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Week 16: Cough > cough > Flashcards

cough Flashcards

1
Q

the amount of gas dissolved in blood will depend on what 2 factors?

A

1) solubility of that gas in blood around alveolus - CONSTANT
2) pressure of that gas in the alveolar air - VARIABLE

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2
Q

what are the 2 reasons for why PO2 in alveoli (100mmHg) differs from atmospheric PO2 (160mmHg)

A

1) atmospheric P becomes saturated with water vapour (diluted by 47mmHg)
2) because of dead space, not all air is fresh with every breath

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3
Q

what is the partial pressure gradients of O2 and CO2 across pulmonary capillaries? - drive gas exchange

A

O2:
- 60mmHg (alveoli 100 > blood 40)
CO2:
- 6mmHg (blood 46 > alveoli 40)

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4
Q

how do we achieve changes in gas pressure from alveoli >pulmonary capillaries >systemic arterial blood

A

varying pulmonary ventilation by controlling the rate and depth of breathing

VE = TV x RF

(typically 500mL x 12/min = 6000mL/min at rest. can achieve 100mL/min during exercise)

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5
Q

what are the key elements of the respiratory control system?

A

sensors: receptors (chemoreceptors in aortic and carotid bodies and medulla - triggered by arterial CO2)
central controller: (pons and medulla in midbrain)
effectors: respiratory muscles

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6
Q

where is the major rhythm generator

A

medulla

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7
Q

how does the pre-Botzinger complex drive inspiration?

A

fires signals to the dorsal respiratory group (fundamental in initiating inhalation) that then fires in bursts, leading to contraction of respiratory muscles. when firing stops you get passive expiration

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8
Q

what happens in active expiration during hyperventilation?

A

increased firing of the dorsal neurones cause the excitation of ventral respiratory group which is normally inactive. Expiratory muscles (internal ICs and abdominal) produce forceful expiration

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9
Q

the basic rhythm set by the pre-Botzinger complex can be modified by what 2 opposing neurons in the pons?

A

1) pneumotaxic centre - controls the rate and pattern of breathing by terminating inspiration
2) apneustic centre - controls the intensity of breathing by prolonging inspiration. promotes inhalation by constant stimulation of DRG

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10
Q

what would happen without the pneumotaxic centre?

A

prolong inspiratory gasps with brief expiration = apneusis

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11
Q

describe how voluntary control of respiration (for speaking, singing, whistling) can be achieved

A

input to medullary control centre from cerebral cortex, bypassing resp.centres. signals sent directly to motor neurones in spinal cord that supply the resp. muscles.

will be overridden by rep.centres if hypo/hyper ventilate to extremes

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12
Q

what are the 4 reflex modifications of breathing (input into medullary control centres)?

A

1) Hering-Breuer reflex: pulmonary stretch receptors inhibit inspiration
2) irritant receptors: initiate reflex bronchial and laryngeal constriction, mucus production
3) Juxta-capillary receptors: respond to vol of fluid inducing changes in resp. rhythm
4) receptors in upper airways initiating cough and sneezes

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13
Q

what nerve stimulates the cough reflex? and what is the cough reflex?

A

vagus n.

  1. up to 2.5L air rapidly inspired
  2. epiglottis and vocal cords close, trapping air in lungs
  3. abs contract, push up against diaphragm. expiratory accessory muscles contract
  4. pressure in lungs increases
  5. epiglottis and vocal cords open suddenly, releasing air at 75-100 mph
  6. force is enough to collapse bronchi and trachea, air ejected through narrow slits
  7. irritant ejected
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14
Q

what chemical is the most important driver in regulating quiet ventilation?

A

PCO2

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15
Q

what is the most likely virus to cause rhinitis?

A

rhinovirus

or coronovirus

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16
Q

what percentage of tonsillitis is viral? and what is the most common bacterial cause?

A

50-80%

streptococcus group A (GABHS)

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17
Q

is pharyngitis (sore throat) usually a viral or bacterial infection?

A

viral. common respiratory viruses = adenovirus, coronavirus, enterovirus and rhinovirus

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18
Q

what is the viral and bacterial cause of otitis media (and mastoiditis)?

A

viral - RSV and rhinovirus

bacteria = streptococcus pneumoniae and haemophilus influenza

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19
Q

what URTI are you likely to get diarrhoea and vomiting ?

A

Otitis media

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20
Q

why would you get sinusitis secondary to viral URTI?

A

occurs as a secondary bacterial infection to common cold (which is usually viral). muscosal swelling prevents muco-ciliary clearance of initial infection. bacterial causes = S.pneumoniae, H.influenza, S,milleri

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21
Q

how does croup present and what is the viral aetiology?

A

stridor, seal like cough, sternal/intercostal recession (possible lethargy, agitation), preceded by fever and coryza. symptoms worse at night. peaks at 2/6months to 6years.

caused by parainfluenza virus

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22
Q

how does epiglottitis present and what is the viral aetiology?

A

rapid onset fever, sore throat, inability to control secretions, classic tripod positioning, difficulty breathing and irritability

caused by haemophilus influenza type b

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23
Q

compare croup and epiglottitis

A

croup vs epiglottitis:

  • onset over days vs hours
  • preceding coryza vs no coryza
  • severe barking cough vs silence
  • able to drink vs not able
  • no drooling vs uncontrollable
  • unwell looking vs toxic, very ill!!
  • fever <38.5 vs >38.5
  • harsh and rasping stridor vs soft and whispering
  • hoarse voice vs muffled
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24
Q

poststreptococcal glomerulonephritis is cause by prior infection with which bacteria?

A

specific nephritogenic strains of group A beta-haemolytic streptococcus (GABHS)

25
Q

what URTI is usually viral in origin (parainfluenza, RSV, adenovirus), in adults causes hoarseness and retrosternal pain and in children a dry cough and inspiratory stridor?

A

tracheitis

26
Q

bronchiolitis is the commonest serious respiratory infection in infancy (rare after 1year). what is the causative agent in 80% of cases? what is the clinical presentation?

A

respiratory syncytial virus (RSV) - highly infectious

coryzal symptoms precede dry cough and increasingly breathlessness (nasal flaring, grunting, use of accessory muscles, difficulty feeding, cyanosis)

27
Q

pneumonia pathogens vary according to age. what is the most likely causative agent in new-borns, infants and >5years?

A

new-borns: from mothers genital tract = group B streptococcus or enterococci

infants: most common is RSV. S.pneumoniae or H.influenza (immunisation against so reduction in incidence, same as epiglottitis)

> 5: mycoplasma pneumoniae, strep.pneumoniae and chlamydia pneumoniae

28
Q

what is an infrequent but serious cause of pneumonia in infants

A

staphyloccocus aureus

29
Q

what is the most common presenting symptoms of pneumonia?

A

fever and struggling to breath.

  • usually precedes URTI
  • cough
  • lethargy
  • poor feeding
  • generally unwell
30
Q

what presenting symptom of possible pneumonia would suggest a bacterial cause

A

localised chest, abdo or neck pain which is a feature of pleural irritation

31
Q

what chest signs would you see in children with pneumonia? compare this to bronchiolitis and asthma

A

pneumonia: reduced movements on affected side, rapid/shallow breaths, dull percussion, crackles and bronchial breathing on auscultation
bronchiolitis: laboured breathing, hyperinflated chest, chest recession. hyper resonant chest and fine crackles in all zones +/- wheeze
asthma: reduced but hyperinflated chest, use of accessory muscles, chest wall retraction, hyper resonant and wheeze

32
Q

in what cases should patients be followed up with a CXR 4-6weeks after pneumonia diagnosis and management

A

evidence of lobar collapse, atelectasis or empyema

33
Q

describe the new-born screening programme for cystic fibrosis (autosomal recessive disorder) and the criteria that must be met for diagnosis

A
  • allows early Rx intervention
  • based on heel-prick immuno-reactive trypsinogen (IRT) level
  • CF suspected if IRT is raised and one pathogenic mutation is found
  • CF is confirmed if IRT is raised and 2 pathogenic mutations are found (e.g G551D)
34
Q

what is the most common cystic fibrosis mutation? what type of mutation is it? and what is its effect?

A
  1. deltaF508
  2. deletion mutation
  3. defects in protein folding. mutant protein is ‘stuck’ in transport system and can’t get to surface of the cell
35
Q

why is R117H a ‘mild’ CF mutation?

A
  • it can be associated with CF, but a higher proportion are found during postnatal screening with no development of CF in childhood
  • therefore, child may develop CF or carry the mild mutation
  • may show some signs later in life e.g. infertility
  • effect of the mutation is dependent on intron 8 splice sites
36
Q

what makes R117H pathogenic?

A

presence of mutation alongside 5T (CFTR genotype) in intron 8 (normal is 7T)

37
Q

compare a normal airway with a CF-airway caused by delF508 or G551D mutation

A

normal: normal CFTR transmembrane protein works like a channel to allow Cl- ions to move in/out cells and maintain a thin, watery layer of mucous

F508del mutation: causes too few or no CFTR channels to reach cell surface. little or no passage of Cl- and thick, sticky mucous. most common GFTR mutation

G551D: creates CTTR channels that reach the cell surface but don’t work correctly. little or no passage of Cl- and thick, sticky mucous. most common gating defect

38
Q

what drug can be used to specifically target G511D mutations?

A

ivacaftor- bind to mutation to encourage dimerization to occur and opening of Cl- channel

39
Q

true or false? if you identify the 2 mutations of CF you can direct the clinical treatment?

A

False. not as simple as that because other factors (environmental and modifier genes) influence the severity

40
Q

what is the most prevalent type of lung cancer?

A

adenocarcinoma(nsclc) in cells lining the alveoli. common in people who have never smoked

41
Q

what is the most common lung cancer in smokers/ almost always caused by smoking?

A

small cell lung cancer in the cells near the bronchi, aggressive

42
Q

changes in what 2 gene types must occur for tumours to arise?

A
  1. oncogene activation (dominant mutation - gain of function). neoplastic driver, only need one copy of gene mutated
  2. tumour suppressor gene inactivation (recessive mutation - loss of function. need both copies of gene mutated)
43
Q

what oncotic behaviour happens in lung cancer that can be exploited in tailoring treatment for patients? name this treatment

A

changes in epidermal growth factor receptor. if mutation leads to too much EGFR, cell driven to pathways of cell proliferation, survival, migration, adhesion and differentiation.

  • there is a different prognosis based on whether tumour expresses EGFR or not
  • if it does can be given Gefitinib; binds to EGFR and inhibits tyrosine kinase activity, therefore, inhibits downstream pathways
44
Q

why do not all patients respond to Gefitinib?

A
  • don’t have mutations in specific area of EGFR protein which is targeted by drug
  • clonality: tumours evolving all the time so variety of mutations in one tumour
  • can develop compensatory mutations against drug = T790M
45
Q

what are the key features of acute and chronic inflammation in lung pathology?

A

acute:

  • causes = infection, aspiration, sepsis, trauma
  • loss of integrity of blood-air barrier
  • endothelial vasodilation (transepithelial neutrophil migration)
  • pro-inflammatory cytotoxic mediators
  • alveolar epithelial permeability compromised = oedema

chronic:

  • follows acute
  • long lasting inflammation
  • driver cells = lymphocytes and macrophages
  • tissue destruction and repair; new vessel formation, fibroblasts->fibrosis, scarring
46
Q

what is a granuloma and relate to TB and sarcoidosis?

A

clump of cells (macrophages + lymphocytes) act together to contain infection.

TB:

  • causes necrotizing granulomas
  • in pulmonary interstitum, compressing surrounding alveoli and destroying parenchyma

Sarcoidosis:
-non-necrosing

47
Q

list 3 mechanisms used by viruses to overcome the host immune system

A

1) antigenic variation -drift or shift
(antigenic drift = accumulation of mutations within the genes Results in a new strain of virus particles which cannot be inhibited as effectively by the antibodies that were originally targeted against previous strains. antigen shift = two or more different strains of a virus combine to form a new subtype having a mixture of the surface antigens of the original strains)

2) inhibition of humoral response
3) immunosuppression of host

48
Q

explain viral immunoevasins and give an example?

A

viral encoded proteins that prevent infected host cells from presenting viral peptides in MHC class I molecules to CD8+ T cells

e.g. the herpes simplex virus 1 protein ICP47 blocks peptide entry into ER. it does this by blocking peptide binding to TAP (transporter on ER that normal facilitated peptide entry to ER during antigen processing and presentation in MHC molecules)

49
Q

latent viruses persist in the host by not replicating - lay dormant. name some latent viruses.

A

Herpes simple - recurrent cold sores

Herpes zoster (varicellar zoster) - chicken pox/shingles

Human papilloma virus (HPV) - cervical cancer

HIV - AIDs

50
Q

what is the type of immune system response to extracellular bacterial pathogen evasion? how might extracellular bacteria evade this type of response?

A

type of response =
ILC type 3 immune response which is driven by neutrophils and TH17 cells
-drive forward opsonizing and complement fixing antibodies
- response activated by host cells recognising microbial associated molecular patterns (MAMPs) on bacteria surfaces

extracellular bacterial evasion strategy =

  • shield it MAPs
  • antigenic variation
  • inhibit opsonization (e.g. secrete compliment degrading factors)
51
Q

name the type of host immune response that fights intercellular bacteria. how might intracellular bacteria evade this response?

A

macrophage and TH1 response (type 1 immune response?):

  • bacterial infected macrophages present to TH1 cells which enhance macrophage activity and attract more TH1 cells, CD8+ cytotoxic T cells and monocytes
  • phagocytosed bacteria fuse with lysosome and degraded

intracellular bacterial evasion strategy:

  • find ways to live inside macrophage
  • resistance against lysosome enzymes e.g. waxy hydrophilic cell wall
52
Q

describe the main features and cellular organisation within TB granuloma - name type of cells and their location

A
  • Mycobacterium tuberculosis is phagocytosed by macrophages but prevents fusion of phagosome and lysosome and is therefore protective
  • followed by granuloma formation
  • chronic low level infection develops requiring TH1 to keep infection from spreading
  • a localised inflammation response develops and a granuloma forms

granuloma:

  • centre core of infected macrophages with fused multinucleated giant cells and surrounded by large macrophages called epithelioid cells
  • core can be necrotic in TB
  • core is surrounded by T cells (CD4+)
53
Q

red flags of acute cough

A

symptoms:
- haemoptysis
- breathlessness
- fever
- chest pain
- weight loss

signs:

  • tachypnoea
  • cyanosis
  • dull chest
  • bronchial breathing
  • crackles

think: pneumonia, lung cancer, LVF

Ix= CXR

54
Q

list some factors involved in emerging infections

A
  • microbial adaption and change - ability to invade and survive
  • ecological - seasonal changes, agricultural exposure, climate change
  • human demographics and behaviours - activities, sex, drugs, migration, poverty and inequalities
  • technology, industry and healthcare - blood transfusions, organ donations, food packaging and rapid dissemination worldwide
  • susceptibility to infection - e.g. malnutrition, hereditary factors
55
Q

what type of atypical pneumonia is associated with birds, poultry and animals?

A

chlamydia psittaci

56
Q

what type of atypical pneumonia is associated with bacteria often found in fresh water? i.e hot water tanks, cooling towers of air-conditioned units?

A

legionella

57
Q

what type of atypical pneumonia is associated with HIV?

A

pneumocystis jirovecii/carinii

58
Q

what is the treatment therapy for community-acquired pneumoccoccal pneumonea not requiring hospital admission? what is used in sever CAP?

A

oral amoxicillin or erythromycin

IV co-amoxiclav and clarythromycin

Week 16: Cough (1 decks)

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