Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CP - JL > Diseases of the Respiratory System > Flashcards

Diseases of the Respiratory System Flashcards

1
Q

what causes tb

A

Mycobacterium TB

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

What happens in primary TB

A

Macrophages phagocytose bacteria - unable to kill them
Macrophages carried back to hilar lymph nodes
Intracellular bacteria growth in bacteria
Disseminated via lymph and bloodstream

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

Where is the most common site for TB to activate

A

The periphery of the mid zone of the lung

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

What is the bodies immune response to TB

A

Mostly cell mediated (not much antibody response)
Granulomas form - central area of epitheliod and histiocyte cells - activates langerhans and macrophages to kill TB
Surrounding lymphocytic cell infiltration
Central area of caseous necrosis - fibrosis and calcification of lesions, bacilli slowly die

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

What are the primary symptoms of TB

A

Influenza like - absent/mild

Do a CXR and tuberculin skin test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How many does TB reactivate in

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is TB called when its read to the hilar lymph nodes

A

Ghon focus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do we histologically diagnose TB

A

Look for granulomas and ZN test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What other tests can we do for TB

A

Skin testing
IFN-gamma release test

But these don’t really look for the active disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What type of tissue samples do we need to test for TB

A

Fresh tissue samples

NOT formalin fixed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can cause reactivation of Tb

A 
Immunosuppression
Alcohol
Malnutrition
Western countries - men over 50
HIV
Silicosis, CRF, gastrectomy
Anti-TNF alpha drugs e.g. infliximab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is tense to keep the tomb walls strong i TB

A

TNF alpha

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

Pathogenesis of TB

A

Coalescing tubercles - central caseous necrosis

Cavitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Where does TB typically reactivate

A

In the apexes of the lungdue to highest oxygen tensions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Symptoms of secondary TB

A

Chornic productive cough - haemoptysis

Weight loss, fever, night sweats

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

How do we treat TB

A

2 months: Isonizaid, rifampicin, pyrazinamide, ethambutol/streptomycin
4 months: Izonizaid, rifampicin

Drug combination reduces risk of resistance

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

What are some extra-pulmonary sites of TB

A 
Pleura
Lymph nodes - enlalrged in chest and neck
Bone - spine
Kidneys
Epididymins
Bran/meninges
Intestine
Pericardium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How can we get intestinal TB

A

Can swallow respiratory pathogens
Or
From unpasterusied milk due to M. Bovis

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

What is atypical TB

A

Non tuberculous mycobacteria
Environmental organism
Lack of person-person complex

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

Describe the effects of mycobacterium avium complex in HIV infected

A

Disseinated disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Descrive the effects of non-HIV infected mycobacterium avid complex

A

Pulmonary TB like

Young children - cervical lymphadentitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe what happens in TB meningitis

A

Inisidious onset
personality change
focal neurological deficit
mild headache/meningism (although the typical fever, night sweats, anorexia and weight loss may be absent)

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

Where does TB multiple in TB meningitis

A

Multiplies at the base of the brain asking basilar inflammation

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

What does the BCG vaccine contain

A

Attenuated M Bovis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How to we treat atypical TB

A

Comibination
Prolonged
Macrolides - clarithromycin/azithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are two TB specific antigens

A

ESAT6

CPF10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How long do we treat extra pulmonary TB

A

Other sites except meningeal = 6 months

Meningial = 12 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What do we also give to treat meningitis and pericarditis with TB infectino

A

Corticosteroids initially

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the 2nd line drugs for TB

A

Amikaxin
Ethionamide
Cycloserine
Fluoroquinolones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are MDR TB resistant to

A

Isonazoid and rifampicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is EDR TB resistatin to

A

Isonazoid and rifampicin

Fluroquionolones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are XDR TB resistant to

A

All first line and 2nd line TB drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What type of bacteria is TB

A

Gram +ve

Slender Bacilli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are mycobacteria different to other bacteria

A

Unusual cell wall - high life content and mycolic acid
Slow growing - divide every 24 hours not 20 minutes
Different staining characteristics - poor uptake of gram stains (form ghost cells)
Retain certain stains without decolorisation by acid/alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How does treatment of mycobacteria different

A

Requires much longer courses of treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How much of the world is infected with TB

A

1/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Why has TB Increased in the developed world

A

HIV infection
Breakdown of control programmes
Increased global migration
Increased travel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What do we call TB if it has disseminated

A

Miliary TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Who does military TB occur in

A

Very young/old/immunocompromised
Primary disaease
Secondary disease - erosion of necrotic tubercle into blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Is TB a notigiable disease

A

YES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Why do we do molecular type profiles on TB

A

To workout who acquired TB from where

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What do we do if there isn’t sputa for us to culture in TB

A

Induced sputa - nevulised saline
Gastric aspirates
Renal - sterile pyuria
CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Is nucleic acid amplification - PCR good for diagnosing TB?

A

Rapid
But less sensitive tan culture
Not 100% specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What does a positive MGIT culture mean for TB

A

Shows speciation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What do the TB specific antigens not cross react with

A

M. Bovis BCG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What causes leprosy

A

M. Leprae

There two extreme clinical forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is Tuberculoid leprosy

A

Th1 type
Macules/plaques on the skin
Nerve: ulnar and common peroneal

Immune system can control it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is lepratomous TB

A

Th2 type
Subcutaneous tissue accumlation
Ear lobes: face -leonine facies

Immune system can’t control it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What can cause pulmonary vasculitis

A

Wegeners & Churg strauss - necrotizing granulomatous vasculitis
Good pastures syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is good pastures syndrome

A

Anti-glomerular basemnt membrane antibodies

Causes intra-alveolar haemorrhage and glomerunephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is bronchietctasis

A

Permanent dilation of the bronco and bronchioles caused by destruction of muscle and elastic tissue
Results from chronic necrotising tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the symptoms of bronchiectasis

A

Cough fever, and foul smelling sputum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is COPD

A

Chronic bronchitis and emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

How do we define chronic bronchitis

A

Cough and sputum for 3 months in each of 2 consecutive years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What histologically changes in chronic bronchitis

A

Mucous gland hyperplasioa and hypersecretion
Infection by secondary low virulence bacteria
Chronic inflammation
Wall weakness/destruction
Centrilobular emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is asthma

A

Chronic airway inflammation

Type 1 hypersensitivity reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the histological changes in asthma

A

Mast cell degranulation
Bronchial wall smooth muscle hypertrophy
Mucous gland hyperplasia and repsiratory bronchiolitis
Causes centrilobular emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is an interstitial lung disease

A

A disease of pulmonary connective tissue e.g the alveolar walls (inflammation and fibrosis)
It is a restrictive lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What occurs in acute interstitial lung disease

A

Diffuse alveolar damage
Death and destruction of type I pneumocytes
Hyperplasia of type II pneumocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What does acute interstitial lung disease look like histologically

A

Acute intersitial pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the symptoms of chronic interstitial lung disease

A 
Dyspnoea
Clubbing
Cachexia
Cough
Honeycombl lung
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What does honeycomb lung show

A

Chronic intersitial lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Causes of chronic interstitial lung disease

A 
Pulmonary fibrosis
Pneumoconiocsis
Sarcodosis
Silicosis
Asbestos
Hypersensitive pneumonitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is pulmonary fibrosis

A

Chronic interstitial lung disease
Usaully occurs sub pleual and lwoer lobes
Histologically intersitial pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what is sarcoidosis

A

Non caseating perilymphatic pulmonary granulomas - fibrosis
Hilar lymph nodes usually affected
Usually get hypercalcaemia and elevated ACE
Commonly young women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What would hypercalcaemia and elevated ACE indicate

A

Sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are pneumoconiocosis

A

the dust disease causing chronic interstitial lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is silicosis

A

a chornic intersitial lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How does silicosis cause disease

A

Silica kills phagocytosing macrophages
Fibrosis and fibrotic noodles in the nodes
Possible TB reactivation and increased risk of lung carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What does asbestos cause

A

Intersitial fibrosis in a usual interisitial pneuomnia fashion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What can cause hypersensitive pneumonitis aka extrinsic allergic alveolitis

A

Farmers lung - due to antimyocytes in hay
Pigeon fanciers lung to pigeon antigens

It is a type II hypersensitivity reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Are the majority of lung cancers malignant or benign

A

90% ar malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are non-small carcinomas

A

Squamous cell
Adenocarcinoma
Large cell neuroendocrine and undifferentiated large cell neuroendorcrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are small cell carcinomas

A

All neuroendocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are carcinoid tumours

A

Low grade neuroendocrine tumours - they are the low grade equicalent of small cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Are carcinoid tumours associated with smoking

A

NO - they are not malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Where do squamous carcinomas occur

A

Mostly central/main/upper lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Histologically what do squamous carcinomas look like

A

Keratinisation - look for keratin pearls
Desmosomes linking cells
Can breach basement membrane
90% occurs in smokine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What would hypercalcaemia due to PTH related peptide indicate

A

squamous carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Where do adenocarcinomas occur

A

more peripherally

they are linked to smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What produce thyroid transcription factors

A

adenocarcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Are bronchioalveolar tumours invasive

A

No they are adenocarcinoma in situ
The spread of well differentiated mucinous/non-mucionues cells on the alveolar wall

Mimics pneumonia
Uncommon to metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What defeines large cell neuroendocrine tumours

A

more than 11 mitotitic figures per 2 sqmm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Are benign or malignant pleural tumours more rare

A

Malignant

benign are rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is malignant mesothelioma associated with

A

Asbestos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

histologically what does a malignant mesothleiuom look like

A

Mixed spindle cell and epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Are metastases common in malignant mesotheliuom

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

How do we define an atypical carcinoid tumours

A

2-10 mitotic figures per 2 sqmm
Much more aggressive than typical carcinoid
70% metastasise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What cancer occurs almost exclusively in smokers

A

Small cell carcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

when do small cell carcinomas usually present

A

At a high stage with lots of metastasises

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is sigh of small cell carcinomas

A

Often release neurosecretory granules with peptide hormones e.g. ACTH

92
Q

What are large cell carcinomas

A

Poorly differentiated epithelial tumours

Can be neuroendocrine - express CD56 and neurosecretory granule proteins (synaptophysin and chromogramin)

93
Q

Common epithelium in the respiratory ttract

A

mostly pseudo stratified ciliated columnar mucous secreting spithelium

94
Q

What is respiratory failure

A

paO2 less than 8kPa

95
Q

What is type 1 respiratory failure

A

Co2 less than 6.3kPA

Hypoxic respiratory drive

96
Q

What is type 2 respiratory failure

A

Co2 greater than 6.3kPa

Hypercapnic respiratory drive

97
Q

What causes stridor

A

Upper airway obstruction - inspiratory noise

98
Q

What causes wheeze

A

distal airway obstruction - expiratory nose

99
Q

What does asbestos cause

A

Mesothelioma, lung cancer and asbestosis (a pulmonary interstitial fibrosis)

100
Q

What do primary lung tumours express

A

Cytokeratin and thyroid transcrption factor

101
Q

What do colorectal secondary tumours express

A

cytokeratin 7 negative, cytokeratin 20 positive

102
Q

what do upper GI tumours express

A

cytokeratin 7 and 20 positive

103
Q

What is metaplastic change in the bronchi

A

Change from pseudo stratified columnar to stratified squamous type that may keratizine like the skin

104
Q

What can cause metaplastic change in the bronchi

A

Irritants like smoke

105
Q

What is thought to be precursors to neuroendocrine lung cancers

A

Carcinoid tumourlets

106
Q

What type of carcinoid tumours are likely to metastasise

A

The atypical carcinoid tumours

typical carcinoid tumours are not benign but distant metastases are rare

107
Q

Differences between typical and atypical carcinoid tumrous

A

typical - grow centrally, organoid bland cells, no necrosis, less than 2 mitotic fiures, associated with multiple endocrine neoplasia syndrome type 1, not associated with smoking

atypical - necrosis, 2-10 mitotic figures per 2 sq., much more aggressive than typical carcinoids

108
Q

How many mitotic figures in large cell neuroendocrine carcinomas

A

More than 11

109
Q

5-hydroxyptamine comes from what type of tumours

A

Carcinoma

110
Q

What is the epidermal growth factor receptor (EGFR) mutations

A

Sensitising mutations in 10% of small cell lung carcinomas

More common in non-smoking and asian women

111
Q

What can we do to treat EGFR

A

use EGFR-tyrosin kinase inhibitors

E.g. Geftinib and Erlotinib

112
Q

What is the analplastic lymphoma kinase gene rearrangement

A

Variable break point on short arm of chromsome 2
Fuses ALK and EML gene
Activates ALK tyrosine kinase

113
Q

who is ALk gene rearrangements seen in

A

Seen in 10% of lung adenocarcinomas

common in non-smoking asian and women

114
Q

What is Crizotnib

A

An ATP analogue that inhibits the ALK gene rearrangement

115
Q

What happens in mesotheliomas

A

Initial noduel and effusion
Later obliterates the pleural cavity growing around the lung - invades the chest wall and lung

But metastasis are loss common

116
Q

How can we differentiate mesotheliomas from adenocarcinomas

A

Due to cellular antigen expressoin

117
Q

what is typical of early malignant mesotheliomas

A

Small plaques on the parietal pleura - difficult to image and tipsy but may produce significant pleural effusion

118
Q

Where do fibrous pleural plaques occur

A

ON lower thoracic wall and diaphragmatic parietal pleura

Associated with low level asbestos exposure - not pre-malignant

119
Q

What is a common cause of bronchopneumonia

A

Often secondary due to compromised defences

often low virulence bacteria or occasionally fungi

120
Q

What causes 90% of lobar pneumonia

A

Strep pneumonia

Uncommon to get confluent segments, red then grey hepatisation, resolution without scarring

121
Q

Who gets klebsiella penumonia

A

Elderly, diabetic and alcoholics

122
Q

What are the TB granulomas like

A

Multinucleated langerhans cells and giant cells and caseous necrosis

123
Q

What type of hypersensitivity reaction is the tuberculin skin test

A

Type IV cell mediated

124
Q

What are the 3 types of emphysema

A

Centrilobular/acinar - due to coal dust and smoking
Panlovular
Paraseptal - upper lobe, sub pleural bullae adjacent to fibrosis, pneumothrax if rupture

125
Q

What is common in the majority of pan lobular emphysemas

A

Anti-trypsin deficienct

126
Q

Do interstitial lung disease increase or decrease lung compliance

A

decrease

127
Q

Where is the cystic fibrosis mutation

A

Mutation in CFTR gene on chromosme 7

128
Q

Cf in the lung

A

Bronchioles distended with mucous
Hyperplasia mucus secreting glands
Multiple repeated infections
Severe chronic bronchitis and bronchiectasis

129
Q

CF in the pancreas

A

exocrine gland and ducts plugged by mucous
Atrophy and fibrosis of the gland
Impaired fat absorption, enzyme secretion, vitamin deficiincies

130
Q

CF in the small bowel, liver, salivary glands and reproductive tract

A

Small bowel - meconium ileus
Liver - plugging of bile cannaliculi causing cirrhosis
Salivary glands - similar to pancreas - atrophy and fibrosis
95% of males infertile

131
Q

How does CF present

A

Abnormallly visous mucus
failure to thrive
pancreatic insufficiency
recurrent intestinal obstruction

132
Q

What is a LRTI

A

An infection below the larynx

133
Q

What are the 4 types of pneumnia

A

Hospital acquired
Community acquired
Ventilator acquired
Aspiration

134
Q

Is the LRTI sterile or non-sterile

A

Should be sterile

135
Q

What can predisspose us to LRTI

A

Loss or supression of cough reflex/swallo
Ciliary defects
Mucuous disroders
Pulmonary oedema
Immunodeficiency
Macrophage function inhibition e.g. smoking

136
Q

What is pneumonia

A

Infection of the lung parenchyma

137
Q

How does acute bronchitis present

A

Cough - dry and retrosternal pain
Dyspnoea
Tachypnoea

138
Q

When is acute bronchitis common

A

Most frequent in winter in children under 5

139
Q

What are the common causes of acute bronchitis

A

Viral - most common, rhinovirus, influenza etc

Bacterial - less common, h. influenza, pneumonia, pertussis

140
Q

How do we treat acute bronchtiis

A

Supportive treatment if healthy
Oxygen and respiratory support if they have a severe diseae or co-morbidity
Antibiotics only if proven bacterial cause

141
Q

How do we diagnose acute bronchitis

A

Diagnostic tests not usually done if mild

If needs be do respiratory secretion to look for a specific cause

142
Q

What is associated with chronic bronchitis

A

Smoking, pollution, allergens

Most common in men and over 40s

143
Q

mediators of chronic bronchitis

A

IInflammation and oedema of airways mediated by exogenous irritants rather than infective agents

Patients can have acute exacerbations mediated by the same infected pathogens

144
Q

If you have obstructed airflow on spirometry and chronic bronchitis what does this mean

A

You have COPD

145
Q

Who does bronchiolitis affect

A

Many childrn
Winter and early spring
Infatns 2-10months

146
Q

What is bronchiolitis

A

Inflammation and oedema of the bronchioles

147
Q

How does bronchiolitis present

A

Acute onset wheeze
Cough
Nasal discharge
Respiratoy distress (grunting, retractions, nasal flaring)

148
Q

What is the most common cause of bronchiolits

A

RSV - 75% of cases

149
Q

How do we diagnose bronchiolitis

A

Chest X-ray

Microbiological diagnsosis - nasopharyngeal aspirate send for viral PCR

150
Q

What is penumonia

A

Infection affecting the most distal airways and alveoli

151
Q

What are the 2 anatomical patterns of pneumonia

A

1) bronchopneumoina - patchy dsitribution of pus centred on inflamed bronchioles and bronchi then subsequent spread to surrounding alveoli

2) Lobar - often affects a large part of entirety of the lobe, 905 due to S. pneumonia
Has a clear line of demarkation

152
Q

Define hospital acquired pneumonia

A

Developed after 48 hours are hospital admissions

If after 5 days think enterbacteriacaece and pseudomonas

153
Q

What is ventilator acquired pneomonia

A

Develops after 48 hours after ET intubation and ventilation

154
Q

Define aspiration pneumonia

A

Resulting from abnormal entry of fluids into the lower respiratory tract
Patient usually has impaired swallow mechanisms

155
Q

Common cause of CAP

A

Person - person (s. pneumonia and h. influenza)
Environment (L. pneumophilia)
Animals (c. pistacci)

156
Q

How can we split CAP

A

Into typical atypical

157
Q

What is atypical CAP

A

Fail to respond to penicillin or sulpha drugs

Mycoplasma pneumonia, legionella, chlamydia, coxiella

158
Q

What is typical CAP

A 
S. pneumonia
H, Influenza
Moraxella
Staph aureus
Klebsiella
159
Q

Presentation of bacterial CAP

A 
Rapid onset
Fever/chills
Productive cough, mucupurulent sputum
Pleurtic chest pain
General malaise

Signs: Tachypnoea, tachycardia, hypotension
Dull to percuss, reduced air entry, bronchial breathing

160
Q

Presentation of Mycobacterium Pneumonia

A

Autumn epidemics
Common in children and young adults
Main symptom is cough
Diagnose with serology

161
Q

Complications of mycobacterium pneumonia

A

Guillian Barre

Peripheral neuropathy

162
Q

Causes of legionella pneumophilia

A

Colonises water pipes

Outbreaks associated with shoes, air conditioning units and de-humidifiers

163
Q

Presentation of legionella pneumophilia

A 
High fevers
rigors
dry cough
Dyspnoea
Vomiting, diarrhoea
Confusion
164
Q

Blood results of legionella pneumophilia

A

Deranged LFTs

SIADH (low sodium)

165
Q

Presentation of chlamydophilia pneumonia

A

More common in elderly

Causes mild penumonia or bronchitis in adolescents and young adults

166
Q

What is chlarmudphilia psittaci associated with

A

Exposure to brds
Consider in those with pneumonia, splenomegaly and history of bird exposure

May also have rash, hepatitis, haemolytic anaemia and reactive arthritis

167
Q

How does influenza present

A

Fever, headache, myalgia, dry cough, sore throat

Convalescence can take 2-3 weeks

168
Q

Who is primary viral prenumonia more common in

A

Those with existing cardiac and lung disorders
Cough, brethaless and cyanosis

secondary bacterial pneumonia may develop after initial period of improvement

169
Q

How do we diagnose influenae

A

PCR

170
Q

Investigations for CAP

A

Sputum gram stain and culture
Blood culture
Pneumococcal and regionally urinary antigen
PCR for viral pathoens, mycoplasma pneumonia and chlamydophilia

171
Q

How to assess severity of CAP

A

CURB

C-confusion
U-Urea
Resp rate
Blood pressute

172
Q

How to prevent LRTIS

A

Pneumococcal vaccinations - patients with chronic heart, lung and kidney disease, may repeat after 5 years

Influenza vaccine

173
Q

Normal URTI flora

A

Strep Viridans
commensal neisseria
Diphterioids
Anaerobes

174
Q

Is nesseiria meningitidis a commensal URTI flora

A

No but can be carried asymptomatically

175
Q

What do get colonisation of in the URTI post antibitoics

A

Pseudomonas and candida

176
Q

How are most URTI transmitte

A

Mainly droplets affecting v. young children and teenagers in winter/viral infections

177
Q

Treatment of URTI

A

1) no treatment
2) delay prescribign
3) only prescribe if risk of complication

178
Q

What causes common cold

A

rhinovirus

also coronoviruses, RSV, enterovirus, parainfluenza, adenovbirus

179
Q

Treatment of common cold

A

No treatment

180
Q

What rhino-sinusitis

A

Post - viral ingection

May also be allergy or non-infective

181
Q

Symptoms of rhino-sinusitis

A

Facial pain
Nasal blockage
Smell Reduction

182
Q

Causes of rhino-sinusitis

A

Secondary bacterial infection from strep pneumonia, ham influenza, strep milleri, anaerobes

183
Q

What are the 3 main microbes causing URTI

A

Strep pneumonia, haem influenza, morexalla catarrhallis

184
Q

What does chronic sinusitis cause

A

osteomyletis, meningitis, cerebral abscesses

185
Q

How do we test for rhino-sinusitis

A

Ct/MRI/X-ray to check fluid level

186
Q

Treatment of rhino-sinusitis

A

Sinus washout - relieves sympomts

Only give antibiotics if proven bacterial

187
Q

What are more the main causes of pharyngitis

A

Viral - RSV, influenza, adenovirus, EBV, HSV1

Bacteria - Strep pyogenes, rarely gonorrhea

188
Q

Symptoms of tonsilits

A

Red tonsils, dysphagia, fever, headache, uvula and exudate, lymphadenopathy

189
Q

Common cause of tonsillitis in children

A

Group A strep infections

Complications of glomerulonephritis and rheumatic/scarlett faever
Supparative complicatinos e.g. ear infection

190
Q

Treatment of tonsillitis in children

A

Penicillin to prevent

191
Q

Symptoms of mono/glandular fever

A

fever and cervical lmphadenopathy

complication: splenic reupture

192
Q

Treatment to avoid in glandular fever

A

ampicillin - get mac-pac rash that is mistaken for allergy

193
Q

diagnosis of mono

A

IgG serology

Paul Brunell test/ PCR

194
Q

What cause diphteria

A

Corynebacterium Diphterhia

195
Q

Symptoms of diphtheria

A

malaris, fever, sore throat

196
Q

Treatment of diphtheria

A

Treat complications with erythromycin/penicillin/antitoxin

197
Q

When do we usually get candida tonsilitis

A

after antibiotics or steroids

198
Q

Symptoms of eppiglotitis

A 
Children 2 -4
Fever
Difficulty speaking (hot potato)
Droolig
Stridor, hoarse
199
Q

Most common cause of epiglottitis

A

H. influenza type B

Now rest bacteria and s. aurues

200
Q

Diagnosis of epiglottitis

A

Lateral neck x-ray - enlarged epiglottis

NOTE do not take swab/examine epiglottis unless intubated

201
Q

Usual cause of acute laryngitis

A

Usually viral or one of the typical 3 bacteria

202
Q

Symptoms of acute laryngitis

A

hoarse voice, globus pharyngitis, fever, myalgia, dysphagia

203
Q

Non infective causes of laryngitsi

A

voice over use and malignancy

204
Q

Cause of croup/acute laryngtracheobronchitis

A

Viral - parainfluenza type 2 and RSV

205
Q

Symptoms of croup

A

Children
Inflammation of larynx and trachea after URTI
only treat symptoms

206
Q

What causes whooping cough

A

Bordatella pertussis

Gram I’ve coccobacillus

207
Q

2 stages of whooping cough

A

1) catarrhal - runny nose, f ever, malaise

2) whooping - a week later with dry non productive cough on exhalation

208
Q

Complications of whooping cough

A

otitis media, pneumonia (secondary or aspiration), convulsions or subconjunctival haemorrhage

209
Q

Treatment of whooping cough

A

Erythromycin (give to household contacts too)

210
Q

What is otitis externa

A

Infection of the external auditor canal

211
Q

Symptoms of otitis eterna

A

Painful, itch, swelling, erythema, otorrhea

212
Q

Causes of acute otitis externa

A

S. aurues or pseudomonas (likely after swimming)

213
Q

Treatment of acute otitis externa

A

Toilet with saline treatment, wick insertion, topical drops

214
Q

Cause of chronic otitis externa

A

Irritation from dram drainage from perforated tympanic membrane

215
Q

Treatment of chronic otitis externa

A

Treat underling cause

Avoid aminoglycosides!! if perforated can cause deafness

216
Q

Cause of malignant otitis externa

A

Pseudomnas aeruginosa
Sever necrotizing, may invade bone/cartilage
Pain and pus
Elderly and immunocompromised more vulnerbale

217
Q

Treatment of malignant otitis externa

A

4-6 weeks and ceftazidime and ciprofloxacin if pseudomonas is the cause

218
Q

Symptoms of otitis media

A 
Common in children
Fever
Pain
Impaired hearing
Red bulging tympanic membrane
219
Q

Causes of otitis media

A

Usually viral or one of the 3 bacteria

220
Q

Treatment of otitis media

A

Supportive or amoxicillin if one of the 3 bacteria

221
Q

What is mastoiditis

A

Inflammation of the mastoid air cells after middle ear infection
Pus collect is cells - may lead to necrosis

222
Q

Signs of mastoiditis

A

Same as acute otitis media BUT pain/swelling over mastoid bone

223
Q

How do we assess mastoiditis

A

Bacteria samples and CT scan

224
Q

How do we treat mastoidis

A

Prolonged antibitics if bone infection

Co-amoxiclav first line treatment

225
Q

What is vin cents angina

A

Deep fascial infections of the head and neck (ludwig and leemers also be aware of)

226
Q

What is similar to concerts angina

A

Ginguvitis and periodontal infections - but we aren’t dentists

227
Q

What do we use to treat vincetn angina

A

penicillin and amocivillin

CP - JL (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions