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Pathology > Basics of the Respiratory System > Flashcards

Basics of the Respiratory System Flashcards

1
Q

Which area of the respiratory system is considered to be extra-pulmonary?

A 
The trachea (generation 0)
The main/primary Bronchi (generation1)
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2
Q

Which part of the branching in the airways does have cartilage and not?

A

The larger airways (Bronchi) have cartilage (generation 1)

The smaller airways (Bronchioles), starting at generation 4, do not have cartilage.

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3
Q

The conducting Zone vs the respiratory zone: the conduction zone finishes at:

A

The terminal bronchioles

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4
Q

The conducting Zone vs the respiratory zone: the conduction zone started at:

A

The respiratory bronchioles

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5
Q

Progression of the respiratory epithelium:

A

Nose: Pseudo-stratified ciliated columnar epithelium
Pharynx: Stratified squamous (provide protection against friction and damage)
Trachea and bronchi: Pseudo-stratified ciliated columnar epithelium
Bronchioles: Cuboidal
Alveoli: Simple squamous.

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6
Q

goblet cells are:

A

mucus producing cells

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7
Q

Type 1 cells:

A

Flattened for gas exchange

Constitute 10% of the alveolar cells BUT cover 95% of alveolar surface area.

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8
Q

Type 2 cells:

A

Cuboidal in shape, produce surfactant contain in the Lamellar bodies.

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9
Q

Pulmonary Surfactant is:

A

a lipoprotein complex (90% lipid, 10% protein)
4 types: SP-A,B,C, and D
Production begins between weeks 24 and 28 gestation.

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10
Q

SP-A and SP-D participate in:

A

the innate immunity (referred as the collectins)

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11
Q

SP-B and SP-C participate in:

A

the biophysical functions of the lung. It is required to his function.

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12
Q

Collectins roles:

A

Collectins is a protein that can bind to bacteria or viral surfaces and facilitates phagocytosis by macrophages.

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13
Q

Innate defenses of the respiratory system:

A
  1. Mucociliary Clearance (trap and move any particles toward the pharynx where it may be swallowed.)
  2. Phagocytosis Macrophage
  3. Phagocytosis Neutrophil (can enter during infection)
  4. Complement (Can enter and bind to bacteria to facilitate phagocytosis)
  5. Reflexe of coughing or sneezing.
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14
Q

Adaptative defenses:

A
  1. Antibody production by plasma cells (specialized B cells)
  2. IgA which is present in mucosal surfaces and IgG which is produced during an infection.
  3. Recruitment of different types of T cells to help contain the infection.
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15
Q

The Nasopharynx-associated lymphoid tissue (NALT) can produce:

A

Antimicrobial factors (AMF) such as enzymes(lysozymes), immunoglobulins, opsonins, and defensins

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16
Q

2 potentials sources of macrophages within the lungs:

A
  1. Alveolar macrophages originated from the york sac characterized by F4/80, CD11c, and Siglec-F.
  2. The Interstitial macrophages originated from the bone marrow (monocytes–>macrophages) characterized by CD11b and F4/80.
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17
Q

The most common viral causes of the common cold are:

A

Rhinoviruses (30-50%)
UNKNOWN (20-30%)
Coronaviruses (10-15%)
Influenza viruses (5-15%)

18
Q

Rhinovirus discovered by Dr. Winston Price in 1957, is structures/functions:

A
  • The Human rhinovirus (HRV) is a single stranded RNA virus with approximately 150 serotypes.
  • It maintly infect the nasal mucosa.
  • The RNA genome is packaged in a protein coat consisting of viral capsid proteins (VP) 1, 2, 3, and 4.
  • The structure of the rhinovirus helps itself attach to the receptor, by forming a “canyon” (allows for an attachment site for the receptor that we have)
  • The rhinovirus bind to the Intracellular adhesion molecule-1 (ICAM-1) in the surface of the cell.
19
Q

DIfference between the different viruse and the rhinovirus in term of consequences?

A

The rhinovirus DO NOT DESTROY the respiratory epithelium.

20
Q

Fomite means:

A

any nonliving object or substance capable of carrying infectious organisms.

21
Q

What went wrong in the study on rhinovirus:

A

The virus was weakened (vaccine) but the consequences of this, is it could adequately stimulate the receptors so there were limited activation and no antibody maturation. (when we get a cold, the virus activates different types of cell surface and intracellular receptors such as TLR4 and 7 which initiate a robust immune response and good antibody affinity maturation.)

22
Q

Are the lung are sterile?

A

No, there is a lot of diversity amoung the microorganisms in the respiratory systems.

23
Q

The bacterial composition changes with lung disease:

A
  • The lung has many microorganisms, but when there is a disease, the proportions are changing.
  • The proteobacteria increase in diseases like asthma, COPD and cystic fibrosis. (including the pathogen pseudomonas)
24
Q

In diseases like asthma, COPD and cystic fibrosis, there is an increase of one type of bacteria, which one?

A

The proteobacteria (including the pathogen pseudomonas)

25
Q

Pertussis (Whooping cough):

A
  • Gram negative coccobacillus
  • Do not survive for long periods in environment, meeds a human reservoir to survive (human-specific pathogen)
  • Fully Immunized at 5months, with booster at 4 and 11.
  • Most dead in younger babies unvaccinated or incompletely vaccinated.
26
Q

Pertussis adhere to the epithelium of the nasopharynx and trachea, and produce different types of toxins, including:

A
  • Pertussis Inhibits phagocytosis
  • Flamentous hemagglutinin and Pertactin which helps adherance to epithelial cells
  • Tracheal cytotoxin which kill epithelial cells
  • Adenylate cyclase toxin which inhibits phagocyte function
  • Type III secretion system which allows pathogens to survive within the respiratory system
  • Lipopolysaccharide
27
Q

3 stages of Whooping Cough:

A
  1. Catarrhal: 1 to 2 week of malaise, rhinorrhea, mild cold. Most contagious periode.
  2. Paroxysmal/Convulsion: 1 to 4 weeks, Cough “whooping sound’’, vomiting and exaustion after coughing fits (called paroxymisms)
  3. Convalescent Stage: Gradual recovery, coughing lessens, but fits of coughing may returns.(2 to 3weeks)
    (Susceptible to other respiratory infections)
28
Q

Diphteria also referred to as the “strangling angel of children” had 2 clinical types:

A
  1. Nasopharyngeal (Formation of a pseudo-membrane causing obstruction)
  2. Cutaneous
29
Q

Cornebacterium diphtheriae will only produce the toxin when:

A
  • It is infected with a corynebacteriophage (carrie the tox gene)
  • When the iron is limited or depreted, the tox gene is derepressd, allowing the toxin to be produce.
30
Q

Diphteria mechanism of action:

A
  • Inhibiting protein synthesis
  • 2 components: A and B.
  • Enter the cell by binding to the toxin receptor, become internalized.
  • the 2 components A and B are separed, toxin A binds to elongation factor-2 (Block the protein synthesis which kill the cell and allows the formation of pseudomembrane)
31
Q

Over factors for children risk of pneumonia:

A
  • Malnutrition**
  • Pre-maturity
  • Poor maternal health
  • Exposure to bio-mass smoke (ex. cooking/heating)
32
Q

Histology during pneumonia look like:

A

the alveoli is filled with inflammatory cells and exudate.

33
Q

Pneumococcal disease include:

A
  • Otitis media
  • Bacteremia
  • Meningitis
34
Q

Cascade of Events in the Lung causing the pathology (pneumonia):

A
  • Bacteria interact with epithelial cells and macrophages, may acuse damage.
  • Secretion of cytokines (chemotactic)
  • Upregulate cell adhesion molecules (help facilitate transmigration of cells from the blood to the lung)
  • Increased neutrophils which release ROS and others factors.
  • Induced necrotic death of infected cells, lung injury.
35
Q

TB contagions:

A
  • mycobacteria tuberculosis is not highly contagious
  • The vast majority of individual encounters the bacteria will never develop the disease (70-90%) and will be eliminated.
36
Q

In the 10-30% of those individual who will contract the TB infection, 2 outcomes are possibles:

A
  1. 90% will have latent TB infection (some may progress to subclinical TB disease or active TB disease, 10%)
  2. 10% will have active TB disease, wich can be fatal,50%.
37
Q

Symptoms of TB infection:

A

Coughing and cough with blood.

38
Q

Latent TB disease vs Subclinical TB disease vs Active TB disease:

A
  1. Latent: TB lives in the body, do not grow, no symptoms, CANNOT spread from one to another person, but can become active TB.
  2. Subclinical: TB disease will be sporadically infectious, no symptoms or mild symptoms.
  3. Active: TB is active, grows, symptoms present, can spread from one persons to another, can cause dead if not treated.
39
Q

Mycobacterium tuberculosis mechanism of action:

A
  • Enter the lung, reach the alveolar space.
  • Encounters aleveolar macrophages (the main cell type in TB infection)
  • Macrophages internalize bacteria, the bacteria hijack the phagosome.
  • TB enter the lung interstitium through epithelial damaged cells or infected macrophages that exits.
  • TB is transported to pulmonary lymph nodes for T cell priming, causing recruitment of more immune cells and the formation of granuloma.
  • Bacteria replicate in the granuloma, but may stay there.
  • Withing the granuloma there is macrophages, foamy macrophages, multinucleated giant cells, T cells, B cells, NK cells, Neutrophils, dendritic cells, fibroblasts and collagen. It bacterial burden, the granuloma will burst.
  • Resulting in dissemination to others organs, include the brain and can reentrering the respiratory tract –>symptoms/active TB.
40
Q

Characteristic lesion of TB:

A

Formation of granuloma.

41
Q

Military TB refer to:

A

an intense systemic dissemination

42
Q

Treatment for TB:

A
  1. Drugs therapy 1e line: Target cell wall synthesis or replication–> RIPE (Rifampin, Isoniazid, Pyrazinamide, Ethambutol)
  2. Vaccination: Bacillus Calmette-Guerin (BCG) protect 50-80% of vaccined people.
  3. 2e line Drugs therapy
  4. Multidrug resistant TB (MDR-TB)

Pathology (23 decks)

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