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Phase 2 > Resp conditions > Flashcards

Resp conditions Flashcards

1
Q

Give examples of 2 organisms that cause TB

A

Mycobacterium tuberculosis
Mycobacterium bovis (unpasteurised milk)
+ africanum, microti

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2
Q

What makes TB a successful pathogen?

A

Thick waxy capsule cell wall is able to resist weak disinfectants and survive on dry surfaces for a long time.
Resistant to phagolysosomal killing by macrophages (- granuloma formation).
Able to remain dormant.

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3
Q

Describe the pathogenesis of primary tuberculosis

A

Inhaled into the lung and ingested by alveolar macrophages.
TB resists phagolysosomal killing and proliferates, releasting cytokines resulting in inflammatory involvement of hilar lymph node.
3 weeks later
Granuloma formation around TB (primary ghon focus) and associated lymph node, known together as the Ghon complex.
Caseous necrosis of complex occurs, and it undergoes fibrosis and calcification (Ranke complex)- visible on CXR.
TB is able to remain dormant within the Ranke Complex for many years = latent TB.
Cell-mediated immunity memory to TB is developed.
Reactivation occurs when the individual is immunocompromised.

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4
Q

Where in the lung is the primary Ghon complex usually found and why?

A

In the apex, as this is less well perfused so the TB comes into contact with fewer immune cells

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5
Q

Describe what may happen if an individual with a latent TB infection is immunocompromised?

How may the TB spread?

A

Reactivation occurs.
Memory T cells release cytokines and TB is able to spread to upper lobes (more O2) ans the immune cells contribute to more areas of caseous necrosis.
These areas cavitate, spreading to the rest of the lung (pulmonary TB) or to the vasculature –> systemic miliary TB.

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6
Q

Describe some features of systemic miliary TB - where is the infection likely to spread, with what effect?

A 
Kidneys - sterile pyuria
Adrenals - addisons
Meninges - meningitis
Lumbar vertebrae - Pott's disease
Liver - hepatitis
Cervical lymph nodes - scrofula
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7
Q

How could you diagnose CNS TB?

A

CSF would contain bacilli on lumbar puncture

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8
Q 
What symptoms might be associated with extrapulmonary TB of the following systems?
GI/abdominal
GU
Bone/spine
CNS
A

GI/abdominal: ascites, ileal malabsorption
GU: epididymitis, frequency, dysuria, haematuria
Bone and spine: pain and swelling of joints, Pott’s
CNS: cranial nerve palsy, raised ICP due to meningeal inflammation, meningitis
Lymph node: swelling +/- discharge

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9
Q

How would you diagnose active TB?

A

CXR: patchy shadows/fibrosis, consolidation. Miliary - normal/miliary shadows.
Sputum/bronchoalveolar lavage: culture
Lumbar puncture for miliary/CNS

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10
Q

How is TB cultured and why?

A

It is acid fast due to waxy cell wall and gram stains weakly, so Ziehl-Nielson is used and appears red if TB.

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11
Q

How would you diagnose latent TB?

A

Mantoux:
Tuberculin injected, stimulates type 4 sensitivity reaction.
Interferon gamma release assays (IGRA) demonstrate exposure but not active infection.

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12
Q

What steps would you take immediately following histology + clinical picture consistent with TB?

A

Notify public health england.
Start treatment without waiting for culture results.
Begin contact tracing.
Isolate until non-infectious.

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13
Q

What is the treatment course for TB (apart from CNS)

A

Rifampicin for 6mo
Isoniazid for 6 mo
Pyrazinamide for first 2 mo
Ethambutol for first 2mo
DOTS: direct observed therapy - medication is taken under supervision.
Individuals must be isolated until no longer infectious, and it is crucial they take the whole course of medication.

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14
Q

Symptoms of pulmonary TB

A 
Cough
Haemoptysis
Chest pain
Breathlessness
systemic features
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15
Q

Define pneumonia

A

lower respiratory tract infection - inflammation of lung parenchyma

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16
Q

Who is at risk of pneumonia?

A 
Extremes of age
Immunocompromised
Individuals with COPD, CHD, diabetes
Impaired swallow
IVDU, alcohol abuse
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17
Q

Describe briefly the pathogenesis of pneumonia

A

Macrophages cannot phagocytose microbe
Release cytokines to recruit neutrophils, filling the alveolar space with dead bacteria + dead neutrophils + tissue fluid + inflammatory proteins = inflammatory exudate or ‘pus’.
This may lead to long term damage to lung parenchyma

18
Q

symptoms of pneumonia

A

CHEST: Cough, potential rusty sputum (characteristic of s. pneumoniae), SOB, pleuritic chest pain
INFECTION: fever, sweats, rigors
SYSTEMIC: weakness, malaise

19
Q

describe the features of pleuritic chest pain

A

Localised, sharp pain that worsens on ddeep breathing and when moving

20
Q

Describe tests used to diagnose pneumonia

A

FBC shows raised WBC,
biochem U+E/LFTs show dehydration
Raised ESR and CRP indicate inflammation
Sample for culture -> microbio for targetted treatment, however management must start before results return.

21
Q

Describe signs of pneumonia

A

Vitals: increased HR, resp rate, decreased BP, fever, dehydration, decreased sats
chest exam: signs of consolidation = dull to percussion, inc. vocal resonance, dec. air entry, crackles/wheeze

22
Q

What scale is used to assess severity of pneumonia and therefore treatment course in CAP?

A 
CURB>65
Confusion
Urea
Resp rate
Blood pressure
>65
0-1 = outpatient, amoxicillin
2 = admit, oral amoxicillin + clarithromycin
3-5 = IV coamoxiclav + clarithromycin
23
Q

Principles of treatment with antibiotics for CAP vs HAP?

A

CAP: narrowest spectrum possible
HAP: start broad spectrum, more likely pt has come into contact with resistant microbes

24
Q

what is parapneumonic effusion and how is it treated?

A

Parapneumonic effusion is any pleural effusion secondary to pneumonia (bacterial or viral) or lung abscess. Pockets of fluid are in the thoracic cavity. If these are filled with pus, it is known as empyema. Treated by drainage.

25
Q

What is a common cause of lung abcess?

A

Metastatic - IVDU
Aspiration
Poor dentition
Secondary to LRTI

26
Q

What is aspiration pneumonia?

A

Inhalation of food/drink/gastric contents causes lung infection.
Often in individuals with compromised gag/cough reflex eg due to alcohol, brain injury or dysphagia.

27
Q

what is meant by COPD?

How are conditions characterised?

A

Group of lung conditions including emphysema and chronic bronchitis characterised by obstruction, progressive nature, not fully reversible, enhanced chronic inflammatory response, and association with smoking.

28
Q

What is emphysema vs chronic bronchitis?

A

Both COPD.
Often coexist.
Emphysema defined by structural changes, chronic bronchitis is a clinical diagnosis based on productive cough.

29
Q

Risk factors for COPD?

A 
Male
Smoker + genetics
Infections
Occupational
Low SE status
air pollution
congenital small lung size
30
Q

Presentation of emphysema vs chronic bronchitis

A

Emphysema ‘pink puffer’
Individual exhales slowly through pursed lips to increase alveolar pressure to prevent collapse. Weight loss, pink (not yet hypoxaemic), dyspnoea, SOB, cough. Develops barrel shaped chest after a while, lungs have poor expansion.
Chronic bronchitis ‘blue bloater’
Highly productive cough
Overweight
Hypoxaemic due to hypercapnia resulting from impaired gas exchange. Productive cough for 3months/year for at least 2yrs. Wheeze, crackles.

31
Q

What is a possible effect of emphysema on the heart?

A

Respiratory failure
Cor pulmonale
Poor gas exchange throughout lungs leads to widespread hypoxic vasoconstriction and pulmonary hypertension. R side of heart has to pump harder to overcome pressure, becomes enlarged = heart failure.

32
Q

What type of resp failure is seen in individuals with COPD?

A

type 2 respiratory failure, hypoxemia (PaO2 <8kPa) with hypercapnia (PaCO2 >7.0kPa).

33
Q

What is the most likely diagnosis in a chronic smoker who has a history of breathlessness and sputum production? What about in a non-smoker?

A

COPD

Asthma in non-smoker, unless family history of alpha 1 antitrypsin deficiency

34
Q

Treatment of COPD?

A

Smoking cessation slows deterioration.
Bronchodilators: SABA salbutamol to reduce acute symptoms, LAMA tiotropin bromide for prevention.

Trial inhaled prednisolone, but risk pneumonia/withdrawal.
O2 therapy
Pulmonary rehab, exercise, good diet
alpha 1 antitrypsin replacement if applicable.
Antibiotics for infections.

35
Q 
Mycobacterium tuberculosis
cause
pathogenesis
symptoms
diagnosis
treatment
A

Caused by mycobacterium tuberculosis. Latent infection in 90-95%, becomes active if an individual is immunocompromised.
Enters alveolar macrophage, proliferates at lung apex. Granuloma forms around TB and associated lymph node with caseous necrosis at centre = ghon complex. Undergoes fibrosis and calcification (visible on CXR). TB may be killed or remain latent, reactivated when immunocompromised - T memory cells produce cytokines - and cavitates, spreading to rest of lung (pulmonary TB) &/or to vasculature (systemic miliary/extrapulmonary TB).
Symptoms - general: chronic illness + fever + weight loss
pulmonary :
cough, chest pain, SOB, haemaptosis
extra:
GI: abdo ascites, ileal malabsorption
hepatitis
lymphadenopathy
CNS: meningitis, CN palsy, tuberculoma, Pott’s disease
Joint pain
Diagnosis - biopsy and culture is definitive: sputum. CXR,. Mantoux test for latent TB - however reacts to BCG vaccine. IGRA more specific.
Treat:
Latent: 6mo isoniazid. Only treat if likely to be immunocompromised (eg steroids, chemo)
Active: 6mo rifampicin + isoniazid, 3mo pyrazinamide + ethambutol. Isolate, contact trace, inform PHE.

36
Q 
COPD
emphysema
cause
symptoms
diagnosis
A

Immune reaction to irritant (cigarette smoke) = protease recruitment, break down collagen and elastin of alveolar walls. Neighbouring alveoli coallesce = reduced surface area, more compliant so collapse under low pressure holding onto trapped air (obstruction)
smoker, male, occupation, pollution, infections, alpha 1 anti-trypsin deficiency (protease inhibitor).
Symptoms:
SOB, dyspnoea, weight loss, cough with some sputum
Diagnosis:
‘pink puffer’. Over time CXR may show barrel chest. FEV1:FVC <0.7 shows obstructive lung disease.Host breathless + smoker.
Treat:
smoking cessation
SABA: salbutamol
LAMA: tiotropium bromide
ICS: prednisolone TRIAL but can exacerbate
O2 therapy
pul rehab, good diet, exercise

37
Q 
chronic bronchitis
pathophysiology
symptoms
diagnose
treatment
A

Reaction to irritant = hypertrophy and hyperplasia of mucous glands and goblet cells. Cilia damaged, mucous build up traps air and leaves individual prone to lung infections.
Productive cough, breathless, dyspnoea.
Clinical diagnosis:
Highly productive cough for 3mo a year, over 2 years. Wheeze, crackles, overweight. Can lead to cor pulmonale due to poor gas exchange = hypoxic vasoconstriction -> pulmonary hypertension.
Treat
Smoking cessation,
SABA: salbutamol
LAMA: tiotropium bromide
ICS: prednisolone TRIAL but can exacerbate
O2 therapy
pul rehab, good diet, exercise

38
Q

Bronchiectasis

A

Chronic inflamation of aiways leads to scarring, airways WIDEN permanently.
This causes a build up of mucus and vulnerability to infection.
Cause:
Infection - pneumonia, TB, measles, pertussis, whooping cough
Cystic fibrosis
Allergic Bronchopulmonary Aspergillosis
Bronchial obstruction - foreign body, tumour
Symptoms:
productive cough, dyspnoea, wheeze, infections, chest pain, exacerbations
Diagnose:
CXR shows dilated bronchi, cysts
Sputum culture for infetions - often heamophilus influenzae, strep pneumoniae, s aureus, p aeruginosa. Spirometry shows obstructive pattern, FEV1:FVC <0.7.
Treat:
mucous clearance - physio, mucolytics, postural drainage
antobiotics - amoxicillin, flucloxacillin for s aureus
azithromycin anti-inflam
Nebulisers and bronchodilators for bad flare ups.
Stop smoking, vaccines, exercise, diet.

39
Q

Pulmonary embolism

Risk

A

Oral contraceptive pill, DVT: immobility, flights, hospital stay/surgery, alcohol, smoking.
Symptoms:
Sharp pleuritic chest pain, SOB, pain, redness and swelling in one leg (DVT).
Diagnosis:
plasma D dimer blood test
Pulmonary CT angiography shows lung perfusion.
Treat:
Depends on severity - OAC warfarin/inject heparin.
Thrombolysis - IV alteplase if severe
Anticoagulants 3mo, clopidogrel.

40
Q

Lung cancer
Most common type
Risk
Diagnosis

A

90% are carcinoma, arising from epithelial cells in the respiratory tract. Most are metastatic.
Non-small cell = most lung cancers
smoking, genetics, radon, asbestos, air pollution, XR/CT.
Diagnose
CXR/CT
Symptoms
usually asymptomatic until late stage.General malaise and weight loss. Cough, chest infections, SOB, extrapulmonary changes.
Treat
not very responsive to chemo. Surgery and radiotheraphy mainstay. Pain management.

Phase 2 (16 decks)

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