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Module 103: The Heart, Lungs and Blood > Theme 4: Lecture 8 - Respiratory infections > Flashcards

Theme 4: Lecture 8 - Respiratory infections Flashcards

1
Q

What is the respiratory tract divided into in terms of infections

A
  • Upper respiratory tract infections

- Lower respiratory tract infections

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2
Q

Describe the innate immunity of the lungs

A
  • Cilia – mucociliary escalator removing debris and pathogens
  • Alveolar macrophages: secrete antimicrobials, engulf and kill pathogens, recruit other immune cells, process and present antigens to T cells
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3
Q

Describe the acquired immunity of the lungs

A
  • B cell/T cell responses (essential for intracellular pathogens, such as mycobacteria, viruses and fungi)
  • IgA secreted by plasma cells interferes with adherence and viral assembly
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4
Q

How do different areas of the lungs differ in terms of the pathogens that they are exposed to

A
  • Lungs constantly exposed to particulate material and microbes from upper airway
  • Lower airways usually devoid of conventional pathogens
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5
Q

What is the body’s response to insult

A

Inflammation

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6
Q

Macro signs of inflammation

A

Redness, heat, pain, swelling and loss of function

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7
Q

Micros signs of inflammation

A

Vasodilation, increased vascular permeability and inflammatory cell infiltration

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8
Q

Name some infections of the upper respiratory tract (5)

A
  • Rhinitis
  • Sinusitis
  • Pharyngitis
  • Tonsillitis
  • Laryngitis
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9
Q

Name some infections of the lower respiratory tract (6)

A
  • Bronchitis
  • Bronchiolitis
  • Pneumonia
  • Pulmonary tuberculosis
  • Pulmonary abscesses
  • Empyema
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10
Q

What is a pulmonary abscess

A

A bit of lung tissue has died and there’s a pus filled abscess in that

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11
Q

What is empyema

A

Pus in the pleural space

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12
Q

What does the rhinovirus cause

A

The common cold

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13
Q

What does the human coronavirus cause

A

common cold

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14
Q

What does the zoonotic coronavirus cause

A

Severe respiratory illness

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15
Q

Transmission of viral URTIs which cause the common cold

A
  • hand contact: virus remains viable for up to 2 hours on skin or several hours on surfaces
  • droplet transmission from sneezing / coughing / breathing
  • IP 2-3 days; symptoms last 3-10ds, and up to 2 weeks in 25% patients.
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16
Q

What causes the symptoms of the common cold

A
  • Bradykinin: intranasal administrationof bradykinin causes a sore throat; it also causes nasal congestion due to vasodilation
  • Sneezing is mediated by stimulation of the trigeminal sensory nerves - histamine mediated
  • Nasal discharge (snot) changes colour with increasing numbers of neutrophils (white ->yellow->green) due to myeloperoxidase
  • Cough is mediated by the vagus nerve – inflammation has to extend to the larynx to trigger this; hyper-reactive response in URTI
  • Cytokines responsible for systemic symptoms such as fever
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17
Q

What are the differences between a cold and an influenza like illness

A
  • A cold appears gradually whereas flu appears quickly, within a few hours
  • A cold affects mainly your nose and your throat whereas flu affects more
  • A cold makes you feel unwell but you’re still ok to carry on as normal and go to work whereas the flu will make you exhausted and too unwell to carry on as normal
  • There’s usually no fever with a cold but high fevers with the flu
  • The flu may have lower respiratory tract features
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18
Q

What is coryza

A

Acute inflammation of the mucus membrane in the nose

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19
Q

What causes influenza

A

Influenza A or B virus

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20
Q

Describe uncomplicated influenza

A

-IP 1-4 days
-Abrupt onset of fever+ cough, headache, myalgia and malaise, sore throat, nasal discharge
-Acutely debilitating.
Fever 38-41OC; otherwise examination often unremarkable

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21
Q

Myalgia

A

Pain in the muscles

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22
Q

What are the risk groups for complications with influenza

A
  • Immunosuppression or chronic medical conditions
  • Pregnancy or 2 weeks postpartum
  • Age <2y or >65y
  • BMI >40
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23
Q

What complications could influenza cause

A
  • Primary viral pneumonia
  • Secondary bacterial pneumonia
  • CNS disease
  • Death (estimated mortality rateamong people infected withinfluenzain the US is about 0.13percent)
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24
Q

What are the 3 problems that a virus must solve in order to survive

A
  • It must know how to replicate inside a cell
  • It must move from one infected cell to a new cell (and a new host) in order to persist in nature
  • It must develop mechanisms to evade host defences (a good way to evade defences is by being intracellular in the first place)
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25
Q

Describe how a virus invades and infects a host cell

A
  • Attachment: Virus binds to a specific receptor on the host cell surface
  • Penetration: The viral nucleic acid enters the cell
  • Synthesis of new components: Viral nucleic acid takes over control of cell metabolism stopping the cell’s normal nucleic acid and protein synthesis. Viral nucleic acid is replicated using nucleotides from the host cell. Protein coats are manufactured using the amino acids of the host cell
  • Assembly: Whole virus particles are made when the nucleic acids are surrounded by the protein coats
  • Release: Many virus particles are released when the cell bursts open or by sow leakage
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26
Q

What allows the influenza virus to enter a cell

A

The influenza virus haemagglutinin surface protein (H) binds sialic acids on cell surface glycoproteins and glycolipids in the respiratory tract. This allows the influenza virus to enter the cell.

27
Q

What allows the influenza virus to escape the cell

A

The neuraminidase (N) on the surface of the virus allows the virus to escape by cleaving sialic acid bonds, otherwise the escaping virions all clump together.

28
Q

What allows the influenza virus to reassort

A

The influenza virus has a segmented genome (8 parts) so can reassort if 2 different viruses infect the same cell.

29
Q

Influenza drift

A

RNA viruses are careless in how they replicate (no checking mechanism) so you get point mutations each time and over time, it slowly changes what’s sitting on the outside of viruses

30
Q

Influenza shift

A

A massive change. This is when a whole segment of the RNA changes and is when you get pandemics because nobody in the population has any immunity

31
Q

What are the options for treatment and prevention of influenza

A
  • Active immunisation against haemagglutinin and neuraminidase components
  • Hand hygiene and droplet precautions
32
Q

What is pneumonia

A
  • Infection of the lung parenchyma

- Alveoli full of inflammation which blocks oxygen transfer

33
Q

What is parenchyma

A

The functioning part of the organ rather than the supporting tissue

34
Q

Symptoms of pneumonia

A
  • Fever, breathlessness, cough, sputum production;
  • Hypoxia, increased respiratory rate;
  • Pleuritic chest pain
  • Sepsis
35
Q

What does diagnosis of pneumonia require

A

Infiltrates on a plain CXR with supporting clinical features

36
Q

What can be seen in radiology of pneumonia

A
  • Consolidation - alveoli and bronchioles completely filled with inflammatory debris / pus / pathogens.
  • Heart borders or diaphragm obscured due to loss of solid-gas interface
  • Air bronchograms - air in larger bronchi outlined by surrounding consolidation.
37
Q

What are the 3 different classification types of pneumonia

A
  • Typical versus atypical – but not very helpful, as there is no feature in an individual patient that helps distinguish between them.
  • Lobar versus bronchopneumonia – also not very helpful; descriptive, but doesn’t help management
  • Community versus hospital-acquired = much more useful, as the pathogens involved differ in their % contribution
38
Q

Name 3 bacterial pathogens that are responsible for community acquired pneumonia (3)

A
  • Streptococcus pneumoniae
  • Mycoplasma pneumoniae
  • Legionella pneumophila
39
Q

Describe community acquired pneumonia caused by streptococcus pneumoniae

A
  • Commonest organism overall to cause community acquired pneumonia
  • Acquired in nasopharynx
  • Asymptomatic carriage in 40-50%
  • smokers more affected than non-smokers
  • Prevention – vaccine
40
Q

Risk factors for getting community acquired pneumonia with streptococcus pneumoniae (7)

A
  • Alcoholics
  • respiratory disease
  • smokers
  • hyposplenism
  • chronic heart disease
  • HIV: 50 to 100 fold increase in invasive pneumococcal disease in HIV+
41
Q

What is streptococcus pneumonia

A

Gram positive cocci

42
Q

What is mycoplasma pneumoniae

A

It lacks a cell wall so is resistant to penicillins and can’t grow on normal lab plates

43
Q

Describe community acquired pneumonia caused by mycoplasma pneumoniae

A
  • Commonest cause of ambulatory ‘atypical pneumonia’
  • Classically young patient, vague constitutional upset, several weeks
  • Extrapulmonary symptoms very common
  • Diagnosis: PCR of throat swab
44
Q

Describe community acquired pneumonia caused by legionella pneumophila

A
  • Can occur as sporadic infection or in outbreaks associated with a contaminated water source (consider travel and nosocomial, meaning originating in a hospital acquisition)
  • Uncommon
  • Can cause severe, life threatening infection
  • Risk factors= smoking and chronic lung disease
  • Diagnosis: Don’t grow on routine culture – need special conditions, and longer. Test for urinary legionella antigen
45
Q

Treatment for community acquired pneumonia caused by legionella pneumophila

A

Macrolides or quinolones

46
Q

Treatment for community acquired pneumonia caused by mycoplasma pneumoniae

A

Macrolides or tetracyclines

47
Q

Describe hospital acquired pneumonia

A

-Definitions vary. New onset at least >48 hours since admission.
-Hospitalised patients become colonised
with hospital bacteria
-These may either be intrinsically more resistant to antibiotics, or have acquired resistance mechanisms.

48
Q

What is hospital acquired pneumonia treated with

A

Broader spectrum antibiotics

49
Q

Treatment for community acquired pneumonia caused by streptococcus pneumoniae

A

Penicillin

50
Q

What causes TB

A

Mycobacterium tuberculosis

51
Q

Describe mycobacterium tuberculosis

A
  • Aerobic bacillus
  • Divides every 16-20 hours (slow) – lab extends culture to 56 days
  • Cell wall, but lacks phospholipid outer membrane therefore does not stain strongly with Gram stain (weakly positive) but retains stains after treatment with acids
  • Referred to as acid fast bacillus (AFB)
52
Q

What are the stains used for mycobacterium tuberculosis

A

Ziehl-Neelsen or auramine-rhodamine

53
Q

Describe infection of TB

A
  • Infection is initiated by the inhalation of aerosol droplets that contain bacteria.
  • The initial stages of infection are characterized by innate immune responses that involve the recruitment of inflammatory cells to the lung.
  • Following bacterial dissemination to the draining lymph node, dendritic cell presentation of bacterial antigens leads to T cell priming and triggers an expansion of antigen-specific T cells, which are recruited to the lung.
  • The recruitment of T cells, B cells, activated macrophages and other leukocytes leads to the establishment of granulomas, which can contain Mycobacterium tuberculosis
54
Q

Describe latent TB

A
  • Dormant bacilli
  • Contained by host defences
  • Non-infectious
  • Asymptomatic
  • Dx by demonstrating host immune response
55
Q

Describe active TB

A
  • Actively replicating bacilli
  • May be infectious (site-dependent)
  • Symptomatic (site-dependent)
  • Dx by isolating AFBs (acid fast bacillus), growing MTB (Mycobacterium tuberculosis) or PCR positive
56
Q

Management of TB

A
  • Cure active disease
  • Reduce spread
  • Prevent reactivation
  • By prompt and adequate treatment, appropriate source isolation and contact tracing
57
Q

Describe the chain of infection of SARS-CoV-2

A
  • SARS-CoV-2 (infectious agent)
  • Humans and other mammals (Reservoir)
  • Coughing, talking and sneezing (Portal of exit)
  • Droplet, aerosol and contact (Mode of transmission)
  • Mouth eyes and nose (Portal of entry)
  • Susceptible people (Susceptible host)
58
Q

What does the spike protein on SARS-CoV-2 do

A

Binds ACE2 receptor on airway epithelial cells

59
Q

What are the 3 cardinal features of SARS-CoV-2

A
  • A new, continuous dry cough;
  • Fever over 37.8OC;
  • Change or loss of sense of smell or taste
60
Q

Risk factors of SARS-CoV-2

A
  • Age (80% of deaths were over 70yrs)
  • Underlying medical problems
  • BAME groups
  • Societal factors eg occupation, household size, deprivation, and access to healthcare
61
Q

When should people with SARS-CoV-2 be admitted to hospital

A
  • Oxygen sats <90%
  • Respiratory rate >30
  • Signs of severe respiratory distress
62
Q

Complications of SARS-CoV-2

A
  • High risk of thromboembolism
  • Glycemic issues – hyperglycemia, DKA (diabetic ketoacidosis)
  • Acute kidney injury
  • Cardiac toxicity
  • Delirium in elderly
63
Q

Treatment for SARS-CoV-2

A
  • Supportive care
  • High flow O2
  • Dexamethasone (a corticosteroid)
64
Q

Prevention for SARS-CoV-2

A
  • PPE
  • Ventilation (environment)
  • Reducing encounters
  • Reducing contact/proximity
  • Handwashing
  • Immunisation

Module 103: The Heart, Lungs and Blood (51 decks)

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