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Respiratory > Week 4 Respiratory > Flashcards

Week 4 Respiratory Flashcards

1
Q

What are the major components of neural control of ventilation?

A

Generation of rhythmic pattern of alternating inspiration and expiration, regulation of rate and depth of ventilation to match changing requirements, modification of respiratory activity for other purposes (voluntary- speech/ involuntary- coughing/sneezing)

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2
Q

Where is the respiratory centre?

A

Located within the brainstem (rostral continuation of spinal cord)

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3
Q

What are the 5 aggregations of neuronal cell bodies in the respiratory centre?

A

Dorsal respiratory group (DRG), ventral respiratory group (VRG), and pre-Botzinger complex within the medulla oblongata, apneustic centre and pneumotaxic centre (in the pons the last two)

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4
Q

Where are the pons and medulla oblongata ?

A

In the brainstem (two different parts)- the pons is rostral to the medulla oblongata

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5
Q

What does the DRG do?

A

It triggers inspiration; with cessation of firing expiration occurs
It also activates the VRG when demands for ventilation increase

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6
Q

What sets the rhythm?

A

pre-Botzinger complex (repetitive self-induced APs)

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7
Q

What does the VRG do?

A

Increases ventilation by firing to get the accessory muscles into action of inspiration and expiration

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8
Q

What does the penumotaxic centre do?

A

Terminates inspiration– by sending signals to the DRG

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9
Q

What does the apneustic centre do?

A

Prevents switching off of inspiratory neurons

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10
Q

What do the stretch receptors in the smooth muscle of airways do, for example the Hering- Breuer reflex do?

A

Inhibition of firing of inspiratory neurons to prevent over-inflation of lungs (stretch receptor in smooth muscle of airways EXAMPLE)

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11
Q

What do mechanoreceptors in airways do?

A

Initiate coughing/ sneezing reflex to remove unwanted material

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12
Q

What do chemoreceptors do?

A

Peripheral chemoreceptors located in: carotid bodies (origin of internal carotid) and aortic bodies (aortic arch)

Central chemoreceptors located in ventral parts of medulla oblongata

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13
Q

What regulates rate and depth of ventilation?

A

medullary centre- e.g. DRG and VRG from signal the body sends

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14
Q

What monitors arterial PO2?

A

Peripheral chemoreceptors- dramatic change in arterial PO2 ( stimulate medullary inspiratory neurons–> increased ventilation (low PO2 depresses all neural function except chemoreceptors- necessary life saving mechanism… only responds to arterial PO2, not O2 bound to Hb)

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15
Q

What is the most important response to elevated arterial PCO2?

A

Stimulation of central chemoreceptors (weak response from peripheral). Central chemoreceptors respond to H+ generated from CO2 in brain ECF rather than PCO2 (CO2 diffuses more readily across the BBB than H+)–> elevated H+ in brain ECF–> stimulation of medullary resp. centre–>stimulation of ventilation (increased removal of CO2 from lungs)

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16
Q

What happens when PCO2 drops below normal?

A

Lowered H+ in brain–> decreased stimulation of medullary respiratory centre by central chemoreceptors–> decreased ventilation

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17
Q

What will very high levels of CO2 in blood do? >75 mm Hg

A

Directly depress neural function–> depression of ventilation–> death

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18
Q

What does H+ directly influence?

A

Peripheral chemoreceptors

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19
Q

What kind of acidosis if increased PCO2

A

Either

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20
Q

What does the Beta-2 adrenoceptor agonists do?

A

Dilate airways via relaxing bronchial smooth muscle.

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21
Q

How do Beta2 agonists work?

A

Inducing production of cAMP–> stimulates key signal transduction pathways for relaxation of airway smooth muscle
Adrenalin binding–> increased adenyl cyclase–> increased cAMP–> activates PKA for example–> inactive MLCK–> bronchodilation

ALSO INCREASES MUCOCILIARY CLEARANCE

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22
Q

How do Phosphodiesterase inhibitors work?

A

Bronchodilation for COPD and asthma. Also raises intracellular cAMP (prevents its breakdown by inhibiting phosphodiesterase mediated breakdown of cAMP). Side effects limit phosphodiesterase use. Side effects include tremor from CNS stimulation, nervousness from the same, diuresis as a result of increased renal blood flow. NARROW THERAPEUTIC WINDOW.

CAUSES relaxation of airways, incrased HR and increase in CO, CNS stimulation
Bronchodilation is not as effective as beta agonists but useful adjunct therapy in asthma and COPD

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23
Q

How do muscarinic receptor antagonists work?

A

Stimulation of PS pathway induces bronchodilation via the M3 muscarinic receptor which is found abundantly in bronchial smooth muscle.

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24
Q

What is the main anti-inflammatory drug in respiratory issues like asthma?

A

Corticosteroids. Longterm low dose is common.

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25
Q

What do mucolytics do?

A

Increase the production of serous mucous in the respiratory tract and make the mucus thinner and less viscous. This contributes to mucociliary clearance in the respiratory tract and thus assists in clearing mucus obstructed airways. Administered by inhalation.

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26
Q

How is feline asthma treated? (Asthma like heaves or recurrent airway obstruction RAO in horses)

A

Bronchodilators and anti-inflammatory

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27
Q

What are the aims of tx in ashma or heaves or RAO?

A

Control inflammation, minimize bronchoconstriction, minimize longterm damage

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28
Q

How does Ca2+ initiate contraction in smooth muscle?

A

Ca2+ binds to calmodulin–> causes active myosin kinase by phosphorylation–> now phosphorylated myosin can bind with actin

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29
Q

How does Ca2+ relax?

A

Ca2+ uptake SR–> myosin loses P–> thin filament/ thick filament disengagement–> relaxation (lattice normal shape)

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30
Q

How do corticosteroids work?

A

decrease inflammatory cells (eosinophils, T-lymphocytes, Mast cells, macrophages, dendritic cells) which also decreases cytokines, also decreases epithelial cells releasing cytokines, endothelial cells allowing gaps??, decreases mucous secretion from mucous glands

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31
Q

What are the defence mechanisms of the upper respiratory tract?

A

*Sneezing, *coughing, *warming and humidification of inspired air by nasal mucousa- prevents desiccation of airway mucosa, promotes mucociliary clearance, and prevents exposure of the lower respiratory tract to cold air, *mechanical filtration (nasal hairs trap large particles, nasal meatuses and coiled arrangement of nasal conchae also trap particles), *mucociliary clearance, *chemical defenses (antimicrobial molecules present in the mucus in the URT), *leukocytes (can be recruited from the circulation), * immune defenses (NALT, B & T lymphocytes, BALT), *normal microflora

32
Q

What size particles are trapped in nasal hairs or nasal meatuses, what size particles make it to the trachea and bronchi, and what size particles could make it to reach the terminal bronchioles and alveoli?

A

particles >10 microns are trapped in the nasal hairs or nasal meatuses
3-10 microns- trachea and bronchi (mucociliary clearance)

33
Q

Where does mucociliary clearance bring material trapped?

A

To the pharynx where it can interact with lymphoid tissue before being swallowed- if it becomes impaired, coughing becomes critical

34
Q

What might impair mucociliary clearance?

A

Upper respiratory tract infection with viruses or bacteria, sustained exposure to cold air or ammonia fumes, and by squamous metaplasia of respiratory epithelium induced by chronic inflammation or toxin exposure (e.g. cigarette smoke)

35
Q

What is primary ciliary dyskinease?

A

Sick cilia syndrom or immotile cilia syndrome- illustrates the defensive importance of mucociliary clearance to respiratory tract health. Rare inherited condition in humans and dogs. Affected animals are predisposed to chronic or recurrent rhinitis, sinusitis, bronchitis, bronchiectasis (permanent dilation of bronchi due to chronic inflammation) and bacterial bronchopneumonia

36
Q

What occurs with abnormally viscous mucus production?

A

Can also prevent normal beating of cilia and hence mucociliary clearance

37
Q

What is cystic fibrosis?

A

In humans, especially Irish (autosomal recessive)- caused by a mutation in a gene that encodes a protein- that regulates the resp. tract mucos, digestive tract secretions, and sweat. Affected patients have airway clogged by viscous mucous and impaired mucociliary clearance–> predisposition to chronic rhinitis, sinusitis, bronchitis, bacterial, and fungal pneumonias and eventually to pulmonary hypertension and cor pulmonale

38
Q

What are some chemical defences of the URT?

A

Lactoferrin- binds to iron rendering unavailable to bacteria; lysozyme; Beta defensins- peptides that are capable of killing bacteria, fungi, and enveloped viruses by creating pores in their membranes; secretory IgA and polysaccharides that block mucosal attachment of bacteria

39
Q

What is NALT?

A

Nasal Associated Lymphoid Tissue - traffic to other lymphoid tissue to promote systemic cellular and humoral immune responses

40
Q

What is the lymphoid tissue called that encircles the oropharynx and the nasopharynx?

A

Waldeyer’s ring

41
Q

What is BALT?

A

Bronchus associated lymphoid tissue- located in bronchial submucosa at branching points where inhaled particles impact on the mucosa- traffic to other lymphoid tissue to promote systemic cellular and humoral immune responses

42
Q

What is chondrodysplasia?

A

Impaired longitudinal growth of the cartilage model of the future skeleton–> dwarfism. abnormal ethmoid bones and turbinates, shortened maxilla.

43
Q

What is holoprosencephaly?

A

Forebrain deformities which typically include agenesis (failure of an organ to develop initially) or severe hypoplasia of the olfactory bulbs and tracts

CYCLOPIA- single large midline eye (due to absence of several cranial bones

WRY NOSE- shortening and lateral deviation of the maxilla- up to 90 degrees

44
Q

What is cheiloschisis?

A

Harelip or cleft lip. Uni or bilateral failure of fusion of the upper lips at the midline philtrum; defect may be superficial or extend into the nostril

45
Q

What is palatoschisis?

A

Cleft palate. A midline defect in the hard and/or soft palate– communication between oral and nasal cavities (usually neonatal death due to inability to suck)

46
Q

What is cystic nasal conchae?

A

Most commonly seen in cattle- uni- or bilateral cysts in the ventral nasal meatuses- composed of mucus filled cavity lined by epithelium. Expand over time to cause progressive air flow obstruction with inspiratory and expiratory noise

47
Q

What is choanal atresia?

A

Uni or bilateral failure of formation of a communicating channel between the nasal cavity and the nasopharynx– common in foals and llama/alpaca crias. Leads to exercise intolerance.

48
Q

What is Brachycephalic Airway Syndrome?

A

Multiple congentical anatomic abnormalities found in brachycephalic dog breeds and short-faced cats:

  • stenotic external nares
  • elongated soft palate
  • everted laryngeal saccules (aka laryngeal ventricles)
  • laryngeal collapse
  • tracheal hypoplasia
49
Q

Why does nasal congestion and hyperaemia occur?

A

Complex vascular plexus in superficial nasal mucosa- present to warm and humidify inspired air- and reclaim moisture and heat from saturated vapour leaving the lungs during expiration. Congestion is a common post mortem , presumably reflecting terminal circulatory failure and pooling of venous blood. Intense nasal (and paranasal sinus) mucosal congestion +/- haemorrhage is a feature of bloat in ruminants. Hyperaemia and oedema of the nasal submucosa is expected in active inflammation.

50
Q

What causes epistaxis?

A

Trauma, FBs, tumours, severe rhinitis, intense sneezing episodes, bleeding disorders (possibly systemic hypertension, right sided congestive heart failure, intra nasal vascular aneurysm, pulmonary haemorrhage (e.g. exercise induced pulmonary haemorrhage in horses), guttural pouch fungal infection (in horses)

51
Q

What is Progressive Ethmoid Haematoma?

A

Unilateral space-occupying mass of organizing haemorrhage and reparative granulation tissue in the submucosa of the ethmoid turbinates. Affects horses especially older TBs and Arabian breeds. Extreme cases it may fill the nasal meatus as far as the external nares or extend into the maxillary sinus.

52
Q

What is Rhinitis?

A

Inflammation of the nasal cavity- localized or component of systemic disease e.g. systemic viral infections. Causes: virus, bacteria, fungi, parasits, FBs, allergens

53
Q

What is acute rhinitis?

A

Nasal mucosa oedema, hyperaemia, and exudation into nasal passages- discharge. Most forms are self limiting and follow chronological sequence from serous to catarrhal to mucopurulent to purulent inflammation followed by complete resolution

54
Q

What is Serous Rhinitis?

A

Serous nasal discharge with FEW leukocytes
Nasal submucosa is oedematous and hyperaemic
Nasal mucosal epithelium may be histologically normal or show evidence of hydropic degeneration with loss of cilia
e.g. exposure to mild nasal irritants, cold air, early stages of viral infections

55
Q

What is Catarrhal Rhinitis?

A

Hours to days- nasal exudate becomes mucoid (catarrhal) due to increased mucous production by goblet cells dna submucosal glands
* Additional recruitment of neutrophils and sloughing of mucosal epithelial cells (+/- bacterial infection) the exudate may become mucopurulent to purulent

56
Q

What is Purulent (Suppurative) Rhinitis?

A

Exudate thickens due to recruitment of large numbers of neutrophils

  • Erosion and ulceration of nasal mucosa
  • typical of many bacterial infections
57
Q

What is Fibrinous Rhinitis?

A
  • severe nasal mucosal injury with marked increase in vascular permeability–> leakage of fibrinogen and neutrophils
  • coagulation of fibrinogen–> pseudomembrane formation
  • e.g. fungal rhinitis, infectious bovine rhinotracheatis (bovine herpesvirus-1), in cattle- Fusobacterium necrophorum infection
58
Q

What is chronic rhinitis?

A

Some forms tend to be persistent e.g. allergic rhinitis, fungal rhinitis

  • progressive fibrosis of nasal submucosa, atrophy of the submucosal seromucoid glands, and hyperplasia +/- squamous metaplasia of the mucosal epithelium
  • +/- formation of proliferative soft tissue masses (granulomas, pyogranulomas, polyps) in the submucosa
  • +/- destruction and atrophy of nasal turbinate bones, deviation of the nasal septum and eventually gross craniofacial deformity (e.g. progressive atrophic rhinitis in pigs)
59
Q

What is Lymphocytic-Plasmacytic Rhinitis?

A

A common uni or bi lateral chronic form of rhinitis in dogs and sometimes cats

  • persistent catarrhal to mucopurulent nasal discharge
  • submucosal infiltrates of lymphocytes and plasma cells
  • Initially triggered by viral, bacterial, or fungal infection, inhaled allergens or FB trauma but inflammation becomes self-sustaining via dysregulation of local immune responses, with ongoing cytokine release and recruitment of additional lymphocytes
60
Q

What is Granulomatous and Pyogranulomatous Rhinitis?

A

Accumulation of submucosal macrophages (+/- multinucleate giant cells) and smaller numbers of lymphocytes, plasma cells, +/- neutrophils or eosinophils

  • may cause formation of grossly protruberant mucosal nodules
  • e.g. chronic allergic rhinitis, chronic fungal infections, FBs, chronic infections in ruminants (Actinobacillus lignieresii)
61
Q

What is Allergic Rhinitis?

A

Dogs, cats, horses, cattle, sheep

  • sneezing, nasal discharge, lacrimation, nose rubbing, heat shaking, epistaxis
  • Type I hypersensitivity to allergens–> exudation of eosinophils and mucus
  • granulomatous (macrophage rich) rhinitis (nasal granuloma) is typical in chronic phase
62
Q

What are Nasal and Nasopharyngeal Polyps?

A

Polyps are masses of well-vascularized reparative connective tissue that can arise within the nasal cavity, nasopharynx, or auditory tubes as a consequence of chronic inflammation

  • common in cats and horses
  • composed of chronically inflamed, oedematous, or fibrous core covered by hyperplastic respiratory epithelium or stratified squamous (metaplastic) epithelium
  • nasal polyp- sneezing, nasal discharge, and protrusion of the polyp through the nares
  • nasopharyngeal polyp- gagging, dysphagia, dyspnoea
  • aural polyp- ataxia (incoordination), unilateral head tilt, drooping of upper eyelid, myosis, enophthalmos (sinking of the eye into orbit), facial nerve paralysis
  • commonly recur if incompletely excised
63
Q

What happens with Extension of Rhinitis?

A

Inflammation may extend from the nasal cavity into the paranasal sinuses (sinusitis), into the nasopharynx (nasopharyngitis) and or along the auditory tubes (to cause otis media and interna- in horses inflamm of the guttural pouches), into underlying nasal bones (osteomyelitis), or through the cribiform plate into the cranial vault to provoke meningitis and encephalitis

64
Q

What is Sinusitis?

A

Inflammation of a paranasal sinus.
Commonly coexists with rhinitis
Frontal and maxillary sinus are most often involved
May go undetected clinically unless it causes facial deformity or it fistulates to the skin surface
* Common in horses (limited drainage of the sinuses- periodontitis to extend to maxillary sinus) and sheep (fly larvae in the sinuses)

65
Q

What is chronic sinus mucocoele or sinus empyema?

A

In acute cararrhal and purulent sinusitis, exudate often occludes the sinus orifices–> impaired drainage–> chronic sinus mucocoele or sinus empyema–> may lead to facial deformity either by pressure effects on bone or by extension of infection into bone as an osteomyelitis

66
Q

What is Nasopharyngitis?

A

Inflamm. and infectious conditions that involve the oral cavity, oropharynx, nasal cavity may extend to involve the nasopharynx–> risk of airway obstruction and asphyxiation or aspiration pneuomia
e.g. ingested FB lodge in oropharynx of dogs, small FBs grass blades in dogs and cats- nasopharynx, in cattle large root crops may lodge in pharynx- asphyxia or pressure necrosis, balling and drenching gun injuries or rough intubation–> perforation of the caudodorsal pharynx–> cellulitis

67
Q

What is pharyngeal/laryngeal lymhpoid hyperplasia?

A

Formation of prominent submucosal lymphoid follicles in the caudal pharynx +/- larynx is common in TB horses under 5 yo. Presumed to reflect chronic antigenic stimulation from exposure to viruses or pesistence of bacteria. In severe cases lymphoid hyperplasia may be accompanied by mucosal bacterial infection and inflammation.

68
Q

What are Guttural Pouch infections?

A

In severe infection, erosion of the medial septum can permit bilateral pouch involvement.
Nasal discharge, epistaxis, painful swelling of the parotid area, abnormally high head carriage, enlargement of regional lymph nodes, dysphagia (difficulty swallowing), stertor

Can be suppurative due to infecton with Steptococcus equi (STRANGLES)

Can be from fungal infections (stabled horses- spores from moudly hay likely- fibrinous or fibrinonecrotising normally)

69
Q

What does guttural pouch empyema lead to?

A

COmpression or inflammation and necrosis of cranial nerves (VII, IX, X, XI, and XII) and/or cervical sympathetic trunk

70
Q

What is Guttural Pouch Tympany?

A

Accumulation of air in the guttural pouch. Uncommon condition of foals up to 1 yo, especially fillies. Abnormal valvular function at the nasopharyngeal orifice of the auditory tube. Usually unilateral. Severe, non-painful and compressible swelling of the parotid area on the affected side.

71
Q

Are most nasal tumours malignant?

A

Yes

72
Q

Which is more common nasal carcinomas or nasal sarcomas?

A

Carcinomas. Nasal lymphoma is common in dogs and cats- probably arises within NALT

73
Q

Where does squamous cell carcinoma arise from?

A

Nasal vestibule, esp. cats

74
Q

Where does Transitional cell carcinoma arie from?

A

Nasal transitional epithelium- dogs esp.

75
Q

Where does olfactory neuroblastoma arise from?

A

Dogs and cats. Caudal nasal cavity from olfactory neuroepithelial cells, neural crest cells, or local components of dispersed neuroendocrine system. Aggressive malignancy that often invades through cribriform plate and into the cerebral cortex.

76
Q

What is the most common tumour of the paranasal sinuses in horses?

A

Squamous cell carcinoma arising in the maxillary sinus. Or same type arising in the guttural pouch

Respiratory (11 decks)

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