Respiratory pathology 2 Flashcards

1
Q

Total time for the treatment if Tb

A

6 months if medication and rehabilitation which involves other members of the MDT

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2
Q

Determinants of Tb

A

Lower income regions
Under nourishment of food
Immunosuppressed people eg HIV
Elderly , neonates and the diabetics
Those with mental health conditions and those in prisons

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3
Q

National epidemiology of Tb

A

Most prevalent in London
With most people being people who were not vaccinated gainst tb with the BCG vaccine

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4
Q

Summary of epidemiology

A

TB incidence over time is falling, 2% per year. But, recent rise ​
TB is still a disease of the poor / social risk factors​
TB is the number 1 killer of communicable diseases​
TB kills more than HIV and Malaria together​
TB is not evenly distributed, globally or nationally​
2/3 of all TB cases (prevalence) in 8 countries​
An estimated 2 billion people are infected worldwide​

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5
Q

Cause TB

A

mycobacteria species for example tuberculosis , M. africanum and mycobacterium.bovis
PRESENT IN SOIL AND WATER

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6
Q

other species of non-tuberculosis mycobacteria

A

Non-tuberculous mycobacteria, NTM-infections / ‘Atypical mycobacteria​
Leprosy (M.leprae)​

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7
Q

characteristics of mycobacteria that cause tuberculosis (AAFBs)

A

Uniquely has a very thick fatty cell wall​
Resistant to acids, alkalis and detergents​
Resistant to neutrophil and macrophage destruction ​
Acid - and alcohol - fast bacilli (AAFB) (Ziehl Neilson stain)​
however not all AAFB are mycobacterium

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8
Q

transmission of tuberculosis

A

airborne only through the laryngeal and pulmonary system
TB in the lymph nodes cannot be spread in other regions in the body

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9
Q

non medicated management of TB

A

good circulation of air in the house ; TB bacteria will remain suspended in air for many hours
outdoors mycobacteria is eliminated by UV radiation and dilution.

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10
Q

ways in which TB is not spread

A

Shaking hands​
Sharing food​
Touching surfaces​
Sharing toothbrushes​
Kissing​

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11
Q

spread of mycobacterium bovis

A

spread through drinking of unpasteurized milk

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12
Q

cells involved in the defence against TB

A

as TB is not sensitive to destruction of macrophage and neutrophils , it can only be destroyed by T helper cells that is lymphocytes.

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13
Q

immunopathology of TB

A

many activated macrophages form epithelioid cells and forms langhan”s giant cells which form granuloma with central necrosis

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14
Q

consequences of the immunological response of t helper cells

A

Eliminates / Reduces number of invading mycobacteria​
Tissue destruction is a consequence of activation of macrophages​

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15
Q

history of dvlpmt of tuberculosis

A

primary infection - helps to build immunity and they are drained on the lymphatic nodes that is the hila lymph nodes , and there are no symptoms , there is development of immunity against tuberculoprotein

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16
Q

primary infection of tuberculosis

A

progressive disease
contained latent
cleared cured

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17
Q

types of primary TB infection

A

tuberculosis bronchopneumonia
miliary tuberculosis

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18
Q

tuberculosis bronchopneumonia

A

there is abnormal enlargement of the hilar node which leads to compression of the bronchi and later on collapse of the lobe has a poor prognosis

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19
Q

milliary tuberculosis

A

there is spread of the bacteria to multiple organs by blood ; presents with widespread small granulomata

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20
Q

post primary disease

A

only present in humans the bacteria enters dormant stage with little to no replication over a prolonged period of time
there is a balanced replication and destruction of the immune mechanisms

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21
Q

spread of tuberculosis

A

primary - progressive primary - milliary , meningeal , pleural TB - post primary pulmonary and skeletal disease - genitourinary and cutaneous TB

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22
Q

clinical presentation of TB

A

Coughing
fever
sweats at night
weight loss

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23
Q

methods of diagnosing active TB

A

chest x ray

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24
Q

presentation of mediastinal lymphadenopathy

A

there is a white patch at the mediastinum just next to the heart

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25
Q

presentation of miliary tuberculosis in an x ray

A

presents as spots on the lung

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26
Q

tests performed to test for TB

A

Sputum; 3 samples, 8-24hrs gap, at least 1 early morning sample​
Induced sputum​
Bronchoscopy with BAL​
Endobronchial ultrasound (EBUS) with biopsy​
Lumbar puncture in CNS TB / biopsy​
Urine in urogenital TB​
Aspirate/biopsy from tissue ( lymph-node, bone, joint, brain, abscess …

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27
Q

clinical management of TB

A

isoniazid
pyrazinamide
rifampicin
ethambutol

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28
Q

rules for prescription of TB

A

Test for HIV, Hepatitis B and C​
Single agent treatment leads to drug resistant organisms within 14 days​
Therapy must continue for at least 6 months​

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29
Q

Standard treatment of TB

A

12 tablets a day for 6 moths
2 moths of all the tablets
4 months of rifampicin and isoniazid
pyridoxine with isoniazid which reduces risk of neuropathy
steroids cause side effects of the CNS , milliary TB , pericardial
vitamin D substitution

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30
Q

side effects of ethambutol

A

Optic neuropathy (check visual acuity)​

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31
Q

Pyrazinamide side effects

A

hepatitis
gout

32
Q

Isoniazid side effects

A

Hepatitis​
Peripheral neuropathy (pyridoxine B6)​

33
Q

rifampicin side effects

A

Orange ‘Irn Bru’ urine/tears/lenses ​
Induces liver enzymes, prednisolone, anticonvulsants​
All hormonal contraceptive methods ineffective​
Hepatitis​

34
Q

side effects of all drugs

A

rashes

35
Q

vaccination against TB

A

BCG vaccination

36
Q

screening of latent TB

A

Contacts of people with active pulmonary or laryngeal TB who are aged ≤65 years As hepatotoxicity risk increases with age those aged 66 years or older: CXR only to rule out active TB only ​

New entrants to Grampian from high incidence areas​

‘Pre-biologics’ (TNF-alpha inhibitors)

37
Q

screening of latent TB

A

Mantoux skin test or Interferon Gamma Release Assay (IGRA) blood test​

38
Q

treatment of latent tuberculosis

A

Rifampicin & Isoniazid for three months, or ​

Isoniazid or Rifampicin only for six months or ​

Rifapentine & Isoniazid once weekly for 12 weeks​

39
Q

possible causes of lung infections

A

microorganism pathogenicity
capacity to resist infection
population at risk that is the removal of the commensal flora

40
Q

upper respiratory tract infections

A

common cold
sore throat
acute laryngotracheobronchitis (croup)
laryngitis
sinusitis
acute epiglottitis

41
Q

acute epiglottitis causative agent

A

haemophilus influenzae ( Virus)
group A beta haemolytic streptococci ( bacteria )

42
Q

lower respiratory tract infections

A

bronchitis
bronchiolitis
pneumonia

43
Q

mechanisms of defence of the respiratory tract

A

macrophage engulfs and destroys the bacteria and the foreign particles , production of mucus , the foreign material is wafted away , coughed up through the cough reflex

44
Q

influenza viral pneumonia

A

influenza virus during a primary attack causes a destruction of the mucociliary escalator system , because of this the commensal flora staph aureus can thrive and not be removed leading to an acute inflammation

45
Q

viral infections in the lungs

A

bronchiolitis
pneumonitis

46
Q

SARS-CoV-2 (COVID19)

A

viral infection where there is inflammation of the bronchioles leading to pneumonia of the lungs

47
Q

classification of pneumonia

A

part of the lung affected
the circumstances that is hospital acquired or community acquired
the type of causative agent

48
Q

hospital acquired pneumonia

A

not sensitive to antibiotics

49
Q

types of pneumonia based on the cause

A

Community Acquired Pneumonia
Hospital Acquired (Nosocomial) Pneumonia
Pneumonia in the Immunocompromised
Atypical Pneumonia
Aspiration Pneumonia
Recurrent Pneumonia

50
Q

anatomical classification of pneumonia

A

bronchopneumonia
segmental pneumonia
lobar pneumonia

51
Q

hypostatic pneumonia

A

fluid retention at the bottom of the lung that causes an optimum environment for the growth of bacteria

52
Q

aspiration pneumonia

A

aspiration of contents that lead to movement of fluids into the inner tubes

53
Q

bronchopneumonia

A

( exudation ) fluid in the bronchi
seen on the x ray as basal patchy opacification
vasodilation of the bronchioles from the inflammatory response

54
Q

lobar pneumonia

A

collapse of an entire lobe caused by an inflammatory response
a whole lobe collapses
exudation of fluid and bleeding
vasodilation of the bronchioles

55
Q

complications of pneumonia

A

1.lung abscess form necrosis of the lung tissue
2.pleural effusion caused by infection of the pleura
3.pleurisy which is the inflammation of the pleura
4.bronchiectasis which is the widening of the bronchi such that there is build up of fluid for
bacterial growth .
5.empyema which is collection of pus in the pleural cavity
6.organisation which leads to development of fibrotic tissue such as the case of cryptogenic organising pneumonia

56
Q

causes of lung abscess

A

1.aspiration pneumonia
2.tumor
3.organism eg staph
4.metastatic pyaemia that is pus movement
5.necrotic lung

57
Q

bronchiectasis

A

Pathological dilatation of Bronchi

58
Q

causes of bronchiectasis

A

Severe Infective Episode
Recurrent Infections - many causes
Proximal Bronchial Obstruction
Lung Parenchymal Destruction

59
Q

most common age group affected by bronchiectasis

A

most start in childhood

60
Q

bronchiectasis

A

COUGH, ABUNDANT PURULENT FOUL SPUTUM, haemoptysis, signs of chronic infection
Coarse crackles, clubbing
Thin section CT
Postural Drainage, Antibiotics, Surgery

61
Q

diagnostic method of bronchiectasis

A

a thin CT section
located at the edge of the lung

62
Q

complications of bronchiectasis

A

suppuration that is the filling up of the bronchi with pus.
haemorrhage - excessive bleeding from systemic blood supply ( blood supply in the bronchi is from brachial artery and therefore high pressure blood )

63
Q

aspiration pneumonia

A

Vomiting
Oesophageal Lesion
Obstetric Anaesthesia
Neuromuscular Disorders
Sedation

64
Q

opportunistic infections

A

infections only present in the immunocompromised such as HIV
Low grade bacterial pathogens
CMV
Pneumocystis jirovecii
Other fungi and yeasts

65
Q

causes of recurrent lung infection

A

Local Bronchial Obstruction

Local Pulmonary Damage

Generalised Lung Disease COPD?
Non-Respiratory Disease (HIV, other)?, Aspiration?

66
Q

abnormal gas exchange

A

type 1 lower partial pressure for oxygen
type 2 lower partial pressure for carbon dioxide
both in the arterial blood

67
Q

consequences of abnormal pulmonary gas exchange

A

shunt
ventilation perfusion mismatch
alveolar hypoventilation
diffusion impairement

68
Q

ventilation perfusion normal values

A

Normally breathing ~4 l/min. Cardiac Output is ~5 l/min so normal V/Q is 4/5 or 0.8

69
Q

what is ventilation perfusion mismatch

A

blood is sent to regions of the lungs where there is less ventilation leading to flow of not fully oxygenated blood back to the lungs
oxygen is given to reverse

70
Q

shunt

A

blood passing too the lungs without any oxygenation
right side of the heart has deoxygenated blood
increase in oxygen doesn`t solve this

71
Q

diseases that display ventilation perfusion abnormality

A

there is oxygenation although the alveoli is abnormal
Bronchitis / Bronchiolitis
Bronchopneumonia
COPD

72
Q

diseases that display shunt system

A

there is no ventilation of the abnormal alveoli
Severe bronchopneumonia
Lobar pattern with large areas of consolidation

73
Q

alveolar hypoventilation

A

Hypoventilation increases PACO2, and thus increases PaCO2
Increase in PACO2 decreases PAO2, which causes PaO2 to fall
Fall in PaO2 due to hypoventilation is corrected by raising FIO2

74
Q

causes of alveolar hypoventilation

A

1.Upper airway or tracheal obstruction
2.Mechanical problems with breathing mechanism (chest wall damage)
3.Functional problems with breathing mechanism (muscle paralysis, diaphragmatic damage)
4.Neurological problems with breathing mechanism
5.Peripheral nerve damage or loss of function
CNS malfunction – opiate poisoning, COPD

75
Q
A