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Year 3 > Block 31 Week 7 > Flashcards

Block 31 Week 7 Flashcards

1
Q

CAP causes

A
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2
Q

CFs of pneumonia?

A
  • fever
  • cough
  • chest pain
  • increased resp rate
  • crackles
  • tachycardia
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3
Q

Ix for pneumonia?

A
  • CXR - to confirm diagnosis/ look for complications e.g. effusions
  • moderate/ severe:
  • blood cultures
  • viral swabs
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4
Q

supportive management of pneumonia?

A
  • Analgesia
  • IV fluids
  • Oxygen as needed
  • Prophylaxis for DVT / PE
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5
Q

pneumonia management - drainage?

A
  • Drainage of effusion if empyema or severe symptoms
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6
Q

Tx of mild pneumonia?

A
  • 1st line: amoxicillin
  • alt: clarithromycin
  • alt: doxycycline
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7
Q

moderate pneumonia - oral/ IV?

A
  • 1st line: amoxicillin + clarithromycin
  • alt: doxycyline
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8
Q

What can be used instead of clarithromycin or doxycycline in moderate pneumonia?

A

Moxifloxacin / Levofloxacin

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9
Q

severe pneumonia drugs are given?

A

IV

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10
Q

Severe CAP first line?

A
  • 1st line: Co-amoxiclav + Clarithromycin
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11
Q

severe CAP alternatives?

A
  • 1st line: Co-amoxiclav + Clarithromycin
  • alt: Cefuroxime + Clarithromycin
  • alt: Benzylpenicillin + Levofloxacin
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12
Q

transmission of COVID-19?

A
  • Major route is respiratory droplets, generated by coughing, sneezing, talking
  • Other routes include aerosols, contact with contaminated surfaces
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13
Q

CFs of Covid?

A
  • Classical URTI symptoms, may progress to severe disease around day 10 of illness
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14
Q

moderate-severe Covid?

A
  • Pronounced inflammatory / pro thrombotic state in critical cases
  • Often little to find on examination
  • cough, fever, SOB, fatigue, chest pain, muscle aches
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15
Q

Ix for Covid?

A
  • Low lymphocytes / platelets
  • AKI
  • Higher d-dimer
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16
Q

RF for mortality from Covid?

A
  • For invasively ventilated patients mortality is around 50%
  • Age is the most consistent and largest risk
  • Men have worse outcomes
  • Ethnicity appears to be a marked risk
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17
Q

CXR for covid?

A
  • clasically there is bilateral interstitial shadowing typical of viral pneumonia
  • takes a long time to resolve - may have persistent shadowing/ fibrosis
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18
Q

supportive care in the management of Covid-19?

A

*Oxygen for hypoxia
*IV fluids
*VTE prevention
*Analgesia

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19
Q

Targeted treatment of covid-19?

A

*Anti viral - Remdesivir
*Anti inflammatory - Dexamethasone

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20
Q

primary TB?

A
  • Typically mild or asymptomatic
  • Mid/lower zone infiltrates, hilar adenopathy, pleural effusion
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21
Q

Secondary TB?

A
  • Tuberculin skin test positive (confounded by BCG)
  • IGRA testing
  • No evidence of active disease
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22
Q

Post-primary TB?

A
  • Active disease; cough, presence of AFB in sputum, fever ~50%, haemoptysis, malaise, anorexia, weight loss, breathlessness
  • Signs of parenchymal disease uncommon until disease advanced
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23
Q

high incidence TB countries?

A
  • india
  • indonesia
  • pakistan
  • china
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24
Q

RF for TB?

A
  • Place of birth
  • HIV
  • Prison inmates/staff,
  • nursing homes
  • homeless shelters,
  • health care workers,
  • substance abuse,
  • immigrant centres & migrant workers camps
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25
Q

medical factors inc TB risk?

A
  • under nutrition
  • smoking
  • cancer
  • HIV
  • taking illicit drugs
  • alcoholism
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26
Q

social factors increasing risk of TB?

A

Single/widowed men, immigration, incarceration, homelessness

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27
Q

CXR of pulmonary TB?

A
  • Upper lobes tend to be affected
  • irregular shadowing
  • cavitation
  • thick irregular walls
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28
Q

microbiological diagnosis of TB?

A
  • positive cultures for M.TB confirm the diagnosis of TB
  • CEPHAID test - detects DNA specific to TB and rifampicin. Results obtained within 90 mins
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29
Q

Mdr-TB means TB resistant to?

A

isoniazid and rifampicin

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30
Q

contact tracing in TB?

A
  • idenficiation of contacts of TB positive individuals
  • national target is for 90% of people with infectious TB to have at least 5 contacts traced
  • pre-entry screening programme for testing of active pulmonary TB in migrants from high incidence countries who apply for visas which reduces importation of active TB
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31
Q

INF-gamma tests?

A
  • quantiferon TB gold - used in place of TB testing for previous infection
  • not confounded by prior BCG vaccine
  • main role is screening for latent disease
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32
Q

what does the INF-G test measure?

A
  • measures cell mediated immune response by looking at INF-g released by T cells in response to TB antigens
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33
Q

TB drugs?

A

*Isoniazid
*Rifampin
*Pyrazinamide
*Ethambutol

RIPE

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34
Q

TB drug regimen?

A
  • Rifampicin, +Isoniazid, +Pyrazinamide, +Ethambutol for 2 months
  • Rifampicin/Isoniazid for 4 months
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35
Q

isoniazid mechanism?

A
  • bactericidal
  • blocks mycolic acid synthesis
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36
Q

isoniazid needs to be taken?

A
  • absorption decreased by fatty acids: needs to be taken 4 hours after food and 1 hour before
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37
Q

Adverse effects of isoniazid?

A
  • hepatitis
  • neuropathy, reduced risk with pyroxidine (vit B6) supplements
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38
Q

rifampicin mechanism?

A
  • bactericidal, inhbitis DNA-dependent RNA polymerase
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39
Q

which drug reduces abs or rifampicin?

A

pyrazinamide

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40
Q

adverse effects of rifampicin ?

A
  • induction of P450 enzymes - increases breakdown of many drugs
  • hepatitis
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41
Q

Pyrazinamide - ? is intrinsically resistant?

A

M bovis

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42
Q

Adverse events of pyrazinamide?

A
  • GI upset and arthralgia - raised uric acid
  • hepatotoxicity
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43
Q

ethambutol?

A
  • weak bacteriostatic drug
  • antacids affect absorption
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44
Q

Adverse effects of ethambutol?

A

Optic neuritis (increased risk with pre-existing eye disease and higher doses than standard regimen)

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45
Q

Adherence to drug Tx - RF?

A
  • social risk factors
  • previous TB
  • MDR
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46
Q

TB drugs that require monitoring?

A
  • rifampicin
  • 2nd line are commonly monitored to avoid toxicity e.g. amikacin, cycloserine
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47
Q

Where are the highest TB rates?

A
  • highest rates of TB in the most deprived groups
  • london has the highest number of TB cases in England followed by the South of England
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48
Q

Tb is concentrated in the following groups:

A
  • the urban poor
  • alcoholics
  • iV drug users
  • homeless
  • prison inmates
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49
Q

how is TB spread?

A
  • inhalation of droplets
  • Infectious particles aerosolized by coughing, sneezing or talking
  • fomites not important
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50
Q

TB - when the antigen load is small?

A
  • granuloma forms
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51
Q

TB - when antigen load is high?

A
  • lymphcoytes, macrophages and granulocytes present is a less organized fashion
  • tissue necrosis may be present - exudative reaction
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52
Q

pathogenesis of TB?

A
  • caseating necrosis is unstable so it tends to liquify and discharge through the bronchial tree producing a TB cavity
  • infectious materal from a cavity results in new exudative foci in other parts of the lung - bronchogenic spread
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53
Q

symtoms of PTB?

A
  • include a productive, prolonged cough (duration of >= 3 weeks),
  • chest pain,
  • hemoptysis.
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54
Q

Systemic symptoms of TB

A
  • Fever, chills, night sweats, appetite loss, weight loss, and easy fatigability
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55
Q

In primary TB, there’s rapid

A

destruction of bactera so the only remaining evidence of infection would be a postive skin test

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56
Q
A
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57
Q

What happens in post-primary TB?

A
  • Immune deficiency including disease, drugs, old age, malnutrition, alcohol etc
  • Reactivation as macrophage/granuloma break up
  • Causes bronchial spread as necrosis occurs
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58
Q

EP TB - metastatic spread to any organ:

A
  • Abdomen
  • Bone
  • Brain
  • Muscle
  • Retina
  • Lymph Node
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59
Q

TB of the spine and kidney?

A
  • TB of the spine may cause pain in the back
  • TB of the kidney may cause blood in the urine.
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60
Q

when should EP TB be considered?

A
  • Extrapulmonary TB should be considered in the differential diagnosis of ill persons who have systemic symptoms and who are at high risk for TB.
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61
Q

sputum collection in TB?

A
  • 3 early morning specimens of sputum on 3 consecutive days
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62
Q

what else can be done to obtain TB specimens?

A
  • bronchoscopy can be done if there’s suspicion of TB and the patient can’t cough up sputum
  • Gastric aspiration can also be used to obtain specimens of swallowed sputum
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63
Q

other tests for TB patients?

A
  • Testing for HIV
  • hep B and C serologic tests if risks present
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64
Q

tests to do when TB Tx is initiated?

A
  • AST
  • ALT
  • bilirubin
  • ALP
  • serum creatinine
  • platelet count
  • Visual acuity and color vision tests (when EMB used)
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65
Q

drug interactions with rifampicin

A
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66
Q

MDR-TB is more likely in:

A
  • people who have a history of Tx with TB drugs
  • contacts of ppl known to have drug resistant TB
  • people from countries where prev of MDR TB is high
  • Persons whose smears or cultures remain positive despite 2 months of therapy with TB drugs;
  • Persons receiving inadequate treatment regimens for > 2 weeks.
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67
Q

extensively drug resistant TB?

A
  • XDR-TB is resistant to fluoroquinoline and at least 3 of the second line drugs (capreomycin, kanamycin, and amikacin), in addition to MDR-TB.
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68
Q

Summary table of the second line therapies in TB Tx

A
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69
Q

CAP =

A
  • refers to pneumonia contracted outside the hospital setting and includes those developing the condition in a nursing home
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70
Q

typical CAP?

A
  • productive cough, fever, pleuritic chest pain
  • most commonly caused by streptococcus pneumoniae
  • can also be caused by haemophilus influenzae
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71
Q

Most common causitive agent of CAP?

A

1) streptococcus pneumoniae
2) haemophilus B

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72
Q

atypical pneumonias?

A
  • These tend to have a more insidious, subacute onset. They often present with a combination of pulmonary and extrapulmonary symptoms
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73
Q

pathogens causing atypical pneumonias?

A
  • Mycoplasma pneumoniae, Legionella pneumophila, Chlamydophila pneumoniae
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74
Q

HAP =

A
  • contracted >48 hrs after hospital admission
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75
Q

causes of HAP?

A
  • Gram-negative bacilli(e.g.Pseudomonas aeruginosa)
  • Staphylococcus aureus
  • Legionella pneumophila
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76
Q

Aspiration of pneumonia?

A
  • caused by inhalation of oropharhngeal or gastric contents
  • typically seen in patients with reduced conciousness level, NM disorders, oesophageal conditions, mechanical interventions such as endotracheal tubes
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77
Q

IC - bacterial pneumonia?

A

typical pathogens and non-tuberculosis mycobacterium.

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78
Q

IC - fungal pathogens?

A

Pneumocystis jirovecii, Aspergillus fumigatus and Cryptococcus neoformans.

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79
Q

IC - viral pathogens?

A

such as varicella zoster virus and cytomegalovirus should be considered.

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80
Q

IC - parisitic pathogens?

A

parasitic pneumonias are very rare and seen almost exclusively in the immunocompromised.

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81
Q

streptococcus pneumonia typically produces a ? pattern of consolidation

A

lobar

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82
Q

sputum

strep pneumonia typically gives?

A
  • It classically gives rust coloured sputum and may be accompanied by the reactivation of cold sores.
  • Urinary antigen tests may be used to diagnose the infection and is unaffected by antibiotics.
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83
Q

mycoplasma pneumoniae?

A
  • lacks a cell wall
  • tends to affect younger demographic
  • occurs in cyclical epidemics
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84
Q

mycoplasma pneumonia causes pneumonia with a prolonged insidious onset that may exhibit EP features:

A
  • Erythema multiforme
  • Arthralgia
  • Myocarditis, pericarditis
  • Haemolytic anaemia
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85
Q

legionella pneumonia?

A
  • gram negative
  • may cause the atypical CAP (lobar) Legionnare’s disease
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86
Q

legionella - exposure to?

A
  • It is encountered in those exposed to contaminated cooling systems, humidifiers and showers.
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87
Q

presentation of legionalla pneumonia?

A
  • Chest symptoms may be preceded by several days of myalgia, headache and fever.
88
Q

Legionnaire’s disease - classical finding?

A
  • hyponatreaemia secondary to SIADH is a classical finding but not always present
89
Q

pseudomonas aeruginosa?

A
  • gram negative bacillus - typically causes HAP
  • In patients with bronchiectasis (e.g. cystic fibrosis) is may cause CAP.
  • opportunistic - rarely causes disease in a healthy person
90
Q

pseudomonas aeruginosa typically causes pneumonia in?

A
  • typically causes pneumonia in IC patients and those with chronic lung disease
  • can lead to bacteraemia
91
Q

pseudomonas aeruginosa - sputum is characteristically?

92
Q

klebsiella?

A
  • gram negative
  • classically causes CAP classically seen in alcoholics
93
Q

klebsiella produces a?

A
  • fast moving lobar pneumonia
94
Q

appearance of sputum with klebsiella pneumonia?

A
  • Sputum may have the characteristic ‘red-currant jelly’ appearance.
95
Q

what is klebsiella resistant to?

A
  • resistant to beta lactams
  • Beta-lactamase stable beta-lactams, cephalosporins and aminoglycosides may be used to treat the infection.
96
Q

Pneumocystis jirovecii?

A
  • fungi
  • aids defining illness that can cause life threatening penumonia
97
Q

Pneumocystis jirovecii causes?

A
  • It causes fever, cough (frequently non-productive) and exertional dyspnoea.
  • Hypoxia and a raised LDH are also common findings.
98
Q

how is Pneumocystis jirovecii pneumonia treated?

A
  • does not respond to antifungals and is instead treated with co-trimoxazole (trimethoprim-sulfamethoxazole).
99
Q

pneumonia is characterised by?

A

cough, SOB and signs of consolidation

100
Q

symptoms of pneumonia?

A
  • Fever
  • Malaise
  • Cough(purulent sputum)
  • Dyspnoea
  • Pleuritic pain
101
Q

respiratory signs of pneumonia?

A
  • Dull percussion note
  • Reduced breath sounds
  • Bronchial breathing(transmission of bronchial sounds to peripheries due to consolidation
  • Coarse crepitations
  • Increased vocal fremitus(increased transmission of ’99’ through consolidated lung)
102
Q

other signs of pneumonia?

A
  • Tachycardia
  • Hypotension
  • Confusion
103
Q

pulmonary complications of pneumonia?

A
  • Parapneumonic effusion
  • Pneumothorax
  • Abscess
  • Empyema
104
Q

EP complications of pneumonia?

A
  • Sepsis
  • Atrial fibrillation
105
Q

Bedside Ix of pneumonia?

A
  • sputum sample
  • urinary sample - urinary antigens: legionella and pneumoccal
  • ECG
106
Q

CURB-65

107
Q

general management of pneumonia?

A
  • O2
  • IV fluids - ppts may be dehydrated
  • analgesia - NSAIDs or opiods
108
Q

Low severity pneumonia Tx?

A
  • amoxicillin
  • doxycycline or clarithromycin if penicillin allergy
  • typical course is 5-7 days
109
Q

intedmediate severity pneumonia?

A
  • dual therapy with beta-lactam (e.g. amoxicillin) and a macrolide (e.g. clarithromycin).
  • Doxycycline may be used as an alternative in those with a penicillin allergy.
110
Q

Typical ab course for intermediate severity pneumonia?

111
Q

high severity pneumonia Tx?

A
  • IV beta-lactamase stable beta-lactam(e.g co-amoxiclav) and a macrolide (e.g. clarithromycin).
112
Q

duration of Tx in high severity pneumonia?

A
  • An antibiotic course of 7-10 days may be extended to 14 or 21 days depending on clinical circumstance.
113
Q

HAP Tx?

A
  • Co-amoxiclav 625mg orally TDS may be used in mild infections.
  • Tazocin (piperacillin/tazobactam) 4.5g IV TDS may be used in severe infections.
114
Q

follow up CXR after pneumonia?

A
  • 11% of smokersover the age of 50 who have pneumoniahave lung cancer.
  • ACXR at 6-8 weekspost-event should be used to screen for underlying lung cancer
115
Q

Streptococcus pneumoniae(pneumococcus)?

A

Accounts for 80% of cases
- Particularly associated with high fever, rapid onset and herpes labialis
- A vaccine to pneumococcus is available

116
Q

Haemophilus influenzae?

A
  • Particularly common in patients with COPD
117
Q

staph aureus?

A
  • Often occurs in patient following influenza infection
118
Q

mycoplasma pneumoniae?

A
  • One of the atypical pneumonias, which often present a dry cough and atypical chest signs/x-ray findings
  • Autoimmune haemolytic anaemia and erythema multiforme may be seen
119
Q

legionella pneuomia?

A
  • Another one of the atypical pneumonias
  • Hyponatraemia and lymphopenia common
120
Q

Pneumocystitis jiroveci?

A

-Typically seen in patients with HIV
- Presents with a dry cough, exercise-induced desaturations and the absence of chest signs

121
Q

latent vs active TB?

A
  • latent: no active disease and not infectious
  • active: symptomatic or progressive disease
122
Q

types of mycobacterium?

A
  • Mycobacterium tuberculosis: main cause of TB in humans
  • Mycobacterium bovis: main cause of TB in cattle and other mammals, can cause human disease
123
Q

post-primary TB?

A
  • also termed reactivation TB. It occurs in patients with latent TB, frequently due to immunocompromise (e.g. AIDs).
  • May be pulmonary (55%) or extra-pulmonary (45%).
124
Q

What happens in primary TB?

A
  • alveolar macrophages phagocytose bacilli which continue to proliferate
  • the Ghon complex (mosy commonly seen in children) may develop which is made up of the ghon focus - a small caseating garnuloma and ipsilateral mediastinal lymph node
125
Q

Cavitating TB on CXR

126
Q

classic triad of pulmonary TB:

A
  • Cough
  • Fever
  • Weight loss
127
Q

lymph node TB?

A
  • most common EP site
  • most commonly affects cervical and supraclavicular nodes
128
Q

Genitourinary TB?

A
  • Sterile pyruria may be seen
  • Other features include:
  • Salpingitis
  • Epididymo-orchitis
  • Renal abscess
129
Q

Miliary TB?

A
  • Miliary TB is the disseminated haematogenous spreadof the bacilli
130
Q

CNS TB?

A
  • TB meningitis
  • TB meningitis tends to present with fever, malaise and headache.
131
Q

TB meningitis CSF results?

A
  • High protein
  • Low glucose
  • Lymphocytosis
132
Q

vertebral TB (Pott’s syndrome)?

A
  • Fever
  • Weight loss
  • Back pain
  • development of kyphosis common
133
Q

Pericardial TB?

A

pericardial effusions or constrictive pericarditis

134
Q

Adrenal TB?

A

TB is the leading cause of Addison’s disease worldwide

135
Q

GI TB?

A

terminal ileitis - peritoneal spread may lead to ascites

136
Q

Mantoux test shows?

A
  • false positive from BCG vaccine
137
Q

Interferon-g is not affected by?

A

previous BCG vaccine

138
Q

Ix for TB

A
  • CXR +/- CT
  • Bronchoscopy and pleural fluid taken for TB microscopcy and culture and cytology
139
Q

Isoniazid mechanism?

A
  • Isoniazid: mycolic acid synethesis inhibitir
140
Q

isoniazid side effects?

A
  • side effects: polyneuropathy (but given with pyroxidine to reduce this risk)
  • may cause hepatotoxicity
141
Q

isoniazid ? CYP450

142
Q

rifampicin?

A
  • RNA polymerase inhibitor
  • Stains secretions pink and may cause hepatotoxicity.
  • It is an inducer of CYP450.
143
Q

Pyrazinamide side effects?

A
  • hepatotoxicity
  • gout
144
Q

ethambutol mechanism?

A
  • inhibits arinosyl transferase needed for cell wall synthesis
145
Q

hepatotoxicity from TB drugs?

A
  • rifampicin, isoniazid and pyrazinamide all associated w hepatotoxicity
  • LFT measurement and serial measurements
146
Q

Tx of latent TB

A
  • 6 months of isoniazidwith pyridoxine (6H)or - preferred if interactions with other meds possible
  • 3 months of isoniazid(with pyridoxine)and rifampicin(3HR) - preferred if patient is younger than 35 if hepatotoxicity is a concern.
147
Q

Prevention of TB?

A
  • Raising awareness - TB education programmes for those in contact with the general public
  • MDT TB teams should raise awareness of TB among under-served and high risk groups and information on symptom recognition and the benefits of diagnosis and treatment
  • national information for the public about TB like PHE and TB alert
148
Q

TB prevention - BCG vaccine?

A
  • improving uptake by identifying eligible groups in line with the DoH’s green book
149
Q

Active TB without CNS involvement drug regimen?

A
  • isoniazid (with pyridoxine), rifampicin, pyrazinamide and ethambutol for 2monthsthen
  • isoniazid (with pyridoxine) and rifampicin for a further 4months.
150
Q

active TB with CNS involvement drug regimen?

A
  • isoniazid (with pyridoxine), rifampicin, pyrazinamide and ethambutol for 2monthsthen
  • isoniazid (with pyridoxine) and rifampicin for a further 10months
151
Q

Approaches to controlling spread of TB
?

A
  • improve vaccination uptake
  • address TB in under-served populations
  • improve access to services and ensure early diagnosis
  • quarentine
  • DOT - directly observed treatment when non-compliance suspected e.g. homeless, alcoholics
152
Q

MDT TB teams should provide data to TB control boards on:

A

screening uptake, referrals and the number of active TB cases identified.

153
Q

TB control boards should?

A
  • control boards should develop TB prevention and control programmes working with commissioners, Public Health England and NHS England
  • TB control boards should be responsible for developing a TB prevention and control programme based on the national strategy and evidence‑based models.
154
Q

roles of the TB control boards?

A
  • TB control boards should plan, oversee, support and monitor local TB control, including clinical and public health services and workforce planning.
155
Q

bronchiectasis =

A
  • abn and irreversible dilatation of the airways
156
Q

bronchiectasis normally results from?

A
  • It normally results from the inflammatory destruction of the elastic and muscular components of the airways.
  • commonly occurs secondary to CF
157
Q

who does bronchiectasis affect more?

A
  • Female > male
  • more common in older age groups especially 70+
158
Q

immune deficiency & bronchiectasis?

A
  • recurrent infective insults combined with poor host immune response increases risk
  • Ig deficiency, panhypogammaglobulinaemia, HIV, malignancy
159
Q

mechanical obstruction and bronchiectasis?

A
  • Airway obstruction can lead to bronchiectasis.
  • Foreign bodies (particularly in children), mucus plugging, stenosis, tumours or lymph nodes can all be responsible.
160
Q

mucocilliary clearance dysfunctions and bronchiectasis?

A
  • primary ciliary dyskinesia
  • young syndrome
161
Q

primary ciliary dyskinesia?

A
  • autosomal recessive
  • characterised by immotile cilia often resulting in recurrent infections and bronchiectasis.
162
Q

primary ciliary dyskinesia is associated with?

A
  • It is associated with early-onset of symptoms (in childhood/ teenage years), otitis media, rhinosinusitis and male infertility.
163
Q

young syndrome?

A
  • is a syndrome characterised by male infertility (obstructive azoospermia), sinusitis and bronchiectasis.
  • relationship with mercury exposure
164
Q

CF and bronchiectasis?

A
  • causes dehydration and depletion of airway surface liquid which is key to normal function of cilia
165
Q

congenital airway defects and bronchiectasis?

A
  • williams-campbell syndrome
  • Mounier-Kuhn syndrome: a
166
Q

Williams–Campbell syndrome?

A

is a rare disease characterised by defective cartilage in the airways (fourth to sixth division) resulting in bronchiectasis.

167
Q

Mounier-Kuhn syndrome?

A

also termed tracheobronchomegaly, it is a rare disease characterised by dilatation of the trachea itself as well as the bronchi.

168
Q

other causes of bronchiectasis?

A
  • RA
  • ABPA - exaggerated immune response to Aspergillus, tends to occur in asthmatics and can lead to bronchiectasis.
  • COPD - repeated infection can lead to bronchiectasis
  • iBD
169
Q

symptoms of bronchiectasis?

A
  • Persistent sputum production - purulent
  • Persistent cough
  • Dyspnoea
  • Haemoptysis
  • Weight loss
170
Q

sputum culture for ? is highly suspicious for bronchiectasis?

A

P aerguinosa

171
Q

signs of bronchiectasis?

A
  • Crackles
  • High pitched inspiratory squeaks
  • Wheeze
  • Clubbing(rare)
172
Q

Dx of bronchiectasis?

A
  • first line: CXR - Typical changes include tram-track airways and ring shadows.
  • CT: diagonistic modality of choice
173
Q

CT scan of bronchiectasis?

A
  • CT: diagonistic modality of choice
  • dilated airways
  • signet sign classicial
174
Q

Bloods for bronchiectasis?

A
  • FBC
  • Renal function
  • Serum immunoglobulins(and serum protein electrophoresis if elevated)
175
Q

Aspergillus fumigatus Ix?

A
  • Serum total IgE
  • Sensitisation assessment(specific IgE or skin prick test)
176
Q

management of bronchiectasis - airway clearance?

A
  • techniques taught by resp physiotherapist
  • active cycle of breathing techniques
177
Q

Mx of B - mucoactives?

A
  • help clearing mucus from airways
  • Isotonic and hypertonic saline may be used and have been shown to improve quality of life
  • oral carbocisteine
178
Q

Mx of B - prophylactic ab?

A
  • > 3 exacerbations per year
  • colistin and gentamicin
  • azithromycin and erythromycin
179
Q

complications of bronchiectasis?

A
  • Infective exacerbation
  • Chronic respiratory failure
  • Haemoptysis(may be massive and life-threatening)
  • Cor pulmonale
  • Pneumothorax
  • # Chest pain
180
Q

CF =

A
  • mutation in CFTR gene found on chromosome 7
  • encodes chroride channels
  • most common in those of white ethnicity
181
Q

pathophys of CF?

A
  • results in dehydration of airway surface fluid resulting in mucociliary dysfunction
  • reduced mucus clearance, airway obstruction and predisposition to infection
  • Recurrent infection leads to chronic bronchitis, damage to the bronchi and eventual bronchiectasis
182
Q

Most common CF mutation?

A
  • most common mutation is the delta-F508 (DF508) mutation
183
Q

CF - pancreatic?

A
  • Pancreatic insufficiency is common in patients with CF and patients can suffer with recurrent acute pancreatitis or chronic pancreatitis.
  • Damage to pancreatic islets may result in CF-related diabetes. Liver impairment is common
184
Q

CF screening?

A

heel prick blood test

185
Q

respiratory symptoms of CF?

A

productive cough and recurrent chest infections

186
Q

CF - pancreatic disease symptoms?

A
  • pancreatic disease - insufficiency with fatty stools and malabsorption.
  • In those with more severe pancreatic disease, autolysis destroys the pancreatic islets leading to CF-related diabetes.
187
Q

CF and GI disease in infants?

A
  • CF is the most common cause of meconium ileus in term infants
188
Q

diagnosis of CF?

A
  • Immuno-reactive trypsin test:the test used at newborn screening
  • Sweat test: can be used in children of any age.
  • Genetic testing: common mutations are screened for,
189
Q

What should be done for pleural effusions?

A

diagnostic tap - diagnostic aspiration

190
Q

What can be used to decide whether ppts w acute bronhitis need ab?

A

CRP > 100 CRP level can be used to guide whether patients with acute bronchitis require antibiotics

191
Q

indications for ab?

A
  • multiple comorbids
  • becoming systemically very unwell
192
Q

BRONCHITIS clinical pattern?

A

Bronchitis follows a clinical pattern of an initial dry cough over 3-4 days followed by a productive cough that usually resolves within 3 weeks.

193
Q

Typical Sx of ARDS?

A

breathlessness, reduced oxygen saturations and auscultation of the chest showing bilateral crackles, is typical of acute respiratory distress syndrome.

194
Q

Decrease in pO2/FiO2in poorly patient with non-cardiorespiratory presentation ->

195
Q

Crackles vs wheeze?

A

Crackles on auscultation imply fluid whereas an asthma exacerbation creates a wheeze as the airways tighten.

196
Q

CO2 retention->

A

CO2 renetion - resp acidosis
low O2

197
Q

pleural plaques?

A

pleural plaques can occur following asbestos exposure and are benign - no follow up required

198
Q

fine end inspiratory crepitations?

A

Fine end-inspiratory crepitations are a common finding in idiopathic pulmonary fibrosis causes by the sudden opening of small airways during inspiration that were held closed in the previous expiration.

199
Q

what points at it being a viral infection?

A

clear sputum, no fever, normal CXR= probably viral infection

200
Q

? is assoc w erthema multiforme

A

Mycoplasma is associated with erythema multiforme

201
Q

which pathogen can cause desaturation on exercise?

A

Pneumocystis jiroveci pneumonia causes desaturation on exercise

202
Q

cold sores ->

A

streptococcus

203
Q

peritoneal dialysis peritonitis?

A

Coagulase-negative Staphylococcus is the most common cause of peritonitis secondary to peritoneal dialysis

204
Q

klebsiella?

A

Klebsiella most commonly causes a cavitating pneumonia in the upper lobes, mainly in diabetics and alcoholics

205
Q

Legionella CP?

A
  • GI symptoms such as diarrhoea, abd painm dry cough, hyponatreamua
206
Q

recent influenza infection->

207
Q

mycoplasma pneumonia?

A
  • young adults
  • sore throat, headache, nausea, abd pain, diarrhoea
208
Q

which 2 pathogens cause cavitating pneumonia?

A

staph a and klebsiella

209
Q

Characteristic features of pneumococcal pneumonia

A
  • rapid onset
  • high fever
  • pleuritic chest pain
  • herpes labialis (cold sores)
210
Q

hyponatreamia, headache and dry cough ->

A

legionella

211
Q

recent flu ->

A

staphyLococcus

213
Q

pneumocystitis jivorci pneumonia Tx?

A

Pneumocystis jiroveci penumonia is treated with co-trimoxazole, which is a mix of trimethoprim and sulfamethoxazole

214
Q

which pathogen can cause cold haem anaemia

A

mycoplasma - pneumonia and CHA

215
Q

which organism causes LRTI in CF?

A

Pseudomonas aeruginosa is an important organism causing LRTI in cystic fibrosis patients

Year 3 (45 decks)

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