COPD Flashcards
COAD
Commonly used clinical term for a group of pathological conditions in which there is (acute or chronic?) partial or complete obstruction to air flow any level from _____ to ________ resulting in functional disability of the lungs
Chronic
trachea to smallest airways
COAD or COPD
⚫_________
⚫______________
⚫__________
⚫______________
Asthma
Chronic bronchitis
Emphysema
Bronchiectasis
ASTHMA
A chronic inflammatory disorder of the airways;
characterised by
⚫ widespread ________ of the airways, with
⚫ marked reduction in the __________________
⚫ Triggered by ________ stimuli.
⚫ Results in recurrent episodes of ________,________,__________ and __________.
⚫ May be ____________________, with or without
treatment
narrowing
inflow and outflow of air
a variety of
coughing, wheezing, breathlessness and chest tightness
reversed partly or completely
Classification of asthma Based on several factors including
A. Aetiology:
_________: ________ induced, Type 1 hypersensitivity
__________: induced by several ___________
Extrinsic; Allergen
Intrinsic; nonimmune factors
Classification of asthma Based on several factors including
Severity: _______,________, or ______
Frequency:_________ or _________
Clinical behaviour: i.e. brittle, difficult, ________ or ________
mild, moderate or severe
intermittent or persistent
steroid dependent or
resistant
Pollen concentrations are highest in the _______ or _________
Afternoon or midday
Pathophysiology
⚫ Asthma attacks are caused by airway
_________________
hyperresponsiveness
Pathophysiology
⚫ Asthma attacks are caused by airway
hyperresponsiveness—that is, an overreaction of the ________ and __________ to various environmental and
physiological stimuli, known as _______.
bronchi and bronchioles;
Pathophysiology
⚫ The most common causes of asthma attacks are extremely (small or large?) and (heavy or light?) weight particles transported through the ____ and inhaled into the lungs.
Small
Light ; air
Pathophysiology of asthma
⚫ When they enter the airways, these particles, known as
environmental triggers, cause ____________ in the airway walls, resulting in an asthma attack
An inflammatory response
Extrinsic/Environmental triggers
⚫ These are called __________.
allergens
ASTHMA: Extrinsic triggers
Allergens produce type ____ hypersensitivity reaction
1
Extrinsic triggers in asthma
⚫ They bind to _____ on the ____ cell in a previously sensitized individual
⚫______ cell _______ & releases inflammatory mediators & chemotactic
factors which cause
⚫ Increased ________ and ______
⚫ Broncho__________
⚫_______ hypersecretion
⚫
IgE; mast
Mast; degranulates
vascular permeability & oedema
constriction; Mucus
Asthma: Extrinsic triggers
These same allergens may cause little or no reaction in nonallergic people
T/F
T
10 Mediators
⚫ The _____ cells release ______ as a 10 mediator
⚫ ______ cells- secrete too much ______.
Mast; histamine
Goblet; mucus
10 Mediators
Histamine causes
⚫ increased ________ leading to ______ and ________
⚫ Broncho_____ - causing more _______
venular permeability
swelling and redness
spasms; narrowing
10 Mediators
Goblet cells- secrete too much mucus.
⚫ Mucus clogs the ________, resulting in _________ and ______
bronchioles
wheezing
Coughing
___________Triggers
These are refered to as intrinsic triggers.
Non-environmental
Non-environmental Triggers / intrinsic triggers. They include:
⚫_________ triggers
⚫ Physical exercise
⚫ Cold weather
⚫ Sometimes __________bring on attacks.
⚫ Chemicals found in _______ or _______
⚫ Intense ________
Physiological
substances in food or drink
food or medicine
emotion
Pathophysiology of asthma
⚫ Extrinsic triggers stimulate ______ nerves in ______ to discharge
⚫ These in turn stimulate the _____ nerve ( _______ nerve) to discharge
⚫ Cause release of inflammatory mediators & chemo tactic factors which
cause
⚫ Macrophage, eosinophil, basophil infiltration &________ activation
⚫ Broncho _______
⚫_______ hypersecretion
afferent
Tracheobronchial tree
vagal; efferent; mast cell
constriction
Mucus
Clinico-Pathologic correlation in asthma
⚫Bronchi and bronchioles become _______ resulting in _______ of airways
⚫_____eases work done to move air in and out of the lungs
⚫Mild chest _______ and _______ develop
⚫__________ starts and increases in pitch; dyspnoea sets in
oedematous; narrowing
Incr; pressure; dry cough
Wheezing
Clinico-Pathologic correlation in asthma
Cough _______ and becomes ______ of thick, stringy mucus.
Inflammation prevents ______________
Cells start to burn oxygen _________, increasing the body’s demand for oxygen.
________ develops. If untreated _____ occurs
intensifies; productive
insufficient oxygen-rich air from getting to the alveoli; at a higher rate
Hypoxaemia; cyanosis
Airway narrowing in asthma
⚫ Release of _______
⚫ Smooth muscle ______
⚫ Increased vascular _________/_______
⚫ Excessive mucous __________
chemical mediators
contraction
permeability/oedema
secretion
MORPHOLOGY of Asthma
Gross:
⚫ ________ lungs
⚫ (Thin or Thick?) , tenacious, adherent mucus in airway
Distended; thick
MORPHOLOGY of asthma
Microscopy:
⚫_________ crystals
⚫_________ spirals
⚫______ bodies
⚫ Hyperplastic bronchial _____________ & increase number of ______ cells
⚫_________ submucosa
Charcot-Leyden
Curschmann
Creola; mucosa and glands ; goblet
Oedematous
MORPHOLOGY of ASTHMA
Microscopy:
⚫ Charcot-Leyden crystals in _________,_______ , strips of _________
⚫ Curschmann spirals- _________ of airway
⚫ Creola bodies- compact clusters of _______ in sputum
mucus plugs, eosinophils
epithelium; mucus cast
epithelial cells
Genetics of asthma
⚫ Research suggests that genetic factors increase the risk of developing the disorder.
T/F
T
Genetics of asthma
Children with a family history of asthma are more likely to develop asthma than other children.
T/F
T
Emphysema
Is the ________ of airspaces (proximal or distal?) to __________
With __________
Without _______
Enlargement
Distal; terminal bronchioles
destruction of their walls
fibrosis
Emphysema occurs With fibrosis
T/F
F
Without fibrosis
Emphysema
A progressive respiratory disease
characterised by coughing, shortness of
breath & wheezing
T/F
T
Classification of Emphysema
Based on morphology
⚫___________
⚫_________
⚫___________
⚫__________
⚫ Mixed (Unclassified)
Panacinar
Centriacinar
Paraseptal
Irregular
Pathogenesis of emphysema
⚫ Cigerette smoking:__________ or _____ imbalance hypothesis
⚫_________ deficiency (genetic)
⚫ Air pollutants
⚫ Infection
Protease-Antiprotease or Proteolysis-Antiproteolysis
Alpha-1-antitrypsin
Smokers’ Emphysema
⚫ Increased number of _______
⚫ Contain __________ & other proteases
⚫ Reduced __________ activity due to
_____________________ enzyme
⚫ Increased activity of _______ & other
enzymes
neutrophils
serine elastase; α1-antitrypsin
oxidation of methionine
trypsin
Smokers’ Emphysema
Unopposed and increased ______ activity
destruction of _______ leads to loss of
___________
permanent ________ of alveoli
(Small or large?) volume of residual air trapped in the lungs
elastolytic; alveolar walls; elastic recoil
dilatation
Large
α1-antitrypsin
Produced in the _______
Is a Circulating ________
Major _______ of _______
liver; glycoprotein
Inhibitor ; proteases
α1-antitrypsin
⚫ In the lungs: inhibits _________
⚫ In the blood:_____% of all antiproteinase activity
neutrophil elastase
90
Molecular genetics of α1-antitrypsin
A1AT def caused by an abnormality of the ______ gene on chromosome ____ (14q32.1)
SERPINA1
14
Molecular genetics of α1-antitrypsin
Amount produced determined by genotype
⚫ Alleles:
⚫_____ , non-mutated
⚫______, glutamate to lysine mutation at position 342
⚫______ glutamate to valine mutation at position 264
PiM
PiZ
PiS
SERPINA1
(Serine Peptidase Inhibitor, Clade A, member 1)
Features of PANACINAR
The acinus is ____________
Destruction of _________
Associated with ___________
Tends to occur in ______ lobes
uniformly affected
alveolar septa
α1-AT deficiency
lower