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VetMed Year 1 > CRS 2 > Flashcards

CRS 2 Flashcards

1
Q

Describe the anatomy and innervation of the diaphragm.

A
  • Diaphragm extends into thoracic cavity
  • Major muscle of inspiration
  • Striated muscle
  • Motor and sensory innervation through phrenic nerve (left and right)
  • From cervical segments of spinal cord
  • separates thorax from abdominal cavity
  • Muscular part is peripheral, tendinous part is central
  • Muscle attached to xiphoid process, to inside of lower costal cartilages and ribs by digitations
  • Crura attach to lumbar vertebrae
  • 3 openings: aortic hiatus, oesophageal hiatus, caval foramen
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2
Q

What are the borders of the thoracic cavity?

A

The first and last ribs and cranially and caudally, and laterally the rib cage.

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3
Q

What is the main difference between the left and right thoracic cavity?

A

More arteries visible on the left, more veins visible on teh right

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4
Q

What divides the left and right thoracic cavities?

A

The mediastinum

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5
Q

List what is present in the left pleural cavity.

A

Sympathetic trunk, aorta, brachiocephalic trunk, oesophagus, vagal nerve, laryngeal recurrens, trachea, vena cava, lymph nodes and thoracic duct, pericardium with the heart

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6
Q

List what is present in the right pleural cavity.

A

Sympathetic trunk, aorta, brachiocephalic trunk, oesophagus, vagal nerve, laryngeus recurrens, trachea, vena cava, azygous vein, lymph nodes, thoracic duct, pericardium with heart.
- Fold for vena cava is called plicae venae cavae
Mediastinal recess for accessory lobe of right lung

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7
Q

Describre the structure of the pleural membranes including the mediastinum.

A
  • Each lung surrounded by pleura (serous membrane)
  • 2 pleural membranes arranged as closed sacs around the lung
  • Same between left and right sac - mediastinum is space between these
  • Surface of lung covered by visceral (pulmonary) pleura (derived from splanchnic mesoderm), reflected around root of lug to become continuous with mediastinal pleura
  • Mediastinal pleura also continuous with diaphragmatic and costal pleura = parietal pleura and line the cavity (derived from somatic mesoderm)
  • Space between parietal and visceral pleura is pleural cavity
  • Contains small amount of serous fluid spread over surface = adhesion + smooth movement
  • Lung not attached to thoracic wall
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8
Q

Describe the function of the pleural membranes including the mediastinum.

A
  • Lung not attached to the thoracic wall
  • Follows movement of pleural membranes
  • Serous fluid allows for adhesion between the pleura
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9
Q

Identify the structures contained within the mediastinum.

A
  • Heart with pericardium
  • Vena cava
  • Trachea
  • Thoracic oesophagus
  • Lymoh nodes
  • Right phrenic nerve
  • Filled with connective tissue
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10
Q

Outline how pathogens have evolved mechanisms for interacting with their hosts.

A
  • Different methods of adhesion, different virulence factors, resistance to immune response
  • Contact between host and pathogen either leads to recognition by the host (internal and external receptors) or production of virulence factors by pathogen
  • Triggers immune response - immunopathology
  • Pathogen detaches, invade and produces toxins which lead to damage
  • Collateral damage caused by immune response
  • Leads to morbidity or mortality
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11
Q

Explain how the signs of infection may be caused bythe pathogen or by the host’s responses.

A
  • Swelling, redness and fever are responses of the host to fight infection
  • Swelling caused by invasion of neutrophils
  • Redness caused by increased blood flow to site of infection (supply more WBCs)
  • Fever is mechanism used to kill pathogens - cannot survive above certain temperatures
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12
Q

Outline the role of virulence genes in bacterial pathogens.

A
  • Genes that code virulence factors
  • Virulence genes can be passed on through plasmid trasfer and phage transduction
  • Hoizontal transfer
  • Virulence factors are what allows the bacteria to survive
  • Without virulence genes, no virulence factors, bacteria will die
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13
Q

Describe virulence factors and explain how they work.

A
  • Virulence factorsare molecules that allow bacteria to adhere, invade, evade host defence, cause tissue damage and replicate or persist in the host
  • Adhesion can be to cells, secretory products, structual components (teeth) or other bacteria (biofilms)
  • Bacterial structures involved may be fimbrae, pili or adhesive macromolecules imbedded in membrane
  • Other structures with adhesive properties: capsules, flagella, proteinaceous fibrils
  • Will usually bind to surface proteins, carbohydrates, host glycolipids/glycoproteins
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14
Q

Explain the process by which tissue invasion occurs.

A
  • Can be opportunistic (injury, procedures, catheters), vector mediated (arthropods)
  • Pathogen produces virulence factors and damaged is caused by toxins
  • Paracytosis = passage through cell layers without penetrating individual cells
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15
Q

Explain the phagocytic process by which bacteria enter host cells.

A
  • Host uptake mechanism (M-cells in gut) or invasion into cells (actin rearrangement, microtubule rearrangement -> forced phagocytosis)
  • Zipper mechanism
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16
Q

Explain the Zipper mechanism by which bacteria enter host cells.

A
  • Bacteria bind to host transmembrane adhesion proteins (integrins, cadeherins)
  • Host attempts to form cell junction
  • Spreads over adhesive surface of bacterium => phagocytosis
  • e.g. Listeria
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17
Q

Explain the trigger mechanisms by which bacteria enter host cells.

A
  • Bacteria inject TTSS effector proteins into host cell
  • Bacterial effector proteins interfere with host cytoskeleton
  • Stimulate actin polymerisation
  • Leads to localised membrane ruffling
  • Shigella and Salmonella are examples
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18
Q

Explain how host bacteria exploit host cell cytoskeletal and metaboic pathways.

A
  • Cytoskeleton used for Zipper and Trigger mechanisms, extracellular attachment and movement within/between cells
  • Cytoplasm viscous and inhibits diffusion
  • Some bacteria use nucleation and assembly of host actin filaments at one pole of bacterium
  • Growing filament generates force
  • Bacteria move 1mm/s
  • Depolymerisation factors in cytosol depolymerise actin again which leads to appearace of an actin tail
  • Some pathogens use monocytes to “hitch a ride”
  • Spread to other tissues
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19
Q

Explain the intracellular movement of bacteria contained in vacuoles

A
  • Salmonella containing vesicles (SCVs) localised along microtubules using molecular moors
  • Both motors (dynein and kinesin) associated with SCVs
  • Position along microtubules is controlled
  • Effector proteins constantly recruiting kinesin
  • Production of Sifa down modulates amount of kinesin on vacuole surface
  • Commonly used by viruses, not well understood in intracellular bacteria
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20
Q

Describe the concept of PAMPs

A
  • Pathogen Associated Molecular patterns
  • Expression of specific components that are then recognised as danger signals
  • Gram -ve: LPS recognised
  • Gram +ve: peptidoglycan
  • Binding of PAMP leads to signalling cascade
  • Activation of host response factors that have already been produced
  • OR activation of transcription factors and then ecpression of host response
  • Both lead to host response
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21
Q

Describe the concept of PRRs

A
  • Pathogen recognition receptors
  • host expression specific receptors that recognise the PAMPs
  • 6 different types of receptors: Toll-like, transmembrane, Nod-like cytoplasmic, C-type lectin, Mannose and Scavenger
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22
Q

Describe the concept of TLRs

A
  • Toll-like receptors
  • Membrane spanning receptors
  • Structure allows signal to go from outside to inside
  • Extracellular section (leucine rich repeats - LRRs)
  • Transmembrane domain that sits in the cell membrane
  • Intracellular section - Toll/IL-1 receptor (TIR) domain that is used for signalling
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23
Q

Outline the types of PAMPs that can elicit an inflammatory response

A
  • Microbial nucleic acids
  • Microbial lipoproteins
  • Microbial carbohydrates
  • Damage associated molecular patterns released from injured cells
  • All cause increase in leukocyte recruitment
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24
Q

Outline the roles of TLR1-TLR9 as pathogen recognition receptors.

A
  • TLRs 1, 2, 3, 4, 5 and 6 localised on cell surface and recognise molecular structures unique to bacteria
  • TLRs 3, 7, 8 and 9 are localised on intracellular compartments (including lysosomes and endosomes) and recognise viral and bacterial nucleic acids
  • TLR2 and 9 are stimulated during asthma
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25
Q

Explain the role of TLR4.

A
  • Recognises LPS, requires LBP, CD14 and MD2
  • LPS binds to LBP, then passed onto CD14
  • CD14 cannot pass through membrane so is passed onto MD-2, then TLR4 so LPS can pass through
  • Signalling through TLR4 requires 4 adapter proteins
  • Essential for host response to gram -ve bacteria
  • Absence leads to resistance to endotoxic shock, but infection by gram -ve bacteria cannot be controlled
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26
Q

Explain the role of TLR2.

A
  • Heterodimer
  • Responds to lipoproteins and lipopeptides from wide range of pathogens
  • Interacts with TLR1, TLR6 or dectin1 to increase specificity
  • Deficiency in TLR2 = increased susceptibility to infection with gram +ve bacteria
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27
Q

Explain the role of TLR5.

A

Recognises bacterial flagellin from gram +ve and -ve bacteria

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28
Q

Explain the role of TLR9.

A
  • Recognises bacterial CpG DNA motives
  • CpG motif consisting of unmethylated CpG dinucleotide generally flanked by 2 5’ purines (A or G) and 2 3’ pyrimidines (T or C)
  • Different for differen species
  • Activation of immune system by bacterial DNA motifs may be utilised in development of adjuvants for vaccines
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29
Q

Explain the role of TLR3.

A
  • Responds to double stranded RNA

- Only other TLR that requires adapter molecule (Trif)

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30
Q

Explain the role of TLR7 and 8.

A

Interacct with single stranded RNAs

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31
Q

How do TLR receptors contribute to hoemostasis on muscosal surfaces populated by commensal bacteria?

A
  • TLR receptor expression on basal surface of epithelial cell
  • Not on apical surface that is in contact with gut lumen and commensal bacteria
  • Prevents reaction to commensals
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32
Q

List clincial syndromes associated with systemic inflammation.

A

Bacteremia/septicaemia, SIRS, shock, sepsis, severe sepsis, MODS

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33
Q

Define bacteremia/septicaemia

A

Presence of viable bacteria in the blood stream

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34
Q

Define SIRS

A

Systemic inflammatory response syndrome

Systemic response to an array of severe clinical insults

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35
Q

Define shock

A

SIRS induced hypotension refractory to fluid resuscitation in association with hypoperfusion

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36
Q

Define sepsis and severe sepsis

A

SIRS due to infection

Severe sepsis is sepsis associated with organ dysfunction, hypoperfusion or hypotension

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37
Q

Define MODS

A

Multi organ dysfunction syndrome

Altered organ function in an acutely ill patient requiring intervention to maintain homeostasis

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38
Q

Explain the processes leading to sepsis, especially pathogen recognition by the host.

A
  • Localised infection becoming systemic
  • Sepsis as complication due to commensal bacteria after breakdown of barrier (often in neonates, some colic cases in horses, long operations, oxygen supply to gut epithelial layer reduced so epitehlial layer breaks down and larger number of bacteria enter blood stream)
  • If a localised infection becomes systemic, will be high systemic levels of mediators which will cause sepsis
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39
Q

Discuss the progession of inflammatory processes and associated pathophysiological damage and how sepsis, SIRs and MODS lead to high mortality

A
  • SIRS and sepsis lead to MODS
  • Infection carried through system by blood
  • Leads to high mortality as organs are destroyed and blood flow is altered
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40
Q

Outline potential therapeutic intervention strategies.

A
  • Early diagnosis
  • Treatment of primary disease process
  • Supportive care
  • Balance to prevent detrimental effects without suppressing beneficial effects
  • Removal or circulation LPS using antibodies or poly myxin B prevents activation of receptors
  • preventing actin of pro-inflammatory cytokines (target TNF alpha, anti TNF alpha antibody, soluble TNF alpha receptor)
  • Targeting IL-1beta (soluble so not likely to be beneficial to all patients)
  • NSAIDS (widely used but no controlled studies to analyse efficacy)
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41
Q

Describe the location of the larynx from palpable topographical landmarks.

A
  • Rostral to the first cartilage on trachea
  • Caudoventral to cricoid cartilage
  • Cranioventral to thyroid cartilage in the midline
  • Caudal to the caudal edge of the lower mandible in the midline of the throat
42
Q

Describe the cartilaginous structures of the larynx and their articulation in mammals.

A
  • 2 arytenoid cartilages
  • thyroid cartilage, cricoid cartilage
  • Cricoarytenoid and cricothyroid joints
  • Also have connection with trachea and hyoid bone through joints, collagenous and elastic ligaments and striated musculature
  • Ligaments of the arytenoid cartilages include rostral vestibular ligament and caudal vocal ligament
43
Q

Describe the cartilaginous structures of teh larynx and their articualtion in birds.

A
  • Cricoid and artyenoid
  • No vocal folds = no creation of sound
  • Glottis can be closed (prevent food entering larynx/trachea)
  • Syrinx used to sound production (tracheal bifurcation)
44
Q

Describe the interactions between larynx, epiglottis and pharynx

A
  • Larynx protected by epiglottis

- Pharynx area that contains larynx, epiglottis and larynx connects nasal part of pharynx and trachea

45
Q

Describe the function of the larynx and its effect on conduction of air to the lungs.

A
  • Connection of nasal part of pharynx and the trachea
  • Breathing
  • Protection of lower airways
  • Swallowing
  • Formation of voice - phonation
  • Allows swallowing to happen at the same time as breathing
46
Q

Describe the innervation of the larynx

A
  • 2 nerves each side
  • Cranial laryngeal and caudal laryngeal
  • Cranial laryngeal (from X) provides teh sensory innervation of laryngeal mucous membrane and motor innervatino of cricothyroideus
  • Caudal laryngeal (X) ascends neck after leaving vagus and innervates all laryngeal muscles except cricothryoideus.
47
Q

Define the relationship between the pharynx and larynx/oesophagus.

A
  • Pharynx is passage that leads to larynx and oesophagus

- Connects pharynx and oesophagus

48
Q

Describe the structure and function of the hyoid apparatus.

A
  • Hyoid apparatus made up of multiple bones
  • Articulate with temporal bone of skull
  • (from skull to larynx) tymapnohyoid, stylohyoid, epihyoid, ceratohyoid, basihyoid, thyrohyoid
  • Suspends larynx
49
Q

What is the function of the closed glottis?

A
  • Closure during swallowing prevents food entering lungs
  • Sudden opening permits coughing
  • Closure important during straining (defecation, parturition, micturition, lifting/pushing)
  • Important for eructation and rumination in ruminants
50
Q

Describe the laryngeal musculature and the actions they have.

A
  • All striated
  • Named same way as ligaments (connected structures)
  • Intrinsics between laryngeal cartilages - respiration + phonation
  • Extrinsics - connect larynx to hyoid bones, pharynx and sternum - swallowing
  • Widening of glottis controlled by intrinsic cricoarytenoideus dorsalis (abducting action)
  • Narrowing controlled by 4 intrinsics: cricothyroideus, arytenoidues transversus, cricoarytenoideus lateralis (adducting), thryoarytenoideus (ventricularis and vocalis)
51
Q

List the ways in which viruses can exploit host cell machinery

A
  • Entering cell
  • Optimising viral replication
  • Transcription
  • Protein synthesis
  • Acquiring lipid envelope
52
Q

Explain how viruses exploit host cell machinery to enter cells

A
  • Enveloped and non-enveloped have different mechanisms
  • Enveloped (retrovirus) fuse directly with host membrane by receptor mediated endocytosis
  • Followed by fusion with endosomal membrane
  • Non-enveloped enter by receptor mediated endocytosis (influenza virus) and pore formation after receptor binding (Piconaviridae)
  • Parts of host cell machinery exploited: host CSM, receptor mediated endocytosis, endosomal maturation steps
53
Q

Explain how viruses exploit host cell machinery to optimise viral replication

A
  • Use host cell ribosoomes to produce viral proteins
  • Host cell DNA polymerase for replication
  • Host cell RNA polymerase for transcription
54
Q

Explain how viruses exploit host cell machinery for transcription.

A
  • Redirect system to produce new virus particles
  • Manipulation for translation to keep host mRNA in nucleius and prevent translation initiative and manipulation for mechanisms of DNA replication
  • e.g. inducing S-phase of cell cycle
  • viruses able to nduce unregulated DNA replication are often oncogenic
55
Q

Give the mechanisms by which enveloped viruses enter host cells.

A
  • Direct fusion with host membrane

- Receptor mediated endocytosis followed by fusion with endosomal membrane

56
Q

Explain the process of direct fusion by which enveloped viruses enter host cells.

A
  • Envelope binds to receptor and coreceptors at neutral pH at plasma membrane
  • Conformational change in viral envelope protein takes place - expose normally buried fusion peptide
  • Releases capsid into cytosol
57
Q

Explain the process of receptor mediated endocytosis by which enveloped viruses enter host cells

A
  • Viral haemagglutinin binds to sialic acid containing surface receptors
  • Loop region and coiled-coil lead to fusion peptides moving near endosomal membrane
  • H+ enter influenza particles through an ion channel
  • Triggers uncoating of viral nucleic acid
58
Q

Give the mechanisms by which non-enveloped viruses can enter host cells.

A
  • Pore formation after receptor binding

- Receptor mediated endocytosis

59
Q

Explain the process of pore formation by which non-enveloped viruses can enter host cells.

A
  • Virus binds to receptor
  • Clatherin mediated endocytosis takes place
  • Conformational change of capsid protein takes place
  • Insert in endosomal membrane and form pore
  • Viral genome exported through pore into cytoplasm
60
Q

Explain the process of receptor mediated endocytosis by which non-enveloped viruses can enter host cells

A
  • Maturation of endosome leads to acidification and reduction of environment
  • Activated viral proteins involved in uncoating process
  • Lysis of endosomal membrane and release of remaining capdis part into cytosol takes place
  • Capsid docks onto nuclear pore complex
  • Viral DNA genome released directly into host nucleus
61
Q

List the ways iin which viruses exploit the host cell cytoskeleton and metabolic pathways

A
  • Alter membrane trafficking
  • Viral movement and spread
  • Viral intracellular movement
  • Axonal transport
  • Intracellular movement using microtubules
62
Q

Explain how viruses exploit the host cell cytoskeleton and metabolic pathways for viral movement and spread

A
  • Local spread - can spread from cell to cell if correct receptors are present
  • Dissemination in host
  • Movemetn into nervous tissue within other infected cells
  • Free movement in fluids (i.e. blood stream)
63
Q

Expalin how viruses exploit the host cell cytoskeleton and metabolic pathways for viral intracellular movement

A
  • Using actin
  • Cytoplasm of mammalian cells is extremely viscous
  • Diffusion of particules like capsids is inhibited
  • Vaccinia virus uses actin nucleation to form an actin comet tail and propel itself through cytoplasm
64
Q

Explain how viruses exploit host cell cytoskeleton and metabolic pathways for axonal transport

A
  • Anterograde and retrograde (kinesin and dynein)
  • Anterograde provides synapse region with proteins
  • retrograde recovers material for lysosomal degradation
65
Q

Explain how viruses exploit host cell cytoskeleton and metabolic pathways for intracellular movement using microtubules.

A
  • Herpes virus
  • Transport virus from cell membrane to nucleus using microtubule based transport by dynein
  • Transport of virus after replication and assembly to cell membrane using kinesin
66
Q

What are the 2 different types of viral evolution?

A
  • Antigenic drift

- Viral reassortment

67
Q

Explain antigenic drift in viral evolution

A
  • Leads to continous change in known viral strains
  • Mistakes occur in replication
  • Means that virus mutates quickly
  • An accumulation of these mutations may significantly change antigens of virus
  • Helps evade immune system (virulence factor)
68
Q

Explain viral reassortment in viral evolution

A
  • Emergence of a new subtype
  • Can occur within antigenic drift
  • Multiple copies form segmented genomes
  • Point mutation on one part of genome changes, making new virus
  • All segments are replicated, randomly assorted, produces new genome and a new virus
  • Leads to rapid changes
69
Q

Describe what happens if 2 different viral strains infect the same cell

A
  • Segmented viral genomes mix prior to packagin
  • Vaccine only protects against one strain
  • Through viral reassortmetn and antigenic drift, next strain will be infectious
  • No protection agains it until a new vaccine is developed
70
Q

Describe the basic features of viruses

A
  • Not cells - proteins plus nucleic acids
  • Can be enveloped or non-enveloped
  • Range in size 20-300nm
  • Nucleic acids surrounded by protein coat
  • Can only replicate by infection of cells
  • Some can only infect particular cell types (receptors) while others can infect many
  • Nucleic acid can be dsDNA, dsRNA, ssDNA or ssRNA
71
Q

Describe the basic features of prions

A

Single proteins

72
Q

What can be used to differentiate viral organisms?

A
  • Nature of genome
  • Capsid symmetry
  • Shape (viewed under EM)
  • Presence of an envelope and other factors
  • Can be classified using the Baltimore classification
73
Q

What are the different viral genomes possible?

A 
ssDNA (+/-)
ssRNA (+/ - retro)
dsRNA (+/-)
ssRNA (ss-)
ssRNA (ss+)
74
Q

What is the general pattern of replication of DNA viruses?

A
  • In nucleus
  • Must first produce mRNA
  • Use host cell enzymes (some encode own RNA polymerase and can replicate own cytoplasm)
  • DNA -> mRNA -> protein
75
Q

Describe the replication of RNA viruses

A
  • In cytoplasm
  • dsRNA: segmented genome transcription in cytoplasm with viral transcriptase (transcription of strand to mRNA (ss+))
  • ssRNA retrpvirus (ss+, enveloped) use self encoded encoded DNA polymerase (reverse transcriptase) to make DNA copy (cDNA) which integrates in host genomes
  • ssRNA (ss+) acts direclt mRNA
76
Q

Describe the replication of ssDNA and dsDNA

A
  • dsDNA -> mRNA -> protein

- ssDNA: synthesis of opposing strands to generate dsDNA -> mRNA -> protein

77
Q

List methods that can be used to identify viruses

A
  • Immunohistochemistry
  • Live virus culture/isolation
  • Virus plaque assay
  • Immune assay detection of virus or positive serology
  • Detection of genetic material
78
Q

Explain how immunohistochemistry can be used to identify viruses

A
  • Antibodies used to label virus
  • Direct primary antibody or indirect primary antibody detected with labelled antibody
  • Antibodies are either enzyme linked and change colour or are flourescent linked
79
Q

Explain how live virus culture or isolation can be used to identify viruses

A
  • Cell culture, fertile egg infection, experimental animals or organ culture
  • Indirect assays can be done or study of diagnositc specimens
  • Sometimes needs confirming by culture
  • Presumptive diagnosis used to decide what culture
80
Q

Explain how virus plaque assays can be used to identify viruses

A
  • Viruses tested on monolayer of susceptible cells
  • Plaque is hole where cells are killed by virus replication
  • Plate out serial dilutions of virus and study cytopathological effects
81
Q

Explain how a haemagglutination assay can be used to identify viruses

A
  • Detemine virus concentration from tissue culture isolate

- Viruses bind receptors of loose cells, link together

82
Q

Explain how immune assay detection or positive serology can be used to identify viruses

A
  • ELISA
  • Only shows previous exposure to virus
  • Cannot show when infection occured
  • False negatives and postives are possible
  • Patient antibodies can block test antibody binding and cross reaction can occur
  • Good knowledge of clinical symptoms, pathology and limitations of test needed
83
Q

Explain how detection of genetic material can be used to identify viruses

A
  • Common use of PCR
  • Amplify virus specific nucleic acids
  • DNA viruses PCR is direct
  • RNA viruses require conversion of RNA to cDNA
84
Q

Explain the role of head position in horses in respiratory defence

A
  • Horses head down most of the time

- Drainage to pharynx to be swallowed or nares to be sneezed out

85
Q

Explain the role of the nares and nasal cavity in respiratory defence

A
  • Size and position differ but hair distribution, density, dilation in exercising limit inhalation of particles
  • Narrow passages of nasal cavity leads to turbulence, particle deposition, swallowed or sneezed out
86
Q

Explain the role of the pharynx in respiratory defence

A
  • Common cavity for food and ingesta
  • Oral cavity ventral, oesophagus dorsal
  • Nasal cavity dorsal, larynx and trachea ventral
  • Means particles can be swallowed
  • Area is rich in draining lymphoid tissues (tonsils)
  • Particles moved towards pharynx to be swallowed and destroyed in stomach
87
Q

Explain the role of the glottis in respiratory defence

A
  • Reflex closure after swallowing

- Prevents larger particles entering lower RT

88
Q

Explain the role of cilia and mucus in respiratory defence

A
  • Form mucociliary escalator
  • Cilia in waves of motion
  • Found in nasal passagest to bronchioles excluding pharynx
  • Mucus consists of aqueous sol layer which covers cilia, mucus gel layer on tips of cilia, contains antibacterial lysozyme
  • Viscous produced by goblet cells
  • Serous by submucosal glands
89
Q

Explain the sneeze reflex

A
  • Particles land on receptors in nasal mucosa
  • Stimulate histamine release
  • Histamine acts on nerve cells (5th nerve of trigeminal ganglion) in mucosa
  • CNS stimulated
  • Large intake of air, rapid release of aerosol from URT leads to particles being expelled
90
Q

Explain the cough reflex

A
  • Stimulated by particles landing on mucus of larynx and trachea
  • High mucus production and irritant gases may also simulate tussis
  • Irritant receptors lie below and between epithelial cells of airways-
  • Vagus nerve communicates with CNS and reflex is initiated
  • Deep inspiration, epiglottis and vocal cords close, elevation of pressure in lungs
  • Sudden, repetitive contaction of abdominal and thoracic muscles
  • When epiglottis and vocal cords open, fast flow of air results
  • Bronchi and tracheal cartilage collapse, narrowing passageways
  • Foreign objects and mucus detach and are forced into mouth and swallowed
91
Q

Explain the role of non-specific antimicrobials in respiratory defence

A
  • Defensins
  • Short chains of amino acids produced by macrophages, neutrophils and epithelium
  • Electrically attracted to microbe, embed into membranes and form pore
  • Kill bacteria, fungi and enveloped viruses
  • Lysozymes in mucus break down cell walls
92
Q

Describe the fate of inhaled particles within the URT

A
  • Larger particles exluded using head position and hairs in nose
  • Smaller particles deposited on mucus and either drain out through the nose or are proprelled on mucociliary escalator to pharynx then swallowed
  • Tiny particles are breathed out
93
Q

Name the major lymph nodes of the neck

A
  • Superficial cervical

- Deep cervical

94
Q

Name the major lymph nodes of the thorax

A
  • Dorsal and ventral thoracic
  • Mediastinal
  • Bronchial
95
Q

Explain the role of lymph nodes in the head and neck in upper respiratory tract defence

A
  • Lymphatic vessels intimately associated with epithelial surfaces
  • Lymph nodes drain respiratory tract mucosa
  • Major lymphoid tissues involved are tonsils, nasopharyx, MALT and BALT
  • Inflammation due to foreign body means antigen presenting cells capture and process antigen
  • Drain to local lymph nodes
  • Immune response stimulated
96
Q

Name major lymph nodes of the head

A
  • Parotid
  • Submandibular
  • Retropharyngeal
97
Q

Describe the histological structure and function of the trachea

A
  • Variable length
  • C-shaped rings of cartilage visible
  • Trachealis msucles on inside of cartilage
  • Fibroelastic tissue, oesophagus may be visible dorsally
  • Laryngeal tissue
  • Ciliated pseudostratified epithelial cells, goblet cells, basal cells, smooth muscle cells, cartilage and bronchial glands
  • Muscle constricts trachea, cartilage holds trachea open,
  • Ciliated and goblet cells make up part of mucociliary escalator
98
Q

Describe the histological structure and function of bronchi

A
  • Lined by mucus membrane
  • Psuedostratified ciliated columnar cells with goblet cells (mucociliary)
  • Narrow layer of connective tissue under epithelium
  • Spiral bands of bronchial smooth muscle (contract when irritant present)
  • Outside bronchial muscle, irregular plates of bronchial cartilage (ensure some air can always flow)
  • Bronchial glands between smooth msucle and cartilage plates surrounded by vascular peribronchial sheath (connective tissue)
99
Q

Describe the histological structure and function of bronchiole

A
  • Cuboidal epithelium, no mucus secreting elements
  • ciliated cells present
  • No cartilage
  • Spiral bronchial muscle well developed
  • Many lymphoid nodules just beneath epithelium
  • Lack vascular sheaths
  • Collateral ventilation - no need for cartilage to hold open
  • No need for mucociliary
  • Few alveoli scattered irregularly along wall
  • At entrance to alveoli simple squamous
  • Bronchial smooth muscle bundles guard entrace to each alveolus
  • Prevent irritants entering
100
Q

Outline how alveolar structure relates to function

A
  • Alveolar duct has alveoli which open on all its sides and has no wall as such
  • Calibre of alveolar duct greater than that of respiratory bronchiole
  • Openings to alveoli guarded by rings of smooth msucle
  • Constrict when irritants detected
  • Prevents irritants or toxins reaching sensitive alveolar tissue
  • Sac is round area at end of dct
  • Cluster of sacs at each duct
  • Increases surface area
  • Outermost surfaces are alveolar epithelial cells
  • Pulmonary capillaries between epithelial sheets
  • Blood gas barrier is single basal lamina
  • Fibre skeleton made up of connective tissue cells and fibres from alveolar interstitium
  • Collagen fibrils and elastic fibres
  • Alveolar wall is blood gas barrier
  • Fluid layer, capillary bed, connective tissue, granular pneumocytes and interalveolar pores

VetMed Year 1 (13 decks)

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