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Year 3 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

symptoms of asthma

A

intermittent dyspnoea, wheeze, cough (often nocturnal), sputum

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2
Q

signs of asthma

A

tachypnoea, audible (widespread, polyphonic) wheeze, hyper inflated chest, hyper-resonant percussion more, decrease air entry,

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3
Q

def dyspnoea

A

shortness of breath

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4
Q

def tachypnoea

A

rapid breathing

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5
Q

tests run for acute attack of asthma

A

PEF
sputum culture
FBC, UE, CRP, blood cultures

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6
Q

tests run for chronic asthma

A

PEF
spirometry
CXR
identifying allergens: skin prick tes, histamine challenge, Aspergillus serology

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7
Q

asthma differential diagnosis

A 
pulmonary oedema ('cardiac asthma')
COPD
large airway obstruction (foreign body, tumour etc)
SVC obstruction, pneumothorax, PE, bronchiectasis, obliterative bronchiolitis
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8
Q

which vaccines to get with asthma

A

influenza and pneumococcal

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9
Q

def peak expiratory flow rate

A

maximal rate that a person can exhale during short maximal expiratory effort after a full inspiration

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10
Q

what are the pathological changes in asthma

A
  • smooth muscle and submucosal glands hypertrophy and hyperplasia
  • infiltration of eosinophils, mast cells and neutrophils
  • globlet cell metaplasia + loss of epithelium (–> mucus plug)
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11
Q

factors contributing to airway narrowing in asthma

A
  1. bronchial muscle contraction
  2. mucosal swelling/inflammation (mast cells and oesinophil degranulation –> release of inflammatory mediators)
  3. increase mucus production
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12
Q

precipitants in asthma

A

-cold air and exercise
-emotion
-allergens
-pollution and irritant dusts, vapours and fumes
-drugs (NSAIDs, beta-blockers)
-diet
infection, smoking exacerbate it

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13
Q

What range should body pH be kept

A

7.35-7.45

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14
Q

how to interpret blood gas results

A
  1. look at pH
  2. look at metabolic component (HCO3)
  3. look at respiratory component (pCO2)
  4. combine all of the above info
  5. check compensation is appropriate
  6. look at pO2 level
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15
Q

FEV1, FVC, FEV1/FVC ratio, RV and RV/TLC in obstructive lung disease

A 
FEV1: (normal or) decreased
FVC:  normal od decreased
FEV1/FVC ratio; decreased (<70%)
\+ coving of the curve (in the flow volume loop)
RV increased
RV/TLC increased
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16
Q

FEV1, FVC, FEV1/FVC ratio, RV and RV/TLC in restrictive lung disease

A 
FEV1: normal or decreased
FVC: decreased
FEV1/FVC ratio: normal or increased (>70%)
RV decreased
RV/TLC decreased
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17
Q

GOLD staging based on FEV1 for COPD

A

GOLD Stage I: FEV1 > 80%
GOLD Stage II: 50% < FEV1 < 80%
GOLD Stage III: 30 < FEV1 < 50
GOLD Stage IV: FEV1 < 30%

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18
Q

causes of clubbing

A 
lung cancer
congenital heart defects
bronchiectasis
CF
lung abscess
infective endocarditis
interstitial lung disease
coeliac disease
cirrhosis
dysentry 
grave's disease
cancers (liver, GI, hodgkin lymphoma)
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19
Q

questions to ask at an annual asthma review?

A
  • difficulty sleeping due to asthma (in the last month)?
  • usual asthma symptoms during the day?
  • has asthma interfered with usual daily activities?
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20
Q

in which conditions do you hear bronchial breathing?

A
  • Consolidation
  • Lobar Collapse with patent bronchus
  • lung Cavity
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21
Q

how do you record serial readings of PEFR and for how long?

A

for diagnosis: 2-4 weeks (twice daily)

for occupational asthma: 2-4 hourly readings over several weeks

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22
Q

complete asthma control definition

A
  • no daytime symptoms
  • no night time waking due to asthma
  • no need for rescue meds
  • no asthma attacks
  • no limitation on activity
  • normal lung function (FEV1/PEF)
  • minimal side effects from meds
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23
Q

asthma treatment

A
  • SABA (for symptoms relief)
  • inhaled corticosteroid as preventer therapy if
    • use of inhaled SABA 3x/week and/or
    • have asthma symptoms 3x/week+ and/or
    • woken at night bt asthma symptoms 1x/week+
  • -> use twice daily at first and then adjust dose (1 dose/day good for maintenance)

if symptoms not well controlled:

  • recheck adherance, tehnique and trigger factors
  • leukotriene receptor antagonist (LTRA) + ICS
  • LABA + ICS
  • MART (single inhalor with ICS and fast acting LABA)

Check this for adults/children

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24
Q

features of acute exacerbation of asthma

A
  • agitation/connsciousness: signs of hypoxia

- signs of exhaustion, cyanosis and use of acessory muscles while at rest

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25
Q

grading of severity of asthma exacerbation

A
  • moderate: PEFR > 50-75% best or predicted and normal speech, with no features of acute severe or life threatening asthma
  • acute severe: PEFR 33-50% best or predicted OR resp rate >/= 25/min (people >12), 30/min (children 5-12) and 40/min (children 2-5) OR pulse rate 110/min (people >12), 125/min (children 5-12) and 140/min (children 2-5) OR inability to complete sentences in one breath, or accessory muscle use OR inability to feed (in infants), w/ O2sats >/= 92%
  • life threatening: PEFR < 33% best or predicted OR O2sats < 92% OR altered consciousness OR exhaustion OR cardiac arrhythmias OR hypotension OR cyanosis OR poor rrespiratory effort OR silent chest OR confusion
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26
Q

acute exacerbation of asthma treatment

A

-O2 (aim 94-98%)
- quadrupling ICS at onset of asthma + oral prednisolone
-SABA: either with nebuliser (5mg (patients>5) and 2.5 mg (pateint 2-5)) or pressurised metered dose inhalor with large volume spacer (adult: 4 puffs initially then 2 puffs every 2 min (up to 10 puffs) repeat every 10-20 min if necessary. for a child: give a puff every 30-60s, up to 10 puffs)
-for life threatening or severe + poor repsonse, add nebulised ipratropium bromide
+magnesium
+ aminophyline (O2sats <92% and rising CO2)

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27
Q

support agencies for domestic violence

A

social services
police adult safeguarding
PCT adult safeguarding units
–> for info on Women’s Refuge accomodation

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28
Q

side effects of ICS

A

hoarse voice
cough
sore throat
oral thrush

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29
Q

side effects of SABA

A 
trembling
nervous tension
headaches
palpitations
muscle cramps
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30
Q

side effects of anticholinergics (ie ipratropium)

A

dry mouth
constipation
cough
headaches

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31
Q

symptoms of COPD

A 
dyspnoea (exertion)
chronic cough 
sputum production
wheeze 
(winter exacerbation)
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32
Q

COPD def

A

airflow obstruction, progressive and not fully reversible + does not change markedly over several months

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33
Q

difference between COPD and asthma

A 
asthma reversible by 15%+
nocturnal cough (diurnal variation) in asthma
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34
Q

COPD causation

A
  • smoking (tobacco, cannabis, biomass fuels etc)

- alpha1 anti trypsin deficiency

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35
Q

pathogenesis of inflammation in COPD

A
  • goblet cell hyperplasia: protease
  • airway narrowing (inflammation and scarring): fibroblasts
  • alveolar destruction (empyema): CD8+ + T cells
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36
Q

what symptoms are associated with what pathophysiology?

A
  • goblet cell hyperplasia: cough and sputum
  • airway narrowing: breathless and wheeze
  • alveolar destruction: breathlessness
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37
Q

COPD signs

A 
tar staining on fingers
central cyanosis
tachypnoae
chest hyper expansion 
reduced lateral and reduced vertical chest expansion 
reduced breath sounds 
wheeze
palpable liver edge
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38
Q

CXR for COPD

A

-often normal
-hyperexpanction (low flat diaphragm and horizontal ribs)
-elongated and narrow heart
(mainly used to exclude other conditions)

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39
Q

CT scan in COPD

A

‘holes’ or bull

bronchial wall thickening

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40
Q

blood gases in COPD

A

T1RF: normal pH, PaO2 and HCO3 and reduced Pa02

T2RF low pH and PaO2 and high PaCO2, HCO3
if raised HCO3: one standing T2RF

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41
Q

natural history of COPD

A
  • progressive decline in lung function
  • progressive dyspnoea and disability
  • right ventricular failure
  • exacerbations
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42
Q

common infective causes of exacerbations in COPD

A 
streptococcus pneumonia 
viruses
moraxella catarrhalis
haemophilia influenza
pseudomonas aeroginosa
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43
Q

drugs given for COPD

A
  • inhaled bronchodilators (SABA, LABA (activate sympathetic NS), anti muscarinics (activate parasympathetic NS))
  • ICS (only for severe or frequent exacerbations)
  • oral theophylline (bronchiodilate)
  • O2
  • mucolytics
  • magnesium
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44
Q

COPD treatment pathway

A
  • anti smoking advice
  • flu and pneumococcal vaccination
  • manage anxiety and depression
  • pulmonary rehab

long term management:

  • SABA + ICS
  • LABA OR short acting anti muscarinic + ICS
  • if FEV1/FVC < 50% or frequent exacerbations: add ICS
  • if still SoB add LABA OR anti muscarinic
  • if still breathless high dose bronchodilators (multi dose SABA or nebuliser)
  • consider O2 therapy (nasal cannula)

if acute exacerbation (community):

  • can give recovery pack or go to hospital
  • antibiotics (if infective exacerbation)
  • oral corticosteroids (if exacerbation in hospital or community)
  • controlled oxygen therapy (T1RF or T2RF)
  • physiotherapy (pos pressure devices to clear sputum)

if acute exacerbation (hospital):

  • the above +
  • nebulised salbutamol and ibutropium
  • NIV
  • IV theophylline
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45
Q

COPD complications

A 
exacerbation
pneumonia
pneumothorax
right ventricular failure 
peripheral neuropathy 
cachexia
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46
Q

how does magnesium work on the lungs

A

physiological Ca channel blocker effect (sympathetic pathway)

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47
Q

name a mucolytic

A

carbocysteine

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48
Q

generic names ICS

A

clenil
QVAR
pulmicort
flixotide

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49
Q

generic names LABA

A

servant

50
Q

generic name LAMA

A

spiriva

51
Q

generic name combination inhaler

A

seretide
symbicort
fostair

52
Q

def T1RF

A

hyperaemic failure: Pa02 <8kPa

underlying pathology i.e. oedema, shunt or infection

53
Q

def T2RF

A

ventilatory failure: PaCO2 > 7

reduced ventilatory effort results in gas trapping

54
Q

pathophysiology of T2RD in COPD

A
  • elastic recoil lost: gas trapping and reduced excretion of carbon dioxide (combined with water to form carbonic acid)
  • lowers pH but as it is progressive, it is compensated by bicarbonate buffer system (kidneys reabsorb more bicarb)
55
Q

clinical features of hypercapnia

A 
dilated pupils
bounding pulse
hand flap 
myoclonus 
confusion 
drowsiness
coma
56
Q

diagnosing COPD pathway

A
  • symptoms
  • spirometry
  • additionally: CXR (exclude other pathologies), FBC (identify anaemia and polycythaemia), BMI (should be btw 20-25 for COPD patients)
57
Q

what is clinical effectiveness of influenza vaccine

A

overall 60-82% with lower protection in elderly subjects

58
Q

how long does it take for influenza vaccine to be effective?

A

10-14 days

59
Q

definition of CAP

A

songs of lower resp tract infection (fever/cough/phlegm/creps or bronchial breathing) + CXR changes

60
Q

how do you assess severity of pneumonia

A 
CURB65
-confusion 
-urea >7 mmol/l
-resp rate > 30
BP (systolic < 90 mmHg or diastolic < 60 mmHg)
-age >/=65
--> get 1 point per feature 
severity score:
0-1: low severity 
-2: moderate
-3-5 high
61
Q

what does NEWS measure?

A 
RR
O2sats
systolic BP
pulse rate
level of consciousness/new confusion 
temperature
62
Q

aetiologies of resp tract infections (upper, lower and pneumonia)

A

upper: primary viral
lower: viral and bacterial
pneumonia: viral, bacterial and fungal

(the higher you go, the most likely it is to be viral)

63
Q

host defence to resp tract infections

A
  • mechanical (nose, larynx, coughing)
  • respiratory epithelium (ciliary beat, mucus, antimicrobial proteins)
  • specific pathogen recognition
  • inflammatory cell recruitment
  • humoral and cell mediated immunity
64
Q

classifications of pneumonia (+ aetiology)

A
  • CAP (G+bact, mycoplasma, influenza)
  • HAP (G-bact, staph, aureus) + ventilator-associated pneumonia (VAP)
  • pneumonia in immunosuppressed host (unusual organisms, fungi)
  • aspiration pneumonia (chemical, mixed flora)
  • termnial pneumonia
65
Q

typical bacteria in CAP

A
  • streptococcus pneumoniae
  • haemophilus influenzae
  • klebsiella pneumonia
  • staphylococcus aureus
66
Q

atypical bacteria in CAP

A
  • mycoplasma pneumoniae
  • legionella pneumophilia
  • chlamydia pneumoniae
  • chlamydia psittaci
67
Q

symptoms of pneumonia

A
  • cough + purulent sputum/red + haemoptysis
  • rigors/fever
  • dyspnoa, orthopnea
  • chest pain (pleuritic, sudden onset, worse on coughing)

non pulmonary symptoms:

  • confusion (elderly, multi morbid patient)
  • abdo pain
  • D&V
  • myalgia and arthralgia
68
Q

signs in pneumonia

A
  • high T°
  • tachypnoea
  • reduced chest expansion on side of infection
  • dull percussion over affected area
  • bronchial breathing
  • focal crackles
  • pleural rub
  • mental confusion
69
Q

investigations in CAP

A
  • O2 sats, ABG
  • sputum culture/throat swab for virus
  • urine pneumococcus and legionella antigen
  • bloods:
    • FBC: WBC, Hb
    • platelets (inflam process)
    • CRP
    • PCT (procalcitonin)
    • U&Es (AKI)
    • lactate (sepsis/shock)
    • LFTs (reduction in liver perfusion associated with sepsis)
  • blood culture
  • CXR
70
Q

treatment for low severity CAP

A

amoxicillin (or doxycycline or clarithromyocin)

71
Q

treatment of moderate severity CAP in hospital

A

amoxicillin and a macrolide (oral or IV)

72
Q

treatment of severe CAP in hospital

A

broad spectrum beta lactase stable antibiotic (i.e. co-amoxiclav) + macrolide

73
Q

complications of CAPs

A
  • parapneumonic effusion
  • infectious complications: empyema, lung assess, metastatic infection
  • VTE
  • worsening of comorbidities
  • SE of antibiotics
  • sepsis
74
Q

how do diagnose HAP

A

new onset symptoms + compatible CXR dvlping after 48h+ of patients admission or within 1 month after discharge

75
Q

difference between early and late onset HAP

A
  • early onset HAP: occurs within 4-5 days of admission and is usually caused by antibiotic sensitive community organism
  • late onset HAP: >5 days: more likely to be caused by antibiotic resistant hospital pathogens
76
Q

bacterial causes of HAP

A
  • enterobacteria (E coli, Klebsiella, enterobacter)
  • staphylococcus aureus
  • pseudomonas
  • environmental gram neg: acinetobacter, stenotrophomons maltrophilia
77
Q

risk factors in developing HAP

A
  • ICU stay, mechanical ventilation
  • prolonged hospital stay
  • severe underlying illness, multiple co-morbidities
  • underlying rest disease
  • abdominal surgery, vomiting/aspiration
78
Q

pathophysiology of bacterial pneumonia

A
  • acute inflammation of lung parenchyma
  • cellular (neutrophil) infiltration
  • inflammatory exudate in th interstitial
  • alveolar oedema and haemorrhage
79
Q

what and which are the ESKAPE pathogens

A

what: pathogens beyond treatment

which:
E. faecium
S. aureus
K. pneumoniae
A. baumanil 
P. aeruginosa
Enterobacter spp
80
Q

how do antibiotics that are mosquito nets or fly swats work?

A

mosquito nets: time dependent

fly swats: dose dependent

81
Q

what is antibiotic stewardship?

A

right drug at the right time

MIND ME
Microbiology guides therapy wherever possible
Indications should be evidence based
Narrowest spectrum required
Dosage appropriate to the site and type of infection
Minimise duration of therapy
Ensure mono therapy in most situations

82
Q

difference between typical and atypical organisms

A

typical organisms can be cultured in lab

atypical ar intracellular and can’t be cultured

83
Q

fungal cause of pneumonia

A

pneumocystis jirovecii (in immunocompromised patients)

84
Q

natural history of patient recovering from pneumonia

A

1 week: fever should have resolved
4 weeks: chest pain and sputum production should be reduced
6 weeks: cough and breathlessness should be reduced
3 months: most symptoms should have resolved but fatigue still may be present
6 months: should be back to normal

85
Q

when should you give antibiotics?

A
  • prophylaxis in immunosuppression (ie to prevent organ rejection)
  • prophylaxis in significant lung, heart, renal, liver or neuromuscular disease
  • prophylaxis in patients >65 w/ 2 of the following: DMT1/2, HF, hospitalisation in the last year or being treated with oral corticosteroids
  • therapy
  • pre-emptive therapy (presumed infection)
86
Q

SEPSIS 6?

A

in:

  • O2
  • IV antibiotics
  • fluid

out:

  • blood culture
  • lactate
  • urine output
87
Q

TB pathology and natural history (primary infection)

A
  • no specific immunity
  • small lung lesion (Ghon focus)
  • regional lymph node involvement
  • haematogenous spread
  • heals with develoment of specific immunity + fibrosis
  • asymptomatic in 90%
88
Q

TB pathology and natural history (post-primary infection)

A
  • reactivation of persisting mycobacteria (latent infection)
  • much greater immune response
  • usually symptomatic
89
Q

TB symptoms

A
  • weight loss
  • fever
  • night sweats
  • cough +/- sputum
  • haemoptysis
  • lymph node enlargement
  • pleuritic pain
  • bone pain
90
Q

investigations in TB

A

-CXR
-ESR/CRP
HIV test
-LFTs (cuz TB can affect liver and drugs given can cause problems in the liver)
-sample for microbiology (sputum smear and culture + aspirate/biopsy i.e. pleura, lymph nodes)
-PCR/histology/cytology
-Mantoux test (for any exposure)
-interferon gamma for active exposure

91
Q

CXR in post primary disease

A
  • upper lobe consolidation
  • hilar pulled up due to fibrosis
  • cavitation
  • volume loss
  • lymphadenopathy
  • pleural effusion
  • pneumothorax
92
Q

def of military TB

A

pulmonary homogenous dissemination of uncontrolled TB infection (usually in the immunocompromised)
poor prognosis

93
Q

what is the pulmonary nodule called in TB and what is it formed by?

A

granuloma:

  • core of caseating necrosis
  • layer of epithelial cells
  • outer layer of lymphocytes
94
Q

def mono-resistance TB

A

resistance to one antituberculosis drugs

95
Q

def poly-resistance TB

A

resistance to more than one antituberculosis drug, other than isoniazid and rifampicin

96
Q

def multidrug-resistance TB

A

resistance to at least isoniazid and rifampicin

97
Q

def extensive drug resistance TB

A

resistance to any fluoroquinolone, and at least one of three injectable second line drugs (capreomycin, kanamycin and amikacin), in addition to multi drug resistance

98
Q

treatment of TB

A

6 months of isoniazid (with pyridoxine) and rifampicin

2 months with pyrazinamide and ethambutol

99
Q

what is TB caused by?

A

mycobacterium tuberculosis complex:

  • M. tuberculosis
  • M. bovis
  • M. africanum
100
Q

3 priorities of TB control

A
  1. detect and treat cases of active TB
  2. detect and treat cases of latent infection (targeted)
  3. offer BCG vaccine (targeted)

(+wider determinants of health: poverty, malnutrition…)

101
Q

risk assessment equation in TB

A

risk = (particles/volume)x exposure time

volume: volume of air/space

102
Q

red flag symptoms in resp

A 
haemoptysis
weight loss
persistent cough 
dyspnoea
pain 
changes in fingers suggesting clubbing 
pain in limb indicating hypertrophic osteoarthopathy
103
Q

non metastatic manifestations of lung cancer

A

-clubbing and hypertrophic pulmonary arthropathy (HPOA)

hormone syndromes:

  • Cushing’s syndrome (ACTH)
  • SIADH (syndrome of inappropriate antidiuretic hormone secretion)
  • hypercalcamia

neuromyopathies:

  • Eaton Lambert syndrome
  • peripheral neuropathy
  • dementia
  • cerebellar syndrome
104
Q

how do you go about breaking bad news

A

SPIKES framework:

  • Setting
  • Patient perception
  • Invitation to continue with information
  • Knowledge in small chunks
  • Empathy for shock/other emotions
  • summarise/strategise
105
Q

why are lungs common site for secondary metastatic cancer?

A

cardiac output going through lungs

106
Q

types of bronchial carcinoma?

A
  • small cell
  • squamous
  • adenocarcinoma
  • large cell
  • alveolar cell carcinoma
  • bronchial adenoma
107
Q

clinical presentation of bronchial carcinoma

A 
cough 
haemoptysis 
chest pain 
breathlessness
stridor 
hoarse voice
weight loss
facial swelling, headaches (SVC obstruction)
108
Q

clinical examination in bronchial carcinoma

A 
weight loss
finger clubbing 
lymphadenopathy 
chest asymmetry 
focal chest signs (consolidation, fluid)
hepatomegaly (metastesis)
neuropathy (non metastatic manifestations)
109
Q

what helps you differentiate between pleural effusion and collapse?

A

mediastinum + trachea

pleural fusion: pushed away
colapse: pulled towards

110
Q

what is Pancoast syndrome?

A

lung tumour arises in apex: grows upwards into base of neck. it can grow into brachial plexus:

  • pain in inner aspect of arm
  • Horner syndrome due to sympathetic nerve supply comes out at T1, reaches lower part of brachial plexus and follows carotid up to eye (pupil is small + droopy, sullen and dry eye on affected side)
111
Q

differential diagnosis to bronchial carcinoma

A

TB
pneumonia
lung metastases from other primary
benign lung tumours

112
Q

investigations in bronchial carcinoma

A 
CXR, CT scan 
bloods (LFTS, FBC, calcium)
fiberoptic bronchoscopy 
percutaneous needle biopsy 
node biopsy 
mediastinoscopy/mediastinotomy
thoracotomy
113
Q

when is bronchial carcinoma inoperable?

A

(-smal cell)

  • distant metastasis
  • mediastinal spread (recurrent laryngeal nerve palsy, phrenic nerve palsy)
  • poor pulmonary function
  • frequent angina/HF
  • psychological failure
114
Q

how do you treat small cell carcinoma?

A

chemotherapy

palliation

115
Q

how do you treat non small cell carcinoma

A
  • surgery
  • radical radiotherapy
  • palliation (symptomatic, radiotherapy and chemotherapy)
116
Q

EGFR and lung cancer?

A

epidermal growth factor receptor: protein found on surface of some NSCLC cells
–> EGFR mutation positive predicts response to specific chemotherapy (gefiinib)

117
Q

where does bronchial carcinoma spread to?

A 
liver
kidney 
pleura
bone 
adrenal glands
118
Q

squamous cell carcinoma?

  • epidemiology
  • location/histology
  • clinical presentation
A
  • smokers
  • more in bronchi (central), (may see desmosomes or keratin accumulation), invade lympathics
  • can secrete hormones (PTH-like CMPD: hyprcalcaemia)
119
Q

adenocarcinoma?

  • epidemiology
  • location/histology
  • presentation
A
  • non smokers
  • peripheral disease, mucus production
  • hypertrophic osteoarthritis triad: clubbing, long bone swelling and arthritis
120
Q

small cell carcinoma?

  • epidemiology
  • presentation
A
  • smokers (exclusively)

- paraneoplastic syndromes: secretes ACTH, ADH, Eaton Lambert

121
Q

what is the commonest cause of high serum calcium

A

malignancy

  • breast cancer cells
  • squamous lung cell carcinoma
  • cholangiocarcinoma
  • multiple myeloma
122
Q

def asbestosis

A

chronic lung condition associated with lung fibrosis that follows chronic exposure to asbestos (thickening and fibrosis of visceral pleura)

Year 3 (7 decks)

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