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OS 213 Respiratory EXAM 1 > Cough and Hemoptysis > Flashcards

Cough and Hemoptysis Flashcards

1
Q

Forced expulsive maneuver usually against a closed glottis, whih is associated sound

A

cough

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2
Q

Cough pellets

A

Broncholiths

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3
Q

Initiation of cough

A

Voluntary cough -cortex

Reflexive cough - vagus nerve and its branches

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4
Q

Most sensitive sites for initiating cough

A

larynx and tracheobronhial tree, esp. carina and branching points

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5
Q

Phases of cough Production

A
  1. Inspiratory
  2. Compressive/ Glottic Closure
  3. Expulsive (Expiratory or explosive)
  4. recovery
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6
Q

Inspiratory phase of coughing

A

1st phase
2.5 L
negative flow rate

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7
Q

Compressive/ Glottic cllosure

A

2nd phase of production
Zero flow rate
Pressure builds up, to as high as 300 mmHg
Positive intrathoracic pressure

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8
Q

Expulsive (Expiratory or explosive)

A 
3rd Phase
1st cough sound heard
Growing, constant, decreasing sub-phases
Positive flow rate
Pressure is highest
120 to 160kph
large pressure differential
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9
Q

Recovery

A

4th phase of coughing

Restorative inspiration

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10
Q

Which phase is not critical to effective coughing?

A

Glottic clossure

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11
Q

Initiation of cough

A
  1. Inflammatory or mechanical changes in the airways
  2. Polymodal Sensosy nerve receptros
  3. Rapid and large changes in lung volumes
  4. Psychological factors
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12
Q

Exaggerated response to harmless or mildly irritating stimuli

A

Cough sensor plasticity

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13
Q

Which nerves are involved in both the efferent and afferent limbs of the cough reflex?

A

Phrenic and Vagus

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14
Q

Medullary cough pattern generatory

A

Nucleus tractus solitarius

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15
Q

Dual primary sensory neuron model of cough induction

A

C fibers - chemical irritants

Mechanoreceptors - sense punctate mechanical forces

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16
Q

Compose most of the bronchopulmonary vagal afferent nerves, with terminals in and around the mucosa surface of the airways

A

Unmyelinated C-fiber nociceptors

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17
Q

Sensitive to bradykinin and activators of the ion channels

A

Unmyelinated C fibers

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18
Q

TRPV1

A

Capsaicin, protons

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19
Q

TRPVA1

A

Ozone, spices, mustard, wasabi-allyl isothiocyanate

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20
Q

Mechanically sensitive “cough receptors”

A

beneath the epithelium in the large airways
Relative insensitive to most chemical mediators
Include Widdicombe cough receptors and lung stretch receptors

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21
Q

Include Widdicombe cough receptors and lung stretch receptors -

A

Rapidly adapting receptors (RARs) and slowly adapting receptors (SARs)

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22
Q

The major afferent pathway

A

Vagus nerve

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23
Q

Stimuli triggering the vagus nerve

A

Ear, pharynx, larynx, trachea, carina, large intrapulmonary bronchi, heart, pericardium, esophagus

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24
Q

Involuntary cough appears to be initiated only from

A

vagal innervation of the airways

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25
Q

Airway afferent nerve fibers originate in the ________-

A

nodose and jugular ganglia

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26
Q

Airway afferents are stimulated by irritants or inflammatory mediators via _______?

A

activation of G protein coupled receptors

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27
Q

Factors contibuting to cough Inefficiency

A
  1. Altered cough mechanics
  2. altered mucous rheology
  3. altered mucociliary function
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28
Q

Altered cough mechanics

A
  1. Expiratory muscle weakness
  2. Inspiratory muscle weakness
  3. Abdominal wall muscle weakness
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29
Q

Altered mucous rheology

A

Adhesiveness

Cohesiveness

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30
Q

Composition of Normal Mucus

A

95% water
3% mucin
1% lipids
<0.3% DNA

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31
Q

Confers viscosity and elasticity

A

Mucin

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32
Q

Liquid-like propertythat resists flow -stickness

A

Viscosity

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33
Q

Solid-like capacity to store energy that moves or deforms the fluid - stringiness

A

Elasticity

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34
Q

MUC genes

A

20 human MUC genes

9 expressed in the human respiratory tract

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35
Q

membrane tethered Mucin

A

MUC 1, MCU 4, MUC 16

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36
Q

Only 3 are classic gel-forming mucins

A

MUC 2 , MUC 5AC, MUC5B

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37
Q

MUC produced mostly at proximal airways by goblet cells

A

MUC5AC

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38
Q

MUC produced by goblet cells throughout airways and by submucosal glands

A

MUC5B

39
Q

Mucin

A

Cysteine-richsecretory mucins stabilized by multiple disulfide bonds _> entangled in a mesh

40
Q

Airway inflammation ->Mucus hypersecretory phenotype

A
  • Decreased mucociliary clearance
  • Increaed luminal mucus
  • Submucosal gland hypertrophy
41
Q

Decreasd mucociliary clearance

A

Goblet cell hyperplasia/mucus metaplasia

Increased plasma exudation

42
Q

Increased luminal mucus

A

Increased mucus synthesis and secretion

Reduced mucin degradation within the airways

43
Q

Submucosal gland hypertrophy

A

Secretion of inflammatory mediators

44
Q

Cystic fibrosis

A

Increased (+++++) inflammatory cells, DNA, Actin, Bacteria

45
Q

Asthma

A

Increased (+++++) mucin

46
Q

Major symptom in chronic bronchitic phenotype II

A

Mucus hypersecretion of COPD (Myeloperoxidase)

myeloperoxidase

47
Q

Sequelae of mucus

A 
Increased Viscosity of mucus
decreased ciliary effectiveness
increased Mucus plugs
Increased Airway Resistance
increased infections
Obstructed bronchioles lead to atelectasis
48
Q

Cough reflex sensitization

A

Viral infection ->Cough reflex becomes hyperreactive-> cough subsides after 2-3 weeks

49
Q

Duration of Cough

A

Acute <3 weeks
Sub-acute : 3-8 weeks
Chronic ->8 weeks

50
Q

Several nerves that are involved in the afferent limb

A

Trigeminal, glossopharungeal, phrenic, and vagus

51
Q

Systematic evaluation of the afferent limb of the cough reflex

A

Anatomic diagnostic protocol

52
Q

drug induced cough

A

ACEI (Captopril, enalapril for HTN)

- accumulation of bradykinin

53
Q

Formerly known as Postnasal drip syndrome

A

Chronic Upper Airway Cough syndrome

54
Q

Complications of cough

A 
Soreness
Syncope
Fractures
Pneumothorax
Exhaustion
Tracheobronchial trauma
Insomnia
Lifestyle change
55
Q

Examples of Non-Specific Cough therapy

A
  1. Antitussive or cough supressant

2. Protrussive

56
Q

Drugs than increase the latency or threshold of the cough center. Affects the afferent Limb of the cough reflex

A

Antitussive or cough supressant

Levodropropizine

57
Q

a cough productive of significant quantities of sputum should usually not be suppressed, since retention of the sputum in the tracheobronchial tree may interfere with distribution of alveolar ventilation and the ability of the lung to resist infection

A

ptrotrussive

  • indicated in cystic fibrosis, bronchiectasis, pneumonia, and post operative atelectasis
58
Q

Controlling Mucus Hypersecretion

A

Increase depth of the sol layer
Alter the consistency of the gel layer
Improve ciliary activity

59
Q

Mucoactive agents

A

Expectorants
Mucoregulators
Mucolytics
Mucokinetics

60
Q

Increase secretion of mucin, Increase the depth f the sol layer and hydration until it can be coughed out

A

Expectorants

hypertonic saline, guaifenesin

61
Q

Decrease neurogenic/airway iflammation

A

Mucoregulators

Anticholinergics, steroids, and macrolides

62
Q

Compounds with sulfhydryl groups that are able to dissociate disulphide bonds -> reduce mucus viscosity

A

“free” sulfhydryl groups -> N-acetylcysteine

“Blocked” sulfhydryl groups _> carbocysteine, erdosteine

Proteolytic enzymes and rhDNAse also breaks up mucus

63
Q

Increase the transportability of mucus through cough

A

improve mucociliary transport

Bronchodilators, surfactants, ambroxol, certain mucolytics

64
Q

Tickle in the throat, throat clearing, hoarseness, nasal congestion

A

Chronic upper airway syndrome

65
Q

Secretions from nose/sinuses stimulate upper airway cough receptors; inflammation increases receptor sensitivity

A

Chronic Upper Airway Cough Syndrome

66
Q

Reversible airflow obstruction in spirometry (FEV1/FVC <75% at least 12% and 200 mL increase in FEV1 or FVC after 2 puffs of SABA)

Low peak flow and at least 15% increase after SABA

A

Cough-variant asthma

67
Q

Cough that worsens when lying supine

A

GERD/LPR

68
Q

Laryngoscopy findings

A

Edema, Erythema, Ventricular obliteration, pseduosulcus, postcricoid hyperplasia

69
Q

Eosinophilic airway inflammation without variable airflow obstruction or airway hyperresponsiveness

A

Non-asthmatic eosinophilic bronchitis (NAEB)

70
Q

Diagnostic tests for NAEB

A

Induced sputum (>3% eosinophils)

71
Q

Diagnostic/therapeutic trial

A

inhaled corticosteroid for >4 weeks

72
Q

Cough that has been present for at last 3-8 weeks following flu-like symptoms, includes tansient post viral BHR, pertussis, cough due to atypical organisms. Consider other diagnoses if cough >8weeks

A

Post infectious cough

73
Q

Likely due to extensive inflammation and disruption of upper and/or lower airway epithelial integrity

A

Post-infectious cough

74
Q

Accumulation of protrussive mediators such as bradykinins and substance P in the respiratory tract with ACEI; bradykinins stimulate production of prostaglandins

A

ACEI- induced cough

75
Q

DDX for dry cough, scratchy throat, feeling of throat obstruction

A

ACEI-Induced cough

76
Q

cough resolves within 1-4 weeks (ave 26 days) If its due to ACE-I intake

A

ACEI-Induced cough

77
Q

Afferent nerve carried by the auricular branch of the vagus nerve innervate the external auditory meatus

A

Arnold reflex

78
Q

Most common cause of mortality in hemoptysis

A

Asphyxiation

79
Q

Massive hemoptysis

A

200-600ml

unquantified amount but with the hemodynamic instability or anemia requiring transfusion

Medical Emergency

80
Q

dark red or brown in clumps, mixed with food, acidic pH, stomachache, abdominal discomfort, nausea, retching

A

hematemesis

81
Q

Why is hemoptysis common>

A

Dual circulation of the lung

82
Q

Most common source of hemoptysis

A

Bronchial arteries (high pressure)

83
Q

Most common etiology of hemoptysis

A

Tracheobronchial disorders

  • diffuse alveolar damage
  • diffuse bleeding in the alveolar space
84
Q

Destruction of cartilaginous support, bronchial artery hypertrophy, expansion of peribronchial and submucosal bronchial arterial apparatus, augmented anastomoses

A

Bronchiectasis

85
Q

Hemoptysis in TB mechanism

A

Bronchial ulceration with necrosis

Rupture of Rasmussen;s aneurysm

86
Q

Pulmonary artery erosion pseudoaneurysm., An aneurysm created by the erosion of a vessel by disease in the lung. Can be simultaneously perfused by teh pulmonary and the systemic circulation. Can be multiple, Diagnosed by spiral CT or pulmonary angiography

A

Ramussen’s aneurysm

87
Q

Primary Pulmonary vascular Disorders

A

Arteriovenous malformmation
Pulmonary embolism
Elevated pulmonary venous pressure
Iatrogenic

88
Q

Miscellaneous/Rare Causes of hemoptysis

A

Cocaine-induced pulmonary hemorrhage
Catamenial hemoptysis
Leptospirosis
Paragonimiasis

89
Q

Seen in free base cocaine users. Associated with diffuse alveolar hemorrhage

A

Cocaine-induced pulmonary hemorrhage

90
Q

Recurrent and coincident with menses, Cause: intrathoracic endometriosis

A

Catamenial hemoptysis

91
Q

TOP main cause of Massive hemoptysis

A

TB, bronchiectasis, Pneumoconiosis, Aspergilloma, Bronchial CA

‘BattleCamp”

92
Q

Putrid smell to the sputum

A

Anaerobic organism

93
Q

Highest value in a patient with hemoptysis + normal or non localizing the bleeding site

A

Bronchoscopy

94
Q

Acute management of Massive Hemoptysis

A 
ABCs
Stop the bleeding
Treat underlying cause
Protect the non bleeding lung
Bronchoscopy
Bronchial artery embolization

OS 213 Respiratory EXAM 1 (19 decks)

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