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PATH300 > Respiratory diseases > Flashcards

Respiratory diseases Flashcards

1
Q

what is the function of gas exchange

A

moving oxygen in body tissues and removing cardon dioxide from cells and blood

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2
Q

describe the muco-cilliary defense of respiratory system

A

cilia lining the airway, thin layer of mucous catches particles/pathogens.
keeps pathogens and mucus away from lower respiratory system

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3
Q

3 functions of respiratory system

A

gas exchange, host-defense, vocalization

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4
Q

what/where is the larynx?

A

voice box. it is the first part of respiratory tract that is it the lower respiratory system

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5
Q

what lung has 3 lobes instead of 2? how many secondary bronchi?

A

right lung = 3 lobes. also 3 secondary bronchi

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6
Q

whats different between bronchi and bronchioles?

A

bronchi have cartilage and mucous glands

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7
Q

where does gas exchange happen

A

respiratory zone

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8
Q

name the order of the type of epithelium from upper to lower respiratory system

A
  • pseudo-stratified ciliated columnar epithelium
  • stratified squamous: in pharynx
  • pseudo-stratified ciliated columnar epithelium (again)
  • cuboidal
  • simple squamous (for gas exchange)
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9
Q

name the cell types and function in mucocilliary defense

A

goblet cells: mucus production
ciliated cells: transporting mucus

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10
Q

what cells help with gas exchange in alveoli? how?

A

endothelial cells; their basement membrane is fused with epithelial cell’s bm.

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11
Q

what structures are in respiratory zone?

A

from respiratory bronchioles to alveoli

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12
Q

how many alveoli are found in the lungs? what surface area?

A

480 million alveoli.
ab 70 m^2 (tennis court)

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13
Q

what are type 1 pneumocytes? features and function

A

have a flattened shape specialized for GAS EXCHANGE. 10% of alveolar cells, but cover 90-95%.
have collagen and elastin for structure.

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14
Q

what are type II pneumocytes? features and function

A

produce pulmonary surfactant.
have microvilli, lamellar bodies, large nucleus, many mitochondria.
make up 18% of alveolar cells, cover 5-10% of alveolar surface area.

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15
Q

what is pulmonary surfactant?

A

lipoprotein complex (90% lipid, 10% protein) that reduces surface tension in the alveoli to prevent alveolar collapse (atelectasis).
stored in lamellar bodies

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16
Q

name the surfactant proteins and their functions

A
  • SP-A and SP-D: innate immunity host defense, facilitate phagocytosis. can directly kill.
  • SP-B and SP-C: required for lung function. prevent atelectasis. not present in infants (causes respiratory distress syndrome)
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17
Q

what do interstitial cells do? (fibroblasts)

A

Help in the secretion of extracellular matrix to provide support/structure for alveoli

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18
Q

what are the innate immune defense techniques in the upper airways?

A
  1. mucociliary clearance (sneezing, filtration in nasal cavity, sinus produce mucus)
  2. NALT: nasal-associated lymphoid tissue produces antimicrobial factors (enzymes, immunoglobulins, opsonins, defensins)
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19
Q

what are the innate immune defense techniques in the lower airways?

A
  1. surfactant: SP-A/D bind to bacterial or viral surfaces to enhance phagocytosis (type II pneumocytes)
  2. macrophages: alveolar and interstitial
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20
Q

describe alveolar vs interstitial macrophages

A

alveolar:
- derived from yolk sac
- stable
- 3-5% of lung cells
- maintain tissue homeostasis and do phagocytosis
- express CD11c
interstitial:
- derived from yolk-sac and bone marrow in adults when needed
- 2% of lung cells
- immunoregulatory functions, less phagocytic
- express CD11b

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21
Q

what can serve as an intermediate to the alveolar macrophage?

A

interstitial fluid differentiated from bone marrow

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22
Q

what happens when alveolar macrophages encounter bacteria?

A

phagocytose & release cytokines that help kill bacteria, recruit other cells, activate interstitial macrophages

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23
Q

what cells are in the adaptive immune response of respiratory tract?

A
  • plasma cells: activated B cells that secrete antibodies such as IgA in the mucosal surfaces of the lungs
  • T and B cells
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24
Q

what are symptoms of rhinitis (common cold)?

A

headaches, sore throat, nasal congestion, and runny nose

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25
Q

risk factors of rhinitis?

A

Smoking, genetics, age, psychological stress, heavy physical training

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26
Q

what % of job absences in the US is due to cold?

A

40% of job absences and 30% of school absences

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27
Q

name examples of viruses associated with the common cold

A

rhinovirus (30-50% of colds), coronavirus, influenza, parainfluenza, adenovirus, enterovirus

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28
Q

describe rhinovirus structure

A

HRV = single-stranded RNA virus with 150 serotypes

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29
Q

why does rhinovirus mostly infect nasal mucosa?

A

optimal replication occurs at 33-35 deg C.
it latch on specific receptors on cell surface via VP1 hydrophobic pocket

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30
Q

how does HRV attach to airway epithelia cell?

A

VP1 viral capsid protein hydrophobic pocket attaches to ICAM-1 -> endosome.
in 10% of cases, low-density lipoprotein receptor LDLR is responsible.

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31
Q

what cytokines are produced from rhinovirus infection?

A

IL-6, IL-8

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32
Q

what signaling intermediates are released after rhinovirus infection?

A

bradykinins, prostaglandins, histamine -> cause inflammation, vasodilation, transudation of plasma, granular secretion -> congestion, cough, sneezing

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33
Q

what different between rhinovirus HRV vs adenovirus and influenza?

A

HRV does not destroy viral respiratory epithelium

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34
Q

definition of a fomite

A

any nonliving object or a substance capable of carrying infectious organisms

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35
Q

what are drugs against rhinovirus?

A
  • Capsid-biding agents: prevent the virus from entering the cells. ex pleconaril, vapendavir, pirodavir
  • Proteolytic enzyme inhibitors: inhibits protease involved in rhinovirus replication. ex: rupintrivir
  • drugs that target ICAM-I and zinc
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36
Q

what version of coronavirus infect human?

A

alpha and beta only (only 7 varieties)

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37
Q

structure of coronavirus?

A

single-stranded RNA virus

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38
Q

describe the protein on coronaviruses

A
  1. nucleocapsid protein N: make nucleocapsid
  2. spike protein S: binding to host cell receptor
  3. envelope protein E: form viral envelope
  4. membrane protein M: central organizer of CoV assembly & envelope shape
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39
Q

what is the receptor for covid entry?

A

angiotensin converting enzyme 2 ACE2

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40
Q

explain ACE2 system of entry?

A

angiotensin 1 gets converted to angiotensin 2 by ACE which can bind to AT1R.AT2R receptors -> vasoconstriction, fibrosis, inflammation, angiogenesis.
then ACE2 convert angiotensin 2 to 1 and 7 -> binds to MAS and has opposit effects to balance both processes.
main point: S protein binds ACE2 receptors to enter the cells

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41
Q

describe the physiological host immune response to SARS-Cov2 infection

A
  1. infection, binds to ACE2 and activates TMPRSS2 which cleaves S protein.
    1.5? PYROPTOSIS: inflammatory form of cell death
  2. chemokine and cytokines (IL-1, 6, 8, type 1 IFN) recruit immune cells (macrophages, DCs)
  3. more cytokine release
  4. cytotoxic antigen-specific T cells are recruited to the lungs
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42
Q

describe the pathological host immune response to SARS-Cov2 infection

A
  1. hyperinflammatory phase = excessive immune cells in the lungs, overproduction of pro-inflammatory cytokines, severe pneumonia in 14% of cases
  2. multiorgan failure = 5% of cases, procoagulant response activated, high neutrophils
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43
Q

covid symptoms

A

fever (88%), dry cough (68%) and fatigue (38%)

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44
Q

4 therapeutic approaches against Covid

A
  1. interfering with glycosylation or receptors/blocking receptors (hydroxychloroquine, chloroquine)
  2. premature termination of RNA transcription (remdesivir)
  3. blockage of protein processing (lopinavir and ritonavir)
  4. blocking cytokine/inflammatory storm
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45
Q

what type of vaccines are the moderna and pfizer vaccines?

A

nucleotide based mRNA vaccines

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46
Q

how do the covid mRNA vaccines work?

A

they cause our APCs to express S proteins -> releases cytokines to create memory B and T cells

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47
Q

what is bacterial dysbiosis?

A

when the lung microbiome changes due to a disease

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48
Q

in what cases is there an increased proportion of proteobacteria?

A

people with asthma, COPD, cystic fibrosis

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49
Q

what is pertussis?

A

whooping cough (violent and intensive)

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50
Q

what are the 3 stages of whooping cough? describe.

A
  1. Catarrhal stage: Highly contagious, lasts 1-2 weeks, resembles the common cold. Symptoms are runny nose, low-grade fever, mild occasional cough
  2. Paroxysmal stage: rapid cough then whooping sound. vomiting, exhaustion. excessive coughing can cause lack of oxygen. lasts 1-10 weeks, still contagious.
  3. Convalescent stage: recovery for 2-3 weeks
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51
Q

what is the most frequent complication of whooping cough in children?

A

pneumonia

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52
Q

how many ppl die of pertussis every year?

A

400 000 children

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53
Q

is there cure for whooping cough?

A

there is a vaccine

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54
Q

How does B. pertussis cause whooping cough?

A

adheres to nasopharynx and trachea epithelium, produces virulence factors that cause ciliary stasis -> bacteria can’t be cleared

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55
Q

what virulence factors are produced by B. pertussis?

A

pertussis toxin: attachment and cell toxicity
filamentous hemagglutinin: facilitates adhesion to epithelial cell
tracheal cytotoxin: kills respiratory epithelial cells
pertactin: adhesion to epithelial cell
adenylate cyclase toxin: inhibits phagocytes
type III secretion system: inhibits defensins to allow pathogen survival

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56
Q

what are the effects of bordetella pertussis on immune cells?

A

inhibit resident airway macrophages, neutrophils, DCs, Treg cells

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57
Q

what are the 2 types of diphteria?

A
  1. nasopharyngeal: formation of pseudomembrane in the back of the throat
  2. cutaneous: lesions on the skin
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58
Q

who and what does diphteria infect?

A

humans; infects nasopharynx and skin

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59
Q

how is diphteria triggered?

A

gram-positive bacillus corynebacterium diphtheriae gets infected with cornybacteriophage carrying a tox gene and produces diphteriatoxin DT.

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60
Q

what is DtxR and how does it work?

A

DtxR normally represses DT and tox gene, stops when there is low iron in the respiratory tract

61
Q

via what receptors does diphteria toxin (A-B toxin) gets internalized?

A

via HB/EGF receptors into endosomes

62
Q

how does A-B toxin (diphetria toxin) work?

A

A facilitates ribosylation -> halts protein synthesis, killing the cell
B binds to the cell receptor, allowing bacterial entry

63
Q

what are diphteria vaccines based on?

A

diphteria toxoid: modified bacterial toxin that induces IgG.

64
Q

describe pneumonia

A

inflammation in the lung parenchyma due to bacteria, viruses, fungi, other (inflamed alveoli)

65
Q

symptoms of pneumonia?

A

chest pain, persistent cough, persistent headaches, and productive phlegm

66
Q

how many children die of pneumonia?

A

more than 2 million children under 5 yo each year.mostly in developping countries

67
Q

risk factors for pneumonia

A

malnutrition, pre-maturity, poor-maternal health, external exposure to biomass smoke and pollution

68
Q

describe the 2 types of pneumonia

A
  1. bronchopneumonia: patchy inflammation in lungs after terminal bronchi
  2. lobar pneumonia: inflammation of one lobe or lung. caused by streptococcus pneumoniae bacteria
69
Q

cascade of events of pneumonia

A
  1. bacteria encounter epithelial and macrophages and pathogens multiply
  2. cytokine secretion
  3. upregulation of adhesion molecules
  4. migration and activation of immune cells like enutrophils
  5. ROS release to fight infection
  6. necrotic death of infected cells if too severe
  7. accumulation of immune cells and fluid
70
Q

what causes tuberculosis?

A

bacteria Mycobacterium tuberculosis.
human are the only known host

71
Q

how is tuberculosis transmitted?

A

airborne disease transmitted by droplets. not highly infectious compared to other diseases

72
Q

what happens to people who are exposed to Mycobacterium tuberculosis?

A

many don’t contract the disease.
come ppl develop latent TB that can be activated later

73
Q

symptoms of tuberculosis

A

Coughing, coughing with blood, fever, fatigue, weight loss, chest pain, chills, night sweats, loss of appetite

74
Q

can latent TB spread?

A

no. no symptoms. TB lives in body but doesn’t grow

75
Q

cascade of events of TB

A
  1. TB is inhaled in alveolar space
  2. alveolar macrophages internalizes bacteria but it hijacks the phagosomes
  3. reaches lung epithelial
  4. gets transported to lymph nodes where it survives in the granuloma (latent)
  5. granuloma breaks = active TB
  6. can spread to other organs (extrapulmonary TB) and dessiminate
76
Q

what does tuberculosis disseminate into?

A

miliary tuberculosis: systemic TB. can re-enter respiratory tract.

77
Q

what are treatments for TB?

A
  • first line therapy drugs and antibiotics present bacteria from replicating
  • second line drugs if first fails
  • multidrug resistant TB
  • vaccination
78
Q

what is the TB vaccine?

A

BCG vaccine: a weakened version of M. bovis

79
Q

name the Obstructive Lung Disease vs. Restrictive Lung Disease

A

obstructive = COPD, Asthma, Cystic Fibrosis
- makes it hard to exhale the air from the lungs
- high mortality rate
restrictive = Pulmonary Fibrosis
- more difficult time filling lungs with air (restricted from fully expanding)

80
Q

what is COPD?

A

combination of emphysema (alveoli destruction) and chronic bronchitis (airways inflammation)

81
Q

is there a cure for COPD?

A

no but it is preventable and treatable

82
Q

what is COPD exacerbations?

A

acute lung attack: worse cough, dyspnea and sputum production, often cause by an infection (ex haemophilus and streptococcus)

83
Q

what has the highest hospitalizations? (healtcare burden)

A

COPD exacerbations

84
Q

what is co-morbidities of COPD?

A

usually COPD + cardiovascular disease and lung cancer. also Osteoporosis, Skeletal muscle dysfunction, Anxiety/depression

85
Q

what is characterized as chronic bronchitis?

A

Mucous production that leads to cough for 3 consecutive months for at least 2 consecutive years.
excessive mucus and inflammation

86
Q

how do airway glands change for people with COPD?

A

submucosal glands enlarge, Goblet cell hyperplasia

87
Q

what does chronic bronchitis do to alveolar attachments? consequence?

A

disrupts them and fibrosis: causes obstruction of small conducting airways

88
Q

describe emphysema

A

Pathological condition with permanent airspace enlargement distal to terminal bronchioles Caused by the irreversible destruction of alveolar structures

89
Q

describe centriacinar vs panacinar emphysema?

A
  • centriacinar = respiratory bronchioles. from cigarette smoke
  • panacinar = alveolar ducts and alveoli. from a1-antti-trypsin deficiency
90
Q

what the 3rd component of COPD? after chronic bronchitis and emphysema

A

small arways disease: remodeling of small peripheral airways (<2mm).
a lot of the airflow limitation is associated with that

91
Q

who is most at risk of COPD?

A

75+ and older people

92
Q

what genes are involved in COPD?

A

a1 antitrypsin deficiency, AAT deficiency

93
Q

what is a1 antitrypsin?

A

Enzyme produced in liver that travels to the lungs.
inhibits neutrophil elastase (usually degrade lungs)

94
Q

COPD environmental risk factors

A

infections, old age, environment, dust, chemicals, cigarette, air pollution

95
Q

what are the main effects of cigarette smoke?

A

mainly affects respiratory bronchioles, centriacinar emphysema

96
Q

how does cigarette cause inflammation?

A

breaches epithelium, interacts with other structural lung cells
activates epithelial cells
triggers production of TNF, IL-6, IL-8 and recruitment of innate and adaptive response cells
damage epithelial barrier
ALL this leads to EMPHYSEMA

97
Q

what t cells are mostly involved in COPD

A

TH1 mostly, TH17

98
Q

how do macrophages contribute to COPD?

A

they release factors like proteases, neutrophils release NE, destroy lung tissue, promote emphysema, activate TGFB which contributes to obstruction,
contribute to lung destruction (elastolysis)

99
Q

what are symptoms of COPD

A

shortness of breath, chronic cough, sputum

100
Q

what is required to diagnose COPD?

A

spirometry: asses airflow limitation

101
Q

what are FEV1 and FVC and how are they affected in COPD

A

FEV1 = forced expiratory volume in 1s. lower in COPD
FVC = forced vital capacity
if FEV/FVC ratio is < 0.7 = obstructive airway disease

102
Q

what are the stages of COPD severity according to FEV/FVC?

A
  • mild, stage 1, FEV1 > 80%
  • moderate: stage 2, FEV1 < 50% to 80%
  • severe, stage 3, FEV1 < 30 to 50%
  • very severe: stage 4, FEV1 <30%
103
Q

what is GOLD?

A

global initiative for chronic obstructive lung disease. goes from GOLD1 (mild) to GOLD 4 (very severe)

104
Q

is COPD reversible?

A

no

105
Q

what medications can be used against COPD? (to relieve symptoms)

A

bronchodilators, corticosteroid, phosphodiesterase inhibitors and methylxanthines (oral)

106
Q

other “treatment” against COPD?

A

oxygen therapy, pulmonary rehabilitation, lung volume reduction surgery

107
Q

definition of asthma + symptoms

A

heterogeneous disease, usually characterized by chronic inflammation.
symptoms = wheezing, coughing, chest
tightness, shortness of breath

108
Q

cool difference between asthma and COPD?

A

asthma is reversible!

109
Q

2 categories of asthma

A
  1. atopic/extrinsic: allergic, most common, 50% of adults have it
  2. non-atopic/intrinsic: non-allergic, inflammation and constriction, can be triggered by virus and inhaled pollutants
110
Q

what is exercise-induced asthma / exercise induced bronchoconstriction?

A

type of non-atopic/intrinsic asthma in 15% of athletes, same symptoms, exercise causes bronchospams and then bronchoconstriction

111
Q

features of asthma

A

airway remodeling, thickened airway wall, increased muscle and mucus secretion, thickened basement membrane, bronchoconstriction
- presence of eosinophils, sub-basement membrane thickening, mucous in the airway lumen

112
Q

name 4 components associated with these
abnormal changes of asthma

A
  1. increased nb of blood vessels
  2. subepithelial fibrosis
  3. increase in SM
  4. increased volume of submucosal glands
113
Q

what is proportional to asthma severity?

A

airway remodeling: look at BM and sub-basement membrane, mucus in lumen, SM size, eosinophils

114
Q

describe the mechanism of asthma

A
  1. allergen activates epithelia cells and cytokines are released
  2. immune cells are recruited -> remodelling
115
Q

what type of hypersensitivity reaction is allergic asthma?

A

type 1 hypersensitivity with type 2 inflammation (Th2)

116
Q

name the cytokines released by Th2 and their function

A

IL-4: stimulates B cells to produce IgE
IL-5: recruits and activates eosinophils
IL-9: enable eosinophil survival
IL-13: stimulates mucus production & goblet cells

117
Q

what happens when DCs present Ag in lymph nodes?

A

CD4+ t cells are primed -> differentiate into follicular helper cells to activate B cells which differentiate into Th2 cells

118
Q

what is Th2 function?

A
  • Secretes IL-4, IL-5, IL-13
  • Induces class switching of plasma cells to secrete IgE
  • Activate mast cell and recruit eosinophil
119
Q

name the Type 2 immune response characteristics

A
  • increased Th2
  • many inflammatory cells
  • leukotrienes responsible for immediate response
  • hyperplasia of the glands
120
Q

what are the predominant cell and cytokines in non-allergic asthma cascade?

A

innate lymphoid cells and IL-5, IL-13

121
Q

what is airway hyperresponsiveness?

A

AHR: clinical feature of asthma responsible for most symptoms.
- predisposition of the airways to narrow excessively in response to stimuli
-> exaggerated response to a bronchoconstrictor

122
Q

what bronchoconstrictors can trigger airway hyperresponsiveness?

A

not normal = exercise, cold air
normal bronchoconstriction = histamine, methacholine

123
Q

what is bronchial provocation test?

A

methalcholine used to cause a 20% fall in FEV1 to calculate the provocation concentration. someone with asthma will be hyperresponsive to this

124
Q

what will be the PC20 value of someone with asthma?

A

PC20 < 8 mg/ml

125
Q

treatments for asthma

A

corticosteroids inhaled alone or with beta 2 agonist

126
Q

what does smoking cause in asthmatic patients?

A

increases symptoms, can’t manage diseases as well, need hospital care, faster decline in its function, reduced responsiveness to steroids and anti-inflammatory meds, alters inflammatory profile (***becomes more neutrophilic than eosinophilic)

127
Q

differences between asthma and COPD mechanism

A

asthma: allergens -> epithelia cells + mast cells -> CD4+, Th2 cells, eosinophils -> bronchoconstriction and airway hyperresponsiveness -> reversible

COPD: smoke ->alveolar macrophages + epithelial cells -> CD8+, T cell, neutrophils -> small airway fibrosis & alveolar destruction -> not reversible

128
Q

what are symptoms of asthma-COPD overlap syndrome?

A
  • Limited reversibility of airway obstruction
  • Hyperinflammation
129
Q

what is cystic fibrosis

A

A multi-system disease that affects the lungs, GI, pancreas and other organs.
respiratory failure is the most common cause of death

130
Q

how do you get CF?

A

inherited genetic mutation in CFTR (chloride channel on apical surface of respiratory and GI epithelium) -> autosomal recessive disorder. get it if both parents are carriers

131
Q

cystic fibrosis symptoms

A
  • Persistent cough with productive, thick mucus
  • Repeat respiratory infections
  • Wheezing and shortness of breath
  • Frequent chest infections
  • Affects multiple organ systems, other organs that rely on SECRETION to do their function (pancreas and GI tract)
  • Sinusitis, nasal polyps
  • Other: Infertility, digestive symptoms, arthritis, osteoporosis
132
Q

what is CFTR and what does it do?

A

cystic fibrosis transmembrane regulator: chloride channel present on apical surface of respiratory and GI epithelium
- regulates fluid and electrolyte transport (Na/Cl levels)
- hydration of organs and mucociliary clearance

133
Q

what does the defect of CFTR cause?

A

mucus is much thicker and stickier and builds up
- no Cl secretion and increased Na absorption
- more than 1000 diseases associated with mutation

134
Q

what is the most common CFTR mutation?

A

deltaF508 class: 90% of CF patients; class II defect

135
Q

how does CF cause damage to lungs?

A

Cycle of chronic inflammation and infection due to mucus obstruction

136
Q

what does a decrease in CFTR cause? leads to CF

A

defective mucociliary clearance

137
Q

what immune cells are recruited in CF?

A

neutrophils are recruited with inflammation

138
Q

what are the treatments for CF?

A

antibiotics, bronchodilators, mucolytic, anti-inflammatories, CFTR drugs (potentiators, correctors, triple combination ex Trikafta

139
Q

describe the restrictive lung disease we talked about

A

pulmonary fibrosis: fatal, chronic, progressive fibrosing interstitial pneumonia of unknown cause.
lungs become scarred and can’t function due to extra ECM

140
Q

how does scarring in pulmonary fibrosis happen?

A

Destruction of lung architecture and deposition of extracellular matrix

141
Q

describe the histology of pulmonary fibrosis

A

honeycombing and dense fibrosis

142
Q

is there a treatment for IPF Idiopathic pulmonary fibrosis?

A

no

143
Q

symptoms of IPF

A

shortness of breath, chronic dry cough, finger clubbing.
occasionally: fatigue, weakness, weight loss

144
Q

what is the theory of IPF pathogenesis?

A

micro injuries to type I and II pneumocytes cause abnormal repair response (epithelial activation, re-epithelization, epithelium tries to repair itself) -> causes TGF-N release -> GFs, cytokines -> myofibroblasts activation

145
Q

what does too much myofibroblasts do?

A

too much ECM production, collagen and fibronectin, stiffening of the lung and scarring

146
Q

what are the main effector cells in pulmonary fibrosis?

A

fibroblasts which differentiate into myofibroblasts

147
Q

what does TGF-B do in the lungs?

A

gets activated, activates smal2/3/4, upregulates several ECM genes

148
Q

what are treatments ish for pulmonary fibrosis?

A

lung transplant
meds: nintedanib, pirfenidone (only slow down progression by lowering TGF-B)

PATH300 (10 decks)

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