Resp - Pathology Of Obstructive Pulmonary Dz

Front 1

obstructive lung dz details

Back 1

-dec airflow from inc resistance
-secondary to obstruction of airway
-anatomic narrowing of airway
-dec elastic recoil

Front 2

PFT in obstructive lung dz

Back 2

-dec FEV1
-nL of inc TLC
-dec FEV1/FVC ratio and TLC not dec

Front 3

what is emphysema

Back 3

permanent enlargement of airspaces with destrution of airspace walls

Front 4

panacinar emphysema clinical features

Back 4

distal acinus (resp bronchioles to terminal alveoli)
-wrose in lower lobes
-can cause clinical airflow obstruction
-alpha 1 - antitrypsin deficiency

Front 5

centriacinar emphysema clinical features

Back 5

-involves central/proximal acini (resp bronchioles) (spares distal alveoli)
-worse in UPPER lobes
-can cuase clinical airflow obstruction
-smokingdistal acinar

Front 6

distal acinar emphysema clinical features

Back 6

-involves distal airspaces (along pleura, along CT septa)
-worse in upper lobes
-no clinical airway obstruction
-spont pneumo in adults ??

Front 7

emphysema pathogenesis

Back 7

excess protease and/or elastase production unopposed by antiprotease regulation

-neutros release elastase, which destroys elastic tissue
-if antiprotease is insufficient, tissue destruction does unchecked

Front 8

smoking and emphysema

Back 8

-inc neutrophils/macs in alveoli
-elastase release from neutros
-inc elastase actibity in macs (not inhibited by alpha-PI)
-oxidants and free radicals in smoke and free radicals from neutros inhibit alpha-PI

Front 9

nL alpha PI phenotype

Back 9

PiMM

Front 10

most common alpha PI phenotype in alpha AT deficiency

Back 10

PiZZ

Front 11

clinical features of emphysema

Back 11

-no sx until loss of 1/2 functioning parenchyma
-dyspnea
-weight loss
-obstructive pattern on PFTs
-pink puffer/ blue bloater
-death (pulm failure, resp acidosis, hypoxia, coma, cor pulmonale, pneumo

Front 12

weird usage of emphysema

Back 12

-compensatory
-mediastinal/interstitial/subQ
-obstructive overinflation

Front 13

what is chronic bronchitis

Back 13

persistent, productive cough for at least 3 consecutive months in at least 2 consecutive years

Front 14

types of chronic bronchitis

Back 14

simple
chronic asthmatic
obstructive chronic

Front 15

pathogenesis of chronic bronchitis

Back 15

-cig smoking + air pollutants inhaled (mucous gland hypersecretionhypertrophy + goblet cell metaplasia)
-inflammation + fibrosis -> obstruction
-frequent co-existent emphysema
-complicated by microbial infection

Front 16

gross morphology of chronic bronchitis

Back 16

-large airway edema + hyperemia
-mucosa (large and small airways) covered by mucinous/mucopurulent secretion

Front 17

micro morphology of chronic bronchitis

Back 17

-mucous gland hyperplasia (+ goblet cell hyperplasia +/- loss of cilia
-inflamm infiltrate
-chronic bronchiolitis (small airway dz)

Front 18

clinical presentation of chronic bronchitis

Back 18

-persistent productive cough
-inc CO2, dec O2, cyanosis
-recurrent infections
-heart failure (cor pulmonale)

Front 19

what is asthma

Back 19

episodic, reversible bronchospasm due to exaggerated broncoconstrictor response

-chronic inflamm dz of airways

Front 20

extrinsic asthma information

Back 20

-type 1 hypersensitivity to extrinsic Ag
-atopic
-occupational
-allergic bronchopulmonary aspergillosis

Front 21

instrinsic style of asthma

Back 21

non-immune trigger
-aspirin
-infection
-cold
-psych stimuli
-stress
-exercise
-inhaled irritants

Front 22

sensitization in atopic asthma

Back 22

-inhaled Ag by dendritic cell to TH2 cell
-TH2 secretes IL4 -> Bcell IgE production
-IL3, IL5, GM-CSF -> eosinophil recruitment
-IgE binds to Fc receptor on mast cell

Front 23

atopic asthma early phase

Back 23

-Ag crosslinks on surface mast cells
-surface mast cells secrete mediators - > open epithelial tight junctions
-Ag penetrates epithelium to cross-link IgE on deep mast cells

Front 24

deep mast cells secretion of mediators results in

Back 24

-inc vascular perm
-inc mucus production
-bronchospasm
-recruit more cells

Front 25

late phase of asthma

Back 25

-more mediator release from leukos, endos, epis
-accumulating eosinophil release: amplifying/sustaining inflamm response without additional Ag exposure

Front 26

intrinsic asthma triggers also affect

Back 26

extrinsic astham sufferers
nL people

-nonimmune mediated bronchospasm, mucus secretion, and edema

Front 27

morphology of asthma

Back 27

-thicker
-more inflamm cells
-hyperplasia of smooth m
-more glands

Front 28

status asthmaticus

Back 28

prolonged attack, refractory to Tx

Front 29

charcot-leyden

Back 29

any complication with excess eosinophils
-asthma

Front 30

curschmann's spirals

Back 30

injury to epi, slough off and in mucous

asthma

Front 31

bronchiectasis

Back 31

permanent dilatation of bronchi and bronchioles due to destruction of muscle and supporting elastic tissue

not primary dz

dx based on hx and CXR

Front 32

forms of dilatation seen in bronchiectasis

Back 32

cylindrical
fusiform (spindle shaped)
saccular

Front 33

predisposing conditions to bronchiectasis

Back 33

bronchial obstruction: tumor, foreign body, mucus impaction

necrotizing or suppurative pneumonia

congenital or hereditary condition: CF, immunodef, primary ciliary dyskinesia

Front 34

morphology of bronchiectasis

Back 34

gorsS:
bronchial dilatation
lower lobes

micro:
-acute and chronic inflamm with exudate
-epithelial ulceration
-abscess formation

Front 35

clinical features of bronchiestasis

Back 35

-severe, persistant cough with mucopurulent sputum +/- blood
-frank hemoptysis
-clubbing of fingers
-obstructive sequelae( dec O2, PHTN, cor pulm)
-mets brain abscess
-reactive amyloidosis