2 Flashcards

Question

bronchiectosis

Answer 1

unrestrained overproduction of mucus secretions that clog airways

Answer 2

abnormal epithelial responses to injury for example goblet cell metaplasia in heavy smokers airways reversible replacement of one cell with another called differentiations so all cells are replaced by goblet cells and there are no cilia etc.

Answer 3

they are associated with severe disease and they block the airways fungus can grow in the plug it can be very fatal cystic fibrosis

Answer 4

a chronic inflammatory disorder recurrent episodes of wheezing, breathlessness, chest tightness and cough,. reversible airflow obstruction can be helped by treatment or by itself.

Answer 5

airway inflammation leads to bronchial hyper responsiveness and the airways narrow due to the constriction of muscle this could trap air in the alveoli this is recurrent reversible airway obstruction

Answer 6

drugs can't enter the bloodstream that come from inhalers

Answer 7

primary care consultations prescriptions and GP service asthma treatments are not automatically free on the NHS

Answer 8

immune disorders such as asthma, crohns and MS infectious diseases such as measles, mumps, and TB because of vaccinations and antibiotics

Answer 9

an increase in hygiene in society has caused an increase in asthma younger siblings are exposed to pathogens at a younger age because older siblings bring them home from school, this will skew their immune system from Th2 to Th1 and make them more likely to have asthma and less likely to have allergies.

Answer 10

you are born with Th2 which is associated with allergies | Th1 is protective

Answer 11

respiratory allergies increased earlier then food allergies

Answer 12

Th2, but these people don't suffer from more allergies like you normally would with Th2 because worm infections are protective against allergens

Answer 13

we have evolved alongside microbes and we are dependant on them, friendly bacteria train the immune system to react appropriately to threats

Answer 14

we have gut flora there are some in the respiratory tract too they develop before we are born and during development we have better sanitations, caesarians and antibiotics and pets

Answer 15

allergens, genetics, work, respiratory infections, smoking, pollutants, medication, food additives, obesity, exercise and stress

Answer 16

heterogenous and polygenic and there are 150 genes identified. if one parent has asthma the risk for the child increases by 25% if two parents have it then the risk increases by 50%

Answer 17

triggering and regulating the immune system (TLR2, 4, 6 and NOD1 and MHCII) regulation of Th2 differentiation (IL4, 13, 5) lung function, remodelling and disease severity positional cloning - IRAKM is for pathogen recognition

Answer 18

obesity- late onset non Th2 phenotype (non allergy) and usually found in older females diet- bacon triggers asthma as it is preserved in nitrites which triggers inflammation vitamin d helps to stop asthma attacks as it stops us catching colds.

Answer 19

respiratory viral infections such as RSV are caught by almost all children, and a small proportion develop a severe disease which will increase the chances of asthma by x4 and it is a major trigger of exacerbations tobacco smoke during pregnancy or second hand causes epigenetic changes that make asthma more likely

Answer 20

Th2 (eosinophilic) - develops from childhood and is associated with allergy. there are non allergic variants such as late onset or exercise induced. non Th2 (non eosinophilic) - obesity, smoking, viruses. they have a neutrophilic characteristic and are associated with more severe disease and are less easy to treat.

Answer 21

the allergen is detected by dendritic cells which are the main antigen presenting cells in the airways. they travel to the lymph nodes and present to the immature Th cells. this will make Th2 lymphocytes which secrete cytokines IL4,5,13. IL4 will cause B cells to produce IgE which go on the surface of mast cells and recognise allergens in the future. If future allergens are detected it will cause release of prostaglandins which cause bronchoconstriction.

Answer 22

mast cells can degranulate and release proteases and cause airway remodelling. IL5 release will cause activation of eosinophils which have inflammatory actions in the airways IL4 and 13 effect smooth muscle cells and epithelial cells

Answer 23

it is activated in response to cigarette smoke, pollutants and viruses which will activate the toll like receptors. this will activate airway epithelial cells and alveolar macrophages. this will lead to cytokine release (IL8) and then the recruitment of neutrophils

Answer 24

release proteases which damage associated cells. Th1 and Th17 cells release cytokines (IL17 which affect monocytes and macrophages and cause them to release more IL8 to recruit more neutrophils) or they affect the mast cells and smooth muscle cells leading to the changes associated with inflammation in the airways.

Answer 25

blood vessels in airways are infiltrated by immune cells because they become leaky and this can cause oedema inflammation and swelling contracted smooth muscle and excess mucus these all lead to decreased lumen diameter

Answer 26

airway inflammation is normally to protect against invaders but asthma is inflammation with no serious infection

Answer 27

infiltration of eosinophils and lymphocytes swelling largened mucus gland and thicker mucus layer airway constriction

Answer 28

asthma it is caused by airway inflammation, which is a dynamic and reversible process where there is innapropriate contraction of the airway smooth muscle.

Answer 29

they give a patient an allergen to inhale and this decreases their FEV1 very quickly but this is reversible, and this is the acute asthmatic response. in 50% of people there is a late asthmatic response several hours later, there is a larger drop in FEV1 and it takes longer to recover to normal. AAR- the allergen binds to membrane bound IgE on mast cells and this causes the release of mediators (histamines, cysteinyl leukotrienes and PGs) and this will lead to bronchoconstriction. LAR- after AAR there is influx of inflammatory cells which are mainly eosinophils and this will cause oedema and bronchoconstriction which is the most damaging.

Answer 30

they can be very damaging and lead to airway remodelling. such as vasodilation, myofibroblast accumulation which release collagen causing collagen deposition on the basement membrane, mucus gland hypertrophy, goblet cells hyperplasia, airway epithelium cells come away from the basement membrane, inflammatory cells fill the airway and the smooth muscle layer will become thickened.

Answer 31

cells proliferate in response to the growth factors PDGF released from inflammatory or epithelial cells thermoplasty can burn away some smooth muscle to treat asthma.

Answer 32

angiogenesis occurs in response to growth factors VEGF and this causes increased muscosal blood flow this can lead to leakage from vessels

Answer 33

IL13 and neutrophil elastase

Answer 34

aberrant repair to persistent injury the basement membrane is thickened due to subepitheilial fibrosis there's release of pro fibrotic mediators such as TGFB from epithelial cells associated with eosinophilic infiltration.

Answer 35

inhalers- inhaled corticosteroids which are non specific and reduce inflammation and dilate the airways. They are long acting B2 agonists which are aimed at the smooth muscle. some patients remain uncontrolled despite having the above treatment, 22-63% of people have poor adherence to ICS. This could be due to young people forgetting to take the medication or people getting better and stopping taking it or poor communication of healthcare. different phenotypes of asthma with different patterns of inflammation may benefit from different treatments

Answer 36

a chronic and progressive disease that is characterised by the development of airflow limitation that is not fully reversible and by an accelerated decline in lung function. This usually results from an abnormal inflammatory response of the lungs to noxious particle or gases.

Answer 37

emphysema- damage to alveoli causing enlarged air spaces in the lungs chronic bronchitis- thickening of bronchial wall and mucus decreasing the airway diameter

Answer 38

commonly affects older people but it can affect all ages smoking is a cause, in lower class countries biomass fuels are the leading cause and it is mainly women that are exposed in households. richer people seem to have more COPD

Answer 39

smoking, air pollution, job, alpha 1 antitrypsin deficiency socio-economic status, alcohol, asthma, exposure primary and secondary smoke low birth weight, family history, atopy, childhood respiratory infections.

Answer 40

that genetics must play a role genes account for 30% of the variation in COPD risk if you smoke and have a first degree relative with COPD you are 3x more likely to develop it yourself if you have a first degree relative with COPD and don't smoke there is no increased risk.

Answer 41

20 CHRNA3 and CHRNA5 this is the nicotinic AchR gene cluster making nicotine addiction likely

Answer 42

a protease inhibitor made in the liver and goes into the bloodstream to the lung it protects the lung from damage caused by neutrophil elastase (released by neutrophils) the deficiency causes a defective protein that cannot be released from the liver so the lungs are more open to damage from smoking etc and because the protein can't leave the liver it will cause liver damage SERPINA1 and the deficiency is autosomal recessive

Answer 43

free radicals and oxidative chemicals in smoke damage the airways the chemicals cause inflammation of the alveolar wall causing loss of elasticity and the airways remain open. the cells begin to break down and create larger airway spaces and this will decrease the surface area and will affect the amount of gas exchange. (emphysema) the lung is like a sponge and soaks up tar.

Answer 44

inflammation of bronchi and fibrosis causing a cough from excess mucus

Answer 45

COPD lung has destroyed alveolar attachments so the airway will collapse and the wall is inflamed and there is excess mucus this is irreversible and occurs with ageing the alveolar attachments hold the airways open

Answer 46

normal smokers without COPD have an increased inflammation mild COPD has more inflammation severe COPD is permanent even if you stop smoking, exacerbations are a feature of COPD in response to pathogens

Answer 47

irritants will cause epithelial cells and macrophages to make chemokines CCL2- recruits monocytes which can differentiate into more macrophages CXCL1+8- recruit neutrophils CXCL9,10,11- recruit T cells and helper and cytotoxic neutrophils and macrophages release proteases such as neutrophil elastase and MMP9 which cause mucus hyper secretion and alveolar destruction epithelial cells make TGFB which causes fibrosis

Answer 48

viruses, bacteria and smoking

Answer 49

smoking creates reactive oxygen species which is damaging to surrounding cells and which creates DAMPs DAMPs can bind to TLRs, HSPs, NLRPs

Answer 50

smoke exposure and inflammatory cell activation it will cause the activation of TFs (NFKB, P38, MAPK) and inflammation. it also causes a decrease in antiproteases and increases TGFB causing fibrosis and emphysema it can cause DNA damage and decreased SIRT1 which maintains genome stability, and this will cause ageing and cancer. it decreases histone deacetylase 2 which causes steroid resistance telomere shortening, mitochondrial dysfunction, stem cell exhaustion

Answer 51

normally FEV1 decreases with age and COPD accelerates this and ageing

Answer 52

patients with COPD are colonised with bacteria normally macrophages kill this bacteria by phagocytosis or efferocytosis (removal of apoptotic cells) in COPD the macrophages are deficient so can't do this and this results in lots of bacteria and inflammation and lots of apoptotic cells

Answer 53

one exacerbation increases the likelihood of more and causes disease progression to death

Answer 54

goblet cell hyperplasia causing increased mucus infiltration of innate and adaptive immune cells, there are lots of neutrophils in COPD there is no basement membrane thickening or increase in smooth muscle like in asthma loss of alveolar attachments and destruction of alveolar airspaces squamous metaplasia of epithelium mucus gland hyperplasia

Answer 55

inflammation increase in fibrosis, but in asthma it is sub epithelial and in COPD it is peribronchial asthma is the only one to have increased smooth muscle and thickened basement membrane and vascular remodelling and connective tissue deposition COPD is the only one to have alveolar disruption and oxidative stress COPD- neutrophils, macrophages, CD8+ T cells asthma- eosinophils, macrophages, CD4+ T cells COPD- IL8, TNFA, IL1B, IL6 and NO asthma- eotaxin and IL4, 5, 13

Answer 56

asthma: COPD: child/teens mid-late adulthood none usually a smoker or ex smoker common level all the time. increases as it develops effective no effect

Answer 57

20% of patients with obstructive airway disease have this and 2% of the general population - COPD patients with increased eosinophil counts and this can be treated by blocking antibodies to cytokines associated with asthma or high dose of inhaled corticosteroids - asthmatic patients who smoke and have predominantly neutrophilic inflammation, this can be treated by macrolides or CXRC2 antagonists to block neutrophil recruitment - asthmatic patients who don't have a dominant cell type and may have increased inflammation, this can be treated by inhaled corticosteroids and b2 agonists

Answer 58

management of a stable disease: reducing exposure to irritants by stopping smoking, bronchodilators to relive symptoms, having a flu vaccine to reduce the chance of exacerbations manage exacerbations by oral antibiotics and corticosteroids to stop infection and inflammation

2 Flashcards

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