A

• Elastic fibres in lung interstitium (collagen &
elastin)
• Surface tension of alveolar lining fluid
(surfactant)

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27
Q

Emphysema:

A

increased lung compliance due to tissue destruction
• reduced interdependence (airway-lung tethering)
• airways collapse more easily during exhale
• breathe at high lung volume (hyperinflation)

steeper the sloop - v. compliant (therefore elastic/stiff)

28
Q

Spirometry

A

performed using a spirometer to measures volume of air moved during inspiration and expiration maneuvers (mL air/min=flow)

(measures airflow)

29
Q

Functional residual capacity (FRC):

A

gas in the lungs at the end of a resting tidal breath

(volume you go down to when you exhale - v. small for someone with condition)

30
Q

(Forced) Vital capacity (VC or FVC):

A

total amount of gas that can be exhaled after a maximal inhalation

(take deepest breath & then exhale all you can - it determines if airflow resis. has changed)

31
Q

What is the Forced Vital Capacity Maneuver?

A

Standard test to assess presence of lung disease: (distinguish’s b/t)
• Obstructive (asthma; emphysema; chronic bronchitis)
• Restrictive (idiopathic pulmonary fibrosis, ILD)

FVC maneuver:
• forced inhalation from FRC to TLC (~1 second) - breath in as much as you can
• follow by forceful exhalation from TLC to RV (~5 seconds) (blow it all out - last 3-4 secs are difficult)

32
Q

Using the FVC Maneuver one can determine:

A

FVC - forced vital capacity. Maximum amount of air forcibly expired after maximum inspiration (how much air can move in & out of lung in total)

FEV1 – volume of gas exhaled during first second (forced expiratory volume in 1 second) (healthy ~ 80% of FVC)

33
Q

FVC Maneuver: Airway Obstruction

In Asthma or COPD:

A

•FEV1:FVC < 70% (if below than asthma or COPD is likely)

• FEV1 decreased
- airway resistance increased

• FVC reduced in severe disease (due to
hyperinflation in COPD) so need FEV1:FVC to isolate airway function!

34
Q

Air has to get to ____ & its not when its severe

A

alveoli

35
Q

What is Obstructive Airway Disease - Asthma?

A

1 reason children go to ER each year

A disorder of the airways characterized by paroxysmal or persistent symptoms (dyspnea, chest tightness, wheeze and cough) with variable airflow limitation & airway hyperresponsiveness to allergic and non-allergic stimuli

• Chronic airway eosinophil/neutrophil inflammation with REVERSIBLE airflow limitation (airway constriction, edema, mucous)

• Without appropriate treatment can be progressive – develop airway remodeling linked with FIXED airway obstruction

36
Q

Asthma shifts to right on curve, so higher R, due to what?

A

• Allergy and inflammation
• Mucus production
• Structural remodeling
• Smooth muscle contraction

36
Q

Asthma shifts to right on curve, so higher R, due to what?

A

• Allergy and inflammation
• Mucus production
• Structural remodeling
• Smooth muscle contraction

37
Q

Risk factors for Asthma

A

Predisposition:
• atopy
• gender
• genetics

Causal Factors:
• in/outdoor allergens
• occupational sensitizers
• respiratory infection

Contributing Factors:
• respiratory infection
• air pollution
• smoking

Triggers:
• smoke & chemical fumes
• cold air, exercise
• aero- & food allergens

38
Q

What does a Typical allergen response look like?

A

• Antigen presentation (innate immunity)
• Tcell maturation & activation (Th1, 2, 17)
• Cytokine and chemokine release
• B cells mature: antibodies (adaptive)
• Recruit eosinophils, neutrophils,
Neutrophil
macrophage
• Mast cell induction & activation (release cytokines, histamine,
lipid mediators)
• Healthy response is self-resolving (active) *****
- disting. asthamatic & healthy response (in severe asthma resolving is compromised - can’t shut it down)

39
Q

What does Asthma look like?

A

• Inflammation excessive and not self-resolving (chronic)
• Skewed towards TH2
• Mast cells, eosinophils, neutrophils
• Pathological mediators cause tissue damage and promote AHR (airway hyperresponsiveness)

40
Q

Asthma Diagnosis requires:

A

• assessment of clinical symptoms / history (how long?)
• Self-reported breathing difficulty (time of day - typ. feel at night) and
triggers (frequency of “attacks”/symptoms)
• Breaths sounds (ex: crackles)
• measurement of airway function

41
Q

What is the preferred diagnosis of athma?

A

spirometry showing REVERSIBLE airway obstruction - measure FEV1/FVC & see if FEV1 changes after a bronchodilator (should show reduced)

& increase in FEV1 after a bronchodilator or after course of controller therapy (should see increase in air after if asthma)

42
Q

What should we look for on a Methacholine Challenge Test for asthma?

A

Pc20 v. low (b/c a healthy person can take lots of methacholine & FEV1 on’t drop much)

43
Q

Measurement of Airway Function: Response to Bronchodilators

A

Spirometry → inhaled or nebulized bronchodilator (eg. 400g salbutamol) → 15+ min → repeat spirometry (>12% increase in FEV1 is positive result)

we see a 34% improvement in FEV1 - therefore 34% airway R & needs a bronchiodilator or corticosteroid or both

44
Q

What do we see in fatal asthma?

A
  • lots of ASM that will make airway smaller
  • excessive mucous production
  • airway wall thickening (fibrosis)
  • airway smooth muscle hypertrophy
45
Q

What does airway remodeling do over time?

A

improve Pc20 (get higher)

46
Q

Obstructive Airway Disease: COPD

Chronic Obstructive Pulmonary Disease:

A

inflammatory lung disease (neutrophilic) that affects airways (bronchitis) and lung parenchyma (emphysema)
• conducting airway wall remodeling, pruning (loss) of terminal
respiratory bronchioles, and alveolar destruction
• Greatly increases lung compliance a significant
component of IRREVERSIBLE airway obstruction

Genetics: Z genotype isn’t good –> means they have v. little of a1-antitrypsin protein circulating in blood which means it doesn’t inhibit endogenous proteins of lung or the ones that neutrophiles release when activated by cigarette smoke

47
Q

What do we see in Emphysema?

A

huge air sacs, therefore LESS SA to gas exchange (get more air into lungs but diffusing capacity is compromised b/c no capillary bed)

& protein for elastic fibres is being degraded by endogenous enzymes

48
Q

Chronic Cigarette Smoking Leads to…

A

Accelerated Loss of Lung Function
- Alveolar loss is IRREVERSIBLE; preventing damage is paramount
- Smoking cessation can re-establish normal rate of decline in lung function (depends when the person stops smoking)

49
Q

Cellular Basis of Inflammation & Tissue Repair in COPD

Alveolar Macrophage:

A
  • Primary defense - increased number in smokers
  • Phagocytes (deposits, dead cells, bacteria)
  • Release cytokines to recruit (IL-8) and activate (TNF) neutrophils
  • Secrete MMP-12 metalloelastase to degrade elastin (modulated by endogenous anti-proteases α1 anti-trypsin (A1AT) & Tissue inhibitors of metalloproteinases (TIMPs)
50
Q

Cellular Basis of Inflammation & Tissue Repair in COPD

Neutrophils (recruited)

A

• Secondary defence: aggressive phagocytes
• Secrete neutrophil elastase and reactive oxygen
species (ROS)
• Elastin degradation and lung cell death/stress

51
Q

How is there increased Small Airway Resistance in COPD?

A

• Mucus production
• Alveolar destruction
• Matrix destruction (aka elastin is destroyed)
• Small airway pruning & collapse
• Increased lung compliance (reduced interdependence)
- easy to inflate lungs, but difficult to come back

cartilage in airways prevent airways from collapsing

52
Q

What does cartilage in the airways do?

A

cartilage in airways prevent airways from collapsing

53
Q

Emphysema: patients breathe at

A

higher FRC to overcome loss of radial force on airways

• peribronchial pressure becomes positive during forced expiration

• at equal pressure point (EPP) airways collapse

• EPP is more easily reached in emphysema

• Pursed lips breathing helps (pop opens airways)

54
Q

Chronic Bronchitis:

A

• Productive cough (disting. b/t asthma & COPD) and wheezing
• Inspiratory & expiratory coarse crackles
• Cardiac: tachycardia common in exacerbations

55
Q

What do the Pulmonary function tests look like in Chronic Bronchitis?

A

• reduced expiratory flows and volumes
• FEV1, FVC, and FEV1/FVC reduced
• airway obstruction NOT responsive to pre-bronchodilators (disting. from asthma)
• expiratory F-V curve shows substantial flow limitation
• increase in RV and FRC
• air trapped due to airway obstruction & early airway closure

56
Q

Emphysema:

A

• Dyspnea & progressive airway obstruction
• Abnormalities of gas exchange (exercise
intolerance) (b/c losing alveoli)
• Decreased breath sounds intensity
• Tachycardia (exacerbations) & pulmonary
hypertension (b/c taking out alveoli but also pulmonary circulation as tissues break down & therefore increase R b/c capillary bed is disappearing)
• Arterial blood gas: loss of the alveolar
capillaries leads to arterial O2 desaturation

57
Q

Pulmonary function tests for emphysema

A

• dynamic airways compression during expiration → reduced FEV1, FVC, and FEV1/FVC (ie. volume they breathe out is less than volume they breath in)
• obstruction NOT responsive to pre-bronchodilators
• flow limitation evident in expiratory F-V curve
• air trapping: increased RV, FRC and TLC

58
Q

What is a hint that its COPD not asthma?

A

FVC reduced in severe disease (hyperinflation in
COPD) so need FEV1:FVC to isolate airway function!

59
Q

What are 2 things to know about Flow-volume loop in emphysema?

A
  1. PEF = peak expiratory flow - in a healthy person it peaks in 1 sec (10L/s) then slows down –> indication of elastic recoil in the lungs
  2. In a person with obstruction - PEF is 2.5L/s & MEF is much lower (in COPD you can breath in, but hard to breath out)
60
Q

Ways to diagnosis emphysema

A
  • Physical exam: Barrel chest, decreased breath sounds
  • Chest X-Ray: can show abnormally large lungs
  • Chest CT Scan: can show small pockets of trapped air
  • Blood tests for: genetic disease evaluation; arterial blood gas; and, white blood cell count (b/c increase in WBCs is linked to infection)
  • Pulmonary function testing
61
Q

Emphysema vs. Chronic Bronchitis clinical presentation

A

Emphysema:
- Severe dyspnea
- Cough after dyspnea
- Sputum not excessive
- Less frequent lung infections
- Terminal resp. failure
- Diffusing capacity (DLCO) decreased

Chronic Bronchitis:
- Mild dyspnea
- Cough before dyspnea
- Copious, purulent sputum
- More frequent lung infections
- Repeated resp. insufficiency
- DLCO less affected (b/c its their airways not alveoli thats affected)

62
Q

COPD Treatment:

A

• Smoking cessation
• Annual influenza vaccination
• Active lifestyle (don’t want to but it can prolong their life)
• Alleviate dyspnea - pharmacologics

management only b/c COPD is paletive/can’t stop

63
Q

Pharmacologic Management of COPD

Bronchodilation (airway smooth muscle relaxation) and reduced mucous production:

A
  • Anti-cholinergics
  • β2 agonists
  • Phosphodiesterase 2 inhibitors
64
Q

Pharmacologic Management of COPD

Control infection, reduce inflammation:

A
  • Antibiotics
  • Anti-inflammatory medications:
    • Inhaled corticosteroids, PDE2 inhibitors
    • Reduce macrophage/neutrophil content

Applied Pathophysiology (34 decks)

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