7-intruduction to respiratory pathology and pneumonia Flashcards

1
Q

what is the major function of lungs?

A

• Major function of the lungs is to excrete carbon dioxide from blood and replenish oxygen

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2
Q

what are the conducting and respiratory zones of the respiratory system?

A
  • -conducting zone (anatomic dead space; i.e., the airways of the mouth, nose, pharynx, larynx, trachea, bronchi, bronchioles, and terminal bronchioles)
  • -respiratory zone (lung parenchyma; i.e., respiratory bronchioles, alveolar ducts, alveolar sacs).
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3
Q

what are the functions of the respiratory system?

A
  • -Ventilation (distribution of air in the airway)
  • -Respiration: gas exchange (absorption of O2 into the blood and release of CO2 into the air)
  • -Immune defense (ciliary clearance, alveolar macrophages, goblet cells)
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4
Q

what is the function of the conducting zone?

A
  • -Conduction of air in and out of the respiratory tree
  • -Anatomic dead space (no gas exchange)
  • -Warms and humidifies air
  • -Mucociliary clearance: ciliated epithelium transports mucus, bacteria, and dust towards the throat, where it is either swallowed or expelled through the mouth
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5
Q

lung parenchyma consists of…

A
  • -Respiratory bronchioles
  • -Alveolar ducts
  • -Alveolar sacs, which contain several pulmonary alveoli surrounded by capillaries
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6
Q

what is the function of lung parenchyma?

A
  • -Oxygen and carbon dioxide exchange across the blood-air barrier
  • -Alveolar macrophages phagocytose fine dust particles (< 2 μm)
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7
Q

what is pneumonia?

A
  • -Inflammatory consolidation of the lung parenchyma caused by the formation of intra-alveolar inflammatory exudate resulting from infection
  • -A respiratory infection characterized by inflammation of the alveolar space and/or the interstitial tissue of the lungs.
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8
Q

what are the pulmonary reflexes?

A
  • Cough reflex
  • Mucociliary apparatus
  • Alveolar macrophages
  • Mucus secretion
  • IgA antibodies
  • Microflora of upper respiratory tract
  • Nasal hairs
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9
Q

how breakdown of pulmonary defenses occurs?

A
1)Loss of cough reflex
Eg Coma; Anaesthesia
2)Injured mucociliary apparatus
Eg Smoking
3)A decrease in alveolar macrophages
Eg Alcohol, smoking
4)Pulmonary congestion/edema
5)Accumulation of secretions
6)Obstruction
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10
Q

what is the pulmonary edema?

A

the accumulation of fluid in the alveoli. The cause can be cardiogenic (e.g., cardiac failure with increased pulmonary capillary pressure) or noncardiogenic (e.g., ARDS, pulmonary embolism, transfusion-related acute lung injury, high altitude, preeclampsia, and opioid overdose). Causes reduced diffusion capacity, hypoxemia, and dyspnea.

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11
Q

what are the causes of secondary pneumonia?

A
  • -Bronchial asthma, COPD, heart failure, cystic fibrosis
  • -Viral upper respiratory tract infections with bacterial superinfection
  • -Anatomical abnormalities such as tubercular caverns, bronchial tumors, or stenosis (post-obstructive pneumonia)
  • -Aspiration (aspiration pneumonia)
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12
Q

CAP vs HAP?

A
  • -pneumonia that is acquired outside of a health care establishment
  • -nosocomial pneumonia, with onset > 48 hours after admission
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13
Q

typical vs atypical pneumonia

A

1) Pneumonia featuring classic symptoms typical findings on auscultation and percussion. Manifests as lobar pneumonia or bronchopneumonia
2) Pneumonia with less distinct classical symptoms and often unremarkable findings on auscultation and percussion. Manifests as interstitial pneumonia

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14
Q

what are the risk factors of pneumonia?

A
1)Personal risk factors
–	Elderly >65 years
–	Smokers
–	Malnourished
–	Immunocompromised
–	Recurrent RTI’s
–	Medications
2)Environmental risk factors
–	Seasonal; more common in Winter
3)Organism virulence
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15
Q

why immobility leads to increase risk of pneumonia?

A

Immobility leads to poor ventilation of the lungs, which increases the risk of bacterial colonization and infection.

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16
Q

what is the pathophysiology of pneumonia?

A
  • -Pulmonary protective mechanisms (cough reflex, mucociliary clearance , alveolar macrophages ) fail → microbial infiltration of the pulmonary parenchyma cannot be prevented
  • -Pathogen infiltrates pulmonary parenchyma → interstitial and alveolar inflammation → impaired alveolar ventilation → Ventilation/perfusion (V/Q) mismatch with intrapulmonary shunting (right to left) → hypoxia due to increased alveolar-arterial oxygen gradient (This effect is worsened if the affected lung is in the dependent position since perfusion is better to the dependent lung than the non-dependent lung)
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17
Q

why there is a right to the left shunt of blood in pneumonia?

A

Caused by continued blood flow to consolidated, poorly ventilated areas, resulting in the passage of blood from the right heart to the left heart without getting oxygenated (i.e. a right to left shunt).

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18
Q

what are the common organisms responsible for pneumonia?

A
1)Bacteria
–	Streptococcus pneumoniae (60% of CAP)
–	Haemophilus influenzae
–	Staphylococcus aureus
–	Mycoplasma pneumoniae (atypical)
–	Legionella pneumophilia (atypical)
2)Viral
–	Influenza pneumoniae
–	Respiratory syncytial virus
3)Fungal
–	Rare; immunocompromised
–	PCP
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19
Q

what are the common causes of typical pneumonia?

A

–Streptococcus pneumoniae (most common)
Most common also in nursing home patients
–Haemophilus influenzae

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20
Q

what are the common causes of atypical pneumonia?

A
  • -Mycoplasma pneumoniae (most common in the ambulatory setting)
  • -Chlamydophila pneumoniae
  • -Legionella pneumophila → legionellosis
  • -Coxiella burnetii
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21
Q

Mycoplasma and Chlamydophila pneumoniae are common in the elderly. True/False

A

False

Mycoplasma and Chlamydophila pneumoniae are common in children and adolescents.

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22
Q

what are the common causes of HAP?

A
  • -Gram-negative pathogens
    1) Pseudomonas aeruginosa
    2) Enterobacteriaceae
  • -Staphylococci (Staphylococcus aureus)
  • -Streptococcus pneumoniae
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23
Q

what is the HAP?

A

Pneumonia that occurs > 48 hours after admission to hospital and did not appear to be developing at that time. A subtype of HAP is ventilator-associated pneumonia that occurs 48–72 hours following endotracheal intubation.

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24
Q

influenza is often complicated by pneumonia caused by?

A

Staphylococcus aureus is often a serious complication of influenza pneumonia in both children and adults.

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25
Q

common causes of pneumonia in immunocompromised patients

A
  • -Encapsulated bacteria
  • -Pneumocystis jirovecii → Pneumocystis jirovecii pneumonia
  • -Aspergillus fumigatus → aspergillosis
  • -Candida species → candidiasis
  • -Cytomegalovirus
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26
Q

Pneumonia in newborn infants is commonly caused by what organisms?

A
  • -Escherichia coli
  • -Group B streptococcus (Streptococcus agalactiae)
  • -Streptococcus pneumoniae
  • -Haemophilus influenzae
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27
Q

what are the routes of infection in pneumonia?

A
  • -Most common: microaspiration (droplet infection) of airborne pathogens or oropharyngeal secretions
  • -Aspiration of gastric acid (Mendelson’s syndrome) , or of food or liquids
  • -Hematogenous dissemination in rare cases (Most likely in the context of staphylococcal infection at a different site, e.g., as a complication of endocarditis)
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28
Q

type 1 vs 2 pneumocytes?

A

1) Type I pneumocytes: thin squamous cells that line the alveoli
- -Comprise 95% of the total alveolar area
- -Connected to each other by tight junctions
- -Form the blood-air barrier, together with the endothelial cells of the capillaries and the basement membrane between the two cells.
2) Type II pneumocytes: cuboidal alveolar cells
- -Comprise 5% of the total alveolar area, but 60% of total number of cells
- -Contain lamellar bodies, which secrete surfactant (surface-activating lipoprotein complex)
- -Mainly composed of the phospholipids dipalmitoylphosphatidylcholine (DPPC or lecithin) and phosphatidylglycerol.
- -Reduces alveolar surface tension and thereby prevents the alveoli from collapsing.
- -Can also proliferate to replace Type I or Type II pneumocytes following lung damage

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29
Q

what are the steps of evolution of signs and symptoms of Pneumonia

A
  • Organisms in alveoli multiply
  • Immune cells attack
  • Influx of white blood cells, protein, fluid, red cells
  • Release of cytokines
  • Release of vasodilators increase vascular permeability causing congestion
  • Alveoli filled with fluid = CONSOLIDATION
  • Hampers O2 flow –>Shortness of breath
  • Bronchoconstriction and increase in mucus secretion stimulates Cough reflex
  • Pain receptor on alveoli –>Chest pain
  • Cytokine release ->Pyrexia
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30
Q

what are the classic lobar pneumonia progression in stages?

A
  • -Congestion (day 1): serous exudate in blood-rich lungs, numerous bacteria evident
  • -Red hepatization (days 2–3): exudate rich in fibrin and inflammatory cells with many bacteria still visible; lungs take on a liver-like texture. Lung loses some spongy quality
  • -Gray hepatization (days 4–7): erythrocytes are degraded but inflammatory cells persist; most bacteria have been destroyed by this stage. The lung is now firm
  • -Resolution (day 8 to week 4): fibrinolysis by enzymatic means and removal of the purulent exudate via productive cough
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31
Q

what is the lobar penumonia?

A

An infection localized to one pulmonary lobe, most commonly caused by Streptococcus pneumoniae, Haemophilus influenzae, gram-negative bacilli, and Staphylococcus aureus.
Affects sections of a lobe
Starts distally and spreads to involve an entire lobe

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32
Q

what are the signs and symptoms of lobar pneumonia?

A
  • -Decrease in chest expansion
  • -Shortness of breath (SOB)
  • -Cough
  • -Chest pain
  • -Pyrexia
  • -Dull to percussion
  • -Tactile fremitus
  • -Bronchial breathing, crackles
  • -Vocal resonance
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33
Q

in red hepatization stage pneumococci are dead. True/False

A

False
• Red Hepatization (2-3 days)
- Exudate of RBCs, neutrophils, and fibrin
- Pneumococci alive
- Lobes are distinctly red, firm and airless, with liver-like consistency
• GrayHepatization (4-6 days)
- Grey, firm lobe with exudate of neutrophils and fibrin
- RBCs disintegrate
- Dying pneumococci

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34
Q

what cells play a major role in regeneration?

A
  • Type II pneumocytes key for regeneration
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35
Q

can scarring occur in pneumonia?

A

Yes, organization

Scarring due to organization of exudate, infiltration of fibroblasts and deposition of collagen

36
Q

what is the bronchopneumonia?

A

mostly descending infection that affects the bronchioles and adjacent alveoli; usually involves the lower lobes or right middle lobe; manifests as typical pneumonia
Primarily caused by pneumococci and/or other streptococci
Necrotizing bronchopneumonia (and pneumatocele) are caused by Staphylococcus aureus and are often preceded by an influenza infection.
• Starts proximally in the BRONCHIOLES
• Patchy infiltrate, often throughout both lungs
• Generally affects the extremes of age: elderly and very young
• Elderly: risk factors include COPD, stroke, immunocompromised
• Young: immature immune system
• Patchy consolidation

37
Q

lobar pneumonia starts proximally or distally?

A

ascends

Starts distally and spreads to involve entire lobe

38
Q

bronchopneumonia starts proximally or distally

A

Starts proximally in the BRONCHIOLES

39
Q

what age groups are at risk for bronchopneumonia?

A

Generally affects the extremes of age: elderly and very young

  • -Elderly: risk factors include COPD, stroke, immunocompromised
  • -Young: immature immune system
40
Q

what are the signs and symptoms of bronchopneumonia?

A

productive cough, pyrexia, chest pain, dyspnoea, crackles on auscultation

41
Q

dullness on percussion indicates?

A

Indicates consolidation in cases of localized pneumonia

42
Q

what is the bronchophony?

A

An abnormal increase in the clarity and pitch of the spoken voice heard over the lung. Bronchophony can indicate the solidification of lung tissue.

43
Q

what is the egophony?

A

A physical examination finding elicited by asking the patient to say “E” while auscultating the lung fields. Characterized by changes on auscultation of an “E” sound to an “A” sound. Suggests the presence of pulmonary consolidation (e.g., from lobar pneumonia).

44
Q

what is the vocile fremitus?

A

A part of the pulmonary examination used to evaluate the conduction of vibrations to the chest wall produced during speech. Palpate the posterior chest wall with the ulnar aspects of both hands while the patient says a phrase such as “toy boat”. Fremitus becomes more pronounced in the presence of consolidation and less pronounced in the presence of effusion or pneumothorax. The examiner can also assess fremitus with a stethoscope on the chest wall (vocal fremitus).

45
Q

what are the complications of bronchopneumonia?

A

Complications include microabscess formation

46
Q

what is atypical pneumonia?

A

Atypical pneumonia is commonly seen in elderly patients and typically takes an indolent course (slow onset) with a non-productive, dry cough. Extrapulmonary symptoms such as fatigue and headache are especially prominent. The most common organisms are Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella pneumophila.
• “Walking pneumonia”
• Interstitial pneumonia
• CXR: Reticulonodular pattern; linear thread like opacities in the lung
• Infiltrate is outside / around the alveoli i.eNO CONSOLIDATION
• Patchy interstitial lymphocytic inflammatory infiltrate
• Symptoms tend to be milder and gradual onset; “flu-like” symptoms
• Cough is non-productive / Dry
• Low-grade pyrexia
• Breath sound: rales
• WCC: normal or only slightly raised
• Other extrapulmonary symptoms: sore throat, myalgia, fatigue, diarrhea

47
Q

CXR pattern in atypical pneumonia?

A

Interstitial pneumonia

CXR: Reticulonodular pattern; linear thread like opacities in the lung

48
Q

in atypical pneumonia, the infiltrate is inside the alveoli. True/False

A

False

Infiltrate is outside / around the alveoli i.eNO CONSOLIDATION

49
Q

the infiltrate in atypical pneumonia is lymphocytic or neutrophilic?

A

Patchy interstitial lymphocytic inflammatory infiltrate

50
Q

what are the common causes of atypical pneumonia?

A

Common pathogens include mycoplasma, legionella, chlamydiae, and viruses such as RSV, influenza, CMV, and adenovirus.

51
Q

what are the features of pneumonia caused by mycoplasma?

A

1) Epidemiology
- -One of the most common causes of atypical pneumonia
- -More common in young individuals
- -Outbreaks may occur in schools, colleges, prisons, and military facilities
2) Clinical features
- atypical pneumonia
- -Generalized papular rash, erythema multiforme
3) Diagnostics
- -Subclinical hemolytic anemia: associated with elevated cold agglutinin titers (IgM)
- -Interstitial pneumonia, often with reticulonodular pattern on CXR
4) Treatment: macrolides, doxycycline, and fluoroquinolones

52
Q

how mycoplasma pneumonia is treated?

A

macrolides, doxycycline, and fluoroquinolones

53
Q

what extra-pulmonary manifestations are characteristic of mycoplasma pneumonia?

A
  • -GBS
  • -encephalitis
  • -bullous myringitis
  • -erythema multiforme
  • -Subclinical hemolytic anemia: associated with elevated cold agglutinin titers (IgM)
54
Q

what is the bullous myringitis?

A

Bullous myringitis is a type of ear infection in which small, fluid-filled blisters form on the eardrum.

55
Q

what is the erythema multiforme?

A

n acute, self-limited, type IV hypersensitivity reaction associated with certain infections (e.g., Mycoplasma pneumoniae, herpes simplex virus, histoplasmosis) and medications. Manifests with lesions that range in severity from localized target lesions without mucosal involvement to extensive mucosal compromise that is potentially life-threatening.

56
Q

what is the GBS?

A

An immune-mediated polyneuropathy that presents with ascending flaccid paralysis that occurs approximately one to two weeks after certain gastrointestinal infections (especially Campylobacter jejuni, H. pylori) or respiratory tract infections (especially Mycoplasma pneumoniae).

57
Q

what is the staccato cough?

A

Patients with mild to moderate illness with chlamydia pneumonia may present with a “staccato cough” (inspiration between each single cough)

58
Q

what is the Legionnaire’s disease?

A

severe form of legionellosis that presents with atypical pneumonia, diarrhea, and neurological manifestations (e.g., confusion, agitation). Bradycardia and hyponatremia are also commonly seen.

59
Q

how legionellosis is contacted?

A

Inhalation of contaminated aerosols

  • -Cold and hot water systems: e.g., those found in hotels, hospitals, and retirement homes
  • -Whirlpools/hot tubs, swimming pools, showers
  • -Air-conditioning systems with contaminated condensed wate
60
Q

howl legionellosis is diagnosed?

A

1) Blood
- -Hyponatremia (serum sodium < 130 mEq/L) and hypophosphatemia are common.
- -Aminotransferases and creatinine may be elevated.
- -Possible thrombocytopenia and leukocytosis
2) Urine
- -Legionella urinary antigen test: the most important diagnostic tool
- -Rapid test, but only detects serogroup 1
- -Hematuria and proteinuria are common
3) Respiratory secretions
- -Gram stain of respiratory secretions shows many neutrophils; usually no organisms identified
- -Requires silver stain
4) Legionella culture: slow; requires buffered (iron and cysteine) charcoal yeast extract agar
- -Results after 3–5 days
5) PCR: high sensitivity, high specificity
6) Serology: A four-fold rise in antibody titer confirms legionellosis. However, the antibody titers have low specificity and sensitivity, and seroconversion can take up to 12 weeks. Therefore, more rapid tests like the urinary antigen test or PCR are used more often.

61
Q

CXR pattern in legionellosis?

A

usually abnormal, diffuse, interstitial infiltrates or unilateral lobar pneumonia!!!!!!!!!!!!!!

62
Q

what is the Pontiac fever?

A

A mild, self-limited disease caused by Legionella infection. Symptoms are difficult to distinguish from the flu and include fever, headache, and muscle aches. Pneumonia is absent.

63
Q

how legionellosis is treated?

A
  • -Legionnaires’ disease should be treated early with antibiotics, especially because of its high mortality rate of 10%.
  • -If legionellosis is verified
  • -Drug of choice: fluoroquinolones (preferably levofloxacin, alternatively moxifloxacin) for 7–10 days
  • -Initial parenteral treatment is recommended for all patients to avoid possibly poor gastrointestinal absorption
  • -Second-line treatment: macrolides (e.g., erythromycin or azithromycin) for 3 weeks
  • -If patients are unresponsive to monotherapy, consider addition of rifampin or tigecycline
64
Q

what is the aspiration pneumonia?

A

Aspiration is the inhalation of foreign material into the respiratory tract. It often occurs after instrumentation of the upper airways or esophagus (e.g., upper GI endoscopy), or secondary to vomiting and regurgitation of gastric content.

  • -Mendelson syndrome: aspiration of gastric acid initially causing tracheobronchitis with rapid progression to chemical pneumonitis
  • -May cause ARDS in extreme cases
65
Q

what are the risk factors of aspiration pneumonia?

A

Predispose to reduced epiglottic gag reflex and dysphagia
o Impaired cough reflex (eg Stroke, neurologic disorder, C2H5OH xs, drug overdose)
o Unconscious
o Pyloric stenosis
o esophageal obstruction
o Hiatus hernia
• Aspirate nonsterile contents eg food, drink, gastric contents (including gastric acid)
• Pneumonia – generally will cause a widespread bronchopneumonia
• Can cause chemical pneumonitis -> further weaken the immune system

66
Q

what neurologic disorders are associated with aspiration pneumonia?

A

Parkinson disease, Alzheimer disease, bulbar involvement in multiple sclerosis, or Guillain-Barré syndrome

67
Q

what pathogens are commonly involved in aspiration pneumonia?

A

mixed infections with anaerobic organisms are common (e.g., Klebsiella)

68
Q

what are the clinical features of aspiration pneumonia?

A

Immediate symptoms: bronchospasms , crackles on auscultation, hypoxemia with cyanosis
Late symptoms: fever, shortness of breath, cough with foul-smelling sputum

69
Q

what parts of the lung are commonly involved in aspiration pneumonia?

A
  • -Radiologic imaging: The lung region in which the infiltrates are seen depends on the patient’s position on aspiration. :
  • -Supine position: the superior segment of the right lower lobe (most common site of aspiration)
  • -Standing/sitting: the posterior basal segment of the right lower lobe
  • -Right lateral decubitus position: posterior segment of the right upper lobe or right middle lobe
70
Q

what are the common pathogens of pneumonia in immunocompromised patients?

A
  • Post organ transplant
  • Chemotherapy
  • AIDS Organisms:
    – Pneumocystis (PCP)
    – Cytomegalovirus (CMV)
    – Unusual mycobacteria
    – Toxoplasma
71
Q

what is the CURB 65 criteria?

A

–Criteria for hospitalization
–Based on CURB-65 score
1)Confusion (disorientation, impaired consciousness)
2)Urea > 7 mmol/L (20 mg/dL)
3)Respiratory rate ≥ 30/min
4)Blood pressure: systolic BP ≤ 90 mm Hg or diastolic BP ≤ 60 mm Hg
5)Age ≥ 65 years
CURB-65 score ≤ 1: The patient may be treated as an outpatient.
CURB-65 score ≥ 2: Hospitalization is indicated.
CURB-65 score ≥ 3: ICU-care should be considered.

72
Q

what is the indication of CT in pneumonia?

A
  • -Indications: inconclusive chest x-ray, recurrent pneumonia
  • -Advantages: more reliable evaluation of circumscribed opacities, pleural emphysema, or sites of colliquation
73
Q

what are the complications of pneumonia?

A
  • Parapneumonic effusion +/_ empyema
  • Abscess
  • Acute confusional state / delirium
  • Septicaemia -> septic shock / multiorgan failure -> death
  • Adult Respiratory Distress Syndrome (ARDS) / Acute lung injury (ALI)
  • Respiratory failure
  • Spread of organisms to other sites eg bacterial endocarditis, otitis, meningitis, arthritis
74
Q

what is the parapneumonic effusion?

A

The presence of fluid in the pleural cavity. Classified as transudative (e.g., due to congestive heart failure, liver cirrhosis) or exudative (e.g., pneumonia, malignancies, pulmonary embolism), depending on the underlying cause. Typically manifests with dyspnea and a dry cough

75
Q

what is the ARDS?

A

A severe inflammatory reaction characterized by noncardiogenic pulmonary edema and injury to alveolar capillaries and endothelial cells. Etiologies include systemic inflammatory response syndrome, trauma, inhalation injury, aspiration pneumonitis, pulmonary infarction, and transfusion-related acute injury.

  • -Initially, hypoxemic respiratory failure with ↓ PaO2 and respiratory alkalosis → PaO2/FiO2 ≤ 300 mm Hg
  • -Hypercapnic respiratory failure develops with disease progression.
  • -Diffuse bilateral infiltrates (perihilar bat wing or butterfly distribution of infiltrates)
76
Q

what is the empyema?

A

• Collection of pus within the pleural cavity
• Complication of pneumonia
• Investigations:
– CXR
– aspirate pleural fluid for cytology and microbiology
Pleural fluid: exudate containing abundant neutrophils.
• Treatment:
– Antibiotics, +/- chest drain +/- surgical decortication if complex

77
Q

how empyema is treated?

A

Antibiotics, +/- chest drain +/- surgical decortication if complex

78
Q

what is lung abscess?

A
  • A localized area of suppurative necrosis within the pulmonary parenchyma, leading to the formation of one or more cavities
  • “necrotizing pneumonia”
  • Anaerobic bacteria are present in almost all lung abscesses
  • Tx: Antibiotic =? surgical drainage if necessary
79
Q

what type of bacteria are commonly present in lung abscess?

A

Anaerobic bacteria are present in almost all lung abscesses

80
Q

what are the causes of lung abscess?

A
–	Aspiration of infected material
–	Aspiration of gastric contents
–	Complication of bacterial pneumonia
–	Bronchial obstruction eg neoplasm
–	Septic embolus
–	Haematogenous spread of bacteria
81
Q

at what lung site commonly abscess develops?

A

Site depends on mode of development i.e aspiration more common on right side (more vertical airways), in posterior segment of upper lobe

82
Q

what are the common pathogens in lung abscess?

A
  • -Most commonly: mixed infections caused by anaerobic bacteria that colonize the oral cavity (e.g., Peptostreptococcus, Prevotella, Bacteroides, Fusobacterium spp.)
  • -Less commonly: monomicrobial lung abscess caused by S. aureus, Klebsiella pneumoniae, Streptococcus pyogenes, Streptococcus anginosus
83
Q

what is the characteristic radiologic finding in lung abscess

A

rregular rounded cavity with an air-fluid level in lung region on aspiration that is dependent on body position.
As the focus of suppuration enlarges, ruptures into airways and may partially drain giving an “air-fluid” level on CXR

84
Q

what are the signs and symptoms of lung abscess?

A

–Fever
–Cough with the production of foul-smelling sputum
–Anorexia, weight loss
–Night sweats
–Hemoptysis
Manifestations include cough, copious amounts of foul-smelling sputum
– Spiking fevers, malaise
– Clubbing, weight loss, anemia
– Secondary amyloidosis in chronic cases
– 10% mortality rate

85
Q

how lung abscess is treated?

A

Antibiotic treatment that covers anaerobes (e.g., ampicillin-sulbactam, carbapenems, or clindamycin )
If medical therapy fails, percutaneous catheter drainage or surgical resection may be considered.

86
Q

what are the complications of lung abscess?

A

– May rupture into pleural space -> bronchopleural fistula or pneumothorax or empyema
– May embolize septic material to brain -> meningitis or brain abscess