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Medicine MBBS year 2 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

state 4 risk factors for lung cancer

A
  1. M>F
  2. 75-90 years peak
  3. smoking history (duration, intensity, time stopped)
  4. lower socioeconomic class
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2
Q

causes of lung cancer?

A

Passive smoking

Asbestos, Radon, indoor cooking fumes, chronic lung disease, immunodeficiency, genetic

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3
Q

where are small cell lung cancers located?
what is their origin?
what are their characteristics?

A
  1. central
  2. from pulmonary neuroendocrine cells. = NET - link to paraneoplastic syndromes e.g. SIADH, cushings
  3. Undifferentiated and highly malignant

“Small NET”

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4
Q

where are adenocarcinomas located?

what is their origin?

A
  1. peripheral

2. from mucus-producing glandular tissue

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5
Q

where are squamous cell carcinoma located?
what is their origin?
what are their characteristics?

A
  1. central
  2. originating from bronchial epithelium
    centrally located - Hilar mass on x-ray
  3. 30%
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6
Q

where are large cell carcinoma located?

what are their characteristics?

A
  1. peripheral

2. undifferentiated -poor prognosis

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7
Q

what is the most common type of lung cancer?

A

adenocarcinoma

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8
Q

which types of lung cancer are central?

A

squamous cell carcinoma and small cell carcinoma are sentral

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9
Q

steps for lung cancer development?

A

hyperplasia -> metaplasia -> dysplasia -> carcinoma in situ -> invasive carcinoma

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10
Q

state 4 oncogenes that lead to the development of cancer

A

EGFR Tyrosine Kinase !!
ALK Tyrosine kinase !!!
ROS1 Tyrosine kinase
BRAF

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11
Q

which oncogene mutation is seen more commonly in smokers?

A

BRAF

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12
Q

what are some symptoms of lung cancer?

A

Cough, hemoptysis, fatigue, breathlessness, weight loss, chest pain

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13
Q

sites of metastasis from lung cancer?

A

Love Affective Boneheads and Braniacs

-> Liver, adrenals, bone, brain. Lymph nodes

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14
Q

What are 5 features of advanced metastatic cancer

A
  1. Neurological features - seizures, focal weakness, spinal cord compression
  2. bone pain
  3. liver failure,
  4. Paraneoplastic syndromes - proteins that tumours secrete into bloodstream - can cause finger clubbing, hypercalcemia from PTH, hyponatremia from SIADH, cushing’s syndrome
  5. Pleural effusion
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15
Q

what are 4 features of advanced lung cancer

A
  1. cahexia
  2. horners syndrome
  3. superior vena cava obstruction
  4. clubbing
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16
Q

how do you diagnose lung cancer?

A

CXR
CT chest and abdomen
PET
biopsy

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17
Q

Why is PET used in lung cancer diagnosis?

A

to exclude occult metastasis

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18
Q

state and describe the WHO performance status stages for lung cancer

A

0 - asymptomatic - fully active (things like chest pain may be present)
1 - symptomatic, restricted in strenous activity but can carry out office work and light work
2 - symptomatic, less than 50 % in bed during day, cant do work
3 - symptomatic, more than 50% in bed during day. limited self care
4. bed bound
5 - death

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19
Q

which performance status stages recieve radical treatment for lung cancer?

A

PS 0-2

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20
Q

distinguish between 3 biopsy methods for LC

A
  1. Bronchoscopy - for tumors of central airway where tissue staging not important
  2. EBUS-TBNA - to stage mediastinum and or achieve tissue diagnosis. You access lymph nodes
  3. CT-guided lung biopsy - to access peripheral lung tumors
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21
Q

what do T N and M represent in tumour staging

A

T - primary tumor site
N - regional lymph node involvement
M - metastasis

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22
Q

what are the different T stages for tumor staging and describe them

A 
T1a - ≤ 1 cm 
T1b - > 1 cm ≤ 2 cm
T1c - > 2 cm ≤ 3 cm 
T2a - > 3cm ≤ 4cm
T2b - > 4 cm ≤ 5cm 
T3 - > 5cm ≤7cm 
T4 -> 7 c m

1-5 = stage by stage

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23
Q

how do you treat early stage lung cancer?

A
  1. surgery

2. radical radiotherapy - if significant co-morbidity or patient declines surgery

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24
Q

how do you treat locally advanced lung cancer involving thoracic lymph nodes?

A
  • surgery + chemotherapy

- radiotherapy + chemotherapy +/- immunotherapy

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25
Q

how do you treat metastatic lung cancer

A
  1. targetable mutation - tyrosine kinase inhibitor. For example if the mutation is in ALK it would be an ALK inhibitor
  2. no targetable mutation. PDL1 positive/ >50 % = immunotherapy
  3. no targetable mutation. PDL1 negative = chemotherapy
  4. palliative care
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26
Q

what imagine will help confirm a staging of T2aN0M0?

A

whole body PET - rule out occult metastais

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27
Q

what are differential diagnosis for cough and lethargy, decreased exercise capacity ?

A

lung cancer, pneumonia, bronchiestasis, TB, pulmonary fibrosis

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28
Q

what 2 additional pieces of information are required before treatment of lung cancer?

A
  1. complete medical history - comorbidities, medication

2. lung function tests

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29
Q

how can tissue diagnosis be carried out in a patient with metastatic lung cancer?

A

US-guided liver Biopsy - lung biopsy has risk of pneumothorax

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30
Q

patient with lung cancer.
performance status 3
has dementia

how do you proceed with treatment?

A

palliative care

  • Systemic treatment rarely given to PS3-4
  • With dementia there is issue of consent to treatment and the ability to report side effects
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31
Q

why is lung cancer frequently only diagnosed at a late stage?

A
  1. Lung tumors have a lot of space to grow unnoticed before they start causing symptoms
  2. Early symptoms are vague and nonspecific - can be dismissed and misattributed
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32
Q

reasons for poor prognosis of lung cancer?

A
  1. late diagnosis
  2. smoking related comorbidity
  3. possible nihilism
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33
Q

what interventions might help reduce deaths from lung cancer?

A
  1. Prevention - further action on smoking e.g. in cars
  2. Early detection of symptomatic disease - public health messaging, increase awareness of GPs to encourage hospital referral
  3. Early detection of asymptomatic disease- screening
  4. Rapid hospital referral & treatment
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34
Q

pneumonia is ….?

A

inflammation and swelling of the alveoli

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35
Q

Cough, sneezing, runny or stuffy nose, sore throat, headache are symptoms of a _____ respiratory tract infection

A

upper

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36
Q

Productive cough, muscle aches, wheezing, breathlessness, fever, fatigue are symptoms of a _______ respiratory tract infection

A

lower

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37
Q

what causes pneumonia?

A

Movement of pathogens from upper respiratory tract and nasopharynx to lower respiratory tract. Aren’t usually caught but could be a sign of poor health in an individual.

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38
Q

what are symptoms of pneumonia?

A

Chest pain, blue tinting of lips, severe fatigue, high fever. other symptoms of lower respiratory tract infection

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39
Q

infants especially in africa and asia present with pneumonia and ____

A

bronchiolitis

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40
Q

______ has the highest annual mortality as a respiratory infection

A

mycobacterium tuberculosis

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41
Q

______ is the most commonly identified pathogen in respiratory illness

A

Rhinovirus

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42
Q

state at least 3 common causes of viral infection

A

Influenza A or B, Respiratory Syncytial virus, Human metapneumovirus, Human rhinovirus, Coronavirus. SARS-COV-2

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43
Q

name a common cause of community acquired pneumonia

A

Streptococcus pneumoniae

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44
Q

streptococcus pneumonia.

It is gram___

Intracellular or extracellular?

A

gram positive
extracellular
opportunistic pathogen

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45
Q

Name a common cause of hospital acquired pneumonia

A 
ecoli, enterobacter spp. 
staphylococcus aureus (also CAP)
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46
Q

Give examples of atypical bacteria causing pneumonia

A
  1. Chlamydia pneumoniae, mycoplasma pneumoniae (CAPs)

2. Legionella pneumophilia

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47
Q

how does streptococcus pneumoniae cause infection?

A

Binds to respiratory epithelium using adhesion molecules, can absorb iron from extracellular environment using metal binding proteins

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48
Q

____, ______, and pneumonia are present in acute bacterial pneumonia

A

bronchitis

bronchiolitis

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49
Q

Describe 2 health risks posed by acute bacterial pneumonia

A
  1. systemic inflammation and bacteremia -> organ infection and dysfunction -> sepsis and or deterioration
  2. lung injury -> hypoxemia -> ARDS
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50
Q

what supportive therapy is given for bacterial pneumonia?

A
  • oxygen, fluids, analgesia
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51
Q

describe how antibiotics are prescribed in CAPs AND HAPS

A
  1. Typical CAPs CRB-65 of 0 - penicillins e.g. amoxicillin- beta lactams that bind proteins in the bacterial cell wall to prevent transpeptidation - only effective against +ve bacteria
  2. Atypical CAPs CRB of 0- macrolides e.g. clarithromycin - bind to bacterial 50s ribosomes to prevent protein synthesis
  3. Any CAP with CRB of 1-2 - amoxicillin + clarithromycin
  4. HAPS - doxycycline (a type of tetracycline, bacteriostatic)
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52
Q

Which bacteria is commonly found in nose of humans?

A

streptococcus pneumoniae

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53
Q

Which bacteria are commonly found in the oropharynx region of the body?

A

Haemophilus spp., staph. Aureus, strep. Pneumoniae

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54
Q

what is a pathobiont?

A

Normally commensal but can cause disease if found in wrong environment/ wrong part of anatomy

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55
Q

___ ____ takes advantage of a change in conditons

A

opportunistic pathogen

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56
Q

what are 3 risk factors for active TB?

A
  1. HIV, alcohol, smoking
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57
Q

persistent cough and chest symptoms may indicate?

A

TB

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58
Q

how does TB spread?

A

In active TB, granulomas form which rupture -> dissemination and transmission

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59
Q

state the 4 antibiotics that are used to treat TB for 6 months.
what are their roles?

A

(R)ifampin - inhibits (R)NA synthesis - blocks RNA polymerase - (r)esistance arising

Isoniazid - inhibits cell wall synthesis by blocking Mycolic Acid synthesis

(P)yrazinamide - disrupts (p)lasma membrane, disrupts energy metabolism. Exact mechanism unknown

Ethambutol - inhibits cell wall synthesis. Inhibits arabinosyl transferase

RIPE!!!

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60
Q

commensal respiratory infections are always viral or bacterial?

A

bacterial

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61
Q

what are serotypes?

A

Viruses that can not be recognized by serum antibodies that recognise another

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62
Q

What part of the respiratory tract does H5N1 avian flu infect?
what does it bind to?

A

Haemagglutinin binds alpha2,3 sialic acids in lower respiratory tract
More severe infections, less transmission

*5 is a lower number than 1

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63
Q

What part of the respiratory tract does H1N1 infect?

what does it bind to?

A

Haemagglutinin binds to alpha2,6 sialic acids in upper respiratory tract

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64
Q

What part of the respiratory tract does SARS-COV-2 infect?

what does it bind to?

A

Binds ACE2 in nasal epithelium
binds ACE2 in type 2 pneumocytes of lower respiratory tract
ACE2 upregulated in smokers

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65
Q

What part of the respiratory tract do rhinoviruses bind

A

Major group bind ICAM-1. Minor group bind LDL receptors

Both in upper respiratory tract

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66
Q

What part of the respiratory tract does respiratory syncytial virus bind?
What does it bind to?

A

F and G proteins bind glycosaminoglycans in IGFR1 and nucleolin receptors
Distributed throughout respiratory tract

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67
Q

compare RSV and influenza infection

A

RSV - recurrence reinfection with similar strains. No vaccine
Influenza - no reinfection by same strain. Vaccine induced immunity wanes

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68
Q

state 4 main causes of severe viral infection

A
  1. highly pathogenic strains (zoonotic)
  2. absence of prior immunity - immunodeficiency, B cell antibody levels
  3. predisposing illness/ condition
    • elderly
    • COPD, asthma
      • diabetes, obesity, pregnancy
  4. genes that cause a loss of function in the interferon pathway
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69
Q

What respiratory virus is the leading cause of infant hospitalization? what does it cause?

A

RSV - causes bronchiolitis

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70
Q

what are risk factors for an infant contacting RSV?

A

congenital heart/lung defect, premature birth

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71
Q

symptoms of RSV in infants

A

Expiratory wheezing, prolonged expiration, coughing, hypoxaemia and cyanosis

72
Q

state 3 treatments for viral infections

A

Vaccines, antivirals, monoclonal antibodies

73
Q

how many serotypes of RSV are there?

A

2 - A and B

74
Q

Why, physiologically, does pneumonia present a more challenging disease than bronchitis and bronchiolitis?

A

gas exchange occurs in alveoli. cellular infiltration or fluid leakage into the airspace prevents exchange

75
Q

what is the alveolar macrophage?

A

specialised resident immune cell in alveoli

76
Q

what happens in prolonged pneumonia

A

Prolonged inflammation will result in a shift from accumulation of neutrophils to lymphocytes (primarily T cells) and macrophages, and monocytes

Innate immune system is not sufficient to rapidly clear an infection from the alveoli so adaptive responses take over to clear

77
Q

what demographic or lifestyle factors increase the risk of penumonia?

A

< 2 years
> 65 years
cigarette smoking
excess alcohol consumption

78
Q

social factors increasing risk pneumonia?

A

contact with children <15 years
poverty
overcrowding

79
Q

medications that increase risk of pneumonia?

A

immunosuppressants e.g. steroids
inhaled corticosteroids
proton pump inhibitors

80
Q

what are specific risk factors for certain pathogens causing pneumonia

A

healthcare work
geographical variation
animal contact

81
Q

explain the CRB65 severity score chart for pneumonia

A

1 point for each of:

  • confusion
  • resipiratory rate ≥ 30/min
  • blood pressure SBP <90 OR DBP ≤60mmHg
  • ≥ 65 years

score of 0 = at home antibiotics
score 1-2 = consider hospital referral
3-4 = urgent hospital admission + antibiotics

82
Q

what can a chest x-ray show in a pneumonia patient?

A

opacities in lungs - fluid and cellular infiltration of alveoli
bilateral blurring of costophrenic recesses - pleural effusion

83
Q

why is chlamydia pneumoniae not treated with beta lactams?

A

Chlamydia pneumoniae is gram negative and due to the difference in the bacterial cell wall is therefore penicillin resistant.

84
Q

treatment for ____ bacteria are usually longer because they have lower replication cycles

A

atypical bacteria

85
Q

in a patient with suspected pneumonia, unresponsive to penicillin and clarithromycin and appearing to be worsening, what is the next step in treatment?

A

invasive mechanical ventilation!

or CPAP or VAV-ECMO

86
Q

based on the SARS-COV2 study in your notes, when is the best time to administer dexamethasone?

A

when patient requires oxygen or largest effect when patient is on mechanical ventilation

87
Q

what is the mechanism of steroids given in pneumonia?

A

suppressing the immune inflammation and thus further lung damage.
- useful in SEVERE pneumonia but not milder disease

88
Q

n comparison to steroids, anti-virals such as Remdesivir, which targets the RNA-dependent RNA polymerase of SARS-CoV-2 and other viruses, are most effective if given prophylactically or very early after infection.
why?

A

Early damage is virus dependent, late damage is immune mediated

89
Q

what are the 4 cardinal features of asthma?

A
  1. wheeze +/- dry cough
  2. atopy
  3. reversible airflow obstruction
  4. airway inflammation
90
Q

describe the airway inflammation seen in asthma

A

oesinophilia - biopsy shows red cell stains

type 2 immune response - lymphocytes

91
Q

what does a flow volume loop of an asthmatic patient look like?

A

blunted expiratory curve

92
Q

describe the pathogenesis of allergic asthma

A

Exposure to allergen causes airway remodelling and inflammation
Increased eosinophils
Increased goblet cells
Increase in matrix and increase in amount and size of smooth muscle cells

93
Q

Why do only some people sensitised to allergies develop asthma?

A

Genetic susceptibility - over-expression of genes like IL33, GSDMB

94
Q

Describe the immunological reaction that happens in asthma when exposed to an allergen

A

Exposure to allergen -> dendritic cells present them to CD4 helper cells using MHCII-> helper cells converted to TH2 which secretes IL5, IL-13, IL-4

95
Q

IL5 in asthma promotes?

A

oesinophilia and increased survival

96
Q

IL4 in asthma promotes?

A

B cell secretion of IgE

Next exposure to allergen - crosslinking of IgE on mast cells and degranulation

97
Q

IL13 in asthma promotes?

A

Increased mucus secretion

98
Q

How do you test for allergen sensitization in asthma

A

Skin prick test - wheal and flare reaction

Blood test - for specific IgEs to allergen of interest

99
Q

How do you test for eosinophilia in asthma?

A
  1. Blood eosinophil count >300 cells /mcl is abnormal
  2. Induced sputum eosinophil count: >2.5% - stain red and bilobar
  3. Exhaled nitric oxide (FeNO) - reduced with corticosteroid asthma treatment
100
Q

What are the nice guidelines for asthma diagnosis?

A
  1. History and examination - asses or confirm wheeze when acutely unwell
  2. Objective tests:
    Spirometry FEV1/FVC ratio < 0.7
    Airway obstruction reversible by >12% using bronchodilator
    (FeNO) >35ppb (children), >40ppb (adults)
101
Q

what 3 things do you think of when treating asthma and which drugs fall under each category

A
  1. Reduce airway eosinophilic inflammation regularly - ICS, Leukotriene receptor antagonists
  2. Bronchodilators for acute symptomatic relief - Beta-2 agonists, Anticholinergic therapies
  3. Severe asthma steroid sparing therapies -
    Anti-IgE antibody - Omalizumab
    Anti-interleukin-5 antibody Mepolizumab or Anti-interleukin-5 receptor antibody which target eosinophils
102
Q

causes of an acute asthma attack?

A

Allergens, pathogens, tobacco smoke, pollution

103
Q

what are the negative changes that occur in an acute asthma attack?

A

Reduced antiviral responses and increased viral replication
Eosinophilic inflammation
Reduced peak expiratory flow rate and increased airway obstruction - wheeze

104
Q

how do anti IgE antibodies work?

A

Bind IgE to prevent interaction with mast cells

105
Q

omalizumab is what type of asthma drug?

A

anti-IgE antibody

106
Q

when is omalizumab prescribed?

A

allergic asthma - Persistent IgE mediated asthma in patients at least 6 years
Total serum IgE between 30-1500

107
Q

what type of drug is mepolizumab?

A

Anti-IL5 antibody - prevents eosinophil differentiation, maturation, activation, survival

108
Q

When is mepolizumab prescribed

A

Severe eosinophilic asthma. At least 6 years old
Blood eosinophils >300 cells/mcl in the last 12 months
At least 4 exacerbations in a year

109
Q

what is the mechanism of B2-agonists?

A

Agonist at β2 adrenergic receptor on airway smooth muscle cells. Activation REDUCES Ca2+ entry and this prevents smooth muscle contraction.

110
Q

side effects of B2 agonists?

A

tremors, palpitations, tachycardia, hypokaleamia at higher doses

111
Q

name a B2 agonist

A

salbutamol - a SABA

112
Q

what is the mechanism of ICS

A

binding to the glucocorticoid receptor in eosinophils

Thus reduction in IL5 production -> eosinophil apoptosis/reduced production

113
Q

give examples of ICS drugs

A

Fluticasone, budesonide, mometasone (nasal spray)

114
Q

side effects of ICS?

A

oral thrush

- systemic side effects - osteoporosis, mood swings, immunosuppression, hyperglycaemia, growth retardation in children

115
Q

describe the mechanism of montelukast

A

Antagonism of CysLT1 leukotriene receptor on eosinophils (mast cells and airway smooth muscle cells)

Thus decreases eosinophil migration, (broncho-constriction and inflammation)

(antileukotriene)

116
Q

which drug is useful as prophylaxis for aspirin induced and exercise induced asthma

A

montleukast

117
Q

First line asthma treatment for <5 children?

How does treatment change with worsening symptoms

A

SABA

  • then first add on ICS
  • the add on LABA
118
Q

why is inhaled salbutamol preferred to oral?

A

you are administering a lower dose as it goes directly to required tissue. Thus reduction in potential side effects.

119
Q

why are nebulisers preferred in asthma treatment

A

Many drug solutions, can deliver combinations, minimal patient cooperation required, can deliver to all patients, concentration and dose can be modified, normal breathing pattern

120
Q

state 4 places where 80% of inhaled sabutamol would go. other than intended target

A
  1. Exhaled
  2. absorption from lungs into blood and binds to plasma protein
  3. mucociliary clearance in lungs
  4. swallowed portion into GI tract
  5. absorption across mucous membrane in oral cavity and pharynx
121
Q

Significant proportion of fluticasone is swallowed. Despite this, the oral bioavailability (proportion of drug reaching plasma VIA the GI tract is less than 1%. Why?

A

first pass hepatic metabolism

122
Q

why is montelukast useful in aspirin induced asthma?

A

NSAIDS block COX enzyme. thus more arachidonic acid is converted to leukotrienes. and montelukast is a leukotriene receptor antagonist

123
Q

what are the 3 components of the respiratory system

A

Nervous system, respiratory muscles, pulmonary

124
Q

what 4 criteria are used to classify ARDS?

A

TIMING - Within 1 week of known clinical insult or worsening respiratory symptoms
CHEST IMAGING - Bilateral opacities not fully explained by effusions, lobar/lung collapse or nodules
ORIGIN OF OEDEMA - not explained by cardiac failure or fluid overload
PF ratio < or equal to 300 mmHg

125
Q

what are chronic causes of respiratory failure?

A 
COPD
Pollution 
Recurrent pneumonia 
Cystic fibrosis 
Pulmonary fibrosis 
Neuro-muscular diseases
126
Q

acute causes of respiratory failure?

A

LRT Infection -viral bacterial,
Aspiration
Trauma
Extra pulmonary - Pancreatitis, Transfusion
Pulmonary vascular disease - emboli, hemoptysis

127
Q

what is type 3 respiratory failure

A

Perioperative respiratory Failure

Most frequent cause = atelectasis Hypoxaemia or hypercapnoea

128
Q

how do you prevent type 3 respiratory failure?

A

Preventing atelectasis: aneasthetic or operative technique, posture,

Reversing atelectasis: incentive spirometry, analgesia, attempts to lower intra- abdominal pressure

129
Q

what is type 4 respiratory failure?

A

shock(hypoperfusion)

130
Q

how do you treat type 4 respiratory failure?

A

optimise ventilation therapy

131
Q

what are the effects of ventilation on each side of the heart?

A

Reduced afterload (good for LV) Increased pre-load (bad for RV)

132
Q

causes of type 1 respiratory failure?

A 
Collapse 
Aspiration  
Pulmonary oedema
Fibrosis 
Pulmonary embolism 
Pulmonary hypertension
133
Q

causes of type 2 respiratory failure?

A 
Nervous system 
Neuromuscular
Muscle failure 
Airway obstruction 
Chest wall deformity
134
Q

state 3 mechanisms of acute lung injury

A
  1. infection
  2. inflammation
  3. immune response
135
Q

describe the inflammation that happens in an acute lung injury

A

Alveolar macrophages release cytokines like TNF alpha and IL8
Protein rich oedema in alveoli builds up
Inactivation of surfactant - alveolus less efficient at expanding

136
Q

describe the immune response that happens in acute lung injury

A

Neutrophils migrate out of blood vessels into interstitium (where they can cause damage) on the way to alveolus/site of cytokine release
Neutrophils secrete proteases which cause damage and fluid build up in interstitium - larger gas exchange distance

137
Q

how do you minimise ventilator induced lung injury?

A

maintaining driving pressure

138
Q

what modalities are used to diagnose ARDS?

A

Lung CT

Lung USS

139
Q

What score is used to determine ARDS severity and what factors are examined?

A 
Murray score:
PF ratio 
CXR 
PEEP
Compliance
140
Q

when do you treat ARDS patients with ECMO?

A

Murray score of 3 or more
When positive pressure ventilation is not appropriate
Reversible disease process

141
Q

disadvantages of ECM0

A

Case selection, not universally available/inequity of provision of care, bleeding: intra-cerebral, venepuncture sites, epistaxis, haemoptysis, Haemolysis, infections from central dwelling canulae, cost.

142
Q

Advantages of ECMO

A

improve oxygen delivery, improve carbon dioxide removal, rest lung and prevent ventilator associated lung injury, resolve respiratory acidosis, reduce multiple organ dysfunction arising from hypoxaemia and hypercapnia

143
Q

Why does additional gas dissolve into blood during dive?

A

Henrys law

144
Q

Which 2 gases increase in partial pressure body during a scuba dive?

A

oxygen and nitrogen

145
Q

Consequences of too much oxygen?

A

toxicity, siezures

146
Q

What happens if a scuba diver ascends too rapidly?

A

Decompression illness:
Nitrogen separates from blood and forms bubbles
Bubbles in joints = joint pain
Bubbles in bloodstream and tissues
Bubbles compress nerves - neurological symptoms

147
Q

how can the effects of gas pressure during scuba diving be mitigated?

A

Change breathing gas

148
Q

What are the functions of pulmonary circulation

A
  1. Gas exchange
  2. Metabolism of vasoactive substances- capillary beds contain ACE which convert Ang1 -> Ang2 AND breaks down bradykinin
  3. Filtration of blood - stops small venous embolisms from becoming arterial embolisms through elimination
149
Q

How do bubbles from venous systems reach the arterial system?

A

Congenital defect - PFO - stroke, MI risk, PE risk

150
Q

Circumstances associated with bypassing the respiratory exchange surface?

A

Foetal circulation
Bronchial circulation
Congenital defect - ASD, PFO, VSD

151
Q

How common is PFO?

A

1 in 4

152
Q

What happens if a diver holds their breath during ascent from 10-30m?

A

Pulmonary barotrauma due to boyle’s law

153
Q

Values show a patient has a Partially compensated respiratory alkalosis with severe hypoxemia. The haemoglobin levels are high. Normal range is 13.8 - 17.2 g/DL. What do you think could have happened to the patient?

A

Climbing a mountain - high Hb levels suggests prolonged exposure to high altitude and low 02

154
Q

46 year old patient in hospital recieveing oxygen through nasal cannula. Hypoxemia, hyperventilation, low PaO2 and PaCO2 observed. could be respiratory alkalosis and metabolic acidosis. what do you think could have happened?

A

bacterial pneumonia

155
Q

name some carcinogens found in tobacco smoke

A

Formaldehyde
Benzene
Ethylene Oxide

156
Q

how does smoking cause gene mutations in lung cancer?

A
  1. Many of the chemicals found in cigarette smoke can form DNA adducts
  2. Normally corrected by anti-tumour genes such as p53 or Rb
  3. Insertion into oncogenes may result in mutation that provides benefit
157
Q

what are some key features of the variola virus

A

It is a DNA virus
It has been eliminated
it is non-zoonotic

158
Q

What are the risk factors for pneumonia but not covid19 mortality?

A

young age, HIV, asthma

159
Q

when do we get the most respiratory infections?

A

up to 5 years old

160
Q

how many serotypes of coronaviruses are there?

A

4

161
Q

how many serotypes of influenza viruses are there?

A

3

162
Q

What are Factors affecting exercise capacity?

A

Neurological (e.g. motor control, coordination)
Respiratory (e.g. ability for lungs to ventilate, for pulmonary perfusion)
Cardiovascular (e.g. ability for heart to receive blood from lungs and to pump to working muscles)
Muscular (e.g. local perfusion, muscle cell enzymes)

163
Q

What is involved in the cardiopulmonary exercise test?

A

Uses a cycle ergometer or treadmill
Intensity is incremental
Undertaken under close clinical supervision in a controlled environment
ECG, ventilation, O2 and CO2 routinely measured
Peak VO2 usually the primary outcome

164
Q

What is involved in a 6-minute walk test

A

Uses a 20-30 m flat course (e.g. corridor)
Objective is to cover greatest distance as possible in six minutes
Externally timed by assessor
Sub-maximal test
Primary outcome is total distance walked in six minutes
Secondary variables may be ‘perceived exertion’ scales, heart rate and pulse oximetry
normal range in 6 minutes - 400-700 meters

165
Q

What is involved in an Incremental shuttle walk test?

A

Uses a 10 m circuit
Externally paced by an audio recording (like bleep test)
Each minute has one extra length than the previous minute
Primary outcome is total distance walked before volitional end
Secondary variables may be ‘perceived exertion’ scales, heart rate and pulse oximetry

166
Q

What treatment should be offered to all people with COPD?

A

Pulmonary rehabilitation - to increase exercise capacity

167
Q

Which people are pulmonary rehabilitation not suitable for?

A

people who are unable to walk
who have unstable angina
who have had a recent myocardial infarction.

168
Q

An assessment for ambulatory oxygen could be carried out using a_____?

A

6MWT

169
Q

The assessment for Long term oxygen therapy (LTOT) defined as >15 hours / day) would include a ________?

A

measure of blood gases

170
Q

What is the effect of Supplemental Oxygen on
Breathlessness?
Exercise capacity?

A

can improve exercise capacity but does not always relieve breathlessness

171
Q

Explain the trends observed in this standard nine panel view for cardiorespiratory variables during an incremental CPET to exhaustion.

A

VE vs VCO2 single straight line graph - VE = minute ventilation, VCO2 = Co2 output in a minute.
The more CO2 you produce, they more you hyperventilate to expel co2.
The slope is an index of exercise capacity
Slope is influenced by fitness levels sex, age, height and weight
Positive y intercept due to Slight ventilation without work due to adrenaline

172
Q

What is the most common cause of ACUTE bacterial infection?

A

Streptococcus pneumoniae

173
Q

Caseating granulomatous inflammation of lungs in __

Non caseating granulomatous inflammation of lungs in ___

A

Tuberculosis

Sarcoidosis

174
Q

The failure of the lungs and heart to provide adequate oxygen is known as what type of respiratory failure?

What is the criteria for it?

A

Type 1 respiratory failure

Hypoxemia refractory to 02 supplementation (PaO2 < 60 mmHg

174
Q

Failure of the lungs to eliminate adequate CO2 all known as pump failure is what type of respiratory failure?

What is the criteria?

A

Type 2 respiratory failure

PaCo2 >45. Hypercapnic

174
Q

decreased alveolar ventilation, for example due to increased dead space causes what respiratory failure?

A

Type 2

175
Q

Increased shunt fraction (QS/QT) due to alveolar flooding is seen in what type of respiratory failure?

A

Type 1

Medicine MBBS year 2 (11 decks)

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