Week 8: Respiratory Flashcards

1
Q

Symptoms of SARS-CoV2

A

Most Common:
* fever
* cough
* tiredness
* loss of taste or smell
Less Common
* sore throat headache
* aches and pains diarrhoea
* a rash on skin, or discolouration of fingers or toes red or irritated eyes
Serious Symptoms
difficulty breathing or shortness of breath loss of speech or mobility, or confusion chest pain

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2
Q

Phase I of SARS-CoV2 infection

A

Infection of epithelial cells
Virus spreading in the respiratory and gastrointestinal tracts,
Early innate immune response (e.g. macrophages and monocytes)
Detection of PAMPs related to SARS-COV2 and activation of PRRs Release of cytokines at local levels
Clinically mild symptoms

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3
Q

Phase II of SARS-CoV2 infection

A

Virus infection leads to cytokine responses
Cytokines production results in influx of various immune cells such as macrophages, neutrophils, and T cells from the circulation into the site of infection
Destructive effects on human tissue resulting from: destabilization of endothelial cell to cell interactions,
damage of vascular barrier,
capillary damage,
diffuse alveolar damage (rapidly progresses to ARDS)
Continuous virus replication and excessive production of cytokines Inflammatory PCD and positive feedback loop resulting in a cytokine storm. Life-threatening damage to host tissues and organs

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4
Q

Covid attached to what cell receptors

A

Primary receptor: ACE2 (Angiotensin-converting enzyme 2) Role: virus attachment to host cell
Co-receptor: TMPRSS2 (A serine protease)
Role: facilitate fusion of virus particle with the host cell

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5
Q

SARS-CoV2 stages of replication

A
  1. Attachment: ACE2
  2. Entry
    Surface fusion: mediated by TMPRSS2 Endocytosis: mediated by ACE2
  3. Release of genome
  4. mRNA & proteins (including RdRp)
  5. Genome replication
  6. Assembly of NC (helical)
  7. Packaging of genome
  8. Released
    (budding into ER and exocytosis)
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6
Q

Acute respiratory distress syndrome

A

a serious lung condition characterised by structural changes in alveolus including fluid builds up and surfactant breaks down.
These physiological changes affect lungs functions and consequently lead to reduced oxygen levels.
Symptom of ARDS:
shortness of breath.
low blood oxygen,
rapid breathing,
rattling sounds in the lungs when breathing.

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7
Q

SARS-CoV2 - Risk factors

A

certain treatments ( eg chemotherapy/immunotherapy)
particular illnesses and conditions
Age, especially if you are over 70 years old
environment smoking
being pregnant being male.

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8
Q

Treatments and prevention for covid

A

Prevention:

  • Vaccination: Primary and booster doses for immunity.
  • Public Health Measures: Masking, hand hygiene, social distancing, and good ventilation.
  • Testing & Contact Tracing: Rapid tests, PCR, isolation, and quarantine.
  • Public Awareness: Education on symptoms and preventive actions.

Treatment:

  • Supportive Care: Symptom relief, oxygen therapy for hypoxemia.
  • Antivirals: Remdesivir, Paxlovid, Molnupiravir for early high-risk cases.
  • Monoclonal Antibodies: For high-risk patients to prevent severe illness.
  • Corticosteroids: Dexamethasone for severe cases needing oxygen.
  • **Anti-inflammatory Agents: **Tocilizumab, Baricitinib for severe inflammation.
  • Complication Management: Anticoagulants, ventilatory support, post-COVID rehabilitation.
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9
Q

Aetiological Classifications of Pneumonia

A
  • Bacterial
  • Viral
  • Aspiration - foreign material eg gastric compounds
  • Atypical - caused by atypical pathogens like Mycoplasma or Chlamydia
  • Opportunistic - occurring in individuals with weakened immune systems, caused by pathogens not typically harmful to healthy individuals.
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10
Q

Acquisition-based Classifications of Pneumonia

A
  • Community acquired - Pneumonia acquired outside of healthcare settings, often caused by common bacteria or viruses.
  • Healthcare acquired- Pneumonia that develops during or after hospitalisation or other healthcare interventions, often involving drug-resistant bacteria.
  • Ventilator associated - Pneumonia developing in patients on mechanical ventilation, often due to hospital- acquired infections.
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11
Q

Clinical features of Pneumonia

A
  • Productive cough
  • Dyspnoea
  • Pluertic chest pain (worsened by deep brething/coughing)
  • Hypoxia
  • Dullness to percussion
  • Decreased breathing sounds
  • Bronchial Breathing
  • Coarse Crackles
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12
Q

Pathophysiology of community acquired pneumonia

A
  1. underlying agent (eg virus/bacteria)
  2. colonisation of nasopharynx
  3. micro aspiration
  4. programmed cell death
  5. release of pro-inflmatory cytokines
  6. systemic inflamatory response
  7. end organ and systemic inflammatory associated damage
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13
Q

Pneumonia complications

A
  • Sepsis
  • Lung abscess
  • Resp failure
  • Kidney failure
  • Neurological effects
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14
Q

Pneumonia Severity parameters

A

S ystolic Blood pressure. (over 90)
M ultilobar CXR involvement
A lbumin over 3.5g/dl
R esp rate over 30 or over 25 if over 50 y/o
T achycardia over 125bpm

C onfusion
O oxygen saturation (2pts)
P h under 7.35

High risk pr needing IRVS = 5-6 points
7+ points = very high risk

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15
Q

Diagnosis of Pneumonia Tests

A
  • CBC High WBC
  • EUCA Impact on renal function
  • Viral Swab
  • Sputum MCS
  • CXR consolidatoon and parapneumonic effusion/empyema
  • Bronchoscopy
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16
Q

role of bronchoscopy in the investigation of pulmonary infection

A
  • Bronchoscopy describes the use of a flexible camera and attached suction device to ‘suck out’ mucous from the lungs.
  • The bronchoscope enters via the oral or nasal cavity and enters the lung through navigation via an attached camera.
  • Sputum MCS and viral PCR are the first line investigations, however, so most patients will not require bronchoscopy upon suspected pneumonia diagnosis.
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17
Q

Management of Pneumonia

A
  • Antibiotics
  • Symptomatic alleviation
  • Supportive management (Oxygen, IV fluids, analgesia)
  • Nutrition assessment
18
Q

Tuberculosis (TB) Pathogenisis

A
  1. M. Tuberculosis enters airway
  2. attempted phagocyotsis by alverolar macrophages
  3. migrates to lymp nodes activating T and B cells
  4. Enables macrophages to differentiate into epithloid cells
  5. Fusion of epithiloid cells to form a Granuloma
  6. M. tuberculosis migrates to lung parenchyma
  7. Granuloma encases bacteria, preventing its spread and proliferation
19
Q

M. Tuberculosis Features

A

Slow growth = hard to culture and treat
Waxy cell wall = protection and resistance to environmental stresses and host immune responses

20
Q

Clinical features of TB

A
  • Chronic Cough
  • Haemoptysis
  • Chest Pain (sharp/aching)
  • Dyspnoea
  • Loss of Appetite
  • Night sweats
  • Fatigue
  • Pallor, wasted appearance, clubbing
21
Q

Extrapulomonary features of TB

A
  • Haematuria Blood in the urine due to TB of the kidney/genitourinary system
  • Headache or confusion due to TB meningitis, a rare complication
  • Back pain Persistent back pain due to TB of the spine or musculoskeletal system
  • Voice hoarseness due to TB of the larynx or the upper airways
  • Abdominal discomfort distension, and bloating due to peritoneal TB
22
Q

TB Diagnosis

A
  • Sputum Microscopy
  • Sputum culture
  • Drug senstivity
  • CXR - fibro nodular changes
23
Q

TB Complications

A
  • Pleural effusion
  • Haematogenous TB
  • Cardiac TB
  • Ocular TB
  • Hepatic TB
  • Gastrointestinal TB
24
Q

Management of TB

A

Always Mutli drug therapy
**Intensive (bactericidal): **Isoniazid, rifampicin, pyrazinamide, ethambutol (treat for 2 months)
Continuation (sterilisation): Isoniazid, rifampicin (treat for 4 months)

25
Q

Directly Observed Therapy (DOT)

A
  • This enables compliance by having the practitioner observe any side effects or issues with the administration
    of the treatment; this can occur via video conference or in-person.
  • DOT is recommended for individuals with cultural barriers, mental or cognitive pathologies, or those who are
    at high risk of fatal consequences if not administered treatment correctly.
26
Q

Acute Vs Chronic chest infection

A

Acute chest infection is defined as infection that lasts <3 weeks in duration; anything longer is defined as a chronic chest infection.

27
Q

Clinical Features of Persistent Chest Infection

A
  • Productive Cough
  • malaise
  • Chest Pain
  • Fever
28
Q

Management of Persistent Chest Infection

A
  • Antibiotics
  • Airway clearance
  • Vaccination
  • Education
  • Smoking cessation
  • Emergceny pack use containig meds and instructions
29
Q

Bronchiectasis

A

Bronchiectasis is a chronic respiratory condition characterised by the abnormal widening and scarring of the airways in the lungs, leading to recurrent infections and mucus build-up.
* Pathologically, bronchiectasis is defined by the presence of permanent and abnormal dilation of the bronchi.
* This usually occurs in the context of chronic airway infection, causing airway inflammation.

30
Q

How does Bronchiectasis devolop

A
  1. Impaired drainage or obstruction meaning mucus can be cleared
  2. Mucus acculuation and bacterial growth
  3. chronic infection and inflamation
  4. tissuse damage
  5. transmural inflammation that goes through tthe full thickenss of the airway wall
31
Q

Clinical Features of Bronchiectasis

A
  • Productive Cough
  • Dyspnoea (worse on exertion)
  • Sleep disturbances
  • Changes in appetite
  • Systemic infection
  • Chest Pain
  • Inspiratory crackles
32
Q

Bronchiectasis Diagnosis

A

Sputum Culture
CXR
Lung function test (obstructive patterns)
CBE to look for infection, inflmation, or anaemia

33
Q

Cystic Fibrosis Epidemiology

A
  • avergae age of diagnoses = 20.2 years
  • most common life-limiting genetic disease in Australia.
  • mostly caucasians
  • 1/25 ppl carry gene
  • 1/2500 babies are born with CF
  • automsomal reccesssive
34
Q

CF Clasifications

A
35
Q

CF Resp Effect

A

CFTR mutations result in the production of thick and sticky mucus in the airways, making it difficult to clear mucus. This leads to chronic airway obstruction, recurrent lung
infections, and progressive lung damage.

36
Q

CF digestive effect

A

In the digestive system, CFTR mutations affect the pancreas, reducing its ability to release enzymes necessary for digestion. This leads to malabsorption of nutrients,
malnutrition, and gastrointestinal issues.

37
Q

CF glandular effect

A

The CFTR protein plays a role in regulating salt and water balance in sweat glands. Mutations in CFTR lead to salty-tasting skin due to elevated salt levels in sweat, which is
a diagnostic feature of cystic fibrosis.

38
Q

CF reproductive effect

A

CFTR mutations can cause infertility in both males and females due to issues with the production and transport of reproductive fluids.

39
Q

Other CF effects

A

CFTR mutations can also affect the liver, leading to complications such as liver disease. Other Additionally, they can impact other organ systems to varying degrees, resulting in a wide
range of symptoms and complications beyond the respiratory and digestive systems.

40
Q

Therapies for CF

A
  • Symptomatic therapy: Treatment aimed at managing and alleviating the symptoms and complications of cystic fibrosis to improve quality of life.
  • CFTR modulator drugs: Medications designed to correct the function of the defective CFTR protein in cystic fibrosis patients, addressing the underlying genetic cause of the disease.
  • Genetic therapies: Emerging treatment approaches that aim to correct or modify the genetic mutations responsible for cystic fibrosis to provide a potential cure or long-term disease management.
41
Q
A