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Year 2 > Resp: Whooping Cough, Pneumonia, TB > Flashcards

Resp: Whooping Cough, Pneumonia, TB Flashcards

1
Q

What is whooping cough caused by

A

Bordatella pertussis

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2
Q

Appearance of bordatella pertussis

A

GRAM-NEGATIVE, ENCAPSULATED COCCOBACILLUS

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3
Q

Name three species that cause whooping cough

A
  1. Bordatella pertussis
  2. Bordatella parapertussis
  3. Bordatella Bronchiseptica
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4
Q

How does whooping cough spread

A

Droplet infection

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5
Q

What virulence factors aid infection by bordatella pertussis

A
  1. Filamentous ham agglutinin and fimbriae aid adherence
  2. Adenylate cyclase toxins inhibit phagocytic chemotaxis and T cell activation
  3. Pertussis toxin is an A/B toxin
  4. Tracheal cytotoxin and dermonecrotic toxin
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6
Q

Role of pertussis toxin

A

Inhibits alveolar macrophage host defence (ADP ribosylates G proteins)

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7
Q

Role of tracheal cytotoxins

A

Epithelial necrosis

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8
Q

What causes chronic inflammation in whooping cough

A
  1. Lymphoid hyperplasia

2. Th17 skewing of mine response

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9
Q

Clinical presentation of whooping cough

A
  1. UNDER 5 with chronic cough
  2. Vomit follows cough
  3. Fever or weight loss
  4. Febrile but vital signs stable
  5. Sub-conjunctival haemorrhage
  6. Lungs clear when auscultation
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10
Q

How long is the incubation period of whooping cough

A

7-10 days

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11
Q

What is the catarrhal phase of whooping cough

A
  1. Patient highly infectious
  2. Cultures from respiratory cultures ar positive
  3. Malaise
  4. Anorexia
  5. Rhinorhoea
  6. Conjunctivitis
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12
Q

What is the paroxysmal phase of whooping cough

A
  1. Begins a week after catarrhal phase
  2. Coughing spasms
  3. Classic inspiratory whoop in younger individuals
  4. Coughing spasms that end in vomiting
  5. Cough for 14 days
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13
Q

What is the paroxysmal phase of whooping cough associated with

A
  1. Pneumonia
  2. Encephalopathy
  3. Sub-conjunctival haemorrhage
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14
Q

What causes the inspiratory whoop

A
  1. Resp tract is compromised by mucus secretion and oedema
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15
Q

How is whooping cough diagnosed

A
  1. Chronic cough + history of contact
  2. PCR tests
  3. Culture of nasopharyngeal swab!!
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16
Q

How is whooping cough treated

A
  1. Antimicrobials (Clarithromycin)
  2. Antibiotics can’t be used in paroxysmal stage
  3. Vaccination (dTap vaccine) at 2,3,4 months and 3-4 years
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17
Q

What is the dTap vaccine

A
  1. Diphtheria
  2. Tetanus
  3. Acellular pertussis
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18
Q

What causes acute laryngotracheobronchitis

A
  1. Parainfluenza virus
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19
Q

What age is affected by acute laryngotracheobronchitis

A

Children under the age of 3

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20
Q

Pathophysiology of acute laryngotracheobronchitis

A
  1. Inflammatory oedema extend sto vocal cords and epiglottis causing narrowing of the airway
  2. Progressive airway obstruction occurs with recession of soft tissue in neck and abdo during inspiration
  3. CYANOSIS
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21
Q

Clinical presentation of acute laryngotracheobronchitis

A
  1. 3 year old
  2. Barking cough
  3. Febrile
  4. Rep rate of 40
  5. Cyanosis
  6. Intercostal recession
  7. Inspiratory stridor
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22
Q

Diagnosis of acute laryngotracheobronchitis

A
  1. Voice is horse with barking cough

2. Audible stridor

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23
Q

How is acute laryngotracheobronchitis treated

A
  1. Nebulised adrenaline

2. Dexamethasone (IM or oral)

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24
Q

Define pneumonia

A
  1. Inflammation of lung substances
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25
Q

What part of the lungs are effected

A

Dial airways and alveoli

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26
Q

What is community acquired pneumonia

A
  1. No underlying immunosuppression or malignancy
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27
Q

What causes community acquired pneumonia

A
  1. Strep pneumoniae
  2. Haemophilus pneumonia
  3. Mycoplasma pneumoniae
  4. Staphylococcu aureus
  5. E.coli
  6. Klebsiella pneumoniae
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28
Q

What is lobar pneumonia

A

When the infection is localised to one whole lobe

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29
Q

What is diffuse pneumonia

A

Multiple lobules and respirartoy bronchioles are affected (bronchopneumonia)

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30
Q

Define hospital-acquired pneumonia

A
  1. New onset of cough with prurulent sputum
  2. X-ray showing consolidation
  3. Patinets staying in beyond 48 hours after admission
  4. Patients in healthcare setting for more than 3 months
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31
Q

What people are effected by hospital-acquired pneumonia

A
  1. Elderly
  2. Ventilator-associated
  3. Post operative
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32
Q

What causative organisms are in HAP

A 
1. AEROBIC GRAM-NEGATIVE bacilli:
Pseudomonas aerguinosa
E.coli
Klebsiella Pneumoniae 
Staph Aureus sue to MRSA
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33
Q

What patients are susceptible to S.aureus infections in hospital (pneumonia)

A
  1. Diabetes Mellitus

2. Head trauma

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34
Q

What is the most common organism causing pneumonia in immunocompromised patients

A

Pneumocystis jiroveci

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35
Q

What is aspiration pneumonia

A
  1. Acute aspiration of gastric contents into the lung which cause intense destruction
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36
Q

Where is aspiration pneumoniae seen

A
  1. Stroke
  2. MG
  3. Bulbar palsies
  4. Lack of consciousness
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37
Q

What is Mendelson syndrome

A

Pneumonia caused by aspiration of anaesthesia

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38
Q

Risk factors of pneumonia

A
  1. Under 16
  2. Over 65
  3. Co-morbidities (HIV, diabetes, CF, COPD)
  4. Smoking
  5. Excess alcohol
  6. IV drug use
  7. Prolonged corticosteroids
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39
Q

How is pneumonia spread

A
  1. Respiratory droplets
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40
Q

Why does pneumococcal pneumonia not respond to penicillin

A

Lack a cell wall

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41
Q

Pathophysiology of pneumonia

A
  1. Bacteria translocate to normally sterile distal airway
  2. Host defence overwhelmed, alveolar macrophages instruct th17 cells to stimulate neutrophilsto secrete pus (inflammatory exudates) into alveolar space
  3. Inflammatory cells are apoptosed (when disease resolves)
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42
Q

What causes pneumonia to become severe

A
  1. Excessive inflammation
  2. Lung injury
  3. Failure to resolve without lung damage
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43
Q

Clinical presentation of pneumonia

A
  1. Fever
  2. Night sweats
  3. Raised resp rate
  4. Productive cough
  5. Absence of upper resp tract symptoms
  6. RIgors
  7. Low BP
  8. Malaise
  9. Anorexia
  10. Dyspnoea
  11. Breathlessness
  12. Coarse crackles on auscultation (consolidation of lung parenchyma)
  13. Dull to percussion
  14. Decreased air entry
  15. Bronchial breath sounds
  16. Dry or productive cough
  17. Prurient sputum (rusty suptum CHARACTERISTIC of strep pneumonia)
  18. Pleuritic chest pain
  19. Cyanosis
  20. Confusion
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44
Q

Differential diagnosis of pneumonia

A
  1. TB or lung cancer
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45
Q

Diagnostic of pneumonia

A
  1. CXR
  2. FBC
  3. U+ E, LFTs
  4. Pulse oximetry / ABG
  5. HIV test
  6. Sputum culture and antibiotic sensitivities with gram stain
  7. Blood culture
  8. Serology
  9. CURB-65 test to assess severity of CAP
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46
Q

Role of FBC in pneumonia

A
  1. Elevated in strep pneumoniae (WCC)

2. ESR and CRP

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47
Q

What is CURB-65

A
  1. Confusion
  2. Urea (greater than 7 mol/L)
  3. Respiratory rate (greater than 30)
  4. BP less than 90 mmHg or 60mmHg diastolic
  5. Age greater than 65
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48
Q

What is a CURB score of 0-1

A

Mild

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49
Q

CURB score of 2

A

Moderate, admit to hospital

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50
Q

CURB score of 3-5

A

Admite, severe and monitor closely

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51
Q

CURB score of 4-5

A

Admission to critical care until

52
Q

How is pneumonia treated

A
  1. Maintain O2 stats between 94-98% - not in COPD though
  2. First dose antibiotics within 4 hours of presentation
  3. Analgesia for pleuritic pain
  4. Amocixillin (4-7 days)
  5. IV co-amoxiclav
53
Q

How is legionella pneumonia treated

A

FLUOROQUINOLONE

54
Q

How is necrotising pneumonia treated

A
  1. IV CLINDAMYCIN
  2. IV LINEZOLID
  3. IV RIFAMPICIN
55
Q

How is pseudomonas aerguinosa pneumonia treated

A
  1. IV ceftazidime with grantamycin
56
Q

How is pneumonia prevented

A
  1. Polysaccharide pneumococcal vaccine
    2> influenza vaccine
  2. Smoking cessation
57
Q

How many subtypes doe the vaccine protect against

58
Q

Complications of pneumonia

A
  1. Respiratory failure 2. Hypotension (dehydration and vasodilation in sepsis)
  2. Parapneumonic effusion and empyema
  3. Pleural effusions
59
Q

How can we tell if empyema has developed from pneumonia

A
  1. Ongoing fever
  2. Failure of WBCa nd CRP to settle on antibiotics
  3. Pain on deep inspiration
  4. Signs of pleural collection (dull percussion and reduced air entry)
60
Q

How do we diagnose pneumonia caused empyema

A
  1. THORACOCENTESIS

2. CXR for pleural effusion

61
Q

What is thoracocentesis

A

Removing fluid from pleural space

62
Q

Appearance of pleural fluid in empyema

A
  1. pH less than 7.2
  2. Fluid is yellow and turbid
  3. Low glucose
63
Q

How is empyema treated

A
  1. Chest drain
  2. CO-amoxiclav
  3. Piperacillin - Tazobactam
  4. Meropenam (anaerobic coverage)
64
Q

What is a lung abscess

A

CAUSED BY PNEUMONIA

Severe localised suppuration within the lungs (cavity seen on CXR)

65
Q

What causes lung abscesses

A
  1. Aspiration (alcoholics, oesophageal obstruction)
  2. Inadequately treated CAP
  3. TB
  4. Foreign body inhalation
  5. Septic emboli (staph)
66
Q

What organisms cause pneumonia lung abscess

A
  1. Strep millers (viridian’s streptococci)
  2. Klebsiella pneumoniae
  3. GRAM NEGATIVE bacteria
67
Q

How is lung abscess treated

A

Antibiotics up to 6 weeks

Surgical Drainage

68
Q

How do most people with HIV die

69
Q

What causes TB

A
  1. Mycobacterium tuberculosis
  2. Mycobacterium bovis (milk is unpasteurised)
  3. Mycobacterium africanum
  4. Mycobacterium microti
70
Q

Characteristics of TB bacteria

A
  1. ACID fast bacilli that need ziehl-neelsen stain
  2. Aerobic
  3. Non motile
  4. non sporing
  5. Thick waxy capsule
  6. Curved bacilli
  7. slow growing
  8. Resistent to phagocytosis - forms granulomata
71
Q

Risk factors of TB

A
  1. HIV
  2. Diabetes mellitus
  3. IVDU
  4. Ageing
  5. Malnutrition
  6. Homeless
  7. Prisons
  8. Smoking
  9. Alcohol
72
Q

How is TB spread

A

Respiratory droplets

73
Q

Do all infected actually develop active TB

74
Q

Do all infected actually develop active TB

75
Q

What is primary TB

A
  1. Once inhaled into lungs, alveolar macrophages ingest bacteria
  2. Bacilli proliferate inside and cause release of chemoattractants and cytokines
  3. Inflammatory infiltrates reach lung
  4. Macrophages present antigen to T cells and we get Type Iv hypersensitivity (granuloma and tissue necrosis)
  5. Lymphocytes and fibrosis
76
Q

What is the initial granuloma known as in the lungs

A
  1. PRIMARY GHON FOCUS
77
Q

Where is primary goon focus found

A

Upper region of the lungs in sub pleural regions

78
Q

Ho wis goon focus seen on a CXR

A

All clarified nodules in lower lobe upper parts and lower parts of upper lobes where bacilli settle

79
Q

Where can primary lesions of TB also be seen

A

Ileocaecal canal

80
Q

What happens to bacilli after primary lesion formation

A

Taken to lymph nodes and secondary lesions develop

81
Q

What is the ghon complex

A
  1. Primary goon focus and caseous lesions in lymph nodes

Caveated areas heal and calcify

82
Q

What do the calcified nodules contain

A

Bacteria which are contained by immune system

83
Q

How do the calcified nodules keep bacteria dormant

A

Hypoxic acidic environment in the granuloma causes them to become dormant (they are aerobic)

84
Q

What is military TB

A

Tb spreads to other organs if it isn’t contained

85
Q

How common is dormant TB

A

VERY - affects 95% of poeple

86
Q

What is latent TB

A
  1. Immune system contains infection and patient develops cell-mediated immunity memory to the bacteria
87
Q

What is reactivation TB

A
  1. Reactivation of latent infection due to depression of host immune system
88
Q

What other types of TB are there

A
  1. GI
  2. TB of bone and spine
  3. Military TB
  4. CNS TB
  5. Pericardila TB
  6. TB of skin
89
Q

Systemic presentation of TB

A
  1. Weight loss
  2. Fever
  3. Anorexia
  4. Night Sweats
  5. Malaise
90
Q

Clinical presentation of pulmonary TB

A
  1. Productive cough
  2. Haemoptysis
  3. Cough more than 3 weeks
  4. Pleuritic pain
  5. Chest pain
  6. Breathlessness
  7. Hoarse voice if laryngeal involvement
91
Q

What is pulmonary TB associated with

A

1/ Consolidation

  1. Pleural effusion
  2. Pulmonary collapse by compression of lobar bronchus by enlarged nodes
92
Q

Clinical presentation of lymph node TB

A
  1. Swelling

2. Discharge

93
Q

Clinical presentation of bone TB

A
  1. Pain or swelling of joint

2. Potts disease (spinal cord/vertebral TB)

94
Q

What is Potts’ disease

A

Disc is avascular and stops receiving nutrients

Collapses

CASEOUS NECROSIS lead stop spinal collapse

95
Q

Presentation of abdo TB

A
  1. Ascites
  2. Abdo lymph nodes
  3. Ileal malabsorption
96
Q

Genito-urinary TB presentation

A
  1. Epdidymitis

2. Frequency, dysuria and haematuria

97
Q

CNS TB presentation

A
  1. Bacilli in CSF and meninges

2. Meningeal inflammation produces thick exudates = strangulation of cranial nerves and raised ICP

98
Q

Diagnostics of TB

A
  1. CXR
  2. Sputum
  3. Bronchoscopy
  4. Histology
  5. Culture
  6. NAAT
  7. Lumbar puncture and CSF examination
99
Q

Role of CXR in TB

A
  1. Nodular shadows in upper zones
  2. Loss of volume
  3. Fibrosis and cavitation seen
  4. Consolidation
  5. Miliary shadows in military TB
100
Q

Role of Sputum in TB

A
  1. Stained with auramine-phenol fluorescent test - bacilli is yellow-orange on a green background
  2. Ziehl-neelsen test for acid fast bacilli
101
Q

Histology in TB

A

Caveating granuloma

102
Q

Culture of sputum in TB

A
  1. Middlebrow agar or Lowenstein-Jensen slopes
103
Q

Role of NAAT in TB

A
  1. Differentiate between TB mycobacteria and non-tuberculosis mycobacteria
104
Q

Diagnosis of latent TB

A
  1. Tuberculin skin test ‘Mantoux’

2. Interferon gamma release assays

105
Q

What is the tuberculin skin test

A
  1. TB antigen injected intradermally
  2. Cell mediated response 48=72 hours after recorded
  3. Stimulates type IV hypersensitivity reaction
  4. Positive = interferon gamma testing
106
Q

When do we get false negatives in skin test

A

Immunosuppressed and military TB won’t react

107
Q

Con of tuberculin skin test

A

False positives

108
Q

What are IGRAs

A
  1. Use antigens specific to M. tuberculosis (ESAT-60 and CFP10) to distinguish between this and environmental mycobacteria)
109
Q

Where should all cases of Tb be reported

A

PUBLIC HEALTH ENGLAND

110
Q

Treatment of TB

A
  1. Begin contact tracing
  2. 6 month treatment (CNS 12 months)

Rifampicin for 6 months
Isoniazid for 6 months
Pyrazinamide for 2 months
Ethambutol for two months

RIPE

111
Q

Role of rifampicin

A
  1. Bactericidal, blocks protein synthesis
112
Q

Role of Isoniazid

A
  1. Bactericidal for rapidly growing bacilli
113
Q

Role of pyrazinamide

A

Bactericidal initially

114
Q

Role of ethambutol

A

Bacteriostatic

115
Q

How do we aid complicance

A

DOTS (Direct Observed therapy ) - medication given under supervision

116
Q

How is TB prevented

A
  1. Case tracing
  2. Detection and treatment of TB via community nursing team
  3. Vaccination (neonatal BCG)
117
Q

What is neonatal BCG

A
  1. Live attenuated vaccine from mycobacterium Bovis that has lost its virulence
118
Q

Causes of alkalosis

A
  1. Vomiting (loss of HCL)
  2. Volume depletion
  3. Alkali ingestion
  4. Hyperaldosteronism
  5. Hyperkalaemia (causes more aldosterone to be released)
119
Q

What causes metabolic acidosis

A

1Renal failure

  1. GI HCO3 loss
  2. Dilution of blood (more water = more H+)
  3. KETOACIDOSIS
120
Q

How do kidneys compensate for respiratory acidosis

A
  1. Increase H+ secretion as NH4+ and release more bicarbonates into plasma
121
Q

How does the kidney compensate in respiratory alkalosis

A
  1. Decrease H+ secretion

2. Decrease in HCO3- reabsorption

122
Q

Hb sat in venous blood

123
Q

Hb sats in arteries

124
Q

What is P(a-a)

A

Alveolar arterial difference of O2

125
Q

Normal P(A-a) O2

A

1-4Kpa (increases with age)

126
Q

What does a high P9A-a) O2 mean

A
  1. Not transferring oxygen properly from alveoli to pulmonary capillaries

Year 2 (155 decks)

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