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Danielle's MD1 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What are some common VIRAL respiratory tract infections?

A
  • common cold (coryza)
  • sore throat (pharyngitis)
  • Tonsillitis
  • Sinusitis
  • Laryngitis
  • Croup
  • acute bronchitis
  • bronchiolitis
  • influenza
  • SARS
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2
Q

What are some common URT syndromes?

A
  • common cold
  • pharyngitis/tonsillitis
  • sinusitis
  • otitis media
  • epiglottitis
  • croup
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3
Q

What are the main actions of exogenous glucocorticoid use in asthma?

A

-decrease inflammatory cell number and activation
(via targetting IL-8, COX2, ICAM-1, NOS2)
-increases activation of anti-inflammatory effectors
(by activating GILZ, MKP-1, IkBalpha)
-decrease probability and severity of asthma episodes

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4
Q

Exogenous glucocorticoid use in asthma targets what specific inflammatory cells?

A
  • decreased activity and recruitment of eosinophils, macrophages, mast cells,
  • decreased cytokine production by macrophages, smooth muscle and fibroblasts
  • decreased collagen production by s muscle and fibroblasts
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5
Q

What are the 2 main categories of glucocorticoids used in asthma?

A
  • inhaled/topical

- oral/systemic

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6
Q

What are some differences between inhaled and oral glucocorticoids?

A

Inhaled

  • start at the effective dose and then step down
  • well tolerated/few SE
  • used in combination with LABAs

Oral

  • either treat for several days for acute asthma or chronically for sever asthma
  • there are dose limiting SE
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7
Q

What are the side effects of inhaled glucocorticoids?

A
  • dysphonia
  • oral candidiasis
  • decreased serum cortisol
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8
Q

What are the side effects of oral glucocorticoids?

A
  • osteoporosis
  • diabetes
  • muscle wasting
  • HT
  • growth suppression
  • suppression of HPA axis
  • eventual atrophy of the adrenal gland with chronic use
  • if you suddenly stop them you can go into withdrawal
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9
Q

Describe the regulation of endogenous glucocorticoids

A

cortisol (an endogenous glucocorticoid) is released from the adrenal gland where is negatively feedbacks to

  • inhibit the hypothalamus from releasing corticotropin releasing hormone,
  • it inhibits the anterior pituitary from releasing corticotropin
  • inhibits the immune system and the CV system
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10
Q

What other 2 drugs can be used to treat asthma other than glucocorticoids?

A

Methylxanthines (eg theophylline)

Phosphodiesterase inhibitors (eg roflumilast)

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11
Q

Briefly explain the mechanism behind using theophylline for asthma

A
  • PDE inhibition/ s muscle relaxant
  • adenosine antagonism
  • HDAC2 activation
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12
Q

What are some side effects of using theophylline in asthma?

A
  • nausea
  • vomiting
  • diarrhea
  • CNS stimulation
  • cardio stimulation–> dysthymia
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13
Q

Describe the steps in asthma therapy

A

Step 1: intermittent inhaled SABA
Step 2: add mildly persistent inhaled glucocorticoid
Step 3: add moderate persistent inhaled LABA
Step 4: increase daily inhaled glucocorticoid, maintain daily LABA, plus theophylline, anti leukotriene and oral glucocorticoid
Step 5: add oral prednisolone

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14
Q

What does GOLD stand for? What is it used for?

A 
Global initiative for chronic 
Obstructive 
Lung
Disease 
-its a way to classify the severity of airflow limitation in people with COPD

GOLD1= mild
GOLD2= moderate
GOLD3=severe
GOLD4= very severe

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15
Q

The alveolar capillary membrane is composed of what

A
  • layer of surfactant
  • type 1 alveolar cells
  • basement membrane (shared)
  • vascular endothelial cell
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16
Q

What are some characteristics of the alveolar capillary membrane?

A
  • thin (o.5 microns)
  • large SA= 50-100m2
  • alveolar volume= 3-6L
  • capillary volume= 80ml
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17
Q

What are some diseases that can disrupt the alveolar capillary membrane?

A
  • inflammation
  • infection
  • fibrosis
  • emphysema
  • fluid
  • cancer
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18
Q

What are the likely physiological effects of disrupting the alveolar capillary membrane?

A
  • abnormal gas exchange
  • abnormal lung mechanics
  • pulmonary vascular complications
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19
Q

Describe the diffussion of gases in the lungs

A
  • diffusion is passive/non E requiring
  • driven by diffs in partial pressures of gases on either side of the membrane
  • rate of diffusion is driven by Ficks Law
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20
Q

What is Ficks law?

A

The rate of diffusion is proportional to [AxD(P1-P2)]/T

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21
Q

Compare the diffusion rate of CO2 to O2

A

CO2 diffusion rate is 20x that of O2

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22
Q

Describe the diffusion of Oxygen

A
  • very fast
  • 0.75 secs at rest
  • 0.25 secs during exercise
  • there is built in redundency (i.e. if we decrease transit time e.g. in exercise, there is still enough time for adequate diffusion of O2)
  • NB normal gas exchange is not diffusion limited, but it in disease states gas exchange is diffusion limited
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23
Q

Describe the phrase: diffusion limitation of oxygen transfer

A
  • oxygen transfer can be diffusion limited in disease states
  • if the a-c membrane is grossly abnormal in severe disease O2 transfer is diffusion limited at rest
  • in moderate disease the O2 transfer is only diffusion limited during exercise
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24
Q

Describe the diffusion of carbon dioxide

A
  • its similar to O2 but 20x faster
  • diffusion limitation only occurs in very severe abnormalities of the membrane
  • when there is an elevated PaCO2 it is due to inadequate alveolar ventilation (VA)
  • PaCO2 is inversely proportional to alveolar ventilation
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25
Q

What are some causes of low PaO2?

A
  • low PiO2
  • low ventilation
  • abnormal gas exchange (via low V/Q, shunt or diffusion impairment)
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26
Q

What are some causes of a high PaCO2?

A

Low ventilation

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27
Q

What are the effects of restrictive lung disease?

A
  • increased sensation of breathing
  • increased elastic WOB
  • decreased lung volume
  • altered pattern of breathing
  • decreased max ventilation
  • abnormal gas exchange that worsens during exercise
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28
Q

Describe the mechanism behind increase sensation and WOB in restrictive lung disease.

A

Inspiration muscles need to generate higher Ps to overcome the stiffness (decreased compliance/ elastic WOB). This leads to

  • recruitment of accessory muscles
  • increased O2 consumption if resp muscles
  • risk of muscle fatigue–> ventilatory failure
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29
Q

What happens to the FVC, FEV1 and FER in restrictive lung disease?

A

FVC is reduced
FEV1 is reduced
FER is normal (because FVC and FEV1 has decreased in proportion)

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30
Q

Minute ventilation is proportional to what…

A

metabolic activity

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31
Q

Describe the type of breaths people take when they have stiff lungs

A

rapid and shallow breaths

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32
Q

In people with restrictive lung disease exercise is often limited by what?

A
  • hypoxia

- pulmonary HT

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33
Q

What reduces surface tension in the alveoli and what happens as a result to this?

A
  • surfactant

- increases the compliance

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34
Q

What are the parameters that describe ventilatory failure?

A

PaO2 50mmHg

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35
Q

What is idiopathic pulmonary fibrosis?

A
  • a fatal interstitial lung disease
  • mean survival= 3 years
  • aka usual interstitial pneumonitis
  • scarring thickens and stiffens alveolar walls leading to impaired oxygen transfer, increased WOB, resp failure
  • drugs used: pirfenidone (TGFbeta modifier), nintedanib (triple kinase inhibitor)
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36
Q

What are the types/causes of pulmonary arterial hypertension?

A
  • idiopathic
  • familial (mutation in BMPII receptors)
  • secondary (chronic hypoxia from: pulmonary fibrosis, COPD, altitude)
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37
Q

What are some treatments for PAH?

A

Endothelin receptor antagonists
-bosentan, sitaxentan, ambisentan

Prostanoids (prostacyclin analgoues)

PDEI
-sildenafil

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38
Q

What is a systematic review?

A
  • lit review that focuses on 1 question
  • steps= identify, selection&appraisal, synthesis
  • has well defined criteria
  • reviews clinical trials and observational data
  • its the highest level of evidence
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39
Q

What is a meta-analysis?

A
  • statistical aspect of a systematic review
  • derives pooled weighted average effect sizes
  • its more quantitative than systematic reviews
  • it mainly takes experimental data
  • it functions to summarise the current lit, increase the power of results, resolve uncertainty, increase precision and answer other questions
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40
Q

What does the identify step in performing a systematic review consist of?

A
  • define a clear question
  • look at PICOT parameters
  • search databases using MESH terms and relevant spelling
  • look at other reference lists
  • look at grey literature
  • adopt inclusion/exclusion criteria
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41
Q

What does the selection&appraisal step in performing a systematic review consist of?

A
  • done by at least 2 independent ppl
  • read all abstracts
  • apply inclusion and exclusion criteria
  • look at full paper
  • access for quality
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42
Q

What does the synthesis step in performing a systematic review consist of?

A

-perform a meta-analysis

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43
Q

Describe what a forest plot is?

A

-quick way to understand systematic reviews
-squares= inidividual studies
area of the square= sample size
horizontal line in the square= CI
verticle line in the square= RR
-diamonds= pooled effects
horizontal width= CI
vertical width= weighted effect size
-line of null effect

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44
Q

What is heterogeneity and what are the different types?

A

Heterogeneity= a test to determine how different the studies being compared are to each other

  • p value>0.05 is good here because it says the studies are similar enough to be pooled i.e. they have failed the heterogeneity test
  • types: statistical heterogeneity, non-statistical heterogeneity
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45
Q

What is statistical heterogeneity?

A
  • measures effect/outcome

- its quantitative

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46
Q

What is non-statistical heterogeneity?

A
  • aka methodological/situational heterogeneity
  • use PICOT
  • its qualitative
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47
Q

What are some common LRT infection syndromes?

A
  • acute bronchitis
  • acute exacerbation of chronic bronchitis
  • bronchiolitis
  • pneumonia (acute bacterial, atypical, others)
  • empyema
  • lung abscess
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48
Q

What causes acute exacerbations of chronic bronchitis?

A

bacterial infection on a compromised lung

  • strept. pneumococci
  • H. influenzae
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49
Q

What causes bronchiolitis?

A

-RSV

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50
Q

What causes acute bacterial pneumonia?

A
  • pneumococci (community derived pneumonia)
  • H. influenzae
  • staph (hospital derived pneumonia)
  • Klebs (hospital derived pneumonia)
  • legionella
  • TB
  • chlamydophila
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51
Q

What causes atypical pneumonia?

A
  • mycoplasma
  • chlamydia
  • M. catarrhalis
  • influenza
  • RSV
  • adenovirus
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52
Q

What causes other pneumonia?

A

Fungi

  • Histoplasma
  • Aspergillus
  • Pneumocystis
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53
Q

What causes lung abcesses?

A
  • mixed anaerobes
  • Staph
  • Klebs
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54
Q

What causes empyema?

A

-staph. aureus

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55
Q

How do you treat pneumonia?

A
  • you need to distinguish between community derived and hospital acquired
  • look at the severity index
  • look at any underlying illnesses
  • look at RFs
  • determine the type of specimen to see if AB treatment is appropriate
  • Pen G/amoxycillin plus doxycycline/macrolide
  • vaccines
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56
Q

What are some common causes of the common cold?

A
  • rhinovirus
  • parainfluenza virus
  • RSV
  • enterovirus
  • coronavirus
  • human metapneumovirus
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57
Q

What are some causes of epiglottitis?

A

-H-influenza type b

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58
Q

What are some causes of croup/laryngio-tracheal bronchitis?

A
  • parainfluenza virus
  • influenza A
  • RSV
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59
Q

What are some causes of otitis media?

A
  • pneumococci
  • H.influenzae
  • M.catarrhalis
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60
Q

What are some causes of sinusitis?

A 
primary= viral
secondary= h.influenzae and strept. pneumoniae
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61
Q

What are some causes of pharyngitis/tonsillitis with nasal involvement?

A

not likely to be bacterial

  • adenovirus
  • enterovirus
  • parainfluenza virus
  • influenza virus
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62
Q

What are some causes of pharyngitis/tonsillitis without nasal involvement?

A
  • adenovirus
  • influenza
  • enterovirus
  • reovirus
  • strept. pyogenes
  • strept. C
  • strept. G
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63
Q

What is a tropism?

A

the anatomical localisation of an infection

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64
Q

List some common routes of entry for viruses

A
  • paraenteral inoculation
  • skin
  • conjunctiva
  • respiratory tract
  • ailmentary tract
  • urogenital tract
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65
Q

What are some barriers in the ailmentary tract that viruses need to overcome?

A
  • sequestration in intestinal contents
  • mucus
  • stomach acidity
  • intestinal alkalinity
  • proteolytic enzymes form pancreas
  • bile
  • IgA
  • scavenging macrophages
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66
Q

What are some barriers in the respiratory tract that viruses need to overcome?

A
  • mucus
  • cilia
  • alveolar macrophages
  • temperature gradient
  • IgA
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67
Q

What are some different mechanisms of viral spread in the body?

A
  • local spread on epithelial surfaces
  • subepithelial invasion and lymphatic spread
  • via the bloodstream
  • infects the foetus
  • infects the baby at birth
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68
Q

Describe the different types of viremia

A

Free in the plasma viremia

  • produced by infected vascular endothelium or released from the liver and spleen
  • neutralised by Ab and removed by macrophages
  • there are 2 stages: 1st small numbers, 2nd large numbers

Cell associated viremia

  • can persist if the viral genome becomes latent
  • avoids CD8 attack when latent
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69
Q

What determines a tropism?

A
  • availability of receptors
  • optimal temp
  • stability in extremes of pH
  • ability to replicate inside macrophages and lymphocytes
  • polarised release
  • presence of activating enzymes
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70
Q

What are some types of viral induced damage to tissues?

A
  • loss of function
  • initiation of apoptosis
  • death of cells directly form viral replication
  • death from toxicity of viral products
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71
Q

What are some signs of immunopathology?

A
  • fever
  • IL-1, TNF
  • increased size of LNs
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72
Q

List some targets for viral evasion strategies

A
  • Ab
  • Ab and T cells
  • T cell priming by DCs
  • CD8 cell recognition
  • complement
  • NK cell recognition
  • Interferon
  • Apoptosis inhibition
  • cytokines
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73
Q

Describe how viruses evade Abs

A

-antigenic variation in B cell epitopes by antigenic drift

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74
Q

Describe how viruses evade Abs and T cells

A

latency

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75
Q

Describe how viruses stop T cell priming by DCs

A
  • blockage of cytokine induced maturation of T cells
  • virus encoded homologue of cytoplasmic tail of TLR4 therefore no signal transduction
  • blockage of T cell stimulation
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76
Q

Describe how viruses evade CD8 T cell recognition

A
  • Ag variation in CD8 epitopes
  • inhibition of proteosome
  • decreased MHC I expression or transcription
  • inhibition of viral peptide release from the ER
  • inhibition of processing and presentation
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77
Q

Describe how viruses evade complement

A

-viral encoded homologues

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78
Q

Describe how viruses evade NK cell recognition

A
  • virus encoded MHC I like molecule
  • upregulation of non-classical class I molecules
  • mutations in ligand for activating receptor
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79
Q

Describe how viruses evade interferon

A

-interfere with PKR pathway by small RNAs, ds RNA binding proteins, PKR binding proteins

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80
Q

Describe how viruses evade cytokines

A
  • virus encoded cytokine receptor homologues
  • intracellular blocking of cytokine production
  • intracellular interference with cytokine function
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81
Q

What are some factors that affect susceptibility to viral infections?

A

Genetic

  • inherited defects
  • receptor genes
  • IFN inducible genes
  • polymorphisms in genes controlling immune responses

Non-genetic

  • age
  • malnutrition
  • hormones and pregnancy
  • dual infections
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82
Q

What are the types of outcomes of a viral infection?

A
  • fatal
  • full recovery
  • recovery but permanent damage
  • persistent infection
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83
Q

What are the stages of viral replication?

A
  • Attachment
  • Penetraction
  • Uncoating
  • Gene transcription
  • Assembly
  • Release
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84
Q

Describe each step of viral replication

A

Attachment
-via carb or protein receptors

Penetration
-by fusion or endocytosis

Uncoating

Gene transcription
-DNA viruses replicate in the nucleus
(protein synthesis)
–early proteins are nonstructural

Assembly
-spontaneous or proteolytic cleavage

Release

  • lysis
  • budding for enveloped viruses
  • secretatory pathway for golgi derived enveloped viruses
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85
Q

What are type I pneumocytes?

A
  • make up the majority of the SA
  • they are the exchange surface
  • have tight junctions
  • simple squamous
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86
Q

What are type II pneumocytes?

A
  • 5% of SA
  • more numerous
  • cuboidal cells
  • short microvili
  • lamellar bodies produce surfactant
  • can replace itself or produce type I pneumocytes
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87
Q

Describe the order of cells in the blood gas barrier from the alveolar lumen to the blood plasma

A
  • alveolar lument
  • surfactant
  • type I pneumocyte
  • basal lamina
  • CT
  • basal lamina
  • endothelial cell
  • plasma
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88
Q

Describe the structure of a bronchus

A
  • thinner walls than the trachea
  • cartilage plates
  • s muscle between lamina propria and submucosa
  • glands
  • lymphoid nodules
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89
Q

Describe the structure of a brionchiole

A
  • NO cartilage
  • 1-2mm diam
  • resp epithelium loses goblet cells and ciliated columnar cells
  • gains clara cells
  • radial CT
  • s muscle
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90
Q

Describe the structure of a terminal brionchiole

A
  • final level of the conducting system
  • NO goblet cells
  • 1-2 layers of s muscle
  • clara cells
  • cuboidal epithelium
  • cilia
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91
Q

Describe the structure of a respiratory brionchiole

A
  • alveoli start to appear–> alveolar ducts
  • epithelium is cuboidal to squamous
  • intermittent wall
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92
Q

Describe the structure of an alveolus

A
  • 200um in diam
  • simple squamous epithelium
  • wall contains capillaries
  • alveoli are connected by pores
  • interalveolar septum
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93
Q

Describe the process of inspiration

A
  • stimulation of the diaphragm by phrenic nerves C3,4,5
  • stimulation of external intercostal muscles by intercostal nerves
  • increase volume of the thorax
  • negative intrapulmonary P
  • sucks air into lungs
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94
Q

Describe the process of expiration

A
  • passive
  • inspiratory muscles relax
  • elastic recoil of lungs
  • generates a positive intrapulmonary P
  • pushes air out
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95
Q

In a normal person FEV1 should be what % of FVC?

A

-greater than 70%

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96
Q

Describe the FVC, FEV1 and FER in people with airflow obstruction

A

FVC is normal but it takes longer to get there
FEV1 is smaller than 70% of FVC
FER is smaller than 70%

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97
Q

Why is it important to match ventilation and perfusion?

A

Because this is when gas exchange is most efficient

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98
Q

What diseases commonly have V/Q mismatch?

A

-COPD and asthma

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99
Q

What are the diff types of V/Q mismatch?

A
  • Low V/Q units

- Shunt

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100
Q

What is the compensatory mechanism done by the body in response to a V/Q mismatch?

A
  • vasoconstriction in areas of low V in order to reduce the hypoxaemic effects
  • this can lead to increased pulmonary artery P
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101
Q

What is the alveolar-arterial gradient?

A

-a measure of the overall efficiency of gas exchange across ALL A-C units

PAO2= PiO2 - (PACO2/RQ)
PiO2= 150
PACO2= PaCO2 from blood gas results
RQ= 0.8

gradient= PAO2-PaO2
PaO2 from blood gas results

normal gradient <15-30

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102
Q

In order to breath what 2 forces must you overcome?

A
  • resistive force

- elastic force

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103
Q

What does hypoxaemia mean?

A

-decreased O2 content of the blood which leads to decreased O2 in the tissues

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104
Q

What does hypercapnemia mean?

A

-increased CO2 which leads to respiratory acidosis

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105
Q

What are the normal blood gas and pH parameters?

A

PaO2 ~100mmHg
PaCO2= 40mmHg
pH= 7.40

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106
Q

What are the different types of validity?

A

Internal validity

  • how well did it answer the q?
  • how did the study deal with bias and confounding?

External validity

  • generalisability
  • use PICOT
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107
Q

Describe intention to treat analysis and what it attempts to minimise

A
  • you assume the subjects remained in the group to which they were originally randomised to, regardless of cross over or drop out
  • is decreases selection bias
108
Q

Describe CI for HR, OR, RR

A

it must NOT include 1

109
Q

Describe CI for absolute risk diffs

A

it must NOT include 0

110
Q

What are some types of errors?

A
  • Type I error (alpha)

- Type II error (beta)

111
Q

What is a type I error (alpha)?

A

When a study says there is an effect when in actual fact there isn’t one
-its due to bias and confounders

112
Q

What is a type II error (beta)?

A

When the study says there is no effect when in actual fact there is one
-its due to the study not having enough power (small sample size)

113
Q

Describe number needed to treat

A

-the number of people needed to undergo the intervention in order to prevent the outcome in one person
NNT= 1/absolute risk or rate reduction

114
Q

Briefly describe the inflammation present in asthma

A
  • Th2 cells
  • mast cells
  • eosinophils
  • some neutrophils
  • mucus hypersecretion–> mucus plug
  • vasodilation
  • bronchoconstriction
  • sensory nerve activation
  • oedema
  • increased vascularity
  • increased subepithelial collagen thickening
115
Q

What are the 4 major groups of hypersensitivity?

A

Type I: immediate hypersensitivity
Type II: antibody mediated
Type III: immune complexes
Type IV: delayed type

116
Q

Describe the 2 phases of a type I hypersensitivity reaction

A

Sensitisation phase

  • DC and IL-33
  • Basophil and IL-4
  • TH2
  • IgE and FCERI

Effector phase

  • immediate phase (release of preformed mediators)
  • delayed phase (lipid mediators)
  • late phase (cytokines)
117
Q

What are some treatments for type 1 hypersensitivity?

A
  • epinephrine
  • inhaled beta agonists
  • corticosteroids
  • antihistamines
  • desensitisation therapy
118
Q

Describe delayed type hypersensitivity

A
  • cell mediated
  • via TH1, IFN-gamma and macrophages
  • has a sensitisation phase
  • Ag persistance–> accumulation of T cells and macrophages
  • 3 examples: contact hypersensitivity, TB and Celiac disease
119
Q

Describe contact hypersensitivity

A

-requires previous exposure
-Ag haptenates to a protein that is normally presented in MHC
-re exposure triggers memory cells and increased IFN-gamma
Eg poison ivy, TB test, eye drop allergy

120
Q

Describe mycobacterium tuberculosis

A
  • inhalation of TB droplet
  • multiplication inside resident alveolar macrophages
  • cytokine production (IL-12, TNF-alpha, IL-1)
  • limited degradation
  • macrophages and DC migrate to the LN–> present TB Ag to T cells
  • activated CD8, TH1 cells produce IFN-gamma –> further activate macrophages
  • persistence of TB–> cyclic cycle–> granuloma formation
121
Q

Describe celiac disease

A
  • to gliadins
  • > 90% are DQ2 positive
  • DQ2 peptide binding cleft is positively charged and therefore binds negatively charged aa
  • gliadins are rich in glutamine
  • unmodified gliadins bind POORLY
  • gliadins modified by tissue transglutaminase 2 cause glutamine–> glutamate
  • can now bind in pocket, presented in MHC II–> effector TH1 response–> IFNgamma–> damage to intestinal wall
122
Q

Where are mast cells located?

A

At sites in contact with the external environment

123
Q

What are some signals for mast cell degranulation?

A
  • poly basic drugs
  • morphine
  • vancomycin
  • allergen
  • stings
  • activated complement
  • neuro peptides
  • hypertonic saline
  • osmotic stimuli
  • UV light/heat
  • mechanical stimulation
124
Q

Describe the degranulation process of mast cells

A
  • allergen binds to already bound IgE
  • cross linking
  • brings FceR1 subunits tog (1alpha, 1beta, 2gamma)
  • lyn tyrosine kinase phosphorylates the ITAMS and other proteins
  • syk tyrosine kinase is recruited–> activated–>produces–> DAG and IP3
  • DAG activates PKC–> granule movement and membrane fusion
  • IP3 increases intercellular calcium–> membrane fusion and cytokine gene expression
125
Q

Describe the 3 phases of the mast cell response

A

Immediate
-preformed mediators
(Histamine)

Delayed
-synthesised mediators
(Cys-LTs, PGD2)

Slow
-changes in gene expression

126
Q

What are some actions of histamine

A

Acting on H1

  • increase in vascular permeability
  • vasodilation
  • mucus secretion
  • bronchospasm
  • pain and itch
  • increased wakefulness

Acting on H2

  • positive inotropic and chronotropic
  • gastric acid secretion
127
Q

What are some inhibitors of mast cell activation?

A
  • PGE2
  • NSAIDs
  • COX2 selective inhibitors
  • cortisol
  • adrenaline
  • disodium cromoglycate/ nedocromil sodium
  • omalizumab
128
Q

What are some inhibitors of mediator production and actions

A
  • glucocorticoids
  • H1 receptor antagonists
  • cysteinyl leukotriene receptor antagonists
129
Q

Describe the actions of glucocorticoids

A
  • induces annexin 1

- decrease mast cell cytokine production

130
Q

Describe the actions of cysteinyl leukotriene receptor antagonists

A

Eg montelukast

-bronchodilator

131
Q

Describe the 3 generations of H1 receptor antagonists

A

1st gen
-sedative

2nd gen

  • non sedative
  • poor CNS entry
  • lacks anti muscarinic activity
  • can cause arrhythmias

3rd gen

  • newer
  • non sedative
  • decrease cardiac events
132
Q

Crepitations indicate what 2 possible pathological processes?

A

-fluid in the lungs
or
-fibrosis

133
Q

What are the 2 main consequences of abnormalities of the pulmonary vessels?

A
  • increased movement of fluid out of pulmonary capillaries and into the alveoli
  • increased P within the pulmonary vessels
134
Q

Describe some characteristics of the pulmonary circulation

A
  • low P ~15mmHg
  • low resistance
  • mostly at the level of the heart
  • thin walled vessels, RA and RV
  • acts as a reservoir for blood
  • pooling of blood occurs on inspiration
  • during ex, pulmonary artery P does NOT increase with increased CO b/c of dilation and recruitment of pulmonary vessels
135
Q

What are the factors that determine fluid movement across the pulmonary capillaries?

A

Starlings forces

  • Hydrostatic P inside (Pc) and outside (Pi) the cap
  • Oncotic P inside (Oc) and outside (Oi) the cap
  • Permeability of the capillary

net fluid out= K[(Pc-Pi)-permeability(Oc-Oi)]

136
Q

What happens to fluid that is in the lungs?

A

Normally there is fluid movement from the caps–> interstitium–> which is then removed by lymphatics. However if this process if overwhelmed and the interstitial fluid rises too high then it will seep into the alveoli

137
Q

What are the effects of pulmonary oedema on lung function?

A

Mechanical effects

  • decreased lung compliance
  • decreased lung vol
  • increased airway resistance
  • increased WOB

Gas Exchange effects
-hypoxaemia due to shunt, low V/Q, and diffusion impairment

Arterial blood gases

  • decreased PaO2 and PaCO2, increased pH
  • if v severe then increased PaCO2 and decreased pH

Pulmonary circulation
-increased pulmonary vascular resistance

138
Q

What are the 2 main causes of pulmonary oedema?

A
  • increased capillary hydrostatic P
  • increased capillary permeability

exaggerating factors= decreased colloid osmotic P, decreased lymphatic drainage

139
Q

Distinguish between diagnostic and screening tests

A

Screening test

  • identify patients who may have the disease
  • high sensitivity (low FN)
  • need to confirm the results with a diagnostic test
  • applied to ppl with no clinical suspicion of disease
  • problem= it will include FP

Diagnostic test

  • confirmation of the disease or otherwise
  • high specificity (low FP)
  • applied to ppl who have a clinical suspicion of the disease
  • problem= it will exclude FN
140
Q

Define sensitivity and its formula

A

= % of ppl with the disease that test positive

Sensitivity= TP/ (TP+FN)

141
Q

Define specificity and its formula

A

= % of ppl without the disease that test negative

Specificity= TN/ (TN+FP)

142
Q

Define positive predictive value and its formula

A

= % of the positive tests that are truly positive

PPV= TP/ (TP+FP)

143
Q

Define negative predictive value and its formula

A

= % of the negative tests that are truly negative

NPV= TN/ (TN+FN)

144
Q

PPV and NPV depend on what factors:

A

-sensitivity
-specificity
-underlying prevalence of the disease
(PPV is proportional to the prevalence, NPV is inversely proportional to the prevalence)

145
Q

What are likelihood rates

A

-they measure the likelihood that a test result would be expected in a patient with the disease compared to a patient without the disease

LR of a positive test= sensitivity/(1-specificity)

LR of a negative test= (1-sensitivity)/specificity

146
Q

Describe the phrase “trade off between sensitivity and specificity”

A
  • Test results are given arbitrary thresholds to define the presence of disease
  • if we lower the threshold–> sensitivity increases and specificity decreases
  • if we increase the threshold–> sensitivity decreases and specificity increases
147
Q

Describe ROC curves

A
  • determines how well a test discriminates people with the disease form people without the disease
  • plot 1-specificity vs sensitivity for various thresholds
  • its a graphical rep of the tradeoff between sens and spec
  • you measure the AUC to determine the quality of the test
    0. 9= excellent quality
    0. 7=fair
    0. 5= fail, no discrimination
148
Q

What are some limitations of screening?

A
  • sometimes they are not cost effective
  • SEs
  • selection bias
  • lead time bias
  • length time bias
149
Q

What is lead time bias?

A

-when a test detects the disease earlier and gives the impression of prolonged survival when actually the outcome of the disease is unchanged

150
Q

What is length time bias?

A

-its more likely to detect non aggressive disease (e.g. slow growing tumours e.g. prostate cancer because the person has lived long enough to be screened and those with more aggressive forms have died before being screened)

151
Q

What are the names of the divisions of a bronchus?

A
  • mainstem
  • lobar
  • segmental
  • subsegmental
152
Q

Describe the cell types found in bronchi–>brionchioles

A
  • resp epithelial cells (tall pseudostratified cilliated columnar cells)
  • goblet cells
  • neuroendocrine cells
  • basal cells
153
Q

Describe the cell types found in alveoli

A
  • alveolar macrophages
  • type I and II pneumocytes
  • fibroblasts
  • inflammatory cells
  • endothelial cells
154
Q

List some obstructive lung diseases

A
  • asthma
  • COPD (chronic bronchitis, emphysema, small airways disease)
  • bronchiectasis
155
Q

List some restrictive lung diseases

A
  • idiopathic pulmonary fibrosis
  • pneumoconiosis
  • sarcoidosis
  • honey comb lung
156
Q

What is the definition of emphysema?

A
  • abnormal, permanent enlargement of air spaces distal to the terminal bronchiole
  • desctruction of the alveolar wall WITHOUT fibrosis
157
Q

What is the definition of chronic bronchitis?

A

-persistent cough, productive of sputum for at least 3 months in 2 consecutive years

158
Q

Describe the morphology of chronic bronchitis

A
  • hypertrophy of mucus secreting goblet glands (xs mucus)
  • increased lymphocytes, macrophages and plasma cells
  • oedema
  • peribronchial fibrosis in small airways
  • possible squamous metaplasia
159
Q

Describe the definition of small airways disease

A
  • caused by cigarette smoke
  • chronic inflammation
  • fibrosis
  • obstruction of terminal brionchioles
  • its a component of COPD
160
Q

What is the definition of bronchiectasis?

A
  • irreversible
  • abnormal dilation of bronchi/bronchioles
  • dilated airways are full of pus
  • severe destructive inflammation
  • loss of surrounding elastic tissue–> airway collapse and obstruction
161
Q

What are the symptoms of bronchiectasis?

A
  • SOB
  • cyanosis
  • episodic fever
  • severe cough with foul smelling sputum
162
Q

What are some causes of bronchiectasis?

A
  • necrotising infections (Staph aureus, influenza, aspergillus)
  • obstruction which increases the risk of infection
  • CF
  • cilia disorders
  • non-infectious inflamm conditions (CT diseases, graft vs host disease)
163
Q

Define restrictive lung disease

A

A group of diverse conditions that have these features:

  • chronic, diffuse, non-infectious
  • restrictive spirometry
  • inflammation and fibrosis of the inter-alveolar septa
  • diffuse reticulo-nodular and or ground glass apperance on a CXR
164
Q

Describe the symptoms of typical influenza

A
  • fever/chills
  • cough
  • headache
  • muscle aches
  • fatigue
  • loss of appetite

CXR is normal

165
Q

Who are the at risk groups for seasonal influenza?

A
  • the young
  • the elderly
  • those with underlying chronic conditions
166
Q

Briefly describe the life cycle of seasonal influenza

A
  • infected droplets from coughing or sneezing enter RT
  • virus binds to sialic acid containing receptors (alpha2-6 linkage to galactose) on non-ciliated resp epithelium via Hemagglutinin (HA)
  • receptor mediated endocytosis via a clatherin coated pit
  • endosome becomes acidic, HA changes confirmation to expose fusion region–> fusion of viral envelope with endosomal membrane
  • 8 RNPs escape
  • travel to nucleus and viral RNA synthesis and mRNA synthesis occurs
  • viral protein synthesis and glycosylation in ER–> golgi (allows surface expression of HA and NA)
  • viruses bud out of cell
  • NA cuts sialic acid receptors on surface so newly formed viruses don’t attach back to the dying cell
  • typtase Clara cuts HA and now the viruses are infectious
167
Q

Describe the pathogenesis of seasonal influenza

A
  • infected droplet enters RT
  • infects non cilliated resp epithelium via sialic acid receptors
  • replicates in URT and LRT but predominately in large airways
  • tissue damage
  • cytokines and IFN
  • IL1–> fever
  • IFN–> malaise, head and muscular aches
  • pre-existing or developing immunity is now sufficient to clear the virus
  • NB later in infection viral replication can occur in ciliated epithelium of trachea and bonchi–> increased risk of secondary bac infection–> death from bac pneumonia
  • or infection can occur within the lung parenchyma–> primary viral pneumonia
168
Q

Describe the time course of seasonal influenza infection

A
  • acute infection
  • 7 days or longer
  • no persistence of virus BUT cough and weakness may last for several weeks
  • incubation period= 1-5 days
  • infectious period= 5-6 days
169
Q

Describe the structure of influenza

A
  • from the orthomyxoviridae family
  • enveloped
  • segmental genome (8 segments)
  • ss -ve sense RNA
  • HA and NA on surface
  • M 1 and 2 channels
  • Non structural protein= anti IFN activity
170
Q

What are some types of influenza viruses?

A

Influenza A

  • further divided into subtypes based on the form of HA and NA they encode
  • 16 diff HA, 9 diff NA
  • only type that can also infect other species
  • causes human influenza

Influenza B
-causes human influenza

Influenza C
-minor human pathogen

171
Q

What are the functions of HA and NA in influenza?

A

HA= the gripper (trimer)

NA= the snipper (tetramer)

172
Q

What influenza subtypes have recently circulated in humans and which are circulating currently?

A
  • H1N1, H2N2, H3N2

- H1N1, H3N2 are currently circulating

173
Q

Despite there being sialic acid containing receptors throughout the body why is influenza confined to the respiratory tract?

A
  • because cleavage of HA can only be done by typtase Clara which is only released by Clara cells in the respiratory tract
  • trytase Clara cuts HA and releaves a hydrophobic fusion peptide
174
Q

Describe the adaptive response to influenza

A

CD8 cells

  • kill infected cells
  • important in recovery
  • immunity is not long lived but can be boosted by repeat exposure
  • doesn’t stop the infection just controls it

Abs

  • speeds clearance of virus
  • inhibits attachment or release of virus
  • Ab and complement mediated lysis of infected cells
  • promotion of phagocytosis
  • immunity is long lived
  • they stop infection unlike CD8 cells
175
Q

Briefly describe antigenic drift in relation to influenza

A
  • it leads to the creation of new strains within a subtype
  • single a.a change because of errors in replication= drift
  • the change can be deleterious, neutral or advantageous
  • its advantageous if they occur at sites on HA and NA where neutralising Abs bind
  • i.e. Abs may not be able to bind any more and so viruses with these mutations will be selected for= antigenic drift
176
Q

Briefly describe the life cycle of seasonal influenza

A
  • infected droplets from coughing or sneezing enter RT
  • virus binds to sialic acid containing receptors (alpha2-6 linkage to galactose) on non-ciliated resp epithelium via Hemagglutinin (HA)
  • receptor mediated endocytosis via a clatherin coated pit
  • endosome becomes acidic, HA changes confirmation and exposes fusion region–> fusion of viral envelope with endosomal membrane
  • 8 RNPs escape
  • travel to nucleus and viral RNA synthesis and mRNA synthesis occurs
  • viral protein synthesis and glycosylation in ER–> golgi (allows surface expression of HA and NA)
  • viruses bud out of cell
  • NA cuts sialic acid receptors on surface so newly formed viruses don’t attach back to the dying cell
  • typtase Clara cuts HA and now the viruses are infectious
177
Q

What are some targets for vaccine induced immunity and for antiviral drugs in the life cycle of influenza?

A
  • Ab attachment to HA (prevents attachment to host cell)
  • Ab to NA blocking efficient release
  • ion channel (M2) blockers (prevents acidification of endosome and therefore endosomal escape)
  • NA inhibitors
178
Q

Name 2 antivirals that are used to block M2 ion channels in influenza

A
  • amantadine

- rimantadine

179
Q

Briefly describe the difference between antigenic drift and antigenic shift

A

Antigenic drift

  • it leads to the creation of new strains within a subtype
  • gentle changes
  • single a.a change because of errors in replication
  • its advantageous only if they occur at sites on HA and NA where neutralising Abs bind
  • i.e. Abs may not be able to bind any more and so viruses with these mutations will be selected for

Antigenic shift

  • big changes
  • sudden appearance of an influenza A virus of a new HA and sometime NA
  • the new HA is often from birds
  • results form genetic reassortment using the mixing vessel (pig) because they contain both the human alpha2-6 linkage and the avian alpha2-3 linkage
180
Q

Describe the influenza vaccine

A
  • inactivated trivalent vaccine
  • inactivated–> only induces Ab responses not CD8
  • contains 3 diff influenza viruses (influenza A H1N1, H3N2 and influenza B)
  • administered intramuscularly
  • grown in fertilised eggs (therefore not for ppl with allergies)
  • needs to be updated each year because of emerging new strains
181
Q

What subtype is the avian flu?

182
Q

What are the effects of pulmonary (artery) HT?

A
  • increased RAP
  • increased systemic venous P–> peripheral oedema, ascites, pleural effusion, right HF if severe
  • RV dilation and hypertophy as compensation but this further increases systemic venous P
183
Q

What are some causes of pulmonary HT?

A
  • increased pulmonary BF
  • increased LA pressure
  • increased pulmonary vascular R (MOST IMPORTANT)
  • -vasoconstriction to compensate for low PAO2
  • -obstruction
  • -obliteration
184
Q

What is the compensation for Respiratory acidosis?

A

Bicarbonate retention

185
Q

What is the compensation for metabolic acidosis?

A

Hyperventilation (lower PaCO2)

186
Q

What is the compensation for respiratory alkalosis?

A

Bicarbonate excretion

187
Q

What is the compensation for metabolic alkalosis?

A

mild hypoventilation

188
Q

Where is the respiratory control centre located?

A

brain stem

  • in the pons and medulla
  • major output is via the phrenic nerves
  • generate automatic rhythm

cortex
-voluntary control

189
Q

Describe the different types of respiratory sensors

A

Central chemoreceptors

  • on medulla
  • surrounded by CSF
  • CSF [H+] reflects CO2 in cerebral capillaries
  • increased PaCO2–> increased CSF [H+]–> increased ventilation
  • doesn’t respond to PaO2

Peripheral chemoreceptors

  • in carotid bodies and aortic bodies
  • respond to decreased PaO2, decreased pH and increased PaCO@–> increased ventilation
  • rapid response

Lung and other receptors

  • pulmonary stretch, irritant, J receptors
  • upper airway receptors, joint and muscle receptors, painful stimuli
190
Q

What are some causes of hypoventilation?

A
  • reduced respiratory centre activity
  • neuromuscular disease
  • chest wall deformity
  • obesity
  • sleep disordered breathing
  • as a consequence of resp muscle fatigue, secondary to severe lung disease
191
Q

Describe the ventilatory response to hypoxia?

A

-there is no change in ventilation until PAO2 is below 50-60mmHg

192
Q

Describe the ventialtory response to exercise

A
  • ventilation increases with work to maintain PaO2 and PaCO2
  • beyond the anaerobic threshold, relative increases in ventilation are because the body is trying to correct the extra H+ production form lactic acid
193
Q

What are the types of sleep disordered breathing?

A
  • obstructive sleep apnoea
  • central sleep apnoea
  • obesity hypoventilation syndrome
194
Q

Define breathlessness

A

-arises when there is a recognition by a subject of an inappropriate relationship between respiratory work and total body work

195
Q

What are some systems approaches to dyspnoea

A
  • respiratory
  • cardiac
  • muscle weakness
  • metabolic
  • anaemia
  • psychogenic
  • MUD (medically undiagnosed dyspnoea)
196
Q

What are some respiratory causes of dyspnoea

A
  • airways disease (upper or lower)
  • alveolar disease
  • pulmonary vascular disease
  • pleural and chest wall disease
  • respiratory muscle disease
197
Q

What millennium development goal number realtes to TB?

198
Q

Describe how the socioeconomic gradient relates to TB risk?

A

-the poorer you are the greater the risk you have for having TB

199
Q

Define pneumonia

A

Any inflammation of the lung

200
Q

Describe 2 patterns of acute bacterial pneumonia

A

acute bronchopneumonia

  • patchy
  • often involves more than 1lobe
  • coughs up purulent sputum
  • fibrin and neutrophil rich exudate

acute lobar pneumonia

  • inflammation in the entire lung
  • red hepatisation–> gray hepatisation
201
Q

What is a lung abscess?

A

Collection/cavity of pus
Caused by:
-aspiration
-obstruction of bronchial tree
-bac pneumonia
-acute bronchopneumonia in debilitated hosts
-haematogenous seeding of the lung from an extra pulmonary infection

202
Q

Describe viral pneumonias

A
  • they don’t produce consolidation
  • can cause bronchiolitis and inflammation of the alveolar septa (lymphocytic rather than neutrophils)
  • most are cytoplasmic which predisposes ppl to secondary bac infections
  • lungs appear heavy, wet, red or boggy
203
Q

Describe 2 examples of chronic infections of the lungs

A

Bronchiectasis

  • dilation of large cartilage containing airways from scar tissue deposition around bronchi–> weakening of the bronchial wall by inflammation
  • permanent
  • poor drainage–> recurrent bac infections and abscesses
  • haemoptysis
  • copious offensive sputum

Pulmonary TB

  • granulomatous inflammation and caseous necrosis
  • type 4 hypersensitivity rxn
  • forms tubercles
204
Q

What are 3 types of pulmonary TB?

A

Primary TB

  • in ppl previously unexposed
  • middle lung segments
  • gohn focus
  • gohn complex
  • self limiting
  • healing by fibrosis

Secondary TB

  • person has already had the disease Ir there is a reactivation of primary TB
  • apical lung segments
  • more severe

Miliary TB

  • numerous small granulomas
  • like little seeds
  • can disseminate to other organs = haematogenous
205
Q

Distinguish between thrombus and clot

A

Thrombus = solid mass of blood components formed DURING LIFE

clot= same but formed POST MORTEM

206
Q

Where can venous thrombi form?

A

In any vein: superficial or deep

Majority are in DEEP veins of the LOWER LIMBS

207
Q

Describe the histology of a venous thrombus

A
  • red bc if RBC

- layered (alternating levels of platelets to RBCs with fibrin throughout)

208
Q

What factors in virchows triad are most important in predisposing to venous thrombosis?

A

Changes in blood constituents (hypercoagulability states)

Changes in BF

209
Q

What are some types of primary hypercoaguability states?

A

(Genetic)
-factor V Leiden mutation (prevents activated protein C from binding to a cleavage site)

-prothrombin III deficiency

  • antithrombin III deficiency
  • protein C deficiency
  • protein S deficiency
210
Q

What are some types of secondary hypercoagulable states.

A
  • surgery
  • trauma
  • burns
  • malignancy
  • obesity
  • smoking
  • hyper oestrogenic states
  • nephrotic syndrome
  • anti phospholipid Ab syndrome
211
Q

What are some fates of venous thrombi?

A

Lysis
Organisation
Recannulisation
Embolism

212
Q

What is an embolus?

A

A mobile mass of material within the vascular system able to lodge within a vessel, occlude it’s lumen and onstruct BF

Thromboembolus= detached piece of thrombus

  • most arise from deep veins in leg
  • can travel to the right side of the heart and enter the pulmonary arterial circulation via the pulmonary artery
213
Q

Describe the characteristics of pulmonary thromboembolism

A
  • effects depends on size of the occluded vessel
  • vein from the outside looks red with pale areas
  • coiled shape (reflects vein of origin)
214
Q

What is the name for an embolism lodged at the bifurcation of the pulmonary artery

A

Saddle embolus

215
Q

What is the major consequence of a small pulmonary thromboembolus? And what does it look like?

A

Pulmonary infarction

  • sharply demarcated
  • wedged shaped
  • base is on pleura
  • red
  • occluded artery is at the apex
216
Q

What clinical signs does a patient present with if they have a small pulmonary thromboembolus without infarction?

A

Unexplained tachycardia and RFs for PE

217
Q

What is sleep?

A

A behavioural state characterised by decreased awareness of the external environment, decreased reactivity to stimuli but with capability to return to wakefulness

218
Q

What are some reasons we sleep?

A
  • health and survival
  • learning and brain development
  • repair and maintenance
  • clearance of metabolites
  • E preservation
  • avoid nocturnal hazards
219
Q

What are the top 3 common sleep problems?

A
  • obstructive sleep apnoea
  • insomnia
  • restless leg syndrome
220
Q

How do you evaluate sleep?

A 
Via polysomnography (PSG)
-looks at EEG, EOG, EMG
221
Q

What is a hypnogram?

A

A graphical representation of sleep

222
Q

What are some common characteristics of a PSG during wake time

A

Eye movements
High levels of muscle activity
High frequency EEG (alpha and beta waves)

223
Q

What are some characteristics of a PSG during stage 1 and 2 sleep?

A

No eye movements
High muscle activity
Lower frequency of EEG (theta waves with sleep spindles and k complexes)

224
Q

What characteristics are on a PSG during stage 3 sleep?

A

No eye movements
Variable levels of muscle activity
Low frequency on EEG (delta=SWS)

225
Q

What are some characteristics of a PSG during REM sleep?

A

REM
low level of muscle activity
Higher frequency EEG (theta)

226
Q

What are some cardiovascular changes that occur during sleep?

A

HR decreases
BP decreases
CO decreases
Metabolic activity decreases

227
Q

What are the theories behind arousals from sleep?

A

Homeostatic vs reflex activation

The evidence supports a waking reflex

  • adaptive reflex
  • provides and evolutionary advantage
228
Q

What does a person with obstructive sleep apnoea’s hypnogram look like?

A

Minimal SWS

No REM sleep

229
Q

Describe the regulation of circadian rhythms

A

Controlled by suprachiasmatic nucleus (SCN)

Zeitgeibers= time givers act as external cues. Eg light inhibits the SCN, a lack of light increases melatonin –> promotes sleep

230
Q

Describe the 2 process model of sleep

A 
Homeostatic process (process S)
-drives sleep 
Circadian process (process C)
-drives arousal

When the 2 process are furthest apart sleep happens. When someone is sleep deprived their amount of SWS and total sleep time increases

231
Q

How does a lack of sleep impair performance?

A
  • slows rxn time
  • reduced vigilance
  • slower info processing
  • reduced short term memory
232
Q

Briefly talk about sleep restriction and deprivation and how one acclimatises to it therefore impairing their subjectiveness

A

Sleep restriction has a cumulative effect on performance.

The more someone is sleep deprived the more they cannot accurately assess their sleepiness

233
Q

What are the 3 functional neurobiological systems that control sleep?

A

Arousal systems

  • within pons/midbrain
  • inhibits sleep promoting system

Sleep promoting system

  • VLPO (ventrolateral pre-optic nucleus)
  • inhibits Orexin neurons and ariusal systems

Orexin neurons

  • in hypothalamus
  • projects onto arousal system
234
Q

Describe species level selectivity

A

-Antimicrobials
-diffs in ribosomes, membranes, cell wall, enzymes and DNA allow selectivity
Eg sulfanilamide and trimethoprim act on the folic acid synthesis pathway at diff points

235
Q

Describe cell level selectivity

A
  • killing cancer cells
  • methotrexate inhibits dihydrofolate reductase
  • it has no effect on bac because they have a diff enzyme
  • it’s an anti cancer drug at high doses
  • it’s immunosuppressive at lower doses
  • it’s teratogenic
236
Q

Describe organ level selectivity

A
  • A combo of a diuretic and a angiotensin system inhibitor with an NSAID leads to acute renal failure via prostaglandin mediated vasodilation to preserve BF in response to hypoxia
  • paraquat a herbicide but also a lung killer because it oxidises other molecules and makes ROS–> damage to membranes, proteins and DNA. Selective to the site of application
  • gentamicin causes nephrotoxicity and ototoxicity. (Inhibits protein synthesis)
237
Q

What are the 2 main types of neoplasia?

A
  • benign

- malignant

238
Q

Paediatric cancers are given what general term?

239
Q

Distinguish between benign and malignant

A

Benign

  • local expansile
  • slow growing
  • well circumscribed
  • can be encapsulated
  • well differentiated
  • unable to metastasise
  • rarely life threatening

Malignant

  • locally invasive
  • destructive growth
  • poorly circumscribed
  • induce desmoplasia in the stroma they invade
  • can have necrosis due to tumour outgrowing its blood supply
  • variable differentiation
  • potential to metastasise
240
Q

What are the ways tumours can spread?

A
  • lymphatic
  • transcoelomic
  • haematogenous
241
Q

What are the histopathologic features of neoplasia?

A

Cytological atypia

  • larger nuclei
  • pleomorphic nuclei
  • coarser nuclear chromatin
  • hyperchromatic nuclei
  • larger nucleoli
  • more mitotic activity

Architectural disorganisation

242
Q

What are the main categories of cell lineage in neoplasia?

A

epithelial cells

  • gladular
  • squamous
  • endocrine

mesenchymal
-smooth muscle

others

243
Q

Describe tumour terminology

A

Prefix= line of differentiation or cell lineage

  • adeno= glandular
  • squamous cell
  • leiomyo= smooth muscle
  • osteo= osteoblastic

Suffix

  • oma= benign
  • carcinoma= epithelial (malignant)
  • sarcoma= mesenchymal (malignant)
244
Q

Describe the types of degree of differentiation in cancer

A

-the extend to which tumour cells resemble their normal counterparts histologically

Well differentiated

  • resemble mature cells
  • less cytologic atypia
  • less mitotic activity
  • architecturally more organised

Poorly differentiated

  • poorly resemble mature cells
  • more cytologic atypia
  • more mitotic activity
  • archietcurally less organised
245
Q

Distinguish between bening tumours and malignant tumours degree of differentiateion

A

-benign tumours are well differentiated

  • malignant tumours may be well differentiated, moderately or poorly differentiated or anaplastic
  • degree of differentiation of a malignant tumours is referred to its grade
246
Q

Define the term premalignant lesion

A
  • aka dysplasia or intraepithelial neoplasia

- = abnormal growth

247
Q

What are the major cancer characteristics of cancer?

A
  • resisting cell death
  • inducing angiogenesis
  • enabling replicative immortality
  • activating invasion and metastasis
  • evading growth suppressors
  • sustaining proliferative signalling
248
Q

What are the emerginc hallmarks and enabling characteristics of cancer?

A

Emerging hallmarks

  • deregulating cellular energetics
  • avoiding immune destruction

Enabling characteristics

  • tumour promoting inflammation
  • genome instability and mutation
249
Q

What are the 4 classes of normal regulatory genes that are commonly mutated in carcinogenesis?

A
  • growth promoting proto-oncogenes
  • growth inhibiting tumour suppressor genes
  • genes that regulate programmed cell death
  • genes involved in DNA repair
250
Q

What are some types of mutations in cancer?

A
  • errors in DNA replication not repaired
  • point mutations
  • amplifications of oncogenes
  • chromosomal rearrangements
251
Q

Name a gene that commonly undergoes oncogenic amplification

252
Q

Name a gene that commonly undergoes oncogenic translocation and fusion

A

BCR and ABL

253
Q

What are the major cell proliferation pathways in cancer?

A

PI3K pathway
-can signal via Ras or independent of Ras

MAPK pathway
-always signal via Ras

254
Q

What is loss of heterozygosity?

A

-the loss of normal function of one allele of a gene in which the other allele was already inactivated

255
Q

The oncogenes Ras and Myc act on what cell cycle checkpoints

A
  • G2 to M

- G1 before S phase

256
Q

What are some strategies to evade apoptosis

A
  • reduced CD95 level (fas receptor)
  • inactivation of death induced signalling complex by FLICE protein
  • up-reg of BCL2 (anti-apoptotic)
  • reduced levels of pro-apoptotic BAX resulting from loss of p53
  • loss of APAF-1
  • up-reg of inhibitors of apoptosis
257
Q

Name the steps involved in metastasis

A
  • detachment of tumour cells from each other (disruption of integrins, E-cadherin, beta and alpha caterin, connexin 43)
  • degradation of ECM
  • attachment to novel ECM components
  • migration of tumour cells
258
Q

What are some effects of metastases

A
  • local lymphadenopathy
  • bone pain
  • hypercalcaemia
  • jaundice
  • seizures
  • weight loss
  • anorexia
259
Q

What is paraneoplastic effects/syndromes?

A

effects not due to effects of the tumour itself

  • cushings syndrome-ACTH (small cell LC, pancreatic C)
  • inappropriate ADH syndrome- ADH (small cell LC)
  • hypercalcaemia- PTH related protein (squamous cell carcinoma of the lung etc)
  • hypoglycamia- insulin
  • polycthemia- erythropoeitin
260
Q

What are some clinical features of LC

A
  • local effects of primary tumour: cough, haemoptysis, wheeze, dyspnoea, pneumonia, Pancoast’s syndrome
  • effects of metastases: bone pain, jaundice, seizures
  • weight loss, anorexia
  • paraneoplastic
261
Q

Name some investigations for LC

A

Hx and examination

blood tests

  • Hb level
  • liver function tests
  • tumour markers
  • -prostate specific Ag
  • -carcinoemryonic Ag (CEA)
  • -alpha fetoprotein

Radiology

Endoscopy

Tissue sampling

  • biopsy
  • cytology
  • histopathology
  • molecular and cytogenetic techniques
262
Q

What are the classification of lung carcinomas?

A

Non-small cell carcinoma

  • squamous cell carcinoma
  • adenocarcinoma
  • large cell carcinoma

Neuroendocrine carcinoma
-Small cell carcinoma

263
Q

What type of LC is the most common?

A

-adenocarcinoma

264
Q

How do you stage cancer?

A

TNM system

  • T= size
  • N= LN metastases?
  • M= metastases?

the TNM components are then combined to give a stage grouping with 4 stages

265
Q

What are some treatment options for cancer?

A
  • surgery
  • radiotherapy
  • chemotherapy
  • targeted therapy (small molecules that inhibit GFs or tyrosine kinase, mAb that target specific proteins or receptors)
  • others e.g. immunotherapies, bone marrow tranplants
266
Q

Describe the EGFR mutations in LC

A
  • a proportion of non-small cell carcinomas are EGFR mutations
  • especially in young non or light smoking female asians
  • targeted therapies= gefitinib, erlotinib

Danielle's MD1 (6 decks)

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