118 - Bronchial Sepsis Flashcards

(110 cards)

1
Q

Define pneumonia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Incidence of pneumonia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Aetiology of pneumonia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

4 classifications of pneumonia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Presentation of pneumonia

A
SOB
Pleuritic chest pain
Cough
Fever
Sputum production
Confusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Patients with pneumonia are generally

A
Pyrexial
Tachypnoeic
Tachycardic
Have reduced lung expansion
Have signs of consolidation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Key complications of pneumonia

A
Respiratory failure
Pneumonia induced pleural effusion
Empyema
Lung abscess
Atrial fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pseudomonas aeriginosa

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Haemophilis influenza

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Legionella pneumonia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Chlamydia psittaci

A

Transmitted by parrots. 1% mortality.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pneumocystis jiroveni pneumonia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Fungal pneumonia

A

Only seen in immunocompromised.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is bronchitis

A

Inflammation of bronchi.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is tracheaitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is pharyngitis

A

Sore throat. Generally minor unless prevents swallowing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is epiglottis
Acute ENT emergency - inflammation of epiglottis (flap to prevent food entering trachea).
26
How to treat epiglottis
``` Limit examinations (can make worse) and secure airway. Particular risk in children. ```
27
Investigations for Community Acquired Pneumonia
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
28
What is CURB-65?
Method of assessing community acquired pneumonia after diagnosis. Can underscore younger patients - need to use with common sense.
29
CURB-65: 1 point given for
C - Confusion - More than normal U - Urea - >7mm/l R - Resp rate >30 B - BP - either
30
Management of CURB-65 score of 0-1
Manage in community. Amoxycillin.
31
Management of CURB-65 score 2
Consider as inpatient or supervised outpatient
32
Management of CURB-65 score 3 or higher
Severe pneumonia. Consider HDU. | IV augmentin/cefuroxine plus IV clarithromycin
33
Impact of poor prognostic features on CURB-65 score.
If 1 then needs IV abx. If 2 or more then treat as severe pneumonia.
34
What are the poor prognostic features that need to be considered with the CURB-65 score
Co-existing disease | Albumin
35
Define hospital acquired pneumonia
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.
36
Investigations/Treatments for Hospital acquired pneumonia
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.
37
Follow up of patients with pneumonia
If no response to abx- review dx and cultures. | If consolidation in smokers. Need to check wasn't hiding cancer.
38
Potential complications of pneumonia
``` Empyema Abscess Pulmonary embolism Pleural effusion Bronchiectasis ARDS - Acute respiratory distress syndrome ```
39
Impact of foetal hiatus hernia on lungs
Presence of GI tract in thorax can prevent lungs from developing correctly
40
Rusty sputum - think
Streptococcus pneumonia
41
Currant jelly sputum - think
Klebsiella
42
In respiratory embryology, Type 2 pneumocytes do what?
Produce surfactant
43
In respiratory embryology. What do Type 1 Pneumocytes do?
Increase surface area
44
What is infant respiratory distress syndrome? What to do about it?
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.
45
When do lung buds start to form?
Embryological week 4 | Clinical week 6
46
When are lungs fully formed?
Lung development continues through last weeks of foetal period
47
Where do lung buds develop?
Bud out from ventral wall of foregut level with future oesophagus
48
What makes lung buds grow?
Increase in [Retinoic acid] produced by adjacent mesoderm. Upregulates transcription factor TBX4 which triggers lung formation and development.
49
What are lungs lined with?
Epithelium derived from endoderm like the gut tube. Internal external surface.
50
What happens in the embryonic stage of lung development.
3-5 weeks. Lung budding and branching.
51
What happens in the pseudo glandular stage of lung development?
6-16 weeks. Branching to form terminal bronchioles. No respiratory bronchioles or alveoli.
52
What happens in the Canalicular stage of lung development.
17-24 weeks. Terminal bronchioles divide into respiratory bronchioles which divide into alveolar ducts.
53
What happens in the Saccular stage of lung development
25 weeks-term. Primitive alveoli form and capillaries establish good blood supply.
54
What happens in the alveolar stage of lung development
More alveoli develop. Mature alveoli have developed epithelial-endothelial contacts
55
Treatment for oesophageal atresia
Surgery always required. Baby will not be able to feed otherwise and is at risk of aspiration pneumonia
56
What is oesophageal atresia?
Abnormalities in separation of oesophagus and trachea. Can occur with or without transoeophageal fissures - abnormal connection between oesophagus and trachea
57
Most common type of oesophageal atresia
90% cases - upper portion of oesophagus ends in line pouch and lower segment forms fistula with trachea.
58
Role of surfactant
Reduces surface membrane tension of alveoli - if not enough then risk of alveolar collapse on expiration.
59
How do pulse oximeters work? Are they the best option?
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
How does haemoglobin bind oxygen?
Harm group - Fe2+ in centre of perforin ring - carries oxygen. Globin - modifies haem to allow binding to be reversible
61
What determines the shape of the oxygen dissociation curve?
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
Why does random movement result in diffusion
More molecules in area of high concentration that can move to area of low concentration.
63
What is Henry's Law?
Partial pressure = [dissolved gas]/solubility coefficent
64
What is a solubility co-efficent?
Some molecules more attracted to water than others. More attracted they are, more can be dissolved at a lowe partial pressure.
65
What is the major limiting factor in movement of gases through tissues?
Rate of gas diffusion through water
66
Factors affecting rate of diffusion through the respiratory membrane?
Membrane thickness Surface area Diffusion coefficient of gas Partial pressure difference between the 2 sides of the membrane
67
What is the diffusing capacity of the respiratory membrane
Ability of respiratory membrane to exchange gas between alveoli and pulmonary blood
68
How to measure diffusing capacity of oxygen
Measure diffusing capacity of CO and then calculate.
69
What is the Bohr effect?
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
What is the Haldane effect?
When O2 brings to haemoglobin - displaces CO2. Opposite of Bohr effect.
71
3 different mechanisms of CO2 transport in the blood
Dissolved in blood Bound to Haemoglobin as carboxyhaemoglobin Transported as a bicarbonate ion
72
How is CO2 transported as a bicarbonate ion?
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
What is sepsis and what can it lead to?
Sepsis - a systemic infection that causes vasodilation. Patient can then go into shock as not enough blood is being pushed around the body.
74
What does palmar erythema indicate
Septic shock. Blood has moved to surface due to vasodilation.
75
How many people in hospital will develop HAP? How many in ITU? How many ventilated patients?
1/100 hospital patients. 1/4 ITU patients. Almost certain to develop if ventilated for a long time.
76
How to differentiate between typical and atypical pneumonia?
No clinically reliable way
77
Highest risk groups for pneumonia
All age groups but elderly, children and the immunocompromised at higher risk
78
Typical pneumonia generally presents with
Abrupt onset, high fever, purulent sputum, focal consolidation
79
Atypical pneumonia generally presents with
Gradual onset, dry cough, myalgia, headache
80
Aspiration pneumonias mostly affect
Alcoholics Patients with impaired consciousness Patients with swallowing problems
81
What can cause pneumonias?
Bacteria Viral Fungal (Rarely) helminth/protozoa
82
Aspiration pneumonias are generally caused by
Anaerobes Gram negative enterobacteria S. aureus
83
Hospital acquired pneumonias are generally caused by
S. aureus Gram negative enterobacteria Pseudomonas Klebsiella
84
Common causes of community acquired pneumonias
Streptococcus pneumonia (60-75%) Haemophilus influenzae Mycoplasma pneumoniae
85
What pneumonia are penicillins ineffective against?
Pseudomonas
86
World's leading cause of death from infectious disease
TB
87
Risk factors for TB
``` Close contact (>8hrs/day) with infected person Immunocomprimised Homeless - 150x national average Drug/alcohol abuse Smoking Healthcare workers ```
88
What causes TB?
Inhalation of causative organism. M tuberculosis M africanum M bovis
89
Geography of TB infection
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
Presentation of primary TB
Usually asymptomatic, can be associated w. mild febrile illness.
91
Presentation of secondary TB
``` Classically: Cough Sputumn production Haemoptysis Fevers Night sweats Fatigue Weightloss ``` Can affect most organs. Elderly patients commonly have non-specific symptoms.
92
Why does TB have such an impact on developing countries?
Mostly affects adults during their most productive years
93
Appearance of TB skin
Erythema nodosum - Inflammation of the fat cells, resulting in red lumps. Generally on the shin.
94
What does TB spine cause?
Vertebral collapse
95
What does TB brain cause?
Chronic meningitis or space occupying lesions can develop
96
What does TB of the adrenal glands cause?
Addison's disease. Now rare in the UK
97
What is primary TB
``` 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
What is secondary TB?
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
What is progressive TB?
Can happen after primary or secondary TB. | TB progresses to widespread cavitations, pneumonitis and lung fibrosis.
100
What is miliary TB?
Acute, diffuse dissemination of tubercle bacilli through the bloodstream, Characteristic millet seed appearance on CXR.
101
Latent TB
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
Investigations for TB
* 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
Treatment for symptomatic TB
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
Major problem with TB treatment is
Non-compliance. Side effects mean patients are likely to stop taking.
105
Rifampicin side effects
Orange body secretions Hepatitis Thrombocytopenia Flu-like symptoms
106
Isoniazid side effects
Peripheral neuropathy Hepatitis Seizures Psychoses
107
Pyrazinamide side effects
Hyperuricaemis Hepatitis Rash Gout
108
Ethambutol side effects
Optic neuritis - can cause blindness | Rashes
109
What is a DOTS strategy?
Directly Observed Treatment, Short-course. | Drugs given by healthcare workers who observe them being taken. Greatly increases compliance.
110
Problems with TB and resistance
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.