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Year 1 SBA revision > 118 - Bronchial Sepsis > Flashcards

118 - Bronchial Sepsis Flashcards

1
Q

Define pneumonia

A

Acute infection of portion of lung involved in gas exchange (Alveoli). High mortality/morbidity.

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2
Q

Incidence of pneumonia

A

5th leading cause of death - most common infectious cause of death. 1/4 ITU pts.

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3
Q

Aetiology of pneumonia

A

Anything that impairs lungs defences is a risk. Huge surface area so at risk from inhaled microbes.

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4
Q

4 classifications of pneumonia

A

Community acquired pneumonia
Hospital acquired pneumonia
Aspiration pneumonia
Pneumonia in immunocompromised patients

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5
Q

Presentation of pneumonia

A 
SOB
Pleuritic chest pain
Cough
Fever
Sputum production
Confusion
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6
Q

Patients with pneumonia are generally

A 
Pyrexial
Tachypnoeic
Tachycardic
Have reduced lung expansion
Have signs of consolidation
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7
Q

Key complications of pneumonia

A 
Respiratory failure
Pneumonia induced pleural effusion
Empyema
Lung abscess
Atrial fibrillation
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8
Q

Pneumonias to treat quickly

A 
Streptococcus - Medical emergency.
S. aureus - drain before abs
M.tuberculosis - isolate if suspect.
Pseudomonas - Penicillin doesn't work
PCP - AIDS defining.
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9
Q

Streptococcus pneumonia

A 
MEDICAL EMERGENCY
Up to 75% UK cases.
Infection in bloodstream so infects whole lobes.
Healthy to dead in hours.
Gram +ve diplococci - stay in pairs.
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10
Q

Staphylococcus aureus

A

Common in IV drug users.
Bunch of grapes appearance.
Upper lobe cavitation.
Forms capsule - need to drain first and then give antibiotics.

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11
Q

Mycobacterium tuberculosis

A

Great mimic - commonly seen in pts who are immunocompromised or who have a travel history. May have millet seed appearance on X-Ray

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12
Q

Pseudomonas aeriginosa

A

Gram -ve affects chronically ill. Pea soup coloured sputum.
Common in cystic fibrosis
Penicillins don’t work.

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13
Q

Haemophilis influenza

A

Bacterial URTI - only an issue in immunocompromised patients. Airborne so spreads along bronchus.

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14
Q

Klebsiella

A

Gram +ve Hospital acquired pneumonia. Mostly in patients with other co-morbidities.
Think alcoholic/COPD
Generally an aspiration pneumonia. Poor prognosis.

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15
Q

E.Coli

A

Not generally seen to cause pneumonia in healthy patients. Aspiration so most common in right lower lobe. Right bronchi shorter and more vertical

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16
Q

Legionella pneumonia

A

Gram -ve. Lives in water. Air conditioning units a risk. Immunocompromised most affected. Up to 30% mortality.
Deranged LFTs

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17
Q

Chlamydia psittaci

A

Transmitted by parrots. 1% mortality.

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18
Q

Pneumocystis jiroveni pneumonia

A

Shows ground glass shadowing on X-Ray. AIDS defining illness.

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19
Q

Fungal pneumonia

A

Only seen in immunocompromised.

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20
Q

What is bronchitis

A

Inflammation of bronchi.

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21
Q

What causes acute bronchitis and how to tell if it is viral or bacterial.

A

Infection - If bacterial, green sputum, if viral - yellow sputum.

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22
Q

What causes chronic bronchitis

A

Smoking - constant inflammation of the airway results in development of fibrous scar tissue over time that narrows the airway.

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23
Q

What is tracheaitis

A

Inflammation of trachea. Usually viral. Barking cough. Not usually treated.

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24
Q

What is pharyngitis

A

Sore throat. Generally minor unless prevents swallowing.

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25
Q

What is epiglottis

A

Acute ENT emergency - inflammation of epiglottis (flap to prevent food entering trachea).

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26
Q

How to treat epiglottis

A 
Limit examinations (can make worse) and secure airway.
Particular risk in children.
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27
Q

Investigations for Community Acquired Pneumonia

A

O2 SATS
Sputum sample - general culture, gram stain, acid fast bacilli (TB) - Don’t wait for results
Urine - check output and dipstick for legionella.
Bloods
ECG
CXR
ABG

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28
Q

What is CURB-65?

A

Method of assessing community acquired pneumonia after diagnosis. Can underscore younger patients - need to use with common sense.

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29
Q

CURB-65: 1 point given for

A

C - Confusion - More than normal
U - Urea - >7mm/l
R - Resp rate >30
B - BP - either

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30
Q

Management of CURB-65 score of 0-1

A

Manage in community. Amoxycillin.

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31
Q

Management of CURB-65 score 2

A

Consider as inpatient or supervised outpatient

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32
Q

Management of CURB-65 score 3 or higher

A

Severe pneumonia. Consider HDU.

IV augmentin/cefuroxine plus IV clarithromycin

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33
Q

Impact of poor prognostic features on CURB-65 score.

A

If 1 then needs IV abx. If 2 or more then treat as severe pneumonia.

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34
Q

What are the poor prognostic features that need to be considered with the CURB-65 score

A

Co-existing disease

Albumin

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35
Q

Define hospital acquired pneumonia

A

Occurs when antibiotics have been taken by the patient previously NOT just pneumonia caught in hospital. Increased risk of resistance so need to treat differently.

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36
Q

Investigations/Treatments for Hospital acquired pneumonia

A

Sputum sample, trachea aspirate and blood culture.
Give empirical antibiotics
If fails to respond - broncheoalveolar lavage with brushings taken. Sample used to determine predominant pathogen.

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37
Q

Follow up of patients with pneumonia

A

If no response to abx- review dx and cultures.

If consolidation in smokers. Need to check wasn’t hiding cancer.

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38
Q

Potential complications of pneumonia

A 
Empyema
Abscess
Pulmonary embolism
Pleural effusion
Bronchiectasis
ARDS - Acute respiratory distress syndrome
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39
Q

Impact of foetal hiatus hernia on lungs

A

Presence of GI tract in thorax can prevent lungs from developing correctly

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40
Q

Rusty sputum - think

A

Streptococcus pneumonia

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41
Q

Currant jelly sputum - think

A

Klebsiella

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42
Q

In respiratory embryology, Type 2 pneumocytes do what?

A

Produce surfactant

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43
Q

In respiratory embryology. What do Type 1 Pneumocytes do?

A

Increase surface area

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44
Q

What is infant respiratory distress syndrome? What to do about it?

A

Not enough surfactant produced. Immaturity of lungs - not enough type 2 pneumocytes. Can give steroids to help develop lungs if think at risk but may also increase risk of premature labour.

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45
Q

When do lung buds start to form?

A

Embryological week 4

Clinical week 6

46
Q

When are lungs fully formed?

A

Lung development continues through last weeks of foetal period

47
Q

Where do lung buds develop?

A

Bud out from ventral wall of foregut level with future oesophagus

48
Q

What makes lung buds grow?

A

Increase in [Retinoic acid] produced by adjacent mesoderm. Upregulates transcription factor TBX4 which triggers lung formation and development.

49
Q

What are lungs lined with?

A

Epithelium derived from endoderm like the gut tube. Internal external surface.

50
Q

What happens in the embryonic stage of lung development.

A

3-5 weeks. Lung budding and branching.

51
Q

What happens in the pseudo glandular stage of lung development?

A

6-16 weeks. Branching to form terminal bronchioles. No respiratory bronchioles or alveoli.

52
Q

What happens in the Canalicular stage of lung development.

A

17-24 weeks. Terminal bronchioles divide into respiratory bronchioles which divide into alveolar ducts.

53
Q

What happens in the Saccular stage of lung development

A

25 weeks-term. Primitive alveoli form and capillaries establish good blood supply.

54
Q

What happens in the alveolar stage of lung development

A

More alveoli develop. Mature alveoli have developed epithelial-endothelial contacts

55
Q

Treatment for oesophageal atresia

A

Surgery always required. Baby will not be able to feed otherwise and is at risk of aspiration pneumonia

56
Q

What is oesophageal atresia?

A

Abnormalities in separation of oesophagus and trachea. Can occur with or without transoeophageal fissures - abnormal connection between oesophagus and trachea

57
Q

Most common type of oesophageal atresia

A

90% cases - upper portion of oesophagus ends in line pouch and lower segment forms fistula with trachea.

58
Q

Role of surfactant

A

Reduces surface membrane tension of alveoli - if not enough then risk of alveolar collapse on expiration.

59
Q

How do pulse oximeters work? Are they the best option?

A

Blood changes colour when oxygenates. Pulse oximeter measures ratio of red:UV light absorption to determine ratios of oxygenated and unoxygenated blood.

Less accurate than ABG

60
Q

How does haemoglobin bind oxygen?

A

Harm group - Fe2+ in centre of perforin ring - carries oxygen.
Globin - modifies haem to allow binding to be reversible

61
Q

What determines the shape of the oxygen dissociation curve?

A

The 4 globes in haemoglobin. 2 alpha and 2 beta. Held together by salt bridges. As O2 bind then salt bridges broken and Haemoglobin relaxes.

This increases the affinity for another O2 molecule to bind to the same haemoglobin.

62
Q

Why does random movement result in diffusion

A

More molecules in area of high concentration that can move to area of low concentration.

63
Q

What is Henry’s Law?

A

Partial pressure = [dissolved gas]/solubility coefficent

64
Q

What is a solubility co-efficent?

A

Some molecules more attracted to water than others. More attracted they are, more can be dissolved at a lowe partial pressure.

65
Q

What is the major limiting factor in movement of gases through tissues?

A

Rate of gas diffusion through water

66
Q

Factors affecting rate of diffusion through the respiratory membrane?

A

Membrane thickness
Surface area
Diffusion coefficient of gas
Partial pressure difference between the 2 sides of the membrane

67
Q

What is the diffusing capacity of the respiratory membrane

A

Ability of respiratory membrane to exchange gas between alveoli and pulmonary blood

68
Q

How to measure diffusing capacity of oxygen

A

Measure diffusing capacity of CO and then calculate.

69
Q

What is the Bohr effect?

A

Increase in CO2 and H+ in blood shifts the Oxygen dissociation curve to the right resulting in release of O2 from blood into tissues where needed.

70
Q

What is the Haldane effect?

A

When O2 brings to haemoglobin - displaces CO2. Opposite of Bohr effect.

71
Q

3 different mechanisms of CO2 transport in the blood

A

Dissolved in blood
Bound to Haemoglobin as carboxyhaemoglobin
Transported as a bicarbonate ion

72
Q

How is CO2 transported as a bicarbonate ion?

A

CO2 in blood reacts with H20 to form carbonic acid. Carbonic acid dissociates into H+ and bicarbonate. H+ combines with haemoglobin and bicarbonate ions are in the plasma. Catalysed by carbonicanhydrase in RBC.

73
Q

What is sepsis and what can it lead to?

A

Sepsis - a systemic infection that causes vasodilation. Patient can then go into shock as not enough blood is being pushed around the body.

74
Q

What does palmar erythema indicate

A

Septic shock. Blood has moved to surface due to vasodilation.

75
Q

How many people in hospital will develop HAP? How many in ITU? How many ventilated patients?

A

1/100 hospital patients.
1/4 ITU patients.
Almost certain to develop if ventilated for a long time.

76
Q

How to differentiate between typical and atypical pneumonia?

A

No clinically reliable way

77
Q

Highest risk groups for pneumonia

A

All age groups but elderly, children and the immunocompromised at higher risk

78
Q

Typical pneumonia generally presents with

A

Abrupt onset, high fever, purulent sputum, focal consolidation

79
Q

Atypical pneumonia generally presents with

A

Gradual onset, dry cough, myalgia, headache

80
Q

Aspiration pneumonias mostly affect

A

Alcoholics
Patients with impaired consciousness
Patients with swallowing problems

81
Q

What can cause pneumonias?

A

Bacteria
Viral
Fungal
(Rarely) helminth/protozoa

82
Q

Aspiration pneumonias are generally caused by

A

Anaerobes
Gram negative enterobacteria
S. aureus

83
Q

Hospital acquired pneumonias are generally caused by

A

S. aureus
Gram negative enterobacteria
Pseudomonas
Klebsiella

84
Q

Common causes of community acquired pneumonias

A

Streptococcus pneumonia (60-75%)
Haemophilus influenzae
Mycoplasma pneumoniae

85
Q

What pneumonia are penicillins ineffective against?

A

Pseudomonas

86
Q

World’s leading cause of death from infectious disease

A

TB

87
Q

Risk factors for TB

A 
Close contact (>8hrs/day) with infected person
Immunocomprimised
Homeless - 150x national average
Drug/alcohol abuse
Smoking
Healthcare workers
88
Q

What causes TB?

A

Inhalation of causative organism.
M tuberculosis
M africanum
M bovis

89
Q

Geography of TB infection

A

95% of cases in the developing world
Africa - most severe buren.
SE Asia/Western Pacific - most new cases occur here.
UK - mostly in ethnic minorities.

90
Q

Presentation of primary TB

A

Usually asymptomatic, can be associated w. mild febrile illness.

91
Q

Presentation of secondary TB

A 
Classically:
Cough
Sputumn production
Haemoptysis
Fevers
Night sweats
Fatigue
Weightloss

Can affect most organs. Elderly patients commonly have non-specific symptoms.

92
Q

Why does TB have such an impact on developing countries?

A

Mostly affects adults during their most productive years

93
Q

Appearance of TB skin

A

Erythema nodosum - Inflammation of the fat cells, resulting in red lumps. Generally on the shin.

94
Q

What does TB spine cause?

A

Vertebral collapse

95
Q

What does TB brain cause?

A

Chronic meningitis or space occupying lesions can develop

96
Q

What does TB of the adrenal glands cause?

A

Addison’s disease. Now rare in the UK

97
Q

What is primary TB

A 
Initial lesion (1-2cm diameter) develops in middle or upper lobes of lung. Ghon complex - focus of primary infection.
After few weeks, initial lesion becomes a tubercle which undergoes necrosis during 'caseation'. The caseous tissue can liquefy, empty into the airway or be transmitted to other parts of the lung allowing bacterial spread.
98
Q

What is secondary TB?

A

Reactivation of the primary infection or reinfection occurs. More common in the immunocompromised. Usually bilateral caveatting lesions as the tubercle follicles develop and new tubercles form.

99
Q

What is progressive TB?

A

Can happen after primary or secondary TB.

TB progresses to widespread cavitations, pneumonitis and lung fibrosis.

100
Q

What is miliary TB?

A

Acute, diffuse dissemination of tubercle bacilli through the bloodstream, Characteristic millet seed appearance on CXR.

101
Q

Latent TB

A

Roughly 1/3 of worlds population. Infected but not yet sick. Cannot transmit the disease. 10% lifetime risk of becoming ill in the future. Higher if malnourished, smoker or immunocomprimised.

102
Q

Investigations for TB

A
  • Sputum test - Acid fast bacilli, culture, PCR (resistance), Need to request TB specific culture.
  • Blood - FBC, ESR, CRP
  • ECG - Normal sinus rhythm?
  • X-Ray
  • Heaf/Mantoux-Tuberculin tests. Won’t work if immunocompromised or miliary TB
  • Histology
103
Q

Treatment for symptomatic TB

A

6 months quadruple therapy supervised by chest physician.
RIPE.
2 months - Rifampicin, isoniazid, pyrazinamide, ethambutol.
Then 4 months rifampicin and isoniazid only if TB fully sensitive.

104
Q

Major problem with TB treatment is

A

Non-compliance. Side effects mean patients are likely to stop taking.

105
Q

Rifampicin side effects

A

Orange body secretions
Hepatitis
Thrombocytopenia
Flu-like symptoms

106
Q

Isoniazid side effects

A

Peripheral neuropathy
Hepatitis
Seizures
Psychoses

107
Q

Pyrazinamide side effects

A

Hyperuricaemis
Hepatitis
Rash
Gout

108
Q

Ethambutol side effects

A

Optic neuritis - can cause blindness

Rashes

109
Q

What is a DOTS strategy?

A

Directly Observed Treatment, Short-course.

Drugs given by healthcare workers who observe them being taken. Greatly increases compliance.

110
Q

Problems with TB and resistance

A

TB - adapts very quickly to develop resistance.
If poor drug availability, poor compliance, inappropriate treatment then resistance likely to develop.
MDR (multi drug resistant) and XDR (Extremely drug resistant) TB now exists.
XDR - worst in Eastern Europe due to partial treatment. No treatments available.

Year 1 SBA revision (37 decks)

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