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COD respiratory diseases Flashcards

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1
Q

What are basal cells?

A

Stem cells of the airways

Differentiate into ciliated and secretory cells

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2
Q

What are ciliated cells?

A

Airway clearance

Removal of debris and pathogens out of the airways

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3
Q

What are goblet cells?

A

Secretes mucous

Which protects the lining of the airways and traps pathogens

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4
Q

What is air-liquid interface (ALI)?

A

Model

Differentiation of basal cells to secretory and ciliated cells upon exposure to air

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5
Q

What is spheroids in Matrigel?

A

Model

Cell differentiation demonstrated by production of mucous

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6
Q

What is Co-Cultures organoids?

A

Powerful to look at cell-cell crosstalk

eg fibroblasts

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7
Q

What are some common respiratory diseases?

A

Obstructive lung diseases eg asthma
Restrictive lung diseases eg Pulmonary fibrosis
Lung cancer

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8
Q

What are obstructive lung diseases?

A

Difficulty getting air out of the lungs
eg asthma
cystic fibrosis

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9
Q

What are restrictive lung diseases?

A

Difficulty getting air into the lungs
eg pulmonary fibrosis
Sarcoidosis

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10
Q

What is the forced vital capacity FVC?

A

Total air volume you can exhale in one forced breath

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11
Q

What is forced expiratory volume in 1 sec FEV1?

A

Air volume you breath out in 1 sec

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12
Q

Obstructive or restrictive diagnosis?
FEV1/FVC ratio <0.7
Reduced speed of breathing out
Narrow airways

A

Obstructive

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13
Q 
Obstructive or restrictive diagnosis?
Normal FEV1/FVC ratio
Reduced amount of air breathed in
Normal speed breathing in
Rigid/unable to expand lungs
A

Restrictive

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14
Q

Describe Chronic Obstructive Pulmonary Disease (COPD)

eg stats

A

Heterogenous disease with different clinical phenotypes and progression course
Usually affecting older people

1.2 million people live with COPD in the UK
3.17 million deaths in 2015
3rd cause of death worldwide but no effective therapy

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15
Q

What are some clinical phenotypes in COPD?

A

PINK PUFFERS

  • (mostly) Emphysema
  • Thin and cold
  • Pink skin
  • Minimal cough
  • Barrel chest
  • Severe breathlessness

BLUE BLOATERS

  • (mostly) Bronchitis
  • Overweight
  • Cyanosis (blue lips)
  • Chronic cough
  • Crackle and wheeze
  • Ankle swelling
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16
Q

Describe COPD as a Premature Aging Disease

A

Ageing lung features: loss of elasticity, enlargement of alveoli

Oxidative stress as key driver

  • > telomere shortening
  • > DNA damage
  • > stem cell exhaustion & senescence
  • > reduced repair & regeneration

Senescent cells secrete inflammatory mediators and proteases ->
senescence-associated secretory phenotype (SASP)

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17
Q

What has been proposed as a new approach for COPD as a Premature Aging Disease?

A

Targeting with anti-ageing drugs (senotherapies)

Awaiting clinical trials in patients

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18
Q

How do you diagnose COPD?

A

Spirometry

The lower the FEV1
is => the worse the COPD is going to be

Chest CT (computed tomography) may help identify emphysema

19
Q

What could be a risk factor for COPD development?

A

Small lungs at birth

20
Q

How is COPD managed?

A

Currently no cure
- Smoking cessation (quit)
- Bronchodilator inhalers: relax & open the airways making breathing easier
- Steroid inhalers: reduce airway inflammation, combined with bronchodilators (triple-therapy)
Pulmonary rehabilitation: exercise and education
Oxygen therapy often required in severe disease
Surgery: lung volume reduction, lung transplantation

21
Q

What are the future directions for COPD?

A

Urgent need for sensitive COPD biomarkers
-> early diagnosis

Need for curative treatments
-> identification of disease drivers & novel regulators

Need for better disease education
-> earlier diagnosis and better management

22
Q

Describe asthma

eg stats

A

Affects people of all ages, often starts in childhood, but can also develop in adults
5.4 million people live with asthma in the UK
420.000 deaths / year (2016)
Reversible disease involving narrowing of the airways (bronchioles)

23
Q

What are some genetic and environmental risk factors associated with asthma?

A
  • > allergens
  • > pollutants
  • > work exposures
  • > cigarette smoke
  • > medication (e.g. aspirin)
  • > stress
  • > exercise
  • > cold air
  • > viruses
  • > obesity
24
Q

What are the 2 asthma subtypes?

A

Atopic = allergic

Non-Atopic =Non- allergic

25
Q

Describe Atopic asthma

A 
Allergic
Extrinsic (triggered by environment)
Most common
Begins in childhood
Elevated IgE - antibodies produced by the immune system
More favourable
Family history
26
Q

Describe Non-Atopic asthma

A 
Non-allergic
Intrinsic (no recognisable allergen)
Non common
Late onset
Normal IgE -antibodies produced by the immune system
More severe
27
Q

What are the key features of asthma?

A 
Airway hyperresponsiveness to a range of stimuli / triggers
Airway inflammation and structural remodelling -> obstruction
Thickened airway wall
Smooth muscle spasm
Mucus hypersecretion
Goblet cell hyperplasia
Immune cells infiltration
(inflammation)
28
Q

Describe airway remodelling in asthma

A

Affects both large and small airways
Triggered by epithelial cells
Recruitment & prolonged activation of immune cells Th2, dendritic cells, macrophages
Increased smooth muscle cell mass & contractility, increased deposition of extracellular matrix
-> structural airway remodelling (thickening, fibrosis)-> obstruction
Activated fibroblasts & smooth muscle cells
Increased number of Goblet cells -> mucus production -> obstruction

29
Q

How is asthma diagnosed?

A

Characteristic pattern of respiratory symptoms
Variable airflow limitation
Variability in lung function
-> peak expiratory flow measurement
Bronchial provocation test (e.g. inhaled methacholine/histamine or exercise stress challenge -> measures how the airways respond to
triggers, assesses airway hyperresponsiveness)
Allergy test (presence of atopy increases probability for asthma)

30
Q

Describe Anti-inflammatory and bronchodilator inhalers

A 
Reliever inhalers = bronchodilator
eg salbutamol
Dilate the airways
Used occasionally
During attack for immediate relief of symptoms

Preventer inhalers = anti-inflammatory
Used regularly eg daily
For prevention of symptoms
Reduces airway swelling

Severe asthma: monoclonal antibodies (e.g. IgE, IL-5, IL-4 receptor)

31
Q

How do bronchodilators work?

A

Different classes & mechanism, but all open (dilate) the airways
▪ Short-acting or long-acting

32
Q

Describe idiopathic pulmonary fibrosis

A

Affects mostly older people (>50 years), more common in males
5000 people diagnosed every year in the UK
30,000 living with IPF in the UK (2016)
Median survival: 2-4 years
Disease involving parenchymal remodelling and progressive ‘scarring’ of the lung
Difficulty breathing and getting oxygen into bloodstream

33
Q

What does idiopathic mean?

A

Unknown cause

34
Q

How do you diagnose IPF?

A

Difficult as symptoms resemble other respiratory diseases & there are many types of interstitial lung diseases (ILDs)
Multidisciplinary team of experts diagnose
Exclusion of other known causes
Spirometry to look for restrictive pattern
DLCO measurement (Lung ability to transfer
gas from inhaled air into
bloodstream (indicates
extend of damage))

35
Q

What are the key features of IPF?

A

High-resolution chest CT scan -> Usual Interstitial Pneumonia pattern
Subpleural reticulation
Honeycombing

Collagen accumulation
Histology: Fibroblastic foci

Lung biopsy (if HRCT not clear)

36
Q

How do you manage IPF

A

No cure
2 drugs approved in 2014 (side effects)
Pirfenidone Nintedanib
Oxygen therapy and pulmonary rehabilitation

37
Q

What are the future directions of IPF?

A

Urgent need for sensitive ILD biomarkers
-> early & accurate diagnosis (potential for disease reversal)
-> identification of rapid progressors
Need for better & curative treatments
-> identification of disease drivers & novel regulators
-> discovery of new drugs without side effects & suitable for severe disease
Need for better disease education (patients & doctors)
-> earlier diagnosis & better management

38
Q

Describe COVID-19

A

Affects people of all ages, but the most dangerous for elderly and vulnerable (associated chronic diseases)
123 million people have been infected worldwide (end of 2020)
2.7 Million deaths so far
Caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2)

39
Q

What are Key Lung Cells Expressing SARS-CoV-2 Entry Proteins?

A

ACE2 & TMPRSS2 expression: nose, oral mucosa, lung (heart, kidney, pancreas, eye, brain, testes) -> potential (but not proof) for infection

40
Q

Describe the Different Expression of Entry Proteins with Age & Disease

A

Expression of ACE2 and TMPRSS2 in nasal and
bronchial airways relative to age and diseases status
children: lower expression than adults
increased expression in smokers, COPD, asthma
and hypertension
May explain differences in disease severity & susceptibility

41
Q

What is fibrosis

A

Excessive scarring in the lung

occurring due to aberrant repair

42
Q

What can we learn from receptor distribution in Covid?

A

Higher expression of receptors in the nose -> increased infectivity of the virus
viral transmissibility dependent on the spatial distribution of receptor accessibility along the respiratory tract
Presence of receptors may explain patients symptoms
eg
> gastrointestinal tract (small intestines): diarrhoea, viral sheading
respiratory tract: cough, pneumonia, acute respiratory distress syndrome
> brain: neurological symptoms: confusion, agitation, memory loss,
psychosis, brain inflammation and swelling, stroke)

43
Q

Expression of ACE2 and TMPRSS2 in nasal and
bronchial airways is relative to age and diseases status
What does this mean for children and smokers?

A

children: lower expression than adults
increased expression in
smokers, COPD, asthma
and hypertension

44
Q

what are the long term effects of covid?

A 
SARS coronaviruses are fibrogenic
exacerbates pulmonary fibrosis
Fibrotic changes observed in patients who recovered from COVID-19
Fibrotic changes visible
on CT scans eg micro-honeycombing

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