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phase 2a mine > resp top tier > Flashcards

resp top tier Flashcards

1
Q

is primary or secondary lung cancer more common

A

secondary

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2
Q

gender association with lung cancer

A

m >f

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3
Q

risk factors for lung cancer

A 
Smoking inc passive
Urban areas
Asbestos 
Chromium
Arsenic
Coal 
Ionising radiation
Genetic risk
HIV
Pre-existing lung disease
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4
Q

types of lung cancer

A

non- small cell carcinoma (main)

  • squamous
  • adenocarcinoma
  • large cell
  • carcinoid tumour

small cell carcinoma

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5
Q

where is lung cancer located

A

mainly bronchial , sometimes pleura

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6
Q

squamous non-small cell carcinoma

  • how does it present
  • spread?
A
  • as obstructive lesion –> infection

- local spread common. metastases widespread but relatively late

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7
Q

adenocarcinoma (non-small cell carcinoma) is strongly associated with what

A

asbestos

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8
Q

small cell carcinoma

  • arises from what
  • secretes what
  • growth/ prognosis
A
  • endocrine cells - kulchitsky cells
  • secrete polypeptides and amines which act as hormones or neurotransmitters
  • Grow rapidly , with widespread metastases. Highly malignant – frequently inoperable at presentation (poor prognosis)
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9
Q

presentation of lung cancer

A 
Cough
Chest pain
Haemoptysis (Red flag)
Dyspnoea , breathlessness, wheeze 
Recurrent infection
finger clubbing
weight loss
anaemia
nodes
headaches
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10
Q

spread of lung cancer and associated symtpoms

A
  • brachial plexus - shoulder/arm pain
  • bone - pain and fractures
  • sympathetic ganglion - horner’s syndrome (eyes)
  • brain - seizures, neurological deficit, headaches
  • abdominal pain
  • left recurrent laryngeal nerve - hoarse voice
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11
Q

investigations of lung cancer

A

CXR

  • round fluffy / spiking shadow
  • hilar enlargement (medial of each lung)
  • Consolidation (= filled with fluid rather than air so is no longer compressible. Appears white)
  • lung collapse
  • pleural effusion

CT/PET - for staging

Bronchoscopy- Biopsy and assess operability

Sputum biopsy

Pleural fluid biopsy

Bloods - FBC low

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12
Q

non small cell carcinoma management

A

Surgery- can be curative (if no metastatic spread)

Chemo (downstages tumours to render them operable. Advanced disease. or post op

Radiotherapy (good for localised squamous cancers. Advanced disease. Or post op

Stop smoking

Remove carcinogens

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13
Q

small cell carcinoma management

A

chemo

Limited disease = Chemo-radio combo
Extensive disease = chemo

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14
Q

what sort of symptom relief / palliative care can you think of that would benefit lung cancer

A
  • corticosteroid (dexamethasone) for superior vena cava obstruction
  • Analgesia
  • Antiemetics
  • Bronchodilators
  • Antidepressants
  • tracheal stenting
  • cryotherapy
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15
Q

treatment for PE- short and long term

A

Immediate - depends on patient condition/signs

  • Oxygen if hypoxic
  • Morphine + antiemetic for pain/ distress
  • IV LMW heparin - anticoagulant
  • IV fluid for hypotension
  • Call ICU
  • Consider thrombolysis if hemodynamically unstable

Long term

  • LMW heparin
  • Anticoagulants - DOAC or warfarin
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16
Q

PE investigations

A

Bloods

  • FBC
  • U/E
  • ** D-dimer = +
  • Baseline clotting
  • ** Troponin levels = raised due to impact on right heart

ABG (decreased PaCO2 and PaO2)

** CT pulmonary angiography (specific, sensitive)

CXR (may be normal. May have dilated pulmonary artery / oligaemia (decreased blood flow through certain segment)

ECG - normal /tachy / RV strain / RBBB
If no other risk factors, consider underlying malignancy

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17
Q

symptoms of PE

A 
Acute breathlessness
Pleuritic chest pain
Haemoptysis
Dizzy
Syncope
Calf pain
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18
Q

signs of PE

A
  • Pyrexia (Fever)
  • Cyanosis
  • Tachypnoea
  • Tachycardia
  • Hypotension
    Raised JVP
    Pleural rub
    Pleural effusion
    Tender hard calf
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19
Q

pathophysiology of PE - the two types

inc cause

A

cause usually = venous thrombi (DVT)

Big

  • Embolus obstructs R ventricular outflow (on way to lungs) - but doesn’t block it i don’t think
  • Pulmonary vascular resistance increases suddenly
  • Causing acute right sided heart failure

Small embolus

  • Blocks terminal peripheral pulmonary vessel
  • May not notice unless causes pulmonary infarction
  • Lung tissue ventilated but not perfused (V/Q mismatch)- impaired gas exchange
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20
Q

risk factors for PE

A
  • DVT
  • Previous PE
  • Thrombophilia
  • Recent surgery - esp abdominal, pelvic, hip replacement, knee replacement
  • Malignancy (If not other risk factors, consider underlying malignancy )
  • Pregnancy / post partum
  • Immobilisation eg leg fracture
  • Combined oestrogen pill / hormone replacement therapy
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21
Q

COPD complications

A
  • Respiratory failure
  • Recurrent infections
  • Pulmonary hypertension → cor pulmonale - enlargement of R heart (heart failure)
  • lung carcinoma
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22
Q

COPD management

A

Smoking cessation - slows deterioration
Avoid infections
Exercise

Bronchodilators = short/long acting beta agonists /muscarinic antagonists:

  • 1st line= SABA/SAMA
  • 2nd line= LABA/LAMA
  • 3rd line= LABA/LAMA + corticosteroid (inhaled/systemic)
  • 4th line= LABA + LAMA + corticosteroid (inhaled/systemic)
  • 5th line= long term oxygen therapy – Need to be careful not to remove the hypoxic drive in blue bloaters

Ventilation
Surgery - lung transplant

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23
Q

investigations into COPD

A
  • ECG - RV/RA hypertrophy
  • ABG - reduced oxygen

Spirometry
= gold standard.
– FEV1/FVC<70%,
– FEV1<80% of predicted

CXR

    • > 6 ribs visible
    • Hyperinflation
    • flattened diaphragm
  • -Large central pulmonary arteries
    • Decreased peripheral vascular markings

CT

    • Bronchial wall thickening
    • Scarring
    • Air space enlargement (dark areas)
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24
Q

symptoms of COPD

A 
Increased sputum production
Chronic cough
Shortness of breath, dyspnoea
Low moor, tired, lethargic
Weight loss
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25
Q

Signs of COPD

A 
Barrel shaped chest - hyperinflation
Ankle swelling 
Tachypnoea
Expiratory wheeze
Use of accessory muscles of respiration eg may lean forward
Decreased expansion
Expiration through pursed lips (prevents alveolar and airway collapse)
Quiet breathing sounds
Cyanosis (if chronic bronchitis)
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26
Q

two appearances of COPD

A

BLUE BLOATER

  • chronic bronchitis
  • capillary bed not damaged
  • compensatory increase in CO and decrease in ventilation leads to hypoxia (blue). Obstruction causes increasing residual lung volume (bloating)

PINK PUFFER

  • emphysema
  • damages capillary bed
  • compensatory hyperventilation (puffing) prevents hypoxia. Lack of cyanosis (pink)
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27
Q

two types of COPD (diseases)

A

CHRONIC BRONCHITIS

  • Airway narrows due to:
  • – Hypertrophy and hyperplasia of mucus secreting glands in bronchial tree
  • –Bronchial wall inflammation
  • –Mucosal oedema - increase in mucus in airway lumen
  • Blue bloaters → compensatory increase in CO and decrease in ventilation leads to hypoxia (blue). Obstruction causes increasing residual lung volume (bloating). (no capillary bed damage)

EMPHYSEMA

  • Lung tissues distal to terminal bronchioles (alveoli) is destroyed : smoking → inflammatory factors released that break collagen and elastin down→ loss of elastic recoil → these collapse following expiration - air trapped.
  • This also causes damage to capillary bed → inability to oxygenate → hyperventilation
  • Pink puffers → compensatory hyperventilation (puffing) prevents hypoxia. Lack of cyanosis (pink)
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28
Q

what type of respiratory failure is associated with COPD

A

Air cannot leave lungs due to obstruction → type 2 respiratory failure (CO2 high, O2 low)

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29
Q

describe COPD nature

A

Usually progressive, poorly reversible
Persistent inflammatory response
obstructive disease - limits airflow

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30
Q

causes of COPD

A

Inflammation caused by

  • -Smoking
  • -Previous infection
  • -Environmental dust
  • -Fumes , pollution

Alpha 1 anti-trypsin deficiency - (more common cause in younger people)

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31
Q

what is Alpha 1 anti-trypsin deficiency

A
  • AAT is a protease inhibitor
  • It protects tissues from inflammatory enzymes (break elastase down causing elastic recoil loss in emphysema)
  • Deficiency = more susceptible to damage from smoke
  • Liver also affected
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32
Q

COPD

  • age
  • gender
  • lifestyle
A

Rare under 35
Smokers
m>f

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33
Q

what put you at higher risk of asthma death

A
  • > 3 classes of treatment
  • Recent admission to hospital / frequent attender
  • Previous near fatal attack
  • Brittle asthma disease (type 1, chronic and sever, type 2 , sudden dips)
  • Psychosocial factors
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34
Q

complications of asthma

A

Pneumonia
Pneumothorax - collapsed lung
Asthma death

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35
Q

immediate treatment of asthma attack

A
  • oxygen
  • salbutamol nebuliser
  • steroids
  • ABG, CXR
  • Monitor response to treatment
  • if deterioration, ITU
  • discharge with asthma action plan, prednisolone, nurse/GP follow up soon and education to prevent readmission
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36
Q

asthma

non pharmacological management

possible surgical treatments

A
  • Avoid triggers and allergens inc occupationally
  • Quit smoking
  • Weight loss
  • Record PEF twice a day
  • Education on self management

Bronchial thermoplasty
Lung transplant

37
Q

asthma pharmacological treatment

A

Bronchodilators

  • treats symptoms, not disease
  • Mainly for non-eosinophilic
  • Short acting used before long acting (depends on disease severity)
  • –Beta agonists - salbutamol
  • –Theophyllines
  • –Long acting beta agonists - salmeterol
  • –Anticholinergics (antimuscarinic bronchodilators) - ipratropium, tiotropium
  • –Leukotriene receptor antagonists = montelukast

Anti-inflammatory

  • reduce airway inflammation
  • decreases mortality
  • Steroids - beclomethasone

Biologics

  • Anti IgE - omalizumab - for atopic disease
  • Anti IL5 - mepolizumab - IL5 needed to make eosinophils
38
Q

steroids for asthma

  • route that is best
  • how to stop and why
  • name 4 side effects
A
  • inhaled
  • need to wean off due to adrenal suppression
  • Diabetes, cataracts, osteoporosis, hypertension, skin thinning, easy bruising, growth retardation, osteonecrosis of femoral head, hoarse voice, oral candida
39
Q

bronchodilators

  • treats symptoms or disease
  • what type are they for mainly
  • which are used for less severity?
  • name 3 examples of types
A
  • treats symptoms, not disease
  • Mainly for non-eosinophilic
  • Short acting used before long acting (depends on disease severity)
  • short/ long acting beta agonists, theophyllines, anticholinergics, antimuscarinics, leukotriene receptor antagonists
40
Q

asthma lung tests

A

Spirometry / peak flow

  • Reduced FEV1
  • FEV1/FVC <70%
  • PEFR (peak expiratory flow rate) reduced more than expected
  • Variability (>20% change 3/7 days)

Exhaled nitric oxide
- FENO (fraction of exhaled nitric oxide) - gives information about eosinophils in lung

Reversibility testing
- Before and after medication taken

Peak flow meter taken home

  • Keep diary of PEFR
  • Diurnal variation!
41
Q

non- lung tests for asthma investigation

A 
examination 
-- may be normal as it is episodic
-- wheeze
-- no crackles/sputum
-- hyperinflated barrel chest
Blood 
count (eosinophils)
Culture
Sputum culture
Atopy and allergy test 
CXR
42
Q

asthma presentation

A
  • Episodic audible wheeze
  • Cough
  • SOB, intermittent dyspnoea
  • Chest tightness
  • Diurnal variation (during day)– worse in morning
  • Symptoms relieve after aspirin / beta blocker
  • Hyperinflated chest (‘barrel’)
  • Tachypnoea
43
Q

how do you grade severe asthma

A

1 major + 2 minor

Major
Treatment with continuous / near continous oral steroids / requirement for high dose inhaled steroids

Minor
Additional daily reliever medication
Beta agonists, theophylline, LTRA
Symptoms needing reliever medication on daily / near daily basis
Persistent airway obstruction (FEV1=20%)
>1 emergency visit per annum
>3 steroid courses per annum
Prompt deterioration with 25% reduction in oral / inhaled steroid dose
Near fatal event in the past§
44
Q

types of asthma

A

eosinophilic / non eosinophilic

also

atopic (Extrinsic) / nonatopic (intrinsic)

45
Q

eosinophilic vs non eosinophilic

A

eosinophilic

  • associated with allergy
  • Triggers cause inflammatory cascade in bronchial tree
  • T cells recruit eosinophils which then cause damage to the epithelium
  • Mast cells, eosinophils, T lymphocytes and dendritic cells increase in the bronchial wall and membranes

non eosinophilic

  • later onset
  • related to smoking and obesity
  • neutrophils rather than eosinophils
  • less understood
46
Q

asthma pathophysiology

A
  • Airflow limitation (reversible but may be chronic - due to remodelling and mucus impaction)- due to obstruction
    • IgE causes mast cells to degranulate and release histamine –> Narrowed due to smooth muscle contraction- bronchospasm as a result
    • Excessive secretions into lumen also obstruct
    • Deposition of collagen and matrix proteins (as a result of inflammation) causes remodelling of airways inc an increased number of goblet cells
  • Airway hyperresponsiveness to range of stimuli
    • Hypersensitivity type 1 reaction
    • IgE produced against stimuli
  • Inflammation of bronchi
    • Inflammation and cellular infiltration causes airway wall thickening
  • -Secretions into lumen as a result
47
Q

what differentiates asthma from COPD

A 
COPD has less diurnal variation
More progresseive SOB
(Has wheeze)
Sputum production
Winter symptoms
48
Q

what does fibrosis have that differentiates it from other stuff like asthma

A

fibrosis has crackles (v distinctive of fibrosis)

49
Q

non -allergic asthma (intrinsic) causes

A

Stress
Cold air
infection

50
Q

provoking factors of asthma attack

A 
Allergens
Infections
Menstrual cycle
Exercise
Cold air
Laughter / emotion
Trauma 
Stress
Some medications - NSAIDs, B blockers
51
Q

pneumonia treatment

A 
O2 maintained 
Analgesia 
Smoking cessation
Antibiotics
- Empirically then MC+S guided
- CAP 
--- Mild = amoxicillin
--- Moderate/severe = amoxicillin + clarithromycin
--- Legionella = fluoroquinolone + clarithromycin (Do not respond to penicillin as they lack cell wall)
-HAP = aminoglycoside + penicillin
52
Q

pneumonia investigations

A

Culture

  • Sputum
  • Blood
  • Urine - inc antigen test
  • Pleural fluid – thoracentesis
Blood
- FBC - elevated WCC
- ESR/CRP raised
- ABG, U/E, LFT for severity 
 serology

CXR

  • Consolidation = filled with fluid, rather than air
  • Extent, severity
  • Listen to chest

CURB65

  • Asseses pneumonia severity – monitor/hospitalise
  • Confusion, urea, RR, BP, age
53
Q

pneumonia symptoms

A 
Common 
Pain
Chest
Pleuritic
Cough
Rusty / green coloured sputum = strep pneumonia
May be purulent sputum
Breathlessness
Fatigue
Also - if these symptoms predominate = ‘atypical pneumonia’
Myalgia
Arthralgia
Headache
Night sweats
Rigors
Malaise 
Anorexia
54
Q

pneumonia signs

A 
Fever 
Consolidation
-dullness to percussion
-Bronchial breathing
Drop in BP
Increased RR
Raised HR
Cyanosis
Confusion
55
Q

pneumonia types

A

CAP (Community)

  • No underlying immunosuppression/ malignancy
  • May be primary or secondary to underlying disease
  • Local or diffuse infection
  • may be atypical (different causative organisms and more prominent extra-pulmonary presentation)

HAP (hospital)

  • Purulent sputum
  • Post admission 48h - 3months
56
Q

pneumonia pathophysiology

A 
Spread by respiratory droplets
Bacteria multiplies in lungs
Acute inflammation
Intense infiltration of neutrophils in and around alveoli and terminal bronchioles
Fluid collects in the lungs
57
Q

pneumonia causes

A 
CAP = community acquired
- Most common
---Main = strep pneumoniae
--- Haemophilus influenzae
--- Staph aureus
--- Klebsiella pneumoniae
- Atypical 
--- Slower onset
--- More prominent extra-pulmonary symptoms and complications
--- Legionella pneumophila
Mycoplasma pneumoniae
Chlamydophila pneumonia

HAP= hospital acquired

  • Early onset = same as CAP
  • Late onset
  • –MRSA
  • –Klebsiella pneumoniae
  • –Pseudomonas aeruginosa

Aspiration

  • inhaled foreign objects that can bring bacteria into the airways
  • Gastric contents inhaled

Can be from virus/ fungi but this is rarer

58
Q

pneumonia risk factors

A
  • Infants
  • Eldely
  • Smoking
  • Existing conditions
  • – COPD and other chronic lung conditions- CF
  • – CV disease, congestive heart disease
  • – Immunocompromised inc HIV
  • –Diabetics
  • Nursing home residents
  • Impaired swallowing
  • Alcoholics and IV drug users
59
Q

prevention of TB

A

Active case finding of patient contacts - reduce infectivity

Vaccination - BCG (variable efficacy so not offered routinely)

60
Q

treatment of TB

A 
Notify public health
Contact tracing
6 months of treatment. 9 if spread to bone. 12 if spread to CNS
- Rifampicin 6months
- Isoniazid 6 months
- Pyrazinamide first 2 months
- Ethambutol first 2 months  (RIPE)
61
Q

TB investigations

A

CXR

  • pleural effusion,
  • typical / patchy/ nodular shadow,
  • Gohn complex (small calcified nodule)
  • Consolidation
  • Fibrosis

Blood/sputum serology

  • Bronchoscopy lavage if no sputum available
  • Ziehl neelsen stain for acid fast bacilli
  • Used for mycobacteria . goes RED/PINK
  • Caseating granuloma*

Nucleic acid amplification – distinguishes causative mycobacteria

  • Miliary – lumbar puncture due to high rate spreading to meninges
  • Latent
  • – tuberculin skin test (mantoux)- wont pick up miliary/ immunosuppressed
  • –Interferon gamma release assays - more accurate (picks up exposure, not active infection)
62
Q

TB main symptoms

A

primary = milder/ asymptomatic

Anorexia
Fatigue
Weight loss
Fever
Night sweats
Cough
Haemoptysis 
Breathlessness
63
Q

extrapulmonary TB symptoms (spread)

A 
Bone pain/ swelling
Ascites 
Lymph node swelling
frequency/ haematuria, dysuria
Meningeal inflammation - raised ICP
May be hoarse voice/ pleuritic pain depending on involvement of laryngeal / pleura
64
Q

TB pathophysiology

A
  • Organisms inhaled
  • Majority of bacteria killed- engulfed by macrophages and stored in granulomas (local granuloma formation). - Macrophages present antigen to T lymphocyte
  • Delayed hypersensitivity reaction occurs
  • Occasionally in GI tract
  • Caseation= diseased, necrosed tissue forms firm dry mass (cheese-like)
  • Cavitation= vapour filled cavities (low presh)
  • Fibrosis
65
Q

types of TB

A

primary = first infection.. usually mild/asymptomatic

miliary TB = initial infection not successfully controlled by caseating granulomas. bacteria multiply. this is more common in infants, immunocomprimised

latent TB = bacteria present but not problematic. in the majority of infected people, the immune system contains the infections and develops cell mediated immunity memory to the bacteria

secondary TB =Dormant organisms reactivate years later due to host immune system reducing
- Age
- Alcohol abuse
- Malignancy
- HIV
- Treatment
- Illness
this is the majority of patient cases

based on features, TB can be pulmonary or extra-pulmonary (Spread)

66
Q

TB causes

A

Mycobacterium tuberculosis
Mycobacterium bovis
(mycobacterium africanum)
(Mycobacterium microti)

67
Q

TB risk factors

A 
High incidence country
Immunosuppression (HIV, chemo)
Diabetes
IV drug user
Ageing
Poverty
Prisons
Smoking 
Alcohol
68
Q

influenza treatment

A

Symptomatic - paracetamol, fluids, tamiflu

Bed rest

69
Q

influenza symptoms

A

Abrupt fever
Aching in limbs
Sore throat
Dry cough

70
Q

influenza cause

A

Influenza = virus
Types = A (most), B, C (mild)
Droplet or direct nasal/eye contact with hands
Antigenic drift – only partial immunity from previous infections. Influenza A can do major and rapid shifts (pandemics)

71
Q

common cold

- infections and cause

A 
Rhinitis
Sinusitis
- Usually viral
- Bacterial  
---strep pneumoniae
---haemophilus influenzae
72
Q

pharyngitis/ tonsilitis causes

A

Viral

  • Rhinovirus
  • Adenovirus
  • EBV
  • HIV acute

Bacteria

  • Lancefield group A - strep pyogenes
  • Neisseria gonorrhoeae
  • Mycoplasma pneumoniae
73
Q

diphtheria cause

A

Corynebacterium diphtheriae

74
Q

epiglotitis cause

A

Haemophilus influenzae unless immunocompromised

75
Q

whooping cough cause + virulence factors

A

Bordetella pertussis

  • ACT toxin - inhibits phagocyte chemotaxis and T cell activation
  • Pertussis toxin - inhibits alveolar macrophage defense
  • Fimbriae - adherence
  • Cytotoxin - causes epithelial necrosis

Bordetella parapertussis and bordetella bronchiseptica (milder)

76
Q

croup cause

A

Parainfluenza virus

measles

77
Q

what causes psuedomembrane (thick, grey ) in tonsils

A

diphtheria

78
Q

what causes pain in ear and into teeth, facial pain and purulent discharge

A

sinusitis

79
Q

what upper resp infection can cause conjunctivitis

A

whooping cough

80
Q

what causes barking cough and crying

what other symptoms are caused by it

A

croup

also
cyanosis
increased RR
intercostal recessions
inspiratory stridor (high pitched wheeze)
81
Q

diphtheria treatment

A

erythromycin and anti-toxin

82
Q

most common cause of COPD exacerbation

A

haemophilius influenza (then strep pneumonia)

83
Q

is pulmonary fibrosis productive

A

non productive

84
Q

what occupation supports pulmonary fibrosis

A

miner

85
Q

tension pneumothorax tracheal deviation goes which way

pleural effusion tracheal deviation goes which way

A

both causes mediastinum shifts away from the side of the pneumothorax/ pleural effusion

86
Q

what sign would you see on pleural effusion Xray

A

meniscus

87
Q

pink frothy sputum

A

pulmonary oedema

caused by HF

88
Q

orthopnea indicates

A

pulmonary oedema

caused by HF

phase 2a mine (38 decks)

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