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Anatomy > Respiratory diseases W11 > Flashcards

Respiratory diseases W11 Flashcards

1
Q

What is the most common chronic respiratory disorder

A

Asthma

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2
Q

What respiratory disease is the leading cause of death

A

Chronic bronchitis and emphysema or pneumonia for respiratory infectious diseases

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3
Q

What is the difference between restrictive and obstructive disorders?:

A

Restrictive: Decreased lung elasticity or other cause - inhibiting lung expansion(cant increase volume and therefore pressure)
* Affects inspiration
Obstructive: Associated with narrowing or obstruction of airways
* Affects expiration

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4
Q

What three diseases are under the category of COPD?

A

Chronic bonchitis
Emphysema
Asthma (variable obstructive airway disease)

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5
Q

From a Dental perspective you need to consider

A

Be able to manage ashtmatic attack or sever allergic reactions in clinic
Be aware that sufferers tend to have more oral health problems
Be aware of the varierty of factors in clinic can trigger attack

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6
Q

What are the symptoms of asthma?

A

Unpredictable, disabling attacks of severe dyspnea, coughing, wheezing, trigged by sudden bronchospams.
May be fatal.
Can be virtually asymptomatic between attacks

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7
Q

What respiratory volumes are affected in asthma?

A

Reduction in FEV (forced expiratory volume) and PEFR (peak expiratory flow rate)
Vital capacity reduced
compliance (stretch) reduced
Recoil reduced
TLC, RV higher

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8
Q

What are some common triggers of asthma?

A

Triggered by exposure to an allergen to which the patient has been previously sensitised
Ex. Foods (nuts, eggs, wheat, shellfish), animal sources (bees, wasps, cats), environmental factors (dust, pollen, mould), medication (antibiotics)

= bronchoconstriction
* Usually stimulus has little to no effect on normal people

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9
Q

What makes someone more susceptible to asthma

A

Underlying chronic inflammation of airways
= damage to airway epithelium
= amplifies neural, inflammatory and immune responses in the airways

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10
Q

Atopic (allergy) Asthma is considered to be a type 1 hypersensitivity reaction. What does this mean?

A

Occurs in individuals who have previously been sensitised to an antigen (not the first time)
Rapid onset - within minutes after rexposure (antigen combines with antibody bound to mast cells or basophils)

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11
Q

What are the three stages to a type 1 hypersensitivity reaction*

A

Exposure to antigen
Sensitisation stage - asymptomatic
Effect stage - anaphylatic or atopic immune response

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12
Q

Describe what occurs in sensitisation stage - what cells specifically?*

A
  • Antigen presenting cells present allergens to Type 2 T-Helper (TH-2) cells
  • TH-2 cells produce cytokines (IL-4) -> turn on IgE producing B cells
  • IgE antibodies attach to surface of mast cells and basophils IMPT
    At lamina propia level
    Immune system is primed for rexposure to the antigen
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13
Q

Describe what occurs in re-exposure (effect) stage - what cells specifically?*

A
  • Basophils and Mast cells are sensitive to allergen (antigen)
  • On rexposure crosslinking of antigen to antibodies = activating mast cell and basophils
  • Release of powerful pro-inflammatory mediators from mast cell and basophils (chemokines, histamines, proteases, IL-4)
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14
Q

Compare the early phase of re-exposure

A

Early phase: minutes after exposure, triggered by cross-linking (antigen-antibodies)
* Epithelial intercellular tight junctions effected = leakage/increased vascular permeability = enhanced antigen penetration through epithelium = more binding to mast cells = more release of pro-inflam mediators = oedema
* Stimulation of sub-epithelial nerve terminals (Vagal nerve - parasympathetic) = bronchoconstriction and **more mucus*

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15
Q

Compare the late phase of re-exposure

A

Late phase: can take hours to come into affect

  • Leukocytes recruited to site of reaction by chemotactic factors and cytokines (released in early phase) = release mediators to begin late phase
  • Eosinophils produce major basic protein and eosinophil cationic protein = toxic to epithelial cells = airway damage and bronchoconstriction
  • Epithelial cells produce eotaxin = chemoattractant/ activator of more eosinophils and T cells
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16
Q

Compare a normal airway to a asthmatic airway (airway remodelling)

A
  • Huge accumulation of mucus in bronchial lumen
  • Increase in the number of mucus secreting cells (goblet cells)
  • Hypertrophy of sub mucousal glands
  • Chronic inflammation because of recruitment of eosinophils, mast cells and macrophages ie. lots of inflam immune cells
  • Thicker basement membrane
  • Hyperthropy and Hypoplasia of smooth muscle cells
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17
Q

Pharmacological interventions (antagonists) prove the major mediators… are involved

A
  • Leukotrienes - prolonged bronchoconstriction, increased vascular permeability, increased mucus secretion
  • Acetylcholine - airway smooth muscle constriction
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18
Q

Pharmacological interventions (antagonists) prove the minor mediators (minor contributors)… are involved. (Antagonising doesn’t have a big effect)

A
  • Histamines - bronchoconstrictor
  • Prostaglandin D - bronchoconstrictor and vasodilation
  • Platelet-activating factor - cause aggregation of platelets and release of serotonin
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19
Q

Describe non-atopic asthma

A

Triggered by respiratory tract infections
Normal IgE, no allergies, normal family history
2nd most common type

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20
Q

What drug is most commonly related to drug-induced asthma

A
  • Aspirin
    Sensitive to NSAID’s and aspirin
    inhibits cyclo-oxygenase pathway
  • Codeine and Morphine
  • Mellitin (bee venom)
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21
Q

What are the two mains types of treatment for asthma

A

Bronchodilators (relivers)
* Relax the airway smooth muscle = bronchodilation
Anti-inflammatory agents (preventers)
* used to manage underlying inflammation

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22
Q

List and describe some examples of Bronchodilators

A

B2-adrenoreceptor agonist (Ventoil) - mimics action of adrenaline - antagonise spasmogens = bronchodilation. Can be used for all patients.
Muscarinic receptor antagonist - prevents bronchoconstriction by acetylcholine. Less effective, useful add on
Methylxanthines Theophylline - bronchodilators and anti-inflam’s but cant inhale

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23
Q

Your patient has selective IgA deficiency. IgA is an antibody. Antibodies are produced by:
1. B cells
1. Plasma cells
1. T helper cells
1. Macrophages

A

Answer Plasma Cells (2)

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24
Q

Where is IgA mostly found?
1. Tissues
1. Lymph nodes
1. Spleen
1. Mucosal surfaces

A

Answer: Mucosal surfaces (4)

25
Q

What is the difference between atopic and non-atopic asthma?

A

Atopic: Allergic
Non-atopic: non-allergic

26
Q

25 year old patient with sever atopic asthma, specifically type 1 hypersensitisty. She is taking corticosteroids as a medication and has noticed some changes to her oral cavity. What are some changes you might idenify in her oral cavity.

A

Increased risk of dental caries and gingivitis (B2 agonists)
xerostomia (B2 agonists)
oral mucosal changes
significantly higher levels of candidiasis - advise patient to rinse mouth with water after using
low bone density
bronchodilators can lead to gastro-reflux -> enamel erosin

27
Q

You need to assess weather Maureen’s asthma is currently sufficiently well controlled before you undertake restoritive work. What questions would be appropriate to ask Maureen/considerations for the patient…

A

Assess the risk on the day, history and severity…
* When was your last ashtma attack?
* How severe was it?
* Have you taken your medications today
Scedule a late morning or late afternoon appointment
Can use bronchodilator as preventitive
Make sure they have brought their ‘reliever’
Provide stress-free environment
Corticosteroid patients - consult risk of infection due to immune supression

28
Q

Maureen suddently starts to cough and wheeze, so you suggest she needs to quickly take her medication. She asks you which inhaler she should use and why?

A

Inhaler (salbutamol/ventolin)
Salbutamol is used to relieve/reverse an asthma attack - need a bronchodilator.

A corticosteroid is used to manage the underlying inflammation - preventor

29
Q

What medications are likely to cause xerostomia in asthma suffers.

A
  • Ventolin: side effect impacts oral health
  • Selective serotonin reuptake inhibitors (SSRI’s) can also cause xerostomia
  • Corticosteroids can cause risk of fungal infections (oral thrush) but xerostomia is not an issue.
30
Q

What are some common drugs that possibly trigger asthma

A

Aspirin - NSAID’s: inhibit fatty-acid cyclooxygenase pathway -> forced to undergo lipooxygenase pathway -> stimulated production of leukotrienes -> leukotrienes will cause bronchoconstriction
Codein - stimulate mast cells -> induce inflammatory response -> bronchocontriction

31
Q

Chronic bronchitis and emphysema often occur together. What is the most significant risk factor for both?

A

Cigarette smoking
Otherwise: long term exposure to lung irritants (chemical vapours, pollutants and dust) and genetic disorder (alpha 1-antitrypsin deficiency can trigger emphysema)

32
Q

What is emphysema?

A

Irreversible enlargement of the airspaces distal to the terminal bronchiole (destruction of alveolar airway walls)
= impaired gas exchange - not enough O2 coming in, too little CO2 exhaled
= overinflation of the lungs (elastic recoil lost -> exhalation effected)

33
Q

Emphysema is classified based on anatomic distribution within the secondary primary lobule. What is the secondary primary lobule?

A

Unit of the lungs supplied by the 12th generation bronchiole. Sac/cluster of acini.

34
Q

What are acini?

A

Acini - subunit of secondary lobule.
gas-exchanging unit of the lung distal to the terminal bronchiole (last conducting airway)
* comprised of respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli.

35
Q

What is a primary lobule

A

Are governed by 1 alveolar duct

36
Q

Compare centrilobular and panacinar emphysema generally

A

centrilobular: central and proximal areas of emphysematous damaged. But surrounded by spared distal alveolar spaces (healthy) lesions common in upper lobe. Common 95% - heavy smoking.
panacinar: involves entire secondary pulmonary lobule

37
Q

Describe panacinar (panolobular) emphysema

A

Whole acini uniformly enlarged (from bronchiole to terminal alveoli)
* Lesions common in lower zones - most severe at base
* Associated with a1-antitrypsin deficiency
* Exacerbated by smoking

38
Q

Describe the causes (pathogenesis) of emphysema

A

Smokers and a1-antitrypsin deficiency = risk factors

Pathogenic triad…
* Oxidative stress (esp from smoke)
* Proteases -> destruction
*Usuaully a1-antitrypsin = protective anti-protease
anti-proteases (deficiency) = no stopping destruction
Imbalance in protease (elastase) and anti-protease activity
* Toxic injury and inflammation

39
Q

Why is smoking a risk factor for emphysema?

A

Smoking, nicotine and noxious gases
= Alveolar macrophages activated (attract neutrophils)
= Increased numbers of activated neutrophils
= release proteases (elastase) -> breakdown connective tissue and release oxygen free radicals
= inhibit a1-antitrypsin activity
=unchecked tissues distruction (elastolytic activity) -> emphysema

40
Q

What are the risk factors and definition of chronic bronchitis?

A

Smoking and pollution
‘chronic cough and excessive sputum production’

41
Q

What are the 2 important factors in the genesis of chronic bronchitis?*

A
  • Chronic irritation by inhaled substances
  • Microbiologic infections
42
Q

Describe the pathology of chronic bronchitis

A

Alteration of mucosal lining of the bronchi…
* increased thickness of airway mucosa
* increase in mucous secreting cells
* inflam. infiltration and fibrosis of bronchial walls
= airways narrowed

43
Q

Describe the progression of chronic bronchitis

A
  1. Respiratory funct. asymptomatic
  2. Eventually, dyspnoea (shortness of breath) on exercertion
  3. Over time - cynanosis (blue nose), hypercapnia (high CO2), hypoxemia (low O2)
  4. Cor pulmonale - pulmonary hypertension and right ventricle enlarged -> heart failure
  5. differentiation airway epithelium (cancer transformation?)
  6. Death from impairment of respiratory funct. with heaps of bacterial infections
    can coexist with emphysema
44
Q

The term ‘pink puffer’ is often interchanged with ____ what are the symptoms?

A

Severe emphysema
* Barrel-chested (overextension of lungs)
* Prolonged expiration
* Sit hunched over to try sqeeze air out
* Breathe through pursed lips
* Low diffusion capacity <- increased respiratory rate
* Weight loss

45
Q

The term ‘blue bloater’ is often interchanged with ____ what are the symptoms

A

Chronic bronchitis
* Recurrent respiratory infections
* Persistant cough with abundant sputum
* Hypercapnia, Hypoxemia
* Cor pulmonale and cyanosis (blue lips and fingers)
* Obese

46
Q

Define pneumonia

A

Infection of the lung parenchyma
= inflammatory reaction in the alveoli and insterstium of the lung
classified by infective agent - bacteria vs virus

47
Q

The vast majority of infections are upper respiratory tract infections caused by bacteria, virus’ or fungus.
A virval lung infection causes damage to bronchial epithelium and obstructs airways with excessive mucus (may also develop superinfection with bacteria)
What are the two most common viruses?

A

Rhinovirus - 60%
Small RNA viruses, infect epithelia cells via ICAM-1, generally confined to upper respiratory tract
&
Influenza
larger more complex virus, binds to host cell membrane

48
Q

What is the treatment for the common cold?

A

Nothing prophylatic, just ‘ride it out’ or relieve symptoms with decongestants (vasocontrictors -> less mucus) or pacaetamol

49
Q

What are the possible treatments for influenza?

A

Amantadine -> inhibits influenza A subtypes
= reduces duration and intensity of symptoms

Zanamivir -> influenza A or B
= inhibits release of virus from infected cells

Tamiflu -> influenza A or B
= decrease viral load and contain infection but side effects

Influenza vaccination -> 3-6 month effectiveness

50
Q

Describe the pathogenesis of pneumonia

A
  • Microbial agents enter the lung, multiple and trigger pulmonary inflam
  • Bacteria invades lung parenchyma -> exudate (puss)
  • Alveolar air space filled with exudate solidifies (consolitdation) -> inflammatory cells invate -> inflammation
51
Q

What is the difference between viral and bacterial pneumonia?

A

Viral: does not produce exudative fluid
Bacterial: exudate (puss) -> solidifies (consolitdation) -> inflammation

52
Q

Compare Bronchopneumonia and lobar pneumonia

A

Broncho
* Patchy consolidation of the lung (part)
* Effects infants and old people (where there is little immune system effect)

Lobar
* Affects large portion or entire lobe
* uncommon

53
Q

What are the normal host defence mechanisms

A

Nasal clearence
* Particles on non-ciliated epithelium (front of airways) removed by sneezing
* Particles on posterior swept by ciliated epithelium to naspharynx to be swallowed

Tracheobronchial (mucocillary) clearence
* Mucocillarly clearence towards oropharynx

Alveolar clearence
* Alveolar macrophages patrol alveoli and phagocytose
* IgA antibodies and IgG antibodies

54
Q

What are the main ‘risk factors’ for pneumonia

A

Impaired defense mechanisms or low host resistance
* Chronic diseases, immune deficiency, immunosupressive agents (corticosteroids)
* Low or supression of cough reflex (coma, drugs)
* Injury to mucocillary apparatus - impaired cilia function or epithelial destruction

55
Q

What are the main symptoms of pneumonia?

A
  • Malaise, fever, cough (sputum)
  • radiological appearence is opaque
56
Q

What is the key to treatment of pneumonia?

A

Identification of organism and its antibiotic sensitivity => determines appropriate therapy
Ex. antibiotics administered with first clinical signs

57
Q

Describe Atypical pneumonia

A

Lack of alveolar exudate
* patchy or unilateral inflammatory changes in the lungs
* less sever symptoms: dry cough, headache

58
Q

What microorganisms tend to cause atypical pneumonia?*

A
  • Mycoplasma pneumoniae (most common)
  • Legionella pneymoniae (legionnaires disease)
  • Coxiella burnetii (Q fever)
59
Q

Describe symptoms of viral pneumonia?

A

Few localised symptoms (possible no cough) -> fever, odema, headache, myalgia, hypoxemia

Anatomy (13 decks)

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