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Year 1 LSS > Respiratory pathology > Flashcards

Respiratory pathology Flashcards

1
Q

Symptoms of lung cancer

A
  • Haemoptysis
  • cough
  • dyspnoea
  • chest/shoulder pain
  • finger clubbing
  • weight loss
  • hoarseness
  • recurrent infections
  • –> if more than 3 weeks –> imaging

Often symptoms only long after a tumor developed

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1
Q

Tumor staging

A

TNM

T= Tumor

  • Size (<1cm = T1, > 3mm =T2)etc.
  • Location: Invasion of surrounding tissue (chest wall, heart), compromising of major vessels (aorta, vena cava)

N= Lymph Nodes

  • No invasion of lymph nodes
  • Invasion of lymph nodes

M= Metastasis

  • No metastases,
  • Mentalities
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2
Q

Pathogenesis of lung cancer (brief summary) + riks factors

A
  1. inactivation of tumor suppressor genes (p53, box (cofactor fo p53)
  2. activation of oncogenes

–> Smoking, Radiation, Asbestos and genetics are risk factors that influence pathogenesis (turn of tumor suppressor genes, activate oncogenes)

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3
Q

Way of imaging/diagnosis in Lung cancer

A
  1. Chest X Ray: Shaddows in lung can be seen –> if abnormal:
  2. Chest CT(sometimes: –> trans-thoracic CT Biopsy –> biopsy via needle, CT lead
  3. Bronchoscopy/Endoscopy –> tumor can be seen + probe can be taken for further diagnosis
    3b: Endobronchial ultrasound

PET scan –> highly metabolic active tissues: marked glucose in scan (tumor = highly active)(additional testing required)

–> Always attempt to do diagnosis and staging together (e.g. via biopsy from lymph node)

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4
Q

Paraneoplastic syndrome

A

Systemic effects of the tumor due to abnormal expression of things

–> would not normally be expressed by this tissue

  1. Endocrine–> Hormones expressed by tumor tissue e.g. Syndrome of inappropriate ADH –> hyponatremia (small cell carcinomas)
  2. Non-endocrine e.g. factors –> coagulation defect
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5
Q

Local and systemic complications of lung tumors

A

Local

Problems with breathing, pain

local invasion and obstruction of tissues–> esophagus, pericardium, pleura, chest wall, branch, airway, major vessels

Systemic:

Spread of metastases

Paraneoplastic syndrome

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6
Q

In which two big groups are Lung cancers classified (+ most important characteristics)

A

Most are carcinomas

  1. Non-small cell carcinomas (+3 subtypes)

less agressive, slowlier devinding

  1. Small cell carcinomas

very agressive, rapid deviding

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7
Q

What are the subclassifications of Non-small cell Carcinomas? (without characteristics) + What is treatment and prognosis

A
  1. Squamous cell carcinoma
  2. Adenocarcinoma
  3. Large cell carcinoma

Often surgery possible, less chemosensitive

Prognosis: Early stage 60% 5Y survival

Late Stage: 5% 5Y survival

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8
Q

Squamous cell carcinoma

A

sub-type of non-small cell carcinoma

smoking –> irritation of epithelium –> metaplasia to more resistant epithelium –> Malignant tumor

often central (bronchial epithelium but recently: also peripheral)

local spread, late metastasis

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9
Q

Adenocarcinoma

A

peripheral, terminal airways and multicentric

more common in female, far east and non-smokers

often EGFR mutation (–> possible target with tyrosine kinase inhibitors) + ALK mutation(young patients)

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10
Q

Large cell carcinomas

A

uncommon

large cells, poorly differentiated

poor prognosis

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11
Q

Small cell carcinomas

A
  • central, near bronchi
  • smoking
  • late diagnosis –> 80% w advanced disease

Treatment: Chemotherapy and radiotherapy (–> very responsive)

Prognosis 2-4 month untreated, 10-20 month treated

–> often paraneoplastic effects

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12
Q

Allergy

A

exaggerated immunological response to a foreign substance (allergen) which is either inhaled, swallowed, injected, or comes in contact with skin/eye.

o Allergy is a MECHANISM, not a disease.

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13
Q

Hypersensitivity

A

exaggerated response.

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14
Q

Intolerance

A

(Non-immunological hypersensitivity)

inability to consume or absorb/metabolize nutrients.

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15
Q

Atopy

A

Atopy – the genetic tendency to develop allergic diseases.

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16
Q

How do hypersensitivity, allergy, atopy and intolerance relate?

A
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17
Q

What is neurophysiology?

A

When CNS creates a sensory impression

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18
Q

What is behavioral psychology?

A

Interpretation of sensory information by the brain leading to sensation

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19
Q

Why do we cough? (causes of cough)

A
  • defense mechanism
  • additional to mucociliary clearing
  • expulsive phase of cough –> high-velocity air flow
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20
Q

Where are cough receptors located?

A

within airway epithelium

the posterior wall of the trachea

pharynx

larynx

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21
Q

What kind of sensory receptors in the lung are there?

What are their characteristics?

Where are they located?

A

1. C-fibre receptor

  • –Larynx, trachea, bronchi, lungs
  • “free” nerve endings
  • release signals after chemical stimulation

2. Rapidly adapting stretch receptors

  • nasopharynx, larynx, trachea, bronchi,
  • small, myelinated fibers
  • Mechanical, chemical irritant stimuli, inflammatory mediators

3. Slowly adapting stretch receptors

  • airway SM
  • Mechanoreceptor –> respond to inflation
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22
Q

Which nerve do all sensory receptor of the lung and airway pass through?

A

Vagus nerve (X)

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23
Q

Afferent neural pathway for cough

A
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24
Q

Efferent neural pahtway for cough

A
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25
Q

What are the three main phases of cough?

A
  1. inspiratory phase
  2. Glottic closure
  3. Expiratory phase
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26
Q

How long is acute cough?

What is a typical cause?

A

less than 3w

Most typical cause is a common cold

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27
Q

When can you speak of chronic cough?

What are the 4 most common reasons?

A

Persistent cough longer than 3weeks

  • Asthma and eosinophilic-associated (25%)
  • Gastro-oesophageal reflux (25%)
  • Rhinosinusitis (postnasal drip) (20%)
  • Idiopathic (10%)

Chronic hypersensitivity syndrome –> increased sensitivity of cough receptors

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28
Q

What is emphysema?

A

Damage start in centre of alveoli sac

–> Destruction –> Try to repair with fibrotic tissue –>Emphysema (holes in lung tissue)

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29
Q

How does alveolar fibrosis occur?

A
  • Type II cells divide in an attempt to repair but they don’t differentiate into Type I cells
  • Fibroblast increase collagen production and
  • Signal Type II cells not to differentiate into Type I cells
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30
Q

Which local effects does lung cancer have?

A

It can invate lung tissue and adjacent structures

–> e.g. CVS system

31
Q

Which systemic effects can lung cancer have?

A

Metastasis can spread distantly

Paraneoplastic effecty –> Effects of hormones that are not meant to be expressed by that tissue

Endocrine: Hormones e.g. ADH in small cell carcinoma

Non-endocrine: coagulation

32
Q

Which risk factors are associated with pneumonia?

A

Age (young and old)

Smoking

Excess alcohol consumption

33
Q

How can you decide, wheater you would admit someone with pneumonia to the hospital or not?

A
34
Q

Which factors influence, wheater pneumonia/ lung infection has a severe or a mild outcome?

A
35
Q

What causes severe flu (over a mild form)?

A
  1. Highly pathogenic strains (zoonotic)
  2. Absence of prior immunity

Innate immunodeficiency (e.g. IFITM3 gene variant)

B cells (antibody- presumably local)

T cells (correlate with peripheral levels?)

  1. Predisposing illness/conditions

Frail elderly

COPD/asthma

Diabetes, obesity, pregnancy etc.

36
Q

How does influenza influence Pneumonia?

A

An influenza infection predisposes to an bacterial pneumonia

37
Q

Which nerves sense pain in the respiratory apparatus?

Where do they senses it from?

A

Trigeminal from Nose

Vagus senses most pain from nose, pharynx, larynx (very little) lung

Spinal nerves –> chest wall

38
Q

How would you treat breathlessness?

A

If possible: Treatment of the course:

But if not:

  • Bronchodilators
  • suppression of breathing center
  • Lun resection
  • pulmonary rehabilitation (increase wellbeing, fitness etc.)
39
Q

What are the three pathogens, that are responsible for most hospital-aquired pneumonias?

A
  • Staphylococcus aureus(28%)
  • Pseudomonas aeruginosa(21.8%)
  • Klebsiella species(9.8%)
40
Q

Which pathogens cause the most Community-aquired pneumonias?

What is special about this?

A

Most of the times not a single pathogen responsible but many infections leading to pneumonia:

  1. Strep. Pneumoniae
  2. Myxoplasmapneumoniae
  3. Staph. Aureus
  4. Chlamydophilapneumoniae
  5. Haemophilus influenzae
41
Q

What is an atypical pneumonia?

What is its significance?

A

Atypical pathogens in pneumonia

  • Mycoplasma pneumoniae
  • Chlamydia pneumoniae
  • Legionella pneumophilia

Atypical bacteria are not covered by penicillinsand requireadditional agents (e.g. macrolides).

42
Q

How could you diagnose a pneumonia?

A
  1. Acute lower respiratory tract symptoms
  2. New focal chest signs and, if in hospital, new CXR changes
  3. >1 systemic feature (fever, shivers, aches and pains, temperature >380C)
  4. No other explanation for illness
43
Q

When should someone who is suspected to have a pneumonia be admitted to hospital?

A
44
Q

How should pneumonia be treted?

A
  • Antibiotics –> as fast as possible
  • O2 (for hypoxia)
  • Fluid (for dehydration)
  • Analgesia (for pain)
45
Q

How would a child with RS V (respiratory syncytial virus) present?

A
46
Q

Who is at risk of RSV infection?

A

RSV= respiratory syncytial virus

Children

Elderly: might lead to winter death

47
Q

What might be the consequence of a viral infection regarding pneumonia?

A

Sometimes a viral infection may make it easier for bacterial pneumonia to show up

–> virus weakens immune system and make tissue more prospone to infection

48
Q

Is Allergy a disease?

A

No, it is a mechanism (immunological hypersenstitivity), not a disease

49
Q

Explain the development of seasonal allergic rhinitis

A
  1. Sensation of Antigen –> First exposure
  2. Hypersensitivity + exaggerated resonse to antigen at 2nd contact –> Increased IL-4, IL-5, Eosinophils
50
Q

What are teh immediate and late response cells that are involved in allergy?

A

Immediate: Mast cells and Basophils

Late response: Eosinophils

51
Q

How can you treat seasonal allergic rhinitis?

A
52
Q

What are the common causes/triggers for allergic asthma or rhinitis?

A

Pollen but also:

53
Q

How does Allergy and Atopy relate to one another?

A

You can be atopic = have IgE against different things but don’t have to be allergic (no allergic response triggered)

54
Q

Which cells are important in medating Atopic responses?

A

Th2 cells are important (–> secrete L4,L5,L13, Eosinophils)

55
Q

Which airways are affected by astma?

A

It is basically an allergic response in the lower airways

56
Q

What is the main immunological cell associated with asthma?

A

Eosinophils (but there are different types)

57
Q

What are the advantages and disadvantages of Immunotherapy in alltergy?

A

Advantages

  • Effective
  • Produces long lasting immunity

Disadvantages

  • Occasional severe allergic reaction
  • Time consuming
  • Standardisation problems
58
Q

Summarise the steps in treatment of an allergic airway disease

A
  1. Avoid Allergen
  2. Anti-allergic medication
  • Anti-histamines
  • Nasal Steroids
  1. Allergen-specific immunotherapy
  • subcutanous
  • sublingual
59
Q

Summarise the mechanism of action of immunotherapy on allergic airway disease

A
  1. Dendritic cells produce other mediators –> Has several effects
  2. Shift from Th2 to Th1 response
  3. Treg cells expressed (regulate and secrete IL-35)
  4. IL-35 induces IL-10 release which has many functions:
60
Q

What is Extrinsic allergic alveolitis?

Explain its mechanism

A

small antigens get immunologically activated in alveoli

–> Triggers different immunological activation

e.g. Farmers lung etc.

61
Q

What happens when there are cilia mutations in the airway?

A

No mucus clearing: often cilia can’t move

–> more prone to severe infections and respiratory failure

62
Q

Which cartilage defects can occur in lung development?

What are their effects?

A
  1. Complete, round cartilage –> Narrowing of airway, might be so narrow that ventilation required
  2. Malacic “floppy” cartilage –> airway collaps very easily –> respiratory distress
63
Q

What is agenesis of a lung?

A

Complete absence of a lung –> no lung or vessels

64
Q

What is aplasia of a lung?

A

Blind ending bronchus –> no lungs or vessels (but still bronchus)

65
Q

What is a hypoplasia in lung development?

Why does this occur

A
  • Bronchi and rudimentary lung are present but
  • Reduced size and number

Because of reduced space in the pulmonary cavity (e.g. diaphragmatic cysts, heart defects etc.)

66
Q

What is Cystic Pulmonary Airway Malformation
CPAM?

A

abnormal differentiation of tissue caulses multiple small cysts

–> often several recurrent pneumonias and infections

67
Q

What is an Intralobar Sequestration?

A

Segments of lung have normal blood supply but no ventilation in segments

–> can get infected

68
Q

What is

Congenital Lobar Emphysema
Congenital Large HyperlucentLobe (CLHL)

A
  • Progressive lobar overexpansion (one lobe too big, compresses everything around in pleural cavity)
  • Underlying cause
  • –Weak cartilage
  • –Extrinsic compression
  • –One way valve effect
  • –Alveoli expand (not disrupted)
69
Q

What level of the respiratory tract is affected by COPD?

Which condition does it affect?

A

Bronchi: Chronic bronchitis

Small airway (<2mm): Small airway fibrosis

Emphysema: Alveoli

70
Q

What happens to the structure of the lung during emphysema?

A

Break down of elastic tissue part of alveoli —> Damage of alveoli (increased air space, decreased tissue (often also by oxidantsn metalloproteases)

71
Q

Why do the small airways collapse, become obstructed and stenosed in COPD?

Which signal/factor is involved in this?

A

Because of small airway fibrosis

–> not functional repair of small chronic inflammation

72
Q

What are the changes in epithelial cell profile and secretions during bronchitis?

A
  1. Hypersecretion of mucus
  2. More goblet cells
  3. more squamous endothelium
  4. hypertrophy of submucosal glands
73
Q

Why would a protease inhibitor help treat COPD?

A

It would

  • reduce inflammation and activation of goblet cells (Chronic bronchitis)
  • stop the formation of new emphysema
  • stop some of the repair process (by reduction of Signaling molecules) (fibrosis of small airway)
74
Q

Why don’t endogenous inhibitors /regulatory proteases work in the regulation of COPD?

A

Because they are broken down by metalloproteases

75
Q

Which substances to Neutrophils and Macrophages secrete that are important in the formation of COPD?

What are its effects?

A

Neutrophils: Elsastases

Macrophages: Metalloproteases + Oxidants

–> Lead to inflammation, emphysema, and triggering of repair mechanism leading to fibrosis

76
Q

Which nerve supplies the larynx and the vocal cords?

A

Superior Laryngeal Nerve

Year 1 LSS (12 decks)

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