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KEY wk 5 lec 2 Flashcards

1
Q

types of obstructive vs restrictive lung diease

A

obstructive:
-bronchial asthma
-COPD (chronic bronchitis and emphysema)
-bronchiectasis

restrictive:
-acute: ARDS (diffuse alveolar damage)
-chronic: idiopathic pulmonary fibrosis

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2
Q

restrictive vs obstructive lung disease

A

obstructive: cant exhale bc airway narrow or obstructed; trap air in lungs (air trapped in alveoli)

restrictive: cant inhale bc lung expansion reduced from stiff lung tissue or impaired respiratory mechanics

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3
Q

pulmonary function tests (2)

A

spirometry
bodyplethysmogrpahy

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4
Q

FEV1/FVC in obstructive vs restrictive

A

obstructive: reduced

restrictive: normal or increase (“physiological”)

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5
Q

TLC (total lung capacity) and RV (residual volume) and FRC (functional residual capacity) in restrictive vs obstructive lung disease

A

obstructive: increased by air trapped (hyperinflation)

restrictive: low lung volumes; decreased both because lung cant expand

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6
Q

bronchial asthma (obstructive)

pathophysiology

irreversible or reversible?

inflammatory cell involved

A

episodic airway obstruction, hyper responsiveness and inflammation

reversible

eosinophils

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7
Q

bronchial asthma “trias” definition

A

chronic inflammation

reversibility of obstructive ventilatory impairment

obstructive ventilatory impairment and bronchial hyperactivity (sx)

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8
Q

risks for bronchial asthma

A

polygenic inheritance (i.e. Beta receptor) and environment and atopy

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9
Q

sx of atopy and test

A

Nose: Allergic rhinitis

Eye: Allergic conjunctivitis

Skin: Eczema

Nose: Hey fever

Allergies (food, contact, inhalation)

Positive skin tests (prick tests)

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10
Q

triggers of bronchoconstrictions

A

allergens

infections in upper airays

inhalatory irritants

anxiety, cold air, GERD, exercise

drugs esp NSAIDS, aspirin

food preservatives (sulphites)

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11
Q

classification of asthma

A

allergic vs non allergic

  1. Allergic - Atopic
  2. Nonallergic – Nonatopic 3. Drug-induced asthma
  3. Occupational asthma
  4. Cardiac asthma
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12
Q

allergic asthma

sx

type _ hypersensitivity

causes

A

kids, hay fever, eczema

type I hypersenstiivity

pollens, dusts, drugs

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13
Q

pathogensis of allergic asthma

ILs? Th_? Ig_?

A

hyperactive airway constricts to stimuli; increase airway resistance

type 1 hypersensitivity

CD4+ and Th2 release IL-4 and IL-5 which then stimulate eosinophils –> produce IgE

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14
Q

nonallergic asthma

what levels are normal

causes

A

adults

NOT type 1 hypersensitivity; IgE is normal

Th17 and Th1 drive infalmmation

exercise, cold air, drugs, GERD, viral (rhinovirus, parainfluenza), hormonal, pregnancy

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15
Q

early vs late stage of asthma

A

early: bronchoconstriction via histamine, prostaglandin, leukotrienes

late: neutrophils release proteases and eosinophils release major basic protein

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16
Q

mechanisms of airway obstruction

A

hyper responsive, inflammation, collagen deposition, smooth muscle constriction vascular proliferation, edema, goblet cell metaplasia and mucus hypersecretion

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17
Q

2 components of airway hyperresponsiveness

A
  1. functional: hyper responsive to direct smooth muscle acting agents like histamine or methacholine
  2. structural: wall thickness (smooth muscle hypertrophy, collagen deposition, edema, inflammation)
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18
Q

gross vs microscopic morphology of asthma

A

gross: status asthmatics= hyperinflated lungs, mucus plugging

microscopic: charcot-leyden crystals (from major basic protein), curschmann spirals, eosinophil infiltrate

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19
Q

spirometry in asthma exacerbation (obstructive)

FEV1/FVC

PEF (peak expiratory flow)

residual volume

and reversibility from

A

FEV1/FVC: reduced

PEF reduced

RV increased

reversible via bronchodilator

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20
Q

spirometry between exacerbations in early vs late asthma

A

early= normal

late=

low peak expiratory flow (PEF)

reduced FEV1/FVC

increase residual volume

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21
Q

arterial blood gases in asthma during exacerbation vs in between exacerbations

A

during: CO2 low; hyperventilate (compensatory), CO2 rises if respiratory failure (later stages)

between: PaO2 and PaCO2 are normal;

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22
Q

classic triad of symptoms in asthma

when are they worse and because of what hormone

A

wheeze, cough, dyspnea

worse or only present at night becasue of cortisol drop

status asthmaticus= prolonged attacks

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23
Q

face findings in asthma

A

Dark rings under the eyes
(“allergic shiners”)

Dark transverse crease on the nose (“allergic salute”)

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24
Q

2 types of COPD

A
  1. chronic bronchitis
  2. emphysema

airflow limitation that’s not reversible; progressive and inflammatory

25
risk factors for COPD
genes (alpha-1-antitrypsin deficiency) tobacco smoke *** BIGGEST occupational dusts air pollution
26
4 evens of COPD
1. inflammatory and immune cell recruitment to airways 2. proteinase damage ECM in airways 3. cell death via oxidant induced damage 4. disordered repair of elastin (emphysema)
27
cellular mechanisms in COPD
chronic bronchitis: larger airways, airway remodelling, mucus secretion emphysema: terminal airways, loss of alveoli, loss of elastin both from apoptosis, inflammation, immune response, oxidants
28
chronic bronchitis time line causes types
productive cough for > 3 months cigarettes irritate airway and increase and hyperplasia of mucus glands, metaplasia of goblet cells, thicken submucosal layer simple, obstructive and asthmatic
29
pathology in chronic bronchitis
airway obstruction air trapping- hyperinflation
30
emphysema what changes to lungs
lose pulmonary parenchyma --> lose elastic recoil --> exhalation; airway collapse --> air trapping lose alveolar septa and airway walls and dilate terminal airways
31
morphology of emphysema
dilation of airspaces bull form in pleural space
32
2 types of emphysema and their causes and what area of lungs are effected
centriacinar emphysema from smoking affect respiratory bronchioles in upper lobes panacinar emphysema from alpha1-antitrypsin deficiency affect alveoli, alveolar ducts, respiratory bronchioles in lower lobes
33
CT patterns of emphysema
1. centrilobular (upper lobe; smoking) 2. pan lobular (diffuse loss, lower lobe; A1 antitrypsin deficiency) 3. paraseptal (smoking)
34
blue bloater vs pink puffer
blue (chronic bronchitis): peripheral edema (fat), RV heart fail, cyanosis, hypercapnia pink (emphysema): hypercapnia, hypoxemia, minimal cyanosis, muscle wasting (skinny)
35
obstructive bronchitis vs emphysema
obstructive bronchitis: -chronic productive cough -hypercapnia -right ventricular failure -peripheral edema emphysema: - dyspnea -hypoxemia -hypercapnia -hyperventilation
36
spirometry on obstructive ventilatory impairment
FEV1 is reduced FVC is normal of slightly reduced FEV1/FVC is reduced to < 0.7
37
complications of COPD
pulmonary hypertension (from hypoxia induced vasospasm) cor pulmonale (right sided heart failure bc of pulmonary hypertension) mismatched ventilation-perfusion (shunt blood to areas of poor ventilation) respiratory failure
38
bronchiectasis (obstructive lung disease) what forms and which is most common
irreversible airway dilation focal or diffuse cylindrical or tubular (most common), varicose or cystic
39
2 compoennts/ causes of bronchiectasis
infection and obstruction infection destroys smooth muscle and elastic fibers of airway wall
40
non infectious vs infectious bronchiectasis and what type of presentation
non-infectious (obstruction of airway) causes focal bronchiectasis 1. extrinsic (compressed by adjacent lymphadenopathy or parenchymal tumor mass) 2. intrinsic (airway tumor or aspirated foreign body) infectious disease or systemic causes diffuse bronchiectasis (I.e HIV immunodeficiniey, mycobacterial, antitrypsin genes, autoimmune, IBD, rheumatoid arthritis, idiopathic)
41
pathogenesis of infectious diffuse bronchiectasis; "vicious cycle hypothesis"
infection susceptibility- poor mucocilliary clearance microbial colonization (p. aeruginosa) severe infection (pneumonia from Bordetella pertussis or Mycoplasma pneumoniae) chronic inflmamtion mediators released from bacteria
42
gross and microscopic morphology in bronchiectasis
gross: dilate away, esp. lower right lobe, airways extend into pleural space microscopic: inflammatory infiltrate and tissue destruction
43
sx and signs of bronchiectasis
dyspnea, chronić cough with sputum, hemoptysis finger clubbing (pulmonary osteoarthropathy), hypoxemia, hypercapnia, chest radiograph shows parallel lines= thickened bronchial walls
44
complications of bronchiectasis
recurrent infections (i.e. antibiotics) hemoptysis --> hemorrhage rare: pulmonary hypertension, abscess formation, amyloidosis
45
restrictive lung disease spirometry findings
reduction of all volumes FEV1/FVC is normal
46
2 categories of restrictive lung disease
extra pulmonary (obesity, chest deformity, kyphoscoliosis) intrapulmonary (primary or secondary, acute ARDS or chronic)
47
intrapulmonary restrictive lung disease cause a reduction in
diffusion capacity
48
pathogenesis of intrapulmonary restrictive lung diseases initial to late phase
environmental, idiopathic, genetic initial phase: inflammation: alveolitis (lymphocytes, neutrophils) late phase: fibrosis: alveoli's (lymphocytes, neutrophils)
49
ACUTE: ARDS (acute restrictive lung disease) - AKA Diffuse Alveolar Damage secondary too findings
short time period (mins to days) second to major systemic insult (i.e. sepsis, shock) diffuse pulmonary infiltrates and hypoxemic respiratory failure) increased vascular permeability necrosis of cells redution in diffusion capacity
50
3 stages of diffuse alveolar damage (ARDS)
1. exudative stage (protein and necrotic cells on alveolar septae form hyaline membranes) 2. proliferative (type II pneumocytes undergo hyperplasia) 3. fibrosis
51
4 main causes of diffuse alveolar damage (ARDS)
1. sever pulmonary infetion 2. aspiration 3. sepsis 4. severe trauma with shock other: viral, acute pancreatitis, acute interstitial pneumonitis....
52
sx and signs of diffuse alveolar damage (ARDS)
dyspnea, pink frothy sputum signs: crackles, hypoxemia, diffuse alveolar infiltrates high mortality -develop fibrosis --> chronic restrictive lung disease - pulmonary hypertension
53
chronic restrictive lung disease
inflam, fibrosis, impaired gas exchange (low diffusing capacity from carbon monoxide), obstructive ventilation impairments (decreased and normal FEV1/FVC)
54
causes of interstitial lung disease
autoimmune (i.e. lupus) idipathic work (asbestosis, silica, coal) drugs
55
chronic idiopathic pulmonary fibrosis (restrictive) findings on x ray (initial and late)
initial: ground-glass (exudates in alveoli) later: honeycomb lung (fibrosis of alveolar septal, parenchyma, and cobblestone pleural surface)
56
7 histological categories of idiopathic interstitial pneumonia
Usual interstitial pneumonia (UIP) Nonspecific interstitial pneumonia (NSIP) Organising pneumonia (OP)* Diffuse alveolar damage (DAD) Desquamative interstitial pneumonia (DIP)** Respiratory bronchiolitis (RB) Lymphocytic interstitial pneumonia (LIP)
57
sx of idiopathic interstitial pneumonia
dyspnea on exertion dry cough tachypnea signs: bibasilar end-inspiratory crackles, finger clubbing, right sided heart failure, diminished lung volume
58
pathogenetic implications for therapy for idiopathic interstitial pneumonia
immunosuppressive therapy (corticosteroids etc) biological therapy (monoclonal antibodies- RTK inhibitors) long term home oxygen therapy lung transplant

BMS250 (52 decks)

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