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year 1 flash cards > clinical symposia - respiratory strand > Flashcards

clinical symposia - respiratory strand Flashcards

1
Q

What are symptoms of asthma?

A

Wheeze, shortness of breath, chest tightness, cough (particularly at night or in early morning), difficulty sleeping, chest pain, vomiting, tremor/hoarse voice

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2
Q

What structures are affected by asthma? How?

A
  • inflammation of the airway
  • hyper-reactive smooth muscle
  • increased basal tone (increased contraction of vessels)
  • mucus hypersecretion
  • mucosal oedema (build up of tissue fluid in the mucosa)
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3
Q

Is asthma a restrictive or obstructive pulmonary disease?

A

Obstructive

The lungs are unable to expel air effectively during exhalation

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4
Q

What would you predict the FEV1/FVC ratio to be?

A

Reduced

As with all obstructive lung disease

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5
Q

Is there likely to be any significant airway reversibility?

A

Yes

Although the airway narrowing is recurring, treatment can reverse this.

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6
Q

How is asthma monitored?

A

Spirometry

Used to measure narrowing of the airways before and after medication.

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7
Q

What signs of asthma may be elicited?

A
  • FEV1/FVC ratio (reduced, measured through spirometry)
  • FeNO test (measures levels of NO in breath showing lung inflammation)
  • Reduced peak flow compared to other individuals of the same age, sex and height
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8
Q

Why may someone with asthma present with a hoarse voice or a tremor?

A
  • overuse of beta agonists
  • overuse of steroids

(Beta agonists can cause a tremor and steroids can cause oral candida, especially if technique is poor)

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9
Q

What is a feature of life-threatening asthma?

A

Paradoxical pulse

this is a large decrease in systolic pressure and pulse wave amplitude during inspiration

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10
Q

What is immediate treatment for an asthma attack?

A
  • oxygen - aim for saturation of 94-98%
  • salbutamol 5mg via an oxygen driven nebuliser
  • ipratropium bromide 0.5mg
  • prednisolone tablets 40-50mg or IV hydrocortisone
  • no sedatives
  • chest x-ray
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11
Q

What triggers asthma?

A
  • tobacco smoke
  • allergens such a dust mites and pets
  • pests
  • mould
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12
Q

How can asthma be managed?

A

Treatment such as relievers or preventers

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13
Q

What are examples of reliever treatment for asthma?

A

Beta-2 adrenoceptor agonists such as salbutamol
- stimulation of airway B2 adrenoreceptors results in relaxation of bronchiole smooth muscle

Antimuscarinics such as ipratropium bromide
- inhibit muscrarinic receptors on smooth muscle causing relaxation of bronchiole smooth muscle

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14
Q

What is an example of a preventer treatment for asthma?

A

Glucocorticoids

  • bind to cytosolic receptors and affect gene transaction and transcription
  • production of potent anti-inflammatory agents and reduce airway hyper-resposonsiveness
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15
Q

Describe the difference between asthma and COPD

A
  • nearly all COPD patients smoke
  • symptoms under 35 more common in asthma
  • chronic productive cough more common in COPD
  • breathlessness is persistent and progressive in COPD
  • variability is more common in asthma
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16
Q

What are the two types of asthma?

A
  • extrinsic (childhood, family history, episodic, positive skin conditions)
  • intrinsic (adulthood, negative skin test, no clear precipitating factors)
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17
Q

What are risk factors of asthma?

A
  • genes
  • maternal smoking
  • pollution
  • obesity
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18
Q

What reduces asthma risk?

A
  • breast feeding

- early exposure to animals

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19
Q

what kind of pulmonary disease is COPD

A

obstructive pulmonary disease

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20
Q

is there any reversibility in COPD

A

no

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21
Q

is COPD of slow or fast progression?

A

slowly progressive

significant airflow obstruction may be present before person aware

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22
Q

how does COPD affect the airways

A
  • chronic inflammation

- large and small airway narrowing

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23
Q

what are 2 the symptoms of COPD

A
  • abnormal mucous (due to irritation/ infection)
  • cough (smokers cough)
  • breathlessness (dyspnoea)
  • sputum production (green)
  • wheeze
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24
Q

what is there main risk factor for COPD?

A

smoking

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25
Q

what is the main disease also associated with COPD

A

emphysema

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26
Q

how does emphysema effect the lungs?

A
  • abnormal, permanent enlargement of airspaces distal to the terminal bronchiole
  • accompanied by destruction of their walls
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27
Q

what is the main symptoms of emphysema and why is this

A

significant breathlessness due to airway collapse in exhalation

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28
Q

what are the risk factors for emphysema and COPD?

A
  • smoking
  • pollution
  • family history (Alpha1-antitrypsin deficiency )
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29
Q

what is alpha1-antitrypsin?

A

glycoprotein produced in liver
protease inhibitor which balances out the action of neutrophil elastase
(some neutrophil elastase needed to clear out debris in alveoli , not too much)

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30
Q

what is alpha1-antitrypsin defiancey?

A

autosomal recessive deficiency in chromsome 14

co-dominant alleles

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31
Q

what can 2 things other than alpah1-antitrypsin effect the amount of neutrophil elastase?

A

smoking

infection

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32
Q

why is abnormal amounts of neutrophil elastase bad?

A

can get trapped in the lungs and cause liver disease

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33
Q

What is bronchiectasis?

A

A disease characterised by a structural abnormality of irreversibly dilated bronchi and large amounts of sputum

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34
Q

What are the types of bronchiectasis?

A
  • cylindrical bronchiectasis (airways don’t taper. They are dilated right out to the periphery)
  • varicose bronchiectasis (tubes get smaller and larger like veins in varicose veins
  • cystic bronchiectasis (fluid in bronchioles)
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35
Q

What would you see on the chest x-ray of an individual with bronchiectasis?

A
  • dilated airways

- signet ring sign showing that the bronchus is larger than the pulmonary artery

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36
Q

What conditions are associated with bronchiectasis?

A
  • cystic fibrosis
  • rheumatoid arthritis
  • immunodeficiency
  • childhood infections such as pneumonia, TB and measles
  • primary ciliary dyskinesia
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37
Q

What are 6 causes of bronchiectasis?

A
  1. Post infection (measles, whooping cough, TB, pneumonia)
  2. Immune deficiency
  3. Allergic bronchopulmonary hypogammagobulinemia ( increased levels of a certain immunoglobulin causing inflammation)
  4. Defective clearance eg in CF or PCK
  5. Aspirations of toxic substances
  6. Mechanical eg tumour (distal bronchiectasis), lymph node (middle lymph node syndrome) or foreign body
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38
Q

What are symptoms of bronchiectasis?

A
  • persistent purulent sputum (purulent = contains puss)
  • haemoptysis
  • breathlessness
  • wheeze
  • sinusitis and nasal symptoms
  • weight loss
  • pleurisy (inflammation of the pleura)
  • nasal polyps
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39
Q

What are signs of bronchiectasis?

A
  • clubbing
  • coarse crackles
  • wheeze

Some people display no signs and bronchiectasis can only be seen on a CT scan

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40
Q

What is clubbing?

A

Tissue at the base of the nail is thickened so the normal angle between the nail base and adjacent ski is obliterated

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41
Q

What are signs of clubbing?

A
  • fluctuation and softening of the nail bed (boggy)
  • loss of angle between the nail bed and fold
  • increased convexity of the nail fold
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42
Q

What conditions are associated with clubbing?

A
  • bronchiectasis
  • lung cancer
  • cystic fibrosis
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43
Q

What investigations can be carried out into bronchiectasis?

A
  • history
  • genetics
  • ciliary beat frequency/ nasal NO
  • sperm analysis
  • sputum (MC&AFB, fungal)
  • autoantibody screen
  • aspergillosis antibodies
  • immunological review
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44
Q

What are treatments for bronchiectasis?

A
  • physiotherapy/ airway clearance
  • mucolytics/ hypertonic saline
  • prompt oral antibiotics
  • IV antibiotics as required
  • nebulised antibiotics
  • annual influenza vaccine
  • immunoglobulin replacement
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45
Q

what kind of disease inheritance is CF?

A

autosomal recessive

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46
Q

what was the first mutation discovered for the CFTR protein?

A

mutation in DF508

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47
Q

what does mutation in DF508 cause?

A
  • deletion of 3 nucleotides spanning positions 507-508 of CFTR gene
  • = loss ignite codon for AA Phe
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48
Q

why is the class of mutation in the CFTR protein key?

A

dictate the therapy undertaken

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49
Q

where are CFTR proteins expressed?

A

airway epithelial cells

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50
Q

on what chromosome is the CFTR gene?

A

chromosome 7

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51
Q

what kind of protein is the does the CFTR gene code for and what’s its function?

A

ion transport channel

regulate chloride bicarbonate and Na transport

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52
Q

what are the effects of the DF508 mutation on the CFTR protein?

A
  • protein produced is abnormal
  • broken down in airway epithelium
  • no CFTR expression
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53
Q

what does the breakdown of the CFTR protein lead to?

A

cant secrete chloride and bicarbonate –> lose inhibitory effect of Na transport –> increased Na absorption –> increased water absorption –> dehydration of airway surface liquid

54
Q

what is mucocillary clearance?

A

protective mechanism that protects the lung from invade particles
particles stick to mucous, propelled to back f throat and swallowed

55
Q

what is ciliopathy?

A

where cilia don’t function properly

56
Q

what does airway surface dehydration cause?

A

-mucocillary disfunction - abnormal mucous Clearence

57
Q

apart from mucocillary disfunction what else can cause abnormal mucous clearance?

A

abnormal mucous and production of DNA from degenerating neutrophils = make secretions very sticky - accumulate in airways

58
Q

what causes mucocillary disfunction ?

A
  • predisposition to infection

- CF also associated with increased inflammatory response which itself causes lung damage

59
Q

is the CFTR gene found all around the body? if so, where?

A 
yes
pancreas
liver 
digestive tract
reproductive tract
skin 
nasal cavity 
lungs
60
Q

why is CF considered a multi system disease?

A

protein found all around the body
can cause:
liver disease, artists, pancreatic insufficiency, male infertility ect

61
Q

how does airway dehydration effect the airway liquid and what is the significance of this?

A

abnormal pH

leads to abnormalities in defensive protein used in infection

62
Q

what are the consequences of airway dehydration?

A 
airway inflammation 
airway infection 
viscous secretions 
lung destruction 
bronchiectasis
63
Q

what is the main test we use to diagnose CF

A

sweat test

-Chloride >60mmol/l (milder cases 30-60

64
Q

why do CF victims have a higher salt content in their sweat and how can we recogniser this ?

A
  • Defective Na/Cl absorption means high sweat salt content
    high amount of Na and Cl as duct impeccable to water absorption
    white crystals form when they sweat
65
Q

what investigations can we do for CF

A
  • genetics- dictate treatment
  • pancreatic function(pancreatic malabsorption, test for faecal elastase, low levels = CF)
  • sperm (obstructive azoospermia)
  • CT scan for bronchiectasis
66
Q

what differnt therapies do we use for CF?

A
  • nebuliser antibiotics
  • oral/ IV antibiotics
  • DNase
  • hypertonic saline
  • pancreatic enzymes
  • insulin ( endocrine disfunction of pancreas too)
  • CFTR modulators
  • Ursodeocycholic acid – reduce liver disease
67
Q

what do nebuliser antibiotics do?

A

fine mist inhaled- eradicate bugs that come up and treat chronic infection such as pseudomonas

68
Q

what are the symptoms of CF?

A
  • Pulmonary exacerbation
  • Increased cough
  • Increased sputum production
  • Change in sputum colour
  • Fever / malaise
69
Q

why may we get a collapsed upper lobe in CF?

A

due to thick secretions

70
Q

what are the signs of CF

A
  • Clubbing
  • Coarse crackles
  • Wheeze
  • Lost weight - infections and pancreatic malabsorption
  • 30% adult have CF diabetes
  • Vision due to vitamin A deficiency
71
Q

is family history important in CF?

A

CRITICAL!!

72
Q

how many different classes of infections do we have for CF and which are the most common?

A

7 classes

2 and 3 most common

73
Q

what is the effect of class 2 mutations on CFTR gene?

A

protein so abnormal not expressed - EG. DF508

74
Q

what is the effect of class 3 mutations on CFTR gene?

A

Called acting mutations - only partially functioned but still expressed

75
Q

what drug do we use for class 3 CFTR mutations

A

CFTR potentilator

76
Q

can we use drugs for class 2 CFTR mutations and if so what?

A

harder as protein not expressed:

  • Tezacaftor/ Lumacaftor + ivacaftor used to increase expression, but this not potent
  • Triple therapy addition of : elaxacaftor to tezacaftor(stabilise and express protein) and invacaftor (mature protein) - significantly effective
77
Q

What are the key symptoms of pneumonia?

A
  • progressive breathlessness
  • ankle swelling
  • cough with green sputum
78
Q

What is the FEV1 and indicator of?

A

FEV1 is a sensitive indicator of lung function

79
Q

What patients are suitable for LTOT (long term oxygen therapy)?

A
  • patients with COPD who have a PO2 <7.3kPa when stable
  • PO2 > 7.3 kPa and <8 kPa when stable and one or more of the following
    — secondary polycythaemia
    — nocturnal hypoxaemia
    — peripheral oedema
    — pulmonary hypertension
80
Q

What is a type 1 respiratory failure?

A

Hypoxia

  • PCO2 normal
  • V/Q mismatch
81
Q

What is a type 2 respiratory failure?

A

Hypoxia and hypercapnoea

  • inadequate alveolar ventilation
  • PCO2 high
82
Q

What does hypoxic drive mean in the context of COPD?

A

The patient needs low oxygen in order to breathe

83
Q

What are the types of COPD?

A
  • pink puffer: maintain normal blood gas at the expense of breathlessness and often with skeletal muscle wastage
  • blue bloater: less breathlessness , but at the expense of abnormal blood gas tensions and right heart failure
84
Q

What are treatments for COPD?

A
  • beta agonists
  • anticholinergic agents
  • inhaled steroids
  • antibiotics
  • mucolytics
  • flu vaccination
  • non-invasive ventilation
  • LTOT
  • pulmonary ventilation
  • lung volume reduction surgery
85
Q

what are the two types of lung cancer?

A

small cell and non-small cell

86
Q

what symptoms are there of lung cancer?

A 
cough
breathlessness
wheeze
stridor (noisy breathing)
haemoptysis 
swallowing difficulties
hoarse voice
chest pain
anorexia
bone pain
neurology
weight loss
87
Q

what are the signs of lung cancer?

A 
weight loss
clubbing
tachypnoea
signs of collapse
lymphodenopathy
SVC obstruction
horner's syndrome
metastatic spread
88
Q

wat is horner’s syndrome?

A

interruption of sympathetic nerve supply to the eye

  • miosis (constricted pupil)
  • partial ptosis (droopy eyelid)
  • anhidrosis (loss of hemifacial sweating)
89
Q

what is SVC obstruction?

A

superior vena cava obstruction

  • large tumours can surround the trachea and block the SVC
  • can cause engorgements - little veins on skin as like with a blocked river, tributaries will form
90
Q

what investigations can you do for lung cancer?

A 
chest x ray
CT scan
PET scan
bronchoscopy
EBUS
perataneous fine needle aspiration
mediastinoscopy
VATS
91
Q

what will a chest x ray do with lung cancer?

A

can usually (70-80% of cases) see the tumour clearly

92
Q

what will a CT scan do with lung cancer?

A

good for confirming diagnosis and staging (can see if there is metastasis)
also in screening for early tumours

93
Q

what will a PET scan do with lung cancer?

A

positron emission tomography

  • system detects gamma rays emitted by a tracer
  • FDG (flurodeoxyglucose)
  • indicates tissue metabolic activity –> can see if benign or malignant and if it has metastasised
94
Q

what will a bronchoscopy do with lung cancer?

A

70% of tumours arise in large bronchi and so can be seen and biopsied by bronchoscopy

  • can take brushing of cells
  • can also go in with forceps and grab a chunk of tumour
95
Q

what is EBUS and for lung cancer?

A

endobronchial ultrasound

  • ultrasound at end of bronchoscope
  • can put needle in lymph nodes to get direct samples
96
Q

what is perataneous fine needle aspiration?

A

for tumours not reached through bronchoscope

CT guided through chest wall to get sample

97
Q

what is mediastinoscopy?

A

looks at mediastinum

98
Q

what is VATS?

A

video assisted thoracoscopic surgery

- telescope between lung and parietal pleura to see outside of lung (good for mesotheliomas)

99
Q

what is treatment for small cell lung cancer?

A

chemotherapy and radiotherapy

100
Q

what is treatment for non-small cell lung cancer?

A

surgery and radiotherapy

chemotherapy for certain tumours

101
Q

can you have targeted drug treatment for lung cancer?

A

advanced cancers

epidermal growth factor receptors in response to chemotherapy in non-small cell

102
Q

what is the survival of lung cancer?

A

one of the lowest survival rates of cancers due to late diagnosis in 2/3 patients

103
Q

what are the causes of lung cancer?

A 
90% due to smoking (increase risk by 8-20 fold)
asbestos exposure
radioactive materials (radon gas)
pyrene, arsenic, nickel, napthalenes
family history
104
Q

what is a paraneoplastic syndrome?

A

syndrome that is a consequence of cancer in the body due to production of chemical signalling molecules (eg hormones) by tumour cells or the immune response to tumour

105
Q

what is ectopic cushings syndrome caused by?

A

ectopic ACTH and ACTH-like substance

106
Q

what is hyponatremial reversible confusion caused by?

A

antidiuretic hormone

107
Q

what is hypercalcaemia caused by?

A

parathyroid hormone-related protein

108
Q

what is pulmonary embolus state caused by?

A

hypercoaguable state

109
Q

what is a pleural effusion?

A

build up of fluid between parietal and visceral pleura

110
Q

what is an exudate pleural effusion?

A

greater amounts of protein

malignancy and infection

111
Q

what is a transudate pleural effusion?

A

lesser amounts of protein

heart failure and nephronic syndrome

112
Q

what is an empyema?

A

inflammatory cells and pus in pleura

113
Q

what is a hydropnuemothorax?

A

pneumothorax and fluid

114
Q

what is a heamothorax?

A

blood in pleura

115
Q

what is chylothorax?

A

lymph in pleura

116
Q

what is pneumonia?

A

an acute lower respiratory infection associated with recently developed radiological signs

117
Q

how can the flu lead to pneumonia?

A

can develop into secondary Bacterial Staphylococcus infection

118
Q

who does pneumonia affect the most?

A

the very young and elderly

119
Q

what are the symptoms of pneumonia?

A 
progressive breathlessness
fever with shivering attacks
left sided sharp pain
general lethargy
chest pain - pleurisy
120
Q

what is pleurisy?

A

sharp pain which is worse on inspiration caused by inflammation of the pleura (basically them rubbing together like sandpaper)

121
Q

what are the signs of pneumonia?

A 
hot, flushed with periferal dilation
chest is dull to percussion and increased breath sounds 
crackles
pleural rub
hypotension
122
Q

why may pneumonia cause hypotension?

A

inflammatory stimulus
decreasing peripheral arterial resistance
cardiac output increases

123
Q

give some organisms that could cause pneumonia?

A 
bacteria - streptococcus pneumoniae, haemophilus influenza, staphylococcus aureus, gm neg bacteria
influenza
chlamydia pnuemoniae and psttaci
legionella pnuemophila
mycoplasma pneumoniae
124
Q

how do you treat pneumonia?

A 
antibiotics/antivirals
O2
analgesia for chest pains
fluids
physiotherapy
nutrition
stop smoking
125
Q

what is the scoring system for predicting complications of pneumonia?

A 
CURBA
Confusion
Urea
Respiratory rate
Blood pressure
Age
126
Q

what test is used for confusion in CURBA?

A

abbreviated mental test

127
Q

what age is risk in CURBA?

A

over 65

128
Q

what CURBA score would be ok for home treatement?
short stay in hospital?
defo hospital as likely severe?

A

0/1
2
3 or more

129
Q

what complication could arise from pneumonia?

A

empayema - pleural effusion of bacteria

130
Q

what is the treatment for empayema?

A

pleural aspiration and drain (may require VATS/ surgery)

TPA to break up empayema for drainage

year 1 flash cards (23 decks)

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