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
What part of the lungs are effected
Dial airways and alveoli
26
What is community acquired pneumonia
1. No underlying immunosuppression or malignancy
27
What causes community acquired pneumonia
1. Strep pneumoniae 2. Haemophilus pneumonia 3. Mycoplasma pneumoniae 4. Staphylococcu aureus 5. E.coli 6. Klebsiella pneumoniae
28
What is lobar pneumonia
When the infection is localised to one whole lobe
29
What is diffuse pneumonia
Multiple lobules and respirartoy bronchioles are affected (bronchopneumonia)
30
Define hospital-acquired pneumonia
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
31
What people are effected by hospital-acquired pneumonia
1. Elderly 2. Ventilator-associated 3. Post operative
32
What causative organisms are in HAP
``` 1. AEROBIC GRAM-NEGATIVE bacilli: Pseudomonas aerguinosa E.coli Klebsiella Pneumoniae Staph Aureus sue to MRSA ```
33
What patients are susceptible to S.aureus infections in hospital (pneumonia)
1. Diabetes Mellitus | 2. Head trauma
34
What is the most common organism causing pneumonia in immunocompromised patients
Pneumocystis jiroveci
35
What is aspiration pneumonia
1. Acute aspiration of gastric contents into the lung which cause intense destruction
36
Where is aspiration pneumoniae seen
1. Stroke 2. MG 3. Bulbar palsies 4. Lack of consciousness
37
What is Mendelson syndrome
Pneumonia caused by aspiration of anaesthesia
38
Risk factors of pneumonia
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
39
How is pneumonia spread
1. Respiratory droplets
40
Why does pneumococcal pneumonia not respond to penicillin
Lack a cell wall
41
Pathophysiology of pneumonia
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)
42
What causes pneumonia to become severe
1. Excessive inflammation 2. Lung injury 3. Failure to resolve without lung damage
43
Clinical presentation of pneumonia
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
44
Differential diagnosis of pneumonia
1. TB or lung cancer
45
Diagnostic of pneumonia
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
46
Role of FBC in pneumonia
1. Elevated in strep pneumoniae (WCC) | 2. ESR and CRP
47
What is CURB-65
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
48
What is a CURB score of 0-1
Mild
49
CURB score of 2
Moderate, admit to hospital
50
CURB score of 3-5
Admite, severe and monitor closely
51
CURB score of 4-5
Admission to critical care until
52
How is pneumonia treated
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
How is legionella pneumonia treated
FLUOROQUINOLONE
54
How is necrotising pneumonia treated
1. IV CLINDAMYCIN 2. IV LINEZOLID 3. IV RIFAMPICIN
55
How is pseudomonas aerguinosa pneumonia treated
1. IV ceftazidime with grantamycin
56
How is pneumonia prevented
1. Polysaccharide pneumococcal vaccine 2> influenza vaccine 3. Smoking cessation
57
How many subtypes doe the vaccine protect against
23
58
Complications of pneumonia
1. Respiratory failure 2. Hypotension (dehydration and vasodilation in sepsis) 3. Parapneumonic effusion and empyema 4. Pleural effusions
59
How can we tell if empyema has developed from pneumonia
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
How do we diagnose pneumonia caused empyema
1. THORACOCENTESIS | 2. CXR for pleural effusion
61
What is thoracocentesis
Removing fluid from pleural space
62
Appearance of pleural fluid in empyema
1. pH less than 7.2 2. Fluid is yellow and turbid 3. Low glucose
63
How is empyema treated
1. Chest drain 2. CO-amoxiclav 3. Piperacillin - Tazobactam 4. Meropenam (anaerobic coverage)
64
What is a lung abscess
CAUSED BY PNEUMONIA | Severe localised suppuration within the lungs (cavity seen on CXR)
65
What causes lung abscesses
1. Aspiration (alcoholics, oesophageal obstruction) 2. Inadequately treated CAP 3. TB 4. Foreign body inhalation 5. Septic emboli (staph)
66
What organisms cause pneumonia lung abscess
1. Strep millers (viridian's streptococci) 2. Klebsiella pneumoniae 3. GRAM NEGATIVE bacteria
67
How is lung abscess treated
Antibiotics up to 6 weeks | Surgical Drainage
68
How do most people with HIV die
TB
69
What causes TB
1. Mycobacterium tuberculosis 2. Mycobacterium bovis (milk is unpasteurised) 3. Mycobacterium africanum 4. Mycobacterium microti
70
Characteristics of TB bacteria
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
Risk factors of TB
1. HIV 2. Diabetes mellitus 3. IVDU 4. Ageing 5. Malnutrition 6. Homeless 7. Prisons 8. Smoking 9. Alcohol
72
How is TB spread
Respiratory droplets
73
Do all infected actually develop active TB
no
74
Do all infected actually develop active TB
no
75
What is primary TB
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
What is the initial granuloma known as in the lungs
1. PRIMARY GHON FOCUS
77
Where is primary goon focus found
Upper region of the lungs in sub pleural regions
78
Ho wis goon focus seen on a CXR
All clarified nodules in lower lobe upper parts and lower parts of upper lobes where bacilli settle
79
Where can primary lesions of TB also be seen
Ileocaecal canal
80
What happens to bacilli after primary lesion formation
Taken to lymph nodes and secondary lesions develop
81
What is the ghon complex
1. Primary goon focus and caseous lesions in lymph nodes Caveated areas heal and calcify
82
What do the calcified nodules contain
Bacteria which are contained by immune system
83
How do the calcified nodules keep bacteria dormant
Hypoxic acidic environment in the granuloma causes them to become dormant (they are aerobic)
84
What is military TB
Tb spreads to other organs if it isn't contained
85
How common is dormant TB
VERY - affects 95% of poeple
86
What is latent TB
1. Immune system contains infection and patient develops cell-mediated immunity memory to the bacteria
87
What is reactivation TB
1. Reactivation of latent infection due to depression of host immune system
88
What other types of TB are there
1. GI 2. TB of bone and spine 3. Military TB 4. CNS TB 5. Pericardila TB 6. TB of skin
89
Systemic presentation of TB
1. Weight loss 2. Fever 3. Anorexia 4. Night Sweats 5. Malaise
90
Clinical presentation of pulmonary TB
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
What is pulmonary TB associated with
1/ Consolidation 2. Pleural effusion 3. Pulmonary collapse by compression of lobar bronchus by enlarged nodes
92
Clinical presentation of lymph node TB
1. Swelling | 2. Discharge
93
Clinical presentation of bone TB
1. Pain or swelling of joint | 2. Potts disease (spinal cord/vertebral TB)
94
What is Potts' disease
Disc is avascular and stops receiving nutrients Collapses CASEOUS NECROSIS lead stop spinal collapse
95
Presentation of abdo TB
1. Ascites 2. Abdo lymph nodes 3. Ileal malabsorption
96
Genito-urinary TB presentation
1. Epdidymitis | 2. Frequency, dysuria and haematuria
97
CNS TB presentation
1. Bacilli in CSF and meninges | 2. Meningeal inflammation produces thick exudates = strangulation of cranial nerves and raised ICP
98
Diagnostics of TB
1. CXR 2. Sputum 3. Bronchoscopy 4. Histology 5. Culture 6. NAAT 7. Lumbar puncture and CSF examination
99
Role of CXR in TB
1. Nodular shadows in upper zones 2. Loss of volume 3. Fibrosis and cavitation seen 4. Consolidation 5. Miliary shadows in military TB
100
Role of Sputum in TB
1. Stained with auramine-phenol fluorescent test - bacilli is yellow-orange on a green background 2. Ziehl-neelsen test for acid fast bacilli
101
Histology in TB
Caveating granuloma
102
Culture of sputum in TB
1. Middlebrow agar or Lowenstein-Jensen slopes
103
Role of NAAT in TB
1. Differentiate between TB mycobacteria and non-tuberculosis mycobacteria
104
Diagnosis of latent TB
1. Tuberculin skin test 'Mantoux' | 2. Interferon gamma release assays
105
What is the tuberculin skin test
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
When do we get false negatives in skin test
Immunosuppressed and military TB won't react
107
Con of tuberculin skin test
False positives
108
What are IGRAs
1. Use antigens specific to M. tuberculosis (ESAT-60 and CFP10) to distinguish between this and environmental mycobacteria)
109
Where should all cases of Tb be reported
PUBLIC HEALTH ENGLAND
110
Treatment of TB
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
Role of rifampicin
1. Bactericidal, blocks protein synthesis
112
Role of Isoniazid
1. Bactericidal for rapidly growing bacilli
113
Role of pyrazinamide
Bactericidal initially
114
Role of ethambutol
Bacteriostatic
115
How do we aid complicance
DOTS (Direct Observed therapy ) - medication given under supervision
116
How is TB prevented
1. Case tracing 2. Detection and treatment of TB via community nursing team 3. Vaccination (neonatal BCG)
117
What is neonatal BCG
1. Live attenuated vaccine from mycobacterium Bovis that has lost its virulence
118
Causes of alkalosis
1. Vomiting (loss of HCL) 2. Volume depletion 3. Alkali ingestion 4. Hyperaldosteronism 5. Hyperkalaemia (causes more aldosterone to be released)
119
What causes metabolic acidosis
1Renal failure 2. GI HCO3 loss 3. Dilution of blood (more water = more H+) 4. KETOACIDOSIS
120
How do kidneys compensate for respiratory acidosis
1. Increase H+ secretion as NH4+ and release more bicarbonates into plasma
121
How does the kidney compensate in respiratory alkalosis
1. Decrease H+ secretion | 2. Decrease in HCO3- reabsorption
122
Hb sat in venous blood
50%
123
Hb sats in arteries
90%
124
What is P(a-a)
Alveolar arterial difference of O2
125
Normal P(A-a) O2
1-4Kpa (increases with age)
126
What does a high P9A-a) O2 mean
1. Not transferring oxygen properly from alveoli to pulmonary capillaries