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Respiratory Block > Pathology of Infectious Disease > Flashcards

Pathology of Infectious Disease Flashcards

1
Q

What is upper respiratory tract composed of?

A

Nasal cavity, pharynx, larynx, trachea ( zone between upper and lower)

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2
Q

What is the lower respiratory tract composed of?

A

Bronchi, lungs, diaphragm.

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3
Q

What is the main defense against viruses?

A

Respiratory tract is the main defense against viruses –> especially the nasal epithelium.

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4
Q

Nasal Cavity does what?

A

The nasal cavity warms, filters, cleans air on it’s way to lungs.

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5
Q

What are the cells making up nasal cavity?

A

Ciliated columnar cells, basal stem cells, goblet cells, neuroendocrine cells.

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6
Q

What respiratory epithelium is made of what?

A

Ciliated cuboidal mucosa +goblet cells

First line of defense: pathogens have to get through mucosa and past the cilia in order to infect the respiratory system.

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7
Q

Larynx

A

Respiratory Epithelium: pseudo-stratified columnar epithelium + goblet cells.

Non-Keratinizing Epithelium: no sero-mucous glands, no lymphoid tissue.

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8
Q

What is the thyroid composed of? What is the epiglottis composed of?

A

Thyroid Cartilage: hyaline cartilage.

Epiglottis: Elastic Cartilage

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9
Q

What is the histology of the trachea and bronchi?

A

There is cartilage, smooth muscle, and epithelium.

The epithelium has goblet cells, basal cells, and ciliated columnar cells.

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10
Q

What is the histology of bronchioles and terminal bronchioles

A

The histology is smooth muscle and simple ciliated columnar epithelium with club cells.

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11
Q

What is the histology of the respiratory bronchioles?

A

Respiratory bronchioles is smooth muscle and respiratory epithelium with club cells and cuboidal ciliated cells and squamous cells

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12
Q

What is the histology of alveolar sacs?

A

The histology is alveolar sacs: Type 1 Pneumocyte, Type 2 Pneumocyte, Alveolar Macrophage, capillary.

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13
Q

What are common patterns of lung disease?

A

Diffuse alveolar damage, granulomatous disease, diffuse interstitial mononuclear cell inflammation (viral pneumo), intra-alveolar supperative inflammation, viral inclusions

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14
Q

What are most URIs?

A

They are viral in nature.

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15
Q

What are the following diseases most likely caused by?

Epiglottitis and Laryngotracheitis:

Pharyngitis:

A
  1. H. Influenza Type B, and Corynebacterium diphtheriae

2. Strep Pyogenes

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16
Q

What is the pathogenesis of bacterial infections of the lung?

A

Elaborate enzymes that damage host cells. Capsules are resistant to phagocytosis and have surface M protein adhesin molecules.

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17
Q

What is the pathogenesis of viral infections?

A

They require entry into host cell for replication causing lysis and inflammation of the cells and tissue.

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18
Q

What is the pathophysiology of SARS Cov- 2?

A
  1. There are hemagglutinin spikes that bind to Sialic acid on the respiratory epithelial cells.
  2. The COVID-19 virus binds to the ACE-2 and Tmpress 2 are cell surface receptors on respiratory epithelial and endothelial cells are used by viruses to enter epithelial cells are used by viruses to enter epithelial cells of the upper airway nasal lining cells.
  3. The ACE-2 receptor causes a host cell: causes there to be multiple effects. Cytokine storm, ACE 2 activation which causes hyper-coagulability and micro-angiopathy. This can cause hypoxia and damage lungs.
  4. Direct viral infection causes rhabdomyolysis and tubular epithelial and podocyte damage causes kidney damage.
  5. Hypoxia and hypotension.
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19
Q

Neuraminidase is used for what by SARS-Covid-2 :

A

To exit the cell.

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20
Q

What cytokine storm?

A

All cases of cytokine storm involve elevated circulated cytokines, acute systemic, inflammatory systems, and secondary organ dysfunction.

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21
Q

How is cytokine storm caused?

A

ACE-2 receptors causes lymphopenia –> which leads to myeloid cell proliferation –> cytokine storm–> hyper-coagulability and microangiopathy –> leads to hypoxia and hypotension leading kidney, lung, and heart injury.

22
Q

Ang 2 causes what?

A

Ang 2 causes vaso-constriction

23
Q

What are the three mechanisms by which bacteria establish infection and damage tissue:

A
  1. They can contact adhere or enter host cells and directly cause death of infected cells. (Streptococcus Pyogenes)
  2. Staphylococcus, Streptococcus, H. Influenzae, Bordatella can release exotoxins and endotoxins that kill at a distance, these bacteria can release enzymes and degrade tissue components damage blood vessels vessels and cause ischemic necrosis
  3. Bacteria can induce host immune response directed against the organisms which can also be the cause of tissue damage (granulomatous inflammation with caseous necrosis and fibrosis as with Myco. Tuberculosis)
24
Q

What is the number one cause of community acquired pneumonia?

A

Strep. Pneumo

25
Q

What is the exotoxin that strep. pneumo uses?

A

Pneumolysin.

26
Q

What is the endotoxin that strep. pneumo uses?

A

Techoic Acid.

27
Q

What is the histopathology of strep pneumo?

A

Pus inflammation with intralveolar PMN leukocytes

28
Q

What does the exotoxin that diphtheria cause?

A

It causes there to be pseudomembrane formation, protein synthesis inhibitions, and necrosis.

29
Q

What are the pathological features of primary and secondary mycobacterium infection?

A

Primary: there is granulomatous infection, caseous necrosis, Ghon complex.

Secondary Infection: reactivation after latency, severe granulomatous inflammation, cavitation, necrosis, and miliary spread.

30
Q

What is the pathogenesis of fungal infections?

A
  1. infection forms one+ nodules
  2. Nodule cavitates
  3. Form necrotizing or non-necrotizing granuloma
  4. Suppurative granuloma
  5. Acute bronchopneumonia
  6. DAD
  7. Intravascular dissemination and damage ( immunocompromised)
31
Q

What are the 3 ways that fungi can enter the body?

A

Primary Mycoses: When spores are inhaled via the respiratory tract.

Subcutaneous: inoculated skin/trauma

Cutaneous/superficial: contamination of skin surface.

32
Q

What are virulence factors of fungal infections?

A

Capsule/adhesion factors, thermal dimorphism, toxin-like substances, capsules and adhesion like capsules, hydrolytic enzymes, and inflammatory stimulants.

33
Q

What is the meaning of interstitial pneumonia?

A

It is when there is pneumonia of the interstitial tissue surrounding the alveolar sacs.

34
Q

What are the general feature of pneumocystic pneumonia?

A

It is interstitial pneumonia that is airborne. Is airborne and occurs exclusively in HIV patients. HIV patient have alveolar thickening which causes impaired gas exchange, which then causes hypoxia.

Granulomatous inflammation is present.

In non-AIDs patients an interstitial pneumonia occurs.

35
Q

What are the tests used to determine pneumocystic pneumonia?

A

BAL (Broncho-alveolar lavage)

Methenamine Silver Stain

36
Q

Parasitic Lung infections examples are:

A

Schistosomiasis, echinococcus (hytatid cyst), amebiasis

37
Q

Parasitic infestation of the lung presents with what type of infiltrates and peripheral presentation?

A

Eosinophilic pulmonary infiltrate and peripheral eosinophilia.

38
Q

How do parasites travel through the body?

A

Travel to the lung most often from skin, can be swallowed and then migrate into the lungs via circulation.

39
Q

What is the pathogenesis of the parasite?

A

Contact of the cyst fluid with the host’s immune system can precipitate life threatening anaphylaxis and other immune complications.

40
Q

What can parasitic cysts cause?

A

chest compression, cough, chest pain, cysts can rupture and spread further

41
Q

What is diffuse alveolar damage?

A

Is when alveolar tissue is damaged causing there to be loss of gas exchange in the tissues causing there to be hypoxia.

42
Q

What are the two types of conditions which lead to DAD?

A

It is Acute Respiratory distress and acute lung injury.

43
Q

When are ARDS and ALI seen?

A

COVID-19, Mycoplasma, pneumocystis, miliary TB, other lung infectinos.

44
Q

How does DAD begin and progress?

A

There is initial pneumocyte and pulmonary lung injury, which causes there to be cytokine storm, injuring tissue.

45
Q

What is a cytokine storm?

A

When there is increased Interleukins, TNF, Chemokines, Interferons. This results in increased edema, inflammation, Fibrin deposition, DAD with hyaline alveolar membranes. Heavy, boggy, and red lungs.

46
Q

If cytokine storm resolves, what happens to lung tissue?

A

granulation tissue and fibrosis.

47
Q

What is the main cause of death for Covid-19?

A

It is diffuse alveolar damage.

48
Q

How is gas exchange impaired in alveoli?

A

There can be ulceration and septal infiltration ( chronic inflammatory cells ), disruption of blood/air barrier.

Hyaline Membrane Formation ( dead cells, fibrin, surfactant that adheres to alveolar wall and forms a gel or “ membrane). This always appears with DAD

49
Q

What are the different types of granulomatous diseases?

A

infectious vs non-infectious, necrotizing vs non-necortizing

50
Q

What is the diagnostic method for ID-ing a granuloma?

A

Acid fast for TB, periodic acid schiff for Fungal

Respiratory Block (12 decks)

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