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PULM > PULM Week 2 > Flashcards

PULM Week 2 Flashcards

1
Q

define hypoxia

A

failure of oxygenation at the tissue and cellular level

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2
Q

define hypoxemia

A

low PO2 in the blood

specifically, hypoxemia is determined by measuring PO2 in the arterial blood (PaO2)

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3
Q

define anoxia

A

total depletion of oxygen levels

extreme form of hypoxia

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4
Q

define asphyxia

A

severely deficient supply of oxygen to the body that arises from abnormal breathing (i.e choking)

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5
Q

list possible causes of hypoventilation

A
  1. depression of the CNS by drugs
  2. inflammation, trauma or hemorrhage in the brainstem
  3. abnormal spinal cord pathway
  4. disease of the motor neurons of the brain stem/spinal cord
  5. disease of nerves supplying the respiratory muscles
  6. disease of the neuromuscular junction
  7. disease of respiratory muscles
  8. abnormality of the chest wall
  9. upper airway obstruction
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6
Q

why will there always be a slight differential between arterial and alveolar PO2?

A
  1. incomplete diffusion
  2. ventilation and perfusion are not perfectly matched even in healthy individuals
  3. a small % of bronchial arterial blood is collected by the pulmonary veins after it has perfused the bronchi and its O2 has been partially depleted
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7
Q

what does an A-a difference of > 10-20 mmHg indicate?

A

lungs aren’t transferring O2 properly

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8
Q

describe the effect on A-a gradient in the following situations, plus whether the patients with these conditions would respond to supplemental O2

  1. low FiO2
  2. alveolar hypoventilation
  3. diffusion abnormality
  4. shunt
  5. V/Q mismatch
A
  1. normal A-a; responsive to supp O2
  2. normal A-a; responsive to O2
  3. normal OR elevated A-a; responsive to O2
  4. elevated (in R->L shunt) A-a; NOT responsive to O2
  5. elevated A-a; responsive to O2
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9
Q

define alveolar hypoventilation

A

low alveolar ventilation

A-a is normal but PaCO2 is elevated

*hypoxemia can be addressed through increasing FiO2 but hypercapnia needs to be addressed through mechanical ventilation

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10
Q

what are diffusion abnormalities and how do they cause hypoxemia

A

in disease states, impaired diffusion can occur when there is increased thickness of the physical separation between alveolar gas and capillary blood and a shorter pulmonary transit time (i.e during exercise)

A-a gradient is normal at rest but may be elevated during exercise

PaCO2 is normal

can be caused by interstitial lung disease

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11
Q

what is a V/Q mismatch and how does it cause hypoxemia

A

most common disease state

involves unequal movement of blood to areas of less perfusion

A-a gradient is elevated but PaCO2 is normal

for efficient gas exchange to occur, air must reach the regions of the lung that are being adequately perfused by blood

normal V/Q ratio for lungs is 0.8-1 (alveolar ventilation is 4 L/min while cardiac output is 5 L/min)

even in healthy lungs the V/Q ratio isn’t perfect because both ventilation and blood are gravity dependent with both increasing as you move down the lungs–> blood flow is 5X more in the bottom versus the top of the lungs, and ventilation is 2X more in bottom versus top

gravity dependent V/Q variations can be as much as 0.7 at bottom vs 0.3 at top

you want more air where there is more blood to perfuse

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12
Q

what body parts/cavities are lined with respiratory mucosa?

A 
upper respiratory tract
nasal tube
auditory tube
larynx
trachea
main bronchi
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13
Q

what are the 4 main types of obstructive lung disease

A

COPD
asthma
bronchiectasis
bronchiolitis obliterans

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14
Q

what are the 4 main symptoms of chronic obstructive airway disease

A

cough

sputum

dyspnea

wheeze

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15
Q

what causes wheezing?

A

airway narrowing, especially due to bronchoconstriction (thus you see it especially in asthma)

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16
Q

what is sputum

A

a mix of saliva, airway lining liquid, mucous and pus expelled from the respiratory system during coughing

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17
Q

what causes sputum production?

A

different disease states caused by infection, smoking or genetics (i.e alpha 1 anti-trypsin deficiency) can lead to pathologies that increase chronic sputum production

may be due to mucous gland enlargement and hyperplasia of goblet cells (i.e in asthma)

chronic inflammation can also lead to formation of pus which could add to mucous to become purulent sputum

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18
Q

what causes foamy sputum?

A

pulmonary edema

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19
Q

how do smoking and inflammation influence sputum production?

A

smoking and inflammation enlarge the mucous glands that line the airway walls in the lungs, causing goblet cell metaplasia and leading to healthy cells being replaced by more mucous secreting cells

inflammation associated with COPD can also damage the muco-ciliary transport system which is responsible for clearing mucous from the airways

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20
Q

causes of dyspnea

A

increased work of breathing due to increased airway resistance–> hypoxemia, hyperinflation

increased resistance can be due to smooth muscle contraction, wall thickening, luminal occlusion, decreased lung elasticity, or obliteration

mediated by inflammatory responses

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21
Q

list and describe the 5 mechanisms of dyspnea

A
  1. SMOOTH MUSCLE CONTRACTION (asthma)–> shortening of the airway’s smooth muscle–> radius of the airway contracts–> decrease in airway diameter–> increased resistance–> dyspnea
  2. THICKENING/REMODELLING (asthma)–> persistent inflammation causes remodelling/thickening of the airway epithelium and basement membrane–> decreased diameter of airway leads to increased resistance and dyspnea
  3. OCCLUSION OF AIRWAY–> i.e due to mucous (asthma)
  4. DECREASED LUNG ELASTICITY–> i.e in COPD, emphysema–> tissues create connective tissue framework–> increased collagen
  5. OBLITERATION–> i.e in bronchiolitis–> destruction–> healing–> fibrosis (obliteration)
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22
Q

clinical definition of COPD

A

progressive development of irreversible airway obstruction

chronic bronchitis + emphysema

hyperinflation of lungs

associated with inflammatory response to noxious particles, especially those in cigarette smoke

onset usually around 40 yo

frequent sputum production

infrequent allergies

symptoms are persistent

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23
Q

what are the diagnostic criteria for COPD

A

productive cough on most days for at least 3 consecutive months in 2 successive years

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24
Q

where does COPD affect in the body

A

central airways, peripheral airways, lung parenchyma, pulmonary vasculature

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25
Q

risk factors for COPD

A

SMOKING

occupational

alpha 1 antitrypsin deficiency

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26
Q

COPD pathogenesis

A

2 forms, but most patients have elements of both

  1. chronic bronchitis–> cough with sputum production for 3 months/2 successive years–> associated with mucous gland hypertrophy and goblet cell metaplasia in cartilaginous airways (bronchi)–> fibrosis and narrowing of airways
  2. emphysema–> permanent enlargement of alveoli and destruction of alveolar walls (without significant fibrosis)–> decrease in elastic recoil–> airways collapse on expiration–> increase in compliance causes easily inspiration but difficult expiration–> caused by imbalance between locally acting proteolytic enzymes released by inflammatory cells and anti-proteolytic mechanisms endogenous to the lungs–> reactive oxygen species damage the parenchyma
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27
Q

what are the differences between

  1. centriacinar
  2. panacinar
  3. distal acinar

COPD

A
  1. centriacinar = proximal acinar central portion, associated with CIGS, upper lobes are affected
  2. panacinar = all parts of acinus, associated with alpha1antitrypsin, lower lobes are affected
  3. distal acinar = alveolar ducts and sacs are involved, common in tall, thin adults in which large bullae can rupture, leading to spontaneous pneumothorax
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28
Q

pathology of COPD

A

inflammatory cells: CD8+ and CD4+T-lymphocytes, neutrophils, macrophages, B-lymphocytes

mediators: LTB4, IL-8, TNF alpha

causing squamous metaplasia and parenchymal damage, glandular enlargement, and goblet cell hyperplasia

dilatation and destruction of air spaces distal to the terminal bronchiole without obvious fibrosis

decreased elastic recoil

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29
Q

symptoms of COPD

A

dyspnea, hypoxia, hyperinflation

chronic cough

sputum production

exertional dyspnea is an early symptom

wheezing and chest tightness is less common

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30
Q

what is the natural history of COPD

A

gradual decrease in FEV1 over time, with episodes of acute exacerbation

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31
Q

COPD on physical exam

A

breath sound intensity decreases

hyperinflation results in increase resonance

crackles at onset of inspiration

ronchi (wheeze)–higher prevalence in patients with dyspnea, not a consistent finding and not related to severity

prolonged expirational time (listen over the larynx–greater than 4 seconds is a severe obstruction)

weight loss

severe sign is barrel chest, pursed lip breathing, emaciation, inguinal hernia, cyanosis, RHF

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32
Q

COPD on spirometry

A

FEV1 low ( doesnt significantly change

increased TLC, FRC, RV due to air trapping

lowered DLCO (due to decreased alveolar surface area and alveolar capillary beds)

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33
Q

COPD on CT and CXR

A

CT–> direct visualization of emphysematous sacs–> can establish and quantify severity of emphysema

CXR–> functional diagnosis–> CXR rules others out, and can only suggest COPD (i.e upon visualization of hyperinflation, flattened diaphragm, cardiac silhouette elongated, increased retrosternal space, hypertranslucency

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34
Q

clinical definition of asthma

A

chronic inflammation disorder of airways that results in episodes of reversible bronchospasm, causing airflow obstruction

onset usually less than 40 yo

smoking is not causal

infrequent sputum production

frequent allergies

symptoms are intermittent and variable

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35
Q

where does asthma effect

A

central and peripheral airways

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36
Q

risk factors for asthma

A 
URTIs
allergens
irritants
drugs
preservatives
cold air
viral infections
atopy
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37
Q

asthma pathogenesis

A

bronchoconstriction mainly, but can also include airway edema, vascular congestion, luminal occlusion with exudates

irritants–> HISTAMINE, leukotrienes, spasmogens, prostaglandins, growth factors etc… –> these cause airway muscle contraction, pulmonary vasculature dilation and leakage, mucous gland secretion, airway remodeling

extrinsic asthma = TYPE I HYPERSENSITIVITY
-involves sensitization with inhalation of allergen–> dendritic cell–> Th2 (IL 4, 5, 13)–> B cell–> IgE binds to mast cells–> deregulation of mast cells with second exposure

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38
Q

describe the early asthmatic response

A

within minutes

mast cells (with histamine, leukotrienes) cause mucosal edema and bronchospasm

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39
Q

describe the late asthmatic response

A

within hours

mast cells (with IL 4, 5, GM-CSF)–> eosinophils (cytokines, leukotrienes)–> tissue inflammation and injury, bronchospasms

*non-asthmatics generate a Th1 response whereas asthmatics generate a Th2 response

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40
Q

what is intrinsic asthma

A

mechanism is unknown, responsive to changes in temperature, exercise etc…

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41
Q

pathology of asthma

A

inflammatory cells: CD4+ lymphocytes, EOSINOPHILS, MAST CELLS, neutrophils, epithelial cells

mediators: LTD4, IL 4 and 5, TNF alpha and many others

fragile epithelium, thickened basement membrane, goblet cell hyperplasia, smooth muscle hypertrophy

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42
Q

symptoms of asthma

A

wheezing, increased on expiration

dyspnea, chest tightness, cough

symptoms are absent between attacks

particularly bad at night and early morning

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43
Q

asthma on the physical exam

A

during attacks:

tachy > 110 bpm

PULSUS PARADOXUS: > 10 mmHg from inspiration to expiration

use of accessory muscles

wheezing

hyperinflation

allergy

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44
Q

asthma spirometry results

A

decreased FEV1

FEV1:FVC >12% ad absolute reversibility

METHADOLINE CHALLENGE TEST–>

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45
Q

asthma on CXR

A

normal

may show some bronchial thickening or mucoid impaction

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46
Q

clinical definition of bronchiolitis obliterans

A

rare and life threatening form of non-reversible obstructive lung disease in which bronchioles are compressed and narrowed due to scarring/inflammation

characterized by submucosal and peribronchiolar fibrosis that causes CONCENTRIC narrowing of the bronchiolar lumen

most commonly seen following inhalation injury, transplantation (of bone marrow or lung) or in the context of rheumatoid lung or inflammatory bowel disease

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47
Q

where does bronchiolitis obliterans affect

A

membranous and respiratory bronchioles

immediately adjacent alveoli

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48
Q

risk factors for bronchiolitis obliterans

A

toxic inhalation

connective tissue disease

chronic infection

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49
Q

pathogenesis of bronchiolitis obliterans

A

edema and accumulated cellular debris causes obstruction of small airways

V/Q mismatch results due to waster perfusion in obstructed areas–> hypoxemia early in the course of the disease–> scarring and inflammation injury to the small airways

respiratory and membranous bronchioles are affected

proliferative and constrictive bronchiolitis–> IRREVERSIBLE flow obstruction (OBLITERATION)–> decreased diffusion capacity–> progressive dyspnea with nonproductive cough

50
Q

pathology of bronchiolitis obliterans

A

inflammatory cells: neutrophils, eosinophils, macrophages, lymphocytes, mast cells

mediators: PROTEASES, REACTIVE OXYGEN, IL-8

smooth muscle hyperplasia, fibrosis, obliterative scarring, increased soft tissue around bronchioles, thickened wall due to inflammatory cells

51
Q

etiology of bronchiolitis obliterans

A

toxic inhalation, infection (RSV or MYCOPLASMA), chrnic rejection, drug reaction, connective tissue disorder, ulcerative colitis

52
Q

symptoms of bronchiolitis obliterans

A

wheezes

INSPIRATIONAL SQUEAKS

hyperinflation

fine crackles

progressive onset of unproductive cough and dyspnea associated with hypoxemia at rest or with exercise

develops rapidly over months

53
Q

natural history of bronchiolitis obliterans

A

disease is irreversible and often requires a lung transplant

54
Q

bronchiolitis obliterans on physical exam

A

crackles may be present

pulmonary function tests show a progressive and irreversible airflow limitation

55
Q

bronchiolitis obliterans spirometry results

A

irreversible flow obstruction

decreased DLCO

56
Q

bronchiolitis obliterans on CT and CXR

A

inspiration CT: CENTRILOBAR WALL THICKENING, bronchiolar dilation, TREE-IN-BUD pattern and GROUND GLASS accentuation pattern

57
Q

clinical definition of bronchiectasis

A

permanent abnormal widening and destruction of the bronchi and bronchiole accompanied by daily production of purulent sputum that is associated with chronic or recurrent infection

hemoptysis, recurrent pneumonia, wheeze

58
Q

bronchiectasis sites of action

A

major bronchi, bronchioles

59
Q

risk factors for bronchiectasis

A

infection, bronchial obstruction, immune deficiency, cystic fibrosis

60
Q

pathogenesis of bronchiectasis

A

inflammation and destruction of structural components of the bronchial wall largely due to mediators released from NEUTROPHILS–> dilated airways become more susceptible to colonization and growth of bacteria–> reinforces the cycle

POST-OBSTRUCTIVE–> interference with mucous clearance leading to infection, inflammation and tissue destruction (i.e tumor, aspirated foreign body, external compression or torsion of lumen)

NON-OBSTRUCTIVE–> prior infection or genetic condition leading to infection (i.e CF, ciliary dyskinesia syndromes i.e “Kartagener’s,” TB, pertussis)

61
Q

pathology of bronchiectasis

A

inflammatory cells: NEUTROPHILS

mediators: immunoglobulins, fibronectins, procoagulants

transmural inflammation, permanent dilatation, neo-vascularization, airway is DISTORTED and may contain mucous, inflammatory cells and debris, goblet cell metaplasia, degeneration and destruction of cartilage, fibrosis and loss of elastin fibers

62
Q

bronchiectasis etiology

A

recurrent infection leading to chronic inflammation, bacterial infection (whooping cough), CF, ciliary dusfunction, foreign bodies, relapsing pylochondritis, inhalation of noxious fumes

63
Q

symptoms of bronchiectasis

A

cough and sputum in >90% of patients

recurrent infection are common (wheezing, cough, weight loss, fever, hemoptysis)

very large sputum production

infective exacerbations

recurrent pleurisy

progressive dyspnea

64
Q

natural history of bronchiectasis

A

surgery and infection treatment

65
Q

bronchiectasis on physical exam

A

course crackles in larger airways

ronchi

wheezes

CLUBBING

severe presents with decreased breath sound and dullness to percussion

postural cough–because affected segments are unresponsive, when people bend down the mucous irritates non affected segments and causes cough

foul smelling sputum if caused by anaerobes

66
Q

spirometry results with bronchiectasis

A

show airway obstruction and AIR TRAPPING

combined obstructive and restrictive effect seen on pulmonary function tests for bronchiectasis

low FEV1 and FEV1:FVC

RV increased

commonly responsive to bronchodilators

abnormal methacholine challenge test

normal or decreased DLCO

67
Q

bronchiectasis on CT and CXR

A

CXR: early phase may be normal

  • TUBULAR SHADOWS from thickened bronchial walls, fibrosis, localized alveolar destruction and collapse
  • may have enlarged air spaces, dilated airways with thickened walls

CT: standard for confirming diagnosis–> shows TAPERING AIRWAYS, and airways ending in dilatations
-SIGNET RIGN SIGN–> bronchial diameter is more than 1.5X larger than the accompanying vessels in x-section

68
Q

what disease does the signet ring sign indicate

A

bronchiectasis

69
Q

indicate the degree to which COPD, asthma, bronchiolitis obliterans and bronchiestasis display the following pathologies

  1. smooth muscle contraction
  2. wall thickening
  3. luminal occlusion
  4. decreased lung elasticity
  5. obliteration
A

COPD–> small amount of SM contraction, wall thickening, luminal occlusion; lots of decreased elasticity and obliteration

Asthma–> lots of smooth muscle contraction; small to large amount of wall thickening; a little bit of luminal occlusion; no evidence of decreased lung elasticity or obliteration

Bronchiolitis obliterans–> a little bit of smooth muscle contraction and luminal occlusion; a bit more of wall thickening; no decreased lung elasticity; lots of obliteration

Bronchiectasis–> a little bit of smooth muscle contraction; a bit more wall thickening and luminal occlusion; no decreased lung elasticity, and some obliteration

  • the only one that shows decreased lung elasticity is COPD
  • the only one that shows extensive SM contraction is asthma
  • the only one that shows NO obliteration is asthma
70
Q

what role does smoking play in the pathogenesis of COPD

A

cigarette smoking increases the concentration of oxidants and thus more reactive oxygen species are generate–> this induces inflammation

inflammatory cells are attracted due to the ROS–> surface adhesion molecules like VCAMs are increased in smokers–> stimulate release of proteolytic enzyme ELASTASE from cells

smoke itself inhibits the action of alpha 1 antitrypsin and tissue inhibitor metalloproteinases (TIMP)

increased accumulation of alveolar macrophages and neutrophils generates more reactive oxygen species and causes oxidative damage

parenchymal inflammation leads to apoptosis and thus decreased lung recoil (emphysema) plus airway inflammation and remodelling (small airway disease) and thus decreased expiratory flow, hyperinflation, and gas exchange abnormalities

71
Q

what causes centriacinar emphysema (centrilobar)

A

smoking (central)

72
Q

what causes panacinar (panlobular) emphysema

A

alpha 1 anti-trypsin deficiency (peripheral)

73
Q

what role does the immune system play in the pathogenesis of asthma

A

primarily allergen driven Th2 response (also viruses and pollutants)

allergen presents to dendritic cell–> presents to a naive T cell–> Th2 and cytokines IL 4, 5, and 13 cause allergic inflammation and increased IgE production

IgE production from B cell goes with mast cells and when allergen is presented again the quick degranulation of the mast cell causes profound bronchoconstriction and inflammation (mucous)

74
Q

what is the role of mast cells in asthma

A

initiate acute bronchoconstrictor responses to allergens via IgE dependent mechanism–> release histamine, cysteinyl-leukotrienes, cytokines, chemokines, growth factors and neutrophils

75
Q

what is the role of eosinophils in asthma

A

are recruited by vascular endothelial cells in the airway–> release of GROWTH FACTORS involved in airway remodelling

76
Q

indications for pulmonary function tests

A
  1. symptoms suggest lung disease–> wheeze, dyspnea, cough–> diagnosis
  2. detect early signs of airflow obstruction in smokers
  3. to follow the course of someone who has established lung disease
  4. to assess risk preoperatively
  5. as part of routine health assessment (i.e like with BP)
77
Q

how is spirometry performed?

A

patient breathes normally through the PNEUMOTACHOGRAPH and then takes a deep breath–> to TLC

then deep expiration for 6 seconds–> to RV

can give measure of forced expiratory volume over 25-75% of FVC, which is more sensitive than FEV1

pneumotachograph = tube with a turbine

78
Q

what does spirometry measure

A

compares to predicted values–> reference standards based on population and matched by age, gender, height, as well as a race/ethnic correction factor

FVC--> L and % predicted
FEV1--> L and % predicted
FEV1:FVC--> % and as % predicted 
Inspiratory capacity (IC)
expiratory reserve volume (ERV)
peak expiratory flow (PEF)
FEF 25-75%--> good for small airway disease assessment
79
Q

what can you NOT determine using spirometry

A

RV, FRC, or TLC

80
Q

normal and diagnostic ranges for FVC

A

normal = 80-120%

70-79% = mild reduction
50-69% = moderate reduction
81
Q

normals and diagnostic ranges for FEV1

A

normal = >75%

60-75% = mild obstruction 
50-59% = moderate obstruction
82
Q

normal and diagnostic ranges for FEF

A

normal = >70%

60-69% = mild obstruction 
40-59% = moderate
83
Q

normal and diagnostic ranges for FEV1:FVC

A

80% or higher = normal

79% or lower = abnormal

84
Q

how do obstructive and restrictive disorders affect:

  1. FVC
  2. FEV1
  3. FEF 25-75%
  4. FEV1:FVC
  5. TLC
A
  1. FVC is normal or decreased in obstructive
    FVC is always decreased in restrictive
  2. FEV1 is decreased in both obstructive and restrictive
  3. FEF 25-75% is decreased in obstructive
    FEF 25-75% is normal or decreased in restrictive
  4. FEV1:FVC is decreased in obstructive
    FEV1:FVC is normal or INCREASED in restrictive
  5. TLC is normal or increased in obstructive
    TLC is decreased in restrictive
85
Q

how do you distinguish between asthma and COPD

A

asthma = episodic

COPD = consistent

86
Q

what is PEF

A

peak expiratory flow

a person’s maximum speed of expiration as measured by w a peak flow meter

87
Q

list drug classes used in the treatment of asthma/COPD

A
  1. B-2 selective agonists (bronchodilation)
  2. inhaled anti-cholinergics
  3. methylxanthines
  4. leukotriene receptor antagonists (LTRAs)
  5. new: monoclonal antibodies and combo therapy
88
Q

name a short acting beta-2 agonist (SABA)

A

salbutamol

89
Q

name a long acting beta-2 agonist (LABA)

A

salmeterol

formoterol

90
Q

MOA of selective B-2 agonists

A

stimulation of B2 receptors in bronchial smooth muscle which results in relaxation–> results in a larger diameter airway

this occurs due to binding of agonist to G-protein coupled receptors that activate adenylate cyclase which causes the conversion of ATP to cAMP (therefore increased cAMP) and bronchodilation

91
Q

results of treatment with B-2 agonists

A

bronchodilation

92
Q

how are B-2 agonists delivered to the system

A

inhaled via a metered dose inhaler (MDI), dry powder inhaler or nebulizer

inhalation delivery gets highest concentration in lungs where the drug is desired and reduces the probability of side effects

salbutamol can also be given in IV and response is rapid (can also be given orally)

systemic uptake is significant and sympathetic stimulation limits dose

93
Q

indications for treatment with a B-2 agonist

A

relief of bronchospasm due to asthma, COPD, anaphylaxis or aspiration

94
Q

contraindications for treatment with a B-2 agonist

A

given with caution to patients in whom tachycardia would be undesirable (i.e in severe CAD or aortic stenosis)

95
Q

SEs of B-2 agonists

A

generally well tolerate

overstimulation of B1 or B2 may cause tachycardia, palpitations, tremor, hypokalemia (because B stimulation is involved with shifting K+ into cells), hyperglycemia (because B stimulation is involved with glucose metabolism)

96
Q

can SABAs and/or LABAs be used as sole treatment in episodic asthma?

what about persistent asthma?

A

SABAs may be used as required as sole therapy for episodic asthma

neither SABAs nor LABAs should be used as sole therapy in persistent asthma, it should be in a combination i.e with other anti-inflammatory meds

97
Q

what is standard therapy for asthma?

A

LABA + inhaled corticosteroid

98
Q

name 2 inhaled anti-cholinergics

A

ipratropium–modified version of atropine

tiotropium–“spirba”

99
Q

MOA of inhaled anti-cholinergics

A

antagonism of MUSCARINIC receptors which prevents bronchoconstriction and reduces secretions

M1 and M3 receptors are blocked which inhibits bronchoconstriction –> BRONCHODILATOR

tiotropium (spirba) is a selective muscarinic antagonist that is longer acting (LAMA)

100
Q

pharmacokinetics of inhaled anticholinergics

A

ipratropium is a quarternary compound that does NOT CROSS hydrophobic membranes easily–> therefore doesn’t readilt cross pulmonary membranes into the blood and therefore there are low levels in systemic circulation

some inhaled drug ends up in the GI but absorption in the GI is very low

compared to salbutamol, onset and duration of action is PROLONGED (likely due to minimum absorption from lungs)–> peak is 30-90 min, with a 6 hour total duration

duration of tiotropium is further prolonged (24 hours) due to slow dissociation from receptors

101
Q

indications for inhaled anti-cholinergics

A

acute asthma (NOT first line), and COPD (acute and chronic maintenance)

102
Q

SEs of inhaled anticholinergics

A

dry mouth
nasal irritation
nose bleeds

103
Q

name 4 inhaled corticosteroids

A 
budesonide (pulmicort)
ciclesonide
fluticasone (flovent)
beclomethasone
triamcinolone
104
Q

how are inhaled corticosteroids made

A

synthetically derived based on CORTISOL

105
Q

MOA of inhaled corticosteroids

A

broad ANTI-INFLAMMATORY effect

bind receptor in cytosol–> move into nucleus–> inhibit transcription of genes that code for pro-inflammatory cytokines, COX2

this inhibition decreases eosinophil activation and recruitment, inhibits production of vasodilators and decreases vascular leakage, increases blood neutrophil counts and decreases the number of lymphocytes, macrophages and thus their functions

decreased phospholipase A2, decreased prostaglandins, decreased leukotrienes

106
Q

main action of inhaled corticosteroids

A

decrease inflammation

107
Q

pharmacokinetics of inhaled corticosteroids

A

highly lipophilic and thus enter cells easily

large first pass effect–> low bioavailability for any drug swallowed

available in a variety of delivery systems including aerosol, dry powder, and liquid nebulizers

108
Q

indications for inhaled corticosteroids

A

asthma–> long term control by limiting frequency and severity of exacerbations
COPD–> severe COPD

109
Q

SEs of inhaled corticosteroids

A

*low systemic absorption

oral candidiasis 
dysphonia (hoarseness)
sore throat 
osteoperosis (when admin in higher doses)
fat redistribution 
hyperglycemia
obesity
110
Q

name 3 methylxanthines

A

theophylline
aminophylline
caffeine

111
Q

MOA of methylxanthines

A

not completely understood

inhibition of PHOSPHODIESTERASE which degrades cCAMP and therefore there is more cAMP available causing bronchodilation

also causes inhibition of release of intracellular CALCIUM and therefore decreased smooth muscle contraction

*causes bronchodilation overall

112
Q

pharmacokinetics of methylxanthines

A

NARROW therapeutic index

many factors affect its rate of absorption (including a number of drug interactions)

serum levels are thus difficult to predict and toxicity may occur unexpectedly

113
Q

indications for methylxanthine therapy

A

SECOND or THIRD line drug for asthma and COPD

also neonatal apnea

114
Q

contraindications for methynxanthine therapy

A

active or symptomatic coronary heart disease because increased cAMP will increase inotropy which will increase O2 demand and use up supply in myocardium

115
Q

SEs of methylxanthines

A 
nausea
vomiting
headache
insomnia
tremor
restlessness
seizures
arrhythmias
116
Q

name one monoclonal Ab used to treat obstructive disease

A

omalizumab

117
Q

MOA of omalizumab

A

prevents interaction of allergen with IgE

118
Q

how do you admin omalizumab

A

subcutaneously every few weeks

119
Q

disadvantages to omalizumab therapy

A

immune reactions possible, and very high cost ($1000/month)

has to be injected

120
Q

omalizumab therapy advantages

A

only have to admin every few weeks

121
Q

why do we care that inhaled corticoseroids cause B-2 receptor upregulation in the lungs?

A

because chronic use of B-2 agonists may lead to receptor downregulation by the body

PULM (9 decks)

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