L13 Pneumonia and Bronchiectasis Flashcards

1
Q

Classification of Pneumonia?

A

Pneumonia is an inflammatory process of the lung c aused by an infectious agent: (bacterial, viral or fungal)

(1) Clinical circumstances

  • Community acquired (typical/atypical)
  • Hospital acquired (nosocomial)
  • Opportunistic

(2) Etiological agent

  • Bacterial
  • Viral
  • Fungal
  • Other

(3) Anatomical pattern

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2
Q

Bronchopneumonia

Characteristics?

Demographics?

Micro-characteristics?

A

Bronchopneumonia

  • Patchy consolidated areas of acute suppurative (pus) inflammation
  • Centered on bronchioles and bronchi - Often multilobar and bilateral
  • Infancy and old age
  • Arises from chronic debilitating illness
  • Neutrophil-rich exudate, fills the bronchi, bronchioles and alveola
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3
Q

Lobar Pneumonia

Characteristics

Demographics

Cause?

Stages?

A

Lobar Pneumonia

Affects a large part of lobe or entire lobe

Typically affects otherwise healthy adults

Rarer now w/ antibiotics

Strep. Pneumoniae (90%)

Stages:

1. Congestion

2. Red Hepatization

3. Gray Hepatization

4. Resolution

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4
Q

Stages of Lobar Pneumonia?

A

1. Congestion

  • Vascular engorgement
  • Intra-alveolar proteinaceous fluid
    • numerous bacteria in alveoli
  • Lung heavy, boggy, red

2. Red Hepatization

  • Massive congestion of lung parenchyma
  • Neutrophils and fibrin fill alveolar spaces
  • Lung appears red, firm, airless, liver-like

3. Gray Hepatization

  • Disintegration of RBCs
  • Fibrosuppurative exudate
  • Gray/brown, dry surface

4. Resolution

  • Occurs at 8-10 days
  • Enzymatic digestion of consolidated exudate
    • Produces semisolid debris
      • Resorbed
      • Ingested by macrophages
      • Coughed up
  • Pleural fibrinous reaction may similarly resolve or undergo organization leaving permanent fibrous adhesions
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5
Q

Host Pneumonia Defence Mechanisms?

A
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6
Q

When does pneumonia infection occur?

A

Infection results when:

  1. Defect in host immunity (intrinsic factor)
  2. Particularly virulent organism (extrinsic)
  • Evasion of muco-ciliary clearance
  • Evasion of macrophage-induced killing
  1. Overwhelming inoculum of infecting organism (extrinsic)
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7
Q

Predisposing Host Factors for Pneumonia (7)

A

Loss of cough reflex

– Neuromuscular disorders

– Cerebrovascular accident

– Coma

• Damage to muco-ciliary apparatus

– Smoking

– Kartagener syndrome

– I_mmotile cilia syndrome_

Accumulation of secretions

– COPD

– Bronchiectasis (CF)

• Pulmonary congestion and oedema

• Decreased alveolar macrophage function

– Alcohol

– Smoking

• Drugs

– Immunosuppressants

– H2 antagonists

• Bronchial obstruction

– Bronchogenic carcinoma

– Foreign body

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8
Q

__________: Chronic necrotizing infection of the bronchi and bronchioles

=> associated with ___________________ of these airways

A

Bronchiectasis: Chronic necrotizing infection of the bronchi and bronchioles

=> associated with abnormal, irreversible dilation of these airways

Weakening/dilatation of lumen of airway => once dilated, does not return to normal

Airways are dilated, up to 4x normal diameter and filled with pus

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9
Q

Bronchietasis is a secondary diesase due to?

A

It is a secondary disease, due to

(1) Obstruction
(2) Persistent severe infection

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10
Q

What part of the lung is usually affected by bronchiectasis?

A

Typically affects Lower Lobes Bilaterally

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11
Q

Pathophysiology of Bronchiectasis (5 Steps)

A

2 main requirements:

– Impaired drainage, airway obstruction or defect in host defense

– Infectious insult

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12
Q

Clinical Features of Bronchiectasis

A

Clinical Features:

Symptoms:

  • Severe persistent cough
  • Production of large volumes of mucopurulent sputum

Signs:

  • Crepitations
  • Wheeze
  • Clubbing of the fingers
  • Cor pulmonale (right ventricular failure)
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13
Q

Investigations of Bronchiectasis?

A

Investigations

Blood tests (Not diagnostic) – Raised WCC and CRP if infective exacerbation

Radiology– CXR/CT thorax

Microbiology– Sputum C+S (Pseudomonas sp)

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14
Q

What causes cystic fibrosis?

A

Multi-system disease caused by a(recessive) genetic mutation in the gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein on Chr. 7q31

=>Thick, viscous secretions in lungs, pancreas, liver, intestine, reproductive tract

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15
Q

Presentation of cystic fibrosis in Adults vs. Children?

A

Presentation in infancy:

–Common mutations in CFTR gene

–Meconium ileus (blockage of the small intestine)

Respiratory symptoms

–Failure to thrive

Presentation in adulthood

–Rare mutations in CFTR gene

Gastrointestinal symptoms

Diabetes mellitus

infertility

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16
Q

Main cause of mortality from cystic fibrosis?

A

Respiratory Disease main cause of mortality (Bronchiectasis, Chronic Bronchitis)

17
Q

Primary causative organisms of Cystic Fibrosis

A

Infection w/

Pseudomonas aeruginosa

Burkholderia cepacia complex

18
Q

Screening for Cystic Fibrosis?

A

Screening

Newborn Heel prick test

DNA analysis

Sweat Chloride Test

Nasal potential differences– Abnormalities in epithelial chloride secretion

19
Q

Treatment of Cystic Fibrosis (Respiratory/GI)

A

Respiratory:

– Antibiotics

– Physiotherapy

– Bronchodilators

– Oxygen

– CFTR potentiators/correctors

Ataluren

permits selective ribosomal read-through of the premature termination codon

=> allows production of full length transcript and CFTR protein.

Lumacaftor

Interacts w/ the CFTR to facilitate its correct folding

=> allow proper trafficking of CFTR to the cell surface.

Ivacaftor

stabilizes the open state of the CFTR => increases channel opening time

– Transplantation

Gastrointestinal:

– Pancreatic enzyme replacement therapy (PERT)

– Fat-soluble vitamin supplementation

20
Q

_______________: permits selective ribosomal read-through of the premature termination codon

=> allows production of full length transcript and CFTR protein.

A

Ataluren: permits selective ribosomal read-through of the premature termination codon

=> allows production of full length transcript and CFTR protein.

21
Q

_______________: Interacts w/ the CFTR to facilitate its correct folding

=> allow proper trafficking of CFTR to the cell surface.

A

Lumacaftor: Interacts w/ the CFTR to facilitate its correct folding

=> allow proper trafficking of CFTR to the cell surface.

22
Q

______________: stabilizes the open state of the CFTR

=> increases channel opening time

A

Ivacaftor: stabilizes the open state of the CFTR => increases channel opening time